A Study on the Key Role of Cadmium Accumulation Induced by PM2.5 Exposure in Renal Injury

摘要

PM2.5 has attracted more and more attention to the damage of the kidney. PM2.5 and heavy metal cadmium both have been proved to play an important role in renal injury. However, the role of heavy metal cadmium in renal injury induced by PM2.5 exposure have not been reported. This research chose serious heavy metal pollution in industrial area and relatively clean living area, starting from the comparison of different regional differences in the cadmium content in PM2.5, through cell experiments in vitro and population studies. The results showed that the survival rate of renal tubular epithelial cells (HK2) was significantly decreased by 100 u g / ml of PM2.5 extract in the living area, while the survival rate of renal tubular epithelial cells was significantly decreased at 50 u g / ml of PM2.5 in industrial area. The results showed that the nephrotoxicity of PM2.5 in industrial area was greater than that in living area. The concentration of PM2.5 and total dust in industrial polluted area and clean living area were analyzed simultaneously. It was found that the concentration of PM2.5 in industrial polluted area was significantly higher than that in living area control group. The contents of some heavy metals (manganese, mercury, cadmium) were significantly higher than those in the control group. The contents of heavy metals in blood or urine of 168 residents (excluding occupational exposure to heavy metals and nephropathy) were measured. It was found that the concentration of urinary cadmium in the observation group was significantly higher than that in the control group, but there was no significant difference in the contents of other heavy metals (blood lead, urine manganese, urine mercury, urinary arsenic) between the two groups. It was found that the concentration of cadmium and metallothionein (MT) was positively correlated with the indexes of renal injury, which reflected the key role of cadmium accumulation induced by PM2.5 in renal injury.