Differential Effects of Wildfire Biomass Smoke Inhalation on Allergic Inflammation in Mice
Citation:
Gavett, S., M. Hargrove, Y. Kim, C. Wood, L. Copeland, J. Dye, R. Jaskot, R. Grindstaff, AND Ian Gilmour. Differential Effects of Wildfire Biomass Smoke Inhalation on Allergic Inflammation in Mice. Society of Toxicology, San Antonio, TX, March 11 - 15, 2018.
Impact/Purpose:
Wildfires annually destroy thousands of homes, burn millions of acres, and threaten human life and health in the United States. Unfortunately, the scale and frequency of wildfires have been increasing over the past 30 years. Furthermore, since wood smoke is recognized by the World Health Organization (WHO) as a probable human lung carcinogen, health risks of short- and long-term exposures to wildfire smoke are becoming of growing concern not only for firefighters but also for the population impacted by smoke. Asthmatics are particularly sensitive to multiple types of air pollutants, including particulate matter (PM) and air toxic compounds, which are released in abundance by wildfires. The purpose of this project is to assess the relative acute toxicity of emissions from distinct fuel types (peat, chaparral (eucalyptus), and red oak) and provide a ranking of effects on pulmonary and allergic asthmatic responses in Balb/cJ mice, a strain which is widely used for the assessment of allergic responses.
Description:
Wildland fires emit high concentrations of airborne particulate matter (PM) and volatile organic compounds which can impact sensitive populations such as asthmatics. Health effects of these biomass emissions may vary significantly depending on fuel type and burn conditions. We assessed the relative acute toxicity of biomass smoke produced from controlled burns of peat, oak, or eucalyptus under smoldering (SM; 510 °C; ~40 mg/m3 PM) or flaming (FL; 640 °C; ~3.5-4 mg/m3 PM) conditions with equivalent carbon monoxide levels in house dust mite (Der p1)-allergic (HDM) Balb/cJ mice. Control and HDM-sensitized mice were all challenged with HDM 1 day before nose-only exposure to air, SM, or FL smoke (1 h/d x 2 d). Lung inflammation and histopathology were assessed in mice necropsied 4 h after the final exposure. Air-exposed HDM-allergic mice had significant increases in bronchoalveolar lavage fluid (BALF) eosinophils (EOS), interleukin (IL)-4, IL-5, and eotaxin compared with air-exposed non-allergic mice. Exposure to SM peat increased BALF neutrophils (PMN; P<0.05) and EOS (not significant) in comparison to air exposure in HDM-allergic mice, despite significantly lower IL-4 and IL-5 (P<0.05). SM peat-exposed HDM-allergic mice also had significantly higher BALF macrophages (MAC), PMN, and EOS (but similar IL-4 and IL-5) compared with FL peat exposure. In contrast to SM peat, both SM oak and SM eucalyptus exposures resulted in lower BALF MAC, PMN, EOS, and IL-4 in comparison to air exposure in HDM-allergic mice. Biochemical markers of lung injury (e.g. protein, LDH, albumin) were generally unchanged or slightly reduced following exposure to any SM or FL compared with air exposure in HDM mice. No consistent changes in BALF cells, cytokines, or biochemical markers were noted in non-allergic groups after SM or FL exposures. We conclude that SM peat emissions potentiate allergic inflammation and may worsen symptoms in sensitive populations to a greater degree than under FL conditions. Greater effects of SM peat emissions may correlate with higher (7-8x) PM polycyclic aromatic hydrocarbon (PAH) levels compared with SM oak or eucalyptus PM PAH levels. (This abstract does not reflect USEPA policy.)