Occupational asthma caused by aluminium welding.

Work-related asthma has been documented in workers employed in the primary aluminium industry and in the production of aluminium salts. The role of aluminium in the development of occupational asthma has, however, never been convincingly substantiated. We investigated a subject who experienced asthmatic reactions related to manual metal arc welding on aluminium. Challenge exposure to aluminium welding with flux-coated electrodes, as well as with electrodes without flux, elicited marked asthmatic reactions. Manual metal arc welding on mild steel did not cause significant bronchial response. The results of inhalation challenges combined with exposure assessments provided evidence that aluminium can cause asthmatic reactions in the absence of fluorides. Awareness of this possibility may be relevant to the investigation of asthma in workers exposed to aluminium.

Occupational asthma due to gas metal arc welding on mild steel.

Occupational asthma has been documented in electric arc welders exposed to manual metal arc welding on stainless steel. A subject is described who developed late and dual asthmatic reactions after occupational-type challenge exposure to gas metal arc welding on uncoated mild steel.

Urinary mandelic acid and hemoglobin adducts in fiberglass-reinforced plastics workers exposed to styrene.

OBJECTIVES: A field study was undertaken to investigate the effects of occupational styrene exposure on mandelic acid excretion and the formation of styrene-7,8-oxide hemoglobin adducts. Especially the sensitivity of a gas chromatography-mass spectrometry method for determining hemoglobin adducts was evaluated. METHODS: Over a four-week period, each individual of a group of 52 fiberglass-reinforced plastics workers was monitored once a week by the simultaneous measurement of styrene in the air and urinary postshift mandelic acid. In addition mandelic acid and hemoglobin adducts were monitored in a group of 24 unexposed referents. At the end of the monitoring period styrene-7,8-oxide adduct formation on N-terminal valine in hemoglobin was examined by gas chromatography-mass spectrometry according to the modified Edman degradation technique. RESULTS: Personal air samples showed an average styrene exposure of 31 mg.m-3. The average postshift mandelic acid was 98 mg.g creatinine-1. For workers not wearing respirators and not showing breath ethanol, the correlation coefficient between styrene and mandelic acid was 0.78. The blood samples were analyzed for styrene-7,8-oxide adducts on hemoglobin. With a detection limit of 10 pmol.g-1, no styrene-7,8-oxide adducts were found under these exposure conditions. CONCLUSION: Adduct formation in humans is less effective than in mice. In comparison with ethylene, styrene is at least 70 times less effective in forming hemoglobin adducts. Investigating adduct formation in humans at or below the exposure levels reported in this study would require a detection limit of about one order of magnitude better.

Cytogenetic analysis of lymphocytes from fiberglass-reinforced plastics workers occupationally exposed to styrene.

In this study a group of 52 workers employed in a plant manufacturing fiberglass-reinforced plastic (FRP) pipes and cisterns, and therefore daily exposed to styrene, were monitored. As a control group 24 non-exposed workers from another factory producing and repairing pallets volunteered to participate. The airborne styrene during the monitoring ranged from 2.2 to 110.1 mg/m3. As a metabolic marker for styrene exposure mandelic acid was measured in the urine and ranged from 11 to 649 mg/g creatinine. From 43 exposed and 15 control workers sister-chromatid exchanges (SCE) and high frequency cell (HFC) data and from 49 exposed and 23 control workers micronucleus (MN) data from peripheral lymphocytes are reported. Although the two groups of workers could clearly be distinguished on the basis of the airborne styrene concentrations and urinary mandelic acid concentrations no differences in any of the cytogenetic markers were found. Correlations between the cytogenetic data and the level of airborne styrene concentrations or urinary mandelic acid levels could also not be demonstrated. Otherwise, smoking increased the SCE frequency. Grouping the workers according to smoking habits showed a statistically significant difference in SCE. Moreover, levels of urinary thiocyanate (SCN), which can be used as a metabolic marker for smoking, showed a significant positive correlation with the number of SCE. This indicates that SCE is a sensitive biomarker and might still be useful in biomonitoring. However, only chronic exposures over a long period would probably be detectable. In this study, where exposure was rather low and the number of working years was small (mean of 2.9 years), cytogenetic effects are probably too low or rare to be detectable with any assay.

Survey of cobalt exposure and respiratory health in diamond polishers.

This cross-sectional study was undertaken after the discovery of cobalt-related fibrosing alveolitis and bronchial asthma in diamond polishers occupationally exposed to cobalt. A total of 194 workers from 10 diamond polishing workshops and 59 workers from three other workshops from the diamond industry (control subjects) were studied; a questionnaire was administered and spirometry was performed. Cobalt exposure was assessed by environmental air sampling using both area and personal sampling and by measuring urinary cobalt concentration. When considered on a workshop basis, these environmental and biologic indices of exposure correlated well with each other. These measurements led to the definition of three cobalt exposure categories: a no exposure group, a low exposure group, and a high exposure group. The high exposure was, however, still below the present threshold limit value for cobalt (50 micrograms/m3). Spirometry showed that indices of ventilatory function (FVC and FEV1) were significantly (p less than 0.05) lower in the group with the highest exposure to cobalt. These differences were not due to differences in smoking habits. The results were confirmed when the data were analyzed by covariance analysis of lung function indices against smoking status, taking mean cobalt exposure in each workshop as a covariate, and when the data were analyzed by multiple regression analysis. This analysis showed that cobalt exposure correlated with decreased pulmonary function. Our results suggest that, during diamond polishing, exposure to cobalt at levels below the current threshold limit value is associated, on a group basis, with measurable effects on lung function parameters. The relationship between these cross-sectional epidemiologic findings and the occurrence of overt lung disease in diamond polishers remains to be established.

Exposure of diamond polishers to cobalt.

Interstitial pulmonary fibrosis due to 'hard metal' exposure is well known, and the presence of cobalt has always been considered as the causative factor. Recently interstitial pulmonary fibrosis has been described in diamond polishing workers. In this study the dust composition in different polisher's workplaces where diamond disks are in use has been determined. Careful investigation showed that the exposure to respirable dust was comparable to that of 'hard metal' workers. The dust consists mainly of iron and cobalt particles and small amounts of silica. No 'hard metals' have been found, and other fibrogenic agents such as beryllium have been excluded. These observations lend support to the hypothesis that crystalline cobalt particles can be responsible for pulmonary fibrosis even in the absence of carbides.

Value of the diagnostic sodium calcium edetate mobilization test as a criterion of lead absorption.

Among the laboratory tests available for the follow-up of lead-exposed workers, the EDTA mobilization test is presently underestimated in the diagnosis of lead intoxication. The authors present the results of regression comparison between the urinary lead excretion 3 h (PbU 3) or 6 h (PbU 6) after EDTA injection and blood lead (PbB), urinary aminolaevulinic acid (ALAU) and urinary lead (PbU). The results were collected from 133 medical examinations of workers exposed to lead, who put in a claim for compensation to the 'Fund of Occupational Diseases' in Belgium. On the basis of the regression curves, PbU 3 and PbU 6 limit values are calculated for different cut-off values of PbB in excessive lead absorption and lead intoxication. For each of these values the 'sensitivity', 'specificity' and 'validity' are calculated. As a result the authors still consider the EDTA mobilization test as a valuable parameter in the diagnosis of lead absorption.

Actual hazard of methyl bromide fumigation in soil disinfection.

Methyl bromide, a highly toxic and ready penetrating fumigant, is widely used against rodents, insects, mites, and a range of pathogenic organisms in soil, compost, and timber. To disinfect soil in greenhouses, methyl bromide is brought under pressure from outside by a vaporiser and blown on to ground under a polyethylene cover. The gas being three times heavier than air easily penetrates the ground. Depending on the local ventilation, a considerable amount of gas evaporates into the surrounding atmosphere, this emission being especially serious during the fumigation procedure and at the removal of the plastic cover. Previously, mechanical injection of methyl bromide on to the ground within closed areas was prohibited, since this technique exposed at least four disinfection workers at a time, who were provided with only a canister respirator, to gas concentrations of over 1000 ppm CH3Br. The present study established that fumigation with methyl bromide also carries risks for the well-protected worker inside, as well as for the one controlling the vaporiser. The concentration during application varies from 30 to 3000 ppm. Concentration in the air declines with time to 4 ppm CH3Br five days after application. Discarding the plastic sheet involves exposure to peak values as high as 200 ppm for a few seconds. On the ninth day after application, milling the soil can expose workers to up to 15 ppm; on the eleventh day no CH3Br concentration in the air could be found.

Dangerous concentrations of methyl bromide used as a fumigant in Belgian greenhouses.

In the disinfection of soil in greenhouses, methyl bromide can be applied to the soil by injection or by fumigation on the surface. The concentrations of methyl bromide in the air are measured, and the differences between each technique discussed. Concentrations during injection vary between 100 and 1,000 ppm with peaks up to 3,000 (10,000 in one case) ppm, but drop below 200 ppm if preventive measures are taken. During fumigation concentrations remain between 100 and 1,000 ppm. Large variations occur within a technique depending on the quality both of the material and operator.