Biological monitoring of occupational exposure to tetrahydrofuran.

Occupational exposure to tetrahydrofuran (THF) was studied by analysis of environmental air, blood, alveolar air, and urine from 58 workers in a video tape manufacturing plant. Head space gas chromatography (GC) with an FID detector was used for determination of THF concentration in alveolar air, urine, and blood. Environmental exposure to THF was measured by personal sampling with a carbon felt passive dosimeter. When the end of shift urinary THF concentrations were compared with environmental time weighted average (TWA) values, urinary THF concentration corrected for specific gravity correlated well with THF concentration in air (r = 0.88), and uncorrected urinary THF concentration gave a similar result (r = 0.86). Correction for creatinine in urine weakened the correlation (r = 0.56). For exposure at the TWA concentration of 200 ppm the extrapolated concentration of THF was 33 mumol/l in blood and 111.9 mumol/l (61 mumol/g creatinine) or 109 mumol/l at a specific gravity of 1.018 in urine. The correlation between exposure to THF and its concentration in exhaled breath and blood was low (r = 0.61 and 0.68 respectively). Laboratory methodological considerations together with the good correlation between urinary THF concentration and the environmental concentration suggest that THF concentration in urine is a useful biological indicator of occupational exposure to THF.     

Monitoring of exposure to cyclohexanone through the analysis of breath and urine.

Occupational exposure to cyclohexanone was studied for 59 workers through the analysis of environmental air, alveolar air, and urinary cyclohexanol. Environmental cyclohexanone exposure was measured by personal sampling with a carbon-felt passive dosimeter. Cyclohexanone in alveolar air and cyclohexanol in urine were determined with gas chromatography with a flame ionization detector. The end-of-shift urinary cyclohexanol levels correlated well with the time-weighted average environmental cyclohexanone values (r = 0.66). Urinary cyclohexanol corrected for creatinine correlated best with cyclohexanone in air (r = 0.77); when corrected for specific gravity, it gave a similar correlation coefficient (r = 0.73). When the time-weighted average of the exposure was 25 ppm, the corresponding calculated concentration for urinary cyclohexanol was 54.5 mg/1, 23.3 mg/g of creatinine, or 43.5 mg/l at a specific gravity of 1.018. The relationship between cyclohexanone exposure and its concentration in exhaled breath was found to be poorer than that for cyclohexanone exposure and the urinary metabolite (r = 0.51).     

Biological monitoring of exposure to low concentrations of styrene

A field study was conducted on 39 male workers exposed to styrene at concentrations below 40 ppm (time weighted average, TWA). Analyses were carried out on environmental air, exhaled air, blood, urine, and two major urinary metabolites of styrene: mandelic acid (MA) and phenylglycoxylic acid (PGA). Head space gas chromatography (GC) with a flame ionization detector (FID) was used for determination of styrene in blood and urine. Postexposure exhaled air was analyzed using capillary GC. Environmental styrene exposure was measured by personal sampling using carbon cloth personal samplers. Urinary metabolites of styrene were determined by high pressure liquid chromatograph (HPLC). When the end-of-shift breath, blood, and urine styrene levels were compared with environmental TWA values, blood styrene correlated best with styrene in air (r = 0.87), followed by breath styrene (r = 0.76). Poor correlation (r = 0.24) was observed between environmental styrene exposure and urine styrene. When styrene metabolites were compared with environmental styrene, the sum of urinary MA and PGA correlated better with styrene in air than MA or PGA alone. The correlations between urinary metabolites and environmental styrene improved when corrected for the specific gravity of urine. Even better correlations were observed when the urinary metabolites were corrected for creatinine. The correlation coefficients for environmental styrene and end-of-shift MA, PGA, and MA + PGA were 0.83, 0.84, and 0.86, respectively. The correlation coefficients between environmental styrene and next morning urinary metabolites fell to 0.47, 0.61, and 0.65 for MA, PGA, and MA + PGA, respectively. These results suggest that determination of the total MA and PGA in urine samples is preferred than separate measurements of MA or PGA. The good correlation between environmental exposure and styrene in the exhaled air also suggests that breath styrene level can be a useful indicator for low level styrene exposure, as the method is specific, noninvasive, and rapid. Urinary styrene seems to be a less reliable indicator for low level styrene exposure. © 1994 Wiley-Liss, Inc.     

Biological monitoring of occupational exposure to methyl ethyl ketone

Summary This study was conducted to evaluate the usefulness of three commonly used methods of biological monitoring for worker exposed to methyl ethyl ketone (MEK) under field conditions using blood, breath and urine. Environmental MEK exposures were measured by personal sampling with carbon-felt dosimeters. The correlation coefficient (r) between the time-weighted average (TWA) MEK concentration in air and the MEK concentration in blood collected at the end of the work shift was 0.85. The correlation coefficient between the TWA MEK level in air and the concentration exhaled in the breath of workers at the end of the work shift was 0.71. The end-of-shift urinary MEK excretion correlated best with the environmental concentration (r = 0.89). Correlations became lower after urine samples had been corrected for urinary creatinine (r = 0.83) or specific gravity (r = 0.73). After 8 h exposure to 200 ppm MEK, the corresponding end-of-shift urinary excretion was 5.11ol/l or 4.11 mg/g creatinine. This value is higher than that previously found in some studies, the difference probably being due to the physical acitivites of the present workers and their extensive skin contact with the solvent. The kinetics of inhaled MEK was also studied in eight subjects. Breath and urine samples were collected during the 8-h work shift on 2 consecutive Mondays. The results showed that urinary MEK excretion rose steadily until the end of exposure, whereas the MEK concentration in exhaled air varied markedly throughout the day. These findings suggest that the determination of MEK levels in end-of-shift urine samples appears to be the most reliable biological indicator of occupational exposure.     

Isopropanol exposure: environmental and biological monitoring in a printing works.

Occupational exposure to isopropanol was studied in 12 workers by testing environmental air, alveolar air, venous blood, and urine during their work shift. Isopropanol, which ranged in environmental air between 7 and 645 mg/m3, was detected in alveolar air, where it ranged between 4 and 437 mg/m3, but not in blood or in urine. Alveolar isopropanol concentration (Ca) was significantly correlated with environmental isopropanol concentration (Ci) at any time of exposure. The value of the arithmetical Ca/ci ratio was 0.418 (SD 0.101). Acetone, which is a metabolite of isopropanol, was found in alveolar air, blood, and urine in concentrations that were higher during exposure than before. Alveolar and blood acetone concentrations were highly correlated with alveolar isopropanol concentrations at any time during exposure. Acetone ranged between 0.76 and 15.6 mg/l in blood, between 4 and 93 micrograms/l in alveolar air, and between 0.85 and 53.7 mg/l in urine. Alveolar (Ca) and blood (Cb) acetone concentrations were highly correlated (r = 0.67), with a Cb/Ca ratio of 101. Alveolar isopropanol uptake ranged between 0.03 and 6.8 mg/min and was highly correlated with environmental isopropanol concentration (r = 0.92). During exposure, acetone eliminated by the lungs ranged between 20 and 273 mg in seven hours and in urine between 0.3 and 9.6 mg in seven hours. Acetonuria was higher the next morning than at the end of exposure.     

Benzene in the blood and breath of normal people and occupationally exposed workers

Benzene was measured in blood and alveolar air of 168 men, aged 20-58 years, subdivided into four groups: blood donors, hospital staff, chemical workers occupationally exposed to benzene, and chemical workers not occupationally exposed to benzene. The group of exposed workers was employed in work places with a mean environmental exposure to benzene of 1.62 mg/M3 (8 hr TWA). Non-exposed workers were employed elsewhere in the same plant, with an environmental exposure to benzene lower than 0.1 mg/M3. Blood and alveolar air samples were collected in the morning, before the start of the work shift for the chemical workers. The group of exposed workers was found to be significantly different from the other three groups, both for blood and alveolar benzene concentrations. The mean blood benzene concentration was 789 ng/l in the exposed workers, 307 ng/l in the non-exposed workers, 332 ng/l in the hospital staff, and 196 ng/l in the blood donors. Apart from the exposed workers, blood benzene concentration was significantly higher in smokers than in non-smokers. The mean alveolar benzene concentration was 92 ng/l in the exposed workers, 42 ng/l in the non-exposed workers, 22 ng/l in the hospital staff, and 11 ng/l in the blood donors. Alveolar benzene concentration was significantly higher in smokers than in non-smokers in the groups of the hospital staff and non-exposed workers, but not in the blood donors and exposed workers. In the three groups without occupational exposure considered altogether, the alveolar benzene concentration correlated significantly with environmental benzene concentration measured at the moment of the individual examinations, both in the smokers (r = .636; p less than .001) and non-smokers (r = .628; p less than .001). In the same three groups and in the exposed workers, alveolar benzene concentration showed a significant correlation with the blood benzene concentration.     

Biological monitoring of occupational exposure to methyl ethyl ketone in Japanese workers

The relationship between occupational exposure to methyl ethyl ketone (MEK) and its concentration in urine and blood was studied in a group of 72 workers in a printing factory. Personal exposure monitoring was carried out with passive samplers during the workshifts. The time weighted average (TWA) concentration of MEK ranged from 1.3 to 223.7 ppm, with a mean concentration of 47.6 ppm. In addition to MEK, toleuene, xylene, isopropyl alcohol, and ethyl acetate were detected as the main contaminants in all samples.At the end of the workshift, urine samples were collected to determine the urinary MEK, hippuric acid (HA), and creatinine, and blood samples were also collected at the same time for determination of MEK. The concentrations of urinary MEK ranged from 0.20 to 8.08 mg/L with a mean of 1.19 mg/L and significantly correlated with TWA concentrations of MEK in the air with a correlation coefficient of 0.889 for uncorrected urine samples. The concentration of MEK in the blood was also significantly correlated with the TWA concentration of MEK with a correlation coefficient of 0.820.From these relationships, MEK concentrations in urine and blood corresponding to the threshold limit value-TWA (200 ppm; ACGIH 1992) were calculated to be 5.1 mg/L and 3.8 mg/L as a biological exposure index (BEI), respectively. Although the BEI for urinary MEK obtained from the present study was higher than that of previous reports and ACGIH's recommendation (2.0 mg/L), the BEI agreed well with a previous study in Japan. On the other hand, the relationship between toluene exposure and urinary HA level, an index of toluene exposure, was also studied at the same time. The urinary concentration of HA corresponding to TWA at 100 ppm was 2.6 g/g creatinine as BEI. This value agreed well with both ACGIH's recommendation (2.5 g/g creatinine) and the values reported by Japanese researchers who have studied Japanese workers. Ethnic differences of MEK metabolism may affect the relationship between exposure and BEI.     

Environmental and occupational exposure to benzene by analysis of breath and blood

Benzene exposure of chemical workers was studied, during the entire workshift, by continuous monitoring of workplace benzene concentration, and 16 hours after the end of the workshift by the measurement of alveolar and blood benzene concentrations and excretion of urinary phenol. Exposure of hospital staff was studied by measuring benzene concentrations in the alveolar and blood samples collected during the hospital workshift. Instantaneous environmental air samples were also collected, at the moment of the biological sampling, for all the subjects tested. A group of 34 chemical workers showed an eight hour exposure to benzene, as a geometric mean, of 1.12 micrograms/l which corresponded, 16 hours after the end of the workshift, to a geometric mean benzene concentration of 70 ng/l in the alveolar air and 597 ng/l in the blood. Another group of 27 chemical workers (group A) turned out to be exposed to an indeterminable eight hour exposure to benzene that corresponded, the morning after, to a geometric mean benzene concentration of 28 ng/l in the alveolar air and 256 ng/l in the blood. The group of hospital staff (group B) had a benzene concentration of 14 ng/l in the alveolar air and 269 ng/l in the blood. Instantaneous environmental samples showed that in the infirmaries the geometric mean benzene concentration was 58 ng/l during the examination of the 34 chemical workers, 36 ng/l during the examination of the 27 chemical workers (group A), and 5 ng/l during the examination of the 19 subjects of the hospital staff (group B). Statistical analysis showed that the alveolar and blood benzene concentrations in the 34 workers exposed to 1.12 microgram/l of benzene differed significantly from those in groups A and B. It was found, moreover, that the alveolar and blood benzene concentrations were higher in the smokers in groups A and B but not in the smokers in the group of 34 chemical workers. The slope of the linear correlation between the alveolar and the instantaneous environmental benzene concentrations suggested a benzene alveolar retention of about 55%. Blood and alveolar benzene concentrations showed a highly significant correlation and the blood/air partition coefficient, obtained from the slope of the regression line, was 7.4. In the group of the 34 chemical workers no correlation was found between the TWA benzene exposure and the urinary phenol excretion.     

Environmental and occupational exposure to benzene by analysis of breath and blood.

Benzene exposure of chemical workers was studied, during the entire workshift, by continuous monitoring of workplace benzene concentration, and 16 hours after the end of the workshift by the measurement of alveolar and blood benzene concentrations and excretion of urinary phenol. Exposure of hospital staff was studied by measuring benzene concentrations in the alveolar and blood samples collected during the hospital workshift. Instantaneous environmental air samples were also collected, at the moment of the biological sampling, for all the subjects tested. A group of 34 chemical workers showed an eight hour exposure to benzene, as a geometric mean, of 1.12 micrograms/l which corresponded, 16 hours after the end of the workshift, to a geometric mean benzene concentration of 70 ng/l in the alveolar air and 597 ng/l in the blood. Another group of 27 chemical workers (group A) turned out to be exposed to an indeterminable eight hour exposure to benzene that corresponded, the morning after, to a geometric mean benzene concentration of 28 ng/l in the alveolar air and 256 ng/l in the blood. The group of hospital staff (group B) had a benzene concentration of 14 ng/l in the alveolar air and 269 ng/l in the blood. Instantaneous environmental samples showed that in the infirmaries the geometric mean benzene concentration was 58 ng/l during the examination of the 34 chemical workers, 36 ng/l during the examination of the 27 chemical workers (group A), and 5 ng/l during the examination of the 19 subjects of the hospital staff (group B). Statistical analysis showed that the alveolar and blood benzene concentrations in the 34 workers exposed to 1.12 microgram/l of benzene differed significantly from those in groups A and B. It was found, moreover, that the alveolar and blood benzene concentrations were higher in the smokers in groups A and B but not in the smokers in the group of 34 chemical workers. The slope of the linear correlation between the alveolar and the instantaneous environmental benzene concentrations suggested a benzene alveolar retention of about 55%. Blood and alveolar benzene concentrations showed a highly significant correlation and the blood/air partition coefficient, obtained from the slope of the regression line, was 7.4. In the group of the 34 chemical workers no correlation was found between the TWA benzene exposure and the urinary phenol excretion.     

o-cresol: a good indicator of exposure to low levels of toluene

This study evaluates the suitability of using urinary excretion of o-cresol (o-CR) as a biological marker of occupational exposure to various concentrations of toluene (TOL). Thirty-eight individuals from three plants involved in the manufacture of paints or inks agreed to participate in the environmental and biological monitoring evaluations, which lasted one to two days. In all, 62 measurements of environmental TOL and urinary o-CR and hippuric acid (HA) levels were made. The eight-hour TOL exposure (time-weighted average [TWA]) ranged from 0 to 111 ppm, depending on plant and job title. TOL exposure was well correlated to post-shift urinary o-CR (r = 0.89) and HA (r = 0.67) levels. At low exposure levels (below 50 ppm), however, o-CR shows a stronger correlation (r = 0.71) than HA (r = 0.24). Based on our results, occupational exposure to 50 ppm of TOL would result in end-of-shift urinary o-CR concentration of 0.72 mumol/mmol creatinine (0.69 mg/L, assuming a urinary creatinine concentration of 1 g/L). This value is of the same order of magnitude as the level proposed by the American Conference of Governmental Industrial Hygienists (ACGIH) in 1998 for exposure to 50 ppm of TOL, namely 0.5 mg/L. Our results suggest that the level of urinary o-CR is a more sensitive index of exposure to low concentrations of TOL than is the urinary concentration of HA.     

Ubiquitous pollution by n-hexane and reference biological levels in the general population

Summary n-Hexane levels were determined by gas chromatography and mass spectrometry in environmental air and in the alveolar air, blood and urine of a group of subjects aged on average of 38 years who had not been occupationally exposed to this hydrocarbon. n-Hexane was found in all environmental air samples examined (n=49), with the mean concentration being 104 ng/l (limit values, 1–279 ng/l). It was also found in all 49 samples of alveolar air, with the mean concentration being 50 ng/l (variation limit, 1–304ng/l). In 64 samples of urine, n-hexane was found in only 50 samples, with the mean concentration being 1,417 ng/l (limit values, 34–8,820 ng/l). In 77 of the 90 blood samples taken, a mean concentration of 608 ng/l was detected (variation limit, 15–7,684ng/l). Particularly the haematic and urinary concentration showed significant differences among the nine groups of individuals classified according to their work activity. The lowest levels were found in the blood and urine of farmers: 270 and 298 ng/l, respectively. The highest values were found for chemical workers (1,377 and 411 ng/1), respectively printers (585 and 2,691 ng/l respectively), and traffic wardens (740 and 8,820 ng/l, respectively). In all, 95% of the determinations of n-hexane yielded values of < 255 ng/l in environmental samples, < 105 ng/l in alveolar air, < 1,475 ng/l in blood and < 5,875 ng/l in urine. A comparison of these data revealed a significant correlation between environmental levels and alveolar (r/s = 0.769; P<0.00001), haematic (r/s = 0.624; P<0.0002), and urinary (r/s = 0.597; P<0.0005) values for n-hexane.     

空气苯浓度与呼出苯及尿酚的关系研究

目的对苯接触水平和接触者可能受到的有害影响进行卫生学评价。方法对１０名苯接触者和６名志愿苯接触者进行研究,用苯呼出气作为生物学监测指标。结果班前呼出苯大多为未检出,班中及班后呼出苯与空气苯时间加权平均浓度均有密切相关;班前尿酚与空气苯时间加权平均浓度无相关,班后尿酚及次晨尿酚均与空气苯ＴＷＡ浓度密切相关;班中、班后呼出苯均与班后尿酚及次晨尿酚密切相关,且以班中呼出苯与班后尿酚的相关性最高（ｒ＝０．９３５３）。呼出苯的快速排出相为脱离接触１０分钟（占班后呼出苯８２．２５％）,其排出稳定相在脱离接触后９０分钟左右。接触空气苯浓度ＴＷＡ７．９～２１７．８ｍｇ／ｍ３时,无论是呼出苯或尿酚在接触后２４小时与空气苯均无相关。结论在呼出苯的快速排出相采集终末呼出气可反映工人当时的接触浓度,采集排出稳定相终末呼出气,其浓度较稳定可反映接触者吸收入血液的浓度,并以此来估测环境浓度与接触水平。呼出苯的呼吸排出规律以及采样方便、无损伤,检出灵敏,呼出苯作为接触水平监测指标较其他指标优越。     

甲苯接触者生物监测指标研究——尿中马尿酸和邻甲酚浓度

对32名职业接触甲苯、18名志愿受试者和77名非职业接触甲苯者的尿中马尿酸及邻甲酚的测定,发现在非接触者中,尿中马尿酸存在日间波动,邻甲酚排出量极少。工人和志愿者接触甲苯后,尿中马尿酸即开始上升,到脱离时达高峰,以后迅速下降,4小时左右降到正常本底水平,班末尿中马尿酸浓度与空气浓度相关(工人:r=0.64,志愿者:r=0.78)。尿中邻甲酚在低浓度接触者中,难以检出,但在高浓度接触时,班末尿中邻甲酚与空气浓度相关(工人;r=0.63,志愿者;r=0.65)。马尿酸和邻甲酚作为甲苯生物监测指标可结合使用。     

Dimethylethylamine in mould core manufacturing: exposure, metabolism, and biological monitoring.

The exposure and metabolism of dimethylethylamine (DMEA) was studied in 12 mould core makers in four different foundries using the Ashland cold box technique. The mean time weighted average (TWA) full work shift DMEA exposure concentration was 3.7 mg/m3. Inhaled DMEA was excreted into urine as the original amine and as its metabolite dimethylethylamine-N-oxide (DMEAO). This metabolite made up a median of 87 (range 18-93) % of the sum of DMEA and DMEAO concentrations excreted into the urine. Occupational exposure did not significantly increase the urinary excretion of dimethylamine or methylethylamine. The data indicate half lives after the end of exposure for DMEA in urine of 1.5 hours and DMEAO of three hours. The postshift summed concentration of DMEA and DMEAO in plasma and urine is a good indicator of the TWA concentration in air during the workday, and might thus be used for biological monitoring. An air concentration of 10 mg/m3 corresponds to a urinary excretion of the summed amount of DMEA and DMEAO of 135 mmol/mol creatinine.     

Dimethylethylamine in mould core manufacturing: exposure, metabolism, and biological monitoring

The exposure and metabolism of dimethylethylamine (DMEA) was studied in 12 mould core makers in four different foundries using the Ashland cold box technique. The mean time weighted average (TWA) full work shift DMEA exposure concentration was 3.7 mg/m3. Inhaled DMEA was excreted into urine as the original amine and as its metabolite dimethylethylamine-N-oxide (DMEAO). This metabolite made up a median of 87 (range 18-93) % of the sum of DMEA and DMEAO concentrations excreted into the urine. Occupational exposure did not significantly increase the urinary excretion of dimethylamine or methylethylamine. The data indicate half lives after the end of exposure for DMEA in urine of 1.5 hours and DMEAO of three hours. The postshift summed concentration of DMEA and DMEAO in plasma and urine is a good indicator of the TWA concentration in air during the workday, and might thus be used for biological monitoring. An air concentration of 10 mg/m3 corresponds to a urinary excretion of the summed amount of DMEA and DMEAO of 135 mmol/mol creatinine.     

Benzyl alcohol as a marker of occupational exposure to toluene

Benzyl alcohol (BeOH) is a urinary metabolite of toluene, which has been seldom evaluated for biological monitoring of exposure to this popular solvent. The present study was initiated to develop a practical method for determination of BeOH in urine and to examine if this metabolite can be applied as a marker of occupational exposure to toluene. A practical gas-liquid chromatographic method was successfully developed in the present study with sensitivity low enough for the application (the limit of detection; 5 microg BeOH /l urine with CV=2.7%). Linearity was confirmed up to 10 mg BeOH/l, the highest concentration tested, and the reproducibility was also satisfactory with a coefficient of variation of 2.7% (n=10). A tentative application of the method in a small scale study with 45 male workers [exposed to toluene up to 130 ppm as an 8-h time-weighted average (8-h TWA)] showed that BeOH in the end-of-shift urine samples was proportional to the intensity of exposure to toluene. The calculated regression equation was Y=50+1.7X (r=0.80, p<0.01), where X was toluene in air (in ppm as 8-h TWA) and Y was BeOH in urine (in microg/l of end-of-shift urine). The levels of BeOH in the urine of the non-exposed was about 50 microg/l, and ingestion of benzoate as a preservative in soft drinks did not affect the BeOH level in urine. The findings as a whole suggest that BeOH is a promising candidate for biological monitoring of occupational exposure to toluene.     

Blood lead concentration, renal function, and blood pressure in London civil servants.

Blood lead concentration was measured in 398 male and 133 female London civil servants not subject to industrial exposure to heavy metals. The relation between blood lead and serum creatinine concentrations and blood pressure were examined. Blood lead concentration ranged from 0.20 to 1.70 mumol/l with a geometric mean concentrations of 0.58 mumol/l in men and 0.46 mumol/l in women (p less than 0.001). In women blood lead concentration increased with age (r = +0.27; p = 0.002). In the two sexes blood lead concentration was positively correlated with the number of cigarettes smoked a day (men r = +0.17 and women r = +0.22; p less than or equal to 0.01), with the reported number of alcoholic beverages consumed a day (men r = +0.34 and women r = 0.23; p less than 0.01), and with serum gamma-glutamyltranspeptidase (men r = +0.23 and women r = +0.14; for men p less than 0.01). Blood lead concentration was not correlated with body weight, body mass index, and employment grade. In men 14% of the variance of blood lead concentration was explained by the significant and independent contributions of smoking and alcohol intake and in women 16% by age, smoking, and alcohol consumption. In men serum creatinine concentration tended to rise by 0.6 mumol/l (95% confidence interval from -0.2 to +1.36 mumol/l) for each 25% increment in blood lead concentration. In men and women the correlations between blood lead concentration and systolic and diastolic blood did not approach statistical significance. In conclusion, in subjects not exposed to heavy metals at work gender, age, smoking, and alcohol intake are determinants of blood lead concentration. At a low level of exposure, lead accumulation may slightly impair renal function, whereas blood pressure does not seem to be importantly influenced. Alternatively, a slight impairment of renal function may give rise to an increase in blood lead concentration.     

Biological monitoring of workers exposed to acetone in acetate fibre plants.

Concentrations of acetone in urine, alveolar air, and blood were measured by gas chromatography with flame ionisation detection for 110 subjects occupationally exposed to acetone (mean 372 ppm) in three factories. Significant relations were found between the time weighted average environmental concentration and the concentration in the biological samples. The strongest correlation was between the concentration of acetone in urine and the degree of exposure (r = 0.71, 95% CI 0.64-0.77). This suggests that urinary acetone concentration is the best biological index of occupational exposure to acetone.     

Biological monitoring of workers exposed to acetone in acetate fibre plants.

Concentrations of acetone in urine, alveolar air, and blood were measured by gas chromatography with flame ionisation detection for 110 subjects occupationally exposed to acetone (mean 372 ppm) in three factories. Significant relations were found between the time weighted average environmental concentration and the concentration in the biological samples. The strongest correlation was between the concentration of acetone in urine and the degree of exposure (r = 0.71, 95% CI 0.64-0.77). This suggests that urinary acetone concentration is the best biological index of occupational exposure to acetone.