Immediately before, immediately after, and the day after the two exposures, participants underwent spirometry and had blood drawn. Ambulatory ECG monitoring was done throughout a 24-hour period.
There were no reports of post-exposure symptoms among the participants.
Changes in biomarkers of inflammation included an increase of 55.7% (95% CI −5.1 to 152.9) in IL-1-beta and a rise of 10.1% (95% CI −0.75 to 22.1) in tumor necrosis factor-alpha.
Even 24 hours after the ozone exposure, blood levels of IL-1-beta were 103.8% (95% CI 32.5 to 213.9) higher than at baseline, and C-reactive protein levels were 65.4% (95% CI 8.1 to 152.9) above pre-exposure levels.
The decrease in the thrombotic marker PAI-1 remained 24 hours after exposure, giving an overall 42.7% reduction (95% CI −65.5 to −5.1).
After 24 hours, plasminogen levels had decreased by 41.5% (95% CI −67.1 to −16).
The researchers also detected a “small but significant” lengthening of the QT interval immediately following ozone exposure, a finding which they noted can increase risk for ventricular tachyarrhythmias and even sudden death.
Additionally, spirometric measures showed changes including a 10.9% (95% CI −6.5 to −15.2) drop in forced expiratory volume in 1 second.
“We believe that the changes in ozone-induced vascular inflammation, fibrinolysis markers, and [heart rate variability] detailed in this study provide the most compelling data to date of the potential for ozone to modulate the cardiovascular system,” wrote Devlin and colleagues.
Potential mechanisms by which ozone might have adverse cardiovascular effects include oxidation of cholesterol in plaque, release of inflammatory mediators from the lung into the bloodstream, and changes to the autonomic nervous system.
“These changes could potentially put a susceptible individual at risk for an adverse clinical event and thus provide biological plausibility to the epidemiology studies that have reported associations between ozone exposure and mortality/morbidity,” the researchers warned in conclusion.