Pneumoproteins and lung function in tunnel workers

Introduction
Tunnel workers are exposed to a mixture of airborne contaminants. Particulate exposure may result in pulmonary inflammation and lung function impairment. Small amounts of the pneumoproteins Clara-cell-protein-16 (CC16), an anti-inflammatory protein secreted along the bronchial tree, and the Surfactant-protein-D (SPD) secreted by the alveolar epithelium, may penetrate the epithelial barrier. Thus, they may function as serum biomarkers of effects on the airways. We hypothesized that exposure during tunneling would cause lung function impairment and alterations in the serum concentrations of the pneumoproteins.

Methods
90 tunnel workers and 51 referents without airborne occupational exposure were examined with lung function tests, blood samples and a questionnaire after an exposure free interval of 12 days, and re-examined after a work period of 9 days. An extensive personal exposure assessment was carried out during the period.

Results
The exposure to particles and α-quartz in the thoracic aerosol fraction ranged from 0.1 to11.3 mg/m3 and from 3 to 919 µg/m3, respectively. Exposure to elemental carbon, a marker of diesel particulates, ranged from 4 to 172 µg/m3 and oil mist from 0.1 to 15 mg/m3. The mean forced expiratory volume in one second (FEV1) declined significantly during follow-up by 64 ml (SD 169) in the exposed workers, compared to 4 ml in the referents. SPD declined significantly by on average 7.1 ng/ml (p=0.003) in the exposed workers, compared to 1.2 ng/ml in the referents. The decline in SPD was related to self-reported hours of work in tunneling during the follow-up period. The concentrations of CC16 measured at the first examination were positively associated with FEV1 percent of predicted, and negatively associated with years of tunnel work.

Discussion
Air exposure in tunnel work appears to have impact on the lung function and the determined concentrations of the pneumoproteins.