Division of Pulmonary, Critical Care, and Sleep Medicine, Department of Medicine, New York University School of Medicine, New York; Bureau of Health Services and Office of Medical Affairs, Fire Department of New York, Brooklyn.
Division of Pulmonary, Critical Care, and Sleep Medicine, Department of Medicine, New York University School of Medicine, New York.
Chest. 2012 Aug;142(2):412-418. doi: 10.1378/chest.11-1202.
The World Trade Center (WTC) collapse on September 11, 2001, produced airflow obstruction in a majority of firefighters receiving subspecialty pulmonary evaluation (SPE) within 6.5 years post-September 11, 2001.
In a cohort of 801 never smokers with normal pre-September 11, 2001, FEV1, we correlated inflammatory biomarkers and CBC counts at monitoring entry within 6 months of September 11, 2001, with a median FEV(1) at SPE (34 months; interquartile range, 25-57). Cases of airflow obstruction had FEV(1) less than the lower limit of normal (LLN) (100 of 801; 70 of 100 had serum), whereas control subjects had FEV(1) greater than or equal to LLN (153 of 801; 124 of 153 had serum).
From monitoring entry to SPE years later, FEV(1) declined 12% in cases and increased 3% in control subjects. Case subjects had elevated serum macrophage derived chemokine (MDC), granulocyte-macrophage colony-stimulating factor (GM-CSF), granulocyte colony-stimulating factor, and interferon inducible protein-10 levels. Elevated GM-CSF and MDC increased the risk for subsequent FEV(1) less than LLN by 2.5-fold (95% CI, 1.2-5.3) and 3.0-fold (95% CI, 1.4-6.1) in a logistic model adjusted for exposure, BMI, age on September 11, 2001, and polymorphonuclear neutrophils. The model had sensitivity of 38% (95% CI, 27-51) and specificity of 88% (95% CI, 80-93).
Inflammatory biomarkers can be risk factors for airflow obstruction following dust and smoke exposure. Elevated serum GM-CSF and MDC levels soon after WTC exposure were associated with increased risk of airflow obstruction in subsequent years. Biomarkers of inflammation may help identify pathways producing obstruction after irritant exposure.
2001 年 9 月 11 日，世界贸易中心（WTC）倒塌，导致在 2001 年 9 月 11 日后的 6.5 年内接受专业肺评估（SPE）的大多数消防员出现气流阻塞。
在一组 801 名从不吸烟且在 2001 年 9 月 11 日前 FEV1 正常的人群中，我们将监测进入 9 月 11 日后 6 个月内的炎症生物标志物和 CBC 计数与 SPE 时的中位 FEV1（34 个月；四分位间距，25-57）相关联。气流阻塞病例的 FEV1 低于正常下限（LLN）（801 例中的 100 例；血清中有 70 例），而对照组的 FEV1 大于或等于 LLN（801 例中的 153 例；血清中有 124 例）。
从监测进入到多年后的 SPE，病例组的 FEV1 下降了 12%，对照组增加了 3%。病例组的血清巨噬细胞衍生趋化因子（MDC）、粒细胞-巨噬细胞集落刺激因子（GM-CSF）、粒细胞集落刺激因子和干扰素诱导蛋白-10 水平升高。升高的 GM-CSF 和 MDC 使随后 FEV1 低于 LLN 的风险增加了 2.5 倍（95%CI，1.2-5.3）和 3.0 倍（95%CI，1.4-6.1），在调整暴露、BMI、2001 年 9 月 11 日的年龄和多形核中性粒细胞的逻辑模型中。该模型的灵敏度为 38%（95%CI，27-51），特异性为 88%（95%CI，80-93）。
炎症生物标志物可能是尘烟暴露后气流阻塞的危险因素。WTC 暴露后不久血清 GM-CSF 和 MDC 水平升高与随后几年气流阻塞的风险增加相关。炎症生物标志物可能有助于识别刺激物暴露后产生阻塞的途径。
