Smokers with airway obstruction are at a higher risk of lung cancer than smokers without airway obstruction. Inflammation plays a key role in lung carcinogenesis. This single-center study prospectively assessed (i) the relationship between smoking exposure and the loss of forced expiratory volume in 1 s (FEV1) in determining lung cancer risk and (ii) the effect of lung cancer on systemic inflammation.
The study group comprised 475 consecutively enrolled patients with cancer who presented with pulmonary or cardiac symptoms. The effects of smoking exposure and FEV1 loss on the predicted lung cancer risk were assessed using multiple logistic regression analysis. C-reactive protein (CRP) was used as a marker of inflammation.
The prevalence of lung cancer was 0.23. The lung cancer risk increased with the number of pack years and FEV1 loss (p < 0.01). Moving from the 5th (−22% of the predicted value) to the 95th percentile of FEV1 loss (56% of the predicted value) increased lung cancer risk from 0.07 to 0.23 (Δ = 0.16) at 0 pack years and from 0.39 to 0.73 (Δ = 0.34) at 70 pack years (95th percentile). The values for Δ peaked at 61 pack years (0.34) and then decreased with a further increase in smoking exposure, without reaching the zero mark. Patients with lung cancer were more likely to have a CRP level above the median (4.05 mg/L) than patients with other cancers (adjusted odds ratio = 2.67).
Systemic inflammation is more pronounced in patients with lung cancer than in patients with other cancers. The effect of FEV1 loss on the patients’ predicted risks of lung cancer increases with increasing smoking exposure. Measurements of FEV1 loss are useful to identify patients facing an increased risk of developing lung cancer.