Agent Name
CAS Number
Major Category
Plumbum; [NIOSH] Lead and inorganic compounds, as Pb; [ACGIH]
Lead Compounds, Inorganic
A heavy, ductile, soft, gray solid; Inorganic lead includes lead oxides, metallic lead, and lead salts (including organic salts such as lead soaps but excluding lead arsenate). [NIOSH]
MINING OR SMELTING: Produce lead fume by primary or secondary smelting--includes brass, copper, and lead foundries and scrap metal recycling operations; MANUFACTURING: Lead-acid battery; crystal glass; lead joints/babbitt; pewter; fishing weights; leaded or stained glass; paint and ink; leaded plastics; ammunition; electronic components (ceramic coated capacitors and resistors); electrical components using fritted glass; lead pipe, sheet, solder, type metal, cable shielding, or anodes; ceramics (mix glaze & fire kiln); mix and weigh lead powders; USING: Weld, cut, braze, grind, sand or blast old paint: houses and buildings (painted before 1978); bridges; ships; steel towers; water, petroleum or underground tanks; Produce lead fume or dust by heating, machining, or spraying lead products; radiator repair; firing ranges; In a 2003 survey of industries using lead in New Jersey, 83% of lead was used to make automotive batteries. The second highest use was metal production (primary and scrap recycling). The third was cable and wire production. The fourth was making leaded compounds in plastics, pastes, and caulks. [PMID 17558800] The highest proportion of adults with high blood leads are employed in manufacturing (72%), construction (14%), and mining (6%). Nonoccupational exposures account for 4% of high blood leads (shooting firearms, remodeling, painting, retained bullets, and lead casting. [Reference #2] In 2010, about 400 children died from lead poisoning in two villages in Nigeria involved in gold extraction from ores containing up to 18% lead. [Nordberg, p. 839]
At blood lead levels above 900 ug/L (90 ug/dl), poisoning can cause acute lead encephalopathy. Peripheral neuropathy results from levels above 600 ug/L (60 ug/dl). Most reports of lead-related symptoms (fatigue, abdominal pain, and arthralgia) begin at blood levels greater than 600 ug/L. Typical concentrations of lead in surface water in the USA is between 5 and 30 ug/L. Typical intake of lead in the USA is 2 to 9 ug per day from food, water, and beverages. "In an analysis of PbB and neurobehavioral test results from 40,000 participants from NHANES III, no statistically significant relationships between blood lead concentration and neurobehavioral test performance were found. . . . Tibia lead, representative of cortical bone, has a residence time of 25 to 30 years and serves as a biomarker of cumulative dose. . . . With additional study, lead in bone could be a viable measure of lead body burden, but at this point in time, the database is insufficient." [ACGIH: BEI Documentation] Heavy lead exposure causes anemia; Lead inhibits hemoglobin synthesis (ALAD and other enzymes), and also shortens lifespan of RBCs with resulting hemolysis. [Nordberg, p. 939-40] Exposure to high air concentrations of lead can precipitate hemolytic anemia. "The anemia of chronic lead toxicity, the primary hematologic effect of lead exposures, is enhanced by shortened red cell survival as well as by inhibition of hemoglobin synthesis." [LaDou, p. 265] At blood levels above 50-60 ug/dl, suppression of heme synthesis causes anemia. [Rom, p. 978] Lead-exposed workers may develop proximal renal tubular damage and progressive renal insufficiency. [Rom, p. 966] Lead can produce slight hepatic injury in experimental animals. [Zimmerman, p. 419] There is strong positive data associating lead exposure with spontaneous abortions and prematurity in pregnant women, neurological dysfunction in children and decreased sperm counts in men. [ATSDR Case Studies #29] The OSHA standard requires periodic determination of blood lead in workers exposed at or above action level (30 ug/m3) for more than 30 days per year. [ATSDR ToxProfiles] About 90% of pre-1940 homes contain lead-based paints, while about 60% of 1960-1979 homes contain significant amounts of lead in paint. The use of lead piping and lead solder in plumbing has been prohibited since 1986. [Coluccio VM. Lead-Based Paint Hazards. Wiley, John & Sons; 1997, p. 8-15] Inorganic lead compounds are probable human carcinogens. Organic lead compounds are not classifiable. [IARC] In contrast to inorganic lead, organic compounds are absorbed readily through the skin and into the CNS. [Sullivan, p. 979] Trabecular lead (measured in the patella) reflects exposure in the last 10 years, while cortical bone (measured in the mid-tibia) reflects lifetime exposure. [PMID 21788910] Tetraethyl & tetramethyl lead (CAS # 78-00-2 & 75-74-1) are covered separately.
Organic lead was added to gasoline in the US until January 1996. Lead allowable in US paint was reduced to 1% in 1971 and to 0.006% in 1977. [ATSDR Case Studies, Lead Toxicity]
Biomedical References

Exposure Assessment

Lead in blood = 200 ug/L (20 ug/100 ml); sampling time not critical; "The BEI cannot be applied to exposure to tetraethyl lead or other organic lead compounds." [TLVs and BEIs]
Skin Designation (ACGIH)
Insufficient data
0.05 mg/m3, as Pb
0.05 mg/m3
0.004 mg/m3, as Pb, inhalable fraction
100 mg/m3
Excerpts from Documentation for IDLHs
Basis for revised IDLH: No inhalation toxicity data are available on which to base an IDLH for lead compounds.
Explanatory Notes
Melting Point = 621 degrees F; Carcinogenicity category is 2A for lead inorganic compounds and 2B for Lead; [IARC]
Half Life
Blood: 1-3 months; whole body: 5 years; [TDR, p. 790] More than 94% of lead is stored in bone with a half-life of years to decades; [PMID 21788910]

Adverse Effects

Hemolytic anemia
Predominantly motor
Hepatoxic (a) from occupational exposure (secondary effect) or (b) in animal studies or in humans after ingestion
Reproductive Toxin
IARC Carcinogen
Probable (2a)
NTP Carcinogen
Anticipated human carcinogen
ACGIH Carcinogen
Confirmed Animal

Diseases, Processes, and Activities Linked to This Agent