Smoking Restrictions in the Homes of Children With Cancer

Abstract

Objectives:

To examine smoking restrictions in households of children with cancer and their effect on biological measures of children’s secondhand smoke exposure (SHSe).

Methods:

A sample of 135 parents of nonsmoking children with cancer who lived with a smoker completed structured interviews.

Results:

Approximately 43% of families prohibited smoking in the home. Children living in homes that prohibited smoking had median cotinine levels that were 71% and 52% lower than did those from homes with no and partial restrictions. Conclusions: Parents should be directed to completely ban all smoking from the home and car to best protect their children from SHSe.

Exposure to secondhand smoke (SHS) is harmful to children’s health and is known to increase morbidity and mortality risks in infants, children, and adult nonsmokers.¹ SHS exposure (SHSe) has been linked to cardiovascular and respiratory disease, increased severity of asthma, increased risk for sudden infant death syndrome,^2,3 and otitis media⁴; and the risk of complication increases with higher levels of exposure.⁵

Children with cancer may be especially vulnerable to these health risks secondary to disease and treatment-related toxicities that may affect their respiratory, pulmonary, and cardiovascular functioning.^6-8 Children newly diagnosed with cancer who reside in smoking households are more likely to present with a history of respiratory and pulmonary problems.⁹ Continued SHSe may exacerbate the pediatric cancer patient’s risk for developing second malignancies.^10-12 Youngsters who are exposed to SHS are also more likely to initiate smoking than are those who are not exposed,^13-16 and adoption of smoking habits can be particularly detrimental to this medically at-risk population.

Policies and regulations that prohibit smoking in public places have largely protected adults from SHSe¹⁷ but do not adequately protect children from exposure to tobacco toxins in their own homes and vehicles, where they spend the majority of their time. In the United States, more than one third of children and adolescents live in homes where residents and visitors smoke regularly, with the majority of SHSe resulting from parental smoking.^18,19 Despite their increased health risks, children with cancer are as likely to live with smokers as healthy children are.⁹ Notably, the household is the primary source of exposure to SHS for infants and children.²⁰ In 2009, 22.8% of nonsmoking US middle and high school students reported exposure in the car within the past 7 days.²¹

Home smoking restrictions (ie, limiting or banning cigarette smoking in the home) have been associated with reduced SHSe among healthy children and children with asthma as quantified by parental report, nicotine dosimeters, and urine cotinine assays.^22-26 Studies have documented that children living in homes with total smoking bans had lower cotinine levels than did children in homes with partial bans or no smoking restrictions.^22-27 Adult smokers who live in homes with strict home smoking restrictions are more likely to decrease their daily cigarette consumption,²⁸ have greater motivation to quit or make a quit attempt,²⁹ and have longer periods of sustained abstinence and successful cessation.^29,30

The adoption of home smoking bans is influenced by the interaction of individual variables, characteristics of the proximal family and social environments, and the overall environmental contexts in which individuals are embedded.³¹ Demographically, the prevalence of home smoking restrictions is lower among rural, low-income, and low SES households.^22,23,28,32 However, bans are more likely if the household includes children^{22,23,28,33,34} or a nonsmoking adult,^22,23,32-34 who often plays a critical role in the establishment of home smoking restrictions. Having a child with a medical condition, such as asthma, residing in the home further increases the likelihood of strict smoking bans.²⁶ The number of smokers in the household is inversely associated with the level of household smoking restrictions.^28,30,32

This is the first study to document the prevalence of smoking restrictions in the households of children who live with smokers and are undergoing treatment for cancer. It also evaluates the effects of home smoking restrictions on reported levels of parent cigarette consumption as well as parent-reported measures and biological assays of child SHSe. Child-related medical variables, as well as family and environmental factors,³⁵ often associated with the adoption of home smoking rules, will be examined in families of children with cancer.

METHODS

Participants

Participants were 135 parents or guardians of a child with cancer who lived with at least one adult smoker who smoked in the home or car at the time of recruitment. Parents/guardians were eligible for participation regardless of their own smoking status. Parents were not required to be the identified smoker in the household to participate in the study. Children were eligible for this study if they were younger than 18 years of age, were receiving active treatment for cancer, were at least 30 days post-diagnosis, and were nonsmokers. Parents of children in medical crisis, who had relapsed, had disease recurrence within the past month, or whose disease had progressed, were not recruited for the study. Recruitment took place in the outpatient clinic of a large pediatric oncology hospital between 2002 and 2008. Eligible families were invited to participate in a randomized intervention trial to reduce SHSe among children with cancer. Parents were compensated for their participation, and children received gift vouchers for providing a urine sample. The data presented represent the baseline data for parents and children who agreed to participate in the trial.³⁶

Procedures

Eligible parents were asked to provide smoking-related information and estimates of their child’s SHSe by completing structured interviews. The parent providing this information was designated as the target parent. Children provided urine samples for cotinine analyses. Informed consent was obtained from all parent participants, and children (aged ≥ 7 years) provided assent. The study was approved by the institutional review board.

Measures

Parent cigarette consumption

Parents reported the number of cigarettes consumed by all persons who smoked in the home and car over the past 7 days. Responses were used to calculate the all-source, 7-day total cigarette consumption, a measure that has been used and validated in prior studies.^37-39

Parent-reported child SHSe

Parents were asked to report on the number of cigarettes to which the child was exposed by all persons who smoked in the home and car for the previous 7 days. Exposure was defined as the number of cigarettes smoked in the same room as the child or in the car when the child was present. Responses were used to calculate the all-source, 7-day total parent-reported child SHSe. This measure has been used extensively in other pediatric populations,^36-38 and acceptable test-retest reliability and validity of parent reports of exposure in children with cancer are reported elsewhere.⁴⁰

Urine cotinine assays

Cotinine is a metabolite of nicotine and a reliable biomarker of recent SHS exposure.³⁸ All samples were obtained from patients in the hospital clinic setting and stored in polyethylene Cryo tubes that were frozen in a standard laboratory freezer at −80 degrees Centigrade. Batched samples were packed in dry ice and shipped to the mass spectrometry laboratories at San Diego State University for analyses. Samples were analyzed for cotinine levels using high-performance liquid chromatography and tandem mass spectrometry methods that are sensitive to low levels of SHSe.⁴¹

Household smoking rules

Household smoking rules were assessed using the following question: “What are the rules, if any, about smoking in your home?” The response options included (1) people can’t smoke in the home (total/complete ban); (2) people can only smoke in certain rooms of the house (partial ban); and (3) there are no rules about smoking at home (no ban). Home smoking restrictions have been similarly assessed in other studies.^30,42 The number of smokers residing in the home was also recorded.

Parental perceived vulnerability

Parents responded to a question that asked about the likelihood that their child would develop serious health problems if exposed to SHS.

Provider communication

Parents were asked how often their child’s health care provider communicated with them about smoking.

Stage of change

Target parents who smoked were classified into the precontemplation, contemplation, or preparation stage^43,44 with respect to intention to quit. For purposes of analyses, precontemplators were combined with contemplators due to similarities in addiction level and history of quit attempts, as done in prior studies.³⁰

Statistical Methods

Descriptive statistics for smoking and exposure outcomes were calculated for the entire sample and according to level of home smoking restrictions. Univariate comparisons were made using the nonparametric Kruskal-Wallis test and the chi-square test or exact chi-square test. Ordinary least squares (OLS) regression models examined the impact of smoking ban on parent report of the child’s 7-day SHSe and cotinine levels. Given the skewed distribution of these variables, data were natural log transformed so that more robust results would be obtained as in prior studies.^38,39,45 One was added to SHSe values prior to transformation given some zero values. Model results were back-transformed by exponentiation, so that presented estimates represent the fold-change in geometric means. Variables significant at alpha = .15 in single-variable models were entered into multivariate models; variables remaining significant at the alpha = .15 level were retained. A logistic model examining variables associated with home smoking restrictions (full ban vs partial/no ban) was also similarly investigated.

RESULTS

Participant Characteristics

Table 1 presents the demographic, medical, and psychosocial characteristics of the study sample according to level of home smoking restrictions and overall. Seventy percent (N = 95) of the parents/guardians participating in the trial were self-reported smokers. Close to 23% of smoking parents/guardians in our study intended to quit in the next 30 days and had made a quit attempt in the previous year (preparation stage). Roughly 68% of parents perceived their child to be at risk for developing serious health problems if exposed to SHS. Sixty percent of all parents reported that their child’s health care provider never talked with them about smoking. This lack of communication did not differ by the smoking status of the target parent, with 57% of smokers reporting that their child’s provider did not talk with them about smoking as compared to 68% of nonsmokers. The majority of our sample had one (48%) or 2 (41%) smokers living in the household. Only one family had 4 smokers. No demographic, child medical, and parent psychosocial variables were significantly associated with level of home smoking restrictions (all p’s > .05).

Table 1.

Family Demographic and Smoking-Related Characteristics According to Level of Smoking Restrictions in the Home

Characteristic	All N = 135	Full N = 58	Partial N = 49	None N = 28	p-value a
Child’s Age (in years)	7.6	6.4	9.3	10.2	.285
Median (range)	(0.4-17.7)	(0.4-17.1)	(0.9-17.3)	(1.0-17.7)
Child’s Gender	71 (52.6)	29 (50.0)	30 (61.2)	12 (42.9)	.261
Male – N (%)
White Child’s Race b– N (%)	102 (75.6)	45 (77.6)	35 (71.4)	22 (78.6)	.698
Child’s Diagnosis
Leukemia/lymphoma	88 (65.2)	37 (63.8)	31 (63.3)	20 (71.4)	.834
Solid tumor	37 (27.4)	17 (29.3)	13 (26.5)	7 (25.0)
CNS	10 (7.4)	4 (6.9)	5 (10.2)	1 (3.6)
Months From Diagnosis	3.0	2.4	2.8	3.7	.299
Median (range)	(1.0-59.5)	(1.0-59.5)	(1.0-37.0)	(1.5-25.1)
Target Parent Age (in years)	33.9	33.2	35.9	32.4	.771
Median (range)	(19.6-61.2)	(22.3-56.9)	(19.9-54.0)	(19.6-61.2)
Target Parent Gender	23 (17.0)	10 (17.2)	6 (12.2)	7 (25.0)	.358
Male – N (%)
White Target Parent’s Race b– N (%)	108 (80.0)	46 (79.3)	39 (79.6)	23 (82.1)	.950
SES – N (%)
High	35 (25.9)	14 (24.1)	15 (30.6)	6 (21.4)
Middle	33 (24.4)	16 (27.6)	14 (28.6)	3 (10.7)	.192
Low	67 (49.6)	28 (48.3)	20 (40.8)	19 (67.9)
Marital Status
Married	78 (57.8)	39 (67.2)	24 (49.0)	15 (53.6)
Divorce/separated	13 (9.6)	7 (12.1)	3 (6.1)	3 (10.7)	.110
Never married	44 (32.6)	12 (20.7)	22 (44.9)	10 (35.7)
# Smokers c – N (%)
0	5 (3.7)	3 (5.2)	2 (4.1)	0 (0.0)	.869
1	65 (48.2)	27 (46.6)	23 (46.9)	15 (53.6)
2	56 (41.5)	24 (41.4)	21 (42.9)	11 (39.3)
3-4	9 (6.7)	4 (6.9)	3 (6.1)	2 (7.1)
Smoking Target Parent – N (%)	95 (70.4)	43 (74.1)	34 (69.4)	18 (64.3)	.633
Perceived vulnerability
Serious health problems   (very likely/likely) – N (%)	92 (68.2)	38 (65.5)	32 (65.3)	22 (78.6)	.413
Provider Communication – N (%)
Many times	16 (11.9)	4 (6.9)	6 (12.2)	6 (21.4)	.082
Sometimes	38 (28.2)	17 (29.3)	10 (20.4)	11 (39.3)
Never	81 (60.0)	37 (66.8)	33 (67.4)	11 (39.3)
Stages of Change d – N (%)
Preparation	21 (22.8)	8 (19.1)	8 (25.0)	5 (27.8)	.876
Contemplation	43 (46.7)	22 (52.4)	14 (43.8)	7 (38.9)
Precontemplation	28 (30.4)	12 (28.6)	10 (31.3)	6 (33.3)

Note.

CNS = central nervous system; SES, socioeconomic status

^aKruskal-Wallis test, chi-square or exact chi-square test

^bWhite and not of Hispanic origin. Remaining patients were black except for 2 whites of Hispanic origin, one Asian, and 3 of more than one race. Remaining parents were black except for one, who was Asian.

^cOnly one family had 4 smokers. Five children lived in nonsmoking homes, but were in family situations where there was regular smoke exposure.

^dOnly captured for smoking target parents (N = 95). Three of these had missing responses. Refers to stage of parental intentions to quit smoking.

Household Smoking Restrictions

A full smoking ban (ie, no smoking allowed) was reported to be in effect in 58 (43%) of the 135 households; 49 (36.3%) had partial smoking restrictions (smoking allowed in specified rooms); and 28 (21%) had no smoking restrictions in the home (smoking allowed) at baseline. There were no significant differences in the number of smokers who resided in the homes of families with full or partial smoking restrictions compared to those with no smoking restrictions (p > .10). Almost 49% of homes with full or partial smoking restrictions had 2-4 smokers living in the home as compared to 46% of those with no smoking restrictions. Sixty-two percent of families with full home smoking bans reported exposing their child in the car as compared to 69% and 75% of families with partial or no smoking restrictions at home, respectively.

Table 2 shows the final logistic regression model predicting full household smoking bans vs partial/no smoking ban combined. Younger age of target parent (p = .003) and younger patient age (p = .001) were associated with an increased odds of a full smoking ban being implemented in the home. There was a trend for target parents who were married to be 2.2 times more likely to establish full smoking bans compared to parents who had never been married (p = .064). Time since diagnosis also met the model inclusion criteria, but was not significant. The final model explained 22% of the variance in the distribution of full home smoking bans.

Table 2.

Predictors of Full Smoking Restrictions in the Home (N = 135) ^a

Effect b	Odds Ratio	95% Confidence Intervals		p-value
Married	2.23	0.95	5.53	.064
Divorced/Separated	2.89	0.75	11.08	.123
Target Parent Age: < 25 years	9.09	2.13	33.33	.003
Patient Age (in years)	0.86	0.79	0.94	.001
Time Since Diagnosis: < 6 months	2.00	0.84	4.77	.116

Note.

^aOutcome is full home restrictions vs partial/no home smoking restrictions combined.

^bReference categories are never married, parent age ≥ 25 years, and ≥ 6 months from diagnosis. Patient age was analyzed as a continuous variable.

Pseudo R-square = .22

Parent-Reported Cigarette Consumption and Child SHSe

The median total number of cigarettes smoked by all sources in the home and car over a 7-day period and related reported exposure and cotinine levels according to level of household smoking restrictions are presented in Table 3. Significant differences were reported in cigarette consumption by smokers across households with different smoking rules (p < .001). No significant differences were found in the number of cigarettes smoked in the car according to level of home smoking restrictions (p > .10). Significant differences were found in cotinine levels obtained from children residing in homes with different smoking restrictions (p = .002).

Table 3.

Median (IQR) Reported All-Source Smoking and Exposure Levels and Cotinine Estimates of Exposure Over 7 Days According to Level of Smoking Restrictions in the Home

All Source	All N = 135	Full N = 58	Partial N = 49	None N = 28	p-valuea
Home
Smoking	18 (0-102)	0 (0-0)	48.5 (5.5-140.5)	75 (45-210)	< .001
Exposure	0 (0-36)	0 (0-0)	2 (0-48)	47.5 (13.5-123.5)	< .001
Car
Smoking	7 (0-23)	8 (0-23)	4 (0-19)	10 (0.5-25)	.391
Exposure	3 (0-14)	3 (0-12)	3 (0-11)	7.5 (0.5-18)	.288
Total
Smoking	42 (7-120)	10 (2-40)	49.5 (22.5-145.5)	102 (59-216)	< .001
Exposure	13 (2-48)	3.5 (0-15)	21 (2-61)	58.5 (24.5-132.5)	< .001
Cotinine (ng/ml)	3.3 (1.5-11.3)	2.1 (1.2-5.4)	6.6 (1.5-15.2)	8.7 (2.8-17.4)	.002

Note.

IQR Interquartile range; ng/ml, nanograms per milliliter

^aNonparametric Kruskal-Wallis test

Smoking exposure was missing for 2 families.

The final multiple variable regression models predicting all-source 7-day total reported exposure and child cotinine levels are shown in Table 4. Compared to households with no ban, those with full smoking bans had a 90% reduction in geometric mean 7-day total exposure (p < .001). Those with partial restrictions had a 76% reduction as compared to those with no bans (p < .001). Geometric mean exposure was 1.9 times higher for children whose target parent was white as compared to those whose parents were not white (p = .045). Children with leukemia had a 47% lower exposure as compared to those with solid or CNS tumors (p = .019). Level of home smoking restrictions, parent race, and child diagnosis accounted for 30% of the variation in 7-day total reported exposure.

Table 4.

Predictors of 7-Day All-Source Reported Exposure and Cotinine

Effect	B a	95% Confidence Intervals		p-value
Reported Exposure (N = 135) b
Full ban	0.10	0.05	0.19	< .001
Partial ban	0.24	0.12	0.48	< .001
White target parent’s race	1.90	1.02	3.57	.045
Leukemia diagnosis	0.53	0.31	0.90	.019
R-square=0.30
Cotinine (N = 133) c
Full ban	0.29	0.19	0.55	< .001
Partial ban	0.67	0.39	1.15	.147
Patient age (in years)	0.96	0.92	1.00	.059
White target parent’s race	1.48	0.89	2.58	.126
High SES	0.45	0.25	0.64	< .001
Married	0.53	0.33	0.85	.010
Divorced/separated	0.46	0.22	0.96	.038
Smoking target parent	2.03	1.29	3.20	.003
High perceived vulnerability	0.49	0.32	0.77	.002
R-square = .40

Note.

SES = socioeconomic status

^aExposure on natural log scale was analyzed, and then results were back-transformed. Therefore, confidence intervals not containing one indicate significant results. One was added to 7-day exposure prior to transformation to address zero exposure values.

^bReference categories are No ban for Ban, Nonwhite for Race, and Solid or central nervous system tumors for Diagnosis.

^cReference categories are No ban for Ban, Male for Gender, low SES for SES, Never married for Married and Divorced/separated, Nonsmoking for Target parent status, and Low perceived vulnerability (score 1-3) for Perceived vulnerability. Patient age was a continuous variable.

The p-values for Full vs Partial ban for all source exposure and cotinine were both p = .002. Results for comparisons with No ban (reference category) are shown above.

Households with full smoking bans were associated with a 71% lower level in children’s geometric mean cotinine values compared to no bans (p < .001) and a 52% lower level compared to partial restrictions (p = .002), whereas partial restrictions were nonsignificantly associated with a 33% lower level compared to no smoking restrictions (p = .147). Greater parent perceptions of health risks from SHSe (p = .002) were associated with lower cotinine levels. There was a 55% lower-level geometric mean cotinine for children from high SES families compared to those from low or middle SES families (p < .001). Children whose target parent was married (p = .010) or divorced/separated (p = .038) had lower cotinine levels as compared to those who were never married. Children whose target parents were smokers had geometric mean cotinine levels that were 2.03 times higher than were those from children whose target parents were not smokers (p = .003). Target parent age and race also met model inclusion criteria, but were not significant. The predictors in Table 4 accounted for 40% of the variance in children’s cotinine levels. Although the number of smokers in the home was significantly associated with cotinine, it was not significant in the multivariate model after adjusting for smoking status of the target parents, which was highly associated with number of smokers.

DISCUSSION

The results of our study show that a significant proportion of children undergoing treatment for cancer are exposed to SHS in their households. Only 43% of families in our study imposed strict smoking rules within the home, similar to results reported for families of children with asthma.^25,26,46 Parents often used incomplete procedures to protect their child from SHSe. These included not smoking in areas where the child sleeps or spends significant time or restricting smoking to a single room in the house not necessarily off limits to the child. Children’s exposure to smoke in the car was also relatively common in our sample, and those living in households with full home smoking restrictions were often exposed in the car. Car exposure is concerning because it is highly concentrated and may reach unhealthy levels that are more toxic than SHSe in the home setting.⁴⁷ Of note is that during the time period when the study data were collected (2000-2008), there was an increase in the number of states that had enacted comprehensive smoke-free laws in public places,^17,21 resulting in better population-level protection from SHSe. However, many children continue to be exposed in domestic settings, which depend on adoption of voluntary smoking restrictions by their families. The finding that many children with cancer live in homes and travel in cars that are not smoke-free is even more disturbing against a background of improved public policy regarding tobacco control.

Full household smoking bans were significantly associated with lower cigarette consumption by smokers in the home as well as lower child SHSe as based on parent report and quantifiable biological cotinine assays. These associations demonstrate construct validity for reported measures, even if not exact estimates of total exposure, as previously reported.^38,40 Significantly lower cotinine levels were observed in children from homes with a full ban on smoking when compared to those obtained from children living in homes with less restrictive smoking conditions. However, more restrictive household smoking rules did not completely eliminate children’s SHSe. This may be due to other sources of exposure not related to the home, such as car exposure, but may be also due to insufficient time since initiation of such rules to see more complete protection from SHSe.

No significant difference was found in the cotinine levels of children residing in homes where smoking was permitted vs those where smoking was partially restricted. Although parent-reported exposure outcomes suggest some benefit for measures that fall short of a full smoking ban (partial ban) relative to no bans, they afford children less protection from SHS, as measured by urinary cotinine. Additionally, partial smoking restrictions are unlikely to offer protection from exposure to high levels of tobacco toxins that are deposited onto household surfaces and that can persist well beyond the period of active smoking.^27,37,48-50 Dust and surface contaminants in homes and cars and their re-emission into the air can be a source of carcinogenic third-hand smoke exposure (TSHe) for children.^49-51

Younger parents, and those living with younger children, were more likely to establish smoke-free homes, as demonstrated in previous studies.^52-54 Younger parents may more readily adopt smoke-free homes because they are more likely to have young children in the household whose health is a primary concern. Parents without the support of a partner may have fewer financial resources and less available backup adult supervision of children in the home. Tobacco education programs should, therefore, consider the barriers experienced by families with limited support in order to promote the adoption of smoking restrictions in homes not likely to have them.

The results from this study should be considered within the context of its limitations. First, estimates of homes with smoking restrictions were based on self-reports and not validated by an objective measure; however, a number of studies have supported the validity of such self-reported data in population surveys.^55,56 It is possible that the hospital setting and collection of information during the child’s cancer treatment influenced the degree of accurate disclosure by parents about their household smoking rules and child’s exposure. Second, the duration of the home bans was not assessed. Further evaluation of the process of and reasons for adopting home smoking restrictions in households of children with cancer, particularly as they relate to the timing of the child’s diagnosis, is warranted. The lower levels of reported exposure among children diagnosed with leukemia in our sample suggest a potential biological, treatment-related, or psychosocial mechanism that should be explored.

Additionally, the collection of children’s urine samples and parent reports of exposure were intended to capture exposure during the same one week prior to assessment. Urine samples were obtained from the child at the time the parent completed the exposure reports for the past 7 days. However, only a single urine sample was obtained at the time of assessment, providing accurate estimates of only recent exposure (2-3 days) due to the short half-life of cotinine. Reliance on a single cotinine sample does not preclude the possibility that estimates of exposure were artificially inflated or reduced if the timing of the urine samples reflected episodic high- or low-level exposure events. For example, children being treated at a smoke-free hospital environment prior to urine sample collection may have had less opportunity for exposure and lower cotinine levels than those of children exposed in other settings prior to their clinic visit. Future studies should require more frequent cotinine measurements to resolve these temporal sampling problems and obtain representative levels of exposure for this patient population.⁵⁷

Of clinical importance is the finding that the majority of parents in our sample had never discussed their smoking habits or their child’s SHSe with their child’s health care provider. This is consistent with low rates of pediatrician tobacco screening and counseling provided across medical settings.^58-60 Advice and counseling about tobacco control may be one of the most cost-effective means of reducing tobacco use or SHSe.⁶¹ Typically, providers ask about smoking and advise smokers to quit. However, child exposure is not fully protected by one parent’s quitting, as most smokers have friends and family members who smoke. Providers should be trained and encouraged to direct parents to establish complete tobacco bans in their homes and cars, even if they remain smokers.³¹ Exposure to hospital settings that promote tighter tobacco control may further encourage personal home smoking bans.