O3C.5 Reduced serum clara cell protein (CC16) as an early pulmonary injury marker for fine particulate matter exposure in occupational population

BackgroundParticulate matter is the key component of air pollutants, mainly produced by emissions of coal-fired plants and road traffic. Exposure to fine particulate matter (PM2.5) 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 PM2.5 exposure.MethodsWe designed a two-stage study. At the first stage, we enrolled 558 coke plant workers with a wide range of PM2.5 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 PM2.5, 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.ResultsSerum CC16 decreased in a dose-response manner in association with both external and internal PM2.5 exposures in two cohorts. In the first stage, serum CC16 levels decreased with increasing duration of occupational PM2.5 exposure history. An IQR (122.0 μg/m3) increase in PM2.5 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 PM2.5 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.ConclusionsReduction of serum CC16 may be a sensitive marker for pulmonary damage in populations with high PM2.5 exposure.

Clara cell protein 16 release from the nasal mucosa in allergic rhinitis, chronic rhinosinusitis, and exposure to air pollutants

Clara cell protein 16 (CC16) is a small protein mainly produced by non-ciliated Clara cells in the respiratory epithelium. It has an anti-inflammatory role in chronic upper and lower airway eosinophilic inflammations. Decreased levels of CC16 are found in the nasal secretions and plasma of patients with chronic eosinophilic inflammatory disorders, such as asthma, allergic rhinitis, and chronic rhinosinusitis with or without nasal polyps, as well as in people exposed to high levels of air pollutants. Intranasal corticosteroid administration suppresses chronic inflammation of the nasal mucosa driven by eosinophils and stimulates local CC16 production. CC16 can be a reliable biomarker of the beneficial effects of perennial allergic rhinitis and chronic rhinosinusitis therapy and of the functional recovery of the nasal mucosa after treatment with topical glucocorticoids.