Page 27

3
Chemistry and Analysis of Arsenic Species in Water, Food, Urine, Blood, Hair, and Nails

In this chapter, the subcommittee describes the chemistry of arsenic and its analysis in water and biological materials. The chapter is divided into four sections. The first section, Arsenic Compounds in Water and Food, provides the reader with general information on the various arsenic species that are now known to be present in food and water and that could be of concern in assessing normal human exposure (i.e., nonoccupational exposure) to arsenic. However, it should be emphasized that many unidentified arsenic species are probably present in the environment, including many in living organisms. It is not an easy task to detect and identify low concentrations of arsenicals, and methods to do so have been developed only in recent years.

The second section, Relevant Chemical Considerations, provides a brief account of arsenic's chemistry that is relevant to considerations of toxicity and carcinogenicity. In the third section, Analysis of Arsenic Compounds, general methods that have been used to analyze arsenic and its species are outlined. The results of applying these methods to the analysis of water and food, respectively, are presented in the sections Arsenic in Water and Arsenic in Food. A separate section discusses the application of these methods to the analysis of arsenic in urine, blood, hair, and nails.

Summary Of Arsenic Compounds In Water And Food

Table 3-1 lists the most important arsenic compounds and species known to be present in water and food consumed by humans. The identified compounds that are not listed are (1) the volatile arsines MexAsH3-x



The National Academies | 500 Fifth St. N.W. | Washington, D.C. 20001
Copyright © National Academy of Sciences. All rights reserved.
Terms of Use and Privacy Statement



Below are the first 10 and last 10 pages of uncorrected machine-read text (when available) of this chapter, followed by the top 30 algorithmically extracted key phrases from the chapter as a whole.
Intended to provide our own search engines and external engines with highly rich, chapter-representative searchable text on the opening pages of each chapter. Because it is UNCORRECTED material, please consider the following text as a useful but insufficient proxy for the authoritative book pages.

Do not use for reproduction, copying, pasting, or reading; exclusively for search engines.

OCR for page 27
Page 27 3 Chemistry and Analysis of Arsenic Species in Water, Food, Urine, Blood, Hair, and Nails In this chapter, the subcommittee describes the chemistry of arsenic and its analysis in water and biological materials. The chapter is divided into four sections. The first section, Arsenic Compounds in Water and Food, provides the reader with general information on the various arsenic species that are now known to be present in food and water and that could be of concern in assessing normal human exposure (i.e., nonoccupational exposure) to arsenic. However, it should be emphasized that many unidentified arsenic species are probably present in the environment, including many in living organisms. It is not an easy task to detect and identify low concentrations of arsenicals, and methods to do so have been developed only in recent years. The second section, Relevant Chemical Considerations, provides a brief account of arsenic's chemistry that is relevant to considerations of toxicity and carcinogenicity. In the third section, Analysis of Arsenic Compounds, general methods that have been used to analyze arsenic and its species are outlined. The results of applying these methods to the analysis of water and food, respectively, are presented in the sections Arsenic in Water and Arsenic in Food. A separate section discusses the application of these methods to the analysis of arsenic in urine, blood, hair, and nails. Summary Of Arsenic Compounds In Water And Food Table 3-1 lists the most important arsenic compounds and species known to be present in water and food consumed by humans. The identified compounds that are not listed are (1) the volatile arsines MexAsH3-x

OCR for page 27
Page 28 TABLE 3-1 Some Arsenic Compounds and Species Known to be Present in Water and Food Consumed by Humans Name Abbreviation Chemical Formula Arsenous acid As(III) H3AsO3 Arsenic acid As(V) H3AsO4 Oxythioarsenic acid   H3AsO3S Monomethylarsonic acid MMA CH3AsO(OH)2 Methylarsonous acid MMA(III) CH3As(OH)2[CH3AsO]n Dimethylarsinic acid DMA (CH3)2AsO(OH) Dimethylarsinous acid DMA(III) (CH3)2AsOH[((CH3)2As)2O] Trimethylarsine TMA (CH3)3As Trimethylarsine oxide TMAO (CH3)3AsO Tetramethylarsonium ion Me4As+ (CH3)4As+ Arsenocholine AsC (CH3)3As+CH2CH2OH Arsenobetaine AsB (CH3)3As+CH2COO- Arsenic-containing ribo- Arsenosugar X-XVa   sides Arsenolipidb   aArsenosugar         R X Y X (CH3)2As(O)- -OH -OH XI (CH3)As(O)- -OH -OPO3HCH2CH(OH)CH2OH XII (CH3)2As(O)- -OH -SO3H XIII (CH3)2As(O)- -OH -OSO3H XIV (CH3)2As(O)- -NH2 -SO3H XV (CH3)3As+- -OH -OSO3H bArsenolipid         R X Y   (CH3)2AsO- -OH -OPO3HCH2CH(OPalm)CH2OPalm

OCR for page 27
Page 29 (Me =CH3, x = 0-3) produced naturally by the action of microorganisms on available arsenicals (Cullen and Reimer 1989); (2) the ethylmethylarsines EtxAsMe3-x (Et=C2H5, x = 1-3) found in natural gas (Irgolic et al. 1991); (3) phenylarsonic acid, C6H5AsO(OH)2, found in shale oil and retort water (Fish et al. 1982); and (4) the undoubtedly numerous arsenicals not yet discovered. The structures of the arylarsenicals that are approved as animal-food additives are shown in Figure 3-1. 4-Hydroxy-3-nitrophenylarsonic acid (3-NHPAA) and p-arsanilic acid (p-ASA) are approved for poultry and swine. 4-Nitrophenylarsonic acid (4-NPAA) and p-ureidophenylarsonic acid (p-UPAA) are approved only for controlling blackhead disease in turkeys (Ledet and Buck 1978; Adams et al. 1994). Melarsoprol, a related arylarsenical, is still the drug of choice for treating secondary trypanosomiasis in humans in rural Africa (Berger and Fairlamb 1994). FIGURE 3-1 Structures of arylarsenicals approved as animal-food additives. 3-NHPAA, roxarsone, 4-hydroxy-3-nitrophenylarsonic acid;  p-ASA,  p-arsanilic acid; 4-NPAA, 4-nitrophenylarsonic acid;  p-UPAA, p-unridophenylarsonic acid As(III) (pKa (negative logarithm of equilibrium constant for dissociation) = 9.23, 12.13, 13.4), As(V) (pKa = 2.22, 6.98, 11.53), MMA (pKa = 4.1, 8.7), DMA (pKa = 6.2), TMA, and TMAO are usually associated with the terrestrial environment, As(III) and As(V) being dominant in water. Unidentified species ("hidden species" not detected by using hydride generation; see section Hidden Arsenic Species), however, can reach up to 22% of total arsenic in river water (Sturgeon et al. 1989), and methylarsenicals can reach up to 59% of total arsenic in lake water (Anderson and Burland 1991). The recent discoveries of AsB, AsC, and Me4As+ in mushrooms (Byrne et al. 1995; Kuehnelt et al. 1997a,b); arsenosugar X in algae (Lai et al. 1997); and oxythioarsenic acid and methylarsenic(III) species MMA(III) and DMA(III) in water (Bright et al. 1994; Hasegawa 1996, 1997; Schwedt and Reickoff 1996a,b) extend the range of identified species. In the marine environment, all the compounds shown in Table 3-1, except

OCR for page 27
Page 30 the oxythioarsenate, have been identified. The most important arsenic compounds in seawater are the inorganic species As(III) and As(V). Those species are usually associated with much lower concentrations of DMA and MMA. In fish, the principal arsenic species is AsB, which is regarded as being ubiquitous. The telost fish Silver Drummer, however, does not contain any AsB, and its principal arsenic species is TMAO (Edmonds et al. 1997). Small amounts of AsC, DMA, MMA, As(V), TMAO, Me4As+, and arsenosugars also are found in marine animals (e.g., Larsen et al. 1993a), although the last two arsenic species can be important in some bivalves. High concentrations of unknown arsenicals have been identified in the abalone (Edmonds et al. 1997). Marine algae contain arsenosugars, principally X-XIII, and 15 arsenosugars have been identified to date. In addition, marine algae contain small amounts of inorganic arsenic and DMA (Francesconi and Edmonds 1997). High concentrations of inorganic arsenic (38-61% of total arsenic) are found in some marine algae, notably Sargassum muticum and Hizikia fusiforme (Morita and Shibata 1990; Francesconi and Edmonds 1997). The arsenolipid (Table 3-1) is a minor component of the brown alga Undaria pinnatifida, an edible seaweed known as Wakame (Shibata et al. 1992), but lipid-soluble arsenicals can reach high concentrations in some species. Relevant Chemical Considerations Is Arsenic Similar to Phosphorus? Arsenic is situated in the Periodic Table in Group 15 (old Group V) below nitrogen and phosphorus. The oxidation state of arsenic in compounds found in the environment is either III or V (Table 3-1), and much of the chemistry of those compounds results from the easy conversion between those two states. The two-electron reduction of arsenate As(V) to arsenite As(III) is favored in acidic solution (E° (standard reduction potential) = 0.56 volts), whereas the reverse is true in basic solution (Eº = -0.67 volts) (Latimer and Hildebrand 1951). In contrast, phosphorus(V) compounds are difficult to reduce. Another major difference between arsenic and phosphorus is the stability of the esters of phosphoric acid to hydrolysis, allowing the existence of, for example, DNA and adenosine 5'-triphosphate (ATP). Esters of As(V) acids are easily hydrolyzed; the half-life in neutral pH is about 30 min. If As(V)OR has a good leaving group such as -P(V) or C(O)R', the half-life falls to seconds. Enzymes can accept arsenate to incorporate into other compounds, such as ATP, but the analogues formed hydrolyze immediately. Thus, arsenate uncouples oxidative metabolism from ATP biosynthesis. That phenome-

OCR for page 27
Page 31 non is believed to account for some of the toxicity of arsenate (Dixon 1997; see Chapter 7). Many As(III) compounds are formulated as RAsX or (R2As)2X (X = 0, S). In the solid state, some of those compounds can be polymeric (e.g., (CH3AsO)3 and (CH3AsS)3), but CH3As(OH)2 and (CH3)2AsOH seem to exist in dilute aqueous solution (Hasegawa 1996, 1997). Affinity Of Arsenic For Sulfur The affinity of arsenic for sulfur is revealed in any list of natural arsenic-containing minerals. Many are sulfides and include As4S4 (realgar), As4S6 (orpiment), and FeAsS (arsenical pyrites, mispickel). That affinity also has been invoked to account for the toxicity of As(III) compounds through the interaction with protein thiols, as shown in Equation 3-1 in Figure 3-2 (see also Chapter 7). Such binding to proteins might inhibit the function of such enzymes as pyruvate dehydrogenase and 2-oxoglutarate dehydrogenase (Knowles and Benson 1983a,b; Dixon 1997). FIGURE 3-2 Affinity of arsenic for sulfur. BAL, British Anti-Lewisite (dimercaprol). The action of dimercaprol, British Anti-Lewisite (BAL), in aiding the elimination of arsenic species from humans, is believed to result from the displacement of bound arsenic from a protein because of the formation of a more stable complex (Equation 3-2). However that action does not necessarily mean that the initial postulate of Equation 3-1 is correct. Binding of the arsenic to BAL could restore the function of an enzyme regardless of how the arsenic was originally bound. Li and Pickart (1995) pointed out that little evidence supports the proposal that the binding of As(III) compounds to

OCR for page 27
Page 32 enzymes is solely or even predominantly that represented in Equation 3-1. Li and Pickart (1995) found that the binding of phenylarsenoxide, (C6H5AsO)n, (which is possibly C6H5As(OH)2 in dilute aqueous solution) to Arg [Arginine]-tRNA protein transferase does not involve vicinal thiols. However, Cys [Cysteine]-31 and Cys-184 seem to be implicated in lecithin-cholesterolacyl transferase (Jauhiainen et al. 1988). The reduction of As(V) compounds by thiols has been well documented (Cullen et al. 1984), but sulfhydryl groups in enzymes do not always affect the reduction (Dixon 1997), presumably because this reductive interaction with sulfhydryl groups requires that more than one sulfhydryl group reach the same arsenic atom (i.e., reduction is a two-electron process). The As(III)-sulfur bond is much more resistant to hydrolysis than the As(III)-oxygen moiety (Sagan et al. 1972; Zingaro and Thomson 1973). Biomethylation of Arsenic Endogenous thiols probably play a critical role in the metabolic conversion of As(III) and As(V) species. It is likely that glutathione (GSH) acts as a reducing agent for As(V) species; the resulting As(III) species can then accept a methyl group from S-adenosylmethionine (SAM) to produce the methylarsenic(V) species in an oxidative-addition reaction, as illustrated in Figure 33 (Cullen and Reimer 1989). This cycle of reduction followed by oxidative addition of a methyl group can be continued, and the end product seems to depend on the organism. This cycle is based on the pioneering studies of Challenger (1951). The end products can be trimethylarsine oxide or trimethylarsine for fungi, the tetramethylarsonium ion for clams, and probably DMA for humans (Cullen and Reimer 1989; Cullen et al. 1994) (see Chapter 5). FIGURE 3-3 Biomethylation of arsenic: SAM as methyldonor, GSH as reducing agent. GSH, glutathione.

OCR for page 27
Page 33 SAM is probably the source of the adenosyl group that is found in the arsenosugars (Francesconi and Edmonds 1997). The As(III) derivatives seem to have the unique ability to accept all three groups that are attached to sulfur in SAM, as illustrated in Figure 3-4. FIGURE 3-4 Reaction of As(III) derivatives with SAM. SAM, S-adenosylemthionine.

OCR for page 27
Page 34 The As(III) species that are intermediates in the biotransformation of arsenic might well be toxic (Hocking and Jaffer 1969; Sheridan et al. 1973; Cullen et al. 1989b) (see Chapter 7). For example, glutathione reductase (GR) is a key enzyme in the metabolism of GSH and is inhibited by the methylarsenic(III) and As(III) species (Delnomdedieu et al. 1994). The action of GR is critical in maintaining the redox status of cells. Some Geochemical Considerations: Absorption and Redox As(III) exists in most natural water as As(OH)3 (pKa = 9.2) and is more mobile than As(V) because it is less strongly absorbed on most mineral surfaces than the negatively charged As(V) oxyanions (H3AsO4; pKa = 2.22, 6.98, 11.53). Iron(III) oxy species are well known to have a high affinity for As(V) (Waychunas et al. 1993; Lumsdon et al. 1984), and As(III) also seems to be adsorbed on some iron(III) surfaces (Sun and Doner 1996). Little is known about the adsorption of As(III) on the terrestrially abundant aluminum oxides and aluminosilicate minerals. Activated alumina has a twofold higher affinity for As(V) than for As(III) at pH 7 (Ghosh and Yuan 1987); negligible removal of As(III) from drinking water is achieved by coagulation with alum (Hering et al. 1997). Kaolinite and montmorillonite also have higher affinities for As(V) than for As(III) (Frost and Griffin 1977). Abiotic oxidation of As(III) is enhanced in the presence of the clay minerals kaolinite and illite, a process that results in strongly bound As(V) species (Manning and Goldberg 1997; Scott and Morgan 1995). Thus, long-term modeling of arsenic mobility in soils and aquifers must consider the effects of pH and mineral conditions, which will influence both adsorption and abiotic oxidation of As(III). Little is known about the adsorption behavior of the organic arsenic species listed in Table 3-1 in spite of the use of the methylarsenicals MMA and DMA and their salts as pesticides, herbicides, and defoliants (Vallee 1973; Nriagu and Azcue 1990). Microbial Activity and Arsenic Mobilization Direct microbial reduction of arsenate to the more mobile arsenite is known for bacterial, algal, and fungal species (Cullen and Reimer 1989; Silver et al. 1993; Diorio et al. 1995). Microbial activity has been implicated in arsenic mobilization from sediments. Iron-reducing bacteria might cause arsenate dissociation from sediment that is solid as a consequence of iron

OCR for page 27
Page 35 oxide dissolution (Lovley et al. 1991). Sulfate-reducing bacteria produce hydrogen sulfide, which might promote arsenate reduction. In recent years, some arsenate-respiring bacteria have been isolated; those include the dissimilatory arsenate-reducer strain MIT-13 (Ahmann et al. 1994) and Chrysiogenes arsenatis native to gold-mine waters (Macy et al. 1996). Ahmann et al. (1997) showed that arsenic-rich anoxic sediments from the Halls Brook storage area are mobilized by native microbial activity. In particular, strain MIT-13 is likely to catalyze that activity. In related experiments, Ahmann et al. (1997) found that microbial activity catalyzed rapid dissolution of arsenic, as As(III), from Fe(II) and Fe(III) arsenates. Free Radical and Peroxy Species It has been suggested that the observed tumor promotional activity of DMA might be due to the action of active oxygen-containing species, such as the dimethylarsenic peroxyl radical (CH3)2As-O-O (Rin et al. 1995; Yamanaka et al. 1996) (see Chapter 7). In fact, not much is known about peroxy species of arsenic, but the proposed As(III) species does not seem to be a plausible entity. Phenylarsonic acid, C6H5AsO(OH)2, can act as an oxygen-transfer agent by reacting with peroxide to form the intermediate peroxy acid C6H5AsO(OH)(OOH) (Jacobson et al. 1979a,b). One compound that was formulated as (CH3)2As-S-S-As(CH3)2, close in structure to the proposed peroxyl radical, turned out to have the structure (CH3)2As(S)-S-As(CH3)2, which has arsenic in two oxidation states (Camerman and Trotter 1964). On that basis and because of the ease of oxidation of DMA(III), (CH3)2As(O)-O or even (CH3)2As(O)-O-O might be more likely candidates for active oxygen-containing species. Related antimony peroxy species have been isolated and characterized (Dodd et al. 1992). Analysis Of Arsenic Compounds The discovery by Scheele in 1775 that arsenic compounds could react under reducing conditions to produce a volatile gas, arsine (AsH3) (Partington 1962), provided a tool to counteract the use of arsenic, usually as the oxide As2O3, for homicide; that use had reached epidemic proportions during the Middle Ages. The discovery led to the development of the Marsh test for arsenic, in which arsine is volatalized out of the reaction mixture and is detected, for example, by decomposition to an arsenic mirror. Alternatively, in the Gutzeit modification, the arsine is brought into contact with a filter

OCR for page 27
Page 36 paper soaked with either silver nitrate or mercuric halide to produce a colored deposit. Both procedures can be made semiquantitative. They are the first applications of an analytical method now referred to as ''hydride generation" that is widely applicable to the analysis of elements that form volatile hydrides when treated with an appropriate reducing agent, usually sodium borohydride (Vallee 1973). In older studies, zinc and hydrochloric acid were used as reducing agents. The Gutzeit method was used in a recently published Japanese study (Tsuda et al. 1995) in which well water was found to contain arsenic in the parts-per-million range—the measurements were made in 1959. A variation of this method, Natelson's method (Natelson 1961), was used in the early study of arsenic in the well water of Taiwan (Tseng et al. 1968). That method uses colorimetric detection and is said to detect arsenic at 40 µg/L. Arsine produced from  arsenate and arsenite is sometimes reacted with silver diethyldithiocarbamate solution to produce a red solution of undetermined chemical nature that can be measured colorimetrically (Vallee 1973; Irgolic 1994; see also Table 3-3). The colorimetric method is easy to use, is inexpensive in terms of equipment and operator costs, and is commonly used by the water-supply industry. For example, Saha (1995) used the colorimetric method for his work on the wells of Bengal, and the method was used in the Lane County, Oregon, study (Morton et al. 1976); however, it has limitations with regard to sensitivity and arsenic speciation. Total-arsenic determination commonly involves oxidation of the sample, by using digestion or ashing, with a mixture of chemicals, including HNO3-H2SO4-H2O2 or HNO3-H2SO4-HCIO4 for wet digestion and MgO-MgNO3 for dry ashing (Irgolic et al. 1995). The arsenic is then determined by using one of a number of methods ranging from hydride generation (colorimetric or spectroscopic detection or neutron activation) to spectrophotometry (e.g., graphite-furnace atomic absorption (GFAA) or inductively coupled plasmaatomic emission spectrometry (ICP-AES)). Hydride Generation with Speciation The commonly used hydride-generation method that is currently applied to the determination of arsenic species is outlined in Figure 3-5. Volatile arsines are produced from a range of inorganic and methylarsenicals in both oxidation states. The four arsines, AsH3 and MexAsH3-x (x = 1-3) are produced from their appropriate precursors and are then quantified following separation if necessary. Bramen and Foreback (1973) and Andreae (1977) were among the first to use this method for arsenic speciation in natural systems.

OCR for page 27
Page 37 FIGURE 3-5 Hydride generation. Arsenic speciation by using hydride generation. UV, ultraviolet. The method involves a derivatization technique, and the number of methyl groups in the evolved arsine, MexAsH3-x, is generally the same as that in the arsenic species before reduction (Andreae 1977). The precursors to the arsines are also generally assumed to be the oxyspecies shown in Table 3-1. That is not necessarily correct. For example, in some sulfur-rich environments, the precursors to the arsines might be such compounds as MeAs(SR)2 (Bright et al. 1994, 1996). An important feature of the hydride-generation reaction is its pH dependence. All the As(III) compounds produce arsines at about pH 6 (Andreae 1977; Bright et al. 1994; Hasegawa 1997). At about pH 1, all the arsenicals are reduced to arsines. By using that difference in reactivity, As(III) and As(V) can be determined in a sample. In the absence of other confounding factors, at intermediate pHs (e.g., in acetic acid) further differentiation between species and oxidation state can be obtained (Cullen et al. 1994). When a mixture of arsines is obtained following hydride generation, the arsines must be separated before quantification can be achieved. Often, in the usual batch-type operation mode, the arsines are trapped at liquid nitrogen temperature (cryofocused) and then separated by using gas chromatography. Alternatively, the cold trapped arsines are allowed to warm up slowly, and the differences in boiling points result in sequential presentation of the four compounds to the detector. In another variation, the hydrides are trapped in cold solvent, and aliquots of the resulting solution are injected into a gas chromatograph. Many detectors have been used for the analysis of the separated arsines.

OCR for page 27
Page 72 625/3-87/013. U.S. Environmental Protection Agency, Risk Assessment Forum, Washington, D.C. Farmer, J.G., and L.R. Johnson. 1990. Assessment of occupational exposure to inorganic arsenic based on urinary concentrations and speciation of arsenic. Br. J. Ind. Med. 47:342-348. Fish, R.H., F.E. Brinckman, and K.L. Jewett. 1982. Fingerprinting inorganic arsenic and organoarsenic compounds in in situ oil shale retort and process waters using a liquid chromatograph coupled with an atomic absorption spectrometer as a detector. Environ. Sci. Technol. 16:174179. Florêncio, M.H., M.F. Duarte, A.M. Bettencourt, M.L. Gomes, and L.F. Vilas Boas. 1997. Electrospray mass spectra of arsenic compounds. Rapid Commun. Mass Spectrom. 11:469-473. Foà, V., A. Colombi, M. Maroni, M. Buratti, and G. Calzaferri. 1984. The speciation of the chemical forms of arsenic in the biological monitoring of exposure to inorganic arsenic. Sci. Total Environ. 34:241-259. Food Additives and Contaminants Committee. 1984. Report on the Review of the Arsenic in Food Regulations. Ministry of Agriculture, Fisheries and Foods, FAC/REP/39. London: Her Majesty's Stationary Office. Francesconi, K.A. and J.S. Edmonds. 1997. Arsenic and marine organisms. Adv. Inorg. Chem. 44:147-189. Frost, R.R. and R.A. Griffin. 1977. Effect of pH on adsorption of arsenic and selenium from landfill leachate by clay minerals. Soil Sci. Soc. Am. J. 41:53-57. Gartrell, M.J., J.C. Craun, D.S. Podrebarac, and E.L. Gunderson. 1985. Pesticides, selected elements, and other chemicals in adult total diet samples, October 1979-September 1980. J. Assoc. Off. Anal. Chem. 68:862-875. GESAMP (IMO/FAO/UNESCO/WMO/WHO/IAEA/UN/UNEP). 1986. Joint Group of Experts on the Scientific Aspects of Marine Pollution. Review of Potentially Harmful Substances; Arsenic, Mercury, and Selenium. Report and Studies. GESAMP Vol. 28. Ghosh, M.M., and J.R. Yuan. 1987. Adsorption of inorganic arsenic and organoarsenicals on hydrous oxides. Environ. Progress 6:150-157. Gunderson, E.L. 1995. FDA total diet study, July 1986-April 1991, dietary intakes of pesticides, selected elements, and other chemicals. J. AOAC Int. 78:1353-1363. Harrison, W. W. and G.G. Clemena. 1972. Survey analysis of trace elements in human fingernails by spark source mass spectrometry. Clin. Chim. Acta 36:485-492. Hasegawa, H. 1996. Seasonal changes in methylarsenic distribution in Tosa

OCR for page 27
Page 73 Bay and Uranouchi Inlet. Appl. Organomet. Chem. 10:733-740. Hasegawa, H.  1997. The behavior of trivalent and pentavalent methyl arsenicals in Lake Biwa. Appl. Organomet. Chem. 11:305-311. Hering, J.G., P.Y. Chen, J.A. Wilkie, and M.L. Elimelech. 1997. Arsenic removal from drinking water during coagulation. J. Environ. Eng. 123:800-808. Heydorn, K. 1970. Environmental variation of arsenic levels in human blood determined by neutron activation analysis. Clin. Chim. Acta 28:349-357. Hindmarsh, J.T. 1998. Hair arsenic as an index of toxicity [abstract]. P. 7 in Book of Abstracts of the Third International Conference on Arsenic Exposure and Health Effects, July 12-15, San Diego, Calif. Hocking, D., and A.A. Jaffer. 1969. Damping-off in pine nurseries: Fungicidal control by seed pelleting. Commonwealth Forest Rev. 48:355-363. Howard, A.G., and S.C. Apte. 1989. Seasonal control of arsenic speciation in an estuarine ecosystem. Appl. Organomet. Chem. 3:499-507. Howard, A.G., and S.D.W. Comber. 1989. The discovery of hidden arsenic species in coastal waters. Appl. Organomet. Chem. 3:509-514. Inoue Y., K. Kawabata, H. Takahashi, and G. Endo. 1994. Determination of arsenic compounds using inductively coupled plasma mass spectrometry with ion chromatography. J. Chromatogr. A 675(1-2): 149-154. Irgolic, K.J. 1994. Determination of total arsenic and arsenic compounds in drinking water. Pp. 51-60 in Arsenic: Exposure and Health, W.R. Chappell, C.O. Abernathy, and C.R. Cothern, eds. Northwood, U.K.: Science and Technology Letters. Irgolic, K.J., D. Spall, B.K. Puri, D. Ilger, and R.A. Zingaro. 1991. Determination of arsenic and arsenic compounds in natural gas samples. Appl. Organomet. Chem. 5:117-124. Irgolic, K.J., H. Greschonig, and A.G. Howard. 1995. Arsenic. Pp 168184 in Encyclopedia of Analytical Science, A. Townshend, ed. London: Academic. Jacobson, S.E., F. Mares, and P.M. Zambri. 1979a. Biphase and triphase catalysis. Arsenated polystyrene as catalysts for Bayer-Villiger oxidation of ketones by aqueous hydrogen peroxide. J. Am. Chem. Soc. 101:69386946. Jacobson, S.E., F. Mares, and P.M. Zambri. 1979b. Biphase and triphase catalysis. Arsenated polystyrene catalysts for the epoxidation of olefins by aqueous hydrogen peroxide. J. Am. Chem. Soc. 101:6946-6950. Jauhiainen, M., K.J. Stevenson, and P.J. Dolphin. 1988. Human plasma lecithin-cholesterol acetyltransferase. The vicinal nature of cysteine 31 and cysteine 184 in the catalytic site. J. Biol. Chem. 263:6525-6533. Jelinek, C.F., and P.E. Corneliussen. 1977. Levels of arsenic in the United

OCR for page 27
Page 74 States food supply. Environ. Health Perspect. 19:83-87. Johnson, L.R., and J.G. Farmer. 1991. Use of human metabolic studies and urinary arsenic speciation in assessing arsenic exposure. Bull. Environ. Contam. Toxicol. 46:53-61. Kaise, T., and S. Fukui. 1992. The chemical form and acute toxicity of arsenic compounds in marine organisms. Appl. Organomet. Chem. 6:155-160. Kalman, D.A., J. Hughes, G. van Belle, T. Burbacher, D. Bolgiano, K. Coble, N.K. Mottet, and L. Polissar. 1990. The effect of variable environmental arsenic contamination on urinary concentrations of arsenic species. Environ. Health Perspect. 89:145-151. Kawabata, K., Y. Inoue, H. Takahashi, and G. Endo. 1994. Determination of arsenic species by inductively coupled plasma mass spectrometry with ion chromatography. Appl. Organomet. Chem. 8:245-248. Knowles, F.C. and A.A. Benson. 1983a. Mode of action of a herbicide. Johnsongrass and methanearsonic acid Sorghum halepense, reduction of methanearsonate to arsenosomethane, inhibition of malic enzymes. Plant Physiol. 71:235-240. Knowles, F.C. and A.A. Benson. 1983b. The biochemistry of arsenic. Trends Biochem. Sci. 8(5):178-180. Koch, I., L. Wang, W.R. Cullen, C.A. Ollson, and K.J. Reimer. 1998. Arsenic Speciation in Yellowknife Biota: Impact on the Terrestrial Environment. Paper presented at the Third International Conference on Arsenic Exposure and Health Effects, July 12-15, San Diego, Calif. Korte, N.E. and Q. Fernando. 1991. A review of arsenic(III) in groundwater. Crit. Rev. Environ. Control 21:1-40. Kuehnelt, D., W. Goessler, and K.J. Irgolic. 1997a. Arsenic compounds in terrestrial organisms I. Collybia maculata, Collybia butyracea, and Amanita muscaria from  arsenic smelter sites in Austria.  Appl. Organomet. Chem. 11:289-296. Kuehnelt, D., W. Goessler, and K.J. Irgolic. 1997b. Arsenic compounds in terrestrial organisms II:  Arsenocholine in the mushroom Amanita muscaria. Appl. Organomet. Chem. 11:459-470. Kumar, U.T., N.P. Vela, and J.A. Caruso. 1995. Multi-element detection of organometals by supercritical fluid chromatography with inductively coupled plasma mass spectrometric detection. J. Chromatogr. Sci. 33:606-610. Lai, V.W.M., W.R. Cullen, C.F. Harrington, and K.J. Reimer. 1997. The characterization of arsenosugars in commercially available algal products including a Nostoc species of terrestrial origin. Appl. Organomet. Chem. 11:797-803.

OCR for page 27
Page 75 Lai, V.W.M., W.R. Cullen, C.F. Harrington, and K.J. Reimer.  1998. Seasonal changes in the arsenic speciation in Fucus species. Appl. Organomet. Chem. 12:243-251. Larsen, E.H., G. Pritzl, and S.H. Hansen. 1993a. Arsenic speciation in seafood samples with emphasis on minor constituents: An investigation using high-performance liquid chromatography with detection by inductively coupled plasma mass spectrometry. J. Anal. Atomic Spectrom. 8:1075-1084. Larsen, E.H., G. Pritzl, and S.H. Hansen. 1993b. Speciation of eight arsenic compounds in human urine by high-performance liquid chromatography with inductively coupled plasma mass spectrometric detection using antimonate for internal chromatographic standardization. J. Anal. Atom. Spectrom. 8:557-563. Latimer, W.M., and J.H. Hildebrand. 1951. Reference Book of Inorganic Chemistry, 3rd Ed. New York: Macmillan. Lawrence, J.F., P. Michalik, G. Tam, H.B.S. Conacher. 1986. Identification of arsenobetaine and arsenocholine in Canadian fish and shellfish by high-performance liquid chromatography with atomic absorption detection and confirmation by fast atom bombardment mass spectrometry. J. Agric. Food Chem. 34:315-319. Le, X.C., and M. Ma. 1998. Short-column liquid chromatography with hydride generation atomic fluorescence detection for the speciation of arsenic. Anal. Chem. 70:1926-1933. Le, X.C., W.R. Cullen, and K.J. Reimer. 1992. Decomposition of organoarsenic compounds by using a microwave oven and subsequent determination by flow injection-hydride generation-atomic absorption spectrometry. Appl. Organomet. Chem. 6:161-171. Le, X.C., W.R. Cullen, and K.J. Reimer. 1993. Determination of urinary arsenic and impact of dietary arsenic intake. Talanta 40:185-193. Le, X.C., W.R. Cullen, and K.J. Reimer. 1994a. Effect of cysteine on the speciation of arsenic by using hydride generation atomic absorption spectrometry. Anal. Chim. Acta 285:277-285. Le, X.C., W.R. Cullen, and K.J. Reimer, K. J. 1994b. Human urinary arsenic excretion after one time ingestion of seaweed, crab and shrimp. Clin. Chem. 40:617-625. Le, X.C., M. Ma, and N.A. Wong. 1996. Speciation of arsenic compounds using high-performance liquid chromatography at elevated temperature and selective hydride generation atomic fluorescence detection. Anal. Chem. 68:4501-4506. Le, X.C., M. Ma, S. Yalcin, N.A. Wong, J. Feldmann, V.W. Lai, and W.R. Cullen. 1998. Stability of Arsenic Species in Urine and Water. Paper

OCR for page 27
Page 76 presented at the Third International Conference on Arsenic Exposure and Health Effects, July 12-15, San Diego, Calif. Ledet, A.E. and W.B. Buck. 1978. Toxicity of organic arsenicals in feedstuffs. Pp. 375-391 in Toxicity of Heavy Metals in the Environment, Part 1. F. W. Oehme, ed. New York: Marcel Dekker. Lerman, S., and T.W. Clarkson. 1983. The metabolism of arsenite and arsenate by the rat. Fundam. Appl. Toxicol. 3:309-314. Li, G.C., W.C. Fei, and Y.P. Yen. 1979. Survey of arsenical residual levels in the rice grain from various locations in Taiwan. Natl. Sci. Council Monthly 7:700-706. Li, J., and C.M. Pickart. 1995. Binding of phenylarsenoxide to Arg-tRNA protein transferase is independent of vicinal thiols.  Biochemistry 34:15829-15837. Liebscher, K., and H. Smith. 1968. Essential and nonessential trace elements. A method of determining whether an element is essential or nonessential in human tissue. Arch. Environ. Health 17:881-890. Lin, T.H., and Y.L. Huang. 1995. Chemical speciation of arsenic in urine of patients with blackfoot disease. Biol. Trace Elem. Res. 48:251-261. Lovley, D.R., E.J.P. Phillips, and D.J. Lonergan. 1991. Enzymatic versus nonenzymatic mechanisms for Fe(III) reduction in aquatic sediments. J. Environ. Sci. Technol. 25:1062-1067. Lu, F.J. 1990. Fluorescent humic substances and blackfoot disease in Taiwan. Appl. Organomet. Chem. 4:191-195. Lu, F.J., and Y.S. Lee. 1992. Humic acid: Inhibitor ofplasmin. Sci. Total Environ. 114:135-139. Lu, F.J., H.P. Hsieh, H. Yamauchi, and Y. Yamamura. 1991. Fluorescent humic substances-arsenic complex in well water in areas where blackfoot disease is endemic in Taiwan. Appl. Organomet. Chem. 5:507-512. Lu, F.J., T.S. Huang, Y.S. Lin, V.F. Pang, and S.Y. Lin. 1994. Peripheral vasculopathy in rats induced by humic acids. Appl. Organomet. Chem. 8:223-228. Lumsdon, D.G., R.A. Fraser, J.D. Russel, and N.T. Livesey. 1984. New infrared band assignments for the arsenate ion adsorbed on synthetic goethite (a-FeOOH) J. Soil Sci. 35:381-386. Macy, J.M., K. Nunan, K.D. Hagen, D.R. Dixon, P.J. Harbour, M. Cahill, and L.I. Sly. 1996. Chrysiogenes arsenatis gen. nov., sp. nov., a new arsenate-respiring bacterium isolated from gold mine wastewater. Int. J. Syst. Bacteriol. 46:1153-1157. Maeda, S. 1994. Biotransformation of arsenic in the freshwater environment. Pp. 155-187 in Arsenic in the Environment. Part 1: Cycling and Characterization, J.O. Nriagu, ed. New York: Wiley Interscience.

OCR for page 27
Page 77 Manning, B.A. and S. Goldberg. 1997. Adsorption and stability of arsenic(III) at the clay mineral-water interface. Environ. Sci. Technol. 31:2005-2011. Mayer, D.R., W. Kosmus, H. Pogglitsch, D. Mayer, and W. Beyer. 1993. Essential trace elements in humans: Serum arsenic concentrations in hemodialysis patients in comparison to healthy controls. Biol. Trace Elem. Res. 37:27-38. Monplaisir, G.M., T. Lei, and W.D. Marshall. 1994. Performance of a novel silica T-tube interface. Anal. Chem. 66:3533-3539. Morita, M., and Y. Shibata. 1990. Chemical form of arsenic in marine macroalgae. Appl. Organomet. Chem. 4:181-190. Morton, W., G. Starr, D. Pohl, J. Stoner, S. Wagner, and P. Weswig. 1976. Skin cancer and water arsenic in Lane County, Oregon. Cancer 37:25232532. Mushak, P., and A.F. Crocetti. 1995. Risk and revisionism in arsenic cancer risk assessment. Environ. Health Perspect. 103:684-689. Natelson, S. 1961. Part II. Methodology. Pp. 113-116 in Microtechniques of Clinical Chemistry, 2nd Ed. Springfield, Ill.: Charles C Thomas. Nissen, P., and A.A. Benson. 1982. Arsenic metabolism in freshwater and terrestrial plants. Physiol. Plant. 54:446-450. NRCC (National Research Council of Canada). 1986. Certified Reference Materials. National Research Council of Canada, Institute for National Measurement Standards, Ottawa, Ont. Nriagu, J.O., and J.M. Azcue. 1990. Food contamination with arsenic in the environment. Pp. 121-143 in Food Contamination from Environmental Sources. J.O. Nriagu and M.S. Simmons, eds. New York: John Wiley & Sons. Odanaka, Y., O. Matano, and S. Goto. 1980. Biomethylation of inorganic arsenic by the rat and some laboratory animals. Bull. Environ. Contam. Toxicol. 24:452-459. Odanaka, Y., N. Tsuchiya, O. Matano, and S. Goto. 1985. Characterization of arsenic metabolites in rice plant treated with DSMA (disodium methanearsonate). J. Agric. Food Chem. 33:757-763. OME (Ontario Ministry of the Environment) 1987. Organic vs Inorganic Arsenic in Selected Food Samples. Rep. 8748-450000-057. Ontario Ministry of the Environment, Hazardous Contaminants Coordination Branch, Toronto, Ont. Palacios, M.A., M. Gomez, C. Camara, and M.A. Lopez. 1997. Stability studies of arsenate, monomethylarsonate, dimethylarsinate, arsenobetaine and arsenocholine in deionized water, urine and clean-up dry residue from urine samples and determination by liquid chromatography. Anal. Chim.

OCR for page 27
Page 78 Acta 340:209-220. Pan, T.C., T.H. Lin, C.L. Tseng, M.H. Yang, and C.W. Huang. 1993. Trace elements in hair of blackfoot disease. Biol. Trace Elem. Res. 39: 117-128. Partington, J.R. 1962. VI. Chemistry in Scandinavia. II. Scheele. Pp. 205234 in A History of Chemistry, Vol. 3. London: Macmillan. Pergantis, S.A., E.M. Heithmar, and T.A. Hinners. 1995. Microscale flow injection and microbore high-performance liquid chromatography coupled with inductively coupled plasma mass spectrometry via a high-efficiency nebulizer. Anal. Chem. 67:4530-4535. Pergantis, S.A.. W.R. Cullen, D.T. Chow, and G.K. Eigendor. 1997a. Liquid chromatography and mass spectrometry for the speciation of arsenic animal feed additives. J. Chromatogr. A 764:211-222. Pergantis, S.A., W. Winnik, and D. Betowski. 1997b. Determination often organoarsenic compounds using microbore high-performance liquid chromatography coupled with electrospray mass spectrometry-mass spectrometry. J. Anal. Atom. Spectrom. 12:531-536. Pergantis, S.A., E.M. Heithmar, and T.A. Hinners. 1997c. Speciation of arsenic animal-feed additives by microbore high-performance liquid chromatography with inductively coupled plasma mass spectrometry. Analyst 122:1063-1068. Pfannhauser, W., and U. Pechanek. 1977. The contamination of food in Austria by toxic heavy metals [in German]. Lebensm. Ernähr. 30:88-92. Pirl, J.N., G.F. Townsend, A.K. Valaitis, D. Grohlich, and J.J. Spikes. 1983. Death by arsenic: A comparative evaluation of exhumed body tissues in the presence of external contamination. J. Anal. Toxicol. 7:216-219. Pyles, R.A. and E.A. Woolson. 1982. Quantitation and characterization of arsenic compounds in vegetables grown in arsenic acid treated soil. J. Agric. Food Chem. 30:866-870. Reimer, K.J., X.C., Le, and W.R. Cullen. 1994. Speciation of arsenic compounds in some marine organisms. Environ. Sci. Technol. 28:15981604. Rin, K., K. Kawaguchi, K. Yamanaka, M. Tezuka, N. Oku, and S. Okada. 1995. DNA-strand breaks induced by dimethylarsinic acid, a metabolite of inorganic arsenics, are strongly enhanced by superoxide anion radicals. Biol. Pharmacol. Bull. 18:45-48. Sagan, L.S., R.A. Zingaro, and K.J. Irgolic. 1972. Alkoxy-, alkylthio-, and (organyseleno)dialkylarsines. J. Organomet. Chem. 39:301-311. Saha, K.C. 1995. Chronic arsenical dermatoses from tube-well water in West Bengal during 1983-87. Ind. J. Dermatol. 40:1-12.

OCR for page 27
Page 79 Schaller, K.H., M. Fleischer, J. Angerer, and J. Lewalter. 1991. Arsenic determination in urine. Pp. 69-80 in Analyses of Hazardous Substances in Biological Materials, J. Angerer and K.H. Schaller, eds. Weinheim, Germany: VCH. Schmitt, V.O., J. Szpunar, O.F. Donard, and R. Lobinski. 1997. Microwave accelerated sample preparation for speciation analysis of organotin compounds in biomaterials. Can. J. Anal. Sci. Spectrosc. 42:33-68. Schoof, R.A., L.J. Yost, E. Crecelius, K. Irgolic, W. Goessler, H.R. Guo, and H. Greene. 1998. Dietary arsenic intake in Taiwanese districts with elevated arsenic in drinking water. Hum. Ecol. Risk Assess. 4:117-135. Schwedt, G., and M. Reickhoff. 1996a. Analysis of oxothio arsenic species in soil and water. J. Prakt. Chem. 338:55-59. Schwedt, G., and M. Reickhoff. 1996b. Separation of thio- and oxothioarsenates by capillary zone electrophoresis and ion chromatography. J. Chromatogr. A 736:341-350. Sckerl, M.M., and R.E. Frans 1969. Translocation and metabolism of MMA-14C in johnsongrass and cotton-D. Weed Sci. 17:421-427. Scott, M.J., and J.J. Morgan. 1995. Reactions of oxide surface. Oxidation of As(III) by synthetic birnessite. Environ. Sci. Technol. 29:1898-1905. Sheppard, B.S., J.A. Caruso, D.T. Heitkemper, and K.A. Wolnik. 1992. Arsenic speciation by ion chromatography with inductively coupled plasma mass spectrometric detection. Analyst 117:971-975. Sheridan, J.E., J.D. Whitehead, and A.G. Spiers.  1973.  Control of mercury-resistant Pyrenophora avenae on seed oats with methyl arsenic sulphide. N.Z. J. Exp. Agric. 1:127-130. Shibata, Y., M. Morita, and K. Fuwa. 1992. Selenium and arsenic in biology: Their chemical forms and biological functions. Adv. Biophys. 28:31-80. Shibata, Y., J. Yoshinaga, and M. Morita. 1994. Detection of arsenobetaine in human blood. Appl. Organomet. Chem. 8:249-251. Shiomi, K., M. Chino, and T. Kikuchi. 1990. Metabolism in mice of arsenic compounds contained in the red alga Porphyra yezoensis. Appl. Organomet. Chem. 4:281-286. Shiomi, K., Y. Sugiyama, K. Shimakura, and Y. Nagashima. 1995. Arsenobetaine as the major arsenic compound in the muscle of two species of freshwater fish. Appl. Organomet. Chem. 9:105-109. Silver, S., G. Ji, S. Broer, S. Dey, D. Dou, and B. R. Rosen. 1993. Orphan enzyme or patriarch of a new tribe: The arsenic resistance ATPase of bacterial plasmids. Mol. Microbiol. 8:637-642. Siu, K.W.M., G.J. Gardner, and S.S. Berman. 1988. Atmospheric pressure chemical ionization and electrospray mass spectrometry of some organo-

OCR for page 27
Page 80 arsenic species. Rapid Commun. Mass Spec. 2:69-71. Siu, K.W.M., R. Guevremont, J.C.Y. le Blanc, G.J. Garnder, and S.S. Berman. 1991. Electrospray interfacing for the coupling of ion exchange and ion-pairing chromatography to mass spectrometry. J. Chromatogr. 554(1/2):27. Smith, H. 1964. The interpretation of the arsenic content of human hair. Forsensic Sci. Soc. J. 4:192-199. Sohrin, Y., M. Matsui, M. Kawashima, M. Hojo, and H. Hasegawa. 1997. Arsenic biogeochemistry affected by eutrophication in Lake Biwa, Japan. Environ. Sci. Technol. 31:2712-2720. Sturgeon, R.E., M.K.W. Siu, S.N. Willie, and S.S. Berman. 1989. Quantification of arsenic species in a river water reference material for trace metals by graphite furnace atomic absorption spectrometric techniques. Analyst 114:1393-1396. Sun, X., and H.E. Doner. 1996. An investigation of arsenate and arsenate bonding structures on goethite by FTIR. Soil Sci. 161:865-872. Tao, S.H., and P.M. Bolger. 1998. Dietary Intakes of Arsenic in the United States. Paper presented at the Third International Conference on Arsenic Exposure and Health Effects, July 12-15, San Diego, Calif. Tay, C.H., and C.S. Seah. 1975. Arsenic poisoning from anti-asthmatic herbal preparations. Med. J. Aust. 2:424-428. Tseng, W.P., H.M. Chu, S.W. How, J.M. Fong, C.S. Lin, and S. Yeh. 1968. Prevalence of skin cancer in an endemic area of chronic arsenicism in Taiwan. J. Natl. Cancer Inst. 40:453-463. Tsuda, T., A. Babazono, E. Yamamoto, N. Kurumatani, Y. Mino, T. Ogawa, Y. Kishi, and H. Aoyama. 1995. Ingested arsenic and internal cancer: A historical cohort study followed for 33 years. Am. J. Epidemiol. 141:198-209. Vahter, M. 1994. Species differences in the metabolism of arsenic compounds. Appl. Organomet. Chem. 8:175-182. Vahter, M., E. Marafante, and L. Dencker. 1984. Tissue distribution and retention of 74As-dimethylarsinic acid in mice and rats. Arch. Environ. Contam. Toxicol. 13:259-264. Vahter, M., G. Concha, B. Nermell, R. Nilsson, F. Dulout, and A.T. Natarajan. 1995. A unique metabolism of inorganic arsenic in native Andean women. Eur. J. Pharmacol. Environ. Toxicol. Pharmacol. 293:455-462. Vallee, B.L. 1973. Arsenic. Air Quality Monographs, No. 73-18. Washington, D.C.: American Petroleum Institute. Vela, N.P. and J.A. Caruso. 1993. Potential of liquid chromatographyinductively coupled plasma mass spectrometry for trace metal speciation.

OCR for page 27
Page 81 J. Anal. Atom. Spect. 8:787-794. Vetter, J. 1994. Data on arsenic and cadmium contents of some common mushrooms. Toxicon 32:11-15. Waychunas G.A., B.A. Rea, C.C. Fuller, and J.A. Davis. 1993. Surface chemistry of ferrihydrite: Part 1. EXAFS studies of the geometry of coprecipitated and adsorbed arsenate. Geochim. Cosmochim. Acta 57:22512269. WHO (World Health Organization). 1989. Arsenic. Pp 155-162. In: Toxicological Evaluation of Certain Food Additives and Contaminants. WHO Food Additive Ser. 24. Cambridge, U.K.: Cambridge University Press. Yalcin, S., and X.C. Le. 1998. Preconcentration and speciation of arsenic species via solid phase extraction cartridges. Paper 384 presented at the 81st Canadian Society for Chemistry Conference and Exhibition, Whistler, B.C., May 31-June 4, 1998. Yamanaka, K., K. Ohtsubo, A. Hasegawa, 1H. Hayashi, H. Ohji, M. Kanisawa, and S. Okada. 1996. Exposure to dimethylarsinic acid, a main metabolite of inorganic arsenics, strongly promotes tumorigenesis initiated by 4-nitroquinoline 1-oxide in the lungs of mice. Carcinogenesis 17:767-770. Yamato, N. 1988. Concentration and chemical species of arsenic in human urine and hair. Bull. Environ. Contam. Toxicol. 40:633-640. Yamauchi, H., and Y. Yamamura. 1984. Metabolism and excretion of orally administered dimethylarsinic acid in the hamster.  Toxicol. Appl. Pharmacol. 74:134-140. Yamauchi, H., K. Takahashi, M. Mashiko, and Y. Yamamura.  1989. Biological monitoring of arsenic exposure of gallium arsenide- and inorganic arsenic-exposed workers by determination of inorganic arsenide and its metabolites in urine and hair. Am. Ind. Hyg. Assoc. J. 50:606-612. Yang, H.L., S.C. Tu, F.J. Lu, and H.C. Chiu. 1994. Plasma protein C activity is enhanced by arsenic but inhibited by fluorescent humic acid associated with blackfoot disease. Am. J. Hematol. 46:264-269. Yost, L.J., R.A. Schoof, and R. Aucoin. 1998. Intake of inorganic arsenic in the North American diet. Hum. Ecol. Risk Assess. 4:137-152. Zhang, X., R. Cornelis, J. De Kimpe, and L. Mees. 1996a. Arsenic speciation in serum of uraemic patients based on liquid chromatography with hydride generation atomic absorption spectrometry and on-line UV photooxidation digestion. Anal. Chim. Acta 319:177-185. Zhang, X., R. Cornelis, J. De Kimpe, L. Mees, V. Vanderbiesen, A. De Cubber, and R. Vanholder. 1996b. Accumulation of arsenic species in serum of patients with chronic renal disease. Clin. Chem. 42(8 Pt 1):1231-1237.

OCR for page 27
Page 82 Zingaro, R.A., and J.K. Thomson. 1973. Thio and seleno sugar esters of dialkylarsinous acids. Carbohydr. Res. 29:147-152.