Module 3: Toxicology - Section 12: Heavy Metals

OHM12.X: Arsenic

ARSENIC:

Arsenic used by humans is obtained in the form of arsenic trioxide, a byproduct of smelting of ores of copper lead and zinc. Arsenical compounds are encountered in among other industries smelting, pesticide industry, wood preservatives, animal feed additives, creation of alloys for lead and copper, semiconductors and glassware manufacture.

The most acutely hazardous exposure scenario is through inhalation of airborne arsine. Arsine or arsenic hydride is formed when arsenic is leached by acid solutions. Arsenicals in pesticides are more likely to be absorbed through the skin or by ingestion. Acute arsenic intoxication is as a result of ingestion or inhalation. Inorganic arsenic results in acute gastrointestinal irritation, producing vomiting, and cramps. Cardiac changes result and patients can develop encephalopathy. Death is due to circulatory collapse. A patient surviving the acute effects can develop delayed systemic toxic effects. A painful peripheral neuropathy may present 2 weeks later with initially with a sensory neuropathy in a glove and stocking distribution progressing to a sensory / motor deficit. Reversible bone marrow suppression can occur with anemia, pancytopenia and or eosinoplhilia. Chronic exposure will result in dermatological, CNS and vascular changes. Dermatological presentations include follicular and eczematous dermatitis due to direct irritation and hyperkeratosis from deposition, or excretion into the sulfhydryl rich epithelium. Mees lines, (transverse white lines across the nail bed), hyperpigmentation, and arsenical keratoses of the palms and soles occur days to weeks after ingestion. Both skin and lung cancers have been associated with human exposure to arsenic. Arsenic associated cancers have a multi-centric association. Arsenic is a recognized human carcinogen, for which there is no animal model.

Peripheral vascular disease may mimic Raynauds' and progress to black foot disease. Additional features may include cardiac suppression, bone marrow suppression and liver damage. Arsenic poisonings in children have been misdiagnosed as Reye's syndrome and in adults as gall bladder disease. Most arsenic poisonings historically have been the results of intentional acts, either suicidal or homicidal uses of pesticides. In occupational settings the use of arsine in microelectronics industry or the generation of arsine gas from exposure of arsenic salts to acids in metallurgy can result in acute hemolytic episodes.

There are no long term stores of arsenic. Urinary arsenic is a measure of acute exposure. A 212 hour specimen after 2 to 3 days of non exposure to arsenic containing food is advised. A concentration of less than 30 ug/l,in the absence of arsenic containing food is considered normal. Urinary excretion of up to 100 to 300 ug/l is not uncommon after ingestion of seafood. Of note, biologic sources of arsenic from seafood are relatively inoccuous as this form af arsenic is typically rapidly excreted and not bioavailable. In acute poisonings urinary excretion is typically well over 1,000 ug/l.

Absorbed arsenic binds to hair and nails and their slow growth can be used to measure arsenic during the preceding months but need to be reviewed carefully due to external contamination.

Chelation with dimercaprol or d-penicillamine can promote excretion in the acute state and DMSA, dimercaptosuccinic acid may be a safe and effective alternative.

Postgraduate Diploma in Occupational Health (DOH) - Modules 3: Occupational Medicine & Toxicology (Basic) by Profs Mohamed Jeebhay and Rodney Ehrlich, Health Sciences UCT is licensed under a Creative Commons Attribution-Noncommercial-Share Alike 2.5 South Africa License. Major contributors: Mohamed Jeebhay, Rodney Ehrlich, Jonny Myers, Leslie London, Sophie Kisting, Rajen Naidoo, Saloshni Naidoo. Source available from here. For any updates to the material, or more permissions beyond the scope of this license, please email healthoer@uct.ac.za or visit www.healthedu.uct.ac.za. Last updated Jan 2007.
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