The acute effects of smoke exposure on inflammatory mediators such as interleukin-10 (IL-10), interleukin-8 (IL-8), and tumor necrosis factor-alpha (TNF-alpha) are not well understood. Our study was designed to measure sputum concentrations of these cytokines in firefighters following low-level smoke exposure. At baseline, participating firefighters underwent blood collection, pulmonary function testing, and sputum induction through inhalation of nebulized hypertonic saline. Study participants later performed overhaul of a structural fire, during which time they wore cartridge respirators and were monitored for smoke exposure. Overhaul involves searching for and extinguishing hidden sources of combustion. One hour following overhaul, blood, pulmonary function data, and induced sputum were again collected. IL-10, IL-8, and TNF-alpha concentrations were measured by enzyme-linked immunosorbent assay (ELISA) in sputum supernatant. In 17 firefighters, baseline sputum IL-10 concentrations were 57.0 +/- 56.8 pg/L, and declined to 16.9 +/- 27.2 pg/L following overhaul (p =.02). No significant changes were observed in sputum IL-8 and TNF-alpha concentrations. Forced vital capacity (FVC) declined significantly in study participants following overhaul. Serum concentrations of Clara-cell protein and surfactant-associated protein A increased significantly following overhaul, indicating increased lung permeability. IL-10 concentrations appear to be exquisitely sensitive to smoke, and studies of IL-10 in sputum should control for recent exposure. Reduced suppression of inflammation by IL-10 may be a mechanism by which low-level smoke exposure causes lung injury.