Katlyn E McGraw1, Daniel W Riggs2, Shesh Rai3, Ana Navas-Acien4, Zhengzhi Xie5, Pawel Lorkiewicz5, Jordan Lynch5, Nagma Zafar6, Sathya Krishnasamy6, Kira C Taylor7, Daniel J Conklin5, Andrew P DeFilippis5, Sanjay Srivastava8, Aruni Bhatnagar9. 1. Christina Lee Brown Envirome Institute, 302 E Muhammad Ali Blvd, Louisville, KY, 40202, USA; Superfund Research Center, 302 E Muhammad Ali Blvd, Louisville, KY 40202, USA; University of Louisville School of Public Health and Information Sciences, USA; Department of Environmental and Occupational Health Sciences, USA. 2. Christina Lee Brown Envirome Institute, 302 E Muhammad Ali Blvd, Louisville, KY, 40202, USA; Superfund Research Center, 302 E Muhammad Ali Blvd, Louisville, KY 40202, USA; University of Louisville School of Public Health and Information Sciences, USA; Department of Epidemiology and Population Health, USA. 3. Christina Lee Brown Envirome Institute, 302 E Muhammad Ali Blvd, Louisville, KY, 40202, USA; Superfund Research Center, 302 E Muhammad Ali Blvd, Louisville, KY 40202, USA; University of Louisville School of Public Health and Information Sciences, USA; Department of Bioinformatics and Biostatistics, 485 E Gray Street, Louisville, KY, 40202, USA. 4. Columbia University Mailman School of Public Health, USA; Department of Environmental Health Science, 722 W 168th St, New York, NY, 10032, USA. 5. Christina Lee Brown Envirome Institute, 302 E Muhammad Ali Blvd, Louisville, KY, 40202, USA; Superfund Research Center, 302 E Muhammad Ali Blvd, Louisville, KY 40202, USA. 6. Christina Lee Brown Envirome Institute, 302 E Muhammad Ali Blvd, Louisville, KY, 40202, USA. 7. University of Louisville School of Public Health and Information Sciences, USA; Department of Epidemiology and Population Health, USA. 8. Christina Lee Brown Envirome Institute, 302 E Muhammad Ali Blvd, Louisville, KY, 40202, USA; Superfund Research Center, 302 E Muhammad Ali Blvd, Louisville, KY 40202, USA; University of Louisville School of Public Health and Information Sciences, USA. 9. Christina Lee Brown Envirome Institute, 302 E Muhammad Ali Blvd, Louisville, KY, 40202, USA; Superfund Research Center, 302 E Muhammad Ali Blvd, Louisville, KY 40202, USA. Electronic address: aruni@louisville.edu.
Abstract
BACKGROUND: Cardiovascular disease (CVD) is the leading cause of mortality worldwide. Exposure to air pollution, specifically particulate matter of diameter ≤2.5 μm (PM2.5), is a well-established risk factor for CVD. However, the contribution of gaseous pollutant exposure to CVD risk is less clear. OBJECTIVE: To examine the vascular effects of exposure to individual volatile organic compounds (VOCs) and mixtures of VOCs. METHODS: We measured urinary metabolites of acrolein (CEMA and 3HPMA), 1,3-butadiene (DHBMA and MHBMA3), and crotonaldehyde (HPMMA) in 346 nonsmokers with varying levels of CVD risk. On the day of enrollment, we measured blood pressure (BP), reactive hyperemia index (RHI - a measure of endothelial function), and urinary levels of catecholamines and their metabolites. We used generalized linear models for evaluating the association between individual VOC metabolites and BP, RHI, and catecholamines, and we used Bayesian Kernel Machine Regression (BKMR) to assess exposure to VOC metabolite mixtures and BP. RESULTS: We found that the levels of 3HPMA were positively associated with systolic BP (0.98 mmHg per interquartile range (IQR) of 3HPMA; CI: 0.06, 1.91; P = 0.04). Stratified analysis revealed an increased association with systolic BP in Black participants despite lower levels of urinary 3HPMA. This association was independent of PM2.5 exposure and BP medications. BKMR analysis confirmed that 3HPMA was the major metabolite associated with higher BP in the presence of other metabolites. We also found that 3HPMA and DHBMA were associated with decreased endothelial function. For each IQR of 3HPMA or DHBMA, there was a -4.4% (CI: -7.2, -0.0; P = 0.03) and a -3.9% (CI: -9.4, -0.0; P = 0.04) difference in RHI, respectively. Although in the entire cohort the levels of several urinary VOC metabolites were weakly associated with urinary catecholamines and their metabolites, in Black participants, DHBMA levels showed strong associations with urinary norepinephrine and normetanephrine levels. DISCUSSION: Exposure to acrolein and 1,3-butadiene is associated with endothelial dysfunction and may contribute to elevated risk of hypertension in participants with increased sympathetic tone, particularly in Black individuals.
BACKGROUND: Cardiovascular disease (CVD) is the leading cause of mortality worldwide. Exposure to air pollution, specifically particulate matter of diameter ≤2.5 μm (PM2.5), is a well-established risk factor for CVD. However, the contribution of gaseous pollutant exposure to CVD risk is less clear. OBJECTIVE: To examine the vascular effects of exposure to individual volatile organic compounds (VOCs) and mixtures of VOCs. METHODS: We measured urinary metabolites of acrolein (CEMA and 3HPMA), 1,3-butadiene (DHBMA and MHBMA3), and crotonaldehyde (HPMMA) in 346 nonsmokers with varying levels of CVD risk. On the day of enrollment, we measured blood pressure (BP), reactive hyperemia index (RHI - a measure of endothelial function), and urinary levels of catecholamines and their metabolites. We used generalized linear models for evaluating the association between individual VOC metabolites and BP, RHI, and catecholamines, and we used Bayesian Kernel Machine Regression (BKMR) to assess exposure to VOC metabolite mixtures and BP. RESULTS: We found that the levels of 3HPMA were positively associated with systolic BP (0.98 mmHg per interquartile range (IQR) of 3HPMA; CI: 0.06, 1.91; P = 0.04). Stratified analysis revealed an increased association with systolic BP in Black participants despite lower levels of urinary 3HPMA. This association was independent of PM2.5 exposure and BP medications. BKMR analysis confirmed that 3HPMA was the major metabolite associated with higher BP in the presence of other metabolites. We also found that 3HPMA and DHBMA were associated with decreased endothelial function. For each IQR of 3HPMA or DHBMA, there was a -4.4% (CI: -7.2, -0.0; P = 0.03) and a -3.9% (CI: -9.4, -0.0; P = 0.04) difference in RHI, respectively. Although in the entire cohort the levels of several urinary VOC metabolites were weakly associated with urinary catecholamines and their metabolites, in Black participants, DHBMA levels showed strong associations with urinary norepinephrine and normetanephrine levels. DISCUSSION: Exposure to acrolein and 1,3-butadiene is associated with endothelial dysfunction and may contribute to elevated risk of hypertension in participants with increased sympathetic tone, particularly in Black individuals.
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