From: The critical role of endothelial function in fine particulate matter-induced atherosclerosis
Reference | Location | Study design | Sample size | Pollutants | PM2.5 Exposure | Evaluation index | Findings or association |
---|---|---|---|---|---|---|---|
[57] | - | Meta-analysis | 9183 | Ambient PM2.5, PM10, PM2.5abs, PMcoarse, NOx, NO2 | - | CIMT | PM2.5 (per 5 μg/m3 increase): CIMT increased by 0.78% (95% CI: -0.18%, 1.75%, p = 0.11). |
[58] | Ohio, United States | Prospective longitudinal cohort | 6575 | Ambient PM2.5, NO2 | Long-term exposure | Angiography | PM2.5 (per 2.2 μg/m3 increase): Mild coronary atherosclerosis (defined as 1 to 2 vessels with ≥ 50% stenosis) OR = 1.43 (95% CI: 1.11-1.83; p = 0.005); Severe coronary atherosclerosis (defined as 3 vessels with ≥ 50% stenosis) OR = 1.63 (95% CI: 1.26 to 2.11; p < 0.001). |
[59] | CA, USA | Cross-sectional | 4238 | PM2.5, traffic noise | Long-term exposure | TAC | PM2.5 (per 2.4 μg/m3 increase): TAC burden increased by 18.1% (95% CI: 6.6 to 30.9%). |
[60] | USA | Longitudinal cohort | 6814 | Ambient PM2.5 NOx, NO2 and black carbon | Long-term exposure | CAC; IMT | PM2.5 (per 5 μg/m3 increase): Coronary calcium progressed by 4.1 Agatson units per year (95% CI: 1.4 to 6.8); Without association with IMT, -0.9 μm per year (95% CI: -3.0 to 1.3). |
[61] | India | prospective, intergenerational cohort | 3278 | Ambient and indoor air pollution | Long-term exposure | CIMT | Ambient PM2.5 (per 1 μg/m3 increase): CIMT increased by 1.79% (95% CI: -0.31 to 3.90) in all participants; CIMT increased by 2.98% (95% CI: 0.23 to 5.72) in men. Indoor air pollution (biomass cooking fuel): CIMT increased by 1.60% (95% CI: -0.46 to 3.65) in all participants |
[62] | - | Meta-analysis | - | PM2.5 | - | CIMT arterial calcification; ankle-brachial index | PM2.5 (per 10 μg/m3 increase): CIMT increased by 22.52 μm (p = 0.06); Without association with arterial calcification (p = 0.44) or ankle-brachial index (p = 0.85). |
[63] | USA | Cross-sectional | 6654 | Ambient PM2.5 and black carbon | 12 months, 3 months 2 weeks Short-term exposure (0-5 days) | HDL-C HDL particle number | No significant association between PM2.5 and HDL-C; PM2.5 (per 5 μg/m3 increase) exposure for 3 months: HDL-P decreased by 0.64 μmol/L (95% CI: -1.01 to -0.26); PM2.5 (per 5 μg/m3 increase) exposure for 2-week: HDL-C increased by -0.86 mg/dL (95% CI: -1.38 to -0.34); HDL-P decreased by 0.29 μmol/L (95% CI: -0.57 to -0.01). PM2.5 (per 5 μg/m3 increase) exposure for 5 days: HDL-P decreased by 0.21 μmol/L (95% CI: -0.38 to -0.04). |
[64] | Beijing, China | Panel study | 40 | Ambient PM2.5 | Short-term exposure (1 day) | Ox-LDL; sCD36 | PM2.5 chloride, strontium, iron (1-day, per 0.51 μg/m3 increase) and nickel (2-day, 2.5 μg/m3 increase): ox-LDL increased by 1.9% (95% CI: 0.2% to 3.7%, p < 0.05) and 1.8% (95% CI: 0.2% to 3.4%), respectively; PM2.5 calcium (1-day, 0.7 μg/m3 increase): sCD36 increased by 4.8% (95% CI: 0.7% to 9.1%). |
[65] | Beijing, China | Cross-sectional | 8867 | Ambient PM2.5, NO2, O3 | Long-term exposure | CAC Score | PM2.5 (per 30 μg/m3 increase): CAC scores increased by 27.2% (95% CI: 10.8% to 46.1%); CAC increased by 42.2% (95% CI: 24.3% to 62.7%) in men, 50.1% (95% CI: 28.8% to 75%) in elderly participants, 62.2% (95% CI: -1.4% to 20.4%) in those with diabetes. |
[66] | Taiwan | Cross-Sectional | 689 | Ambient PM10, PM2.5, PM2.5abs, NO2, NOx | Long-term exposure | CIMT | PM2.5abs (per 1.0 x 10-5/m): Maximum left CIMT increased by 4.23% (95% CI: 0.32% to 8.13%, p < 0.05); PM2.5 mass concentration was not associated with CIMT. |
[67] | Toronto | Cohort study | 30 | Urban PM2.5 and O3 | Short-term exposure (2 h) | HOI; Blood pressure; | PM2.5 (exposure for 2h, 1h after exposure): Association with HOI (p = 0.078); HOI associated with systolic blood pressure (p = 0.05). |
[68] | USA | Cross-sectional, longitudinal | 5276 | PM2.5 | Long-term exposure | CIMT | PM2.5 concentration (per 2.5 μg/m3 increase): Increased IMT progression (5.0 μm/y, 95% CI: 2.6 to 7.4 μm/y); PM2.5 concentration (per 1 μg/m3 reduce): Slowed IMT progression (-2.8 μm/y, 95%CI: -1.6 to -3.9μm/y). |
[69] | USA | Cross-sectional | 5488 | Ambient PM2.5 | Long-term exposure | CIMT | PM2.5 (sulfur, silicon, EC and OC): Association: CIMT Sulfur (0.022 mm, 95% CI: 0.014 to 0.031); silicon (0.006 mm, 95% CI: 0.000 to 0.012); OC (0.026 mm, 95% CI: 0.019 to 0.034). |
[70] | South India | Cross-sectional | 7000 | PM2.5 | - | CIMT | PM2.5 (per 1 μg/m3 increase): Association: CIMT. |
[71] | Germany | Cohort study | 4814 | Traffic- related air pollution and noise | Long-term exposure | TAC | No associations between PM2.5 and TAC |
[72] | USA | Longitudinal | 165675 | Ambient PM (PM10, PM2.5, PM2.5-10) | Long-term exposure; Short-term exposure | Leukocyte Counts and Composition | PM2.5 (per 10 μg/m3 increase, exposure for 1-month): Increased: leukocyte count (12 cells/μl, 95%CI: -9 to 33), granulocyte proportion (1.2%, 95% CI: 0.6% to 1.8%); Decreased: CD8+ T cell (-1.1%, 95%CI: -1.9% to -0.3%); PM2.5 (per 10 μg/m3 increase, exposure for 12-month): Increased: leukocyte count (28 cells/μl, 95%CI: -20 to 75), granulocyte proportion (1.1%, 95% CI: -0.2% to 2.4%); Decreased: CD8+ T cell (-1.3%, 95%CI: -2.4% to -0.1%); |
[38] | USA | Longitudinal | 6814 | Ambient PM2.5 | Long-term exposure; Short-term exposure | Serum CRP, IL-6, fibrinogen, D-dimer, soluble E-selectin, sICAM -1 | Long-term exposure to PM2.5 ( per 10 μg/m3 increase): Association: inflammation and fibrinolysis (CRP, fibrinogen and E-selectin); Increased: e.g. IL-6 (6%, 95%CI: 2% to 9%). Short-term exposure to PM2.5: Association: inflammation, coagulation and endothelial activation. |
[73] | Netherlands | Prospective cohort | 750 | Air pollutants (PM2.5, NO2, black smoke, SO2) | Long-term exposure | CIMT; PWV; AIx | PM2.5 (per 5 μg/m3 increase): CIMT increased by 0.94% (95% CI: -.2.59% to 4.47%); PWV increased by 0.64% (95% CI: -4.71% to 6.01%); AIx increased by 10.17% (95% CI: -37.82% to 58.17%); |
[74] | USA | Cohort study | 3996 | PM2.5, PM10 | Long-term exposure | radial artery pulse wave and carotid artery ultrasound | Long-term particle mass exposure: Not appear to be associated with greater arterial stiffness. |
[75] | Australian | Cross-sectional | 606 | Ambient PM2.5, NO2 | Long-term exposure | CCS | PM2.5 (per μg/m3 increase): Association: CCS (≥ 100): (OR 1.20, 95% CI: 1.02 to 1.43); CCS (≥ 400): (OR 1.55, 95% CI: 1.05 to 2.29). |
[76] | Germany | Cross-sectional | 4291 | Ambient PM2.5, PM10 | Long-term exposure | Arterial blood pressure (BP) | Per IQR of PM2.5 (2.4 μg/m3): Systolic BP increased by 1.4 mmHg (95% CI: 0.5 to 2.3); Diastolic BP increased by 0.9 mmHg (95% CI: 0.4 to 1.4). |
[77] | Switzerland | Cross-sectional | 1503 | Ambient PM10, PM2.5, UFP | Long-term exposure | CIMT | Vehicular source of PM2.5: CIMT increased by 1.67% (95% CI: -0.30 to 3.47%). |
[78] | USA | Cross-sectional | 6256 | Ambient PM2.5 (EC, OC, silicon, and sulfur) | Long-term exposure | CIMT, PM2.5 components EC, OC, silicon, and sulfur | Per IQR increase of PM2.5: Association/increase: CIMT PM2.5 (14.7 μm, 95% CI: 9.0 to 20.5); OC (35.1 μm, 95% CI: 26.8 to 43.3); EC (9.6 μm, 95% CI: 3.6 to 15.7); Sulfur (22.7 μm, 95% CI: 15.0 to 30.4). |
[79] | Seoul, Korea | Cohort study | 364 | Ambient PM2.5 | Long-term exposure | Coronary computed tomographic angiography | PM2.5 (per 1 μg/m3 increase): Increase/association: HRP (aHR 1.62, 95% CI: 1.22 to 2.15, p < 0.001); fibrofatty and necrotic core component (aHR 1.41, 95% CI: 1.23 to 1.61, p < 0.001); total plaque volume progression (aHR 1.14, 95% CI: 1.05 to 1.23, p = 0.002). |
[80] | USA | Cross-sectional | 417 | Ambient PM2.5,O3 | Long-term exposure | CIMT | PM2.5 (per 1 μg/m3 increase): CIMT increased by 4.28 μm/y (95% CI: 0.02 to 8.54μm/y). |
[81] | Germany | Prospective cohort | 4494 | Traffic and PM2.5 | Long-term exposure | CAC | Possible association between PM2.5 exposure and CAC |
[82] | USA | Cohort study | 3506 | Ambient PM2.5 | Long-term exposure | TAC, AAC | No consistent associations between PM2.5 and TAC, AAC |
[83] | Taiwan | Prospective cohort | 30034 | Ambient PM2.5 | Long-term exposure | CRP | PM2.5 (per 5 μg/m3 increase): Association: systemic inflammation CRP increased by 1.31% (95% CI: 1.00% to 1.63%) |
[84] | North Carolina | Cross-sectional | 861 | PM10, PM2.5, NO2, O3 | - | CIMT | No associations between PM2.5 and CIMT. |
[85] | Detroit, MI; Oakland, CA; Pittsburgh, PA; Chicago, IL; and Newark, NJ | Cohort study | 1188 | PM2.5, O3 | Long-term exposure | CIMT, IAD, plaque presence and plaque index | PM2.5 (1 μg/m3 higher 5-year mean): CIMT increased 8 μm (95% CI: 1.0 to 15.1), adjusting for cardiovascular disease risk factors; No significant associations between PM2.5 and IAD; No associations between PM2.5 and plaque presence or plaque index. |
[86] | German | Cohort study | 4814 | PM2.5, PM10 | Long-term exposure | CIMT | PM2.5 (interdecile range increase 4.2μg/m3): CIMT increased 4.3% (95% CI: 1.9% to 6.7%); PM10 (interdecile range increase 6.7μg/m3): CIMT increased 1.7% (95% CI: -0.7% to 4.1%). |
[87] | Sichuan, China | Longitudinal study | 205 | Household air pollution (PM2.5 and BC) | Short-term exposure (48 h) | BP, PP, cfPWV, AIx | PM2.5 (1-ln (μg/m3) increase): Association: SBP; PP; cfPWV (-0.1 m/s, 95% CI -0.4 to 0.2) with no difference; slightly higher AIx (1.1%, 95% CI -0.2 to 2.4). |
[88] | Puno, Peru | Cross-sectional | 266 | Householdbiomass fuel | long-term exposure | Measure 24 h indoor PM2.5, CIMT, Carotid plaque, BP | Biomass fuel exposure: Increased: CIMT (0.66 vs 0,60 mm, p < 0.001); carotid plaque prevalence (26% vs 14%, p < 0.05); systolic BP (118 vs 111 mm Hg, p < 0.001); median household PM2.5 (280 vs 14 μg/m3, p < 0.001). |
[39] | Taiwan, China | Prospective panel atudy | 117 | Ambient PM2.5, NO2 | - | baPWV, hsCRP | PM2.5 (10 μg/m3 increases at 1 day lag): Association: baPWV (2.1%, 95% CI: 0.7%-3.6%; 2.4%, 95% CI: 0.8%-4.0%); No significant association between NO2 and baPWV. |
[89] | USA | Cross-sectional | 798 | PM2.5 | long-term exposure | CIMT | PM2.5 (10 μg/m3 increases): CIMT increased (5.9%, 95% CI: 1 to 11%); Adjustment of age, never smokers, ≥ 60 years of age women: the strongest associations with CIMT increased (15.7%, 95% CI: 5.7 to 26.6%). |
[90] | USA | Cross-sectional | 1147 | PM2.5 | long-term exposure | calcium scores | PM2.5 (10 μg/m3): Aortic calcification (RR=1.06; 95% CI: 0.96 to 1.16); Long-term residence near a PM2.5 monitor (RR=1.10; 95% CI: 1.00 to 1.22). |
[91] | USA | Cohort study | 5172 | PM2.5 | long-term exposure | CIMT | PM2.5 (12.5 μg/m3 increases): CIMT increased 1 to 3%. |
[81] | Geman | Prospective cohort study | 4494 | PM2.5 | long-term exposure | CAC | PM2.5 (3.91 μg/m3): CAC higher 17.2% (95% CI: -5.6 to 45.5%). |
[92] | Hebei, China | Cross-sectional | 752 | Indoor PM2.5, CO, SO2 | Long-term exposure | CIMT, IL-8, CRP, TNF-α, SAA1 | Smoky coal combustion-derived indoor air pollutants: Increased: systemic inflammation; The risk of carotid atherosclerosis RR = 1.434 (95% CI: 1.063 to 1.934, p = 0.018). |