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

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This cross-sectional study investigated associations between environmental arsenic exposure, sweat chloride concentration (a measure of cystic fibrosis transmembrane conductance regulator [CFTR] function), and pulmonary function in 269 adults in Dhaka, Bangladesh. Drinking water arsenic concentrations were measured by graphite furnace atomic absorption spectrometry (GF-AAS); toenail arsenic (the primary long-term exposure metric) was measured by ICP-MS. Spirometry was conducted using ATS guidelines. Sweat chloride was collected by iontophoresis and measured within 48 hours.

Key numbers

  • n = 269 (90% of 300 enrolled); 166 completed spirometry meeting ATS quality standards.
  • Drinking water arsenic: median 41.0 µg/L (2001-2003), 138.5 µg/L mean; median 82.5 µg/L at follow-up (2018-2022), mean 166.9 µg/L.
  • Toenail arsenic (long-term average): median 4.7 µg/g (IQR 2.2-10.4 µg/g).
  • Sweat chloride mean: 49.1 mmol/L (SD 16.8); 25.7% had sweat chloride 60 mmol/L or above.
  • Participants with sweat chloride 60 mmol/L or above had higher toenail arsenic (median 8.2 µg/g) versus those below (4.1 µg/g), p = 0.024.
  • In models adjusted for age, sex, smoking, and education: a one-unit µg/g increment in toenail arsenic concentration was associated with 0.59 mmol/L higher sweat chloride concentration, p less than 0.001.
  • Airflow obstruction (FEV1/FVC less than 0.7) was present in 19.9% (33 of 166) of participants who completed spirometry.
  • Toenail arsenic was associated with increased odds of airflow obstruction (OR: 1.97, 95% CI: 1.06-3.67, p = 0.03) in unadjusted analysis.
  • Sweat chloride did not statistically mediate the arsenic-airflow obstruction association.
  • LOD for toenail arsenic: 0.002 µg/g.

Methods (brief)

Sampling: adults from a 2001-2003 arsenic skin lesion study, re-contacted 2018-2022 at Dhaka Community Hospital. Toenail ICP-MS (Dartmouth Trace Element core facility for 2001-2003; Harvard T.H. Chan for follow-up). Drinking water GF-AAS (Bangladesh University of Engineering and Technology for 2001-2003; ICP-MS for follow-up). Sweat chloride by iontophoresis (ATS-DLD 1978 questionnaire for symptoms; EasyOne Air handheld spirometers). Participants excluded if lung cancer or active pulmonary tuberculosis on chest radiography. CFTR sequencing performed on 45 of 69 participants with elevated sweat chloride; none had pathogenic CFTR mutations consistent with cystic fibrosis diagnosis.

Evidence fitness

Supports: establishing that environmental arsenic exposure via contaminated drinking water is associated with impaired CFTR function (elevated sweat chloride) and obstructive lung disease in a high-exposure adult population. Documents a proposed mechanism (arsenic-induced CFTR degradation) relevant to understanding non-dietary inhalation and systemic arsenic toxicity pathways. Limitation: cross-sectional design; arsenic exposure via water, not food; Bangladesh setting with very high arsenic concentrations not representative of dietary exposure in low-arsenic settings.

Limitations

Single time point for spirometry; arsenic exposure primarily from drinking water (food contribution not measured); high-exposure context (median drinking water arsenic far above WHO 10 µg/L guideline); sweat chloride mediation analysis underpowered; COVID-19 pandemic interrupted enrollment midway; no CFTR gene mutations found, confirming the sweat chloride elevation is not genetic cystic fibrosis.

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