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The effects of tobacco smoke on respiratory symptoms among young adults in the Children's Health Study II

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The effects of tobacco smoke on respiratory symptoms among young adults in the Children's Health Study II

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Content THE EFFECTS OF TOBACCO SMOKE ON RESPIRATORY SYMPTOMS
AMONG YOUNG ADULTS IN THE CHILDREN’S HEALTH STUDY II
by
G rade R. Neuman
A Thesis Presented to the
FACULTY OF THE GRADUATE SCHOOL
UNIVERSITY OF SOUTHERN CALIFORNIA
In Partial Fulfillment o f the
Requirements for the Degree
MASTER OF SCIENCE
(APPLIED BIOSTATISTICS AND EPIDEM IOLOGY)
M ay 2006
Copyright 2006 Gracie R. Neuman
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UMI Number: 1437853
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DEDICATION
To Barbara and Bruce Gordon
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ACKNOW LEDGEMENTS
I wish to thank my committee chair and mentor, Dr. Frank Gilliland, for his
unwavering support, interest, and guidance from the very beginning and throughout
the entire process o f completing this manuscript. I am thankful for his research
support and the great opportunity to work as his research assistant. M y gratitude
goes to members o f m y thesis committee, Dr. W endy M ack and Dr. Rob McConnell,
for their valuable comments and careful review o f this manuscript. I thank
Dr. Wendy M ack for her friendship and common interest in the welfare o f animals. I
appreciate the warm nudge and encouragement received from Dr. Stan Azen to work
as a teaching assistant in order to gain more hands-on experience with statistics and
to increase m y knowledge o f epidemiology. I thank all the professors in my classes
who imparted to me their indomitable spirit and love for biostatistics and
epidemiology. I thank Made Wenten for generously sharing his time and his
tremendous reassurance throughout the whole process, and the friendship he so
willingly provided. I thank Miwa Kawakubo and Ling Yao for their great SAS
troubleshooting skills and their boundless patience. I am grateful for Lisa Grossman
for always being so optimistic and for cheering me on.
This work would not have been possible without the strong support and
encouragement o f m y family. I thank m y parents who have instilled in me a sense of
purpose and responsibility and my in-laws who are a constant source o f cheer and
happiness. I thank m y husband and best friend, Dr. B. Clifford Neuman, for his
unshakable support, friendship, and love throughout this project. Thank you all for
your generous support and your belief in me.
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TABLE OF CONTENTS
IV
DEDICATION............................................................................................................................. ii
ACKNOW LEDGEM ENTS.....................................................................................................iii
LIST OF TA BLES...................................................................................................................... v
ABSTRACT .................................................................................................................. vii
Chapter
I. INTRODUCTION............................................................................................. 1
FIGURE 1......................................................................................................... 5
II. M ETH ODS.......................................................................................... 12
III. RESU LTS..........................................................................................................17
IV. D ISCUSSION ...................................................................................................48
BIBLIOGRAPHY......................................................................... 55
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Table 1:
Table 2:
Table 3:
Table 4:
Table 5:
Table 6A:
Table 6B:
Table 6C:
Table 7:
Table 8 :
Table 9:
Table 10:
Table 11:
Table 12:
v
LIST OF TABLES
Role o f active smoking and environmental tobacco smoke
exposure on asthma symptoms 7
Selected characteristics o f participants with never,
former, and current asthma status, CHS II, 1999-2003 18
Personal smoking by gender and asthma status,
CHS II Participants 20
Personal smoking patterns by asthma indicators 21
Personal smoking pattern by asthma symptoms 23
Respiratory symptoms in non-smokers and smokers
exposed to environmental tobacco smoke at home, CHS II 25
Respiratory symptoms in non-smokers and smokers
exposed to environmental tobacco smoke at work, CHS II 26
Respiratory symptoms in non-smokers and smokers
exposed to social environmental tobacco smoke, CHS II 27
Percentage o f non-smokers and smokers exposed to
second-hand smoke 29
Percentage o f non-smokers exposed to second-hand
smoke at home, work, or social environments stratified
by asthma status, CHS II 31
Second-hand smoke exposure in non-smoking females
and males by asthma status, CHS II 32
ETS exposure patterns in non-smokers by
asthma indicators 34
Second-hand smoke exposure pattern in non-smokers
by asthma symptoms 36
Percentage o f non-smokers and smokers by
physician-diagnosed asthma exposed to second-hand smoke 37
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Table 13:
Table 14:
Table 15:
Table 16:
Effects o f active smoking on asthma symptoms
in the past 12 months among CHS II participants,
adjusted odds ratios and 95% Cl
Effects o f tobacco smoke exposure at hom e on
asthma symptoms in the past 12 months among
CHS II participants, adjusted odds
ratios and 95% Cl
Effects o f tobacco smoke exposure at work on
asthma symptoms in the past 12 months among
CHS II participants, adjusted odds
ratios and 95% Cl
Effects o f social tobacco smoke exposure on
asthma symptoms in the past 12 months among CHS II
participants, adjusted odds ratios and 95% Cl
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ABSTRACT
VII
Comparatively few studies have evaluated the contribution o f environmental
tobacco smoke to the aggravation o f asthma in young adults. Our aims are: (1)
characterize asthma-smoking association; (2) determine the effect ETS exposure on
asthma in non-smoking young adults. Data from participants (N=T,628) in the
Children’s Health Study II between ages 12 and 28 was examined. We observed a
marked contrast in the association between personal smoking and congestion and
phlegm in participants with (OR, 2.0; 95% Cl 1.1-3.2) and without physician-
diagnosis of asthma (OR, 3.6; 95% C l 2.6-5.0). Exposure to social second-hand
smoke among young adults was significantly associated with congestion or phlegm
(OR, 1.8; 95% C l 1.2 to 2.6), wheezing without a cold (OR, 1.8; 95% Cl 1.3 to 2.4),
and wheezing after exercise (OR, 2.0; 95% Cl 1.4 to 2.8). These findings point to a
need for improving respiratory health o f young adults by reducing tobacco smoke
exposure.
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1
I. INTRODUCTION
Asthma has been recognized as one o f the most common chronic conditions
in the United States with more than 1.5 million emergency department visits,
500,000 hospitalizations, and 5,500 deaths per year (NIH 2004). Asthma affects an
estimated 4.8 million children across the country. The onset o f asthma usually
occurs between the ages of 5 to 15 years. Recent surveys reveal a rising asthma
prevalence among children in this age range, up from 42.8 per 1,000 in 1980 to 74.4
per 1,000 in 1993-1994 (NIH 2004).
Although widely studied, asthma etiology and the basis for the increasing
prevalence have not yet been clearly established (Carter 1998). Environmental
factors, such as air pollution and indoor allergens, have been shown to be important
factors to the onset and course o f asthma (Mazaik 2002). Several studies have
focused on the association between asthma and atopic disease with factors related to
the home environment, such as molds, SHS, house dust mite, animal dander, use of
N 02-producing heating appliances like gas- or oilstoves without a flue, and
environmental tobacco smoke (Bardana 2001).
Over recent years researchers have learned more about the pathogenesis of
asthma, leading to an evolving definition for the disease. For many years asthma
was considered primarily as a broncho spastic condition. It was believed that
bronchioconstriction was due to smooth muscle contraction in the airway. Airway
narrowing occurs in asthmatics and is due to several factors such as bronchospasm,
edema o f the airway, increased mucus secretions, cellular infiltration o f airway
walls, and injury o f airway epithelium. More recent studies have shown that
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obstructive airways may be the result o f an inflammatory process. The National
Heart, Lung, and Blood Institute (NHLBI) recently defined asthma as a chronic
inflammatory disease(Zeffren 1996). The inflammation causes airway
hyperresponsiveness resulting in narrowed airways and decreased airflow to lung
tissues.
Researchers studying the biological mechanism for asthma have described it
as an inflammatory response that is characterized by infiltration of the airway wall
with mast cells, lymphocytes, and eosinophils (W ills-Karp 1999). In genetically
susceptible individuals the inflammatory process has been hypothesized to be due to
inappropriate immune responses to common aeroallergens. CD4+ T cells and Th2
play an important role in the pathogenesis by releasing cytokines such as IL-4, IL-5,
and IL-13 (Corrigan 1990). These cytokines trigger a cascade o f numerous
inflammatory mediators that individually or in concert with other immune cells
induce changes in the airway wall (Gerblich 1991).
Studies have reported cellular and structural changes, known as airway
remodeling, in the airway walls of asthmatics (Bento 1998; Vignola 2004; Bai 2005).
Airway remodeling indicates structural changes in the composition, quantity and
organization o f the cellular and molecular structure o f the airway wall. Airway
remodeling leads to changes such as epithelial fragility, goblet cell hyperplasia,
enlarged submucosal mucus glands, angiogenesis, increased matrix deposition in the
airway wall, increased airway smooth muscle mass, wall thickening, and
abnormalities in elastin (Bai 2005). Disruption of alveolar attachments and
adventitial thickening may augment airway narrowing (M auad 2004). Structural
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3
changes may also increase narrowing by alteration o f smooth muscle dynamics
through limitation o f the ability o f smooth muscle to periodically lengthen (Hirst
2004).
Researchers believe asthma to be a chronic episodic disease that is initiated
early in childhood (Silverman 1993). Chronic wheezing associated with atopy and
inflammation may indicate asthma in young children (Gem 1995). Exposure to
allergens in sensitized children is reported to trigger an immediate and late cellular
airway reaction and bronchial obstruction (Holgate 1985). In adulthood, high
exposures to new allergens, such as occupational allergens may mimic the
sensitization process occurring in early life (Jarvis 1996). Other environmental
factors in adulthood, such as exposures to irritants, have been suggested as important
risk factors for persistent asthma in adulthood (Busse 1995).
Although it is one o f the most common childhood illnesses, there are no
objective diagnostic tests for a clinical syndrome like asthma. The assessment and
diagnosis of asthma is complicated. Frequently, the diagnosis o f asthma in suspected
individuals involves a detailed family history o f asthma, the child’s medical history,
physical exam, chest x-ray, blood tests and sputum studies, allergy prick skin test,
use o f asthma medications, and pulmonary function tests such as spirometry and
methacholine challenge test.
As part of the diagnostic procedure, objective assessment of pulmonary
function is often by spirometry. A spirometer device is used to measure timed
expired and inspired volumes to assess whether there is airflow obstruction and
whether this condition may be reversible over a short time period. Spirometry
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4
measurements are made before and after a patient inhales a bronchiodilator, which
causes airways to expand allowing air to pass freely. Figure 1 shows the common
measurements made for spirometry analyses. In some instances, asthma may be
suspected if measurements fall below normal for a person’s age and improves
significantly after treatment with a bronchiodilator drug.
Another diagnostic tool that assesses airway obstruction and asthma
symptoms is the methacholine challenge test. Asthma symptoms are deliberately
triggered by inhalation of aerosolized methacholine through a nebulizer for 2
minutes. M ethacholine causes the airways to spasm and narrow in asthmatic
individuals. Below-normal spirometric measurements at this point may indicate
asthma. During the test, increasing amounts o f methacholine aerosol mist are
inhaled before and after spirometry. A positive methacholine test indicates the
presence o f asthma if the lung function is reduced by 2 0%.
The link between smoking and asthma has been a focus o f recent studies
(Vesterinen 1988; Brook 1993; Thomson 2004). Inhaled tobacco smoke is known to
trigger asthma as irritating chemical substances settle on the moist lining of the
airways. With an estimated 13% to 35% of adolescents smoking tobacco, smoking is
a major health risk for young adults. A report in 1994 from the Centers for Disease
Control and Prevention found that an estimated 3.1 million adolescents were current
smokers (CDC 1994). Tobacco smoking has been reported to begin primarily by age
16 with most initial use occurring before high school graduation. A report by the
2004 National Youth Tobacco Survey of about 28,000 U.S. students showed that
about 12% of middle and 28% of high school students were current tobacco users
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5
FIGURE 1
Common measurements made using a spirometer
FEVj
< 1 >
E
3
O
>
VC (vital capacity) is the m axim um volum e of air which can be
exhaled or inspired during either a forced (FVC) or a slow (VC)
procedure
FEVi (forced expired volum e in one second) is the volum e expired in
the first second of maximal expiration after a m axim al inspiration and
is a useful measure of how quickly full lungs can be em ptied.
FEVi/VC is the FEVi expressed as a percentage of the VC or FVC
(whichever volum e is larger) and gives a clinically useful index of
airflow lim itation.
FEF2 5 -7 5 % is the average expired flow over the middle half of the FVC
Procedure and is regarded as a more sensitive measure of small
airways narrowing than FEVi.
U nfortunately FEF2 5-7 5% has a wide range of norm ality, is less
reproducible than FEVi, and is difficult to interpret if the VC (or FVC) is
reduced or increased.
Source: National Asthma Council Spirometry Handbook, July 2004
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o >
E
3
s
FVC
FEV i
0 1
, FE V i
Time (seconds) Time (seconds)
6
(CDC 2004). Trends in cigarette smoking among high school students (grades 9-12)
between 1991 and 1999 showed a significant increase from 27.5% in 1991 to 34.8%
in 1999, with some leveling or decline later in the decade (CDC 2000). Smoking
prevalence among female adolescents began exceeding males in the mid-1970s. The
prevalence has now become similar in both genders (CDC 2000)
Recent interest has focused on the effects of direct exposure to tobacco
smoke through personal smoking. Table 1 lists common respiratory effects often
linked to active smoking. Personal cigarette smoking is associated with bronchial
hyper-responsiveness, frequent bronchial irritation symptoms, increased sensitization
to certain work-related agents, and decline in lung function in adults, and
aggravation o f acute asthma episodes.
The role o f smoking in asthmatics has received particular interest because of
the relationship between smoking and chronic obstructive pulmonary disease
(COPD). Smoking has adverse health effects on individuals with asthma by
increasing cough, inflammation of the airways, and aggravation o f asthma
symptoms. Active cigarette smoking and asthma interact to increase severity of
symptoms and accelerate decline in lung function (Thomson 2004). A study on the
prevalence of bronchial hyperresponsiveness and asthma among adult smokers found
that personal smoking resulted in bronchial irritation and increased bronchial
responsiveness (Burney 1987).
Although much is known about triggers of asthma, researchers have yet to
completely explain the causes of this respiratory illness. Genetics, allergens, and
environmental factors are known to play a role in asthma development and
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TABLE 1
Role of active smoking and environmental tobacco smoke exposure
on asthma symptoms
7
Active smoking and asthma
• Increased bronchial responsiveness
• Frequent bronchial irritation symptoms
• Increased sensitization to occupational agents
• Aggravation o f acute episodes
• Association with asthma severity
• Risk factor for asthma
• Exaggerated decline in lung functions
• Role in development of fixed airway obstmction and chronic obstructive pulmonary disease
(COPD)
Environmental tobacco smoke exposure and asthma
• Aggravation and occurrence o f increased prevalence of respiratory symptoms
• Bronchial hyper-responsiveness in adults
• Aggravation of asthma symptoms
• Precipitation of acute episodes
• Risk factor for development of asthma (both children and adults)
Source: Jindal et al, 2004
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8
aggravation. Active smoking has been postulated to be a risk factor for asthma and
the development o f chronic obstructive pulmonary disease (COPD). Rasmussen et
al reported that the development o f asthma in asymptomatic teenagers over a 6-yr
period was independently associated with active tobacco smoking (OR, 2.1; 95% Cl
1.2-3.8) (Rasmussen 2000). A retrospective study o f 15,813 randomly sampled
adults found that, in females but not in males, tobacco smokers had an increased
incidence rate (OR, 1.6; 95% Cl 1.1-2.2) compared to never-smokers for adult-onset
asthma (Plaschke 2000).
Chemical compounds in cigarette tobacco may act to trigger asthma
aggravation. Cigarette smoking may modify inflammation that is associated with
asthma. Because asthmatics have sensitive lung airways, smoking cigarettes narrows
these airways leading to increased risk o f asthma symptoms. Active smoking in
young adults is associated with a reduced rate o f lung growth and reduced lung
function (CDC 1994). Adolescent smokers are significantly more likely than
nonsmokers to experience shortness of breath, coughing spells, phlegm production,
wheezing, and diminished physical health. Cigarette smoking during childhood and
adolescence may contribute to increased risk for respiratory symptoms and chronic
obstructive pulmonary disease (CDC 1994).
Another source o f tobacco smoke exposure is from second-hand smoke.
Environmental tobacco smoke is a known source o f indoor air pollutants in homes,
workplaces, and social settings. SHS contains high concentrations o f ammonia,
benzene, nicotine, carbon monoxide, and many carcinogens (Eriksen 1988).
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9
About 78% o f adolescents from a 1993 M assachusetts Tobacco Survey
reported having been exposed to SHS during the preceding week (Biener 1997). An
estimated 33% of non-smokers have reported being exposed to SHS more
increasingly in public spaces (Perez 2004). Non-smokers who are chronically
exposed to SHS have been postulated to have health risks similar to those of light
smokers (Eriksen 1988). Detectable serum cotinine level (2-13ng/ml) in 3,300 non-
smokers showed that 28 percent of 18-30 year-olds were exposed to SHS
(W agenknecht 1993). This study also reported that blacks compared to whites had a
higher self-reported SHS exposure at home (hrs/wk).
Data are accumulating on the role of second-hand smoking on asthma
reported. Exposure to indoor air pollutants have shown significant associations with
airway and allergic responses (Cunningham 1996). SHS has been found to
contribute to the occurrence o f aggravation o f respiratory symptoms, bronchial
responsiveness, precipitation o f acute asthma episodes, and aggravation o f asthma
symptoms leading to increased frequency of attacks and asthma medication use in
children and adults (Al-Dawood 2001; Eisner 2002; Li 2005). One study reported
that SHS has lead to an increase in health care utilization and cost (Janson 2004).
A possible joint effect o f genetic susceptibility to asthma and exposure to
environmental tobacco smoke may exist to increase the risk for the disease.
The presence of parental atopy and environmental tobacco smoke exposure produced
a 2 -fold increase in risk for both bronchial obstruction and asthma in children
(Jaakkola 2001). Exposure to maternal smoking is associated with adverse
respiratory health effects, such as asthma and wheezing (Cook 1999). Maternal and
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10
even grandmatemal smoking during pregnancy was reported to increase the risk of
childhood asthma (Li 2005).
Second-hand smoke may be a risk factor for the development of asthma both
in children and adults. In particular, the association between second-hand smoke and
the occurrence o f respiratory symptoms in children is relatively strong. The effects
on children include pneumonia, bronchitis, increased severity o f attacks among
asthmatics, possible induction o f asthma in asymptomatic individuals, small
reductions in lung function, and upper respiratory tract irritation (Jinot 1996).
Children o f smoking parents have more respiratory infections, more hospitalizations
for bronchitis and pneumonia, and a lower rate of growth in lung function compared
to children of non-smoking parents (Cook 1999).
Effects of SHS exposure on adult asthma have not been as extensively
researched as those in children. Studies in adult populations have provided
inconsistent results. Exposure to SHS has been shown to exacerbate symptoms in
adults with preexisting allergies, chronic lung conditions, and angina (Eriksen 1988).
In non-smoking adults, SHS exposure is associated with eye, nose, and throat
irritation, and wheezing, symptoms o f bronchitis, shortness o f breath, and decreased
lung function. An 8-year longitudinal study o f a Finnish population of never
smokers ages 15-40 to examine the effects of SHS exposure at home and at work did
not find SHS exposure to have any physiologically-relevant effect on the volume of
air exhaled during the first second o f a forced expiratory procedure (FEVi) or the
average flow (or speed) of air coming out of the lung during the middle portion of
the expiration (FEF25-75) (Jaakkola 1995). However, a later paper from the same
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11
study reported evidence of adverse respiratory effects, with cumulative incidence of
respiratory symptoms consistently higher among SHS exposed subjects compared to
the reference group (Jaakkola 1996). Conflicting finding in other studies testing the
effects o f SHS on chronic respiratory symptoms in adults may be due to the fact that
these studies were conducted on selected groups or with pooled data from different
countries (Janson 2001).
One research study working to elucidate the causes of respiratory illnesses in
young adults is the University o f Southern California Children’s Health Study II, a
follow-up phase o f the Children’s Health Study (CHS). The CHS II study was
launched in August 1998 to examine the effects o f chronic exposure to ambient air
pollutants on respiratory health. Dietary and genetic factors were measured to
determine the impact o f these factors on children’s susceptibility to respiratory
problems. Participants completed a health questionnaire, dietary questionnaire (DQ),
and an update sheet providing address and residential history. Buccal cell samples
for DNA from participants were obtained for genotyping to investigate family
history of asthma. The purpose of the present analysis was to investigate the effects
of exposure to tobacco smoke on respiratory symptoms among young adults.
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II. METHODS
1. Study Design and Subject Selection
The Children’s Health Study II (CHS II) offered a unique opportunity to
understand the health effects o f active and passive smoking on the occurrence of
asthma symptoms in young adults. Subjects in the present study were participants in
the larger University o f Southern California Children’s Health Study (CHS). Details
o f the CHS has been described previously (Peters 1999). Briefly, the CHS is a
population-based study that recruited children from public school classrooms from
grades 4, 7, and 10 in 12 communities to examine the determinants o f respiratory
health. Initiated in 1993, the CHS was designed as a ten-year longitudinal
investigation o f the respiratory health o f school-age children in southern California.
Factors of interest were students’ respiratory health, patterns o f physical activity, and
exposure to tobacco smoke and other forms o f air pollution. The study was
conducted in twelve communities across southern and central California: Atascadero,
Santa Maria, Lompoc, Long Beach, Lancaster, Upland, M ira Loma, San Dimas,
Riverside, Lake Gregory, Lake Elsinore, and Alpine. These communities were
selected because they represented a spectrum o f air quality profiles, were roughly
similar in socioeconomic level, and had cooperative school district personnel.
Subjects were recruited in local schools. Recruitment presentations were
made in fourth, seventh and tenth grade classrooms. The goal was to obtain at least
90% class participation. Upon entry, parents of the children completed a baseline
questionnaire that extensively probed their child’s respiratory health history,
exposure to tobacco smoke and other elements, and demographic information. The
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subjects performed yearly lung function tests at school and completed yearly update
questionnaires. To date, over 6000 children have participated in the study.
A subset of the Children’s Health Study, the Children’s Health Study II
(CHS II), is a second follow-up phase o f the CHS. It was conducted between
January 1999 and July 2003 to investigate the respiratory health outcomes in young
adults. The CHS II study included 3,489 subjects who were currently participating
in the Children’s Health Study. Current CHS participants (1,792 female and 1,697
male subjects) completed a dietary questionnaire (DQ) and contributed buccal cells.
Moved or graduated participants completed a health questionnaire, updated personal
information, and a completed residential history, in addition to the DQ and the
buccal cell collection. In the follow up phase, 346 (171 females and 176 males)
declined to participate. We were unable to contact 1,515 (747 female and 767 male)
subjects. O f the 1,628 subjects that participated, 874 were females and 754 were
males. Subjects ranged from 12 to 26 years, and are U.S. residents with a current
address and phone number.
2. Definition of terms
In this analysis, information about personal smoking and second hand smoke
exposure was taken from the CHS II questionnaire. Recruitment for CHS II
participants took place twice a month in groups o f 20. CHS II include subjects who
are 18 years old or older, living on their own, or living with parents. Subjects who
are 17 years old or younger were followed through letters addressed to the parents.
All the CHS participants were mailed a self-administered questionnaire. Trained
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14
interviewers collected information on the questionnaire by telephone interviews for
approximately half o f participants who did not return the questionnaire.
Current congestion or phlegm, current wheeze, and current exercise-induced
wheeze were based on self-reported symptoms in the past 12 months. Current
wheeze was defined as the presence o f wheezing with or without cold, or wheezing
during exercise or play in the previous 12 months. Asthma status was based on self-
report o f a physician diagnosis o f asthma. Respondents were classified as currently
having asthma (current asthma) if they answered the following two questions
affirmatively: “Has a doctor ever said you had asthma?” and “Do you still have
asthma?” Respondents who reported ever being told they had asthma but who no
longer had asthma were classified as formerly having asthma (former asthma).
Respondents who had never been told that they had asthma were classified as never
having had asthma (never asthma).
Personal smoking by participants was defined as a history o f ever smoking
more than 100 cigarettes. Participants were categorized as ever smokers if they
answered yes to “Do you currently smoke cigarettes?” and yes to “Have you smoked
at least 5 packs of cigarettes in your lifetime (Pack=20 cigarettes)?” Ever-smokers
were classified as ex-smokers if they answered no to “Do you currently smoke
cigarettes?” but yes to “Have you smoked at least 5 packs o f cigarettes in your
lifetime (Pack=20 cigarettes)?” Participants who answered no to both o f these
questions were classified as never smokers. Participants were asked to provide
information on the number o f cigarettes smoked each day (< Vi pack or > V 2 pack).
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Using questionnaire items about current household, work, and social smoking
status we collected second-hand smoke exposure information. The following
questions were asked: “Does anyone in your household currently smoke tobacco
while you are at home?”, “Not counting yourself, how many members smoke in the
house?”, “How many hours a day on average do you breath their tobacco smoke?”,
“On average, how smoky is that household area?”, Do you currently breath tobacco
smoke o f others in your workplace?”, On average, how smoky is your work area?”,
“Other than at home or work, do you spend time around people who smoke on a
regular basis?”, and “How many hours a day on average?” .
All demographic data was taken from the CHS II questionnaire. Four age
groups, ages <15 years, 16-18 years, 19-21 years, and >22, were defined to provide
proportionately equal categories. Participant’s race or ethnic background was
defined as being one of the following three groups: non-Hispanic white, Hispanic, or
Other ethnicity. The education level of the participants was grouped into three
categories: up to high school, some college, and college or graduate degree.
Allergies (No/Yes) and current hay fever (No/Yes) were also assessed by self-report.
3. Statistical Methods
In this analysis, the primary analysis is the association between tobacco
smoke and respiratory symptoms in the past 12 months in young adults. Univariate
tests of association between demographic and smoking variables were conducted
using data from all CHS II subjects. Chi-square tests o f associations were first
performed. Unconditional logistic regression models were fitted to assess the
individual effects of active smoke and SHS exposures on the occurrence o f current
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asthma symptoms (yes/no). Respondents were classified as currently having asthma
(current asthma) if they answered yes to two questions: “Has a doctor ever said you
had asthma?” and “Do you still have asthm a?” On the basis o f the study design and
a priori consideration o f potential confounders, models included terms for asthma
status (never, former, current asthma), age (<15 years, 16-18 years, 19-21 years,
>22), gender (M vs. F), ethnicity (non-Hispanic white, Hispanic, other ethnicity),
allergies (No/Yes), and current hay fever (No/Yes). If the estimates of the tobacco
smoke effects changed by at least 10% when a covariate was included in the base
model, the covariate was included in the final model. Stratified analyses were
performed separately for smokers and non-smokers when testing the effects of
second-hand smoking on asthma symptoms. Unconditional logistic regression was
conducted separately by strata defined by asthma status. In addition, unconditional
logistic regression models with appropriate smoking-by-asthma interaction terms
were tested using likelihood ratio was performed (Hosmer 1989). All tests were
two-sided at a 5% significance level. Analyses were conducted using SAS STAT
software (version 9.0, SAS Institute Inc., Cary, NC).
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17
III. RESULTS
We analyzed the data for 874 females and 754 males in the CHS II. The
demographic characteristics, household SHS exposure, and personal smoking status
are shown in Table 2. There were more women (53.7%) than men (46.3%) in the
study population. The distribution of never, former, and current asthma subjects did
not differ by age (p=0.80) or race (p=0.06). There was significant difference in
asthma association by gender (p<0.01). The majority o f the study participants were
non-Hispanic whites (58.2%) followed by Hispanic-white (27.6%). The other race
category (15.3%) included subjects who are African-Americans, Native Americans,
and Asians (Chinese, Japanese, Korean, Filipino, Vietnamese, or East Asian).
Subjects were between 12 and 28 years o f age at the time o f their interview in the
CHS II and their mean age was 19.7 (standard deviation 3.3 years). Over 60 percent
o f participants had completed high school, and 33 percent had some college
education. Subjects with current asthma reported a statistically higher percentage of
having allergies (78%) and hay fever (71%) compared to those who were former and
never asthmatics (p<0.01). SHS exposure at home, work, or social environments did
not differ significantly by asthma status (p-values>0.05). More participants reported
being exposed to household and social SHS than to work SHS. The percent of
current tobacco smokers among (23.5%), former (22.6%), or never asthmatics
(21.6%) were not statistically different (p=0.96). Thus, in this sample current
asthmatics continued to smoke despite having respiratory problems. These
percentages underscore the additive nature of smoking since subjects with current
asthma smoke as much as those who formerly or never had asthma.
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Table 2
Selected characteristics of participants by never, former, and current asthma status,
Children’s Health Study II, 1999-2003
Characteristic
Never
N %
Asthma Status
Former
N %
Current
N %
P-value*
ALL (N=l ,623) 1264 12.3 159 oo
200 12.3
(5 missing)
Gender
Female 686 54.3 67 42.1 118 59.0 <0.01
Male 578 45.7 92 57.9 82 41.0
Race/ethnicity
Non-Hispanic White 727 57.5 93 58.5 113 56.5 0.06
Hispanic white 344 27.2 51 32.1 47 23.5
Other 193 15.3 15 9.4 40 20.0
Age (years)
<15 166 13.1 22 13.8 28 14.0 0.80
16-18 406 32.1 59 37.1 70 35.0
19-21 307 24.3 32 20.1 47 23.5
>22 385 30.5 46 28.9 55 27.5
Education, yr
High school 765 60.5 90 56.6 122 61.0 0.45
Some college 427 33.8 54 34.0 66 33.0
College or graduate 72 5.7 15 9.4 12 6.0
Personal Smoke
Never 868 68.7 109 68.5 133 66.5 0.96
Ex 123 9.7 14
°0
OO
20 10.0
Current 273 21.6 36 22.6 47 23.5
Household ETS
No 865 68.4 104 65.4 126 63.0 0.26
Yes 399 31.6 55 34.6 74 37.0
Work ETS
No 1093 86.6 146 91.8 175 87.5 0.18
Yes 169 13.4 13 8.2 25 12.5
Social ETS
No 731 57.8 95 59.8 111 55.5 0.71
Yes 533 42.2 64 40.2 89 44.5
Allergies
No 833 66.0 85 53.5 44 22.0 <0.01
Yes 429 34.0 74 46.5 156 78.0
Hay Fever
No 758 60.2 92 58.2 58 29.0 <0.01
Yes 500 39.7 66 41.8 142 71.0
* Chi-sq (2)-test of difference in proportions between never, former, and current asthmatics
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19
Active Smoking Patterns
W ithin males and females, there was no significant association between
personal smoking variables and asthma status (Table 3). W e observed a higher
percentage of currently smoking females with current asthma (16%) compared to
currently smoking males with current asthma (10.7%). More females who smoked
> Vi pack/day were currently asthmatic (17.3%) than were males who smoked > X A
pack/day (9.7%). In our study population there were more females (45%) than males
(55%) who are current smokers (p<0.001). Among female participants the
proportion of current smokers (16.2%) with current asthma is not significantly
different than among never smokers (12.9%) or ex-smokers (13.3%) (p=0.82). This
pattern is also observed among male participants where the proportion o f current
asthmatics is similar among never (10.8%) and current (10.7%) smokers. Data seem
to suggest that current asthmatic females tend to smoke >X A pk/day o f cigarettes and
smoke occasionally on some days compared to current asthmatic males who tend to
smoke < l A pk/day o f cigarettes and smoke everyday. Compared to current asthmatic
males in the same age range, about 18 percent o f females who first began smoking
between ages 14-16 years have current asthma.
Personal smoking by participants was not statistically significantly
associated with asthma indicators such as physician-diagnosed asthma, seeing a
doctor or medical practitioner for asthma, visiting an emergency room or staying
overnight in the hospital for asthma, or using medication for asthma in the previous
12 months (Table 4). Comparable percent were observed between ever and never
smokers for asthma indicators assessed.
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20
Table 3
Personal smoking by gender and asthma status,
Children’s Health Study II
Number (% total), n= 1,628
Fem ales
(N=874)
M ales
(N=754)
A sthm a Status A sthm a Status
N ever Form er Current N ever Form er Current
686 (78.8) 67 (7.7) 118(13.5) 578 (76.9) 92 (12.2) 82 (10.9)
N ever smokers
Ever sm okers
X 2 p-value
506 (79.6)
180 (76.6)
0.60
48 (7.5)
19(8.1)
82 (12.9)
3 6 (15.3)
362 (76.4)
2 1 6 (7 7 .7 )
0.78
61 (12.9)
31 (11.1)
51 (10.8)
31 (11.1)
N ever smokers
Ex-sm okers
Current sm okers
X 2 p-value
506 (79.6)
58 (77.3)
122 (76.2)
0.82
48 (7.5)
7 (9.3)
12(7.5)
82 (12.9)
1 0(13.3)
2 6 (1 6 .2 )
362 (76.4)
65 (79.3)
151 (77.0)
0.86
61 (12.9)
7 (8.5)
24 (12.2)
51 (10.8)
10(12.2)
21 (10.7)
N ever & Ex-sm okers
Current sm okers
X 2 p-value
564 (79.3)
122 (76.2)
0.54
55 (7.7)
12(7.5)
9 2 (1 2 .9 )
2 6 (1 6 .2 )
427 (76.8)
151 (77.0)
0.99
6 8 (1 2 .2 )
24 (12.2)
61 (11.0)
21 (10.7)
N ever & Ex-sm okers
Current (<'/2 pk/day)
Current (> 'A pk/day)
X 2 p-value
563 (79.3)
82 (75.9)
40 (76.9)
0.81
55 (7.7)
9 (8.3)
3 (5.8)
92 (1 3 .0 )
17(15.7)
9 (17.3)
427 (76.8)
76 (73.8)
75 (80.6)
0.84
68 (12.2)
15 (14.6)
9 (9.7)
61 (11.0)
12(11.6)
9 (9.7)
N ever sm okers
Some days
Every day
X 2 p-value
552 (79.1)
65 (80.2)
68 (7.8)
0.74
55 (7.9)
4 (4.9)
8 (0.9)
91 (13.0)
12(14.8)
15(1.7)
4 1 4 (7 6 .7 )
73 (78.5)
90 (76.3)
0.66
67 (12.4)
13 (14.0)
12(10.2)
5 9 (10.9)
7 (7.5)
16(13.6)
Current sm okers
Age first started, yr
<13
14-16
17-19
>20
X 2 p-value
18 (72.0)
44 (73.3)
47 (77.0)
13 (93.0)
0.82
2 (8.0)
5 (8.3)
5 (8.2)
0 (0)
5 (20.0)
11 (18.3)
9 (14.7)
1 (7.0)
27 (73.0)
58 (79.4)
53 (73.6)
12 (92.3)
0.82
6 (16.2)
6 (8.2)
11 (15.3)
1 (7.7)
4 (10.8)
9 (12.3)
8 (11.1)
0 (0)
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21
Table 4
Personal smoking pattern by asthma indicators
Number (% total), N= 1,628
Asthma Indicators
Personal Smoke N (% total) MD Asthma
Diagnosis
MD visit in
12 mos
ER visit in
12 mos
Medication
use in 12
mos
Never smokers 1113 (68.4) 243 (21.8) 62 (5.6) 11(1.0) 100 (8.9)
Ever smokers 515 (31.6) 118 (22.9) 29 (5.6) 10(1.9) 51 (9.9)
X 2 p-value 0.63 0.87 0.28 0.83
Never smokers 1113 (68.4) 243 (21.8) 62 (5.6) 11(1.0) 100 (8.9)
Ex-smokers 157 (9.6) 34 (21.7) 11 (7.0) 3(1.9) 16(10.2)
Current smokers 358 (22.0) 84 (23.5) 18(5.0) 7 (2.0) 35 (9.8)
X 2 p-value 0.80 0.73 0.60 0.93
Never & Ex- 1270 (78.0) 277 (21.8) 73 (5.8) 14(1.1) 116(9.1)
Current smokers 358 (22.0) 84 (23.5) 18(5.0) 7 (2.0) 35 (9.8)
X 2 p-value 0.51 0.52 0.41 0.80
Never & Ex-smoker 1270 (78.0) 277 (21.9) 73 (5.8) 14(1.1) 116(9.2)
Current (< Vipk/day) 213 (13.1) 54 (25.3) 13 (6.1) 5 (2.4) 27(12.7)
Current (> Vipk/day) 145 (8.9) 30 (20.7) 5 (3.4) 2(1.4) 8 (5.5)
X p-value 0.47 0.57 0.52 0.21
Non-smokers 1241 (76.3) 273 (22.0) 70 (5.6) 14(1.1) 113 (9.1)
Some days 175 (10.8) 37(21.1) 10(5.7) 3(1.7) 17(9.7)
Every day 210 (12.9) 51 (24.3) 11(5.3) 4(1.9) 21 (10.0)
X 2 p-value
Current smokers
Age first started
0.71 0.88 0.79 0.92
<13 63 (3.9) 17 (27.0) 3 (4.8) 2 (3.2) 7(11.1)
14-16 133 (8.2) 31 (23.3) 7(5.3) 2(1.5) 14(10.5)
17-19 134 (8.2) 34 (25.4) 8 (6.0) 3 (2.2) 13 (9.7)
>20 27 (1.7) 2 (7.4) 0(0) 0 (0) 1 (0.7)
X 2 p-value 0.27 0.58 0.46 0.70
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22
On the other hand, we found that in Table 5 smoking tobacco cigarettes was
highly associated with asthma symptoms such as cough, phlegm, and wheeze (all p-
values <0.001). Compared to never smokers, 17 percent o f smokers reported having
a cough for three months in the previous 12 months, 31 percent had congestion or
coughed up phlegm, 65 percent had wheezing or whistling with a cold, 30 percent
had wheezing or whistling without a cold, and 37 percent had wheezing or whistling
after play or exercise. The association was stronger with increasing numbers o f
cigarettes smoked daily. Smoking tobacco cigarettes daily also showed a
substantially larger effect on respiratory symptoms compared to never smokers or to
smokers who smoked a few days during the week. Research has shown that age at
first starting smoking is associated with asthma symptoms. In the CHS II sample,
early age at initiating smoking was associated with higher prevalence o f asthma
symptoms. Among smokers who started smoking when they were <13 years old,
about 78 percent experienced wheezing or whistling with a cold, and over 50 percent
had wheezing after play or exercise. However, with these unadjusted associations it
is unclear whether age at first starting smoking or the amount o f tobacco smoke per
day was independently associated with these asthma symptoms.
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23
Table 5
Personal smoking pattern by asthma symptoms
Number (% total), N= 1,628
Asthma symptoms
Personal Smoke Cough 3
mos in
last 12
Congestion
or phlegm
Wheezy or
whistling
with cold
Wheezy or
whistling
without cold
Wheezing
after play or
exercise
Never smokers
Ever smokers
X2 p-value
mos
64 (5.8)
88(17.1)
<0.0001
148(13.3)
158 (30.7)
<0.0001
495 (44.5)
337 (65.4)
<0.0001
206 (18.5)
157 (30.5)
<0.0001
311 (28.0)
190 (36.9)
0.0003
Never
Ex-smokers
Current smokers
X2 p-value
64 (5.8)
16(10.2)
72 (20.1)
<0.0001
148(13.3)
37 (23.6)
121 (33.9)
<0.0001
495 (44.5)
101 (64.3)
236 (66.0)
<0.0001
206 (18.5)
35 (22.3)
122 (34.1)
<0.0001
311 (28.0)
50(31.8)
140 (39.1)
0.0004
Never & Ex-
Current smokers
X2 p-value
80 (6.3)
72 (20.1)
<0.0001
185 (14.6)
121 (33.9)
<0.0001
596 (47.0)
236 (65.9)
<0.0001
241 (19.0)
122 (34.1)
<0.0001
361 (28.4)
140 (39.1)
0.0001
Never & Ex-smoker
Current (< ‘ Apk/day)
Current (> ‘ Apk/day)
X2 p-value
80 (6.3)
33 (15.5)
39 (26.9)
<0.0001
185 (14.6)
57 (26.9)
64 (44.1)
<0.0001
594 (46.9)
129 (60.6)
107 (73.8)
<0.0001
241 (19.0)
60 (28.2)
62 (42.8)
<0.0001
361 (28.5)
80 (37.6)
60 (41.4)
0.0005
Never smokers
Some days
Every day
X2 p-value
75 (6.0)
25 (14.3)
52 (24.8)
<0.0001
173 (14.0)
39 (22.4)
94 (44.8)
<0.0001
579 (46.7)
102 (58.3)
151 (71.9)
<0.0001
232 (18.7)
45 (25.7)
86(41.0)
<0.0001
350 (28.2)
62 (35.4)
89 (42.4)
<0.0001
Current smokers
Age first started
<13
14-16
17-19
>20
X2 p-value
21 (33.3)
24(18.0)
21 (15.7)
6 (22.2)
<0.0001
31 (49.2)
47 (35.3)
35 (26.3)
8 (29.6)
<0.0001
49 (77.8)
90 (67.7)
81 (69.4)
15 (55.6)
<0.0001
32 (50.8)
38 (28.6)
46 (34.3)
6 (22.2)
<0.0001
32 (50.8)
52 (39.1)
48 (35.8)
8 (29.6)
0.0003
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24
Second-hand Smoke Exposure
The results o f tests of associations between home SHS exposure and asthma
symptoms in never smokers and ever smokers in the CHS II study are shown in
Table 6A. There were statistically significant associations between home SHS and
asthma symptoms among smokers (p<0.05), but these associations were not apparent
among non-smokers (p>0.05). Over 36 percent o f smokers who were exposed to
home SHS reported having had a cough for 3 months in the previous year, 70 percent
experienced wheezing or whistling with a cold, and 41 percent had wheezing after
play or exercise compared to smokers who were not exposed to home SHS.
Environmental tobacco smoke exposure at work was not statistically associated with
asthma symptoms (Table 6B, all p>0.05).
However, we found statistically significant associations between social SHS
exposure and asthma symptoms in both non-smoking and smoking participants.
Among non-smokers in Table 6C, about 9 percent of study participants exposed to
social SHS reported having a cough for 3 months in the previous year compared to 4
percent in the SHS unexposed (p<0.01), 17 percent o f exposed subjects had
congestion or coughed up phlegm compared to 12 percent o f unexposed subjects
(p=0.01), 50 percent o f exposed subjects to social SHS had wheeze or whistling with
a cold compared to 43 percent o f SHS unexposed subjects (p=0.04), 23 percent of
SHS exposed subjects had wheeze or whistling without a cold compared to 17
percent o f unexposed subjects (p=0.03), and 35 percent if SHS exposed subjects had
wheeze after play or exercise compared to 25 percent o f unexposed subjects
(pO .O l).
Reproduced with permission of the copyright owner. Further reproduction prohibited without permission.
25
Table 6A
Respiratory symptoms in non-smokers and smokers exposed to environmental tobacco
smoke at home, Children’s Health Study II
Home ETS Exposure
Sym ptom s N ever sm okers
N =1113
U nexposed Exposed U nexposed
E ver Smokers
N=515
Exposed
C ough for 3 m os in
previous 12 m os
No
Yes
X 2( l) p-value*
804 (94.4)
48 (5.6)
0.75
244 (93.8)
16 (6.2)
2 1 2 (8 6 .2 )
34 (13.8)
0.06
215 (79.9)
54 (21.1)
Congestion or phlegm
No
Yes
X 2( l) p-value
739 (86.8)
112(13.2)
0.79
225 (86.2)
3 6 (1 3 .8 )
184 (75.1)
61 (24.9)
0.01
172 (63.9)
97 (36.1)
W heeze or w histling w ith cold
No
Yes
X 2( l) p-value
477 (56.0)
374 (43.9)
0.50
140 (53.6)
121 (46.4)
96 (39.0)
150 (61.0)
0.04
82 (30.5)
187 (69.5)
w ithin past wk
w ithin past m onth
w ithin past 12 mos
> 12 mos
X 2(4) p-value
3 5 (4 .1 )
52 (6.1)
2 1 6 (2 5 .3 )
71 (8.3)
0.50
13 (5.0)
22 (8.4)
68 (26.0)
1 6(6.1)
22 (8.9)
23 (9.3)
84 (34.1)
21 (8.5)
0.11
3 8 (1 4 .1 )
3 2 (1 1 .9 )
100 (37.2)
17(6.3)
W heeze or w histling without cold
N o
Yes
X 2( l) p-value
697 (81.8)
155(18.2)
0.62
21 0 (8 0 .5 )
51 (19.5)
179 (72.8)
67 (27.2)
0.13
179 (66.5)
90 (33.5)
w ithin past wk
w ithin past m onth
w ithin past 12 m os
> 12 months
X 2(4) p-value
29 (3.4)
26 (3.1)
79 (9.3)
29 (3.4)
0.36
10(3.8)
14 (5.4)
19(7.3)
11 (4.2)
14(5.7)
9 (3.7)
3 7 (1 5 .0 )
7 (2.9)
0.12
16 (6.0)
25 (9.3)
44 (16.4)
9 (3.4)
W heeze after play or exercise
No
Yes
X 2( l) p-value
623 (73.2) 178 (68.2)
228 (26.8) 83 (31.8)
0.11
167 (67.9)
79 (32.1)
0.03
158 (58.7)
111 (41.3)
w ithin past wk
w ithin past m onth
w ithin past 12 mos
> 12 mos
X 2(4) p-value
3 7 (4 .4 ) 18(6.9)
4 1 (4 .8 ) 17(6.5)
1 09(12.8) 38 (14.6)
4 1 (4 .8 ) 10(3.8)
0.26
13 (5.3)
1 6(6.5)
4 2 (1 7 .1 )
8 (3.3)
0.12
18(6.7)
3 0 (1 1 .2 )
47 (17.5)
16 (6.0)
*Chi-square test of difference in proportions between SHS exposed and unexposed groups
Reproduced with permission of the copyright owner. Further reproduction prohibited without permission.
26
Table 6B
Respiratory symptoms in non-smokers and smokers exposed to environmental tobacco
smoke at work, Children’s Health Study II
W ork ETS Exposure
Sym ptom s N on-sm okers
N=1113
U nexposed Exposed
Sm okers
N=515
U nexposed Exposed
C ough for 3 m os in
previous 12 mos
No
Yes
X 2( l) p-value*
951 (94.4)
56 (5.6)
0.62
97 (93.3)
7 (6.7)
342 (83.4)
6 8 (1 6 .6 )
0.52
84 (80.8)
2 0 (1 9 .2 )
C ongest or phlegm
No
Yes
X 2( l) p-value
873 (86.7)
134(13.3)
0.82
91 (87.5)
12(12.5)
290 (70.7)
120 (29.3)
0.13
65 (63.1)
38 (36.9)
W heeze or w histling w ith cold
No
Yes
X 2( l) p-value
559 (55.5)
448 (44.5)
0.89
57 (54.8)
47 (45.2)
141 (34.4)
269 (65.6)
0.97
36 (34.6)
68 (65.4)
w ithin past wk
w ithin past m onth
w ithin past 12 mos
> 12 mos
X 2(4) p-value
45 (4.5)
66 (6.6)
254 (25.2)
81 (8.0)
0.76
3 (2.9)
8 (7.7)
30 (28.8)
6 (5.8)
45 (11.0)
41 (10.0)
152 (37.1)
31 (7.6)
0.60
15 (14.4)
14(13.5)
32 (30.8)
7 (6.7)
W heeze or whistling w/o cold
No
Yes
X 2( l ) p-value
820 (81.3)
188(18.7)
0.74
86 (82.7)
18(17.3)
291 (71.0)
1 19(29.0)
0.20
67 (64.4)
37 (35.6)
w ithin past wk
w ithin past m onth
w ithin past 12 mos
> 1 2 months
X 2(4) p-value
33 (3.3)
37 (3.7)
91 (9.0)
3 8 (3 .8 )
0.50
6 (5.8)
3 (2.9)
7 (6.7)
2 (1 .9 )
19 (4.6)
28 (6.8)
6 2 (1 5 .1 )
13 (3.2)
0.16
11 (10.6)
5 (4.8)
19(18.3)
3 (2.9)
W heeze after play or exercise
No
Yes
X 2( l) p-value
727 (72.2)
280 (27.8)
0.67
73 (70.2)
31 (29.8)
257 (62.7)
153 (37.3)
0.61
68 (65.4)
36 (34.6)
w ithin past wk
w ithin past m onth
w ithin past 12 mos
> 12 mos
X 2(4) p-value
50 (5.0)
52 (5.2)
132(13.1)
46 (4.6)
0.99
5 (4.8)
6 (5 .8 )
15 (14.4)
5 (4.8)
22 (5.4)
39 (9.5)
73 (17.8)
19(4.6)
0.53
9 (8.6)
6 (5.8)
16(15.4)
5 (4.8)
*Chi-square test of difference in proportions between SHS exposed and unexposed groups
Reproduced with permission of the copyright owner. Further reproduction prohibited without permission.
Table 6C
Respiratory symptoms in non-smokers and smokers exposed to social environmental
tobacco, Children’s Health Study II
Social ETS Exposure
Sym ptoms
Cough for 3 mos in last year
No
Yes
X 2( l) p-value*
N on-sm okers
N = 1 113
U nexposed Exposed
763 (95.5) 285 (91.0)
36 (4.5) 28 (8.9)
<0.01
Sm okers
N=515
U nexposed
129 (92.8)
10 (7.2)
<0.01
Exposed
298 (79.3)
78 (20.7)
C ongest or phlegm
No
Yes
X 2( l ) p-value
705 (88.3)
93 (11.6)
0.01
259 (82.5)
55 (17.5)
111 (79.9)
28 (20.1)
<0.01
245 (65.3)
130 (34.7)
W heeze or w histling w ith cold
No
Yes
X 2( l) p-value
458 (57.4)
340 (42.6)
0.04
159 (50.6)
155 (49.4)
5 8 (4 1 .7 )
81 (58.3)
0.04
120 (31.9)
256 (68.1)
w ithin past wk
w ithin past m onth
within past 12 m os
> 12 mos
X 2(4) p-value
30 (3.7)
51 (6.4)
189 (23.6)
68 (8.5)
0.04
18(5.7)
23 (7.3)
95 (30.2)
19(6.0)
7 (5.0)
12(8.6)
51 (36.7)
11 (7.9)
0.03
53 (14.1)
43 (11.4)
133 (35.4)
27 (7.2)
W heeze or w histling w/o cold
No
Yes
X 2( l) p-value
664 (83.1)
135 (16.9)
0.03
243 (77.4)
71 (22.6)
107 (77.0)
32 (23.0)
0.03
251 (66.8)
125 (33.2)
w ithin past week
w ithin past m onth
w ithin past 12 mos
> 12 months
X2(4) p-value
27 (3.4)
22 (2.7)
65 (8.1)
30 (3.7)
0.08
12 (3.8)
18 (5.7)
33 (10.5)
10(3.2)
3 (2.2)
4 (2.9)
23 (16.5)
6 (4.3)
0.04
27 (7.2)
30 (8.0)
58(15.4)
10 (2.7)
W heeze after play or exercise
No
Yes
X 2( l) p-value
596 (74.7)
202 (25.3)
<0.01
205 (65.3)
109 (34.7)
103 (74.1)
36 (25.9)
<0.01
222 (59.0)
154(41.0)
w ithin past week
w ithin past m onth
w ithin past 12 mos
> 12 mos
X 2(4) p-value
36 (4.5)
33 (4.1)
95 (11.9)
38 (4.8)
<0.01
19(6.1)
25 (8.0)
52(16.6)
13(4.1)
5 (3.6)
4 (2.9)
23 (16.5)
4 (2.9)
<0.01
26 (6.9)
42 (1 1 .2 )
66(17.5)
20 (5.3)
*Chi-square test of difference in proportions between SHS exposed and unexposed groups
Reproduced with permission of the copyright owner. Further reproduction prohibited without permission.
28
Social SHS exposure among smokers showed similar statistically significant
associations with asthma symptoms (all p<0.05). Our results suggest that the
association between second-hand smoke and asthma symptoms is more evident in
social SHS exposure than in either home or work exposure.
The proportions o f non-smokers exposed to home SHS and social SHS were
higher than work SHS (Table 7). This exposure pattern was again more evident for
smokers where the percentage o f home SHS and social SHS exposure was much
larger than work SHS exposure. Smokers (52%) were twice as likely as non-
smokers (23%) to be exposed to home SHS. Current smokers (61 %) were more
likely to report being exposed to home SHS compared to ex-smokers (31%) and non-
smokers (23%), and nearly 15 percent o f smokers were exposed to 2 or more
household smokers at home compared to only 5 percent of non-smokers (p<0.01;
data not shown). In the workplace, 20 percent o f smokers reported being exposed to
second-hand tobacco smoke while only 9 percent of non-smokers were exposed. We
found that 73 percent o f smokers compared to 28 percent o f non-smokers reported
being exposed to SHS in social environments. The SHS exposure patterns by
smoking status were not statistically significant different between females and males
(Table 7). Both females and males were similarly exposed to SHS at home, work, or
social environments.
About 17 percent of non-smoking and 22 percent o f smoking subjects
reported being exposed less than 1 hr a day to smokers at places other than at home
or work. Male smokers (7%) were more likely to report spending more than 3 hrs
around other smokers in the workplace compared to female smokers (3.4%).
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29
Table 7
Percentage of non-smokers and smokers exposed to second-hand smoke
Number (% total), N=l,628
Non-smokers fN==1113) Smokers (N=515)
Females Males Females Males
Total (%) N (%) N (%) Total (%) N (%) N (%)
Home ETS
No 852 (76.5) 488 (76.5) 364 (76.6) 246 (47.8) 112(47.5) 134 (48.0)
Yes 261 (23.5) 150 (23.5) 111 (23.4) 269 (52.2) 124 (52.5) 145 (52.0)
X2 p-value* 0.96 0.90
Work ETS
No 1008 (90.6) 581 (91.2) 427 (89.9) 410(79.6) 199 (84.7) 211 (75.6)
Yes 104 (9.4) 56 (8.8) 48 (10.1) 104 (20.4) 36(15.3) 68 (24.4)
X2 p-value 0.46 0.01
Social ETS
No 799 (71.8) 465 (72.9) 334 (70.3) 139 (27.0) 68 (28.8) 71 (25.5)
Yes 314(28.2) 173 (27.1) 141 (29.7) 376 (73.0) 168 (71.2) 208 (74.5)
X2 p-value 0.35 0.39
Home ETS
< lh r 45 (4.1) 20 (3.2) 25 (5.3) 24 (4.8) 10 (4.4) 14(5.1)
1-3 hrs 26 (2.4) 15 (2.4) 11 (2.4) 39 (7.8) 15 (6.6) 24 (8.8)
>3 hrs 36 (3.3) 19(3.0) 17 (3.6) 50 (10.0) 27(11.9) 23 (8.5)
X2 p-value 0.31 0.50
Work ETS
< lh r 68 (6.1) 38 (6.0) 30 (6.3) 52(10.1) 20 (8.5) 32(11.5)
1-3 hrs 22 (2.0) 11(1.7) 11 (2.3) 24 (4.7) 8 (3.4) 16 (5.7)
>3 hrs 14(1.3) 7 (1.1) 7 (1.5) 28 (5.5) 8 (3.4) 20 (7.2)
X2 p-value 0.82 0.06
Social ETS
< lhr 191 (17.2) 110(17.2) 81 (17.0) 112(21.8) 55 (23.3) 57 (20.4)
1-3 hrs 84 (7.6) 40 (6.3) 44 (9.3) 119(23.1) 52 (22.0) 67 (24.0)
>3 hrs 39 (3.5) 23 (3.6) 16 (3.4) 145 (28.2) 61 (25.8) 84 (30.1)
X2 p-value 0.32 0.56
Smoky at Home
A little 80 (7.3) 37 (5.9) 43 (9.2) 77(15.4) 34(15.0) 43 (15.8)
Fairly-very 26 (2.4) 17 (2.7) 9 (1.9) 36 (7.2) 18 (7.9) 18 (6.6)
X2 p-value 0.09 0.84
Smoky at Work
A little 81 (7.3) 44 (6.9) 37 (7.8) 79(15.4) 25 (10.6) 54(19.3)
Fairly-very 22 (2.0) 11(1.7) 11 (2.3) 24 (4.7) 11(4.7) 13 (4.7)
X2 p-value 0.65 0.02
*Chi-square test for gender-by SHS association
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30
More smokers reported smoky household (7.2% vs 2.4%) and work environments
(4.6% vs 1.9%) than non-smokers (p<0.001; data not shown). Over 15 percent of
smokers reported that their home and work environment were a little bit smoky
compared to only 7 percent o f non-smokers. Again smokers were more likely to be
living and working in environments that were fairly to very smoky compared to non-
smokers (p<0.01).
There was no statistically significant difference in SHS exposure patterns for
non-smokers by asthma status (Table 8, all p>0.05). SHS exposure at home, work,
or social settings was similar for subjects who were never, former, or current
asthmatics. Less than 10 percent o f non-smokers reported exposure to work SHS
compared to 23 percent home and 28 percent social SHS (Table 8).
Analyses o f SHS exposure patterns by gender also did not reveal statistically
significant differences among non-smoking subjects who were never, former, or
current asthmatics (Table 9, all p>0.05). Current asthmatic females on average were
somewhat more likely to be exposed to environmental tobacco smoke in the
workplace or in social environments than current asthmatic males. In females, a
larger percentage o f participants with current asthma compared to those with former
asthma reported breathing between 1-3 hrs/day tobacco smoke at home. But this
difference in proportions was not observed in males where instead more former
asthmatics reported breathing between 1-3 hrs/day tobacco smoke at home compared
to current asthmatics. Among those participants reporting having spent more than 3
hrs/day on average with smokers in social settings, 22 percent were non-smoking
asthmatic females and 33 percent were non-smoking asthmatic males.
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31
Table 8
Percentage of non-smokers exposed to second-hand smoke at home, work, or social
environments stratified by asthma status, Children’s Health Study II
Number (% total), N = l,l 13
A s th m a S ta tu s
ETS exposure Never (N=868) Former (N=109) Current (N=133)
Home
No
Yes
X2 p-value 0.34
N (%)
670 (77.2)
198 (22.8)
N (%)
84 (77.1)
25 (22.9)
N (%)
95 (71.4)
38 (28.6)
Work
No
Yes
X2 p-value 0.33
782 (90.2)
85 (9.8)
103 (94.5)
6 (5.5)
121 (91.0)
12 (9.0)
Social
No
Yes
X2 p-value 0.83
621 (71.5)
247 (28.5)
81 (74.3)
28 (25.7)
96 (72.2)
37 (27.8)
Daily ETS, hrs
Home
<1 hr
1-3 hrs
>3 hrs
X2 p-value 0.41
29 (3.4)
20 (2.3)
29 (3.4)
6 (5.5)
3 (2.7)
3 (2.7)
10(7.7)
3 (2.3)
4(3.1)
Work
<1 hr
1-3 hrs
>3 hrs
X2 p-value 0.35
52 (6.0)
21 (2.4)
12(1.4)
5 (4.6)
1 (0.9)
0(0)
10(7.5)
0(0)
2(1.5)
Social
<1 hr
1-3 hrs
>3 hrs
X2 p-value 0.09
157(18.1)
66 (7.6)
24 (2.8)
14(12.8)
10(9.2)
4(3.7)
19(14.3)
8 (6.0)
10(7.5)
Smoky at Home
A little
Fairly-very
X2 p-value 0.73
58 (6.8)
20 (2.3)
9 (8.3)
3 (2.7)
13 (10.1)
3 (2.3)
Smoky at Work
A little
Fairly-very
X2 p-value 0.47
64 (7.4)
20 (2.3)
5 (4.6)
1 (0.9)
11 (8.3)
1 (0.7)
Reproduced with permission of the copyright owner. Further reproduction prohibited without permission.
Table 9
Second-hand smoke exposure in non-smoking females and males
by asthma status, Children’s Health Study II
32
ETS N (%)
Home
No
Yes
X2 p-value
Work
No
Yes
X2 p-value
Social
No
Yes
X2 p-value
Daily ETS
Home
<1 hr
1-3 hrs
>3 hrs
X2 p-value
Work
<1 hr
1-3 hrs
>3 hrs
X2 p-value
Social
<1 hr
1-3 hrs
>3 hrs
X2 p-value
Smoky Home
A little
Fairly-very
X2 p-value
Work
A little
Fairly-very
X2 p-value
Never
(N=506)
Females
Asthma
Former
(N=48)
36 (75.0)
12 (25.0)
45 (93.7)
3 (6.2)
39(81.2)
9 (18.7)
1 (2 . 1)
1 (2 .1)
2 (4.2)
2 (4.2)
1 (2 . 1)
0 (0)
6(12.5)
2 (4.2)
1 (2 . 1)
3 (6.2)
1 (2 . 1)
3 (6.2)
0 (0)
Current
(N=82)
56 (68.3)
26 (31.7)
74 (90.2)
8 (9.8)
61 (74.4)
21 (25.6)
7 (8.9)
2 (2.5)
2 (2.5)
7 (8.5)
0 (0)
1 ( 1.2)
12(14.6)
4 (4.9)
5 (6.1)
9(11.4)
2 (2.5)
7 (8.5)
1 ( 1.2)
Never
(N=362)
276 (76.2)
86 (23.8)
0.92
321 (88.7)
41 (11.3)
0.26
257 (71.0)
105 (29.0)
0.90
17(4.8)
8 (2 .2)
14(3.9)
0.89
24 (6.6)
11 (3.0)
6 (1.7)
0.54
66(18.2)
32 (8.8)
7(1.9)
0.07
33 (9.3)
6(1.7)
0.93
31 (8.6)
10(2.9)
0.44
Males
Asthma
Former
(N=61)
48 (78.7)
13 (21.3)
58 (95.1)
3 (4.9)
42 (68.8)
19(31.1)
5 (8.2)
2 (3.2)
1 (1.6)
3 (4.9)
0 (0)
0 (0)
8(13.1)
8 (13.1)
3 (4.9)
6 (9.8)
2(3.3)
2 (3.3)
1 ( 1.6 )
Current
(N=51)
39 (76.5)
12(23.5)
47 (92.2)
4 (7.8)
35 (68.6)
16(31.4)
3 (6.0)
1 (2 .0)
2 (4.0)
3 (5.9)
0 (0)
1 (2 .0)
7(13.7)
4 (7.8)
5 (9.8)
4 (8.0)
1 (2.0)
4 (7.8)
0 (0)
394 (77.9)
1 1 2 (22.1)
0.16
461 (91.3)
44 (8.7)
0.79
364 (71.9)
142 (28.1)
0.36
12 (2.4)
12 (2.4)
15 (3.0)
0.14
28(5.5)
10 (2.0)
6 (1 .2 )
0.73
91 (18.0)
34 (6.7)
17(3.4)
0.65
25 (5.0)
14(2.8)
0.28
33 (6.5)
1 0 (2 .0)
0.80
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33
More non-smoking female asthmatics than former asthmatics were likely to be in
smoky home and work environments.
There was no significant association between SHS exposure patterns o f non-
smokers and asthma indicators shown in Table 10. Among non-smoking participants
exposed to household smokers, 25 percent had been diagnosed with asthma by a
physician, 32 percent had visited a doctor or health care provider in the last 12
months for their asthma, 45 percent had visited the emergency room or stayed in the
hospital for their asthma, and 32 percent had used medications for their asthma in the
previous year. Higher proportion o f participants who visited the doctor for their
asthma, seen in the ER for their asthma in the previous 12 months, and used asthma
medication use were exposed to household compared to work SHS. Non-smokers
reporting >3 hrs per day exposure in social settings had a higher percent o f subjects
with a physician diagnosis o f asthma (27%) compared to work exposure (8%).
Our findings suggested that both the home and social environments were
important sources o f SHS exposure for non-smokers who have asthma compared to
the work environment. About 32 percent o f on-smoking subjects who saw a doctor
or medical practitioner for their asthma in the previous year were exposed to SHS at
home and 21 percent were exposed in social setting compared to only 7 percent
exposure in the workplace (Table 10). About 3 to 6 percent non-smoking subjects
who had used medication (inhalers, pills, etc.) for their asthma were exposed to >3
hrs a day on average to SHS at home (3%), work (2%), or social setting (6%).
Reproduced with permission of the copyright owner. Further reproduction prohibited without permission.
Table 10
ETS exposure patterns in non-smokers by asthma indicators
34
ETS N(%) MD Asthma
Asthma Indicators
MD visit in ER visit in Medications
Diagnosis Previous 12 mos Previous 12 mos Previous 12 mos
Home N=243 N=62 N =11 N=100
No 180 (21.1) 42 (4.9) 6 (0.7) 68 (8.0)
Yes 63 (24.1) 20 (7.7) 5(1.9) 32(12.3)
X2 p-value 0.30 0.24 0.18 0.10
Work
No 224 (22.2) 58(5.8) 10(1.0) 90 (8.9)
Yes 19(18.3) 4 (3.8)
1 (1-0)
10(9.6)
X2 p-value 0.35 0.59 0.64 0.40
Social
No 178 (22.3) 49 (6.1) 8(1.0) 72 (9.0)
Yes 65 (20.7) 13 (4.2) 3(1.0) 28 (9.0)
X2 p-value 0.57 0.44 0.87 0.79
Daily ETS
Home
<1 hr 16 (35.6) 5(11.1) 1 (2.2)
10(22.2)
1-3 hrs 6(23.1) 1 (3.9) 1 (3.8) 1 (3.9)
>3 hrs 7 (19.4) 4(11.1) 1 (2.8) 3 (8.3)
X2 p-value 0.15 0.12 0.13 0.06
Work
<1 hr 16(23.5) 3 (4.4) 1(1.5) 10(14.7)
1-3 hrs 1 (4.5) 0(0) 0(0 ) 0(0)
>3 hrs 2(14.3) 1 (7.1) 0(0 ) 0(0)
X2 p-value 0.21 0.49 0.58 0.18
Social
<1 hr 33 (17.3) 7 (3.7) 2(1-0) 15 (7.9)
1-3 hrs 18 (21.4) 3 (3.6)
1 (1-2)
7 (8.3)
>3 hrs 14 (35.9) 3 (7.9) 0(0 ) 6(15.8)
X2 p-value 0.07 0.18 0.20 0.30
Smoky at home
A little 22 (27.5) 6(7.5)
1(1.2)
10(12.5)
Fairly-very 6(23.1) 3(11.5) 1 (3.8) 3 (11.5)
X2 p-value 0.44 0.38 0.38 0.68
Smoky at work
A little 17(21.0) 3 (3.7)
1 (1-2)
9(11.1)
Fairly-very 2(9.1) 1 (4.5) 0(0) 1 (4.5)
X2 p-value 0.33 0.36 0.68 0.51
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35
In Table 11 we found that compared to unexposed participants those exposed
to social SHS reported statistically significantly higher percentage of coughing for 3
months in previous year (9% vs.4.5%), congestion or phlegm (17.5% vs. 11.7%),
wheeze or whistling including times with a cold (49.4% vs.42.6%), wheeze or
whistling including times without a cold (22.6% vs. 16.9%), and wheeze after play or
exercise (34.7% vs. 25.3%). There was significant difference in the proportions of
participants exposed to social SHS for <1 hr, 1-3 hrs, and >3hrs. Exposure to social
second-hand tobacco smoke anywhere between one to three hours was more
common among participants reporting symptoms of cough for 3 months during the
last 12 months (15.5%), wheeze including times when they did have a cold (56%),
and wheezing after play or exercise (39%). A similar pattern for the primary
outcomes assessed was not observed for home SHS or work SHS exposure.
Analyses showed non-significant effects o f exposure to home or work environment
(all p-values >0.05).
We did not find statistically significant differences in the pattern o f second
hand smoke exposure in the home between participants with and without physician-
diagnosed asthma (Table 12). About 21 percent of unexposed at home reported
having been diagnosed by a physician for asthma compared to 24 percent among
those who reported living with household smokers (p=0.11). Among both non
smoking and smoking participants, exposure to home tobacco smoke did not vary by
physician-diagnosed asthma status (non-smokers, p=0.30; smokers, p=0.26). Similar
associations exposure to second-hand tobacco smoke in the workplace and social
environments were seen (all p>0.05). However, statistically significant finding were
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36
Table 11
Second hand smoke exposure pattern in non-smokers by asthma symptoms
Asthma symptoms
ETS N (%) Cough for 3
months in last
12 mos
Congestion
or phlegm
Wheezy or
whistling with
cold
Wheezy or
whistling
without cold
Wheezing
after play or
exercise
Home Exposure
No 48 (5.6) 112(13.2) 374(43.9) 155 (18.2) 228 (26.8)
Yes 16(6.1) 36(13.8) 121 (46.4) 51 (19.5) 83 (31.8)
X2 p-value 0.76 0.79 0.49 0.62 0.12
Work Exposure
No 56 (5.6) 134(13.3) 448 (44.5) 188 (18.7) 280 (27.8)
Yes 7 (6.7) 13 (12.5) 47 (45.2) 18(17.3) 31 (29.8)
X2 p-value 0.62 0.82 0.89 0.74 0.67
Social Exposure
No 36 (4.5) 93 (11.7) 340 (42.6) 135(16.9) 202 (25.3)
Yes 28 (9.0) 55(17.5) 155(49.4) 71 (22.6) 109 (34.7)
X2 p-value <0.01 0.01 0.04 0.03 <0.01
Daily ETS
Home Exposure
<1 hr 4 (8.9) 8(17.8) 23 (51.1) 11 (24.4) 18(40.0)
1-3 hrs 0(0) 4(15.4) 11 (42.3) 4(15.4) 8 (30.8)
>3 hrs 3 (8.6) 4(11.1) 25 (69.4) 9 (25.0) 11 (30.6)
X2 p-value 0.40 0.79 0.02 0.50 0.29
Work Exposure
<1 hr 4 (5.9) 9(13.2) 31 (45.6) 13 (19.1) 20 (29.4)
1-3 hrs 2(9.1) 3 (13.6) 9 (40.9) 2(9.1) 6 (27.3)
>3 hrs 1(7.1)
1 (7-1)
7 (50.0) 3 (21.4) 5 (35.7)
X2 p-value 0.92 0.92 0.96 0.70 0.92
Social Exposure
<1 hr 13 (6.8) 31 (16.2) 84 (44.0) 25 (22.3) 65 (34.0)
1-3 hrs 13 (15.5) 15 (17.9) 47 (55.9) 41 (34.4) 33 (39.3)
>3 hrs 2(5.3) 9(23.1) 24 (61.5) 59 (26.1) 11 (28.2)
X2 p-value <0.01 0.05 0.02 0.06 0.01
Smoky at Home
A little 5 (6.3) 12(15.0) 37 (46.2) 16 (20.0) 26 (32.5)
Fairly-very 2 (8.0) 4(15.4) 21 (80.8) 8 (30.8) 10(38.5)
X2 p-value 0.87 0.86 <0.01 0.24 0.29
Smoky at Work
A little 6 (7.4) 9(11.1) 35 (43.2) 18 (22.2) 24 (29.6)
Fairly-very 1 (4.5) 4(18.2) 11 (50.0) 0(0) 7(31.8)
X2 p-value 0.79 0.67 0.85 0.06 0.87
Reproduced with permission of the copyright owner. Further reproduction prohibited without permission.
37
Table 12
Percentage of non-smokers and smokers by physician-diagnosed asthma
exposed to second-hand smoke
Number (% total), N=l,628
Non-smokers (N =1113) Smokers (N=515)
Physician-diagnosed Asthma
No Yes
Physician-diagnosed Asthma
No Yes
Home ETS
No 672 (78.9) 189 (21.1) 195 (79.3) 51 (20.7)
Yes 198 (75.9) 63 (24.1) 202 (75.1) 67 (24.9)
X2 p-value 0.30 0.26
Work ETS
No 784 (77.8) 224 (22.2) 312(78.8) 98 (23.9)
Yes 85 (81.7) 19(18.3) 84 (80.8) 20(19.2)
X2 p-value 0.35 0.31
Social ETS
No 621 (77.7) 178 (22.3) 110(79.1) 29 (20.9)
Yes 249 (79.3) 65 (20.7) 287 (76.3) 89 (23.7)
X2 p-value 0.57 0.50
Home ETS
< lhr 29 (64.4) 16(35.6) 17(70.8) 7 (29.2)
1-3 hrs 20 (76.9) 6(23.1) 33 (84.6) 6(15.4)
>3 hrs 29 (80.6) 7(19.4) 38 (76.0) 12 (24.0)
X2 p-value 0.15 0.60
Work ETS
< lhr 52 (76.5) 16(23.5) 40 (76.9) 12(23.1)
1-3 hrs 21 (95.4) 1 (4.5) 21 (87.5) 3 (12.5)
>3 hrs 12 (85.7) 2(14.3) 23 (82.1) 5 (17.9)
X2 p-value 0.21 0.55
Social ETS
< lh r 158 (82.7) 33 (17.3) 96 (85.7) 16(14.3)
1-3 hrs 66 (78.6) 18(21.4) 84 (70.6) 35 (29.4)
>3 hrs 25 (64.1) 14(35.9) 107 (73.8) 38 (26.2)
X2 p-value 0.07 0.03
Smoky at Home
A little 58 (72.5) 22 (27.5) 66 (85.7) 11 (14.3)
Fairly-very 20 (76.9) 6(23.1) 22 (61.1) 14(38.9)
X2 p-value 0.44 0.01
Smoky at Work
A little 64 (79.0) 17(21.0) 63 (79.7) 16(20.2)
Fairly-very 20 (90.9) 2(91) 20 (83.3) 4(16.7)
X2 p-value 0.33
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38
observed for social exposure to SHS. Among smokers, participants without
physician-diagnosed were not significantly more exposed to social SHS compared to
those who had asthma diagnosed by a physician (p=0.57). About 21 percent of non
smoking asthmatics reported being exposed to social SHS from 1 to 3 hrs/day while
almost 36 percent had more than 3 hrs/day (p=0.07).
Personal Smoking and Asthma Symptoms
A multivariable model was developed to investigate the association of
tobacco smoke and current asthma symptoms. Potential determinants o f asthma
symptoms such as asthma status, age, race/ethnicity, gender, education, allergies, hay
fever, and personal smoking history were considered. The independent variables
found to be statistically significant predictors o f asthma symptoms in univariate
models were included as variables in the multivariable model.
Table 13 displays the results o f analyses of the relationship between active
smoking and asthma symptoms. Analyses were conducted separately by physician-
diagnosed asthma status. The table displays odds ratios and 95% confidence
intervals for the association o f personal smoking with current asthma symptoms
including congestion or phlegm, wheezing or whistling with a cold, wheezing or
whistling without a cold, and wheezing after play or exercise. We found a greater
association of smoking with current asthma symptoms in participants without
physician-diagnosed asthma than in subjects with clinical diagnosis of asthma.
Results showed higher odds ratios in non-asthmatics compared to asthmatics for the
primary symptom outcomes evaluated. Among non-asthmatics, ever smokers were
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Table 13
Effects of active smoking on asthma symptoms
in the past 12 months among CHS II participants
Adjusted Odds Ratios, and 95% Confidence Intervals (95% Cl)*
Congestion or Phlegm Wheeze with Cold Wheeze without Cold Wheeze after exercise
Active Smoking
N=l,628
MD Asthma diagnosis MD Asthma diagnosis MD Asthma diagnosis MD Asthma diagnosis
No Yes No Yes No Yes No Yes
Never smoker 1.0 1.0 1.0 1.0 1.0 1.0 1.0 1.0
Ever smoker 3.6 (2.6-5.0) 2.0(1.1-3.2) 2.7 (2.1-3.5) 1.7 (0.9-3.2) 2.7 (1.9-3.9) 1.6 (0.9-2.6) 1.9 (1.4-2.5) 1.4 (0.8-2.3)
p-interaction 0.01 0.07 0.04 0.05
Never smoker 1.0 1.0 1.0 1.0 1.0 1.0 1.0 1.0
Ex-smoker 2.4(1.5-4.0) 1.2 (0.5-2.9) 2.6 (1.7-3.9) 1.2 (0.4-3.3) 1.2 (0.7-2.3) 1.5 (0.7-3.5) 1.3 (0.8-2.2) 1.5 (0.7-3.7)
Current smoker 4.2 (3.0-6.0) 2.3 (1.3-4.1) 2.7 (2.0-3.6) 2.0 (0.9-4.2) 3.6 (2.5-5.2) 1.6 (0.9-2.8) 2.2 (1.6-3.0) 1.4 (0.8-2.4)
p-interaction 0.03 0.13 0.04 0.11
Never and Ex-smoker 1.0 1.0 1.0 1.0 1.0 1.0 1.0 1.0
Current smoker 3.6 (2.6-5.0) 2.2(1.3-4.0) 2.4(1.8-3.2) 2.0 (0.9-4.1) 3.4 (2.4-4.9) 1.5 (0.9-2.6) 2.1 (1.5-2.8) 1.3 (0.1-2.2)
p-interaction 0.05 0.40 0.01 0.04
Packs per day
No current smoke 1.0 1.0 1.0 1. 0 1.0 1.0 1.0 1.0
< 'A pack 2.4(1.6-3.7) 1.7 (0.9-3.4) 1.7 (1.2-2.4) 2.0 (0.9-5.0) 2.4 (1.5-3.8) 1.2 (0.6-2.2) 1.9(1.3-2.7) 1.1 (0.6-2.1)
> Zi pack 6.0 (3.9-9.3) 3.6 (1.5-8.2) 4.0 (2.6-6.3) 1.7 (0.5-5.5) 5.3 (3.3-8.5) 2.5 (1.0-6.1) 2.4 (1.5-3.7) 1.6 (0.7-4.1)
p-interaction 0.19 0.32 0.09 0.14
p-trend <0.01 0.01 <0.01 0.12 <0.01 0.04 <0.01 0.29
*Adjusted for allergies (Yes vs. No), current hay fever (Yes vs. No), age (<15, 16-18, 19-21, >22), race (Non-Hisp White, Hispanic White, Other),
sex (M vs F)
co
40
3.6 times more likely to have congestion or phlegm com pared to non-smokers. The
association appeared stronger for current smokers (OR=4.2; 95% Cl, 3.0-6.0). For
non-asthmatic smokers, the odds ratios for congestion or phlegm were 2.4 (1.6-3.7)
for smoking < Vi packs per day and 6.0 (3.9-9.3) for those smoking > Vi packs per
day. Asthmatic smokers were 2.0 times more likely to have congestion or phlegm
compared to non-smokers. Asthmatic ex-smokers had a lower risk o f congestion or
phlegm (OR=1.2; 95% Cl, 0.5 to 2.9) than current smokers (OR=2.3; 95% Cl, 1.3 to
4.1). Smoking more cigarettes per day increased the risk for congestion or phlegm.
The odds ratio for < Vi packs per day was 1.7 (0.9-3.4) and for > Vi packs per day is
3.6 ( 1 . 5 - 8.2). There was evidence o f an increasing trend in symptom prevalence for
congestion or phlegm with increasing cigarettes smoked per day for both non
asthmatics and asthmatics ( p t r e n d < 0 . 0 1 ) . Significant interactions between smoking
and physician diagnosed asthma status were observed for asthma outcomes such as
congestion or phlegm and wheezing with a cold ( p i n t e r a c t i o n < 0 . 0 5 ) .
Similar results for wheezing including times with a cold were obtained. The
effects o f smoking did not differ by physician-diagnosed asthma status. Among non
asthmatic smokers, the association o f active smoking was statistically significant
(OR, 2.7; 95% Cl, 2.1 to 3.5) whereas in asthmatics the association did not reach
statistical significance (OR=1.7; 95% Cl, 0.9 to 3.2). W ith increasing Vi pack of
cigarettes smoked, there was no evidence o f an increasing trend in risk for wheezing
with a cold in asthmatics (p=0.12), but there was a statistically significant trend for
non-asthmatics (p<0.01).
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41
Tobacco smoking had a greater effect on asthma symptoms such as wheezing
including times without a cold and wheezing after play or exercise in non-asthmatic
smokers than in asthmatic smokers. The associations with personal smoking differed
in regard to physician-diagnosed asthma status (p<0.05). The odds ratio for
wheezing without a cold in current smokers who did not have physician-diagnosed
asthma was 3.6 (2.5-5.2), whereas the odds ratio for current smokers who did have
physician-diagnosed asthma was 1.6 (0.9-2.8). There was a statistically significant
trend in risk for wheezing without a cold for both asthmatic and non-asthmatic
smokers per increase in cigarettes smoked (p<0.05). Results for wheezing after play
or exercise were similar to those observed for the other current asthma symptoms.
The association of smoking was again seen to be stronger in non-asthmatic smokers
compared to asthmatic smokers and showed an increasing dose response with respect
to increasing cigarette smoked.
Second-hand Smoking and Asthma Symptoms
W e investigated the association o f exposure to SHS at home, at work, and in
social environments on current asthma symptoms such as congestion or phlegm,
wheeze including times with a cold, wheeze including times without a cold, and
wheezing after play or exercise. Although smokers tended to show higher odds
ratios than to non-smokers, there were no significant interactions by smoking status
for SHS exposure (all pinteraction >0.05). W e analyzed these associations separately in
smokers and non-smokers, by current and ex-smoking status, and by the number of
packs smoked daily.
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42
Household SHS Exposure
Among non-smokers, exposure to any household SHS was not significantly
associated w ith any o f the primary asthma outcomes o f interest (Table 14). Having
one household smoker (OR=1.8; 95% Cl 1.0 to 3.2) and having two or more
household smokers (O R =l .4; 95% Cl 0.7 to 2.6) was only w eakly and non-
significantly associated w ith wheezing with a cold. Duration o f exposure (<1 hr, 1-3
hrs, or >3 hrs) to SHS at home did not show a dose response relationship with
asthma symptoms except with wheezing with a cold where an upward trend was
observed (p=0.01). In particular, there was an elevated risk (OR=3.4; 95% Cl 1.6 to
7.3) for >3 hrs exposure among non-smokers. Household smokiness did not produce
a statistically significant trend (p>0.05). Among smokers exposure to SHS produced
overall higher risk for having the asthma symptoms compared among non-smokers.
Work SHS Exposure
We investigated the effects o f second-hand smoke on current asthma
symptoms in non-smoking and smoking working adults. In the CHS II study 54
percent o f females (N=497) and 46 percent o f males (N =431) were currently
employed. Among working females, 23% were between the ages o f 16-18, about
34% were between ages 19-21, and 42 % were 22 years and older. More than 59% of
these working females reported having current asthma. Among working males, 25%
were between the ages o f 16-18, 27% were between ages 19-21, and 46% were 22
years and older. Over 40% o f working males had current asthma.
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Table 14
Effects of tobacco smoke exposure at home on asthma symptoms in the past 12 months among CHS II Participants
Adjusted Odds Ratios, and 95% Confidence Intervals (95% Cl)*
Congestion or Phlegm W heeze w ith Cold W heeze w ithout Cold W heeze after exercise
H om e SH S E xposure
N =1628 N on-sm okers Sm okers N on-sm okers Sm okers N on-sm okers Sm okers N on-sm okers Sm okers
H ousehold Sm okers
No 1.0 1.0 1.0 1.0 1.0 1.0 1.0 1.0
Yes 1.0 (0.7-1.5) 1.7(1.1-2.5) 1.0 (0.8-1.4) 1.4 (1.0-2.1) 0.9 (0.6-1.3) 1.4 (0.9-2.1) 1.1 (0.8-1.6) 1.5 (1.0-2.3)
Location
N o sm okers at hom e 1.0 1.0 1.0 1.0 1.0 1.0 1.0 1.0
O utside only 0.9 (0.5-1.7) 1.7(1.1-2.8) 0.8 (0.5-1.3) 1.3 (0.8-2.1) 0.7 (0.4-1.4) 1.1 (0.6-1.9) 1.2 (0.7-2.0) 1.5 (0.9-2.6)
Inside only 1.2 (0.6-2.3) 1.5 (0.8-3.0) 1.1 (0.7-1.9) 1.2 (0.6-2.2) 0.8 (0.4-1.7) 1.0 (0.5-2.1) 0.7 (0.4-1.4) 1.3 (0.7-2.5)
Both 1.1 (0.6-2.0) 1.7(1.0-2.8) 1.3 (0.8-2.2) 1.8 (1.0-3.1) 1.1 (0.6-2.2) 1.9 (1.1-3.4) 1.4 (0.8-2.5) 1.6 (0.9-2.8)
N um ber household
sm okers
N o household sm okers 1.0 1.0 1.0 1.0 1.0 1.0 1.0 1.0
1 m em ber 0.8 (0.4-1.9) 1.3 (0.7-2.7) 1.8(1.0-3.2) 2 .2 (1 .0 -5 .0 ) 1.5 (0.7-3.2) 1.4 (0.7-3.1) 1.5 (0.8-2.8) 1.2 (0.6-2.4)
2 or m ore m em bers 1.5 (0.7-3.2) 1.7(1.0-2.9) 1.4 (0.7-2.6) 1.4 (0.8-2.4) 0.7 (0.3-2.7) 1.9(1.1-3.4) 1.0 (0.5-2.0) 1.6 (0.9-2.8)
p - t r e n d 0.51 0.04 0.09 0.15 0.84 0.02 0.65 0.09
H ours exposed per day
N o household sm okers 1.0 1.0 1.0 1.0 1.0 1.0 1.0 1.0
< 1 hr 1.2 (0.6-2.7) 1.1 (0.5-2.8) 1.1 (0.6-2.2) 1.1 (0.4-2.7) 0.9 (0.4-2.3) 0.9 (0.3-2.7) 1.3 (0.6-2.7) 0.7 (0 .3 -2 .1)
1-3 hrs 1.2 (0.5-3.6) 0.9 (0.5-1.9) 1.0 (0.4-2.2) 1.5 (0.7-3.0) 0.7 (0.2-2.4) 1.6 (0.8-3.4) 1.1 (0.4-2.9) 1.5 (0.8-3.2)
>3 hrs 0.9 (0.3-2.5) 2.7 (1.5-5.0) 3.4 (1.6-7.3) 2.1 (1.0-4.3) 1.7 (0.7-4.3) 2 .4 (1 .2 -4 .6 ) 1.2 (0.5-2.9) 1.8 (0.9-3.5)
p - t r e n d 0.95 0.01 0.01 0.03 0.50 0.01 0.49 0.05
Sm oky at H om e
No household sm okers 1.0 1.0 1.0 1.0 1.0 1.0 1.0 1.0
A little 1.1 (0.6-2.1) 1.4 (0.8-2.4) 1.0 (0.6-1.7) 1.3 (0.8-2.3) 0.9 (0.4-1.8) 1.5 (0.9-2.8) 1.1 (0.6-1.9) 1.1 (0.6-2.0)
Fairly-very 1.3 (0.4-3.9) 2 .0 (1 .0 -4 .0 ) 5 .9 (2 .2 -1 6 .3 ) 2 .6 (1 .0 -6 .5 ) 2.3 (0.9-6.0) 2.2 (1.0-4.8) 1.8 (0.7-4.4) 2.5 (1.2-5.3)
p - t r e n d 0.62 0.03 0.01 0.03 0.30 0.02 0.30 0.04
*M odels are adjusted for asthm a status (never, form er, current), age (<15, 16-18, 19-21, >22), race (N on-H ispanic W hite, H ispanic W hite, Other), sex (M vs F)
it*.
co
44
We found that exposure to second-hand smoke at work was not associated with any
o f the asthma symptoms in non-smokers or smokers (Table 15). Duration of
exposure times (<1 hr, 1-3 hrs, or >3 hrs) to SHS at work also did not show a dose
response relationship with any o f the asthma symptoms investigated (p>0.05). Our
results suggested that second-hand tobacco smoke exposure in the workplace is not a
risk factor for having current asthma symptoms in young adults.
Social SHS Exposure
We found that association between exposure to social second-hand smoke
and having current asthma symptoms were similar for both non-smokers and
smokers (Table 16). Among non-smokers, there were statistically significant
associations between social SHS and congestion or phlegm (OR, 1.8; 95% Cl 1.2 to
2.6), wheezing including times without a cold (OR, 1.8; 95% Cl 1.3 to 2.4), and
wheezing after play or exercise (OR, 2.0; 95% Cl 1.4 to 2.8). Duration o f exposure
to second-hand smoke in social settings other than at home or work showed a dose
response relationship with the asthma symptoms for congestion or phlegm and for
wheezing with a cold but not for wheezing without a cold or wheezing after exercise.
The odds o f having congestion or phlegm for someone exposed to < 1 hr to social
SHS was 1.7 times the odds o f having congestion or phlegm in someone with no
social SHS exposure. Exposure to 1-3 hrs o f second-hand smoke in a social setting
was significantly associated with wheezing including times with a cold (non-
smokers: OR, 1.9; 95% Cl 1.2 to 3.0; smokers: OR, 1.3; 95% Cl 0.8-2.2) and without
a cold (non-smokers: OR, 2.5; 95% Cl 1.3 to 4.5; smokers: OR, 1.5; 95% Cl 0.8-
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Table 15
Effects of Tobacco Smoke Exposure at Work on Asthma Symptoms
in the past 12 months among Currently Employed CHS II Participants
Adjusted Odds Ratios, and 95% Confidence Intervals (95% Cl)*
Currently Congestion or Phlegm Wheeze with Cold Wheeze without Cold Wheeze after exercise
employed
N=928
Non-smokers Smokers Non-smokers Smokers Non-smokers Smokers Non-smokers Smokers
ETS at Work
No 1.0 1.0 1.0 1.0 1.0 1.0 1.0 1.0
Yes 0.9 (0.5-1.9) 1.3 (0.8-2.3) 0.9 (0.6-1.5) 1.2 (0.7-2.0) 1.1 (0.6-2.2) 1.4 (0.8-2.5) 1.4 (0.8-2.5) 0.9 (0.5-1.6)
Hours exposed
No ETS at work 1.0 1.0 1.0 1.0 1.0 1.0 1.0 1.0
< 1 hr per day 0.9 (0.4-2.0) 0.9 (0.4-1.8) 0.9 (0.5-1.6) 1.1 (0.5-2.1) 1.0 (0.5-2.3) 1.2 (0.6-2.5) 1.1 (0.6-2.3) 0.7 (0.4-1.5)
1-3 hrs per day 1.4 (0.4-5.2) 2.5 (1.0-6.4) 1.0 (0.4-2.6) 1.9 (0.7-5.1) 1.0 (0.3-4.7) 2.2 (0.8-5.8) 2.4 (0.9-6.7) 1.1 (0.4-2.9)
>3 hrs per day 0.6 (0.1-4.6) 1.7 (0.7-4.0) 0.9 (0.3-3.2) 0.9 (0.4-2.3) 1.7 (0.4-8.2) 1.2 (0.5-3.2) 1.7 (0.4-7.0) 1.0 (0.4-2.7)
p-trend 0.83 0.09 0.84 0.63 0.59 0.27 0.12 0.98
Smokiness
No ETS at work 1.0 1.0 1.0 1.0 1.0 1.0 1.0 1.0
A little 0.8 (0.4-1.8) 1.1 (0.6-1.9) 0.8 (0.5-1.4) 1.1 (0.6-1.9) 1.4 (0.7-2.9) 1.5 (0.8-2.7) 1.2 (0.6-2.3 0.9 (0.5-1.7)
Fairly-very 1.5 (0.4-5.9) 3.4 (1.3-9.2) 1.1 (0.4-3.0) 2.0 (0.7-6.0)
—
1.3 (0.4-3.9) 3.1 (1.0-9.2) 0.9 (0.3-2.7)
p-trend 0.90 0.06 0.76 0.28 0.75 0.29 0.08 0.75
*Models are adjusted for asthma status (never, former, current), age (<15, 16-18, 19-21, >22), race (Non-Hispanic White, Hispanic White, Others),
sex (M vs F)
un
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Table 16
Effects of social tobacco smoke exposure on asthma symptoms
in the past 12 months among CHS II participants
Adjusted Odds Ratios, and 95% Confidence Intervals (95% Cl)*
Social SHS
Exposure
N=1628
Congestion or Phlegm Wheeze with Cold Wheeze without Cold Wheeze after exercise
Social ETS
Non-smokers Smokers Non-smokers Smokers Non-smokers Smokers Non-smokers Smokers
No 1.0 1.0 1.0 1.0 1.0 1.0 1.0 1.0
Yes 1.8 (1.2-2.6) 2.0 (1.2-3.2) 1.4 (1.0-1.8) 1.5 (1.0-2.2) 1.8 (1.3-2.4) 1.7(1.1-2.8) 2.0(1.4-2.8) 2.0 (1.2-3.2)
Hours exposed
No social ETS 1.0 1.0 1.0 1.0 1.0 1.0 1.0 1.0
< 1 hr per day 1.7(1.1-2.6) 1.4 (0.8-2.6) 1.2 (0.8-1.7) 1.2 (0.7-2.0) 1.6 (1.0-2.6) 1.1 (0.6-2.2) 2.1 (1.4-3.2) 2.2(1.2-4.0)
1-3 hrs per day 1.9 (1.0-3.5) 2.0(1.1-3.5) 1.9 (1.2-3.0) 1.3 (0.8-2.2) 2.5 (1.3-4.5) 1.5 (0.8-2.9) 2.6 (1.6-4.5) 2.0 (1.1-3.5)
>3 hrs per day 2.2(1.0-5.0) 2.5 (1.5-4.3) 1.5 (0.7-3.1) 2.0 (1.2-3.4) 1.3 (0.5-3.2) 2.4 (1.4-4.4) 0.6 (0.2-1.6) 1.9(1.1-3.3)
p-trend 0.01 0.01 0.02 0.01 0.06 0.01 0.08 0.06
*Models are adjusted for asthma status (never, former, current), age (<15, 16-18, 19-21, >22), race (Non-Hispanic White, Hispanic White, Others),
sex (M vs F)
4 *
C T l
2.9). Compared to no exposure to social SHS, exposure to either <1 hr or 1-3 hrs of
social SHS produced more than a 2-fold increase in risk for wheezing after play or
exercise for both non-smokers and smokers.
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48
IV. DISCUSSION
A substantial body o f literature has documented the effects o f tobacco smoke
exposure on childhood respiratory morbidity, yet few studies have investigated the
associations between active and passive tobacco smoke exposure and asthma-related
symptoms in young adults. Our findings on the effects o f both active and passive
tobacco smoke on respiratory symptoms are consistent with a growing body o f
evidence that supports the independent effect o f active cigarette smoking (Troisi
1995; Strunk 1998; Toren 1999; Plaschke 2000; Rasmussen 2000; Thomson 2004)
and environmental tobacco smoke exposure (White 1980; W iedemann 1986; Eriksen
1988; Cook 1997; Strunk 1998; Cook 1999; Eisner 2002; Kurz 2004; Cantani 2005)
on the occurrence and exacerbation o f asthma symptoms.
Our study found an association between personal smoking and aggravation of
current asthma symptoms. The associations with active smoking varied by
physician-diagnosed asthma status. Our results showed higher odds ratios for
smokers without a physician-diagnosed o f asthma compared to smokers with a
physician-diagnosis of asthma on a range o f asthma and wheezing outcomes. This
is consistent with a general belief that tobacco is a risk factor for asthma among
smokers since asthmatics are believed to be non-smokers. This may be due to the
fact that physicians generally advise individuals with asthma not to smoke.
Adolescents with asthma would therefore be expected to smoke less than adolescents
without asthma. Our finding is consistent with a study that found that young adults
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49
with asthma smoke less than those without asthma (Brook 1993). Higher prevalence
of smoking among asthmatics increased the risk for having asthma symptoms.
Current smokers were at higher risk for having asthma symptoms than ex
smokers and never smokers. The odds of having these asthma symptoms increased
with the number o f cigarettes smoked. These differences were not accounted for by
allergy status, current hay fever, age, race, or gender.
The effects o f SHS exposure in asthmatic adults is less clear compared to the
effects in asthmatic children because of conflicting results reported from different
studies. Some case-control studies found no association between SHS exposure and
asthma in adults (Hu 1997; Kronqvist 1999; Janson 2001). Significant associations
o f physician-diagnosed ‘ever asthm a’ and ‘current asthm a’ were reported for both
maternal and paternal smoking in 1,469 young adults (Hu 1997). Another study
examined the relationship between asthma and SHS exposure in adults using
inhalation challenge tests. Shephard et al reported that after 2 hours of SHS
exposure some asthmatic adults experienced shortness of breath and wheezing or
tightness of the chest. A similar study demonstrated a significant linear decrease in
pulmonary function among asthmatic subjects exposed to SHS for an hour whereas
no change was found in control subjects (Dahms 1981). Evidence from a
population-based Swedish study suggested a possible association between childhood
SHS exposure and respiratory disease later in adulthood (Larsson 2001).
Exposure to second-hand smoke has been shown to increase the risk of
respiratory infections, visits to physicians and emergency rooms, and hospital
admissions (Cook 1999). Our results supports these findings; we found that
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50
exposure to social SHS is associated with increased risk for cough for 3 months in
the previous year (p<0.01), having congestion or phlegm (p=0.01), and wheeze or
whistling in the chest including times with a cold (p=0.04), without a cold (p=0.03),
or after play or exercise (p<0.01). Exposure at home to more than 3 hours o f SHS
produced a statistically significant association (p=0.02). Exposure to any SHS for
more than 1 hr/day resulted in significant association with all respiratory outcomes
investigated. Participants without physician-diagnosed asthma were more likely to
be exposed to social SHS than to those who had physician-diagnosed asthma.
W e found a 1.5-fold increase in risk of asthma-related symptoms among young
adults exposed to two or more household smokers. These findings are consistent
with the fact that SHS is a mixture o f respiratory toxins that has been shown to
increase the risk and severity o f respiratory infections, airway obstruction, and
respiratory inflammation (Janson 2001). In our study sample, we did not find that
home or work SHS to have a strong relationship with respiratory symptoms possibly
because of the age group o f our cohort and the environment in which they spend
considerable time. Further research will elucidate the mechanisms for SHS effects
providing clarity on the respiratory risk from SHS exposure on young adults with
asthma.
Despite increasing evidence to suggest that SHS causes respiratory illness in
adults (White 1991; Tredaniel 1994; Jaakkola 1995), there are few papers which
support a strong association between workplace exposure to SHS and current asthma
symptoms in adults. For example, White et al reported in 1991 that workplace SHS
was more strongly related to respiratory symptoms than household exposure.
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51
However, our study we observed that social SHS exposure was more associated with
current asthma symptoms than home and workplace exposure. The difference in our
results and theirs may be explained by the fact that workplace exposure has
dramatically declined after California legislature passed a new smoking law in 1994
that prohibited smoking o f tobacco products in all enclosed places o f employment.
Statistics from 1996 from California Department o f Health Services showed that 90
percent of California adults employed indoors were protected from second-hand
smoke exposure. This may explain why we observed no statistically significant
association with workplace second-hand tobacco smoke exposure and current asthma
symptoms.
We observed an independent association o f social SHS exposure among non-
smokers with the risk o f asthma symptoms. This is consistent with studies that found
that young adults occasionally smoke at parties, on weekends, and with friends. The
Center for Disease Control and Prevention (CDC) reported in 1996 that 34.8 percent
o f the nation’s high school students had smoked in the previous month. The
association increased with increasing hours of exposure to social SHS exposure.
Substantial evidence from various studies points to SHS exposure as being causally
associated with asthma exacerbations (Strachan 1998). However, this relationship
was not as statistically significant for home or work SHS exposure in young adults of
this study population but was statistically more significant for social SHS exposure
as evidenced by the high odds ratios obtained for both non-smokers and smokers.
This result is useful in spotlighting the adverse effects o f social SHS exposure on
asthma symptoms among young adults.
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52
Some limitations from our study may influence the interpretation of our
results. Findings from the CHS II study are based on cross-sectional data that were
collected at cohort entry and may be subject to selection bias, information bias, and
problems with temporality inherent in cross-sectional studies. Exposure to tobacco
smoke was assessed using questionnaire responses and was not independently
validated by objective measurements. However, exposure estimates based on
questionnaire responses have been validated (Coultas 1990).
Recalling the use o f tobacco smoke is unlikely to produce misclassification of
exposure since respondents were asked to provide information on current tobacco
use. Although differential misclassification of exposure to environmental tobacco
smoke does occur in cross-sectional studies, it is improbable that bias from this type
o f misclassification would have explained our findings since study participants were
not informed o f study objectives and questionnaires were carefully designed so not
to introduce such bias. Exposure to environmental tobacco smoke was assessed
using questionnaire responses about household, work, and social sources and was not
validated by objective measurements such as cotinine levels. Again, the validity of
exposure estimates based on questionnaire responses has been found to provide
reasonably valid estimates o f actual tobacco smoke exposure because self-reported
smoking and serum cotinine concentrations have been found to be highly correlated
(Stick 1996).
One reason for the conflicting results observed in various studies could be
attributed to the lack of agreement for the epidemiological definition of asthma. In
most questionnaire-based surveys, self-reported asthma is commonly used to define
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53
asthma. This might underestimate the true population prevalence according to one
study (Toraen 1993). Several epidemiological studies relied instead on the presence
of new onset o f wheezing as a more sensitive indicator o f asthma in adults
(Leuenberger 1994; Jaakkola 1996). In our study, asthma status was ascertained by
self-report of physician-diagnosed asthma using self-completed questionnaires. The
diagnosis of asthma by a physician depends on several factors such as access and use
of medical care and on physician diagnostic practices (Burr 1975; Dodge 1980).
In studies o f asthma in children such as the Children’s Health Study, parents
often are asked to complete questionnaires about their child’s asthma symptoms.
W ith longitudinal studies o f asthma, children reach an age when they complete the
questionnaire themselves as in the case o f the Children’s Health Study II. Hedman et
al found that the agreement between parental and self-completed questionnaires
about asthma in teenagers was generally very high (Hedman 2005). These authors
reported that the change in methodology from parental to self-completed
questionnaire did not affect the results in the study. The highest results in both
absolute agreement and kappa-value were reached by the questions on diagnosis of
asthma (98.9% and 0.93), use of asthma medicines (95.5% and 0.78), and whether
the child ever had asthma (97.2% and 0.86) (Hedman 2005). Based on these
findings, it is unlikely that our results were biased due to misclassification of the
outcome variables.
Conclusion
Our study found that active smoking and passive exposure to second-hand
smoke increased the risk for having current asthma symptoms. Compared to non
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54
smokers, the effect o f SHS on asthma symptoms is much worse among smokers
because smokers have larger and more direct exposure to toxins found in cigarettes.
The adverse effect o f SHS is stronger for current smokers compared to either ex
smokers or non-smokers. The effect shows an increasing dose-response relationship
(p-trend<0.01). Among non-smokers, exposure to social SHS resulted in a
significantly higher proportion o f participants with current asthma symptoms
compared to no social SHS exposure. There was a statistically significant
association with current asthma symptoms and being exposed to social SHS. An
increasing dose-response relationship was also seen with increasing duration of
exposure (p-trend <0.05).
As a result, there appears to be a need for tobacco cessation and control
programs to reduce tobacco smoke exposure in young adults. Better interventions
will serve to reduce the impact o f tobacco exposure in susceptible individuals.
Preventive actions could encompass smoking cessation, smoking prevention, pulling
tobacco advertisements aimed at young adults, increasing taxation on tobacco, and
adopting stringent nonsmoking policies in schools and public places. Particularly,
preventing social SHS exposure in non-smokers may significantly protect the
respiratory health o f young adults.
Reproduced with permission of the copyright owner. Further reproduction prohibited without permission.
55
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Asset Metadata

Creator Neuman, Gracie R. (author)

Core Title The effects of tobacco smoke on respiratory symptoms among young adults in the Children's Health Study II

Degree Master of Science

Degree Program Applied Biostatistics and Epidemiology

Publisher University of Southern California (original), University of Southern California. Libraries (digital)

Tag Health Sciences, Epidemiology,health sciences, public health,OAI-PMH Harvest

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Permanent Link (DOI) https://doi.org/10.25549/usctheses-c16-53637

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