Epidemiological and toxicological evidence indicates that fine particulate matter (PM2.5, particulate matter < 2.5 µm in aerodynamic diameter) causes cardiopulmonary toxicity; however, its neurotoxic effects remain unclear. The objective of this study was to investigate the role of the neurofilament light (NEFL) serum polypeptide in neurotoxicity. 6-month-old male Sprague Dawley (SD) rats were exposed to traffic-related PM1 (< 1 µm in aerodynamic diameter; 16.3 µg m–3) and gaseous pollutants (via high-efficiency particulate air, HEPA) for 3 and 6 months through a whole-body exposure system. According to our observations, the levels of interleukin (IL)-4, IL-10, and tumor necrosis factor (TNF)-α in the serum of the rats significantly increased (p < 0.05) after 3 months of exposure to PM1, whereas that of NEFL polypeptide significantly increased (p < 0.05) after 3 and 6 months of exposure. Additionally, increases in the IL-2, IL-6, IL-10, IL-17a, TNF-α, and interferon (IFN)-γ levels after 3 and/or 6 months of exposure to this pollutant (p < 0.05) were observed in the cerebrospinal fluid (CSF). In terms of their respective levels, the IL-6 correlated well with the CSF IL-2 and IL-10; the TNF-α correlated well with the CSF IL-6, IL-17a, TNF-α, and IFN-γ; and the NEFL polypeptide correlated well with the CSF IL-2, IL-4, IL-6, IL-10, IL-17a, TNF-α, and IFN-γ. In summary, systemic neuroinflammatory and immune responses in rats occurred after chronic exposure to PM1. Hence, NEFL polypeptide in serum may be a suitable biomarker for neurotoxicity caused by chronic exposure to this pollutant.
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