Wenchang Zhao

Mercury levels and estimated total daily intakes for children and adults from an electronic waste recycling area in Taizhou, China: Key role of rice and fish consumption

In order to assess the potential health risks of Hg pollution, total mercury (T-Hg) and methyl mercury (MeHg) concentrations were determined in air, dust, surface soil, crops, poultry, fish and human hair samples from an electronic waste (e-waste) recycling area in Taizhou, China. High concentrations of T-Hg and MeHg were found in these multiple matrices, and the mean concentration was 30.7 ng/m(3) of T-Hg for atmosphere samples, 3.1 μg/g of T-Hg for soil, 37.6 μg/g of T-Hg for dust, 20.3 ng/g of MeHg for rice and 178.1 ng/g of MeHg for fish, suggesting that the e-waste recycling facility was a significant source of Hg. The inorganic Hg (I-Hg) levels (0.84 μg/g) in hair samples of e-waste workers were much higher than that in the reference samples. Pearsons correlation coefficients showed that strong positive correlations (p<0.01) between hair I-Hg and time staying in industrial area (r=0.81) and between MeHg and fish consumption frequency (r=0.91), imply that workers were mainly exposed to Hg vapor through long-time inhalation of contaminated air and dust, while other population mainly exposed to MeHg through high-frequency fish consumption. The estimated daily intakes of Hg showed that dietary intake was the major Hg exposure source, and Hg intakes from rice and fish were significantly higher than from any other foods. The estimated total daily intakes (TDIs) of MeHg for both children (696.8 ng/(kg·day)) and adults (381.3 ng/(kg·day)) greatly exceeded the dietary reference dose (RfD) of 230 ng/(kg·day), implying greater health risk for humans from Hg exposures around e-waste recycling facilities.

Urban ambient air quality investigation and health risk assessment during haze and non-haze periods in Shanghai, China

Abstract Haze pollution has attracted much interest during the past decade for its significant effects on visibility, public health, and even global climate. The main objective of this study is to investigate ambient air quality during haze and non– haze periods and related health hazard for the local residents in Shanghai, China. Different levels, seasonal patterns, and health–risks of air pollutants (PM 10 , NO 2 , and SO 2 ) in haze and non–haze periods were observed. The results showed that the average PM 10 , NO 2 , and SO 2 concentrations were 110.9 μg/m 3 , 67.7 μg/m 3 , and 48.8 μg/m 3 in haze periods and 63.6 μg/m 3 , 45.3 μg/m 3 , and 27.5 μg/m 3 in non–haze periods, respectively. Due to a combination of increased emissions from heating sources coupled with meteorological conditions, PM 10 , NO 2 , and SO 2 levels were highest in winter and lowest in autumn. For the potential health risk analysis, the residents have been divided into four age categories namely, infants, children (1 year), children (8–10 years) and adults. The analysis took into account age–specific breathing rates, body weights for different age categories. Health risks for all age groups in haze periods were higher than those in non–haze periods, and the local residents suffered from the highest health risks due to NO 2 in haze periods.

Prenatal low-dose methylmercury exposure impairs neurite outgrowth and synaptic protein expression and suppresses TrkA pathway activity and eEF1A1 expression in the rat cerebellum.

Methylmercury (MeHg) is a highly neurotoxic environmental chemical that can cause developmental impairments. Human fetuses and neonates are particularly susceptible to MeHg toxicity; however, the mechanisms governing its effects in the developing brain are unclear. In the present study, we investigated the effects of prenatal and lactational MeHg exposure on the developing cerebellum in rats. We demonstrated that exposure to 5ppm MeHg decreased postnatal expression of pre- and postsynaptic proteins, suggesting an impairment in synaptic development. MeHg exposure also reduced neurite outgrowth, as shown by a decrease in the expression of the neurite marker neurofilament H. These changes were not observed in rats exposed to 1ppm MeHg. In order to define the underlying mechanism, we investigated the effects of MeHg exposure on the tropomyosin receptor kinase (Trk) A pathway, which plays important roles in neuronal differentiation and synapse formation. We demonstrated suppression of the TrkA pathway on gestation day 20 in rats exposed to 5ppm MeHg. In addition, down-regulation of eukaryotic elongation factor 1A1 (eEF1A1) was observed on postnatal day 1. eEF1A1 knockdown in differentiating PC12 cells impaired neurite outgrowth and synaptic protein expression, similar to the results of MeHg exposure in the cerebellum. These results suggest that suppression of the TrkA pathway and subsequent decreases in eEF1A1 expression induced by prenatal exposure to MeHg may lead to reduced neurite outgrowth and synaptic protein expression in the developing cerebellum.

Neurobehavioral effects, c-Fos/Jun expression and tissue distribution in rat offspring prenatally co-exposed to MeHg and PFOA: PFOA impairs Hg retention.

Exposure to methylmercury (MeHg) and perfluorooctanoic acid (PFOA) can occur simultaneously as both contaminants are found in the same food sources, especially fish, seafood, marine mammals and milk. The aim of this study was to assess the effects of exposure to MeHg (10 μg mL(-1) in drinking water) and PFOA (10 μg mL(-1) in drinking water) from gestational day 1 to postnatal day (PND) 21, alone and in combination, on neurobehavioral development and the expression of c-Fos/Jun in different brain regions in the offspring. Our findings showed that exposure to MeHg alone, and exposure to MeHg combined with PFOA significantly induced cliff avoidance reflexes and negative geotaxis reflexes. And these effects appeared to be greater following exposure to MeHg alone. MeHg and/or PFOA exposure did not significantly impair motor coordination functions, or cause significant changes in c-Fos expression in the hippocampus and cerebellum, and spatial learning tests were similar to those in the controls, thus it was impossible to determine whether combined exposure to MeHg and PFOA had any additional effects on both hippocampus and cerebellum regions. However, a significant increase in the frequency of line crossing was observed in rats treated with MeHg or PFOA alone, and there were no significant differences between the MeHg+PFOA-treated group and the controls, suggesting that PFOA was antagonistic to MeHg toxicity in the locomotor activity test. Co-exposure to MeHg and PFOA decreased all tissue Hg concentrations in pups compared to the group exposed to MeHg only, suggesting that PFOA impaired Hg retention in different tissues.

Accumulation of mercury, selenium and PCBs in domestic duck brain, liver and egg from a contaminated area with an investigation of their redox responses

PCBs and methylmercury (MeHg) are two of the most ubiquitous contaminants in the Qingzhen (QZ) area of Guizhou province. The estimated tolerable daily intakes (TDIs) of total mercury (T-Hg), MeHg, PCBs and Se from contaminated rice, eggs and fish by Chinese people in QZ showed that both MeHg and PCBs exceeded the corresponding safety limits. Pearsons correlation analyses of mercury and Se in all duck tissues showed that there were high correlations with T-Hg or MeHg and Se in QZ samples. However, the molar ratio between T-Hg and Se in brain tissues was close to 1, suggesting that Se is antagonistic to mercury toxicity only in brain tissues. Biochemical analyses showed that both superoxide dismutase and glutathione peroxidase increased in the brain, whereas in the liver and egg these enzymes decreased. However, lipid peroxidation and H2O2 generation in liver and egg tissues showed contrary responses, where significant increases in these tissues were seen relative to controls. Mercury and PCBs co-accumulation in liver and egg tissues gave rise to large numbers of free radicals as well as aggravated alkyl free radicals, superoxide radical and nitric oxide, thereby resulting in oxidative stress in these tissues. It can be concluded that an adaptive response of the redox defense system is present in brain tissues, as opposed to a general break down of the redox defense system in liver and egg. The results obtained in this study will provide basic information on exposure and risk assessment in local residents.

Assessment of neurotoxic effects and brain region distribution in rat offspring prenatally co-exposed to low doses of BDE-99 and methylmercury

Exposure to polybrominated diphenyl ether (PDBE) and methylmercury (MeHg) can occur simultaneously as both contaminants are found in the same food sources, especially fish, seafood, marine mammals and milk. The aim of this study was to assess the effects of exposure to low levels of MeHg (2.0 μg mL(-1) in drinking water) and BDE-99 (0.2 mg kg(-1) d(-1)) from gestational day 6 to postnatal day (PND) 21, alone and in combination, on neurobehavioral development and redox responses in offspring. The present study demonstrated an interaction due to co-exposure with low doses of MeHg and BDE-99 enhanced developmental neurotoxic effects. These effects were manifested as the delayed appearance of negative geotaxis reflexes, impaired motor coordination, and induction of oxidative stress in the cerebellum. In particular, the cerebellum may be a sensitive target for combined MeHg and BDE-99 toxicity. The neurotoxicity of low dose MeHg was exacerbated by the presence of low dose of BDE-99. It is concluded that prenatal co-exposure to MeHg and BDE-99 causes oxidative stress in the cerebellum of offspring by altering the activity of different antioxidant enzymes and producing free radicals. Hg retention was not affected by co-exposure to BDE-99. However, MeHg co-exposure seemed to increase BDE-99 concentrations in selected brain regions in pups compared to pups exposed to BDE-99 only. These results showed that the adverse effects following prenatal co-exposure to MeHg and BDE-99 were associated with tissue concentrations very close to the current human body burden of this persistent bioaccumulative compound.