Hellenic karst waters: geogenic and anthropogenic processes affecting their geochemistry and quality.

Karst hydrosystems represent one of the largest global drinking water resources, but they are extremely vulnerable to pollution. Climate change, high population density, intensive industrial, and agricultural activities are the principal causes of deterioration, both in terms of quality and quantity, of these resources. Samples from 172 natural karst springs were collected in the whole territory of Greece. To identify any geogenic contamination and/or anthropogenic pollution, analyses of their chemical compositions, in terms of major ions and trace elements, were performed and compared to the EU limits for drinking water. Based on chloride content, the collected karst springs were divided into two groups: low-chloride (< 100 mg L-1) and high-chloride content (> 100 mg L-1). An additional group of springs with calcium-sulfate composition was recognised. Nitrate concentrations were always below the EU limit (50 mg L-1), although some springs presented elevated concentrations. High contents in terms of trace elements, such as B, Sr, As, and Pb, sometimes exceeding the limits, were rarely found. The Greek karst waters can still be considered a good quality resource both for human consumption and for agriculture. The main issues derive from seawater intrusion in the aquifers along the coasts. Moreover, the main anthropogenic pollutant is nitrate, found in higher concentrations mostly in the same coastal areas where human activities are concentrated. Finally, high levels of potentially harmful trace elements (e.g. As, Se) are very limited and of natural origin (geothermal activity, ore deposits, etc.).

[Acute poisoning with carbon dioxide: report of 2 fatal cases]. / Intossicazione acuta da anidride carbonica: descrizione di due casi mortali.

BACKGROUND: Carbon dioxide (CO2), a very high density gas, tends to stratify at the lowest levels of the atmosphere. It can be produced by neutral geothermal emissions, fermentative processes or by human and industrial activity. When carbon dioxide concentrations rise to a very high level in a confined and poorly ventilated space, the anoxic hazard is a very important cause of severe accidents that can involve workers and rescuers. At CO2 levels higher than 20% there is a very high risk of a fatal accident, also considering the odourless feature of this gas. OBJECT: Two fatal accidents in workers are described which occurred during inspection of a concrete well, built as a part of sewerage network in a rural area. In the weeks after the accident, composition and concentration of gases inside the well were analysed. We also considered the influence of an organic fertilizer called "pollina" which was found on the ground around the concrete well, in order to ascertain whether fermentation could alter the gas composition inside the well. METHODS: Samples of air and water were collected in the well and samples of the organic fertilizer (pollina) on the ground surrounding the concrete well were also taken. Different quantities of organic fertilizer (pollina) with or without water were incubated in airtight glass bottles and placed in a dark room at 20 degrees C temperature; analysis of air inside the glass bottles was performed after 7 and 18 days of incubation. All the samples of air and water were analysed by gas-chromatographic-mass-spectrometry. RESULTS: Analysis of the air samples collected inside the well after 2, 16 and 18 weeks after the accident showed a low concentration of O2 (range 4.2-9%), a high concentration of CO2 (range 5.9-12.3%), a normal level of N2 (range 78-85%) and a concentration of N2O between 0.03 and 0.19%. In water collected 2 weeks after the accident at the bottom of the concrete well, CO2 and N2O concentrations of respectively 222 mg/L and 2 mg/L were measured. In the bottles with "pollina" we found, at different times of incubation, high concentrations of CO2 (highest value 25.2%), low levels of O2 (lowest value 0.5%) and negligible concentrations of N2O (< 0.015%). CONCLUSIONS: All these findings suggest that the atmosphere inside the concrete well was altered by the fermentative processes of pollina. The death of the two workers, caused by a poorly oxygenated atmosphere with a high concentration of carbon dioxide, can be classified under the confined space hypoxic syndrome (CSHS).

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.

[Guidelines for assessment and management of risks caused by benzene for workers at gas stations]. / Linee guida per la valutazione e la gestione dei rischi da benzine per la salute dei lavoratori addetti alle stazioni di servizio carburanti.

The European regulations classify gasoline as "carcinogenic agent" because of its content of benzene (> 0.1%). Consequently the preventive and protective actions towards the petrol station attendants prescribe, before all, the elimination of the agent or the reduction of the exposure and the risk to the minimum. Well known are currently a series of preventive measures able to produce appreciable reduction of the risk: reduction of the benzene content of gasoline, vapor recovery systems, self-areas or do-it-yourself, specific procedures for working. Exposure assessment is an essential step in order to establish the need for further preventive measure and to verify their efficacy. The exposure levels to gasoline of the petrol station attendants can be influenced by a variety of factors other than benzene air concentrations and therefore biological monitoring can give some sensible advantage in respect to air monitoring. Dosage of benzene in expired air, in urine, or in blood give a very good estimation of the exposure to benzene but they are not test largely practicable today, because analytical, economical, organizational reasons. Recent studies suggest that the dosage in urine of trans,trans muconic acid (ttMA) or phenil mercapturic acid can be useful biomarkers of recent exposure, even at low levels of exposure such as in filling stations. Exposure conditions to gasoline vapors in filling stations are rapidly changing thanks to some technological innovations and legal restrictions and the exposure levels are much below the occupational air standards, Toxicological and epidemiological data (although not yet conclusive at low doses) suggest to carry out however health and epidemiological surveillance programs for the working population. A program for the health surveillance and biological monitoring is here proposed: a clinical examination, integrated with haematological tests and biological monitoring tests, must be carried out in pre-employment and subsequently repeated yearly in the highest exposure conditions. When the exposure levels should decrease the examinations could be carried out every two years.

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.

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.

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.

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.

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.

[Chrono-thermometry in the diagnosis of Raynaud-like vasculopathies caused by prolonged use of vibrating tools]. / La cronotermometria nella diagnosi delle vasculopatie Raynaud-simili da uso prolungato di strumenti vibranti.

Raynaud's phenomenon may be secondary to several different pathological conditions. In some cases it is favoured by occupational exposure to vibration of the upper arms. The diagnosis of Raynaud's phenomenon requires clinical information together with specific technical investigations. This report presents the results of 232 chrono-thermometric tests performed on 157 workers exposed to vibrations during the use of different kinds of tools. Seventy-five subjects not exposed to vibrations of the upper arms but with suspected Raynaud's syndrome were also tested. Chrono-thermometry enabled us to distinguish between three different subgroups of subjects exposed to vibrations: 61 workers with "normal" chrono-thermometry, 33 subjects with "pathological" vascular reactivity to cold in some fingers and 63 workers with such reactivity in all fingers. Similarly the 75 patients not exposed to vibration could also be divided into three groups. No statistical difference was found between the chrono-thermometric results obtained from the exposed and non-exposed subjects when divided into the three subgroups. The overall analysis of the combined results of the different kinds of tests (capillaroscopy plus a vascular reactivity test) is discussed.

Biological monitoring of acrylonitrile exposure.

This study reports the results obtained with the environmental and biological monitoring of 34 workers exposed to acrylonitrile (ACN). Occupational exposure was monitored during 8-h work shifts with both active and diffusive personal samplers which yielded comparable results. The median exposure was 78 micrograms/m3. The ACN concentration in urine collected at the end of the work shifts correlated significantly with the environmental exposure. The ACN concentration in the pre-shift urine samples (median 3.6 micrograms/l) was lower than that found in the post-shift samples (median 10.9 micrograms/l), but higher than in the urine of non-exposed people (median 0.45 microgram/l). Smoking is an important confounding factor in monitoring exposure to ACN. The ACN concentration in urine provides reliable information about occupational and non-occupational exposure to ACN. Aspects of the mechanism of ACN excretion in urine are also discussed.

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.

[Environmental exposure and blood levels of benzene in gas station attendants. Comparison with the general population]. / Esposizione ambientale e livelli ematici di benzene negli addetti agli impianti di distribuzione carburanti. Confronto con la popolazione generale.

Environmental benzene levels were measured in 26 petrol stations using both active and passive stationary and personal samplers. Simultaneously, benzene levels were measured in the petrol station operators on blood samples collected at the end of the work shift and the following morning before starting work. The petrol stations belonged to various different oil companies and were studied both during the winter (9 stations) and in the summer (17 stations). The environmental levels measured with active samplers in the 26 stations were on average 256 ng/l, were significantly lower (98 ng/l) in winter and higher (326 ng/l) in summer. The blood levels of benzene in 77 workers at the end of the work shift were on average 548 ng/l, were significantly lower (306 ng/l) in winter and higher (651 ng/l) in summer. The following morning, blood levels of benzene were lower than those found at the end of the work shift, on average 249 ng/l in winter and 427 ng/l in summer. Smokers had higher benzene levels than non-smokers, both in winter at the end of the work shift (617/170 ng/l) and the following morning (506/137 ng/l), and in summer at the end of the shift (742/517 ng/l) and the following morning (535/233 ng/l). A comparison with a sample of 243 "normal" subjects of the general population showed that their mean blood level of benzene of 165 ng/l was significantly lower than the level found in petrol station workers the morning after the work shift (364 ng/l).

[Urban air pollutant exposure among traffic policemen]. / Esposizione agli inquinanti dell'aria urbana dei vigili municipali.

Exposure to dusts and benzene was studied in 65 traffic policemen. Samples of total dusts showed that mean personal exposure was 0.44 (SD = 0.30) mg/m3, with peaks of about 2 mg/m3. Exposure to 1-nitropyrene (1-NP), the main compound occurring in emissions from diesel engines, which was estimated from concentrations in dusts collected with high-flow samplers, was 0.28 (SD = 0.19) ng/m3 (range: 0.06-1.24 ng/m3). The mean concentration of benzene in the breathing zone was 41 (SD = 20) micrograms/m3, although a level of 100 micrograms/m3 was slightly exceeded in one subject. In urine samples collected before and after workshifts, two biological indicators of exposure to benzene were measured, urinary benzene and urinary trans, trans-muconic acid (MA). The mean values of urinary benzene before and after workshift were similar (98, SD = 81 and 83, SD = 55 ng/l; n = 63; Wilcoxon's T-test = not significant), while a moderate increase in the metabolite was observed (MA = 0.08, SD = 0.11; 0.11, SD = 0.09 mg/g creatinine, in pre- and post-shift samples respectively; Wilcoxon's T-test, z = 3.00; p < 0.01). The levels of exposure to dusts and 1-NP deriving from diesel engine emissions were comparable to those of other occupational groups with this type of risk (garage mechanics, workers operating diesel engine machinery, etc.). Traffic police exposure to benzene was similar to that of the whole population of Padova (40 micrograms/m3, mean annual 24-hour value). However, the values of urinary MA, like those reported by other authors for non-smoker controls, increased after the workshift, indicating low occupational exposure to this pollutant. It should be noted that traffic police exposure to benzene is much lower than that of other occupational categories, e.g., fuel pump distributors.

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.

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.

Blood and urine concentrations of chemical pollutants in the general population.

The concentration of 9 environmental chemical pollutants in the general population was measured in blood and urine. For the 9 different pollutants, the blood samples tested varied from 88 for acetone to 431 for benzene. Urine samples varied from 48 for styrene to 213 for n-hexane. Six of these agents (benzene, toluene, styrene, n-hexane, acetone and carbon disulphide) were present in all or almost all (100-94%) blood samples. The three chlorides (chloroform, trichloroethylene and tetrachloroethylene) were present only in 60-85% of samples. After acetone, with blood concentrations in microgram/1 (mean 840 microgram/l), the highest mean blood levels were those of toluene (1097 ng/l), chloroform (955 ng/l) and n-hexane (642 ng/l). Trichloroethylene and free carbon disulphide showed similar values (458 and 438 ng/l, respectively). Finally, benzene, styrene and tetrachloroethylene showed the lowest values (262, 217 and 149 ng/l, respectively). There was generally a significant difference between rural and urban workers in terms of blood benzene (200 ng/l vs 264 ng/l), trichloroethylene (180 ng/l vs 763 ng/l) and tetrachloroethylene (62 ng/l vs 263 ng/l). In a group of subjects potentially exposed to industrial solvents, classed as chemical workers, blood benzene, toluene, chloroform and n-hexane were significantly higher than in rural and urban workers. Smokers showed a significantly higher blood concentration than non-smokers for benzene (381 ng/l vs 205 ng/1), toluene (1431 ng/l vs 977 ng/l), and n-hexane (838 ng/l vs 532 ng/l). All or almost all urine samples (100-92%) contained all the compounds except trichloroethylene and tetrachloroethylene, present in 79% and 76% of samples, respectively (table 2). Urinary concentrations of all compounds did not differ significantly between rural and urban workers. Benzene and toluene were significantly higher in in urine of smokers than of non-smokers. Chloroform and n-hexane showed significantly higher urinary than blood values. Excluding acetone, with urinary and blood concentrations in pg/l, chloroform, toluene and n-hexane showed the highest mean concentrations both in blood and in urine.

Effects of disulfiram on serum dopamine-beta-hydroxylase and blood carbon disulphide concentrations in alcoholics.

The aim of this study was to investigate the effects of single and repeated disulfiram doses on serum dopamine-beta-hydroxylase activity and blood carbon disulphide concentrations in a group of abstinent alcoholics. The increase in the blood concentration of carbon disulphide was dose dependent after the oral administration of 100-400 mg of disulfiram. Free carbon disulphide peaked at 12 h while the protein-bound fraction increased at least up to 24 h. Both single (100-400 mg p.o.) and repeated (200 mg daily p.o. for ca. 1 month) administrations failed to inhibit the activity of serum dopamine-beta-hydroxylase. The repeated daily administration of 200 mg of disulfiram also had no influence on copper-activated serum dopamine-beta-hydroxylase, which was the same before and after 1-month treatment period. Contrary to the disulfiram group, the activity of the copper-activated enzyme in the serum of abstinent alcoholics declined significantly during the same 30 days.

Carbon disulfide in blood: a method for storing and analysing samples.

Concentrations of free and acid-labile carbon disulfide in human blood were determined by gas chromatography mass-spectrometry. Carbon disulfide was measured in the blood of 62 subjects not occupationally exposed to the solvent, and in 27 subjects treated with disulfiram (which is partially biotransformed into carbon disulfide). In blood, a small part of carbon disulfide is free (it can be analysed without any blood treatment); most carbon disulfide is bound ("acid labile" carbon disulfide), and requires acid hydrolysis to become free and detectable. During the first phase of our study, stored samples of blood (storage at 4 degrees C for 15-40 days) were used. Later, we analysed fresh blood samples. A significant decrease in carbon disulfide was found in stored samples in comparison to fresh samples. During storage, free and acid-labile carbon disulfide in blood decreased respectively to 26% and 27% of the initial concentration within a month. In fresh samples, free carbon disulfide concentrations in blood showed a median of 139 ng/l in normal subjects. Acid-labile carbon disulfide concentrations were much higher (median 2743 ng/l). Free and acid-labile carbon disulfide in blood were closely correlated (r = 0.9358). Blood samples stored at -80 degrees C maintained a constant concentration of carbon disulfide over almost three weeks.

[Blood interface in environmental and occupational exposure to industrial chemical pollutants]. / L'interfaccia ematica nell'esposizione ambientale e professionale a inquinanti chimici industriali.

The concentration of 12 environmental chemical pollutants was measured in the blood of the general population. With reference to the 12 different pollutants, the blood samples tested varied from 88 for acetone to 431 for benzene. Nine of these agents (benzene, toluene, styrene, cumene, xilene, n-hexane, nitrous oxide (N20), acetone and carbon disulphide) were present in all or almost all (100-94%) blood samples. The three chlorides (chloroform, trichloroethylene and tetrachloroethylene) were present only in 60-85% of samples. After acetone and carbon disulphide, with blood concentrations in microgram/l (mean 840 micrograms/l and 2.4 micrograms/l respectively), the highest mean blood levels were those of toluene (1097 ng/l), chloroform (955 ng/l), N2O (915 ng/l), and n-hexane (642 ng/l). Trichloroethylene and free carbon disulphide had similar values (458 and 438 ng/l, respectively). Finally, benzene, styrene and tetrachloroethylene had the lowest values (262, 217 and 149 ng/l, respectively). There was generally a significant difference between rural and urban workers in terms of blood benzene (200 ng/l vs. 264 ng/l), trichloroethylene (180 ng/l vs 763 ng/l) and tetrachloroethylene (62 ng/l vs. 263 ng/l). In a group of subjects potentially exposed to industrial solvents, classed as chemical workers, blood benzene, toluene, chloroform and n-hexane were significantly higher than in rural and urban workers. Smokers showed a significantly higher blood concentration than non-smokers for benzene (381 ng/l vs. 205 ng/l), toluene (1431 ng/l vs. 976 ng/l) and n-hexane (803 ng/l vs. 505 ng/l).