Abstract
Airborne fine and ultrafine particulate matter (PM) are often generated through widely-used thermal processes such as the combustion of fuels or the thermal decomposition of waste. Residents near Superfund sites are exposed to PM through the inhalation of windblown dust, ingestion of soil and sediments, and inhalation of emissions from the on-site thermal treatment of contaminated soils. Epidemiological evidence supports a link between exposure to airborne PM and an increased risk of cardiovascular and pulmonary diseases. It is well-known that during combustion processes, incomplete combustion can lead to the production of organic pollutants that can adsorb to the surface of PM. Recent studies have demonstrated that their interaction with metal centers can lead to the generation of a surface stabilized metal-radical complex capable of redox cycling to produce ROS. Moreover, these free radicals can persist in the environment, hence their designation as Environmentally Persistent Free Radicals (EPFR). EPFR has been demonstrated in both ambient air PM2.5 (diameter < 2.5 µm) and in PM from a variety of combustion sources. Thus, low-temperature, thermal treatment of soils can potentially increase the concentration of EPFR in areas in and around Superfund sites. In this review, we will outline the evidence to date supporting EPFR formation and its environmental significance. Furthermore, we will address the lack of methodologies for specifically addressing its risk assessment and challenges associated with regulating this new, emerging contaminant.
Highlights
Residents near Superfund sites are exposed to fine and ultrafine particles through a variety of routes, including inhalation of windblown dust, ingestion of soil and sediments, and inhalation of emissions from the on-site thermal treatment of contaminants
Findings from this study suggested that PM2.5 derived from fossil fuel combustion was associated with both short-term and long-term health effects
PM2.5 originating from residual oil combustion and traffic sources were associated with short-term health effects, while PM2.5 derived from coal combustion was correlated with long-term health consequences [3]
Summary
Residents near Superfund sites are exposed to fine and ultrafine particles through a variety of routes, including inhalation of windblown dust, ingestion of soil and sediments, and inhalation of emissions from the on-site thermal treatment of contaminants. A notable example is the association between decreased lung function and increased prevalence of chronic obstructive pulmonary disease (COPD) and respiratory infections reported in populations exposed to particulates from the combustion of biomass fuels for cooking [33,34] In another example, the National Particle Component Toxicity (NPACT) initiative sought to determine an association between PM levels and health effects, and utilized data from the EPA’s Chemical. Studies have shown elevations in ischemic heart disease in trucking industry workers exposed chronically to particulate emissions [38], and PM emitted from diesel engines is associated with a wide range of heavy metals [39,40] These exposures were associated with elevated plasma biomarkers for oxidative stress and inflammation [41], suggesting that these factors may play a role in the biological mechanisms of action of these PM. We believe that the metal is important as an entity necessary to form the pollutant-particle systems responsible for EPFR formation, and that different metals impart differences in radical formation and stability in the environment and in the host
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