Abstract
Background: Exposure to different levels of lead (Pb) has been demonstrated to elicit varied degrees of pathogenicity in animal models. But this is yet to be demonstrated in human beings. The present study determined the levels serum Pb, immunoglobulin classes, total plasma peroxide, nitric oxide and C-reactive protein in three groups of professionals exposed to different levels of lead.
Methods: Thirty–eight Pb-exposed workers, including 18 battery chargers (BC), 10 spray painters (SP) and 10 mechanics (MC) volunteered to participate in this study. Fifteen apparently healthy health workers of University College Hospital, Ibadan, Nigeria, served as controls. Serum levels of immunoglobulins G,M,A (IgG, IgM and IgA respectively) and C-reactive protein (CRP) were determined using single radial immunodiffusion techniques, Pb was determined using atomic absorption spectrophotometry technique, while total plasma peroxides (TPP) and nitric oxide (NO) were determined using spectrophotometry methods in the study groups (BC, SP and MC) and controls.
Results: The study shows significantly (p<0.05) higher levels of Pb in the BC and SP (BC> SP) compared with the controls. The mean levels of serum TPP was significantly (p<0.05) higher in BC, SP and MC compared with the controls. Significantly (p<0.05) lower levels of IgM were observed in BC, SP and MC compared with the controls. The serum levels of IgG was significantly (p<0.05) lower in BC and SP (BC< SP) but not in MC (p>0.05) when compared with the controls. There were no significant (p>0.05) differences in the levels of IgA in BC, SP and MC compared with the controls. Also, there were no significant (p>0.05) differences in the serum levels of NO observed in BC, SP and MC compared with the controls. But the mean levels of CRP were significantly (p<0.05) higher in BC, SP and MC (BC> SP> MC) compared with the controls. Significant (p<0.05) correlations were observed between serum Pb and IgG in BC (r= -0.50, p = 0.04) and between serum Pb and IgM in MC (r=-0.85, p=0.002).
Conclusion: It could be concluded in this study that the nature of a profession determines the level of Pb in the exposed workers. Oxidative stress and inflammation are possible consequences of Pb exposures, while the toxicity effects of Pb on serum IgG and IgM may depend on the levels of Pb exposures.
Keywords: lead-exposures, immunoglobulin classes, oxidative stress, CRP.
Résumé
Contexte: Il a été démontré que l’exposition à différents niveaux de plomb (Pb) induit divers degrés de pathogénicité dans des modèles animaux. Mais cela n’a pas encore été démontré chez les êtres humains. La présente étude a déterminé les niveaux de Pb sérique, les classes d’immunoglobulines, le peroxyde de plasma total, l’oxyde nitrique et la protéine C-réactive dans trois groupes de professionnels exposés à différents niveaux de plomb.
Méthodes: Trente-huit travailleurs exposés au plomb, dont 18 chargeurs de batterie (BC), 10 peintres en aérosol (SP) et 10 mécaniciens (MC) se sont portés volontaires pour participer à cette étude. Quinze agents de santé apparemment en bonne santé du Collège Hospitalier Universitaire, Ibadan, Nigéria, ont servi de témoins. Les taux sériques d’immunoglobulines G, M, A (IgG, IgM et IgA respectivement) et de protéine C-réactive (CRP) ont été déterminés à l’aide de techniques d’immunodiffusion radiale unique, le Pb a été déterminé en utilisant la technique de spectrophotométrie d’absorption atomique, tandis que les peroxydes de plasma totaux (TPP) et l’oxyde nitrique (NO) ont été déterminés à l’aide de méthodes de spectrophotométrie dans les groupes d’étude (BC, SP et MC) et les témoins.
Résultats: L’étude montre des niveaux significativement plus élevés (p <0,05) de Pb dans BC et SP (BC>SP) par rapport aux témoins. Les niveaux moyens de TPP sérique étaient significativement (p <0,05) plus élevés dans BC, SP et MC par rapport aux témoins. Des taux d’IgM significativement plus faibles (p <0,05) ont été observés dans BC, SP et MC par rapport aux témoins. Les taux sériques d’IgG étaient significativement (p <0,05) plus faibles dans BC et SP (BC <SP) mais pas en MC (p> 0,05) par rapport aux témoins. Il n’y avait pas de différences significatives (p> 0,05) dans les niveaux d’IgA dans BC, SP et MC par rapport aux témoins. De plus, il n’y avait pas de différences significatives (p> 0,05) dans les taux sériques de NO observés dans BC, SP et MC par rapport aux témoins. Mais les niveaux moyens de CRP étaient significativement (p <0,05) plus élevés dans BC, SP et MC (BC> SP> MC) par rapport aux témoins. Des corrélations significatives (p <0,05) ont été observées entre Pb sérique et IgG dans BC (r = -0,50, p = 0,04) et entre Pb sérique et IgM dans MC (r = -0,85, p = 0,002).
Conclusion: On pourrait conclure dans cette étude que la nature d’une profession détermine le niveau de Pb chez les travailleurs exposés. Le stress oxydatif et l’inflammation sont des conséquences possibles des expositions au Pb, tandis que les effets de toxicité du Pb sur les IgG et IgM sériques peuvent dépendre des niveaux d’exposition au Pb.
Mots clés: Expositions au plomb, classes d’immunoglobulines, stress oxydatif, CRP.
Correspondendence: Dr. M.O. Akiibinu, Department of Biochemistry and Chemistry, Caleb University, Lagos. Nigeria. Email: akiibinumoses@yahoo.com
References
The National Academy Press. In the book: Improving Health in the community: A role for performance monitoring, 5th edition, chapter A4: Environmental and Occupational lead poisoning (2019).
DeCicco JM. and Kliesch J. ACEEE’s Green Book: The Environmental guide to Cars and Trucks.
Environmental Protection Authority (EPA), Victoria (2019). Lead exposure and your health. 1, USA.
WHO Fact sheets on Lead poisoning and Lead (2018).
Gilian SR, Zaidi SR, Batool M, Bhatti DA and Mahmood J. Report on CNS: toxicity caused by metal poisoning. Pakistan Journal of Pharmaceutical Sciences, 2015; 28 (4), 1417-1423.
Falk H. Internatiuonal environmental health for the pediatrician: Case study of lead poisoning. Pediatrics. 2003;112:259-264.
Fewtrell LJ, Prüss-Ustün A, Landrigan P and Ayuso-Mateos JL. Estimating the global burden of disease of mild mental retardation and cardiovascular diseases from environmental lead exposure. Environ Res. 2004;94: 120-133.
Gao D, Mondal TK and Lawrence DA. Lead effects on development and function of bone marrow-derived dentritic cells promote Th2 immune responses. Toxicol Appl Pharmacol. 2007; 222(1): 69-79.
Shafiq-ur-Rehman S. Lead-induced regional lipid peroxidation in brain. ToxicolLett 1984; 21: 333-337
Garcia-Arenas G, Claudio L, Perez-Severiano F and Rios C. Lead acetate exposure inhibits nitric oxide synthase activity in capillary and synaptosomal fractions of mouse brain. Life Sciences & Medicine & Toxicological Sciences. 1999 Aug;50(2):244-248
Vaziri ND and Sica DA. Lead-induced hypertension: role of oxidative stress. Curr Hypertens Rep. 2004; 6: 314-320.
Michael JK and Charles EB, In basic and clinical pharmacology. Seventh edition. Appleton and Lange Stanford Connecticut; 1998, pg 956.
Khalil-Manesh F, Gonick HC, Cohen AH, et al. Experimental model of lead nephropathy. I. Continuous high-dose lead administration . Kidney Int. 1992;41(5):1192.
Gelman BB. Michaelson IA and Bus JS. The effect of lead on Oxidative haemolysis and erythrocyte defence mechanisms in the rat. Toxicol. Appl. Pharmacol. 1978; 45: 199-129.
Lawrence DA, and MCCabe MJ Jr. Immunomodulation by metals. Int Immunopharmacol. 2002; 2(2-3):293-302.
Vaziri ND, Oveisi F and Ding Y. Role of increased oxygen free radical activity in the pathogenesis of uremic hypertension. Kidney Int 1998; 53: 1748-1754.
Ercal N, Gurer-Orhan H, and Aykin-Burns N. Toxic metals and oxidative stress. Part 1. Mechanisms involved in metal-induced oxidative damage. Curr Top Med Chem 2001;1:529-539
Albert E. Sobel H and Yuska DD. Peters, and Benjamin Kramer. The Biochemical Behavior of Lead. Nutrition Classics, The Journal of Biological Chemistry, 1940; 132: 239-265.
Dietart RR and Piepenbrink MS. Lead and immune function. Crit Rev Toxicol. 2006; 36(4): 359-385.
Salimonu LS, Ladipo AO, Adeniran SO and Osunkoya BO. Serum immunoglobulin levels in normal premature newborns and their mothers. Intl J. Gynaecol. Obstet. 1978. 16:119-123.
Wanchu A, Khullar M, Bhatnagar A, et al. Pentoxiphylline Reduces Nitric Oxide Production among Patients with HIV Infection. Immunology Letters. 2000;74:121-5.
Harma M. Harma M. and Enel O. Increased oxidative stress in patients with hydatidiform mole. Swiss Med. Wkly,2003;133:563-566.
Kenako J.J. Clin. Biochem of Animal 4th edition. Kenako JJ editor Academic press Inc. New York 1999; pp. 932.
Thomas PM. Trace metals. In the Tietz textbook of clinical chemistry. 3rd editionNB Saunders Co. Philadelphia; 1999. 982-998.
David E.J, Robert P. Clickner JY. et al. The prevalence of Lead-Based Paint Hazrds in U.S. Housing. Environmental Health Perspectives. 2002. 110;10.
Mielke HW and Reagan PL. Soil is an important pathway of human exposure. Environ Health Perspect. 1998;106 Suppl 1;217-29.
Stroop DM, Dietrich KN, Hunt AN, et al. Lead-based paint health risk assessment in dependent children living in military housing. Public Health Rep.Public Health Rep. 2002;117(5);446-52
Jacobs DE.; Clickner RP.; Zhou JY. et al. “The prevalence of lead-based paint hazardsmin U.S . housing”. Environmental Health Perspectives 2002; 110 (10): A599-606.
Arinola OG. and Akiibinu MO. The levels of antioxidants and some trace metals in Nigerians that are occupationally exposed to chemicals. Indian Journal of Occupational and Environmental Medicine. 2006; 10:60-63.
Kitman, J. “The Secret History of Lead. The Nation. Retrieved. 2000; 8-17-2009.
Geoffrey Lean. “ UN hails green triumph as leaded petrol is banned throughout Africa”. The Independent. 2006.
Ribarov SR and Benov LC. Relationship between the hemolytic action of heavy metals and lipid peroxidation. Biochim Biophys Acta 1981;640:721-726.
Ghaffari S. oxidative stress in the regulation of normal and neoplastic hematopoiesis. Antioxidant and redox signaling 2008; 10 (11) 1923-1940.
Miller T.E., Golemboski K.A., Ha R.S., et al. Developmental exposure to lead cause persistent immunotoxicity in Fischer 344 rats. Toxicology Science. 1998; 42(2): 129-35.
Heo Y, Parsons PJ and Lawrence DA. Lead differentially modifies cytokine production in vitro and in vivo. Toxicol Appl Pharmacol. 1996;138(1): 149-145.
Ercal N, Rachel N P, Treeratphan PM. et al. . “A role for oxidative stress in suppressing serum immunoglobin levels in lead-exposed Fisher 344 rats”, Archives Environmemtal Contamination Toxicology, 2000; 39: 2: 251-256.
Dardenne M. Zinc and immue function. Eur J Clin Nutr. 2002;56 Suppl 3:S20-3.
Faith RE, Luster MI and Kimmel CA. Effect of chronic developmental lead exposure on cell-mediated immune functions. Clin Exp Immunol. 1979; 35(3): 413-420.
White J.M and Harvery DR. Defective synthesis of alpha – and beta – globin chains in lead poisoning. Nature (Lond). 1972;236,71-73.
McCabe MJ Jr and Lawrence DA. Lead, a major environmental pollutant, is immunomodulatory by its differential effects on CD4+ T cells subsets. Toxicol Appl Pharmacol. 1991; 111(1):13-23.
Sarasua SM, Vogt RF, Henderson LO, Jones PA and Lybarger JA. Serum immunoglobulins and lymphocyte subset distributions in children and adults living in communities assessed for lead and cadmium exposure. J Toxicol Environ Health A. 2000; 12; 60(1): 1-15.
Halliwell B. What nitrates tyrosine? Is nitrotyrosine specific as a biomarker of peroxynitrate formation in vivo? FEBS Lett 1997; 411:157-160.
Quinn MR and Harris CL. Lead inhibits Ca2+-stimulated nitric oxide synthase activity from rat cerebellum. Neurosci Lett. 1995;196:65-68.
Blazka ME, Harry GJ and Luster MI. Effect of lead acetate on nitrite production by murine brain endothelial cell cultures. Toxicol Appl Pharmacol. 1994;126:191-194.
Harvey C. Gonick; Yaoxian Ding; Steven C. Bondy; Zhenmin Nil; ; Nosratola D. Vaziri. Lead-Induced Hypertension. 1997; 30: 1487-1492
Gabay C and Kushner I. Acute-phase proteins and systematic responses to inflammation. N Engl J Med. 1999; 340: 448-454.
Yiangou M and Papaconstantinou J. The differential induction of alpha 1-acid glycoprotein and serum amyloid A genes by heavy metals. Biophys Acta. 1993: 19;1174(2): 123-32.
Ross R. The pathogenesis of atherosclerosis: a perspective for the 1990s. Nature. 1993; 362:801-809.