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接触生物气溶胶的垃圾收集工和污水处理工人体内的克拉拉细胞蛋白和表面活性蛋白B

Clara cell protein and surfactant protein B in garbage collectors and in wastewater workers exposed to bioaerosols.

作者信息

Steiner D, Jeggli S, Tschopp A, Bernard A, Oppliger A, Hilfiker S, Hotz P

机构信息

Occupational and Environmental Medicine Unit, Sumatrastrasse 30, 8006, Zurich, Switzerland.

出版信息

Int Arch Occup Environ Health. 2005 Apr;78(3):189-97. doi: 10.1007/s00420-004-0586-2. Epub 2005 Mar 16.

Abstract

OBJECTIVES

Inhalation of bioaerosols has been hypothesised to cause "toxic pneumonitis" that should increase lung epithelial permeability at the bronchioloalveolar level. Serum Clara cell protein (CC16) and serum surfactant protein B (SPB) have been proposed as sensitive markers of lung epithelial injury. This study was aimed at looking for increased lung epithelial permeability by determining CC16 and SPB in workers exposed to bioaerosols from wastewater or garbage.

METHODS

Subjects (778 wastewater, garbage and control workers; participation 61%) underwent a medical examination, lung function tests [American Thoracic Society (ATS) criteria], and determination of CC16 and SPB. Symptoms of endotoxin exposure and several potential confounders (age, gender, smoking, kidney function, obesity) were looked for. Results were examined with multiple linear or logistic regression.

RESULTS

Exposure to bioaerosols increased CC16 concentration in the wastewater workers. No effect of exposure on SPB was found. No clue to work-related respiratory diseases was found.

CONCLUSIONS

The increase in CC16 in serum supports the hypothesis that bioaerosols cause subclinical "toxic pneumonitis", even at low exposure.

摘要

目的

有假设认为,吸入生物气溶胶会导致“中毒性肺炎”,进而在细支气管肺泡水平增加肺上皮通透性。血清克拉拉细胞蛋白(CC16)和血清表面活性蛋白B(SPB)被认为是肺上皮损伤的敏感标志物。本研究旨在通过检测接触废水或垃圾生物气溶胶的工人的CC16和SPB,寻找肺上皮通透性增加的情况。

方法

研究对象(778名废水、垃圾处理工人及对照工人;参与率61%)接受了医学检查、肺功能测试[美国胸科学会(ATS)标准],并检测了CC16和SPB。调查了内毒素暴露症状及几个潜在混杂因素(年龄、性别、吸烟、肾功能、肥胖)。结果采用多元线性或逻辑回归分析。

结果

废水处理工人接触生物气溶胶后CC16浓度升高。未发现暴露对SPB有影响。未发现与工作相关的呼吸系统疾病线索。

结论

血清中CC16升高支持了生物气溶胶即使在低暴露水平也会导致亚临床“中毒性肺炎”的假设。

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