Toxicity, Arsenic ?>

Toxicity, Arsenic

Toxicity, Arsenic
Introduction


Background

Arsenic is a heavy metal with a name derived from the Greek word arsenikon, meaning potent. Arsenic is ubiquitous, found in air, water, fuels, and marine life. The daily human intake of arsenic contained in food ranges from 0.5-1 mg, with the greatest concentrations coming from fish and crustaceans. Arsenic has been used for a variety of purposes. For a long time, arsenic was considered the perfect poison because it is odorless, tasteless, and resembles sugar. Throughout history, arsenic was thought to have claimed the lives of many, including Britanicus, Pope Pius III, Pope Clemente XIV, and Napoleon Bonaparte. Arsenic has been used for the treatment of ulcers, tuberculosis, syphilis, and many other ailments. More recently, arsenic has been used as an insecticide, fungicide, rodenticide, and wood preservative. Arsenic also has been used to manufacture glass and semiconductors.
Pathophysiology

Arsenic exists in metalloid, arsenite (trivalent), and arsenate (pentavalent) valences and in arsine gas. The inorganic (trivalent) compound is absorbed more readily than the organic (pentavalent) forms because of its high lipid solubility. Absorption primarily occurs through the gastrointestinal tract; however, some absorption occurs through the skin. Once arsenic is in the body, it binds to hemoglobin, plasma proteins, and leukocytes and is redistributed to the liver, kidney, lung, spleen, and intestines. Over a period of weeks, deposits may be found in skin, hair, nails, bone, muscle, and even nervous tissue.

Arsenic produces cellular damage through a variety of mechanisms. Arsenic binds to enzyme sulfhydryl groups and forms a stable ring, which deactivates the enzyme. The process of deactivating the enzyme causes widespread endothelial cell damage, vasodilation, and leakage of plasma. Massive transudation of fluid into the bowel lumen, mucosal vesicle formation, and tissue sloughing may result in large gastrointestinal fluid losses. Arsenic binds to dihydrolipoic acid, a pyruvate dehydrogenase cofactor, blocking the conversion of pyruvate to acetyl coenzyme A and inhibiting gluconeogenesis. Arsenic competes with phosphates for adenosine triphosphate, forming adenosine diphosphate monoarsine, causing the loss of high-energy bonds.

In some forms, arsenic is caustic, exerting a direct toxic effect on blood vessels and large organs. Long-term exposure results in nerve damage and may lead to lung, skin, or liver cancer. Once inhaled, arsine gas combines with hemoglobin in RBCs, causing severe hemolysis and anemia. Patients develop hemoglobinuria and hematuria within several hours of exposure.
Frequency
United States

Approximately 1000 cases of arsenic exposure are reported annually. Many more cases of chronic arsenic exposure probably go unreported.
International

Thousands of people are exposed to arsenic in the form of contaminated drinking water, foodstuffs, and industrial pollution.
Mortality/Morbidity
Acute arsenic intoxication resulting in a fatality is rare. Survivors may have severe disabilities secondary to organ damage.
Chronic exposure, from weeks to months, can have devastating effects. Patients may develop encephalopathy, painful paresthesias, myocarditis, pericarditis, peripheral vascular disease (ie, blackfoot disease), lung cancer, renal failure, anemia, brittle nails exhibiting Mees lines, or hyperpigmentation (especially of the eyelids, neck, axillae, and groin).
Clinical
History
Exposure may be homicidal, suicidal, occupational, or environmental in nature.
A thorough examination of the patient’s history, including questions about use of chemicals at work, gardening supplies, dietary supplements, and home remedies, is essential when trying to determine the source of exposure.
Physical
Findings depend on the chronicity of exposure.
Patients with acute exposure usually develop symptoms within 30 minutes. They present with gastrointestinal distress characterized by nausea, vomiting, abdominal pain, and profuse watery or bloody diarrhea. Patients often are hypotensive and tachycardic and may complain of a metallic taste in their mouth and have a garlic odor on their breath.1 Patients frequently exhibit signs of delirium upon examination.
Patients with chronic arsenic exposure often present with the complaint of painful paresthesias. Neuropathy results in diminished sensitivity to pinprick, light touch, temperature, and vibration and in motor deficits in a stocking-glove distribution. Muscle wasting and foot drop sometimes are noted. Other examination findings include cyanosis of distal extremities, pallor from anemia, hyperpigmentation of skin, and Mees lines. Patients may develop cardiovascular effects, diabetes mellitus, or cancer as well.
Patients with acute arsine gas exposure present with headache, nausea, vomiting, diarrhea, and abdominal pain. Patients often develop dyspnea and severe jaundice.
Causes
Accidental or intentional ingestion of insecticides, rodenticides, and other compounds containing arsenic is more likely to result in an acute intoxication.
Environmental exposure to contaminated drinking water or food and industrial exposures are more likely to result in chronic effects.

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