Impaired endothelial function assessed by flow-mediated vasodilatation in workers occupationally exposed to lead

Environmental Toxicology and Pharmacology

Volumn 29, Issue 3, 2010, Pages 266-270

  Poreba, Rafał ^a   Poreba, Małgorzata ^a   Gać, Paweł ^a   Pilecki, Witold ^a   Andrzejak, Ryszard ^a  

^a WROCLAW MEDICAL UNIVERSITY   (Poland)

Author keywords

Endothelium; Flow mediated dilation; Lead; Occupational exposition

Indexed keywords

LEAD;

ADULT; ARTERY DIAMETER; ARTERY INTIMA; ARTICLE; BLOOD SAMPLING; BRACHIAL ARTERY; CLINICAL ARTICLE; CONTROLLED STUDY; ENDOTHELIAL DYSFUNCTION; HUMAN; ISCHEMIA; MALE; METAL INDUSTRY; OCCUPATIONAL EXPOSURE; PRIORITY JOURNAL; SMELTER; STATISTICAL ANALYSIS; VASODILATATION;

EID: 77951977343     PISSN: 13826689     EISSN: None     Source Type: Journal    
DOI: 10.1016/j.etap.2010.03.001     Document Type: Article

References (48)

1. Anderson T.J. Prognostic significance of brachial flow-mediated vasodilation. Circulation 2007, 115:2373-2375.
2. Andrzejak R., Poreba R., Derkacz A. Effect of chronic lead poisoning on the parameters of heart rate variability. Med. Pr. 2004, 55:139-144.
3. Asselbergs F.W., van der Harst P., Jessurun G.A., Tio R.A., van Gilst W.H. Clinical impact of vasomotor function assessment and the role of ACE-inhibitors and statins. Vasc. Pharmacol. 2005, 42:125-140.
4. Bhatnagar A. Environmental cardiology: studying mechanistic links between pollution and heart disease. Circ. Res. 2006, 99:692-705.
5. Cardenas A., Roels H., Bernard A.M., et al. Markers of early renal changes induced by industrial pollutants. II. Application to workers exposed to lead. Br. J. Ind. Med. 1993, 50:28-36.
6. Carmignani M., Boscolo P., Poma A., Volpe A.R. Kininergic system and arterial hypertension following chronic exposure to inorganic lead. Immunopharmacology 1999, 44:105-110.
7. Celermajer D.S., Sorensen K.E., Georgakopoulos D., et al. Cigarette smoking is associated with dose-related and potentially reversible impairment of endothelium-dependent dilation in healthy young adults. Circulation 1993, 88:2149-2155.
8. Celermajer D.S., Sorensen K.E., Gooch V.M., et al. Non-invasive detection of endothelial dysfunction in children and adults at risk of atherosclerosis. Lancet 1992, 340:1111-1115.
9. Chang H.R., Chen S.S., Chen T.J., Ho C.K., Chiang H.C., Yu H.S. Lymphocyte β2-adrenergic receptors and plasma catecholamine levels in lead-exposed workers. Toxicol. Appl. Pharmacol. 1996, 139:1-5.
10. Cheng Y., Schwartz J., Vokonas P.S., Weiss S.T., Aro A., Hu H. Electrocardiographic conduction disturbances in association with low-level lead exposure (the normative aging study). Am. J. Cardiol. 1998, 82:594-599.
11. Corretti M.C., Anderson T.J., Benjamin E.J., et al. International brachial artery reactivity task force. Guidelines for the ultrasound assessment of endothelial-dependent flow-mediated vasodilatation of the brachial artery: a report of the International Brachial Artery Reactivity Task Force. J. Am. Coll. Cardiol. 2002, 39:257-265.
12. Ding Y., Vaziri N.D., Gonick H.C. Lead-induced hypertension. II. Response to sequential infusions of l-arginine, superoxide dismutase, and nitroprusside. Environ. Res. 1998, 76:107-113.
13. Dorman R.V., Freeman E.J. Lead-dependent effects on arachidonic acid accumulation and the proliferation of vascular smooth muscle. J. Biochem. Mol. Toxicol. 2002, 16:245-253.
14. Dursun N., Arifoglu C., Süer C., Keskinol L. Blood pressure relationship to nitric oxide, lipid peroxidation, renal function, and renal blood flow in rats exposed to low lead levels. Biol. Trace Elem. Res. 2005, 104:141-150.
15. Fischbein A., Luo J.C., Solomon S.J., Horowitz S., Hailoo W., Miller A. Clinical findings among hard metal workers. Br. J. Ind. Med. 1992, 49:17-24.
16. Fujiwara Y., Kaji T. Possible mechanism for lead inhibition of vascular endothelial cell proliferation: a lower response to basic fibroblast growth factor through inhibition of heparin sulfate synthesis. Toxicology 1999, 133:147-157.
17. Gonick H.C., Ding Y., Bondy S.C., Ni Z., Vaziri N.D. Lead-induced hypertension: interplay of nitric oxide and reactive oxygen species. Hypertension 1997, 30:1487-1492.
18. Harris R.A., Padilla J., Hanlon K.P., et al. The flow-mediated dilation response to acute exercise in overweight active and inactive men. Obesity 2008, 16:578-584.
19. 2+ in calmodulin. Arch. Toxicol. 1983, 54:61-70.
20. Hertz-Picciotto I., Croft J. Review of the relation between blood lead and blood pressure. Epidemiol. Rev. 1993, 15:352-373.
21. Hotter G., Fels L.M., Closa D., Roselló J., Stolte H., Gelpí E. Altered levels of urinary prostanoids in lead-exposed workers. Toxicol. Lett. 1995, 77:309-312.
22. Karatzis E.N., Ikonomidis I., Vamvakou G.D., et al. Long-term prognostic role of flow-mediated dilatation of the brachial artery after acute coronary syndromes without ST elevation. Am. J. Cardiol. 2006, 98:1424-1428.
23. Karpoff L., Vinet A., Schuster I., et al. Abnormal vascular reactivity at rest and exercise in obese boys. Eur. J. Clin. Invest. 2009, 39:94-102.
24. Kasperczyk S., Przywara-Chowaniec B., Kasperczyk A., Rykaczewska-Czerwinska M., Wodniecki J., Birkner E. Function of heart muscle in people chronically exposed to lead. Ann. Agric. Environ. Med. 2005, 12:207-210.
25. Lustberg M., Silbergeld E. Blood lead levels and mortality. Arch. Intern. Med. 2002, 162:2443-2449.
26. Malvezzi C.K., Moreira E.G., Vassilieff I., Vassilieff V.S., Cordellini S. Effect of l-arginine, dimercaptosuccinic acid (DMSA) and the association of l-arginine and DMSA on tissue lead mobilization and blood pressure level in plumbism. Braz. J. Med. Biol. Res. 2001, 34:1341-1346.
27. Matsushima Y., Takase B., Uehata A., et al. Comparative predictive and diagnostic value of flow-mediated vasodilation in the brachial artery and intima media thickness of the carotid artery for assessment of coronary artery disease severity. Int. J. Cardiol. 2007, 117:165-172.
28. Menke A., Muntner P., Batuman V., Silbergeld E.K., Guallar E. Blood lead below 0.48micromol/L (10microg/dL) and mortality among US adults. Circulation 2006, 114:1388-1394.
29. Navas-Acien A., Guallar E., Silbergeld E.K., Rothenberg S.J. Lead exposure and cardiovascular disease-a systematic review. Environ. Health Perspect. 2007, 115:472-482.
30. Navas-Acien A., Selvin E., Sharrett A.R., Calderon-Aranda E., Silbergeld E., Guallar E. Lead, cadmium, smoking, and increased risk of peripheral arterial disease. Circulation 2004, 109:3196-3201.
31. Nawrot T.S., Thijs L., Hond E.M., Roels H.A., Staessen J.A. An epidemiological re-appraisal of the association between blood pressure and blood lead: a meta-analysis. J. Hum. Hypertens. 2002, 16:123-131.
32. Niinuma Y., Sakai T., Yanagihara S., et al. A modified FEP (free erythrocyte protoporphyrin) test. Sangyo Igaku. 1981, 23:254-259.
33. Patrick L. Lead toxicity part II: the role of free radical damage and the use of antioxidants in the pathology and treatment of lead toxicity. Altern. Med. Rev. 2006, 11:114-127.
34. Piomelli S. A micromethod for free erythrocyte porphyrins: the FEP test. J. Lab. Clin. Med. 1973, 81:932-940.
35. Prentice R.C., Kopp S.J. Cardiotoxicity of lead at various perfusate calcium concentrations: functional and metabolic responses of the perfused rat heart. Toxicol. Appl. Pharmacol. 1985, 81:491-501.
36. Revis N.W., Zinsmeister A.R., Bull R. Atherosclerosis and hypertension induction by lead and cadmium ions: an effect prevented by calcium ion. Proc. Natl. Acad. Sci. U.S.A. 1981, 78:6494-6498.
37. Rodríguez-Iturbe B., Vaziri N.D., Herrera-Acosta J., Johnson R.J. Oxidative stress, renal infiltration of immune cells, and salt-sensitive hypertension: all for one and one for all. Am. J. Physiol. 2004, 286:F606-616.
38. Schober S.E., Mirel L.B., Graubard B.I., Brody D.J., Flegal K.M. Blood lead levels and death from all causes, cardiovascular disease, and cancer: results from the NHANES III mortality study. Environ. Health Perspect. 2006, 114:1538-1541.
39. Schwartz J. Lead, blood pressure, and cardiovascular disease in men and women. Environ. Health Perspect. 1991, 91:71-75.
40. Schwartz J. Lead, blood pressure, and cardiovascular disease in men. Arch. Environ. Health 1995, 50:31-37.
41. Sharp D.S., Becker C.E., Smith A.H. Chronic low-level lead exposure. Its role in the pathogenesis of hypertension. Med. Toxicol. 1987, 2:210-232.
42. Staessen J.A., Bulpitt C.J., et al. Hypertension caused by low-level lead exposure: myth or fact?. J. Cardiovasc. Risk 1994, 1:87-97.
43. Tanriverdi H., Evrengul H., Kuru O., et al. Cigarette smoking induced oxidative stress may impair endothelial function and coronary blood flow in angiographically normal coronary arteries. Circ. J. 2006, 70:593-599.
44. Vander A.J. Chronic effects of lead on the renin-angiotensin system. Environ. Health Perspect. 1998, 78:77-83.
45. Vaziri N.D., Ding Y., Ni Z. Compensatory up-regulation of nitric-oxide synthase isoforms in lead-induced hypertension; reversal by a superoxide dismutase-mimetic drug. J. Pharmacol. Exp. Ther. 2001, 298:679-685.
46. Victery W., Vander A.J., Shulak A.M. Lead hypertension and the renin-angiotensin system in rats. J. Lab. Clin. Med. 1982, 99:354-362.
47. Weinhold B. Environmental cardiology: getting to the heart of the matter. Environ Health Perspect. 2004, 112:A880-A887.
48. Yamamoto C., Miyamoto A., Sakamoto M., Kaji T., Kozuka H. Lead perturbs the regulation of spontaneous release of tissue plasminogen activator and plasminogen activator inhibitor-1 from vascular smooth muscle cells and fibroblasts in culture. Toxicology 1997, 117:153-161.