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Polychlorinated dibenzo-p-dioxins (PCDDs), polychlorinated dibenzofurans (PCDFs), mono-ortho and non-ortho polychlorinated biphenyls (dioxin-like PCBs) were determined in samples of human fat tissue from nine Italian obese patients. The toxicity equivalent (TEQ) values ranged from 9 to 25pgTEQg−1 lipid (WHO-TEF values, 2005 [Van den Berg, M., Birnbaum, L.S., Denison, M., De Vito, M., Farland, W., Feeley, M., Fiedler, H., Hakansson, H., Hanberg, A., Haws, L., Rose, M., Safe, S., Schrenk, D., Tohyama, C., Tritscher, A., Tuomisto, J., Tysklind, M., Walker, N., Peterson, R.E., 2006. The 2005 World Health Organization reevaluation of human and mammalian Toxic Equivalency Factors for dioxins and dioxin-like compounds. Toxicol. Sci. 93, 223–241]), the contribution of dioxin-like PCBs was more than 30% of the total TEQ values. The obese body burdens varied from 6 to 11ngTEQkg−1 body weight (BW), exceeding the estimated steady-state body burden 5ngTEQkg−1 BW, based on lipid adjusted serum concentrations from several populations in the mid-1990s, calculated in the risk assessment US EPA document. [Copyright &y& Elsevier]

Fine airborne particulate matter (PM 2.5 ) has been repeatedly associated with adverse health effects in humans. The PM 2.5 soluble fraction, and soluble metals in particular, are thought to cause lung damage. Literature data, however, are not consistent and the role of leachable metals is still under debate. In this study, Winter and Summer urban PM 2.5 aqueous extracts, obtained by using a bio-compatible solution and different contact times at 37 °C, were used to investigate cytotoxic effects of PM 2.5 in cultured lung epithelial cells (A549) and the role played by the leachable metals Cu, Fe, Zn, Ni, Pb and Cd. Cell viability and migration, as well as intracellular glutathione, extracellular cysteine, cysteinylglycine and homocysteine concentrations, were evaluated in cells challenged with both PM 2.5 extracts before and after ultrafiltration and artificial metal ion solutions mimicking the metal composition of the genuine extracts. The thiol oxidative potential was also evaluated by an abiotic test. Results demonstrate that PM 2.5 bioactive components were released within minutes of PM 2.5 interaction with the leaching solution. Among these are i) low MW (<3 kDa) solutes inducing oxidative stress and ii) high MW and/or water-insoluble compounds largely contributing to thiol oxidation and to increased homocysteine levels in the cell medium. Cu and/or Ni ions likely contributed to the effects of Summer PM 2.5 extracts. Nonetheless, the strong bio-reactivity of Winter PM 2.5 extracts could not be explained by the presence of the studied metals. A possible role for PM 2.5 water-extractable organic components is discussed., (Copyright © 2017 Elsevier Ltd. All rights reserved.)

Polychlorinated dibenzo-p-dioxins (PCDDs), polychlorinated dibenzofurans (PCDFs), mono-ortho and non-ortho polychlorinated biphenyls (dioxin-like PCBs) were determined in samples of human fat tissue from nine Italian obese patients. The toxicity equivalent (TEQ) values ranged from 9 to 25 pg TEQ g(-1) lipid (WHO-TEF values, 2005 [Van den Berg, M., Birnbaum, L.S., Denison, M., De Vito, M., Farland, W., Feeley, M., Fiedler, H., Hakansson, H., Hanberg, A., Haws, L., Rose, M., Safe, S., Schrenk, D., Tohyama, C., Tritscher, A., Tuomisto, J., Tysklind, M., Walker, N., Peterson, R.E., 2006. The 2005 World Health Organization reevaluation of human and mammalian Toxic Equivalency Factors for dioxins and dioxin-like compounds. Toxicol. Sci. 93, 223-241]), the contribution of dioxin-like PCBs was more than 30% of the total TEQ values. The obese body burdens varied from 6 to 11 ng TEQ kg(-1) body weight (BW), exceeding the estimated steady-state body burden 5 ng TEQ kg(-1) BW, based on lipid adjusted serum concentrations from several populations in the mid-1990s, calculated in the risk assessment US EPA document.