READ: Most Comprehensive ETS Report -
40,000-67,000 Deaths/Yr
The National Cancer Institute (NCI) has just issued what it describes
at "the most comprehensive report on the health risks of secondhand smoke
ever conducted. " In it the NIH concludes that:
* ETS kills between 40,000 and 68,000 Americans each year
* ETS causes lung cancer, sinus cancer, and heart disease deaths
* ETS may cause cervical cancer, spontaneous abortions, cystic fibrosis,
and other conditions
* Even outdoor exposure can present a serious problem
Reprinted below, in a form in which it can easily be downloaded,
searched, and reprinted, is a word-for-word copy of the entire
Executive Summary. Also included -- and presented first on this page
-- are a table showing the many different diseases caused by ETS,
and a chart showing the number of people killed or made ill each year by
ETS.
HEALTH EFFECTS ASSOCIATED WITH EXPOSURE TO ENVIRONMENTAL
TOBACCO SMOKE (ETS)
EFFECTS CAUSALLY ASSOCIATED WITH ETS
Developmental Effects:
Fetal Growth: Low birthweight or small for gestational age
Sudden Infant Death Syndrome (SIDS)
Respiratory Effects:
Acute lower respiratory tract infections in children
( e.g., bronchitis and pneumonia)
Asthma induction and exacerbation in children
Chronic respiratory symptoms in children
Eye and nasal irritation in adults
Middle ear infections in children
Carcinogenic Effects:
Lung Cancer
Nasal Sinus Cancer
Cardiovascular Effects:
Heart disease mortality
Acute and chronic coronary heart disease morbidity
EFFECTS WITH SUGGESTIVE EVIDENCE OF A CAUSAL ASSOCIATION WITH
ETS EXPOSURE
Developmental Effects:
Spontaneous abortion
Adverse impact on cognition and behavior
Respiratory Effects:
Exacerbation of cystic fibrosis
Decreased pulmonary function
Carcinogenic Effects:
Cervical cancer
SOURCE: NIH MONOGRAPH 10
US Estimated Annual Morbidity and Mortality in US Nonsmokers Associated with ETS
CONDITION
Developmental Effects
Low birthweight 9,700-18,600 cases
Sudden Infant Death
Syndrome (SIDS) 1,900-2,700 deaths
Respiratory Effects in Children
Middle ear infection 0.7-1.6 million
physician office visits
Asthma induction 8,000-26,000 new cases
Asthma exacerbation 400,000-1,000,000 children
Bronchitis or pneumonia 150,000-300,000 cases
in infants and toddlers 7,500-15,000
(18 months and under) hospitalizations
136-212 deaths
Cancer
Lung 3,000 deaths
Nasal sinus N/A
Cardiovascular Effects
Ischemic heart disease 35,000-62,000 deaths
SOURCE: NIH MONOGRAPH 10
EXECUTIVE SUMMARY
Exposure to environmental tobacco smoke (ETS) has been linked to a variety
of adverse health outcomes. Many Californians are exposed at home, at work,
and in public places. In the comprehensive reviews published as Reports
of the Surgeon General and by the U.S. Environmental Protection Agency
(U.S. EPA) and the National Research Council (NRC), ETS exposure has been
found to be causally associated with respiratory illnesses -- including
lung cancer, childhood asthma, and lower respiratory tract infections.
Scientific knowledge about ETS-related effects has expanded considerably
since the release of the above-mentioned reviews. The state of California
has therefore undertaken a broad review of ETS covering the major health
endpoints potentially associated with ETS exposure: perinatal and postnatal
manifestations of developmental toxicity, adverse impacts on male and female
reproduction, respiratory disease, cancer, and cardiovascular disease.
A "weight of evidence" approach has been used, in which the body of evidence
is examined to determine whether or not it can be concluded that ETS exposure
is causally associated with a particular effect. Because the epidemiological
data are extensive, they serve as the primary basis for assessment of ETS-related
effects in humans. The report also presents an overview on measurements
of ETS exposure (particularly as they relate to characterizations of exposure
in epidemiological investigations) and on the prevalence of ETS exposure
in California and nationally.
ETS, or "secondhand smoke," is the complex mixture formed from the escaping
smoke of a burning tobacco product and smoke exhaled by the smoker. The
characteristics of ETS change as it ages and combines with other constituents
in the ambient air. Exposure to ETS is also frequently referred to as "passive
smoking," or "involuntary tobacco smoke" exposure. Although all exposures
of the fetus are "passive" and "involuntary," for the purposes of this
review, in utero exposure resulting from maternal smoking during pregnancy
is not considered to be ETS exposure.
GENERAL FINDINGS
ETS is an important source of exposure to toxic air contaminants indoors.
There is also some exposure outdoors in the vicinity of smokers. Despite
an increasing number of restrictions on smoking and increased awareness
of health impacts, exposures in the home, especially of infants and children,
continue to be a public health concern. ETS exposure is causally associated
with a number of health effects. Listed in Table ES.1 are the developmental,
respiratory, carcinogenic, and cardiovascular effects for which there is
sufficient evidence of a causal relationship—including fatal outcomes such
as sudden infant death syndrome and heart disease mortality, as well as
serious chronic diseases such as childhood asthma. There are, in addition,
effects for which evidence is suggestive of an association, but further
research is needed for confirmation. These include spontaneous abortion,
cervical cancer, and exacerbation of asthma in adults (Table ES.1). Finally,
it is not possible to judge on the basis of the current evidence the impact
of ETS on a number of endpoints including congenital malformations, changes
in female fertility and fecundability, male reproductive effects, rare
childhood cancers, and cancers of the bladder, breast, stomach, brain,
hematopoietic system, and lymphatic system.
Many Californians are exposed to ETS, and the number of people adversely
affected may be correspondingly large. Table ES.2 presents morbidity and
mortality estimates for health effects causally associated with ETS exposure.
For cancer, cardiovascular, and some respiratory endpoints, estimates are
derived from figures published for the U.S. population, assuming that the
number affected in California would be 12 percent of the total. The estimates
for middle ear infection, sudden infant death syndrome, and low birthweight
were derived using information on prevalence of ETS expo-sure in California
and the U.S. Relative risk estimates (RR) associated with some of these
endpoints are small, but because the diseases are common, the overall impact
can be quite large. A relative risk estimate of 1.3 for heart disease mortality
in nonsmokers is supported by the collective evidence; this estimate corresponds
to a lifetime risk of death of roughly 1 to 3 percent for exposed non-smokers
and approximately 4,000 deaths annually in California. The relative risk
estimate of 1.2 to 1.4 associated with low birthweight implies that ETS
may impact fetal growth of 1,200 to 2,200 newborns in California, roughly
1 to 2 percent of newborns of nonsmokers exposed at home or at work. ETS
may exacerbate asthma (RR Å 1.6 to 2) in 48,000 to 120,000 children
in California. Large impacts are associated with relative risks for respiratory
effects in children such as middle ear infection (RR Å 1.62) and
lower respiratory disease in young children (RR Å 1.5 to 2). Asthma
induction (RR Å 1.75 to 2.25) may occur in as many as 0.5 to 2 percent
of ETS-exposed children. ETS exposure may be implicated in 120 SIDS deaths
per year in California (RR Å 3.5), with a risk of death approaching
0.1 percent for infants exposed to ETS in their homes. Lifetime risk of
lung cancer death related to ETS-exposed nonsmokers may be about 0.7 percent
(RR Å 1.2). For nasal sinus cancers, observed relative risks have
ranged from 1.7 to 3.0, but future studies are needed to confirm the magnitude
of ETS-related risks.
SPECIFIC FINDINGS AND CONCLUSIONS: EXPOSURE MEASUREMENT AND PREVALENCE
ETS is a complex mixture of chemicals generated during the burning and
smoking of tobacco products. Chemicals present in ETS include irritants
and systemic toxicants such as hydrogen cyanide and sulfur dioxide; mutagens
and carcinogens such as benzo[a]pyrene, formaldehyde, and 4-aminobiphenyl;
and the reproductive toxicants nicotine, cadmium, and carbon monoxide.
Many ETS constituents have been identified as hazardous by state, federal,
and international agencies. To date, over 50 compounds in tobacco smoke
have been identified as car-cinogens and six identified as developmental
or reproductive toxicants under California's Proposition 65 (California
Health and Safety Code 25249.5 et seq.).
Exposure assessment is critical in epidemiological investigations of
the health impacts of ETS, and in evaluating the effectiveness of strategies
to reduce exposure. Exposure can be assessed through the measurement of
indoor air concentrations of ETS constituents, through surveys and questionnaires,
or more directly through the use of personal monitors and the measurement
of biomarkers in saliva, urine, and blood. There are advantages and disadvantages
associated with the various techniques, which must be weighed in interpreting
study results. One important consideration in epidemiologic studies is
misclassification of exposure. Studies on the reliability of questionnaire
responses indicate that qualitative information obtained is generally reliable,
but that quantitative information may not be. Also, individuals are often
unaware of their ETS exposure, particularly out-side the home. In studies
using both self-reporting and biological markers, the exposure prevalence
was higher when determined using biological markers.
Available data suggest that the prevalence of ETS exposure in California
is lower than elsewhere in the U.S. Among adults in California, the workplace,
home, and other indoor locations all contribute significantly to ETS exposure.
For children, the most important single location is the home. Over the
past decade, ETS exposures in California have decreased significantly in
the home, workplace, and in public places. Over the same period, restrictions
on smoking in enclosed worksites and public places have increased (e.g.,
Gov. Code, Section 19994.30 and California Labor Code, Section 6404.5),
and the percentage of the adults who smoke has declined. Decreases in tobacco
smoke exposure may not be experienced for some population subgroups, as
patterns of smoking shift with age, race, sex, and socioeconomic status.
For example, from 1975 to 1988, the overall smoking prevalence among 16
to 18 year olds declined, but after 1988 the trend reversed.
PERINATAL MANIFESTATIONS OF DEVELOPMENTAL TOXICITY
ETS exposure adversely affects fetal growth, with elevated risks of
low birth weight or "small for gestational age" observed in numerous epidemiological
studies. The primary effect observed, reduction in mean birthweight, is
small in magnitude. But if the distribution of birthweight is shifted lower
with ETS exposure, as it appears to be with active smoking, infants who
are already compromised may be pushed into even higher risk categories.
Low birth-weight is associated with many well-recognized problems for infants
and is strongly associated with perinatal mortality.
The impact of ETS on perinatal manifestations of development other than
fetal growth is less clear. The few studies examining the association between
ETS and perinatal death are relatively non-informative, with only two early
studies showing increased risk associated with parental smoking, and with
the sparse data on stillbirth not indicative of an effect. Studies on spontaneous
abortion are suggestive of a role for ETS, but further work is needed,
particularly as a recent report did not confirm the findings of four earlier
studies. Although epidemiological studies suggest a moderate association
of severe congenital malformations with paternal smoking, the findings
are complicated by the use of paternal smoking status as a surrogate for
ETS exposure, since a direct effect of active smoking on sperm can-not
be ruled out. In general, the defects implicated differed across the studies,
with the most consistent association seen for neural tube defects. At this
time, it is not possible to determine whether there is a causal association
between ETS exposure and this or other birth defects.
POSTNATAL MANIFESTATIONS OF DEVELOPMENTAL TOXICITY
Numerous studies have demonstrated an increased risk of sudden infant
death syndrome, or "SIDS," in infants of mothers who smoke. Until recently
it has not been possible to separate the effects of postnatal ETS exposure
from those of pre-natal exposure to maternal active smoking. Recent epidemiological
studies now have demonstrated that postnatal ETS exposure is an independent
risk factor for SIDS.
Although definitive conclusions regarding causality cannot yet be made
on the basis of available epidemiological studies of cognition and behavior,
there is suggestive evidence that ETS exposure may pose a hazard for neuropsychological
development. With respect to physical development, while small but consistent
effects of active maternal smoking during pregnancy have been observed
on height growth, there is no evidence that postnatal ETS exposure has
a significant impact in otherwise healthy children. As discussed in greater
detail below, developmental effects of ETS exposure on the respiratory
system include lung growth and development, childhood asthma exacerbation,
and, in children, acute lower respiratory tract illness, middle ear infection,
and chronic respiratory symptoms.
FEMALE AND MALE REPRODUCTIVE TOXICITY
Though active smoking by women has been found to be associated with
decreased fertility in a number of studies, and tobacco smoke appears to
be anti-estrogenic, the epidemiological data on ETS exposure and fertility
are not extensive and show mixed results, and it is not possible to determine
whether ETS affects fecundability or fertility. Regarding other female
reproductive effects, while studies indicate a possible association of
ETS exposure with early menopause, the analytic methods of these studies
could not be thoroughly evaluated, and therefore at present, there is not
firm evidence that ETS exposure affects age at menopause. Although associations
have been seen epidemiologically between active smoking and sperm parameters,
conclusions cannot be made regarding ETS exposure and male reproduction,
as there is very limited information avail-able on this topic.
RESPIRATORY EFFECTS
ETS exposure produces a variety of acute effects involving the upper
and lower respiratory tract. In children, ETS exposure can exacerbate asthma,
and increases the risk of lower respiratory tract illness and acute and
chronic middle ear infection. Eye and nasal irritation are the most commonly
reported symptoms among adult nonsmokers exposed to ETS. Odor annoyance
has been demonstrated in several studies.
Regarding chronic health effects, there is compelling evidence that
ETS is a risk factor for induction of new cases of asthma as well as for
increasing the severity of disease among children with established asthma.
In addition, chronic respiratory symptoms in children—such as cough, phlegm,
and wheezing—are associated with parental smoking. While the results from
all studies are not wholly consistent, there is evidence that childhood
exposure to ETS affects lung growth and development, as measured by small
but statistically significant decrements in pulmonary function tests; associated
reductions may persist into adulthood. The effect of chronic ETS exposure
on pulmonary function in otherwise healthy adults is likely to be small
and is unlikely by itself to result in clinically significant chronic disease.
However, in combination with other insults (e.g., prior smoking history,
exposure to occupational irritants or ambient air pollutants), ETS exposure
could contribute to chronic respiratory impairment in adults. In addition,
regular ETS exposure in adults has been reported to increase the risk of
occurrence of a variety of lower respiratory symptoms.
Children are especially sensitive to the respiratory effects of ETS
exposure. Children with cystic fibrosis are likely to be more sensitive
than healthy individuals. Several studies of patients with cystic fibrosis,
a disease characterized by recurrent and chronic pulmonary infections,
suggest that ETS can exacerbate the condition. Several studies have shown
an increased risk of atopy (a predisposition to develop IgE antibodies
against common allergens, which can then be manifested as a variety of
allergic conditions) in children of smoking mothers, though the evidence
regarding this issue is mixed.
CARCINOGENIC EFFECTS
The role of ETS in the etiology of cancers in nonsmokers was explored,
as smoking is an established cause of a number of cancers (lung, larynx,
oral cavity, esophagus, and bladder), and a probable cause of several others
(cervical, kidney, pancreas, and stomach). Also, ETS contains a number
of constituents which have been identified as carcinogens.
Reviews published in the 1986 Report of the Surgeon General, by the
National Research Council in 1986, and by the U.S. EPA in 1992 concluded
that ETS exposure causes lung cancer. Three large U.S. population-based
studies and a smaller hospital-based, case-control study have been published
since the completion of the U.S. EPA review. The population-based studies
were designed to, and have successfully, addressed many of the weaknesses
for which the previous studies on ETS and lung cancer have been criticized.
Results from these studies are compatible with the causal association between
ETS exposure and lung cancer already reported by the U.S. EPA, Surgeon
General, and National Research Council. Of the studies examining the effect
of ETS exposure on nasal sinus cancers, all three show consistent associations,
presenting strong evidence that ETS exposure increases the risk of nasal
sinus cancers in nonsmoking adults. Further study is needed to characterize
the magnitude of the risk of nasal sinus cancer from ETS exposure.
The epidemiological and biochemical evidence suggests that expo-sure
to ETS may increase the risk of cervical cancer. Positive associations
were observed in two of three case-control studies, and a statistically
non-significant positive association was observed in the only cohort study
conducted. Findings of DNA adducts in the cervical epithelium as well as
nicotine and cotinine in the cervical mucus of ETS-exposed nonsmokers provides
biological plausibility.
For other cancer sites in adults, there has been limited ETS-related
epidemiological research in general; there is currently insufficient evidence
to draw any conclusion regarding the relationship between ETS exposure
and the risk of occurrence. A review of the available literature clearly
indicates the need for more research. For example, although compounds established
as important in the etiology of stomach cancer are present in tobacco smoke,
only a single cohort study has been performed for this site. Precursors
of endogenously formed N-nitroso compounds suspected of causing brain tumors
are present in high concentrations in ETS, and the one cohort and two case-control
studies available suggest a positive association, but the results are based
on small numbers and may be confounded by active smoking. In biochemical
studies of nonsmokers, higher levels of hemoglobin adducts of the established
bladder carcinogen, 4-amino-biphenyl, have been found in those exposed
to ETS. However, no significant increases in bladder cancer were seen in
the two epidemiological studies (case-control) conducted to date, although
both studies were limited in their ability to detect an effect. Several
compounds in tobacco smoke are associated with increased risk of leukemia,
but only one small case-control study in adults, reporting an increased
risk with ETS exposure during child-hood, has been performed. Finally,
all four studies on ETS exposure and breast cancer suggest an association,
but in two of the studies the associations were present only in select
groups, and in three studies there is either no association between active
smoking and the risk of breast cancer, or the association for active smoking
is weaker than for passive smoking. Moreover, there is no indication of
increasing risk with increasing intensity of ETS exposure. Still, results
from a recent study suggest that tobacco smoke may influence the risk of
breast cancer in certain susceptible groups of women, an association which
requires further investigation.
Regarding childhood cancers, it is unclear whether parental smoking
increases risk, either overall or for specific cancers such as acute lymphoblastic
leukemia or brain tumors, the two most common cancers in children. The
lack of clarity is due to the conflicting results reported and the limitations
of studies finding no association. The epidemiological data on ETS exposure
and rare childhood cancers also provide an inadequate foundation for making
conclusions regarding causality. Some studies in children found small increased
risks in relation to parental smoking for neuroblastoma, Wilm's tumor,
bone and soft-tissue sarcomas, but not for germ cell tumors. Studies to
date on these rare cancers have been limited in their power to detect effects.
The impact of ETS exposure on childhood cancer would benefit from far greater
attention than it has received to date.
CARDIOVASCULAR EFFECTS
The epidemiological data from prospective and case-control studies conducted
in diverse populations, in males and females and in western and eastern
countries, are supportive of a causal association between ETS exposure
from spousal smoking and coronary heart disease (CHD) mortality in nonsmokers.
To the extent possible, estimates of risk were determined with adjustment
for demographic factors and often for other factors related to heart disease—factors
such as blood pressure, serum cholesterol level, and obesity index. Risks
associated with ETS exposure were almost always strengthened by adjustment
for other cofactors. For nonsmokers exposed to spousal ETS compared to
nonsmokers not exposed, the risk of CHD mortality is increased by a factor
of 1.3. The association between CHD and risk is stronger for mortality
than for non-fatal out-comes, including angina.
Data from clinical studies suggest various mechanisms by which ETS causes
heart disease. In a number of studies wherein nonsmokers were exposed to
ETS, carotid wall thickening and compromise of endothelial function were
similar to, but less extensive than those experienced by active smokers.
Other effects observed include impaired exercise performance, altered lipoprotein
profiles, enhanced platelet aggregation, and increased endothelial cell
counts. These findings may account for both the short- and long-term effects
of ETS exposure on the heart.
Reviewed: June 3, 2004
This information is presented as a public service by:
Action on Smoking and Health (ASH)
2013 H Street NW / Washington, DC 20006 / (202) 659-4310
A national nonprofit, scientific and educational organization founded in 1967.
All donations are fully tax deductible.
Dedicated to Mr. and Mrs. Warren Wells
