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Linda Irvine a Department of Child Health, Ninewells Hospital and
Medical School, Dundee DD1 9SY, b Department of Epidemiology
and Public Health, Ninewells Hospital and Medical School, c Department of Medicine, Ninewells
Hospital and Medical School, d Wallacetown Health Centre, Dundee DD4 6RB, e Nicotine Laboratory,
Wardalls Grove, London SE14 5ER
Correspondence to: L Irvine
lirvine{at}eph.dundee.ac.uk
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Abstract |
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Objective:
To investigate whether parents of
asthmatic children would stop smoking or alter their smoking habits to
protect their children from environmental tobacco smoke.
Design:
Randomised controlled trial.
Setting:
Tayside and Fife, Scotland.
Participants:
501 families with an asthmatic child
aged 2-12 years living with a parent who smoked.
Intervention:
Parents were told about the impact of
passive smoking on asthma and were advised to stop smoking or change
their smoking habits to protect their child's health.
Main outcome measures:
Salivary cotinine
concentrations in children, and changes in reported smoking habits of
the parents 1 year after the intervention.
Results:
At the second visit, about 1 year after the baseline visit, a small decrease in salivary cotinine concentrations was found in both groups of children: the mean decrease in the intervention group (0.70 ng/ml) was slightly smaller than that of the
control group (0.88 ng/ml), but the net difference of 0.19 ng/ml had a
wide 95% confidence interval (
0.86 to 0.48). Overall, 98% of
parents in both groups still smoked at follow up. However, there was a
non-significant tendency for parents in the intervention group to
report smoking more at follow up and to having a reduced desire to stop smoking.
Conclusions:
A brief intervention to advise parents
of asthmatic children about the risks from passive smoking was
ineffective in reducing their children's exposure to environmental
tobacco smoke. The intervention may have made some parents less
inclined to stop smoking. If a clinician believes that a child's
health is being affected by parental smoking, the parent's smoking
needs to be addressed as a separate issue from the child's health.
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Key messages
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Introduction |
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The adverse effects of passive smoking on the respiratory system of children has been shown in infancy1 and throughout childhood.2 Asthmatic children have more severe disease if their parents smoke.3
Many asthmatic children are exposed to high levels of tobacco smoke at home.4 Exposure mainly depends on proximity to smokers, and young children who spend much of their time with parents that smoke are particularly vulnerable.
The harmful effects of active smoking are now well known through campaigns,5 but whether the risks from passive smoking are appreciated is unproved. Clinicians have been advised to counsel parents about the harmful effects of passive smoking on their children.6 It is not clear whether this advice encourages parents to reduce their children's exposure to tobacco smoke.
We aimed to investigate whether a brief intervention informing parents
about the harmful effects of smoking on childhood asthma encouraged
them to stop smoking or to modify their smoking habits to protect their children.
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Participants and methods |
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Recruitment
We invited 123 general practices in Tayside and Fife to
take part in our study: 73 (59%) agreed to participate, and these
practices identified 1047 potential families for our study. Families
were considered eligible if they had a child aged 2-12 years with
documented asthma who lived with a parent or guardian who smoked.
Children were identified from asthma registers or from repeat
prescribing of asthma drugs. We chose the lower age limit of 2 years to
ensure that asthma had been definitely diagnosed, and we chose the
upper age limit of 12 years to minimise the number of children who were
actively smoking.
Sample size
We aimed to reduce the proportion of children with high
salivary cotinine concentrations. Cook et al7 showed that
86% of children exposed to adults who smoke have salivary cotinine
concentrations greater than 0.6 ng/ml. To detect a decrease in cotinine
concentrations from 86% to 74% in children with concentrations greater than 0.6 ng/ml as being significant at the 5% level, with a
power of 90%, we would require 248 children in both the control group
and the intervention group.
Data collection
The families were visited at home on two occasions
at baseline and then about 1 year later
by two research nurses (LI and
KG). At baseline each research nurse recruited half of the study
population. At the second visit each nurse visited those families
recruited by her colleague, thus the nurses remained blind to baseline
information. A questionnaire was completed by the index parents at both
visits. Information was collected on family socioeconomic factors, the
child's asthma, smoking habits of the index parent, and overall
exposure of the child to tobacco smoke. Saliva samples were obtained
from the parents and the children on both occasions to measure cotinine
concentrations, the major metabolite of nicotine.8 Our
methods have been reported.4
Intervention
On giving their written consent, the families were
randomised to either an intervention group or a control group. The
intervention was designed to be brief, on the basis of a method reported by Russell et al.9 At the baseline visit, parents in the intervention group were given information on passive smoking. This was followed by a discussion on asthma, passive smoking, the
effects of environmental tobacco smoke, and the potential benefits to
the child when tobacco smoke is avoided. Financial and health benefits
were also discussed. The parents were (a) given information
on how to seek help to stop smoking, (b) advised that if
they could not stop smoking then smoking in a different room or outside
the home could help to protect their child, and (c) advised
that their child's exposure to tobacco smoke could further be reduced
by discouraging visitors from smoking in the home. The parents were
given a leaflet (the first in a series of three) that was specifically
designed to reinforce the information given and that included
information on seeking help to stop smoking. The parents were also
given a commercially available leaflet by The Advisory Council on Drug
and Alcohol Education (TACADE). At 4 and 8 months after the baseline
visit, they were sent the second and third leaflets by post with a
letter encouraging them to stop smoking.
Follow up
Families were revisited at home about 1 year after the
initial visit. We chose a 1 year follow up to assess the long term
effects of the intervention.
Data analysis
We analysed the data with SPSS for Windows. As the
children's cotinine concentrations were highly skewed, we used the
conventional logarithmic transformation.7 However, as the
difference in cotinine concentrations (baseline minus follow up) was
approximately normally distributed, we made no transformation for the
analyses of change in cotinine concentration. To compare the
intervention and control groups at baseline and to detect differences
between the groups at follow up, we used the
2
test and t tests.
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Results |
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Randomisation
We compared those factors we had identified4 as having an influence on cotinine concentrations in children (table
1). These were: the child's age, smoking habits of the index parent,
contact with other smokers, and the home environment. The groups were
similar for age, sex, socioeconomic factors, and smoking status of the
parents. The children's mean cotinine concentrations showed that both
groups had been similarly exposed to tobacco smoke: 2.83 ng/ml in the
intervention group and 2.91 ng/ml in the control group (geometric
mean).
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Cotinine concentrations
The children showed a small decrease in cotinine concentrations at the second visit: the mean decrease in the
intervention group (0.70 ng/ml) was slightly smaller than in the
control group (0.88 ng/ml), but the net difference of 0.19 ng/ml had a wide 95% confidence interval (
0.86 to 0.48).
Parental cotinine concentrations had increased marginally in both
groups by the second visit. Although the mean increase was slightly
larger in the intervention group (3.1 ng/ml) than in the control group
(1.8 ng/ml), the net difference of 1.3 ng/ml again had a wide
confidence interval (
26.4 to 23.9).
Changes in reported smoking
We assessed the changes in smoking habits by comparing the
difference in responses to identical questions at baseline and follow
up. At follow up, more parents in the intervention group (59, 28%)
reported smoking less frequently in the same room as their child than
parents in the control group (49, 22%; table 2). Similarly, 104 parents (49%) in the intervention group and 84 parents (38%) in the
control group reported smoking less in the home at follow up. These
differences were non-significant. However, more parents in the
intervention group (58, 27%) smoked more cigarettes per day at the end
of the study period than parents in the control group (47, 21%).
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Impact of the study
We asked the parents if our study had encouraged them to
think about stopping smoking or changing their smoking habits: 114 parents (54%) in the intervention group and 122 parents (56%) in the
control group said that it had. When asked how much they wanted to stop
smoking at follow up, however, only 31 parents (15%) in the
intervention group compared with 51 parents (24%) in the control group
expressed a greater desire to stop smoking than at baseline (P=0.06).
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Discussion |
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Our study showed that informing parents of the harmful effects of passive smoking was ineffective in persuading them to reduce the exposure of their children to tobacco smoke. Cotinine concentrations in the children had decreased by the end of follow up in both groups, but by the same margin. The decrease was of the order we would expect from the ageing of the children by 1 year.4 The intervention also failed to increase either the number of attempts by parents to stop smoking or the numbers who had stopped at 1 year. Slightly more parents in the intervention group reported smoking less frequently in the presence of their child. The effect of this was weak as the cotinine concentrations were not correspondingly changed. Fewer parents in the intervention group (30/206; 15%) reported an increased desire to stop smoking at the end of the study than parents in the control group (51/217; 24%), but this difference was non-significant (P=0.06). Similarly, more parents in the intervention group (58/213; 21%) than in the control group (47/222; 27%) reported smoking more overall at the end of the study than they had at baseline. These findings are consistent with the theory that patients are resistant to information or advice when it is not being sought. 10 11 As Butler said "telling patients what to do can make them feel challenged and provoke them to assert control by continuing their unhealthy behaviours with renewed vigour. Patients often erect barriers in response to the attempted imposition of a medical agenda."12
Ours is the first study to report the effect of a brief intervention on
parents of asthmatic children in which an objective measure of exposure
to tobacco smoke
salivary cotinine concentrations
was used. A small
scale study on asthmatic children did not report changes in cotinine
concentrations.13 Other trials have studied non-asthmatic
children. One study of newborn infants found a non-significantly higher
cotinine concentration in the intervention group than in the control
group.14 Another small study advising parents of ways to
reduce the exposure of their children to environmental smoke showed no
significant effect on the children's cotinine concentrations,15 but this was flawed because follow up
measurements of continine concentrations were not available for half of
the children. A larger study that monitored passive exposure of
preschool children to tobacco smoke by self report rather than by
cotinine concentrations, found no effect on parental smoking
behaviour.16
Our intervention was designed to be brief
that is, a package that
could be easily delivered to parents in a clinical setting. Possibly a
more intensive intervention repeated on several occasions could have
been more effective. However, a recent systematic review showed that
more intensive advice was no more successful in encouraging smoking
cessation than brief advice.17
The overall cessation rate of 3% in our study was slightly lower than
that of unaided smoking cessation (7%) reported in two
recent meta-analyses.
17 18
Several explanations may apply. We recruited smokers who were not seeking help to stop smoking.19 Several factors that are associated with poor
success at quitting were apparent in our study. These were young age
(mean age 33 years),20 being female,21 having
a partner who smoked,22 and low social
class.23 Finally, parents may regard the home as the only
place where they are free to make choices about their smoking as more
restrictions on smoking in public places are enforced.
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Conclusion |
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Our study has shown that a brief intervention
focusing on children's health is not sufficient to achieve a long term
change in parental smoking. The intervention may have made some parents less inclined to stop smoking. Brief interventions on smoking cessation
targeted at the smoker's health may have a modest
impact,24 but interventions aimed at the health of a third
party
in this case the parent's child
seemed ineffective.
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Acknowledgments |
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We thank the general practitioners and staff from the practices in Tayside and Fife who helped identify families suitable for our study.
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Footnotes |
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Funding: The Wellcome Trust (grant number 039282/Z/93/Z).
Competing interests: None declared.
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References |
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| 2. | Cook DG, Strachan DP. Parental smoking and prevalence of respiratory symptoms and asthma in school aged children. Thorax 1997; 52: 1081-1094[Abstract]. |
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Strachan DP.
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| 23. | Fowler G. Smoking among women from socially deprived backgrounds. Maternal Child Health 1994:340-4. |
| 24. | Law M, Tang JL. An analysis of the effectiveness of interventions intended to help people stop smoking. Arch Intern Med 1995; 155: 1933-1941[Abstract]. |
(Accepted 30 March 1999)
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