Maternal exposure to polychlorinated biphenyls and the secondary sex ratio: an occupational cohort study

Though commercial production of polychlorinated biphenyls was banned in the United States in 1977, exposure continues due to their environmental persistence. Several studies have examined the association between environmental polychlorinated biphenyl exposure and modulations of the secondary sex ratio, with conflicting results. Our objective was to evaluate the association between maternal preconceptional occupational polychlorinated biphenyl exposure and the secondary sex ratio. We examined primipara singleton births of 2595 women, who worked in three capacitor plants at least one year during the period polychlorinated biphenyls were used. Cumulative estimated maternal occupational polychlorinated biphenyl exposure at the time of the infant's conception was calculated from plant-specific job-exposure matrices. A logistic regression analysis was used to evaluate the association between maternal polychlorinated biphenyl exposure and male sex at birth (yes/no). Maternal body mass index at age 20, smoking status, and race did not vary between those occupationally exposed and those unexposed before the child's conception. Polychlorinated biphenyl-exposed mothers were, however, more likely to have used oral contraceptives and to have been older at the birth of their first child than non-occupationally exposed women. Among 1506 infants liveborn to polychlorinated biphenyl-exposed primiparous women, 49.8% were male; compared to 49.9% among those not exposed (n = 1089). Multivariate analyses controlling for mother's age and year of birth found no significant association between the odds of a male birth and mother's cumulative estimated polychlorinated biphenyl exposure to time of conception. Based on these data, we find no evidence of altered sex ratio among children born to primiparous polychlorinated biphenyl-exposed female workers

Evaluating the Role of the Steroid and Xenobiotic Receptor (SXR/PXR) in PCB-153 Metabolism and Protection against Associated Adverse Effects during Perinatal and Chronic Exposure in Mice.

BACKGROUND:Polychlorinated biphenyls (PCBs) are environmental toxicants; PCB exposure has been associated with adverse effects on wildlife and humans. However, the mechanisms underlying these adverse effects are not fully understood. The steroid and xenobiotic receptor [SXR; also known as the pregnane X receptor (PXR) and formally known as NR1I2] is a nuclear hormone receptor that regulates inducible metabolism of drugs and xenobiotics and is activated or inhibited by various PCB congeners. OBJECTIVES:The aim of this study was to investigate the effects of exposure to PCB-153, the most prevalent PCB congener in human tissues, on SXR knockout mice (SXRKO) and to elucidate the role of SXR in PCB-153 metabolism and promotion of its harmful effects. METHODS:Wild-type (WT) and SXRKO mice were chronically or perinatally exposed to a low dose (54μg/kg/d) of PCB-153. Blood, livers, and spleens were analyzed using transcriptome sequencing (RNA-seq) and molecular techniques to investigate the impacts of exposure on metabolism, oxidative stress, and hematological parameters. RESULTS:SXRKO mice perinatally exposed to PCB-153 displayed elevated oxidative stress, symptoms of hemolytic anemia, and premature death. Transcriptomal analysis revealed that expression of genes involved in metabolic processes was altered in SXRKO mice. Elevated levels of the PCB-153 metabolite, 3-OH-PCB-153, were found in exposed SXRKO mice compared to exposed WT mice. Blood hemoglobin (HGB) levels were lower throughout the lifespan, and the occurrence of intestinal tumors was larger in SXRKO mice chronically exposed to PCB-153 compared to vehicle and WT controls. DISCUSSION:Our results suggest that altered metabolism induced by SXR loss of function resulted in the accumulation of hydroxylated metabolites upon exposure to PCB-153, leading to oxidative stress, hemolytic anemia, and tumor development in a mouse model. These results support a major role for SXR/PXR in protection against xenobiotic-induced oxidative stress by maintaining proper metabolism in response to PCB-153 exposure. This role of SXR could be generally applicable to other environmental toxicants as well as pharmaceutical drugs. https://doi.org/10.1289/EHP6262

Placental transfer of a hydroxylated polychlorinated biphenyl and effects on fetal and maternal thyroid hormone homeostasis in the rat

Earlier studies at our laboratory indicated that several hydroxylated polychlorinated biphenyls (OH-PCBs) detected in human blood could specifically inhibit thyroxine (T4) transport by competitive binding to the thyroid hormone transport protein transthyretin (TTR) in vitro. In the present study we investigated the effects of prenatal exposure to 5 mg/kg body weight of [14C]-labeled or unlabeled 4-OH-2,3,3',4',5-pentachlorobiphenyl (4-OH-CB107), one of the major metabolites of PCBs detected in human blood, from gestation days (GD) 10 to 16 on thyroid hormone status and metabolism in pregnant rats and their fetuses at GD 17 and GD 20. 4-OH-CB107 is a metabolite of both 2,3,3',4,4'-pentachlorobiphenyl (CB-105) and 2,3',4,4',5-pentachlorobiphenyl (CB-118). We were able to show the accumulation of 4-OH-CB107 in the fetal compartment. The fetal/maternal ratios at GD 20 in liver, cerebellum, and plasma were 11.0, 2.6, and 1.2, respectively. The 14C-4-OH-CB107-derived radioactivity in plasma was bound to TTR in both dams and fetuses. Fetal plasma TT4 and FT4 levels were significantly decreased at GD 17 and GD 20 (89 and 41␛espectively at GD 20). Fetal thyroid stimulating hormone levels were increased by 124 at GD 20. The T4 concentrations in fetal forebrain homogenates at GD20 were reduced by 35°but no effects could be detected on brain T3 concentrations. The deiodination of T4 to T3 was significantly increased in fetal forebrain homogenates at GD 17, and unaltered at GD 20. In addition, no alterations were observed in maternal and fetal hepatic T4-UDP-glucuronosyltransferase activity, type I deiodinase activity, and EROD activity. In conclusion, exposure of pregnant rats to 4-OH-CB107 results in the distribution of the compound in the maternal and fetal compartment, which is probably caused by the binding of the PCB metabolite to TTR. Consequently, TT4 levels in fetal plasma and brain samples were reduced. Despite reductions in fetal brain T4 levels, the active hormone (T3) in fetal brains remained unaffected

Prevention and control of contaminants of industrial processes and pesticides in the poultry production chain

The reduction in levels of organochlorine pesticide residues in food of animal origin in the past 30 years has been achieved especially by controlling entrance via the feed chain. A further reduction was achieved by registration and use of less persistent pesticides both for direct treatment of animals and of plant material. The remaining problems (e.g. dioxins and PCB's) are much harder to tackle. They are either of a ubiquitous nature and their impact might be enlarged by the present welfare trend requiring more contact of the animals with their environment, or they are of a sporadic nature making checking and control quite hard to execute. The present public demand for a farm animal production that is in balance with the animals' needs and a residue free product adds even more complications to the system

Degradation of Askarel (PCB Blend) by Indigenous Aerobic Bacteria Isolates from Dumpsites in Ore, Ondo State.Nigeria.

The removal of toxic industrial products such as polychlorinated biphenyls (PCBs) perchloroethylene (PCE) and trichloroethylene (TCE) in soils has become a daunting and necessary task. These compounds adsorb onto organic matter in the environment, making decontamination using traditional approaches difficult or ineffective. The use of microbes to transform these contaminants to non toxic degradation products is an alternative and imperative approach due to the prevalence of such organisms within the environment. In this study; the use of bacteria in the microbial degradation of polychlorinated biphenyls blend (Askarel) was explored. The notable bacteria isolated from dumpsites in Ore, Ondo state were identified using morphological and biochemical characteristics. These include: Pseudomonas, Micrococcus, Corynebacteria, Bacillus, Achromobacter and Arthrobacter species. The bacterial isolates potential to utilize Polychlorinated biphenyls blend (Askarel) as carbon source was investigated for twenty-one days period. From the results obtained, there was a general decrease in the pH and increase in mean Optical density (O.D); were the mean pH and O.D readings ranged between (3.08-6.02 and 0.060-0.557) respectively

Chemical signatures of the Anthropocene in the Clyde Estuary, UK: sediment hosted Pb, 207/206 Pb, Total Petroleum Hydrocarbons (TPH), Polyaromatic Hydrocarbon (PAH) and Polychlorinated Bipheny (PCB) pollution records

The sediment concentrations of total petroleum hydrocarbons (TPHs), polyaromatic hydrocarbons (PAHs), polychlorinated biphenyls (PCBs), Pb and 207/206Pb isotope ratios were measured in seven cores from the middle Clyde estuary (Scotland, UK) with an aim of tracking the late Anthropocene. Concentrations of TPHs ranged from 34 to 4386 mg kg−1, total PAHs from 19 to 16 163 μg kg−1 and total PCBs between less than 4.3 to 1217 μg kg−1. Inventories, distributions and isomeric ratios of the organic pollutants were used to reconstruct pollutant histories. Pre-Industrial Revolution and modern non-polluted sediments were characterized by low TPH and PAH values as well as high relative abundance of biogenic-sourced phenanthrene and naphthalene. The increasing industrialization of the Clyde gave rise to elevated PAH concentrations and PAH isomeric ratios characteristic of both grass/wood/coal and petroleum and combustion (specifically petroleum combustion). Overall, PAHs had the longest history of any of the organic contaminants. Increasing TPH concentrations and a concomitant decline in PAHs mirrored the lessening of coal use and increasing reliance on petroleum fuels from about the 1950s. Thereafter, declining hydrocarbon pollution was followed by the onset (1950s), peak (1965–1977) and decline (post-1980s) in total PCB concentrations. Lead concentrations ranged from 6 to 631 mg kg−1, while 207/206Pb isotope ratios spanned 0.838–0.876, indicative of various proportions of ‘background’, British ore/coal and Broken Hill type petrol/industrial lead. A chronology was established using published Pb isotope data for aerosol-derived Pb and applied to the cores

Signaling in a polluted world: oxidative stress as an overlooked mechanism linking contaminants to animal communication

The capacity to communicate effectively with other individuals plays a critical role in the daily life of an individual and can have important fitness consequences. Animals rely on a number of visual and non-visual signals, whose production brings costs to the individual. The theory of honest signaling states that these costs are higher for low than for high-quality individuals, which prevents cheating and makes signals, such as skin and plumage colouration, indicators of individual’s quality or condition. The condition-dependent nature of signals makes them ideally suited as indicators of environmental quality, implying that signal production might be affected by contaminants. In this mini-review article, we have made the point that oxidative stress (OS) is one overlooked mechanism linking exposure to contaminants to signaling because (i) many contaminants can influence the individual’s oxidative balance, and (ii) generation of both visual and non-visual signals is sensitive to oxidative stress. To this end, we have provided the first comprehensive review on the way both non-organic (heavy metals, especially mercury) and organic (persistent organic pollutants) contaminants may influence either OS or sexual signaling. We have also paid special attention to emerging classes of pollutants like brominated flame-retardants and perfluoroalkoxy alkanes in order to stimulate research in this area. We have finally provided suggestions and warnings for future work on the links among OS, sexual signaling and contaminant exposure

Polychlorinated biphenyl 153 exacerbates nonalcoholic fatty liver disease in C57BL/6 mice.

Polychlorinated biphenyls (PCBs) are persistent environmental pollutants which are detectable in the serum of all American adults. Amongst PCB congeners, PCB 153 has the highest serum level. PCBs have been dose-dependently associated with suspected nonalcoholic fatty liver disease (NAFLD), obesity and metabolic syndrome in epidemiological studies. The purpose of this study is to determine if PCB 153 induces NAFLD in mice fed a control diet (CD), and exacerbates NAFLD in mice fed a high fat diet (HFD). C57BL6/J mice were fed either control or 42% milk fat diet for 12 weeks with or without PCB 153 coexposure (50 mg/kg i.p. x 4). Glucose tolerance tests were performed, and plasma/tissues were obtained at necropsy for measurements of adipocytokine levels, histology, and gene expression microarrays. In mice fed CD, the addition of PCB 153 had little to no effect on any of the measured parameters. In contrast, PCB 153 co-exposure in high fat-fed mice was associated with dramatically increased visceral adiposity, hepatic steatosis and increased plasma adipokines including adiponectin, leptin, resistin and plasminogen activator inhibitor-1 levels. Likewise, co-exposure reduced expression of hepatic genes implicated in ~oxidation while increasing the expression of genes associated with lipid biosynthesis. Regardless of diet, PCB 153 had no effect on insulin resistance or tumor necrosis factor alpha levels. However, HFD+PCB 153 appeared to induce an endoplasmic reticulum (ER) stress response. Therefore, PCB 153 is an obesogen which exacerbates hepatic steatosis; alters adipocytokines; and disrupts normal hepatic lipid metabolism when administered with HFD. Because all U.S. adults have been exposed to PCB 153, this particular nutrient-toxicant interaction potentially impacts on the progression of human NAFLD