Biomedical Engineering Reference
In-Depth Information
Table 1
Calculated Concentrations of Some Major Components in Gas-Phase
Cigarette Smoke and Their Levels When Deposited in Respiratory Tract Lining
Fluid (RTLF)
In cigarette
(mmol
=
cig)
Component
In RTLF (mM)
Aldehydes
Acetaldehyde
20
2000
Formaldehyde
1.5
150
Acrolein
0.8
80
Crotonaldehyde
0.2
20
Nitrogen oxide
Nitric oxide
12
1200
Nitrogen dioxide
1.0
100
Organic free radicals (alkyl,
alkoxyl, peroxyl)
0.02
2.0
1
l0
17
radicals
=
cig
ΒΌ
0.02 mmol radicals
=
cigarette (11), assuming complete deposition in
respiratory tract lining fluid.
content of MPO in neutrophils, which correlates with the degree of pulmon-
ary dysfunction (13). MPO activity also has a negative correlation with
FEV
1
in patients with COPD, suggesting that neutrophil MPO-mediated
oxidative stress may play a role in the pathogenesis of COPD (13).
Alveolar macrophages obtained by bronchoalveolar lavage (BAL)
fluid from the lungs of smokers are more activated compared with those
obtained from non-smokers. One manifestation of this is the release of
increased amounts of ROS such as O
2
-
and H
2
O
2
(1,14). Exposure to cigar-
ette smoke in vitro has also been shown to increase the oxidative metabolism
of alveolar macrophages. Subpopulations of alveolar macrophages with a
higher granular density appear to be more prevalent in the lungs of smokers
and are responsible for the increased O
2
-
production by smoker's macro-
phages (1).
The generation of ROS in epithelial lining fluid may be further
enhanced by the presence of increased amounts of free iron in the airspaces
in smokers. This is relevant to COPD since the intracellular iron content of
alveolar macrophages is increased in cigarette smokers and is increased
further in those who develop chronic bronchitis, compared with non-smo-
kers (15). In addition, macrophages obtained from smokers release more
free iron in vitro than those from non-smokers (16). The lungs of smokers
contain darkly pigmented areas of high ESR spin heme iron, non-heme iron,
and carbon-centered radicals (7). This mechanism may be responsible for
the excess iron that accumulates in the alveolar macrophages of smokers.
Eosinophils have been shown to be prominent in the airway walls of
both in stable and mild exacerbations of bronchitis. Bronchoalveolar lavage
