Dataset Information

Environmental exposure to volatile organic compounds is associated with endothelial injury.

ABSTRACT:

Objective

Volatile organic compounds (VOCs) are airborne toxicants abundant in outdoor and indoor air. High levels of VOCs are also present at various Superfund and other hazardous waste sites; however, little is known about the cardiovascular effects of VOCs. We hypothesized that ambient exposure to VOCs exacerbate cardiovascular disease (CVD) risk by depleting circulating angiogenic cells (CACs).

Approach and results

In this cross-sectional study, we recruited 603 participants with low-to-high CVD risk and measured 15 subpopulations of CACs by flow cytometry and 16 urinary metabolites of 12 VOCs by LC/MS/MS. Associations between CAC and VOC metabolite levels were examined using generalized linear models in the total sample, and separately in non-smokers. In single pollutant models, metabolites of ethylbenzene/styrene and xylene, were negatively associated with CAC levels in both the total sample, and in non-smokers. The metabolite of acrylonitrile was negatively associated with CD45^dim/CD146⁺/CD34⁺/AC133⁺ cells and CD45⁺/CD146⁺/AC133⁺, and the toluene metabolite with AC133⁺ cells. In analysis of non-smokers (n = 375), multipollutant models showed a negative association with metabolites of ethylbenzene/styrene, benzene, and xylene with CD45^dim/CD146⁺/CD34⁺ cells, independent of other VOC metabolite levels. Cumulative VOC risk score showed a strong negative association with CD45^dim/CD146⁺/CD34⁺ cells, suggesting that total VOC exposure has a cumulative effect on pro-angiogenic cells. We found a non-linear relationship for benzene, which showed an increase in CAC levels at low, but depletion at higher levels of exposure. Sex and race, hypertension, and diabetes significantly modified VOC associated CAC depletion.

Conclusion

Low-level ambient exposure to VOCs is associated with CAC depletion, which could compromise endothelial repair and angiogenesis, and exacerbate CVD risk.

SUBMITTER: Riggs DW

PROVIDER: S-EPMC10045232 | biostudies-literature | 2022 Feb

REPOSITORIES: biostudies-literature

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Publications

Environmental exposure to volatile organic compounds is associated with endothelial injury.

Riggs Daniel W DW Malovichko Marina V MV Gao Hong H McGraw Katlyn E KE Taylor Breandon S BS Krivokhizhina Tatiana T Rai Shesh N SN Keith Rachel J RJ Bhatnagar Aruni A Srivastava Sanjay S

Toxicology and applied pharmacology 20220116

<h4>Objective</h4>Volatile organic compounds (VOCs) are airborne toxicants abundant in outdoor and indoor air. High levels of VOCs are also present at various Superfund and other hazardous waste sites; however, little is known about the cardiovascular effects of VOCs. We hypothesized that ambient exposure to VOCs exacerbate cardiovascular disease (CVD) risk by depleting circulating angiogenic cells (CACs).<h4>Approach and results</h4>In this cross-sectional study, we recruited 603 participants w ...[more]

PMID: 35045333

Similar Datasets

Project description:BackgroundCardiovascular 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.ObjectiveTo examine the vascular effects of exposure to individual volatile organic compounds (VOCs) and mixtures of VOCs.MethodsWe 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.ResultsWe 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.DiscussionExposure 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.

Dataset Information

Environmental exposure to volatile organic compounds is associated with endothelial injury.

Objective

Approach and results

Conclusion

Publications

Environmental exposure to volatile organic compounds is associated with endothelial injury.

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