Epidemiological studies likely need to consider PM2.5 composition even if total outdoor PM2.5 mass concentration is the exposure of interest.

Background: Outdoor fine particulate air pollution, <2.5 µm (PM2.5) mass concentrations can be constructed through many different combinations of chemical components that have varying levels of toxicity. This poses a challenge for studies interested in estimating the health effects of total outdoor PM2.5 (i.e., how much PM2.5 mass is present in the air regardless of composition) because we must consider possible confounders of the version of treatment-outcome relationships. Methods: We evaluated the extent of possible bias in mortality hazard ratios for total outdoor PM2.5 by examining models with and without adjustment for sulfate and nitrate in PM2.5 as examples of potential confounders of version of treatment-outcome relationships. Our study included approximately 3 million Canadians and Cox proportional hazard models were used to estimate hazard ratios for total outdoor PM2.5 adjusting for sulfate and/or nitrate and other relevant covariates. Results: Hazard ratios for total outdoor PM2.5 and nonaccidental, cardiovascular, and respiratory mortality were overestimated due to the confounding version of treatment-outcome relationships, and associations for lung cancer mortality were underestimated. Sulfate was most strongly associated with nonaccidental, cardiovascular, and respiratory mortality suggesting that regulations targeting this specific component of outdoor PM2.5 may have greater health benefits than interventions targeting total PM2.5. Conclusions: Studies interested in estimating the health impacts of total outdoor PM2.5 (i.e., how much PM2.5 mass is present in the air) need to consider potential confounders of the version of treatment-outcome relationships. Otherwise, health risk estimates for total PM2.5 will reflect some unknown combination of how much PM2.5 mass is present in the air and the kind of PM2.5 mass that is present.

Biomass Burning as a Source of Ambient Fine Particulate Air Pollution and Acute Myocardial Infarction.

BACKGROUND: Biomass burning is an important source of ambient fine particulate air pollution (PM2.5) in many regions of the world. METHODS: We conducted a time-stratified case-crossover study of ambient PM2.5 and hospital admissions for myocardial infarction (MI) in three regions of British Columbia, Canada. Daily hospital admission data were collected between 2008 and 2015 and PM2.5 data were collected from fixed site monitors. We used conditional logistic regression models to estimate odds ratios (ORs) describing the association between PM2.5 and the risk of hospital admission for MI. We used stratified analyses to evaluate effect modification by biomass burning as a source of ambient PM2.5 using the ratio of levoglucosan/PM2.5 mass concentrations. RESULTS: Each 5 µg/m increase in 3-day mean PM2.5 was associated with an increased risk of MI among elderly subjects (≥65 years; OR = 1.06, 95% CI: 1.03, 1.08); risk was not increased among younger subjects. Among the elderly, the strongest association occurred during colder periods (<6.44°C); when we stratified analyses by tertiles of monthly mean biomass contributions to PM2.5 during cold periods, ORs of 1.19 (95% CI: 1.04, 1.36), 1.08 (95% CI: 1.06, 1.09), and 1.04 (95% CI: 1.03, 1.06) were observed in the upper, middle, and lower tertiles (Ptrend = 0.003), respectively. CONCLUSION: Short-term changes in ambient PM2.5 were associated with an increased risk of MI among elderly subjects. During cold periods, increased biomass burning contributions to PM2.5 may modify its association with MI.

Ambient PM2.5 and risk of emergency room visits for myocardial infarction: impact of regional PM2.5 oxidative potential: a case-crossover study.

BACKGROUND: Regional differences in the oxidative potential of fine particulate air pollution (PM2.5) may modify its impact on the risk of myocardial infarction. METHODS: A case-crossover study was conducted in 16 cities in Ontario, Canada to evaluate the impact of regional PM2.5 oxidative potential on the relationship between PM2.5 and emergency room visits for myocardial infarction. Daily air pollution and meteorological data were collected between 2004 and 2011 from provincial monitoring sites and regional estimates of glutathione (OP(GSH)) and ascorbate-related (OP(AA)) oxidative potential were determined using an acellular assay based on a synthetic respiratory tract lining fluid. Exposure variables for the combined oxidant capacity of NO2 and O3 were also examined using their sum (Ox) and a weighted average (Ox (wt)) based on their redox potentials. RESULTS: In total, 30,101 cases of myocardial infarction were included in the analysis. For regions above the 90(th) percentile of OP(GSH) each 5 µg/m(3) increase in same-day PM2.5 was associated with a 7.9 % (95 % CI: 4.1, 12) increased risk of myocardial infarction whereas a 4.1 % (95 % CI: 0.26, 8.0) increase was observed in regions above the 75(th) percentile and no association was observed below the 50(th) percentile (p-interaction = 0.026). A significant 3-way interaction was detected with the strongest associations between PM2.5 and myocardial infarction occurring in areas with high regional OP(GSH) and high Ox (wt) (p-interaction < 0.001). CONCLUSIONS: Regional PM2.5 oxidative potential may modify the impact of PM2.5 on the risk of myocardial infarction. The combined oxidant capacity of NO2 and O3 may magnify this effect.

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.

Exposure assessment for estimation of the global burden of disease attributable to outdoor air pollution.

Ambient air pollution is associated with numerous adverse health impacts. Previous assessments of global attributable disease burden have been limited to urban areas or by coarse spatial resolution of concentration estimates. Recent developments in remote sensing, global chemical-transport models, and improvements in coverage of surface measurements facilitate virtually complete spatially resolved global air pollutant concentration estimates. We combined these data to generate global estimates of long-term average ambient concentrations of fine particles (PM(2.5)) and ozone at 0.1° × 0.1° spatial resolution for 1990 and 2005. In 2005, 89% of the world's population lived in areas where the World Health Organization Air Quality Guideline of 10 µg/m(3) PM(2.5) (annual average) was exceeded. Globally, 32% of the population lived in areas exceeding the WHO Level 1 Interim Target of 35 µg/m(3), driven by high proportions in East (76%) and South (26%) Asia. The highest seasonal ozone levels were found in North and Latin America, Europe, South and East Asia, and parts of Africa. Between 1990 and 2005 a 6% increase in global population-weighted PM(2.5) and a 1% decrease in global population-weighted ozone concentrations was apparent, highlighted by increased concentrations in East, South, and Southeast Asia and decreases in North America and Europe. Combined with spatially resolved population distributions, these estimates expand the evaluation of the global health burden associated with outdoor air pollution.