A reliable and sensitive graphite furnace atomic absorption spectrometry (GFAAS) method with Zeeman background correction was developed for the analysis of aluminium in serum and urine in the biological monitoring of aluminium exposure. The method is based on platform atomisation in pyrolytically coated graphite tubes after fourfold dilution with nitric acid. For serum analysis, a matrix matched standard curve is prepared and for urine the method of standard additions is used. The within-run imprecision (C.V.) for serum and urine was 3% and 5%, and the between-day imprecision, 6% and 7.2%, at a concentration level of 4.0 mumol/l. The between-day imprecision for urinary aluminium was 15.7% at a concentration level of 0.24 mumol/l. The detection limits were 0.02 mumol/l for serum and 0.07 mumol/l for urine. During 1 year of participation in TEQAS external quality assessment scheme of the Robens Institute for Health and Safety (Guildford, UK) for serum aluminium the maximum cumulative performance score was achieved. For urinary aluminium a certificate in the external quality control scheme of the German Society of Occupational Medicine was obtained. The mean concentration of aluminium in a non-exposed population, who did not use antacid drugs, was 0.06 mumol/l (S.D. 0.03, range 0.02-0.13, n = 21) in serum, and 0.33 mumol/l (S.D. 0.18, range 0.07-0.82, n = 44) in urine. The upper reference limit for aluminium in a healthy, non-exposed population was estimated to be 0.1 mumol/l in serum and 0.6 mumol/l in urine.
The exposure of Finnish tank lorry drivers to methyl tert-butyl ether (MTBE) and tert-amyl methyl ether (TAME) during loading of gasoline was studied using biological and breathing-zone sampling. During the field measurements in October 1994 and August 1995 the gasolines (95, 98, 99 RON) contained MTBE to 5.2-11.8% and TAME to 0-6%.
The geometric mean (GM) breathing-zone concentration of MTBE was 4.3 mg/m3 (n = 15) in October and 6.4 mg/m3 (n = 20) in August. The GM concentration of TAME, measured only in August, was 0.98 mg/m3. The mean loading/sampling times were 37 and 35 min, the mean wind speeds were 0.8 and 0.6 m/s, and the mean air temperatures were -4.9 degrees and + 14.1 degrees C, respectively. Blood samples collected on average at 20 min after gasoline loading/exposure showed an MTBE concentration of 143 nmol/l (GM, n = 14) in October and 213 nmol/l (GM, n = 20) in August. Pearson's coefficient of correlation (r) between the MTBE breathing-zone concentrations and MTBE in blood was 0.86 (P = 0.0001) in October and 0.81 (P = 0.00001) in August. No correlation was found between MTBE in air and the metabolite tert-butanol (TBA) in blood. MTBE, but not TBA, in urine samples collected on average at 2.5 h after exposure showed a correlation with MTBE in air. The concentrations of TAME and its metabolite tert-amyl alcohol were below the quantitation limits (
Past and present exposure to nickel was studied in an electrolytic nickel refinery, where an increased incidence of nasal cancer had been reported, using nickel analyses in air, blood and urine. Genotoxic effects were studied using analysis of micronuclei from acridine orange-stained smears from the buccal mucosa of the workers. Workers used respirators or masks in tasks where the exposure was expected to be high. Inside the mask, nickel concentrations were 0.9-2.4 micrograms m-3 in such tasks. In those tasks where masks were not used, nickel concentrations in the breathing zone were 1.3-21 micrograms m-3. Air-borne nickel concentrations (stationary sampling) varied between 230 and 800 micrograms m-3 in 1966-1988 with no systematic change; thereafter lower concentrations (170-460 micrograms m-3) have been observed. After-shift urinary concentrations of nickel were 0.1-2 mumol l-1; they showed no correlation with nickel concentrations in the air. Concentrations of nickel in the urine were still elevated after a 2-4 week vacation. The frequency of micronucleated epithelial cells in the buccal mucosa of nickel refinery workers was not significantly elevated by comparison with referents. No relationship was observed between micronucleus frequencies and levels of nickel in air, urine or blood.
The scheme consists of analyses for phenol,2,5-hexanedione, and mandelic, trichloroacetic and methylhippuric acids in urine. The present participants are 31 laboratories from 14 countries. Samples are prepared by pooling urine obtained from occupationally exposed workers or by spiking with appropriate pure metabolites. Four sets of samples at two concentration levels for each analyte are distributed annually. The report includes information on the arithmetic means, standard deviations and CVs for overall results and separately for different methods. During the last three years, the CVs have varied rather non systematically, being 21-31% for mandelic acid, 24-26% for trichloroacetic acid, 24-35% for phenol, 55-110% for 2,5-hexanedione and 44-50% for methylhippuric acid.
A worksite survey was conducted in all 38 Finnish electroplating plants. All workers (n = 163) who worked with nickel plating (bath workers, hangers and solution makers) were interviewed with a questionnaire about symptoms of nickel dermatitis, hand dermatitis, and about protective measures, atopy, etc. Patch testing with nickel sulfate was done with the TRUE TestTM method. All the workers, 94 men and 69 women, answered the questionnaire. The mean age of women was 41.1 years, and of men 43.1 years, respectively. Men had longer occupational exposure to nickel (14 years) than women (10 years). Most workers used protective gloves. 35% of women and 30% of men reported present or past hand dermatosis. 19% reported a history of atopic dermatitis. 15% of women (n = 8) and 4% (n = 2) of men had an allergic patch test reaction to nickel sulfate. 70% of those with an allergic patch test reaction to nickel reported past or present hand eczema. The prevalence of nickel allergy among the electroplaters was similar to that of patients in patch test clinics in Finland. An allergic patch test reaction to nickel sulfate does not necessarily oblige an electroplater to change jobs.
To evaluate the neuropsychological effects of current low level and previous higher levels of exposure to lead and evaluate the relation between effects of lead and bone lead.
A neuropsychological test battery was given to 54 storage battery workers with well documented long term exposure to lead. The effect was studied in two subgroups: those whose blood lead had never exceeded 2.4 mmol/l (the low BPbmax group, n = 26), and those with higher exposure about 10 years earlier (the high BPbmax group, n = 28). In both groups, the recent exposure had been low. Correlations between the test scores and the indices of both long term and recent exposure--including the content of lead in the tibial and calcaneal bone--and covariance analyses were used to assess the exposure-effect relation. Age, sex, and education were controlled in these analyses.
Analyses within the low BPbmax group showed a decrement in visuospatial and visuomotor function (block design, memory for design, Santa Ana dexterity), attention (digit symbol, digit span), and verbal comprehension (similarities) associated with exposure to lead and also an increased reporting of subjective symptoms. The performance of the high BPbmax group was worse than that of the low BPbmax group for digit symbol, memory for design, and embedded figures, but there was no reporting of symptoms related to exposure, probably due to selection in this group. No relation was found between the output variables and the tibial lead concentration. The calcaneal lead concentrations were related to the symptoms in the low BPbmax group.
Neuropsychological decrements found in subjects with high past and low present exposure indicate that blood lead concentrations rising to 2.5-4.9 mmol/l cause a risk of long lasting or even permanent impairment of central nervous system function. Milder and narrower effects are associated with lower exposures; their reversibility and time course remain to be investigated. History of blood lead gives a more accurate prediction of the neuropsychological effects of lead than do measurements of bone lead.
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An occupational hygiene survey was made in 38 nickel plating shops in Finland and exposure to nickel was studied by means of biological measurements and, in three shops, by using air measurements. The average after-shift urinary nickel concentration of 163 workers was 0.16 mumol l.-1 (range 0.001-4.99 mumol l.-1). After the 1-5 week vacation the urinary nickel concentration was higher than the upper reference limit of non-exposed Finns indicating that a part of water-soluble nickel salts is accumulated in the body. Urinary nickel concentrations in the shops considered clean in the industrial hygiene walk-through were not different from those observed in the shops considered dirty. The correlation between the concentrations of nickel in the air and in the urine was low, and the amount of nickel excreted in the urine exceeded the calculated inhaled amounts, indicating exposure by other routes such as ingestion.