Routes of exposure to lead include contaminated air, water, soil, food, and consumer products. Occupational exposure is a common cause of lead poisoning in adults. One of the largest threats to children is lead paint that exists in many homes, especially older ones; thus children in older housing with chipping paint are at greater risk. Prevention of lead exposure can range from individual efforts (e.g. removing lead-containing items such as piping or blinds from the home) to nationwide policies (e.g. laws that ban lead in products or reduce allowable levels in water or soil).
Elevated lead in the body can be detected by the presence of changes in blood cells visible with a microscope and dense lines in the bones of children seen on X-ray. However, the main tool for diagnosis is measurement of the blood lead level; different treatments are used depending on this level. The major treatments are removal of the source of lead and chelation therapy (administration of agents that bind lead so it can be excreted).
No safe threshold for lead exposure has been discovered—that is, there is no known amount of lead that is too small to cause the body harm.
Lead poisoning was among the first known and most widely studied work and environmental hazards. One of the first metals to be smelted and used, lead is thought to have been discovered and first mined in Anatolia around 6500 BCE. Its density, workability, and corrosion-resistance were among the metal's attractions.
In the second century BCE the Greek botanist Nicander described the colic and paralysis seen in lead-poisoned people. Dioscorides, a Greek physician who lived in the first century CE, wrote that lead makes the mind "give way".Lead was used extensively in Roman aqueducts from about 500 BCE to 300 CE Julius Caesar's engineer, Vitruvius, 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 is produced by it, and this is said to be harmful to the human body." Gout, prevalent in affluent Rome, is thought to be the result of lead, or leaded eating and drinking vessels. Sugar of lead was used to sweeten wine, and the gout that resulted from this was known as saturnine gout.
After antiquity, mention of lead poisoning was absent from medical literature until the end of the Middle Ages. In 1656 the German physician Samuel Stockhausen recognized dust and fumes containing lead compounds as the cause of disease, called since ancient Roman times morbi metallici, that were known to afflict miners, smelter workers, potters, and others whose work exposed them to the metal.
The painter Caravaggio might have died of lead poisoning. Bones with high lead levels were recently found in a grave likely to be Caravaggio's grave. Paints used at the time contained high amounts of lead salts. Caravaggio is known to have indulged in violent behavior, as caused by lead poisoning.
In 17th-century Germany, the physician Eberhard Gockel discovered lead-contaminated wine to be the cause of an epidemic of colic. He had noticed that monks who did not drink wine were healthy, while wine drinkers developed colic, and traced the cause to sugar of lead, made by simmering litharge with vinegar. As a result, Eberhard Ludwig, Duke of Württemberg issued an edict in 1696 banning the adulteration of wines with litharge.
In 18th century Boston, lead poisoning was fairly frequent on account of the widespread drinking of rum, which was made in stills with a lead component (the "worm"). Also in the 18th century, "Devonshire colic" was the name given to the symptoms suffered by people of Devon who drank cider made in presses that were lined with lead. Lead was added to cheap wine illegally in the 18th and early 19th centuries as a sweetener. The composer Beethoven, a heavy wine drinker, suffered elevated lead levels (as later detected in his hair) possibly due to this; the cause of his death is controversial, but lead poisoning is a contender as a factor.
With the Industrial Revolution in the 19th century, lead poisoning became common in the work setting. The introduction of lead paint for residential use in the 19th century increased childhood exposure to lead; for millennia before this, most lead exposure had been occupational. An important step in the understanding of childhood lead poisoning occurred when toxicity in children from lead paint was recognized in Australia in 1897. France, Belgium and Austria banned white lead interior paints in 1909; the League of Nations followed suit in 1922. However, in the United States, laws banning lead house paint were not passed until 1971, and it was phased out and not fully banned until 1978.
The 20th century saw an increase in worldwide lead exposure levels due to the increased widespread use of the metal. Beginning in the 1920s, lead was added to gasoline to improve its combustion; lead from this exhaust persists today in soil and dust in buildings. Blood lead levels worldwide have been declining sharply since the 1980s, when leaded gasoline began to be phased out. In those countries that have banned lead in solder for food and drink cans and have banned leaded gasoline additives, blood lead levels have fallen sharply since the mid-1980s.
The levels found today in most people are orders of magnitude greater than those of pre-industrial society. Due to reductions of lead in products and the workplace, acute lead poisoning is rare in most countries today; however, low level lead exposure is still common. It was not until the second half of the 20th century that subclinical lead exposure became understood to be a problem. During the end of the 20th century, the blood lead levels deemed acceptable steadily declined. Blood lead levels once considered safe are now considered hazardous, with no known safe threshold.