US EPA

3275174 

Journal Article 

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

Weichenthal, S; Lavigne, E; Evans, G; Pollitt, K; Burnett, RT 

2016 

0 

Environmental Health
ISSN: 0013-9270 

15 

46 

English 

27012244 

10.1186/s12940-016-0129-9 

WOS:000372776200001 

is supplemented by 3449410 - Supplementary material

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 (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 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 90th percentile of OPGSH each 5 mu g/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 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 O-x(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 O-3 may magnify this effect. 

Particulate matter; Oxidative potential; Myocardial infarction; Case-crossover