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Exposure to environmental contaminants can result in profound effects on the host immune system. One class of environmental toxicants, known as dioxins, are persistent environmental contaminants termed “forever chemicals”. The archetype toxicant from this group of chemicals is 2, 3, 7, 8-tetrachlorodibenzo-p-dioxin (TCDD), an immunotoxicant that activates the aryl-hydrocarbon receptor pathway leading to a variety of changes in immune cell responses. Immune cell functions are crucial to the development and maintenance of healthy reproduction. Immune cells facilitate tolerance between at the maternal-fetal interface between the parent and the semi-allogenic fetus and help defend the gravid reproductive tract from infectious assault. Epidemiological studies reveal that exposure to environmental contaminants (such as TCDD) are linked to adverse reproductive health outcomes including endometriosis, placental inflammation, and preterm birth. However, little is known about the molecular mechanisms that underpin how environmental toxicant exposures impact immune functions at the maternal-fetal interface or within the reproductive tract in general. This review presents the most recent published work that studies interactions between dioxin or TCDD exposure, the host immune system, and reproduction.

Breast cancer (BC) is the most common cancer in women, with metastasis as the leading cause of mortality. Persistent organic pollutants (POPs) may increase BC aggressiveness, but mechanisms remain unclear. This study examined the link between POP exposure and BC progression. We analyzed tumor samples from 89 BC patients in the METAPOP cohort, measuring 42 POPs, including dioxins, polychlorinated biphenyls (PCBs), and polybromodiphenylethers (PBDEs). Transcriptomic analysis identified genes differentially expressed in relation to POP exposure and BC aggressiveness (tumor size, metastatic risk, lymph node involvement, and estrogen receptor status). RNA sequencing of 89 tumors identified 4931 genes differentially expressed with ER status, 283 with tumor size, and 99 with metastasis. Key enriched pathways included immune response, extracellular matrix remodeling, and cell cycle regulation. Gene set enrichment analysis revealed significant overlap in pathways regulating the cell cycle, immune response, and BC hallmarks. Findings suggest that POP exposure alters tumor biology, promoting an aggressive phenotype. This study provides novel insights into the role of environmental pollutants in BC progression, emphasizing the need for further research on how POPs contribute to tumor aggressiveness.

Northern Lights against POPs tells the many-faceted scientific, policy, legal, and advocacy story that led to the Stockholm convention. Unique in its perspective, scope, and breadth, it reveals the key links among environmental and health science, international politics, advocacy, law, and global negotiations. Never before have public health concerns articulated by northern Indigenous peoples in Canada and throughout the circumpolar Arctic had such a direct impact on global policy-making. Authors show how research on POPs (persistent organic pollutants) in the Arctic from the mid-1980s influenced international negotiations and analyze the potential for the convention to be effective. Contributors include elected representatives, researchers, civil servants, Indigenous people who participated in the negotiations, and scientists who provided the compelling Arctic data that prompted the United Nations Environment Programme to sponsor negotiations. Contributors include David Anderson (Minister of the Environment, Canada); Nigel Bankes (University of Calgary); John Buccini (Consultant, former chair of the Global POPs Negotiations); Sheila Watt-Cloutier (Inuit Circumpolar Conference-Canada); Barry Commoner, Paul Woods Bartlett, Holger Eisl, Kimberly Couchot (Center for the Biology of Natural Systems, Queens College, City University of New York); Eric Dewailly (Laval University); David Downie (Director of Educational Partnerships, Columbia Earth Institute, Columbia University, New York); Terry Fenge (Inuit Circumpolar Conference-Canada); Henry Huntington (Consultant, Anchorage) and Michelle Sparck (Circumpolar Conservation Union, Washington, D.C.); Harriet Kuhnlein, Laurie Chan (Centre for Indigenous Peoples' Nutrition and Environment, McGill University), and Olivier Receveur (formerly Centre for Indigenous Peoples' Nutrition and Environment, McGill University); Lars-Otto Reiersen (Arctic Monitoring and Assessment Programme Secretariat,Oslo); Henrik Selin (Massachusetts Institute of Technology); David Stone, Russell Shearer (Northern Contaminants Program, Department of Indian Affairs and Northern Development, Canada); Klaus Topfer (Executive Director, United Nations Environment Programme).

Persistent organic pollutants (POPs) are xenobiotic chemicals of global concern due to their long-range transport capabilities, persistence, ability to bioaccumulate, and potential to have negative effects on human health and the environment. Identifying POPs in both the environment and human body is therefore essential for assessing potential health risks, but their diverse range of chemical classes challenge analytical techniques. Currently, platforms coupling chromatography approaches with mass spectrometry (MS) are the most common analytical methods employed to evaluate both parent POPs and their respective metabolites and/or degradants in samples ranging from d rinking water to biofluids. Unfortunately, different types of analyses are commonly needed to assess both the parent and metabolite/degradant POPs from the various chemical classes. The multiple time-consuming analyses necessary thus present a number of technical and logistical challenges when rapid evaluations are needed and sample volumes are limited. To address these challenges, we characterized 64 compounds including parent per- and polyfluoroalkyl substances (PFAS), pesticides, polychlorinated biphenyls (PCBs), industrial chemicals, and pharmaceuticals and personal care products (PPCPs), in addition to their metabolites and/or degradants, using ion mobility spectrometry coupled with MS (IMS-MS) as a potential rapid screening technique. Different ionization sources including electrospray ionization (ESI) and atmospheric pressure photoionization (APPI) were employed to determine optimal ionization for each chemical. Collectively, this study advances the field of exposure assessment by structurally characterizing the 64 important environmental pollutants, assessing their best ionization sources, and evaluating their rapid screening potential with IMS-MS.

Background Prenatal maternal plasma persistent organic pollutant (POP) concentrations have been associated with neonatal outcomes. However, the underlying mechanisms remain unknown. Placental epigenetic mechanisms may be involved, but no prior epigenome-wide studies have investigated the impact of maternal POPs on placental DNA methylation. We studied the association between maternal plasma POP concentration in early pregnancy and epigenome-wide placental DNA methylation among 260 pregnant women from the NICHD Fetal Growth Studies. Results Our analysis focused on POPs with more than 80% plasma concentrations above the limit of quantification, including 3 organochlorine pesticides (hexachlorobenzene, trans-nonachlor, p,p’ -dichlorodiphenyldichloroethylene), 1 polybrominated diphenyl ether (PBDE 47), 3 polychlorinated biphenyls (138/158, 153, 180), and 6 poly- and perfluorinated alkyl substances (PFASs) (perfluorodecanoic acid, perfluorohexanesulfonic acid, perfluorononanoic acid, perfluorooctanesulfonic acid, perfluoroundecanoic acid (PFUnDA)). Using 5% false discovery rate, POPs were associated with a total of 214 differentially methylated CpG sites (nominal p values ranging from 2.61 × 10 −21 to 2.11 × 10 −7 ). Out of the 214 CpG sites, 24 (11%) were significantly correlated with placental expression of 21 genes. Notably, higher PFUnDA was associated with increased methylation at 3 CpG sites (cg13996963, cg12089439, cg18145877) annotated to TUSC3 , and increased methylation at those 3 CpG sites was correlated with decreased expression of TUSC3 in the placenta. Increased methylation at cg18145877 ( TUSC3 ) and decreased expression of TUSC3 were correlated with shorter birth length. Out of the 214 CpG sites, methylation at 44 CpG sites was correlated ( p value < 0.10) with at least one neonatal anthropometry measure (i.e., birth weight, birth length, and head circumference). Seven CpG sites mediated ( p value < 0.05) the association between PBDE 47 and neonatal anthropometry measures. Genes annotating the top differentially methylated CpG sites were enriched in pathways related to differentiation of embryonic cells (PBDE 47) and in pathways related to brain size and brain morphology (PFASs). Conclusions DNA methylation changes in the placenta were significantly associated with maternal plasma POPs concentration. The findings suggest that placental DNA methylation and gene expression mechanism may be involved in the prenatal toxicity of POPs and their association with neonatal anthropometry measures.

Purpose of Review Evidence suggests neurotoxicity of endocrine disrupting chemicals (EDCs) during sensitive periods of development. We present an overview of pediatric population neuroimaging studies that examined brain influences of EDC exposure during prenatal period and childhood. Recent Findings We found 46 studies that used magnetic resonance imaging (MRI) to examine brain influences of EDCs. These studies showed associations of prenatal exposure to phthalates, organophosphate pesticides (OPs), polyaromatic hydrocarbons and persistent organic pollutants with global and regional brain structural alterations. Few studies suggested alteration in functional MRI associated with prenatal OP exposure. However, studies on other groups of EDCs, such as bisphenols, and those that examined childhood exposure were less conclusive. Summary These findings underscore the potential profound and lasting effects of prenatal EDC exposure on brain development, emphasizing the need for better regulation and strategies to reduce exposure and mitigate impacts. More studies are needed to examine the influence of postnatal exposure to EDC on brain imaging.

Examines what we know about the relationship between organic chemicals and human disease Organic chemicals are everywhere: in the air we breathe, the water we drink, and the food we eat.They are also found in a myriad of common household and personal care products.

In recent years, new advanced oxidation processes based on the electrochemical technology, the so-called electrochemical advanced oxidation processes (EAOPs), have been developed for the prevention and remediation of environmental pollution, especially focusing on water streams. These methods are based on the electrochemical generation of a very powerful oxidizing agent, such as the hydroxyl radical (•OH) in solution, which is then able to destroy organics up to their mineralization. EAOPs include heterogeneous processes like anodic oxidation and photoelectrocatalysis methods, in which •OH are generated at the anode surface either electrochemically or photochemically, and homogeneous processes like electro-Fenton, photoelectro-Fenton, and sonoelectrolysis, in which •OH are produced in the bulk solution. This paper presents a general overview of the application of EAOPs on the removal of aqueous organic pollutants, first reviewing the most recent works and then looking to the future. A global perspective on the fundamentals and experimental setups is offered, and laboratory-scale and pilot-scale experiments are examined and discussed.

The aim of the present study was to evaluate the contamination levels of some classes of persistent organic pollutants in free-range hen eggs and to estimate the related human dietary exposure in a site of national interest, characterized by a serious state of environmental pollution in the Bussi sul Tirino area in central Italy. For these purposes, 17 samples of free-range hen eggs collected in home-producing farms located in the site of national interest territory were analyzed for 17 polychlorinated dibenzo-p-dioxins and dibenzofurans (PCDD/Fs), 12 dioxin-like polychlorinated biphenyls (dl-PCBs), and 6 non-dioxin-like PCBs (ndl-PCBs). Dietary exposure was assessed assuming a standard consumption of eggs per week. The concentration of ∑PCDD/Fs plus dl-PCBs ranged from 0.463 to 8.028 pg toxic equivalent g-1 fat, whereas the mean contamination level of the ∑ndl-PCBs ranged from 0.234 to 7.741 ng toxic equivalent g-1 fat. PCDD/Fs and PCBs contamination levels were lower than maximum values established by the Commission Regulation (European Union) 1259/2011, except for one sample. The estimated weekly intake, calculated to evaluate the contribution in terms of the monitored pollutants of the locally produced eggs to the diet, was lower than the tolerable weekly intake established by the European Food Safety Authority.