PEDIATRICS Vol. 101 No. 2 February 1998, p. e8
ELECTRONIC ARTICLE:
The Burden of Environmental Tobacco Smoke Exposure on the
Respiratory Health of Children 2 Months Through 5 Years of Age in the
United States: Third National Health and Nutrition Examination Survey,
1988 to 1994
,
, and
From the * Center for Primary Care, Agency for Health Care
Policy and Research, Rockville, Maryland;
Klemm Analysis Group, Inc,
Hyattsville, Maryland; § National Center for Health Care Statistics,
Centers for Disease Control and Prevention, Hyattsville, Maryland; and
National Institute of Child Health and Human Development, National
Institutes of Health, Bethesda, Maryland.
| |
ABSTRACT |
|---|
|
|
|---|
Objective. To measure the effect of environmental tobacco smoke (ETS) on respiratory health in a national sample of young children.
Methods. The study evaluated children 2 months through 5 years of age participating in the Third National Health and Nutrition Examination Survey, 1988 to 1994. The group was a representative sample of the US population (N = 7680). A parental report of household smoking or maternal smoking during pregnancy ascertained ETS exposure. Respiratory outcomes were based on parental report of wheezing, cough, upper respiratory infection, or pneumonia in the last 12 months and chronic bronchitis or physician-diagnosed asthma at any time. Logistic regression was used to adjust for age, sex, race/ethnicity, birth weight, day care, family history of allergy, breastfeeding, education level of head of household, and household size.
Results. Approximately 38% of children were presently
exposed to ETS in the home, whereas 23.8% were exposed by maternal
smoking during pregnancy. ETS exposure increased chronic bronchitis and three or more episodes of wheezing among children 2 months to 2 years
old and asthma among children 2 months to 5 years old. For household
exposure, a consistent effect was seen only at
20 cigarettes smoked
per day. Adjusted odds ratios for increased risk (95% confidence
interval) for household exposures (
20 cigarettes smoked per day vs
none smoked) and maternal prenatal exposure (prenatal smoking vs no
smoking), respectively, for children 2 months to 2 years old were
chronic bronchitis, 2.5 (1.6, 4.1); 2.2, (1.6, 3); three or more
episodes of wheezing, 2.7 (1.7, 4.2), 2.1 (1.5, 2.9); and for children
2 months to 5 years old were asthma, 2.1 (1.4, 3.2); 1.8 (1.3, 2.6).
Reported use within the past month of prescription medications for
asthma (
-agonists or inhaled steroids) was not different between
those with asthma reporting ETS exposure and those reporting no
exposure; percent of patients with asthma reporting use of medication
by household exposure was 0, 25.7%; 1 to 19 cigarettes smoked per day,
32.9%; and
20 cigarettes smoked per day, 23.1%; percent of patients with asthma reporting use of medication by maternal smoking during pregnancy was no, 28.9%; yes, 22.7%. Among children 2 months to 2 years of age exposed to ETS, 40% to 60% of the cases of asthma, chronic bronchitis, and three or more episodes of wheezing were attributable to ETS exposure. For diagnosed asthma among children 2 months through 5 years old, there were 133 800 to 161 600 excess cases. Among exposed children 2 months through 2 years of age, there
were 61 000 to 79 200 excess cases of chronic bronchitis and 126 700
to 172 000 excess cases of three or more episodes of wheezing.
Conclusions. ETS exposure is common among children in the United States. The reported prevalence of asthma, wheezing, and chronic bronchitis was increased with ETS exposures. No statistically significant increase in the prevalence of upper respiratory infection, pneumonia, or cough was associated with ETS exposure. ETS exposure has little effect on the respiratory health of children between 3 and 5 years of age, with the exception of asthma. ETS appears to increase the prevalence of asthma rather than the severity as measured by medication use. These findings reinforce the need to reduce the exposure of young children to ETS.
Key words: environmental tobacco smoke (ETS), asthma, wheeze, chronic bronchitis, children, attributable risk.
Environmental tobacco smoke (ETS) is a highly prevalent
respiratory irritant. A recent metaanalyses concluded that ETS plays an
important role in the health of children.1 However, in
regard to respiratory health, the report noted there were gaps in the literature. Many of the samples studied were small and may not have
been suitable to generalization. Few studies have data on the many
factors that contribute to respiratory health in the first 5 years of
life (eg, birth weight, socioeconomic status, family history of atopy,
day care attendance, and so forth), thus making it impossible to
identify the independent contribution of ETS. The effect of ETS appears
to change depending on the age studied. Much of the work in young
children has focused on the first year of life, when a strong effect
has been reported consistently.2 The few studies that
have attempted to evaluate the change in the effect of ETS over the
first 5 or so years of life have found the effect of ETS is limited
primarily to the first several years of life.5,6
The Third National Health and Nutrition Examinations Survey (NHANES
III), a representative sample of the US population, offered a unique
dataset in which information on ETS exposure, respiratory health, and
cofactors was collected. The objectives of these analyses are to
evaluate the effect of ETS exposure on the reported respiratory health
of children 2 months through 5 years of age in the United States while
taking into account the relevant cofactors and to calculate the
excessive number of cases of the various respiratory conditions
attributable to ETS exposure.
Study Population and Sample Design
NHANES III was conducted from 1988 to 1994 by the National
Center for Health Statistics of the Centers for Disease Control and
Prevention, Atlanta, GA.7 A stratified multistage
clustered probability design was used to select a sample of the
civilian noninstitutionalized US population Demographic Characteristics
Age at the time of interview is reported as age in years at the
last birthday, except for children <1 year of age, for whom age in
months is reported. Self-reported race/ethnicity was categorized as
non-Hispanic white, non-Hispanic black, Mexican-American, or other. The
education level of the head of the household was the highest grade
completed. Household size was based on the number of persons living in
the house regardless of relationships.
Variable Definition
Parents were asked whether the child was ever breastfed or fed
breast milk and the age when the child stopped breastfeeding completely. Children who were breastfed until at least 1 month of age
were classified as ever breastfed. A family history of allergies was
the self-report of asthma or hay fever at any age in either biologic
parent. Day care was defined as attendance at a day care center or
nursery school where there were six or more children for at least 10 hours per week for 1 or more months. Birth weight was derived from
birth certificates (87.2%) and maternal report at the time of the
household interview (12.8%), when the birth certificate was not
available. Birth weight was used as a categoric variable in the
analyses: <2500 g, ETS Exposure
Reported ETS exposure was classified in two different ways:
current household exposure and maternal smoking at any time during the
pregnancy. Current household exposure was defined as the total number
of cigarettes smoked by household members in the house per day. Smoking
by visitors or guests was not asked. Three categories were defined:
none, 1 to 19 cigarettes smoked per day, and It was not possible to identify the mother among the reported smokers
in the household. However, information was collected on the biologic
mother's smoking during pregnancy. Maternal smoking during pregnancy
was used as a surrogate for current maternal smoking, because a high
percent of women who smoking during pregnancy continue smoking through
at least the first 5 years of the child's life.9,10
Statistical Methods
All estimates were calculated using the sampling weights to
represent children 2 months through 5 years of age in the United States. The sampling weights were created to adjust for unequal probabilities of selection and adjusted to account for nonresponse and
poststratified to the US population as estimated by the Bureau of the
Census. Statistical analyses were performed using
SUDAAN,11 a program that adjusted for the complex
sample design when calculating variance estimates. All confidence
intervals shown are at the 95% level.
Modeling and Attributable Risk
The association between exposure and outcome was evaluated by
analyzing stratified two-way contingency tables, testing the hypothesis
of independence versus general association. Linear contrasts were used
to evaluate differences in outcome proportions between groups exposed
to ETS and those not exposed. Logistic regression models were then
developed to account for other factors that might affect the
association between ETS exposure and each respiratory outcome. Separate
models were developed for the age groups 2 months through 2 years, 3 years through 5 years, and 2 months through 5 years, which included
main effects other than exposure only when they or interactions between
them were significant at P < .05.
Finally, the proportion of the prevalence of each outcome among exposed
groups that can be attributed to ETS was calculated from the logistic
model parameters.12 The resulting proportions were
multiplied by the estimates of the exposed population to obtain the
number of excess cases attributable to ETS. Totals for observations
with missing values were distributed among the categories in proportion
to the distributions of outcome by exposure for the sample of
observations with complete information.
Response Rate of the Interview Sample
Among white, black, and Mexican-American children 2 months
through 5 years of age (N = 8238) selected for
the NHANES III sample, 94.2% (n = 7763)
participated in the interview. Of those participating in the interview,
98.9% (n = 7680) had complete information on ETS exposure. The nonresponse for all other variables used in the
analyses within the group with complete data on ETS exposure was
<2.1%.
Exposure to ETS varied by the measure evaluated. Based on current
household exposure, 61.6% of the children lived in homes with no smoke
exposure, whereas 23.9% lived in homes where 1 to 19 cigarettes were
smoked per day and 14.5% in homes where Among all children, diagnosed asthma, chronic bronchitis, and three or
more episodes of wheezing increased with increased ETS exposure,
regardless of which measure of exposure was used (Table
1). For household exposure, the effect
was seen most consistently when ETS exposure was TABLE 1
![]()
INTRODUCTION
Top
Abstract
Introduction
Methods
Results
Discussion
Conclusion
References
![]()
METHODS
Top
Abstract
Introduction
Methods
Results
Discussion
Conclusion
References
2 months of age. A total
of 81 locations were selected for inclusion in the final sample. The
protocol included a home interview followed by a physical examination
in a mobile examination center. The study was approved by the National
Center for Health Statistics' Institutional Review Board.
2500 g. Medication use was defined as
the self-reported use of
-agonists or inhaled steroids within the
month before the household interview. Asthma and chronic bronchitis
required the self-report of a physician's diagnosis at any time in the
past. The number of self-reported episodes of wheezing or whistling in
the chest, cough, and upper respiratory infection (URI) during the past
12 months were categorized into two groups: none to two, and three or
more. Self-reported pneumonia during the past 12 months was categorized
as none, one or more, because of its infrequent occurrence.
20 cigarettes smoked per
day. Previous analyses from NHANES III reported that household exposure
was significantly associated with serum cotinine levels and accounted
for most of the explained variance in the regression models among
participants
4 years of age.8
![]()
RESULTS
Top
Abstract
Introduction
Methods
Results
Discussion
Conclusion
References
20 cigarettes were smoked
per day. Smoking during pregnancy was reported by 23.8% of the
biologic mothers. Mexican-American children were exposed to the lowest
levels of ETS, whereas non-Hispanic white children were exposed to the
highest levels. Little difference was seen by age or sex.
20 cigarettes per
day. Exposure to
20 cigarettes appeared to be protective for URI,
whereas smoking during pregnancy had no effect. The negative
association of ETS with URI disappeared after adjusting for
breastfeeding, day care, and race (data not shown). Pneumonia and three
or more episodes of cough showed no significant association to ETS and
were excluded from additional analyses.
Percent of Children 2 Months to 5 Years of Age With Respiratory
Outcomes by ETS Exposure
The effect of ETS varied by age (Table 2). When the sample was divided into two age groups (children 2 months to 2 years of age and children 3 years to 5 years of age), ETS was associated with diagnosed asthma, chronic bronchitis, and three or more episodes of wheezing in the younger age group. In the older age group, only the association between ETS and diagnosed asthma remained statistically significant.
|
Logistic regression analyses were performed to evaluate the role of
potential confounders on the relationship observed between ETS and
respiratory outcomes (Table 3). Models
were created for the all-ages group of children, for children 2 months
to 2 years of age, and for children 3 years to 5 years age groups
separately, using both definitions of ETS exposure. When ETS was
defined as household exposure, the strongest effect was seen
consistently in the 2 months to 2 years age group among children living
in households where
20 cigarettes were smoked per day, with the exception of diagnosed asthma, for which the adjusted odds ratios were
similar in the younger and older age groups. Similar results were seen
when ETS was defined as smoking during pregnancy.
|
Additional analyses investigated whether exposure to ETS increased the
use of asthma medication among children with asthma. Reported use
within the past month of prescription medications for asthma
(
-agonists or inhaled steroids) was not different between those with
asthma reporting ETS exposure and those reporting none; percent of
those with asthma reporting use of medication by household exposure:
none, 25.7%; 1 to 19 cigarettes smoked per day, 32.9%; and
20
cigarettes smoked per day, 23.1% (P > .4);
percent of those with asthma reporting use of medication by maternal
smoking during pregnancy: no, 28.9%; yes, 22.7%
(P > .30).
Attributable Risk
The excess number of cases attributable to ETS exposure after adjustment for the relevant confounders was calculated. The findings were similar regardless of the measure of ETS. The attributable risks ranged from 0.4 to 0.6 among children exposed to ETS at age 2 months to 2 years (Fig 1); that is, among children exposed, 40% to 60% of the cases of asthma, chronic bronchitis, and three or more episodes of wheezing were attributable to ETS exposure. For diagnosed asthma among children 2 months through 5 years old, there were 133 800 to 161 600 excess cases, whereas among children 2 months through 2 years old, there were 61 000 to 79 200 excess cases of chronic bronchitis, and 126 700 to 172 000 excess cases of three or more episodes of wheezing.
|
| |
DISCUSSION |
|---|
|
|
|---|
ETS exposure in the home is widespread among US children <6 years
of age (38%), and it plays an important, independent role in the
respiratory health of children
2 years of age. The levels of exposure
reported here are lower than those from the 1988 Child Health
Supplement (CHS) of the National Health Interview Survey (NHIS), in
which 42% of children
5 years of age were currently living in a
household with a smoker.13 Part of the difference may
be attributable to the ~1.2% decrease in smoking levels between 1988 and 1992 among women >18 years of age in the United
States.14
There is no ideal method to quantify a child's exposure to ETS.
Comparison of self-report with cotinine measures have found that both
give equivalent results when classifying children in regards to ETS
exposure.15 At the first well-child visit (6 to 8 weeks
of age), urine cotinine levels
10 µg/L were found in 8% of
nonsmoking homes, 44% in homes where someone other than the mother
smoked, 91% where only the mother smoked vs 96% where the mother and
another household member smoked.19 The authors concluded
that a screening questionnaire about household smoking was sufficient
to define a group of infants with urine cotinines
10 µg/L. Previous
analyses on Phase I (1988 to 1990) of NHANES III showed that among
children 4 to 11 years of age, serum cotinine levels were higher in
children with reported household exposure versus those with none
reported.8
Reported smoking during pregnancy has been shown to be an excellent surrogate measure for current maternal smoking during at least the first 5 years of life. A telephone follow-up study performed on participants from the 1985 NHIS reported that 70% of women who quit smoking during any part of their pregnancy resumed smoking within 1 year of delivery, with >93% of those resuming in the first 6 months.10 Data from the 1970 Child Health and Education Study in the United Kingdom, a birth cohort of all children born from April 5 to 11, 1970, found that >90% of the women who smoked during pregnancy were still smoking when their child reached 5 years of age.9
The number of smokers in the house is highly correlated with cotinine levels among children.20,21 However, maternal smoking has been shown to be the chief source of ETS exposure for children in the home.17,21 Maternal smoking behavior influences the smoking behavior of others. In a study of 433 infants at age 18 days, 75% of smoking mothers smoked near their infant and the amount smoked near the infant by the mother was correlated with the amount smoked by others near the infant.22
Day care does not seem to be a significant source of ETS exposure. Among English school children 5 to 7 years of age, only 8.7% of the children received child care from a smoker, and in 66% of the cases, the parent was also a smoker.21 Among children with asthma 8 months through 13 years of age studied in an allergy clinic, reported ETS exposure in day care was not an important determinant of the child's cotinine level once household exposure was accounted for.16 However in a nationwide study, day care has been shown to be an important factor contributing to the number of respiratory infections experienced by children 6 weeks through 17 months of age.23
In addition to the potential misclassification with respect to ETS exposure, a number of other issues may influence the findings of this study. Self-report was used to classify individuals in regards to their respiratory problems. Misunderstanding of the questions or use of unfamiliar terms may have resulted in nondifferential misclassification, which would tend to obscure any underlying association. Conversely, the effect of smoking on ETS may be attributable to an overreporting of symptoms by parents who smoke. Lebowitz and Burrows24 reported that the association between ETS and smoking exposure was no longer significant after controlling for the respiratory symptoms of the parents. Other studies have reported that the association of ETS on respiratory symptoms is not eliminated when taking into account parental respiratory symptoms.5,25 Finally, either the low prevalence of some of the respiratory effects or a small true effect of ETS on a particular respiratory outcome would reduced the power of this study to detect any true difference between the exposed and unexposed groups.
The NHANES III data add to the growing literature that with the
exception of asthma, the respiratory effects of ETS are limited to the
first few years of life among children
5 years of age. The reported
incidence of pneumonia and bronchitis was influenced by ETS only during
the first year of life in a birth cohort of >2200 children in England
followed to age 5 years.5 Maternal smoking was associated
with an increased rate of medical consultations for
bronchitis
pneumonia and maternal report of lower respiratory symptoms only in the first 2 years of life after adjustment for confounders in a birth cohort of ~1100 children followed annually from birth to 6 years of age in the Christchurch, New Zealand Child
Development Study.6 Although pneumonia was not
statistically significantly related to ETS in the NHANES III, even in
the 0 to 2 years age group, there appeared to be a tendency for
pneumonia to increase with increasing ETS exposure.
Similar results are seen from analyses of studies focusing on active
wheezing or wheezy bronchitis. In a case-control study of children 2 months to 16 years of age presenting to an emergency room with
wheezing, ETS exposure (salivary cotinine
10 ng/mL) was found to be
associated only with wheezing in children <2 years of
age.26 A case-control study of children 4 months to 4 years of age hospitalized for the first time for wheezy bronchitis
reported that parental smoking, especially maternal, was an important
factor in children <18 months of age.18 Data from the 1987 National Medical Expenditure Survey showed that maternal smoking was
significantly associated with asthma and wheezing combined only in the
0 to 2 years age group but not in the 3 to 18 years age
group.27
Only diagnosed asthma is associated with ETS exposure during the first 5 years of life. Interestingly, wheezing, the major symptom of asthma, was not associated with ETS in the older group. Other studies have reported previously that ETS exposure approximately doubles the prevalence of asthma in children.28,29 However, studies linking ETS to the incidence of asthma have found conflicting results. In Arizona, ETS exposure was associated only with the development of asthma if the mother had <12 years of education, but not among the children of more highly educated women.30 In Canada, only children with atopic dermatitis exposed to ETS developed asthma, whereas others exposed to ETS did not develop asthma31 and in New Zealand, ETS was not associated with the development of asthma.32
The role of ETS exposure on asthma severity is unclear. A previous
report from the 1981 CHS of the NHIS reported that ETS was associated
with the greater use of physician-prescribed asthma medication in the
last 2 weeks,29 whereas no association was seen in the
NHANES III. The variation in defining medication use may explain the
differences. In the 1981 CHS, a parent had to report the use of any
medication prescribed by a physician for asthma. This form of the
question does not eliminate the reporting of over-the-counter
medications such as decongestants or cough suppressants. The NHANES III
asked specifically about the name of the medication; the parent could
either show the bottle or report the name verbally. In our analyses, we
looked specifically at
-agonists and inhaled steroids, which are
specific therapies for asthma. It is also possible that a sufficient
number of sample persons whose asthma was aggravated by ETS avoided
exposure to ETS and thus remove any association between ETS and
severity in this cross-sectional study.
Studies using other measures of severity have reported conflicting results. Lower pulmonary functions and more reported acute exacerbations were found with ETS exposure among patients with asthma attending an allergy clinic.16 Among low-income urban children with asthma in New York City (average age, 9 years), passive smoking was associated with emergency room visits for asthma, but not with hospitalizations or abnormalities in pulmonary function.33 The effects of ETS on severity of asthma varied with age among patients evaluated at a Canadian allergy clinic. In the youngest group (1 to 6 years of age), no significant effect was found with exposure to smoke; in the middle age group (7 to 11 years of age), the children of smokers had an increase in their asthma score; and in the oldest group (12 to 17 years of age), the asthma symptom score was increased and the pulmonary functions were decreased in the children exposed to smoke.34 In a recent report on 22 children (mean age, 5 years) followed for 1 month after being hospitalized for asthma, children living with a smoker reported 1.9 fewer days of daytime symptoms than those not living with a smoker (P < .05); however, no statistically significant difference was found in the mean number of nighttime symptoms.35 Other studies reporting changes in ETS exposure did not find an association with acute attacks of asthma.36,37
A previous study used a national dataset to estimate the number of excess cases of disease from ETS. Approximately 38 000 excess cases of asthma and wheezing in children <18 years of age were reported from the 1987 National Medical Expenditure Survey.27 This probably is an overestimate because ETS was statistically significantly associated with ETS exposure only in children 0 to 2 years of age. However, the nonsignificant association in the older age group was included in their calculation.27 Our findings indicate ~13 400 to 16 200 excess cases of asthma among children 2 months through 5 years old. Among children 2 months through 2 years old, there were ~61 000 to 79 000 excess cases of chronic bronchitis and 127 000 to 172 000 cases of three or more episodes of wheezing.
| |
SUMMARY |
|---|
|
|
|---|
ETS exposure is common among children in the United States. The reported prevalence of asthma, wheezing, and chronic bronchitis was increased with ETS exposures. No statistically significant increase in the prevalence of URI, pneumonia, or cough was associated with ETS exposure. The exposure has little effect on the respiratory health of children 3 years through 5 years of age with the exception of asthma. ETS appears to increase the prevalence of asthma rather than the severity, as measured by medication use. These findings reinforce the need to reduce the exposure of young children to ETS.
| |
FOOTNOTES |
|---|
Received for publication May 1, 1997; accepted Oct 17, 1997.
Reprint requests to (P.J.G.) Agency for Health Care Policy and Research, CPCR, Room 502, 2101 E Jefferson St, Rockville, MD 20852.
| |
ABBREVIATIONS |
|---|
ETS, environmental tobacco smoke. NHANES III, the Third National Health and Nutrition Examination Survey. CHS, Child Health Supplement. NHIS, National Health Interview Survey. URI, upper respiratory infection.
| |
REFERENCES |
|---|
|
|
|---|
-
DiFranza JR,
Lew RA
Morbidity and mortality in children associated
with the use of tobacco products by other people.
Pediatrics.
1996;
97:560-568
[Abstract/Free Full Text] - Harlap S, Davies AM Infant admissions to hospital and maternal smoking. Lancet. 1974; 1:529-532[Medline]
- Leeder SR, Corkhill R, Irwig LM, Holland WW Influence of family factors on the incidence of lower respiratory illness during the first year of life. Br J Prev Soc Med 1976; 30:203-212[Medline]
-
Pedreira FA,
Guandolo VL,
Feroli EJ,
Mella GW,
Weiss IP
Involuntary smoking and incidence of respiratory illness during the first year of
life.
Pediatrics.
1985;
75:594-597
[Abstract/Free Full Text] - Colley JRT, Holland WW, Corkhill RT Influence of passive smoking and parental phlegm on pneumonia and bronchitis in early childhood. Lancet. 1974; 2:1031-1034[CrossRef][Medline]
- Fergusson DM, Hons BA, Horwood LJ Parental smoking and respiratory illness during early childhood: a six-year longitudinal study. Pediatr Pulmonol. 1985; 1:99-106[Medline]
- National Center for Health Statistics Plan and operation of the Third National Health and Nutrition Examination Survey, 1988-1994. Vital Health Stat. 1994; 1:32
-
Pirkle JL,
Flegal KM,
Bernert JT,
Brody DJ,
Etzel RA,
Maurer KR
Exposure of the US population to environmental tobacco smoke. The Third National Health and Nutrition Examination Survey, 1988-1991.
JAMA.
1996;
275:1233-1240
[Abstract/Free Full Text] -
Taylor B,
Wadsworth J
Maternal smoking during pregnancy and lower
respiratory tract illness in the early life.
Arch Dis Child.
1987;
62:786-791
[Abstract/Free Full Text] -
Fingerhut LA,
Kleinman JC,
Kendrick JS
Smoking before, during, and
after pregnancy.
Am J Public Health.
1990;
80:541-544
[Abstract/Free Full Text] - Shah BV, Barnwell BG, Bieler GS. SUDAAN User's Manual. Release 7.0. Research Triangle Park, NC: Research Triangle Institute; 1996
- Kleinbaum DG, Kupper LL, Morgenstern H. Epidemiologic Research Principles and Quantitative Methods. Belmont, CA: Lifetime Learning Publications; 1982:160
- Overpeck MD, Moss AJ. Children's Exposure to Environmental Cigarette Smoke Before and After Birth: Health of Our Nation's Children, United States, 1988. Hyattsville, MD: National Center for Health Statistics; 1991. Advance data from Vital and Health Statistics publication 202
- National Center for Health Statistics. Health, United States, 1994. Hyattsville, MD: US Public Health Service; 1995
- Greenberg RA, Haley NJ, Etzel RA, Loda FA Measuring the exposure of infants to tobacco smoke. Nicotine and cotinine in urine and saliva. N Engl J Med. 1984; 310:1075-1078[Abstract]
-
Chilmonczyk BA,
Salmun LM,
Megathlin KN,
Association between
exposure to environmental tobacco smoke and exacerbations of asthma in
children.
N Engl J Med.
1993;
328:1665-1669
[Abstract/Free Full Text] - Bakoula CG, Kafritsa YJ, Kavadias GD, Objective passive-smoking indicators and respiratory morbidity in young children. Lancet. 1995; 346:280-281[CrossRef][Medline]
- Rylander E, Pershagen G, Eriksson M, Bermann G Parental smoking, urinary cotinine, and wheezing bronchitis in children. Epidemiology. 1995; 6:289-293[Medline]
-
Chilmonczyk BA,
Knight GJ,
Palomaki GE,
Pulkkinen AJ,
Williams J,
Haddow JE
Environmental tobacco smoke exposure during infancy.
Am J Public Health.
1990;
80:1205-1208
[Abstract/Free Full Text] -
Jarvis MJ,
Strachan DP,
Feyerabend C
Determinants of passive smoking
in children in Edinburgh, Scotland.
Am J Public Health.
1992;
82:1225-1229
[Abstract/Free Full Text] -
Cook DG,
Whincup PH,
Jarvis MJ,
Strachan DP,
Papacosta O,
Bryant A
Passive exposure to tobacco smoke in children aged 5-7 years:
individual, family, and community factors.
Br Med J.
1994;
308:384-389
[Abstract/Free Full Text] - Greenberg RA, Bauman KE, Glover LH, Ecology of passive smoking by young infants. J Pediatr. 1989; 114:774-780[CrossRef][Medline]
-
Hurwitz ES,
Gunn WJ,
Pinsky PF,
Schonberger LB
Risk of respiratory
illness associated with day-care attendance: a nationwide study.
Pediatrics.
1991;
87:62-69
[Abstract/Free Full Text] -
Lebowitz MD,
Burrows B
Respiratory symptoms related to smoking habits
of family adults.
Chest.
1976;
69:48-50
[Abstract/Free Full Text] - Weiss ST, Tager IB, Speizer FE, Rosner B Persistent wheeze. Its relation to respiratory illness, cigarette smoking, and level of pulmonary function in a population sample of children. Am Rev Respir Dis. 1980; 122:697-707[Medline]
-
Duff AL,
Pomeranz ES,
Gelber LE,
Risk factors for acute wheezing
in infants and children: viruses, passive smoke, and IgE antibodies to
inhalant allergens.
Pediatrics.
1993;
92:535-540
[Abstract/Free Full Text] -
Stoddard JJ,
Miller T
Impact of parental smoking on the prevalence of
wheezing respiratory illness in children.
Am J
Epidemiol.
1995;
141:96-102
[Abstract/Free Full Text] -
Gortmaker SL,
Walker DK,
Jacobs FH,
Ruch-Ross H
Parental smoking and
the risk of childhood asthma.
Am J Public Health.
1982;
72:574-579
[Abstract/Free Full Text] -
Weitzman M,
Gortmaker S,
Walker DK,
Sobol MA
Maternal smoking and
childhood asthma.
Pediatrics.
1990;
85:505-511
[Abstract/Free Full Text] -
Martinez FD,
Cline M,
Burrows B
Increased incidence of asthma in
children of smoking mothers.
Pediatrics.
1992;
89:21-26
[Abstract/Free Full Text] - Murray AB, Morrison BJ It is children with atopic dermatitis who develop asthma more frequently if the mother smokes. J Allergy Clin Immunol. 1990; 86:732-739[CrossRef][Medline]
-
Horwood LJ,
Fergusson DM,
Hons BA,
Shannon FT
Social and familial
factors in the development of early childhood asthma.
Pediatrics.
1985;
75:859-868
[Abstract/Free Full Text] - Evans D, Levison MJ, Feldman CH, Clark NM, Wasilewski Y, Levin B, Mellins RB The impact of passive smoking on emergency room visits of urban children with asthma. Am Rev Respir Dis. 1987; 135:567-572[Medline]
-
Murray AB,
Morrison BJ
Passive smoking by asthmatics: its greater
effect on boys than on girls and on older than on younger children.
Pediatrics.
1989;
84:451-459
[Abstract/Free Full Text] -
Abulhosn RS,
Morray BH,
Llewellyn CE,
Redding GJ
Passive smoke
exposure impairs recovery after hospitalization for acute asthma.
Arch Pediatr Adolesc Med.
1997;
151:135-139
[Abstract/Free Full Text] - Ehrlich R, Kattan M, Godbold J, Childhood asthma and passive smoking. Urinary cotinine as a biomarker of exposure. Am Rev Respir Dis. 1992; 145:594-599[Medline]
- Ogborn CJ, Duggan AK, DeAngelis C Urinary cotinine as a measure of passive smoke exposure in asthmatic children. Clin Pediatr. 1994; 33:220-226
Pediatrics (ISSN 0031 4005). Copyright ©1998 by the American Academy of Pediatrics
This article has been cited by other articles:
![]() |
M. D. Klinnert, A. H. Liu, M. R. Pearson, M. C. Ellison, N. Budhiraja, and J. L. Robinson Short-term Impact of a Randomized Multifaceted Intervention for Wheezing Infants in Low-Income Families Arch Pediatr Adolesc Med, January 1, 2005; 159(1): 75 - 82. [Abstract] [Full Text] [PDF] |
||||
| ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||






