Lung-retained contaminants,urinary chromium and nickel among stainless steel welders

Summary The magnetic method of measuring the amount of lung retained contaminants as well as urinary chromium and nickel determinations have been performed among 83 stainless steel (SS) welders who have used matural metal arc (MMA) and tungsten inert gas (TIG) welding techniques. The welders were divided into four groups according to the time percentage used for MMA welding. Only exposure to MMA/SS welding fumes resulted in clearly elevated chromium concentrations in the urine, the correlation coefficient between the values of urinary chromium and MMA/SS percentage being very significant (P < 0.001). Among the smokers the urinary chromium values were increased (P < 0.05) perhaps owing to contaminated cigarettes. In many workplaces the urinary chromium values of several welders exceeded the value of 30 g/l which is the recommended reference value in Finland. Owing to the solubility properties of nickel compounds in SS welding fumes urinary nickel concentrations were only slightly elevated among MMA/SS welders, and therefore, the urinary nickel determinations do not reflect the level of exposure to nickel compounds. The measured average remanent magnetic field of the chest area correlated well (P < 0.01) with the use of the MMA technique. A very significant correlation (P < 0.001) existed between the average remanent magnetic fields of the chest and the urinary chromium values of MMA/SS welders.     

Monitoring of chromium and nickel in biological fluids of grinders grinding stainless steel

Objective Stainless steel (SS) welders usually spend some of their working time grinding, to finish and smoothen the welding groove. The aim of this study was to investigate possible relations between the concentrations of nickel (Ni) and chromium (Cr) in the work atmosphere generated by grinders grinding SS, and to compare the air levels to the levels of Cr and Ni in their biological fluids. Hereby, it might be possible to identify the contribution of grinding to the levels of Cr and Ni in biological fluids in SS welders. Also the airborne levels of Cr and Ni in SS grinders were compared to corresponding levels in SS welders. Method/design The subjects examined in this study were selected among SS grinders not performing welding. Nine grinders were monitored for 1 workweek, measuring Cr and Ni in air, blood and urine. They were questioned about their exposure to Cr and Ni during their working careers. Results Air levels of total Cr up to 95 μg/m³ and Ni levels up to 25 μg/m³ were measured. Chromium^VI (Cr^VI) was detectable only in five air samples; the levels in the remaining samples were below the detection limit. The levels of Cr in blood and urine were also low. The levels of Ni in urine were close to those for MMA and MIG/MAG SS welders. In spite of high levels of total Cr and Ni observed in air, the levels found in biological fluids were low. The Cr levels in more than 50% of the whole blood and red cell samples and about 1/3 of the Cr–plasma levels were below the detection limits. The mean blood levels for Cr were 0.43, 0.60 and 0.35 μg/l, in whole blood, plasma and red cells, respectively. The mean levels for Cr in the urine was 1.6, 1.4 and 1.4 μg/g creatinine for the first void, just before and just after work. For Ni the mean blood levels were 0.87 μg/l in whole blood and 0.68 μg/l in plasma. The mean levels and ranges of Ni from the first void, just before and after work in urine were 3.79 μg/g creatinine, 3.39 and 4.56, respectively. The Cr concentrations found in whole blood, plasma and red cells were approximately the same as those found in the unexposed controls and among TIG SS welders, while the urinary levels were somewhat higher, but still lower than in the welders applying other welding techniques. The mean levels of Ni in the urine of grinders were higher than those of welders, except for SS welders welding the MIG/MAG-method. Conclusion SS Grinding seems not to contribute significantly to the uptake of Cr, which may be explained by the fact that most of Cr in the air is present in the metallic (0-valent) or trivalent form, and hardly any as Cr^VI, and therefore hardly being taken up in the airways. The grinders’ uptake of Ni seems to take place to the same extent as in SS welders.     

Occupational chronic exposure to metals

Summary External and internal chromate exposure of 103 stainless steel welders who were using manual metal arc welding (MMA), metal inert gas welding (MIG) and both methods, were measured by ambient and biological monitoring. At the working places the maximum chromium trioxide concentrations were 80 g/m³. The median values were 4 g/m³ (MMA) and 10 g/m³ (MIG). The median chromium concentrations in erythrocytes, plasma and urine of all welders were < 0.60, 9.00 and 32.50 g/l. For biological monitoring purposes, chromium levels in erythrocytes and simultaneously in plasma seem to be suitable parameters. According to our results, chromium levels in plasma and urine in the order of 10 and 40 g/l seem to correspond to an external exposure of 100 g chromium trioxide per cubic metre, the technical guiding concentration (TRK-value). Chromium concentrations in erythrocytes greater than 0.60 g/l indicate an external chromate exposure greater than the TRK-value.     

Occupational chronic exposure to metals

Summary Stainless steel welders (n = 103) were examined. To estimate external exposure, personal air sampling was used. Internal exposure was quantified by the determination of nickel levels in erythrocytes, plasma and urine. Men and women (n = 123) were examined for control purposes. In the plasma and erythrocytes of the controls the nickel concentration was below the level of detection (< 1.81 μg/l). The element concentrations in urine were between < 0.1 and 13.3 μg/l. Of the controls 95% showed nickel levels in urine below 2.2 μg/l (reference value). The average concentration of nickel in the air was 93 ± 81 μg/m³. The average concentration of nickel in the plasma samples was 4.9 ± 4.0 μg/l (95th percentile 12.8 μg/L). In erythrocytes nickel could not be detected. The nickel concentrations in the urine of the welders were 18.5 ± 28.5 μg/l on average (95th percentile 52.5 μg/l). Only a weak correlation between the nickel levels of plasma and urine could be detected (C_urine = 2.07 + 8.45 C_plasma; r = 0.294; p < 0.01). Based on our results and on the reported literature a future limit value for the nickel concentration in urine should lay between 30 and 50 μg/l. This value corresponds to an external exposure of 500 μg nickel per cubic metre.     

Urinary N -acetyl-β-glucosaminidase as an indicator of renal dysfunction in electroplating workers

Objectives: To investigate chromium-induced renal dysfunction in electroplating workers. Methods: A cross-sectional study was used to evaluate four biochemical markers of renal function. A total of 178 workers were divided into 3 comparable groups consisting of 34 hard-chrome plating workers, 98 nickel-chrome electroplating workers, and 46 aluminum anode-oxidation workers, who represented the reference group. Ambient and biological monitoring of urinary chromium were performed to measure exposure concentrations. Results: Overall, urinary chromium concentrations were highest among hard-chrome plating workers (geometric mean 2.44 μg/g creatinine), followed by nickel-chrome electroplating workers (0.31 μg/g creatinine) and aluminum workers (0.09 μg/g creatinine). Airborne chromium concentrations were also highest in the hard-chrome plating area (geometric mean 4.20 μg/m³), followed by the nickel-chrome electroplating area (0.58 μg/m³) and the aluminum area (0.43 μg/m³). A positive correlation was found between urinary chromium and airborne concentrations (r = 0.54, P < 0.01). Urinary concentrations of N-acetyl-β-d-glucosaminidase (NAG) were also highest among hard-chrome plating workers (geometric mean 4.9 IU/g creatinine), followed by nickel-chrome workers (3.4 IU/g creatinine) and aluminum workers (2.9 IU/g creatinine). The prevalence of “elevated” NAG (>7 IU/g creatinine) was significantly highest among hard-chrome plating workers (23.5%), then among nickel-chrome workers (7.1%) and aluminum workers (8.7%). Differences in β₂-microglobulin, total protein, and microalbumin were not significant. Conclusion: The author's evidence indicates that NAG is an early indicator of renal dysfunction in hard-chrome plating workers.     

Biomonitoring of manganese in blood, urine and axillary hair following low-dose exposure during the manufacture of dry cell batteries

Objectives: A cross-sectional study was carried out on 100 workers from three different workplace areas in a dry cell battery manufacturing plant and on 17 currently nonexposed referents, to examine the relationship between the external exposure to manganese dioxide (MnO₂) and the body burden of manganese in blood, urine and hair. Methods: Inhalable dust was measured gravimetrically after stationary active sampling. Manganese was analyzed in dust samples, blood, urine and axillary hair by atomic absorption spectro- metry. Results: The average air concentrations of manganese in the three workplace areas were 4 μg/m³ (range: 1–12 μg/m³), 40 μg/m³ (12–64 μg/m³) and 400 μg/m³ (137–794 μg/m³). Manganese in blood and axillary hair correlated with airborne manganese in group-based calculations but not on an individual level. The manganese concentrations varied between 3.2 μg/l and 25.8 μg/l in the blood (mean: 12.2 ± 4.8 μg/l) and between 0.4 μg/g and 49.6 μg/g in hair (mean: 6.2 ± 6.2 μg/g in the proximal sequence), respectively. The results for the nonexposed referents were 7.5 ± 2.7 μg/l (mean) in the blood (range: 2.6–15.1 μg/l) and 2.2 ± 1.8 μg/g (mean) in axillary hair (range: 0.4–6.2 μg/g). In these matrices, manganese differed significantly between the highly exposed workers and both the reference and the low-exposure group. Manganese in blood revealed the lowest background variance. No differences for manganese in urine were observed between workers (mean: 0.36 ± 0.42 μg/l, range: 0.1–2.2 μg/l) and referents (mean: 0.46 ± 0.47 μg/l, range: 0.1–1.7 μg/l). Conclusions: Manganese in blood is a specific and suitable parameter for the biomonitoring of MnO₂ exposure, although its validity is limited to group-based calculations. Urinary manganese failed to allow a differentiation between exposed workers and referents. The suitability of manganese analysis in hair for biomonitoring purposes suffers from a relatively great background variation as well as from analytical problems. Received: 11 December 1998 / Accepted: 17 July 1999     

Urinary beryllium – a suitable tool for assessing occupational and environmental beryllium exposure?

Objectives: The reasons for the slow progress and lack of new knowledge in the biological monitoring of beryllium (Be) are to be found in the presumed small number of working activities involving exposure to the metal, and the lack of adequate analytical methods. The reference values for urinary Be reported earlier in the literature appear to be too high, due to the poor specificity and sensitivity of the adopted methods. The aim of this study was to correlate Be air concentrations and Be urinary levels to ascertain whether the biological indicator was suitable for assessing occupational exposure to the metal. Methods: To investigate the relationship between the Be concentrations in air and those excreted in urine, we examined 65 metallurgical workers exposed to very low levels of the metal, and 30 control subjects. The exposed workers were employed in two electric steel plants and two copper alloy foundries. The alloys were produced in electric furnaces, starting with scrap containing Be as an impurity. The Be concentrations in the air were monitored by area samplers and the levels of Be in the urine of the workers were determined in samples taken at the end of the shift. Both determinations were carried out by ICP-MS. Results: The median airborne Be concentrations in the copper alloy plants were 0.27 μg/m³ in the furnace area and 0.31 μg/m³ in the casting area. Median values of 0.03 to 0.12 μg/m³ were determined in the steel plants, the relatively wide range probably due to differing amounts of Be in the scrap. Regression analysis was performed on the median values from four work areas and the corresponding urinary samples. A significant correlation was found for the relationship between external and internal exposure. The urinary Be levels were in the range between 0.12 and 0.15 μg/l with observation of the recommended TLV-TWA for inhalable dust of 0.2 μg/m³ (0.2 μg/l at the upper 95th percentile). Conclusions: Sufficient data are not currently available to be able to propose a BEI for urinary Be. Our results show that new investigations are necessary to improve the evaluation of dose indicators and the relationship between external and internal exposure to Be. Received: 15 May 2000 / Accepted: 8 September 2000     

Reference values of urinary chromium in Italy

Objective: The paper describes the results of a polycentric study for the assessment of reference values of urinary chromium (U-Cr) in the Italian population. Method: A total of 890 subjects (58.3% males and 41.7% females) were selected on the basis of standardized criteria in eight different areas of Italy. Urinary chromium was determined on morning spot samples collected using standardized procedures. The U-Cr was determined independently by three laboratories using an Electrothermic atomization-Atomic Absorption Spectrometry (ETA-AAS) method with a detection limit of 0.05 μg/l, adopting – for the statistical analysis – the median value of the results of the three laboratories. The between-laboratories within-subjects standard deviation was 0.049 μg/l. Due to the high proportion (approx. 28%) of undetectable chromium levels, the geometric mean (GM) and geometric standard deviation (GSD) were estimated using a procedure of linear interpolation. The analysis of the effects of some variables (sex, age, center, residence, smoking and drinking habits) on the U-Cr values was also performed, by multiple regression analysis after logarithmic transformation, using GM and SD. Results: The reference value of U-Cr was of 0.08 μg/l as an estimated GM, whereas the expected distribution ranged from not detectable (nd) (95% CI = nd–0.06) to 0.24 μg/l (95th percentile; 95% CI = 0.20– 0.31). Among the variables studied, only geographical area and sex significantly influenced the U-Cr levels. In subjects selected in the provinces of Bari and Venice values of U-Cr were significantly lower than those determined in subjects residing in other areas. Conclusions: From our investigation the reference values for U-Cr were lower than those obtained in previous investigations. In addition it confirms a further reduction in U-Cr levels following the previous decline reported in the 1970s and 1980s. In over 20 years U-Cr values in the general population dropped from values greater than 1 μg/l to values between 0.5 and 0.2 μg/l. The reasons of this progressive decline cannot be attributed in our opinion to a reduced intake of the metal, but mainly to the improvement in analytical instrumentation and methods. A further decrease may be ascribed to a more accurate definition of the reference groups and to a better control of pre-analytical factors. Considering that the reference values for U-Cr are much lower than those determined some decades ago, toxicological studies in order to verify the significance of biological limit values currently suggested for chromium seem to be necessary. Received: 26 November 1996 / Accepted: 7 February 1997     

Monitoring of chromium and nickel in biological fluids of stainless steel welders using the flux-cored-wire (FCW) welding method

Objective: This study was undertaken to investigate the exposure to chromium (Cr) and nickel (Ni) in flux-cored wire (FCW) welders welding on stainless steel (SS). Method/design: Seven FCW welders were monitored for 3 days to 1 workweek, measuring Cr and Ni in air, blood, and urine. The welders were questioned about exposure to Cr and Ni during their whole working careers, with emphasis on the week of monitoring, about the use of personal protective equipment and their smoking habits. Results: The air concentrations were mean 200 g/m³ (range 2.4–2,744) for total Cr, 11.3 g/m³ (<0.2–151.3) for Cr^VI, and 50.4 g/m³ (<2.0–416.7) for Ni during the workdays for the five welders who were monitored with air measurements. The levels of Cr and Ni in biological fluids varied between different workplaces. For Cr in whole blood, plasma, and erythrocytes, the mean levels after work were 1.25 (<0.4–8.3) and 1.68 (<0.2–8.0) and 0.9 (<0.4–7.2) g/l, respectively. For Ni most of the measurements in whole blood and plasma were below the detection limits, the mean levels after work being 0.84 (<0.8–3.3) and 0.57 g/l (<0.4–1.7), respectively. Mean levels for Cr and Ni in the urine after work were 3.96 (0.34–40.7) and 2.50 (0.56–5.0) g/g creatinine, respectively. Conclusion: Correlations between the Cr^VI levels measured in air and the levels of total Cr in the measured biological fluids were found. The results seem to support the view that monitoring of Cr in the urine may be versatile for indirect monitoring of the Cr^VI air level in FCW welders. The results seem to suggest that external and internal exposure to Cr and Ni in FCW welders welding SS is low in general.     

Comparison between blood and urinary toluene as biomarkers of exposure to toluene

Objectives: To compare blood toluene (TOL-B) and urinary toluene (TOL-U) as biomarkers of occupational exposure to toluene, and to set a suitable procedure for collection and handling of specimens. Method: An assay based on headspace solid-phase microextraction (SPME) was used both for the determination of toluene urine/air partition coefficient (λ_urine/air) and for the biological monitoring of exposure to toluene in 31 workers (group A) and in 116 non-occupationally exposed subjects (group B). Environmental toluene (TOL-A) was sampled during the work shift (group A) or during the 24 h before specimen collection (group B). Blood and urine specimens were collected at the end of the shift (group A) or in the morning (group B) and toluene was measured. Results: Toluene λ_urine/air was 3.3 ± 0.9. Based on the specimen/air partition coefficient, it was calculated that the vial in which the sample is collected had to be filled up to 85% of its volume with urine and 50% with blood in order to limit the loss of toluene in the air above the specimen to less than 5%. Environmental and biological monitoring of workers showed that the median personal exposure to toluene (TOL-A) during the work-shift was 80 mg/m³, the corresponding TOL-B was 82 μg/l and TOL-U was 13 μg/l. Personal exposure to toluene in environmentally exposed subjects was 0.05 mg/m³, TOL-B was 0.36 μg/l and TOL-U was 0.20 μg/l. A significant correlation (P < 0.05) was observed between TOL-B or TOL-U and TOL-A (Pearson's r=0.782 and 0.754) in workers, but not in controls. A significant correlation was found between TOL-U and TOL-B both in workers and in controls (r=0.845 and 0.681). Conclusion: The comparative evaluation of TOL-B and TOL-U showed that they can be considered to be equivalent biomarkers as regards their capacity to distinguish workers and controls and to correlate with exposure. However, considering that TOL-U does not require an invasive specimen collection, it appears to be a more convenient tool for the biological monitoring of exposure to toluene. Received: 20 October 1999 / Accepted: 4 March 2000     

Risk of lung cancer in workers producing stainless steel and metallic alloys

Objectives: The mortality of workers involved in the production of stainless and alloyed steel from 1968 to 1992 was studied, in order to investigate the risk of lung cancer due to exposure to metals, i.e. iron oxides, chromium and/or nickel compounds. Methods: The study design was a historical cohort mortality study and a nested case-control study concerning lung cancer. Standardized mortality ratios (SMRs) were computed using regional mortality rates as an external reference for comparing observed and expected numbers of deaths, adjusting for age, sex and calendar time. Conditional logistic regression was used to estimate odds ratios (ORs). Occupational exposure was assessed through the complete job histories of cases and controls and a specific job-exposure matrix. Results: The cohort comprised 4,288 male and 609 female workers. The observed overall mortality was significantly lower than expected [649 deaths; SMR = 0.91; 95% confidence interval (CI) 0.84–0.98]. No significant SMR was observed for mortality from lung cancer (54 deaths; SMR = 1.19; CI 0.88–1.55). The case-control study was based on 54 cases and 162 individually matched controls. Smoking habits were available for 71%. No lung cancer excess was observed for exposure to (1) metals and/or their compounds, i.e. iron (OR = 0.94, CI 0.48–1.86), chromium and/or nickel (OR = 1.18, CI 0.62–2.25), and cobalt (OR = 0.64, CI 0.33–1.25), (2) acid mists (OR = 0.43, CI 0.17–1.10), and (3) asbestos (OR =  1.00, CI 0.54–1.86). With respect to exposure to polycyclic aromatic hydrocarbons (PAHs) and silica, which are often found together in workplaces, (1) high and statistically significant lung cancer excesses were observed, the ORs being 1.95 (CI 1.03–3.72) and 2.47 (CI 1.28–4.77) respectively, (2) quantitative exposure parameters revealed upward trends reaching statistical significance (P < 0.05), and (3) adjustments for tobacco consumption did not reveal any confounding factors from smoking. Conclusion: This study failed to detect any relationship between lung cancer and exposure to iron, chromium, nickel and/or their compounds. High and statistically significant relative risks, along with increasing trends, were observed for simultaneous exposure to PAHs and silica. Received: 12 April 1999 / Accepted: 2 October 1999     

Exposure to cobalt and nickel in the hard-metal production industry

Objective The shortage of cobalt (Co) on the metal market forced the industry to add nickel (Ni) to Co as a binding agent for the sintering of hard metal. This change enabled us to study (1) the exposure to Ni powder and (2) the effect of Ni on Co uptake (and vice versa). Methods Equal amounts of Co and Ni were used in the mixture in a plant employing 50 workers. Both personal ambient-air samples and single-void urine samples were taken twice in the same week, i.e., on Monday and Thursday. Atomic absorption spectroscopy (AAS) was used for analyses. Results The airborne availability of Ni (mean value 41.65 ± 6.29 μg/m³) was 2-fold that of Co (mean value 21.85 ± 24.25 μg/m³), although the two series of data (n = 20) were significantly correlated. Even if the Co and Ni urinary concentration values (n = 45) recorded on Monday morning and Thursday evening were significantly correlated, at the end of the week there was a 3-fold increase, specifically, from 7.3 to 22.28 μg/l, in Co elimination (a significant difference) and a 30% increase in Ni elimination from 11.98 to 15.83 μg/l. Moreover, on Monday morning, 90% of Ni urinary concentration values were higher than those of Co as opposed to only 33% on Thursday evening. In the six cases in which both airborne and urine determinations were performed on the 2 days, no significant relationship was found between external exposure and biological monitoring data. Conclusions Although Ni uptake was variable, it was generally low, whereas Co uptake was substantial, as had previously been observed in the same plant when Co was the only binder under use. It was therefore possible to rule out any influence of Ni exposure on Co uptake and to suggest the contrary, as has been demonstrated in bacterial species and in rats using everted intestinal sacs. Received: 18 March 1997 / Accepted: 2 October 1997     

Cadmium in the blood and seminal fluid of nonoccupationally exposed adult male subjects with regard to smoking habits

Blood cadmium (B-Cd) and seminal fluid cadmium (Sf-Cd) were measured in 120 adult male subjects not occupationally exposed to cadmium (Cd), comprising 42 nonsmokers (including nine former smokers) and 78 smokers. The respective median and range values were: 0.46 (0.19–1.49) μg/l of B-Cd and 0.54 (0.17–1.67) μg/l of Sf-Cd in nonsmokers, and 4.33 (0.49–13.33) μg/l of B-Cd and 0.85 (0.29–3.56) μg/l of Sf-Cd in smokers. Both indicators showed a highly significant difference in Cd exposure between the groups (P<0.0001), although the increase in B-Cd was considerably more pronounced than that of Sf-Cd in smokers compared with nonsmokers. The results suggest a nonlinear relationship (log Sf-Cd/log B-Cd: r=0.501, P<0.0001), rather than linear relationship (Sf-Cd/B-Cd: r=0.430, P<0.0001), between the indicators. Significant correlations were found between smoking habits, i.e., the number of cigarettes per day, and an increase in B-Cd in smokers (r=0.296, P<0.01) and in all 120 subjects (r=0.685, P<0.0001), as well as between smoking habits and an increase in Sf-Cd in smokers (r=0.378, P<0.001) and in all 120 subjects (r=0.488, P<0.0001). Both indicators are necessary for evaluation of individual internal Cd dose, since they appear to differ in reflecting recent and long-term cumulative Cd exposure and/or the amount of Cd at the site(s) of its effect(s) in the body. Received: 30 September 1996 / Accepted: 18 February 1997     

Indoor Environmental Differences between Inner City and Suburban Homes of Children with Asthma

We conducted this study to compare environmental exposures in suburban homes of children with asthma to exposures in inner city homes of children with asthma, to better understand important differences of indoor pollutant exposure that might contribute to increased asthma morbidity in the inner city. Indoor PM₁₀, PM_2.5, NO₂, O₃, and airborne and dust allergen levels were measured in the homes of 120 children with asthma, 100 living in inner city Baltimore and 20 living in the surrounding counties. Home conditions and health outcome measures were also compared. The inner city and suburban homes differed in ways that might affect airborne environmental exposures. The inner city homes had more cigarette smoking (67% vs. 5%, p < .001), signs of disrepair (77% vs. 5%, p < .001), and cockroach (64% vs. 0%, p < .001) and mouse (80% vs. 5%, p < .001) infestation. The inner city homes had higher geometric mean (GM) levels (p < .001) of PM₁₀ (47 vs. 18 μg/m³), PM_2.5 (34 vs. 8.7 μg/m³), NO₂ [19 ppb vs. below detection (BD)], and O₃ (1.9 vs. .015 ppb) than suburban homes. The inner city homes had lower GM bedroom dust allergen levels of dust mite (.29 vs. 1.2 μg/g, p = .022), dog (.38 vs. 5.5 μg/g, p < .001) and cat (.75 vs. 2.4 μg/g, p = .039), but higher levels of mouse (3.2 vs. .013 μg/g, p < .001) and cockroach (4.5 vs. .42 U/g, p < .001). The inner city homes also had higher GM airborne mouse allergen levels (.055 vs. .016 ng/m³, p = .002). Compared with the homes of suburban children with asthma, the homes of inner city Baltimore children with asthma had higher levels of airborne pollutants and home characteristics that predispose to greater asthma morbidity. Simons, Curtin-Brosnan, and Eggleston are with the The Johns Hopkins University School of Medicine, Baltimore, MD, USA; Buckley and Breysse are with the The Johns Hopkins Bloomberg School of Public Health, Baltimore, MD, USA; Simons is with the Divisions of Allergy and Immunology, Albany Medical College, Albany, NY, USA.     

Evaluation of biological monitoring among stainless steel welders

Summary Ten manual metal arc (MMA) high alloy stainless steel (SS) welders were studied during one week and the concentrations of chromium (Cr) and nickel (Ni) were determined in their urine and blood. Stationary and personal air samples were collected from the immediate work environment; they covered the entire work period. Spot urine samples were collected during the follow-up period. Whole blood and plasma samples were taken from the workers before and after one shift, and the retention rate of magnetic dust in the lungs was estimated with magnetopneumography. On the basis of the results, indices of short-term exposure to Cr and Ni were evaluated. Urinary Cr and Ni concentrations (corrected to creatinine) reflect both the body burden caused by long-term and short-term exposure to easily soluble fractions of these metals. The results indicated that the use of Cr and Ni urinary analyses as indices of short-term exposure is not as dependable as previously assumed. The Cr and Ni concentrations in whole blood and plasma did not correlate with the measured exposure, but the daily mean increase in the Cr concentration reflected exposure to total Cr and Cr (VI) very well. The large variation in the Cr concentration of the morning urine (0.01–2.7 mol/l) and blood (0.05–1.43 mol/l) indicated large personal variations of body burden among the exposed welders. The retention rate of magnetic dust in the lungs correlated well (P<0.01) with the daily mean increase of Cr in blood. Very good correlations (P<0.001) were found between the retention rate of magnetic dust and the personal air samples of Cr and Cr (VI).     

Carcinogenicity assays of wood dust and wood additives in rats exposed by long-term inhalation

Objective: This study evaluates whether wood dust and/or wood preservatives develop a carcinogenic potential against the tissues of the airways of rats. Methods: The formation of tumors of the respiratory tract after exposure to wood dust was studied in six groups of approximately 60 female Fischer 344 rats exposed by long-term inhalation to mean concentrations of (1) 18 mg/m³ of untreated oak wood dust, (2) wood preservatives containing ca. 1 μg/m³ lindane and 0.2 μg/m³ of pentachlorophenol (PCP) in the exposure air, or lindane and 18 μg/m3 of PCP (group lindane/PCP vapors, and group oak wood treated with lindane/PCP), (3) 21 or 39 μg/m³ of sodium dichromate (calculated as CrO₃, group chromate aerosol and group oak wood with chromate), and 72 μg/m³ of N-nitrosodimethylamine vapors as positive control. The negative control group consisted of 115 animals (sham-exposed). Results: Tumors of the nasal cavity developed in two rats exposed to chromate aerosol or in combination with wood dust (2/102, 2%). Malignant tumors of the lower respiratory tract were induced only in exposed groups of rats (three adenocarcinomas of the lung and four bronchiolar lung carcinomas, 7/254, 2.8%). More respiratory tract tumors were observed in rats exposed to chromate or wood with chromate (5/102, 5%), also in groups exposed to oak wood dust (oak untreated, oak + chromate, oak + lindane/PCP; together 5/155, 3.2%). Analysis of `unpreserved' oak wood dust revealed up to 5 μg/m³ of chromate. When this exposure was taken into account, eight of nine animals with respiratory tract tumors (including nasal cavity) had exposure to chromate, while only one tumor occurred in the group lindane/PCP. Otherwise the incidence of systemic tumors was increased in animals exposed to lindane/PCP, due in particular to a significantly increased incidence of liver tumors (OR=3.7; 1.24–11.3; P=0.019). Fatal (mucoepidermoid) tumors were induced by N-nitrosodimethylamine (NDMA) in the positive control (14/46, 30%). No such tumors of the respiratory tract were observed in the negative control. Conclusions: Tumors in the respiratory tract were found only in exposed animals, predominantly in the groups which inhaled oak wood dust and chromate stain. Chromate may play a decisive role for the etiology of tumors of the nasal cavity in wood workers. This assumption should be supported by further dose-response studies. Received: 23 May 2000 / Accepted: 13 September 2000     

Exposure-response relationships in rhinitis and conjunctivitis caused by methyltetrahydrophthalic anhydride

Objective: To examine exposure-response relationships in the occurrence of symptoms of the eyes and airways in workers exposed to methyltetrahydrophthalic anhydride (MTHPA). Methods: A population of 111 workers from 2 condenser plants (A and B) using epoxy resin with MTHPA underwent a questionnaire survey and serology investigations, and data obtained on 95 subjects in assembly and inspection lines were analyzed for this study. Results: In all, 24 (65%) of 37 workers in plant A and 38 (66%) of 58 workers in plant B had positive MTHPA-specific IgE. The air levels of MTHPA detected in assembly and inspection lines were higher in plant A than in plant B (geometric mean 25.5–63.9  and 4.93–5.49 μg/m³, respectively). IgE-sensitized workers in each plant had significantly (P < 0.05) more complaints regarding the eyes and nose than did unsensitized workers, suggesting that there is an IgE-mediated mechanism in most of these symptoms. The sensitized workers in plant A had higher frequencies for symptoms of the eyes, nose, and pharynx than did those in plant B (P < 0.02). Furthermore, only 15% of persons often displayed work-related symptoms among the 20 symptomatic workers in plant B as compared with 73% of the 26 symptomatic workers in plant A (P < 0.0001). These results can be explained by the difference in the MTHPA levels measured in the lines between the two plants. In plant B the minimal level of MTHPA that was associated with work-related symptoms was 15–22 μg/m³, which was lower than the geometric mean levels detected in assembly and inspection lines in plant A. Conclusions: These results suggest that MTHPA exposure at levels above 15 μg/m³ should be avoided to prevent the development of occupational allergic diseases in most workers. Received: 4 May 1998 / Accepted: 4 August 1998     

Determination of N-nitrosodiethanolamine in urine by gas chromatography thermal energy analysis: application in workers exposed to aqueous metalworking fluids

 Objective: The aim of this study was to describe a detailed and validated methodology designed for the analysis of carcinogenic N-nitrosodiethanolamine (NDELA) down to sub-μg/l levels in urine and its application to a number of workers exposed to NDELA-contaminated aqueous metalworking fluids (MWF). Methods: Following a work-up procedure based on solid-phase extraction of NDELA, the urinary extracts were analysed without derivatization by gas chromatography on a polar wide-bore column with chemiluminescent detection using a thermal energy analyser (TEA). N-Nitroso-(2-hydroxypropyl)amine was used as an internal standard. The method was applied to 12 workers using “nitrite-free” or “nitrite-formulated” MWF and to 15 unexposed subjects. The NDELA content of the MWF was also determined using a similar, but simpler method able to easily quantify NDELA down to at least 0.1 mg/l. Results: Contamination by NDELA traces of some chemicals used for the sample preparation, particularly ethyl formate, must be carefully checked since it can give rise to false-positive results of up to 1 or 2 μg/l. The response was linear in the range of 0–500 μg/l. Between 0.5 and 10 μg/l, the recovery rate was close to 95%, while repeatability ranged from 12.5 to 6.4% (n = 5). The detection limit was 0.3 μg/l (Signal/noise = 3). No detectable NDELA could be observed in the control workers. There was no significant increase in NDELA levels at the end of shift spot samples from an exposed worker over 1 week. Higher NDELA concentrations were found in two workers (4.3 and 10.7 μg/l) exposed to “nitrite-formulated” fluids (contaminated with 65 and 18 mg NDELA per l, respectively) than in nine workers (range, 0.4–1.3 μg/l exposed to “nitrite-free” fluids with lower levels of NDELA (range, 0.5–6.6 mg/l). Conclusion: The detailed methodology described in this work and applied to a limited industrial situation was found to be suitable for monitoring NDELA in the urine of workers exposed to aqueous MWF. A much larger screening has been undertaken with the aim of obtaining better information on the real exposure of workers sometimes exposed to “nitrite-formulated” fluids that are still used. Received: 8 December 1998 / Accepted: 3 April 1999     

Urinary elimination of nickel and cobalt in relation to airborne nickel and cobalt exposures in a battery plant

Objective To estimate the relationship between Ni concentrations in the ambient air and in the urine, at a battery plant using nickel hydroxide. Methods Workers occupationally exposed to a mixture of nickel hydroxide, metallic cobalt and cobalt oxyhydroxide dust were studied during two consecutive workdays. Air levels of Ni and Co in total dust were determined by personal sampling in the breathing zone. Both metals in air were sampled by Teflon binder filters and analyzed by inductively coupled plasma absorption emission spectrophotometry. Urine was collected from 16 workers immediately before and after the work shift. Urinary Ni and Co concentrations were measured by electrothermal atomic absorption spectrometry. Results A poor correlation was seen between Co in the air and in post-shift urine (r = 0.491; P < 0.01), and no correlation was found between Ni in the air and in post-shift urine (r = 0.272; P = 0.15), probably due to the use of respiratory protection. The subjects were exposed to higher levels of Ni than Co (Ni (mg/m³) = −0.02 + 7.41 Co (mg/m³), r = 0.979, P < 0.0001). Thus, exposure to Co at 0.1 mg/m³ should produce a Ni level of 0.7 mg/m³. According to section XIII of the German list of MAK and BAT Values, a relationship between exposure to Co and urinary Co excretion, Co (μg/l) = 600 Co (mg/m³), has been established and the relationship between soluble or insoluble Ni salts in the air and Ni in urine was as follows: Ni (μg/l) = 10 + 600 Ni (mg/m³) or Ni (μg/l) = 7.5 + 75 Ni (mg/m³). Assuming nickel hydroxide to be soluble and to be insoluble, the Ni concentrations corresponding to Ni exposure at 0.7 mg/m³ were calculated as 430 and 60 μg Ni/l, respectively. Similarly, exposure to Co at 0.1 mg/m³ should result in Co urinary concentrations of 60 μg Co/l. On the other hand, a good correlation was found between Co and Ni in post-shift urine (Ni (μg/l) = 9.9 + 0.343 Co (μg/l), r = 0.833, P < 0.0001). On the basis of this relationship, the corresponding value found in our study was 0.343 × 60 μg Co/l + 9.9 = 30.5 μg Ni/l. This value was close to that calculated by the equation for a group of insoluble compounds, but about 14 times lower than that calculated by the equation for a group of soluble compounds. Conclusions Our results suggest that exposure to nickel hydroxide yields lower urine nickel concentrations than the very soluble nickel salts, and that the grouping of nickel hydroxide might be reevaluated. Therefore, to evaluate conclusively the relationship between nickel hydroxide dust in the air and Ni in post-shift urine, further studies are necessary.     

Biological monitoring of workers exposed to 4,4′-methylene-bis-(2-orthochloroaniline) (MOCA)

Objective: The objective of the study was to validate a new and simple method to determine MOCA in the urine of exposed workers. Methods: The separation, identification and quantification of urinary MOCA were performed in spiked urines by a sensitive and practical high-performance liquid chromatography (HPLC) method and applied to urine samples of 11 workers occupationally exposed to MOCA; the postshift urinary levels of MOCA in their urine samples with and without hydrolysis, “total” and “free” MOCA respectively, were determined. In addition, we investigated the use of citric or sulfamic acid as preservatives of urine samples. Results: The “total” and “free” MOCA were extracted with isooctane from hydrolysed and nonhydrolysed 20-ml urine samples respectively. After evaporation, the residue was dissolved in 4 ml of 2 · 10⁻² M aqueous hydrochloric acid and analysed by an isocratic HPLC system using both ultraviolet (UV) detection at 244 nm and electrochemical detection working in oxidation mode (0.9 V) with an Ag/AgCl reference electrode. Mobile phase (50% acetonitrile in water containing 0.4% acetate buffer solution pH = 4.6) was used to complete the 20-min analysis. “Free” and “total” MOCA were chromatographed on a reversed-phase C8 column (5 μm; 250 mm × 4 mm). The standard curve of MOCA was linear over the range 5–500 μg/l in human urine. The detection limit was 1 μg/l for a 20-μl injection volume; the repeatability ranged from 5.6 to 1.3% (n = 6) for spiked urines at 5 and 500 μg/l, with a percentage recovery of 94 ± 3%. The reproducibility of the method was 7.3% (n = 4) for spiked urine at 10 μg/l. The use of sulfamic acid as a preservative of urine samples is important to improve the precision and accuracy of the analysis. Conclusion: The results indicate that these analytical procedures using conventional apparatus may be used routinely and reliably with large numbers of urine samples for biological monitoring of the exposure to MOCA. The occupational exposure to MOCA in some factories in France is studied in the second part of this work. Received: 10 November 1998 / Accepted: 25 March 1999