Matte TD

Idioma: Español
Referencias bibliográficas: 30
Paginas: 220-224
Archivo PDF: 79.99 Kb.

RESUMEN

El plomo es un elemento que no tiene ninguna función fisiológica conocida en los seres humanos, pero cuyos efectos adversos inciden sobre una diversidad de procesos bioquímicos esenciales. Existe evidencia considerable acerca de los efectos adversos sobre la salud de los niños del plomo en niveles que son comunes a distintas poblaciones en todo el mundo. La intoxicación aguda por plomo, que ocasiona encefalopatía, a pesar de no ser frecuente, sí pone en riesgo la vida y requiere de un tratamiento agresivo y oportuno. Es necesario tenerla presente en el diagnóstico diferencial de toda enfermedad no explicada que incluya anemia, convulsiones, letargo, dolor abdominal, o vómito recurrente. Existe una gran cantidad de niños que padecen los efectos subclínicos crónicos debidos a la exposición de bajo nivel al plomo, y que incluyen un desarrollo cognitivo deficiente, trastornos en la conducta, ligera deficiencia en la agudeza auditiva, y talla reducida. La evidencia disponible indica que las únicas intervenciones efectivas para evitar la intoxicación de bajo nivel por plomo son aquellas que se aplican para controlar la exposición a este metal.

REFERENCIAS (EN ESTE ARTÍCULO)

1. Patterson C, Ericson J, Manea-Krichten M, Shirahata H. Natural skeletal levels of lead in Homo sapiens sapiens uncontaminated by technological lead. Sci Total Environ 1991;107:205-236.

2. The National Academy of Sciences Committee on Measuring Lead in Critical Populations. Measuring lead exposure in infants children and other critical populations. Washington DC: National Academy Press, 1993.

3. Landrigan PJ, Carlson JE, Bearer CF, Cranmer JS, Bullard RD, Etzel RA et al. Children’s health and the environment: A new agenda for prevention research. Environ Health Perspect 1998;106 Suppl 3: 787-794.

4. Goering PL. Lead-protein interactions as a basis for lead toxicity. Neurotoxicology 1993;14:45-60.

5. Markovac J, Goldstein GW. Lead activates protein kinase C in immature rat brain microvessels. Toxicol Appl Pharmacol 1988;96:14-23.

6. Suzuki T. Protein kinases involved in the expression of long-term potentiation. Int J Biochem 1994;26:735-744.

7. Markovac J, Goldstein GW. Picomolar concentrations of lead stimulate brain protein kinase C. Nature 1988;334:71-73.

8. US Environmental Protection Agency. Air quality criteria for lead. Research Triangle Park (NC): USEPA, Office of Research and Development, EPA600/8-83-028F, 1986.

9. US Centers for Disease Control and Prevention. Fatal pediatric lead poisoning—New Hamphshire, 2000. MMWR Morb Mortal Wkly Rep 2001;50:457-459.

10. Center for Disease Control and Prevention. Preventing lead poisoning in young children: A statement by the Centers for Disease Control, October 1991. Atlanta (GA): US Department of Health and Human Services, Public Health Service, CDC, 1991.

11. American Academy Of Pediatrics Committee On Drugs. Treatment Guidelines for Lead Exposure in Children. Pediatrics 1995;96:155-160.

12. Schwartz J. Low-level lead exposure and children’s IQ: A metaanalysis and search for a threshold. Environ Res 1994;65:42-55.

13. Pocock SJ, Smith M, Baghurst P. Environmental lead and children’s intelligence: A systematic review of the epidemiological evidence. BMJ 1994;309:1189-1197.

14. Centers for Disease Control and Prevention. Strategic Plan for the Elimination of Childhood Lead Poisoning. Atlanta (GA) US Department of Health and Human Services, 1991.

15. Needleman HL, Schell A, Bellinger D, Leviton A, Allred EN. The long-term effects of exposure to low doses of lead in childhood. An 11-year follow-up report. N Engl J Med 1990;322:83-88.

16. Rice DC. Behavioral effects of lead: Commonalities between experimental and epidemiologic data. Environ Health Perspect 1996;104 Suppl 2:337-351.

17. Schwartz J, Otto D. Blood lead, hearing thresholds, and neurobehavioral development in children and youth. Arch Environ Health 1987;42:153-160.

18. Landrigan PJ, Baker EL Jr, Feldman RG, Cox DH, Eden KV, Orenstein WA. Increased lead absorption with anemia and slowed nerve conduction in children near a lead smelter. J Pediatr 1976;89:904-910.

19. McElvaine MD, Orbach HG, Binder S, Blanksma LA, Maes EF, Krieg RM. Evaluation of the erythrocyte protoporphyrin test as a screen for elevated blood lead levels. J Pediatr 1991;119:548-550.

20. Schwartz J, Landrigan PJ, Baker EL. Lead-induced anemia: Dose-response relationships and search for a threshold. Am J Public Health 1990;80: 165-168.

21. Chisholm JJ Jr, Harrison HC, Eberlien WR, Harrison HE. Aminoaciduria, hypophosphatemia, and rickets in lead poisoning: Study of a case. Am J Dis Child 1955;89:159-168.

22. Loghman-Adham M. Aminoaciduria and glycosuria following severe childhood lead poisoning. Pediatr Nephrol 1998;12:218-221.

23. Henderson DA. A follow-up of cases of plumbism in children. Aust Ann Med 1954;3:219-224.

24. Inglis JA, Henderson DA, Emmerson BT. The pathology and pathogenesis of chronic lead nephropathy occurring in Queensland. J Pathol 1978;124:65-76.

25. Bernard AM, Vyskocil A, Roels H, Kriz J, Kodl M, Lauwerys R. Renal effects in children living in the vicinity of a lead smelter. Environ Res 1995;68:91-95.

26. Loghman-Adham M. Renal effects of environmental and occupational lead exposure. Environ Health Perspect 1997;105:928-939.

27. Schwartz J. Lead, blood pressure, and cardiovascular disease in men. Arch Environ Health 1995;50:31-37.

28. Frisancho AR, Ryan AS. Decreased stature associated with moderate blood lead concentrations in Mexican-American children. Am J Clin Nutr 1991;54:516-519.

29. Ballew C, Khan LK, Kaufmann R, Mokdad A, Miller DT, Gunter EW. Blood lead concentration and children’s anthropometric dimensions in the Third National Health and Nutrition Examination Survey (NHANES III), 1988-1994. J Pediatr 1999;134:623-630.

30. Shukla R, Dietrich KN, Bornschein RL, Berger O, Hammond PB. Lead exposure and growth in the early preschool child: A follow-up report from the Cincinnati Lead Study. Pediatrics 1991;88:886-892.