Asthma Management and Environmental Tobacco Smoke Exposure Reduction in Latino Children: A Controlled Trial
Objectives. This study tested the efficacy of coaching to reduce environmental tobacco smoke (ETS) exposure among asthmatic Latino children.
Design. After asthma management education, families were randomly assigned to no additional service (control condition) or to coaching for ETS exposure reduction (experimental condition).
Setting. The study was conducted in San Diego, California.
Participants. Two hundred four Latino children (ages 3–17 years) with asthma participated.
Intervention. Approximately 1.5 hours of asthma management education was provided; experimental families also obtained 7 coaching sessions (∼45 minutes each) to reduce ETS exposure.
Outcome Measures. Reported ETS exposure and children’s urine cotinine were measured.
Results. Parents in the coached condition reported their children exposed to significantly fewer cigarettes than parents of control children by 4 months (postcoaching). Reported prevalence of exposed children decreased to 52% for the coached families, but only to 69% for controls. By month 4, mean cotinine levels decreased among coached and increased among control children. Cotinine prevalence decreased from 54% to 40% among coached families, while it increased from 43% to 49% among controls. However, cotinine levels decreased among controls to the same level achieved by coached families by the 13-month follow-up.
Conclusions. Asthma management education plus coaching can reduce ETS exposure more than expected from education alone, and decreases in the coached condition may be sustained for about a year. The delayed decrease in cotinine among controls is discussed.
Asthma prevalence and incidence rates have increased worldwide.1 US prevalence has increased 75% from 1980 to 1994,2 with the greatest increase during this period taking place among children up to 4 years (160% increase) and 5 to 14 years (74% increase). Poor minorities make up a disproportionate percentage of the increase in prevalence and incidence, and they have corresponding increases in severity of illness and mortality.3
In California, asthma is the most common cause of childhood hospitalizations,4 and poverty is the single most important risk factor for asthma hospitalization.5 Because Latinos in California are a relatively youthful population, Hispanic communities are particularly affected by increasing rates of asthma among the young.6 Latinos presently account for 32% of California’s population and ∼44% of the State’s children.7,8 At current rates of growth, Latinos, the fastest growing ethnic group in California,9 will comprise the majority of Californians within 40 years. Because about 1 in 3 families was without health insurance coverage in 1998,10 the potential impact of asthma among Latino children on the State is substantial.6 Clearly, more investigation and services to control asthma among Latino children are warranted.
Exacerbation of asthmatic symptoms is dependent, in part, on exposure to triggers, such as allergens, and irritants, such as environmental tobacco smoke (ETS).1 The World Health Organization has concluded that there is no evidence for a “safe” level of exposure to ETS11 and has estimated that the health of half of the world’s children is threatened by exposure to ETS.12 US prevalence ranges from 43% of children living in homes with a smoker,13 to state-specific estimates up to 34%. These suggest a US nationwide total of ∼15 million children and adolescents exposed to ETS.14 Childhood exposure rates in other countries include ∼43% in Australia,15 33% in Canada,16 and 41% in the United Kingdom.17 In addition to asthma, ETS exposure increases children’s risk of upper respiratory tract infections, otitis media, and sudden infant death syndrome.18–20 Meningitis infection21 is another possible consequence. Children’s annual medical care costs from ETS exposure were $703 to $897 million in the United States, $239.5 million in Canada, and $267 million in Great Britain (each in 1997 dollars).22 Approximately 20% of US children’s asthma is exacerbated by ETS exposure.23
To date, efforts to reduce ETS exposure for children exposed in their homes have been tested for children with respiratory disease and children without known respiratory or other serious illnesses. Our assumption is that these studies have been directed, implicitly, to families for whom smoking cessation is most difficult and for whom protecting the child from ETS has not been achieved. We believe most families, especially those with an ill child, quit smoking and/or adopt procedures to protect their children from ETS exposure. If these assumptions are correct, the majority of ETS intervention studies have addressed a subsample of the community for which cessation and/or changes in ETS exposure has been the most difficult. These are the subset of the population for whom more than community education and more than incidental physician advice may be required to protect their children from ETS exposure.24,25
Five previous trials have demonstrated significant decreases in children’s ETS exposure after parent counseling/coaching. Greenberg and colleagues26 studied children with pulmonary illness and decreased parent-reported exposure. However, urine cotinine (a major metabolite of nicotine) increased. Hovell and colleagues27,28 obtained a decrease in reported ETS exposure (verified by air nicotine assays) for asthmatic children that were sustained over 2 years, but did not report cotinine outcomes. Hovell and colleagues also achieved similar decreases in reported exposure among children free of asthma from low-income white, African American, and Latino families.29 Cotinine levels increased among control children and decreased slightly among those whose mothers obtained coaching for ETS exposure reduction. Emmons and associates30 used motivational interviewing/counseling with low-income minority families whose children were exposed to ETS in the home and reported significantly decreased ETS exposure as measured by nicotine dosimeter estimates from 1 of 2 rooms in the home. However, this study did not report cotinine or parent-reported ETS change. Wilson and colleagues31 were the first to combine children’s cotinine feedback with repeated counseling, reducing asthmatic children’s asthma-related health care use. However, this study did not report significant changes in ETS exposure based on parent reports, nicotine dosimeter, or cotinine assays. These studies suggest that coaching parents can decrease their child’s exposure to ETS, but only 1 has confirmed this with a biological marker of exposure.
The present study extended previous research by using urine cotinine as an outcome measure of in-home coaching (similar to our previous counseling) for low-income Latino families with an asthmatic child exposed to ETS. This study also extended the literature to date by providing coaching to the mother of the target child even if the mother was not the smoker (72%) in the family. We hypothesized that coaching plus asthma management education would decrease children’s reported exposure and urine cotinine more than asthma management education alone.
Families were eligible if they had an asthmatic child 1) from 3 to 17 years of age, 2) whose natural parent(s) was Latino or Hispanic, 3) who lived in a home with at least one smoker, and 4) who had reported exposure to at least 6 cigarettes in the previous week. We adopted 6 cigarettes of ETS exposure to insure sufficient exposure to maximize our probability of detecting differences between controls and coached groups.
Families were recruited from San Diego County, California, with cooperation from multiple agencies and through media. Sources included agencies of the San Diego County supplemental nutrition program for Women, Infants & Children, community clinics, public schools, health fairs, newspaper ads, radio announcements, and flyers/posters. Interested families were contacted by telephone for screening. Twelve hundred telephone screenings, spanning February 1997 through March 1999, identified 317 potential families based on child’s age, parent ethnicity, child’s diagnosis of asthma, and a smoker living in the home (Fig 1). Of these, 281 completed an additional screening conducted in their home. Sixty-seven were ineligible, and 58 of these were ineligible because of the child’s ETS exposure falling below 6 cigarettes/week. During the subsequent baseline interview (n = 214), another 10 families were identified as ineligible; leading to 204 who officially entered the study. One caregiver in each household completed interviews, participated in asthma education, and if assigned, participated in ETS coaching. Ninety-eight percent of these “target” caregivers were the children’s mothers. (For convenience, we refer to these caregivers simply as “mothers.”)
Timeline and Random Assignment
A total of 6 measurement interviews were conducted: baseline, 1 week post-asthma education (week 2), post-ETS coaching (month 4), and follow-ups at months 7, 10, and 13. All families were provided with asthma management education the week after the first baseline measures. One week after the asthma management education, all families repeated another complete battery of measures and were then assigned at random to coaching or control conditions. An Excel (Microsoft, Redmond, WA) computer-generated list of random 3-digit numbers was constructed by clinic site (stratum), including 1 stratum for all “other” recruitment sources (eg, media). Participants were assigned to the coaching condition and control condition based on numbers ending with even and odd digits, respectively. Research assistants notified families assigned to the intervention. Control families were unaware of coaching procedures and continued in the study for measurement purposes only. Interviewers were blind to group assignment and investigators were blind to results until all data were collected.
Trained Latina assistants delivered asthma management education in English or Spanish. The curriculum covered the cause of asthma, methods of control, and medication use, adapted from the 1994 Allergy and Asthma Foundation of America manual “You Can Control Asthma.” Education was offered as 1 or 2 in-home sessions (total time in minutes: mean: 108; standard deviation: 24) with as many family members as possible attending. Asthma education included a review of common asthma triggers in the home, including recommendations to reduce triggers (eg, minimize dust, keep pets outside), and to reduce ETS exposure. In addition, recommendations were provided for implementing environmental controls, such as obtaining plastic pillowcases and encasing mattresses, and for administration of maintenance and rescue medications. As part of the asthma education parents were advised not to expose their child to smoke, not to smoke in the home, and to quit if possible. However, no specific advice was provided as to how to achieve changes in tobacco use. Educators stressed the importance of ongoing medical care to manage asthma and referred families to available medical services as appropriate. Families were given a medication plan form and encouraged to bring it to the child’s next medical visit to help establish an asthma management plan with a physician. Peak flow meters were provided to all children and educators demonstrated how to use them and supervised the child’s practice using peak flow meters. Improvements in knowledge, decreased exposure to triggers, including ETS, and increased use of controller medication following asthma education was validated and reported earlier.32
Coaching for ETS reduction was based on previous research experience.27,29 The intervention was labeled “coaching” because it more accurately describes this activity than does the previous term, “counseling.” The process of behavior change requires ongoing shaping toward the “target” behavior, and, once established, usually requires ongoing support for maintenance. Hence, the process is akin to coaching sports, in which ongoing guidance is required to improve performance and to help adapt to unforeseen challenges. Families in the coaching condition were told that the goal was to help them reduce/eliminate their child’s exposure to ETS. Although coaches explained that smoking cessation was the means by which the greatest decrease in their child’s ETS exposure and simultaneous reduction in the parent’s risk could be achieved, attempting to quit was not required for participation in the study. This approach seemed especially important in light of the fact that 72% of the mothers were not smokers and, thus, needed training to reduce the child’s exposure from all sources in the home. In our previous ETS studies, we tested 6 to 7 sessions, and in each instance an important proportion of families had not yet reduced their child’s exposure to near zero by the time the intervention ended. Thus, for this study, coaching was provided for 7 in-home 30- to 45-minute sessions over 3 months plus a “booster” phone call. Coaching included contingency contracting and shaping procedures.33 Contingency contracts detailed target behaviors to be attained and rewards that family members provided for one another for achieving objectives.
At the first coaching session, mothers set long-term behavioral goals for reducing children’s ETS exposure and signed 3-month contingency contracts. Coaches explained the behavior shaping process, and, during each session, mothers reported the residents’ recent smoking behavior and the children’s exposure on pictorial charts. Mothers were provided with no-smoking signs and stickers to serve as cues to reduce exposure. Prescription-like forms were completed to set 2-week goals for each family. In subsequent sessions, coaches reviewed individual progress and negotiated possible solutions to reported barriers to ETS exposure reduction. For example, if the mother complained that the child did his homework near the father while he smoked, the mother might offer a special “prize” if the child completed homework in another room. Other objectives and strategies were then discussed, and a revised 2-week goal was determined. Contingencies for caregiver behavior included praise and congratulations from coaches as outcomes for progress. During the last session, mothers were assisted in writing final goals/objectives for maintaining or for attempting additional decreases in ETS exposure.
To build rapport, engender trust, and provide continuity, the same person who conducted the asthma education served as a coach for families assigned to the intervention. Coaches were nonprofessional Latinas from the same community with limited college experience and a few who were completing their masters in public health or psychology. All were trained during an 8-hour workshop. All participated in weekly case review meetings, where individual families were discussed and where supervisors and investigators provided suggestions for coaching approaches that might work with particular individuals and where supervisors and investigators provided feedback to enhance coaching skills more generally.
Families assigned to the control condition participated only in repeated measurements and asthma management education.
The baseline interview included information regarding demographics, general medical and asthma status, smoking and ETS exposure history. Detailed smoking and ETS exposure measures were obtained at each follow-up interview. The tobacco assessment covered a 1-week recall period. Because the majority (ie, 72%) of mothers were not smokers, and to improve proxy reports,34,35 a “time-line follow-back” (TLFB) interview procedure was created, similar to those used for other health risk behaviors.36–39 This involved the interviewer asking the mother to report the detailed activities of the target child from the time of awakening to going to sleep for each of 7 days, starting with the day before the interview and then reviewing each of the 6 preceding days. Interviewers first probed for special days or events that might be more memorable “anchors” (eg, birthdays, visitors, illnesses, etc). More routine activities were then recorded. For each discrete activity (such as “eating breakfast”) and less specific activities (such as “visiting grandma”), the interviewer asked whether the child was exposed to tobacco smoke, who the smoker was (target participant, other parent, other relative, other nonrelative), and to how many cigarettes the child was exposed. They reported exposure by others living in and visiting the home, and from all smokers outside of the home. Reported exposure was the number of cigarettes smoked while the child was in the same room or car as the smokers. The TLFB interview covered the week concurrent with the collection of the children’s urine samples.
Children’s average daily exposure to all ETS sources was computed based on the TLFB interview. Acceptable 5-day test-retest reliability (r = 0.69; P < .001) and validity in relation to the children’s urine cotinine (r = 0.34–0.47; all P < .001) were obtained. This is similar to correlations from other studies.40,41
Child’s Urine Cotinine
Urine was analyzed for cotinine at the Centers for Disease Control and Prevention, using isotope-dilution liquid chromatography-tandem mass spectrometry with a limit of detection of <50 parts per trillion (0.05 ng/mL).42 Children’s samples were collected using a sterile urine collection cup. Samples were frozen at −20°C and packed in dry ice for shipping. The laboratory was blind to participant identification and group assignment.
For each measurement period, the urine samples were collected the day of the interview (supervised by a research assistant), 2 days before the interview (collected by the mother alone), and 4 days before the interview (supervised by a research assistant). Mothers were taught how to obtain a clean catch, provided with containers, and instructed to store the urine in their freezer for later retrieval by the research assistant. The mean of the 3 samples was computed for analysis for the target week to obtain more stable estimates of each child’s cotinine for the week.
All cotinine analyses were performed in accordance with Clinical Laboratory Improvement Act guidelines in the Division of Laboratory Science, National Code for Environmental Health (Centers for Disease Control and Prevention), and all results were from runs confirmed to be in statistical control by quality control/quality assurance evaluations. Assay validity was periodically confirmed by an in-house proficiency-testing program using National Institute for Standards and Technology cotinine in urine Reference Material #8444 (NIST, Gaithersburg, MD), and also blank urine samples spiked with known amounts of cotinine perchlorate. In addition, reliability estimates for split-half urine samples resulted in correlations exceeding r = 0.99 (P < .001). Among the 3 samples collected 2 days apart each, within the week (ie, test-retest), high reliability (Pearson’s r = 0.84–0.86; all P < .001) was obtained, and the combination of all measures provided the most reliable estimate (intraclass correlation coefficient for an averaged measure = 0.94; 95% confidence interval: 0.93–0.96) of cotinine level for the target week.
Air Nicotine Monitors, Bogus Pipeline Measures
Air nicotine dosimeters43,44 were placed in 3 rooms where children’s greatest ETS exposure was reported. Monitors were used primarily as a “bogus pipeline” procedure45 to sensitize mothers to possible confirmation of their reports and to enhance reporting accuracy. Monitors consisted of a 37-mm diameter cassette similar to ones used in previous studies.43,44 Monitors were placed on lamp shades and other convenient places as near to the smoker as possible in each room. Because of limited resources, active nicotine dosimeters (Yale University Environmental Health Sciences, New Haven, CT) were used only for 20% of the sample and only for baseline and posttest measures. The remaining 80% of the sample received inactive dosimeters (Lermer, Garwood, NJ).
Parent’s Saliva Cotinine
Saliva samples were obtained only from mothers who reported quitting during the course of the study. These samples were used to confirm reported cessation. Saliva was collected from each quitter at the visit when she reported quitting, and each subsequent follow-up visit that she reported having remained quit. Saliva was collected using the Episcreen saliva collection device (Epitope Co; Beaverton, OR). After collection the samples were shipped to the Neurochemistry Laboratory, Dartmouth-Hitchcock Medical Center (Lebanon, NY), where they were stored at −70°C until assayed. Cotinine was analyzed by enzyme-linked immunoassay available in kit form from STC Corp (Bethlehem, PA). The assay is a competitive microplate assay for determination of cotinine in saliva. A 5-point standard curve was run with each plate. The standards were analyzed in duplicate and range from 1 to 100 ng/mL. Saliva samples were diluted as needed and reanalyzed to provide results that may be quantified from the standard curve. Quality assurance and blank samples were assayed with standards and samples regularly. Cessation was judged as “verified” if the cotinine level was <10 ng/mL. The manufacturer of the test kits (OraSure Technologies, Inc, Bethlehem, PA) reported a limit of detection of 3 ng/mL.
Analyses followed the intent-to-treat rule. Families that dropped before randomization were excluded from outcome analyses. Urine cotinine and parent-report measures were subjected to logarithmic transformations to adjust for skewed distributions and heterogeneous residual variances. The statistical analyses were based on the generalized estimating equations (GEE) approach46 with time as a within-subjects factor, group (coaching, usual care), a between-subjects factor, and the group x time interaction to capture differential change over time. Time intervals between interviews, and the duration of the coaching intervention, varied among participants. The GEE strategy preserves the interindividual variability in the follow-up assessments to be modeled as the number of days that elapsed since the postintervention interview. GEE models are particularly suited for this design, because they do not require repeated measures to be equally spaced from one another, and they retain cases with missing data over time.
The xtgee module of Stata 747 was used to estimate these models. For quantitative response variables (level of exposure), the identity link function, Gaussian error distribution, and exchangeable correlation structures were specified. For dichotomous response variables (prevalence of exposure), the logit link function, binomial error distribution, and exchangeable correlation structures were specified. To determine the immediate coaching effects, we investigated differential change from baseline to the end of the coaching intervention (4-month measures). To investigate maintenance of change, we tested change from the 4-month measure to the 13-month measure. We hypothesized that ETS exposure may change in a curvilinear fashion in response to the intervention such that a larger decline occurs immediately after the intervention, followed by smaller declines and possible increases. To model such curvilinear change patterns, linear, quadratic, and cubic terms of time (ie, days since intervention) were entered to test for linear, quadratic, and cubic main effects of time and time-by-group interactions.
No significant differences between assigned groups were found for any of 30 baseline variables (including demographics, child’s health and health care utilization, and child’s ETS exposure), suggesting successful random assignment.
Cohort Retention and Tests for Differential Attrition
Eleven families dropped out of the study before randomization (resulting n = 193 for analysis). Five families (3 control, 2 coaching) dropped between randomization and the final measure at month 13. The 16 total dropouts did not differ from completers on 29 of the same 30 tested baseline variables, suggesting little or no sampling bias attributable to attrition. However, nonmaternal participants were more likely than mothers to drop out of the study (6% [12 of 197] of mothers dropped out of the study, compared with 57% [4 of 7] of nonmaternal participants who dropped out). As stated above, attrition also did not differ by group assignment.
Of the 97 families assigned to the experimental group, 95 (98%) mothers completed all 7 face-to-face coaching sessions.
Table 1 shows the demographic characteristics of the mothers and children for the 193 families randomized in the study. The majority of the sample was of Mexican descent, less than half of the mothers had completed high school, ∼35% of the families had no medical insurance, and 58% were covered by government programs for low-income families. The majority of asthmatic children took medication for asthma, but few were prescribed inhaled corticosteroids. Over half attended the emergency department or were hospitalized for respiratory problems in the last year. The families were predominantly low income and first generation immigrants from Mexico with limited education and limited access to medical care.
Immediate Coaching Effect
Figure 2 shows a decline in the number of cigarettes/day to which the children were exposed. After the asthma education sessions, ETS exposure decreased between baseline and the 2-week measure by essentially the same magnitude for both the control and the coached groups. After random assignment, the slope for reported ETS exposure sharply decreased for the coached group compared with the controls, between the 2-week measure and the 4-month postcoaching measure. GEE analyses for parent-reported exposure levels revealed a significant time × group interaction (linear effect of time P < .01), indicating that exposure levels in the coaching group dropped from a mean of 2.25 to 0.57 cigarettes/day, approximately a 75% decrease in baseline level, whereas exposure levels decreased less in the usual care group, from a mean of 2.12 to 1.11 cigarettes/day, about a 50% decrease from baseline level.
To better understand the practical significance of these changes in average levels of reported exposure, we defined a dichotomous exposure variable that takes on a value of 0 for parent-reports of zero cigarettes of exposure (ie, not exposed) and a value of 1 for parent-reports of 1 or more cigarettes of exposure (ie, exposed). Figure 3 shows the decline in proportion of children exposed to ETS in each group. Again, statistically significant time × group interaction effects (linear P < .05; quadratic P < .05) indicated a decline in ETS exposure from 97% to 52% in the coaching group and a less dramatic decline from 93% to 69% in the control group, by the fourth month measure.
Urine Cotinine Levels
Figure 4 shows a decline in level of cotinine over time for the coaching group and an increase in level, similar in magnitude, for the asthma management control group. Findings from the GEE analyses for urine cotinine levels revealed a significant linear time × group interaction (P < .05), indicating that urine cotinine levels in the coaching group dropped from 1.44.to 1.19 ng/mL, while cotinine levels increased in the usual care group from 1.17 to 1.35 ng/mL.
Similar to parent-reported exposure, we defined a dichotomous exposure variable that takes on a value of 0 for urine cotinine levels less than or equal to 1.00 ng/mL (ie, not exposed) and a value of 1 for cotinine levels >1.00 ng/mL (ie, exposed). The cut point of 1.00 ng/mL was based on the average cotinine level found in nonsmoking children who live in homes where no smoking occurs (range: 0.6–1.8 ng/mL13,48–50 converted from serum and saliva cotinine values to urine cotinine values using ratios of 5:1 for serum and 1.1:1–1.4:1 for saliva51). For those with less than or equal to 1.00 ng/mL, our label of “not exposed” means that they seem similar to children from other studies13,48,49 who were reportedly not exposed to ETS in the home. They may be exposed to residential or nonresidential ETS at very low levels or several days before assessment, or exposed to other sources such as nicotine off-gassing from surfaces, dietary exposure, etc. This low level may represent the lowest exposure level attainable by prevention of residential exposure to ETS. GEE analyses revealed a statistically significant linear time × group interaction effect (P < .01), indicating a decline in ETS exposure prevalence from 54% to 40% in the coaching group and an increase from 43% to 49% in the control group (Fig 5). These findings suggest that coaching resulted in more children avoiding all ETS exposure in their home than did control procedures.
Maintenance and Follow-up Effects
In the coaching group, average parent-reported exposure levels continued to decline over the follow-up period from 0.57 to 0.47 cigarettes/day. In the usual care group, the level declined from 1.11 to 0.71 cigarettes/day. The GEE analyses for parent-reported exposure revealed significant group (P < .05) and time (linear P < .01) main effects. In combination, these findings indicate that exposure levels continued to decline in both groups and that the coaching intervention effect persisted to the 13-month follow-up measure.
These findings were confirmed in GEE analyses of the dichotomous reported exposure prevalence variable. Statistically significant time (linear P < .01) and group (P < .05) main effects indicated that the exposure prevalence based on parent-reports declined approximately the same in both groups during the follow-up period, from 52% to 45% in the coaching group and from 69% to 54% in the usual care group. Thus, group differentials in level and trajectory were sustained through follow-up for prevalence based on reported number of cigarettes to which children were exposed.
Urine Cotinine Levels
In the coaching group, average urine cotinine levels continued to decline over the follow-up period from 1.19 to.97 ng/mL. In the usual care group, mean level declined from 1.35 to 0.86 ng/mL. Findings from the GEE analyses for urine cotinine levels revealed a significant linear time × group interaction (P < .05). Similarly, a significant linear time × group interaction effect (P < .05) indicated that the exposure prevalence based on urine cotinine levels declined over the follow-up period from 40% to 32% in the coaching group and from 49% to 31% in the usual care group to essentially the same prevalence level. Inspection of the patterns of change during the follow-up period shows that each group’s trajectory was different from one another from the post-measure at 4 months through the 7-month follow-up measure. This suggests maintenance of effects from coaching and no additional (beyond that attributable to asthma management education plus measurement effects) decrease in cotinine among the control families at the 7-month follow-up. The coached families’ cotinine remained essentially stable from month 7 to month 13, but the controls decreased to essentially the same levels.
Mothers’ Smoking and Cessation
Seventeen mothers (8 coaching, 9 control: χ2 not significant) who were daily smokers at baseline reported quitting during the study. Saliva was collected from only 13 mothers (5 coaching, 8 control): every one of these quits was confirmed via cotinine assays. Nine of the 13 mothers also provided saliva collections at subsequent visits (range: 1–4 repeat collections). All repeated cotinine assays confirmed maintenance of cessation. GEE models of the child’s cotinine changes were recomputed including smoking status of mothers (daily smoker versus occasional or nonsmoker) as a potential moderator. In none of the 4 models did mother’s smoking status reach significance, and the variable was deleted from the final models.
The Department of Health and Human Services has reported health service disparities for low-income and minority populations.52 A large proportion of the racial/ethnic differences in asthma prevalence in the study by Litonjua et al53 was explained by factors related to income, area of residence, and level of education. Children living in poverty are at increased risk for asthma hospitalization.5,54 Differential medical care utilization rates and higher asthma-related hospitalization and mortality rates have been documented for Latinos, and several studies have shown that racial/ethnic effects persist when socioeconomic status is controlled.55 Lower rates of medical insurance, partly because of less job-based insurance,56,57 cultural and language barriers,58,59 and lack of citizenship60 result in inferior access to health care for Latinos. Inadequate care for asthma serves to perpetuate existing asthma, contributing to illness, reduced quality of life, and hospitalizations for Latinos.61 Christiansen et al62 reported a high prevalence of asthma-related symptoms in a sample of San Diego Latino school children from socioeconomically disadvantaged families. The present sample of Latino families seems to come from such a population, with limited education, limited medical insurance, and limited medical services for their asthmatic child. Control of ETS exposure among high-risk Latinos could improve their children’s asthma management and the families’ quality of life.
This study’s procedural fidelity was confirmed by documentation of reliability and validity of measures, by high cohort retention (188/204 = 92% at the 13-month measure), by successful random assignment and by no apparent sampling bias because of the few who were lost to follow-up. In addition, the measurement staff, the coaching staff, the families, and the investigators were blind to experimental conditions, substantially reducing the likelihood of bias.
This study was designed to determine the efficacy of coaching Latino parents to reduce their asthmatic child’s ETS exposure. Five other trials demonstrated significant decrease in ETS exposure associated with similar coaching procedures.26,27, 29–31 However, this is the first to show that ETS can be decreased for Latino asthmatic children as demonstrated by both change in reported and cotinine estimates of ETS exposure. This is also the first to demonstrate that coaching for families in which ∼72% of the mothers were not smokers resulted in significant decreases in ETS exposure. This is also the first study to show the effect of coaching for ETS exposure reduction after a relatively extensive in-home asthma management education program that included tobacco as one of the “triggers” to be avoided.
The coached families decreased their children’s cotinine, whereas cotinine levels increased in the usual care group. These results suggest that coaching is efficacious—a conclusion supported by the results from the previous controlled trials. This result is all the more profound given the relatively low level of exposure observed at the baseline measures.
It is not surprising that the absolute level of exposure reported and that implied by cotinine assays was relatively low at baseline (eg, geometric mean of ∼2.25 cigarettes/week) for this sample. This was probably attributable to relatively low rates of smoking among Mexican immigrants in general,63,64 and because the majority of the mothers were nonsmokers, limiting ETS exposure to that coming from fathers and other family members. Under these circumstances the mothers were provided with coaching and then were responsible in most instances for changing other family members’ smoking practices or removing the child from the presence of others when they were smoking. This may be especially difficult in families where the mother is expected to defer to the father. Low exposure levels at baseline make it difficult to further reduce exposure and to detect differential changes in ETS exposure. Despite the low baseline exposure levels, this study was able to demonstrate that coaching may be efficacious even for families where the mother (who is typically the recipient of coaching) is not a smoker, and for families where the children are exposed to relatively low levels of ETS before asthma management and coaching for ETS reduction.
The effects of coaching as assessed by cotinine show relatively small differences between the posttest means (eg, 1.19 ng/mL and 1.35 ng/mL) for the 2 experimental conditions. This raises questions about clinical significance. Risks from ETS exposure among asthmatic children can be assumed to be both acute and cumulative. It is not yet known how low a dose of exposure can be tolerated by an asthmatic child without suffering acute exacerbations of his/her asthma. If such a dose exists, it likely depends on many other variables, including the severity of asthma, concurrent exposure to other triggers, and the activity of the child at the time of exposure. Thus, it is difficult to define a safe level of exposure for acute outcomes.
For asthmatic and children free of asthma, cumulative exposure to ETS has been associated with a wide-range of morbidity, and it may be instrumental in promoting smoking as a teen or early adult. Again, the details concerning a threshold dose that defines clinically significant cumulative dose that may increase risk is not yet known. This likely depends on many factors, including individual differences, critical periods of exposure (eg, infancy), as well as the duration and acute and cumulative dose of tobacco smoke to which a child may be exposed. Because tobacco smoke contains several recognized toxins and carcinogens, and because the particle size of the smoke alone may be considered toxic, the best public health and preventive medicine policy may be to assume no safe level of ETS exposure.11,65,66
Nevertheless, differences between 1.19 ng/mL and 1.35 ng/mL might not represent real differences in an individual’s cotinine level and would not be likely to convey a real difference in risk, even if both levels represent increased risk compared with no exposure. This logic implies that changes in an individual’s cotinine from 1.19 ng/mL to 1.35 ng/mL or vice versa, would not represent a clinically important change in level or risk. However, these differences in this study represent mean estimates of population differences. The distribution around these means suggests that substantially fewer children among coached families were exposed to relatively high levels of nicotine. Results also represent the trajectory of change in cotinine for the 2 groups during the intervention period—increasing for the controls and decreasing after coaching. These patterns imply that without coaching, cumulative exposures would be substantially higher, while the coached families would be substantially lower over time. The continued decrease among coached families during the follow-up period confirmed the generalization of cumulative change observed during the coached condition. If these patterns and generalizations are correct, coaching can be expected to reduce ETS exposure cumulatively to near zero and to sustain this level long enough to make a clinically meaningful decrease in risk for the population, even if it is not yet possible to predict which individual children might benefit.
Follow-up analyses showed that subsequent to the coaching phase, the experimental group families obtained additional decreases in ETS exposure (by report and cotinine measures), albeit at a slower rate, and stabilized at a mean exposure of ∼0.5 cigarettes from parent reports. Control families showed a mean of ∼0.7 cigarettes of exposure and this stable difference between conditions is consistent with our previous findings of maintenance of coaching effects28,29 and suggest lasting effects after coaching. The mean cotinine for children in the coaching condition decreased and stabilized at ∼1.10 ng/mL during the 9-month follow-up. This sustained low level achieved after coaching suggests maintenance of the coaching effects and supports the same conclusion based on the reported level of ETS exposure.
The control families’ children showed a mean cotinine level of 1.35 ng/mL at the end of the intervention phase. This level did not change appreciably between the 4-month and 7-month follow-up measures. The sustained higher level of cotinine among controls for the first 3 or more months of follow-up confirms the level of ETS exposure was greater for the controls than coached families for at least 3 months. During this same period, the average cotinine level continued to drop slightly in the coached condition. This pattern of results contributes to a judgment of both an initial coaching effect and maintenance of the group differential for at least 3 months.
However, additional follow-up results were somewhat puzzling in that the control group’s mean cotinine level decreased between the 7-month and 13-month follow-up measure to near 1.0 ng/mL on average. This decrease in the middle of the follow-up period is difficult to explain.
Because the study involved sequential recruitment over about 2 years, the decrease in cotinine visible in the follow-up period took place at very different calendar times across participants. This suggests that the change is attributable to study participation experience, and not to a single event that took place at one point in time. This design feature essentially rules out a discrete confounding event, such as other tobacco control interventions. This anomaly may not be explainable without replication in future studies that include assessment of measurement reactivity and other possible confounding variables, especially those related to cumulative time in the study.
The effects of coaching and the possible effects of measurement and/or asthma management education are all the more powerful, given the conditions under which they were tested. Latino families tend not to expose their children to as much ETS as other racial/ethnic groups.63,64 The families recruited to this trial underwent extensive screening and asthma management education before they were assigned at random to coaching or control conditions, a process followed by, and possibly accounting for, a relatively low average level of ETS exposure for both groups at the “precoaching” measure. Both groups reported their child exposed to an average of ∼2 cigarettes/day, and both showed a mean of <1.5 ng/mL cotinine at the same measure. Baseline reported levels of ETS exposure approximated the levels achieved by the end of coaching in previously reported trials.27,29 The low baseline cotinine levels approached the levels that could represent background exposure (eg, 1.0 ng/mL). These unexpected results of our selection and screening procedures reduced the “room for improvement” by approaching practical floor levels of ETS exposure and thereby reduced the power to detect change, let alone differential change in ETS exposure. Thus, the significant group by time changes observed for coaching and for follow-up periods is more remarkable. These findings suggest that the changes observed are both real and reflect compelling “intervention” effects, effects that might yield greater decreases for Latino children exposed to higher ETS levels.
Finally, this study was conducted in California, a state with one of the largest and most aggressive anti-tobacco control programs ever initiated.67–69 The initial effects of coaching and the possible effects of asthma management education and/or measures over the follow-up period might be attributable, in part, to independent effects or interactions with statewide anti-tobacco control efforts. Although investigators outside California have found similar results for coaching effects, no long-term follow-up studies have been conducted to date outside California. Thus, it remains important to replicate the coaching and “control” conditions in this study in other states and to do so with at least 1 year of follow-up assessment, to determine possible maintenance or continued decreases in ETS exposure in communities where tobacco control programs are less extensive.
The importance of the current findings is underscored by a recent $1.5 million public health initiative by the US Environmental Protection Agency to promote prevention of children’s residential ETS exposure.70 This is the sixth trial to verify reduction in ETS exposure among children and the first to do so using cotinine outcome measures for Latino children with asthma. Results demonstrated that asthma management education plus coaching for ETS exposure reduction decreased ETS exposure more than asthma management alone. These data confirmed that coaching is efficacious. The follow-up assessment showed that children’s ETS exposure continued to decrease over time and stabilized by the 10- to 13-month follow-up measures. This shows maintenance of the initial decrease in ETS exposure. However, follow-up measures for controls show a different and unexpected pattern, where after 3 or more months of stable and relatively high ETS exposure, a decrease in cotinine level was observed. This result raises questions about possible delayed effects of participating in asthma management education, reactivity to repeated measures, and possibly nonspecific effects of participation in trials in general. Replication of the current study and follow-up will be required to verify coaching results with Latino families with an asthmatic child, and future studies should explore the degree to which time in the trial (or factors related to time in the trial) are associated with changes in reported or cotinine estimates of ETS exposure during follow-up.
Assessment of the effects of coaching plus asthma management versus asthma management alone showed essentially the same pattern of results obtained in our last ETS trial for which we had both reported and cotinine outcome measures.29 The overall intervention effects also replicate all of the methodologically strong trials to date that have tested coaching/counseling interventions. Thus, we believe these results support the conclusion that coaching Latino mothers with an asthmatic child exposed to tobacco smoke in their home is efficacious for reducing the child’s ETS exposure. Future studies should determine the effects of similar asthma management education plus ETS coaching when used in clinical practices. Future studies also should test the effects of combining ETS coaching with smoking cessation counseling, especially for parents who are not initially inclined to quit. Results from this study suggest that ETS exposure can be reduced reliably by coaching and that once reduced levels remain low for almost a year. This sets the stage for larger-scale trials with sufficient power to test the effects of lowering ETS on morbidity among asthmatic or other children with compromised health status.
This research was supported by grant HL52835 (to Dr Hovell) from the National Heart, Lung, and Blood Institute, National Institutes of Health; and by discretionary funds from the Center for Behavioral Epidemiology and Community Health.
- ↵National Institutes of Health. Global Strategy for Asthma Management and Prevention: NHLBI/WHO Workshop Report. National Heart, Lung, and Blood Institute, National Institutes of Health; 1995. NIH Publ. No. 95-3659
- ↵Mannino DM, Homa DM, Pertowski CA, et al. Surveillance for Asthma—United States, 1960–1995. MMWR Morb Mortal Wkly Rep.1998;47(SS-1) :1– 28
- ↵English PB, Von Behren J, Harnly M, Neutra RR. Childhood asthma along the United States/Mexican border: hospitalizations and air quality in two California counties. Pan Am J Public Health.1998;3 :392– 399
- ↵Flegal C. Confronting Asthma in California’s Latino Communities. San Francisco, CA: Latino Issues Forum; 1999
- ↵US Census Bureau. Census 2000 Data for the State of California. Available at: http://www.census.gov/press-release/www/2001/tables/redist_ca.html
- ↵State of California, Department of Finance. County Population Projections with Age, Sex and Race/Ethnic Detail. Sacramento, CA; December 1998
- ↵State of California, Department of Finance. County Population Projections with Race/Ethnic Detail. Sacramento, CA; December 1998
- ↵Schauffler H, Brown R, McMenamin S, Cubanski J, Rice T. The State of Health Insurance in California, 1998. Berkeley, CA: Health Insurance Policy Program, Center for Health and Public Policy Studies, University of California, Berkeley, and UCLA Center for Health Policy Research; 1999
- ↵World Health Organization. Air Quality Guidelines for Europe. 2nd ed. WHO Regional Publications; 2000. European Series No. 91
- ↵World Health Organization, Division of Noncommunicable Diseases, Tobacco Free Initiative. International consultation on environmental tobacco smoke (ETS) and child health. Consultation Report. 1999. Available at: http://tobacco.who.int/en/health/int-consult.html. Accessed August 29, 2001
- ↵National Health and Medical Research Council. The Health Effects of Passive Smoking. Canberra, Australia: NHMRC; 1997
- ↵Physicians for a Smoke-Free Canada. One in three kids’ health at risk from household smoke, doctors warn. 1999. Available at: http://www.smoke-free.ca/eng_home/news_press_Jun99.htm. Accessed August 29, 2001
- ↵Jarvis MJ. Children’s exposure to passive smoking: survey methodology and monitoring trends. Background paper. 1999. Available at: http://tobacco.who.int/en/health/background-papers-ets.html. Accessed August 29, 2001
- ↵US Department of Health and Human Services (PHS), NIH, US Environmental Protection Agency. Respiratory Health Effects of Passive Smoking: Lung Cancer and Other Disorders. Washington, DC: Office of Research and Development, Office of Air and Radiation, 1993. NIH Publ. No. 93-3605
- ↵Adams EK, Melvin C, Merritt R, Worrall B. The Costs of Environmental Tobacco Smoke (ETS): An International Review. Available at: http://tobacco.who.int/en/health/background-papers-ets.html. Accessed August 29, 2001
- ↵US Environmental Protection Agency. Respiratory Health Effects of Passive Smoking: Lung Cancer and Other Disorders. US Environmental Protection Agency, Office of Research and Development, Office of Health and Environmental Assessment; 1992. EPA Publ. No. EPA/600/6-90/006F
- ↵Hovell MF, Zakarian JM, Wahlgren DR, Matt GE. Reducing children’s exposure to environmental tobacco smoke: the empirical evidence and directions for future research. Tobacco Control.2000;9(suppl 2) :40– 47
- ↵Hovell MF, Wahlgren DR, Zakarian JM, Matt GE. Reducing children’s exposure to environmental tobacco smoke: a review and recommendations. In: Watson RR, Witten M, eds. Environmental Tobacco Smoke. Boca Raton, FL: CRC Press; 2001
- ↵Hovell MF, Zakarian JM, Matt GE, Hofstetter CR, Bernert JT, Pirkle J. Effect of counseling mothers on their children’s exposure to environmental tobacco smoke: randomised controlled trial. Br Med J.2000;321 :337– 342
- ↵Emmons KM, Hammond SK, Fava JL, Velicer WF, Evans JL, Monroe AD. A randomized trial to reduce passive smoke exposure in low-income households with young children. Pediatrics.2001;108 :18– 24
- ↵Mattaini MA, Thyer B, eds. Finding Solutions to Social Problems: Behavioral Strategies for Change. Washington, DC: American Psychological Association; 1996
- ↵Matt GE, Wahlgren DR, Hovell MF, et al. Measuring ETS exposure in infants and young children through urine cotinine and memory-based parental reports: empirical findings and discussion. Tobacco Control.1999;8 :282– 289
- ↵Hovell MF, Zakarian JM, Wahlgren DR, Meltzer SB, Matt GE, Emmons K. Measurement of environmental tobacco smoke exposure: trials and tribulations. Tobacco Control.2000;9(suppl 3) :22– 28
- ↵Bernert JT, Turner WE, Pirkle JL, et al. Development and validation of sensitive method for determination of serum cotinine in smokers and nonsmokers by liquid chromatography/atmospheric pressure ionization tandem mass spectrometry. Clin Chem.1997;43 :2281– 2291
- ↵Diggle PJ, Liang KY, Zeger SL. Analysis of Longitudinal Data. Oxford, United Kingdom: Clarendon Press; 1995
- ↵Stata Corp. Stata Statistical Software: Release 7.0. College Station, TX: Stata Corporation; 2000
- ↵Jarvis MJ, Russell MAH, Feyerabend C, et al. Passive exposure to tobacco smoke: saliva cotinine concentrations in a representative population sample of nonsmoking schoolchildren. Br Med J (Clin Res Ed).1985;291 :927– 929
- ↵Cook DG, Whincup DH, Jarvis MJ, et al. Passive exposure to tobacco smoke in children 5–7 aged years: individual, family, and community factors. Br Med J.1994;308 :384– 389
- ↵Floro JN, Mexia MC, Matt GE. The validity of proxy-reported second-hand smoke exposure in children. Poster presentation at the Western Psychological Association 80th Annual Convention; April 13-April 16, 2000; Portland, OR
- ↵Benowitz NL. Cotinine as a biomarker of environmental tobacco smoke exposure. Epidemiol Rev.1996;18 :188– 204
- ↵US Department of Health and Human Services. Strategic Research Plan to Reduce and Ultimately Eliminate Health Disparities: Fiscal Years 2002–2006. Washington, DC: National Institutes of Health; 2000
- ↵Brown ER, Wyn R, Ojeda VD. Noncitizen Children’s Rising Uninsured Rates Threaten Access to Health Care. Policy Brief. Los Angeles, CA: UCLA Center for Health Policy Research; 1999
- ↵Levan R, Brown ER, Hays N, Wyn R. Disparity in Job-based Health Coverage Places California’s Latinos at Risk of Being Uninsured. Policy Brief. Los Angeles, CA: UCLA Center for Health Policy Research; April 1999
- ↵Wood PR, Hidalgo HA, Prihoda TJ, Kromer ME. Hispanic children with asthma: morbidity. Pediatrics.1993;91 :62– 69
- ↵National Coalition of Hispanic Health and Human Services Organizations (COSSMHO). Hispanic environmental health: ambient and indoor air pollution. Otolaryngol Head Neck Surg.1996;114 :256– 264
- ↵Gergen PJ, Fowler JA, Maurer KR, Davis WW, Overpeck MD. 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. Pediatrics.1998;101(2) . Available at: http://www.pediatrics.org/cgi/content/full/101/2/e8
- ↵Berman BA, Wong GC, Bastani R, et al. Household smoking behavior and ETS exposure among children with asthma in low-income, minority households. Addict Behav. In press
- ↵California Environmental Protection Agency. Health Effects of Exposure to Environmental Tobacco Smoke. Sacramento, CA: California Environmental Protection Agency, Office of Environmental Health Hazard Assessment. September 1997
- ↵European Environment Agency. Children’s Health and Environment: A Review of Evidence. A Joint Report From the European Environment Agency and the WHO Regional Office for Europe. Luxembourg: Office for Official Publications of the European Communities; 2002. Environmental issue report no. 29
- ↵Traynor MP, Glantz SA. California’s tobacco tax initiative: the development and passage of Proposition 99. J Health Polit Policy Law.1996;21 :543– 585
- Tobacco Control Section. California Tobacco Control Update. Sacramento, CA: California Department of Health Services; 2000. Available at: http://www.dhs.cahwnet.gov/ps/cdic/ccb/tcs/index.htm. Accessed September 7, 2001
- ↵EPA Administrator Whitman to announce new environmental health initiative to protect children from secondhand smoke [press release]. Consumer Federation of America Foundation. Available online: http://www.consumerfed.org/epa_ets_pressconf.pdf. Accessed October 16, 2001
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