Raymond L W
Division of Pulmonary and Critical Care Medicine, Department of Medicine, Baylor College of Medicine, Houston, TX USA.
Chest. 1996 Apr;109(4):1010-8. doi: 10.1378/chest.109.4.1010.
Seven repair technicians (RT, site A) repeatedly exposed to facsimile machine fume developed recurring sore throat, fever, lymphadenopathy, chest tightness, dry cough, and dyspnea. The fume concentration was low (0.6 mg/m3 of breathing-zone air) but it contained butyl methacrylate (BMA), a known skin sensitizer. Although chest radiographs were normal, three of the seven RT-A had lung crackles and spirometric abnormalities, and increased serum levels of immunoglobulins IgE or IgM. Symptoms and most other abnormalities improved when exposure to BMA was stopped. We later evaluated workers in two other sites (B and C). Six RT-B had daily contact with BMA fume (0.14 to 0.40 mg/m3 of air) at a field repair depot. Six administrative and six sales staff members (AS-B, SS-B) without regular fume exposure served as controls. All RT-B had elevated serum IgE levels (202+/-69 U/mL [SEM]; normal <41 U/mL). IgE and fume levels were positively correlated (r=0.83). four RT-B had lung crackles, but few symptoms and normal results of spirometry. The crackles cleared 8 weeks after substitution of a BMA-free paper, but IgE levels remained high (201+/-69). The nonexposed AS-B and SS-B had no crackles. Their IgE levels were normal (19+/-4 U/mL [SEM]; p<0.01). The crackles suggest BMA fume might have caused inflammation in terminal airways units. The significance of the IgE elevations is also uncertain since this class of antibodies is usually associated with asthma, not pneumonitis. In view of these uncertainties, BMA was eliminated from the facsimile transceiver process. Follow-up of group C workers (n=32) found no symptoms, lung crackles, or abnormal results of spirometry. However, IgE concentrations were elevated in 15 and remained so for 21 months, perhaps because of continuing exposure to residual low levels of BMA. These findings suggest that BMA-bearing facsimile fume caused increased IgE levels in RT at sites A, B, and C, and might have resulted in permanent lung injury if such exposure had continued.
七名维修技术员（RT，A站点）反复接触传真机烟雾后，出现了反复的喉咙痛、发热、淋巴结病、胸闷、干咳和呼吸困难。烟雾浓度很低（呼吸区空气中为0.6毫克/立方米），但其中含有甲基丙烯酸丁酯（BMA），一种已知的皮肤致敏剂。尽管胸部X光片正常，但七名A站点的维修技术员中有三人出现肺部啰音和肺功能异常，血清免疫球蛋白IgE或IgM水平升高。停止接触BMA后，症状和大多数其他异常情况有所改善。我们随后评估了另外两个站点（B和C）的工人。六名B站点的维修技术员在一个现场维修站每天接触BMA烟雾（空气中0.14至0.40毫克/立方米）。六名行政人员和六名销售人员（AS-B，SS-B），他们没有经常接触烟雾，作为对照组。所有B站点的维修技术员血清IgE水平均升高（202±69 U/mL[标准误]；正常<41 U/mL）。IgE水平与烟雾浓度呈正相关（r = 0.83）。四名B站点的维修技术员有肺部啰音，但症状较少，肺功能检查结果正常。更换无BMA的纸张8周后，啰音消失，但IgE水平仍然很高（201±69）。未接触烟雾的AS-B和SS-B没有啰音。他们的IgE水平正常（19±4 U/mL[标准误]；p<0.01）。啰音表明BMA烟雾可能导致了终末气道单位的炎症。IgE升高的意义也不确定，因为这类抗体通常与哮喘有关，而非肺炎。鉴于这些不确定性，BMA被从传真收发过程中去除。对C组工人（n = 32）的随访发现没有症状、肺部啰音或肺功能异常检查结果。然而，15人的IgE浓度升高，并持续了21个月，这可能是因为持续接触残留的低水平BMA。这些发现表明，含BMA的传真烟雾导致A、B和C站点的维修技术员IgE水平升高，如果继续接触，可能会导致永久性肺损伤。
