Lead Poisoning – Source, Investigation & Detection Method
Lead, mercury, arsenic and cadmium are ranked first, second, third and sixth respectively in the U.S. Agency for Toxic Substances and Disease Registry which lists all hazards present in toxic waste sites according to their prevalence and severity of toxicity. Lead poisoning has widely contributed in the death of many people across the globe.
Metals such as lead and mercury are xenobiotic and can exert toxic effect at any level of exposure. Other metals such as copper and selenium are trace elements and are essential for normal metabolic function, however at high levels these are toxic.
Lead:- The twentieth century saw the greatest-ever exposure of the general population to lead and an extraordinary amount of new research on lead toxicity. The Centers for Disease Control and Prevention reported that one million children in the US have lead blood levels high enough to cause irreversible damage to their health.
Source:- Lead exposure is chiefly via paints, cans, plumbing and leaded gasoline. Other environmental sources include leafy vegetables grown in lead-contaminated soil, improperly glazed ceramics, lead crystal and certain herbal remedies.
Metabolism:- Elemental lead and inorganic lead compounds are absorbed via ingestion and inhalation; organic lead (tetraethyl lead, additive in gasoline) is absorbed through skin as well. Children absorb 50% of lead ingested compared to 10% absorbed by adults. Lead crosses the blood brain barrier and placenta and accumulates in bone and soft tissues; the skeleton contains >90% of the body’s total lead burden. Up to 99% of lead in blood is present in the red cells bound to hemoglobin. Lead is excreted in urine and feces and is also present in sweat, saliva, breast milk, hair and nails. The half life of lead in blood is 25 days, in soft tissues 40 days and in bone >25 years.
Clinical Toxicology:- In children symptoms of lead toxicity appear at blood levels > 80 ug/dL and include abdominal pain, anorexia, irritability followed by lethargy, pallor, ataxia and slurred speech. In severe cases convulsions, coma and death occur due to generalized cerebral edema and renal failure. Subclinical lead poisoning can cause mental retardation and deficits in language, cognitive function, balance, behaviour and school performance. Lead’s effect on intellectual capacity is probably dose-related and occurs at levels below 30ug/dL and is greatest when exposure is of long duration.
In adults symptoms are apparent at levels >80ug/dL and include abdominal pain, headache, irritability, joint pain, fatigue, anemia, peripheral motor neuropathy and deficits in short term memory. A lead line on gums is sometimes seen after prolonged exposure to high doses. Chronic subclinical exposure causes interstitial nephritis, tubular damage with inclusion bodies, hyperuricemia, decrease glomerular filtration and chronic renal failure.
Lead levels between 7 and 35 ug/dL are associated with increase blood pressure.
Lead that is dormant in bone may pose a threat at times of increased bone resorption such as pregnancy, lactation and osteoporosis. Hyperthyroidism can cause lead toxicity by mobilizing lead accumulated in bone.
In children lead levels should be maintained at <10ug/dL and in adults <40ug/dL.
In the US measurement of blood levels in children 6 months to 5 years of age is mandated; workers with occupational exposure to lead are also required to have blood lead levels monitored.
Investigations:- Anemia is usually normochromic and normocytic; basophilic stippling may be present.
Heme precursors (delta aminolevulinic acid) in plasma and urine can be elevated at blood lead levels as low as 15ug/dL In children azotemia and pyuria can occur and in adults elevated serum creatinine and decreased creatinine clearance. Lead lines ie increased metaphyseal plate density of long bones develops in children.
Prolonged nerve conduction time occurs due to peripheral demyelination.
Estimation of blood lead levels is required for definitive diagnosis of lead poisoning and for monitoring dangerous levels in asymptomatic individuals in order to prevent irreversible damage in both adults and children.
Detection Methods:- Colorimetric methods and anode stripping voltametry have been replaced by atomic absorption spectrophotometry for routine analysis of blood lead levels. Flame atomic absorption could detect blood levels of 60ug/dL; this was improved with the use of the Delves cup but was not very reproducible as it was operator dependent. With the development of Graphite Furnace atomic absorption (GFAA) the detection capability was improved 200 times (0.1 ppb). A major advantage of the GFAA is automation with very little off-line sample preparation. Another major advantage is decreased interference from matrix components that are driven off before atomization at 2700oC, hence very low levels of lead can be accurately determined. The next major milestone in AS was the development of Zeeman correction which compensates for nonspecific
Absorption and structured background produced by complex biological matrices like blood and urine; this allows for the use of aqueous standards. GFAA has been the accepted method for blood lead estimation for more than 20 years.
ICP-MS is 50-100 times more sensitive than GFAA, however cost is a limiting factor for routine clinical use.
With the use of AAS the blood lead level considered dangerous in children was lowered from 60 ug/dL to 10ug/dL; AAS has also helped in identifying the environmental sources of contamination.
Modern AAS instrumentation has in addition helped enormously in understanding other trace elements such as the toxic effects of arsenic and chromium and the nutritional benefit of selenium and has impacted on the quality of human lives.
