Respiratory Treatment and Prevention (Advances in Experimental Medicine and Biology)

study protocol. Durak et al. ( 2000 ) have
investigated serum markers of oxidative stress
in healthy subjects after smoking full flavor and
full flavor low tar cigarettes (23 mg and 12 mg tar
content, respectively) and demonstrated a lower
burden of oxidative stress after smoking the lat-
ter. The cigarettes used in our study had 6 mg tar
content. We may assume that lower tar and nico-
tine content induce smaller alterations in the
cytokine profile of biological samples from
smokers.
Interestingly, the present results showed a
negative relationship between EBC TNF-αcon-
centration after smoking and FEV 1 /FVC in
healthy smokers. To our knowledge, this correla-
tion has not been reported before. This relation-
ship suggests that monitoring of TNF-αlevel in
smokers may be useful in the identification of
subjects at risk for COPD. TNF-αis considered a
major player in connective tissue damage in
response to CS (Comandini et al. 2009 ), promot-
ing COPD-related inflammation at the local and
systemic levels (Go ́rska et al. 2010 ; Tanni
et al. 2010 ). The influence of smoking on annual
FEV 1 decline has been well documented
(Fletcher and Peto 1977 ), and a decreased
FEV 1 /FVC ratio is the main functional criterion
for COPD diagnosis (GOLD 2015 ). Therefore, it
seems that smoking young subjects who demon-
strate a relationship between FEV 1 /FVC and air-
way inflammation markers involved in the
pathogenesis of COPD should be the target for
smoking-cessation initiatives and COPD screen-
ing programs. That is supported by a review of
Kotz et al. ( 2007 ) who provide evidence that
smoking has early negative effects on lung func-
tion in young smokers with a short smoking
history.
Our study has several limitations. Firstly,
there was a significant difference between both
analyzed groups in terms of smoking history.
This was imposed by one of the aims of the
study, i.e., the comparison of the effect of CS in
young healthy smokers and patients with COPD.
Healthy subjects obviously had to have a less
relevant smoking history, mainly due to a shorter
time of smoking. Secondly, our measurements
were performed only at two time points, i.e.,

before and 60 min after smoking. Serial

measurements could better reflect the airway

inflammatory response to CS over time, but

their application in the clinical setting is rather

difficult due to time duration and cost. Our study

aimed at the evaluation of a rapid airway inflam-

matory response to CS exposure, hence we chose

the assessment at two time points.

5 Conclusions

Acute cigarette smoke exposure does not

increase the concentration of TNF-α, IL-1β, and

malondialdehyde in the exhaled breath conden-

sate in both smoking COPD patients and healthy

asymptomatic smokers. Short-term cigarette

smoke-induced oxidative stress is higher in

young smokers than in COPD patients, what

indicates a greater susceptibility to cigarette

smoke content of young smokers.

Acknowledgements The authors would like to thank

Piotr Korczynski for his assistance in the preparation of

the manuscript.

Conflicts of Interest The authors declare no conflict of

interest related to the contents of this article.

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