Wood smoke exposure induces a pulmonary and systemic inflammatory response in firefighters.
Epidemiological studies report an association between exposure to biomass smoke and cardiopulmonary morbidity. The mechanisms for this association are unclear. The aim of the present study was to characterise the acute pulmonary and systemic inflammatory effects of exposure to forest fire smoke. Seasonal forest firefighters (n = 52) were recruited before and/or after a day of fire-fighting. Exposure was assessed by questionnaires and measurement of carbon monoxide levels (used to estimate respirable particulate matter exposure). The pulmonary response was assessed by questionnaires, spirometry and sputum induction. Peripheral blood cell counts and inflammatory cytokines were measured to define the systemic response. Estimated respirable particulate matter exposure was high (peak levels >2 mg x m(-3)) during fire-fighting activities. Respiratory symptoms were reported by 65% of the firefighters. The percentage sputum granulocytes increased significantly from 6.5 to 10.9% following fire-fighting shifts, with concurrent increases in circulating white blood cells (5.55x10(9) to 7.06x10(9) cells x L(-1)) and band cells (0.11x10(9) to 0.16x10(9) cells x L(-1)). Serum interleukin (IL)-6, IL-8 and monocyte chemotactic protein-1 levels significantly increased following fire-fighting. There were no changes in band cells, IL-6, and IL-8 following strenuous physical exertion without fire-fighting. There was a significant association between changes in sputum macrophages containing phagocytosed particles and circulating band cells. In conclusion, acute exposure to air pollution from forest fire smoke elicits inflammation within the lungs, as well as a systemic inflammatory response.
Swiston
J R
JR
The James Hogg iCAPTURE Centre for Cardiovascular and Pulmonary Research, University of British Columbia, St. Paul's Hospital, 1081 Burrard Street, Vancouver, BC, V6Z 1Y6, Canada.
Davidson
W
W
Attridge
S
S
Li
G T
GT
Brauer
M
M
van Eeden
S F
SF
D000293:Adolescent; D000328:Adult; D002248:Carbon Monoxide / Q000032:analysis; D015331:Cohort Studies; D005260:Female; D005390:Fires; D006306:Health Surveys; D006801:Humans; D007249:Inflammation / Q000097:blood; D016676:Macrophages, Alveolar / Q000145:classification / Q000276:immunology*; D008297:Male; D008875:Middle Aged; D016273:Occupational Exposure / Q000009:adverse effects*; D011014:Pneumonia / Q000209:etiology / Q000276:immunology*; D012120:Respiration Disorders / Q000209:etiology / Q000276:immunology; D012906:Smoke / Q000009:adverse effects* / Q000032:analysis; D013147:Spirometry; D013183:Sputum / Q000166:cytology* / Q000276:immunology; D014197:Trees
D012906:Smoke; D002248:Carbon Monoxide