The impact of tobacco use on mortality and morbidity
is well known. As far back as 1982, the Surgeon General
of the United States Public Health Service has concluded
that cigarette smoking is the major single cause of cancer
mortality in the United States. Recently, the World Health
Organization (WHO) reported in 2010 that almost one
billion people and 250 million women are daily smokers.
The tobacco epidemic kills 5.4 million people in average
per year from lung cancer, heart disease, and other illnesses,
and approximately 650,000 of these deaths are caused by
second-hand smoke. If this smoking trend continues, there
will be more than 8 million deaths every year, with more
than 80% of tobacco-related deaths in developing countries
by 2030. Consequently, tobacco will kill a billion people due
to smoking-related disease during this century, with tobacco
use-related cancers being one of the main causes of death.
Tobacco use is by far the most widespread factor causing
exposure to known carcinogens and death from cancer
and is therefore a model for understanding mechanisms of
cancer induction. A causal relationship was reported between
active smoking and cardiovascular diseases, respiratory diseases, reproductive disorders, and several types of cancers,
including cancers of the lung, bladder, cervix, esophagus,
kidney, larynx, mouth, pancreas, stomach, and leukemia [1].
Although it might seem obvious that carcinogens associated
with the use of tobacco products have caused numerous
cancers, the effects of cancer genes, protein complexes,
cellular circuitry, and signal transduction pathways are often
According to the report from the International Agency
for Research on Cancer in 2010, cigarette smoke contains a
diverse array of 4,000 chemicals, 250 of which are known
to be harmful, and more than 60 known carcinogens have
been detected in mainstream cigarette smoke, and most of
the same carcinogens are also present in second-hand smoke.
The most potent of these carcinogens are polycyclic aromatic hydrocarbons and nicotine-specific metabolites, such
as 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone (NNK)