a) Ventricular tachycardia, ventricular bigeminy, and ventricular fibrillation have been described after acute arsenic ingestion (Lai et al, 2005; Brayer et al, 1997; Goldsmith, 1980; Peterson & Rumack, 1977; St Petery et al, 1970) .
b) QRS morphology of the ventricular dysrhythmia is often consistent with torsade de pointes (Lai et al, 2005; Beckman et al, 1991; Goldsmith, 1980; St Petery et al, 1970).
c) Abrupt respiratory failure and asystole developed in a 21-year-old man who ingested 4 grams of arsenic (Moore et al, 1994a).
d) CASE REPORT: Sinus tachycardia (114 bpm) was reported in a 3-year-old boy who ingested approximately 5 mL of an herbicide containing 47.6% monosodium methylarsonate (Roth et al, 2011).
e) RETROSPECTIVE REVIEW: According to a retrospective review of 155 patients who ingested corrosive arsenic-based depilatory (CABD) agents, cardiac dysrhythmias were reported in 10% of the patients. Analysis of CABD has shown that it consists of approximately 25% arsenic sulfide (Farzaneh et al, 2011).

a) ECG changes have included QT prolongation, left axis deviations, peaked T waves, and also deeply inverted T waves (Lai et al, 2005; Gousios & Adelson, 1959; Heyman et al, 1956).
b) Abnormal ECG changes, including ST elevation, flat T, and prolonged QT intervals, were reported in infants following consumption of dried milk powder contaminated with arsenic. Analysis of a sample of milk powder estimated the arsenic concentration to be 4 to 7 mg/L (Dakeishi et al, 2006).

a) CHRONIC EXPOSURE: Interstitial myocarditis resulting in fatal ventricular arrhythmias has been reported after chronic exposure to arsenic (Hall & Harruff, 1989).

a) CHRONIC EXPOSURE: A study of Taiwan residents who drank artesian well water containing high amounts of arsenic found chronic arsenic exposure to be related to ischemic heart disease in a dose-dependent manner. Mortality attributed to ischemic heart disease gradually declined over 17 to 20 years following cessation of consumption of the well water (Chang et al, 2004).

a) Hypotension and tachycardia are common early signs (Shum et al, 1995; Schoolmeester & White, 1980).
b) Hypotension from gastrointestinal fluid loss or myocardial depression may develop after acute ingestion (Lai et al, 2005; Moore et al, 1994a).
c) CASE SERIES: Three patients, including a pregnant woman at 38 weeks gestation, developed hypotension (80 to 100/40 to 70 mmHg), respiratory distress, severe rash, blisters, oliguria, anuria, and leukopenia following dermal application, from neck to toe, of an isopropyl solution that contained 30% arsenic instead of the prescribed 25% benzyl benzoate for treatment of scabies. Despite intensive supportive therapy, all of the patients died, including the fetus, within 72 hours post-application (Majid Cheraghali et al, 2007).
d) RETROSPECTIVE REVIEW: According to a retrospective review of 155 patients who ingested corrosive arsenic-based depilatory (CABD) agents, hypotension was reported in 10% of the patients. Analysis of CABD has shown that it consists of approximately 25% arsenic sulfide (Farzaneh et al, 2011).

a) CHRONIC EXPOSURE: A dose-related increased incidence of hypertension was found in a Taiwanese population with chronic arsenic exposure in drinking water (Chen et al, 1995).
b) A cross-sectional analysis was conducted to evaluate the association between arsenic exposure from drinking water and blood pressure using baseline data of 10,910 participants in the Health Effects of Arsenic Longitudinal Study in Bangladesh (October 2000 to May 2002). Results suggested that the effect of low-level arsenic exposure on blood pressure is nonlinear and may be more pronounced in persons with lower intake of nutrients related to arsenic metabolism and cardiovascular health (Chen et al, 2007).
c) A cross-sectional study involving 8790 postpartum women who were exposed to arsenic in drinking water showed that as arsenic concentrations increased from 21 to 50, 51 to 100, and greater than 100 mcg/L, systolic blood pressure also increased by 1.88 mmHg (95% CI, 1.03 to 2.73), 3.90 mmHg (95% CI, 2.52 to 5.29), and 6.84 mmHg (95% CI, 5.40 to 8.28), respectively as compared with women in the control group (drinking water arsenic concentration of 20 mcg/L or less). Diastolic blood pressure also increased with increasing drinking water arsenic concentrations, with a change of 2.10 mmHg (95% CI, 1.37 to 2.84), 2.72 mmHg (95% CI, 1.53 to 3.92), and 3.17 mmHg (95% CI, 1.92 to 4.41), respectively, as compared with women in the control group (Kwok et al, 2007).

a) CHRONIC: Peripheral vascular function to cold stress, measured by finger systolic blood pressure before and after ice-water immersion, was significantly improved after a reduction in arsenic exposure from drinking water (Pi et al, 2005).

a) A retrospective review of cases from 1950 to 2000, comparing patients from an arsenic-exposed region (region II) in Chile with a non-arsenic-exposed region (region V) in Chile showed that the mortality rates from acute myocardial infarction (AMI) were significantly increased in region II during 1958 to 1970 (considered the peak exposure period, prior to installation of an arsenic removal plant), with a rate ratio (RR) in men of 1.48 (95% CI, 1.37 to 1.59) and a RR in women of 1.26 (95% CI, 1.14 to 1.4). From 1971 to 2000, the RR gradually decreased to a final recorded RR in men of 1.21 (95% CI, 1 to 1.47) and a RR in women of 0.90 (95% CI, 0.71 to 1.14). The RR for AMI, comparing region II and region V, varied according to gender and age. Within the peak exposure period of 1958 to 1970, the RR was the greatest in men and women aged 30 to 39 years, at 2.27 (95% CI, 1.61 to 3.20) and 2.51 (95% CI, 1.43 to 4.42), respectively. In comparison with lung and bladder cancer (2 prevalent cancers following arsenic exposure), excess deaths due to AMI were greater during the peak exposure period (1958 to 1970) with 452 in men and 129 deaths in women, as compared with 71 deaths in men and 19 in women for lung cancer and 17 deaths in men and 10 in women for bladder cancer (Yuan et al, 2007).

a) A 45-year-old woman developed acute respiratory distress and multiorgan failure following an intentional ingestion of between 8 and 16 g of sodium arsenite. The patient gradually improved with dimercaprol therapy and supportive care; however, residual quadriplegia occurred (Bartolome et al, 1999).
b) Acute respiratory failure presumably from severe weakness of respiratory muscles was reported in a patient with severe arsenic poisoning (Greenberg et al, 1979). The problem progressed despite dimercaprol therapy and required ventilatory assistance for 1 month.
c) Breathlessness was associated with asymmetric bilateral phrenic nerve involvement secondary to arsenic poisoning from contaminated opium in a 35-year-old opium addict (Bansal et al, 1991).
d) Abrupt respiratory failure and asystole developed in a 21-year-old man who ingested 4 grams of arsenic (Moore et al, 1994a).

a) Pulmonary edema, either noncardiogenic from capillary leaking or cardiogenic from myocardial depression, may occur and be life-threatening.
b) CASE REPORTS: Three patients developed respiratory distress, hypotension, and burns and blistering of the skin following dermal application, from neck to toe, of an isopropyl alcohol solution containing arsenic 30% instead of the prescribed benzyl benzoate 25% for treatment of scabies. Despite intensive supportive therapy, all 3 patients continued to deteriorate clinically and subsequently died within 72 hours postapplication (Majid Cheraghali et al, 2007).
c) Adult respiratory distress syndrome (ARDS) has been reported (Bollinger et al, 1992)(Schoolmeester & White, 1980; Zaloga et al, 1970).

a) Acute inhalation exposure may result in irritation of the upper respiratory tract (Hathaway et al, 1996; ACGIH, 1996a).
b) CHRONIC EXPOSURE: Following chronic arsenic exposure through water contamination, asthmatic bronchitis (ie, cough, expectoration, breathlessness, restrictive asthma) has been reported in India. The causality is not well-defined (Rahman et al, 2001).

a) Chronic arsenic exposure due to ingestion of contaminated ground water was studied in 107 subjects. Twenty cases (68.9%) had an obstructive pattern of lung involvement (7 mild; 9 moderate; 4 severe), 8 cases (27.6%) had a mixed obstructive-restrictive pattern and 1 (3.5%) had only a restrictive pattern (Majumdar et al, 2004).

a) CHRONIC EXPOSURE: Bronchiectasis, as identified by high-resolution computed tomography, was reported in individuals following chronic exposure to arsenic in drinking water (Mazumder et al, 2005).
b) A retrospective study comparing the mortality rates in Antofagasta, Chile during a period of high arsenic exposure in the drinking water (1958 to 1971) with the rest of Chile found that the standardized mortality ratio (SMR) for bronchiectasis in patients born just before the period of exposure (1950 to 1957), and exposed during early childhood, was 12.4 (95% CI, 3.3 to 31.7). For those individuals born during the exposure period (1958 to 1970) and who were exposed in utero, the SMR was 46.2 (95% CI, 21.1 to 87.7), suggesting increased mortality in adults from bronchiectasis following chronic arsenic exposure from drinking water while in utero as compared with exposure during early childhood (Smith et al, 2006).

a) A 3-year-old boy developed vomiting within 30 minutes of ingesting 3 Python brand "snakes" (fireworks) which contained arsenic and looked like candy. He became obtunded within 1 hour. Neurological exam was nonfocal, and pupils were 5 mm and reactive. Blood glucose was 125 mg/dL. The patient was provided supportive care and mentation began to clear within several hours. He returned to baseline within 10 hours of ingestion. No permanent sequelae was reported (Brayer et al, 1997).
b) A 4-month-old developed vomiting within 10 minutes of ingesting arsenic. He was comatose within 6 hours of ingestion; he was unresponsive and died 36 hours after ingestion (Lai et al, 2005).
c) RETROSPECTIVE REVIEW: According to a retrospective review of 155 patients who ingested corrosive arsenic-based depilatory (CABD) agents, an altered level of consciousness was reported in 13.5% of the patients. The consciousness levels ranged from grade I (awake, lethargic, or sleeping, but arousable) to grade IV (unresponsive to pain, flaccid paralysis, and absent brainstem reflexes and respirations). Analysis of CABD has shown that it consists of approximately 25% arsenic sulfide (Farzaneh et al, 2011).

a) Toxic delirium and encephalopathy are complications of significant acute (Duenas-Laita et al, 2005; Quatrehomme et al, 1992; Jenkins, 1966) and chronic (Morton & Caron, 1989; Freeman & Couch, 1978) arsenic poisoning. The encephalopathy may be permanent and result in cortical atrophy 1 to 6 months after exposure (Fincher & Koerker, 1987).
b) PREVENTION: Early institution of chelation therapy may not be successful in preventing arsenic encephalopathy (Fincher & Koerker, 1987). However, British anti-lewisite has been reported to reverse the encephalopathy seen after chronic arsenic exposure (Beckett et al, 1986; Freeman & Couch, 1978).

a) CHRONIC EXPOSURE: A cross-sectional study was performed to determine the possible influence of long-term arsenic exposure on the development of cognitive function in adolescents. Neurobehavioral tests included continuous performance test (CPT), symbol digit (SD), pattern memory (PM), and switching attention (SA). After adjusting for education and sex, pattern memory and switching attention were significantly affected by long-term arsenic exposure. The authors, however, state that the limitations of the study require replication to confirm this conclusion (Tsai et al, 2003).
b) A follow-up study, conducted 14 years after 381 infants developed arsenic poisoning following consumption of dried milk powder contaminated with arsenic, showed that the children continued to have a variety of abnormal neurologic findings as compared with unexposed individuals of approximately the same age, including higher rates of severe mental retardation and an increase in the prevalence of epilepsy. Analysis of a sample of the dried milk determined that the arsenic concentration was 4 to 7 mg/L, with a total ingested dose of approximately 60 mg (Dakeishi et al, 2006).

a) CASE REPORT: A toxic polyneuropathy resulting in quadriparesis has been reported within 2 weeks of beginning use of an arsenic-containing homeopathic preparation (Chakraborti et al, 2003).

a) ONSET: Peripheral neuropathy is common after either acute or chronic arsenic poisoning (Duenas-Laita et al, 2005; Mukherjee et al, 2005; Tsuji et al, 2004; Nazmul Ahasan HAM, 2001; Guha Mazumder et al, 1992). After acute exposure peripheral neuropathy usually begins 1 to 3 weeks later (Hahn et al, 2000; Goebel et al, 1990; Le Quesne & McLeod, 1977; Heyman et al, 1956).
b) INITIAL SIGNS: Peripheral neuropathy usually begins as paresthesias of the soles of the feet, then the hands, progressing proximally over the next few days (Heyman et al, 1956). Severe muscle weakness and wasting then develops, causing severe disability (OSHA, 1988; Le Quesne & McLeod, 1977). In a case of arsenic poisoning from burning pressure-treated wood, symptoms in an 11-year-old boy were limited to bilateral pain and tingling of the feet along with difficulty sleeping and walking secondary to the pain (Hahn et al, 2000).
c) CASE REPORT: Paresthesias, generalized weakness, vomiting, and abdominal pain occurred in a 16-year-old girl following intentional ingestion of up to 240 mL of an herbicide containing monosodium methylarsonate 47%. The patient was administered a bolus dose of British anti-lewisite approximately 12 hours postingestion, followed by administration of Dimercaptosuccinic acid for 14 days. The patient's condition improved and she was transferred to a psychiatric institution; however, mild paresthesia in her hands and feet persisted at her 6-week follow-up (Roth et al, 2011).
d) DIFFERENTIAL: The syndrome may initially be confused with Guillain-Barre (Kim et al, 2012; Gherardi et al, 1990; Donofrio et al, 1987a). Facial nerves are commonly involved in Guillain-Barre and almost never affected in arsenic poisoning (Jenkins, 1966).
e) PAIN: The paresthesias may be painful and are frequently described as severe burning pain in a stocking and glove distribution.
f) Physical findings of arsenic neuropathy usually include prominently decreased sensation to touch, pinprick, and temperature, frequently in a stocking and glove distribution (Kelafant et al, 1993; Heyman et al, 1956); loss of vibration sense is also common; profound muscle weakness and wasting, distal more so than proximal, is also seen (Hahn et al, 2000; Donofrio et al, 1987a; Heyman et al, 1956); wrist drop, foot drop, and fasciculations may be seen (Heyman et al, 1956).
g) Electrodiagnostic studies of arsenic neuropathy have shown a reduction of motor conduction velocity and marked abnormalities of sensory nerve action potentials (Le Quesne & McLeod, 1977).
h) Nerve biopsy may demonstrate various stages of axonal degeneration without demyelination (Le Quesne & McLeod, 1977) or with demyelination (Donofrio et al, 1987a).
i) Dimercaprol (BAL) does not seem to reverse arsenic neuropathy (Donofrio et al, 1987a; Le Quesne & McLeod, 1977; Heyman et al, 1956); recovery is usually very slow and incomplete. It has been claimed that if BAL is administered within hours of ingestion, however, neuropathy may be prevented (Jenkins, 1966), although this is not true for all cases (Marcus, 1987).
j) CASE REPORT: A 35-year-old man with acute arsenic neuropathy with asymmetric bilateral phrenic nerve involvement made a significant recovery with D-penicillamine (250 mg/3 times daily) therapy (Bansal et al, 1991).
k) CASE REPORT: A patient with chronic exposure to an arsenical pesticide presented with peripheral neuropathy and macrocytosis but without anemia (Heaven et al, 1994).
l) CASE REPORT: A 39-year-old woman developed progressive weakness and peripheral neuropathy leading to quadriplegia and requiring mechanical ventilation following an unknown type of exposure to arsenic. Analysis of her serum and urine revealed elevated arsenic (As) concentrations (290 mcg/kg [normal less than 2 mcg/kg] and 2000 mcg/L [normal less than 10 mcg/L], respectively). The patient slowly improved clinically following chelating therapy with DMSA; however, 5 years following intoxication, the patient continued to have residual paresthesias and weakness in her hands and distal lower extremities (Stenehjem et al, 2007).
m) CASE SERIES: In a large survey of arsenic poisoning from various water supplies in India, 37.3% (n=154 cases; total 413 subjects) of individuals developed clinical neuropathies. Of those cases, 80.5% (n=124 cases) had a sensory neuropathy and 30 cases had a motor component (Rahman et al, 2001).
n) CASE SERIES: In a study of 137 subjects chronically exposed to arsenic in drinking water, arsenic exposure was associated with elevated toe vibration threshold. Urinary arsenic and cumulative arsenic index were both significantly associated with elevated toe vibration threshold (Hafeman et al, 2005).
o) CASE REPORTS: Numbness in all 4 extremities were reported in 3 patients (a 45-year-old woman, her 23-year-old son, and a 5-year-old child) following dermal application, from neck to toe, of an isopropyl alcohol solution containing arsenic 30% instead of the prescribed benzyl benzoate 25% for treatment of scabies. The patients also experienced vomiting, pruritus, and blistering of the skin. With symptomatic and supportive therapy, all of the patients recovered and were discharged within 5 days postadmission; however, numbness of the extremities continued to persist (Majid Cheraghali et al, 2007).
p) RETROSPECTIVE REVIEW: According to a retrospective review of 155 patients who ingested corrosive arsenic-based depilatory (CABD) agents, neuropathy was reported in 8.6% of the patients. Analysis of CABD has shown that it consists of approximately 25% arsenic sulfide (Farzaneh et al, 2011).
q) CASE REPORT: A 74-year-old woman, with existing idiopathic peripheral neuropathy, presented to a neurology clinic with worsening of her peripheral neuropathy of her lower extremities. Prior to presentation, toxicologic analysis of her blood and urine indicated elevated concentrations of arsenic. Following a 5-day abstention of fish and shellfish, a repeat urinalysis reported elevated urine arsenic (622.1 nmol/L; reference range less than 534 nmol/L). Medication history of the patient revealed that she had been taking greater than the recommended dosages of gingko biloba, fish oil, omega-3, and glucosamine. After discontinuing all supplements, a repeat urinalysis, conducted 1 month later, showed that the arsenic concentration was 57.5 nmol/L. At five months follow-up, the patient reported improvement, with a return of sensation and recovery of some motor function (Barton & McLean, 2013).
r) CASE REPORT: A 43-year-old man presented to the emergency department with a 5-day history of progressive quadriparesis. For 25 days prior to presentation, the patient had been taking an herbal medication to treat psoriasis. Five days after cessation of medication, he experienced bilateral arm weakness and hand paresthesia progressing to his lower extremities bilaterally. Electrodiagnostic studies indicated an acquired demyelinating polyradiculoneuropathy. An initial diagnosis of Guillain-Barre syndrome was made; however, screening for heavy metals showed an elevated urinary arsenic concentration (240.7 mcg/L), suggesting arsenic-induced neuropathy, mimicking Guillain-Barre syndrome (Kim et al, 2012).

a) CHRONIC EXPOSURE: Among a Taiwanese population chronically exposed to high levels of arsenic in drinking water, there was an increased prevalence of cerebrovascular disease, particularly cerebral infarction (Chiou et al, 1997).

a) CASE REPORT: A 45-year-old woman intentionally ingested between 8 and 16 g of sodium arsenite and developed multiorgan failure (ie, respiratory, renal, hepatic, and hematologic), along with neurological deterioration. During the first hospital day the patient was treated with dimercaprol (300 mg/3 times daily and increased to 200 mg every 4 hours) and received supportive care. The patient gradually improved, but permanent quadriplegia occurred (Bartolome et al, 1999).
b) CASE REPORT: A 39-year-old woman developed progressive weakness and peripheral neuropathy leading to quadriplegia and requiring mechanical ventilation following an unknown type of exposure to arsenic. Analysis of her serum and urine revealed elevated arsenic (As) concentrations (290 mcg/kg [normal less than 2 mcg/kg] and 2000 mcg/L [normal less than 10 mcg/L], respectively). The patient slowly improved clinically following chelating therapy with DMSA; however, 5 years following intoxication, the patient continued to have residual paresthesias and weakness in her hands and distal lower extremities (Stenehjem et al, 2007).

a) Upward gaze-evoked nystagmus was reported in 3 women following chronic exposure of diphenylarsinic acid, an organoarsenic compound, in the drinking water. Other neurologic signs and symptoms that developed included ataxia, myoclonus of the extremities with diffuse hyperreflexia, speech disturbances, and sleep disorders. The nystagmus spontaneously resolved following cessation of exposure to the contaminated water (Nakamagoe et al, 2006).

a) In a cross-sectional study of 602 children (6 to 8 years of age) living within 3.5 km of a metallurgy smelter complex in the city of Torreon, Mexico, cognitive and neurobehavioral function was evaluated. Of these children, 591 had complete anthropometry, iron, and zinc status by biochemical measurements in serum, blood lead concentration (PbB), and arsenic in urine, and 557 completed several cognitive performance tests. Linear and logistic regression adjusted for hemoglobin concentration, PbB, and sociodemographic confounders showed a significant inverse association between urine arsenic concentration and Visual-Spatial Abilities with Figure Design, the Peabody Picture Vocabulary Test, the WISC-RM Digit Span subscale area, Visual Search, and Letter Sequencing Tests. It was concluded that arsenic contamination can affect children's cognitive development independent of any effect of lead (Rosado et al, 2007).

a) A decrease in intellectual function, as measured by a number of different neuropsychiatric tests including the Wechsler Intelligence Scale for Children, the Primary Scale of Intelligence, and the Total Sentence Recall test, has been reported in children following recent exposures to arsenic in drinking water and in food (vonEhrenstein et al, 2007; Wasserman et al, 2007).

a) CASE REPORT: A 54-year-old woman presented with worsening alopecia and memory loss. She also experienced diarrhea, nausea, vomiting, fatigue, a erythematous rash bilaterally on her lower extremities, and onycholysis. A spot urine sample indicated an arsenic concentration of 83.6 mcg/g creatinine (normal less than 50 mcg/g creatinine). A review of the patient's medication history revealed that she had been taking kelp supplements for treatment of menopause (2 to 4 tablets/day for 1 year). Analysis of a kelp supplement sample showed an arsenic concentration of 8.5 mg/kg. Discontinuation of the supplements resulted in complete resolution of her symptoms. A repeat spot urine sample, obtained 2 months after the first urine sample, revealed an arsenic level of 25 mcg/L (normal 0 to 50 mcg/L) (Amster et al, 2007).

a) CASE REPORT: A 5-year-old child experienced itching, severe erythema, blisters, vomiting, fever, and seizures following dermal application, from neck to toe, of an isopropyl solution that contained arsenic 30% instead of the prescribed benzyl benzoate 25% for treatment of scabies. With symptomatic and supportive therapy, the patient recovered and was discharged 4 days postadmission (Majid Cheraghali et al, 2007).

a) Early symptoms within hours following significant exposure to arsenic include abdominal pain, nausea, vomiting, profuse bloody or watery diarrhea (sometimes described as "rice water-like") (Cox & Orledge, 2011; Roth et al, 2011; Majid Cheraghali et al, 2007; Lai et al, 2005; Tsuji et al, 2004; Bartolome et al, 1999; Brayer et al, 1997; Moore et al, 1994a; Quatrehomme et al, 1992), pain in the extremities and muscles, weakness, and flushing of the skin. A sensation of burning and dryness of the oral and nasal cavities may occur.
b) Stool or emesis may have a garlic-like odor (Lee et al, 1995).
c) Hematemesis may develop with severe poisoning (Lai et al, 2005).
d) RETROSPECTIVE REVIEW: According to a retrospective review of 155 patients who ingested corrosive arsenic-based depilatory (CABD) agents, gastric pain, nausea and vomiting, and diarrhea were reported in 64.5%, 27%, and 20% of the patients, respectively. Analysis of CABD has shown that it consists of approximately 25% arsenic sulfide (Farzaneh et al, 2011).

a) Hepatocellular injury may occur after severe acute arsenic poisoning but is not common (Lai et al, 2005; ACGIH, 1991; Donofrio et al, 1987a). Mitotic activity of hepatocytes may be a common postmortem finding of arsenic poisoning (Mackell et al, 1985).
b) Hepatomegaly was reported in 61 infants who ingested dried milk powder contaminated with arsenic (Dakeishi et al, 2006).
c) CHRONIC TOXICITY

a) Mildly elevated AST concentrations (64 to 238 units/L) were reported in 5 of 7 teenagers (ages ranging from 15 to 18 years) who unintentionally ingested an unknown amount of herbicide containing monosodium methylarsonate 24%, mistakenly used as cooking oil. The AST concentrations peaked 3 days postingestion and normalized within 2 weeks (Cox & Orledge, 2011).

a) CASE REPORT: A 4-year-old child presented with abdominal pain and vomiting after ingesting an unknown amount of a chromated copper arsenate wood preservative containing 13.3% chromium, 7.8% copper, and 11.3% arsenic. Severe chemical burns were observed with an upper esophagogastroduodenal endoscopy. Fulminant liver and kidney failure were reported the next day. Due to hepatic encephalopathy, intubation and mechanical ventilation were necessary. The patient's initial blood arsenic concentration, obtained 3 days post-ingestion, was 206 mcg/L. Sodium 2,3-dimercaptopropane-1-sulfonate was administered intravenously in order to increase the urinary excretion of arsenic; however, liver transplantation was considered the only viable option. In order to extract as much as possible the amount of protein and erythrocyte-bound arsenic and minimize the risk of toxicity to the transplanted liver, plasmapheresis and erythrocyte apheresis were performed, however, the blood arsenic concentration could not be reduced by plasmapheresis and was only reduced by 11% with erythrocyte apheresis. Liver transplantation was successful and the patient recovered uneventfully (Breuer et al, 2015).

a) Oliguria, anuria, hematuria, proteinuria (Majid Cheraghali et al, 2007; Schoolmeester & White, 1980; Zaloga et al, 1970), acute tubular necrosis, renal failure have occurred following acute arsenic exposure (Breuer et al, 2015; Lai et al, 2005; Bartolome et al, 1999; Moore et al, 1994a; Vaziri et al, 1980; Giberson et al, 1976), and chronic renal insufficiency from cortical necrosis has been described (Gerhardt et al, 1978).
b) A prospective study, involving 100 arsenic-exposed subjects, showed an increased incidence in hematuria, urinary ketones, and urinary bilirubin in subjects exposed to arsenic concentration of 50 to 150 mcg/L as compared with those subjects exposed to arsenic concentrations less than 50 mcg/L. It is suggested that these urinary effect parameters may be useful as biomarkers of arsenic-induced renal injury; however further studies are warranted (Dalal et al, 2008).

a) CHRONIC EXPOSURE: A study was conducted to determine the association between arsenic exposure and erectile dysfunction and involved sending questionnaires to 2 groups of men. The first group consisted of 66 men who were at least 50 years of age and living in an arsenic-endemic area in Taiwan. The second group consisted of 111 men who were at least 50 years of age and living in a non-arsenic-endemic area. The questionnaire included standardized questions regarding demographics, lifestyle factors, and disease records, as well as an International Index of Erectile Function (ILEF-5) questionnaire used to measure the level of erectile function in each participant. The results of the study showed that the prevalence of erectile dysfunction (ED) was greater in the arsenic-endemic area (83.3%) as compared with the non-arsenic-endemic area (66.7%). The odds ratio (OR) in the greater than 50 parts per billion (ppb) arsenic-exposed group was 3.4 (95% CI, 1.1 to 10.3), indicating a significant risk of ED in those subjects as compared with those individuals with exposure to arsenic at a concentration of 50 ppb or less, and the risk of developing severe ED (ILEF of 7 or greater) was also significantly higher in the greater than 50 ppb group with an OR of 7.5 (95% CI, 1.8 to 30.9) after adjusting for free testosterone and other risk factors of ED (Hsieh et al, 2008).

a) Acute hemolysis may occur after acute arsenic poisoning (Kyle & Pease, 1965). It is usually Coombs negative; abnormalities of developing normoblasts are also common (Ringenberg et al, 1988).

a) CHRONIC EXPOSURE: A 51-year-old woman developed severe Coombs-negative intravascular hemolytic anemia with hemosiderinuria after long-term ingestion of a traditional Chinese medicine containing arsenic. Urine arsenic level was elevated. She was treated with red cell exchange without sequelae (Lee et al, 2004).

a) Arsenic can disturb erythropoiesis and myelopoiesis (OSHA, 1988). After either acute or chronic arsenic exposure, pancytopenia may be seen (Rezuke et al, 1991; Kyle & Pease, 1965; Kjeldsberg & Ward, 1972; Bartolome et al, 1999). However, isolated anemia may also be seen.
b) The anemia is usually normochromic and normocytic but may be hypochromic and microcytic (Kyle & Pease, 1965).
c) Bone marrow aspirate may demonstrate pronounced erythroid hyperplasia similar to that seen with pernicious anemia (Selzer & Ancel, 1983).
d) Basophilic stippling and rouleau formation of red cells may also be seen (Kyle & Pease, 1965).

a) CHRONIC TOXICITY: Aplastic anemia and acute myelogenous leukemia have been described after chronic arsenic exposure (Kjeldsberg & Ward, 1972).

a) ACUTE: Decreases in the hemoglobin and hematocrit values were the only sequelae possibly associated with an acute ingestion of approximately 1.2 grams arsenic as sodium arsenate in a 44-year-old woman (Chan & Matthews, 1990).
b) CHRONIC: Anemia has also been reported after chronic arsenic exposure (Rahman et al, 2001; Guha Mazumder et al, 1992).

a) CASE REPORT/CHRONIC EXPOSURE: A patient presented with macrocytosis and peripheral neuropathy but without anemia after chronic exposure to an arsenical pesticide (Heaven et al, 1994).

a) CASE REPORT: Leukopenia and thrombocytopenia have been reported following use of an arsenic-containing homeopathic preparation (Chakraborti et al, 2003).

a) Leukopenia was reported in 3 patients following dermal application, from neck to toe, of an isopropyl alcohol solution that contained arsenic 30% instead of the prescribed benzyl benzoate 25% for the treatment of scabies (Majid Cheraghali et al, 2007).

a) A 4-month-old developed evidence of disseminated intravascular coagulation within 11.5 hours of ingesting arsenic. He died 36 hours after ingestion despite aggressive chelation and resuscitation(Lai et al, 2005).

a) IN VITRO: Tests of human whole blood lymphocytes exposed to arsenite and arsenate in concentrations similar to those found in the blood of exposed humans revealed a dose-related inhibition of proliferation (Gonsebatt et al, 1992).

a) Skin findings after either acute or chronic arsenic poisoning may include flushing, diaphoresis, diffuse pigmentation, hyperkeratosis of palms and/or soles, peripheral edema, hyperpigmentation, hypopigmentation, leuko-melanoderma, brawny desquamation, and exfoliative dermatitis (Dakeishi et al, 2006; Tsuji et al, 2004; Ahasan, 2001; Huang et al, 1998a; Hutton & Christians, 1983; Schoolmeester & White, 1980; Zaloga et al, 1970; Heyman et al, 1956) .
b) ENDEMIC ARSENISM: Outbreaks of arsenic poisoning from water are common in the West Bengal and Bangladesh countries, and it was found that clinical symptoms often did not manifest until 6 months to 10 years after exposure. The first signs and symptoms of chronic exposure were related to dermatologic changes. Arsenical skin lesions included melanokeratosis, diffuse melanosis, spotted melanosis (raindrop pigmentation), leukomelanosis, and keratosis. Minor dermatological changes included buccal mucous membrane pigmentation, nonpitting edema, and red eyes (without signs or symptoms of inflammation) (Mukherjee et al, 2005; Rahman et al, 2001).
c) INCIDENCE: In a review of 648 cases of patients with cutaneous lesions, 17 (2.6%) had cutaneous lesions associated with long-term arsenic exposure. Of those, 15 patients (88%) had asthma, of whom 14 (93%) ingested Chinese proprietary medicines which contained inorganic arsenic and the remaining patients had a history of ingesting well water contaminated with arsenic (Wong et al, 1998).
d) CASE REPORT: A 54-year-old woman presented with worsening alopecia and memory loss. She also experienced diarrhea, nausea, vomiting, fatigue, an erythematous rash bilaterally on her lower extremities, and onycholysis. A spot urine sample indicated an arsenic concentration of 83.6 mcg/g creatinine (normal less than 50 mcg/g creatinine). A review of the patient's medication history revealed that she had been taking kelp supplements for treatment of menopause (2 to 4 tablets/day for 1 year). Analysis of a kelp supplement sample showed an arsenic concentration of 8.5 mg/kg. Discontinuation of the supplements resulted in complete resolution of her symptoms. A repeat spot urine sample, obtained 2 months after the first urine sample, revealed an arsenic level of 25 mcg/L (normal 0 to 50 mcg/L) (Amster et al, 2007).
e) CASE REPORT: A 73-year-old man, from Thailand, presented with several dermal lesions, including basal cell carcinoma at the lower abdomen, arsenical keratoses on his left forearm and knee, and punctate palmoplantar keratosis. Analysis of his pubic hair and nails revealed elevated arsenic concentrations of 4.76 and 3.29 mcg/g, respectively (normal less than 3 mcg/g). The lesions resolved following treatment with imiquimod 5% cream. A review of the patient's history revealed that he had long-term exposure to Thai proprietary medicines, presumably containing arsenic (Boonchai, 2006).

a) Sixty-seven people became ill after eating arsenic-laced curry at a festival in Japan. Four of the victims died. During the acute stage of the poisoning, 56% of the patients developed dermatologic signs and symptoms. Conjunctival hemorrhage was observed in 15 patients, facial edema in 13 patients, acral desquamation in 11 patients, maculopapular eruptions in the intertriginous areas in 8 patients, transient flushing erythema in 5 patients, and herpesvirus infection in 3 patients. Histopathological examination of the maculopapular eruptions revealed moderate to marked perivascular infiltration with endothelial swelling (Uede & Furukawa, 2003).

a) CHRONIC EXPOSURE: Basal cell and squamous cell cancers of the skin may also be seen years after exposure (Ahasan, 2001; Sass et al, 1993; Renwick et al, 1981; Wagner et al, 1979; Jackson & Grainge, 1975). Merkel cell carcinoma has also been associated with chronic arsenism in a small number of patients (Lien et al, 1999).

a) Melanosis and keratosis have been reported following use of arsenic-containing homeopathic preparations (Chakraborti et al, 2003; Tsuji et al, 2004).

a) Transverse white striae of the nails (Mees lines) may be seen after acute or chronic exposure (Duenas-Laita et al, 2005; Sass et al, 1993). Mees lines commonly take 5 weeks to appear above the cuticle and advance 1 mm per week afterwards, allowing the approximation of the time of acute exposure (Heyman et al, 1956).

a) Shingles have been reported following arsenic poisoning (Jenkins, 1966).

a) SENSITIZATION: Arsenic pentoxide can cause contact dermatitis (OSHA, 1988).
b) CASE REPORT: The organic arsenical pesticide cacodylic acid has caused airborne contact dermatitis (Bourrain et al, 1998).

a) CASE REPORT: A 54-year-old woman presented with worsening alopecia and memory loss. She also experienced diarrhea, nausea, vomiting, fatigue, an erythematous rash bilaterally on her lower extremities, and onycholysis. A spot urine sample indicated an arsenic concentration of 83.6 mcg/g creatinine (normal less than 50 mcg/g creatinine). A review of the patient's medication history revealed that she had been taking kelp supplements for treatment of menopause (2 to 4 tablets/day for 1 year). Analysis of a kelp supplement sample showed an arsenic concentration of 8.5 mg/kg. Discontinuation of the supplements resulted in complete resolution of her symptoms. A repeat spot urine sample, obtained 2 months after the first urine sample, revealed an arsenic level of 25 mcg/L (normal 0 to 50 mcg/L) (Amster et al, 2007).

a) CASE SERIES: Seven patients developed dermal toxicity, including pruritus, severe rash, burns, blisters, and bullae, following dermal application, from neck to toe, of an isopropyl solution containing arsenic 30% instead of the prescribed benzyl benzoate 25% for the treatment of scabies. Three patients, including a pregnant woman (38 weeks gestation) subsequently developed hypotension and respiratory distress and died within 72 hours following application of the solution. The other 4 patients received symptomatic and supportive therapy and were discharged 4 to 5 days postadmission (Majid Cheraghali et al, 2007).
b) CASE REPORT: Severe chemical burns were reported, following an upper esophagogastroduodenal endoscopy, in a 4-year-old boy who ingested an unknown amount of a chromated copper arsenate (CCA) wood preservative, containing 13.3% chromium, 7.8% copper, and 11.3% arsenic (Breuer et al, 2015).

a) Disruption of the normal oxidative intermyofibrillar network (involving type I fibers), perifascicular hypercontracted fibers, increased vacuolization in approximately 30% of fibers, abnormally enlarged mitochondria with loss of cristae, and abundant lipid vacuoles separating the myofibrils has been found on muscle biopsy (Fernandez-Sola et al, 1991).
b) CASE REPORT: Mild rhabdomyolysis (CPK 1200 units/L) developed in a 21-year-old man who ingested 4 grams of arsenic (Moore et al, 1994a).

a) CHRONIC TOXICITY: Myalgia and myopathy have been reported following chronic exposure and are considered rare events (Rahman et al, 2001).

a) CHRONIC EXPOSURE: A dose-related increase in prevalence of diabetes mellitus has been seen in residents of areas where arsenism is hyperendemic and in workers exposed to arsenic at a copper smelter (Coronado-Gonzalez et al, 2007; Rahman et al, 1998; Rahman & Axelson, 1995; Lai et al, 1994). However, there was no increased incidence of diabetes mellitus among Swedish art glass workers with chronic arsenic exposure (Rahman et al, 1996)
b) RETROSPECTIVE ANALYSIS: Data from the Canadian Health Measures Survey was collected from 2007 to 2009 to evaluate the association between arsenic exposure (based on urinary arsenic concentration) and the prevalence of type 2 diabetes in adults. The analysis included 3151 participants (ages 20 to 79 years) and were divided into 3 groups: prediabetes (n=831; fasting glucose level between 100 and 125 mg/dL or hemoglobin A1c (HbA1c) 5.7% and 6.4%), type 2 diabetes (n=225; fasting glucose level 126 mg/dL or greater or HbA1c 6.5% or greater), and the control group (n=2054; not diabetic or prediabetic). There was no data on 41 patients. According to urinary arsenic quartiles (less than 5.71 mcg/L, 5.71 to 11.20 mcg/L, 11.21 to 22.98 mcg/L, and 22.99 mcg/L and greater), there is a 1.8-fold higher risk for type 2 diabetes in patients at the highest urinary arsenic quartile (22.99 mcg/L or greater) than for those patients at the lowest urinary arsenic quartile (less than 5.71 mcg/L), after adjusting for age and gender, diabetes risk factors, urinary creatinine, and seafood consumption. Similarly, there is 2.1-fold higher risk for prediabetes in patients at the highest urinary arsenic quartile than for those patients at the lowest urinary arsenic quartile, indicating a positive association between arsenic exposure and the prevalence of prediabetes and type 2 diabetes. However, causal inference is limited due to the cross-sectional design of the study and the absence of long-term assessment of arsenic exposure (Feseke et al, 2015).

a) Hyperglycemia was observed following IV infusion of arsenic in the treatment of leukemia (Tsuji et al, 2004).

a) A 4-month-old infant developed hyperglycemia (serum glucose 286 mg/dL 6 hours after ingestion) after a lethal arsenic ingestion (Lai et al, 2005).

a) Arsenic (inorganic) is teratogenic in rodents at doses of 20 mg/kg or greater.
b) In mice, the combination of maternal restraint stress and arsenic (in the form of sodium arsenate at 20 mg/kg IP on day 9) produced roughly twice the incidence of exencephaly than either agent alone (Rasco & Hood, 1994).
c) There have been many studies on the reproductive effects of arsenic and its compounds in laboratory animals. Typically they can cause birth defects at high doses which may have been toxic to the mothers. Birth defects have been found in chickens (sodium ortho arsenate) (Ridgway & Karnofsky, 1952), in hamsters (disodium arsenate) (Ferm, 1971), in mice (sodium arsenate and sodium arsenite) (Baxley, 1981; Hood & Bishop, 1972), and in rats (sodium arsenate) (Beaudoin, 1974).
d) IP injection of 40 mg/kg arsenate on days 7 and 8 of gestation induced 90 to 100 percent neural tube defects in the susceptible strain LM Bc of mice. Analysis of gene expression showed increased transcription of bcl-2 and p53 on day 9, compared with controls. This result suggests that arsenic induces neural tube defects in mice via inhibition of cell proliferation, rather than by inducing apoptosis. Whether or not arsenic can induce neural tube defects in humans is controversial (Wlodarczyk et al, 1996).
e) Generally the maximum activity for inducing birth defects in animals was at doses which were equally toxic to the mothers (OTA, 1985). Arsenite was more active than arsenate, but both were less active orally than when injected (OTA, 1985).
f) The teratogenicity of arsenate was antagonized by sodium selenite in hamsters (Barlow & Sullivan, 1982), a finding consistent with the general antagonism between these two families of compounds. Heat was synergistic with arsenic in hamsters. Chelating agents which are known to remove arsenic from the body, such as BAL (2,3-dimercaptopropanol), reduced the teratogenicity of sodium arsenate in mice (Barlow & Sullivan, 1982).

a) An increased number of spontaneous abortions, preterm births, and low birth weight infants occurred in women who were exposed to arsenic in drinking water during pregnancy at concentrations ranging from 284 to 1474 mcg/L (Mukherjee et al, 2005).
b) A systematic review and meta-analysis found that high levels of arsenic in the groundwater is associated with an increased risk of spontaneous abortion, stillbirth, neonatal mortality, and infant mortality, as well as a significant reduction in birth weight; the association between arsenic exposure and preterm delivery was inconclusive. Analysis of data from 6 studies on spontaneous abortion showed that populations exposed to high arsenic concentrations (greater than 50 mcg/L) in groundwater had a significant nearly 2-fold increased risk of spontaneous abortion, while the findings for populations exposed to low to moderate levels of arsenic in groundwater or tap water were inconclusive. Analysis of data from 8 studies showed that populations exposed to high arsenic levels in groundwater had a significant 77% increased risk of stillbirth; 1 study conducted in a population with low-to-moderate arsenic exposure (less than 50 mcg/L) found a significant 4 times increased risk of stillbirth. Analysis of data from 5 studies examining neonatal mortality in populations exposed to high arsenic levels in groundwater found a significant 51% increased risk of neonatal mortality and 7 studies on infant mortality showed a significant 35% increased risk of infant mortality with high arsenic exposure. Analysis of data from 4 studies on birth weight showed that environmental arsenic exposure was associated with a significant reduction in birth weight of 53.2 g. The causal association between arsenic exposure and adverse pregnancy outcomes, including infant mortality, is limited by the number of studies on dose response (Quansah et al, 2015).

a) Acute ingestion of arsenic in a female with a 30-week pregnancy has been reported to result in the death of the infant born 4 days after the poisoning (Lugo et al, 1969). The child apparently died of hyaline membrane disease but did have elevated tissue levels of arsenic. It seems apparent that arsenic can cross the placenta.
b) Associations between arsenic exposure in populations living near or working in smelters and an increased incidence of spontaneous abortions and stillbirths have been reported, but the studies are difficult to interpret because multiple chemical exposures were involved (Golub et al, 1998) Sholot et al, 1996).
c) There was an increased incidence of stillbirths in an Hispanic population in central Texas where arsenical agricultural products had been produced for 60 years (Ihrig et al, 1998).
d) Maternal exposure, during pregnancy, to drinking water contaminated with arsenic, has resulted in an increased risk of infant death and fetal loss. The risk of infant death, in particular, appeared to be significantly directly proportional to the amount of exposure to arsenic during pregnancy (Rahman et al, 2007).

a) Early chelation therapy is thought to have abrogated the toxic effect of an acute arsenic ingestion in a woman and her 20-week fetus (Daya et al, 1989).

a) In a study of women living near a copper smelter, placental arsenic levels increased with increasing arsenic levels in the environment (Tabacova et al, 1994). Higher levels of arsenic exposure were associated with a lower percentage of reduced compared with total glutathione levels in maternal and cord blood, suggesting reduced antioxidant protection.
b) A similar study did not find increased arsenic body burdens in pregnant Swedish women (Jakobsson-Lagerkvist et al, 1993).

a) A prospective cohort study was conducted, involving two groups of pregnant women. The first group was exposed to drinking water arsenic levels of 40 mcg/L and the second group was exposed to drinking water arsenic levels of less than 1 mcg/L . During the first trimester of pregnancy, anemia, as measured by at least one hemoglobin level, appeared to occur more frequently in the high arsenic level-exposed group as compared with the low arsenic level-exposed group (10.3% (n=242) versus 6.9% (n=248)) and also appeared to be more prevalent as the pregnancy progressed to the third trimester (46% (n=274) versus 17.5% (n=240)) (Hopenhayn et al, 2006). During pregnancy, the most common type of anemia is primarily due to iron or folate deficiency. In this study, analysis of 150 women demonstrated that serum transferrin receptor and folate measurements did not differ between the two groups; therefore, the differences in anemia rates between the two groups are most likely not a result of iron or folate deficiency, but may be associated with an increase in arsenic intake.

a) A prospective cohort study, involving 52 pregnant women, was conducted to determine an association between arsenic exposure and birth weight. The women were recruited from a region within Bangladesh that was highly contaminated with arsenic. Maternal hair, toenails, and drinking water samples were collected at the first prenatal visit and within 2 weeks after birth. Comparison of maternal and newborn arsenic concentrations showed that there was a significant correlation between maternal hair samples taken at the first prenatal visit and newborn hair samples (0.32; p=0.04), although there was no significant correlation between maternal hair samples taken within 2 weeks after birth and newborn hair samples. There was also no significant correlation between maternal nail samples taken at the first prenatal visit or within 2 weeks after birth and newborn nail samples. However, linear regression analyses demonstrated a significant negative association between maternal hair arsenic concentrations at the first prenatal visit and newborn birth weight (-193.5 +/-90 g; p=0.04); for every 1 mcg/g increase in arsenic, the birthweight decreased by 194 grams (Huyck et al, 2007).

a) In a population of women living in an area of the Argentinean Andes where drinking water contains about 200 mcg/L of arsenic, the average breast milk arsenic concentration was 2.3 mcg/kg fresh weight (range: 0.83 to 7.6 mcg/kg). Urinary arsenic concentrations in 2 nursing infants were low (17 and 47 mcg/L), indicating that inorganic arsenic is not secreted to any significant extent in breast milk, as maternal blood and urine arsenic levels were 10 and 320 mcg/L, respectively (Concha et al, 1998).
b) Arsenic is transferred across the placenta and into breast milk (Barlow & Sullivan, 1982). There may be some risk to nursing infants of mothers exposed to arsenic from evidence in Japanese children who drank arsenic-contaminated powdered milk and who may have suffered problems in later brain development (Barlow & Sullivan, 1982).

a) Listed as: Arsenic and inorganic arsenic compounds
b) Carcinogen Rating: 1

a) Another study found a dose response relationship between the amount of arsenic in well water and the mortality rate from kidney, bladder, liver and lung cancer (Chen et al, 1992).
b) Another study of populations in Taiwan exposed to high concentrations of arsenic in artesian well water found a dose response relationship between the estimated cumulative arsenic exposure and the incidence of lung and bladder cancers and of all cancers combined (Chiou et al, 1995). Patients with Blackfoot disease had an increased risk of cancer.

a) CASE SERIES: In a review of 648 patients with cutaneous lesions associated with long-term arsenic exposure, 7 patients developed squamous cell carcinoma (SCC). One patient had a history of carcinoma of the larynx before skin lesions appeared. The authors observed the following risk factors: ingestion of arsenic at an older age and were more likely to have palmar arsenical keratoses compared with those without SCC (Wong et al, 1998).

a) Concentrations of arsenic in 24-hour urine in a male agricultural worker exposed to arsenic from the immersion of his foot in a storage container of concentrated arsenic acid ranged from a high of 2,500 mcg to a low of 160 mcg (McWilliams, 1989).

a) Mussels gave significant elevations of urinary monomethyl- and dimethylarsonic acid, while ray, cod, and place did not (Buchet et al, 1994).
b) In order to accurately determine urinary arsenic levels, patients should abstain from consuming seafood for 72 to 96 hours prior to urine collection. Also, with samples that contain elevated total arsenic concentrations, laboratories should perform speciation (determination of arsenic as organic or inorganic) prior to reporting results (Kales et al, 2006).

a) HAIR/NAIL: Arsenic has been demonstrated in hair and nails within hours after exposure (Lander et al, 1965). NOTE: Hair is continually exposed to the external environment and the presence of a chemical may not be indicative of inhalational or oral exposure.
b) Normal concentration of arsenic in hair and nails is less than 1 mg/kg (Baselt, 1997).
c) Many commercial laboratories performing hair analyses for consumers have not been shown to yield consistent and reliable results (Barrett, 1985).
d) If hair is sent for arsenic quantitation, pubic hair instead of scalp hair should be sent because of the possibility of scalp hair being contaminated with arsenic from the environment (Jenkins, 1966).
e) A comparison of the mean air arsenic concentrations of each occupational exposure group with corresponding arsenic levels in fingernails was highly correlated (Agahian et al, 1990).
f) In a Finnish population, hair arsenic content correlated well with chronic or past exposure to arsenic in drinking water. Hair arsenic concentration increased 0.1 mg/kg for each increase of 10 mcg/L of arsenic in drinking water or 10 to 20 mcg/day of arsenic intake (Kurttio et al, 1998).

a) Persons exposed to high levels of arsenic in drinking water had a significantly increased presence of micronuclei in exfoliated bladder cells, even when exposures were near the USA Maximum Contaminant Level (MCL) of 50 mcg of arsenic per liter of water (or 100 mcg in a 24-hour urine) (Moore et al, 1997; Rahman et al, 2001).

a) A sweat chloride test is a diagnostic test for cystic fibrosis. An elevated sweat chloride level will indicate dysfunction of the cystic fibrosis transmembrane conductance regulator (CFTR), which is a protein that acts as a chloride channel to regulate fluid transport in the lung and pancreas, as well as other organs. Cell culture studies have demonstrated that arsenic can also cause CFTR degradation.

a) CHRONIC TOXICITY: Other diagnostic studies which may be beneficial (based on a patient's clinical presentation) include: ultrasonography of the abdomen, upper gastrointestinal endoscopy, lung function tests, nerve conduction studies (Rahman et al, 2001).

a) Consider lavage more than 60 minutes after ingestion of sustained-release formulations and substances known to form bezoars or concretions.

a) SEIZURE CONTROL: Is mandatory prior to gastric lavage.
b) AIRWAY PROTECTION: Place patients in the head down left lateral decubitus position, with suction available. Patients with depressed mental status should be intubated with a cuffed endotracheal tube prior to lavage.

a) Use small aliquots of liquid. Lavage with 200 to 300 milliliters warm tap water (preferably 38 degrees Celsius) or saline per wash (in older children or adults) and 10 milliliters/kilogram body weight of normal saline in young children(Vale et al, 2004) and repeat until lavage return is clear.
b) The volume of lavage return should approximate amount of fluid given to avoid fluid-electrolyte imbalance.
c) CAUTION: Water should be avoided in young children because of the risk of electrolyte imbalance and water intoxication. Warm fluids avoid the risk of hypothermia in very young children and the elderly.

a) Complications of gastric lavage have included: aspiration pneumonia, hypoxia, hypercapnia, mechanical injury to the throat, esophagus, or stomach, fluid and electrolyte imbalance (Vale, 1997). Combative patients may be at greater risk for complications (Caravati et al, 2001).
b) Gastric lavage can cause significant morbidity; it should NOT be performed routinely in all poisoned patients (Vale, 1997).

a) Loss of airway protective reflexes or decreased level of consciousness if patient is not intubated, following ingestion of corrosive substances, hydrocarbons (high aspiration potential), patients at risk of hemorrhage or gastrointestinal perforation, or trivial or non-toxic ingestion.

a) WHOLE BOWEL IRRIGATION/INDICATIONS: Whole bowel irrigation with a polyethylene glycol balanced electrolyte solution appears to be a safe means of gastrointestinal decontamination. It is particularly useful when sustained release or enteric coated formulations, substances not adsorbed by activated charcoal, or substances known to form concretions or bezoars are involved in the overdose.
b) CONTRAINDICATIONS: This procedure should not be used in patients who are currently or are at risk for rapidly becoming obtunded, comatose, or seizing until the airway is secured by endotracheal intubation. Whole bowel irrigation should not be used in patients with bowel obstruction, bowel perforation, megacolon, ileus, uncontrolled vomiting, significant gastrointestinal bleeding, hemodynamic instability or inability to protect the airway (Tenenbein et al, 1987).
c) ADMINISTRATION: Polyethylene glycol balanced electrolyte solution (e.g. Colyte(R), Golytely(R)) is taken orally or by nasogastric tube. The patient should be seated and/or the head of the bed elevated to at least a 45 degree angle (Tenenbein et al, 1987). Optimum dose not established. ADULT: 2 liters initially followed by 1.5 to 2 liters per hour. CHILDREN 6 to 12 years: 1000 milliliters/hour. CHILDREN 9 months to 6 years: 500 milliliters/hour. Continue until rectal effluent is clear and there is no radiographic evidence of toxin in the gastrointestinal tract.
d) ADVERSE EFFECTS: Include nausea, vomiting, abdominal cramping, and bloating. Fluid and electrolyte status should be monitored, although severe fluid and electrolyte abnormalities have not been reported, minor electrolyte abnormalities may develop. Prolonged periods of irrigation may produce a mild metabolic acidosis. Patients with compromised airway protection are at risk for aspiration.

a) One study has reported no significant adsorption to activated charcoal, but specific quantities bound were not stated (Mitchell et al, 1989).
b) Sodium arsenite (0.65 millimolar) and sodium arsenate (1.7 millimolar) were NOT adsorbed to activated charcoal (in a ratio of 1:10) to any measurable extent in an aqueous acidic solution (simulated gastric juice) that was incubated at 37 degrees C for 30, 60, 120, and 240 minutes in an in vitro model (Al-Mahasneh QM & Rodgers GC, 1990).
c) Solutions incubated for 120 and 240 minutes at pH 10 to 12 (simulated intestinal juices) showed adsorption of 75% to 80% (Al-Mahasneh QM & Rodgers GC, 1990).

a) DIMERCAPROL/BAL IN OIL: INDICATIONS: Used for the treatment of mercury (inorganic and elemental), arsenic, and gold poisoning. It is also used in combination with Edetate Calcium Disodium injection to treat patients with severe lead poisoning (Prod Info BAL In Oil intramuscular injection, 2008). Dimercaprol is contraindicated in methyl mercury poisoning (Howland, 2002; Clarkson, 1990).
b) MILD ARSENIC OR GOLD POISONING: DOSE: 2.5 mg/kg 4 times daily for 2 days, 2 times on the third day, and once daily thereafter for 10 days. SEVERE ARSENIC OR GOLD POISONING: DOSE: 3 mg/kg every 4 hours for 2 days, 4 times on the third day, then twice daily thereafter for 10 days. Administered by deep intramuscular injection only (Prod Info BAL In Oil intramuscular injection, 2008).
c) MERCURY POISONING: DOSE: 5 mg/kg initially, then 2.5 mg/kg 1 or 2 times daily for 10 days. Administered by deep intramuscular injection only (Prod Info BAL In Oil intramuscular injection, 2008).
d) ACUTE LEAD ENCEPHALOPATHY: DOSE: 4 mg/kg is given alone in the first dose and thereafter at 4-hour intervals with Edetate Calcium Disodium injection administered at a separate site. For less severe poisoning, dimercaprol dose can be decreased to 3 mg/kg after the first dose. Administered by deep intramuscular injection only. Continue the treatment for 2 to 7 days depending on clinical response (Prod Info BAL In Oil intramuscular injection, 2008). Therapy is generally switched to a less toxic oral chelator as soon as tolerated.
e) ADVERSE EFFECTS: Common effects include pain at the injection site and fever (especially in children). Other effects include hypertension, tachycardia, nausea, vomiting, headache, burning sensations of the mouth and throat, a sensation of constriction in the throat, chest, or hands, conjunctivitis, lacrimation, salivation, tingling of the extremities, diaphoresis, abdominal pain, and anxiety. Dimercaprol injection contains peanut oil. Avoid in patients with peanut allergy (Prod Info BAL In Oil intramuscular injection, 2008). Adverse effects are dose related; they develop in 1% of patients receiving 2.5 mg/kg every 4 to 6 hours, 14% of patients receiving 4 mg/kg every 4 to 6 hours and 65% of patients receiving 5 mg/kg every 4 to 6 hours (Eagle & Magnuson, 1946).
f) PRECAUTIONS: It is generally contraindicated in patients with hepatic insufficiency, with the exception of postarsenical jaundice (Prod Info BAL In Oil intramuscular injection, 2008). May cause hemolysis in G6PD deficient patients. BAL metal chelate disassociates in acid environment; urinary alkalinization is usually recommended. Do not administer with iron therapy as BAL iron complex may cause vomiting (Howland, 2002).

a) CHILDREN: BAL has been reported to result in clinical improvement and decrease in hospital days in children poisoned with arsenic (Woody & Kometani, 1948). It has also been reported to effect complete recovery in a woman and her 20-week fetus after an acute ingestion of inorganic arsenic by the mother (Daya et al, 1989).
b) ANIMALS: BAL has been shown to reduce the organ deposition of arsenic in a rabbit model using subcutaneous injections of Lewisite at the LD10 and LD40 and 4 doses of BAL of 35 mg/kg each (Snider et al, 1990).

a) PEDIATRIC: Initial dose is 10 mg/kg or 350 mg/m(2) orally every 8 hours for 5 days (Prod Info CHEMET(R) oral capsules, 2011).
b) ADULT: Succimer is not FDA approved for use in adults, however it has been shown to be safe and effective when used to treat adults with poisoning from a variety of heavy metals (Fournier et al, 1988a). Initial dose is 10 mg/kg or 350 mg/m(2) orally every 8 hours for 5 days (Prod Info CHEMET(R) oral capsules, 2011).

a) The manufacturer recommends monitoring liver enzymes and complete blood count with differential and platelet count prior to the start of therapy and at least weekly during therapy (Prod Info CHEMET(R) oral capsules, 2011).
b) Succimer therapy did not worsen preexisting borderline abnormal liver enzyme levels in a prospective evaluation of 15 children with lead poisoning (Kuntzelman & Angle, 1992).

a) Succimer has been shown to have a safety ratio of 20 times greater than BAL. The total dosage of BAL is limited by its intrinsic toxicity, and the greater safety ratio of succimer allows for longer and more prolonged dosing of succimer (Inns & Rice, 1993).
b) CHRONIC ENVIRONMENTAL ARSENIC POISONING: In a randomized placebo-controlled clinical trial, succimer was NOT EFFICACIOUS in improving a clinical scoring system, skin lesions, or various biochemical laboratory measurements when administered to patients in India with chronic arsenic poisoning from drinking contaminated groundwater (Guha Mazumder et al, 1998).
c) CASE REPORT: In a patient treated with succimer (30 mg/kg/day for 5 days) for long-term ingestion of arsenic, plasma concentrations were unchanged after treatment and renal excretion of arsenic increased 1.5-fold (Fournier et al, 1988).
d) CASE REPORT: A 39-year-old woman developed progressive weakness and peripheral neuropathy leading to quadriplegia and requiring mechanical ventilation following an unknown type of exposure to arsenic. Analysis of her serum and urine revealed elevated arsenic (As) concentrations (290 mcg As/kg [normal less than 2 mcg/kg] and 2000 mcg As/L [normal less than 10 mcg/L], respectively). Despite succimer therapy, 10 mg/kg administered 3 times daily for a total of 33 days over a 45-day period, the patient only showed slow clinical improvement with continued residual paresthesias and weakness in her hands and distal lower extremities 5 years following intoxication(Stenehjem et al, 2007).
e) CASE REPORT: An intravenous preparation of succimer was used to treat a 26-year-old man with multi organ system failure after acute trivalent arsenic overdose. A solution was prepared with 1.6 grams of succimer diluted in 50 mL of sterile water and titrated with 10 N NaOH to pH 7.2 to 7.4 and filtered through a 0.22 micron filter. The solution was administered in 500 mL of 0.9% saline solution as an infusion over 1 hour at a dose of 20 mg/kg/day for 5 days followed by 10 mg/kg/day. The succimer solution was also given via peritoneal dialysis, 20 milligrams/liter of dialysate with 12 L exchanged daily for 5 days (Hantson et al, 1995).

a) 1 to 1.5 g/day given orally in 4 divided doses (Nelson, 2011).

a) 15 to 30 mg/kg/day in 3 to 4 divided doses. Initially, a small dose may be given to minimize side effects and then increased gradually (eg, 25% of the desired dose in week 1, 50% in week 2, and the full dose by week 3) (Caravati, 2004; Prod Info DEPEN(R) titratable oral tablets, 2009).

a) SERIOUS ADVERSE EFFECTS: Nephrotic syndrome, hypersensitivity reactions, leukopenia, thrombocytopenia, aplastic anemia, agranulocytosis, cholestatic hepatitis, and various autoimmune responses (Prod Info DEPEN(R) titratable oral tablets, 2009; Feehally et al, 1987; Kay, 1986).

a) CHILDREN: D-penicillamine has been successfully used in acute arsenic poisoning in children (Peterson & Rumack, 1977; Kuruvilla et al, 1975; Watson et al, 1981).
b) ANIMALS: In an experimental animal model, mice and guinea pigs were injected subcutaneously with 8.4 milligrams/kilogram arsenic trioxide and 30 minutes later 0.7 millimole/kilogram (104.5 milligrams/kilogram) of d-penicillamine was administered. D-penicillamine was found to lack effectiveness in this model (Kreppel et al, 1989).

a) SUMMARY: Unithiol (DMPS) is used in Europe as a chelating agent for heavy metal poisonings (Kruszewska et al, 1996). It appears to be an effective chelator of arsenic in experimental animals (Inns et al, 1990; Kreppel et al, 1990; Aposhian et al, 1984; Hsu et al, 1983; Aposhian et al, 1981) and humans (Goebel et al, 1990; Kew et al, 1993; Moore et al, 1994a; Zilker et al, 1999).
b) INTRAVENOUS DOSING: The dosing regimen depends on the severity of poisoning (Prod Info DIMAVAL(R) IV, IM injection, 2004). See UNITHIOL MANAGEMENT for further information.
c) DMPS/INDICATIONS: Chelating agent for heavy metal toxicities associated with arsenic, bismuth, copper, lead and mercury (Blanusa et al, 2005).
d) DMPS/DOSING
e) SOURCES
f) CASE SERIES/CHRONIC TOXICITY: In a small (n=10) prospective, randomized, placebo-controlled, single-blind study of untreated patients with chronic arsenicosis following groundwater contamination, unithiol treatment was found to improve some clinical parameters (i.e., weakness, pigmentation and lung disease), and to increase total urinary excretion of arsenic. The treatment dose was 100 mg unithiol (orally) given four times per day for 1 week and repeated in the 3rd, 5th and 7th week of the study (Mazumder et al, 2001).
g) CASE REPORT: A 33-year-old woman developed arsenic poisoning as evidenced by a 1.5 year-history of peripheral neuropathy, pancytopenia, ventricular tachycardia, skin rash, and nail changes. Laboratory data revealed a blood arsenic concentration of 5.6 mcg/dL. Despite administration of succimer, the neuropathy continued to progress to facial paresis, severe weakness in all 4 extremities, and respiratory failure. Succimer was then discontinued, and unithiol was initiated at a dosage regimen of 250 mg IV every 4 hours. Twenty-four hours after beginning unithiol therapy, urinary excretion of arsenic increased to 300 mcg/L from a baseline of 101 mcg/L. Within 48 hours, the patient's neuropathy improved and, 10 days later, she was discharged in a wheelchair. At her 3-month follow-up, the patient continued to have residual paresthesias and weakness in her lower extremities, but she was able to walk without assistance, and by 1 year she was back at work with mild residual weakness and paresthesiae(Wax & Thornton, 2000a).

a) DOSE: Begin at 5 micrograms per kilogram per minute progressing in 5 micrograms per kilogram per minute increments as needed (Prod Info dopamine hcl, 5% dextrose IV injection, 2004). If hypotension persists, dopamine may need to be discontinued and a more potent vasoconstrictor (eg, norepinephrine) should be considered (Prod Info dopamine hcl, 5% dextrose IV injection, 2004).
b) CAUTION: If ventricular dysrhythmias occur, decrease rate of administration (Prod Info dopamine hcl, 5% dextrose IV injection, 2004). Extravasation may cause local tissue necrosis, administration through a central venous catheter is preferred (Prod Info dopamine hcl, 5% dextrose IV injection, 2004).

a) PREPARATION: 4 milligrams (1 amp) added to 1000 milliliters of diluent provides a concentration of 4 micrograms/milliliter of norepinephrine base. Norepinephrine bitartrate should be mixed in dextrose solutions (dextrose 5% in water, dextrose 5% in saline) since dextrose-containing solutions protect against excessive oxidation and subsequent potency loss. Administration in saline alone is not recommended (Prod Info norepinephrine bitartrate injection, 2005).
b) DOSE

a) Obtain an ECG, institute continuous cardiac monitoring and administer oxygen. Evaluate for hypoxia, acidosis, and electrolyte disorders (particularly hypokalemia, hypocalcemia, and hypomagnesemia). Lidocaine and amiodarone are generally first line agents for stable monomorphic ventricular tachycardia, particularly in patients with underlying impaired cardiac function. Amiodarone should be used with caution if a substance that prolongs the QT interval and/or causes torsades de pointes is involved in the overdose. Unstable rhythms require immediate cardioversion.

a) LIDOCAINE/INDICATIONS
b) LIDOCAINE/DOSE
c) LIDOCAINE/MAJOR ADVERSE REACTIONS
d) LIDOCAINE/MONITORING PARAMETERS

a) AMIODARONE/INDICATIONS
b) AMIODARONE/ADULT DOSE
c) AMIODARONE/PEDIATRIC DOSE
d) ADVERSE EFFECTS

a) Withdraw the causative agent. Hemodynamically unstable patients with Torsades de pointes (TdP) require electrical cardioversion. Emergent treatment with magnesium (first-line agent) or atrial overdrive pacing is indicated. Detect and correct underlying electrolyte abnormalities (ie, hypomagnesemia, hypokalemia, hypocalcemia). Correct hypoxia, if present (Drew et al, 2010; Neumar et al, 2010; Keren et al, 1981; Smith & Gallagher, 1980).
b) Polymorphic VT associated with acquired long QT syndrome may be treated with IV magnesium. Overdrive pacing or isoproterenol may be successful in terminating TdP, particularly when accompanied by bradycardia or if TdP appears to be precipitated by pauses in rhythm (Neumar et al, 2010). In patients with polymorphic VT with a normal QT interval, magnesium is unlikely to be effective (Link et al, 2015).

a) Magnesium is recommended (first-line agent) for the prevention and treatment of drug-induced torsades de pointes (TdP) even if the serum magnesium concentration is normal. QTc intervals greater than 500 milliseconds after a potential drug overdose may correlate with the development of TdP (Charlton et al, 2010; Drew et al, 2010). ADULT DOSE: No clearly established guidelines exist; an optimal dosing regimen has not been established. Administer 1 to 2 grams diluted in 10 milliliters D5W IV/IO over 15 minutes (Neumar et al, 2010). Followed if needed by a second 2 gram bolus and an infusion of 0.5 to 1 gram (4 to 8 mEq) per hour in patients not responding to the initial bolus or with recurrence of dysrhythmias (American Heart Association, 2005; Perticone et al, 1997). Rate of infusion may be increased if dysrhythmias recur. For persistent refractory dysrhythmias, a continuous infusion of up to 3 to 10 milligrams/minute in adults may be given (Charlton et al, 2010).
b) PEDIATRIC DOSE: 25 to 50 milligrams/kilogram diluted to 10 milligrams/milliliter for intravenous infusion over 5 to 15 minutes up to 2 g (Charlton et al, 2010).
c) PRECAUTIONS: Use with caution in patients with renal insufficiency.
d) MAJOR ADVERSE EFFECTS: High doses may cause hypotension, respiratory depression, and CNS toxicity (Neumar et al, 2010). Toxicity may be observed at magnesium levels of 3.5 to 4.0 mEq/L or greater (Charlton et al, 2010).
e) MONITORING PARAMETERS: Monitor heart rate and rhythm, blood pressure, respiratory rate, motor strength, deep tendon reflexes, serum magnesium, phosphorus, and calcium concentrations (Prod Info magnesium sulfate heptahydrate IV, IM injection, solution, 2009).

a) Institute electrical overdrive pacing at a rate of 130 to 150 beats per minute, and decrease as tolerated. Rates of 100 to 120 beats per minute may terminate torsades (American Heart Association, 2005). Pacing can be used to suppress self-limited runs of TdP that may progress to unstable or refractory TdP, or for override refractory, persistent TdP before the potential development of ventricular fibrillation (Charlton et al, 2010). In a case series overdrive pacing was successful in terminating TdP associated with bradycardia and drug-induced QT prolongation (Neumar et al, 2010).

a) Potassium supplementation, even if serum potassium is normal, has been recommended by many experts (Charlton et al, 2010; American Heart Association, 2005). Supplementation to supratherapeutic potassium concentrations of 4.5 to 5 mmol/L has been suggested, although there is little evidence to determine the optimal range in dysrhythmia (Drew et al, 2010; Charlton et al, 2010).

a) Isoproterenol has been successful in aborting torsades de pointes that was resistant to magnesium therapy in a patient in whom transvenous overdrive pacing was not an option (Charlton et al, 2010) and has been successfully used to treat torsades de pointes associated with bradycardia and drug induced QT prolongation (Keren et al, 1981; Neumar et al, 2010). Isoproterenol may have a limited role in pharmacologic overdrive pacing in select patients with drug-induced torsades de pointes and acquired long QT syndrome (Charlton et al, 2010; Neumar et al, 2010). Isoproterenol should be avoided in patients with polymorphic VT associated with familial long QT syndrome (Neumar et al, 2010).
b) DOSE: ADULT: 2 to 10 micrograms/minute via a continuous monitored intravenous infusion; titrate to heart rate and rhythm response (Neumar et al, 2010).
c) PRECAUTIONS: Correct hypovolemia before using; contraindicated in patients with acute cardiac ischemia (Prod Info Isuprel(TM) intravenous injection, intramuscular injection, subcutaneous injection, intracardiac injection, 2013).
d) MAJOR ADVERSE EFFECTS: Tachycardia, cardiac dysrhythmias, palpitations, hypotension or hypertension, nervousness, headache, dizziness, and dyspnea (Prod Info Isuprel(TM) intravenous injection, intramuscular injection, subcutaneous injection, intracardiac injection, 2013).
e) MONITORING PARAMETERS: Monitor heart rate and rhythm, blood pressure, respirations and central venous pressure to guide volume replacement (Prod Info Isuprel(TM) intravenous injection, intramuscular injection, subcutaneous injection, intracardiac injection, 2013).

a) Mexiletine, verapamil, propranolol, and labetalol have also been used to treat TdP, but results have been inconsistent (Khan & Gowda, 2004).

a) Avoid class Ia antidysrhythmics (eg, quinidine, disopyramide, procainamide, aprindine), class Ic (eg, flecainide, encainide, propafenone) and most class III antidysrhythmics (eg, N-acetylprocainamide, sotalol) since they may further prolong the QT interval and have been associated with TdP.

a) To minimize barotrauma and other complications, use the lowest amount of PEEP possible while maintaining adequate oxygenation. Use of smaller tidal volumes (6 mL/kg) and lower plateau pressures (30 cm water or less) has been associated with decreased mortality and more rapid weaning from mechanical ventilation in patients with ARDS (Brower et al, 2000). More treatment information may be obtained from ARDS Clinical Network website, NIH NHLBI ARDS Clinical Network Mechanical Ventilation Protocol Summary, http://www.ardsnet.org/node/77791 (NHLBI ARDS Network, 2008)

1) A 30-year-old man survived an ingestion of 6 ounces of "Blue Ball Rat Killer" containing 1.5 percent arsenous oxide (2150 mg metallic arsenic per 6 ounces), ethanol, and intranasal cocaine use with aggressive therapy (fluid resuscitation, chelation therapy, and hemodialysis) (Fesmire et al, 1988).
2) LACK OF EFFECT: A 32-year-old woman developed only epigastric discomfort and paresthesias in the lower extremities following ingestion of about 2 grams of sodium arsenate; urine arsenic level was 14 mg/L about 13 hours postingestion (Hernandez et al, 1998).
3) A 45-year-old woman survived an ingestion of sodium arsenite between 8 and 16 g (serum arsenic concentration was 300 mcg/L on admission). Residual quadriplegia did occur (Bartolome et al, 1999).

1) A 16-year-old girl developed vomiting, agitation, abdominal pain, generalized weakness, and paresthesias after intentionally ingesting up to 240 mL of an herbicide containing 47% monosodium methylarsonate. The patient's condition improved following chelation therapy; however, mild paresthesia in her hands and feet continued to persist at her 6-week follow-up (Roth et al, 2011).
2) A 3-year-old boy experienced 3 episodes of vomiting after ingesting 5 mL of an herbicide containing 47.6% monosodium methylarsonate. An ECG demonstrated sinus tachycardia (114 bpm). He received dimercaptosuccinic acid for the next 15 days. Other than the initial episodes of vomiting, the patient remained asymptomatic throughout his hospital stay and at his follow-up exam 10 days post-discharge (Roth et al, 2011).

a) Hemodialysis patients had higher serum arsenic levels (2.3 to 79.8 ng/ml) than did normal subjects (0.132 to 4.783 ng/ml) in one study (Kimpe et al, 1993). Packed red blood cell arsenic levels were 2.1 to 68.4 ng/g and 0.51 to 14.44 ng/g for dialysis patients and controls respectively.

a) Concentrations of arsenic in urine, blood, and gastric fluid after admission in a worker buried in arsenic trioxide for about 10 minutes were 1.9, 3.4, and 550 mg/L, respectively (Gerhardsson et al, 1988).
b) Tissue concentrations in micrograms/gram wet weight of arsenic at autopsy of a worker who was buried for about 10 minutes in arsenic trioxide were brain (frontal cortex) 0.3, myocardium (left ventricle) 1.2, kidney (cortex) 1.4, lung (peripheral) 2.9, liver 3.8, and blood 2.3 (Gerhardsson et al, 1988).

a) A 3-year-old child had a blood arsenic concentration of 1.8 mg/L at 5.5 hours after accidental ingestion of approximately one mouthful of a 44% solution of sodium arsenite (Saady et al, 1989).
b) A 25-year-old man who died after ingesting 8 g of di-arsenic-trioxide had a serum arsenic concentration of 0.15 mg/L the day of ingestion (Quatrehomme et al, 1992).
c) A 45-year-old woman had an initial serum arsenic concentration of 300 mcg/L following an ingestion of sodium arsenite between 8 and 16 g. The patient survived with residual neurologic injury (i.e., quadriplegia) (Bartolome et al, 1999).
d) A 54-year-old woman had a urine arsenic concentration of 83.6 mcg/g creatinine (normal <50 mcg/g creatinine) after chronically ingesting 2 to 4 kelp supplement tablets daily over a 1-year period (Amster et al, 2007).
e) A 3-year-old boy ingested 5 mL of an herbicide containing 47.6% monosodium methylarsonate and had a blood arsenic concentration of 654.8 mcg/L, obtained 8 hours post-ingestion (Roth et al, 2011).
f) Seven teenagers (ages ranging from 15 to 18 years) unintentionally ingested an unknown amount of herbicide containing 24% monosodium methanearsonate, mistakenly used as cooking oil. Their blood arsenic concentrations, obtained approximately 7 hours post-ingestion, ranged from 348 to 613 mcg/mL (Cox & Orledge, 2011).

1) Arsenic
b) Adopted Value

1) Listed as: Arsenic (inorganic compounds, as As)
2) REL:
3) Listed as: Arsenic, organic compounds (as As)
4) REL:
5) IDLH:

1) ACGIH (American Conference of Governmental Industrial Hygienists, 2010): A1 ; Listed as: Arsenic
2) ACGIH (American Conference of Governmental Industrial Hygienists, 2010): A1 ; Listed as: Arsenic and inorganic compounds, as As
3) EPA (U.S. Environmental Protection Agency, 2011): A ; Listed as: Arsenic, inorganic
4) IARC (International Agency for Research on Cancer (IARC), 2016; International Agency for Research on Cancer, 2015; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2010; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2010a; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2008; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2007; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2006; IARC, 2004): 1 ; Listed as: Arsenic and inorganic arsenic compounds
5) NIOSH (National Institute for Occupational Safety and Health, 2007): Ca ; Listed as: Arsenic (inorganic compounds, as As)
6) NIOSH (National Institute for Occupational Safety and Health, 2007): Not Listed ; Listed as: Arsenic, organic compounds (as As)
7) MAK (DFG, 2002): Category 1 ; Listed as: Arsenic and inorganic arsenic compounds: Metallic arsenic
8) MAK (DFG, 2002): Category 1 ; Listed as: Arsenic and inorganic arsenic compounds
9) NTP (U.S. Department of Health and Human Services, Public Health Service, National Toxicology Project ): K ; Listed as: Arsenic Compounds, Inorganic

1) Listed as: Arsenic, inorganic compounds (as As); see 29 CFR 1910.1018
2) Table Z-1 for Arsenic, inorganic compounds (as As); see 29 CFR 1910.1018:
3) Listed as: Arsenic, organic compounds (as As)
4) Table Z-1 for Arsenic, organic compounds (as As):

a) 46,200 mcg/kg -- ataxia, gastrointestinal hypermotility, diarrhea

a) 25-47 mg/kg (OHM/TADS, 2001)
b) 145 mg/kg -- ataxia, gastrointestinal hypermotility, diarrhea

a) 13,390 mcg/kg

a) 15 mg/kg (OHM/TADS, 2001)
b) 112 mg/kg (OHM/TADS, 2001)
c) 763 mg/kg -- ataxia, gastrointestinal hypermotility, diarrhea

a) Induce emesis with Syrup of Ipecac, 10 to 30 mL orally or hydrogen peroxide 5 to 25 mL orally repeated in 5 to 10 minutes if there is no response. DOGS ONLY may receive apomorphine 0.05 to 0.10 mg/kg IV, IM or subcutaneously.
b) Gastric lavage may be performed using tap water or normal saline.
c) Administer activated charcoal, 5 to 50 g, orally, as a slurry in water.
d) Then administer Milk of Magnesia 1 to 15 mL orally, mineral oil 2 to 15 mL orally, sodium sulfate 20%, 2 to 25 g orally or magnesium sulfate 20% 2 to 25 g orally, for catharsis.

a) Give 250 to 500 g of activated charcoal in a water slurry, orally, to adsorb the toxic agent.
b) Administer an oral cathartic: mineral oil (1 to 3 liters), 20% sodium sulfate (25 to 10,000 g), 20% magnesium sulfate (25 to 1,000 g), or milk of magnesia (20 to 30 mL).
c) Ruminants (cattle and sheep) cannot be made to vomit. Horses should not be made to vomit.
d) Unabsorbed arsenic in the digestive tract of the horse will bind to orally administered sodium thiosulfate for eventual excretion in the feces (Oehme, 1987).

1) Begin treatment immediately.
2) Keep animal warm.
3) Sample vomitus, blood, urine, and feces for analysis.
4) If skin exposure has occurred, wash animal thoroughly with a mild detergent and flush with copious amounts of water.

1) DOGS/CATS
2) LARGE ANIMALS

1) POSTMORTEM - Liver and kidney tissues with arsenic concentrations of greater than 10 parts per million, on a wet weight basis, are diagnostic (Oehme, 1987).