Lauren Pinault

Oxidative burden of fine particulate air pollution and risk of cause-specific mortality in the Canadian Census Health and Environment Cohort (CanCHEC).

BACKROUND Fine particulate air pollution (PM2.5) is known to contribute to cardiorespiratory mortality but it is not clear how PM2.5 oxidative burden (i.e. the ability of PM2.5 to cause oxidative stress) may influence long-term mortality risk. METHODS We examined the relationship between PM2.5 oxidative burden and cause-specific mortality in Ontario, Canada. Integrated PM2.5 samples were collected from 30 provincial monitoring sites between 2012 and 2013. The oxidative potential (% depletion/µg) of regional PM2.5 was measured as the ability of filter extracts to deplete antioxidants (glutathione and ascorbate) in a synthetic respiratory tract lining fluid. PM2.5oxidative burden was calculated as the product of PM2.5 mass concentrations and regional estimates of oxidative potential. In total, this study included 193,300 people who completed the Canadian long-form census in 1991 and who lived within 5km of a site where oxidative potential was measured. Deaths occurring between 1991 and 2009 were identified through record linkages and Cox proportional hazard models were used to estimate hazard ratios (and 95% confidence intervals) for interquartile changes in exposure adjusting for individual-level covariates and indirect-adjustment for smoking and obesity. RESULTS Glutathione-related oxidative burden was associated with cause-specific mortality. For lung cancer specifically, this metric was associated with a 12% (95% CI: 5.0-19) increased risk of mortality whereas a 5.0% (95% CI: 0.1, 10) increase was observed for PM2.5. Indirect adjustment for smoking and obesity decreased the lung cancer hazard ratio for glutathione-related oxidative burden but it remained significantly elevated (HR=1.07, 95% CI: 1.005, 1.146). Ascorbate-related oxidative burden was not associated with mortality. CONCLUSIONS Our findings suggest that glutathione-related oxidative burden may be more strongly associated with lung cancer mortality than PM2.5 mass concentrations.

Spatial associations between socioeconomic groups and NO2 air pollution exposure within three large Canadian cities.

Previous studies of environmental justice in Canadian cities have linked lower socioeconomic status to greater air pollution exposures at coarse geographic scales, (i.e., Census Tracts). However, studies that examine these associations at finer scales are less common, as are comparisons among cities. To assess differences in exposure to air pollution among socioeconomic groups, we assigned estimates of exposure to ambient nitrogen dioxide (NO2), a marker for traffic-related pollution, from city-wide land use regression models to respondents of the 2006 Canadian census long-form questionnaire in Toronto, Montreal, and Vancouver. Data were aggregated at a finer scale than in most previous studies (i.e., by Dissemination Area (DA), which includes approximately 400-700 persons). We developed simultaneous autoregressive (SAR) models, which account for spatial autocorrelation, to identify associations between NO2 exposure and indicators of social and material deprivation. In Canadas three largest cities, DAs with greater proportions of tenants and residents who do not speak either English or French were characterised by greater exposures to ambient NO2. We also observed positive associations between NO2 concentrations and indicators of social deprivation, including the proportion of persons living alone (in Toronto), and the proportion of persons who were unmarried/not in a common-law relationship (in Vancouver). Other common measures of deprivation (e.g., lone-parent families, unemployment) were not associated with NO2 exposures. DAs characterised by selected indicators of deprivation were associated with higher concentrations of ambient NO2 air pollution in the three largest cities in Canada.

Associations between fine particulate matter and mortality in the 2001 Canadian Census Health and Environment Cohort

Background: Large cohort studies have been used to characterise the association between long‐term exposure to fine particulate matter (PM2.5) air pollution with non‐accidental, and cause‐specific mortality. However, there has been no consensus as to the shape of the association between concentration and response. Methods: To examine the shape of this association, we developed a new cohort based on respondents to the 2001 Canadian census long‐form. We applied new annual PM2.5 concentration estimates based on remote sensing and ground measurements for Canada at a 1 km spatial scale from 1998 to 2011. We followed 2.4 million respondents who were non‐immigrants aged 25–90 years and did not reside in an institution over a 10 year period for mortality. Exposures were assigned as a 3‐year mean prior to the follow‐up year. Income tax files were used to account for residential mobility among respondents using postal codes, with probabilistic imputation used for missing postal codes in the tax data. We used Cox survival models to determine hazard ratios (HRs) for cause‐specific mortality. We also estimated Shape Constrained Health Impact Functions (a concentration‐response function) for selected causes of death. Results: In models stratified by age, sex, airshed, and population centre size, and adjusted for individual and neighbourhood socioeconomic variables, HR estimates for non‐accidental mortality were HR = 1.18 (95% CI: 1.15–1.21) per 10 &mgr;g/m3 increase in concentration. We observed higher HRs for cardiovascular disease (HR=1.25; 95% CI: 1.19–1.31), cardio‐metabolic disease (HR = 1.27; 95% CI: 1.21–1.33), ischemic heart disease (HR = 1.36; 95% CI: 1.28–1.44) and chronic obstructive pulmonary disease (COPD) mortality (HR = 1.24; 95% CI: 1.11–1.39) compared to HR for all non‐accidental causes of death. For non‐accidental, cardio‐metabolic, ischemic heart disease, respiratory and COPD mortality, the shape of the concentration‐response curve was supra‐linear, with larger differences in relative risk for lower concentrations. For both pneumonia and lung cancer, there was some suggestion that the curves were sub‐linear. Conclusions: Associations between ambient concentrations of fine particulate matter and several causes of death were non‐linear for each cause of death examined. HighlightsAssociations between PM2.5 and mortality were examined in a new Canadian cohort.Hazard ratios between NAC mortality and PM2.5 were 1.18 per 10 &mgr;g/m3 increase.The shape of the concentration‐response curve was non‐linear for all causes of death examined.

Impact of Oxidant Gases on the Relationship between Outdoor Fine Particulate Air Pollution and Nonaccidental, Cardiovascular, and Respiratory Mortality

Outdoor fine particulate air pollution (PM2.5) is known to increase mortality risk and is recognized as an important contributor to global disease burden. However, less is known about how oxidant gases may modify the chronic health effects of PM2.5. In this study, we examined how the oxidant capacity of O3 and NO2 (using a redox-weighted average, Ox) may modify the relationship between PM2.5 and mortality in the 2001 Canadian Census Health and Environment Cohort. In total, 2,448,500 people were followed over a 10.6-year period. Each 3.86 µg/m3 increase in PM2.5 was associated with nonaccidental (Hazard Ratio (HR) = 1.095, 95% CI: 1.077, 1.112), cardiovascular (HR = 1.088, 95% CI: 1.059, 1.118), and respiratory mortality (HR = 1.110, 95% CI: 1.051, 1.171) in the highest tertile of Ox whereas weaker/null associations were observed in the middle and lower tertiles. Analysis of joint non-linear concentration-response relationships for PM2.5 and Ox suggested threshold concentrations between approximately 23 and 25 ppb with Ox concentrations above these values strengthening PM2.5-mortality associations. Overall, our findings suggest that oxidant gases enhance the chronic health risks of PM2.5. In some areas, reductions in Ox concentrations may have the added benefit of reducing the public health impacts of PM2.5 even if mass concentrations remain unchanged.

Global estimates of mortality associated with long-term exposure to outdoor fine particulate matter

Significance Exposure to outdoor concentrations of fine particulate matter is considered a leading global health concern, largely based on estimates of excess deaths using information integrating exposure and risk from several particle sources (outdoor and indoor air pollution and passive/active smoking). Such integration requires strong assumptions about equal toxicity per total inhaled dose. We relax these assumptions to build risk models examining exposure and risk information restricted to cohort studies of outdoor air pollution, now covering much of the global concentration range. Our estimates are severalfold larger than previous calculations, suggesting that outdoor particulate air pollution is an even more important population health risk factor than previously thought. Exposure to ambient fine particulate matter (PM2.5) is a major global health concern. Quantitative estimates of attributable mortality are based on disease-specific hazard ratio models that incorporate risk information from multiple PM2.5 sources (outdoor and indoor air pollution from use of solid fuels and secondhand and active smoking), requiring assumptions about equivalent exposure and toxicity. We relax these contentious assumptions by constructing a PM2.5-mortality hazard ratio function based only on cohort studies of outdoor air pollution that covers the global exposure range. We modeled the shape of the association between PM2.5 and nonaccidental mortality using data from 41 cohorts from 16 countries—the Global Exposure Mortality Model (GEMM). We then constructed GEMMs for five specific causes of death examined by the global burden of disease (GBD). The GEMM predicts 8.9 million [95% confidence interval (CI): 7.5–10.3] deaths in 2015, a figure 30% larger than that predicted by the sum of deaths among the five specific causes (6.9; 95% CI: 4.9–8.5) and 120% larger than the risk function used in the GBD (4.0; 95% CI: 3.3–4.8). Differences between the GEMM and GBD risk functions are larger for a 20% reduction in concentrations, with the GEMM predicting 220% higher excess deaths. These results suggest that PM2.5 exposure may be related to additional causes of death than the five considered by the GBD and that incorporation of risk information from other, nonoutdoor, particle sources leads to underestimation of disease burden, especially at higher concentrations.