LEAD POISONING By F.Ahmadzadeh occupational medicine
especialist
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Lead is an ancient metal. Because of its malleability and low
melting point, humans have used lead since prehistoric times to
make statues, jewelry, water pipes, and drinking vessels. In the
mid-1970s, nearly 200,000 tons of lead were consumed annually in
gasoline in the United States. Virtually all of this lead was
emitted into the environment from vehicles in a finely particulate
form and caused widespread contamination of air, dust,soil,
drinking water and food crops.
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OCCUPATIONAL LEAD EXPOSURE In the United States more than 3
million workers are estimated by NIOSH to be potentially exposed to
lead in their work. Occupational exposure to lead is regulated in
the United States by the OSHA lead standard, first promulgated in
1978. This standard sets limits on air-borne lead exposure as well
as on permissible levels of lead in blood.
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Major occupations associated with risk of inorganic lead
poisoning
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A major industrial group that previously had been exempted from
the protection of the United States lead standard were construction
workers. Major outbreaks of lead poisoning were observed among
workers who cut leadpainted steel structures such as bridges with
oxyacetylene torches and among renovation workers who remove lead
paint from older homes. In 1993, the OSHA lead standard was
extended to cover the construction and demolition trades.
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Measurement of occupational exposure Assessment of occupational
exposure to inorganic lead requires measurement of lead levels in
both air and blood. The OSHA standard (1993) for the permissible
exposure level of lead in workplace air is 50 micrograms/m3,
expressed as an 8-hour time-weighted average. This standard can no
longer be considered adequately protective of workers health,
because lead toxicity has been observed in workers whose lead
exposures do not exceed the current OSHA standard. Fetal lead
poisoning can occur in the offspring of female lead workers well
below this level.
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Measurement of the blood lead level complements determination
of lead levels in air. By the OSHA lead standard, anyone found to
have a blood lead level of 50 micrograms/dl or above must be
removed from the high-exposure job (termed medical removal
protection). A worker is not allowed to return to a high-exposure
job until the blood lead level has fallen to below 40 Gr/dl.
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Air: Air lead standard in the United States is 1.5 gr/m3
ENVIRONMENTAL LEAD EXPOSURE Motor vehicles were the major
contributor of lead emissions to the air (TEL). MTBE (Methyl
tert-butyl ether) Ethanol
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Paint: Some lead compounds are colorful and are used widely in
paints and lead paint is a major route of lead exposure in children
Soil May be caused by: 1. broken-down lead paint, 2.residues from
lead-containing gasoline, 3.used engine oil 4.Pesticides used in
the past 5.from nearby industries such as foundries or
smelters
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Water 1.From the atmosphere or soil ( end up in groundwater and
surface water.) 2.from plumbing and fixtures (chloramines, which
were adopted as a substitute for chlorine disinfectant due to fewer
health concerns, increase corrositivity ) In the US, 1420% of total
lead exposure is attributed to drinking water. safe drinking water
standard for lead is 0.15 mg/l (15 parts per billion).
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Lead-containing products Lead can be found in products such as
kohl, an ancient cosmetic. from some toys. In 2007, millions of
toys made in China were recalled from multiple countries owing to
safety hazards including lead paint. Lead is commonly incorporated
into herbal remedies such as Indian Ayurvedic.Ayurvedic
preparations and remedies of Chinese origin.
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In the general population, children are the group most heavily
exposed and most susceptible to the toxic effects of lead. Who is
most Vulnerable to the Effects of Lead?
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Exposure to lead can cause behavior problems and learning
disabilities in young children and can also affect the health of
adults. Imported toys tainted with lead have made news recently.
The lead can be both in the paint and in the plastic itself.
Sucking or chewing on the toy -- or getting lead on the hands --
can be enough to poison a child. www.recalls.gov
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The mean blood lead level of children in the United States is
about 3 micrograms/dl. A decline of 90% in bloodlead levels
occurred among American children from 1976 to 1997 as a consequence
of removal of lead from gasoline. According to the Centers for
Disease Control and Prevention (CDC), blood lead levels of 10
micrograms/dl and higher in children indicate excessive exposure.
Blood leadlevels of 10 g/dl and above are associated with
subclinical lead toxicity in children.
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Lead-based paint is the major concentrated, high-dose source of
lead for American children. Since 1979, the maximum allowable
concentration of lead in domestic paint has been regulated by the
United States Consumer Product Agency at 0.06 parts per million.
The new dust standard : 40 micrograms/ft2 for floors 250
micrograms/ft2on window sills Below 400 ppm in soil of play areas
1200 ppm average for bare soil in the rest of the yard.
CLINICAL EFFECTS IN ADULTS Acute inorganic lead toxicity
Intense occupational exposure to lead over a brief period of time.
abdominal colic, constipation, fatigue, hemolytic anemia,
peripheral neuropathy, alteration of central nervous system
function Signs and symptoms
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gingival lead line acute encephalopathy with coma, convulsions,
and papilledema may occur ;
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In milder cases : only fatigue, headache or personality changes
may be evident as manifestations of the neurologic toxicity of
lead. Mild liver involvement, limited to modest elevations in serum
glutamic-oxaloacetic transaminase (SGOT). musculoskeletal pains and
arthritic. Basophilic stippling in the red blood cells. (occur in
blood lead level 70 micrograms/dl or more)
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Chronic inorganic lead toxicity Arthralgias Myalgias Headache
Weakness Depression loss of libido, impotence, Vague
gastrointestinal difficulties. Thyroid and adrenal function often
are depressed. Hypertension Sperm counts can be depressed in men
and fertility reduced in women. Signs and symptoms
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Renal function may reveal impairment of glomerular clearance;
decreased tubular urate clearance resulting in hyperuricemia is
common. Late effects of inorganic lead intoxication include :
chronic renal failure, gout, chronic encephalopathy, and
hypertension. Subclinical toxicity( low-dose exposure ) May cause
harmful effects to health in the absence of symptoms and signs that
are evident on the standard Clinical examination.
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1.Hematologic toxicity Anemia : presence of anemia is not
required for a diagnosis of lead poisoning The severity and
prevalence of lead-induced anemia are correlated directly with the
blood lead level in both adults and children. The effects of lead
on organ system Function
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Lead-induced anemia is the result of multiple mechanisms:
impairment of heme biosynthesis : 1.Inhibition of the cytoplasmic
enzyme, d-aminolevulinic acid dehydratase (ALA-D). 2.The
mitochondrial enzyme ferrochelatase. That results accumulation of
zinc protoporphyrin [ZPP]) in the erythrocytes. Acceleration of red
blood cell destruction. inhibition of erythopoietin production in
the kidney.
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2.Neurologic toxicity (Neurologic toxicity of lead in adults)
Peripheral motor neurologic toxicity: 1. Extensor muscle palsy with
wrist drop or ankle drop 2. Asymmetry Unlike other toxic
neuropathies, this motorneuropathy may show leftright
asymmetry.
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Mild to moderate sensory dysfunction also may be evident in
lead neuropathy, and in such cases the clinical picture is one of
mixed motorsensory neuropathy, often with asymmetric features. In
the central nervous system( high-dose acute exposure to lead )
causes encephalopathy characterized clinically by obtundation coma,
and convulsions Among persons who recover from acute lead
encephalopathy, a high proportion are left with significant
neuropsychologic deficits, including reduced intelligence,
shortened attention span, and instability of mood.
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Impairment in central neurologic function in adults at doses
insufficient to produce clinical encephalopathy: -Fatigue
-Short-term memory loss -Depressed mood
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3.Renal toxicity Acute Fanconi syndrom Vit.D defficiency At
blood lead levels below 25 gm/dl, lead inhibits the metabolic
activation (hydroxylation) of vit. D At blood lead levels of 4080
gm/dl, lead induces the formation of dense intranuclear inclusion
bodies consisting of a lead protein complex in cells lining the
proximal tubules.
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Hyperuremic gout resulting from increased reabsorption of uric
acid by the tubular cells. Chronic nephropathy, which may progress
to kidney failure. Chronic low-level lead exposure: abnormal
urinary excretion of n-acetyl glucosaminidase (NAG) 4. hypertension
long-term, high-dose exposure to lead associated with an increased
incidence of hypertension and cerebrovascular disease
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5.Reproductive toxicity of lead Decreased sperm counts,
abnormal sperm morphology, and decreased sperm motility when lead
levels were above 40 micrograms/dl. increased incidence in
spontaneous abortion among female lead workers as well as in the
wives of male lead workers. lead may cause neurologic damage to the
fetus at blood levels as low as 510 micrograms/dl, substantially
below the current OSHA standard for blood levels of lead in
Workers.
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The prevention of fetal lead encephalopathy requires that blood
lead levels of prospective mothers be kept below 10 micrograms/dl,
not only during pregnancy but also in the years preceding
conception. If a woman who has previously had elevated blood lead
levels wishes to become pregnant, it may be reasonable to recommend
either an x-ray Fluorescence examination of bone to determine body
burden of lead.
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6.Carcinogenicity group 2A probable human carcinigen Renal
cancer Brain tumor
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Organic lead TEL use as antiknock in gasoline TEL produce a
syndrom difrenet from inorganic lead poisoning Cause : insomnia,
anorhexia, muscle irritability,aggitated encephalopathy,tremor and
ataxia
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Clinical evaluation Clinical evaluation strategy for adult The
diagnosis of in organic lead intoxication in adults requires: 1-
demonstration of excess lead absorption 2-documentation of
impairment in an organ system consistent with the effect of lead
3-exclution of other cause of impairment
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Lead is not distributed homogeneously in the human body It is
dispersed amonge several physiologically distinct compartment.
Blood lead Lead Distribution in human body 1% of body burden half
life 36 days Single best indicator of recent lead absorption Normal
adult lead level is below 10gr/dl Clinical symptom appear at 30-40
gr /dl At 50 gr /dl worker must immediately remoev from exposure
and they can not return to work their level have fallen below 40
g/dl
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Lead in calcified tissue of skeleton and teeth: 90-99% of
absorpted lead ( 70% in children). Half life 15-20 years. blood
lead level appears principally to reflect release of stored from
deep tissue compartment to blood. K-shell x-ray fluorescence (XRF)
analysis is a accurate, non-invasive and relatively rapid
assessment of chronic lead exposure.
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Zinc protoporphyrin (ZPP) or free erythrocyte protoporphyrin
(FEP) levels reflect the toxic effect of lead on the erythrocytic
enzyme ferrochelatase. A combination of normal FEP value and high
blood lead level indicates very recent exposure that has not yet
had opportunity to poison heme metabolism. Because the ZPP level
remains elevated long after the blood lead level has fallen, this
test does not discriminate between recent and past exposure. Zinc
protoporphyrin
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the diagnosis of lead poisoning cannot await the appearance of
anemia Anemia: Basophilic stippling in the red blood cells is seen
in most patients with acute hemolysis and occasionally in patients
with chronic hemolytic syndromes; it is not specific to lead
poisoning. Basophilic stippling: Lead lines on the gums are
uncommon except in cases of severe poisoning and may be difficult
to recognize in patients with poor dental hygiene. Lead lines:
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Complete blood counts and routine blood chemistry should be
performed as baseline in asymptomatic workers. Other baseline tests
include creatinine clearance,BUN, and uric acid. Blood pressure
should be measured regularly. Blood lead levels should be obtained
on a periodically. If the whole blood lead levelexceeds 40
micrograms/dl, tests should be repeatedmonthly; blood lead levels
over 50 micrograms/dl require immediate removal of workers from
lead-exposure, andthey may not return to work in a lead-exposed job
until there have been two lead-levels below 40 micrograms/dl
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Measurement of the urine lead level is of little value in
monitoring populations exposed to inorganic lead; the test is too
highly variable to be reliable. Hair lead hair lead analysis is not
considered reliable for monitoring purposes. urine lead
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Clinical evaluation strategy: organic lead Organic lead (TEL)
intoxication is difficult to diagnose without a history of
exposure. Blood or urine lead levels and FEP levels are not
predictably elevated in TEL poisoning.
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MANAGEMENT Management of acute lead poisoning in adults:
Immediate removal from exposure to lead. chelation (intravenous
calcium EDTA and Oral chelation with DMSA ). Chelation should be
considered for blood levels greater than 80 micrograms/dl,
especially when there are central or peripheral nervous system
effects. For blood lead levels of 6080 micrograms/dl, decisions
regarding chelation should be made on a case-by-case basis.
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Management of chronic lead Intoxication Studies are needed to
confirm whether chelation therapy of adults with chronic lead
intoxication results in amelioration of long-term effects such as
gout, hypertension or renal insufficiency, The administration of
chelating agents to persons with chronic lead intoxication must be
approached with great care, because they often have impairment of
renal function. Chronic administration of oral chelation agents to
workers who continue to be exposed to unacceptably high levels of
lead in their work has been used by some unscrupulous employers as
a means of reducing blood lead levels while not reducing levels of
lead in air in the workplace.
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Management of organic lead poisoning The treatment for TEL
poisoning is primarily support; chelation with calcium EDTA has
been tried with variable efficacy. Sedation and careful observation
are required in severe cases, often for prolonged periods.
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Prevention of occupational lead Poisoning Air-born exposure to
both organic and inorganic lead in the workplace must be strictly
limited by enclosure of hazardous processes, ventilation, and other
engineering controls. OSHA lead standard mandates that occupational
exposures to lead be held below 50 gr/m3 of air, expressed as an
8-hour, TWA. However, studies have shownclearly that toxic adverse
effects can occur in lead workers at levels of exposure below this
standard.
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clinical or subclinical toxic effects can occur at and below
the current biologic exposure limitof 50 micrograms/dl of whole
blood. A physician may remove a worker with a lower blood level if
lead Poisoning is diagnosed and restrict the worker from return to
Exposure until approved by the physician.