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1.
Per- and poly-fluoroalkyl substances (PFAS) and female reproductive outcomes: PFAS elimination, endocrine-mediated effects, and disease.
Rickard, BP, Rizvi, I, Fenton, SE
Toxicology. 2022;:153031
Abstract
Per- and poly-fluoroalkyl substances (PFAS) are widespread environmental contaminants frequently detected in drinking water supplies worldwide that have been linked to a variety of adverse reproductive health outcomes in women. Compared to men, reproductive health effects in women are generally understudied while global trends in female reproduction rates are declining. Many factors may contribute to the observed decline in female reproduction, one of which is environmental contaminant exposure. PFAS have been used in home, food storage, personal care and industrial products for decades. Despite the phase-out of some legacy PFAS due to their environmental persistence and adverse health effects, alternative, short-chain and legacy PFAS mixtures will continue to pollute water and air and adversely influence women's health. Studies have shown that both long- and short-chain PFAS disrupt normal reproductive function in women through altering hormone secretion, menstrual cyclicity, and fertility. Here, we summarize the role of a variety of PFAS and PFAS mixtures in female reproductive tract dysfunction and disease. Since these chemicals may affect reproductive tissues directly or indirectly through endocrine disruption, the role of PFAS in breast, thyroid, and hypothalamic-pituitary-gonadal axis function are also discussed as the interplay between these tissues may be critical in understanding the long-term reproductive health effects of PFAS in women. A major research gap is the need for mechanism of action data - the targets for PFAS in the female reproductive and endocrine systems are not evident, but the effects are many. Given the global decline in female fecundity and the ability of PFAS to negatively impact female reproductive health, further studies are needed to examine effects on endocrine target tissues involved in the onset of reproductive disorders of women.
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2.
Environmental Determinants of Type 1 Diabetes: From Association to Proving Causality.
Quinn, LM, Wong, FS, Narendran, P
Frontiers in immunology. 2021;:737964
Abstract
The rising incidence of type 1 diabetes (T1D) cannot be ascribed to genetics alone, and causative environmental triggers and drivers must also be contributing. The prospective TEDDY study has provided the greatest contributions in modern time, by addressing misconceptions and refining the search strategy for the future. This review outlines the evidence to date to support the pathways from association to causality, across all stages of T1D (seroconversion to beta cell failure). We focus on infections and vaccinations; infant growth and childhood obesity; the gut microbiome and the lifestyle factors which cultivate it. Of these, the environmental determinants which have the most supporting evidence are enterovirus infection, rapid weight gain in early life, and the microbiome. We provide an infographic illustrating the key environmental determinants in T1D and their likelihood of effect. The next steps are to investigate these environmental triggers, ideally though gold-standard randomised controlled trials and further prospective studies, to help explore public health prevention strategies.
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3.
Perspective on prenatal polychlorinated biphenyl exposure and the development of the progeny nervous system (Review).
Wang, Y, Hu, C, Fang, T, Jin, Y, Wu, R
International journal of molecular medicine. 2021;(2)
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Abstract
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.
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Mitochondrion: a sensitive target for Pb exposure.
Han, Q, Zhang, W, Guo, J, Zhu, Q, Chen, H, Xia, Y, Zhu, G
The Journal of toxicological sciences. 2021;(8):345-358
Abstract
Pb exposure is a worldwide environmental contamination issue which has been of concern to more and more people. Exposure to environmental Pb and its compounds through food and respiratory routes causes toxic damage to the digestive, respiratory, cardiovascular and nervous systems, etc. Children and pregnant women are particularly vulnerable to Pb. Pb exposure significantly destroys children's learning ability, intelligence and perception ability. Mitochondria are involved in various life processes of eukaryotes and are one of the most sensitive organelles to various injuries. There is no doubt that Pb-induced mitochondrial damage can widely affect various physiological processes and cause great harm. In this review, we summarized the toxic effects of Pb on mitochondria which led to various pathological processes. Pb induces mitochondrial dysfunction leading to the increased level of oxidative stress. In addition, Pb leads to cell apoptosis via mitochondrial permeability transition pore (MPTP) opening. Also, Pb can stimulate the development of mitochondria-mediated inflammatory responses. Furthermore, Pb triggers the germination of autophagy via the mitochondrial pathway and induces mitochondrial dysfunction, disturbing intracellular calcium homeostasis. In a word, we discussed the effects of Pb exposure on mitochondria, hoping to provide some references for further research and better therapeutic options for Pb exposure.
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The effect of endocrine disruptors on the reproductive system - current knowledge.
Czarnywojtek, A, Jaz, K, Ochmańska, A, Zgorzalewicz-Stachowiak, M, Czarnocka, B, Sawicka-Gutaj, N, Ziółkowska, P, Krela-Kaźmierczak, I, Gut, P, Florek, E, et al
European review for medical and pharmacological sciences. 2021;(15):4930-4940
Abstract
OBJECTIVE Chemicals that disrupt the endocrine homeostasis of the human body, otherwise known as endocrine disruptors (EDCs), are found in the blood, urine, amniotic fluid, or adipose tissue. This paper presents the current knowledge about EDCs and the reproductive system. MATERIALS AND METHODS The article is an overview of the impact of EDCs and their mechanism of action, with particular emphasis on gonads, based on the information available on medical databases (PubMed, Web of Science, EMBASE and Google Scholar, EMBASE and Web of Science) until May 2021. RESULTS EDCs occur in everyday life, e.g., they are components of adhesives, brake fluids, and flame retardants; they are used in the production of polyvinyl chloride (PVC), plastic food boxes, pacifiers, medicines, cosmetics (bisphenol A, phthalates), hydraulic fluids, printing inks (polychlorinated biphenyls - PCBs), receipts (bisphenol A, BSA) and raincoats (phthalates); they are also a component of polyvinyl products (e.g. toys) (phthalates), air fresheners and cleaning agents (phthalates); moreover, they can be found in the smoke from burning wood (dioxins), and in soil or plants (pesticides). EDCs are part of our diet and can be found in vegetables, fruits, green tea, chocolate and red wine (phytoestrogens). In addition to infertility, they can lead to premature puberty and even cause uterine and ovarian cancer. However, in men, they reduce testosterone levels, reduce the quality of sperm, and cause benign testicular tumors. CONCLUSIONS Therefore, this article submits that EDCs negatively affect our health, disrupting the functioning of the endocrine system, and particularly affecting the functioning of the gonads.
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The Dark Side of the Force: When the Immune System Is the Fuel of Tumor Onset.
Digifico, E, Balinzo, S, Belgiovine, C
International journal of molecular sciences. 2021;(3)
Abstract
Nowadays, it is well accepted that inflammation is a critical player in cancer, being, in most cases, the main character of the process. Different types of tumor arise from sites of infection or chronic inflammation. This non-resolving inflammation is responsible for tumor development at different levels: it promotes tumor initiation, as well as tumor progression, stimulating both tumor growth and metastasis. Environmental factors, lifestyle and infections are the three main triggers of chronic immune activation that promote or increase the risk of many different cancers. In this review, we focus our attention on tumor onset; in particular, we summarize the knowledge about the cause and the mechanisms behind the inflammation-driven cancer development.
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Environmental and Genetic Risk Factors of Congenital Anomalies: an Umbrella Review of Systematic Reviews and Meta-Analyses.
Lee, KS, Choi, YJ, Cho, J, Lee, H, Lee, H, Park, SJ, Park, JS, Hong, YC
Journal of Korean medical science. 2021;(28):e183
Abstract
BACKGROUND The prevalence of congenital anomalies in newborns in South Korea was 272.9 per 100,000 in 2005, and 314.7 per 100,000 in 2006. In other studies, the prevalence of congenital anomalies in South Korea was equivalent to 286.9 per 10,000 livebirths in 2006, while it was estimated 446.3 per 10,000 births during the period from 2008 to 2014. Several systematic reviews and meta-analyses analyzing the factors contributing to congenital anomalies have been reported, but comprehensive umbrella reviews are lacking. METHODS We searched PubMed, Google Scholar, Cochrane, and EMBASE databases up to July 1, 2019, for systematic reviews and meta-analyses that investigated the effects of environmental and genetic factors on any type of congenital anomalies. We categorized 8 subgroups of congenital anomalies classified according to the 10th revision of the International Statistical Classification of Diseases (ICD-10). Two researchers independently searched the literature, retrieved the data, and evaluated the quality of each study. RESULTS We reviewed 66 systematic reviews and meta-analyses that investigated the association between non-genetic or genetic risk factors and congenital anomalies. Overall, 269 associations and 128 associations were considered for environmental and genetic risk factors, respectively. Congenital anomalies based on congenital heart diseases, cleft lip and palate, and others were associated with environmental risk factors based on maternal exposure to environmental exposures (air pollution, toxic chemicals), parental smoking, maternal history (infectious diseases during pregnancy, pregestational and gestational diabetes mellitus, and gestational diabetes mellitus), maternal obesity, maternal drug intake, pregnancy through artificial reproductive technologies, and socioeconomic factors. The association of maternal alcohol or coffee consumption with congenital anomalies was not significant, and maternal folic acid supplementation had a preventive effect on congenital heart defects. Genes or genetic loci associated with congenital anomalies included MTHFR, MTRR and MTR, GATA4, NKX2-5, SRD5A2, CFTR, and 1p22 and 20q12 anomalies. CONCLUSION This study provides a wide perspective on the distribution of environmental and genetic risk factors of congenital anomalies, thus suggesting future studies and providing health policy implications.
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[Oral cavity as a target and a marker of environmental exposures: diseases diagnosed during adulthood].
Babajko, S, Lescaille, G, Radoï, L, Thu Bui, A, Baaroun, V, Boyer, E, Delbosc, S, Chardin, H, Barouki, R, Coumoul, X
Medecine sciences : M/S. 2020;(3):231-234
Abstract
The oral cavity is one of the main route for environmental contaminations associated to many chronic diseases via alimentation, medications and respiration. Other factors may also impact the oral environment, some of them are endogenous, like microbiota, hormones and saliva, and others are exogenous, like dental materials and pathogens.
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Bisphenol A and Phthalates in Diet: An Emerging Link with Pregnancy Complications.
Filardi, T, Panimolle, F, Lenzi, A, Morano, S
Nutrients. 2020;(2)
Abstract
Endocrine-disrupting chemicals (EDCs) are exogenous substances that are able to interfere with hormone action, likely contributing to the development of several endocrine and metabolic diseases. Among them, Bisphenol A (BPA) and phthalates contaminate food and water and have been largely studied as obesogenic agents. They might contribute to weight gain, insulin resistance and pancreatic β-cell dysfunction in pregnancy, potentially playing a role in the development of pregnancy complications, such as gestational diabetes mellitus (GDM), and adverse outcomes. Pregnancy and childhood are sensitive windows of susceptibility, and, although with not univocal results, preclinical and clinical studies have suggested that exposure to BPA and phthalates at these stages of life might have an impact on the development of metabolic diseases even many years later. The molecular mechanisms underlying this association are largely unknown, but adipocyte and pancreatic β-cell dysfunction are suspected to be involved. Remarkably, transgenerational damage has been observed, which might be explained by epigenetic changes. Further research is needed to address knowledge gaps and to provide preventive measure to limit health risks connected with exposure to EDCs.
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10.
Mutational Landscape and Environmental Effects in Bladder Cancer.
Hayashi, T, Fujita, K, Hayashi, Y, Hatano, K, Kawashima, A, McConkey, DJ, Nonomura, N
International journal of molecular sciences. 2020;(17)
Abstract
Bladder cancer is the most common cancer of the urinary tract. Although nonmuscle-invasive bladder cancers have a good prognosis, muscle-invasive bladder cancers promote metastases and have a poor prognosis. Comprehensive analyses using RNA sequence of clinical tumor samples in bladder cancer have been reported. These reports implicated the candidate genes and pathways that play important roles in carcinogenesis and/or progression of bladder cancer. Further investigations for the function of each mutation are warranted. There is suggestive evidence for several environmental factors as risk factors of bladder cancer. Environmental factors such as cigarette smoking, exposure to chemicals and gases, bladder inflammation due to microbial and parasitic infections, diet, and nutrition could induce several genetic mutations and alter the tumor microenvironment, such as immune cells and fibroblasts. The detailed mechanism of how these environmental factors induce carcinogenesis and/or progression of bladder cancer remains unclear. To identify the relationship between the mutations and the lifestyle could be useful for prevention and treatment of bladder cancer.