Abstract
OBJECTIVES: Understanding patterns of parental tobacco use and their association with child exposure can help us target interventions more appropriately. We aimed to examine the association between parental smoking practices and cotinine levels of hospitalized children.
METHODS: This is a secondary analysis of data collected from parents of hospitalized children, recruited for a cessation intervention randomized controlled trial. Smoking parents were identified by using a medical record screening question. Parent-reported demographics and smoking habits were compared to child urine cotinine by using geometric means and log-transformed cotinine levels in multivariable linear regression analyses.
RESULTS: A total of 213 patients had complete baseline parent-interview and urine cotinine data. The median age was 4 (interquartile range: 1–9); 57% were boys; 56% were white, 12% were Black, and 23% were multiracial; 36% identified as Hispanic. Most families (54%) had 1 smoker in the home; 36% had 2, and 9% had ≥3. Many (77%) reported having a ban on smoking in the home, and 86% reported smoking only outside. The geometric mean cotinine level of the cohort was 0.98 ng/mL. Higher cotinine levels were associated with more smokers in the home (ratio of 2.99) and smoking inside the house (ratio of 4.11).
CONCLUSIONS: Having more smokers in the home and parents who smoke inside are associated with increased smoke exposure; however, even children whose families who smoke only outside the home have significant levels of cotinine, a marker for toxin exposure.
Tobacco smoke exposure (TSE) remains an important cause of disease in children. Although smoking rates in adults have decreased, 18% of children have a parent who smokes tobacco in the home, and 38% of children from ages 3 to 11 have detectable cotinine in their urine.1,2 TSE impacts many childhood diseases; it increases the risk and severity of bronchiolitis,3,4 asthma,5,6 influenza,7 and pneumonia.8 The risk of TSE is not confined to respiratory illness; it has also been associated with the development of gastroenteritis in young children.9 TSE is associated with a significant overall increase in hospitalization.10,11
TSE can be from secondhand smoke, which occurs in the presence of a lit cigarette, or from thirdhand smoke, in which the residue of the smoke remains in the air, textiles, floors, and other surfaces after the cigarette is extinguished.
Cotinine is a metabolite of nicotine and is a specific biomarker for exposure to tobacco smoke. It has been used clinically to monitor TSE;12,13 however, it is still not widely available, and, thus, we often must rely on parent report. Even low levels of cotinine have been associated with asthma exacerbations,14 decreased antioxidant levels,15 and lower cognitive testing scores.16 Understanding how parents use tobacco and how this influences biological evidence of TSE among hospitalized children may improve the effectiveness of counseling and improve delivery of smoking cessation interventions, including screening, provision of nicotine replacement therapy, and brief motivational interviewing17,18 in child health care settings, especially when we have to rely only on parent report. In particular, it may allow us to target interventions at more high-risk children and provide feedback on possible exposure levels. The specific aims for this study were to describe parental smoking behaviors in our sample and explore how parental smoking behaviors related to child cotinine level.
Methods
This is a secondary analysis of baseline data from a randomized controlled trial of a smoking cessation intervention for parents of hospitalized children, which took place at an ∼400-bed university affiliated children’s hospital in the Midwest United States, between December 2014 and April 2018. We used an electronic medical record–based screening question: “Does anyone who lives in your home or who cares for your children smoke?”; any family with a positive response was eligible to be approached for recruitment. A study team member assessed for parental smoking status and eligibility. Children from ages 0 to 17 were eligible for participation if they had at least 1 parent who was a current cigarette smoker. Families were excluded if there were concerns about custody or if the child was unable to produce urine. Consent (and assent for children >7 years) was obtained for participation, and families were given a $25 gift card at the baseline visit. The study was approved by the affiliate institutional review board.
After consent, the participant completed the baseline exposure and smoking behavior survey. We used validated measures for assessing pediatric TSE and parental tobacco use from the American Academy of Pediatrics Julius B. Richmond Center of Excellence.19 The questions included standard demographic information about both the parent and child and information about other potential sources of exposure and smoke-free home and car rules. Exposure was not defined in the question stem but was explained if the parent was confused. We also asked if parents used electronic cigarettes (e-cigarettes) every day, some days, or not at all. The child’s diagnosis for the hospitalization (primary and any secondary) was pulled from the electronic medical record.
Baseline Urine Collection
We collected urine from patients at enrollment using cotton balls placed in the diaper, a catheter (if already in place for routine care), a urine bag applied by a trained study team member, or a specimen cup or hat (for older children). Urine was stored in a −80° freezer, and aliquots were batched shipped on dry ice via overnight transportation to the Tobacco Biomarkers Core Facility at the University of California, San Francisco, for analysis of cotinine by using liquid chromatography–tandem mass spectrometry; the limit of quantification (LOQ) was 0.05 ng/mL.20
Analysis
Patients were identified as having a respiratory illness by using the Agency for HealthCare Research and Quality Clinical Classification Software Refined (CCSR) for ICD-10-CM Diagnoses.21 Single imputation was used for values below the LOQ, replacing those missing values with the LOQ divided by 2. The characteristics of the pediatric participants were summarized with count (percent) for categorical data and median (interquartile range) or mean (SD) for continuous data. Because of its skewed distribution, cotinine values were log-transformed for analyses. Transformed means and their confidence intervals were back-transformed to obtain geometric means and confidence intervals. Linear regression was used to examine the relationship between parental smoking practices and log-transformed cotinine values. Multivariable linear regression was used to examine the association of parental smoking practices with log-transformed cotinine levels, while adjusting for age, sex, ethnicity, race, and parental education. Data were analyzed by using SAS version 9.4 (SAS Institute, Inc, Cary, NC) software. All statistical tests were performed with a level of significance of 0.05.
Results
Of 1989 families who were eligible after in-person screening, 263 (13%) agreed to participate in the randomized controlled trial (Fig 1) from which these data were subsequently analyzed. Of these, 214 had both complete survey data and cotinine data. Of the 21 adolescents in the study, 1 had a cotinine level >10 ng/mL (a level indicating they were an active smoker) and was excluded; 213 were included in these analyses. Overall, the median age was 4 year, and 57% were boys. The racial and ethnic composition was the following: 56% white, 12% Black, and 23% multiracial, with 36% reporting Hispanic or Latino ethnicity (Table 1). A majority (57%) were admitted for respiratory illness diagnoses. The geometric mean cotinine level of the cohort was 0.98 ng/mL, with a range from 0.025 to 115.76 ng/mL.
Main randomized controlled trial Consolidated Standards of Reporting Trials diagram.
Geometric Mean Cotinine Levels by Demographics and Reported Exposure
Most of the parents reported having 1 smoker in the home (54%), whereas 36% had 2 and 9% had ≥3 (Table 1). We asked parents about their child’s recent TSE; 33% had been exposed in the previous 24 hours. In the previous 7 days, 31% had been exposed to tobacco smoke at home, 30% in the parent’s car, and 36% in an outdoor public place. When asked “Where do you smoke tobacco when you are at home,” most parents (85%) reported smoking outside only; slightly fewer (73%) responded no when asked “Over the past 3 months, has anyone smoked tobacco anywhere inside your home.” A total of 22% reported using e-cigarettes some days or every day. A total of 77% reported having a ban on smoking in the home, but only 34% did not allow smoking in the car.
There were significant differences in cotinine level by demographics (Table 1); boys had a lower geometric mean than girls (0.82 ng/mL vs 1.24 ng/mL; P = .047), and Black children had a higher cotinine level (2.13 ng/mL), compared with white children (0.81 ng/mL; P = .004). The number of smokers in the home was significantly associated with higher cotinine levels: 0.72 ng/mL for children with 1 smoker in the home, compared with 1.24 ng/mL for children with 2 smokers in the home (P = .01) and 2.24 ng/mL for children with ≥3 (P = .002). Reported recent exposure was also associated with higher cotinine levels. Children with exposure in the past 24 hours had a mean cotinine level of 1.32 ng/mL, compared with 0.81 ng/mL with no exposure (P = .03), and children exposed in the home in the past 7 days also had higher cotinine levels (1.50 ng/mL vs 0.80 ng/mL; P < .01). Children in families in which smoking was not allowed in the home had a lower cotinine level than those in which it was allowed (0.84 ng/mL vs 1.64 ng/mL; P = .007), as did those in homes in which no one had smoked in the previous 3 months (0.83 ng/mL vs 1.85 ng/mL; P < .001). Cotinine levels did not vary by parental e-cigarette use or by whether the child was admitted for respiratory illness versus nonrespiratory illness. In a multivariable regression analysis, the numbers of smokers in the home (ratio of 2.99 for >2 vs 1), smoking in the home (ratio of 4.11 for inside versus outside only), and Black race (ratio of 2.25 versus white children) were significantly associated with elevated cotinine (Fig 2). We assessed for collinearity using correlations; ρ statistics were <0.5 for all variables.
Multivariate predictors of increased cotinine level. CI, confidence interval; SHS, secondhand smoke.
Discussion
We found high levels of TSE, as measured by cotinine, in our cohort of hospitalized children who have at least 1 parent who smokes tobacco. We found a strong association between higher cotinine levels and the number of smokers in the home, exposure in the past 24 hours, and exposure in the past 7 days. Because cotinine tests are not widely available for clinical use, we currently must rely on proxy measures to assess the risk of exposure. These findings suggest that a few simple questions about exposure may be able to identify children at risk for higher exposure levels and are consistent with previous studies in which researchers have found that the number of smokers in the home correlates with cotinine levels22,23 and that parent report can be used to assess exposure.24,25 There are limitations to parent report, most of which will result in underreporting, as has been seen in previous studies.26 Parents may not recognize that a child is being exposed,27 especially if they do not see or smell the smoke, such as when the smoking happens outside or when the parent is not home to detect others smoking in the home. Adult smokers tend to underreport their own tobacco use.28 Biochemical validation is, thus, recommended to confirm cessation, usually with expired carbon monoxide or urine or saliva cotinine.29 However, carbon monoxide has not been demonstrated to be an accurate proxy for secondhand exposure in children, and the widely available, clinically approved cotinine tests lack the sensitivity to detect low levels of exposure. Until a commercially available sensitive clinical test for cotinine is made available for children, we will continue to have to rely on parent report.
Although we found significantly lower levels of exposure in children whose parents did not allow smoking in the home, they still had cotinine levels that may be high enough to cause harm, suggesting that thirdhand smoke plays an important role in exposure. The Surgeon General has stated that there is no safe level of exposure to tobacco smoke.30 Although having a home smoking ban and only smoking outdoors may have reduced the TSE of children in the study, it did not completely protect the children in the home from exposure. However, in our study, we did provide additional empirical support for the American Academy of Pediatrics policy recommending exposure reduction when complete elimination of TSE is not possible.
This complements data from Matt et al,30 who found that infants of mothers who smoked only outside still had significantly elevated urine cotinine levels. We did not see that parental use of e-cigarettes in addition to tobacco smoking was associated with an increase in cotinine level; further research is needed, particularly in families that use only e-cigarettes, to understand the relationship between secondhand e-cigarette aerosol and children’s health.
Consistent with previous studies, we found that African American children had higher levels of cotinine compared with that of white children, even when controlling for smoking behaviors. Researchers have hypothesized that the higher levels found in African Americans are due to differences in the metabolism of cotinine,31 but it is unclear whether this is associated with higher morbidity. We also found that boys had higher levels of cotinine than girls; however, this association was not found in the final model and, thus, likely represents confounding.
Because our parents were participating in a randomized controlled trial, we were limited to children of parents who were willing to participate in an intervention; this may have biased the sample to lower-exposure households because of social desirability, in addition to the overall risk of reporting bias. If this is the case, the true exposure is likely higher. Our enrollment rates were low and, likely, overrepresented parents who wanted to quit smoking and may have already been decreasing their use. We also only recruited families in which there was a parent who smoked tobacco, and, thus, we cannot compare levels with nonexposed children. Many of the questions relied on parental report of other people’s behavior in the home. We did not assess child smoking behaviors and may have not excluded light intermittent teen-aged smokers. This study may not be generalizable outside of a hospitalized population of children in the Midwest United States.
Conclusions
Parent report is a good, if not perfect, measure of exposure in children who have a parent who smokes. Smoking outside does not completely eliminate children’s exposure to tobacco. Dual use of e-cigarettes and combusted tobacco was not associated with a lower cotinine level in children. The hospitalization of a child represents an important opportunity to help parents engage in smoking cessation programs. Hospitals should invest in evidence-based programs to help parents quit, including mandatory screening for exposure and provision of nicotine replacement therapy and brief motivational interviewing.
Acknowledgments
We thank Cordelia R. Elaiho, MPH, for article preparation.
Footnotes
FINANCIAL DISCLOSURE: The authors have indicated they have no financial relationships relevant to this article to disclose.
FUNDING: Funded by the National Cancer Institute grant R01CA181207 (to Dr Wilson), the Flight Attendant Medical Research Institute (through a grant to the American Academy of Pediatrics), and the Children’s Hospital Colorado Research Institute. Funded by the National Institutes of Health (NIH).
POTENTIAL CONFLICT OF INTEREST: The authors have indicated they have no potential conflicts of interest to disclose.
References:
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