Table 3. PM-induced neuronal dysfunction on brains of AD disease models.

Year	Particle type and source	Mouse	Sex	Age	Exposure condition	Conc.	Observation	Citation
				Start ~ end		(μg/m3)
2008	CAPs collected near freeway I-10 in the Los Angeles, CA	APOE-/-	M	1.5-month-old ~	5 h/day	30.4	Increased AP1, NF-κB, GFAP, and pJNK/JNK ratio in cortical tissue after either lower or higher exposure.	[67]
				3-month-old	3 days/week	114.2
					6 weeks
2017	nPM collected near highway 101 in the Los Angeles, CA	E3FAD	F	2-month-old ~	5 h/day	468.0	1. Increased Aβ protein load and oligomers in the cortex of E4FAD.	[18]
		E4FAD		7-month-old	3 days/week
							2. Selective neuronal atrophy (lower neurite density) in the CA1 of hippocampus of E3FAD and wild type mice.
					15 weeks
							3. Decreased synaptic proteins (GluR1) in the hippocampus of all three types of mice.
2019	UFP collected near roadway in Rochester, NY	3xTg-AD	M	12.5-month-old ~	4 h/day	57.0	1. Protracted detriments in spatial learning, reference memory, and short-term memory independent of underlying AD genotype.	[66]
				13.0-month-old	4 days/week
					2 weeks
							2. UFP worsened olfactory discrimination in 3xTgAD mice
2020	nPM collected near highway I-110 in the Los Angeles, CA	J20-hAPPswe	M	Unknown	5 h/day	300.0	1. Increased Aβ40, Aβ42, and Aβ load n the cortex as well as increased APP in the lipid raft of the cortex.	[36]
					3 days/week
					10 weeks
							2. Increased lipid oxidation (4-HNE) in the cortex.

CAPs: concentrated ambient particles; GFAP: glial fibrillary acidic protein; UFP: ultrafine particulate matter; nPM: nano-scale PM; E3FAD: 5xFAD^{+/ −} /human APOE ε3/ε3; E4FAD: 5xFAD^{+/ −} /human APOE ε4/ε4; GluR1: glutamate receptor subunit