[接触致敏金属引起的职业病]。

Y Kusaka
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引用次数: 29

摘要

由职业接触致敏金属引起的疾病,包括铂(Pt),铑(Rh),镍(Ni),铬(Cr),钴(Co),金(Au),汞(Hg),锆(Zr)和铍(Be)。由金属引起的过敏反应是根据库姆斯和盖尔的分类来描述的。未证实致敏潜力的金属,如果报告非常罕见或缺乏令人信服的过敏证据,则不讨论。致敏金属是半抗原,它们本身不能作为抗原。有证据表明,金属与循环蛋白或组织蛋白结合会产生新的抗原。另一种假设是,这些金属干扰了免疫反应的抗原识别步骤。金属的免疫调节作用或免疫毒性也可能与金属诱发的超敏反应有关。职业性暴露于Pt、Rh、Ni、Cr和Co可通过I型过敏反应引起过敏性哮喘,其中受影响个体的血清显示针对精神-人血清白蛋白偶联物的特异性IgE抗体。一些接受金盐治疗的类风湿关节炎患者发生II型和/或III型过敏反应引起的肾小球肾炎、血小板减少症或粒细胞缺乏症。职业性接触汞可引起肾小球肾炎,其中III型反应参与其中。接触金属后,皮肤也会发生IV型超敏反应:接触Ni、Cr、Co、Rh和Hg可诱发过敏性接触性皮炎;皮肤肉芽肿是由接触Zr和Be形成的。它也是肺部的致敏剂,导致肉芽肿病。金属过敏性疾病的诊断是在金属抗原的过敏试验的基础上进行的,包括皮肤试验、特异性抗体的放射过敏原吸附试验、淋巴细胞转化试验、巨噬细胞迁移抑制试验和激发试验。特应性是诱发因素,吸烟是诱发金属诱发哮喘的危险因素。遗传因素在金属接触性皮炎发展中的证据是相互矛盾的,尽管动物模型暗示遗传因素与某些金属的皮肤致敏和Be的呼吸致敏有关。皮肤刺激、前臂损伤、特应性皮炎并发症及伴随的其他药物致敏是皮炎预后的决定因素。本文综述了工业金属过敏反应引起的职业病的流行病学报告,包括患病率和过敏表现。有一篇铂减敏治疗铂哮喘患者的临床试验报告。评价金属敏化电位的预测方法已经发展起来,人们正在寻求更客观地量化电位的新方法。
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[Occupational diseases caused by exposure to sensitizing metals].

Diseases caused by occupational exposure to sensitizing metals including platinum (Pt), rhodium (Rh), nickel (Ni), chromium (Cr), cobalt (Co), gold (Au), mercury (Hg), zirconium (Zr) and beryllium (Be) are reviewed. Allergic reactions induced by the metals are described according to the classification by Coombs and Gell. Metals with unproven sensitizing potential are not discussed if reports on these are either very rare or devoid of convincing evidence for allergic involvement. The sensitizing metals are haptens which are not themselves able to act as antigens. There is evidence that combination of the metals with circulating or tissue protein gives rise to new antigens. An alternative hypothesis is that these metals interfere with the antigen recognition step of the immune response. Immunomodulatory effects or immunotoxicity of the metals may be also involved in metal-induced hypersensitivity. Occupational exposure to Pt, Rh, Ni, Cr, and Co causes allergic asthma via type I allergic reaction in which serum from affected individuals shows specific IgE antibodies against mental-human serum albumin conjugates. Some rheumatoid arthritis patients treated with gold salt therapy develop glomerulonephritis, thrombocytopenia, or agranulocytosis, which arise from type II and/or type III allergic reactions. Occupational exposure to mercury causes glomerulonephritis in which involvement of type III reaction is suggested. Type IV hypersensitivity reaction of the skin also takes place following exposure to the metals: allergic contact dermatitis is evoked by exposure to Ni, Cr, Co, Rh, and Hg; cutaneous granuloma is formed by contact with Zr and Be. Be is also a sensitizer of the lungs, resulting in granulomatous disease. Diagnosis of metal-induced allergic diseases is made on the basis of allergological tests with metal antigens including skin tests, radioallergosorbent test for specific antibody, lymphocyte transformation test, macrophage migration inhibition test, and provocation test. Atopy is a predisposing factor and smoking is a risk factor for developing metal-induced asthma. Evidence for genetic factors in the development of metal contact dermatitis is conflicting, although animal models implicate genetic factors in skin sensitization with some metals and respiratory sensitization with Be. Skin irritation, forearm injury, complication with atopic dermatitis and concomitant sensitization to other agents are determinants for prognosis of the dermatitis. Epidemiological reports of occupational diseases from allergic reactions to metals in industries are reviewed with respect to prevalence and allergic manifestations. There is a report on a clinical trial of hyposensitization with Pt in a platinum asthma patient. Predictive methods for evaluating sensitization potential of metals have been developed and new methods, which quantify potential more objectively, are sought.

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