Is the Exhaled Breath Temperature Sensitive to Cigarette Smoking?

The smoking habit is accompanied by an acute inflammatory response which follows tissue injury. It would be desirable to find a non-invasive inflammatory marker that would simplify the task of studying and monitoring smokers more simply and allow us to identify populations at risk of contracting Chronic Obstructive Pulmonary Disease (COPD). Today's expectations regarding research focus on issues ranging from inflammatory markers to those of exhaled breath temperature (EBT) are considerable. That said, although the EBT has been largely studied in asthma and COPD, there have not been any studies thus far that have analysed the effect of cigarette smoking on the EBT. Bearing this in mind, in this longitudinal study we aim to analyse the EBT in current smokers, monitor the effects both of cigarette smoking on EBT and of what happens after smoking cessation. Twenty-five (25) smokers (59.5 ± 3.1 yrs, 12 M) who participated in a multi-disciplinary smoking cessation programme and 25 healthy never-smokers (58.7 ± 2.9, 13 M) underwent EBT measurement. EBT values were higher in smokers before smoking (T0) than in never-smokers [34.6 (34.2-35) vs 33.2 (32.4-33.7)°C, p < 0.001. The smokers repeated measurement 5 minutes after smoking a cigarette (T1) and 2 hours after (T2). They repeated EBC measurement after 1 week (T3) and then after 3 months (T4) from smoking cessation. EBT is higher in smokers compared to controls. EBT increases after cigarette smoking and progressively decreases with the increase of time from when the last cigarette was smoked. Thus, we can conclude that EBT is increased in smokers and also sensitive to the acute effect of cigarette smoke.

Exhaled breath temperature in NSCLC: could be a new non-invasive marker?

The exhaled breath temperature (EBT) has been proven to be the expression of airways inflammation as well as of the increased vascularity. Although both these conditions characterize lung cancer pathogenesis, this is the first study where the EBT has been analysed in patients affected by non-small-cell lung cancer. The aim of this study was to verify whether and how the lung cancer being examined influences the EBT for possible future clinical implications. Eighty-two consecutive subjects with a radiological suspicion of lung cancer were enrolled and underwent standard diagnostic and staging procedures for cancer. EBT was measured in all the subjects at the enrolment with the X-Halo device. Forty patients resulted as affected by lung cancer while 42 as false-positive (controls). We found a higher EBT in NSCLC patients compared to healthy subjects. The EBT was correlated with number of packs/year and associated with the stage of lung cancer. We identified a cut-off value for the EBT that is able to screen patients with lung cancer with a high sensitivity and specificity. Our results suggest that lung cancer causes an increase in the EBT, which, whether confirmed and validated, could become a new non-invasive clinical tool in the screening and monitoring of this disease.

Cigarette smoke and increased COX-2 and survivin levels in exhaled breath condensate of lung cancer patients: how hot is the link?

UNLABELLED: One of the most current intriguing hypotheses on lung cancerogenesis envisages a role for inflammation as a possible trigger of both epithelial-mesenchymal transition and cancer development. Cigarette smoke has been suggested to be the main factor underlying the inflammation of the airways described in lung cancer patients. Cycloxygenase and survivin, a COX-2 dependent factor of apoptosis resistance, seem to play a key role in this regard. PURPOSE: The aim of this study was to study COX-2 and survivin in the airways of lung cancer patients and in those of a group of smokers in a view to increasing our understanding of the link between smoking, airway inflammation and lung cancer. PATIENTS AND METHODS: 70 NSCLC patients (28 smokers, 26 ex-smokers and 16 non-smokers) and 30 healthy subjects (20 smokers and 10 non-smokers) were enrolled in the study. Both COX-2 and survivin concentrations were measured in the exhaled breath condensates of all the subjects under study using EIA kits. RESULTS: Higher levels of exhaled survivin and COX-2 were found in NSCLC patients compared to healthy smokers and non-smokers. These levels were observed to be significantly elevated in smokers (patients with lung cancer and healthy) and ex-smokers compared to non-smokers and exhibited a positive correlation with the number of cigarettes smoked expressed as pack/year. A correlation was also found between exhaled COX-2 and survivin and the progression of cancer. CONCLUSIONS: We support the hypothesis that cigarette smoke be strongly connected to the inflammation of the airways observed in lung cancer patients. On the basis of the results obtained the use of exhaled breath condensate COX-2 and survivin levels could be suggested as two potential markers within an early non-invasive screening of populations of smokers at risk of lung cancer.