LEAD
LEAD, ELEMENTALThis record contains information for lead in its zero valence state only.
For general toxicity and environmental fate of lead ions and lead compounds,
refer to the LEAD COMPOUNDS record; for compound-specific information, to the
appropriate individual record, e.g., lead iodide, lead phosphate, etc.Evidence for Carcinogenicity:
CLASSIFICATION: B2; probable human carcinogen.
BASIS FOR CLASSIFICATION: Sufficient animal evidence. Ten rat bioassays and one
mouse assay have shown statisticlly significant increases in renal tumors with
dietary and subcutaneous exposure to several soluble lead
salts. Animal assays provide reproducible results in several laboratories, in
multiple rat strains with some evidence of multiple tumor sites. Short term
studies show that lead affects gene
expression. Human evidence is inadequate. HUMAN CARCINOGENICITY DATA:
Inadequate. ANIMAL CARCINOGENICITY DATA: Sufficient. /Lead
and compounds/
A3; Confirmed animal carcinogen with unknown relevance to humans. /Lead,
elemental, and inorganic compounds, as Pb/
Human Toxicity Excerpts:
TOXIC BY INGESTION & INHALATION OF DUST OR
FUME.
SEVERE POISONING IS PRODUCED THROUGH EXPOSURE TO FUMES FROM LEAD
FURNACES IF FUMES ARE ALLOWED TO ESCAPE & FROM DUST FROM DROSSING.
MOST ... LEAD EXPOSURE STUDIES INVOLVE
LEAD OXIDE DUST OR THE FUME OF
METALLIC LEAD. SOME REPORTS HAVE
INDICATED THAT THE DUSTS OF CERTAIN INSOLUBLE LEAD
COMPOUNDS, SUCH AS THE SULFIDE & CHROMATE, WERE LESS HAZARDOUS THAN MORE
SOLUBLE FORMS OF LEAD.
ONE OF 2 /EPIDEMIOLOGICAL/ STUDIES ON METALLIC LEAD
WORKERS SHOWED NO EXCESS OF CANCER DEATHS. THE OTHER SHOWED A SLIGHT (ALTHOUGH
SIGNIFICANT) EXCESS OF DEATHS DUE TO CANCERS OF DIGESTIVE SYSTEM & RESP
SYSTEM AMONG SMELTER WORKERS BUT NOT AMONG WORKERS IN LEAD-ACID
BATTERY FACTORY. AS 60% OF MEMBERS OF SMELTER WORKERS COHORT WERE HIRED AFTER
1950, FURTHER FOLLOW-UP OF THIS COHORT IS WARRANTED, IN ORDER TO DETERMINE MORE
RELIABLY IF THERE IS AN EXCESS RISK.
Cases of lead poisoning due to
retained bullets are reported only rarely but represent potentially
life-threatening reactions. ... Almost all cases in USA have involved the
dissolution of a single bullet over several mo to more than 20 yr. ... Bullets
in joint spaces are ... more likely to cause toxic complications than are
bullets lodged in soft tissues.
LEAD METAL FOREIGN BODIES IN EYE OR ... ORBIT IN HUMANS ... HAVE
BEEN CONSIDERED TO CAUSE LITTLE REACTION & RARELY ANY TOXIC EFFECT. CLINICAL
EXPERIENCES WITH VARIOUS INTRAOCULAR FOREIGN BODIES PRESENTED IN DETAIL WITH
HISTOLOGIC STUDIES ... INDICATED THAT LEAD
METALLIC FOREIGN BODIES CAUSED MINIMAL INFLAMMATORY REACTION, MAINLY MECHANICAL
INJURY. ... /IN ANOTHER REPORT IT WAS/ CONCLUDED THAT LEAD
FRAGMENTS IN PATIENTS WERE WELL TOLERATED IN THE EYE & IN THE ORBIT &
THAT THEY SHOULD NOT BE REMOVED UNLESS THEY WERE IN THE ANTERIOR CHAMBER. ...
/A/ CASE /IS DESCRIBED/ IN WHICH ... A SMALL LEAD
SHOT WAS ALLOWED TO REMAIN IN THE VITREOUS, THE VISION RETURNED TO NORMAL AS
BLOOD IN THE VITREOUS ABSORBED OR SETTLED IN THE COURSE OF A YEAR. ... IN ONE
CASE, WHICH APPEARS TO HAVE BEEN QUITE EXCEPTIONAL ... A PATIENT WITH A LEAD
SHOT BEHIND ONE GLOBE HAD IMPAIRED VISION IN THAT EYE. THIS WAS ASSUMED TO BE
DUE TO A TOXIC EFFECT OF LEAD. WHETHER
THIS INTERPRETATION WAS CORRECT OR NOT, A SIGNIFICANT IMPROVEMENT OF VISION WAS
REPORTED WHEN SYSTEMIC & TOPICAL TREATMENT WITH
2,3-DIMERCAPTOPROPANSULFONATE SODIUM WAS STARTED 5 YEARS AFTER THE INJURY.
In a cross-sectional study, the neurobehavioral effects of low-level lead
exposure were evaluated in a group of 59 lead
workers compared with 59 matched controls. The groups were not significantly
different in age, education level, sleep pattern, or use of alcohol. The mean
blood lead level in the exposed group
was 2.37 umol/l (50 ug/100 ml) which was similar to the previous three years
(2.36, 2.36, and 2.32 umol/l, respectively). The mean duration of exposure was
8109 hrs. Visual sensory function was affected, and perhaps as a consequence
sustained attention and psychomotor tasks were performed more slowly by the lead
exposed group. Cognitive functions were also impaired, with sensory store and
short term memories, and learning abilities all showing deficits in lead
workers. Multiple linear regression analysis relating to lead
workers test performance and their lead
exposure showed that performance on the sensory store memory test alone was
significantly related to exposure.
The activities of erythrocyte (rbc) arginase,
pyrimidine 5'- nucleotidase (P5N), and deoxypyrimidine 5'-nucleotidase (dP5N)
were compared in 16 lead workers and
14 age-matched controls as correlates of blood lead
(PbB) and unextracted zinc protoporphyrin (EP). Subjects with blood lead
of 0.9-2.5 uM (19-52 ug/dl) had 6.5 + or - 0.6 IU of pyrimidine 5'-nucleotidase
activity with uridine monophosphate (UMP) as substrate, significantly less
(p< 0.001) than the 12.0 + or - 0.7 IU activity of controls with blood lead
0.3-0.6 uM (6-12 ug/dl). Erythrocyte pyrimidine 5'-nucleotidase was
significantly correlated with blood lead
(r= 0.75). There were no significant differences in erythrocyte arginase or
deoxypyrimidine 5'-nucleotidase activity.
In a cross-sectional study of 20 gun-metal
foundry workers (mean age 47 yr) the subclinical neurophysiological effects of
exposure to lead, zinc, copper, and
tin were evaluated by "short-latency" somatosensory evoked potential (SSEP).
Controls were age and height-matched males without occupational exposure to lead.
Range of employment was 1-16 yr (mean 10 yr). In exposed workers, mean blood lead
was 42 ug/dl, mean zinc plasma 95 ug/dl, mean copper plasma 105 ug/dl, and mean
urinary tin 28 ug/l. In workers, the interpeak latency of SSEP in the
cervico-spino-bulbar region (N9(Erb)-N13 latency) was significantly prolonged
(p< 0.05), and the MCV and SCV in the forearm were significantly slowed
(0.01< p< 0.05) when compared with controls. The yield of urinary lead
following challenge with Ca-EDTA was positively related to SSEP latency in the
cervico-spino-bulbar region and inversely related to hematocrit (p< 0.05).
The interpeak latency in the upper central nervous system (N13-20 latency) was
inversely related to zinc concentration in erythrocytes. Latency up to the Erbs
point was inversely related to urinary zinc. MCV and SCV in the palm were
positively related to erythrocyte zinc concentration and plasma copper
concentration, respectively (p< 0.05). It appears that zinc antagonizes the
central and peripheral neurophysiologic dysfunction caused by lead,
and similarly copper antagonizes the peripheral sensory nerve dysfunction.
Battery workers (N= 18), who were exposed to
high airborne lead levels, /were
compared/ with cement workers (N= 18), who were exposed to ambient lead
levels. Blood lead urinary lead,
semen lead, and zinc protoporphyrin
concentrations were markedly elevated (p< 0.001) in battery workers. Battery
workers had a significantly shifted (p< 0.025) frequency distribution of
sperm count (median count, 45 vs 73x10x6 cells/cc, respectively). ... These
results suggest a direct toxic effect of increased lead
absorption on sperm production or transport in man.
Lead containing particles in ambient air have an aerodynamic
diameter of approx 0.1-1.0 um, & the predicted deposition in the airway is
about 35%. This is questionable for smaller particles (< 0.1 um) which are
mainly deposited by diffusion. Actual measurements of deposition in human
volunteers gave results that differed considerably depending on the physical
& chemical properties of the inhaled aerosol. ... A deposition of approx 25%
/was observed/ after exposure to particles with a mass median aerodynamic
diameter of 0.25 um. ... A deposition in the resp tract of about 60% /was
observed/ in persons close to a motorway, where particles were about 0.03 um in
diameter. This figure is consistent with lab expt carried out by the same
authors, in which subjects inhaled radioactively labeled particles of about the
same size. When volunteers inhaled lead
particles near urban roads where the particle size was larger (0.2-2.0 um),
deposition was about 50%. Based on available data, it seems reasonable to
conclude that the rate of deposition of airborne lead
in the general population is approx 30-50%, depending on particle size &
ventilation rates.
There is no evidence that inhaled lead
/as a trace substance in the environment/ has local effects on the respiratory
system in man ... .
Dissolution of lead from lead
soldered joints in water pipes frequently occurs where water is soft or acidic.
/SRP: Thereby contributing to long term chronic exposure to the general
population./
Most lead poisoning in children occurs
between ages 1 and 5 years. There is a higher incidence of child-related lead
poisoning during the warmer months.
Chronic exposure to lead has been
found to produce infertility, germinal epithelium damage, oligospermia and
testicular degeneration, decreased sperm motility, and prostatic hyperplasia.
There is convincing evidence that lead
is transferred to neonates via maternal milk. It appears that maternal milk
might be a source of lead for the
neonates, particularly when metal levels are elevated in the mother.
Arthralgia, often associated with muscle aches and pain, is a frequent symptom
in lead poisoning. Although generally
thought to appear mainly in chronic poisoning, joint pain is often reported even
by persons exposed briefly (weeks) who have relatively low blood lead
concentrations. It is a symptom that ... frequently indicates that the blood lead
concentration is on the rise.
... The EPA concluded that blood levels in the
range of 50-70 ug/dl are associated with a 5-point reduction in IQ, even among
asymptomatic children and after controlling for potential confounding factors.
/Researchers/ reported on a cohort of 132 young adults whose levels of dentine lead
were measured in primary school. Young people whose childhood dentine levels
were greater than 20 ppm were found to be at a markedly higher risk of dropping
out of high school and having reading disabilities, than the low-lead
exposure group, whose dentine lead
levels had been less than 10 ppm. Other measures of performance affected
included vocabulary and grammatical reasoning, absenteeism, hand-eye
coordination (poorer) and reaction time (slowed).
The earliest subjective symptoms /of lead
poisoningin working adults/ are diffuse and include weariness at the end of the
day. The patient is moody and irritable and may fall asleep watching television.
Often he loses his interest in leisure-time activities. Such mild symptoms
frequently occur with blood-lead
levels below 80 ug/100 ml.
... 49 long-term lead-exposed
workers were compared to 27 low-exposed workers through a number of psychologic
tests. After controlling for age, the exposed group performed worse on tests
measuring memory, learning, and reaction time, while impaired performance was
not detected in reasoning, perceptual speed, and psychomotor ability.
... /Researchers/ found impaired performances
on tests of verbal concept formation, perceptual performance, and memory in a lead-exposed
group with present lead concentrations
between 40 and 60 ug/100 ml.
A study of 260 infants prospectively followed
from birth suggests that the expected stature of a child born to a mother with a
prenatal blood lead concentration over
7.7 ug/dL is about 2 cm shorter at 15 mos of age if, potentially, the infant
also incurred a 10 ug/dL blood level increase during the 3- to 15-month interval
of life.
Moderate effects on follicle stimulating
hormone and luteinizing hormone have been correlated with lead
levels over about 50 ug/dL.
The relative risk of preterm delivery at
exposure levels of 14 ug/dL or greater was 8.7 times the risk at levels of up to
8 ug/dL in one prospective study. A Cincinnati study noted a half-week's
reduction in gestation for every 10 ug/dL increment in blood lead.
Lead
has an adverse effect on fetuses, particularly in the later stages of
development. Distribution of lead in
fetal tissues was examined in a case in which a woman was exposed during
pregnancy. The female worker was exposed to lead
dust for 8 hr daily when conception occurred. ... Measurements of lead
content were started after the end of the exposure and continued for 6 months
until normal values were obtained. Because of half-life of nearly 20 days for lead
elimination from blood, the estimated body burden at the end of exposure was
about 1200 ppb. The fetal tissue samples contained between 0.4 (brain) and 7.9
(liver) ug Pb/g dry weight. The fetal lead
was stored mainly in bone, blood, and liver.
Goyer found inclusion bodies in renal biopsies
of two lead industry workers who had
excess lead exposure, but only
subclinical signs of lead toxicity in
the form of weakness, nausea, some abdominal colic, and blood lead
values of about 100 ug/dl.
Finnish men were biologically monitored for lead
exposure. The cases (213 spontaneous abortions) and controls (300 births) were
identified from medical registers in Finland. The results did not show a
statistically significant relationship between spontaneous abortion and paternal
lead exposure among all the study
subjects. However, a significant increase in the risk of those women whose
husbands had been monitored (blood lead
equal to or greater than 1.5 umol/l) during or close to the time of
spermatogenesis was observed.
Small increases in blood pressure have been
related to adults with PbB levels down to 7 ug/dl.
... PbB concentrations in excess of 60 ug/100
g ... have been associated with peripheral neuropathy, gastrointestinal
disturbances and anemia. ... Nerve conduction velocities ... /decreases/ in
workers with maximal blood leads between 50 and 70 ug/100 g.
Food and Environmental Agents: Effect on
Breast-Feeding: Reported Sign or Symptom in Infant or Effect on Lactation: Lead:
Possible neurotoxicity. /From Table 7/
Medical Surveillance:
... Comparative advantages of /the biological
indicator/ delta-aminolevulinic acid dehydratase in typical (variable)
occupational exposure conditions included: the highest sensitivity at low and
relatively high lead (Pb) exposure
levels; better reflection of biologically active Pb as opposed to blood lead
(particularly compared to delta-aminolevulinic acid and coproporphyrin); higher
specificity compared to other indicators of Pb effect; and generally higher
reliability with regard to biologically and methodologically induced variations.
...
Populations at Special Risk:
SRP: Law enforcement officers are subject to
potential intoxication while firing weapons in an indoor firing range.
Lead
toxicity is of special concern to workers, such as miners and smelters,
automobile finishers, foundry and storage battery workers, typesetters, sheet
metal workers, and spray painters. Lead
... may also be a contaminant in moonshine whiskey.
Probable Routes of Human Exposure:
... MOST SEVERE HAZARD OCCURS IN SPRAYING OF
MOLTEN LEAD ... GRINDING OR POWER
SANDING ... SOLDER & POURING OF LEADED IRON & STEEL ... MIXING &
WEIGHING OF LEAD POWDERS.
PRINCIPAL TYPES OF PRIMARY INDUSTRIES WITH
OCCUPATIONAL EXPOSURE ... ARE LEAD
SMELTING & REFINING, STORAGE BATTERY MANUFACTURE, WELDING & STEEL
CUTTING & PRINTING. HIGHEST EXPOSURES ... OCCUR IN SMELTING & REFINING
OF LEAD. MOLTEN LEAD
& LEAD ALLOYS ARE BROUGHT TO HIGH
TEMP, RESULTING IN VAPORIZATION OF LEAD.
Emergency Medical Treatment:
Emergency Medical Treatment:
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The following Overview, *** LEAD ***, is relevant for this HSDB record chemical. |
| Life Support: |
o This overview assumes that basic life support measures
have been instituted.
|
| Clinical Effects: |
0.2.1 SUMMARY OF EXPOSURE
0.2.1.1 ACUTE EXPOSURE
A) WITH POISONING/EXPOSURE
1) Lead poisoning can affect almost every organ system.
Organ systems primarily affected include the central
and peripheral nervous systems, cardiovascular,
gastrointestinal, renal, endocrine, and hematologic
systems. Lead can also adversely impact reproductive
functioning and the developing fetus and child. The
signs or symptoms may be varied and non-specific, and
the clinician needs to consider the constellation of
complaints and findings that may suggest lead
poisoning as the diagnosis. Symptoms may be absent
despite significant poisoning.
a) ACUTE TOXICITY - Common in young children with a
history of pica. Symptoms can include: anorexia,
vomiting, malaise, and convulsions; may cause
permanent brain damage and reversible renal injury.
1) The ingestion of rapidly absorbed salts causes an
acute syndrome of hepatic injury, hemolysis,
anorexia, vomiting, malaise, and seizures due to
increased intracranial pressure, as well as, chronic
exposure effects.
b) CHRONIC TOXICITY - Children show weight loss,
weakness, and anemia. The first signs in children may
be subtle neurobehavioral deficits adversely
affecting classroom behavior and social interaction.
Adults manifest vague gastrointestinal and CNS
complaints; wristdrop and colic rarely occur.
0.2.1.2 CHRONIC EXPOSURE
A) The hazard of exposure to lead is particularly serious
in small companies or operations, often employing no
more than three or four workers, engaged in radiator
repair, leaded or stained glass production,
laboratories, or ceramics.
B) Lead poisoning in adults is usually occupational or
hobbies related due to inhalation of lead containing
dust, fumes or vapors. Upon inhalation, absorption
takes place easily from the respiratory tract and
symptoms develop relatively quickly as compared to oral
ingestion.
C) Subtle neurological/neurophysiological effects have
been demonstrated in workers with blood lead levels
below 60 microgram per 100 milliliter of blood.
D) The onset of symptoms of chronic lead poisoning often
is gradual. The major organ systems affected are the
nervous system, red blood cells, and kidneys.
E) Signs and symptoms include:
1. Abdominal tenderness
2. Anemia
3. Anxiety
4. Disturbance of the gastrointestinal tract (includes
constipation, anorexia, and rarely excruciating colic)
5. Facial pallor
6. Forgetfulness and/or poor concentration
7. Glomerular sclerosis
8. Hypotension
9. Insomnia
10. Interstitial fibrosis
11. Irreversible vascular sclerosis
12. Lassitude
13. Motor weakness (which may lead to paralysis of the
extensor muscles of the wrist and ankles)
14. Pallor of the eye grounds
15. Tubular cell atrophy
16. Weight loss and/or malnutrition
F) Lead poisoning diagnosis is supported when lead content
of blood is greater than 50 mcg/dL, and if urine is
greater than 80 mcg/dL.
G) Lead poisoning has been misdiagnosed as chronic fatigue
syndrome in some patients, due to the presenting signs
and symptoms.
H) PEDIATRIC - Children have been considered a risk group
for lead toxicity, mainly due to the neurophysiological
or neuro-cognitive deficits that may result.
I) Signs and symptoms for children include weight loss,
weakness, and anemia. Encephalopathy occurs frequently
in children who have ingested inorganic lead compounds.
0.2.3 VITAL SIGNS
0.2.3.1 ACUTE EXPOSURE
A) WITH POISONING/EXPOSURE
1) Chronic lead exposure may cause hypertension and gout.
0.2.7 NEUROLOGIC
0.2.7.1 ACUTE EXPOSURE
A) WITH POISONING/EXPOSURE
1) In young children, developmental defects, including
learning disabilities and behavioral abnormalities,
can occur without symptoms at blood lead levels at or
even below 10 micrograms/deciliter.
2) At higher levels of exposure headache, fatigue,
irritability and malaise may occur. At high levels,
generally above 100 mcg/dL, encephalopathy, seizures
and focal neurologic findings with imminent risk of
death, permanent mental retardation, and motor
deficits may occur.
0.2.7.2 CHRONIC EXPOSURE
A) During chronic exposure to lead, the concentration in
the brain is relatively low comparing to other soft
tissues such as aorta, liver, and kidneys. However,
inorganic lead does pass the blood brain barrier.
B) Low levels of lead impair neurotransmission. Lead
exposure has been shown to be associated with lowered
IQ in children, cephalopathy, and peripheral nervous
paralysis.
0.2.8 GASTROINTESTINAL
0.2.8.1 ACUTE EXPOSURE
A) WITH POISONING/EXPOSURE
1) CHRONIC LEAD EXPOSURE: Abdominal pain, nausea,
anorexia, vomiting, constipation, diarrhea, and a
metallic taste in the mouth have been reported with
chronic toxicity. Severe and paroxysmal colic
characterized by a rigid and retracted abdomen may
occur.
0.2.8.2 CHRONIC EXPOSURE
A) Gastrointestinal problems are the most commonly
reported effects of lead. When there is no obvious
history of lead exposure, the severe symptoms in the
gastrointestinal system may aid in the diagnosis of
lead poisoning. Even gunshot wounds have been reported
to display gastrointestinal symptoms.
B) Gastrointestinal absorption of lead varies widely and
depends on other substances present in the diet.
0.2.9 HEPATIC
0.2.9.1 ACUTE EXPOSURE
A) WITH POISONING/EXPOSURE
1) Hepatic injury has been associated with acute lead
poisoning, but is uncommon in chronic poisoning.
0.2.10 GENITOURINARY
0.2.10.1 ACUTE EXPOSURE
A) WITH POISONING/EXPOSURE
1) In acutely ill patients, proteinuria, glucosuria, and
aminoaciduria may occur, and reversible kidney damage
has been reported. In individuals chronically exposed
to lead, signs and symptoms can include tubular
damage, azotemia, and gout. Decreased sperm count in
males has also been described.
0.2.10.2 CHRONIC EXPOSURE
A) Chronic exposure can result in kidney disease with few
symptoms appearing until extensive and permanent damage
has occurred.
0.2.13 HEMATOLOGIC
0.2.13.1 ACUTE EXPOSURE
A) WITH POISONING/EXPOSURE
1) Lead interrupts several steps in heme synthesis
resulting in anemia. With some lead salts, hemolysis
is possible. RBCs occasionally show endoplasmic
clumping known as stippling. Iron deficiency is common
in lead poisoned children.
0.2.13.2 CHRONIC EXPOSURE
A) Anemia is an early indication of chronic exposure to
lead.
0.2.14 DERMATOLOGIC
0.2.14.2 CHRONIC EXPOSURE
A) Cutaneous absorption of lead is limited.
0.2.15 MUSCULOSKELETAL
0.2.15.1 ACUTE EXPOSURE
A) WITH POISONING/EXPOSURE
1) CHRONIC LEAD EXPOSURE: Muscle and joint pain are
common complaints with chronic lead poisoning.
Radiographic lead lines may be seen in the metaphyses
in chronically poisoned children. Most of the body
burden of lead is stored in bone.
0.2.16 ENDOCRINE
0.2.16.1 ACUTE EXPOSURE
A) WITH POISONING/EXPOSURE
1) Lead exposure has been associated with decreased
stature, decreased growth hormone secretion, decreased
levels of 1,25 dihydroxy vitamin D, and increased
catecholamine levels.
0.2.17 METABOLISM
0.2.17.1 ACUTE EXPOSURE
A) WITH POISONING/EXPOSURE
1) CHRONIC LEAD EXPOSURE: Hyperuricemia may be seen after
chronic lead poisoning.
0.2.19 IMMUNOLOGIC
0.2.19.2 CHRONIC EXPOSURE
A) Low levels of lead can impair immune system function.
0.2.20 REPRODUCTIVE HAZARDS
A) Lead is transferred across the placenta. It can affect
reproduction in males and females, and affects
neurodevelopmental milestones in children with both
prenatal and postnatal exposure.
0.2.21 CARCINOGENICITY
0.2.21.1 IARC CATEGORY
A) IARC Carcinogenicity Ratings for CAS7439-92-1 (IARC,
2004):
1) IARC Classification
a) Listed as: Lead
b) Carcinogen Rating: 2B
1) The agent (mixture) is possibly carcinogenic to
humans. The exposure circumstance entails exposures
that are possibly carcinogenic to humans. This
category is used for agents, mixtures and exposure
circumstances for which there is limited evidence of
carcinogenicity in humans and less than sufficient
evidence of carcinogenicity in experimental animals.
It may also be used when there is inadequate
evidence of carcinogenicity in humans but there is
sufficient evidence of carcinogenicity in
experimental animals. In some instances, an agent,
mixture or exposure circumstance for which there is
inadequate evidence of carcinogenicity in humans but
limited evidence of carcinogenicity in experimental
animals together with supporting evidence from other
relevant data may be placed in this group.
2) IARC Classification
a) Listed as: Lead compounds, inorganic
b) Carcinogen Rating: 2A
1) The agent (mixture) is probably carcinogenic to
humans. The exposure circumstance entails exposures
that are probably carcinogenic to humans. This
category is used when there is limited evidence of
carcinogenicity in humans and sufficient evidence of
carcinogenicity in experimental animals. In some
cases, an agent (mixture) may be classified in this
category when there is inadequate evidence of
carcinogenicity in humans and sufficient evidence of
carcinogenicity in experimental animals and strong
evidence that the carcinogenesis is mediated by a
mechanism that also operates in humans.
Exceptionally, an agent, mixture or exposure
circumstance may be classified in this category
solely on the basis of limited evidence of
carcinogenicity in humans.
3) IARC Classification
a) Listed as: Lead, organic compounds
b) Carcinogen Rating: 3
1) The agent (mixture or exposure circumstance) is not
classifiable as to its carcinogenicity to humans.
This category is used most commonly for agents,
mixtures and exposure circumstances for which the
evidence of carcinogenicity is inadequate in humans
and inadequate or limited in experimental animals.
Exceptionally, agents (mixtures) for which the
evidence of carcinogenicity is inadequate in humans
but sufficient in experimental animals may be placed
in this category when there is strong evidence that
the mechanism of carcinogenicity in experimental
animals does not operate in humans. Agents, mixtures
and exposure circumstances that do not fall into any
other group are also placed in this category.
0.2.22 GENOTOXICITY
A) Exposure to lead has been reported to cause chromosome
aberrations in humans, rats, and monkeys, but mixed
exposures were involved in the human study.
B) Varying results of genotoxicity tests with lead and its
compounds may be due to differing solubilities,
different specificities of the tests, or possible
indirect genotoxic mechanisms. The potential
genotoxicity of lead remains unclear.
|
| Laboratory: |
A) Elevation of blood lead level is essential to the
diagnosis of childhood and industrial cases. Children
with a blood lead level of 45 mcg/dL or greater require
medical intervention and chelation.
B) Children with venous BLLs of 20 mcg/dL or greater or with
venous BLLs of 15-19 mcg/dL that persist for at least 3
months should receive medical evaluation and treatment.
Chelation therapy should be instituted in all children
with a blood lead level of 45 mcg/dL or greater using
venous blood lead measurement.
C) Obtain a CBC to assess for anemia and perform a
peripheral smear. Hypochromia and basophilic stippling
suggest lead intoxication, but they are non-specific and
their absence does not rule out the diagnosis.
D) Employees whose blood lead level is equal to or greater
than 50 mcg/100 g shall be temporarily removed from
exposure until their blood lead level is at or below 40
mcg/dl.
|
| Treatment Overview: |
0.4.2 ORAL EXPOSURE
A) ACUTE EXPOSURE
1) ACTIVATED CHARCOAL: Administer charcoal as a slurry
(240 mL water/30 g charcoal). Usual dose: 25 to 100 g
in adults/adolescents, 25 to 50 g in children (1 to 12
years), and 1 g/kg in infants less than 1 year old.
2) Consider gastric lavage in patients with recent
ingestion of liquid or powdered products.
3) GASTRIC LAVAGE: Consider after ingestion of a
potentially life-threatening amount of poison if it can
be performed soon after ingestion (generally within 1
hour). Protect airway by placement in Trendelenburg and
left lateral decubitus position or by endotracheal
intubation. Control any seizures first.
a) CONTRAINDICATIONS: Loss of airway protective reflexes
or decreased level of consciousness in unintubated
patients; following ingestion of corrosives;
hydrocarbons (high aspiration potential); patients at
risk of hemorrhage or gastrointestinal perforation;
and trivial or non-toxic ingestion.
4) WHOLE BOWEL IRRIGATION - Perform whole bowel irrigation
if there is evidence of radiopaque material on
abdominal radiographs. Administer a polyethylene glycol
balanced electrolyte solution orally. Adults: 2 liters
initially followed by 1 liter/hour. Repeat the x-ray to
determine if radiopaque material has been removed (N.B.
lead may remain in the GI tract even though rectal
effluent has been clear for several hours or even
days). Children: 500 mL initially followed by 500
mL/hour until rectal effluent is clear and radiopaque
material is removed.
5) Obtain a blood lead level; repeat in 48 hours and as
needed thereafter.
6) Chelation should be considered in patients with large
ingestions or highly elevated blood lead levels.
B) ACUTE OR CHRONIC EXPOSURE
1) OBTAIN BLOOD LEAD LEVEL - Hospitalize any child with a
BLL of 45-69 micrograms/deciliter (mcg/dL) and symptoms
(significant CNS or protracted gastrointestinal
symptoms), or with BLL of greater than or equal to 70
mcg/dL, with or without symptoms ( CDC, 1997).
2) Chelation therapy should be instituted in all patients
with a blood lead level of 45 micrograms/deciliter (2.2
micromoles/liter) or greater using venous blood lead
measurement. The child should be in a lead-safe
environment before beginning chelation therapy ( CDC,
1997).
3) CALCIUM EDTA PROVOCATION TEST - May be useful in
determining necessity for therapeutic chelation in
children with blood lead levels of 25 to 44 mcg/dL.
This may be performed as an outpatient if the patient
remains in the clinic. Because of the difficulties in
administering the test and the uncertainties in
interpreting results it is not as widely used as in the
past.
4) CHELATION THERAPY
a) Chelation therapy should be instituted in all patients
with a blood lead level of 45 micrograms/deciliter
(2.2 micromoles/liter) or greater using venous blood
lead measurement. If a capillary sample is used and
BLL is elevated, a second BLL by venipuncture should
be performed before starting chelation therapy. The
child should be in a lead-safe environment before
beginning chelation therapy. Returning the individual
to a contaminated environment may result in
re-accumulation of the metal ( CDC, 1997). Symptoms
and signs, along with the EP and blood lead level,
determine the route, dose, and agent to be used for
chelation.
b) BAL (dimercaprol) - 3 to 5 mg/kg/dose deep IM every 4
hours for 2 days; then every 4 to 6 hours for 2 more
days; then every 4 to 12 hours up to an additional 7
days.
c) CALCIUM EDTA - 50 to 75 mg/kg/day deep IM in 3 to 6
divided doses for up to 5 days. EDTA should only be
administered after BAL in patients with encephalopathy
or children with levels >69 mcg/dL.
d) D-PENICILLAMINE - 250 mg 4 times a day PO for up to 5
days. Do not exceed 40 mg/kg/day. OSHA prohibits
prophylactic chelation therapy in workers
occupationally exposed to lead.
e) DMSA - Initial pediatric dose is 10 mg/kg or 350
mg/m(2) orally every 8 hours for 5 days; reduced to
every 12 hours for an additional 2 weeks. OSHA
prohibits prophylactic chelation therapy in workers
occupationally exposed to lead.
5) ESTABLISH ADEQUATE FLUID BALANCE with a urine flow of 1
to 2 mL/kg/hour, unless encephalopathy present or
suspected, or increased intracranial pressure noted on
CT. Do not force fluids if neuro compromise possible.
6) PERFORM A NEUROLOGICAL EXAM with particular reference
to the presence of encephalopathy; particularly after
starting EDTA, mental status may worsen; observe
carefully.
7) CEREBRAL EDEMA - May be managed by ventilation and the
administration of 1.5 g/kg of 20% mannitol IV over 20
minutes. Dexamethasone: up to 1 to 2 mg/kg/day IV in
divided doses. Spinal tap may be dangerous in the
presence of increased intracranial pressure.
8) SEIZURES: Administer a benzodiazepine IV; DIAZEPAM
(ADULT: 5 to 10 mg, repeat every 10 to 15 min as
needed. CHILD: 0.2 to 0.5 mg/kg, repeat every 5 min as
needed) or LORAZEPAM (ADULT: 2 to 4 mg; CHILD: 0.05 to
0.1 mg/kg).
a) Consider phenobarbital if seizures recur after
diazepam 30 mg (adults) or 10 mg (children > 5 years).
b) Monitor for hypotension, dysrhythmias, respiratory
depression, and need for endotracheal intubation.
Evaluate for hypoglycemia, electrolyte disturbances,
hypoxia.
9) FOR ENCEPHALOPATHY, institute BAL followed 4 hours
later by EDTA in the maximum dose. Administer EDTA as a
continuous infusion over 24 hours.
10) Although chelation therapy is associated with
significant decrease in BLL, surgery may be considered
to remove lead foreign bodies.
|
| Range of Toxicity: |
A) A preterm infant with severe congenital lead poisoning
(cord blood lead 7.6 mcmol/L or 157.5 mcg/dL; BLL of 11.8
mcmol/L) recovered following chelation therapy.
B) A man with a history of schizophrenia developed severe
lead poisoning (BLL 391 mcg/dL) after ingesting 206
22-caliber lead bullets. He recovered following
aggressive GI decontamination and chelation therapy.
|
Antidote and Emergency Treatment:
Basic treatment: Establish a patent airway.
Suction if necessary. Watch for signs of respiratory insufficiency and assist
ventilations if necessary. Administer oxygen by nonrebreather mask at 10 to 15
L/min. Monitor for shock and treat if necessary ... . Anticipate seizures and
treat if necessary ... . For eye contamination, flush eyes immediately with
water. Irrigate each eye continuously with normal saline during transport ... .
Do not use emetics. For ingestion, rinse mouth and administer 5 mL/kg up to 200
mL of water for dilution if the patient can swallow, has a strong gag reflex,
and does not drool. Administer activated charcoal ... . /Lead
and related cmpds/
Advanced treatment: Consider orotracheal or
nasotracheal intubation for airway control in the patient who is unconscious.
Use hyperventilation to help control increased intracranial pressure. Start an
IV with lactated Ringer's to support vital signs. For hypotension with signs of
hypovolemia, administer fluid cautiously. Watch for signs of fluid overload ...
. Treat seizures with diazepam (Valium) ... . Use proparacaine hydrochloride to
assist eye irrigation ... . /Lead and
related cmpds/
The treatment of lead
poisoning is based on the prompt termination of exposure and on the use of
chelating agents. The first requirement is categoric. The second is determined
by the severity of poisoning; at present, the greatest issue is whether a
symptomatic patients should be treated or not. The most commonly used
therapeutic chelating agents are CaEDTA, BAL, and D-penicillamine can be given
... . /SRP: DMSA should also be considered./ It is not easy to judge which
method is superior. ... /Lead/
Animal Toxicity Studies:
Evidence for Carcinogenicity:
CLASSIFICATION: B2; probable human carcinogen.
BASIS FOR CLASSIFICATION: Sufficient animal evidence. Ten rat bioassays and one
mouse assay have shown statisticlly significant increases in renal tumors with
dietary and subcutaneous exposure to several soluble lead
salts. Animal assays provide reproducible results in several laboratories, in
multiple rat strains with some evidence of multiple tumor sites. Short term
studies show that lead affects gene
expression. Human evidence is inadequate. HUMAN CARCINOGENICITY DATA:
Inadequate. ANIMAL CARCINOGENICITY DATA: Sufficient. /Lead
and compounds/
A3; Confirmed animal carcinogen with unknown
relevance to humans. /Lead, elemental,
and inorganic compounds, as Pb/
Non-Human Toxicity Excerpts:
Lead
particles have been well tolerated in the eyes of dogs & rats. ... Lead
particles in the anterior chamber in rabbits became coated with purulent exudate
& sometimes were extruded through the cornea at the limbus. In the vitreous
humor in rabbits a similar purulent reaction was observed, causing the vitreous
to shrink & the retina to separate.
LEAD
POWDER SUSPENDED IN CORN OIL WAS ADMIN TO MALE & FEMALE FISCHER 344 RATS BY
STOMACH TUBE (10 MG TWICE/MO FOR 12 MO). CONTROL RATS WERE GIVEN 0.5 ML OF CORN
OIL BY STOMACH TUBE ACCORDING TO SAME SCHEDULE. ONE LYMPHOMA & 4 LEUKEMIAS
WERE FOUND IN 5/47 LEAD-TREATED RATS;
THIS DID NOT DIFFER SIGNIFICANTLY FROM THE INCIDENCE OF 3 LYMPHOMAS IN 29
CONTROLS. NO OTHER NEOPLASMS WERE REPORTED IN TREATED OR CONTROL RATS.
LEAD
POWDER SUSPENDED IN TRIOCTANOIN WAS ADMIN IM TO 25 MALE & 25 FEMALE FISCHER
RATS AS 9 MONTHLY INJECTIONS OF 10 MG, THEN 3 MONTHLY INJECTIONS OF 5 MG. EQUAL
NUMBER OF VEHICLE CONTROLS WERE USED. 1 TREATED FEMALE DEVELOPED FIBROSARCOMA AT
SITE OF IMPLANTATION ... THE LYMPHOMA RATE WAS SAME IN TREATED AS IN CONTROL
ANIMALS.
TWELVE SHEEP WERE EXPOSED TO FINELY POWDERED
METALLIC LEAD IN THEIR DIET (DOSES,
0.5 TO 16 MG/KG BODY WT) DURING ENTIRE ... PREGNANCY; BLOOD LEVELS WERE ABOUT
0.4 MG/L, WITHOUT RESULTING IN DEATH. NINE ANIMALS SERVED AS CONTROLS. RATE OF
LAMBING WAS 18% IN EXPOSED (27% ABORTIONS) & 100% IN UNEXPOSED SHEEP (NO
ABORTIONS). NO MALFORMATIONS WERE REPORTED. ... /IT WAS CONCLUDED THAT/ CHRONIC LEAD
POISONING IN SHEEP CAUSED ABORTION, MISCARRIAGE & TRANSITORY STERILITY.
THERE WAS NO SIGNIFICANT EXCESS OF CHROMOSOME
DAMAGE IN CULTURED LEUKOCYTES OBTAINED FROM 9 COWS ACCIDENTALLY INTOXICATED WITH
MIXTURE OF HEAVY METALS & SHOWN TO HAVE TOXIC LEVELS OF LEAD
IN LIVER & KIDNEYS.
Waterfowl can become poisoned by ingesting 6-8
buckshot from frequently hunted shorelines. Natural sources of lead
such as galena or soils are not particularly toxic but can add to the total body
burden.
In waterfowl, lead
shot ingestion causes anorexia, loss of wt, weakness, lethargy, diarrhea, coma,
& quiet death. ... Progressive tachycardia /has been observed/ in geese as
the birds became more & more ill. Some geese developed ECG abnormalities.
In geese chronically poisoned with lead
shot, microscopic degenerative lesions appear in the myocardium before any ECG
abnormalities are manifested. Lesions include upper GI impaction with plant
materials, emaciation, distended gallbladder, flabby hemorrhagic heart,
discolored friable liver, & enteritis. Lesions in mallard ducks given lead
shot include destruction of proventricular epithelium, bone medullary osteocytes,
& pectoral muscle cells. Renal proximal tubules contain intranuclear
inclusions. Mallard ducks also may develop encephalopathy & peripheral
neuropathy.
Metallic lead
in the form of weights or foil can cause poisoning, as also can shot; duck
frequently dredge up shot from the mud at the bottom of ponds. Lead
shot in muscle is usually encapsulated, & systemic poisoning from it is
unlikely. Nevertheless, lead shot
dropped by anglers on river banks is a serious cause of poisoning in swans. ...
Vegetation in the neighborhood of a smelter engaged in melting down old battery
plates had a lead content of up to
3200 ppm. ... Vegetation near a busy highway may contain 500 ppm of lead
due to contamination by exhaust fumes. It should be noted that in these cases
the lead is only a surface
contaminant; significant quantities of the element cannot be taken up by
vegetation from lead-bearing soil,
although the latter has itself caused poisoning in small animals.
Birds (fowls, ducks, geese & pigeons) are
all susceptible to lead poisoning.
They show anorexia & ataxia, followed by excitement & loss of condition.
Egg production, fertility, & hatchability decrease; & mortality may be
high.
It is doubtful whether the term "toxic
dose" has any real meaning when it is applied to a substance such as
/elemental/ lead /in its ionic form/,
as it is affected by so many different factors. Among these are environment,
nutrition, disease & age, the last of these being considerably more
important, as young animals are considerably more sensitive than old ones. There
is also a seasonal variation. Over half the cases of lead
poisoning in cattle in Scotland occur in the spring. Similar effects have been
noted for dogs. ... Even more important is the fact that lead
is both cumulative & ubiquitous. All living creatures are continually
absorbing it, & the "toxic" dose is only the amount necessary to
bridge the gap between this normal intake & a potentially dangerous level.
... Three or four lead shots will kill
a duck, 10 a goose.
The acute oral lethal single dose of lead
in ... calves /is/ 50-600 mg/kg as lead
or lead salts. ... Solid lead
is not as toxic as /the/ more soluble salts, which are more readily absorbed.
Eleven pregnant squirrel monkeys were
perorally exposed to lead during the
latter two-thirds of pregnancy (mean blood lead
0.54 ug/ml (2.61 umol/l), range 0.39-0.82 ug/ml (1.88-3.96 umol/l), at a dosing
regime producing no maternal toxic symptoms. Lesions similar to lead
encephalopathy and growth retardation of the fetal cerebrum were seen in some of
the offspring, as well as neurological and behavioral symptoms at adult age.
Cerebral lead levels in offspring (an
abortion, stillborns, a sacrificed full-term fetus, and a neonatal death) were
between 0.1-0.7 ug/g. Pre- and perinatal mortality, and prematurity, was
increased, and the size of the offspring at birth was reduced. The head
circumference tended to be reduced postnatally.
... Animal studies indicate that relatively
high levels of lead exposure interfere
with resistance to infectious disease.
ORAL ADMIN OF LEAD
TO RATS INHIBITED ACTIVITY OF DELTA-AMINOLEVULINIC ACID DEHYDRATASE. EDTA
TREATMENT OF RATS GIVEN LEAD CAUSED
REACTIVATION OF LIVER DELTA-AMINOLEVULINIC ACID DEHYDRATASE.
Studies have been conducted with nestling
kestrels in which oral intubations were administered daily for the first 10 days
post-hatching. A high mortality from metallic lead
was observed with 525 mg/kg, reduced growth was observed with 125 mg/kg, and
altered physiology was observed with 25 mg/kg. /From table/
Ecotoxicity Values:
LC50 Japanese quail (Coturnix japonica), males
or females, 14 days old, oral (5-day ad libitum in diet) >5,000 ppm; at 1000,
2236 & 5000 onset of toxic signs began at 7, 7 & 7 days and remissed at
11, 11 & 12 days, respectively, no mortality was observed; control
references were dieldrin & dicrotophos; corn oil diluent was added to diet
at ratio of 2:98 by wt; (extreme concentrations: 1,000-5,000 ppm) /Lead
metal, 100%/
Metabolism/Pharmacokinetics:
Absorption, Distribution & Excretion:
Only 1 to 2% of ingested lead
is absorbed from the GI tract because it can form rather insoluble compounds,
even within the gut. Acid conditions favor dissolution of lead
& its compounds.
... Metallic lead
shot or bullets lodged in tissues do not dissolve readily because tissue pH is
not low enough.
The absorption rate of deposited lead
depends on various factors, particularly on the physiochemical form of lead
in particles. There is ... no evidence of lead
accumulation in the lung, & any lead
compound once deposited is eventually absorbed or transferred to the
gastrointestinal tract.
Only a very minor fraction of particles over
0.5 um in mean maximal external diameter are retained in the lung but are then
cleared from the respiratory tract & swallowed. ... The percentage of
particles less than 0.5 um retained in the lung increases with reduction in
particle size. About 90% of lead
particles in ambient air that are deposited in lung are small enough to be
retained. Absorption of retained lead
through alveoli is relatively efficient & complete.
A group of 109 male workers occupationally
exposed to both antimony (as Sb2O3) and lead
in the glass-producing industry were examined for levels of these metals in
whole blood and urine. The workers were divided into four groups based on
specific work activities: melter (n= 32), batch mixer (n= 45), craftsman (n= 8),
and glass washer (n= 24). Blood and urine samples were collected at the end of a
shift. Concentrations of lead in the
blood ranged from 70 to 680 ug/l. Median values for melters, batch mixers,
craftsmen, and glass washers were 220, 340, 275, and 170 ug/l, respectively. A
significant difference (p< 0.05) was found only between the batch mixers and
glass washers. The urinary lead values
ranged from 7 to 110 ug/l with median values for melters, batch mixers,
craftsmen, and glass washers of 35, 43, 24, and 42 ug/l, respectively. A
significant difference was found between only the batch mixers and craftsmen
(p< 0.05). Exposure rates for lead
were not given.
... Two human volunteers were given 212Pb
intravenously. There was no lead in
the feces during the first 24 hr, whereas the urine contained 4.42% of the dose.
The figures for the second 24 hours, however, were 1.5% and 1.42%, respectively,
which indicates that the fecal route may contribute as much as the urinary one
to total excretion.
Other possible routes for lead
excretion include sweat, milk, hair, nails, desquamating epithelia, and teeth.
As much as 90% of ingested lead
is not absorbed and is excreted in the feces. The urine is the primary vehicle
for excretion of absorbed lead, but a
smaller proportion may be excreted in the bile.
An inverse relationship was found between
diets containing metallic lead of
particle sizes </= 250 um and absorption in rats.
Biological Half-Life:
The first half-time of lead
in blood after the cessation of exposure is 35-40 days, while for the lead
in long bones, the half-time is around 20 yr.
Mechanism of Action:
The ability of a number of metals and organic
chemicals to induce metallothionein synthesis in primary cultures of rat
hepatocytes was tested to determine whether metallothionein induction in vivo
results from a direct effect of the agent on the liver or as a result of an
indirect, physiological response to the agent. Hepatocytes were exposed to
metals (zinc, cadmium, mercury, manganese, lead,
cobalt, nickel, and vanadium) or org cmpd. Ethanol, urethane,
L-2-oxothiazolidine-4-carboxylate, or dexamethasone and were assayed for
metallothionein by the cadmium/mercury radioassay. Cell viability was monitored
by protein synthesis activity and cellular potassium ion concn. Increases in
metallothionein concn were noted for zinc (22 fold), mercury (6.4 fold), cadmium
(4.8 fold), cobalt (2.4 fold), nickel (22 fold), and dexamethasone (4.5 fold).
However, even at max tolerated concn, manganese, lead,
vanadium, ethanol, urethane, and L-2-oxothiazolidine-4-carboxylate did not
increase metallothionein. Thus, zinc, cadmium, mercury, cobalt, nickel, and
dexamethasone induce metallothionein in vitro and are direct inducers of
metallothionein synthesis in hepatic tissue. In contrast, manganese, lead,
ethanol, urethane, and L-2-oxothiazolidine-4-carboxylate, which did not increase
the metallothionein content of hepatocytes, apparently do so in vivo by an
indirect mechanism.
Interactions:
Female Swiss mice were exposed to lead
in the drinking water at concentrations ranging from 0 to 1000 ppm for 105 or
280 day periods of time. The effect of lead
on urethane induced pulmonary adenoma formation was evaluated in the 105 day
study. Urethane induced sleeping times observed following ip injection of
urethane (1.5 mg/g) after 3 weeks of lead
exposure were not altered by lead
indicating that lead did not affect
the rate of urethane elimination. Pulmonary adenoma formation was evaluated 84
days later. Lead exposure did not
affect the number of tumors produced, nor did it alter the mean tumor diameter
in the lead treatment groups.
Immunosuppressive activity of lead did
not enhance urethane induced adenoma formation. In the 280 day study, leukemia
was observed in all treatment groups. Mortality was greater in the lead
exposed mice. Mice exposed to 50 or 1000 ppm lead
had 41.6% and 58.3% more deaths associated with the virus. The median survival
time was also reduced in the lead
exposed mice. Immunosuppressive effects of lead
increased expression of the murine lymphocytic leukemia virus.
Cultured C6 rat glioma cells were exposed to lead
acetate (0, 1, 10, or 100 uM) for 3-4 days. Cells were analyzed for changes in
viability and intracellular lead,
iron, and copper concentrations after lead
treatment was discontinued. Lead
uptake did not affect intracellular iron or copper concentrations. Unlike C6
cells, however, astroglia showed elevations of intracellular iron or copper
after lead treatment. C6 cells appear
to be an adequate model for selected events in glial toxicosis, such as lead
stimulated protein synthesis in oligodendroglia and lead
uptake in astroglia, but not lead
induced alterations of intracellular copper and iron in astroglia.
The distribution of iv admin lead
(50 nmol/kg) was studied by means of autoradiography and impulse counting in
pregnant C57BL mice (day 18 of gestation) treated orally with dithiocarbamates.
Diethyldithiocarbamate, disulfiram or thiram (2X1 mmol/kg) or vehicle (gelatin)
alone, was given by gavage 2 hr before & immediately after injection of lead.
All the dithiocarbamates changed the distribution pattern of lead.
Disulfiram had the greatest effect at 24 hr after lead.
The pattern of changes in lead
distribution is consistent with the formation in the body of lipid sol. Lead-dithiocarbamate
complexes that pass biological barriers more easily than inorganic lead
(to brain, fetus, melanocytes, etc), probably are followed by a dissociation of
the complexes in the tissues.
Chelating agents, zinc salts, and selenium
preparations have been utilized with some success in attempts to reduce
absorption and/or increase the excretion of absorbed lead.
... Both selenium and vitamin E have been shown to be involved in decreasing the
toxic effect of lead in rats.
Pharmacology:
Interactions:
Female Swiss mice were exposed to lead
in the drinking water at concentrations ranging from 0 to 1000 ppm for 105 or
280 day periods of time. The effect of lead
on urethane induced pulmonary adenoma formation was evaluated in the 105 day
study. Urethane induced sleeping times observed following ip injection of
urethane (1.5 mg/g) after 3 weeks of lead
exposure were not altered by lead
indicating that lead did not affect
the rate of urethane elimination. Pulmonary adenoma formation was evaluated 84
days later. Lead exposure did not
affect the number of tumors produced, nor did it alter the mean tumor diameter
in the lead treatment groups.
Immunosuppressive activity of lead did
not enhance urethane induced adenoma formation. In the 280 day study, leukemia
was observed in all treatment groups. Mortality was greater in the lead
exposed mice. Mice exposed to 50 or 1000 ppm lead
had 41.6% and 58.3% more deaths associated with the virus. The median survival
time was also reduced in the lead
exposed mice. Immunosuppressive effects of lead
increased expression of the murine lymphocytic leukemia virus.
Cultured C6 rat glioma cells were exposed to lead
acetate (0, 1, 10, or 100 uM) for 3-4 days. Cells were analyzed for changes in
viability and intracellular lead,
iron, and copper concentrations after lead
treatment was discontinued. Lead
uptake did not affect intracellular iron or copper concentrations. Unlike C6
cells, however, astroglia showed elevations of intracellular iron or copper
after lead treatment. C6 cells appear
to be an adequate model for selected events in glial toxicosis, such as lead
stimulated protein synthesis in oligodendroglia and lead
uptake in astroglia, but not lead
induced alterations of intracellular copper and iron in astroglia.
The distribution of iv admin lead
(50 nmol/kg) was studied by means of autoradiography and impulse counting in
pregnant C57BL mice (day 18 of gestation) treated orally with dithiocarbamates.
Diethyldithiocarbamate, disulfiram or thiram (2X1 mmol/kg) or vehicle (gelatin)
alone, was given by gavage 2 hr before & immediately after injection of lead.
All the dithiocarbamates changed the distribution pattern of lead.
Disulfiram had the greatest effect at 24 hr after lead.
The pattern of changes in lead
distribution is consistent with the formation in the body of lipid sol. Lead-dithiocarbamate
complexes that pass biological barriers more easily than inorganic lead
(to brain, fetus, melanocytes, etc), probably are followed by a dissociation of
the complexes in the tissues.
Chelating agents, zinc salts, and selenium
preparations have been utilized with some success in attempts to reduce
absorption and/or increase the excretion of absorbed lead.
... Both selenium and vitamin E have been shown to be involved in decreasing the
toxic effect of lead in rats.
Environmental Fate & Exposure:
Probable Routes of Human Exposure:
... MOST SEVERE HAZARD OCCURS IN SPRAYING OF
MOLTEN LEAD ... GRINDING OR POWER
SANDING ... SOLDER & POURING OF LEADED IRON & STEEL ... MIXING &
WEIGHING OF LEAD POWDERS.
PRINCIPAL TYPES OF PRIMARY INDUSTRIES WITH
OCCUPATIONAL EXPOSURE ... ARE LEAD
SMELTING & REFINING, STORAGE BATTERY MANUFACTURE, WELDING & STEEL
CUTTING & PRINTING. HIGHEST EXPOSURES ... OCCUR IN SMELTING & REFINING
OF LEAD. MOLTEN LEAD
& LEAD ALLOYS ARE BROUGHT TO HIGH
TEMP, RESULTING IN VAPORIZATION OF LEAD.
Natural Pollution Sources:
LEAD
RARELY OCCURS IN THE ELEMENTAL STATE, BUT EXISTS ... IN A NUMBER OF ORES ...
ALSO OCCURS IN VARIOUS URANIUM & THORIUM MINERALS, ARISING FROM RADIOACTIVE
DECAY.
Pb derived from the decay of radon. /Inorganic
lead/
Metallic lead
is naturally occurring and is the end product of three natural radioactive
elements uranium (206), thorium (208), and actinium (207)(1).
Milk Concentrations:
Other possible routes for lead
excretion include ... milk....
Environmental Standards & Regulations:
Acceptable Daily Intakes:
Tolerable intake of lead
for preschool children should be less than the 3 mg/wk recommended provisionally
for adults. ... /Inorganic lead/
0.007 mg/kg (WHO) /Lead;
from table/
CERCLA Reportable Quantities:
Persons in charge of vessels or facilities are
required to notify the National Response Center (NRC) immediately, when there is
a release of this designated hazardous substance, in an amount equal to or
greater than its reportable quantity of 10 lb or 4.54 kg. The toll free number
of the NRC is (800) 424-8802; In the Washington D.C. metropolitan area (202)
426-2675. The rule for determining when notification is required is stated in 40
CFR 302.4 (section IV. D.3.b).
RCRA Requirements:
D008; A solid waste containing lead
may or may not become characterized as a hazardous waste when subjected to the
Toxicity Characteristic Leaching Procedure listed in 40 CFR 261.24, and if so
characterized, must be managed as a hazardous waste.
Atmospheric Standards:
National primary and secondary ambient air
quality standard for lead and its
compounds, measured as elemental lead
is: 1.5 ug/cu m, maximum arithmetic mean averaged over a calendar quarter. /Lead
and its compounds, as Pb/
Listed as a hazardous air pollutant (HAP)
generally known or suspected to cause serious health problems. The Clean Air
Act, as amended in 1990, directs EPA to set standards requiring major sources to
sharply reduce routine emissions of toxic pollutants. EPA is required to
establish and phase in specific performance based standards for all air emission
sources that emit one or more of the listed pollutants. Lead
compounds are included on this list. /Lead
compounds/
Clean Water Act Requirements:
Toxic pollutant designated pursuant to section
307(a)(1) of the Clean Water Act and is subject to effluent limitations. /Lead
and inorganic and organic lead
compounds/
Designated as a hazardous substance under
section 311(b)(2)(A) of the Federal Water Pollution Control Act and further
regulated by the Clean Water Act Amendments of 1977 and 1978. These regulations
apply to discharges of this substance.
Federal Drinking Water Standards:
EPA 15 ug/l (Action Level)
State Drinking Water Guidelines:
(AZ) ARIZONA 20 ug/l
(ME) MAINE 20 ug/l
FDA Requirements:
The FDA action level of lead
is 7.0 ug/ml of leaching soln for pottery (ceramics) flatware (avg of 6 units);
5.0 ug/ml of leaching soln for small hollowware (any one of 6 units); 2.5 ug/ml
of leaching soln for large hollowware (any one of 6 units); 7.0 ug/ml of
leaching soln if product intended for use by adults for silver-plated hollowware
(avg of 6 units); and 0.5 ug/ml of leaching soln if product intended for use by
infants and children for silver-plated hollowware (one or more of 6 units).
/Inorganic lead/
Chemical/Physical Properties:
Molecular Formula:
Pb
Molecular Weight:
207.2
Color/Form:
Bluish-white, silvery, gray metal. Highly
lustrous when freshly cut, tarnishes upon exposure to air. Cubic crystal
structure.
Boiling Point:
1740 deg C
Melting Point:
327.4 deg C
Density/Specific Gravity:
11.34 @ 20 deg C/4 deg C
Heat of Vaporization:
206 cal/g @ 1740 deg C
Vapor Pressure:
1.77 mm Hg @ 1000 deg C
Viscosity:
Viscosity of molten lead
(327.4 deg C) 3.2 centipoises, (400 deg C) 2.32 cP, (600 deg C) 1.54 cP, (800
deg C) 1.23 cP.
Other Chemical/Physical Properties:
VAPOR PRESSURE: 10 MM HG AT 1162 DEG C; 100 MM
HG AT 1421 DEG C; 400 MM HG AT 1630 DEG C
Very soft and malleable, easily melted, cast,
rolled, and extruded. Density (at mp) 10.65 g/cu cm. Heat capacity (20 deg C):
0.031 cal/g/deg C. Resistivity (microohm-cm) at 20 deg C: 20.65; at 100 deg C:
27.02; at 320 deg C: 54.76; at 330 deg: 96.74. Standard electromotive force (aq)
Pb/Pb2+ +0.126 v. Coefficient of linear expansion (0-100 deg C) 29X10-6, (20-300
deg C) 31.3X10-6, (-183 deg C to +14 deg C) 27X10-6; thermal conductivity varies
from 0.083 at 50 deg C to 0.077 at 225 deg C. Hardness 1 on Mohs' scale; Brinell
hardness (high purity Pb) 4.0.
Reacts with hot concd nitric acid, with
boiling concd hydrochloric or sulfuric acid. Attacked by pure water, weak
organic acids in the presence of oxygen. Resistant to tap water, hydrofluoric
acid, brine, solvents.
Chemical Safety & Handling:
Fire Potential:
Flammable in the form of dust when exposed to
heat or flame.
Toxic Combustion Products:
When heated ... it emits highly toxic fumes of
lead.
Explosive Limits & Potential:
Moderately explosive in the form of dust when
exposed to heat or flame.
Hazardous Reactivities & Incompatibilities:
CAN REACT VIGOROUSLY WITH OXIDIZING MATERIALS.
Ground mixtures of sodium carbide and ... lead
... can react vigorously.
... Trituration in a mortar of disodium
acetylide with finely divided lead may
be violent, carbon being liberated.
... Reaction with chlorine trifluoride at
ambient or slightly elevated temp is violent, ignition often occurring.
Mixtures of trioxane with 60% hydrogen
peroxide solution are detonable by heat or shock, or spontaneously after contact
with metallic lead. The latter may be
... /due/ to the heat of oxidation of lead.
... Reacts violently or explosively with fused
ammonium nitrate below 200 deg C.
... Lead
containing dry-box gloves may ignite in nitric acid environment.
Finely divided lead
produced by reduction of the oxide with furfural vapor at 290 deg C is
pyrophoric and chemically reactive.
A solution of sodium azide in copper pipe with
lead joints formed copper azide and lead
azide, both detonating compounds.
REACTS WITH HOT CONCN NITRIC ACID, BOILING
CONCN HYDROCHLORIC & SULFURIC ACIDS
Strong oxidizers, hydrogen peroxide, acids.
Incompatible with NaN3; Zirconium ...
Hazardous Decomposition:
When heated to decomposition it emits highly
toxic fumes of lead.
Immediately Dangerous to Life or Health:
100 mg/cu m
Protective Equipment & Clothing:
Wear appropriate personal protective clothing
to prevent skin contact.
Wear appropriate eye protection to prevent eye
contact.
Recommendations for respirator selection. Max
concn for use: 0.5 mg/cu m. Respirator Class(es): Any air-purifying respirator
with a high-efficiency particulate filter. Any supplied-air respirator.
Recommendations for respirator selection. Max
concn for use: 1.25 mg/cu m. Respirator Class(es): Any supplied-air respirator
operated in a continuous flow mode. Any powered, air-purifying respirator with a
high-efficiency particulate filter.
Recommendations for respirator selection. Max
concn for use: 2.5 mg/cu m. Respirator Class(es): Any air-purifying, full-facepiece
respirator with a high-efficiency particulate filter. Any supplied-air
respirator that has a tight-fitting facepiece and is operated in a
continuous-flow mode. Any powered, air-purifying respirator with a tight-fitting
facepiece and a high-efficiency particulate filter. Any self-contained breathing
apparatus with a full facepiece. Any supplied-air respirator with a full
facepiece.
Recommendations for respirator selection. Max
concn for use: 50 mg/cu m. Respirator Class(es): Any supplied-air respirator
operated in a pressure-demand or other positive-pressure mode.
Recommendations for respirator selection. Max
concn for use: 100 mg/cu m. Respirator Class(es): Any supplied-air respirator
that has a full facepiece and is operated in a pressure-demand or other
positive-pressure mode.
Recommendations for respirator selection.
Condition: Emergency or planned entry into unknown concn or IDLH conditions:
Respirator Class(es): Any self-contained breathing apparatus that has a full
facepiece and is operated in a pressure-demand or other positive-pressure mode.
Any supplied-air respirator that has a full facepiece and is operated in a
pressure-demand or other positive-pressure mode in combination with an auxiliary
self-contained breathing apparatus operated in pressure-demand or other
positive-pressure mode.
Recommendations for respirator selection.
Condition: Escape from suddenly occurring respiratory hazards: Respirator
Class(es): Any air-purifying, full-facepiece respirator with a high-efficiency
particulate filter. Any appropriate escape-type, self-contained breathing
apparatus.
Preventive Measures:
Control of exposure to toxic materials in
ceramics is important because of the large variety of toxic materials /including
lead tetroxide/. Dust control is of
paramount importance. This is accomplished by good local exhaust ventilation,
careful handling and storage of materials and proper clean-up techniques. The
area should have general dilution ventilation, but also local exhaust systems
for dry clay and glaze mixing, liquid glaze spraying and for the kiln emissions.
All dry clays and glazes should be stored in sealed containers (not in ripped
open paper bags). Plastic garbage cans with lids, on wheels, or similar
containers can be used. All materials should be handled in a manner that
prevents the creation of dusts. Premixed liquid glazes should be used and work
done with materials in the wet form as much as possible. Good housekeeping is
essential to keep the dust level down. There must be no dry sweeping or
vacuuming in the studio, as this will resuspend settled dust that can be inhaled
by the artists. Wet mopping, wet wiping and wet vacuuming or high efficiency
particulate air (HEPA) filtered vacuuming is recommended. Protective equipment
such as respirators, heat resistant gloves, eye protection, emergency showers
and fire extinguishers are recommended around kilns. Proper studio design is
important to insure that adequate ventilation, proper storage areas, handwashing
sinks, safety equipment and other facilities are provided and safety hazards are
avoided. Personal hygiene is also important. Artists should not eat, drink or
smoke in the studio. Clothes should be washed daily. Hands and particularly
nails should be washed frequently throughout the day, especially before eating,
drinking, smoking or leaving the studio for the day.
Cloakroom accommodation should be provided for
personal protective equipment with separate accommodation for clothing taken off
during working hours. Washing accommodation, including bathing accommodation
with warm water, should be provided and used. Time should be allowed for washing
before eating. Arrangements should be made to prohibit eating and smoking in the
vicinity of lead processes and
suitable messrooms should be provided.
SRP: Local exhaust ventilation should be
applied wherever there is an incidence of point source emissions or dispersion
of regulated contaminants in the work area. Ventilation control of the
contaminant as close to its point of generation is both the most economical and
safest method to minimize personnel exposure to airborne contaminants.
SRP: Contaminated protective clothing should
be segregated in such a manner so that there is no direct personal contact by
personnel who handle, dispose, or clean the clothing. Quality assurance to
ascertain the completeness of the cleaning procedures should be implemented
before the decontaminated protective clothing is returned for reuse by the
workers. All contaminated clothing should not be taken home at end of shift, but
should remain at employee's place of work for cleaning.
The worker should wash daily at the end of
each work shift.
Work clothing that becomes wet or
significantly contaminated should be removed or replaced.
Workers whose clothing may have become
contaminated should change into uncontaminated clothing before leaving the work
premises.
Stability/Shelf Life:
TARNISHES ON EXPOSURE TO AIR; ATTACKED BY PURE
WATER, WEAK ORG ACIDS IN PRESENCE OF OXYGEN; RESISTANT TO TAP WATER,
HYDROFLUORIC ACID, BRINE, SOLVENTS
Cleanup Methods:
Environmental considerations: Water spill:
Neutralize with agricultural lime (CaO), crushed limestone (CaCO3), or sodium
bicarbonate (NaHCO3). Adjust pH to neutral (pH= 7). Use mechanical dredges of
lifts to remove immobilized masses of pollutants & precipitates.
Environmental considerations: Land spill: Dig
a pit, pond, lagoon, or holding area to contain liquid or solid material. /SRP:
If time permits, pits, ponds, lagoons, soak holes, or holding areas should be
contained with a flexible impermeable membrane liner./ Cover solids with a
plastic sheet to prevent dissolving in rain or fire fighting water.
... Described treatment of wastewater from a
tetraethyl lead manufacturing process.
Two major categories of waste were inorganic lead
wastewaters and organic lead
wastewaters. After sedimentation in a holding basin to recover solid lead
and lead oxide, the inorganic lead
waste fraction (66.1 mg/l) was effectively treated by coagulation with ferric
and ferrous sulfate. /Inorganic lead/
Disposal Methods:
Generators of waste (equal to or greater than
100 kg/mo) containing this contaminant, EPA hazardous waste number D008, must
conform with USEPA regulations in storage, transportation, treatment and
disposal of waste.
Precipitation is the preferred treatment
process for removing toxic heavy metals from electroplating waters.
Precipitation processes include hydroxide, lime and/or sulfide treatment.
Chemical reduction is used to treat complex metals such as nickel, copper,
hexavalent chromium waste, soluble lead,
silver, metal containing cyanide, and mercury. Adsorption has shown potential
for treating and polishing aqueous metal bearing wastes. Activated carbon,
activated alumina, and iron filings are all applicable adsorbents. Alkaline
chlorination and incineration are effective cyanide destruction treatments.
Evaporation, ion-exchange, reverse osmosis, electrodialysis, and electrolytic
recovery are waste reduction and recovery techniques applicable to metal bearing
hazardous streams.
The following wastewater treatment
technologies have been investigated for lead:
Concentration process: Biological treatment. /Lead/
The following wastewater treatment
technologies have been investigated for lead:
Concentration process: Chemical precipitation. /Lead/
The following wastewater treatment
technologies have been investigated for lead:
Concentration process: Reverse osmosis. /Lead/
The following wastewater treatment
technologies have been investigated for lead:
Concentration process: Activated carbon. /Lead/
The following wastewater treatment
technologies have been investigated for lead:
Concentration process: Miscellaneous sorbents. /Lead/
Occupational Exposure Standards:
OSHA Standards:
The employer shall assure that no employee is
exposed to lead at concentrations
greater than 50 ug/cu m averaged over an 8-hr period. If an employee is exposed
to lead for more than 8 hr in any work
day, the permissible exposure limit, as a TWA for that day, shall be reduced
according to the following formula: Maximum permissible limit (in ug/cu m)= 400
divided by the number of hours worked in the day. /Lead,
inorganic, as Pb/
Threshold Limit Values:
8 hr Time Weighted Avg (TWA): 0.05 mg/cu m. /Lead,
elemental, and inorganic compounds, as Pb/
Excursion Limit Recommendation: Excursions in
worker exposure levels may exceed three times the TLV-TWA for no more than a
total of 30 min during a work day, and under no circumstances should they exceed
five times the TLV-TWA, provided that the TLV-TWA is not exceeded. /Lead,
elemental, and inorganic compounds, as Pb/
A3; Confirmed animal carcinogen with unknown
relevance to humans. /Lead, elemental,
and inorganic compounds, as Pb/
Biological Exposure Index (BEI): Determinant: lead
in blood; Sampling Time: not critical; BEI: 30 ug/100 ml. [Note: Women of child
bearing potential, whose blood Pb exceeds 10 ug/dl, are at risk of delivering a
child with a blood Pb over the current Centers for Disease Control guideline of
10 ug/dl. If the blood Pb of such children remains elevated, they may be at
increased risk of cognitive deficits. The blood Pb of these children should be
closely monitored and appropriate steps should be taken to minimize the child's
exposure to environmental lead.] /Lead,
elemental/
NIOSH Recommendations:
Recommended Exposure Limit: 10 hr
Time-Weighted avg: 0.1 mg/cu m.
Air concentrations should be maintained so
that worker blood lead remains less
than 0.06 mg PB/100 g of whole blood.
Immediately Dangerous to Life or Health:
100 mg/cu m
Other Occupational Permissible Levels:
Australia: 0.15 mg/cu m (as Pb) (1990);
Federal Republic of Germany: 0.1 mg/cu m total dust (as Pb), short-term level 1
mg/cu m, 30 min, once per shift, Pregnancy group B, a risk of damage to the
developing embryo or fetus must be considered to be probable, to minimize the
potential risk, a BAT value of 30 ug/dl blood has been evaluated specifically
for women under 45 years old (1991); Sweden: 0.1 mg/cu m, total dust, 0.05 mg/cu
m, respirable dust (1989); United Kingdom: 0.15 mg/cu m (1991).
Manufacturing/Use Information:
Major Uses:
Main uses are in the manufacture of storage
batteries, ammunition, nuclear and x-ray shielding devices, cable covering,
ceramic glazes, noise control materials, bearing, brass and bronze, casting
metals, solders, pipes, traps, and bends.
Construction material for tank linings,
piping, and other equipment handling corrosive gases and liqs used in the manuf
of sulfuric acid, petr refining, halogenation, sulfonation, extraction,
condensation; for x-ray and atomic radiation protection; manuf of tetraethyllead,
pigments for paints, and other organic and inorganic lead
compds; bearing metal and alloys; storage batteries; in ceramics, plastics, and
electronic devices; in building construction; in solder and other lead
alloys; in the metallurgy of steel and other metals.
Lead
and lead compounds was used in solder
applied to water distribution pipes and to seams of cans used for food, in some
traditional remedies, in bottle closures for alcoholic beverages and in ceramic
glazes and crystal tableware.
Manufacturers:
ASARCO, Incorporated, Hq, 180 Maiden Lane, New
York, NY 10038 (212) 510-2000. Production sites: Glover, MO 63646; Denver CO
80216
The Doe Run Co., hq, 1801 Park 270 Drive,
Suite 300, St. Louis, MO 63146 (314) 453-7100. Production site: Boss, MO 65440
Cominco Alaska Incorporated, (wholely owned
subsidiary of Cominco Ltd.,Toronto, Canada)
Hecla Mining Company, Coeur d'Alene, ID
Pegasus Gold, Inc., Spokane, WA.
Methods of Manufacturing:
The lead
mineral in most crude ores is separated from the gangue and other valuable
minerals. Occasionally, the ores are sufficently rich in lead
and low in impurities to be smelted directly. The primary operation of ore
dressing are crushing, grinding, and concentration (beneficiation). The first
step is a size reduction of the mined ore to liberate the desired minerals from
interlocking gangue. Primary (gyratory or jaw) and secondary (gyratory or roll)
crushers are employed. Wire-mesh screens bypass the finer material & return
the oversize for recrushing. Further comminution is accomplished by wet grinding
in horizontal, cylindrical mills containing steel balls, rods, or flint pebbles.
Autogenous grinding is employed occasionally. Classifiers that depend on
differences in settling rates in air or water are used in closed circuit with
grinding mills to recirculate oversize for regrinding.
Gravity concentration ... /such as/ the
separation of ore from gangue using jigs, heavy-medium separation, or tables, is
applicable to lead ores. These
techniques are often combined with the more widely used flotation process.
Flotation ... makes it possible to selectively separate ... the gangue ...
/&/ other valuable minerals from the lead
ore, such as sphalerite (zinc sulfide). For flotation the ore is ground to a
size sufficiently fine that the surface forces of adhesion to the bubbles,
supplied for buoyancy, overcome the force of gravity. ... The ground & sized
ore is discharged from classifiers to a conditioning tank in which the slurry is
mixed with the required chemicals, & then passed to the flotation cells in
which air is forced up through the slurry, forming bubbles to which the galena
adheres. The floated galena is trapped in the top froth & eventually
skimmed. ... The lead concentrate
skimmed from the cell is dewatered & thickened to a moisture content of 50%.
Vacuum filtering further decreases the moisture to 15% ... .
... /The/ series of processes ... /used to/
produce commercial grade of lead /from
lead concentrate include/
blast-furnace smelting (sintering ... /&/ smelting) ... drossing (soda
process ... /&/ continuous drossing) ... refining (pyrometallurgical methods
... /&/ electrolytic refining) ... /& the/ imperial smelting process
(none in the USA).
General Manufacturing Information:
The Bureau of Mines is investigating a
leach-electrolysis technique to produce lead
from galena concentrates without sulfur emissions. The concentrate is leached
with a hot FeCl3-NaCl solution to obtain a filtrate containing more than 99% of
the lead & a residue of elemental
sulfur & gangue material. Pure PbCl2 crystallizes out of the leach solution
on cooling & is electrolyzed in a relatively low temp fused-salt cell to
yield lead metal & chlorine gas.
New developments in the refining of lead
in general have focused on improvements & adaptions of the traditional
pyrometallurgical & electrorefining processes, & esp on the conversion
of batch processes into continuous processes. Completely continuous refining
operations are the goal of these efforts.
The recovery of lead
from scrap is an important source for the lead
demands of the USA & rest of the world. In the USA, 50% of the lead
requirements are satisfied by recycled lead
products. The ratio of secondary to primary lead
increases with increasing lead
consumption for batteries. The well-organized collecting channels forecast a
stable & growing future for lead.
... The principal types of scrap are battery plates, drosses, skimmings, &
industrial scrap such as solders, babbitts, cable sheathing, etc. Some of this
material is reclaimed by kettle melting & refining. ... Most scrap is a
combination of metallic lead & its
alloying constituents mixed with compounds of these metals, usually oxides &
sulfates. ... Most recycled lead
derives from scrap lead batteries
since >50% of the lead consumed in
the USA is in the form of lead
batteries. About 90% is reclaimed; hence, the bulk of the recycling industry is
centered on the processing of lead
battery scrap.
At present, battery scrap is converted to
impure lead or lead
alloys by pyrometallurgical processes employing blast, reverberatory, or rotary
furnaces. In many plants, a furnace combination is used. ... The overall
recovery of the metallic components of scrap in plants having both reverberatory
& blast furnaces is over 95%. ... The decisions being made by the operators
of secondary smelters as to which procedures will be designed into new plants or
installed in updating old plants are strongly influenced by the introduction of
new grid alloys, such as calcium alloys, low-antimony alloys (2-3%), &
strontium alloys, to replace the traditional 5-7% antimonial alloys, & by
air pollution standard requirements.
The projected world and USA demand for lead
in the year 2000, including that supplied from recycled lead,
is est at approx 9X10+6 and 2.2X10+6 tonnage/yr, respectively. This is an annual
growth rate of about 3% for the world & 1.5% for the USA. The demand in the
developing nations is expected to grow at a faster rate than in the
industrialized nations. If these estimates are correct, the lead
industry in the USA would have to increase by 50 to 60%. The cumulative demand
for primary lead in the world from
1973 to 2000 has been est at 140X10+6 tons. The est world reserves of 150X10+6
tons are sufficient to supply this demand.
The economics of USA lead
prodn, both primary & recycled, are markedly influenced by government
regulations concerning lead concn in
air. Compliance with those standards has been costly, and if more limiting
standards are imposed, can result in a reduction of present smelter capacity
& set limits on future expansion.
Stricter regulations concerning lead
emissions and ambient air lead levels,
as well as the need to reduce capital and operating costs have lead
to the development of alternative lead
smelting processes to replace the sinter-blast furnace combination. Four
processes have reached the stage of being promoted for commercial use, namely:
Kivcet, QSL, Isamelt, and Boliden Kaldo. These processes have the potential
advantages of meeting proposed in-plant hygiene requirements, utilizing the heat
of combustion and thereby reducing energy costs, reduction in capital and
operating costs through the use of high intensity vessels, and the production of
low volumes of process gas of high SO2 content through the use of large amounts
of oxygen.
1997 Production by state: Missouri, 412,000
metric tons; Montana, 9,230 metric tons; and Colorado, Idaho, Illinois, New
York, and Tennessee (combined), 26,600 metric tons.
1997: Lead
recovered from new scrap, 63,700 metric tons; old scrap, 1,040,000 metric tons,
of which 991,000 metric tons comes from batteries.
The princpal U.S. lead
producers, ASARCO, Inc. and The Doe Run Co., account for 75% of domestic mine
production and 100% of primary lead
production. Both companies employ sintering/blast furnace operations at their
smelters and pyrometallurigical methods in their refineries.
The most important ore mineral is galena, PbS
(87% Pb), followed by anglesite, PbSO4 (68% Pb), and cerussite, PbCO3 (77.5% Pb).
The latter two minerals result from the natural weathering of galena.
Although lead
is a relatively rare element, the occurrence of concentrated and easily
accessible lead ore deposits is
unexpectedly high.
Formulations/Preparations:
Grade: high purity (less than 10 ppm
impurity); pure (99.9+); powdered (99% pure); pig lead;
paste. Forms available: ingots, sheet, pipe, shot, buckles or straps, grids,
rod, wire, etc; paste; powder; single crystals.
Low bismuth, low silver, pure lead.
99.995% lead (ASTM B29-92) (for
chemical applications requiring low bismuth and silver contents). Specifications
(max allowable metal, wt%: Sb, As, Sn, 0.0005 each; Cu, 0.0010; Ag, 0.0010; Bi,
0.0015; Zn, 0.0005; Te, 0.0001; Ni, 0.0002; Fe, 0.0002.
Refined pure lead.
99.97% lead (ASTM B29-92) (for lead
battery applications). Specifications (max allowable metal, wt%: Sb, As, Sn,
0.0005 each; Cu, 0.0010; Ag, 0.0025; Bi, 0.025; Zn, 0.0005; Te, 0.0001; Ni,
0.0002; Fe, 0.001.
Pure lead.
99.94% lead (ASTM B29-92).
Specifications (max allowable metal, wt%: Sb, As, Sn, 0.001 each, 0.002 total;
Cu, 0.0015; Ag, 0.005; Bi, 0.05; Zn, 0.001; Ni, 0.001; Fe, 0.001.
Chemical copper-lead.
99.90% lead (ASTM B29-92) (for
applications requiring corrosion protection and formability). Specifications
(max allowable metal unless range is given, wt%: Sb, As, Sn, 0.001 each, 0.002
total; Cu, 0.040-0.080; Ag, 0.020; Bi, 0.025; Zn, 0.001; Ni, 0.002; Fe, 0.002.
Impurities:
ASTM requires pig lead
to be 99.85 to 99.90% pure; impurities consist of silver, copper, arsenic,
antimony, tin, zinc, iron, and/or bismuth.
After softening /lead
bullion/, the impurities that may still remain in the lead
are silver (about 0.2%), gold (about 0.006%), copper, tellurium, platinum
metals, & bismuth (up to 0.1%). Although these concentrations may be
tolerable for some lead applications,
their market value encourages separation & recovery.
Consumption Patterns:
Transportation-automotive batteries, gasoline
additives, 70%; construction, ammunition, electrical uses, TV glass, and paint,
25%; ceramics, type metal, ballast or weights, and tubes or containers, 5%
(1986)
COMPONENT OF LEAD
OXIDE BATTERIES, 36.5%; COMPONENT OF ANTIMONIAL LEAD
BATTERIES, 29.1%; CHEM INT FOR LEAD
ALKYLS, 11.1%; CHEM INT FOR PIGMENTS, 5.7%; AMMUNITION, 4.1%; SOLDER, 2.6%;
SHEET LEAD, 1.4%; CABLE COVERING,
1.4%; OTHER METAL PRODUCTS, 6.3%; OTHER, 1.8% (1982)
Lead
consumption in the USA by product in approx metric tons for 1979: ammunition,
52,884; bearing metal, 12,230; brass & bronze, 15,569; cable covering,
15,623; caulking lead, 4,055; casting
metals, 9,365; pipes, traps, bends, 2,942; sheet lead,
6,545; solders, 40,429; storage battery grids, posts, etc, 309,838; storage
battery oxides, 337,412; terne metal, 4,722; pigments, 82,788; antiknock
additives, 186,947.
Lead
consumption in the USA by product in approx metric tons for 1978: ammunition,
55,776; bearing metal, 9,510; brass & bronze, 16,502; cable covering,
13,851; caulking lead, 9,909; casting
metals, 3,611; pipes, traps, bends, 10,479; sheet lead,
12,626; solders, 68,391; storage battery grids, posts, etc, 412,568; storage
battery oxides, 466,714; terne metal, 3,778; pigments, 91,643; antiknock
additives, 178,333.
Lead
consumption in the USA by product in approx metric tons for 1977: ammunition,
61,961; bearing metal, 10,873; brass & bronze, 15,148; cable covering,
13,705; caulking lead, 8,725; casting
metals, 5,428; pipes, traps, bends, 10,555; sheet lead,
15,205; solders, 58,320; storage battery grids, posts, etc, 416,709; storage
battery oxides, 441,387; terne metal, 1,491; pigments, 90,703; antiknock
additives, 211,295; annealing, weights, galvanizing ballast, 21,478; other uses,
35,812.
Lead
consumption in the USA by product in approx metric tons for 1976: ammunition,
66,659; bearing metal, 11,851; brass & bronze, 14,207; cable covering,
14,452; caulking lead, 11,317; casting
metals, 6,085; pipes, traps, bends, 12,509; sheet lead,
22,170; solders, 57,447; storage battery grids, posts, etc, 348,221; storage
battery oxides, 397,859; terne metal, 1,447; pigments, 95,792; antiknock
additives, 217,507; annealing, weights, galvanizing ballast, 24,401; other uses,
29,351.
By class of products, 1997: Metal products,
7.8%; Storage Batteries, 86.9%; Miscellaneous, including other oxides, 5.3%.
By product, 1997: Ammunition, shot and
bullets, 3.46%; Bearing metals, 0.16%; Brass and bronze, billets and ingots,
0.28%; Cable covering, power and communication, 0.31%; Caulking lead,
building construction, 0.087%; Casting metals 1.14%; Pipes, traps and extruded
products, 0.12%; Sheet lead, 1.19%;
Solder, 0.60%; Storage batteries, 86.9%; Other metal products, 0.47%; Other
oxides, 4.18%; Miscellaneous uses, 0.53%.
U. S. Production:
Between 1960 & 1978, mine prodn in the USA
... increased from 232,00 to 541,000 tonnage. The large increase occurred from
1968 to 1970 with the coming on stream of mines & smelters in the newly
developed Missouri lead belt. Domestic
mine prodn in 1978 accounted for 70% of the USA primary lead
prodn.
(1977) 1.31X10+12 G
(1978) 541,000 metric tons (mine production);
776,000 metric tons (refined production with some secondary lead
included)
(1982) 1.09X10+12 G
(1986) 1.26x10+12 g
1997: Recoverable lead
from mines (after smelting and refining), 448,000 metric tons; Primary lead
(refined; domestic ores and base bullion), 343,000 metric tons; Secondary lead
(lead content), 1,110,000 metric tons.
U. S. Imports:
(1977) 2.30X10+11 G
(1982) 9.50X10+10 G
(1986) 1.20X10+10 g
1997: Lead
in ore and concentrates, 17,800 metric tons; Lead
in base bullion, 25 metric tons; lead
in pigs, bars, and reclaimed scrap, 265,000 metric tons. (lead
content)
U. S. Exports:
(1977) 8.90X10+9 G
(1982) 5.56X10+10 G
(1986) 1.40X10+10 g
1997: Lead
ore and concentrates, 42,200 metric tons; Lead
materials, excluding scrap, 104,000 metric tons. (lead
content)
Laboratory Methods:
Clinical Laboratory Methods:
MICRODETERMINATION OF LEAD
IN BLOOD & URINE BY ANODIC STRIPPING VOLTAMMETRY EQUIPPED WITH MERCURY
ELECTRODE. NO INTERFERENCE WAS FOUND WITH COEXISTING IONS FOUND IN URINE. /TOTAL
LEAD/
High performance liquid chromatography assay
of RBC UMPase activity is a sensitive and rapid assay that appears to meet
criteria for a reliable clinical laboratory index of blood lead
concentrations. /Total lead/
Lead
concentrations (ug/g wet weight) in human bone (tibia) were measured
noninvasively in vivo employing an x-ray fluoresence technique. Forty-five
workers who had been chronically exposed to lead
(mean duration of employment 20.9 yr) were found to have a mean bone lead
content of 52.9 ug/g wet weight (range 0-198 ug/g). Blood lead,
urinary lead excretion after EDTA
chelation, zinc protoporphyrin, and unstimulated urinary lead
excretion were also evaluated. The correlation coefficients (r) between bone lead
measurements (as assayed by x-ray fluoresence) and blood lead,
zinc protoporphyrin, or unstimulated urinary lead
were 0.44 (p=0.004), 0.39 (p=0.015), and 0.40 (p=0.01) respectively. The
correlation coefficient between x-ray fluoresence (XRF) findings and lead
excretion following Ca-EDTA administration was 0.69 (p<0.001). /Total lead/
Biological indicator of exposure to lead
or lead compounds. Analyte: Lead.
Matrix: blood or tissue. Method: Inductively-coupled argon plasma-atomic
emission spectroscopy. Wavelength: 220.4 nm. Precision: 0.85. This method is
useful for monitoring the blood of workers exposed to several metals
simultaneously. This is a simultanous multielemental analysis, but is not
compound-specific. /Total lead/
Biological indicator of exposure to lead
& lead compounds. Analyte: Lead(II)-APDC
(ammonium pyrrolidine dithiocarbamate) complex. Matrix: blood or urine.
Technique: atomic absorption, air/acetylene. Quality control: commercial
controls, pooled urine or blood, urine corrected for creatinine. Extraction:
APDC-MIBK (methyl isobutyl ketone). Range: 5 to 150 ug/100 g blood; 5 to 150 ug/100
ml urine. Precision: 0.05. This procedure quantitates Pb(2+) in blood or urine
to assess body burden, injury to the hematopoietic system, & to comply with
Federal regulations. Blood lead is the
preferred biological indicator of lead
absorption. The optimum working range is 0.1 to 1.5 ug Pb/g or per ml urine.
Interferences: Phosphate, EDTA, & oxalate can sequester lead
and cause low lead readings. /Total lead/
Sampling Procedures:
Airborne particulate lead
is sampled with a high-volume air sampler (as high as 2 cu m/min) for a period
of 24 hr and analyzed by atomic absorption spectrometry. Gross particulate
loading is determined by weighing the filter before and after sample collection.
Additional supplemental samplers include the following: 1) dichotomous sampler -
to fractionate samples into two size ranges, since there are distinct
differences in the effects of small and large particles on humans; 2) tape
sampler - to monitor airborne particulates for shorter time intervals (for
source and transport studies).
Analyte: Lead.
Matrix: Air. Sampler: Filter (0.8-um cellulose ester membrane). Flow rate: 1 to
4 l/min. Vol: min, 200 l at 0.05 mg/cu m; max, 1200 l. Stability: stable.
Shipment is routine. Range studied: 0.13 to 0.4 mg/cu m; 0.15 to 1.7 mg/cu m
(fume). Overall precision: 0.072; 0.068 (fume). The working range is 0.25 to 0.5
mg/cu m for a 400 l air sample. The method is applicable to elemental lead,
including lead fume, & all other
aerosols containing lead. This is an
elemental analysis, not compound specific.
Special References:
Special Reports:
CHISOLM JJ JR, D BARLTROP; RECOGNITION &
MANAGEMENT OF CHILDREN WITH INCR LEAD
ABSORPTION; ARCHIVES OF DISEASES IN CHILDHOOD 54: 249-62 (1979). REVIEW WITH
DISCUSSION ON MANAGEMENT & RECOGNITION OF INCREASED LEAD
ABSORPTION IN CHILDREN
USEPA; Ambient Water Quality Criteria Doc: Lead
(1980) EPA 440/5-80-057
USEPA; Air Quality Criteria for Lead
(1977) EPA 600/8-77-017
USEPA; Intermedia Priority Pollutants Guidance
Document Lead (1982)
Nat'l Research Council Canada; Effects of
Chromium in the Canadian Envir (1976) NRCC No.15017
WHO; Environ Health Criteria: Lead
(1977)
USEPA; Air Quality Criteria for Lead
I-IV (1986) EPA-600/8-83/028aF
McInnes G; Airborn Lead
Concentrations and the Effect of Reductions in the Lead
Content of Petrol (1986)
National Academy of Sciences; Lead
in the Human Environment (1980)
USEPA; Health Effects Assessment for Lead
(1984) PB86-134665
DHHS/ATSDR; The Nature and Extent of Lead
Poisoning in Children in the United States: A Report to Congress (7/88)
WHO; Environmental Health Criteria 119:
Principles and Methods for the Assessment of Nephrotoxicity Associated with
Exposure to Chemicals (1991)
DHHS/FDA; Guidance Document for Lead
in Shellfish (1993)
U.S. Dept Health & Human Services/Agency
for Toxic Substances & Disease Registry; Toxicological Profile for Lead
(Update) (1993) ATSDR/TP-92/12
Synonyms and Identifiers:
Related HSDB Records:
Synonyms:
CI pigment metal 4
**PEER REVIEWED**
CI 77575
**PEER REVIEWED**
KS-4
**PEER REVIEWED**
LEAD
**PEER REVIEWED**
Lead
flake
**PEER REVIEWED**
Lead
metal
**PEER REVIEWED**
Lead
S2
**PEER REVIEWED**
Olow
(Polish)
**PEER REVIEWED**
Pb-S 100
**PEER REVIEWED**
PLUMBUM
**PEER REVIEWED**
Formulations/Preparations:
Grade: high purity (less than 10 ppm
impurity); pure (99.9+); powdered (99% pure); pig lead;
paste. Forms available: ingots, sheet, pipe, shot, buckles or straps, grids,
rod, wire, etc; paste; powder; single crystals.
Low bismuth, low silver, pure lead.
99.995% lead (ASTM B29-92) (for
chemical applications requiring low bismuth and silver contents). Specifications
(max allowable metal, wt%: Sb, As, Sn, 0.0005 each; Cu, 0.0010; Ag, 0.0010; Bi,
0.0015; Zn, 0.0005; Te, 0.0001; Ni, 0.0002; Fe, 0.0002.
Refined pure lead.
99.97% lead (ASTM B29-92) (for lead
battery applications). Specifications (max allowable metal, wt%: Sb, As, Sn,
0.0005 each; Cu, 0.0010; Ag, 0.0025; Bi, 0.025; Zn, 0.0005; Te, 0.0001; Ni,
0.0002; Fe, 0.001.
Pure lead.
99.94% lead (ASTM B29-92).
Specifications (max allowable metal, wt%: Sb, As, Sn, 0.001 each, 0.002 total;
Cu, 0.0015; Ag, 0.005; Bi, 0.05; Zn, 0.001; Ni, 0.001; Fe, 0.001.
Chemical copper-lead.
99.90% lead (ASTM B29-92) (for
applications requiring corrosion protection and formability). Specifications
(max allowable metal unless range is given, wt%: Sb, As, Sn, 0.001 each, 0.002
total; Cu, 0.040-0.080; Ag, 0.020; Bi, 0.025; Zn, 0.001; Ni, 0.002; Fe, 0.002.
EPA Hazardous Waste Number:
D008; A waste containing lead
may (or may not) be characterized a hazardous waste following testing by the
Toxicant Extraction Procedure as prescribed by the Resource Conservation and
Recovery Act (RCRA) regulations. /Lead/
Administrative Information:
Hazardous Substances Databank Number:
231
Last Revision Date: 20030214
Last Review Date: Reviewed by
SRP on 5/20/1999
Update History:
Complete Update on 02/14/2003, 1 field
added/edited/deleted.
Complete Update on 11/08/2002, 1 field added/edited/deleted.
Complete Update on 07/22/2002, 2 fields added/edited/deleted.
Complete Update on 01/14/2002, 1 field added/edited/deleted.
Complete Update on 08/09/2001, 1 field added/edited/deleted.
Complete Update on 05/16/2001, 1 field added/edited/deleted.
Complete Update on 09/12/2000, 1 field added/edited/deleted.
Complete Update on 06/12/2000, 1 field added/edited/deleted.
Complete Update on 06/01/2000, 87 fields added/edited/deleted.
Field Update on 02/02/2000, 1 field added/edited/deleted.
Field Update on 09/21/1999, 1 field added/edited/deleted.
Field Update on 08/26/1999, 1 field added/edited/deleted.
Field Update on 05/04/1999, 1 field added/edited/deleted.
Field Update on 02/11/1999, 1 field added/edited/deleted.
Field Update on 11/20/1998, 1 field added/edited/deleted.
Field Update on 11/17/1998, 1 field added/edited/deleted.
Complete Update on 06/02/1998, 1 field added/edited/deleted.
Complete Update on 10/17/1997, 1 field added/edited/deleted.
Complete Update on 08/13/1997, 1 field added/edited/deleted.
Complete Update on 05/08/1997, 1 field added/edited/deleted.
Complete Update on 03/27/1997, 1 field added/edited/deleted.
Complete Update on 02/18/1997, 1 field added/edited/deleted.
Complete Update on 10/12/1996, 1 field added/edited/deleted.
Complete Update on 05/03/1996, 3 fields added/edited/deleted.
Complete Update on 04/16/1996, 6 fields added/edited/deleted.
Complete Update on 01/18/1996, 1 field added/edited/deleted.
Complete Update on 10/23/1995, 1 field added/edited/deleted.
Complete Update on 02/14/1995, 1 field added/edited/deleted.
Complete Update on 02/01/1995, 1 field added/edited/deleted.
Complete Update on 12/19/1994, 1 field added/edited/deleted.
Complete Update on 09/26/1994, 1 field added/edited/deleted.
Complete Update on 09/01/1994, 1 field added/edited/deleted.
Complete Update on 08/17/1994, 1 field added/edited/deleted.
Complete Update on 08/11/1994, 1 field added/edited/deleted.
Complete Update on 03/25/1994, 1 field added/edited/deleted.
Complete Update on 02/02/1994, 1 field added/edited/deleted.
Complete Update on 01/17/1994, 1 field added/edited/deleted.
Complete Update on 11/05/1993, 1 field added/edited/deleted.
Complete Update on 10/28/1993, 1 field added/edited/deleted.
Complete Update on 08/17/1993, 4 fields added/edited/deleted.
Field Update on 08/03/1993, 1 field added/edited/deleted.
Field Update on 05/25/1993, 1 field added/edited/deleted.
Field Update on 01/20/1993, 1 field added/edited/deleted.
Field update on 12/11/1992, 1 field added/edited/deleted.
Complete Update on 12/10/1992, 1 field added/edited/deleted.
Complete Update on 12/03/1992, 1 field added/edited/deleted.
Complete Update on 11/23/1992, 1 field added/edited/deleted.
Complete Update on 11/04/1992, 1 field added/edited/deleted.
Complete Update on 07/29/1992, 1 field added/edited/deleted.
Complete Update on 05/15/1992, 1 field added/edited/deleted.
Complete Update on 04/27/1992, 1 field added/edited/deleted.
Complete Update on 01/23/1992, 1 field added/edited/deleted.
Complete Update on 07/11/1991, 1 field added/edited/deleted.
Complete Update on 01/07/1991, 7 fields added/edited/deleted.
Field update on 11/09/1990, 1 field added/edited/deleted.
Field update on 05/18/1990, 1 field added/edited/deleted.
Field Update on 01/15/1990, 1 field added/edited/deleted.
Complete Update on 01/11/1990, 6 fields added/edited/deleted.
Field update on 12/29/1989, 1 field added/edited/deleted.
Complete Update on 07/12/1989, 89 fields added/edited/deleted.
Complete Update on 02/24/1988, 11 fields added/edited/deleted.
Complete Update on 04/17/1987