Lung Disease in Chinese Textile Workers

摘要 在美国，来自多个行业的至少500万工人可能暴露于空气中。 内毒素急性内毒素暴露产生动态气流阻塞的特征。然而，健康 长期接触的影响尚不清楚。一些慢性内毒素暴露的研究已经确定了一个 1秒用力呼气量（FEV1）加速下降，这是慢性阻塞性肺疾病的标志 肺疾病（COPD）。然而，即使是对慢性暴露的研究，也往往持续不到十年， 人们对停止接触后肺部疾病的发展轨迹、潜在的机制、 疾病的严重程度，以及慢性暴露的肺外效应。这种竞争延续的目标是 是完成一项36年的纵向研究，研究对象是919名纺织工人， 中国上海的地理区域。这一独特的群体包括暴露于高水平的棉花工人， 工作场所内毒素与对照丝绸工人暴露于不可检测水平的内毒素， 终生不吸烟者的比例很高。自1981年以来，他们已经评估了灰尘和内毒素 暴露和呼吸结果。所有的工人现在都退休了，但74.2%的人仍然活着， 30年调查，预计35岁时进行可比的随访参与。先前的延续 这项研究的循环使我们能够描述工作场所内毒素的持续有害影响， 工人退休。呼吸系统不良反应包括肺功能恢复受损，FEV1加速 下降，气道狭窄增加，胸部计算机显示肺肿块和肺密度增加 X线断层扫描（CT），这可能代表持续的肺部炎症。这些发现提出了新的问题： 持续性炎症是否在疾病进展中起作用， 暴露停止，以及长期内毒素暴露是否导致肺外疾病。我们 总体假设是先前累积的工作场所内毒素暴露导致持续性肺部疾病 在由于全身、肺实质和气道炎症而停止暴露后， 肺外健康影响。这一修订后的提案扩大了其范围，以回应批评， 评估一组密集的炎症生物标志物，并考虑空气污染和其他 变量对研究普遍性很重要。我们的研究结果对于设计有效的预防措施至关重要。 程序.本提案涉及的诺拉部门包括：农业、制造业、医疗保健、 服务和建筑。所涉及的跨部门方案是呼吸系统疾病和全球 合作。

ABSTRACT At least 5 million workers in the United States from several sectors are potentially exposed to airborne endotoxin. Acute endotoxin exposure produces features of dynamic airflow obstruction. However, the health effects of long-term exposure remain unclear. A few studies of chronic endotoxin exposure have identified an accelerated decline in forced expiratory volume at 1 second (FEV1), a hallmark of chronic obstructive pulmonary disease (COPD). Even studies of chronic exposure, though, tend to span less than a decade, and little is known about the trajectory of lung disease after exposure cessation, the mechanisms underlying disease severity, and the extra-pulmonary effects of chronic exposure. The goal of this competing continuation is to complete a 36-year longitudinal study of a stable, closed cohort of 919 textile workers living in the same geographical region of Shanghai, China. This unique cohort comprises cotton workers exposed to high levels of workplace endotoxin with matched control silk workers exposed to non-detectable levels of endotoxin, both with a high proportion of lifetime non-smokers. Since 1981, they have been evaluated for dust and endotoxin exposure and respiratory outcomes. All workers are now retired, but 74.2% of those still alive participated in the 30-year survey, with comparable follow-up participation expected at 35 years. The previous continuation cycle of this study enabled us to describe the persistent deleterious effects of workplace endotoxin even after worker retirement. Adverse respiratory effects include impaired lung function recovery with accelerated FEV1 decline, increased airway narrowing, and increased lung mass and lung density on chest computed tomography (CT), which likely represents persistent lung inflammation. These findings raise new questions: whether persistent inflammation plays a role in disease progression, whether disease is reversible after exposure cessation, and whether long-term endotoxin exposure leads to extra-pulmonary disease. Our overarching hypothesis is that prior cumulative workplace endotoxin exposure leads to persistent lung disease after exposure cessation due to systemic, lung parenchymal, and airway inflammation, and also results in extra-pulmonary health effects. This revised proposal has expanded its scope in response to critiques to evaluate a dense panel of inflammatory biomarkers, as well as consideration of air pollution and other variables important to study generalizability. Our research results are essential to devising effective preventive programs. The NORA sectors addressed in this proposal include: agriculture, manufacturing, healthcare, services, and construction. The cross-sector programs addressed are respiratory disease and global collaborations.