Page 75 - Organic Electronics in Sensors and Biotechnology

52 Cha pte r T w o

role in a wide range of inflammatory illnesses has been recently
1–3
highlighted. In the following, a brief overview of both the toxic
and physiological role of the above-mentioned inorganic gases is
reported.
Carbon monoxide is a colorless and odorless gas produced during
the incomplete combustion of organic fuels (natural gas, wood, petrol,
and charcoal). In urban context, motor vehicle emissions are the pri-
mary source of CO, and about 90% of the CO released in such condi-
tion is due to road traffic. Average carbon monoxide concentration in
the outdoor air is about 100 ppb, but it may reach up to 200 ppm in the
urban areas during rush hours.
The toxicity of carbon monoxide resides in its greater capability
to bond hemoglobin with respect to the oxygen, eventually reducing
the amount of oxygen that human cells need for mitochondrial respi-
ration. Progressive exposures to CO can result in fatigue, angina,
reduced visual perception, reduced dexterity, and finally death. The
elderly, children, and people with preexisting respiratory diseases are
particularly susceptible to carbon monoxide pollution. The recom-
mended exposure limit set by the Occupational Safety and Health
Administration (OSHA) is 50 ppm during a typical 8 h day with a
ceiling level of 200 ppm.
Despite the toxic effects, CO has a potential protective role against
oxidative stress. CO is produced endogenously in the human body
4, 5
by a class of enzymes known as heme oxygenase (HO-1 and HO-2). 6
HO enzymes are activated by various stimulant factors including
proinflammatory cytokines and nitric oxide. HO-1 catalyzes the ini-
7
tial and rate-determining step in the oxidative degradation of heme
to the antioxidant bilirubin. Employing NADPH (reduced nicotina-
mide adenine dinucleotide phosphate) and molecular oxygen, the
HO-1 enzyme cleaves a meso carbon of the heme molecule, produc-
ing biliverdin, free iron, and CO. Biliverdin is subsequently converted
to bilirubin by the bilirubin reductase. CO produced in the bilirubin
synthesis has several biological activities including stimulation of the
guanylate cyclase, which eventually activates the immunodefensive
mechanisms against inflammatory diseases. CO is normally present in
the exhaled air of healthy subjects at detectable concentrations of 1 to
3 ppm, while it increases up to 3 to 7 ppm in patients with inflamma-
8
tory pulmonary diseases such as bronchial asthma, bronchiectasis,
upper respiratory tract infections, and seasonal allergic rhinitis. 3, 8
Treatments with inhaled and oral corticosteroids, which have been
shown to reduce airway inflammation, have been associated with a
reduction in the exhaled levels of CO in asthma patients. Based on
9
these findings, it has been proposed that the measurements of CO
concentration in exhaled air may serve as an indirect marker of air-
way inflammation. Moreover, recent reports demonstrated an
increase of exhaled CO concentrations also in other diseases such as
cystic fibrosis and diabetes mellitus. 10–11