Tesfaigzi Yohannes, Singh Shashibhushan P, Foster Jennifer E, Kubatko Justin, Barr Edward B, Fine Philip M, McDonald Jacob D, Hahn Fletcher F, Mauderly Joe L
Lovelace Respiratory Research Institute, 2425 Ridgecrest Drive SE, Albuquerque, New Mexico 87108, USA.
Toxicol Sci. 2002 Jan;65(1):115-25. doi: 10.1093/toxsci/65.1.115.
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.
在美国许多地区，木烟是空气污染的一个重要来源，流行病学数据表明木烟水平升高与健康影响之间存在因果关系。本研究旨在提供有关新墨西哥州一个美国原住民社区亚慢性木烟暴露潜在呼吸道健康反应的信息。因此，本研究在相似的燃烧条件和木烟颗粒浓度下使用同类型木材，以模拟该社区观察到的情况。将雄性挪威大鼠每天暴露3小时，每周5天，持续4周或12周，分别暴露于作为对照的空气中，或暴露于浓度为1或10毫克/立方米的矮松木烟颗粒中。木烟由细颗粒（<1微米）组成，这些细颗粒形成更大的链和聚集体，其尺寸分布在<1微米部分为63 - 74%，在>1微米部分为26 - 37%。颗粒结合物质主要由碳组成，大多数鉴定出的有机化合物由糖和木质素衍生物组成。高暴露组的肺功能，特别是一氧化碳弥散能力和肺阻力，受到了一定影响。在暴露组的喉部观察到轻度慢性炎症和鳞状化生。肺泡巨噬细胞增生和色素沉着的严重程度随烟雾浓度和暴露时间的延长而增加，肺泡间隔略有增厚。低暴露组在90天后，气道内衬的黏液细胞内容物从过碘酸希夫阳性物质变为阿尔辛蓝阳性物质。这些观察结果共同表明，暴露于木烟会在雄性挪威大鼠身上引起轻微但显著的变化。需要进一步研究以确定暴露于木烟是否会加剧类似哮喘的症状，这些症状类似于居住在使用木炉取暖和做饭家庭中的儿童所描述的症状。
