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OCR for page 263
7
EXPOSURE TO ENVIRONMENTAL
TOBACCO Smoke
Involuntary exposure to environmental tobacco smoke (ETS),
or passive smoking, has been extensively investigated with re-
spect to its potential health effects, particularly on respiratory
health. There is a significant body of research on its potential ef-
fects regarding the incidence, prevalence, and exacerbation of es-
tablished asthma. While attention has focused upon possible as-
sociations with childhood asthma, associations with asthma in
adults also have been investigated. The following analysis relies
heavily on several very detailed and comprehensive reviews, in-
cluding those of the U.S. Environmental Protection Agency (EPA)
(U.S. EPA, 1992), the California EPA s Office of Environmental
Health Assessment (California EPA, 1997), the World Health Or-
ganization (WHO) International Consultation on Environmental
Tobacco Smoke (ETS) and Child Health (WHO, 1999), the report
of the United Kingdom s Scientific Committee on Tobacco and
Health (SCOTH, 1998), and the series of ten meta-analyses (to
date) of the health effects of ETS by Cook, Strachan, and col-
leagues (Anderson and Cook, 1997; Cook et al., 1998; Cook and
Strachan, 1997, 1998, 1999; Strachan and Cook, 1997, 1998a-1998c).
263
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264
CLEARING THE AIR
DEFINITION OF ENVIRONMENTAL TOBACCO SMOKE (ETS}
Environmental tobacco smoke has been defined (Daisey et al.,
1994) as:
. . . the smoke to which non-smokers are exposed when they are in
an indoor environment with smokers. It is composed largely of
sidestream tobacco smoke (SS), the smoke emitted by the smolder-
ing end of a cigarette between puffs, with minor contributions from
exhaled mainstream smoke (the smoke which is directly inhaled by
the smoker) and any smoke that escapes from the burning part of
the tobacco during puff-drawing by the smoker. ETS differs from
SS in that it is highly diluted and dispersed within a room and it
undergoes aging.
Tobacco smoke contains many chemical products with known
or suspected adverse health effects. These products include eye
and respiratory irritants, systemic toxicants, mutagens and car-
cinogens, and reproductive toxicants (California EPA, 1997~. ETS
consists of solid particulates, and semivolatile and volatile organic
compounds (VOCs). The solid particulates have a mean diameter
of 0.32,um (National Research Council, 1986~. "The aging process
includes volatilization of nicotine, which is present in the particu-
late phase in mainstream smoke but is almost exclusively a com-
ponent of the vapor phase of ETS" (U.S. EPA, 1992~. The mean
and standard deviation of the total emission factor for PM 2 5, de-
termined for six commercial cigarettes and Kentucky reference
cigarette 1R4F, is 8,100 + 2,000 ,ug per cigarette. Bacterial endot-
oxin (lipopolysaccharide), previously associated with environ-
mental lung diseases, has been reported to be a respirable con-
stituent of both mainstream and sidestream smoke (Hasday et al.,
1999~.
Significant amounts of nearly 30 volatile organic compounds
have been measured, including acetaldehyde, formaldehyde,
nicotine, 3-viny~pyridine, toluene, pyridine, benzene, pyrrole, xy-
lene, 2-butanone (methyl ethyl ketone iMEK]), phenol, and oth-
ers. Many of the more volatile VOCs (such as aldehydes) remain
in the air for prolonged periods of time following the smoking of
a cigarette (at least four hours) and do not appear to undergo
significant chemical reactions within this period. Some of the less
volatile compounds and particulates appear to decrease over time
OCR for page 265
EXPOSURE TO ENVIRONMENTAL TOBACCO SMOKE
265
due to deposition as well as ventilation effects. With the excep-
tion of nicotine, the emission factors for VOCs are significantly
greater in ETS than in SS (U.S. EPA, 1992~.
Additional information on the physical and chemical proper-
ties of ETS and the biological activities can be found in the U.S.
and California EPA reports (California EPA, 1997; U.S. EPA, 1992~.
FACTORS CONTROLLING EXPOSURE TO ETS
Variations in Concentration of ETS in Indoor Environments
Exposure Assessment
Nicotine and particulate matter (PM), in addition to carbon
monoxide, have been the constituents most extensively measured
as a means of assessing ETS concentrations in indoor air. Nicotine
is considered an adequate tracer for PM under certain conditions,
and, possibly, for VOCs ranging from slightly to very volatile
compounds (Dailey, 1999~. Among the documented conditions
influencing the concentration of nicotine are emission rates, ven-
tilation, and (for VOCs/SVOCs) resorption and Resorption from
surfaces (Dailey, 1999~. The EPA (1992) and Guerin et al. (1992)
summarized more than 25 studies of nicotine concentration in
more than 100 different indoor environments and found that the
average concentrations of nicotine ranged from 0.3 to 30,ug/m3, a
hundredfold difference. In residences with one or more smokers,
the typical range was from 2 to 10 ,ug/m3, typically being higher
in winter than in summer. Bars and smoking sections of commer-
cial airplanes recorded the highest levels up to 50-75 ,ug/m3,
although nonsmoking regulations and ordinances have signifi-
cantly altered this. In general, the concentrations of nicotine have
been found to increase with the number of smokers and number
of cigarettes consumed in a given indoor environment (U.S. EPA,
1992~.
One study involving personal monitor measurement of
approximately 100 individuals in 16 metropolitan areas in the
United States reported mean 24-hour time weighted average nico-
tine concentrations of 3.28 ,ug/m3 for those exposed to ETS both
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266
CLEARING THE AIR
at work and away from work; 1.41,ug/m3 for those exposed away
from work only; 0.69 ,ug/m3 for those exposed at work only; and
0.05 ,ug/m3 for those exposed at neither location Jenkins et al.,
1996; Jenkins and Counts, 1999~. Particulate concentrations, un-
like nicotine, are not specific to ETS as a source. However, al-
though not unique to the combustion of tobacco, the quantity of
respirable particulates produced by cigarette smoking, is large-
significantly greater than the amounts produced by other com-
mon combustion sources within the home, such as wood-burning
fireplaces, gas stoves, and kerosene space heaters (California EPA,
1997~. Respirable suspended particles in homes with at least one
smoker average about 20-100 ,ug/m3 higher than the levels in
similar nonsmoking homes. The highest concentrations have been
reported in restaurants and bars a maximum of 1,379,ug/m3 and
a range of average concentrations of 35-986 ,ug/m3 (U.S. EPA,
1992~. Ott et al. (1996) documented a 77°/O decrease in the average
concentration of respirable suspended particles in a northern
California tavern after a prohibition against smoking was insti-
tuted. In addition to the influence of the number of smokers and
the amount smoked on the concentration of ETS in a given indoor
environment, concentration is affected by the ventilation rate.
Long-term exposure to ETS has been of most concern from
the standpoint of effects on lung development and cancers. How-
ever, ETS concentration varies over an extreme spatial and tem-
poral range in indoor and outdoor environments, making it in-
feasible to comprehensively assess the ETS exposure history of an
individual over their lifetime by direct exposure assessment or
air sampling in all of the relevant environments. Critical aspects
of this history can, however, be determined and more compre-
hensive and accurate assessment is often feasible for infants and
very young children. Because of the difficulties involved, epide-
miologists have tended to use questionnaires and interviews to
determine individual history with regard to ETS exposure, classi-
fying people into categorical groups to provide a semiquantitative
measure of exposure. Direct measurement of exposure at or near
the breathing zone is often done via personal monitors and can
provide an assessment of integrated exposure, but this is feasible
for monitoring only over a relatively limited period of time.
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EXPOSURE TO ENVIRONMENTAL TOBACCO SMOKE
Biomarkers of Exposure
267
The most direct assessment of exposure involves the measure-
ment of ETS constituents or their breakdown products in body
fluids. To date, the most reliable of these biomarkers is cotinine, a
metabolite of nicotine (Benowitz, 1999~. Cotinine has an average
half-life of approximately 16-19 hours (Benowitz and Jacob, 1994;
larvis et al., 1988), making it highly useful for the assessment of
integrated ETS exposure over the two to three days prior to the
measurement. In infants and children, the half-life is appreciably
longer, from approximately 40 hours in children more than 18
months old to approximately 65 hours in neonates (U.S. EPA,
1992~. Because urinary cotinine excretion varies markedly among
individuals as a result of renal function, urinary flow rate, and
urinary pH (Benowitz et al., 1983), results often are expressed as
nanograms of cotinine per milligram of creatinine, rather than
simply in nanograms per milliliter of fluid. However, the produc-
tion of creatinine is a function of muscle mass; hence excretion
varies with age, sex, and other individual factors. In particular,
the low level of creatinine produced in children means that the
cotinine-to-creatinine ratios in children may fall into the range
reported for active smokers (Watts et al., 1990~.
The levels of exposure of nonsmokers to ETS are sufficient
that nicotine and cotinine are detectable in their urine, blood, and
saliva (Benowitz, 1996~. Values are typically in the range of 0.5 to
10-15 ng/mL in the saliva and plasma, respectively, of nonsmok-
ers, with urinary concentrations approximately three times
higher as much as 50 ng/mL or more (Guerin et al., 1992; U.S.
EPA, 1992~. A cutoff of 90 ng/mL has been used to distinguish
active smokers from exposed and unexposed nonsmokers
(Cummings et al., 1990), and studies consistently have been able
to distinguish active smokers from exposed and unexposed non-
smokers Jarvis et al., 1987~. It has been more difficult to distin-
guish exposed from non-exposed non-smokers for a variety of
reasons related to the validity of self-reported smoking status and
ETS exposure, variability in nicotine metabolism, variability in
sampling procedures, and the limits of sensitivity of the assay
methods used (Idle, 1990~. Increasing levels of cotinine have been
generally found to be associated with increasing levels of self
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268
CLEARING THE AIR
reported ETS exposure (NRC, 1986; U.S. DHHS, 1986; U.S. EPA,
1992~.
As would be expected from the results of measurement of
ambient concentrations of nicotine, the maximum reported expo-
sure levels have occurred in bars and restaurants and on commer-
cial airline flights approximately 30 ng/mg creatinine (Mattson
et al., 1989~. One study in which adults in an enclosed area were
exposed to sidestream smoke from four cigarettes being smoked
simultaneously and injected into the room continuously by ma-
chine, with ventilation conditions equivalent to those in the aver-
age office environment, found the air concentration of nicotine
rapidly reached a stable level of 280,ug/m3. Average nicotine con-
centration in saliva reached a maximum of 880 ng/mL after 60
minutes of exposure, and cotinine concentrations reached 3.4 ng/
mL in serum and 55 ng/mg creatinine in urine, a little more than
six hours after exposure.
A number of studies have compared biomarkers in active
smokers with those in exposed and nonexposed nonsmokers.
larvis and Russell (1984), for example, found mean urinary
cotinine levels in these three groups of 1,390.0,7.7, and 1.6 ma/
mL, respectively (p < .001 between exposed and nonexposed non-
smokers). Cotinine concentrations of self-reported smokers and
nonsmokers have generally been found to overlap.
In infants and children exposed to ETS, levels of cotinine have
been found to be significantly higher in exposed than in
nonexposed children. Direct exposure assessment has detected
cotinine in the urine on the first day of life in neonates of both
active smokers and ETS-exposed nonsmokers with significantly
higher levels in the latter than in neonates of unexposed non-
smokers Jordanov, 1990~. Henderson et al. (1989) found that air
nicotine concentration in the home was significantly associated
with the average log urinary cotinine level (r = 0.68, p = .006~.
Greenberg et al. (1989) found a median concentration of 121 ng
cotinine/mg creatinine (range 6-2,273 ng cotinine/mg creatinine)
in children with any detectable cotinine. Chilmonczyk et al. (1990)
found median levels of urinary cotinine of 1.6 mg/mL in non-
smoking households, 8.9 mg/mL where someone other than the
mother smoked, 28 mg/mL where only the mother smoked, and
43 mg/mL where both the mother and someone else smoked.
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EXPOSURE TO ENVIRONMENTAL TOBACCO SMOKE
Exposure Prevalence
269
In reviewing studies of ETS exposure prevalence, the Califor-
nia EPA (1997) concluded, "Taken as a whole, the various studies
[at least 10 separate investigations including large representative
sample surveys] . . . indicate that within California and the United
States, exposure to ETS was widespread during the time period
of the studies (1979 through 1992~. Analysis of ETS exposure
within California indicated that the workplace, home, and other
indoor locations contributed significantly to the exposure of
adults. For children, the home was the most important single lo-
cation contributing to ETS exposure. In all studies using both self-
reporting and a biological marker (cotinine level) as measures of
exposure, prevalence was higher when determined using the bio-
logical marker." It further cited indirect evidence that "the preva-
lence of ETS exposure in the rest of the U.S. population is higher
than that in California."
It is particularly noteworthy that despite aggressive antismok-
ing education and regulation, and documented reductions in
smoking rates (to 16.7% of the adult population in 1995 [CDHS,
1995~), in 1992 an estimated 9.4% of California women pregnant
within the previous five years had smoked throughout pregnancy,
and an estimated 19.6% of those 17 years of age may be exposed
to ETS in their homes (Pierce et al., 1994~. By inference from stud-
ies of adult smoking, it also would appear that the rates may be
appreciably higher in specific subpopulations.
Influence of Activity Patterns on Exposure
The activity patterns of both children and adults have been
studied in relation to exposure to ETS. For all ages, the home is
the location in which the average person spends the most time
921 minutes per day for adults and 1,078 minutes per day for
children in California. Time within the home is spent primarily in
the bedroom an average of 524 minutes per day for adults and
674 minutes per day for children (Wiley et al., 1991~. The next
greatest amounts of time are spent by children in school or child
care (an average of 109 minutes for all children and 330 minutes
for those attending school), in other people's homes (80 minutes
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270
CLEARING THE AIR
average and 251 minutes for those doing this), and in-transit (69
minutes overall and 83 minutes for those traveling). Overall, chil-
dren spend an average of 1,230 min. (20.5 hours) each day in-
doors, 141 minutes outdoors, and 69 minutes in enclosed transit.
Infants and other children ages 2 and under spend the most time
indoors (an average of 21.6 hours), but somewhat less in enclosed
transit (48 minutes). For adults, the times are 1,253 minutes in-
doors, 73 minutes outdoors, and 111 minutes in enclosed trans-
portation, with time in the workplace replacing time spent in
school or child care by children.
For children, the home is clearly the most likely source of ex-
posure to ETS and the place that the child is most likely to sleep.
While smoking is not permitted in schools or day care facilities
and is prohibited in some states in licensed child care in private
homes when children are present, the fact that many children are
in nonlicensed child care arrangements or in states or communi-
ties where smoking prohibitions are not well enforced means that
significant regular exposure may occur in home settings. Expo-
sure during travel in the private automobile is another potential
source of exposure.
For adults, research in California (Lum, 1994a, 1994b) has
shown that exposure in the workplace is the most prevalent loca-
tion for exposure of nonsmokers to ETS, with the home as the
second most prevalent location. To the extent that workplaces
adopt antismoking regulations, this exposure source may dimin-
ish in importance. The private automobile represents another po-
tentially significant location for adult exposure.
It is possible for both adults and children to be exposed to
ETS the majority of the time they are indoors, both during the day
and at night. For the average preschool child, this could be virtu-
ally all of the time, for the school-aged child as many as 15.5 hours
a day, and for adults anywhere from 12 hours (for those working
in a nonsmoking environment) to 24 hours for those working as
well as living in environments in which smoking is permitted.
The only reliable exception would be time spent in school, public
buildings, or public transit where smoking is prohibited. There is
no reason to believe that the activity patterns of persons with
asthma differ significantly from those of nonasthmatics, except
for the possibility of their having lower activity levels that could
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EXPOSURE TO ENVIRONMENTAL TOBACCO SMOKE
271
result in more time spent indoors and hence greater exposure to
any ETS present in indoor environments. Further, there are ques-
tions as to whether the sensitization of children to allergens (e.g.,
dust mites, cockroaches) in the home environment may be in-
creased by the presence of ETS, as well as whether increased time
spent in the indoor environment, if this occurs, results in greater
exposure to ETS as well as to indoor allergens.
One study of children between the ages of 2 and 12 in Scot-
land, having at least one parent who smoked, found that salivary
cotinine levels were nondetectable in only four children, all of
whom had only a father who smoked (Irvine et al., 1997~. In the
remaining 493 children, the levels ranged from 0.5 ng/mL (barely
detectable) to 21.2 ng/mL, with a mean of 4.35 ng/mL. The au-
thors cite two studies in which levels of 14.3 ng/mL or higher
have been taken as indicative of active smoking by a child. How-
ever, 13 of the 18 children who scored between 14.3 and 21.2 ng/
mL were younger than 6 years of age and are presumed not to be
active smokers. This study found that the age of the child, cotinine
level and self-reported amount smoked in the home by the index
parent, self-reported frequency of smoking in the same room as
the child, whether the index parent's partner smoked, whether
the child had contact with other smokers, the number of persons
per room in the home, and whether the home had a yard or gar-
den were all significantly and independently related to the child's
cotinine level.
EVIDENCE OF A RELATIONSHIP
BETWEEN ETS AND ASTHMA
Action of ETS on the Lungs
Tobacco smoke, whether mainstream, sidestream, or ETS, is a
lung irritant. From a pathophysiologic point of view, active smok-
ing is associated with significant structural changes in both the
airways and the pulmonary parenchyma (U.S. DHHS, 1984), in-
cluding hypertrophy and hyperplasia of the upper airway mu-
cous glands, leading to an increase in mucous production with
associated increased prevalence of cough and phlegm. Chronic
inflammation of the smaller airways also occurs, leading to bron
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272
CLEARING THE AIR
chial obstruction. In addition, airway narrowing may occur con-
sequent to destruction of the alveolar walls, decreased Jung elas-
ticity, and development of centrilobular emphysema (U.S. EPA,
1992~. Smoking also may increase mucosal permeability to aller-
gens, increasing total and specific immunogiobulin E (IgE) levels
(Zetterstrom et al., 1981) and blood eosinophi] counts (Halonen et
al., 1982~.
The adverse health effects and pathophysiologic changes as-
sociated with active smoking have been observed at low-dose ex-
posures, suggesting that ETS might have similar adverse effects,
a suspicion that was heightened by the fact that ETS contains
some volatile substances in greater quantities than are found in
mainstream smoke (U.S. EPA, 1992~. In addition, since large pro-
portions of the population are involuntarily exposed to ETS, in-
cluding more susceptible infants and children, the index of suspi-
cion for adverse effects of ETS is high. Exposures early in life,
when the lung is undergoing significant growth and remodeling,
could plausibly alter Jung development and increase the risk of
various respiratory illnesses, including asthma. It is also plausible
that, in addition to the marked susceptibility of young lungs, there
is variable individual susceptibility in other respects, including
genetic predisposition, lung injury such as bronchopulmonary
dysplasia consequent to premature birth, and greater contact with
a primary caregiver who smokes.
Maternal Active Smoking During Pregnancy
Exposure of the fetus to the products of maternal tobacco
smoking is a form of "environmental" exposure to tobacco smoke,
although not in the same proportions as in airborne ETS and not
to all constituents of ETS (notably, not the particulates). It is plau-
sible that virtually all products of active maternal smoking that
enter the bloodstream of the mother, including products arising
from mainstream and sidestream smoke, cross into the fetus
through the placenta with a diffusion gradient. This has been con-
firmed in the case of carbon monoxide (Longo, 1970) and cotinine.
A biomarker for nicotine exposure, cotinine has been detected in
the amniotic fluid of ETS-exposed women and the urine of their
neonates in significantly higher concentrations than in
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EXPOSURE TO ENVIRONMENTAL TOBACCO SMOKE
. .
273
nonexposed nonsmoking women Jordanov, 1990~. Transplacen-
tal passage of the bloodborne products of passive maternal ETS
exposure also would be expected, although at lower levels and
with a different chemical com Position than if the mother were an
active smoker.
Active maternal smoking has been associated with reduced
size of the placental arteries (Asmussen, 1979), a reduction in av-
erage birthweight of 75~00 am. (Abell et al., 1991; Asmussen,
1979; Lodrup Carisen et al., 1997; Miiner et al., 1999; Sherwood et
al., 1999; Wang et al., 1997), and altered lung function measured
shortly after birth (Lodrup Carisen et al., 1997~. Small but statisti-
cally significant deficits in forced expiratory volume in one sec-
ond (FEVER and other spirometric indices (forced vital capacity
[FVC], mid expiratory flow iMEF], and end expiratory flow [EEF])
have been fairly consistently demonstrated in school-aged chil-
dren (data reviewed in Cook and Strachan, 1999) and as early as
three days after birth (Lodrup Carisen et al., 1997), thereby
strongly implicating maternal smoking during pregnancy as the
cause of these deficits. However, in Turkey, where there is heavy
smoking by men and virtually none by women, exposure of chil-
dren also has been associated with significant deficits in lung
function (e.g., Bek et al., 1999~. Experimental studies in animals
have demonstrated that ETS exposure of pregnant rats is associ-
ated with reduced Jung volume, number of saccules and septal
crests, and elastin fibers in fetal lungs (Collins et al., 1985~. More
recently, Sekhon et al. (1999) reported that nicotine alone, when
administered to pregnant rhesus monkeys, altered the expression
of nicotine receptors in the developing fetal lung, leading to lung
hyperplasia with structural alterations and reduced complexity
of the gas-exchange surface.
ETS and Children's Respiratory Health
Recent reviews of an extensive body of cross-sectional, case-
control, and longitudinal epidemiologic research on the effects of
parental smoking on children's respiratory health have come to
very similar, although not identical, conclusions. These reviews
include both systematic, quantitative meta-analyses (Cook and
Strachan, 1999) and narrative reviews (California EPA, 1997; U.S.
OCR for page 287
EXPOSURE TO ENVIRONMENTAL TOBACCO SMOKE
287
the outset of the study, and no intervention effect was observed.
This differential self-reported exposure of infants of maternal
smokers was not, however, accompanied by a significant differ-
ential in the cotinine-to-creatinine ratios of the intervention and
control children. In fact, the proportion with detectable urine
cotinine levels tended to increase over the year of follow-up in
both groups. The incidence of all acute lower respiratory illnesses
(ALRIs) and of severe acute respiratory illnesses did not decrease
in the intervention group, and in fact, there was a small but statis-
tically significant difference in all ALRIs favoring the control
group. There was a significant difference in the frequency of per-
sistent lower-respiratory symptoms in the maternal smoking
subsample, but only where the head of household had a high
school education or less. The authors interpret the results as indi-
cating that mothers took steps to protect the infant from exposure
by removing them from the vicinity of the smoker and that the
infants were nevertheless subsequently exposed to residual nico-
tine but not to other ETS products, "which may be more likely
than nicotine to have acute and chronic toxicity for passive smok-
ers." The authors did not discuss whether parental report could
have been biased in the direction of reduced reporting of expo-
sure, and the unplanned subgroup analysis means that the posi-
tive results with regard to persistent lower-respiratory symptoms
are merely suggestive.
Chilmonczyk et al. (1992) reported an unsuccessful phy-
sician's office-based intervention strategy that used feedback from
the physician to the parent on infant urine cotinine measurements
in an attempt to reduce the infant's exposure to ETS. The 6% re-
duction of urine cotinine levels for the intervention group at fol-
low-up two months later was not statistically significant. This lack
of success was in contrast to the investigator's previous success
in getting women to stop smoking during pregnancy based on
feedback on their own urine cotinine levels (Haddow et al., 1991),
suggesting there may be greater motivation and ability of women
to cease smoking and eliminate exposure of their fetus than to
prevent exposure of infants and older children. An earlier unsuc-
cessfu] attempt to reduce passive smoking in infancy was re-
ported by Woodward et al. (1987~.
Hovell et al. (1994) and Wahigren et al. (1997) have reported
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288
CLEARING THE AIR
that among children with asthma, a preventive medicine counsel-
ing intervention was associated with a greater reduction in self-
reported and air monitor-verified ETS exposure than a monitored
or usual care control condition. McIntosh et al. (1994) did not re-
port a significant benefit of a cotinine-assisted, minimal-contact
intervention.
Where positive results and promising interventions have been
reported, there is a need for replication and, if possible, extension
to other populations. Extensions of interventions should be made
to populations including those who tend to be more resistant to
cessation efforts and may be more typical of those whose children
are being exposed to significant levels of ETS and are at risk for
poor asthma outcomes for a variety of reasons. Wilson et al. (1996)
i]
have found that both adults with asthma who smoke and smok-
ing parents of children with asthma are less likely than nonsmok-
ers to attend an asthma education program, making it less likely
that they will modify the child's exposure or experience the other
benefits of such asthma education programs.
None of the studies to date that have investigated educational
nterventions to reduce ETS exposure have extended this to in-
clude asthma outcomes either doctor-diagnosed asthma or
wheezing illness incidence, or the prevalence or exacerbations of
established asthma. Until this is done, it leaves unanswered the
question of whether any ETS exposure reduction that may be
achieved is sufficient to alter these disease outcomes, as well as
whether there is any safe ETS exposure level. This is particularly
important when the intervention aims to reduce infant exposure
by means other than cessation of smoking by all caregivers and
others in the child's environment. For this reason it also is impos-
sible to directly answer questions regarding the cost-effectiveness
of mitigation and prevention strategies.
CONCLUSIONS REGARDING ETS SOURCE CONTROL OR
MITIGATION: FEASIBILITYAND BENEFITS
Conclusions Regarding the Effects of
Complete Avoidance of ETS Exposure
Based on reasoning from the epidemiologic evidence pre
OCR for page 289
EXPOSURE TO ENVIRONMENTAL TOBACCO SMOKE
289
sensed above, the following conclusions can be reached regard-
ing the potential benefits of essentially complete avoidance of ETS
exposure, if this could be achieved:
· There is sufficient evidence to conclude that complete
avoidance of ETS exposure would be associated with a lower like-
lihood of exacerbations of asthma in preschool children with es-
tablished asthma.
· There is limited evidence suggesting that complete avoid-
ance of ETS exposure would be associated with a lower likeli-
hood of exacerbations of asthma in older children and adults.
· There is sufficient evidence to conclude that complete
avoidance of ETS exposure, if this could be achieved, would re-
duce the probability of the development of wheezing with respi-
ratory illness in younger children.
· There is limited or suggestive evidence that complete
avoidance of ETS exposure, if this could be achieved, would re-
duce the likelihood of the persistence of asthma or of new-onset
asthma in children and adults.
Conclusions Regarding Mitigation Through Source Control
· There is sufficient evidence to conclude that increased ven-
tilation and air-cleaning methods are technologically capable of
reducing the concentration of ETS particulates in indoor air.
· There is no evidence as to how readily the necessary venti-
lation and air-cleaning methods or technologies would be
adopted and how effectively they actually would be used to re-
duce ETS concentration.
· There is no evidence of whether interventions designed to
encourage the use of the requisite ventilation and air-cleaning
methods would be associated with a reduction in ETS concentra-
tion, in the exposure of persons with asthma to ETS, or in asthma
prevalence or exacerbations.
· There is inadequate evidence to conclude that interven-
tions intended to establish smoke-free homes where a family
member has asthma and to require smokers to smoke only out-
doors are associated with a reduction in ETS exposure or asthma
exacerbations.
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CLEARING THE AIR
RES"RCH NEEDS
A better understanding is needed of the mechanisms by
which ETS and its individual constituents may
· impair the normal development of the airways in the fetus,
· promote allergic sensitization,
· promote respiratory infections,
· promote early wheezing illness, and
· (possibly) induce pathophysiologic changes that may pro-
mote the establishment of asthma.
Research is also needed to understand the nature of the inter-
actions, both at the population or epidemiologic level and at the
molecular and cellular levels, between the genetic predispositions
to allergic sensitization and bronchial hyperresponsiveness and
ETS exposure as they relate to the development of asthma. The
respective roles of antenatal and postnatal exposure to ETS in the
pathophysiologic changes associated with asthma and other res-
piratory illnesses are in need of further investigation.
Behavioral research also is needed to better understand the
factors that lead to the initiation of smoking in adolescents, espe-
cially young women, and to the maintenance of smoking in preg-
nant women and mothers. Additionally, there is a need to develop
more effective interventions to achieve sustained pre- and post-
natal smoking cessation in pregnant women and mothers, espe-
cially those whose children are at higher risk of developing
asthma due to their family history, socioeconomic status, and
place of residence. Since ETS exposure of children at greatest risk
for adverse asthma outcomes (especially low-income and minor-
ity children of African-American ancestry) may come from other
caregivers as well as the mother or parents (i.e., other family mem-
bers with whom the mother and child live and from day care pro-
viders), interventions must be developed that will be effective in
reducing the child's exposure from all sources. The effectiveness
of ETS exposure reduction interventions in actually improving
asthma outcomes should be evaluated as well.
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Representative terms from entire chapter:
tobacco smoke
