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Erratum: assessing long-term exposure in the California Teachers Study.

In an article published in Environmental Health Perspectives (Ostro et al. 2010), we analyzed the relationships of long-term exposure to fine particulate matter ([less than to equal to] 2.5 [micro]m in aerodynamic diameter; [PM.sub.2.5]) and its components with mortality in a cohort of > 100,000 active and retired female professionals participating in the California Teachers Study (CTS) cohort. We used a Cox proportional hazards model in which pollution exposure was measured as a continuous variable over the study period. Monthly average pollutant concentrations were obtained for each participant from measurements at the nearest [PM.sub.2.5] monitor within either 8 or 30 km of her geocoded residential address. Each participant was assigned a single exposure value over the follow-up period, defined as the average pollutant concentration from the beginning of the observation period (1 June 2002) to the woman's date of death, loss to follow-up, or study termination (31 July 2007). Thus, exposure assignment was dependent on the duration of follow-up for each participant.

In our article (Ostro et al. 2010), we reported associations of mortality from all causes, cardiopulmonary disease, and ischemic heart disease (IHD) with [PM.sub.2.5] mass and several of its components. However, the estimated hazard ratios (HRs) were generally higher than those reported from previous cohort studies (Dockery et al. 1993; Eftim et al. 2008; Krewski et al. 2009; Laden et al. 2006; Pope et al. 1995). Part of this difference was likely due to the nature of the exposure assignment. Most previous cohort studies have assigned the same exposure period to all study subjects, regardless of when deaths occurred. Thus, estimated exposures for some study participants in several studies occurred after their deaths. In addition, exposures have usually been assigned to participants based on their residential address at enrollment only, without taking into account exposure changes that may have occurred throughout the study period or when participants relocated. Finally, many previous studies measured exposure for only a subset of the years during which the cohort was followed. In an effort to reduce these aspects of exposure misclassification, we estimated exposures beginning prior to the cohort follow-up period, continuing to the end of the study or until the participant died or relocated out of state, incorporating updated exposure assignments when the subjects moved.

Importantly, measured concentrations of several pollutants in California declined substantially from 2002 through 2007; annual average [PM.sub.2.5], organic carbon (OC), and nitrates decreased by around 30% each. These marked decreases in ambient [PM.sub.2.5] concentrations resulted in lower average exposure estimates for cohort members who survived to the end of our study. Thus, the exposure assigned to a participant who died at time t would tend to be greater for events occurring early in the observation period, compared with the long-term average exposures of the participants who comprised the remainder of the risk set (i.e., those who were still part of the cohort study at time t and who subsequently experienced lower ambient pollution levels).

We have reanalyzed the CTS data using time-dependent pollution metrics--in which the exposure estimates for everyone remaining alive in the risk set were recalculated at the time of each death--in order to compare their average exposures up to that time with that of the individual who had died. In this way, decedents and survivors comprising the risk set had similar periods of pollution exposure, without subsequent pollution trends influencing the surviving women's exposure estimates.

As in our previous study (Ostro et al. 2010), we restricted the sample in this reanalysis to women living within 30 km of one of eight fixed-site monitors in the U.S. Environmental Protection Agency's Speciation Trend Network (STN), resulting in a study population of almost 44,000 women. Residential addresses from study enrollment forward were geocoded and linked with monthly pollutant averages at the nearest STN monitor to generate estimates of long-term exposure. We also used the same set of individual and ecological covariates in a Cox proportional hazards model as was used in the original study. Pollutants entered separately into the model included [PM.sub.2.5] mass, elemental carbon (EC), OC, sulfate, nitrate, iron, potassium, silicon, and zinc. We used data on primary cause of death from August 2002 through July 2007 to examine the relationships between pollutants and mortality from all causes and cardiopulmonary, pulmonary, and IHDs.

The results are summarized in Erratum Table 1, scaled to the interquartile range (IQR) for each pollutant. HRs were significantly attenuated from our previous results. No associations were observed between all-cause mortality and [PM.sub.2.5] or its components. For cardiopulmonary mortality, we observed significant associations for [PM.sub.2.5] mass, nitrate, sulfate, and silicon, with more modest associations for zinc. [PM.sub.2.5] mass and all of its components were associated with mortality from IHD, whereas none of the pollutants was associated with pulmonary mortality. This Erratum Table 1 should replace Table 5 in our previous article (Ostro et al. 2010).
Erratum Table 1. Association between mortality outcomes and
[PM.sub.2.5] and its components using a 30-km buffer (n = 43,220).

                                         All-cause (ICD-10 codes, all
                                            except S-Z) (n = 2,519)

Pollutant       IQR ([mu]g/[m.sup.3])      HR (95% CI)       p-Value

[PM.sub.2.5]             6.1             1.03 (0.98-1.10)     0.26

EC                       0.65            1.02 (0.93-1.12)     0.65

OC                       0.84            1.00 (0.95-1.04)     0.91

Sulfate                  2.2             1.06 (0.97-1.16)     0.18

Nitrate                  3.2             1.03 (0.98-1.09)     0.27

Iron                     0.13            1.01 (0.93-1.11)     0.77

Potassium                0.07            1.01 (0.94-1.08)     0.85

Silicon                  0.03            1.02 (0.99-1.06)     0.22

Zinc                     0.01            1.03 (0.96-1.11)     0.45

                 Cardiopulmonary         Ischemic heart disease
              (ICD-10 codes, I00-I99,   (ICD-10 codes, I20-I25)
                J00-J98) (n = 1,357)            (n = 460)

Pollutant       HR (95% CI)    p-Value    HR (95% CI)    p-Value

[PM.sub.2.5]  1.11(1.03-1.21)   0.01    1.31(1.14-1.50)  < 0.01

EC            1.07(0.94-1.22)   0.28    1.46(1.17-1.83)  < 0.01

OC            1.04(0.98-1.11)   0.19    1.13(1.01-1.25)    0.03

Sulfate       1.14(1.01-1.29)   0.03    1.48(1.20-1.82)  < 0.01

Nitrate       1.11(1.03-1.19)   0.01    1.27(1.12-1.43)  < 0.01

Iron          1.05(0.93-1.19)   0.40    1.39(1.13-1.72)  < 0.01

Potassium     1.06(0.97-1.17)   0.22    1.27(1.07-1.49)  < 0.01

Silicon       1.05(1.00-1.10)   0.04    1.11(1.02-1.20)    0.01

Zinc          1.09(0.98-1.20)   0.10    1.33(1.12-1.58)  < 0.01

                   Pulmonary (ICD-10,
                codes J00-J98) (n = 355)

Pollutant         HR (95% CI)      p-Value

[PM.sub.2.5]    1.02(0.87-1.19)     0.84

EC              0.88(0.68-1.15)     0.35

OC              0.95(0.84-1.06)     0.35

Sulfate         1.04(0.82-1.31)     0.77

Nitrate         1.04(0.90-1.20)     0.58

Iron            0.88(0.69-1.13)     0.32

Potassium       0.90(0.74-1.09)     0.27

Silicon         0.98(0.89-1.08)     0.71

Zinc            0.97(0.79-1.18)     0.74

ICD-10, International Classification of Diseases, 10th Revision (World
Health Organization 1993). Values shown are HRs [95% confidence
intervals (CIs)] and p-values scaled to the IQR of each pollutant. All
models are adjusted for smoking status, total pack-years, body mass
index, marital status, alcohol consumption, second-hand smoke exposure
at home, dietary fat, dietary fiber, dietary calories, physical
activity, menopausal status, hormone replacement therapy use, family
history of myocardial infarction or stroke, blood pressure medication
and aspirin use, and neighborhood contextual variables (income, income
inequality, education, population size, racial composition,

Compared with our previous results (Ostro et al. 2010), these updated [PM.sub.2.5] HRs are more consistent with several other published estimates of mortality risks, which are scaled to an increment of 10 [micro]g/[m.sup.3] of long-term average [PM.sub.2.5] and summarized in Erratum Table 2. For example, relative to our revised HR of 1.19 for cardiopulmonary disease, analogous HRs from previous studies include 1.09 (95% CI, 1.03--1.16) from the American Cancer Society-Cancer Prevention II (ACS) cohort (cardiopulmonary disease; Pope et al. 2004), 1.28 (95% CI, 1.13-1.44) from the Harvard Six Cities study (cardiovascular disease; Laden et al. 2006), and 1.10 (95% CI, 0.94-1.28) from the Los Angeles subcohort of the ACS study (cardiopulmonary disease; Jerrett et al. 2005). Much higher HRs were observed in the observational study of the Women's Health Initiative cohort for cardiovascular and IHD mortality (Miller et al. 2007).
Erratum Table 2. Comparative HRs (95% CIs) associated with a
10-[micro]g/[m.sup.3] change in long-term exposure to [PM.sub.2.5]
in several cohort studies conducted in the United States.

Authors               Exposure assessment             All causes

Ostro et al.    From 1 year prior to follow-up    1.06 (0.96-1.16) (a)
(this report)   until event (either death or end
                of study), time-dependent

Ostro et al.    From 2 months prior to study      1.84 (1.66-2.05) (a)
(2010)          through event month

Pope et al.     Four years prior to or at start   1.06 (1.02-1.11)
(2002, 2004)    of follow-up and 2 years after
                end of follow-up

Laden et al.    Multiyear average concurrent      1.16 (1.07-1.26)
(2006)          with follow-up

Miller et al.   One year in middle of follow-up

Jerrett et al.  One year at end of follow-up      1.15 (1.03-1.29)

Eftim et al.    Three-year average concurrent     1.21 (1.15-1.27)
(2008)          with follow-up

Chen et al.     Four-year moving average prior
(2005)          to event

Puett et al     One year prior to event           1.26 (1.02-1.54) (a)

Authors       Cardiovascular    Cardiopulmonary        IHD

Ostro et                       1.19 (1.05-1.36)  1.55 (1.24-1.93)
al. (this                      (a)               (a)

Ostroetal.                     2.05 (1.80-2.36)  2.89 (2.27-3.67)
(2010)                         (a)               (a)

Pope et al.  1.12 (1.08-1.15)  1.09 (1.03-1.16)

Laden et     1.28 (1.13-1.44)
al. (2006)

Miller et    1.76 (1.25-2.47)                    2.21 (1.17-4.16)
al. (2007)   (a)                                 (a)

Jerrett et                     1.10 (0.94-1.28)  1.32 (1.05-1.66)
al. (2005)

Eftim et
al. (2008)

Chen et al.                                      1.42 (1.06-1.90)
(2005)                                           (a)

Puett et al                                      2.02 (1.07-3.78)
(2009)                                           (a)

HRs are scaled to 10-[micro]g/[m.sup.3] change in [PM.sub.2.5], in
contrast to Table 1, in which HRs are scaled to the pollutant
interquartile range.
(a) Women only.

These revised results still support the existence of elevated risks of [PM.sub.2.5]-associated cardiopulmonary disease and IHD, and illustrate the importance of considering the impact of long-term pollution trends in modeling estimates of exposure.

The authors declare they have no actual or potential competing financial interests.

Bart Ostro

California Office of Environmental Health Hazard Assessment

Oakland, California


Peggy Reynolds

Debbie Goldberg

Andrew Hertz

Cancer Prevention Institute of California

Berkeley, California

Richard T. Burnett

Hwashin Shin

Health Canada

Ottawa, Ontario, Canada

Edward Hughes

Edward Hughes Consulting

Ottawa, Ontario, Canada

Cynthia Garcia

California Air Resources Board Sacramento, California

Katherine D. Henderson

Leslie Bernstein

City of Hope

Duarte, California

Michael Lipsett

California Department of Public Health

Richmond, California


Chen LH, Knutsen SF, Shavlik D, Beeson WL, Petersen F, Ghamsary M, et al. 2005. The association between fatal coronary heart disease and ambient particulate air pollution: are females at greater risk? Environ Health Perspect 113:1723-1729.

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Eftim SE, Samet JM, Janes H, McDermott A, Dominici F. 2008. Fine particulate matter and mortality: a comparison of the Six Cities and American Cancer Society cohorts with a Medicare cohort. Epidemiology 19:209-216.

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Ostro B, Lipsett M, Reynolds P, Goldberg D, Hertz A, Garcia C, et al. 2010. Long-term exposure to constituents of fine particulate air pollution and mortality: results from the California Teachers Study. Environ Health Perspect 118:363-369.

Pope CA III, Burnett RT, Thun MJ, Calle EE, Krewski D, Ito K, et al. 2002. Lung cancer, cardiopulmonary mortality, and long-term exposure to fine particulate air pollution. JAMA 287:1132-1141.

Pope CA III, Burnett RT, Thurston GD, Thun MJ, Calle EE, Krewski D, et al. 2004. Cardiovascular mortality and long-term exposure to particulate air pollution: epidemiological evidence of general pathophysiological pathways of disease. Circulation 109:71-77.

Pope CA III, Thun MJ, Namboodiri MM, Dockery DW, Evans JS, Speizer FE, et al. 1995. Particulate air pollution as a predictor of mortality in a prospective study of U.S. adults. Am J Respir Crit Care Med 151:669-674.

Puett RC, Hart JE, Yanosky JD, Paciorek C, Schwartz J, Suh H, et al. 2009. Chronic fine and coarse particulate exposure, mortality and coronary heart disease in the Nurses' Health Study. Environ Health Perspect 117:1697-1701.

World Health Organization 1993. International Classification of Diseases, 10th Revision. Geneva:World Health Organization.
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Title Annotation:Correspondence
Publication:Environmental Health Perspectives
Article Type:Correction notice
Date:Jun 1, 2011
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