Gannon P F, Burge P S
Department of Respiratory Medicine, East Birmingham Hospital.
Br J Ind Med. 1993 Sep;50(9):791-6. doi: 10.1136/oem.50.9.791.
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.
A surveillance scheme of physicians likely to see cases of occupational asthma.
The West Midlands Region of the United Kingdom.
Workers with occupational asthma diagnosed within the boundaries of the West Midlands Region.
Demographic data, employer, agent to which exposed, date of diagnosis, method of diagnosis, proposed mechanism of asthma, and employment state.
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%).
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.
研究特定地理区域内职业性哮喘的总体发病率和特定发病率;审核职业性哮喘的诊断情况;确定哮喘的可能发病机制;并确定诊断时工人的就业状况。
针对可能诊治职业性哮喘病例的医生的监测方案。
英国西米德兰兹地区。
在西米德兰兹地区范围内被诊断为职业性哮喘的工人。
人口统计学数据、雇主、接触的致病因子、诊断日期、诊断方法、哮喘的可能发病机制以及就业状况。
检测到每年每百万普通工人中新增43例(95%置信区间CI 35 - 52)确诊病例。特定职业的发病率各不相同,从每百万喷漆工中的1833例(95%CI 511 - 2990)到每百万职员中的8例。按地区卫生局划分的特定发病率从索利哈尔的每百万103例到南沃里克郡的每百万普通工人中的14例不等。工人诊断时接触的致病因子通常已得到充分认识(异氰酸酯20.4%,面粉8.5%,松香8.3%)。最常用的诊断方法是连续呼气峰值流速(PEF)测量。其使用情况各不相同(专科单位72%,普通胸科医生50%,赔偿委员会48%)。在专科中心未进行PEF读数的病例中,4%的工人仍在接触致病因子,因此本可进行有效的PEF读数;胸科医生诊治的病例中有16%,赔偿委员会诊治的病例中有2%。在专科单位之外,其他诊断方法很少使用。56%的报告医生认为哮喘的发病机制是过敏,而认为是刺激的占18%。28%的工人在诊断时接触了疑似致病因子,38%的工人要么长期请病假、已退休,要么已失业。在专科中心,1991年变革前被认定可获法定赔偿的致病因子接触工人中,获得赔偿并由赔偿委员会上报该方案的比例(38%)高于胸科医生诊治的病例(9%)。
这些已确认的发病率可能低估了实际发病率。它们突出了高危职业,并表明一些地区卫生局存在诊断不足的情况。它们表明诊断方法在专科中心之外未得到充分利用,且哮喘的发病机制通常被认为是过敏性的。