Local and Systemic Inflammation May Mediate Diesel Engine Exhaust-Induced Lung Function Impairment in a Chinese...

Area of Science:

• Environmental Health
• Pulmonary Medicine
• Toxicology

Background:

• Diesel exhaust (DE) is a primary source of ambient particulate matter, known to impair lung function.
• Understanding the inflammatory mechanisms linking DE exposure to lung function deficits is crucial for public health.
• Previous studies highlight potential roles for local and systemic inflammation in respiratory diseases.

Purpose of the Study:

• To assess the contribution of local (FeNO, CC16) and systemic (CRP, IL-6) inflammation to diesel exhaust-induced lung function impairment.
• To investigate dose-response and time-course relationships between DE exposure and inflammatory markers.
• To establish benchmark doses for internal DE exposure for regulatory risk assessment.

Main Methods:

• A cohort study comparing diesel engine testers (DETs) with non-DETs, including current and former smokers.
• Assessment of urinary metabolites, fraction of exhaled nitric oxide (FeNO), serum inflammatory markers (CC16, CRP, IL-6), and spirometry.
• Mediation analysis to quantify the role of inflammatory markers in lung function differences; dose-response and time-course analyses.

Main Results:

• DETs showed significantly reduced CC16 (19% decrease) and increased CRP (94% increase) compared to non-DETs (p < 10-4).
• Dose-response and time-course relationships confirmed the link between DE exposure and these inflammatory markers (p < .04 and p < .005, respectively).
• Circulating CC16 and CRP explained 43% of the lung function (FEV1) difference between DETs and non-DETs (p < .001); an inverse dose-dependent relationship was found for FeNO and cigarette smoke exposure (p = .0003).

Conclusions:

• Local (CC16) and systemic (CRP) inflammation are key mediators contributing to lung function impairment in diesel exhaust-exposed populations.
• The study recommends benchmark doses for urinary phenanthrols (1.0261-1.4513 μg/g creatinine) for regulatory risk assessment of DE exposure.
• Findings suggest that inflammatory processes driven by DE exposure may contribute to the development of obstructive lung diseases.