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Community and environment as determinants of health
Published in Ben Y.F. Fong, Martin C.S. Wong, The Routledge Handbook of Public Health and the Community, 2021
Thomas Man-chi Dao, Bean S.N. Fu
Altogether, the POPs, such as polychlorinated biphenyls (PCBs) and polybrominated biphenyls (PBBs), polycyclic aromatic hydrocarbons (PAHs), and organochlorine pesticides like dichlorodiphenyltrichloroethane (DDT), can have a direct chemical toxic effect when humans consume the polluted water. PCBs and PBBs are endocrine-disrupting compounds. They can potentially affect people’s reproductive system and the newborn’s outcome, although there are still insufficient research findings to prove any causative pathology. The POPs can also enter and accumulate in the food chain, which ultimately affects human beings when various types of seafood are consumed, especially when people ingested bivalves and small fish as a whole, microplastics and POPs can be easily absorbed because they are concentrated in the guts of marine organisms.
Diseases of the Nervous System
Published in George Feuer, Felix A. de la Iglesia, Molecular Biochemistry of Human Disease, 2020
George Feuer, Felix A. de la Iglesia
Entry of polychlorinated (PCB) and polybrominated biphenyls (PBB) into the human body results in neurological symptoms.121 Polychloro or polybromobiphenyls are very stable, highly fat soluble compounds and stay in living organisms for a long time. In 1968, an outbreak of PCB toxicity occurred in Japan (Yoshu disease) caused by PCB-contaminated rice oil used for cooking. Affected individuals developed peripheral neuropathy, acne-form skin eruptions, and pain and numbness in the limbs.423
Habitual Abortion
Published in E. Nigel Harris, Thomas Exner, Graham R. V. Hughes, Ronald A. Asherson, Phospholipid-Binding Antibodies, 2020
Dwight D. Pridham, Christine L. Cook
Polychlorinated biphenyls (PCBs) and polybrominated biphenyls (PBBs) are utilized as heat exchangers, plasticizers and fire retardants. They are biodegraded very slowly if at all and tend to concentrate in the food chain. Most experience in humans stems from a contamination of cooking oil in Japan with PCBs at levels of 2000 to 3000 ppm. Over a thousand people were poisoned, and two stillbirths occurred out of thirteen deliveries in exposed women.200 In a widespread PBB contamination of livestock feed with subsequent transmission to humans in Michigan, stillbirths were noted in livestock but not humans.176
Sex differences in the association of measures of sexual maturation to common toxicants: Lead, dichloro-diphenyl-trichloroethane (DDT), dichloro-diphenyl-dichloroethylene (DDE), and polychlorinated biphenyls (PCBs)
Published in Annals of Human Biology, 2021
Casey N. West, Lawrence M. Schell, Mia V. Gallo
Several articles provide accessory information concerning sexual maturation in both boys and girls. For boys’ testicular volume maturation staging, one analysis reports decreased testicular volume for age in association with NDLmPCBs and DDE exposure (Grandjean et al. 2012). Two additional analyses report delays in testicular volume development in association with BLL (Williams et al. 2010; Khalaf et al. 2019). Another analysis found a reduction in testosterone levels of adolescent boys after correction for Tanner stages (Schell et al. 2014). A study of prenatal exposure to polybrominated biphenyls found an acceleration in age at menarche (Blanck et al. 2000). In addition, some studies on sexual maturation also reported hormone levels, which are not the focus of this paper. These findings support the observed disruptions in maturation. In one analysis, oestradiol levels in girls are negatively associated with both PCB and DDT levels (Su et al. 2012). Decreases in free-androgen index levels in girls, as well as a decrease in follicle numbers, are found to be associated with increased sum PCB levels (Kristensen et al. 2016). While these studies are not the focus of this review, they are supporting evidence for disruptions from increased toxicant exposure.
Rodent genetic models of Ah receptor signaling
Published in Drug Metabolism Reviews, 2021
Rachel H. Wilson, Christopher A. Bradfield
The aryl hydrocarbon receptor (AHR) is a central paradigm of modern toxicology (Bradshaw and Bell 2009; Zhou 2016). This ligand activated transcription factor is a member of the PER-ARNT-SIM (PAS) superfamily of environmental sensors and is essential for the adaptive metabolism of many xenobiotic compounds, including polycyclic aromatic hydrocarbons (PAHs) like benzo(a)pyrene (BaP). The AHR participates in this biology through the induction of phase I xenobiotic metabolizing enzymes including members of the cytochromes P450 family (e.g. Cyp1a1, Cyp1a2, and Cyp1b1) and phase II enzymes such as glucuronosyltransferase (Figure 1). In addition to adaptive metabolism, the AHR plays a central role in the toxicity of common polyhalogenated pollutants including 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) and related polychlorinated and polybrominated biphenyls. The adaptive and toxic pathways often overlap, as AHR-mediated induction of detoxification enzymes like Cyp1a1 and Cyp1b1 metabolize ligands such as BaP to yield toxic diol epoxide intermediates (Gelboin 1980). The mechanism of AHR-mediated toxicity of other ligands, such as TCDD, remains unclear. The dependence of many widespread environmental pollutants on AHR activation has made this signaling pathway the focus of many toxicological studies (Figure 1). A testament to this interest is the observation that a literature search cross referencing ‘AHR’ and ‘toxicology’ yields over 2000 results (Web of Science, June 10 2020).
The tryptophan derivative 6-formylindolo[3,2-b]carbazole, FICZ, a dynamic mediator of endogenous aryl hydrocarbon receptor signaling, balances cell growth and differentiation
Published in Critical Reviews in Toxicology, 2018
Recently, FICZ has proven to be potently embryotoxic toward fish and birds. FICZ is a strong agonist of fish AHR2, inducing CYP1A and CYP1B1 in zebrafish embryos approximately fivefold more potently than the polybrominated biphenyl PCB126 (Jonsson et al. 2009). Wincent et al. (2016) demonstrated that FICZ dramatically increased mortality and the incidence and severity of pericardial edema and circulatory failure, while reducing hatching and blocking inflation of the swim bladder in zebrafish embryos. Importantly, these toxic manifestations were only seen when CYP1A was inhibited by morpholino antisense oligonucleotides or α-naphthoflavone (αNF), this latter compound augmenting the mortality caused by FICZ even at concentrations as low as 5 pM (Wincent et al. 2016). Proper development of zebrafish embryos appears to require crosstalk between the AHR and the Wnt/β-catenin pathway (Yin et al. 2011; Yoshioka et al. 2011) and this latter pathway was a key target for FICZ during early zebrafish development (Wincent et al. 2015).