Di Stefano F, Verna N, Di Giampaolo L, Schiavone C, Di Gioacchino G, Balatsinou L, Burge P S, Boscolo P, Di Gioacchino M
Department of Medicine and Science of Aging, Section of Allergy, Clinical Immunology and Occupational Medicine, University G. D'Annunzio, Chieti, Italy.
Int J Immunopathol Pharmacol. 2004 May-Aug;17(2 Suppl):77-82. doi: 10.1177/03946320040170S213.
Occupational asthma is defined as variable airflow obstruction and airways hyperresponsiveness caused by exposure to agents present in the workplace. Low molecular weight agents such as isocyanates, aldehydes, anhydrides, colophony, dyes, persulphate, amines, acrylates and metals are steadily increasing as causative agents of occupational asthma. Isocyanates, aldehydes and anhydrides my cause sensitisation through an IgE mediated response in some workers. These agents act as haptens which combine with a carrier protein to form a complete antigen. Assays for the detection of specific IgE are standardized for very few agents and have a good specificity, but poor sensitivity. The diagnosis of occupational asthma relies not only on a suggestive hystory showing that asthma is caused or exacerbated specifically by work exposure, but in most cases needs to be confirmed by objective means. Combined monitoring of lung function parameters, such as peak expiratory flow rate at the work site and non specific bronchial hyperresponsiveness during and away from exposure, is necessary. The "gold standard" for confirming a diagnosis in an individual worker still remains the specific bronchoprovocation test, which has now reached a high degree of sensitivity, specificity and reproducibility for agents such a s isocyanates. In occupation asthma due to low molecular weight agents there are no individual risk factors which could predict the susceptibility to develop the disease. The primary prevention is based on appropriate interventions tn the workplace. The strict medical surveillance of workers may allow the early diagnosis and removal from further exposure in order to prevent morbidity and disability.
职业性哮喘的定义是因接触工作场所中存在的物质而导致的可变气流受限和气道高反应性。低分子量物质，如异氰酸酯、醛类、酸酐、松香、染料、过硫酸盐、胺类、丙烯酸酯和金属，作为职业性哮喘的致病因素正在稳步增加。异氰酸酯、醛类和酸酐可能通过一些工人中IgE介导的反应引起致敏。这些物质作为半抗原，与载体蛋白结合形成完全抗原。用于检测特异性IgE的检测方法仅针对极少数物质进行了标准化，具有良好的特异性，但敏感性较差。职业性哮喘的诊断不仅依赖于提示性病史，表明哮喘是由工作接触特异性引起或加重的，而且在大多数情况下需要通过客观手段来证实。有必要联合监测肺功能参数，如工作场所的呼气峰值流速以及接触期间和接触后非特异性支气管高反应性。在个体工人中确诊的“金标准”仍然是特异性支气管激发试验，该试验目前对异氰酸酯等物质已达到高度的敏感性、特异性和可重复性。在由低分子量物质引起的职业性哮喘中，没有个体风险因素可以预测患该病的易感性。一级预防基于工作场所的适当干预措施。对工人进行严格的医学监测可以实现早期诊断，并使其脱离进一步接触，以预防发病和残疾。
