Analyzing the impact of phthalate and DINCH exposure on fetal growth in a cohort with repeated urine collection

Ouidir, Marion; Jedynak, Paulina; Rolland, Matthieu; Lyon-Caen, Sarah; Thomsen, Cathrine; Sakhi, Amrit K.; Sabaredzovic, Azemira; Bayat, Sam; Slama, Rémy; Philippat, Claire

doi:10.1016/j.envint.2024.108584

Environment International

2024

DOI: 10.1016/j.envint.2024.108584

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Analyzing the impact of phthalate and DINCH exposure on fetal growth in a cohort with repeated urine collection

Marion Ouidir,

Paulina Jedynak,

Matthieu Rolland

et al.

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2024

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Cited by 3 publications

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Neonatal exposure to phthalates and their alternatives and associated thyroid disorders: Levels, potential health risks, and mechanisms

Chen,

Weng,

et al. 2024

Journal of Environmental Sciences

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Neonatal exposure to phthalates and their alternatives and associated thyroid disorders: Levels, potential health risks, and mechanisms

Chen,

Weng,

et al. 2024

Journal of Environmental Sciences

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DINCH Exposure Triggers Inflammatory, Oxidative, and Apoptotic Pathways in the Liver of Long-Evans Lactating Rats and Their Offspring

Íñigo-Catalina,

Linillos-Pradillo,

Schlumpf

et al. 2024

IJMS

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1,2-cyclohexane dicarboxylic acid diisononyl ester (DINCH) is a non-phthalate plasticizer used as a replacement of di(2-ethylhexyl) phthalate (DEHP) in daily usage items. It is not known whether continuous exposure to low doses of DINCH can lead to hepatic alterations, the liver being the organ responsible for its metabolism. The aim of this study was to evaluate the activation of inflammatory and apoptotic pathways in the liver of lactating dams after DINCH exposure, and whether these effects may be observed on postnatal day 6 (PND6) offspring. Two doses of DINCH were tested by oral administration to the following three groups of Long-Evans rats: control, DINCH-lower dose (LDINCH, 30 mg/kg b.w./day), and DINCH-high dose (HDINCH, 300 mg/kg b.w./day). Inflammatory mediators (IL-1β, TNF-α, NF-κB), mitochondrial transcriptional factors (PPARγ and PGC-1α), oxidative stress markers (SOD, CAT, GSSG/GSH), and components of the mitochondrial apoptotic pathway (PUMA, BAX, BAD, Bcl-2, Bcl-xL, Cytochrome c, APAF-1, Caspase-3, AIF) were assessed by the gene and protein expression in the liver of lactating dams and offspring. Exposure to LDINCH promoted the release of pro-inflammatory cytokines such as IL-1β and TNF-α and raised oxidative stress levels (GSSG/GSH), as well as increased Caspase-3 levels and reduced anti-apoptotic proteins (Bcl-2 and Bcl-xL), both in lactating dams and PND6 offspring. Thus, constant exposure to lower doses of DINCH can disrupt inflammatory and oxidant/antioxidant homeostasis, leading to hepatic tissue damage in lactating dams and having a perinatal effect in PND6 offspring.

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Short-Half-Life Chemicals: Maternal Exposure and Offspring Health Consequences—The Case of Synthetic Phenols, Parabens, and Phthalates

Rousseau-Ralliard,

Bozec,

Ouidir

et al. 2024

Toxics

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Phenols, parabens, and phthalates (PPPs) are suspected or known endocrine disruptors. They are used in consumer products that pregnant women and their progeny are exposed to daily through the placenta, which could affect offspring health. This review aims to compile data from cohort studies and in vitro and in vivo models to provide a summary regarding placental transfer, fetoplacental development, and the predisposition to adult diseases resulting from maternal exposure to PPPs during the gestational period. In humans, using the concentration of pollutants in maternal urine, and taking the offspring sex into account, positive or negative associations have been observed concerning placental or newborn weight, children’s BMI, blood pressure, gonadal function, or age at puberty. In animal models, without taking sex into account, alterations of placental structure and gene expression linked to hormones or DNA methylation were related to phenol exposure. At the postnatal stage, pollutants affect the bodyweight, the carbohydrate metabolism, the cardiovascular system, gonadal development, the age of puberty, sex/thyroid hormones, and gamete quality, but these effects depend on the age and sex. Future challenges will be to explore the effects of pollutants in mixtures using models and to identify the early signatures of in utero exposure capable of predicting the health trajectory of the offspring.

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Analyzing the impact of phthalate and DINCH exposure on fetal growth in a cohort with repeated urine collection

Cited by 3 publications

References 78 publications

Neonatal exposure to phthalates and their alternatives and associated thyroid disorders: Levels, potential health risks, and mechanisms

Neonatal exposure to phthalates and their alternatives and associated thyroid disorders: Levels, potential health risks, and mechanisms

DINCH Exposure Triggers Inflammatory, Oxidative, and Apoptotic Pathways in the Liver of Long-Evans Lactating Rats and Their Offspring

Short-Half-Life Chemicals: Maternal Exposure and Offspring Health Consequences—The Case of Synthetic Phenols, Parabens, and Phthalates

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