Rationale: Tropospheric ozone (O 3 ) is potentially associated with cardiovascular disease risk and premature death. Results from longterm epidemiological studies on O 3 are scarce and inconclusive.Objectives: In this study, we examined associations between chronic ambient O 3 exposure and all-cause and cause-specific mortality in a large cohort of U.S. adults.Methods: Cancer Prevention Study II participants were enrolled in 1982. A total of 669,046 participants were analyzed, among whom 237,201 deaths occurred through 2004. We obtained estimates of O 3 concentrations at the participant's residence from a hierarchical Bayesian space-time model. Estimates of fine particulate matter (particulate matter with an aerodynamic diameter of up to 2.5 mm [PM 2.5 ]) and NO 2 concentrations were obtained from land use regression. Cox proportional hazards regression models were used to examine mortality associations adjusted for individual-and ecological-level covariates. Measurements and Main Results:In single-pollutant models, we observed significant positive associations between O 3 , PM 2.5 , and NO 2 concentrations and all-cause and cause-specific mortality. In two-pollutant models adjusted for PM 2.5 , significant positive associations remained between O 3 and all-cause (hazard ratio [HR] per 10 ppb, 1.02; 95% confidence interval [CI], 1.01-1.04), circulatory (HR, 1.03; 95% CI, 1.01-1.05), and respiratory mortality (HR, 1.12; 95% CI, 1.08-1.16) that were unchanged with further adjustment for NO 2 . We also observed positive mortality associations with both PM 2.5 (both near source and regional) and NO 2 in multipollutant models.Conclusions: Findings derived from this large-scale prospective study suggest that long-term ambient O 3 contributes to risk of respiratory and circulatory mortality. Substantial health and environmental benefits may be achieved by implementing further measures aimed at controlling O 3 concentrations.

Exposure to green space has been associated with better physical and mental health. Although this exposure could also influence cognitive development in children, available epidemiological evidence on such an impact is scarce. This study aimed to assess the association between exposure to green space and measures of cognitive development in primary schoolchildren. This study was based on 2,593 schoolchildren in the second to fourth grades (7-10 y) of 36 primary schools in Barcelona, Spain (2012-2013. Cognitive development was assessed as 12-mo change in developmental trajectory of working memory, superior working memory, and inattentiveness by using four repeated (every 3 mo) computerized cognitive tests for each outcome. We assessed exposure to green space by characterizing outdoor surrounding greenness at home and school and during commuting by using high-resolution (5 m × 5 m) satellite data on greenness (normalized difference vegetation index). Multilevel modeling was used to estimate the associations between green spaces and cognitive development. We observed an enhanced 12-mo progress in working memory and superior working memory and a greater 12-mo reduction in inattentiveness associated with greenness within and surrounding school boundaries and with total surrounding greenness index (including greenness surrounding home, commuting route, and school). Adding a traffic-related air pollutant (elemental carbon) to models explained 20-65% of our estimated associations between school greenness and 12-mo cognitive development. Our study showed a beneficial association between exposure to green space and cognitive development among schoolchildren that was partly mediated by reduction in exposure to air pollution. neurodevelopment | greenness | cognition | built environment | school

Background Evidence suggests that longer-term exposure to air pollutants over years confers higher risks of cardiovascular morbidity and mortality than shorter term exposure. One explanation is that cumulative adverse effects that develop over longer durations lead to the genesis of chronic disease. Preliminary epidemiological and clinical evidence suggest that air pollution may contribute to the development hypertension and type 2 diabetes. Methods and Results We used Cox proportional hazards models to assess incidence rate ratios (IRRs) and 95% confidence intervals (CI) for incident hypertension and diabetes associated with exposure to fine particulate matter (PM2.5) and nitrogen oxides (NOx) in a cohort of African American women living in Los Angeles. Pollutant levels were estimated at participant residential addresses with land use regression models (NOx) and interpolation from monitoring station measurements (PM2.5). Over follow-up from 1995-2005, 531 incident cases of hypertension and 183 incident cases of diabetes occurred. When pollutants were analyzed separately, the IRR for hypertension for a 10 μg/m3 increase in PM2.5 was 1.48 (95% CI 0.95-2.31) and the IRR for the interquartile range (12.4 parts per billion) of NOx was 1.14 (95% CI 1.03-1.25). The corresponding IRRs for diabetes were 1.63 (95% CI 0.78-3.44) and 1.25 (95% CI 1.07-1.46). When both pollutants were included in the same model, the IRRs for PM2.5 were attenuated and the IRRs for NOx were essentially unchanged for both outcomes. Conclusions Our results suggest that exposure to air pollutants, especially traffic-related pollutants, may increase the risk of type 2 diabetes and possibly of hypertension.