ABSTRACT
The public health education in Japan was practiced with the construction of the nation during Japanese modernization from the Meiji. After Second World War, it is practiced over wide study field based on the new Constitution of Japan and the way from U.S.A. , for example community organization. These performance contributed to the popularization and the development of public health. After high economic growth the system of public health was structured with deregulation and the progress of decentralization of power. At last Japan achieved the highest health standard in the world. However the public health education is more complicated for the variation of Japanese society from the end of 20th century. Furthermore in 21st century we are asked the development of comprehensive public health education system, for example the graduate school of public health, with the wide education system as ever.
ABSTRACT
<p><b>AIM</b>To 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.</p><p><b>METHODS</b>Diets 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.</p><p><b>RESULTS</b>Histological 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.</p><p><b>CONCLUSION</b>The 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.</p>
Subject(s)
Animals , Male , Mice , Body Weight , Copper , Metabolism , Diethylhexyl Phthalate , Metabolism , Pharmacology , Iron , Metabolism , Kidney , Metabolism , Lipid Peroxidation , Liver , Metabolism , Mice, Inbred ICR , Nitrogen Oxides , Metabolism , Pancreas , Metabolism , Spermatogenesis , Testis , Metabolism , Testosterone , Blood , Zinc , MetabolismABSTRACT
<p><b>OBJECTS</b>We 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.</p><p><b>METHODS</b>The 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.</p><p><b>RESULTS</b>Chlorpyrifos 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).</p><p><b>CONCLUSIONS</b>The 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.</p>
ABSTRACT
Objects: We 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. Methods: The 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. Results: Chlorpyrifos in indoor air in the control houses was not detected (ND<1 ng/m3, n=3), while 41 of 43 houses with termiticide application showed 1−350 ng/m3. Although the chlorpyrifos concentrations in these 41 houses did not exceeded the indoor air quality guideline of 1000 ng/m3, but 3 houses were higher than the guideline 100 ng/m3 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). Conclusions: The 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.