A Controlled Trial of an Environmental Tobacco Smoke Reduction Intervention in Low-Income Children With Asthma

A Controlled Trial of an Environmental Tobacco Smoke Reduction Intervention in Low-Income Children With Asthma* Sandra R. Wilson, PhD; Eileen G. Yamada, MD, MPH; Reddivalam Sudhakar, MD; Lauro Roberto, MD; David Mannino, MD, FCCP; Carolina Mejia, BA; and Nancy Huss, RN Study objectives: To determine the effectiveness of a cotinine-feedback, behaviorally based education intervention in reducing environmental tobacco smoke (ETS) exposure and health-care utilization of children with asthma. Design: Randomized controlled trial of educational intervention vs usual care. Setting: The pediatric pulmonary service of a regional pediatric hospital. Participants: ETS-exposed, Medicaid/Medi-Cal-eligible, predominantly minority children who were 3 to 12 years old and who were seen for asthma in the hospital’s emergency, inpatient, and outpatient services departments (n ⴝ 87). Intervention: Three nurse-led sessions employing behavior-changing strategies and basic asthma education and that incorporated repeated feedback on the child’s urinary cotinine level. Measurements: The primary measurements were the urinary cotinine/creatinine ratio (CCR) and the number of acute asthma medical visits. The secondary measurements were number of hospitalizations, smoking restrictions in home, amount smoked, reported exposures of children, and asthma control. Results: The intervention was associated with a significantly lower odds ratio (OR) for more than one acute asthma medical visit in the follow-up year, after adjusting for baseline visits (total visits, 87; OR, 0.32; p ⴝ 0.03), and a comparably sized but nonsignificant OR for one or more hospitalization (OR, 0.34; p ⴝ 0.14). The follow-up CCR measurement and the determination of whether smoking was prohibited inside the home strongly favored the intervention group (n ⴝ 51) (mean difference in CCR adjusted for baseline, ⴚ0.38; p ⴝ 0.26; n ⴝ 51) (60; OR [for proportion of subjects prohibiting smoking], 0.24; p ⴝ 0.11; n ⴝ 60). Conclusions: This intervention significantly reduced asthma health-care utilization in ETSexposed, low-income, minority children. Effects sizes for urine cotinine and proportion prohibiting smoking were moderate to large but not statistically significant, possibly the result of reduced precision due to the loss of patients to active follow-up. Improving ETS reduction interventions and understanding their mechanism of action on asthma outcomes requires further controlled trials that measure ETS exposure and behavioral and disease outcomes concurrently. (CHEST 2001; 120:1709 –1722) Key words: asthma; behavior change; children; controlled trial; cotinine; education; environmental tobacco smoke; low-income Abbreviations: CCR ⫽ cotinine/creatinine ratio; ED ⫽ emergency department; ETS ⫽ environmental tobacco smoke; ICS ⫽ inhaled corticosteroid; IRB ⫽ institutional review board; OR ⫽ odds ratio; ORa ⫽ adjusted odds ratio; ORu ⫽ unadjusted odds ratio; VCH ⫽ Valley Children’s Hospital

tobacco smoke (ETS) exposure E nvironmental has adverse consequences for respiratory health, and there is a well-documented association between long-term ETS exposure and the exacerbation of

asthma in children.1–3 The meta-analysis by Cook and Strachan3 concluded that parental smoking was associated with the increased prevalence of asthma and respiratory symptoms and that, among children who

*From the Department of Health Services Research (Dr. Wilson and Ms. Mejia), Palo Alto Medical Foundation Research Institute, Palo Alto, CA; Chronic Disease Control Branch (Dr. Yamada), California Department of Health Services, Sacramento, CA; Pediatric Pulmonary Department (Drs. Sudhakar and Roberto, and Ms. Huss), Valley Children’s Hospital, Madera, CA; and US Centers for Disease Control and Prevention (Dr. Mannino), Atlanta, GA. This research was supported by award No. U60/CCU912212

from the US Centers for Disease Control and Prevention and by the Medi-Cal Special Projects Section and Tobacco Control Section, California Department of Health Services. Manuscript received October 13, 2000; revision accepted March 29, 2001. Correspondence to: Sandra R. Wilson, PhD, Department of Health Services Research, Palo Alto Medical Foundation Research Institute, 795 El Camino Real, Ames Bldg, Palo Alto, CA 94301; e-mail: [email protected] CHEST / 120 / 5 / NOVEMBER, 2001

1709

had already developed asthma, parental smoking was associated with more severe disease that increased the incidence of emergency department (ED) visits, lifethreatening attacks, and asthma symptoms.3 Other expert reviews have drawn similar conclusions,4 – 6 most recently that maternal smoking during pregnancy is associated with an increased likelihood of wheezing with respiratory illness and contributes to the development of asthma in very young children. The fact that adverse health consequences of ETS exposure for children with asthma have been documented in virtually all the relevant studies suggests that the current prevalence and intensity of exposure are clinically important, despite overall decreases in the rate of smoking in the US population. The California Tobacco Survey, for example, found that in 1996, 87% of all California children and adolescents were “protected” from ETS exposure in the home by restrictions on smoking or by a complete ban.7 However, only 65% of families with a child 0 to 5 years of age in which there was a smoker reported that they restricted or prohibited smoking in the home. In those families in which all adults smoked, only 40% claimed they restricted or prohibited smoking inside the home. California smoking rates are lower than those in many other states2 and countries, suggesting that exposure is even greater elsewhere. In addition, the rates of both smoking7 and asthma morbidity and mortality8 –11 tend to be elevated in urban areas with high levels of poverty and/or minority populations. Daily passive smoke exposure was reported in one third of children from families of low socioeconomic status who had asthma in a Baltimore sample.12

Interventions to Reduce ETS Exposure in Children Legal, regulatory, and taxation changes, antismoking education programs, and smoking cessation assistance that incorporates nicotine replacement therapy have been associated with a reduction in the overall smoking rates in the United States, but reductions in the rates among young women, especially those with less education, have lagged behind those of men.13 Attempts to encourage nonvolunteer female smokers of childbearing age, including pregnant women and new mothers, to quit smoking or to modify household smoking habits to reduce infant and early childhood exposure have had very mixed results.14 –21 However, even women who abstain during pregnancy do not cease permanently, because approximately two thirds resume smoking.22,23 Efforts to decrease relapses have had limited success.24 –26 1710

Several controlled trials27–30 of ETS reduction interventions have been reported that have specifically targeted families of children with asthma. The success of these interventions has been mixed, and ETS exposure has been assessed in a variety of ways. Although one study27 measured ETS concentration in the home environment, most have failed to confirm parental self-report with objective measures of the child’s exposure and/or have failed to measure asthma outcomes, making it difficult to assess the clinical significance of any changes that may have occurred in the child’s exposure. Both the use of feedback to the caregiver on the child’s exposure (via urine cotinine measurement) and behaviorally based counseling have shown promise, but these techniques have not been used in combination. The present study reports the results of a controlled trial comparing a behaviorally based, nurseadministered, individual feedback and counseling intervention to reduce the ETS exposure of children with asthma who were 3 to 12 years of age and were from low-income, predominantly minority families. All of the children were at risk, having been seen for acute asthma in an urgent-care setting, hospital ED, or inpatient hospital setting in the previous year. A key feature of the intervention was repeated feedback to the parents, over a period of approximately 5 weeks, on the results of four successive urine cotinine measurements to inform them of the initial level of exposure of the child and the success of their efforts to reduce this exposure. The primary outcomes investigated were emergency/urgent healthcare utilization for asthma and ETS exposure as indexed by the child’s urine cotinine/creatinine ratio (CCR). Asthma hospitalization, parental reporting on whether smoking was allowed in the home and on the child’s exposure, and several indicators of asthma control also were examined on an exploratory basis. Materials and Methods Subjects Eligibility: Eligible children had the following characteristics: (1) age between 3 and 12 years; (2) had been examined because of acute asthma within the preceding year in the ED or urgent-care (Peds Plus) clinics and/or had been admitted to the inpatient service of the Valley Children’s Hospital (VCH) (VCH had been located in Fresno County, CA, until its new facility [in-patient services, ED, and specialty clinics] opened just across the Fresno-Madera County line in September 1998; the Peds Plus outpatient clinics remained in their original community locations); (3) were Medi-Cal (California’s Medicaid program)eligible; (4) were exposed to ETS, per the caregiver report; and (5) had caregivers who spoke either English or Spanish. VCH electronic records were searched to identify children who were 3 to 12 years of age who had been seen for acute asthma between January 1996 and June 1997. Of the 867 families Occupational and Environmental Health

contacted, 25 (3%) were not Medi-Cal-eligible and 568 (66%) had no reported ETS exposure. Eight-seven families (31% of those who were eligible) agreed to participate and were enrolled. The study was reviewed annually and approved by the Institutional Review Board (IRB) of the VCH and the Committee for the Protection of Human Subjects of the California State Health and Welfare Agency. The consent process informed parents of the following: (1) that the study was directed at children who had emergency or other unscheduled visits for acute asthma exacerbations and were regularly exposed to ETS; and (2) samples of the child’s urine would be taken periodically and “analyzed for cotinine, a substance found in the urine of a person who has breathed tobacco smoke.” Data Collection Instruments: At baseline and at the 6-month and 12-month follow-up visits, the primary caregiver provided data by personal interview on family demographic characteristics, the child’s asthma history, current symptoms, activity limitations, environmental factors, and medication regimen (ie, a complete listing of asthma medications, dosages, and schedules). The caregiver reports included the following: (1) the types of tobacco products smoked, the amount smoked, and the relationship of the child to each smoker who lived in or regularly visited the home; (2) the degree to which the child was exposed to ETS; and (3) any restrictions on smoking in the home (eg, smoking not allowed inside the home, only allowed in certain locations inside the home, or not restricted). Families received $10 each time that they completed the scheduled data collection at baseline, 6 months, and 12 months, and the child received a small bag of inexpensive, age-appropriate toys. Pulmonary Function: For children who were developmentally able to provide a valid measurement, lung function was tested prior to and 5 min after the administration of two puffs of a ␤-adrenergic bronchodilator at baseline and at the 12-month follow-up visit. (Postbronchodilator testing was erroneously omitted at enrollment for 17 children because the laboratory initially continued its standard procedure of omitting this measurement when the initial value of the FEV1 was ⬎80% of predicted.) Testing was performed by the VCH Pulmonary Function Laboratory using standardized methods and equipment that met American Thoracic Society requirements (V˙max series pneumotach, using a bi-directional flow-sensing mechanism; SensorMedics, Yorba Linda, CA). Normal (predicted) values were those of Polgar and Promadhat.31 Urine Cotinine: Assays for urine cotinine and creatinine were performed for both intervention and control children at enrollment and at the 6-month and 12-month follow-ups by the VCH Clinical Laboratory using a radioimmunoassay (Coti-Traq; International Diagnostic System Corp; St. Joseph, MI).32 Children in the intervention group also contributed urine samples at each intervention session. Asthma Medications: This study was conducted through the Pediatric Pulmonary Service of VCH. Each child was examined at enrollment by a pediatric pulmonary specialist (R.S. or L.R.), and baseline pulmonary function testing was ordered. Most children had been receiving episodic urgent medical care and/or general medical care from primary-care physicians in the community. Many were on drug regimens that were clearly inadequate, as evidenced by their baseline lung function, symptoms, activity limitations, and prior acute health-care utilization (see “Results” section). In light of their poorly controlled asthma and high risk, it was considered medically and ethically requisite that an adequate regimen be prescribed for each child at the outset of the study, and from a design standpoint, this helped assure that there would be comparable management in both experimental

groups. Where necessary, the medication regimen was adjusted on the basis of history, physical examination, and pulmonary function results such that all children were prescribed a regimen consistent with national guidelines.33 Health-Care Utilization: For all eligible children, the dates on which the child was seen in the VCH Peds Plus clinic (pulmonary department or ED) or in the inpatient service for asthma, another respiratory condition, or a nonrespiratory condition were obtained from VCH records. Health-care utilization was measured by (1) the number of visits for asthma and (2) the number of times the child was hospitalized for asthma and the number of days of each hospitalization in the year prior to enrollment in the study (baseline) and in the follow-up year. Randomization: Following baseline data collection, participants were randomized equally to the intervention group (n ⫽ 44) or control group (n ⫽ 43) using a randomization design with blocks of length four. This avoided long strings of assignments to either group while ensuring that the assignment of any participant was not predictable from the preceding assignments. Intervention and Control Conditions Intervention: The ETS exposure-reduction intervention consisted of three behaviorally based counseling sessions spaced over approximately 5 weeks. Each session (outlined in the “Appendix”) followed a written protocol for a nurse-educator to instruct the caregiver(s). This protocol included instruction about asthma and its treatment, including environmental controls, and was designed to ensure a basic understanding of the inflammatory nature of the disease and the role of ETS in exacerbating and sustaining that inflammation. A variety of behavior-changing strategies were used, which were adaptable to the circumstances of the individual family. These strategies included monitoring of the time and circumstances of the child’s ETS exposure, role modeling and role-playing of interactions with (other) smokers to secure their cooperation in reducing the child’s exposure, personal feedback on progress, and contingency contracting. Exposure recall covered the day of the session and each of the 3 days preceding the session, extending beyond the 16- to 19-h half-life of cotinine in the body and the somewhat longer half-life in children.34 –37 When the cotinine results were presented to the parent at the next session, the caregiver and interventionist reviewed the 4-day ETS exposure recall taken the same day as the urine sample. To help caregivers, especially nonsmokers, address exposure reduction with other (smoking) family members, the caregiver was asked whether those persons could be invited to the third session and whether the invitation should be issued by the caregiver or the nurse. To the extent that the children were developmentally able, they also were involved in learning about asthma and the problems of ETS exposure and played an asthma “Jeopardy”-like game along with the caregiver to demonstrate what they had learned. Usual Care: Subsequent to the initial medication adjustment, control group children received usual medical care in the Pediatric Pulmonary Clinic. Caregivers were given basic information about asthma and their medication regimen by a regular clinic nurse who was not otherwise involved in the study. Inflammation and bronchoconstriction were described, and questions about asthma and its treatment were answered. Enrollment cotininetesting results were not volunteered, and there was no specific focus on ETS reduction except for the statement (which is a part of the usual care in this clinic) that the exposure of children to ETS is to be avoided, especially children with asthma. If cotinine test results were specifically requested, the parent was told whether cotinine had been detected but not its concentration. As is usual in this hospital-based clinic, the parents of children in both the treatment and control groups were informed about CHEST / 120 / 5 / NOVEMBER, 2001

1711

the three-session small group Wee Wheezers38 asthma education classes being offered at VCH and were encouraged to attend. At the 12-month follow-up, six parents of children in the control group and two parents of children in the treatment group reported having attended such classes. Statistical Analysis Descriptive statistics were examined for each study variable. A natural log transformation was applied when the outcome measures were skewed, (eg, for the CCR). When the skew was more extreme, nonparametric methods were used. Because of the highly skewed distributions of the number of asthma visits, children were classified in each of the 2 years (pre-enrollment and postenrollment) as having more than one visit per year or fewer than or equal to one visit per year (one being the minimum number, pre-enrollment, for eligibility). The proportions of children with higher utilization then were compared between the intervention and control groups using logistic regression. Because of the seasonal variability in asthma and the correspondence of the 12-month active follow-up with the end point of the year-long health-care utilization follow-up, the analyses focused on the 12-month follow-up. Study hypotheses were tested using logistic regression (dichotomous variables) or t tests (continuous variables), with and without adjustment/control for baseline differences on the outcome variable. All analyses were performed by intent to treat and, except as noted below, were performed using computer software (SAS, version 6.12; SAS Institute; Cary, NC). The analysis used all cases for which a particular outcome variable was available. In addition, the analyses of all the outcome measures were repeated for the subset of children for whom cotinine data were available at 12 months.

Attrition rates on the cotinine data were equivalent in the intervention and control groups (see “Results” section). Asymptotic tests of the significance of treatment effects can be unreliable in logistic regression models that adjust for an influential baseline covariate. We used the nonparametric bootstrap estimates of confidence intervals by Efron and Tibshirani39 to check the results. The bootstrap analyses were performed with a general nonparametric bootstrapping routine (S-Plus, version 4.0; MathSoft; Cambridge, MA).

Results Characteristics of Sample Demographic Characteristics: The sample consisted of approximately equal numbers of male and female children (Table 1). Approximately 44% of the sample was Hispanic and 38% was black. One third of the primary caregivers (28 of 87 caregivers) had not graduated from high school, and only 3 caregivers were college graduates. None of these demographic characteristics differed significantly between the intervention and control groups. Smoking Practices: The primary maternal caregiver (who was not always the child’s natural mother) was a smoker in 61% of intervention group families and in 42% of control families (p ⫽ 0.07). An average

Table 1—Baseline Characteristics of Intervention and Control Group Participants Characteristics Age, yr* Sex† Male Female Race† White Black Asian-Pacific, Native American, Other Hispanic (not elsewhere classified)‡ Ethnicity† Hispanic Non-Hispanic Education level (primary caregiver)† Less than 12th grade High school graduate Some college/trade school 4-yr college graduate or higher ⬎ 1 acute asthma visit†§ Maternal caregiver smokes† Smoking allowed inside the home† Smokers in home,†㛳 No. Cigarettes smoked per day,§ No.

Intervention (n ⫽ 44)

Control (n ⫽ 43)

p Value

7.2 (2.5)

7.5 (2.7)

0.62

25 (56.8) 19 (43.2)

19 (44.2) 24 (55.8)

0.24

16 (36.4) 14 (31.8) 8 (18.2) 6 (13.6)

15 (34.9) 19 (44.2) 2 (4.7) 7 (16.3)

0.22

19 (43.2) 25 (56.8)

19 (44.2) 24 (55.8)

0.92

15 (34.9) 6 (14.0) 20 (46.5) 2 (4.7) 16 (37.2) 18 (41.9) 18 (41.9) 2.09 (0.95) 27 (18.5)

0.69

13 (30.0) 10 (22.7) 20 (45.5) 1 (2.3) 22 (50.0) 27 (61.4) 15 (34.1) 2.32 (0.96) 27 (18.2)

0.23 0.07 0.46 0.27 0.88

*Values given as mean (SD). †Values given as No. (%). ‡Separate questions were asked concerning race and ethnicity. The majority of Hispanics responded to the question regarding race by checking white or black or other. A smaller proportion wrote in “Hispanic” but did not indicate race. §Baseline year signifies 12 months preceding enrollment. 㛳Refers to all adult smokers living in or frequently visiting the home. 1712

Occupational and Environmental Health

of 27 cigarettes (1.35 packs) was smoked per day by all residents and frequent visitors in the homes. Smoking was allowed inside the homes of 34% of intervention group children and 42% of control children (p ⫽ 0.46). Where smoking was not allowed, the exposure was reported to occur in other homes where the child spent substantial amounts of time (eg, those of the child’s father, grandparents, or childcare provider). ETS exposure was assessed by the urine CCR, after natural log transformation. At baseline, the log of the child’s urine cotinine level (Table 2) was significantly predicted by whether the child’s maternal caregiver was a smoker (p ⫽ 0.006), whether smoking was allowed in the home (p ⫽ 0.0005), how much tobacco smoke the caregiver reported that the child was exposed to on a typical day (p ⫽ 0.01), and by the total number of cigarettes smoked per day by persons living in or frequently visiting the child’s home (p ⫽ 0.003). These relationships also were observed when the

cotinine level was corrected for excretion (ie, when predicting the log CCR). When these four variables were entered together into a multivariate regression for predicting the log urine cotinine level, the first three variables were retained, together accounting for only 38% of the variance in the log cotinine level (p ⬍ 0.0001). The urine cotinine level reflects nicotine exposure within a relatively brief time span. Assays of single urine samples do not quantify the average exposure over long periods of time and may not capture intermittent high exposure levels. Despite the overall association between cotinine level and caregiverestimated ETS of the child, 47% of children whose parents reported that the child typically was exposed to a “moderate” or “large” amount of tobacco smoke (ie, generally children living in homes where smoking was permitted) had measured cotinine levels at baseline that were quite low (ie, ⱕ 10 ng/mL). This apparent discrepancy may reflect parental awareness

Table 2—Intervention and Control Group Means and Proportions on Primary and Secondary Outcome Variables, Including Group Differences and ORs at 12-Month Follow-up, With and Without Adjustment for Baseline Differences* Intervention

Control

Intervention Effect Unadjusted

Measure Primary outcomes ⬎ 1 acute medical visit/year All participants Those with 12-mo cotinine data CCR, ng/mg㛳 Secondary outcomes Any hospitalization in year Smoking allowed in home Activity limitations (any reported)†† Cigarettes smoked per day㛳††‡‡ Symptom-free days per 2 wk†† Nights awakened per 2 wk†† FEV1, % predicted

Diff

OR

p Value

0.48 0.21

0.11† 0.01†

Adjusted Diff

OR

p Value

0.32 0.16

0.03†‡ 0.01†§

No.

Baseline

Follow-up

No.

Baseline

Follow-up

44 25

50.0 52.0

29.6 36.0

43 26

37.2 50.0

46.5 73.1

25

1.82 (1.05)

1.27 (1.31)

26

2.34 (1.11)

1.93 (1.24)

44

27.3

6.8

43

23.3

16.3

0.38

0.18

0.34

0.14#

30

27.7

10.0

30

40.0

30.0

0.26

0.06

0.24

0.11**

30

56.7

40.0

29

62.1

50.0

0.67

0.44

0.64

0.39

28

2.76 (0.99)

2.52 (1.10)

29

2.98 (1.26)

2.57 (0.99)

⫺0.05

0.86

0.09

0.67

29

5.41 (5.32)

7.66 (5.43)

29

5.86 (5.99)

7.93 (6.17)

⫺0.27

0.86

⫺0.22

0.88

29

3.00 (3.91)

3.07 (3.99)

27

4.89 (5.42)

4.15 (5.45)

⫺1.08

0.40

⫺0.37

0.76

18

80.28 (21.56) 84.00 (21.78)

21

74.10 (18.84) 79.48 (21.17)

4.52

0.52

⫺0.41

0.93

⫺0.66

0.07¶

⫺0.38

0.26¶

*Values given as percentages or mean (SD), unless otherwise indicated. Diff ⫽ difference. †Logistic regression. ‡Relation between having ⬎ 1 visit in baseline year and having ⬎ 1 visit in follow-up year (OR, 6.2; p ⬍ 0.0001; n ⫽ 87). §Relation between having ⬎ 1 visit in baseline year and having ⬎ 1 visit in follow-up year (OR, 4.5; p ⫽ 0.03; n ⫽ 87). 㛳Statistical tests performed on natural logarithm transformed values. Numbers shown are in log units. ¶t test. #Relation between having ⱖ 1 hospitalization in baseline year and having ⱖ 1 hospitalization in follow-up year (OR, 3.9; p ⫽ 0.05). **Relation between having a nonsmoking policy at baseline and having a nonsmoking policy at follow-up (OR, 49.18; p ⬍ 0.001; n ⫽ 60). ††Parental report. ‡‡Total number of cigarettes smoked per day by persons residing in or frequently visiting the home. CHEST / 120 / 5 / NOVEMBER, 2001

1713

of patterns of ETS exposure that were not reflected in that specific urine sample. Medication Regimen: The medication regimen was “stepped up” for a total of 54 of the 87 children (62%) as a result of physician assessment at the enrollment visit. The proportions that were stepped up were comparable between the two groups (intervention group, 61%; control group, 63%). The following levels of asthma severity implied by the resultant regimens, using the criteria of the National Asthma Education and Prevention Program guidelines (mild intermittent, prn bronchodilator alone; mild persistent, prn bronchodilator and low-dose inhaled corticosteroid [ICS], or cromolyn/nedocromil, or leukotriene modifier; moderate persistent, prn bronchodilator and medium-dose ICS or low-tomedium dose ICS with or without a long-acting ␤-agonist or theophylline; severe persistent, prn bronchodilator and oral steroids with or without ICS, a long-acting ␤-agonist, or theophylline) also were comparable: 1. Intervention group: mild intermittent, 12%; mild, 45%; moderate, 43%; and severe persistent, 0%; and 2. Control group: mild intermittent, 12%; mild, 44%; moderate, 42%; and severe persistent, 2%. Intervention Participation: A total of 32 of the 44 intervention families (73%) attended all three sessions, 2 other families (5%) attended two sessions, 5 families (11%) attended one session, and 5 families (11%) failed to attend any sessions. The mean time between the first and third sessions was 37.3 days (SD, 11.4 days). Follow-up: All randomized patients (n ⫽ 87) were observed (passively) through their medical records over the entire follow-up year. At the 12-month follow-up, interview data were obtained in person or by phone for 60 participants (69%). Twenty-seven patients were unavailable for active follow-up, despite aggressive attempts to retain them, but were not unavailable for follow-up by medical records. Urine samples were obtainable for 51 of these participants (59% of the randomized sample). The rates of retention in active follow-up did not differ between those for the intervention and control groups (30 for each group for the interview data and 25 and 26, respectively, for the urine samples). There was a tendency for those who contributed follow-up urine data to have lower CCRs at baseline (mean, 14.3; SD, 17.5) than those who did not (mean, 24.3; SD, 33.2; p ⫽ 0.07). Attrition was not 1714

significantly associated with a patient’s race, gender, or degree of health-care utilization for asthma in the baseline year. Primary Outcome Measures Acute Medical Visits: The proportion of children with more than one asthma-related medical visit decreased in the intervention group from 50.0% in the baseline year to 29.6% in the follow-up year, as contrasted with a slight increase, from 37.2 to 46.5%, in the control group (Table 3). The odds ratio (OR), adjusted for baseline visits, was 0.32 (p ⫽ 0.03) [ie, the odds of having more than one visit were reduced by approximately two thirds in the intervention group compared with the control group]. The bootstrap results revealed that the 95% confidence interval for the difference between the intervention and control group follow-ups in log odds, and adjusting for baseline visits, did not include zero. This supports the validity of the asymptotic results from the logistic regression analysis despite the overall strong association that exists, as would be expected, between baseline asthma visits and follow-up visits (OR, 6.2; p ⫽ 0.0005). When similar analyses were performed for the subset of children with cotinine results available for the 12-month follow-up as well as for the baseline (n ⫽ 51) [Table 2], the effects of the intervention were even more pronounced (ie, lower ORs) and were statistically significant despite the reduced sample size. The proportions of patients in the intervention group with more than one visit decreased from 52.0 to 36.0%, whereas those in the control group increased from 50.0 to 73.1% (unadjusted OR [ORu], 0.21; p ⫽ 0.01; adjusted OR [ORa], 0.16; p ⫽ 0.01). Again, the bootstrap results supported the validity of the asymptotic results, despite the strong overall association between baseline and follow-up visits (OR, 4.5; p ⫽ 0.03). Cotinine Level: Intervention-control differences at follow-up in the log urine CCR, unadjusted for the baseline values, favored the intervention group (difference, ⫺0.66; p ⫽ 0.07; Table 3). However, when adjusted for the baseline values, the interventioncontrol difference was not statistically significant (difference, ⫺0.38; p ⫽ 0.26). Compared with the health-care utilization results for the full sample, this comparison has reduced precision due to the unavailability of patients for follow-up (intervention group, 25 patients; control group, 26 patients with cotinine data at 12-month follow-up). The difference corresponds to a 46% greater reduction in the CCR in the intervention group than in the control group. Occupational and Environmental Health

Table 3—Urine Cotinine and CCR at Baseline in Relation to Caregiver Report of Smokers and Smoking Practices Cotinine, ng/mL Variables Maternal caregiver smokes No Yes Smoking allowed inside the home No Yes Child’s typical daily exposure None Moderate amount Large amount Cigarettes smoked,‡ No.

CCR, ng/mg

No. (%)

Mean (SD)

p Value*

Mean (SD)

p Value*

45 (51.7) 42 (48.3)

9.5 (12.8) 24.6 (31.8)

0.006

10.8 (11.5) 25.5 (32.2)

0.006

54 (62.1) 33 (37.9)

10.0 (16.3) 29.2 (32.8)

0.0005

11.2 (15.6) 30.3 (33.3)

0.0005

11 (12.6)† 59 (67.8) 15 (17.2) 27.0 (18.3)§

5.1 (9.7) 16.1 (23.7) 29.3 (35.1) 17.3 (25.6)

0.014 0.003

8.4 (12.6) 15.9 (23.1) 33.5 (35.2) 18.4 (25.5)

0.008 0.006

*Significance test applied to linear regression coefficient— cotinine (or CCR) regressed on the variable in question. †Only 3 of the 11 caregivers who claimed their child was not exposed said that smoking was prohibited in their home. Six of the 11 caregivers were smokers. Five of these were light smokers (1– 4 cigarettes per day). One smoked 15 cigarettes per day and had a male partner, a relative, and friends who smoked, but said smoking was not allowed in the home. In all five cases in which the maternal caregiver was not a smoker, her male partner was a smoker. Nine of the 11 caregivers also reported that a friend who visited their home or someone else in a location where their child spent time was a smoker. The average amount of time spent by these children in those locations was 11 h/wk). ‡Combined numbers of cigarettes smoked per day by all household residents, relatives and friends who are frequent visitors, and persons in other locations where child regularly spends time. §Values given as mean (SD).

Secondary Outcome Measures Hospitalization: The proportions of children who were hospitalized for asthma in the baseline year (intervention group, 27.3%; control group, 23.3%) decreased to 6.8% and 16.3% in the follow-up year. A trend toward relatively lower odds of hospitalization in the intervention group was observed whether or not the analyses adjusted for baseline hospitalization, but it did not achieve the 0.05 level of significance (ORu, 0.38 [p ⫽ 0.18]; ORa, 0.34 [p ⫽ 0.14]). For the intervention group, the total number of hospitalizations was 12 in the baseline year and 3 in the follow-up year. For the control group, the total number of hospitalizations was 10 in the baseline year and 7 in the follow-up year. Hospitalization in the baseline year was significantly associated with hospitalization in the following year (OR, 3.9; p ⫽ 0.05). Prohibition of Smoking Within the Home: Among those patients with follow-up interview data (n ⫽ 60), the proportion of parents who allowed smoking in the home decreased from 27.7 to 10.0% in the intervention group and from 40.0 to 30.0% in the control group (Table 3). The ORu was 0.26 (p ⫽ 0.06), and the ORa was 0.24 (p ⫽ 0.l1). Amount of Smoking: The intervention supported, but did not emphasize, smoking cessation as a goal. It concentrated on eliminating smoking in all the indoor environments that would be frequented by the child (eg, houses or cars). Not surprisingly, there was

only a small change between the baseline data and the data at the 12-month follow-up for the reported total number of cigarettes smoked by persons living in or frequently visiting the home in both groups, and there was no intervention-control difference (unadjusted difference, 0.05 [p ⫽ 0.86]; adjusted difference, 0.09 [p ⫽ 0.67]; Table 3). Asthma Control: The following four indicators of asthma control were analyzed on an exploratory basis (Table 2): reported activity limitations; symptomfree days (in the preceding 2 weeks); parental nocturnal awakening due to the child’s asthma (in the preceding 2 weeks); and lung function (ie, the percent predicted FEV1). The sample size is quite small for pulmonary function tests, since the younger children and, in this population, even some of the older children (with apparent developmental delays) were unable to correctly perform the test and, therefore, could not be tested. None of these measures showed a significant effect of the intervention, although baseline-adjusted group differences at 12 months for all measures except symptom-free days favored the intervention group. Changes in Health-Care Utilization in Relation to Changes in Cotinine Level and Smoking Rules in the Home: Ideally (ie, assuming that the decrease in asthma health-care utilization was mediated entirely by a decrease in ETS exposure and that ETS exposures were measured without error), statistically controlling for the change in exposure should elimCHEST / 120 / 5 / NOVEMBER, 2001

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inate the significant association between the intervention and health-care utilization. However, this was not observed. The intervention effect on acute asthma visits remained when either of two covariates assessing exposure was included in the model. Prior to including the change in smoking restrictions in the model (n ⫽ 60 cases with follow-up interview data), the ORa was 0.20 (p ⫽ 0.01) and the ORu was 0.25 (p ⫽ 0.01). When the change in smoking restrictions was added, the ORs were essentially unchanged (ORa, 0.20 [p ⫽ 0.01]; ORu, 0.26 [p ⫽ 0.01]). Similarly, when the change in CCR was included (n ⫽ 51 cases with follow-up cotinine values), the results did not differ from those shown in line 2 of Table 3, which do not include the change in CCR in the model.

Discussion We found that an educational intervention that emphasized reduction in ETS exposure and that used a variety of motivational, instructional, and other aides to promote behavior change was associated with significantly lower odds of having more than one acute medical visit for asthma (OR, 0.32; p ⫽ 0.03 [after controlling for baseline visits]) and also with a nonsignificant trend toward lower odds of hospitalization (OR, 0.34; p ⫽ 0.14). Using statistical bootstrap procedures, we confirmed that these logistic regression results were not a statistical artifact of the inherent tendency for the level of health-care utilization to be correlated from 1 year to the next. This result is both statistically and clinically significant, especially for a population of very low-income, ETS-exposed, minority children with a history of acute exacerbations. One fourth of the children had been hospitalized for asthma in the preceding year. The population also was composed entirely of nonvolunteer families, that is, families who were not in the process of seeking assistance with exposure reduction, smoking cessation, or asthma control when they were recruited. Individuals in the intervention and control groups were comparable in terms of their pharmacologic regimens and were provided with comparable medical management throughout the study, yet comparable reductions in health-care utilization were not observed among participants in the control group. In this medical setting, a small-group asthma education program was being offered on a regular basis to the community. Six control group families and two intervention group families enrolled in this program over the course of the study, which potentially could have tended to reduce the differences between the two groups. That program mentions the 1716

need to avoid ETS exposure but does not emphasize it or provide additional assistance in accomplishing that goal. Nevertheless, the ETS reduction intervention was associated with health-care utilization benefits substantially exceeding those of the control group. To our knowledge, this is the first report of an educational intervention that explicitly targets ETS reduction in exposed children that has demonstrated a reduction in the number of acute visits for asthma under controlled conditions. Although we have not carried out a formal cost-benefit analysis, the reduction in the numbers of acute visits appears to justify the modest cost in nursing time, and the possible reduction in inpatient care, if confirmed, would provide further economic justification. We made the ad hoc observation that the benefits of the intervention were even more pronounced (ORa, 0.16; p ⫽ 0.01) when the comparison was restricted to the subset (approximately 59%) of the children in the intervention group and the control group whose families cooperated with all the active data collection requirements of the study during the follow-up. Within the intervention group, those who participated in the active follow-up also proved more likely to attend intervention sessions, supporting the conclusion that the observed reduction in healthcare utilization was in some manner directly related to exposure to the intervention. For the subgroup with follow-up cotinine data, no baseline difference in cotinine levels or the number of smokers in the home was observed between children in the intervention and control groups. Failure to participate in active follow-up was associated with greater ETS exposure at baseline in both experimental groups but was unrelated to participants’ race, gender, or baseline health-care utilization. In focusing on the group that complied with the follow-up requirements, one is presumably comparing a subset of the families in the intervention and control groups that were somewhat more positively predisposed toward the goals and requirements of the study. In the framework of the transtheoretical model of stages of change,40 a higher proportion of these individuals may have been at the “contemplation” stage with regard to changing smoking practices, rather than the “precontemplation” stage. Nevertheless, within this subset, children of the control group families showed little or no reduction in health-care utilization simply as a result of their participation in the study and the data collection, whereas those exposed to the intervention showed a marked reduction. The point estimate of the effect of the intervention on the proportion of families allowing smoking in the home (OR, 0.24) is even larger than the estimate of the effect on utilization but is not statistically significant (p ⫽ 0.11). The reduced statistical precision Occupational and Environmental Health

due to the loss to follow-up may account for the failure to detect an effect on this outcome as well as in the CCR. The change in the CCR favored the intervention group, and the effect size (ie, the adjusted difference divided by the control group baseline SD) was moderately large (⫺0.38/1.11 ⫽ ⫺0.34 SD) but was not statistically significant (p ⫽ 0.26). It is possible that a reduction in ETS exposure, on the order of the effect size observed in the present study, may be clinically significant, if not statistically significant in a sample of only 51 cases. We did not demonstrate a statistically clear mechanism that would account for the effects of the intervention on asthma outcomes by its effect on measures of exposure. Compared to the main outcome (health-care utilization), which was measured on all subjects, the exposure variables were measured only on about two thirds of the subjects at follow-up. Furthermore, the less-than-perfect association among the measures of exposure indicates that there is considerable variation associated with these measures. When an intervening variable on the causal pathway between treatment and outcome is measured with error, the test of the mechanistic hypothesis loses precision and can give a falsenegative result. These considerations cause us to be cautious in the interpretation of the apparently negative results with respect to the hypothesis that the effects of the intervention on health-care utilization are entirely or in part due to a reduction in ETS exposure. Larger studies, with more complete follow-up and even greater attention to reduction of error in the measurement of ETS exposure, are necessary to adequately evaluate the hypothesis that some or all of the clinical effect of our intervention is due to measurable effects on exposure. Nevertheless, we recognize that there may well be other explanations for the positive clinical effects of the intervention. Some behavior change associated with the intervention, other than ETS exposure reduction, could have mediated the reduction in health-care utilization, in whole or in part. For example, although both groups were on similar medication regimens, the intervention group might have been more adherent to those medications, or might have made additional modifications in their home environment, or might have responded more quickly and appropriately to the onset of asthma symptoms than the control group. If this were the case, the importance of the finding of an overall clinical benefit associated with the intervention would remain, but the interpretation of the underlying mechanism would be quite different. Resolving the questions on which this study fails to be statistically clear (ie, on the questions of the mechanism) will require further controlled trials in

which objective data are concurrently gathered on family asthma-management behaviors (eg, medication adherence and other environmental control practices), as well as on ETS exposure and asthma outcomes (eg, symptoms, lung function, activity limitations, and health-care utilization). We suggest that it also would be important to measure the stage of change of the caregiver with regard to smoking cessation and the prohibition of smoking in the home at the outset and at the conclusion of the study. With permission, stage data might also be gathered from those caregivers who decline to participate. This information could help to identify the segment of the ETS-exposed population that is reached by such an intervention and could reveal whether certain types of caregivers are more responsive to the intervention than others and whether the intervention is able to move participants from a precontemplation stage to contemplation and action. The measurement of all the key links in the presumed causal chain initiated by any environmental exposure reduction intervention is clearly critical to improving such interventions and to understanding the mechanisms involved in any associated clinical benefits. Methodologic Issues in Evaluation of Exposure Reduction Interventions Observing very marked differential improvement in asthma health-care utilization, coupled with failing to demonstrate a statistically significant difference in ETS exposure reduction or asthma symptoms, raises yet other important methodological issues for exposure mitigation research, regardless of whether the exposure is to ETS or some other agent in indoor air that exacerbates asthma. The effectiveness of previous attempts to reduce ETS exposure has been mixed, as noted earlier. Convincing reductions in ETS exposure have not been reported. Where a reduction has been noted,27 the reduction was in home air concentration rather than in personal exposure, and there was only a very limited concurrent assessment of asthma symptoms and no assessment of asthma health-care utilization. Consequently, the clinical significance of any ETS exposure reduction that might have been achieved is unknown. The present results pose a different issue. We have noted the possibility that the intervention improved health-care utilization through some mechanism other than ETS exposure reduction. However, the latter interpretation cannot be ruled out, especially given the relatively large effect size and the relatively small sample. The dose-response relationship between reductions in ETS exposure and improvements in asthma outcomes is unknown at present. Modest reductions in ETS exposure actually may CHEST / 120 / 5 / NOVEMBER, 2001

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have important benefits in children with hyperreactive airways, and decreases sustained during the winter months may be especially important since that is the time when children and smokers tend to be indoors, ventilation is poorer, and viral respiratory tract infections are most prevalent. Further, prenatal exposure and the duration of prior exposure may modify the dose-response relationship. If these considerations are important, the failure of most ETS reduction studies to measure asthma outcomes as well as exposure, coupled with a relatively high variance in the measure of exposure and the rather low statistical power in some instances, may result in an underestimation of the value of such interventions. Future studies need to be appropriately powered to detect modest differences in exposure, and the measurement of exposure should span several seasons of the year. Conversely, a very small reduction in exposure or indoor concentration might prove statistically significant in a study with a very large sample but may have little clinical significance. The only way to guard against the misinterpretation of the results of such studies is to gather concurrent data on ETS exposure and disease outcomes. There is an additional measurement issue. While cotinine is the best available biomarker of ETS exposure, single, intermittent urine samples provide a relatively crude index of both typical and maximal exposure. We observed that 30% of the children from homes where smoking was not restricted had a measured cotinine level at baseline ⱕ 10 ng/mL. Similarly low levels were obtained at baseline in 47% of the children whose parents reported that they had moderate or heavy exposure. While it is possible that some of these parents may have overestimated the child’s exposure, it seems more likely that these children actually had exposure that was much higher at certain times than would be suggested by the measured value. If that is the case, the exposure and exposure-reduction signals conveyed by the results of isolated urine cotinine measurements might be relatively weak. This sampling problem could be remedied by more frequent or more carefully targeted measurements (eg, more frequent measurements during the fall and winter seasons). Adherence to such frequent measurements may be low, however, except in more motivated families, and the measurements themselves may be reactive. The limitations of infrequent urine cotinine tests as a measure of typical exposure may seem to imply that providing feedback on cotinine levels as part of the intervention is questionable. However, the problems that arise in its use as an outcome measure are primarily due to temporal sampling problems, rather than to any insensitivity or unreliability of the assay in the range of cotinine levels in which we are 1718

interested (notwithstanding the complexities of the assays and of nicotine metabolism and excretion).41 In the present intervention, the results of cotinine measurements were always communicated to the caregiver in conjunction with a review of the parent’s report of the child’s exposure history during the period leading up to that report, which was given on the day the urine sample was taken. In this way, high or low values could be interpreted and discussed, and the parent could be reinforced for a reduction or queried further if there was an apparent discrepancy between the assay value and the reported exposure. In some cases, such queries prompted the recall of previously unreported exposure (eg, that a sister’s boyfriend, a chain smoker, had moved into the home), which then uncovered the need for a new strategy to eliminate exposure. When used in this manner, the cotinine level results had face validity to the parents and nurse educator and were wellaccepted. Other family members also appeared to be more readily convinced of the reality and importance of the exposure by the laboratory results than by the caregiver’s assertions. Smoking by Other Family Members and Friends In this population, only about half of the maternal caregivers smoked, and, typically, those who did so were not the only smokers in the home. To reduce exposure, caregivers typically had to negotiate behavior changes by other adults. Some children were exposed when staying in their second (paternal) home but not in the maternal home. Many mothers and their children lived with the mother’s parent(s), who were smokers, and were dependent on them for financial support, shelter, or childcare. Some children lived in homes in which boyfriends, girlfriends, and other acquaintances of family members were present frequently, sometimes for prolonged periods of time, and they lacked authority over these individuals and had limited capacity to monitor their smoking practices when the caregiver was not present. In one instance, the child’s caregiver was the grandmother, who did not smoke but was also the caregiver to two other elderly, physically and emotionally handicapped relatives who both smoked. These caregivers, particularly the younger mothers, typically lacked the skills needed to address these issues effectively. In some cases, older family members discounted their opinions on the relationship of ETS to the child’s asthma. The intervention attempted to develop those skills through modeling and role playing, and it provided additional support using such strategies as a written prescription from the physician that the child was not to be exposed to ETS and by providing “smoke-free zone” window Occupational and Environmental Health

stickers. Where relevant, the nurse invited the (other) smokers to attend the third session and to participate in the education in order to gain their cooperation with a prohibition against smoking in the home, if not in smoking cessation. It was very apparent that, without this tailored assistance, little change was likely to occur. The subjective impression of the nurse educator, as recorded in her progress notes, was that these strategies were very clearly beneficial in a number of instances. Study Participation and Generalization of the Results Wilson et al38 reported that maternal smokers were less likely than nonsmokers to enroll in an asthma education research study and, if enrolled and randomized to the intervention, were less likely to attend education sessions than were nonsmokers.40 We observed here that children whose families did not comply with the follow-up assessments had greater baseline ETS exposure than those who were retained but were no more likely to have a maternal caregiver who smoked (children with cotinine data at follow-up, 47%; children without cotinine data at follow-up, 50%). We could not determine whether children whose parents declined to participate in the study at all may have had still greater exposure than did participants, because we lacked the necessary data on nonparticipants. The results of any intervention study that recruits nonvolunteers (ie, individuals who were not identified by virtue of their seeking assistance with ETS reduction or smoking cessation) necessarily generalize only to those willing to participate. It is likely that those who are contemplating or willing to contemplate making changes in smoking practices are more likely to participate in such a study than those who are at a precontemplation stage, hence the results of the experiment may generalize only to the former population. In the case of smokers in particular, there is apparent resistance to participation in such research. Some families may have been sensitized to the issue of passive smoke exposure in previous contacts with the health-care system. One parent who did participate feared that continuing to expose the child to ETS might result in intervention by Child Protective Services. Given these concerns and the increased concentration of smokers in lower-income and lowereducation populations, the rates of participation and retention in the present study are not surprising. They mirror the experience in other studies recruiting nonvolunteer subjects into smoking cessation programs and recruiting low-education populations into research in general. Our participation rate of 31%, for example, is only slightly lower than that of

Irvine et al30 (47.9%), who recruited a population in Scotland having 16% college graduates for a study with far fewer demands in terms of time and invasiveness. To date, most childhood ETS exposure reduction research predominantly has involved white populations with higher education and income levels, whereas the present sample was predominantly minority, exclusively Medi-Cal-eligible, and resided in an agricultural region experiencing a double-digit unemployment rate. It is likely that special strategies will be needed to move parents who are at a precontemplation stage with regard to smoking cessation or prohibition of smoking in the home to the point of contemplation. An intervention of this nature might have greater acceptance in a clinical (ie, nonresearch) setting, where meetings with the nurse could be approached as a normal component of the care of children with asthma. A research setting poses special challenges due to the burdens of data collection and to the detail and formality of the consent procedures. The extent of advance disclosure in ETS reduction intervention studies has varied. Notwithstanding the differences in the criteria of investigators and IRBs for informed consent that are implicit in these variations, full disclosure most likely decreases the willingness to participate on the part of some caregivers. Published reports of ETS reduction interventions should carefully describe the recruitment and disclosure procedures and should document participation rates in order to define the limitations of generalization of the results. ACKNOWLEDGMENT: The authors acknowledge the contributions of the participating families and of Patricia Springer, RN, Pediatric Pulmonary Department, Monica Dibble, RRT, RPFT, and Terry Driscoll, RRT, CPFT, of the Pulmonary Function Laboratory, Eldon Swanson, Supervisor of the Immunology Laboratory, and Leo Baranda and Christine Davies of the Information Services Department, all of VCH, Madera, CA, for their assistance with the identification of patients, recruitment and follow-up, laboratory testing, and the extraction of data from hospital records. Marvin Bohnstedt, PhD (retired), served as the initial principal investigator for the California Department of Health Services. Joy Grado, then at the San Joaquin Valley Health Consortium, assisted in the management of the project. Robert Wells, PhD, VCH Director of Research, served as Chair of the VCH IRB. The expert counsel and assistance provided by Philip Lavori, PhD, biostatistical consultant, is also very gratefully acknowledged. Wayne Shoumaker, PhD, provided assistance with data analysis.

Appendix: Outline of the Behaviorally Based Counseling and Cotinine-Feedback Intervention Session 1 I. Introduction a. Overview of the program b. Identify problems that the parent has in managing the child’s asthma II. Asthma pathophysiology CHEST / 120 / 5 / NOVEMBER, 2001

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a. Explain how the lungs and breathing system work b. Explain how this system is affected during and after an acute asthma episode c. Explain inflammation and how to prevent and control it d. Explain the effects of irritants/allergens on the lungs e. Explain what it means to control asthma: environmental control and medications f. Parental practice in explaining asthma to someone else III. Understand the cumulative effects of asthma triggers a. Water pitcher demonstration to explain the cumulative effects of asthma triggers b. Explain how to prevent symptoms IV. Eliminate the child’s exposure to ETS a. Complete a 4-day ETS exposure recall: recognizing how and where the child is being exposed to tobacco smoke b. Explain the cotinine test as a measure of tobacco smoke exposure c. Review cotinine test results collected at enrollment and provide a copy of the result to parents to take home d. Explain the relationship between the initial cotinine result and the 4-day ETS exposure prior to that (initial) test e. Identify smokers and locations that have the highest priority in reducing the child’s ETS exposure f. Role play situations if the parent seems to lack effective negotiation strategies and if negotiation is required with another person g. Provide parent with “no smoke exposure” prescription and “smoke free zone” stickers, and discuss how they might be used h. Complete a “behavioral contract” with the parent to reduce the child’s exposure to ETS in the next 2 weeks V. Offer to answer medication questions in the next visit or a follow-up phone call VI. Wrap up a. Plan follow-up phone call in about a week b. Give card with name and phone number for questions or problems Session 2 I. Review of progress a. Discuss progress and problems II. Use of metered-dose inhaler a. Review written instructions on inhaler use b. Demonstrate use of (placebo) inhaler with the child and have the parent use the “inhaler usage skills checklist” during the demonstration c. Discuss inhaler-use techniques, and answer any questions III. Review of asthma pathophysiology with the child (if possible) and the adult(s) a. Review the “Picture of My Body and What Happens With Asthma” handout b. If the patient is an older child, have the child practice explaining asthma to a friend c. Demonstrate with a straw how difficult it is to breathe when the child gets asthma d. Review “My Early Warning Signs” and “My Asthma Triggers” handout 1720

e. Discuss what the child can do to avoid tobacco smoke (as appropriate) and explain the importance of indoor air problems affecting asthma IV. Understand the role of tobacco smoke exposure in asthma symptoms a. Determine whether there are any misconceptions and/or disagreements within the family about asthma b. Show the “Poisoning Our Children” video,42 and then discuss the ideas and answer questions from the video c. Discuss the severity of the child’s asthma V. Progress in eliminating the child’s exposure to tobacco smoke a. Review progress on the behavioral contract b. If participants who were not at session 1 are present, explain what cotinine is and what it means. Review the cotinine test results collected before the last session, and provide a copy of the results to the parents to take home c. Explain the relationship between the last cotinine result and the 4-day ETS exposure prior to the test, and compare them to the initial cotinine results and exposure d. Complete a new 4-day ETS exposure recall e. As appropriate to circumstances, reinforce the efforts of the family, discuss barriers, role play negotiation with (another) smoker, and/or offer to personally call other smokers to invite them to the next session f. Establish one or two goals for the period between sessions 2 and 3, referring to the 4-day ETS exposure and complete behavioral contract VI. Wrap up a. Answer questions b. Plan follow-up phone call in about a week c. Encourage family to phone if questions or problems arise Session 3 I. Review of asthma status and understanding of asthma a. Discuss progress and problems b. Play “Asthma Jeopardy” to review and reinforce the mastery of basic asthma facts by the parent(s) and child II. Review progress in eliminating the child’s exposure to tobacco smoke a. If participants were not at previous sessions, explain what cotinine is and what it means b. Show “Secondhand Smoke Revised” video, and discuss the ideas with the family c. Review the cotinine test results collected before the last session, and provide a copy of the result to parents to take home d. Explain the relationship between the last cotinine results and the 4-day ETS exposure prior to the test, and compare it to previous cotinine results and exposures e. Complete a new 4-day ETS exposure recall f. As appropriate to circumstances, reinforce the efforts of the family, discuss barriers, role play, and/or offer to personally call other smokers to discuss ETS exposure reduction g. Give California Department of Health Services “Take Charge” card with the telephone number for the California Smokers’ Helpline Occupational and Environmental Health

III. Review the asthma action plan given to the parent(s) at the enrollment medical visit a. Review the child’s action plan with the parent(s) (eg, how to recognize the symptoms of asthma in order to take the appropriate action) IV. Encourage participation in asthma education classes a. Give parent(s) a written announcement with the schedule of the next class series, along with the physician’s “education prescription” V. Wrap up a. Review all elements covered b. Answer questions

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33 National Asthma Education and Prevention Program. Expert panel report 2: guidelines for the diagnosis and management of asthma. Bethesda, MD: National Institutes of Health, April 1997; publication No. 97– 4051 34 Jarvis MJ, Russell MAH. Measurement and estimation of smoke dosage to non-smokers from environmental tobacco smoke. Eur J Respir Dis 1984; 133(suppl):68 –75 35 Benowitz NL, Jacob P III. Metabolism of nicotine to cotinine studied by a dual stable isotope method. Clin Pharmacol Ther 1994; 56:483– 493 36 Benowitz NL. Biomarkers of environmental tobacco smoke exposure. Environ Health Perspect 1999; 107(suppl):349–355 37 Jarvis MJ, Russell MA, Benowitz NL, et al. Elimination of cotinine from body fluids: implications for noninvasive measurement of tobacco smoke exposure. Am J Public Health 1988; 78:696 – 698

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