Аннотация:Background Particulate matter is the key component of air pollutants, mainly produced by emissions of coal-fired plants and road traffic. Exposure to fine particulate matter (PM 2.5 ) pollution is associated with increased morbidity and mortality for respiratory diseases. However, few population-based studies have been conducted to assess the alterations of circulating pulmonary proteins due to long-term PM 2.5 exposure. Methods We designed a two-stage study. At the first stage, we enrolled 558 coke plant workers with a wide range of PM 2.5 exposure levels as the exposed group and 210 controls in China. Pulmonary injury was measured by lung function and serum Clara cell protein (CC16), surfactant protein A (SP-A), and surfactant protein D (SP-D). Linear regression models were used to assess the associations between PM 2.5 , pulmonary injury markers, and lung function. At the second stage, significant initial findings were validated by an independent diesel engine exhaust (DEE) cohort with 50 DEE exposed workers and 50 controls. Results Serum CC16 decreased in a dose-response manner in association with both external and internal PM 2.5 exposures in two cohorts. In the first stage, serum CC16 levels decreased with increasing duration of occupational PM 2.5 exposure history. An IQR (122.0 μg/m 3 ) increase in PM 2.5 was associated with a 5.76% decrease in serum CC16, whereas an IQR (1.06 μmol/mol creatinine) increase in urinary 1-OHP concentration was associated with a 5.36% decrease in serum CC16 in the COE cohort. In the validation stage, the concentration of serum CC16 in PM 2.5 exposed group were 22.42% lower than that of the control and an IQR (1.24 μmol/mol creatinine) increase in urinary 1-OHP concentration was associated with a 12.24% decrease in serum CC16 in DEE cohort. Conclusions Reduction of serum CC16 may be a sensitive marker for pulmonary damage in populations with high PM 2.5 exposure.
