Abstract

BackgroundArsenic (As) is an established toxic metal, but its effect on longitudinal lung function change among occupational workers is less conclusive. Methods1243 participants were recruited in a coke-oven plant and followed up from 2010 to 2014. Each individual provided 20 mL morning urine sample at baseline, which was then used for urinary levels of As (U–As) and polycyclic aromatic hydrocarbon (PAH) metabolites detecting. Lung function levels at both baseline and the end of follow-up were determined. Multiple linear regression models were used to analyze the associations between U–As with annual lung function changes, and to evaluate the joint effects of U–As with cigarette smoking and regular physical exercise. ResultsAmong all participants, each 2-fold increase in U–As was associated with −12.09 (95%CI: −19.37, −4.81) mL, −0.32% (95%CI: −0.54%, −0.10%), −15.04 (95%CI: −24.62, −5.46) mL, and −0.36% (95%CI: −0.64%, −0.08%) annual changes in reduced forced expiratory volume in 1 second (FEV1), percent predicted FEV1 (ppFEV1), forced vital capacity (FVC), and percent predicted FVC (ppFVC), respectively. These effects were more pronounced among coke-oven workers with smoking (especially heavy smoking with pack-years≥15) and without regular physical exercise. Compared to low-As-exposed (≤4.70 μg/mmol creatinine) non-smokers with regular physical exercise, the high-As-exposed (>4.70 μg/mmol creatinine) smokers without regular physical exercise had the worst annual declines in FEV1 [β (95%CI) = −69.01 (−106.67, −31.34) mL], ppFEV1 [β (95%CI) = −1.94% (−3.02%, −0.87%)], FVC [β (95%CI) = −78.66 (95%CI: −129.46, −27.86) mL], and ppFVC [β (95%CI) = −1.80% (−3.23%, −0.37%)]. ConclusionsThe findings in our prospective cohort study suggested the positively linear dose-response relationship of U–As with annual lung function decline. The adverse effects of As could be enhanced by cigarette smoking and attenuated by regular physical exercise. Specific emphasizes on tobacco control and physical exercise were suggested to prevent As exposure induced pulmonary impairment.

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