Environmental Public Health Division, National Health and Environmental Effects Research Laboratory, U.S. Environmental Protection Agency, Research Triangle Park, NC, 27711, USA.
National Research Council, Washington, DC, 20001, USA.
Arch Toxicol. 2019 Jun;93(6):1501-1513. doi: 10.1007/s00204-019-02450-5. Epub 2019 Apr 20.
The characteristics of wildland fire smoke exposures which initiate or exacerbate cardiopulmonary conditions are unclear. We previously reported that, on a mass basis, lung toxicity associated with particulate matter (PM) from flaming smoke aspirated into mouse lungs is greater than smoldering PM. In this study, we developed a computer-controlled inhalation system which can precisely control complex biomass smoke emissions from different combustion conditions. This system was used to examine the toxicity of inhaled biomass smoke from peat, eucalyptus, and oak fuels generated under smoldering and flaming phases with emissions set to the same approximate concentration of carbon monoxide (CO) for each exposure (60-110 ppm), resulting in PM levels of ~ 4 mg/m for flaming and ~ 40 mg/m for smoldering conditions. Mice were exposed by inhalation 1 h/day for 2 days, and assessed for lung toxicity at 4 and 24 h after the final exposure. Peat (flaming and smoldering) and eucalyptus (smoldering) smoke elicited significant inflammation (neutrophil influx) in mouse lungs at 4 h with the peat (flaming) smoke causing even greater lung inflammation at 24-h post-exposure. A significant alteration in ventilatory timing was also observed in mice exposed to the peat (flaming) and eucalyptus (flaming and smoldering) smoke immediately after each day of exposure. No responses were seen for exposures to similar concentrations of flaming or smoldering oak smoke. The lung toxicity potencies (neutrophil influx per PM mass) agreed well between the inhalation and previously reported aspiration studies, demonstrating that although flaming smoke contains much less PM mass than smoldering smoke, it is more toxic on a mass basis than smoldering smoke exposure, and that fuel type is also a controlling factor.
野火烟雾暴露引发或加重心肺疾病的特征尚不清楚。我们之前的研究报告表明,从燃烧的烟雾中吸入到小鼠肺部的烟尘颗粒(PM)与闷烧 PM 相比,与肺部毒性的关联更大。在这项研究中,我们开发了一种计算机控制的吸入系统,可以精确控制来自不同燃烧条件的复杂生物质烟雾排放。该系统用于检查泥炭、桉树和橡木燃料在闷烧和燃烧阶段下产生的吸入性生物质烟雾的毒性,排放的一氧化碳(CO)浓度相同,每种暴露情况(60-110 ppm),导致 PM 水平为4 mg/m3 用于燃烧,40 mg/m3 用于闷烧条件。小鼠通过吸入暴露 1 小时/天,2 天,最后一次暴露后 4 小时和 24 小时评估肺毒性。泥炭(燃烧和闷烧)和桉树(闷烧)烟雾在 4 小时内引起了小鼠肺部明显的炎症(中性粒细胞浸润),而泥炭(燃烧)烟雾在暴露后 24 小时甚至引起更大的肺部炎症。在每天暴露后立即暴露于泥炭(燃烧)和桉树(燃烧和闷烧)烟雾的小鼠中,还观察到通气时间的明显改变。对类似浓度的燃烧或闷烧橡木烟雾的暴露没有反应。吸入和先前报道的吸入研究之间的肺毒性效价(每 PM 质量的中性粒细胞流入)非常吻合,这表明尽管燃烧烟雾的 PM 质量远低于闷烧烟雾,但它在质量基础上比闷烧烟雾暴露更具毒性,而且燃料类型也是一个控制因素。