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Lead poisoning natural history, complications and prognosis

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Aksiniya Stevasarova, M.D.. Leena Josephin Jetty, M.B.B.S[2]

Overview[edit | edit source]

If left untreated, 100% of patients with [lead poisoning] may progress to develop seizures, unconsciousness and death.

Natural History, Complications, and Prognosis[edit | edit source]

Natural History[edit | edit source]

Complications[edit | edit source]

Central nervous system and neuromuscular symptoms usually result from intense exposure, while gastrointestinal symptoms usually result from exposure over longer periods.[2] Signs of chronic exposure include loss of short-term memory or concentration, depression, nausea], abdominal pain, loss of coordination, and numbness and tingling in the extremities.[3][unreliable medical source?] Fatigue, problems with sleep, headaches, stupor, slurred speech, and anemia are also found in chronic lead poisoning.[1] A "lead hue" of the skin with pallor and/or lividity is another feature of chronic lead poisoning.[4][5] A blue line along the gum with bluish black edging to the teeth, known as a Burton line, is another indication of chronic lead poisoning.[6] Children with chronic poisoning may refuse to play or may have hyperkinetic or aggressive behavior disorders.[1] Visual disturbance may present with gradually progressing blurred vision as a result of central scotoma, caused by toxic optic neuritis.[7]

  • Studies conducted in the recent past have confirmed that long term exposure of low levels of lead, which were previously determined to be safe are a major risk factor for atherosclerotic cardiovascular disease in adults and cognitive deficits in children. The effects of exposure to lead on long term basis varies in children and adults.

Complications

Effects on Growth and Development[edit | edit source]

  • Lead exposure is found to be a risk factor for preterm birth ,a 10 microgram elevation in blood lead levels is associated with 70 % increase in preterm birth.For those with Vitamin D deficiency this risk is even more elevated.
  • Lead exposure is associated with reduced I.Q ,with higher reductions occurring at relatively low levels of exposure.[8]
  • Childhood exposure to Lead is a known risk factor for anti social disorders ,including
    • In Adults:
  • Higher blood or bone levels are found to be congruently associated with accelerated cognitive decline; especially in those withAPOE4 alleles, drawing suspicion that it may have a role as a risk factor for late onset Alzheimer’s disease.

CVS[edit | edit source]

  • Lead causes cellular changes that are characteristic for hypertension and atherosclerosis.Is is a leading risk factor for death from cardiovascular disease. *Laboratory studies revealed endothelial cells incubated in lead for 72 hours at concentrations of 0.14 to 8.2 μg per liter showed signs of membrane damage , which is the earliest finding in the natural history of atherosclerosis.
  • Studies revealed that the risk of death from cardiovascular disease and coronary artery disease increased sharply at levels below 50 μg per liter, when adjusted for other risk factors.
Hypertension[edit | edit source]
  • The incidence of hypertension in the U.S decreased tremendously during the phaseout of leaded gasoline.
  • The usual factors like smoking, antihypertensive medicines, obesity, or even the larger size of the cuff used to measure blood pressure in persons with obesity — did not explain the decline.but it was observed that the median blood lead levels dropped by 100 μg per litre over a period of 18 years, which point towards the role of Lead in the causation of hypertension[9]

CVS[edit | edit source]

  • Lead causes cellular changes that are characteristic for hypertension and atherosclerosis.Is is a leading risk factor for death from cardiovascular disease. *Laboratory studies revealed endothelial cells incubated in lead for 72 hours at concentrations of 0.14 to 8.2 μg per liter showed signs of membrane damage , which is the earliest finding in the natural history of atherosclerosis.
  • Studies revealed that the risk of death from cardiovascular disease and coronary artery disease increased sharply at levels below 50 μg per liter, when adjusted for other risk factors.
Hypertension[edit | edit source]
  • The incidence of hypertension in the U.S decreased tremendously during the phaseout of leaded gasoline.
  • The usual factors like smoking, antihypertensive medicines, obesity, or even the larger size of the cuff used to measure blood pressure in persons with obesity — did not explain the decline.but it was observed that the median blood lead levels dropped by 100 μg per litre over a period of 18 years, which point towards the role of Lead in the causation of hypertension[9]

Prognosis[edit | edit source]

  • Prognosis is generally related to the extent and duration of lead exposure.[10]

Effects of lead on the physiology of the kidneys and blood are generally reversible; its effects on the central nervous system are not.[11] While peripheral effects in adults often go away when lead exposure ceases, evidence suggests that most of lead's effects on a child's central nervous system are irreversible.[12] Children with lead poisoning may thus have adverse health, cognitive, and behavioral effects that follow them into adulthood.[13]

References[edit | edit source]

  1. 1.0 1.1 1.2 Invalid <ref> tag; no text was provided for refs named Pearce07-EurNeurol
  2. 2.0 2.1 2.2 2.3 2.4 2.5 Invalid <ref> tag; no text was provided for refs named Brunton07-31
  3. Invalid <ref> tag; no text was provided for refs named Patrick06
  4. James, William; Berger, Timothy; Elston, Dirk (2005). Andrews' Diseases of the Skin: Clinical Dermatology. (10th ed.). Saunders. ISBN 0-7216-2921-0. :859
  5. El Safoury, OmarSoliman; Abd El Fatah, DinaSabry; Ibrahim, Magdy (2009). "Treatment of periocular hyperpigmentation due to lead of kohl (surma) by penicillamine: A single group non-randomized clinical trial". Indian Journal of Dermatology. 54 (4): 361. doi:10.4103/0019-5154.57614. ISSN 0019-5154. PMID 20101339.
  6. Rambousek (2008) p.177
  7. Fintak, David R. (30 January 2007). "Wills Eye Resident Case Series". Archived from the original on 14 July 2014.
  8. Canfield RL, Henderson CR, Cory-Slechta DA, Cox C, Jusko TA, Lanphear BP (April 2003). "Intellectual impairment in children with blood lead concentrations below 10 microg per deciliter". N Engl J Med. 348 (16): 1517–26. doi:10.1056/NEJMoa022848. PMC 4046839. PMID 12700371.
  9. 9.0 9.1 Wright JD, Stevens J, Poole C, Flegal KM, Suchindran C (June 2010). "The impact of differences in methodology and population characteristics on the prevalence of hypertension in US adults in 1976-1980 and 1999-2002". Am J Hypertens. 23 (6): 620–6. doi:10.1038/ajh.2010.40. PMC 5774853. PMID 20339353.
  10. Chisolm (2004) p. 223
  11. Invalid <ref> tag; no text was provided for refs named Rubin08-267
  12. Bellinger, DC (2004). "Lead". Pediatrics. 113 (4 Suppl): 1016–22. doi:10.1542/peds.113.4.S1.1016 (inactive 2018-05-20). PMID 15060194.
  13. Woolf, AD; Goldman, R; Bellinger, DC (2007). "Update on the clinical management of childhood lead poisoning". Pediatric clinics of North America. 54 (2): 271–94, viii. doi:10.1016/j.pcl.2007.01.008. PMID 17448360.

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