In this study, we recruited 49 subjects from one village close to an electronic waste (e-waste) site (exposed group) and another located 50 km away from the e-waste site (control group). We found that serum levels of polybrominated diphenyl ethers (median PBDEs, 382 ng/g lipid weight; range, 77-8452 ng/g lipid weight) and thyroid-stimulating hormone (median TSH, 1.79 microIU/mL; range, 0.38-9.03 microIU/mL) and frequencies of micro-nucleated binucleated cells (MNed BNC; median, 5% per hundred; range, 0-96% per hundred) were significantly higher in the exposed group than in the control group (158 ng/g, range of 18-436 ng/g, and p < 0.05; 1.15 microIU/mL, range of 0.48-2.09, and p < 0.01; and 0% per hundred, range of 0-5% per hundred, and p < 0.01, respectively). A history of working with e-waste was significantly associated with increased MNed BNC frequencies (odds ratio (OR), 38.85; 95% confidence interval (CI) = 1-1358.71, p = 0.044), independent of years of local residence, a perceived risk factor. However, there was no association between PBDEs exposure and oxidative DNA damage. Therefore, the exposure to PBDEs at the e-waste site may have an effect on the levels of TSH and genetoxic damage among these workers, but this needs to be validated in large studies.
The striking 3-4:1 male predominance of esophageal squamous cell carcinoma (ESCC) has not yet been well explained. Our hypothesis is that the changes in level of estrogen and/or subtype of estrogen receptor (ER) may exert a protective factor in esophageal carcinogenesis and prognosis of ESCC. Radioimmunoassay (RIA) was used to determine the serum level of estradiol in healthy cohort from high-incidence area (HIA) and low-incidence area (LIA) for esophageal cancer as well as patients with ESCC from HIA in Henan, northern China. The ERβ expression profiling during the multi-stage progression of ESCC pathogenesis was evaluated by immunohistochemistry (IHC). Both males and females from HIA had significant decreases of serum estradiol in high-risk subjects predisposing for ESCC compared to healthy counterparts from LIA (P < 0.01). Furthermore, patients with ESCC from HIA developed the lowest level of estradiol (P < 0.01). ERβ expressed in precursor lesions of ESCC and changed quantitatively and qualitatively with disease progression during the multi-stages process of esophageal carcinogenesis. High frequency of ERβ expression was correlated with less aggressive potential of clinical behavior (P = 0.012, 0.015 for lymph node metastasis and tumor stage, respectively). This study indicates that lower serum level of estradiol may represent higher predisposition for development of ESCC, and ERβ expression and/or nuclear location may predict better outcome for patients with ESCC. The present results provide clues to explain the striking gender difference for ESCC, which warrants further investigations on potential applications of estrogen or analogs in prevention of ESCC.
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