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    DOI: 10.1542/peds.2009-0690; originally published online January 18, 2010;2010;125;e261Pediatrics

    Beebe and Judith OwensKimberly Yolton, Yingying Xu, Jane Khoury, Paul Succop, Bruce Lanphear, Dean W.

    ChildrenAssociations Between Secondhand Smoke Exposure and Sleep Patterns in

    http://pediatrics.aappublications.org/content/125/2/e261.full.html

    located on the World Wide Web at:The online version of this article, along with updated information and services, is

    of Pediatrics. All rights reserved. Print ISSN: 0031-4005. Online ISSN: 1098-4275.Boulevard, Elk Grove Village, Illinois, 60007. Copyright 2010 by the American Academypublished, and trademarked by the American Academy of Pediatrics, 141 Northwest Point

    publication, it has been published continuously since 1948. PEDIATRICS is owned,PEDIATRICS is the official journal of the American Academy of Pediatrics. A monthly

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    Associations Between Secondhand Smoke Exposureand Sleep Patterns in Children

    WHATS KNOWN ON THIS SUBJECT:Adult and adolescent

    smokers report difficulties with sleep. Young children who are

    exposed to tobacco smoke have poorer sleep quality. Children

    with asthma report more sleep problems and are more sensitive

    to the respiratory effects of tobacco smoke.

    WHAT THIS STUDY ADDS: We report significant associations

    between SHS exposure, as measured with a biological marker

    (serum cotinine levels), and sleep problems in children with

    asthma. Reduction in SHS exposure is an area with the potential

    for significant impact in the pediatric population.

    abstractOBJECTIVES: The objective of this study was to investigate the relation-

    ship between exposure to secondhand smoke (SHS) and child sleep

    patterns among a group of children with asthma who were exposed

    regularly to tobacco smoke at home.

    METHODS: We studied 219 children who were enrolled in an asthma

    intervention trial and were exposed regularly to SHS. Serum cotinine

    levels were used to measure exposure to tobacco smoke, and sleep

    patterns were assessed through parent reports using the ChildrensSleep Habits Questionnaire. Covariates in adjusted analyses included

    gender, age, race, maternal marital status, education, and income,

    prenatal tobacco exposure, maternal depression, Home Observation

    for Measurement of the Environment total score, household density,

    asthma severity, and use of asthma medications.

    RESULTS: Exposure to SHS was associated with sleep problems, in-

    cluding longer sleep-onset delay (P .004), sleep-disordered breath-

    ing (P .02), parasomnias (P .002), daytime sleepiness (P .022),

    and overall sleep disturbance (P .0002).

    CONCLUSIONS: We conclude that exposure to SHS is associated with

    increased sleep problems among children with asthma. Pediatrics2010;125:e261e268

    AUTHORS:Kimberly Yolton, PhD,

    a

    Yingying Xu, MS, MA,

    a

    Jane Khoury, PhD,b Paul Succop, PhD,c Bruce Lanphear,

    MD, MPH,d Dean W. Beebe, PhD,e and Judith Owens, MDf

    Divisions of aGeneral and Community Pediatrics andbBiostatistics and Epidemiology, andeBehavioral Medicine and

    Clinical Psychology, Department of Pediatrics, Cincinnati

    Childrens Hospital Medical Center, Cincinnati, Ohio;cDepartment of Environmental Health, University of Cincinnati,

    Cincinnati, Ohio;dFaculty of Health Sciences, Simon Frasier

    University and British Columbia Childrens Hospital, Vancouver,

    Canada; andfDepartment of Pediatrics, Brown University,

    Providence, Rhode Island

    KEY WORDS

    passive smoking, environmental exposure, sleep, child, asthma

    ABBREVIATIONS

    CSHQChildrens Sleep Habits Questionnaire

    ORodds ratio

    CIconfidence interval

    SHSsecondhand smoke

    HOMEHome Observation for Measurement of the Environment

    www.pediatrics.org/cgi/doi/10.1542/peds.2009-0690

    doi:10.1542/peds.2009-0690

    Accepted for publication Aug 3, 2009

    Address correspondence to Kimberly Yolton, PhD, Cincinnati

    Childrens Hospital Medical Center, Division of General and

    Community Pediatrics, 3333 Burnet Ave, ML 7035, Cincinnati, OH

    45229-3039. E-mail: [email protected]

    PEDIATRICS (ISSN Numbers: Print, 0031-4005; Online, 1098-4275).

    Copyright 2010 by the American Academy of Pediatrics

    FINANCIAL DISCLOSURE: The authors have indicated they have

    no financial relationships relevant to this article to disclose.

    ARTICLES

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    Appropriate sleep quality and quantity

    are increasingly being recognized as

    critical elements for many aspects

    of child health and development. For

    children, inadequate sleep has been

    linked with poor school performance,1

    somatic complaints,1 behavior prob-lems,25 and mental health problems.1,6

    In addition, sleep problems during

    childhood are associated with in-

    creased incidence of anxiety and de-

    pression, aggressive behaviors, and

    attention problems in adulthood,

    which suggests a lasting impact of

    sleep problems on mental health.7

    Poor childhood sleep also predicts the

    development of obesity and its associ-

    ated morbidities,8,9 which indicatesan important influence on health

    outcomes.

    More than 25% of children experience

    some type of sleep problem during

    childhood.1,1012 Among children with

    asthma, the prevalence of sleep

    problems is higher, with 40% to 60%

    having some difficulty.13,14 Children

    with asthma are nearly 4 times more

    likely to experience sleep-disordered

    breathing,15 which results in sleepdisruption and decreased sleep effi-

    ciency,16 reduced sleep quality, in-

    creased nighttime activity levels,17 and

    more difficulties with daytime sleepi-

    ness.16,18 Sleep efficiency has been

    shown to improve with effective treat-

    ment of asthma symptoms,16 but even

    children with clinically stable asthma

    have worse sleep quality and more

    daytime sleepiness than do children

    without asthma.19

    Tobacco exposure is a risk factor for

    sleep problems in adolescents and

    adults. Cigarette smoking is associ-

    ated with changes in sleep architec-

    ture, with smokers experiencing

    longer latency to sleep initiation and

    lighter sleep.20 Adult and adolescent

    smokers report more sleep problems,

    such as trouble initiating sleep, main-

    taining sleep, difficulty waking, and

    daytime sleepiness.2124 Women who

    smoke during pregnancy are more

    likely to report insufficient sleep, diffi-

    culty initiating sleep, early morning

    waking, short sleep duration, snoring,

    and excessive daytime sleepiness,

    compared with pregnant women whodo not smoke. Interestingly, women

    who are nonsmokers but are exposed

    to secondhand smoke (SHS) during

    pregnancy also report more difficul-

    ties with sleep, including insufficient

    sleep, difficulty initiating sleep, and

    short sleep duration, compared with

    those not exposed.25

    This effect of SHS on sleep in adult

    women raises concerns about the po-

    tential impact on children whose fam-ily members smoke. There is little re-

    search on the influence of tobacco

    smoke exposure on sleep patterns in

    childhood. Young children who are ex-

    posed to tobacco smoke either prena-

    tally or postnatally are reported to

    have poorer sleep quality26 and more

    symptoms of sleep-disordered breath-

    ing,27 compared with those who are

    not exposed. Because tobacco smoke

    is a known contributor to asthma se-verity,2830 exposure to SHS may have a

    particularly marked effect on the sleep

    of children with asthma. Although this

    possibility has received little empirical

    investigation, SHS exposure has been

    associated with increased night wak-

    ings in children with asthma.31 A major

    limitation of these studies linking SHS

    and sleep difficulties in children26,27,31

    is the fact that they relied on parent

    reports of exposure, instead of more-precise and more-objective biological

    markers of tobacco exposure.

    The objective of this study was to ex-

    amine the relationship between SHS

    exposure and sleep patterns among a

    group of children with asthma. We

    used a biomarker of tobacco expo-

    sure, serum cotinine levels, to quan-

    tify exposure objectively and a vali-

    dated pediatric sleep survey32 to

    characterize sleep patterns. We hy-

    pothesized that children with asthma

    who were exposed to higher levels of

    SHS would exhibit more sleep prob-

    lems, as reported by parents, com-

    pared with children with lower levels

    of exposure.

    METHODS

    This study used the Cincinnati Asthma

    Prevention Study, an asthma interven-

    tion trial based on environmental mod-

    ifications to the home in the form of

    high-efficiency particulate air clean-

    ers, and outcomes focused on asthma

    symptoms, health care utilization, and

    pulmonary function. For the current

    study, SHS exposure, child sleep pat-terns, and potential covariates were

    measured before initiation of the

    asthma intervention.

    Recruitment and enrollment proce-

    dures for the 6- to 12-year-old children

    are described in detail elsewhere.33

    Briefly, all children in the sample had

    physician-diagnosed asthma that had

    been treated within the previous year

    and exposure to SHS from 5 ciga-

    rettes per day at home, according toparent report. Children were identified

    on the basis of hospital and clinic bill-

    ing records, and parents of 1678 chil-

    dren were contacted for completion of

    a screening survey and request for

    participation, if eligible. Children were

    excluded if they had other respiratory

    diseases, heart disease, mental retar-

    dation, or other serious conditions

    barring participation in the study. Of

    the 348 eligible participants, 232 en-rolled and completed the main study

    (67% participation rate), and 219 had

    complete data pertinent to the current

    study and were retained for the analy-

    sis. Protocols were approved by the in-

    stitutional review board.

    We collected detailed survey data re-

    garding the childs daily exposure to

    SHS in the home, car, and other loca-

    tions, including hours of exposure,

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    number of cigarettes per day, whether

    the child was in the same room during

    smoking, and whether windows were

    open during car exposure. SHS expo-

    sure also was measured objectively by

    using serum cotininelevels detected in

    samples collected at the baselinehome visit, which represent our pri-

    mary measure of exposure. Cotinine, a

    metabolite of nicotine, is a reliable

    biomarker of exposure to tobacco

    smoke.34 Serum levels provide a short-

    term view of exposure over the previ-

    ous 48 to 72 hours. However, because

    of stability of exposure patterns over

    time, a one-time cotinine measure-

    ment is considered representative of

    typical daily exposure.34 Cotinine levelsin serum were measured by the Cen-

    ters for Disease Control and Preven-

    tion with published methods involving

    high-performance liquid chromatog-

    raphy linked to atmospheric-pressure

    chemical ionization-tandem mass

    spectrometry.35 We applied a logarith-

    mic base 2 transformation for analysis

    of serum cotinine levels because of

    the skewed distribution of the raw

    data. This provides for simpler inter-pretation of the coefficients from the

    regression analyses, in which there is

    an increase in the sleep scale equal to

    the coefficient for log cotinine level for

    each doubling of the cotinine level.

    The Childrens Sleep Habits Question-

    naire (CSHQ)3 was used to measure

    child sleep patterns within the previ-

    ous 2 weeks, as reported by the pri-

    mary caregiver. The CSHQ yields a to-

    tal sleep disturbance score and scoresfor 8 scales (ie, bedtime resistance,

    sleep-onset delay, sleep duration, sleep

    anxiety, night wakings, parasomnias,

    sleep-disordered breathing, and daytime

    sleepiness). This instrument is used in

    clinical and research settings to pro-

    vide a broad description of child sleep

    patterns. Internal consistency mea-

    sures for the entire scale are high

    ( 0.68 for a community sample and

    0.78 for a clinical sample), and

    test-retest reliabilities among the

    scales are high (r 0.620.79). A total

    CSHQ score of41 has sensitivity of

    0.80 and specificity of 0.72, properly

    classifying 80% of a group with clini-

    cally relevant sleep disorders. To en-sure uniform thorough completion,

    this measure was administered in

    an interview in which caregiver re-

    sponses were recorded by a trained

    research assistant.

    Asthma severity was reported as mild,

    moderate, severe, or very severe by

    the childs caregiver. Severe and very

    severe categories were combined be-

    cause of small group sizes. Parent

    report of asthma symptoms is an ef-fective means of characterizing child

    asthmaand is notenhancedby asthma

    diaries or pulmonary function test-

    ing.36 Parents also reported asthma

    medication use by the child, includ-

    ing use of short-acting bronchodila-

    tors, long-acting inhaled steroids,

    and orally administered steroids

    prescribed for treatment of acute

    exacerbations.

    Other measured covariates were ma-ternal depression (Beck Depression In-

    ventory II)37 and quality of the home en-

    vironment, measured with the Home

    Observation for Measurement of the

    Environment (HOME) instrument for

    elementary school-aged children.38

    The HOME instrument is primarily an

    observational tool that assesses the

    quality of the home environment, in-

    cluding physical characteristics, vari-

    ety of stimulation, and nurturing be-havior from the parent, and was

    completed at a 12-month follow-up

    visit. For 14 participants, this assess-

    ment was missing and imputed values

    generated with SOLAS 3.0 (Statistical

    Solutions, Cork, Ireland), on the basis

    of age, race, and gender, were used.

    Univariate analyses involved inspec-

    tion of frequencies and estimation of

    means and associated SDs. Because of

    nonnormal distributions, serum cotin-

    ine levels are reported as geometric

    means and 95% confidence intervals

    (CIs), and household income is re-

    ported as median and 25th and 75th

    percentile values. We used linear re-

    gression for the daytime sleepinessand total sleep disturbance scales. The

    distributions of the other sleep scales

    reflected varying degrees of nonnor-

    mality; therefore, responses were di-

    chotomized, at approximately the 75th

    percentile value, and logistic regres-

    sion was used. For each outcome mea-

    sure, 3 models were developed, to

    reflect (1) the simple bivariate associ-

    ation between exposure and sleep, (2)

    the association after adjustment forall covariates (age, gender, race, ma-

    ternal smoking during pregnancy,

    marital status, maternal education,

    household income, household density,

    number of siblings, maternal depres-

    sion, HOME score, asthmaseverity, and

    asthma medication use), and (3) the

    association after adjustment for im-

    portant covariates, representing the

    most statistically parsimonious final

    model. For the final models, age, gen-

    der, and asthma severity were re-

    tained irrespective of statistical signif-

    icance. Other covariates were retained

    if they accounted for significant vari-

    ance on the given sleep scale (P .05).

    Also, if removal of the covariate from

    the model was associated with a

    10% change in the regression coeffi-

    cient for serum cotinine levels, then it

    was retained in the model. SAS 9.1

    (SAS Institute, Cary, NC) was used for

    all analyses.

    RESULTS

    Descriptive information on the sample

    is summarized in Table 1. The mean

    age of the subjects at the baseline visit

    was 9.4 years. Sixty-one percent of the

    children were boys, and 56% were re-

    ported to be black. Childrenin thesam-

    ple were exposed to a median of 13

    cigarettes per day in their homes, as

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    reported by their parents, and the geo-

    metric mean serum cotinine level for

    the sample was 1.16 ng/mL. The corre-

    lation between serum cotinine levelsand parent-reported exposure was

    0.39 (P .0001) for the full sample.

    Mean values for overall sleep distur-

    bance and sleep scale scores for

    children in our sample fell between

    the clinical and control samples re-

    ported by Owens et al.32 Internal con-

    sistency for the sleep measure also

    was comparable to the findings of

    Owens et al.32 Surprisingly, 93% of

    the children in the sample had a

    CSHQ total sleep disturbance score

    (41) that would be considered clin-

    ically relevant. The mean sleep timereported by parents was 9.6 hours

    per night.

    In bivariate analyses, the associations

    between the logarithm of serum cotin-

    ine levels and child sleep patterns

    were significant for bedtime resis-

    tance, sleep anxiety, parasomnias,

    sleep-disordered breathing, daytime

    sleepiness, and total sleep distur-

    bance but not for sleep-onset delay or

    sleep duration (Table 2). There was no

    association between total duration of

    nighttime sleep and serum cotinine

    levels.

    In multivariate analyses including all

    potential covariates of child sleep pat-

    terns, we found that higher levels of

    SHS exposure were significantly asso-

    ciated with higher scores (ie, more

    problems) on the sleep-onset delay,

    parasomnias, daytime sleepiness, and

    total sleep disturbance scales. Final

    models, including only covariates that

    had a relationship with the sleep scale

    of interest or affected the coefficient

    for cotinine levels, revealed significant

    associations between SHS exposure

    andincreases in sleep-onset delay, para-somnias, sleep-disordered breathing,

    daytime sleepiness, and overall sleep

    disturbance (Table 2).

    Several covariates remained in our

    final models because of associations

    with sleep scales. Increasing age

    was significantly associated with de-

    creased bedtime resistance, more

    problems with sleep duration, less

    sleep anxiety, and lower overall sleep

    disturbance. More-severe asthma was

    associated with more problems with

    sleep duration and more-frequent

    night wakings. Maternal smoking

    during pregnancy was associated

    with decreased sleep-onset delay. A

    nonmarried parent was associated

    with fewer parasomnias and in-

    creased daytime sleepiness. Lower

    family income was associated with de-

    creased sleep duration and decreased

    daytime sleepiness. Higher levels ofmaternal depression were associated

    with more-frequent parasomnias,

    increased daytime sleepiness, and

    greater overall sleep disturbance.

    More siblings and increased housing

    density were associated with de-

    creased sleep-disordered breathing.

    Finally, the use of long-term inhaled

    asthma medications was associated

    with fewer parasomnias.

    TABLE 1 Sample Characteristics (N 219)

    Age, mean SD, y 9.4 1.8

    Male, n(%) 134 (61.2)

    Race, n(%)

    Black 122 (55.7)

    White 92 (42.0)

    Other 5 (2.3)

    Parent education, n(%)

    High school graduate or less 143 (65.3)

    Any college 76 (34.7)

    Parent marital status, n(%)

    Married or living with someone 91 (41.6)

    Divorced, separated, or widowed 37 (16.8)

    Single, never married 91 (41.6)

    Household income, median (interquartile range), $ 25 000 (15 00045 000)

    Asthma severity, n(%)

    Mild 51 (23.2)

    Moderate 105 (48.0)

    Severe/very severe 63 (28.8)

    Maternal smoking during pregnancy, n(%)

    None 73 (33.3)

    Until pregnancy recognition 32 (14.6)

    Throughout pregnancy 114 (52.1)No. of cigarettes smoked in home daily, median (interquartile range) 13 (920)

    Serum cotinine level

    Geometric mean (95% CI), ng/mL 1.16 (0.1013.07)

    Median (interquartile range), ng/mL 1.45 (0.562.69)

    HOME score, mean SD 46.9 8.1

    Maternal depression score, mean SD 12.4 9.9

    Behavior Assessment System for Children-2 score within clinical range

    (70), n(%)

    Externalizing symptoms 41 (18.8)

    Internalizing symptoms 58 (26.6)

    Behavior symptoms 46 (21.1)

    Sleep pattern score, mean SD

    Bed resistance 8.9 2.7

    Sleep-onset delay 1.6 0.8

    Sleep duration 4.4 1.7

    Sleep anxiety 5.7 1.8

    Night waking 4.3 1.3

    Parasomnias 9.6 2.1

    Sleep-disordered breathing 4.2 1.4

    Daytime sleepiness 15.5 3.3

    Total sleep disturbance 51.6 8.2

    Total sleep disturbance raw score of41, n(%) 203 (92.7)

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    We found cotinine level-gender inter-

    actions for the sleep-onset delay (odds

    ratio [OR]: 0.63; P .011) and sleep

    anxiety (OR: 1.47; P .05) scales;

    therefore, we performed gender-

    stratified regression analyses for

    those scales, controllingfor the covari-

    ates retained in the final models for

    the full sample. For boys, a statistically

    significant relationship was found be-

    tween serum cotinine levels and

    higher scores for sleep anxiety (OR:

    1.54; P .003). For girls, a statistically

    significant relationship was found be-

    tween serum cotinine levels and sleep-

    onset delay (OR: 1.54; P .008).

    DISCUSSION

    For children with asthma, we found

    that SHS exposure was associated

    with greater parent-reported sleep

    problems. Specifically, as SHS expo-

    sure increased, parents reported that

    their children had longer delays in

    sleep onset, more-frequent parasom-

    nias and sleep-disordered breathing,

    increased daytime sleepiness, and

    greater overall sleep disturbance.

    Two sleep scales showed significant

    gender-cotinine level interactions. In

    regression analyses stratified accord-

    ing to gender, greater exposure to SHS

    was associated with greater sleep anx-

    iety in boys and greater sleep-onset

    delay in girls.

    SHS exposure was associated with in-

    creased incidence of parasomnias in

    this sample of children. Parasomnias

    reflect partial arousal from either non-

    rapid eye movement or rapid eye

    movement sleep and, although usually

    benign, can be highly distressing tochildren and their families. More than

    80% of preschoolers experience para-

    somnias, but their incidence de-

    creases with age.39 Adult men who

    smoke report more nightmares and

    disturbing dreams than do men who

    do not smoke, but there has been no

    reported association for women.24

    Boys in our study experienced greater

    sleep anxiety with increasing SHS ex-

    posure. Nighttime fears are reportedby upto 79% of 8- to 16-year-old youths.

    In contrast to our findings, however,

    they have been reported more fre-

    quently among girls (72%) than boys

    (55%).40 For girls in our study, greater

    SHS exposure was associated with

    greater sleep-onset delay, which is con-

    sistent with reports that both men and

    women who smoke cigarettes have in-

    creased difficulty initiating sleep.41 No

    other studies have investigated the rela-

    tionship between SHS and sleep-onset

    delays among children.

    The exact mechanism through which

    SHS exposure may affect childrens

    sleep is not clear. We briefly explore 3

    possible explanations, that is, exacer-

    bation of respiratory symptoms, nico-

    tine arousal mechanisms, and symp-

    toms of abstinence. In adults, smokingis known to exacerbate respiratory

    disorders such as obstructive sleep

    apnea,24,42 and SHS exposure has been

    associated with increased snoring in

    pregnant women.25 Among children,

    parent-reported maternal smoking is

    associated with increased snoring,27

    and nighttime respiratory symptoms

    are exacerbated by exposure to SHS.31

    Indeed, higher levels of SHS exposure

    were associated with more sleep-disordered breathing among children

    in our study. It is likely that SHS

    exposure acts as an upper airway

    irritant, increasing symptoms of sleep-

    disordered breathing and thus contrib-

    uting to overall sleep disturbances

    among children with asthma.

    Although adolescent and adult smokers

    report disturbances in sleep,2224,41,43 a

    clear causal relationship between to-

    TABLE 2 Associations Between Serum Cotinine Levels (Independent Variable) and Childrens Sleep (Dependent Variable) in Logistic and Multiple

    Regression Analyses (N 219)

    Sleep Scale (Cutoff Point) Bivariate Association Between

    Serum Cotinine Levels and Sleep

    Outcomes

    Full Model of Association

    Between Serum Cotinine Levels

    and Sleep Outcomes Including

    All Covariates

    Final Model of Association

    Between Serum Cotinine Levels

    and Sleep Outcomes Including

    Significant Covariates

    OR or (95% CI) P OR or (95% CI) P OR or (95% CI) P

    Bed resistance (10) 1.29 (1.091.53) .003 1.34 (0.951.88) .093 1.21 (0.9951.47) .056Sleep-onset delay (2) 1.07 (0.921.24) .39 1.50 (1.082.06) .014 1.53 (1.152.03) .004

    Sleep duration (5) 1.00 (0.861.17) .98 1.19 (0.871.63) .27 1.12 (0.921.37) .24

    Sleep anxiety (7) 1.28 (1.071.53) .006 0.90 (0.651.24) .51 1.06 (0.811.38) .68

    Night wakings (5) 1.09 (0.931.28) .28 1.10 (0.811.50) .54 1.09 (0.921.31) .32

    Parasomnias (12) 1.62 (1.232.12) .0005 1.91 (1.093.34) .023 1.95 (1.362.79) .0002

    Sleep-disordered breathing (5) 1.29 (1.081.54) .005 1.33 (0.941.89) .11 1.26 (1.041.52) .02

    Daytime sleepiness 0.40 (0.150.64) .002 0.51 (0.080.94) .021 0.33 (0.050.61) .022

    Total sleep disturbance 1.40 (0.811.99) .0001 1.42 (0.372.47) .009 1.14 (0.541.74) .0002

    Childage, gender, and asthmaseveritywere included in allanalyses.Other covariateswere included if theywere statisticallyrelevantto the sleepscale of interest and included the following

    considerations: maternal race, marital status, education, income, smoking during pregnancy, and depression, HOME inventory total score, household density (house volume per persons),

    number of siblings, and use of asthma medication (including short-acting inhaled medicines, long-acting inhaled medicines, and orally administered steroids). Multivariate regression

    analyses were used for analysis of daytime sleepiness and total sleep disturbance ( reported); all other analyses used logistic regression analyses of dichotomized sleep scales (OR

    reported).

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    bacco and sleep disorders has been

    difficult to establish.42 Nicotine is a

    stimulant that may contribute to in-

    creased arousal and attention among

    smokers, likely by stimulating neuro-

    transmission of acetylcholine and trig-

    gering activation of the dopaminergicsystem in the brain.42,44 Nicotine is as-

    sociated with altered sleep architec-

    ture, resulting in reduced sleep time

    and efficiency, longer sleep latency,

    lighter sleep, and reduced rapid eye

    movement sleep.20,45

    Frequent night wakings among smok-

    ers often are attributed to withdrawal

    during sleep. During the early stages

    of smoking abstinence, adult smokers

    experience difficulty falling asleep, re-duced sleep efficiency, and longer la-

    tency to rapid eye movement sleep.46

    Colrain et al47 reported increased

    night wakings and sleepiness as the

    most-consistent findings of research

    on smoking cessation. Insomnia, sleep

    disturbance, and anxiety also are

    symptoms of nicotine withdrawal

    listed in the Diagnostic and Statistical

    Manual of Mental Disorders, Fourth

    Edition.48 These symptoms in manyways resemble those reported in our

    sample. It is possible that children ex-

    posed to SHS experience a degree

    of nicotine withdrawal during sleep,

    which results in disruptions in the

    normal sleep process. Although with-

    drawal symptoms among children ex-

    posed to SHS have, to our knowledge,

    not been noted in the literature, sev-

    eral studies presented evidence that

    newborns who were exposed prena-

    tally to tobacco experienced nicotine

    withdrawal shortly after birth.4951 This

    area requires further study.

    SHS exposure results in a much

    smaller amount of nicotine intakethan active smoking. Studies of SHS

    effects on sleep have included re-

    ports of sleep disturbances among

    adult men,41 pregnant women,25 and

    preschool-aged children,26 which in-

    dicates that even small amounts of ex-

    posure to nicotine, as would occur in

    SHS exposure, are sufficient to affect

    sleep adversely. Our study contributes

    additional evidence that SHS affects

    sleep among school-aged childrenwith asthma.

    This study is not without limitations. All

    children in the study had asthma, and

    the results may not be generalizable

    to populations of children without

    asthma. However, these results may

    be reflective of risks from SHS expo-

    sure for the 9% of children in the

    United States today who have asthma.52

    All children in this study were exposed

    to SHS, and we can generalize our find-ings only to exposed children. The de-

    gree of exposure varied widely in our

    sample, and there was no evidence of

    curvilinear or threshold effects that

    might suggest a safe level of SHS ex-

    posure. In addition, national data sug-

    gest that more than one half of chil-

    dren are exposed to SHS.53 Our sleep

    data were derived from parent reports

    only. Additional study in this area

    should include use of child-reported

    sleep problems and additional mea-

    sures of sleep patterns, such as

    polysomnography, actigraphy, or de-

    tailed sleep diaries. Finally, we had

    no information on prematurity in thissample, which could be an important

    contributor to sleep problems.54,55

    CONCLUSIONS

    Among children with asthma, expo-

    sure to SHS affects sleep negatively,

    as evidenced by greater sleep-onset

    delays, more-frequent parasomnias,

    more sleep-disordered breathing, in-

    creased daytime sleepiness, and

    greater overall sleep disturbance. Theconsequences of inadequate sleep in

    children are not trivial. Sleep distur-

    bances have been linked with in-

    creased behavior problems,25 mental

    health problems,1,6 and poor school

    performance1 in children. In addition,

    effects of poor sleep in childhood can

    persist into adulthood in the form of

    obesity8,9 and behavior and mood dis-

    orders.7 Reduction in SHS exposure is

    an area with the potential for signifi-cant impact for physical and emotional

    health and school performance in the

    pediatric population.

    ACKNOWLEDGMENTS

    This work was supported by grants

    from the National Institutes of Health

    (grants R21 ES12952-01 and R01

    HL65731).

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    DOI: 10.1542/peds.2009-0690; originally published online January 18, 2010;2010;125;e261Pediatrics

    Beebe and Judith OwensKimberly Yolton, Yingying Xu, Jane Khoury, Paul Succop, Bruce Lanphear, Dean W.

    ChildrenAssociations Between Secondhand Smoke Exposure and Sleep Patterns in

    ServicesUpdated Information &

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