Most Lead contamination occurs via oral ingestion of contaminated food or water or by children mouthing or eating Lead-containing substances. The degree of absorption of oral Lead depends upon stomach contents (empty stomach increases uptake) and upon the essential element intake and Lead status.

Deficiency of zinc, calcium or iron increases Lead uptake. Transdermal exposure is significant for Lead-acetate (hair blackening products). Inhalation has decreased significantly with almost universal use of non-leaded automobile fuel. Lead accumulates in extensively in bone and can inhibit formation of heme and hemoglobin in erythroid precursor cells. Bone Lead is released to soft tissues with bone remodeling that can be accelerated with growth, menopausal hormonal changes, osteoporosis, or skeletal injury.

Low levels of Lead may cause impaired vitamin D metabolism, decreased nerve conduction, and developmental problems for children including: decreased IQ, hearing impairment, delayed growth, behavior disorders, and decreased glomerular function.

Transplacental transfer of Lead to the fetus can occur at very low Lead concentrations in the body. At relatively low levels, Lead can participate in synergistic toxicity with other toxic elements (e.g. cadmium, mercury).

Excessive Lead exposure can be assessed by comparing urine Lead levels before and after provocation with Ca-EDTA (iv) or oral DMSA.

Urine Lead is higher post-provocation to some extent in almost everyone. Whole blood analysis reflects only recent ongoing exposure and does not correlate well with total body retention of Lead. However, elevated blood Lead is the standard of care for diagnosis of Pb poisoning (toxicity).