Abstract

Background: Cardiovascular disease (CVD) is the leading cause of mortality worldwide. Exposure to air pollution, specifically PM2.5, is a well-established risk factor for CVD. However, the contribution of gaseous pollutant exposure to CVD risk is less clear.Methods: To examine the cardiovascular effects of volatile organic compounds (VOCs) on vascular function, we measured urinary metabolites of acrolein (CEMA and 3-HPMA), 1,3-butadiene (DHBMA and MHBMA3), and crotonaldehyde (HPMMA) in 309 nonsmokers with varying levels of CVD risk, recruited from a preventive cardiology clinic. On the day of enrollment, we measured blood pressure (BP), reactive hyperemia index (RHI - a marker of endothelial dysfunction), and urinary levels of biogenic amines and their metabolites.Results: We found that the urinary levels of 3-HPMA, DHBMA, and HPMMA were higher in White than Black participants. Levels of DHBMA and HPMMA were higher in women than men. Using generalized linear models, we found that 3-HPMA was positively associated with systolic BP (0.98 per SD of 3HPMA; CI: 0.04, 1.91; P=0.04). The relationship found in the total cohort remained significant for Black participants, despite lower levels of urinary 3-HPMA in this population. Associations between VOC metabolites and BP were independent of PM2.5 exposure and BP medications. For each IQR of 3-HPMA or DHBMA, there was a 3.3% (CI: -6.18, -0.37; p-value: 0.03) or a 4.0% (CI: -7.72, -0.12; P=0.04) decrease in RHI. Urinary levels of MHBMA3 were positively associated with a 2.92% increase in urinary epinephrine (CI: 0.48, 5.37; P=0.02). Although the association between VOC metabolites and BP were independent of urinary catecholamines, it was stronger in participants with higher urinary levels of epinephrine.Conclusions: Taken together, these findings suggest that exposure to VOCs (acrolein, 1,3-butadiene, and crotonaldehyde) may lead to endothelial dysfunction particularly in those with a higher sympathetic tone, and contribute to risk of hypertension.

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