This document discusses the history and health effects of smoking. It begins with the origins of tobacco use among Native Americans and its spread to Europe. It then discusses the addictive properties of nicotine and how cigarettes effectively deliver nicotine to the brain. The document outlines the various health risks of smoking such as increased risk of lung cancer, COPD, and heart disease. It also discusses challenges with smoking cessation and methods that can be used to help people quit smoking such as nicotine replacement therapies, bupropion, and varenicline. The document concludes by discussing approaches to harm reduction for smokers unable or unwilling to quit.

1. SMOKING & IT’S ILL
EFFECTS
DR. FIROZ A HAKKIM
DEPT. OF PULMONARY MEDICINE

3. Nicotiana tabacum

4.  Native Americans discovered the use of the tobacco plant,
Nicotiana tabacum, during antiquity.
 By the time Columbus arrived in America, tobacco use was
widespread throughout the western hemisphere and was well
integrated into Native American cultures.
 Production of tobacco and its trade represented a major
economic activity in the pre-ColumbianAmericas.
 Early European explorers learned of the tobacco plant from
Native Americans, and by the mid-seventeenth century
tobacco was widely used in Europe.
History of cigarette

6.  Nicotine is a potent euphoriant
 Nicotine also has number of other effects on the central nervous
system(CNS).
 nicotine can improve task performance and attention time by
measurable degrees in non habituated individuals and may have
beneficial effects on cognition.
 Nicotine can also ameliorate anxiety and depression and induce a
sense of well-being while causing a state of arousal.
 nicotine can attenuate pain.
 Unfortunately, nicotine is also highly addictive.

8. (Source: www.willwilliams.co.uk/common-issues/smoking/whats-in-a-cigarette)

9. NICOTINE ADDICTION
 Nicotine exerts its biologic effects on “nicotinic” receptors, a
subset of cholinergic receptors whose endogenous ligand is
acetylcholine.
 (alpha4)(beta2) receptor is believed to be most important in
the addicting effects of nicotine.

10.  Smoking is a particularly effective means of delivering
nicotine to induce psychoactive effects.
 When the drug is inhaled into the lungs its lipid solubility
allows it to be rapidly absorbed across the alveolar surface
into the pulmonary capillary blood.
 This results in a very rapid increase in nicotine levels in
arterial circulation.
 Consequently, at the level of receptors in the brain, nicotine
concentration rises very rapidly following inhalation of a
cigarette.
 This type of pharmacodynamics maximizes not only the
psychoactive potential of nicotine, but is also important in its
addictive potential.

11. Reasonsto Smoke
Some want to act cool or act like
someone special or dangerous
They want to get attention
They are curious about cigarettes
Peer pressure
They are stressed or nervous

12. SOCIAL AND CULTURAL
ASPECTS OFSMOKING
 Experience a child has with the initial attempts at smoking appears
to be important, as is an individual’s attitude toward smoking (i.e.,
the “image” of the smoker, peer pressure, parental cigarette use, and
availability.
 Use of tobacco products has become well integrated into modern
cultures worldwide.
 Tobacco is a multi–billion dollar industry.
 tobacco is a crucial cash crop in an agricultural economy.
 In addition, the manufacture, distribution, marketing, and sale of
tobacco products employ many individuals worldwide.
 Taxation on tobacco products has become an important means for
the support of many governments. Thus, any changes in tobacco
usage are likely to have economic impacts well beyond any health
effects.

13. MASTER SETTLEMENT AGREEMENT
 was signed into effect in 1998.
 It served as a measure to recuperate what states had lost through
Medicaid expenditures due to smoking-related illnesses and as a
measure to fine the tobacco industry for deceitful actions.
 Four major United States tobacco companies awarded 46 states $206
billion dollars to be paid over 25 years.
 States have failed to use the funding for tobacco control causes
,instead using it to fill budget deficits or support other state programs.

15. SMOKING AS A PUBLIC HEALTH
PROBLEM
 number of deaths attributed to cigarette smoking in the United States
has been estimated to be in excess of 400,000 annually.
 becoming more common in the developing world, where smoking
prevalence has been increasing.
 tobacco smoke contains compounds that can disrupt DNA, causing
both mutations and altering gene expression, bind to and disrupt
proteins, and alter cellular lipids.

22. Smoking & COPD
 Heavy smokers are at greater risk of developing COPD.
 Low doses are also likely hazardous, as symptoms of bronchitis
and increased risk for COPD have been associated with passive
smoke exposure.
 Expiratory airflow in cigarette smokers decreases twice as fast in
smokers (40 ml/y) than nonsmokers (20 ml/y).
 COPD is a major risk factor for acute cardiac events with even
minor decrements in lung function being associated with
increased cardiac risk.

23.  Emphysema likely develops from lung damage, which can be
a result of direct injury from oxidants in cigarette smoke, and
the action of oxidants released by inflammatory cells
recruited into the lung as a result of smoke exposure.
 Smoke-generated oxidants may also disrupt the anti-
protease protective mechanisms of the lung, creating a milieu
more susceptible to protease-induced damage.
 When damage induced by smoking is not balanced by
appropriate repair mechanisms, emphysema may result

25.  Inflammation induced by cigarette smoke appears capable of
stimulating both acute production of secretions and inducing
long-term anatomic changes in the airway.
 Changes such as goblet cell metaplasia may predispose to a
hypersecretory state.
 Others,such as peribronchial fibrosis, may result in airflow
obstruction.

26. MALIGNANCY & SMOKING
 Risk for developing lung cancer is increased about 20-fold in
smokers compared to nonsmokers.
 lung cancer risk increases with amount smoked and, most
importantly, with the duration of smoking.
 The increased risk of lung cancer among passive smokers
again is suggestive that even low-dose exposures to
cigarette smoke carry significant risk.
 Both tumor initiators and tumor promoters are present in
cigarette smoke.

28. SMOKING CESSATION
 Comprehensive tobacco control programs, including bans on
advertising ,restriction of sales to minors, and increased price for
cigarettes, also appear to be having an effect in reducing
smoking.
 BehavioraLApproaches
 A sense of empowerment and control over the behavior is vital to
making and succeeding in a quit attempt.
 Individual and group counseling, education, aversive
conditioning, psychotherapy, transcendental meditation, sensory
deprivation, hypnosis, and desensitization

29. STAGES OF SMOKING
CESSATION
Precontemplation Smokers are not interested in
quitting smoking and will likely
be non responsive to direct
intervention
Contemplation considering quitting smoking and
may be receptive to a physician’s
advice about the risks and
benefits of quitting
Preparation smokers are actively preparing to
quit.
Action encompasses both initial
abstinence and the 6-month post
cessation period
Maintenence Commences after the 6-month
abstinence period

30. Pharmacologic Treatment
 Nicotine Replacement Therapies
tablets, polacrilex (gum), transdermal systems
,nasalspray ,inhalers, and nicotine toothpicks.
 Buproprion
an antidepressant.
act by potentiating dopaminergic and noradrenergic
signaling.
currently recommended dose is 150 mg daily for 3 days
followed by 150 mg twice daily.
The quit date should be after a week of therapy so that
blood levels areestablished.

33.  clonidine and nortriptyline, are supported by guidelines for
“off-label” use as secondary agents.
 Varenicline is an (alpha4)3(beta2)2 receptor partial agonist
that has looked promising.
 Nicotine vaccines
antibodies bind nicotine reversibly.
By slowing the delivery of nicotine to the brain, the
vaccine would distort the pharmacokinetics of a cigarette.

34.  two critical factors required for successful abstinence are that
smokers must have a reason for quitting and the ability to
quit.

36. Fagerstrom Test for Nicotine
Dependence

37.  Tobacco Withdrawal Period
first 3 days of abstinence
peak during the first 72 hours, and then
gradually subside over a 3-to4-week period.
These symptoms can include restlessness,
anxiety, difficulty concentrating, irritability, frustration,
depression, and almost unrelenting craving for cigarettes.

38. Health Benefits of Smoking
Cessation
 rapid reduction in acute myocardial events.
 reduction in complications of atherosclerotic vascular disease.
 risk for the development of lung cancer appears to decrease
gradually following cessation.
 improvement in lung function.
 significant improvement in FEV1 in the first year following
cessation.

39. HARM REDUCTION
 Controversial approach for smokers who are unwilling or
unable to quit
 the health consequences may be partially addressed by
reducing the exposure to smoke derived toxins.
 (1)administration of agents to counteract the effects of
cigarette smoking;
 (2) smoking reduction; and
 (3) development of a less toxic cigarette.

41. SLIDESHARE.NET
FIROZ HAKKIM