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The rapid development of the electronics industry to create huge profits and wealth at the same time waste production is also huge increase at an alarming rate, especially in abandoned home appliances, communications and electronic instruments and other electronic waste is staggering. Such as electronic waste or disposed of improperly, which contains large amounts of toxic chemicals such as PBDEs (polybrominated diphenyl ethers, PBDEs), heavy metals may be released to the environment as a new source of pollution on human health posed a potential threat. PBDEs are widely used as a flame retardant added electronic products, easy to enter the environment through various means, electronic waste is an important common pollutants. Humans through the respiratory tract, gastrointestinal tract and skin contact and other means exposure to PBDEs. In this study, Wang et al reported that the level of exposure to soil PBDEs 0.26 ~ 824 ng / g, the other relevant report data 10 to 60 times. In recent years, many countries have been reported in the biological sample (human serum, milk and fat) has been detected PBDEs, and its content is increasing year by year. Studies have shown that, PBDEs have endocrine disrupting effects, liver toxicity, neurotoxicity, and reproductive and developmental toxicity. But its toxicity mechanism is unclear, especially PBDEs pollution on human health effects research is still very limited. Although e-waste and other pollutants PBDEs have become more health problems brought attention, but so far about e-waste environmental exposure to biological effect of population is very limited. Based on this, this study in southern China through a 10-year history of electronic waste contaminated areas of maternal and neonatal thyroid hormone and hormone receptor mRNA levels and the corresponding level of testing to reveal e-waste pollution on local residents potential health hazards. The first part of the e-waste pollution on the general population of endocrine disrupting effects Objective: To investigate the electronic waste dismantling area residents thyroid hormones and sex hormones. Methods: During August 2005 to December in southern China has more than 10 years history of electronic waste dismantling areas and about 50km away from the area without significant industrial pollution, agricultural areas were randomly selected residents 58 (exposed group) and 80 (control group). Chemiluminescence analysis by immunohistochemistry (Immunochemiluminometric assay, ICMA) assay, including two residents free three serum thyroid hormone triiodothyronine (freetriiodothyronine, FT3), free four triiodothyronine (free thyroxine, FT4), thyroid stimulating hormone (thyroid stimulating hormone, TSH) and sex hormones, including estrogen (estradiol, E2), progesterone (progesterone, Pro), testosterone (testerone, Testo) level, and its possible influencing factors were analyzed. Results: The serum FT4 level exposure group than the control group (P lt; 0.01), but TSH levels higher (P lt; 0.01). Male subjects, serum E2 and Testo exposed group were lower than the control group (P lt; 0.05); female subjects, exposure to higher levels of serum Pro (P lt; 0.05). Further analysis of the factors that may affect endocrine function and found that e-waste dismantling occupational exposure history elevated TSH levels may be a risk factor (OR = 3.88, P lt; 0.01); gender (female) (OR = 0.39, P lt; 0.05) and has a household situation (OR = 0.33, P lt; 0.05) may be a protective factor FT3 levels decreased. Conclusion: Electronic waste environmental exposures may affect local residents thyroid hormones and sex hormones. The second part of the e-waste pollution on maternal endocrine disrupting effects Objective: To investigate the electronic waste dismantling area of ??maternal and reproductive hormones and thyroid hormone receptor expression level changes. Methods: in December 2005 to July 2006 in southern China has more than 10 years history of electronic waste dismantling areas and away from the area, about 50km geographical conditions, habits similar urban MCH were randomly selected from the local maternal 48 ( exposed group) name and 45 (control group). Using radioimmunoassay of serum thyroid hormones including FT3, FT4, TSH and reproductive hormones, including E2, Pro, Testo, follicle stimulating hormone (follicle stimulating hormone, FSH) and luteinizing hormone (luteinizing hormone, LH) using real-time Quantitative PCR determination of placental tissue TRα1, TRβ1, TSHR, ERα, ERβ, PR mRNA expression levels. Results: ① exposure group maternal serum FT4 levels than the control group (P lt; 0.05); but TSH levels higher (P lt; 0.05). ② exposed group and Pro maternal serum E2 levels were higher (P lt; 0.05). ③ exposure group placenta TRα1, TRβ1 mRNA expression levels than the control group (P lt; 0.05 and 0.01); But TSHR mRNA expression level was higher (P lt; 0.01). ④ exposure group placenta ERα, ERβmRNA expression levels were higher (P lt; 0.01); But PR mRNA expression levels than the control group (P lt; 0.05). Conclusion: Electronic waste environmental exposures may on maternal and reproductive hormone levels of thyroid hormone receptor expression and impact. The third part of the e-waste pollution on neonatal endocrine disrupting effects Objective: To explore? Discuss e-waste recycling area newborn and reproductive hormones and thyroid hormone receptor expression levels. Methods: in December 2005 to July 2006 in southern China has more than 10 years history of electronic waste dismantling areas and away from the area, about 50km geographical conditions, habits similar urban MCH were born to mothers randomly selected local Neonatal 48 (exposed group) and 45 (control group). Using radioimmunoassay of serum FT3, FT4, TSH and E2, Pro, Testo level; using real-time quantitative PCR determination of umbilical cord tissue TRα1, TRβ1, TSHR, ERα, ERβ, PR mRNA expression levels. Results: ① exposure group cord serum FT4 levels than the control group (P lt; 0.05); but TSH levels higher (P lt; 0.05). ② exposure group cord blood serum E2 and Pro levels were higher (P lt; 0.05). ③ exposure group placenta TRα1, TRβ1 mRNA expression levels than the control group (P lt; 0.05, P lt; 0.01); But TSHR mRNA expression level was higher (P lt; 0.01). ④ exposure group umbilical cord tissue ERα, ERβmRNA level higher (P lt; 0.01), PR mRNA levels were lower than the control group (P lt; 0.05). Conclusion: Electronic waste environmental exposures may neonatal thyroid hormone and reproductive hormone levels and receptor expression impact. The fourth part of maternal and neonatal effects of endocrine disruptors on Correlation Analysis Objective: To study the indicators of maternal and neonatal hormonal correlation between methods: Spearman analysis of maternal serum and cord serum thyroid hormone and reproductive hormone levels between correlation. Results: ① maternal serum FT4, TSH levels were with cord blood serum FT4, TSH levels were positively correlated, cord blood serum FT3 and FT4 were positively correlated. ② maternal serum E2, TSH levels were with cord blood serum E2, TSH levels were positively correlated; ③ cord blood serum E2 and P were positively correlated, E2 and P were associated with TSH levels were positively correlated. ④ maternal serum HPL, cord blood GH levels were positively correlated with birth weight (P lt; 0.05). Conclusion: Maternal exposure to environmental pollution caused by electronic waste Hormone Changes in hormone levels may affect the newborn. The fifth part of e-waste pollution on maternal and neonatal levels of oxidative stress Objective: To investigate the electronic waste dismantling area of ??maternal and neonatal changes in the level of oxidative stress in vivo methods: malondialdehyde (malondialdehyd, MDA), glutathione glutathione catalase (glutathione peroxidase, GSH-PX), superoxide dismutase (superoxide dismutase, SOD) kits serum MDA, GSH-PX, SOD and other indicators of oxidative stress. Results: The exposed group of maternal and neonatal serum MDA increased (P lt; 0.01), SOD activity decreased (P lt; 0.01); placenta and umbilical cord tissue MDA content increased (P lt; 0.01), SOD and GPX activity decreased (P lt; 0.05, P lt; 0.01), maternal serum and tissue MDA, SOD, GPX levels were and neonatal MDA, SOD, GPX (P lt; 0.05) levels were positively correlated. Conclusion: E-waste pollution of the environment may induce maternal and neonatal oxidative stress produced by the body. In summary, the e-waste contamination may have affected the local residents endocrine system. The results of this study reveal improper e-waste treatment and disposal has affected local residents thyroid hormones and sex hormone levels and the corresponding hormone receptor mRNA levels and oxidative stress induced by the corresponding reaction. Therefore, in-depth understanding of mechanisms of toxicity of PBDEs to identify the environmental impact of PBDEs and health hazards to the early establishment of POPs pollution hazard assessment and early warning systems have extremely important scientific significance.
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