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Differential parental exposure to polystyrene microplastics from weaning period to maturity: Immune homeostasis dysregulation in F1 offspring
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When rat parents drank water containing microplastics for three months, their babies were born with disrupted gut bacteria and weaker immune systems, even though the babies themselves were never directly exposed. Interestingly, the effects differed depending on whether the mother, father, or both parents were exposed, with mother's exposure causing the most damage to offspring's immune organs and gut health. While this is animal research, it raises concerns that microplastic exposure before pregnancy could affect children's immune development in ways that might not show up until later.
The effects of long-term parental microplastic exposure on offspring immunity remain unclear. This study investigated how different parental exposure patterns affect immune status in F1 offspring. Parental rats were divided into four groups: paternal, maternal, dual-parental, and control. Treated groups received polystyrene microplastics (5 mg/L) in drinking water for 90 days. F1 offspring were raised under standard conditions until 8 weeks of age, after which fecal samples, thymus, spleen, and serum were collected for immune evaluation. Maternal microplastic exposure significantly disrupted gut microbiota α-diversity, dysbiosis index, and composition in F1 offspring (all P < 0.05). These changes were accompanied by decreased RBCs and PLT counts, elevated serum TNF-α, reduced thymic CD3 + and CD4 + T cells, and downregulated IL-10 mRNA and NF-kB protein expression. Histological examination revealed blurred corticomedullary boundaries, sparse cellularity, and lymphocyte vacuolization in the thymus, along with thinning of the periarteriolar lymphatic sheaths in the spleen, further indicating immune imbalance. Paternal and dual-parental exposure also induced gut microbiota dysbiosis and reduced thymic CD4 + T cells. Paternal exposure upregulated Th17-related RORγt and TNF-α mRNA in the thymus, whereas dual-parental exposure decreased thymic Nrf2 protein, splenic CD4 + /CD8 + ratios, and white pulp area. Thymic pathology was observed in both groups. In conclusion, our findings suggest that prolonged parental exposure to microplastics may disrupt immune homeostasis in F1 offspring by altering gut microbiota composition and modulating oxidative stress or inflammatory responses. Moreover, the extent of these effects varies with the different parental exposure patterns.
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Researchers exposed pregnant and lactating mice to polystyrene microplastics and found that maternal exposure disrupted the breast milk microbiome, reducing beneficial bacteria like Ligilactobacillus while increasing potentially harmful ones. Offspring from exposed mothers showed altered gut colonization, excessive weight gain, reduced immune markers, and compromised intestinal barrier integrity, suggesting microplastics may affect infant development through changes in breast milk composition.
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Researchers found that mice exposed to polyethylene microplastics during pregnancy transferred particles to offspring, and those offspring showed impaired antiviral immune responses. The findings suggest that maternal microplastic exposure can programme immune dysfunction in the next generation through disruption of developing immune systems.
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This study found that when male mice were exposed to polystyrene microplastics during the nursing period, both the adult mice and their offspring showed changes in immune cell populations in the spleen. The microplastics altered the balance of different types of immune cells, suggesting the immune system was being disrupted. This is especially concerning because it shows that microplastic exposure during early life can affect immune development in the next generation.
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Researchers exposed pregnant mice to polystyrene microplastics during pregnancy and nursing and found significant metabolic disruptions in both the mothers and their offspring across two generations. The microplastics altered lipid metabolism, gut microbiota composition, and key metabolic signaling pathways. The study suggests that microplastic exposure during critical developmental windows may have lasting health consequences that pass to future generations.
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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.
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