Nanoplatics (NPs), particularly polystyrene (PS)-NPs, can traverse the placental barrier upon maternal exposure, leading to bioaccumulation in both dam and offspring organs, and inducing widespread transplacental toxicity. The distribution and toxicity of NPs are influenced by a variety of factors, including NP properties (type, size, and charge), exposure parameters (dose, route, and timing), and biological variables (model and co-exposures). Due to their minute size, NPs pose significant threats to multiple systems in animal models. In rodent studies, reproductive and endocrine toxicity primarily manifests as placental dysfunction, impaired embryo implantation, increased miscarriage rates, and gonadal toxicity in offspring, mechanisms for which are suggested to involve oxidative stress, endocrine disruption, and dysregulated calcium homeostasis. Reported neurotoxicity, characterized by aberrant cortical architecture, hippocampal dysfunction, and learning and memory deficits, is mediated by mechanisms such as oxidative stress and ferroptosis, neurotransmitter disruption, gut-brain axis dysregulation, and pathological protein aggregation. In the cardiovascular system, studies suggest PS-NPs induce offspring cardiac fibrosis, apoptosis, and functional impairments, demonstrating marked sex-specific dimorphism potentially driven by ferroptosis. And PS-NPs have been shown to disrupt glycolipid metabolism in animal models, leading to offspring metabolic disorders. Furthermore, evidence from non-mammalian models, notably Caenorhabditis elegans, reveals transgenerational toxicity. Critically, the consequences of early-life NP exposure are long-lasting, potentially elevating susceptibility to various diseases in adulthood. This review comprehensively summarizes the toxicological profiles of NPs during the critical windows of gestation and lactation, underscoring the need for more robust research and a systematic approach to risk assessment.
Jing He (Thu,) studied this question.