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Secondhand
Smoke
"While smokers may have the right to smoke,
nonsmokers should have the right to be protected from
harm resulting from the action of smokers"
Proffessor Adi Gazdar, M.D.,
W. Ray Wallace Distinguished Chair in Molecular Oncology
Research,
Department of Pathology,
Southwestern Medical School
Secondhand smoke is considered to be a combination
of:
sidestream smoke (smoke released from burning
end of cigarette), plus exhaled
mainstream smoke (smoke exhaled by the smoker).
Sidestream smoke is generated at lower temperatures and
under different conditions than mainstream smoke, and
therefore contains higher concentrations of many of the
toxins found in cigarette smoke, and at least 250 of these
chemicals in secondhand smoke are known to be toxic or
carcinogenic (including formaldehyde, benzene, vinyl chloride,
arsenic, ammonia, and hydrogen cyanide), according to
estimates from the National Toxicology Program, with over
50 of these known and classified to be carcinogenic:
- Polynuclear aromatic hydrocarbons (PAHs) (such as
Benzo[a]pyrene)
- N-Nitrosamines (such as tobacco-specific nitrosamines)
- Aromatic amines (such as 4-aminobiphenyl)
- Aldehydes (such as formaldehyde)
- Miscellaneous organic chemicals (such as benzene and
vinyl chloride) and
- Inorganic compounds
(such as those containing metals like arsenic, beryllium,
cadmium, lead, nickel and radioactive polonium-210)
so when nonsmokers are exposed to secondhand smoke, they
are in fact inhaling many of the same carcinogens inhaled
by smokers themselves
Major
Conclusions of the 2006 Surgeon General Report on Secondhand
Smoke:
The Health Consequences of Involuntary Exposure to Tobacco
Smoke: A Report of the Surgeon General.
U.S. Department of Health and Human Services,
Centers for Disease Control and Prevention,
National Center for Chronic Disease Prevention and Health
Promotion,
Office on Smoking and Health, 2006.
(Also available: Executive
Summary).
- Exposure:
- Millions of Americans are exposed to secondhand
smoke.
- There is no risk-free level of exposure to
secondhand smoke:
even small amounts of secondhand smoke
exposure can be harmful to people’s health:
- Short exposures to secondhand smoke, such
as even a short time in a smoky room, can cause
blood platelets to become stickier, damage the
lining of blood vessels, decrease coronary flow
velocity reserves, and reduce heart rate variability,
potentially increasing the risk of a heart attack.
- Secondhand smoke contains many chemicals that
can quickly irritate and damage the lining of
the airways. Even brief exposure can result
in upper airway changes in healthy persons,
triggering respiratory symptoms, including cough,
phlegm, wheezing, and breathlessness, and can
lead to more frequent and more asthma attacks
in children who already have asthma, and children
exposed to secondhand smoke are also at an increased
risk for acute respiratory infections, ear problems,
and severe asthma.
- A smoke-free environment is the only way
to fully protect nonsmokers from the dangers
of secondhand smoke.
- Separating smokers from nonsmokers, cleaning
the air, and ventilating buildings cannot eliminate
exposure of nonsmokers to secondhand smoke:
- Conventional air cleaning systems can remove
large particles, but not the smaller particles
or the gases found in secondhand smoke.
- ASHRAE (American Society of Heating, Refrigerating
and Air-Conditioning Engineers, the preeminent
U.S. authority on ventilation issues, has concluded
that ventilation technology cannot be relied on
to control health risks from secondhand smoke
exposure.
- Health Hazards of Exposure:
- Secondhand smoke (SHS) has been designated
as a known human carcinogen by the U.S. EPA, the
National Toxicology Program and the International
Agency for Research on Cancer (IARC), with several
compounds in tobacco smoke identified by IARC as
known human carcinogens (Group 1).
In addition, the National Institute for Occupational
Safety and Health has concluded that secondhand
smoke is an occupational carcinogen.
- SHS exposure causes disease and premature death
in non-smokers:
- Exposure of adults to secondhand smoke has
immediate adverse effects on the cardiovascular
system and causes coronary heart disease and
lung cancer.
- Breathing secondhand smoke for even a short
time can have immediate adverse effects on the
cardiovascular system and interferes with the
normal functioning of the heart, blood, and
vascular systems in ways that increase the risk
of a heart attack.
- Secondhand Smoke Exposure
in the Home:
- The home is a major location of secondhand
smoke exposure for adults and the place where
children are most exposed to secondhand smoke.
- Secondhand smoke exposure in the home has
been consistently linked to a significant increase
in both heart disease and lung cancer risk among
adult nonsmokers.
- Eliminating smoking in indoor spaces is the
only way to fully protect nonsmokers from secondhand
smoke exposure.
- Smoke-free rules in homes and vehicles can
reduce secondhand smoke exposure among children
and nonsmoking adults.
- Risk of Exposure:
- Nonsmokers exposed to secondhand smoke at home
or at work increase their risk of developing heart
disease by 25 - 30 percent.
- Nonsmokers exposed to secondhand smoke at home
or at work increase their risk of developing lung
cancer by 20 - 30 percent.
Testing
for Exposure to Secondhand Smoke
- Currently, as observed by Georg Matt at San Diego
State University and colleagues (Matt GE, Wahlgren DR,
Hovell MF, et al. Measuring
environmental tobacco smoke exposure in infants and
young children through urine cotinine and memory-based
parental reports: empirical findings and discussion.
Tob Control. 1999 Autumn;8(3):282-9), there is no means
by which the harmful components of ETS can be directly
measured in the organs of interest (like the lungs).
Therefore, indirect measures of secondhand smoke exposure
have been developed,
- Cotinine is the major metabolite (that is,
breakdown (by-)product) of nicotine in th body, being
generated from nicotine metabolically in the liver and
then released into the bloodstream, and so analyzing
the cotinine level in either the blood, saliva, or urine
provides a reliable objective quantitative measure exposure
to nicotine; and although nicotine itself is rapidly
metabolized (short half-life), cotinine is metabolized
and eliminated at a much slower rate, thus extending
the window of detection for several days, typically
48 - 96 hours (Curvall M, Elwin CE, Kazemi-Vala E, Warholm
C, Enzell CR.
The pharmacokinetics of cotinine in plasma and saliva
from non-smoking healthy volunteers. Eur J Clin
Pharmacol. 1990;38(3):281-7. Simoni M, Baldacci S, Puntoni
R, et al. Plasma,
salivary and urinary cotinine in non-smoker Italian
women exposed and unexposed to environmental tobacco
smoking (SEASD study). Clin Chem Lab Med. 2006
May;44(5): 632-638).
- Serum (blood), salivary or urinary levels of cotinine
therefore most closely reflect the effective ingested
dose of nicotine absorbed from secondhand smoke (both
saliva and cotinine levels have been shown to
be highly correlated with blood levels, and so allow
these simpler and more accessible test to substitute
for a serum assay, as demonstrated by Neil Benowitiz
at UCSF (in Benowitz NL. Biomarkers
of environmental tobacco smoke exposure. Environ
Health Perspect. 1999 May;107 Suppl 2:349-55), who concluded
that "cotinine levels provide valid and quantitative
measures of average ongoing human ETS [environmental
tobacco smoke] exposure over time".
- Although the amount of cotinine may not be directly
related to the amount of the disease-causing constituents,
such as benzo(a)pyrene, to which a non-smoker was exposed
(California Environmental Protection Agency Office of
Environmental Health Hazard Assessment (OEHHA). Health
Effects of Exposure to Environmental Tobacco Smoke),
cotinine is nonetheless a surrogate
marker of other toxins produced by the burning of tobacco
such as benzene, formaldehyde, and others, and thus
assesses assess cumulative exposure over days, as demonstrated
by Jaakkola & Jaakkola (Jaakkola MS, Jaakkola JJ.
Assessment
of exposure to environmental tobacco smoke [pdf].
Eur Respir J. 1997 Oct;10(10):2384-97) who concluded
that cotinine measurement was suitable for assessment
of cumulative doses over short exposure periods of several
days duration, serving as serve as a measure for the
combined but not separate toxic components of secondhand
smoke exposure (Benowitz NL. Biomarkers
of environmental tobacco smoke exposure. Environ
Health Perspect. 1999 May;107 Suppl 2:349-55. Also Hovell
MF, Zakarian JM, Wahlgren DR, Matt GE, Emmons KM. Reported
measures of environmental tobacco smoke exposure: trials
and tribulations. Tob Control. 2000;9 Suppl
3:III22-8).
- TobacAlert (from Nymox) is a leading over-the-counter
home test for urinary cotinine levels, one whose instructions
explicitly recognize its use for the detection of recent
second hand smoke exposure. In urine, cotinine values
between 11 ng/mL and 30 ng/mL are taken to be associated
with light active smoking or secondhand exposure, while
levels in active smokers typically achieve 500 ng/mL
or above.
Evidence-based Research on Secondhand Smoke (SHS)
- Secondhand Smoke and Cardiovascular
Disease
SHS Adverse Cardiovascular
Impact
The adverse cardiovascular impact of secondhand smoke
has been supported in cohort and case control studies
which find a 30% excess risk of fatal and non-fatal
coronary heart disease in nonsmokers exposure to secondhand
smoke (Law & Wald, Prog Cardiovasc Dis (2003): Environmental
tobacco smoke and ischemic heart disease). And
both epidemiological and laboratory data indicates that
the risk of acute myocardial infarction and coronary
heart disease associated with exposure to tobacco smoke
is non-linear at low doses, increasing rapidly with
relatively small doses such as those received from secondhand
smoke - or actively smoking one or two cigarettes a
day (Pechacek et al., BMJ (2004): How
acute and reversible are the cardiovascular risks of
secondhand smoke?), and even such small exposures
significantly and rapidly increase platelet aggregation
and induce other adverse arterial and hemodynamic changes
(and the activation and aggregation of platelets, and
consequent formation of a thrombus or clot obstructing
arterial blood supply to part of the heart are established
precipitants of acute myocardial infarction). Furthermore,
the ATTICA study found that concentrations of known
biomarkers of inflammation such as white blood cells,
C reactive protein, homocysteine, fibrinogen, and oxidized LDL
cholesterol in subjects exposed to secondhand smoke
are similar to those observed in active smokers, with
increase in overall inflammation, a precursor of atherosclerotic
plaque (Panagiotakos et al., Am J Med (2004): Effect
of exposure to secondhand smoke on markers of inflammation:
the ATTICA study; see also Valkonen & Kuusi,
Circ (1998): Passive
Smoking Induces Atherogenic Changes in Low-Density Lipoprotein)
who found that exposure of nonsmokers to secondhand
smoke breaks down serum antioxidant defense, leading
to a cascade of accelerated lipid peroxidation, LDL
modification, and accumulation of LDL cholesterol in
human macrophages, and these processes may be the pathophysiological
basis for the epidemiological evidence of increased
CHD risk among passive smokers.
Sensitivity to Low Exposure
The lowness of the exposure level needed to induce significant
adverse cardiovascular events is suggested in the research
of Otsuka et al. who found that just 30 minutes of exposure
to a typical dose of secondhand smoke induces changes
in arterial endothelial function (in terms of coronary
flow velocity reserve (CFVR)) in exposed nonsmokers
of a magnitude similar to those measured in active smokers
(Otsuka et al. JAMA (2004): Acute
Effects of Passive Smoking on the Coronary Circulation
in Healthy Young Adults), thus inducing coronary
circulation endothelial dysfunction. And as concluded,
the cardiovascular system (platelet and endothelial
function, arterial stiffness, atherosclerosis, oxidative
stress, inflammation, heart rate variability, energy
metabolism, and increased infarct size) is astonishingly
sensitive to the toxins in secondhand smoke, given that
the effects of even brief (minutes to hours) passive
smoking are often nearly as large (averaging 80% to
90%) as chronic active smoking (Barnoya & Glantz,
Circ (2005): Cardiovascular
Effects of Secondhand Smoke - Nearly as Large as Smoking).
The ultra-sensitivity is highlighted by the observation
that despite the fact that the dose of smoke delivered
to active smokers is 100 times or more that delivered
to a passive smoker, the relative risk of coronary heart
disease (CHD) is barely different, being 1.78 for smokers,
and still 1.31 for passive smokers (Law et al., BMJ
(1997): Environmental
tobacco smoke exposure and ischaemic heart disease:
an evaluation of the evidence).
Underlying Mechanisms
The underlying mechanisms of these adverse cardiovascular
impacts of secondhand smoke are complex, and includes
activation of platelet activity (increased platelet
aggregability), endothelial dysfunction, increased arterial
stiffness, lowered HDL, proinflammatory and pro-infection
activity, atherosclerosis progression, increased infarct
size, increased oxidative stress and decreased antioxidant
defense, mitochondrial DNA damage, heart rate variability
(HRT), insulin resistance, and decreased energy production
in the heart muscle, and a decrease in the parasympathetic
output to the heart. Some of the these, and other mechanisms
are elaborated on below:
- polycyclic aromatic hydrocarbons (PAHs) in cigarette
smoke, already recognized as potential environmental
procarcinogens, and recently shown to induce acceleration
of atherogenesis (Kurzee & Ramos, Circ Res (2001):
Constitutive
and Inducible Expression of Cyp1a1 and Cyp1b1 in Vascular
Smooth Muscle Cells - Role of the Ahr bHLH/PAS Transcription
Factor).
- adverse increase in carotid intimal thickening,
via increased arterial expression of inducible nitric
oxide synthase (iNOS), mediated at least in part by
aryl hydrocarbon receptor (AhR) signaling (Anazawa
et al., Arterioscler Thromb Vasc Biol (2005): Effect
of Exposure to Cigarette Smoke on Carotid Artery Intimal
Thickening - The Role of Inducible NO Synthase);
inactivation of nitric oxide, possibly related to
acute endothelial dysfunction, may be an underlying
mechanism in the adverse cardiovascular sequelae of
secondhand smoke (on secondhand smoke and endothelial
dysfunction, see also Maresh et al., Physiol Genomics
(2005):
Tobacco smoke dysregulates endothelial vasoregulatory
transcripts in vivo), and Celermajer et al.,
N Eng J Med (1996): Passive
Smoking and Impaired Endothelium-Dependent Arterial
Dilatation in Healthy Young Adults) who found
that passive smoking was associated with dose-related
impairment of endothelium-dependent dilatation in
otherwise healthy young adults, suggesting early arterial
damage).
- free radicals, inducing oxidative stress, that may
modulate the expression of both acute and chronic
phenotypes of smoking-induced vascular disease (see
McNamara & Fitzgerald's (Circ Res (2001): Smoking-Induced
Vascular Disease - A New Twist on an Old Theme)
thoughtful commentary on this and related issues);
see also the review of Raupach et al. (Sur Heart J
(2006):
Secondhand smoke as an acute threat for the cardiovascular
system: a change in paradigm); as observe,
the acute vascular responses to tobacco smoke may
be secondary in part to oxidative stress, which can
generate reactive oxygen species (ROS) such as superoxide
anion, and these ROS may react with nitric oxide to
form peroxynitrite, an eNOS activity uncoupler.
- atherosclerosis-mediated tissue damage following
ischemia or myocardial infarction, by virtue of accelerated
atherosclerotic lesion development consequent to the
increased platelet activity stimulated by secondhand
smoke (Glantz & Parmley, JAMA (1995): Passive
smoking and heart disease. Mechanisms and risk).
- secondhand smoke induces altered cardiac autonomic
function: heart rate variability (HRV) in healthy
people has been shown to decrease by 12% after 2 hours
of breathing secondhand smoke in an airport lounge,
with HRV being an established predictor of cardiac
death or arrhythmic events after myocardial infarction
(Pope et al., Environ Health Perspect (2001): Acute
Exposure to Environmental Tobacco Smoke and Heart
Rate Variability).
- SHS and Respiratory Disease
(Lung Cancer and COPD (Chronic Obstructive Pulmonary
Disease))
Even as of the beginning of 2004, over 50 studies (Veneis
et al., J Natl Cancer Inst (2004):
Tobacco and Cancer: Recent Epidemiological Evidence)
have shown that there is a clear dose-response relationship
consistent with a causal association between exposure
to secondhand smoke and the development of lung cancer
among never smokers (and urinary levels of nicotine,
cotinine, 4-(methylnitrosamino)-1-(3-pyridyl)-butanol
(NNK), a tobacco-specific carcinogen, and its glucuronide
(NNAL-Gluc) are elevated in nonsmoking women exposed
to secondhand smoke compared to those who were not exposed),
as found by the early review of Hackshaw et al. (BMJ
(1997): The
accumulated evidence on lung cancer and environmental
tobacco smoke) who concluded that based on epidemiological
and biochemical evidence on exposure to secondhand tobacco
smoke, coupled with the supporting evidence of tobacco
specific carcinogens in the blood and urine of exposed
nonsmokers provides compelling confirmation that "breathing
other people’s tobacco smoke is a cause of lung
cancer", also confirmed in the Veneis JNCI
review (see above). And the recent review of Thomas
et al. (Chest (2005): Lung
Cancer in Women - Emerging Differences in Epidemiology,
Biology, and Therapy) found that secondhand
(environmental) smoke accounts for approximately 3,000
lung cancer deaths each year in the United States among
nonsmokers, confirming the findings of the seminal EPIC
study (Veneis et al. BMJ (2005): Environmental
tobacco smoke and risk of respiratory cancer and chronic
obstructive pulmonary disease in former smokers and
never smokers in the EPIC prospective study)
which had previously found that secondhand smoke (or
ETS: environmental tobacco smoke) is a significant risk
factor for both lung cancer and other respiratory diseases.
From an updated meta-analysis by IARC the risk is approximately
25% greater than expected for women (based on data from
46 studies that included 6257 lung cancer case subjects)
and 35% greater than expected for men (IARC Monographs
V. 83 (2004): Tobacco
Smoke and Involuntary Smoking [pdf]). See also
the editorial commentary (BMJ (2005): Evidence
is unfavourable for passive smoking) which cites
correlations of secondhand smoke with cancer of the
lung, pharynx, and larynx, as well as chronic obstructive
pulmonary disease or emphysema, stroke, ischaemic heart
disease, and all cause mortality, and the editorial
of Ichiro Kawachi (BMJ (2005): More
evidence on the risks of passive smoking), and
E Cetti (Thorax (2005): Further
evidence on the dangers of exposure to second hand tobacco
smoke) who speculates that given the overwhelming
weight of the evidence, it may now or soon be possible
to reclassifying secondhand smoke-related deaths as
"poisoning". And it has been independently
established that secondhand smoke is associated with
chronic obstructive pulmonary disease: as Eisner at
al. concluded in their recent study (BMC Pulm Med (2006):
Directly
measured secondhand smoke exposure and COPD health outcomes),
"There is no question that cigarette smoking
is the dominant risk factor for COPD and is the most
important factor driving the progression of airflow
obstruction. Our results implicate SHS exposure as another
important factor influencing disease severity and health
status in this health condition".
Furthermore, Adi Gazdar (Cancer Cell (2003): Environmental
tobacco smoke, carcinogenesis, and angiogenesis - A
double whammy?) observes that given that it
has been established (Zhu et al., Cancer Cell (2003):
Second hand smoke stimulates tumor angiogenesis and
growth) that secondhand smoke promotes tumor
growth, tumor angiogenesis, and an increase in growth
factors and cells known to contribute to tumor angiogenesis,
suggesting that the oncogenic effects of secondhand
smoke are mediated in part by angiogenic effects of
nicotine (and remember that the concentration of nicotine
in sidestream smoke is greater than its concentration
in mainstream smoke), then it can be concluded that
not only is secondhand smoke harmful, but it is associated
with many diseases other than cancer, and that given
all the evidence it must be held that "while
smokers may have the right to smoke, nonsmokers should
have the right to be protected from harm resulting from
the action of smokers".
Finally, more recently, Peng Yin and colleagues (Lancet
(2007): Passive
smoking exposure and risk of COPD among adults in China:
the Guangzhou Biobank Cohort Study) measured
passive smoking at home and at the workplace in terms
of density and the duration of exposure, finding that
four subjects who were highly exposed to passive smoking,
defined as more than 40 hours per week for more than
5 years, were 48% more likely to present with COPD (Chronic
Obstructive Lung Disease) than were unexposed subjects.
The accompanying Lancet commentary by Ana Menenez and
Pedro Hallal (Lancet (2007): Role
of passive smoking on COPD risk in non-smokers)
conclude that "These results suggest that future
anti-smoking policies should, in addition to targeting
active smoking, also consider addressing passive smoking"
and that these "findings, added to what is already
known about the harmful effects of passive smoking,
suggest that urgent strategies to reduce this exposure
are needed".
- SHS and Diabetes
We have already observed above that increased insulin
resistance is recognized to increase the heart disease
risk, and the IRAS study showed that exposure to secondhand
smoke can lead to an increase in insulin resistance
(Henkin et al., Ann Epidemiol (1999): Cigarette
Smoking, Environmental Tobacco Smoke Exposure and Insulin
Sensitivity: The Insulin Resistance Atherosclerosis
Study), and more recently another related adverse
effect secondhand smoke has been found, namely an increased
risk of glucose intolerance: Houston et al. (BMJ (2006):
Active and passive smoking and development of glucose
intolerance among young adults in a prospective cohort:
CARDIA study) in their 15 year prospective study
found that both active and passive smokers are more
likely than nonsmokers to develop clinically relevant
glucose intolerance or diabetes, with the association
of such exposure with diabetes being greatest among
white men and women. See also the accompanying editorial
by Panagiotakos & Pitsavos (BMJ (2006): Passive
smoking's role in diabetes) who notes that never
smokers with secondhand smoke exposure experienced 35%
higher risks of developing glucose intolerance than
never smokers without passive exposure, concluding that
sensibly that given the current state of matters, "most
nonsmokers wish not to be exposed to tobacco smoke against
their will".
- Other Health Hazards Evidenced
in the Report of the Surgeon General 2006
The Report of the Surgeon General 2006 (see above) also
presents methodologically compelling evidence and on
that basis concludes that:
- secondhand smoke exposure could increase the
risk for sudden infant death syndrome (SIDS),
- there is a causal relationship between secondhand
smoke exposure from parental smoking and lower
respiratory illnesses in infants and children
- there is a causal relationship between parental
smoking and middle ear disease in children,
including acute and recurrent otitis media
and chronic middle ear effusion
- there is a causal relationship between parental
smoking and cough, phlegm, wheeze, and breathlessness
among children of school age
- there is a causal relationship between parental
smoking and ever having asthma among children
of school age
- there is a causal relationship between secondhand
smoke exposure from parental smoking and the onset
of wheeze illnesses in early childhood
- there is a causal relationship between maternal
smoking during pregnancy and persistent adverse
effects on lung function across childhood
- there is a causal relationship between exposure
to secondhand smoke after birth and a lower level
of lung function during childhood.
- Other Health Hazards Independently
Evidenced
- Leukemia
Kasim et al. (Epidemiology (2005): Environmental
Tobacco Smoke and Risk of Adult Leukemia)
found that the risk for one type of leukemia, chronic
lymphocytic leukemia, was clearly associated with
secondhand smoke exposure
- Increased Metabolism
and Thyroid Hormone Levels
Giorgos Metsios and colleagues (J Clin Endocrinol
Metab (2007): A
Brief Exposure to Moderate Passive Smoke Increases
Metabolism and Thyroid Hormone Secretion)
found that just one hour of passive smoking at
bar/restaurant levels induces significant increases
in metabolism and thyroid hormone levels.
- Alzheimer's Disease /
Dementia
Research presented by Thaddeus Haight at the University
of California and colleagues (28 April–5 May
2007 Annual Metting of the American Academy of Neurology
(2007): Effects
of Second-Hand Smoke and Cardiovascular Disease
on Incident Dementia in Participants from the Cardiovascular
Health Study) at 2007 annual meeting of
the American Academy of Neurology (AAN) suggests
thatchronic exposure to secondhand smoke is associated
with increased risk of Alzheimer disease and other
forms of dementia, based on data compiled from the
Cardiovascular Health Study, a national study of
cardiovascular disease risk factors, concluding
that higher levels of lifetime SHS exposure are
associated with greater risk of incident Alzheimer's
Disease / dementia in the elderly, and in addition
pose a significant risk in individuals with underlying
carotid artery disease. Furthermore, those with
a more than 30 years lifetime exposure had a 30%
greater risk for developing dementia in comparison
with the no-exposure group, and that within this
high exposure group, those with subclinical cardiovascular
disease (carotid artery stenosis) had an even higher
risk, nearly two and a half times that of the no-exposure
group.
- Glucose Intolerance
Thomas Houston and colleagues (BMJ (2006): Active
and passive smoking and development of glucose intolerance
among young adults in a prospective cohort: CARDIA
study) found a role of both active and passive
smoking in the development of glucose intolerance
in young adulthood, a precursor of diabetes and
atherosclerotic disease.
- Breast Cancer
Chisato Nagata and colleagues (Jpn J Clin Oncol
(2006): Tobacco
Smoking and Breast Cancer Risk: An Evaluation Based
on a Systematic Review of Epidemiological Evidence
among the Japanese Population) concluded
from an appraisal of the medical literature that
both active and passive tobacco smoking may increase
the risk of breast cancer, confirming earlier findings
to the same effect based on epidemiological data
by Tomoyuki Hanaoka and colleagues (Int J Cancer
(2005): Active
and passive smoking and breast cancer risk in middle-aged
Japanese women).
Smoking Cessation
- Background
 About
half of all long-term smokers die prematurely from smoking's
adverse events: cancer, cardiovascular disease, lung
disease, or other serious illnesses (Henningfield et
al., CA Cancer J Clin (2005): Pharmacotherapy
for Nicotine Dependence), with at least another
40,000 nonsmokers dying each year in the U.S. as a direct
consequence of involuntary exposure to environmental
(secondhand) smoke (Centers for Disease Control and
Prevention (CDC), MMWR Morb Mortal Wkly Rep (2002):
Annual
Smoking-Attributable Mortality, Years of Potential Life
Lost, and Economic Costs --- United States, 1995--1999),
a number now considered likely the underestimate the
true adverse impact on nonsmokers (see the Surgeon General
The
Health Consequences of Involuntary Exposure to Tobacco
Smoke 2006 Report, above).
- Available Smoking Cessation
Products
In addition to other modalities and counseling (see
Molyneux et al, Thorax (2003): Clinical
trial comparing nicotine replacement therapy (NRT) plus
brief counselling, brief counselling alone, and minimal
intervention on smoking cessation in hospital inpatients),
public guidelines suggest that pharmacotherapy should
be offered to "all smokers trying to quit"
(U.S. Public Health Service (PHS) Report (2000): Treating
Tobacco Use and Dependence - Clinical Practice Guideline
[pdf]; also published in alternate form in JAMA (2000):
A Clinical Practice Guideline for Treating Tobacco
Use and Dependence - A US Public Health Service Report).
There are currently seven smoking cessation assistive
products approved by the FDA for the treatment of tobacco
dependence:
- six forms of nicotine replacement therapy (NRT)
which is the therapeutic use of nicotine-containing
medications that replace, at least partially, nicotine
formerly obtained from smoking, providing nicotine-mediated
neuropharmacologic effects, and
- a sustained-release antidepressant.
- nicotine transdermal patch
- nicotine gum
- nicotine lozenge
- sublingual tablet
- nicotine nasal spray
- nicotine vapor inhale
- bupropion (Wellbutrin SR, Zyban)
- Emerging Therapies:
A number of additional agents are being studies for
their potential use in smoking cessation: (1) rimonaban
is a unique cannabinoid receptor agonist showing promise
both in smoking cessation and independently for weight
control, and given that many smokers who quit show a
tendency to gain weight, this dual-mode agent may be
of particular benefit, decreasing the likelihood of
relapse during a quit attempt during which weight gain
is a disincentive; (2) varenicline, a partial
agonist of nicotinic receptors, that has also shown
benefit in achieving and sustaining smoking abstinence;
(3) there are currently three antinicotine vaccines
in various stages of clinical trials (TA-NIC, NicVAX,
and Nicotine-Qbeta), designed to induce antibodies against
the nicotine molecule preventing the drug from reaching
neural receptors that produce the normal effects of
smoking; (4) some antidepressants besides bupropion
may be of value (in particular, nortriptyline
and doxepin), as well as the noradrenergic agonist
clonidine.
In conclusion, smoking cessation interventions are receiving
considerable intensive research interest at this time,
and new developments may help to transform the therapeutic
landscape in the near future.
Consumer Resources:
- Smokefree.gov
(from Health and Human Services)
Provides authoritative information and professional
assistance for people trying to quit smoking.
- Treating
Tobacco Use and Dependence
(from the Agency for Healthcare Research and Quality
(AHRQ))
A clinical practice guideline issued in June 2000 by
the Public Health Service (PHS) providing evidence-based
information on first-line pharmacologic therapies and
counseling for patients trying to quit smoking.
- Tobacco Information
and Prevention Source (TIPS)
(from the Centers for Disease Control and Prevention
(CDC))
Publications, data and statistics, educational materials,
public health information campaigns, and more from the
Office on Smoking and Health.
- Involuntary
Smoking Database
A searchable database of research abstracts of the key
articles on secondhand smoking and disease outcomes
that are cited in the 2006 Surgeon General’s Report
(see above), reflecting the most recent findings in
the scientific literature, along with qualitative data,
and quantitative data charted graphically.
- Smoke-free
Homes Program
A resource from the Environmental Protection Agency
(EPA) promoting a smoke-free environment at home.
- Tobacco
Cessation - You Can Quit Smoking Now!
Provides up to date information and extensive resource
links to help people quit smoking, and to help health
care professionals treat tobacco use and dependence.
- Smoking
Cessation
Extensive collection of categorized resource links on
smoking cessation, from MedlinePlus.
- Products
To Help You Stop Smoking
Clear illustrated guide to each of the smoking cessations
products (all the nicotine replacement therapies (NRTs)
and the antidepressant bupropion.
- Quit
Smoking Action Plan
An easy-to-follow three-step plan for quitting smoking
from the American Lung Association, each step illustrated
with detailed charts.
- SLATI: State
Legislated Actions on Tobacco Issues
Unique comprehensive and searchable database of smoking
laws, tobacco laws and public smoking policy, including
a state-by-state clickable map., from the American Lung
Association.
- Smoking
Cessation
Collection of government resources on quitting smoking
from the National Institute of Health (NIH).
- New
York State Smokers’ Quitline
1-866-NY-QUITS (1-866-697-8487)
A service of NYS, the quitline is staffed by trained
Quitline Specialists to help with smoking quit plans,
and provides information for NYS residents about local
stop smoking programs at various hospitals and other
centers, and will also provide a free starter kit of
nicotine patches, gum or lozenges for eligible NYS smokers.
- New
York State Smokers' Quitsite
Comprehensive site providing extensive resources for
NYS residents to help quit smoking.
Best Strategy for Quitting Smoking: A Survival Guide
STEP ONE: Start with the Nicotine
Transdermal Patch
This form of nicotine replacement therapy is the
easiest to deal with, applied anywhere between waist
and neck (like upper arm or shoulder). According to
studies, the most effective is the NicoDerm CQ
patch, (21 mg/24 hours) which comes in 7-, 14-, and
21-mg / per day dose strengths, intended to be worn
for 24 hours.
- Which Strength To Choose?
The rule with the NicoDerm CQ patch is that if you're
a smoker who uses more than 10 cigarettes a day:
- start with the 21-mg/day patch for the first
6 weeks
- after that, switch to the 14-mg/day strength
for 2 weeks
- then after the eight week, use the 7-mg dose
for another 2 weeks, thus ending the smoking cessation
process after 10 weeks.
- How Many Hours Per Day To Wear?
- This patch is designed to be worn for 24 hours,
but you can remove it after 16 hours, before bedtime,
if you find your sleep is disturbed.
- If you can tolerate it, and most people can,
wear throughout the day, because it will control
cravings, not only during the morning hours (so-called
morning craving), but also throughout the day,
and the full-day approach yields greater reductions
in anxiety, irritability, and restlessness.
STEP TWO: While On the Patch,
Supplement with "Rescue" Nicotine Gum for
Breakthrough Cravings
- How To Get Over Breakthrough Cravings
- The nicotine patch is designed to work smoothly
throughout the 24-hour day, but occasionally you
might get an especially strong "breakthrough
craving" sometime during the day, so a good
trick is to use the nicotine gum as a rescue aid
to get over the intense craving.
- And remember, such breakthrough cravings are
often triggered situationally, as by seeing
someone else smoke, or when emotionally upset, or
a stressful meeting or encounter, and many smokers
find these episodes of sudden craving difficult
to resist, so instead of giving in, let the nicotine
gum get you over the craving, no matter how often
this may happen.
- How Many Hours Per Day To Chew?
Here's the rule:
- For smokers who use less than 25 cigarettes
per day, use the 2-mg dose of the nicotine gum
- For smokers who regularly smoke more than 25
cigarettes per day, use the 4-mg dose.
- When in doubt, or if your a very heavy smoker
or experience very intense cravings, use the 4-mg
dose which will be more effective.
STEP THREE: For Highly Dependent
Smokers, Add Bupropion (Wellbutrin / Zyban) to the Nicotine
Patch
- If you're a very heavy smokers (two or more packs
a day), or if you know you're very dependent because
you've already tried quitting and failed or relapsed
after a while, then a very effective trick is to combine
both the nicotine patch plus the antidepressant called
bupropion (brand names: Wellbutrin, Zyban); this is
a prescription product that's been found very effective
by itself for quitting smoking, but the combo with
the patch is amazingly effective for "hard"
cases.
- The dose is 150 mg per day for three days, then
twice per day for seven to 12 weeks, as needed.
SUMMARY of the Three Step Quit Smoking Program
- The Program:
- Use the nicotine patch, and supplement it as
needed with the nicotine gum to get over any breakthrough
cravings;
- if you are very dependent, then speak to you
doctor about adding Wellbutrin / Zyban.
- This three step program for quitting takes about
10 - 12 weeks, and represents the best advice for
the most effective regimen,
based on the best evidence to date.
- To learn more about which part of this program (nicotine
patch, nicotine gum, and antidepressant, if needed),
check out the consumer resources above, and of course
if you're going to need the antidepressant (a prescription-only
product),
check with doctor to make sure it's appropriate for
you and your health condition.
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