Table 1.

Human studies on the association of inflammation and/or oxidative stress with air pollution.

First Author/Year	Population/Cohort	Air Pollutants	Major Outcomes	Ref.
Liu, 2021	40 chronic obstructive pulmonary disease patients and 75 controls	PAHs	A one fold increase in hydroxylated PAHs was associated with a 4.1–15.1% elevation of malondialdehyde, which was stronger in subjects with impaired lung function.	[18]
Abohashem, 2021	503 subjects without cardiovascular disease	PM2.5	Higher PM2.5 was associated with increased risk for major adverse cardiovascular events, mediated by an increase in leucopoietic activity and arterial inflammation.	[21]
Ni, 2021	740 subjects	PM2.5	Acute increases in PM2.5 were associated with increased soluble lectin like oxidized LDL receptor-1, but not with nitrite.	[46]
Nassan, 2021	456 men	PM2.5 species	Acute increases in PM2.5 species were associated with metabolic pathways involved in inflammation, oxidative stress, immunity, and nucleic acid damage and repair.	[19]
Mann, 2021	299 children	Traffic related air pollutants (sum of PAH456, NO2, elemental carbon, PM2.5)	Acute increases in traffic related air pollutants were associated with 8-isoprostane.	[22]
Prunicki, 2020	100 subjects	PM2.5, NO, NO2, CO, PAHs	Air pollutants were associated with oxidative stress, acute inflammation, altered hemostasis, endothelial dysfunction, monocyte enrichment, and diastolic blood pressure.	[23]
Riggs, 2020	100 subjects	PM2.5	A 10 μg/m3 increase in PM2.5 was associated with a 12.4% decrease in reactive hyperemia index (95% CI −21.0–−2.7). Increased PM2.5 was associated with elevated F-2 isoprostane metabolite, angiopoietin 1, vascular endothelial growth factor, placental growth factor, intracellular adhesion molecule-1, and matrix metalloproteinase-9 as well as reduced vascular adhesion molecule-1.	[47]
Li, 2019	73 subjects	PM2.5, BC, NO2, CO	Increases in air pollutants were associated with reductions in circulating high density lipoprotein cholesterol and apolipoprotein A-I, as well as elevations in HDL oxidation index, oxidized LDL, malondialdehyde, and C-reactive protein.	[48]
Lin, 2019	26 subjects	PAHs	Increases in 5-, 12-, and 15-hydroxyeicosatetraenoic acid, as well as 9- and 13-hydroxyoctadecadienoic acid, were observed. Decreases in paraoxonase and arylesterase, as well increases in C-reactive protein and fibrinogen, were observed.	[49]
Balmes, 2019	87 subjects	O3	Acute O3 exposure did not alter C-reactive protein, monocyte–platelet conjugates, and microparticle associated tissue factor activity, whereas increases in endothelin-1 and decreases in nitrotyrosine were observed.	[50]
Han, 2019	60 subjects with prediabetes and 60 healthy subjects	PM2.5	Acute exposure to PM2.5 resulted in increased exhaled NO, white blood cells, neutrophils, interleukin-1α, and glycated hemoglobin. Compared to healthy subjects, prediabetic subjects displayed pronounced PM2.5 associated systemic inflammation, elevated systolic and diastolic blood pressure, impaired endothelial function, and elevated fasting glucose.	[51]
Xia, 2019	215 pregnant women	PM2.5	Acute increases in PM2.5 and lead constituent were associated with endothelial dysfunction (increased endothelin-1, E-selectin, and intracellular adhesion molecule-1) and inflammation (increased interleukin-1β, interleukin-6, tumor necrosis factor-α). Endothelial dysfunction and elevated inflammation were partially mediated by the effect of PM2.5 and lead constituent on blood pressure.	[52]
Li, 2019	3820 subjects	PM2.5, BC, O3, sulfate, NOX	Negative associations of acute PM2.5 and BC with P-selectin, of O3 with monocyte chemoattractant protein 1, and of sulfate and NOx with osteoprotegerin were found.	[53]
Li, 2017	3996 subjects	PM2.5, sulfate, NOx, BC, O3	Acute increases in PM2.5 and sulfate were associated with increased C-reactive protein, which was also true for NOx in case of interleukin-6 and for BC, sulfate, and O3 in case of tumor necrosis factor receptor 2. Conversely, BC, sulfate, and NOx were negatively associated with fibrinogen, and sulfate was negatively associated with tumor necrosis factor α.	[24]
Mirowsky, 2017	13 subjects with coronary artery disease	O3	Per acute IQR increase in O3, changes in tissue plasminogen factor (6.6%, 95% CI 0.4–13.2), plasminogen activator inhibitor-1 (40.5%, 95% CI 8.7–81.6), neutrophils (8.7%, 95% CI 1.5–16.4), monocytes (10.2%, 95% CI 1.0–20.1), interleukin-6 (15.9%, 95% CI 3.6–29.6), large artery elasticity index (−19.5%, 95% CI −34.0–−1.7), and the baseline diameter of the brachial artery (−2.5%, 95% CI −5.0–0.1) were observed.	[54]
Pope 3rd, 2016	24 subjects	PM2.5	Episodic increases in PM2.5 were associated with increased endothelial cell apoptosis, an anti-angiogenic plasma profile, and elevated circulating monocytes, and T, but not B, lymphocytes.	[55]
Wu, 2016	89 subjects	PM2.5, NO2	Acute increases in PM2.5 were associated with brachial–ankle pulse wave velocity, whereas no association was found for NO2. NO2 was associated with increased C-reactive protein.	[56]

PAHs: polycyclic aromatic hydrocarbons, PM_{(diameter size)}: particulate matter, NO₂: nitrogen dioxide, NO: nitric oxide, CO: carbon monoxide, BC: black carbon, O₃: ozone, NO_x: nitrogen oxides, IQR: interquartile range, CI: confidence interval.