Investigations of PM2.5 Long-term Exposure and Subclinical Atherosclerosis in Women: An Overview
DOI:
https://doi.org/10.17140/EPOJ-7-129Keywords:
Particulate matter, Air pollution, Long-term exposure, Subclinical atherosclerosis, Coronary artery calcification, Women’s healthAbstract
Background/Aim
Evidence demonstrates that coronary artery calcification (CAC) is a biological marker for cardiovascular disease (CVD) risk prediction. Acute cardiovascular effects of temporary and chronic environmental particle exposures sensitive to ≤2.5 micrometers in diameter (here termed “PM2.5”) have been well-studied. However, there is less information on the long-term effects of PM2.5 exposures on the earlier pre-clinical stage of CVD, especially in women (in whom it is also established experience frequent cardiovascular late- and under-diagnoses). This phase of pre-diagnosis pathological activity is classified as subclinical atherosclerosis (SCA) unless and until a patient meets established clinical diagnostic criteria. In this systematic review, we summarize reported as sociations of long-term PM2.5 and SCA exposure, with investigators placing an emphasis on gender differences in any documented associations.
Methods
We conducted a comprehensive literature review for articles published from 2007 to 2022 that reported associations of long-term PM2.5 and SCA and evaluated each study with areas of particular focus including study designs, populations at risk, and exposure measures.
Results
Investigations representing four cohorts yielded equivocal findings related to long-term PM2.5 exposure and CAC. Three cohorts reported positive associations between long-term PM2.5 and CAC development/progression. Two studies supported a strongly positive associations among women or postmenopausal women for PM2.5 on CAC. Studies, however, evaluating PM2.5 exposure associations with carotid intima-media thickness (another biomarker of SCA), reflect increases in both men and women with ↑PM2.5 levels but reporting no gender differences in PM2.5 exposure and this measure of SCA.
Conclusion
Our study identifies important gaps in current knowledge synthesis including different methods of PM2.5 estimation and linkage, a lack of consensus of what constitutes long-term air pollution, and the selection of important covariates and intermediate variables. Our aim is to outline best practices going forward in the investigation of PM2.5 long-term exposure and SCA in women.
References
Achilleos S, Kioumourtzoglou MA, Wu CD, Schwartz JD, Koutrakis P, Papatheodorou SI. Acute effects of fine particulate matter constituents on mortality: A systematic review and meta-regression analysis. Environ Int. 2017; 109: 89-100. doi: 10.1016/j. envint.2017.09.010
Du Y, Xu X, Chu M, Guo Y, Wang J. Air particulate matter and cardiovascular disease: The epidemiological, biomedical and clinical evidence. J Thorac Dis. 2016; 8 (1): E8-E19. doi: 10.3978/j. issn.2072-1439.2015.11.37
Talbott EO, Rager JR, Benson S, et al. A case-crossover analysis of the impact of PM2.5 on cardiovascular disease hospitalizations for selected cdc tracking states. Environ. Res. 2014; 134: 455-465. doi: 10.1016/j.envres.2014.06.018
Amsalu E, Wang T, Li H, et al. Acute effects of fine particulate matter (PM2.5) on hospital admissions for cardiovascular disease in beijing, china: A time-series study. Environ Health. 2019; 18(1): 70. doi: 10.1186/s12940-019-0506-2
Talbott EO, Zborowski J, Rager J, Stragand JR. Is there an inde-pendent effect of polycystic ovary syndrome (PCOS) and meno-pause on the prevalence of subclinical atherosclerosis in middle aged women? Vasc Health Risk Manag. 2008; 4(2): 453-462. doi: 10.2147/vhrm.s1452
Dabass A, Talbott EO, Rager JR, et al. Systemic inflammato-ry markers associated with cardiovascular disease and acute and chronic exposure to fine particulate matter air pollution (PM(2.5)) among US NHANES adults with metabolic syndrome. Environ Res. 2018; 161: 485-491. doi: 10.1016/j.envres.2017.11.042
El Khoudary SR, Greendale G, Crawford SL, et al. The menopause transition and women’s health at midlife: A prog-ress report from the Sstudy of Women’s Health Across the Na-tion (SWAN). Menopause. 2019; 26(10): 1213-1227. doi: 10.1097/ GME.0000000000001424
Auro K, Joensuu A, Fischer K, et al. A metabolic view on meno-pause and ageing. Nat Commun. 2014; 5(1): 4708. doi: 10.1038/ ncomms5708
Bai Y, Sun Q. Fine particulate matter air pollution and athero-Systematic Review | Volume 7 | Issue 1| Talbott EO, et al sclerosis: Mechanistic insights. Biochim Biophys Acta. 2016; 1860(12): 2863-2868. doi: 10.1016/j.bbagen.2016.04.030
Toth PP. Subclinical atherosclerosis: What it is, what it means and what we can do about it. Int J Clin Pract. 2008; 62(8): 1246- 1254. doi: 10.1111/j.1742-1241.2008.01804.x
Budoff MJ, Achenbach S, Blumenthal RS, et al. Assessment of coronary artery disease by cardiac computed tomography: a scientific statement from the American Heart Association Com-mittee on Cardiovascular Imaging and Intervention, Council on Cardiovascular Radiology and Intervention, and Committee on C. Circulation. 2006; 114(16): 1761-1791. doi: 10.1161/CIRCULA-TIONAHA.106.178458
Otsuka F, Sakakura K, Yahagi K, Joner M, Virmani R. Has our understanding of calcification in human coronary atherosclerosis progressed? Arterioscler Thromb Vasc Biol. 2014; 34(4): 724-736. doi: 10.1161/ATVBAHA.113.302642
Stürzlinger H, Antony K, Pichlbauer E. Computed tomogra-phy for the measurement of coronary calcification in asymptom-atic risk patients. GMS Health Technol Assess. 2006; 2: Doc11.
Hamanaka RB, Mutlu GM. Particulate matter air pollution: effects on the cardiovascular system. Front Endocrinol (Lausanne). 2018; 9: 680. doi: 10.3389/fendo.2018.00680
Montiel-Dávalos A, de JesúsIbarra-Sánchez M, Ventura-Gal-legos JL, Alfaro-Moreno E, López-Marure R. Oxidative stress and apoptosis are induced in human endothelial cells exposed to ur-ban particulate matter. Toxicol in Vitro. 2010; 24(1): 135-141. doi: 10.1016/j.tiv.2009.08.004
Yang X, Feng L, Zhang Y, et al. Cytotoxicity induced by fine particulate matter (PM(2.5)) via mitochondria-mediated apoptosis pathway in human cardiomyocytes. Ecotoxicol Environ Saf. 2018; 161: 198-207. doi: 10.1016/j.ecoenv.2018.05.092
Mills NL, Donaldson K, Hadoke PW, et al. Adverse cardiovas-cular effects of air pollution. Nat Clin Pract Cardiovasc Med. 2009; 6(1): 36-44. doi: 10.1038/ncpcardio1399
Mori H, Torii S, Kutyna M, Sakamoto A, Finn AV, Virmani R. Coronary artery calcification and its progression: What does it really mean? JACC Cardiovasc Imaging. 2018; 11(1): 127-142. doi: 10.1016/j.jcmg.2017.10.012
Blaha MJ, Mortensen MB, Kianoush S, Tota-Maharaj R, Cainzos-Achirica M. Coronary artery calcium scoring: Is it time for a change in methodology? JACC Cardiovasc Imaging. 2017; 10(8): 923-937. doi: 10.1016/j.jcmg.2017.05.007
Akoumianakis I, Antoniades C. Impaired vascular redox sig-naling in the vascular complications of obesity and diabetes mel-litus. Antioxid Redox Signal. 2019; 30(3): 333-353. doi: 10.1089/ ars.2017.7421
Rao X, Zhong J, Brook RD, Rajagopalan S. Effect of particu-late matter air pollution on cardiovascular oxidative stress path-ways. Antioxid Redox Signal. 2018; 28(9): 797-818. doi: 10.1089/ ars.2017.7394
Antoniades C, Shirodaria C, Leeson P, et al. MTHFR 677 C>T Polymorphism reveals functional importance for 5-me-thyltetrahydrofolate, not homocysteine, in regulation of vascular redox state and endothelial function in human atherosclerosis. Circulation. 2009; 119(18): 2507-2515. doi: 10.1161/CIRCULA-TIONAHA.108.808675
Antoniades C, Shirodaria C, Warrick N, et al. 5-Methyltetra-hydrofolate rapidly improves endothelial function and decreases superoxide production in human vessels: Effects on vascular tet-rahydrobiopterin availability and endothelial nitric oxide synthase coupling. Circulation. 2006; 114(11): 1193-1201. doi: 10.1161/CIR-CULATIONAHA.106.612325
Shire JD, Marsh GM, Talbott EO, Sharma RK. Advances and current themes in occupational health and environmental public health surveillance. Annu Rev Public Health. 2011; 32: 109-132. doi: 10.1146/annurev-publhealth-082310-152811
U. S. Environmental Protection Agency (EPA). Outdoor Air Quality Data. https://www.epa.gov/outdoor-air-quality-data/air-data-basic-information. Accessed November 3, 2022
McMillan NJ, Holland DM, Morara M, Feng J. Combining nu-merical model output and particulate data using bayesian space-time modeling. Environmetrics. 2010; 21(1): 48-65. doi: 10.1002/ env.984
U.S. Centers for Disease Control and Prevention (CDC). Pub-lic Health Air Surveillance Evaluation (PHASE) Project. https:// www.cdc.gov/nceh/tracking/phase.htm. Accessed November 3,
Dabass A, Talbott EO, Venkat A, et al. Association of ex-posure to particulate matter (PM2.5) air pollution and biomark-ers of cardiovascular disease risk in adult NHANES Participants (2001-2008). Int J Hyg Environ Health. 2016; 219(3): 301-310. doi: 10.1016/j.ijheh.2015.12.002
Kerimray A, Azbanbayev E, Kenessov B, Plotitsyn P, Alim-bayeva D, Karaca F. Spatiotemporal variations and contributing factors of air pollutants in almaty, kazakhstan. Aerosol Air Qual Res. 2020; 20(6): 1340-1352. doi: 10.4209/aaqr.2019.09.0464
Cressie NA. Statistics for spatial data. In: Statistics for Spa-tial Data. NY, USA: John Wiley & Sons Ltd; 1993: 1-26. doi: 10.1002/9781119115151.ch1
Slawsky E, Ward-Caviness CK, Neas L, et al. Evaluation of PM(2.5) air pollution sources and cardiovascular health. Environ Epidemiol. 2021; 5(3): e157. doi: 10.1097/EE9.0000000000000157
Di Q, Koutrakis P, Schwartz J. A hybrid prediction model for PM2.5 mass and components using a chemical transport model and land use regression. Atmos Environ. 2016; 131: 390-399. doi: doi: 10.1016/j.atmosenv.2016.02.002
Benjamin EJ, Muntner P, Alonso A, et al. Heart disease and stroke statistics-2019 update: A report from the American Heart Associa-tion. Circulation. 2019; 139. doi: 10.1161/CIR.0000000000000659
Dai W, Ming W, Li Y, et al. Synergistic effect of a physiological ratio of estradiol and testosterone in the treatment of early-stage atherosclerosis. Arch Med Res. 2015; 46(8): 619-629. doi: 10.1016/j. arcmed.2015.11.003
El Khoudary SR, Wildman RP, Matthews K, Thurston RC, Bromberger JT, Sutton-Tyrrell K. Progression rates of carotid intima-media thickness and adventitial diameter during the meno-pausal transition. Menopause. 2013; 20(1): 8-14. doi: 10.1097/ gme.0b013e3182611787
Duan C, Talbott EO, Broadwin R, et al. Residential exposure to PM2.5 and ozone and progression of subclinical atherosclero-sis among women transitioning through menopause: The study of women’s health across the nation. J Women’s Heal. 2019; 1-10. doi: 10.1089/jwh.2018.7182
Bell G, Mora S, Greenland P, Tsai M, Gill E, Kaufman JD. As-sociation of air pollution exposures with high-density lipoprotein cholesterol and particle number: The multi-ethnic study of ath-erosclerosis. Arterioscler Thromb Vasc Biol. 2017; 37(5): 976-982. doi: 10.1161/ATVBAHA.116.308193
Tepper PG, Randolph Jr, JF, McConnell DS, et al. Trajectory clustering of estradiol and follicle-stimulating hormone during the menopausal transition among women in the Study of Women’s Health across the Nation (SWAN). J Clin Endocrinol Metab. 2012; 97(8): 2872-2880. doi: 10.1210/jc.2012-1422
Matthews KA, Crawford SL, Chae CU, et al. Are changes in cardiovascular disease risk factors in midlife women due to chron-ological aging or to the menopausal transition? J Am Coll Cardiol. 2009; 54(25): 2366-2373. doi: 10.1016/j.jacc.2009.10.009
Mendelsohn, M. E, Karas, R. H. The protective effects of es-trogen on the cardiovascular system. N Engl J Med. 1999; 340(23): 1801-1811. doi: 10.1056/NEJM199906103402306
Christensen A, Pike CJ. Menopause, obesity and inflammation: Interactive risk factors for alzheimer’s disease. Front Aging Neurosci. 2015; 7: 130. doi: 10.3389/fnagi.2015.00130
Wang M, Hou Z, Xu H, et al. Association of estimated long-term exposure to air pollution and traffic proximity with a marker for coronary atherosclerosis in a nationwide study in China. JAMA Netw Open. 2019; 2(6): 1-13. doi: 10.1001/jamanet-workopen.2019.6553
Kim SY, Sheppard L, Kaufman JD, et al. Individual-level con-centrations of fine particulate matter chemical components and subclinical atherosclerosis: A cross-sectional analysis based on 2 advanced exposure prediction models in the multi-ethnic study of atherosclerosis. Am J Epidemiol. 2014; 180(7): 718-728. doi: 10.1093/aje/kwu186
Kaufman JD, Adar SD, Barr RG, et al. Association between air pollution and coronary artery calcification within six metropolitan areas in the usa (the multi-ethnic study of atherosclerosis and air pollution): A longitudinal cohort study. Lancet. 2016; 388(10045): 696-704. doi: 10.1016/S0140-6736(16)00378-0
Hoffmann B, Moebus S, Möhlenkamp S, et al. residential exposure to traffic is associated with coronary atherosclerosis.Circulation. 2007; 116(5): 489-496. doi: 10.1161/CIRCULATIONAHA.107.693622
Diez Roux AV, Auchincloss AH, Franklin TG, et al. Long-term exposure to ambient particulate matter and prevalence of subclini-cal atherosclerosis in the multi-ethnic study of atherosclerosis. Am J Epidemiol. 2008; 167(6): 667-675. doi: 10.1093/aje/kwm359
Dorans KS, Wilker EH, Li W, et al. Residential proximity to major roads, exposure to fine particulate matter, and coronary ar-tery calcium. Arterioscler Thromb Vasc Biol. 2016; 36(8); 1679-1685. doi: 10.1161/ATVBAHA.116.307141
Sun M, Kaufman JD, Kim SY, et al. Particulate matter components and subclinical atherosclerosis: Common approaches to estimating exposure in a multi-ethnic study of atherosclerosis cross-sectional study. Environ Health. 2013; 12: 39. doi: 10.1186/1476-069X-12-39
Adar SD, Sheppard L, Vedal S, et al. Fine particulate air pol-lution and the progression of carotid intima-medial thickness: a prospective cohort study from the multi-ethnic study of athero-sclerosis and air pollution. PLoS Med. 2013; 10(4): e1001430. doi: 10.1371/journal.pmed.1001430
Künzli N, Jerrett M, Mack WJ, et al. Ambient air pollution and atherosclerosis in los angeles. Environ Health Perspect. 2005; 113(2): 201-206. doi: 10.1289/ehp.7523
Hennig F, Geisel MH, Kälsch H, et al. Air pollution and pro-gression of atherosclerosis in different vessel beds—results from a prospective cohort study in the Ruhr Area, Germany. Environ Health Perspect. 2020; 128(10): 1-9. doi: 10.1289/EHP7077
Erbel R, Eisele L, Moebus S, et al. Die Heinz nixdorf recall studie. Bundesgesundheitsblatt Gesundheitsforschung Gesundheitsschutz. 2012; 55(6): 809-815. doi: 10.1007/s00103-012-1490-7
Tsao CW, Vasan RS. Cohort Profile: The Framingham Heart Study (FHS): Overview of milestones in cardiovascular epidemi-ology. Int J Epidemiol. 2015; 44(6): 1800-1813. doi: 10.1093/ije/ dyv337
Hennig F, Guntert B, Steinmuller C, et al. Are air pollution and traffic noise independently associated with atherosclerosis: The heinz nixdorf recall study. Eur Heart J. 2013; 35(13): 853-860. doi: 10.1093/eurheartj/eht426 Systematic Review | Volume 7 | Issue 1| Talbott EO, et al
Bergen S, Sheppard L, Sampson PD, et al. A National Predic-tion Model for PM2.5 component exposures and measurement er-ror-corrected health effect inference. Environ Health Perspect. 2013; 121(9): 1017-1025. doi: 10.1289/ehp.1206010
Kim SY, Sheppard L, Bergen S, et al. Prediction of fine particu-late matter chemical components with a spatio-temporal model for the multi-ethnic study of atherosclerosis cohort. J Expo Sci Environ Epidemiol. 2016; 26(5), 520-528. doi: 10.1038/jes.2016.29
Künzli N, Jerrett M, Garcia-Esteban R, et al. Ambient air pol-lution and the progression of atherosclerosis in adults. PLoS One. 2010; 5(2): e9096. doi: 10.1371/journal.pone.0009096
Bauer M, Moebus S, Mhlenkamp S, et al. Urban particulate matter air pollution is associated with subclinical atherosclerosis: results from the HNR (Heinz Nixdorf Recall) study. J Am Coll Cardiol. 2010; 56(22): 1803-1808. doi: 10.1016/j.jacc.2010.04.065
Sutton-Tyrrell K, Kuller LH, Meilahn E, Matthews KA, Bunker C, Lassila HC. Carotid atherosclerosis in premenopausal and post-menopausal women and its association with risk factors measured after menopause. Stroke. 1988; 29(6): 1116-1121. doi: 10.1161/01. str.29.6.1116
Green R, Broadwin R, Malig B, et al. Long- and short-term exposure to air pollution and inflammatory/hemostatic markers in midlife women. Epidemiology. 2016; 27(2): 211-220. doi: 10.1097/ EDE.0000000000000421
Wu X, Basu R, Malig B, et al. Association between gaseous air pollutants and inflammatory, hemostatic and lipid markers in a cohort of midlife women. Environ Int. 2017; 107(2): 131-139. doi: 10.1016/j.envint.2017.07.004
Hu FB, Grodstein F, Hennekens CH, et al. Age at natural menopause and risk of cardiovascular disease. Arch Intern Med. 1999; 159(10): 1061-1066.
Cabrera-Rego JO, Navarro-Despaigne D, Staroushik-Morel L, Diaz-Reyes K, Lima-Martinez MM, Iacobellis G. Association be-tween endothelial dysfunction, epicardial fat and subclinical ath-erosclerosis during menopause. Clin Investig Arterioscler. 2018; 30(1): 21-27. doi: 10.1016/j.arteri.2017.07.006
Ostro B, Malig B, Broadwin R, et al. Chronic PM2.5 exposure and inflammation: Determining sensitive subgroups in mid-life women. Environ Res. 2014; 132(510): 168-175. doi: 10.1016/j.en-vres.2014.03.042
Röhrl C, Stangl H. Cholesterol metabolism-physiological regu-lation and pathophysiological deregulation by the endoplasmic reticulum. Wien Med Wochenschr. 2018; 168(11-12): 280-285. doi: 10.1007/s10354-018-0626-2
Ley SH, Li Y, Tobias DK, et al. Duration of reproductive life span, age at menarche, and age at menopause are associated with risk of cardiovascular disease in women. J Am Heart Assoc. 2017; 6(11): e006713. doi: 10.1161/JAHA.117.006713
El Khoudary SR, Santoro N, Chen HY, et al. Trajectories of es-tradiol and follicle-stimulating hormone over the menopause tran-sition and early markers of atherosclerosis after menopause. Eur J Prev Cardiol. 2016; 23(7): 694-703. doi: 10.1177/2047487315607044 Submit your article to this journal | https://openventio.org/submit-manuscript/
El Khoudary SR, Wildman RP, Matthews K, Thurston RC, Bromberger JT, Sutton-Tyrrell K. Endogenous sex hormones impact the progression of subclinical atherosclerosis in women during the menopausal transition. Atherosclerosis. 2012; 225(1): 180- 186. doi: 10.1016/j.atherosclerosis.2012.07.025
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