The health effects of environmental tobacco smoke
Since the early 1970s, medical and environmental health journals have published
numerous articles presenting evidence on the health effects of environmental
tobacco smoke. A number of major medical research agencies including Australia’s
National Health and Medical Research Council (NHMRC) have reviewed this evidence
to draw conclusions on the health effects of passive smoking. This section
provides a brief overview of the evidence. A complete list of the major reviews
on ETS and passive smoking is in Appendix C.
More information
Overview of evidence on the major health effects of ETS exposure
Epidemiological evidence linking ETS with ill-health is supported by knowledge
of the chemical make-up of ETS and its biological effects. It is estimated
that tobacco smoke contains over 4000 chemical compounds, including 43 known
carcinogens (cancer causing agents). [30]
It is generally accepted within the scientific community that there is no
safe dose for a carcinogen.
Furthermore, many tobacco smoke constituents are pharmacologically active,
toxic and mutagenic (facilitating genetic mutations). Given the similarity
of the chemical composition of ETS and mainstream tobacco smoke, it is plausible
that non-smokers exposed to ETS will be at risk of contracting the same diseases
as active smokers.
Cardiovascular disease
Since the mid 1980s, an increasing number of studies have implicated exposure
to ETS as a risk factor for heart disease. Indeed, all the recent major reports
on the effects of passive smoking have arrived at this conclusion.
The mechanisms by which ETS causes heart disease in non-smokers are thought
to be similar to those by which heart disease is caused in active smokers.
For example, a 1991 NSW study has shown that exposure to ETS increases fibrinogen
concentrations in non-smokers. [31]
Fibrinogen contributes to blood clotting by increasing the aggregation of
platelets (cell fragments that contribute to the formation of blood clots).
This increases the likelihood of a thrombus (a blood clot in the vascular
system) as well as damage to the lining of the coronary arteries. Even a low
exposure to ETS can significantly increase platelet aggregation in non-smokers,
to levels approaching those of regular smokers. [32]
One of the major chemical constituents of tobacco smoke known to contribute
to heart disease is carbon monoxide (CO). When carbon monoxide is inhaled,
it binds to haemoglobin (a protein in the blood which normally transports
oxygen to body tissues) thus starving the tissues of oxygen.
The NHMRC review cited evidence that increased exposure to carbon monoxide
is associated with angina in people with established heart disease and, perhaps
more significantly, with potentially fatal cardiac dysrhythmias (disturbances
of the heart’s electrical rhythm). [33]
Other significant findings from the medical literature
- The NHMRC found that ‘the risk of heart attack or death from coronary
heart disease is 24% higher in never-smokers who live with a smoker compared
with unexposed never-smokers.’ [34]
A 1999 US analysis of 18 studies found a 25% increased risk of heart disease
among non-smokers exposed to ETS. [35]
- A major US study in 1997 found a strong link between exposure to ETS and
the progression of atherosclerosis, with exposure to ETS associated with
a 20% progression while active smoking was associated with a 50% progression.
[36]
- Another major 1997 US study noted the growing evidence of various mechanisms
for a causal association between ETS and heart disease. This evidence includes
compromised exercise performance among non-smokers exposed to ETS, as well
as carotid (artery) wall thickening and compromised endothelial function
(the endothelium is the layer of cells that line the blood vessels and the
cavities of the heart). [37]
- Researchers at the University of Helsinki found in a 1998 study that exposure
to ETS can significantly reduce antioxidant levels in the blood. Antioxidants
prevent damage by highly active oxygen radicals (free radicals) which
combine with cholesterol in the blood to form an oxidised cholesterol which
is more inclined to stick to blood vessel walls, contributing to atherosclerosis.
[38]
- A 1999 Australian and Finnish study suggests that the damaging effect
of ETS on the arteries may be only partially reversible in young adults.
Among the study group, cessation of exposure to ETS for more than two years
was associated with improved arterial function. However, arterial function
did not return to normal as measured in a control group who had neither
actively or passively smoked. [39]
- In 1992, a US National Institute for Occupational Health and Safety review
stated that ‘individual lifetime excess risks of heart disease death due
to ETS of one to three per 100 can be compared with much lower excess risks
of one death per 100,000 which are often used for determining environmental
limits for other toxins.’ [40]
- In a US review paper published in 1991, it was estimated that approximately
10 times as many deaths occur from ETS-induced heart disease as from ETS-induced
lung cancer. [41]
Lung cancer
Cigarette smoking is the major cause of lung cancer. Around 5000 Australians
die annually from tobacco induced lung cancer. [42]
Passive smoking is also a risk factor for lung cancer—albeit a somewhat smaller
risk factor than active smoking.
Evidence for a link between ETS exposure and lung cancer is provided by epidemiological
research. Other evidence includes the knowledge that sidestream smoke (smoke
emitted from a burning cigarette) contains many of the carcinogenic compounds
found in mainstream smoke (smoke inhaled directly into a smoker’s lungs).
Furthermore—although sidestream smoke becomes diluted once it enters the atmosphere—it
contains many carcinogens in greater concentrations than does mainstream smoke.
[43] The presence of carcinogen biomarkers
of tobacco smoke exposure in the bodies of non-smokers after exposure to ETS
provides further evidence of an uptake of carcinogens from ETS. [44]
Based on a review of the evidence, the US Department of Health and Human
Services National Toxicology Program’s Ninth Report on Human Carcinogens
2000 concluded that ETS is a ‘known human carcinogen’. [45]
Significant findings
- The NHMRC reviewed over 40 epidemiological studies from a number of countries
on ETS and lung cancer. Most of these focused on lung cancer in women who
had never smoked. The NHMRC concluded: ‘that passive smoking causes lung
cancer is biologically plausible, the evidence is coherent and consistent,
and dose–response relationships are present’. [46]
- After reviewing the evidence, the UK Government’s Scientific Committee
on Tobacco and Health concluded in its 1998 report that exposure to ETS
is a cause of lung cancer and that, in those with long-term exposure, the
increased risk is in the order of 20–30%. [47]
- A 1997 Californian Environmental Protection Authority report on the health
effects of ETS identified a causal association between ETS exposure and
lung cancer. [48]
- In 1998 a major European study conducted by the International Agency for
Research on Cancer found elevated lung cancer risks associated with long
term exposure to ETS in the home and in the workplace[*],
estimated at 16% and 17% respectively greater than for subjects not exposed.
[49] Again, a dose–response relationship
was identified. The study’s key author, Dr Paolo Boffetta, stated that the
study provided further evidence of a causal link between passive smoking
and lung cancer. [50]
- Research showing that benzo[a]pyrene—a chemical constituent of tobacco
smoke—damages the P53 tumour suppressor gene provides further evidence for
a link between ETS and lung cancer. [51]
- A 1990 USEPA review of ETS-related lung cancer risk assessments noted
that the risk was ‘about 57 times greater than the combined estimated cancer
risk from all the hazardous outdoor air pollutants currently regulated by
the USEPA’. [52]
Stroke
A number of studies have found a link between active smoking and stroke.
[53,54,55]
A major New Zealand study conducted in 1999 found that passive smoking was
associated with an increased risk of approximately 82% for non-smokers exposed
to ETS. The authors stated that their finding provides support for efforts
to reduce the prevalence of passive smoking. [56]
Breast cancer
A number of studies have indicated an association between passive smoking
and breast cancer, although little direct evidence has been demonstrated.
[57,58,59]
A 1999 US study found significantly increased risks among women who had been
exposed to tobacco smoke (both actively and passively) before 12 years of
age. Among the women who had been early passive smokers the increased risk
was four-and-a-half times that of never exposed women, while the risk among
the early active smokers was seven-and-a-half times that of those never exposed.
The authors of the study suggested that a possible mechanism may involve the
susceptibility of early-age breast tissue to the chemical mutagens in tobacco
smoke.
However a more recent study that the authors claimed to be particularly compelling
because of its large sample and prospective design as compared with most earlier
studies, found no association between exposure to ETS and breast cancer. Though
the study did find a small, not statistically significant increased risk of
breast cancer mortality among women who were married before age 20 to smokers.
[60]
The findings of recent studies suggest a need for further research into any
possible relationship between breast cancer and exposure to tobacco smoke.
Respiratory health effects in adults
The NHMRC examined the evidence on the relationship between ETS and respiratory
illness in adults. Studies reviewed by the NHMRC showed that acute upper and
lower respiratory symptoms were common.
Upper respiratory symptoms included:
- nasal symptoms
- sore throat and hoarseness.
The lower respiratory symptoms most commonly reported were:
- chronic cough
- chronic phlegm
- shortness of breath (see below for asthma)
- chest illness.
Irritation of the eyes was another common symptom.
In summary, the NHMRC stated that:
…adult non-smokers exposed to ETS frequently experience symptoms
resulting from irritation of the upper and lower respiratory tract. Small
decreases in lung function, both acutely and chronically, are often evident,
with larger decreases occurring in subjects with asthma. Subtle, but statistically
significant, effects of ETS on adult respiratory health probably exist, and,
while the magnitude of the effect of ETS on adult lung function appears small,
it may be important in people with co-existing diseases. [61]
In its landmark 1993 report Respiratory Health Effects of Passive Smoking:
Lung cancer and other disorders, the USEPA came to similar conclusions.
One of its primary findings was:
Passive smoking has subtle but significant effects on the respiratory health
of non-smoking adults, including coughing, phlegm production, chest discomfort,
and reduced lung function. [62]
Significant findings
- A 2000 study found that invasive pneumococcal disease was associated
with both active smoking and passive smoking. The increase in risk was reported
to be 51% for active smokers and 17% for passive smokers. [63]
- A study into the respiratory health of Californian bartenders after the
state-wide introduction of smoking bans in bars and taverns found significant
and rapid improvements in pulmonary (lung) function as well as reduced respiratory
symptoms. [64]
Asthma
There is evidence that ETS can exacerbate asthma in those who already suffer
from it. As one study concluded, ‘the control of asthma is poor and morbidity
greater in adult patients with asthma exposed to ETS at home and/or at work’.
[65]
Asthma in children is discussed below.
Respiratory health effects in children
There is evidence to suggest that babies and children are particularly susceptible
to the health effects of ETS, and that these effects commonly manifest as
lower respiratory illness. Lower respiratory illnesses common in childhood
include:
- croup
- tracheo-bronchitis
- bronchiolitis
- asthma
- pneumonia.
Significant findings
- The NHMRC, the WHO and the USEPA agree that the weight of evidence suggests
a causal relationship between ETS exposure in the home and lower respiratory
tract infections in young children (up to two years old). [66,67,68]
- During the past decade the evidence linking ETS with asthma in childhood
has grown.
- The USEPA’s review of the evidence as at 1992 concluded that passive
smoking is causally associated with additional episodes and increased
severity of asthma in children who already have it. The USEPA also found
that the evidence suggested a causal association between ETS and new
cases of childhood asthma, although it was not conclusive. [69]
- By 1997, the NHMRC was able to conclude that ‘the evidence now supports
a causal relationship between ETS and asthma in children’. It notes
that ‘the association of passive smoking and childhood asthma is most
consistent at high exposures’ and that there is ‘some evidence that
the strength of the association between ETS and asthma symptoms is greater
in older children, which may be a consequence of cumulative, prolonged
exposure’. [70]
- The NHMRC found that there is increasing evidence of a link between ETS
and sudden infant death syndrome (SIDS). The report notes that the findings
are consistent among several studies from several different countries, that
a dose–response relationship has been documented and there are plausible
mechanisms by which ETS may have an influence on SIDS. It concluded that
the evidence indicates a causal association between ETS and SIDS. [71]
- Another effect of ETS exposure in young children is to reduce lung function.
According to the NHMRC, this effect appears to be greater among children
with pre-existing respiratory illnesses such as asthma. [72]
ETS and pregnancy
The effects of smoking on the foetus are well documented. According to one
major review, low birthweight babies, spontaneous abortions and a range of
other complications of pregnancy and labour occur more frequently in smokers.
[73]
A biological explanation for such outcomes may lie in the ability of the
toxic constituents of tobacco smoke, such as nicotine and carbon monoxide,
to cross the placenta. [74] A 1990
study which measured the level of cotinine (the major metabolite of nicotine)
in the amniotic fluid and urine of pregnant women found that amniotic cotinine
levels were eight times higher in active smokers and two-and-a-half times
higher in passive smokers than in non-smokers not exposed to ETS. [75]
Nicotine is known to affect foetal heart rate and breathing movements. [76]
Carbon monoxide reduces the amount of oxygen reaching the foetus. [77]
There have been a number of studies of passive smoking by non-smoking women
during pregnancy. The studies indicate that exposure to ETS during pregnancy
may affect foetal growth, resulting in reduced birthweight. [78]
Otitis media with effusion (glue ear) in children
Otitis media with effusion (glue ear) occurs more often among children of
smoking parents. The symptoms of glue ear include inflammation with discharge
from the middle ear, difficulty in hearing and earache.
The NHMRC concludes that, on balance, there is a causal link between ETS
and glue ear, although little is known about the biological mechanisms involved.
[79]
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Footnotes
* The study did not take into account recreational exposure to ETS.
