Potential occupational exposure of parents to endocrine disrupting chemicals, adverse birth outcomes, and the modification effects of multi-vitamins supplement and infant sex

Zhang, Huanhuan; Li, Yanqiu; Zhang, Xiao‐Xin; Chen, Weiyi; Liang, Qianhong; Li, Changchang; Knibbs, Luke D.; Huang, Cunrui; Wang, Qiong

doi:10.1016/j.ecoenv.2022.113314

Cited by 4 publications

(2 citation statements)

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“…Our findings are consistent with epidemiological studies linking parental exposure to persistence organic pollutants and other environmental chemicals to low birth size in offspring in humans [13][14][15][16]25 . In our model, the reduced birth weight in offspring of DDT-exposed males was associated with impaired fetal growth and placenta size.…”

Section: Discussionsupporting

confidence: 91%

“…Epidemiological studies link pre-conception paternal exposure to persistence organic pollutants and other environmental chemicals to low birth size in offspring in humans 13,14 15 16 . Low birth weight is often a result of placenta defects, yet there is a lack of studies investigating the link between paternal exposure to environmental toxicants and placenta development.…”

Section: Introductionmentioning

confidence: 99%

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Paternally-induced environmental programming of placenta development, offspring birth weight and health phenotypes in a mouse model

Chen,

da Cruz,

Nascimento

et al. 2023

Preprint

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Mounting evidence suggests that environmentally induced epigenetic inheritance occurs in mammals and that traits in the progeny can be shaped by parental environmental experiences. Epidemiological studies link parental exposure to environmental toxicants, such as the pesticide DDT, to health phenotypes in the progeny, including low birth and increased risk of chronic diseases later in life. Here, we show that the progeny of male mice exposed to DDT in the pre-conception period are born smaller and exhibit sexual dimorphism in metabolic function, with male offspring developing both glucose intolerance and insulin resistance compared to controls. These phenotypes in DDT offspring were linked to reduced fetal growth and placenta size as well as placenta-specific reduction of glycogen levels and the nutrient sensor and epigenetic regulator OGT, with more pronounced phenotypes observed in male placentas. However, placenta-specific genetic reduction of OGT only partially replicates the metabolic phenotype observed in offspring of DDT-exposed males. Our findings reveal a role for paternal pre-conception environmental experiences in shaping placenta development and in fetal growth restriction. While many questions remain, our data raise the tantalizing possibility that placenta programming could be a mediator of environmentally induced intergenerational epigenetic inheritance of phenotypes and needs to be further evaluated.

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