Neuropathy arsenic causing

Melarsoprol given intravenously in patients with trypanosomiasis can cause a peripheral neuropathy within 2-5 weeks (SEDA-14, 243). It also causes a reactive arsenical encephalopathy in 3-5% of patients with trypanosomiasis (SEDA-13, 834) (6). 

Heyman A, Pfeiffer JB, Willett RW, et al Peripheral neuropathy caused by arsenical intoxication. N Engl J Med 254 401-409, 1956 Jenkins RB Inorganic arsenic and the nervous system. Brain 89 479-498,1966 Krainer L, Black DAK, McGill RJ, et al Arsenical encephalopathy in Indian troops. 

C. Neuropathy. A variety of dmgs and poisons can cause sensory or motor neuropathy, usually after chronic repeated exposure (Table 1-20). Some agents (eg, arsenic and thallium) can cause neuropathy after a single large exposure. 

Skin lesions, which emerge gradually over a period of 1-10 years, typically begin with a characteristic pattern of spotted ( raindrop pigmentation on the torso and extremities, followed after several years by the development of hyperkeratotic changes on the palms and soles. Skin lesions may occur after lower doses than those causing neuropathy or anemia. Arsenic-related skin cancer, which includes squamous cell carcinoma, Bowen s disease, and basal cell carcinoma, is characteristically multicentric, and in non-sun-exposed areas. 

Established causes of peripheral neuropathy include lead, arsenic, mercury, carbon disulfide (mentioned earlier in connection with ASHD), n-hexane, and certain organophosphates. 

Arsenic (CAS 7440-38-2) irritating to eyes and skin hyperplgmenta-tion, hyperkeratoses, and skin cancers have been dexribed. A general cellular poison. May cause bone marrow suppression, peripheral neuropathy, and gastrointestinal, liver, and cardiac injury. Some arsenic compounds have adverse effects on fetal development in test animals. Exposure linked to skin, respiratory tract, and liver cancer in workers (IARC 1). See also p 115. 0.01 mg/m (as As) A1 OSHACA NIOSH CA 5 mg/m (as As) Elemental forms vary In appearance. Crystals are gray. Amorphous fomes may be yellow or black. Vapor pressure is very low—about 1 mm Hg at 372°C (701°F). 

PAA is an acrylate polymer formed from the monomer acrylamide, which is a neurotoxin that causes peripheral neuropathy. Non-polymerised remnants of acrylamide in PAA pose some potential risks. It is claimed that, people unintentionally absorb around 25 pg of acrylamide daily from the environment, which may account for a significant number of cancer cases. Although there is no solid proof so far for a connection between acrylamide intake and cancer, it remains under investigation, and acrylamide can still be considered as a probable human carcinogen. On a health hazard spectrum, acrylamide registers 2 (3 = a very high hazard to health 2 = a medium hazard, and 1 = harmful to health arsenic scores highly at 2.3, while one of the lowest scores is ammonia at 1.0) [37]. 

Complications include hemolytic anemia, renal failure, hyperkalemia, and death. Overwhelming exposures cause rapid death from massive hemolysis. Most deaths occur from renal failure in patients who survive acute exposure. Patients surviving acute arsine exposiue may develop chronic arsenic toxicity, including anemia and peripheral neuropathy. 

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