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Impact of maternal microplastic exposure on offspring lung structure and function: Insights into transcriptional misregulation and the TGF-β/α-SMA pathway
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Pregnant rats exposed to polystyrene microplastics in their drinking water produced offspring with lung damage visible just 7 days after birth, including plastic deposits and collapsed air sacs. By 120 days, the offspring developed lung changes resembling emphysema, even though they were never directly exposed to microplastics after birth. This study provides evidence that a mother's microplastic exposure during pregnancy can cause lasting lung damage in her children.
The "Developmental Origins of Health and Disease" (DOHaD) theory suggests that prenatal exposure to harmful environmental factors may impair fetal tissue development, increasing the risk of diseases later in life. This study investigated the effects of prenatal exposure to polystyrene microplastics (PS-MPs) on offspring lung development. Pregnant Sprague-Dawley rats were randomly assigned to receive PS-MPs in drinking water until delivery, with a control group receiving standard water. Offspring were assessed at 7 and 120 d after birth without further PS-MPs exposure. Histopathological examination at 7 d revealed PS-MPs deposits, alveolar collapse, and inflammation in lung tissue. Gene expression analysis showed disruptions in tight junctions, transcriptional regulation, and transforming growth factor-beta (TGF-β) pathways. By day 120, lung dysfunction and structural changes, consistent with emphysema were observed. These findings demonstrate that prenatal PS-MPs exposure adversely affects lung development potentially increasing the risk of respiratory diseases. Public health measures should address the potential hazards of microplastics to fetal health.
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SD rats exposed to mixed polystyrene micro(nano)plastics via intratracheal administration at escalating doses over time developed pulmonary fibrosis and mitochondrial dysfunction, with severity linked to dose. The findings demonstrated a clear biological pathway connecting inhaled microplastic exposure to lung injury.
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Pregnant rats that inhaled micro- and nanoplastic particles throughout gestation passed them to their offspring, with plastic particles detected in pup tissues after birth. This is one of the first studies to show that inhaled microplastics can cross the placental barrier during pregnancy and persist in offspring, raising concerns about prenatal exposure from airborne plastic pollution.
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Researchers found that rat pups exposed to polystyrene microplastics before birth showed significant oxidative stress and metabolic disruption in their lung tissues. The prenatal exposure altered nucleic acid metabolism and amino acid profiles in the lungs of newborn pups. Encouragingly, treatment with melatonin significantly improved lung function and reduced tissue damage in the affected offspring.
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Researchers exposed pregnant mice to nanoscale polystyrene particles through inhalation and tracked where the particles traveled. They found that the nanoplastics crossed from the lungs into the bloodstream and accumulated in both placental and fetal tissues, confirming that inhaled plastic nanoparticles can reach developing offspring during pregnancy.
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