Background

Smoke from biomass burning in different environments has been shown to contribute to adverse respiratory health effects, including airway infections. Wood smoke particles induce pro-inflammatory and cytotoxic effects in vitro. Short-term exposure studies to wood smoke in humans have yielded inconclusive results, but suggest a cytotoxic response.

Aims and objectives

Our aim was to further characterize early airway responses following wood smoke exposure in healthy humans and to clarify the underlying mechanisms.

Methods

Fourteen healthy, non-smoking participants were included in a double-blinded randomised cross-over exposure study. Participants were exposed on two occasions, with at least 3 weeks apart, to filtered air and to sooty, polycyclic aromatic hydrocarbon-rich wood smoke at a concentration of 409±43 µg/m³ for 2 hours. Bronchoscopy with bronchial wash (BW) and bronchoalveolar lavage (BAL) was performed 6 hours after exposure. Differential cell counts and analysis of lactate dehydrogenase (LDH) in BW and BAL-fluid were executed. Phagocytic function among BAL-cells was assessed ex vivo.

Results

Wood smoke caused increased levels of LDH in BAL-fluid 6 h after exposure. Phagocytosing cells from BAL following wood smoke exposure displayed decreased phagocytic capacity (p=0.02) and viability (p=0.03) when compared with cells after air exposure.

Conclusion

We report decreased phagocytosis and an increase in LDH in BAL after wood smoke exposure. Our findings suggest a cytotoxic response to wood smoke and may lend support to the epidemiological evidence of increased incidence of respiratory infections as a consequence of biomass burning.