Arsenic exposure is associated with elevated sweat chloride concentration and airflow obstruction among adults in Bangladesh: A cross-sectional study.

Arsenic is associated with lung disease and experimental models suggest that arsenic-induced degradation of the chloride channel CFTR (cystic fibrosis transmembrane conductance regulator) is a mechanism of arsenic toxicity. We examined associations between arsenic exposure, sweat chloride concentration (measure of CFTR function), and pulmonary function among 269 adults in Bangladesh. Participants with sweat chloride ≥ 60 mmol/L had higher arsenic exposures than those with sweat chloride < 60 mmol/L (water: median 77.5 µg/L versus 34.0 µg/L, p = 0.025; toenails: median 4.8 µg/g versus 3.7 µg/g, p = 0.024). In linear regression models, a one-unit µg/g increment in toenail arsenic was associated with a 0.59 mmol/L higher sweat chloride concentration, p < 0.001. Among the entire study population, after adjusting for covariates including age, sex, smoking, education, and height, toenail arsenic concentration was associated with increased odds of airway obstruction (OR: 1.97, 95%: 1.06, 3.67, p = 0.03); however, sweat chloride concentration did not mediate this association. Our findings suggest that sweat chloride concentration may serve as novel biomarker for arsenic exposure, warranting further investigation in diverse populations, and that arsenic likely acts on the lung through mechanisms other than inducing CFTR dysfunction. Alternative mechanisms by which environmental arsenic exposure may lead to obstructive lung disease, such as arsenic-induced direct lung injury and/or increase lung proteinase activity, require additional exploration in future work.