THE TOXICITY OF LEAD

The Toxicity of Lead

The Toxicity of Lead

Lead has been mined and used in industry and in household products for centuries. The dangers of lead toxicity, the clinical manifestations of which are known as plumbism, have been known since ancient times. The twentieth century has seen both the greatest-ever exposure of the general population to lead and an extraordinary amount of new research on lead toxicity.

Populations are exposed to lead chiefly via paints, cans, plumbing fixtures, and leaded gasoline. The intensity of these exposures, while recently decreased by regulatory actions, remains high in some segments of the population because of the deterioration of lead paint used in the past and the entrainment of lead from paint and vehicle exhaust into soil and house dust. Many other environmental sources of exposure exist, such as leafy vegetables grown in lead-contaminated soil, improperly glazed ceramics, lead crystal, and certain herbal folk remedies. Many industries, such as battery manufacturing, demolition, painting and paint removal, and ceramics, continue to pose a significant risk of lead exposure to workers and surrounding communities.

New research on lead toxicity has been stimulated by advances in toxicology and epidemiology as well as by a shift of emphasis in toxicology away from binary outcomes (life/death; 50 percent lethal dose) to grades of function, such as neuropsychological performance, indices of behavior, blood pressure, and kidney function.

Lead ranks second in the list of prioritised hazardous substances issued by the U.S. ATSDR (Agency for Toxic Substances and Disease Registry) in 1999. The noxious effects of this metal have long been well known, especially as regards acute forms of poisoning. However, as for many other contaminants, the threshold level of safety has been drastically lowered recently. Until approximately 30 years ago, chronic lead poisoning was defined by blood lead levels above 80(gr/dl, while today a lead level of 30(gr/dl in blood is considered excessive and levels at or above 10(gr/dl (0.1 ppm) are considered potentially harmful, particularly in children.

Once absorbed by the body, mainly through breathing and feeding, lead is not metabolised, but mostly expelled. The remaining portion (about 20%) settles into the tissues and notably:

in the blood, where it is carried almost exclusively by the erythrocytes

in mineral tissues (bones and teeth), where it deposits

in soft tissues (kidneys, bone marrow, liver and brain) (Ragan 2009 40-5)

The presence of lead in the blood stream (inside the red blood cells and mostly linked to haemoglobin) provokes anaemia. This disease cannot be considered a symptom, but rather a delayed sign of lead poisoning. Through the blood, lead reaches all other tissues. Because of its capacity to "mimic" calcium (see mechanisms), lead is stored in the bones and becomes a stable bone component, particularly in the case of insufficient calcium intake. This lead deposit may be mobilised and return into the blood stream under particular states of physiological stress (pregnancy, breast-feeding, diseases), but also as a consequence of greater calcium intake in the diet. This stable presence of lead in bones makes recovery from lead poisoning extremely slow, ...