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Effects of Lead Poisoning in Children and Adults
THRESHOLD LIMIT VALUE (TLV/TWA): 0.15 MG/M3 ( PPM)
TOXICITY: LD50 (IPR-RAT)(MG/KG) - 630
Target organs : Kidneys, Blood, Brain.
Anorexia-loss of appetite
Lead-line in gum
Same as above plus :
High blood pressure
Metal fume fever
Reduced sperm count
Teratogenic effects : congeitive abnormalities
Lead occurs in the earth's crust as Galena (PbS). The other lead minerals are all associated with Galena. White lead
ore (PbS) is a decomposition product of Galena. The atomic weight of lead is 207.20 and its atomic number is 82. Density is
11.35 gm/cc and Melting point is 327.50 deg C. the Boiling point is 1740 deg C.
Lead metal exists commercially as granules, pellets, lead shots, dust, foil or sheet. Due to handling and friction,
inhalation of lead metal fumes and lead metal dust can cause irritation to skin, eyes, nose, throat and bronchi.
However, although inhaled fumes can be absorbed through the respiratory system, the inhaled doses are eventually absorbed
into the gastrointestinal tract and do not accumulate in the lungs.
Exposure to lead foil and metal sheet pose no hazard unless it is heated. If lead metal is heated, fumes will be released
and inhalation will cause fume-metal fever with flu-like symptoms.
Occupational and domestic exposure to lead may come from lead based paints, airborne emissions from mines and
smelters, gas petrol fuel (anti-knock), bullets, fishing sinkers, and water-pipes joint and fittings.
Lead toxicity also occurs by oral ingestion of lead contaminated food or water and by children sucking, licking or
swallowing lead contaminated substances.
lead toxicity in children
Lead poisoning occurs when too much lead is absorbed into the body by inhalation or ingestion. Toxic leves of lead in children
can have physiological and pathological effects resulting in development disorder and behavioral problems. Lead poisoning can affect nearly every system in the body. Because lead poisoning often occurs with no obvious symptoms, it frequently goes unrecognized. Lead poisoning can cause learning disabilities, behavioral problems, and, at very high levels, seizures, coma, and even death.
The following may occur with lead poisoning :
Poor vitamin D metabolism, erythroid precursor cell enzymology, erythrocyte protoposphyrin, headaches and decreased nerve velocity.
High level doses give metallic taste, loss of appetite, constipation, poor haemoglobin synthesis, colic, anemia, nephrotoxic effects
(difficult renal excretion of uric acid), neuropathy and encephalopathy.
Inorganic lead can penetrate the blood brain barrier in children and cause encephalopathy. Organic lead compounds sch as
tetramethyl and tetraethyl lead can also cross the blood brain barrier and cause cerebral dysfunction.
There is incidence that lead easily accumulates in the bone and inhibits the formation of red blood cells and may cause anemia.
Lead absorption increases in the body when the stomach is empty or there is a deficiency of zinc, copper or iron in the body.
Lead can increase in synergistic toxicity in the presence of cadmium and mercury.
Approximately 434,000 U.S. children aged 1-5 years have blood lead levels greater than the CDC recommended level of 10 micrograms of lead per deciliter of blood.
Lead encephalopathy is a life-threatening complication of lead poisoning that can occur in young children who have very high BLLs (blood-lead level) >70--100 µg/dL.
Nonspecific symptoms (e.g., lethargy, sporadic vomiting, and constipation) can occur at BLLs >50--70 µg/dL and may precede the abrupt onset of frank encephalopathy characterized by persistent vomiting, ataxia, altered consciousness, coma, and seizures. Anemia with basophilic stippling also suggest lead poisoning.
However, symptoms or signs cannot be used to reliably diagnose or exclude lead poisoning; a BLL must be measured whenever lead poisoning is suspected.
In young children, BLLs >70 µg/dL or elevated BLLs with symptoms suggesting encephalopathy require prompt inpatient treatment with chelating agents to rapidly reduce BLLs. Providing appropriate intensive care for children with encephalopathy can prevent death, although severe permanent brain damage can occur despite treatment .
"Fatal Pediatric Lead Poisoning"
CDC:Centers for Disease Control and Prevention
lEAD Toxicity in Adults
|Blood Level||Reactions to Lead.|
|10ug/dL||Increased blood pressure, harmful effects on fetus, joint and muscle.|
|40ug/dL||Kidney damage and damage to blood formation.|
|60ug/dL||Anemia, nerve damage, constipation, stomach pain, fatigue, memory and concentration problems, clumsiness, drowsiness, sleep problems.|
|>80ug/dL||Blue line on gums, uncontrollable shaking of hands, wrist and footdrop, hallucinations, brain damage, coma, and death.|
There can be a difference in neurologic manifestations or sequelae between an adult exposed
to lead as an adult, and an adult exposed as a child when the brain was developing.
Childhood neurologic effects, including possibly ADHD, may persist into adulthood. Other
than this, many of the neurologic symptoms experienced by children may also be experienced
by lead-exposed adults, although the thresholds tend to be higher.
Lead encephalopathy may occur at extremely high BLLs, e.g., 460 µg/dL (Kehoe 1961).
Precursors of encephalopathy, such as dullness, irritability, poor attention span, muscular
tremor,loss of memory, and hallucination, may occur at lower BLLs.
Less severe neurologic and behavioral effects have been documented in lead-exposed workers
with BLLs ranging from 40 to 120 µg/dL. These effects include malaise; forgetfulness;
irritability; lethargy; impaired concentration; depression and mood changes; increased
nervousness; headache; fatigue; impotence; decreased libido; dizziness; weakness; and
paresthesia; as well as diminished reaction time, visual motor performance, hand dexterity,
IQ scores, and cognitive performance (ATSDR 1999).
There is also some evidence that lead exposure may affect adults’ postural balance and
peripheral nerve function (ATSDR 1997a, 1997b; Arving et al. 1980; Haenninen et al. 1978;
Hogstedt et al. 1983; Mantere et al. 1982; Valciukas et al. 1978).
Slowed nerve conduction and forearm extensor weakness (wrist drop), as late signs of lead
intoxication, are more classic signs in workers chronically exposed to high lead
Acute toxicity with large amounts of lead may lead to ataxia, delirium, convulsions, seizures, coma and death.
1. "Case Studies in Environmental Medicine
Lead Toxicity "
ASTD:Agency for Toxic Substances and Disease Registry.
2. British Medical Bulletin:familywellnesshq/