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Poison group analysis

TABLE 16.1. Comparison of Order of Examination for Poison Groups, Target Specimens, and Methods Commonly Used in Systematic Toxicological Analysis... [Pg.314]

Pesticide poisoning incidents from 1959-68 in Uzbekistan were analyzed. The acute poisoning analysis permitted us to divide sufferers into three groups the first indudes workers who have direct contact with pestiddes the second includes collective farm workers who worked in the fields shortly after the crops were treated and the third includes people who suffered the effects of pestiddes introduced into their bodies through water, food, and inhalation. [Pg.61]

Adverse effects on the thyroid have not been observed in children, however. In a study of inner-city children, linear regression analysis revealed that there was no association between PbB levels and either thyroxin or free thyroxin (Siegel et al. 1989). Similar findings were reported by Huseman et al. (1992) in a group of 12 children from the Omaha Lead and Poison Prevention Program with PbB levels in the range of 41 to 72 pg/dL. Siegel et al. (1989) offered four possible explanations to account for this apparent... [Pg.287]

L/mole). It cross-reacts at >90% with saxitoxin but at <1% with neosaxitoxin. This antibody, when used in an anti-rabbit IgG "second antibody" radioimmunoassay format, can detect pmole quantities of saxitoxin. This assay has been shown to be a simple and efficient method for the analysis of saxitoxin in clam extracts. The lack of antibody cross-reactivity to the neosaxitoxin sub-group of the paralytic shellfish poisons limits the general utility of the assay to neurophysiology studies and to certain clam species which preferentially accumulate saxitoxin. However, the radioimmunoassay serves as a good precursor in the development of an enzyme immunoassay for the paralytic shellfish poisons. [Pg.181]

Lewis and coworkers have also made significant contributions to the understanding of the MCS reaction via the use of surface studies72. XPS and AES analysis of catalytically active surfaces showed that zinc causes a restructuring of the Cu3Si surface. Additionally, zinc enrichment is enhanced by the addition of SnCLt. Lead is a well known poison for the direct reaction and the Lewis group found that lead suppressed enrichment of the Cu3Si surface in zinc and silicon. [Pg.1589]

If borate is found to be present, transfer the centrifugate from Group II to a small crucible, heat to expel hydrogen sulphide (do not evaporate to dryness), and allow to cool. Add 2-3 drops concentrated hydrochloric acid and 5-6 drops methanol, and heat on a water bath until the solution is almost evaporated to dryness. Repeat the addition of hydrochloric acid and methanol, and evaporate to dryness on the water bath. If borate is the only interfering ion, dissolve the residue in 2 ml of 2m hydrochloric acid, and continue the analysis for cations. The borate is volatilized as methyl borate (poisonous). [Pg.494]

Although investigation should always precede analysis, there is no need to wait for full completion of tile questionnaire because some poisons are so common that they should always be eliminated. These include ethanol, aspirin, paracetamol, barbiturates, and carbon monoxide. Many of tiiese can be checked by rapid analytical probing tests before a full group screen is applied. Completion of the following analytical probing tests will, in many cases, provide clues to the nature of the poison. [Pg.40]

Rapid onset of symptoms, followed by serious illness or death is the most valuable clue to the presence of this group. The probable identity of the particular poison may be indicated by the nature of the symptoms (Table 2). Physical evidence at the scene (e.g. bottles, residues in cups, etc., tubes of adhesives, and plastic bags with characteristic odours) frequently leaves little doubt of the nature of the intoxicant, if the material is submitted within 48 hours. If deadi has been delayed for several days by hospital treatment, it is imperative to obtain for analysis any antemortem samples taken on admission to hospital, no matter how small. [Pg.43]

If several days have elapsed before the body is discovered, there is a tendency to tiiink that analysis for volatile poisons would be futile. In fact it should be one of the first groups to be checked. The presence of alcohols, toluene, and halogenated hydrocarbons... [Pg.43]

Azaspiracid (AZA-1) and related compounds were involved in a nnmber of recent hnman intoxifications, cansing DSP-like symptoms. The toxic syndrome is called azaspiracid poisoning (AZP). The LC-MS analysis of AZA-1 was reported by Draisci et al. [125]. Isocratic elntion with 85% acetonitrile in 0.03% aqneons TFA from a 1.0-imn-ID Cig colnnm at 30 pl/min was performed. [M+H] was observed at m/z 842. In MS-MS, three snbsequent water losses were observed, next to several other minor fragments. The irrstrumental detection limit was 20 pg, which is cortsiderably better than the conventional mottse bioassay (2.8 pg). Lehane et al. [126] reported the analysis of AZA-1 and fom related compounds in shellfish down to 0.05 pg/ml. The same group compared various SPE methods [127]. They developed a CRM procedtrre with an ion-trap irrstrument for the determination of... [Pg.403]

The deactivation of Group VIII metal catalysts by thiophene poisoning In ethylbenzene hydrogenation has been studied. With the exception of Pt, the sequence of sulfur resistance found, Pt < Pd < N1 < Rh < Ru, correlates with the decreasing order of the density of states at the Fermi level. This behavior is explained by a competitive adsorption of both ethylbenzene and thiophene on the metal sites, which is related to the basicity of the organic compounds and the electronic structure of the metals. This hypothesis is supported by XPS analysis of both the fresh and poisoned catalysts. [Pg.499]


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See also in sourсe #XX -- [ Pg.314 ]




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Poison analysis

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