Lead

Optimal result: 0 – 1.2 µg/g creatinine

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).

A percentage of assimilated Lead is excreted in urine. Therefore the urine Lead level reflects recent or ongoing exposure to Lead and the degree of excretion or endogenous detoxification processes.

Sources of Lead include:

- old lead-based paints,

- batteries,

- industrial smelting and alloying,

- some types of solders,

- Ayruvedic herbs,

- some toys and products from China and Mexico,

- glazes on (foreign) ceramics,

- leaded (anti-knock compound) fuels,

- bullets and fishing sinkers,

- artist paints with Pb pigments,

- and leaded joints in municipal water systems.

Urinary lead (Pb) provides an indication of recent or ongoing exposure to the toxic metal, and endogenous detoxification to a lesser extent. Low level Pb exposure is particularly problematic for the developing nervous system.

Dust and paint chips from Pb-based paint in older buildings are the most common sources of Pb exposure for children. Some types of artificial turf and rubber playground surfaces can also contain Pb. Imported toys and costume jewelry tainted with Pb can be an issue. Imported non-glossy, vinyl mini-blinds are known to contain lead. Water is a common source of exposure for Pb. Old plumbing, especially from 1930 or earlier, is a significant source for chronic exposure to Pb. Plumbing in very new homes may also be problematic, due to the use of leaded solder to join copper pipes. Well water may also be contaminated with Pb in pump components or the well seal. Old pipes that supply water to buildings may contaminate water with Pb.

Foods are not commonly contaminated with Pb, but imported candies or foods containing chili or tamarind may be contaminated with Pb. Lead has been reported to be present in chocolate (the darker the higher), cocoa powders, and some chocolate flavored whey protein concentrates. Some Ayurvedic medications have been found to contain high levels of Pb and other toxic metals. Pb may get into foods or
liquids that have been stored in ceramics, pottery, china, or leaded-crystal.

Sources of air-borne Pb include: waste incinerators, utilities, and lead-acid battery manufacturer, and ore and metals processing. The highest air concentrations of Pb are usually found near lead smelters. Fishing tackle, ammunition, indoor firing ranges, and some art/hobby supplies may contribute to Pb exposure. Transdermal Pb absorption is slight, except for high absorption of lead acetate that may be present in hair darkening products and certain tattoo inks.

Pb has pathological, neurotoxic, nephrotoxic, cardiovascular and carcinogenic effects that may be manifested with chronic low-level exposure. Pb may also affect the body’s ability to utilize the essential elements calcium, magnesium, and zinc. Sustained Pb exposures may have adverse effects on memory, cognitive function, nerve conduction, and metabolism of vitamin D. Infants and children are especially vulnerable to Pb-induced developmental disorders, and behavior problems are associated with lower levels of blood Pb than previously acknowledged; lower of IQ, hearing loss, and poor growth. Pb is transferred across the placenta, and into breast milk.

Lead exposure and toxicity is commonly assessed by elevated blood lead. However blood lead may only reveal isolated exposures as the half-life of Pb in circulation is only about 1 month. Hair elemental analysis may provide information regarding Pb exposure over the past 2-4 months. Urine porphyrin analysis may reveal Pb-induced disruption of heme biosynthesis (physiological impact). Chelation may acutely increase the urinary Pb excretion.

Lead
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