Lead, inorganic
| 1. NAME |
| 1.1 Substance |
| 1.2 Group |
| 1.3 Synonyms |
| 1.4 Identification numbers |
| 1.4.1 CAS number |
| 1.4.2 Other numbers |
| 1.5 Brand names, Trade names |
| 1.6 Manufacturers, Importers |
| 2. SUMMARY |
| 2.1 Main risks and target organs |
| 2.2 Summary of clinical effects |
| 2.3 Diagnosis |
| 2.4 First-aid measures and management principles |
| 3. PHYSICO-CHEMICAL PROPERTIES |
| 3.1 Origin of the substance |
| 3.2 Chemical structure |
| 3.3 Physical properties |
| 3.4 Other characteristics |
| 4. USES/CIRCUMSTANCES OF POISONING |
| 4.1 Uses |
| 4.2 High risk circumstance of poisoning |
| 4.3 Occupationally exposed populations |
| 5. ROUTES OF ENTRY |
| 5.1 Oral |
| 5.2 Inhalation |
| 5.3 Dermal |
| 5.4 Eye |
| 5.5 Parenteral |
| 5.6 Others |
| 6. KINETICS |
| 6.1 Absorption by route of exposure |
| 6.2 Distribution by route of exposure |
| 6.3 Biological half-life by route of exposure |
| 6.4 Metabolism |
| 6.5 Elimination by route of exposure |
| 7. TOXICOLOGY |
| 7.1 Mode of Action |
| 7.2 Toxicity |
| 7.2.1 Human data |
| 7.2.1.1 Adults |
| 7.2.1.2 Children |
| 7.2.2 Relevant animal data |
| 7.2.3 Relevant in vitro data |
| 7.2.4 Workplace standards |
| 7.2.5 Acceptable daily intake (ADI) and other guideline levels |
| 7.3 Carcinogenicity |
| 7.4 Teratogenicity |
| 7.5 Mutagenicity |
| 7.6 Interactions |
| 8. TOXICOLOGICAL ANALYSES AND BIOMEDICAL INVESTIGATIONS |
| 8.1 Material sampling plan |
| 8.1.1 Sampling and specimen collection |
| 8.1.1.1 Toxicological analyses |
| 8.1.1.2 Biomedical analyses |
| 8.1.1.3 Arterial blood gas analysis |
| 8.1.1.4 Haematological analyses |
| 8.1.1.5 Other (unspecified) analyses |
| 8.1.2 Storage of laboratory samples and specimens |
| 8.1.2.1 Toxicological analyses |
| 8.1.2.2 Biomedical analyses |
| 8.1.2.3 Arterial blood gas analysis |
| 8.1.2.4 Haematological analyses |
| 8.1.2.5 Other (unspecified) analyses |
| 8.1.3 Transport of laboratory samples and specimens |
| 8.1.3.1 Toxicological analyses |
| 8.1.3.2 Biomedical analyses |
| 8.1.3.3 Arterial blood gas analysis |
| 8.1.3.4 Haematological analyses |
| 8.1.3.5 Other (unspecified) analyses |
| 8.2 Toxicological Analyses and Their Interpretation |
| 8.2.1 Tests on toxic ingredient(s) of material |
| 8.2.1.1 Simple Qualitative Test(s) |
| 8.2.1.2 Advanced Qualitative Confirmation Test(s) |
| 8.2.1.3 Simple Quantitative Method(s) |
| 8.2.1.4 Advanced Quantitative Method(s) |
| 8.2.2 Tests for biological specimens |
| 8.2.2.1 Simple Qualitative Test(s) |
| 8.2.2.2 Advanced Qualitative Confirmation Test(s) |
| 8.2.2.3 Simple Quantitative Method(s) |
| 8.2.2.4 Advanced Quantitative Method(s) |
| 8.2.2.5 Other Dedicated Method(s) |
| 8.2.3 Interpretation of toxicological analyses |
| 8.3 Biomedical investigations and their interpretation |
| 8.3.1 Biochemical analysis |
| 8.3.1.1 Blood, plasma or serum |
| 8.3.1.2 Urine |
| 8.3.1.3 Other fluids |
| 8.3.2 Arterial blood gas analyses |
| 8.3.3 Haematological analyses |
| 8.3.4 Interpretation of biomedical investigations |
| 8.4 Other biomedical (diagnostic) investigations and their interpretation |
| 8.5 Overall Interpretation of all toxicological analyses and toxicological investigations |
| 8.6 References |
| 9. CLINICAL EFFECTS |
| 9.1 Acute poisoning |
| 9.1.1 Ingestion |
| 9.1.2 Inhalation |
| 9.1.3 Skin exposure |
| 9.1.4 Eye contact |
| 9.1.5 Parenteral exposure |
| 9.1.6 Other |
| 9.2 Chronic poisoning |
| 9.2.1 Ingestion |
| 9.2.2 Inhalation |
| 9.2.3 Skin exposure |
| 9.2.4 Eye contact |
| 9.2.5 Parenteral exposure |
| 9.2.6 Other |
| 9.3 Course, prognosis, cause of death |
| 9.4 Systematic description of clinical effects |
| 9.4.1 Cardiovascular |
| 9.4.2 Respiratory |
| 9.4.3 Neurological |
| 9.4.3.1 CNS |
| 9.4.3.2 Peripheral nervous system |
| 9.4.3.3 Autonomic nervous system |
| 9.4.3.4 Skeletal and smooth muscle |
| 9.4.4 Gastrointestinal |
| 9.4.5 Hepatic |
| 9.4.6 Urinary |
| 9.4.6.1 Renal |
| 9.4.6.2 Others |
| 9.4.7 Endocrine and reproductive systems |
| 9.4.8 Dermatological |
| 9.4.9 Eye, ears, nose, throat: local effects |
| 9.4.10 Haematological |
| 9.4.11 Immunological |
| 9.4.12 Metabolic |
| 9.4.12.1 Acid-base disturbances |
| 9.4.12.2 Fluid and electrolyte disturbances |
| 9.4.12.3 Others |
| 9.4.13 Allergic reactions |
| 9.4.14 Other clinical effects |
| 9.4.15 Special risks |
| 9.5 Others |
| 9.6 Summary |
| 10. MANAGEMENT |
| 10.1 General principles |
| 10.2 Relevant laboratory analyses and other investigations |
| 10.2.1 Sample collection |
| 10.2.2 Biomedical analysis |
| 10.2.3 Toxicological analysis |
| 10.2.4 Other investigations |
| 10.3 Life supportive procedures and symptomatic treatment |
| 10.4 Decontamination |
| 10.5 Elimination |
| 10.6 Antidote treatment |
| 10.6.1 Adults |
| 10.6.2 Children |
| 10.7 Management discussion |
| 11. ILLUSTRATIVE CASES |
| 11.1 Case reports from literature |
| 11.2 Internally extracted data on cases |
| 11.3 Internal cases |
| 12. ADDITIONAL INFORMATION |
| 12.1 Availability of antidotes |
| 12.2 Specific preventive measures |
| 12.3 Other |
| 13. REFERENCES |
| 14. AUTHOR(S), REVIEWER(S), DATE(S) (INCLUDING UPDATES), COMPLETE ADDRESSES |
1. NAME
1.1 Substance
Inorganic lead
1.2 Group
Non-ferrous metal
1.3 Synonyms
C.I. 77575
C.I. pigment metal
KS-4
lead flake
lead S2
Plumbum (Pb)
1.4 Identification numbers
1.4.1 CAS number
7439-92-1
1.4.2 Other numbers
DOT 1794
RTECS OF7525000
1.5 Brand names, Trade names
Not applicable.
1.6 Manufacturers, Importers
Not applicable.
(NIOSH, 1978; Budavari, 1989; Sax, 1989)
2. SUMMARY
2.1 Main risks and target organs
Exposure occurs from breathing air, drinking water, and eating
foods that contain lead. Inhalation of lead fumes or of fine
lead particles is the most important route of absorption in
the working environment and general atmosphere. Chronic low-
dose lead exposure exerts subtle neuropsychiatric,
reproductive and renal effects and children are particularly
susceptible.
Acute poisoning may follow ingestion of lead-containing paint
by children (pica). The possible effects of low-dose of lead
in adults is still unclear. Hypertension, gout, nephropathy,
and neurotoxic symptoms may be related to lead exposure.
Target organs
Lead interferes with the haem biosynthetic pathway, producing
haematological effects, and competes at the molecular level
with calcium. The central nervous system and kidneys are
particularly sensitive to lead. The central and peripheral
nervous systems are affected; gastrointestinal structures are
also damaged; and there is strong evidence of effects on the
reproductive system. Lead also may have a role as a cofactor
in carcinogenesis (Putnam, 1986; Sax, 1989; ATSDR, 1990; Goyer,
1990).
2.2 Summary of clinical effects
Poisoning by inorganic lead compounds presents as three main
clinical pictures: chronic poisoning; acute poisoning; and
asymptomatic poisoning, occurring during childhood.
Acute poisoning from a single exposure is rare but may result
from the ingestion of solutions of soluble lead salts (lead
acetate, lead carbonate). The primary symptoms are related to
local irritation of the gastrointestinal tract and include:
vomiting and abdominal colic. Pain in the legs, cramps and
paresthesiae may follow, with shock, haemolytic anaemia and
renal dysfunction. Depression, coma and death occur within 1
to 2 days.
Lead is a cumulative poison and the acute symptoms are
commonly a manifestation of chronic poisoning. Chronic
symptomatic poisoning (plumbism) causes abdominal colicky
pains, anorexia, nausea, vomiting, metallic taste, blue line
on the gum margins, anaemia, peripheral neuropathy (wrist
drop), convulsions and encephalopathy.
In childhood, lead poisoning may be asymptomatic. There may be
elevated levels of lead in the blood but symptoms are delayed.
The so-called developmental syndrome, with cognitive and
behavioural changes, is the consequence of the absorption of
lead, mainly from pica. Anaemia is often a common
manifestation. It is very important to implement chelation
therapy soon after diagnosis (Prerovska, 1974; Gilman, 1990;
Garrettson, 1990).
2.3 Diagnosis
Diagnosis of poisoning is based on history of exposure and the
clinical signs and symptoms described above. Chronic
poisoning may be asymptomatic for some time. Many laboratory
tests are used for the diagnosis of lead poisoning. Many
laboratory tests are used for the diagnosis of lead poisoning.
Blood: complete blood count (basophilic stippling of red
cells); whole-blood lead levels; red cell delta-aminolevulinic
acid dehydratase activity; free erythrocyte protoporphyrin.
Urine: 24-hour urine lead levels; Urinary delta-aminolevulinic
acid; Urinary coproporphyrin; Lead in urine after calcium
disodium EDTA mobilization test.
Hair: determination of lead levels.
Sample collection: a 24-hour specimen of urine is preferable
to a single specimen; the blood sample should be taken and
stored in specially cleaned glass-ware; samples of hair should
be properly washed.
2.4 First-aid measures and management principles
The main emphasis of management is on symptomatic treatment of
life-threatening effects and chelation therapy with EDTA, BAL,
DMSA or pencillamine depending on the particular case and
antidote availability.
If acute poisoning by inorganic lead occurs, remove patient
from further exposure, send for medical assistance, remove and
discard contaminated clothing, wash skin with soap and copious
amounts of water. If the patient has seizures, control
convulsions with appropriate drug regimen, and treat
symptomatically.
After oral ingestion and unless vomiting is extensive, if the
patient is obtunded, convulsing, comatose, insert an oro- or a
naso-gastric tube and lavage after endotracheal intubation.
In the case of lead encephalopathy, calcium disodium may be
indicated, as well as in cases of acute poisoning by ingestion,
or in acute episodes during chronic poisoning.
Chronic poisoning: combined treatment BAL and edetate calcium
disodium is indicated in adults with blood lead levels up to
1000 µg/L. Interrupt treatment for 2 days and, if the blood
lead level remains high, restart edetate; subsequently, d-
penicillamine may be given for 3 to 6 months.
Children with blood lead levels up to 700 ug/L should be
treated with combined BAL and edetate calcium disodium; BAL
may be discontinued after 3 days if the blood lead is < 500
ug/L but edetate should be continued for 5 days. Long term
chelation with penicillamine in children should be limited to
2 months.
3. PHYSICO-CHEMICAL PROPERTIES
3.1 Origin of the substance
Lead is a naturally occurring metal in the earth's crust. Its
compounds can be found in all parts of the environment. It
occurs in the earth's crust chiefly as minerals such as
galena, anglesite, cerussite, mimetite and pyromorphite. A
large number of inorganic lead compounds is represented by
acetate, antimonate, arsenate, arsenite, azide, bromate,
bromide, butyrate, chlorate, chloride, chromate, dioxide,
fluoride, formate, hexafluorosilicate, hydroxide,
hypophosphite, iodide, lactate, molybdate, monoxide, nitrate,
oxalate, phosphate, selenate, selenite, sesquioxide, sodium
thiosulphate, subacetate, sulfate, sulfide, telluride,
tetraacetate, tetrafluoride, tetroxide, thiocyanate, tungstate
and vanadate.
3.2 Chemical structure
Chemical name: Lead
Molecular weight: 207.2
Structural formula: not applicable
3.3 Physical properties
Boiling point: 1740 C (at 760 mmHg)
Melting point: 327.4 C
Flash point: not applicable
Autoignition temperature: Lead is combustible in powder
form
Relevant density: 11.34 at 20 C
Vapour pressure: 1.77 mmHg at 1000 C
Solubility: Lead nitrate, chlorate and, to a lesser
degree, chloride are soluble in water.
Other salts are poorly soluble in water,
but many are dissolved by acids
Explosive limits: Lead azide explodes at 350 C
Viscosity: (Molten lead at 327.4 C) 3.2
centipoises
Molecular Structural
Name CAS Number Weight Formula Solubility Other
---- ---------- --------- ---------- ---------- -----
Lead 301-04-2 325.28 C4H6O4Pb Alcohol pH of
Acetate Water water
Glycerol sol=5.5-
6.5
Lead Pb3(SbO4)2 Insoluble
Antimonate in water
Lead 7784-40-9 PbHAsO4 Insoluble
Arsenate in water;
soluble in
HNO3
Lead 10031-13-7 Pb(ASO2)2 Insoluble Explosive
Arsenite in water;
soluble in
HNO3
Lead 13424-46-9 291.26 Pb(N3)2 Soluble in
Azide water and
acetic acid
Lead Pb(BrO3)2 Soluble in
Borate water;
soluble in
HNO3
Lead 34018-28-5 463.01 Pb(BrO3)2
Bromate
Lead 367.04 Br2Pb
Bromide
3.4 Other characteristics
Normal state at room temperature: solid, heavy, ductile metal.
Colour: blueish-white, silvery, grey metal.
Dangers associated with vapours: vapours form at 550-600 C
and combine with oxygen in air to form lead oxide.
Present in work atmosphere as fumes, mists (for instance,
produced by spray painting) and dusts.
Lead reacts vigorously with oxidizing materials. Contact with
hydrogen peroxide or active metals such as sodium or potassium
may cause fire or explosion. Toxic fumes may be released in a
fire involving inorganic lead. Attacked by pure water or weak
organic acids in the presence of oxygen.
Pollution of the environment occurs through the smelting and
refining of lead, the burning of fuels containing lead
additives, and the smelting of other metals and the burning of
coal and oil.
The transport and distribution of lead is mainly via air. The
fraction that remains airborne (about 20%) is widely
dispersed. The concentration of lead in air varies from 2-4
µg/m3 in large cities to less than 0.2 µg/m3 in suburban and
rural areas (WHO, 1972; WHO, 1977; ACGIH, 1986; Budavari,
1989).
4. USES/CIRCUMSTANCES OF POISONING
4.1 Uses
Lead can be used in its pure form or combined with other
elements to form a variety of organic and inorganic
compounds. Metallic lead is used in storage batteries,
solders, ammunition, shielding systems for protection
from X-rays and radiation, lining tanks, and pipes. It
is a major component of many alloys such solders, type
metals, and bronzes. Lead inorganic salts are used in
insecticides, pigments, paints, enamels, glazes, glass,
plastics, rubber compounds (WHO, 1977; Glenn, 1986;
Putnam, 1986; Sax, 1989).
4.2 High risk circumstance of poisoning
Non-occupationally exposed individuals are exposed to
inorganic lead compounds primarily from ingestion of food and
water. Inhalation of airborne lead originating in dusts and
fumes is still a very important environmental source. Leaded
gasoline is an important cause of contamination and is
reviewed in the monograph on organic lead.
Domestic sources include contamination of food and beverages
from contact with utensils as earth-glazed pottery; ingestion
of lead-containing paint by children (pica); and use of herbal
medicines contaminated with lead (WHO, 1977; Glenn, 1986; Sax,
1989).
4.3 Occupationally exposed populations
Lead is the most widely used non-ferrous metal and a large
number of occupations may be associated with risk of exposure.
Workers may be exposed to metallic and inorganic lead
compounds in a wide variety of occupations, including mining,
smelting and refining operations; high-temperature lead
applications such as steel welding and spray coating; lead
grinding, cutting or discing; battery manufacturing and
recycling; radiator repair shops; production of paints,
ceramics and glazes, enamels and rubbers; car refinishing or
paint removal associated with building renovation; plumbing
and tank cleaning, etc..
The Occupational Safety and Health Administration has
identified over 120 occupations in which workers may be
exposed to lead (Federal Register, 1978). Lead poisoning is
one of the commonest occupational diseases, specially when
preventative measures are not established (WHO, 1977; Glenn,
1986; Sax, 1989).
5. ROUTES OF ENTRY
5.1 Oral
Accidental or deliberate ingestion of lead compounds may
occur. Lead may be ingested on contaminated food, drinks and
cigarettes, or lead particles trapped in the upper respiratory
tract may be swallowed. 5-15% of ingested inorganic lead is
absorbed from the gastrointestinal tract; the rest passes
through the body unabsorbed, and is eliminated in the faeces.
Absorption can increase to as much as 45% under fasting
conditions (Putnam, 1986) and 53% in infants and young
children (WHO, 1977). Decreased calcium and zinc levels
increase lead absorption, and iron appears to enhance it.
Naphthenate, acetate and some oxides of lead are rapidly and
more completely absorbed (Garrettson, 1990). Gastrointestinal
absorption of lead occurs by acid solubilization (Ellenhorn,
1988) and it seems that lead transport across the digestive
mucosa is similar to that of calcium (Gilman, 1990).
5.2 Inhalation
Inhalation of fumes, dusts, mists, and vapours of lead should
be considered as a major route of entry - from 50 to 70% of
the particles that reach the respiratory tract are absorbed,
depending on the particles (less than 1 µm), their
concentration and the ventilation rate (Putnam, 1986; Budavari,
1989; Gilman, 1990).
5.3 Dermal
Dermal absorption is not an efficient process, for inorganic
compounds of lead (Sax, 1989).
5.4 Eye
Not relevant.
5.5 Parenteral
One case of self-injection of lead acetate has been reported
(Sixel-Dietrick, 1985).
5.6 Others
Not relevant.
6. KINETICS
6.1 Absorption by route of exposure
Accidental or deliberate ingestion of lead compounds may
occur. Lead may be ingested on contaminated food, drinks and
cigarettes, or lead particles trapped in the upper respiratory
tract may be swallowed. Between 5-15% of ingested inorganic
lead is absorbed through the gastrointestinal tract. The rest
passes through the body unabsorbed, and is eliminated in the
faeces. Absorption can increase to as much as 45% under
fasting condition (Putnam, 1986) or 53% in infants and young
children (53%) (WHO, 1977). Decreased calcium and zinc levels
increase lead absorption, and iron appears to enhance it.
Naphthenate, acetate and some oxides of lead are rapidly and
more completely absorbed (Garrettson, 1990). Gastrointestinal
absorption of lead occurs by acid solubilization (Ellenhorn,
1988) and it seems that lead transport across the digestive
mucosa is similar to that of calcium (Gilman, 1990).
Inhalation of fumes, dusts, mists, and vapours of lead should
be considered as a major route of entry - from 50 to 70% of
the particles that reach the respiratory tract are absorbed,
depending in large part of the size of the particles (less
than 1 µm), their concentration and the ventilation rate
(Putnam, 1986; Gilman, 1990). Dermal absorption is not an
efficient process for inorganic compounds of lead (Sax, 1989).
6.2 Distribution by route of exposure
Lead is distributed according to a three-compartmental
pharmacokinetic model. Blood and soft tissues represent the
active pool and bones the storage pool. Lead is distributed to
kidney tubular epithelium and to liver, and redistributed to
bone, teeth, and hair; the long bones contain more lead and
about 95% of the body load is stored in the skeleton. The
largest part of circulating lead is bound to haemoglobin in
erythrocytes and the concentration of lead in erythrocytes is
about 16 times greater than in plasma (WHO, 1977).
Factors affecting the distribution of calcium, such as
phosphate intake, also affect the distribution of lead in
bones (a high intake of phosphate favours the storage in the
skeleton while a low intake promotes the redistribution from
bones to soft tissues) (Ellenhorn, 1988; Gilman, 1990;
Garrettson, 1990).
Lead has an affinity for the organic osteoid substance of bone
rather than its mineral components (Flood et al., 1988). In
certain circumstances (infection, wasting disease, pregnancy)
lead may be mobilized from storage sites in bone. Under
conditions of continuous intake over long periods of time, a
near-steady state is achieved with respect to
intercompartmental distribution (WHO, 1977).
6.3 Biological half-life by route of exposure
The biological half-life of lead is extremely difficult to
estimate (WHO, 1977). The half-life of lead in erythrocytes
is 35 days; in soft tissues (kidney, liver, and nervous
tissue) the half-life is 40 days; the half-life in bone is 20
to 30 years (Ellenhorn, 1988: Garrettson, 1990).
The half-life in blood reaches a steady state in about 6
months. The time required for accumulation of toxic
concentrations is inversely proportional to lead intake: a
daily intake of 2.5 mg will achieve a toxic level after 4
years whereas daily ingestion of 3.5 mg achieves similar
levels in only a few months (Gilman, 1990).
6.4 Metabolism
Inorganic lead compounds and elemental lead are not modified
by organic biochemical processes.
6.5 Elimination by route of exposure
The rate of excretion of lead is low. Renal clearance of
unchanged lead is essentially by glomerular filtration but at
high levels some active tubular transport occurs. Urinary
excretion accounts for 76% of daily losses, while
gastrointestinal secretions for 16% and hair, nails, sweat and
other routes for 8% (WHO, 1977; Ellenhorn, 1988).
When calcium disodium EDTA is administered the lead normally
excreted in the faeces is not transferred to the renal route.
Instead, the urinary lead arises from the removal of lead
deposited in organic tissue (Prerovska et al., 1974).
7. TOXICOLOGY
7.1 Mode of Action
Lead combines with sulfhydryl groups on proteins and
interferes with some biochemical processes. The enzymes
involved in the pathways of haem, myoglobin, cytochromes, and
catalases, are inhibited by lead. In the blood very low
concentrations of lead inhibit the synthesis of haem and
reduces the life span of erythrocytes. In the nervous system,
lead disrupts mitochondrial function. In the kidney, lead
produces lesions of the proximal tubules and the loop of Henle
(WHO, 1977; Hodgson et al., 1987; Ellenhorn, 1988; Gilman,
1990).
7.2 Toxicity
7.2.1 Human data
7.2.1.1 Adults
The dose of lead required to cause adverse
effects is rarely, if ever, known. The lead
blood level confirms a causal link between
likely exposure and an effect (WHO, 1977).
Fatal poisoning occurs with lead acetate and
lead carbonate in doses exceeding 30 g (Gosselin,
1984). Accumulation and toxicity occur if >
0.5 mg/day is absorbed. The fatal dose is
estimated at 500 mg of absorbed lead (Noji &
Kelen, 1989).
The lowest observed adverse effect level (LOAEL)
in human volunteers exposed to particulate lead
(inhalation) is 3.2 µg/m3. The LOAEL in human
volunteers is 20 µg/kg/day of lead acetate daily
for 21 days (0.2 mg/kg/day) (ATSDR, 1990).
Inhalation: Lowest toxic concentration in
humans - 10 µg/m3.
7.2.1.2 Children
Death from lead poisoning has occurred in
children at blood lead levels of 1250 µg/L or
higher. The LOAEL for children (causing
developmental toxicity) is 100 µg/L in blood.
This level is associated with diminishing IQ
score in children (Sax, 1989; ATSDR, 1990).
7.2.2 Relevant animal data
The lowest lethal dose for the dog is 191 mg/kg Pb; for
the guinea-pig is 313 mg/kg Pb (Sax, 1989).
Lowest Toxic Dose oral rats: 790 mg/kg
Lowest Toxic Dose oral rats: 1100 mg/kg (over 14 days)
Lowest Toxic Dose inhalation rats: 10 mg/m3/24 h
Lowest Lethal Dose intraperitoneal (rat): 1000 mg/kg
Lowest Lethal Dose oral (pigeon): 160 mg/kg (Sax, 1989)
7.2.3 Relevant in vitro data
Lead salts did not induce chromosomal aberrations in
human lymphocytes in vitro (IARC, 1987).
7.2.4 Workplace standards
Permissible Exposure Limit (PEL): 50 µg/m3 (NIOSH,
1978).
Recommended Exposure Limit (REL) Time Weighted Average
(TWA): 100 µg/m3 (NIOSH, 1978).
TLV-TWA (Threshold Limit Values-Time Weighted Average)
inorganic dusts and fumes, as Pb: 150 µg/m3 (ACGIH,
1990).
7.2.5 Acceptable daily intake (ADI) and other guideline levels
Provisional maximum tolerable weekly intake of lead:
adults, 3 mg per person or 50 µg/kg body weight;
children 25 µg/kg body weight (FAO/WHO, 1987).
In Great Britain, the amount of lead in food is
generally restricted to a maximum of 1 ppm with the
exception of food specially prepared for infants and
children, where the limit is 0.2 ppm (Ministry Agric.
Fish & Food, 1982).
7.3 Carcinogenicity
At very high concentrations, lead displays some carcinogenic
activity in experimental animals. The evidence for
carcinogenicity in humans is inadequate (IARC, 1987).
7.4 Teratogenicity
There have not been any adequate animal studies to provide
evidence to support the suggestion that lead may have a
teratogenic effect. In humans, one case has been reported of
neuromuscular abnormalities and failure to grow in one child;
this was attributed to lead poisoning as a result of the
consumption of lead by the pregnant mother (WHO, 1977).
7.5 Mutagenicity
Studies of chromosomal aberrations in people exposed to lead
have given conflicting results: positive results have been
published concerning workers in lead battery industries and
lead smelters but other studies have given negative results.
Lead salts do not induce chromosomal aberration in human
lymphocytes in vitro. They do not cause aneuploidy in
Drosophila, mutation or gene conversion in yeast or mutation
or DNA damage in bacteria (IARC, 1987).
7.6 Interactions
Interactions between lead and other environmental pollutants
occur. Lead forms lead sulfate in both water and air in the
presence of the sulfate ion (ATSDR, 1990).
Lead and disulfiram increase brain lead concentrations, and
depress Purkinje neuron function in the rat (Oskarsson et al.,
1986). Lead brain levels are increased after long-term
treatment with lead and dithiocarbamate or thiuram derivatives
in rats (Oskarsson & Lind, 1985).
8. TOXICOLOGICAL ANALYSES AND BIOMEDICAL INVESTIGATIONS
8.1 Material sampling plan
8.1.1 Sampling and specimen collection
8.1.1.1 Toxicological analyses
8.1.1.2 Biomedical analyses
8.1.1.3 Arterial blood gas analysis
8.1.1.4 Haematological analyses
8.1.1.5 Other (unspecified) analyses
8.1.2 Storage of laboratory samples and specimens
8.1.2.1 Toxicological analyses
8.1.2.2 Biomedical analyses
8.1.2.3 Arterial blood gas analysis
8.1.2.4 Haematological analyses
8.1.2.5 Other (unspecified) analyses
8.1.3 Transport of laboratory samples and specimens
8.1.3.1 Toxicological analyses
8.1.3.2 Biomedical analyses
8.1.3.3 Arterial blood gas analysis
8.1.3.4 Haematological analyses
8.1.3.5 Other (unspecified) analyses
8.2 Toxicological Analyses and Their Interpretation
8.2.1 Tests on toxic ingredient(s) of material
8.2.1.1 Simple Qualitative Test(s)
8.2.1.2 Advanced Qualitative Confirmation Test(s)
8.2.1.3 Simple Quantitative Method(s)
8.2.1.4 Advanced Quantitative Method(s)
8.2.2 Tests for biological specimens
8.2.2.1 Simple Qualitative Test(s)
8.2.2.2 Advanced Qualitative Confirmation Test(s)
8.2.2.3 Simple Quantitative Method(s)
8.2.2.4 Advanced Quantitative Method(s)
8.2.2.5 Other Dedicated Method(s)
8.2.3 Interpretation of toxicological analyses
8.3 Biomedical investigations and their interpretation
8.3.1 Biochemical analysis
8.3.1.1 Blood, plasma or serum
8.3.1.2 Urine
8.3.1.3 Other fluids
8.3.2 Arterial blood gas analyses
8.3.3 Haematological analyses
8.3.4 Interpretation of biomedical investigations
8.4 Other biomedical (diagnostic) investigations and their
interpretation
8.5 Overall Interpretation of all toxicological analyses and
toxicological investigations
8.6 References
9. CLINICAL EFFECTS
9.1 Acute poisoning
9.1.1 Ingestion
Acute poisoning from a single exposure is rare and may
result from the ingestion of soluble lead salts. Acute
episodes are frequently a manifestation of chronic
poisoning. Primary symptoms are related to
gastrointestinal irritation and include anorexia,
vomiting, abdominal colic. Pain in the legs, cramps and
paresthesiae may follow. Shock, haemolytic anaemia and
renal dysfunction are observed. Headache and
hypertension have been reported in adults (Gosselin,
1984; Ellenhorn, 1988; Noji & Kelen, 1989; Garrettson;
1990).
9.1.2 Inhalation
Inhalation of lead oxides, fumes or of fine lead
particles is the most important route of absorption in
the working environment (Fischbein, 1983). However,
acute episodes with systemic symptoms are exceptional.
9.1.3 Skin exposure
Not relevant.
9.1.4 Eye contact
Not relevant.
9.1.5 Parenteral exposure
One case of lead acetate intravenously injected has been
described (Sixel-Dietrick et al., 1985).
9.1.6 Other
Not relevant.
9.2 Chronic poisoning
9.2.1 Ingestion
Chronic poisoning by ingestion causes a number of
symptoms: abdominal colicky pains, anorexia, nausea,
vomiting, metallic taste, blue line on the gum margins,
anaemia, peripheral neuropathy, irritability, lethargy,
convulsions, encephalopathy conditions. Chronic
nephritis and hypertension have been described. Two
groups are particularly affected: adults exposed
occupationally, and children. The symptoms are not
specific to lead poisoning and should be considered as
signs of poisoning if exposure and working conditions
indicate the possibility of increased lead absorption.
Three major clinical syndromes of chronic poisoning are
described: the gastrointestinal type, the neuromuscular
type and the cerebral type. The cerebral syndrome is
most often seen in childhood and is associated with
encephalopathy. However, many of the signs and symptoms
described are features common to all types (ILO, 1983;
Gosselin, 1984; Ellenhorn, 1988; Garrettson, 1990).
9.2.2 Inhalation
The main route of entry in industrial exposure is the
respiratory tract. However, bad conditions of hygiene
and living in the neighbourhood of small industries
which use lead can affect general population, especially
children.
The clinical picture of chronic plumbism by inhalation
is similar to that described after chronic ingestion:
fall-off in physical fitness, fatigue, sleep disturbance,
headache, aching bones and muscles, vomiting, abdominal
colic, obstipation, decreased appetite. Anaemia,
peripheral nerve disturbances and acute encephalopathy
may develop in children (ILO, 1983; Gosselin, 1984;
Ellenhorn, 1988; Garrettson, 1990).
9.2.3 Skin exposure
Not relevant.
9.2.4 Eye contact
Not relevant.
9.2.5 Parenteral exposure
An unusual case of lead poisoning due to intravenous
injection has been reported (Sixel-Dietrick et al.,
1985).
9.2.6 Other
Unusual cases of lead chronic poisoning have been
reported after liberation into the circulation, over
periods of many years, of lead from retained bullets,
(Gosselin, 1984).
9.3 Course, prognosis, cause of death
After chelation therapy, complete recovery may take up to 1
year. Long-term effects include neurological deficits,
chronic nephritis, nephrotic syndrome and saturnine gout.
In children, subtle behavioural, cognitive and neurological
deficits (developmental syndrome) become evident many years
after the exposure to lead and mortality in lead
encephalopathy is as high as 25%. A large number of patients
surviving lead encephalopathy have neurological sequelae,
mental retardation, EEG abnormalities, seizures, cerebral
palsy, optical atrophy, or dystonia musculorum deformans
(Chisolm & Barltrop, 1979). Death is caused by a multitude of
factors as anaemia, infection, immunologic impairment,
bleeding from gastrointestinal tract, kidney failure,
hypertension and central nervous system effects. Malignant
neoplasms are statistically more common among battery plant
workers (Gosselin, 1984; Putnam, 1986; Ellenhorn, 1988; Noji &
Kelen, 1989; Goyer, 1990).
9.4 Systematic description of clinical effects
9.4.1 Cardiovascular
Acute: arterial hypertension may be present. Shock
syndrome due to massive gastrointestinal loss of fluids.
Chronic: arterial hypertension. Peripheral
vascoconstriction.
9.4.2 Respiratory
Acute: not relevant.
Chronic: not relevant.
9.4.3 Neurological
9.4.3.1 CNS
Acute: Paresthesiae, pain, muscle weakness.
Encephalopathy (rare): severe headache,
convulsions, delirium, coma.
Chronic: Fatigue, sleep disturbance, headache,
irritability, lethargy. Slurred speech, stupor,
ataxia, convulsions. Hyperkinetic and
aggressive behaviour disorders. Also in
children: refusal to play and learning
regression.
Lead encephalopathy (more common in children):
vertigo, ataxia, headache, insomnia,
restlessness and irritability. Delirium, tonic-
clonic convulsions, coma. Increased
intracranial pressure.
9.4.3.2 Peripheral nervous system
Acute: Paresthesiae, pain, muscle weakness.
Chronic: Paresthesiae, pain, muscle weakness;
lead palsy involves the most active muscles,
including paralysis of the radial nerve with
"wrist drop". The afferent nerves are not
affected: there is no loss of sensation and no
pain. Slowing of nerve conduction by segmental
demyelination.
9.4.3.3 Autonomic nervous system
Acute and chronic: Lead affects cholinergic,
dopaminergic, and noradrenergic functions in
brain.
9.4.3.4 Skeletal and smooth muscle
Acute and chronic: Smooth muscles of the gut
are affected, producing intestinal colic.
Effects on skeletal muscles, especially in the
limbs, cause weakness, tremors and paralysis.
9.4.4 Gastrointestinal
Metallic taste, thirst. The lead line (Burton or blue
line) consists of a deposit of dark blue-grey lead
sulfide in the gums about 1 mm from the margins. It
does not occur in edentulous gums. Nausea, vomiting,
anorexia, constipation. Vomitus with milky appearance
(indicating the presence of lead chloride). Sometimes
black stools due to lead sulfide. Lead colic (very
intense intermittent abdominal cramps) is associated
with severe obstipation and vomiting. Many cases are
wrongly diagnosed as acute disease.
9.4.5 Hepatic
Transient elevation of transaminases.
9.4.6 Urinary
9.4.6.1 Renal
Swelling of proximal tubular cells with
correspondent impairment of function. Amino-
aciduria, glycosuria, and phosphaturia (Fanconi
syndrome). Retention of uric acid. Chronic
nephritis. Nephrotic syndrome may occur.
9.4.6.2 Others
Not relevant.
9.4.7 Endocrine and reproductive systems
Animal studies demonstrate irregular oestrous cycles in
female rats and testicular damage in male rats. Some
data suggest that high-level exposure to lead may cause
abortion and stillbirth among pregnant women. Lead may
induce decreased sperm counts. There is currently no
reliable information concerning the risk of adverse
effects on the offspring following lead exposure in men.
9.4.8 Dermatological
Not relevant.
9.4.9 Eye, ears, nose, throat: local effects
Acute: Not relevant.
Chronic: Retinal stippling.
9.4.10 Haematological
Basophilic stippling occurs in erythrocytes by
aggregation of ribonucleic acid. Anaemia in chronic
lead poisoning results from decreased life span of red
cells and from inhibition of haem synthesis. Lead
inhibits haem formation at several points, mainly at
the steps involving dependent sulfhydryl enzymes such
as delta-aminolevulinate, dehydratase and
ferrochelatase. This causes hypochromic microcytic
anaemia, which is more frequently observed in children.
9.4.11 Immunological
Immune effects have been observed in animals but not in
humans.
9.4.12 Metabolic
9.4.12.1 Acid-base disturbances
Not relevant.
9.4.12.2 Fluid and electrolyte disturbances
After massive ingestion of soluble lead
products there is a large gastrointestinal
loss of fluids, with fluid and electrolyte
disturbances.
9.4.12.3 Others
Saturnine gout is a consequence of
hyperuricaemia, due to renal dysfunction.
Inhibition of guanine aminohydrolase (guanase)
by lead may also be responsible for saturnine
gout.
9.4.13 Allergic reactions
Not relevant.
9.4.14 Other clinical effects
Pallor of the face; retinal stippling; appearance of
premature aging.
9.4.15 Special risks
Pregnancy, breast-feeding, enzyme deficiencies: there
is no reliable evidence of a risk of spontaneous
abortion and still-birth. Lead crosses the placenta
and fetal blood concentrations at birth approximate to
those of the mother. Lead is also excreted in human
milk. In animals, low-level exposure to lead during
prenatal or postnatal life results in retarded growth.
Inhibition of gama-glutamyl transpeptidase and adenyl
cyclase activity has been demonstrated in rats (WHO,
1977; ILO, 1983).
9.5 Others
Not relevant.
9.6 Summary
10. MANAGEMENT
10.1 General principles
- Acute poisoning
Poisoning by inorganic lead compounds is rare, but in case
of ingestion of large quantities of soluble compounds, or
exposure to fumes or vapours, it is mandatory to remove the
patient from further exposure. Remove and discard
contaminated clothing. Gastric lavage is preferred to
emesis (Noji & Kelen, 1989); administer a cathartic
(magnesium sulphate). Administer atropine for abdominal
pain but an opioid may sometimes be necessary. Treat lead
colic with calcium gluconate 10% IV. If the patient is
obtunded, convulsing or comatose, insert an oro- or a naso-
gastric tube and lavage after endotracheal intubation.
If the patient is convulsing, administer diazepam, 0.1 mg/kg
IV, to a maximum dose of 10 mg. A comatose or convulsive
state indicates increased intracranial pressure. Use of
mannitol, steroids and hypothermia, and referral to a
neurosurgical unit may then be necessary.
Administer intravenous fluids. Monitor vital signs.
- Chronic poisoning: remove the patient from further
exposure and treat symptomatically. Individuals with blood
lead levels > 600 µg/L must be removed from the work place.
General supportive treatment is to maintain airway and
respiration. Start artificial respiration at the first sign
of respiratory failure. Administer oxygen if cyanosis is
present. Correct dehydration.
The specific pharmacological treatment is chelation therapy
using calcium disodium edetate (EDTA), penicillamine, and
dimercaprol (BAL).
Chelation therapy is indicated in all symptomatic patients
and patients whose blood lead levels exceed 700 µg/L. EDTA
is administered in doses of 50 to 75 mg/kg/day in two
divided doses of IM or in saline infusion IV slowly, for 5
days.
In case of lead encephalopathy: BAL should be used in doses
of 2.5-4 mg/kg IM every 4 hours. EDTA is started 4 hours
after the first dose of BAL, in intravenous continuous
infusion. This therapy should be continued for 5 days.
Gosselin, 1984; Putman, 1986; ACHIH, 1986; Ellenhorn, 1988;
Noji & Kelen,
1989; Gilman, 1990; ATSDR, 1990; Goyer, 1990; Garrettson,
1990.
Acute poisoning by ingestion or acute episodes during
chronic poisoning: EDTA by slow intravenous drip or in
divided doses IV. Continue for 5 days.
In adults with blood levels up to 1000 µg/L give combined
treatment with intramuscular BAL and intravenous EDTA for 5
days. Interrupt treatment for 2 days and restart EDTA if
blood lead levels remain high (> 1000 µg/L); penicillamine
should then be given for 3-6 months (20 mg/kg/day oral
route). In children with blood levels up to 700 µg/L, use
combined treatment with BAL plus EDTA. Therapy with BAL may
be discontinued after 3 days if blood lead level is < 50
g/dl. EDTA should be continued for 5 days. Long-term
chelation with penicillamine in children should be limited
to 2 months.
Problems with chelators are:
- oral chelators may promote lead absorption from the
gastrointestinal tract.
- the chelator-lead complex is nephrotoxic. Urine output
must be monitored and chelation should be stopped if renal
impairment.
- chronic chelation therapy with EDTA or penicillamine
promotes loss of essential metals.
- intramuscular injection of EDTA is painful. Multiples
sites should be used.
- BAL may cause local pain, nausea, vomiting.
Hypertension is described after BAL therapy. Antihistamines
may be administered.
- d-penicillamine causes alteration of taste, neutropenia,
allergic rashes, aplastic anaemia, nephropathy, hepatitis
(Gosselin, 1984; Noji & Kelen, 1989; Gilman, 1990;
Garrettson, 1990; Volans & Henry, 1984).
10.2 Relevant laboratory analyses and other investigations
10.2.1 Sample collection
Blood and urine should be collected at any time. It
is essential to avoid contamination: needles,
containers, and anticoagulants must be lead-free. A
24-hour urine specimen is preferable.
10.2.2 Biomedical analysis
Lead in blood and urine.
Red cell delta-aminolevulinic acid dehydratase
activity.
Free erythrocyte protoporphyrin.
Urinary delta-aminolevulinic acid.
Urinary coproporphyrin.
Full blood count (red cells, white cells, platelets;
haemoglobin and reticulocytes count).
Radiographs of bones (children).
Abdominal X-rays after ingestion.
Electroencephalogram.
Determination of lead in hair.
(Kopito et al., 1967; ILO, 1983; Gosselin, 1984;
Ellenhorn, 1988; Noji & Kelen, 1989; Garrettson,
1990).
10.2.3 Toxicological analysis
No data available.
10.2.4 Other investigations
10.3 Life supportive procedures and symptomatic treatment
Make a proper assessment of airway, breathing, circulation
and neurological status of the patient.
Maintain a clear airway. Aspirate secretions from airway.
Control convulsions with diazepam 0.1 mg/kg.
Open and maintain at least one intravenous route.
Administer intravenous fluids. Monitor vital signs.
Increased intracranial pressure in encephalopathy may
require mannitol, steroids (dexamethasone), and
neurosurgical assistance.
10.4 Decontamination
After ingestion, if convulsions are not imminent, induce
emesis or perform gastric lavage. Do not induce emesis if
the vehicle of the product is a petroleum distillate.
To induce emesis use syrup of ipecac. Gastric lavage may be
performed if emesis fails, bearing in mind the possible risk
of imminent convulsions. The decision to induce emesis
depends on a knowledge of the constituents of the product.
Gastric lavage may be preferred in case of soluble inorganic
lead compounds.
Administer a saline cathartic (magnesium sulphate, 15 to 30
g in water).
After inhalation, management is symptomatic and supportive:
Remove from exposure and ensure the airway and ventilation.
Supportive measures include oxygen and artificial
respiration.
Skin - remove of all contaminated clothes and wash the skin
and hair.
Eyes - extensive eye irrigation with water or saline should
also be performed.
10.5 Elimination
Chelation therapy will promote the excretion of inorganic
lead through urine. A good urinary output is mandatory.
Haemodialysis is indicated in cases of impaired renal
function.
10.6 Antidote treatment
10.6.1 Adults
The antidotes which may be used are:
- Calcium disodium edetate (CaNa2EDTA): 1 to 2 g
daily (non-convulsing or comatose) 2 to 4 g daily
(convulsing or comatose) in two divided doses
intramuscularly or IV in saline infusion, slowly for
5 days.
- Succimer (DMSA): 10 mg per kg body weight per os,
every 8 hours for 5 days, then every 12 hours for an
additional 14 days. The course of treatment may be
repeated if necessary, after an interval of two weeks
(Reynolds, 1993).
- Dimercaprol (BAL): 2.5 to 4 mg/kg/dose
intramuscularly every 4 hours, for 48 hours; then,
every 6 hours, for 48 hours; and every 6 to 12 hours
for more 7 days.
- d-penicillamine: 250 mg 4 times daily for 5 days.
Doses in long-term treatment should not exceed 40
mg/kg/day.
10.6.2 Children
Children with blood lead levels up to 700 ug/L should
be treated with combined BAL and edetate calcium
disodium; BAL may be discontinued after 3 days if the
blood lead is < 500 ug/L but edetate should be
continued for 5 days. Long term chelation with
penicillamine in children should be limited to 2
months. (Gosselin, 1984; Ellenhorn, 1988; Noji &
Kelen, 1988; Garrettson, 1990; Gilman, 1990; Volans &
Henry, 1984).
- Calcium disodium edetate (CaNa2EDTA):
50 mg/kg/day in two divided doses (non-convulsing
child) 75 mg/kg/day in two divided doses
(convulsing child) intramuscularly or IV in saline
infusion, slowly for 5 days.
- Dimercaprol (BAL): 2.5-4 mg/kg/dose
intramuscularly every 4 hours, for 48 hours; then,
every 6 hours, for 48 hours; and every 6 to 12
hours for more 7 days.
- Succimer (DMSA): to be completed.
- d-penicillamine: 20-40 mg/kg/day (maximum 1 g/dat)
may be given for 3-6 months.
10.7 Management discussion
Alternatives, controversies and research needs: chelation
therapy is effective in removing lead from soft tissues but
not from bone. Significant quantities of lead are present
in bone and intercurrent illness may mobilise toxic
quantities of lead into soft tissue, thereby exacerbating
the symptoms of poisoning. When chelating agents are given
orally, the risks include depletion of essential metals due
to rapid mobilization and impaired absorption from the
digestive system.
Lead poisoning in childhood is a chronic disease and
currently it is accepted that even very low blood levels of
lead may induce developmental deficits. Screening programs
to detect these cases are required. (Gosselin, 1984; Noji &
Kelen, 1989; Gilman, 1990; Garrettson, 1990).
11. ILLUSTRATIVE CASES
11.1 Case reports from literature
Lead poisoning from cocktail glasses: a man and his wife
acquired plumbism by drinking repeatedly from cocktail
glasses decorated with lead-based paint (Natelson & Fred,
1976).
Lead poisoning in children of lead workers: 38 in 91
children (41.8%) presented lead blood levels up to 300 µg/L
and 10 with lead blood levels higher than 800 µg/L. The
source of contamination was lead dust carried home on
parents contaminated work clothing (Baker et al., 1977).
Lead intoxication in an adult caused by chinese herbal
medication: a patient was diagnosed severe lead poisoning
caused by ingestion of herbal medication from Hong Kong
(Lightfoote et al., 1977).
11.2 Internally extracted data on cases
A man was admitted to hospital with severe epigastric pain.
An abdominal explorative surgery was performed. No elements
corroborated the presumptive diagnosis of perforated peptic
ulcer. As he was a worker in a smeltery, lead poisoning was
suspected after the detection of basophil stippling in
erythrocytes and a blue line in the gums. Blood lead levels
were 124 µg/L. Chelation therapy was instituted with
calcium disodium EDTA 2 g a day IV, during 5 days. He
recovered from the acute crisis, but manifested sequels of
impaired muscular strength in the right forearm. The
measurement of peripheral motor nerve conduction radial
velocity was reduced.
11.3 Internal cases
12. ADDITIONAL INFORMATION
12.1 Availability of antidotes
12.2 Specific preventive measures
Use protective clothes (including shoes).
The protective clothes and shoes must not leave plant.
Avoid skin contact with lead dust and fume.
Avoid contact of lead with oxidizers (such as perchlorates,
peroxides, permanganates, chlorates and nitrates) and
chemically active metals (such as potassium, sodium,
magnesium and zinc) since violent reactions occur.
Insist in personal hygiene: do not smoke, do not eat, do not
drink in contaminated environment.
Eating facilities must be separated from working areas.
Face and hand coverings should be made of impermeable
material.
Medical surveillance program for lead: pre-employment and
pre-placement examination, periodical examination, clinical
tests, record-keeping and health education.
Immediate cleaning up of spills. Floors should be wetted
with a fine spray to avoid stirring up dust.
Storage receptacles should be kept covered to reduce fumes
and dust.
Measurement of lead air levels (ILO, 1983; Glenn, 1987).
- Non-occupational exposure:
Avoid non-industrial ceramics for foodstuff.
Do not allow small children to swallow chips of deteriorated
paint.
Measures of prevention involving Public Health must concern:
- Control of lead in drinking water.
- Treatment of public water systems to decrease
contamination from plumbing.
- Control of lead emissions in air.
(ATSDR, 1990).
12.3 Other
The hazards of lead exposure are reported to have been well
known as early as the second century BC, when exposure
occurred due to the use of lead in plumbing, cooking
utensils, and as a "sweetener" of wines. The overt symptoms
of poisoning, including colic, encephalopathy, anaemia, and
renal disease, were well known.
Lead poisoning remains a serious problem. It is often
associated with poverty, misuse, ignorance, and bad working
conditions. Lead poisoning is one of the commonest
occupational diseases.
Over the last 20 years subclinical effects have been
described following the development of sensitive methods to
detect cognitive and behavioural changes, especially in
children.
Concern about environmental contamination has led to a
reduction in the lead content of gasoline and control of
occupational exposure; the average blood level of lead in
the population in the USA has now declined by nearly 50%.
- First aid summary
Induce vomiting, if spontaneous vomit is not prompt and
profuse. Ipecac syrup may be administered by mouth.
Dose of ipecac syrup:
Children: 6-18 months 10 ml
18 months to 12 years 15 ml
Adolescents and adults: 30 ml
The decision to induce emesis depends on knowledge of the
constituents of the product: emesis is not recommended if
the vehicle is a petroleum distillate. Do not induce emesis
if the patient's conscious level is imparied or if fits are
likely. A sample of vomitus should be collected in a clean
bottle.
Gastric lavage may be performed if emesis is not induced
even when the product contains kerosene or a related
petroleum distillate.
A purgative may be given to remove the ingested compound.
Inhalation of vapours and fumes: Treatment is symptomatic
and supportive. Maintain an airway and ventilation;
supportive measures include oxygen and artifical respiration
(Gosselin, 1984; Noji & Kelen, 1989; Garrettson, 1990).
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14. AUTHOR(S), REVIEWER(S), DATE(S) (INCLUDING UPDATES), COMPLETE
ADDRESSES
Author: Alberto Furtado Rahde
Rua Riachuelo 677 ap. 201
90010 Porto Alegre
Brazil
Telephone: 55-512-275419
Facsimile: 55-512-246563
Date: December 1991
Reviewer:
Peer Review: Newcastle-upon-Tyne, United Kingdom, February 1992
Finalized at the IPCS: May 1994