Sixty patients with occupational asthma due to exposure to toluene diisocyanate (TDI) were re-evaluated, five years after the initial diagnosis had been confirmed by a specific bronchial provocation challenge. During both examinations the severity of asthmatic symptoms and the need for antiasthma treatment were graded and lung function tests, measurement of airway responsiveness to methacholine (PD15), and skin tests with common inhalant allergens were carried out. The evolution of the disease was established on the basis of the increase or decrease in asthmatic symptoms, requirements for medication, and FEV, and PD,5methacholine between the two examinations. At follow up 17 patients (group A, 28-3%) had carried on working in the same environment after relocation to jobs with only occasional exposure to TDI; 15 of them used protective respiratory devices. The remaining 43 (group B, 71-7%) avoided further inhalation of TDI by moving to another sector. Group A showed a significant decrease in FEV, and PD,5 methacholine and significant increases in the severity of symptom score and requirement for medication; 13 subjects (76 5%) were worse, four (23-5%) were stable, and no one had recovered or improved. Group B showed significantly less severe symptoms and a threefold increase in PD,5 methacholine; 12 subjects (28-2%) totally recovered, 10 (23 2%) improved, 16 (37 2%) were stable, and five (1 1-6%) were worse. In group B the duration of exposure to TDI and of symptoms before the initial diagnosis delineated the patients who recovered from those who did not improve; intermediate values in these features characterised the subjects who improved but did not recover. It is inferred that complete removal
Lead levels in whole blood and in plasma were measured in 64 non-exposed and in 29 exposed subjects with signs and symptoms of varying severity. Lead was determined by atomic absorption spectrophotometry after chelation with ammonium pyrrolidine dithiocarbamate and extraction with methyl isobutyl ketone. The method has a sensitivity of 04 ,ug/l00 ml (0.02 ,umol/l) for whole blood and of 0-2 ,g/100 ml (0.01 O,mol/l) for plasma and is reliably accurate and precise. Plasma lead increases progressively and significantly with the increase of whole blood lead, while its relative percentage in the plasma remains practically constant at all concentrations in whole blood. In exposed subjects a highly significant correlation was found between lead in plasma and lead in urine (r = 0 549) but the correlation coefficient was higher for whole blood lead versus urinary lead (r = 0 938). Aminolevulinic acid excretion in urine appeared to be significantly related to plasma lead concentration (r = 0-563) but to a greater extent to whole blood levels (r = 0-801). There was no significant correlation between lead in plasma and the logarithm of aminolevulinic acid dehydratase. The hypothesis is advanced that plasma lead, the more biologically active fraction of the metal, could be related to different individual sensitivities which would condition the development of toxic effects in various organs at different levels of lead.Although normally considered to be a single compartment (Rabinowitz et al., 1976) blood contains lead (Pb) in two forms, a non-diffusible form bound to erythrocytes and a diffusible form in plasma. Because of the uneven distribution of the metal between red blood cells and plasma, two physiological pools may be considered to exist. The diffusible form, because of its greater bioavailability, is likely to influence lead concentration of the other compartments directly and, as a consequence, to produce critical effects in the various organs, with the possible exception of erythrokinetic effects.There is little information so far relating to plasma lead levels; this may be attributable either to the technical difficulties involved in their measurement or to the lack of evidence of correlation with whole blood concentrations (Ambrosi and Chiantera, 1962;Rosen et al., 1974) Varying concentrations have been reported for serum lead: in adults, Ambrosi and Chiantera (1962) found levels ranging from 4-0 to 8-6 pug/100 ml (019-0-41 ,umol/l) in non-exposed subjects and from 5-0 to 13(),ug/100 ml (0 24-063 ,umol/l) in workers showing toxic effects, by using a dithizone method. Butt et al. (1964) by means of an emission spectrochemical technique, estimated lead values of 3 9, 2-7 and 2-8 ,ug/10O ml (0-19, 0-13 and 0(13 ,utmol/l) respectively in three non-exposed groups. Lloyd Davies and Rainsford (1967) reported figures of 1-2 ug (0-05-01 ,umol/l) of lead in serum of nonexposed subjects and of 3-4 Htg/100 ml (0-14-0-19 ,tmol/l) at whole blood values of 100 ,ug/100 ml (4-83 ,umol/l). In children, Robinson et...
In sensitized subjects, provocation tests to latex may induce severe systemic reactions and even anaphylactic shock. It is probable that part of the risk is due to the difficulty in grading the stimulating dose and in starting from very low levels of exposure. To identify the aetiological agent of work-related asthma in four nurses with previous allergic contact urticaria to latex surgical gloves dusted with cornstarch powder, we performed a specific bronchial provocation test study, based on exposure on three different days to nonpowdered latex surgical glove extract, powdered latex surgical glove extract and cornstarch powder extract, respectively. Extracts were nebulized in increasing concentrations in a 7 m3 challenge room, in the absence of the patients. The initial extract concentration was a tenfold dilution of the predetermined skin test end-point in the individual undergoing challenge, and the highest concentration was the undiluted extract. After exposure, the patients' forced expiratory volume in one second (FEV1) was monitored for 2 h. If FEV1 decreased by at least 15%, the next scheduled exposure was not carried out and FEV1 was monitored over a period of 24 h. Whereas nebulization of cornstarch powder extract caused no bronchial reaction in the patients, nebulization of nonpowdered latex surgical glove extract induced immediate bronchoconstriction in two subjects as an undiluted solution, and nebulization of powdered latex surgical glove extract induced immediate bronchoconstriction in all subjects at the 1:10 dilution. No systemic reaction was elicited by the bronchial provocation challenges. Our results demonstrate that airborne powder from latex gloves can be an inhalative occupational hazard.(ABSTRACT TRUNCATED AT 250 WORDS)
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