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Effect of Gestational and Passive Smoke Exposure on Ear Infections in Children
Judith E. C. Lieu, MD;
Alvan R. Feinstein, MD
Arch Pediatr Adolesc Med. 2002;156:147-154.
ABSTRACT
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Objective To estimate the relative risk for otitis media (OM) in children from
environmental tobacco smoke (passive exposure), maternal smoking during pregnancy
(gestational exposure), or both.
Design Analysis of data from a national cross-sectional health survey, utilizing
questionnaire information and serum cotinine measurements.
Participants Children younger than 12 years (N = 11 728) in the Third National
Health and Nutrition Examination Survey (NHANES III), conducted from 1988-1994.
Main Outcome Measures Occurrence and recurrence of ear infections.
Results The cumulative incidence of ear infections was 69%. Of all participants,
38% were exposed to passive smoke, 23% were exposed to gestational smoke,
and 19% were exposed to combined passive and gestational smoke. The occurrence
of any ear infection was not increased by passive smoke exposure (adjusted
risk ratio [RR], 1.01; 95% confidence interval [CI], 0.95-1.06), but was slightly
increased by gestational (adjusted RR, 1.08; 95% CI, 1.01-1.14) and combined
(adjusted RR, 1.07; 95% CI, 1.00-1.14) smoke exposures. The risk of recurrent
ear infections ( 6 lifetime episodes) was significantly increased with
combined smoke exposure (adjusted RR, 1.44; 95% CI, 1.11-1.81). Other risk
factors for ear infection identified in multivariable analysis were race/ethnicity,
poverty-income ratio of 2.00 or more, attendance in day care, history of asthma,
and presence of allergic symptoms.
Conclusions Passive smoke exposure was not associated with an increased risk of
ever developing an ear infection in this study. The increased risk found with
gestational and combined smoke exposures has marginal clinical significance.
For recurrent ear infections, however, combined smoke exposure had a clinically
and statistically significant effect.
INTRODUCTION
OTITIS MEDIA (OM) is a common complication of upper respiratory tract
infections in young children.1 Among the risk
factors often associated with recurrent OM are a family history of OM, child
care outside the home, presence of siblings, early onset of OM, atopy, male
sex, not being breastfed, and parental smoking.1-13
Exposure to environmental tobacco smoke (ETS), often called passive
smoking, is thought to increase the risk of OM, possibly through an effect
on mucociliary clearance. Agius et al2 found
that in patients who had chronic OM with effusion, ciliary beat function was
impaired with, but not without, passive smoke exposure. Other possible mechanisms
include goblet cell hyperplasia with mucus hypersecretion and alteration of
phagocytic antibacterial defenses in conjunction with some viral infections.14 The role of ETS in children's middle ear disease
(eg, acute OM, recurrent OM, or OM with effusion) has been clinically investigated
in numerous cohort studies,3, 5, 9, 14-23
case-control studies,7, 10, 24-36
and cross-sectional surveys8, 12, 37-45
and has been summarized in multiple reviews46-47
and meta-analyses.4, 48-49
Quantitative synthesis of results in the 3 meta-analyses suggests a small
to moderate risk increase from parental smoking, with estimates ranging from
a risk ratio (RR) of 1.19 for middle ear disease to an odds ratio (OR) of
1.74 for recurrent OM (3 episodes).
Of the studies that do show a link between ETS and OM, several have
suggested that maternal, but not paternal, smoking increases the risk of OM.5, 12, 16-17,29, 50
Of 4 studies that have investigated the association between maternal smoking
during pregnancy and OM, 2 have suggested that the incidence of OM increased
with gestational smoke exposure, as distinguished from maternal smoking postpartum.8, 12, 17, 50
Maternal smoking during pregnancy is generally known to be associated
with increased adverse neonatal events51-53
and increased childhood morbidity, such as depressed neonatal respiratory
function and increased incidence of childhood asthma.54-63
Gestational smoking is also associated with cord blood immune function alterations
in newborns, including reduction in natural killer cell activity,64 decreased neutrophil counts,65
and elevated levels of IgA, IgM, and IgG.66
Because OM is considered a complication of an upper respiratory tract infection,
it is pathophysiologically plausible that maternal smoking during pregnancy
would increase the risk of OM. The current study was conducted to answer the
question: Does maternal smoking during pregnancy and/or subsequent passive
smoke exposure raise the risk of OM in children?
PARTICIPANTS AND METHODS
DATA SOURCE
We used data from the Third National Health and Nutrition Examination
Survey (NHANES III), a national cross-sectional health survey performed from
1988-1994. The survey included 33 994 persons aged 2 months and older
who represented the noninstitutionalized civilian population of the United
States. Details of the complex sampling design, data collection, and weighting
approach have been described elsewhere.67 Briefly,
NHANES III used a stratified, multistage probability sample design, with oversampling
of young children (age <5 years), older persons (age >59 years), non-Hispanic
black persons, and Mexican Americans. To obtain a distribution of participants
similar to the US population as a whole, sampling weights were applied during
the analysis to incorporate the differential probabilities of selection and
include adjustments for noncoverage and nonresponse.67
To generate estimates of risk for OM in children, the current analysis is
limited to the 11 728 survey participants younger than 12 years.
DEFINITION OF VARIABLES
In the NHANES III interviews on demographic characteristics, the family
reference person (ie, head of household) marked race/ethnicity as non-Hispanic
white, non-Hispanic black, or Mexican American. Any person who did not choose
a category was considered to be "other." A poverty-income ratio (PIR), calculated
as the reported household annual income divided by the poverty threshold defined
by the US Census Bureau with adjustment for family size, was coded as a continuous
variable in the NHANES III database. For our analysis, the PIR was demarcated
into 3 ordinal categories: less than 1.00, 1.00 to 1.99, and 2.00 or more.
Educational level completed by the family reference person was coded in the
NHANES III database as "never attended school or kindergarten only" or in
individual levels of 1 to 17 years, with 17 entered for those with 17 or more
years of schooling. For the current analysis, educational level was categorized
as less than 7 years (primary or no schooling), 7 to 12 years (at least some
secondary school), and more than 12 years (at least some college).
For each child, all information was given by a proxy respondent (ie,
mother, father, sibling, grandparent, aunt or uncle, or other). Age of the
child was recorded in the survey in months or years and analyzed in the current
study by year. Day care attendance was defined in the survey as ever having
attended a day care center with at least 6 children and whether attendance
was less than 10 or at least 10 hours per week. Child's birth weight was divided
into 3 ordinal categories: less than 2500 g, 2500 to 4100 g, and more than
4100 g. For children younger than 6 years, questions were asked about whether
breastfeeding had ever occurred, and if so, the child's age when it completely
stopped.
For the question, "Did [the child] ever have an ear infection or an
earache?" a positive response was followed by questions about whether a physician
ever treated the child for an ear infection; whether tubes were placed for
treatment; and the number of episodes, coded in the survey as 1, 2, 3 to 5,
or 6 or more episodes. Any positive response was counted as an ear infection,
and we defined recurrent ear infections as at least 6 episodes18
and nonrecurrent as 1 to 5 episodes. Because other investigators have considered
3 or more ear infections to be recurrent, an analysis using this definition
of recurrence was also done separately.
The presence of comorbid conditions—asthma, chronic bronchitis,
and hay fever—was ascertained by the question, "Did a doctor ever say
that [the child] had . . . ?" Presence of allergic symptoms was elicited by
the questions, "During the past 12 months, has [the child] had any episodes
of stuffy, itchy, or runny nose? Watery, itchy eyes?"
Passive cigarette smoke exposure in the NHANES III survey was determined
by questions about the existence and number of persons who currently smoked
cigarettes in the household. We coded any passive exposure as yes or no for
the presence of smokers in the household and quantified it by summing the
number of smokers and the number of cigarettes they smoked per day. Maternal
smoking during pregnancy (ie, gestational exposure) was ascertained in the
survey by asking whether the mother smoked at any time while pregnant with
the child. A positive response was followed by a question about whether she
quit or refrained from smoking for the rest of the pregnancy. We then created
a composite variable for the combination of passive smoking and gestational
smoke exposure. For this composite variable, exposure was categorized as neither
passive nor gestational, passive only, gestational only, or both passive and
gestational (ie, combined).
To quantify the dose of passive cigarette smoke exposure in another
way, we examined the NHANES III results for children's values of serum cotinine,
a metabolite of nicotine. Because this test was performed only on children
who participated from 1988-1991, serum cotinine measurements were available
for only 60% of the total survey population. Furthermore, because serum cotinine
was not measured in children younger than 4 years, 5982 children were excluded
from the serum cotinine analysis. Data from 1825 children were thus used for
the analysis of serum cotinine. Concentrations were determined by the NHANES
III survey in a 2-step process. The enzyme immunoassay method was used as
a screening method for differentiating "low" (<25 ng/mL) and "high" (25
ng/mL) cotinine concentrations. Based on the low or high concentrations on
enzyme immunoassay, liquid chromatography/mass spectrometry analysis was performed
on all specimens. Serum cotinine concentrations greater than 10 to 20 ng/mL
generally indicate active smokers.68
STATISTICAL ANALYSIS
All analyses for this study were done using SUDAAN software (Research
Triangle Institute, Research Triangle Park, NC) to incorporate sampling weights
(ie, primary sampling unit and strata information) consistent with the complex
design of the NHANES III survey.67 This method
of statistical adjustment, incorporating the sampling weights, produced a
weighted cumulative incidence that estimates the proportion of children who
ever had ear infections nationally. Bivariate comparisons of the cumulative
incidence of ear infections were assessed using  2 tests and
crude RRs with 95% confidence intervals (CIs) for dichotomous independent
variables. The logistic regressions produced ORs and 95% CIs for categorical
independent variables after they were converted to "dummy" binary variables.
For continuous serum cotinine level, medians and interquartile ranges were
used.
A second method of statistical adjustment, a multivariable adjustment,
controlled for the effect of multiple independent variables. Demographic,
baseline, and comorbidity variables were used in the multivariable logistic
regression models. For OR calculations in the logistic regression models,
the reference groups were non-Hispanic whites for the race/ethnicity variable,
female sex, and normal birth weight (ie, 2500-4100 g). The adjusted ORs obtained
from logistic regression were converted into adjusted RRs for ear infections
(any, recurrent, and nonrecurrent) because they all had cumulative incidences
of more than 10% in this population. The conversion, performed with an equation
provided by Zhang and Yu,69 was done because
the OR for relatively common outcomes will either overestimate RRs more than
1 or underestimate those less than 1 (ie, provide estimates farther away from
1 than the true RR). The 95% CIs for adjusted RRs were correspondingly converted
from ORs using the same equation. Multiple stratification tables were used
to examine possible interactions between the independent variables in affecting
the cumulative incidence of any ear infections.70
RESULTS
ANY EAR INFECTION
The US cumulative incidence of any ear infection in children younger
than 12 years was 69.1%, affecting similar proportions of men and women (Table 1). The rates of ear infection rose
from 34.1% among those younger than 1 year to a maximum of 77.2% among 5-year-olds
before decreasing to 69.5% among 11-year-olds (data not shown). In bivariate
analysis, the risk of having any ear infection was lower in non-Hispanic blacks,
Mexican Americans, and those of other race than in non-Hispanic whites. Both
increasing PIR and level of educational attainment by the head of household
increased the risk for any ear infection in children. The risk also increased,
as expected, with attendance in day care but was not affected by whether the
child attended day care less than 10 or 10 or more hours per week (data not
shown). Birth weight less than 2500 g was associated with a decreased rate
of ear infections, but breastfeeding for longer than 4 months was not. In
addition, history of asthma and allergic symptoms were significantly associated
with an increased cumulative incidence of any ear infections, although chronic
bronchitis and hay fever were not. Of the variables significantly associated
with any ear infections in bivariate analysis, only educational level of head
of household did not continue to be a significant factor in multivariable
analysis (data not shown).
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Table 1. Effect of Demographic, Baseline, and Exposure Variables on
Cumulative Incidence of Ear Infections in Children Younger Than 12 Years*
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PASSIVE SMOKE EXPOSURE
Any passive smoke exposure occurred in 38%, any gestational smoke exposure
in 23%, and combined passive and gestational smoke exposure in 19% of children
younger than 12 years. Although any passive smoke exposure at home had no
statistically significant association with an increased risk of any ear infection
in children (adjusted RR, 1.01; 95% CI, 0.95-1.06), any maternal smoking during
pregnancy did confer a small increased risk for developing any ear infections
(adjusted RR, 1.08; 95% CI, 1.02-1.14) (Table 2). Whether the mother quit smoking during pregnancy did not
significantly alter the cumulative incidence of any ear infections in bivariate
analysis (74.5% for children whose mothers did quit vs 73.6% for those whose
mothers continued to smoke). Defining any ear infections as only those treated
by physicians decreased the cumulative incidence to 66.9% (data not shown).
This definition, however, did not change the risk of exposure to passive smoke
(adjusted RR, 1.01; 95% CI, 1.95-1.06) or maternal smoking during pregnancy
(adjusted RR, 1.08; 95% CI, 1.01-1.15).
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Table 2. Type of Smoke Exposure and Cumulative Incidence of Any Ear
Infection*
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DOSE OF PASSIVE SMOKE EXPOSURE
The dose of smoke exposure was quantified according to the number of
persons smoking at home, the number of cigarettes smoked at home, and the
composite variable of passive and gestational exposures (Table 3). The median serum cotinine levels rose with each increasing
ordinal category of passive smoke exposure, confirming the accuracy of statements
regarding the dose exposures. The occurrence of any ear infections was not
related to the number of persons (2 test for linear trend,
0.29; P<.60) or number of cigarettes smoked at
home (2 test for linear trend, 1.06; P<.40),
but there was a slight statistically significant increase in cumulative incidence
(adjusted RR, 1.07; 95% CI, 1.00-1.14) for combined exposure.
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Table 3. Smoke Exposure, Serum Cotinine Levels, and Cumulative Incidence
of Any Ear Infection*
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When the dose of passive smoke exposure was quantified according to
serum cotinine levels, no significant dose response was found in the cumulative
incidence of any ear infections (2 test for linear trend,
1.15; P<.30) (Table 4). Although the unadjusted RR for those with a serum cotinine
level less than 3 to 4 ng/mL was 1.14, the 95% CI included 1, and the RRs
for higher serum cotinine levels decreased rather than increased. Only the
unadjusted RRs are given to avoid numerical instability from too few denominator
degrees of freedom for the full multivariable logistic regression model.71
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Table 4. Effect of Serum Cotinine Levels on Cumulative Incidence of
Any Ear Infection*
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We analyzed the potential effect of comorbid conditions (asthma, chronic
bronchitis, hay fever, or allergic symptoms), passive smoke exposure, and
the cumulative incidence of any ear infections in multiple stratification
tables (data not shown). Within subgroups of children with these comorbid
conditions, however, passive smoke did not significantly change the cumulative
incidence of any ear infections.
RECURRENT EAR INFECTIONS
Table 5 presents the effect
of tobacco exposure on nonrecurrent vs recurrent ear infections. Their cumulative
incidence was not significantly altered by any passive smoking alone, but
any maternal smoking during pregnancy increased the risk of recurrent over
nonrecurrent ear infections. Furthermore, in the analysis of the composite
exposure variable, only the presence of both passive and gestational smoke
exposure produced a significantly increased risk of recurrent ear infection
(adjusted RR, 1.41; 95% CI, 1.09-1.78). Expressed as the number needed for
1 extra effect (calculated as the reciprocal of the absolute difference in
cumulative incidence between those who were and were not exposed to both passive
and gestational smoke),72 21 children must
be so exposed to result in 1 excess case of recurrent ear infections. However,
within the subgroup of children with recurrent ear infections, exposure to
passive smoke (crude RR, 0.97; 95% CI, 0.73-1.28), maternal smoking during
pregnancy (crude RR, 1.09; 95% CI, 0.78-1.53), or both (crude RR, 1.08; 95%
CI, 0.73-1.57) did not result in higher rates of tympanostomy tube placement
than no exposure. Only the unadjusted RRs are given here for the tympanostomy
tube placement data to avoid numerical instability from too few denominator
degrees of freedom for the full multivariable logistic regression model.71
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Table 5. Cumulative Incidence of Nonrecurrent vs Recurrent Ear Infections
by Type of Home Smoke Exposure*
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If the definition of recurrent was 3 or more ear infections, passive
smoking still did not significantly raise the risk of recurrent ear infections
(adjusted RR, 1.03; 95% CI, 0.90-1.24). Exposure to maternal smoking during
pregnancy or combined exposure continued to significantly increase the risk
of recurrent ear infections (adjusted RR, 1.19; 95% CI, 1.03-1.35; and adjusted
RR, 1.18; 95% CI, 1.01-1.36, respectively) with this definition of recurrence.
Other risk factors associated with recurrent ear infections differed
slightly from the risk factors associated with any ear infections. The risk
of recurrent ear infections continued to be lower among non-Hispanic blacks
(adjusted RR, 0.28; 95% CI, 0.22-0.36), Mexican Americans (adjusted RR, 0.52;
95% CI, 0.43-0.63), and those of other race (adjusted RR, 0.59; 95% CI, 0.34-0.98)
than in non-Hispanic whites; higher among those with a PIR of 2.00 or more
(adjusted RR, 1.76; 95% CI, 1.32-2.28) than those with a PIR less than 1.00;
higher in those attending day care (adjusted RR, 1.62; 95% CI, 1.31-1.96);
and higher in those with asthma (adjusted RR, 1.64; 95% CI, 1.32-2.09) or
allergic symptoms (adjusted RR, 1.68; 95% CI, 1.32-2.09 for nasal or ocular symptoms; and adjusted RR, 2.19; 95% CI, 1.78-2.65 for nasal and ocular symptoms). Educational level of the head of
household, birth weight, and breastfeeding duration were not significant factors
in multivariable analysis, but male sex had a small effect (adjusted RR, 1.23;
95% CI, 1.02-1.47).
COMMENT
Our results suggest that maternal smoking during pregnancy may be a
risk factor for ear infections and that the combination of gestational and
passive smoke exposure moderately increases the risk of recurrent ear infections.
Prior studies examining the effect of maternal smoking during pregnancy vs
ETS have reported conflicting results. In a cohort study that followed 5627
women from their first prenatal visit to 5 years postdelivery, Stathis et
al50 found that any amount of maternal smoking
at the first prenatal visit was associated with increased risk of acute ear
infections at 5 years postdelivery (1-9 cigarettes/d: OR, 1.6; 95% CI, 1.1-2.5;
10-19 cigarettes/d: OR, 2.6; 95% CI, 1.6-4.2; and 20+ cigarettes/d: OR, 3.3;
95% CI, 1.9-5.9). Smoking at the first prenatal visit was also associated
with increased subacute infections (1-9 cigarettes per day: OR, 1.7; 95% CI,
1.0-3.0; 10-19 cigarettes per day: OR, 2.6; 95% CI, 1.4-5.0; and 20+ cigarettes
per day: OR, 2.8; 95% CI, 1.3-6.0), and smoking 20 or more cigarettes per
day was associated with increased risk of ear surgery (OR, 2.9; 95% CI, 1.3-6.6).
Smoking during the third trimester and at 6 months and 5 years postdelivery,
however, did not increase the risk of acute OM, subacute ear infections, or
ear surgery. Ey et al17 followed up 1013 infants
from birth to 1 year of age and found that compared with children whose mothers
did not smoke, recurrent OM occurred more frequently in children whose mothers
were heavy smokers both during pregnancy and after delivery (32%), but not
when mothers smoked only during pregnancy (15%). In a cross-sectional study
of 2065 children aged 2 to 6 years, maternal smoking during the first
3 months of pregnancy increased the proportion of children who had acute OM
(RR, 1.16; P<.05).12
Smoking during the last 6 months of pregnancy also significantly raised the
proportion of children with acute OM, although the difference was "less striking."
In a study that used data from 2 cross-sectional surveys done in 1981 and
1988, recurrent OM occurred in 23.8% of children whose mothers smoked during
pregnancy and 22.7% of those whose mothers did not (OR, 1.1; 95% CI, 0.9-1.2).8
The current result for the effect of passive smoke exposure on any ear
infections is not consistent with the results of the 3 meta-analyses synthesizing
studies on passive smoking and OM.4, 48-49
Several explanations may account for this difference. One is that the true
effect of passive smoking on ear infections (if any exists) is probably small
(ie, RR <1.5), and uncontrolled confounding in this study may have moved
the estimated RR from a theoretical 1.25 to 1.01 in the current analysis.
Most children have an ear infection at some point, so looking at the cumulative
incidence of any ear infection may ultimately result in a RR near 1.0 for
risk factors that do not have a large impact. Another possible explanation
is that the risk attributed to parental smoking found in previous studies
may actually be driven by the combined effect of maternal smoking during pregnancy
and ETS during childhood, as found in the current study, but not separated
out. The magnitude of the effect of combined gestational and passive exposure
in this study (adjusted RR, 1.41) is in the same range as the results of the
3 meta-analyses. Those results showed small to moderate increased risk from
parental smoking, ranging from a RR of 1.19 for middle ear disease to an OR
of 1.74 for recurrent OM (ie, 3 episodes).4, 48-49
Because ORs poorly estimate the true RR when the prevalence or incidence of
an outcome exceeds 10%, the OR of 1.74 can be converted69
to an RR of 1.42 to 1.51 (for an estimated recurrent OM cumulative incidence
in the range of 20%-30%).
A limitation of this study is that ear infections are reported by proxy
in a questionnaire in the NHANES III survey, rather than documented by a physician.
Consequently, earache without ear infection, otitis externa, and ear-pulling
behavior in an infant may be included in proxy-reported "ear infections."
The cumulative incidence of "doctor-treated" ear infections in NHANES III,
however, was not significantly different from self-report (66% for any "doctor-treated"
ear infections vs 69% for self-report). We chose not to use the cumulative
incidence of "doctor-treated" ear infections because the questions regarding
the numbers of episodes of ear infections, which were used to define recurrence,
were based on self-report. In addition, when the National Health Interview
Survey used the same method of proxy-report, the 12-month cumulative incidence
of acute ear infections in 1994 was found to be 62.7% in those younger than
5 years,73 a result appropriately less than
the 69.1% noted in our study for ever having ear infections.
Other factors that may affect the accuracy of questionnaire-reported
ear infections include the number of infections, the duration of recall, and
the characteristics of the respondents. Daly et al74
found that compared with medical records, parents tended to overestimate the
number of episodes if they reported 6 or more episodes and underestimate them
if they reported fewer episodes. Pless and Pless75
showed that younger parents tended to recall more accurately than older parents
and mothers were more accurate than fathers. Alho76
found that questionnaire-based data tended to damp the associations between
various risk factors and acute OM. These same studies, however, have found
good to excellent concordance between parental report and medical records
for OM, suggesting that parental report is a reasonably valid approach.74-76 Also, when the analysis
in the current study was repeated in children younger than 3 years, a subgroup
in whom recall bias should be less, the results for passive smoking (adjusted
RR, 1.03; 95% CI, 0.97-1.09) and gestational smoking (adjusted RR, 1.08; 95%
CI, 1.02-1.14) are similar to those for the entire population.
Other limitations of the NHANES III data are that smoking behavior by
caregivers may be underreported and that only household exposures are noted
for ETS, without recognition of exposures in other settings (eg, a private
baby-sitter). Underreporting of smoke exposure may bias the analysis of the
effect of ETS on ear infections toward the null. A recent report using NHANES
III data examined the possible discrepancy between self-reported cigarette
smoking status and serum cotinine levels in adults, however, and concluded
that "self-reported smoking status among adult respondents to a population-based
survey conducted in a private medical setting is accurate."77
Because this current study used the same data source as that report, bias
from underreport likely has minimal effect on our results. The NHANES III
questionnaire does not differentiate among maternal, paternal, and other sources
of ETS within the home. Nevertheless, in Table 3, the children's median serum cotinine levels, a physiologic
measurement, show appropriately corresponding increases with the reported
doses of smoke exposure according to the number of persons who smoke and the
cumulative number of cigarettes. Therefore, ETS exposure inside the home significantly
influences serum cotinine levels in children and probably accounts for most
of the smoke exposure.
Additional limitations of this study come from the cross-sectional design
of the NHANES III survey. Although gestational smoke exposure necessarily
came before the onset of ear infections, ETS was ascertained at the time of
the survey rather than before the onset of infections. A potential association
between ETS and ear infections may be biased toward the null if children with
ear infections came from more households with ETS exposure in the past and/or
children without ear infections came from more households without ETS in the
past. Similarly, ear infection status was ascertained at the time of the survey
rather than at the time of infection, so that bias toward the null could occur
if fewer caregivers from smoking households recalled children having ear infections
than from nonsmoking households.
The socioeconomic and demographic risk factors in this study are similar
to those in another national cross-sectional survey of OM.8
In particular, rates of ear infections were inversely correlated with non-Hispanic
black and Mexican American race/ethnicity, but directly correlated with increasing
income levels. Two other studies have found elevated rates of OM with increasing
income16 and socioeconomic status.5 In contrast, however, another study found that rates
of OM or middle-ear effusion were increased by low socioeconomic status and
black race.9 The small statistically significant
increase of OM in the male sex has been documented in multiple reports.3, 5-6,8, 11, 16-17,36
Other important risk factors for recurrent ear infections in this study
include attendance in day care, which is almost universally found in other
studies of OM, and the presence of allergy or allergic symptoms, which is
usually found if these symptoms are studied. Breastfeeding, however, was not
a protective factor in this study, a phenomenon found in many studies5, 7-8,11, 13, 16, 18, 21-22,25, 35-36,39, 41, 44
but not in others that are often quoted.3, 6, 9, 17, 31
The heterogeneity of the sampled population in the NHANES III survey allowed
multiple socioeconomic and demographic factors to be analyzed simultaneously
and may account for the differences found in these factors.5, 7-8,11, 13, 16, 18, 21-22,25, 35-36,39, 41, 44
In conclusion, passive smoke exposure was not associated with an increased
risk of children ever experiencing ear infections in this study. The increased
risk found with gestational and combined smoke exposures has marginal clinical
significance. For recurrent ear infections, however, combined gestational
and passive smoke exposure had a clinically and statistically significant
effect, which may partially explain why maternal but not paternal smoking
has been found in some studies to increase the cumulative incidence of OM.
The results suggest that attempts to decrease the recurrence of OM should
consider interventions against maternal smoking during and after pregnancy.
| What This Study Adds
Although ETS exposure has been associated with a small increased risk
of OM in children, prior studies examining the effect of maternal smoking
during pregnancy vs ETS on the risk of ear infections in children have reported
conflicting results. These studies have not been able to determine the effect
of both of types of passive smoke exposures separately and in combination.
The study found that for recurrent ear infections, combined exposure
to ETS and maternal smoking during pregnancy had a clinically and statistically
significant effect. However, ETS was not associated with an increased risk
of children ever experiencing ear infections in this study, and the increased
risk found with maternal smoking during pregnancy and combined smoke exposures
had marginal clinical significance. The results suggest that attempts to decrease
the recurrence of otitis media should consider interventions against maternal
smoking both during and after pregnancy.
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AUTHOR INFORMATION
Accepted for publication October 25, 2001.
This study was presented at the Robert Wood Johnson Clinical Scholars
Program National Meeting, Fort Lauderdale, Fla, November 9, 2000.
Corresponding author and reprints: Judith E. C. Lieu, MD, Department
of Otolaryngology–Head and Neck Surgery, Washington University School
of Medicine, 1 Children's Place, Room 3S35, St Louis, MO 63110 (e-mail: lieuj{at}msnotes.wustl.edu).
From the Robert Wood Johnson Clinical Scholars Program, Yale University
School of Medicine, New Haven, Conn. Dr Lieu is now with the Department of
Otolaryngology–Head and Neck Surgery, Washington University School of
Medicine, St Louis, Mo.
Dr Feinstein died October 24, 2001.
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