An ex vivo approach to the differential parenchymal responses induced by cigarette whole smoke and its vapor phase.

Using a rat lung slice model, this study compared the stress responses induced by cigarette whole smoke (WS) to that induced by the vapor phase (VP) of the smoke. Following a 3-day exposure, lung slices exposed to 4, 10 and 20% WS retained 85, 42 and 16% relative survival respectively in comparison to the air-exposed ones. Consistently, histological observations revealed concentration-related alveolar damages in the lung slices. Expression of 5 stress-response genes was examined following a single 30 min exposure to 4% WS or VP. WS exposure resulted in 4, 11 and 50-fold induction of IL-1β, kinin type I receptor (B₁R) and CYP1A1 genes, respectively, while CYP1B1 and TNF-α genes expression was found only two times higher in comparison to VP group. Since cigarette WS consists of particulate and vapor phases, these results highlight the preferential or synergistic role of the particulate phase in the induction of IL-1β, B₁R and CYP1A1 genes and that VP did not have comparable effects on expression of these genes. However, both phases fairly contributed to the induction of CYP1B1 and TNF-α genes. VP was the fraction responsible for the toxic effect since WS did not produce further toxicity. The 4% whole smoke deposited about 7.1 μg/cm² of total particulate matter (TPM) to the exposure chamber which may account for observed differential stress responses in the lung slices.