Carbon disulfide exposure induced lung function reduction partly through oxidative protein damage: A cross-sectional...

Carbon disulfide (CS₂) exposure has been associated with lung function reduction in occupational population. However, evidence on the general population with relatively low CS₂ exposure is lacking and the mechanism involved remains largely unknown. Urinary CS₂ metabolite (2-mercaptothiazolidine-4-carboxylic acid, TTCA) and lung function were determined in the urban adults from the Wuhan-Zhuhai cohort at baseline in 2011-2012 and were repeated every 3 years. Cross-sectional and longitudinal associations between TTCA and lung function were estimated using linear mixed models. Inflammation and oxidative damage biomarkers in blood/urine were measured to evaluate their potential mediating roles involved. Cross-sectionally, participants in the highest quartile of TTCA level showed a 0.64% reduction in FEV₁/FVC and a -308.22 mL/s reduction in PEF, compared to those in the lowest quartile. Longitudinally, participants with consistently high TTCA level had annually -90.27 mL/s decline in PEF, compared to those with consistently low TTCA level. Mediation analysis revealed that plasma protein carbonyl mediated 49.89% and 22.10% of TTCA-associated FEV₁/FVC and PEF reductions, respectively. Conclusively, there was a cross-sectional and longitudinal association between CS₂ exposure and lung function reduction in the general urban adults, and protein carbonylation (oxidative protein damage) partly mediated lung function reduction from CS₂ exposure.