Background: Approximately 2.9 million deaths are attributed to ambient fine particle air pollution around the world each year (PM_2.5). In general, cohort studies of mortality and outdoor PM_2.5 concentrations have limited information on individuals exposed to low levels of PM_2.5 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 PM_2.5 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 PM_2.5. 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 PM_2.5 exposure estimates, and mortality incidence to 2016. Cox proportional hazard models were used to estimate the relationship between non-accidental mortality and ambient PM_2.5 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 PM_2.5 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 PM_2.5 were increased for males, those under age 65, and non-immigrants. Hazard ratios for PM_2.5 and mortality were attenuated when gaseous pollutants were included in models. Conclusions: Outdoor PM_2.5 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 PM_2.5 concentrations.

Ambient fine particulate matter (PM2.5) is associated with a wide range of acute and chronic health effects, including increased risk of respiratory infection. However, evidence specifically related to novel coronavirus disease (COVID-19) is limited. COVID-19 case counts for 111 Canadian health regions were obtained from the COVID-19 Canada Open Data portal. Annual PM2.5 data for 2000–2016 were estimated from a national exposure surface based on remote sensing, chemical transport modelling and ground observations, and minimum and maximum temperature data for 2000–2015 were based on a national interpolated surface derived from thin-plate smoothing splines. Population counts and sociodemographic data by health region were obtained from the 2016 census, and health data (self-rated health and prevalence of smoking, obesity, and selected chronic diseases) by health region, were obtained from the Canadian Community Health Survey. Data on total number of COVID-19 tests and changes in mobility comparing post-vs. pre-introduction of social distancing measures were available by province. Data were analyzed using negative binomial regression models. After controlling for province, temperature, demographic and health characteristics and days since peak incidence by health region, long-term PM2.5 exposure exhibited a positive association with COVID-19 incidence (incidence rate ratio 1.07, 95% confidence interval 0.97–1.18 per μg/m3). This association was larger in magnitude and statistically significant in analyses excluding provinces that reported cases only for aggregated health regions, excluding health regions with less than median population density, and restricted to the most highly affected provinces (Quebec and Ontario). We observed a positive association between COVID-19 incidence and long-term PM2.5 exposure in Canadian health regions. The association was larger in magnitude and statistically significant in more highly affected health regions and those with potentially less exposure measurement error. While our results generate hypotheses for further testing, they should be interpreted with caution and require further examination using study designs less prone to bias.

A mobile laboratory equipped with state-of-the-art gaseous and particulate instrumentation was deployed across the Greater Toronto Area (GTA) during two seasons. A high-resolution time-of-flight chemical ionization mass spectrometer (HR-TOF-CIMS) measured isocyanic acid (HNCO) and hydrogen cyanide (HCN), and a high-sensitivity laser-induced incandescence (HS-LII) instrument measured black carbon (BC). Results indicate that on-road vehicles are a clear source of HNCO and HCN and that their impact is more pronounced in the winter, when influences from biomass burning (BB) and secondary photochemistry are weakest. Plume-based and time-based algorithms were developed to calculate fleet-average vehicle emission factors (EFs); the algorithms were found to yield comparable results, depending on the pollutant identity. With respect to literature EFs for benzene, toluene, C2 benzene (sum of m-, p-, and o-xylenes and ethylbenzene), nitrogen oxides, particle number concentration (PN), and black carbon, the calculated EFs were characteristic of a relatively clean vehicle fleet dominated by light-duty vehicles (LDV). Our fleet-average EF for BC (median: 25 mg kg${}_{\mathrm{fuel}}^{-\mathrm{1}}$ ; interquartile range, IQR: 10–76 mg kg${}_{\mathrm{fuel}}^{-\mathrm{1}}$ ) suggests that overall vehicular emissions of BC have decreased over time. However, the distribution of EFs indicates that a small proportion of high-emitters continue to contribute disproportionately to total BC emissions. We report the first fleet-average EF for HNCO (median: 2.3 mg kg${}_{\mathrm{fuel}}^{-\mathrm{1}}$ , IQR: 1.4–4.2 mg kg${}_{\mathrm{fuel}}^{-\mathrm{1}}$ ) and HCN (median: 0.52 mg kg${}_{\mathrm{fuel}}^{-\mathrm{1}}$ , IQR: 0.32–0.88 mg kg${}_{\mathrm{fuel}}^{-\mathrm{1}}$ ). The distribution of the estimated EFs provides insight into the real-world variability of HNCO and HCN emissions and constrains the wide range of literature EFs obtained from prior dynamometer studies. The impact of vehicle emissions on urban HNCO levels can be expected to be further enhanced if secondary HNCO formation from vehicle exhaust is considered.

A growing number of studies observe associations between the amount of green space around a mother’s home and positive birth outcomes; however, the robustness of this association and potential pathways of action remain unclear. To examine associations between mother’s residential green space and term birth weight within the Canadian Healthy Infant Longitudinal Development (CHILD) study and examine specific hypothesized pathways. We examined 2510 births located in Vancouver, Edmonton, Winnipeg, and Toronto Canada. Green space was estimated around mother’s residences during pregnancy using Landsat 30 m normalized difference vegetation index (NDVI). We examined hypothesized pathways of: (1) reduction of environmental exposure; (2) built environment features promoting physical activity; (3) psychosocial conditions; and (4) psychological influences. Linear regression was used to assess associations between green space and term birth weight adjusting first for a comprehensive set of confounding factors and then incrementally for pathway variables. Fully adjusted models showed non-statistically significant increases in term birth weight with increasing green space. For example, a 0.1 increase in NDVI within 500 m was associated with a 21.5 g (95% CI − 4.6, 47.7) increase in term birth weight. Associations varied by city and were most robust for high-density locations. For the two largest cities (Vancouver and Toronto), we observed an increase in birth weight of 41.2 g (95% CI 7.8, 74.6) for a 0.1 increase in NDVI within 500 m. We did not observe substantial reductions in the green space effect on birth weight when adjusting for pathway variables. Our results highlight the need to further characterize the interactions between green space, urban density and climate related factors as well as the pathways linking residential green space to birth outcomes.

Industrial sources contribute a significant proportion of anthropogenic particulate matter (PM) emissions, producing particles of varying composition that may differentially impact health. This study investigated the in vitro toxicity of ambient PM collected near industrial sites in relation to particle size and composition. Size-fractionated particles (ultrafine, PM0.1–2.5, PM2.5–10, PM>10) were collected in the vicinity of steel, copper, aluminium, and petrochemical industrial sites. Human lung epithelial-like A549 and murine macrophage-like J774A.1 cells were exposed for 24 h to particle suspensions (0, 30, 100, 300 μg/cm2). Particle potency was assessed using cytotoxic (resazurin reduction, lactate dehydrogenase (LDH) release) and inflammatory (cytokine release) assays, and regressed against composition (metals, polycyclic aromatic hydrocarbons (PAHs), endotoxin). Coarse (PM2.5–10, PM>10) particle fractions were composed primarily of iron and aluminium; in contrast, ultrafine and fine (PM0.1–2.5) fractions displayed considerable variability in metal composition (especially water-soluble metals) across collection sites consistent with source contributions. Semi-volatile and PM-associated PAHs were enriched in the fine and coarse fractions collected near metal industry. Cell responses to exposure at equivalent mass concentrations displayed striking differences among sites (SITE x SIZE and SITE x DOSE interactions, p < 0.05), suggesting that particle composition, in addition to size, impacted particle toxicity. While both J774A.1 and A549 cells exhibited clear particle size-dependent effects, site-dependent differences were more pronounced in J774A.1 cells, suggesting greater sensitivity to particle composition. Plotting particle potency according to cytotoxic and inflammatory response grouped particles by size and site, and showed that particles of similar composition tended to cluster together. Cytotoxic effects in J774A.1 cells correlated with metal and PAH content, while inflammatory responses were associated primarily with endotoxin content in coarse particles. Industrial sources produce particulate emissions with varying chemical composition that differ in their in vitro potency in relation to particle size and the levels of specific constituents.