Active Smoking, Environmental Tobacco Smoke and
Bronchitic Symptoms among Adolescents in Taiwan: a
prospective cohort study
Jer-Min Chena,b, Bing-Fang Hwangc, Yang-Ching Chena,b, Yungling Leo Leea,d
a
Institute of Epidemiology and Preventive Medicine, College of Public Health,
National Taiwan University, Taipei, Taiwan
b
Department of Family Medicine, Taipei City Hospital, Taipei, Taiwan
c
Department of Occupational Safety and Health, College of Public Health, China
Medical University, Taichung, Taiwan
d
Institute of Biomedical Sciences, Academia Sinica, Taipei, Taiwan
Jer-Min Chen, MD; e-mail: airobo33@gmail.com
Bing-Fang Hwang, PhD; e-mail: bfhwang@mail.cmu.edu.tw
Yang-Ching Chen, MD; e-mail: melisa26@gmail.com
Correspondence to:
Yungling Leo Lee, MD, PhD
Institute of Epidemiology and Preventive Medicine, College of Public Health,
National Taiwan University, No.17, Xuzhou Road, 516R, Taipei 100, Taiwan;
Tel:
+886-2-3366-8016
Fax:
+886-2-2392-0456
E-mail:
leolee@ntu.edu.tw
Page 1
Key words: adolescents, smoking, tobacco smoke pollution, asthma, bronchitis
Word counts: abstract: 194; main text: 2,877
Page 2
ABSTRACT
Objective
The study investigates the association between active smoking, exposure to
environmental tobacco smoke (ETS) and the development of bronchitis and bronchitic
symptoms among adolescents.
Methods
A prospective cohort study was conducted with 4,134 adolescents aged 12-14 from
the Taiwan Children Health Study in 14 communities in Taiwan since 2007. Parents
or guardians completed written questionnaires regarding demographic information,
household ETS and respiratory symptoms at baseline. The adolescents themselves
completed identical questionnaires on respiratory outcomes in the 2009 survey.
Associations between active smoking, exposure to ETS and the 2-year incidence of
respiratory outcomes were analyzed by multiple Poisson regression models, taking
overdispersion into account.
Results
Active smoking was associated with an increased risk of developing chronic cough
and chronic phlegm. We found significant dose-response associations between the
duration of smoking, the numbers of cigarettes and the onset of bronchitic symptoms.
Exposure to ETS was a significant risk factor for the development of chronic cough.
Among asthmatic adolescents, exposure to ETS was associated with an additional risk
for the onset of chronic phlegm.
Conclusion
This study demonstrates that active smoking and exposure to ETS are associated with
higher risks for developing bronchitic symptoms among adolescents.
Page 3
Introduction
Smoking and exposure to environmental tobacco smoke (ETS) are serious and
growing public health problems worldwide (CDC, 2006). The increasing prevalence of
regular smoking up to 10% among youths was found in some countries (Warren et al.,
2009), and more than 50% of children in Taiwan live with smokers (Wen et al., 2005).
Both active smoking and exposure to ETS are linked to a multitude of respiratory
diseases and symptoms (Strachan and Cook, 1998; Withers et al., 1998). These illnesses
include chronic bronchitis and associated symptoms can have a marked influence on the
performance of children in school (Liberty et al., 2010) and are associated with poorer
exercise capacity, incident airflow limitation and increased mortality risk later in life
(Martinez et al., 2014; Guerra et al., 2009).
Most previous studies designed to determine the effects of smoking on asthma and
other bronchitic symptoms have been conducted among older participants with a long
history of smoking (Forey et al., 2011). The evidence for an association between smoking
and bronchitis among adolescents has been limited, and most of these studies are
cross-sectional in design (Forey et al., 2011); thus, causal inferences have been difficult
to establish. Some studies have concluded that active smoking increases the risk of
developing bronchitis and bronchitic symptoms (Karunanayake et al., 2011; Withers et al.,
1998), while others have found weak associations (Eagan et al., 2002; Frank et al., 2007).
Previous studies have also suggested that ETS is a substantial risk factor for the incidence
of respiratory diseases. However, Stoddard and Miller reported that younger children may
be more affected by ETS than older children (Stoddard and Miller, 1995) and
longitudinal data on adolescents has remained scarce. Many adolescents with a history of
asthma or wheezing disorders have taken up smoking and have a continued exposure to
ETS. Numerous studies have shown that tobacco smoke can cause decrements in lung
function and can increase the frequency of asthma attacks (Cook and Strachan, 1999).
Trédaniel et al. has reported that there was no sufficient evidence to infer a causal
relationship between ETS exposure and respiratory symptoms among adults with asthma
(Trédaniel et al., 1994).
In the present study, we used a longitudinal study with a nationally representative
sample to investigate the relationship between cigarette smoking and ETS exposure and
Page 4
the incidence of bronchitis and bronchitic symptoms. We also assessed the risk of
developing respiratory symptoms associated with ETS exposure in asthmatic participants.
Page 5
Materials and Methods
Study design
The Taiwan Children Health Study (TCHS) is a prospective study of the
determinants of children’s respiratory health. The details of the design and methods of
this study have been described in previous publications (Tsai et al., 2010). In brief, a total
4,134 seventh-grade children were enrolled into the study from public schools in 14
communities covering different parts of Taiwan in 2007. Parents or guardians of each
participant completed a self-administered questionnaire that provided demographic
information, respiratory health conditions, tobacco smoke exposure and household
environmental characteristics at cohort entry. The cohort participants were followed up
on during the school visit in 2009 with an updated questionnaire that contained identical
questions concerning respiratory outcomes. The study was approved by the Institutional
Review Board at the National Taiwan University Hospital and complied with the
principles outlined in the Declaration of Helsinki.
Definition of respiratory health outcomes
Questions regarding respiratory diseases were modified from the questionnaire
used in the Children’s Health Study in Southern California (McConnell et al., 1999). The
respiratory health outcomes of interest were bronchitis and bronchitic symptoms.
Participants who were disease-free at baseline and who reported a “yes” answer to the
question: “Has a physician ever diagnosed you as having bronchitis?” on the follow-up
questionnaire were classified as having new-onset bronchitis. Chronic cough was defined
on the follow-up questionnaire by the questions: “During the past 12 months, have you
had a cough first thing in the morning that lasted for as much as 3 months in a row?” or
“During the past 12 months, have you had a cough at other times lasting at least 3 months
in a row?”. The presence of new-onset chronic phlegm was determined by a “yes” answer
to the following question: “Other than with colds, did you usually seem congested in the
chest or bring up phlegm?”.
We also assessed the association between active smoking, ETS and new-onset
bronchitic symptoms among asthmatic adolescents. An asthmatic participant was defined
as someone who reported a positive answer to the questions: “Has a physician ever
Page 6
diagnosed your child as having asthma?” or “During the past 12 months, has this child
had a wheezing or whistling sound in the chest?” on the baseline questionnaire.
Personal smoking history and environmental tobacco smoke exposures
Information on the personal smoking behavior of each adolescent was obtained by
a confidential interview that was conducted by experienced field staff during the baseline
school visits. Personal smoking was defined as a history of smoking more than 100
cigarettes during the participant’s lifetime. The report of weekly smoking amount was
classified as nonsmokers, infrequent (1 to 6 cigarettes) and regular smokers (7 or more
cigarettes). The amount of yearly smoking was also categorized into 3 groups: none,
1-299 cigarettes and 300 or more cigarettes.
We obtained information about the smoking status of each participant’s parents,
adult household members and regular visitors. Current ETS exposure was defined as
someone who was exposed to smoke continuously prior to the date of baseline interview.
We categorized the intensity of ETS exposure into 2 groups: the amount of daily smoking
exposure and the percentage of lifetime exposed to ETS. The amount of daily ETS
exposure was categorized as none, 1-10 cigarettes and 11 or more cigarettes and the
percentage of ETS exposure was determined by 20% of a person’s lifetime.
Statistical analysis
The incidence of new cases of respiratory outcomes was calculated using the
number of new cases divided by the person-years at risk over a 2-year period of
follow-up. The relationships between active smoking and ETS and the incidence of
respiratory diseases were analyzed by Poisson regression models. To account for
overdispersion of incidence rates in Poisson models, the scale parameter was adjusted
using Pearson chi-square statistics (Le, 2003). Based on the study design and our a priori
considerations of potential confounders, we introduced age, gender, parental history of
asthma, parental history of atopy, maternal smoking during pregnancy and community
into all of our models. If the estimates of smoking effects changed by more than 10%
when a covariate was introduced into the base models, then the covariate was included in
the final models. Participants with missing covariate information were included in the
Page 7
models using missing indicators. To investigate the effects on the relationship between
active smoking and ETS and new-onset respiratory diseases among asthmatic adolescents,
we conducted a stratified analysis using likelihood ratio tests to examine the interactive
effects between tobacco smoke and personal history with or without asthma/wheeze. All
analyses were carried out using SAS software version 9.1 (SAS institute, Cary, NC,
USA).
Page 8
Results
A total of 3,909 participants completed the follow-up questionnaire, with a
follow-up rate of 94.6%. The loss to follow-up of participants was mostly due to families
moving out of the school district area based on interviews with the school staff and on
telephone interviews with the families of participants. Because of baseline respiratory
conditions and missing or “not known” answers to questions on three bronchitic
outcomes, 3664 bronchitis-free, 3680 chronic cough-free and 3704 chronic phlegm-free
participants were recruited at cohort entry. Table 1 shows the distribution of selected
characteristics among participants in the separate respiratory health outcomes. At cohort
entry, the proportion of gender was almost equal (51.1% female and 48.9% male) and the
majority of children were 12 years of age. Exposure to maternal smoking in pregnancy
was reported for 3.7% of the cohort. More than 40% of the children were exposed to ETS
and 5.6% of the children had an active smoking habit.
The number of new cases of bronchitis, chronic cough and chronic phlegm were 59,
278 and 363 after a 2-year follow-up. The incidence of bronchitis was 8.1/1000
person-years, the incidence of chronic cough was 37.9/1000 person-years and the
incidence of chronic phlegm was 49.2/1000 person-years for chronic phlegm.
The rate ratio (RR) and the 95% confidence interval (CI) for bronchitis and
bronchitic symptoms in relation to active smoking are shown in Table 2. We found that
active smoking was positively associated with new-onset chronic cough (RR = 1.72; 95%
CI: 1.11 to 2.64) and chronic phlegm (RR = 1.64; 95% CI: 1.11 to 2.43). We observed a
dose-response relationship between duration, weekly and yearly amounts of smoking and
the incidence of bronchitic symptoms. Children who smoked cigarettes for more than one
year had an increased risk for developing chronic cough (RR = 2.07, 95%: CI: 1.12 to
3.82) and chronic phlegm (RR = 2.23, 95% CI: 1.32 to 3.79) when compared with
nonsmokers. Consistent with the risk associated with active smoking assessed on a
duration basis, adolescents who reported active smoking on a weekly basis (more than 7
cigarettes per week) and yearly basis (more than 300 cigarettes) were at a 2.21-fold and
2.10-fold increased risk for the incidence of chronic cough.
Table 3 shows the association between ETS and the onset of bronchitic symptoms.
In our cohort, exposure to ETS was significantly related to chronic cough (RR = 1.31,
Page 9
95% CI: 1.03 to 1.67). The percentage of current ETS exposure also showed a trend
toward increased risk of developing chronic cough. Restricting the analysis to
participants without a history of asthma did not substantially alter the above findings
(Appendix Table 1 and 2).
We also analyzed our data for the incidence of asthma and wheezing disorders in the
TCHS cohort. Similar risks were observed between active smoking and ETS and
wheezing disorders; however it is difficult to make this conclusion firmly because of
small numbers of cases over the 2-year period of follow-up (Appendix Table 3).
In further analyses, we observed the increased risk for new-onset chronic phlegm
among asthmatic adolescents who had been exposed to ETS (Table 4). Children who had
a history of asthma or wheeze and who were exposed to current ETS had an increased
risk (RR = 1.98; 95% CI: 1.09 to 3.60) when they were compared with unexposed
non-asthmatic adolescents (p for interaction = 0.02).
Page 10
Discussion
Our population-based prospective study demonstrates that active smoking and
exposure to ETS significantly increase the risk of new-onset bronchitic symptoms among
adolescents. Active smoking was associated with the development of chronic cough and
chronic phlegm. The increased duration and the weekly and yearly amount of active
smoking showed significant trends in the risk of developing bronchitic symptoms. The
exposure to ETS increased the risk of new-onset chronic phlegm in participants with a
personal history of asthma or wheeze. To the best of our knowledge, this is the first
longitudinal study that has identified an association between active smoking and ETS and
bronchitis/bronchitic symptoms among adolescents.
In the current study, we enrolled a large nationally representative population cohort
and had a very high follow-up rate (94.6%). Some individual and environmental factors,
such as maternal smoking during pregnancy (Gilliland et al., 2001), family history of
asthma or atopy (Lee et al., 2003; Sears et al., 1996), body mass index (Nystad et al.,
2004) and socio-economic status (Ellison-Loschmann et al., 2007), may have affected the
development of respiratory diseases, and we adjusted the above covariates in our Poisson
regression models to minimize these potentially confounding effects.
Cigarette smoke has complex effects on the proinflammatory and immune responses
in the pulmonary system. Chronic inflammation, consisting of the enlargement of the
mucous glands and the remodeling of the bronchi, reflects a deregulated healing process
in the tissue that is damaged by the inhalation of tobacco smoke (Hogg et al., 2004). This
process causes the development of a chronic cough, mucus hypersecretion and phlegm
production in the airways. Previous research suggested that chronic cough and phlegm
are not only an important cause of school absence and medical use in childhood
(Spee-van der Wekke et al., 1998), but also associated with poorer exercise capacity, the
higher incidence of chronic obstructive pulmonary disease and increased mortality risk
later in life (Martinez et al., 2014; de Marco et al., 2007; Guerra et al., 2009).
Our finding that there is an increased risk of the incidence of bronchitic symptoms
after the onset of active smoking is consistent with previous evidence showing that
tobacco smoke causes adverse effects on respiratory health. Karunanayake et al. (2011)
found an increased risk of developing cough and phlegm with a risk of 2.04 and 2.02 in
Page 11
individuals in the 20-70-year-old age group in rural Canada. Withers et al. (1998) noted
that regular smoking was positively associated with late-onset cough, but was not
significantly associated with persistent cough in children aged 6-8 years. However, Eagan
et al. (2002) observed a weak association between smoking and the development of
chronic cough among Norwegian participants aged 15 to 70. Previous research suggested
that being 50 years of age or older was an independent risk factor of the incidence of
bronchitic symptoms (Eagan et al., 2002). The majority of evidence regarding the
cigarette smoking effects came from the studies of elderly cohorts, and longitudinal data
on adolescents or children has remained scarce. In our study, active smoking showed
significant trends in the risks of developing chronic cough and chronic phlegm in
adolescents. There was no significant association observed between the incidence of
bronchitis and active smoking in our study; however, the small numbers of bronchitis
cases may explain this observation. Yeatts et al. (2003) reported that current smoking and
exposure to ETS were positively associated with undiagnosed wheezing among
adolescents. Therefore, underreporting, possibly due to the underdiagnosis of respiratory
diseases is a possible reason for the observed lack of an association.
We also assessed the effect of exposure to household ETS on the risk of developing
respiratory diseases. In Taiwan, children are not typically exposed to ETS in school due
to the legislative ban on public smoking; therefore, household exposure is likely the
predominant source of ETS. A previous meta-analysis has suggested that maternal
smoking is a stronger risk factor for the incidence of respiratory illness in early childhood
than it is for the incidence of respiratory illness at school age (Strachan and Cook, 1998).
We found a significant association between ETS and the onset of chronic cough in our
study. These smaller effects may reflect the decreasing level of exposure to ETS from
household sources as children age.
We found that exposure to ETS was associated with an additional risk for the onset
of bronchitic symptoms among asthmatic adolescents. Exposure to ETS and active
smoking can aggravate the severity of respiratory diseases and can increase
hospitalization rates. However, asthmatic status in childhood does not prevent smoking
initiation in adulthood (Vignoud et al., 2011), and many asthmatic children are still
exposed to high levels of tobacco smoke at home (Irvine et al., 1997). Previous research
Page 12
has suggested that it remains controversial whether ETS exposure is associated with
chronic respiratory symptoms and decrements in lung function among asthmatic adults
(Trédaniel et al., 1994). In our study, adolescents with a history of asthma or wheeze and
who were exposed to ETS had the greatest risk of developing chronic phlegm when they
were compared with un-exposed non-asthmatic adolescents. Similarly, Schwartz et al.
(2000) reported that exposure to ETS was associated with increases in respiratory
symptoms including cough and phlegm production among younger asthmatic children in
Finland. We observed a protective effect against developing bronchitic symptoms
between an asthmatic history and a regular smoking habit in adolescents. The possible
explanation for this is that a reduced severity of asthma was observed among asthmatic
smokers at baseline when they were compared with asthmatic non-smokers; thus, the
“healthy smoker” effect might account for this inverse association.
Our study has some limitations. The measurement of active smoking and ETS
exposure by questionnaire may be relatively imprecise. However, the validity of exposure
estimates based on questionnaire responses has been found to provide reasonably valid
data and Spanier et al. (2011) observed that the parental reporting of ETS may
underestimate the risk of respiratory diseases in children. Another limitation to this study
is the potential misclassification of respiratory diseases that may lead to underestimation
of the effect estimates. A self-reported respiratory outcome questionnaire has been
demonstrated to be valid and repeatable and has been widely used in epidemiologic
studies (Burney et al., 1989). It is possible that bronchitic symptoms, including cough and
phlegm may mimic the symptoms of an asthmatic attack and may, therefore, lead to an
overestimation of the risk. However, this seems unlikely because the effect estimates did
not change substantially when we restricted the analyses to adolescents without a history
of asthma at baseline (Appendix table 1 and 2).
In conclusion, we performed a large, high follow-up rate longitudinal study to
discover that active smoking and exposure to ETS are important risk factors for the
incidence of bronchitic symptoms in adolescents. Moreover, asthmatic adolescents who
are exposed to ETS have an additional risk of developing bronchitic symptoms. Effective
tobacco control efforts focusing on the prevention of smoking initiation and the reduction
Page 13
of ETS exposure are urgently needed to reduce the adverse impact on respiratory health
in adolescents.
Page 14
Conflict of interest statement
The authors declare that there are no conflicts of interests.
Acknowledgment
This work was partially supported by grants #98-2314-B-002-138-MY3 and
#96-2314-B-006-053 from the Taiwan National Science Council. The sponsors had no
role in the design of the study, the collection and analysis of the data, or in the
preparation of the manuscript.
Page 15
References
Burney, P.G., Laitinen, L.A., Perdrizet, S., et al., 1989. Validity and repeatability of the
IUATLD (1984) Bronchial Symptoms Questionnaire: an international comparison. Eur.
Respir. J. 2, 940-945.
CDC. The health consequences of involuntary exposure to tobacco smoke: a report of
the Surgeon General. Atlanta, GA: US Department of Health and Human Services, CDC;
2006 [Available at http://www.ncbi.nlm.nih.gov/books/NBK44324/pdf/TOC.pdf
[Accessed April 2014]].
Cook, D.G., Strachan, D.P., 1999. Health effects of passive smoking-10: Summary of
effects of parental smoking on the respiratory health of children and implications for
research. Thorax 54, 357-366.
de Marco, R., Accordini, S., Cerveri, I., et al., 2007. Incidence of chronic obstructive
pulmonary disease in a cohort of young adults according to the presence of chronic cough
and phlegm. Am. J. Respir. Crit. Care Med. 175, 32-39.
Eagan, T.M., Bakke, P.S., Eide, G.E., Gulsvik, A., 2002. Incidence of asthma and
respiratory symptoms by sex, age and smoking in a community study. Eur. Respir. J. 19,
599-605.
Ellison-Loschmann, L., Sunyer, J., Plana, E., et al., 2007. Socioeconomic status, asthma
and chronic bronchitis in a large community-based study. Eur. Respir. J. 29, 897-905.
Forey, B.A., Thornton A.J., Lee, P.N., 2011. Systematic review with meta-analysis of the
epidemiological evidence relating to COPD, chronic bronchitis and emphysema. BMC
Pulm. Med. 11, 36.
Frank, P.I., Hazell, M.L., Morris, J.A., Linehan, M.F., Frank, T.L., 2007. A longitudinal
study of changes in respiratory status in young adults, 1993-2001. Int. J. Tuberc. Lung
Dis. 11, 338-343.
Gilliland, F.D., Li, Y.F., Peters, J.M., 2001. Effects of maternal smoking during
pregnancy and environmental tobacco smoke on asthma and wheezing in children. Am. J.
Respir. Crit. Care Med. 163, 429-436.
Guerra, S., Sherrill, D.L., Venker, C., Ceccato C.M., Halonen, M., Martinez, F.D., 2009.
Chronic bronchitis before age 50 years predicts incident airflow limitation and mortality
risk. Thorax 64, 894-900.
Page 16
Hogg, J.C., Chu, F., Utokaparch, S., et al., 2004. The nature of small-airway obstruction
in chronic obstructive pulmonary disease. N. Engl. J. Med. 350, 2645-2653.
Irvine, L., Crombie, I.K., Clark, R.A., et al., 1997. What determines levels of passive
smoking in children with asthma? Thorax 52, 766-769.
Karunanayake, C.P., Rennie, D.C., Pahwa, P., Chen, Y., Dosman, J.A., 2011. Predictors
of respiratory symptoms in a rural Canadian population: A longitudinal study of
respiratory health. Can. Respir. J. 18, 149-153.
Le, C.T., 2003. Introductory Biostatistics. John Wiley & Sons, Hoboken, NJ.
Lee, Y.L., Lin, Y.C., Hsiue, T.R., Hwang, B.F., Guo, Y.L., 2003. Indoor and outdoor
environmental exposures, parental atopy, and physician-diagnosed asthma in Taiwanese
schoolchildren. Pediatrics 112, e389.
Liberty, K.A., Pattemore, P., Reid, J., Tarren-Sweeney, M., 2010. Beginning school with
asthma independently predicts low achievement in a prospective cohort of children. Chest
138, 1349-1355.
Martinez, C.H., Kim, V., Chen, Y., et al., 2014. The clinical impact of non-obstructive
chronic bronchitis in current and former smokers. Respir. Med. 108, 491-499.
McConnell, R., Berhane, K., Gilliland, F., et al., 1999. Air pollution and bronchitic
symptoms in Southern California children with asthma. Environ. Health Perspect. 107,
757-760.
Nystad, W., Meyer, H.E., Nafstad, P., Tverdal, A., Engeland, A., 2004. Body mass index
in relation to adult asthma among 135,000 Norwegian men and women. Am. J.
Epidemiol. 160, 969-976.
Schwartz, J., Timonen, K.L., Pekkanen, J., 2000. Respiratory effects of environmental
tobacco smoke in a panel study of asthmatic and symptomatic children. Am. J. Respir.
Crit. Care Med. 161, 802-806.
Sears, M.R., Holdaway, M.D., Flannery, E.M., Herbison, G.P., Silva, P.A., 1996.
Parental and neonatal risk factors for atopy, airway hyper-responsiveness, and asthma.
Arch. Dis. Child. 75, 392-398.
Spanier, A.J., Kahn, R.S., Xu, Y., Hornung, R., Lanphear, B.P., 2011. Comparison of
biomarkers and parent report of tobacco exposure to predict wheeze. J. Pediatr. 159,
776-782.
Page 17
Spee-van der Wekke, J., Meulmeester, J.F., Radder J.J., Verloove-Vanhorick S.P., 1998.
School absence and treatment in school children with respiratory symptoms in the
Netherlands: data from the Children Health Monitoring System. J. Epidemiol.
Community Health. 52, 359-363.
Stoddard, J.J., Miller, T., 1995. Impact of parental smoking on the prevalence of
wheezing respiratory illness in children. Am. J. Epidemiol. 141, 96-102.
Strachan, D.P., Cook, D.G., 1998. Health effects of passive smoking. 6. Parental smoking
and childhood asthma: longitudinal and case-control studies. Thorax 53, 204-212.
Trédaniel, J., Boffetta, P., Saracci, R., Hirsch, A., 1994. Exposure to environmental
tobacco smoke and adult non-neoplastic respiratory diseases. Eur. Respir. J. 7, 173-185.
Tsai, C.H., Huang, J.H., Hwang, B.F., Lee, Y.L., 2010. Household environmental
tobacco smoke and risks of asthma, wheeze and bronchitic symptoms among children in
Taiwan. Respir. Res. 11, 11.
Vignoud, L., Pin, I., Boudier, A., et al., 2011. Smoking and asthma: disentangling their
mutual influences using a longitudinal approach. Respir. Med. 105, 1805-1814.
Warren, C.W., Lea, V., Lee, J., Jones, N.R., Asma, S., McKenna, M., 2009. Change in
tobacco use among 13-15 year olds between 1999 and 2008: findings from the Global
Youth Tobacco Survey. Glob. Health Promot. 16 (2 Suppl.), 38-90.
Wen, C.P., Levy, D.T., Cheng, T.Y., Hsu, C.C., Tsai, S.P., 2005. Smoking behaviour in
Taiwan, 2001. Tob. Control 14 (Suppl. 1), i51-i55.
Withers, N.J., Low, L., Holgate, S.T., Clough, J.B., 1998. The natural history of
respiratory symptoms in a cohort of adolescents. Am. J. Respir. Crit. Care Med. 158,
352-357.
Yeatts, K., Davis, K.J., Sotir, M., Herget, C., Shy, C., 2003. Who gets diagnosed with
asthma? Frequent wheeze among adolescents with and without a diagnosis of asthma.
Pediatrics 111, 1046-1054.
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Table 1
Baseline characteristics of the study population, Taiwan Children Health Study, 2007.
Selected characteristics at
study entrya
Gender
Boys
Girls
Age, years
12
13
14
Parental incomeb
≦400,000
400,000～800,000
＞800,000
Parental history of asthma
Yes
No
Parental history of atopyc
Yes
No
Maternal smoking during pregnancy
Yes
No
BMI classification
Underweight
Normal
Overweight
Obese
Current ETS
Yes
No
Active smoking
Yes
No
Bronchitis-free
cohort
(N=3,664)
n
%
Chronic coughfree cohort
(N=3,680)
n
%
1768
1896
48.2
51.8
1791
1889
48.7
51.3
1803
1901
48.7
51.3
2914
729
8
80.0
19.9
0.2
2948
711
8
80.1
19.3
0.2
2956
725
8
79.9
19.6
0.2
1205
1372
811
35.6
40.5
23.9
1199
1382
826
35.2
40.6
24.2
1198
1395
833
35.0
40.7
24.3
94
3570
2.6
97.4
102
3578
2.8
97.2
104
3600
2.8
97.2
863
2801
23.6
76.4
916
2764
24.9
75.1
919
2785
24.8
75.2
140
3524
3.8
96.2
137
3543
3.7
96.3
135
3569
3.6
96.4
1465
1054
497
629
40.2
28.9
13.6
17.3
1464
1061
495
641
40.0
29.0
13.5
17.5
1478
1062
503
640
40.1
28.8
13.6
17.4
1564
2075
43.0
57.0
1568
2090
42.9
57.1
1595
2086
43.3
56.7
202
3446
5.5
94.5
199
3464
5.4
94.6
201
3486
5.5
94.5
Abbreviation: ETS, environmental tobacco smoke.
a
Number of subjects does not add up to total N because of missing data.
b
New Taiwan dollars per year ($1 US = $ 30 New Taiwan).
c
Atopy is defined as allergic rhinitis or atopic dermatitis.
Page 19
Chronic phlegmfree cohort
(N=3,704)
n
%
Table 2
Effects of active smoking on bronchitis and bronchitic symptoms, Taiwan Children Health Study, 2007-2009.
Bronchitis
IR
RR
No
8.0
1
Yes
10.0 1.26
95% CI
Chronic cough
IR
RR
95% CI
Chronic phlegm
IR
RR
95% CI
Active smokinga
36.4 1
(0.44, 3.60)
60.9 1.72
47.9 1
(1.11, 2.64)
72.5 1.64
(1.11, 2.43)
Duration
None
8.0
1
≦1 year
9.4
1.22
(0.29, 5.17)
61.9 1.70
(0.96, 3.00)
65.4 1.49
(0.87, 2.57)
＞1 year
6.7
0.91
(0.12, 6.75)
73.3 2.07
(1.12, 3.82)
96.7 2.23
(1.32, 3.79)
p for trend
36.4 1
0.97
47.9 1
0.003
0.001
Amount smoked weekly
None
8.0
1
＜7
4.8
0.62
(0.08, 4.57)
58.8 1.60
(0.88, 2.88)
66.0 1.52
(0.88, 2.63)
≧7
13.2 1.80
(0.43, 7.59)
77.9 2.21
(1.23, 3.99)
92.1 2.05
(1.19, 3.53)
p for trend
36.4 1
0.72
47.9 1
0.002
0.003
Amount smoked yearly
None
8.0
1
＜300
8.0
1.02
(0.24, 4.35)
67.5 1.80
(1.09, 2.98)
73.6 1.65
(1.03, 2.66)
≧300
9.6
1.33
(0.18, 9.86)
68.6 2.10
(0.98, 4.50)
90.0 2.15
(1.10, 4.20)
p for trend
36.4 1
0.88
0.003
47.9 1
0.003
Abbreviations: IR, incidence rate per 1000 person-years; RR, rate ratio; and CI, confidence interval.
a
Models are adjusted for age, sex, parental history of asthma, parental history of atopy, maternal smoking during
pregnancy, body mass index, ETS exposure and community.
Page 20
Table 3
Effects of environmental tobacco smoke (ETS) on bronchitis and bronchitic symptoms, Taiwan Children Health
Study, 2007-2009.
Bronchitis
95% CI
Chronic cough
IR
RR
95% CI
Chronic phlegm
IR
RR
IR
RR
95% CI
No
8.9
1
Yes
7.0
0.72
None
8.9
1
≦10
8.6
0.90
(0.48, 1.65)
44.9 1.36
(1.06, 1.76)
52.5 1.16
(0.93, 1.45)
＞10
1.6
0.14
(0.01, 1.35)
41.7 1.22
(0.79, 1.88)
50.2 1.09
(0.74, 1.59)
Current ETS
33.9 1
(0.42, 1.25)
43.8 1.31
47.2 1
(1.03, 1.67)
51.5 1.14
(0.92, 1.41)
Daily amount of ETS
p for trend
Percent of ETS
33.9 1
0.08
47.2 1
0.04
0.24
a
None
8.9
1
≦20%
6.1
0.68
(0.35, 1.32)
43.3 1.06
(0.70, 1.62)
50.4 1.12
(0.88, 1.43)
＞20%
9.2
0.84
(0.40, 1.75)
45.3 1.24
(0.90, 1.70)
55.2 1.20
(0.89, 1.61)
p for trend
33.9 1
0.44
0.02
47.2 1
0.13
Abbreviations: IR, incidence rate per 1000 person-years; RR, rate ratio; and CI, confidence interval.
Models are adjusted for age, sex, parental history of asthma, parental history of atopy, maternal smoking during
pregnancy, body mass index, smoking habit and community.
a
Average percent of ETS in lifetime.
Page 21
Table 4
Joint effects of exposure to environmental smoke (ETS), active smoking and personal history of asthma or
wheeze at baseline on the incidence on bronchitic symptoms, Taiwan Children Health Study, 2007-2009.
Current ETSa
Unexposed
RR
Chronic cough
Asthma/wheeze
No
1
Yes
1.43
95% CI
(0.91, 2.26)
p for interaction
Chronic phlegm
Asthma/wheeze
p for interaction
Active smokingb
Exposed
No
RR
95% CI
RR
1.23
(0.94, 1.60)
1
1.40
(0.76, 2.57)
1.85
95% CI
(1.34, 2.53)
0.28
No
1
Yes
0.86
(0.54, 1.36)
Yes
RR
95% CI
2.01
(1.27, 3.16)
0.32
(0.07, 1.40)
0.03
1.03
(0.81, 1.29)
1
1.98
(1.09, 3.60)
1.34
(0.99, 1.81)
0.02
1.91
(1.29, 2.87)
0.17
(0.02, 1.31)
0.03
Abbreviations: RR, rate ratio; and CI, confidence interval.
a
Models are adjusted for age, sex, parental history of asthma, parental history of atopy, maternal smoking during
pregnancy, smoking habit, body mass index and community.
b
Models are adjusted for age, sex, parental history of asthma, parental history of atopy, maternal smoking during
pregnancy, ETS exposure, body mass index and community.
Page 22