Long-Term Maternal Exposure to Triclosan Provokes Pulmonary Fibrosis in Mouse Offspring

Triclosan (TCS) is a broad-spectrum antibacterial agent that is widely used as an additive in personal care products. Due to its extensive application, TCS has been frequently detected in human samples, posing potential health risks. To investigate the adverse effects on offspring following maternal exposure to TCS, 4-week-old female mice were exposed to TCS via daily gavage until the end of lactation. The results showed that the birth weight, 21-day survival rate, and skeletal length of offspring were all significantly reduced. Morphological examinations revealed distinct inflammatory infiltrations in the liver, kidney, and spleen of the F1 mice. However, the lungs exhibited abnormal alveolar cells, interstitial hyperplasia, and thickened vascular walls. Further investigations uncovered fibrosis, collagen deposition, fibroblast proliferation, and myofibroblast augmentation in the lungs of the mouse offspring. The enhancement of apoptosis, necroptosis, and pyroptosis in the lungs indicated the involvement of PANoptosis in pulmonary injury. RNA sequencing analysis predicted that the Hedgehog and PI3K-Akt signaling pathways might be the potential toxicological mechanisms underlying maternal TCS exposure-induced pulmonary damage in mouse offspring. This study highlights the toxic effects of TCS on offspring and provides special insights into the health risks associated with TCS exposure.