Air pollution and mortality in a large, representative U.S. cohort: multiple-pollutant analyses, and spatial and temporal decompositions.

BACKGROUND: Cohort studies have documented associations between fine particulate matter air pollution (PM2.5) and mortality risk. However, there remains uncertainty regarding the contribution of co-pollutants and the stability of pollution-mortality associations in models that include multiple air pollutants. Furthermore, it is unclear whether the PM2.5-mortality relationship varies spatially, when exposures are decomposed according to scale of spatial variability, or temporally, when effect estimates are allowed to change between years. METHODS: A cohort of 635,539 individuals was compiled using public National Health Interview Survey (NHIS) data from 1987 to 2014 and linked with mortality follow-up through 2015. Modelled air pollution exposure estimates for PM2.5, other criteria air pollutants, and spatial decompositions (< 1 km, 1-10 km, 10-100 km, > 100 km) of PM2.5 were assigned at the census-tract level. The NHIS samples were also divided into yearly cohorts for temporally-decomposed analyses. Cox proportional hazards models were used to estimate hazard ratios (HRs) and 95% confidence intervals (CIs) in regression models that included up to six criteria pollutants; four spatial decompositions of PM2.5; and two- and five-year lagged mean PM2.5 exposures in the temporally-decomposed cohorts. Meta-analytic fixed-effect estimates were calculated using results from temporally-decomposed analyses and compared with time-independent results using 17- and 28-year exposure windows. RESULTS: In multiple-pollutant analyses, PM2.5 demonstrated the most robust pollutant-mortality association. Coarse fraction particulate matter (PM2.5-10) and sulfur dioxide (SO2) were also associated with excess mortality risk. The PM2.5-mortality association was observed across all four spatial scales of PM2.5, with higher but less precisely estimated HRs observed for local (< 1 km) and neighborhood (1-10 km) variations. In temporally-decomposed analyses, the PM2.5-mortality HRs were stable across yearly cohorts. The meta-analytic HR using two-year lagged PM2.5 equaled 1.10 (95% CI 1.07, 1.13) per 10 µg/m3. Comparable results were observed in time-independent analyses using a 17-year (HR 1.13, CI 1.09, 1.16) or 28-year (HR 1.09, CI 1.07, 1.12) exposure window. CONCLUSIONS: Long-term exposures to PM2.5, PM2.5-10, and SO2 were associated with increased risk of all-cause and cardiopulmonary mortality. Each spatial decomposition of PM2.5 was associated with mortality risk, and PM2.5-mortality associations were consistent over time.

Mortality risk associated with greenness, air pollution, and physical activity in a representative U.S. cohort.

Several cohort studies suggest greenness is associated with decreased mortality risk. Potential confounding by or interactions between physical activity and air pollution remains unclear. This study evaluates associations of greenness, air pollution, and physical activity with mortality risk and investigates confounding and effect modification across these key risk factors. National Health Interview Survey (NHIS) data covering 1997-2014 were linked to the National Death Index to generate a cohort of 403,748 individuals with 39,528 deaths. Greenness, represented by census-tract Normalized Difference Vegetation Index (NDVI) for the seasonal period of May-October, was averaged over the years 2003-2016. Air pollution was estimated by census-tract level PM2.5 concentrations from 1999 to 2015. Cox Proportional Hazard Models were used to estimate hazard ratios (HR) for differences in greenness, air pollution, and physical activity. Alternative models that evaluated potential confounding and stratified models that evaluated effect modification were examined. Mortality risks were associated with PM2.5 (HR = 1.14, 95% CI: 1.09-1.19 per 10 µg/m3) and physical inactivity (1.49, 1.44-1.54 relative to sufficiently active), but not with greenness (1.01, 0.99-1.03 per IQR). The PM2.5-mortality association was mitigated at high levels of greenness (1.05, 0.91-1.22). There was no strong evidence of confounding between air pollution, physical activity, and greenness. However, stratified analysis suggested effect modification for PM2.5 and NDVI by physical activity. A significant protective greenness-mortality association was observed for only highly active individuals (0.91, 0.86-0.96). Also, relatively high PM2.5-mortality HRs were observed for more physically active individuals (1.25, 1.12-1.40). PM2.5 air pollution and physical inactivity are robustly associated with mortality risk. Greenness may be most beneficial and air pollution relatively harmful to highly active individuals. This analysis provides evidence that, in addition to not smoking, being physically active and living in a clean, green environment contributes to improved health and reduced risk of mortality.

Fine particles exposure and cardiopulmonary morbidity in Jeddah: A time-series analysis.

Health effects linked to PM2.5, have been extensively studied in developed countries of Europe and N. America. However, little has been done in Saudi Arabia and the Middle East. This study evaluated the morbidity risk for cardiovascular (CVD) and respiratory (RD) diseases, associated with PM2.5 exposure in Jeddah, Saudi Arabia. 24-h PM2.5 sampling was conducted at 3 sites for 6 weeks quarterly from Apr 8th, 2013-Feb 18th, 2014 with simultaneous hospital data collection. The relative risks (RRs) for cardiopulmonary morbidity at different moving averages (MAs) of lagged exposures were estimated using a generalized linear time-series model. Elevated risks for RD were associated with recent PM2.5 exposures (0-2 days). RD prevalence was highest in children 0-14 years. Overall, RD morbidity risk ranged from 1.081 (CI: 1.005-1.162) to 1.096 (CI: 1.023-1.173) at MAs_2-4; male, 1.081 (CI: 1.019-1.146) to 1.087 (CI: 1.020-1.159) at MAs_2-3, and female, 1.086 (CI: 1.007-1.172) to 1.093 (CI: 1.017-1.175) at MAs_2-4. Generally, females 0-14 years were the most at risk for RDs with RR = 1.097 (CI: 1.025-1.174) to 1.148 (CI: 1.049-1.257). CVD morbidity risk was highest in ER visits with overall RR = 1.057 (CI: 1.005-1.111) to 1.137 (CI: 1.065-1.213) across all MAs; male, 1.060 (CI: 1.007-1.204) to 1.131 (CI: 1.060-1.208); female, 1.065 (CI: 1.008-1.125) to 1.116 (CI: 1.045-1.192). PM2.5 exposure showed significantly increased cardiopulmonary morbidity risk, accentuating the severe health effects associated with elevated PM2.5 in Jeddah. Overall, females (0-14 years) were more at risk for RD morbidity than males. CVD morbidity risk was relatively higher in males than females, with highest risk observed in age-groups above 40 years.

Air pollution and cardiovascular disease.

An escalating body of epidemiologic and clinical research provides compelling evidence that exposure to fine particulate matter air pollution contributes to the development of cardiovascular disease and the triggering of acute cardiac events. There are 3 potential mediating pathways that have been implicated, including "systemic spillover," autonomic imbalance, and circulating particulate matter constituents. Further support that the increased morbidity and mortality attributed to air pollution comes from studies demonstrating the adverse cardiovascular effects of even brief periods of exposure to secondhand smoke. Accordingly, persons with known or suspected cardiovascular disease, the elderly, diabetic patients, pregnant women, and those with pulmonary disease should be counseled to limit leisure-time outdoor activities when air pollution is high. Recognizing the insidious and pervasive nature of air pollution, and the associated odds ratios and population attributable fractions for this widely underappreciated chemical trigger of acute cardiovascular events, may serve to maximize the potential for cardiovascular risk reduction by addressing at least a portion of the 10%-25% incidence of coronary disease that is unexplained by traditional risk factors.