This was our first study to test an intervention that promoted both SHSe reduction and smoking cessation. It was based on past SHSe trials, where we noticed unprompted higher short-term quit rates for experimental families compared with controls (Hovell et al., 1994
). These observations fit the BEM in that SHSe counseling involved shaping parents to reduce their smoking frequency around the child. These shaping and sensitizing procedures, theoretically, could motivate parents to quit (Laraway, Snycerski, Michael, & Poling, 2003
). In the present study, the addition of smoking cessation counseling with SHSe counseling resulted in more short-term quits among counseled families than controls, suggesting that SHSe counseling can offer a foundation for promoting experimentation with quitting. Parents’ reports of exposure and smoking levels showed moderate and significant correlations with children’s urine cotinine levels and home air nicotine in the present trial, equivalent to those found in our past studies (Emerson et al., 1995
; Matt et al., 2000
). These findings confirm our previous observations that parents’ reports of smoking and SHSe rates can be as reliable and valid as cotinine biomarkers or nicotine assays.
Our results confirm previous research demonstrating the efficacy of counseling for children’s SHSe reduction among diverse races/ethnicities. This study demonstrated sustained decreases in SHSe in the counseled group. These results suggest that children and their families would benefit if such services were implemented in clinical or community settings, including WIC programs, which serve over 8 million low-income women, infants, and children nationwide. Three states, including California, pioneered using SHSe as a criterion for determining nutritional risk and provided SHSe counseling with WIC services, although this criterion was eliminated at the recommendation of a scientific review panel (Committee on the Scientific Evaluation of WIC Nutrition Risk Criteria, Institute of Medicine, 1996
Children’s cotinine concentration showed a decrease in both study conditions that was not significantly different by group over time. This finding is consistent with a number of studies (Gehrman & Hovell, 2003
; Greenberg et al., 1994
; Roseby et al., 2002
). However, it departs from two of our previous trials. One showed stable cotinine levels for the experimental children, while levels increased for controls, suggesting a prevention effect (Hovell et al., 2000
). In the other (Hijos Sanos
), cotinine concentrations decreased significantly more for the counseled group than for controls by postintervention; but late in the follow-up period, controls decreased to similar levels, suggesting a delayed reactivity effect (Hovell, Meltzer, et al., 2002
). These patterns across studies suggest that reduction in children’s cotinine is not yet reliably obtained. This may be due to a number of complications.
The definition of reported “exposure” for our trials has been that a child was in the same indoor room or a car when a cigarette was smoked. A child was not considered “exposed” to cigarettes that were smoked on a porch or balcony with a door open to the home, or anyplace inside the home when the child was not present in the same room. Yet children may be in close proximity to a room where smoking occurs or they may enter a room soon after cigarettes are smoked. Because tobacco smoke disperses quickly throughout a residence, our parent-reported outcome measure was not as inclusive in measuring all sources of SHSe as was urinary cotinine. Evidence to date suggests that SHSe should be defined by any smoking in the home or car, even when children are not present.
Nicotine contamination and thirdhand exposure
Home contamination may also have contributed to the failure to obtain a differential decrease in children’s urine cotinine concentration. Since this trial was conducted, we have learned more about the behavior of nicotine in indoor environments. Volatile SHSe components such as nicotine sorb into surfaces within minutes of emission, contaminating furniture, carpets, walls, clothes, and skin (Daisey, 1999
). Subsequently, SHSe components are re-emitted from contaminated surfaces into the air over months (Van Loy, Riley, Daisey, & Nazaroff, 2001
). Our research has found that indoor surfaces, dust, and air in smokers’ homes showed nicotine concentrations 5–7 times higher than nonsmokers’ homes, and homes of smokers who reported always smoking outside had intermediate levels of contamination (Matt et al., 2004
). Cars of smokers without car smoking bans showed significantly higher levels of nicotine in dust, on surfaces, and in the air compared with nonsmokers’ cars with smoking bans (p
< .001), and dust and surface nicotine in cars of smokers who had imposed car smoking bans were at similar levels as for smokers’ cars without bans (Matt et al., 2008
). Young children are at high risk of SHSe through dust and surface contamination because they spend more time near floors. They exhibit mouthing (e.g., hand–mouth, toy–mouth) and pica behaviors (i.e., ingesting nonfood objects), increasing risk via ingestion and skin contact with contaminated objects. Thus, parents cannot easily eliminate contamination sources of children’s exposure unless they discontinue all smoking in the home and car. The nonsignificant Group × Time interactions for mothers’ and all indoor smoking in the present trial indicate that the counseling interventions we have tested to date may not have focused sufficiently on this goal.
One of the prerequisite steps in establishing a complete home smoking ban may be to direct counseling to all family members. The planned intervention might have been more effective in helping parents achieve entirely smoke-free homes if more family members had participated. Mothers enrolled their families in the study and counselors encouraged all family members, especially smokers, to participate in counseling sessions. All were eligible to receive free nicotine replacement products. Yet other family members seldom participated.
Measurement and methodological issues
A source of reduced power for the trial may have been measurement reactivity in both conditions. Our first SHSe trial tested limited measures (interviews and air nicotine monitors), full measures (adding diary monitoring of parent smoking and children’s exposure and asthma symptoms), and full measures plus counseling (Wahlgren et al., 1997
). That study showed that measurement alone may have accounted for about 50% of the total decrease in SHSe. The current study shows that about two thirds of the experimental effect may be accounted for by measurement reactivity. Results from Hijos Sanos
might reflect counseling effects as well as measurement reactivity in the experimental condition and delayed measurement reactivity in the control condition. The decrease in cotinine levels for both groups in our current study raises the possibility that measures alone were partly responsible and that counseling was not powerful enough to cause detectable differential decreases for cotinine outcomes in the context of measurement reactivity.
Partial exposure to counseling
Another source of reduced power may have been incomplete counseling due to dropouts and families that were changing slowly and could not reach substantive reductions in the time available. Almost half of families assigned to the experimental condition did not complete all the 14 offered sessions. At the end of the intervention period, 65% of families in the experimental condition still reported child SHSe. This implies that these counseling procedures provided as a routine clinical service might result in greater reductions in SHSe and a larger proportion and longer duration of quit attempts, as clinical services typically continue as long as there is need and would not be curtailed due to a research timeline. Another possible source of reduced power in the current trial might have been the combination of cessation and SHSe counseling. It is possible that the inclusion of cessation services and parents’ quit attempts distracted the counselors and/or parents from protecting children from SHSe.
Finally, smoking cessation rates following experimental interventions have decreased over time. This may be due to greater recalcitrance in the remaining smokers, who persist in smoking despite increasing social, regulatory, and medical pressures to quit (Irvin & Brandon, 2000
). Our participants reported serious life events, including difficulties with sustaining housing (26.7%), employment (27.9%), or telephone service (22.7%); their own or a family member’s incarceration (23.3%) or alcohol or other drug abuse (24.0%); domestic violence (11.6%); and problems with child custody (7.8%). Therefore, these low-income families experienced significant life challenges that may have compounded their difficulties with attending counseling sessions and quitting smoking or reducing children’s SHSe. Such high-risk families may require even more intensive clinical interventions to make larger changes in quit rates and children’s differential cotinine reduction.
Recommendations for future research
Future studies should be directed to removing all smoking from the home, car, and other environments. Studies need to be supported to test more powerful services by continuing counseling and shaping processes until children’s SHSe is eliminated and total smoking bans are enacted. Future interventions should consider additional methods to ensure involvement from all family members, especially smokers, including the possibility of providing incentives for each individual’s participation and/or for confirmed abstinence from smoking (Donatelle et al., 2004
). Longer follow-up periods are recommended so that reductions in home contamination might be reflected in children’s cotinine concentration. Future studies should also be supported to test factorial models of no counseling, SHSe counseling, smoking cessation counseling, combined counseling, and measurement reactivity effects. At present, we are unable to determine the comparable efficacy of our past interventions that provided parents only with counseling for reducing children’s SHSe with the combined intervention tested in this study. Similar SHSe counseling procedures should be tested in states that do not yet have well-established tobacco control programs. It is conceivable that they might prove more powerful in these states due to inclusion of families who have not already quit due to local policies. However, it is also plausible that counseling might be synergistic with long-term and intensive statewide efforts to control tobacco, making clinical outcomes more likely for counseled families in states with strong tobacco control programs. The degree and direction of moderation of counseling effects due to statewide tobacco control policies warrant formal analysis. Such studies will inform the need for policies in other states and help highlight moderating effects of such policies for counseling services.
This combined SHSe and smoking cessation intervention demonstrated promising outcomes for reducing children’s SHSe and mothers’ smoking, and increasing mothers’ short-term quits. These results extend previous findings and suggest that adding smoking cessation services to SHSe counseling may increase experimentation with quitting and contribute to subsequent long-term abstinence.