Biomedical subjects

F Brugnone

Publications and source records attributed to F Brugnone.

At least 19 recordsLinked to original sources

PubMed2001

Analysis of urinary N-acetyl-S-(N-methylcarbamoyl)cysteine, the mercapturic acid derived from N,N-dimethylformamide.

Human biotransformation of the industrial solvent N,N-dimethylformamide gives raise to N-acetyl-S-(N-methylcarbamoyl)cysteine (AMCC) which has the longest half-life (about 23 h) among urinary metabolites of N,N-dimethylformamide. It could be used for monitoring industrial exposure over several workdays, by measuring it in urine samples collected at the end of the working week. This is consistent with the suggestions of the American Conference of Governmental Industrial Hygienists, which established a limit of 40 mg/l for the year 2000. An easy, cheap and user-friendly method has been developed for determination of urinary AMCC. Unlike currently available methods, it requires neither a time-consuming preparation phase nor gas chromatographic analysis with a nitrogen-phosphorus or mass detector. The method uses high-performance liquid chromatography (HPLC), with an UV detector at 436 nm. A 10-microl volume of urine is added to a carbonate-hydrogen carbonate buffer and mixed with a dabsyl chloride solution in acetonitrile. The reaction between AMCC and the reagent is performed at 70 degrees C for 10 min. The 'dabsylated' product is stable for at least 12 h. After brief centrifugation, the solution is ready for HPLC analysis using a C18 column (250 x 4.6 mm, 5 microm). The method is sensitive (detection limit 1.8 mg/l) and specific. It identified urinary AMCC in urine of 40 subjects not exposed to N,N-dimethylformamide with a median concentration of 3.9 mg/l. In urine samples from 20 workers exposed to N,N-dimethylformamide (5-40.8 mg/m3), AMCC concentrations ranged from 16 to 170 mg/l. Industrial toxicology laboratories with limited instrumentation will be able to use it in the biological monitoring of workers exposed to N,N-dimethylformamide.

Acetylcysteine↗

PubMed1999

Benzene in blood as a biomarker of low level occupational exposure.

The occupational airborne exposure to benzene of 150 workers employed in petrol stations and a refinery plant was assessed using personal sampling pumps. All workers provided blood samples after the end of work and on the following morning before resuming work. Benzene concentrations in the blood of 243 non-occupationally-exposed subjects were also measured. The median occupational benzene exposure for all 150 workers studied was 80 micrograms/m3. Overall median blood benzene of all workers was 251 ng/l at the end of the shift, and 174 ng/l the following morning. The benzene concentrations measured in blood collected the following morning proved to be significantly lower than those measured at the end of the shift. Median blood benzene for the 243 'normal' subjects was 128 ng/l, which was significantly lower than that measured in the workers before a new work shift. The median blood benzene concentration was significantly higher in smokers than in non-smokers, both in the general population (210 ng/l vs. 110 ng/l) and in the exposed workers at the end of the shift (476 ng/l vs. 132 ng/l) and the following morning (360 ng/l vs. 99 ng/l). End-of-shift blood benzene correlated significantly with environmental exposure; this correlation was better in the 83 non-smokers than in the 67 smokers. In non-smokers with the median benzene occupational exposure of 50 micrograms/m3, no difference was found in blood benzene concentration in exposed and non-exposed subjects.

Adolescent↗

PubMed1999

Biological monitoring of occupational exposure to cyclohexane by urinary 1,2- and 1,4-cyclohexanediol determination.

OBJECTIVES: This article reports the results obtained with the biological and environmental monitoring of occupational exposure to cyclohexane using 1,2-cyclohexanediol (1,2-DIOL) and 1,4-DIOL in urine. The kinetic profile of 1,2-DIOL in urine suggested by a physiologically based pharmacokinetic (PBPK) model was compared with the results obtained in workers. METHODS: Individual exposure to cyclohexane was measured in 156 workers employed in shoe and leather factories. The biological monitoring of cyclohexane exposure was done by measurement of 1,2-DIOL and 1,4-DIOL in urine collected on different days of the working week. In all, 29 workers provided urine samples on Monday (before and after the work shift) and 47 workers provided biological samples on Thursday at the end of the shift and on Friday morning. Another 86 workers provided biological samples at the end of the work shift only on Monday or Thursday. RESULTS: Individual exposure to cyclohexane ranged from 7 to 617 mg/ m3 (geometric mean value 60 mg/m3). Urinary concentrations of 1,2-DIOL (geometric mean) were 3.1, 7.6, 13.2, and 6.3 mg/g creatinine on Monday (pre- and postshift), Thursday (postshift) and Friday (pre-shift), respectively. The corresponding values recorded for 1,4-DIOL were 2.8, 5.1, 7.8, and 3.7 mg/g creatinine. A fairly close, statistically significant correlation was found between environmental exposure to cyclohexane and postshift urinary 1,2-DIOL and 1,4-DIOL on Monday. Data collected on Thursday and Friday showed only a poor correlation to exposure with a wide scatter. Both metabolites have a urinary half-life of close to 18 h and accumulate during the working week. CONCLUSIONS: Comparison between data obtained from a PBPK model and those found in workers suggests that 1,2-DIOL and 1,4-DIOL are urinary metabolites suitable for the biological monitoring of industrial exposure to cyclohexane.

Cyclohexanes↗

PubMed1999

Influence of GSTM1 genotypes on anti-BPDE-DNA adduct levels in mononuclear white blood cells of humans exposed to PAH.

OBJECTIVE: Association between genetic deletion polymorphism of GSTM1 (*0/*0 or active) and levels of anti (+/-)-r-7,t-8-dihydroxy-t-9,10-oxy-7,8,9,10-tetrahydrobenzo[a]pyrene (anti-BPDE)-DNA adducts in the peripheral blood lymphocyte plus monocyte fraction (LMF) of PAH-exposed subjects was investigated. METHODS: A total of 94 Caucasian subjects comprised the sample population: 13 coke-oven workers, 19 chimney sweeps, 36 aluminum-anode plant workers, and 26 non-occupationally PAH-exposed subjects (controls). PAH exposure was assessed in each group by means of the urinary excretion of 1-pyrenol (mean group levels 1.2, 0.7, 0.3, and 0.1 mumol/mol creatinine in coke-oven workers, chimney sweeps, aluminum-anode plant workers, and control subjects, respectively). Anti-BPDE-DNA adducts were detected by HPLC/fluorescence analysis of anti-BPDE tetrols (tetrol I-1) released after acid hydrolysis of DNA samples. RESULTS: In coke-oven workers the percentage of cases with adduct levels exceeding the 95th percentile control value (4.4 adducts/10(8) nucleotides) was significantly higher in the subgroup with the null GSTM1 genotype (*0/*0) (100%) than in that with active GSTM1 (43%; chi 2 test, P < 0.05). In the other groups with different and lower levels of PAH exposure the percentages of positive samples were always higher in the subgroup with GSTM1 *0/*0 than in the active one, although the differences were not statistically significant. Univariate (odds ratio) and multivariate (relative risk) analyses showed that the risk of having high anti-BPDE-DNA levels increased with occupational exposure to PAH. Such risks, moreover, were further significantly increased by the lack of GSTM1 activity (RR = 5.94; CI = 1.15-30.7; P < 0.05). In coke-oven workers, chimney sweeps, and aluminum workers, respectively, the multiplicative effect of the null genotype with occupational PAH exposure gives risks of 162 (= 27.2 x 5.94), 10 (= 1.70 x 5.94), and 3 (= 0.50 x 5.94) times higher probability (risk) of high BPDE-DNA adduct formation than that of non-exposed subjects with the active GSTM1 genotype. CONCLUSION: Our results indicate a greater risk of anti-BPDE-DNA adduct formation resulting from occupational high-level PAH-exposure in GSTM1 null (GSTM1 *0/*0) workers.

7,8-Dihydro-7,8-dihydroxybenzo(a)pyrene 9,10-oxide↗

PubMed1999

HPLC/fluorescence determination of anti-BPDE-DNA adducts in mononuclear white blood cells from PAH-exposed humans.

The aim of this study was to compare (+/-)-r-7,t-8-dihydroxy-t-9,10-oxy-7,8,9,10-tetrahydrobenzo[a]pyrene (anti-BPDE)-DNA adduct levels in groups of humans subjected to various levels of polycyclic aromatic hydrocarbon (PAH) (benzo[a]pyrene) exposure. An HPLC/fluorescence method was applied to detect specifically anti-BPDE-DNA adducts in mononuclear white blood cells [lymphocyte plus monocyte fraction (LMF)] from humans exposed to PAHs. A total of 130 subjects comprised the sample population: 26 psoriatic patients (3 days after clinical coal tar treatment of the skin), 15 coke oven workers, 19 chimney sweeps, 36 aluminium anode plant workers and 34 non-occupationally PAH-exposed subjects (controls). PAH exposure was assessed in each group by means of the urinary excretion of 1-pyrenol (mean group levels: 1.2, 0.7, 0.3, 65.0 and 0.1 micromol/mol creatinine in coke oven workers, chimney sweeps, aluminium plant anode workers, psoriatic patients and non-occupationally PAH-exposed subjects, respectively). HPLC/fluorescence analysis of BPDE-DNA adducts showed that the percentage of subjects with adduct levels exceeding the 95 percentile control subject value (8.9 adducts/10(8) nucleotides) was significantly high in coke oven workers (46.7%) and chimney sweeps (21.0%) (chi2 test, P < 0.01 and P < 0.05, respectively) but not in aluminium plant workers (11.1%) and psoriatic patients (0%). The increase in BPDE-DNA adduct levels in LMF (Ln values) was significantly related to chronic inhalatory and high PAH exposure (linear multiple regression analysis, F = 6.37, P < 0.01; t = 4.2, P < 0.001). Skin acute (or short-term) and high PAH exposure, charcoal-grilled meat consumption and smoking habit did not seem to influence BPDE-DNA adduct formation in LMF.

7,8-Dihydro-7,8-dihydroxybenzo(a)pyrene 9,10-oxide↗

PubMed1998

Benzene in environmental air and human blood.

OBJECTIVE: To study the blood benzene levels resulting from environmental and occupational benzene exposure. METHODS: Benzene in venous blood was measured in 243 nonoccupationally exposed subjects ("normal" people) and in 167 workers occupationally exposed to benzene. All exposed workers gave blood samples at the end of the work shift and on the following morning before resuming work. Blood benzene was assayed by gas chromatography (GC)-mass spectrometry. Occupational benzene exposure was monitored by environmental personal samplers and measured by GC analysis. RESULTS: The mean occupational benzene exposure for all 167 workers studied was 186 ng/l (58 ppb; range 5 1535 ng/l, 2-500 ppb). Overall, the mean blood benzene level of all workers was 420 ng/1 at the end of the shift and 287 ng/l on the morning thereafter. The blood benzene levels measured the morning after turned out to be significantly lower (t=3.6; P < 0.0001) than those measured at the end of the shift. The mean blood benzene level of the 243 "normal" subjects was 165 ng/l, which was significantly lower than that measured in the workers on the morning thereafter (t=5.8: P < 0.0000001). The mean blood benzene concentration was significantly higher in smokers than in nonsmokers in both the general population (264 versus 123 ng/l) and in the exposed workers. In the group of nonsmoking workers, whose workplace exposure to benzene was lower than 100 ng/l, blood benzene levels were similar (210-202 ng/l) to those measured in the nonsmoking general population (165 ng/l). End-of-shift blood benzene correlated significantly with environmental exposure (y=0.91x + 251; r=0.581; n=162; P < 0.00001). Finally, there was also a significant correlation between blood benzene measured at the end of the shift and that determined on the morning thereafter (y=0.45x + 109; r=0.572; n=156; P < 0.00001). CONCLUSION: Nonsmoking workers occupationally exposed to benzene at environmental levels lower than 100 ng/l (mean 35 ng/l) and the nonsmoking general population exposed to ubiquitous benzene pollution have similar blood benzene concentrations. This suggests that it is impossible to distinguish between occupational and environmental exposure when the benzene level in the workplace is less than 100 ng/l.

Air Pollutants↗

PubMed1997

Acute arsine intoxication as a consequence of metal burnishing operations.

The report concerns a 30-year-old factory worker, employed in a small galvanizing plant for over ten years in the burnishing, copper- and nickel-plating of small metal articles for the shoe industry. Acute arsine poisoning was attributed to the use of a dilute solution of CuSO4 (3%), HCl (32%), and As2O3 (2%) for burnishing metal (Fe-Zn) shoelace eyelet holes, in the absence of local exhaust ventilation and with no respiratory protection. Arsine caused severe intravascular hemolysis with a rapid drop in hematocrit and hemoglobin levels. Other body organs were involved as a result of the hypoxic effect of anemia and hemolysis, or as a direct toxic effect of the arsine itself. Our experience confirms that exchange transfusion is capable of rapidly arresting the adverse effects of arsine. The importance of preventive measures and worker information to avoid acute arsine poisoning is emphasized.

Adult↗

PubMed1995

Blood toluene as a biological index of environmental toluene exposure in the "normal" population and in occupationally exposed workers immediately after exposure and 16 hours later.

Blood toluene was measured in a group of 100 workers occupationally exposed to a mean 8-h environmental toluene concentration of 128 micrograms/l (34 ppm), and in a group of 269 "normal" subjects without occupational exposure to toluene. The mean blood toluene of the workers at the end of the shift and the following morning, after 16 h, was 457 and 38 micrograms/l, respectively. The normal subjects had a blood toluene level of 1.1 micrograms/l. On the basis of the highly significant correlation between blood toluene and occupational exposure, it can be calculated that environmental toluene exposure of 188 and 377 micrograms/l (50 and 100 ppm) gives end-of-shift blood toluene levels of 690 and 1390 micrograms/l, respectively. The corresponding blood toluene levels on the following morning are 50 and 100 micrograms/l, respectively.

Environmental Exposure↗

PubMed1995

Nitrous oxide in blood and urine of operating theatre personnel and the general population.

Nitrous oxide (N2O) was assayed in 676 urine samples and 101 blood samples provided after exposure by operating theatre personnel from nine hospitals. The blood and urine assays were repeated in 25 subjects 18 h after the end of exposure. For 80 subjects, environmental N2O was also measured during intraoperative exposure. Mean urinary N2O in the 676 subjects at the end of exposure was 40 micrograms/l (range 1-3805 micrograms/l); in 10 of the 676 subjects, urinary N2O was in the range 279-3805 micrograms/l (mean 1202 micrograms/l). The 98th percentile was 120 micrograms/l. Mean blood N2O at the end of exposure, measured in 101 subjects, was 21 micrograms/l (median 16 micrograms/l, range 1-75 micrograms/l). Blood and urine N2O (1.5 micrograms/l and 4.9 micrograms/l, respectively) in 25 subjects, 18 h after exposure, was significantly higher than in occupationally non-exposed subjects (blood 0.91 microgram/l, urine 1 microgram/l). Environmental exposure was significantly related to blood and urinary N2O (r = 0.59 and r = 0.64, respectively). Blood and urinary N2O were significantly related to each other (r = 0.71), and were equivalent to about 25% of the environmental exposure level. The mean urinary N2O of 1202 micrograms/l in 10/676 subjects was not related to environmental exposure in the operating theatre. The highest urinary N2O levels measured in these 10/676 subjects could be explained by an asymptomatic urinary infection.

Environmental Exposure↗

PubMed1994

Blood acetone concentration in "normal people" and in exposed workers 16 h after the end of the workshift.

Acetone levels were measured by gas chromatography mass spectrometry (GC-MS) in environmental and alveolar air, blood and urine of 89 non-occupationally exposed subjects and in three groups of workers exposed to acetone or isopropanol. Acetone was detected in all samples from non-exposed subjects, with mean values of 840 micrograms/l in blood (Cb), 842 micrograms/l in urine (Cu), 715 mg/l in alveolar air (Ca) and 154 ng/l in environmental air (Ci). The ninety-fifty percentiles were 2069 micrograms/l in Cb, 2206 micrograms/l in Cu and 1675 ng/l in Ca. The blood/air partition coefficient of acetone was 597. Correlations were found in Cb, Cu and Ca. In specimens sampled at the end of the workshift from subjects occupationally exposed to acetone, a correlation was found in the blood, urine, alveolar and environmental air concentrations. The blood/air partition coefficient of acetone was 146. On average, the blood acetone levels of workers were 56 times higher than the environmental exposure level, and the concentration of acetone in alveolar air was 27% more than that found in inspiratory air. The half-life for acetone in blood was 5.8 h in the interval of 16 h between the end of the workshift and the morning after. The morning after a workshift with a mean acetone exposure of 336 micrograms/l, blood and urinary levels were 3.5 mg/l and 13 mg/l, respectively, which were still higher than those found in "normal" subjects. It can be concluded that endogenous production of acetone and environmental exposure to acetone or isopropanol do not affect the reliability of biological monitoring of exposed workers, even 16 h after low exposure.

Acetone↗

PubMed1993

Blood concentrations of carbon disulphide in dithiocarbamate exposure and in the general population.

Blood carbon disulphide (CS2), both free and total, was determined by gas chromatography-mass spectrometry in 112 "normal" subjects and in 20 subjects employed in a dithiocarbamate factory, comprising ten blue-collar workers involved in dithiocarbamate production and ten white-collar office staff. The ten production workers were examined over two workshifts, the first at the beginning of the week (Monday) and the second after an intervening period of at least 1 day. Three blood samples were taken for each shift studied, one prior to starting work, one at the end of the shift and the third 16 h after the end of the shift (on the following morning). The mean CS2 blood levels measured in the 112 normal subjects was 663 ng/l for the free fraction and 3178 ng/l for the total. In 16 blood samples taken from the ten dithiocarbamate factory office workers, the mean free and total CS2 blood levels were 846 and 4140 ng/l, respectively, i.e. not significantly different from those observed in the normal subjects. At the end of the first 8-h shift, the ten dithiocarbamate factory production workers had free and total CS2 values of 1070 and 8471 ng/l, respectively, which were significantly higher than those observed prior to starting work (240 and 4738 ng/l). All the total CS2 levels measured in the shop-floor workers, with the sole exception of the values recorded prior to the start of the Monday shift (4738 ng/l), ranged from 7047 to 8471 ng/l and were significantly higher than those measured in the white-collar staff (4140 ng/l).

Adult↗

PubMed1993

Reference values for blood toluene in the occupationally nonexposed general population.

Blood toluene was measured by gas chromatography--mass spectrometry in 232 occupationally nonexposed subjects, consisting of 126 rural and 106 urban workers, and 37 chemical workers. Mean blood toluene was significantly lower in rural (698 ng/l) and urban workers (984 ng/l) than in chemical workers (2789 ng/l). Blood toluene was not significantly different between the rural and urban workers or among the urban workers with different jobs. Smokers had significantly higher levels (median 606 ng/l) than nonsmokers (median 424 ng/l). Subjects who had smoked at least one cigarette in the last 2 h before blood sampling had significantly higher blood toluene (median 1170 ng/l) than those who had not smoked during this time (median 693 ng/l), for whom the level was not significantly different from that in nonsmokers. Blood toluene in the total population was less than 2863 ng/l in 95% cases.

Adult↗

PubMed1993

Blood styrene concentrations in a "normal" population and in exposed workers 16 hours after the end of the workshift.

Blood styrene was measured by a gas chromatography-mass spectrometry method in 81 "normal people" and in 76 workers exposed to styrene. In the normal subjects, styrene was also tested in alveolar and environmental air. Styrene was found in nearly all (95%) blood samples. Average styrene levels in the normal subjects were 221 ng/l in blood (Cb), 3 ng/l in alveolar air (Ca) and 6 ng/l in environmental air (Ci). Styrene levels did not differ significantly between smokers and nonsmokers, 95% of values being below 512 ng/l in Cb, 7 ng/l in Ca and 15 ng/l in Ci. In workers with an average exposure to styrene of 204 micrograms/l, at the end of the workshift, mean blood styrene concentration was 1211 micrograms/l. In blood samples collected at the end of the Thursday shift, styrene levels were significantly higher (1590 micrograms/l) than those found at the end of the Monday shift (1068 micrograms/l). A similar difference was found in samples taken the morning after exposure (60 and 119 micrograms/l, respectively). Significant correlations between blood and environmental styrene were found both at the end of the shift and the morning after exposure (r = 0.61 and 0.41, respectively). In workers occupationally exposed to styrene, 16 h after the end of the workshift, blood styrene (94 micrograms/l) was significantly higher than that found in the normal subjects (0.22 microgram/l). The half-life of blood styrene was 3.9 h.

Adult↗

PubMed1993

Biochemical and physiological aspects of 2,5-hexanedione: endogenous or exogenous product?

This article reports results regarding two different physiological aspects of 2,5-hexanedione (2,5-HD). The first is the relationship between "free" 2,5-HD (the fraction of "real" 2,5-HD) and "total" 2,5-HD (2,5-HD obtained from acid hydrolysis) in urine and blood of workers exposed to n-hexane. The second part of the study is an attempt to clarify "physiological" excretion of 2,5-HD in subjects not occupationally exposed to n-hexane. The concentration of free 2,5-HD in urine of workers exposed to n-hexane is about 8% of total urinary 2,5-HD. In blood, free 2,5-HD is about 50% of the total. The serum concentration range of total and free 2,5-HD in workers from whom blood was taken was 33-418 micrograms/l and 14-283 micrograms/l respectively. In subjects not exposed to n-hexane, urinary concentration of 2,5-HD ranged between 0.17 and 0.98 mg/l, the urinary excretion rate between 0.23 and 0.57 microgram/min, and renal clearance between 14 and 66 ml/min. The blood concentration of 2,5-HD in nonexposed subjects was 6-30 micrograms/l. Fluctuations typical of a circadian rhythm were not observed for 2,5-HD in blood or urine. We think that 2,5-HD is mainly a product of intermediate metabolism in the human body. Only a minimal part could derive from n-hexane as a ubiquitous micropollutant.

Circadian Rhythm↗

PubMed1993

Biological monitoring of occupational exposure to n-hexane by measurement of urinary 2,5-hexanedione.

Occupational exposure to n-hexane in shoe factory workers was monitored by measuring urinary 2,5-hexanedione, the major metabolite of this solvent and the probable cause of peripheral neuropathy in exposed workers. Solvent pollution was monitored in the work environments of 189 employees, of whom 123 (65%) worked in Alicante, Spain, and 66 (35%) in Veneto, Italy. 2,5-Hexanedione was measured in spot urine samples collected from workers at the end of the shift. Information on working conditions was obtained from a previous study. A significant linear correlation was found between mean environmental concentration of n-hexane and urinary concentration of 2,5-hexanedione. The variability in the correlation may have been due to the variable use of protective clothing (gloves), and to variations in exposure during the working week. In numerous workers, percutaneous absorption of n-hexane represented as much as 50% of the total absorbed dose. Urinary concentrations of 2,5-hexanedione tended to increase during the working week. Simultaneous exposure to n-hexane and toluene tended to reduce urinary excretion of 2,5-hexanedione, whereas exposure to n-hexane and methyl ethyl ketone tended to increase excretion of the metabolite.

Adolescent↗

PubMed1992

Reference values for blood benzene in the occupationally unexposed general population.

Blood benzene was determined by gas chromatography-mass spectrometry in 431 "normal" subjects, subdivided into 155 rural subjects and 276 urban subjects. Blood benzene (mean value 262 ng/l) was significantly lower in rural (200 ng/l) than in urban (296 ng/l) workers, as well as differing significantly between 293 non-smokers and 138 smokers (205 ng/l and 381 ng/l, respectively). Among non-smokers, values were significantly higher (307 ng/l) in 76 chemical workers. In the total study population, in 95% of cases blood benzene was less than 718 ng/l, the 95th percentile being 514 ng/l in non-smokers vs 901 ng/l in smokers and 576 ng/l in rural vs 822 ng/l in urban subjects. Within each population subgroup, the difference between non-smokers and smokers was statistically significant, except among office workers (non-smokers 234 ng/l, smokers 304 ng/l). Blood benzene (y) was directly proportional to the number of cigarettes smoked (x) (y = 201 + 12x; r = 0.44; n = 431), and inversely proportional to the interval between the last cigarette and the time at which the blood samples was taken (z) (log y = 6.167-0.0015z; r = -0.461; n = 135). The blood half-life of benzene was about 8h. The multiple correlation between blood benzene (Cb), number of cigarettes per day (x) and time since the last cigarette (z) is: Cb = 417 + 7.2x - 0.41z (n = 135; R = 0.20; P less than 0.00001).

Adult↗

PubMed1992

Blood concentration of carbon disulphide in "normal" subjects and in alcoholic subjects treated with disulfiram.

Assay of free and acid labile carbon disulphide (free and total CS2 respectively) in human blood was performed by gas chromatography/spectrometry. The method used a large dynamic head space volume and a "cryogenic trap". Blood CS2 concentration was measured in 42 subjects not occupationally exposed to CS2 (group A) and in 11 alcoholic subjects (group B) treated with disulfiram. Free CS2 concentration showed a mean value of 261 ng/l in the 42 subjects in group A and 9482 ng/l in eight subjects of group B. Total CS2 concentration was 897 ng/l and 40,084 ng/l in groups A and B respectively. Differences between the groups were highly significant for concentrations of both free and total CS2. Total CS2 concentration was about four times as high as free CS2 concentration in both groups. A significant correlation was found between free and total CS2 concentration both in group A and in group B. In the alcoholic subjects (group B), blood concentrations of both free and total CS2 were related to time of sampling after treatment with disulfiram.

Alcoholism↗

PubMed1991

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

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, 1-304 ng/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, 15-7,684 ng/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/l), 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 less than 255 ng/l in environmental samples, less than 105 ng/l in alveolar air, less than 1,475 ng/l in blood and less than 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 less than 0.00001), haematic (r/s = 0.624; P less than 0.0002), and urinary (r/s = 0.597; P less than 0.0005) values for n-hexane.

Adult↗