China
Africa
Explore chapters and articles related to this topic
Lifestyle and Diet
Published in Chuong Pham-Huy, Bruno Pham Huy, Food and Lifestyle in Health and Disease, 2022
Chuong Pham-Huy, Bruno Pham Huy
Dioxins can be generated either naturally or by human activities (198–200). In nature, dioxins are produced through forest fires or volcanic activities. In industrial processes like chlorine bleaching of pulp paper and manufacturing of chlorinated pesticides, these compounds are produced accidentally. The incomplete combustion of municipal and domestic waste, the burning of chlorine-containing materials such as plastics, and the burning of fuels (wood, coal, or oil) produce dioxins (198–200). Heating systems in homes and emissions from cars also generate small amounts of dioxins.
Different kinds of infertility, possible reasons for infertility
Published in Elisabeth Hildt, Dietmar Mieth, In Vitro Fertilisation in the 1990s, 2018
Hans-Rudolf Tinneberg, Ulrich Göhring
The list of possibly toxic agents would be too long for this chapter. The Reproductive Toxicology Center at the Columbia Hospital for Women Medical Center, Washington D.C., USA provides up to date information on the current scientific knowledge, since the disaster of Seveso in Northern Italy where massive amounts of mainly tetrachlorodibenzodioxin (TCDD), a highly lipophilic substance with a long half-life, were released into the air. Dioxins are unintentional byproducts produced primarily in the synthesis of certain chemicals and combustion processes. The chemicals involved consist of chlorphenoxy herbicides such as 2,4,5-trichlorophenoxyacetic acid, the disinfectant hexachlorophene and polychlorinated biphenols (PCBs) which were used as dielectric fluids in capacitators and transformers. High levels of dioxins have also been found in technical grade pentachlorophenol (PCP) used primarily as a pesticide and wood preservative.
Work in progress
Published in Richard Lawson, Jonathon Porritt, Bills of Health, 2018
Richard Lawson, Jonathon Porritt
In humans, the only effect that is generally accepted with certainty to result from dioxin exposure is chloracne, a painful eruptive skin condition. This was widespread around Seveso, the Italian region contaminated by a leak from a chemical plant. Birth defects were not seen as many mothers had preventive abortions. US servicemen contaminated by Agent Orange, a defoliant sprayed on the countryside in the Vietnam war, complained of reproductive effects, but failed to get a causal link officially accepted until 1996. It must be said that had the US war machine accepted responsibility it would have been faced with a huge compensation bill, and the perception remains that the true effects have been covered up.
The protective effects of capsaicin on oxidative damage-induced by 2,3,7,8-tetrachlorodibenzo-p-dioxin in rats
Published in Drug and Chemical Toxicology, 2022
Muhammed Fatih Doğan, Neşe Başak Türkmen, Aslı Taşlıdere, Yasemin Şahin, Osman Çiftçi
Dioxins are emitted into the atmosphere as undesirable products of diverse oxidation and industrial processes and constitute an important class of environmental toxicants (White and Birnbaum 2009). Dioxins emitted from the environment are first collected in plant tissues and then in human tissues by the biomagnification process. Among the dioxins, the most toxic compound 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD), which is usually transferred to humans through animal products, such as meat and milk (Ciftci and Ozdemir 2011). The TCDD half-life is known to be very long in humans and it is estimated to vary between 7 and 12 years (Patrizi and Cumis 2018). The main cause of TCDD toxicity is its binding to the aryl hydrocarbon receptor (AhR), known as an intracellular ligand-dependent transcription factor (Kolluri et al. 2017). Some in vivo research represent that exposure to TCDD reasons a diversity of adverse effects on the central nervous system (Unkila et al. 1995), immune system (Neubert et al. 1994), reproductive system (Elsayed et al. 2019), heart (Fujisawa et al. 2019), and liver (Roth et al. 1994). In addition, oxidative stress caused by AHR activation is a prominent factor in TCDD toxicity (Reichard et al. 2005). Studies showing that exposure to TCDD causes oxidative damage in many tissues, such as the heart, kidney, and liver support this hypothesis (Jin et al. 2008, Ciftci et al. 2012, Kalaiselvan et al. 2016).
The interplay between aryl hydrocarbon receptor, H. pylori, tryptophan, and arginine in the pathogenesis of gastric cancer
Published in International Reviews of Immunology, 2022
Marzieh Pirzadeh, Nastaran Khalili, Nima Rezaei
An interesting finding is that the role of AHR in cell proliferation depends on the phenotype of the cell. In other words, cell phenotype can be a strong determinant for AHR to either promote cell proliferation, showing its oncogenic potential or to inhibit proliferation, demonstrating its tumor-suppressive activity [68]. These dual effects of AHR have been investigated in multiple studies. In a study it was reported that treatment with Dioxin, a group of highly toxic chemical compounds, caused the human mammary carcinoma MCF-7 and mouse hepatoma Hepa-1 cells to aggregate in the G1 phase. This aggregation was accomplished through AHR and p300 interaction, which led to p300 displacement from E2F-dependent promoters, driving cell cycle inhibition. This repression is caused through AHR interaction with retinoblastoma protein [69]. A similar study performed by Peng et al. revealed that treatment of AGS cells in a dose and time-dependent manner with TCDD, a potent AHR agonist, puts a growth arrest at the G1-S phase of the cell cycle, implicating AHR as a probable therapeutic target for gastric cancer development [11]. Nevertheless, TCDD itself is a carcinogenic substance inducing a wide range of responses like induction of CYP1A1, immunotoxicity, liver damage, etc. [70]. It has been shown that an AHR modulator, 3,3 Diindolylmethane, also induces apoptosis in gastric cancer SGC7901 cell line [71].
Does the environment affect menopause? A review of the effects of endocrine disrupting chemicals on menopause
Published in Climacteric, 2023
The evidence presented points to an important association between environmental contaminants and accelerated ovarian aging/early menopause derived from both epidemiologic and basic studies (summarized in Table 1) and indicates the need for additional well-designed studies that are relevant to a range of human exposures. While effects documented in epidemiologic studies are relatively small, mixtures of environmental toxins to which we are all exposed have received little attention. Moreover, the delay in childbearing in populations across the world speaks to the importance of even small changes in ovarian aging and the age of menopause. While we may not be able to prevent all exposures, there are important actions that can be taken on a personal [96] and societal [97] level. BPA exposure can be reduced by use of plastics and food cans labeled as BPA-free, use of glassware for microwaving/cooking and storing food [98], and avoidance of handling paper receipts. Phthalate exposure can be reduced be avoiding plastics in food preparation and storage and by using fragrance-free personal care products. Dioxin exposure can be minimized by replacing bleached paper products with cloth. Dietary exposure to pesticides on produce can be avoided by peeling produce or soaking produce in sodium bicarbonate (baking soda) for 15 min [99]. While a balanced diet is essential for overall health, it is important to know where our food, especially fish, is sourced and monitor the potential for high levels of contamination [100]. Finally, it is important that we all play a role in reducing our global exposure to toxic chemicals for ourselves and our patients.