Environmental exposure to volatile organic compounds is associated with endothelial injury

Riggs, Daniel W.; Malovichko, Marina V; Gao, Hong; McGraw, Katlyn E.; Taylor, Breandon S.; Krivokhizhina, Tatiana; Shesh, N.; Keith, Rachel J.; Bhatnagar, Aruni; Srivastava, Sanjay

doi:10.1016/j.taap.2022.115877

Cited by 16 publications

(12 citation statements)

References 76 publications

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“…The mean age was 50 ± 12 years, and the mean BMI was 28.8 ± 6.9 kg/m 2 . Forty-three percent of the participants were smokers (urinary cotinine level >40 μg/g creatinine), 63% were hypertensive, and 17% were diabetics. No significant differences were observed in the demographics and clinical characteristics of smokers and nonsmokers.…”

Section: Resultsmentioning

confidence: 99%

“…Urinary cotinine levels were measured to determine the current smoking status of the study subjects. Participants with urinary cotinine level >40 μg/g creatinine were regarded as smokers. , Demographic information (Table ) including age, sex, race, cotinine level, creatinine level, tobacco product usage, and medical information was obtained through the questionnaires. The study was approved by the University of Louisville Institutional Review Board (IRB 15.1260).…”

Section: Methodsmentioning

confidence: 99%

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Global Profiling of Urinary Mercapturic Acids Using Integrated Library-Guided Analysis

Xie

Gao

Keith

et al. 2023

Environ. Sci. Technol.

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Urinary mercapturic acids (MAs) are often used as biomarkers for monitoring human exposures to occupational and environmental xenobiotics. In this study, we developed an integrated library-guided analysis workflow using ultraperformance liquid chromatography–quadrupole time-of-flight mass spectrometry. This method includes expanded assignment criteria and a curated library of 220 MAs and addresses the shortcomings of previous untargeted approaches. We employed this workflow to profile MAs in the urine of 70 participants40 nonsmokers and 30 smokers. We found approximately 500 MA candidates in each urine sample, and 116 MAs from 63 precursors were putatively annotated. These include 25 previously unreported MAs derived mostly from alkenals and hydroxyalkenals. Levels of 68 MAs were comparable in nonsmokers and smokers, 2 MAs were higher in nonsmokers, and 46 MAs were elevated in smokers. These included MAs of polycyclic aromatic hydrocarbons and hydroxyalkenals and those derived from toxicants present in cigarette smoke (e.g., acrolein, 1,3-butadiene, isoprene, acrylamide, benzene, and toluene). Our workflow allowed profiling of known and unreported MAs from endogenous and environmental sources, and the levels of several MAs were increased in smokers. Our method can also be expanded and applied to other exposure-wide association studies.

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Section: Resultsmentioning

confidence: 99%

Section: Methodsmentioning

confidence: 99%

Global Profiling of Urinary Mercapturic Acids Using Integrated Library-Guided Analysis

Xie

Gao

Keith

et al. 2023

Environ. Sci. Technol.

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“…In animal models, mice exposed to volatile benzene exhibited a higher risk of developing cardiovascular diseases than those that breathed filtered air [ 26 ]. Benzene was found to be negatively correlated with many types of circulating angiogenic cells (CD45 dim /CD146 + /CD34 + cells) in human samples [ 11 ]. Abplanalp et al found that mice inhalation of volatile benzene exhibited increasing plasma levels of low-density lipoproteins and decreasing plasma levels of circulating angiogenic cells (Flk-1+/Sca-1+) [ 26 ].…”

Section: Discussionmentioning

confidence: 99%

Association of the blood levels of specific volatile organic compounds with nonfatal cardio-cerebrovascular events in US adults

Jing,

Chen,

Yang

et al. 2024

BMC Public Health

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Background Cardio-cerebrovascular diseases constitute a major global public health burden. Volatile organic compounds (VOCs) exposure has become progressively severe, endangering human health and becoming one of the main concerns in environmental pollution. The associations of VOCs exposure with nonfatal cardio-cerebrovascular events have not been identified in observational study with a large sample size, so we aim to examine the association in US adult population. Methods Adults aged > 18 years with complete data regarding selected blood levels of VOCs (including benzene, ethylbenzene, o-xylene, and m-/p-xylene) and nonfatal cardio-cerebrovascular events were included in the analysis (n = 3,968, National Health and Nutrition Examination Survey, NHANES, 2013–2018 survey cycle). Participants were classified into low- and high-exposure based on whether above selected VOCs low limit detect concentration or median value. Weighted multivariate logistic analyses and subgroup analyses were used to detect the association between selected VOCs exposure and nonfatal cardio-cerebrovascular events in US adults. Results Weighted multivariate logistic analyses showed that the high-VOCs exposure group had an increased risk of nonfatal cardio-cerebrovascular events compared with the low-VOCs exposure group; the adjusted odds ratios (OR) and 95% confidence intervals (CI) of nonfatal cardio-cerebrovascular events for the high-VOCs exposure group were 1.41 (0.91, 2.19), 1.37 (0.96, 1.95), 1.32 (0.96, 1.82), and 1.17 (0.82, 1.67) for benzene, ethylbenzene, o-xylene, and m-/p-xylene, respectively, which was not significant assuming statistical significance at a 0.05 significance level (95% CI) for a two-tailed test. Lastly, we found high-VOCs exposure was associated with increased incidence of nonfatal cardio-cerebrovascular events in both daily smokers an non-daily smokers (p-interaction > 0.01), but the association was not statistically significant in non-daily smokers. Conclusions This study found that VOCs (benzene, ethylbenzene, o-xylene, and m-/p-xylene) exposure was associated with increased incidence of nonfatal cardio-cerebrovascular events in US adults, and the results need to be confirmed by larger cohort studies.

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“…28 VOCs are primarily produced by human activity, particularly the burning of fossil fuels and have been linked with endothelial injury. 29 Along with continued increases in VOCs, increasing ambient temperatures lead to increases in ground O 3 , and by 2030, the maximum daily O 3 concentrations are expected to spike to 1 to 5 ppb throughout the United States. 2 These increases are projected to contribute to an additional tens of thousands of O 3 -related morbidity and mortality annually.…”

Section: Compendium On Environmental Impacts On Cardiovascular Health...mentioning

confidence: 99%

Environmental Impacts on Cardiovascular Health and Biology: An Overview

Blaustein,

Quisel,

Hamburg

et al. 2024

Circulation Research

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Environmental stressors associated with human activities (eg, air and noise pollution, light disturbance at night) and climate change (eg, heat, wildfires, extreme weather events) are increasingly recognized as contributing to cardiovascular morbidity and mortality. These harmful exposures have been shown to elicit changes in stress responses, circadian rhythms, immune cell activation, and oxidative stress, as well as traditional cardiovascular risk factors (eg, hypertension, diabetes, obesity) that promote cardiovascular diseases. In this overview, we summarize evidence from human and animal studies of the impacts of environmental exposures and climate change on cardiovascular health. In addition, we discuss strategies to reduce the impact of environmental risk factors on current and future cardiovascular disease burden, including urban planning, personal monitoring, and mitigation measures.

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Environmental exposure to volatile organic compounds is associated with endothelial injury

Cited by 16 publications

References 76 publications

Global Profiling of Urinary Mercapturic Acids Using Integrated Library-Guided Analysis

Global Profiling of Urinary Mercapturic Acids Using Integrated Library-Guided Analysis

Association of the blood levels of specific volatile organic compounds with nonfatal cardio-cerebrovascular events in US adults

Environmental Impacts on Cardiovascular Health and Biology: An Overview

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