Humans have been mining and using this heavy metal for thousands of years, poisoning themselves in the process due to accumulation and exposure. These dangers have long been known, though the modern understanding of their full extent and the small amount of lead necessary to produce them is relatively recent; blood lead levels once considered safe are now considered hazardous, with no known threshold. Reducing these hazards requires both individual actions and public policy regulations.
Lead was first mined in Asia Minor (today Turkey) about 6500 BC. A 6000- to 8000-year-old lead necklace was found in the ancient city site of Anatolia. Lead's easy workability, low melting point and corrosion-resistance were among its attractions.
Lead toxicity was first recognized as early as 200 B.C. Nicander of Colophon wrote of lead-induced anemia and colic in 250 B.C. Gout, prevalent in affluent Rome, is thought to be the result of lead, or leaded eating and drinking vessels. Lead was used in makeup. Sugar of lead (lead(II) acetate) was used to sweeten wine, and the gout that resulted from this was known as saturnine gout.
Aulus Cornelius Celsus, writing ca. A.D. 30, listed white lead on a list of poisons with antidotes (beside cantharides, hemlock, hyoscyamus, poisoned mushrooms, and a swallowed leech), and claimed it could be remedied by mallow or walnut juice rubbed up in wine. Despite his awareness of lead's toxicity, citing many contemporary authorities, Celsus recommended its use in a wide range of ointments applied to wounds to stop bleeding and reduce infection or inflammation.
Julius Caesar's engineer, Vitruvius, who also served his successor Caesar Augustus, reported, "Water is much more wholesome from earthenware pipes than from lead pipes. For it seems to be made injurious by lead, because white lead, a pigment base produced by soaking lead in vinegar until a soft paste, is produced from it; and this is said to be harmful to the human body. It should be noted that the prevalence of lead poisoning, at least that caused by drinking water containing lead, in ancient Rome is far less than what is traditionally believed. The hardness of Rome's water caused heavy deposits of calcium carbonate to form on pipes and in turn prevented the lead of the pipes from coming into contact with the water, thus reducing the chance of getting lead poisoning from drinking water. The calcium deposits takes some time to collect. Older homes have the potential for less lead exposure where new homes with fresh pipes, connections and construction residue have a good potential for lead poisoning of occupants.
In 17th-century Germany, an Ulm physician noticed that monks who did not drink wine were healthy, while wine drinkers developed colic. The culprit was sugar of lead, made by simmering litharge with vinegar.
In 18th-century Boston, lead poisoning was fairly frequent on account of the widespread drinking of rum in that city, which was distilled in stills with one component (the "worm") made of lead.
Devon colic was an affliction caused by lead poisoning which was suffered by the cider drinking people of Devon during the 17th and 18th centuries.
Chinese alchemists found that lead could be rendered harmless by soaking it in blood and firing it (citation needed). When this process was repeated several times it provided a protective coat that lead could not pass. The only notable use of this measure was by martial artists so they could use the heavy metal as weights for training.
Today, most exposure in developed countries is the result of occupational hazards, leaded paint, and leaded gasoline (which continues to be phased out in most countries). Lead poisoning interferes with the normal development of the brain.
The term "lead poisoning" is sometimes used as a euphemism for gunshot wounds, as almost all bullets are mainly composed of lead. Despite this, bullets lodged in the body rarely cause significant levels of lead poisoning. Bullets lodged in the joints are the exception, as they deteriorate and release lead into the body over time.
In humans, lead toxicity sometimes causes the formation of a bluish line along the gums, which is known as the "Burton's line", although this is very uncommon in young children. Blood film examination may reveal "basophilic stippling" of red blood cells, as well as the changes normally associated with iron-deficiency anemia (microcytosis and hypochromia). However, basophillic stippling is also seen in unrelated conditions, such as megaloblastic anemia caused by vitamin B12 (colbalamin) and folate deficiencies.
Lead affects the peripheral and central nervous system. The most common sign of peripheral neuropathy due to chronic lead poisoning is painless wristdrop (weakness of the extensor muscles of hand) which usually develops after many weeks of exposure.
A direct link between early lead exposure and extreme learning disability has been confirmed by multiple researchers and child advocacy groups.
A May 2000 study by economic consultant Rick Nevin theorizes that lead exposure explains 65% to 90% of the variation in violent crime rates in the U.S.. A July 2007 paper by the same author claims to show a strong association between preschool blood lead and subsequent crime rate trends over several decades across nine different countries. These results were discussed in a July 2007 Washington Post article, reviving interest in the subject. Nevin's results reflect peer reviewed findings by Dartmouth Political Scientist Roger D. Masters, and similar work is being done by other researchers. Amherst economist Jessica Reyes' working paper and Masters' work are both pre-publication and available online.
Lead is removed from the body extremely slowly (mainly through urine, normally at a rate of 0.5 µmol/l), causing accumulation in the tissues. 95% of the absorbed lead is deposited as a lead phosphate complex in the skeletal bones.
Most lead poisoning symptoms are thought to occur by interfering with an essential enzyme Delta-aminolevulinic acid dehydratase, or ALAD. ALAD is a zinc-binding protein which is important in the biosynthesis of heme, the cofactor found in hemoglobin. Lead poisoning also inhibits the enzyme ferrochelatase which catalyzes the joining of protoporphyrin IX and Fe2+ to form a Heme. Genetic mutations of ALAD cause the disease porphyria, a disease which was highlighted in the movie The Madness of King George. Lead poisoning is sometimes mistaken for porphyria but the distinction is that lead poisoning usually causes anemia while true porphyria does not.
An article on Lead Encephalopathy on Emedicine states:
Lead also interferes with excitatory neurotransmission by glutamate, which is the transmitter at more than half the synapses in the brain and is critical for learning. The glutamate receptor thought to be associated with neuronal development and plasticity is the N-methyl-D-aspartate (NMDA) receptor, which is blocked selectively by lead. This disrupts long-term potentiation, which compromises the permanent retention of newly learned information.
The January 2004 edition of Scientific American magazine contained an article on schizophrenia that said the latest research:
... implies that their brain circuits reliant on NMDA receptors are out of kilter. If reduced NMDA receptor activity prompts schizophrenia's symptoms, what then causes this reduction? The answer still remains unclear.
However, a Johns Hopkins report by Tomas Guilarte stated:
It has been known for some time that lead is a potent inhibitor of the NMDA receptor, a protein known to play an important role in brain development and cognition. In this study we demonstrate that lead exposure decreased the amount of NMDA receptor gene and protein in a part of the brain called the hippocampus.
Ezra Susser and his colleagues at Columbia University in New York followed 12,000 children born in Oakland, California, between 1959 and 1966, whose mothers had given samples of blood serum while they were pregnant, which were frozen and stored for later analysis. They found that children who had been exposed to high levels of lead in the womb were more than twice as likely to go on to develop schizophrenia. Their research was presented at the 2004 annual meeting of the American Association for the Advancement of Science in Seattle, Washington.
Lead poisoning can also be fatal.
Lead has also been found in drinking water. It can come from plumbing and fixtures that are either made of lead or have trace amounts of lead in them. In 2004, seven reporters from The Washington Post discovered high levels of lead in the drinking water in Washington, D.C. The team won an award for investigative reporting for a series of articles about this contamination.
Exposure to metallic lead such as small lead objects, can rarely lead to an increase in blood lead levels if the lead is retained in the gastrointestinal tract or appendix.
Lead can also be found in some imported cosmetics such as Kohl, from the Middle East, India, Pakistan, and some parts of Africa, and Surma from India and from imported toys, such as many made in China. There are also risks of elevated blood lead levels caused by folk remedies like Azarcon which contains 95 percent lead and is used to "cure" empacho. For more information about less common causes of elevated blood lead levels, see footnote.
Lead may be contracted through the mucous membranes through direct contact to mouth, nose, eyes, and breaks in skin.
"In 1998, the US Government instituted regulations which limit the amount of lead in toys and other consumer products which are expected to be used by infants to 0.06% (or 600 ppm).
Ten µg/dL (micrograms /deciliter) was adopted by CDC in 1991 as an action level for children, an advisory level for environmental and educational intervention, though the agency acknowledges that "Recent studies have suggested possible neurodevelopmental effects concentrations of less than 10 µg/dL." There are requirements that children receiving Medicaid be screened. Most states ask or require primary care physicians and persons in charge of screening programs to report both presumptive and confirmed cases of lead toxicity to the appropriate health agency. This is to ensure abatement of the lead source, education of the patient, and remediation steps are undertaken. In some states, the clinical laboratories performing blood lead testing are required to report cases of lead toxicity.
In 2006 the Lead Poisoning Reduction Act was introduced to protect children from lead poisoning by requiring all non-home-based child care facilities (i.e. Head Start and kindergartens) to be lead-safe within five years .
In early 2008, the watchdog Food and Drug Administration ordered several US retail stores and malls to remove bindi and sindoor from their shelves due to concerns over high lead and other harmful chemical contents.
The NIOSH Adult Blood Lead Epidemiology and Surveillance (ABLES) program, a state-based surveillance program of laboratory-reported adult blood lead levels works to reduce the rate of adults (age 16 or older) who have blood lead levels of 25 micrograms per deciliter (mcg/dL) or greater.
Lead contaminated soil can pose a risk through direct ingestion, uptake in vegetable gardens, or tracking into homes. Uncontaminated soil contains lead concentrations less than 50 ppm but soil lead levels in many urban areas exceed 200 ppm. (AAP 1993) The EPA’s standard for lead in bare soil in play areas is 400 ppm by weight and 1200 ppm for non-play areas. This regulation applies to cleanup projects using federal funds. The soil screening level (SSL) for lead represents a conservative estimate for a level that would be protective of public health in residential soils based on an analysis of the direct ingestion pathway for children.
EPA has set drinking water standards with two levels of protection. The maximum contaminant level goal (MCLG) is zero. This is the level determined to be safe by toxicological and biomedical considerations, independent of feasibility. EPA’s final rule establishes an action level is set at 15 µg/L. The use of lead solder and other lead-containing materials in connecting household plumbing to public water supplies was banned by EPA as of June 1988.
FDA has set a number of action levels (enforceable) and levels of concern for lead in various food items. These levels are based on FDA calculations of the amount of lead a person can consume without ill affect. FDA has set an action level of 0.5 µg/mL for lead in products intended for use by infants and children and has banned the use of lead-soldered food cans.
House paint contained up to 50% lead before 1955. Federal law lowered the amount of lead allowable in paint to 1% in 1971. The CPSC has limited since 1977 the lead in most paints to 0.06% (600 ppm by dry weight). Paint for bridges and marine use may contain greater amounts of lead.
Both the federal government and the state of Massachusetts are considering (as of September 2007) action against lead in children’s jewelry. "But Mr. Durbin said he was disappointed with Ms. Nord and the safety commission, which he said did not appear to be attacking the problem aggressively enough, including moving too slowly to institute and enforce a ban on lead in children’s jewelry. He also mocked a new agreement with Chinese officials to block lead in toys, saying that the Chinese government told his office the policy had long been in place."
Additionally, a comparative study of chelating agents showed that vitamin C (ascorbic acid), along with DMSA, CDTA and DMPS increased survival in an animal model of lead intoxication, while EGTA, N-acetyl-L-cysteine (NAC) and various other agents did not. High serum levels of vitamin C have been associated with a decreased prevalence of elevated blood lead levels and intervention with supplemental vitamin C was shown to markedly decrease lead levels in smokers (mean: 81%). Authors hypothesize, however, that this effect might be due to an inhibition of lead absorption.