Schwartz D A, Galvin J R, Dayton C S, Stanford W, Merchant J A, Hunninghake G W
Department of Internal Medicine, University of Iowa, Iowa City 52242.
J Appl Physiol (1985). 1990 May;68(5):1932-7. doi: 10.1152/jappl.1990.68.5.1932.
We evaluated whether restrictive lung function among asbestos-exposed individuals with pleural fibrosis was caused by radiographically inapparent parenchymal inflammation and/or parenchymal fibrosis. All 24 study participants were sheet metal workers who were nonsmokers with normal parenchyma on posteroanterior chest radiograph. These subjects had either normal pleura (n = 7), circumscribed plaques (n = 9), or diffuse pleural thickening (n = 8). After controlling for age, years in the trade, and pack-years of smoking, we found that sheet metal workers with diffuse pleural thickening had a lower forced vital capacity (P less than 0.001), total lung capacity (P less than 0.01), and CO-diffusing capacity of the lung (P less than 0.05) than those with normal pleura. Similarly, sheet metal workers with circumscribed plaques were found to have a reduced forced vital capacity; however, because of the small number of study subjects, this difference (regression coefficient = -11.0) was only marginally significant (P = 0.06). Although circumscribed plaque and diffuse pleural thickening were both associated with a lymphocytic alveolitis and a higher prevalence of parenchymal fibrosis on high-resolution computerized tomography (HRCT) scan, neither a lymphocytic alveolitis nor the finding of parenchymal fibrosis on HRCT scan influenced the relationship between pleural fibrosis and restrictive lung function. We conclude that pleural fibrosis is associated with restrictive lung function and abnormally low diffusion that appears to be independent of our measures of parenchymal injury (chest X-ray, bronchoalveolar lavage, and HRCT scan).(ABSTRACT TRUNCATED AT 250 WORDS)
我们评估了患有胸膜纤维化的石棉暴露个体的限制性肺功能是否由影像学上不明显的实质炎症和/或实质纤维化引起。所有24名研究参与者均为钣金工人,他们不吸烟,后前位胸部X光片显示实质正常。这些受试者的胸膜要么正常(n = 7),要么有局限性斑块(n = 9),要么有弥漫性胸膜增厚(n = 8)。在控制了年龄、行业工作年限和吸烟包年数后,我们发现,与胸膜正常的钣金工人相比,有弥漫性胸膜增厚的工人其用力肺活量(P < 0.001)、肺总量(P < 0.01)和肺一氧化碳弥散量(P < 0.05)更低。同样,发现有局限性斑块的钣金工人用力肺活量降低;然而,由于研究对象数量较少,这种差异(回归系数 = -11.0)仅具有边缘显著性(P = 0.06)。尽管局限性斑块和弥漫性胸膜增厚均与淋巴细胞性肺泡炎以及高分辨率计算机断层扫描(HRCT)上实质纤维化的较高患病率相关,但HRCT扫描上的淋巴细胞性肺泡炎和实质纤维化发现均未影响胸膜纤维化与限制性肺功能之间的关系。我们得出结论,胸膜纤维化与限制性肺功能以及异常低的弥散相关,这似乎独立于我们对实质损伤的测量指标(胸部X光、支气管肺泡灌洗和HRCT扫描)。(摘要截断于250字)