Co-exposure to ambient PM_2.5 plus gaseous pollutants increases amyloid β1–42 accumulation in the hippocampus of male and female rats

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 (PM_2.5) plus gaseous pollutants on amyloid β1–42 (Aβ1–42) accumulation as a biomarker of AD. Three groups including exposure group 1 (PM_2.5 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 PM_2.5, O₃, SO₂, and NO₂ was measured continuously. The concentration of O₃, NO₂, and SO₂ via UV fluorescence method and concentration of PM_2.5 via beta attenuation method were monitored. Concentration of metals in PM_2.5 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 PM_2.5 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 PM_2.5 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 PM_2.5 was Al > Ca > Cu > Cd > Na > Fe > Cr > Ni > Mn > Pb. Also, sum concentration of 16-PAHs in the PM_2.5 was 45.7 ± 37.15 ng/m³. Exposure to ambient PM_2.5 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 PM_2.5 can increase the risk of Alzheimer’s disease.

Keywords:

• Alzheimer’s disease
• co-exposure
• in-vivo model
• PM2.5
• amyloid β1-42

Disclosure statement

No potential conflict of interest was reported by the authors.

Additional information

Funding

This study is based on data from the Ph.D. Thesis of Yadolah Fakhri. School of Public Health and Safety, Shahid Beheshti University of Medical Sciences, Tehran, Iran was the financial provider of this investigation project [Grant number #11421].