Ultrafine particles are not major carriers of carcinogenic PAHs and their genotoxicity in size-segregated aerosols

Some studies suggest that genotoxic effects of combustion-related aerosols are induced by carcinogenic polycyclic aromatic hydrocarbons (c-PAHs) and their derivatives, which are part of the organic fraction of the particulate matter (PM) in ambient air. The proportion of the organic fraction in PM is known to vary with particle size. The ultrafine fraction is hypothesized to be the most important carrier of c-PAHs, since it possesses the highest specific surface area of PM. To test this hypothesis, the distribution of c-PAHs in organic extracts (EOMs) was compared for four size fractions of ambient-air aerosols: coarse (1 < dae < 10μm), upper (0.5 < dae < 1 μm), and lower (0.17 < dae < 0.5 μm) accumulation aerosol particles and ultrafine particles (dae < 0.17). High-volume aerosol samples were collected consecutively in four localities that differed in the level of environmental pollution. The genotoxicity of EOMs was measured by analysis of DNA adducts induced in an a cellular assay consisting of calf thymus DNA with/without rat liver microsomal S9 fraction coupled with 32P-postlabelling. The upper accumulation fraction was the major size fraction in all four localities, forming 37-46% of the total PM mass. Per m3 of sampled air, this fraction also bound the largest amount of c-PAHs. Correspondingly, the upper accumulation fraction induced the highest DNA-adduct levels. Per PM mass itself, the lower accumulation fraction is seen to be the most efficient in binding DNA-reactive organic compounds. Interestingly, the results suggest that the fraction of ultrafine particles of various ambient-air samples is neither a major carrier of c-PAHs, nor a major inducer of their genotoxicity, which is an important finding that is relevant to the toxicity and health effects of ultrafine particles, which are so extensively discussed these days.