The URL can be used to link to this page

Browse Search

Home My WebLink About20173887.tiffEXHIBIT INVENTORY CONTROL SHEET Case USR17-0043 - CACTUS HILL RANCH COMPANY, CIO SIMON CONTRACTORS, INC. Tyler Exhibit Page # Submitted By Description (Cont'd from 2017-3886) CE. 2 Kelly Huff Email of Opposition, dated 11/8/2017 CF. 3 Ray and Joan Glabach Email of Opposition, dated 11/8/2017 CG. 4 Caitlyn Moore Email of Opposition, dated 11/8/2017 CH. 5-18 Linda Tufts Public Comments and Petition of Opposition, 11/8/2017 Cl. 19-35 Laura Doyle Packet of Clean Air information, 11/8/2017 CJ. 36 Laura Doyle Doctor's Note re: Air Pollution, 11/8/2017 CK. 37-42 Laura Doyle Batch Plant maps (Front Range), 11/8/2017 CL. 43-55 Laura Doyle Endangered Species information, 11/8/2017 CM. 56-195 Laura Doyle Large Packet w photos. 11/8/2017 CN. 196-197 Laura Stretch Public Comments. 11/8/2017 2017-3887 Tisa Juanicorena From: Sent: To: Cc: Subject: Please add to the case file. Thank you Kim Ogle Wednesday, November 08, 2017 5:37 AM Tisa Juanicorena; Esther Gesick Johnson, Anne FW: Regarding the Proposed Asphalt and Cement Plant (Simon Concrete) From: Kelly Huff [mailto:huff.kelly@gmail.com] Sent: Tuesday, November 7, 2017 10:09 PM To: Esther Gesick <egesick@weldgov.com>; Kim Ogle <kogle@weldgov.com> Subject: Regarding the Proposed Asphalt and Cement Plant (Simon Concrete) To Whom It May Concern, I am writing to voice my strong opposition to the permanent asphalt and cement plant located at HWY 257 an WCR 80.5. Allowing such a plant so close to residential and city limits will negatively impact our community. This plant will bring with it dust and air pollution, contamination of groundwater and agricultural irrigation canals, as well as noise. traffic. and light pollution. According to the EPA. "The cement sector is the third largest industrial source of pollution, emitting more than 500,000 tons per year of sulfur dioxide, nitrogen oxide. and carbon monoxide " If the current proposed location is allowed, prevailing winds will blow these pollutants directly towards the center of Severance and Windsor. This type of dust and air pollution will significantly contribute to respiratory and health problems of Severance and Windsor residents. In addition to the air pollution, I am highly concerned about the contamination of groundwater and agricultural irrigation canals. At the informational meeting on October 30th, we were informed that the waste water would be held and treated in unlined retention ponds only 25 feet from the current irrigation canal. Once this waste water is treated. it will then be released into the irrigation canal. This irrigation canal flows east for livestock and crop irrigation. I am appalled that we would allow our water. crops and livestock to be subject to such pollutants. We were also told at the informational meeting that the plant will operate 24/7 if contracts demand. This will cause noise and light pollution that will negatively effect residents that live nearby. In addition. the 250 round trips made by large truck equates to a truck coming or going every 86 seconds. These constant "ins and outs" from a dirt road are dangerous to other drivers on HWY 257 We live in one of the fastest growing areas in the US. This plant, and the negative aspects it brings with it. will most definitely stunt the rapid growth the communities of Severance and Windsor are experiencing. People will choose to live. shop. and visit away from this plant. I urge you to act in the best interests of Weld County residents and immediately stop the operation of the asphalt and cement plant located at HWY 257 and WCR 80 5. Thank you. Kelly Huff Tisa Juanicorena From: Sent: To: Subject: Esther Gesick Wednesday, November 08, 2017 5:15 AM Tisa Juanicorena; Kim Ogle FW: USR 17-0043. Nov. 6. Simon Concrete Original Message From: Joan Glabach [mailto:glabjoan@yahoo.com] Sent: Tuesday, November 7, 2017 8:53 PM To: Esther Gesick <egesick@weldgov.com> Subject: USR 17-0043. Nov. 6. Simon Concrete We attended the above meeting. We hoped to be heard and listened to. Most of us had sent emails and made phone calls regarding this matter. We know of many people who could not attend due to jobs, illness, or other commitments.. So they took their valuable time and wrote emails or letters. My husband and I personally delivered our letter along with three photos of the area on Thursday, Nov. 2. The clerks were very helpful and assured us all letters and emails would go into packets for the Commissioners and Planners. But on Nov. 6 there was very little evidence that any of this material had been presented to the Commissioners. The Weld Co. Planner gave a lengthy summary of the submittal by Simon Concrete. No letters or emails were mentioned. Then we had to endure close to two hours of presentation by Simon Concrete. With 50 people waiting in the audience, who were obviously there to protest the Plant, the Commissioners had the arrogance to take a two hour lunch. Most of us left and returned. Some gave up or had other commitments. When we began again Simon Concrete still had the floor. About 2:30 it was finally our turn. Each speaker was allowed 3 minutes. We were adjourned at 3:30 due to a Commissioner needing to leave. Quite a workday! This meeting was very one sided toward putting a cement plant in the midst of our pastoral, rural neighborhood. Speakers were told not to get emotional. How do you do that when the place you have lived in for many years changes in a negative way? Some people in attendance have ranched or farmed there for generations. Please take the time to read our letters and emails. Ray andJoan Glabach 37076 Soaring Eagle Circle Sent from my iPad 1 Tisa Juanicorena From: Sent: To: Subject: Esther Gesick Wednesday, November 08, 2017 5:13 AM Tisa Juanicorena; Kim Ogle FW: Cement Plant Severance From: caitlyn christie [mailto:caitil0@sbcglobal.net] Sent: Tuesday, November 7, 2017 8:31 PM To: Esther Gesick <egesick@weldgov.com> Subject: Cement Plant Severance Dear Esther, I would like to voice my disapproval of the Cement Plant on Highway 257. I am very concerned about the ditch running near the property and the air pollution from the plant. The increase in truck traffic will also be a huge determinant to those living in the area. This decision is not in the best interest of Severance and Weld County residents. I strongly urge the board to reconsider. Thank you, Caitlyn Moore 1 (56(zn 5cj Cic. I� W hy did Simon Contractors choose this site? W hen choosing a site for the temporary facility where you have to use generators, propane bottles and haul water in, why would infrastructure for electrical, water and gas be a factor? W hy has there been almost no complaints raised to the temporary site? What production level have they operated at in the past few months? Why haven't they started preparing recyclables, and grinding concrete into useable materials? Why has production been minimal since the hearing on October 25th? My point is this was never intended to be a temporary batch plant. The intention was to get operational "as temporary" and stay under the radar of the community, thereby minimizing local complaints. The extent of the full level operations of this plant are yet to be revealed to the public, waiting until after the permanent status has been approved. At this point, when full operation begins, it is too late for us to voice our concerns. I have heard the question raised by the Commissioners several times, "Did you complain or have concerns with the temporary site?" I live 3/4 of a mile from the site and I did not file a formal complaint. I called the landowner when they started preparing the ground. I was informed that the plant was going in to help with a road construction project on hwy 85 and it was only a temporary site. Since I was assured it was only temporary, why file a complaint. I tried to be "a good neighbor", accept their presence along with the inconveniences that resulted from traffic, noise, dust, and safety because it would not be here permanently. I learned on Oct 21 from one of my neighbors , the same way the majority of the neighbors found out, that the temporary status may be changing to permanent and a hearing was coming up in less than a week to make a determination on the permanent application request. Again, I called the landowner to verify if what I was being told was correct. The answer I received was that they had already signed a 10 year least with Simon Contractors? My question is how is this possible when the property is zoned agricultural and the current permit is only for temporary use? All of the questions I have raised seem to be able to be answered by the same response - The intention has always been to establish a permanent site, and try to do it without any resistance from the community by staying under the radar and misleading the public as to the nature of their intentions. Our community has been good neighbors to the property owner and Simon Contractors, but we feel that we have deceived in this process. I asked that you would protect our neighborhood from becoming industrialized by denying this application and assisting Simon Contractors in finding a more suitable location. Linda Tufts 39124 County Rd 19 It is so difficult to express all of the thoughts, emotions, and concerns swirling through my heart and mind about the issue of the asphalt plant becoming a permanent fixture in my neighborhood, and trying to express it all in 3 minutes. I ask you to think about your own experiences and see if you can remember a time when you had to deal with a situation that would impact your quality of life yet you had little control over resolving that situation. Did you have a pit in your stomach? Have difficulty sleeping at night thinking about how your circumstances might change as a result? That is what many of us are experiencing in this situation. We moved to a rural property to have a rural lifestyle. Many of us were raised on farms and ranches and want to pass that lifestyle on to our children. What we did not move to the country to experience was having industrial companies in our backyard. If this permit application is approved, will it open the door to further industrial applications moving into our area? In the months the asphalt plant has been in operation, my family has had a few concerning encounters with the trucks coming in and out of the plant, which have expressed to the management of Simon Contracting at the open house. These issues involve the trucks cutting off drivers approaching the intersection as the exit the plant, trucks turning the corner short when exiting hwy 257 which would result in a collision if the car would not move to yield to the truck, and trucks parking at the intersection blocking oncoming traffic from entering Hwy 257. This is my third time in this room listening to discussion on this application. On October 25th, I heard the commissioners question an applicant about parking 3 additional delivery trucks on his property, and whether or not these trucks turning into his property have an adequate turning radius. . Yet I have not heard these questions or concerns raised to this applicant. There will be substantially more than 3 trucks going in and out of this property each day. On Monday, November 6th I heard you, as commissioners remark to an applicant that being a good neighbor means doing more than meeting the minimum requirements but going above and beyond. If you do approve this application, which we are all praying you do not, I hope ask that you do require this applicant to go above and beyond the minimum requirements. That you would require landscaping standards similar to what you have required with previous applicants such as DCP, that you would find enforceable ways to ensure dust requirements are met, that noise limits be set at residential levels of 55 for daytime and 50 at night from the property line to protect any current and future residential property neighbors. Another concern that has not been addressed is the impact on the residential water use. I fully empathize with the concerns for the agricultural water use. also have concerns about the plant's impact on my household water. They are requesting a 2" water tap from North Weld County Water and will use up to 25,000 gallons of water per day. Many of us already have water pressure issues. Our water pressure is so low that we can't take a shower and water our lawns, or run our dishwasher and do laundry at the same time. What impact will adding this water tap to our current water line have on those of us that are further down the line? The questions just keep flooding my mind. I implore each of you to think about us, your constituents when making this decision. Do what is best for the people you represent not necessarily what is best for a company's bottom line. We, the undersigned, oppose the approval of a special use permit for the purpose of housing a permanent ashphalt and concrete batch plant at the corner of Hwy 257 and CR 80.5. First & Last Name (printed) Signature Address Email 1 ►�16 AvrYie <*/1 >S eci) 7 ',Jr, 7 P fio 70-, `'' 2 -1I E DLMEXZ- n-1(1- 3g -)bur R\O rt (l R 14-SoUL is @M JJ CO 3 'U 54 I n WHOUri 371r O sC o f ie c e c// 4:14eiroeivsfin �lQ /�1 G? t J 4 14/O tios,‘,7 A O6se / . - a — 4 ((7( 91,1% ig - r p; i*kk4 6fi. 5 3 S► c a 5 ar-ma . Z951 1 r 1 �a 1 ii i,5 54 r rya n: l.� 0- 1 ,► -� 6 $j' I%c4ep1'..., L3rMy1L n Iron �h wLlei it/die/7 ie/7 en(94o me o 7 AO e1)/ P /flo#Ir ->'Y74Lnk '7690 �jrnn ell 8 --\ \iir \ l � � ♦ " \ ' -� LA\ 5 �s� freed'av ✓ ��W m5O, car/ 9J≤t Ne6,d J �_ �� ' fly/C Bair zr ? A47;00s WAM/.� 10 hea4 6 kr:5A e&til ofirnte -(___c arC7 CZ O harte15-tset/6 li lieent i �j9' (..75g- & c.,e / 9 r2�.Kea //V th n SN Ce N Thr, 2%� 11 i , / 12 8eik-e-17, iiv 398 av L' j°1 jJ13 L L rn: % c,' a'0 1. C�.n, 1-2' g.� 1.7121/A 370'' 17 ..1 l� _enell U11,13 ,13 49 it ciP kvCCcz4 . 14 O c �e len Af l a_(409v--?a/ 8' 15 �l ( > i,+'ycd,---- -- 6_3 7 6 c r 72 6 i,ii is errL --) I of rid/ n r qr.' / ��-�`,"- ettfkitjet �'( L____Las\--- Cet i i� ^/\/y///o svah�//sewmP _ - �<c- - - / �cc 17 .J /-it%I ��'f t G(� c'�, i �r 6 44- i r✓ l� ( /c� 1� 7 el,[ job / IP1ti7 01,( ` C (ii Nc 1-G" L6)-(1'' 18 `) f ; ,ti i J/)/) , ' )Zr 7 / Z •._ - / 1 ile)11-_ `' /. `l ! i.19 '/ � I, ' ' hit li- /lilt 1 afn �� rN 9.3—C (� C(Lc�1 �,�y�j61., fsci(iLte[L'h2�4-00._jCie- 20 -c Y cc clef' iti,v 1 / _-- 7/ .� / / .-, I ..- ° trio., c'g»,71 -c 7 0/11 ti We, the undersigned, oppose the approval of a special use permit for the purpose of housing a permanent ashphalt and concrete batch plant at the corner of Hwy 257 and CR 80.5. • First & Last Name (printe Signature Address Email 1 /.e. A LocA2G-6 ?ea Cie Fic rawer h L.dr henariilfi cm G— cti 2 gRA CCIfiro Sic rr 1;',4--17 3 7/3-7 1) IC /cg .-sJ,� kil ( y t'/- c j c - `l ✓ d de ✓ S 769.1 3 '�tze -hit r e -1"4-► a� Li -c3 -17D SIC u,u..„ 1 -. Ms *k Siet*.eeklyvk . cc, t,titi r 4 Let( r1�- 'aevrvt-- f sflce Cc / C7 At/To-GeV uo(• cem -e-C(ca.,?i7Ortir, 5 V a 0 6 (O144, 4, c...-1-1 7.-a-11,'Lli !ell elleAt<L) i 7 07 b Soft r' Fttc (e C , Q i c% k b' CC 1 a IZ0 e. crop, 6 C4+4\ 'er"t ✓LC_ t1/, 5 l Ja'M Lt. -►ti 1/2'-)1t7( Lcilia_ 1 r+,_ aI,ti /1Zs a) ;Gist C7 ri - Li/ii O 4is'/ 7 II( \ t \ J 51 .,.� �1, _ Y &vCOrt {-T 4- //," ; 77(0; �(-�V/'"S 1, k jPA eil.�t. 3`�� [% te5"91 . Coe 8 �?-s'' 6e1j5c,i ex746am Sa,, x/66 6:70x4;1., 876 Cno 4q ' ✓ 9 iRs"-7 77-K P t« 4v aka G' /�tfr. Y&( rht . 10 161-y friter� ,� 8IciC St�.� • y � � Cr ' liar- Auk' ,-oinc .6444 n I, ' / Qa/ �, �/ <� '' my �'AKIWI) l j / ! � �iJZ C�� /7r 12 • iy y<≥' e5/< Ma / 49‘, � e.. 13 �14't� k-rk-CAT)t; r `-\,J /1 ZRS5 tkk IL €50.3 jai/ :11 ��b5Y-k0Ci 14 -1----it-#114- 4-intektvt nu_ ox______, , ea---- 15 1 ./ A - % 4 rid Clic-. L;in "Ar'a )i-ed. PA vi .c�� 16 v v C'.1Pt FCC) 4 a3 Al £ w 5 4s —es g .C�Y-i'�G ! c- %je 393 U 41" KV` /9 eee / / t.. 17 t " 1' l c he l l e iI Y1 9 /Lz.l = c it 2319 O { !I (F '2 c 7 , G t'C'c'k , Legurp_i, eh\ lic t �� l • cht4 a t ( . tts✓1 18 Paix\ Vi V\ `, Wile t il,,,ek IS7,GReel r Il.L`ail kikc( (atI \AcA0.feel 19 il-4--)ii (/ An , 1 \A/CA /14.4 l -`I it (> 17. I) frill ii (,e wL'3j(-. 20 o. `e- w,-‘ r G4.(cL& L‘.( - • .G`* 77G9)-1 W,/ S- - � �� //-� We, the undersigned, oppose the approval of a special use permit for the purpose of housing a permanent ashphalt and concrete batch plant at the corner of Hwy 257 and CR 80.5. Firs Last Name printed) Sig atur Address Email 1 i �� dtif ( 140g 7741-1A gb� �3 2 — 3 9°SC �ctiCc-it 04--hoe...2. fret C )" SztaA L i 4 < < 1ZS-- 3 /'zii( &Lae/ .J 4 c( sji Ad7Vo076' /94 IM/ 2 �44Vto 5 iZ1k ITS n 7(3)3 5 YAatc C kfrke1A 1 L-4 C-`ALOCnnl.ZC ` 6 C 1 }4 ,j t ce ;rte`-''' l 7 1 Vc hodiscizziresiz,bea4tri Pc 7 \ '\c_V\G i I ics -r: 1 e3 V/51c WCF 1 8 PhA SoSr:E.04‘ Kr (7. ioSO 3 ze9 cr.,e, A 52. 9 *ICU_ aptile i Cr e-c-Lspc-co Tocit orzgii, t•cu( 5 10 )(II- i 1 n fJ / ,, ti; 2 ,,c- Meic, . 3 $ ? tS T t /9 c -A e. /c i IF - 11 gat.) I v ` & O 01264414- ?105' in cli LI z D4,,,v o lkii r7 r/40, 601ne 12 7A`1a- Pl et I,J 10 / 0;�7 (A na,Svr gtb(ue5 (� M)14tS ✓). 6.14t, vi ≤T'0. rinr13 a *fp CwM 7 Co fact , e s I MS y% .ca.“ in . 14 fr v4. cmirite2.Ar) Ina `n�.v77 /4A!! I$ eta e� $140 y1" G 1,061 /i. C �-� 15 thH %Ac,tt<� I 7241 3ng6 EXI, 64 6014 Ycsz`f /y(/-11c:ti •Ati ci t_e 16 CO ,((I'I u ti -y�,jorv.� x] J (0-7 'P�AZ-o i=.�Gc-t Ci �U (cl,(-2L--) Trcc 5v !`4fi1 i Nr., pl� f 17 L--)a-'r C ( C f `' C1,MA4A-A,M (el I ct rb Cri iY arlc Ct,3 ? Ifu 'r, (0.1/ 18 gA4Alic.c. t*,}see fr,2 efirAteakRow /A/ b� t S&L€ 4-761-040ikko, A � _ __ 19 pepa CarfSeao 4 dan cart solks-ciszlet, / I 11+9 CP-1-7Cc. 0440<ser-05So 20 ' - : 11 Al w , c4 0,4a. ets -b.tii . Q - ti r We, the undersigned, oppose the approval of a special use permit for the purpose of housing a permanent ashphalt and concrete batch plant at the corner of Hwy 257 and CR 80.5. First & Last Name (printed) Signature Address Email 1 • > 1&tky F N 3-7 67 Diet L -L GKO---riN yS)k rr-&-P‘el 2 Pa/lIti`d3 (P099 dno IDA 10 P -g -Q ) r:7-0, Cie, ilst--k-vui - ik lief,J- 3 --�Al L Sn G -:e, ri e-!�( g -!`a -e 779-e9, 4 Like__ cl 6 S z (Jc uke l,,, r, e - .Ca ,6 -i\ G/4/1;11-111Al-7 1'e/41'757 -1//t_ % `7�/ r je;_edcf re) irph ri 50;7 57) 0) ro a re:A lectie c., AW/g7,1ZA/ r\&! , -37( et sogib-itsLuSCg Ci rG( f' a diiectiQkcsoAiQOf cc,-, 7 4rvt5 jOk4cov\ 8 9 10 11 12 13 14 15 16 17 18 19 20 We, the undersigned, oppose the approval of a special use permit for the purpose of housing a permanent ashphalt and concrete batch plant at the corner of Hwy 257 and CR 80.5. First & Last Name (printed) Signature Address Email 1 „a-42 37C--.3="? & /g () " hrt- <. ,a.1t..--, acx) je113nrJccflA r a.t C. -5002AA1 2 F--' ��b �R 0.SL-/--F — 3 3 ._ .5:> A t; r F -i4 cpc. C�? . t 6.�6. 3J cccK 5t I `� 5 t ealare ,t4a �...r--� . 3 Rot-'- / cv 2-Zv. i Ala ✓ S70a'? fic-d-r /.teat/c (33✓ %„t -'k fr is, I , tsa4- 4 Dcl idc �� 3) CA/2_So i h13 tic l€ C ---:-t EMYc . K") `e6ri'i ,1 ,Cvt-1 , ; n 6 Meac3rcn LA, i 2 y Cr I °j rnectonettefiskici. hcO. COON 7 Cc:NJ..sz L CQ h i Sc� L) i : 3 ?r!/ co( 7O c ssh RI fr I. f R) t'`,' ,45cy 411)>571ip 8 ej1� Ccn\\o c7o n SocellioirC(147c-f- LJF+0 9 Ted a (Y6 I I o (YL.AA,V(IX-- i 10 ')J k \ �) A aLQL,ck_Co 37x).5 cccn4--i ' fe C r r T1)fkJc1SnCc 11 ��'� A1,13t_,\,a.,21,4_t___� - p L�� ,� R �3 s f 12 L vL / 4" / .567 -To I &O . 14 Re (JoW&cLAWAlaheALASI ''6'1LL �� i , 13 (kEd � ✓l 1(„44.. ^ J Gvc o C��L , 7,, ,,2 4 ( i l✓i.k> `_° h t°�l �7e1-.4-0. t!"9"--- 14 �4,' 4„ Jftli ��. ` , i i,/?i 1.'' �G,%/.� � y/ ;A 6V/11i l� ii 15 1 L 9 SO 6 Cite 0 • (d /(7 hi t u r7 �Y°�`> 6 404 • LIB Jen L7 rtT i /iL /�rl 16 g4 -}J ni I ►'�4 h�� `% �I M, (A, vi !~ • Coil -0S Y1n + k' wt. C C c .i�..: I , carw ! li�,c� 17 S F.�.)r � S f� t- 9043.0 Cr g o -� c J) r , 5 I o-nc_.S fool -23 % ��r 18 -y7knitt, - r �Q C eg tO F11eico ' C 4�ti ia049C Yti1ca 19 ` 0 &fl W L ,( g �I r4_ , io A ' d ,� de .� c 4- Oita' /. l v V� l_�,�� p� y 20 li7cr %�' %` ✓ % �� -=` m We, the undersigned, oppose the approval of a special use permit for the purpose of housing aO > � ashphalt and concrete batch plant at the corner of Hwy 257 and CR 80.5. First & Last Name Address Email 1 e. Dontef 18322_ ciQ 19, f fl OA vi S ratctoner cJ J ltitlt ( 1 Caw 2 Arc bon/6R. 303z:z. Gc i` dzi„v S mam Ft►e-r ,'ne�-(4c.6)N,-( i 3 4 5 6 7 8 9 10 11 12 13 14 15 16 17 18 19 20 21 22 23 24 25 We, the undersigned, oppose the approval of a special use permit for the purpose of housing a permanent ashphalt and concrete batch plant at the corner of Hwy 257 and CR 80.5. First & Last Name (printed) Signature Address Email 1 n (NJ' C-'4ro e. o kx- n e9 tD cpstssb 2 (oey, _ ( ck)n kNN ci��VttA) L LTe trAe,, cc!, _ , _ , / 5 D, C: R 7' C'1.) 5 S-Ci 3 4 5 6 7 8 9 10 11 12 13 14 15 16 17 18 19 20 We, the undersigned, oppose the approval of a special use permit for the purpose of housing a permanent ashphalt and concrete batch plant at the corner of Hwy 257 and CR 80.5. First & Last Name (printed) .Signature Address Email 1 D u>n Ma Do\t3tLI8`�OS X05 Z4 �I tJ Y1 wed 11 QLoc C2g)o�� 1 Z 2 ,' /11A175 bfthq go`‘ Gimp I L i 3 _, C_L_Th �v �- -'S mac- l Le �,.� Sr ® act �� 4 it/3767yc- cy r --k-urclk kz c1 -v d jrn c,U tory , fiS4.- /.3 T s v.c 5 L, nd1/4 (-). 3l4 , 2 v -k.-n"s enionaii , C;brr1 oc I.9 6_ 6 7 8 9 10 11 12 13 14 15 16 17 18 19 20 Westford Clean Air: Asphalt Plants and Property Values How Much Money Will Westfor... Page 1 of 2 G. More Next Bloc, Westford Clean Air THURSDAY. MAY 7. 2015 Asphalt Plants and Property Values How Much Money Will Westford Lose? (Presented at the Town of Westford's Zoning Board of Appeals.)in Executive Summary Westford Residents stand to lose 75.6 Million Dollars in Property Values. Although we cannot definitively know how an asphalt plant will affect Westford, we can make an educated prediction. We can use the values lost from an actual asphalt plant, and calculate a projected affect on Westford. Based on actual loss. Westford residents are likely to lose a combined 75.6 million dollars in homeowner property value, which would be the equivalent of 1 2 million dollars in tax revenue annually for the town. Create B Documents: • • Research from Pineola. NC, where property values before the introduction of an asphalt plant were an average of 27% higher than values post -asphalt plant. • • Excel Spreadsheet of tax assessment home :aiues on streets :n Westford that are within a one -mile radius of the asphalt plant. (Available upon request.) Documented Decrease in Home Value The Blue Ridge Environmental Defense League documented a 27% decrease in property values near an asphalt plant in Pineola, NC. Based on tax -assessor's documents from between 1995 (before the increase in asphalt production) and 1996 (after the increase), these properties lost 27% value Ore property lost 56% of its value due to the plant. 13L[.IE RIDGE: ENVIRONMENTAL DEFENSE I:PAGI-r': Cir1..4 1.ra.L. ^�1<..�s in. -. ti"- ..,,t .a .,,; n.,,r'F!b'.rl- hi:.'6 V.:-ba •1:'.it' •n Properties ilex Around Pineola tsphalt Plant From Avrbry roomy Tn Department DATA .Tannary 26. ?anI All pa -trek 'oIIt .y 0. 1,. ,.. in. 1• .•.r•• t I •.. .. I T:- .,_ J r:ac• .. A.1..:. r• r - F 7.7 •• -g•-• -tint : •.:•I,•' ci f Actual Losses from Asohalt Pram Homes Affected The proposed asphalt plant is on 540 Groton Road Westford MA. We l'mited the projected loss to only those homes on streets within a mile radius of the proposed plant. We used Westford's tax assessments for the year 2015 The total value of houses to be affected is $280.052,454. Russells Way, Sweet Wood, Betty Lane Forrest Rd. Chandler Rd. Caldwell Drive. Morrison Lane. Ledge Road, Christy Lane, Quarry Hill Road. Danley Drive. Tyler Road, Vineyard Road, Curren Drive, Perham Circle. Rolling Meadow Lane, Links Road. Doris Road, Blacksmith Drive, Fernwood Drive. Emerson Road, Byrne Avenue Gassett Road, Lake Shore Drive North. Pine Tree Trail, Pollyanna Lane Lawson Road. Moore Avenue. Briarwood Drive, and Oak Hill Road numbers 46-124. Conclusion LABELS Property Values (2) Traffic (1) BLOG ARCHIVE P. 2016 (1) ♦ 2015 (4) ♦ May (4) Asphalt Plants and Pro Values How Much N Asphalt Traffic: Effect c Property Values The Proposed Asphalt is less than a mile a. 5 Reasons Why Westfc Needs an Asphalt PI http://www.westfordcleanair.or<g'2015/05/asphalt-plants-and-property-values-how.html 11/7/2017 Westford Clean Air: Asphalt Plants and Property Values How Much Money Will Westfor... Page 2 of 2 Westford's property values on roads within a mile of the proposed asphalt plant total $280,052,454 If those homes lose 27% of their value, these Westford homeowners will lose $75,614,162.58 in property value, which would be the equivalent of 1.2 million dollars in tax revenue annually for the town 75.6 million dollars poses a significant detrimental increase for those homeowners in particular. and losing 1 2 million dollars in tax leverue annually also poses a significant detrimental increase to the town in general. Addendum 27% may be an underestimate These calculations only take into account the -somas near the asphalt pant. Many more homes will be affected. For example since I live 1.2 miles from the plant, my house does no: fail witnin the one -mile radius, and altnough I did not include my home in the calculations here. I do intend to move if the plant comes to town. which means there will be additional losses that are not in these calculations. So. Keep in mind that the scope o' the problem is much larger than these numbers suggest. Pineola's 27% home value loss occurred from an increase in the amount of asphalt produced at an existing plant. Pineola already had an asphalt plant. In 1995 Pineola's plant produced 150 tons/hour. The property values decreased by 27% after the plant increased production to 325 tons/hour. Since Ne,A port Material s proposed aspnatt plant will be able to produce 400 tons/hour, which is significantly more than Pineola's. a 2- 'go •oss could easily oe an unoerestimate 111 Presented at tree To -fir of Y,est'ac•d s Inning Board of Appeal - :.r: _Z;, '!a, ._t rdtp.OVA" westforarragcvrpagtst;overnrnentAowndepartmenisJt a'as .-t1eesV.estayotvl _zca -_r. Posted by Wenoy Welsh . 5.52 AM Labels. Property Values No comments Post a Comment Ente: Comment as Seieel profile.. vj Publish Pre' ,ew Newer Post Subscribe to: Post Comments 'Atom) 444 Home Older Post ;rte;) I,.. •,an by Kingg€' http://vvww.westfordcleanair.org/20 1 5/05/asphalt-plants-and-property-values-how.html 1 1/7/2017 Westford Clean Air: Asphalt Traffic: Effect on Property Values Page 1 of 2 3- More Next Blogf> Westford Clean Air THURSDAY. MAY 7 2015 Create B Asphalt Traffic: Effect on Property Values (Presented at the Town of Westford's Zoning Board of Appeals )[1] Executive Summary Westford residents will lose property value if the asphalt plant is allowed into Westford. Included here, is a tax assessor's document, that clearly shows a 15% decrease in taxable valt. a to a home near an asphalt plant in Portsmouth NH due to traffic. Documents: • Below is part of a document obtained from the assessor's office of the city of Portsmouth, NH. (The full document is on the next page.) This assessors cocument shows the negative effect of traffic on property value. In this case. the assessed value decreased by 15% as a result of excessive traffic. Traffic Increase There is no argument that traffic will increase due to the proposed asphalt plant Newport Materials has a current limit of 150 truck trips a day with their current product. If the asphalt plant is approved, Newport will have an additional 250 truck trips a day with a high percentage of those trucks carrying 20-24 tons of asphalt each That would lead to 400 truck trips per day. This Property is Near a Similar Asphalt Plant This particular property location is very significant This property is close to the plant that Newport Materials has claimed is a good example of the type of asphalt plant that it would build in Westford This property is one half mile from the Pike Industries' asphalt plant at 650 Peverly Hill Rd, Portsmouth, NH Many other properties near Pike Industries' plant have losses due to excessive traffic. You can find more documented property value losses at the City of Portsmouth: http://cityofportsmouth com/assessors/manualfVor3-4AAolume3ValidRes;salescombosmall/smvalidresia►es101-200.pdf Conclusion If Newport Materials is allowed to build an asphalt plant in Westford, Westford residents near the plant should expect at least a 15% decrease in the value of their homes FILL) REM) B 1TH SECTION" ;d: \ea:cv..; 20 huh -15% Traffic 9;4 _u09 tl 11 13 2000 CU Conu 0.000 LABELS Property Values (2) Traffic (1) BLOG ARCHIVE ► 2016 (1) ♦ 2015 (4) V May (4) Asphalt Plants and Pro Values How Much N Asphalt Traffic: Effect c Property Values The Proposed Asphalt is less than a mile a. 5 Reasons Why Westfc Needs an Asphalt PI http://www.westfordcleanair.org/?015/05/asphalt-traffic-affect-on-property.html 11/7/2017 Westford Clean Air: Asphalt Traffic: Effect on Property Values Page 2 of 2 n.port. 1 ... P•. M:1 I II \\1111 ND .1... III &PII PM: OHM •1JI \•..• V••• I M MI• %Ww161112$ y•n .M Lilt• I.11 I.. 0, •.! Ito' I 4 I Mrl•1D.M111.2Y1.1• 11J1 (IttLN IMINa Para ( IJIJln) ITl1AYl4a /M.4110\ ci aJntatsiuwta7 ••••I-• 11411 •M•• I1• U ...4 •.N •••...•r. . ... nq..w i.1. %SS ••'M Iv 111•.1 I Itr 1 r ' Vitae.' NI •111•71 !PM Ira I PIw J11• [WS,•••I IoW nM MAM Plow n.afVu( R•, •M nlMllw.. I . \n .•14•. 1 •410‘ II nM Sal ..:N 1.44 .Ise•• S.i. •ta in 400 Io tyl et: S. 1II• O- WPM•..•1•:II.• 1•.•P 1. re u,l VYI• .Ul1• VISION 1i11 I II.. MM aad MO up Ile W anM/t 14Nt•u .w •1 ul•• • IM• tvinalSM \M 1(111 MOWS.* 1\v . Fitt, ..1•L 68,4. •• 011••••• %% 11\11 N1 N1 P PN4S PULS Nails •• ••II'..tlglH P•11•1• • M ir.l•..1 gm.s. IMVI•.•I I.M!11•• u1\I 4411 OAP :.Ye n fl— • • so *AV. I SW MM• l M •MI .n- Mb M I..M T•.M. antral A ••N tin P11(1 II Ia• l*K3 Nya(Iil.\A llff rum M•:•.. • MMwy 7.8 ••• ... .. .. _ •_..1 _. 'a • 1 IONS III P 1). 14tH pw .'JM M•I I•P •_••MCI MO t. '•• C a v •- la/ r w ton&tll— uvula 1\Y/.t%W •It /hit .0•••••• M lr.tiyrw•.w Si. ./M1.("ara•••.I .. 4114 MNP 15111 J.q'MMYT c•. 1101 \.I.I II ad ',al . -• \I 111 YNYI ltlidpl \Y'- ••1111\HI,IWi •,+r II•• • • w Ii. 4, I.Itryyy: PI.. 1. •• .1 _ • V.•••••5 \•1 I •.• •Ta••1 'OM %PM• if MMIM M1/•'.J flu IH/LFMitcs *B?Olt too ••••••• • :SUN r .. 4.. ♦ • ♦. ..p1 .I III ••.r✓M•.•• •r It 4 •atI•IPwPs ,...• ..... •.1. 11A• . IS* - lam L1•PCI•l I n1 4110•111 1,0• '• ... P•. 1./1• 11) Presentee at the To. of Kn:. _ . r ning Board a? aneea:s _ . r..• ..... http/Avwwwestfardmigcv/;.ages•;awe-^'Iertdtoa•ndepa•terents/c_a'. -7 CA) dl/= - Posted by Wendy Welsh 527 AM Labels: Property Values Traffic No comments: Post a Comment E:.trc Comment as. Select profile. , v) Publish Newer Post . • a•• •.a- ••• • I l l.. I..✓/—i I •—e MS Preview Subscribe to: Post Comments (Atom) Home Older Post • Powereel by (If http://www.westfordcleanai r.org/2015/05/asphalt-traffic-affect-on-property.html 11/7/2017 Property Values Decrease When a Quarry is Built Page 1 of 4 Main Menu Home I Our Fight I Legal =-r quarry W= LMRA Home Lower Miloford Residents Association I''IIew, Tarr v Facts Our Friends Contact Us the aggregate is extracted water storage capacity is lost. Aggregate operations are characterized by the release of significant amounts of particular matter (i.e. dust) and noise pollution from extraction and processing activities as well as smog precursors and greenhouse gases from the operation of heavy equipment and machinery The heavy truck traffic to and from aggregate sites is often a serious hazard and nursar:ce affecting people over areas, and is a si http://crushthequarry .org/index.php?option=com_content&view=article&id=63 :property -v... 11 /7/2017 Property Values Decrease When a Quarry is Built Page 2 of 4 source of air pollution itself --Pembina Institute, 2005 Los:: Nnise Home Qt,arry Facts Real Estate Property Values Decrease When a Quarry is Built Volunteer r.. 4... -- a- *High 1111111117 ;-7 t".; SIN:- VOLUNTEERt Lower Milford Township. HeN us fight for You can he'c with fundraisers. programs n!icity, and leadersh.p 3.c,i up to help LMRA. Spend as much time as you would litre. Zoning Board Hearings on Quarry Delayed The Zoning Board Hearings regarding the application to build a quarry at West Mill Hil has been postponed until there is a resolution of the appeal of the Commonwealth Court of the Planning Commision decision. The Township has appealed the decision and LMRA has joined in the appeal. Since the decision has a important influence on how both parties will proceed, it was agreed to wait to see what the outcome will be before proceeding. Property Values Decrease When a Quarry is Built Property va; ies drop when a quarry is built. Over the past twenty years, the evidence is clear. Scientific methods have been developed to account for other factors such as the size and location of the property. the local environn-nertage of the hu„se etc., so that the effect of property value changes _red only by the quarry can be calculated. The value of property decreases n-c-st within the immediate vicinity but will be felt several miles away. Homes witnin a quarter mile will drop by about 30%. A mile away the value of non.es will decrease oy about 13%, Home as far as 3 miles away can expect :: L .out a 0° o drop in value. a Loss in Real Estate Value 2 Mmes from Quarry 2.3 s 1.s Library • Documents • Legal Matters • Presentations • Newsletters • Miscellaneous http://crushthccl tua rry . org/index . php?option=corn_content&view=article&id=63 :property -v... 11/7/201 7 Property Values Decrease When a Quarry is Built Page 3 of 4 On average, property within a mile of the quarry will lose about 19% of its value as soon as a quarry begins For example a S350,000 home will lose about $67,000 if it is within a mile of the quarry. For Lower Milford Township, this loss translates to more that $6 million loss in property value with its attendant loss in local taxes, change in the type and mix of new construction, and other effects. These losses do not account for loses in other areas where truck traffic. dust. noise will contribute to Further loss in property value. There have been several studies that have confirmed this cata unequivocally. Quarry operators, including witnesses for Geryville Materials. try tc refute that fact. They claim there is not effect when quarries are o:.ilt. This certainly goes against common sense — would you pay the same ar:our: for a rouse with a quarry in :he neighborhood and the sarr.e house without a quarry'- But it also goes against the actual data. Quarry operators compare property values in one of two ways: • It compares values in two locations Out do ;,ot account for differences in the type of environment. They compara homes in an inaustna area or a lower income housing area with nomes ir.1.;-,e quarry area which were more rural cr .es:dential thus cornrn z ling s r. g icr p`,ce. -hey then claim homes are comparable in value. not taking into account the loss when the quarry came into existence. • They look at the property appreciation over time pointing out that the value of the properties grow at about the same rate as homes further away from the quarry. They also point out that there is development that occurs in the area. Both are true. The loss in value occurs wren a quarry first comes to the area. This loss persits essentially forever. However. the property after the initial loss will grow at about the same as other more desiraole areas Development also occurs in that area cut it is of less value, e.g., step malls, small subdivision homes, industrial companies seeking fewer regulations for the manufacturing processes they use. The consulting company C4SE looked L. 3 cases where no; -he values were purported to remain the same once , .,.. : ry was L..i;t. 5 cases. They found that the methodology used was fla.. eo i did not coo. I. -or otter factors. That is, the cornarison was more .1kt. .oarin j apples a:iu oranges. In one, done by the Bureau of Mines, they ::.hat the va!Les sc:ualty decreased in 4 of the 5 areas the Bureau claimea remained the same. it the remaining study by the Bureau, the study was in an area that already was neavily industrialized and so a quarry did not atect the overall quality of one area. Lower Milford i c r.r, ,:;ip will lose in a .a .;:ty of ways. • It will lose a small amount in real Este taxes The quarry rezoned to industhal will not bring in more :ax revenue to offset that lost •, :he surrounding properties. That is bect.:,se the equipment and s:u.'age facilities are temporary and not subject to real estate tax. Property owners will have to n ,aKe up the revenue. Cf:.ourse, .i.e Schoei District will lose even more. This time the School District residents will nave to make up for the loss. • It will have to provide more municipal services such as Fire. EMT. and Police as well as legal services to nave them comply win our ordinances. It will raise taxes even if Geryville agrees to relocate and support financially the extra services. Other areas, have shown that the training costs for specialized services and the need to recruit often end in non - volunteer services which the Township has to maintain • It will affect to safety of our citlzs"5 .Additional traffic win increase the number of accidents in the Township on Kings Highway and Limeport Pike. When accidents occur cue to uck traffi:, °ate has shown the accident is either minor or very servo -us. There are no accidents that http://crushthequa:ry .org/index.ptip?optialir-co n__c ontent&view=article&id=63 :property -v... 11/7/2017 Property Values Decrease When a Quarry is Built Page 4 of 4 causes non -serious injury or moderate damage. We can expect more residents dying. Lower Milford Township will chage dramatically, none for the better, if a quarry is permitted. How much value in property loss will you encounter. Check the map below to see where you will live if a quarry is built on West Mill Hill. Then as a rough guide use a 15 I3SS if you Lye with a mile (red circle) of the quarry, and use a 9% loss if you live between 1 and 3 miles (black circle) from the quarry. The only winners will be Geryville Materials investors and Haines & Kibblehouse who purportedly will be the quarry operators. help us You membership helps pay for our legal defense. Also, strong community support is notice to Geryville Materials that we will not permit destruction of our Township. rase consider helping. Click here to join or donate Lower Milford Residents Association Copyright 2012 http://crushthequarry.org/index.php?option=com_content&view=article&id=63 :property -v... 11/7/2017 Healthy Workplaces and Healthy Homes - Information - Delaware Health and Social Serv... Page 1 of 14 Str (http://delaware. Listen Current Suspected Overdose Deaths in Delaware for 2017: 191 (http://www.helpisherede.com/#intro) (http://app.na.readspeaker.com/cgi-bin/rsent? customerid=7262&lang=en_us&readid=main_content&url=/dhss/dph/hsp/hwtopics. html) Delaware Healthy Workplaces Asbestos Information Additional Resources http://www.dhss.delaware.gov/dph/hsp/hwtopics.html 11/7/2017 Healthy Workplaces and Healthy Homes - Information - Delaware Health and Social Serv... Page 2 of 14 General Asbestos is a Information group of (http://delaware.goV'nerals wit" fibrous crystals which occur naturally in the environment. Asbestos is used in applications that benefit from sound and thermal insulation. Though not officially banned in the United States, there are regulations that forbid uses in many applications and the use of asbestos has steadily decreased over the last few decades. However, due to both Oast and present use of asoestos, workers in the construction, stobuilding, au :omotive arc other industries remain at risk for exposure. Asbestos FAQ S ch ttp://ww��.avvm.celaware.gov/AQM/Asbestos/Pages/AsbestosFA px) NIOSH ToxFAQs Asbestos (http://www.atsdr.cdc.gov/tfacts61.html) http://www.dhss.delaware.gov/dph/hsp/hwtopics.html 11/7/2017 Healthy Workplaces and Healthy I Iomes - Information - Delaware Health and Social Serv... Page 3 of 14 Uses Asbestos was historically (http://delaware.goV d as an insulation arc fire retardant. Common applications include plumbing insulation, floor tile and adnesive, exterior shingles and automotive brake pads. Health Asbestos is a Effects known human carcinogen and exposure isunked to lung cancer, asbestosis arm mesothelioma. OS - Exposure Limits and Guidelines Carcinogen Please use the back button on your web browser to return to the previous page. Asphalt and Asphalt Products Information Additional Resources General Asphalt is a ,:;la`K, sticky liquid present Information ir, petroleum oe _ ,sits. R'ocuced by distillation of true oi! asphalt is widely used in a variety of applications. Asphalt is typically used as an adhes;ve hold *oge:'per aggregate ma,e als such as sand and gravel. S�Ch NIOSH Health and Safety Topic - Asphalt (http://www.cdc.gov/niosh/topics/asphalt/) http://www.dhss.delaware.gov/dph'hsp/hwtopics.html 11/7/2017 Healthy Workplaces and Healthy Homes - Information - Delaware Health and Social Serv... Page 4 of 14 Uses Road surfaces are the most common r• f h t: ,U Roofing use c. asphat: � � the .: . ?._,� , � ,g and (http://delaware.govhingles account for most of the rest use. Health Effects Workers can be exposed to asphalt fumes when the material is heated for application. Exposure to asphalt fumes has been '.inked to eye, skin and respirator`, rract irritation. There is evidence r_nat exposure to asphalt products and fumes can cause cancer. NIOSH • • Exposure Limits and Guidelines 5 mg/m3 (15 -minute) Carcinogen Please use the back button on your web browser to return to the previous page. Asthma Information General Asthma is a respiratory disease. It creates Information narrowing of : e air passages that results in difficult breath nng, tightness of the chest, coughing, c eats-i-souncs such as wheezing. Occupational asti}ma refer: to asthma that is caused oy orea:ning in spe: c agents in the workplace. Ccc,.pational asthma is the most common lung condition re,ated to occupationsi exposures on -.e developed vior'td. Treatment Swift diagnes s including identifying the agent or situation likely :r, trigger an attack, is important. Eliminating exposure, or reducing risk of exposure, ano -allowing a coctor's recommeno3r"s can orevenr long-term problems. Additional Resources S�h US EPA - Asthma (http://www.epa.gov/asthma/) CDC - Asthma (http://www.cdc.gov/asthma/) Please use the back button on your web browser to return to the previous page. http://www.dhss.delaware.a-ov/dphihspihwtopies.html 11/7/2017 Healthy Workplaces and Healthy Homes - Information - Delaware Health and Social Serv... Page 5 of 14 Carbon Monoxide (http://delaware.gov) General Information Information Carbon monoxe (CO) is a colorless, odorless gas. CO is produced by combustion and is releases in exhaust from vehicles, generators, etc. CO can also oe released from natura' sc� rces such as forest fires and volcanic activity. Such Additional Resources US EPA - Carbon Monoxide (http://www.epa.gov/iaq/co.html) Uses CO is widely in ndus!_lia applications. Exposure Limits Ranging from metal and fuel processing to and Guidelines production of otner gases and compounds, OSHA CO is a very common indust' .al gas. Health haling carbon monoxide gas can :ead to Effects headache, dizziness, mild nausea, and onfusion. Hg•- eves can :",E_ rata., causing death within r- nutes. NIOSH 50 mg/m3 (TWA) 40 mg/m3 (TWA) Please use the back button on your web browser to return to the previous page. Chromium (Hexavalent Chrom Information General Information Chormium ;s common eleme in the environment often found try valent chromium (Cr-'` or hexavalent chromium (Cr- Cr---1 is a nuthe,__ essential to goo° health ins smaH ; amounts. Cr6) Additional Resources Chromium FAQ vvy.v1.dhss.Celaware.gov/dhss/dph/files/chromiumfaq.pdf) [ Text of Chromium FAQ (http://www.dhss.aelaware.gov/dhss/dph/files/chromiumfaq.txt) a T SDR Chrom ToxFAQ (http://www.atsdr.cdc.gov/tfacts7.pdf) NIOSH - tinromium (http://vvww.cdc.gov/niosh/topics/hexchrom/) http://www.dhss.delaware.goviclphihsp/hvitopics.html 11/7/2017 Healthy Workplaces and Healthy Homes - Information - Delaware Health and Social Serv... Page 6 of 14 Uses Cr''3 and Cr' are important (http://delaware.go�raustrial metais NIOSH used in chrome plating, leather orocessing, cve`= and pigments and wood preservation. Health inhaling Effects hexavalent chromium at hgn concentrations can irritatte the nose ana throat, trigger asthma attacks and !eac to ung cancer Eating or crir contamire:ec foods can the stomach me damage the He - or Kidneys. Exposure Limits and Guidelines Carcinogen 0.001 mg/m3 (TWA) Please use the back utton on your web browser to return to the previous page. Diesel Exhaust Information Additional Resources Such http://www.dhss.delaware.gov/ dp'. `hsp/hwtopics.html 11/7/2017 Healthy Workplaces and Healthy Homes - Information - Delaware Health and Social Serv... Page 7 of 14 General Diesel exhaust is a Information complex rrix:ure cf (http://delaware.govcpmpounds and includes diesel particulate matter (DPM). DPM is a group } of fine {� oarticles ides that are easily inhaled deep into the lungs. Diesel S ch Exhaust FAQ (http://www.dnss.delaware.gov/dhss/dph/files/dieselexfaq.pdf) Sources Diesel exhaust released by ve*:les and equipment OSHA operating cn fuel. Heavy construction eouiornent, NIOSH generators arr even some oassenger venic.es are examples o- diesel exhaust sources. Health Snort term Effects exposure ro r.esei exhaust can cause eye irritation and breathing problems. Lon_ term exposure increase your r::s' of cancer and Exposure Limits and Guidelines None Carcinogen Please use the back button on your web browser to return to the previous page. Hazardous Drugs Information Additional Resources http://www.dhss.delaware.gov/dphthsp/hwtopics.html 11/7/2017 Healthy Workplaces and Healthy Homes - Information - Delaware Health and Social Serv... Page 8 of 14 General in :ne US, Information mHions of (http://delaware.g(M'lth care workers are exposed to hazardous drugs everyday. From preparing doses in a ob rmacy to acmHnisterin drugs and disposing of waste, there are numerous tasKs :bar risk exoosure to dangerous drugs. Medic? Personnel are at Tisk from exposure by n ha ation, nJection via puncture wcj^d or acicenral neecle stick a nc absorption wren skin is co ,st:tea. Uses Drugs and onarmaceutica!s are used everyday to prolong and Mnrnve the quality of life. Safe Handling of Hazardous Drugs intto://wvvw.guideline.gov/summary/summary.aspx? doc_id=4152&nbr=3180&ss=6) Hospital e -Tool Pharmacy Module nttp://wviN csha.gov/SLTC/etools/hospital/pharmacy/pharmacy.html) Preventing Occupational to Antineop!astic and Other Hazardous Drugs in Health Care Settings (http://www.cdc.gov/niosh/dots/2004-165/) Persona! Protective Equipment for Health Workers Who Work itr—azardous Drugs (http://www.cdc.gov/niosh/dots/wp- so:utions/2009-106/pdfs/2009-106.pdf) http://www.dhss.dela«are.gov/dpivhspihwtopics.htlnl 11/7/2017 Healthy Workplaces and Healthy Homes - Information - Delaware Health and Social Serv... Page 9 of 14 Health Accidental ar,c Effects ,n:encora� (http://delaware.gog,'s'use of drugs and oharrnaceutica. products have wide range of serious and ootentially fats ne th effects. The specific effects cts are dependent on Mold -rte . r. spec11c cc noounc arc do Teout car ;ncL_Ide skin irritation respiratory orcolems, eeproductive disorders and cancer. Please use the back button on your web browser to return to the previous page. Information Additional Resources Str General Mold is a natural part of the environment. US EPA Mold Information V Dios are f,r.r0;, the grcup crgan:sms Information tn,a: help decd„ rose organ+c matter. Molds (http://www.epa.gov/mold/index.html) require r no s:..r - o grow, our. under the condt'ons can grcvv on a variety of CDC Mold S. r:=ces. T ese T_^ .-iuGe `.end, drywall, Information '_r^iture, o;-icener organic sources. (htto://www.cdc.gov/mold/basics.htm) http://www.dhss.delaware.gov/dphlhspihwtopicsehtml 11/7/2017 • ■ Cheyenne Regional Medical Center Hospitalist Service 214 E. 23rd St. • Cheyenne, WY 82001 • Phone: (307) 432-6629 • Fax: (307) 432-6634 Chandrasekhar Chada, MD Rajesh Kunadharaju, MD Houssam Marwany, MD Ann Lopez, MD Mompoloki Nkhumane, MD Prasangika Ranasinghe, MD Daniel Rivard, MD Rudraraju, MD Rodolphe Taby, MD Sahar Abdelgader, MD Cherry Valino, MD Judd Dawson, DO Doug Tucker, DO Yojna Singh, MD NPI# Vinod Yalamanchili, MD by, MD Alpeshkumur Pate►, Paula Thornton, NP Scott Horton, ACNP DEA#1 Name..Laura C - DOB...�.2 !. j i i 66 .J Date II I C 1! Lo r1 Address Diagnosis Code: to 'W ING rr a t inn C., Co y.C Y. : L- i vatik.A Lila owl a tiov,.O s ,ri. e itot. C-- CA ricAr te,c11-1.,, t co ca,n. et /Vire otycii,ornAi, 1-24 t 1 �� _ 25.49 w _�. JAN 0-7 O 00 Q 1- 0 0 Signature ■ a EXHIBIT 14-5 �' ci-ecoLt3 Red Feather Lakes Lc f&rs-e. As IQ (a -t - S { u)cLr rt :#!organ O EXHIBIT iCK R -cog Asphalt Specialties Co. - Locations Page 1 of 2 SPECIALTIES CO. I Ionic > Locations LOCALLY OWNED AND OPERATED Development --- Commercial --- Retail --- Heavy Highway/Municipal About Us Capabilities Projects Environment Subcontractors Locations Material Sales Industry News Employment Community Contact Us Links Locations Asphalt Specialties Plant Locations and Service Area !Mao Ra A $froo. lot • / • 0 • • L n• 4.T iMY Arvada dye em Wwl IM Gown - Ras,. , ,' ' / 1 Denver €13 A4N0ri • L.,•.••••• 6-3 :.e•ww wan.. Eny.•p0$ U.N$$••• • canna air LN RN •R{••. PM 4 Asphalt Plants 4, Aggregate and Mines tV Inert Fill Main Office 10100 Dallas St. Henderson, CO 80640 Map Image ..,roan» Cw.n... Parr. turn ,.. 4c000• Fin C - Can. owl Pokes I pq '144 I • "y. http://www.asphaltspecialties.com/page.cfm/ID/19/Locations/ 11/8/2017 Asphalt Specialties Co. - Locations Page 2 of 2 Asphalt Plants Asphalt Plant #1 9113 Quince St. Henderson, CO 80640 Mao Aggregate and Mines Turnpike Aggregate and Mines 599 State Highway 52 Erie, CO 80516 Map Image Aggregate and Mines Chavers Recycle Yard 12367 Weld County Rd. 8 Ft. Lupton, CO 80621 Mao Inert Fill Speer Inert Fill 12021 Brighton Rd. Henderson, CO 80640 Map About Us I Capabilities Asphalt Plant #2 11401 WCR 9 3/4 Firestone CO 80504 Mao Nelson Aggregate and Mines 6755 Weld County Rd 26 Longmont, CO 80504 Map Asphalt Plant #3 6550 Huron St. Denver, CO 80221 Mao Chavers Aggregate and Mines 12367 Weld County Rd. 8 Ft. Lupton, CO 80621 Map DADS Recycle Yard 3500 S Gun Club Rd Aurora, CO 80018 Projects I Subcontractors I Industry News I Contact Us Copyright © 2017 - Asphalt Specialties Company. All Rights Reserved. http://www.asphaltspecialties.com/page.cfm/ID/19/Locations/ 11/8/2017 Contacts — BURNCO Colorado I Bestway Concrete & Aggregate Page 1 of 3 Grand Mesa National Forest c North Dispatch 1970.587.9305 South Dispatch 1303.637.0900 0 Hours I M -F 6am-Spm CZ Apply to be a Driver f G+ ANVdWO3 ODN!SI1B V BESTWAY CONCRETE & AGGREGATE Medicine Bow National Forest Medicine Dow•Routt National Forests White River National Forest Rocky Mountain National Park Arapaho & Roosevelt National Forests and Pike and San Isabel National V ....n:n n.. r/..nn..- WINDSOR 32744 Co Hwy 13, Windsor, CO 80550 0 HOME ABOUT PROJECTS BLOG MORE D Pawnee National Grassland CONCRETE LOCATIONS North Dispatch 1970.587.9305 I South Dispatch 1303.637.0900 DENVER HENDERSON JEFFCO/GOLDEN 5901 York St, Denver, 10040 Dallas St. 10888 CO -93. Golden, CC) 80216 Henderson, CO 80640 CO 80403 MILLIKEN TITAN/LITTLETON FIRESTONE NISSEN 315 Frontier Ct, Milliken, CO 80543 9681 Titan Park Cir, Littleton, CO 80125 11401 County Rd 9 3/4, Longmont, CO 80504 AGGREGATE LOCATIONS Aggregate Dispatch 1303.651.6409 CO RD 58 & 47 1/2, Greeley. CO 80631 Map dnottaiDailiPeogle http://burnco-usa.com/colorado/contacts/ 11/8/2017 Simon Contractors Locations Page 1of1 one Dark , .I. A M 0URAI VAT I NI billings Simo{,1`Contractors Locations ; P E `_ {i l i P �e WYOMING car Fort Collins 0 Denver O I Grand COLORADO Mapdate 'e?ojIe.INEGI Terms 50mi STANDING ROCK RESERVATION CHEYENNE RIVER RESERVATION SOUTH DAKOTA NEBRASKA 9f 9 9 9 United States J Sioux Falls. Siouxx City Omaha o' Lincoln https://www.google.com/maps/d/embed?mid=1 J_zc6UCFM3gzr 1 W34AXeJsXmCJO&11=4... 11/8/2017 Page 1of1 EXHIBIT ICL https://upload.wikimedia.org/wikipedia/commons/thumb/c/c7/Cynomys_ludovicianus_-Pai ... 11/8/2017 Colorado Parks & Wildlife - Threatened and Endangered List Page 1 of 5 COLORADO PARKS & WILDLIFE Things To Do Learn Places To Go About Us Buy Et Apply Threatened and Endangered List COMMON NAME AMPHIBIANS Boreal Toad Couch's Spadefoot Great Plains Narrowmouth Toad Northern Cricket Frog Northern Leopard Frog Plains Leopard Frog Wood Frog BIRDS American Peregrine Falcon Bald Eagle Burrowing Owl SCIENTIFIC NAME Bufo boreas boreas Scaphiopus couchii Gastrophryne olivacea Acris crepitans Rana pipiens Rana blairi Rana sylvatica STATUS* Falco peregrinus anatum Haliaeetus leucocephalus Athene cunicularia SE SC SC SC SC SC SC SC SC ST http://cpw.state.co.us/learn/Pages/SOC-ThreatenedEndangeredList.aspx 11/8/2017 Colorado Parks & Wildlife - Threatened and Endangered List Page 2 of 5 Columbian Sharp -Tailed Grouse Ferruginous Hawk Greater Sage Grouse Greater Sandhill Crane Gunnison Sage -Grouse Least Tern Lesser Prairie -Chicken Long -Billed Curlew Mexican Spotted Owl Mountain Plover Plains Sharp -Tailed Grouse Piping Plover Southwestern Willow Flycatcher Western Snowy Plover Western Yellow -Billed Cuckoo Whooping Crane FISH Arkansas Darter Bonytail Brassy Minnow Colorado Pikeminnow Colorado River Cutthroat Trout Colorado Roundtail Chub Tympanuchus phasianellus columbianus Buteo regalis Centrocercus urophasianus Grus canadensis tabida Centrocercus minimus Sterna antillarum Tympanuchus pallidicinctus Numenius americanus Strix occidentalis lucida Charadrius montanus Tympanuchus phasianellus jamesii Charadrius melodus circumcinctus Empidonax traillii extimus Charadrius alexandrinus Coccyzus americanus Grus americana SC SC SC SC SC FE, SE FT, ST SC FT, ST SC SE FT, ST FE, SE SC SC FE, SE Etheostoma cragini Gila elegans Hybognathus hankinsoni Ptychocheilus Lucius Oncorhynchus clarki pleuriticus Gila robusta ST FE, SE ST FE, ST SC SC http://cpw.state.co.us/learn/Pages/SOC-ThreatenedEndangeredList.aspx 11/8/2017 Colorado Parks & Wildlife - Threatened and Endangered List Page 3 of 5 Common Shiner Flathead Chub Greenback Cutthroat Trout Humpback Chub Iowa Darter Lake Chub Mountain Sucker Northern Redbelly Dace Plains Minnow Plains Orangethroat Darter Rio Grande Chub Rio Grande Cutthroat Trout Rio Grande Sucker Razorback Sucker Southern Redbelly Dace Stonecat Suckermouth Minnow MAMMALS Black -Footed Ferret Black -Tailed Prairie Dog Botta's Pocket Gopher Gray Wolf Grizzly Bear Luxilus cornutus Platygobio gracilus Oncorhynchus clarki stomias Gila cypha Etheostoma exile Couesius plumbeus Catostomus playtrhynchus Phoxinus eos Hybognathus placitus Etheostoma spectabile Gila pandora Oncorhynchus clarki virginalis Catostomus plebeius Xyrauchen texanus Phoxinus erythrogaster Noturus flavus Phenacobius mirabilis ST SC FT, ST FE, ST SC SE SC SE SE SC SC SC SE FE, SE SE SC Mustela nigripes Cynomys ludovicianus Thomomy bottae rubidus Canis lupus Ursus arctos SE FE, SE SC SC FE, SE FT, SE http://cpw.state.co.us/learn/Pages/SOC-ThreatenedEndangeredList.aspx 11/8/2017 Colorado Parks & Wildlife - Threatened and Endangered List Page 4 of 5 Kit Fox Lynx Northern Pocket Gopher Preble's Meadow Jumping Mouse River Otter Swift fox Townsend's Big -Eared Bat Wolverine REPTILES Triploid Checkered Whiptail Midget Faded Rattlesnake Longnose Leopard Lizard Yellow Mud Turtle Common King Snake Texas Blind Snake Texas Horned Lizard Roundtail Horned Lizard Massasauga Common Garter Snake MOLLUSKS Rocky Mountain Capshell Cylindrical Papershell Vulpes macrotis Lynx canadensis Thomomys talpoides macrotis Zapus hudsonius preblei Lontra canadensis Vulpes velox Corynorhinus townsendii pallescens Gulo gulo SE FT, SE SC FT, ST ST SC SC SE Cnemidophorus neotesselatus Crotalus viridis concolor Gambelia wislizenii Kinosternon flavescens Lampropeltis getula Leptotyphlops dulcis Phrynosoma cornutum Phrynosoma modestum Sistrurus catenatus Thamnophis sirtalis SC SC SC SC SC SC SC SC SC SC Acroloxus coloradensis SC Anodontoides ferussacianus SC http://cpw.state.co.us/learn/Pages/SOC-ThreatenedEndangeredList.aspx 11/8/2017 Colorado Parks & Wildlife - Threatened and Endangered List Page 5 of 5 *Status Codes • FE = Federally Endangered • FT = Federally Threatened • SE = State Endangered • ST = State Threatened • SC = State Special Concern (not a statutory category) Resources • Species Profiles Colorado's State Wildlife Action Plan (SWAP) itLynx kitten. The approved State Wildlife Action Plan identifies priority species Et habitats that need conservation efforts in the state, £t potential conservation actions that can address threats these species Et habitats face. »Read More http://cpw.state.co.us/learn/Pages/SOC-ThreatenedEndangeredList.aspx 11/8/2017 RESULTS Database Summary Table 2 provides a summary of the 17 data sources that contributed to this study's baseline. The total prairie dog town acreage compiled in this study's GIS database is 314,114 acres. However, this includes all prairie dogs towns that were active and inactive, as well as towns that were "no longer present" (i.e.. lost to agriculture land conversion, urbanization, or reverted to shod -grass prairie). As shown in Table 2. a total of 38% of the acreage contained in the baseline was field checked as part of this study. The other sources listed in Table 2 are for acreages that were either too recent to warrant field checking. or they represent prairie dog towns that could not be field -checked because of resource limitations (time and budget) and accessibility issues (no nearby roads, or on private land). Table 2. Database Source Summar Source Area in Acres Percent of Area Black -tailed Prairie Dog Study (2000) 120.202 38.3% Boulder County Open Space 1,021 0.3% Boulder Mountain Parks 183 0.1% Colorado Bird Observatory 85,754 27.3% CDOW - Archival Data from Bissell et al. (1979) 34.496 11.0% CDOW - Volunteer Contributions 2.739 0.9% CDOW - Denver Area Study (Weber) 36.894 11.7% City of Boulder 1,505 0.5% City of Fort Collins 801 0.3% DOD - Pueblo Chemical Depot 1,962 0.6% DOD - Fort Carson 2,147 0.7% Denver County Environmental Health Dept. 439 0.1% Fossil Creek RMP (EDAW) 35 0.0% CDOW - Northeast WRIS Data 10.498 3.3% USFS - Comanche National Grassland 1.375 0.4% USFS - Pawnee National Grassland 1.008 0.3% USFWS - 1991 Northeast Colorado Study 11.081 3.5% USFWS - Rocky Mountain Arsenal 1.975 0.6% Total 314,114 100% Includes all colonies: i.e., active, inactive. no longer present. and unknown status. 2. The "Black -tailed Prairie Dog Study" refers to prairie dog towns that were field checked as part of this study. The acreages shown from all other contributors represents prairie dog towns that were either too recent to require field checking. or that were not field checked because of accessibility and resource limitations. Final Report Black -Tailed Prairie Dog Study of Eastern Colorado Page 18 2000 Field Survey Accomplishments Surveys for this study were conducted during July through August 2000. The entire eastern plains and Front Range regions of Colorado were subdivided into 5 separate survey areas, with an experienced wildlife biologist assigned the role of field checking prairie dog towns in each. The reader is reminded that, due to resource limitations (budget and time), it was not possible to field verify every prairie dog colony included in this study's baseline. Through consultation with CDOW, it was decided to set an overall 25% field verification goal, with older data and larger towns being assigned higher priorities for field checking. The survey statistics presented in Table 3 demonstrate that. based on the 100,284 acres surveyed, a 31.9% level of field checking was achieved for previously documented towns. Also. EDAW surveyors were able to identify an additional 220 new prairie dog towns, comprising 20,444 acres of "new" (previously undocumented) active acreage. These two categories combined result in the overall total of 38% that was field checked. Gratitude should also be expressed again to the Colorado Bird Observatory staff, which contributed details concerning 527 new prairie dog towns that they mapped as part of their ongoing statewide burrowing owl survey efforts. Table 3. Survey Accomplishments in 2000 Status Number of Colonies Area in Acres Percent of Area Surveyed in This Study 749 100,284 31.9% Surveyed By Another Agency Within The Last 2 Years 1.367 38,557 12.3% Surveyed By Another Agency Between 3 and 5 Years 1.335 22,756 7.2% Not Surveyed (Not Visited in the Last 5 Years) 880 46,320 14.7% New Colony Added As Part of Study - EDAW 220 20,444 6.5% New Colony Added As Part of Study - CBO/CDOW 527 85,754 27.3% Total 5,078 314,114 100.0% Another important statistic not shown in Table 3 is the percent of "very old" information that was updated by this study's survey efforts. Prior to field survey, the acreage of black -tailed prairie dog towns that were over 10 years old was about 90,000 acres, or about 28% of the baseline. EDAW surveyors were able to field verify and update 60% of these. Post -Survey Summary of Database The GIS database was updated with information gathered during the July/August 2000 field surveys. The updating involved changes to prairie dog town status, size, and number. It also included some "final compilation" adjustments, where towns from different sources that were nearby were either combined or split. The Final Report Black -Tailed Prairie Dog Study of Eastern Colorado Page 19 updated database includes190,423 acres of active black -tailed prairie dog towns, as shown in Table 4. Table 4. Colony Status Following 2000 Field Surveys Status Number of Colonies Area in acres Active 2,578 190,423 Inactive 1.109 21,599 Unknown Status 1,022 57,056 No Longer Present 292 45,037 Total 5,001 314,114 Variability in Colony Status Because it was not possible to update the status of all prairie dog towns included in the study's baseline, it was necessary to assign a portion to an "unknown status" category. As shown in Table 4, this category amounted to 57,056 acres, or 18% of the updated baseline. Although the "unknown status" towns were not field checked, trends from the 2000 field surveys would suggest that a large portion of this acreage was probably still active. Table 5 provides a breakdown of the changes in colony status since the time of last survey. Table 5. Changes in Colony Status Since Last Survey Status Number of Colonies Percent of Colonies Area In Acres Percent of Area Colony Still Active 360 48% 42.441 42% Colony Now Inactive 97 13% 12.806 13% Colony No Longer Present 292 39% 45,037 45% Total 749 100% 100,284 100% Most of the older data sets compiled into the baseline did not include a "colony status" field. so it is assumed that those towns were active at the time they were mapped. Total Active and Inactive Prairie Dog Acreage Using data from Table 5. "pro -ratings" were applied to the unknown status colonies so that a portion of the older data that was not updated in 2000 could be reasonably included in total active and inactive acreage figures. Based on a finding that 42% of the previously documented colonies were found to be still active in the 2000 field survey, this factor was applied to the acreage of colonies with "unknown status" from Table 4. The results of this approach are shown in Table 6, which reports a total active acreage figure of 214.570 acres for the study. Because this study only addresses known prairie dog towns, the true active acreage figure for the entire state is certainly higher. Final Report Black -Tailed Prairie Dog Study of Eastern Colorado Page 20 Table 6. Statewide Results — Active and Inactive Acreage Status Number of Colonies Acreage2 Active 3,069 214,570 Inactive 1,241 28,884 1. Includes pro -rated portions of older, unchecked colonies that are of "unknown status". 2. Includes only prairie dog towns that were part of this study's baseline. These figures can, therefore, be viewed as a minimum known amount for the state. Active Prairie Dog Town Size Size statistics were generated for known active prairie dog towns. These numbers were generated directly from the database, using only recent (1995 - present) information. The total number of active prairie dog towns involved in this analysis is 2,581. The minimum active colony size is 0.04 acres. The maximum active colony size is 4,129 acres. The average colony size is 75 acres. Table 7 provides a breakdown of active colonies by size category. Table 7. Black -tailed Prairie Do a Town Size A P '' ! • 0 • n.�ize..� . .five Size Number of Towns Percent Less than 1.0 acre 294 11% Between 1.1 and 20.0 acres 1021 40% Between 20.1 and 100.0 acres 794 31% Between 100.1 and 200.0 acres 255 10% Between 200.1 and 500.0 acres 152 6% Between 500.1 and 1000.0 acres 45 2% Greater than 1,000.0 acres 17 1% Total 2578 100% County -by -County Results For the 29 counties that comprise the range of the black -tailed prairie dog in eastern Colorado, Table 8 provides a county -by -county summary of total active, inactive. and potential habitat acreage. Each statistic is further split by private and public land ownership, with public lands including only state and federal properties. Final Report Black -Tailed Prairie Dog Study of Eastern Colorado Page 21 Table 8. County -by -County Summary of Black -tailed Prairie Dog Acreage' Count Active Towns Inactive Towns Potential Habitat y3 Private Public Private Public Private Public Adams 10.927 2,338 387 1,185 79.159 22.968 Arapahoe 2.663 1,700 152 3 110,562 1 31,817 Baca 11,776 2,584 190 43 501.281 199.283 Bent 12,782 4,288 259 122 581.990 134.772 Boulder 11,511 16 1.542 5 19.703 287 Cheyenne 8,145 1,032 171 17 260.760 24.495 Crowley 12.146 1,373 327 40 302,901 61.703 Denver _ 2,157 91 450 59 4,381 606; Douglas 6,679 203 515 2 55,919 2.348 Elbert 223 - 54 - 538,504 66.096 El Paso 748 1,250 278 695 290,690 131.225 Fremont 2.352 447 296 104 94,428 11.853 Huerfano - - - - 374.007 32.900 Jefferson 4,656 187 0 39.375 3.782 777 Kiowa 7.162 1.799 1.126 359 203.626 50.913 Kit Carson 8.106 136 51 2 298,753 29.688 Larimer 1,484 68 146 64 144.838 24.602 Las Animas 1,488 689 250 28 1.414,436 332.556 Lincoln 5.013 254 146 1 818,834 115.266 Logan 6.584 1,805 4.708 649 273.619 35.972 Morgan 6.297 495 995 84 96.355 17.026 Otero 2,324 1.047 66 99 360.807 267.351 Phillips 1.836 2 161 - 12,746 1.510 Prowers 10.951 1,793 83 2 358,920 30.739 Pueblo 12,100 10,096 2.967 4,021 664,124 203.768 Sedgwick 2,496 110 35 32 66,913 7,207 Washington 1,222 0 40 0 264,130 33.266 Weld 16.399 3,715 1,614 2,165 638,393 275.674 Yuma 4.320 2.266 717 528 149,607 14.844 TOTALS2 174,549 39,783 18,503 10,309 9,019,759 2,164,517 1. Includes all active and inactive acreage. as well as pro -rated portions of older, unchecked colonies of unknown status. Because data relating to local government ownership was not readily available, the public lands category includes only state and federal lands from BLM's 150,000 land ownership layer. 2. Totals here are slightly different from previous totals because of rounding errors and the number of calculations involved in generating 29 sets of county statistics. 3. County boundaries are from USGS 1:50.000 county topographic series. As indicated in Table 8, there is a wide range of variability in prairie dog active. inactive, and potential habitat acreage between the 29 counties. With regards to total active acreage, the top 10 counties were: Pueblo (22,196 acres), Weld (20,114 acres), Bent (17,070 acres), Baca (14,360 acres), Crowley (13,519 acres), Adams (13,265 acres), Prowers (12,744 acres), Boulder (11,527 acres). Cheyenne (9.177 acres), and Kiowa (8,961 acres). Final Report Black -Tailed Prairie Dog Study of Eastern Colorado Page 22 With regards to total inactive acreage. the top 10 counties were: Pueblo (6,988 acres). Logan (5,357 acres), Weld (3,779 acres), Adams (1.572 acres). Boulder (1.547 acres), Kiowa (1,485 acres), Yuma (1,245 acres), Morgan (1,079 acres). El Paso (973 acres). and Jefferson (777 acres). With regards to total potential habitat acreage, the top 10 counties were: Las Animas (1,746,992 acres), Lincoln (934,100 acres), Weld (914, 067 acres), Pueblo (867,892 acres). Bent (716,762 acres), Baca (700.564 acres), Otero (628.158 acres), Elbert (604,600 acres). El Paso (421.915 acres). and Huerfano (406.907 acres). Caution should be exercised in reading too much into the county statistics. While the active and inactive acreages being reported are accurate, they reflect only what is known about prairie dog towns in a given area. And, what is known may simply be a function of level of survey effort. To help test this hypothesis, it was decided to total all active and inactive black -tailed prairie dog acreages for each county, and then express that number as a percent ratio of total available habitat. This number can be considered a "known percent occupancy rate", with occupancy referring to acreage surveyed and documented as having prairie dogs present at one point in time in recent years (i.e., thus. both active and inactive acreage is included). The highest "occupancy rates" were recorded for the following six counties: Boulder (65%), Denver (55%), Adams (15%). Phillips (14%), Jefferson (13%), and Douglas (13%). The lowest "occupancy rates" were recorded for Washington. Las Animas. Elbert, and Huerfano, with each being less than 1%. These numbers indicate that "occupancy rate" certainly can be a function of the level of historic survey effort applied to different geographic regions. For example, Baca County. a county traditionally considered as having a high density of prairie dogs, only rated a 2% rate: that was based on having 700,000 acres of potential habitat, but only 14,000 documented "prairie dog acres". In comparison, Boulder County is at 65%, having about 11,000 "prairie dog acres". but only 20,000 acres of potential habitat. Other obvious factors, besides survey effort, that could affect species occupancy in a given county are plague, control efforts, and habitat fragmentation. Other Sensitive Species Sightings While there were several observations of swift fox (Vulpes velox) and ferruginous hawks (Buteo regalis) by field survey staff. the only "other sensitive species sighting" worth reporting here is data related to burrowing owl (Athene cunicularia) occurrence. This is because it was the one species that was sighted quite frequently, and the sightings could be closely tied to a given location Burrowing owls in Colorado are very dependent on black -tailed prairie dog colonies. Both live in the short grass prairie habitat of the eastern plains, and Final Report Page 23 Black -Tailed Prairie Dog Study of Eastern Colorado burrowing owls use the prairie dog burrows and tunnels for nest sites and escape cover. During the process of field -checking prairie dog town locations and status, survey staff observed burrowing owls on 72 of the 756 towns that were visited, which equates to a 9.5% "occupancy rate". Final Report Page 24 Black -Tailed Prairie Dog Study of Eastern Colorado , EXHIB N�EaARL1!MMI� . u5R } Qoq Blue Smoke Control from Asphalt Plants Provides a Real -World Solution to Current Emi... Page 1 of 4 Home // Asphalt // Asphalt Plants // Blue Smoke Control Plants Provides a Real -World Solution to Current Emissions Problems Blue Smoke Control Plants Provides a Real -World Solution to Current Emissions Problems At some point warm mix asphalt may be routinely specified by state DOTs, and will likely provide an answer to issues with blue smoke - but a simple and cost-effective solution for asphalt plants is available today to control blue smoke. JULY 9, 2009 https://www.forconstructionpros.com/asphalt/plants/article/10292426/blue-smoke-control-... 11/8/2017 Blue Smoke Control from Asphalt Plants Provides a Real -World Solution to Current Emi... Page 2 of 4 VIEW GALLERY Mike Butler Butler -Justice, Inc. It is often the case with a new technology that excitement over its benefits is tempered by the need for additional research before use becomes widespread. While we all know that warm mix asphalt (WMA) isn't exactly new, interest in its use is growing as certain benefits - including reduced emissions - emerge. Yet we also know that greater acceptance of WMA will take time. Forward -thinking producers have begun to view plant options that will allow production of WMA. But the routine specification of warm mix designs is still a long way off as state DOTs wait for additional research on long-term benefits. At the same time, companies that want to meet future regulations - and also be good environmental stewards and good neighbors - are looking for real -world solutions they can apply today to the problem of blue smoke produced in their existing HMA plants. A Solution Working to meet the need for better control equipment, Blue Smoke Control, a division of Butler -Justice, Inc., of Anaheim, Calif., developed its system to capture blue smoke from numerous points, including transfer points, silo filling and truck loading. The collector features seven stages of filtration, with the final high -efficiency filter being 95% efficient at capturing particles as small as .03 microns (creating a filter that is equivalent to HEPA quality). But this high -efficiency filter is only the final component of the system. Because blue smoke is a vapor at high temperatures, a well -engineered ducting system incorporates the infusion of ambient air at key points to help coalesce the tiny droplets of oil (blue smoke) into a larger droplet that can be filtered out by the Blue Smoke Collector. The coalesced oil is drained from the filters via gravity and collected in a sump. In some asphalt plants, the collector pulls as much as five gallons of coalesced oil per day from the silo filling and truck load -out areas. https://www.forconstructionpros.com/asphalt/plants/article/ 10292426/blue-smoke-control-... 11/8/2017 Blue Smoke Control from Asphalt Plants Provides a Real -World Solution to Current Emi... Page 3 of 4 Since its introduction in 2002, a growing number of companies in California and across the U.S. are aggressively installing the Blue Smoke Control system in order to become a good neighbor today - without the need to build a new plant or expand an old one. To date, Blue Smoke Control has more than 50 of its collectors installed in the continental U.S., Hawaii, Mexico and Australia. Alternative Solutions Asphalt producers have fought blue smoke over the years with a variety of filtering and collecting systems. Typical systems used over the years include electrostatic precipitators, heating ventilating and air conditioning -type (HVAC) filter units, baghouse-type devices with a bag coating substance that resembles "kitty litter," and a recycle system that directs the blue smoke laden air into the combustion zone of the asphalt plant burner. The intent of the latter is to incinerate the oil droplets. But each of these technologies has shortcomings that can create headaches of their own for producers - including their cost, efficiency, maintenance issues, waste disposal problems and fire hazards. The Concern Over Blue Smoke Across the U.S., but especially along the West Coast, environmental groups who have armed themselves with quick but questionable information that they've gained from the Internet seem eager to oppose any proposed new hot mix asphalt (HMA) plant. They ignore the fact that over the past 40 years, asphalt production has increased more than 250% while total emissions have been reduced 97%. And they ignore that in 2002, the EPA de -listed asphalt manufacturing as a source category for hazardous air pollutants. These oppositional groups have a very visible target - the blue haze that hovers over hot asphalt and carries much of the characteristic asphalt odor. We all know this haze as blue smoke. As air pollution agencies also focus their attention on blue smoke, asphalt producers across the country are preparing themselves for new regulations. Routine specification of RAP, rubberized asphalt and polymer blends creates special concern because these specialty mixes are known to produce blue smoke. At some point, after its long-term wear properties are better evaluated, WMA may be routinely specified by state DOTs, and will likely provide an answer to issues with blue smoke. But a simple and cost-effective solution available today to control blue smoke is the Blue Smoke Control system. https://www. forconstructionpros.com/asphalt/plants/article/ l 0292426/blue-smoke-control-... 11/8/2017 Blue Smoke Control from Asphalt Plants Provides a Real -World Solution to Current Emi... Page 4 of 4 Mike Butler, Butler Justice Inc. Call (714) 696-7599 ore -mail, mikebVbutlerjustice.com. https://www.forconstructionpros.com/asphalt/plants/article/ 10292426/blue-smoke-control-... 11/8/2017 lung damage from pollution - PubMed - NCBI Page 1 of 4 PubMed v lung damage from pollution Format: Summary Sort by. Most Recent Per page 20 nud Arivtaa Best matches for lung damage from pollution: DNA -damage effect of polycyclic aromatic hydrocarbons from urban area, evaluated in lung fibroblast cultures. Teixeira EC et al. Environ Pollut. (2012) Ambient particulate air pollution from vehicles promotes lipid peroxidation and inflammatory responses in rat lung. Pereira CE et al. Braz J Med Biol Res. (2007) Effects of ultrafine petrol exhaust particles on cytotoxicity, oxidative stress generation, DNA damage and inflammation in human A549 lung cells and murine RAW 264.7 macrophages. Durga M et al. Environ Toxicol Pharmacol. (2014) Sevitc 1 to our new best match sort order Search results Items: 1 to 20 of 435 1. Potential application of the oxidative nucleic acid damage biomarkers in detection of diseases. Guo C. Ding P. Xie C, Ye C. Ye M, Pan C, Cao X. Zhang S, Zheng S. Oncotarget. 2017 Sep 8;8(43):75767-75777. doi: 10.18632/oncotarget.20801. eCollection 2017 Sep 26. Review. PMID: 29088908 Free PMC Article ❑ Effect of Particulate Matter Air Pollution on Cardiovascular Oxidative Stress Pathways. 2 Rao X, Zhong J, Brook RD, Rajagopalan S. Antioxid Redox Signal. 2017 Oct 30. doi: 10.1089/ars.2017.7394. [Epub ahead of print] PMID: 29084451 3 4. Urban particulate matter stimulation of human dendritic cells enhances priming of na�ve CD8 T lymphocytes. Pfeffer PE. Ho TR. Mann EH, Kelly FJ. Sehlstedt M. Pourazar J. Dove RE, Sandstrom T. Mudway IS. Hawrylowicz CM. Immunology. 2017 Oct 16. doi: 10.1111/imm.12852. [Epub ahead of print] PMID: 29044495 Genotoxicity of airborne PM2 F, assessed by salmonella and comet assays in five cities of the Emilia- Romagna (Italy) mutagenicity monitoring network. Bocchi C, Bazzini C, Fontana F, Pinto G, Casson' F. Environ Mol Mutagen. 2017 Oct 11. doi: 10 1002/em.22141. [Epub ahead of print] PMID: 29023966 https://www.ncbi.nlm.nih.gov/puhmed/`?term=lung+damage+from+pollution 11/7/2017 lung damage from pollution - PubMed - NCBI Page 2 of 4 5 6 Biomass burning in the Amazon region causes DNA damage and cell death in human lung cells. de Oliveira Alves N. Vessoni AT, Quinet A. Fortunato RS, Kajitani GS. Peixoto MS. Hacon SS. Artaxo P. Saldiva P. Menck CFM, Batistuzzo de Medeiros SR. Sci Rep. 2017 Sep 7:7(1):10937. doi: 10.1038/s41598-017-11024-3. PMID: 28883446 Free PMC Article Protective effects of chebulic acid on alveolar epithelial damage induced by urban particulate matter. Lee KW, Nam MH, Lee HR. Hong CO, Lee KW. BMC Complement Altern Med. 2017 Jul 19:17(1):373. doi: 10.1186/s12906-017-1870-5. PMID: 28724416 Free PMC Article Ultrafine particles CUFPs) from domestic wood stoves: genotoxicity in human lung carcinoma A549 7. cells. Marabini L. Ozgen S, Turacchi S, Aminti S, Arnaboldi F, Lonati G, Fermo P, Corbella L, Valli G. Bernardoni V. Dell'Acqua M. Vecchi R, Becagli S, Caruso D, Corrado GL. Marinovich M. Mutat Res. 2017 Aug:820:39-46. doi: 10.1016/j.mrgentox.2017.06.001. Epub 2017 Jun 16. PMID: 28676265 Lung damage analyzed by machine vision on tissue sections of mice. 8. Tao C. Zhang Y. Arch Toxicol. 2017 Jul 3. doi: 10.1007/s00204-017-2023-9. [Epub ahead of print] PMID: 28674726 Air pollution and genomic instability: The role of particulate matter in lung carcinogenesis. 9 Santibanez-Andrade M. Quezada-Maldonado EM. Osornio-Vargas A. Sanchez -Perez Y, Garcia -Cuellar CM. Environ Pollut. 2017 Oct;229:412-422. doi: 10.1016/j.envpol.2017.06.019. Epub 2017 Jun 13. Review. PMID: 28622661 Particulate matter air pollution and liver cancer survival. 10. Deng H. Eckel SP, Liu L, Lurmann FW, Cockburn MG, Gilliland FD. Int J Cancer. 2017 Aug 15:141(4):744-749. doi: 10.1002/ijc.30779. Epub 2017 Jun 7. PMID: 28589567 Industrial PM2 ri cause pulmonary adverse effect through RhoA/ROCK pathway. 11. Yan J, Lai CH, Lung SC, Chen C, Wang WC, Huang PI, Lin CH. Sci Total Environ. 2017 Dec 1:599-600:1658-1666. doi: 10.1016/j.scitotenv.2017.05.107. Epub 2017 May 19. PMID: 28535594 Lung inflammation and genotoxicity in mice lungs after pulmonary exposure to candle light 12. combustion particles. Skovmand A, Damiao Gouveia AC. Koponen IK. Moller P, Loft S, Roursgaard M. Toxicol Lett. 2017 Jul 5;276:31-38. doi: 10.1016/j.toxlet.2017.04.015. Epub 2017 Apr 29. PMID: 28465192 The nexus between urbanization and PM2 5 related mortality in China. 13. Liu M. Huang Y. Jin Z. Ma Z. Liu X. Zhang B. Liu Y, Yu Y, Wang J. Bi J. Kinney PL. https://www.nchi.nlm.nih.gov/pubmed/`?term=lung+damage+from+pollution 11/7/2017 lung damage from pollution - PubMed - NCBI Page 3 of 4 Environ Pollut. 2017 Aug;227:15-23. doi: 10.1016/j.envpol.2017.04.049. Epub 2017 Apr 25. PMID: 28454017 Comparison of gene expression profiles induced by fresh or ozone -oxidized black carbon particles in 14. A549 cells. An J, Zhou Q, Qian G, Wang T, Wu M, Zhu T, Qiu X, Shang Y, Shang J. Chemosphere. 2017 Aug;180:212-220. doi: 10.1016/j.chemosphere.2017.04.001. Epub 2017 Apr 1. PMID: 28410501 PM<sub>2.5</sub>-induced alterations of cell cycle associated gene expression in lung cancer cells 15. and rat lung tissues. Zhao H, Yang B, Xu J, Chen DM, Xiao CL. Environ Toxicol Pharmacol. 2017 Jun;52:77-82. doi: 10.1016/j.etap.2017.03.014. Epub 2017 Mar 24. PMID: 28384515 TRIM36 hypermethylation is involved in polycyclic aromatic hydrocarbons -induced cell transformation 16. He Z, Li D, Ma J, Chen L, Duan H, Zhang B, Gao C, Li J, Xing X, Zhao J, Wang S, Wang F, Zhang H, Li H, Chen S, Zeng X, Wang Q, Xiao Y, Zheng Y, Chen W. Environ Pollut. 2017 Jun;225:93-103. doi: 10.1016/j.envpol.2017.03.001. Epub 2017 Mar 27. PMID: 28359976 ( 1 Risk factors for persistence of lower respiratory symptoms among community members exposed to 17. the 2001 World Trade Center terrorist attacks. Jordan HT, Friedman SM, Reibman J, Goldring RM, Miller Archie SA, Ortega F, Alper H, Shao Y, Maslow CB, Cone JE, Farfel MR, Berger KI. Occup Environ Med. 2017 Jun;74(6):449-455. doi: 10.1136/oemed-2016-104157. Epub 2017 Mar 24. PMID: 28341697 Free PMC Article ❑ Smoking modify the effects of polycyclic aromatic hydrocarbons exposure on oxidative damage to 18. DNA in coke oven workers. Yang J, Zhang H, Zhang H, Wang W, Liu Y, Fan Y. Int Arch Occup Environ Health. 2017 Jul;90(5):423-431. doi: 10.1007/s00420-017-1206-2. Epub 2017 Feb 8. PMID: 28181029 Polydatin protects the respiratory system from PM? c exposure. 19. Yan XD, Wang QM, Tie C, Jin HT, Han YX, Zhang JL, Yu XM, Hou Q, Zhang PP, Wang AP, Zhang PC, Gao Z, Jiang JD. Sci Rep. 2017 Jan 9;7:40030. doi: 10.1038/srep40030. PMID: 28067267 Free PMC Article jlmpacts of airborne particulate matter and its components on respiratory system health]. 20. Cao LM, Zhou Y, Zhang Z, Sun WW, Mu G, Chen WH. Zhonghua Yu Fang Yi Xue Za Zhi. 2016 Dec 6;50(12):1114-1118. doi: 10.3760/cma.j.issn.0253-9624.2016.12.018. Review. Chinese. PMID: 28057119 Back to top https://www.ncbi.nlm.nih.gov/pubmed/?term=lung+damage+from+pollution 11/7/2017 1. MAIN FACTS (km) pLifoict IfuLD.t.t-L HEALTH AND SAFETY ISSUES `1 n « %/k -C"L. 2. THE PLANT IS NOT A STERILE ONE- HAS STEAM, TOXINS, DUST AND GASES, METALS AND PARTICULATES 3. PM 10/ DEADLY IS PM 2.5 IT PENETRATES THE RESP SYSTEM WITHOUT BEING CAUGHT BY UPPER RESPIRATIORY SAFETY FACTORS AND IS ABLE TO PENETRATE DEEP INTO THE LOWER LOBES AND CAUSE PERM DAMAGE 4/ THERE IS NO SAFE LEVEL OF PM 2.5 IT CAUSES THE MOST DAMAGE FACT 48 TOXIC COMPOUNDS, METALS, PARTICULATES AND GASES ARE FORMED AT THIS SITE AND PUT INTO THE ENVIRONMENT 1. LETTER FROM DR PATEL- DOCUMENTED AND PUBLISHED ARTICLES ON PM 2.5 2. POLLUTION/ DUST ON LUNG EFFECTS NATIONAL JEWISH ----40 PUB MED ARTICLES 3. OCC HEALTH ARTICLES OSHA SITE HANDBOOK MSDS... EPA SILICA WARNINGS 4. Main health issues - 5. NOISE LEVEL TO STAY AT RES LEVEL. LIMIT WORK HOURS TO 7A -7P WE HAVE A RIGHT TO SLEEP/ KIDS SAFETY/ BE OUT IN NEIGHBORHOOD -WALK DOG WITHOUT HEAVY TRUCK TRAFFIC OR DANGERS 6. LEACHING OF SITE WITH BENZE, LEAD AND FORMALDEHYDE 7. WE ARE OVERSERVICED !N THE AREA OF CEMENT/ ASPHALT PLANTS -WHAT IS THE RUSH TO PUT THIS HERE.. THIS IS A WANT BY SIMON....NOT A NEED FOR THE AREA.. NEED COMPATIABILITY STUDY BEFORE DECISION.. --- 8. IF THEY ARE WILLING TO HAUL WATER OFF SITE.. THEY SHOULD BE WILLING TO USE THEIR FORT MORGAN SITE AS A HIGH VOLUME SITE FOR OVERTIME AND LARGER PROJECTS. 9. POORLY THOUGHT.. OIL AND GAS WELL W FRACKING 300 FT FROM A ASHPHALT AND HOT OIL STORAGE AREA WITH A PROPANE TANK THE SIZE OF A SMALL SUBMARINE= EXPLOSION POTENTIAL WHAT IS THE SITE STUDY, EVACUATION AND HYDRANT HAZMAT PLANS? OR IS IT THE GENERAL 10. EPA IS TO MONITOR SUCH INDUSTRIES BUT OUR DOCTORS AND HOSPITALS ARE THE ONES WHO CARE FOR THE RESIDENTS AND PUBLIC AT LARGE THAT DEVELOPS SYMPTOMS LUNG DISEASE AND CANCER FROM SUCH SITES. It is notable that medicine and practicing doctors be allowed to have imput on the safety as well as PUB Med. JAMA, New England Journal of Med. 11. Benzene handout and peaches into water table.. "fund set up for contamination clean up efforts 12. Condit- work time 7a -7p 13. Odor control w cherry vanilla additives 9.0 um - lO.Opm 52 Pharynx 47pm 5r84si1 Trachea and pAmary brcnci 31 pm — 4.7 pm Secindary bronci 2.I pm 13 pm Terminal bronc•i 6.1 t�111 a 2.a 1,:rn 0.65 pm fl PREGNANT WOMEN EARl/LUNG E: DIABETES IVES IORS LOREN FANTS ATRISKPEOPIE/INCREASED EFFECTS Nat- • • • • • • • Q • • • . • •* • •.° • ASTHMA ist a PREMATURE INFANT MOF REARI DISEA RESP ILLNE LUNG PREMA DEATH ng ozone can trigger chest pain, coughing, throat irritation. and worsen emphysema and asthma. particulate pollution can result in respiratory illness, cardiovascular disease (heart disease and strokes )n death. (Source: Ozone Basic Information. U.S. EPA/ Particulate Matter. Basic Information. U.S. EPA) Particulate Matter (PM) liar CASSIPA.•Sef ..ad..Nq..a PM is a complex mixture of extremely small particles and liquid droplets Chemically it comprises a number of components including acids (such as nitrates and sulfates), organic compounds (OC), elemental carbon (EC), transition metals, soil, fugitive dust and sea -spray. Fine fraction Coarse fraction (PM25) • Etarratal sad ° maak Cartes o Sulphate p Nitrate • traaranhun ■ C rl.rldrc is Insoluble ■nt,acrab ■ Ns. K.Mt. (;a (PM2 5-PMlo) Approximate chemical composition of Particulate Matter N PM size is directly linked to their potential for causing health problems. The smaller the more lethal. The Magnitude and Source of Air Emissions from Asphalt Blowing Operations David C. Trumbore Owens Coming. Asphalt Technology Laboratory, Summit. 11.60501 The US EPA has developed emission factors for estimating the emissions of filterable particulate, total organic compounds, and carbon monoxide from asphalt blowing operations These are published by the EPA in a series called AP -d2, which con- tain factors for many manufacturing processes. The emission factors for asphalt blowing are acknowledged by the EPA to be of poor quality. Owens Corning has taken extensive data in various manufacturing facilities and an asphalt Pilot Plant to provide more information on air emissions from these opera- tions. The results of that work clearly show that the current AP - 42 emission factors for asphalt processed by air blowing are deficient in that they omit significant emissions of SO1 and overestimate particulate and CO emissions, and potentially underestimate both VOC and NO„ emissions. In fact, SOc which is not addressed by AP -42, is the major air emission contributed by the fumes from fir asphalt blowing process when those fumes are incinerated The sources of SO„from air blowing are discussed in detail in this paper. The impact of incineration temperature on carbon monoxide is dso illustrat- ed With the exception of hU, the hazardous air pollutants encountered in tie asphalt blowing process are minimal. INTRODUCTION The use of asphalt as a material is prevalent throughout recorded history. The commercial use of air blown asphalt, also known as oxidized asphalt, dates from the late 19th century ( I j. Oxidized asphalt is produced by blow - ing air through hot petroleum residuum. which can core from vacuum dis- tillation tow ers. atm ospheric tow ers or solvent extraction units. A t the start of the batch. input residuum is typically pum ped through a direct fired non - contact preheater to achieve tern peratures over 400°F (204°C), and into reac• lion vessels called oxidizers, or alternately, stills or convertors. Air is injected into the oxidizer and dispersed through perforated pipes. Air flow is typically in the range of 15 to 50 cfm /ton (0.008 to 0.026 m 3/sec/Mg) of asphalt and the oxidizer is typically operated between 400 and 550°F (between 204 and 288°C) [2]. Oxygen is consumed by the reaction of air with the petroleum residuum, resulting in fumes exiting the oxidizer at less than 10% oxygen content. Many theories exist as to the specific chemistry of the asphalt blow- ing reaction, with no consensus as to what is really happening. It is clear that in the asphalt blowing reaction oxygen functionality is added to the asphalt molecules; the apparent molecular weight of the asphalt increases; and compounds like hydrogen sulfide, methane, water, carbon monoxide, and carbon dioxide are released [3,4,5]. In addition to the gases formed, the high air flows both evaporate and entrain oily materials from the residuum, which can condense further down the process. fhese are referred to in this article as process oils. Fumes from asphalt blowing processes are typically treated with a variety of separation devices to remove condensing or entrained process oil, and then are incinerated. The most commonly used catalyst for the reaction is ferric chloride, although most oxidized asphalt is produced without any catalyst. Air blowing of residuum results in an increase in Ring and Ball Softening Point (ASTM D36) and Brookfield Viscosity (ASTM D4402), and a decrease in Penetration (ASTM 05). The product is unique in that its combination of properties cannot be produced by any other refinery process. That is, if the softening point of the residu- um is raised by distillation or solvent extraction the material is far more brittle than if the softening point is raised by air blowing. Oxidized asphalt is used for the manufacture of asphalt shingles; and in built-up roof construction, adhesives, corrosion protection, waterproofing, and a wide variety of specialty applications. The two highest volume prod- ucts made using this process, shingle coating and BURA Type III asphalt, typically see a softening point increase during the blowing process from an initial value of less than 100°F (38°C ) to a final value of 200°F (93 °C) or higher. Title V of the 1990 Clean Air Act required the accurate estimation of emissions from all U.S. manufacturing processes, and placed the burden of proof for that estimate on the process owner. In response to Title V, Owens Corning (OC) analyzed existing data and conducted extensive testing of their asphalt blowing processes in plant and pilot plant scale to develop the best possible emission factors. This paper is the result of that work, and it is our hope that it will lead to improved AP -42 emission factors for the asphalt blowing process. Environmental Progress (Vol.17, No.1) Table 1. Test Methods Used in Sampling Air Blowing Emissions EPA Method # Items Measured Using Method Sample and velocity traverses 2 Stack gas velocity & flow 3 Dry molecular weight 3 A Oxygen & Carbon dioxide 4 Stack moisture 5 Particulate 5A Particulates 6C Sulfur oxides 7E Nitrogen oxides 10 Carbon Monoxide 25A Total gaseous organic (VOCs) 26 Hydrogen chloride 26A Hydrogen chloride 29 Inorganic compounds 202 Condensible particulate 0010 Semi -volatile HAPs TEST METHODS Testing of emissions from Owens Coming's asphalt blowing processes was done using the EPA test methods outlined in Table 1. AP -42 Emission Factors The Emission Factor and Inventory Group (EF1G) in the U. S Environ- mental Protection Agency's (EPA) Office of Air Quality Planning and Stan- dards (OAQPS) develops and maintains a database of emission factors for manufacturing processes. These emission factors are published in a series known as AP -42 [6]. As part of this process the emission factors have been assigned a quality rating. AP -42 emission factors for limited pollutants exist for the asphalt blowing process [7]. The factors are available for ftlterablepar- ticulates (PM), total organic compounds (VOC), and carbon monoxide (CO). They are summarized in Table 2. These emission factors have been assigned "D" or `E' ratings, indicating they are no better than "Engineering Judgment" in acaiacy. More specifically a "D" rating indicates below aver- age quality based on a small number of possibly non-random facilities with evidence of test variation. An "E" rating indicates poor quality based on unproved test methods, and issues with a low number of data points, ran- domness, and variability. An 'E' rating is the lowest rating given to emission factors by AP -42 [61 The asphalt blowing AP -42 factors are for both satu- rant and coating asphalt manufacture. The rest of this article only addresses the coating factors, which are larger in proportion to their longer processing times. Owens Corning Plant Testing Results The results of emission testing for Criteria Pollutants done on 33 differ- ent occasions in 14 different Owens Coming plant locations are shown in Table 3. The processes shared common process conditions: 15 to 30 cfm/ton (0.008 to 0.016 m3/sec/Mg) air injection and 460 to 510°F (238 to 266°C) reaction temperature, common control equipment (fumes bubbled through a liquid seal in a knock out tank followed by gas fired incineration in an incineration chamber designed for adequate turbulence), and were processed to a common end point (coating asphalt). Widely variable input petroleum residuum were used in the tests. There was no catalyst used in any of the tests reported in Table 3. In all but one case, each data point is the average of three determinations, taken during three separate process times, with the same input residuum, under as similar as possible process condi- tions. The exception to that is the case of the PM data for plant J from 1984 to 1994. In this case an average of 83 different determinations were used to avoid skewing the overall PM data for only one plant configuration. Averages and other statistics for each criteria pollutant are given at the bottom of Table 3. The arithmetic mean and median are included for each pollutant. The geometric mean is also included in Table 3, and could in some cases be appropriate because of the exponential nature of the depen- dence of the emissions data on some process conditions. As can be seen in Table 3, the arithmetic mean is the most conservative estimate and all further analyses in this paper use it as the most representative value of the data set. These data are the basis of what we believe to be improved emission factors for asphalt blowing, and in lieu of other available data, we recommend the arithmetic means be accepted as new emission factors for asphalt blowing with gas incineration. When used to estimate emissions, the emission factors are adjusted depending on the configuration and the amount of data existing for that particular plant. For example, the average value plus two or three standard deviations are often used to ensure that the estimate is greater than the actual emission. CONTRIBUTION OF INC1NERAT1ON FUEL TO EMISSIONS I u apply the data of Table 3 to p u ss using fud oil, rather than natur- al gas, for incineration requires that the contribution of the fuel burned be recognized This is done by calculating the incremental emissions from the Pollutant Table 2. US EPA Emission Factors for Asphalt Blowing Emissions from AP -42 (7) Method Control Equipment Saturant Asphalt Coating Asphalt Emission Factor Rating Filterable PM Filterable PM Total Organic Compounds Total Organic Compounds Carbon Monoxide Carbon Monoxide EPA 5A EPA 5A EPA 25A EPA 25A none incineration none incineration none incineration 6.6 lb/ton' 0.27 lb/ton 1.3 lb/ton 0.0043 lb/ton I lb/ton = 0.5 kg/Mg 2unclear what product was manufactured. 24 lb/ton 0.81 lb/ton 3.4 lb/ton 0.017 lb/ton 0.27 lb/ton2 3.7 lb/ton2 E D E D E E 54 Spring 1998 Environmental Progress (Vol. 17, No. I) Table 3. Emission Factor Data for Asphalt Blowing to Coating with Gas Incineration Plant SOx (lb/ton) A A B C C C D F F F H i I 1 1 1 h L L L M M M M M M M M M N P P S Co (lb/ton) NOx (lb/ton) VOC PM Comments (lb/ton) (lb/ton) Year Tested 0.63 0.43 0.06 0.88 0.72 0.07 0.11 0.95 0.08 0.84 0.09 0.02 0.66 0.002 0.08 0.01 0.86 0.95 0.65 0.34 0.77 0.33 0.10 0.02 0.05 1.03 3.2 0.03 0.76 0.95 0.93 1.15 1.15 0.17 0.12 0.01 0.02 0.21 0.12 2.00 0.04 Summary SOx Arithmetic Mean Geometric Mean Median Std Dev Arith. Mean+3s Minimum Maximum Number 0.08 0.02 0.002 0.17 0.02 0.06 0.08 0.07 0.07 0.07 0.06 0.01 0.18 0.05 0.10 0.14 0.11 0.18 0.02 0.08 0.12 0.11 0.002 0.02 0.001 0.04 0.23 0.25 0.03 0.06 0.07 0.07 0.04 0.03 0.002 0.06 al NOX YQC PM 0.86 0.59 0.05 0.03 0.10 0.84 0.18 0.04 0.01 0.08 0.87 0.27 0.05 0.02 0.07 0.16 0.83 0.03 0.03 0.06 1.34 3.09 0.16 0.14 0.29 0.63 0.002 0.02 0.001 0.02 1.15 3.20 0.12 0.10 0.25 12 18 11 12 24 Incinerator @1550F Incinerator @1550F 3 oxidizers 2 oxidizers 2 oxidizers Incinerator @ 1400F Incinerator @ 1450F Incinerator @ 1500F 2 oxidizers 1996 2 oxidizers 1996 1996 1988 1994 Incinerator @ 15001. 1992 1988 1990 1990 1990 2 oxidizers 1994 1993 Incinerator @ 1625F 1993 average of 83 PM tests 1984-1994 Incinerator @1550F 1992 1995 1986 1993 1994 1997 1992 1988 1994 1995 1996 1995 1995 1995 1995 1996 2 oxidizers 1984 1993 4 oxidizers 1993 '1 lb/ton = 0.5 kg/Mg, °C = (°F-32)*5/9 alternate fuel by using AP -42 emissions factors for combustion [891 and adding that source of emissions to the data in Table 3 for gas incineration. The incremental emissions subtract the gas combustion emissions from the fuel al cantxrsstion emissions. Table 4 contains asphalt blowing emission favor data measured in four plats using heavy fie! oil. To illustrate the tech- nique descnlbad above, the average of the measurements in these plants is compered to an average predicted by adjusting the gas incineration average Fran Table 3 with lid oil emissions fa a typical fuel oil usage rate. Environmental Progress (Vol. 17, No. 1) Spring 1998 55 Table 4. Evaluation of Emission Factors for Air Blowing Coating Asphalt with Heavy Fuel Oil Incineration Plant SOx CO NOX VOC PM Year (1b/ton)' (lb/ton) (lb/ton) (lb/ton) (lb/ton) F Q Q Q X P 1.38 1.14 1.50 2.87 0.31 0.02 0.00 1.25 0.37 0.12 0.19 0.04 0.15 0.01 0.01 0.01 0.00 0.03 1985 0.28 1989 0.30 1994 0.35 1994 0.09 1993 1993 Average 1.72 0.39 0.13 0.01 0.21 1lb/ton = 0.5 kg/Mg Gas Data Averages from Table 3 Adjusted fir Biel Oil Emissions. SOx Co NO, VOC PM (Ib/ton)1 (lb/ton) (lb/ton) (lb/ton) (lb/ton) 1.53 0.60 0.14 0.03 0.14 CRITERIA POLLUTANT SUMMARY Table 5 summarizes the comparisons between current AP -42 emission factors for asphalt blowing, the data gathered by Owens Coming on 33 occa- sions in 14 plants using gas incineration, and estimated values for the contri- bution of the gas fuel that is burned in the incinerator. The key conclusions from this comparison follow 1. It is clear from the data in Table 5 that the omission of a sulfur oxide (SOt) emission factor for the asphalt blowing process from AP -42 ignores what is usually the largest criteria pollutant from this process. The average value in all our testing is 0.86 lb SO/ton asphalt (0.43 kg/Mg) with gas fueled incinerators without using catalysts. This represents a significant route of SOx that should be accounted for in all asphalt blowing operations. 2.The AP -42 factor for carbon monoxide (CO) of 3.7 lb/ton (1.85 kg/NV is obviously based on poor incineration as it is excessively high for normal processes In all of our testing on gas systems with adequate incirrera- tion turbulence and without any catalyst the average CO factor was 0.59 lb/ton (0.295 kg/Mg). Our one value close to AP -42, 3.2 lb/ton (1.6 kgt in plant M. was reduced to less than 0.2 lbWton (0.1 kg/Mg) by rais- ing the incineration temperature 100 °F (38°C). The sensitivity of CO to incineration temperature will be disaEsed below. 3.The AP -42 factor for volatile organic compounds (VOC) of 0.017 lb/ton (0.0085 kg/Mg) is achievable (5 out of 12 measurements we took went less than that value), but is approximately one half of the average mea- sured value. This factor should be increased. 4. The AP -42 value for particulate material (PM) is much too high. Our largest reading in 24 tests was still less than 1/3 the AP -42 value and our aver- age was 11 the AP -42 value. 5. The contribution of fuel burning to nitrogen oxide (NO%) emissions gives an order of magnitude estimate of NO, emissions in the asphalt blow- ing process. Some additive emissions appear to be warranted from the data, but this omission from the AP -42 factors is not a serious one. 6. Based on comparisons in Table 4, asphalt blowing emission factors based on gas incineration systems can be used as approximate estimates for systems using alternate fuels by adding the emission contribution of the alter- nate fuel calculated using AP -42 for combustion. SOURCES OF SPECIFIC ASPHALT BLOWING EMISSIONS Sulfur Oxides SO, emissions in the asphalt blowing process come from three sources: I .The fuel used to incinerate the asphalt blowing fumes contains sulfur compounds which are oxidized on incineration to produce SOx emissions. 2. Some process oil is carried over as condensable vapor or droplets in the fume stream and, when burned, the sulfur, which exists primarily as thio- phenes, is oxidized to produce SO, emissions. 3. Hydrogen sulfide (H,S) is formed in the asphalt blowing process and that material oxidizes in the fume strew n and in the incinerator to produce SOx emissions. The incineration fiel component is quite small when using nab as shown in Table 5. Estimates of the magnitude of the other two compo- nents can be made from observations of results of experiments to reduce these emissions The use of H,S scavengers in the asphalt blowing process to tic up the H2S component of the emission has been seen to give a maximum reduction in SO emissions of about 70 to 80% in a gas incineration situa- tion [ 10). This would indicate that the contribution of the release of 1-12S in the process is about 70 to 80% of the emission in a gas incineration system. Similarly, unpublished work with filtration of pilot scale asphalt blowing fumes indicated that completely eliminating droplet carryover in an asphalt blowing process with gas incineration reduced SO, emissions by 20 to 30%. Therefore, in a gas incineration system the contributions to SO% emissions could reasonably be estimated as indicated in Table 6. Table 5. Summary of Emission Factors for Asphalt Blowing Process Making Coating SO% (lb/ton)' Co (lb/ton) NO% (lb/ton) VOC (lb/ton) PM (lb/ton) AP -42 Factor (Table 2) Average OC Emission for Gas Incineration (Table 3) Range of OC Values (Table 3) Contribution from gas fuel estimated with AP -42 (8) omitted 0.86 0.63 to 1.15 0.0002 3.7 omitted 0.017 0.81 0.59 0.002 to 3.2 0.05 0.03 0.02 to 0.12 0.001 to 0.10 0.10 0.02 to 0.25 0.007 0.03 0.002 0.004 Table 6. Sources of SOx in Asphalt Blowing - Table 7. Effect of Incineration Temperature on Carbon Monoxide Emissions Typical Values Source of SOx Typical Contribution Gas fuel for incinerator H2S release from Asphalt During Blowing Carryover of process oil containing thiophene sulfur <0.1% of the total SOx 70 to 80% of the total SO 20 to 30% of the total SOx 0.5 0.45 0.4 0.35 0.3 0.25 0.2 0.15 0.1 1.5 2 2.5 3 3.5 lapnt Asphalt Soifer Content(%) Y axis denotes SOx Emission (lb/ton Is Pilot Plant) 4 45 FIGURE 1. Correlation of input asphalt sulfur content With SOx emissions. Eight different crude sources used in study. Correlation coefficient = 0.09(1 lb/ton = 0.5 kg/Mg). Because of the strong contribution of some input petroleum residu- um sulfur to SOx. an investigation was done to determine if the total sulfur content of input residuum, which is easily measured, would cor- relate with SOx emissions. To determine this a series of input residuum made with different crude oils were brought to Owens Corning's asphalt blowing pilot plant and oxidized under identical conditions, with determination of emission factors for SOx. The results of these tests are shown in Figure 1, a plot of pilot plant SOx emissions versus total sulfur content of the input asphalt. It is clear that no correlation exists, implying that only a small, unidentified, component of the sul- fur in the asphalt is responsible for the 142S release and subsequent SOx emission. Plant M M M 1.2 L CO Emission Incineration Factor Temperature (lb/ton)' (°F)' 1.15 1400 0.17 1450 0.12 1500 2.15 1450 0.17 1550 �I Ib:tun = 0.5 kg/M g. °C = CF -32)85/9 - The L plant data was taken with ferric chloride as a catalyst and is therefore not included in the Table 1 data set. Carbon Monoxide Large amounts of carbon monoxide can be emitted from the asphalt blowing process when the incineration conditions are less than optimum in terms of residence time, incineration temperature and fume turbulence. In Table 7 the efleui of incineration temperature is shown for two asphalt blow- ing processes where the incineration residence time and turbulence are acceptable. As can be seen, the emission of carbon monoxide is wry sensitive to a relatively small change in temperature. In general, we have found that for incinerators with more than 0.5 seconds of residence time and chambers designed to promote turbulence, incineration temperatures in the 1450 to 1550°F (788 to 843°C) range are necessary to achieve very low CO levels. From the data in Table 7, plant M needs to run at least 1450°F (788°C ) while plant L needs to run 1550°F (843°C) to achieve emission factors under 0.2 lb/ton (0.1 kg/Mg). A small amount of CO is detectable in the flutes prior to the incinerator, but the major source for CO emissions is incomplete combustion of hydro- carbons to (bon dioxide (CO3). Hydrocarbon Emissision - Particulate and VOCs From the description of the asphalt blowing process, it is not surprising that the fumes entering the incinerator contain significant amounts of hydrocarbons. The reactions that occur in the process create lower molecular weight hydrocarbons that remain as vapor or condense at some point in the fume system. The incineration process does a good job of combusting these Table 8. Measured Incineration Destruction Efficiencies for Hydrocarbons in the Air Blowing Process Plant # Samples Averaged Residence Time (seconds) Incineration Temperature Destruction Efficiency (OF)1 C S S S S 3 4 4 5 4 0.7 0.5 1500 1500 1500 1500 1500 98.9% 98.1% 97.9% 98.7% 99.2% '°C = (°F-32)=5/9 Environmental Progress (Vol.17, No.1) Spring 1998 57 Table 9. Sampling Data for HAPs Emissions from Asphalt Blowing (1 lb/ton = 0.5 kg/Mg). Plant Year Fuel Comments Hazardous Air Pollutant Hydrogen chloride Ggneral Inorganic HAPS Antimony Arsenic Bery l lium Cadmium Chromium Cobalt Lead Manganese Nickel Phosphorus Selenium General Organic HAPS Benzene Toluene Ethyl Benzene Xylene III TCE methyl chloride vinyl chloride ethyl chloride methylene chloride chloroform Di-n-butylphthalate Dibenzofuran bis(2-ethylhexy l )phthalate isophorone 4-nitrophenol phenol o -cresol p -cresol Polycyclic Organic Matter 2-methylnaphthalene Acenaphthene (ACEP) Acencphthylene (ACEY) Anthracene (ANTH) Benz (A) anthracene (BENA) Benzo (B) Fluoranthene (BENB) Benzo(G,H,1) Preylene (BENG) Benzo (K) Floouranthene (BENK) Benzo (A) Pyrene (BEZA) Benzo(e)pyrene Chrysene (CHRY) Dibenz (A,H) Anthracene (DIBN) Fluoranthene (FLUO) Indeno (1,2,3-C,D) Pyrene (INDE) Naphthalene (NAPH) Phenathrene (PHEA) Pyrene (PYRE) O P L L Q Q M 1992 1990 1984 1994 1994 1994 1994 1995 gas gas gas gas gas BD Oil #5 Fuel gas Ferric No Ferric Ferric (Ih/ton) (lb/ton) (lb/ton) (lb/ton) (lb/ton) (lb/ton) (lb/ton) (lb/ton) 0.0E+00 0.0E+00 4.2E-05 0.0E+00 2.6E-04 1.3E-02 0.0E+00 6.7E-09 0.0E+00 0.0E+00 0.0E+40 0.0E+00 0.0E+00 0.0E+00 0.0E+00 0.0E+00 0.0E+00 0.0E+00 5.9E-06 0.0E+00 0.0E+00 M 1995 gas No Ferric (lb/ton) 8.2E-03 2.5E-01 3.6E-02 8.4E-03 7.7E-03 1.9E-01 4.0E-02 1.0E-06 8.5E-07 8.5E-09 5.7E-07 3.2E-05 3.2E-06 5.5E-06 2.8E-04 4.1E-06 8.1E-07 8.2E-04 I.3E-04 2.1E-04 8.7E-05 5.5E-05 1.3E-03 1.0E-04 2.5E-06 3.8E-05 9.6E-06 3.0E-06 1.6E-05 1.4E-05 2.4E-06 8.7E-06 7.7E-07 2.8E-06 6.3E-07 6.3E-07 6.2E-09 6.2E-09 4.3E-06 4.1E-06 7.3E-06 7.4E-07 8.9E-06 2.2E-06 1.3E-05 4.7E-05 4.1E-06 9.9E-05 2.4E-04 6.3E-06 2.2E-06 2.5E-06 6.3E-07 6.3E-07 .5E-03 8.8E-05 7.9E-04 9.7E-05 7.7E-05 1.3E-03 1..2E-04 3.0E-06 6.1E-06 8.4E-06 2.5E-06 I.1E-05 7.4E-06 2.5E-06 5.7E-06 9.0E-04 1.2E-05 3.4E-04 1.2E-05 1.0E-02 1.2E-02 1.7E-04 9.0E-06 2.1E-05 2.2E-05 2.1E-05 4.7E-06 4.6E-08 8.2E-08 3.6E-05 2.5E-06 2.7E-07 8.4E-08 2.5E-08 6.7E-09 2.5E-09 5.6E-08 8.0E-09 6.2E-09 7.1E-09 7.9E-09 2.0E-08 2.2E-08 1.0E-08 1.4E-08 1.3E-05 2.5E-06 6.5E-09 2.0E-08 5.3E-05 2.5E-05 8.0E-05 6.9E-06 7.3E-06 2.5E-06 8.9E-07 9.9E-07 6.4E-08 6.4E-07 7.8E-09 1.8E-08 58 Spring 1998 Environmental Progress (Vol.17, No.1) ) to CO and CO2 as indicated by the data in Table 8, which was taken by measuring total hydrocarbons entering the incinerator and total leaving to get a destruction efficiency. Because of the nature of the process there is an insignificat amount of inorganic components in the particulate emissions. HAZARDOUS AIR POLLUTANTS TEST RESULTS In addition to testing on criteria pollutants, Owens Corning has done extensive testing on the emissions of hazardous air pollutants (HAPs) from the asphalt blowing process. This testing, done in six plants on nine occa- sions, is summarized in Table 9. On different occasions four basic classes of HAPs have been measured: I. hydrogen chloride, 2. general inorganic HAPs, 3. general organic HAPs, and 4. polycyclic organic matter (POM). Table 9 is organized around those groupings. The data show that the use of ferric chloride as a catalyst significantly increases hydrogen chloride emissions from the 0.007 to 0.04 lb/ton (0.0035 to 0.02 kg/Mg) emission factor level without ferric chloride use to 0.19 to 0.25 lb/ton (0.095 to 0.125 kg/Mg) with the catalyst This is an important omission from AP -42 and should be added for ferric chloride catalyzed asphalt blowing. The source of this chloride is fine HO in the ferric solution and the reaction of ferric chloride to ferrous chloride as part of the mecha- nism of catalysis1111. 1 11. Only a fraction of the HCI available from these tw o sources is actually evolved. The rest takes part in as yet unidentified reactions in the asphalt. Emissions of general inorganic materials can be seen to be very small. in the range of 0.000000006 to 0.0002 lb/ton (0.000000003 to 0.0001 kg/M g). Emissions of general organic materials were very In with the exception of ethyl benzene and one measurement of benzene. w hich were in the range of 0.01 to 0.013 lb/ton (0.005 to 0.0065 kg/Mg). Clearly more severe incineration conditions can reduce these values. and this is indicated in other measurements of benzene emissions which were as low as 0.000012 lb/ton (0.000006 kg/Mg). Emissions of POM were all extremely low ranging in measurement from 0.000000005 to 0.00008 lb/ton (0.0000000025 to 0.00004 kg/Mg). CONCLUSIONS From the data presented in this paper the following conclusions have been reached: 1. Current AP -42 emission factors for asphalt blowing ignore important emissions of sulfur oxides. This is usually the largest emission from the process. The emission of sulfur oxides are not correlated with total sulfur in the input residuum. In a gas incineration system the source of sulfur oxides are approximately 70 to 80% from l l2S released in the asphalt blowing reac- tion, 20 to 30% from entrained or condensing oils, and almost no contribu- tion from the fuel used for incineration. 2. Current AP -42 emission factors for asphalt blowing ignore hydrogen chloride emissions, which are important when ferric chloride is used as a cata- lyst in the process. 3. Current AP -42 emission factors for asphalt blowing overestimate the emissions of particulate and carbon monoxide in a well designed process. Carbon monoxide emissions can be dramatically reduced with small inc ee s ' incineration temperature above a certain threshold temperature, timismamme in an incinerator with adequate residence time and turbulence. In our experience that threshold temperature is approximately 1400 to 1500°F (760 to 816 °C). 4. Emissions of hazardous air pollutants, other than hydrogen chloride, from the asphalt blowing process are insignificant LITERATURE CITED I. Byerley, F.X., U.S. Patent 524,130 (Aug. 1894). 2. Corbett, L.W., "Manufacture of Petroleum Asphalt", Chapter 4, in "Bituminous Materials: Asphalts, Tars and Pitches, Volume H: Asphalts", edited by Arnold Hoiberg, Robert Krieger Publishing Co., Huntington, New York (1979). 3. Boduszynski, M.M., "Asphaltenes in Petroleum Asphalt: Composition and Formation", Chapter 7, in "The Chemistry of Asphaltenes", pp. 119 to 135, American Chemical Society, Washington, D.C. (1981). 4. Haley, G.A., "Changes in Chemical Composition of a Kuwait Short Residue during Air Blowing", Analytical Chemistry, 47 (14), pp. 2432-2437, (Dec. 1975). 5. Corbett, L.W.. "Reaction Variables in the Air Blowing of Asphalt", Ltd Eng. Chem Process. Des. Dev., I4 (2), pp. 181-187,(1975). 6. U.S. Environmental Protection Agency, "Introduction to 5th edition of AP -42 Emission Factors", U.S. EPA, January, 1995, from the Internet at http://www.epa.gov/ttn/chief/ap42m enu.htm l (accessed 8/8/97). 7. U.S. Environmental Protection Agency, Chapter 11 of the 5th edition ofAP-42 Emission Factors, U.S. EPA, "Mineral Products Industry, Section 2, Asphalt Roofing" Tables 11- 2.2 and 11-2.4, January, 1995, from the Internet at http://www.epa.gov/ttn/chief/ap42menu.html (accessed 8/8/97). 8. U.S. Environmental Protection Agency, Chapter 1 of the 5th edition of AP -42 Emission Factors, U.S. EPA, "External Combustion Sources - Section 4, Natural Gas", Tables 1.4- 1,2 &3, October, 1996, from the Internet at http://www.epa.gov/ttn/chief/ap42menu.htmI (accessed 8/8/97). 9. U.S. Environmental Protection Agency, Chapter 1 of the 5th edition ofAP-42 Emission Factors, U.S. EPA, "External Combustion Sources - Section 3, Fuel Oil", Tables 1.3-1,2, October, 1996, from the Internet at http://www.epa.gov/ttn/chief/ap42menu.html (accessed 8/8/97). 10. Marzari, J. A., M. Franzen, and J. Smith, "Method for reducing sulfur emissions in processing air -blown asphalt", U.S. Patent 5,611,910 (Mar.18, 1997). 11 Kudryavtseva, 1.N., D. Rozental, and V. Proskuryakov, "Influence of ferric chloride on oxidation of bitumens and their components", Lensovet Leningrad Technological Institute. Translated from Diurnal Prikladnoi Khirnii, 44 (10), pp. 2229-2235, (Oct. 1971). Environmental Progress (Vol. 17, No. 1) Spring 1998 59 I' O Wirierre A Missouri Department of Natural Resources "Integrity and excellence in all we do' Air Quality Construction Permits If you want to set up or change an asphaltic concrete (hot mix asphalt) plant, you probably need an air construction permit from the Missouri Department of Natural Resources or local air pollution control agency office. If so, you must have this permit before you begin construction, set up or modification of your asphalt plant. The most common air pollutants from hot mix asphalt plants are particulate matter (PM, ), sulfur dioxide (SO..), nitrogen oxides (NO), volatile organic compounds (VOCs), carbon monoxide (CO) and hazardous air pollutants (HAPs). PM._ is particulate matter with a diameter of no more than 10 microns. National Ambient Air Quality Standards (NAAQS) limit the concentrations of PM._. SO_, NO and CO in the air to protect public health. The construction permit rule applies to any asphalt plants set up, constructed or modified after May 13, 1982, that have potential emissions of any pollutant exceeding the deminimis level. Potential emissions are calculated assuming the plant operates at maximum capacity 24 hours per day, 365 days per year. For PM,,; the deminimis emissions rate is 15 tons per year. For NO„ SOS and VOCs it is 40 tons per year. For CO it is 100 tons per year. And for HAPs it is 10 tons per year for any individual HAP and 25 tons per year for the combination of all HAPs released from the installation. To get this permit, you need to complete air construction permit application forms and submit the forms to the Department of Natural Resources' Air Pollution Control Program (APCP) or your local air pollution control agency, listed below. Application forms in the Application for Authority to Construct include Emissions Unit Information forms and worksheets for storage piles, haul roads, fuel tanks and heaters. Applications must also include the location of the plant and a drawing or map of the site layout with the length and position of haul roads, storage piles and plant equipment. You will need to list the process equipment that will be used. the date it was manufactured, the serial number and the maximum rated design performance of each piece of process equipment. If you haven't purchased the equipment, describe the plant you intend to set up with detailed equipment specifications. You will also be asked the expected daily and annual asphalt production and fuel use. The application fee is $100, and technical review time is charged at $50 per hour. New portable plants are permitted using the same procedure, except that portable plants may have multiple sites permitted in their original construction permit by including information on each proposed plant site with the application. A plant with a portable construction permit may operate indefinitely at the first permitted site, but upon moving the equipment to a new site, it may not operate more than two years without applying to convert to a stationary plant. Relocation of permitted portable plants requires a Portable Source Relocation Request to the APCP or the local agency. If the site was approved in the initial permit, the relocation request is processed in seven days. If it is a new site, the request may take up to 21 days to process and ambient impact analysis is required. A $200 review fee is also required. When the APCP or the local air pollution control agency receives a permit application, the staff reviews it for completeness. This is called the administrative review. Administrative review will take no more than 30 days. However, if the application is incomplete, the total time from your t original submittal to final approval may be longer. If the application is found to be incomplete, you will receive a request for more information. When that information is received, the administrative review may take up to an additional 30 days. Once the agency determines that the application is complete, the staff will conduct a technical review. There are different types of permits and levels of permit review depending on the type of operation being permitted. The length of time needed for technical review of your permit application will depend on the type of permit. Construction permit applications for a typical asphalt plant can take up to 90 days to process. although most take less time. Again, the 90 -day clock stops each time the permit is returned to you for corrections or revisions. Air Pollution Control Agencies City of St. Louis: Division of Air Pollution Control (314) 613-7300 St. Louis County: St. Louis County Department of Health (314) 615-8983 City of Springfield: Air Pollution Control Authority (417) 864-1000 Kansas City: Kansas City Health Department Air Quality Section (816) 513-6314 Elsewhere in Missouri: Department of Natural Resources Air Pollution Control Program (573) 751-4817 Remember r An air construction permit is probably needed before setting up, constructing or modifying a hot mix asphalt plant. It can take several months to get this permit. For More Information Missouri Department of Natural Resources Environmental Assistance Office P.O. Box 176 Jefferson City, MO 65102-0176 1-800-361-4827 or (573) 526-6627 www.dnr.mo.9ov/oac/env assistance.htm EMECIA-1) Health Effects of Particulate Air Polk, don 2200 Wilson Boulevard * Suite 310 * Arlington, VA * (202) 296-4797 October 14, 2014 This report compiles and summarizes recent studies and research programs that have been conducted on the effects of air pollution particulate matter on human health. Executive Summary PM Effects on Respiratory and Cardiovascular Systems • Study Finds Black Carbon Linked to Increased Cardiovascular Risk (p.2) • A Systematic Review and Meta -Analysis of Outdoor Particulate Matter Exposure and Lune Cancer (p. 3) • Exposure to Particulate Pollution Associated With Lune Cancer (n. 3) • HF.I Publishes Two Comprehensive Studies on Health Effects of PM (n. 4) • China Study Shows PM 1 Air Pollution Most Harmful (p. 5) • Air Pollution Linked With Thickening of the Arteries, Cardiovascular Problems (p. 6) • Detailed diesel exhaust characteristics including particle surface area and lunE deposited dose for better understanding of health effects in human chamber exposure studies (p. 7) • Study Finds Increasing Emergency Room Visits for Stroke by Elevated Levels of Fine Particulate Constituents • Cell Cycle Alterations Induced by Urban PM2.5 in Bronchial Epithelial Cells (p. 8) • Air Pollution and Hospital Emergency Room and Admissions for Cardiovascular and Respiratory Diseases in Dona Ana County, New Mexico (p. 9) • A Case -Crossover Study on Ambient Fine Particulate Air Pollution Triggers ST -Elevation Myocardial Infarction (p. 9) • Study Associates Air Pollution to Irregular Heartbeat and Lune Blood Clots (p. 10) • Study Finds Living in Areas Polluted with Fine Particles Raises Lung Cancer Risk (p. 11) • Increased Ultrafine Particles and Carbon Monoxide Concentrations Are Associated with \sthma Exacerbation Among Urban Children (p. 12) • New Study Finds Strong Association between Exposure to Fine PM and Cardiovascular Mortality. (p. 13) • Effects of Concentrated Ambient Particles on Normal and Hypersecretory Airways in Rats (p. 13) • WHO Releases Report on Health Effects of PM (p. 151 t Itrafine PM • Researchers Publish Study on PM2.5 Constituents and Hospital Visits in Shanghai (p. 15) • Epidemiological Evidence on Human Effects of Ultrafine Particles (p. 16) • HEI Releases New Report on Health Effects of Ultrafine Particles (p. 16) • Study Identifies Toxicity of Fine and Ultrafine PM from Specific Sources (p. 17) • Predicting Primary PM2.5 and PM0.1 Trace Composition for Epidemiological Studies in California (p. 18) • Researchers find Ultrafine Particles Have Independent Health Impacts from Larger Particles (p. 19) PM and Premature Mortality • SCAOMD Releases Latest Air Toxics Study, Concludes 57% Drop in Cancer Risk Since 2005 (p. 19) • NASA Map Shows Deadliest Places on Earth Associated with PM2.5 Air Pollution (p. 20) 1 Executive Summary (continued) • New Study Finds Association Between Reductions in PM2.5 Levels and Improved Life Expectancy in U.S. (p. 21) • EPA Research Finds Exposure to Ozone and PM2.5 Can Lead to Premature Death (p. 21) • Modeling Source -Attributable Health Impacts of Ambient Particulate Matter Exposure: Global Premature Mortality from Surface Transportation Emissions in 2005 (p. 22) PM Effects on Cognitive and Neurological Functions • Study Warns on Possible Air Pollution Link to Neuroinflammatorv, Alzheimer and Parkinson's Pathologies in Children (p. 23) • Study Links PM2.5 Exposure to Physical Changes in Brain (p. 23) • Neurotoxicitv of Traffic -related PM on Human Brain Structure (p. 241 • Exposure to Vehicle Emissions Results in Altered Blood Brain Barrier Permeability and Expression of Matrix Metalloproteinases and Tight Junction Proteins in Mice (p. 25) • New Study Finds Air Pollution Linked to Cognitive Decline in Later Years (p. 26) • Study Links PM Air Pollution to Autism, Schizophrenia (p. 27) • Associations between Traffic -Related Black Carbon Exposure and Attention in a Prospective Birth Cohort of Urban Children (p. 27) • Convergence of Human, Animal, and In Vitro Studies on the Effects of Air Pollution on the Brain (p. 28) PM Effects on Human Reproduction • New Study Concludes that Carbon Nanoparticles in PM2.5 Can Lead to Miscarriage (p. 29) • Study Finds Air Pollution Exposure in Second Trimester May Increase Asthma Risk in Children (n.29) • Adverse Reproductive Health Outcomes and Exposures to Gaseous and Particle Matter Air Pollution in Pregnant Women (p. 30) PM from Alternative Fuels • Study Reports that Biodiesel PM May Have Greater Adverse Health Effects Than Diesel (p. 31) • Study Characterizes PM Toxicity from Diesel Passenger Cars Using DPF and Biodiesel Fuel (p. 32) • Characteristics of Particulate Matter Emissions from a Current Technology Natural Gas Engine (p. 33) U.S. EPA and California ARB Funded Research Proiects on the Health Effects of PM • U.S. EPA Clean Air Research Centers Awarded Funding to Investigate Health Effects of Air Pollution (p. 33) PM EFFECTS O\ RESPIRATORY AM) CARDIOVASCULAR SYSTEMS Study Finds Black Carbon Linked to Increased Cardiovascular Risk According to a new international study led by McGill University Professor Jill Baumgartner, black carbon (BC) from incomplete biomass and fossil fuel combustion is the most strongly light -absorbing component of particulate matter air pollution and a major climate -forcing emission. The study suggests that BC may also increase the risk of cardiovascular disease. The team's findings are published in the August 2014 Proceedings of the National Academy of Sciences of the United States (PNAS). China's PM air pollution significantly exceeds health guidelines and is driven by industrial emissions, motor vehicles, and household use of biomass and coal fuels. Baumgartner and her colleagues measured the daily exposure to different types of air pollutants, including black carbon, in 280 women (mean age 51.9 years) in China's rural Yunnan province, where biomass fuels are commonly used. They found that BC exposure from biomass smoke is more strongly associated with blood pressure, which directly impacts cardiovascular risk, than total PM mass, and that co -exposure to motor vehicle emissions may strengthen BC's impact. Air 2 pollution mitigation efforts focusing on reducing combustion pollution are likely to have major benefits for climate and human health. The researchers outfitted women with wearable air samplers that collected fine particulate matter. The particulate samples were then analyzed for different pollutant types, including black carbon. The women's blood pressure, salt intake, physical activity, body mass index, and their proximity to highways were also measured. In addition, the researchers found that women living closer to highways and exposed to both wood smoke and traffic emissions had three times higher blood pressure than women who lived away from highways. BC had the strongest association with systolic blood pressure (SBP), followed by PM mass and water-soluble organic mass. The team also found that effect of BC on SBP was almost three times greater in women living near the highway. More information on this is available at: https://www.mcgill.ca/newsroom/channels/news/black-carbon-linked-risk-cardiovascular- disease-238419. A Systematic Review and Meta -Analysis of Outdoor Particulate Matter Exposure and Lung Cancer —Particulate matter in outdoor air pollution was recently designated a Group 1 carcinogen by the International Agency for Research on Cancer (IARC). This determination was based on the evidence regarding the relationship of PM2.5 and PMI0 0 to lung cancer risks. However, the IARC evaluation did not include a quantitative summary of the evidence. The goal of this review was to provide a systematic review and quantitative summary of the evidence regarding the relationship between PM and lung cancer. The researchers conducted a meta -analyses of studies examining the relationship of exposure to PM2.5 and PM 10 with lung cancer, incidence and mortality. In total, 18 studies met their inclusion criteria and provided the information necessary to estimate the change in lung cancer risk per 10 gg/m3 increase in exposure to PM. They used random -effects analyses to allow between -study variability to contribute to meta -estimates. The results of these analyses, and the decision of the IARC Working Group to classify outdoor air pollution as a Group 1 carcinogen, further justify efforts to reduce exposures to air pollutants, which can arise from many sources. The Global Burden of Disease collaboration estimated that approximately 3.22 million deaths were caused by exposure to air pollution in 2010, an increase from 2.91 million deaths attributed to air pollution in 1990. Cancers of the trachea, bronchus, or lung represent approximately 7% of total mortality attributable to PM2.5 in 2010. The results of the meta -analysis provided in this study could be useful for better quantifying the burden of lung cancer associated with air pollution. A copy of the study, published in Environmental Health Perspectives in September 2014 is available at: http://ehp.niehs.nih.gov/wp-content/uploads/I 22/9/ehp.1408092.pdf. Exposure to Particulate Pollution Associated With Lung Cancer — Exposure to particulate air pollution is associated with lung cancer incidence, according to a prospective 3 analysis of data from 17 European cohort studies. Researchers set out to assess the association between long-term exposure to ambient air pollution and lung cancer incidence across nine European countries. This study, Prospective Analyses from the European Study of Cohorts for Air Pollution Effects (ESCAPE), was published in the journal Lancet Oncology in August 2013. Air pollution was assessed by land -use regression models for particulate matter of less than 10 gm, less than 2.5 µm, and between 2.5 gm and 10 gm, as well as nitrogen oxides, soot and two traffic indicators. The 312,944 people included in the analysis equated to 4,013,131 person -years at risk. Within the 12.8 -years follow-up, there were 2,095 cases of incident lung cancer. A significant association was found between lung cancer risk and exposure to particulate matter of less than 10 gm (HR=1.22; 95% Cl, 1.03-1.45); the HR for particulate matter of less than 2.5 gm was 1.18 (95% Cl, 0.96-1.46). The HR for the association between adenocarcinomas and exposure to particulate matter of less than 10 gm was 1.51 (95% CI, 1.10- 2.08), and the HR for association between adenocarcinomas and exposure to particulate matter of less than 2.5 gm was 1.55 (95% CI, 1.05-2.29). Researchers reported no association between lung cancer and nitrogen oxide concentration (HR=1.01; 95% CI, 0.95-1.07) or traffic intensity on the nearest street (HR= 1.00; 95% CI, 0.97-1.04). Researchers noted the study may have been limited because data for previous lung disease were not obtained. "Previous lung disease might be associated with both air pollution concentrations and the risk for lung cancer," they wrote. In an accompanying editorial, Takashi Yorifuji, MD, of the department of human ecology at Okayama University Graduate School of Environmental and Life Science in Japan, and Saori Kashima, PhD, of the department of public health and health policy at the Institute of Biomedical and Health Sciences at Hiroshima University in Japan, wrote: "At this stage, we might have to add air pollution, even at current concentrations, to the list of causes of lung cancer and recognize that air pollution has large effects on public health ... Fortunately, like tobacco smoking, it is a controllable factor." The study was funded by the European Community's Seventh Framework Program. More information on this is available at: http://www.ncbi.nlm.nih.gov/pubmed/23849838. HEI Publishes Two Comprehensive Studies on Health Effects of PM — In October 2013, the Health Effects Institute (HEI) published two new comprehensive studies on the health effects of PM and its components. Despite previous claims that certain sources of fine PM air pollution (PM2.5) may be less toxic than others, the results of the two studies lead to the overall conclusion that no source can yet be excluded as having no health effects. These nationwide studies, funded as part of HEI's National Particle Component Toxicity (NPACT) initiative, are the most systematic effort ever to combine epidemiologic and toxicologic research to investigate whether "all particles are created equal" and therefore deserve the same level of public health and regulatory attention. The studies found links between adverse health effects, particularly on the cardiovascular system, and sulfate particles (primarily from coal combustion) and, to a somewhat lesser extent, 4 traffic sources. But the HEI NPACT Review Panel, 14 experts who subjected the studies to in ense, independent peer review, cautioned that the results "do not provide compelling evidence that any specific source, component, or size class of PM may be excluded as a possible contributor to PM toxicity." The panel went on to note that a "better understanding of exposure and health effects is needed before it can be concluded that regulations targeting specific sources or components of PM2.5 will protect public health more effectively than continuing to follow the current practice of targeting PM2.5 mass as a whole." HEI launched the NPACT initiative in response to calls from its sponsors, at both the U.S. EPA and industry, for answers to these important questions about PM and health. Following extensive planning and intense scientific competition, two teams, led by Morton Lippmann from New York University and Sverre Vedal from the University of Washington - Seattle, were selected to conduct detailed toxicologic and epidemiologic investigations across the U.S. of air pollution and its effects on cardiovascular and other health outcomes. Lippmann and colleagues conducted four coordinated toxicologic and epidemiologic studies. They analyzed heart rate variability and atherosclerosis as well as markers of inflammation and oxidative stress in animals and human cells exposed to PM samples from five geographic regions in the U.S. In epidemiologic studies, they exam short-term effects on mortality and hospital admissions associated with PM2.5 emission in 150 U.S. cities; they also evaluated associations between long-term exposure to PM and mortality from cardiovascular and respiratory diseases and lung cancer for participants in the American Cancer Society's Cancer Prevention Study population. Their study has provided new insights into the toxicity of PM components and source categories and identified the coal combustion, residual oil combustion, traffic, and metals source categories as most consistently associated with adverse health effects. However, other components and source categories could not be definitively excluded as having no adverse effects. Vedal and colleagues studied the cardiovascular effects of PM components, with a focus on traffic sources. They analyzed data from the Multi -Ethnic Study of Atherosclerosis and the Women's Health Initiative Observational Study cohorts, and they also exposed mice to combinations of mixed vehicular engine emissions and non -vehicular PM. They found strong evidence for associations of PM2.5, organic carbon, and sulfur with subclinical and clinical outcomes in the cohorts, with weaker evidence for elemental carbon. Their toxicologic study provides strong evidence for effects of mixed vehicular engine emissions and, to a lesser extent, exhaust gases on vascular markers in mice; non -vehicular PM induced few effects. For a copy of the press release announcing the two NPACT studies, go to: www.healtheffects.org/Pubs/H El -N PACT- PressRelease-October-30-20 13 .pdf. An executive summary of the two studies is available at: www.healtheffects.org/Pubs/NPACT- ExecutiveSummary.pdf. China Study Shows PM1 Air Pollution Most Harmful — A recent study led by Chinese scientists shows a strong link between smaller air pollution particles and a range of serious health conditions. Scientists said the smaller the airborne particles, the more likely they are to cause illness, suggesting the need for monitoring particulate matter of 1 micron or less in diameter, a 5 category of pollution rarely monitored. In recent years, many locations across China have been blanketed with heavy air pollution, raising public health concerns. In the study, published in the public health journal Environmental Health Perspectives in October 2013, researchers from the School of Public Health at Fudan University in Shanghai have demonstrated correlations between PM2.5 pollution and the incidence of particular illnesses. Researchers spent about two years collecting data in a medium-sized city in northern China, measuring levels of PM in 23 size categories ranging from 0.25 microns to 10 microns. They then plotted the health conditions of residents in the city against the concentrations of particles of different sizes found in their locations. Among the key findings was that those areas with larger concentrations of smaller particles showed higher incidences of particular illnesses, such as cardiovascular diseases. The fine particles measuring between 0.25 to 0.5 microns in diameter accounted for about 90% of the total number of particles found in the air during the study. Kan Haidong, a professor at the School of Public Health at Fudan University, said the smaller the particle, the higher the concentration in any given volume of air and so the greater the number of particles coming into contact with tissues inside the body. Kan said the smaller particles can also pass through the blood -air barrier in the lungs. entering the blood as toxins, and causing cardiovascular disease. He also said that smaller particles in the body can harm the regulation of the human nervous system. More information on this is available at: usa.chinadaily.com.cn/china/2013- 10/28/content_ I7061997.htm. Air Pollution Linked With Thickening of the Arteries, Cardiovascular Problems - Air pollution has been linked to heart attacks, strokes and atherosclerosis ("hardening of the arteries"), thanks to research published in PLOS Medicine in April 2013. The study found that high concentrations of fine particulate air pollution (PM2.5) were linked with faster thickening of artery walls. The thickening was found in the inner walls of the carotid artery. This is the main blood vessel providing blood to the head, neck and brain. The team also found that reductions in particulate levels were linked to a slower progression of blood vessel thickness. Blood vessel thickness is a symptom of atherosclerosis, and is present throughout the body even for people without obvious symptoms of heart disease. "Our findings help us to understand how it is that exposures to air pollution may cause the increases in heart attacks and strokes observed by other studies," said Sara Adar, John Searle Assistant Professor of Epidemiology, University of Michigan School of Public Health. The research was conducted by a team led by Adar and Joel Kaufman, Professor of Environmental and Occupational Health Sciences and Medicine, University of Washington. The researchers investigated 5362 people aged between 45 to 84 years old from six U.S. metropolitan areas as part of the Multi -Ethnic Study of Atherosclerosis and Air Pollution (MESA Air). They took ultrasound measurements of blood vessels 3 years apart. All participants in the study had no known heart disease. The researchers found that on average, the thickness of the carotid vessel increased by 14 gm each year. Thickening of the inner two layers of this key blood vessel, which supplies blood to the head, neck and brain, occurred more quickly following exposure to higher 6 concentrations of fine particulate air pollution. The researchers said the thickness of the carotid artery is an indicator of how much atherosclerosis is present in the arteries throughout the body. "Linking these findings with other results from the same population suggests that persons living in a more polluted part of town may have a 2 percent higher risk of stroke as compared to people in a less polluted part of the same metropolitan area," Adar said. In response to the findings, Nino Kuenzli, of the University of Basel in Switzerland, said in a news release that the study "further supports an old request to policy makers -- namely that clean air standards ought to comply at least with the science -based levels proposed by the World Health Organization." More information on this is available at: http://www.plosmedicine.org/article/info%3Adoi%2F 10.1371 %2Fjournal.pmed.1001430. Detailed diesel exhaust characteristics including particle surface area and lung deposited dose for better understanding of health effects in human chamber exposure studies — Several diesel exhaust (DE) characteristics, comprising both particle and gas phase, recognized as important when linking with health effects, are not reported in human chamber exposure studies. In order to understand effects of DE on humans there is a need for better characterization of DE when performing exposure studies. This study, published in Atmospheric Environment in April 2014, aims to determine and quantify detailed DE characteristics during human chamber exposure. Additionally to compare to reported DE properties in conducted human exposures. A wide battery of particle and gas phase measurement techniques have been used to provide detailed DE characteristics including the DE particles (DEP) surface area, fraction and dose deposited in the lungs, chemical composition of both particle and gas phase such as NO, NO2, CO, CO2, volatile organic compounds (including aldehydes, benzene, toluene) and polycyclic aromatic hydrocarbons (PAHs). Eyes. nose and throat irritation effects were determined. Exposure conditions with PM1 (<1 µm) mass concentration 280 µg m 3, number concentration 4 X 105 cm3 and elemental to total carbon fraction of 82% were generated from a diesel vehicle at idling. When estimating the lung deposited dose it was found that using the size dependent effective density (in contrast to assuming unity density) reduced the estimated respiratory dose by 132% by mass. Accounting for agglomerated structure of DEP prevented underestimation of lung deposited dose by surface area by 37% in comparison to assuming spherical particles. Comparison of DE characteristics reported in conducted chamber exposures showed that DE properties vary to a great extent under the same DEP mass concentration and engine load. This highlights the need for detailed and standardized approach for measuring and reporting of DE properties. Eyes irritation effects, most probably caused by aldehydes in the gas phase, as well as nose irritation were observed at exposure levels below current occupational exposure limit values given for exhaust fumes. Reporting detailed DE characteristics that include DEP properties (such as mass and number concentration, size resolved information, surface area, chemical composition, lung deposited dose by number, mass and surface) and detailed gas phase including components known for their carcinogenic and irritation effect (e.g. aldehydes, benzene, PAHs) can help in determination of key parameters responsible for observed health effects and comparison of chamber exposure studies. 7 More information on this is available at: http://www.sciencedirect.com/science/article/pii/S 1352231013008546. Study Finds Increasing Emergency Room Visits for Stroke by Elevated Levels of Fine Particulate Constituents — The association between PM2.5 and stroke remain inconsistent. Researchers conducted a time -series study to evaluate emergency room visits for ischemic and hemorrhagic stroke in relation to PM2.5 and its constituents. Generalized additive models were used to model the counts of daily ER visits for ischemic and hemorrhagic strokes among patients admitted to the National Taiwan University Hospital from January 1, 2004 to August 31, 2008. Exposure variables included PM2.5 and the four constituents, nitrate, sulfate, organic carbon (OC), and elemental carbon (EC). 12,982 ischemic stroke and 3,362 hemorrhagic stroke cases were identified during the study period. For hemorrhagic stroke, the strongest relative risks (RRs) of ER visits were 1.19 for an interquartile range (IQR) increase in 3 -day average nitrate and EC. For ischemic stroke, increased RRs of ER visit of 1.21 and 1.81 were observed in the warm season for an IQR increase in 3 -day average of OC and EC, respectively. PM2.5 and OC were associated with increased RRs of ER visits for ischemic stroke among patients aged 65 years or older and female patients. The researchers concluded that PM2.5 constituents, rather than PM2.5 mass, are more closely related to ER visits for hemorrhagic stroke. Both PM2.5 mass and its chemical constituents are associated with ER visits for ischemic stroke in the warm season, among patients older than 65 years, and female patients. A copy of the study, Increasing Emergency Room Visits for Stroke by Elevated Levels of Fine Particulate Constituents published in March 2014, is available for purchase at: http://www.sciencedirect.com/science/article/pii/S0048969713014897. Cell Cycle Alterations Induced by Urban PM2.5 in Bronchial Epithelial Cells — This study explores and characterizes cell cycle alterations induced by urban PM2.5 in the human epithelial cell line BEAS-2B, and elucidates possible mechanisms involved. In October 2013, the International Agency for Research on Cancer (IARC) classified outdoor air pollution as carcinogenic to humans. PM is a well-known air pollutant and its adverse effects on human health are well established. Increased levels of PM have been associated with exacerbation of airways disease in patients with asthma and Chronic Obstructive Pulmonary Disease (COPD). There is a growing evidence linking long-term exposure to fine PM fraction with increased risk of cardiovascular mortality and lung cancer. However, the understanding of the mechanisms by which PM exerts its various adverse effects is still incomplete and detailed in vitro studies are highly needed. In vitro studies have demonstrated that PM may inhibit cell growth, by reducing proliferation and/or causing cell death. The reduced proliferation has been linked to an arrest in various steps of the cell cycle. Cell cycle progression can be blocked and/or delayed in response to various genotoxic stresses, but also to structural dysfuctions of various proteins. Researchers have observed that exposure to 25 pg/cm2 of Milan winter PM2.5 for 20 hours induced a mitotic arrest resulting in cell death by apoptosis in human bronchial epithelial 8 cells. Effects involved in DNA -damaged response were detected at the low doses 5 and 7.5 gg/cm2. A further characterization of PM -induced cell cycle and mitotic alterations is important when trying to explain PM -induced chromosomal alterations, as well as its association with an increased risk of lung cancer. In this study, the effects of Milan winter PM2.5 on the cell cycle progression were characterized using the low dose 7.2 gg/cm2. The cells were exposed to a low dose (7.5 gg/cm2) of PM2.5 for different time points, and the cell cycle progression was analyzed by fluorescent microscopy and flow cytometry. The researchers concluded that Milan winter PM2.5 rapidly induces severe cell alterations, resulting in increased frequency of cells with double nuclei and micronuclei. This effect is related to the metabolic activation of PM2.5 organic chemicals, which cause damages to DNA and spindle apparatus. This study was published in the journal Particle and Fibre Toxicology in December 2013. More information on this study is available at: http://www.particleandfibretoxicology.com/content/10/1, 63. Air Pollution and Hospital Emergency Room and Admissions for Cardiovascular and Respiratory Diseases in Dona Ana County, New Mexico — Dona Ana County in New Mexico regularly experiences severe air pollution episodes associated with windblown dust and fires. Residents of Hispanic/Latino origin constitute the largest population group in the region. Researchers investigated the associations of ambient PM and ozone with hospital emergency room and admissions for respiratory and cardiovascular visits in adults. The researchers used trajectories regression analysis to determine the local and regional components of particle mass and ozone. The researchers found that the sources within 500 km of the study area accounted for most of particle mass and ozone concentrations. Sources in Southeast Texas, Baja California and Southwest U.S. were the most important regional contributors. Increases of cardiovascular emergency room visits were estimated for PM 10 and PM 10-2.5 for all adults during the warm period (April to September). When high PM 10 mass concentrations were excluded, strong effects for respiratory emergency room visits for both PM 10 and PM2.5 were computed. The analysis indicated effects of PM 10, PM2.5 and ozone on emergency room visits during the April to September period in a region impacted by windblown dust and wildfires. This study was published in Environmental Research in February 2014. More information on this study is available at: http://www.sciencedirect.com/science/article/pii/S0013935 113002077. A Case -Crossover Study on Ambient Fine Particulate Air Pollution Triggers ST - Elevation Myocardial Infarction — Previous studies investigating triggering of myocardial infarction by PM concentrations have, in most cases, reported an increased risk of myocardial infarction associated with increases in PM on the same and previous day. Similar acute effects 9 of fine particulate air pollution have been reported for other cardiovascular outcomes. Some studies of myocardial infarction and PM have used symptom onset time, rather than the arrival time at the emergency room, to define myocardial infarction onset, thereby providing a better estimate of the myocardial infarction onset time and less exposure error. Using hospital admissions data, researchers reported that myocardial infarction/PM2.5 association may be limited to transmural infarctions. The researchers found a 10% increase risk of transmural infarction, but not non-transmural infarctions associated with each 10.8% µg/m3 increase in the PM2.5 concentration in the preceding 24 hours. The researchers hypothesized that this may be due to differences in response to air pollution by myocardial infarction type. However, transmural and non-transural myocardial infarction are estimations of assumed injury to the myocardium, whereas acute coronary syndromes attempt to describe the spectrum of physiologic events occurring in coronary arteries during an acute ischemic event. Therefore, in order to better understand the relationship between the acute pathophysiologic process of myocardial infarction and increased air pollutant concentrations, researchers sought to study acute coronary syndromes (i.e. ST segment elevation myocardial infarction [STEMI] , non -ST segment elevation myocardial infarction [NSTEMI], and unstable angina) to reflect the spectrum of pathophysiologic events occurring. STEMI is most often the result of plaque rupture followed by thrombus formation and coronary artery lumen occlusion. The researchers found a significant 18% increase in the risk of STEMI associated with each 7.1 µg/m3 increase in PM2.5 concentration in the previous hour prior to acute coronary syndrome onset, with smaller, non -significantly increased risks associated with increased fine particle concentrations in the previous 3, 12, and 24 hours. The researchers found no pattern with NSTEM I. Estimates of the risk of STEMI associated with interquartile range increases in ultrafine particle and accumulation mode particle number concentrations in the previous 1 to 96 hours were all greater than 1.0, but not statistically significant. Patients with pre-existing hypertension had a significantly greater risk of STEMI associated with increased fine particle concentration in the previous hour than patients without hypertension. Researchers concluded that increased fine particle concentrations in the hour prior to acute coronary syndrome onset were associated with an increased risk of STEMI, but not NSTEMI. Patients with pre-existing hypertension and other cardiovascular disease appeared particularly susceptible. Further investigation into mechanisms by which PM can preferentially trigger STEMI over NSTEMI within this rapid time scale is needed. This study was published in the journal Particle and Fibre Toxicology in January 2014. More information on this is available at: http://www.particleandfibretoxicology.com/content/11/1/1. Study Associates Air Pollution to Irregular Heartbeat and Lung Blood Clots — A new study linked air pollution to irregular heartbeat and lung blood clots. But its impact on directly boosting the risk of heart attacks and stroke is rather less clear. The evidence suggests that high levels of certain air pollutants are associated with a higher risk of cardiovascular problems, but exactly how this association works has not been clarified. 10 The research team set out to explore the short-term biological impact of air pollution on cardiovascular disease, using data from three national collections in England and Wales for the 2003-2009 period. These were the Myocardial Ischaemia National Audit Project (MINAP), which tracks hospital admissions for heart attack/stroke; hospital episode statistics (HES) on emergency admissions; and figures from the Office of National Statistics (ONS) on recorded deaths. Some 400,000 heart attacks recorded in MINAP; more than 2 million emergency admissions for cardiovascular problems; and 600,000 deaths from a heart attack/stroke were linked to average levels of air pollutants over a period of 5 days using data from the monitoring station nearest to the place of residence. Air pollutants include carbon monoxide, nitrogen dioxide, particulate matter (PM 10 and PN12.5) sulfur dioxide, and ozone. Information on ambient daily temperatures, recorded by the UK Meteorological Office, was also factored in. No clear link with any air pollutant was found for cardiovascular deaths, with the exception of PM2.5 which was linked to an increased risk of irregular heart rhythms, irregular heartbeat and blood clots in the lungs. Only nitrogen dioxide was linked to an increased risk of a hospital admission for cardiovascular problems, including heart failure, and an increased risk of a particular type of heart attack in the MINAP data. However, there does not seem to be a clear link between PM levels and heightened risk of atrial fibrillation and pulmonary embolism. This study was published in the BIM British Medical Journal in June 2014. More information on this is available at: http://www.sciencedaily.com/releases/2b 14/06/ 140604203052.htm. Study Finds Living in Areas Polluted with Fine Particles Raises Lung Cancer Risk — A new research concludes that nonsmoking women who live many years in communities polluted with fine particles have an elevated risk of lung cancer. The study, which is the largest to date to examine the link, adds to mounting evidence that chronic exposure to soot may raise the risk of lung cancer, particularly among nonsmokers. Led by Harvard University researchers, the study estimated exposures of 103,650 U.S. women to three sizes of airborne particulates. They calculated how many women contracted cancer (2,155) between 1994 and 2010, and analyzed the pollution levels near their homes for the previous six years. All sizes of particle pollution, particularly the smallest (PM2.5), were linked to an increased risk of lung cancer. For every small (10 µg/m3) increase in PM2.5 the risk of lung cancer increased 37% among nonsmoking women or women who had quit smoking at least 10 years earlier, which was published online in the journal Environmental Health Perspectives. The sources of the pollutants varied. Although the research suggested that traffic played a role in the higher cancer risk, the finding was not scientifically significant because too few women in the study lived near major roads. According to the American Lung Association, more than 46 million Americans, or almost 15%, live in areas with unhealthful year-round levels of fine particle pollution. U.S. areas with the highest levels include the Los Angeles region, California's Central Valley, Chicago and Houston. In this study, about half of the women lived in the Northeast. The research doesn't prove air pollution causes lung cancer. But it is the latest of multiple human health studies that have linked fine particles to lung cancer. Such studies 11 prompted the International Agency for Research on Cancer to classify PM as carcinogenic to humans in 2013. The researchers didn't have personal exposure for the women. Instead, they estimated their exposures by plugging local air quality data into models that took into account how close the women lived to major roads, as well as nearby industries and weather conditions. Edelman of the American Lung Association said the study's strength was that it looked at a period of six years of exposure instead of a snapshot in time. However, one researcher said the study didn't look far enough back in the women's past. Previous exposures may be more important because cancer can develop over a period of decades. The study uses "more or less current exposure to categorize long-term response," said Fred Lipfert, an environmental engineer formerly of the Brookhaven National Laboratory who has published multiple articles on air pollution and health. The other problem is that the study doesn't take into consideration indoor air pollution. Laden agreed that past exposures are important, but the scientists were limited by the data. PM were not routinely measured a decade or two ago. A copy of the study, published in the Environmental Health Perspectives in June 2014, is available at: http://ehp.niehs.nih.gov/wp-content/uploads/advpub/2014/6/ehp. l 307490.pdf. Increased Ultrafine Particles and Carbon Monoxide Concentrations Are Associated with Asthma Exacerbation Among Urban Children — Increased air pollution concentrations have been linked to several asthma -related outcomes in children, including respiratory symptoms, medication use, and hospital visits. However, few studies have examined effects of ultrafine particles in a pediatric population. This study's primary objective was to examine the effects of ambient concentrations of ultrafine particles on asthma exacerbation among urban children and determine whether consistent treatment with inhaled corticosteroids could attenuate these effects. The researchers also explored the relationship between asthma exacerbation and ambient concentrations of accumulation mode particles, fine particles (PM2.5), carbon monoxide, sulfur dioxide and ozone. The researchers hypothesized that increased 1-7 day concentrations of ultrafine particles and other pollutants would be attenuated among children receiving school -based corticosteroid therapy. The researchers conducted a pilot study using data from 3 to 10 year old children participating in the School -Based Asthma Therapy trial. Using a time -stratified case -crossover design and conditional logistic regression, the researchers estimated the relative odds of a pediatric asthma visit treated with prednisone associated with increased pollution concentrations in the previous 7 days. They re -ran these analyses separately for children receiving medications through the school -based intervention and children in a usual care control group. The study found that interquartile increases in ultrafine particles and carbon monoxide concentrations in the previous 7 days were associated with increase in the relative odds of a pediatric asthma visit, with the largest increases observed for 4 -day mean ultrafine particles and 7 -day mean carbon monoxide. Relative odds estimates were larger among children receiving school -based inhaled corticosteroid treatment. The researchers observed no such associations with accumulation mode particles, black carbon, fine particles, or sulfur dioxide. Ozone concentrations were inversely associated with the relative odds of a pediatric asthma visit. 12 The researchers concluded that the findings suggest a response to markers of traffic pollution among urban asthmatic children. Effects were strongest among children receiving preventive medications through school suggesting that this group of children was particularly sensitive to environmental triggers. Medication adherence alone may be insufficient to protect the most vulnerable from environmental asthma triggers. However, more research is needed to confirm this finding. This study was published in the journal Environmental Research in February 2014. More information on this is available at: http://www.sciencedirect.com/science/article/pii/S0013935113002028. New Study Finds Strong Association between Exposure to Fine PM and Cardiovascular Mortality — A new study in Environmental Research published in July 2014 demonstrates a strong association between exposure to fine particles emitted from fuel -burning engines and C -reactive protein (CRP), which is directly linked to deaths from cardiovascular disease. The study conducted by scientists at the California Environmental Protection Agency's Office of Environmental Health Hazard Assessment (OEHHA) is among the first to link long- term exposure to fine particle air pollution (PM2.5) to elevated levels of CRP. High levels of CRP are key indicators of inflammation, which is the body's response to inhaled irritating fine particles and is strongly associated with heart disease and stroke. The study's link between PM2.5 and CRP provides a plausible explanation for the previously documented connection between PM2.5 and cardiovascular mortality. The study, "Chronic PM2.5 exposure and inflammation: Determining sensitive subgroups in mid-life women," found that: • Diabetics and smokers experience particularly large effects of PM2.5 on CRP. • People with low incomes, high blood pressure, or who are using hormone therapy may also be more vulnerable to PM2.5. • Statin medication and moderate alcohol consumption can reduce the impact of PM2.5 on CRP. The study analyzed data from 3.000 women observed over a five-year period from the Study of Women's Health Across the Nation cohort. Women recruited from six different metropolitan areas throughout the U.S. provided blood samples every year of the study. The researchers were able to isolate the effect of air pollution after taking into account other factors that might affect CRP. More information on this study is available at: http://www.ncbi.nlm.nih.gov/pubmed/24792413. Effects of Concentrated Ambient Particles on Normal and Hypersecretory Airways in Rats — Epidemiological studies have reported that elevated levels of particulate air pollution in urban communities are associated with increases in attacks of asthma based on evidence from hospital admissions and emergency department visits. Principal pathologic features of chronic B airway diseases, like asthma, are airway inflammation and mucous hypersecretion with excessive amounts of luminal mucus and increased numbers of mucus -secreting cells in regions of the respiratory tract that normally have few or no mucous cells. The overall goal of the study was to understand the adverse effects of urban air fine particulate matter on normal airways and airways compromised with airway inflammation and excess mucus. The project was specifically designed to: 1) examine the chemical and physical characteristics of PM2.5 and other airborne pollutants in the outdoor air of a local Detroit community with a high incidence of childhood asthma; 2) determine the effects of this community -based PM2.5 on the airway epithelium in normal rats compromised with pre-existing hypersecretory airway diseases; and 3) identify the chemical or physical components of PM2.5 that are responsible for PM2.5-induced airway inflammation and epithelial alterations in these animal models. Two animal models of airway disease were used to examine the effects of PM2.5 exposure on pre-existing hypersecretory airways. A mobile air monitoring and exposure laboratory equipped with inhalation exposure chambers for animal toxicology studies, air pollution monitors, and particulate collection devices was used in this investigation. The mobile laboratory was parked in a community in southwestern Detroit during the summer months when particulate air pollution is usually high (July and September 2000). The researchers monitored outdoor air pollution in this community daily, and exposed normal and compromised rats to concentrated PM2.5 from this local urban atmosphere. Rats in the inhalation studies were exposed for 1 day or for 4 or 5 consecutive days (10 hours/day) to either filtered air (controls) or concentrated ambient particles (CAPs) delivered by a Harvard ambient fine particle concentrator. Rats were killed 24 hours after the end of the exposure. Biochemical, morphometric, and molecular techniques were used to identify airway epithelial and inflammatory responses to CAPs. 1'he Harvard concentrator effectively concentrated the fine ambient particles from this urban atmosphere (10-30 times) without significantly changing the major physicochemical features of the atmospheric particles. Daily CAPs mass concentrations during the 10 -hour exposure period in July ranged from 16 to 895 µg/m3 and in September ranged from 81 to 755 µg/m'. In general, chemical characteristics of ambient particles were conserved through the concentrator into the exposure chamber. Single or repeated exposures to CAPs did not cause adverse effects in the nasal or pulmonary airways of health rats. Variable airway responses to CAPs exposure were observed in rats with preexisting allergic airway disease induced by ovalbumin (OVA) sensitization and challenge. Only OVA -challenged rats exposed to CAPs for 5 consecutive days in September 2000 has significant increases in airway mucosubstances and pulmonary inflammation compared to saline-challenged/air-exposed control rats. OVA - challenged rats that were repeatedly exposed to CAPs in July 2000 had only minor CAP -related effects. In only the September 5 -day exposure protocol, PM2.5 trace elements of anthropogenic origin were recovered from the lung tissues of CAPs-exposed rats. Recovery of these specific trace elements was greatest in rats with OVA -induced allergic airway disease. Additional laboratory experiments using intratracheal instillations of ambient PM2.5 samples were performed to identify bioactive agents in the CAPs to which rats had been exposed in the inhalation exposure component. Because the most pronounced effects of CAPs inhalation 14 were found in rats with OVA -induced allergic airways exposed in September, researchers ambient PM2.5 samples that were collected on 2 days during the September CAPs inhalation exposures to use for instillation. The results from this instillation component did not suggest what fractions of the CAPs may have been responsible for enhancing OVA -induced airway mucosubstances and pulmonary inflammation observed in the inhalation exposure component. In summary, inhaled CAPs-related pulmonary alterations in the affected OVA -challenged rats appeared to be related to the chemical composition, rather than the mass concentration, to which the animals were exposed. Results of the trace element analysis in the lungs of CAPs-exposed rats exposed in September suggested that air particles derived from identified local combustion sources were preferentially retained in allergic airways. These results demonstrate that short- term exposures to CAPs from this southwestern Detroit community caused variable responses in laboratory rats and suggest that adverse biological responses to ambient PM2.5 may be associated more closely with local sources of particles and weather patterns than with particle mass. This study was published by the Health Effects Institute in August 2004. More information on this is available at: http://www.ncbi.nlm.nih.gov/pubmed/15543855. WHO Releases Report on Health Effects of PM — In July 2014, the World Health Organization (WHO) released a report on the health effects of PM. The report notes that one issue of concern is that monitoring of PM is very limited in the countries of eastern Europe, the Caucasus and central Asia. The paper summarizes the evidence about the health effects of air pollution from PM and presents the policy implications, the aim being to stimulate policy -makers to develop more effective strategies to reduce air pollution and its health effects in those countries. A copy of the paper is available at: http://www.euro.who.int/_data/assets! pd f_fi 1e/0006/189051 /Health-effects-of-particulate- matter-final-Eng.pdf?ua=1. ULTRAFINE PM Researchers Publish Study on PM2.5 Constituents and Hospital Visits in Shanghai — This month, Chinese researchers published the results of a study that examined the short-term association between PM2.5 constituents and emergency room visits in Shanghai, China. The researchers measured daily concentrations of PM2.5, organic carbon (OC), elemental carbon (EC), and eight water-soluble ions between January 1, 2011 and December 31, 2012. They analyzed the data using overdispersed generalized linear Poisson models. During the study period, the mean daily average concentration of PM2.5 in Shanghai was 55 µg/m3. Major contributors to PM2.5 mass included OC. EC, sulfate, nitrate, and ammonium. For a 1 -day lag, an interquartile range increment in PM2.5 mass (36.47 µg/m3) corresponded to 0.57% increase of emergency room visits. In the three models used, the researchers found significant positive associations of emergency room visits with OC and EC. Their findings suggest that PM2.5 constituents from the combustion of fossil fuel may have an appreciable influence on health impact attributable to PM2.5. More information on this is available at: pubs.acs.org/doilabs/ 10.1021 / es5013 05 k :' journalCode=esthag. 15 Epidemiological Evidence on Human Effects of Ultrafine Particles — Evidence from epidemiologic studies linking ambient concentrations of particulate matter to morbidity and mortality influenced the guidelines for air quality standards worldwide. With the improvement of measurement techniques, clearer effects were observed with smaller particle sizes. Based on these effects and results from animal studies on the potential toxicity of ultrafine particles, recent epidemiologic studies focus on the health effects of particles which are less than 100 nm in diameter. However, most of the studies are ongoing and only few results have been available so far. Six panel studies with patients suffering from chronic pulmonary diseases have been performed in Germany, Finland and the United Kingdom. Overall, a decrease of peak expiratory flow and an increase of daily symptoms and medication use was found for elevated daily particle concentrations. Effects were seen with both fine and ultrafine particles. One large study on daily mortality from Germany showed comparable effects of fine and ultrafine particles in all size classes considered. However, fine particles showed more immediate effects while ultrafine particles showed more delayed effects on mortality. The limited number of epidemiological studies suggest that there are health effects of fine and ultrafine particles which might be independent of each other. The study reviewed more than 30 references. This study was published in the journal of Aerosol Medicine in July 2004. More information on this is available at: http://online.liebertpub.com/dui/abs/ ! 0.1089/089426802320282310. HEI Releases New Report on Health Effects of Ultrafine Particles — On January 23, 2013, the Health Effects Institute (HEI) released a new report that concludes that, while there have been a growing number of laboratory and field studies of the effects of ultrafine particles (UFPs), "toxicologic studies in animals, controlled human exposure studies, and epidemiologic studies to date have not provided consistent findings on the effects of exposures to ambient levels of UFPs, particularly in human populations." The report, "Understanding the Health Effects of Ambient Ultrafine Particles," concludes that the "current evidence does not support a conclusion that exposures to UFPs alone can account in substantial ways for the adverse effects that have been associated with other ambient pollutants such as PM2.5." The expert panel formed by HEI reviewed over 300 siiidies, and the final report was peer reviewed by 10 outside experts. According to Dan Greenbaum. president of HE1, "there is extensive evidence today that the complex mix of fine airborne particulate matter, PM2.5, can contribute to a variety of cardiovascular respiratory and other ►;eaith effects. But despite a large number of studies of the smallest particles (particles less than 0.1 microns in diameter), our expert panel found that the evidence to date has not confirmed the hypothesis of some in the scientific community that these ultrafine particles are the principle reason for these broader PM2.5 health effects." Particulate matter emissions are a complex mixture, containing particles of a variety of sizes and composition, and there have been continuing questions from the scientific and policy communities about whether some components or characteristics of that mixture, or particles from some sources, are more toxic and deserving of priority efforts for control. The ultrafine particles, which are emitted from a variety of sources, including traffic, industry, and cooking, have gained 16 special attention because of their potential for traveling deeper into the lungs, into the bloodstream, and into the brain. They are important as well because a number of regulatory actions in Europe and the U.S. have required new filters on diesel engines to reduce UFP emissions, while at the same time fuel economy rules are encouraging the use of more fuel - efficient gasoline engines that may increase UFP emissions. A copy of the report is available at: pubs.healtheffects.org/view.php?id=394. Study Identifies Toxicity of Fine and Ultrafine PM from Specific Sources — In May 2012, ARB and the Electric Power Research Institute (EPRI) released a report they commissioned by investigators at the University of California, Davis, that looks at how to distinguish health effects caused by different types of fine and ultrafine airborne particulate matter (PM) from different sources. This is among the first studies to examine the toxicology of particles according to their source of or;gin. Previous research has linked fine and ultrafine particles to asthma, heart disease, and other adverse health effects. These particles, produced by emissions from many different sources, including traffic, industrial processes, wood -burning fireplaces, and gas- and coal-fired power plants, combine in the atmosphere and are affected by sunlight and other meteorological variables. National Ambient Air Quality Standards (NAAQS) do not distinguish between these sources since they are based solely on mass in a given particle size range. In addition, the mixing makes it difficult to determine which compounds in PM may be responsible for specific health effects. The research was conducted by Dr. Anthony Wexler, director of the Air Quality Research Center at the University of California, Davis. Dr. Wexler used a single particle mass spectrometer and ten particle samplers to capture ambient particles. He then developed novel methods to extract PM from the filter and polyurethane foam substrates, so that as much as the PM was extracted from the substrates and hydroscopic and hydrophobic compounds in the PM were extracted evenly. Laboratory mice were exposed to the separated particles, and their responses were monitored for signs of toxicity by Dr. Kent Pinkerton, a professor of pediatrics at the UC Davis School of Medicine. The analysis showed different levels of toxicity for different PM samples, associated with a variety of sources, such as traffic and wood smoke. Most of the toxicity was associated with automobile and cooking sources in both seasons, while in the winter toxicity was also associated with secondary compounds. Ultrafine particles were more potent inducers of inflammatory markers and cell death than larger particles. Broadly, the study found that: • Based on particle size, ultrafne PM was a more potent inducer of inflammatory and cytotoxic response compared to submicron fine PM on a per mass basis. • For pulmonary inflammation and cytotoxicity, samples containing PM from vehicular sources or metals had the highest biological response for summer samples, while PM from vehicular sources, regional processes background, and nighttime inversions had the highest response for winter samples. 17 • In general, the same PM sample produced greater inflammatory and cytotoxic responses in lung, samples than in the blood samples under the conditions used in this study. • Analysis of systemic inflammation did not reveal major differences between the collected samples. On February 19, 2013. Drs. Wexler and Pinkerton held a seminar to discuss this study at the Cal/EPA building in Sacramento. A copy of the final report is available at: www.arb.ca.2ov/research/apripast/CG-331.pdf. and a copy of the presentation slides presented during the seminar is available at: www.arb.ca.g.ov/research/seminars/wexler5/wexler5.pdf. Predicting Primary PM2.5 and PM0.1 Trace Composition for Epidemiological Studies in California - Epidemiological studies have identified positive correlations between exposure to ambient airborne PM and increased health risk. Recent studies have attempted to link these health effects to particle size and/or composition using exposure estimates based on the measured ambient PM 10 or PM2.5 concentrations from central site monitors, which are usually spare in time, space, chemical composition, and source origin information. Important particle size distribution and chemici_1 composition information is not routinely available, especially for the ultrafine particle size fraction (PM0.1) that has been shown to have greater toxicity than larger particles. A more accurate estimate of exposure to detailed particle size fractions and chemical components would improve the power of future epidemiological studies. A variety of statistical and mechanical modeling techniques have been proposed to improve the accuracy of exposure estimates to air pollution. Land Use Regression models have been developed to predict the spatial distribution of exposure to primary traffic PM on scales of hundreds of meters, but corresponding regression models for other important particle sources have not been widely demonstrated. Regression models also do not directly address the issues of data sparseness in time, particle size. and particle composition. Some land use regression models and dispersion models have been developed to predict the spatial distribution of exposure to primary traffic PM on scales of hundreds of meters, but corresponding regression models for other important particle sources have not been widely demonstrated. The objective of this study is to develop the University of California — Davis_Primary (UCD_P) CTM to predict detailed particle size, composition, and source information over a 7 - year period that can be used in subsequent epidemiological studies for PM0.1 and PM2.5. California is chosen as the focus area for the study because it has a large population exposed to high PM concentrations, accurate PM emissions inventories, and comprehensive ambient measurements for model evaluation. The ability of UCD_P predictions for mass and chemical component concentrations in the PNMU.: and PM2.5 factions is evaluated against ambient measurements; a companion study will evaluate the model ability for PM source apportionment. The predicted and measured daily PM2.5 EC concentrations exhibited seasonal variation at the seven available monitoring. sites with lower values during the summer and higher values during the winter. 18 More information on this study, published in the journal Environmental Science Technology in April 2014, is available at: http://pubs.acs.org/doi/abs/10.1021/es404809i. Researchers find Ultrafine Particles Have Independent Health Impacts from Larger Particles — Using a quasi -experimental opportunity offered by greatly restricted air pollution emissions during the 2008 Beijing Olympics compared to before and after the Olympics, a team of U.S. and Chinese researchers conducted a study to compare ultrafine particles (UFPs) and fine particles (PM2.5) in their associations with biomarkers reflecting multiple pathophysiological pathways linking exposure and cardiorespiratory events. Number concentrations of particles (13.0-764.7 nm) and mass concentrations of PM2.5 were measured at two locations within 9 km from the residence and workplace of 125 participating Beijing residents. Each participant was measured 6 times for biomarkers of autonomic function (heart rate, systolic and diastolic blood pressures), hemostasis (von Willebrand factor, soluble CD40 ligand, and P-selectin), pulmonary inflammation and oxidative stress (exhaled nitric oxide and exhaled breath condensate pH, malondialdehyde, and nitrite), and systemic inflammation and oxidative stress (urinary malondialdehyde and 8-hydroxy-2' -deoxyguanosine, plasma fibrinogen, and white blood cells). Linear mixed models were used to estimate associations of biomarkers with UFPs and PM2.5 measured 1-7 days prior to biomarker measurements (lags). The researchers found that the correlation coefficient for UFPs at two locations (~9 km apart) was 0.45, and at the same location, the correlation coefficient for PM2.5 vs UFPs was — 0.18. Changes in biomarker levels associated with increases in UFPs and PM2.5 were comparable in magnitude. However. associations of certain biomarkers with UFPs had different lag patterns compared to those with PM2.5. suggesting that the ultrafine size fraction (≤100 nm) and the fine size fraction (~100 nm to 2.5 µm) of PM2.5 are likely to affect PM -induced pathophysiological pathways independently. The findings suggest that number concentrations of UFPs monitored in a central site may be useful in a panel study design that mainly relies on within -person comparisons and when subjects work and resides within a relatively small area (<9 km radius). The results of this study suggest that particle emission controlling policies need to consider both the ultrafine and the fine size fraction of PM2.5 in order to protect human health. The complete study results are published in Environmental Science & Technology, published in March 2014: http://pubs.acs.orgidoi/full/10.1021/es5006016. PM AND PREMATURE MORTALITY SCAQMD Releases Latest Air Toxics Study, Concludes 57% Drop in Cancer Risk Since 2005 — The South Coast Air Quality Management District has released its Multiple Air Toxics Exposure Study IV (MATES IV) report, a monitoring and evaluation study conducted in the South Coast Air Basin. The study is a follow up to previous air toxics studies in the Basin and is part of the SCAQMD Governing Board Environmental Justice Initiative. 19 The MATES IV Study consists of several elements. These include a monitoring program, an updated emissions inventory of toxic air contaminants, and a modeling effort to characterize risk across the basin. The study focuses on the carcinogenic risk from exposure to air toxics. It does not estimate mortality or other health effects from particulate exposures. The report concludes that the Southern California's air is getting healthier and with that the risk of developing cancer from inhaling toxins has fallen significantly. Compared to previous studies of air toxics in the Basin, this study found decreasing air toxics exposure, with the estimated Basin -wide population -weighted risk down by about 57% from the analysis done for the MATES III time period in 2005. Concerted efforts to reduce emissions from diesel trucks and other vehicles account for much of the drop. However, risks persist from toxic pollutants such as diesel PM and benzene. Air management district officials noted that calculations of cancer risk from the particles have been underestimated. The California Office of Environmental Health Hazard Assessment found that actual cancer risk due to the toxins tracked in the study is about three times greater than current state guidelines suggest. Those findings are being reviewed and the guidelines could be updated in 2015, which would increase the cancer risk figures the air district has reported over the years. The area of greatest concern remains around the ports of Los Angeles and Long Beach where thousands of trucks and ocean-going vessels carry goods near neighborhoods. Air - associated cancer risk there is at least double that of other urban areas of Los Angeles, Orange, Riverside, and San Bernardino counties. A copy of the MATES IV report is available at: www.agmd.gov/docs/default-source/air- quality/air-toxic-studies/mates-iv/mates-iv-draft-report-10-1-14.pdf?sfvrsn=4. A SCAQMD press release announcing the report is available at: www.agmd.gov/home/library/public- information/2014-news-arch i ves/mates- i v -pr. NASA Map Shows Deadliest Places on Earth Associated with PM2.5 Air Pollution — A newly published map based on NASA -sponsored computer modeling of air quality shows the regions of the planet that suffer the highest annual premature death rates associated with levels of fine particulate air pollution (PM2.5). The global map was put together by Jason West, an earth scientist at the University of North Carolina, who is investigating the health impacts of air pollution. Based on models put together by West and his team, he estimates that 2.1 million premature deaths each year across the globe are the result of exposure to fine particulates that are emitted by motor vehicles, industrial smokestacks, and other sources. The highest levels of fine particulate emissions are found in East Asia, India, Indonesia, the Philippines, and some parts of Central Europe where mortality rates due to fine particulate pollution approach 1,000 premature deaths per square kilometer each year. Areas that are relatively "safe" from mortality associated with particulate emissions include the southeastern United States and interior regions of South America. Both of these regions have significantly reduced the levels of agricultural burning over the past 100 years. This graphic representation of global fine particulate air pollution, released in September 2013, is available at: v v, vv .theatlanticcities.com/technology/2013/09/heres-where- youre-most-likely-die-air-pollution/69461. The scientific study on which the map is based is available here: iopscience.iop.org/174S-9326/83/034005/article. 20 New Study Finds Association Between Reductions in PM2.5 Levels and Improved Life Expectancy in U.S. — A new study led by researchers at the Harvard School of Public Health (HSPH) has found an association between reductions in fine particulate matter and improved life expectancy in 545 counties in the U.S. from 2000 to 2007. It is the largest study to date to find beneficial effects to public health of continuing to reduce air pollution levels in the U.S. Controlling for socioeconomic status, smoking prevalence, and demographic characteristics, the results showed that a decrease of 10 micrograms per cubic meter in the concentration of PM2.5 during the period from 2000 to 2007 was associated with an average increase in life expectancy of 0.35 years in 545 U.S. counties. The study, which appears in the journal Epidemiology published in December 2012, looked at the effect on health of fine particulate matter (PM2.5). Numerous studies have shown associations between acute and chronic exposure to fine particle air pollution and cardiopulmonary disease and mortality. Studies have also shown that reductions in air pollution are associated with reductions in adverse health effects and improved life expectancy. Air pollution has been declining steadily in the U.S. since 1980, but the rate has slowed in the years since 2000. The HSPH researchers wanted to know whether the relatively smaller decreases in PM2.5 levels since 2000 are still improving life expectancy. The research expanded on a 200x) study published in the New England Journal of Medicine by some of the same authors mat found that reduced air pollution was associated with increased life expectancy in 211 urban counties. This new study looked at more recent data, more than two -and -a -half times as many counties, and included both rural and urban areas. The findings showed that there's a stronger association between declining air pollution and increased life expectancy in more urban, densely populated areas than in rural areas. The results also suggested that reduced levels of air pollution may be more beneficial to women than to men. As to why there was a stronger association between reductions in PM2.5 and improvements in life expectancy in urban areas, the researchers speculated that the composition of the particulates there may be different from that in rural areas. More information on this is available at: www.eurekalert.org/pub releases/2012- 12/hsop-dap 120312.php. EPA Research Finds Exposure to Ozone and PM2.5 Can Lead to Premature Death — According to research completed last year by EPA scientists, exposure to ozone and fine particulate matter (PM2.5) can lead premature death in populations that are not already gravely ill, which proponents say could help justify stricter ambient air standards for the two criteria pollutants. The research, published in the January 2012 edition of the journal Risk Analysis, finds that 130,000 to 340.000 premature deaths are attributable to exposure. The paper, "Estimating the National Public Heath Burden Associated with Exposure to Ambient PM2.5 and Ozone," indicates that "premature mortality attributable to poor air quality is not associated only with those already near death (sometimes called mortality displacement)," the Society for Risk Analysis said in a February 6, 2012 statement announcing the work. "These findings are in agreement with many other studies, shoving that improved air quality has yielded a direct positive impact on life expectancy and does not affect only those individuals near the end of life." 21 According to the paper, "among populations aged 65-99, we estimate nearly 1.1 million life -years lost from PM2.5 exposure and approximately 36,000 life -years lost from ozone exposure. These results show that despite significant improvement in air quality in recent decades, recent levels of PM2.5 and ozone still pose a nontrivial risk to public health." The findings also show greater health effects in urban areas, including New York, Pittsburgh, and Houston, than elsewhere. EPA researchers note that their findings are based on 2005 data and that they do not take into account air qual:t) improvements since then. One source says the research shows there is need for more work to be done in reducing PM2.5 and ozone levels, and it may boost EPA's efforts to tighten the ambient air quality limits for these pollutants The release of the study comes as EPA sent a February 3, 2012 letter to House Energy and Commerce Chairman Fred Upton (R -MI) noting that people are dying at PM2.5 levels below the current PM2.5 national ambient air quality standard. The letter is in response to December 14 questions Upton raised about the agenc} 's cost -benefit analysis of its air regulations. One environmentalist says EPA's reply to Upton's questions ``make it crystal clear that the current national fine particle soot standard is far too weak. Indeed, EPA reports that people are dying from breathing particle soot levels that are 'significantly below' the arbitrary Bush standard..." To view the study, go to: onlineiibcary.wiley.com/doi/10.1111/j.1539- 6924.2011.01630.x/ful I. Modeling Source -Attributable Health Impacts of Ambient Particulate Matter Exposure: Global Premature Mortality from Surface Transportation Emissions in 2005 — Outdoor exposure to ambient particulate matter was responsible for 3.2 million annual premature deaths in 2010 and is among the top ten leading risk factors for early death. While comprehensive air quality management is an effective strategy for air quality control in much of the developed world, the capacity to implement this approach in the developing world is generally weak. Nonetheless, developing countries have demonstrated an ability to enact sector - specific measures as a means of bottom -up air quality control. This study addresses the ongoing lack of information on sector -specific health impacts from ambient particulate matter exposure in order to inform new air quality improvement measures. The focus of this analysis is on the surface transportation sector. This study introduces the Transportation Attributable Fraction (TAF), a relative value that expresses the fraction of ambient PM concentrations attributable to surface transportation at any point in space and time. In 2005 the researchers estimate the global population -weighted average TAF was 8.5%, representing an average exposure of 1.75 µg/m3 per person. Approximately 247,000 annual premature deaths were attributable to surface transportation emissions, dominated by China, the U.S., the European Union and India. The global average crude mortality rate was 3.8 deaths per 100.000 and was highest in Western and Central Europe. The researchers concluded that the surface transportation emissions were a significant global source of premature deaths in 2005. The study demonstrated how sector -specific health burden can be estimated using outputs from the Global Burden of Disease or other estimates of ambient PM health burden. More information on this is available at: http://www.healtheffects.org/Pubs/AnnualConferenceBook2014.pdf. PM EFFECTS ON COGNITIVE: AND 'NI;t RO1.OGICAL FuNcTioNS Study Warns on Possible Air Pollution Link to Neuroinflammatory, Alzheimer and Parkinson's Pathologies in Children - According to a study led by University of Montana Professor Lilian Calderon-Garciduenas and her colleagues, children living in polluted megacities are at increased risk for brain inflammation and neurodegenerative changes, including Alzheimer or Parkinson's disease. Calderon-Garciduenas and her team compared 58 serum and cerebrospinal fluid samples from a control group living in a low -pollution city and matched them by age, gender, socioeconomic status, education levels achieved by their parents to 81 children living in Mexico City. The results found that the children living in Mexico City had significantly higher serum and cerebrospinal fluid levels of autoanti bodies against key tight junction and neural proteins, as well as combustion -related metals. The breakdown of the blood-bra;n barrier and the presence of autoantibodies to important brain proteins will contribute to the iieurointlammation observed in urban children and raises the question of what role air pollution plays in a 400% increase in multiple sclerosis cases in Mexico City, making it one of the main diagnoses for neurology referrals. Calderon-Garciduenas points out that there is a need for a longitudinal follow-up study to determine if there is a relationship bezv en the cognition deficits and brain MRI alterations previously reported in Mexico City children, and their autoimmune responses. What is clear, however, is that the children are suffering from immune dysregulation. Once there is a breakdown in the blood -brain barrier, not only will particulate matter enter the body but it also opens the door to harmful neurotoxins, bacteria and viruses. The autoimmune responses are potentially contributing to the neuroinfla amatory and Alzheimer's and Parkinson's pathology they are observing in young urban cnildreii. While the study focused on children living in Mexico City, others living in cities where there are alarming levels of air pollution suctz as Los Angeles, Philadelphia -Wilmington, New York City, Salt Lake City, Chicago, Tokyo. Mumbai, New Delhi or Shanghai, among others, also face major health risks. In the L.S.. 200 million people live in areas where pollutants such as ozone and fine PM exceed the standards. More information on this is available at: http://iospress.metapress.com/conten /xx65 82688105j48h/?p=823f040ead0940a8a2bd 15295c6a8 ffe&pi=0. Study Links PM2.5 Exposure to Physical Changes in Brain - According to new research in mice, long-term exposure tc, air pollution can lead to physical changes in the brain, as well as learning and memory problems ana even depression. Laura Fonken, lead author of the 1 study and a doctoral student in neuroscience at Ohio State University, stated that, while other studies have shown the damaging effects of polluted air on the heart and lungs, this is one of the first long-term studies to show the negative impact on the brain. For this study, Fonken and colleagues in Ohio State's Department of Neuroscience collaborated with researchers in the university's Davis Heart and Lunch Research Institute. In previous studies in mice, the Davis research group found that tine air particulate matter causes widespread inflammation in the body, and can be linked to high blood pressure, diabetes, and obesity. This study, published in October 2011, aimed to extend their research on air pof!ution to the brain. In the new study, mice were exposed to either filtered air or polluted air for six hours a day, five days a week, for 10 months. The polluted air contained fine particulate matter. The concentration of particulate matter that the mice were exposed to was equivalent to what people may be exposed to in some polluted urban areas. After 10 months of exposure to the polluted or filtered air, the researchers performed a variety of behavioral tests on the animals. The researchers also performed tests on the nippocampal area of the mice's brains. Results showed clear physical differences in the hippocampi of the mice who were exposed to polluted air compared to those who weren't. In addition, several of the co-authors of this study from the Davis research center found that chronic exposure to polluted air leads to widespread inflammation in the body, which is linked to a variety of health problems in humans, including depression. The study found evidence that this low-grade inflammation is evident in the hippocampus. A copy of this study is available for purchase at: www.nature.com/mp/journalivaopineuramtifuli/inp201176a.html. Neurotoxicity of Traffic -related PM on Human Brain Structure - This epidemiologic study aimed to investigate whether late -life exposures to particulate air pollutant affect: the risk for mild cognitive impairment (MC!)/dementia: and MRI-measured brain volumes. Exposures to ambient PM are a novel environmental determinant of cognitive functions of elderly. Recent data from animal studies highlighted the neurotoxicity of PM exposures near roadways. However, very little is known about the putative adverse effects of traffic -related PM exposure on aging brains. Diesel exhaust, an important contributor of ambient PM exposure from traffic sources, has well -documented neurotoxic etlects in animals. The study examined whether diesel PM exposure affects different brain regic;ns involved in human cognition, focused on association brain and hippocampus. The researchers selected an ongoing, well -characterized and geographically -diverse population of older women, the Women's Health Initiative Memory Study (WHIMS) cohort. Structural brain MRI scans were obtained in 2005-2006 (aged 71-89 years) to quantify the volumes of gray matter and normal -appearing white matter of 1,403 WHIMS participants. Annual diesel PM exposure was assigned to each residential census tract in a nationwide spatiotemporal mapping of yearly diesel PM estimates. The researchers had previously used a generalized additive model to conduct census tract -specific temporal interpolation of diesel PM estimate and complete the nationwide spatiotemporal mapping of annual diesel PM exposures in 1996-2005. This approach was informed by the results of 4 -level hierarchical models/spatiotemporal analyses of diesel PM estimates given by the EPA National -Scale Air 24 Toxics Assessment Program. which employed motor vehicle emission simulators and air pollution dispersion models. The study showed that older women with higher cumulative exposures to diesel PM, compared to those with lower exposures. had smaller volumes of gray matter volumes associated with higher cumulative exposures were found in all three associated cortices (frontal, parietal, and temporal). Over the interquartile range of cumulative exposure to diesel PM from on -road mobile sources (0.32 µg/m'), the multicovariate-adjusted difference in mean frontal gray matter volume was 3.08 cm3, adjusting for geographic region, demographic features, socioeconomic status, lifestyle, and clinical characteristics including cardiovascular disease risk factors. The researchers found no statistically significant difference in the hippocampal volume associated with diesel PM exposure. The researchers concluded that 1 :nuings from their cross-sectional analyses support the hypothesized neurotoxic effects of traffic: -related PM on association cortices. The observed smaller gray matter volume associated with diesel PM exposure was consistent with the emerging data on synaptic neurotoxicity in animals with PM exposures near roadways. More information on this is available at: http://www.healtheffects.orwiPubs/A:1r ualConicrenceBook2U 14. pd f. Exposure to Vehicle Emissions Results in Altered Blood Brain Barrier Permeability and Expression of Matrix Metalloproteinases and Tight Junction Proteins in Mice — Traffic -generated air pollution -exposure is associated with adverse effects in the central nervous system (CNS) in both human exposures and animal models, including neuroinflammation and neurodegeneration. While alterations in the blood brain barrier (BBB) have been implicated as a potential mechanism of air pollution-inJLccd CNS pathologies, pathways involved have not been explained. Recent studies report a positive correlation between exposure to high levels of air pollution and increased hospital admissions/occurrence for cerebrovascular events such as stroke. Air pollution exposure has also oven associated with other adverse effects on the CNS including neuroinflammation and neurodegeneration, which are associated with dementia -related disorders such as Alzheimer's disease and Parkinson's disease. With stroke being the third leading cause of death in the Western -world, as well as the leading cause of adult disability; and with the prevalence of neurological disorders such as AD and PD, which effect more than 4 million people in the U.S. and an estimated 27 million worldwide, it is critical to identify risk factors, including environmental, which may cause progression of these pathologies. While the pathways associated with air pollution-xposure induced effects on the CNS are not fully understood, recent studies suggest that pollutants, including those derived from vehicular emissions, may disrupt the integrity of'the I3BB. BBB disruption, and resulting alteration in permeability, has been implicated in the pathology of neurodegenerative disease, states of neuroinflammation, rev in, andior hemorrhagic transformation during ischemic stroke. The goal of this study. publisl„u in December 20; 3, was to determine whether inhalation exposure to mixed vehicle exhaust G.iV* E j mediates alterations in BBB permeability, activation 25 of matrix metalloproteinases (MMP)-2 and -9, and altered tight junction (TJ) protein expression. The data from this study indicate that inhalation exposure to traffic -generated air pollutants promotes increased MMP activity and degradation of TJ proteins in the cerebral vasculature, resulting in altered BBB permeability and expression of neuroinflammation markers. More information on this is available at: http://www.particleandfibretoxicologyscorn/content/10/1/62. New Study Finds Air Pollution Linked to Cognitive Decline in Later Years — According to a new study, particulate matter in vehicle exhaust and other sources of air pollution may hasten cognitive decline in older adults. Jennifer Ailshire who co -wrote the report is with the Center for Biodemography and Population Health and the Andrus Gerontology Center at the University of California in Los Angeles. She. along with Philippa Clarke of the Institute for Social Research at the University of Michigan, Ann Arbor, say that based on their results, improvements in air quality may be an important strategy for reducing age -related cognitive decline. There has been some evidence that people living in more polluted areas have greater rates of cognitive decline, and the link is not explained by wealth and other social factors, the researchers point out in the Journals of Gerontology: Series B, published in June 2014. They gathered information from one wave of a large ongoing survey started in 1986, and focused their analysis on 780 participants who were 55 years of age or older at the time of the 2001/2002 survey. Routine measurement of air pollution by census tract did not start until the late 1990s. Cognitive function was measured by ,path and memory tests and participants got a score based on the number of cognitive errors they made. Air pollution levels for each participant's neighborhood were calculated using fine particulate levels reported by the EPA's Air Quality System. Ailshire and Clarke found the average PM2.5 concentrations in the study's participants' environments were 13.8 µg/m3, which is above the EPA's air quality standard of 12 µg/m3. Then they compared the cognitive error scores to pollution levels and found that people living in high pollution areas, with 15 pg/m' or moce of PM2.5 had error scores 1.5 times those of the participants who lived in low pollution arias with no more than 5 µg/m3. The authors note that poverty and other social factors as well as health problems can influence cognitive function. And poorer neighborhoods tend to be more polluted. But after the researchers adjusted for education, employment, gender, marital status and several other factors, the differences in cognitive error rates remained. Scientists believe that PM may affect cognitive function in older adults by its harmful effects on the cardiovascular system, which is connected to the brain through blood vessels, and possibly by directly acting on the brain itself. More information on this is available at: http://psychsocgerontology.oxtordjournals.orgicontent/early/2014/06/05/geronb. zbu064.short?rs s=1. 36 Study Links PM Air Pollution to Autism, Schizophrenia — According to a new study published in the journal Environmental Health Perspectives, particulate matter in air pollution may irritate very young brains enough to cause problems. When mice younger than 2 weeks old were exposed to very small particle pollutants, their brains showed damage that is c"nsistent with brain changes in humans with autism and schizophrenia. Research on mice doesn't always translate to humans. But Deborah Cory-Slechta, professor of environmental medicine at the University of Rochester Medical Center and lead researcher in the study, said the results could lead to regulations on even the smallest types of pollutant particles. Schizophrenia is a mental illness that interferes with a person's ability to think clearly, manage emotions, make decisions and relate to others. Autism, and autism spectrum disorder, are terms for complex disorders in brain development. The disorders are present in varying degrees, and include difficulties in social situations, verbal and nonverbal communication, and repetitive behavior. The causes of both are a source of controversy and confusion. The University of Rochester `ileciicat Center research built on other studies that have shown a link between air pollution ar.d autism in children. Cory-Slechta noted in 2013 study in JAMA Psychiatry, formerly .4i -chives of General Psychiatry, that reported children who lived with high levels of traffic -related air pollution during their first year were three times as likely to develop autism. The medical center's research took a new direction in trying to show whether ultrafine particles would damage the brain, and if so, how. The National Institute of Environmental Health Sciences, part of gr±e National Institute of Health, financed the three-year study. Larger particles regulated by the- EPA actually are less harmful because the nose and lungs keep them out of the bloodstream. But very fine particles, which aren't regulated, can slip through, travel through the lungs and be picked up in the bloodstream. The researchers exposed mice for specific periods of time to levels of air pollution found during rush hour in cities such as Los Angeles. Boston, Atlanta, and New York City. One group of mice was examined 24 hours after its final exposure, another group 40 days later and a third group 270 days later. There was evidence of permanent inflammation and high level of neurotransmitter that is seen in humans with autism and schizophrenia. However, that doesn't mean a line exists between pollution and brain disorders. More information on this is avai lat)ie at.. http://www.urmc.rochester.eUL. i 00. Associations between Traffic -Related Black Carbon Exposure and Attention in a Prospective Birth Cohort of Urban Children — Ambient air pollution may have neurotoxic effects in children. Data examining association between traffic -related air pollution and attention remain sparse. 17 Researchers examined the associations between black carbon (BC), a marker of traffic particles, and attention measures ascertained at 7-14 years of age among 174 children in a birth cohort based in the Boston, MA, area. The researchers estimated the BC levels using a validated spatial -temporal land -use regression model based on residence during children's lifetime. The children completed the Conner's Continuous Performance Test (CPT) measuring omission errors, commission errors, and hit reaction time (HRT), with lighter scores indicating increased errors or slower reaction time. Multivanabie-adjusted linear regression analyses were used to examine associations between BC and each attention outcome. The children in the study were primarily Hispanic (56%) and Caucasian (41%); 53% were boys. The researchers found a positive association between higher BC levels with increased commission errors and slower 1IRT. adjusting for child IQ, age, sex, blood lead level, maternal education, pre- and postnatal tobacco smoke exposure, and community -level social stress. Notably, the association was weaker, though still positive, for the highest BC quartile relative to the middle two quartiles. Sex -stratified analysis demonstrated statistically significant associations between BC and both commission errors and HRT in boys, but BC was not significantly associated with am of the CPI outcomes in girls. In this population of urban children. the researchers found associations between BC exposure and higher commission errors anc slower reaction time. These associations were overall more apparent in boys than girls. More information on this study, published in the journal Environmental Health Perspectives in June 2013, is available at: http://www.ncbi.nlm.nih.gov; pmc/articics/Piv1CS70199W. Convergence of Human, Animal, and In Vitro Studies on the Effects of Air Pollution on the Brain — In addition to increased morbidity and mortality caused by respiratory and cardiovascular diseases, air pollution may also negatively affect the brain and contribute to central nervous system diseases. A major constituent of ambient ultrafine PM is represented by traffic -related air pollution, mostly ascribed to diesel exhaust. Human epidemiological studies and controlled animal studies have sho ti. a-. t: tat exposure to air pollution may lead to neurotoxicity. In addition to a variety o.oehav ioral abnormalities, two prominent effects caused by air pollution are oxidative stress and iieuroinflammation, which are seen in both humans and animals and are confirmed by in vitro s tidies. Human and animal studies suggest that air pollution (and diesel exhaust) may cause developmental neurotoxicity and may contribute to the etiology of neurodevelopmental disorders. including autistic spectrum disorders. In addition, air pollution exposure has been associated w itn increased expression of markers of neurodegenerative disease pathologies. More information on this study, published in the _journal BioMed Research International in 2014, is available at: http://w i.cornijournais,bmri/2014/736385/. 78 PM EFFECTS ON HuNIAN REPRODI t 'HUN New Study Concludes that Carbon Nanoparticles in PM2.5 Can Lead to Miscarriage — A research team at Lanzhou University has found that carbon nanoparticles can pass through the placental barrier, causing damage to an unborn baby and leading to miscarriage, according to China Science Daily. The research result has been published in Scientific Reports in March 2014. Dr Qi Wei, main author of the report, said tests on pregnant laboratory rats have proved that carbon nanoparticles can cross the placental barrier and invade the fetus' body, causing estradiol secretion to increase, and hormone secretion and blood vessels to decrease, which will delay the fetus' development, and lead to stillbirth and miscarriage. Professor Wu Wangsuo, corresponding author of the report, said research results have proved that carbon nanoparticles cause damage the fetus. The research has directly verified that particulate pollutants, PM2.5 included, can cause harm to pregnant people, Wu said, and warned those exposed to severe particle contamination. The paper also suggested treatments for pregnancy -related disease caused by pollutants, Wu added. A copy of the study is available at: http://www.nature.com/srep/2014/ 143 311/srcp04352/fulltsrep04352.html. Study Finds Air Pollution Exposure in Second Trimester May Increase Asthma Risk in Children — According to a new study presented at the 2014 American Thoracic Society International Conference in San Diego. children who are exposed in utero to high levels of PM air pollution during the second trimesi.er of pregnancy may be at greater risk of developing asthma in early childhood. The study was published in May 2014. Fetal lung growth and structui-ai development occurs in stages, the researchers explained, thus timing of exposure may have di r erential effects on postnatal disease risk. They assessed the windows of susceptibility to particulate air pollution exposure during pregnancy on childhood asthma onset in a prospective urban birth cohort. The study included 430 full -term (%37 weeks gestation at birth) children followed to age 7 years and their mothers. Daily exposure to air pollution from sources including traffic, power plants, and other industrial sources consisting of fine panicles in the prenatal period was estimated based on where these mothers Iiked. These fine particle have been linked to the greatest health risk and previous studies have suggested that effects on pregnant women can be transferred to the growing baby. Children's physician -diagnosed asthma was ascertained by maternal reports up to age 7 years. The team examined associations between weekly averaged prenatal PM2.5 levels and children's asthma using distributed lag models. This modeling framework describes delayed effects between predictors and an outcome and estimates associations at each week while adjusting for exposures at other weeks. assuming that the associations varying smoothly over time during gestation. Effect modification by (gender and maternal pre -pregnancy obesity was also examined. The researchers found that exposure to higher levels of fine particles in the second trimester was most strongly associated with increased asthma onset among the children, particularly for those born to non -obese mothers. The effect of maternal obesity, another known risk factor of childhood asthma onset, may be so strong that it was difficult to determine additional effects of air pollution among children born to obese mothers in this setting, the researchers noted. Separately, a study in the American Journal of Respiratory and Critical Care Medicine reported that exposure to high levels of traffic -related air pollution is associated with changes in the right ventricle of the heart that may contribute to the known connection between air pollution exposure and heart disease. The study involved 3,896 participants in the Multi -Ethnic Study of Atherosclerosis who were free of clinical cardiovascular disease and who underwent cardiac magnetic resonance imaging (MRI). Using estimated exposure to outdoor N0x at the homes of participants over the year preceding MRI, the authors found that increased exposure to N0x was associated with an approximately 1.0 g (5%) increase in right ventricular mass and a 4.1 mL (3%) increase in right ventricular end -diastolic volume. More information on this is atiaiiable at: http://ww,w.eurekalert.org/pub_releases/2014- 05/ats-ape051214.php. Adverse Reproductive Health Outcomes and Exposures to Gaseous and Particle Matter Air Pollution in Pregnant Women — This study aimed to identify sources and components of air pollution mixtures unit contribute most to the adverse reproductive outcomes and to determine the effect modification by socioeconomic factors, race, and body mass index. California birth certificate data (?„01-2008) were obtained with maternal address at delivery, geocoded at parcel level wl►ei'i ver possible. Primary PM concentrations were modeled for 2000-2006, by emission sources and size fractions (PM0. 1 , PM2.5, and PM 10). Secondary particles for 2000-2008 were also modeled. with less detail on source origin. Monthly ambient ozone, NO? and PM2.5 from EPA monitoring network (2000-2008) were interpolated using Bayesian Kriging. The researchers studied the relationships between low birth weight (LBW) in term born babies and interpolated 03, NO2, and PN12.5, modeled primary PM by source and composition and traffic density in Los Angeles County. using generalized additive models adjusting for potential confounders. The researchers found that in Los Angeles, slightly increased (LBW) risk are associated with primary PM2.5 and PMVi0.1 mass, v, ith se, eral sources (especially gasoline, wood burning and commercial meat cooking) of primary PM, and with species of primary PM (elemental and organic carbon), K, Fe, Cr, Ni, Ti). Slightly increased LBW risks are also associated with measured total PM2.5, NO-, and local traffic indices, but not with 03. Stronger associations are 30 observed in infants born to Hispanic women, and women with low socioeconomic status, chronic hypertension, diabetes and high BM I. Preterm birth risk increased by 9-10% and 17% for interpolated NO? and 03, and interpolated total PM2.5, respectively, per inter -quartile range increase in entire pregnancy exposure in California women. Associations with modeled primary PM are weaker but statistically significant. For primary PM2.5, the strongest associations by source are for onroad gasoline, followed by onroad diesel. offroad gasoline and commercial meat cooking. Overall, associations appear slightly higher for PM0. I than for PM2.5. For PM2.5 composition, the strongest positive associations with preterm birth risk are observed for nitrate, ammonium, and secondary organic aerosols. followed by elemental carbon, organic carbon and potassium, with metals showing weak and generally non -significant associations. For PM0.1, 8-11% increased risk is observed per inter -quartile range exposure of Al, Ti, V, Si, and SOA. Associations are generally higher in lower socioeconomic status and African American populations. The researcher found a modest influence of traffic and meat -cooking related pollution on term low birth weight, and a strongez influence on preterm birth. Both secondary pollutants and species in primary PM are strongly associated with preterm birth. More information on this is available at: http://www.healtheffects.ordArchiv.2AnnCont2011 Poster pdfs/Wu.pdf. PM FROM ALTERNATIVE Ft.EI,S Study Reports that Siodiesdl Prvi May Have Greater Adverse Health Effects Than Diesel — A recent publication in the ACS journal Environmental Science & Technology, published in September 2013, characterized PM generated from petroleum diesel and a blend of 20% soy -derived biodiesel (B20) using the same engine and operating conditions and conducted experiments in two human cell cultures. as well as female mice. They found that, although the PM mass from the B20 fuel was a facto i' iu o lower than: 30, the concentrations of inflammatory mediators in the in vitro ct;l:s and bronchoalveolar lavage fluid of mice were 20- 30% higher in the B20 -treated cells on an equivalent mass basis. The work was published by researchers from the University of Vermont using a 1.9 -liter VW light -duty engine operated over a 9 -mode steady-state test cycle. Particle measurements were made using a scanning mobility particle sizer. The BO particles exhibited a single mode distribution centered around 51 nm whereas the 820 PM nad a mode at 32.2 nm and a larger 51 nm shoulder. The surface area of the 820 particles was about two times higher than the BO particles. The BO particles consisted or 54% non -polar compounds of n-alkanes, alkenes, and a mixture of 16 PAHs. The polar compounds in the BO were primarily esters, ketones, and acids. In contrast, the B20 PM was made up o 68% polar compounds and the PAH content was reduced by a factor of two relative to the BO particles. Furthermore, the content of benzo(a)pyrene, a Class 1 carcinogen (accoruing to IARC), was two times higher in BO compared to B20. Both the in vitro and in vivo inflammation response from cytokine/chemokine data to an equal mass of PM resulted in a higher response to B20 PM, suggesting that biodiesel PM may be associated with more significant health outcomes. The authors suggest that the mechanism for the greater inflammatory response and reactive oxygen species (ROS) in the mice and cells treated with B20 PM may be linked to the larger polar or soluble organic component in B20 exhaust. The smaller size and higher surface area of B20 PM may also be a contributor 1:o the adverse health effects observed in this study. The full reference for this publication is: Naomi K. Fukagawa, Muyao Li, Matthew E. Poynter, Brian C. Palmer, Erin Parker, John Kasumba, and Britt A. Holmen (2013), "Soy Biodiesel and Petrodiesel Emissions Differ in Size, Chemical Composition and Stimulation of Inflammatory Responses in Cells and Animals," Environmental Science & Technology, doi: 10.1021 /es403 146c, pubs.acs.org/doi/abs/10.1021/es403146c. Studv Characterizes PM Toxicity from Diesel Passenger Cars Using DPF and Biodiesel Fuel — A European study nubl isined recently in the Journal of Environmental Science and Technology looked at the influence of 1'M control technology and fuel types on PM emissions and health effects. The overall conclusions showed that both the use of a DPF and the use of B50 fuel reduced the PM mass emissions from the diesel light -duty vehicles; however, the biodiesel fuel did not reduce the hazard of engi►ie emissions while the DPF did on a per distance driven basis as indicated by reduced cytotoxicity, oxidative stress, and pro -inflammatory potential. The PM emissions from two diesel passenger cars certified to Euro 4 emission standards were characterized over four test cycles made up of composites containing the Urban Driving Cycle, Extra Urban Driving Cycle, and Artemis Urban and Artemis Rural Road Cycles. The 2.2 L Honda Accord was equipped with a DOC and an underfloor deNOx catalyst; the 2.0 L Peugeot 407 came with a DOC, an iron -based metal fuel additive, and an uncatalyzed DPF. The vehicles were fueled with petroleum diesel containing 10 ppm sulfur and a 50% blend of petroleum diesel and rapeseed -derived biodiesel. PM from om a constant volume sampling (CVS) system was collected on filters using a' high volu,rie sample:. PM samples were extracted and a number of toxicity responses were measured, including: oxidative potential, cytotoxicity, and pro - inflammatory markers. The following obsen ations N \ e: made by the authors and further discussed in the paper: • Use of B50 reduced PM mass by 50% and PM emission rates were reduced by 95% using a DPF, dropping emissions below the Euro 5 limit. • Per unit mass, PM from B50 caused more cytotoxicity and greater release of pro - inflammatory markers than petroleum diesel and on an equal mass basis may be more harmful. This was reduced on a kilometer basis. • PM from DPF-equipped vehicles contains higher fraction of semi-volatiles which contributes >70% of the oxidative activity. This resulted in a higher pro - inflammatory response and cytotoxicity per mass of post-DPF PM versus non -filtered PM. However, on a per kilometer basis, PM emissions from a DPF-equipped vehicle were less cytotoxic with iovver oxidative potential. The toxic potential of PM can differ depending on the method or metric used and the authors suggest that a harmonized test protocol be used to compare results from different studies to allow conclusions on the impact on human health risks to be analyzed. The complete reference for this paper is: Gerlofs-Nijland. M.E. et al, "Cell Toxicity and Oxidative Potential of Engine Exhaust Particulates — Impact of Using Particulate Filter or Biodiesel Fuel Blend," Environ. Scr. Tuchtiol., DOI: 10.1021/es305330y, 4/18/13, www.unboundmedicine.com/medliiie/citation, 23597117/Cell toxicity and_oxidative_potential of engine exhaust_particles impact of using particulate filter or biodiesel fuel blend . Characterization of Particulate Matter Emissions from a Current Technology Natural Gas Engine - A team of researchers conducted experiments to characterize the particulate matter size distribution, nuamoer concentration, and chemical composition emitted from transit buses powered by a EPA 2010 -compliant, stoichiometric heavy-duty natural gas engine equipped with a three-way catalyst (TWC). Results of the particle -size distribution showed a predominant nucleation mode centered close to 10 nm. PM mass in the size range of 6.04 to 25.5 nm correlated strongly with mass of lubrication-oil-uerived elemental species detected in the gravimetric PM sample. Results from oil analysis indicated an elemental cc.1rnpos tion that was similar to that detected in the PM samples. The source of elemental species in the oil sample can be attributed to additives and engine wear. Chemical speciation of PIvl showed that lubrication -oil -based additives and war metals were a major fraction of the PM, mass emitted from the buses. The results of the study indicate the possible existence of nanoparticies below 25 rim formed as a result of lubrication oil passage through the combustion chambe . Additionally, the result of oxidative stress analysis on the PM samples indicated strong co!-i el. tions v. ith both the PM mass calculated in the nanoparticle-size bin and the mass elemental species that can be linked to lubrication oil as the source. More information on this stuc.y, published in the journal Environmental Science & Technology in June 2014, is available al. iltip://pubs.acs.org/doi/abs/10.1021/es5005973. U.S. EPA AND C:ALIFORNI .ARB 1" \ f) RE sE: ARCH PROJECTS ON THE HEALTH EFFECTS OF PM U.S. EPA Clean Air Research Centers Awarded Funding to Investigate Health Effects of Air Pollution — The U.S. EPA Clean Air Research Center has awarded funding to the following organizations to research the health effects of air pollution. A list of EPA funded research projects on air pollution effects on health is available at: http://www.epa.gov/ncer/claresi. • University of Washington center fvf Clean Air Research (UW CCAR): Project Amount: $8,000,000: Project P erbd: December 1, 2010 through November 30, 2015. The UW CCAR is focused o,-, the cardioNdascular health effects of near -roadway pollution, a complex mixture of particle, vapor and gas phase components that vary by vehicle emission source, road surface, extent of physical aging and the type and degree of atmospheric processing and photochemical reactions. This exposure scenario is not only known to be of considerable health importance, it also serves as a prototypical case for developing research approaches to dealing with multi -pollutant exposure -effect relationships. The researchers' aim is to integrate exposure, epidemiological, toxicological, clinical, and statistical sciences to study cardiovascular hazards of fresh and aged roadway emissions and significantly advance their understanding of the components and reaction procucts that cause these effects. Researchers from four institutions are joining in a multi -disciplinary effort to study health effects of near-roadvyay pollution in line with current efforts to move from a single - pollutant to a multi -pollutant perspective. The Center consists of five highly -integrated research projects and two facility cores (including a Biostatistics Core) that together have the following six tasks: 1) to characterize real -world near -roadway pollutant concentrations, particle size disirioutions and chemical composition; 2) to simulate realistic contrasting near-roacm ay multi -pollutant exposure atmospheres for laboratory animal and human studies; 3) to identify cardiovascular and immunologic effects and the pathogenic mechanisms of near-rcoauway exposures using animal models; 4) to identify cardiovascular and immunologic effects of near -roadway exposures in human clinical studies; 5) to identify effects of long-term exposure to traffic -derived particle and gases on sub -clinical measures of cardiovascular disease and DNA methylation in a multi- ethnic population; and 6) to cJcelop a statistical and methodological framework for studying health effects ofmuttu-pollutant mixtures. The Center program of research addresses at least three of the research questions posed in the Request for Appiicau�on (RFA): 1) pollutant health effects in a multi - pollutant context; 2) biological mechanisms underlying health effects; and 3) exposure - response relationships. identifying the most hazardous components of near -roadway exposures will allow more focused. coordinated and effective air pollution health policy based on sound science to reu,Jc2 h:altn impacts of this multi -pollutant exposure. More information on this is ava::uole at: http://cfpub.epa.gov 'ncer abstra..t index.cfm/fus :action/display.abstractDetail/abstract/9 282/report/O. • Great Lakes Air Center for Inter; native Environmental Research (GLACIER): Project Amount: $7,999,875; Project Period: January 1. 2011 through December 31, 2015. GLACIER is a multi-disciplinai.: center with the objective to explore one of the most prevalent and important global health -environmental interfaces: the interrelationships between facets of the cardiometaholic syndrome (CMS) and air pollution. CMS is among the leading causes of death a4 -.J !Heats to world o. ide health. In tandem, exposure to air pollution. most notably tine particle matter remains highly prevalent and ranks among the leading causes of global mottaiitti. inter -relationships and health impacts of this growing confluence between tiles: tv c1 epidemics are of tremendous importance to elucidate. The researchers' previous research has elucidated that PM2.5 exposure plays a critical, yet under -appreciated, role in eliciting or exacerbating several key facets of the CMS, including elevating blood pressure. impairing vascular function, and even worsening metabolic insulin sensitivity and adiposity over a chronic duration. The researchers have also found that the location of exposure, multi -pollutant context, and constituents within PM2.5 affect the responses. The full extent and importance of inter -relationships between CMS and air pollution, individual susceptibility, specific pollution components, multi -pollutant atmospheres. PM2.5-ozone coexposures, and underlying mechanisms of toxicity are all key issues remaining to be clarified. The researchers' center's overall hypothesis is that PM2.5 and ozone are: l ) capable of eliciting multiple important adverse cardiometabolic health effects that are dependent on; 2) the local multi -pollutant milieu; 3) an individual's pre-existiri cardiovascular (CV) and metabolic condition; and 4) the interactive toxicity of PM2.5 and ozone coexposure. In conjunction with core facilities. GLACIER consists of 3 controlled exposure projects that each addresses specific aspects of zne CMS -air pollution interface. The projects are scientifically integrated and Jci.aclive which will foster synergistic insights and cohesive synthesis of conclusions. The Lxposure Characterization Core (ECC) is an integral part of all three Projects of the Great Lakes Air Center for Integrative Environmental Research. In coordination with aid support of the GLACIER Research Projects, the ECC will provide measurements of multi -pollutant exposures for both human subject (Project 1) and animal toxicology (Project 2 and 3) studies. The overall objectives of the ECC are to: 1) determine the mass, size. a1,a chemical composition of pollutants for each exposure period; 2) determine the atmospheric emission sources responsible for the observed exposure concentrations: and 3) provide a detailed assessment of the differences in air pollution composition, sources. aria chemistry between each of the exposure sites across each of the Projects. The or,,c ct yes of the GLACIER BDMC are to provide guidance for the statistical design and analysis of studies and ata management services that allow for the integration of the data into a single platform that facilitates timely analysis for GLACIER investigations and projects. Specific aims for this Core are: 1) to assist GLACIER investigators with statistical and data aspects of their research by providing expertise in the design, conduct arid analysis of studies in Project 1-3; 2) to establish a database for each project on a secure computerized system; and 3) to implement a website to allow data import and expori in a secured, controlled environment with a user- friendly interface. Project I aims to clarify in ilc:mmmariCite. mechanisms of adverse CMS responses and the concentration -response relations,uip of acute exposures to differing PM2.5 mixtures. Project 2 aims to determine the short-term CV, autonomic and airway toxicity in rats exposure to differing PM2.5 mixtures. Project 3 expands on the main theme b) determining the CMS toxicity of differing longer -term exposures in mice. Bach project wilt also investigate the role of pre-existing susceptibility and the comparative effects of PM2.5 mixtures derived from 2-3 dissimilar multi -pollutant milieus of re._:o1-iiii importance. Toxic effects of PM2.5, ozone, each alone and in combination, will he evaluated at each location. The researchers will address: 1) temporal -response relationships to pollutant exposure and the development of CMS: 2) CMS effects of ozone and fine particle mixtures from 3 differing locations and their interactive toxicity; 3) the role of obesity and pre-existing cardiometabolic abnormalities in individual susceptibility; 4) concentration -response relationships for particles and ozone: and 5) mechanisms whereby air pollutants elicit CV and metabolic health effects. Their results will provide critical insights into the health effects of PM2.5, ozone, anu their co -exposures in a multi -pollutant context. More information on this is avai iabe at: http://cfpub.epa.gov /nccr_abstracts, indcx.cfm/fuscaction/display.abstractDetail/abstract/9 281 /report/0. • Multi -Scale Assessment of Health Effects of Air Pollution Mixtures Using Novel Measurements and Models: Project Amount: $7.999,779; Project Period: October 1, 2010 through September 30. 20 . A multi -institutional, multi -disciplinary Center is proposed to address critical issues relating to the public health impacts of ambient air pollution. The overarching theme of the Center is a focus on characterizing ambient air pollution mixtures and elucidating their role in human health risk associated with air pollution. Novel measurements and modeling approaches will be applied in the context of a tiered multi -scale assessment of the health risks of mixtures characterized based on: 1) biological considerations (oxidants); 2) environmental ;'management (sources); 3) evidence -based considerations (traffic emissions); 4) empirncai assessment (data -based approach). Four Research Projects in oc 3.upporzed by three Cores: an Administrative Core, an Air Quality Core and a Biostatistics Core. Project 1 vv ill develop and deploy instrumentation to measure oxidants (including aerosol reactive oxygen species) and other species of interest to better unuerstana their origins and atmospheric transformation and for use in characterizing mixtures for the three health studies. Project 2 will make direct use of these measurements to confirm associations witn markers of oxidative stress in commuters. Project 3 and 4 will use a combination of measurements and modeled air quality estimates in large population studies, with Project 3 investigating questions regarding risks of in utero and early life exposures to air pollutant mixtures in two major new birth cohorts and Project. 4 assessing underlying consistencies in morbidity associations across selected cities that have comprehensive daily air pollution characterization. The health projects inciude assessment of potentially sensitive and vulnerable subpopulations. More information on this is avaitaote at: http://cfpub.epa.gov/ncer_ar,stit ;s: indcx.cfm/fuseact ion/display.abstractDetail/abstract/9 280/report/0. • Air Pollution Mixtures: Health Effects Across Life Stages: Project Amount: $7,997,561; Project Period: Jar►uar\ 1, 2011 through December 31, 2015. The main objectives of the prop._>seci Center are: I ) to investigate the acute and chronic health effects across life stages of six exposure metrics (short- and long-term exposures 36 to individual pollutants. pollution sources and multi -pollutant mixtures) on: cognitive/neuropsychological function. cardiovascular/endothelial function, inflammation, birth weight/growth. and CVD-related hospitalization/mortality, and 2) to identify susceptibility and vulnerability factors that modify these effects. Project 1 will investigate the toxicity of air pollutant mixtures in Boston, focusing on the identification of pollutant charactcr;stics that are responsible for the most toxic effects, including: individual components, combinations of components (mixtures), formation processes, and source types. Exposures will be generated using a novel integration of the ambient particle concentrator and photochemical chamber technologies. Sprague- Dawley rats will be exposed and toxicity will be assessed by changes in: in vivo oxidant response, blood pressure. inflammation. and vascular reactivity. Project 2-5 will examine the health effects of the six exposure metrics on multiple integrated specific health outcomes. Project 2 will examine effects of these exposure metrics on cognitive and neuropsychological function:,ardiovascular and endothelial function; inflammation; and oxidative stress among elderly individuals living in New England enrolled in the Normative Aging Study. Project 3 vii; investigate effects of the six metrics on cognitive impairment and interference. as vet: as vascular and endothelial function, among middle- aged and older adults living ;n New England enrolled in the Framingham Offspring and Third Generation Study. Project 4 wili investigate effects of the metrics on somatic growth, blood pressure. card10 ascular fitness, and cognition, in the Viva ongoing prebirth study of over 1.300 children from Eastern Massachusetts. Project 5 will estimate mortality and hospitalization :-isics in nundreds of counties across the U.S. It will also study two cohorts in New En4tandi to: 1) estimate risks of adverse birth outcomes using approximately 700.000 live births; and 2) assess mortality and morbidity risks using 2.3 million Medicare enrollees. hest ;projects (2-5) will study the modifying effect of measures of susceptibility and vulnerability and will link outcomes to the same pollution mixtures across all .ife stages. More information on this is ava,:abte at: http://cfpub.epa.gov - necr_absirac Ls/ indt x.cfm/fuseactioni d isplay.abstractDetail/abstract/9 283/report/0. ARB Funded Research Projects on the Health Effects of PM — ARB has funded the following research projects to study the eifccts of PM on human health. A complete list of ARB funded research projects are availabl-: at: !ittp:• .www'.arb.ca.gov,'research/research- results.php?category=Health%20Exposure. • Co -Exposure to PM and 03: Puknonary C Fiber Platelet Activation in Decreased HRV: Contractor: LUC Da\ is. i'rincipai Investigator: Fern Tablin; Project Status: Active. Fine particulate matter (PM2.5.) anc ozone (03) appear to be responsible for the majority of serious health effects related tc air pollution exposure, although little is known about how these pollutants cause adverse health effects, or whether or not they have interactive or synergistic effects onneaizi ei.cir.oinLs. The Jc,_;:,ctive of this study is to examine a hypothesized mechanistic pthilwva'v for the cardio ascular effects of ozone and PM2.5, and to examine whether the et e.cts of co -exposure to these pollutants are additive or 37 synergistic in laboratory animals. Normal and spontaneously hypertensive rats with implanted telemetry units that record the electrocardiogram and breathing pattern will be exposed for six hours to filtered air. and PM2.5 and 03 alone and in combination. At the end of exposure, multiple endpoints related to platelet, vascular endothelial, heart rate variability, cardiac arrhythmia, and nervous system function will be evaluated to assess the contribution of each mechanistic pathway to the health effects observed. Analyses will compare responses to ozone done and PM2.5 alone to responses to filtered air and the combined exposure (PM 2.:; and G3). More information on this is a. a;1able at: http:-`' v w.arb.ca.goviresearch/single- project.php?row id -55194. • Cardiovascular Effects of Multi -Pollutant Exposure: Mechanisms and Interactions: Contractor: UC Irvine: Principal Investigator: Michael Kleinman; Project Status: Active. The objective of this study is to .j, yestigate the atherosclerotic potential of ambient PM2.5 from the In ine. CA area. Both intact particles and particles denuded of the semi - volatile constituents of PM2.5 '\ ill be used with and without concurrent exposure to ozone in a mouse model of atne•� :sclerosis. The principle goals are to elucidate the role of the semi -volatile components of PN 2.5 and ozone in the progression of atherosclerosis, and the extern. tc. whier. concomitant ozone exposure interacts with disease progression. More information on this is project.php?row_id= u5184. at: http://vv' '% .arb.ca.gov/research/single- • Risk of Pediatric Asthma Morbidity from Multi -pollutant Exposures: Contractor: UC Irvine; Principal Investigator: Ralph Delfino, Project Status: Active. One of ARB's goals is the p, racc:ion► of sensitive populations, such as children, from air pollution impacts. Many studies nave shown a link between PM exposure and asthma morbidity outcomes in children. While these studies have contributed to ARB's understanding of the health of particle exposure in children, several issues regarding the biolo?icaily act., \J.. components of PM remain to be addressed. For example, there is limited inf ,!•ma:ion on the health effects of two important classes of particles in California. pcirna; `. ( yrgar is aerosols ( i 7A) directly emitted from combustion sources; and secondary orgyrdc aerosol (SOA). which are largely photochemically- produced. These classes of u,geiiiIc aerosols have different spatial and temporal variability and they arc miniitiail\ correlated with each other in southern California. The study aims to analyze the pos.;irne relationship between asthma morbidity using hospital data for 7,954 children with t:sthina, and both regional and local exposures to PM including POA and S0A. "Lab ..t.11l be studied using PM predictions generated by regional air quality models. "1-1\.1 vv iii nc estimated for three particle sizes, including ultrafine, PM2.5, and PM 10 with estimates of the contributions of specific sources of PM. Other air pollutants suer; as ozone. nitrogen oxides, and carbon monoxide will also be estimated. The sway will evaluate whether temporal and spatial variations of PM2.5 sources and species ate ec ftLe association between PM2.5 mass concentrations and emergency department visits ana hospital admissions for asthma. It will also 38 evaluate the association bemeen air pollution susceptibility, including asthma recurrence and socioeconomic status and demographic factors. The study will leverage the daily POA and SOA exposure data from the University of California, Davis/California Institute of Technology Source Oriented Chemical Transport Model. The study is expected to provide new information on the association of asthma morbidity with multiple local and regional air pollutants and general particle composition. Findings will be relevant to efforts by ARB to control Plv.2.5 by assessing the importance of sources and components that are related to health outcOrnes. More information on this is &'y ai lab:e http://www.arb.ca.gov/research/single- project.php?row_iu= oDU31. • Health Effects of Central Valley Particulate Matter: Contractor: UC Davis; Principal Investigator: Anthony Wexler; Project Status: Active. Epidemiological studies have demonstrated that respiratory and cardiovascular health effects are most associated with particulate matter levels one to three days prior to the advent of adverse health responses. However, the temporal patterns for development of pulmonary and cardiovascuiat ft:sparse; se; appear to differ. Little is understood as to whether adverse changes in respiratory and cardiovascular endpoints represent independent effects that have different time courses for development, or whether they represent a continuum oi :i;at share common biological pathways and are inter- related. In addition. past studies nave, evaluated all endpoints at the same time post - exposure. Because of this, little i± i:fU'v1 n about the time course for development of respiratory and cardiovascular elects. This project will involve a series of experiments in the Central Valley of California designed to investigate how time lags in exposure increase or diminish pulmonary and cardiovascular responses in a species of mouse model that has similar pulmonary ana systemic responses to PM as are observed in humans. The hypothesis of tnis project is that local pulmonary inflammatory responses in the airways of the lung precedes. and then initiates vascular inflammation and subsequent platelet acti, ation. Plate et activation is a key factor in formation of thrombi (clots) in the systemic circuiaiion. 1eaaing to heart attacks and stroke, which are among the leading causes of prema:,.r,: death that. have been associated with PM exposure. The results of this project will pro.v ide critical data on the biological mechanisms through which PM adversely impacts nenith. and will specifically address the key question of the lack of concordance betvveerz respiratory and cardiovascular endpoints. This study will provide important informatioa That ‘A ill help to explain the biological basis of epidemiological associations h t,\cen adverse health outcomes and PM, and provide needed biological support for set.:e and national ambient air quality standards for PM. More information on this is available at: I►ttp://www.arb.ca.gov/research/single- project.php?row_id=64x54. • Location Specific Systemic health Effects of Ambient Particulate Matter: Contractor: UC Davis: Principal Investigator: Dennis Wilson; Project Status: Completed. Previous work by the contraLtol and otters demonstrates induction of a systemic pro - inflammatory and pro -c: agu i ant state in response to inhalation of environmental 39 particulate matter. This work demonstrated PM exposure activated platelets to an enhanced state of reactivity and suggested this could be a key factor in adverse cardiovascular events. This project evaluated pulmonary inflammation and systemic inflammatory and platelet responses to tine and ultrafine ambient PM collected from an urban (Sacramento) and rural (Davis) location. The objective of these experiments was to determine whether prior chelation of transition metals with deferoxamine mesylate (DFM) or binding of bacterial source endotoxin by polymyxin B reduce pulmonary and systemic responses to Piv12.5. Tnc contractor hypothesized those inflammatory responses to a more transition metal rich urban source PM2.5 would be inhibited more by metal chelation while rural source PiV1 _11.5 would be more affected by endotoxin binding. Adult mice were given intratrachea, instiilation of collected PM2.5 and pulmonary pathology, systemic cytokine concentrations. and platelet activation were evaluated 24 hours later. To better assess contributions o.* aromatic hydrocarbons, oxidants or pro -inflammatory responses to biologically active ,Material like endotoxin, the contractor used laser capture microscopy to probe specific anatomic locations in lung for gene responses associated with each of these coniponenrs. ► hp results support the following conclusions: o Urban source PM2.5 were significantly more pro -inflammatory than an equivalent dose by mass of rural source ?'M2.5. o DFM pre-treatment of ,aban source PM2.5 did not decrease PM induced pulmonary inflarnmmtion;. o Treatment with DFiVi alone led to significant systemic platelet activation. o Pulmonary inflammatur Ty responses to bolt, urban and rural source PM2.5 were inhibited by pre-incuhaticn P VI2.5 with polymyxin B. o In contrast to several prior animal experiments that demonstrated significant activation of circulati:i2. platelets after exposures to concentrated ambient particulates for two-vi�cks in the field, this study with a single exposure dose found no evidence of piatei i activation in response to instilled PM2.5 at 24 hours after exposure. o Urban source PM2.5 :ra iscription of genes associated with polycyclic aromatic hydrocarbGii reactive oxygen species response elements and inflammation in sma1i ,)u1nmonary arterioles and alveolar parenchyma. A copy of the final report, published in January 2014, is available at: http://www.arb.ca.2ovii i e seau ; a. pasu' I 0- s 02. pu f. • Cardiopulmonary Health Effects: Toxicity o>≤ Semi -Volatile and Non -Volatile Components of Ultrafine PM: Contractor: UC Irvine; Principal Investigator: Michael Kleinman; Project Status: COmnipleted. The goal of the project was to dL:r; mine whether or not the toxicity of ultrafine (UFP) particle depends on the concentration and composition of semi -volatile and non-volatile factions of the PM. the researchers tested the h) po thesis that adverse effects of exposure to these UFP, which are primµril) emitted by cornoustion sources and are highly enriched in semi -volatile components. ti\ ; it b3 significantly attenuated by removal of those components from the aerosol. the researchers used a unique mobile in vivo rodent exposure system in comhina.cion _v\ ith a particle concentrator and thermal denuder to study the cardiopulmonary d1 is is of L l T, before and after the removal of the semi - 40 volatile components. The study used genetically modified mice that had impaired lipid metabolism and were therefore predisposed to the development of atherosclerotic -like plaques. Exposures were 6 hours/day. 4 days per week for 8 weeks and were conducted near the University of Southern California campus in central Los Angeles. Detailed chemical and physical characterization examinations of the concentrated ambient UFP (CAP) and thermally denuded CAPs were conducted. The thermal denuder removed more than 60% of the particle -associated organic compounds (OC) but did not remove the non-volatile components such as elemental carbon (EC) or trace metals. Exposure to undenuded CAPs accelerated the ueveioprrment of atherosclerotic plaque in the genetically modified mice, characterized bydecreased arterial lumen diameters and increased incorporation of lipids in arterial walls. The lumen diameters and arterial wall lipid contents in the genetically modi;:ec: mice exposed to thermally denuded CAPs suggested significantly less plaque development than in the mice exposed to undenuded CAPs and were not different from plaque !eveis in genetically modified mice exposed to purified air, as controls. In addition. heart rate variability was decreased in the mice exposed to undenuded CAPs but not in fir mice exposed to either purified air or denuded CPAs. in a separate experiment genetically modified mice were exposed to air, denuded CAPs and the particle free organic compounds (PFO) that were stripped from the CAPs in the thermodenuder and deliverer Lc; the exposure system. This study demonstrated that the organic compound. independent or the presence of particles, played an active role in the acceleration of plaque development. Cholesterol and low density lipoprotein -cholesterol (LDL) levels were relativel,, :-.ig:-! in the genetically modified mice, as would be expected. Exposure to undenuded GAF's. uc;-:u;lea CAPs and PFO all induced increased levels of both cholesterol and LDi. iu the ,ert4m of these mice, but only the undenuded CAPs and the PFO cause significant serum lipid peroxidation, which is a known contributor to plaque formation. The researiers concluded that the organic constituents of UFP contribute to the accelerated de• e!c p:nen: of atherosclerotic plaque in arteries, lipid oxidation is an important mechai;;bnn of action in ?,M -induced coronary artery disease, and that removal of the organic c..rr, pounds from PM greatly ameliorates plaque development associated wiu; air pollution exposure. These findings suggest the emission control measures that remove a;ta sequester or destroy organic constituents of combustion generated aerosols could benefit public health because coronary artery disease is a leading contributor nears-re:ated deaths, which represents about 50% of deaths, annually, in Califon -Ala an t other states as well. A copy of the fina: i rte .'t, pubi:s:rcu iai April 20 i 3. is available at: http://www.arb.ca.2ov..-esearchr.-.0-)i- pa -K/07 -307.1)A • Toxicity of Source -Oriented Ambient Submicron Particulate Matter: Contractor: UC Davis; Principal Investigator: Anthony Wexler; Project Status: Completed. Current National Ambient Air Quality Standards for particulate matter regulate the mass concentration of particles in the _.trnc'sphere. Thei e is growing evidence that different sources of these particles have different levels of toxicity. In this work, a system was developed for collecting source: c;r iernted particles tom the atmosphere suitable for toxicity testing. Briefly a si,Ig.le r)a:tie,e mass spectrometer identified particle sources in 41 real time; the mass spectrometer selected a ChemVol associated with each source category to collect size -selected PM while those particles were being observed. This system was operated in Fresno, CA during the summer of 2008 and winter of 2009. The toxicity of the collected samples was assessed in a mouse model. Samples were chemically analyzed to associate them with sources prevalent in Fresno, CA. Most of the toxicity was associated with automobile and cooking sources in both seasons while in the winter toxicity was also associated ,vith secondar_, compounds. A copy of the final ieport, puc>l►siiea in May 2012, is available at: http://www.arb.ca.govit-eseacen, .:,-.r past/G6-33 i .pdf. f. • Systemic Platelet Activation ai Mice Exposed to Fine Particulate Matter: Contractor: UC Davis; Principal Investigator: Fern Tablin; Project Status: Completed. The contractor conducted five separate experiments designed to define the effects of ambient particles on the car. i-ava!;cular system. Mice were exposed to concentrated ambient particles (CAPs) less than 2.5 microns in diameter or instilled with PM2.5 from the Fresno, California area. Control an;n►ais were exposed to filtered air or physiological saline. Studies were conduc.cdl during summer and winter in both urban and rural areas. The three CAPS experiments'A.cce conducted in winter 2008, summer 2008, and evaluated the effects of CAI's „ ascu;ar and hemostatic systems. Later studies examined the effects of short-R.-inh v;-vo instillation of PM2.5 that was collected during the CAPS experiments. in al! s«,3Tea. it was determined the production of systemic inflammatory cytokines to e\ altm:c the extent of pulmonary, coronary and systemic inflammation. Platelet upreguiautiuor; and activation in response to agonist was evaluated by flow cytometry. They detexv Wiled the expression and activation of key platelet integrins and the extent of alp;ia w,ar,ule and lysosomal grandule secretion. Complete blood counts were performed. Lw;g tissue was evaluated for change in gene expression either by gene array or b, laser capture micro -dissection. Particle exposed animals showed platelet activation ir, st ides compared to control animals, while proinflammatory cytokines \;. ere p:edoininantly upregulated in the winter CAPs and winter instilled exposures. Expo,uie to winter PM appears to activate different physiological outcomes :han sun -.m -if exposures. A copy of the final repot. pug;iislr.ee in February 231 1, is available at: http: v, ww.arb.ca.<zo\ <'r :seal �i; at: past/07-337.pcif. • Extended Analyses of Air Po;6k.3 ticsn and Cardiovascular Disease in the California Teachers Study Cohort: Contractor: Department of Health Services; Principal investigator: Michael Lipselt. Status: Completed. Several studies have report i 2s:. :aticns between long-term exposure to air pollution and mortality. A number of important questions remain, however, regarding the impact of how long-term exposure S :- .casure.i. tiie exisLedee of critical windows of exposure, the relative importance of va: io i s c„ns.ituents of PM, the relationship of chronic exposure to new cases di:;easy:. _u10 the shape of the concentration -response function linking fine particulate math •;..,c. a-.:oriality. As an extension of previous work, researchers developed estirnE:et. cd :ong-term air pollution exposure at the residences of over 100,000 female participants in the longitudinal California Teachers Study (CTS). The researchers examined associations between several exposure metrics and the following outcomes: all -cause mortality. cause -specific mortality (principally diseases of the cardiovascular and respiratory systems), as well as new causes of both fatal and non- fatal heart attacks and stroke. To derive the pollutant exposure metrics, the researchers linked the CTS participants- ,.1da ess :s with monthly estimates of long-term exposure to PM2.5, PM 10, ozone. carbon mut oxide, nitrogen dioxide, nitrogen oxides, and sulfur dioxide. The main analyses'examiced potential relationships of mortality and disease incidence with long-term resicn:ia' exposures to PM 10, ozone, CO, NO2, NOx, and SO2 from 1996 through 2005. and to 'N12.5 beginning in 1999, when the latter pollutant began to be systematically measured statewide. 'articipants' addresses were linked as well with several cross-sectiona, measures of potential traffic -related exposures from the year 2000. The researchers analyzed these relationships while adjusting for many individual —level and neighbors occ variables, and undertook a variety of sensitivity analyses. The researchers found e,evatcd risks b.-svt een long-term exposure to PM2.5 and mortality from ischemic heart disease as „ et; as incidence of stroke, particularly among women who were post-menopausai at basc,ine. Long-term exposures to PM10, ozone and NOx were associated with elevated risks of ischemic heart disease mortality. PM 10 exposure was also linked incident stroke. l'he association of ozone with mortality was most likely due to its strong correlations ',>,Hitli ?I'4 l U and PM2.5. Among never -smokers, NOx exposure was associated witi: elevated risks of cardiovascular and ischemic heart disease mortality. The researchers aid n. -,r find that women who had diabetes or who were overweight or obese kvzre a incL cased risk of PM2.5-associated effects. Traffic density, a measure of the estimated nwnh;:r of vehicle miles traveled within 150 meter of a participant's residence. was associated with all -cause, cardiopulmonary and cardiovascular moctalit .‘ . In aGLt ucna1 analyses Cif associations between long-term exposure to PM2.5 u;.0 ,nor,.lit_ . t►ne researchers hound that: 1) the exposure -response relationship was best descrn)eci iinear: and 2) significant effect estimates were evident by one year of exposure. wit; u; :tagn,tude of the association leveling off with increasing duration. This swu«y pro, ides additional evidence that long-term exposure to air pollution is associated with mortality from heart disease and demonstrates as well that exposure to PM is associated i:h me incidence of new cases of stroke. A copy of the final report. pa -hi_ lc° .n Jetober 2011, is available at: http:i, %\ ,,w.arb.ca._ov.. r. sea:.: t • Spatiotemporal Analysis of A:z' f'o,ititior, and Mortality in California Based on the American Cancer Society Cohort: Contractor: University of California, Berkeley; Principal Investi_ator: ierrett v:;ehae l: Project Status: Completed. Studies using the America:Society (ACS; Cancer Prevention II (CPS II) cohort to assess the relation between particulate air pollution and mortality rank among the most influential and widen cited. i !.e original study, a reanalysis that introduced new random effects methods and spatial analytic tecnnique.s, and recent studies with longer follow-up and improved exposure assig„incnt_ have all demonstrated statistically significant and substantively large air pollution effects on all -cause and cause -specific mortality. Due to this robust association and a lack of other large cohort studies on the long-term effects, the ACS studies have proven important to government regulatory interventions and health burden assessments. Currently, there are no ACS statewide studies in California that investigate whether the risks are similar zo or different from those reported in the ACS CPS II analyses. Existing estimates con yes ;i'om either national -level ACS studies, in which the California subjects comprise less than 15% of the total national sample, or from select metropolitan or county areas of California, where questions remain about their generalizability to the rest of the state. A need exists to investigate whether the results hold across California. Addlitionall acne of the existing ACS studies have used high - resolution exposure assignment er investigated the temporal dimensions of the dose - response relationship. in this stuci,. -one researchers used advanced exposure modeling to reduce problems of measurement :error. and they investigated time windows of exposure. The researchers identified mo:e .:han 76.000 California subjects in the ACS cohort to serve as the study pcpu,_alert ,20,432 deaths with an 18 year follow-up ending in 2000). These subjects were widely distributed across California, giving comprehensive coverage for much of the population cif the state. for the first time in using the ACS CPS II data, the researchers have geocoded subjects to their home address to refine their exposure assignment. The researchers assessed the association between air pollution and several causes of death, including cardicvascu1ar (CVD). ischemic heart disease (IHD), respiratory, lung cancer, and oti er causes. The researchers also evaluated all -cause mortality. The researchers assessed the association between air pollution and death using standard and multileN el Cox proportional hazards models. Control was also applied for residence in the five largest ur'r.,a a conu: bations. which potentially have different mortality rates than non-►ire:rupc'lita,a areas. The researchers concluded Inat tuiccn together, the results from this investigation indicate consistent and robust effect:; i.,f and other pollutants commonly found in the combustion -source mixiure tl; ,-)N42.5, on deaths from CVD and 1HD. The researchers also found significant association t}etv<een PM2.5 and all causes of death, although these findings were sensitive to model specification. In Los Angeles, where the monitoring network is capable of d :tect:;.g i,1Lraurban variations in PM2.5, the researchers observed large effects on death from al causes, VD. 1HD. and respiratory disease. These results were consistent with past AC. S a! gal yses and with finding from other national or international studies rev iewec in th;s report. The strongest results were from a land use regression estimate of D?. is generally thought to represent traffic sources, where significantly elevated effects were round on deaths from all causes, CVD, IHD, and lung cancer. The researchers thereto, c conclude that combustion -source air pollution is significantly associatcu ',-vith prcn:al .ire death in this large cohort of Californians. A copy of the final report. pL ic!,hed in November 2011. is available at: http://www .arb.ca.:\ ,...JSeart.i1: _thr. paJL: Gb-33G.1;�1f. • Effects of Inhaled Fine Particles on Lung Growth and Lung Disease: Contractor: UC, Irvine; Principal Investigator: Michael Kleinman; Project Status: Completed. The Children's Health Study (CHS). conducted by the University of Southern California, has reported significant associations between reduced lung function growth and exposures to NO2. acid vapor. PM2.5. and elemental carbon. The primary objective of this study was to use any animal triode! to test the hypothesis that chronic PM2.5 exposure during the period of rapid growth and development can lead to reduced growth in pulmonary function that is relatal Jo oxidative stp..ss and tissue injury. The researchers studied changes in the development of the mouse Ling and lung function during chronic exposure to concentrated ambient PM2.5 using a mouse model. The mice were exposed from 3 weeks to 1 i weeks of age. . ne study also evaluated whether observed deficits in lung -unction persisted for up :t• �1to weeks after exposure was terminated. Mice that were exposed to concentrate`. fine particles (CAPS) for eight weeks had reduced pulmonary function. measurota as increased respiratory resistance, that persisted for up to 2 weeks after the termination o ::xposure. The researchers preserved tissue, blood and bronchoalveolar lavage tluia st:mples for later analyses to investigate the relationship between pulmonary unotien -:ref;;: its aria alterations in lung structure, biochemical mediators of oxidative stress and in,iammation, as well as alteration in gene expression that might be associated with ;u.ig development. = he researchers also examined the associations between particle chemical composition. particle physical characteristics and particle concentrations and cbse.-ved changes in pulmonary function. There were two sets of exposures: the first exoos.,res x. re performed at "high" concentration (PM2.5, 243 µg/m'; number concentraion_ •)3.000 particles/cc) and the second exposures were at "low" concentration ('N12.3. 56 rn : particle number 83,000 particles/cc). Both y studies produced signi icam increases in resistance. Particle mass concentrations in the low study were nearly I /5`n die high study. :however the particle number concentrations were nearly tnz sa:rio. suggesting :nat high concentrations of ultrafine particles were present au;ing both sets of exposures. There were methodological differences between die two sets ur exposures, novvever the results suggest that the ultrafine components of PNMi=.. z it;a.v oc more st►•o►,gly associated with the observed decreases in resistance in the 1 -.4 -exposed develluping lung than are larger -sized particle components. A copy of the final report, pu31i:silec in June 20;0, is available at: http:. vwvv.arb.ca.a.,\..eseu.,,i:::cp ,,art U5-342.,)c:i • Cardiovascular Health Effects of Fine and Ultrafine Particles During Freeway Travel: Contractor: L,U Los a.r..eles: Principal investigator: William Hinds; Project Status: Completed. A 24 -month study of huma:-. _-eT nse two-hour exposures to freeway air in Southern California was conducted. :1 nine -passenger van was modified with a high -efficiency filtration system that dr.:iverej ; iiiered or unfiltered air to an exposure chamber inside the van. State-of-the-art instrumer=;_ v,cre used to measure concentration and size distribution of fine and ultras inc particles and the concentration of other pollutants associated with motel- •\;..;:iecr. volunteer subjects (average age 71 years) rode for two hours each in filtered and uuniTered air on two freeways, I-405 and I-710. Double-blind health assessments included 24 -hour ambulatory ECG, blood biochemistry, blood pressure, and lung function. Mean unfiltered particle number concentration was 107,500 particles/cm' for 1-710 and 77.800 particles/cm3 for 1-405; mean PM2.5 mass was 51.4 and 44.5 µg/m', respectively. Filtration reduced particle count greater than 95% but did not remove gases. Atriai ectopic beat incidence during and after exposure decreased 20% on average watt; Filtered air compared to unfiltered air. Individual responses related most strongly w particle count. Blood markers NT pro-BNP and VEGF decreased 30% on average in fil,e,: d air comparcu to unfiltered air. A copy of the final rcpert, p.,hlishcd in January 20;0. is available at: http:;,'www.arb.ca. gur c pasts j4-324 .pd • Ultrafine Particulate Matter iid Cardiurespir-atory Health: Contractor: UC Irvine; Principal Investigator: Ralph Dcilino: Project Status: Completed. This is the first study cunductec in California among vulnerable individuals with coronary artery disease on tni: ac ite ;:a:-�iovascu ar health effects of exposures near subject residences to size -fractionated particles and to particle characteristics linked to mobiles sources. The researone! ; conducted a co iiprehcnsive PM monitoring effort for a repeated -measures panel studhy. aimed at evaluating acute cardiovascular health effects of exposure to PM. They! iollo\ 04 nonsmoking `iderly individuals with coronary artery disease living in rei.irement :,. o-li:1,,a:1iues in the Los Angeles Air Basin in California. Subjects were follcwed -.vith i2 vvv eekly blood draws for biomarkers and over 10 days with ambulatory electrcicaroic. ranhs and blood pressure monitors. This project supplements the exposure a:;s;s-.,-.-+e.« =or an NII-i-Funded study. The researchers found the contribution of mobile same t:, to indoor Ply i ,: vels was similar to their corresponding outdoor estimates. Analysis of uie relation between PM redox activity and blood bion-narkers was iarY,e:s nonsiuniNieant. dowev i. analysis of health outcomes and direct air measurements revealed that primary combustion markers [elemental -black carbon, primary organic carbon. CC.' were positively associated with blood pressure, electrocardiographic depression (an indicator of cardiac ischemia), biomarkers of systemic !nflainmaiion. and platelet activation, and were inversely associated with eryttirocyte antaAicant enzymes. Particle number and particle < 0.25 µm were more strongly associate,: v.th biomarkers than particles 0.25-2.5 µm. Biomarker associations were stronger for ind!otor exposures R) EC and PN of outdoor origin than uncharacterized indoor exposures. Overall results suggest that current regulations of particle mass may not comp!ei: 1 :epre_sent particle size fractions and components important to protect puH is Lain- o.• b uinerabie populations. This likely includes particles < 0.25 µni and components Ili -aced to fresh traffic emissions, including indoor infiltrated pattic cs fr ni rsonilt sources. A copy of the final report., in. April 2009, is available at: �� . http://www.arb.ca.ilo%. �o � ; ese,: _.-� ,; >-.r na:�� 03-329 9 :_,d . • Air Pollution and lair Disease in the California Teachers Study Cohort: Contractor: California Depari me.11 of Public Health; Principal Investigator: Michael Lipsett; Project Status: Corno!eL :ti 46 There are few studies examining association between long-term exposure to air pollution and adverse health outcomes. In an ongoing cohort study of over 100,000 female participants in the California Teachers Study (CTS), the researchers developed estimates of long-term air pollution exposures at the subjects' residences and examined associations between these exposure estimates and the following health outcomes: total mortality, cardiopulmonary Iat_:ia :liLy, and incidence of both fatal and non -fatal heart attacks and stroke. in audition. examined the potential impacts of several traffic metrics on these outcomes. 1;a : Jt.: to derive the pollutant to multiple air pollutants, including PM2.5, PM1b. U. anc: several gases (including ozone, CO, NO2), and traffic related exposures from the year _C)A or iater. They analyzed these relationships while adjusting for many individual lc,ei anu neighbornod variables, and undertook a variety of sensitivity analyses. The cscat ciers round strong and consistent associations of PM2.5 not only w i n total any: cardiopu„►zonary mortality, but also with incidence of heart attacks and stroke. They aiso identified somewhat less consistent relationships oetwzen one of more of these adverse outcomes and PM10, 0, CO, NO2 and ozone. Most of the traffic metrics were not associated with these outcomes. This study provides additional evidence that Ion& -ter::: exposure to air pollutant is associated with mortality, and demonstrates as ‘vei, thEa exposure to several combustion related pollutants is associated with the ;ticidencc a, new cases of heart attacks and stroke. A copy of the final report. pLaaiisheu in October 2007, is available at: -,ttp:,'/www.arb.ca.gcr, L-csec.•-t 1.. :.;is,,ui-3I:}.pol. • Particulate Air Pollution aa(1 °+iorbidiiyy in t1:4 California Central Valley: A High Particulate Pollution Region: Contractor: Kaiser Permanente, Northern California Region; Principal ins astiga.tc_.,,.: \Jan Den Eeden; Project Status: Completed. The goal of this study :\ as t,n the :elatio:.ship between particulate air pollution and morbidity among the K.,iser Permanente (KP) membership who reside in the Central Valley (CV) of C a: i forma. ! :.:Ai 1, P:'vi monitoring in the Central Valley was instituted as the > o, en-;Oer i 96 Cif a special monitoring program by the ARB. The combination of the amb::r air poilut on data collected as part of the enhanced monitoring and the moi-bidiay UL:.a. a.ora Kaiser Permanente provided an excellent opportunity to expi ;ie this resa.:nsn p in an area with varied PM. The researchers cencucted tire. -series analyses examining the association between daily ambient measures of 1'M (in, ;..ki:j,_ PM chemica: components), other criteria air pollutants (e.g., ozone. NO). ani CD) and daily admissions to the emergency room or hospitalization for respirator:, }n cardiovascular conditions among members of Kaiser Permanente, Northern California Region (KPNC) living in the Central Valley of California. Only those .KPN;a,:;nocrs no resided in an area where exposure could be assigned using one or more The study period was+rem 9v6 to Jec: rnher 2000. r Cl i PIvt monitoring stations were included in the study. Exposure was assigned ;asee on c:acn KKP member's residential zip code and linked to the city where a monitoring stati.:in \\,as in ;,lace. Morbidity data were derived from computerized data sources et K..m ; er PJe. n -ma ►ent::. Each health event of interest was identified and the age. gender and diagnosis ascertained. Outcome events were classified into one of three categories: cardio\ ascular, acute and chronic respiratory conditions, and two types of admissions: hospitalizations and emergency room visits. Preliminary analyses of the data included graphical techniques and bivariate analyses. Non - parametric smooths were developea that first fit confounding variables to each set of outcome data. These factors included long -wave terms (time), day -of -week, temperature, and humidity. In addition, because there were four population centers in this study a set of indicator variables for celv..er .‘,as also included. Consistent adverse health effects s were observed between a variety of air pollution metrics and acute and chron;c respirator,, hcspiaaiizations and emergency room visits among Kaiser Permanente members i ;ing .n the Central :valley of California. These associations were consistent across type of analysis and type of admission. Of the pollutant studied PM 10 and P M"2.5 were consistently associated with increases in hospitalizations and cm ;ergeney room visits for acute and chronic respiratory conditions. To a lesser extent CO and NO: :ere associated with increases in admissions for all outcomers in their study. In contrr.st to the PM ► 0 and PIVI2.5 results, the researchers did not find convincing evidence a,: association between the coarse fraction of PM and their outcomes. In addition. theft results for cardiovascular admissions were inconsistently or not at all ass, c.aica w,th the pollutants studied. Some of their pollutant - outcome associations were in In, notably. ozone. site direction from what they expected, most A copy of the final report, published in July 2002, is available at: http://\\• \w.arb.ca.s!3v,i.seGr ; ; .r pais - s03.udf. • A Critical Review of the Particulate Matter Toxicology Literature For Senate Bill 25 Review of the Particulate Matter Standard: Contractor: UC Davis; Principal Investigator: Kent hi -Act -ton: ,):'0rect Status: Completed. The California Eiv :ttnneir_,, .':cC_ecLen .A.�_enc' has been charged with reviewing the ambient air quality standards for fiNi and sulfates to ensure they are protective of childre.a. Toxicoiog ; s:..the p a critical eeirmponent of the overall standards review process. T oxicolog. studies u:.t. ,l:oy ide information essential for identifying which components or characteristics ofiL,\I air pollution may be more harmful or more closely associated with the acl'yarse licaan cr :.,:.s seen in epidemiological studies of human populations exposed to a►nbieet le;/elam uRM. Toxicology studies can also provide valuable information on the Holofaieal necnanisi; s involved in causing adverse health effects in animals and nL mar posto to PM. -fishis report provides a critical review of the peer reviewed .\ is , log_ i ne:'ature as it pertains to PM and PM component exposure. It is not an exhausti sUDin•iar., or all roxicologv studies conducted using PM or PM components. The repor: ref►ccts focused effort co examine the results of toxicology studies that the authors belie., e i 1 ne ;host neip:ill in aadressing the ongoing air quality standards review in Cat: 'orn ►:. ce the completion of this report in 2002, the majority of the toxicology studies re` iewv:3I6Lnd associations between exposure to PM of many different sizes and c 3mposi:iuuns : esu;tca in direct effects on the respiratory tract. These effects include general as \Nt l; os site specific cell and tissue injury, increased production 48 of inflammatory biochemical species leading to increased pulmonary inflammation, increases in airway tissue reactivity. leading to exacerbation of existing respiratory conditions, typically in compromised animal models. Changes have also been noted in immune cell populations or function that may lead to increased host susceptibility to respiratory infections. A copy of the report, publisned 1n May 2002, is available at: http:/, www.arb.ca.2.av, past/0O-327 .pd 49 AFSCME>r-7 Health & Safety Fact Sheet e ASPHALT Asphalt is a dark brown or black substance derived from crude oil. It may be a solid, a semi- solid, or a liquid and is a strong adhesive. Asphalt is often mistakenly confused with "tar," "coal tar," or "pitch" because the appearance is similar and the substances may be used interchangeably in many industrial processes. Tar and pitch are derived from coal products which are chemically and physically different. Other names for asphalt include road tar, road binder, mineral pitch, petroleum pitch, petroleum asphalt, and seal -coating material. Asphalt is used for road paving, roofing tar, roll -roofing, roofing felt, shingles, pipe covering, floor tile, waterproofing, and many other products and processes. Its use will determine what other substances are blended with it and what health and safety hazards are associated with it. There are two primary types of asphalt: • Straight -run asphalt or asphalt cement: Straight -run asphalt is used for paving roads, airport runways and parking lots. Because of its solid to semi -solid nature, it must first be "cut" with a solvent to bring it to a more liquid state; this is known as Cut Back Asphalt. Highway workers are most likely to use straight run asphalt. • Air -blown or oxidized asphalt: Air -blown asphalt has a high softening point and is used primarily in roofing, pipe covering, and similar situations. HAZARDS There are two main hazards associated with asphalt: • Fire and explosion hazards, and • Health hazards associated with skin contact, eye contact, and/or inhalation of fumes and vapors FIRE AND EXPLOSION HAZARDS Most of the fire and explosion hazard associated with asphalt comes from the vapors of the solvent mixed into the asphalt, not the asphalt itself. The hazard is determined by the flammable or explosive nature of the solvent used and how fast it evaporates. The flashpoint (FP) of a chemical or mixture is the combined measure of this flammable or explosive potential. The flashpoint is the lowest temperature at which enough of the chemical evaporates to form a mixture with air which can be ignited by a spark. The lower the flash point, the higher the fire and explosion hazard. If the flash point is below the room temperature, the chemical is a potential bomb. The flash point -- and therefore, the fire or explosion hazard -- can be determined, in part, by the type of asphalt used. There are three types of cut asphalt. The type and amount of solvent (or oil) added determines the properties of the final mix. • Rapid -Curing Asphalt (RC) is blended asphalt which has been "cut" with a "low - flash" (highly flammable) petroleum solvent. This low flash solvent quickly evaporates, allowing the "RC" mixture to rapidly set and harden. Examples of solvents commonly used in "RC" mixtures include: Benzene (FP = 12°F), Dioxin (FP = 81-90°F); and Naphtha (FP = 107°F), (FP = 54°F), Toluene (FP = 40°F), Xylene. • Medium -Curing Asphalt (MC) is blended asphalt which has been "cut" with a solvent with a flash point over 170°F. • Slow -Curing Asphalt (SC) is blended asphalt which has been "cut" with a low - flash oil having a flashpoint of over 250°F. The FP of the asphalt and solvent mix will be higher than the FP of the solvent alone. Remember, the lower the FP, the greater the explosion hazard. Table 1 illustrates the various grades of RC, MC, and SC asphalt mixes and their relative flash points. HEALTH HAZARDS OF ASPHALT • Acute (short-term) health effects: Skin or eye contact may cause inflammation and skin rashes, changes in skin coloration, and an acne -like condition at hair follicles and skin pores. FLASH. POINT REQUIREMENTS FOR ASPHALTIC MATERIALS* Type and Grade of Material Flash Point (deg.F) Rapid -Curing Liquid Asphalt Grades RC -250, 800, and 3,000 Medium -Curing Liquid Asphalt Grade MC -70 Grades MC -250, 800, 3,000 Slow -Curing Liquid Asphalt Grade SC -70 Grade SC -250 Grade SC -800 Grade SC -3,000 80 + 100+ 150 + 150+ 175 + 200 + 225 + *Adapted from NSC Data Sheet 1-215-80, Asphalt Asphalt fumes are created when asphalt is heated. Fumes contain very small, solid, airborne particles which are easily inhaled by the worker. Inhalation of asphalt fumes can cause irritation to the nose, throat and lungs. Fumes may also contain hydrogen 2 sulfide vapors, which are very toxic, as well as the vapors generated by the solvents used to "cut" the asphalt. (See below). Exposure to sunlight or other ultraviolet light (such as welding) may make these skin conditions worse. • Chronic (long term) health effects: Asphalt cement also causes rashes and other skin conditions, possibly including skin cancers. In addition, asphalt particles left on the hands may accidentally get into the eyes causing severe irritation to the eyes. Hot asphalt may also cause severe bums if splashed onto exposed skin. ASPHALT -EXPOSURE LIMITS • The National Institute for Occupational Safety and Health (NIOSH) has recommended that the Short Term Exposure Limit (STEL) for exposure to asphalt fumes should be set at 5 milligrams per cubic meter of air (mg/m3) measured during any 15 minute period. • The Occupational Safety and Health Administration (OSHA) has not adopted a standard for worker exposure to asphalt fumes despite the fact that the NIOSH recommendation was made in 1977. • The American Conference of Governmental Hygienists (ACGIH) standard (Threshold Limit Value, or TLV) is 5 milligrams per cubic meter of air (mg/m3) averaged over eight hours. HEALTH HAZARDS OF SOLVENT VAPORS Vapors from solvents that are used to "cut" asphalt can also present serious health hazards. The solvent vapors generated by heating asphalt are often more toxic than the asphalt fumes themselves. Solvents will evaporate out of the mix at a wide range of temperatures. Heating of the asphalt mix speeds up the evaporation process. The faster the solvent evaporates, the easier it is to inhale. In order to understand the hazards of asphalt, it is necessary to know which solvent is used in the mixture, how fast the substance evaporates and how toxic the substance is. The boiling point of a chemical determines how fast the substance evaporates. The lower the boiling point, the easier it evaporates and the easier it is to inhale. The toxicity of a substance refers to the effects of that substance on the human body. As indicated above, OSHA, NIOSH and ACGIH recommend exposure limits for chemicals. OSHA's standards are called PELs (Permissible Exposure Limits). OSHA's PELs arc enforceable by law in states where public employees are covered by OSHA or by OSHA -approved state plans. (Some state plans may have PELs which are more stringent than federal OSHA's PELs.). ACGIH calls its limits TLVs (Threshold Limit Values). TLVs are only recommendations. not mandates. In theory, a highly toxic chemical will have a very low PEL. In reality, however, many PELs are outdated and do not take into account new studies about health effects. Others are only based on a chemical's irritant properties instead of its ability to cause cancer or other serious health effects. It is important to remember that a variety of sources must be checked to determine the toxicity of a chemical and discover the safest exposure limit. Remember, legal does not mean safe. The names of the asphalt -cutting solvents, their boiling points and any exposure limits should be listed on the Material Safety Data Sheet. Listed below are three solvents commonly used in asphalts, their boiling points, health effects and exposure limits. • Benzene (BP 176°F) is known to cause leukemia, a cancer of the white blood cells, and a serious blood disorder called aplastic anemia which can lead to leukemia. Benzene has also been shown to cause skin cancer in animal studies. The OSHA PEL has recently been changed to 1 part benzene per million parts air (ppm) with a 5 ppm STEL. This means that exposures must average 1 ppm over an eight hour day, but cannot average more than 5 ppm over any 15 minute period. The ACGIH TLV is still 10 ppm. • Divxane (BP 214°F) is very toxic to the liver and kidneys and has been shown to cause cancer in laboratory testing. OSHA PEL: 25 ppm, averaged over 8 hours; ACGIH TLV: 25 ppm. • Toluene (BP 231°F) may cause kidney and liver damage in high concentrations, as well as a skin condition called dermatitis. It is safer to use than benzene. OSHA PEL: 100 ppm (averaged over an eight hour day), STEL: 150 ppm for 15 minutes. This means that the average exposure over an eight -hour work day cannot exceed 100 ppm and cannot average more than 150 ppm over any 15 minute period. ACGIH TLV: 100 ppm. STEL: 150 ppm. Again, in order to understand the health effects of asphalt, it is important to find which solvent was used to "cut" the asphalt mix. Remember that an "RC" mix contains the most dangerous solvents; an "MC" is less dangerous, and an "SC" is the least dangerous of the asphalt mixes. All required and recommended exposure limits (OSHA, NIOSH and ACGIH) should be checked. Remember, the legal limit (OSHA PEL) is not necessarily the safe limit. SAFE WORK PROCEDURES 1. Training All workers exposed to asphalt fumes should be trained about hazards and safe work procedures. This training should include specific information about the solvents used in mixing the asphalt. 2. Material Safety Data Sheets (MSDSs) should be made available to each employee assigned to work with or near asphalt processes. The MSDS should include specific information on the solvents present in the asphalt mix and should list all pertinent information including Flash Point, Boiling Point, acute and chronic effects of all chemical ingredients in the solution, protective equipment, as well as other fire and emergency cleanup information. (4)4 3. Engineering Controls • Substitution. The best method of controlling exposure to asphalt fumes and solvent vapors is to substitute a safer asphalt mix. If explosion hazards are a problem in a paving operation, MC -250 may be substituted for RC -250. The flashpoint of the mix is nearly doubled, which means that the mix is less likely to ignite. If the toxicity of the chemical is a problem, the employer may be able to order an asphalt mixture which contains a less toxic solvent (e.g. toluene for benzene). Finally, if a less toxic solvent cannot be substituted in the mix, a less volatile solvent may be. Less volatile means that the boiling point of the new solvent will be higher, so less will evaporate into inhalable particles. • Enclosure. Enclosing the process where the asphalt is used is not possible in road paving and roofing operations. However it may be possible for smaller operations such as pipe covering processes. • Mechanization and Automation. Certain parts of asphalt processes may be mechanized. For example, stirring asphalt in a tar kettle exposes the worker to asphalt fumes, solvent vapors, and potentially severe burns; mechanical devices can accomplish this task without exposing the employee to such risks. • Local Exhaust Ventilation. Local exhaust ventilation may be an effective way to control worker exposure to fumes and vapors, particularly in areas where enclosure of the operation is impossible. • General Dilution Ventilation. General dilution ventilation involves flooding a work area with uncontaminated air in an attempt to remove contaminants from the workers' breathing zone. However the use of fans and blowers set up for this purpose, are often not adequate to remove the contaminants. This is generally not the most effective way of removing contaminants from the worker's breathing zone, but may be used to supplement local exhaust ventilation. 4. Respiratory Protection. While engineering controls are the preferred method for controlling worker exposure to fumes and vapors, respirators should be worn where this is not possible. In selecting the proper respirator, it is important to know all of the hazards to which workers may be exposed. A NIOSH-approved dust respirator will control exposure to asphalt fumes, but will do nothing to protect the worker against exposure to the toxic vapors given off by the solvent in the mix. In situations where vapors are present, a full -face mask respirator with organic vapor and particulate cartridges should be used. Because of the possibility of eye irritation a half -face mask respirator would be inadequate. IMPROPER USE OF RESPIRATORS IS DANGEROUS. The employer must have a (5) _ written respirator program that takes into account workplace conditions, requirements for worker training, respirator fit testing, and medical exams, as described in OSHA standard 29 CFR 1910.134. 5. Protective Clothing. Protective clothing is necessary to protect workers from asphalt burns and irritation. In addition, many of the solvents used to cut asphalt are readily absorbed through unprotected skin into the bloodstream, where they can travel throughout the body and cause damage to many different organs. NIOSH recommends that workers wear thermally -insulated gloves, long sleeve shirts, long cuffless trousers and metal -toed safety shoes when working with hot asphalt. Clothing should be loose -fitting, collars should be closed, and sleeves rolled down. Safety shoes should be at least 15 centimeters (cm) high and should be laced so that no openings are left through which hot asphalt may reach the skin. 6. Face and Eye Protection. Face and eye protection are recommended whenever hot asphalt is used. A face shield (8" minimum) should be worn when handling heated asphalt if a full face respirator is not worn. When liquid asphalt is hand -sprayed on road surfaces as "tack coat" or "prime coat," spraying equipment should have flexible hoses and long handles. 7. Barrier Creams and Lotions. When applied to the skin, barrier creams and lotions leave a thin film, which acts as a barrier against skin irritants. They should not be substituted for protective clothing, but may be useful along with other protective measures. 8. Fire and Explosion Hazards • The solvents which make asphalt an RC, MC, or SC mixture will determine the flammability limits of the mixture. For example, RC -250, with a flashpoint near 80°F will generate flammable vapors at a much lower temperature than will MC -3000. Extreme caution must be exercised when heating RC mixes. Smoking, lighted matches, torches, and other possible ignition sources must be kept away from areas where vapors are being produced. • Welding and brazing on tar -kettles, tanks, or other vessels which either contain or have contained asphalt is DANGEROUS. Only qualified personnel should do such welding. The welder must be familiar with safe procedures for welding tanks that have contained flammable liquids. September, 2011 For more information about protecting workers from workplace hazards, please contact the AFSCME Research & Collective Bargaining Department, Health and Safety Program at (202) 429-1215. You can also contact our office located at 1625 L Street, NW Washington, DC 20036. (6) _ emu., Moat)) t43 39 c..1945”, g 19 I'3 d vs 3 cl 'text cx.)t--a, rieQUA (OkIktlia WAla Qv% 63 et cccvs-si 4 391 rusk LS11,TC01g ti4IMN't CO a`1 ' es).-fp Esp,sti 'me Lerk€ Lso CLu-Qs(cZ Pyr- Jsr--t Asesi ms( pea, (mai 444 (audit, -(2(2. \ bacL Wfus c24.4fr fr-Ito 1,) :4,45C tLc d � ti w '�5 ��j S3a t �o.Pta%Vktk) 2- atit\,-(Th iteito k-Nt9 Quata siNe- z) LaiRkAti Ake `max _o--1-4.-62tekr 4-0 .4r 642/ SJ, s�� Air pollution within legal limits still can be deadly for older adults Association of Health... Page 1 of 2 Association of Health Care Journalists CENTER FOR EXCELLENCE IN HEALTH CARE JOURNALISM Air pollution within legal limits still can be deadly for older adults BY LIZ SEEGERT I SEPTEMBER 1, 2017 Al Gore's new movie, "An Inconvenient Sequel, Truth to Poo,e.," delves into t. -.e most recent effects of climate change on humans and nature. (Watch the official trailer here.) Among those most affected by a thinning ozone layer, rising temperatures and increased air pollution are older adults. Recent research finds that even air pollution within legal limits could mean an early death for older residents. Increased air pollution already is hi A 13 -year Harvard School of Public Health st ,_ A 3.` map' 1 tes indicates that outcomes for older adults could oe c L cal. Researchers found that for every 10 percent increase in tiny particulate matter (PMI's, c partic es smaller than 2.5 microns in diameter), the risk of early death increased by approximately 2 percent. This risk was apparent even in areas where pollution evels were below the EPA's National Ambient Air Quality Standards (NAAQS). Additionally, men, blacks, and low-income populations had higher risk estimates from PM2.5 exposure compared with the national average, with blacks having mortality risks three times higher than the national average. Many elderly people already struggle with chronic obstructive pulmonary disease (COPD), asthma, the after-effects of pneumonia, bronchitis, and other respiratory conditions. In addition, as people age they are less able to compensate for the effects of environmental hazards. Air pollution exacerbates pulmonary conditions, ma<ing it nearly impossible at times for older adults to even take a walk around the block. While the EPA has been removing ' Y. c ,. on its website, you can still find information about the dangerous effects of air noi!ution on older adults' health. "Air pollution, like ozone, particle pollution (PM), and especially fine particle pollution (PM2.5), is most likely to affect the health of older adults, I.. Fine particle pollution has been {inked to premature death, cardiac arrhythmias and heart attacks, asthma attacks, and the development of chronic bronchitis. Ozone, even at low levels, can https://healthjournaiism.org/blog/2017/09/air-pollution-within-legal-limits-still-can-be-dea... 11/6/2017 Air pollution within legal limits still can be deadly for older adults j Association of Health... Page 2 of 2 aggravate respiratory diseases. This can lead to increased use of medication, more visits to health care providers, admissions to emergency rooms and hospitals and even death." The findings are supported by additional research conducted in the United States and elsewhere. Air pollution impacts ca•' ra! : or: in rural older adults and has been linked to increased incidence of ve and entia. Psychological stress can amplify thes is. In 2016, the World Health. C, ganizatien reporter that 90 percent of people worldwide live in areas with hazardous air ollution. Toxicity of particular matter increases as air tempers rL res rise, according to the Harvard study. Additionally, "particles from traffic were found to be more toxic than other types, indicating a need for further reductions from vehicie poliution." Researchers hope these findings will lead to new pcl?cies to protect vulnerable populations against the increasing deadly effects of air pollution. As global warming continues to affect cur planet, mate change has become a matter of life and death. Journalists may want to explore how teir communities are addressing air pollution. Here are some questions to ask: • Are there alternative transportation, options to cars for older adults? • Are emergency departments seeing more seniors with respiratory problems during high -ozone alert days? • Are cooling centers available for elderly and mn=rs with breathing problems on bad air days? • Are activists stepping up to address clhma_e change anc health in your area? Facebook Ln k This entry was posted in Aging, Public e:nd tagged air, climate change, envirormert, pollution, ser c Log in to comn er. This post has been shared! You have shared this post with doylegreg5@aol.com https://healthjournalism.org/blog/2017/09/air-pollution-within-legal-limits-still-can-be-dea... 11/6/2017 Asphalt Plant Health Concerns Page 1 of 3 HOM1 You Can I Icip NcV,s Coveraue Lisbon ZBA, Issues and Discussion Health Issues with an Asphalt Plant Nearby Here are some short quotes and abstracts from articles referencing the health problems that occur with working, and/or living near an Asphalt Plant. Asphalt and Diesel Exhaust Fumes " Over a half -million workers are exposed to fumes from asphalt, a petroleum product used extensively in road paving, rooting, siding. and concrete work. Health effects from exposure to asphalt fumes include headache, skin rash, sensitization, fatigue, reduced appetite, throat and eye irritation, cough. and skin cancer. " Reference: Asphalt Fumes - Lffited Suites Department of Labor, Occupational Safety and Health Administration Reference: Hot Mix Asphalt Plants - Tract: Loading and Unloading " The primary emission sources associated with Hot Mix Asphalt(HMA) production are the dryers, hot bins, and mixers, which emit particulate matter (PM) and a variety of gaseous pollutants. Other emission sources found at HMA plants include storage silos, which temporarily hold the HMA; truck load -out operations, in which the HMA is loaded into trucks for hauling to the job site; liquid asphalt storage tanks; hot oil heaters, which are used to heat the asphalt storage tanks; and > and emissions, which consist of fugitive emissions from the HMA in truck beds. Emissions also result from vehicular traffic on paved and unpaved roads, aggregate storage and handling operations, and vehicle exhaust. " " The PM emissions associated with HMA production include the criteria pollutants PM -10 (PM less than 10 micrometers in aerodynamic diameter) and PM -2.5, hazardous air pollutant (HAP) metals, and HAP organic compounds. The gaseous emissions associated with HMA production include the criteria pollutants sulfur dioxide (SO 2 ), nitrogen oxides (NO x ), carbon monoxide (CO), and volatile organic compounds (VOC), as well as volatile HAP organic compounds. " Reference: r.PA - Hot Mix : _-,p :1t Assessment Summary of Research on Dlesk.: and : Toxic Smell "It smells." http://stoppresbyasphaltplant.org/Health.phtml 11/6/2017 Asphalt Plant Health Concerns Page 2 of 3 "While a state study indicates the air quality in a neighborhood next to a controversial paving plant meets safety standards, neighbors say their problems with the plant are as much about quality of life as quality of air. The odor of asphalt coming from the R.C. & Sons paving plant has been a prime complaint of several residents of the nearby Grandvie\\ neighborhood." Bangor Daily - It si is k. but \ lame Asphalt Plant meets standards " Dr. Mitchell said that tiny particles in asphalt production plant emissions can cause lung damage, exacerbate breathing condir'cros and ultimately cause more severe problems. " New York Tin;_`; Article - Who Wants Lo Livc -Near an Asphalt Plant Noise Here are typical noise emissions from a Hot -Mix Asphalt Plant. Noise Level Distance from Center of Plant 85 dBA 78 dBA 70 dBA 63 dBA 55 dBA 46 dBA 36 dBA 24 dBA 50 feet (measured reference level) 100 feet 200 feet 400 feet 8CCI feet 1,600 feet 3,200 feet 6.400 feet We do not knm - the assumptions that went into the measurements in this noise summary table. Looking at the California study. we do not know, the age or size/capacity of the plant(s) measured. Remember that newer plants are quieter. and older plants make more noise. Reference: Full Document - C .tram. - •, ;aww @1 ilifornia Overall Health Effects " The complex chemical composition of asphalt makes it difficult to identify the specific component(s) responsible for adverse health effects observed in exposed workers. Known carcinogens have been found in asphalt fumes generated at worksites. Observations of acute irritation in workers from airborne and dermal exposures to asphalt fumes and aerosols and the potential for chronic health effects. including cancer, warrant continued diligence in the control of exposures. Reference: CI)(_. - Hazard R.2% ! '\\ of Occupational Exposure to Asphalt What [At Federal Government Regulates on Asphalt Plants and Air Quality What federal rules apply to asphalt plants') http://stoppresbyasphaltplant.org/Health.phtmi 11/6/2017 Asphalt Plant Health Concerns Page 3 of 3 • Asphalt plant emissions of particulate matter (PM2.5 and PM 10, carbon monoxide, sulfur dioxide. nitrogen dioxide, and lead must not exceed National Ambient Air Quality Standards (NAAQS ) at the property bounciai-) . • Asphalt plants manufactured after June 11, 1973, are subject to 40 CFR 60 Subpart I -New Source Performance Standards for Hot Mix Asphalt Plants. NSPS, Subpart I limits only the emissions of particulate matter from material haddling systems. • On November 8, 2002 . LSEPA ren-ioveu Asphalt Hot Mix Production from the Source Category List for which development of National Emission Standards for Hazardous Air Pollutants Standar( is required. Reference: No:tit Caroling. Lei , is it. n i u; i::y -- Air l'oxics and Asphalt Plants Web Sites With More information. Here are addition web sites that have information on Asphalt Plants and health effects. • Hot Mix Asphalt Plants - Stak hci.:. i i'pinions Report - I_ S EPA • Fact Sheet - Hot Mix Asphalt Ha m-. - Orcon Department of Environmental Quality • Preventing Pollution at Hot Mix 1 -lams - . Guide to Environmental Compliance and Pollution Prevention for Asphalt Plants in i'✓1 State of Missouri • Asphalt Plant Pollution - Blue Ridge Environmental Report • Road Pa n Aspha:t - e \ ! :an:;)shire - Fact Sheet • Asphalt - Hazardous 1 -LL:: Shetc - :. iITT New Jersey • North C'a<Aina I)i" si in (.; Ai :Iii\ - 'Jr Toxics and Asphalt Plants Copyright ©2017 NHParc.org We are PARC - Protectors of the Arnrnonoosuc River Corridor in Lisbon. New Hampshire. You can contact PARC at PARC P.O. Box 515 Sugar Hill, New Hampshire. 03586 Fiscal Agent: Peter Nightingale Phone #: (603) 6i 6-9292 http://stoppresbyasphaltplant.org!Health. phtml 11/6/2017 NAAQS Table I Criteria Air Pollutants I US EPA Page 1 of 3 We've made some changes to EPA.gov. If the information you are looking for is not here, you may be able to find it on the EPA Web Archive or the January 19, 2017 Web Snapshot. United state► CIP Env toy mental P►a,,KGCrn AD nc NAAQS Table The Clean Air Act, which was last amended in 1990, requires EPA to set National Ambient Air Quality Standards (40 CFR part 50) for pollutants considered harmful to public health and the environment. The Clean Air Act identifies two types of national ambient air quality standards. Primary standards provide public health protection, including protecting the health of "sensitive" populations such as asthmatics, children, and the elderly. Secondary standards provide public welfare protection, including protection against decreased visibility and damage to animals, crops, vegetation, and buildings. The EPA has set National Ambient Air Quality Standards for six principal pollutants, which are called "criteria" air pollutants. Periodically, the standards are reviewed and may be revised. The current standards are listed below. Units of measure for the standards are parts per million (ppm) by volume, parts per billion (ppb) by volume, and micrograms per cubic meter of air (µg/m3). Pollutant [links to historical tables of NAAQS reviews] Primary/ Secondary Carbon Monoxide (CO) primary Averaging Time 8 hours 1 hour Lead (Ph) primary and secondary Rolling 3 month average Nitrogen Dioxide (NO2.1 primary 1 hour Level 9 ppm 35 ppm 0.15 µg/m' 100 ppb Form Not to be exceeded more than once per year Not to be exceeded 98th percentile of 1 -hour daily maximum concentrations, averaged over 3 years https://www.epa.gov/criteria-air-pollutants/naaqs-table 11/6/2017 NAAQS Table I Criteria Air Pollutants I US EPA Page 2 of 3 Pollutant 'links to historical tables of NAAQS reviews] Primary/ Secondary Averaging Time Level Form primary and secondary 1 year `-'1 Annual Mean 53 ppb Ozone (O3) primary and secondary 8 hours Li Annual fourth - highest daily maximum 8 -hour concentration, averaged over 3 years 0.070 ppm Particle PM2.5 primary 1 year 12.0 µg/m3 annual mean, averaged over 3 years secondary 1 year 15.0 µg/m3 annual mean, averaged over 3 years Pollution primary and secondary 24 hours 35 µg/m3 98th percentile, averaged over 3 years (PM) PM10 primary and secondary 24 hours 150 µg/m3 Not to be exceeded more than once per year on average over 3 years Sulfur Dioxide (SO2) primary 1 hour Lu 99th percentile of 1 -hour daily maximum concentrations, averaged over 3 years 75 ppb secondary 3 hours 0.5 ppm Not to be exceeded more than once per year https://www.epa.gov/criteria-air-pollutants/naaqs-table 11/6/2017 NAAQS Table I Criteria Air Pollutants I US EPA Page 3 of 3 (1) In areas designated nonattainment for the Pb standards prior to the promulgation of the current (2008) standards, and for which implementation plans to attain or maintain the current (2008) standards have not been submitted and approved, the previous standards (1.5 µg/m3 as a calendar quarter average) also remain in effect. (2) The level of the annual NO2 standard is 0.053 ppm. It is shown here in terms of ppb for the purposes of clearer comparison to the 1 -hour standard level. (3) Final rule signed October 1, 2015, and effective December 28, 2015. The previous (2008) O3 standards additionally remain in effect in some areas. Revocation of the previous (2008) O3 standards and transitioning to the current (2015) standards will be addressed in the implementation rule for the current standards. (4) The previous SO2 standards (0.14 ppm 24 -hour and 0.03 ppm annual) will additionally remain in effect in certain areas: (1) any area for which it is not yet 1 year since the effective date of designation under the current (2010) standards, and (2)any area for which an implementation plan providing for attainment of the current (2010) standard has not been submitted and approved and which is designated nonattainment under the previous SO2 standards or is not meeting the requirements of a SIP call under the previous SO2 standards (40 CFR 50.4(3)). A SIP call is an EPA action requiring a state to resubmit all or part of its State Implementation Plan to demonstrate attainment of the required NAAQS. Menu of Control Measures for NAAQS Implementation The Menu of Control Measures (MCM) provides state, local and tribal air agencies with the existing emission reduction measures as well as relevant information concerning the efficiency and cost effectiveness of the measures. State, local and tribal agencies will be able to use this information in developing emission reduction strategies, plans and programs to assure they attain and maintain the National Ambient Air Quality Standards (NAAQS). The MCM is a living document that can be updated with newly available or more current data as it becomes available. • Menu of Control Measures LAST UPDATED ON DECEMBER 20, 2016 https://www.epa.gov/criteria-air-pollutants/naaqs-table 11/6/2017 ilrNEW JERSEY DEPARTMENT H EALTH -oil I1 SENIOR SERVICES New Jersey Department of Health and Senior Services HAZARDOUS SUBSTANCE FACT SHEET Common Name: CAS Number: DOT Number: DOT Hazard Class: ASPHALT 8052-42-4 NA 1999 (Asphalt) UN 1999 (Tars, Liquid) 3 (Flammable) HAZARD SUMMARY * Asphalt can affect you when breathed in. * Extracts of certain Asphalts have been shown to cause cancer in animals. * Asphalt fumes can irritate the eyes on contact. * Breathing Asphalt fumes can irritate the nose, throat and lungs causing coughing, wheezing and/or shortness of breath. * Contact can irritate and cause severe burns of the skin and may cause dermatitis and acne -like lesions. * Exposure to Asphalt fumes can cause headache, dizziness, nausea and vomiting. * Long-term contact can cause skin pigment change which is made worse by sunlight exposure. * Cutback and Rapid Curing Asphalt are FLAMMABLE and FIRE HAZARDS. * Asphalt is derived from Petroleum. Asphalt and Coal Tar Pitch are different. If you are actually working with Coal Tar chemicals, CONSULT THE NEW JERSEY DEPARTMENT OF HEALTH AND SENIOR SERVICES HAZARDOUS SUBSTANCE FACT SHEETS ON COAL TAR PITCH AND COAL TARS. * Asphalt, Oxidized (CAS # 64762-93-4) is a carcinogen. CONSULT THE NEW JERSEY DEPARTMENT OF HEALTH AND SENIOR SERVICES HAZARDOUS SUBSTANCE FACT SHEET ON ASPHALT, OXIDIZED. IDENTIFICATION Asphalt is a blackish -brown solid, semi -solid or liquid, depending on the formulation or mixture of Asphalt used. Asphalt fumes are produced during the manufacture and heating of Asphalt, which is used for road building and roofing, and in rubber and adhesives. REASON FOR CITATION * Asphalt is on the Hazardous Substance List because it is cited by ACGIH, DOT, NIOSH, IARC and NFPA. * Definitions are provided on page 5. RTK Substance number: 0170 Date: January 2001 Revision: April 2007 HOW TO DETERMINE IF YOU ARE BEING EXPOSED The New Jersey Right to Know Act requires most employers to label chemicals in the workplace and requires public employers to provide their employees with information and training concerning chemical hazards and controls. The federal OSHA Hazard Communication Standard (29 CFR 1910.1200) requires private employers to provide similar training and information to their employees. * Exposure to hazardous substances should be routinely evaluated. This may include collecting personal and area air samples. You can obtain copies of sampling results from your employer. You have a legal right to this information under the OSHA Access to Employee Exposure and Medical Records Standard (29 CFR 1910.1020). * If you think you are experiencing any work -related health problems, see a doctor trained to recognize occupational diseases. Take this Fact Sheet with you. WORKPLACE EXPOSURE LIMITS NIOSH: The recommended airborne exposure limit is 5 mg/m3, which should not be exceeded during any 15 -minute period. ACGIH: The recommended airborne exposure limit is 0.5 mg/m3 (for the inhalable fraction of the Benzene -soluble aerosol), averaged over an 8 - hour workshift. WAYS OF REDUCING EXPOSURE * Where possible, enclose operations and use local exhaust ventilation at the site of chemical release. If local exhaust ventilation or enclosure is not used, respirators should be worn. * Wear protective work clothing. * Wash thoroughly immediately after exposure to Asphalt and at the end of the workshift. * Post hazard and warning information in the work area. In addition, as part of an ongoing education and training effort, communicate all information on the health and safety hazards of Asphalt to potentially exposed workers. ASPHALT page 2 of 6 This Fact Sheet is a summary source of information of all potential and most severe health hazards that may result from exposure. Duration of exposure, concentration of the substance and other factors will affect your susceptibility to any of the potential effects described below. HEALTH HAZARD INFORMATION Acute Health Effects The following acute (short-term) health effects may occur immediately or shortly after exposure to Asphalt: * Asphalt fumes can irritate the eyes on contact. * Breathing Asphalt fumes can irritate the nose, throat and lungs causing coughing, wheezing and/or shortness of breath. * Contact can irritate and cause severe burns of the skin and may cause dermatitis and acne -like lesions. * Exposure to Asphalt fumes can cause headache, dizziness, nausea and vomiting. Chronic Health Effects The following chronic (long-term) health effects can occur at some time after exposure to Asphalt and can last for months or years: Cancer Hazard * While Asphalt has not been identified as a carcinogen, it should be HANDLED WITH CAUTION since extracts of certain Asphalts have been shown to cause cancer in animals. Reproductive Hazard * According to the information presently available to the New Jersey Department of Health and Senior Services, Asphalt has not been tested for its ability to affect reproduction. Other Long -Term Effects * Long-term contact can cause skin pigment change which is made worse by sunlight exposure. * Asphalt fumes can irritate the lungs. Repeated exposure may cause bronchitis to develop with cough, phlegm, and/or shortness of breath. MEDICAL Medical Testing Before beginning employment and at regular times after that, for those with frequent or potentially high exposures, the following are recommended: * Lung function tests Any evaluation should include a careful history of past and present symptoms with an exam. Medical tests that look for damage already done are not a substitute for controlling exposure. Request copies of your medical testing. You have a legal right to this information under the OSHA Access to Employee Exposure and Medical Records Standard (29 CFR 1910.1020). Mixed Exposures * Because smoking can cause heart disease, as well as lung cancer, emphysema, and other respiratory problems, it may worsen respiratory conditions caused by chemical exposure. Even if you have smoked for a long time, stopping now will reduce your risk of developing health problems. Conditions Made Worse By Exposure * Exposure to sunlight may make skin effects of Asphalt worse. WORKPLACE CONTROLS AND PRACTICES Unless a less toxic chemical can be substituted for a hazardous substance, ENGINEERING CONTROLS are the most effective way of reducing exposure. The best protection is to enclose operations and/or provide local exhaust ventilation at the site of chemical release. Isolating operations can also reduce exposure. Using respirators or protective equipment is less effective than the controls mentioned above, but is sometimes necessary. In evaluating the controls present in your workplace, consider: (1) how hazardous the substance is, (2) how much of the substance is released into the workplace and (3) whether harmful skin or eye contact could occur. Special controls should be in place for highly toxic chemicals or when significant skin, eye, or breathing exposures are possible. In addition, the following controls are recommended: * Where possible, automatically pump liquid Asphalt from drums or other storage containers to process containers. * Before entering a confined space where Asphalt may be present, check to make sure that an explosive concentration does not exist. Good WORK PRACTICES can help to reduce hazardous exposures. The following work practices are recommended: * Workers whose clothing has been contaminated by Asphalt should change into clean clothing promptly. * Contaminated work clothes should be laundered by individuals who have been informed of the hazards of exposure to Asphalt. * Eye wash fountains should be provided in the immediate work area for emergency use. * If there is the possibility of skin exposure, emergency shower facilities should be provided. * On skin contact with Asphalt, immediately wash or shower to remove the chemical. At the end of the workshift, wash any areas of the body that may have contacted Asphalt, whether or not known skin contact has occurred. ASPHALT page 3 of 6 * Do not eat, smoke, or drink where Asphalt is handled, processed, or stored, since the chemical can be swallowed. Wash hands carefully before eating, drinking, applying cosmetics, smoking, or using the toilet. PERSONAL PROTECTIVE EQUIPMENT WORKPLACE CONTROLS ARE BETTER THAN PERSONAL PROTECTIVE EQUIPMENT. However, for some jobs (such as outside work, confined space entry, jobs done only once in a while, or jobs done while workplace controls are being installed), personal protective equipment may be appropriate. The OSHA Personal Protective Equipment Standard (29 CFR 1910.132) requires employers to determine the appropriate personal protective equipment for each hazard and to train employees on how and when to use protective equipment. The following recommendations are only guidelines and may not apply to every situation. Clothing * Avoid skin contact with Asphalt. Wear protective gloves and clothing. Safety equipment suppliers/manufacturers can provide recommendations on the most protective glove/clothing material for your operation. * All protective clothing (suits, gloves, footwear, headgear) should be clean, available each day, and put on before work. Eye Protection * Wear indirect -vent, impact and splash resistant goggles when working with liquids. * Wear a face shield along with goggles when working with corrosive, highly irritating or toxic substances. * Contact lenses should not be worn when working with this substance. Respiratory Protection IMPROPER USE OF RESPIRATORS IS DANGEROUS. Such equipment should only be used if the employer has a written program that takes into account workplace conditions, requirements for worker training, respirator fit testing, and medical exams, as described in the OSHA Respiratory Protection Standard (29 CFR 1910.134). * Where the potential exists for exposure over 0.5 mg/m3, use a NIOSH approved full facepiece respirator with an organic vapor cartridge and particulate prefilters. Increased protection is obtained from full facepiece powered -air purifying respirators. * If while wearing a filter or cartridge respirator you can smell, taste, or otherwise detect Asphalt, or if while wearing particulate filters abnormal resistance to breathing is experienced, or eye irritation occurs while wearing a full facepiece respirator, leave the area immediately. Check to make sure the respirator -to -face seal is still good. If it is, replace the filter or cartridge. If the seal is no longer good, you may need a new respirator. * Be sure to consider all potential exposures in your workplace. You may need a combination of filters, prefilters or cartridges to protect against different forms of a chemical (such as vapor and mist) or against a mixture of chemicals. * Where the potential exists for exposure over 5 mg/m3, use a NIOSH approved supplied -air respirator with a full facepiece operated in a pressure -demand or other positive - pressure mode. For increased protection use in combination with an auxiliary self-contained breathing apparatus operated in a pressure -demand or other positive -pressure mode. HANDLING AND STORAGE * Prior to working with Asphalt you should be trained on its proper handling and storage. * Asphalt, when HEATED, can give off toxic Hydrogen Sulfide gases. * Asphalt may ignite or explode when mixed with NAPHTHA, other VOLATILE SOLVENTS, and LIQUID OXYGEN. * Asphalt is not compatible with OXIDIZING AGENTS (such as PERCHLORATES, PEROXIDES, PERMANGANATES, CHLORATES, NITRATES, CHLORINE, BROMINE and FLUORINE). * Store in tightly closed containers in a cool, well -ventilated area. • Sources of ignition, such as smoking and open flames, are prohibited where Cutback and Rapid Curing Asphalt are used, handled, or stored. * Metal containers involving the transfer of Cutback and Rapid Curing Asphalt should be grounded and bonded. * Use only non -sparking tools and equipment, especially when opening and closing containers of Cutback and Rapid Curing Asphalt. QUESTIONS AND ANSWERS Q: If I have acute health effects, will I later get chronic health effects? A: Not always. Most chronic (long-term) effects result from repeated exposures to a chemical. Q: Can I get long-term effects without ever having short- term effects? A: Yes, because long-term effects can occur from repeated exposures to a chemical at levels not high enough to make you immediately sick. Q: What are my chances of getting sick when I have been exposed to chemicals? A: The likelihood of becoming sick from chemicals is increased as the amount of exposure increases. This is determined by the length of time and the amount of material to which someone is exposed. Outiioor enthusiasts fighting plan for gravel mine, asphalt plant near Colorado River in Ea... Page 1 of 7 NEWS > ENVIRONMENT Outdoor enthusiasts fighting plan for gravel mine, asphalt plant near Colorado River in Eagle County J at. 4 • 1 I • •I /fir ••'�•`Y. • -. -0 • ! i ...!'r --r s- _ .r -..O....:.s.o -'- .�'_•�±Ti"rtF'��',•. '.-. ti.! L� -ay.. :.J_ J• I . I H _ . r 4111. Jason Blevins, The Denver Post A kayaker paddles upstream on the Colorado River near Dotsero next to a pasture that has been preserved as open space. The landowner of that pasture, Karl Berger, is asking for the Town of Gypsum's approval to develop a gravel pit on the mesa above the river. By JASON BLEVINS I jblevins@denverpost.com I The Denver Post PUBLISHED: December 11, 2016 at 5:37 pm I UPDATED: December 11, 2016 at 5:39 pm http://www.denverpost.com/2016/12/1 1 /gravel-mine-asphalt-plant-colorado-river-eagle-co... 11 /7/2017 Oi door enthusiasts fighting plan for gravel mine, asphalt plant near Colorado River in Ea... Page 2 of 7 GYPSUM — A plan to develop a gravel pit mine and asphalt plant on a sage brush mesa above the Colorado River is roiling Eagle County river users and open -space advocates who have spent years fighting to protect the corridor from development. Grand Junction asphalt paving firm Elam Construction and landowner Karl Berger are asking the Gypsum Town Council to annex more than 150 acres above the Colorado River and issue a special permit to allow the company to develop a 10 -year pit mine and asphalt plant that could produce and process 230,000 tons of aggregate a year for construction in the growing Eagle Valley. The plan calls for a 30 -foot -deep terraced mine near the confluence of Deep Creek and the Colorado River, bordered by county open space and Bureau of Land Management land. Dotsero, in unincorporated Eagle County, has cultivated a recreation -rich reputation as the "gateway to the Colorado River and Flat Tops Wilderness" and a portal to some of the state's best fishing, hunting, camping and floating. Upstream, local open space efforts have preserved hundreds of acres of riverfront ranchland as open space for recreation, wildlife and water protection. Berger has spent many years clearing the lower parcel of his 166 -acre Coyote Ranch along the banks of the Colorado River. He removed old mining and railroad debris, then graded, seeded and irrigated a pasture. He has hosted the annual America Cup World Fly Fishing Championships on the land for the last two years. Last month, he inked a $190,000 deal with Eagle County Open Space and Proposed gravel pit Gypsum's town council on Tuesday will discuss plans for a gravel mine and asphalt plant on part of the Coyote Ranch near the confluence of Deep Creek and the Colorado River. n Week (' t S my %`1°r�` .rr' Eagle Rivet Gypsum •- • r J N mile ommi The Denver Post The Denver Post the Eagle Valley Land Trust to protect the pasture, assuring that the 6,000 feet of riverfront and 38 acres can never be developed. He wants to do the same rehabilitation to the roughly 130 acres he owns above the river. Elam Construction, after 10 years, will grade the mesa, plant native grasses and return the sage -brush and scrub oak mesa to green pasture. http://www.denverpost.com/2016/ 12/ 11 /gravel-mine-asphalt-plant-colorado-river-eagle-co... 11/7/2017 Outdoor enthusiasts fighting plan for gravel mine, asphalt plant near Colorado River in Ea... Page 3 of 7 "Do I want a gravel pit on my property? Not necessarily. But these guys, Elam, they are promising to do all the heavy lifting and pay for it and put my land into the condition you see along the river," said Berger, who has raised three kids in the Eagle Valley. Berger said lie understands the concern from river lovers about impacts. He said he spent five years negotiating with Elam Construction to assure operational safeguards and developing reclamation plan that will restore the land as a working ranch. "It's a special stretch of river," said Berger, who said the ranch was in terrible shape in 2004 when he bought it from a mine operator with plans to unearth a limestone deposit in the middle of the Flat Tops, using the ranch as a processing area. "I'm a land reclamation guy. I'm not some evil industrialist. I feel absolutely blessed that I am a steward of that piece of property." The beauty of Berger's Coyote Ranch is something everyone in Eagle County can agree on. Since 2011, Eagle County's mill -levy -funded open space program and Great Outdoors Colorado have spent more than $10 million acquiring more than 1,300 acres of riverfront ranch land along the Colorado River above Dotsero. The county has protected more than 6 miles of riverfront as well as water rights. The county has built four boat ramps along the idyllic stretch of river from State Bridge to Dotsero, where the Eagle River joins the Colorado River. The goal of the deal with Berger was to protect scenic corridors, water rights and riparian habitat on the acreage, said Toby Sprunk, the director of the Eagle County Open Space program. "This was a relatively small but very important property," Sprunk said. River advocates fear not just the plant, but its potential threat to years of conservation work along the river corridor. "The precedent here certainly concerns me," said Nathan Fey, the Colorado director for American Whitewater, which has spent a decade laboring to secure a federal Wild and Scenic River designation for the Upper Colorado. "I don't think this is the right location. What is the risk of contamination from the asphalt plant?" Elam Construction, in a mid -November presentation to the town, said its 10 -year plan would benefit the Eagle Valley's construction industry by providing high -quality sand and gravel that could "minimize the monopoly on the valley" — where B&B Excavating controls most of the supply of aggregate for new construction — while supporting local contractors and roadway improvements. http://www.denverpost.com/2016/12/l 1 /gravel-mine-asphalt-plant-colorado-river-eagle-co... 11 /7/2017 O idoor enthusiasts fighting plan for gravel mine, asphalt plant near Colorado River in Ea... Page 4 of 7 The Town of Gypsum has seen its aggregate costs for new projects climb 20 percent in the last two years. Last month the town got a letter from its aggregate supplier that prices were climbing another 7 percent next year. Most contractors and road builders have to import gravel from Garfield and Mesa counties to the west. The town wants to encourage land uses that mirror Dotsero's renown as a gateway to some of the finest recreation in Colorado, Gypsum town manager Jeff Shroll said. The gravel pit won't necessarily do that and it won't make the town any money. But it could improve the valley's aggregate market, saving local contractors and Eagle County municipalities money. "It's always a concern if there's not competition on a very needed commodity," Shroll said. Still, he admits the gravel pit plan was not expected. "This caught us a little bit flatfooted," he said, noting that the town's approval could include strict contingencies and safeguards above and beyond state and federal guidelines. "The annexation opens the door to negotiate a little more on our behalf and the public's behalf." Elam Construction has filed permits with the Colorado Department of Transportation for a new access road, the state Division of Reclamation. Mining and Safety, the Army Corps of Engineers and the Colorado Department of Public Health and Environment. The dry pit - known as a terrace pit — will not require water for operations and will discharge only stormwater. Elam and Berger have developed mitigation strategies to reduce noise, dust, traffic and visual impacts, which include a paved access road, dust -settling irrigation and berms blocking views of the mining and buildings. "There's nothing more possibly we can do to make this thing more non- impactful," Berger said. Eagle County in 2012 released a community plan for Dotsero. The plan — developed after meetings and surveys with the region's residents and landowners — noted that Dotsero "is perceived by many as a location where land uses 'pushed' from upper valley communities have found an affordable home." http://www.denverpost.com/2016/12/1 1 /gravel-mine-asphalt-plant-colorado-river-eagle-co... 11 /7/2017 O�Itdoor enthusiasts fighting plan for gravel mine, asphalt plant near Colorado River in Ea... Page 5 of 7 With a gravel pit in Eagle, a biomass facility that turns beetle kill into electricity and a massive gypsum wallboard plant in Gypsum, the downvalley communities of the Eagle Valley are home to industrial operations that no longer fit the area around Vail and Beaver Creek resorts. The Dotsero community plan recognized this perception and elevated recreation as a potential economic engine that could guide development in the area. Gypsum, which annexed a private water ski lake in Dotsero five years ago, envisions a future where the town has a role in guiding development on its western border. Commercial development, according to the community plan, should "provide opportunities for businesses that would support or enhance the reputation of Dotsero as a recreational destination and portal to the Colorado River corridor." The plan designated Berger's Coyote Ranch as a potential residential and agricultural area, where future land use should "avoid negative impacts from utility installations and resource extraction operations." Eagle County's board of commissioners in October penned a letter to Gypsum planners expressing concerns that the mining operation"may permanently alter" recreational, rural and agricultural attributes identified in the county's community plan for Dotsero. The commissioners cited potential mining impacts to Dotsero's Two Rivers Village residential community, recreation along the river, air and water quality issues. traffic, night lighting and damage to scenic corridors. While the commissioners said the proposal "appears inconsistent with several policy goals" — like the Dotsero community and open space plan — they did like the long-term plan to convert the property back to rangeland and wildlife habitat. Local river advocates have been trumpeting a call to arms against not necessarily the asphalt plant, but its proximity to open space and the river. "It makes no sense to put a pit beside a conservation easement, especially in that location," said Greta Campanale, who regularly rafts and kayaks that stretch of the Colorado River with her family. "I understand the financial incentive, and also that this is a finite period of time, but it's not a good enough argument to support that kind of operation so close to the river." http://www.denverpost.com/2016/ 12/11 /gravel-mine-asphalt-plant-colorado-river-eagle-co... 11 /7/2017 Lqaorte nsidents: Our town, gravel pit don't mix Page 1 of 4 Thanks for supporting local journalism (Photo: Valerie Mosley/The Coloradoan) SUBSCRIBE NOW (HTTP://OFFERS.COLORADOAN.COM/SPECIALOFFER?GPS- SOURCE-BENBNOV&UTM_MEDIUM=NANOBAR&UTM_SOURCE-BOUNCE- EXCHANGE&UTM_CAMPAIGN=THANKSGIVING17) For $29/yr. VENUS Laporte residents: Our town, gravel pit don't mix Jacy Marmaduke, jmarmadukeiecoloradoan.com Published 8:01 a.m. MT April 3, 2017 I Updated 9:59 a.m. SIT April 4, 2017 Living near a gravel mining operation can be the pits. Or can it? Fullscreen A Northern Colorado concrete company is trying to convince Laporte residents that a proposed gravel pit and concrete batch plant can coexist peacefully with their comrPHO O&4iflei> tRetdyMIXbusiness model doesn't mix with their way of life. gravel pit hopes to expand to Laporte Residents are worried about dust, increased traffic, noise and water impacts from the 123 -acre site located about a half -mile west of Taft Hill Road just north of Larimer County Road 54G And they're reluctant to believe project organizer Loveland Ready -Mix's promises to mitigate those impacts because they say gravel operations have burned their community before. "These plans will say, 'We're going to use berms and plant vegetation and do all these things,"" said Terry Waters, a Laporte resident who was involved with previous gravel pit opposition efforts. "And they don't do it." More: RMNP chief: 'It's becoming harder to accomplish our mission' (/story/news/2017/03/31/rocky-mountain-national-park-chief-s-becoming-harder- accomplish-our-mission/99702920/) The fight puts the spotlight on a crushing reality confronting a growing Front Range: The bigger we get, the more roadwork we need, and all that gravel and concrete has to come from somewhere. The Colorado Geological Survey mapped all the gravel resources in the state decades ago. Most of it is near riverbeds, like the Poudre River — and a lot of it is gone. "It's getting to harder and harder to find (sites for pits)," said Stephanie Fancher, Loveland Ready -Mix co-owner. "I know for neighbors, it's not their problem that we're trying to find a dwindling resource and utilize it. But that's the reality of the situation." Loveland Ready -Mix picked the Laporte site in part because of its proximity to construction projects north of the company's existing sites in Loveland, Boulder and Johnstown, Fancher said. Mining at the proposed Laporte facility, which must be approved by Larimer County commissioners, would continue for 10 to 12 years, depending on demand. Fancher hopes the concrete batch plant would be a permanent fixture. Batch plants measure and weigh concrete materials that are mixed inside cement trucks. About 250 area residents packed a recent community meeting about the project. The meeting bordered on rowdy at times as opponents questioned Loveland Ready -Mix about the project, held up signs and took frequent breaks for applause, prompting a few threats of ending the gathering early. "How many signatures do we need to say 'no'?" was a common refrain. Among opponents' concerns: http://www.coloradoan.com/story/news/2017/04/03/can-gravel-pit-coexist-laporte-residents/99839876/ 11/7/2017 Laporte rf sidents: Our town, gravel pit don't mix Page 2 of 4 • i ne site s proximity to scnoois ana a rarm::�l.afcne is rouare miaaie ana elementary scnoois are less tnan a mile west or the raciiity site, ana Native Hill Farm's new 50 -acre F' NM*0&4 9 J?9JRc9!dt'ifT2 h1Sm • Air quality impacts of dusaitip r ripTF rdniiO vKADOAN.COM/SPECIALOFFER?GPS- • Traffic: The facility would altitataiSINS03\16CRV6.44G,cranOVANOritIttialWaffeittottattOttbaread that residents say is already EXCHANGE&UTM_CAMPAIGN=THANKSGIVING17) overcrowded. • Water: Laporte's water table is relatively close to grounpi lleve 4yi_ng_residents are more susceptible to basement and crawlspace or flooding. Residents are also concerned about potentialrimpac s to th it water wells. • Noise, especially if the facility operates during the weekends and at night as initially requested Fancher, a Loveland native, is sure her company can be a good neighbor to Laporte residents. Responding to the traffic concerns, she said the traffic increase would be much smaller than if the site became a residential subdivision, which was the previous plan for the land. Turning the area into a subdivision would have added upward of 2,000 trips each day, or an increase of about 67 percent, but developers changed their plans when faced with the cost and complications of adding water and sewer lines to the site. Join now for as low as $29 / yr Subscribe Now (http://offers.coloradoan.com✓specialoffer? gps- source=BEAZnov&utm_mediurrl=agilityzone&utm_source=bounce- exchange&utm_campaign=UyVEB2017) Among the company's mitigation strategies: • Watering to prevent excess dust • Placing berms around the mine site to cut down on noise and limit visibility from the road • Reclaim the pits once they're mined by turning them into ponds and planting native vegetation around the area • Monitor water levels around the site to avoid harming neighbors' wells and basements • Backing off the request to allow 24 -hour and weekend operation The company's Loveland facility is less than a half -mile from Namaqua Elementary School and hasn't received any complaints from parents, Fancher said. Thompson School District representatives said they haven't received any recorded complaints. Fancher said gravel mining would be conducted in small patches of about 10 acres, further reducing the facility's footprint. "All we can do is try to educate people," she said. "We don't want to come in and ruin your life and your business. That's not what we're about." Residents are unswayed. They say they've heard those mitigation strategies before — from Aggregate Industries, a company that mined gravel at the Stegner property just west of North Taft Hill Road about a half -mile south of US 287. Despite complaints from neighbors, the operator performed noisy work on weekends, flooded basements and produced a lot of dust without watering, neighbors said. More: Losses from Colorado mine spill may be less than feared (/story/news/local/colorado/2017/04/03/losses-colorado-mine-spill-may-less-than- feared/100006468/) Aggregate Industries representatives couldn't be reached for comment. Aggregate "gave mining a bad name," said Bill Seaworth, a neighbor of the Stegner pit. But he said mining can coexist with communities if it's done right. Seaworth's property just south of the old Stegner pit is surrounded by gravel pits past and present. "Ninety percent of it is up to the operator," he said, noting some operators follow regulations while others don't. Gravel miners must obtain a state air pollution permit and undergo regular county inspections. Residents can also call county officials to file complaints. Neighbors of Loveland Ready -Mix's Loveland facility, which includes a gravel pit and batch plant, said they hadn't noticed any negative impacts. http://www.coloradoan.com/story/news/2017/04/03/can-gravel-pit-coexist-laporte-residents/99839876/ 11/7/2017 L,orte residents: Our town, gravel pit don't mix fft Page 3 of 4 uerelc ts&cner, wno lives about a quarter -mile sown 44pPKSor pits at me rams', s�+aia rnoust ana noise naven t Peen issues ror nis ramny. in a rew years, L velana Ready -Mix will begin mining slightly farther sei SRE #ipipnn9 A lUPt�c9tt7?f4 worried about that, either. SUBSCRIBE NOW (HTTP://OFFERS.COLORADOAN.COM/SPECIALOFFER?GPS- "I know a lot of people were upset abostotipecagnilmogtenitynyymeitdaimitiestentaIM itiogggicatitteriposcis." EXCHANGE&UTM_CAMPAIGN=THANKSGIVING17) Buy Photo Owner Stephanie Fancher shows a handful of gravel at Loveland Ready Mix gravel pit on Monday, March 27, 2017. (Photo: Valerie Mosley/The Coloradoan) Fancher said she and her colleagues are planning meetings and tours with concerned Laporte residents. They're also continuing to work with county planners to finish a project proposal for the planning commission. Meanwhile, opponents are getting organized. They've held community meetings, are contacting commissioners and have gathered more than 1,200 signatures on a petition opposing the project. Signatures alone can't stop the project, but the opponents hope the opposition effort will help prove the facility is incompatible with the community, one of the key criteria for the commissioners' final decision. Laporte is a community close to nature and wildlife, they say, where people would rather putter in their gardens or go for a bike ride than stay indoors. Residents keep their windows open to stay cool during hot days and enjoy the symphonies of bird calls and breezes. They're worried that industrial operations are chipping away at their unique way of life. "I've tried looking for places to move," Waters said. "There's just nothing out there like this. And why should we have to move when we don't want to? For all of its quirks, this is our home." What happens to gravel pits once all the gravel is mined out? A state law passed in 1977 put an end to the practice of abandoning spent gravel pits by requiring reclamation of mining sites. Today, an operator must post a bond with the state that is returned only after reclamation work, such as grading and planting native plants to re -vegetate a site, is completed and the permit closed. The reclamation and treatment a pit receives depends upon its next use, but many become ponds used for water storage or recreation. The complexities of state law on water ownership also come into play. City of Fort Collins Natural Areas along the Poudre River with ponds that are remnants of gravel -mining operations include the North Shields Ponds, Kingfisher Point and Arapaho Bend, among many others. http://www.coloradoan.com/story/news/2017/04/03/can-gravel-pit-coexist-laporte-residents/99839876/ 11/7/2017 Laporte residents: Our town, gravel pit don't mix .o. Page 4 of 4 0, ,e e _e rnalism fill,4114" 1:11L.,SU $SCRIBE NOW (HTTP://OFFERS.COLORADOAN.COM/SPECIALOFFER?GPS- �$QURCE=BENBNOV&UTM_MEDIUM=NANOBAR&UTM_ URCE=BOUNCE- EXCHANGE&UTM_CAMPAIGN=THANKSGIVINGI7) For $29/yr. _z • F -N .. gravel pa site (123 acres) 1 ✓., yfw • ; eul_.. 1 +tyrf ' yi i . .L' a-:. , A map of the proposed site for a gravel pit and batch plant in Laporte. (Photo: Jacy Marmaduke/rhe Coloradoan) Read or Share this story: http://noconow.co/2nAiPXn (JIiIy ciao http://www.coloradoan.com/story/news/2017/04/03/can-gravel-pit-coexist-Laporte-residents/99839876/ 11/7/2017 Page 1 of 1 Silicosis: Occupational lung disease Silicosis is an often fatal lung disease caused by breathing dust con tain ing crystalline silica particles, a basic component of sand and granite.. There is no cure for silicosis. and treatment options are limited. However, the condition can be prevented if measures are taken to reduce exposure. Symptoms At -risk occupations Continued exposure: > Construction Shortness 01 breath > Fever Bluish skin at the ear lobes or lips As the disease progresses: Fatigue • Ettreme shortness or breath Loss of appetite > Chest pain • Respiratory failure sotto U S. Dirsattnat of I. ate Ott '*aI aW SaK.t aM Mai A Sal Mist LA* OW O w or Silica dust particles can embed themselves in the alveolar sacs deep in the lungs where they cannot be tinted by rnutouS of coughing Mining Sando:asting b- Masonry Demo,ttion Man iacturing of glass and metal products Plumbing a- Paenl i I t' rt e '- Inhaling the dust can cause scar tau+e to loran in the lungs that reduces the lungs' ability to extract oxygen from the air. ti .w♦ lawn*, :*r.%aalab float http://image.slidesharecdn.com%occupationalhealthfinal-151 109103746-1val-app6891 /95/o... 11/7/2017 Silicosis Symptoms, Causes, and Risk Factors I American Lung Association Page 3 of 7 What Are the Symptoms of Silicosis? Symptoms of silicosis can appear from a few weeks to many years after exposure to silica dust. Symptoms typically worsen over time as scarring in the lungs occurs. Cough is an early symptom and develops over time with exposure to silica that is inhaled. In acute silicosis, you may experience fever and sharp chest pain along with breathing difficulty. These symptoms can come on suddenly. In chronic silicosis, you may only have an abnormal chest X-ray in the beginning and then slowly develop a couch and breathing difficulty. More than a third of people with silicosis have phlegm production and cough. Chronic bronchitis -like symptoms may occur, and the lungs have additional sounds called wheezes and crackles. As extensive scarring progresses over time, you may see signs of chronic lung disease such as leg swelling, increased breathing rate, and bluish discoloration of the lips. What Causes Silicosis? Silicosis is caused by exposure to crystalline silica, which comes from chipping, cutting, drilling, or grinding soil, sand, granite, or other minerals. Any occupation where the earth's crust is disturbed can cause silicosis. A long list of occupations are known that expose workers to crystalline silica that is inhaled. These include: • Various forms of mining, such as coal and hard rock mining • Construction work • Tunnel work • Masonry • Sand blasting http://www.lung.org/lung-health-and-diseases/lung-disease-lookup/silicosis/silicosis-sympt... 11/7/2017 . Silicosis Symptoms, Causes, and Risk Factors I American Lung Association Page 4 of 7 • Glass manufacturing • Ceramics work • Steel industry work • Quarrying • Stone cutting What Are Risk Factors of Silicosis? Breathing crystalline silica causes silicosis and the main risk factor is exposure to silica dust. You can prevent silicosis by limiting exposure. There are national guidelines on exposure limits over a lifetime of working. If you work in a job that exposes you to silica dust, your employer must, by law, give you the correct equipment and clothing you need to protect yourself You are responsible for using italways—and for taking other steps to protect yourself and your family as you leave your job site and head home. NIOSH also recommends that medical examinations occur before job placement or upon entering a trade, and at least every 3 years thereafter. Patients with silicosis have an increased risk of other problems, such as tuberculosis, lung cancer, and chronic bronchitis. If you are a smoker, quitting may help, as smoking damages the lungs. When to See Your Doctor Any person who works in industries with exposure to inhaled silica should get regular health checkups and be monitored for signs and symptoms of lung disease. In addition, if you have a cough, phlegm, or breathing difficulty that is not improving, you should http://www.lung.org/lung-health-and-diseases/lung-disease-lookup/silicosis/silicosis-sympt... 11/7/2017 S licosis Symptoms, Causes. and Risk Factors I American Lung Association Page 5 of 7 be closely evaluated by your doctor. Some people with acute silicosis also have fever, weight loss, and fatigue. Previous Next CHEST FOUNDATION This content was developed in partnership with the CHEST Foundation, the philanthropic arm of the American College of Chest Physicians. Lung Health & Diseases Lung Disease Lookup Silicosis Learn About Silicosis Silicosis Symptoms, Causes, and Risk Factors Diagnosing and Treating Silicosis Living With Silicosis Questions to Ask Your Doctor About Silicosis Ask An Expert Questions about your lung health? Need help finding healthcare? Call 1-800-LUNGUSA. http://www.lung.org/lung-health-and-diseases/lung-disease-lookup/silicosis/silicosis-sympt... 11/7/2017 Page 1of1 Pneumoconiosis: it This is an occupational disease where dust or particulate matter is inhaled. t This causes the formation of pulmonary fibrosis. Types: Silicosis is caused by inhaling silicon dioxide (sand). Asbestosis occurs as the result of inhaling asbestos dust. Patients who present with this disease possesses very distinct radiopaque pleural plaques. Black lung disease is caused by inhaling coal dust. http://slideplayer.com/slide/5735151 /19/images/16/Pneumoconiosis:+This+is+an+occupati... 11/7/2017 Page 1 of 1 Workplace diseases and their causes... Chemicals • Diseases Deaths DALYs Chemicals involved in acute poisonings Asbestos Occupational lung carcinogens, e.g. arsenic, silica, chromium Occupational Ieukaemogens, e.g. benzene Dust and fumes Unintentional poisonings Mesothelioma and other cancers Lung cancer Leukaemia COPD, asthma 30,000 110,000 110,000 650,000 1,500,000 1,000,000 7,500 110,000 375,000 3,800,000 IOMb' P russ-Ustun A. Vickers C, Haetkger P, et al. Knowns and unknowns on burden of disease due to chemicals:a systematic review. Environmental Health 2011:10:9. https://image.slidesharecdn.com/orpdisease-cherrie-140522094958-phpapp02/95/what-sho... 11/7/2017 Page 1 of 1 Rh.initis and laryngitis Large particles ore daposrled in the nose, pharynx. and larynx. More soluble gases (Lg., sulfur dioxidel am absorbed by upper respiratory tract mucous membranes, causing - W edema and mucus hypersecretiion. Tracheitis, bronchitis, and bronchrolitis Large particles (more than 10 dun in diameter) are deposited and then cleared by cilia. Small particles and fine fibers are doposilud in bronchioles and bifurcations of alveolar ducts. Lass soluble gases penetrate to deeper small airways. Asthma and chronic obstructive pulmonary disease Allergens and irritants are deposited in large airways by turbulent lh�w..."using chronic inflammatory changes Cancer Carcinogens (asbestos and polycyclic aromatic hydrocarbonug carne into contact with bronchial epithelial cells, causing mutations in proto•or.cogenes and tumor -suppressor genes. More than one such contact results in malignant transformation. Interstitial disease Srnalt particles Bess than 10 firs in diameter) and fibers am dtrpoxti/sd in terminal bronchioles, alveolar ducts, and alveoli Penetration to the irrterstnrum results in fibroais and the formation of granulomas. Nasal cavity .Pharyn Larynx Trachea Bronchus http://www.nejm.org/na101 /home/literatum/publisher/mms/journals/content/nejm/2000/nej... 11 /7/2017 The impact of PM2.5 on the human respiratory system Page 1 of 8 journal of Thoracic Disease J Thorac Dis. 2016 Jan; 8(1): E69 —E74. doi: 10.3978/]. issn.2072-1439.2016.01.19 PMCID: PMC4740125 The impact of PM2.5 on the human respiratory system Yu-Fei Xing, Yue-Hua Xu, Min-Hua Shi, and Yi-Xin Lian. Department of Respiratory Medicine, Second Affiliated Hospital of Soochow University, Suzhou 215004, China {Corresponding author. Contributions: (I) Conception and design: YX Lian; (II) Administrative support: MH Shi; (Ill) Provision of study materials or patients: YH Xu, MH Shi; (IV) Collection and assembly of data: YF Xing; (V) Data analysis and interpretation: YX Lian; (VI) Manuscript writing: All authors; (VII) Final approval of manuscript: All authors. Correspondence to: Yi-Xin Lian. Department of Respiratory Medicine, Second Affiliated Hospital of Soochow University, Suzhou 215004, China. Email: lynelian@163.com. Received 2015 Sep 14; Accepted 2015 Dec 10. Copvriaht 2016 Journal of Thoracic Disease. All rights reserved. This article has been cited by other articles in PMC. Abstract Go to: Recently, many researchers paid more attentions to the association between air pollution and respiratory system disease. In the past few years, levels of smog have increased throughout China resulting in the deterioration of air quality, raising worldwide concerns. PM2.5 (particles less than 2.5 micrometers in diameter) can penetrate deeply into the lung, irritate and corrode the alveolar wall, and consequently impair lung function. Hence it is important to investigate the impact of PM2.5 on the respiratory system and then to help China combat the current air pollution problems. In this review, we will discuss PM2.5 damage on human respiratory system from epidemiological, experimental and mechanism studies. At last, we recommend to the population to limit exposure to air pollution and call to the authorities to create an index of pollution related to health. Keywords: Air pollution, PM2.5, respiratory system, China Background Go to: Recently, with accelerated urban development and modernization, air pollution is worsening and its impact on human health has become a main research topic. Air pollutants include gaseous pollutants and particle matters (PM). The pathogenicity of PM is determined by their size, composition, origin, solubility and their ability to produce reactive oxygen. Studies (I) have shown that smog is generally caused by high concentrations of fine particles (particle size less than or equal to 2.5 btm, referred to as PM2.5) or aerosols. It has been found that PMs with an aerodynamic diameter smaller than 10 gm have a greater impact on human health. One group of PM identified, PM2.5, have small diameters, however large surface areas and may therefore be capable of carrying various toxic stuffs, passing through the filtration of nose hair, reaching the end of the respiratory tract with airflow and accumulate there by diffusion, damaging other parts of the body through air exchange in the lungs. What's more, adults exposed to other high levels of ambient air pollution, for example PM 10 and coarse particulate, also have shown increased prevalence of respiratory disease. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4740125/ 11/6/2017 The impact of PM2.5 on the human respiratory system Page 2 of 8 Recently, a growing number of studies in toxicology, epidemiology and other related fields have demonstrated that respirable particles are closely related to the incidence of human diseases and mortality rate. The "Harvard six Cities Study", published in 1996, revealed that PM2.5 was one of the causative factors of human non -accidental death. In this study, PM2.5 was positively related to daily morality of humans, particularly the elderly (RR =1.5%, 95% CI: 1.1-1.9%) (2). The study provides evidence supporting the linear relationship between non -accidental death and PM2.5. Patients with respiratory diseases account for a large proportion of these non -accidental deaths caused by air pollution. Given that PM2.5 causes asthma, respiratory inflammation, jeopardizes lung functions and even promotes cancers, its impact on human respiratory system should not be dismissed (3-5). In this review, we will discuss PM2.5 damage on human respiratory system from epidemiological, experimental and mechanism studies. Epidemiological evidence of PM2.5 damage on human respiratory Go to: system After twenty years of epidemiological studies, scientists have revealed a significant correlation between fine particle pollutants and respiratory morbidity and mortality (6). A report from the last century illustrated that increased PM concentration in the air may directly lead to an elevated morbidity and mortality of a population (7,8). In European Union countries, PM2.5 decreased the average life span by 8.6 months (9). After investigating 29 European countries, Analitis (10) found that respiratory mortality increased by 0.58% for every 10 µg/m3 increase of PM l0. It was recently reported that the prevalence rate of respiratory diseases increased by 2.07%, while hospitalization rate raised by 8% accordingly, when the daily PM2.5 increased by 10 µg/m3 (11,12). This study also reported that elevated air particle pollutants were directly associated with more serious symptoms of respiratory tract diseases, undermined lung function and raised morbidity and mortality of cardiopulmonary diseases. Furthermore, this correlation was more obvious in the elderly, pregnant women, adolescents, infants, patients with a history of cardiopulmonary problems and other susceptible populations (13-15). Scientists in Canada and the US found that long-term exposure to PM2.5 significantly increased not only the chances of cardiopulmonary problems but also the mortality of lung cancers US17). Indeed a study conducted for 7 years (from 2000 to 2007) in the US indicated that the average life span was extended by 0.35 years for every 10 gg/m3 decrease of PM2.5 (18). From the American Cancer Society, Pope and coworkers (19) collected a set of data, based on 500,000 adults living in large cities. They concluded that the overall mortality and mortality of cardiopulmonary diseases as well as lung cancer increased by 4%, 6% and 8%, respectively, for every 10 µg/m3 PM2.5 increase, after ruling out smoking, diet, drinking, occupation and other risk factors. In addition, a cohort study by the American Cancer Society tracked 1.2 million American adults for 26 years [1982-2008] and found that the mortality of lung cancer increased by 15-27% when PM2.5 air concentrations increased by 10 µg/m3 (20). This risk was even higher among patients with chronic lung diseases. More strikingly, the results of 11 cohort studies in Europe revealed that the population hazard ratio (HR) of lung adenocarcinoma was 1.55 (95% CI: 1.05-2.29), for each increase of PM2.5 by 5 gg/m3 (21). In 2011, after balancing smoking and other interfering factors, a study 22) of 63,520 people from 6 regions in 3 states in Japan demonstrated that a higher incidence of respiratory diseases, in particular pneumonia, were closely related to long-term exposure to particles in the air. Yadav et al. (23) revealed that the morbidity of asthma, influenza and acute respiratory tract infection increased notably during outbreaks of smog. Compared with Western countries, research into the hazard of PM2.5 in China began just 10 years ago. It has been reported that PM2.5 mainly occurs in the Beijing -Tianjin -Hebei Economic Zone, the https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4740125/ 11/6/2017 The impact of PM2.5 on the human respiratory system Page 3 of 8 Yangtze River Delta, the Pearl River Delta region, the three northeastern provinces, the Sichuan Basin, and other densely populated areas. It has seriously affected public health both physically and emotionally. Data from the program (http://stateair.net/web/mission/1/) which tracks daily PM2.5 concentrations on the grounds of the U.S. Embassy in Beijing in the winter months from 2010 to 2014 showed that daily PM2.5 concentrations exceeded 100 µg/m3 for more than half of the days and reached as high as 744 µg/m3, more than 20 times the US Environmental Protection Agency's (EPA) 24 -hour standard for PM2.5 of 35 µg/m3. Surveys in Beijing, Shanghai, Guangzhou and other areas in China (24-29) displayed a strong linear correlation between daily mortality (including non -accidental death) and PM2.5 levels. In addition, the daily mortality significantly increased with increased fine PM concentration. A meta -analysis on the current dose -response relationship of particle exposure and morbidity showed that morbidity increased by 0.38% with each increase of PMI0 0 by 10 µg/m3 (29). Using meta -analysis, Qian et al. (21) studied the epidemiological literature published between 1995 and 2003. It was concluded that for every 100 µg/m3 increase of PM2.5, the morbidity of residents increased by 12.07%. The authors also showed that respiratory outpatient visits increased during smog outbreaks (32). Therefore, the impact of particles in the air on the human respiratory system is a worldwide issue of concern. Experimental evidence of PM2.5 damage on the respiratory system Go to: In animal studies, Phipps (33) exposed two groups of mice to either air or cigarette smoke for 5 weeks. After intratracheal injection of streptococcus pneumoniae, bacteria counts in mice lungs after cigarette exposure were 4 times in 24 hours and 35 times in 48 hours higher than the control group, respectively. One study in China found that air pollution could cause damage, lose and dysfunction of rat tracheal cilia, resulting in infection and a declined nonspecific immune defense, and that these mice were then prone to secondary infection (34). In addition, many studies have focused on the impact of PM2.5 on alveolar macrophages. Jalava et al. collected air particles from 6 cities in Europe and cultured them with mice macrophages in vitro for 24 hours. The viability of alveolar macrophages decreased significantly with a PM0.2-2.5 range from 300 pg/mL to 150 g/mL. Furthermore, alveolar macrophages TNF-a expression increased with increased particle concentration (35). Renwick et al. carried out intratracheal instillation on rats with fine particles and ultrafine particle suspensions (125 and 500 µg per rat, respectively). A LDH cytotoxicity study indicated that the viability of alveolar macrophages was severely damaged when the fine particle concentration reached 500 µg per rat (36). In another study, alveolar macrophages were harvested by instilling PM2.5 suspension (300,750, 2,000, 5,000 µg per rat) into the trachea of Wistar rats. The results indicated that the phagocytize rate and phagocytic index were remarkably lower with increased particle concentrations (37). Additional study (38) has reported that PM2.5 significantly reduces phagocytosis of alveolar macrophages both in vitro and in vivo. Mechanism study of PM2.5 and human respiratory system _ Go to: Recently, the mechanisms of the damaging effects of PM2.5 on the respiratory system have been investigated including: I. Injury from free radical peroxidation: earlier studies showed that the free radicals, metal and the organic components of PM2.5 can induce free radical production to oxidize lung cells, which may be the primary cause of body injury (39-1. In 1996, Donaldson and Beswick, etc. reported that the surface itself of environmental particles can produce free radicals. In addition, that the PM2.5 surface was rich in iron, copper, zinc, manganese, and other transition elements, as well as polycyclic aromatic hydrocarbons and lipopolysaccharide, etc. These components can increase https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4740125/ 11/6/2017 The impact of PM2.5 on the human respiratory system Page 4 of 8 free radical production in the lung, consume antioxidant ingredients and cause oxidative stress (39). Many studies (43) have confirmed that the reactive oxygen species (ROS) generated by particles, particularly by water soluble particles, produce hydroxyl radical (• OH) by activating metals. Hydroxyl radicals are the main factor causing oxidative damage of DNA. When damaged DNA is not effectively repaired in time, it can induce teratogenesis carcinogenesis, mutagenesis and other irreversible damages. Mehta et al. (44) found that particles could not only damage DNA and suppress DNA repair, but could also promote the replication of damaged DNA fragments and consequently prompt carcinogenesis; II. Imbalanced intracellular calcium homeostasis: calcium is one of the important second messengers that mediates and regulates cell functions both physiologically and pathologically. Abnormally high calcium concentrations activates a series of inflammatory reactions, leading to inflammation and cell damage. PM2.5 induces excessive production of free radicals or ROS and decreases the antioxidant capacity of cells, resulting in the peroxidation of lipids on the cell membrane and the elevation of intracellular Cat concentrations. In addition, increased intracellular Cat+ concentrations can further elevate free radical or ROS production (45). Brown et al. 46 showed that it is possible that ROS-mediated regulation of intracellular Cat+ concentrations may be one of the mechanisms of PM2.5-induced cell damages. Xing (47) also indicated that cell apoptosis and necrosis were related to over expression of Cat} -sensitive receptors; III. Inflammatory injury: it has been wildly reported that PM2.5 is related to inflammatory cytokines whereby it stimulates overexpression of a number of transcription factor genes and inflammation - related cytokine genes that cause inflammatory injury. Sigaud et al. (4$) found that PM2.5-induced inflammation led to an increase in the number of neutrophils. Gripenback et al. (49) reported that exposure to pine dust caused an increase in the number of eosinophils, T cells and mastocytes in bronchoalveolar lavage fluid and in 2003, Gordon (50) showed that PM2.5 and its microenvironment influenced the phenotype and function of two types of alveolar macrophages. The first of these macrophages, known as M1 polarized alveolar macrophage, is primarily induced by Thl-type cytokines (IL -12, IFN-y) and pathogens in the body and promote inflammation. The second of these macrophages, M2 polarized alveolar macrophage, is closely related to the Th2 type cytokines (IL -4 and IL -13) and the immunomodulatory cytokine (IL -10), which primarily inhibit inflammation. It has been reported that human alveolar macrophages treated with PM2.5 express high levels of MI -associated cytokines (IL -12, IFN-y) and low levels of M2 -associated cytokines (IL -4, IL -10 and IL -13) (51-53). These results indicate that cytokines can both induce neutrophil, T cell and eosinophil migration to the lungs and other tissues, and on their own, migrate to the lung, exhibiting higher cell activities, releasing more inflammatory cytokines and chemokines. The interactions between inflammatory cells and cytokines can damage lung cells synergistically. Consequently, the mechanism of action of PM2.5 in the damage to human health remains one of the primary focuses of many current studies. Several studies have illustrated how one single component of PM2.5 can influence human health, whilst others investigated the details of how an imbalance of key inflammatory cytokines can lead to certain lung diseases. Few studies have, however, investigated the pathogenesis of PM2.5 as a whole. Integration of the fragmented information from previous studies will provide a great deal of knowledge in the understanding of the harm to human health of PM2.5. Prevention of P M2.5 damage to the respiratory system Go to: Understanding how PM2.5 leads to respiratory diseases will assist in preventing and diagnosing the corresponding health issues and the evolution of more effective methods and technologies for the treatment of PM2.5-induced diseases. China is currently facing severe air pollution in the transition phase of industrialization and urbanization. Less than 1% of the 500 largest cities in China can meet the air quality guidelines recommended by the World Health Organization. Seven of these cities were https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4740125/ 11/6/2017 The impact of PM2.5 on the human respiratory system Page 5 of 8 ranked among the ten most polluted cities in the world (54). There has been mounting concern on the part of the government and the population of China generally as to the consequences of such high levels of air pollution, which are so high as to greatly limit visibility. The high levels of pollution was related to the linearity of the health effects (55). Consequently, controlling air pollution is an arduous and long-term task. It is therefore proposed that the following guidelines be in place to address increased PM2.5 concentrations and/or an increase in smog levels: I. Remain indoors, close all windows and doors and if going outside, wear a qualified mask and minimize the duration or intensity of outdoor activities; II. Sensitive populations (the elderly and those with pre-existing cardiopulmonary problems) should be more cautious of PM2.5 pollution and minimize outdoor PM2.5 exposure; III. Patients with chronic cardiopulmonary problems should increase their medication dosage and pay close attention to their health to prevent severity of their symptoms during an increase in smog; IV. As oxidative stress is one of the main pathogenic mechanisms of PM2.5, taking antioxidant supplements or nutritious food (for example, w-3 fatty acids in fish oil); V. Chinese environmental authorities could launch a "smog health index", referring to the Canadian "air quality health index" by Environment Canada (EC). Such an index may instruct members of the public to prepare early and correctly thereby minimizing the health threats of smog. Acknowledgements None. Footnotes Go to: Conflicts of Interest: The authors have no conflicts of interest to declare. References Go to: Go to: 1. Zhang XY, Sun JY, Wang YQ, et al. Factors contributing to haze and fog in China. Chin Sci Bull (Chin Ver) 2013;58:1178-87. 2. Schwartz J, Dockery DW, Neas LM. Is daily mortality associated specifically with fine particles? J Air Waste Manag Assoc 1996;46:927-39. [PubMed] 3. Samoli E, Analitis A, Touloumi G, et al. Estimating the exposure -response relationships between particulate matter and mortality within the APHEA multicity project. Environ Health Perspect 2005;113:88-95. [PMC free article] [PubMed] 4. Ostro B, Broadwin R, Green S, et al. Fine particulate air pollution and mortality in nine California counties: results from CALFINE. Environ Health Perspect 2006;114:29-33. PMC free article] [PubMed] 5. Lewis TC, Robins TG, Dvonch JT, et al. Air pollution -associated changes in lung function among asthmatic children in Detroit. Environ Health Perspect 2005;113:1068-75. [PMC free article] [PubMed] 6. Brunekreef B, Holgate ST. Air pollution and health. Lancet 2002;360:1233-42. [PubMed] 7. Nemery B, Hoet PH, Nemmar A. The Meuse Valley fog of 1930: an air pollution disaster. Lancet 2001;357:704-8. [PubMed] 8. Helfand WH, Lazarus 1, Theerman P. Donora, Pennsylvania: an environmental disaster of the 20th century. Am J Public Health 2001;91:553. [PMC free article] [PubMed] https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4740125/ 11/6/2017 The impact of PM2.5 on the human respiratory system Page 6 of 8 9. Orru H, Maasikmets M, Lai T, et al. Health impacts of particulate matter in five major Estonian towns: main sources of exposure and local differences. Air Quality, Atmosphere & Health 2011;4:247- 58. 10. Analitis A, Katsouyanni K, Dimakopoulou K, et al. Short-term effects of ambient particles on cardiovascular and res-piratory mortality. Epidemiology 2006;17:230-3. [PubMed] 11. Zanobetti A, Franklin M, Koutrakis P, et al. Fine particulate air pollution and its components in association with cause -specific emergency admissions. Environ Health 2009;8:58. [PMC free article] [PubMed] 12. Dominici F, Peng RD, Bell ML, et al. , Fine particulate air pollution and hospital admission for cardiovascular and respiratory diseases. JAMA 2006;295:1127-34. [PMC free article] [PubMed] 13. Huynh M, Woodruff TJ, Parker JD, et al. Relationships between air pollution and preterm birth in California. Paediatr Perinat Epidemiol 2006;20:454-61. [PubMed] 14. Martinelli N, Girelli D, Cigolini D, et al. Access rate to the emergency department for venous thromboembolism in relationship with coarse and fine particulate matter air pollution. PLoS One 2012;7:e34831. -PMC free article] PubMed] 15. de Oliveira BF, Ignotti E, Artaxo P, et al. Risk assessment of PM(2.5) to child residents in Brazilian Amazon region with biofuel production. Environ Health 2012;11:64. [PMC free article] [PubMed] 16. Schwartz J. Harvesting and long term exposure effects in the relation between air pollution and mortality. Am J Epidemiol 2000;151:440-8. [PubMed] 17. Franklin M, Koutrakis P, Schwartz P. The role of particle composition on the association between PM2.5 and mortality. Epidemiology 2008;19:680-9. [PMC free article] [PubMed] 18. Correia AW, Pope CA, 3rd, Dockery DW, et al. Effect of air pollution control on life expectancy in the United States: an analysis of 545 U.S. counties for the period from 2000 to 2007. Epidemiology 2013;24:23-31. -PMC free article] [PubMed] 19. Pope CA, 3rd, Burnett RT, Thun MJ. Lung cancer, cardiop-ulmonary mortality, and long-term exposure to fine particu-late air pollution. JAMA 2002;287:1132-41. [PMC free article [PubMed] 20. Turner MC, Krewski D, Pope CA, 3rd, et al. Long-term ambient fine particulate matter air pollution and lung cancer in a large cohort of never -smokers. Am J Respir Crit Care Med 2011;184:1374-81. [PubMed] 21. Raaschou-Nielsen O, Andersen ZJ, Beelen R, et al. Air pollution and lung cancer incidence in 17 European cohorts: prospective analyses from the European Study of Cohorts for Air Pollution Effects (ESCAPE). Lancet Oncol 2013;14:813-22. [PubMed] 22. Katanoda K, Sobue T, Satoh H, et al. An association between long-term exposure to ambient air pollution and mortality from lung cancer and respiratory diseases in Japan. J Epidemiol 2011;21:132- 43. [PMC free article] [PubMed] 23. Yadav AK, Kumar K, Kasim A, et al. Visibility and incidence of respiratory diseases during the 1998 haze episode in Brunei Darussalam. Pure and Applied Geophysics 2003;160:265-77. 24. Xu X, Gao J, Dockery DW, et al. Air pollution and daily mortality in residential areas of Beijing, China. Arch Environ Health 1994;49:216-22. [PubMed] 25. Huang W, Tan J, Kan H, et al. Visibility, air quality and daily mortality in Shanghai, China. Sci Total Environ 2009;407:3295-300. [PubMed] https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4740125/ 11/6/2017 The impact of PM2.5 on the human respiratory system Page 7 of 8 26. Yang C, Peng X, Huang W, et al. A time -stratified case -crossover study of fine particulate matter air pollution and mortality in Guangzhou, China. Int Arch Occup Environ Health 2012;85:579-85. [PubMed] 27. Qian Z, He Q, Lin HM, et al. Association of daily cause -specific mortality with ambient particle air pollution in Wuhan, China. Environ Res 2007;105:380-9. [PubMed 28. Ma Y, Chen R, Pan G, et al. Fine particulate air pollution and daily mortality in Shenyang, China. Sci Total Environ 2011;409:2473-7. [PubMed] 29. Wong CM, Ou CQ, Chan KP, et al. The effects of air pollution on mortality in socially deprived urban areas in Hong Kong, China. Environ Health Perspect 2008;116:1189-94. [PMC free article] [PubMed] 30. Kan HD, Cheng BH. Analysis of exposure -response relationships of air particulate matter and adverse health outcomes in China. Journal of Environment and Health 2002;19:422-4. 31. Qian XL, Kan HD, Song WM, et al. Meta -analysis of association between air fine particulate matter and daily mortality. Journal of Environment and Health 2005;22:246-8. 32. Li N, Peng XW, Zhang BY, et al. Relationship between air pollutant and daily hospital visits for respiratory diseases in guangzhou: a time -series study. Journal of Environment and Health 2009;26:1077-80. 33. Phipps JC, Aronoff DM, Curtis JL, et al. Cigarette smoke exposure impairs pulmonary bacterial clearance and alveolar macrophage complement -mediated phagocytosis of Streptococcus pneumoniae. Infect Immun 2010;78:1214-20. [PMC free article] [PubMed] 34. Zhou Y, Wang RQ, Zhao S, et al. Effect on cytokines and ultrastructure in rats exposed to mixed air pollutants. Journal of Shenyang Medical College 2009;11:6-12. 35. Jalava PI, Salonen RO, Pennanen AS, et al. Heterogeneities in inflammatory and cytotoxic responses of RAW 264.7 macrophage cell line to urban air coarse, fine, and ultrafine particles from six European sampling campaigns. Inhal Toxicol 2007;19:213-25. [PubMed] 36. Renwick LC, Brown D, Clouter A, et al. Increased inflammation and altered macrophage chemotactic responses caused by two ultrafine particle types. Occup Environ Med 2004;61:442-7. [PMC free article] [PubMed] 37. Huang NH, Wang Q, Xu DQ. Immunological effect of PM2.5 on cytokine production in female Wistar rats. Biomed Environ Sci 2008;21:63-8. [PubMed] 38. Miyata R, van Eeden SF. The innate and adaptive immune response induced by alveolar macrophages exposed to ambient particulate matter. Toxicol Appl Pharmacol 2011;257:209-26. [PubMed] 39. Donaldson K, Beswick PS. Free radical activity associated with the surface of the particles: a unifying factor in deter -mining biological activity. Toxicol Lett 1996;88:293-8. [PubMed] 40. Greenwell LL, Moreno T, Jones TP, et al. Particle -induced oxidative damage is ameliorated by pulmonary antioxidants. Free Radic Biol Med 2002;32:898-905. [PubMed] 41. Rahman I, Macnee W. Role of oxidants/antioxidants in smoking -induced lung diseases. Free Radic Biol Med 1996;21:669-81. [PubMed] 42. Kelly FJ. Oxidative stress: its role in air pollution and adverse health effects. Occup Environ Med 2003;60:612-6. PMC free article] [PubMed] https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4740125/ 11/6/2017 The impact of PM2.5 on the human respiratory system Page 8 of 8 43. Valavanidis A, Fiotakis K, Bakeas E, et al. Electron paramagnetic resonance study of the generation of reactive oxygen species catalysed by transition metals and quinoid redox cycling by inhalable ambient particulate matter. Redox Rep 2005;10:37-51. [PubMed] 44. Mehta M, Chen LC, Gordon T, et al. Particulate matter inhibits DNA repair and enhances mutagenesis. Mutat Res 2008;657:116-21. [PMC free article] [PubMed] 45. Kim YK, Jung JS, Lee SH, et al. Effects of antioxidants and Ca2+ in cisplatin-induced cell injury in rabbit renal cortical slices. Toxicol Appl Pharmacol 1997;146:261-9. [PubMed] 46. Brown DM, Donaldson K, Borm PI, et al. Calcium and ROS-mediated activation of transcription factors and TNF-acytokine gene expression in macrophages exposed to ultrafine particles. Am J Physiol Lung Cell Mol Physiol 2004;286:L344-53. [PubMed] 47. Xing WJ, Kong FJ, Li GW, et al. Calcium -sensing receptors induce apoptosis during simulated ischaemia-reperfusion in Buffalo rat liver cells. Clin Exp Pharmacol Physiol 2011;38:605-12. [PubMed] 48. Sigaud S, Goldsmith CA, Zhou H, et al. Air pollution particles diminish bacterial clearance in the primed lungs of mice. Toxicol Appl Phannacol 2007;223:1-9. [PMC free article [PubMed] 49. Gripenback S, Lundgren L, Eklund A, et al. Accumulation of eosinophils and T -lymphocytes in the lungs after exposure to pinewood dust. Eur Respir J 2005;25:118-24. [PubMed] 50. Gordon S. Alternative activation of macrophages. Nat Rev Immunol 2003;3:23-35. [PubMed] 51. He M, Ichinose T, Yoshida S, et al. Urban particulate matter in Beijing, China, enhances allergen - induced murine lung eosinophilia. Inhal Toxicol 2010;22:709-18. [PubMed] 52. Park EJ, Roh J, Kim Y, et al. PM 2.5 collected in a residential area induced Thl-type inflammatory responses with oxidative stress in mice. Environ Res 2011;111:348-55. [PubMed] 53. Yoshizaki K, Brito JM, Toledo AC, et al. Subchronic effects of nasally instilled diesel exhaust particulates on the nasal and airway epithelia in mice. Inhal Toxicol 2010;22:610-7. [PubMed] 54. Asian -Development -Bank, 2013. Toward an Environmentally Sustainable Future: Country Environmental Analysis of the People's Republic of China. Available online: http://www. Adb.Org/publications/toward-environmental ly-sustainable-future-countryenvironmental-analysis-prc 55. Aunan K, Pan XC. Exposure -response functions for health effects of ambient air pollution applicable for China -- a meta -analysis. Sci Total Environ 2004;329:3-16. [PubMed] Articles from Journal of Thoracic Disease are provided here courtesy of AME Publications https://www.ncbi.nIntnih.gov/pmc/articles/PMC4740125/ 11/6/2017 Maternal exposure to fine particulate air pollution induces epithelial-to-mesenchymal tran... Page 1 of 2 PubMed Format: Abstract Toxicol Lett. 2017 Feb 5:267:11-20. doi: 10.1016/j.toxlet.2016.12.016. Epub 2016 Dec 29. Full text links El I S F [ FULL -TEXT ARTICLE Maternal exposure to fine particulate air pollution induces epithelial-to-mesenchymal transition resulting in postnatal pulmonary dysfunction mediated by transforming growth factor-13/Smad3 signaling. Tang W1, Du L2, Sun W2, Yu Z3, He F2, Chen J2, Li X2. Li X2, Yu L2, Chen D4. Author information Abstract Fine particles from air pollution. also called particulate matter. less than 2.5 micrometers in diameter (PM2.5), are a threat to child health. Epidemiological investigations have related maternal exposure to PM2.5 to postnatal respiratory symptoms, such as frequent wheezing, chronic cough, and lung function decrements. However, only few experimental animal studies have been performed to study the effects of PM2.5.The aim of this study was to investigate the effects of maternal exposure to PM2.5 on postnatal pulmonary dysfunction in a rat model and to examine the mechanism of PM2.5-induced morphological pulmonary changes.Timed pregnant Sprague-Dawley rats were treated with PM2.5 (0.1, 0.5, 2.5, or 7.5mg/kg) once every three days from day 0 to 18 of pregnancy. After delivery, pups were sacrificed on postnatal day (PND)1 and 28. The effects of transforming growth factor -beta (TGF-R) on epithelial-mesenchymal transition (EMT) were determined by immunohistochemistry, Western blotting, and quantitative RT-PCR. The offspring underwent pulmonary function measurements on PND28, lung tissues were histopathologically examined, and markers of oxidative stress were measured. Maternally PM2.5-exposed offspring pups displayed significant decreases in lung volume parameters, compliance, and airflow during expiration on PND28. The PM2.5-exposed group showed interstitial proliferation in lung histology. significant oxidative stress in lungs, and up -regulation of TGF- p-induced EMT via increased vimentin and a -smooth muscle actin and decreased E-cadherin levels on PND1 and PND28.These results suggest that EMT up -regulation mediated by the TGF-p/Smad3 pathway plays a role in postnatal pulmonary dysfunction associated with maternal exposure to PM2.5. Copyright © 2016 Elsevier Ireland Ltd. All rights reserved. https://www.nebi.nlm.nih.gov/pubmed/28041981 11/6/2017 Maternal exposure to fine particulate air pollution induces epithelial-to-mesenchymal tran... Page 2 of 2 KEYWORDS: EMT; Offspring; PM2.5; Pulmonary dysfunction PMID: D: 28041981 DOI: 10.1016/j.toxlet.2016.12.016 [Indexed for MEDLINE] MeSH terms, Substances LinkOut - more resources PubMed Commons PubMed Commons home 0 comments How to join PubMed Commons https://www.ncbi.nlm.nih.gov/pubmed/28041981 11/6/2017 Fine particulate matter air pollution and atherosclerosis: Mechanistic insights. - PubMed -... Page 1 of 2 PubMed Format: Abstract Full text links Biochim Biophys Acta. 2016 Dec;1860(12):2863-8. doi: 10.1016/j.bbagen.2016.04.030. Epub 20 Fine particulate matter air pollution and atherosclerosis: Mechanistic insights. Bai Y1, Sun Q2. Author information Abstract BACKGROUND: Atherosclerosis is a progressive disease characterized by the accumulation of lipids and fibrous plaque in the arteries. Its etiology is very complicated and its risk factors primarily include genetic defects, smoking, hyperlipidemia, hypertension, lack of exercise, and infection. Recent studies suggest that fine particulate matter (PM2.5) air pollution may also contribute to the development of atherosclerosis. SCOPE OF REVIEW: The present review integrates current experimental evidence with mechanistic pathways whereby PM2.5 exposure can promote the development of atherosclerosis. MAJOR CONCLUSIONS: PM2.5-mediated enhancement of atherosclerosis is likely due to its pro -oxidant and pro -inflammatory effects, involving multiple organs. different cell types, and various molecular mediators. GENERAL SIGNIFICANCE: Studies about the effects of PM2.5inhalation on atherosclerosis may yield a better understanding of the link between air pollution and major cardiovascular diseases, and provide useful information for policy makers to determine acceptable levels of PM2.5 air quality. This article is part of a Special Issue entitled Air Pollution, edited by Wenjun Ding, Andrew J. Ghio and Weidong Wu. Copyright © 2016 Elsevier B.V. All rights reserved. KEYWORDS: Air pollution; Atherosclerosis: Fine particulate matter: Inflammation; Oxidative stress PMID: D: 27156486 DOI: 10.1016/j. bbaden.2016.04.030 [Indexed for MEDLINE] https://www.ncbi.nlm.nih.gov/pubmed/27156486 11/6/2017 Fine particulate matter air pollution and atherosclerosis: Mechanistic insights. - PubMed -... Page 2 of 2 Publication types, MeSH terms, Substances, Grant support LinkOut - more resources PubMed Commons PubMed Commons home 0 comments How to join PubMed Commons https://www.ncbi.nlm.nih.gov/pubmed/27156486 11/6/2017 Direct effects of airborne PM2.5 exposure on macrophage polarizations. - PubMed - NCBI Page 1 of 2 PubMed u aranumarnatkasest Format: Abstract Full text links Biochim Biophys Acta. 2016 Dec;1860(12):2835-43. doi: 10.1016/j.bbagen.2016.03.033. Epub 2 1,\, l t l� ULL-TEXT ARTICLE Direct effects of airborne PM2.5 exposure on macrophage polarizations. Zhao Q1, Chen H2, Yang T2, Rui W3, Liu F3, Zhang F3, Zhao Y4, Ding W5. Author information Abstract BACKGROUND: Exposure of atmospheric particulate matter with an aerodynamic diameter less than 2.5µm (PM2.5) is epidemiologically associated with illnesses. Potential effects of air pollutants on innate immunity have raised concerns. As the first defense line, macrophages are able to induce inflammatory response. However, whether PM2.5 exposure affects macrophage polarizations remains unclear. METHODS: We used freshly isolated macrophages as a model system to demonstrate effects of PM2.5 on macrophage polarizations. The expressions of cytokines and key molecular markers were detected by real-time PCR. and flow cytometry. The specific inhibitors and gene deletion technologies were used to address the molecular mechanisms. RESULTS: PM2.5 increased the expression of pro -inflammatory cytokines granulocyte - macrophage colony -stimulating factor (GM-CSF), interleukin-6 (IL -6), interleukin-1 R (IL -1p), tumor necrosis factor alpha (TNFa). PM2.5 also enhanced the lipopolysaccharide (LPS) -induced M1 polarization even though there was no evidence in the change of cell viability. However. PM2.5 significantly decreased the number of mitochondria in a dose dependent manner. Pre-treatment with NAC, a scavenger of reactive oxygen species (ROS), prevented the increase of ROS and rescued the PM2.5-impacted M1 but not M2 response. However, mTOR deletion partially rescued the effects of PM2.5 to reduce M2 polarization. CONCLUSIONS: PM2.5 exposure significantly enhanced inflammatory M1 polarization through ROS pathway, whereas PM2.5 exposure inhibited anti-inflammatory M2 polarization through mTOR-dependent pathway. GENERAL SIGNIFICANCE: The present studies suggested that short-term exposure of PM2.5 acts on the balance of inflammatory M1 and anti-inflammatory M2 macrophage polarizations. which may be involved in air pollution -induced immune disorders and https://www.ncbi.nlm.nih.gov/pubmed/27041089 11/6/2017 Direct effects of airborne PM2.5 exposure on macrophage polarizations. - PubMed - NCBI Page 2 of 2 diseases. This article is part of a Special Issue entitled Air Pollution, edited by Wenjun Ding, Andrew J. Ghio and Weidong Wu. Copyright © 2016 Elsevier B.V. All rights reserved. KEYWORDS: Inflammation; Macrophages; PM(2.5); Polarization; ROS PMID: 27041089 DOI: 10.1016/j.bbagen.2016.03.033 [Indexed for MEDLINE] Publication type, MeSH terms, Substances LinkOut - more resources PubMed Commons PubMed Commons home 0 comments How to join PubMed Commons https://www.ncbi.nlm.nih.gov/pubmed/27041089 11/6/2017 DDAH1 plays dual roles in PM2.5 induced cell death in A549 cells. - PubMed - NCBI Page 1 of 2 PubMed Format: Abstract Full text links IELSEV I ER FiffieflIffdalinBiochim Biophys Acta. 2016 Dec;1860(12):2793-801. doi: 10.1016/j.bbagen.2016.03.022. Epub 2u r 16 ivr' DDAH1 plays dual roles in PM2.5 induced cell death in A549 cells. Wang H1, Guo Y1, Liu L1, Guan L1, Wang T1, Zhang L1. Wang Y1, Cao J1, Ding W1, Zhang F2, Lu Z3. Author information Abstract BACKGROUND: Dimethylarginine dimethylaminohydrolase 1 (DDAH1) is an enzyme that can degrade asymmetric dimethylarginine (ADMA), an endogenous nitric oxide synthase (NOS) inhibitor. Emerging evidence suggests that alterations in the ADMA-DDAH1 pathway are involved in environmental pollution induced airway inflammation. However. the role of DDAH1 in protection against cytotoxicity of ambient airborne particulate matter is unclear. METHODS: We examined the influence of DDAH1 expression on oxidative stress and cell apoptosis in human type II alveolar epithelial A549 cells exposed to PM2.5 (particulate matter with an aerodynamic diameter less than 2.5µM). RESULTS: We found that PM2.5 exposure for 48h significantly decreased DDAH1 expression. However, knockdown of DDA.H1 prior to PM2.5 exposure actually attenuated the cytotoxicity of PM2.5. Cytoprotection in DDAH1 deficient cells was due to increased reactive oxygen species, activation of PI3K-AKT and mitogen-activated protein kinase (MAPK) pathways, subsequent activation of nuclear factor erythroid-2-related factor 2 (Nrf2) and this caused a subsequent reduction in PM2.5 induced oxidative stress relative to control. DDAH1 depletion also repressed the induction of inducible NOS (iNOS) in PM2.5-exposed cells and knockdown of iNOS protected cells against PM2.5 induced cell death. Interestingly, overexpression of DDAH1 also exerted a protective effect against the cytotoxicity of PM2.5 and this was associated with a reduction in oxidative stress and upregulation of the anti-apoptotic protein Bcl-2. CONCLUSIONS: Our data indicate that DDAH1 plays dual roles in protection against cytotoxicity of PM2.5 exposure. apparently by limiting PM2.5 induced oxidative stress. GENERAL SIGNIFICANCE: Our findings reveal new insights into the role(s) of the DDAH1/ADMA in pulmonary protection against airborne pollutants. This article is part of a https://www.ncbi.nlm.nih.gov/pubmed/26996393 1 1 /6/2017 DDAH1 plays dual roles in PM2.5 induced cell death in A549 cells. - PubMed - NCBI Page 2 of 2 Special Issue entitled Air Pollution, edited by Wenjun Ding, Andrew J. Ghio and Weidong Wu. Copyright © 2016 Elsevier B.V. All rights reserved. KEYWORDS: DDAH1; Nrf2; PM(2.5); ROS; iNOS PMID: D: 26996393 DOI: 10.1016/j.bbagen.2016.03.022 [Indexed for MEDLINE] Publication type, MeSH terms, Substances LinkOut - more resources PubMed Commons PubMed Commons home 0 comments How to join PubMed Commons https://www.ncbi.nlm.nih.gov/pubmed/26996393 11/6/2017 DHEC: Effects on Health, Environment Page 1 of 3 00 South Carolina Department of Health and Environmental Control 0 About Us Health Environment For Business Food Safety Vital Records TAIRSIKPr2-aii4aaapt DHEC > Environmen... > Air... > Most Commo... > Particulat... > Effects On Health, Environment Effects on Health, Environment Concentrations of PM that measure near or above the National Ambient Air Quality Standards can have adverse effects on human health and our environment. Effects on Health PM can have significant impacts on the health of sensitive groups. High PM levels particularly affect children, people with lung disease, and people who are active outdoors. These pollutants are small enough to invade our respiratory system as we breathe in polluted air. They can damage lung tissues when they reach the alveoli, which are the tiny air sacs where we take in oxygen and unload carbon dioxide (see image below). This reduces lung capacity. Particles 10 micrometers in diameter and smaller (also called PM10) pose the greatest problems, because they can get deep into the lungs, and some may even get into the bloodstream. Among these particles are "fine particles," which are 2.5 micrometers in diameter and smaller (also called PM2.5). These fine particles can affect both the lungs and the heart. Children are at risk because their lungs are still developing and because they spend more time outdoors, and the elderly are also sensitive to the harmful effects of PM pollution. However, there is some risk for all of us. Scientific studies have linked breathing PM to serious health problems, including: http://www.scdhec.gov/HomeAndEnvironment/Air/MostCommonPoll utants/ParticulateMa... 11 /6/2017 DHEC: Effects on Health, Environment Page 2 of 3 • Respiratory symptoms, such as irritation of the airways, coughing or difficulty breathing; • Decreased lung function; • Aggravated asthma; • Development of chronic bronchitis; • Irregular heartbeat; • Nonfatal heart attacks; and • Premature death in people with heart or lung disease. Both short and long term exposure to PM, primarily PM2.5, can lead to these health problems. Short term exposure is measured on a daily basis. Effects such as nonfatal heart attacks and premature death are the result of repeated short term exposures, rather than a single instance of exposure to high PM levels. Long term exposure is measured on an annual basis. For more information on the health effects of wildfire smoke, see DHEC's wildfires webpage. Related Topics and Resources • Protect Your Lungs From Wildfire Smoke • Particle Pollution and Your Health (Brochure) • Particle Matter Pollution (Fact Sheet) U.S. EPA Resources • Asthma Information (EPA) • Burnwise - How Fine Particles Can Affect Your Health (EPA) Effects on Environment PM pollution can reduce visibility (haze) and build up in the atmosphere, soils, plants, and animals. http://www.scdhec.gov/HomeAndEnvironment/Air/MostCommonPollutants/ParticulateMa... 11 /6/2017 DHEC: Effects on Health, Environment Page 3 of 3 Visibility Impairment PM pollution is the major cause of reduced visibility (haze) in parts of the United States, including many of our treasured national parks and wilderness areas. The U.S. Environmental Protection Agency Regional Haze program addresses visibility. Pictured to the right is Cape Romain National Wildlife Refuge; hover your cursor over the image to compare visibility on a clear day versus a hazy one. (Images provided courtesy of the U.S. Fish and Wildlife and National Park Service Visibility Programs.) Atmospheric Depostion Particles can be blown by wind over long distances where they then settle on the ground or in water. This settling action is called called deposition. Effects of PM deposition include: • increasing acidity of bodies of water like lakes and streams, • altering the nutrient balance in coastal waters and large river basins, • depleting the nutrients in soil and groundwater, • damaging sensitive forests and farm crops, and • affecting the diversity of ecosystems. Aesthetic Damage Over time, some particulate matter can stain and damage stone and other materials through deposition. This includes culturally important objects like monuments and statues. Aesthetic damage can also be caused by acid rain. About Us Regulations News Releases Calendar Pay Invoices Accessibility, Nondiscrimination, Privacy Request Documents (FOI) Careers Contact © 2017 South Carolina Department of Health and Environmental Control. All Rights Reserved. 2600 Bull Street, Columbia. SC 29201 (803) 898-DHEC (3432) http://www.scdhec.gov/HomeAndEnvironment/Air/MostCommonPollutants/ParticulateMa... 11 /6/2017 D H E C ! Fact Sheet =1, PROMOTE PROTECT PROSPER South Carolina Department of Health and Environmental Control • www.scdhec.gov Particulate Matter What is it? Particulate matter (PM) is made of solid particles and liquid droplets that are in the air. Where does it come from? Particulate matter can come from many places. In general, any type of burning of materials or any dust - generating activities are sources of particulate matter. Here are some examples: • Smoke (from semi -trucks, fireplaces, industrial plant smoke stacks) • Burning wood, diesel, and oil • Swirls of dirt that form when the wind blows • Construction activities Does it come in different sizes? Particulate matter comes in many different sizes. Larger particles come mostly from the soil. Smaller particles come from burning of fossil fuels, like gasoline in cars and coal used by power plants. What are the health effects of breathing in particulate matter? The smaller the particles, the more dangerous they are because they can travel deeper into the lungs. Breathing in particulate matter can cause: • Breathing problems due to damage and irritation to the lungs. • Aggravation of asthma, lung, or heart disease in people who already suffer from these problems. • Difficulty breathing in children and the elderly. • Chronic bronchitis. • Irritation of eyes, throat, skin, and nose. What are the environmental effects of particulate matter? Particulate matter can cause decreased visibility. In the eastern U.S., visibility in some areas has been reduced to 14-24 miles. Natural visibility should be about 90 miles in these areas. The airborne particles can also damage buildings. How can you protect yourself and the environment from particulate matter? • Try to stay away from dust that has recently been stirred up and from smoky areas. • Carpool, walk, or bike whenever possible. • Keep cars well tuned and maintained. • Conserve electricity. For more information, visit: http://www.scdhec.gov/environment/baq/AirPollutants/effects.asp http://www.epa.gov/particles/ DHEC's Bureau of Air Quality, Innovations Section provides information on environmental topics. Readers are encouraged to reproduce this material. For more information about air quality issues, please call (803) 898-4123 or visit our website at www.scdhec.gov/baq. Please send written correspondence to: DHEC's Bureau of Air Quality, Innovations Section, 2600 Bull Street, Columbia, SC 29201. SPARE THE AIR south carolina CR-008070 4/11 Assessment of Irritative Effects of Fumes of Bitumen on the Airways by using Non-Invas... Page 4 of 4 Information-. ! Open access Authors Editors Librarians Societies Help and info Help FAQs Press releases Contact us Commercial services Copyright © 2017 Informa UK Limited conditions Accei_,H>ibility Registered in S Howick Overview Open Journals Open Select Cogent OA Connect with Taylor & Francis OD nokies Terms & http://www.tandfonline.com/doi:Laos. 1 U. i USU/ i 54> 020701 334798 11/7/2017 Page 1 of 1 (dates A Clean Swee lam ad' (Wards] �rill on3 http://www.vecelliogroup.com/images/VanG-2007Q4-layout_Page-1 .jpg 11/7/2017 Page 1 of 1 Table 1. Baseline Characteristics of the Study Participants. Characteristic Female sex — no. (%) Age — yr Mean Range Height — cm Body -mass indext White race — no. (%) 1: FEV, — % of predicted value Atopy — no. (%) Methacholine PC20— mg/mIll Treatment with inhaled corticosteroids — no. (%) Unlimited exercise tolerance — no. (%) Asthma affected by exercise — no. (%) Yes Not sure Asthma affected by traffic fumes — no. (%) Yes Not sure All Participants (N =60) 29 (48) 32 19-55 172±8.8 23.2±3.7 47 (78) 88.9±10.8 42 (84) 2.82±2.47 37 (62) 51 (85) 44 (73) 4 (7) 17 (28) 30 (50) Participants with Mild Asthma (N=31) 14 (45) 31 20-49 172±8.4 23.2±3.6 26 (84) 93.4±6.9 24 (89) 2.73±2.43 12 (39) 28 (90) 20 (65) 3 (10) 7 (23) 19 (61) Participants with Moderate Asthma (N=29) P Value 15 (52) 0.61 34 19-55 171±9.3 23.2±3.9 21 (72) 84.1±12.3 18 (78) 2.92±2.56 25 (86) 23 (79) 24 (83) 1 (3) 10 (34) 11 (38) 0.13 0.67 0.98 0.28 <0.001 0.31 0.78 <0.001 0.23 0.27 0.19 * Plus —minus values are means ±SD. P values are for comparisons according to the severity of asthma. FEV1 denotes forced expiratory volume in 1 second. j The body -mass index is the weight in kilograms divided by the square of the height in meters. Race was self -reported. Ten participants (six with moderate asthma) did not have skin -prick tests. 11 Methacholine PC20 denotes the concentration of methacholine required to provoke a 20% decrease in the FEV1. http://www.nejm.org/na101 /home/literatum/publisher/mms/journals/content/nejm/2007/nej... 11/7/2017 Respiratory Effects of Exposure to Diesel Traffic in Persons with Asthma — NEJM Page 1 of 5 NEJM CASES IN PRIMARY CARE DOWNLOAD NOW > HOME ` ARTICLES & MULTIMEDIA ISSUES SPECIALTIES & TOPICS FOR AUTHORS CME ORIGINAL ARTICLE Respiratory Effects of Exposure to Diesel Traffic in Persons with Asthma James McCreanor, M R.C.P . Paul Cuilinan. M u Mary J Nieuwennuiisen, Ph D . James Stewart -Evans. M Sc , Eleni Malharou. M Sc . Lars Jarup Ph D . Robert Harrington M S Magnus Svartengren, M D In-Kyu Han, M P H.. Pamela Ohman-Strickland, Ph D Kian Fan Chung, M.D . and Junteng hang. Ph 0 N Engl J Med 2007, 3572348-23581 December 6, 2007 DOI 10 1056/NEJMoa071535 Share: Abstract Article References Citing Articles (384) Air pollution from road traffic is a serious health hazard, and particulates from diesel exhaust have become cause for increasing concern Epidemiologic studies have demonstrated associations between ambient particulate matter and respiratory -associated morbidity and mortality; these effects may be greater among persons with preexisting respiratory disease, including asthma.1 2 Diesel engines emit relatively low concentrations of carbon monoxide and carbon dioxide, but as compared with gasoline engines of similar size, diesel engines can generate more than 100 times the number of particles per distance traveled' and are major contributors to atmospheric particulate pollution. In urban environments, almost 90% of traffic -generated particulate matter is from diesel exhaust.4 5 Many urban residents, including those with increased susceptibility to the effects of air pollution, have short-term exposure to diesel traffic during normal activities. Studies of humans in exposure chambers have shown that controlled exposure to diesel exhaust can provoke increased airway resistance° 7 and bronchial inflammatory changes.&t1 Such studies are limited by their artificial nature, however, and the small numbers of study participants have typically been healthy. We explored the effects of roadside traffic exposure on people with mild or moderate asthma, of differing severity, on a busy city street where traffic is entirely diesel -powered. We tested the hypothesis that short-term, ambient exposures to diesel traffic would lead to a reduction in lung function and a worsening of symptoms, accompanied by increased inflammation in the lungs. METHODS Participants Using advertising and volunteer databases, we recruited 60 adults with asthma, none of whom were smokers; 31 had mild asthma and 29 had moderate asthma, as defined by the Global Initiative for Asthma.12 Each participant had intermittent wheezing and airway hyperresponsiveness to methacholine; the concentration of methacholine required to provoke a 20% decrease (PCP) in the forced expiratory volume in 1 second (FEV1) was <8 mg per milliliter. The participants were studied during periods of asthmatic stability, defined by the absence of exacerbations, respiratory infections, and treatment with oral corticosteroids for 4 weeks or more During the study, the participants took their usual asthma medications. The project was approved by the ethics committee at Brompton Hospital, London, and the institutional review board at the Robert Wood Johnson Medical School, New Brunswick, New Jersey. Written informed consent was provided by all participants Study Design In this randomized, crossover study, participants walked for 2 hours (10:30 a.m. to 12:30 p.m.) along the western end of Oxford Street, London's busiest shopping street, where only diesel -powered buses and taxicabs are permitted, or through the traffic -free, western part of the nearby 142 -hectare (about 350 -acre) Hyde Park. Participants walked about 6 km during each exposure, at a steady pace on predefined paths, resting for 15 minutes every half hour Exposure sessions, separated by more than 3 weeks, were confined to weekdays between November and March (2003 to 2005) to avoid pollen seasons: rainy days were also avoided. Equal numbers of participants were randomly Welcome Guest Renew. Subscnbe or Create Account Sign in VTI4� p', i'sgmategi- li Mll4COO. I Keyword, Title, Author, or Citation TOOLS SUBSCRIBE OR RENEW TODAY* POF Print Download Citation Slide Set Supplementary Material QAdvanced Search E -Mad Save Article Alert Repnnts Permissions Snare/Bookmark RELATED ARTICLES EDITORIAL Health Effects of Airborne Particulate Matter December 6. 2007 M Lippmann TOPICS Asthma Pulmonary/Critical Care MORE IN Research December 6, 2007 k :: cejkcr ■.. porch .. VIEW THE LATEST SALARY FIGURES IN YOUR SPECIALTY TRENDS Most Viewed (Last Week) ORIGINAL ARTICLE MGMT Gene Silencing and Benefit from Temozolomide in Glioblastoma [52.054 views] March 10. 2005 I M E Hegi and Others ORIGINAL ARTICLE PCI Strategies in Patients with Acute Myocardial Infarction and Cardiogenic Shock (31,954 views] October 30. 2017 I H Thiele and Others IMAGES IN CLINICAL MEDICINE HIV Infection Manifesting as Proximal White Onychomycosis [22,963 views] November 2, 2017 1 E. G0mez-Moyano and V Crespo-Erchiga More Trends http://www.nejm.org/doi/full/10.1056/NEJMoa071535 11/7/2017 Respiratory Effects of Exposure to Diesel Traffic in Persons with Asthma — NEJM Page 2 of 5 assigned to each exposure sequence. The study had an estimated 90% power to detect a minimum difference in FEVI response of 5.7% in each asthma -severity group between the two sites. Clinical Measurements Participants measured their peak expiratory flow on a mini —Wright meter and recorded asthma symptoms 1 week before and after each exposure session; during the week before each exposure, they wore a diffusion tube to measure individual exposure to nitrogen dioxide throughout the week. At Royal Brompton Hospital, baseline measurements of FEV1, forced vital capacity (FVC), and forced expiratory flow at 25 to 75% of vital capacity (FEF25_,5) were performed with the use of a spirometer (Vitalograph); the fraction of exhaled nitric oxide (FeNo) was recorded with the use of a chemiluminescence analyzer (Aerocrine). Exhaled breath condensate from tidal breathing was obtained with the use of a standardized breath -condensate collector (ECoScreen, Jaeger), and its pH was measured after de -aeration with argon. Participants were driven for approximately 10 minutes to the exposure sites in a gasoline -powered car. On arrival and hourly during each session, we made further spirometric measurements; on completion of each session, we asked participants to record any asthmatic symptoms. After returning to the hospital, we repeated spirometric and FeNo measurements regularly for 5 hours and measured responsiveness to methacholine; participants recorded any asthma symptoms over the ensuing 12 hours. The next morning, we repeated measurements of lung function and FeNo and collected samples of sputum induced by inhalation of a 3% sodium chloride solution from an ultrasonic nebulizer. Total cell counts were performed on a homogenized sputum sample with the use of 0.1% dithiothreitol, and differential cell counts were performed on 400 nonsquamous cells on cytospin slides. Supernatants were kept at -80`C for analysis of interleukin-8, myeloperoxidase, and eosinophil cationic protein with the use of commercially available immunoassay kits (IL -8 DuoSet, R&D Systems; and TiterZyme and UniCAP, Pharmacia Diagnostics AB; respectively). Exposure Measurements Throughout each exposure session, we measured number concentrations of ultrafine particles, using a real-time condensation particle counter (Model 3007, JSI) equipped with a ribbon laser light - scattering optical system (range, 0 to 100,000 particles per cubic centimeter; accuracy, ±20%). We collected fine particles smaller than 2.5 pm in aerodynamic diameter (PM25) on quartz -fiber filters, using an air sampler (16 liters per minute) The filters were used first to determine PM25 mass concentration gravimetrically and were then analyzed for elemental carbon according to National Institute for Occupational Safety and Health guidelines (method 5040) (Sunset Laboratory). With a sampling pump, we collected nitrogen dioxide on C18 Sep -Pak cartridges coated with potassium hydroxide and triethanolamine and subsequently analyzed the sample using ion chromatography.13 Temperature and relative humidity sensors, along with all air monitors, were located on a pushcart beside the participants. Statistical Analysis Descriptive summaries of exposure and health outcomes included means (±SD) for normally distributed variables and medians with ranges for other variables. Correlations between pollutants were examined. Associations between exposure and health outcomes were examined through comparative analysis (Oxford Street vs. Hyde Park) and pollutant -specific. exposure -response analyses. A repeated - measures, mixed -effects linear regression model was constructed to estimate average values for health outcomes, with the use of an interaction term for the categorical variables of site and time to examine the effect of the exposure site on changes in lung -function or inflammatory biomarkers.14 A random effect for individual participants accounted for similarities across sessions for each person. A spatial -power covariance structure was used to model correlations between the unequally spaced repeated measurements within each session with a decay in the strength of correlation, depending on the time between measurements. With the use of the Akaike information criterion, this structure proved to model the data adequately relative to an unstructured correlation matrix. Additional covariates, including temperature and relative humidity and, where necessary, age, sex, body -mass index, and race or ethnic group were entered as covariates. Type 3 F tests of the site —time interaction produced P values representing the overall significance of the effect of site on changes in responses over time; contrasts of means were used to examine differences between sites in changes from baseline to particular time points. To study potential effect modifiers, we tested interactions between them and site —time interaction and conducted stratified analyses. Because pollutant concentrations varied within and between sites, we performed pollutant -specific, exposure -response analyses using mixed models, as described above. In these models, we regressed the percent change from baseline in each of the lung -function and inflammatory- biomarker variables against pollutant concentrations averaged over each exposure session. Separate, single -pollutant models for PM25, elemental carbon, ultrafine particles, and nitrogen dioxide were generated. Subsequently, we used two -pollutant models, in which two of the four pollutants were analyzed simultaneously. RESULTS CareerCenter PHYSICIAN JOBS Novemoer 7, 2017 Primary Care Primary Care LOMPOC Cardiology NON INVASIVE CARDOLOGIST - GEISINGER - LEWISTOWN HOSPITAL PORT MATILDA Critical Caro Medicine Interventional Pulmonary - Murray, LIT - Intermountain Medical Center UTAH Chiefs / Directors / Dept. Meads DIRECTOR PEDIATRIC ENDOCRINOLOGY DANVILLE Pediatrics, General Pediatric Surgeon - Major New York Teaching Hospital STATEN ISLAND Primary Care Primary Care Physician - State College, Pa. STATE COLLEGE nejmcareercenter.org Sign up for FREE Alerts and Updates (REIM Catalyst FREE ARTICLE COLLECTION Physician Burnout: The Root of the Problem and the Path to Solutions > DOWNLOAD NOW Catalyst MestaA sa 'I- p a an/ PS MYIMr• http://www.nejm.org/doi/ful1/10.1056/NEJMoa071535 11/7/2017 Respiratory Effects of Exposure to Diesel Traffic in Persons with Asthma — NEJM Page 3 of 5 As anticipated, participants with mild asthma had a higher baseline FEV, than those with moderate asthma. They were also less likely to report limited exercise tolerance or symptoms provoked by exercise or traffic fumes (Table 1). TABLE 1 Median weekly nitrogen dioxide exposures were not significantly different before exposure at the two sites (Table 2). Participants had significantly higher exposures to PM?5, ultrafine particles. elemental carbon, and nitrogen dioxide on Oxford Street than in Hyde Park. Spearman's rank -correlation coefficients for exposures to the four pollutants were as follows: 0.58 for the correlation of nitrogen dioxide with both ultrafine particles and elemental carbon, 0.62 for the correlation of PM25 with ultrafine particles. and 0.84 for the correlation of ultrafine particles with elemental carbon. (Complete information is provided in Table Al of the Supplementary Appendix, available with the full text of this article at www.nejm.org.) Average daily peak expiratory flow, symptoms. and use of asthma medication did not differ significantly in the week before exposures at the two sites. Similarly, there were no significant differences between the sites in mean FEV,, FVC, or FEF?5_,5 at baseline in the hospital or on arrival at the site (Table 2). On the whole, changes over time in mean FEV, and FVC differed significantly between the sites (P=0.04 and P=0.01, respectively), but there were no significant differences between sites in the changes in FEF25 _75. Mean FEV, (percent of the predicted value) was lower after 1 hour of exposure at both sites. The subsequent decrement was greater and more sustained for Oxford Street, with a maximal decline at 2 hours (-6.1%, vs. -1.9% for Hyde Park; P<0.001). The differences between sites remained significant at every time point (P<0.05) until 22 hours after exposure. Among participants with moderate asthma, the decline in FEV, was greater for Oxford Street than for Hyde Park, but the difference was not significant. Baseline Characteristics of the Study Participants. TABLE 2 The pattern for mean FVC (percent of predicted value) was similar (Figure 1), with a maximum drop after 2 hours (-5.4% for Oxford Street vs. -1.6% for Hyde Park, P<0.005). The differences in changes in FVC between the two sites were significant at each time point between 2 and 5 hours after the start of exposure (P<0.05) and were significantly greater among participants with moderate asthma than among those with mild asthma (P=0 008). There were no significant differences in the mean change in FEF:5_75 (percent of predicted value) between sites or in the methacholine PC20 value 5 hours after exposure. Changes in respiratory symptoms during and after exposures were small. Participants with mild asthma reported more symptoms after exposures on Oxford Street (both immediately afterward and 5 hours afterward) than after exposures in Hyde Park, but the differences were not significant. The use of treatments for asthma relief over the 7 -day period after exposure did not differ significantly between the two sites. Exposure Measurements for Oxford Street and Hyde Park and Lung Function before Exposure. FIGURE 1 Mean Percent Changes in FEV, and FVC during and after Exposure on Oxford Street and in Hyde Park. There were no significant differences in the changes in mean Few, between exposures on Oxford Street and those in Hyde Park There were greater decreases in the pH of exhaled breath condensate after exposure on Oxford Street — 1.16%. as compared with 0.88% in Hyde Park at 3 hours, and -1.90% as compared with 0.04% in Hyde Park at 6 hours (Figure 2). The changes were not significantly greater among participants with moderate asthma. FIGURE 2 The sputum myeloperoxidase concentration at 24 hours was higher after exposure on Oxford Street (24.5 ng per milliliter) than after exposure in Hyde Park (4.2 ng per milliliter, P=0.01) (Figure 2). Sputum neutrophil counts and interleukin-8 concentrations were strongly correlated with myeloperoxidase (P<0.001 for both comparisons), and each was higher after Oxford Street exposures; only in the case of sputum neutrophil counts (for all participants), however, was this difference significant. There were no significant differences in sputum eosinophil counts or eosinophil cationic protein levels. We found no consistent evidence of an interaction between these health outcomes and the other variables listed in Table 1 (and Table A2 in the Supplementary Appendix). Reductions in FEV,, FVC. FEF25_75, and exhaled breath condensate pH were associated with ultrafine-particle exposures at most time points (Figure 3); these reductions were also associated, although less consistently, with elemental carbon exposures (for ultrafine particles, P=0 02, P=0.27, P=0.11, and P=0.03, respectively; for elemental carbon. P=0.04. P=0.11, P=0.32, and P=0.24, respectively). Elemental carbon exposures were also associated with increases in FeNo concentrations (P=0 06) For nitrogen dioxide, the associations were similar but less pronounced: for PM25, there were no consistent associations. Increased sputum myeloperoxidase concentrations Mean Changes in Exhaled Breath Condensate pH, Sputum Neutrophil Counts, Supernatant Interteukin-8, and Supematant Myeloperoxidase before and after Exposure on Oxford Street and in Hyde Park FIGURE 3 http://www.nejm.org/doi/full/10.1056/NEJMoa071535 11/7/2017 Respiratory Effects of Exposure to Diesel Traffic in Persons with Asthma — NEJM Page 4 of 5 were associated with ultrafine-particle exposure (P=0.03). There were no associations between sputum cell counts or interleukin-8 and any of the pollutant constituents. After adjustment for copollutants in the two -pollutant models, the effects of ultrafine particles and elemental carbon remained the most consistent and were significant (Table A3 in the Supplementary Appendix). Point Estimates and 95% CI of the Percent Change in Health End Points per Incremental Change in Pollutant Components. DISCUSSION We examined the functional and inflammatory effects on asthma of real -life exposure to roadside diesel traffic. In adults with asthma, walking for 2 hours at a leisurely pace along a street where only diesel -powered vehicles were permitted resulted in a significant but essentially asymptomatic reduction in lung function. Although the changes were small, they were greater than those provoked by walking in a nearby park and were more pronounced among study participants whose asthma was more severe. These changes were accompanied by inflammatory changes in sputum and exhaled breath condensate The inflammatory response was predominantly neutrophilic, with raised levels of myeloperoxidase and interleukin-8 in sputum supernatants; we did not detect, even in participants with more severe asthma, an eosinophilic response characteristic of asthmatic inflammation. In association with the drop in FEV,, we found a twofold increase in exhaled -breath -condensate hydrogen ions after exposure on Oxford Street. Acute asthma may be accompanied by airway acidification, with an increase in hydrogen ions by a factor of more than 100,15 perhaps reflecting inhibition of local epithelial proton pumps dunng airway inflammation.'° Thus, intracellular acidosis related to the inflammatory process may be reflected in reduced airway pH.17 It has been suggested that any harmful respiratory effects of acute exposure to diesel exhaust are attributable more to its particulate content than to its gaseous content.18 In addition to coarse particles (2.5 to 10 pm in diameter), diesel exhaust contains, in far greater numbers, ultrafine particles (<0.1 pm in diameter). In our study the most consistent relationships between changes in respiratory variables and specific pollutant concentrations were for ultrafine particles and elemental carbon, a finding consistent with growing evidence that the adverse respiratory effects of diesel - generated particles are attributable to those in the very small size range.1a-23 With their higher ratio of surface area to mass, ultrafine particles can adsorb greater fractions of potentially toxic substances onto their surface, and they are deposited more deeply and in greater numbers within the lung than are larger particles. Furthermore. the carbon core of elemental carbon particles is highly adsorptive.24 Differences in the concentrations of ultrafine particles and elemental carbon between Oxford Street and Hyde Park were substantially larger than the differences in concentration between PM25 and particles less than 10 pm in diameter. However, our findings cannot be taken as a demonstration of a causal association with ultrafine particles and elemental carbon, since these may simply be a sensitive proxy for the entirety of a roadside diesel -traffic exposure, which is composed not only of the complex diesel exhaust mixture but also of resuspended coarse, thoracic particles (small enough to enter the thorax) from road dust and engine or tire debris, which we did not measure. Previous studies of the direct effects of diesel exnaust on asthma in humans have been conducted under laboratory conditions, with fresh diesel fumesfrom which gaseous constituents may have been removed ("scrubbed"), or reconstituted diesel exhaust material delivered to subjects in an exposure chamber.6 7 11.25-27 The findings of these studies have not been entirely consistent, and none of them have demonstrated an effect on spirometric lung function, despite the use of much higher concentrations of diesel particles than those we measured on Oxford Street. The discrepancies between the findings of other studies and our own may be due to the complexity of the natural pollutant mixture we studied, with interactions between particulates and other pollutants, or to the possibility that reconstituted or scrubbed diesel exhaust mixtures substantially reduce the proportion of ultrafine particles. In addition, we studied people with more severe asthma. Svartengren et al.,28 in a realistic study of brief exposure to traffic pollution in a road tunnel, also failed to find any effect on FEV, but reported more symptoms than we observed. Personal exposures to PM25 and nitrogen dioxide were much higher in that study, but the study participants had milder asthma than did the participants in our study. On the other hand, the inflammatory responses we observed, particularly the increase in sputum neutrophils and myeloperoxidase, were similar in nature to those in studies of controlled, chamber exposures.8.1o,26.28 Our primary motive was to understand the effects of typical exposures to an urban atmosphere dominated by diesel exhaust. To this end, we selected a setting where only diesel traffic was allowed and used a randomized, crossover design limited to the winter months to avoid confounding exposure to pollens, thereby removing or controlling for most important confounding factors. Nonetheless, we recognize some limitations of our study, including the impossibility of blinding participants and the inability to exclude the possibility of subjective responses, particularly with symptom reporting. However, the internal consistency of our findings and the changes in variables over which the participants had no control make it very improbable that our results arose entirely from a subjective bias. Another difficulty arises from potentially confounding exposures that we did not measure. For example. a walk on Oxford Street is likely to be a more stressful experience than a walk in a quiet park, and it is possible that some of the responses we measured were induced by factors associated with stress, particularly noise 29 In addition, because we did not study a reference http://www.nejm.org/doi/ful1/10.1056/N EJMoa07153 5 11/7/2017 Respiratory Effects of Exposure to Diesel Traffic in Persons with Asthma — NEJM Page 5 of 5 group of people without asthma, we cannot be sure that our findings are specific to people with asthma, although the more pronounced responses in the participants with more severe disease suggest that the findings are specific. Finally, we did not study exposure to gasoline -powered traffic and therefore cannot conclude that diesel traffic is more toxic than other types. Our observations serve as a direct demonstration and explanation of the epidemiologic evidence that associates exposure to diesel traffic with the severity of asthma and of the symptoms that many patients with asthma report after exposure to diesel exhaust. The changes in our primary end point (FEV1) were small and unaccompanied by clinically significant symptoms but would be more important in patients with more compromised lung function Without further study, however, we do not believe that these findings should deter most patients with asthma from visiting or working in busy urban environments. Our design has considerable advantages over orthodox chamber studies and could readily be adapted to assess therapeutic strategies in the prophylaxis of traffic responses in asthma or other cardiorespiratory diseases. Supported by the Health Effects Institute through a Research Agreement (02-9) with the University of Medicine and Dentistry of New Jersey Dr. Cullinan reports serving as a member of the Expert Advisory Panel for Air Quality Standards for the U.K. government. Dr Chung reports receiving advisory -board fees from Astra-Zeneca, GlaxoSmithkline, Novartis, Merck, and Mundi-Pharma, consulting fees from Gilead. and research support from GlaxoSmithKline. No other potential conflicts of interest relevant to this article were reported. We thank the volunteers who took part in this study. Sally Meah for her help with recruitment and clinical measurements at Royal Brompton Hospital, and Frank Speizer and Terry Tetley for helpful advice. SOURCE INFORMATION From the National Heart and Lung institute. Imperial College, and Royal Brompton Hospital (J.M., P.C., K.F C.) and the Department of Epidemiology and Public Health. Imperial College (J.S.-E., E M., L.J.) — all in London, the Center for Research in Environmental Epidemiology, Barcelona (M.J N ); the University of Medicine and Dentistry of New Jersey School of Public Health. Piscataway (R H. I -K H., P O -S . J.Z ); and the Department of Public Health Sciences, Karolinska Institutet, Stockholm (M S.). Address reprint requests to Dr. Cullman at the Department of Occupauonal and Environmental Medicine. National Heart and Lung Institute. lb Manresa Rd., London SW3 SLR. United Kingdom, oratp.cullinan@impenalac.uk. CONTENT: Home I Current Issue I Articles 1 Issue Index I Specialties & Topics I Multimedia & Images I Archive 1812-1989 INFORMATION FOR: Authors I Reviewers I Subscribers I Institutions I Media I Advertisers I Agents SERVICES: Subscribe 1 Renew I Pay Bill I Activate Subscription I Create or Manage Account I Alerts I RSS & Podcasts I Submit a Manuscript I Mobile RESOURCES: Physician Jobs I Reprints 1 Conventions ► NEJM Knowledge+ I NEJM Journal Watch I NEJM Catalyst 1 NEJM Resident 360 I NEJM Yi Xue Qian Van I NEJM Group NEJM: About I Product Information 1 Editors & Publishers 1200th Anniversary 1 Terms of Use 1 Privacy Policy I Copyright I Permissions I Advertising Policies I FAQs I Help I Contact Us CME: Weekly CME Program I Browse Weekly Exams I Your CME Activity I Purchase Exams I Review CME Program Earn CME Credits » Over 300eiams available A Follow us In O Tim Tube ._.opyngta *2017 Massachusetts Medical Society. All rights reserved @EJM http://www.nejm.org/doi/full/10.1056/NEJMoa071535 11/7/2017 is State Water Resources Control Board Division of Water Quality GAMA Program GROUNDWATER INFORMATION SHEET Benzene The purpose of this groundwater information sheet is to provide general information regarding a specific constituent of concern (COC). The information provided herein relates to wells (groundwater sources) used for public drinking water, not water served at the tap. GENERAL INFORMATION Constituent of Concern Benzene Aliases Annulene, Benzole, Phene, Phenyl hydride, Pyrobenzole. Cyclohexatriene Chemical Formula C5H6 CAS No. 71-43-2 Storet No. 34030 Summary Benzene is a regulated chemical with an established California State Maximum Contaminant Level (MCL) in drinking water of 1 pg/L. Benzene is a colorless highly flammable liquid that evaporates quickly into air and dissolves slightly in water. It is found in crude oil and gasoline. but also occurs naturally in volcanic gases and smoke resulting from forest fires. Benzene is a known carcinogen both in humans and in laboratory animals. Based on SWRCB data from 2007 to 2017, 8 active and standby public water supply wells (of 8,997 tested) had at least one detection of benzene above the MCL. Revised November 2017 1 ♦ State Water Resources Control Board Division of Water Quality GAMA Program REGULATORY AND WATER QUALITY LEVELS' Type Agency Concentration Federal MCL US EPA2 5 pg/L California State MCL SWRCB3 1 pg/L Detection Limit for Purposes of Reporting (DLR) SWRCB3 0.5 pg/L Others: CA Public Health Goal (PHG) Cancer Potency Factor (1/106 cancer risk) OEHHA4 OEHHA 0.15 pg/L 0.35 pg/L 'These levels generally relate to drinking water; other water quality levels may exist. For further information, see A Compilation of Water Quality Goals. 17th Edition (SWRCB. 2016). 2 US EPA — United States Environmental Protection Agency 3SWRCB - State Water Resources Control Board 4OEHHA — Office of Environmental Health Hazard Assessment SUMMARY OF DETECTIONS IN PUBLIC WATER WELLS 5 Detection Type Number of Groundwater Sources Number of active and standby public water wells with benzene concentrations6 > 1 pg/L 8 of 8,997 wells tested. County with most detections of benzene in active and standby public water wells with concentrations >1 pg/L King County (2 wells), and one well from each of the following counties: Fresno, Kern, Los Angeles, San Bernardino. San Joaquin. Sonoma. and Yuba. Based on 2007-2017 public standby ana active well (groundwater sources) data collected by the SWRCB. 6 Groundwater from active and standby wells is typically treated to prevent exposure to chemical concentrations above the MCL. Data from private domestic wells and wells with less than 15 service connections are not available. Revised November 2017 2 State Water Resources Control Board Division of Water Quality GA MA Program ANALYTICAL INFORMATION Method Detection Limit Note US EPA 502.2 0.01 pg/L Gas chromatography with photoionization and electrolytic conductivity detectors. US EPA 8260/524.2 0.04 µg/L Gas chromatography/mass spectrometry. US EPA Method 8260 is used at Leaking Underground Fuel Tank (LUFT) sites US EPA 8020 " 2 Jq/L Gas chromatography with photo -ionization detector Known Limitations to Analytical Methods US EPA Method 8020 can detect benzene but may yield false positives when other volatile organic compounds are present and co -elute in the same chromatographic range. The presence of benzene should be confirmed by US EPA Method 524.2 or Method 8260 prior to use of Method 8020 for a long-term monitoring program. Public Drinking Water Testing Requirements Benzene is a regulated chemical for drinking water sources, with monitoring and compliance requirements (Title 22. Section 64431. et seq.). OCCURRENCE Anthropogenic Sources Benzene is a naturally occurring chemical found mostly in crude oil and gasoline. Benzene in unleaded gasoline is typically around 1 percent of the total volume By 2007, the worldwide annual demand for benzene was approximately 40 million tons. Most of it is used to produce styrene and cumene; chemicals used in the manufacturing of plastics, resins, adhesives and nylon. It is estimated that approximately 6 million tons of benzene was used annually in the USA in the 1990s. Benzene can be released to groundwater from leaking underground fuel storage tanks and piping, atmospheric depos Lion, fuel spills during transportation, and leaks at refineries. Underground storage tanks or piping releases make up the majority of the releases that have impacted groundwater. Studies have shown that atmospheric deposition of benzene Revised November 20 1 State Water Resources Control Board Division of Water Quality GAMA Program results only in trace concentrations in surface waters. In contrast, point sources of benzene contamination such as underground storage tank sites may result in benzene concentrations in the milligrams per liter (mg/L) range. Natural Sources Benzene occurs naturally in the environment as a product of incomplete combustion of carbon -rich materials. Benzene is also present in petroleum oil deposits and in gases associated with volcanic eruptions and forest fires. History of Occurrence Benzene replaced lead as a gasoline additive for its anti -knock properties. Concerns about negative health effects related to air quality led to the limitation of benzene content in gasoline to about 1 percent. US EPA regulations had further lowered the benzene content to 0.62 percent in 2011. Based on a SWRCB data query in October 2017 using GeoTracker GAMA, 26 active and standby public water wells out of approximately 10.000 sampled had benzene detections above the State MCL at least once since 1984. The maximum measured concentration was 180 µg/L. Contaminant Transport Benzene can volatilize into air from soil and water. Once in the Characteristics atmosphere, benzene breaks down (biodegrades) within a few days. in soil and groundwater; the biodegradation process is slower. Benzene is slightly soluble in water and can migrate �'-.rough the soil column into groundwater. Because benzene is a tight non -aqueous phase liquid (LNAPL) it can collect on top of the water table. Benzene biodegradation in groundwater can take days to years, depending on oxygen concentration, temperature, and the presence of favorable bacteria. Revised November 2017 State Water Resources Control Board Division of Water Quality GAMA Program REMEDIATION & TREATMENT TECHNOLOGIES Several effective remediation technologies remove benzene and other gasoline compounds from soil and groundwater. These include: Soil Vapor Extractor. ,,'SVIE) — Effective in reducing benzene in the unsaturated zone due to the high vapor pressure. Air Sparging — Used in conjunction with soil vapor extraction. This can also oxygenate the groundwater and stimulate biodegradation of dissolved contaminants. In -situ Oxidation — Relies on the capacity of certain chemicals (e.g. hydrogen peroxide combined with iron) to rapidly oxidize organic molecules in water. Bioremediation — Most effective under aerobic conditions. Flushing (Pump and Treat) — Extracts contaminated groundwater and treats at the surface using air stripping, activated carbon, or advanced oxidation systems. For drinking water, the most common treatment options are air stripping, activated carbon filters. and advanced oxidation (combinations of ultraviolet light. chemical oxidants. and catalysts). There are other emerging technologies for the remediation and treatment of benzene and gasoline compounds including permeable reactive barriers and thermal treatment. HEALTH EFFECT INFORMATION Exposure to benzene can occur through the lungs (inhalation), gastrointestinal tract (ingestion), and through skin (dermal contact). Health effects depend on two main factors: length of exposure and concentration (amount of benzene a person is exposed to). Brief exposure to very high levels of benzene in air can result in death, while breathing lower levels can cause drowsiness confusion, dizziness, headaches, tremors and unconsciousness. The major effect of benzene exposure is to the blood. Long term exposure to benzene can affect the body's ability to produce red blood cells. When the bone marrow is affected, the result is usually a form of leukemia. It can also cause blood (hematologic) diseases. anemia. and cancers of blood -forming organs. The most common long-term health effects associated with benzene exposure are: • Acute Myelogenous Leukemia (AML) in which cancer cells are present in the blood and bone marrow. • Acute Lymphocytic Leukemia (ALL) in which the cancer affects the cells that make the lymphocytes for the bone marrow. • Chronic Myelogenous Leukemia (CML) in which the leukemia develops from the white blood cells reducing the body's ability to fight disease and infection. Revised November 2017 State Water Resources Control Board Division of Water Quality GAMA Program KEY REFERENCES 1. 2. 3. 4. 5. 6. California State Water Resources Control Board, A Compilation of Water Quality Goals, 17th Edition (SVVRCB, 2016). http://www.waterboards.ca.gov/water issues/programs/water quality goals/index.sht ml Office of Environmental Health Hazard Assessment -California Environmental Protection Agency Public Health Goal for BENZENE In Drinking Water https://oehha.ca.gov/media/downloads/water/chemicals/phq/benzenefinphq 0.pdf State Water Resources Control Board. California Drinking Water -Related Laws http://www.waterhoards.oa.gov/drinkinq water/certlic/drinkinqwater/Lawbook.shtml State Water Resources Control Board. GeoTracker GAMA Online Database http://www.waterboaras.ca.gov/water issues/proqrams/gama/qeotracker gama.shtml US Environmental Protection Agency, Technologies-Remediation, http://www.clu- in.org/remediation/ US Environmental Protection Agency. 2012. Water, Benzene Health Advisory, https://nepis.epa.gov/Exe/ZyPDF.cgi/P100N01 H.PDF?Dockey=P100N01 H.PDF Revised November 2017 State Water Resources Control Board Division of Water Quality GAMA Program • 6 S. r k • Water Boards t • if 33 93 •r Active and Standby Division of Drinking Water Wells 2007-2017 Benzene • > 1 µg/L (CA MCL) (8) All Sampled Wells (8,997) Regional Board Boundaries County Boundaries ..,....; I.- Y 1••' ytaP... Cana by Os State WS bard September 2017 i i:E D`:orme. Npm1vda C 0cetSann'n Active and standby public drinking water wells that had at least one detection of benzene above the MCL, 2007-2017, 8 wells. (Source: Public well data in GeoTracker GAMA) Revised November 2017 In accordance to the Commissioner's request that the public state only facts, I bring the following forward: FACT: Given the impact that a permanent facility like this will have to the community, beyond the Cactus Hill properties that flank the facility on 3 of the 4 sides of the operation, the community was ill- informed and given very little time to respond. This is evidenced by the fact that when word finally did get out a few days prior to the scheduled final hearing, the county began receiving letters and numerous citizens showed up at the Oct 25th Meeting. Response continued to build as Simons/Tetra Tech at the request of the commissioners sent out invites to those within a mile of the site to its first and what appears to be its final meeting with the community. The 12 days at best that public was given is not enough to time for an organized, fact filled, evidence based response. We would have appreciated having the luxury of time that Tetra Tech in preparing its 260+ document so that we could provide statements from our experts, gather fact based evidence and perform our own site analysis. Twelve days is not enough time especially considering this is not our actual job. FACT: The community was under the impression that the facility was temporary while hwy 85 was being resurfaced. Many when ask compared the concept to what we witnessed a couple years ago when a batch operation came in for construction on Hwy 14. They came in, did the job and left! Do not hold us at fault that we did not call to voice concerns nor pass judgement because we did not file complaints. We tolerating an operation that was supposed to come in, do the job and leave. I seriously doubt there is anyone in this room that has hasn't tolerated something and remained silent because they knew that it was temporary. FACT: The majority of those who have come before you to voice their disapproval for this operation reside in unincorporated Weld County.tWe voted you the commissioners in to represent our interests - our economic interests, our health and safety and our well being. You are all we have. .� V- lufs C,' O.Ar7c,\l ,'J iA.J r-tvrltr orc'Aft � �� ,J nRfl �e,4 r Ai 7! !7c.ik m101/4 -267 - FACT: Our site analysis if given the time t conduct would have contained the following criteria — away 1��'` wi'1 ► S St^4 compatible from irrigation laterals, areas compatib�ith similar operations (aka Industrial), enough real estate to allow adequate berming, landscaping and barrier walls. Costs and convenience would have been a consideration but certainly NOT the driving factor shown in Tetra Tec/Simons analysis. FACT: Research overwhelmingly states that PM 2.5 is hazard to our health. Tetra Tec's hired scientist 11 -f\.4V V 7 can state all he wants about the toxins and r Asphalt Rep who swooped in from Elbert County to market the joys of living near an asphalt plant cannot deny the hazard PM 2.5 imposes on our community. If we had been afforded the time, our 260+ document would have had an entire section devoted to this concern. Enforcing the control of this hazardous dust and other particulates is the responsibility of Weld County. Do you really have the bandwidth to enforce this and protect the health of our residential and agricultural community? FACT: Lawn mowers are loud! And guess what also can cause hearing loss when exposed for 8 hours or more and would have occupied another section of our document. Imagine listening to that on a summer night, laying in bed with your windows open (if you dare to risk the PM 2.5 hazard). No current resident or future one wants to listen to that 24/7! EXHIBIT C IV 05k i 7-_cjctt 3 So these are just a few of the facts that I have been given time to present. However, if you chose to continue to push forward this ill-conceived and ill- planned operation that , then for the record we want the operation to abide by the following restrictions: Make no mistake this is by no means an endorsement for this project and if it comes to fuition as proposed, it will be a black mark on Weld County. There is not a resident who came forward who does not feel that they were left in the dark, duped and/or forgotten. For the record: The operation be regulated at the residential area decibel limits stated by our laws. This is to protect current and future residents .37,-;," 5 4.1,--y-7 J7 tk ou- a e\ fa i.f4*dt mil A complete landscaping, berming and barrier design be incorporated into the plans. What was proposed is nominal at best. Precedent with the DCP operation indicates that we the citizens, the community deserve to this eye sore and hazardous operation mitigated to the fullest extent. And despite the narrow L, I' 1 / 'r • h -► iS s9 t/ - , i/&JcaC fci eiktiVnq l:' eL In the event of accident on hwy 257 and/hwy 14, truck traffic to the operation is NOT routed to through the CR80.5, 19, 80, 21 or 78. Abide byWater Supply and Storage opinion that Residents are provided updated list of the appropriate contacts and numbers to register violations and complaints. Rest assured the community will no longer be silent. Hello