Inhalation exposure to polystyrene nanoplastics induces chronic obstructive pulmonary disease-like lung injury in mice through multi-dimensional assessment.

Nanoplastics are widely distributed in indoor and outdoor air and can be easily inhaled into human lungs. However, limited studies have investigated the impact of nanoplastics on inhalation toxicities, especially on the initiation and progression of chronic obstructive pulmonary disease (COPD). To fill the gap, the present study used oronasal aspiration to develop mice models. Mice were exposed to polystyrene nanoplastics (PS-NPs) at three concentrations, as well as the corresponding controls, for acute, subacute, and subchronic exposure. As a result, PS-NPs could accumulate in exposed mice lungs and influence lung organ coefficient. Besides, PS-NPs induced local and systemic oxidative stress, inflammation, and protease-antiprotease imbalance, resulting in decreased respiratory function and COPD-like lesions. Meanwhile, PS-NPs could trigger the subcellular mechanism to promote COPD development by causing mitochondrial dysfunctions and endoplasmic reticulum (ER) stress. Mechanistically, ferroptosis played an important role in the COPD-like lung injury induced by PS-NPs. In summary, the present study comprehensively and systematically indicates that PS-NPs can damage human respiratory health and increase the risk for COPD.

The hepatotoxicity assessment of micro/nanoplastics: A preliminary study to apply the adverse outcome pathways.

Plastic pollution has become a significant global problem over the years, leading to the continuous decomposition and accumulation of micro/nanoplastics (MNPLs) in the environment. As a result, human exposure to these MNPLs is inevitable. The liver, in particular, is highly susceptible to potential MNPL toxicity. In this study, we systematically reviewed the current literature on MNPLs-induced hepatotoxicity and collected data on toxic events occurring at different biological levels. Then, to better understand the cause-mechanism causality, we developed an Adverse Outcome Pathway (AOP) framework for MNPLs-induced hepatotoxicity. The AOP framework provided insights into the mechanism of MNPL-induced hepatotoxicity and highlighted potential health risks such as liver dysfunction and inflammation, metabolism disorders and liver fibrosis. Moreover, we discussed the potential application of emerging toxicological models in the hepatotoxicity study. Liver organoids and liver-on-chips, which can simulate the structure and function of the liver in vitro, offer a promising alternative platform for toxicity testing and risk assessment. We proposed combining the AOP framework with these emerging toxicological models to improve our understanding of the hepatotoxic effects of MNPLs. Overall, this study performed a preliminary exploration of novel toxicological methodologies to assess the hepatotoxicity of MNPLs, providing a deeper understanding of environmental toxicology.

Nanomaterials-induced toxicity on cardiac myocytes and tissues, and emerging toxicity assessment techniques.

The extensive production and use of nanomaterials have resulted in the continuous release of nano-sized particles into the environment, and the health risks caused by exposure to these nanomaterials in the occupational population and the general population cannot be ignored. Studies have found that particle exposure is closely related to cardiovascular disease. In addition, there have been many reports that nanomaterials can enter the heart tissue, accumulate and then cause damage. Therefore, in the present article, literature related to nanomaterials-induced cardiotoxicity in recent years was collected from the PubMed database, and then organized and summarized to form a review. This article mainly discusses heart damage caused by nanomaterials from the following three aspects: Firstly, we summarize the research 8 carbon nanotubes, etc. Secondly, we discuss in depth the possible underlying mechanism of the damage to the heart caused by nanoparticles. Oxidative stress damage, mitochondrial damage, inflammation and apoptosis have been found to be key factors. Finally, we summarize the current research models used to evaluate the cardiotoxicity of nanomaterials, highlight reliable emerging technologies and in vitro models that have been used for toxicity evaluation of environmental pollutants in recent years, and indicate their application prospects.