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Biomedical subjects

R Alexandersson

Publications and source records attributed to R Alexandersson.

34 records · Page 2Linked to original sources
PubMed1987

Effects of exposure to vehicle exhaust on health.

Exposure to combustion engine exhaust and its effect on crews of roll-on roll-off ships and car ferries and on bus garage staff were studied. The peak concentrations recorded for some of the substances studied were as follows: total particulates (diesel only) 1.0 mg/m3, benzene (diesel) 0.3 mg/m3, formaldehyde (gasoline and diesel) 0.8 mg/m3, and nitrogen dioxide (diesel) 1.2 mg/m3. The highest observed concentration of benzo(a)pyrene was 30 ng/m3 from gasoline and diesel exhaust. In an experimental study volunteers were exposed to diesel exhaust diluted with air to achieve a nitrogen dioxide concentration of 3.8 mg/m3. Pulmonary function was affected during a workday of occupational exposure to engine emissions, but it normalized after a few days with no exposure. The impairment of pulmonary function was judged to have no appreciable, adverse, short-term impact on individual work capacity. In the experimental exposure study, no effect on pulmonary function was observed. Analyses of urinary mutagenicity and thioether excretion showed no sign of exposure to genotoxic compounds among the occupationally exposed workers or among the subjects in the experimental study.

Air Pollutants↗
PubMed1986

Lung function and rhizopus antibodies in wood trimmers. A cross-sectional and longitudinal study.

Pulmonary function was studied in 66 wood trimmers exposed to organic dust (moulds) after a month of no exposure (summer vacation) and then three and 27 months later, and also during a working week. The results of forced expirometry and single breath nitrogen washout were compared with those obtained in local controls and in larger reference materials. The forced vital capacity (FVC) and forced expired volume in one second (FEV1) were reduced by an average of 0.4 and 0.31, respectively, after one month of no exposure, however, the nitrogen washout variables showed no clear changes. Repeated measurements three months later on a Monday morning after two days of no exposure showed a further reduction in FVC and FEV1 by an average of 0.21 in a sawmill with high exposure to moulds (10 colony-forming units/m3), but not in another sawmill with ten times lower exposure. Further recordings 27 months later (Monday morning before work) displayed no further worsening in any spirometric variable. No change in lung function was noted after one day of work (Monday morning to Monday evening), but a further reduction in FVC of an average of 0.31 was seen in non-smokers at the end of the week, with apparent resolution over the weekend. The impairment was more obvious at the sawmill with higher air concentrations of organic dust than at the other sawmill. It is concluded that wood trimmers may develop restrictive pulmonary dysfunction, which might be explained by an immunopathological reaction to heavy mould exposure.

Adult↗
PubMed1985

Symptoms and lung function in low-exposure to TDI by polyurethane foam manufacturing.

A cross-sectional investigation was performed in seven polyurethane foam manufacturing factories. Lung function tests were performed at the factories by spirometric and nitrogen wash-out methods. Sixty-seven persons were investigated before and after the work shift, and exposure to toluene diisocyanate (TDI) was evaluated by subject-carried sampling equipment on the same day. The day mean exposure to TDI was 0.008 mg/m3 (0.001 ppm). In the non-smokers there was an increased frequency of symptoms from the airways reported in the exposed subjects as compared to the unexposed controls. There were, however, no signs of acute or chronic effects on the lung function measured by spirometric and nitrogen wash-out methods, which could not be explained by smoking.

Adult↗
PubMed1983

Exposure to terpenes: effects on pulmonary function.

Forty-eight subjects exposed to terpenes (mean air concentration 258 mg m-3) and 47 unexposed subjects, all employed at sawmills, were studied with regard to symptoms and pulmonary function. Dyspnoea and chest oppression were significantly increased in the exposed subjects compared to the unexposed controls. A reduced FEV1, on spirometry and an increased CV% and slope of the alveolar plateau (phase III) on single breath nitrogen washout were seen on Monday morning before exposure to terpenes. There was no correlation between exposure time (duration of employment) and lung function impairment. A day of industrial exposure to terpenes caused no further change in any lung function variable. The unexposed controls showed normal spirometry and nitrogen washouts. The findings indicate a slight stable lung function impairment of an obstructive nature which does not necessarily undergo further deterioration with increased duration of exposure.

Adult↗
PubMed1982

Pulmonary function after long-term exposure to trichlorophenol.

Symptoms and pulmonary function were evaluated in subjects exposed to trichlorophenol. Symptoms from upper airways and chest were more common among those exposed than in control subjects (60% and 10%, respectively) Significantly reduced forced expired flow at 75% of vital capacity [exposed: 5.721/s (5.08-6.85), mean and range; reference: 6.451/s (5.77-8.40), P less than 0.05] and increased closing volume [exposed: 25.2% (19.5-36.0), reference: 17.1% (12.0-23.5), P less than 0.01] were measured while other spirometric variables and the transfer factor of the lung for CO were normal. Increased elastic recoil pressure of the lung and signs of lung tissue engagement in X ray were noticed in two subjects. Blood and liver tests were normal. The findings suggest an irritating effect on the lung by trichlorophenol, and it cannot be excluded that long-term exposure may produce pulmonary fibrosis.

Adult↗
PubMed1981

Pleural plaques and lung function in construction workers exposed to asbestos.

Respiratory symptoms and pulmonary function have been evaluated in construction workers exposed to asbestos and in control subjects. Group I displayed pleural plaques but not lung tissue involvement on X-ray, group II had the same history of asbestos exposure as the previous group but had no pleural plaques, nor any lung tissue involvement, and group III constituted non-exposed control subjects. Chronic bronchitis and productive cough were 4-5 times more frequent in group I compared to group III, while non-productive cough was rare. Conventional spirometry gave no significant differences between exposed and non-exposed subjects, while expiratory flow rates during the latter half of the expiration (MEF50, MEF25) were reduced in group I. Closing volume (CV) was markedly increased in group I and the transfer factor of the lung for CO was slightly reduced. The static transpulmonary pressure - lung volume curve was much the same for all three groups. The difference in CV, MEF50, and MEF25 was greater between exposed and non-exposed non-smokers than between exposed and non-exposed smokers. No significant differences were noticed between those in group II and the control group III. The findings indicate that asbestos exposure whcih elicits pleural plaques, may cause pulmonary dysfunction, representing a disease of the small airways.

Aged↗
PubMedDate not supplied

Exposure to formaldehyde: effects on pulmonary function.

Forty-seven subjects exposed to formaldehyde (mean air concentration 0.45 mg/m3) and 20 unexposed subjects, all of whom were employed at a carpentry shop, were studied with regard to symptoms and pulmonary function. Symptoms involving eyes and throat as well as chest oppression were significantly more common in the exposed subjects than in the unexposed controls. Spirometry and single breath nitrogen washout were normal Monday morning before exposure to formaldehyde. A reduction in forced expiratory volume in 1 sec by an average of 0.2 L (P = .002), percent forced expiratory volume by 2% (P = .04), maximum midexpiratory flow by 0.3 L/sec (P = .04) and an increase in closing volume in percentage of vital capacity by 3.4% (P - .002) were seen after a day of work and exposure to formaldehyde, suggesting bronchoconstriction. Smokers and nonsmokers displayed similar changes in spirometry and nitrogen washout.

Adult↗
PubMedDate not supplied

Exposure to naphthalene-diisocyanate in a rubber plant: symptoms and lung function.

Twenty-three subjects exposed to naphthalene-diisocyanate (NDI, [mean air concentration 0.002-0.007 mg/m3]) were examined with regard to symptoms and pulmonary function. Irritation of the eyes, cough, and exertion dyspnea were more common in exposed subjects than in unexposed controls. Closing volume, as a percentage of vital capacity (CV%), was 6% higher than the reference value (P = .01) on Monday morning after 2 days with no exposure to NDI. The other lung function variables were normal. Two days of industrial exposure caused no further change in any lung function variable. The difference between measured and expected CV% increased with age in the exposed subjects. Five employees who had complained of severe symptoms during NDI exposure and who, therefore, had been transferred to other tasks with no exposure to NDI, displayed marked increases in CV% and a reduction in the forced vital capacity by an average of 0.6 L. Smokers and nonsmokers displayed similar lung function changes.

Adult↗
PubMedDate not supplied

Exposure, lung function, and symptoms in car painters exposed to hexamethylendiisocyanate and biuret modified hexamethylendiisocyanate.

Individuals who paint cars often complain to doctors about respiratory problems. Car painters are exposed to isocyanates, especially hexamethylendiisocyanate (HDI), and biuret modified HDI (HDI-BT). The mean exposure to HDI-BT was 115 micrograms/m3 in the air (range 10-385 micrograms/m3), which exceeds the time-weighted Swedish threshold level of 90 micrograms/m3. Exposure to HDI was about 1.0 microgram/m3 with brief peaks. This study investigated the effect of HDI and HDI-BT on lung function and included two control groups: (1) car platers, exposed to the same solvents and grinding dust as car painters, but not to isocyanates, and (2) car mechanics (controls), not exposed to the mentioned agents. Car painters and car platers were compared to car mechanics on Monday before work. Acute effects of car painting were tested by comparing the lung function values on Monday morning with those on Friday afternoon. Pulmonary function was evaluated by means of spirometry and a single breath nitrogen washout. Spirometry in painters and platers did not differ from that in controls, i.e., car mechanics. Closing volume in relation to vital capacity (CV%) was increased in car painters, suggestive of a "small airways disease" on Monday before work and tended to increase during a work week. Car platers did not differ from controls.

Adult↗
PubMedDate not supplied

Blood and urinary concentrations as estimators of cobalt exposure.

Methods for determining low levels of cobalt in blood and urine within a normal range have been developed. Mineralizing by using small amounts of nitric acid, ion exchange separation, and electrothermal atomic absorption measurements are the techniques used. The normal content of cobalt is 8.5 nmol/L (range 1.7-20.4 nmol/L) in blood and 6.8 nmol/L (range 1.7-37.3 nmol/L) in urine in a nonoccupational cobalt-exposed group. After exposure, cobalt is excreted rapidly in urine. When exposure is relatively high, there is rapid continuous decrease in excretion for about 24 hr followed by a slower excretion phase. When exposure is low, the excretion of cobalt in urine is relatively constant but may be 4-10 times higher than in non-exposed persons. The slow excretion can continue at least 4 wk after exposure. Variations of cobalt concentrations in blood are smaller but follow the exposure. When blood and urine concentrations of cobalt were compared on a Friday afternoon, the correlation coefficient was 0.82. When the average exposure to cobalt for the whole week was compared with the cobalt concentration in urine, the correlation coefficient on Friday afternoon was 0.79 and on Monday morning 0.81. For blood, the correlation coefficient was 0.87 on Friday afternoon and 0.76 on Monday morning.

Adult↗
PubMedDate not supplied

Respiratory hazards associated with exposure to formaldehyde and solvents in acid-curing paints.

Thirty-eight employees exposed to formaldehyde when working with acid-hardening lacquers and 18 nonexposed control persons employed at the same company were examined to determine lung function (spirometry and nitrogen washout), total immunoglobulin blood concentration, and work-related symptoms. The mean exposure to formaldehyde during an 8-hr workday was 0.40 mg/m3 air, and the mean exposure to peak values was 0.70 mg/m3. Mean exposure to solvents was low, i.e., approximately 1/10 of the hygienic effect. Eye, nose, and throat irritation was more common in exposed persons than in controls. Monday morning, after two exposure-free days, forced vital capacity (FVC) values were found to have declined by 0.24 L and forced expiratory volume in 1 sec (FEV1.0) by 0.21 L, compared with normal values. There was a weak correlation between the individual concentration of IgG and decrease in FVC and FEV1.0. No significant changes were noted in any other lung function variable before a workshift, and no lung function changes were noted over a full workshift. Deviations in FVC and FEV1.0 values did not correlate to peaks or mean exposures or employment time.

Adult↗
PubMedDate not supplied

Pulmonary function in wood workers exposed to formaldehyde: a prospective study.

Employees exposed to formaldehyde in the woodworking industry (N = 47) and nonexposed control subjects (N = 20) were examined in 1980 by spirometry and the nitrogen washout technique. A transient impairment of lung function was noted over a work shift. Five years later, 21 subjects were still experiencing exposure to formaldehyde. A transient decrease in lung function was again found over a work shift, as evidenced by a reduction in forced mid-expiratory flow (FEF25-75) of 0.15 l/s and an increase in closing volume (CV%) of 3.0% in nonsmokers. Significant decreases in forced expired volume in 1 s as a percent of forced vital capacity (FEV1.0/FVC) and FEF25-75 were also noted over the 5 y in nonsmokers (0.4% and 0.2 l.s/y, respectively, after correction for normal aging). After 4 wk of no exposure (holidays), FEF25-75 and forced expired vital capacity (FVC, FEV1.0) returned to normal in the smoking group. Lung function in smokers improved less during the holiday. A dose-response relationship was found between exposure to formaldehyde and decrease in lung function. Thus, industrial exposure to formaldehyde causes transient lung function impairment over a work shift, with a cumulative effect over the years. The impairment, however, can be reversed with 4 wk of no exposure.

Adult↗