The spatial distribution, health risk, and cytotoxicity of metal(loid)s in contaminated field soils: The role of Cd in human gastric cells damage.

The spatial distribution and pollution level of heavy metal(loid)s in soil (0-6 m) from a typical industrial region in Jiangmen City, Southeast China was investigated. Their bioaccessibility, health risk, and human gastric cytotoxicity in topsoil were also evaluated using an in vitro digestion/human cell model. The average concentrations of Cd (87.52 mg/kg), Co (106.9 mg/kg), and Ni (1007 mg/kg) exceeded the risk screening values. The distribution profiles of metal(loid)s showed a downward migration trend to reach a depth of 2 m. The highest contamination was found in topsoil (0-0.5 m), with the concentrations of As, Cd, Co, and Ni being 46.98, 348.28, 317.44, and 2395.60 mg/kg, respectively, while Cd showed the highest bioaccessibility in the gastric phase (72.80 %), followed by Co (21.08 %), Ni (18.27 %), and As (5.26 %) and unacceptable carcinogenic risk. Moreover, the gastric digesta of topsoil suppressed the cell viability and triggered cell apoptosis, evidenced by disruption of mitochondrial transmembrane potential and increase of Cytochrome c (Cyt c) and Caspases 3/9 mRNA expression. Bioaccessible Cd in topsoil was responsible for those adverse effects. Our data suggest the importance to reduce Cd in the soil to decrease its adverse impacts on the human stomach.

Organophosphorus Flame Retardant TCPP Induces Cellular Senescence in Normal Human Skin Keratinocytes: Implication for Skin Aging.

Tris (1-chloro-2-propyl) phosphate (TCPP) is one of the most frequently detected organophosphorus flames in the environment. Continuous daily exposure to TCPP may harm human skin. However, little is known about the adverse effects of TCPP on human skin. In this study, we first evaluated the detrimental effects and tried to uncover the underlying mechanisms of TCPP on human skin keratinocytes (HaCaT) after 24 h exposure. We found that TCPP caused a concentration-dependent decrease in HaCaT cell viability after exposure to 1.56-400 µg/mL for 24 h, with an IC50 of 275 µg/mL. TCPP also promoted the generation of intracellular reactive oxygen species (ROS) and triggered DNA damage, evidenced by an increase of phosphorylated histone H2A.X (γH2A.X) in the nucleus. Furthermore, the cell cycle was arrested at the G1 phase at 100 µg/mL by upregulation of the mRNA expression of p53 and p21 and downregulation of cyclin D1 and CDK4 expression. Additionally, both the senescence-associated-ß-galactosidase activity and related proinflammatory cytokine IL-1ß and IL-6 were elevated, indicating that TCPP exposure caused cellular senescence may be through the p53-dependent DNA damage signal pathway in HaCaT cells. Taken together, our data suggest that flame-retardant exposure may be a key precipitating factor for human skin aging.