Environmental health perspectives
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Environ. Health Perspect. · Sep 2006
Comparative StudyExposure to phthalates in neonatal intensive care unit infants: urinary concentrations of monoesters and oxidative metabolites.
We previously demonstrated that among 54 infants in neonatal intensive care units, exposure to polyvinyl chloride plastic medical devices containing the plasticizer di(2-ethylhexyl) phthalate (DEHP) is associated with urinary concentrations of mono(2-ethylhexyl) phthalate (MEHP) , a DEHP metabolite. In this follow-up report, we studied the neonates' exposure to DEHP-containing devices in relation to urinary concentrations of two other DEHP metabolites, and to urinary concentrations of metabolites of dibutyl phthalate (DBP) and benzylbutyl phthalate (BzBP) , phthalates found in construction materials and personal care products. ⋯ Inclusion of the oxidative metabolites MEHHP and MEOHP strengthened the association between intensiveness of product use and biologic indices of DEHP exposure over that observed with MEHP alone.
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Controversy remains regarding the relationship between ambient ozone and mortality worldwide. In mainland China, the largest developing country, there has been no prior study investigating the acute effect of O3 on death risk. Given the changes in types of air pollution from conventional coal combustion to the mixed coal combustion/motor vehicle emissions in China's large cities, it is worthwhile to investigate the acute effect of O3 on mortality outcomes in the country. ⋯ O3 pollution has stronger health effects in the cold than in the warm season in Shanghai. Our analyses also strengthen the rationale for further limiting levels of O3 pollution in outdoor air in the city.
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Environ. Health Perspect. · May 2006
Correspondence: Dimethylamine Borane Neurotoxicity and Authors' Response.
Correspondence on Dimethylamine Borane Neurotoxicity and authors' response.
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Environ. Health Perspect. · Apr 2006
Lead increases lipopolysaccharide-induced liver-injury through tumor necrosis factor-alpha overexpression by monocytes/macrophages: role of protein kinase C and P42/44 mitogen-activated protein kinase.
Although lead and lipopolysaccharide (LPS), both important environmental pollutants, activate cells through different receptors and participate in distinct upstream signaling pathways, Pb increases the amount of LPS-induced tumor necrosis factor-alpha (TNF-alpha). We examined the cells responsible for the excess production of Pb-increased LPS-induced TNF-alpha and liver injury, and the roles of protein kinase C (PKC) and p42/44 mitogen-activated protein kinase (MAPK) in the induction of TNF-alpha. Peritoneal injection of Pb alone (100 micromol/kg) or a low dose of LPS (5 mg/kg) did not affect serum TNF-alpha or liver functions in A/J mice. ⋯ Pb+LPS coexposure stimulated the phosphorylation of p42/44 MAPK and the expression of TNF-alpha in CD14+ cells of cultured mouse whole blood, peritoneal macrophages, and RAW264.7 cells. Moreover, blocking PKC or MAPK effectively reduced Pb+LPS-induced TNF-alpha expression and liver injury. In summary, monocytes/macrophages were the cells primarily responsible for producing, through the PKC/MAPK pathway, the excess Pb-increased/LPS-induced TNF-alpha that caused liver injury. alpha.