Abstract

Exposure to air pollution increases the risk of neurodegenerative disorders (ND) like Alzheimer’s disease (AD). The current in-vivo model study was undertaken to investigate the effects of co-exposure to ambient fine particulate matter (PM2.5) plus gaseous pollutants on amyloid β1–42 (Aβ1–42) accumulation as a biomarker of AD. Three groups including exposure group 1 (PM2.5 plus gaseous pollutants), exposure group 2 (gaseous pollutants alone) and control group (air with standard condition) were designed. Exposure time was 5 h per day (9.00 am to 14.00 pm) for 4 days per week for 3 months periods of exposure. The concentration of PM2.5, O3, SO2, and NO2 was measured continuously. The concentration of O3, NO2, and SO2 via UV fluorescence method and concentration of PM2.5 via beta attenuation method were monitored. Concentration of metals in PM2.5 including Al, Ca, Na, Cr, Mn, Pb, Cd, Ni, Fe, and Cu by inductively coupled plasma mass spectrometry (ICP-MS) and polycyclic aromatic hydrocarbons (PAHs) in PM2.5 by gas chromatography-mass spectrometry (GC-MS) were measured. The concentration of Aβ1–42 in the hippocampus of male and female rats was measured by enzyme-linked immunosorbent assay (ELISA) method. The concentration of PM2.5 in the 3 months exposure significantly was higher than WHO recommended level (p value <.05), However concentration of SO2, O3, and NO2 in the 3 months exposure significantly was lower than WHO recommended level (p value <.05). The order of metals in the PM2.5 was Al > Ca > Cu > Cd > Na > Fe > Cr > Ni > Mn > Pb. Also, sum concentration of 16-PAHs in the PM2.5 was 45.7 ± 37.15 ng/m3. Exposure to ambient PM2.5 plus gaseous pollutants significantly increased the concentration of Aβ1–42 in male and female rats after 3 months. There is no significant difference in concentration Aβ1-42 between male and female rats after 3 months. The results of current study indicate that exposure to urban ambient PM2.5 can increase the risk of Alzheimer’s disease.

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