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May 2004
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Passive smoking and lung cancer. 2
Passive smoking
and heart disease. 3
Other
circulatory diseases. 4
Passive smoking and respiratory diseases. 4
The impact of passive smoking on children. 4
Other effects of passive smoking. 5
Policy Implications. 5
Public Places. 5
Workplace. 6
Children. 6
Estimate of UK
impact of passive smoking. 6
Tobacco Industry Approach. 6
Conclusion. 7
Breathing
other people's smoke is called passive, involuntary or second‑hand
smoking. The non-smoker breathes "sidestream" smoke from the
burning tip of the cigarette and "mainstream" smoke that has been
inhaled and then exhaled by the smoker.
Environmental tobacco smoke (ETS) is a major source of indoor air pollution. Tobacco smoke contains over 4000 chemicals,
some of which have marked irritant properties and some 60 are known or suspected carcinogens
(cancer causing substances).[1]
Evidence of the health impact of passive smoking has
been building up over the past two decades.
During the 1980s, a number of comprehensive reviews of the effects of
passive smoking were published. These
include reports by the US National Research Council, [2], the 1986 Report of the US Surgeon General, [3], the National Health and
Medical Research Council of Australia [4] and the UK Independent Scientific Committee
on Smoking and Health [5]. This culminated in a
major review by the US Environmental Protection Agency [6] published in 1992 which
classified ETS as a class A (known human carcinogen).
More recently, further major reviews on passive
smoking have been published. These include studies by the UK
Government-appointed Scientific Committee on Tobacco and Health[7] (SCOTH), a World Health Organization (WHO)
consultation report on Environmental Tobacco Smoke and Child Health,[8] a report by the California Environmental
Protection Agency[9] (EPA)
and a review by the International Agency for Research on Cancer (IARC). [10] The California EPA identified passive smoking as a risk factor
for the following:
Childbirth and infancy
Low birthweight
Cot death (SIDS)
Illnesses in children
Middle ear infection
Asthma (induction & exacerbation)
Bronchitis (induction & exacerbation)
Pneumonia (induction & exacerbation)
Illnesses in adults
Heart disease
Stroke
Lung cancer
Nasal cancer
The California EPA report also identified
a link between passive smoking and the following:
Spontaneous abortion (miscarriage)
Adverse impact on learning and behavioural
development in children
Meningococcal infections in children
Cancers and leukaemia in children
Asthma exacerbation in adults
Exacerbation of cystic fibrosis
Decreased lung function
Cervical cancer
More than 50 studies of passive smoking and lung
cancer risk in never smokers have been published over the past 25 years. Most show an increased risk, especially
among people with a high level of exposure.
To evaluate this information, meta-analyses have been conducted
whereby the relative risks from the individual studies are pooled
together. These meta-analyses show
that there is a statistically significant risk of lung cancer risk among non-smokers
living with smokers. The risk is in
the order of 20% for women and 30% for men.
Furthermore, studies of non-smokers exposed to environmental tobacco
smoke at work show an increased risk of lung cancer of the order of 16 to 19
per cent. The IARC review led the
authors to conclude that “This evidence is sufficient to conclude that
involuntary smoking is a cause of lung cancer in never smokers.”10
Hackshaw et
al [11] analysed 37 published epidemiological studies of the
risk of lung cancer (4626 cases) in non-smokers. The review found that the excess risk of
lung cancer in life-long non-smokers who lived with a smoker was 24 per
cent (95% confidence interval: 13% to
36%). Adjustment for factors such as
diet had little overall effect.
Tobacco specific carcinogens in the blood of the non-smokers provided
clear evidence of the effect of passive smoking. In addition, the study found a dose-response
relationship between a non-smoker’s risk of lung cancer and the number of cigarettes
and years of exposure to the smoker.
The authors concluded that “The
epidemiological and biochemical evidence on exposure to environmental tobacco
smoke, with the supporting evidence of tobacco specific carcinogens in the
blood and urine of non-smokers exposed to environmental tobacco smoke,
provides compelling confirmation that breathing other people’s tobacco smoke
is a cause of lung cancer.”
A
major European study of non-smokers’ exposure to ETS also found a small
increased risk of lung cancer in non-smokers who work in a smoky environment
or live with a spouse who smokes. The study by Boffetta et al[12] was conducted
in 12 centres from seven European countries.
A total of 650 patients with lung cancer and 1542 control subjects up
to 74 years of age were asked about their exposure to ETS during childhood,
adulthood, at home, in the workplace, in vehicles and in public places. The study found that exposure during
childhood was not associated with an increased risk of lung cancer: odds
ratio (OR) for ever exposure = 0.78 (95% confidence interval: 0.64 -
0.96). The OR for exposure to spousal
ETS was 1.16 (95% CI: 0.93 - 1.44). No
clear dose response relationship could be demonstrated for cumulative spousal
ETS exposure. The OR for workplace exposure was 1.17 (95% CI: 0.94 - 1.45) with
possible evidence of increasing risk of duration of exposure. Although the increased risk of lung cancer
is small, the findings are within the range of a 10-30% increase in risk
found in other major studies of lung cancer and ETS exposure.
A review of the evidence to date on passive smoking
and lung cancer risk, including the above studies, by the UK’s Scientific
Committee on Tobacco and Health (SCOTH) concluded: “that
long term exposure of non-smokers to ETS caused an increase risk of lung
cancer which, in those living with smokers, is in the region of 20-30%”.
The report of the California EPA drew similar
conclusions after reviewing evidence from major US studies. The reports states: “Taken together, the recent studies provide additional evidence that
ETS exposure is causally associated with lung cancer. The consistency of the findings in the five
recent studies and the meta-analysis result of the US EPA indicate about a 20
per cent increase risk of lung cancer in non-smokers.”
Evidence of a
link between passive smoking and heart disease began to be established in the
mid 1980’s. The first qualitative
reviews were included in the Report of the US Surgeon General, 1986 and the report of
the US National Research Council, 1986.
Both reviews concluded that an association between ETS and coronary
heart disease (CHD) was biologically plausible but the epidemiological
evidence was inconclusive.
Studies by
Glantz and Parmley[13]
[14]
in the early 1990s estimated that heart disease caused by passive smoking was the third leading preventable
cause of death in the United States, ranking behind active smoking and
alcohol abuse, and that non-smokers
living with smokers had an increased risk of heart disease of around
30%.
Analysis of a
large sample in the United States also showed an elevated heart disease
risk of around 20%[15]. Given how widespread heart disease is in non-smokers,
a 20% additional risk is very significant.
The authors concluded:
If true, ETS might account for an
estimated 35 000 to 40 000 heart disease deaths per year in the United States.
Since then,
studies have shown conclusively that not only does exposure to ETS increase
the risk of heart disease in non-smokers but that the risks are non-linear.
It would appear that even a small exposure to tobacco has a large effect on heart disease,
with further exposure having a relatively small additional effect. This may be explained by the fact that
exposure to ETS causes the blood to thicken - a phenomenon known as platelet
aggregation. New research has shown
that even half an hour’s exposure to environmental tobacco smoke by
non-smokers is enough to adversely affect cells lining the coronary
arteries. The dysfunction of these
endothelial cells contributes towards the narrowing of arteries and a
reduction in blood flow. [16]
Unlike the risk
for lung cancer, where the risk is roughly in proportion to smoke exposure,
passive smokers’ risk of heart disease may be as much as half that of someone
smoking 20 cigarettes a day even though they only inhale about 1% of the
smoke.
A
review of 19 published studies of
the risk of heart disease by Law et al[17] found that non-smokers have an
overall 23 per cent increased risk of heart disease when living with a
smoker, after adjusting for confounding factors such as diet. The authors
also found that the immediate effect of a single environmental exposure was
to increase risk by an estimated 34%.
This compares with a risk of 39% from smoking one cigarette per
day.
In
a study by He et al[18] the authors reviewed 18 epidemiological studies and
found that, overall, nonsmokers exposed to environmental tobacco smoke had a
relative risk of coronary heart disease of 1.25 (ie a 25 per cent increased
risk compared with nonsmokers not exposed).
The relative risk for men was 1.22
and women 1.24. Non-smokers
exposed to tobacco smoke at home had an overall risk of 1.17, while at work
the risk was found to be 1.11.
While the risk of heart disease in non-smokers
exposed to ETS is proportionally large, it would appear that some of the
early damage to arteries caused by smoking may be reversible in healthy
adults if further tobacco smoke exposure is avoided for at least a year.[19] The study by Raitakari et al in Australia
found that most improvement in the former passive smokers was evident after 2
years of cessation of passive smoking.
Research in New
Zealand by Bonita et al
revealed that passive smoking as well
as active smoking increases the risk of stroke.[20] The study found passive smoking exposure
increased the risk of stroke in non-smokers by 82% ( odds ratio = 1.82; 95% confidence
interval = 1.34-2.49). The risk was
significant in men (OR = 2.10; 95% CI
1.33-3.32) and in women (OR = 1.66; 95% CI: 1.07-2.57). By comparison, active smokers had a
fourfold risk of stroke compared with people who had never smoked or had
stopped smoking more than 10 years earlier and who were not exposed to
ETS (OR = 4.14; 95% CI 3.04-6.63.) Given that stroke
is a common condition, this means that passive smoking is having a serious health
impact on non-smokers.
Passive smoking
has subtle but significant effects on the respiratory health of non-smoking
adults, including increased coughing, phlegm production, chest discomfort and
reduced lung function. For people with
asthma, ETS can cause serious problems as cigarette smoke is a common trigger
for asthma attacks. There are 3.5
million people with asthma in the UK and ETS causes difficulties for up to
80% of them.[21]
Adults exposed
to ETS at home or in the workplace have a 40-60% increase in the risk of
asthma compared with adults who are not exposed in these places. Passive
smoking as a cause of chronic
obstructive pulmonary disease (COPD) in non-smokers has been demonstrated in
a number of studies, although the magnitude of the association is small. This may be a reflection of the lack of
data and complexity of designing studies to measure the effects of
non-malignant respiratory diseases.[22]
The review by the California EPA notes that recent studies suggest
that ETS may make a significant contribution to the development of chronic
respiratory symptoms in non-smoking adults.
According to the World Health Organization, almost
half the world’s children (700 million) are exposed to tobacco smoke by the
1.2 billion adults who smoke. A
consultation document issued by the WHO concluded that passive
smoking is a cause of bronchitis, pneumonia, coughing and wheezing, asthma
attacks, middle ear infection, cot death, and possibly cardiovascular and
neurobiological impairment in
children.8
Approximately half of all children in the UK are
exposed to tobacco smoke in the home.
Young children are particularly vulnerable to the health impact of
passive smoking. In its 1992 report,
“Smoking and the Young”, the Royal College of Physicians estimated that
17,000 children under the age of five are admitted to hospital every year in
the UK as a
result of illnesses resulting from passive smoking.[23]
For young children, the major source of tobacco
smoke is smoking by parents and other household members. Maternal smoking is usually the largest
source of ETS because of the
cumulative effect of exposure during pregnancy and close proximity to the
mother during early life. Results from
more than 40 studies of the impact of parental smoking on lower respiratory
tract illnesses in children have shown that children whose mothers smoke are
estimated to have a 1.7-fold (95% CI = 1.6 – 1.9) higher risk of respiratory illnesses than children of
non-smoking mothers. Paternal smoking
alone causes a 1.3-fold (95% CI = 1.2 - 1.4) increase in risk.
Maternal smoking during pregnancy is a major cause
of sudden infant death syndrome (SIDS)
as well as other health effects including low birth weight and reduced lung
function. In addition, the WHO
consultation document notes that ETS exposure among non-smoking pregnant
women can cause a decrease in birth weight and that infant exposure to ETS
may contribute to the risk of SIDS.
Asthma is the most common chronic disease of
childhood. Both asthma and respiratory
symptoms (wheeze, breathlessness and phlegm) are increased among children
whose parents smoke. | 
