No abstract

Urine samples were collected from 64 men and 88 women in shoe factories and printing plants at the end of a seven hour day shift in the latter half of a week in spring. Urine samples were also taken from 43 men and 88 women in the same factories but who were not exposed to solvents. Exposure to benzene during the shift was monitored by passive dosimeters. Both phenol in urine and benzene in activated carbon were analysed with FID gas chromatographs. The urinary concentrations of phenol were linearly related to the time weighted average concentrations of benzene in the breathzone air; the variation was so small that those exposed to 10 ppm benzene could be separated from the non-exposed at least on a group basis when the phenol concentration was corrected either for creatinine concentration or for specific gravity. The urinary phenol concentrations corresponding to lOppm benzene were 47T5mg/1 (as observed), 57-9mg/g creatinine, or 46-6 mg/l (specific gravity 1*016).Benzene is considered to be a cause of human leukaemia' and occupational as well as nonoccupational exposure to this chemical has been a focus of keen attention. Among the biological indicators of exposure to benzene, urinary phenol has been most frequently used although it may be inferior to benzene in blood in its sensitivity and specificity,2 3 probably because urine is apparently much more readily available from factory workers than venous blood, and this is especially so in the case of the -general population. The existing data on the quantitative relation between exposure to benzene and urinary phenol excretion are, however, usually hampered by the technical limitations prevailing at the time of the study such as the low specificity of urinary phenol determination, the inability to measure average exposure during work, the small number of subjects, or a combination of these factors.2The present study was initiated to establish the quantitative exposure excretion relation, using passive samplers to determine the time weighted average exposure intensity of exposure to benzene and FID gas chromatography for the specific meaAccepted 21 January 1986 surement of phenol in urine. The results of studies with similar methodology have been described for toluene hippuric acid/o-cresol4 and tetrachloroethylene total trichloro compounds.5 Materials and methods EXAMINEESThe factory survey was conducted in the latter half of a week in spring. The workers exposed to benzene were 64 men (aged 26-9 + 8-4 years as arithmetic mean + arithmetic standard deviation (AM + ASD)) and 88 women (29-9 + 8-5 years) in five workshops in two shoe factories and two small printing plants. Control subjects were 43 men (39 3 + 119 years) and 88 women (26 9 + 8-4 years) who worked in the same factories but had not been exposed to solvents. Those under medical treatment with drugs were excluded. COLLECTION AND ANALYSES OF URINE SAMPLESEach subject was asked to pass urine at about 1300. The urine sahilple for analysis was collected at about 1500 when the seven hour shift was ...

Time weighted average concentrations of benzene in breathing zone air (measured by diffusive sampling coupled with FID gas chromatography) and concentrations ofcatechol and quinol in the urine (collected at about 1500 in the second half of a working week and analysed by high performance liquid chromatography) were compared in 152 workers who were exposed to benzene (64 men, 88 women). The concentration of urinary metabolites was also determined in 131 nonexposed subjects (43 men, 88 women). There was a linear relation between the benzene concentrations in the breathing zone and the urinary concentrations of catechol and quinol (with or without correction for urine density) in both sexes. Neither catechol nor quinol concentration was able to separate those exposed to benzene at 10 ppm from those without exposure. The data indicated that when workers were exposed to benzene at 100 ppm about 25% ofbenzene absorbed was excreted into the urine as phenolic metabolites, ofwhich 1 3 2%, 1*6%, and 10-2% are phenol, catechol, and quinol, respectively.As early as 1953, Parke and Williams identified catechol and quinol, in addition to phenol, in the urine of rabbits given '4C-benzene by mouth.' Regarding the biological monitoring by means of urine analysis, however, attention has been focused on phenol as an indicator of exposure to benzene.2 Other phenolic urinary metabolites such as catechol and quinol are ignored, probably because of the technical difficulties in their analysis. A high performance liquid chromatographic (HPLC) method for the simultaneous determination of catechol and quinol34 has been applied in our laboratory to the analysis of urine samples obtained from workers exposed to benzene, and the excretion of the two metabolites was related to the intensity of exposure to benzene. The results are presented in this report compared with previous findings5 on excretion of phenol. Materials and methods EXAMINEES AND URINE COLLECTIONUrine samples previously analysed for phenol5 were used. In brief, urine samples were collected from 152 workers (64 men, 88 women)

Over 100 workers exposed to trichloroethylene (TRI) mostly at less than 50 ppm during the production or vapor degreasing operation and about an equal number of the non-exposed control workers were examined for subjective symptoms, hematology, serum biochemistry, and sugar, protein and occult blood in urine. Essentially all the clinico-laboratory tests stayed normal, and there was no significant difference in the findings between the exposed and the controls. Thus, no clinically significant effects of TRI exposure were found in the blood and liver functions among the exposed workers as compared with the controls. The prevalence of the subjective symptoms was, however, significantly higher in the exposed group than in the controls, and dose-response relationship could be established in some selected symptoms such as nausea, heavy feeling in the head, forgetfulness, tremor in extremities, cramp in extremities and dry mouth, although the exposure was low. The findings warrant further attention to the effects of TRI especially on the central nervous system at the concentration lower than, e.g., 50 ppm.

While this study is larger than previous investigations and includes workers with a wide range of exposures to benzene, the estimates of risk, as measured by statistical confidence intervals, are still fairly broad, and would benefit from the larger numbers that could be provided by continued follow-up of this population. Nevertheless, the study confirms earlier findings of increased risk for ANLL and aplastic anemia among benzene-exposed workers, provides the first substantial evidence that MDS is linked to benzene exposure, and provides evidence that benzene increases risk for ANLL/MDS at lower levels of exposure than had previously been demonstrated. Currently we are evaluating the potential for extending the follow-up of workers included in this study. A new study would include expanded data collection for cases of hematopoietic malignancy and related disorders and for an appropriate control series.