Medscape is available in 5 Language Editions – Choose your Edition here.


Arsenic Toxicity

  • Author: Steven Marcus, MD; Chief Editor: Asim Tarabar, MD  more...
Updated: Mar 27, 2014

Practice Essentials

Arsenic poisoning occurs through industrial exposure (see the image below), from contaminated wine or moonshine, or due to malicious intent. It may also occur through heavy metal contamination of herbal preparations and so-called nutritional supplements. A resurgence of interest in arsenic as a medicinal agent for the treatment of acute promyelocytic leukemias, multiple myeloma, myelodysplastic syndromes, and assorted resistant solid tumors may potentially contribute to arsenic toxicity.[1]

Black water urine from a patient with massive hemo Black water urine from a patient with massive hemolysis secondary to arsine exposure at a gas tank cleaning operation.

See Clues on the Skin: Acute Poisonings, a Critical Images slideshow, to help diagnose patients based on their dermatologic presentations.

Signs and symptoms

Arsenic exposure is usually associated with suicide, malicious intent, homicide, or occupational exposure. A detailed history to determine the exposure includes the following:

  • Careful work history on individuals with a painful peripheral neuropathy
  • Careful history regarding dietary and nutritional habits (eg, use of nutritional supplements and ayurvedic medicines, alcohol abuse) and hobbies

Clinical effects of arsenic toxicity depend on the chronicity (eg, acute, chronic) and type of poisoning (eg, arsenic, trivalent arsenic, arsine gas). Frequently, patients exposed to arsenic have a garlic smell to their breath and tissue fluids.

Acute severe arsenic poisoning manifests with the following signs and symptoms:

  • Tachycardia, hypotension, and even shock
  • Altered mental status, delirium, coma, seizures (acute encephalopathy)

Trivalent arsenic poisoning manifests with the following signs and symptoms:

  • Acute exposure: Cholera-like gastrointestinal (GI) symptoms of vomiting (often bloody) and severe diarrhea (may be rice-watery, often bloody); these patients will experience acute distress, dehydration (often), and hypovolemic shock
  • Chronic toxicity: Insidious; may manifest as a classical dermatitis (hyperkeratosis with a classical "dew drops on a dusty road" appearance) or peripheral neuropathy (usually a painful, symmetrical paresthesia with stocking-glove distribution); commonly, hepatic and renal damage
  • Fingernails: Whitish lines (Mees lines) that look like those from traumatic injuries

Arsine gas exposure manifests with an acute hemolytic anemia and striking chills.

See Clinical Presentation for more detail.


Laboratory testing

  • Complete blood count: Microcytic hypochromic anemia common; with arsine exposure, acute hemolytic anemia is the rule
  • Serum electrolyte levels, including calcium and magnesium
  • Type and screen or cross-match blood: For transfusion in patients exposed to arsine gas
  • Plasma arsenic concentrations: Helpful, but results usually not available until treatment decision has been made
  • Urinalysis: Urine spot test for arsenic and 24-hour urine collection for total arsenic excretion; patient must not have consumed seafood for at least 3 days prior to urine collection; laboratory must “speciate” the arsenic into organic and inorganic moieties, because the inorganic form is responsible for symptoms and signs of arsenic toxicity
  • Urine pregnancy test
  • Serum acetaminophen levels

Other studies

  • Abdominal x-ray: May reveal radio-opaque densities; may resemble an upper GI series
  • Nerve conduction studies: May confirm peripheral neuropathy
  • Electrocardiography: May reveal cardiac arrhythmias/failure from arsenic toxicity

See Workup for more detail.


Treatment of acute arsenic toxicity is supportive. Chelation therapy is imperative in all symptomatic patients; however, the use of chelators in patients exposed to arsine gas is controversial.

  • Support airway, breathing, and circulation
  • Hemodynamic stabilization: May include infusing large amounts of crystalloid solutions and the use of blood products
  • Acute arsenic ingestions: Orogastric lavage if the patient presents rapidly or plain radiography indicates that arsenic is present in the stomach; whole bowel irrigation with polyethylene glycol may be effective to prevent GI tract absorption of arsenic
  • Definitive chelation therapy; may be controversial for argine gas toxicity
  • Hemodialysis


The following chelating agents are used in the management of arsenic toxicity:

  • Dimercaprol
  • Succimer
  • Dimerval

See Treatment and Medication for more detail.



Arsenic, element 33, has a long and nefarious history; its very name has become synonymous with poison. In the 15th and 16th centuries, the Italian family of Borgias used arsenic as their favorite poison for political assassinations. Some even have suggested that Napoleon was poisoned by arsenic-tainted wine served to him while in exile.

The metal was reported as the causative agent in an outbreak of food-borne illness after a church gathering in which the coffee urn was apparently criminally contaminated with arsenic. This highlights the need for an index of suspicion when multiple individuals present to an emergency department temporally related and with similar symptoms and circumstances.[2]

Arsenic is typically considered a heavy metal and shares many toxic characteristics with the other heavy metals (eg, lead, mercury). Arsenic is ubiquitous in the environment. It ranks 20th in abundance in the earth's crust, 14th in seawater, and 12th in the human body.[3] In nature, arsenic exists in the metallic state in 3 allotropic forms (alpha or yellow, beta or black, gamma or grey) and several ionic forms.

Arsenic has been used as a medicinal agent, a pigment, a pesticide, and an agent of criminal intent. In the form of chromated copper arsenate (CCA), it was used until recently as part of the treatment to render architectural wood immune to pest infestation. This product was banned for use in the United States by the Environmental Protection Agency (EPA) in 2003. A great deal of the treated wood continues to exist in the form of decks and other structures exposed to the elements. Data suggest that a significant quantity of arsenic may leach out from such wood into landfills and into the interiors of homes with existing CCA-treated decks.[4, 5, 6] The durability of the CCA-treated wood suggests that such exposures may continue for decades. There is evidence in the rodent model that exposure to this compound, CCA, may produce significant renal pathology. Today, arsenic is primarily used in the production of glass and semiconductors.

Arsenic may be found as a water or food contaminant, particularly in shellfish and other seafood, and often contaminates fruits and vegetables, particularly rice.

Today, arsenic poisoning occurs through industrial exposure, from contaminated wine or moonshine, or because of malicious intent. The possibility of heavy metal contamination of herbal preparations and so-called nutritional supplements must also be considered. There has been a resurgence of interest in arsenic as a medicinal agent for treatment of acute promyelocytic leukemias, multiple myeloma, myelodysplastic syndromes, and assorted resistant solid tumors.[1]

An association between exposure to arsenic and the development of Alzheimer disease has been proposed.[7] In addition, an apparent link exists between arsenic exposure and gestational diabetes and potential long-term effects on the infants born to mothers consuming arsenic-contaminated water among other during pregnancy.[8, 9]

Because arsenic has been involved in geopolitics, an estimated 100 million people are at risk of exposure to unacceptable arsenic levels in either well water or ground water. Numerous "outbreaks" of excessive arsenic in water and food from an assortment of natural and anthropological causes have occurred. This has become a major public health issue in the developing world, primarily Bangladesh and surrounding countries, where many thousands of individuals have precancerous arsenic-related disease.



Inorganic forms of arsenic are more toxic than organic forms. The trivalent forms are more toxic and react with thiol groups, while the pentavalent forms are less toxic but uncouple oxidative phosphorylation. Very few organ systems escape the toxic effects of arsenic.

Trivalent inorganic arsenic inhibits pyruvate dehydrogenase by binding to the sulfhydryl groups of dihydrolipoamide. Consequently, conversion of pyruvate to acetyl coenzyme A (CoA) is decreased, citric acid cycle activity is decreased, and production of cellular ATP is decreased. Trivalent arsenic inhibits numerous other cellular enzymes through sulfhydryl group binding. Trivalent arsenic inhibits cellular glucose uptake, gluconeogenesis, fatty acid oxidation, and further production of acetyl CoA; it also blocks the production of glutathione, which prevents cellular oxidative damage.

Effects of pentavalent inorganic arsenic occur partially because of its transformation to trivalent arsenic; toxicity proceeds as outlined above. More importantly, pentavalent arsenic resembles inorganic phosphate and substitutes for phosphate in glycolytic and cellular respiration pathways. Consequently, high-energy phosphate bonds are not made, and uncoupling of oxidative phosphorylation occurs. For example, in the presence of pentavalent arsenic, adenosine diphosphate (ADP) forms ADP-arsenate instead of ATP; the high-energy phosphate bonds of ATP are lost.

Arsenic has been shown to produce oxidative stress. In a small pilot study of environmentally exposed children, arsenic altered monocyte superoxide anion production and inhibited nitric oxide production.[10]

Arsenic trioxide has been shown to cause a significant prolongation of cardiac action potential duration at many levels of repolarization producing conduction delay and increased triangulation. Electrolyte imbalance appears to enhance this toxicity.[11] The drug appears to inactivate endothelial nitric oxide synthase, leading to a reduction in production and bioavailability of nitric oxide. It also has been associated with inducing/accelerating atherosclerosis, increasing platelet aggregation and reducing fibrinolysis.[12]

Arsenic is listed as a presumed carcinogenic substance based on the increased prevalence of lung and skin cancer observed in human populations with multiple exposures (primarily through industrial inhalation).



United States

According to the American Association of Poison Control Centers' (AAPCC) National Poisoning Data System (NPDS), in 2010, there were 927 human exposures related to arsenic (excluding pesticides) and 67 exposures related to arsenic-containing pesticides. The majority of the pesticide exposures occurred in children younger than 5 years (43 [65%] of 67), whereas more than 58% of the nonpesticide exposures occurred in adults (539 of 927).[13]


Worldwide, up to 100 million people are at risk of exposure to arsenic from excessive arsenic in drinking water. In Bangladesh, more than 95% of the water supply to over 138 million people is potentially arsenic contaminated at levels exceeding the US EPA and WHO action limits.[14] If international efforts at elimination of the risk are unsuccessful, it is estimated that a substantial proportion of the Bangladesh population will develop arsenic-related diseases such as pulmonary and skin cancers as well as cardiovascular and renal disease.

In addition to the concentration of arsenic in the water, the prevailing diet existing in the affected areas may place the citizens at increased risk for toxicity from the arsenic. The population was recently surveyed and those individuals who had diets deficient in certain B vitamins and antioxidants appeared to have greater risk of arsenic dermatoses. An inverse correlation was found between consumption of vitamins A, C, and E, riboflavin and folic acid, and the existence of dermatological manifestations or chronic arsenic exposure.[15]



According to the American Association of Poison Control Centers' (AAPCC) National Poisoning Data System (NPDS), 6 individuals suffered major effects and 3 died from exposure to nonpesticide arsenic exposure in 2011. Two of the 3 deaths were the result of suicides. There were no serious effects seen in the pesticide exposures.


Men are more likely to experience industrial arsenic exposure than women.


As in many reported cases of poisoning, the majority of reports of exposure to arsenic-containing pesticides occur with children younger than 6 years as the victim (274 of 379 in the NPDS 2007 data), whereas, when nonpesticide arsenic exposure is involved, the majority are in adults older than 19 years (645 of 1165).[13]

Contributor Information and Disclosures

Steven Marcus, MD Professor, Department of Preventive Medicine and Community Health, Associate Professor, Department of Pediatrics, Rutgers New Jersey Medical School, Rutgers University School of Biomedical and Health Sciences; Executive and Medical Director, New Jersey Poison Information and Education System; Consulting Staff, Departments of Pediatrics and Internal Medicine, University Hospital; Consulting Staff, Department of Pediatrics, Newark Beth Israel Medical Center

Steven Marcus, MD is a member of the following medical societies: Academy of Medicine of New Jersey, American Academy of Clinical Toxicology, American Academy of Pediatrics, American College of Emergency Physicians, American College of Medical Toxicology, American Medical Association, Medical Society of New Jersey

Disclosure: Nothing to disclose.

Specialty Editor Board

John T VanDeVoort, PharmD Regional Director of Pharmacy, Sacred Heart and St Joseph's Hospitals

John T VanDeVoort, PharmD is a member of the following medical societies: American Society of Health-System Pharmacists

Disclosure: Nothing to disclose.

Michael J Burns, MD Instructor, Department of Emergency Medicine, Harvard University Medical School, Beth Israel Deaconess Medical Center

Michael J Burns, MD is a member of the following medical societies: American Academy of Clinical Toxicology, American College of Emergency Physicians, American College of Medical Toxicology, Society for Academic Emergency Medicine

Disclosure: Nothing to disclose.

Chief Editor

Asim Tarabar, MD Assistant Professor, Director, Medical Toxicology, Department of Emergency Medicine, Yale University School of Medicine; Consulting Staff, Department of Emergency Medicine, Yale-New Haven Hospital

Disclosure: Nothing to disclose.

Additional Contributors

David C Lee, MD Research Director, Department of Emergency Medicine, Associate Professor, North Shore University Hospital and New York University Medical School

David C Lee, MD is a member of the following medical societies: American Academy of Emergency Medicine, American College of Emergency Physicians, American College of Medical Toxicology, Society for Academic Emergency Medicine

Disclosure: Nothing to disclose.

  1. Emadi A, Gore SD. Arsenic trioxide - An old drug rediscovered. Blood Rev. 2010 Jul-Sep. 24(4-5):191-9. [Medline]. [Full Text].

  2. Gensheimer KF, Rea V, Mills DA, Montagna CP, Simone K. Arsenic poisoning caused by intentional contamination of coffee at a church gathering--an epidemiological approach to a forensic investigation. J Forensic Sci. 2010 Jul. 55(4):1116-9. [Medline]. [Full Text].

  3. Mandal BK, Suzuki KT. Arsenic round the world: a review. Talanta. 2002 Aug 16. 58(1):201-35. [Medline].

  4. Sigmon C, Patch S. A pilot survey of in-service home arsenic tracked in from chromated copper arsenate-treated decks. J Environ Health. 2010 Jan-Feb. 72(6):18-22. [Medline].

  5. Matos RC, Vieira C, Morais S, Pereira ML, Pedrosa J. Toxicity of chromated copper arsenate: a study in mice. Environ Res. 2010 Jul. 110(5):424-7. [Medline].

  6. Kamchanawong S, Veerakajohnsak C. Arsenic, chromium, and copper leaching from CCA-treated wood and their potential impacts on landfill leachate in a tropical country. Environ Technol. 2010 Apr 1. 31(4):381-94. [Medline].

  7. Gong G, O'bryant SE. The Arsenic Exposure Hypothesis for Alzheimer Disease. Alzheimer Dis Assoc Disord. 2010 May 13. [Medline].

  8. Ettinger AS, Zota AR, Amarasiriwardena CJ, Hopkins MR, Schwartz J, Hu H, et al. Maternal arsenic exposure and impaired glucose tolerance during pregnancy. Environ Health Perspect. 2009 Jul. 117(7):1059-64. [Medline]. [Full Text].

  9. Vahter M. Effects of Arsenic on Maternal and fetal Health. Annu Rev Nutr. June 2009. 29:381-399. [Medline]. [Full Text].

  10. Luna AL, Acosta-Saavedra LC, Lopez-Carrillo L, Conde P, Vera E, De Vizcaya-Ruiz A, et al. Arsenic alters monocyte superoxide anion and nitric oxide production in environmentally exposed children. Toxicol Appl Pharmacol. 2010 Jun 1. 245(2):244-51. [Medline].

  11. Raghu KG, Yadav GK, Singh R, Prathapan A, Sharma S, Bhadauria S. Evaluation of adverse cardiac effects induced by arsenic trioxide, a potent anti-APL drug. J Environ Pathol Toxicol Oncol. 2009. 28(3):241-52. [Medline].

  12. Balakumar P, Kaur J. Arsenic exposure and cardiovascular disorders: an overview. Cardiovasc Toxicol. 2009 Dec. 9(4):169-76. [Medline].

  13. Bronstein AC, Spyker DA, Cantilena LR Jr, Green JL, Rumack BH, Dart RC. 2010 Annual Report of the American Association of Poison Control Centers' National Poison Data System (NPDS): 28th Annual Report. Clin Toxicol (Phila). 2011 Dec. 49(10):910-41. [Medline].

  14. Ng JC, Moore MR. Arsenic in drinking water: a natural killer in Bangladesh and beyond. An urgent alternative watershed management strategy is needed. Med J Aust. 2005 Dec 5-19. 183(11-12):562-3. [Medline]. [Full Text].

  15. Zablotska LB, Chen Y, Graziano JH, Parvez F, van Geen A, Howe GR, et al. Protective effects of B vitamins and antioxidants on the risk of arsenic-related skin lesions in Bangladesh. Environ Health Perspect. 2008 Aug. 116(8):1056-62. [Medline].

  16. Yoshimura Y, Endo Y, Shimoda Y, Yamanaka K, Endo G. Acute Arsine Poiosning Confirmed by Speciation Analysis of Arsenic Compounds in the Plasma and urine by HPLC-ICP-MS. J Occupational Health. Nov 2011. 53:45-49. [Medline]. [Full Text].

  17. Amster E, Tiwary A, Schenker MB. Case report: potential arsenic toxicosis secondary to herbal kelp supplement. Environ Health Perspect. 2007 Apr. 115(4):606-8. [Medline].

  18. Borak J, Hosgood HD. Seafood arsenic: implications for human risk assessment. Regul Toxicol Pharmacol. 2007 Mar. 47(2):204-12. [Medline].

  19. Duenas-Laita A, Perez-Miranda M, Gonzalez-Lopez MA, et al. Acute arsenic poisoning. Lancet. 2005 Jun 4-10. 365(9475):1982. [Medline].

  20. Fesmire FM, Schauben JL, Roberge RJ. Survival following massive arsenic ingestion. Am J Emerg Med. 1988 Nov. 6(6):602-6. [Medline].

  21. Gerhardt RE, Crecelius EA, Hudson JB. Moonshine-related arsenic poisoning. Arch Intern Med. 1980 Feb. 140(2):211-3. [Medline].

  22. Graeme KA, Pollack CV Jr. Heavy metal toxicity, Part I: arsenic and mercury. J Emerg Med. 1998 Jan-Feb. 16(1):45-56. [Medline].

  23. Hall JC, Harruff R. Fatal cardiac arrhythmia in a patient with interstitial myocarditis related to chronic arsenic poisoning. South Med J. 1989 Dec. 82(12):1557-60. [Medline].

  24. Lai MW, Boyer EW, Kleinman ME, et al. Acute arsenic poisoning in two siblings. Pediatrics. 2005 Jul. 116(1):249-57. [Medline].

  25. Lech T, Trela F. Massive acute arsenic poisonings. Forensic Sci Int. 2005 Jul 16. 151(2-3):273-7. [Medline].

  26. Moon KA, Guallar E, Umans JG, Devereux RB, Best LG, Francesconi KA, et al. Association Between Exposure to Low to Moderate Arsenic Levels and Incident Cardiovascular Disease: A Prospective Cohort Study. Ann Intern Med. 2013 Sep 24. [Medline].

  27. Muckter H, Liebl B, Reichl FX, et al. Are we ready to replace dimercaprol (BAL) as an arsenic antidote?. Hum Exp Toxicol. 1997 Aug. 16(8):460-5. [Medline].

  28. Navarro B, Sayas MJ, Atienza A, Leon P. An unhappily married man with thick soles. Lancet. 1996 Jun 8. 347(9015):1596. [Medline].

  29. Severo R. Albany consumer unit calls sealant a health peril. NY Times Mag. 1976 Dec 30. 42.

  30. Stenehjem AE, Vahter M, Nermell B, Aasen J, Lierhagen S, Morland J. Slow recovery from severe inorganic arsenic poisoning despite treatment with DMSA (2.3-dimercaptosuccinic acid). Clin Toxicol (Phila). 2007 May. 45(4):424-8. [Medline].

  31. Stiles S. Arsenic in drinking water, even at low to moderate levels, ups CVD mortality. Heartwire. September 23, 1013. Available at Accessed: September 27, 2013.

Black water urine from a patient with massive hemolysis secondary to arsine exposure at a gas tank cleaning operation.
All material on this website is protected by copyright, Copyright © 1994-2016 by WebMD LLC. This website also contains material copyrighted by 3rd parties.