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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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Effects of environmental and occupational lead toxicity and its association with iron metabolism.
Słota, M, Wąsik, M, Stołtny, T, Machoń-Grecka, A, Kasperczyk, S
Toxicology and applied pharmacology. 2022;:115794
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Abstract
BACKGROUND Discrepancies are present in the findings from clinical trials evaluating a physiological role of iron status in the lead-exposed population. OBJECTIVE The purpose of this article was to summarize the current understanding of cellular mechanisms of lead toxicity and present a comprehensive review of existing clinical trials related to associations of lead poisoning and iron status. Although an association of iron metabolism pathways that are affected by lead intoxication has been studied, there are still aspects that remain to be elucidated. The existence of additional Pb uptake pathways besides DMT1 transporter-mediated is postulated to non-specifically regulate lead absorption. METHODS Authors performed a systematic search of PubMed, EMBASE® and Web of Science databases to identify studies that reported an association between health risks of non-organic lead that are associated with iron status markers as possible effect modifier. RESULTS There were 58 studies that met the pre-defined inclusion criteria for the systematic review. There is a strong body of evidence supporting the hypothesis that alleviated blood lead level can be correlated with a reduced body iron store and increasing the risk of anemia. This association is of a high significance in cases of a young adolescent, weaker in groups of older children and often without a statistical significance in adults. DISCUSSION Discrepancies in the observations may result from different specificities of lead absorption pathways in children and adults, as well as the power of the statistical tests in varying population sizes. It may be assumed that the extent of iron deficits coupled together with source, timing, and severity of lead exposure, significantly influence the correlation between these factors. Some of the intervention programs of counteracting lead poisoning by iron supplementation proved to be effective and may be a promising prevention strategy for the exposed population.
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Role of Endocrine-Disrupting Chemicals in the Pathogenesis of Non-Alcoholic Fatty Liver Disease: A Comprehensive Review.
Cano, R, Pérez, JL, Dávila, LA, Ortega, Á, Gómez, Y, Valero-Cedeño, NJ, Parra, H, Manzano, A, Véliz Castro, TI, Albornoz, MPD, et al
International journal of molecular sciences. 2021;(9)
Abstract
Non-alcoholic fatty liver disease (NAFLD) is considered the most common liver disorder, affecting around 25% of the population worldwide. It is a complex disease spectrum, closely linked with other conditions such as obesity, insulin resistance, type 2 diabetes mellitus, and metabolic syndrome, which may increase liver-related mortality. In light of this, numerous efforts have been carried out in recent years in order to clarify its pathogenesis and create new prevention strategies. Currently, the essential role of environmental pollutants in NAFLD development is recognized. Particularly, endocrine-disrupting chemicals (EDCs) have a notable influence. EDCs can be classified as natural (phytoestrogens, genistein, and coumestrol) or synthetic, and the latter ones can be further subdivided into industrial (dioxins, polychlorinated biphenyls, and alkylphenols), agricultural (pesticides, insecticides, herbicides, and fungicides), residential (phthalates, polybrominated biphenyls, and bisphenol A), and pharmaceutical (parabens). Several experimental models have proposed a mechanism involving this group of substances with the disruption of hepatic metabolism, which promotes NAFLD. These include an imbalance between lipid influx/efflux in the liver, mitochondrial dysfunction, liver inflammation, and epigenetic reprogramming. It can be concluded that exposure to EDCs might play a crucial role in NAFLD initiation and evolution. However, further investigations supporting these effects in humans are required.
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Per- and polyfluoroalkyl substances exposure during pregnancy and adverse pregnancy and birth outcomes: A systematic review and meta-analysis.
Gao, X, Ni, W, Zhu, S, Wu, Y, Cui, Y, Ma, J, Liu, Y, Qiao, J, Ye, Y, Yang, P, et al
Environmental research. 2021;:111632
Abstract
BACKGROUND Exposure to per- and polyfluoroalkyl substances (PFAS) during pregnancy has been suggested to be associated with adverse pregnancy and birth outcomes; however, the findings have been inconsistent. We aimed to conduct a systematic review and meta-analysis to provide an overview of these associations. METHODS The online databases PubMed, EMBASE and Web of Science were searched comprehensively for eligible studies from inception to February 2021. Odds ratios (ORs) and 95% confidence intervals (CIs) were pooled using random- or fixed-effects models, and dose-response meta-analyses were also conducted when possible. FINDINGS A total of 29 studies (32,905 participants) were included. The pooled results demonstrated that perfluorooctane sulfonate (PFOS) exposure during pregnancy was linearly associated with increased preterm birth risk (pooled OR per 1-ng/ml increase: 1.01, 95% CIs: 1.00-1.02, P = 0.009) and perfluorononanoate (PFNA) and perfluorooctanoate (PFOA) exposure showed inverted U-shaped associations with preterm birth risk (P values for the nonlinear trend: 0.025 and 0.030). Positive associations were also observed for exposure to perfluorodecanoate (PFDA) and miscarriage (pooled OR per 1-ng/ml increase: 1.87, 95% CIs: 1.15-3.03) and PFOS and preeclampsia (pooled OR per 1-log increase: 1.27, 95% CIs: 1.06-1.51), whereas exposure to perfluoroundecanoate (PFUnDA) was inversely associated with preeclampsia risk (pooled OR per 1-log increase: 0.81, 95% CIs: 0.71-0.93). Based on individual evidence, detrimental effects were observed between PFDA exposure and small for gestational age and between PFOA and PFOS and intrauterine growth restriction. No significant associations were found between pregnancy PFAS exposure and other adverse pregnancy outcomes (i.e., gestational diabetes mellitus, pregnancy-induced hypertension, low birth weight, and large and small for gestational age). INTERPRETATION Our findings indicated that PFOS, PFOA and PFNA exposure during pregnancy might be associated with increased preterm birth risk and that PFAS exposure might be associated with the risk of miscarriage and preeclampsia. Due to the limited evidence obtained for most associations, additional studies are required to confirm these findings.
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Associations between exposure to heavy metals and the risk of chronic kidney disease: a systematic review and meta-analysis.
Jalili, C, Kazemi, M, Cheng, H, Mohammadi, H, Babaei, A, Taheri, E, Moradi, S
Critical reviews in toxicology. 2021;(2):165-182
Abstract
We performed a systematic review and meta-analysis to examine the relationship between heavy metals (HMs) exposure and the risk of chronic kidney disease (CKD). Databases of Web of Science, Embase, MEDLINE, and Scopus were searched through June 2020 to identify studies assessing the relationships between exposure to HMs (i.e. cadmium, lead, arsenic, mercury) and the risk of CKD, evaluated by decreased estimated glomerular filtration rate (eGFR) and/or increased proteinuria risks in adults (≥18 years). Data were pooled by random-effects models and expressed as weighted mean differences and 95% confidence intervals. The risk of bias was assessed by the Newcastle-Ottawa scale (NOS). Twenty-eight eligible articles (n = 107,539 participants) were included. Unlike eGFR risk (p = 0.10), Cadmium exposure was associated with an increased proteinuria risk (OR = 1.35; 95% CI: 1.13, 1.61; p < 0.001; I2 = 79.7%). Lead exposure was associated with decreased eGFR (OR = 1.12; 95%CI: 1.03, 1.22; p = 0.008; I2 = 87.8%) and increased proteinuria (OR = 1.25; 95% CI: 1.04, 1.49; p = 0.02; I2 = 79.6) risks. Further, arsenic exposure was linked to a decreased eGFR risk (OR = 1.55; 95% CI: 1.05, 2.28; p = 0.03; I2 = 89.1%) in contrast to mercury exposure (p = 0.89). Only two studies reported the link between arsenic exposure and proteinuria risk, while no study reported the link between mercury exposure and proteinuria risk. Exposure to cadmium, lead, and arsenic may increase CKD risk in adults, albeit studies were heterogeneous, warranting further investigations. Our observations support the consideration of these associations for preventative, diagnostic, monitoring, and management practices of CKD.
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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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Selection of Endophytic Strains for Enhanced Bacteria-Assisted Phytoremediation of Organic Pollutants Posing a Public Health Hazard.
Karaś, MA, Wdowiak-Wróbel, S, Sokołowski, W
International journal of molecular sciences. 2021;(17)
Abstract
Anthropogenic activities generate a high quantity of organic pollutants, which have an impact on human health and cause adverse environmental effects. Monitoring of many hazardous contaminations is subject to legal regulations, but some substances such as therapeutic agents, personal care products, hormones, and derivatives of common organic compounds are currently not included in these regulations. Classical methods of removal of organic pollutants involve economically challenging processes. In this regard, remediation with biological agents can be an alternative. For in situ decontamination, the plant-based approach called phytoremediation can be used. However, the main disadvantages of this method are the limited accumulation capacity of plants, sensitivity to the action of high concentrations of hazardous pollutants, and no possibility of using pollutants for growth. To overcome these drawbacks and additionally increase the efficiency of the process, an integrated technology of bacteria-assisted phytoremediation is being used recently. For the system to work, it is necessary to properly select partners, especially endophytes for specific plants, based on the knowledge of their metabolic abilities and plant colonization capacity. The best approach that allows broad recognition of all relationships occurring in a complex community of endophytic bacteria and its variability under the influence of various factors can be obtained using culture-independent techniques. However, for practical application, culture-based techniques have priority.
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Susceptibility to COVID-19 in populations with health disparities: Posited involvement of mitochondrial disorder, socioeconomic stress, and pollutants.
Yao, Y, Lawrence, DA
Journal of biochemical and molecular toxicology. 2021;(1):e22626
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Abstract
SARS-CoV-2 is a novel betacoronavirus that has caused the global health crisis known as COVID-19. The implications of mitochondrial dysfunction with COVID-19 are discussed as well as deregulated mitochondria and inter-organelle functions as a posited comorbidity enhancing detrimental outcomes. Many environmental chemicals (ECs) and endocrine-disrupting chemicals can do damage to mitochondria and cause mitochondrial dysfunction. During infection, SARS-CoV-2 via its binding target ACE2 and TMPRSS2 can disrupt mitochondrial function. Viral genomic RNA and structural proteins may also affect the normal function of the mitochondria-endoplasmic reticulum-Golgi apparatus. Drugs considered for treatment of COVID-19 should consider effects on organelles including mitochondria functions. Mitochondrial self-balance and clearance via mitophagy are important in SARS-CoV-2 infection, which indicate monitoring and protection of mitochondria against SARS-CoV-2 are important. Mitochondrial metabolomic analysis may provide new indicators of COVID-19 prognosis. A better understanding of the role of mitochondria during SARS-CoV-2 infection may help to improve intervention therapies and better protect mitochondrial disease patients from pathogens as well as people living with poor nutrition and elevated levels of socioeconomic stress and ECs.
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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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Pharmacokinetics of fluoride in human adults: The effect of exercise.
Mahmood, M, Azevedo, LB, Maguire, A, Buzalaf, M, Zohoori, FV
Chemosphere. 2021;:127796
Abstract
The literature is sparse in terms of the effect of exercise on the pharmacokinetics of fluoride (F) in humans. In a 4-treatment repeated measures cross-over study, we investigated F pharmacokinetics following no exercise (control) and three exercise intensity conditions (light, moderate and vigorous) in healthy adults. At a pre-experimental session, 8 participants (18-30y) residing in a non-fluoridated-area, underwent a VO2 max test to guide the three exercise intensities for the experimental sessions. Participants were on a F-free regime one week before and throughout the four experimental weeks. We measured urinary F excretion (UFE), maximum plasma concentration (Cmax), lag time of Cmax (Tmax), and Area Under the Curve (AUC) for plasma F concentration against time, following F ingestion then no, light, moderate and vigorous exercise. Results showed no statistically significant difference in Tmax among all sessions; whereas Cmax for moderate exercise (226.2 ng/ml) was significantly higher than for no (27.0 ng/ml; p < 0.001), light (105.6 ng/ml; p = 0.016) and vigorous (94.2 ng/ml; p = 0.008) exercise. Mean AUC over 0-90 min following F ingestion was also significantly higher in moderate exercise than for no (p < 0.001), light (p = 0.004) and vigorous (p = 0.001) exercise. Mean UFE over 0-14h was 638.8, 718.7, 574.6 and 450.5 μg for no, light, moderate and vigorous exercise, with no statistically significant differences among different sessions. In conclusion, this human experimental study suggests that moderate exercise may increase the fraction of F absorbed systemically which is therefore available to produce a biological effect. Future studies should be conducted with larger samples, different age groups and using different F doses.