Correlation of exposure to volatile organic compounds with myocardial infarction: A Cross-sectional study based on NHANES 2011-2018.

Myocardial infarction (MI), commonly referred to as a heart attack, ranks among the foremost causes of death worldwide. The contribution of exposure to volatile organic compounds (VOCs) to MI is still not well established. This study aims to examine how urinary metabolites of 19 volatile organic compounds (mVOCs) correlate with MI risk in the ordinary population. The data were extracted from the National Health and Nutrition Examination Survey spanning from 2011 to 2018, a nationally representative program conducted by the Centers for Disease Control and Prevention (CDC) to collect and assess the health and nutritional status of the non-institutionalized U.S. population through interviews and physical examinations. The relationship between a single mVOC and MI was analyzed by applying a logistic regression model. The nonlinear relationship between a single mVOC and MI was investigated with the help of a restricted cubic spline regression model. The overall association between mVOCs and MI was examined using a weighted quantile sum (WQS) regression model. The analysis included 5,211 participants, among whom 209 experienced MI, with mVOC levels assessed. A positive association between N-acetyl-S-(3-hydroxypropyl)-L-cysteine (3HPMA) [OR, 1.95; 95% CI, (1.06, 3.58)] and MI incidence was observed after adjustment for potential confounders. Similarly, N-acetyl-S-(2-cyanoethyl)-L-cysteine (CYMA) was also significantly associated with MI incidence [OR, 1.8; 95% CI, (1.14, 2.83)]. Each incremental unit increase in WQS was linked to a 20.4% rise in MI risk (95% CI, 1.05, 1.38). Among them, N-acetyl-S-(3,4-dihydroxybutyl)-L-cysteine (DHBMA), N-acetyl-S-(2-carboxyethyl)-L-cysteine (CEMA), CYMA, N-acetyl-S-(phenyl-2-hydroxyethyl)-L-cysteine (PHEMA), 3HPMA, and 3- and 4-methylhippuric acid (3,4MHA) were identified as key contributors, with DHBMA showing the highest weight (0.27). mVOCs are metabolic derivatives of VOC exposure, with common sources including industrial emissions, environmental pollution, and tobacco combustion. The findings revealed a significant association between urinary mVOCs and MI, implying exposure to these compounds may be linked to an increased MI risk.