Personal exposure to fine particulate matter, lung function and serum club cell secretory protein (Clara)
2017
Wang, Cuicui | Cai, Jing | Chen, Renjie | Shi, Jingjin | Yang, Changyuan | Li, Huichu | Lin, Zhijing | Meng, Xia | Liu, Cong | Niu, Yue | Xia, Yongjie | Zhao, Zhuohui | Li, Weihua | Kan, Haidong
The underlying mechanisms about the association between ambient fine particulate matter (PM2.5) and lung function were unclear. Few epidemiological studies have evaluated the potential mediating effects of serum club cell secretory protein (Clara) (CC16), a biomarker of pulmonary epithelium integrity.To evaluate the short-term effect of personal PM2.5 exposure on lung function and to explore the potential mediating role of CC16 in this effect.We enrolled 36 healthy, nonsmoking college students for a panel study in Shanghai, China from December 17, 2014 to July 11, 2015. We measured personal and real-time exposure to PM2.5 for 72 h preceding each of four rounds of health examinations, including lung function test and serum CC16 measurement. We used linear mixed-effect models to examine the effects of PM2.5 on lung function and CC16 over various lag times. Furthermore, we analyzed the mediating effect of CC16 in the association between PM2.5 and lung function.Average PM2.5 exposure ranged from 36 to 52 μg/m3 across different lag periods. PM2.5 exposure was negatively associated with lung function and positively associated with serum CC16 concentration. The effect of PM2.5 on CC16 occurred earlier than that on lung function. For instance, an interquartile range (IQR) increase in 0–2 h average exposure to PM2.5 was significantly associated with a 4.84% increase in serum CC16; and an IQR increase in 3–6 h average exposure to PM2.5 was significantly associated with a 1.08% decrease in 1-sec forced expiratory volume. These effects lasted up to 24 h after exposure. Increased serum CC16 contributed 3.9%–36.3% of the association between PM2.5 and impaired lung function.Acute exposure to PM2.5 might induce an immediate decrease in lung function by virtue of the loss of pulmonary epithelium integrity.
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