It is therefore imperative to differentiate between smoke and non-smoke PM 2.5 when assessing impacts on public health. All the above compounds in wildfire smoke tend to generate more free radicals and thus have a greater potential to cause inflammation and oxidative stress in the lung than urban ambient particulate from the same region 20, 21. Wildfire particulate matter is mostly carbonaceous (with 5–20% elemental carbon and at least 50% organic carbon 17, 18) and has more oxidative potential than ambient urban particulate due to the presence of more polar organic compounds 19. In vitro and in vivo studies have shown that mechanisms that may explain wildfire-specific PM higher toxicity include inflammation, oxidative stress 15, or increased respiratory infection by altering pulmonary macrophages activity 16. Though the differential toxicity of wildfire PM 2.5 as compared to other ambient sources of PM 2.5 is not well understood 11, 12, 13, recent animal toxicological studies suggest that particulate matter from wildfires is more toxic than equal doses from other sources such as ambient pollution 14, 15. This is also true in other regions of the world, as in the WHO Air Quality Guidelines (AQG) 10 for example. Current air quality standards specific to PM 2.5 from the Clean Air Act Amendments do not distinguish the sources of emission or chemical composition, implicitly considering PM 2.5 from wildfires and from other sources (e.g., ports, industrial plants, and traffic emissions) to be equally harmful to human health. Levels of wildfire PM 2.5 can greatly exceed those of ambient PM 2.5, spiking episodically within a short period of time (e.g., hours after the onset of a wildfire), and such high exposure levels may generate important health impacts. Wildfire PM 2.5 in the US is projected to increase with climate change along with the associated burden on human health 9. PM 2.5 in the United States has decreased in past decades due to environmental regulations 5, 8, with the exception of wildfire-prone areas 5. PM 2.5 can be inhaled into the deepest recesses of the lungs 6 and may enter the bloodstream impairing vital organs including the lungs 7. Our conclusions point to the need for air quality policies to consider the variability in PM 2.5 impacts on human health according to the sources of emission.įine particulate matter, i.e., particles with aerodynamic diameter ≤2.5 μm (PM 2.5), is the main component of wildfire smoke 1 that impacts public health 2, 3, 4, 5. We found increases in respiratory hospitalizations ranging from 1.3 to up to 10% with a 10 μg m −3 increase in wildfire-specific PM 2.5, compared to 0.67 to 1.3% associated with non-wildfire PM 2.5. Here, we isolate the wildfire-specific PM 2.5 using a series of statistical approaches and exposure definitions. Assessing whether PM 2.5 from wildfires is more or less harmful than PM 2.5 from other sources is a pressing public health concern. Air quality regulations however assume that the toxicity of PM 2.5 does not vary across different sources of emission. Recent toxicological studies suggest that wildfire particulate matter may be more toxic than equal doses of ambient PM 2.5. Fine particulate matter, PM 2.5, in wildfire smoke adversely impacts human health. Wildfires are becoming more frequent and destructive in a changing climate.
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