Section of Pulmonary, Critical Care and Sleep Medicine, Department of Medicine, West Virginia University, Morgantown, WV, USA.
Department of Radiology, West Virginia University, Morgantown, WV, USA.
Int J Chron Obstruct Pulmon Dis. 2023 Apr 1;18:431-446. doi: 10.2147/COPD.S397667. eCollection 2023.
Cigarette smoking (CS)-related monocytosis contributes to the development of chronic lung injuries via complex mechanisms. We aim to determine correlations between measures of CS and monocytes, their capacities to predict chronic lung diseases, and their associations with mortality.
A single-center retrospective study of patients undergoing surgical resection for suspected lung nodules/masses was performed. CS was quantified as cigarettes smoked per day (CPD), duration of smoking, composite pack years (CPY), current smoking status, and smoking cessation years. A multivariate logistic regression analysis was performed.
Of 382 eligible patients, 88% were ever smokers. In this group, 45% were current smokers with mean CPD of 27.2±40.0. CPY and duration of smoking showed positive linear correlations with percentage monocyte count. Physiologically, CPY was associated with progressive obstruction, hyperinflation, and reduced diffusion capacity (DL). Across the quartiles of smoking, there was an accumulation of radiologic and histologic abnormalities. Anthracosis and emphysema were associated with CPD, while lung cancer, respiratory bronchiolitis (RB), emphysema, and honeycombing were statistically related to duration of smoking. Analysis using consecutive CPY showed associations with lung cancer (≥10 and <30), fibrosis (≥20 and <40), RB (≥50), anthracosis and emphysema (≥10 and onwards). Percentage monocytes correlated with organizing pneumonia (OP), fibrosis, and emphysema. The greater CPY increased mortality across the groups. Significant predictors of mortality included percentage monocyte, anemia, GERD, and reduced DL.
Indices of CS and greater monocyte numbers were associated with endpoints of chronic lung disease suggesting a participation in pathogenesis. Application of these easily available metrics may support a chronology of CS-induced chronic lung injuries. While a relative lesser amount of smoking can be associated with lung cancer and fibrosis, greater CPY increases the risk for emphysema. Monocytosis predicted lung fibrosis and mortality. Duration of smoking may serve as a better marker of monocytosis and associated chronic lung diseases.
与吸烟有关的单核细胞增多症通过复杂的机制导致慢性肺损伤的发展。我们旨在确定吸烟量和单核细胞之间的相关性，它们预测慢性肺部疾病的能力，以及它们与死亡率的关系。
对因疑似肺结节/肿块而行手术切除的患者进行了一项单中心回顾性研究。吸烟量以每天吸烟的支数（CPD）、吸烟持续时间、复合包年数（CPY）、当前吸烟状况和戒烟年数来衡量。进行了多变量逻辑回归分析。
在 382 名合格患者中，88%为曾吸烟者。在这组患者中，45%为当前吸烟者，平均 CPD 为 27.2±40.0。CPY 和吸烟持续时间与单核细胞百分比呈正线性相关。从生理上讲，CPY 与进行性阻塞、肺气肿和弥散能力降低（DL）有关。在吸烟的四分位数中，存在放射学和组织学异常的积累。炭末沉着症和肺气肿与 CPD 相关，而肺癌、呼吸性细支气管炎（RB）、肺气肿和蜂窝肺与吸烟持续时间有统计学上的关联。使用连续 CPY 进行分析显示与肺癌（≥10 且<30）、纤维化（≥20 且<40）、RB（≥50）、炭末沉着症和肺气肿（≥10 且持续存在）相关。单核细胞百分比与机化性肺炎（OP）、纤维化和肺气肿相关。CPY 越高，各组的死亡率越高。死亡率的显著预测因子包括单核细胞百分比、贫血、胃食管反流病（GERD）和 DL 降低。
吸烟指数和更高的单核细胞数量与慢性肺部疾病的终点相关，提示其参与发病机制。应用这些易于获得的指标可能有助于支持 CS 引起的慢性肺损伤的时间顺序。虽然相对较少的吸烟可能与肺癌和纤维化有关，但 CPY 越高，患肺气肿的风险就越大。单核细胞增多症预测肺纤维化和死亡率。吸烟持续时间可能是单核细胞增多症和相关慢性肺部疾病的更好标志物。
