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.     

Urinary nickel as bioindicator of workers' Ni exposure in a galvanizing plant in Brazil

Objectives: We measured urinary nickel (U-Ni) in ten workers (97 samples) from a galvanizing plant that uses nickel sulfate, and in ten control subjects (55 samples) to examine the association between occupational exposure to airborne Ni and Ni absorption. Methods: Samples from the exposed group were taken before and after the work shift on 5 successive workdays. At the same time airborne Ni (A-Ni) was measured using personal samplers. Ni levels in biological material and in the airborne were determined by a graphite furnace atomic absorption spectrometry validated method. In the control group the urine samples were collected twice a day, in the before and after the work shift, on 3 successive days. Results: Ni exposure low to moderate was detected in all the examined places in the plant, the airborne levels varying between 2.8 and 116.7 μg/m³ and the urine levels, from samples taken postshift, between 4.5 and 43.2 μg/g creatinine (mean 14.7 μg/g creatinine). Significant differences in U-Ni creatinine were seen between the exposed and control groups (Student's t test, P ≤ 0.01). A significant correlation between U-Ni and A-Ni (r = 0.96; P ≤ 0.001) was detected. No statistical difference was observed in U-Ni collected from exposed workers in the 5 successive days, but significant difference was observed between pre- and postshift samples. Conclusions: Urinary nickel may be used as a reliable internal dose bioindicator in biological monitoring of workers exposed to Ni sulfate in galvanizing plants regardless of the day of the workweek on which the samples are collected. Received: 28 January 1999 / Accepted: 10 July 1999     

Acute nickel toxicity in electroplating workers who accidently ingested a solution of nickel sulfate and nickel chloride

Thirty-two workers in an electroplating plant accidently drank water contaminated with nickel sulfate and chloride (1.63 g Ni/liter). Twenty workers promptly developed symptoms (e.g., nausea, vomiting, abdominal discomfort, diarrhea, giddiness, lassitude, headache, cough, shortness of breath) that typically lasted a few hours but persisted 1-2 days in 7 cases. The Ni doses in workers with symptoms were estimated to range from 0.5 to 2.5 g. In 15 exposed workers who were tested on day 1 postexposure, serum Ni concentrations ranged from 13 to 1,340 micrograms/liter and urine Ni concentrations ranged from 0.15 to 12 mg/g creatinine. Ten subjects (with initial urine Ni concentrations greater than 0.8 mg/g creatinine) were hospitalized and treated for 3 days with intravenous fluids to induce diuresis, resulting in a mean elimination half-time (T1/2) for serum Ni of 27 hours (SD +/- 7 hour), which was significantly shorter (p less than .001) than the mean T1/2 of 60 hours (SD +/- 11 hours) in 11 subjects who did not receive intravenous fluids. Laboratory tests showed transiently elevated levels of blood reticulocytes (N = 7), urine albumin (N = 3), and serum bilirubin (N = 2). All subjects recovered rapidly, without evident sequellae, and returned to work by the eighth day after exposure.     

Behavioral interventions to reduce nickel exposure in a nickel processing plant

Nickel is a widely-used material in many industries. Although there is enough evidence that occupational exposure to nickel may cause respiratory illnesses, allergies, and even cancer, it is not possible to stop the use of nickel in occupational settings. Nickel exposure, however, can be controlled and reduced significantly in workplaces.

The main objective of this study was to assess if educational intervention of hygiene behavior could reduce nickel exposure among Indonesian nickel smelter workers. Participants were randomly assigned to three intervention groups (n = 99). Group one (n = 35) received only an educational booklet about nickel, related potential health effects and preventive measures, group two (n = 35) attended a presentation in addition to the booklet, and group three (n = 29) received personal feedback on their biomarker results in addition to the booklet and presentations. Pre- and post-intervention air sampling was conducted to measure concentrations of dust and nickel in air along with worker's blood and urine nickel concentrations. The study did not measure significant differences in particles and nickel concentrations in the air between pre- and post-interventions. However, we achieved significant reductions in the post intervention urine and blood nickel concentrations which can be attributed to changes in personal hygiene behavior. The median urinary nickel concentration in the pre-intervention period for group one was 52.3 µg/L, for group two 57.4 µg/L, and group three 43.2 µg/L which were significantly higher (p< = 0.010) than those measured in the post-intervention period for each of the groups with 8.5 µg/L, 9.6 µg/L, and 8.2 µg/L, respectively. A similar pattern was recorded for serum nickel with significantly (p < 0.05) higher median concentrations measured in the pre-intervention period for group one 1.7 µg/L, and 2.0 µg/L for group 2 and group 3 compared with the post intervention median serum nickel levels of 0.1 µg/L for all groups.

The study showed that educational interventions can significantly reduce personal exposure levels to nickel among Indonesian nickel smelter workers.     

Serum and urinary aluminium levels of workers in the aluminium industry

We have measured serum aluminium and urinary aluminium/creatinine ratios in 235 aluminium workers and 44 controls to examine the association between occupational exposure to airborne aluminium and aluminium absorption. Serum and urine samples were taken before and after a 3- to 5-day work shift. Occupational exposure was estimated from aluminium measurements of respirable and total particulates in air. Median exposure values were 25 and 100 μg m⁻³, respectively. Serum aluminium and urinary aluminium/creatinine ratios did not change significantly during the shift; however, both pre-shift and post-shift serum aluminium and urinary aluminium/creatinine ratios were increased in the exposed group. Occupational exposure was associated with serum aluminium increments of 1.32μg l.⁻¹ (P = 0.01) pre-shift, and 0.96μg l.⁻¹ (P = 0.08) post-shift. Greater and more significant differences were seen between exposed and controls for the urinary aluminium/creatinine ratios [5.67 μg g⁻¹ (P < 0.01) pre-shift; 8.01 μg g⁻¹ (P < 0.01) post-shift]. Urinary aluminium/creatinine ratios were greater in plants with higher aluminium exposures. These results are consistent with the systemic absorption of aluminium from occupational exposure and suggest the presence of a sensitive uptake process for airway aluminium.     

Ambient monitoring and biomonitoring of workers exposed to N-methyl-2-pyrrolidone in an industrial facility

Objectives: The exposure of seven workers and three on-site study examiners to N-methyl-2-pyrrolidone (NMP) was studied in an adhesive bonding compound and glue production facility. Methods: Airborne NMP was analysed by personal and stationary sampling on activated charcoal tubes. NMP and its main metabolites, 5-hydroxy-N-methyl-2-pyrrolidone (5-HNMP) and 2-hydroxy-N-methylsuccinimide (2-HMSI), were analysed in pre-shift and post-shift spot urine samples by gas chromatography-mass spectrometry. The workers were examined with respect to irritation of the eyes, the mucous membranes and the skin, and health complaints before and after the work-shift were recorded. Results: The time-weighted average concentration of NMP in most work areas varied between 0.2 and 3.0 mg/m³. During the manual cleaning of stirring vessels, valves and tools, 8-h TWA exposures of up to 15.5 mg/m³ and single peak exposures of up to 85 mg/m³ were observed. NMP and its metabolites were detected in two pre-shift urine specimens. NMP and 5-HNMP concentrations in post-shift urine samples of five workers and three on-site study examiners were below 125 μg/g creatinine and 15 mg/g creatinine, respectively, while two vessel-cleaning workers showed significantly higher urinary NMP concentrations of 472 and 711 μg/g creatinine and 5-HNMP concentrations of 33.5 and 124 mg/g creatinine. 2-HMSI was detectable in four post-shift samples (range: 1.6–14.7 mg/g creatinine). The vessel cleaner with the highest NMP exposure reported irritation of the eyes, the upper respiratory tract and headaches. Conclusions: The results of this study indicate a relatively low overall exposure to NMP in the facility. An increased uptake of NMP occurred only during extensive manual vessel cleaning. Health complaints associated with NMP exposure were recorded in one case and might be related to an excessive dermal exposure due to infrequent and inadequate use of personal protective equipment.     

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.     

Children’s Exposure to Metals: A Community-Initiated Study

In 2007, it was shown that the shipping of lead (Pb) through Esperance Port in Western Australia resulted in contamination and increased Pb concentrations in children. A clean-up strategy was implemented; however, little attention was given to other metals. In consultation with the community, a cross-sectional exposure study was designed. Thirty-nine children aged 1 to 12 years provided samples of hair, urine, drinking water, residential soil and dust. Concentrations of nickel (Ni) and Pb were low in biological and environmental samples. Hair aluminium (Al) (lower than the detection limit [DL] to 251 μg/g) and copper (Cu) (7 to 415 μg/g), as well as urinary Al (<DL to 210 μg/L), manganese (Mn) (<DL to 550 μg/L), and Cu (<DL to 87 μg/L), were increased for a small number of participants. Concentrations of nickel (Ni) in urine, soil, and dust decreased with increasing distance from the port, as did soil Pb concentrations. The results suggest exposure to Ni and Pb was limited in children at the time of sampling in 2009. Further investigation is required to determine the source(s) and significance of other increased metals concentrations.     

Acute respiratory health effects among cement factory workers in Tanzania: an evaluation of a simple health surveillance tool

Objectives: The effects of cement dust exposure on acute respiratory health were assessed among 51 high exposed and 33 low exposed male cement workers. The ability of the questionnaire to diagnose acute decrease in ventilatory function was also assessed. Methods: Acute respiratory symptoms were recorded by interview using a structured optimal symptom score questionnaire. Peak expiratory flow (PEF) was measured preshift and postshift for each worker with a Mini-Wright PEF meter. Personal respirable dust (n=30) and total dust (n=15) were measured with 37-mm Cyclone and 37-mm closed-faced Millipore cassette. Twenty-nine workers had concurrent respirable dust, PEF and questionnaire on the same day. Results: The geometric means of personal respirable dust and total dust among high exposed were 4.0 and 13.2 mg/m³, respectively, and 0.7 and 1.0 mg/m³ among low exposed. High exposed workers had more acute cough, shortness of breath and stuffy nose than the low exposed. Mean percentage cross-shift decrease in PEF was significantly more pronounced among high exposed workers than low exposed (95% CI 1.1, 6.1%). For workers with concurrent respirable dust, PEF and questionnaire assessment, an exposure–response relationship was found between log-transformed respirable dust and percentage cross-shift decrease in PEF (4.5% per unit of log-respirable dust in mg/m³ ; 95% CI 3.3, 5.6%). Respirable dust exposure ≥2.0 mg/m³ versus <2.0 mg/m³ was associated with increased prevalence ratio for cough (7.9) and shortness of breath (4.2). Shortness of breath was associated with the highest sensitivity (0.87) and specificity (0.83) for diagnosing a percentage cross-shift decrease in PEF of ≥10%. Conclusion: The observed acute respiratory health effects among the workers are most likely due to exposure to high concentrations of irritant cement dust. The results also highlight the usefulness of the questionnaire for health surveillance of the acute respiratory health effect.     

Assessment of the permissible exposure level to manganese in workers exposed to manganese dioxide dust.

The prevalence of neuropsychological and respiratory symptoms, lung ventilatory parameters, neurofunctional performances (visual reaction time, eye-hand coordination, hand steadiness, audioverbal short term memory), and several biological parameters (calcium, iron, luteinising hormone (LH), follicle stimulating hormone (FSH), and prolactin concentrations in serum, blood counts, manganese (Mn) concentration in blood and in urine) were examined in a group of workers (n = 92) exposed to MnO2 dust in a dry alkaline battery factory and a matched control group (n = 101). In the battery plant, the current exposure of the workers to airborne Mn was measured with personal samplers and amounted on average (geometric mean) to 215 and 948 micrograms Mn/m3 for respirable and total dust respectively. For each worker, the lifetime integrated exposure to respirable and total airborne Mn dust was also assessed. The geometric means of the Mn concentrations in blood (MnB) and in urine (MnU) were significantly higher in the Mn exposed group than in the control group (MnB 0.81 v 0.68 microgram/100 ml; MnU 0.84 v 0.09 microgram/g creatinine). On an individual basis, MnU and MnB were not related to various external exposure parameters (duration of exposure, current exposure, or lifetime integrated exposure to airborne Mn). On a group basis, a statistically significant association was found between MnU and current Mn concentrations in air. No appreciable difference between the exposed and the control workers was found with regard to the other biological measurements (calcium, LH, FSH, and prolactin in serum). Although the erythropoietic parameters and serum iron concentration were in the normal range for both groups, there was a statistically significant trend towards lower values in the Mn exposed workers. The prevalences of reported neuropsychological and respiratory symptoms, the lung function parameters, and the audioverbal short term memory scores did not differ between the control and exposed groups. The Mn workers, however, performed the other neurofunctional tests (visual reaction time, eye-hand coordination, hand steadiness) less satisfactorily than the control workers. For these tests, the prevalences of abnormal results were related to the lifetime integrated exposure to total and respirable Mn dust. On the basis of logistic regression analysis it may be inferred that an increased risk of peripheral tremor exists when the lifetime integrated exposure to Mn dust exceeds 3575 or 730 micrograms Mn/m3 x year for total and respirable dust respectively. The results clearly support a previous proposal by the authors to decrease the current time weighted average exposure to Mn dust.     

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     

Assessment of the permissible exposure level to manganese in workers exposed to manganese dioxide dust.

The prevalence of neuropsychological and respiratory symptoms, lung ventilatory parameters, neurofunctional performances (visual reaction time, eye-hand coordination, hand steadiness, audioverbal short term memory), and several biological parameters (calcium, iron, luteinising hormone (LH), follicle stimulating hormone (FSH), and prolactin concentrations in serum, blood counts, manganese (Mn) concentration in blood and in urine) were examined in a group of workers (n = 92) exposed to MnO2 dust in a dry alkaline battery factory and a matched control group (n = 101). In the battery plant, the current exposure of the workers to airborne Mn was measured with personal samplers and amounted on average (geometric mean) to 215 and 948 micrograms Mn/m3 for respirable and total dust respectively. For each worker, the lifetime integrated exposure to respirable and total airborne Mn dust was also assessed. The geometric means of the Mn concentrations in blood (MnB) and in urine (MnU) were significantly higher in the Mn exposed group than in the control group (MnB 0.81 v 0.68 microgram/100 ml; MnU 0.84 v 0.09 microgram/g creatinine). On an individual basis, MnU and MnB were not related to various external exposure parameters (duration of exposure, current exposure, or lifetime integrated exposure to airborne Mn). On a group basis, a statistically significant association was found between MnU and current Mn concentrations in air. No appreciable difference between the exposed and the control workers was found with regard to the other biological measurements (calcium, LH, FSH, and prolactin in serum). Although the erythropoietic parameters and serum iron concentration were in the normal range for both groups, there was a statistically significant trend towards lower values in the Mn exposed workers. The prevalences of reported neuropsychological and respiratory symptoms, the lung function parameters, and the audioverbal short term memory scores did not differ between the control and exposed groups. The Mn workers, however, performed the other neurofunctional tests (visual reaction time, eye-hand coordination, hand steadiness) less satisfactorily than the control workers. For these tests, the prevalences of abnormal results were related to the lifetime integrated exposure to total and respirable Mn dust. On the basis of logistic regression analysis it may be inferred that an increased risk of peripheral tremor exists when the lifetime integrated exposure to Mn dust exceeds 3575 or 730 micrograms Mn/m3 x year for total and respirable dust respectively. The results clearly support a previous proposal by the authors to decrease the current time weighted average exposure to Mn dust.     

Elimination kinetics of metals after an accidental exposure to welding fumes

Objective We had the opportunity to study the kinetics of metals in blood and urine samples of a flame-sprayer exposed to high accident-prone workplace exposure. We measured over 1 year, the nickel, aluminium, and chromium concentrations in blood and urine specimens after exposure. On this basis, we evaluated the corresponding half-lives. Methods Blood and urine sampling were carried out five times after accidental exposure over a period of 1 year. The metals were analysed by graphite furnace atomic absorption spectrometry and Zeeman compensation with reliable methods. Either a mono-exponential or a bi-exponential function was fitted to the concentration-time courses of selected metals using weighted least squares non-linear regression analysis. The amount excreted in urine was calculated integrating the urinary decay curve and multiplying with the daily creatinine excretion. Results The first examination was carried out 15 days after exposure. The mean aluminium concentration in plasma was 8.2 μg/l and in urine, 58.4 μg/g creatinine. The mean nickel concentration in blood was 59.6 μg/l and the excretion in urine 700 μg/g creatinine. The mean chromium level in blood was 1.4 μg/l in urine, 7.4 μg/g creatinine. For the three elements, the metal concentrations in blood and urine exceeded the reference values at least in the initial phase. For nickel, the German biological threshold limit values (EKA) were exceeded. Conclusions Aluminium showed a mono-exponential decay, whereas the elimination of chromium and nickel was biphasic in biological fluids of the accidentally exposed welder. The half-lives were as follows: for aluminium 140 days (urine) and 160 days (plasma); for chromium 40 and 730 days (urine); for nickel 25 and 610 days (urine) as well as 30 and 240 days (blood). The renal clearance of aluminium and nickel was about 2 l/h estimated for the last monitoring day.     

Reference values for cobalt, copper, manganese, and nickel in urine among women of the general population in Japan

Objective: The present study was initiated to establish the reference levels of Co, Cu, Mn, and Ni in urine of women in the general Japanese population. Methods: Stored urine samples were subjected to the analysis. The samples were collected from 1,000 adult women all over Japan, who had no occupational exposure to these elements. Co, Cu, Mn, and Ni in urine were analyzed by graphite furnace atomic absorption spectrometry. The concentrations were distributed log-normally, and were presented in terms of geometric mean (GM) and geometric standard deviation, as observed or after correction for creatinine concentration or a specific gravity of urine of 1.016. Results: The GM values of observed levels (i.e., with no correction for urine density) and of the levels after correction for creatinine (cr) concentration (values in parenthesis) were 0.68 g/l (0.60 μg/g cr) for Co, 13.4 g/l (11.8 g/g cr) for Cu, 0.14 μg/l (0.12 g/g cr) for Mn and 2.1 g/l (1.8 g/g cr) for Ni. There was a life-long age-dependent increase in Cu. Mn levels reached the maximum at 60 to 69 years of ages. In contrast, age-dependency was not substantial in Co and Ni. Conclusions: Comparison with values reported in literatures for other areas showed that Co and Ni levels in urine of Japanese women are higher than, Cu level is comparable with, and Mn level is lower than others. The reasons for high Co and Ni levels deserve further study.     

Biological monitoring of workers exposed to low levels of 2-butoxyethanol

Objectives: (1) To assess the value of urinary butoxyacetic acid (BAA) measurement for the monitoring of workers exposed to low concentration of 2-butoxyethanol (BE); (2) to evaluate the in vivo effect of low occupational BE exposure on the erythrocyte lineage; and (3) to test the possible influence of genetic polymorphism for cytochrome P450 2E1 (CYP 2E1) on urinary BAA excretion rate. Methods: Thirty-one male workers exposed to BE in a beverage package production plant were examined according to their external (BE) and internal (BAA) solvent exposure. The effect of this exposure on erythrocyte lineage [red blood cell numeration (RBC), hemoglobin (Hb), hematocrit (Htc), mean corpuscular volume (MCV), mean corpuscular hemoglobin (MCH), mean corpuscular hemoglobin concentration (MCHC), haptoglobin (Hp), reticulocyte numeration (Ret) and osmotic resistance (OR)], hepatic [aspartate aminotransferase (GOT), alanine aminotransferase (GPT)] and renal [plasmatic creatinine, urinary retinol binding protein (RBP)] parameters was also investigated. DNA purified from whole blood was used for CYP 2E1 genotyping. Results: Average airborne concentration of BE was 2.91 mg/m³ (0.59 ppm) with a standard deviation of 1.30 mg/m³ (0.27 ppm). There was a relatively good correlation between external and internal exposure estimated by measuring BAA in post-shift urine samples (average 10.4 mg/g creatinine; r=0.55;P=0.0012). Compared with a matched control group (n=21) exposed workers had a statistically significant decrease (3.3%;P=0.03) in Hct while MCHC was increased (2.1%;P=0.02). No significant difference was observed either in other erythroid parameters or in hepatic and renal biomarkers. One exposed individual exhibited a mutant allele with increased cytochrome P450 oxidative activity which coincided with a very low urinary BAA excretion. Conclusions: Single determination of BAA in post-shift urine samples can be used to assess exposure to low levels of BE. A slight but significant effect on erythroid parameters suggesting membrane damage was observed in exposed workers. The influence of the genetic polymorphism for CYP 2E1 deserves further investigation for the interpretation of urinary BAA measurements. Received: 6 December 1996 / Accepted: 21 February 1997     

Distribution of nickel in lungs from former nickel workers

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 μg g⁻¹ dry wt. Biopsies collected on the center of the lower right lobe had an average nickel concentration of 82 ± 252 μg g⁻¹. The average nickel concentration detected in the right and left bronchus was 5.9 ± 11.6 and 3.8 ± 6.0 μg g⁻¹, respectively. Lung tissue obtained from ten people not connected to the refinery had an average nickel concentration of 0.74 ± 0.44 μg 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. Received: 20 November 1997 / Accepted: 21 April 1998     

Urinary hexane diamine as an indicator of occupational exposure to hexamethylene diisocyanate

The occupational exposure of 19 men to hexamethylene diisocyanate (HDI) vapour was monitored during one 8-h shift. It ranged from 0.30 to 97.7 μg/m³. This was compared with the urinary output of hexane diamine (HDA) liberated by acid hydrolysis from its conjugates in post-shift samples. The excretion varied from 1.36 to 27.7 μg/g creatinine, and there was a linear association of HDI air concentration with urinary HDA excretion. The validity of the urinary analysis was confirmed by simultaneous blind analysis in another laboratory. The results had an excellent linear concordance. Thus, it seems that while the gas chromatographic-mass spectrometric detection method requires sophisticated apparatus, the results are very useful to occupational health practices. A biological exposure index limit of 19 μg HDA/g creatinine in a post-shift urine specimen is proposed as an occupational limit level of HDI monomer (time-weighted average=75 μg/m³). Most importantly, biological monitoring of HDA is sensitive enough to be used at and below the current allowable exposure limit levels.     

Biological surveillance of workers exposed to dimethylformamide and the influence of skin protection on its percutaneous absorption

Summary Two studies were carried out among workers exposed to dimethylformamide (DMF) in an acrylic fiber factory. The first study involved 22 exposed workers and 28 control workers. Blood was examined at the beginning and at the end of a working week for the presence of biological signs of liver dysfunction. Pre- and post-shift urine samples were also collected during 1 week for determination of N-methylformamide (NMF) concentration. The airborne concentration of DMF was determined at different work places during the same period. On prevention of direct skin contact with DMF solution a significant correlation was found on a group basis between the concentration of DMF vapor and the NMF concentration in post-shift urine samples. When the concentration of NMF in post-shift urine samples from a group of workers does not exceed 30 mg/g creatinine, then their integrated exposure is probably below 60 mg/m³ × h (10 mg/m3 for 6 h). This exposure appears to be safe with regard to the risk of liver damage but does not necessarily preclude episodes of alcohol intolerance in some workers.During a second study, NMF concentrations in pre- and post-shift urine samples were followed-up in seven workers during three weeks when different personal protective devices were used. In an acrylic fiber factory, skin absorption was found to be more important than inhalation in the overall exposure to the solvent when no personal protective devices were used. The use of impermeable gloves with long sleeves appears to be the best method of preventing skin absorption of DMF. Silicone or glycerol barrier creams are less effective and should not be recommended.Part of this work was presented at the First International Congress on Toxicology in Toronto 1977     

Evaluation of take-home organophosphorus pesticide exposure among agricultural workers and their children

We analyzed organophosphorus pesticide exposure in 218 farm worker households in agricultural communities in Washington State to investigate the take-home pathway of pesticide exposure and to establish baseline exposure levels for a community intervention project. House dust samples (n = 156) were collected from within the homes, and vehicle dust samples (n = 190) were collected from the vehicles used by the farm workers to commute to and from work. Urine samples were obtained from a farm worker (n = 213) and a young child (n = 211) in each household. Dust samples were analyzed for six pesticides, and urine samples were analyzed for five dialkylphosphate (DAP) metabolites. Azinphosmethyl was detected in higher concentrations (p < 0.0001) than the other pesticides: geometric mean concentrations of azinphosmethyl were 0.53 micro g/g in house dust and 0.75 micro g/g in vehicle dust. Dimethyl DAP metabolite concentrations were higher than diethyl DAP metabolite concentrations in both child and adult urine (p < 0.0001). Geometric mean dimethyl DAP concentrations were 0.13 micro mol/L in adult urine and 0.09 micro mol/L in child urine. Creatinine-adjusted geometric mean dimethyl DAP concentrations were 0.09 micro mol/g in adult urine and 0.14 micro mol/g in child urine. Azinphosmethyl concentrations in house dust and vehicle dust from the same household were significantly associated (r2 = 0.41, p < 0.0001). Dimethyl DAP levels in child and adult urine from the same household were also significantly associated (r2 = 0.18, p < 0.0001), and this association remained when the values were creatinine adjusted. The results of this work support the hypothesis that the take-home exposure pathway contributes to residential pesticide contamination in agricultural homes where young children are present.     

Airflow limitation among workers in a labour-intensive coal mine in Tanzania

Objectives To describe the relationship between cumulative respirable dust and quartz exposure and lung functioning among workers in a labour-intensive coal mine. Methods The study population comprised 299 men working at a coal mine in Tanzania. Lung function was assessed using a Vitalograph alpha III spirometer in accordance with American Thoracic Society recommendations. Multiple linear regression models were developed to study the relationship between forced expiratory volume in 1 s (FEV₁), forced vital capacity (FVC) and FEV₁/FVC and the cumulative dust or quartz exposure while adjusting for age, height and ever smoking. To evaluate trends for dose response, cumulative exposure concentrations for respirable dust and quartz were ranked and categorized in quartiles and the highest decile, with the first quartile as the reference group. Logistic regression models were used to determine odds ratios for FEV₁/FVC < 0.7 and FEV₁% < 80 for categories of cumulative dust or quartz exposure. Results The prevalence of FEV₁/FVC < 0.7 among the workers was 17.3%. Workers in the development team (20.5%) had the highest prevalence of FEV₁% < 80%. The estimates of the effects of cumulative exposure on FEV₁/FVC were −0.015% per mg years m^–3 for respirable dust and –0.3% per mg years m^–3 for respirable quartz. In logistic regression models, the odds ratios for airway limitation (FEV₁/FVC < 0.7) for the workers in the highest decile of cumulative dust and quartz exposure versus the referents were 4.36 (95% confidence interval: 1.06, 17.96) and 3.49 (0.92, 13.21), respectively. The upper 10% of workers by cumulative dust and quartz exposure also had higher odds ratios for predicted FEV₁% < 80% than the reference group odds ratio: 10.38 (1.38, 78.13) and 14.18 (1.72, 116.59), respectively. The results must be interpreted with caution due to a possible healthy worker effect and selection bias. Conclusion Exposure to respirable coal mine dust was associated with airway limitation as measured by FEV₁/FVC and predicted FEV₁%.