Arsenic speciation in the urine and hair of individuals exposed to airborne arsenic through coal-burning in Guizhou, PR China

Research Center for Environmental Risk, National Institute for Environmental Studies, 16-2 Onogawa, Tsukuba, 305-8506, Ibaraki, Japan.
Toxicology Letters (Impact Factor: 3.26). 02/2003; 137(1-2):35-48. DOI: 10.1016/S0378-4274(02)00379-X
Source: PubMed


The extent of exposure of residents of Changqing (Guizhou, PR China) to arsenic through coal-burning was investigated. Despite the low coal-arsenic content (56.3+/-42.5 mg As kg(-1)) when compared with coals collected at different location and times from the same province, more than 30% of the study subjects have shown symptoms of arsenicosis. Coal, urine, hair, and water samples were collected in mid-September 2001 and analysed for arsenic. The average urinary and hair-arsenic concentrations in the exposed subjects were 71.4+/-37.1 microg As g(-1) creatinine (control 41.6+/-12.1) and 7.99+/-8.16 mg kg(-1), respectively. A positive correlation between the hair and urinary-arsenic concentration (R(2)=0.601) was found. There was no significant difference between females and males for both urinary and hair-arsenic concentrations. Females were found to have a higher dimethylarsinic acid but lower percentages of inorganic arsenic and monomethylarsonic acid in their urine than males.


Available from: Amjad Shraim
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    • "Arsenic (As) is a highly toxic substance at high, acute exposures, but is also well-known for its negative health outcomes under chronic, low-to-mid-level exposure (Ratnaike 2003, Bräuner et al 2014, Das et al 2014, James et al 2014). Drinking water is generally the primary source of exposure to arsenic in areas with elevated arsenic in groundwater or surface water, although other exposure sources include food, soil and air (Canadian Council of Ministers of the Environment 1997, Schoof et al 1999, Shraim et al 2003). The World Health Organization (WHO) has recommended a maximum contaminant limit (MCL) of As in drinking water of 10 μg l −1 (World Health Organization (WHO) 2008). "
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    ABSTRACT: A new portable x-ray fluorescence (XRF) screening tool was evaluated for its effectiveness in arsenic (As) quantification in human finger and toe nails ([Formula: see text]). Nail samples were measured for total As concentration by XRF and inductively coupled plasma-mass spectrometry (ICP-MS). Using concordance correlation coefficient (CCC), kappa, diagnostic sensitivity (Sn) and specificity (Sp), and linear regression analyses, the concentration of As measured by XRF was compared to ICP-MS. The CCC peaked for scaled values of fingernail samples, at 0.424 (95% CI: 0.065-0.784). The largest kappa value, 0.400 (95% CI: -0.282-1.000), was found at a 1.3 μg g(-1) cut-off concentration, for fingernails only, and the largest kappa at a clinically relevant cut-off concentration of 1.0 μg g(-1) was 0.237 (95% CI: -0.068-0.543), again in fingernails. Analyses generally showed excellent XRF Sn (up to 100%, 95% CI: 48-100%), but low Sp (up to 30% for the same analysis, 95% CI: 14-50%). Portable XRF shows some potential for use as a screening tool with fingernail samples. The difference between XRF and ICP-MS measurements decreased as sample mass increased to 30 mg. While this novel method of As detection in nails has shown relatively high agreement in some scenarios, this portable XRF is not currently considered suitable as a substitute for ICP-MS.
    Physiological Measurement 11/2015; 36(12):2443-2459. DOI:10.1088/0967-3334/36/12/2443 · 1.81 Impact Factor
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    • "As (Li et al., 2012). In practice, however, adverse drainage from coal-mine tips is not as critical an environmental problem as from coal combustion and its products (e.g., Shraim et al., 2003; Ruhl et al., 2009). This is likely a function of the capacity of organic compounds and iron oxyhydroxides contained within the coal to complex contaminants and thus mitigate toxicity (Dang et al., 2002). "
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    Applied Geochemistry 12/2014; 51. DOI:10.1016/j.apgeochem.2014.09.010 · 2.27 Impact Factor
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    • "As described below, the specific mechanism of arsenic methylation has yet to be clarified and remains under debate. Most of the arsenic metabolites including iAs V , iAs III , MMA V , and DMA V are excreted in the urine, with DMA V being the most abundantly detected urinary metabolite (Shraim et al. 2003). Intracellular iAs III and MMA III appear to inhibit AS3MT, especially the second methylation activity (from MMA to DMA). "
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    ABSTRACT: Arsenic is a worldwide environmental pollutant and a human carcinogen. It is well recognized that the toxicity of arsenicals largely depends on the oxidoreduction states (trivalent or pentavalent) and methylation levels (monomethyl, dimethyl, and trimethyl) that are present during the process of metabolism in mammals. However, presently, the specifics of the metabolic pathway of inorganic arsenicals have yet to be confirmed. In mammals, there are two possible mechanisms that have been proposed for the metabolic pathway of inorganic arsenicals, oxidative methylation, and glutathione conjugation. Oxidative methylation, which was originally proposed in fungi, is based on findings that arsenite (iAs(III)) is sequentially converted to monomethylarsonic acid (MMA(V)) and dimethylarsinic acid (DMA(V)) in both humans and in laboratory animals such as mice and rats. However, recent in vitro observations have demonstrated that arsenic is only methylated in the presence of glutathione (GSH) or other thiol compounds, which strongly suggests that arsenic is methylated in trivalent forms. The glutathione conjugation mechanism is supported by findings that have shown that most intracellular arsenicals are trivalent and excreted from cells as GSH conjugates. Since non-conjugated trivalent arsenicals are highly reactive with thiol compounds and are easily converted to less toxic corresponding pentavalent arsenicals, the arsenic-glutathione conjugate stability may be the most important factor for determining the toxicity of arsenicals. In addition, "being a non-anionic form" also appears to be a determinant of the toxicity of oxo-arsenicals or thioarsenicals. The present review discusses both the metabolism of arsenic and the toxicity of arsenic metabolites.
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