Wood Smoke Exposure Induces the Activation of Bronchoalveolar Lavage Lymphocytes

Introduction: Exposure to air pollution is associated with respiratory morbidity and mortality. Biomass combustion, including wood smoke, is a major source of indoor and outdoor air pollution. However, the underlying mechanisms between wood smoke-induced airway inflammatory responses and adverse health effects are not fully understood. Aim and Objectives: To investigate lymphocyte subtypes and their activity in bronchoalveolar lavage (BAL) from healthy volunteers exposed to emissions from incomplete wood smoke combustion. Methods: Fourteen healthy volunteers were exposed to both wood smoke at a particulate matter (PM1) concentration of ~450 µg/m3, from a wood stove firing birch log, and filtered air for two hours, on two separate occasions. Bronchoscopies with sampling of BAL cells for flow cytometry analysis were performed 6 hours after each exposure. Cells were stained with fluorochrome-conjugated antibodies for CD3, CD4, CD8, CD25, CD127, CD69, CD56 and CD16. Results: Total lymphocyte numbers were not changed between exposures. Numbers of CD4 and CD8 cells expressing CD25 were increased following wood smoke exposure (p = 0.026 for both), as were CD4CD25CD127 cells (p = 0.035). NKT cells (CD3CD56CD16) tended to increase after wood smoke exposure (p = 0.056). Conclusions: Acute exposure to sooty wood smoke from incomplete combustion induced increased activation of lymphocyte subtypes in the airways. These findings may be linked to the development and worsening of respiratory diseases, as a consequence of long-term exposure to wood smoke.