1 Introduction
Cigarette smoking is responsible for 6 million
deaths each year (WHO 2016 ). The 2012 data
indicate that 21 % of the world population aged
15 and more smoked. It is estimated that approx-
imately 32.4 % of men and 23.7 % of women
were smokers in Poland in 2015 (WHO 2016 ).
The impact of smoking on general health is well
documented. Despite numerous anti-tobacco
campaigns, prevalence of smoking-related
diseases is alarming. Chronic obstructive pulmo-
nary disease (COPD), for which smoking is the
major risk factor, was the world’s sixth leading
cause of death in 1990 and is presumed to rank
fourth by 2030 (GOLD 2015 ). Smoking is also
the main risk factor for lung cancer, a leading
cancer worldwide in both genders (WCRF 2016 ).
COPD and lung cancer usually develop after
many years of exposure to tobacco, therefore the
vast majority of studies focus on the long-term
effect of smoking. Exposure to cigarette smoke
(CS) increases the production of a variety of
compounds which trigger a complex inflamma-
tory response leading to structural changes in the
respiratory tract. The proinflammatory
compounds include tumor necrosis factor α
(TNF-α), interleukin 1β(IL-1β), granulocyte-
macrophage colony stimulating factor
(GM-CSF), interleukin 8 (IL-8), transforming
growth factor β (TGF-β), metalloproteinases,
cathepsins, neutrophil elastase, and reactive oxy-
gen species (Rovina et al. 2013 ).
Research on the acute effect of cigarette
smoke is less extensive. Smoking is followed
by instant changes the physico-chemical
properties of exhaled breath condensate causing
an increase in its electric conductivity (Koczulla
et al. 2010 ), changes in pH, in markers of oxida-
tive stress, and in the cytokine and chemokine
profiles (Konstantinidi et al. 2015 ). It has been
documented that acute exposure to CS stimulates
the release of IL-1βand TNF-αby peripheral
blood mononuclear cells (Ryder et al. 2002 ),
increases the plasma level of malondialdehyde
(MDA), a marker of oxidative stress, and reduces
the plasma antioxidant potential (Durak
et al. 2000 ). There is evidence that CS elicits
the production of IL-1β by peripheral blood
mononuclear cells in in vitro (Ryder
et al. 2002 ). CS also causes short-term alterations
in the cellular composition of induced sputum in
healthy intermittent smokers (van der Vaart
et al. 2005 ). Studies involving bronchoalveolar
lavage fluid have shown that CS stimulates influx
of dendritic cells, mononuclear cells, and
neutrophils to the airways (van der Toorn
et al. 2013 ; Lommatzsch et al. 2010 ), and an
increase of oxidative stress (van der Vaart
et al. 2004 ). The evaluation of the inflammatory
response to acute CS exposure has been
performed at various time intervals, ranging
from 5 to 15 min (Koczulla et al. 2010 ; Ryder
et al. 2002 ) to 8 days (van der Vaart et al. 2005 )
after smoking. Some studies consist of serial
measurements (Koczulla et al. 2010 ; van der
Vaart et al. 2005 ).
Given different biologic samples tested and
different time points at which the effect of short
term smoking on the airways has been
investigated, we undertook this study to evaluate
the level of TNF-α, IL-1β, and MDA in exhaled
breath condensate (EBC), as measures of inflam-
mation and oxidative stress burden, in response
to acute CS exposure, i.e., 60 min after smoking a
single cigarette, in smokers suffering from
COPD and in healthy smokers.2 Methods2.1 Study DesignThe study protocol was approved by the Bioeth-
ics Committee of the Medical University of
Warsaw in Poland (permit #KB/106/2013). All
the study participants signed informed consent.
The study involved two groups: smoking patients
with stable COPD and young healthy asymptom-
atic smokers. In each group, EBC was collected74 M. Maskey-Warze ̨ chowska et al.