British Journal of Industrial Medicine最新文献

Objective: To study the general and specific incidence of occupational asthma within a defined geographic area; to audit the diagnosis of occupational asthma; to determine proposed mechanisms of asthma; and to determine the employment state of workers at diagnosis.

Design: A surveillance scheme of physicians likely to see cases of occupational asthma.

Setting: The West Midlands Region of the United Kingdom.

Subjects: Workers with occupational asthma diagnosed within the boundaries of the West Midlands Region.

Main measures: Demographic data, employer, agent to which exposed, date of diagnosis, method of diagnosis, proposed mechanism of asthma, and employment state.

Results: A recognised incidence of 43 (95% confidence interval CI 35-52) new cases per million general workers per year was detected. Specific occupational incidences varied from 1833 (95% CI 511-2990) per million paint sprayers to eight per million clerks. Specific incidence by District Health Authority varied from 103 in Solihull to 14 per million general workers in South Warwickshire. Agents to which workers were exposed at the time of diagnosis were generally well recognised (isocyanates 20.4%, flour 8.5%, colophony 8.3%). The most commonly used method of diagnosis was serial peak expiratory flow (PEF) measurement. Its use varied (specialist unit 72%, general chest physicians 50%, compensation board 48%). Workers were still exposed and therefore could have usefully performed PEF readings in 4% of cases where they were omitted from the specialist centre, 16% seen by chest physicians, and 2% seen by the Compensation Board. Other methods of diagnosis were used only infrequently outside the specialist unit. Fifty six per cent of reporting physicians considered that the mechanism of asthma was allergy compared with 18% who believed that it was irritation. Twenty eight per cent of workers were exposed to the suspected causative agent at the time of diagnosis, 38% were either on long term sickness absence, had retired, or had become unemployed. More workers (38%) who were exposed to agents recognised for statutory compensation before the 1991 changes seen at the specialist centre reach compensation and were reported to the scheme by the Compensation Board than those seen by chest physicians (9%).

Conclusions: These recognised incidences are likely to be an underestimate of the true incidence. They highlight at risk occupations and suggest underdiagnosis in some District Health Authorities. They suggest that diagnostic methods are underused outside specialist centres and that the mechanism of asthma is generally considered to be allergic.

The question of lung damage as a result of exposure to silicon carbide (SiC) was investigated by inhalation experiments to obtain information on the qualitative response of lung tissue to the test substance (SiC). For comparison, quartz, kaolinite, and tempered clay dusts were used. The indices for the effects of the dusts studied were organ weights, numbers of bronchoalveolar cells, lung surfactant phospholipid concentrations including subfractions, and lung clearance. Exposure to the test samples was carried out according to the Essen inhalation model in two independent series. The results of the two series were similar: Compared with sham controls, exposure to SiC did not affect the indices studied. Even at a low dose (a quarter of the SiC dose) quartz gave pronounced deviations in all indices. In particular, an increase in granulocytes indicated toxic properties of the dust. The long term elimination of quartz from the lung was worse than that of SiC. The kaolinite and tempered clay dusts were intermediate between SiC and quartz based on several of the indices studied. It is concluded that SiC is deposited practically inert in the lung.

The mortality from ischaemic heart disease was studied in a prospective cohort of 1725 shipyard workers exposed to asbestos. The analyses were stratified for age and smoking habits and restricted to men. In agreement with other findings, men with impaired lung function had a significantly higher risk (relative risk (RR) = 3.5) of dying from ischaemic heart disease than men with normal lung function. Men with asbestosis or suspected asbestosis had a significantly higher risk (RR = 3.1) of dying from ischaemic heart disease than men without asbestosis. Thus asbestosis or suspected asbestosis also seemed to be a risk factor for ischaemic heart disease. This finding was independent of respiratory function. There was no increased risk for ischaemic heart disease in men with compared with men without pleural plaques. Men with production of phlegm or sputum and wheezing or whistling had no increased risk for ischaemic heart disease compared with men without these symptoms. In the group with normal lung function men with dyspnoea had a significantly higher risk of dying from ischaemic heart disease than men without dyspnoea. The findings for men with asbestosis or suspected asbestosis indicated a further risk factor besides impaired lung function, in persons exposed to asbestos. Perhaps this risk factor is due to lesions of the pericardium with consequences for heart function.

An investigation was conducted to examine the reliability (reproducibility) of self reported occupational histories obtained from a cohort of 326 capacitor manufacturing workers who had participated in an epidemiological study relating health abnormalities to exposure to polychlorinated biphenyls (PCBs). For a subsample of the cohort (n = 164) in which occupational histories were obtained twice (in 1976 and 1979), reliability of cumulative exposure to PCBs ranged from 93.6% for the early PCB period (1947-70) to 95.7% for the late PCB period (1971-6). These respective reliabilities were lower, however, for workers who changed jobs often. Workers above the median value of a weighted job change index had early and late reliabilities of 89.9% and 83.6% respectively. Reliability is a relevant factor when calculating power or sample size during the planning stage of epidemiological studies, for interpretation or adjustment of estimates in the analysis stage, or for determination of study feasibility.

The elimination of mercury (Hg) in blood was investigated in 14 chloralkali workers exposed to metallic Hg vapour for 1-24 (median 10) years. Blood and urine samples were collected on several (median eight) occasions during a period of 17-26 days. The initial Hg concentrations were about 80 nmol/l in whole blood (B-Hg) and 17 nmol/mmol creatinine in urine (U-Hg). The decrease in Hg in whole blood, plasma (P) and erythrocytes (Ery) was best characterised by a two compartment model. In a model with a common half life for all subjects, the best fit for B-Hg was obtained with half lives of 3.8 days for a fast phase and 45 days for a slow phase. The half life of the fast phase was shorter for P-Hg than for Ery-Hg, whereas the opposite was the case for the slow phase. The half lives of the slow phases in whole blood and plasma were longer, and the relative fractions of the slow phases were higher (about 50%) after long term exposure than those (about 20%) reported after brief exposure. Slower elimination indicates higher accumulation of Hg in organs with long half lives, and possibly the presence of at least one additional, even slower compartment. The U-Hg fluctuated substantially during the sampling period, and average concentrations decreased only slightly.

Silicon carbide (SiC) dust and other dusts for comparison were injected intratracheally at a high dose (50 mg) into rats and the response of the lungs and the lymph nodes was studied after an appropriate experimental period. The indices studied were: histological changes in the lung and lymph nodes, organ weights, the formation of collagenous fibres, and the appearance of quartz typical areas. According to several epidemiological investigations and previous experimental animal studies, SiC produces silicogenic (fibrogenic) effects. No changes in the tissues studied in terms of damaging fibrogenic effects could be found after eight months (first series) and three and 12 months (second series). In particular, the histological findings and the absence of quartz typical areas as well as the quantitative determination of collagen fibres show that SiC had no harmful effects on tissues. Based on these results, the extent to which other exposures during the production of SiC can be responsible for the established radiological alterations is discussed. Without doubt the following may be confounders: SiC fibres, crystalline SiO2 (quartz, cristobalite, tridymite), and possibly gaslike emissions (SO2). From the hygienic medical point of view the workplaces during SiC manufacture should be examined carefully. The substance SiC dust as such can be considered as inert from the experimental results based on qualitative and extremely sensitive procedures. A revision of the present threshold value for SiC in ther German MAK list is called for.