Toxicity of Arsenic

Toxicity of Arsenic

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  Arsenic o Arsenic isan element and naturally occurring mineral o Ubiquitous in the environment o A solid metalloid and has a low solubility
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  Arsenic o Exists infour common valence states:  As (0) (metalloid arsenic , 0 oxidation state)  As (III) (trivalent, 3 oxidation state, such as Arsenites )  As (V) (pentavalent, 5 oxidation state, such as Arsenates )  Arsine gas
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  Sources of Arsenic VolcanoesSmelting of metals Rocks and mineral deposits Industrial processes Forest fires Fossil fuel burning Ground water Waste incineration Mineral extraction Sources Natural Anthropogeni c
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  Uses of Arsenic Pesticidesand insecticides Arsenic trioxide may be found in pesticides and defoliants. Electronic industry Gallium arsenide and arsine gas are used in semiconductor devices. Used in wood preservatives.
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  Uses of Arsenic •Drugs and chemical treatments. • Metal and other industrial processes. • Found in foods, especially in sea foods. • Colouring dyes and cosmetics.
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  o Inorganic arsenicis generally more toxic than organic arsenic. o Arsenite and Arsenate are the inorganic forms such as Arsenic trioxide, Sodium arsenate, Arsenic sulphide, Copper arsenate, etc. o Arsenobetaine and Arsenocholine are the organic forms known as “ Fish arsenic” found in seafood. o Arsine gas is the most toxic arsenical. Poisonous compounds of Arsenic
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  Arsenic exposure  Ingestion Arsenic containing foods – meat, fish, seafood  Drinking well water  Drugs  Inhalation  Burning of fossil fuel containing arsenic  Cotton gins  Emission from industrial operations  Smelters  Pesticides  Tobacco smoke  Dermal  Preserved wood products  Clothes using dyes
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  Toxicity by form Arsenicis a known human carcinogen. It can cause cell injury and death by multiple mechanisms. Toxicity may vary by the forms:  metalloid arsenic is generally regarded as nonpoisonous due to its insolubility in water and body fluids.  Trivalent, methylated, and relatively less ionizable arsenic metabolites may be capable of interacting with cellular targets such as proteins and even DNA.  The half life of inorganic arsenic in humans is about 10 hours.  After inhalation, arsine gas rapidly binds to red blood cells, producing irreversible cell membrane damage.
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  Effects of arsenicexposure Because it targets widely dispersed enzyme reactions, arsenic affects nearly all organ systems : 1. Gastrointestinal and Hepatic effects  GI effects are generally the result of ingestion.  GI lesion appears to be increased permeability of the small blood vessels, leading to fluid loss and hypotension.  Extensive inflammation and necrosis in stomach and intestine.  Hemorrhagic gastroenteritis may develop, with bloody diarrhea.  Toxic hepatitis with elevated liver enzyme levels.  Chronic arsenic ingestion may lead to cirrhotic portal hypertension.
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  2. Cardiovascular effects Acute arsenic toxicity may cause diffuse capillary leakage and cardiomyopathy, resulting in shock.  Hypertension with long-term exposure to arsenic.  Increased cardiovascular mortality in occupationally exposed groups. 3. Neurologic effects  Arsenic poisoning can cause peripheral neuropathy which leads to increased sweating, muscle cramps, numbness and spontaneous pain.  Sensory effects, particularly painful dysesthesia occur in moderate poisoning.  Weakness and paralysis may occur in more severe poisoning.  Cranial nerves are rarely affected.  Encephalopathy has been reported after both acute chronic exposure.
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  4. Dermal effects Skin lesions occurring most frequently in arsenic exposed humans are- hyperkeratosis, hyperpigmentation and skin cancer.  Patchy hyperpigmentation, a pathologic hallmark of chronic exposure may be found anywhere on the body.  Arsenical hyperkeratosis occurs most frequently on the palm and soles.  Skin cancer over a long-term exposure. 5. Renal effects  Severe acute arsenic poisoning may cause acute tubular necrosis with acute renal failure.  Chronic renal insufficiency from cortical necrosis has been reported.  There is limited strength of association between chronic arsenic exposure and renal cancer.  Arsine gas is more nephrotoxic than arsenic. however, both can cause acute tubular necrosis.
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  6. Respiratory effects Irritation of the respiratory mucosa.  Erosive lesions of mucosa including nasal septum perforation due to prolonged exposure of airborne arsenic.  Lung cancer has been associated with chronic arsenic exposure. 7. Carcinogenic effects In humans, chronic arsenic ingestion may cause cancers of the  Bladder  Kidney  Liver  Lung  Prostate, and  Skin Arsenic exposure also associated with tumors of the bladder, kidney, liver, lung, and prostate.
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  Arsenic in Indiaand Bangladesh Well water contaminated by natural sources containing arsenic has been reported to be the cause of arsenic toxicity throughout the world. Arsenic in drinking water has attracted much attention since recognition in the 1990s of its wide occurrence in well-water in Bangladesh. About 20% of wells in Bangladesh are contaminated and an estimated 80 million people are dependent on those wells for domestic purposes and affected by arsenic poisoning.
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  Standards for arsenicexposure The U.S Environment Protection Agency (EPA) adopted the standards for arsenic in workplace, food, and drinking water. the permissible limit for arsenic: • Workplace - 10µg of inorganic arsenic /m³ of air • Drinking water - 10 ppb • Food - 0.5 ppm to 2 ppm in seafood and other animal foods.