BACKGROUND: Recent studies have provided compelling evidence that exposure to brominated flame retardants (BFRs) can adversely affect human health. We aim to explore the potential impact of BFRs on adiposity and central obesity. METHODS: Data from the National Health and Nutrition Examination Surveys (NHANES) cycles conducted between 2009 and 2014 was used to study the connections between variables. After filtering, we analyzed a sample of 4,110 adults aged 20 years and above. Our goal was to examine the potential association between BFRs and consequences and investigate the part played by oxidative stress and inflammatory markers as intermediaries. To achieve this, we used advanced statistical methods such as weighted quantile sum (WQS) regression, quantile-based g-computation (QGC), and the Bayesian kernel machine regression (BKMR). RESULTS: The findings showed that among the examined chemicals, exposure to PBDE85 (weight: 41%), PBDE100 (24%), and PBB153 (23%) may be the dominant contributors to general obesity risk. Upon controlling for all variables that could impact the results, it was found that the QGC outcomes indicated a positive correlation between exposure to mixtures of brominated flame retardants and the occurrence of abdominal obesity (OR = 1.187, 95% CI: 1.056-1.334, p = 0.004). Significant contributions were made by PBDE85 (52%), PBB153 (27%), and PBDE100 (21%). Mediation analysis shows that lymphatic cells (LC) and albumin (ALB) partially mediate the link between brominated flame retardants and obesity. The results of BKMR are generally consistent with those of WQS and QGC. CONCLUSION At a population level, our research has revealed a noteworthy correlation between BFRs and obesity. However, further investigation is required through prospective cohort studies and in-depth mechanistic exploratory studies.
Humans ; Flame Retardants/adverse effects* ; Oxidative Stress/drug effects* ; Adult ; Male ; Female ; Middle Aged ; Inflammation/epidemiology* ; Obesity/chemically induced* ; Biomarkers/blood* ; Nutrition Surveys ; Mediation Analysis ; Young Adult ; United States/epidemiology* ; Environmental Exposure/adverse effects* ; Aged ; Environmental Pollutants/adverse effects* ; Halogenated Diphenyl Ethers/adverse effects*

Objective: To explore the effects of prenatal exposure to polybrominated diphenyl ethers (PBDEs) on placental size and birth outcomes. Methods: Based on the perspective Wenzhou Birth Cohort, this nested case-control study included 101 fetal growth restriction (FGR) and 101 healthy newborns. Maternal serum samples were collected during the third trimester and measured for PBDEs by gas chromatography tandem mass spectrometry. The basic information of mother-newborn pairs was collected from questionnaires, whereas the placental size and birth outcomes of newborns were obtained from hospital records. Results: A total of 19 brominated diphenyle ether (BDE) congeners were detected in maternal serum samples. Higher concentrations of BDE-207, -208, -209, and ∑ Conclusion A negative association was found between PBDE levels in maternal serum and placental size and birth outcomes. Prenatal PBDE exposure may be associated with elevated risk of the incidence of FGR birth.
Case-Control Studies ; China/epidemiology* ; Female ; Fetal Growth Retardation/epidemiology* ; Halogenated Diphenyl Ethers/blood* ; Humans ; Incidence ; Infant, Newborn ; Placenta/physiology* ; Pregnancy ; Risk Factors

Objective To discuss the effects of polybrominated diphenyl ethers （PBDEs） exposure in e-waste dismantling region on the human body and provide data support for the identification of environmental health damage to residents in the e-waste dismantling region. Methods Adults in an e-waste dismantling region （exposed group, 54 participants） and a control region （control group, 58 participants） were selected, questionnaires were carried out and blood and urine samples were collected. Blood PBDEs, blood lipids, blood routine, blood lead, urine cadmium, urine chromium and urine nickel were detected. T-test was utilized to compare the differences of PBDEs between the two groups. Multivariate analysis were utilized to compare the differences between the two groups in blood routine indexes. Linear regression was used to analyze the relationship between PBDEs and blood routine. Results Exposure levels of PBDEs were significantly higher in the exposed group （240.00 ng/g, adjusted mass fraction of blood lipids, thereafter） than in the control group （93.00 ng/g, P<0.05）. There was no statistical significance in the differences in most blood routine indexes of the two groups （ P>0.05）, and their reference values were all within normal ranges. Mean platelet volume, plateletcrit, basophils percentage, absolute value of basophils, and mean corpuscular hemoglobin concentration were higher in the exposed group than in the control group （P<0.05）. Platelet distribution widths were lower in the exposed group than in the control group and below the normal reference range （P<0.05）. Conclusion PBDEs exposure in e-waste dismantling region tend to change platelet morphology, the number of basophils, and mean corpuscular hemoglobin concentration, and may pose potential health hazards to local residents.
Adult ; China ; Electronic Waste/analysis* ; Environmental Monitoring ; Halogenated Diphenyl Ethers/toxicity* ; Human Body ; Humans

Increasing prevalence of childhood obesity poses threats to the global health burden. Because this rising prevalence cannot be fully explained by traditional risk factors such as unhealthy diet and physical inactivity, early-life exposure to endocrine disrupting chemicals (EDCs) is recognized as emerging novel risk factors for childhood obesity. EDCs can disrupt the hormone-mediated metabolic pathways, affect children’s growth and mediate the development of childhood obesity. Many organic pollutants are recently classified to be EDCs. In this review, we summarized the epidemiological and laboratory evidence related to EDCs and childhood obesity, and discussed the possible mechanisms underpinning childhood obesity and early-life exposure to non-persistent organic pollutants (phthalates, bisphenol A, triclosan) and persistent organic pollutants (dichlorodiphenyltrichloroethane, polychlorinated biphenyls, polybrominated diphenyl ethers, per- and polyfluoroalkyl substances). Understanding the relationship between EDCs and childhood obesity helps to raise public awareness and formulate public health policy to protect the youth from exposure to the harmful effects of EDCs.
Adolescent ; Diet ; Endocrine Disruptors* ; Global Health ; Halogenated Diphenyl Ethers ; Humans ; Metabolic Networks and Pathways ; Pediatric Obesity* ; Polychlorinated Biphenyls ; Prevalence ; Public Health ; Risk Factors

OBJECTIVEThis paper is to assess the current status of polybrominated diphenyl ethers (PBDEs) contamination in the environment in China and estimate the exposure to PBDEs in non-occupational populations.

METHODSA total of 80 research papers published from January 2001 to October 2013 were selected. Geographic information system (GIS) was used in mapping PBDE concentrations and distributions in environmental media. Ni's model was applied to calculate ∑PBDE-intake via the intakes of contaminated food, water and air in the Pearl River Delta and Yangtze River Delta.

RESULTSBDE-209 was found to be the major PBDE congener in the environmental media and food in China. PBDE concentrations varied among different areas, among which the contamination in Guangdong Province was most serious. Daily intake of ∑PBDEs was 225.1-446.0 ng/d for adults in the Pearl River Delta, which was higher than the intake for those living in the Yangtze River Delta (148.9-369.8 ng/d).

CONCLUSIONAtorvastatin can attenuate LPS-induced TNF-α expression and production by activating HO-1 via the ERK and p38 MAPK pathways, suggesting that atorvastatin can be used in treatment of inflammatory diseases such as sepsis, especially in those with atherosclerotic diseases.

China ; Diet ; Environmental Pollutants ; analysis ; Food Contamination ; analysis ; Geographic Information Systems ; Halogenated Diphenyl Ethers ; analysis ; Humans ; Inhalation Exposure ; analysis

Eleven recently completed toxicological studies were critically reviewed to identify toxicologically significant endpoints and dose-response information. Dose-response data were compiled and entered into the USEPA's benchmark dose software (BMDS) for calculation of a benchmark dose (BMD) and a benchmark dose low (BMDL). After assessing 91 endpoints across the nine studies, a total of 23 of these endpoints were identified for BMD modeling, and BMDL estimates corresponding to various dose-response models were compiled for these separate endpoints. Thyroid, neurobehavior and reproductive endpoints for BDE-47, -99, -209 were quantitatively evaluated. According to methods and feature of each study, different uncertainty factor (UF) value was decided and subsequently reference doses (RfDs) were proposed. Consistent with USEPA, the lowest BMDLs of 2.10, 81.77, and 1698 µg/kg were used to develop RfDs for BDE-47, -99, and -209, respectively. RfDs for BDE-99 and BDE-209 were comparable to EPA results, and however, RfD of BDE-47 was much lower than that of EPA, which may result from that reproductive/developmental proves to be more sensitive than neurobehavior for BDE-47 and the principal study uses very-low-dose exposure.
Animals ; Female ; Halogenated Diphenyl Ethers ; toxicity ; Male ; Mice ; Rats ; Reference Standards ; Toxicity Tests

OBJECTIVETo study the protective effects of N-acetylcysteine (NAC) against oxidative injury in the brain tissue of mice induced by decabromodiphenyl ether (PBDE-209) and the expression of mitogen activated protein kinase (MAPK)-related proteins in the hippocampus.

METHODSTwenty-one male BALB/c mice were randomly divided into three groups with seven mice in each group: solvent control group, PBDE-209 group with gavage of 500 mg/kg PBDE-209, and PBDE-209 +NAC group which received intraperitoneal injection of 100 mg/kg NAC 0.5 h before exposure to PBDE-209. Mice were sacrificed 6 weeks after exposure. Malondialdehyde (MDA) level, superoxide dismutase (SOD) activity, and glutathione (GSH) level in the cerebral cortex, hippocampus, cerebellum, and striatum, as well as the protein expression of extracellular signal-regulated kinase (ERK), phosphorylated ERK (p-ERK), p38 MAPK (p38), and phosphorylated p38 (p-p38) in the hippocampus, were determined by Western blot.

RESULTSCompared with the hippocampal and cerebellar levels of MDA in control group [(4.91±1.60) and (2.42±1.41) nmol/mg pro] and PBDE-209+NAC group [(6.16±1.03) and (2.83±0.85) nmol/mg pro], the MDA levels in PBDE-209 group [(12.12±6.39) and (4.24±1.15) nmol/mg pro] were significantly increased (P < 0.05). The striatum MDA level in PBDE-209 group [(12.92±4.30) nmol/mg pro] was significantly increased as compared with that of the control group [(4.05±2.23) nmol/mg pro] (P < 0.05). The hippocampal SOD activity of PBDE-209 group [(59.29±37.09) U/mg pro] was reduced significantly as compared with those of the control group [(93.28±21.75) U/mg pro] and PBDE-209+NAC group [(98.92±21.54) U/mgpro] (P < 0.05). The GSH levels in the cerebral cortex, striatum, and cerebellum in PBDE-209 group [(40.98±13.19), (24.46±11.30), and (3.55±1.55) mg GSH/g pro] were significantly reduced as compared with those of the control group [(75.79±26.51), (44.52±13.15) and (8.01±3.23) mg GSH/g pro] and the PBDE-209+NAC group [(89.86±28.39), (39.01±9.05) and (10.34±2.58) mg GSH/g pro] (P < 0.05). Western blot results showed that the ratios of p-p38/p38 and p-ERK/ERK in the hippocampus were significantly higher in the PBDE-209 group than in the control group and PBDE-209+NAC group (P < 0.05).

CONCLUSIONAntioxidant NAC has a protective effect against PBDE-209-induced brain injury in mice to some extent, and reduces the expression of MAPK-related proteins.

Acetylcysteine ; pharmacology ; Animals ; Antioxidants ; metabolism ; pharmacology ; Brain ; drug effects ; metabolism ; Extracellular Signal-Regulated MAP Kinases ; metabolism ; Glutathione ; metabolism ; Halogenated Diphenyl Ethers ; toxicity ; Hippocampus ; metabolism ; Male ; Malondialdehyde ; metabolism ; Mice, Inbred BALB C ; Mitogen-Activated Protein Kinases ; metabolism ; Oxidation-Reduction ; Phosphorylation ; p38 Mitogen-Activated Protein Kinases ; metabolism

OBJECTIVES: This study was conducted to determine the depositional characteristics of several tree barks, including Ginkgo (Ginkgo biloba), Pine (Pinus densiflora), Platanus (Platanus), and Metasequoia (Metasequoia glyptostroboides). These were used as passive air sampler (PAS) of atmospheric polybrominated diphenyl ethers (PBDEs). METHODS: Tree barks were sampled from the same site. PBDEs were analyzed by highresolution gas chromatography/high-resolution mass spectrometer, and the lipid content was measured using the gravimetric method by n-hexane extraction. RESULTS: Gingko contained the highest lipid content (7.82 mg/g dry), whereas pine (4.85 mg/g dry), Platanus (3.61 mg/g dry), and Metasequoia (0.97 mg/g dry) had relatively lower content. The highest total PBDEs concentration was observed in Metasequoia (83,159.0 pg/g dry), followed by Ginkgo (53,538.4 pg/g dry), Pine (20,266.4 pg/g dry), and Platanus (12,572.0 pg/g dry). There were poor correlations between lipid content and total PBDE concentrations in tree barks (R2=0.1011, p =0.682). Among the PBDE congeners, BDE 206, 207 and 209 were highly brominated PBDEs that are sorbed to particulates in ambient air, which accounted for 90.5% (84.3-95.6%) of the concentration and were therefore identified as the main PBDE congener. The concentrations of particulate PBDEs deposited on tree barks were dependent on morphological characteristics such as surface area or roughness of barks. CONCLUSIONS: Therefore, when using the tree barks as the PAS of the atmospheric PBDEs, samples belonging to same tree species should be collected to reduce errors and to obtain reliable data.
Ginkgo biloba ; Halogenated Diphenyl Ethers* ; Plant Bark* ; Trees

OBJECTIVETo investigate the effect of maternal decabromodiphenyl ether (BDE-209) exposure on the sexual development in male offspring rats.

METHODSTwenty-four pregnant Sprague-Dawley rats were randomly divided into three BDE-209 exposure groups and one control group. The three BDE-209 exposure groups were given BDE-209 (100, 300, and 900 mg/kg) by gavage on gestational days 12∼18, and the control group was given corn oil. The body weight and body length of each newborn male rat was measured at postnatal days 4, 10, 16, and 21. Twelve newborn male rats were randomly selected from each group; anogenital distance was measured at postnatal day 21, serum testosterone was measured, and the organ coefficient of testis was calculated.

RESULTSThe newborn male rats in all exposure groups showed declining trends in body weight and body length compared with those in the control group, and the 900 mg/kg BDE-209 exposure group had significantly lower body weight and body length than the control group at postnatal days 4, 10,16, and 21 (P < 0.01). At postnatal day 21, the 100, 300, and 900 mg/kg BDE-209 exposure groups had anogenital distances of 17.82±2.35 mm, 16.32±1.66 mm, and 15.80±1.34 mm, respectively, demonstrating a significant decrease with increased exposure dose (P < 0.05), but no significant difference was found when comparing these values with that of the control group (16.64±2.38 mm) (P > 0.05). There were no significant differences in serum testosterone and organ coefficients of testis and epididymis between the control group and BDE-209 exposure groups (P > 0.05).

CONCLUSIONMaternal exposure to BDE-209 has adverse effect on the growth of male offspring rats, but it leads to no significant changes in sexual development.

Animals ; Female ; Halogenated Diphenyl Ethers ; toxicity ; Male ; Pregnancy ; Prenatal Exposure Delayed Effects ; Rats ; Sexual Development ; drug effects

This review surveys the recent literature on the neurodevelopmental impacts of chemical exposures during pregnancy. The review focuses primarily on chemicals of recent concern, including phthalates, bisphenol-A, polybrominated diphenyl ethers, and perfluorinated compounds, but also addresses chemicals with longer histories of investigation, including air pollutants, lead, methylmercury, manganese, arsenic, and organophosphate pesticides. For some chemicals of more recent concern, the available literature does not yet afford strong conclusions about neurodevelopment toxicity. In such cases, points of disagreement among studies are identified and suggestions provided for approaches to resolution of the inconsistencies, including greater standardization of methods for expressing exposure and assessing outcomes.
Air Pollutants ; Arsenic ; Biphenyl Compounds ; Child ; Halogenated Diphenyl Ethers ; Humans ; Manganese ; Neurobehavioral Manifestations ; Pesticides ; Pregnancy