Background: Decision making regarding air pollution can be better informed if air quality impacts are traced back to individual emission sources. Adjoint or backward sensitivity analysis is a modeling tool that can achieve this goal by allowing for quantification of how emissions from sources in different locations influence human health metrics.Objectives: We attributed short-term mortality (valuated as an overall “health benefit”) in Canada and the United States to anthropogenic nitrogen oxides (NOx) and volatile organic compound (VOC) emissions across North America.Methods: We integrated epidemiological data derived from Canadian and U.S. time-series studies with the adjoint of an air quality model and also estimated influences of anthropogenic emissions at each location on nationwide health benefits.Results: We found significant spatiotemporal variability in estimated health benefit influences of NOx and VOC emission reductions on Canada and U.S. mortality. The largest estimated influences on Canada (up to $250,000/day) were from emissions originating in the Quebec City–Windsor Corridor, where population centers are concentrated. Estimated influences on the United States tend to be widespread and more substantial owing to both larger emissions and larger populations. The health benefit influences calculated using 24-hr average ozone (O3) concentrations are lower in magnitude than estimates calculated using daily 1-hr maximum O3 concentrations.Conclusions: Source specificity of the adjoint approach provides valuable information for guiding air quality decision making. Adjoint results suggest that the health benefits of reducing NOx and VOC emissions are substantial and highly variable across North America.

Background Approximately 2.9 million deaths are attributed to ambient fine particle air pollution around the world each year (PM2.5). In general, cohort studies of mortality and outdoor PM2.5 concentrations have limited information on individuals exposed to low levels of PM2.5 as well as covariates such as smoking behaviours, alcohol consumption, and diet which may confound relationships with mortality. This study provides an updated and extended analysis of the Canadian Community Health Survey-Mortality cohort: a population-based cohort with detailed PM2.5 exposure data and information on a number of important individual-level behavioural risk factors. We also used this rich dataset to provide insight into the shape of the concentration-response curve for mortality at low levels of PM2.5. Methods Respondents to the Canadian Community Health Survey from 2000 to 2012 were linked by postal code history from 1981 to 2016 to high resolution PM2.5 exposure estimates, and mortality incidence to 2016. Cox proportional hazard models were used to estimate the relationship between non-accidental mortality and ambient PM2.5 concentrations (measured as a three-year average with a one-year lag) adjusted for socio-economic, behavioural, and time-varying contextual covariates. Results In total, 50,700 deaths from non-accidental causes occurred in the cohort over the follow-up period. Annual average ambient PM2.5 concentrations were low (i.e. 5.9 μg/m3, s.d. 2.0) and each 10 μg/m3 increase in exposure was associated with an increase in non-accidental mortality (HR = 1.11; 95% CI 1.04–1.18). Adjustment for behavioural covariates did not materially change this relationship. We estimated a supra-linear concentration-response curve extending to concentrations below 2 μg/m3 using a shape constrained health impact function. Mortality risks associated with exposure to PM2.5 were increased for males, those under age 65, and non-immigrants. Hazard ratios for PM2.5 and mortality were attenuated when gaseous pollutants were included in models. Conclusions Outdoor PM2.5 concentrations were associated with non-accidental mortality and adjusting for individual-level behavioural covariates did not materially change this relationship. The concentration-response curve was supra-linear with increased mortality risks extending to low outdoor PM2.5 concentrations.

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Background:Ambient fine particulate air pollution with aerodynamic diameter ≤2.5 μm (PM2.5) is an important contributor to the global burden of disease. Information on the shape of the concentration–response relationship at low concentrations is critical for estimating this burden, setting air quality standards, and in benefits assessments.Objectives:We examined the concentration–response relationship between PM2.5 and nonaccidental mortality in three Canadian Census Health and Environment Cohorts (CanCHECs) based on the 1991, 1996, and 2001 census cycles linked to mobility and mortality data.Methods:Census respondents were linked with death records through 2016, resulting in 8.5 million adults, 150 million years of follow-up, and 1.5 million deaths. Using annual mailing address, we assigned time-varying contextual variables and 3-y moving-average ambient PM2.5 at a 1×1 km spatial resolution from 1988 to 2015. We ran Cox proportional hazards models for PM2.5 adjusted for eight subject-level indicators of socioeconomic status, seven contextual covariates, ozone, nitrogen dioxide, and combined oxidative potential. We used three statistical methods to examine the shape of the concentration–response relationship between PM2.5 and nonaccidental mortality.Results:The mean 3-y annual average estimate of PM2.5 exposure ranged from 6.7 to 8.0 μg/m3 over the three cohorts. We estimated a hazard ratio (HR) of 1.053 [95% confidence interval (CI): 1.041, 1.065] per 10-μg/m3 change in PM2.5 after pooling the three cohort-specific hazard ratios, with some variation between cohorts (1.041 for the 1991 and 1996 cohorts and 1.084 for the 2001 cohort). We observed a supralinear association in all three cohorts. The lower bound of the 95% CIs exceeded unity for all concentrations in the 1991 cohort, for concentrations above 2 μg/m3 in the 1996 cohort, and above 5 μg/m3 in the 2001 cohort.Discussion:In a very large population-based cohort with up to 25 y of follow-up, PM2.5 was associated with nonaccidental mortality at concentrations as low as 5 μg/m3. https://doi.org/10.1289/EHP5204