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Current Topics in Developmental Biology 2023There is credible evidence that environmental factors influence individual risk and/or severity of autism spectrum disorders (hereafter referred to as autism). While it... (Review)
Review
There is credible evidence that environmental factors influence individual risk and/or severity of autism spectrum disorders (hereafter referred to as autism). While it is likely that environmental chemicals contribute to the etiology of autism via multiple mechanisms, identifying specific environmental factors that confer risk for autism and understanding how they contribute to the etiology of autism has been challenging, in part because the influence of environmental chemicals likely varies depending on the genetic substrate of the exposed individual. Current research efforts are focused on elucidating the mechanisms by which environmental chemicals interact with autism genetic susceptibilities to adversely impact neurodevelopment. The goal is to not only generate insights regarding the pathophysiology of autism, but also inform the development of screening platforms to identify specific environmental factors and gene×environment (G×E) interactions that modify autism risk. Data from such studies are needed to support development of intervention strategies for mitigating the burden of this neurodevelopmental condition on individuals, their families and society. In this review, we discuss environmental chemicals identified as putative autism risk factors and proposed mechanisms by which G×E interactions influence autism risk and/or severity using polychlorinated biphenyls (PCBs) as an example.
Topics: Humans; Gene-Environment Interaction; Autism Spectrum Disorder; Polychlorinated Biphenyls
PubMed: 36707213
DOI: 10.1016/bs.ctdb.2022.11.001 -
Environmental Science & Technology Sep 2020We measured the concentrations of 205 polychlorinated biphenyl (PCB) congeners in 26 food items: beef steak, butter, canned tuna, catfish, cheese, eggs, french fries,...
We measured the concentrations of 205 polychlorinated biphenyl (PCB) congeners in 26 food items: beef steak, butter, canned tuna, catfish, cheese, eggs, french fries, fried chicken, ground beef, ground pork, hamburger, hot dog, ice cream, liver, luncheon meat, margarine, meat-free dinner, milk, pizza, poultry, salmon, sausage, shrimp, sliced ham, tilapia, and vegetable oil. Using Diet History Questionnaire II, we calculated the PCB dietary exposure in mothers and children participating in the AESOP Study in East Chicago, Indiana, and Columbus Junction, Iowa. Salmon had the highest concentration followed by canned tuna, but fish is a minor contributor to exposure. Other animal proteins are more important sources of PCB dietary exposure in this study population. Despite the inclusion of few congeners and food types in previous studies, we found evidence of a decline in PCB concentrations over the last 20 years. We also found strong associations of PCB congener distributions with Aroclors in most foods and found manufacturing byproduct PCBs, including PCB11, in tilapia and catfish. The reduction in PCB levels in food indicates that dietary exposure is comparable to PCB inhalation exposures reported for the same study population.
Topics: Animals; Aroclors; Cattle; Chicago; Child; Food Contamination; Humans; Indiana; Iowa; Polychlorinated Biphenyls
PubMed: 32816464
DOI: 10.1021/acs.est.0c03632 -
Critical Reviews in Toxicology Mar 2015Abstract The metabolism of polychlorinated biphenyls (PCBs) is complex and has an impact on toxicity, and thereby on the assessment of PCB risks. A large number of... (Review)
Review
Abstract The metabolism of polychlorinated biphenyls (PCBs) is complex and has an impact on toxicity, and thereby on the assessment of PCB risks. A large number of reactive and stable metabolites are formed in the processes of biotransformation in biota in general, and in humans in particular. The aim of this document is to provide an overview of PCB metabolism, and to identify the metabolites of concern and their occurrence. Emphasis is given to mammalian metabolism of PCBs and their hydroxyl, methylsulfonyl, and sulfated metabolites, especially those that persist in human blood. Potential intracellular targets and health risks are also discussed.
Topics: Animals; Environmental Exposure; Environmental Pollutants; Humans; Polychlorinated Biphenyls
PubMed: 25629923
DOI: 10.3109/10408444.2014.999365 -
Frontiers in Endocrinology 2023Polychlorinated biphenyls (PCBs), organic lipophilic pollutants that accumulate through diet and increase with age, have been associated with polycystic ovary syndrome...
INTRODUCTION
Polychlorinated biphenyls (PCBs), organic lipophilic pollutants that accumulate through diet and increase with age, have been associated with polycystic ovary syndrome (PCOS) and shown to affect microRNA (miRNA) expression. This work aimed to determine if PCBs were associated with circulating miRNAs and whether there were any correlations with serum PCB/miRNA levels and hormonal changes.
METHODS
29 non-obese PCOS and 29 healthy control women, with similar age and body mass index (BMI), had their serum miRNAs measured together with 7 indicator PCBs (PCB28, PCB52, PCB101, PCB118, PCB138, PCB153, PCB180) using high resolution gas chromatography coupled with high resolution mass spectrometry.
RESULTS
In the combined study cohort, four miRNAs (hsa-miR-139-5p, hsa-miR-424-5p, hsa-miR-195-5p, hsa-miR-335-5p) correlated with PCBs, but none correlated with metabolic parameters. hsa-miR-335-5p correlated with FSH. When stratified, 25 miRNAs correlated with PCBs in controls compared to only one (hsa-miR-193a-5p) in PCOS; none of these miRNAs correlated with the metabolic parameters of BMI, insulin resistance, or inflammation (C-reactive protein, CRP). However, of these 25 miRNAs in controls, hsa-miR-26a-5p, hsa-miR-193a-5p, hsa-miR-2110 and hsa-miR-195-5p positively correlated with luteinizing hormone (LH), hsa-miR-99b-5p and hsa-miR-146b-5p correlated with estradiol, hsa-miR-193a-5p correlated with progesterone, hsa-miR-195-5p correlated with follicle stimulating hormone (FSH), and hsa-miR-139-5p and hsa-miR-146b-5p negatively correlated with anti-müllerian hormone (AMH) (all <0.05). hsa-miR-193a-5p in PCOS cases correlated with estradiol.
CONCLUSION
In this cohort of women, with no difference in age and BMI, and with similar PCB levels, the miRNAs correlating to PCBs associated with menstrual cycle factors in healthy menstruating controls versus the anovulatory PCOS subjects. The PCB-associated miRNAs did not correlate with non-reproductive hormonal and metabolic parameters. This suggests that PCB effects on miRNAs may result in changes to the hypothalamo-ovarian axis that may thus affect fertility.
Topics: Humans; Female; Polycystic Ovary Syndrome; Polychlorinated Biphenyls; MicroRNAs; Follicle Stimulating Hormone; Circulating MicroRNA; Estradiol
PubMed: 37790603
DOI: 10.3389/fendo.2023.1233484 -
Environmental Research Nov 2022In 1973-74, a polybrominated biphenyl (PBB) flame retardant mixture was shipped to Michigan livestock feed mills in place of a nutritional supplement and contaminated...
In 1973-74, a polybrominated biphenyl (PBB) flame retardant mixture was shipped to Michigan livestock feed mills in place of a nutritional supplement and contaminated the food supply. Following the accident, the Michigan PBB Registry was established to study the long-term health effects of halogenated compounds and is now led by a community-academic partnership. PBB exposure is associated with altered DNA methylation in sperm, which may lead to adverse birth outcomes in children whose fathers have increased levels of serum PBB or polychlorinated biphenyl (PCB). Paternal PBB and PCB levels of men enrolled in the Michigan PBB Registry (n = 155) were analyzed against matched offspring birthweight and gestational age (n = 336). Birthweight and gestational age were dichotomized at the 25th percentile and 37 weeks, respectively, and paternal PBB and PCB levels were examined as continuous measures and divided into tertiles. Associations of offspring birthweight and gestational age with paternal PBB and PCB serum concentrations were modeled using multivariable linear spline and log-risk regression, adjusting for family clustering, paternal health and lifestyle factors, maternal PBB, and PCB serum concentrations, sex, and offspring gestational age (for birthweight). Fathers in the middle and upper PBB and PCB tertiles had increased risks for lowest quartile birthweight compared to the first tertile, with adjusted risk ratios (aRR) = 1.67 (95% CI: 0.93, 2.99) and aRR = 2.06 (95% CI: 1.12, 3.79) for PBB, and aRR = 1.47 (95% CI: 0.79, 2.75) and aRR = 1.34 (95% CI: 0.70, 2.54) for PCB, respectively. Elevated paternal PBB levels were not associated with an increased risk for preterm birth, while PCB levels were associated with a small, but not significant, decrease in gestational age, β = -0.37 (95% CI: -0.76, 0.03) weeks per log unit increase PCB. The findings suggest that increased paternal PBB and PCB levels negatively impact offspring birthweight, and paternal PCB levels may negatively impact gestational age.
Topics: Birth Weight; Child; Environmental Pollutants; Fathers; Female; Humans; Infant; Infant, Newborn; Male; Polybrominated Biphenyls; Polychlorinated Biphenyls; Premature Birth; Semen
PubMed: 36041536
DOI: 10.1016/j.envres.2022.114215 -
Environmental Science and Pollution... Feb 2016The pathology of cardiovascular disease is multi-faceted, with links to many modifiable and non-modifiable risk factors. Epidemiological evidence now implicates exposure... (Review)
Review
The pathology of cardiovascular disease is multi-faceted, with links to many modifiable and non-modifiable risk factors. Epidemiological evidence now implicates exposure to persistent organic pollutants, such as polychlorinated biphenyls (PCBs), with an increased risk of developing diabetes, hypertension, and obesity; all of which are clinically relevant to the onset and progression of cardiovascular disease. PCBs exert their cardiovascular toxicity either directly or indirectly via multiple mechanisms, which are highly dependent on the type and concentration of PCBs present. However, many PCBs may modulate cellular signaling pathways leading to common detrimental outcomes including induction of chronic oxidative stress, inflammation, and endocrine disruption. With the abundance of potential toxic pollutants increasing globally, it is critical to identify sensible means of decreasing associated disease risks. Emerging evidence now implicates a protective role of lifestyle modifications such as increased exercise and/or nutritional modulation via anti-inflammatory foods, which may help to decrease the vascular toxicity of PCBs. This review will outline the current state of knowledge linking coplanar and non-coplanar PCBs to cardiovascular disease and describe the possible molecular mechanism of this association.
Topics: Animals; Cardiovascular Diseases; Humans; Oxidative Stress; Polychlorinated Biphenyls
PubMed: 25877901
DOI: 10.1007/s11356-015-4479-6 -
International Journal of Environmental... Feb 2023Polychlorinated diphenyl ethers (PCDEs) are a class of synthetic halogenated aromatic compounds, which have gradually attracted widespread attention due to potential... (Review)
Review
Polychlorinated diphenyl ethers (PCDEs) are a class of synthetic halogenated aromatic compounds, which have gradually attracted widespread attention due to potential environmental risks to humans and ecosystems. This paper presents a literature review of research on PCDEs using PubMed, Web of Science and Google Scholar as search engines/databases with no constraints on publishing year or number. A total of 98 publications on the sources, environmental levels, environmental behavior and fate, synthesis and analysis and toxicology of PCDEs were retrieved. Existing studies have shown that PCDEs widely exist in the environment with the ability of long-range transport, bioaccumulation and biomagnification, which are almost comparable to polychlorinated biphenyls. They can elicit adverse effects including hepatic oxidative stress, immunosuppression, endocrine disorders, growth retardation, malformations, reduced fertility and increased mortality in organisms, among which some seem to be related to the activation of the aryl hydrocarbon receptor. PCDEs can be metabolized into other organic pollutants, such as hydroxylated and methoxylated PCDEs and even polychlorinated dibenzo--dioxins and furans through biotransformation, photolysis and pyrolysis reactions in the environment. Compared with reviews on PCDEs published previously, some new information and findings are summarized in this review, such as new sources, current environmental exposure levels, main metabolism pathways in aquatic organisms, acute toxicity data for more species and relationships between structural parameters and toxicity and bioaccumulation potentials of PCDE congeners. Finally, current research deficiencies and future research perspectives are proposed to facilitate the assessment of health and ecological risks of PCDEs.
Topics: Humans; Halogenated Diphenyl Ethers; Ecosystem; Environmental Pollutants; Polychlorinated Biphenyls; Environmental Exposure
PubMed: 36900991
DOI: 10.3390/ijerph20053982 -
Chemosphere Nov 2022From the 1950s to the 1970s, three Superfund sites discharged polychlorinated biphenyl (PCB)-contaminated waste upstream of the Mohawk Nation at Akwesasne, resulting in... (Review)
Review
From the 1950s to the 1970s, three Superfund sites discharged polychlorinated biphenyl (PCB)-contaminated waste upstream of the Mohawk Nation at Akwesasne, resulting in PCB contamination of groundwater, soil, and sediment in the surrounding area. Given the persistence of PCBs in the environment and in human tissues, there are continued concerns regarding PCB exposures and the potential for adverse health effects in the community. We developed an evidence map of PCB research at Akwesasne in order to characterize the available data and to highlight potential research needs. Human health and exposure biomarker studies were identified from a literature search based on population, exposure, comparator, and outcome (PECO) criteria. Data extracted from references that met the inclusion criteria after full-text review included study characteristics (e.g., sample size, study design, sampling years), details on PCB measurements (e.g., analytical method, number of congeners analyzed, method detection limits), and results (e.g., PCB levels and summary of study conclusions). We identified 33 studies, conducted between 1986 and 2013, that examined PCB exposure characteristics and health effects in residents of the Akwesasne Mohawk Nation. Organizing this literature into an evidence map including information on study cohort, congener groupings, exposure biomarker characteristics, and health effects allowed us to identify research gaps and to suggest future research priorities for the community. We identified current PCB exposure levels and PCB source characterization as major uncertainties, both of which could be addressed by new studies of PCB concentrations in environmental media.
Topics: Cohort Studies; Environmental Exposure; Humans; Indians, North American; Outcome Assessment, Health Care; Polychlorinated Biphenyls
PubMed: 35764106
DOI: 10.1016/j.chemosphere.2022.135454 -
International Journal of Molecular... Aug 2021The developmental origins of health and disease concept illustrates that exposure in early life to various factors may affect the offspring's long‑term susceptibility... (Review)
Review
The developmental origins of health and disease concept illustrates that exposure in early life to various factors may affect the offspring's long‑term susceptibility to disease. During development, the nervous system is sensitive and vulnerable to the environmental insults. Polychlorinated biphenyls (PCBs), which are divided into dioxin‑like (DL‑PCBs) and non‑dioxin‑like PCBs (NDL‑PCBs), are synthetic persistent environmental endocrine‑disrupting chemicals. The toxicological mechanisms of DL‑PCBs have been associated with the activation of the aryl hydrocarbon receptor and NDL‑PCBs have been associated with ryanodine receptor‑mediated calcium ion channels, which affect neuronal migration, promote dendritic growth and alter neuronal connectivity. In addition, PCB accumulation in the placenta destroys the fetal placental unit and affects endocrine function, particularly thyroid hormones and the dopaminergic system, leading to neuroendocrine disorders. However, epidemiological investigations have not achieved a consistent result in different study cohorts. The present review summarizes the epidemiological differences and possible mechanisms of the effects of intrauterine PCB exposure on neurological development.
Topics: Environmental Exposure; Environmental Pollutants; Female; Humans; Infant, Newborn; Nervous System; Nervous System Malformations; Polychlorinated Biphenyls; Pregnancy; Prenatal Exposure Delayed Effects
PubMed: 34132363
DOI: 10.3892/ijmm.2021.4983 -
Epigenetics Apr 2020Anniston, Alabama was home to a major polychlorinated biphenyl (PCB) production facility from 1929 until 1971. The Anniston Community Health Survey I and II (ACHS-I...
Anniston, Alabama was home to a major polychlorinated biphenyl (PCB) production facility from 1929 until 1971. The Anniston Community Health Survey I and II (ACHS-I 2005-2007, ACHS-II 2013-2014) were conducted to explore the effects of PCB exposures. In this report we examined associations between PCB exposure and DNA methylation in whole blood using EPIC arrays (ACHS-I, n = 518; ACHS-II, n = 299). For both cohorts, 35 PCBs were measured in serum. We modelled methylation versus PCB wet-weight concentrations for: the sum of 35 PCBs, mono-ortho substituted PCBs, di-ortho substituted PCBs, tri/tetra-ortho substituted PCBs, oestrogenic PCBs, and antiestrogenic PCBs. Using robust multivariable linear regression, we adjusted for age, race, sex, smoking, total lipids, and six blood cell-type percentages. We carried out a two-stage analysis; discovery in ACHS-I followed by replication in ACHS-II. In ACHS-I, we identified 28 associations (17 unique CpGs) at p ≤ 6.70E-08 and 369 associations (286 unique CpGs) at FDR p ≤ 5.00E-02. A large proportion of the genes have been observed to interact with PCBs or dioxins in model studies. Among the 28 genome-wide significant CpG/PCB associations, 14 displayed replicated directional effects in ACHS-II; however, only one in ACHS-II was statistically significant at p ≤ 1.70E-04. While we identified many novel CpGs significantly associated with PCB exposures in ACHS-I, the differential methylation was modest and the effect was attenuated seven years later in ACHS-II, suggesting a lack of persistence of the associations between PCB exposures and altered DNA methylation in blood cells.
Topics: Adult; Alabama; CpG Islands; DNA Methylation; Environmental Exposure; Environmental Pollutants; Female; Health Surveys; Humans; Male; Middle Aged; Occupational Exposure; Polychlorinated Biphenyls
PubMed: 31607210
DOI: 10.1080/15592294.2019.1666654