Oxidative potential, cytotoxicity, and intracellular oxidative stress generating capacity of pm10: A case study in south of italy

Long and short-term exposure to atmospheric particulate matter (PM) has detrimental effects on human health. The effective mechanisms leading to PM toxicity are still not fully under-stood, even if it is known that physical-chemical properties, strongly influenced by sources and atmospheric processes, are known to play an important role. In this work, PM10 samples were collected, at an urban background site in southern Italy, to determine cytotoxicity (using MTT test on A549 cells), genotoxicity (using the comet assay), and intracellular oxidative stress on A549 cells exposed for 24 h to aqueous extracts of PM10 samples. Organic carbon (OC) and elemental carbon (EC) content of PM10 and acellular determination of oxidative potential with DTT assay were performed to compare results of acellular and cellular biological assays. Cellular (OSGCV and MTTV ) and acellular (OPDTT V) outcomes, normalized in volume, are well correlated (statistically significant results) with carbon content suggesting that combustion sources play an important role in determining cellular oxidative stress and cytotoxicity of PM10 . Even if the number of data is limited, genotoxicity results are well correlated (Pearson r > 0.95) with OSGCV and MTTV, and a weaker, but statistically significant correlation was observed with OPDTT V. OSGCV is well correlated with the cell mortality observed with the MTTV test and a lower, but still statistically significant correlation is observed between MTTV and OPDDT V. A statistically significant correlation was found between OPDTT V and OSGCV results. When the outcomes of the cellular and acellular assay are compared normalized in mass (i.e., intrinsic values), the correlations become significantly weaker suggesting that the different sources acting on the site produces particulate matter with different toxicological potential influencing differently the biological tests studied.