In the present medical practice a poisoning by lead is usually proved by measuring the concentration of Pb (II) ions in blood and urine and by the determination of d-aminolevulic acid (ALA) as well as by a semiquantitative determination of the porphyrines content in urine. The above analytical procedures are time-consuming and relatively expensive. The present communication describes the procedures used for obtaining independent analytical results in following the detoxication of the organism after a lead poisoning. It has been found that the quantity of Pb(II) ions determined in urine and blood and that of d-aminolevulic acid and of porphyrines in urine are not independent. A correlation was e.g. found between the porphyrine and the d-aminolevulic acid content. Thus the determination of one of last-mentioned substances is superfluous. The correlation analysis made it possible to propose a simplification and an acceleration of following the detoxication process in a patient.
A procedure is described for microwave mineralization of urine or faeces samples as replacement for wet mineralization. The new method uses a sodium peroxosulfate solution at pressures lower than 4 MPa in two consecutive mineralizations for 60 and 30 s. For complete decomposition, it is necessary to boil the mixture once again with a sodium peroxosulfate solution and evaporate it to dryness. The results obtained are about 5-10 % higher than those from classic mineralization, which indicates a more thorough decomposition of the matrix. The time required for microwave mineralization (ca. 30 min) is substantially shorter than that for wet mineralization. The same method can be used in determination of metals in urine simultaneously (e.g. cadmium, thallium, copper, and lead).
A procedure of pretreatment of urine samples with active carbon for voltammetric determination of thiodiglycolic acid is described. The procedure enables rapid distinguishing uncontaminated samples from those contaminated above a certain limit.
Abstract Chromosome analysis was conducted for peripheral lymphocytes of 23 printers exposed to toluene concentrations of 590 mg/m3 in a rotary machine workshop and to rotogravure printing inks. The percentages of aberrant cells were 2.30 in the printers and 1.46 in the control group (n = 22) (p < .05). The concentration of hippuric acid in printers was significantly higher than in the control group (p < .01), and the level of blood toluene at the end of the workshift was 0.500 mg/l. The authors also examined rotogravure printing inks—considered a potential source of genotoxic polycyclic aromatic hydrocarbons because they contained carbon black—their use in printing plants, and previous documentation of increased chromosomal aberrations in rotogravure printers. Only milligrams of fluorene and phenanthrene per gram of the printing inks were found; no polycyclic aromatic hydrocarbons with carcinogenic properties were discovered in the inks. The authors used Salmonella typhimurium indicator strains TA 98, TA 100, TA 1537, and YG 1041 in spot tests and indicator strains TA 98 and TA 100 in plate-incorporation assays to determine that there was no bacterial mutagenicity of all four colors of rotogravure inks. Urinary mutagenicity, which was evaluated with a microsuspension assay containing YG 1041 indicator strain both in the presence and absence of metabolic activation, was also studied. No significant difference in bacterial mutagenicity was found between the exposed and control groups. The increased percentage of aberrant cells in printers can be explained by exposure to genotoxicants that are not excreted in urine. Toluene was the most likely cause of the aberration.
Abstract Presented herein are the results of follow-up examinations of 13 workers performed in 1996–30 yr following 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) intoxication in a herbicide production plant. In these workers, the current mean plasma level of 2,3,7,8-TCDD, measured by high-resolution gas chromatography/high-resolution mass spectrometry, was 256 pg/gm lipid (range = 14–760 pg/gm lipid). This mean value corresponded to an estimated concentration of approximately 5,000 pg/gm plasma fat that existed about 30 years ago. Such a mean plasma level indicates that this group was one of the most heavily exposed groups to 2,3,7,8-TCDD described in the literature. Patients with persistent chloracne had significantly higher plasma levels of 2,3,7,8-TCDD than persons without chloracne. A significant, positive correlation was found between plasma levels of 2,3,7,8-TCDD in 1996 and levels of cholesterol and plasma lipids that existed since 1974. During 1996, there was a significant positive correlation between 2,3,7,8-TCDD and levels of beta-lipoproteins, cholesterol, and triglycerides. Also in 1996, significant correlations were found between neuropsychological variables and plasma levels of 2,3,7,8-TCDD. Other significant correlations were observed between neuropsychological variables and (1) the highest levels of triglycerides (i.e., since the year 1989), (2) levels of triglycerides in 1996, (3) levels of cholesterol at the first examination (i.e., 1969–1970), (4) highest level of cholesterol since the year 1969, and (5) cholesterol levels in 1996. Such correlations are biologically plausible, and they provide evidence of impaired cognitive performance (i.e., memory first), with a concurrent increase of plasma lipid levels. Abnormal electromyography, electroencephalography, and visual evoked potentials were observed in 23%, 54%, and 31 %, respectively, of former workers. Abnormal electroencephalography findings occurred more frequently in workers who had 2,3,7,8-TCDD blood levels that exceeded 200 pg/gm plasma fat than in workers with 2,3,7,8-TCDD values lower than 200 pg/gm plasma fat (p < .025). Frequency of polyneuropathic EMG abnormalities decreased from 38% in the 1970s to 23% in 1996. Improvement of conduction velocity in the tibial nerve was statistically significant (p < .05).
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