1. LEAD POISONING
By F.Ahmadzadeh
occupational medicine especialist

2. Lead is an ancient metal
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.

3. 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.

4. Major occupations associated with risk of inorganic lead poisoning

5. 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.

6. 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 .

7. 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 µGr/dl.

8. ENVIRONMENTAL LEAD EXPOSURE
Air:
Air lead standard in the United States is 1.5 µgr/m3
Motor vehicles were the major contributor of lead emissions to the air (TEL).
MTBE (Methyl tert-butyl ether)
Ethanol

9. and lead paint is a major route of lead exposure in children
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:
broken-down lead paint,
residues from lead-containing gasoline,
used engine oil
Pesticides used in the past
from nearby industries such as foundries or smelters

10. 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, 14–20% of total lead exposure is attributed to drinking water .
safe drinking water standard for lead
is 0.15 mg/l (15 parts per billion).

11. 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.
preparations and remedies of Chinese origin.

12. Who is most Vulnerable to the Effects of Lead?
In the general population, children are the group most heavily exposed and most susceptible to the toxic effects of lead.

13. 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.

14. 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 µg/dl and above are associated with
subclinical lead toxicity in children.

16. 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.

17. Hand-held portable blood lead instruments
portable, hand-held x-ray fluorescence (XRF) detectors.

18. CLINICAL EFFECTS IN ADULTS
Acute inorganic lead toxicity
Intense occupational exposure to lead over a brief period
of time .
Signs and symptoms
abdominal colic,
constipation,
fatigue,
hemolytic anemia,
peripheral neuropathy,
alteration of central nervous
system function

19. gingival lead line
acute encephalopathy with coma,
convulsions, and papilledema may occur;

20. only fatigue, headache or personality changes may be evident
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)

21. Chronic inorganic lead toxicity
Signs and symptoms
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.

22. 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.

23. The effects of lead on organ system Function
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.

24. 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.

25. 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 left–right asymmetry.

28. Mild to moderate sensory dysfunction also may be evident
in lead neuropathy, and in such cases the clinical picture is
one of mixed motor–sensory 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.

29. Impairment in central neurologic function in adults at
doses insufficient to produce clinical encephalopathy:
-Fatigue
-Short-term memory loss
-Depressed mood

30. 3.Renal toxicity Acute Fanconi syndrom Vit .D defficiency
At blood lead levels below 25 µgm/dl, lead
inhibits the metabolic activation (hydroxylation) of vit. D
At blood lead levels of 40–80 µgm/dl, lead induces the
formation of dense intranuclear inclusion bodies consisting
of a lead protein complex in cells lining the proximal tubules.

31. 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

32. 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 5–10 micrograms/dl, substantially below the current
OSHA standard for blood levels of lead in Workers.

33. 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 .

34. 6.Carcinogenicity
group 2A – probable human carcinigen
Renal cancer
Brain tumor

35. 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

36. 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

37. Lead Distribution in human body
Lead is not distributed homogeneously in the human
body It is dispersed amonge several physiologically
distinct compartment.
Blood lead
Single best indicator of recent lead absorption
half life 36 days
1% of body burden
Normal adult lead level is below 10µgr/dl
Clinical symptom appear at µgr /dl
At 50 µgr /dl worker must immediately remoev from
exposure and they can not return to work their level
have fallen below 40 µg/dl

38. 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.

41. Zinc protoporphyrin
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.

42. Anemia:
the diagnosis of lead poisoning cannot await the appearance of anemia
Basophilic stippling:
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.
Lead lines:
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.

43. 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 untilthere have been two lead-levels
below 40 micrograms/dl

44. urine lead
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.

45. 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.

46. 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 60–80 micrograms/dl, decisions
regarding chelation should be made on a case-by-case
basis.

47. 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.

48. 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.

49. 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 µgr/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.

50. 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.

52. THANKS FOR ATTENTION