To assess the effects of ambient particulate matter (PM) air pollution on risk of fatal coronary heart disease (CHD) in persons characterized as a sensitive subgroup, e.g. persons with known respiratory disease. The Adventist Health Study on Smog (AHSMOG) is a cohort study of 3769 nonsmoking, adults who have been followed for 22 years. A total of 806 persons free of CHD, stroke or diabetes at baseline and who reported having symptoms of asthma, some kind of bronchial condition, or emphysema on one of the 4 follow-up questionnaires (1977, 1987, 1992, 2000) constitute the study population. Monthly concentrations of ambient air pollutants were obtained from monitoring stations (PM10, Ozone, SO2, and NO2) or airport visibility data (PM2.5) and interpolated to zip code centroids of work and residence locations. PM10-2.5 concentrations were calculated as the differences between PM10 and PM2.5. Time-dependent Cox proportional hazards regression was used for analyses. Analyses were controlled for a number of potential confounders available from a detailed lifestyle questionnaire at baseline and for environmental tobacco smoke and other personal sources of air pollution available from the 4 subsequent questionnaires. Elevated risk of fatal CHD was found for all ambient PM fractions with the highest risk estimates for coarse fraction (PM10-2.5). The relative risk (RR) for fatal CHD with each 10 μg/m3 increase in PM10-2.5 was 2.1 (95% confidence interval (CI): 1.3, 3.3) in the single pollutant model and 2.2 (95 % CI: 1.3, 3.8) in the two-pollutant model with ozone. Risk appeared to be stronger in females than in males. High ambient concentrations of PM, especially coarse fraction, are associated with increased risk of fatal CHD among persons with known chronic respiratory disease (asthma, bronchial condition, or emphysema). The risk appears to be stronger in females than in males.

The purpose of this study was to assess the effect of long-term ambient particulate matter (PM) on risk of fatal coronary heart disease (CHD). A cohort of 3,239 nonsmoking, non-Hispanic white adults was followed for 22 years. Monthly concentrations of ambient air pollutants were obtained from monitoring stations [PM < 10 microm in aerodynamic diameter (PM10), ozone, sulfur dioxide, nitrogen dioxide] or airport visibility data [PM < 2.5 microm in aerodynamic diameter (PM2.5)] and interpolated to ZIP code centroids of work and residence locations. All participants had completed a detailed lifestyle questionnaire at baseline (1976), and follow-up information on environmental tobacco smoke and other personal sources of air pollution were available from four subsequent questionnaires from 1977 through 2000. Persons with prevalent CHD, stroke, or diabetes at baseline (1976) were excluded, and analyses were controlled for a number of potential confounders, including lifestyle. In females, the relative risk (RR) for fatal CHD with each 10-microg/m3 increase in PM2.5 was 1.42 [95% confidence interval (CI), 1.06-1.90] in the single-pollutant model and 2.00 (95% CI, 1.51-2.64) in the two-pollutant model with O3. Corresponding RRs for a 10-microg/m3 increase in PM(10-2.5) and PM10 were 1.62 and 1.45, respectively, in all females and 1.85 and 1.52 in postmenopausal females. No associations were found in males. A positive association with fatal CHD was found with all three PM fractions in females but not in males. The risk estimates were strengthened when adjusting for gaseous pollutants, especially O3, and were highest for PM2.5. These findings could have great implications for policy regulations.

The relationship between ambient air pollution and cardiovascular disease is currently a topic of debate. If there is a relationship, this could have great implications for policy regulations. Methods To study the health effect of long-term ambient air pollution, a cohort of 6,338 nonsmoking, white California Seventh-day Adventists was followed with respect to health outcomes from 1977. To be included in the study, participants must have lived within 10 miles of their 1977 address for the previous 10 years. At baseline in 1977, a comprehensive lifestyle and diet questionnaire was completed and the cohort was followed with update of residence and workplace in order to assess monthly averages of ambient air pollutants throughout the study period. Exposure to environmental tobacco smoke, dusts and fumes in the workplaces, and time spent outdoors was assessed through self-administered questionnaires in 1977, 1987, and again in 1992. The risk of fatal coronary heart disease (CHD) (ICD: 410–414) was ascertained between 1977 and 1992 through matching with death certificates obtained from the National Death Index (NDI). Monthly indices of particulate ambient air pollutant concentrations (PM10, PM2.5, SO4,) wre obtained from the California Air Resource Board monitoring stations from 1973–1992, and interpolated to zip code centroids. Cox proportional hazards were used to estimate relative risks (RR) of CHD death associated with an interquartile range (IQR) increase in mean concentrations of each ambient air pollutant averaged over the 5-year period immediately preceding death. The analyses excluded those with prevalent CHD at baseline and was controlled for age, pack-years of past cigarette smoking, history of diabetes, history of hypertension, BMI, years of education, and total exercise level. Results Elevated risk of fatal CHD was found for all pariculate ambient air pollution levels with the highest risk estimates for PM2.5.Conclusion Significant risk of fatal CHD death was found for PM10, PM2.5 and SO4. As has been found for other air pollution-disease outcomes in this study, the associations were stronger in males than in females. This could partly be due to the fact that the men in this study report spending more time outdoors than females. Our data has not yet been analyzed using multipollutant models to determine the relative effects of each pollutant, nor has the model been adjusted for differences in dietary habits. We have detailed dietary information at baseline, and adjustment for relevant dietary practices will be done to determine whether diet modifies the observed relationship between ambient particulate air pollution and risk of fatal CHD. The observed relationships are strong and could have implications for public health policy. However, further studies are needed to confirm these findings in other studies.

Abbey, D; Burchette, R; Petersen, F; Knutsen, S; Peters, J; Hayes, C Author Information

Cancer incidence and mortality in a cohort of 6 000 Seventh-day Adventist nonsmokers who were residents of California were monitored for a 6-y period, and relationships with long-term ambient concentrations of total suspended particulates (TSPs) and ozone (O3) were studied. Ambient concentrations were expressed as mean concentrations and exceedance frequencies, which are the number of hours during which concentrations exceeded specified cutoffs (e.g., federal and California air quality standards). Risk of malignant neoplasms in females increased concurrently with exceedance frequencies for all TSP cutoffs, except the lowest, and these increased risks were highly statistically significant. An increased risk of respiratory cancers was associated with only one cutoff of O3, and this result was of borderline significance. These results are presented in the context of setting standards for these two air pollutants.