Plumbism, or lead toxicity, was recognised as early as 370 BCE when hipprocrates coined the term "lead colic" (Gracia & Snodgrass, 2007). Lead's use and exposure peaked with the discovery of tetra-ethyl lead (TEL) as an anti-knocking agent for gasoline in 1924 (Gracia & Snodgrass, 2007). Despite consistent documentation of the adverse effects of TEL on the health of factory workers and the population as a whole, it was not until the 1970's that TEL was banned in gasoline in the United States (Gracia & Snodgrass, 2007). Although, a significant decline in blood lead levels has been reported since 1970, there remains concern as to the exact threshold by which adverse effects will occur (Gracia & Snodgrass, 2007).
The United States Centre for Disease Control and Prevention define elevated blood level concentrations for children as exceeding 10 μg/dL (Gracia & Snodgrass, 2007). Nonetheless, there is evidence to suggest that blood lead concentrations <5 μg/dL can significantly reduce the intelligence quotient (IQ) of children (Canfield, Henderson, & Cory-Slechta, 2003). This being so, it is concerning that no blood threshold at which the IQ of infants and young children is lowered has been established (Gracia & Snodgrass, 2007). Moreover, when we consider that the bone skeletal lead levels of pre-industrialised humans (4000 years ago) was 0.016 μg/dL, more than 300 times lower than the 5 μg/dL considered normal today, it is no surprise that we should be alarmed (Gracia & Snodgrass, 2007).
Sources of lead include coal mining, petroleum and coal product manufacturing; cement, lime, plaster and concrete manufacturing; ceramic and glass manufacturing; iron and steel manufacturing; manufacture of electronic parts, plastics, batteries, rubbers and metals; pigments, dyes, paints and coatings; household exposure: water pipes (older buildings) and lead based paints; soil, dust and water (Gracia & Snodgrass, 2007). It is reported that many urban centres and industralised contaminated areas contain more than 200 ppm (parts per million) of lead (Gracia & Snodgrass, 2007). There is evidence to suggest that children's blood lead concentrations rise 3 to 7 μg/dL for every 1000 ppm rise in their environmental soil or dust concentration (Lanphear, Burgoon & Rust, 1998). Interestingly, the United States Environmental Protection Agency informs us that 1200 ppm in areas of a yard, where children should not be playing is appropriate (Gracia & Snodgrass, 2007).
Jorup (2003) reports that lead exposure may lead to memory deterioration, prolonged reaction time and reduced ability to understand; reduced nerve conduction and reduced skin sensitivity (hypersensitivity and allergens); and behavioural disturbances, learning and concentration difficulties. Moreover, long term exposure may give rise to kidney damage (Jorup, 2003).
Canfield, R.L., Hendersen, C.R. & Cory-Slechta, D.A. 2003. Intellectual impairment in children with blood concentrations below 10 micrograms per decilitre. New England Journal of Medicine. 348, 1517-1526.
Gracia, R.C. & Snodgrass, W.R. 2007. Lead toxicity and chelation therapy. American Journal of Health-System Pharmacology, 64, 45-53.
Jorup, L. 2003. Hazards of heavy metal contamination. British Medical Bulletin, 68, 167-182.
Lanphear, B.P., Burgoon, D.A. & Rust S.W. 1998. Environmental exposures to lead and urban children's blood lead levels. Environmental Resources, 76, 120-130.