BackgroundRegional differences in the oxidative potential of fine particulate air pollution (PM2.5) may modify its impact on the risk of myocardial infarction.MethodsA 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 (OPGSH) and ascorbate-related (OPAA) 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 (Oxwt) based on their redox potentials.ResultsIn total, 30,101 cases of myocardial infarction were included in the analysis. For regions above the 90th percentile of OPGSH each 5 μg/m3 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 75th percentile and no association was observed below the 50th 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 OPGSH and high Oxwt (p-interaction < 0.001).ConclusionsRegional 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.Electronic supplementary materialThe online version of this article (doi:10.1186/s12940-016-0129-9) contains supplementary material, which is available to authorized users.

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Background: We do not currently understand how spatiotemporal variations in the composition of fine particulate air pollution [fine particulate matter with aerodynamic diameter ( )] affects population health risks. However, recent evidence suggests that joint concentrations of transition metals and sulfate may influence the oxidative potential (OP) of and associated health impacts. Objectives: The purpose of the study was to evaluate how combinations of transition metals/OP and sulfur content in outdoor influence associations with acute cardiovascular events. Methods: We conducted a national case-crossover study of outdoor and acute cardiovascular events in Canada between 2016 and 2017 (93,344 adult cases). Monthly mean transition metal and sulfur (S) concentrations in were determined prospectively along with estimates of OP using acellular assays for glutathione ( ), ascorbate ( ), and dithiothreitol depletion ( ). Conditional logistic regression models were used to estimate odds ratios (OR) [95% confidence intervals (CI)] for across strata of transition metals/OP and sulfur. Results: Among men, the magnitudes of observed associations were strongest when both transition metal and sulfur content were elevated. For example, an OR of 1.078 (95% CI: 1.049, 1.108) (per ) was observed for cardiovascular events in men when both copper and S were above the median, whereas a weaker association was observed when both elements were below median values ( , 95% CI: 1.007, 1.031). A similar pattern was observed for OP metrics. was not associated with acute cardiovascular events in women. Discussion: The combined transition metal and sulfur content of outdoor influences the strength of association with acute cardiovascular events in men. Regions with elevated concentrations of both sulfur and transition metals in should be examined as priority areas for regulatory interventions. https://doi.org/10.1289/EHP9449

Limited toxicity data on electronic cigarette (ECIG) impede evidence-based policy recommendations. We compared two popular mixed fruit flavored ECIG-liquids with and without nicotine aerosolized at 40 W (E-smoke) with respect to particle number concentrations, chemical composition, and response on physiologically relevant human bronchial and alveolar lung mucosa models cultured at air–liquid interface. E-smoke was characterized by significantly increased particle number concentrations with increased wattage (25, 40, and 55 W) and nicotine presence. The chemical composition of E-smoke differed across the two tested flavors in terms of cytotoxic compounds including p-benzoquinone, nicotyrine, and flavoring agents (for example vanillin, ethyl vanillin). Significant differences in the expression of markers for pro-inflammation, oxidative stress, tissue injury/repair, alarm anti-protease, anti-microbial defense, epithelial barrier function, and epigenetic modification were observed between the flavors, nicotine content, and/ or lung models (bronchial or alveolar). Our findings indicate that ECIG toxicity is influenced by combination of multiple factors including flavor, nicotine content, vaping regime, and the region of respiratory tree (bronchial or alveolar). Toxic chemicals and flavoring agents detected in high concentrations in the E-smoke of each flavor warrant independent evaluation for their specific role in imparting toxicity. Therefore, multi-disciplinary approaches are warranted for comprehensive safety profiling of ECIG.

Background: Regional differences in the oxidative potential of fine particulate air pollution (PM 2.5) 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 PM 2.5 oxidative potential on the relationship between PM 2.5 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 NO 2 and O 3 were also examined using their sum (O x) and a weighted average (O x 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 PM 2.5 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 PM 2.5 and myocardial infarction occurring in areas with high regional OP GSH and high O x wt (p-interaction < 0.001). Conclusions: Regional PM 2.5 oxidative potential may modify the impact of PM 2.5 on the risk of myocardial infarction. The combined oxidant capacity of NO 2 and O 3 may magnify this effect.