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Perinatal exposure to nano-polystyrene: deleterious imprinting on inflammatory bowel diseases
Summary
When pregnant and nursing mice were fed tiny plastic particles (nanoplastics, like those found in our food and water), their offspring grew up with a higher risk of severe gut inflammation later in life, even though the exposure happened only early on. This suggests that plastic exposure during pregnancy and breastfeeding could set the stage for digestive diseases like colitis much later in life, raising concerns about how early-life plastic exposure might affect human gut health long-term.
The extent of production and use of plastics leads to release of nanoplastics (NPL) into the environment, where they undergo weathering that could alter their toxicological properties. NPL enter the human food chain via contaminated food, and food packaging, and within the body they are known to pass through epithelial barriers. In parallel to the increasing exposure to plastics, the incidence of non-communicable diseases, including intestinal diseases, is rising worldwide. This study focuses on how oral exposure of gestating and lactating female mice to 50 nm polystyrene beads, pristine (PS50) or weathered (PS50w) affects intestinal function in offspring. Two aspects of intestinal function were studied: oral tolerance and the onset of intestinal disorders. Gestating mice received 1.25 mg of PS50 or PS50w by oral gavage administered daily from gestational day 15. Exposure was continued during lactation until pups were weaned (Postnatal Day, PND21). To study oral tolerance, offspring were exposed to ovalbumin (OVA) both orally and systemically. To study intestinal disorders, colitis was induced by exposure to Dextran Sulfate Sodium (DSS) from PND63. Perinatal exposure to PS50 or PS50w had no impact on mortality of gestating or lactating dams or sex ratio in litters, but did lead to increased body weight at PND63 in offspring. No impact on tolerance to OVA was observed. However, macroscopic scores for DSS-induced colitis in adult offspring were significantly worsened in both sexes. In this context, in male offspring, PS50w was more deleterious than PS50. Early-life exposure to PS50 or PS50w has long-lasting consequences on gut physiology, and effects show sexual dimorphism. The results presented raise questions on the kinetics of later-life effects linked to perinatal PS50 and PS50w exposure, and introduce the notion of imprinting.