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Results are reported of X-ray diffraction analysis of extracts derived from lungs of two nickel refinery workers and of three stationary air samples collected inside a nickel refinery. Since environmental samples from the 1950s and 1960s do not exist, two archived production control samples from that period were also analyzed. Because nickel has been found in respiratory tissue of workers retired for more than twenty years, it was likely that the residual nickel compounds must be rather insoluble. Preliminary surveys showed that sulfur was not present in the lung tissue deposits and thus water-soluble and sulfidic nickel were therefore extracted from the ten process samples before the X-ray analysis. A common compound that was found in all 10 samples was trevorite. This is a spinel-type mineral, much like magnetite where the divalent iron is replaced by nickel. It may be formed when trivalent iron reacts with nickel at 1100 degrees C. It has magnetic properties and is very insoluble. Samples from the lungs were obtained by burning off the organic tissue at 630 degrees C. Due to a relatively high detection limit for the X-ray diffraction technique, we were initially not able to detect any mineral nickel compound. But when particles extracted with a magnet were analyzed, a very clear diffraction pattern of trevorite was identified. The main residue after the magnetic separation had a low concentration of nickel (4 microg g(-1)), which suggests that trevorite was the dominating, if not the only, nickel compound present. In addition, chemical analyses were performed on 13 tissue samples from one single lung; one from each main bronchus, two from each lobe, and an additional one from the lower right lobe. Statistical testing showed a highly significant correlation between the five elements determined: Ni, Co, Cu, Fe and Cr. This suggests that these metals are isomorphous and substitute for each other in the mineral structure. These results may indicate that the nickel left in the lungs some years after exposure is trevorite, and may be biologically inert. However, further speciation of nickel compounds in the lungs seems warranted, and trevorite should be tested for its potential toxic effects.

The tobacco plant contains nickel and several other toxic metals, most probably absorbed from the soil, fertilizing products or from pesticides. It has been stated that nickel in a burning cigarette might form the volatile, gaseous compound, nickel tetracarbonyl, and thereby be introduced into the respiratory tract. Accordingly, the main objective of the present study was to find out if nickel content in inhaled smoke from ordinary cigarettes and nickel-contaminated cigarettes handmade by nickel process workers might be a supplementary source of nickel exposure to cigarette smoking process workers leading to additional risk of occupational respiratory cancer in these workers. Blood and urine samples from 318 randomly selected employees from Falconbridge Nickel Refinery in Kristiansand, Norway, allocated to 197 smokers and 121 non-smokers, were analysed for nickel content. Nickel quantities in tobacco from various cigarette brands, from nickel-contaminated cigarettes made by process workers or from cigarettes added known amounts of various nickel salts were analysed before being smoked. The cigarettes were smoked in a smoking machine device applying an electrostatic filter. Blood and urine, tobacco, ash and precipitates in the filter from the main stream smoke of the cigarettes were analysed for nickel quantities by atomic absorption spectrometry methods as previously described by the authors. The nickel concentrations in blood plasma and urine were quite similar among smokers and non-smokers, 6.2 and 48.1 microg L(-1) in smokers, and 6.4 and 50.5 microg L(-1) in non-smokers respectively. We recovered 1.1% or even less of nickel in the mainstream smoke after smoking the entire cigarettes without leaving any butt. Most of the tobacco nickel was recovered in the ash. We conclude that the inhaled nickel in the working atmosphere is probably the main source of the nickel exposure to the respiratory tract in these workers. It remains to be determined why cigarette smoking still seems to be a decisive cofactor in the development of respiratory tract cancer in nickel workers.

People working in the nickel refining industry are known to have a higher concentration of nickel in lung tissue than the general population. To be able to evaluate a potential nickel exposure from other sources, e.g., welding, it is important to have sufficient data on what is normal for a local population. Several local factors such as the content of nickel in air and soil can have a significant impact on this so-called normal value. As almost all surgical equipment contains nickel, the sampling process can in itself be a source of contamination. The scope of this work was to investigate if there was any measurable contamination from the sampling instruments routinely used in hospitals, and if the presence of a nickel refinery had any effect on the nickel content in the lungs of the general population. Autopsy lung tissue samples were collected in situ from 50 people who had lived in the county of Vest Agder in Norway. Two samples were collected from each person; one with a regular scalpel (Swann-Norton) and forceps, and one with a titanium knife and plastic forceps. None of the persons had any known connection to the nickel refinery. The samples were collected at random and no special attention was given to age, sex and place of residence. The autopsies were performed according to Norwegian law and in understanding with the next of kin. The arithmetic mean value +/- s of nickel was 0.64 +/- 0.56 microgram g-1 and 0.29 +/- 0.20 microgram g-1 dry weight, respectively, for samples collected with a regular scalpel and a titanium knife (P < 0.0001). For people who lived 8 km and closer to the refinery by the time of death, the nickel content was 0.41 +/- 0.19 microgram g-1 and for those who had lived between 8 and 70 km away from the refinery it was 0.18 +/- 0.13 microgram g-1 (P < 0.015). No statistical difference was established between results for males and females. Previous investigations have shown that the nickel content in lung tissue varies in the so-called normal population. This work has shown that factors such as sampling equipment and place of residence have an impact on the results. It thus demonstrates that reliable background values can presumably only be obtained by collecting samples from individuals not exposed to known environmental nickel sources and to use nickel-free instruments in the sampling process.

Objective: The purpose of this work was to study the distribution of nickel within lung tissue obtained from nickel-exposed people and to evaluate the use of only one single sample for determination of the nickel burden of the lung., Methods and Materials: The material used was lung tissue obtained from 15 former nickel refinery workers who had been exposed to a variety of nickel compounds such as Ni3S2, NiO, Ni0, NiSO4, and NiCl2. Ten samples taken from different locations of the lung as well as from the right and left bronchus and from the right lower lobe (total 13 samples per individual) were analyzed for nickel by electrothermal atomic absorption spectrometry. Samples obtained from ten people not connected to the refinery served as a reference group., Results: The arithmetic mean value +/-SD for nickel concentration was 50+/-150 microg g(-1) dry wt. Biopsies collected on the center of the lower right lobe had an average nickel concentration of 82+/-252 microg g(-1). The average nickel concentration detected in the right and left bronchus was 5.9+/-11.6 and 3.8+/-6.0 microg g(-l), respectively. Lung tissue obtained from ten people not connected to the refinery had an average nickel concentration of 0.74+/-0.44 microg g(-1)., Conclusions: The significant findings based on log-normal distribution of the nickel concentration were as follows: (1) samples obtained from the right lung showed no significant difference from samples taken from the left lung-a comparison of the nickel concentration detected in all the lung lobes showed that no single lobe differed from another; (2) the concentration of nickel found in the main bronchus of the refinery workers, although elevated, was significantly lower than the concentration detected in the remaining tissue; and (3) one single biopsy did not reflect the nickel burden of the lung.

Earlier work-related lung and nasal cancer studies included estimates of exposures to different nickel species in the refinery. Based on the metallurgy, only insoluble nickel was believed to be present around the roasters but mixed exposure was assumed in most areas, including the tankhouse. Occasional leaching tests of samples from the roaster area have indicated the presence of soluble nickel. This study reports on five parallel sets of dust samples collected from different floors with standard equipment and treated as follows. Two sets were leached with an ammonium citrate buffer at pH 4.4. Undissolved material was treated with HClO4/HNO3, evaporated to dryness and dissolved in HCl, Ni, Cu, Co, Fe, Se, and As were determined in both fractions. Water soluble Ni was found in all samples, ranging from 5-35%. Sulfate in the solutions correlated nearly stoichiometrically to the total metal content. The three remaining sets were investigated by, respectively, differential leaching, X-ray diffraction and scanning electron microscopy. The percentage of soluble nickel found by differential leaching corresponded well with those obtained by the simplified procedure. X-Ray diffraction analysis showed the presence of NiSO4.6H2O as well as oxides of Ni and Cu. This study indicates mixed exposures also in the roaster area. It also clearly indicates that basing exposure on the metallurgy alone can lead to serious misjudgements. The impact of this new information on the interpretation of cancer incidence at this refinery must await the analysis in an ongoing case-reference study.

Nasal epithelial dysplasia is considered a precancerous state. From 1976 through 1989, regular screening for such lesions has been performed among workers at the Falconbridge nickel refinery in Kristiansand. The longitudinal data thus obtained have been evaluated to ascertain to what extent, if any, pre-existing dysplasia can regress when exposure to nickel is reduced. A total of 418 pairs of observations were available from 243 workers. Interpretation of the data is complicated by the fact that dysplasia may remain undetected in small biopsies and the probability of detection of existing dysplasia was, therefore, incorporated into the two-state Markov model. Transition probability rates were estimated by maximum likelihood. The results suggest that regression of dysplasia has taken place and that regression rates increased with time. This finding probably reflects a decreased exposure resulting from a combination of a reduction in airborne nickel, improved personal hygiene and allocation of workers with dysplasia to work in areas with lower nickel exposure. Our results indicate that the chance of developing carcinomas related to nickel exposure is reduced. There are, however, indications that dysplasias continue to develop at a low rate.

One of the basic problems in monitoring exposure of nickel refining workers has been the unclear correlation between plasma nickel, urine nickel, and airborne nickel during the eight-hour work period or throughout the 24-hour day. In previous studies the authors have demonstrated the value of biological sampling in an occupational health program in the nickel processing industry. Whether a single plasma or single urine sample is an adequate gauge of exposure or whether 24-hour urine specimens or a three-day average plasma level are more accurate indices remained to be determined. The purpose of this paper is to report the results of studies of diurnal variations which affect the significance of single biological samples. In addition, data gathered on the correlation of plasma and urine nickel levels with soluble and insoluble nickel compounds in the atmosphere are presented.

The objective of the present investigation was to study the influence of the occupational nickel exposure on the concentration of nickel in nasal mucosa, plasma and urine. Plasma, urine and biopsy specimens of nasal mucosa from 318 nickel workers, 15 retired nickel workers and 57 non-exposed controls were analyzed for nickel by atomic absorption spectrometry. The results showed that nickel exposure led significantly to raised nickel concentration in nasal mucosa, plasma and urine both in active and retired nickel workers. The average nickel concentration in the nasal mucosa was highest in workers exposed to the highest atmospheric nickel concentration, inhaled as nickel subsulphide and oxide dust. Workers exposed to aerosols of nickel chloride and sulphate at a lower atmospheric nickel concentration had, on the other hand, the highest mean nickel concentration in plasma and urine. The mucosal, plasma and urine nickel concentration were significantly correlated to duration of nickel exposure. The accumulated nickel in the nasal mucosa was retained for years after termination of the nickel exposure, and slowly released with an estimated half-life of 3.5 years.

We describe and evaluate a method for determining nickel in plasma and urine by atomic absorption spectrometry. Proteins are precipitated with trichloroacetic acid and sulfuric acid; ammonium pyrrolidinedithlocarbamate is used as the chelating agent for nickel, and methyl isobutyl ketone as extraction solvent. The results were compared with results obtained by the acid-digestion technique for removing proteins and other organic substances. Analyses for both plasma and urine were better by the present procedure. The mean and standard deviation for nickel in plasma from 15 healthy individuals was 2.13 +/- 0.58 microgram/liter by this method. For nickel in urine from 15 healthy men the mean and standard deviation was 4.45 +/- 1.9 microgram/liter. The coefficient of variation for plasma was 11.9%, and for urine 12.2% in 10 analyses of the same plasma and urine with the protein-precipitation procedure, as compared with 26.0 and 38.2%, respectively, by the acid-digestion technique.

We describe a method for determining the nickel content of small tissue samples by flameless atomic absorption spectrophotometry in this case biopsy specimens from human palatine tonsils. Contact between tissue samples and metallic objects was avoided, except for the use of biopsy forceps (Type No. 8150.00 Wolf, stainless steel) for collecting samples, to imitate the actual procedure when small biopsy specimens are removed from the nasal mucosal membranes in nickel workers for histopathological and chemical investigations. Nickel contamination from this instrument was insignificant at the precision of the present procedures. The mean concentration of nickel in 15 tonsils was 13.5 +/- 7.0 (SD) microng/100g (wet wt). The mean nickel concentration in eight different samples of the same tonsil was 5.6 +/- 2.7 (SD microng/100 g.

Lung specimens from 39 nickel refinery workers autopsied during the period from 1978 to 1984 were analyzed for nickel. Fifteen of the workers were employed in the Roasting and Smelting Department, where exposure to nickel was predominantly in the form of nickel-copper oxides, Ni3S2 and metallic dust. The remaining 24 men worked in the Electrolysis Department. Exposure in this group was considered to be mostly to the water-soluble compounds, NiSO4 and NiCl2, but also to a lesser degree to water-insoluble nickel compounds such as nickel-copper oxides and sulphides. The arithmetic mean +/- SD for nickel concentration in lung tissues expressed in micrograms g-1 dry wt for the 39 workers was 150 +/- 280. In the workers employed in the Roasting and Smelting Department, the average nickel concentration was 330 +/- 380; for those who worked in the Electrolysis Department it was 34 +/- 48. Lung tissue from 16 autopsied persons not connected with the refinery had an average nickel concentration of 0.76 +/- 0.39. Statistical analysis based on log-normal distributions of the measured nickel concentrations allowed three major conclusions to be formulated: (1) nickel refinery workers exhibit elevated nickel levels in lung tissues at autopsy; (2) workers of the Electrolysis Department and the Roasting Smelting Department constitute distinct groups with respect to the accumulation of nickel in lung tissue; (3) workers who were diagnosed to have lung cancer had the same lung nickel concentrations at autopsy as those who died of other causes.

Nasal histology and nickel concentration in the plasma and urine of nickel workers were reexamined after 4 a for an evaluation of the effect of improvements in the refining process and work conditions. Ninety-eight (31%) nickel workers who were part of a previous study were reexamined. In addition, 33 of the original 38 workers with nasal epithelial dysplasia were studied for possible regression of the histological changes. Reduction in the atmospheric content of nickel and improved hygienic conditions lowered the concentration of nickel in plasma and urine by approximately 50%. The mean histological score and frequency of dysplasia was virtually the same in the two investigations, 12 and 13%, respectively. Nasal biopsies are of limited diagnostic value in the examination of individual cases. However, the method seems to be of value in identifying and monitoring groups of persons with increased risk of developing nasal carcinoma.