“..significant occurrence of environmentally persistent free radicals in particulate matter samples collected from coal-burning activities, automobile exhaust, and biomass burning activities was detected”
Environmentally persistent free radicals (EPFRs) are toxic products of incomplete combustion. They form on particulate matter through interactions with aromatic hydrocarbons and their formation is promoted by metal oxides1. Unlike free radicals, EPFRs are not highly reactive and so can persist in the environment for several months, or even indefinitely.
EPFRs can cause DNA damage, cardiac toxicity and oxidative stress and be detrimental to human health through negative effects on the pulmonary, immune, and cardiovascular systems2,3. It is possible that fine airborne particulate matter may carry EPFRs deep into the respiratory tract and lungs, where they may have adverse effects on human health. Indeed, EPFRs on particulate matter are known to be more cytotoxic than well-known individual organic pollutants1. The extended lifespan of EPFRs mean that, even though they are less destructive per se than free radicals , they have greater opportunity to cause damage in humans. In addition, EPFRs may induce the generation of the more harmful reactive oxygen species2,4.
The huge potential for EPFRs to cause harm to humans has led to extensive research to determine their prevalence and nature within particulate matter. EPFRs have been detected in great quantities in atmospheres containing high levels of man-made particulate matter. This suggests that their distribution may be altered in haze conditions. Haze is the term used to describe an atmosphere in which dust, smoke, and other dry particulates obscure the clarity of the sky. Haze conditions are becoming increasingly common in Beijing and in 2015, the level of atmospheric particulate matter was 8 times that of the Chinese National Ambient Air Quality Standard.
The health impact of haze conditions cannot be definitively determined since the levels and particle-size distributions of EPFRs in airborne particulate matter is not known. In order to allow better evaluation of the potential health risks caused by haze conditions, a study has measured the level of exposure to EPFRs on fine particles in haze and non-haze conditions in Beijing5.
Samples of particulate matter were collected on haze days and also non-haze days. The quantities of EPFRs and their particle-size distributions were determined by electron paramagnetic resonance (EPR) spectroscopy using a Bruker EMX-plus X162 band EPR spectrometer. In addition, particulate matter collected from atmospheres with high levels of fossil fuel combustion, eg, coal burning, vehicle exhaust, waste incineration, were also assessed for EPFR content using EPR spectroscopy.
The EPR spectroscopy analyses revealed that the average concentration of EPFRs in the airborne particulate matter collected on haze days was two orders of magnitude higher than the levels previously reported in the US atmosphere. By using EPR spectroscopy to determine the high levels of EPFRs from in the samples collected in areas with extensive fossil fuel combustion, the technology enabled the researchers to support the theory that this may be a primary source of EPFRs in airborne particulate matter.
Furthermore, the highest levels of EPFRs were found in the fine (diameter <1 μm) fraction of particulate matter, which is most likely to reach deep into the lungs when inhaled. In agreement with previous studies, the EPFRs from the samples collected in this study had an average half-life of around 2 months.
The findings in this study thus provide a basis for assessing the potential risks of EPFRs. Particular attention is required in areas of extensive human activities where levels of EPFRs are likely to be highest. In addition, the persistence of EPFRs mean that they have the potential for long-term adverse effects on both the environment and human health.
- Lomnicki S, et al. Copper Oxide-Based Model of Persistent Free Radical Formation on Combustion-Derived Particulate Matter. Environ. Sci. Technol. 2008;42:4982 4988.
- Chuang GC, et al. Environmentally Persistent Free Radicals Cause Apoptosis in HL-1 Cardiomyocytes. Cardiovasc Toxicol. 2017;17(2):140 149.
- Dugas TR; et al. Addressing Emerging Risks: Scientific and Regulatory Challenges Associated with Environmentally Persistent Free Radicals. Int. J. Environ. Public Health 2016;13:573.
- Gehling W, et al. Hydroxyl Radical Generation from Environmentally Persistent Free Radicals (EPFRs) in PM2.5. Environ. Sci. Technol. 2014;48:4266 4272.
- Yang L, et al Highly Elevated Levels and Particle-Size Distributions of Environmentally Persistent Free Radicals in Haze-Associated Atmosphere. Environ. Sci. Technol. 2017;51(14):7936–7944.