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Updated: Jan 9, 2026

Generation of a Chronic Obstructive Pulmonary Disease Model in Mice by Repeated Ozone Exposure
Published on: August 25, 2017
Risk of venous thromboembolism associated with short-term exposure to fine particulate matter (PM2.5) and ozone air
Scott C Woller1,2, Scott M Stevens1,2, Joseph R Bledsoe3,4
1Department of Medicine, Intermountain Medical Center, Intermountain Health, Salt Lake City, Utah, USA.
Background:
While established associations between air pollution and adverse cardiovascular outcomes are known, it remains uncertain whether short-term exposure to air pollution is a risk factor for venous thromboembolism (VTE). The risk of VTE associated with pollution seasonality (summer wildfire season vs winter inversion season) is not understood.
Objectives:
The aim of this study was to assess for an association between short-term exposure to air pollution and VTE.
Methods:
We queried the electronic data warehouse of an integrated healthcare system for VTE occurrence from January 1, 2008, to March 31, 2022, at 11 hospitals on Utah's Wasatch Front. We described air pollution based on small particulate matter (PM2.5) and ozone exposures stratified by day and rolling multiday blocks. We described VTE outcomes in relation to wildfire season (June-October) and inversion season (November-March). We hypothesized that there would be no increased risk of VTE on high PM2.5 days and high ozone days compared with low PM2.5 days and low ozone days.
Results:
Among 25,083 VTE cases, no significant association was observed between short-term PM2.5 air pollution and VTE. Only lag 2-day ozone exposure was associated with an increased VTE risk (odds ratio [OR], 1.03 per +10 parts per billion; 95% CI, 1.01-1.06; P = .02). During the wildfire season, elevated ozone was associated with an increased odds of VTE at lag 1-day (OR, 1.05; 95% CI, 1.00-1.10; P = .0545), mean 3-day lagged average (OR, 1.06; 95% CI, 1.00-1.13; P = .05), and mean 7-day lagged average (OR, 1.09; 95% CI, 1.01-1.18; P = .037).
Conclusion:
We found little evidence that short-term air pollution exposure increases VTE risk. However, short-term PM2.5 and short-term ozone exposure may variably confer risk for VTE when stratified by wildfire and inversion seasons.
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