Arsenic Toxicity of Food Chain

Arsenic can enter through the food chain through drinking water or the food crops raised in arsenic contaminated soil (Fig. 12.2). There are evidences of elevated arsenic levels in the rice grain in regions of West Bengal and Bangladesh where rice fields are irrigated with arsenic contaminated waters (Rahman et al. 2009; Duxbury et al. 2003; Williams et al. 2005; Islam et al. 2004; Khan et al. 2009). Apart from rice crop, elevated levels of arsenic contamination in vegetables was also reported from Bangladesh (Williams et al. 2006). Global normal range of 0.08-0.2 mg As kg-1 has been suggested for rice (Zavala and Duxbury 2008) but values may reach as high as 1.8 mg As kg-1 have been found in Bangladesh rice (Meharg and Rahman 2003). The most notable case was observed in India and Bangladesh where over 50 million people were exposed to highly contaminated water or food (Hossain 2006). There have been reports of up to 2 mg kg-1 of arsenic accumulated in grains and up to 92 mg kg-1 of arsenic in straws (Abedin et al. 2002). Zhong et al. (2011) reported that there are different controls on the unloading of inorganic As and dimethylarsinic acid (DMA) in rice grain; the latter accumulated mainly in the caryopsis before flowering, whereas inorganic As was mainly transported into the caryopsis during grain filling. However, Carey et al. (2010) reported that arsenite was retained in the ovular vascular trace and DMA dispersed throughout the external grain parts and into the endosperm.

Arsenic being an carcinogenic element interferers with the cellular components in living creatures. Therefore, long-term intake of arsenic contaminated water and food would cause severe damage to the various metabolic systems in the living body. Arsenic (e.g., As3+) is a potentially hazardous toxic element that interacts with sulfhydryl groups of proteins and enzymes (to denature the proteins and enzymes within the cells; Gebel 2000; Graeme and Pollack 1998) and reactive oxygen species in the cells, consequently causing cell damage (Ahmed et al. 2006). Arsenic can interfere with essential enzymatic functions and transcriptional events in cells, leading ultimately to "multitude of multisystemic noncancer effects that might ensue" (NRC 1995). For example, oxidative stress induced by trivalent methylated arsenicals inhibits glutathione (GSH) reductase (Styblo et al. 1997) and thioredoxin reductase (Lin et al. 1999) with subsequent impairment of cellular protective mechanism against oxidants. While depletion of cellular GSH sensitizes cells to arsenicals and may also contribute to cell transformation (Shimizu et al. 1998), thioredoxin depletion affects gene expression due to the fact that it modulates DNA binding activity of some transcriptional factors (Powis et al. 2000). Arsenite is known to inhibit more than 200 enzymes in the body (Abernathy et al.

1999) and, because arsenate has a similar structure as phosphate, it can substitute for phosphorus in the body, which can lead to replacement of phosphorus in the bone for many years (Arena and Drew 1986; Ellenhorn and Barceloux 1988). Because arsenate is hydrolyzed easily (in the cell), it prevents subsequent transfer of phosphate to adenosine diphosphate (ADP) to form adenosine triphosphate (ATP; the energy currency of the cell) and thus depletes the cell of its energy (Winship 1984). Arsine, the most toxic of the arsenicals (Buchet and Lauwerys 1983; Leonard 1991), is known to cause hemolysis of red blood cells, leading to hemolytic anemia, which is primarily responsible for the development of oliguria renal failure (Fowler and Weissberg 1974; Fowler 1977). It has been suggested that arsine interaction with sulfhydryl group of proteins and enzymes (Levinsky et al. 1970) may be responsible for inhibition of erythrocyte sodium-potassium pump. It also is known that arsenic decreases DNA repair process (Brochmoller et al.

2000) and, hence, enhances susceptibility to cancer (e.g., skin cancer; Wei et al. 1994) and non-cancer-related diseases (Feng et al. 2001).

Arsenic toxicity could affect a wide variety of organisms, including humans (Cervantes et al. 1994). Chronic arsenic effects in humans have been well documented and reviewed (e.g., Pershagen 1983). Organs most affected are those involved with arsenic in absorption, accumulation, and/or excretion. These organs are the gastrointestinal tract, circulatory system, liver, kidney, skin, tissues very sensitive to arsenic and those tissues secondarily affected (e.g., heart; Squibb and Fowler 1983). Signs of chronic arsenic toxicity include dermal lesions (e.g., hyperpigmentation, hyperkeratosis, desquamation, and loss of hair; Zaloga et al. 1985), peripheral neuropathy, skin cancer, and peripheral vascular disease. These signs have been observed mostly in populations whose drinking water contains arsenic (Tseng 1977; Tseng et al. 1968; Zaldivar 1980; Zaldivar and Ghai 1980; Cebrian et al. 1983; Smith et al. 2000). Among these symptoms, dermal lesions were most dominant, and were also known to occur within a period of about 5 years. The skin is known to localize and store arsenic because of its high keratin content, which contains several sulfhydryl groups to which As3+ may bind (Kitchin 2001) and may be the reason for its sensitivity to arsenic toxic effect. A study of Tseng (1977) in the Province of Taiwan (China) established a clear dose-response relationship between arsenic and dermal lesions, Blackfoot disease (BFD; a peripheral vascular disorder) and skin cancer. From several studies ( Chen and Wu 1962; Chi and Blackwell 1968; Tseng 1977; Chen et al. 1988; Engel et al. 1994), it has been established that peripheral vascular diseases are associated with arsenic in well water in Taiwan. However, vascular disease has also been reported among German vintners (Grobe 1976), inhabitants of Antofagasta and Chile (Borgono et al. 1977). Skin cancers, including in situ cell carcinoma (or Bowen's disease), invasive cell carcinoma, and multiple basal cell carcinomas, are all known to be associated with chronic arsenic exposure (Shneidman and Belizaire 1986; ATSDR 1990). Chen et al. (1995) observed that hypertension was linked to long-term arsenic ingestion as well as cerebrovascular disease (i.e., cerebral infection). Other effects are hematopoietic depression, anhydremia (due to loss of fluid from blood into tissue and the gastrointestinal tract), liver damage characterized by jaundice, portal cirrhosis and ascites, sensory disturbance and peripheral neuritis, anorexia and loss of weight (Webb 1966). Although the effects of arsenic, as recounted previously, result in several kinds of diseases, it certainly may also impact adversely on the immune system, which may predispose to viral/bacterial infections. Several of such diseases resulting from alterations of the immunologic surveillance may not have been known to be due to arsenic and therefore may not have been attributed to arsenic effects. A probing into this area is therefore appropriate. The toxicity of specific arsenic chemical species is mentioned later (Oremland and Stolz 2005).

Arsenic occurs in four oxidation states: As5+, As3+, As0, and As3-. The two highest oxidation states are the most common in nature, whereas the two lowest are rare.

Arsenate: This oxyanion is an analog of phosphate, and as such it is a potent inhibitor of oxidative phosphorylation, the key reaction of energy metabolism in metazoans, including humans.

Arsenite: The most toxic of arsenic oxyanions. It readily binds to reactive sulfur atoms (SH goups) of many enzymes, including those involved in respiration.

Arsenic trioxide (As2O3): The most common form of arsenic used for a variety of agricultural, manufacturing, and medical purposes. It is highly toxic, and being soluble in water, as well as colorless and tasteless, it has proved useful in criminal homicide. During the eighteenth century it gained so much notoriety that it was referred to as "inheritance powder."

Methylated forms of arsenate and arsenite: Compounds, such as methylarsonic acid (MMAV), monomethylarsonous acid (MMAIII), and dimethylarsenic acid (DMAV) are produced by algae and as excretory products of animals. They have varying degrees of toxicity, depending on their chemical form and the oxidation state of the arsenic that they contain. They occur in low concentrations in the environment.

Arsines: Arsenic in the 3- oxidation state, occurring as highly toxic gases, such as H3As and (CH3)3As. Very little is known about the natural cycles of these substances, as they occur at very low concentrations in the environment.

Organoarsenic compounds: Naturally occurring substances, such as arseno-betaine, are molecular analogs of osmotic-regulating compounds, such as betaine, where arsenic substitutes for the original nitrogen atom. They commonly occur in several marine animals, including shellfish and elasmobranchs. Their physiological role in these organisms is unknown, but they are benign and are not toxic to animals that eat these organisms, including humans.

Synthetic organoarsenic compounds: Substances, such as roxarsone (4-hydroxy-3-nitrophenylarsonic acid), are used as palliatives included in the feed of massraised swine and poultry. They are benign, do not accumulate in these organisms, and are ultimately excreted. However, their subsequent breakdown by bacteria in soils will release As(V) into the environment.

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