BACKGROUND:

Tobacco smoke exposure (TSE) harms children, who are often “captive smokers” in their own homes. Project Zero Exposure is a parent-oriented, theory-based intervention designed to reduce child TSE. This paper reports on findings from the pilot study, which was conducted in Israel from 2013 to 2014.

METHODS:

The intervention consisted of motivational interviews, child biomarker and home air quality feedback, a Web site, a video, and self-help materials. The primary outcome was child TSE as measured by hair nicotine. Secondary outcome measures were air nicotine and particulate matter, parental reports of TSE, parental smoking behavior, and TSE child protection. A single-group pre- and posttest design was used.

RESULTS:

Twenty-six of the 29 recruited families completed the study. The intervention was feasible to implement and acceptable to participants. Among the 17 children with reliable hair samples at baseline and follow-up, log hair nicotine dropped significantly after the intervention (P = .04), hair nicotine levels decreased in 64.7% of children, and reductions to levels of nonexposed children were observed in 35.3% of children. The number of cigarettes smoked by parents (P = .001) and parent-reported child TSE declined (P = .01). Logistical issues arose with measurement of all objective measures, including air nicotine, which did not decline; home air particulate matter; and hair nicotine.

CONCLUSIONS:

A program based on motivational interviewing and demonstrating TSE and contamination to parents in a concrete and easily understandable way is a promising approach to protect children from TSE. Further research is needed to enhance current methods of measurement and assess promising interventions.

Forty percent of children worldwide are exposed to the harmful effects of tobacco smoke.1 The consequent public health burden is enormous and includes an increased risk of upper and lower respiratory disease, sudden infant death syndrome, early asthma onset, ear infections, slower lung development in children, and an increased risk for uptake of smoking among the children of smoking parents.2 Most exposure of young children is caused by smoking in the home, with the greatest risk for increased lower respiratory illness caused by maternal smoking.2 

Although many countries have enacted legislation to protect nonsmokers from tobacco smoke exposure (TSE) in public places,3 the protection of vulnerable children within their own homes is more complex. Legal measures to control the home environment are unlikely to be passed or implemented in liberal democracies, where the private sphere is not commonly regulated.4 Voluntary approaches to child protection have resulted in modest benefit. Systematic reviews with meta-analyses have revealed that interventions designed to increase parental cessation for the purpose of child protection were somewhat effective, however, most parents continued to smoke, leaving the majority of children unprotected.5 Programs aimed at convincing parents to change their smoking behaviors around children were beneficial when child exposure was assessed by parental report, but not by child biomarkers.6 In addition, although home air quality improved for intervention group participants, tobacco smoke pollution remained in some homes in all studies.7 Consequently, although there is a broad consensus about the need to protect children from tobacco smoke,2,8,10 the key to protecting most children with smoking parents from TSE has eluded the scientific community.11 

The current multiphase research project is aimed at developing, piloting, implementing, and assessing a parent-oriented, theory-based intervention to protect young children from TSE.12 The program, called Project Zero Exposure, uses a phased system for the development of lifestyle interventions.13,15 Early developmental phases included systematic literature reviews5,7 and qualitative research.7,16 On the basis of early findings revealing that parents may be unaware of the true extent of exposure,16 we focused the developed program on providing objective information about child exposure via biomarkers and home air quality, in the context of motivational interviews (MIs). The goal of the pilot study was to assess the feasibility of the developed intervention and obtain an estimate of intervention effectiveness. Baseline findings from the pilot study about home air monitoring have previously been reported.17 In the current article, we describe the pilot study and report on changes in all outcomes from baseline to follow-up.

Approval for the trial was received from the Tel Aviv University Ethics Committee, the Ministry of Health, and the Asaf HaRofeh Hospital Helsinki Committee. Approval for recruitment from areas adjacent to NA’AMAT day care centers was received from the national educational supervisor of the NA’AMAT day care center network. Written informed consent was obtained from all participants during the first home visit. The trial is registered in the National Institutes of Health Clinical Trials Registry (identifier NCT01335178).

The pilot was conducted in Israel from 2013 to 2014 by using a 1-group, pre- and posttest design to assess the acceptability and feasibility of the intervention program, to test all intervention components and research instruments in a real-world setting, and to estimate the expected changes in outcome variables.

Parents from families in which smoking occurred were recruited to the study between March and September 2013 from areas adjacent to NA’AMAT child day care centers by using the snowball technique. Eligibility criteria included having a child up to the age of 8 with sufficient hair for a sample, at least 1 smoking parent in the family, and willingness to join the research and provide a hair sample. Once a parent agreed to participate, the spouse or partner was also invited to participate. Families received a gift certificate worth ∼$70 as compensation for their time.

The intervention was designed to (1) allow objective assessment of child TSE, via biomarkers (hair nicotine) and measurement of home air quality (air nicotine, and particulate matter [PM2.5], as measured by a SidePak and/or Dylos monitor), (2) provide feedback to parents on objective levels of child exposure and home air quality, and (3) use MIs as the primary tools for communication with parents. A summary of the intervention protocol is presented in Fig 1.

FIGURE 1

Timeline of intervention.

FIGURE 1

Timeline of intervention.

As in previous studies in which feedback was used,6,18,25 the aim of providing objective information about tobacco smoke was to convince parents that their children were indeed exposed to tobacco smoke, so that they would take steps to protect them. MI was adopted because it is a well-established method for behavioral change that has been previously used to encourage parents to protect their children from TSE.6 The goals of the MIs, which were scheduled for baseline, 1, and 3 months, were to explore and resolve the ambivalence of parents regarding their smoking behavior around their children, in light of the new information they received about exposure, and to create realistic plans for changing exposure levels of the children. Through the MIs, information on second- and thirdhand smoking was provided, and a decisional balance tree was used to highlight positive and negative aspects of current smoking habits and to help parents come to a decision of what could contribute most to reducing their child’s exposure.

Follow-up phone calls were conducted every other week for the first 3 months of the intervention, and monthly thereafter, until the close of the intervention. Final visits were scheduled for 6 months after the baseline visit. The program included a Web site to enable interactivity between parents and project staff (parents.org.il); and various self-help materials, including a booklet, a video clip, a magnet about smoke-free homes, and car air fresheners.

The protocol for demonstrating home tobacco smoke pollution evolved over the course of the study. At the beginning, we used the technique of continuous PM2.5 monitoring publicized by authors of the Scottish Reducing Families’ exposure to Second-hand smoke in the Home study.20 The method involved leaving a SidePak monitor in the home to continuously monitor PM2.5 over a 24-hour period and then discussing the findings with the parents. Because of problems with the method, including large variations in PM2.5 levels and sensitivity to air pollutants other than tobacco,17 and complaints from participants about the noise, we switched to real-time PM2.5 monitoring, as was done in a previous study conducted in Armenia.19 Real-time monitoring involved turning on the SidePak monitor in the home, having a parent light a cigarette in their usual place while the machine was running, and showing the parent the results immediately.

Feedback on hair nicotine was shown with a graph that included 1 bar for the child’s level of hair nicotine and another bar for the levels of hair nicotine from children in nonsmoking families, taken from the values provided by Wipfli et al.26 Although we originally planned to provide feedback about hair nicotine levels at 3 months after recruitment to the study, logistical difficulties prevented us from providing the information until the end of the pilot study.

The primary outcome was the change in exposure to tobacco smoke during the study, as assessed by differences in log hair nicotine from baseline to the close of the study. Use of hair nicotine to assess child exposure has become increasingly popular in the past decade.26,27 Hair nicotine sampling is noninvasive and, according to our qualitative research, likely acceptable to parents.7 Hair nicotine is stable for long periods of time and reflects long-term exposure of the individual (∼1 cm of hair growth per month).28 Hair samples were collected from the participating children from the back of the head, as closely as possible to the scalp, at baseline and at 6 to 9 months postintervention. Analysis was performed by gas chromatography with mass spectrometer detection at Johns Hopkins University. Before analysis, hair samples were washed by using laboratory procedures to reduce the impact of nicotine found on the hair surface. We used Floresco’s cutoff of 0.2 ng/mg to discriminate between exposed and unexposed children.28 

We assessed home air quality by measuring home air nicotine and PM2.5. Passive nicotine dosimeters were placed in central areas in the participants’ homes for ∼7 days to measure home air nicotine at baseline and 6 to 10 (mean: 8.5) months after the trial began. After dosimeter collection, the monitors were stored at −20°C and then shipped to Mass Spectrometry Services at San Diego State University for analysis. Cumulative nicotine levels were adjusted for the number of days of measurement.

PM2.5 was measured in all homes by using SidePak monitors (SidePak Personal Aerosol Monitor AM510; TSI, Inc, St Paul, MI)20 and in some homes by using a Dylos monitor.29 The original protocol called for 24-hour continuous monitoring of PM2.5 with the SidePak monitor at baseline, 1, and 3 months, for the purpose of feedback and assessment of the intervention. Because of the aforementioned difficulties, the 24-hour monitoring was conducted at baseline and 1 month, but not at 3 months.

Face-to-face interviews with participants were conducted at baseline and 1, 3, and 6 months after the intervention began.

We were interested in measuring child TSE, smoking behavior in the home, and home smoking rules, as well as parental smoking behavior. Obtaining this information was complicated by the lack of standardized questions regarding TSE at the time of the research. To assess home smoking, we used questions developed and validated by Johansson et al30 and adapted to the Israeli context. To assess child exposure, we used the method of Wilson et al,21 which is based on ascertaining child location and smoking in that location during the previous 24 hours (S. Davis, PhD, personal communication, 2013). The question on home smoking bans was informed by the US Social Climate Survey.31 Questions on parental smoking behavior were taken from national standardized surveys conducted in Israel.32 

We used the set of questions employed by the B. I. and Lucille Cohen Institute for Public Opinion Research of Tel-Aviv University to collect data on age, sex, education, ethnicity, religion, religiosity, and income. The final questionnaire was reviewed by a panel of 7 public health professionals.

Child 24-Hour Exposure

Exposure was reported on a per-time-period basis during the course of the previous day (morning at home, on way to nursery or school, at nursery or school, on way home, afternoon at home, afternoon activity out, evening, at night while asleep). We calculated the summary measure by assigning 1 point for each time period during which the child was exposed, which could add up to a possible total score of 8 points.

Child Past-Month Exposure

We asked a general question about exposure in the past month and assigned points according to frequency (1 point for never, 2 for rarely, 3 for once a week, 4 for several times a week, 5 for once a day, and 6 for several times a day).

Home Smoking

We assigned points for increasing frequency of exposure in various places around the home (0 = never, 1 = less than once a month, 2 = at least once a month, 3 = at least once a week, 4 = several times a week, 5 = daily, and 6 = several times a day) for each of the following locations: anywhere around the home (including balconies), inside the house, on closed balconies, on open balconies, in the child’s room, in the stairwell, in the garden, in the car, in the car when the child is present. The maximum possible score was 36.

We also asked about smoking rules around the home. Answers were classified by using the following categories: home smoking ban, home ban when children are present, or no rules.

We present descriptive statistics on the sociodemographic variables and on all outcomes at baseline and at other collected time points. As in previous studies of TSE,21,33 we used the natural log transformation for hair and air nicotine because of the nonnormal underlying distributions of these variables. For log hair nicotine and log air nicotine, we analyzed the pre-post difference by using the paired t test. Regarding log hair nicotine, the nicotine content (in nanograms) in some samples was lower than the limit of detection (LOD). The resulting LOD for nicotine concentration, defined as the nicotine content in nanograms divided by the hair mass in milligrams, varied across children because the amount of hair in the samples varied. In our analysis, the nicotine concentration for these samples was taken to be one-half the LOD value. An alternative analysis (not reported here) based on the truncated normal distribution revealed similar conclusions. In response to notifications by the laboratory that some hair nicotine values were of questionable reliability because of the small amount of hair in the sample, we conducted analyses with and without the questionable values.

We used the paired t test to assess changes in parent-reported continuous measures, McNemar’s test to assess changes in parent-reported categorical measures (smoking rules in the home, percentage of daily smokers, mothers and fathers), and the sign test to assess changes in parent-reported smoking around the house.

We conducted analyses with SAS version 9.4 (SAS Institute, Inc, Cary, NC) and SPSS version 23 (IBM SPSS Statistics, IBM Corporation).

Of the 74 parents who expressed interest in hearing about the program, 29 agreed to participate and provided baseline data. One baseline questionnaire was lost. Two families dropped out after the first meeting, and 1 family dropped out because of family illness. Ninety percent of participants were managed until the end of the study. Twenty-seven families received at least 1 MI, and 20 received at least 2. In 14 families, both parents participated in the intervention. Full protocol adherence information is provided in Fig 2.

FIGURE 2

Flow of participants through trial.

FIGURE 2

Flow of participants through trial.

The mean age of the children was 3.5 (±2.1) years (range: 1–8.5 years); 12 were boys and 16 were girls. All but 1 of the families were Jewish. Four (14%) classified themselves as religious or Haredi; 10 (34%) classified themselves as traditional; and 13 (46.4%) classified themselves as secular. Self-reported socioeconomic status classifications included much below average (21.4%), a little below average (14.3%), average (10.7%), and above average (53.5%). Full-time employment status was applicable to 64.3% of mothers and 82.1% of fathers. Five (17.9%) mothers and 5 (17.9%) fathers had a high school education; the remainder had post–high school education. Parents lived together in 89.3% of families.

The MIs were well-received by the participants, who also expressed great interest in child hair nicotine levels. The air nicotine levels were of less interest to the parents. The Web site was used only infrequently. Because the laboratory staff analyzed the samples in batches, we were delayed in providing feedback from the hair and air samples to participants.

Hair nicotine data are presented in Table 1 and in Fig 3 for all children with data at baseline or follow-up. Among the 26 children who had data for both baseline and follow-up, the mean difference (post-pre) was −0.48 (SD = 2.07, P = .25). Eight of the 26 children had levels lower than the LOD at baseline. Of the 18 with levels greater than the LOD at baseline, hair nicotine decreased in 72.2% (13/18).

TABLE 1

Objective Measures of TSE and Pollution Over Time

PreinterventionPostinterventionChangeP (Paired t Test)
Log hair nicotine All observations N 28 26 26 .25 
Mean −0.88 −1.24 −0.48 
SD 1.27 1.51 2.07 
Median −0.83 −1.34 −0.50 
25th percentile −2.10 −2.42 −2.09 
75th percentile 0.35 −0.15 0.11 
Observations with <10 mg of hair removed N 27 17 17 .04 
Mean −0.93 −1.65 −1.04 
SD 1.27 1.41 1.88 
Median −1.07 −1.52 −1.05 
25th percentile −2.11 −2.83 −2.64 
75th percentile 0.27 −0.38 0.00 
Log air nicotine All observations N 27 25 24 .16 
Mean −3.69 −3.23 0.57 
SD 1.85 1.04 1.93 
Median −3.94 −3.34 0.63 
25th percentile −4.95 −3.89 −0.43 
75th percentile −2.55 −2.68 1.77 
PreinterventionPostinterventionChangeP (Paired t Test)
Log hair nicotine All observations N 28 26 26 .25 
Mean −0.88 −1.24 −0.48 
SD 1.27 1.51 2.07 
Median −0.83 −1.34 −0.50 
25th percentile −2.10 −2.42 −2.09 
75th percentile 0.35 −0.15 0.11 
Observations with <10 mg of hair removed N 27 17 17 .04 
Mean −0.93 −1.65 −1.04 
SD 1.27 1.41 1.88 
Median −1.07 −1.52 −1.05 
25th percentile −2.11 −2.83 −2.64 
75th percentile 0.27 −0.38 0.00 
Log air nicotine All observations N 27 25 24 .16 
Mean −3.69 −3.23 0.57 
SD 1.85 1.04 1.93 
Median −3.94 −3.34 0.63 
25th percentile −4.95 −3.89 −0.43 
75th percentile −2.55 −2.68 1.77 
FIGURE 3

Exposure of children to tobacco smoke as assessed by hair nicotine in nanograms per milligram, before and after trial. T1, Time 1, baseline; T3, Time 2, follow-up. a Samples <10 mg.

FIGURE 3

Exposure of children to tobacco smoke as assessed by hair nicotine in nanograms per milligram, before and after trial. T1, Time 1, baseline; T3, Time 2, follow-up. a Samples <10 mg.

The laboratory staff who analyzed the hair samples noted that results from 9 samples were questionable because of a hair mass <10 mg, far lower than the 30 mg of hair used for validation of the assay. Of the 26 children with pre- and postvalues, 17 had ≥10 mg of hair at both baseline and follow-up. Among these 17 children, hair nicotine decreased in 64.7% (11/17) of children during the trial, with reductions to values lower than the 0.2-ng/mg level for nonexposed children in 35.3% (6/17) of children. The mean difference was −1.04 (SD = 1.88, P = .04). Four of the 17 children had levels lower than the LOD at baseline. Among the remaining 13 children, 11 (84.6%) had levels that decreased during the study, and 6 (46.2%) had levels that decreased to values lower than the 0.2-ng/mg level.

The measurement of air nicotine was more complex than anticipated, with difficulties regarding shelf life and frozen storage encountered during the baseline measurement.17 A new type of dosimeter (CS Medical LLC, Creedmoor, NC) was sent to us for some of the postintervention samples because parts for the dosimeters of the old type (3M Detection Solutions, Oconomowoc, WI) were no longer available. Subsequent to the analysis of the postintervention samples, the laboratory staff alerted us to possible inaccuracies caused by low air nicotine levels and LODs for some samples.

Data on log air nicotine at pre- and postintervention, and the change in levels, are presented in Table 1. Air nicotine measured by dosimeters did not change significantly after intervention (P = .16).

As previously documented,17 we observed a substantial amount of statistical noise in the PM2.5 readings, much of it related to nontobacco sources. There was no significant change in PM2.5 values recorded by the SidePak between baseline and the 1-month visit. (Mean [SD]: Baseline: 0.015 (0.008) mg/m3, n = 24; Follow-up: 0.027 (0.035) mg/m3, n = 24, P = .11).

We did not measure PM2.5 at the 3-month visit because of the problems mentioned and because of complaints from participants about noise levels.

As shown in Tables 2 and 3, improvements were observed in almost all parent-reported measures, although most did not reach statistical significance. Child exposure in the past month decreased significantly (P = .01). Past 24-hour exposure decreased, but not significantly, from pre- to postintervention (P = .08). Household exposure frequency decreased, but the change was not statistically significant (P = .19). Nonsignificant reductions in household exposure were observed in almost all areas of the home.

TABLE 2

Parent-Reported Measures of Child Exposure–Related Variables Over Time

Baseline1 mo After Intervention Start3 mo After Intervention StartMean Change, T1–T3P (Difference, T1–T3)
Exposures, mean (SD), n 
No. cigarettes smoked (mother + father)a 23.02 (12.27), 27 16.73 (11.60), 26 18.68 (9.33), 25 −7.11 (9.15), 23 .001 
Child exposure (last 24 h)a 2.32 (1.36), 28 1.76 (1.36), 25 1.52 (1.16), 25 −0.63 (1.66), 24 .08 
Child exposure (last mo)a 5.07 (1.33), 28 3.85 (1.85), 26 4.08 (1.78), 25 0.92 (1.64), 24 .01 
Household exposure frequencya 17.96 (7.07), 28 14.08 (6.95), 26 15.76 (7.58), 25 −2.21 (8.04), 24 .19 
Daily smokers, % 
Mothersb 53.6 34.6 30.8 −22.8 .03 
Fathersa 82.1 80.8 84.6 +2.5 1.00 
Baseline1 mo After Intervention Start3 mo After Intervention StartMean Change, T1–T3P (Difference, T1–T3)
Exposures, mean (SD), n 
No. cigarettes smoked (mother + father)a 23.02 (12.27), 27 16.73 (11.60), 26 18.68 (9.33), 25 −7.11 (9.15), 23 .001 
Child exposure (last 24 h)a 2.32 (1.36), 28 1.76 (1.36), 25 1.52 (1.16), 25 −0.63 (1.66), 24 .08 
Child exposure (last mo)a 5.07 (1.33), 28 3.85 (1.85), 26 4.08 (1.78), 25 0.92 (1.64), 24 .01 
Household exposure frequencya 17.96 (7.07), 28 14.08 (6.95), 26 15.76 (7.58), 25 −2.21 (8.04), 24 .19 
Daily smokers, % 
Mothersb 53.6 34.6 30.8 −22.8 .03 
Fathersa 82.1 80.8 84.6 +2.5 1.00 

T1, Time 1, baseline; T3, Time 3, follow-up.

a

Paired t test.

b

McNemar’s test.

TABLE 3

Parent-Reported Smoking Around the Home

Daily Smoking Around the HouseNo. Reporting Several Times/d (Positive/Total)Post–Pre ChangeaSign Test Pa
Preintervention (%)Postintervention (%)0+
Anywhere around home (inside and out) 23/27 (85.2) 16/26 (61.5) 14 .11 
Inside the house (excluding balconies) 5/28 (17.9) 2/26 (7.7) 19 .22 
Closed balcony 4/14 (28.6) 2/26 (7.7) 10 .48 
Open balcony 8/18 (44.4) 8/26 (30.8) 12 1.00 
Child’s bedroom 0/28 (0.0) 0/26 (0.0) 25 — 
Stairway 1/24 (4.2) 0/26 (0.0) 13 .29 
Garden and/or yard 14/26 (53.9) 10/26 (38.5) 11 10 .03 
Car 10/28 (35.7) 7/26 (26.9) 12 .60 
Car when child present 0/28 (0.0) 0/26 (0.0) 20 1.00 
Daily Smoking Around the HouseNo. Reporting Several Times/d (Positive/Total)Post–Pre ChangeaSign Test Pa
Preintervention (%)Postintervention (%)0+
Anywhere around home (inside and out) 23/27 (85.2) 16/26 (61.5) 14 .11 
Inside the house (excluding balconies) 5/28 (17.9) 2/26 (7.7) 19 .22 
Closed balcony 4/14 (28.6) 2/26 (7.7) 10 .48 
Open balcony 8/18 (44.4) 8/26 (30.8) 12 1.00 
Child’s bedroom 0/28 (0.0) 0/26 (0.0) 25 — 
Stairway 1/24 (4.2) 0/26 (0.0) 13 .29 
Garden and/or yard 14/26 (53.9) 10/26 (38.5) 11 10 .03 
Car 10/28 (35.7) 7/26 (26.9) 12 .60 
Car when child present 0/28 (0.0) 0/26 (0.0) 20 1.00 

—, not applicable.

a

Based on parents who reported on both occasions.

The number of homes with some type of smoking rules (eg, no smoking inside or no smoking with children present) increased from 82.1% at baseline to 92.3% at follow-up, although this was not significant (McNemar’s P = .13). In 6 families, 1 or both parents quit smoking; 5 families implemented a car smoking ban; and 5 families reported moving the location of their smoking away from the children (eg, to the garden or roof instead of balcony).

The mean number of cigarettes smoked daily by mothers and fathers combined decreased significantly from baseline to follow-up. This change was largely caused by the change in mothers’ habits: 15 mothers smoked daily at baseline and 8 smoked daily at follow-up, whereas 23 fathers smoked daily at baseline and 22 smoked daily at follow-up. The mean change in the number of cigarettes smoked daily was −7.1 (SD: 9.2).

This intervention, which was designed to persuade parents to protect their children from TSE, was feasible to implement and acceptable to the participants, after minor modifications were made. Among children with reliable hair samples at baseline and follow-up, log hair nicotine dropped significantly after the intervention (P = .04), hair nicotine levels decreased in 64.7% of children, and reductions to nondetectable levels were observed in 35.3% of children. The number of cigarettes smoked by parents (P = .001) and parent-reported child TSE declined (P = .01). Home air nicotine did not decrease.

The novelty of this intervention was in the use of multiple means to demonstrate child exposure, including home PM2.5, home air nicotine, and child hair nicotine, in the context of MI. Yet, the difficulties that we encountered when using the different types of objective measures were of concern. The 24-hour continuous monitoring of PM2.5 used by previous researchers20 was dropped both as a feedback tool and as an endpoint because of high levels of variability and a lack of specificity to tobacco smoke. Air nicotine measurements were complicated by unanswered questions about storage, transport, and shelf life of the monitors, LODs, and multiple analyses of data. Analyses of hair nicotine were complicated by differences in treatment of LOD levels between baseline and follow-up samples and by low hair weight samples.

Of the 4 outcomes measured (hair nicotine, air nicotine, PM2.5 continuous measurement, and PM2.5 real-time measurement), hair nicotine was the most practical for intervention evaluation, whereas PM2.5 real-time measurement and hair nicotine were both useful for feedback to parents.

The decreases in objectively-measured child exposure levels observed in this trial, combined with the enormous interest shown by parents regarding the results of their children’s hair samples (which were not available until the end of the trial), reveal that child TSE surveillance may be a powerful motivating factor for behavioral change among parents. Because taking serum specifically for the purpose of measuring TSE might meet with some resistance,7 hair, urine, or saliva should be considered, and serum should be considered in the event that it is also being drawn for other purposes. In clinical settings, child TSE feedback could be provided by trusted pediatricians, resulting in an enhanced health system and parental and societal awareness of the actuality of child exposure. With increased awareness, parents and societies could be motivated to change social norms about smoking around children, and these changes could result in further reductions of smoking around children. The initial cost of TSE monitoring might be more than recovered by reductions in the need for health care services.

Population or system-wide monitoring of child TSE, with feedback via clinicians or others to parents and perhaps children, should be aided by improvements in TSE measurement science. The ideal method for monitoring would be sensitive, specific, and low-cost and could be used to provide immediate measurement of both current and long-term exposure to tobacco smoke, with the possibility of recording changes over time. None of the commonly employed measures can be used to achieve these goals. SidePak and Dylos monitors are used to measure PM2.5 in the air, which is not specific to tobacco smoke. Passive air monitors are used to measure air nicotine in a cumulative manner, and measurements must be analyzed in laboratories, necessitating expense and a time delay in the provision of results. Hair nicotine samples can be used to provide cumulative evidence of exposure and also require the costs and time for laboratory analysis; in addition, measurement issues including rate of hair growth, hair pigmentation, and laboratory cleaning have been noted.2 Using urinary cotinine requires researchers to retrieve multiple samples to fully describe 1 child’s exposure (some researchers suggest that as many as 9 to 12 samples may be required34), and analysis must be conducted in a laboratory. Several recent innovations are promising: a real-time nicotine air detector recently became available for commercial use,35 and a PM2.5 measurement system that uses sound and light to demonstrate exposure is under development.36,37 The possibility of using mobile phones for these measurements, which has been done for other aspects of digital health, is intriguing. Advances in measurement science could contribute to regular monitoring of pediatric populations, with feedback to parents accompanied by clinician advice on how to better protect children. Finally, researchers in Scotland conducting work on the provision of air quality feedback to parents will likely make important contributions to the public health and medical communities on reducing child TSE.38 

This was a small trial designed to test feasibility and acceptability of the intervention. It was not designed to provide a definitive answer to whether the intervention is effective, nor could it differentiate between the effects of MI and provision of feedback on air quality and child exposure. Observed changes in outcome measures may have occurred for reasons unrelated to the intervention, such as seasonal variations in exposure, child growth, changes in social norms regarding TSE, or differences in laboratory techniques. It is also possible that the changes were caused directly by trial participation and/or the measurement that took place in the context of the trial.

To protect children from the hazards of tobacco smoke, parents need to eliminate tobacco smoke from their homes and cars and prevent exposure of children in all settings. We examined a strategy involving MI and demonstrating TSE and contamination to parents in a concrete and easily understandable way. The results obtained with this strategy are promising but must be rigorously tested before widespread implementation in pediatric primary care and community settings.

     
  • LOD

    limit of detection

  •  
  • MI

    motivational interview

  •  
  • PM2.5

    particulate matter

  •  
  • TSE

    tobacco smoke exposure

Dr Rosen initiated the research, conceptualized and designed the study, obtained funding with colleagues, and drafted most of the initial manuscript; Prof Guttman assisted with obtaining funding, contributed to the design of the intervention, and critically revised the manuscript; Ms Myers was a motivational interviewer, performed statistical analyses, and wrote parts of the manuscript; Ms Brown created the motivational interview protocol, trained the other interviewers, was a motivational interviewer, and reviewed the manuscript; Ms Ram was a motivational interviewer and reviewed the manuscript; Prof Hovell contributed to the design of the intervention and to the design and conduct of the study and edited the initial manuscript; Prof Breysse was responsible for the analysis of the baseline hair nicotine samples and reviewed the manuscript; Dr Rule was responsible for the analysis of the follow-up hair nicotine samples and reviewed the manuscript; Dr Berkovitch obtained Helsinki (institutional review board) approval for the trial and reviewed the manuscript; Prof Zucker assisted with the conceptualization and design of the study and with obtaining funding, held overall responsibility for statistical aspects of the study and ran some analyses, and critically edited the initial manuscript; and all authors approved the final manuscript as submitted and agree to be accountable for all aspects of the work.

This trial has been registered at www.clinicaltrials.gov (identifier NCT01335178).

FUNDING: Funded by the Flight Attendant Medical Research Institute (Award 072086_YCSA) and the Sackler Faculty of Medicine at Tel Aviv University.

1
Oberg
M
,
Jaakkola
MS
,
Woodward
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,
Peruga
A
,
Prüss-Ustün
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Competing Interests

POTENTIAL CONFLICT OF INTEREST: The authors have indicated they have no potential conflicts of interest to disclose.

FINANCIAL DISCLOSURE: The authors have indicated they have no financial relationships relevant to this article to disclose.