Background: Individuals are exposed to various volatile organic compounds (VOCs) in their surroundings. VOCs were associated with some cardiovascular and metabolic diseases, but the effects on blood pressure (BP) have not yet been clarified. This study aimed to ascertain the relationship between the urine levels of VOCs and the prevalence of hypertension (HTN) in the general population.
Methods: This analysis utilized data from 4156 participants aged from 20 to 79 years in 2013-2018 National Health and Nutrition Examination Survey (NHANES). Exposure to VOCs was assessed through measurements of urinary VOC metabolites, with 16 VOCs selected for analysis. The relationships between VOCs and the risk of HTN in patients were examined through the weighted logistic regression and the weighted linear regression models. Generalized additive models were employed to analyze potential nonlinear associations between VOCs and the risk of HTN. Additionally, subgroup analyses and intergroup interaction tests were conducted.
Results: A total of 4156 participants with 16 VOCs were finally included for analysis. Multivariable logistic regression showed that ln-transformed urine levels of N-acetyl-S-(2-cyanoethyl)-L-cysteine (CYMA) [odds ratio (OR) 1.54; 95% confidence interval (CI) 1.18-2.02], N-acetyl-S-(3-hydroxypropyl)-L-cysteine (3HPMA; OR 1.33; 95% CI 1.03-1.74), N-acetyl-S-(4-hydroxy-2-butenyl)-L-cysteine (MHBMA3; OR 1.68; 95% CI 1.29-2.20), and N-acetyl-S-(1-phenyl-2-hydroxyethyl)-L-cysteine + N-acetyl-S-(2-phenyl-2-hydroxyethyl)-L-cysteine (PHEMA; OR 1.55; 95% CI 1.19-2.00) were significantly associated with an increased risk of HTN in US general population. A nonlinear relationship and a threshold effect were only observed between ln (N-acetyl-S-(2-hydroxypropyl)-L-cysteine or 2HPMA) and HTN. There was a significantly positive correlation between ln(2HPMA) and HTN when ln(2HPMA) at least 5.29. Sub-analysis revealed that there was a more pronounced association in the elderly group (age ≥60 years), the overweight group (BMI ≥25), and the alcohol consumption group.
Conclusion: Our work presents novel epidemiological evidence supporting the establishment of the relationship between environmental pollutants and HTN, highlighting hitherto ignored positive correlations between nonoccupational VOC exposure and the entire population's risk of HTN.
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