Table 4.

The effects of particulate matter on inflammation, oxidative stress, adhesion molecules, and thrombosis: Evidence from clinical studies.

Models	Exposure/Method	Results			Interpretation	References
		Inflammation	Coagulation & Adhesion Molecules	Blood Parameters
Healthy young adults (N = 16) Mean age 25 y	Inhalation of # Petrodiesel exhaust (PDE) # Mixture of biodiesel 30% and 70% of petrodiesel from rapeseed methyl ester (RME30) # Biodiesel 100% from rapeseed methyl ester (RME100) For 1 h Evaluation at 2, 4, 8, 24 h after exposure		↔ tPA ↔ thrombus formation	↔ Hb, WBC, platelet	Inhalation exposure of biodiesel formulation (RME30, RME100) did not alter coagulation and blood cell parameters in comparison to PDE.	[77]
# Healthy adults (N = 15) Mean age: 28 y # Metabolic syndrome patients (N = 17) mean age 40 y	Inhalation of # DEP # Filtered fresh air (control) for 2 h Evaluate at pre-exposure, 7 and 22 h after exposure	↔ MMP-9 ↔ IL-1β ↔ IL-6 ↔ IL-10	↔ E-selectin ↔ ICAM-1, VCAM-1	# Both healthy and metabolic syndrome subjects: ↑ Hct ↔ Hb, RBC ↑ platelet ↔ WBC	Short-term DEP exposure resulted in hemoconcentration & thrombocytosis but did not affect inflammatory response and endothelial cell activation in both healthy and metabolic syndrome subjects.	[71]
Healthy adults (N = 73) Mean age 23.3 y	Ambient air pollution in an urban area, Beijing, China Evaluate the PM level at 1, 2, 3, 5, and 7 d MA	# PM2.5: ↑ sRAGE ↑ MIP-1α, β ↔ IL-1β, CRP # BC: ↑ sRAGE ↑ MIP-1α, β ↔ IL-1β, CRP	# PM2.5: ↑ P-selectin ↑ sCD40L ↔ PT ↑ FDP # BC: ↑ P-selectin ↔ sCD40L ↓ PT ↑ FDP		Exposure to higher ambient air pollution was associated with increased inflammatory biomarkers and heightened thrombogenicity.	[69]
Healthy young adults (N = 125) Mean age 24.2 y	Ambient air pollution in Beijing, China # Pre-Olympic period # During Olympics (Strict pollution control) # Post-Olympics period Evaluate the PM level at 1, 12, 24, 48, 96 h		# PM2.5, EC: ↑ P-selectin, sCD40L ↑ fibrinogen, VWF # OC: ↑ P-selectin, ↔ sCD40L ↑ fibrinogen, VWF # Pre- vs. During Olympic period: ↓ P-selectin, sCD40L ↔ fibrinogen ↓ VWF # During vs. post-Olympic period: ↑ P-selectin, ↔ sCD40L ↔ fibrinogen ↔ VWF	# PM, OC, EC: ↔ WBC # Pre- vs. During Olympic period: ↔ WBC # During vs. post-Olympic period: ↔ WBC	The restricted air pollution control markedly reduced PM, which was associated with decreased platelet activation and prothrombotic state. The alteration of PM level did not affect WBC count.	[76]
Elderly individuals with either CVD, or COPD and healthy individuals (N = 47) Mean age 78 y	Ambient air pollution fine PM outside of each individuals’ homes Seattle, WA, USA Evaluation of the PM level at the zero d and 1 d MA	↔ CRP ↑ MCP-1	↔ fibrinogen ↔ D-dimer		The effects of low ambient levels of PM on inflammation or thrombosis were not significant in elderly individuals.	[70]
Healthy elderly (N = 704) Mean age 73.2 y	Ambient Air Pollution in Boston, USA Evaluate the PM level at 4, 24 h, 3, 7, 14, 21, and 28 d MA	# PM2.5: ↔ CRP # BC: ↔ CRP	# PM2.5: ↑ ICAM-1, VCAM-1 ↔ fibrinogen # BC: ↑ ICAM-1, VCAM-1 ↑ fibrinogen		Short-term (1–3 d MA), and intermediate-term (7–28 d MA) exposure to traffic-related air pollution were associated with alteration of adhesion molecules, reflecting acute inflammatory and endothelial responses.	[73]
Adult patients undergoing cardiac catheterization due to stable IHD or ACS (N = 135) Mean age 61.4 y	Ambient air pollution Rochester, NY, USA Evaluate the PM level at 1, 12, 24, 48, 72, and 96 h MA	# PM2.5: ↑ CRP # Delta-C, AMP: ↔ CRP # BC: ↑ CRP # UFP: ↔ CRP	# PM2.5, Delta-C, BC: ↑ PF4 ↑ fibrinogen ↔ VWF, D-dimer # AMP ↑ PF4 ↑ fibrinogen ↔ P-selectin ↔ VWF, D-dimer # UFP: ↓ PF4 ↑ fibrinogen ↔ P-selectin ↔ VWF, D-dimer		The high PM was generally associated with an increase in biomarkers of systemic inflammation and coagulation.	[72]
Patients with CAD or at least two CVD comorbid diseases (HT, DM, hyperlipidemia) (N = 61) Mean age 62.3 y	Ambient air pollution In an urban area, Taipei City, Taiwan Evaluate the PM level at 1 to 3 d MA	# PM2.5, OC, EC: ↔ hsCRP	# PM2.5: ↔ fibrinogen ↔ D-dimer # OC, EC: ↔ fibrinogen ↑ D-dimer		Short-term exposure (1–3 d) to urban pollution triggered systemic inflammatory and thrombotic response in high-risk CVD patients.	[75]
DM type II (N = 30) Mean age 56.5 y	Acute exposure to ambient PM in Rochester, NY, USA Evaluate the PM level at 1, 12, 24, 48, 96 h		# PM2.5, AMP: ↔ TBXB2 ↔ ADP-, and collagen-induced platelet aggregation # UFP: ↔ TBXB2 ↔ ADP-induced platelet aggregation ↓ collagen-induced platelet aggregation at 48–96 h MA # BC: ↓ TBXB2 at 48–96 h MA ↔ ADP-, and collagen-induced platelet aggregation		High UFP levels were associated with reduced platelet response, whereas PM2.5, AMP, and BC resulted in a trend of increased platelet aggregation.	[78]

ACS: acute coronary syndrome, ADP: adenosine diphosphate, AMP: accumulation mode particles, BC: black carbon, CAD: coronary artery disease, COPD: chronic obstructive pulmonary disease, CRP: C-reactive protein, CVD: cardiovascular disease, d: days, DEP: diesel exhaust particles, DM: diabetes mellitus, E-selectin: endothelial cell adhesion molecule, EC: elemental carbon, FDP: fibrin degradation product, h: hours, Hb: hemoglobin, Hct: hematocrit, hsCRP: high sensitivity C-reactive protein, HT: hypertension, ICAM-1: intercellular adhesion molecule, IHD: ischemic heart disease, IL-1β: interleukin-1β, IL-6: interleukin-6, IL-10: interleukin-10, MA: moving average, MCP-1: monocyte chemoattractant protein-1, MIP-1: macrophage inflammatory protein-1, MMP-9: matrix metallopeptidase 9, OC: organic carbon, PF4: platelet factor 4, PM: particulate matter, PM_2.5: particulate matter in diameter <2.5 µm, PMN: polymorphonuclear cells, PT: prothrombin time, RBC: red blood cells, sCD40L: soluble CD40 ligand, sRAGE: soluble receptor for advanced glycation end products, TBXB2: thromboxane B2, tPA: tissue plasminogen activator, UFP: ultrafine particles, VCAM-1: vascular cell adhesion molecule, VWF: von Willebrand factor, WBC: white blood cells, y: years.