Association Between Volatile Organic Compound Metabolites in Urine and Adult Lung Function: Evidence From NHANES 2011-2012.

OBJECTIVES: Volatile organic compounds (VOCs) have been reported to be associated with adverse respiratory outcomes during daily exposure at low levels. However, the main contributors among the numerous VOCs and tobacco as the possible sources of VOCs in the general population have not been fully revealed. Here, we aimed to examine the association between urinary VOCs metabolites (UM-VOCs) mixtures and adult lung health. METHODS: We used data from the National Health and Nutrition Examination Survey (NHANES) for the years 2011-2012 and aimed at 16 UM-VOCs. Initially, we used linear regression to evaluate the association between a single compound and lung health. Next, we utilized the BKMR model to assess the overall effect and attempt to understand the potential modifying effects of smoking. RESULTS: Our linear regression analysis suggested that the majority of the UM-VOCs were inversely related to lung function. In multivariable linear regression models, each one-unit increase in natural log-transformed urinary concentrations (μg/mmol Cr) of AMCC, CYMA, MHBMA3, 3HPMA, AAMA, and MA was associated with an absolute decrease in 1 s/forced vital capacity (FEV1/FVC) ratio of 3.5, 1.6, 2.3, 3.0, 3.2, and 4.6 percentage points, respectively (all p < 0.05). Moreover, 3HPMA and HPMMA were positively correlated with wheeze symptom, while 2MHA and 3MHA + 4MHA were negatively correlated with fractional exhaled nitric oxide (FeNO), respectively. BKMR model results showed that UM-VOC mixtures exhibited a negative correlation with FEV1/FVC and FeNO. Urinary AMCC and CYMA were identified as the most important contributors to the decline in FEV1/FVC and FeNO, respectively. Subsequently, we found UM-VOCs of higher concentration in smokers, and stratified BKMR analyses revealed an effect modification by smoking status. CONCLUSIONS: /FVC ratios and lower FeNO levels in a population-based study. This association was primarily observed among smokers, suggesting that tobacco smoke may be a significant contributor to VOC exposure.