Perspective on halogenated organic compounds.

BackgroundPer- and polyfluoroalkyl substances (PFAS) and polybrominated diphenyl ethers (PBDEs) are endocrine disrupting chemicals with widespread exposures across the U.S. given their abundance in consumer products. PFAS and PBDEs are associated with reproductive toxicity and adverse health outcomes, including certain cancers. PFAS and PBDEs may affect health through alternations in telomere length. In this study, we examined joint associations between prenatal exposure to PFAS, PBDEs, and maternal and newborn telomere length using mixture analyses, to characterize effects of cumulative environmental chemical exposures.MethodsStudy participants were enrolled in the Chemicals in Our Bodies (CIOB) study, a demographically diverse cohort of pregnant people and children in San Francisco, CA. Seven PFAS (ng/mL) and four PBDEs (ng/g lipid) were measured in second trimester maternal serum samples. Telomere length (T/S ratio) was measured in delivery cord blood of 292 newborns and 110 second trimester maternal whole blood samples. Quantile g-computation was used to assess the joint associations between groups of PFAS and PBDEs and newborn and maternal telomere length. Groups considered were: (1) all PFAS and PBDEs combined, (2) PFAS, and (3) PBDEs. Maternal and newborn telomere length were modeled as separate outcomes.ResultsT/S ratios in newborn cord and maternal whole blood were moderately correlated (Spearman ρ = 0.31). In mixtures analyses, a simultaneous one quartile increase in all PFAS and PBDEs was associated with a small increase in newborn (mean change per quartile increase = 0.03, 95% confidence interval [CI] = -0.03, 0.08) and maternal telomere length (mean change per quartile increase = 0.03 (95% CI = -0.03, 0.09). When restricted to maternal–fetal paired samples (N = 76), increasing all PFAS and PBDEs combined was associated with a strong, positive increase in newborn telomere length (mean change per quartile increase = 0.16, 95% CI = 0.03, 0.28). These associations were primarily driven by PFAS (mean change per quartile increase = 0.11 [95% CI = 0.01, 0.22]). No associations were observed with maternal telomere length among paired samples.ConclusionsOur findings suggest that PFAS and PBDEs may be positively associated with newborn telomere length.

Polychlorinated dioxins and dibenzofurans (PCDD/F), polybrominated dioxins and dibenzofurans (PBDD/F), polychlorinated biphenyls (PCB), polybrominated diphenyl ethers (PBDE), and per- and polyfluoroalkyl substances (PFAS) in German breast milk samples (LUPE 8)

Traditional and new POPs in environments along the Bohai and Yellow Seas: An overview of China and South Korea

Alternatives to PFASs: perspectives on the science.

Accumulation of brominated flame retardants and polychlorinated biphenyls in human breast milk and scalp hair from the Philippines: Levels, distribution and profiles

Indoor spaces contain several classes of persistent organic chemicals, including per- and polyfluoroalkyl substances (PFAS), polybrominated diphenyl ethers (PBDEs), polychlorinated biphenyls (PCBs), and organochlorine pesticides (OCPs). However, concentrations of PFAS and persistent chemical mixtures and their associations with building characteristics on college campuses are understudied. We collected dust from 43 nonresidential spaces on four U.S. college campuses in 2016 and evaluated associations of room characteristics (carpeting, upholstered furniture, and years since last furnished) with dust concentrations of PFAS, PBDEs, PCBs, and OCPs. Nine PFAS, twelve PBDEs, two PCBs, and four OCPs were each detected in at least 75% of the spaces, including several chemicals (e.g., DDT) that have been banned for decades. Concentrations were correlated within and, in some cases, between chemical classes. Wall-to-wall carpeting (compared to rooms without wall-to-wall carpeting) was associated with higher concentrations of six individual PFAS and a mixture of PFAS, and the number of pieces of upholstered furniture was associated with increased concentrations of a mixture of PBDEs. These findings indicate that carpeting and furniture are current sources of PFAS and PBDEs, respectively. Building and finish materials should be carefully selected to avoid exposure to persistent chemicals.

The exposure to several compounds such as polychlorinated biphenyls (PCBs), organochlorine pesticides (OCPs), organophosphorus pesticides (OPs), polycyclic aromatic hydrocarbon (PAHs), perfluoroalkyl substances (PFASs) and polybrominated diphenyl ethers (PBDEs) is a public health issue. The European Union (EU) recommended that its member states monitor the presence of emerging contaminants, like PBDEs and PFASs, in food and in the environment to obtain an accurate estimation of exposure. The tissues of wild animals exposed to these compounds can represent a suitable indicator of environmental pollution. The aim of this work is to evaluate: (i) the occurrence of PCBs, PBDEs, PFASs, PAHs, OCPs and OPs in four game animals’ meat (chamois, red deer, wild boar and roe deer); (ii) interspecies differences and (iii) human exposure. Muscle samples from seventy-nine animals were collected during the hunting season in a Northern Italy mountain area at altitudes ranging from 300 to 2500 meters above sea level. The analyses were performed with gas chromatography-mass spectrometry (GC-MS/MS) and ultra-performance liquid chromatography – tandem mass spectrometry (UHPLC-MS/MS). No PBDEs were found in the samples. OCPs, OPs and PCBs were detected in almost all samples at different concentration ranges, showing higher frequency in ungulate species than in wild boar. PFAs were found only in wild boar. Anthracene and benzopyrene, among PAHs, were found only in chamois, at low concentrations. The lack of an accurate pattern of exposure as well as variable consumption by hunters does not allow accurate risk characterisation. However, a low risk for consumers can be indicated due to the frequent detection of contaminants only at trace levels, the scarce prevalence of high concentrations of some contaminants and the low consumption of game animal meat. In conclusion, the organisation of a control plan on residues in game animals would be advisable.

Halogenated organic pollutants in aquatic invertebrate - Fish food webs: Global distributions and trophic magnification.

Organohalogen Pollutants and Human Health

The notion that some substances in the environment can damage the nervous system has an ancient history. The neurotoxicity of lead was recognized more than 2,000 years ago by the Greek physician Dioscerides, who wrote, “Lead makes the mind give way.” In the intervening millennia many other substances have been added to the list of known or suspected neurotoxicants. Despite this accumulation of knowledge, there is still much that isn’t understood about how neurotoxicants affect the developing brain, especially the effects of low-dose exposures. Today researchers are taking a hard look at low-dose exposures in utero and during childhood to unravel some of the mysteries of impaired neurodevelopment. About 17% of school-age children in the United States suffer from a disability that affects their behavior, memory, or ability to learn, according to a study published in the March 1994 issue of Pediatrics by a team from the Centers for Disease Control and Prevention (CDC). The list of maladies includes attention deficit/hyperactivity disorder (ADHD), autistic spectrum disorders, epilepsy, Tourette syndrome, and less specific conditions such as mental retardation and cerebral palsy. All are believed to be the outcome of some abnormal process that unfolded as the brain was developing in utero or in the young child. These disorders have an enormous impact on families and society. According to the 1996 book Learning Disabilities: Lifelong Issues, children with these disorders have higher rates of mental illness and suicide, and are more likely to engage in substance abuse and to commit crimes as adults. The overall economic cost of neurodevelopmental disorders in the United States is estimated to be $81.5–167 billion per year, according to a report published in the December 2001 issue of EHP Supplements. Potentially even more disturbing is that a number of epidemiologic studies suggest that the incidence of certain disorders is on the rise. In the United States, the diagnosis of autistic spectrum disorders increased from 4–5 per 10,000 children in the 1980s to 30–60 per 10,000 children in the 1990s, according to a report in the August 2003 Journal of Autism and Developmental Disorders. Similarly, notes a report in the February 2002 issue of CNS Drugs, the diagnosis of ADHD grew 250% between 1990 and 1998. The number of children in special education programs classified with learning disabilities increased 191% between 1977 and 1994, according to an article in Advances in Learning and Behavioral Disabilities, Volume 12, published in 1998. So what is going on? The short answer is that no one really knows. There’s not even consensus on what the soaring rates actually mean. Heightened public awareness could account for the surge in the numbers, or it may be that physicians are getting better at diagnosing the conditions. Some autism researchers believe the rise in that condition’s prevalence simply reflects changes in diagnostic criteria over the last 25 years. On the other hand, some scientists believe that the rates of neurodevelopmental disease are truly increasing, and that the growing burden of chemicals in the environment may play a role. With that in mind, investigators are considering the effects of gene–environment interactions. A child with a mild genetic tendency toward a neurodevelopmental disorder might develop without clinically measurable abnormalities in the absence of environmental “hits.” However, children in industrialized nations develop and grow up in a veritable sea of xenobiotic chemicals, says Isaac Pessah, director of the University of California, Davis, Center for Children’s Environmental Health and Disease Prevention. “Fortunately,” he says, “most of us have a host of defense mechanisms that protect us from adverse outcomes. However, genetic polymorphisms, complex epistasis, and cytogenetic abnormalities could weaken these defenses and amplify chemical damage, initiating a freefall into a clinical syndrome.” Pessah cites the example of autism. He says susceptibility for autism is likely conferred by several defective genes, no one of which can account for all the core symptoms of social disinterest, repetitive and overly focused behaviors, and problems in communication. Could multiple genetic liabilities and exposure to a chemically complex environment act in concert to increase the incidence and severity of the condition? Despite the uncertainties, many scientists believe it would be wise to err on the side of caution when it comes to a research agenda. As Martha Herbert, a pediatric neurologist at Harvard Medical School, puts it, “Even though we may have neither consensus nor certainty about an autism epidemic, there are enough studies coming in with higher numbers that we should take it seriously. Environmental hypotheses ought to be central to research now. The physiological systems that have been harmed by environmental factors may also point to treatment targets, and this might be a great way to help the children.”

Multiple stressors and reproductive success of tree swallows: Perfluoroalkyl acids, chemical mixtures, and ecological factors.

When it comes to feeding the newborn, human milk is, from an evolutionary perspective, the biological norm, the time-tested standard of care. The health benefits to the infant of breast-feeding have been amply documented; numerous studies strongly indicate significantly decreased risks of infection, allergy, asthma, arthritis, diabetes, obesity, cardiovascular disease, and various cancers in both childhood and adulthood. Among the more fundamental disadvantages of not being breastfed is a loss of immunologic protection afforded by maternal colostrum, a “pre-milk” fluid secreted only during the first days after delivery, as well as numerous other bioactive factors that help protect the infant through the first two years of life, when the immune and nervous systems are incompletely developed. Nevertheless, given the tendency for persistent organic pollutants (POPs), pesticides, heavy metals, and other contaminants to accumulate in human milk, researchers and parents alike are asking whether the nursling’s exposure to these pollutants might reduce or even override the health benefits.

Polychlorinated dibenzo-p-dioxins/furans (PCDD/Fs), polychlorinated biphenyls (PCBs), and polybrominated diphenyl ethers (PBDEs) in breast milk from Zhejiang, China

Background: Epidemiological research investigating the impact of exposure to plastics, and plastic-associated chemicals, on human health is critical, especially given exponentially increasing plastic production. In parallel with increasing production, academic research has also increased exponentially both in terms of the primary literature and ensuing systematic reviews with meta-analysis. However, there are few overviews that capture a broad range of chemical classes to present a state of play regarding impacts on human health. Methods: We undertook an umbrella review to review the systematic reviews with meta-analyses. Given the complex composition of plastic and the large number of identified plastic-associated chemicals, it was not possible to capture all chemicals that may be present in, and migrate from, plastic materials. We therefore focussed on a defined set of key exposures related to plastics. These were microplastics, due to their ubiquity and potential for human exposure, and the polymers that form the matrix of consumer plastics. We also included plasticisers and flame retardants as the two classes of functional additive with the highest concentration ranges in plastic. In addition, we included bisphenols and per- and polyfluoroalkyl substances (PFAS) as two other major plastic-associated chemicals with significant known exposure through food contact materials. Epistemonikos and PubMed were searched for systematic reviews with meta-analyses, meta-analyses, and pooled analyses evaluating the association of plastic polymers, particles (microplastics) or any of the selected groups of high-volume plastic-associated chemicals above, measured directly in human biospecimens, with human health outcomes. Results: Fifty-two systematic reviews were included, with data contributing 759 meta-analyses. Most meta-analyses (78%) were from reviews of moderate methodological quality. Across all the publications retrieved, only a limited number of plastic-associated chemicals within each of the groups searched had been evaluated in relevant meta-analyses, and there were no meta-analyses evaluating polymers, nor microplastics. Synthesised estimates of the effects of plastic-associated chemical exposure were identified for the following health outcome categories in humans: birth, child and adult reproductive, endocrine, child neurodevelopment, nutritional, circulatory, respiratory, skin-related and cancers. Bisphenol A (BPA) is associated with decreased anoclitoral distance in infants, type 2 diabetes (T2D) in adults, insulin resistance in children and adults, polycystic ovary syndrome, obesity and hypertension in children and adults and cardiovascular disease (CVD); other bisphenols have not been evaluated. Phthalates, the only plasticisers identified, are associated with spontaneous pregnancy loss, decreased anogenital distance in boys, insulin resistance in children and adults, with additional associations between certain phthalates and decreased birth weight, T2D in adults, precocious puberty in girls, reduced sperm quality, endometriosis, adverse cognitive development and intelligence quotient (IQ) loss, adverse fine motor and psychomotor development and elevated blood pressure in children and asthma in children and adults. Polychlorinated biphenyls (PCBs), polybrominated diphenyl ethers (PBDEs) but not other flame retardants, and some PFAS were identified and are all associated with decreased birth weight. In general populations, PCBs are associated with T2D in adults and endometriosis, bronchitis in infants, CVD, non-Hodgkin's lymphoma (NHL) and breast cancer. In PCB-poisoned populations, exposure is associated with overall mortality, mortality from hepatic disease (men), CVD (men and women) and several cancers. PBDEs are adversely associated with children's cognitive development and IQ loss. PBDEs and certain PFAS are associated with changes in thyroid function. PFAS exposure is associated with increased body mass index (BMI) and overweight in children, attention deficit hyperactive disorder (ADHD) in girls and allergic rhinitis. Potential protective associations were found, namely abnormal pubertal timing in boys being less common with higher phthalate exposure, increased high-density lipoprotein (HDL) with exposure to mono(2-ethyl-5-oxohexyl) phthalate (MEOHP) and reduced incidence of chronic lymphocytic lymphoma (a subtype of NHL) with PCB exposure. Conclusions: Exposure to plastic-associated chemicals is associated with adverse outcomes across a wide range of human health domains, and every plastic-associated chemical group is associated with at least one adverse health outcome. Large gaps remain for many plastic-associated chemicals. Recommendations: For research, we recommend that efforts are harmonised globally to pool resources and extend beyond the chemicals included in this umbrella review. Priorities for primary research, with ensuing systematic reviews, could include micro- and nanoplastics as well as emerging plastic-associated chemicals of concern such as bisphenol analogues and replacement plasticisers and flame retardants. With respect to chemical regulation, we propose that safety for plastic-associated chemicals in humans cannot be assumed at market entry. We therefore recommend that improved independent, systematic hazard testing for all plastic-associated chemicals is undertaken before market release of products. In addition because of the limitations of laboratory-based testing for predicting harm from plastic in humans, independent and systematic post-market bio-monitoring and epidemiological studies are essential to detect potential unforeseen harms.

Halogenated hydrocarbons include polychlorinated biphenyls (PCBs), dioxins, furans, DDT, polybrominated biphenyls (PBBs), polybrominated diphenyl ethers (PBDEs), and PFAS. These compounds are widely dispersed in the environment, are biologically and environmentally persistent, and are detected in the bodies of virtually all humans. Consumption of contaminated foods, most notably seafood from contaminated waters as well as red meat and chicken, is the main route of human exposure. For the PBDEs, contaminated house dust is additional source of exposure. Halogenated hydrocarbons cross the placenta from mother to baby, and they concentrate in breast milk. Injury to the developing brain is the most serious health consequence of early-life exposure to halogenated hydrocarbons. Babies born to mothers with increased body burdens of PCBs have decreased IQ scores and problems with visual recognition. Deficits in executive functioning, and symptoms of attention deficit hyperactivity disorder and autism spectrum disorders can become evident at higher levels of exposure. PBDEs appear to produce similar effects. National governments can reduce exposures to halogenated hydrocarbons by curtailing or banning their manufacture and use, establishing programs for monitoring the food supply, and controlling environmental releases. Local governments can control the spread of PCBs into school environments by requiring timely removal of PCB-containing fluorescent light ballasts and can ban use of PBDEs. Although human breast milk can contain high concentrations of halogenated hydrocarbons, the advantages of breastfeeding outweigh this hazard except in cases of extreme exposure. Authoritative bodies such as the American Academy of Pediatrics continue to strongly recommend breast feeding.