Rationale: Several studies have linked long-term exposure to particulate air pollution with increased cardiopulmonary mortality; only two have also examined incident circulatory disease.

Objectives: To examine associations of individualized long-term exposures to particulate and gaseous air pollution with incident myocardial infarction and stroke, as well as all-cause and cause-specific mortality.

Methods: We estimated long-term residential air pollution exposure for more than 100,000 participants in the California Teachers Study, a prospective cohort of female public school professionals. We linked geocoded residential addresses with inverse distance-weighted monthly pollutant surfaces for two measures of particulate matter and for several gaseous pollutants. We examined associations between exposure to these pollutants and risks of incident myocardial infarction and stroke, and of all-cause and cause-specific mortality, using Cox proportional hazards models.

Measurements and Main Results: We found elevated hazard ratios linking long-term exposure to particulate matter less than 2.5 μm in aerodynamic diameter (PM2.5), scaled to an increment of 10 μg/m3 with mortality from ischemic heart disease (IHD) (1.20; 95% confidence interval [CI], 1.02–1.41) and, particularly among postmenopausal women, incident stroke (1.19; 95% CI, 1.02–1.38). Long-term exposure to particulate matter less than 10 μm in aerodynamic diameter (PM10) was associated with elevated risks for IHD mortality (1.06; 95% CI, 0.99–1.14) and incident stroke (1.06; 95% CI, 1.00–1.13), while exposure to nitrogen oxides was associated with elevated risks for IHD and all cardiovascular mortality.

Conclusions: This study provides evidence linking long-term exposure to PM2.5 and PM10 with increased risks of incident stroke as well as IHD mortality; exposure to nitrogen oxides was also related to death from cardiovascular diseases.

Background

Although recent reviews have suggested active smoking to be a risk factor for breast cancer, the association with passive smoke exposure remains controversial. This risk association was explored in a large prospective study of women, the California Teachers Study.

Methods

Detailed lifetime information on passive smoke exposure by setting (home, work, or social) and by age of exposure were collected in 1997 from 57,523 women who were lifetime nonsmokers and had no history of breast cancer. In the ensuing decade, a total of 1,754 women were diagnosed with invasive breast cancer. Cox proportional hazards models were fit to estimate hazard ratios (HRs) and 95% confidence intervals (95% CI) associated with several lifetime passive smoke exposure metrics.

Results

For all breast cancer, measures of higher lifetime passive smoking intensity and duration were associated with non-statistically significant HRs of 1.11 to 1.14. For postmenopausal women, HRs for lifetime low, medium and high cumulative exposure were 1.17 (95%CI 0.91, 1.49), 1.19 (95%CI 0.93, 1.53), and 1.26 (95% CI 0.99, 1.60). For women exposed in adulthood (age ≥20) risk was elevated at the highest level of cumulative exposure (HR=1.18, 95% CI 1.00, 1.40), primarily among postmenopausal women (HR=1.25, 95% CI 1.01, 1.56). A statistically significant dose response was detected when analysis was restricted to women with moderate to high levels of passive smoke exposure.

Conclusion

These results suggest that cumulative exposures to high levels of side stream smoke may increase breast cancer risk among postmenopausal women who themselves have never smoked tobacco products.

Background

Several studies have reported associations between long-term exposure to ambient fine particulate matter (PM) and cardiovascular mortality. However, the health impacts of long-term exposure to specific constituents of PM2.5 (PM with aerodynamic diameter ≤ 2.5 μm) have not been explored.

Methods

We used data from the California Teachers Study, a prospective cohort of active and former female public school professionals. We developed estimates of long-term exposures to PM2.5 and several of its constituents, including elemental carbon, organic carbon (OC), sulfates, nitrates, iron, potassium, silicon, and zinc. Monthly averages of exposure were created using pollution data from June 2002 through July 2007. We included participants whose residential addresses were within 8 and 30 km of a monitor collecting PM2.5 constituent data. Hazard ratios (HRs) were estimated for long-term exposure for mortality from all nontraumatic causes, cardiopulmonary disease, ischemic heart disease (IHD), and pulmonary disease.

Results

Approximately 45,000 women with 2,600 deaths lived within 30 km of a monitor. We observed associations of all-cause, cardiopulmonary, and IHD mortality with PM2.5 mass and each of its measured constituents, and between pulmonary mortality and several constituents. For example, for cardiopulmonary mortality, HRs for interquartile ranges of PM2.5, OC, and sulfates were 1.55 [95% confidence interval (CI), 1.43–1.69], 1.80 (95% CI, 1.68–1.93), and 1.79 (95% CI, 1.58–2.03), respectively. Subsequent analyses indicated that, of the constituents analyzed, OC and sulfates had the strongest associations with all four outcomes.

Conclusions

Long-term exposures to PM2.5 and several of its constituents were associated with increased risks of all-cause and cardiopulmonary mortality in this cohort. Constituents derived from combustion of fossil fuel (including diesel), as well as those of crustal origin, were associated with some of the greatest risks. These results provide additional evidence that reduction of ambient PM2.5 may provide significant public health benefits.

Hazardous air pollutants (HAPs) are compounds shown to cause cancer or other adverse health effects. We analyzed population-based childhood cancer incidence rates in California (USA) from 1988 to 1994, by HAP exposure scores, for all California census tracts. For each census tract, we calculated exposure scores by combining cancer potency factors with outdoor HAP concentrations modeled by the U.S. Environmental Protection Agency. We evaluated the relationship between childhood cancer rates and exposure scores for 25 potentially carcinogenic HAPs emitted from mobile, area, and point sources and from all sources combined. Our study period saw 7,143 newly diagnosed cancer cases in California; of these, 6,989 (97.8%) could be assigned to census tracts and included in our analysis. Using Poisson regression, we estimated rate ratios (RRs) adjusted for age, race/ethnicity, and sex. We found little evidence for elevated cancer RRs for all sites or for gliomas among children living in high-ranking combined-source exposure areas. We found elevated RRs and a significant trend with increasing exposure level for childhood leukemia in tracts ranked highest for exposure to the combined group of 25 HAPs (RR = 1.21; 95% confidence interval, 1.03, 1.42) and in tracts ranked highest for point-source HAP exposure (RR = 1.32; 95% confidence interval, 1.11, 1.57). Our findings suggest an association between increased childhood leukemia rates and high HAP exposure, but studies involving more comprehensive exposure assessment and individual-level exposure data will be important for elucidating this relationship.

We analyzed population-based childhood cancer incidence rates throughout California in relation to agricultural pesticide use. During 1988-1994, a total of 7,143 cases of invasive cancer were diagnosed among children under 15 years of age in California. Building on the availability of high-quality population-based cancer incidence information from the California Cancer Registry, population data from the U.S. Census, and uniquely comprehensive agricultural pesticide use information from California's Department of Pesticide Regulation, we used a geographic information system to assign summary population, exposure, and outcome attributes at the block group level. We used Poisson regression to estimate rate ratios (RRs) by pesticide use density adjusted for race/ethnicity, age, and sex for all types of childhood cancer combined and separately for the leukemias and central nervous system cancers. We generally found no association between pesticide use density and childhood cancer incidence rates. The RR for all cancers was 0.95 [95% confidence interval (CI), 0.80-1.13] for block groups in the 90th percentile and above for use of pesticides classified as probable carcinogens, compared to the block groups with use of < 1 lb/mi(2). The RRs were similar for leukemia and central nervous system cancers. Childhood leukemia rates were significantly elevated (RR = 1.48; 95% CI, 1.03-2.13) in block groups with the highest use of propargite, although we saw no dose-response trend with increasing exposure categories. Results were unchanged by further adjustment for socioeconomic status and urbanization.