Heavy Metal Poisoning: Lead

U.S. Agency for Toxic Substances and Disease Registry lists toxic substances according to their prevalence and the severity of their toxicity and lead is in number one position. Recently the development of K-X-ray fluorescence (KXRF) instruments has made it possible to measure bone lead levels (which, in turn, reflect cumulative exposure over many years, as opposed to blood lead levels, which reflect recent exposure). High bone lead levels measured by KXRF are associated with increased risk of hypertension in both men and women. High maternal bone lead levels were found to cause lower birth weight, head circumference, birth length, and lower neurodevelopmental performance in children by age 2.   

Sources of lead poisoning:  Manufacturing of auto batteries, ceramics, fishing weights, lead crystal, demolition of lead-painted houses and bridges; stained glass making, soldering, environmental exposure to paint chips, plumbing, firing ranges (from bullet dust), food or water from lead pipes are the main sources of lead poisoning.  Contaminated herbal remedies, candies and exposure to the combustion of leaded fuels also contribute to the lead poisoning.

Lead can be absorbed through ingestion or inhalation and organic lead (e.g., tetraethyl lead) is absorbed through skin. In blood lead is concentrated in RBCs. Distributed in soft tissue, with ½ life of about 30 days. 15% of lead is sequestered in bone with ½ life of more than 20 years. Lead is excreted mainly in urine, but also appears in other fluids including breast milk.

 Toxicity: Acute poisoning with blood lead levels (BPb) of more than 60–80 µg/100ml can cause impaired neurotransmission and neuronal cell death, which lead to central and peripheral nervous system effects. If blood lead level is more than 80 µg/100ml it can cause acute encephalopathy with convulsions, coma, and death. 

Subclinical exposure of lead in children (BPb 25–60 µg/100ml) is associated with anemia, mental retardation, language deficit, motor function, balance, behavior, hearing, and school performance. Impairment of IQ can occur at even lower levels.

In adults, chronic subclinical exposures (BPb 40 µg/100ml) are associated with an increased risk of anemia, demyelinating peripheral neuropathy (mainly motor), and impairments of reaction time, hypertension, and ECG conduction delays. Chronic renal failure, diminished sperm counts and spontaneous abortions in females is seen.

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Posted by - October 28, 2008 at 1:27 am

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Heavy Metal Poisoning: Cadmium

Cadmium poisoning can be a serious health problem from mining of cadmium. There was serious cadmium poisoning from contamination of food and water by mining effluents in Japan, in 1946 lead to outbreak of “itai-itai” (“ouch-ouch”) disease. The disease was so named because of cadmium-induced bone toxicity that led to painful bone fractures.

Sources of arsenic poisoning: Metal plating, battery, pigment, smelting, and plastics industries and incineration of these products are the main sources of cadmium poisoning. Tobacco smoking and consumption of food that concentrate cadmium like grains and cereals are also important source of cadmium poisoning.

Clinical manifestations: Acute cadmium inhalation causes pneumonitis 4–24 hours after inhalation and acute ingestion causes gastroenteritis. Chronic exposure causes anosmia (loss of smell), yellowing of teeth, emphysema, microcytic hypochromic anemia that do not respond to iron therapy, proteinuria (protein in urine), calciuria (calcium crystals in urine), leading to chronic renal failure, osteomalacia, and fractures.

Symptoms of cadmium poisoning due to inhalation include chest pain, breathlessness, fever, pulmonary edema, nausea and high pulse rate. Symptoms due to ingestion are nausea, vomiting, cramps, and diarrhea.

Diagnosis: If poisoning is due to recent exposure, serum cadmium is about 5µg/dL. Urinary cadmium (10µg/g creatinine) and/or urinary ?2-microglobulin more than 750µg/g creatinine (but urinary ?2-microglobulin also increased in other renal diseases such as pyelonephritis, so it is not reliable).

Treatment: There is no effective and specific treatment for cadmium poisoning. Chelation is not useful and dimercaprol can aggravate renal toxicity. So the main management is further avoidance of exposure to cadmium and supportive therapy. Vitamin D is given for osteomalacia.

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Posted by - October 21, 2008 at 4:01 pm

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Heavy Metal Poisoning: Arsenic

Metals like arsenic pose a significant threat to health through occupational as well as environmental exposures. U.S. Agency for Toxic Substances and Disease Registry ranks arsenic third, according to its prevalence and severity.

Sources of arsenic poisoning: Smelting and microelectronics industries, pesticides, fungicides, herbicides, contamination of deep-water wells, coal, incineration of these products and folk remedies are the main sources of arsenic poisoning. Water pollution is a source of arsenic poisoning.

 Acute arsenic poisoning can cause necrosis of intestinal mucosa with resulting hemorrhagic gastroenteritis, fluid loss, hypotension, delayed cardiomyopathy, acute tubular necrosis and hemolysis. Chronic arsenic poisoning can cause diabetes, vasospasm (spasm of blood vessels), peripheral gangrene due to peripheral vascular insufficiency, peripheral neuropathy, and cancer of skin, liver, lung, bladder and kidney.

Lethal dose: The lethal dose of arsenic is 120–200 mg in adults and 2 mg/kg in children.

Clinical manifestations: Nausea, vomiting, abdominal pain, diarrhea, coma, delirium and seizure can be seen. Typical garlic like odor is characteristic sign in arsenic poisoning. Mees’ lines (transverse white striae of the fingernails), hyperkeratosis, hyperpigmentation, sensory and motor polyneuritis and distal weakness also seen.

Diagnosis: Radiopaque sign on abdominal X-ray; ECG shows QRS broadening, QT prolongation, ST depression, T-wave flattening; 24-h urinary arsenic 50 µg/day; (no seafood x 24 h); if recent exposure, serum arsenic 7 ?g/100ml. High arsenic in hair or nails.

Treatment: In acute poisoning ipecac is given to induce vomiting. Gastric lavage (remove stomach content) and activated charcoal is given along with symptomatic treatment. Dimercaprol is given every 4 hourly at the dose of 3-5 mgs/kg intramuscularly for two days and every 6 hourly for 1 day, than twice a day for 10 days. Alternative to dimercaprol is oral succimer.

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Posted by - October 13, 2008 at 1:50 am

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