Lead Compounds ^(a)

Hazard Summary-Created in April 1992; Revised in January 2000

Please Note: The main sources of information for this fact sheet are EPA's Integrated Risk Information System (IRIS), which contains information on the carcinogenic effects of lead, and the Agency for Toxic Substances and Disease Registry's (ATSDR's) Toxicological Profile for Lead.

Uses

The primary use of lead is in the manufacture of batteries. (1)
Lead is also used in the production of metal products, such as sheet lead, solder (but no longer in food cans), and pipes, and in ceramic glazes, paint, ammunition, cable covering, and other products. (1)
Tetraethyl lead was used in gasoline to increase the octane rating until lead additives were phased out and eventually banned from use in gasoline in the U.S. by the EPA by 1996. (1)

Sources and Potential Exposure

The largest source of lead in the atmosphere has been from leaded gasoline combustion, but with the phasedown of lead in gasoline, air lead levels have decreased considerably. Other airborne sources include combustion of solid waste, coal, and oils, emissions from iron and steel production and lead smelters, and tobacco smoke. (1,2)
Exposure to lead can also occur from food and soil. Children are at particular risk to lead exposure since they commonly put hands, toys, and other items in their mouths, which may come in contact with lead-containing dust and dirt. (1,2)
Lead-based paints were commonly used until 1978 and flaking paint, paint chips, and weathered paint powder may be a major source of lead exposure, particularly for children. (1,2)
Lead in drinking water is due primarily to the presence of lead in certain pipes, solder, and fixtures. (1,2)
Exposure to lead may also occur in the workplace, such as lead smelting and refining industries, steel and iron factories, gasoline stations, and battery manufacturing plants. (1,2)
Lead has been listed as a pollutant of concern to EPA's Great Waters Program due to its persistence in the environment, potential to bioaccumulate, and toxicity to humans and the environment. (3)

Assessing Personal Exposure

The amount of lead in the blood can be measured to determine if exposure to lead has occurred. (1,2)
The level of lead in the blood is measured in micrograms per deciliter (µg/dL).
Exposure to lead can also be evaluated by measuring erythrocyte protoporphyrin (EP), a component of red blood cells known to increase when the amount of lead in the blood is high. This method was commonly used to screen children for potential lead poisoning. (1,2)
Methods to measure lead in teeth or bones by X-ray fluorescence techniques are not widely available. (1)

Health Hazard Information

Acute Effects:

Death from lead poisoning may occur in children who have blood lead levels greater than 125 µg/dL and brain and kidney damage have been reported at blood lead levels of approximately 100 µg/dL in adults and 80 µg/dL in children. (1,2)
Gastrointestinal symptoms, such as colic, have also been noted in acute exposures at blood lead levels of approximately 60 µg/dL in adults and children. (1,2)
Short-term (acute) animal tests in rats have shown lead to have moderate to high acute toxicity. (4)

Chronic Effects (Noncancer):

Chronic exposure to lead in humans can affect the blood. Anemia has been reported in adults at blood lead levels of 50 to 80 µg/dL, and in children at blood lead levels of 40 to 70 µg/dL. (1,2)
Lead also affects the nervous system. Neurological symptoms have been reported in workers with blood lead levels of 40 to 60 µg/dL, and slowed nerve conduction in peripheral nerves in adults occurs at blood lead levels of 30 to 40 µg/dL. (1,2)
Children are particularly sensitive to the neurotoxic effects of lead. There is evidence that blood lead levels of 10 to 30 µg/dL, or lower, may affect the hearing threshold and growth in children. (1,2)
Other effects from chronic lead exposure in humans include effects on blood pressure and kidney function, and interference with vitamin D metabolism. (1,2,5)
Animal studies have reported effects similar to those found in humans, with effects on the blood, kidneys, and nervous, immune, and cardiovascular systems noted. (1,2,5)
EPA has not established a Reference Concentration (RfC) or a Reference Dose (RfD) for elemental lead or inorganic lead compounds. (6)
EPA has established a Reference Dose (RfD) for tetraethyl lead (an organometallic form of lead) of 1 x 10^-7 milligrams per kilogram body weight per day (mg/kg/d) based on effects in the liver and thymus of rats. The RfD is an estimate (with uncertainty spanning perhaps an order of magnitude) of a daily oral exposure to the human population (including sensitive subgroups) that is likely to be without appreciable risk of deleterious noncancer effects during a lifetime. It is not a direct estimator of risk, but rather a reference point to gauge the potential effects. At exposures increasingly greater than the RfD, the potential for adverse health effects increases. Lifetime exposure above the RfD does not imply that an adverse health effect would necessarily occur. (7)
EPA has medium to low confidence in the RfD due to (1) medium to low confidence in the study on which the RfD for tetraethyl lead was based because, although only a few animals per sex per dose level were tested, a good histopathologic exam was conducted and a dose-severity was observed; and (2) medium to low confidence in the data base because some supporting information was available. (7)

Reproductive/Developmental Effects:

Studies on male lead workers have reported severe depression of sperm count and decreased function of the prostate and/or seminal vesicles at blood lead levels of 40 to 50 µg/dL. These effects may be seen from acute as well as chronic exposures. (1,5)
Occupational exposure to high levels of lead has been associated with a high likelihood of spontaneous abortion in pregnant women. However, the lowest blood lead levels at which this occurs has not been established. These effects may be seen from acute as well as chronic exposures. (1,5)
Exposure to lead during pregnancy produces toxic effects on the human fetus, including increased risk of preterm delivery, low birthweight, and impaired mental development. These effects have been noted at maternal blood lead levels of 10 to 15 µg/dL, and possibly lower. Decreased IQ scores have been noted in children at blood lead levels of approximately 10 to 50 µg/dL. (1,2)
Human studies are inconclusive regarding the association between lead exposure and other birth defects, while animal studies have shown a relationship between high lead exposure and birth defects. (1,5)

Cancer Risk:

Human studies are inconclusive regarding lead exposure and an increased cancer risk. Four major human studies of workers exposed to lead have been carried out; two studies did not find an association between lead exposure and cancer, one study found an increased incidence of respiratory tract and kidney cancers, and the fourth study found excesses for lung and stomach cancers. However, all of these studies are limited in usefulness because the route(s) of exposure and levels of lead to which the workers were exposed were not reported. In addition, exposure to other chemicals probably occurred. (1,2,6)
Animal studies have reported kidney tumors in rats and mice exposed to lead via the oral route. (1,2,5,6)
EPA considers lead to be a Group B2, probable human carcinogen. (6)

Physical Properties

Lead is a naturally occurring, bluish-gray metal that is found in small quantities in the earth's crust. (1,2)
Lead is present in a variety of compounds such as lead acetate, lead chloride, lead chromate, lead nitrate, and lead oxide. (1,2)
Pure lead is insoluble in water; however, the lead compounds vary in solubility from insoluble to water soluble. (1,2)
The chemical symbol for lead is Pb and the atomic weight is 207.2 g/mol. (1)
The vapor pressure for lead is 1.0 mm Hg at 980 °C. (1)

Conversion Factors (only for the gaseous form):
To convert concentrations in air (at 25°C) from ppm to mg/m³: mg/m³ = (ppm) × (molecular weight of the compound)/(24.45). For lead: 1 ppm = 8.5 mg/m³.

Health Data from Inhalation Exposure

ACGIH TLV--American Conference of Governmental and Industrial Hygienists' threshold limit value expressed as a time-weighted average; the concentration of a substance to which most workers can be exposed without adverse effects.
LC₅₀ (Lethal Concentration₅₀)--A calculated concentration of a chemical in air to which exposure for a specific length of time is expected to cause death in 50% of a defined experimental animal population.
NIOSH REL--National Institute of Occupational Safety and Health's recommended exposure limit; NIOSH-recommended exposure limit for an 8- or 10-h time-weighted-average exposure and/or ceiling.
NIOSH IDLH -- NIOSH's immediately dangerous to life or health concentration; NIOSH recommended exposure limit to ensure that a worker can escape from an exposure condition that is likely to cause death or immediate or delayed permanent adverse health effects or prevent escape from the environment.
NAAQS--National Ambient Air Quality Standard. NAAQS set by EPA for pollutants that are considered to be harmful to public health and the environment; the NAAQS for lead is 1.5 µg/m³, maximum arithmetic mean averaged over a calendar quarter.
OSHA PEL--Occupational Safety and Health Administration's permissible exposure limit expressed as a time-weighted average; the concentration of a substance to which most workers can be exposed without adverse effect averaged over a normal 8-h workday or a 40-h workweek.

The health and regulatory values cited in this factsheet were obtained in December 1999.
^aHealth numbers are toxicological numbers from animal testing or risk assessment values developed by EPA.
^bRegulatory numbers are values that have been incorporated in Government regulations, while advisory numbers are nonregulatory values provided by the Government or other groups as advice. OSHA and NAAQS numbers are regulatory, whereas NIOSH and ACGIH numbers are advisory.

References

Agency for Toxic Substances and Disease Registry (ATSDR). Toxicological Profile for Lead (Update). Draft for Public Comment. Public Health Service, U.S. Department of Health and Human Services, Atlanta, GA. 1997.
Agency for Toxic Substances and Disease Registry (ATSDR). Case Studies in Environmental Medicine, Lead Toxicity. Public Health Service, U.S. Department of Health and Human Services, Atlanta, GA. 1992.
U.S. Environmental Protection Agency. Deposition of Air Pollutants to the Great Waters. First Report to Congress. EPA-453/R-93-055. Office of Air Quality Planning and Standards, Research Triangle Park, NC. 1994.
U.S. Department of Health and Human Services. Registry of Toxic Effects of Chemical Substances (RTECS, online database). National Toxicology Information Program, National Library of Medicine, Bethesda, MD. 1993.
U.S. Department of Health and Human Services. Hazardous Substances Data Bank (HSDB, online database). National Toxicology Information Program, National Library of Medicine, Bethesda, MD. 1993.
U.S. Environmental Protection Agency. Integrated Risk Information System (IRIS) on Lead and Compounds (Inorganic). National Center for Environmental Assessment, Office of Research and Development, Washington, DC. 1999.
U.S. Environmental Protection Agency. Integrated Risk Information System (IRIS) on Tetraethyl Lead. National Center for Environmental Assessment, Office of Research and Development, Washington, DC. 1999.
National Institute for Occupational Safety and Health (NIOSH). http://www.cdc.gov/niosh/npg/npg.html. U.S. Department of Health and Human Services, Public Health Service, Centers for Disease Control and Prevention. Cincinnati, OH. 1997.
Occupational Safety and Health Administration (OSHA). Occupational Safety and Health Standards, Toxic and Hazardous Substances. Code of Federal Regulations 29 CFR 1910.1025. 1998.
American Conference of Governmental Industrial Hygienists (ACGIH). 1999 TLVs and BEIs. Threshold Limit Values for Chemical Substances and Physical Agents, Biological Exposure Indices. Cincinnati, OH. 1999.

^a Human exposure to lead occurs through a combination of inhalation and oral exposure, with inhalation generally contributing a greater proportion of the dose for occupationally exposed groups, and the oral route generally contributing a greater proportion of the dose for the general population. The effects of lead are the same regardless of the route of exposure (inhalation or oral) and are correlated with internal exposure, as blood lead levels. For this reason, this fact sheet will not discuss the exposure in terms of route but will present it in terms of blood lead levels.

Lead Compounds (a)