Cigarette Smoking, and Blood Monocyte Count Correlate with Chronic Lung Injuries and Mortality

Abstract

Background

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.

Methods

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.

Results

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_CO). 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_CO.

Conclusion

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.

Keywords:

• smoking
• monocyte
• pulmonary fibrosis
• lung cancer
• mortality
• emphysema

Abbreviations

AM, alveolar macrophage; BMI, body mass index; CAD, coronary artery disease; CBC, complete blood count; CL, centrilobular; CS, cigarette smoking; COPD, chronic obstructive pulmonary disease; CPD, cigarettes smoked per day; CPY, composite pack years; DIP, desquamative interstitial pneumonia; DLCO, diffusing capacity for carbon monoxide; FEV₁, forced expiratory volume in one second; FVC, forced vital capacity; GGO, ground glass opacity; HC, honeycombing; HSD, honest significant difference; ILAs, interstitial lung abnormalities; ILD, interstitial lung disease; IPF, idiopathic pulmonary fibrosis; IQR, interquartile range; MCH, mean corpuscular hemoglobin; MCHC, mean corpuscular hemoglobin concentration; MCV, mean corpuscular volume; OP, organizing pneumonia; PAD, peripheral artery disease; PBM, peribronchiolar metaplasia; PFT, pulmonary function test; PS, paraseptal; PY, pack years; Q1 to 4, quartile 1 to 4; RBC, red blood cell; RB-ILD, respiratory bronchiolitis-ILD; RV, residual volume; TB, traction bronchiectasis; TLC, total lung capacity; WBC, white blood cell.

Data Sharing Statement

All data generated or analyzed during this study are included in this published article.

Ethics Statements

Ethics committee: the study protocol was approved by the Institutional Review Board of West Virginia University (ID 2010131995). The written informed consent was waived by the IRB considering its qualification for exempt research category 4: “secondary research”. The identifiable private information was recorded by the investigators in such a manner that the identity of the human subjects could not readily be ascertained directly or through identifiers linked to the subjects, the investigator did not contact the subjects, and the investigator did not re-identify subjects. The data related to study was collected confidentially to maintain HIPAA compliance. All ethical standards were adhered in accordance with the Declaration of Helsinki.

Acknowledgments

Authors sincerely thank Esra Alshaikhnassir, MD, from the Department of Pathology, West Virginia University for the photomicrographs representing lung histology findings.

Author Contributions

All authors made a significant contribution to the work reported, whether that is in the conception, study design, execution, acquisition of data, analysis and interpretation, or in all these areas; took part in drafting, revising or critically reviewing the article; gave final approval of the version to be published; have agreed on the journal to which the article has been submitted; and agree to be accountable for all aspects of the work.

Disclosure

The authors declare they have no financial or non-financial competing interests in this work.

Additional information

Funding

There is no funding to report.