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Justice, environmental health laws and relations between people
Published in Friedo Zölzer, Gaston Meskens, Ethics of Environmental Health, 2017
Quite alarming and surprising is that animal data have shown that some ill-timed exposures during development of reproductive organs can cause transgenerational harms. Exposure of male rats during reproductive organ development to some pesticides and bisphenol A (individually) causes sperm damage, sterility, prostate disease, kidney disease, immune system abnormalities, testis abnormalities and tumour development (e.g. breast) (Anway et al. 2006; Anway et al. 2008). Analogous results were seen in female rats exposed in utero. Exposure in utero to one toxicant can cause polycystic ovarian disease (infrequent ovulation, multiple persistent ovarian cysts [seen in 6–18 per cent of women], and primary ovarian insufficiency [POI]). These conditions can persist through four generations, making them transgenerational (Nilsson et al. 2012).
Epigenotoxicity: a danger to the future life
Published in Journal of Environmental Science and Health, Part A, 2023
Farzaneh Kefayati, Atoosa Karimi Babaahmadi, Taraneh Mousavi, Mahshid Hodjat, Mohammad Abdollahi
According to the studies performed on 24 umbilical cord blood measuring the level of dichlorodiphenyltrichloroethane (DDT), 1,131 CpG sites with different methylation levels were revealed, including 690 hypermethylation regions and 441 hypomethylation regions in 589 genes. Exposure to DDT increased the level of methylation at the CpG sites of the BRCA1 gene (responsible for repairing DNA), reducing its level of expression.[35] Thus, epigenetic processes resulting from maternal organochlorine pesticides (OCP-DDT) exposure reduces fetal development. The more they contact this substance, the higher the level of DNA methylation and the lower the level of gene expression.[35] The most common ovarian diseases that threaten fertility and women’s health are polycystic ovary syndrome (PCOS) and Primary ovarian insufficiency (POI). Exposure to several environmental toxins could increase the relative epigenetic inheritance of ovarian diseases. It was shown that lncRNAs and small non-coding RNAs (sncRNAs) express differentially in ovarian granulosa cells purified from F3 generation rats after ancestral DDT exposures.[36] Exposure to pesticides such as dichloroacetic acid and trichloroacetic acid reduced methylation in mice’s c-jun and c-myc promoter regions. Global DNA hypomethylation has also been observed in high levels of blood. In addition, increased acetylation of H3 and H4 nucleus histones has been observed by a chlorinated organic pesticide.[37]