Pb exposure is a well-known risk factor for inflammation including vessels. In our study, we aimed to investigate the relationship between Pb levels of exposed workers and the severity of inflammation/endothelial dysfunction. We analyzed the correlation between blood lead level and the markers of endothelial damage. There was a significant correlation between blood lead levels and vascular cell adhesion molecule-1 (VCAM-1). Elevated levels of blood lead also show correlation with soluble CD40 ligand (sCD40L). The strongest correlation was with sE-selectin. Association between lead exposure and markers of cardiovascular injury may help to predict cardiovascular effects of lead earlier and to protect workers who are exposed to lead.
___
1. Yusuf S, Ounpuu S. Tackling the growing burden of atherosclerotic cardiovascular diseases. Eur J Cardiovasc Prev Rehabil. 2003;10:236-9.
2. Kim H, Kim S, Han S, et al. Prevalence and incidence of atherosclerotic cardiovascular disease and its risk factors in Korea: a natiowide populationbased study. BMC Pub Health. 2019;19:1112.
3. Amer MS, Khater MS, Omar OH, et al. Association between Framingham score and subclinical atherosclerosis among elderly with both type 2 diabetes mellitus and healthy subjects. Am J Cardiovasc Dis. 2014;4:14-9.
4. Arsenault J, Rana JS, Lemieux I, et al. Physical activity, the Framingham risk score and risk of coronary heart diseases in men and women of the EPIC-Norfolk study. Atherosclerosis. 2010;209:261-5.
5. Ji X, Leng X, Dong Y, et al. Modifiable risk factors for carotid atherosclerosis: a meta-analysis and systematic review. Ann Transl Med. 2019;7:632.
6. Bress AP, Colantonio LD, Booth JN, et al. Modifiable risk factors versus age on developing high predicted cardiovascular disease risk in blacks. J Am Heart Assoc. 2017;6:pii:e005054.
7. Stefanidis C, Antoniou CK, Tsiachris D, et al. Coronary atherosclerotic vulnerable plaque: Current perspectives. 2017;6:e005543.
8. Nakagawa K, Nakashima Y. Pathological intimal thickening in human atherosclerosis is formed by extracellular accumulation of plasma-derived lipids and dispersion of intimal smooth muscle cells. Atherosclerosis. 2018;274:235-42.
9. Back M, Yurdagul A, Tabas I, et al. Inflammation and its resolution in atherosclerosis: mediators and therapeutic opportunities. Nar Rev Cardiol. 2019;16:389-406.
10. Hicken MT, Adar SD, Hajat A, et al. Air pollution, cardiovascular outcomes, and social disadvantage: The Multiethnic Study of Atherosclerosis. Epidemiology. 2016;27:42-50.
11. Asgary S, Movahedian A, Keshvari M, et al. Serum levels of lead, mercury and cadmium in relation to coronary artery disease in the elderly: A crosssectional study. Chemosphere. 2017;180:540-4.
12. Barry V, Steenland K. Lead exposure and mortality among US workers in a surveillance program: Results from 100 additional years of follow-up. Environ Res. 2019;177:108625.
13. Hwang SJ, Ballantyne CM, Sharrett AR, et al. Circulating adhesion molecules VCAM-1, ICAM-1 and E-selectin in carotid atherosclerosis and incident coronary heart diseases cases: The Atherosclerosis Risk in Communities (ARIC) study. Circulation. 1997;96:4219-25.
14. Peter K, Weirich U, Nordt TK, et al. Soluble vascular cell adhesion molecule-1 (VCAM-1) as potential marker of atherosclerosis. 1999;81:38- 43.
15. Ponthieux A, Herbeth B, Droesch S, et al. Biological determinants of serum ICAM-1, E-selectin and L-selectin levels in health subjects: the Stanislas study. Atherosclerosis. 2004;172:299-308.
16. Blaha M, Kresjek J, Blaha V, et al. Selectins and monocyte chemotactic peptides as the markers of atherosclerosis activity. Physiol Res. 2004;53:273-8.
17. Cockerill GW, Huehns TY, Weerasinghe A, et al. Elevation of plasma highdensity lipoprotein concentration reduces interleukin-1-induced expression of E-selectin in an in vivo model of acute inflammation. Circulation. 2001;103:108-12.
18. Antczak AJ, Singh N, Gay SR, et al. IgG-complex stimulated platelets: source of sCD40L and RANTES in initiation of inflammatory cascade. Cell Immunol. 2010;263:129-33.
19. Prasad KS, Andre P, He M, et al. Soluble CD40L ligand induces beta3 integrin tyrosine phosphorylation and triggers platelet activation by outside-in signalling. Proc Natl Acad USA. 2003;100:12367-71.
20. Pankiw-Bembenek O, Zalewksi J, Goralczyk T, et al. A history of early stent thrombosis is associated with prolonged clot lysis time. Thromb Haemost. 2012;170:513-20.
21. Hu H, Pepper L, Goldman R. Effect of repeated occupational exposure to lead, cessation of exposure, and chelation on levels of lead in bone. Am J Ind Med. 1991;20:723-35.
22. Slupsky JR, Kalbas M, Willuweit A, et al. Activated platelets induce tissue factor expression on human umbilical vein endothelial cells by ligation of CD40. Thromb Haemost. 1998;80:1008-14.
23. Songdei N, Winters PC, McCabe MJ Jr, et al. A population-based assessment of blood lead levels in relation to inflammation. Environ Res. 2010;110:272-7.
24. Navas-Acien A, Gallar E, Silbergelg EK, et al. Lead exposure and cardiovascular disease – A systematic review. Environ Health Perspect. 2007;115:472-82.
25. Metrka, E. Lead (Pb) exposure enhances expression of factors associated with inflammation. Int J Mol Scie. 2018;19:1813.
26. Chowdry R, Ramond A, O’Keefe LM, et al. Environmental toxic metal contaminants and risk of cardiovascular disease: systematic review and meta-analysis. BMJ. 2018;362:k3310.
27. Gergei I, Kalsch T, Scharnagl H, et al. Association of soluble CD40L with short-term and long-term cardiovascular and all-cause mortality: The Ludwigshafen Risk and Cardiovascular Health and all-cause mortality. Atherosclerosis. 2019;291:127-31.