Search PubMed⌕ Search

Biomedical subjects

S Skerfving

Publications and source records attributed to S Skerfving.

At least 145 records · Page 8Linked to original sources

Cadmium concentration in the kidney cortex of occupationally exposed workers measured in vivo using X-ray fluorescence analysis.

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.

Adult↗

Relation between lung function, exercise capacity, and exposure to asbestos cement.

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.

Asbestos↗

Measurement of lung density by x-ray computed tomography. Relation to lung mechanics in workers exposed to asbestos cement.

We measured lung density by means of x-ray computed tomography and lung mechanics in 33 workers exposed to asbestos cement and in 39 normal subjects. The exposed group showed evidence of lung fibrosis with reduced static lung volumes and lung compliance, although only three subjects had signs of interstitial fibrosis at standard chest radiography. Lung density was significantly increased in the exposed workers compared to control subjects, with greater differences between nonsmokers than between smokers. Lung density correlated inversely with static lung volumes. There was no appreciable difference in the regional distribution of lung density between exposed workers and control subjects. We conclude that lung density is often increased in workers with mild asbestosis, even in the presence of a normal chest radiograph. Measurement of lung density may be of value in the evaluation of asbestos-exposed workers for assessment of the extent of parenchymal disease.

Asbestosis↗

Kinetics of lead in blood after the end of occupational exposure.

The sum of two exponential functions was fitted to the decay of blood lead (PbB) level after the end of lead exposure. For two subjects who had not formerly been occupationally exposed to lead but who had been exposed to a single short heavy dose, the fast compartment (probably soft tissues) had a biological half-time of 27 and 44 d, respectively. For 20 lead workers after the end of occupational exposure, the corresponding median was 29 (range 7-63) d. For 21 ex-lead workers, the median biological half-time of the slow compartment was 5.6 (range 2.3-27) years. There was significant interindividual variation in both the fast and the slow half-time. This finding probably means a considerable variation in risk at a certain exposure level. In the lead workers, the PbB fraction corresponding to the slow compartment had a median as high as 1.8 (range 0.7-2.7) mumol/l, which constituted more than half of the total PbB. This fraction was associated with exposure history, and with the lead level in the skeleton, the latter determined in vivo by an X-ray fluorescence method. The data thus indicate a rather rapid turnover of the skeletal lead pool, a phenomenon which may affect the PbB level considerably.

Adult↗

Decreasing lead exposure in Swedish children, 1978-84.

Blood-lead levels were determined, each summer during the period 1978-1984, in children from Scania in Southern Sweden. A total of 1395 determinations were made. The average blood-lead concentration was 55 (range 14-250) micrograms 1(-1). There was a statistically significant decrease over time, both in rural and urban areas, averaging about 4 micrograms 1(-1) per year. Lead exposure has thus decreased remarkably. One possible explanation is the contemporary, considerable reduction of the alkyl lead content of petrol.

Child↗

Allergy to laboratory animals in laboratory technicians and animal keepers.

The prevalence of allergy to laboratory animals (LAA) was investigated in laboratory technicians and animal keepers. In a questionnaire 41 of 101 technicians reported symptoms provoked by work with laboratory animals. On clinical investigation 30 were found to have symptoms and signs related to contact with animals, and allergy was confirmed by radioallergosorbent tests (RAST) and skin tests in 19. All had rhinitis and 10 also had bronchial asthma. Forty seven other technicians who had stopped working with laboratory animals showed the same relative numbers of respiratory tract symptoms and of confirmed allergy to laboratory animals as did those currently handling animals. Seven of 23 animal keepers had work related symptoms. LAA symptoms were found in four and confirmed animal allergy in two. All four animal keepers with animal related symptoms had rhinitis, none had bronchial asthma. Positive animal RAST and skin tests were found only among people with animal related symptoms. A history of atopic disease was commoner among those with positive animal test results than among those with negative test results. No relation between smoking and the development of allergy to laboratory animals emerged. Simple prophylactic measures often sufficed to help technicians with animal related symptoms to remain at work.

Adult↗

Phthalic anhydride-induced occupational asthma.

Out of 118 workers exposed to phthalic anhydride (PA) dust for 2 months or more in four plants producing alkyd and/or polyunsaturated polyester resins, 28 (24%) suffered from work-related rhinitis, 13 (11%) from chronic productive bronchitis, and 21 (28%) from work-associated asthma. Asthma was generally preceded by rhinitis and was mostly of late type. 3 out of 11 asthmatics had a PA-positive skin test. In 2 subjects the presence of antibodies was demonstrated by the Prausnitz-Küstner test. 4 out of 25 heavily exposed subjects without asthma had a nonspecific bronchial hyperreactivity. The results did not indicate any significant 'healthy worker selection' as regarding rhinits and asthma. Chronic productive bronchitis was common and was more prevalent among former workers than among present employees, indicating a selection of nonreacting subjects in the plant. The time-weighted average breathing zone PA levels in two plants were between 3 and 13 mg/m3 during different direct PA handling operations and less than 0.3 mg/m3 at other kinds of work. In 2 subjects, positive bronchial provocation was obtained by short-term exposure to 0.5 and 6 mg PA/m3, respectively.

Asthma↗

Mortality and cancer morbidity among workers in a chemical factory.

A retrospective cohort study was performed on a group of 664 male workers employed for at least one month during the period 1942-1979 in a chemical factory. Both established and suspected carcinogens had been handled in the plant, primarily piperazine, but also urethane, ethylene oxide, formaldehyde, and organic solvents. A significantly increased mortality, compared with the regional death rate, was observed in the cohort. The increase was mainly due to violent deaths and cardiovascular diseases. No rise in death rates was observed for asthma, bronchitis or emphysema, in spite of other evidence of a high risk of occupational asthma, due to exposure to piperazine. A statistically significant increase in cancer morbidity was observed for malignant lymphoma/myelomatosis when an induction latency time of at least 10 years was used. Furthermore, an increase in bronchial cancer was noted, but it was statistically significant only when an induction-latency time of at least 15 years was used. A case-referent study within the cohort did not reveal any significant association between any specific chemical exposure and cancer morbidity.

Adult↗

Exposure in welding of high nickel alloy.

Nickel (Ni) levels in air during welding of high-Ni alloy (75% Ni) were very high (mean 0.44 mg/m3, range 0.07-1.1 mg/m3; 20 person-days of measurements). In six welders the Ni level in urine after four weeks of vacation was slightly but statistically significantly enhanced as compared to ten unexposed controls (means 8.7 vs 5.1 micrograms/l; P less than 0.005). The level on Monday mornings increased somewhat during a period of six weeks of high-Ni alloy welding (mean 13 micrograms/l; P less than 0.05). The level was slightly higher Thursday afternoon (mean 18 micrograms/l; P less than 0.0001). The data indicate the existence of a very slow pool of Ni in the body in addition to a faster one. There was no correlation between Ni levels in air and urine. Thus, in spite of the very high Ni levels in air, urinary Ni levels were thus of little use for biological monitoring of exposure and risk during high-Ni alloy welding. All eleven welders studied reported one or more symptoms (irritation of upper airways, headache, tiredness) as occurring more often (P less than 0.006) during high-Ni welding than when welding ordinary stainless steel. Lung-functions studies were normal.

Adult↗

Phthalate ester exposure--air levels and health of workers processing polyvinylchloride.

Exposure to phthalic acid esters (PAE; mainly di-(2-ethylhexyl), diisodecyl and butylbenzyl phthalates) of workers in a polyvinyl chloride processing industry ranged from 0.02 to 2 mg/m3 in different job categories. The workers excreted slightly but significantly higher levels of PAE metabolites in urine than controls. In 54 workers studied clinically, there were no indications of peripheral nerve or respiratory system effects. Some biochemical tests were abnormal; these should be studied further.

Adult↗

Visual disturbances after experimental human exposure to triethylamine.

Two volunteers were exposed to various airborne concentrations of triethylamine. Levels of 18 mg/m3 for eight hours caused subjective visual disturbances (haze and halos) and objective corneal oedema. The effects faded within hours after the end of exposure. The visual disturbances are unpleasant and may cause accidents at work and in traffic after the end of work.

Adult↗

Systemic reactions associated with polyisocyanate exposure.

A spray-painter suffered attacks of chills, fever, general malaise, dyspnea and wheezing, headache, arthralgia, and leucocytosis a few hours after exposure to aerosols of varnishes containing two different polyisocyanates based upon monomers of hexamethylene or toluene diisocyanate. Immunologic studies revealed an increase in the serum immunoglobulin G level, but no specific antibodies against isocyanates conjugated to human serum albumin. The polyisocyanate level in the workroom air was high [a time-weighted average of 4.2 mg/m3, corresponding to 17 mumol NCO (isocyanate groups)/m3], the toluene diisocyanate monomer level being much lower (a time-weighted average of 0.03 mg/m3, corresponding to 0.3 mumol NCO/m3).

Aerosols↗

Piperazine-induced airway symptoms: exposure-response relationships and selection in an occupational setting.

The heterocyclic secondary amine piperazine is known to cause asthma. In a cohort of 602 workers, employed during the period 1942-1979, at a chemical industry where piperazine is handled, a study conducted by means of a mailed questionnaire showed a strong exposure-response relationship as to frequency of work-related airway symptoms indicating asthma. In the most exposed group about a third of the workers had experienced such symptoms. Age, length of employment, smoking habits, and previous work-related asthmatic symptoms, but not atopy, modified the response. Further, there was an association between piperazine exposure and chronic bronchitis. In the most exposed group every fourth subject had chronic bronchitis. The frequency was modified by smoking habits; atopy was a confounder. Although many subjects, especially high-exposed ones, left work because of airway symptoms, there was no difference in occurrence of airway symptoms between former and present employees, ie, no "healthy worker selection" ("survivor population effect").

Asthma↗

Lead in finger-bone analysed in vivo in active and retired lead workers.

In 75 active lead workers the median lead level in finger-bone (bone-Pb), as determined in vivo by an X-ray fluorescence method, was 43 micrograms/g (range less than 20-122). In 32 retired workers the median level was even higher, 59 micrograms/g (range less than 20-135), which indicates a slow turnover rate of lead in finger-bone. This was confirmed in 18 of the "active" workers, in whom bone-Pb was studied in connection with an exposure-free period. In spite of a significant decrease in blood-lead levels (B-Pb), no systematic change of bone-Pb occurred. There was an increase of bone-Pb with time of employment, but with a large interindividual variation. No association was found between bone-Pb and present B-Pb in the active lead workers. However, in the retired ones, B-Pb rose with increasing bone-Pb. The bone-lead pool thus causes an "internal" lead exposure.

Adult↗

Elimination of chromium in urine after stainless steel welding.

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.

Adult↗

No cytogenetic effects in lymphocytes of stainless steel welders.

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.

Adult↗