# Appendix H Public Hearing Record

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## Public Hearing Record i The Charlotte-Gastonia-Rock Hill, NC-SC 8-Hour Ozone Appendix H North Carolina Reasonable Further Progress Demonstration November 30, 2009 

# Table of Contents

Hearing Officer’s Report ..................................................................................................... ...........1
Comment Letter: 10/15/2009, Kenneth Geathers, TAC Chair; Cabarrus Rowan Metropolitan Planning Organization .......................................................................................................10
Comment Letter: 11/13/2009, Eldewins M. Haynes, Air Quality Specialist for Charlotte DOT ..11
Comment Letter: 11/13/2009, Richard A. Schu tt, Chief of Air Planning Branch US Environmental Protectio n Agency Region 4 ....................................................................13
Comment Letter: 11/19/2009, June Bl otnick, Director of “Clean Ai r Carolina” submitted article “Long-Term Ozone Exposure and Mortality” (from www.nejm.org March 12, 2009) ....14
Comment Letter: 11/19/2009, June Bl otnick, Director of “Clean Ai r Carolina” submitted article “Is Healthy Air in Charlotte’s Future” ...............................................................................25
Comment Letter: 11/13/2009, J. David Farren, Senior Attorney, Director of Regional Transport Initiative, with Thomas Gremillion, Associ ate Attorney Sothern Environmental Law Center ........................................................................................................................ .........27
Letter: 11//2009, B. Keith Overcash, Response to US Environmental Protection Agency Region 4 11/13/2009 comment letter .............................................................................................48
Letter: 11//2009, B. Keith Overcash, Response to Southern Environmental Law Center 11/13/2009 comment letter ................................................................................................49

The Charlotte Observer Affidavit .............................................................................................. ....51

## Public Hearing Record ii The Charlotte-Gastonia-Rock Hill, NC-SC 8-Hour Ozone Appendix H North Carolina Reasonable Further Progress Demonstration November 30, 2009 

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## Metrolina RFP Demonstration Hearing Report November 19 2009 b.doc R. P. Fisher 

## MEMORANDUM
TO: Keith Overcash, Director, DAQ
FROM: Robert P. Fisher, RAQS, Washington RO

DATE: November 19, 2009
SUBJECT: Hearing Officer’s Report and Recommendations The North Carolina 8-Hour Ozone Reasonable Further Progress (RFP) Demonstration for the Charlotte-Gastonia-Rock Hill, NC-SC 8-Hour Ozone Nonattainment Area

As requested in an October 9, 2009 email from Ke ith Overcash, I served as the public hearing officer for the draft North Carolina 8-Hour Ozone RFP Demonstration for the CharlotteGastonia-Rock Hill, NC-SC 8-Hour Ozone Nonattainment Area.
The hearing was held on November 13, 2009 at th e Mecklenburg County Ai r Quality Office at 700 N. Tryon Rd in Charlotte, NC. Two (2) peopl e requested time to present oral comments out of approximately 6 people atte nding the hearing (not including NCDAQ or LUESA DAQ staff). I am recommending that this SIP be submitted to EPA with appropriate consideration of the hearing officer’s recommendations.
Four (4) people submitted written comments dur ing the public comment period. As announced at the hearing, the publ ic comment period officially closed on November 13, 2009. All comments are included in the hearing record. These comments and the hearing registration forms have been emailed to Laura Boothe , acting Chief of the DAQ Planning Section.
Attached is a copy of the hear ing report for the RFP Demonstr ation. The report contains a summary of the comments received, responses to the comments, th e hearing officer’s recommendations, the written comments received, and the p ublic notice.

I wish to thank DAQ staff member s who assisted me in my se arch for information and who assisted in the hearing: Laur a Boothe and George Bridgers; al so Ron Slack of the Mooresville Regional Office.

cc: Laura Boothe

# Hearing Officer's Report

North Carolina Division of Air Quality

Public Hearing on November 13, 2009

. 

# For The North Carolina 8-Hour Ozone Reasonable Further Progress Demonstration for the Charlotte-Gastonia- Rock Hill, NC-SC 8-Hour Ozone Nonattainment Area



# November 19, 2009

Robert P. Fisher - Hearing Officer Regional Air Quality Supervisor Washington Regional Office Washington, North Carolina

Robert P. Fisher

, 

## ((/I~/~ 'f



### Date

Metrolina RFP Demonstration Hearing Report November 19 2009.doc Page 2 of9

## Metrolina RFP Demonstration Hearing Report November 19 2009 b.doc R. P. Fisher 

# Overview & Introduction

On November 13, 2009 a public hearing was held for the draft North Carolina 8-Hour Ozone Reasonable Further Progress (RFP) Demonstration for the Charlo tte-Gastonia-Rock Hill, NC-SC 8-Hour Ozone Nonattainment Area (Cabarru s, Gaston, Lincoln, M ecklenburg, Rowan, Union Counties and Coddle Creek and Davidson Town ships in Iredell County). The hearing was conducted in Auditorium 1 at the Mecklenburg County Services Center , 700 North Tryon Street, Charlotte, North Carolina. The purpose of the public hearing was to inform interested parties about the RFP Demonstration and solicit comment s from the public. The public comment period closed on November 13, 2009.
According to the public hearing registration forms, a total of six (6) people attended the hearing, not including North Carolina Division of Air Qu ality (NCDAQ) or Land Use and Environmental Services Agency (LUESA) Mecklenburg County Airy Quality (MCAQ) staff, and two (2) people requested time to present oral comments. Written comments were received from the Cabarrus Rowan Metropolitan Planning Organization (CRMPO ), Charlotte Department of Transportation (CDOT), the United States Environmental Protection Agency (USEPA), Southern Environmental Law Center (SELC ), and Clean Air Carolina.

Kenneth Geathers, TAC Chair of CRMPO, submitted written comments received on October 15, 2009. Eldewins M. Haynes, Air Quality Specia list with the CDOT submitted comments via email on November 13, 2009. Also on November 13, 2009, Richard A. Schutt, Chief of Air Planning Branch of USEPA, Region 4, submitted co mments via email. June Blotnick, Director of “Clean Air Carolina” submitted two articles dir ectly to the hearing officer at the hearing. J. David Farren, Seniour Attorney, Director of Re gional Transportation Ini tiative, with Thomas Gremillion, Associate Attorney, both of the S ELC, submitted written comments via email on November 13, 2009.

Based on the information contained in th is report, I recommend the following:

I recommend that the “North Carolina 8- Hour Ozone Reasonable Further Progress Demonstration for the Charlotte-Gastonia-Rock Hill, NC-SC 8-Hour Ozone Nonattainment Area (Cabarrus, Gaston, Lincoln, Mecklenburg, Ro wan, Union Counties and Coddle Creek and Davidson Townships in Iredell County)” be approved for submittal to the USEPA after addressing the hearing officer’s recommendations as described in the body of this report.

### Metrolina RFP Demonstration Hearing Re port November 19 2009 b.doc Page 2 of 9 

## Hearing Officer’s Report For The North Carolina 8-Hour Ozone Reasonable Further Progress Demonstration for the Charlotte-Gastonia-Rock Hill, NC-S C 8-Hour Ozone Nonattainment Area

November 19, 2009

Robert P. Fisher
On November 13, 2009 a public hearing was held for the draft North Carolina 8-Hour Ozone Reasonable Further Progress (RFP) Demonstration for the Charlo tte-Gastonia-Rock Hill, NC-SC 8-Hour Ozone Nonattainment Area (Cabarru s, Gaston, Lincoln, M ecklenburg, Rowan, Union Counties and Coddle Creek and Davidson Town ships in Iredell County). The hearing was conducted in Auditorium 1 at the Mecklenburg County Services Center , 700 North Tryon Street, Charlotte, North Carolina. The purpose of the public hearing was to inform interested parties about the RFP Demonstration and solicit comment s from the public. The public comment period closed on November 13, 2009.
Background (borrowed from the draft plan)
In July 1997, the United States Environmental Protection Agency (USEP A) promulgated a new 8-hour ozone NAAQS, setting a standard at 0.08 parts per million (ppm) averaged over an 8- hour period. Section 182(b)(1) of the Cl ean Air Act Amendments (CAAA) mandates a 15 percent volatile organic compounds (VOC) emi ssion reduction, accounting for growth, in the first six years after the baseli ne year (2002) for Moderate an d above ozone nonattainment areas. Thus, for the Charlotte-Gastonia-Rock Hill, NC -SC 8-hour ozone nonattainment area (referred to as the Metrolina area), a RFP analysis between 2 002 and 2008 is required.
The methodology the North Carolina Division of Air Quality (NCDAQ) us ed to calculate the RFP target levels of VOC emissions is base d on the method developed in the CAAA, while taking into account the restrict ions on creditable emissions and the need to use the 2002 inventory as a baseline. Since th e actual 2008 VOC emissions were ca lculated to have been well below the target level, RFP is demonstrat ed for the Metrolina nonattainment area.
The NCDAQ must also show continued progre ss from 2008 through the attainment date. To do so, the NCDAQ calculated the expect ed benefits from the fleet turnover for the on-road and offroad mobile sectors. Based on modeling emissions for 2009 and 2011, the NCDAQ expects approximately 14 tons per day of nitrogen oxi des (NOx) emissions reductions from fleet turnover, demonstrating continued reasonable further progress toward attainment beyond 2008.
Another requirement of the RFP demonstration is that VOC motor vehicle emission budgets (MVEBs), for transportation conformity purposes, need to be set for the RFP milestone year 2008. This means that the level of emissions estimated by the North Carolina Department of Transportation or the metropolitan planning orga nizations for the Transportation Improvement Program and Long Range Transportation Plan must not exceed the MVEBs as defined in this

### Metrolina RFP Demonstration Hearing Re port November 19 2009 b.doc Page 3 of 9 

## RFP demonstration. The NCDAQ is setting MVEB , for transportation conformity purposes, as county budgets within the Metrolina nonattainment area. For purposes of SIP strengthening, the NCDAQ has additionally esta blished NOx MVEBs for 2008.
Summary of Public Hearing and Comment Period
According to the public hearing registration forms, a total of six (6) people attended the hearing, not including NCDAQ or Land Use and Environm ental Services Agency (LUESA) Mecklenburg County Airy Quality (MCAQ) staff, and two (2) pe ople requested time to present oral comments. Written comments were received from the Cabarrus-Rowan Metropolitan Planning Organization (CRMPO), the Charlotte Department of Tr ansportation (CDOT), the USEPA, Southern Environmental Law Center (SELC ), and Clean Air Carolina (formerly Carolinas Clean Air Coalition). It is my opinion that the concerns ra ised by the interested parties can be adequately addressed by the NCDAQ.
The public comment period was open until 11:59PM on November 13, 2009. Two people spoke at the public hearing: June Blotnick, Director of Clean Air Carolina; and Thomas Gremillion, Associate Attorney for the SELC. During the pub lic comment period the Hearing officer did not receive any phone calls commen ting on the public notice.

Kenneth Geathers, TAC Chair CRMPO, submitted written comments received on October 15, 2009. Thomas Gremillion, Associate Attorney fo r the SELC submitted via email a written version of the oral comments he presented on November 13, 2009. June Blotnick, Director of Clean Air Carolina, at the hearing submitted to th e Hearing Officer two articles: one about public health effects of long-term ozone exposure; a nd the other about air po llution levels in the Charlotte area. Eldewins M. Haynes, Air Qual ity Specialist with the CDOT submitted comments via email on November 13, 2009. Also on November 13, 2009, Richard A. Schutt, Chief of Air Planning Branch of US EPA Region 4 submitted comments via email.

The following is a summary of the pertinent co mments, with regard to NCDAQ’s jurisdiction, raised by all parties involved in the public hearing process along with the Hearing Officer’s opinions and recommendations. Some comments received were very extensive and touched on a number of somewhat related issu es. This report does not attempt to address comments that are not applicable to the R FP demonstration SIP.
Clean Air Carolina (CAC): June Blotnick, Director of Cl ean Air Carolina, provided oral comments at the public hearing. Ms. Blotnick stated that CAC had signed on to the Southern Environmental Law Center’s writte n comments, which are discussed below. The issues raised in the CAC comments were the health issues surro unding ozone and the increase in adult onset asthma. Ms. Blotnick stated th at the NCDAQ needed to be much more proactive and that the revised RFP SIP did not establish any new programs. Ms. Blotnick stated that the State needed to do something because what has been done is notworking and she provided to articles relating to health issues and ozone. These articles are attached to this report.

### Metrolina RFP Demonstration Hearing Re port November 19 2009 b.doc Page 4 of 9 

## Hearing Officer’s Response: The CAC were more directed at health issues relating to ozone. The NCDAQ disagrees with Ms. Blotnick’s st atement that the programs that have been established are not working. North Carolina ha s continued to see improvements in the air quality due to programs that have been establis hed. When designations were made for the 1997 8-hour ozone standards, the majority of the m onitors across the State were violating the standard. Today, only one monitor in the State is slightly above th e 1997 standard, and this monitor observed clean data in 2009. Her one co mment relevant to the RFP SIP was that the revised RFP SIP did not establish any new programs. This revision was not to address new programs but rather address an issue that the US EPA recently raised with the original RFP SIP. The hearing officer does not believe any action, re garding the RFP SIP, is needed to address the CAC comments.

CDOT : CDOT submitted written comments receiv ed on November 13, 2009 that in general supports the RFP SIP. CDOT believes that re gional motor vehicle emission budgets (MVEBs) would be more appropriate; however they co nceded that they can work with the MVEBs recommended in the RFP SIP.
Hearing Officer’s Response: No further action is required by the NCDAQ.

CRMPO: CRMPO submitted written comments received on October 15, 2009, which endorsed the RFP SIP and corresponding county leve l MVEBs for Cabarrus and Rowan Counties.
Hearing Officer’s Response: No further action is required by the NCDAQ.

USEPA: The USEPA submitted written comments received on November 13, 2009. The first comment requested that the NCDAQ provide the source of data us ed to develop the population estimates for Coddle Creek and Davidson townships used to adjust the partial county estimates for Iredell County. The second comment requested that the NCDAQ indicate the list of specific Maximum Achievable Control Technology standa rds that were used to develop the 2008 inventory for the nonattainment area.
Hearing Officer’s Response: The USEPA comments do not hi ghlight anything controversial that cannot be addressed by the NCDAQ prior to the final submittal. The hearing officer recommends that the NCDAQ address the comments prior to the final submittal.

SELC: SELC submitted written comments receivedon November 13, 2009 and also spoke at the public hearing reiterating th eir written comments. Since there were numerous comments from SELC, the comments will be generally grouped and addressed separately by the hearing officer. The first comment incorporated by reference the comments SELC sent to South Carolina officials on their portion of the attainment demonstration.
Hearing Officer’s Response: These comments all deal with an attainment demonstration for the area and are not applicable to the RFP SIP. Ther efore, these comments will not be addressed in this hearing officer’s report.

### Metrolina RFP Demonstration Hearing Re port November 19 2009 b.doc Page 5 of 9 

## SELC: SELC stated that the NCDAQ should voluntar ily reclassify the Metrolina region to “Serious” nonattainment since the area has effectively failed to m eet the applicable attainment date for the 1997 8-hour ozone standard.
Hearing Officer’s Response: This comment is not applicable to the RFP SIP; however, the NCDAQ disagrees that the region should be recl assified to Serious. Although the region’s 3- year design value is slightly over the 1997 8-hour ozone standard, the region has clean data for 2009 and the NCDAQ believes that the area meets the requirements necessary request a 1-year extension of the attainment date. The hearing officer does not believe any action, regarding the RFP SIP, is needed to address this comment.

SELC: The proposed RFP SIP retroactively es tablishes MVEBs for the year 2008. SELC recommends refocusing air quality resources on pros pective strategies to improve air quality and meet future attainment challenges instead of a retrospective analysis that falls outside the regulatory scheme contemplated by the Clean Air Act (CAA).
Hearing Officer’s Response: The CAA requires that volati le organic compounds (VOC) MVEBs be set for the RFP milestone year, which, for a m oderate nonattainment area, is 2008. In the original RFP SIP submitted to the USEPA on 6/ 15/07, the NCDAQ had not set MVEBs since we believed that the mobile source VOC emissions we re insignificant to ozone formation. In September 2009, the USEPA informed the NCD AQ that they would not approve the insignificance finding for the Metrolina nonattainment area. Th erefore, in order to meet the CAA requirements, the NCDAQ had to revise the RFP SIP to include MVEBs for 2008. The hearing officer does not believe any action, regarding the RFP SIP, is needed to address this
comment.

SELC: SELC states “The “purpose of ‘reasonable further progress’ is to ensure attainment by the applicable attainment date. ... ... But the Metrolin a area has now conclusively failed to meet the applicable attainment date for the 1997 effec tive ozone air quality standard of 84 parts per billion (ppb). Consequently, the proposed RFP-SIP is of questio nable relevance to solving the Metrolina area’s ozone problem. ... ... ... Submi ssion of the proposed RFP-SIP would not only fail to advance the Metrolina area’s progress in meeting existing legal requirements, it would also delay efforts to attain even stronger anticipated standards, which will be a major challenge for the region.”
Hearing Officer’s Response: The purpose of the RFP SIP is to demonstrate that the region is making progress in reducing ozone precursors and making progress to wards attaining the standard. The CAA requires the first RFP SIP to re duce VOC emissions by 15% within six years of the base year. The RFP SIP clearly demonstrates this reduction. The RFP SIP was submitted to the USEPA on time and this revision is to addr ess an issue with the RFP SIP that the USEPA recently informed the NCDAQ about. It is un clear how addressing the USEPA’s concern with the original RFP SIP would fail to advance th e Metrolina area’s pr ogress in meeting the standard or delay efforts to attain any future standard. The hearing officer does not believe any action, regarding the RFP SIP, is needed to address this comment.

### Metrolina RFP Demonstration Hearing Re port November 19 2009 b.doc Page 6 of 9 

## SELC: The proposed RFP-SIP will not help the st ate to qualify for an extension of the attainment deadline beca use it is untimely.
Hearing Officer’s Response: The original RFP SIP was submitted to the USEPA on time and has been waiting for action by the USEPA. The intension of the proposed revisions to the RFP SIP are to address issues recently raised by the USEPA on the original submission and not to help the State qualify for an extension of the atta inment deadline. The hearing officer does not believe any action, regarding the RFP SIP, is needed to address this comment.

SELC: South Carolina officials’ failure to collaborate on the pr oposed RFP SIP underscores the inappropriateness of the plan as well.
Hearing Officer’s Response: The RFP SIP must be submitted by each state for their portion of the nonattainment area. The NCDAQ has decided to move forward with addressing the USEPA concerns with the North Carolina RFP SIP and it will be up to South Carolina to address any comments from the USEPA regarding their RFP SIP. The hearing officer does not believe any action, regarding the RFP SIP, is needed to address this comment.

SELC: The proposed RFP SIP is a distraction from the challenge of cl eaning up the Metrolina area’s unhealthy air – now the worst smog in the South. North Carolina officials should prepare a new SIP revision consistent wi th the Metrolina area’s legally required bump-up to “Serious” status and the State should focus efforts on ac tually achieving the tough new standards on the horizon.
Hearing Officer’s Response: Although SELC believes the proposed revisions to the RFP SIP is a distraction from the challenge of improving ai r quality, this revision is required by the USEPA in order for the RFP SIP to be approved. The USEPA is reconsidering what the ozone standard should be set at and it will be 2010 before a new standard is promulgated. However, the NCDAQ is not waiting until a new standard is established before starting the SIP process. The NCDAQ has already started modeling analysis effo rts to determine what additional controls will be needed to meet whatever le vel the standard is established at . Additionally, the NCDAQ has been working to reduce the mobile sector of emissions by developing an idle reduction rule for heavy duty vehicles and applying for and being awarded competi tive diesel emission reduction grants from the USEPA. These diesel emission re duction grant funds will be used to reduce the on-road as well as off-road mobile source sector emissions. The hearing officer does not believe any action, regarding the RFP SIP, is needed to address this comment.

Recommendation: Based on the information contained in this re port, I recommend approva l of the draft North Carolina 8-Hour Ozone Reasonable Further Prog ress Demonstration for the Charlotte-GastoniaRock Hill, NC-SC 8-Hour Ozone NonattainmentArea (Cabarrus, Gaston, Lincoln, Mecklenburg, Rowan, Union Counties and Coddle Creek and Davidson Townships in Iredell County).

### Metrolina RFP Demonstration Hearing Re port November 19 2009 b.doc Page 7 of 9 

## Attachments to Report: (1) Kenneth Geathers, TAC Chair, CRMPO written comments dated October 15, 2009.

(2) Eldewins M. Haynes, Air Quality Speciali st for the CDOT written comments dated November 13, 2009.

(3) Richard A. Schutt, Chief of Air Planning Br anch of USEPA, Region 4, written comments dated November 13, 2009.

(4) June Blotnick, Director of “Clean Air Caro lina” submitted two articles directly to the hearing officer at the hearing:

a. “Long-Term Ozone Exposure and Morta lity” (Downloaded from www.nejm.org March 12, 2009) b. “Is Healthy Air in Charlotte's Future?”

(5) J. David Farren, Seniour Attorney, Director of Regional Transporta tion Initiative, with Thomas Gremillion, Associate Attorney, bot h of the SELC written comments dated November 13, 2009.

lab/rpfl' heN EWE N G LAN 0 J 0 URN A L of M E 0 I C I N E

II ORIGINAL ARTICLE


# Long-Term Ozone Exposure and Mortality

MichaelJerrett, Ph.D., Richard T. Burnett, Ph.D., C. Arden Pope III, Ph.D., I<azuhiko Ita, Ph.D., George Thurston, Sc.D., Daniell<rewski, Ph.D., Yuan Ii Shl, M.D., Eugenia Calle, Ph.D., and Michael Thun, M.D.

ABSTRACT

BACKGROUND 

### Although many studies have linked elevations in tropospheric ozone to adverse health outcomes, the effect oflong-term exposure to ozone on air pollution-related mortality remains uncertain. We examined the potential contribution of exposure to ozone to the risk of death from cardiopulmonary causes and specifically to death from respiratory causes.

METHODS 

### Data from the study cohon of the American Cancer Society Cancer Prevention Study II were correlated with air-pollution data from 96 metropolitan statistical areas in the United States. Data were analyzed from 448,S50 subjects, with l1S,777 deaths in an IS-year follow-up period. Data on daily maximum ozone concentrations were obtained from April 1 to September 30 for the years 1977 through 2000. Data on concentrations of fine particulate matter (particles that are ~.5 JLm in aerodynamic diameter [PM2.J) were obtained for the years 1999 and 2000. Associations between ozone concentrations and the risk of death were evaluated with the use of standard and multilevel Cox regression models.

RESULTS 

### In single-pollutant models, increased concentrations of either PM2.5or ozone were significantly associated with an increased risk of death from cardiopulmonary causes. In two-pollutant models, PM2.5was associated with the risk of death from' cardiovascular causes, whereas ozone was associated with the risk of death from respiratory causes. The estimated relative risk of death from respiratory causes that was associated with an increment in ozone concentration ofl0 ppb was 1.040 (95% confidence interval, 1.010 to 1.067). The association of ozone with the risk of death from respiratory causes was insensitive to adjustment for confounders and to the type of statistical model used.

CONCLUSIONS 

### In this large study, we were not able to detect an effect of ozone on the risk of death from cardiovascular causes when the concentration ofPM2.5was taken into account.We did, however, demonstrate a significant increase in the risk of death from respiratory causes in association with an increase in ozone concentration.

N ENGLJ MED 360;11 NEJM.ORG MARCH 12,2009

Downloaded from _.nejm.org by on March 12, 2009 . Copyright e 2009 Massachusetts Medical Society. ADrights reserved. II

From the University of California, Berkeley (MJ.); Health Canada, Ottawa (R.T.B.); Brigham Young University, Provo, UT (C.A.P.); New York University School ofMedicine, New York (K.I., G.T.); the University of Ottawa, Ottawa (D.K., Y.S.); and the American Cancer Society, Atlanta (E.C., M.T.). Address reprint requests toDr. Jerrett at the Division of Environmental Health Sciences, School of PublicHealth, University of California, 710 University Hall, Berkeley, CA 94720, or at jerrett@berkeley.edu.

N EnglJ Med 2009;360:1085-95. ~ 0 2009A_~ Medit:oISociety.

1085rhe NEW ENGLAND JOURNAL o(MEDICINE

TUDIES CONDUCTED OVER THE PAST 15 

### years have provided substantial evidence that long-term exposure to air pollution is a risk factor for cardiopulmonary disease and death.1-5Recent reviews of this literature suggest that rrne particulate matter (particles that are ~2.5 #Lm in aerodynamic diameter [PM2.J) has a primary role in these adverse health effects.6,7The particulate-matter component of air pollution includes complex mixtures of metals, black carbon, sulfates, nitIates, and other direct and indirect byproducts of incomplete combustion and high-temperature industrial processes. Owne is a single, well~efined pollutant, yetthe effect of exposure to owne on air pollutionrelated mortality remains inconclusive. Several studies have evaluated this issue, but they have been short-term studies,8-10have fuiled to show

a

. 

### statistically significant effect, 1,3 

### or have been 

### based on limited mortalitydata. 11 

### Recentreviews by the Environmental Protection Agency (EPA)12and the National Research CouncilB have questioned the overall consistency of the availabledata correlating exposure to ozone and mortality. Similar conclusions about the evidence base for the long-term effects of owne on mortality were drawn by a panel of experts in the United Kingdom.14 Nonetheless, previous studies have suggestedthat a measurable efrect of owne may exist, particularly with respect to the risk of death from cardiopulmonary causes. In one of the larger studies, owne was significantly associated with death from cardiopulmonary causes15 but notwith death from ischemic heart disease. However, the estimated effect of ozone on the risk of death from cardiopulmonary causes in this study was attenuated when PM2.5was added to the analysis in copoQutant models. On the basis of suggested effects of ozone on the risk of death from cardiopulmonary causes (which includes

. 

### death from respiratory causes) but an absence of evidence fur effects of ozone on the risk of death from ischemic heart disease, we hypothesized that ozone might have a primary effect on the risk of death from respiratory causes.

METHODS

HEALTH, MORTALITY, AND CONFOUNDING DATA 

### Our study used data from the American CancerSociety Cancer Prevention Study n (CPS II) cohort.16 The CPS n cohort consists of more than

1086 

### 1.2 million participants who were enrolled byAmerican Cancer Society volunteers between September 1982 and February 1983 in all 50 states,the District of Columbia, and Puerto Rico. Enrollment was restricted to persons who were at least 30 years of age living in households with at leastone person 45 years of age or older. After providing written informed consent, the participantscompleted a confidential questionnaire that included questions on demographic characteristics,smoking history, alcohol use, diet, and educatiOn.17Deaths were ascertained until August 1988 by personal inquiries of family members by thevolunteers and thereafter by linkage with the National Death Index. Through 1995, death certificates were obtained and coded fur cause of death. Beginning in 1996, codes for cause of death were provided by the National Death Index.18The study population fur our analysis included only those participants in CPS n who resided in U.S. metropolitan statistical areas within the 48 contiguous states or the District of Columbia(according to their address at the time of enrollment) and fur whom data were available from at least one pollution monitor within their metr0-politan area. The study was approved by the 0ttawa Hospital Research Ethics Board, Canada. Data on "ecologic" risk factors at the level ofthe metropolitan area representing social variables (educational level, percentage ofhomes with air conditioning, percentage of the populationwho were nonwhite), economic variables (household income, unemployment, income disparity), access to medical care (number of physicians andhospital beds per capita), and meteorologic variables were obtained from the 1980 U.S. Censusand other secondary sources (see the Supplementary Appendix, available with the full text of this article at NE}M.org). These ecologic risk factors, as well as the individual risk factors collected in the CPS n questionnaire, were assessed as p0- tential confuunders of the effects of owne.3,5,19,20

ESTIMATES OF EXPOSURE TO AIR POLLUTION 

### Ozone data were obtained from 1977 (5 years befure the identification of the CPS n cohort) through 2000 fur all air-pollution monitors inthe study metropolitan areas from the EPA'sAerometric .Information Retrieval System. Ozone dataat each monitoring site were collected on an hourly basis, and the daily maximum value fur the site was determined. All available daily maximum values fur the monitoring site were averaged over

N ENGLJ MEO 360;11 NEJM.ORG MARCH 12, 2009

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### each quarter year. The quarterly average values were reported for each monitor only when at least 75% of daily observations for that quarter were available. The averages of the second (April throughJune) and third Guly through September) quarters were calculated for each monitor if both quarterly averages were available. The periodfrom April through September was selected because ozone concentrations tend to be elevated during the warmer seasons and because £ewer data were available for the cooler seasons. The average of the second and third quarterly averages for each year was then computed for all the monitors within each metropolitan area to form a single annual time series of air-pollution measurements fur each metropOlitan area fur theperiod from 1977 to 2000. In addition, a summary measure of long-term exposure to ambient warm-season ozone was dermed as the average of annual time-series measurements during theentire period from 1977 to 2000. Individual measures of exposure to ozone were then dermed by assigning the average for the metropolitan area to each cohort member residing in that area. Data on exposure to PM:z..swere also obtainedfrom the Aerometric Information Retrieval System database for the 2-year period from 1999 to 2000 (data on PM2.s were not available before 1999 for most metropolitan areas).s The average concentrations of PM:z..swere included in our analyses to distinguish the effect of particulates from that of ozone on outcomes.

STATISTICAL ANALYSIS

### Standard and multilevel random-effects Cox proportional-hazard models were used to assess therisk of death in relation to exposures to pollution. The subjects were matched according to age (in years), sex, and race. A total of 20 variables with 44 terms were used to control for individual characteristics that might confound or modify the association between air pollution and death. These variables, which were considered to be of potential importance on the basis of previous studies, included individual risk.fuctors for whichdata had been collected in the CPS n questionnaire. Seven ecologic covariates obtained from the 1980 U.S. Census (median household income, the proportion of persons living in households with an income below 125% of the poverty line, the percentage of persons over the age of16 years who were unemployed, the percentage of adults with less than a high-school [12th-grade] education, the percentage of homes with air conditioning, the Gini coefficient of income inequality [ranging from 0 to I, with 0 indicating an equal distribution of income and 1 indicating that one person has all the income and everyone else has no income2o:J,and the percentage of persons who were white) were also included. These variables were included at two levels: as the average for the metropolitan statistical area and as the clifrerencebetween the average for the ZIP Code of residence and the average for the metropolitan statistical area. Additional sensitivity analyses wereundertaken for ecologic variables that were available for only a subgroup of the 96 metropolitanstatistical areas (see the Supplementary Appendix). Models were estimated for either ozone or PM2.s.In addition, models with both PM:z..sand QZOnewere estimated. In additional analyses, our basic Cox models were modified by incorporating an adjustment fur community-level random effects, which allowedus to take into account residual variation in mortality among communities.21 The baseline hazard function was modulated by a community-specific random variable representing the residual risk ofdeath for subjects in that community after individual and ecologic risk fuctors had been controlled for (see the Supplementary Appendix). A formal analysis was conducted to assess whether a threshold existed for the association between exposure to ozone and the risk of death (see the Supplementary Appendix). A standard threshold model was postulated in which there was no association between exposure to ozone and the risk of death below a specified threshold co~ntration~aMearassocia~~nthe logarithmic scale of the proportional-hazards model) above the threshold. The question of whether specific time windowswere associated with the health effects was investigated by subdividing the follow-up interval into four periods (1982 to 1988, 1989 to 1992, 1993 to 1996, and 1997 to 2000). Exposures were matched for each of these periods and also tested for alQ-year average on the basis of the 5-year followup period and the 5 years befure the follow-up period (see the Supplementary Appendix).

RESULTS

The analytic cohort included 448,850 subjects residing in 96 metropolitan statistical areas (Fig. 1).

N ENGLJ MED 360;11 NEJM.ORG MARCH 12,2009 1087

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# fJ

o Colorado Springs 

# G

Portlani.:.t 

# r

Providence



# ~

" LasVeg<1ls 

# .

.. Angeles-longBeach 

## .hoen;,



# ~ EIPaso 

# . . .h,evepon.

. cb:<illcksonvillC!: Ozone (ppb)

.

. Houst~n N"'<


# ~ . o 33.3-53.1 

# ~ sanAnt~"'o 

# .~ ,,"



# . 53.2-57.4 

### tJc 7
Ch . FO~ lauderdalt>-Hollywood orpus flstl i


# . 57.5-62.4



# . 62.5-104.0 ,... Wichita o



# . 

# .

Figure 1. Ozone Concentrations in the 96 Metropolitan Statistical Areas in Which Members ofthe American Cancer Society Cohort Resided in 1982. The average exposures were estimated from 1 to 57 monitoring sites within each metropolitan area from April 1 to September 30 for the years 1977 through 2000.

1088 In 1980, the populations of these 96 areas ranged

from 94,436 to 8,295,900. Data were available on the concentration of ambient ozone from all 96 areas and on the concentration of PM2.s from 86areas. The average number of air-pollution monitors per metropolitan area was 11 (range, 1 to 57), and more than 80% of the areas had 6 or more monitors. The average ozone concentration for each metropolitan area during the interval trom 1977 to 2000 ranged trom 33.3 ppb to 104.0 ppb (Fig. 1). The highest regional concentrations were in Southern California and the lowest in the PacificNorthwest and parts ofthe Great Plains. Moderately elevated concentrations were present in many areas of the East, Midwest, South, and Southwest.The baseline characteristics of the study population, overall and as a function of exposure to ozone, are presented in Table 1. The mean age of the cohort was 56.6 years, 43.4% were men, 93.7% were white, 22.4% were current smokers, and 30.5% were former smokers. On the basis of estimates from 1980 Census data, 62.3% of homes had air conditioning at the time of initial data collection. During the 18-year follow-up period (from initial CPS II data collection in 1982 through the end of follow-up in 2000), there were 118,777 deaths in the study cohort (Table 2). Of these,58,775 were trom cardiopulmonary causes, including 48,884 from cardiovascular causes (of which 27,642 were due to ischemic heart disease) and 9891 £fom respiratory causes. In the single-pollutant models, exposure to ozone was not associated with the overall risk of

. death (relative risk, 1.001; 95% confidence inter

### val [CI],0.996 to 1.007) (Table 3). However, it was significantly correlated with an increase in the risk of death from cardiopulmonary causes. A

N ENGl) MED 360;11 NE)M.ORG MARCH 12, 2009

Downloaded from www.nejm.org by on March 12,2009. Copyright@ 2009 Massachusetts Medical Society. All rights reserved.Table 1. Baseline Characteristics of the Study Population in the Entire Cohort and According to Exposure to Ozone.'"

Entire Cohort Variable (N=448,850) Concentration of Ozone 33.3-53.1 ppb 53.2-57.4 ppb 57.5---62.4 ppb 62.5-104.0 ppb (N

= 126,206) (N =95,740) (N

= 106,545) (N=120,359)

No.ofMSAs 96 24 24 24 24

No. ofMSAs with data on PM2.s 86 21 20 23 22 Concentration ofPM2.s (j.Ig/m3) 11.9x2.5 13.h2.9 14.h2.1 15.4x3.2

Individual risk factors Age (yr) 56.6xlO.5 56.hlO.4 56.4xlO.7 56.h10.4 56.9x10.5 Male sex (%) 43.4 43.5 43.1 43.5 43.2 White race (%) 93.7 94.3 95.1 93.9 91.8 Education (%) Less than high school 12.1 11.5 13.6 12.1 11.6 High school 30.6 30.2 33.6 32.1 27.4 Beyond high school 57.3 58.3 52.8 55.8 61.0 Smoking status

Current smokers Percentage of subjects 22.4 22.0 23.5 22.2 21.9 No. of cigarettes/day 22.0x12.4 22.0x12.3 22.0x12.5 22.2x12.5 21.9x12.4 Duration of smoking (yr) 33.5Il1.0 33.4xlO.8 33.4x11.1 33.4x11.0 33.9x11.2 Started smoking <18 yr of age (%) 9.6 9.3 10.5 9.4 9.3 Started smoking ;,18 yr of age (%) 13.2 13.3 13.4 13.3 13.0

Former smokers Percentage of subjects 30.5 31.2 30.8. 29.5 30.4 No. of cigarettes/day 21.6x14.7 2L6x14.6 22.2x15.1 21.6x14.6 21.h14.6 .Duration of smoking (yr) 22.2x12.6 22.h12.5 22.6x12.6 22.0x12.5 22.401012.7 Started smoking <18 yr of age (%) 11.9 11.8 12.7 11.5 11.8 Started smoking ;,18 yr of age (%) 18.5 19.3 17.9 17.9 18.5 Exposure to smoking (hr/day) 3.h4.4 3.2x4.4 3.4x4.5 3.4x4.5 3.h4.4 Pipe or cigar smoker only (%) 4.1 4.0. 4.2 4.3 3.8
Marital status (%)

Married 83.5 84.2. 83.0 83.7 83.1 Single 3.6 3.4 4.0 3.8 3.2 Separated, divorced, or widowed 12.9 12.4 13.0 12.5 13.7 OZONE AND AIR POLLUTION-RELATED MORTALITY

10-ppb increment in exposure to ozone elevated the relative risk of death from the following causes: cardiopulmonary causes (relative risk, 1.014; 95% CI, 1.007 to 1.022), cardiovascular causes (relative risk, 1.011; 95% CI, 1.003 to 1.023), ischemic heart disease (relative risk, 1.015; 95% CI, 1.003 to 1.026), and respiratory causes (relative risk, 1.029; 95% CI, 1.010 to 1.048).Inclusion of the concentration of PM2.5 measured in 1999 and 2000 as a copoIIutant (Table 3) attenuated the association with exposure to ozonefor all the end points except death from respiratory causes, for which a significant correlation persisted (relative risk, 1.040; 95% CI, 1.013 to 1.067). The concentrations of ozone and PM2.5 were positively correlated (r=O.64 at the subject level and r=0.56 at the metropolitan-area level),resulting in unstable risk estimates for both pollutants. The concentration of PM2.5 remainedsignificantly associated with death from cardioN ENGlJ MEO 360;11 NEJM.ORG MARCH 12, 2009 1089

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Table 1. (Continued.)

Entire Cohort Variable (N=448,850) Concentration of Ozone 33.3-53.1 ppb 53.2-57.4 ppb 57.5-62.4 ppb 62.5-104.0 ppb (N

= 126,206) (N =95,740) (N

= 106,545) (N

= 120,359) Body.mass index"! 25.h4.1 25.h4.1 25.h4.2 25.h4.1 24.8z4.0 level of occupational exposure to particulate matter (%):j:

0 50.7 50.9 50.0 50.8 51.0
13.3 13.4 13.1 13.3 13.3

2 11.4 11.5 10.8 11.4 11.9

3 4.6 4.7 4.8 4.6 4.5
4 6.1 6.2 6.2 6.1 6.0
5 4.2 4.2 4.3 4.1 4.1

6 1.1 1.0 9.5 1.4 8.4
Not able to ascertai n 8.6 8.2 1.2 8.4 0.9 Self. reported exposure to dust or fumes (%) 19.5 19.5 19.8 19.7 19.1 level of dietary.fat consumption (%)~

0 14.5 13.7 14.9 14.1 15.3

1 15;9 15.8 16.5 15.6 15.9

2 17.4 17.6 17.7 17.2 17.1

3 21.2 21.8 21.1 21.3 20.8

4 30.9 31.1 29.8 31.9 30.9 level of dietary.fiber consumption (%)~

0 16.6 16.0 17.5 16.7 16.6
19.9 19.4 20.5 20.1 19.7

2 18.8 18.6 19.2 19.1 18.5
3 22.8 23.0 22.4 22.8 22.7
4 21.9 23.0 20.4 21.3 22.5 Alcohol consumption (%)

Beer

Drinks beer 22.9 24.3 23.2 22.9 21.4
Does not drink beer 9.7 9.5 9.3 9.5 10.2
No data 67.4 66.2 67.5 67.6 68.4 liq uor
Drinks liquor 28.0 30.4 27.9 25.4 27.9 Does not drink liquor 8.8 8.4 8.5 10.1 9.2
No data 63.2 61.2 63.6 65.5 62.9
Wine

Drinks wine 23.5 25.4 22.5 21.1 24.3
Does not drink wine 8.9 8.7 8.8 9.3 9.1
No data 67.6 65.9 68.7 69.6 66.6

1090 N ENGLJ MED 360;11 NEJM.ORG MARCH 12,2009

Downloaded from www.nejm.org by on March 12,2009. Copyright @ 2009 Massachusetts Medical Society. All rights reserved.Table 1. (Continued.)

Entire Cohort Variable (N =448,850) Concentration of Ozone

33.3-53.1 ppb 53.2-57.4 ppb 57.5-62.4 ppb 62.5-104.0 ppb (N

= 126,206) (N=95,740) (N

= 106,545) (N

= 120,359)
Ecologic risk factors

II Nonwhite race (%) 11.601016.8 10.501016.4 9.301015.5 10.201016.0 15.901018.3

Home with air conditioning (%) 62.301027.0 55.401031.2 59.401024.0 65.301024.8 69.h24.3

High-school education or greater (%) 51.70108.2 53.50107.9 52.40107.5 50.80107.2 50.00109.5

Unemployment rate (%) 11.70103.1 12.h3.4 11.30102.6 11.30102.9 11.80103.4

Gini coefficient ofincome inequality** 0.3 70100.04 0.370100.05 0.3 70100.04 0.370100.04 0.380100.04

Proportion of population with income 0.120100.08 0.lhO.08 0.12po0O.08 0.110100.07 0.130100.09

<125% of poverty line
Annual household income (thousands 20.70106.6 21.90107.1 19.80106.0 21.20106.7 19.70106.3

ofdollars)H OZONE AND AIR POLLUTION-RELATED MORTALITY

* MSA denotes metropolitan statistical area, and PM,.. fine particulate matter consisting of particles that are 2.5 /-1m or less in aerodynamic diameter. Plus-minus values are means otSD. Because of rounding, percentages may not total 100. All baseline characteristics included in the survival model are listed (age, sex, and race were includes as stratification factors). The model also includes squared terms for the number of cigarettes smoked per day and the number of years of smoking for both current and former smokers and a squared term for body-mass index. 

### t The body-mass index is the weight in.kilograms divided by the square of the height in meters. :j: Occupational exposure to particulate matter increases with increasing index number. The index was calculated by assigning a relative level of exposure to 'PM,.. associated with a cohort member's job and industry. These assignments were performed by industrial hygienists on the basis of their knowledge of typical exposure patterns for each occupation and specific job." § Dietary-fat consumption increases with increasing index number. Dietary information from cohort members was used to define the level of fat consumption according to five ordered categories.'o



### ~ Dietary-fiber consumption increases with increasing index number. Dietary information from cohort members was used to define the level of fiber consumption according to five ordered categories."

II For the ecologic variables, the model included terms for influences at the level of the average for the metropolitan statistical area and atthe level of the difference between the value for the ZIP Code of residence and the average for the metropolitan statistical area to represent between- and within-metropolitan area confounding influence. Some values for ecologic variables and individual variables differ, although they appear to measure the same risk factor. For example, for the entire cohort, the percentage of whites as listed under individualvariables is 93.7, whereas the percentage of nonwhites as listed under ecologic variables is 11.601016.8. This apparent contradiction is explained by the fact that the former is an exact figure based on the individual reports of the study participants in the CPS II questionnaire, whereas the latter is a mean (otSD) for the population based on Census estimates for each metropolitan statistical area.

** The Gini coefficient is a statistical dispersion measure used to calculate income inequality. The coefficient ranges from 0 to I, with 0 indicating an equal distribution of income and 1 indicating that one person has all the income and everyone else has no income.20 A coefficient of 0.37 indicates that on average there is a measurable inequality in the distribution of income among the different income groups within the MSAs. 

### tt Average household incomes for the cohort and for each quartile of ozone concentration were calcu.lated from the median household income for the metropolitan statistical area.

pulmonary causes, cardiovascular causes, ami ischemic heart disease when ozone was includedin the modeL The association of ozone concentrations with death from respiratory causes re

### mained significant after adjustment for PM2.5' Risk estimates for ozone-related death from respiratory causes were insensitive to the use of a random-effects survival model allowing for spatial clustering within the metropolitan areaand state of residence (Table lS in the Supplementary Appendix). The association between increased ozone concentrations and increased risk of death from respiratory causes was also insensitive to adjustment for several ecologic variablesconsidered individually (Table 2S in the Supplementary Appendix).Subgroup analyses showed that environmental temperature and region of the country, butnot sex, age at enrollment, body-mass index, education, or concentration of PM2.5' significantly modified the effects of ozone on the risk of death from respiratory causes (Table 4). Figure 2 illustrates the shape of the relationbetween exposure to ozone and death from reN ENGLJ MED 360;11 NE)M.ORG MARCH 12,2009 1091

Downloaded from www.nejm.org by on March 12, 2009 . Copyright@ 2009 Massachusetts Medical Society. All rights reserved.Concentration of Ozone 33.3-53.1 ppb 53.2-57.4 ppb 57.5-62.4 ppb 62.5-104.0 ppb (N

= 126,206) (N=95,740) (N

= 106,545) (N

= 120,359)

number of deafhs 32,957 25,642 27,782 32,396 16,328 12,621 13,544 16,282 13,605 10,657 11,280 13,342 7,714 6,384 6,276 7,268 2,723 1,964 2,264 2,940 The NEW ENGLAND JOURNAL oJ MEDICINE

Table 2. Number of'Deaths in the Entire Cohort and According to Exposure to Ozone.

Cause of Death Entire Cohort (N =448,850)

Ischemic heart disease Respiratory 118,777 58,775 48,884 27,642 9,891 Any cause Cardiopulmonary
Cardiovascular

Table 3. Relative Risk of Death Attributable to a lO-ppb Change in the Ambient Ozone Concentration, '4'

Any cause Cardiopulmonary Respiratory
Cardiovascular
Ischemic heart disease 1.00l (0.996-1.007)
1.014 (1.007-1.022)
1.029 (1.010-1.048)
1.011 (1.003-1.023)
1.015 (1.003-1.026) 1.001 (0.996-1.007)

1.016 (1.008-1.024) 1.027 (1.007-1.046) 1.014 (1.005-1.023) 1.017 (1.~1.029) PM2.5 (86 MSAs)

re/afill6 risk (95% 0)
1.048 (1.024-1.071) 1.129 (1.094-1.071) 1.031 (0.955-1.113) 1.150 (1.111-1.191) 1.211 (1.15~1.268) Two-Pollutant Model:!:

Ozone (86 MSAs) PMz.s (86 MSAs) Cause of Death Single-Pollutant Modelt Ozone (96 MSAs) Ozone (86 MSAs)

0.989 (0.981~.996) 0.992 (0.982-1.003) 1.040 (1.013-1.067)
0.983 (0.971~.994) 0.973 (0.95~.988) 1.080 (1.048-1.113)
1.153 (1.104-1.204)
0.927 (0.83~1.029)
1.206 (1.150-1.264)
1.306 (1.22~1.390)

* MSA denotes metropolitan statistical area, and PM2.5 fine particulate matter consisting of particles that are 2.5 jlm or less in aerodynamic diameter. Ozone concentrations were measured from April to September during the years from 1977 to 2000, with follow-up from 1982 to 2000; changes in the concentration of PM2.5 of 10 jig per cubic meter were recorded for members of the cohort in 1999 and 2000. These models are adjusted for all the individual and ecologic risk factors listed in Table 1. For the ecologic variables, the model included terms for influences at the level of the average for the metropolitan statistical area and at the level of the difference between the value for the ZIPCode of residence and the average for the metropolitan statistical area to represent between- and within-metropolitan area confounding influence. The risk of death was stratified according to age (in years), sex, and race.

t The single-pollutant models were based on 96 metropolitan statistical areas for which information on ozone was available and 86 metropolitan statistical areas for which information on both ozone and fine particulate matter was available. :j:The two-poliutant models were based on 86 metropolitan statistical areas for which information on both ozone and fine particulate matter was available.



### spiratory causes. There was limited evidence that

a threshold model specification improved model fit as compared with a nonthreshold linear model(P=O.06) <Table 3S in the Supplementary Appendix). Because air-pollution data from 1977 to 2000 were averaged, exposure values for persons who died during this period are based partly on data that were obtained after death had occurred. Further investigation by dividing this interval into specific time windows of exposure revealed nosignificant difference between the effects of earlier and later time windows within the period of follow-up. Allowing for a 10-year period of exp0- sure to ozone (5 years of follow-up and 5 years before the follow-up period) did not appreciablyalter the risk estimates <Table4S in the Supplementary Appendix). Thus, when exposure valueswere matched more closely to the follow-up period and when exposure values Were based on data obtained before the deaths, there was little change in the results.

DISCUSSION


### Our principal rmding is that ozone and PM2..S contributed independently to increased annual mortality rates in this large, U.S. cohort study in analyses that controlled for many individual and ecologic risk factors. In two-poUutant models that

1092 N ENGLJ MED 360;11 NEJM.ORG MARCH 12, 2009

Downloaded from _.nejm.org by on March 12, 2009 . Copyrighte 2009 Massachusetts Medical Society. AI rights reserved.Table 4. Relative Risk of Death from Respiratory Causes Attributable to a 1O-ppb Change in the Ambient Ozone Concentration, Stratified According to Selected Risk Factors.1\'

%of P Value Subjects Relative Risk of Effect Stratification Variable in Stratum (95% CI) Modification

Sex 0.11

Male 43 1.01 (0.99-1.04)

Female 57 1.04 (1.03-1.07) Age at enrollment (yr) 0.74

<50 26 1.00 (0.90-1.11)

50-65 54 1.03 (1.01-1.06)

>65 20 1.02 (1.00-1.05)

Education 0.48 High school or less 43 1.02 (1.00-1.05) Beyond high school 57 1.03 (1.01-1.06) Body-mass indext 0.96



# . <25.0 53 1.03 (1.01-1.06)

25.0-29.9 36 1.03 (0.99-1.06)

«30.0 11 1.03 (0.96-1.10)
PM2.5 CIIg/m'):t: 0.38

<14.3 44 1.05 (1.01-1.09)

>14.3 56 1.03 (1.00-1.05)
Region' 0.05

Northeast 24.8 0.99 (0.92-1.07)

Industrial Midwest 29.7 1.00 (0.91-1.09)

Southeast 21.0 1.12 (1.05-1.19) Upper Midwest 5.2 1.14 (0.68--1.90)

Northwest 7.7 1.06 (1.00-1.13)

Southwest 3.9 1.21 (1.04-1.40)

Southern California 7.8 1.01 (0.96-1.07) External temperature rq:t:' 0.01

<23.3 24 0.96 (0.90-1.01)

>23.3 to <25.4 29 0.97 (0.87-1.08)

>25.4 to <28.7 22 1.04 (0.92-1.16)

>28.7 25 1.05 (1.03-1.08) OZONE AND AIR POLLUTION-RELATED MORTALITY



### included ozone and PM2.5'

ozone was significantly associated only with death from respiratory

causes. For every lO-ppb increase in exposure to ozone, we observed an increase in the risk of death from respiratory causes of about 2.9% in single-pollutant models and 4% in two-pollutantmodels. Although this increase may appear moderate, the risk of dying from a respiratory causeis more than three times as great in the metropolitan areas witJI the highest ozone concentrations as in those with the lowest ozone concentrations. The effects of ozone on the risk of death from respiratOry causes were insensitive to adjustment for individual, neighborhood, and metropolitan-area confounders or to differences in multilevel-model specifications. There is biologic plausibility for a respiratory effect of ozone. In laboratory studies, ozone can increase airway inflammation24 and can worsenpulmonary function and gas exchange.25 In addition, exposure to elevated concentrations of tropospheric ozone has been associated with numerous adverse health effects, including theinduction26 and exacerbation27,28of asthma, pulmonary dysfunction,29,30and hospitalization for respiratory causes.31 Despite these observations, previous studies linking long-term exposure to ozone with deathhave been inconclusive. One cohort study conducted in the Midwest and eastern United Statesreported an inverse but nonsignificant association between ozone concentrations and mortality.1Subsequent reanalyses of this study replicatedthese findings but also suggested a positive association with exposure to ozone during warmseasons.3 A study of approximately 6000 nonsmoking Seventh-Day Adventists living in Southern California showed elevated risks among men 

### after long-term exposure to ozone, 11 

### but this finding was based on limited mortality data. Previous studies using the CPS II cohort havealso produced mixed results for ozone. An earlier examination based on a large sample of more than 500,000 people fiom 117 metropolitan areasand 8 years of follow-up indicated nonsignificant results for the relation between ozone and death from any cause and a significant inverse association between ozone and death fiom lung cancer. A positive association between death fiom cardiopulmonary causes and summertime exp0- sure to ozone was observed in single-pollutant * PM2.5 denotes fine particulate matter consisting of particles that are 2.5 /-1m or less in aerodynamic diameter. Ozone exposures for the cohort were mea.sured from April to September during the years from 1977 to 2000, with followup from 1982 to 2000, with adjustment for individual risk factors, and with baseline hazard function stratified according to age (single-year groupings), sex, and race. These analyses are based on the single-pollutant mOdel for ozone shown in Table 3. Because of rounding, percentages may not total 100. 

### t The body-mass index is the weight in kilograms divided by the square of the height in meters.:t:Stratum cutoff is based on the median of the distribution at the metropolitanarea level, not at the subject level. 

# , Definitions of regions are those used by the Environmental Protection Agency.' 

# , External temperature is calculated as the average daily maximum temperature recorded between April and September from 1977 to 2000.

N ENGL) MED 360;11 NE)M.ORG MARCH 12,2009 1093

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0.2

...

.. ii!

.. 0.1 ::J 

### ." li

'" . '

. ' . ,

. .'

. ,



### . - 

### . - . - . - . .-

. - .

-

~; ,;" 0.0
- - --- -.-.-.---.-....--.-.-.--- -,-,-,-'-'-

- 40 60 80 100 Daily I.Hr Maximum Ozone Level(ppb). 1977-2000

Figure 2. Exposure-Response Curve for the Relation between Exposure to Ozone and the Risk or Death &om Respiratory Causes. The curve is based on a natural spline with 2 df estimated from the residual relative risk of death within a metropolitan statistical area (MSA) acco~ingto a random-effects survival model. The dashed lines indicate the 95% confidence interval of fit, and the hash marks indicate the ozone levels of each ofthe 96 MSAs.

models. but the association with ozone was non

### significant in two-pollutant models.3 Further analyses based on 16 years of fullow-up in 134cities produced similarly elevated but nonsignificant associations that were suggestive of e£-fects of summertime auf)' to September) exposure to ozone on death from cardiopulmonary causes.5 The increase in deaths from' respiratory causes with increasing exposure to ozone may represent a combination of short-term effects of ozone onsusceptible subjects who have influenza or pneumonia and long-term effects on the respiratory system caused by airway inflammation,24 with subsequent loss of lung function in childhood,32 young adulthood,33,34and possibly later life.35If exposure to ozone accelerates the natural loss of adult lung function with age, those exposed to higher concennations of ozone would be at ~er risk of dying from a respiratory-related syndrome.In our two-poIIutant models, the adjusted estimates of relative risk fur the effect of ozone on the risk of death from caldiovascuIar causes were significantly less than 1.0, seemingly suggesting a protective effect. Such a beneficial influence ofozone, however, is unlikely from a biologic standpoint. The association of ozone with cardiovascular end points was sensitive to adjustment fur exposure to PM2.5' making it difficult to deter1094 

### mine precisely the independent contributions of these copollutants to the risk of death. Therewas notable collinearity between the concentrations of Ozone and PM2.5"Furthermore, measurement at central monitors probably represents population exposure toPM2.5more accurately than it represents exposure to ozone. OzOne concennation tends to varyspatially within cities more than does PM2.5concennation, because of scavenging of ozone by nitrogen oxide near roadways.36In the presence of a high density of local naffic, the measurement error is probably higher for exposure to ozone than fur exposure to PM2.5'The effects of ozone could therefore be confuunded by the presence ofPM2.5because of collinearity between the measurements of the two pollutants and the higher 

### precisionof measurements of PM2.5.37 

### Measurements of PM2.5were available only for the end of the study fullow-up period (1999 and 2000). Widespread collection of these databegan only after the EPAadopted regulatory limits on such particulates in 1997. Since particulate air pollution has probably decreased .in most metropolitan areas during the follow-up intervalof our study, it is likely that we have underestimated the effect of PM2.5in our analysis. A limitation of our study is that we were not able to account for the geographic mobility of the population during the fullow-up period. We had infurmation on home addresses fur the CPS n cohort only at the time of initial enrollment in 1982 and 1983. Census data indicate that duringthe interval between 1982 and 2000, approximately 2 to 3% of the population moved from one state to another annually (with the highest rates in an age group younger than that of our study population). 38 

### However, any bias due to afailure to account fur geographic mobility is 1ikely to have attenuated, rather than exaggerated, the effects of ozone on monaIity. In summary, we investigated the effect of tr0- pospheric ozone on the risk of death from any cause and cause-specific death in a large cohon, using data from 96 metropolitan statistical areas across the United States and controlling fur theeffect of particulate air poIIutants. We were unable to detect a significant effect of exposure to ozone on the risk of death from cardiovascular

. 

### causes when particulates were taken into. account, but we did demonstrate a significant e£- feet of exposure to ozone on the risk of death from respiratory causes.

N ENGLJ MED 360;11 NEJM.ORG MARCH 12, 2009

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. Copyright @ 2009 Massachusetts Medical Society. All rights reserved.OZONE AND AIR POLLUTION-RELATED MORTALITY

Supported by the Health Effects Institute. Dr. Krewski reports receiving grant support from the Natural Sciences and Engineering Research Council of Canada as holder of the Industrial Research Chair in Risk Science. This chair isfunded by a peer-reviewed university-industry partnership program. No other potential conflict of interest relevant to this article was reported. We thank the National Institute of Environmental Health Sciences for providing grant support (ES0026O) to the New York University School of Medicine. This article is dedicated to the memory of our coauthor and friend, Dr. Jeanne Calle, who died unexpectedly on February 17, 2009.

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Reanalysis of the Harvard Six Cities 15. Krewski 0, Jerrett M, Burnett RT, et Fine JM. Summertime haze air pollution Study and the American Cancer Society at. Extended fullow-up and spatial analy- and children with asthma. Am J Respir Study of Particulate Air Pollution and Mar- sis of the American Cancer Society study Crit Care Med 1997;155:654-60. tality: a special report of the institute's linking particulate air pollution and mar- 29. Spektor OM, Lippmann M, Lioy PJ, etParticle Epidemiology Reanalysis Project. tality. Bostun: Health Etreets Institute (in al. Etreets of ambient ozone on respiraPart II. Sensitivity analyses. Cambridge, press). tory function in active, normal children. MA: Health Etreets Institute, 2000. 16. American Cancer Society. Cancer pre- Am Rev Respir Dis 1988;137:313-20. 4. Miller KA, Siscovick OS, Sheppard L, vention study overviews. '(Accessed Febru- 30. Tager lB, Balmes J, Lurmann F, Ngo et at. Long-term exposure to air pollution ary 17, 2009, at http://www.cancer.org/L.AlcornS.Kiinzli N. Chronic exposure and incidence of cardiovascular events in docroot/RES/contenrJRES_6_2_Srudy_ to ambient ozone and lung function in women. N Engl J Med 2007;356:#7-58. Overviews.asp?) young adults. Epidemiology 2005;16:751-9. 5. Pope CA ill, Burnett RT, Thun MJ, et al. 17. Thun MJ, Calle BE, Namboodiri MM, 31. Yang Q, Chen Y, Shi Y, Burnett RT,Lung cancer, cardiopulmonary mortality, et at. Risk factors fur fatal colon cancer in McGrail KM, Krewski D. Association beand long-term exposure to fine particuJate a large prospective study. J NatI Cancer tween ozone and respiratory admissions. air pollution. JAMA 2002;287:1132-41. Inst 1992;84:1491-500. among childten and the elderly in Van6. Brook RD, Franklin B, Cascio W, etal. J.I.. Calle BE, Terrell DO. Urility of the Na- couver, Canada. Inhal Toxicol 2003;15: Air pollution and cardiovascular disease: tional Death Index for ascertainment of 1297-308. a statement fur healthcare professionals mortality among Cancer Prevention Study 32. Rojas-Martinez R. Perez-Padilla R. from the Expert Panel on Population and II participants. Am J Epidemioll993;137: OIaiz-Femandez G, et al. Lung function Prevention Science of the American Heart 235-41. growth in children with long-term expoAssociation. Circulation 2004;109-.2655-71. 19. 1errett M, Burnett RT, Willis A, et al. sure to air pollutants in Mexico City. Am J 7. Pope CA III, Dockery OW. Health ef.. Spatial analysis of the air pollution-mar- Respir Crit Care Med 2007;176:377-84.fects of fine particulate air pollution: lines tality relationship in the context of eco- 33. Galizia A, Kinney PI.. Long-term resithat connect. J Air Waste Manag AsSOC logic confuunders. J Toxicol Environ dence in areas ofhigh ozone: associarions 2006;56:709-42. Health A 2003;66:1735-77. with respiratory health in a nationwide8. Bell ML, Dominici F, Samet1M. A meta- 20. Willis A, Krewski 0, Jerrett M, Gold- sample of nonsmoking young adults. Enanalysis of time-serles studies of ozone berg MS, Burnett RT. Selection of ecologic viron Health Perspect 1999;107:675-9.and mortality with comparison to the Na- covariates in the American Cancer Society 34.. Chen C, Arjomandi M, Balmes J, Tagtional Morbidity, Mortality, and Air Pollu- study. J Toxicol Environ Health A 2003; er lB, Holland N. Efrects of chronic and tion Srudy. Epidemiology 2005;16:436-45. 66:1563-89. acute ozone .exposure on lipid peroxida9. Ito K, De Leon SF, Lippmann M. Asso- n. Ma R. Krewski 0, Burnett RT. Ran- tion and antioxidant capacity in healthy ciations between ozone and daily mortal- dam efrects Cox models: a Poisson model- young adults. Environ Health Perspect ity: analysis and meta-analysis. Epidemi- ling approach. Biometrika 2003;90:157-69. 2007;115:1732-7. ology 2005;16:446-57. 22. Siemiatyclri J, Krewski 0, Shi Y, Gold- 35. Ackermann-Liebrich U, Leuenberger 10. Levy ]I, Chemerynsld SM, Sarnat]A. berg MS, Nadon L, Lakhani 1. ConrroI- P, Scbwartz J, et at. Lung function and Ozone exposure and mortality: an empiric ling fur potential confuunding by

~- long term exposure to air pollutants in Bayes metaregression analysis. Epidemi- tional exposures. J Toxicol Environ Health Switzerland. Am J Respir Crit Care Med ology 2005;16:458-68. A 2003;66:1591-603. 1997;155:122-9.11. Abbey DE, Nishino N, McDonnell WF, 23. Chao A, Thun MJ, Jacobs EJ, Henley 36. McConnell R. Berhane K, Yao L, Luret al. Long-term inhaJable particles and SJ, Rodriguez C, Calle BE. Cigarette smok- mann FW, Awl E, Perm; 1M. Predicting other air pollutants related to mortality in ing and colorectal cancer mortality in the residential ozone deficits from nearby nonsmokers. Am J Respir Crit Care Med Cancer Prevention Srudy IL J NatI Cancer traffic. Sci Total Environ 2006;363:166-74. 1999;159:373-82 Inst 2000;92:1888-96. 37. Zidek]V, Wong H, Le NO, Burnett 1.12. Review of the national ambient air . 24. Mudway IS, KclIyFJ. An investigation of. Causality: measurement error and multiquality standards fur ozone: poIicy assess- inhaled ozone dose and the magnitude of collinearity in epidemiology. Environmetment of scientific and technical infurma- airway infI2mmJlt1()1'1in healthy adults. Am rics 1996;7:441-51. tion. Research Triangle Park, NC: Envi- J Respir Crit Care Med 2004;169:1089-95. 38. Schachter J. Geographical mobility: ronmental ProtectionAgency, 2007. (Report 25. Brown JS, Bateson TF, McDonnell WF. population characteristics. March 1999 to no. EPA-452/R-07-OO7.) Effects of exposure to 0.06 ppm ozone on March 2000. Current population reports 13. Committee on Estimating Mortality FEYI in humans: a secondary analysis of PPL-l#. Washington, DC: Census Bureau, Risk Reduction Benef'tts from Decreasing existing data. Environ Health Perspect May 2001. (Accessed February 17, 2009, at Tropospheric Ozone Exposure. Estimat- 2008;116:1023-6. http://wwW.census.gm/prodI2OO1pubsi ing mortality risk reduction and economic 26. McConnell R. Berhane K, Gilliland F, p20-538.pdf.) benefits from conrrolling ozone air pollu- et al. Asthma in exercising children ex- ~ 0 2Of19 ft_"'- M8Ii<oI.-". N ENGLJ MED360;11 NEJM.ORG MARCH12, 2009 1095

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### OCTOBER 2009 I Vol. 39, No.9 

# Mecklenburg Medicine

A Publication of the Mecklenburg County Medical Society

I 

## www.meckmed.org



# ,.

...

I 

# \ \



# /J\~ Mecklenburg County Medical Society. Mecklenburg Medical Alliance and Endowment

Founders of: Bioethics Resource Group, Ltd., Hospitality House of Charlotte, Teen Health Connection, MedAssist of Mecklenburg, Physicians Reach Qut Mecklenburg County Medical Society

# Is Healthy Air in Charlotte's Future?

By Stephen R. Keener, MD, MPH, and Maeve E. O'Connor, MD 

# D. oes it seem like you are seeing more

patients with respiratory problems today . than you were 10 years ago? That's not just your imagination. There has been a noticeable increase in asthma and cardiovascular disease in the Charlotte region in the last few years. according to the American Lung Association (ALA). The poor state of Charlotte's air is partly to blame. Health professionals are wise to be informed of the current trends in regional air quality and how they may be impacting patient health. In the American Lung Association's 2009 State of the Air report, the Charlotte metro region's air ranked eighth worst in terms of ozone pollution when compared to the nation's dirtiest cities, up from last year's 13th spot According to the 2009 report, there was a 5 percent increase in the number of pediatric asthma cases and a 21 percent increase in adult asthma cases over the 2008 numbers. The ALA report also gives Charlotte a failing grade for its high levels of particle pollution. Fine particles are of special concern to those with cardiovascular problems. The number of cases of cardiovascular disease noted in the 2009 report increased 13 percent from the 2008 report. Since the early 199Os, the Charlotte region has been in violation of the EPA's health-based standard for ozone and, while our region's air quality has improved somewhat, it's far from healthy. The Clean Air Act requires the EPA to consider ouly medical findings, not the cost of compliance, in setting federal air pollution standards. Medical research continues to show stronger correlations between dirty air and poor health, and standards are beginning to get more stringent Regional air quality doesn't meet the 1m standard of .080 parts per million (ppm), nor does it meet the current standard of .075 ppm set last year by the EPA. It's expected the EPA will adjust the standard again within the coming year. Clearly, our region has a long way to go before our air quality can be considered healthy during ozone season. Research shows physicians have a right to be concerned about Charlotte's high ozone numbers. New research from Princeton University reveals exposure to ozone levels currently considered safe e.075 ppm) has been shown to significantly impair lung function in healthy individuals. Researchers also found inhalation of .070 ppm ozone for 6.6 hours, well under the current EPA standard, can induce significant reduction in FEY I 

## - the volume of air a person can forcibly eXhale in the first second

- according to a report in the Aug. 1 issue of the American Journal of Respiratory and Critical Care Medicine. "The acute inhalation of ambient concentrations of ozone induces several health effect~, including airway irritation and inflammation, decrements in pulmonary function, and symptoms of respiratory discomfort," Edward S. Schelegle, PhD, of the University of California Davis, and colleagues assert. The researchers found statistically significant decrements in FEY I and increases in total subjective symptoms scores (P«J.05) after exposure to mean ozone concentrations of .070, .080 and .087 ppm. Another concern for an ozone hotspot like Charlotte is long-term exposure to high ozone levels. An article entitled "Long-term Ozone Exposure and Mortality" published in the March 2009 issue of the New Engl<md Journal of Medicine, reports on a'study which analyzed 448,850 subjects over an 18-year period. Researchers concluded that prolonged exposure to ozone and/or particulate matter is linked to increased mortality rates. Every .010 ppm of additional ozone raises the death rate due to respiratory disease by 4 percent In high ozone cities like. Charlotte, researchers found citizens have as much as a 30 percent higher chance of dying from respiratory illness. The risk for other nonfatal respiratory diseases also is elevated. This study adds to the literature that already documents the increase of asthma and heart attacks when ozone levels peak. Ozone is not the only danger lurking in Charlotte's air. Fine particulate matter, which is smaller than 10 microns, or one-tenth the diameter of a human hair, is especially harmful. These microscopic substances are too small to be filtered by the nose and mouth and can enter directly into the bloodstream. The burning of fossil fuels in power plants and vehicles, especially diesef engines, is a major contributor to fine particle pollution. The link between fine particles and cardiopulmonary disease has been established for two decades. In June, the Health Effects Institute (HEI) published an extended analysis of the American Cancer Society's study linking particulate air pollution and mortality. This new appraisal of

. existing studies shows mortality rates among people exposed to the particles are twice as high as previously thought The analysjs was conducted by a team of resear«hers from the University of Ottawa, led by Dr. Daniel Krewski. The current EPA maximum annual average standard for fine particles is 15.0 micrograms per cubic meter. California has set a more stringent annual average standard of 12.0. Mecklenburg County fine particulate matter levels are 14.9 micrograms per cubic meter. Our entire community needs to come together if we are to solve this major public health problem. Physicians have an important role to play. Your voice is stronger than you might think! Public officials value and respect the testimony of physicians who know the serious impact air pollution has on patient health. Clean Air Carolina (formerly Carolinas Clean Air Coalition), a local nonprofit organization working to improve air quality, has started a new initiative, Medical Advocates for Healthy Air, to provide health professionals an avenue for getting involved in the quest for clean air. Simple actions

- like adding your name to a medical sign-on letter supporting stronger regulation of air toxies, or submitting a joint letter to the editor or Op-ed column on the dangers diesel pollution from old school

buses has on children's health 

### - can make a difference in raising awareness. Educating your patients, colleagues and family members about the link between air pollution and illness also is an extremely important public service you can provide. More than 75 health professionals statewide have gotten involved in this effort and many more are needed if we are to have an impact Lawrence W. Raymond, MD, Carolinas Medical Center, Maeve E. O'Connor, MD, Carolina Asthma and Allergy, and Stephen R. Keener, MD, Mecklenburg County Health Department are three of the leaders of this new initiative. We invite you to join us as we work together to help restore healthy air for the residents of the Charlotte region.

.1. State of the Air: 2009. American Lung Association. April 29, 2009. www.stateoftheair. org/2009/stateslnorth-caro1ina. State of the Air:" 2008. American Lung Association, May 2, 2008. www.stateoftheair/2008/ stateslnorth-carolina. 2. Scheiegle E, et al "6.6-hour inhalation of ozone concentrations from 60 to 87 parts per billion in healthy humans" American Journal of Respiratory and Critical Care Medicine, 2009; 180: 265-72 3. Jerrett M. "Long-Term Ozone Exposure and Mortality", New England Journal of Medicine,



## - 360;11. March 12,2009. 4. Barringer, Felicity. "Analysis finds Elevated Risk from Soot Particles in tbe Air". The New York Tunes. June 3, 2009.

Mecklenburg Medicine. October 2009 I 15