Arsine is gradually converted to arsenite (As3+), then methylated into monomethylarsonic and dimethylarsinic acids. It is primarily excreted in the urine. (T21)
Arsine enters the bloodstream and crosses the alveolo-capillary membrane into red blood cells. Here it preferentially binds to hemoglobin and is oxidized to an arsenic dihydride intermediate and elemental arsenic, both of which are hemolytic agents. Arsine also depletes the reduced glutathione content of the red blood cells, resulting in the oxidation of sulfhydryl groups in hemoglobin and red cell membranes. These effects produce membrane instability, resulting in hemolysis. Arsine may also inhibit catalase, which leads to the accumulation of hydrogen peroxide. This destroys red cell membranes and may contribute to arsine-induced conversion of Fe+2 to Fe+3, which also impairs oxygen transport. (L11)
Acute poisoning with arsenic is marked by severe abdominal pain, nausea and vomiting, diarrhea, muscle cramps, metallic taste and extreme thirst, followed by stupor, coma, cardiovascular collapse and death. Death can occur within 24 hours of exposure, but with sublethal doses, survival is possible and liver injury may arise 24 to 48 hours after the acute ingestion. Other symptoms include conjunctival and respiratory tract inflammation, epistaxis, rash, renal insufficiency and painful neuropathy. The characteristics of the liver injury have not been well defined, but are likely similar to those with acute iron poisoning, with a clinical phenotype of acute hepatic necrosis, marked elevations in serum aminotransferase levels, early onset of hepatic failure and rapid recovery in cases without early fatality.
Chronic, lower dose exposure to arsenic can be toxic and result in arsenosis, a syndrome marked by fatigue, nausea and vomiting, abdominal crampy pain, weakness, stupor, seizures and neuropathy. Skin manifestations are frequent and characteristic with chronic excessive exposure marked by hyper- and hypo-pigmentation, a "rain-drop" pattern of skin discoloration, skin dryness and exfoliation, keratosis of the palms and soles, and skin cancers. Arsenic is also deposited in the hair and nails, where it can be detected even after it is no longer measureable in urine. Liver injury can also occur with chronic arsenic exposure, typically with appearance of signs and symptoms of portal hypertension, without obvious cirrhosis (idiopathic or noncirrhotic portal hypertension). The clinical onset of noncirrhotic portal hypertension is often insidious with weight loss, fatigue and abdominal swelling and minor, nonspecific elevations in serum enzymes, followed by appearance of variceal hemorrhage or ascites. Features of portal hypertension (ascites, variceal hemorrhage) rather than hepatic failure (jaundice, encephalopathy or coagulopathy) predominate. Symptoms generally improve slowly upon withdrawal of arsenic exposure and long term survival is not uncommon, although porto-caval shunting may be needed to manage portal hypertension and variceal hemorrhage. Serum enzyme elevations and jaundice are uncommon, but may occur. Chronic exposure is usually due to environmental contamination, from elevated arsenic levels in water due to run-offs from mining or storage of arsenic containing compounds such as herbicides and pesticides. When arsenic was still being used as a medicinal agent, cases of chronic poisoning were linked to use of Fowler's solution for psoriasis and asthma and arsphenamine for syphilis generally after 5 to 25 years of use. Furthermore, some cases became clinically apparent several years after the arsenical was stopped and at a time that arsenic could no longer be detected in urine, tissue or hair samples. Chronic arsenic exposure has also been linked to cirrhosis, although the contribution of alcohol and other chronic liver diseases in reported cases could not be excluded. Chronic exposure has also been linked to liver cancer, including hepatic angiosarcoma and hepatocellular carcinoma. Other long term complications of arsenic exposure include skin discoloration, palmar and plantar keratosis, peripheral neuropathy, and skin and lung cancer which can arise several decades after exposure. Patients presenting with noncirrhotic portal hypertension due to arsenic frequently have other manifestations of its chronic toxicity such as skin discoloration, palmar keratosis and skin cancers.
Arsenic trioxide (Trisenox) given intravenously as therapy of acute promyelocytic leukemia has had limited use, but hepatotoxicity has been reported in 8% to 47% of patients, generally in the form of mild and transient serum enzyme elevations that resolve even with continuation of treatment. Nevertheless, more severe hepatic injury has been reported including cases of acute liver failure, although the clinical features of the injury and relatedness to the therapy were not well defined.
Likelihood score: A[HD] (well known cause of chronic liver injury when given in high dosess).
CLASSIFICATION: A; human carcinogen. BASIS FOR CLASSIFICATION: Based on sufficient evidence from human data. An increased lung cancer mortality was observed in multiple human populations exposed primarily through inhalation. Also, increased mortality from multiple internal organ cancers (liver, kidney, lung, and bladder) and an increased incidence of skin cancer were observed in populations consuming drinking water high in inorganic arsenic. HUMAN CARCINOGENICITY DATA: Sufficient. ANIMAL CARCINOGENICITY DATA: Inadequate. /based on former classification system/
来源:Hazardous Substances Data Bank (HSDB)
毒理性
致癌性证据
A1：已确认的人类致癌物。/砷和无机砷化合物，如As/
A1: Confirmed human carcinogen. /Arsenic and inorganic compounds, as As/
Evaluation: There is sufficient evidence in humans that arsenic in drinking-water causes cancers of the urinary bladder, lung and skin ... Overall evaluation: Arsenic in drinking-water is carcinogenic to humans (Group 1). /Arsenic in drinking-water/
Normal values of arsenic in urine, ... vary from 0.013-0.046 mg/L, to 0.13 mg/L, to 0.25 mg/L. The urinary excretion, in mg/L, of elements that are freely eliminated by this route, such as ... arsenic, is at most 2.5-5 times the occupation exposure in mg/cu m of air. It is apparent that biological monitoring for arsenic by urinalysis would be of limited value in determining whether or not the NIOSH recommended standard ... was being met or exceeded.
Process for separating arsenic from acid solutions containing it
申请人：Consiglio Nazionale Delle Richerche
公开号：US04701311A1
公开（公告）日：1987-10-20
A process for the selective extraction of arsenic from acid solutions containing other metals comprising treating the solutions with polyhydroxybenzene derivatives in organic diluent; mono- and di- alkyl derivatives containing at least four alkyl carbon atoms of pyrocatechol and pyrogallic acid are particularly contemplated for use in the removal of arsenic from strongly acid copper-containing electrolyte solutions.
CATALYST FOR PRODUCING UNSATURATED ALDEHYDE BY OXIDATION OF LOWER OLEFIN AT HIGH SPACE VELOCITY
申请人：Wang Jian
公开号：US20110295041A1
公开（公告）日：2011-12-01
A method of preparing a catalyst for producing acrolein by oxidation of propylene at high space velocity, said catalyst is a Mo—Bi—Fe—Co based composite metal oxide. Producing unsaturated aldehyde via partial oxidation of lower unsaturated olefin at high space velocity using said catalyst is suitable for process with or without off-gas recirculating. Said catalyst is prepared by co-precipitation, the reaction conditions for using said catalyst to produce unsaturated aldehyde are, the space velocity of unsaturated lower olefin relative to catalyst being 120˜200 h-1(STP), reaction temperature being 300˜420° C. and absolute pressure being 0.1˜0.5 MPa; a single-stage unsaturated lower olefin conversion ratio of greater than 98.0% and carbon oxide yield of less than 3.3% with an overall yield of unsaturated lower aldehyde and acid of greater than 94.0% are obtained. The process to prepare the said catalyst is simple, easy to be repeated, and capable of industrial scale-up.
Catalyst for producing unsaturated aldehyde by oxidation of lower olefin at high space velocity
申请人：Wang Jian
公开号：US08481790B2
公开（公告）日：2013-07-09
A method of preparing a catalyst for producing acrolein by oxidation of propylene at high space velocity, said catalyst is a Mo—Bi—Fe—Co based composite metal oxide. Producing unsaturated aldehyde via partial oxidation of lower unsaturated olefin at high space velocity using said catalyst is suitable for process with or without off-gas recirculating. Said catalyst is prepared by co-precipitation, the reaction conditions for using said catalyst to produce unsaturated aldehyde are, the space velocity of unsaturated lower olefin relative to catalyst being 120˜200 h-1(STP), reaction temperature being 300˜420° C. and absolute pressure being 0.1˜0.5 MPa; a single-stage unsaturated lower olefin conversion ratio of greater than 98.0% and carbon oxide yield of less than 3.3% with an overall yield of unsaturated lower aldehyde and acid of greater than 94.0% are obtained. The process to prepare the said catalyst is simple, easy to be repeated, and capable of industrial scale-up.
ARSENIC COMPLEXES FOR POTENTIAL DIAGNOSTIC APPLICATIONS
申请人：Jurisson Silvia S.
公开号：US20160083408A1
公开（公告）日：2016-03-24
The present invention provides radioactive arsenic complexes useful in diagnostic and therapeutic applications and methods for forming those arsenic complexes.
本发明提供了用于诊断和治疗应用的放射性砷复合物，以及形成这些砷复合物的方法。
Aluminum containing precipitating agent for precious metals and method
申请人：American Chemical & Refining Co., Inc.
公开号：US04092154A1
公开（公告）日：1978-05-30
A precipitating agent for precipitating precious metals such as gold from aqueous cyanide solution of the precious metal ions includes aluminum powder and a reducing agent such as sodium hydrosulfite, sodium borohydride or hydrazine. The precipitating agent may also include an alkali metal carbonate, such as potassium carbonate, as an activator. The precipitating agent efficiently reduces the precious metal ions to elemental metal for recovery and also consumes a portion of the cyanide content, which is often high in such solutions. The method of use includes adjusting the precious metals cyanide solution to a high pH, adding the precipitating agent with agitation, preferably in incremental portions of the amount required. The solution is allowed to stand to permit the precipitated metal to settle, and the metal is separated from the solution.
