Abstract
BackgroundExposure to zinc was suggested to be associated with pulmonary damage, but whether zinc exposure affects lung function remains unclear.ObjectivesTo quantify the association between urinary zinc and lung function and explore the potential mechanisms.MethodsUrinary zinc and lung function were measured in 3917 adults from the Wuhan-Zhuhai cohort and were repeated after 3 years of follow-up. Indicators of systemic inflammation (C reactive protein), lung epithelium integrity (club cell secretory protein-16) and oxidative damage (8-hydroxy-2′-deoxyguanosine and 8-isoprostane) were measured at baseline. Linear mixed models were used to estimate the exposure–response relationship between urinary zinc and lung function. Mediation analyses were conducted to assess mediating roles of inflammation and oxidative damage in above relationships.ResultsEach 1-unit increase in log-transformed urinary zinc values was associated with a 35.72 mL decrease in forced vital capacity (FVC) and a 24.89 mL decrease in forced expiratory volume in 1 s (FEV1) in the baseline analyses. In the follow-up analyses, there was a negative association between urinary zinc and FVC among participants with persistent high urinary zinc levels, with an estimated change of −93.31 mL (95% CI −178.47 to −8.14). Furthermore, urinary zinc was positively associated with restrictive ventilatory impairment. The mediation analyses suggested that C reactive protein mediated 8.62% and 8.71% of the associations of urinary zinc with FVC and FEV1, respectively.ConclusionUrinary zinc was negatively associated with lung function, and the systemic inflammation may be one of the underlying mechanisms.
Funder
Key Program of the National Natural Science Foundation of China
National Natural Science Foundation of China’s Major Research Program
Subject
Pulmonary and Respiratory Medicine
Cited by
28 articles.
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