• T V Larson and J Q Koenig.
• Department of Civil Engineering, University of Washington, Seattle 98195.
• Annu Rev Public Health. 1994 Jan 1; 15: 133-56.

AbstractIn conclusion, this review reveals much about the constituents and fate of wood smoke but not enough about the health effects. Animal toxicological studies show that wood smoke exposure can disrupt cellular membranes, depress macrophage activity, destroy ciliated and secretory respiratory epithelial cells, and cause aberrations in biochemical enzyme levels. With respect to the human epidemiological data, the literature summarized in Table 4 shows a coherence of the data from young children, with 7/8 studies especially in children with asthma, reporting increased respiratory symptoms, lower respiratory infection, and decreased pulmonary function as a result of exposure to wood smoke. As Bates (6) has discussed, coherence of the data, although not amenable to statistical tests, carries the weight of linkage and plausibility. These adverse respiratory effects associated with wood smoke exposure also comply with many of Brandon Hill's aspects of association necessary to establish causation (40). There is strength of association, consistency (7/8 studies showing positive associations), temporality, plausibility, coherence, and analogy (using ETS exposure; 70, 94). A biological gradient has not been shown, although one is suggested in the study of pulmonary function in wildfire fighters. We conclude that the preponderance of the data suggest a causal relationship between elevated wood smoke levels and adverse respiratory health outcomes in young children.

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