Objective: Developmental exposure to dioxin-like compounds has been associated with cognitive and motor impairments in children. These toxicants have been shown to be thyroid toxicants in animal studies. Therefore, the objective of this study was to quantify the overall dioxin-like activity in maternal serum and determine the association between dioxin-like activity and thyroid hormone levels.
Study Design: Cross-sectional examination of serum from pregnant women (n = 150) attending a prenatal diagnosis clinic between January 2002 and December 2003.
Results: Serum dioxin-like activity was measured in 145 of 150 (96.7%) maternal serum samples. The mean (+/- SEM) serum lipid-adjusted dioxin-like activity was 0.34 +/- 0.01 pg/g. Multiple regression analysis failed to demonstrate a relationship between maternal serum dioxin-like activity and serum thyroid hormone levels.
Conclusion: Dioxin-like activity is quantifiable in an overwhelming majority of second-trimester maternal serum samples but there was no relationship between dioxin-like activity and thyroid hormone levels in our study population.
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http://dx.doi.org/10.1016/j.ajog.2005.08.013 | DOI Listing |
PeerJ
December 2024
Department Aquatic Ecotoxicology, Johann Wolfgang Goethe Universität Frankfurt am Main, Frankfurt, Germany.
Sixty percent of discrete surface water bodies in Europe do not meet the requirements for good ecological and chemical status and in Germany, the situation is even worse with over 90% of surface water bodies failing to meet the threshold. In addition to hydromorphological degradation, intensive land use and invasive species, chemical pollution is primarily considered to be responsible for the inadequate ecological status of the water bodies. As a quantitatively important source of micropollutants, wastewater treatment plants (WWTPs) represent an important entry path for chemical stressors.
View Article and Find Full Text PDFEnviron Sci Technol
December 2024
State Key Laboratory of Environmental Chemistry and Ecotoxicology, Research Center for Eco-Environmental Sciences, Chinese Academy of Sciences, Beijing 100085, China.
Chemosphere
December 2024
Department of Civil, Urban, Earth, and Environmental Engineering, Ulsan National Institute of Science and Technology (UNIST), Ulsan, 44919, Republic of Korea. Electronic address:
The spatial distribution and contamination patterns of polychlorinated dibenzo-p-dioxins and dibenzofurans (PCDD/Fs) and polychlorinated biphenyls (PCBs) in soil and pine needles from the multi-industrial city of Ulsan, South Korea were assessed. The mean concentrations of Σ PCDD/Fs, Σ dl-PCBs, and Σ I-PCBs were 78 pg/g dw, 90 pg/g dw, and 453 pg/g dw in the soil and 6 pg/g ww, 31 pg/g ww, and 166 pg/g ww in the pine needles, respectively. The mean concentrations of PCDD/Fs, dl-PCBs, and I-PCBs in the soil at industrial sites (138, 184, and 453 pg/g dw) were significantly higher than those at urban (47, 33, and 186 pg/g dw) and suburban sites (48, 49, and 234 pg/g dw).
View Article and Find Full Text PDFMar Pollut Bull
December 2024
Department of Marine Environmental Engineering, National Kaohsiung University of Science and Technology, Kaohsiung, Taiwan. Electronic address:
The objective of this study is to comprehensively characterize persistent organic pollutants (POPs) in seawater at Kaohsiung Harbor, focusing on their concentrations, partitioning behaviors, and profiles in both particle and liquid phases. We analyzed 100 L seawater for each sample, finding total dioxin-like toxicity (PCDD/Fs + PCBs + PBDD/Fs) ranging from 0.00936 to 0.
View Article and Find Full Text PDFbioRxiv
October 2024
Michigan State University, Department of Biochemistry and Molecular Biology, East Lansing, MI 48823, USA.
Epidemiological evidence suggests an association between dioxin and dioxin-like compound (DLC) exposure and human liver disease. The prototypical DLC, 2,3,7,8-tetrachlorodibenzo--dioxin (TCDD), has been shown to induce the progression of reversible hepatic steatosis to steatohepatitis with periportal fibrosis and biliary hyperplasia in mice. Although the effects of TCDD toxicity are mediated by aryl hydrocarbon receptor (AHR) activation, the underlying mechanisms of TCDD-induced hepatotoxicity are unresolved.
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