Rui Deng

1. Ambient temperature is a fundamental environmental factor with profound implications for both planetary ecosystems and human health (Romanello et al., 2022). Its influence spans the natural and ...

Respiratory diseases continue to be a major global concern, with allergies and asthma often discussed as critical areas of study. While the role of environmental risk factors, such as non-allergenic pollutants and high humidity, in asthma induction is often mentioned, there is still a lack of thorough research on their co-exposure. This study aims to investigate the adjuvant effect of ultrafine carbon black (30–50 nm) and high humidity (70% relative humidity) on the induction of allergic asthma. A mouse model of asthma was established using ovalbumin, and airway hyperresponsiveness, remodeling, and inflammation were measured as the endpoint effects of asthma. The mediating role of the oxidative stress pathway and the transient receptor potential vanilloid 1 pathway in asthma induction was validated using pathway inhibitors vitamin E and capsaicin, respectively. Co-exposure to ultrafine carbon black and high humidity had a significant impact on metabolic pathways in the lung, including aminoacyl-tRNA biosynthesis, glycerophospholipid metabolism, and ATP-binding cassette transporters. However, administering vitamin E and capsaicin altered the effects of co-exposure on the lung metabolome. These results offer new insights into the health risk assessment of co-exposure to environmental risk factors and provide an important reference point for the prevention and treatment of allergic asthma. Graphical abstract

Asthma is a chronic respiratory disease that is highly sensitive to environmental pollutants, including engineered nanoparticles (NPs). Exposure to NPs has become a growing concern for human health, especially for susceptible populations. Toxicological studies have demonstrated strong associations between ubiquitous NPs and allergic asthma. In this review, we analyze articles that focus on adverse health effects induced by NPs in animal models of allergic asthma to highlight their critical role in asthma. We also integrate potential mechanisms that could stimulate and aggravate asthma by NPs. The toxic effects of NPs are influenced by their physicochemical properties, exposure dose, duration, route, as well as the exposure order between NPs and allergens. The toxic mechanisms involve oxidative stress, various inflammasomes, antigen presenting cells, immune cells, and signaling pathways. We suggest that future research should concentrate on establishing standardized models, exploring mechanistic insights at the molecular level, assessing the combined effects of binary exposures, and determining safe exposure levels of NPs. This work provides concrete evidence of the hazards posed by NPs in animals with compromised respiratory health and supports the modifying role of NPs exposure in allergic asthma. Graphical Abstract: