In a population of women residing in Metropolitan Statistical Areas in the northeastern region of the United States, all-cause mortality was statistically significantly associated with average PM10 exposures in the time period 3–48 months prior to death. The association was strongest with average PM10 exposure in the 24 months prior to death (hazard ratio = 1.16, 95% CI: 1.05, 1.28) and weakest with exposure in the month prior to death (hazard ratio = 1.04, 95% CI: 0.98, 1.11). Risk of fatal CHD was significantly associated with chronic exposure to PM10. The association of greatest magnitude occurred with mean exposure in the 24 months prior to death (hazard ratio = 1.42, 95% CI: 1.11, 1.81). We did not find an association between nonfatal myocardial infarctions and PM10 exposure in this population.
We examined the effects of potential confounders on these health outcomes, with physical activity and smoking attenuating the strength of the relation. Risk of all-cause mortality and fatal CHD associated with PM10 in the 12 months before death was significantly elevated after adjustment for smoking status and pack-years, body mass index, diabetes, family history of myocardial infarction, hypercholesterolemia, hypertension, and median census tract family income and house value. Controlling for physical activity in addition to these factors resulted in elevated, but nonsignificant risks of all-cause mortality and fatal CHD. Few previous studies have controlled for physical activity, and mechanisms underlying this attenuation are unclear.
Examination of possible effect modification showed that the association between fatal CHD and long-term PM10 exposure was influenced by body mass index and smoking. Women with a higher body mass index were at increased risk of fatal CHD associated with PM10. Women who had never smoked showed the strongest risk, regardless of body mass index. These results suggest that the health effects of smoking may mask the impact of air pollution. Reductions in PM10 levels may produce greater benefits in healthier populations.
Our observations are consistent with a growing body of literature on chronic particulate matter exposure, cardiovascular events, and mortality. The size fraction in these studies varies (PM10
or particulate matter <2.5 μm in diameter (PM2.5
)), precluding direct comparisons in some cases. In the extended Harvard Six Cities Study (4
) and the American Cancer Society Study (6
), the adjusted hazard ratios for a 10-μg/m3
change in PM2.5
exposure were 1.14 (95% CI: 1.06, 1.22) and 1.06 (95% CI: 1.02, 1.11), respectively. Eftim et al. (3
) evaluated the association between all-cause mortality and fine particulates by using Medicare data in the same counties. They observed a 10.9% (95% CI: 9.0, 12.8) increase in all-cause mortality for a 10-μg/m3
increase in PM2.5
in the American Cancer Society Study counties and a 20.8% (95% CI: 14.8, 27.1) increase in the Harvard Six Cities Study counties.
In a case-control study of Swedish men and women using 30-year averaged, traffic-related PM10
, Rosenlund et al. (19
) did not find an association with nonfatal myocardial infarctions (odds ratio = 0.92, 95% CI: 0.71, 1.19 for an approximately 5-μg/m3
change in PM10
). For fatal myocardial infarction, there was a nonsignificant elevated risk (odds ratio = 1.39, 95% CI: 0.94, 2.07) (19
). Results from our study were stronger than those in this study, which included both genders. The Adventist Health Study on Health Effects of Smog showed associations of fatal CHD with PM10
, and PM10–2.5
for women but not for men (20
The relation between chronic PM2.5
exposure and cardiovascular events was examined in the Women's Health Initiative observational study (5
). Although results are not directly comparable, a significant increase in deaths from CHD and a nonsignificant increased risk of first myocardial infarction were also found. Similar to our study, the authors of this study observed effect modification by body mass index. The overall associations were higher than those reported here, likely because of differences in the particle size studied.
The time pattern of the association we found is interesting. Distributed lag-time series analyses of PM10
exposure out to a month prior to death (21
) reported larger associations than those seen a few days preceding death, very similar to our findings regarding monthly exposure variables. Recent reanalyses of the Harvard Six Cities Study (23
) examined whether previous findings are due to decades of exposure or shorter-term changes. The reported association was with exposure in the previous 2 years. These results indicate a developing coherence of the air pollution mortality literature, and the mortality risk benefits from reducing air pollution would be expected within a few years of intervention.
Most previous cohort studies have not examined the effect of physical activity on the association of particulate exposure with all-cause mortality and fatal CHD (1
). It was assessed in the Women's Health Initiative study, which did not find evidence of confounding (5
). Whether physical activity is a confounder, is a risk modifier, or is in the causal pathway warrants further exploration.
can deposit in the thoracic area of the respiratory system. The biologic mechanisms through which PM10
contributes to mortality and CHD are not clearly understood. Hypothesized pathways include oxidative stress (25
) and inflammation leading to accelerated atherosclerosis (26
) or endothelial dysfunction (28
), and ischemic responses in the myocardium (28
Limitations of our study include potential bias from obtaining initial information through self-report. Use of medical records, interviews, autopsy reports, and death certificate information reduces the possibility, and it is unlikely that underreporting would be associated with exposure. Findings may differ for other geographic areas. Selecting the northeastern region of the United States enabled us to focus on contiguous states with a denser and more evenly distributed study population than in other regions of the country. The similarity of sources and model complexity increased accuracy but necessitated initial assessment and validation in a smaller area. We did not adjust for additional ambient pollutants. Particulate exposures were assigned by geocoded residential locations; however, work locations were unavailable. In addition, we were unable to determine time spent outdoors, housing characteristics, or whether nurses were living at reported addresses year-round. Some addresses were unable to be geocoded because of abbreviations and the like. High correlations between time windows of exposure (ρ > 0.95 for correlations of all measures between 12 and 48 months) and potential residual confounding by incomplete adjustment for season limited our ability to determine the most relevant time period. Although estimates of pollution exposure were available on a monthly basis, covariates were assessed only every 2 years.
Through a combination of updated covariates, improved outcome assessment, and more accurate long-term exposure assessment, the current study provides valuable information on the associations of chronic PM10 exposure with all-cause mortality and CHD. We identified women nonsmokers with a higher body mass index as a potentially susceptible population. Most importantly, with residential addresses that were updated every 2 years and monthly predictions from our geographic information system–based exposure model, we had the unique opportunity to assess exposures on a finer spatial and temporal scale than in previous long-term studies. Finally, our findings add to a growing coherence of the literature across multiple time scales indicating that the public health benefits of reducing particle concentrations will be realized within years, not decades, of the reduction. This study also suggests that measures taken to limit particulate air pollution should benefit population health over extended periods of time.