OBJECTSWe carried out an investigation to clarify the real state of indoor air pollution by chlorpyrifos (termiticide) and exposure to chlorpyrifos of residents by measuring its urinary metabolite 3,5,6-trichloro-2-pyridinol (TCP) as an exposure index, such as biological monitoring.

METHODSThe investigation was conducted in 43 individual houses with termiticide application (whether the termiticide was chlorpyrifos is uncertain) and 3 control houses without any termiticide application in Kagawa, Japan. Urine samples were collected from 46 healthy adult residents of the aforementioned houses.

RESULTSChlorpyrifos in indoor air in the control houses was not detected (ND<1 ng/m(3), n=3), while 41 of 43 houses with termiticide application showed 1-350 ng/m(3). Although the chlorpyrifos concentrations in these 41 houses did not exceeded the indoor air quality guideline of 1000 ng/m(3), but 3 houses were higher than the guideline 100 ng/m(3) for children in Japan. Urinary TCP concentrations of 0.1-7.8 ng/mg·creatinine were detected in 41 residents from the 41 houses where chlorpyrifos had been detected. The chlorpyrifos concentration and the urinary TCP revealed a positive correlation (r=0.5468, p<0.01, n=41).

CONCLUSIONSThe immediate health hazard from air born chlorpyrifos in the examined houses was negligible, but the findings suggest that it is necessary to monitor chemicals which may contaminate indoor air and to assess the risk of prolonged exposure to such chemicals. The measuring of urinary metabolite TCP of chlorpyrifos via biological monitoring would be useful, allowing comprehensive evaluation of the exposure to chlorpyrifos in indoor air.

AIMTo determine the biochemical effect of di-(2-ethylhexyl) phthalate (DEHP) on testes, liver, kidneys and pancreas on day 10 in the process of degeneration of the seminiferous epithelium.

METHODSDiets containing 2% DEHP were given to male Crlj:CD1(ICR) mice for 10 days. The dose of DEHP was 0.90 +/- 0.52 mg/mouse/day. Their testes, livers, kidneys and pancreata were examined for detection of mono-(2-ethylhexyl) phthalate (MEHP), nitrogen oxides (NOx) produced by peroxidation of nitric oxide (NO) with free radicals, and lipid peroxidation induced by the chain reaction of free radicals.

RESULTSHistological observation and serum analysis showed the presence of severe spermatogenic disturbance, Leydig cell dysfunction, liver dysfunction and dehydration. Unexpectedly, the concentration of MEHP in the testes was extremely low compared with that in the liver. However, the concentration of the NOx in the testes was as high as the hepatic concentration. Furthermore, free radical-induced lipid peroxidation was histochemically detected in the testes but not in the liver.

CONCLUSIONThe results indicate that DEHP-induced aspermatogenesis is caused by the high sensitivity of the testicular tissues to MEHP rather than the specific accumulation or uptake of circulating MEHP into the testes.

Animals ; Body Weight ; drug effects ; Copper ; metabolism ; Diethylhexyl Phthalate ; analogs & derivatives ; metabolism ; pharmacology ; Iron ; metabolism ; Kidney ; drug effects ; metabolism ; Lipid Peroxidation ; drug effects ; Liver ; drug effects ; metabolism ; Male ; Mice ; Mice, Inbred ICR ; Nitrogen Oxides ; metabolism ; Pancreas ; drug effects ; metabolism ; Spermatogenesis ; drug effects ; Testis ; drug effects ; metabolism ; Testosterone ; blood ; Zinc ; metabolism