Cardiopulmonary toxicity of peat wildfire particulate matter and the predictive utility of precision cut lung slices

Abstract

BackgroundEmissions from a large peat fire in North Carolina in 2008 were associated with increased hospital admissions for asthma and the rate of heart failure in the exposed population. Peat fires often produce larger amounts of smoke and last longer than forest fires, however few studies have reported on their toxicity. Moreover, reliable alternatives to traditional animal toxicity testing are needed to reduce the number of animals required for hazard identification and risk assessments.MethodsSize-fractionated particulate matter (PM; ultrafine, fine, and coarse) were obtained from the peat fire while smoldering (ENCF-1) or when nearly extinguished (ENCF-4). Extracted samples were analyzed for chemical constituents and endotoxin content. Female CD-1 mice were exposed via oropharyngeal aspiration to 100 μg/mouse, and assessed for relative changes in lung and systemic markers of injury and inflammation. At 24 h post-exposure, hearts were removed for ex vivo functional assessments and ischemic challenge. Lastly, 8 mm diameter lung slices from CD-1 mice were exposed (11 μg) ± co-treatment of PM with polymyxin B (PMB), an endotoxin-binding compound.ResultsOn an equi-mass basis, coarse ENCF-1 PM had the highest endotoxin content and elicited the greatest pro-inflammatory responses in the mice including: increases in bronchoalveolar lavage fluid protein, cytokines (IL-6, TNF-α, and MIP-2), neutrophils and intracellular reactive oxygen species (ROS) production. Exposure to fine or ultrafine particles from either period failed to elicit significant lung or systemic effects. In contrast, mice exposed to ENCF-1 ultrafine PM developed significantly decreased cardiac function and greater post-ischemia-associated myocardial infarction. Finally, similar exposures to mouse lung slices induced comparable patterns of cytokine production; and these responses were significantly attenuated by PMB.ConclusionsThe findings suggest that exposure to coarse PM collected during a peat fire causes greater lung inflammation in association with endotoxin and ROS, whereas the ultrafine PM preferentially affected cardiac responses. In addition, lung tissue slices were shown to be a predictive, alternative assay to assess pro-inflammatory effects of PM of differing size and composition. Importantly, these toxicological findings were consistent with the cardiopulmonary health effects noted in epidemiologic reports from exposed populations.

Review of emissions from smouldering peat fires and their contribution to regional haze episodes

“…Ultrafine particles (UFP, particles with an aerodynamic diameter #0.1 mm) can deposit deep in the lungs by diffusion and can enter the blood through the alveoli of the lung (Lighty et al 2000). Recently, a cardiopulmonary toxicity study showed that PM 10 from smouldering peat fires induced larger lung inflammatory responses, whereas UFP caused significant adverse cardiac effects (Kim et al 2014).…”

Computational study of critical moisture and depth of burn in peat fires

“…More recent figures estimate that the average annual carbon footprint is equivalent to 15% of manmade emissions (Poulter et al 2006). Moreover, pollutants in smouldering haze substantially increase the risk of cardiopulmonary diseases in the human population (Rappold et al 2011;Kim et al 2014).…”

Comparative chemistry and toxicity of diesel and biomass combustion emissions

“…These effects were associated with OC content, because the ultrafine PM obtained during the smoldering, but not the glowing, phase had >3 times higher OC content [32]. Forest wildfire PM toxicity is also associated with OC content [33][34][35], although it should be noted that different fuels may produce similar OC content but have a gradation in toxicity depending on the presence (or absence) of specific organic species [32]. Because of the variation in fuels and combustion conditions, there are still many uncertainties about the toxicity of biomass or wildfire smoke PM, although the limited evidence available reveals that, beyond the effect of carbon monoxide poisoning, toxicity outcomes are most strongly associated with organic compounds.…”

“…In contrast, ultrafine PM collected during the wildfire did not induce lung inflammation but caused cardiovascular effects in an ischemia reperfusion injury model. These effects were associated with OC content, because the ultrafine PM obtained during the smoldering, but not the glowing, phase had >3 times higher OC content [32]. Forest wildfire PM toxicity is also associated with OC content [33][34][35], although it should be noted that different fuels may produce similar OC content but have a gradation in toxicity depending on the presence (or absence) of specific organic species [32].…”