Rolf Alexandersson

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.

Exposure to terpenes: Effects on pulmonary function

SummaryForty-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 111) 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.

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.

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.

Lung function and rhizopus antibodies in wood trimmers

SummaryPulmonary 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 (FEV 1) 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.

Small airways function in aluminium and stainless steel welders

SummaryThe effect of welding fumes on small airways was studied in 25 male subjects who welded in aluminium (Al) and to some extent also in stainless steel (SS). Despite a low exposure to welding fumes as compared to the permissible exposure limits, excretion of Al in urine was found to be increased in all subjects (median value: 0.29 mmol/mol creatinine on Friday afternoon, as compared to an upper reference level of 0.10 mmol/mol creatinine). In addition, the welders displayed increased prevalences of work-related eye and airways (pharyngitis and non-specific bronchial hyper-reactivity) symptoms, as compared to 25 matched controls. Short-term welders (≤ 2.5 years) had more symptoms related to the upper airways than did long-term welders, which may indicate a selection. Spirometry, closing volume and volume of trapped gas (VTG) did not deviate. However, after methacholine inhalation, the long-term welders had a significantly steeper slope of the alveolar plateau on the single-breath nitrogen wash-out test, and a slight increase in VTG, as compared to the short-term welders and the controls. These findings may indicate a welding fume-induced increase in the reactivity of the small airways. Because Al welding was far more frequent than SS welding, an association with the former seems likely.

Impeded lung function in moulders and coremakers handling furan resin sand

SummaryA total of 39 moulders and coremakers exposed to furan resin sand and 27 unexposed local controls were examined by lung-function tests before and after a work shift. In all, 28 of the subjects exposed to furan resin sand and the control group were evaluated by dynamic spirometry and nitrogen washout. The remaining 11 subjects exposed to furan resin sand were studied using both static and dynamic spirometry and the CO single-breath technique. The time-weighted average exposure to furfuryl alcohol was about 7 mg/m3, with peak values exceeding the present Swedish short-term exposure limit (40 mg/m3). The exposure to respirable dust and formaldehyde as time-weighted over the shift was < 2 mg/m3 and 0.4 mg/m3, respectively, in all groups. During the work shift studied, the 28 exposed subjects had more complaints of airway symptoms than did the controls, showing an average decrease of 0.21 in forced vital capacity but no fall in any other lung-function variable. The remaining 11 exposed subjects demonstrated a post-shift decrease in total lung capacity. The results indicate an acute restrictiveness induced by exposure to furan resin sand, but the underlying mechanism is unclear. Chronic impairment of lung function was not observed.

Serum IgE and lung function in workers exposed to phthalic anhydride

SummaryA total of 23 phthalic anhydride (PA)-exposed workers (air levels up to 17 mg/m3) showed significantly (P<0.01) more workrelated symptoms in their eyes (48% vs 6%) and nose (39% vs 0) than did 18 unexposed control subjects. Two of the exposed workers had PA-associated asthma. Surprisingly, the control group exhibited significantly (P<0.05) more symptoms of nonspecific bronchial hyperreactivity (44% vs 13%). The exposed workers showed significantly higher levels of total serum IgE (medians, 32 vs 15 kIU/l, P<0.05), although values for specific IgE against PA did not differ. This may indicate that such exposure can facilitate the entry of common allergens. There was a significant difference in PA-specific IgG [enzyme-linked immunosorbent assay (ELISA) ratios 0.21 vs 0.12; P<0.01]. There were no differences in lung function with regard to vital capacity (VC) and forced expiratory volume (FEV1), closing volume expressed as a percentage of VC (CV%), volume of trapped gas (VTG) before and after inhalation of metacholine, or carbon monoxide transfer factor (TLCO), whereas exposed workers displayed significantly higher late expiratory flow rates (MEF5O and MEF25). In a [99mTc]-diethylenetriamine penta-acetate (DTPA) clearance test, there was no difference between exposed subjects and controls. In summary, exposure to PA did not cause subclinical effects of the lungs. Subjects with lower-airway symptoms showed lower FEV1, MEF50, and MEF25 values and higher VTG (after metacholine) than did those without symptoms. Six subjects with chronic bronchitis displayed significantly (P<0.05) higher VTG (before metacholine) and TLCO, than those without this ailment. Thus, VC, CV and the [99m99mTc]-DTPA test were not affected by the lung disorder.

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

SummaryA 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.

Pulmonary function after long-term exposure to trichlorophenol

SummarySymptoms 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: 5.721A (5.08–6.85), mean and range; reference: 6.451A (5.77–8.40), P < 0.05] and increased closing volume [exposed: 25.2% (19.5–36.0), reference: 17.l% (12.0–23.5), P < 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.