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Table 1 Epidemiological studies on the association between PM2.5 exposure and atherosclerosis

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).

  1. Note: Short-term exposure means the period of exposure is less than 3 months; Long-term exposure means the period of exposure is longer than 3 months
  2. AAC abdominal aortic calcium agatston score, aHR adjusted hazard ratio, AIx augmentation index, BC black carbon, BP Blood pressure, CAC coronary artery calcification, CCS Coronary artery calcium score, cfPWV carotid-femoral PWV, CI confidence interval, CIMT carotid intima-media thickness, CRP C-reactive protein, EC elemental carbon, HDL-P high-density lipoprotein cholesterol particle matter, HOI HDL oxidant index, HDL-C high-density lipoprotein cholesterol, HRP high-risk plaque, IAD inter-adventitial diameter, IMT intima-media thickness, IL interleukin, O3 ozone, IQR interquartile, NO nitrogen dioxide, OC organic carbon, Ox-LDL oxidized low-density lipoprotein, OR odds ratio, PM2.5abs absorbance levels of PM2.5, PNacc particle number of accumulation mode particles, PP pilse pressure, UFP ultrafine particles (< 0.1μm), TAC thoracic aortic calcium agatston score, SBP systolic blood pressure, sCD36 soluble cluster of differentiation 36, sICAM-1 soluble Intercellular Adhesion Molecule-1, SO2 sulfur dioxide, PWV Pulse wave velocity, baPWV brachial-ankle pulse wave velocity