Urinary polycyclic aromatic hydrocarbon metabolites, Club cell secretory protein and lung function

Area of Science:

• Environmental Health
• Pulmonary Medicine
• Toxicology

Background:

• Exposure to polycyclic aromatic hydrocarbons (PAHs) is linked to decreased lung function.
• The precise mechanisms underlying this association remain incompletely understood.
• Investigating biomarkers like Club cell secretory protein (CC16) is crucial for elucidating these pathways.

Purpose of the Study:

• To examine the potential role of Club cell secretory protein (CC16) as a mediator in the relationship between PAH exposure and lung function decline.
• To assess how CC16 levels influence the association between PAH metabolites and lung function over time.

Main Methods:

• Utilized data from 3384 adults in the Wuhan-Zhuhai cohort with a three-year follow-up.
• Employed linear mixed models to analyze dose-response relationships between urinary monohydroxylated PAH metabolites (OH-PAHs) and lung function/plasma CC16.
• Conducted mediation analysis to evaluate CC16's role and assessed lung function changes in relation to OH-PAHs and CC16 levels.

Main Results:

• Increased exposure to high and low molecular weight OH-PAHs was associated with reductions in FEV1 and FVC.
• These negative associations were significant primarily in individuals with lower CC16 levels (<15.83ng/ml).
• CC16 levels decreased with higher ∑HMW OH-PAHs, and CC16 mediated 22.13% of the association between ∑HMW OH-PAH and FVC.

Conclusions:

• Club cell secretory protein (CC16) plays a significant role in the association between high molecular weight PAHs and FVC.
• Individuals with low plasma CC16 levels are at higher risk of lung function decline when exposed to elevated levels of high molecular weight PAHs.
• Findings underscore the importance of CC16 as a biomarker for PAH-induced respiratory effects.