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CHEMINFO Record Number: 131
CCOHS Chemical Name: Lead acetate

Acetic acid, lead (2+) salt
Anhydrous lead acetate
Dibasic lead acetate
Lead diacetate
Lead acetate trihydrate
Lead (II) acetate
Lead dibasic acetate
Neutral lead acetate
Normal lead acetate
Plumbous acetate
Salt of Saturn
Sugar of lead
Acétate de plomb

Chemical Name French: Acétate de plomb anhydre
Chemical Name Spanish: Di(acetato) de plomo
CAS Registry Number: 301-04-2
Other CAS Registry Number(s): 6080-56-4
UN/NA Number(s): 1616
RTECS Number(s): AI5250000
EU EINECS/ELINCS Number: 206-104-4
Chemical Family: Lead and compounds / organic lead compound / saturated aliphatic monocarboxylic acid salt / alkanoic acid salt / acetic acid salt / acetate
Molecular Formula: C4-H8-O4-Pb2
Structural Formula: (CH3-CO2-)2.Pb++; (CH3-CO2-)2.Pb++.3H2O


Appearance and Odour:
White or colourless crystalline solid, flakes, granules or powder.(39,41- 43) Commercial grades are frequently brown or gray lumps.(39) Slight acetic acid odour.(43)

Odour Threshold:
Not available

Warning Properties:
Information not available for evaluation.

Lead (II) acetate is commercially available as the anhydrous salt (Pb(CH3COO)2) (CAS 301-04-02) and the trihydrate (Pb(CH3COO)2.3H2O) (CAS 6080- 56-4), which is the main commercial form.(41) It is available in reagent, purified and technical grades. Typical trace impurities are iron and chlorides.(39)

Uses and Occurrences:
Lead acetate trihydrate is used in the preparation of basic lead carbonate, lead chromate and lead salts of higher fatty acids; as a mordant in cotton dyes; as a water repellant; as a component in combined toning and fixing baths for daylight printing papers and for treating awnings and outdoor furniture to prevent removal of mildew and rot-proofing agents by rain or laundering. It is also used in the preparation of rubber antioxidants; as a processing agent in the cosmetic, perfume and toiletry industries; as a component of colouring agents for adhesives; and in the preparation of organic lead soaps used as driers of paints and inks. Anhydrous lead acetate is used for the preparation of other lead salts.(41)


White crystalline solid or brown or gray lumps. Slight acetic acid odour. Will not burn. Can decompose at high temperatures forming acetic acid and lead/lead oxides. DANGER OF CUMULATIVE EFFECTS if inhaled or ingested. Symptoms may include headache, fatigue, nausea, abdominal cramps, joint pain, metallic taste in the mouth, vomiting and constipation or bloody diarrhea. Can cause harmful effects to the nervous system. SUSPECT CANCER HAZARD - may cause cancer. REPRODUCTIVE HAZARD - may cause harmful effects in the unborn child; may have serious adverse effects on the male and female reproductive systems. MUTAGEN - may cause genetic damage.


Effects of Short-Term (Acute) Exposure

One case report describes moderate exposure to inorganic lead while sandblasting lead-based paint for twelve-hours. Symptoms included headache, fatigue, nausea, abdominal cramps, and joint pain.(1) Other health effects such as a metallic taste in the mouth, vomiting and constipation or bloody diarrhea might also be expected to occur.(2) Harmful effects due to short-term exposure to inorganic lead compounds are rarely seen any more because of strict controls used in workplaces where lead exposure might occur.
Lead accumulates in the body and inorganic lead compounds are well known to cause significant health effects following long-term (chronic) exposure. If a significant amount of lead has accumulated in the body, symptoms of long-term toxicity may develop after what may seem to be a short-term acute exposure.(3) For more information, refer to "Effects of Long-Term (Chronic)/Exposure" below.

Skin Contact:
Inorganic lead compounds are not known to cause skin irritation and are poorly absorbed through the skin.(1,4)

Eye Contact:
Concentrated solutions or high levels of dust or fumes of lead acetate may cause irritation, although there is no relevant human or animal information available. Water solutions of lead acetate caused clouding and white, chalky crusting of the cornea and eyelid, when applied to people who had previously injured corneas.(5)

Symptoms of ingestion of a very large dose over a short time period may include headache, fatigue, nausea, abdominal cramps, and joint pain. Other health effects such as a metallic taste in the mouth, vomiting and constipation or bloody diarrhea might also be expected to occur.(2) Reports of effects following short-term ingestion in adults are very rare, particularly now that strict controls are used in workplaces where lead exposure might occur.
Cases of ingestion of inorganic lead compounds by children are commonly reported. Children are much more susceptible to the effects of lead than adults and, therefore, effects observed in children are not necessarily relevant to adults.

Effects of Long-Term (Chronic) Exposure

Long-term health effects of inorganic lead compounds, including lead acetate, are similar following inhalation or ingestion. Inorganic lead compounds, like lead acetate, are poorly absorbed through the skin.

Blood lead levels are often used as a general indicator of how much exposure to lead has occurred. As a result, blood lead levels are provided in most reports which discuss the potential health effects of exposure to inorganic lead compounds, rather than airborne levels. The relationship between airborne lead levels and blood lead levels is complicated and depends many factors, including other sources of lead exposure and individual physical differences. Several studies indicate that an airborne exposure of 0.05 mg/m3 compares to a blood lead level of approximately 30-40 micrograms/deciLitre (range 20-60 micrograms/deciLitre).(6,7)
Average blood lead levels of adults with no occupational exposure vary widely depending upon factors such as smoking habits, nutritional status, geographic area, and recreational exposures (for example, the use of firearms). In most industrialized countries, blood lead levels in adults without occupational exposure are typically less than 20-30 micrograms/deciLitre.(8) In this review, blood lead levels below 50 micrograms/deciLitre are considered to reflect relatively low lead exposure; blood lead levels of 51-100 micrograms/deciLitre reflect moderate lead exposure, and blood lead levels above 100 micrograms/deciLitre would reflect high lead exposure. Many jurisdictions require that workers be monitored more closely or be removed from exposure if their blood lead levels exceed a certain level. Contact your regulatory jurisdictions for information.

Long-term lead toxicity is commonly referred to as "plumbism" and may include effects on the following body systems.

Nervous System:
CENTRAL NERVOUS SYSTEM: Central nervous system (CNS) or brain function has been harmed in workers with long-term, low-level lead exposure.(9) Symptoms typically occur with low to moderate exposure and include forgetfulness, irritability, tiredness, headache, fatigue, impotence, decreased libido (sexual drive), dizziness, and depression. Repeated exposure to moderate to high levels can cause encephalopathy (a progressive degeneration of certain parts of the brain). Early symptoms of encephalopathy include dullness, irritability, poor attention span, headache, muscular tremor, loss of memory and hallucinations. More severe symptoms occur at very high exposures and include delirium, lack of coordination, convulsions, paralysis, coma and death.(1)
Repeated exposed to inorganic lead compounds can affect behaviour. Lead smelter workers with long-term exposure to low levels of lead have experienced altered mood states.(10) Effects at moderate exposures include disturbances in hand-eye coordination, reaction times, visual motor performance, and mental performance.(1,11)
Disturbances to vision have been observed in workers after months to years of overexposure to inorganic lead compounds. Symptoms range from very slight visual changes to a gradual decrease in vision, with slow recovery or, in some instances, progression to blindness.(5)
Changes in hearing ability have also been reported in lead-exposed workers, particularly those with moderate to high exposure.(12)

PERIPHERAL NERVOUS SYSTEM: Peripheral nerve function (nerves of the arms and legs) has been harmed in workers exposed to low to moderate levels of inorganic lead. Effects were shown to be reversible following a 5-month exposure.(1,6) However, only partial recovery may occur, particularly if lead exposure continues or treatment is not carried out.(2)
Peripheral neuropathy (loss of myelin which insulates the nerves) has been observed following long-term overexposure to inorganic lead compounds. This disorder is often referred to as "lead palsy" and symptoms include weakness of the arms and legs and weakness and paralysis of the wrist, fingers and ankles. Decreased hand dexterity (measured by finger tapping speed) has been reported in workers with low to moderate exposure to inorganic lead.(13,40) Footdrop and wristdrop (an inability to hold the foot or hand extended) commonly occur with higher exposures.(2)

Skin Sensitization:
Lead acetate is not known as a skin sensitizer. Two case reports of lead-exposed workers developing dry, red, itchy skin (dermatitis) and then testing positive in patch tests with lead acetate cannot be evaluated due to insufficient details.(18)

Heart/Blood Vessels:
Inorganic lead can cause harmful effects to certain types of blood cells, including reduced hemoglobin production and reduced life span and function of red blood cells. Reduced hemoglobin production has been associated with low-level exposure to inorganic lead in the workplace.(6) Hemoglobin is the molecule responsible for carrying oxygen to body tissues. With moderate exposures, anemia has been observed in lead- exposed workers.(14)
Low, moderate or high exposures to inorganic lead compounds may increase blood pressure, particularly in men.(1,6,14)
No firm conclusions can be drawn from two studies in which electrocardiographic (ECG) abnormalities were observed in employees with moderate exposure to inorganic lead compounds.(1) Details on study design are not available for one study. The other study only examined a relatively small number of employees (95).

Digestive System:
Effects on the gastrointestinal tract tend to be observed following high exposure to inorganic lead compounds, although they have sometimes been noted in workers with moderate exposure. Symptoms include loss of appetite, inflammation of the stomach walls (gastritis) and colic, with severe abdominal pain, cramps, nausea, vomiting, constipation, anorexia (loss of appetite), weight loss and decreased urination.(1) In severe cases of lead exposure, a deposit of lead occurs in the gums near the base of the teeth. This deposit is visible as a blue-gray line.

Kidneys/Urinary System:
Reversible kidney injury has been observed in some workers with repeated low exposure to inorganic lead compounds.(1,4,14) Irreversible kidney damage has been observed following long-term, moderate exposures.(4,15) An increased number of deaths due to kidney disease were observed in smelter and lead production workers with moderate lead exposure.(1,16)

Endocrine System:
Whether or not long-term exposure to inorganic lead is associated with harmful effects on thyroid and immune system function has not been well studied yet and the available evidence is weak.(1,4,7,15) In one study, firearm instructors with low exposure to inorganic lead had reduced numbers of some types of immune system cells. This observation is a very early indicator of impaired immune response.(17) With moderate levels of exposure, workers had more colds and flu infections, but did not have impaired antibody production.(1)


Inorganic lead compounds are probably carcinogenic to humans.(54)
The International Agency for Research on Cancer (IARC) has concluded there is limited evidence for the carcinogenicity of exposure to inorganic lead compounds to humans. IARC evaluated the available epidemiological evidence and found 6 occupational cohort studies of high-exposed workers to be particularly informative. One study showed a statistically significant two-fold excess of lung cancer among smelter workers, but this excess may have been caused by exposure to arsenic. In four studies, there was a fairly consistent 30-50% excess of stomach cancer. However, it is possible that other factors (e.g. ethnicity, dietary habits) played a role in the stomach cancer excesses. Five studies reported findings for kidney cancer. In one study, there was a statistically significant two-fold excess of kidney cancer. All five studies were based on small numbers of deaths. Four studies reported findings of tumours of the brain and nervous system, but there was no consistent pattern in these studies. In a separate cohort of workers, a nested case-control study showed a statistically significant, positive dose-response relationship between blood lead concentrations and the risk for glioma; this cohort had lower exposures to lead than the other occupational cohorts. All of these studies were also based on small numbers of deaths.(54)
Another comprehensive review of more than twenty human studies involving workers exposed to inorganic lead compounds in battery industries, smelters, pigment factories, printing trades and the glass manufacturing industry concluded that there was a significant excess risk of overall cancer (stomach, lung, and bladder cancers), but not cancer of the kidney.(20)

The International Agency for Research on Cancer (IARC) has concluded that this chemical is probably carcinogenic to humans (Group 2A).

(Inorganic lead compounds)

The American Conference of Governmental Industrial Hygienists (ACGIH) has designated this chemical as an animal carcinogen (A3).

The US National Toxicology Program (NTP) has listed this chemical as reasonably anticipated to be a human carcinogen.

(Lead and Lead Compounds)

Teratogenicity and Embryotoxicity:
Inorganic lead exposure during pregnancy has historically been associated with significant harmful effects on pregnancy, including increased miscarriages and stillbirths.(1,4,21) Many of these historical reports involved exposure to very high levels of lead, as well as other environmental, social and lifestyle characteristics which may have caused or contributed to the observed effects. Lead exposure which has not also caused significant toxicity in the mother has not been clearly associated with teratogenic or embryotoxic effects.(7,22,23,24)
Several non-occupational studies indicate that low to moderate exposure to lead during pregnancy and in early childhood, can produce harmful effects on neurobehavioural development and IQ, a measure of intelligence.(16,25) Two animal studies have also shown subtle neurobehavioural effects following exposures which did not cause harmful effects in the mothers.(26,27)
Reduced birth weight and shorter pregnancy may also be related to low level lead exposure. However, this literature is inconsistent and no firm conclusions can be drawn.(7,22,28)

Reproductive Toxicity:
Significant harmful effects have been reported in the male reproductive system following low to moderate exposures. Harmful effects on the female reproductive system have not been clearly demonstrated following low to moderate lead exposure. Harmful reproductive effects have been reported in both men and women following high level exposures.
Despite limitations in human population studies, the overall literature suggests that moderate lead exposures are associated with significant male reproductive effects, such as low sperm count and abnormal sperm structure and mobility. Recent reviews conclude that lead is a male reproductive toxicant, producing reduced fertility, at exposure levels that produce a blood lead level exceeding 40 microg/dL or a level exceeding 25 microg/dL for a period of years.(29,30,56,57,60) There is moderate evidence that adverse male reproductive effects (reduced fertility, lowered sperm counts and increased numbers of abnormal sperm) may occur at even lower exposure levels.(56,58,60) In Yugoslavia, 101 male workers exposed to low to high levels of inorganic lead had reduced semen volume and density; reduced total, mobile and viable sperm; and increased numbers of abnormal sperm.(16) Another study of 150 male workers with moderate to high, long-term exposure to inorganic lead compounds showed signs of reduced fertility, as measured by reduced viability of spermatozoa, low sperm counts and abnormal sperm structure.(31) Similar effects have been observed in animal studies.
Associations between workplace exposure of the father and an increased rate of miscarriage or fetal death have also been reported.(32,33) A critical review of the literature which relates these effects directly to the male (that is, through the sperm) indicates the information is limited and incomplete and that published results are conflicting.(7) Therefore, no firm conclusions can be drawn. Historically, these effects have been related to poor hygiene procedures resulting in exposure of a pregnant woman to lead which has been carried home on her partner's work clothing.
There are historical reports of reduced fertility and menstrual disorders in women with relatively high lead exposures.(7,30) There are no recent human studies which meet current scientific standards. Animal studies are inconclusive.

Lead acetate is considered mutagenic, based on positive results observed in both the somatic and germ cells of animals exposed by relevant routes of exposure. Several studies have reported positive results (chromosomal aberrations) in the white blood cells of workers with low to moderate exposure. Other studies have shown no increase in chromosomal aberrations in workers with similar exposures.(1)

Toxicologically Synergistic Materials:
Significantly increased kidney toxicity was reported in rats given lead acetate and selected nitroso- or amide-type chemicals.(19) Nutritional status and exposure to other metals such as calcium, phosphorous, iron, zinc and copper may influence lead absorption and toxicity.(1)

Potential for Accumulation:
Inorganic lead compounds are absorbed into the body following inhalation or ingestion. It is estimated that 30-50% of inhaled lead and that 5-15% of ingested lead is absorbed. The amount of lead absorbed is affected by many factors, including particle size (inhalation), as well as age, nutritional status and time of last meal (ingestion). Inorganic lead compounds are poorly absorbed through the skin. Once absorbed, inorganic lead compounds are distributed throughout the body. They can readily cross the placenta, reaching the unborn child. The majority of absorbed lead is excreted in the urine and feces. Small amounts are also excreted in sweat, hair, fingernails and breast milk. Some lead is not excreted, but is stored in the bones and accumulates in the body. It can take more than 20 years for half of the inorganic lead in the bones to be removed from the body after the last exposure to lead. Lead which is released from the bones can cause health effects, even if there is no current exposure to lead. In some cases, lead can be rapidly released from the bones because of fractures, infections or other stresses on the body.(1,2,4,7,14)


This chemical is very toxic. Take proper precautions to ensure your own safety before attempting rescue (e.g. wear appropriate protective equipment). Remove source of contamination or move victim to fresh air. Immediately obtain medical attention.

Skin Contact:
Avoid direct contact. Wear chemical protective clothing, if necessary. As quickly as possible, remove contaminated clothing, shoes and leather goods (e.g. watchbands, belts). Flush with lukewarm, gently flowing water for 5 minutes. Obtain medical advice.

Eye Contact:
Avoid direct contact. Wear chemical protective gloves, if necessary. DO NOT allow victim to rub eye(s). Let the eye(s) water naturally for a few minutes. Have victim look right and left, and then up and down. If particle/dust does not dislodge, flush with lukewarm, gently flowing water for 5 minutes or until particle/dust is removed, while holding the eyelid(s) open. If irritation persists, immediately obtain medical attention. DO NOT attempt to manually remove anything stuck to the eye(s).

NEVER give anything by mouth if victim is rapidly losing consciousness, is unconscious or convulsing. Have victim rinse mouth thoroughly with water. DO NOT INDUCE VOMITING. If vomiting occurs naturally, have victim rinse mouth with water again. Immediately obtain medical attention.

First Aid Comments:
All first aid procedures should be periodically reviewed by a doctor familiar with the material and its conditions of use in the workplace.

Lead acetate can accumulate in the body and cause significant long-term health effects. Medical advice should be sought following any exposure.

Note to Physicians:
Many jurisdictions have specific regulations for lead. These regulations may include requirements for medical surveillance programs, including pre- employment and pre-placement examinations, periodic medical examinations, clinical tests, health education and record keeping. Obtain detailed information from the appropriate government agency in relevant jurisdictions.


Flash Point:
Not combustible (will not burn).

Lower Flammable (Explosive) Limit (LFL/LEL):
Not applicable

Upper Flammable (Explosive) Limit (UFL/UEL):
Not applicable

Autoignition (Ignition) Temperature:
Not applicable

Sensitivity to Mechanical Impact:
Not sensitive. Stable metal.

Sensitivity to Static Charge:
Not applicable. Not combustible.

Combustion and Thermal Decomposition Products:
Acetic acid and lead/lead oxides.(44)

Fire Hazard Summary:
Lead acetate does not burn or support combustion. Heating lead acetate to high temperatures may produce acetic acid and lead oxides. Well-sealed containers may rupture violently when exposed to fire or excessive heat for sufficient time.

Extinguishing Media:
Does not burn. Use fire extinguishing agents suitable for materials which are burning.

Fire Fighting Instructions:
Evacuate area and fight fire from a safe distance. Approach fire from upwind to avoid hazardous vapours and toxic decomposition products.
Closed containers may rupture violently when exposed to the heat of the fire. If possible, isolate materials not yet involved in the fire, and move containers from the fire area if this can be done without risk, and protect personnel. Otherwise, fire-exposed containers or tanks should be cooled by application of water spray. Application should begin as soon as possible and should concentrate on any unwetted portions of the container. Apply water from the side and from a safe distance until well after the fire is out. For a massive fires, consider using unmanned hose holders or monitor nozzles. In any case, stay away from the ends of tanks involved in the fire.

Protection of Fire Fighters:
Lead acetate and its decomposition products are hazardous to health. Do not enter without wearing specialized protective equipment suitable for the situation. Firefighter's normal protective clothing (Bunker Gear) will not provide adequate protection. A full-body encapsulating chemical resistant suit with positive pressure self-contained breathing apparatus (MSHA/NIOSH approved or equivalent) may be necessary.


NFPA - Comments:
NFPA has no listing for this chemical in Codes 49 or 325.


Molecular Weight: 325.28 (anhydrous); 379.33 (trihydrate)

Conversion Factor:
Not applicable

Physical State: Solid
Melting Point: 280 deg C (536 deg F) (anhydrous) (40,41,45); 75 deg C (167 deg F) (trihydrate) (41,45)
Boiling Point: Decomposes at 200 deg C (392 deg F) (trihydrate) (41,42,45)
Relative Density (Specific Gravity): 3.25 at 20 deg C (water = 1) (anhydrous) (45); 2.55 (water = 1) (trihydrate) (41,42,45)
Solubility in Water: Very soluble - 44.3 g/100 mL at 20 deg C (anhydrous) (41,42,45); 45.61 g/100 mL at 15 deg C (trihydrate) (41,42,45)
Solubility in Other Liquids: Very soluble in glycerol; very slightly soluble in ethanol (anhydrous) (44). Insoluble in ethanol (trihydrate) (41,42,45)
Coefficient of Oil/Water Distribution (Partition Coefficient): Not available
pH Value: 5.5-6.5 (5% aqueous solution at 25 deg C) (43)
Vapour Density: Not applicable
Vapour Pressure: Probably essentially zero.
Saturation Vapour Concentration: Not applicable
Evaporation Rate: Not available. Probably very low at normal temperatures.
Critical Temperature: Not available


Lead acetate is normally stable. It absorbs carbon dioxide from the air.(44) May decompose on exposure to light or excessive heat.(44) Upon heating, the trihydrate loses some of its water of crystallization.(41) Above 100 deg C, it begins to lose some acetic acid and it decomposes completely at 200 deg C.(43)

Hazardous Polymerization:
Does not occur

Incompatibility - Materials to Avoid:

NOTE: Chemical reactions that could result in a hazardous situation (e.g. generation of flammable or toxic chemicals, fire or detonation) are listed here. Many of these reactions can be done safely if specific control measures (e.g. cooling of the reaction) are in place. Although not intended to be complete, an overview of important reactions involving common chemicals is provided to assist in the development of safe work practices.

STRONG OXIDIZING AGENTS (e.g. perchlorates, peroxides) - reaction may be violent. Risk of fire and explosion.(44)
STRONG ACIDS (e.g. sulfuric acid) - reaction may be vigorous or violent, giving off acetic acid.(44)
STRONG BASES (e.g. sodium hydroxide, potassium hydroxide) - reaction may be vigorous or violent.(44)
POTASSIUM BROMATE - react to form the lead acetate-lead bromate double salt, which is explosive and very sensitive to friction.(46)

Hazardous Decomposition Products:
Acetic acid

Conditions to Avoid:
Generation of airborne dusts and mists, high temperatures.

Corrosivity to Metals:
Dry lead acetate is probably not corrosive. Lead acetate solutions are corrosive to gray cast iron, steel and aluminum at normal temperatures, and to copper, bronze and brass at higher temperatures (93 deg C).(47)


Standard animal toxicity values (for example, LD50s) are not available for lead acetate.
In rats, the minimum lethal dose is 11000 mg/kg.(34)

Eye Irritation:

No conclusions can be drawn from studies where rabbit eyes were damaged before lead acetate was applied.(5) No other information was located.

Effects of Long-Term (Chronic) Exposure:

Extensive studies on the long-term health effects of lead acetate on animals have not been conducted because effects in humans have been well-defined. Repeated oral exposure to lead acetate has reduced survival and caused harmful blood, kidney, nervous system and immune effects in experimental animals.(1,4) A dose-dependent decrease in survival time was observed in mice fed 0.5 to 4.0% in their diets.(35) Kidney damage was observed in rats given 37 mg/kg/day lead acetate in their drinking water for 76 weeks.(1) Suppression of the immune system was observed in rats with blood lead levels of 29.3 micrograms/deciLitre.(4)

The International Agency for Research on Cancer (IARC) has determined that the evidence for carcinogenicity to animals is sufficient for inorganic lead compounds.(54)
Kidney tumours have been observed following oral administration of lead acetate to rats. In a series of well conducted studies, kidney tumours occurred in 5/50 male rats that received 27 mg lead/kg/day, in 10/20 males that received 56.5 mg lead/kg/day and in 16/20 males and 7/20 females that received 105 mg/kg/day. No kidney tumours were observed in controls or in rats given 0.9-7.0 mg/kg/day.(1,19)

Teratogenicity, Embryotoxicity and/or Fetotoxicity:
Numerous studies have investigated the effect of lead acetate on pregnancy outcome in animals.(1,4) In the majority of studies, maternal toxicity was not evaluated and, therefore, the studies have not been reviewed here. Some of the remaining studies have shown significant harmful effects in the offspring (teratogenicity, stillbirths and spontaneous abortions), but only at exposures that also caused significant toxicity in the mothers. Other studies were not reviewed due to the use of non-relevant routes of exposure (for example, injection) or design problems which limit the relevance of the results. Two studies have shown neurobehavioural effects in the offspring of rats at oral exposures which did not produce maternal toxicity.(26,27)
Subtle behavioral effects were observed in the offspring of rats given 200 or 400 mg/L lead acetate in drinking water 14 days prior to mating and during pregnancy and nursing.(27) In another study, learning ability (maze measurements) was impaired in the offspring of male and/or female rats administered 500 mg/kg/day lead acetate orally for 60 days prior to mating and, for females, during pregnancy and nursing.(26) Although the exposure to lead acetate occurred during mating, pregnancy and nursing, the reported effects are likely predominantly related to exposure during pregnancy. This conclusion is based on a number of considerations, including the fact that inorganic lead compounds readily cross the placenta, the evidence of embryotoxic/teratogenic effects in teratology studies conducted at maternally toxic doses of lead acetate, recognition of the central nervous system as a target organ for inorganic lead compounds, and the observation that lead acetate has not been demonstrated to be a germ cell mutagen.

Reproductive Toxicity:
Lead is a reproductive toxin in animals. Altered testicular structure, effects on sperm, and effects on hormonal and biochemical processes have been observed in male animals.(1,29,35) Results of studies on female animals are inconclusive.(16,36) Effects on fertility have been observed in multi-generation studies, but only at doses which also have caused toxicity in the parents.(37)
Abnormal sperm were observed in male mice administered 1.0% lead acetate in the diet for 8 weeks.(35) Sperm count and diameter of seminiferous tubules were reduced in rats given 45 mg/kg lead as lead acetate in their drinking water for 60 days. Testicular wasting and cellular degeneration were observed at 90 mg/kg/day. Effects were not seen at 22 mg/kg. Reversibility of these effects not addressed.(1,29) Fertility was not affected in male mice given lead acetate in their drinking water at concentrations ranging from 0.1 to 1000 mg lead/L for 9 months (21) or in rats administered 0.3% lead acetate in drinking water for 70 days (38). Irregular reproductive cycles were observed in female rats administered 5 or 100 micrograms/day of lead acetate in the diet for 30 days. At the high dose, ovarian cysts and decreased numbers of corpus luteus were also observed.(36) Firm conclusions cannot be drawn from this study because the results were not statistically analyzed. In another study, long-term exposure to lead, with blood lead levels of approximately 35 micrograms/decilitre, resulted in decreases in circulating reproductive hormones in female monkeys, but did not affect menstruation.(16) Significant impairments in reproduction were not observed in several one- or two-generation studies in which animals were administered lead acetate in the diet or drinking water.(4) In a two-generation study, the number of first pregnancies and the number of offspring/litter were decreased when male and female rats were fed a diet containing high levels (1.0%) of lead as lead acetate. Parental toxicity was not evaluated in this study, but would have been expected at the dose level administered.(37)

Lead acetate is mutagenic, based on positive results obtained in both the somatic and germ cells of animals exposed by relevant routes of exposure.
Male mice were administered 200 or 400 mg/kg purified lead acetate in their diet once daily for 5 days. A dose-dependant, statistically significant increase in chromosomal aberrations (with and without gaps) was observed in the bone marrow cells of mice evaluated after 1, 7 or 14 days exposure to both doses. A dose-dependant, statistically significant increase in the percentage of metaphases with chromosomal abnormalities was also observed in spermatocytes from mice evaluated after 24 and 48 hours exposure to both doses.(50) Male rats were orally dosed with 10 mg/kg lead acetate (analytical grade) in distilled water for 4 weeks (5 times/wk). Untreated and distilled water control groups were used. Treatment with lead acetate significantly increased numerical aberrations in the bone marrow cells, but not the number of structural aberrations (with or without gaps).(51) Male mice were exposed to by inhalation to 6.8 mg/m3 (cited as 0.0068 microg/cc) lead acetate aerosol (particle size less than 1 microm) once for 60 minutes (Group 1), for three 60-minute periods over 2 weeks (Group 2), for five 60-minute periods over 3 weeks (Group 3) or for seven 60-minute periods over 4 weeks (Group 4). Control animals inhaled deionized water for the same time periods. DNA damage (single strand breaks and alkali labile sites) was analyzed using the Comet assay. Statistically significant increases in DNA damage were observed in lung cells of exposed animals in Groups 1 and 3, but not 2 and 4, due to high variability. Statistically significant increases in DNA damage were observed in kidney cells of exposed animals in Groups 2, 3 and 4, in liver cells from animals in all exposed groups, and in brain and bone marrow cells from exposed animals in Groups 2 and 4.(53) This study is limited by the use of only 1 exposure concentration. In a non-standard, but well-conducted test, male rats were given a single oral dose of 160 mg/kg or 3 doses of 107 mg/kg lead acetate (99% pure). The rats were partially nephrectomized and injected intravenously with folic acid to increase the proliferative activity of the kidney cells. A significant increase in DNA damage, as measured by the Comet Assay, was observed in kidney cells from animals exposed to 107 mg/kg. A significant increase in micronucleated cells was observed in kidney cells from animals in both dose groups.(52)
Lead acetate is not mutagenic in bacteria or yeast. Positive and negative results have been obtained in cultured mammalian cells.(1)


Selected Bibliography:
(1) Agency for Toxic Substances and Disease Registry. Toxicological profile for lead. TP-92/12. US Department of Health and Human Services, 1993
(2) The Report on the Designation of Lead in Ontario. Occupational Health and Safety Division, Ontario Ministry of Labour, July 1981
(3) Gosselin, R.E., et al. Clinical toxicology of commercial products. 5th ed. Williams and Wilkins, 1984. p. III-226 to III-239
(4) Cohen, A.J., et al. Review of lead toxicology relevant to the safety assessment of lead acetate as a hair colouring. Food and Chemical Toxicology. Vol. 29, no. 7 (1991). p. 485-507
(5) Grant, W.M., et al. Toxicology of the Eye. 4th ed. Charles C. Thomas, 1993. p. 884-895
(6) Lead. In: Documentation of the threshold limit values and biological exposure indices. 6th ed. American Conference of Governmental Industrial Hygienists, 1991. p. 847-852, BEI-99 to BEI-104
(7) Nearing, J.N. Health effects of inorganic lead with an emphasis on the occupational setting: an update. Ontario Ministry of Labour, 1987
(8) The Commission on Lead in the Environment. Health effects of lead. Edited by M.C.B. Hotz. The Royal Society of Canada, Sept. 1986
(9) Hirata, M., et al. Effects of lead exposure on neurophysiological parameters. Environmental Research. Vol. 63, no. 1 (Oct. 1993). p. 60-69
(10) Maizlish, N.A., et al. Neurobehavioural evaluation of Venezuelan workers exposed to inorganic lead. Occupational and Environmental Medicine. Vol. 52, no. 6 (June 1995). p. 408-414
(11) Balbus-Kornfeld, J.M., et al. Cumulative exposure to inorganic lead and neurobehavioural test performance in adults: an epidemiological review. Occupational and Environmental Medicine. Vol. 52, no. 1 (Jan. 1995). p. 2-12
(12) Otto, D.A., et al. Auditory and visual dysfunction following lead exposure. NeuroToxicology. Vol. 14, no. 2-3 (Summer/Fall 1993). p. 191-208
(13) Matsumoto, T., et al. Relations between lead exposure and peripheral neuromuscular functions of lead-exposed workers: results of tapping test. Environmental Research. Vol. 61, no. 2 (May 1993). p. 299-307
(14) Toxic effects of metals: lead. In: Casarett and Doull's Toxicology: the basic science of poisons. 5th ed. Edited by M.O. Amdur, et al. McGraw- Hill, 1995. p. 703-709
(15) Gennart, J.P., et al. Assessment of thyroid, testes, kidney and autonomic nervous system function in lead-exposed workers. International Archives of Occupational and Environmental Health. Vol. 64, no.1 (1992). p. 49-57
(16) Goyer, R.A. Lead toxicity: current concerns. Environmental Health Perspectives. Vol. 100 (Apr. 1993). p. 177-187
(17) Fischbein, A., et al. The immune system as target for subclinical lead related toxicity. British Journal of Industrial Medicine. Vol. 50, no. 2 (Feb. 1993). p. 185-186
(18) Cronin, E. Contact dermatitis. Churchill Livingstone, 1980. p. 337- 338
(19) International Agency for Research on Cancer. Lead and lead compounds: lead and inorganic lead compounds (Group 2B). In: IARC monographs on the evaluation of carcinogenic risks to humans. Suppl. 7. Overall Evaluations of Carcinogenicity: an updating of IARC monographs volumes 1 to 42. World Health Organization, 1987. p. 230-232
(20) Fu, H., et al. Cancer and occupational exposure to inorganic lead compounds: a meta-analysis of published data. Occupational and Environmental Medicine. Vol. 52, no. 2 (Feb. 1995). p. 73-81
(21) International Agency for Research on Cancer. Lead and lead compounds. In: IARC monographs on the evaluation of carcinogenic risks to humans. Vol. 23. Some metals and metallic compounds. World Health Organization, July 1980. p. 325-415
(22) Ernhart, C.B. A critical review of low-level prenatal lead exposure in humans. 1. Effects on the fetus and newborn. Reproductive Toxicology. Vol. 6, no. 1 (1992). p. 9-19
(23) Ernhart, C.B. A critical review of low-level prenatal lead exposure in humans. 2. Effects on the developing child. Reproductive Toxicology. Vol. 6, no. 1 (1992). p. 21-40
(24) Bellinger, D. Teratogen update: lead. Teratology. Vol. 50, no. 5 (Nov. 1994). p. 367-373
(25) Hatch, M.C. Prenatal and postnatal exposure to lead in relation to infant development: A review. Division of Standards Development and Transfer Technology, National Institute for Occupational Safety and Health, Jan. 1992 (NIOSH Purchase Order No. 0009139428)
(26) Brady, K., et al. Influence of parental lead exposure on subsequent learning ability of offspring. Pharmacology Biochemistry and Behavior. Vol. 3, no. 4 (Sept. 1975). p. 561-565
(27) Taylor, D.H., et al. Low level lead (Pb) exposure produces learning deficits in young rat pups. Neurobehavioral Toxicology and Teratology. Vol. 4, no. 3 (1982). p. 311-314
(28) Andrews, K.W., et al. Prenatal lead exposure in relation to gestational age and birth weight: a review of epidemiologic studies. American Journal of Industrial Medicine. Vol. 26, no. 1 (July 1994). p. 13-32
(29) Winder, C. Lead, reproduction and development. NeuroToxicology. Vol. 14, no. 2-3 (Summer/Fall 1993). p. 303-318
(30) Tas, S., et al. Occupational hazards for the male reproductive system. Current Reviews in Toxicology. Vol. 26, no. 3 (1996). p. 261-307
(31) Lancranjan, I., et al. Reproductive ability of workmen occupationally exposed to lead. Archives of Environmental Health. Vol. 30, no. 8 (Aug. 1975). p. 396-401
(32) Savitz, D.A., et al. Review of epidemiologic studies of paternal occupational exposure and spontaneous abortion. American Journal of Industrial Medicine. Vol. 25, no. 3 (Mar. 1994). p. 361-383
(33) Kristensen, P., et al. Perinatal outcome among children of men exposed to lead and organic solvents in the printing industry. American Journal of Epidemiology. Vol. 137, no. 2 (Jan. 15, 1993). p. 134-144
(34) Venugopal, B., et al. Metal toxicity in mammals. Volume 2. Chemical Toxicity of metals and metalloids. Plenum Press, 1978. p. 185-195
(35) Eyden, B.P., et al. Long-term effects of dietary lead acetate on survival, body weight and seminal cytology in mice. Bulletin of Environmental Contamination and Toxicology. Vol. 20, no. 3 (Sept. 1978). p. 266-272
(36) Hilderbrand, D., et al. Effect of lead acetate on reproduction and metabolism. Trace Substances in Environmental Health. Vol. 6 (1972). p. 237- 246
(37) Stowe, H.D., et al. The reproductive ability and progeny of F1 lead- toxic rats. Fertility and Sterility. Vol. 22, no. 11 (Nov. 1971). p. 755-760
(38) Pinon-Lataillade, G., et al. Effect of ingestion and inhalation of lead on the reproductive system and fertility of adult male rats and their progeny. Human and Experimental Toxicology. Vol. 12, no. 2 (Mar. 1993). p. 165-172
(39) Report on Carcinogens. 11th ed. US Department of Health and Human Services, Public Health Service, National Toxicology Program
(40) International Programme on Chemical Safety. Inorganic lead. Environmental Health Criteria 165. World Health Organization, 1995
(41) Carr, D.S., et al. Lead compounds: lead salts. In: Kirk-Othmer encyclopedia of chemical technology. 4th ed. Vol. 15. John Wiley and Sons, 1995. p. 141-143
(42) Carr, D.S. Lead compounds. In: Ullmann's encyclopedia of industrial chemistry. 5th completely revised ed. Vol. A 15. VCH Verlagsgesellschaft, 1990. p. 249-250
(43) Budavari, S, ed. The Merck index: an encyclopedia of chemicals, drugs, and biologicals. 12th ed. Merck and Co. Inc., 1996. p. 922-923
(44) The Sigma-Aldrich library of chemical safety data. Ed. II. Vol. 1. Sigma-Aldrich Corporation, 1988. p. 2070C,D
(45) Weast, R.C., ed. Handbook of chemistry and physics. 66th ed. CRC Press, 1985-1986. p. B-105
(46) Urben, P.G., ed. Bretherick's handbook of reactive chemical hazards. 5th ed. Vol. 1. Butterworth-Heinemann Ltd., 1995. p. 539
(47) Corrosion data survey: metals section. 6th ed. National Association of Corrosion Engineers, 1985. p. 76-4 to 77-4
(48) European Communities. Commission Directive 98/98/EC. Dec. 15, 1998
(49) NIOSH pocket guide to chemical hazards. NIOSH, June 1994. p.184
(50) Aboul-Ela, E.I. The protective effect of calcium against genotoxicity of lead acetate administration on bone marrow and spermatocyte cells of mice in vivo. Mutation Research. Vol. 516 (2002). p. 1-9
51) Nehéz, M., et al. Simultaneous action of cypermethrin and two environmental pollutant metals, cadmium and lead, on bone marrow cell chromosomes of rats in chronic administration. Ecototoxicology and Environmental Safety. Vol. 45 (2000). p. 55-60
(52) Robbiano, L., et al. Correlation between induction of DNA fragmentation and micronuclei formation in kidney cells from rats and humans and tissue-specific carcinogenic activity. Toxicology and Applied Pharmacology. Vol. 161 (1999). p. 153-159
(53) Valverde, M., et al. Genotoxicity induced in CD-1 mice by inhaled lead: differential organ response. Mutagenesis. Vol. 17, no. 1 (2002). p. 55-61
(54) International Agency for Research on Cancer (IARC). IARC monographs on the evaluation of carcinogenic risks to humans. Vol. 87. Inorganic and organic lead compounds. World Health Organization, Mar. 8, 2004. Available at: <>
(55) Apostoli, P., et al. Male reproductive toxicity of lead in animals and humans. Occupational and Environmental Health. Vol. 55, no. 6 (June 1998). p. 364-374
(56) Bellinger, D.C. Teratogen update: lead and pregnancy. Birth Defects Research (Part A). Vol. 73 (2005). p. 409-420
(57) Bonde, J.P. and Apostoli, P. Any need to revisit the male reproductive toxicity of lead? Occupational and Environmental Medicine. Vol. 62 (2005). p. 2-3
(58) Agency for Toxic Substances and Disease Registry (ATSDR). Toxicological profile for lead. PB-99/166704. US Department of Health and Human Services, 1999
(59) Landrigan, P., et al. The reproductive toxicity and carcinogenicity of lead: a critical review. American Journal of Industrial Medicine. Vol. 38 (2000). p. 231-243
(60) Sallmen, M. Exposure to lead and male fertility. International Journal of Occupational Medicine and Environmental Health. Vol. 14, no. 3 (2001). p. 219-222

Information on chemicals reviewed in the CHEMINFO database is drawn from a number of publicly available sources. A list of general references used to compile CHEMINFO records is available in the database Help.

Review/Preparation Date: 1997-10-02

Revision Indicators:
Chronic health effects 1997-12-01
US transport 1998-03-01
TLV comments 1998-08-01
EU Class 2000-04-01
EU Risk 2000-04-01
EU Safety 2000-04-01
TDG 2002-05-29
TLV basis 2004-01-11
PEL-TWA transitional 2004-01-29
PEL-TWA final 2004-01-29
PEL final comments 2004-01-29
Toxicological info 2004-03-15
Mutagenicity 2004-03-15
WHMIS proposed classification 2004-03-15
WHMIS health effects 2004-03-15
Engineering controls 2004-04-08
Carcinogenicity 2004-08-25
WHMIS detailed classification 2004-08-25
Emergency overview 2004-08-25
Bibliography 2005-09-26
Reproductive toxicity 2005-09-26

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