Low-level subchronic exposure to wood smoke exacerbates inflammatory responses in allergic rats.

Epidemiological studies have implicated wood smoke as a risk factor for exacerbating asthma. However, comparisons of findings in animal models with those in humans are currently not possible, because detailed clinically relevant measurements of pulmonary function are not available in animal studies. Brown Norway rats were immunized with ovalbumin and exposed to either filtered air or wood smoke at 1 mg particulate matter/m(3) for 70 days and challenged with allergen during the last 4 days of exposure. Baseline values for dynamic lung compliance were lower while functional residual capacity was increased in rats exposed to wood smoke compared to rats exposed to filtered air. IFN-gamma levels were reduced and IL-4 levels increased in the bronchoalveolar lavage fluid and blood plasma, inflammatory lesions in the lungs were 21% greater, and airway mucous cells/mm basal lamina were non-significantly increased in rats exposed to wood smoke compared to controls. Collectively, these studies suggest that the pulmonary function was affected in rats by exposure to wood smoke and this decline was associated with only minor increases in inflammation of the lung. Therefore, this animal model may be useful to elucidate the mechanisms of the decline in pulmonary function caused by environmental pollutants when asthmatics are exposed to allergen.

Health effects of subchronic exposure to low levels of wood smoke in rats.

Wood smoke is a significant source of air pollution in many parts of the United States, and epidemiological data suggest a causal relationship between elevated wood smoke levels and health effects. The present study was designed to provide information on the potential respiratory health responses to subchronic wood smoke exposures in a Native American community in New Mexico. Therefore, this study used the same type of wood under similar burning conditions and wood smoke particle concentrations to mimic the conditions observed in this community. Brown Norway rats were exposed 3 h/day, 5 days/week for 4 or 12 weeks to air as control, or to 1 or 10 mg/m3 concentrations of wood smoke particles from pinus edulis. The wood smoke consisted of fine particles (< 1 microm) that formed larger chains and aggregates having a size distribution of 63-74% in the < 1-microm fraction and 26-37% in the > 1-microm fraction. The particle-bound material was primarily composed of carbon, and the majority of identified organic compounds consisted of sugar and lignin derivatives. Pulmonary function, specifically carbon monoxide-diffusing capacity and pulmonary resistance, was somewhat affected in the high-exposure group. Mild chronic inflammation and squamous metaplasia were observed in the larynx of the exposed groups. The severity of alveolar macrophage hyperplasia and pigmentation increased with smoke concentration and length of exposure, and the alveolar septae were slightly thickened. The content of mucous cells lining the airways changed from Periodic Acid Schiff- to Alcian Blue-positive material in the low-exposure group after 90 days. Together, these observations suggest that exposure to wood smoke caused minor but significant changes in Brown Norway rats. Further studies are needed to establish whether exposure to wood smoke exacerbates asthmalike symptoms that resemble those described for children living in homes using wood stoves for heating and cooking.