OCCUPATIONAL ASTHMA

OCCUPATIONAL ASTHMA
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DOI:
10.2307/3432381
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发表时间:
1995-09-01
影响因子:
10.4
通讯作者:
CHANYEUNG, M
CHANYEUNG, M
中科院分区:
环境科学与生态学1区
文献类型:
--
作者:
CHANYEUNG, M

文献摘要

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在空气排放物中发现的许多有毒化合物可能会导致支气管收缩。在工作场所,工人暴露在这些化合物中,浓度往往要高得多。其中一些化合物起到了增敏剂的作用。这些都是。一些化合物通过产生针对该化合物或其蛋白结合物的特异性IgE抗体来诱发哮喘,而另一些化合物则通过尚未确定的免疫机制诱发哮喘。一些化合物。当吸入高浓度时。作为刺激物,可能通过引起急性呼吸道炎症而产生支气管收缩。后一种情况称为反应性呼吸道功能障碍综合症(RADS)或刺激性哮喘。职业性哮喘是研究成人哮喘发病机制和自然病史的极佳模型,因为可以确定致病因素,可以完全避免,并且可以测量或估计暴露。
Many toxic compounds found in air emissions may induce bronchoconstriction. In the workplace, workers are exposed to these compounds, often in much higher concentrations. Some of these compounds act as sensitizers. Of these. some compounds induce asthma by producing specific IgE antibodies to the compound or its protein conjugate, while others induce asthma through yet unidentified immunologic mechanisms. Some compounds. when inhaled in high concentrations. act as irritants and produce bronchoconstriction probably by inducing acute airway inflammation. The latter condition is called Reactive Airways Dysfunction Syndrome (RADS) or irritant-induced asthma. Occupational asthma is an excellent model to study the pathogenesis and the natural history of adult onset asthma because the responsible agent can be identified, complete avoidance is possible, and exposure can be measured or estimated.