Abstract
Air and light pollution contribute to fetal abnormalities, increase prevalence of cancer, metabolic and cardiorespiratory diseases, and central nervous system (CNS) disorders. A component of air pollution, particulate matter, and the phenomenon of dim light at night (dLAN) both result in neuroinflammation, which has been implicated in several CNS disorders. The combinatorial role of these pollutants on health outcomes has not been assessed. Male C3H/HeNHsd mice, with intact melatonin production, were used to model humans exposed to circadian disruption by dLAN and contaminated environmental air. We hypothesized exposure to 2.5 μm of particulate matter (PM2.5) and dLAN (5lx) combines to upregulate neuroinflammatory cytokine expression and alter hippocampal morphology compared to mice exposed to filtered air (FA) and housed under dark nights (LD). We also hypothesized that exposure to PM2.5 and dLAN provokes anxiety-like and depressive-like responses. For four weeks, four groups of mice were simultaneously exposed to ambient concentrated PM2.5 or FA and/or dLAN or LD. Following exposure, mice underwent several behavioral assays and hippocampi were collected for qPCR and morphological analyses. Our results are generally comparable to previous PM2.5 and dLAN reports conducted on mice and implicate PM2.5 and dLAN as potential factors contributing to depression and anxiety. Short-term exposure to PM2.5 and dLAN upregulated neuroinflammatory cytokines and altered CA1 hippocampal structural changes, as well as provoked depressive-like responses (anhedonia). However, combined, PM2.5 and dLAN exposure did not have additive effects, as hypothesized, suggesting a ceiling effect of neuroinflammation may exist in response to multiple pollutants.