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Home My WebLink About20162648.tiffCLR-34 Neighborhoods Assn. July 26, 2016 Ms. Julie Cozad Weld County Board of Commissioners 1150 O St Greeley, CO 80632 Dear Commissioner Cozad: RECEIVED AUG 1 0 2016 WELD COUNTY COMMISSIONERS As you are aware, the CLR-34 Neighborhoods Assn. is a non-profit organization that represents the interests of the larger community that surrounds the proposed Martin Marietta Materials (11./IMM) "Highway 34 Project". This includes both sections of Indianhead Estates, Coyote Ridge and Lakota Lakes as well as the individual homes and businesses located along WCR 13 and WCR 56. One of our responsibilities is to educate and represent this group of several hundred residents regarding the impacts of the changing land use in this area, and especially their health, safety and welfare. As such, we wish to take the strongest possible exception to the description of the dust -related complaints that Mr. Phil Brewer expressed in the attached letter to Mr. Ken Houlden at CDPHE. This is an example of Mr. Brewer's consistent hostility to the residents who will be adjacent to the MMM aggregate distribution and processing facility. The condescending attitude expressed and the complete misrepresentation of the facts of the complaints leave us deeply concerned that the County has no intention to protect our health, safety and welfare or to enforce the County and State regulations that will apply to this facility. Mr. Brewer's assertion that there was no violation is misleading at best, and in reality, completely misrepresents the facts. Mr. Brewer neglects to acknowledge that the complaints were called in on July 7, 2016, but representatives of the County did not visit the site until 2PM the next day, by which time MMM had started to do dust suppression using water trucks that suddenly appeared. However, at the time of the complaints, MMM was doing no dust suppression, and in fact, we found considerable evidence that the MMM site was in violation of the requirements of the GP -03. In particular, we documented visible clouds of dust crossing the property line, which is explicitly a violation according to section II.B.1.a(i) of that permit: II.B.1.a. THE FOLLOWING PARTICULATE EMISSIONS CONTROL MEASURES SHALL BE USED FOR ENFORCEMENT PURPOSES ON THE SOURCES COVERED BY THIS PERMIT, AS REQUIRED BY THE AIR QUALITY CONTROL COMMISSION REGULATION NO 1. THIS SOURCE IS SUBJECT TO THE FOLLOWING EMISSION GUIDELINES: COArvivelown t c a..}-; a n s s-/(5/ I(o ce. cca.C Se)), PL. (-re) HL, CP(3) 9-/13/QO Cn 2016-2648 1/4 && 00-13 CLR-34 Neighborhoods Assn. II.B.1,a,(i) All Activities - Visible emissions not to exceed 20%, no off -property transport of visible emissions. In addition, we have photographic evidence that the "opacity" standard was likely violated, as per the same section of the GP03. Since July 7, we have continued to observe considerable fugitive dust at the site, although additional complaints have not yet been filed. On some days, a reasonable effort at fugitive dust suppression through watering has been done. Contrary to Mr. Brewer's implication that our concerns are based on "heresay" [sic], "fear", "misinformation", and "Nimby", we have gone to some lengths to make sure that our complaints are valid, whether regarding dust or any other environmental impact. We have reviewed and understand the GP03 permit requirements, and intend to judge MMM's activities based only on those criteria. The tone of Mr. Brewer's letter is condescending and apparently intended to communicate to Mr. Houlden, the CDPHE Permit Engineer, that by going through the motions of accepting public input, our concerns can then be ignored. Particularly telling is the following comment: "Every possible environmental deviation or subtle insult to the clarity of the air or the health of the area is going to be reported to us," The suggestion seems to be that this is an annoyance at best and inappropriate or a waste of his time at the least. What Mr. Brewer fails to understand is that MMM does NOT have any right to have any negative impact on our health whatsoever!! The recent report from the University of Washington (Kaufmann et al., The Lancet. 25 May 2016), sponsored by the EPA and the National Institutes of Health, makes it clear that there is no safe level of small particulate pollution, i.e. PM2.5. Small particulate pollution will be one of the largest health threats from this facility, and we do NOT intend to stand by and allow our health to be compromised because of the attitude of persons such as Mr. Brewer and the management of MMM. And, if MMM is in violation of either Colorado or EPA air quality standards, we have not only a right but a responsibility to report those violations and attempt to make sure that they are eliminated by working with the proper authorities who actually have enforcement responsibility. 2/4 CLR-34 Neighborhoods Assn. Simply reporting the issues to MMM is insufficient, as then the complaints can be suppressed or ignored, as they have been in the past. And, if the County is not going to take these issues seriously, then we will be forced to escalate the reporting of documented violations to a level of enforcement that is sufficiently concerned that the violations are eliminated. Hopefully, going forward, we can expect a more professional response and level of concern to which we are entitled as taxpayers and Weld County residents. This project is going to have numerous, wide -spread, negative impacts, and we must be able to count on the County to protect our Health, Safety and Welfare during this entire process. We hope that you will agree and will take the necessary steps to assure that this is the case. Respectfully, Board of Directors CLR-34 Neighborhoods Assn. l Ls David W. Kisker, President {= , John Cummings, Vice President Sue Thomas, Secretary/Treasurer Anita Corner, At Large Board Member /jL> Mel Bickling, At Large Board Member Attachments: Email sequence from Phil Brewer to Ken Houlden GP03 Permit GP03 letter issued to Martin Marietta Seattle Times Article regarding PM2.5 health impacts Lancet Journal article regarding PM2.5 health impacts 3/4 CLR-34 Neighborhoods Assn. Cc: Tom Parko Commissioner Sean Conway Commissioner Steve Moreno Bruce Barker, Weld County Attorney 4/4 File from Accela, USRI5-0027 Diana Aungst Subject 7-2016 dust complaint From: Phillip Brewer Sent: Friday, July 15, 2016 4:14 PM To: Tom Parka Jr. <tparko@co.weld.co.us> Subject: FW: Martin Marietta Materials Hwy 34 project Tom: My apology. 1 did not think to include you on this reply, so here it is. J. Phillip (Phil) Brewer Environmental Specialist III Weld County Department of Public Health and Environment Environmental Health Services 1555 N 17th Avenue Greeley, CO 80631 970-356-4000, x 2227 (office & messages) 970-304-6411 (Fax) 970-590-7702 (c, M -F, 8 am - 5pm) pbrewer@co.weld.co.us Confidentiality Notice: This electronic transmission and any attached documents or other writings are intended only for the person or entity to which it is addressed and may contain information that is privileged, confidential or otherwise protected from disclosure. If you have received this communication in error, please immediately notify sender by return e-mail and destroy the communication. Any disclosure, copying, distribution or the taking of any action concerning the contents of this communication or any attachments by anyone other than the named recipient is strictly prohibited. From: Phillip Brewer Sent: Friday, July 15, 2016 4:01 PM To: 'Houlden - CUPHE, Kenneth' <kenneth.houlden@state.co.us> Cc: Trevor Jiricek <tjiricek@co.weld.co.us>; Lauren Light (Ilight@co.weld.co.us) <Ilight@co.weld.co.us>; James Taloumis <jtalournis@co.weld.co.us>; Julie Cozad <jcozad@co.weld.co.us> Subject: RE: Martin Marietta Materials Hwy 34 project Well, Ken, your message is of interest to me. Here are some things that may be of interest to you: 1. I sat through 27 hours of Weld County Planning Commissions and Weld County Board of County Commissioners hearings last fall. These were held to help determine if this project should be given a USR to proceed with development. 2. 1 heard a lot of testimony based on "heresay", "fear", "misinformation", and "Nimby". There was "scientific" testimony from both sides. Emmett Malone provided me with meterological information that we studied and understood but did not present at the meetings (1 told Emmett that I would not present his information ----that if his information was needed, we would send an invitation to him to come and present his own interpretation of wind roses. 1 3. The first two complaints were received here at the WCDPHE this week. The complainants live in the indianhead subdivision to the east. This was the place where a lot of the "negative" testimony came from during the hearings. 4. The two complaints were based on their observations of fugitive dust "blowing all over". The site is undergoing initial land preparations. 5. We investigated the complaints in the presence of 4 or 5 MMM representatives. The MMM people have reached out to the lndianhead Estates residents requesting their calls whenever they have concerns. They provided contact information to the residents. 6. We have contact information for the MMM people as well. 7 The complaints were not verified as valid ---the emissions were not out of compliance with the GPO3 permit terms. More than 24 hours after the complaints, and after MMM was notified. My suggestion to you is this: I think that it would be wise to have or solicit public comment on each and every portion of this permitting review whether the analyses of data trigger it or not. The residents Vf the Indianheac JubeAkisiJI I re rinn ,4111ni,Inrr o1L JLI LAILI IIILII IS ever; phase and activity of this prnjert Every possible L Y1.1 phase JV and activity I this I V �.t. environmental deviation or subtle insult to the clarity of the air or the health of the area is going to be reported to us. The residents "need' to know their input is valued, solicited, and welcomed. They need to be able to provide "public comment". If we don't include them, I believe later there will be some sharp statements about them being excluded from the on- going planning and permitting activities. This could have a significant long term negative effect in our area. We need to involve them more than "normal". We need to "include" them whenever we can. I think that we go out of our way to announce the public input request. Somehow we must assure that every resident in that subdivision is informed of the opportunity for public comment. Phil J. Phillip (Phil) Brewer Environmental Specialist Ili Weld County Department of Public Health and Environment Environmental Health Services 1555 N 17th Avenue Greeley, CO 80631 970-356-4000, x 2227 (office & messages) 970-304-6411 (Fax) 970-590-7702 (c, M -F, 8 am - 5pm) PbIrewericci}co.wI_.,Id_rc.as Confidentiality Notice: This electronic transmission and any attached documents or other writings are intended only for the person or entity to which it is addressed and may contain information that is privileged, confidential or otherwise protected from disclosure. if you have received this communication in error, please immediately notify sender by return e-mail and destroy the communication. Any disclosure, copying, distribution or the taking of any action concerning the contents of this communication or any attachments by anyone other than the named recipient is strictly prohibited. 2 From: Houlden - CDPHE, Kenneth[mailto:kenneth.houlden@state.co.us] Sent: Friday, July 15, 2016 3:23 PM To: Philip Brewer cpbrewereco.weid.co.us> Cc: Chip Hancock - CDPHE cr.hancockea state.co.us>; Roland Hea - CDPHE <roland.hea a@state.co.us> Subject: Martin Marietta Materials Hwy 34 project Good afternoon Phil I spoke to Shannon McMillan today and she said that you are familiar with the Highway 34 project and the public interest surrounding it. Would you be able to give an overview from your personal dealing with this site as to the interest from the community and neighbors? We are trying to decide whether there is enough interest to send this to public comment for the first portion of the project which currently doesn't trigger it through regular means. The first phase of permitting (aside from the land development) would be a concrete batch plant and the transloading of aggregate. The second phase will be an BMA plant application that would probably follow in a year that will most likely be going to public comment for being a synthetic minor source. Anything you might be able to help with in regard to this would be appreciated. Thank you, E.C. Houlden Permit Engineer Construction Permits COLORADO Air Pollution Control Division Department of Public -Health 8 Environment P 303.691..4092 I F 303.782.0278 4300 Cherry Creek Drive South, Denver, CO 80246-1530 kenneth.houiden@state.co. us I www.colorado.gov/cdphe/apcd NOTE: As of January 1, 2014, the Colorado Air Pollution Control Division no longer accepts blank or incomplete APENs. Additional fees may apply if an APEN is submitted without the necessary information. An application with missing information may result in longer processing times. Please note that all APEN submissions should be completed using forms currently supplied by the Division (See Reg. 3, Part A, Section IJ.A). Current APEN forms can be found at: httpsd/www.colorada.gavfcdphelAPENforms 3 STATE OF COLORADO COLORADO DEPARTMENT OF PUBLIC HEALTH AND ENVIRONMENT AIR POLLUTION CONTROL DIVISION TELEPHONE: (303) 692-3150 GENERAL CONSTRUCTION PERMIT Land Development Projects . ti PERMIT NO: GPO3 FINAL APPROVAL Modification `I eesr_e ;- t .r...< November 10, 2009 R K Hancock III, P.E. Date Issued Permitting Section Supervisor Note: See the Land Development General Permit Guidance document available through the Division's Small Business Assistance Program for further information on demonstrating compliance with the requirements of this permit. I. General Permit Applicability I.A. I.B. 1. C. The owner or operator of any land development activity that can comply with all of the operating conditions described in Section II of this permit and meet all requirements of this Section I may register for this general permit. Land development refers to all land clearing activities, including but not limited to land preparation such as excavating or grading, for residential, commercial, or industrial development, or oil and gas exploration and production. Land development does not include mining operations or the disturbance of contaminated soils. Land development activities that are less than 25 contiguous acres and less than 6 months in duration are exempt from permitting and do not need to report air emissions to the Division. For these projects, operators must use appropriate control measures to minimize the release of fugitive dust from the site. II. Operating Terms and Conditions Il.A. Emission Limitations I I.A.1. Project will not exceed 1850 acres in size. Any project over 1850 acres will be subject to a Construction Permit and Public Notice proceedings. II.B. General Operating Conditions 11.8.1. Particulate emissions Control Plan ll,B.1.a. THE FOLLOWING PARTICULATE EMISSIONS CONTROL MEASURES SHALL BE USED FOR ENFORCEMENT PURPOSES ON THE SOURCES COVERED BY THIS PERMIT, AS REQUIRED BY THE AIR QUALITY CONTROL COMMISSION REGULATION NO 1. THIS SOURCE IS SUBJECT TO THE FOLLOWING EMISSION GUIDELINES: LAND DEVELOPMENT GENERAL PERMIT Page 1 of 4 Permit Number GP03 Colorado Department of Public Health and Environment Final Approval Air Pollution Control Division II. B.1.a. (i) All Activities - Visible emissions not to exceed 20%, no off -property transport of visible emissions. II.B,1.a.(ii) Haul Roads - No off -property transport of visible emissions shall apply to on -site haul roads, the nuisance guidelines shall apply to off -site haul roads. II.B.1.a.(iii) Haul Trucks - There shall be no off -property transport of visible emissions from haul trucks when operating on the property of the owner or operator. There shall be no off -vehicle transport of visible emissions from the material in the haul trucks when operating off of the property of the owner or operator. .b. Control Measures I I. B.1. b. (i) All unpaved roads and other disturbed surface areas on site must be watered as necessary to prevent off -property transport of visible fugitive particulate emissions. II.B.1.b.(ii) Vehicle speed on all unpaved roads and disturbed areas shall not exceed a maximum of 30 mph, Speed limit signs shall be posted. 11 in .4 L J:::\ I. ..l -..-II [.r. .••.•.a.a.r.v,nM .,,hr.vi 41an torie'nnnrl irnernentie '2f1 nn Hese ner VI 11.0. i . u.I I ill-) car U r■•VI f\ °LAIvitI.eo .7I ion iic IIFOCI I I ICU YYI IC.11 11 IQ TV IF i.� 4.7f.JL+�+%J mind.... nd +J tJIW %Ail iry T.'. hour. II.B,1.b.(iv) All disturbed surface areas shall be revegetated within one year and according to the information submitted by the applicant with the permit application. II.B.1.b.(v) Gravel entryways shall be utilized to prevent mud and dirt carryout onto paved surfaces. Any mud and dirt carryout onto paved surfaces shall be cleaned up daily. II .B.1.c. Other control measures recommended by the Division, but not required for general permitting I . B.1. c. (i) Foundation soil shall be compacted on a daily basis to within 90% of maximum compaction. II.B.1.c,(ii) Silt fencing shall be installed prior to overlotting along all property borders that are adjacent to developed areas. II.B.1.c.(iii) Surface area disturbed shall be minimized as described in the information submitted by the applicant with the permit application. Ill. General Recordkeepinq III.A. The records in this section shall be maintained on site_ III.B The current version of this general construction permit. 111.0. The most recently submitted Air Pollutant Emission Notice (APEN). lI I.D. The general permit registration approval letter. 1V. General Permit Terms and Administration IV.A. General Terms IV.A.1. Land development owner/operator agreement to Particulate Emissions Control Plan (II.B.1) will result in issuance of general permit approval letter. LAND DEVELOPMENT GENERAL PERMIT Page 2 of 4 Permit Number GP03 Colorado Department of Public Health and Environment Final Approval Air Pollution Control Division IV.A.2. A land development general permit will be valid for five (5) years from the initial date of the approval letter issuance. Any project exceeding five years will be required to file an APEN update after five years. IV.A_3. One APEN will be submitted per project. Multiple phases may be covered under a single APEN provided that the entire project is less than the 1850 acres. IV.A.4. APEN and General Permit Fees IV.A.4.a. Total fees for a land development APEN and General Permit will be $202.90. These fees will arise from two sources: IV.A,4.a.(i) An APEN filing fee in the amount of $152.90 per APEN filed (Please note that the APEN filing fee is subject to change by the Colorado State Legislature) and IV.A.4.a.(ii) A general permit fee of $50.00 for each APEN filed. IV.A.5. A revised Air Pollutant Emission Notice (APEN) shall be filed: (Reference: Regulation No. 3, Part Al Section II.C.) IV.A.5.a. Whenever there is a change in the owner or operator of any facility, process, or activity; or IV.A.5.b. No later than 30 days before the five-year term of the existing APEN expires. IV.A.6. This permit is granted subject to all rules and regulations of the Colorado Air Quality Control Commission and the Colorado Air Pollution Prevention And Control Act C.R.S. (25-7-101 et seq), to those general and specific terms and conditions included in this document. Rt./0cl Unless specifically stated otherwise, the general and specific conditions contained in this permit have been determined by the Division to be necessary to assure compliance with the provisions of Section 25-7-114.5(7)(a), C.R.S. IV.A.8. Each and every condition of this permit is a material part hereof and is not severable. Any challenge to or appeal of, a condition hereof shall constitute a rejection of the entire permit and upon such occurrence, this permit shall be deemed denied ab initio. IV.A.9. Violation of the terms of a permit or of the provisions of the Colorado Air Pollution Prevention and Control Act or the regulations of the AQCC may result in administrative, civil or criminal enforcement actions under Sections 25-7-115 (enforcement), -121 (injunctions), -122 (civil penalties), -122.1 (criminal penalties), C.R.S. IV.A.10. Registration under this permit is approved in reliance upon the accuracy and completeness of information supplied by the applicant and is conditioned upon operation of the source, in accordance with this information and with representations made by the applicant or applicant's agents. It is valid only for the equipment and operations or activity specifically identified on the general permit registration. IV.B. Registration Certification IV.B.1_ Conditional certification of a registration under this general permit is effective from the date the complete registration request is received by the Division. A complete registration request consists of all General Permit application materials required by the Division including, but not limited to, an impact analysis that demonstrates, that the APEN requested emissions from the proposed source or modification will not cause or contribute to concentrations of air pollutants in ambient air in violation of any applicable state or national ambient air quality standard. The owner or operator may commence construction and operation of the land development project as represented in the registration upon submission of the completed registration request. In the LAND DEVELOPMENT GENERAL PERMIT Page 3 of 4 Permit Number GP03 Colorado Department of Public Health and Environment Final Approval Air Pollution Control Division event the land development project does not qualify for registration under the general permit or is demonstrated to violate an applicable ambient air quality standard, the owner or operator accepts the liability of commencing these activities. IV.C. Registration Modification IV.C,1. in order to modify operations under the general permit, the owner or operator must submit a new general permit application and APEN to the Division. This application will detail the changes being made to the project. Reasons for submitting a modification include, but are not limited to: IV_C.I.a. Increase in project size resulting in greater emission. IV.C.1.b. Increase in the duration of the project resulting in fugitive particulates being released longer than initially reported. IV.C.1.c. An increase in the amount of paving being performed on the site. IV.C.1.d. A decrease in dust control measures being implemented from those initially reported. IV r) Registration Revision /Termination IV D.1 IV. D.2. The Division may deny or revoke registration under the general permit under the circumstances specified in Regulation No. 3, Part B, Section IIl.I.3.c, A registration under this general permit may be reissued to a new owner by the Division as provided in Regulation No. 3, Part B, Section II.B. upon a request for transfer of ownership and the submittal of a revised APEN and the required fees. IV.D.3. Registration under this general permit is voluntary. The permittee may withdraw or cancel a registration under this general permit at any time by notifying the Division in writing. iv_E. uenerai Permit Revision ! I errriiriailuri iV.E, IV.E.2. IV.E.3. IV.E.4. This generai permit remains in &reci until revised of terrrinaled by the Division in accordance with the provisions of Regulation No. 3. After public notice and comment as provided by Regulation No. 3, Part B, Section III.1.7., the Division may revise this general permit in order to add or delete requirements or limitations to the permit. This public notice shall be conducted in a manner consistent with the provisions of Regulation No. 3, Part B, Section I11.C,4. If a revised general permit is issued by the Division, any existing registration to use the general permit will be automatically converted to a registration to use the revised general permit, provided that the permittee continues to meet all requirements of the revised general permit. Persons not wishing to continue coverage under the revised general permit shall have the option of applying for an individual permit as required by Regulation No. 3, Part B. If the Division terminates this general permit, it will provide written notice to affected registrants prior to the termination of the general permit. The notice will advise registrants that they must apply for an individual permit as required by Regulation No. 3, Part B. Permit History Final Approval issued October 17, 2008. Modification 1: Removal of requirement that owner or operator receive division approval prior to commencement of project. LAND DEVELOPMENT GENERAL PERMIT Page 4 of 4 COLORADO Department of Public Health Et Environment Dedicated to protecting and improving the health and environment of the people of Colorado March 10, 2016 Walt Wright Martin Marietta 10170 Church Ranch Way, Suite 201 Westminster, CO 80021 RE: Land Development GP03 General Permit Approval for Package #338804 Dear Mr. Wright, The Colorado Air Pollution Control Division approves land development general permit registration for the sites listed in the table below. Please refer to general permit GP03 for all applicable requirements, limitations, terms and conditions. A copy of the general permit may be obtained via the Internet at the following web address: https: //www.colorado.gov/ pacific Icdphe/general-air-permits AIRS ID Site Name e Actual Location City County Approval Expiration 124-4595-001 Highway 34 6433 CR 56 £x 27486 CR 13 Weld 10/08/2020 12:00:00 AM If you have any questions regarding this letter, please contact me directly at (303)692-3242. Sincerely, YVIdeitV Aaron Moseley Permit Engineer Stationary Sources Program Air Pollution Control Division 4300 Cherry Creek Drive S., Denver, Co 80246-1530 P 303-692-3090 www.colorado.gov/cdphe John W. Hickenlooper, Governor 1 Larry Walk, MD, MSPH, Executive Director and Chief Medical Officer i S. ft- JoNiei Mecca id U -led study pinpoints how air pollution harms your heart (..�i a:e is ••:�i��' (Ilialis itt: i`'e :1f 7.s, :,i.3-:i' .. ' jPC:1CILL•c i•':U)' 2 5.'K'6' http://www. seattl eti mes.corn/sea ttl e-news/hea lth/uw-I ed-study-pinpoints-how-air -pol luti on -ha rms- your-heart/ a 7 of .... T i't!C:fg./'.C J:eu' al: SC':!' Dr. Joel Kaufman of the University of Washington led a to -year study of 6,000 people in six cities that found air pollution accelerates deposits of calcium in heart arteries, a known cause of heart attack and stroke. Scientists have known for years that long-term exposure to air pollution raises the risk of heart disease, but a highly anticipated study led by a University of Washington environmental health expert finally explains why. In a decade long analysis involving more than 6,000 people in six states, Dr. Joel Kaufmann found that people living in areas with more outdoor pollution built up calcium in the arteries of their hearts faster than those who lived elsewhere increasing a known risk for heart attack and stroke. "On average we found a 20 percent acceleration in the rate of the calcium deposits," said Kaufman, 54, director of the UW's occupational and environmental medicine program. "I would say the results are a little more clear-cut and dramatic than I expected when I started this." The $30 million study, funded by the U.S. Environmental Protection Agency and the National Institutes of Health, is the largest to measure both metrics of air - pollution exposure and health markers over time. Results were published Tuesday in the journal The Lancet. It relied on data collected through the Multi -Ethnic Study of Atherosclerosis and Air Pollution (MESA Air), which studies the effects of pollution in six U.S. metropolitan areas: Baltimore, Chicago, Los Angeles, New York, St. Paul, Minn., and Winston-Salem, N.C. Through what authors of an accompanying Lancet editorial called "meticulous measurements," Kauf van's analysis looked at the exposure of participants to the fme particulate matter present in pollution, tiny bits less than 2.5 microns in diameter, too small to be seen with the naked eye. Those fine particles are referred to as PM 2.5. The study, which tracked air quality in participants' communities and near their homes, also measured exposure to nitrogen oxide and nitrogen dioxide and black carbon or soot, pollutants typically associated with traffic. Participants also visited study clinics multiple times to collect health measurements. In a complicated conclusion, the researchers found that for every 5 micrograms per cubic meter higher concentration of PM 2.5, or for every 35 parts per billion higher concentration of oxides of nitrogen, participants saw an increase of 4 units per year of a marker for coronary -artery calcium, called the Agatston score. In plain language, that means the higher the concentrations of pollutants, the faster participants developed atherosclerosis, a condition commonly known as hardening of the arteries. Overall, the increase from those sources accounted for a 20 percent acceleration in the rate of the calcium deposits, Kaufman said. "Another way to look at it is this: A move from an area with low pollution to an area with high pollution could be associated with an increased rate of 10 to 20 percent in atherosclerosis," Kaufman explained. Researchers also analyzed pollution in relation to another potential marker of cardiovascular disease, the thickness of the inner layers of the carotid artery, but found no effect. The study drew praise from experts in air pollution and heart disease. It answers questions raised by scientists since the 1990s, when research first showed that people who lived in areas with high levels of pollution suffered more heart disease and stroke that those who lived elsewhere. "The exact mechanism by which pollution has effects on heart and cardiovascular disease has been unknown," said Dr. Russell Luepker, a Mayo professor at the University of Minnesota's School of Public Health. "This is a first attempt from an extremely good study." Dr. Robert Brook, a cardiologist with the University of Michigan Health System, said the findings of the new study "would be hard to overstate." They mean that air pollution is not just a trigger of heart attacks or strokes over a few days in high -risk or sick people who would have had such episodes anyway, but it's also a cause of harm over years. "This is THE study we have all been waiting to see the results of during the past decade," Brook said in an email. "I am in awe of the study." Kaufman's research has implications for public -health policy in the U.S. and abroad. During the study period, from 2002 to 2012, air -pollution levels actually improved in the U.S., in large part because of reductions in allowed ambient particulate levels. The I.S. now permits an annual average of 12 micrograms per cubic meter of PM 2.5, about half the European standard of 25 micrograms per cubic meter, "This is a public -health success story," Kaufman said. But the new evidence also shows that there's no safe level of pollution, no exposure that doesn't increase heart disease risk, he added. 'Even though things are clean and getting better, there's still more work to do." JoNel Aleccia: 206-464-2906 or jaleccitraseatrt1ethnes.coral. On Twitter JoNel Aleccia Articles Association between air pollution and coronary artery calcification within six metropolitan areas in the USA (the Multi -Ethnic Study of Atherosclerosis and Air Pollution): a longitudinal cohort study Joel D Kaufman, Sara D Adar, R Graham Barr, Matthew Budo f f, Gregory I Burke, Cynthia L Curl, Martha L Dauiglus, Ana V Diez Roux, Amanda] Gossett, David R JacobsJr, Richard Kronmal, Timothy V Larson, Ana Navas-Acien, Casey Olives, Paul D Sampson, Lianne Sheppard, David 5Siscovick, James H Stein, Adam A Szpiro, Kara/ E Watson Summary Background Long-term exposure to fine particulate matter less than 2.5µm in diameter (PM, ,) and traffic -related air pollutant concentrations are associated with cardiovascular risk. The disease process underlying these associations remains uncertain. We aim to assess association between long-term exposure to ambient air pollution and progression of coronary artery calcium and common carotid artery intiirna-media thickness. Methods In this prospective 10 -year cohort study, we repeatedly measured coronary artery calcium by CT in 6795 participants aged 45-84 years enrolled in the Multi -Ethnic Study of Atherosclerosis and Air Pollution (MESA Air} in six metropolitan areas in the USA. Repeated scans were done for nearly all participants between 2002 and 2005, for a subset of participants between 2005 and 2007, and for half of all participants between 2010 and 2012. Common carotid artery intima-media thickness was measured by ultrasound in all participants at baseline and in 2010-12 for 3459 participants. Residence -specific spatio-temporal pollution concentration models, incorporating community - specific measurements, agency monitoring data, and geographical predictors, estimated concentrations of PMZ.s and nitrogen oxides (NOJ between 1999 and 2012. The primary aim was to examine the association between both progression of coronary artery calcium and mean carotid artery intima-media thickness and long-term exposure to ambient air pollutant concentrations (PMz-S, NOx, and black carbon) between examinations and within the six metropolitan areas, adjusting for baseline age, sex, ethnicity, socioeconomic characteristics, cardiovascular risk factors, site, and CT scanner technology. Findings In this population, coronary calcium increased on average by 24 Agatston units per year (SD 58), and intima- media thickness by 12 µm per year (10), before adjusting for risk factors or air pollutant exposures. Participant - specific pollutant concentrations avenged over the years 2000-10 ranged from 9.2-22.6 µg PM2.5/m3 and 7.2-139.2 parts per billion (ppb) NO,. For each 5 pg PM,.,/m3 increase, coronary calcium progressed by 4-1 Agatston units per year (95% CI 1.4-6.8) and for each 40 ppb NO„ coronary calcium progressed by 4.8 Agatston units per year (0.9-8.7). Pollutant exposures were not associated with intima-media thickness chime. The estimate for the effect of a 5µg/m3 higher long-term exposure to PM2_5 in intima-media thickness was -0-9 pm per year (95% CI -3-0 to 1.3). For 40 ppb higher NO„, the estimate was 0.2 pin per year (-1.9 to 2.4). Interpretation Increased concentrations of PM2.5 and traffic -related air pollution within metropolitan areas, in ranges commonly encountered worldwide, are associated with progression in coronary calcification, consistent with acceleration of atherosderrosis. This study supports the case for global efforts of pollution reduction in prevention of cardiovascular diseases. Funding US Environmental Protection Agency and US National Institutes of Health. Introduction Particulate air pollution and traffic -related air pollutants are associated with overall mortality, cardiovascular mortality, and cardiovascular disease events. In particular, long-term exposure to high concentrations of air pollutants has been associated with risk of myocardial infarction and stroke.' However, previous studies of cardiovascular disease and air pollution have had short follow-up duration, have often been limited by between - city exposure contrasts without precisely accounting for within -city variation, and have comprised secondary analyses of existing data sets collected to test other hypotheses. Furthermore, the underlying pathological process has not been well established, leaving the biological plausibility of these findings open to question. To reduce uncertainties in the understanding of the potential health effects of ambient air pollutants, the US Environmental Protection Agency (EPA) supported an unprecedented effort to characterise pollutant exposures in participants of the National Heart, Published Wine May 24, 2016 http://dx.doi.org/10.10161 50140-6736(16)00378-0 See Online/Comment http://dx.doi.org/10,1016/ 50140-6736(16)30375-0 Department of Enviran roerrtal and occupational Health Sciences (Prof) D Kaufman MD, A JGassettMS, C0lionPhD, Prof L Sheppard PhD), Department of Epidemiology (Prof) D Kaufman), Department of Medicine (Prof) D Kaufman, Prof Emeritus D S Siscovick MD), Department of H1astatfstks (Prof R Kronmal PhD, Prof L Sheppard PhD, A A Szpiro PhD), Department of civil and Environmental Engineering (Prof T V Larson PhD), and Department of Statistics (Prof P D Sampson), University of Washington, Seattle. WA, USA; Department of Epidemiology, University of Michigan, Ann Arbor, M4 USA (SD Adar ScD); Department of Medicine and Department of Epidemiology, Columbia University New York, NY, USA (R G Barr MD); Los Angeles Biomedical Research Institute at Harbor, UCLA Medical Center, Torrance, CA, USA (Prof M Rudoff MD); Division of Public Health Sciences, Wake Forest University, Winston-Salem, NC, USA (Prof G L Burke MD); Department of Community and Frrvionn ental Health, Boise State University, Boise, ID, USA (C L Curl PhD); Fcnberg School ofMedicu.4 Northwesod.r tkihie sit c Evanston, it, USA (Prof M L Daviqius MD); Institute for Minority Health Research, Urriversityof Illinois at Chicago, Chicago, IL, USA (Prof M L Davigkrs); School of www.theiancet.corn Published online May 24, 21316 http://dx.doi_org/io.1o16/50140-6736(16)00378-0 1 Articles Public Health, Drexel University, PA. USA (Prof AV Diez Roux MD); School of PublicHealth, Division of Epidemiology and Community tfeatth, University of Minnesota, Minneapolis, MN, USA (Prof D Rix -ohs PhD); Departinentofi swuonanerstal Health Sciences, (elms Hopkins University, Baltimore, MD, USA (A Navas -Aden MD); New York Academy of Medicine, New Yak, NY, USA (Prof D S Siscovick Emeritus); Department of Medicine, University ofWisconsin School of Medidne and Public Health, Madison, WI, USA (Rut) H Stein MD); and Department of Medicine Division ofCadiology, University of California las Angeles, Los CA, USA (Prof K E Watson MD) Corre-spondencetoo Prof Joel D Kaufman, University of Washington, Seattle, WA 98105, USA joelk@unradington.edu Research in context Evidence before this study At study launch, there was no literature on progression of atherosclerosis in relation to long-term exposure to air pollution; the studywas in cesponsetothe US Environmental Protection Agency's Request For Applications for a prospective observational study of cardiovascular disease initiation and progression associated with long-term exposureto ambient particulate matter and other air pollutants in a population -based sample. Although previous research has been considered to be consistent with a causal relationship between particulate matter air pollution and ischaernic heart disease events and mortality, these studies had substantial limitations and biological plausibility has continued to be questioned Previous studies have had short follow-up durations, little attentionto fine -scale variation in pollutant exposure, and comprised secondary analyses of existing datasets collected to test other hypotheses. Added value of this study This study provides important new information about the underlying biological processes of long-term exposure to air Lung, and Blood Institute's Multi -Ethnic Study of Atherosclerosis (MESA)! The re Rllltant study (the Multi -Ethnic Study of Atherosclerosis and Air Pollution, IMI cA Airti} tactari a nrinn them accnr,tinnc of air r- ---- - n r pollution concentrations, specifically particulate matter of less than t c l :': A;. .lwr 1PM G1 nitrnaPn nylaPe Yi J..VV Yawaa • z �•lf, a vyvaa (NO„), and black carbon, with progression of subclinical arteriosclerosis. We report the association between long- term exposure to ambient air pollution and progression of coronary artery calcium and common carotid artery intima-media thickness. Methods Study design and participants The designs of the MESA' and MESA Aie studies have been described previously. Briefly, MESA recruited a cohort of 6814 participants with no history of clinical cardiovascular disease from four ethnic groups (Hispanic, black, white, and Chinese), with sex balance and uniform age distribution (range 45-84 years at recruitment) in six areas of the USA: Baltimore, MD; Chicago, IL; Los Angeles County, CA; New York City, NY; St Paul, MN; and Winston-Salem, NC. Community - based strategies that varied by clinical centre were used to recruit participants. Recruitment and baseline examinations were done between July 17, 2000, and Aug 29, 2002. Between Feb 22, 2005, and May 9, 2007, MESA Air recruited 257 additional participants in Rockland County, NY (grouped as being from the same area as New York City, NY participants); Riverside County, CA (grouped as being from the same area as Los Angeles County, CA participants); and a coastal area of Los Angeles County, CA, to add heterogeneity in air pollutant concentrations and their association with cardiovascular disease, ttuough repeated assessment of coronary artery cakif cation by CT (a surrogate of atherosclerosis extent} in a cohort and with an unprecedented effort to characterise air pollutant exposures. The study was specifically designed to address the hypothesis that air pollutants would be associated with progression in subclinical atherosclerosis. Exposures assessed i n this study are low and relevant for understanding the health effects of ambient environments occurring nowadays in high -income, low-income, and rapidly industrialising countriess. Implications of math. evidence Together with accumulating observational evidence of the relationship between ambient pollutants and cardiovascular disease events, this study substantially advances the case for global efforts to reduce exposures to ambient air pollutants. pollution exposures. The study protocol was approved by the institutional review board at each of the six study centres, and participants provided written informed rnncent rrnnn their arrival at the c t-urly clinic -r - Rrnraririrac All participants received CT scans at baseline to measure coronary artery calcium as previously describe&.& Repeated scans were done for nearly all participants between 2002 and 2005, for a subset of participants between 2005 and 2007, and for half of all participants between 2010 and 2012. CT technology diffcd between clinical centres and over time.; A four -density calibration phantom was imaged with each scan to enhance comparability of images between scanners and to scale the voxels in each composite scan before the calculation of coronary artery calcium scores. Scans were scored in the Harbor -UCLA Los Angeles Biomedical Research Institute by the Agatston method! To measure the common carotid artery intima-media thickness, one ultrasound and transducer model (Logiq 700, MI2L, GE Medical Systems, Waukesha, WI, USA) were used at all sites in all examinations.' Images were read by the University of Wisconsin Carotid Ultrasound Reading Center. Baseline images were read only for participants with images from the 2010-12 examination.6 Exposure assessment The MESA Air pollution measurement and modelling methods have been described previously.vm MESA Air measured ambient PM,.„ NO„, nitrogen dioxide (NO2), and black carbon (assessed by light absorption) at 27 long-teiui sites, in community snapshot locations (simultaneous 2 www.thelartcet.com Published online May 24, 2016 http:/ldx.doi orgf 10.1016!50140-6736(16)00378-0 Articles i 2 -week measurements collected on three occasions), and outside 697 participants' homes between 2005 and 2009 to supplement measurements from. Environmental Protection Agency Air Quality System monitoring locations. Participants reported all residential addresses from 1980 to 2012. Community -specific spatio-temporal models were developed to predict pollutant con- centrations at participants' residences for each fortnight from 1999 to 2012, with statistical methods to accommodate irregular monitoring data and incorporate all monitoring results. These models explained 90-97% of the variation (model -fit R2) in measurements at participant homes. The cross -validated R2 values (assessing out -of -sample validation) for predictions from the area -specific models at residence locations varied by site. Median (range) R2 values for these models were 0-79 (0.54- 0.85) for PM2.5, 0.78 (0.45--4.90) for NO2, 0-72 (0.50-0.92) for NOy, and 0.67 (O.51-0.78) for black carbon. These R2 values at participants' homes leverage temporal as well as spatial variability. R2 values from the Winston-Salem, NC NewYe* City, NY Baltimore. MD St Paul, MN Chicago, IL Cos Angeles County, CA Year 2000-10 PM,s (pg jar'); 13.5 (0.4) 14-5 (1.9) 13.7 (o -B) 10.6 (0.6) 141(1.0) 174 (13) n Baseline 1008 1166 1005 1027 1143 1446 Follow-up 897 1007 847 898 1004 1182 Follow-up time (years) 644(3.5) 6.6(3.4) 5-60-6) 6.5 (34) 6-6 (3.5) 5.5 (34) Co onaryarterycaldum Baseline (Agatstan score) 143 (403) 131(413) 186 (462) 172 (474) 121 012) 129 (374) Progression (Agatston peryear)f 26 (61) 22 (60) 26 (63) 26 (60) 22 (47) 21(52) Demographics Age (years) Male Ethnicity White Chinese Black Hispanic Education level Less than high school High school Some college ortea nical University or graduate Smoking status Never Former Present General health characteristics Body -mass index (kg/m2) Systolic blood pressure (ram Hg) HDt_chcrllesterol (mrnolli_) Total cholesterol (mmoljL) LOL cholesterol (mmollUt) Hypertension Statin use Diabetes Normal Impaired fasting glucose Diabetic 62 (10) 471(47%) 547 (54%) 458 (45%) 3 (0%) 76 (3%) 211(21%) 314(31%) 407 (40%) 412 (41%) 43S(43%) 161(16%) 29 (5) 133 (22) 1.32 (0.39) 4-89 (088) 2.95 (0.78) 553(55%) 164 (16%) 769 (76%) 120 (12%) 119 (12%) 62 (10) 63 (10) 521(45%) 471(47%) 281(24%) 2 (0%) 395 (34%) 488 (42%) 271(23%) 222 (19%) 322 (28%) 351(30%) 564 (48%) 429 (379% 173 (15%) 29 (5) 124 (20) 1.37 (0.39) 499 (0.91) 343 (0.83) 538446%) 197 (17%) 831(71%) 169 (14%) 165 (14%) 60(10) 547 (49%) 62 (10) 63 (10) 537 (47%) 695 (48%) 498 (50%) 590 (57%) 542 (47%) 303 (27%) 507 (50%) 298 (26%) 112 (11%) 202 (20%) 303 (30%) 388 (39%) 432 (43%) 423 (42%) 150 (15%) 29 (6) 128 (21) 1.32 (039) 4.97 (4.93) 303 (080) 515(51%) 193 (19%) 721(72%) 155 (15%) 126(13%) 437(43%) 194 (19%) 224 (22%) 359(35%) 250 (24%) 430 (42%) 405 (39%) 192 (1.9%) 29 (5) 122 (20) 1-27 (0.36) 5.17 (0.93) 3.10 (0-$0) 357(35%) 126 (12%) 776 (76%) 133 (13%) 118(11%) 84(7%) 89 (8%) 278 (24%) 692 (61%) 543 (48%) 451(39%) 149 (13%) 220 (15%) 490 (34%) 166 (11%) 570 (39%) 472 (33%) 261(18%) 375 (26%) 338 (236) 872 (60%) 422 (29%) 152 (12%) 27 (5) 27 (5) 124(21) 127(23) 1.40 (0.41) 1.27 (036) 5.04(093) 507(0.96) 3.03 (0-80) 3.05 (0.85) 435 (38%) 626 (43%) 165 (14%) 196 (14%) 908 (79%) 136(12%) 98 (9%) 964(67%) 242 (17%) 240 (17%) Data are mean (SD)or n (%). All percentages are caiculatedus+ngthe baseline as the denominator. PM -tine particulate matter less than 2.5 hem in diameter. HDlmlrigh density Lpoprotein. W1 4owdensity lk,oprotein. *Average of 2 -week predictions iromlanuary, 2000, to December, 2010, generated at each participant's baseline address tBasedon irxfnridually-derived slopes Table: Participant dmeactest sties at baseline and unadjusted longitudinal outcomes by fieldcentre, for partidptrttsincluded inthe analysis ofcoronary artery calcification www.theiancet.com Published online may 24, 2016 http://dx doi•org►14.1016/50140-6736(16)00378.0 3 Articles c v -o w LL California III lnols Minnesota Maryland NewYork North Carolina Overall IQR I-- 6 -14 to I I 20 30 PM,5 (ig/m3) 02,9-15.7) a 4, --1 oao r r I 4 4 25 75 125 NO, (pph) (21.4-57.3) oonl to rte 30 50 NO, (ppb) (3.1-8-26.4) 0 awl frExp a f -- ark I r t15 1.5 Black carbon (µg/rn3) (0.5-12) Figure 2: Long-term outdoorair pollutant concentrations by area Pollutant concentrations are averaged over the time hetwrsen the first and last CT scan, Frondedtnthe nearest full year. Roves rmrerthe is -6th percentile (tQR) with a centre line for the median concentration. Whiskers extend to the highest observation within 3 IQR of the box, with more extreme observations shown as points. Black carbon was measured by light absorption coefficient, where 0-5x104 m'twas approximately equivalent to 0-5 pg/m3 of elemental carbon. PM,, fine particulate matter less than 2.5 pm in diameter. NO„=nitrogen oxides. NO_=nitrogendioxide. ppb=parts per billion. cross -validation of the measured long -teen fixed sites • +t n weir suuuar.- MESA Air participants completed detailed question- naires at recruitment and after life changes, including moving homes. Examples of items queried included heating choices, air conditioner use, and window opening, and time spent indoors and outdoors, during summer and winter.9 Responses, meteorology, and an outdoor PM2.5 tracer (particulate sulphur assessed in concurrent samples inside and outside selected homes) were used to predict the fraction of ambient PM2.5 infiltrating homes.t° Indoor PM2.5 exposures were calculated as the predicted fortnight's outdoor PM,.; concentration multiplied by the weather -specific and residence -specific infiltration fraction. An individually -weighted exposure to ambient- derived PM2.5 (PM2.5ia„) for each fortnight was calculated by time -weighting the outdoor concentration by time spent outdoors, and indoor exposure by time spent indoors. Long-term exposures were the average of fortnightly residence -specific predictions from recruitment to follow-up for each examination. Year 2000 concentrations at the baseline address were used to model baseline cross-sectional relationships. Outdoor concentrations of black carbon were generated only for the years 2006-48 because comparable air quality system data were not available at other times (EPA's measurement method for black carbon was not comparable to the study -specific measurement method). Long-term black carbon avenges were calculated by weighting the residence -specific 2006-08 means by the amount of time participants lived at each location between their examinations. Statistical analysis •-r0 7 7 • 7 1 7 7 7 The siuuy was designed to tie auequaieiy puweieu to detect air pollutant effects of 2 Agatston units per year or 7 pm per year intitna-media thickness per iu pg per m3 PM2.5, based on pollution contrasts observed between MESA communities before 2003. The associations of progression of coronary artery calcium and mean intima-media thickness with long-term average outdoor pollutant concentrations (PM25, NO,, and black carbon) were the primary interests, with NO, and ambient -derived PM2.5 assessed as secondary. The primary adjustment model included baseline age, sex, ethnicity, site, CT scanner type (in the coronary artery calcium analysis), body -mass index (BMI), physical activity, smoking and second-hand smoke exposure (both time -varying), employment outside the home, total cholesterol, high density lipoprotein (H DL), triglycerides, statin use (time -varying), neighbourhood socioeconomic index, level of education, income, and the interactions between these variables and study time. Participants were censored at the time of coronary revascularisation procedures for analysis of coronary artery calcium. Additional models incorporated information on blood pressure and diabetes. A mixed model jointly analysed both the cross-sectional association between air pollution and the outcomes at baseline examination and the relationship between air pollution and the rate of progression -u Repeated measurements were modelled as a function of study time, with time -varying exposures modelled as an interaction with time to obtain a rate, Participant -specific 4 www.thelancet.cam Published online May 24, 2016 httttc/ldx.dot.org/10.1016/50140-6736(16)0037*-o Articles i PM,5 (P9/m9 ti{ - IS Baltimore, Mtn PM,. PM,5 ritirThamr roms�� ifs Y1di�'� masta St Paul, MN PM�5 98 Lns Angeles, CA Pik. Winaon-Salem, NC PMT, NewYork City, NY Chicago, IL PM�5 NO (ppb) — 50 37 Baltimore, MD NO, 13 to St Paul, MN NO. Los Angeles, CA No, No Y Winston-Salem, NC NO, NewYork City, NY Chicago, IL NO. Figure 2: Maps of predicted PM,,s and NO concentrations for 2005 in the MESA Air wmn>N hies,. by the city of the clinical site contrasts are smoothed in these figures, which might attenuate the visibility of fine -scale variation. Participant residential locations are shown by black dots, filtered to protecttheirprivacy. PM,5,-fine particulate matter less than 2-S pm in diameter, N{.=nitrogen codelt3,. ppb=arts per billion. random intercepts and slopes were included, along with random intercepts for neighbourhood clusters. We investigated potential effect modification by sex, ethnicity, obesity (BMI <30 kg/rnZ vs BMI 2:30 kg/m2), age category (10 -year intervals), smoking status, hypertensive status, diabetes status, EWDL cholesterol concentration (HDL cholesterol <1.03 mmol/L vs HDL cholesterol ≥1.04 mmol/L), total cholesterol (total <5 -17 mmol/L, total 5.17-64 21 mmol/L, or total >6.21 mmol/L), and LDL cholesterolconcentration (LDL cholesterol <2. 59 mmol/L, LDL cholesterol 2- 59--3.36 rtimol/L, LDL cholesterol 3.36-4-14 mmol/L, or LDL cholesterol >4.14 nunol/L). Evidence for effect modification was assessed by including three-way interaction terms between study time, the effect modifier, and air pollution concentration. A concentration -response curve was generated using a thin plate regression spline with five degrees of freedom for long-term average PM2.s concentrations. We also examined the relationship between pollutants and relative progression of coronary artery calcium, using a ln(Agatston score plus 25) transformation of the outcome. Role of the funding source This study was overseen by a Steering Committee and an External Scientific Advisory Committee (ESAC). The primary fiinder of MESA Air, the US Environmental Protection Agency, had ex -officio representation on the E SAC. The fonder had no role in data collection, analysis, interpretation, or writing of the study reports. All authors were provided complete access to the data and all authors share responsibility for the decision to submit the manuscript. Results Ofthe 7060 participants ini#iallyenrolled, 5834 underwent at least two examinations and had sufficient data to be included longitudinally in the analysis of coronary artery calcium. 961 participants were included only at baseline. The mean age of the cohort at baseline was 62 years (SD 10), and 3593 (53%) of the 6795 participants assessed were women. Overall, the cohort included 2678 (39%) white, 795 (12%) Chinese, 1824 (2796) black, and 1498 (22%) Hispanic participants (table). The differences in population characteristics between sites, notably in ethnicity and level of education, reflect purposefully implemented sampling strategies; differences in smoking rates reflect community differences. Mean follow-up time for participants with at least two coronary artery calcium measurements was 6.2 years (SD 3.5) and for those with intima-media thickness measurements from at least two timepoints was 9.2 years (1.8). Figure 1 shows summary statistics of air pollutant concentrations in the year 2000 and over follow-up. Long- term average levels of pollution were lower than levels of pollution in 2000. Mean concentrations also varied between sites by pollutant, with PKS concentrations being highest in Los Angeles County and lowest in St Paul, and NO„ and NO, being highest in New York City and lowest in Winston-Salem (figure 1). Figure 2 www.thelancet.com Published online May 24, 2016 http://dx.dol.arg/10.1016/50140-b736(16)00378-0 5 I artistes A Air pollutant PM25 (S pg/m3) NO„ (40 ppb) NO, (10 ppb) Black carbon' (0.5 pg(m) p Agatston units peryear B 20- 15- 10- 5- 0- -5 - D California D Illinois O Minnesota D Maryland LI New York © North Carolina -4 -7. 0 2 4 a tl 10 Agatston units per year a 12 1 I 1 1 I I 1 I 14 lb tt1 Long-term average PM2,r (fig/m3) 20 Figure 3 Long-term average air pollutant concentrationsand cmmnaryartery calcium progression (A)The linear longitudinal association of fine particulate matter (PM,,), nitrogenoxides (NOx), nitrogen dioxide (NO,), and black carbon, with coronary artery cakium progression (Agatston units peryear), from linear mixed models adyusted for age, sex, ethnicity, city, income, employment outsidethe home, smoking status, second-hand smoke exposwe, physical activity, adiposity, cholesterol, stain use, neighbourhood socioeconomic index, income, education and scannertype. (R)The concentration -response nlrvpwith 95% Cls for the overall change in and coronary artery calcium (lxrlgresdem rate associated with long-term average PM,, concentrations).The curve is basedon a mixed model that includesathin plate regression spline with five degrees of freedom to more flexibly assess the potentially non-linear association.The relationship at the extremes is less certain and might rely on concentrations that are recorded only in one geographical region; the highest and lowest 5% of overall concentrations have been trimmed for visualisation. The histogram at the bottom of the right panel shows the relative overall distribution of long-term PM,s concentrations in the cohort, with different colours representing each clinic location. *Black carbon as measured by light absorption coefficient, where t}5 x1©'rn is approximately equivalentto 7 7 I •.7 ' •. shows uetweeu-cny anti wiuun-Lay emyussure cunirasis see Online for appendix ofconcentrations ofPM2.5 and NO„ in 2005 (appendixp 11). ne mean progression rate over follow-up for coronary artery calcium was 24 Agatston units per year (SD 58) and for intima-media thickness was 12 pm per year (10); at baseline, coronary artery calcium scores were 145 Agatston units (407). Because the intima-media thickness analysis was restricted to participants who returned for ultrasound scans during the last examination, participants with intima-media thickness data were on average 2 years younger, more educated, and less likely to have diabetes than were those included in the coronary artery calcium analysis (appendix p 15). In the primary analysis adjusted for potential confounders, a 5 pg jrn3 higher PM2.5 concentration was associated with 4.1 Agatston units per year (95% CI 1-4-6.8) increased rate of coronary artery calcium progression (figure 3). A 40 parts per billion (ppb) higher NOx concentration was associated with a 4-8 Agatston units per year (0-9-8-7) increased rate of coronary artery calcium progression, and a 10 ppb higher NO, concentration was associated. with 2.7 Agatston units peryear (-0.3 to 5.7) increased rate of coronary artery calcium progression. Neither black carbon nor ambient -derived PM,.., were associated with coronary artery calcium progression (0.1 Agatston units per year for a 0.5µg/rn3 higher black carbon concentration [-3.8 to 4.1] and 1.0 Agatston units per year for a 5 pg fm3 higher ambient -derived PM,.5 exposure (-1.9► to 3.9)). Results were similar in models incorporating blood pressure and diabetes status. rouutaia exposures were Hui assotlawit with uliirna- media thickness change. The estimate for the effect of a 5 }igloo higher long-term exposure to PM2.5 in intima- media thickness was —0.9 pm per year (95% CI -3.0 to 1.3). For 40 ppb higher NOR, the estimate was 0.2 pin per year (-1.9 to 2.4). Results for both outcomes were consistent in sensitivity analyses. The associations of PM2.5 and NOx with coronary artery calcium progression were attenuated with widened confidence intervals if one was adjusted for the other. Exposure to outdoor PM2.5, NOR, NO„ and ambient -derived PM2.5 were all positively associated with relative coronary artery calcium progression (appendix P 13). The concentration -response function between outdoor PM,.; and coronary artery calcium progression concentration suggests attenuation of the association at higher concentrations (figure 3). Evidence for effect modification by several factors was weak and inconsistent between PM2., and NOR, although it suggested that the effects of exposures to these pollutants might be greater in older, non -obese, and hypertensive individuals (figure 4). Discussion In this multi -ethnic prospectively studied population, ambient concentrations of PM2.; and NOx were strongly associated with accelerated atherosclerosis, as shown by assessment of coronary artery calcium over a 10 -year period. Air pollution was not associated with progression of intima-media thickness. This study benefited from 6 www.thelancet.00m Published online May 24, 2016 httplitlx.doi.org/10.101650140-6736(16)003711-0 Articles i state-of-the-art exposure estimation at the time and location of each residence during follow-up and incorporated high -quality information about potential confounding factors, inducting time -varying covariates such as statin use. The cohort -focused air quality monitoring effort and spatio-temporal modelling methods enabled us to generate individually resolved exposures and examine relationships between athero- sclerosis progression and air pollution over time, using within -city contrasts with an unprecedented level of accuracy. These results provide important evidence that long-term exposure to these ambient air pollutants is associated with atherosclerosis progression in the coronary arteries and can explain previous findings that pollutants are associated with cardiovascular events and mortality. Exposures during follow-up of this cohort were low by historical and international standards. The present US National Ambient Air Quality Standards72 permit annual average PM,., concentrations of 12 pg/m1 and the European Union Air Quality Standards11 permit 25 pg/m3, whereas the mean ambient PM2,5 concentration that participants in our study were exposed to over 2000-10 was 14.2 Rims (range 9.2-22.6). The con- centrations in rapidly industrialising countries are substantially higher:1° Calcified plaques in the coronary arteries have been consistently associated with cardiovascular disease in both clinical trials and observational research's Coronary artery calcium is a very strong risk marker of future ischaemic vascular events. Although most often studied as a one -lime measure of atherosclerotic extent and plaque burden,' change in coronary artery caldmu also predicts subsequent ischaemic events! Risk factors that accelerate coronary artery calcium progression (including age, male sex, adiposity, systolic blood pressure, smoking, and diabetes) are also strong predictors of sub- sequent ischaemic events° Coronary artery calcium measurements might represent more mature athero- sclerotic lesions than forming or vulnerable plaques. The association between coronary artery calcium progression and air pollution has not been reported, although the plausibility of a causal relationship between air pollution and atherosclerosis is suggested through several mechanisms." In a cross-sectional analysis in the the Heinz -Nixdorf Recall study," coronary artery calcium was higher in individuals living near roads than in those who did not live near major roads. Our findings provide evidence that exposure to air pollution is associated with coronary artery calcium progression. Although coronary artery calcium progression was associated with PM2.5 and NOx, it was not associated with black carbon. Unlike the other pollutants, for which exposures were estimated between 1999 and 2012, black carbon exposures were limited to only spatial contrasts in 2006-08; hence, analyses could not capture the decreasing trends in pollutant concentrations recorded Women Men White Chinese Black Hispanic 45-54 years' 55-64 years' 65-74 years' 275 years' Not diabetic Impaired fasting glucose Diabetic No hypertension at baseline Hypertension at baseline BMI s30 kgim't BMI >30 kg/rn't HDL s1.03 mmat/Lf HDL 4.03 mmol/Lt Total cholesterol <5.17 mnwl/Lt Total cholesterol 5.17-6.21 mmol/Lt Total cholesterol >6 21 rnmoi/Lt 101 cholesterol <2.59 mmol/L# LDL cholesterol 2.59-3.36 mmol/Lt 101 cholesterol 336-444 mmol/Lf LDL cholesterol >4.14 mmol/Lt Never smokers Farmersmoker Current smoker ■ ■ ■ I 1 I I 1 T 1 -2 0 2 4 6 8 10 12 Change in coronary artery calcium progression per 5 pg/rn3 PM,5 (Agatston per year) Foxe* Assoriatiun between pollutant oonoerrtmtionsand coronary artery calcium progression. by imam participant dwacteristks The shaded region Indicates the 95% confidence lateral for theoverall association per 5 pe lm' of PM,5.'tinearadjustments for age were replaced with rategories.tlinearadjustmentsforadipositywere replaced with indicator for body -mass index >30 kg/m'. fianear acijustrnents for cholesterol were replaced with categories. 94ot adjusted for pack -years or second-hand smoke. during follow-up!' Additionally, coronary artery calcium progression was not as strongly associated with NO, as it was with total NOx. The total NOx is highest in the most near -road environments (measured in previous research as proximity to a major roadway or time in traffic); 2 and might better represent the group of primarily emitted traffic -related air pollutants present in these locations. Therefore, characterisation of NO,, exposure might be a better way to capture the effects of the near -road environ- ment on health. We noted a somewhat stronger association between PM2.5 and coronary artery calcium progression in hypertensive, in non -obese, and in individuals older than 65 years. The findings with age and hypertension suggest a synergistic association between air pollutants and these two strong risk factors for progression of atherosclerosis, though this association was not found for other strong risk factors such as diabetes or elevated cholesterol levels. The finding that pollutant associations with coronary www.thelancetoom Published online May 24, 2016 http://dx.doLong/10.1016/50140-6736(16)00378-0 7 Articles Fora full list of participating MESA investigators and institutinots see hrgx!}wnw. ,mesa-nhibi.cug artery calcium progression appeared stronger in non - obese participants is not what would be expected because iuflannnatory and metabolic consequences of obesity are thought to share mechanistic pathways with those of air pollutants." Although this study's sample size and precision provided adequate statistical power for the primary comparisons, analyses of effect modification were less well powered. Our findings for the effect of pollutants on coronary artery calcium progression were robust to a variety of sensitivity analyses and did not differ depending on stages of control of potential confounding variables. This result strengthens our confidence in these associations. In addition, air pollutant relationships were recorded whether the outcome was measured as an absolute or relative change in calcification. Although absolute change in the extent of calcifications was our a -priori outcome choice, assessment of the outcome as a relative change did suggest additional associations with NO, and ambient -derived PM2.5 that were not observed with the absolute change outcome. An association between air pollution and progression of carotid wall thickness has been noted in some, but not all, previous studies.2'2' An interim analysis's in MESA showed that exposure to a 2.5 pgJm3 higher PM2.5 concentration was associated with a 5 pin per year increase in intima- media thickness progression; the interim study used a tlULCtVIIt appioa it Ul irriagc drliltySla, a less -developed approach to exposure estimation, and a much shorter rr 1 � 1 x � r � period or follow-up. An observational stoup-- within clinical trial data showed associations between PAM 5 and intima- media thickness progression in some subgroups. Carotid wall thickness is a challenging outcome for observational studies because the change in intima-media thickness over time is small relative to the measurement error at each timepoint. The mechanism by which air pollution might accelerate atherosclerosis might also be unrelated to intima-media thickness, which is a marker of arterial injury rather than atherosclerosis per se? Unlike coronary artery calcium, change over time in intima-media thickness is not predictive of subsequent cardiovascular disease events in observational studies, although it is a commonly used outcome in pharmaceutical studies In MESA participants, coronary artery calcium has been a much stronger predictor of subsequent corollary heart disease events than intima-media thiekness.J° The MESA cohort provides an extraordinarily well characterised population in terms of potential confounders of the relationship between air pollution and cardiovascular disease. Nevertheless, residual confounding by unmeasured factors remains a possibility. Additionally, though we chose a -priori exposures and outcomes of interest, the presence of more than one exposure and outcome in our analyses could be criticised for including multiple comparisons. This study focused on the health effects of ambient - derived air pollutants on cardiovascular health. Our primary exposure metrics focused on concentrations of pollutants outside homes, although individuals spend time in specific micro -environments, including indoors. We developed the ambient -derived PM,., measure specifically to address this issue, to better characterise actual exposure to ambient PM2_5 by adjusting outdoor concentrations by time spent indoors and infiltration of particles into the home. Because these predictions tepiesent the product of two different modifiers of outdoor concentration (each imperfectly assessed and not available for all study participants) we believe that the additional error in exposure estimation was the primary driver for the weak associations reported for ambient -derived PM, 3. Full characterisation of time -location patterns and indoor exposures is notoriously difficult. Ascertainment of highly resolved, individualised micro -environmental exposure estimates over several years of follow-up is elusive, hence our primary exposure estimation approach relies on outdoor concentrations. In conclusion, evidence from this study provides strong biological support for the observation that long- term exposures to outdoor particulate matter and traffic - related air pollution, specifically PM2.; and Nil„, are related to �+tyhe development of atherosclerotic cardio- vascular disease. Contributors •t • •. . t - .t the t tit 'Ali authors contributed substantially to tun: kuntepuun vi design lil nit manuscript or the acquisition, analysis, or interpretation of data for the manuscript: All authors contributed to critical revision of the manuscript for important intellectual content. All authors approved the final version submitted JDK directed the MESA Air investigator team and the remaining investigators are listed alphabetically. Declaration of interests We declare no competing interests - Acknowledgments This research has been supported by a grant from the US Environmental Protection Agency's (EPA's) Science to Achieve Results (STAR) programme. This publication was developed under Assistance Agreement nnmher RD831697 awarded by the EPA to the University of Washington (WA, USA). It has not been formally reviewed by EPA. The views expressed in this document are solely those of the authors and do not necessarily reflect those of the Agency. EPA does not endorse any products or commercial services mentioned in this publication. MESA and work in this manuscript was supported by the National Heart, Lung, and Blood Institute (NHLBZ) through the fallowing grants and contracts: N01 -IBC -95159, N01 -HC -9576O, NO1-HC-95161, N41 HC -95162, NO1-HC-95163, N01 -HC -95164, N41 -HC -95165, NO1-HC-95166, NO1-HC-95167, NO1-HC-95168, N01 -HC -95169 by the National Center for Research Resources through ULI-TR-000040 and. UL1-` R-001079; and by the National Institute of Environmental Health Sciences th nazgh PSOES015915, P30ES(t7033, and K24ES013195. We thank the MESA Air participants as well as the staff and investigators ofthe MESA study fur their valuable contributions,. We also thank the members of our Fiternal Scientific Advisory Committee ittee (appendix) for their dedication and contributions to our work_ References1 Hoek C, Krishnan RM, Beelen R, et aL Long -terra air pollution exposure and cardio- respiratory mortality: a review Environ Health 2013; 12: 43_ 2 Bild DE, Bhtemke DA, Burke CL, et aL Multi -Ethnic Study of Atherosclerosis: objectives and design. Arn j Ella:mid 2002; 15& 871.81. 8 www.thelancet.com Published online May 24, 2016 fittp://dx.dobarg/101.016/50140-6736(16)4203713-0 Articles i 3 Kaufman ID, Mar SD, Allen RW, et al Prospective study of particulate air pollution exposures. subclinicai atherosclerosis, and clinical cardiovascular disease: The Multi -Ethnic Study of Alhem,sclerosis and Air Pollution (MESA Air). Ann f Epidemia4 2012; 176:825-37 4 Carr JJ, Nelson JC, Wong ND, et al, Calcified coronary artery plaque measurement with cardiac CT in population -based studies: standardized protocol of Multi -Ethnic Study of Atherosclerosis (MESA) and Coronary Artery Risk Development in Young Adults (CARDLA) study. Radiology 2005; 234: 35-43. 5 Budoff Mj, McClelland RL, Chung H, et al. Reproducibility of coronary attery calcified plaque with cardiac 64-MDCT: the Multi -Ethnic Study of Atherosclerosis. AIR Am). Roentgen°, 2009;19L- 613-07. 6 Tattersall MC, Gossett A, Karcarz CE, et al. Predictors of carotid thickness and plaque progression during a decade: the Multi -Ethnic Study of Atherosclerosis. Stroke 2014; 45: 3257-62. 7 Cohen M, Mar S. Allen R. et al. Approach to estimating participant pollutant exposures in the Multi -Ethnic Study of Atherosclerosis and Air Pollution (MESA Aix). Ertvimn Sci Ticlrno( 2009; 43:4687-93. 8 Kellen JP, Olives C, Kits. SY, et ale A unified spatiotemporal modeling approach for predicting concentrations of multiple air pollutants in the Multi -Ethnic Study of Atherosclerosis and Air Pollution. Environ. Health Perspect 2015; 123: 301-09. 9 Spilt ENV, Curl CL, Allen RW, et al. Three -location patterns of a diverse population ofolder adults: The Multi -Ethnic Study of Atherosclerosis and Air Pollution (MESA Air). J Expo Sci Eirviras Epidemiot 2015; published online April 29. DU1:10.1038/jes1015.29. 10 Allen RW, Mar SD, Avol E, et aL Modeling the residential infiltration of outdoor PM(2.5) in the Multi -Ethnic Study of Atherosclerosis and Mr Pollution (MESA Air). Environ Health Perspet 2012;120: 824-30. 11 Cassett Al, Sheppard 1, McClelland RL, et al. Risk factors for long-term coronary artery calcium progression in the Multi-Edmic Study of Atherosclerosis. J Am Heart Assoc 2015; 4: e001726. 12 United Statn Environmental Protection Agency. National ambient air quality standards for particulate matter: Fed gist 2013; 78: 3086-286. 13 Directive 2008/50/EC of the European Parliament and of the Council of 21 May 2008 on ambient air quality and cleaner air for Europe. http//eur-lexoumpa.eu(legakontent/EN/TXT/HTML/ ?urinCELE :3200 LA050&frnn EN (accessed April 30, 2015). 14 Brauer 14, Amara M, Burnett RT, et al. Exposure assessment for estimation of the global burden of disease attributable to outdoor air pollution. Ertvinm Sci Te chnol 2012; 46:652-60. 15 McEvoy JW, Blabs M J. Deflippis AP, et al. Coronary artery calcium progression: an important clinical measurement:?? A review of published reports../ Am Cott Carotid 2010; 54: 1613-22. 16 Sangiotgi G, Runtberger JA, Severson A, et at Arterial calcification and not lumen stenosis is Inertly co�l�� with atherosclerotic plaque burden in humans: a histologic study of 723 coronary artery segments using nondecakifying methodology. J Atn Cott Cardioi 1998; 3k 126-33. 17 Kronmal RA. McClelland RL, Detcano R, et al. Risk factors for the progression of coronary artery calcification in asymptomatic subjects —results from the Multi -Ethnic Study ofAtherosclerosis (MESA). Circulation 2007; 115: 2722-30. 18 Shaw LJ, Narula J, Chandrashekhar Y The never-ending story on coronary calcium: is it predictive, punitive, or protective? J Am Coll Cardio, 2015; 65:1283.85. 19 Cosseiman XE, Navas-Acien A, Kaufman JD. Envirnttunental factors in cardiovascular disease. Nat Rev Candid 2015;12: 627-42. 20 Hoffmann B, Moebus 5, Mobdenkamp S. et al. Residential exposure to traffic is associated with coronary atherosclerosis. Circulation 2007; 116: 489--96. 21 Murphy D, Chow J, Leibensperger E. et al. Decreases in elemental carbon and fine particle mass in the United States. Atoows Client Phys 2011,11.: 467916. 22 Karner AA, Eisinger DS, Niemeier DA. Near -roadway air quality: synthesizing the findings from real world data. Environ Sci Technol 2010; 44: 5334 44_ 23 Leutvta V, Uitetwaal C, Beeien R, et aL icing -terns lure to air pollution and vascular damage in yrtttatg adults. Epidemiology 2010; 2k 512-20. 24 Gan WQ, Allen RW, Brauer M, Davies 41W, Mancini GB, Dear SA. Long-term eposure to traffic -related air pollution and progression of carotid artery atherosclerosis: a prospective cohort study. BMJ Open 2014; 4c e004743. 25 Mar SD, Sheppard L, Vedal S. et al. Fine particulate air pollution and the progression of carotid intima-medial thickness: a prospective cohort study from. the Multi-Ethnnic Study of Atherosclerosis and Air Pollution. PIA'S Med 2013; 10: e1001430. 26 Krinzli N, Jerzett M, Garcia -Esteban R. et al. Ambient air pollution and the progression of atherosclerosis in adults. PLUS One 2010; 5: e9096. V Stein JH, Korean CE, Hurst RT, et al. Use of carotid ultrasound to identify subclinical vascular disease and evaluate cardiovascular disease risk: a consensus statement from the American Society of Echocardiography Carotid Intinn-Media Thickness Task Force. Endorsed by the Society for Vascular Medicine. J Am Sot Echouudi gr 2008; it 93-111. 28 Den Ruijter HM, Peters SA, Anderson TJ, et al. Common carotid intima-media thickness measurements in cardiovascular risk prediction: a meta -analysis. J Mn Med Assoc 2012; Mt 796-803. 29 Lorenz MW, Polak IF, Kavousi M, et at Carotid intima-media thickness progression to predict cardiovascular events in the general population (the PROC-IMTcollaborativ+e project): a meta -analysis of individual participant data. Lancet 2012; 379: 2053-62. 30 Gepner AD, Young IL Delaney JA, et at Comparison of coronary artery calcium presence, carotid plaque presence, and carotid intima-media thickness for cardiovascular disease prediction in the Multi -Ethnic Study of Atherosclerosis. Circ Esc Imaging 2015; 8: e002262. www.thelancetcom Published online May 24, 2016 http://dx.doi.org/10.1016/501404236(16)00378-0 9 Hello