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Lead poisoning is a problem that won’t go away…

March 25, 2013

Even though the toxic element lead was banned from household paint, toys, and gasoline more than 30 years ago, lead poisoning is still prevalent today. Check out this article from that explores this ever present problem.

Lead—non-biodegradable, soft, malleable, and heat and corrosion resistant—is environmentally omnipresent. Its known properties made it an ideal metal for the automobile, paint, smelting, ceramics, plastics, and toy industries at one time.1,2Unfortunately, lead is toxic to humans. Humans neither need lead nor derive benefits from it. Although lead toxicity has been a global concern since the industrial revolution in the late 1800s, civilization has been unable to prevent or control it satisfactorily. Overall incidence of lead poisoning among American children has fallen from 4.4% in the early 1990s to 1.4% in 2004.3 In 2002, around 10 of every 100,000 of adults had lead toxicity.4,5 

Venous blood lead levels (BLLs) of 10 mcg/dL and 25 mcg/dL have been considered toxic in children and adults respectively.4-7 Since any level of lead can cause toxicity, the CDC announced a new, lower reference value for children in June 2012: 5 mcg/dL. Infants and children absorb a higher fraction of lead than adults do when exposed, increasing their vulnerability.8 Approximately 450,000 American children have BLLs >5 mcg/dL.9 It is still a problem.

Diagnosis and Clinical Presentation 
Lead exposure can start with prenatal maternal-fetal transmission.10 Outside the womb, children may inhale (or eat) lead dust, often present in street debris, soil, and most frequently, aged house paint.11-14 Lead-based paint was phased out in the 1970s, lowering but not eliminating risk of exposure by this means.14 Old pipes sometimes leach lead into drinking water.12,13 Lead hazards are disproportionately found in low-income housing.15 Adults rarely develop lead poisoning, but risk is increased in workers in industries that use or manufacture lead-based products.16,17

Health care providers use many tests to identify lead poisoning. In addition to the BLL, a blood smear may show basophilic stippling ribosomal clusters.18,19 Increased urinary aminolevulinic acid concentrations are also reliable indicators.20 Plain film radiographs can reveal visible lead lines in patients’ long bones.10,12,17,19,21 Astute clinicians sometimes diagnose lead poisoning after seeing a blue line along patients’ gums (Burton’s line) that forms when lead reacts with sulfur ions released by oral bacteria.22

Lead affects every organ system, causing an unpredictable variety of symptoms.18,21-23 The nervous system is most sensitive (centrally in children, peripherally in adults),24-26 but lead affects hematopoietic, hepatic, and renal systems, producing serious disorders. Acute lead poisoning’s classic symptoms include colic, encephalopathy, anemia, neuropathy, and Fanconi syndrome (abnormal glucose, phosphates, and amino acid excretion).8,27Sometimes, classic signs and symptoms are absent, confusing the clinical picture.

Chronic lead exposure is slowly progressive, creating cognitive and neurobehavioral abnormalities that irreversibly reduce IQ even if BLLs are well below the old CDC standard.15 Rising BLLs correlate with diminished achievement on intelligence tests.6,28 Lower BLLs (from 3 mcg/dL to 8 mcg/dL) can cause mild IQ decreases or attention-deficit hyperactivity disorder. Higher levels (over 40 mcg/dL) may completely stop neurobehavioral development and cause toxic encephalopathy.6,18,28 Adults can also develop cognitive and neurobehavioral consequences after an acute exposure or low-level, exposure for months to years.29,30 Table 1 describes other neurologic symptoms.

In other systems, lead wreaks havoc. Anemia is a common problem—lead inhibits hemoglobin synthesis pathways and shortens erythrocyte life-span, which manifests as fatigue.18,19Hypertension may occur after acute or chronic exposure; ischemic coronary heart disease, cerebrovascular accidents, and peripheral vascular disease also can occur.31-33 Acute nephropathy with hypertension, gout, and proximal tubule dysfunction are also common.18 If it becomes chronic, end-stage renal disease are possible.18,20,34

Gastrointestinal symptoms (discomfort, constipation, or vomiting) may be vague and nonspecific at low exposures. Higher BLLs cause recurrent, severe abdominal pain called lead colic.19,20

Lead poisoning manifests in the ocular system as cataracts.35 Decreased libido, infertility, abnormal spermatogenesis or impotence,17,18 and musculoskeletal and endocrine complaints are possible.12,16

Since many lead toxicities are irreversible, the best strategy is prevention, individual intervention, and public health coordination.36-38 The main preventive measure is screening children at high risk. When prevention fails, clinicians use BLL to manage lead toxicity in children (Table 2).

Chelators increase urinary lead excretion and extract lead from blood and tissue, including the brain.36-38 If effective, they alleviate acute encephalopathy, vomiting, abdominal pain, anemia, and renal insufficiency. They cannot reverse neurologic complications.39-41

  • Dimercaprol cannot be used in patients with hepatic insufficiency or peanut allergies. Caution is needed in children with renal impairment, hypertension, or G6PD deficiency. Adverse effects (AEs) include nausea and vomiting (N/V), headache, tachycardia, and leukopenia. Concurrent iron therapy will increase N/V, and must be stopped.37,38
  • Calcium disodium versenate is considered second line because it may increase CNS lead concentration and subsequently elevate intracranial pressure, but can be given intravenously (IV) or intramuscularly (IM). IV administration creates constant chelation and is less painful than IM. AEs include local injection site reactions, fever, hypercalcemia, renal insufficiency, and excretion of other essential minerals.36-38
  • Succimer is an oral water-soluble dimercaprol analogue associated with fewer AEs than parenteral chelators. AEs include rash, neutropenia, elevated transaminases, and gastrointestinal upset. Patients may object to succimer’s sulfur odor, and opening the capsules and sprinkling the beads onto food or dissolving in juice can help.36-38
  • The oral copper chelator D-penicillamine also chelates lead in children with low-level toxicity; this is an off-label use. AEs include nausea and vomiting, transient neutropenia and thrombocytopenia, rash, abdominal pain, and abnormal liver function. If drug-induced rash develops, therapy may need to be stopped. 36-38,42Chelation’s efficacy in adults with lead toxicity is unclear.17 Treatment starts with identifying the exposure source, removing it, then using chelation in patients with a BLL greater than 80 mcg/dL; between 60 and 80 mcg/dL with symptoms; or between 40 and 60 mcg/dL if symptoms continue after the exposure source is removed.43

Why Won’t It Go Away?
Lead poisoning is more likely in low income areas, and in children who suffer from poor nutrition.44 Lead is everywhere, and almost impossible to remove entirely from the body once it enters. There is no safe blood level and fixing this problem is very costly. This is why public health strategy is essential: it targets areas where lead poisoning is likely, and encourages preventive strategies like sequestering industries dealing with lead apart from inhabited areas and banning the use of lead when appropriate replacements are available.


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