Association between Exposure to Environmental Tobacco Smoke and Exacerbations of Asthma in Children
Barbara A. Chilmonczyk, Luis M. Salmun, Keith N. Megathlin, Louis M. Neveux, Glenn E. Palomaki, George J. Knight, Andrea J. Pulkkinen, and James E. Haddow
Background Exposure to environmental tobacco smoke, as reportedby parents, has been linked to diminished pulmonary functionand more frequent exacerbations of asthma in children with thedisease. Further insight into this association might be gainedby using urine cotinine levels to measure actual exposure.
Methods We measured urine cotinine levels in 199 children withasthma; 145 also underwent pulmonary-function studies. A parentanswered questions about each child's exposure to environmentaltobacco smoke. Acute exacerbations of asthma during the precedingyear were documented through blinded review of medical records.Possible confounding factors were accounted for by the use ofmultivariate analysis and by comparisons of serum theophyllinelevels in exposed and unexposed children.
Results The median urine cotinine levels were 5.6 ng per milliliterin the 116 children reported not to have been exposed to tobaccosmoke, 13.1 ng per milliliter in the 53 children exposed tocigarette smoking by the mother or other persons, and 55.8 ngper milliliter in the 30 children exposed to cigarette smokingby the mother and other persons. Acute exacerbations of asthmaincreased with exposure, whether such exposure was reportedby a parent or identified on the basis of the cotinine level;the relative risks for the highest as compared with the lowestexposure category were 1.8 (95 percent confidence interval,1.4 to 2.2) for reported exposure and 1.7 (95 percent confidenceinterval, 1.4 to 2.1) for exposure indicated by cotinine levels.The forced expiratory volume in one second (FEV1), the forcedexpiratory flow between 25 and 75 percent of vital capacity,and the ratio of FEV1 to forced vital capacity also decreasedwith increases in both measures of exposure.
Conclusions Measurement of urine cotinine levels provides furtherevidence of an association between exposure to environmentaltobacco smoke and pulmonary morbidity in children with asthma.These data emphasize the need for systematic, persistent effortsto stop the exposure of children with asthma to environmentaltobacco smoke.
Asthma is the most common chronic lung disorder in children;it affects approximately 2 million to 5 million children inthe United States. Exposure to environmental tobacco smoke hasbeen reported to affect children with asthma adversely in avariety of ways; its effects include a decrease in pulmonaryfunction,1,2,3 an increase in airway reactivity,1,2,3,4,5,6and an increase in the frequency of visits to the emergencyroom for treatment of acute exacerbations of asthma7. Threestudies have suggested that children exposed to environmentaltobacco smoke may have a higher-than-average risk of asthma8,9,10.
To date, the published studies that have examined the consequencesof exposure to environmental tobacco smoke in children withasthma have relied exclusively on parents' reports of theirsmoking habits. Even reliable parental reports of exposure toenvironmental tobacco smoke could be relatively inaccurate,however, as a measure of children's actual inhalation of suchsmoke. Although this inaccuracy is not likely to interfere withanalyses comparing exposed and unexposed groups, it could makeit difficult to detect a dose-response relation. If cotininemeasurements were found to be consistent with parental reportsof children's exposure to environmental tobacco smoke, thismeasurement could provide additional validation for publishedstudies that have linked reported exposure to pulmonary morbidity.Moreover, if a dose-response relation were identified betweenmorbidity and cotinine levels, this relation would strengthenthe argument in favor of causality and lessen the possibilitythat exposure to environmental tobacco smoke serves only asa marker for other environmental or socioeconomic factors.
We used urine cotinine levels in addition to parental reportsto examine these questions further in a population of childrenwho were receiving ongoing specialized care for asthma. Cotinine,a metabolic derivative of nicotine, is excreted in the urineand serves as an accurate, short-term quantitative measure ofthe intake of tobacco smoke. The circulating half-life of cotinineis approximately 24 hours11,12. In this study, pulmonary-functionmeasurements and acute exacerbations of asthma were the health-relatedend points analyzed in relation to both parental reports ofexposure to environmental tobacco smoke and urine cotinine concentrations.
Methods
Study Population
From February 20 through May 9, 1992, 204 children with asthma(age, 8 months to 13 years) and the parents who accompaniedthem to routine visits at a large allergy-asthma practice inPortland, Maine, were asked by the office staff whether theywere willing to take part in a clinical study. The study hadbeen approved by the institutional review boards of the Foundationfor Blood Research and the Maine Medical Center. A total of199 pairs of children and parents agreed to participate, andthe parents gave written consent. At enrollment, each parentfilled out a questionnaire, and a urine sample was obtainedfrom each child. In addition to obtaining demographic data aboutthe child, the questionnaire sought information on the following:the parents' occupations and years of education completed; thenumber of people in the household; the age at which the childwas given a diagnosis of asthma; the child's current medicationstatus; the child's school status; use of day care outside ofthe home; smoking at the day-care site, including an estimateof the amount; the current smoking status of the accompanyingparent, including the number of cigarettes smoked per day andthe estimated number of hours per week of smoking in the home;and the current smoking status of all others in the household,including the estimated number of cigarettes (or cigars or pipes)smoked per day.
Pulmonary-function tests were also performed at enrollment inthe 145 children who were capable of performing the forced expiratorymaneuver. All the children's medical records were reviewed ina blinded fashion to determine the number of acute exacerbationsof asthma during the 12 months before enrollment and to obtaininformation about use of medications. Using published guidelinesfrom the National Heart, Lung, and Blood Institute,13 we classifiedasthma as mild in 47 of the children (23.6 percent), moderatelysevere in 145 (72.9 percent), and severe in 7 (3.5 percent).
Urine Cotinine and Creatinine Analyses
Urine samples were frozen and stored to be analyzed in batches.The measurement of cotinine was performed with use of an iodine-125competitive radioimmunoassay, the details of which have beenpreviously reported14. Creatinine was also measured in eachsample, with use of a commercially available kit (Sigma Diagnostics,St. Louis).
Statistical Analysis
In an earlier study,15 urine cotinine levels were found to beconsistent with exposure to environmental tobacco smoke at alevel of 10 ng per milliliter (57 nmol per liter) or higher.Continuous variables were compared by t-test after appropriatetransformations of the data. Categorical variables were comparedwith the chi-square test. Cotinine levels were corrected forthe concentration of the urine by fitting the relation betweenthe log cotinine level and the log creatinine level,16 withuse of a second-order curve. The dose-response relation betweenthe two measures of exposure to environmental tobacco smokeand the results of the four pulmonary-function tests was assumedto be linear. Stepwise multivariate linear-regression analysiswas, therefore, used to estimate the extent of the change inpulmonary function associated with increasing levels of exposure.In this analysis we controlled for the mother's age and educationlevel and the child's age, sex, and attendance at day care.To allow a direct comparison between reported exposure and cotininelevels, the cotinine cutoff points were chosen to include thesame number of children in each category of cotinine intakeas dictated by the reported exposure categories. All analyseswere performed with the BMDP statistical package17.
Results
Table 1 compares selected characteristics of the study populationaccording to the presence or absence of reported exposure toenvironmental tobacco smoke. According to parental reports,83 (42 percent) of the children were exposed to environmentaltobacco smoke. Boys predominated in both the nonexposed andthe exposed categories. In households where exposure to environmentaltobacco smoke was reported, the average age of the mothers wasyounger, they had fewer years of education, and children's enrollmentin day care was more frequent. Urine cotinine measurements weresignificantly higher when exposure to environmental tobaccosmoke was reported.
Table 1. Characteristics of Children with Asthma, According to Parental Reports of Exposure to Environmental Tobacco Smoke.
Figure 1 shows urine cotinine concentrations in relation toexposure to environmental tobacco smoke as reported by the parents.The median cotinine concentrations increased monotonically inthe three defined categories (no exposure to environmental tobaccosmoke, exposure to smoking by the mother or other persons, andexposure to smoking by the mother and other persons). Of the116 cotinine measurements in the group with no reported exposureto environmental tobacco smoke, 100 were below 10 ng per milliliter,a level previously established as consistent with minimal exposure;except for 1 cotinine measurement of 40 ng per milliliter (228nmol per liter), the highest level in this group was 20 ng permilliliter (114 nmol per liter). Of the 30 cotinine measurementsin the group with the highest reported level of exposure (smokingby the mother and other persons), all were above 10 ng per milliliter,and all but 3 were above 20 ng per milliliter. Cotinine measurementsin the intermediate-exposure group (smoking by the mother orother persons) were less consistent, indicating more variableintake of tobacco smoke. Reported exposure to environmentaltobacco smoke in the day-care setting did not add measurablyto the children's cotinine levels, over and above householdexposure. Table 2 shows the extent to which parental reportsof exposure to environmental tobacco smoke correlated with measurementsof cotinine in urine. Overall, when the cutoff level of 10 ngper milliliter was used for urine cotinine, the two methodsagreed for 164 of the 199 children.
Figure 1. Relation between Reported Exposure to Environmental Tobacco Smoke and Urine Cotinine Concentrations in 199 Children with Asthma.
Urine cotinine concentrations (corrected for the creatinine concentration) are represented on a logarithmic scale. Three mutually exclusive levels of exposure to environmental tobacco smoke reported by parents are shown. Solid circles identify children in day-care settings in which exposure to environmental tobacco smoke was reported. The horizontal line at 10 ng of cotinine per milliliter is an arbitrary demarcation point, above which exposure to environmental tobacco smoke was considered substantial. Median cotinine levels are indicated for the three exposure levels. To convert values for cotinine to nanomoles per liter, multiply by 5.7.
Table 2. Agreement between Urine Cotinine Levels and Reported Exposure to Environmental Tobacco Smoke in Children with Asthma.
Table 3 demonstrates that, as reported exposure to environmentaltobacco smoke increases, acute exacerbations of asthma increaseand pulmonary function decreases. A monotonic pattern of increasedmorbidity was found for acute exacerbations of asthma but notfor the measures of pulmonary function. The observed changesin the four measures of morbidity due to asthma for each increasein the category of exposure to environmental tobacco smoke wereinitially analyzed with use of simple linear regression analysis(observed) and then further analyzed with use of a multivariatelinear regression model that included the mother's age and educationlevel and the child's age, sex, and day-care attendance (adjusted).The 95 percent confidence intervals for the adjusted estimatesindicate that three of the four measures of morbidity were significantlyworse with increasing exposure to environmental tobacco smoke.For the number of acute exacerbations in the previous year,the adjusted relative risk for the highest as compared withthe lowest exposure category was 1.8 (95 percent confidenceinterval, 1.4 to 2.2).
Table 3. Current Pulmonary Function and Number of Acute Exacerbations of Asthma during the 12 Months before Enrollment, According to Reported Exposure to Environmental Tobacco Smoke.
Table 4 repeats the analyses in Table 3, but in this case weused urine cotinine measurements, rather than parental reports,to measure the intake of environmental tobacco smoke. The sametrends were found as in Table 3, but a monotonic pattern wasfound for both the increase in acute exacerbations of asthmaand the decrease in the measures of pulmonary function. Afteradjustment for potential confounders, the 95 percent confidenceintervals for three of the four measures indicated that significantlyincreased morbidity due to asthma was associated with the actualintake of environmental tobacco smoke. The relative risk forthe number of acute exacerbations of asthma in the previousyear in the highest as compared with the lowest intake categorywas 1.7 (95 percent confidence interval, 1.4 to 2.1), afteradjustment for possible confounders.
Table 4. Current Pulmonary Function and Number of Acute Exacerbations of Asthma during the 12 Months before Enrollment, According to Intake of Environmental Tobacco Smoke as Defined by the Urine Cotinine Level.
The extent to which the information provided by reported exposureto environmental tobacco smoke overlaps with that provided bycotinine measurements can be examined by testing the effectof adding one of these measures (cotinine levels or reportedexposure) to a multivariate model that already contains theother, along with possible confounders. When reported exposurewas tested in relation to acute exacerbations of asthma in thismultivariate model, it added significant predictive power (F= 5.99, P = 0.02), whereas cotinine levels did not (F = 0.05,P = 0.8). In relation to pulmonary function, neither cotininelevels nor reported exposure added significant predictive powerto a model already containing the other (for reported exposure:F = 0.35, P = 0.6 for the relation to the forced expiratoryvolume in one second [FEV1]; F = 0.48, P = 0.5 for the relationto the forced expiratory flow between 25 and 75 percent of vitalcapacity [FEF25-75]; and F = 1.01, P = 0.3 for the relationto the ratio of FEV1 to forced vital capacity [FVC]; for cotininemeasurements: F = 2.82, P = 0.1 for the relation to FEV1; F= 1.73, P = 0.2 for the relation to FEF25-75; and F = 2.01,P = 0.2 for the relation to FEV1:FVC).
Theophylline was prescribed for 104 of the 199 children withasthma during the year before enrollment, including 45 (54 percent)of the 83 exposed to environmental tobacco smoke and 59 (51percent) of the 116 not exposed. Serum theophylline levels wereavailable for 27 of the exposed children and 36 of the unexposedchildren. When more than one measurement was available for agiven child during the preceding year, only the first was includedin the analysis. Measurable theophylline levels were presentin all 63 of the children. The mean serum theophylline levelsof 11.37 µg per milliliter (62.5 µmol per liter)in the exposed children and 11.42 µg per milliliter (62.8µmol per liter) in the unexposed children were similar(t = -0.04, P = 0.97).
Discussion
Data from this study provide further validation of publishedreports that exposure to environmental tobacco smoke adverselyaffects the health of children with asthma1,2,3,4,5,6,7,8,9,18.Furthermore, the cotinine measurements in this study group provideinformation not previously available: parental reports indicatingno exposure to environmental tobacco smoke were consistent withcotinine measurements 86 percent of the time, and parental reportsindicating exposure were consistent with measured levels 77percent of the time. Discrepancies between parental reportsand cotinine measurements might be explained by incomplete knowledgeof exposure, on the one hand, or variability in environmentalconditions leading to diminished inhalation of environmentaltobacco smoke, on the other. Purposeful misreporting of smokinghabits is unusual11,12. Cotinine is a measure of actual recentintake of smoke from cigarette products and, as such, will notalways agree with the reported smoking habits of nearby persons.
Significant increases in the frequency of acute exacerbationsof asthma were found whether exposure to environmental tobaccosmoke was identified on the basis of parental reports or urinecotinine levels, and monotonic dose-response patterns were evidentwith both methods. Significant reductions in pulmonary functionwere also found, whether exposure to environmental tobacco smokewas assessed on the basis of parental report or cotinine level,and linear dose-response patterns were evident when the exposurewas defined by the cotinine level. The linear dose-responsepatterns provide further evidence of a causal relation betweenexposure to environmental tobacco smoke and pulmonary morbidityin children with asthma.
Some or all of the morbidity associated with exposure to environmentaltobacco smoke may be attributable to the differences betweenthe exposed and unexposed populations (Table 1). This possibleconfounding was taken into account in the multivariate analysessummarized in Table 3 and Table 4. The observed and adjustedvalues for each of the variables measured were not very different,indicating that, at most, only a small proportion of the observedrelation can be explained by confounding.
The theophylline levels in a subgroup of the study populationserved as a measure of compliance; they provide evidence thatthe exposed and unexposed children followed medical advice similarly.These levels were obtained in a nonstandardized fashion as partof routine management, and in nearly all instances the childrenhad been treated with theophylline for a considerable periodof time.
Our findings are consistent with the results of studies of infantsand children without asthma, in which more frequent respiratoryinfections and diminished pulmonary function were found to beassociated with reported exposure to environmental tobacco smoke19,20,21,22,23,24,25,26,27.Dose-response relations have been identified between the degreeof exposure to environmental tobacco smoke reported by parentsand pulmonary function in one cohort of children with asthma1,2and in several studies of children without asthma22,23,24,27.
The urine cotinine levels in the current study indicate thatparental reports are reliable when used to screen for exposureto environmental tobacco smoke in children with asthma. Theseobservations provide further support for the results of publishedstudies that rely on parental reports in examining the relationof exposure to environmental tobacco smoke and pulmonary morbidity.Urine cotinine levels can provide additional information whenexposure to environmental tobacco smoke is reported, both inassessing the degree of actual intake (with its attendant risks)and in monitoring efforts to reduce exposure. The evidence thatenvironmental tobacco smoke has a causal role in asthma-relatedmorbidity is sufficiently strong, and the adverse pulmonaryeffects are sufficiently great, that systematic efforts to reduceinhalation of environmental tobacco smoke are warranted forchildren with asthma.
Supported by a grant from the Maine Medical Center ResearchDepartment and by internal funding from the Foundation for BloodResearch.
We are indebted to Josephine Williams, data-management analystat the Foundation for Blood Research, for her assistance incoordinating the collection of data and patient samples; tothe office staff of Megathlin, Sigler, and Chilmonczyk for theirassistance in patient enrollment, urine collection, and dataretrieval; and to Robert Sigler, M.D., for referring some ofthe patients in the study.
Source Information
From the Foundation for Blood Research, Scarborough, Me. (B.A.C., L.M.N., G.E.P., G.J.K., A.J.P., J.E.H.); and the Maine Medical Center, Portland (B.A.C., L.M.S., K.N.M.).
Address reprint requests to Dr. Haddow at the Foundation for Blood Research, P.O. Box 190, Scarborough, ME 04070-0190.
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