Epidemiology studies indicated that air pollution has been associated with adverse neurological effects in human. Moreover, the secretion of glucocorticoid (GC) affects the mood regulation, and the negative feedback of hippocampal glucocorticoid receptors (GR) inhibits the GC secretion. Meanwhile, the over secretion of GC can interfere the immune system and induce neurotoxicity. In the present study, the human test showed that the secretion of the cortisol in plasma was elevated after exposure in heavy air pollution. In the mouse model, we found that breathing the highly polluted air resulted in the negative responses of the mood-related behavioral tests and morphology of hippocampus, as well as the over secretion of GC in plasma, down regulation of GR, and up-regulation of cytokine and chemokine in the hippocampus. When considering the interrelated trends between the hippocampal GR, inflammatory factors, and plasmatic GC, we speculated that PM_2.5 exposure could lead to the increased secretion of GC in plasma by decreasing the expression of GR in hippocampus, which activated the inflammation response, and finally induced neurotoxicity, suggesting that PM_2.5 exposure negatively affects mood regulation. When combined with the results of the human test, it indicated that exposure to ambient air particles increased the risk of mental disorder.

The symptoms of asthma, breathlessness, insomnia, etc. all have relevance to pulmonary rhythmic disturbances. Epidemiology and toxicology studies have demonstrated that exposure to ambient air particles can result in pulmonary dysfunction. However, there are no data directly supporting a link between air pollution and circadian rhythm disorder. In the present study, we found that breathing highly polluted air resulted in changes of the molecular clock genes expression in lung by transcriptome profiling analyses in a rodent model. Compared to those exposed to filtered air, in both pregnant and offspring rats in the unfiltered group, key clock genes (Per1, Per2, Per3, Rev-erbα and Dbp) expression level decreased and Bmal1 expression level increased. In both rat dams and their offspring, after continuous exposure to unfiltered air, we observed significant histologic evidence for both perivascular and peribronchial inflammation, increased tissue and systemic oxidative stress in the lungs. Our results suggest that chronic exposure to particulate matter can induce alterations of clock genes expression, which could be another important pathway for explaining the feedbacks of ambient particle exposure in addition to oxidative stress and inflammation.

2,2′,4,4′-tetrabromodiphenyl ether (BDE-47) is a widely used brominated flame retardant belonging to persistent organic pollutants (POPs). After being released into the marine environment, BDE-47 can cause a range of toxic effects on marine organisms through bioaccumulation, biomagnification, and intergenerational transmission. These effects include lethality, impaired motility, photosynthetic toxicity, immune damage, liver toxicity, developmental impairments, and reproductive toxicity. This article reviews the latest research progress on the toxic effects and molecular mechanisms of BDE-47 mentioned above. The primary mechanisms underlying its toxicity include oxidative stress, DNA damage, cellular apoptosis, impaired metabolism, and activation of the MAPK signaling cascade.

The various industries, sectors, and citizens’ daily lives have undergone significant changes after the outbreak of the COVID-19 pandemic. The researchers collected and analyzed PM_2.5 samples including secondary inorganic ions (SO₄²⁻, NO₃⁻, and NH₄⁺, namely SNA), organic carbon (OC), elemental carbon (EC), and other 16 metal elements in Beijing in 2019 (before the pandemic) and 2020 (after the pandemic). The particulate matter (PM_2.5) concentration in the autumn and winter of 2020 is 21.16 µg/m³ and 14.05 µg/m³ lower than in 2019, respectively. The contribution of six sources of pollution, including coal combustion, secondary sources, transportation-related sources, dust, Industrial I, and Industrial II, were analyzed using the Positive Matrix Factorization (PMF) model. Due to the impacts of the COVID-19 pandemic, more and more people are choosing private transportation, such as private cars, instead of public transportation. As a result, the contribution of PM_2.5 pollution related to transportation increased after the pandemic. The metal elements measured during the sampling period represent only a very small fraction (1%) of PM_2.5. However, their health risk to humans cannot be ignored because of the toxicity of some metallic elements, and the carcinogenic risks induced by metal elements in PM_2.5 exceeded the safety threshold (>10⁻⁶) during the autumn and winter of 2019 and 2020. Arsenic (As) contributes the most to carcinogenic risk, so controlling arsenic emissions is the primary approach to reducing cancer risk in Beijing. Considering the contribution to the health risk from various sources obtained in PMF, coal combustion is the most significant contributor to cancer risk. Therefore, serious consideration should be given to controlling coal combustion at the local and regional levels to reduce health risks in Beijing.