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Purpose: The main aim of this study was to investigate the cobalt (Co) concentrations in urine along 4 months and their relationship with Co concentrations in blood and haemoglobin (adducts) in 34 workers from a hard metal manufacturing plant where metallic Co and Co oxide were used. Furthermore, the excretion kinetics of Co was investigated and the half-lives of Co in blood, plasma and urine were calculated along 18 days of non-exposure in the same workers., Methods: Co was analysed, in all biological samples, by ICP/MS., Results: Wide fluctuations in the urinary Co concentration were observed throughout the work shift and during the work week. A highly significant linear correlation was found between Co concentration (geometrical mean) in urine samples provided each Thursday (end shift) during 16 subsequent weeks and levels of Co-haemoglobin adducts or blood Co concentrations at the end of the same period. The Co elimination kinetics in globin calculated along 18 days without Co exposure was slow, being related to the physiological metabolism of haemoglobin, while in blood, plasma and urine Co half-lives were 12.3, 9.1 and 5.3 days, respectively., Conclusion: Co concentrations in haemoglobin or blood are highly related to the geometrical mean concentration of urinary Co when samples are collected weekly for several subsequent weeks. The biological monitoring of occupational exposure to Co in hard metal facilities provides reliable results by using the Co concentrations in haemoglobin or in whole blood. The urinary findings, though, do not show the same reliability because of their wide daily and weekly fluctuations.

Aim: To unravel key aspects of the use of lanthanide-doped nanoparticles (NPs) in biomedicine, the interaction with immune and brain cells., Materials & Methods: Effects of citrate-stabilized CaF 2 and SrF 2 : Yb, Er NPs (13-15 nm) on human dendritic cells and neurons were assessed in vitro. In vivo distribution was analyzed in mice at tissue and ultrastructural levels, and with glia immunophenotyping., Results: The NPs did not elicit dendritic cell activation and were internalized by cultured neurons, without viability changes. After intravenous injection, NPs were found in the brain parenchyma, without features of glial neuroinflammatory response., Conclusion: Lanthanide-doped NPs do not activate cells protagonists of systemic and brain immune responses, are endocytosed by neurons and can cross an intact blood-brain barrier.

Interest in the amount of metal ion intake from dental alloys has grown. Fixed orthodontic appliances usually include brackets, bands, and archwires made of stainless steel, nickel-titanium, or nickel-cobalt alloys, and these can release metal ions. The purpose of this study was to investigate the biocompatibility in vivo of fixed orthodontic appliances, evaluating the presence of metal ions in oral mucosa cells, their cytotoxicity, and their possible genotoxic effects. Mucosa samples were collected by gentle brushing of the internal part of the right and left cheeks of 55 orthodontic patients and 30 control subjects who were not receiving orthodontic treatment. The cells were immediately prepared for cell viability and the comet assay. Nickel and cobalt cellular content was quantified by inductively coupled plasma mass spectrometry (ICP-MS). The results indicate that nickel and cobalt concentrations were 3.4-fold and 2.8-fold higher, respectively, in the patients than in the controls; cellular viability was significantly lower in the patients than in the controls, and there was a significant negative correlation with metal levels. The biologic effects, evaluated by alkaline comet assay, indicated that both metals induced DNA damage (more cells with comets and apoptotic cells). There were significant positive correlations between (1) cobalt levels and the number of comets and apoptotic cells, (2) nickel levels and number of comet cells, and (3) cobalt levels and comet tails. This study corroborates that nickel and cobalt released from fixed orthodontic appliances can induce DNA damage in oral mucosa cells.

Acrylonitrile (ACN) is a solvent widely used in industry especially as raw material in the manufacturing of acrylic fibres, clothes and domestic furniture. It is also used in manufacturing of resins (ACN-butadiene-styrene...) and for production of nitrilic elastomers. Some researchers proposed the biological monitoring of occupational exposure to ACN by measuring the solvent in the urine, but results were widely spread especially in relation to the analytical method used. This article reports the main aspects that can reduce the variability of results. We checked several ACN solutions in water and urine after heating at 90 degrees C for 1, 3, 5, 8 and 16 hours. Water solutions maintained their ACN concentration in all the checked conditions, while urine concentrations of ACN in urine deceased during the conditioning time until 80% of their initial concentration. The analysis of ACN in urine provided by workers potentially exposed to ACN and by control subjects gave median results of 1.9 and 2.0 micrograms/g creat, without any statistical difference. The results split in relation to the smoking habit showed a statistic difference: the median values of ACN were 1.7 and 4.7 micrograms/g creat, respectively among the 175 non-smokers and 57 smokers.

Objectives: To investigate and compare alveolar, blood, and urine concentrations of 1,3-butadiene, 2,5 dimethylfuran, and benzene, in non-occupational exposure to these products., Methods: Benzene, 2,5-dimethylfuran and 1,3-butadiene were measured in the breath, blood, and urine samples of 61 subjects living in small mountain villages. All 61 were regularly employed as forestry workers. Sampling was done during the long winter-season non-working period. Samples were collected after overnight rest and analysed by headspace and GC-mass spectrometry methods., Results: The median 1,3-butadiene level was 1.2 ng/l (range: <0.8-13.2 ng/l) in alveolar air, 2.2 ng/l (range: <0.5-50.2 ng/l) in blood, and 1.1 ng/l (range: <1-8.9 ng/l) in urine. The median benzene level was 5.7 ng/l (range: <1-24.9 ng/l) in alveolar air, 62.3 ng/l (range: 33.5-487.2 ng/l) in blood, and 63.4 ng/l (range: 25.8-1099.1 ng/l) in urine. The median 2,5-dimethylfuran level was 0.5 ng/l (range: <1-12.5 ng/l) in alveolar air, 2.5 ng/l (range: <5-372.9 ng/l) in blood, and 51.8 ng/l (range: <5-524.9 ng/l) in urine. In several cases, 2,5-dimethylfuran levels were below the detection limit in alveolar air and blood, especially in non-smokers. 1,3-Butadiene, 2,5-dimethylfuran and benzene levels were significantly higher in smokers than non-smokers in all biological media., Conclusions: 1,3-Butadiene and benzene, as ubiquitous pollutants, are detectable and quantifiable in human alveolar air, blood and urine. 2,5-Dimethylfuran, which is not a usual environmental pollutant, is almost always detectable in biological media, but only in smokers.

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).

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.

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).

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.

In order to study solvent exposure in shoe factories, 43 kinds of glues and 22 solvent products used in footwear manufacturing were analyzed. A gas chromatographic spectrometric method was used to identify the mixtures of solvents contained in glues and their diluents. Acetone, ethylacetate and cyclohexane were the solvents more frequently found in glues. Cyclohexane represented on average about 40% of the solvent mixture. Methyl ethyl ketone, 3-methylpentane and 2-methylpentane were often present in glues (45-52% of the samples), but only in a few cases were they associated with n-hexane. N-hexane and methylcyclopentane were found in 32% of the glue samples. N-hexane represented 47% of the solvents only in one glue. Most of the glues contained less than 10% n-hexane. Other solvents (dichloropropane, toluene, trichloroethane, butyl acetate, iso-butyl acetate and 2,2-dimethylbutane) were found in few glue samples or in low percentages. The 22 solvents used as glue diluents were mainly acetone, ethylacetate, dichloromethane and methyl ethyl ketone. The results suggest that solvent exposure in shoe factories has changed compared with data reported about 10 years ago. Biological monitoring of shoe factory workers should measure exposures to the specific solvents found in each factory, especially acetone, cyclohexane, ethylacetate and methyl ethyl ketone.