Baur X, Chen Z, Liebers V
Research Institute for Occupational Medicine (BGFA), Institute at the Ruhr-Universität Bochum, Germany.
Clin Exp Allergy. 1998 May;28(5):537-44. doi: 10.1046/j.1365-2222.1998.00276.x.
Only a few threshold limit values exist at present for allergens in the workplace known to cause bronchial asthma. This contrasts with the great number of occupational asthma cases observed in industrialized countries. Recently published studies provide clear evidence for exposure intensity response relationships of occupational allergens of plant, microbiological, animal or man-made origin. If allergen exposure levels fall short of determined limit values, they are not associated with an increased risk of occupational asthma. Corresponding data are available for wheat flour (1-2.4 mg/m3), fungal alpha-amylase (0.25 ng/m3), natural rubber latex (0.6 ng/m3), western red cedar (0.4 mg/m3) and rat allergens (0.7 microg/m3). It is suggested to stipulate legally binding threshold limit values (TLV/TWA) on this basis in order to induce more effective primary preventive measures. If no reliable data on the health risk of an occupational airborne noxa exist, the lowest reasonably practicable exposure level has to be achieved. Appropriate secondary preventive measures have to be initiated in all workplaces contaminated with airborne allergens. Verified exposure-response relationships provide the basis for risk assessment and for targeted interventions to reduce the incidence of occupational asthma also in consideration of cost benefit aspects. 'Occupational asthma is a disease characterized by variable airflow limitation and/or airway hyperresponsiveness due to causes in a working environment. These causes can give rise to asthma through immunological or non-immunological mechanisms. Up to 15% of all asthma cases are of occupational origin or have at least a significant causal occupational factor. According to the New Zealand part of the European Respiratory Health Survey, an increased risk of asthma prevalence was found for several occupations such as laboratory technicians, food producers, chemical workers, plastic and rubber workers. The Spain part of this study comprising 2646 Spanish subjects showed an asthma risk to be attributed to occupational exposures between 5 and 6.7%. Main asthma-inducing agents in the workplace are flour, grain and feed dust, animal dander/urinary proteins and isocyanates. Further, several inhalative irritants such as chlorine, acid or alkaline aerosols play a pivotal role. Many low molecular weight chemicals have irritative as well as allergenic effects on the airways, e. g. isocyanates and acid anhydrides. In addition to chronic or repetitive exposures, also singular accidental exposure to high concentrations of irritative or toxic airborne substances can cause occupational asthma. This condition is frequently called reactive airways dysfunction.
目前,已知会导致支气管哮喘的工作场所过敏原仅有少数几个阈限值。这与工业化国家中观察到的大量职业性哮喘病例形成了鲜明对比。最近发表的研究为植物、微生物、动物或人造来源的职业过敏原的暴露强度-反应关系提供了明确证据。如果过敏原暴露水平低于确定的限值,则与职业性哮喘风险增加无关。小麦粉(1 - 2.4毫克/立方米)、真菌α淀粉酶(0.25纳克/立方米)、天然橡胶乳胶(0.6纳克/立方米)、西部红雪松(0.4毫克/立方米)和大鼠过敏原(0.7微克/立方米)都有相应的数据。建议在此基础上规定具有法律约束力的阈限值(时间加权平均阈限值),以便采取更有效的一级预防措施。如果不存在关于职业性空气污染物健康风险的可靠数据,则必须实现最低合理可行的暴露水平。在所有被空气传播过敏原污染的工作场所都必须启动适当的二级预防措施。经过验证的暴露-反应关系为风险评估以及有针对性的干预措施提供了依据,这些干预措施还考虑到成本效益方面,以降低职业性哮喘的发病率。“职业性哮喘是一种因工作环境中的因素导致气流受限和/或气道高反应性多变的疾病。这些因素可通过免疫或非免疫机制引发哮喘。所有哮喘病例中,高达15%是职业性起源的,或至少有一个重要的职业性致病因素。根据欧洲呼吸健康调查的新西兰部分,发现一些职业如实验室技术员、食品生产者、化学工人、塑料和橡胶工人患哮喘的风险增加。这项研究的西班牙部分涉及2646名西班牙受试者,结果显示职业暴露导致哮喘的风险在5%至6.7%之间。工作场所主要的哮喘诱发剂是面粉、谷物和饲料粉尘、动物皮屑/尿液蛋白以及异氰酸酯。此外,一些吸入性刺激物如氯气、酸性或碱性气溶胶也起着关键作用。许多低分子量化学物质对气道有刺激性和致敏性,例如异氰酸酯和酸酐。除了慢性或重复性暴露外,单次意外暴露于高浓度的刺激性或有毒空气传播物质也可导致职业性哮喘。这种情况通常被称为反应性气道功能障碍。