Department of Occupational & Environmental Health, School of Public Health, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, Hubei, China.
Key Laboratory of Environment and Health, Ministry of Education & Ministry of Environmental Protection, and State Key Laboratory of Environmental Health (Incubating), School of Public Health, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, Hubei, China.
Thorax. 2020 Sep;75(9):771-779. doi: 10.1136/thoraxjnl-2019-213909. Epub 2020 Jul 6.
Exposure to zinc was suggested to be associated with pulmonary damage, but whether zinc exposure affects lung function remains unclear.
To quantify the association between urinary zinc and lung function and explore the potential mechanisms.
Urinary 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.
Each 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.
Urinary zinc was negatively associated with lung function, and the systemic inflammation may be one of the underlying mechanisms.
有研究提示锌暴露与肺损伤有关，但锌暴露是否影响肺功能尚不清楚。
定量分析尿锌与肺功能的关系，并探讨潜在机制。
本研究纳入了来自武汉-珠海队列的 3917 名成年人，测量了其尿锌和肺功能，并在 3 年随访后重复测量。在基线时还测量了全身炎症标志物（C 反应蛋白）、肺上皮完整性标志物（克拉细胞分泌蛋白 16）和氧化损伤标志物（8-羟基-2'-脱氧鸟苷和 8-异前列腺素）。采用线性混合模型估计尿锌与肺功能之间的暴露-反应关系。采用中介分析评估炎症和氧化损伤在上述关系中的中介作用。
在基线分析中，尿锌每增加 1 个单位，用力肺活量（FVC）降低 35.72 毫升，1 秒用力呼气量（FEV1）降低 24.89 毫升。在随访分析中，在持续高尿锌水平的参与者中，尿锌与 FVC 呈负相关，估计变化值为-93.31 毫升（95%CI-178.47 至-8.14）。此外，尿锌与限制性通气障碍呈正相关。中介分析表明，C 反应蛋白分别介导了尿锌与 FVC 和 FEV1 关联的 8.62%和 8.71%。
尿锌与肺功能呈负相关，全身炎症可能是其潜在机制之一。
