LEAD POISONING ( Health Tips)

 Lead is used in a variety of industrial and commercial products such as paints, cans, plumbing fixtures, leaded gasoline, improperly glazed ceramics, lead crystals, leafy vegetables grown in lead contaminated soil and storage batteries.

Lead produces adverse effects on CNS, GIT and blood.

METABOLISM

Lead is absorbed into the blood where 95-99% is sequestered in red cells, where it is bound to hemoglobin. Therefore lead is measured in whole blood rather than in serum. The largest proportion of absorbed lead is incorporated into skeleton; however it also appears in nails, hair, sweat, saliva and breast milk.

Toxicity occurs due to its affinity for cell membrane and mitochondria. Therefore it interferes mitochondrial phosphorylation. Na+ K+ and calcium ATPase.

CLINICAL FEATURES

CHILDREN

Symptomatic

Symptomatic toxicity in children develops usually at blood level of 80 ug/dl and is characterized by:

• Abdominal pain and irritability followed by lethargy, anorexia, pallor (due to anemia), ataxia and slurred speech.
• Convulsion, coma and death due to generalized cerebral edema and renal failure occur in severe cases.

Subclinical toxicity

Subclinical toxicity occurs at blood level>30ug/dl and causes learning disorders in children and motor neuropathy.

It presents with mental retardation, selective deficits in language, cognitive function, balance, behavior and school performance. Maximum impact occurs at around age 2 years.

ADULTS

Symptomatic

Symptomatic toxicity in adults develops when the blood lead level is >80ug/dl for period of weeks and is characterized by:

• Abdominal pain, headache, irritability, joint pain, fatigue, anemia, peripheral motor neuropathy (e.g foot drop, wrist drop), deficits in short-term memory and ability to concentrate.
• Lead-line appears on gingival-tooth border after prolonged high level exposure.

Chronic Subclinical

• Chronic Subclinical intoxication causes:
• Interstitial nephritis, tubular damage, hyperuricemia (with increased risk of gout) and chronic renal failure.
• Hypertension.

FOR BOTH CHILDRENAND ADULTS

• Increased bone level is a risk factor for bone diseases, anemia and hypertension.
• Hyperthyroidism may causes lead toxicity by mobilizing stores of lead in bones.

INVESTIGATIONS

1. Blood lead level:

·         Less than 10 ug/dl is considered non-toxic.

• Levels between 10-25 ug/dl is associated with impaired neurobehavioral development in children.
• Levels of 25-50 ug/dl may be associated with headache, irritability and Subclinical toxicity.
• Levels of 50-70 ug/dl are associated with moderate toxicity.
• Levels >70-100 ug/dl are associated with severe poisoning.

2. Blood CP: microcytic anemia with basophilic stippling.
3. Blood protoporphyrin: elevated.
4. Gamma aminolevillinic acid (heme precursor) increases in plasma and urine.
5. Nerve conduction velocity (NCV): prolonged nerve conduction time due to peripheral demyelination usually of extensor muscles of hand and feet.
6. X-ray bone: increased density at metaphyseal plate and growing long bones (lead lines) can develop in children.
7. UCE: adults chronically exposed to lead can develop elevated serum creatinine.

MANAGEMENT

Emergency measure

Coma: maintain airway, other management of unconscious patient.

Convulsion: anticonvulsion therapy.

Activated charcoal and endoscopic removal for recent acute ingestion.

Chelating agents

EDTA, dimercaprol and penicillamine.

Indications for chelation: blood lead level > 55 ug/dl in children and 80 ug/dl in adults.