Arsenic toxic forms

Arsine is the most acutely toxic form of arsenic. It binds with oxidized hemoglobin, causing profound hemolysis of sudden onset. Inhalation of 250ppm may be fatal within 30 minutes, whereas 10-50 ppm may cause anemia and death with more prolonged exposure. Human experience has indicated that there is usually a delay of 2-24 hours after exposure before the onset of headache, malaise, weakness, dizziness, and dyspnea, with abdominal pain, nausea, and vomiting. Dark red urine is frequently noted 4—6 hours after exposure. This often progresses to brown urine, with jaundice appearing at 24-48 hours after exposure. 

The toxic forms of arsenic are mainly (Section III,A) compounds of the type R—AsX2, where X is a ligand that is easily displaced by thiols. Many such compounds are volatile, and this increases their hazard. As mentioned in Section VII,A,2, one such compound, Cl2As— CH2—AsC12, is a convenient intermediate in the synthesis of the diphosphate analogue H203As—CH2—As03H2. Obviously, its distillation and that of any similar compound should be performed in a fume... 

Elemental arsenic is used in alloys of lead and copper, in semiconductors, and as an additive to the grid metal in storage batteries. Arsenic compounds have been used as pesticides and wood preservatives [4]. Although arsenic is most well known for its use as a poison, some evidence suggests that trace amounts may be essential for good health [5]. Inorganic forms of arsenic are more toxic than the organic forms arsenite, As (III), is the most toxic form of the element, followed by arsenate, As (V), monomethylarsenate, and dimethylarsenate. 

Arsine, the most toxic form of arsenic, exhibits some characteristics that may make it useful as a chemical warfare (CW) agent. Arsine is a colorless, odorless, nonirritating gas and is 2.5 times denser than air (Henriksson et al, 1996 Pullen-James and Woods, 2006 Thomas and Young, 2001). At concentrations above 0.5 ppm, a garlic-like odor may be noted, but arsine is toxic at much lower concentrations. Acute arsine poisoning due to inhalation of arsine gas (AsHs) is rare but has no known antidote. It is the most acutely toxic form of arsenic causing rapid and severe hemolysis immediately on exposure. The mechanisms of hemolysis are not completely understood. Arsine has a short half-life (27-96 h) and is converted to various arsenic derivatives. Although it... 

Arsine is supposed to be the most toxic form of arsenic. The acute toxicity of arsine is high in different species... 

Arsenic toxicity from drinking water is a major public health concern in many countries throughout the world. If exposure is to the inorganic form, the kidneys are the target organ due to its involvement in in vivo biotransformation and elimination. Very few clinical cases of toxicity are reported in humans. Most clinical cases of toxicosis are reported in animals, especially cattle and dogs, by... 

A strong base. Vigorous reaction with 1,2,4,5-tetrachlorobenzene has caused many industrial explosions and forms the extremely toxic 2,3,7,8-tetrachlorodibenzodioxin. Mixmres with aluminum + arsenic compounds form the poisonous gas arsine. Potentially explosive reaction with bromine, 4-chlorobutyronitrile, 4-chloro-2-methylphenol (in storage), nitrobenzene + heat, sodium tetrahydroborate, 2,2,2-trichloroethanol, zirconium + heat. Reacts to form explosive products with ammonia + silver nitrate (forms silver nitride), N,N -bis(trinitroethyl)urea (in storage), cyanogen... 

Arsenic in aquatic environments is usually more concentrated in sediments and pore water than in the overlying water column (Ahmann et al., 1997 Smedley and Kinniburgh, 2002 Williams, 2001). The most abundant forms of arsenic are arsenate [As(V)] and arsenite [As(III)], but methylated forms can occur in mine-impacted environments (i.e., methylarsenic acid and dimethylarsenic acid) (Smedley and Kinniburgh, 2002) see Chapter 9.02. The principal pathway of arsenic toxicity is through dietary exposure to sediment and suspended particulates by fish, followed by human consumption. Environmental exposure to arsenic is a causal factor in human carcinogenous and other related health issues. Chronic exposure symptoms in humans include hyperkeratosis, hyperpigmentation, skin malignancies, and peripheral arteriosclerosis. Water provides the dominant pathway for arsenic exposure in humans (Williams, 2001). 

Most arsenic compounds are highly toxic, causing dermatitis, acute and chronic poisoning, and possibly cancer. Arsenic is found in virtually all soil and other environmental matrices [16]. Arsenic is present in coal, pesticides, preservatives, etc. Arsenite, a commercial form of arsenic, is one of the most toxic forms of arsenic. 

Simpler procedures mainly starting with liquids (water, urine, blood, other body fluids) often suffice in that they permit a quick determination of the sum or of toxic forms of arsenic - that is. As ", As, MMA and DMA in laboratory routine. More sophisticated procedures, however, are required for scientific investigations on arsenic metabolism in humans, animals and plants and the identification and quantification of hitherto unknown arsenic species in the environment - a research field that is now just at its beginning. 

Since in very many cases the differentiation between totai arsenic, inciuding fish-derived arsenobetaine and toxic forms of arsenic, is the most important task, this approach wiil be described in as much detail as possible and some of the other procedures are outlined and references given for the reader s further information. 

The reduced species (arsenite) is more toxic than the oxidized species (arsenate) since it may react with sulfhydryl groups of cysteine in structure and enzyme proteins. Therefore oxidation of arsenite in (micro)organisms is an important protective mechanism which is described for various species of the genus Pseudomonas, Xantho-monas and Achromobacter. However, some bacteria are able to reduce arsenate to the more toxic form arsenite. This process is described for some strains of Pseudomonas fluorescens and Anabaena oscillaroides (Cullen and Reimer, 1989). 

Note Hydrogen gas can react with inorganic arsenic to form the highly toxic gas arsine ]... 

Recent studies using cultured cells have shown that MMA(III) and DMA(lll) are at least as toxic as the inorganic arsenic species (97-102). The methylated trivalent arsenic species are also proposed to be the proximate or ultimate genotoxic forms of arsenic (103). Thus, there has been much interest in the determination of these metabolites in humans. The observation of MMA(III) and DMA(III) species in human urine, together with these studies on arsenic toxic effects, indicates that methylation of arsenic may not be entirely a detoxification process for humans, as previously believed (104,105). Toxicological consequences of MMA(lll) and DMA(III) in humans need to be further examined. 

All ars operons encode an ArsC arsenate reductase enzyme. However, as mentioned above, there are two sequence-unrelated families of arsenate reductases whose role is to reduce less toxic As(V) to more toxic As(lll) (21,34,36). It is only As(lll) and not As(V) that is pumped out from the cells by the ArsB transport protein. It seems counterintuitive from an environmental biology or metabolic chemistry point of view to convert a less toxic compound to a more toxic form. We have speculated that arsenite pumping activity evolved prior to the existence of oxygen in the atmosphere, and ArsC evolved only after an oxidizing atmosphere developed (8). At that point arsenite would spontaneously oxidize to arsenate, presenting a selective pressure for evolution of a reductase. The two types of arsC genes are positioned last in all ars operons shown in Fig. 2. The... 

It is well established that microbiota plays a very significant role in the various transformations of arsenic, including mineralization/immobilization, oxidation/ reduction, and methylation/demethylation. Some of these biotransformations lead to less toxic forms of arsenic that can be used in the detoxification of the arsenic-contaminated environments. Biomethylation of arsenic results in formation of mono-, di-, and trimethylarsines which are volatile however, these gaseous arsenic forms are also toxic. In developing a bioremediation strategy to clean the... 

Arsenic interrupts some of your body s most basic and common biochemical pathways. Arsenic, particularly As " and As + oxides, interferes with the citric acid cycle and respiration (specifically reduction of NAD-I- and ATP synthesis— see Biochemistry ). If that weren t enough to kill you, and it probably is, arsenic also boosts the level of hydrogen peroxide in your body, which causes another whole set of problems. Unfortunately, these toxic forms of arsenic are not only water soluble but can be found in well water from natural sources and man-made contamination from mining. 

---