Documents determination in urine 12 results

"Objectives The aims were to study the toxicokinetics of 5-hydroxy-N-methyl-2-pyrrolidone (5-HNMP) in blood and urine after exposure to N-methyl-2-pyrrolidone (NMP) and to study the suitability of 5-HNMP as a biomarker for assessing NMP exposure.Methods Six male volunteers were exposed for 8 hours to NMP concentrations of 0, 10, 25, and 50 mg/m3. Blood and urine were sampled before, during, and up to 40 hours after exposure. Aliquots of urine and plasma were purified, derivatized, and analyzed for 5-HNMP on a gas chromatograph/mass spectrometer in the electron impact mode.Results The mean plasma concentration [P-(5-HNMP)] after 8-hour NMP exposure to 10, 25, and 50 mg/m3 was 8.0, 19.6, and 44.4 mmol/l, respectively. The mean urinary concentration [U-(5-HNMP)] for the 2 last hours of exposure was 17.7, 57.3, and 117.3 mmol/mol creatinine, respectively. The maximal P-(5-HNMP)and U-(5-HNMP) concentrations occurred 1 hour and 0-2 hours, respectively, after the exposure. The half-times of P-(5-HNMP) and U-(5-HNMP) were 6.3 and 7.3 hours, respectively. The 5-HNMP urinary concentrations were 58% of the calculated retained dose. There was a close correlation (r) between P-(5-HNMP) (r=0.98) and U-(5-HNMP) (r=0.97) with NMP exposure.Conclusion 5-HNMP is an excellent biomarker for assessing exposure to NMP. Its plasma and urinary half-times (6-7 hours), the minimal risk for contamination during sampling in occupational settings, and the close correlation of P-(5-HNMP) and U-(5-HNMP) with NMP exposure makes 5-HNMP suitable for monitoring exposure to NMP. 5-HNMP in plasma is recommended."

Background The aim of the study was to evaluate whether cadmium concentrations in kidney (K-Cd), blood (B-Cd) or urine (U-Cd) could reveal previous occupational cadmium exposure at a metal smelter. Methods The study included 90 smelters and 35 controls (B-Cd and U-Cd determination). In a subgroup (N = 33), K-Cd was also determined. Results B-Cd (median 4.6; range 0.5-53 nmol/L), U-Cd (0.29; 0.04-1.9 mol/mol creatinine) and K-Cd (14; 3-61 g/g wet weight) were similar to reported concentrations in the general Swedish population. In the subgroup, significant associations (P<0.001) were obtained between B-Cd and K-Cd (r = 0.70), U-Cd and K-Cd (r = 0.60) and between U-Cd and B-Cd (r = 0.62). Multiple regression analyses revealed smoking as the major predictor of K-Cd, B-Cd, and U-Cd. B-Cd and U-Cd were both associated with the duration of employment at the smelter. Conclusions There was no statistically significant evidence of previous occupational exposure at the smelter from measurement of K-Cd.

Volume 1
A detailed guide to the biological monitoring of occupational exposures to selected metals, solvents, pesticides, and other chemicals. Addressed to occupational health professionals and the managers of analytical laboratories, the book aims to promote the use of biological monitoring as an integral part of efforts to safeguard occupational health and safety. To this end, chapters draw on the latest scientific knowledge to identify recommended biomarkers of exposure and provide technical advice on the best methods of sampling and analysis. Recommended principles and methods reflect the consensus reached by a large number of experts.

The book opens with a discussion of basic principles governing the use of biological monitoring to obtain reliable data on exposure levels and the related risks to health. Topics covered include the concept of internal dose, three main approaches to monitoring, the types of data required, and the unique value of biological monitoring when used in conjunction with ambient monitoring. Advice on methodological procedures is provided for the implementation of sampling, analytical methods, and the interpretation of results. The importance of quality assurance is addressed in the second chapter, which gives particular attention to common sources of error in the selection, collection, storage, and transport of specimens, during the analysis of samples, and in the recording, reporting, and interpretation of results. Sources of certified reference materials for use in analytical laboratories are presented in a table.

Against this background, the main part of the book provides guidelines for the biological monitoring of exposure to four metals, eight solvents, the organophosphorus pesticides, and carbon monoxide and fluorides. Individual chemicals were selected on the basis of criteria pertaining to their frequency of use, toxicity, routes of absorption, knowledge about human metabolism, relationship between exposure and established biomarkers, and the existence of Occupational Biological Reference Values.

Guidelines for each chemical follow a common framework. The chemical is first introduced in terms of its physical and chemical properties, possible occupational and non-occupational exposures, data on toxicokinetics and toxic effects, and a comparison of currently available biological indicators of exposure. Recommended biomarkers are then discussed in terms of suggested methods of sampling and analysis, and guidelines for the interpretation of test results. The book concludes with a tabular presentation of monitoring methods and biological limit values, as proposed by three different agencies, for some 60 commonly used industrial chemicals.

Volume 2
Provides guidelines for the biological monitoring of occupational exposure to four metals (aluminium, arsenic, cobalt, and nickel), three solvents (benzene, methanol, and methylene chloride), two groups of pesticides (dithiocarbamates and pyrethroids), aromatic amines, and polycyclic aromatic hydrocarbons. Guidelines for each chemical follow a common framework. The chemical is first introduced in terms of its physical and chemical properties, possible occupational and non-occupational exposures, data on toxicokinetics and toxic effects, and a comparison of currently available biological indicators of exposure. Recommended biomarkers are then discussed in terms of suggested methods of sampling and analysis, and guidelines for the interpretation of test results.

This study describes the exposure of coke plant workers to hydrocarbons. Aromatic hydrocarbons (AHs) and polycyclic aromatic hydrocarbons (PAHs) in the breathing zone air and their oxygenated metabolites in the urine of coke plant workers are qualitatively and quantitatively determined. Concentrations of benzene, toluene, naphthalene, m+p-xylene, o-xylene and 14 different PAHs were measured at the different workplaces by personal air sampling. O-cresol, 1- and 2-naphthol, methylhippuric acid, and 1-hydroxypyrene were determined in hydrolyzed urine of workers collected after the work shift. The gas chromatography-mass spectrometry (GC/MS) method was applied to identify AHs in air and in urine samples. Time-weighted values of exposure to aromatic hydrocarbons at a coke plant were: benzene (0.06-9.82 mg/m3), toluene (0.05-4.71 mg/m3), naphthalene (0.01-3.28 mg/m3), o-xylene (0.01-1.76 mg/m3) and m + p-xylene (0.01-2.62 mg/m3). At the coke batteries, the total concentration of PAHs ranged from 7.27 to 21.92 g/m3. At the sorting department, the total concentration of PAHs were about half this value. Concentration of the urinary metabolites (naphthols and methylhippuric acid) detected in workers at the tar distillation department are three times higher than those for the coke batteries and sorting department workers. A correlation between inhaled toluene, naphthalene, xylene, and urinary excretion of metabolites has been found. Time-weighted average concentrations of AHs in the breathing zone air show that exposure levels of the workers are rather low in comparison to exposure limits. The 1-hydroxypyrene concentration is below 24.75 mol/mol creatinine. The GC/MS analysis reveals the presence of AHs, mainly benzene and naphthalene homologues. It has been found that coke plant workers are simultaneously exposed to the mixture of aromatic and polycyclic hydrocarbons present in the breathing zone air of a coke plant. Exposure levels are significantly influenced by job categories. Compounds identified in the urine appear to be the products of the hydroxylation of AHs present in the air as well as unmetabolized hydrocarbons.