INTRODUCTION

Tobacco smoke or simply put, Environmental tobacco smoke (ETS) is generated

by the combustion or smoking of tobacco products. It is composed of side stream

smoke (SS), emitted from the smouldering tobacco between puffs, and exhaled

mainstream smoke (MS) from the smoker. When a cigarette is smoked, roughly

half of the smoke generated is SS and the other half MS (USEPA, 1992)

ETS, SS and MS are complex mixtures of over 4000 compounds. These include

more than 40 known or suspected human carcinogens, such as 4-aminobiphenyl, 2-

naphthylamine, benzene, nickel, and a variety of polycyclic aromatic hydrocarbons

(PAHs) and N-nitrosamines. A number of irritants, such as ammonia, nitrogen

oxides, sulfur dioxide and various aldehydes, and cardiovascular toxicants, such as

carbon monoxide, nicotine and some PAHs, are also present (USEPA, 1992)

While ETS, SS and MS are qualitatively similar with respect to chemical

composition, the absolute and relative quantities of the constituents can differ

substantially (USEPA, 1992) A major quantitative difference is that ETS is a

diluted mixture of SS and exhaled MS. In addition, because SS is produced at

lower temperatures and under more reducing conditions than MS, many

carcinogens and other toxicants are generated in greater amounts in SS than in MS.

For example, N- nitrosodimethylamine, a potent animal carcinogen, is emitted in

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quantities 20–100 times greater in SS than in MS (Brunneman, 1977), and SS:MS

ratios of about 7–30 for the known human carcinogens 4- aminobiphenyl and 2-

naphthylamine have been measured (Luce,1993). These quantitative differences

are consistent with animal and genotoxicity studies, suggesting that SS is more

potent than MS per unit of tobacco smoked (Wynder, and Hoffman, 1967)

Concerns about the health effects of ETS generally focus on the unsolicited

exposures of nonsmokers. Although active smokers are likely to be the most

heavily exposed to ETS, and a portion of their smoking-attributable excess health

risks may actually result from heavy ETS exposures, the added risk to smokers

from passive smoking is expected to be relatively insignificant compared to their

voluntary risk from active smoking.

This seminar work therefore X – rayed the social and health effects of tobacco

smoking in public places

COMPOSITION OF TOBACCO

Tobacco products contains around 5000 toxic substances. Most important and

dangerous constituents are:

1. Nicotine

2. Carbon Monoxide

3. Tar
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Nicotine is the major cause of the predominant behavioral effects of tobacco. It is a

poisonous substance leads to addiction. Nicotine influences and reinforces all

tobacco-use behavior. After absorption, nicotine travels rapidly to the brain, in a

matter of seconds, therefore, the psycho-active rewards associated with smoking

occur quickly and these rewards are highly reinforced. Nicotine binds to the

receptors in the brain where it influences the cerebral metabolism. Nicotine is then

distributed throughout the body, mostly to skeletal muscles. Development of

tolerance to its own actions is similar to that produced by other addictive drugs.

Carbon mono-oxide reduces the amount of oxygen blood can carry and causes

shortness of breath. Tar is a sticky residue which contains benzopyrene, one of the

deadliest cancer causing agents known. Other compounds are carbon dioxide,

nitrogen oxides, ammonia, volatile nitrosamines, hydrogen cyanide, volatile sulfur

containing compounds, volatile hydrocarbons, alcohols, aldehydes and ketones.

Some of these compounds are known to cause cancers of various organs of the

body (Talhoult et. al., 2011)

FORMS OF TOBACCO INTAKE

1. Cigarette - Most common and most harmful

2. Bidi – Most commonly used form in India

3. Cigar

4. Hookah (Hubble bubble)

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 5. Sheesha

6. Tobacco chewing

7. Kreteks (clove cigarettes)

8. Snuff – Moist & Dry

9. E-cigarette – recent intruder in the list

When non-smokers are exposed to smoke containing nicotine and toxic chemicals

emitted by smokers it is called passive smoking or exposure to second hand smoke.

SOURCES AND OCCURRENCE IN INDOOR AIR

The sole source of ETS is the combustion of tobacco products. ETS is nearly

ubiquitous in most societies. Exposure occurs in indoor air wherever there is

smoking of tobacco products – in homes, workplaces, vehicles and public places.

The degree of exposure depends on the number of smokers and the amount of

tobacco smoked, as well as size and ventilation characteristics of the indoor space

and the duration of exposure

ROUTES OF EXPOSURE

The only route of exposure of concern for ETS is inhalation.

TOXICOKINETICS

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The many compounds in ETS will have different toxicokinetic and metabolic

pathways. Vapour and particulate phases of constituents will also have different

patterns of absorption and retention. Highly soluble gases, such as formaldehyde,

will be almost completely absorbed in the upper respiratory tract, especially during

nasal breathing, while those with low solubility, such as carbon monoxide, will be

slowly absorbed from the alveoli (NRC, 1986). Diffusion in the alveolar region of

the lung is the major deposition mechanism for small particles in the size range of

those in ETS; the deposition efficiency is estimated to be about 10% for ETS

particles (DHHS, 1986).

Some compounds may elicit health effects without metabolic activation, while

others may require activation. Carbon monoxide, for example, can directly bind to

hemoglobin and decrease the oxygen-carrying capacity of the blood. Nicotine can

also directly affect the cardiovascular system. Carcinogenic tobacco-specific N-

nitrosamines, on the other hand, require metabolic activation (Hecht and

Hoffmann, 1986). The uptake and metabolism by ETS-exposed nonsmokers of

three major classes of carcinogens found in tobacco smoke, aromatic amines,

nitrosamines and PAHs, has been elucidated in recent publications. Hammond in

1993, reported that levels of hemoglobin adducts of the aromatic amine 4-

aminobiphenyl in nonsmokers increased significantly with increasing ETS

exposure and that nonsmokers in the highest exposure quartile had adduct levels

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that were about 18% of those in smokers. Such high relative levels are consistent

with observations that 4-aminobiphenyl concentrations are up to 30 times greater

in SS than in MS. Hecht in 1993 examined levels of metabolites of the tobacco-

specific nitrosamine 4- (methylnitrosamino)-1-(3-pyridyl)-1-butanone (NNK) in

the urine of nonsmokers exposed to sides tream smoke. They demonstrated that

mean levels of specific metabolites in the urine of nonsmokers were significantly

higher after ETS exposure than at baseline. Crawford in 1994, observed that

PAH-albumin adducts were significantly higher in young children of smoking

mothers than in those of nonsmoking mothers. Children whose mothers smoked

had roughly 40% of the excess adduct levels (i.e. above the levels in subjects with

no smokers in the household) of their smoking mothers. PAHs are not specific to

tobacco smoke; however, Crawford also found, using limited measures of dietary,

residential and occupational sources of PAHs, that ETS was the most important

contributor to PAH-albumin adduct levels in nonsmokers. Excretion of tobacco

smoke components is predominantly through ventilation and urinary and fecal

excretion. Some studies have shown that the mutagenic potential of urine is

increased by ETS exposure (Bos, 1983)

HEALTH EFFECTS OF TOBACCO SMOKING

Effects on Experimental Animals and In Vitro Test System

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Carcinogenic effects

The carcinogenicity of tobacco smoke has been demonstrated in a number of

lifetime animal bioassays: inhalation studies in the hamster, intrapulmonary

implantations in the rat, and skin-painting in the mouse (DHHS, 1986). The

Syrian golden hamster has been the most useful animal inhalation model for

studying smoking- induced carcinogenesis. The hamster is refractory to the

induction of lung tumours by known carcinogens; however, inhalation of MS

induces carcinomas of the larynx in a dose-related manner (Bernfeld, 1979). There

are no lifetime animal inhalation studies of ETS or SS.

Mutagenic effects

Tobacco smoke is genotoxic in virtually every in vitro system tested (Demarini,

1983), providing strong supportive evidence for its carcinogenic potential. IARC in

1986 concluded that there was “sufficient” evidence in short-term tests for genetic

activity (mutation and chromosomal effects) for both cigarette smoke and cigarette

smoke condensate. Whole SS (Ong, 1984) and extracts of ETS collected from

indoor air (Löfrot) have also been shown to be mutagenic in Salmonella

typhimurium. Claxton in 1989 found that SS accounted for approximately 60% of

the total S. typhimurium mutagenicity per cigarette, 40% from particulates and

20% from semivolatiles.

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Cardiovascular effects

Subchronic and acute exposures to tobacco smoke and various tobacco smoke

constituents have been shown to elicit a wide variety of cardiovascular effects in

several animal species. These effects have been comprehensively reviewed by

Glantz and Parmley in 1995 and include promotion of atherosclerosis, activation of

platelets and leukocytes, exacerbation of ischaemia/reperfusion injury, and

reduction of respiration by myocardial mitochondria. The development of

atherosclerosis in response to exposure to tobacco smoke, as well as to some

individual constituents of tobacco smoke (e.g. PAHs), has been demonstrated in a

number of animal models. Penn in 1994 exposed young cockerels intermittently

for 16 weeks to SS levels equivalent to ETS exposures under heavy smoking

conditions. The number (not statistically significant) and size (statistically

significant) of plaque-containing abdominal aorta segments in the exposed animals

was increased over control levels, suggesting that short-term ETS exposures are

sufficient to enhance plaque development. Furthermore, the increase in plaque size

was not as great as that observed under higher exposure conditions, suggesting the

existence of an exposure– response relationship. Zhu in 1993 also demonstrated

that ETS increases atherosclerosis in the lipid- and cholesterol-fed rabbit model.

The percentage of arterial surface area that was covered by atherosclerotic plaques

was increased by ETS in an exposure-related manner in the aorta and pulmonary

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artery; the increase was independent of serum triglyceride, cholesterol and high-

density lipoprotein (HDL) cholesterol levels. Animal studies also indicate that

exposure to tobacco smoke increases platelet activation, which can contribute to

the development of atherosclerosis and thrombosis (DHHS, 1993). Sun in 1994

and Zhu in 1993 reported significantly shorter bleeding times in rabbits exposed to

tobacco smoke compared with control rabbits. Both groups also reported that

bleeding times were reduced by a similar magnitude for all exposure groups,

suggesting a saturation of the effect of tobacco smoke on platelets. Tobacco smoke

has also been shown to increases leukocyte activation, which can also contribute to

the development of atherosclerosis. Other animal studies suggest that ETS causes

exacerbation of ischaemia/reperfusion injury

Other toxicological

Other toxicological effects observed in experimental animals include reproductive

and immune system effects. For example, Rajini in 1994 exposed pregnant rats

intermittently to SS and observed small but significant reductions in mean pup

weight in the resulting litters. A study of immune system effects (Ortega, 1994)

revealed both a reduction in the number of alveolar macrophages with phagocytic

activity and a decrease in the phagocytic efficiency of these activated macrophages

in mice after acute exposure to the smoke of just one cigarette.

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Effects on humans

Epidemiological studies of ETS and chronic diseases such as lung cancer and heart

disease are faced with the difficulties of discriminating between exposed and

unexposed subjects and estimating past exposures. Never-smoking women are the

most common subjects of these studies, because the prevalence of smoking in

women has historically been less than that of men. Furthermore, most researchers

consider the smoking status of the husband to be the best single surrogate of past

ETS exposure for adult female never-smokers. In general, home exposure has been

found to be the greatest single source of exposure contributing to total ETS

exposure (Riboli, 1990). Other exposure surrogates used, such as exposure at work

or during childhood, tend to be less reliable because workplace exposure is less

stable and the exposure sources are more difficult to recall over time, especially

when proxy interviews are the source of exposure information (Stockwell, 1992).

Two forms of exposure misclassification exert a downward bias on relative risk

estimates in ETS epidemiology studies and make ETS-related health effects

difficult to detect. In the first, an individual classified as “exposed” based on

spousal smoking status may actually receive little exposure; in the second, an

“unexposed” person may receive considerable exposure from sources other than

the spouse (e.g. workplace or social exposures). In most Western societies, ETS is

so ubiquitous that recruitment of a truly “unexposed” group is impossible. Spousal

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or home exposure is generally a better surrogate of total ETS exposure in more

traditional societies such as Greece and Japan, with historically high male and low

female smoking prevalences. Such countries may offer the best opportunities for

studying the effects of long-term exposure to ETS. A potential source of upward

bias, known as smoker (status) misclassification bias, arises because some current

or former smokers will be misclassified as people who have never smoked (never-

smokers). Smokers thus misclassified would be more likely to develop lung cancer

and to be married to smokers (i.e. classified as “exposed” in ETS studies) than true

never-smokers. Smoker misclassification rates reported from population survey

studies suggest that this bias, if it exists in the lung cancer studies, could explain an

increase in risk of 10–15% in some studies. There is a substantial database on a

variety of non-cancer respiratory effects and reduced birth weight, and there are a

few recent studies on sudden infant death syndrome. Each of these health effects is

discussed below:

Lung cancer

The evidence on ETS and lung cancer has been assessed by many health

organizations, all of which concluded that exposure to ETS increases the risk of

lung cancer. The US Environmental protection Agency (EPA) declared ETS to be

a known human lung carcinogen based on the total weight of evidence:

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  similarities in chemical composition between ETS and MS, including over

40 known or suspected human carcinogens;

 the known lung carcinogenicity of MS, with clear exposure–response

relationships down to low levels and no evidence of a threshold;

 supporting evidence from animal bioassays and genotoxicity tests;

 measured exposure to, and bodily uptake of, ETS constituents

The consistent exposure-related increases in risk seen in so many epidemiological

studies from different countries using different designs (USEPA, 1992)

Non-cancer respiratory health effects

Children

Acute respiratory illnesses are one of the leading causes of morbidity and mortality

during infancy and childhood. They may also weaken the lung and predispose it to

asthma and other chronic respiratory diseases and lower levels of respiratory

function later in life. Considering the known adverse acute and chronic effects of

active smoking on the respiratory system, it is plausible that exposure to ETS could

similarly adversely affect the immature system of infants, and that continued

exposure could be a major risk factor in disease development throughout life

(USEPA, 1992)

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Nearly all studies of ETS in children focus on the level of parental, and especially

maternal, smoking. Parental smoking is generally a very good surrogate for total

ETS exposure in young children, although exposure misclassification could be an

important source of downward bias in studies of older children (Spitzer, 1990)

At least 150 epidemiological studies on ETS and non-cancer respiratory health

effects in children have been published in the last 25 years. Several reviews

(Spitzer, 1990) have already assessed the database, and there is strong consensus

that ETS affects the developing respiratory system and causes an increased risk of

the following health effects:

 lower respiratory tract infections (e.g. bronchitis, bronchiolitis and

pneumonia) in infants and young children;

 chronic middle-ear effusion in young children;

 increased frequency and severity of asthma attacks in asthmatic children;

 irritation of the upper respiratory tract;

 reduced lung function.

Several recent studies on respiratory effects in children are especially noteworthy

because they ascertain biomarker evidence of ETS exposure, in addition to

questionnaire data such as asthma, middle ear effusions, bronchitis and reduced

lung function (Strachan1989). The biomarker data correlate well with the

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questionnaire data and the various respiratory effects, validating the use of

questionnaire data and also supporting the direct association between recent ETS

exposure and non-cancer respiratory health effects.

Adults.

A number of reviews have concluded that adult nonsmokers exposed to ETS may

experience small reductions in lung function and an increased frequency of

respiratory symptoms. A review by Tredaniel in1994 found no consistent evidence

for an association between ETS and chronic respiratory symptoms or chronic

obstructive pulmonary disease, including asthma, although decreased lung function

from ETS exposure was noted. Other studies have reported symptoms of acute

irritation of the eyes and respiratory tract associated with ETS exposure (Weber,

and Grandjea, 1987).

Decreased birth weight

It is well established that maternal smoking during pregnancy is causally

associated with low birth weight, in an exposure-related manner. Maternal

smoking has been reported to cause an average decrease in birth weight of 150–

200g. This is supported by evidence from animal studies. The most widely

accepted hypothesis for this effect on fetal development is that smoking induces

fetal hypoxia, probably mediated, at least in part, by carbon monoxide and/or

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nicotine. Carbon monoxide is known to decrease the oxygen-carrying capacity of

hemoglobin. Fetal hemoglobin has a higher affinity for carbon monoxide than

adult hemoglobin, and the impact on the fetus is more severe than on the mother as

fetal tissues receive even less oxygen. Nicotine is a vasoconstrictor and is believed

to decrease placental perfusion, which could also lead to low fetal tissue

oxygenation. A number of studies have shown that pregnant nonsmokers exposed

to ETS also have an increased risk of delivering babies with lower birth weights.

While most of the decreases in birth weight are of small magnitude and do not

achieve statistical significance, the studies demonstrate a consistent pattern, even

after adjusting for major potential confounders and considering potential smoker

misclassification bias. The decrease in mean birth weight associated with ETS

exposure generally ranges from 10 - 110g, with an average decrease of about 35g.

Increased cotinine levels have been measured in the amniotic fluid of pregnant

nonsmokers exposed to ETS, as well as in the urine of their newborn infants on the

first day of life, confirming that the fetus is exposed to ETS constituents (Jordano,

1990)

Sudden infant death syndrome (SIDS)

Sudden infant death syndrome (SIDS) is the sudden, unexpected and inexplicable

death, usually during sleep, of infants aged 1 month to 1 year. In developed

countries, this is the most common cause of post-neonatal death. Maternal smoking
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has been consistently shown to be a major risk factor, independent of low birth

weight and other potential confounders. The etiology is, by definition, unknown;

however, one of the proposed mechanisms by which tobacco smoke may

contribute to SIDS involves the reduction of infants’ hypoxia tolerance. Milerad in

1995 observed that nicotine administration decreased the hyperventilatory response

to hypoxia in young lambs

Cardiovascular effects

A number of recent reviews have assessed the evidence on ETS exposure and

cardiovascular disease and concluded that ETS causes such disease in nonsmokers.

Quantitative risk estimates of 35000 to 40000 ETS-attributable heart disease deaths

per year for never-smokers and long-term former smokers in the United States.

Mechanistic studies have shown that there is evidence of cardiovascular effects in

humans of acute ETS exposures. The major effects include decreased oxygen-

carrying capacity resulting in decreased exercise ability and, potentially ischaemia,

as well as increased platelet activation, endothelial damage, altered lipoprotein

levels and increased arterial wall thickness, which can promote atherosclerosis and,

in the case of platelet activation, thrombosis. Ischaemia, atherosclerosis and

thrombosis increase the risk of myocardial infarction and other serious

cardiovascular effects (Steenland, 1992)

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Risk factors for tobacco initiation

1. Biological:

 Developmental aspects of adolescent age group include (a) establishing

independence and autonomy, (b) forming a coherent self-identity and (c)

adjusting to psycho-social changes associated with physical maturation.

 Gender: tobacco use is more common among males in India.

2. Psychological:

Low emotional stability and risk taking behavior are more common in tobacco

users. Existence of some mental disorders also increases the risk of tobacco use.

3. Social and Environmental:

Parental influence, lower education status, attraction towards role models, cultural

practices, etc.

RISKS FROM SMOKING

The chart below gives the various risks and effects seen in the human body as a

result of smoking

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Therapy for tobacco cessation at the individual level

Therapy for tobacco-cessation can be broadly classified into two types: a)

pharmacological and b) non-pharmacological.

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A. Pharmacological:

1. Nicotine Replacement Therapy: The general principle of nicotine

replacement therapy is to present the patient with a safer and more

therapeutically manageable form of the nicotine that directly alleviates the

signs and symptoms of withdrawal and craving. Nicotine chewing gum is a

very common method. There are other nicotine delivery systems available:

 Transdermal patches for delivery of nicotine through the skin.

 Nasal nicotine solution

 Nicotine vapour inhalers (smokeless tobacco).

Nicotine lozenge and sub-lingual tablets are also available as a form of nicotine

replacement therapy. These devices increase quitting rates by approximately 1.5 to

2 times, regardless of setting.

2. Other Pharmacological Therapies: It includes anti depressants and

symptomatic treatment. Pharmacological strategies have a useful role in alleviating

withdrawal symptoms.

B. Behavioural treatment: There are number of techniques which can be used to

manage the cessation of tobacco use.

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 1. Psychoeducation is providing information about the tobacco and its effects

on human body. Discussing about the changes occur due to nicotine use are

also informed to the user. This helps the patient to accept the corrective

method.

2. Aversion therapy: Aversion procedures involve pairing of smoking with

unpleasant imagery scripts with electric shock, or with the unpleasant effects

produced by smoking itself. These techniques are designed to create

aversions to cigarette smoke-effective reactions characterized by distaste,

disgust, fear, or displeasure. Such reactions reduce the incentive to smoke.

3. Social support: Spouses of the smokers are also included in smoking

cessation program to teach them how to be supportive of clients’ quitting

program.

CONCLUSION

Tobacco smoking is really a dangerous activity considering the effects that result

from it. Being a first hand and /or second hand smoke all have one effect or the

other. The various effects caused by tobacco smoking are alarming and cannot be

over stressed hence its use should be discouraged.

RECOMMENDATION

 The use of tobacco should be enacted by the Government

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  There should be ban of public smoking

 Advertisement, sponsorship and promotion of tobacco and its products

should be discouraged

 Sales of tobacco should be prohibited to minors (under age of 18)

 The slogan ‘smokers are liable to die young should be alarmed)

REFERNCES

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