Table 6.
Particulate Matter and Atherosclerotic Plaque Formation: Literature Summary
| Authors, Year | Methods | Main Findings |
|---|---|---|
| Du et al. 2018 | ApoE−/− mice fed normal or high-fat chow and exposed to PM2.5 or filtered air for 8h/d, 7d/wk, for 16 wks. | PM2.5 increased aortic root plaques and plaque area, ox-LDL, LDL-C, apoplipoprotein B, and serum and aortic CD36. Decreased HDL-C, apolipoprotein A1 |
| Miller et al. 2017 | Healthy humans exposed to gold nanoparticles for 2h during exercise. Carotid endarterectomy patients exposed to gold 2x for 2h before surgery | Gold in blood and urine, excised carotid plaques Particles in blood and liver, with the smallest particles in the highest quantities |
| Bell et al., 2017 | MESA-Air participants | PM2.5 decreased HDL particle number but not HDL cholesterol. |
| Cao et al. 2016 | Review | Increased reactive oxygen species (ROS) or an adaptive response to oxidative stress in mediating particle-induced cell formation |
| Wang et al. 2016 | 4800 participants | Living < 150 m from major roadways increased CIMT, not CAC or AAC |
| Akintoye et al. 2016 | Meta-analysis investigating the effect of PM2.5 | PM2.5 increased CIMT, not arterial calcification or ABI |
| Kaufman et al. 2016 | PM2.5 and NOx measured in subjects aged 45–84 years | PM2.5 increased coronary calcification progression, no effect on CIMT |
| Ramanathan et al. 2016 | Healthy participants | PM2.5 significantly decreased the anti-oxidant capacity of HDL in participants with a higher pre-exposure anti-oxidant capacity |
| Keebaugh et al. 2015 | ApoE-/- mice exposed to CAP for 5 hr/day, 4 days/wk for 8 weeks | Increased plaque area and lipid content in brachiocephalic artery, increase serum MDA, decreased HRV |
| Cao et al. 2015 | Human THP-1 derived macrophages exposed to DEP | DEP increased intracellular reduced GSH, lipid droplet formation, and led to lysosomal dysfunction |
| Morales-Barcenas et al. 2015 | Airway epithelial A549 cells exposed to PM10 from industrial zone (IZ) or commercial zone (CZ) | PM10 increased protease activity and invasiveness. CZ PM10 increased MMP-2 after 24 hr exposure |
| Su et al 2015 | 689 adults | PM2.5, PM10, NO2, and NOx increased subclinical atherosclerosis |
| Du et al. 2015 | Human monocyte-derived macrophage and Chinese hamster ovary cell lines | Smaller HDL particles were the most efficient at removing cholesterol from macrophages. |
| Rao et al. 2014 | ApoE−/− and LDLR−/− exposed to PM2.5 or filtered air for 6 months | PM2.5 increased 7-ketocholesterol in plasma and aortic plaques; increased CD36 in macrophages in plaques |
| Armijos et al. 2014 | 287 healthy children | Increased CIMT in children <100 meters from the nearest heavily trafficked road compared to those living ≥ 200 meters away |
| Gan et al. 2014 | 509 healthy subjects | No associations between TRAP and progression of carotid atherosclerosis |
| Li et al. 2013 | LDLR−/− exposed to inhalational UFPs or FA for 5h/d, 3d/wk for 10 wks | Exposure to UFP decreased plasma HDL, paraoxonase activity, HDL anti-oxidant capacity. Increased ox-LDL, free oxidized fatty acids, triglycerides, TNF-alpha, plaque lesion, cross-sectional plaque area in aortic sinus |
| Chen et al. 2013 | ApoE−/− exposed to PM or filtered air | Increased serum total cholesterol, LDL, TNF-alpha, C-reactive protein. Increased aortic plaque area and TNF-alpha and IL-6 in BAL of PM mice |
| Toth et al. 2013 | Review | Low HDL-C identifies patients at elevated risk, and much investigation suggests that HDL may play a variety of antiatherogenic roles |
| Li et al. 2013 | Fat-fed low density lipoprotein receptor-null (LDLR⁻/⁻) mice exposed to filtered air (FA) or UFPs for 10 weeks | UFP exposure promoted proatherogenic lipid metabolism and reduced HDL antioxidant capacity |
| Miller et al. 2013 | ApoE−/− mice and wild-type mice exposed to (35 μL) DE or saline 2 days/wk for 4 wks. | DEP in both strains increased neutrophils in BAL and Nrf2 in liver |
| Wilker et al. 2013 | 380 elderly men | Black carbon increased CIMT |
| Lund et al. 2011 | ApoE−/− mice exposed to inhalational filtered air or whole engine emissions | Increased ox-LDL, vascular ROS, MMP-9, macrophage infiltration, endothelin-1 |
| Bai et al. 2011 | ApoE−/− mice exposed to (200 mg/m3) PM2.5 or FA, 6h/day, 5 days/wk for 7wks. | Increased oxidative stress (iNOS, nitrotyrosine, CD36) and lipid and DNA oxidation in PM2.5 mice |
| Kunzli et la. 2011 | Review | CIMT is a useful candidate for cross-sectional and longitudinal studies investigating the role of air pollution in atherogenesis |
| Campen et al. 2010 | ApoE−/− mice exposed to DE or FA for 6 h/day for 50 days. | DE increased MMP-9, ET-1 mRNA, collagen, and macrophages in DE vessels. |
| Tranfield et al. 2010 | Watanabe heritable hyperlipidemic rabbits exposed to instilled (5 mg) PM10 or saline for 2 days/wk for 4 wks. | Ultrastructural plaque analysis showed increased foam cells, fragmented or absent dense ECM, increased endothelial-foam cell contact |
| Bauer et al. 2010 | 3,380 adults | PM2.5 increased CIMT and atherosclerosis |
| Ying et al. 2009 | ApoE−/− mice exposed to CAPs PM2.5 or FA | Increased aortic expression of NADPH oxidase subunits, iNOS, superoxide generation, protein nitration |
| Floyd et al. 2009 | ApoE-/- mice exposed to FA or CAPs for 6 h/day, 5 days/wk for 5 months | CAPs-induced changes to inflammation, proliferation, cell cycle, hematological system, and cardiovascular pathways |
| Yatera et al. 2008 | Watanabe heritable hyperlipidemic rabbits exposed to intratracheal PM10 2x/wk for 1 month | PM10 increased the number of monocytes in the endothelium over plaques, in plaques, and in the smooth muscle beneath plaques |
| Sun et al. 2008 | Human bronchial epithelial cells, hSMCs, monocytes exposed PM2.5 and PM0.1. ApoE−/− exposed to PM2.5 or FA for 6 hr/day, 5 day/wk for 6 months | PM2.5 and UFP increased TF protein. PM2.5 increased TF and macrophages in plaques |
| Araujo et al. 2008 | ApoE−/− mice exposed to UFP, PM2.5, or FA 5 hrs/ day, 3 days/wk for total of 75 hrs. | UFP increased the number and size of atherosclerotic lesions infiltrated w/ foam cells, reduced HDL’s anti-inflammatory effect, and increased MDA and Nrf2 in the liver |
| Lund et al. 2007 | ApoE-/- mice exposed by inhalation to FA, PM whole exhaust or filtered exhaust | Increased aortic MMP-3, MMP-7, and MMP-9 mRNA, tissue inhibitor of MMP-2, ET-1 and HO-1. ROS in arteries, not plasma, of PM exposed mice |
| Sun et al. 2005 | 28 ApoE−/− exposed to PM2.5 or FA for 6 h/day, 5 days/wk for 6 mo. | PM2.5 increased vasoconstriction to phenylephrine and serotonin, attenuated Ach-vasodilation, increased iNOS, macrophage infiltration, ROS, and 3-nitrotyrosine |
| Miyata et al. 2003 | New Zealand White rabbits with abdominal aorta balloon injury followed by PM10 or saline exposure for 4 wks ± lovastatin(5mg/kg/day) | PM10 exposure accelerated balloon catheter induced plaque formation, increased intimal macrophages, and lipid accumulation |
Abbreviations: AP: Augmentation Pressure, AIx: Augmentation Index, Tr: time to wave reflection, FMD: flow-mediated dilation, BP: blood pressure, NMD: endothelial-independent nitroglycerin-mediated dilatation, MVRI: microvascular responsiveness index, OC: organic carbon, EC: elemental carbon, TiO2: titanium dioxide, SNP: sodium nitroprusside, FID: flow-induced dilation, ROFA: residual oil fly ash, BAL: bronchoalveolar lavage, MPO: myeloperoxidase, hSMCs: human smooth muscle cells, TF: tissue factor, CIMT: carotid intima-media thickness, TRAP: traffic-related air pollution, ABI: ankle-brachial index, CAC: coronary artery calcification, AAC: abdominal aortic calcification, MDA: malondialdehyde, CRP: c-reactive protein, CK: creatine kinase