Heavy Metal Poisoning

Heavy Metal Poisoning: Uncommon Types

Heavy Metal Poisoning by arsenic, cadmium, lead and mercury has been already discussed. Here we will discus about heavy metal poisoning by uncommon poisoning by heavy metals. Uncommon heavy metal poisoning includes poisoning by aluminum, chromium, cobalt, manganese, nickel, selenium, thallium, tin etc. The poisoning due to the above mentioned heavy metals is relatively rare and there is uncertainty regarding their potential toxicities.
Aluminum Poisoning:

It can cause encephalopathy in patients with severe renal disease who are undergoing dialysis. High levels of aluminum are found in the cerebral cortex and hippocampus of patients with Alzheimer’s disease. High levels of aluminum are also found in the drinking water and soil of areas with a high incidence of Alzheimer’s disease. But it cannot be proved that aluminum is the causative factor or contributing factor in the development of Alzheimer’s disease.

Chromium Poisoning:

It is a corrosive. Workers of chromate and chrome pigment production industries have a greater risk of lung cancer due to chronic exposure to chromium. Hexavalent chromium is mainly responsible.

Cobalt Poisoning:

cobalt chloride was once used as fortifier of beer which led to outbreaks of fatal cardiomyopathy among heavy consumers. Now it is no more used and there are very rare incidences of cobalt poisoning due to it.

Manganese Poisoning:

Chronic exposure to manganese can cause Parkinsonian syndrome. Parkinsonian syndrome is seen in persons like miners, dry-battery manufacturers, and arc welders. It is seen within 1–2 years of occupational exposure. Gait disorders, postural instability, tremor, expressionless face and psychiatric symptoms can be seen.
Nickel Poisoning:

Nickel exposure can cause allergic reaction and chronic exposure by inhalation of nickel compounds with low aqueous solubility like nickel subsulfide and nickel oxide in occupational settings can cause is an increased risk of lung cancer.

Selenium Poisoning:

Overexposure to selenium can cause local irritation of the respiratory system, gastrointestinal irritation and eyes, hepatitis, loss of hair, depigmentation, and peripheral nerve damage.

Thallium Poisoning:

Thallium can be absorbed through ingestion, inhalation and also through skin. Thallium is used in insecticides, metal alloys, and fireworks. Severe poisoning occurs after a single ingested dose of more than 1g or more than 8 mg/kg. Nausea and vomiting, abdominal pain, and blood in vomit occur before confusion, psychosis and coma.

Asbestos Exposure:

Asbestos is absorbed through inhalation. Asbestos was used in building insulation through the late 1970’s. Asbestos is the leading cause of mesothelioma, a rare form of cancer that develops from the cells of the mesothelium.

Treatment:

The principle of treatment is same like other heavy metal poisoning. Chelating agents and symptomatic treatment should be given. Gastric lavage (removing stomach contents) can be done if poisoning is by ingestion. Being metal all are radio opaque and X-ray helps in diagnosis and extent of heavy metal in stomach.

In thallium poisoning Prussian blue prevents absorption and is given orally at 250 mg/kg in divided doses. Thallium poisoning may be less severe when activated charcoal is used to interrupt its enterohepatic circulation (liver and intestinal circulation of poison). Other measures include forced diuresis, treatment with potassium chloride to promote renal excretion of thallium, and peritoneal dialysis.

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Posted by - December 22, 2008 at 1:34 pm

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Mercury Poisoning: Treatment

Sign & Symptoms of Mercury Poisoning: Chronic exposure to metallic mercury vapor produces characteristic intension tremor. It can also produce Mercurial erethism (excitability, insomnia, timidity, memory loss, and delirium known as “mad as a hatter”).  Decreased motor speed, visual scanning, and decreased verbal and visual memory, visuomotor (visual & motor) coordination are seen on neurobehavioral tests. Toxicity from elemental or inorganic mercury exposure begins when blood level is more than 3.6 µg/100 ml and urine levels more than 15µg/100 ml.

Organic mercury exposure is measured by mercury levels in blood in acute poisoning and mercury levels in hair in chronic poisoning. 

If children are exposed to mercury in any form (organic, inorganic, vaporized or ingested) may develop acrodynia known as “pink disease” that include flushing, itching, swelling, irritability, hypertension, high pulse rate, excessive salivation, perspiration, weakness, morbilliform rashes, desquamation of palms and soles.

Treatment: Acute ingestion of mercury is treated by gastric lavage or by inducing vomiting (with gag reflex which is by touching the pharynx or by hypertonic saline or drugs that cause vomiting). Polythiol resin is given which binds to mercury in the gastrointestinal tract (GIT) and reduce absorption from GIT. Chelating agent (bind metals into stable cyclic compounds with relatively low toxicity and enhances their excretion) like dimercaprol (British Anti Lewisite or BAL), 24 mg/kg per day IM in divided doses, penicillamine or DMSA (succimer or dimercaptosuccinic acid) should be given. Chelating agents are given as several 5 day courses which are separated by few days of rest days. If renal failure develops, treat with hemodialysis or peritoneal dialysis.

Chronic inorganic mercury poisoning is treated with N-acetyl penicillamine.

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Posted by - December 12, 2008 at 3:39 pm

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Heavy Metal Poisoning: Mercury

Mercury is the only metal which is present in liquid form. The toxicity of low level organic mercury exposure is mainly manifested by neurobehavioral performance. Mercury is excreted in urine and feces and has a ½ life in blood of about 60 days. But, deposits in the kidney and brain may remain for many years. Elemental mercury (Hg°) is not absorbed well. But, it can volatilize into highly absorbable vapor. Inorganic mercury is absorbed through the gastro intestinal tract and skin. Organic mercury is well absorbed by ingestion and inhalation and it is a major source of mercury poisoning.

Sources of Mercury poisoning: Metallic, mercuric mercury (Hg°, Hg+, Hg2+) and mercurous mercury exposures occur in some chemical, metal-processing, electrical equipment industries and automotive industries. Mercury is also present in thermometers, dental amalgams and batteries. Mercury can also be spread by waste incineration. Mercury present in environment is converted to organic mercury from inorganic mercury by bacteria. This organic mercury is than taken up by planktons, algae and fungi which are food for sea fishes like tuna, swordfish, and other pelagic fish. These sea foods when consumed by humans in large amount can lead to slow mercury poisoning.

Toxicity: Acute inhalation of mercury vapor can cause pneumonitis and pulmonary edema (water in lungs) which may cause death. It can also cause polyneuropathy and CNS (central nervous system) symptoms. Acute ingestion of inorganic mercury can cause gastroenteritis, nephritic syndrome, acute renal failure, hypertension, and cardiovascular collapse. Death usually occurs at a dose of 10–42 mg/kg. Acute ingestion of organic mercury causes gastroenteritis, arrhythmias (rhythm disturbance of heart beat), and lesions in the basal ganglia and gray matter. Chronic inhalation of mercury vapor causes CNS toxicity (mercurial erethism) lower exposures impair renal function, motor speed, memory, coordination.

High exposure of mercury during pregnancy can cause severe mental retardation due to derangement of fetal neuronal migration. Mild exposures of mercury during pregnancy (from fish like tuna, swordfish, and other pelagic fish consumption) are associated with reduced neurobehavioral performance in offspring.

Dimethylmercury is highly toxic (supertoxic) and is found in research labs. A few drops of exposure via skin absorption or inhaled vapor can cause severe cerebellar degeneration which lead to death.

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Posted by - November 29, 2008 at 12:46 am

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Lead Poisoning: Treatment

Clinical manifestations of lead poisoning: Abdominal pain, lethargy, anorexia, irritability, anemia, Fanconi’s syndrome, pyuria (pus in urine), azotemia in children with blood lead level of more than 80µg/100ml. Epiphyseal plate “lead lines” can be seen on X-ray of long bones. Convulsions, coma, and death can occur if blood lead level is more than 120µg/100ml. CDC Atlanta, USA recommends screening of all children at the time of crawling age (about 6 months) source identification and intervention is begun if the BPb (blood lead level) is more than 10 µg/100ml. Neurodevelopmental delays are seen at BPb of 40–80 µg/100ml. Headaches, arthralgias (joint pain), myalgias, depression, impaired short-term memory, loss of libido are common symptoms of lead poisoning. Examination may reveal a “lead line” at the gum-tooth border, pallor, wrist drop.

Diagnosis: Diagnosis is mainly by history, clinical symptoms and blood lead levels.  Laboratory tests may reveal a normocytic, normochromic anemia, an elevated blood protoporphyrin level, and motor delays on nerve conduction. In the U.S., regular testing of lead-exposed workers with removal if BPb is more than 40 µg/100ml is mandatory. K-X-ray fluorescence (KXRF) instruments have made it possible to measure bone lead levels which can diagnose a chronic lead poisoning even if it is at subclinical level.

Treatment: Source of the poisoning should be identified and corrected. Chelation is recommended with oral DMSA (succimer). Severe toxic cases should be hospitalized and IV (intravenous) or IM (intramuscular) chelation with edentate calcium disodium (CaEDTA) is administered. Dimercaprol is given to prevent worsening of encephalopathy. Correction of dietary deficiencies of iron, calcium, magnesium, and zinc lower lead absorption and also can improve the toxic condition. Vitamin C is a weak and natural chelating agent.

Chelation should be done or not in children with asymptomatic lead poisoning (blood lead level 20-40 µg/100ml) are not clear.

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Posted by - November 8, 2008 at 2:00 pm

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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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