Total and cause-specific mortality in cohorts of asbestos-cement workers and referents between 1907 and 1985.
Explore the source record for details and available documents.
Biomedical subjects
Publications and source records attributed to H Welinder.
Explore the source record for details and available documents.
An N2 wash-out technique was used to estimate the small airways function in 22 male workers, exposed to the asthma-inducing amine piperazine, and in 22 referent subjects, with similar smoking habits and age. The volume of trapped gas (VTG) was determined before and after a bronchial provocation with an aerosol of 0.25 ml 0.01% metacholine solution. No difference in VTG was observed between the piperazine-exposed workers and the referent subjects, either before or after the metacholine provocation. This indicates that a time-weighted average (TWA) exposure of about 0.1 mg piperazine/m3 does not cause small airways disease in non-asthmatic workers. Further, age and smoking habits were significantly associated with VTG.
A method for in vivo X-ray fluorescence analysis of the cadmium concentration in the kidney cortex has been improved and tested in 20 selected male occupationally cadmium-exposed workers (duration of exposure 7-39 years). The concentration of cadmium in kidney cortex ranged from 47 to 317 (median 141) micrograms/g. The concentration of cadmium in blood was 32-160 (median 64) nmole/liter, cadmium in urine was 2.5-13 (median 5.4) nmole/mmole creatinine, and beta 2-microglobulin in urine was 3.3-68 (median 14) micrograms/mmole creatinine. In individuals, the relationship between duration of exposure, time-integrated exposure, and cadmium level in urine on the one hand and cadmium level in the kidney on the other varied considerably. Direct in vivo analysis of the concentration of cadmium in the kidney cortex is therefore valuable as a complement to the other tests when monitoring cadmium exposure. Our method is sensitive, practically free from risk, and can b performed by routine at low costs.
A group of 137 male workers with known exposure (mean 20 fibre years per millilitre) to asbestos cement who had symptoms or signs of pulmonary disease was studied together with a reference group of 49 healthy industrial workers with no exposure to asbestos. Lung function measurements were made at rest and during exercise. Evidence of lung fibrosis was found as well as of obstructive airways disease in the exposed group compared with the reference group. Asbestos cement exposure was related to variables reflecting lung fibrosis but not to variables reflecting airflow obstruction. Smoking was related to variables reflecting obstructive lung disease. Exercise capacity was reduced in the exposed workers and was related to smoking and to lung function variables, reflecting obstructive airways disease. There was no significant correlation between exercise capacity and exposure to asbestos cement.
The presence of specific IgE antibodies against conjugates between human serum albumin and piperazine, a compound previously known to cause occupational asthma, and N-methyl-piperazine, respectively, was demonstrated by RAST, RAST inhibition and skin prick tests in 2 asthmatic subjects occupationally exposed to these agents.
In 5 out of 72 (7%) workers exposed to the asthma-inducing amine piperazine, specific IgE antibodies against a conjugate between human serum albumin and piperazine were demonstrated with RAST and RAST inhibition techniques. No specific antibodies were found in 64 nonexposed workers at the same plant, and in 60 healthy reference subjects. Eight out of the 72 (11%) exposed employees had unequivocal histories of piperazine-associated asthma, but only 4 of them had specific IgE antibodies against piperazine. However, there was a statistically significant association between specific antibodies and disease, as 4 out of 5 RAST-positive subjects were asthmatics, as compared with 4 out of the 67 RAST-negatives (p = 0.0003). The 4 RAST-positive asthmatics had been exposed to piperazine for between 6 and 168 months before their asthma started, as compared with induction times of less than a month for the 4 RAST-negatives. This discrepancy may reflect different pathogeneses for piperazine-associated asthma; either type-I allergy, pseudo-allergic reactivity or nonspecific irritative effect on the bronchi. The RAST-positive subjects did not differ from other employees as regards smoking habits but had significantly elevated levels of total serum IgE (p = 0.004).
The presence of specific IgE (immunoglobulin E) antibodies against a conjugate between human serum albumin and a reactive azo dye (Levafix Goldgelb E-3GA, Reactive Orange 67) was demonstrated by the radioallergosorbent test (RAST), RAST inhibition, and skin prick tests in an occupationally exposed subject with symptoms of mainly rhinoconjunctivitis.
The effects of organic solvents on 50 male workers exposed 5-46 (mean 18) years were studied with a cross-sectional design. Referents were matched pairwise according to age and education. An analysis of confounders confirmed good comparability between the two groups. As indicators of organic brain dysfunction regional cerebral blood flow was measured and the power spectrum of the subjects' electroencephalograms was analyzed, the former being reduced 4% and the latter showing increased power in the delta and beta bands in the exposed group. Symptoms of brain dysfunction were significantly more frequent among the exposed subjects and showed an exposure-effect relationship. Neuropsychological tests revealed definite indication of brain dysfunction in 14% of the exposed subjects in comparison to none in the reference group. The exposed subjects performed significantly worse than the referents in tests measuring focused attention abilities. A neurophysiological examination of the peripheral nervous system showed no difference between the groups. Clinical chemistry demonstrated no differences that could be explained by solvent exposure.
Seventeen male manual metal-arc stainless steel welders (mean exposure time 20 years) had far higher levels of chromium in urine than individually matched controls (medians 23 vs 1.5 mumol/mol creatinine; 10.5 vs 0.7 microgram/g creatinine). However, there were no signs of kidney damage in tests of function of tubuli (beta-hexosaminidase, lysozyme, and beta 2-microglobuline) or glomeruli (albumine clearance).
Nine retired (on an average of four years) stainless steel welders had higher (p less than 0.001) urinary chromium levels [mean 7 (range 3-13) mumol/mol of creatinine] than 21 nonexposed referents [mean less than or equal to 1.5 (range less than 0.6-7) mumol/mol of creatinine] but did not differ in this respect from 14 active welders studied at the end of a 31-d vacation (mean 9, range 4-17). This result shows the existence of a slow compartment for chromium in the body. Urinary chromium on time after the end of exposure was analyzed mathematically by use of an exponential two-compartment model. Good fits were obtained, showing the existence of a fast compartment in addition to the slow one. For four welders followed for 31 d, the biological half-time of the slow compartment ranged from 14 d to infinity. For 12 welders followed for 60 h, the fast compartment had a median half-time of 7 (range 4-35) h. For 19 welders there was a significant (p less than 0.01) correlation between chromium in air (total and soluble hexavalent) and urinary chromium (rs = 0.68 and 0.64). However, the variation of urinary chromium on chromium in air was considerable, especially at chromium air levels at or below the hygienic standards. Correction for urinary chromium levels on Monday morning did not decrease the variation.
In 24 manual metal arc stainless steel welders (means: exposure time 19 years, 100 electrodes/d, air chromium level 81 micrograms/m3, urinary chromium 47 mumol/mol creatinine) and 24 matched referents, lymphocytes in peripheral blood were analyzed for cytogenetic effects. No statistically significant differences were observed as to frequency of cells with breaks and fragments (1.5% for the welders, 1.9% for the referents); gaps and isogaps (1.8 vs 2.0%); interchanges, dicentrics, rings and markers (0.8 vs 0.5%); total number of cells with structural aberrations (4.1 vs 4.4%); hyperdiploidy (0.3 vs 0.2%); or total number of cells with aberrations (4.4 vs 4.6%). Neither were there any differences in the frequencies of micronuclei (7.8 vs 7.9 per mille) or sister chromatid exchanges (11 vs 12 per cell) in lymphocytes of peripheral blood.
A new micronucleus method based on the analysis of lymphocytes with preserved cytoplasm revealed an increased frequency of micronuclei in 38 workers employed in a plant producing styrene-modified polyester resin as compared to the frequency in 20 referents (5.9 vs 3.6%). The time-weighted average of the styrene concentration in the workroom air varied between 1 and 36 ppm (mean 13 ppm) during the last year and correlated well to low urinary levels of mandelic acid, which ranged from 9 to 316 mg/g of creatinine (mean 65 mg/g of creatinine).
Explore the source record for details and available documents.
Thirty-three styrene exposed workers from three different industrial sites were examined with electroencephalography and motor and sensory neurography. The three groups had respective styrene exposures of clearly above the threshold limit value (50 ppm), at about this level, and clearly below it. The neurophysiological results were compared with those of a group of normal controls and a group of 17 patients judged to suffer from sequelae after long-term heavy exposure to organic solvents (mainly painters). Ten subjects in the styrene group presented signs of a mild sensory neuropathy with polyphasic sensory responses of a low amplitude. The same pattern was commonly found among the reference group heavily exposed to solvents. The ten subjects in the styrene group with mild polyneuropathy had a significantly higher age and significantly heavier styrene exposure than the rest of the group. Age difference could not explain the difference in the neurophysiological parameters, and therefore the contributing role of styrene exposure has to be considered. The electroencephalographic analysis showed no changes of the dominant alpha frequency. An increased amount of diffuse slow activity was seen in many of the heavily exposed mixed-solvent cases and was seen in some of the styrene-exposed cases without a clear relation to degree of exposure. An increased occurrence of fast activity in central and precentral areas of the brain was found in the styrene group, as well as in the mixed-solvent group. This pilot study indicates that the same type of neurophysiological changes from the strictly normal are seen among workers exposed to styrene as those found among a group of patients judged to suffer from sequelae after chronic exposure to various organic solvents. The neurophysiological "profile" is (a) sensory nerve responses with low amplitude and long duration, (b) somewhat low sensory conduction velocities, (c) close to normal motor neurographic findings, and (d) an increased amount of fast activity in central and precentral regions in the electroencephalogram in combination with normal occipital alpha activity.
144 industrial workers were investigated for the presence of Staphylococcus aureus in the upper respiratory tract because 53 of them had complained of chronic throat discomfort. Significantly more patients with subjective throat complaints harboured Staph. aureus in the nose (49.1%) and throat (32.1%) than patients without such symptoms (27.4% and 9.9%, respectively). No Staph. aureus were found in throat swab cultures from 21 randomly selected individuals working in a similar factory where no chronic throat discomfort was reported and only 2 throat carriers of Staph. aureus were found among 66 medical undergraduates investigated. The staphylocci belonged to several different phage type patterns and could not be recovered on sedimentation plates or from machines or products. In the light of these and other findings it was suggested that the staphylocci accentuated an already existing damage of the mucous membrane of the throat, but seemed not to be the primary cause of the discomfort.