Air pollution is progressively identified as a non-negligible environmental risk factor for mental health [1]. Atmospheric particulate matter (PM) is comprised of a complex mixture of components such as heavy metal elements and toxic chemical compounds. PM10, with aerodynamic diameters <10 μm, can be inhaled by mankind, and is primarily generated from sources including road dust, agricultural dust, and construction and demolition sites [2]. PM10 comprises inorganic, organic, and biological compounds, and can be deposited in the respiratory airway, and the fine particles manifest serious fractional deposition in the alveoli [3]. Epidemiological studies have shown that long-term exposure to PM10 can cause extensive damage and even cancerous changes in the respiratory, immune, and endocrine systems [[4], [5], [6], [7]]. For example, Park et al. found that PM10 might trigger Th1-shifting immune response, and might disturb reproduction through lung hypoxia [8].

In addition to affecting the peripheral system, some research has shown that PM damages brain function primarily through the respiratory system and gut microbiome [9,10]. There is increasing emphasis on the potential hazards of PM exposure, particularly in relation to its effects on the central nervous system. PM10 could increase the risk of ischemia-like injuries in the brain and induce developmental neurotoxicity and neurodegeneration [[11], [12], [13], [14]]. In addition, emerging evidence to indicate that long-term exposure to heavy air pollution may unfavorably influence cognitive development, depression and psychological well-being by altering neuronal morphology [[15], [16], [17], [18]]. There is plenty of evidence to suggest a positive association between PM2.5 and mental disorders [17,19]. Oxidative stress and inflammation in the central nervous system have been identified as significant factors in the relationship between psychosis pathophysiology and PM exposure [15,17]. For instance, studies have demonstrated correlations between PM exposure and neuroinflammation markers, such as glial involvement and oxidative damage, in both humans and animal models [[20], [21], [22], [23], [24], [25]].

Nuclear factor E2-related factor-2 (Nrf2), a crucial transcription factor, plays a vital role in regulating cellular antioxidant defenses. Nrf2-mediated antioxidant responses can be activated in response to reactive oxygen species (ROS) induced by fine particulate matter (PM2.5), leading to an anti-oxidative stress effect [26]. Liu et al. found that PM induced oxidative stress led to lung injury via disturbing the phosphoinositide 3-kinase/serine/threonine-protein kinase/Nrf2 pathway, which could be protected by administrating fibroblast growth factor 10 [27]. Collectively, these findings demonstrate the significant impact of PM on brain function and provide evidence supporting the hypothesis of a link with clinically relevant mental disorders. Nevertheless, the specific mechanisms underlying the neurotoxic effects of PM remain poorly understood.

In this study, we collected PM10 samples and pursued the potential toxic mechanism of PM10 on the mental behavior of rats. Our present study aimed to clarify an association between different PM10 exposure concentrations and the heightened risk of anxiety-like behavior.