Report on Carcinogens, Twelfth Editiona€„ (2011)
Lead and Lead Compounds
CAS No. 7439-92-1 (Lead)
No separate CAS No. assigned for lead compounds as a class
Reasonably anticipated to be human carcinogens
First listed in the Eleventh Report on Carcinogens (2004)
Also known as Pb
Introduction
The compounds lead phosphate and lead acetate were first listed in the Second
Annual Report on Carcinogens in 1981 as reasonably anticipated to be human
carcinogens based on sufficient evidence of carcinogenicity in experimental
animals. The listing of lead and lead compounds supersedes the previous listing
of lead phosphate and lead acetate in the Report on Carcinogens and applies to
lead and all lead compounds.
Carcinogenicity
Lead and lead compounds are reasonably anticipated to be human carcinogens
based on limited evidence of carcinogenicity from studies in humans and
sufficient evidence of carcinogenicity from studies in experimental animals.
Cancer Studies in Humans
Lead exposure has been associated with increased
risk of lung, stomach, and urinary-bladder cancer in diverse human populations
(Fu and Boffetta 1995, Steenland and Boffetta 2000, NTP 2003). The strongest
epidemiological evidence is for lung and stomach cancer,which are consistently
but weakly associated with occupations and industries entailing lead exposure
and with indices of individual lead exposure, including job history and
biological monitoring of occupationally exposed and general populations. However,
most studies of lead exposure and cancer reviewed hadlimitations, including
poor exposure assessment and failure to control for confounding by other factors
that could increase the risk of cancer (such as lifestyle factors and
concurrent occupational exposure to other carcinogens), and did not demonstrate
relationships between the level or duration of exposure and the magnitude of
cancer risk. The crude exposure measures
used in most studies, such as treating whole plants or occupations
as having uniform exposure, may have limited the magnitude of risk
estimates, most of which were modest. Evidence from epidemiological studies
therefore is compatible with small increases in the risk
of lung or stomach cancer; however, this evidence must be weighed
against the potential for confounding by factors such as smoking, diet
or coexposure to arsenic.
Cancer Studies in Experimental Animals
Lead compounds caused tumors in several species of experimental animals, at
several different tissue sites, and by several different
routes of exposure. Carcinogenicity was observed in studies with
inorganic lead compounds, both soluble (lead acetate and lead subacetate) and
insoluble (lead phosphate, lead chromate), and with tetraethyl lead (an organic
lead compound). Lead caused cancer in rats
and/or mice exposed orally, by injection, or perinatally (via the placenta or
lactation). Benign and malignant kidney tumors (adenoma
carcinoma, and adenocarcinoma) were most frequently associated
with lead exposure, and tumors of the brain, hematopoietic system,
and lung were reported in some studies (IARC 1980,1987).
Lead subacetate administered in the diet caused benign and malignant kidney
tumors (adenoma and carcinoma or adenocarcinoma
in mice and rats of both sexes and brain tumors (glioma) in rats, and its
administration by intraperitoneal injection caused benign lung tumors (adenoma) in mice. Lead acetate
administered in thediet or drinking water caused benign and malignant kidney
tumors (adenoma and carcinoma) in rats and increased the incidence of virus-induced
lymphocytic leukemia in mice. After pregnant mice were given lead acetate in
the drinking water from gestation day 12 to four weeks postpartum, the offspring
showed a dose-related increase in proliferative lesions of the kidneys
(including atypical hyperplasia, adenoma, and adenocarcinoma) (Waalkes et al.
1995).
Rats exposed to lead phosphate by subcutaneous
injection (alone or followed by intraperitoneal injection) developed benign or
malignant kidney tumors (adenoma or carcinoma). Rats exposed to lead chromates
by subcutaneous injection developed cancer at the injection site (sarcoma), and
administration of lead chromates by intramuscular injection caused kidney cancer
(renal-cell carcinoma) (IARC 1990). (Because lead chromate is also a hexavalent
chromium compound, it is also included in the listing for Chromium Hexavalent Compounds.)
Tetraethyl lead administered by subcutaneous injection caused lymphoma in
female mice. Exposure to lead naphthenate, lead carbonate, lead arsenate, lead
nitrate, and metalliclead (as lead powder) did not significantly increase tumor
incidences in experimental animals (IARC 1980).
Studies on Mechanisms of Carcinogenesis
Exposure of rodents to lead compounds also increased the incidence
or accelerated the appearance of kidney tumors induced by other carcinogens,
including N-ethyl-N-hydroxyethylnitrosamine and N-(4′fluoro-4-biphenyl)acetamide. Higher incidences of kidney and liver
cancer were observed in rats fed diets containing lead subacetate
and 2-acetylaminofluorene than in rats fed either lead subacetate or
2-acetylaminofluorene alone (IARC 1980, 1987).
Absorption of lead is affected by age, the chemical form of the
lead, and minerals in the diet (e.g., iron, calcium, and zinc) (ATSDR
1999). Gastrointestinal absorption of lead is greater in children than
in adults (Hammad et al. 1996). Once absorbed, lead is distributed to
blood plasma, the nervous system, and soft tissues. It subsequently is
redistributed and accumulates in bone; 75% to 90% of the lead body
burden is found in bones and teeth.
In studies of humans occupationally exposed to lead, there is evidence to
suggest that lead damages chromosomes or DNA. In most
studies, lead caused micronucleus formation, chromosomal aberrations, and DNA
damage, but studies on sister chromatid exchange
gave conflicting results. Genetic studies on humans environmentally
exposed to lead also gave conflicting results. Lead did not cause mutations in
bacteria, and results from test systems using mammalian
cells were conflicting. Lead caused chromosomalaberrations in most
studies in plants or mammals, both in vitro and in vivo. It caused
DNA damage or fragmentation in mammals in vivo and in cell-free
systems (in the presence of hydrogen peroxide), but mammalian in
vitro studies gave conflicting results. Lead also inhibited the activity
of DNA and RNA polymerase in cell-free systems and in mammalian
cell cultures. Conflicting results were observed for sister chromatid
exchange and micronucleus formation in mammalian test systems
(in vitro and in vivo) (ATSDR 1999, NTP 2003).
The mechanisms by which lead causes cancer are not understood.
Lead compounds do not appear to cause genetic damage directly, but
may do so through several indirect mechanisms, including inhibition
of DNA synthesis and repair, oxidative damage, and interaction with
DNA-binding proteins and tumor-suppressor proteins (NTP 2003).
National Toxicology Program, Department of Health and Human Services
Report on Carcinogens, Twelfth Editiona€„ (2011)
Properties
Substance
Elemental lead is an odorless, silver-bluish-white metal that is insoluble in
water (Budavari et al. 1996, Lide and Frederikse 1998, HSDB
2009). It is soft, highly malleable, ductile, and a relatively poor conductor
of electricity. It is resistant to corrosion but tarnishes upon
exposure to air. Lead exists in the valence states of +2 and +4 and has
four naturally occurring stable isotopes: 204Pb, 206Pb, 207Pb, and 208Pb
Inorganic lead compounds usually consist of lead in the divalent state
(+2), and the chemistry of divalent lead is similar tothat of group
2 metals (beryllium, magnesium, calcium, strontium, and barium).
Lead compounds may be divided between those compounds that
are relatively soluble in water and those that are relatively insoluble in
water. Compounds are considered soluble or insoluble based
on the following criteria: (1) If a solubility
constant (Ksp) is available, a compound with a value greater than or equal to
the Ksp for
lead chloride (1 × 10–4) is considered soluble. (2) If a Ksp is not
available, a compound is considered soluble if more than 2 g of the
compound dissolves in 100 mL of water. (3) If no numeric solubility data
are available, the compounds are considered soluble or insoluble according to
the general rules of solubility.
The major soluble lead compounds are lead acetate, lead acetate
trihydrate, lead chloride, lead nitrate, and lead subacetate; all are soluble
in water, and lead acetate trihydrate is miscible with water. Lead
acetate exists as colorless or white crystals, granules, or powders that
are soluble in glycerol and slightly soluble in ethanol. Lead acetate
trihydrate occurs as white crystals that are slightly soluble in ethanol and
acetone. Lead chloride exists as a white crystalline powder
that is insoluble in ethanol. Lead nitrate occurs as colorless or white
crystals that are insoluble in nitric acid. Lead subacetate is a white
heavy powder that is soluble in ethanol (HSDB 2009).
The major insoluble lead compounds include 17 inorganic lead
compounds. Lead arsenate, lead azide, lead bromide, lead fluoride
lead phosphate,lead stearate, lead sulfate, and lead thiocyanate occur as white
powders, crystals, or needles. Lead carbonate occurs as
colorless rhombic crystals, and lead fluoborate occurs as a colorless
crystalline powder. Lead chromate, lead iodide, lead naphthenate, lead
oxide, and lead styphnate occur as yellow to reddish-yellow powder
crystals, or paste. Lead sulfide occurs as metallic black cubic crystals, and
lead tetraoxide is a bright-red heavy powder. Lead arsenate
lead fluoride, and lead phosphate are soluble in nitric acid, and lead
arsenate, lead carbonate, lead oxide, lead phosphate, lead sulfate, and
lead thiocyanate are soluble in potassium hydroxide or other alkalis. Lead
bromide, lead iodide, lead oxide, lead phosphate, and lead
sulfate are insoluble in alcohol, and lead fluoborate decomposes in
alcohol. Lead tetraoxide is soluble in hydrochloric and acetic acids
and insoluble in ethanol. The reported melting points of these compounds range
from 100°C (lead naphthenate) to 1,170°C (lead sulfate). All of the insoluble
inorganic lead compounds have high boiling
points (up to 1,470°C); however, lead carbonate decomposes before
it boils, and lead azide explodes at 350°C. Most of these compounds
have high specific gravities, ranging from 6.2 for lead sulfate to 9.53
for lead oxide, but a few have lower specific gravities, including lead
naphthenate (1.15), lead fluoborate (1.75), and lead thiocyanate (3.82)
(HSDB 2009, Akron 2010).
Tetraethyl lead and tetramethyl lead are insoluble organic lead
compounds. They both exist ascolorless liquids and are
soluble in
benzene, ethanol, and diethyl ether. The octanol-water partition coefficients
are 4.15 for tetraethyl lead and 2.97 for tetramethyl lead
(HSDB 2009). The following table lists physical and chemical properties for
lead, the major soluble inorganic lead compounds, and the
organic lead compounds.
Lead
Leada€„acetate
Leada€„acetatea€„trihydrate
Leada€„chloride
Leada€„nitrate
Leada€„subacetatea€„
Tetraethyla€„leada€„
Tetramethyla€„leada€„
Specific gravity
Melting pt.
Boiling pt.
11.34
3.25
2.55
5.85
4.53
NR
1.659
1.995
327°C
280°C
75°C
501°C
470°C
75°C
–136.8°C
–30.2°C
1,740°C
dec
200°Ca€„(dec)
950°C
dec
dec
200°C
110°C
Source:a€„HSBDa€„2009.a€„deca€„=a€„decomposes.a€„NRa€„=a€„nota€„reported.
Use
In worldwide metal use, lead ranks behind only iron, copper, aluminum, and zinc
(Howe 1981). Its largest use is in lead-acid storage
batteries for motor vehicles and general industry. Lead metal also is
commonly used for ammunition, cable covering, piping, brass and
bronze, bearing metals for machinery, and sheet lead (ATSDR 1999).
All of the major soluble lead compounds have industrial uses. Lead
acetate is used as a water repellent, for mildew protection, and as a
mordant for cotton dyes. Lead acetate trihydrate is used in varnishes
chrome pigments, and as an analytical reagent, and lead chloride is
used in asbestos clutch or brake linings, as a catalyst, and as a flame
retardant. Lead nitrate is used in the manufacture of matches and
explosives, as a heat stabilizer in nylon, and as a coating onpaper for
photothermography. Lead subacetate is used in sugar analysis and for
clarifying solutions of organic substances (HSDB 2009).
The insoluble lead compounds also have a variety of uses. Lead
azide and lead styphnate both are used in munitions manufacture.
Lead carbonate, lead fluoride, lead fluoborate, and lead naphthenate
are used as catalysts, with additional uses in the electronic and optical
industries (lead fluoride), in coatings for thermographic copying
(lead carbonate), as a curing agent for epoxy resins (lead fluoborate),
and as a varnish drier (lead naphthenate). Lead phosphate and lead
stearate both are used as stabilizers in the plastics industry. Lead
iodide and lead sulfate are used in photography; lead iodide is also
used in thermoelectric materials, and lead sulfate
with zinc in galvanic batteries. Lead oxide and lead sulfide are used in
ceramics; lead
oxide is also used as a vulcanizing agent in rubber and plastics, and
lead sulfide as a humidity sensor in rockets. Lead chromate is used
as a pigment in paints, rubber, and plastics; lead tetraoxide is used
in plasters, ointments, glazes, and varnishes; and lead thiocyanate is
used in the manufacture of safety matches and cartridges. Lead arsenate
formerly was used as an insecticide and herbicide, but no current uses were
found.
Organic lead (including tetraethyl lead and tetramethyl lead) was
widely used in the United
States as an anti-knock additive in
motorvehicle fuels until the U.S. Environmental Protection Agency initiated a
phase-out of leaded gasoline inthe early 1970s. By 1988, the
total lead used in gasoline had been reduced to 1% of the 1970 level
in 1996, the use of lead in fuel for on-road motor vehicles was totally
banned. Despite the legislated end to use of lead as a gasoline additive and
reductions in some other uses of lead, overall U.S. lead consumption continued
to grow until 1999, mainly because of increased
production of lead-acid batteries (ATSDR 1999), but has since been
on a general decline (USGS 2009, 2010, Guberman 2010).
Production
Lead is refined from mined ore, which occurs most frequently in
the form of lead sulfide, also known as galena (Howe 1981). Mined
lead ore is crushed and ground, and a lead concentrate is formed by
separation of the various minerals. The lead concentrate is shipped
to a primary smelter for refining. At the smelter, lead concentrates
are sintered, roasted, and refined into lead metal that is 99.99% pure.
National Toxicology Program, Department of Health and Human Services
Report on Carcinogens, Twelfth Editiona€„ (2011
However, secondary lead, produced from recycled scrap (primarily
from lead acid batteries), accounts for the majority of lead produced
in the United States.
In 2009, 400,000 metric tons (882 million pounds) of lead was
mined in the United States,
a slight decline from levels over the previous four years (USGS 2010). Primary
lead production in the United
States has declined steadily over the past several decades, from a high
of 626,000 metric tons (1.4 billion pounds) in 1970 to 115,000 metric tons (254
millionpounds) in 2009 (USGS 2009, 2010). In contrast, secondary lead
production has increased steadily over the same
period, from 450,000 metric tons (992 million pounds) in 1970 to
1,120,000 metric tons (2.5 billion pounds) in 2009, when it accounted
for about 90% of the total refined lead produced in the United States.
In 2009, five lead mines in Missouri, plus
lead-producing mines in
Alaska and Idaho,
yielded most of the mined lead in the United States.
Lead was processed at one smelter-refinery in Missouri. Of the 21
plants that produced secondary lead, 15 accounted for over 99% of
secondary production (USGS 2010).
From 1980 to 1999, lead consumption in the United States rose
steadily from 906,000 metric tons (2 billion pounds) to 1,760,000
metric tons (3.9 billion pounds), but consumption has since generally
declined; in 2009, it was 1,420,000 metric tons (3.1 billion pounds).
In 2009, lead was consumed at 76 manufacturing plants, with leadacid battery
production accounting for 88% of U.S. lead consumption. U.S. imports
and exports of lead have fluctuated widely over
the past several decades. Imports have ranged from a low of 85,000
metric tons (187 million pounds) in 1980 to a high of 365,000 metric tons (805
million pounds) in 2000; imports in 2009 were 275,000
metric tons (606 million pounds). Exports of refined lead metal have
ranged from a low of 5,000 metric tons (11 million pounds) in 1976 to
a high of 164,000 metric tons (362 million pounds) in 1980; exports
in 2009 were 85,000 metric tons (187 million pounds) (USGS 2010).Lead acetate
was first produced in the United States in 1944; however, little production
information was found. Three companies reported production of an undisclosed
amount of lead acetate in 1977.
Production volumes were estimated at over 6,810 kg (15,000 lb) in
1978 and over 2,270 kg (5,000 lb) in 1982, and U.S. imports were
113 kg (250 lb) in 1978 and 39,300 kg (87,000 lb) in 1982 (IARC
1980, HSDB 2009). Lead nitrate was first commercially produced in
the United States
in 1943, and imports of 480,000 kg (1.06 million
pounds) were reported in 1978. Commercial production of lead subacetate was
first reported in the United
States in 1947; no production
data were found (IARC 1980).
Lead carbonate has been produced commercially in the United
States since the 1600s; in 1976, U.S. production
was 1.48 million kilograms (3.3 million pounds), with imports in 1978 of
178,000 kg
(392,000 lb) (IARC 1980). U.S.
exports of lead carbonate in 2002
were 779,071 kg (1.7 million pounds) (USITC 2003). U.S. production of lead oxide in
1976 was 120 million kilograms (260 million
pounds), with imports of 20 million kilograms (44 million pounds
(IARC 1980). U.S.
imports of lead oxides in 2002 totaled 3.9 million
kilograms (8.6 million pounds), and exports totaled 1.7 million kilograms (3.7
million pounds) (USITC 2003). Commercial production
of lead naphthenate in the United
States was first reported in 1944.
Production of lead naphthenate was 8.2 million kilograms (18.1 million pounds)
in 1969, dropping to 2.2 million kilograms (4.9 million
pounds) in1977. U.S. production of lead tetraoxide in 1976 was 18
million kilograms (39.7 million pounds), with imports of 800,000
kg (1.8 million pounds) in 1976 and 1 million kilograms (2.2 million
pounds) in 1979, and exports were estimated at 1 million to 15 million
kilograms (2.2 million to 33 million pounds) in 1977 (IARC 1980).
Tetraethyl lead was first produced commercially in the United
States in 1923. Production was 266 million kilograms (590 million pounds) in 1964,
dropping to 148 million kilograms (330 million pounds) in 1977. U.S. imports of
tetraethyl lead in 1978 were
17,000 kg (37,500 lb). Commercial production of tetramethyl lead in
the United States
began in 1960; 54 million kilograms (119 million
pounds) was produced in 1977, and 13,800 kg (30,400 lb) was imported in 1974
(IARC 1980).
Exposure
The routes of environmental exposure to lead resulting
in its absorption into the body are inhalation (with 30% to 50% of the inhaled
dose
absorbed into the bloodstream), ingestion (with 8% to 15% of the
ingested dose absorbed into the bloodstream) and, to a limited extent, dermal
contact. Lead is released to the environment from both
natural and anthropogenic sources; however, most exposure results
from anthropogenic sources (e.g., mining, smelting, industrial
uses).
Lead exists in various inorganic and organic forms, which affect its
environmental fate, transport, and bioavailability. Regardless of the
form, however, lead is not degraded and remains available for exposure. In the
mid 1980s, combustion of leaded gasolinecontributed
about 90% of all anthropogenic lead emissions, but the percentage
decreased sharply through the late 1990s as a result of the phase-out
of leaded gasoline (ATSDR 1999, EPA 2003). Over 90% of the lead
released from the combustion of leaded gasoline was in the form of
inorganic lead halides (e.g., lead bromochloride), while less than 10%
was in the form of organic lead alkyls (e.g., tetraethyl lead). Tetraalkyl lead
compounds once accounted for 5% to 10% of the total particulate lead present in
the atmosphere but are no longer present in
significant quantities. Industrial processes, particularly lead smelters, are
now the primary source of lead emissions and accounted for
more than 78% of emissions in 2001 (EPA 2003).
According to EPA’s Toxics Release Inventory, over 4,000 facilities
released almost 22 million pounds of lead and 482 million pounds of
lead compounds to the environment in 2007 (TRI 2009). Concentrations
of lead in the air in the United
States declined by 97% between
1976 and 1995 and by 57% between 1993 and 2002 (ATSDR 1999, EPA
2003). Ambient concentrations are highly variable but may exceed
10 μg/m3 near industrial sources such as smelters (ATSDR
1999). A
1991 survey of lead levels in U.S.
urban air found a maximum quarterly mean concentration of
approximately 0.08 μg/m3. Lead concentrations typically are
lower in rural areas. In 1995, the estimated U.S
mean air lead concentration was 0.04 μg/m3 (EPA 1996). The estimated
daily average intake of lead by inhalation in 1991 was 2 μg for
an adult living in a U.S.urban setting, significantly lower than estimates from
the early 1980s (ATSDR 1999).
Lead concentrations in U.S.
drinking water generally are below
5 μg/L. Lead also is found in food, cigarette smoke, and alcoholic
beverages. Levels in food have declined since the elimination of
leadsoldered food cans between 1979 and 1989 (ATSDR 1999). In 1990,
the estimated daily intake of lead from consumption of food, water,
and beverages was approximately 4 μg for children aged 2 years or
younger, 6 to 9 μg for children aged 14 to 16, 6 to 9 μg
for adults aged
25 to 30, and 2 to 8 μg for adults aged 60 to 65. For young
children
the most common source of environmental lead exposure is direct
ingestion of paint chips and lead-laden dust and soil released from
aging painted surfaces. These sources can contribute an additional
daily intake of 5 μg for a toddler engaging in normal hand-to-mouth
activity (CDC 1997, Lanphear et al. 1998).
The most common route of occupational exposure to lead is inhalation of lead
fumes or lead-laden dusts in air and absorption of lead
through the respiratory system. Lead may also be ingested and abNational
Toxicology Program, Department of Health and Human Services
Report on Carcinogens, Twelfth Editiona€„ (2011
sorbed via the gastrointestinal tract (Bress and Bidanset 1991, Stauber
et al. 1994). The National Institute for Occupational Safety and Health
has estimated that more than three million Americans potentially are
occupationally exposed to some form of lead (Staudinger and Roth
1998). Occupations havingfrequent high exposure to lead include
battery-production worker, battery-recycling worker, foundry worker,
lead chemical worker, lead smelter and refinery worker, leaded-glass
worker, pigment worker, and radiator-repair worker. Occupations
with a moderate frequency of high exposure include firing-range
instructor, house renovator, lead miner, newspaper printer, plastics
worker, rubber worker, and steel welder or cutter. Occupations with
a low frequency of high exposure include automobile-repair worker
cable-production worker, construction worker, demolition worker,
firing-range participant, flame-solder worker, plumber or pipe fitter,
pottery-glaze producer, ship-repair worker, and stained-glass
producer (Fu and Boffetta 1995, ATSDR 1999). For U.S. industries
identified by the Occupational Safety and Health Administration as
having significant airborne lead in the workplace, the mean concentration
ranged from 165 μg/m3 at secondary smelters to 200 μg/m3
at storage-battery plants and brass, bronze, and copper foundries
(Froines et al. 1990).
Regulations
Consumer Product Safety Commission (CPSC
Accessible parts of products designed or intended primarily for children 12 and
younger may not
contain more than 300 ppm of lead; products exceeding this level are banned
hazardous
substances.
Paint or any other surface-coating materials for consumer use shall not contain
lead at levels greater
than 90 ppm.
Toys and other items for child use that bear paint with lead at levels greater
than 0.06% of the total
weight of the solid ordried paint film are banned.
Furniture articles for consumer use that bear paint with lead
at levels greater than 0.06% of the total
weight of the solid or dried paint film are banned.
Metal-cored candlewicks containing more than 0.06% lead by weight in the metal,
and candles with
such wicks, are banned.
Department of Transportation (DOT
Numerous specific lead compounds, and lead compounds not otherwise specified,
are considered
hazardous materials and marine pollutants, and special requirements have been
set for marking,
labeling, and transporting these materials.
Environmental Protection Agency (EPA
Clean Air Act
National Ambient Air Quality Standards: National primary and secondary ambient
air quality standard
= 1.5 μg/m3 for lead and lead compounds.
National Emissions Standards for Hazardous Air Pollutants: Lead compounds are
listed as a hazardous
air pollutant.
New Source Performance Standards: Manufacture of tetraethyl lead and
tetramethyl lead is subject to
provisions for the control of volatile organic compound emissions.
Prevention of Accidental Release: Threshold quantity (TQ) = 10,000 lb for
tetramethyl lead.
Urban Air Toxics Strategy: Lead compounds are identified as one of 33 hazardous
air pollutants that
present the greatest threat to public health in urban areas.
Mobile Source Air Toxics: Lead compounds are listed as a mobile source air
toxic for which regulations
are to be developed.
As defined by the Clean Air Act, gasoline which contains lead additives or
contains lead at a
concentration greater than0.05 g/gal shall not be sold for use in motor
vehicles.
Clean Water Act
Biosolids Rule: Limits have been established for lead in biosolids (sewage
sludge) when used or
disposed of via land application or incineration.
Effluent Guidelines: Lead and lead compounds are listed as toxic pollutants.
Numerous lead compounds are designated as hazardous substances.
Comprehensive Environmental Response, Compensation, and Liability Act
Reportable quantity (RQ) = 10 lb for lead, lead acetate, lead chloride, lead
fluoborate, lead fluoride,
lead iodide, lead nitrate, lead phosphate, lead stearate, lead subacetate, lead
sulfate, lead sulfide,
lead thiocyanate, and tetraethyl lead; = 1 lb for lead arsenate.
Emergency Planning and Community Right-To-Know Act
Toxics Release Inventory: Lead and lead compounds are listed substances subject
to reporting
requirements.
Reportable quantity (RQ) = 10 lb for tetraethyl lead; = 100 lb for tetramethyl
lead.
Threshold planning quantity (TPQ) = 100 lb for tetraethyl lead and tetramethyl
lead.
Federal Insecticide, Fungicide, and Rodenticide Act
All registrations for pesticides that have lead
arsenate as an active ingredient have been canceled.
Resource Conservation and Recovery Act
Characteristic Hazardous Waste: Toxicity characteristic leaching procedure
(TCLP) threshold = 5.0 mg/L
Listed Hazardous Waste: Waste codes for which the listing is based wholly or
partly on the presence of
lead or lead compounds = F035, F037, F038, K002, K003, K005, K046, K048, K049,
K051, K052,
K061, K062, K064, K069, K086, K100, K176,P110, P116, U144, U145, U146.
Lead and lead compounds are listed as hazardous constituents of waste.
Safe Drinking Water Act
Treatment technique, action level = 0.015 mg/L for lead.
Numerous requirements have been established to reduce exposure to lead in
drinking water due to
lead leaching from lead pipes and lead fittings.
Toxic Substances Control Act
A seller must disclose to the purchaser of a home any known lead-based paint
hazards.
Comprehensive regulations have been developed to prevent lead-based paint
poisoning in certain
residential structures.
Food and Drug Administration (FDA
A conspicuous label shall be on the surface of ornamental or decorative
ceramics that contain lead
warning that the vessel is not for food use and may be harmful if used for
such.
A number of food additives generally recognized as safe are permitted for use
in foods for human
consumption providing maximum lead levels do not exceed concentrations
prescribed in
21 CFR 84.
Action levels for lead in ceramic ware, hollowware, cups, mugs, and pitchers
range from 0.5 to 7 μg/mL
of leaching solution.
Lead acetate hair coloring must provide warning labels and may be safely used
in cosmetics intended
for coloring hair on the scalp if lead levels do not exceed 0.6% (weight to
volume).
Lead solder may not be used in food packaging.
Maximum allowed levels of lead in various color additives used in food, drugs,
cosmetics, and medical
devices are provided 21 CFR 73 and 74.
Maximum permissible level of lead in bottled water = 0.005 mg/L.
Select foodadditives are permitted for use in animal feed with maximum lead
levels ranging from
10 to 30 ppm.
Restrictions on the use of lead in various food additives are prescribed in 21
CFR 172.
Limits on the use of lead in feed and drinking water of animals are prescribed
in 21 CFR 584.
Tin-coated lead foil capsules shall not be used for wine bottles.
Department of Housing and Urban Development (HUD
HUD’s Lead-Based Paint Disclosure Rule requires that a seller or lessor
disclose to the purchaser the
presence of any lead-based paint in a home for sale, provide an EPA pamphlet on
the health
effects of lead, provide records on lead-based paint used in home, and provide
a 10-day period to
conduct a home inspection for lead-based paint or lead-based paint hazards.
HUD has established regulations to implement the provisions set forth in the
Residential Lead-Based
Paint Hazard Reduction Act. In part, the goals of these regulations are to
develop a national
strategy to build the infrastructure necessary to eliminate lead-based paint
hazards in all housing
as expeditiously as possible, and to ensure that the existence of lead-based
paint hazards is taken
into account in the development of government housing policies and in the sale,
rental, and
renovation of homes and apartments.
Occupational Safety and Health Administration (OSHA
While this section accurately identifies OSHA’s legally enforceable PELs for
this substance in 2010,
specific PELs may not reflect the more current studies and may not adequately
protect workers.
Permissible exposure limit(PEL) = 0.050 mg/m3 for
metallic lead, inorganic lead compounds, and
organic lead soaps.
Comprehensive standards have been developed for occupational exposure to
metallic lead, all
inorganic lead compounds, and organic lead soaps.
Guidelines
American Conference of Governmental Industrial Hygienists (ACGIH
Threshold limit value – time-weighted average (TLV-TWA) = 0.05 mg/m3
for lead, inorganic lead
compounds, and lead chromate; = 0.15 mg/m3 for tetramethyl lead;
= 0.1 mg/m3 for tetraethyl
lead.
Consumer Product Safety Commission (CPSC
Manufacturers are requested to eliminate the use of lead that may be accessible
to children from
products used in or around households, schools, or in recreation.
It is recommended that before purchasing products for resale, importers,
distributors, and retailers
make assurances that those products do not contain lead that may be accessible
to children.
National Institute for Occupational Safety and Health (NIOSH)
Recommended exposure limit (REL) = 0.05 mg/m3 (as metallic lead) for
metallic lead, lead oxides, and
lead salts (including organic salts such as lead soaps but excluding lead
arsenate); = 0.002 mg/m3
(as arsenic) for lead arsenate (15-min exposure) (listing for inorganic arsenic
compounds).
Immediately dangerous to life and health (IDLH)
limit = 100 mg/m3 (as metallic lead).
National Toxicology Program, Department of Health and Human Services
Report on Carcinogens, Twelfth Editiona€„ (2011)
Air concentrations should be maintained so that worker blood-lead levels remain
at less than0.06 mg
Pb/100 g of whole blood.
References
Akron.
2010. The Chemical Database. The Department of Chemistry at
the University of
Akron. https://ull.
chemistry.uakron.edu/erd and search on CAS number. Last
accessed: 3/23/10.
ATSDR. 1999. Toxicological Profile for Lead (Final
Report). Agency for Toxic Substances and Disease Registry.
https://www.atsdr.cdc.gov/toxprofiles/tp13.pdf.
Bress WC, Bidanset JH. 1991. Percutaneous in vivo and in vitro absorption of
lead. Vet Hum Toxicol 33(3):
212-214.
Budavari SM, O’Neal J, Smith A, Heckelman PE,
eds. 1996. The Merck Index, 12th ed. Whitehall, NJ:
Merck
& Company.
CDC. 1997. Update: blood lead levels—United States
1991-1994. Morbid Mortal Wkly Rep 46(7): 141-146.
EPA. 1996. National Air Quality and Emissions Trends
Report, 1995. U.S.
Environmental Protection Agency.
https://www.epa.gov/airtrends/aqtrnd95/report.
EPA. 2003. Lead. In Latest Findings on National Air
Quality: 2002 Status and Trends. U.S. Environmental
Protection Agency.
https://www.epa.gov/airtrends/aqtrnd02/2002_airtrends_final.pdf. p. 17.
Froines JR, Baron S, Wegman DH, O’Rourke S. 1990. Characterization
of the airborne concentrations of
lead in U.S.
industry. Am J Ind
Med 18(1): 1-17.
Fu H, Boffetta P. 1995. Cancer and occupational exposure to inorganic lead
compounds: a meta- analysis
of published data. Occup Environ Med 52(2): 73-81.
Guberman DE.
2010. Lead [Advance Release]. In Minerals Yearbook, Vol.
I, Metals and Minerals. U.S
Geological Survey.
https://minerals.usgs.gov/minerals/pubs/commodity/lead/myb1-2008-lead.pdf.Hammad
TA, Sexton M, Langenberg P. 1996. Relationship between blood
lead and dietary iron intake in
preschool children. A cross-sectional study.
Ann Epidemiol 6(1): 30-33.
Howe HE. 1981. Lead. In Kirk-Othmer Encyclopedia of
Chemical Technology, 3rd ed, vol. 14. New York
John Wiley & Sons. pp. 98-139.
HSDB. 2009. Hazardous Substances Data Bank. National Library of Medicine. Last
updated: 5/20/99. https://
toxnet.nlm.nih.gov/cgi-bin/sis/htmlgen?HSDB and search on CAS number or
compound name.
IARC. 1980. Lead and lead compounds. In Some Metals
and Metallic Compounds. IARC Monographs on
the Evaluation of Carcinogenic Risk of Chemicals to Humans, vol. 23. Lyon, France:
International Agency
for Research on Cancer. pp. 325-415.
IARC. 1987. Lead and lead compounds. In Overall Evaluations of Carcinogenicity. IARC Monographs
on the
Evaluation of Carcinogenic Risk of Chemicals to Humans, suppl 7. Lyon, France:
International Agency for
Research on Cancer. pp. 230-232.
IARC. 1990. Chromium and chromium compounds. In Chromium, Nickel, and Welding. IARC
Monographs on
the Evaluation of Carcinogenic Risks to Humans, vol. 49. Lyon, France:
International Agency for Research
on Cancer. pp. 49-256.
Lanphear BP, Matte TD, Rogers
J, Clickner RP, Dietz B, Bornschein RL, et al. 1998. The contribution of
lead-contaminated house dust and residential soil to children’s blood lead
levels. A pooled analysis of 12
epidemiologic studies. Environ Res 79(1): 51-68.
Lide DR, Frederikse HPR, eds. 1998. CRC Handbook of Chemistry
and Physics. New York:
CRC Press.
NTP.2003. Report on Carcinogens Background Document for Lead and Lead
Compounds. National Toxicology
Program. https://ntp.niehs.nih.gov/ntp/newhomeroc/roc11/Lead-Public.pdf.
Stauber JL, Florence
TM, Gulson BL, Dale LS. 1994. Percutaneous absorption of inorganic lead
compounds.
Sci Total Environ 145(1-2): 55-70.
Staudinger KC, Roth VS. 1998. Occupational lead poisoning. Am
Fam Physician 57(4): 719-726, 731-732.
Steenland K, Boffetta P. 2000. Lead and cancer in humans: where are we now? Am J Ind
Med 38(3): 295-299.
TRI. 2009. TRI Explorer Chemical Report. U.S. Environmental
Protection Agency. https://www.epa.gov/
triexplorer/ and select Lead.
USGS. 2009. Lead statistics. In
Historical Statistics for Mineral and Material Commodities in the United
States. U.S. Geological Survey. Last updated: 11/5/09.
https://minerals.usgs.gov/ds/2005/140/lead.pdf.
USGS. 2010. Lead. In Mineral
Commodity Summaries. U.S.
Geological Survey. https://minerals.usgs.gov/
minerals/pubs/commodity/lead/mcs-2010-lead.pdf. 2 pp
USITC. 2003. USITC Interactive Tariff and Trade DataWeb. United States International Trade Commission.
https://dataweb.usitc.gov/scripts/user_set.asp and search on HTS nos. 283670 and
282490. Last accessed
2003.
Waalkes MP, Diwan BA, Ward JM, Devor DE, Goyer RA. 1995. Renal tubular tumors
and atypical hyperplasias
in B6C3F1 mice exposed to lead acetate during gestation and lactation occur
with minimal chronic
nephropathy. Cancer Res 55(22): 5265-5271.
National Toxicology Program, Department of Health and Human Services