Clearing the Air Asthma and Indoor Air Exposures (2000) / Chapter Skim
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7 Exposure to Environmental Tobacco Smoke
7 Exposure to Environmental Tobacco Smoke
Pages 263-297
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From page 263... ...
, the World Health Organization (WHO) International Consultation on Environmental Tobacco Smoke (ETS)
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From page 264... ...
Tobacco smoke contains many chemical products with known or suspected adverse health effects. These products include eye and respiratory irritants, systemic toxicants, mutagens and carcinogens, and reproductive toxicants (California EPA, 1997~.
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From page 265... ...
, 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~.
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From page 266... ...
However, although not unique to the combustion of tobacco, the quantity of respirable particulates produced by cigarette smoking, is largesignificantly greater than the amounts produced by other common 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.
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From page 267... ...
, and studies consistently have been able to distinguish active smokers from exposed and unexposed nonsmokers Jarvis et al., 1987~. It has been more difficult to distinguish 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~.
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From page 268... ...
, 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 nonsmokers)
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From page 269... ...
In all studies using both selfreporting and a biological marker (cotinine level) as measures of exposure, prevalence was higher when determined using the biological marker." It further cited indirect evidence that "the prevalence of ETS exposure in the rest of the U.S.
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From page 270... ...
For children, the home is clearly the most likely source of exposure 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 communities where smoking prohibitions are not well enforced means that significant regular exposure may occur in home settings.
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From page 271... ...
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 garden 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.
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From page 272... ...
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)
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From page 273... ...
ETS and Children's Respiratory Health Recent reviews of an extensive body of cross-sectional, casecontrol, 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)
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From page 274... ...
summarize their earlier general conclusions (Cook and Strachan, 1997, 1998; Cook et al., 1998; Strachan and Cook, 1997, 1998a-1998c) as follows: Overall, there is a very consistent picture with odds ratios for respiratory illnesses and symptoms and middle ear disease of between 1.2 and 1.6 for either parent smoking, the odds usually being higher in pre-school than school-aged children and higher for maternal smoking than for paternal smoking.
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From page 275... ...
There is, at present, some inconsistency with regard to the interpretation of studies that have attempted to separate the influence of maternal smoking during pregnancy from postnatal maternal smoking. Separation of the effects is difficult since those who smoke during pregnancy are very likely to continue to do so after the birth of the child, although some smokers may quit during the first trimester and abstain for the remainder of the pregnancy, often resuming thereafter.
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From page 276... ...
[7] Sudden infant deaths 2.13 (1 .8E NOTE: Numbers in square brackets are numbers of studies on which pooled odds ratios (OR)
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From page 277... ...
EXPOSURE TO ENVIRONMENTAL TOBACCO SMOKE Tory 277 % Cl) Mother Only OR (95% Cl)
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From page 278... ...
A possibly more delayed development of asthma in some non-ETS-exposed children would not dilute the observed relationship between ETS exposure and early wheezing. Dose-Response Relationship Between ETS Exposure and Asthma As summarized in Table 7-1 and noted above, the OR for asthma prevalence when both parents smoke tends to be higher than when only the mother smokes, which in turn is higher than when only the father smokes.
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From page 279... ...
. The relative risks associated with these four situations with respect to tobacco smoke in the home (i.e., both parents smoke, only the mother smokes, only the father smokes, neither parent smokes)
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From page 280... ...
In the limited number of studies that have been able to separate the effects of maternal active smoking during pregnancy from the effects of ETS exposure after birth, evidence suggests that while both exposures are detrimental maternal smoking during pregnancy has the stronger adverse effect. · There is limited or suggestive evidence of a relationship
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From page 281... ...
· There is inadequate or insufficient evidence to determine whether or not an association exists between ETS exposure and the development of asthma in school-age children. EVIDENCE REGARDING MEANS OF SOURCE MITIGATION OR PREVENTION Ventilation and Air Cleaning At present, source control appears to be the only reliably effective means of preventing ETS exposure.
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From page 282... ...
Source Control If all ETS exposure were eliminated for fetuses, infants, and children, and for persons of any age who have already developed asthma, it is reasonable to assume that the population risk of developing wheezing with respiratory infections and the risk of asthma exacerbations would decrease to the levels currently observed among similar persons who are not exposed. This conclusion, however, is inferred primarily from the epidemiologic data comparing persons from homes with smokers to those living in homes with no smoker.
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From page 283... ...
After several years of substantial decline among adolescents in four ethnic minority groups, smoking prevalence increased during the l990s among African-American and Hispanic youth (CDC, 1998~. These trends and the success of efforts at smoking prevention and cessation among young women in particular are especially relevant to the issue of avoiding antenatal and postnatal exposure of children to maternal smoking.
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From page 284... ...
With regard to smoking cessation attempts in the clinical setting, strong cessation messages from clinicians, structured in relation to the readiness and personal needs of the patients and utilizing nicotine replacement therapy and supplementary educational and behavioral interventions, have been associated with an increase in both initial and sustained quit rates in controlled trials
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From page 285... ...
Odds ratios are lowest for gum, rising to ~2.0 for the transdermal patch, and 2.92 and 3.05 for nasal spray and inhaled nicotine (Cepeda-Benito, 1993; Fiore et al., 1994; Law and Tang, 1995; Li Wan Po, 1993; Silagy et al., 1994; Tang et al., 1994; Viswesvaran and Schmidt, 1992~. Smoking Cessation Interventions in Pregnant Women As discussed above, maternal smoking, in particular, has been associated with adverse respiratory and asthma outcomes.
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From page 286... ...
Intervention effects were considered separately for families where the mother smoked and families where the mother did not smoke. Among those randomized, when the mother smoked the intervention was associated with significantly lower self-reported exposure of the infant to tobacco smoke from the mother and from nonmaternal household members.
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From page 287... ...
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)
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From page 288... ...
None of the studies to date that have investigated educational nterventions to reduce ETS exposure have extended this to include 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.
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From page 289... ...
Conclusions Regarding Mitigation Through Source Control · There is sufficient evidence to conclude that increased ventilation 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 ventilation and air-cleaning methods or technologies would be adopted and how effectively they actually would be used to reduce ETS concentration.
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From page 290... ...
Research is also needed to understand the nature of the interactions, 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 respiratory illnesses are in need of further investigation.
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From page 291... ...
1996. Cotinine as a biomarker of environmental tobacco smoke exposure.
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From page 292... ...
1992. An unsuccessful cotinine-assisted intervention strategy to reduce environmental tobacco smoke exposure during infancy.
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1998. Environmental tobacco smoke and adult asthma.
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From page 294... ...
1994. Reduction of environmental tobacco smoke exposure among asthmatic children: a controlled trial.
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1986. Environmental Tobacco Smoke: Measuring Exposures and Assessing Health Effects.
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From page 296... ...
1994. Meta-analysis on efficacy of nicotine replacement therapies in smoking cessation.
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From page 297... ...
1997. Reduction of environmental tobacco smoke exposure in asthmatic children.
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