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

Abstract

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.

Genome-wide transcriptional analysis of cardiovascular-related genes and pathways induced by PM2.5 in human myocardial cells

“…As far as we know, oxidative stress is the main mechanism for PM 2.5 -caused toxicity (Dai et al 2016;Weichenthal et al 2016). In addition, inflammation, changes in blood viscosity, dysfunction of myocardial cell ion channel, and cardiac autonomic nerve also have a toxic effect on the cardiovascular Fig.…”

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

“…27 Therefore, one explanation for the observed trend of increased MI risk across tertiles of biomass contributions to PM 2.5 may be that the oxidative potential of PM 2.5 is increased when biomass contributions are greater. Indeed, at least two recent studies support this hypothesis.…”

Ambient Size Distributions and Lung Deposition of Aerosol Dithiothreitol-Measured Oxidative Potential: Contrast between Soluble and Insoluble Particles

“…Positive associations between cardiorespiratory health end points and OP measured with the dithiothreitol (DTT) assay (OP DTT ) have been reported (units for OP DTT are loss of DTT per time per volume of air sampled). 5–7 Physiologically relevant assays, glutathione (OP GSH ) and ascorbic acid (OP AA ) (both antioxidants found in lung fluid), tested in a synthetic respiratory tract lining fluid model, show mixed results; OP GSH has been associated with lung cancer mortality 8 and myocardial infarction, 9 while OP AA was not. In other studies, neither OP GSH nor OP AA was associated with respiratory function 10,11 or cardiorespiratory mortality.…”