Neuropathology changed by 3- and 6-months low-level PM_2.5 inhalation exposure in spontaneously hypertensive rats

Epidemiological evidence has linked fine particulate matter (PM_2.5) to neurodegenerative diseases; however, the toxicological evidence remains unclear. The objective of this study was to investigate the effects of PM_2.5 on neuropathophysiology in a hypertensive animal model. We examined behavioral alterations (Morris water maze), lipid peroxidation (malondialdehyde (MDA)), tau and autophagy expressions, neuron death, and caspase-3 levels after 3 and 6 months of whole-body exposure to urban PM_2.5 in spontaneously hypertensive (SH) rats.

SH rats were exposed to S-, K-, Si-, and Fe-dominated PM_2.5 at 8.6 ± 2.5 and 10.8 ± 3.8 μg/m³ for 3 and 6 months, respectively. We observed no significant alterations in the escape latency, distance moved, mean area crossing, mean time spent, or mean swimming velocity after PM_2.5 exposure. Notably, levels of MDA had significantly increased in the olfactory bulb, hippocampus, and cortex after 6 months of PM_2.5 exposure (p < 0.05). We observed that 3 months of exposure to PM_2.5 caused significantly higher expressions of t-tau and p-tau in the olfactory bulb (p < 0.05) but not in other brain regions. Beclin 1 was overexpressed in the hippocampus with 3 months of PM_2.5 exposure, but significantly decreased in the cortex with 6 months exposure to PM_2.5. Neuron numbers had decreased with caspase-3 activation in the cerebellum, hippocampus, and cortex after 6 months of PM_2.5 exposure.

Chronic exposure to low-level PM_2.5 could accelerate the development of neurodegenerative pathologies in subjects with hypertension.