Association between children’s secondhand co-exposure to tobacco and cannabis smoke and elevated urinary cotinine levels: a cross-sectional analysis
Social and Behavioral Sciences, Barnett College of Public Health, Temple University, Philadelphia, Pennsylvania, USA
Chapman University, Orange, California, USA
The City University of New York, New York, New York, USA
University of Rochester School of Medicine and Dentistry, Rochester, New York, USA
Abstract
Background
Cannabis use is far more common among adults who smoke tobacco than adults who do not, and its use is increasing among people who smoke tobacco with children living in the home. Given the well-established evidence that caregiver smoking is the primary source of children’s secondhand exposures to these products, the increasing trend in caregiver co-use is raising public health concerns about children’s co-exposure. Emerging data indicates that adult co-use is linked to additive health consequences, such as elevated nicotine and other tobacco-related toxicant blood levels, relative to use of only tobacco. It is unknown whether children’s co-exposure leads to similar additive consequences. This study examined whether children’s co-exposure to secondhand tobacco and cannabis smoke related to higher urinary levels of cotinine (the primary nicotine metabolite) relative to children exposed to only tobacco smoke.
Methods
This study performed a cross-sectional analysis of baseline data from the ‘Babies Living Safe and Smokefree’ tobacco intervention randomised controlled trial. All participants (N=396) included low-income mothers who smoked tobacco daily and were primary caretakers of young children (<6 years old). Multivariable regression was performed to test the hypothesis that maternal co-smoking would relate to children’s elevated cotinine levels in a model including potential confounding variables (eg, children’s mean daily tobacco smoke exposure, maternal nicotine dependence level).
Results
Mean participant age was 30.11+6.52 years old, and their children’s age was 30.24+20.0 months old. In the past 7 days, 146 (36.9%) participants reported smoking cannabis on at least 1 day. Multivariable regression modelling showed that maternal co-smoking was associated with higher children’s cotinine levels (p=0.04).
Conclusions
Maternal co-use of tobacco and cannabis, relative to tobacco smoking only, is associated with higher cotinine levels in their children. Given that caregiver smoking is the primary source of young children’s exposure to both tobacco and cannabis, clinicians and the public could be better informed about the potential additive health risks of co-exposure without diluting existing health messaging and prevention efforts focused on use and exposure risks related to each product independently. Results point to the need for sustained public health efforts to reduce children’s exposure to these toxicants.
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Keywords: Public Health, Primary Prevention, Risk Assessment, Cross-Sectional Studies
Article notes
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Received 2025 Aug 5; Accepted 2026 Feb 2; Collection date 2026.
Boxed Text
WHAT IS ALREADY KNOWN ON THIS TOPIC
- Adult co-smoking of tobacco and cannabis is linked to additive tobacco-related health risks. For example, blood levels of tobacco-related toxicants in adults are higher among current co-users of tobacco and cannabis compared with those who only smoke tobacco. Caregiver’s secondhand smoke (from either tobacco or cannabis) is the primary source of young children’s exposures to those products, but few studies have examined co-exposure risks.
WHAT THIS STUDY ADDS
- Young children (≤6 years old) of mothers who smoked tobacco daily and smoked cannabis within the last 7 days had significantly higher mean urinary cotinine (primary nicotine metabolite) than children whose mothers only smoked tobacco daily.
HOW THIS STUDY MIGHT AFFECT RESEARCH, PRACTICE OR POLICY
- Public health advocates and clinicians have become keenly aware of the wide array of tobacco smoke exposure-related child health consequences, and emerging data points to health consequences associated with children’s exposure to secondhand cannabis smoke. Results of this study suggest that co-exposure may increase risks even further. This study could inspire researchers to broaden their examination of the potential additive negative child health consequences of co-exposure as well as the biobehavioural and social mechanisms that could explain this association. Regarding practice implications, results could prompt paediatric clinicians to consider expanding best practice guidelines for tobacco intervention to include screening and health education around secondhand cannabis exposure. In addition, public health programming could expand health messaging about the harms of children’s exposures to tobacco and cannabis, while paediatric health advocates could work to enhance smoke-free air policies and laws to include cannabis smoke restrictions in subsidised housing, childcare centres and vehicles.
Introduction
Tobacco and cannabis are among the most commonly used psychoactive substances in the USA.1 While rates of tobacco smoking have declined over recent decades, 28.3 million (11.5%) US adults still smoke2 and nearly 40% of US children aged 3–11 years old show biological evidence of tobacco smoke exposure (TSE).1 3 4 In contrast, the prevalence of cannabis smoking has climbed during this time. The most recent surveillance data suggests that 58.9 million US adults have either smoked or vaped cannabis in the last month (ie, 12.4 million (36.5%) adults 18–25 years old; 46.5 million (20.8%) adults >26 years old).5 The prevalence of cannabis use is significantly higher among adults who smoke tobacco than those who do not smoke.6 7 A recent study of Behavioural Risk Factor Surveillance System surveys suggested that adults who currently smoke tobacco were more than two times as likely to use cannabis either frequently (6.2% vs 3.0%) or daily (10.1% vs 4.0%) compared with adults who never smoked tobacco.8 Moreover, among adult caregivers who smoke tobacco, nearly 30% report cannabis smoking regularly compared with less than 1% of parents who never smoke tobacco.9 10 The primary sources of young children’s secondhand tobacco and cannabis smoke exposures are caregiver smoking in the home, often that which occurs in social contexts.10,12 In addition, many low-income communities evidence higher prevalence of adult co-use13 and greater likelihood of children’s residential secondhand smoke exposures than more affluent areas.14,18 Thus, children dwelling in low-income communities bear the greatest public health burden related to co-exposure.
Independent consequences of children’s secondhand tobacco and cannabis smoke exposures
Children’s secondhand exposure to either tobacco or cannabis smoke is linked to numerous health and developmental consequences as described below.
Secondhand TSE: Research over the past few decades has firmly established that children’s TSE is a risk factor for numerous acute and chronic paediatric health consequences across developmental periods.12 19 20 For example, since 2000, the WHO has maintained there is no safe level of TSE21 due to its links to lung cancer, heart disease, respiratory illnesses and cardiometabolic risks. In addition to physical health consequences, children’s TSE is linked to neurodevelopmental and behavioural problems, such as attention deficit, conduct difficulty and emotional dysregulation.22 Moreover, exposed children have a greater likelihood of future tobacco use than children raised in smoke-free homes23 as they experience intensified neurological reactivity to nicotine that increases their vulnerability to future nicotine dependence.23,25
Cotinine is the primary metabolite of nicotine and is the most specific and sensitive biomarker of children’s TSE.26 In addition, cotinine levels are positively correlated to elevated TSE-related health risks in children.27 Well-established predictors of elevated cotinine in children include: (1) greater amount of parental tobacco smoking (eg, cigarettes smoked per day, nicotine dependence level), (2) more residents who smoke tobacco in the home, (3) higher levels of parent-reported TSE from all potential sources and (4) less frequent parental efforts to protect their children from TSE (eg, prohibiting smoking around their children).
Secondhand cannabis smoke exposure (CSE): Compared with TSE, secondhand CSE has yet to become firmly established as a modifiable risk factor for child health and remains insufficiently integrated within public health advocacy and prevention intervention frameworks. Part of the challenge is that many adults misperceive that secondhand CSE is safe compared with TSE.28,30 However, like TSE, CSE extends to individuals who are in proximity to a person who smokes cannabis via respiratory and dermal pathways.31 32 A 2025 systematic review presents emerging evidence that prenatal and early-life cannabis exposure may confer similar paediatric health vulnerabilities as TSE, including impairments in emotional regulation and behavioural functioning in young children.33 Other recent studies highlight that children are increasingly exposed to secondhand cannabis smoke in their homes.11 34 Importantly, secondhand cannabis smoke contains many of the same carcinogens and respiratory irritants as tobacco smoke, in addition to cannabis’ primary psychoactive compound, tetrahydrocannabinol (THC).16 35 Moreover, compared with residential tobacco smoke, cannabis smoke can generate four times higher PM2.5 particle concentrations.36 (PM2.5 particles are tiny airborne pollutants, 2.5 micrometers or less in diameter, that originate from combustion and dust and cause inflammation linked to asthma and cardiovascular disease). CSE also increases risk of paediatric respiratory infections, cognitive impairment and behavioural problems.37,39 Cannabinoids from secondhand cannabis smoke have been detected on surfaces indoors, after smoke is no longer visible.40 This evidence parallels thirdhand tobacco smoke, which contains nicotine, carcinogens and other tobacco toxicants that are absorbed on hard surfaces (eg, floors, clutter), dust and fabrics—then remitted into the air over months after tobacco smoke has cleared the air.41
Consequences of children’s co-exposure
Although the psychoactive compounds in tobacco and cannabis differ, secondhand smoke constituents from both products share similarities that could create additive exposure-related health risks.35 In one study of co-exposed 0–3 years old children,42 THC blood levels were associated with cotinine blood levels (≥2.0 ng/mL; p=0.0001), suggesting that co-exposed children absorb the psychoactive constituents of both tobacco and cannabis smoke. These results support earlier evidence of potential additive exposure risks among co-exposed children.10 16
While there remains a dearth of research examining the effects of children’s co-exposure, examining evidence of potential additive consequences of co-use among adults43 may point to possible parallels in children. For example, compared with smoking either substance, co-smoking increases carcinogen exposure and cardiovascular risk and lowers lung function.44 45 In addition, compared with tobacco smoking alone, co-use leads to additive tobacco-specific toxicant blood levels (eg, nicotine, cotinine, tobacco-related volatile organic compounds) as well as toxicants from both products (eg, polycyclic aromatic hydrocarbons).1718 46,48
A potential mechanism underlying elevated tobacco toxicant levels among adults who co-smoke is cannabis’ inhibitory effects on multiple nicotine metabolism pathways, resulting in slower nicotine metabolism.49 50 Slower nicotine metabolism leads to higher sustained nicotine and nicotine metabolite blood levels per cigarette smoked. This mechanism may partially explain why co-users demonstrate greater use and dependence of tobacco and worse cessation outcomes34 51 compared with people who smoke tobacco only.
Purpose
Recent evidence suggests that adults who co-use tobacco and cannabis have higher sustained blood levels of tobacco-related toxicants (eg, cotinine) than adults who only use tobacco. However, it remains unknown whether there are parallel risks related to children’s co-exposure. Therefore, this study compared urinary cotinine levels among children whose mothers co-smoked tobacco and cannabis versus mothers who only smoked tobacco in the past 7 days. Based on evidence in adult people who smoke tobacco and cannabis, we hypothesised that urinary cotinine among children who were co-exposed would be significantly higher than children who were only exposed to secondhand tobacco smoke in the last 7 days.
Methods
Overview
Data for this study were obtained from cross-sectional baseline data collected during the Babies Living Safe and Smokefree (BLiSS) randomised controlled trial52 and funded by the National Cancer Institute within the US National Institute of Health (NIH). (The National Cancer Institute (NCI/NIH) was not involved in the conduct of the study or interpretation of results.) Between 2015 and 2020, the BLiSS trial tested the efficacy of a multilevel intervention for mothers who smoke tobacco initiated in 10 safety net community clinics in Philadelphia, Pennsylvania, USA, that administered the Special Supplemental Nutrition Programme for Women, Infants and Children (WIC). Nutrition counsellors screened all participants for tobacco use and advised people who smoke about TSE dangers and benefits of TSE protections. Mothers interested in treatment were referred to the trial. Participants were eligible if they smoked tobacco daily, >18 years old, received WIC services, spoke English and had a child <6 years old exposed to tobacco smoke at home. Exclusion criteria included pregnancy or presenting with issues (eg, low literacy) that could interfere with the ability to provide informed consent. Prior to trial randomisation, consented participants (N=396) completed a structured telephone-based baseline interview from which the cross-sectional data for this study were extracted and analysed. This sample size was determined via approved power analysis as described in the trial protocol.53 Blinded research staff conducting the structured interviews included bachelor’s degree and master’s degree-level professionals. Interview staff were trained and supervised by the study principal investigators in rigorous quality control procedures that included achieving and maintaining 95% accuracy in delivering standardised, scripted interview procedures and questions to minimise data collection bias. Interviews were recorded and data were double entered and verified to maximise accuracy and data quality. Outcome and covariate measures were chosen for their strong psychometric properties and consistent use in the adult tobacco and child TSE intervention literature.
Measures
All outcome (dependent variable)
Children’s urinary cotinine: participants collected their child’s urine following standardised instructions designed to minimise sample contamination. Urinary cotinine assays used a validated high-performance liquid chromatography with tandem high-resolution mass spectrometry procedure (0.1 ng/mL limit of quantitation).52 We adjusted cotinine values to normalise the distribution for subsequent analysis. First, we winsorised six extreme outliers by equating their values with the cotinine value nearest the third SD above the mean (>466 ng/mL). Then, we log-transformed the winsorised data.
Independent variable
Any cannabis smoking by participants (‘co-smoking’) in the last 7 days: Participants’ cannabis smoking was assessed via single self-report item capturing any cannabis smoking by the participants (‘How many days in the last 7 days did you smoke marijuana at home?’). Because of the skewed distribution toward 0 days, we dichotomised co-smoking as 1=‘any cannabis smoking and daily tobacco smoking’ versus 0=‘only daily tobacco smoking’ in the last 7 days.
Covariates
The following cotinine-related factors were chosen for multivariable analysis due to evidence of their association with child cotinine from prior published analyses using the same BLiSS trial dataset.52 54
Mean daily TSE from all sources in the last 7 days was assessed using validated, structured timeline follow-back interview methods.55 Participants estimated, over each day, the number of cigarettes to which their child was exposed from their and other individuals’ tobacco smoking, in any location.
Parent’s exposure protection (‘PREP’) behaviours: Participants’ efforts to protect their children from secondhand tobacco smoke were assessed using the 11-item PREP scale.53 PREP measures the frequency (1=never to 4=often) with which participants engaged in behaviours to reduce or eliminate their child’s TSE (eg, ‘ask people to not smoke around child’, ‘post ‘no smoking’ signs around home’). Higher item sum scores (range=11–44) indicate more frequent TSE protection behaviours.
The total number of people who smoke tobacco living at home was assessed via a single item.53
Nicotine dependence was assessed with a single item from the Fagerström Test for Cigarette Dependence (FTCD)56 asking how soon participants smoke after waking to produce a continuous variable: within 5 min, 6–30 min, 31–60 min or after 60 min.
Statistical analysis
Statistical analyses were performed using the R statistical software.57 Three cases had missing cotinine values and were eliminated from all analyses. Descriptive univariate analyses included between-group comparisons among people who smoke tobacco and cannabis versus people who smoke tobacco only across 12 participant characteristics, using t-tests for continuous variables, χ2 tests for categorical variables and a Bonferroni correction (from 0.10 to 0.01) to adjust the critical significance level due to multiple comparisons. Multiple regression was performed to test our co-use—child cotinine association hypothesis, modelling children’s adjusted cotinine levels based on maternal co-smoking and the covariates outlined above. Estimated regression coefficients were standardised and two-tailed t-tests were used to assess significance of each predictor (=0.05). Multicollinearity was tested using variance inflation factors.
Patient and public involvement
Neither patients nor the public were involved in the design or conduct of this study.
Results
Sample characteristics
Among 396 low-income mothers who smoke tobacco, 146 (36.9%) reported also smoking cannabis in at least 1 out of the last 7 days. The mean participant age was 30.11+6.52 years old, and their mean child’s age was 30.24+20.0 months old. Participants smoked 8.88+5.43 mean cigarettes per day and exposed their children to 5.79+7.49 mean cigarettes per day. Also, 70.1% of participants were black/African American, 34.1% had a high school education or less, 58.3% were unemployed, 50% had at least one other person who smokes living at home and 87.6% reported at least some residential smoking restrictions. Before log transformation, children’s mean winsorised raw cotinine level was 28.92+86.42 ng/mL. Table 1 shows no between group differences between participants who co-smoked and those who only smoked tobacco in established determinants linked to child cotinine (eg, mean number of cigarettes smoked per day).
| Variable | Group | n | Mean (SD) | t | P value |
|---|---|---|---|---|---|
| Participant tobacco cigarettes smoked per day | Co-smokers | 146 | 8.67 (6.02) | 1.32 (df 391) | 0.55 |
| Tobacco-only | 250 | 9.01 (5.07) | |||
| Total child TSE (all sources and places) | Co-smokers | 146 | 5.46 (7.18) | −0.68 (df 394) | 0.50 |
| Tobacco-only | 250 | 5.99 (7.68) | |||
| Total number of people who smoke tobacco living in home | Co-smokers | 146 | 1.71 (0.84) | 0.28 (df 394) | 0.78 |
| Tobacco-only | 250 | 1.69 (0.84) | |||
| TSE protection (PREP) | Co-smokers | 146 | 33.68 (4.93) | −1.39 (df 394) | 0.167 |
| Tobacco-only | 250 | 34.42 (5.18) | |||
|
Co-smokers vs
tobacco only | χ2 | P value | |||
| Employment | Working | 165 | 36.4% vs 63.6% | 0.06 (df=1) | 0.44 |
| Unemployed | 231 | 37.6% vs 63.4% | |||
| Education | >High school | 153 | 36.2% vs 63.8% | 0.12 (df=1) | 0.73 |
| HS or less | 243 | 37.1% vs 62.9% | |||
Multivariable modelling results
Multiple regression results shown in table 2 support our hypothesis. There was a significant, positive association between maternal co-smoking and child cotinine (p=0.04) independent of confounds. Among the other covariates, higher reported TSE accounted for the greatest variance in child cotinine level, followed by FTCD and number of people who smoke tobacco living at home. Only the PREP score was not significantly associated with child cotinine in the model. Variance inflation factor values on all predictors ranged from 1.01 to 1.11, indicating negligible collinearity and no concern for coefficient instability.
| Predictor | Estimate | SE | 95% CI | P value | ||
|---|---|---|---|---|---|---|
| LL | UL | |||||
| Maternal co-smoking (yes) | 0.12 | 0.058 | 0.005 | 0.23 | 0.10 | 0.04 |
| Number of people who smoke at home | 0.12 | 0.035 | 0.047 | 0.18 | 0.16 | 0.001 |
| Reported TSE (all sources) | 0.018 | 0.004 | 0.010 | 0.026 | 0.22 | <0.001 |
| PREP score | −0.008 | 0.006 | −0.02 | 0.003 | −0.07 | 0.16 |
| FTCD (ref=within 5 min) | ||||||
| Within 6–30 min | 0.0005 | 0.06 | −0.13 | 0.13 | 0.0004 | 0.99 |
| Within 30–60 min | −0.282 | 0.08 | −0.44 | −0.12 | −0.17 | <0.001 |
| After 60 min | −0.273 | 0.10 | −0.46 | −0.086 | −0.14 | 0.005 |
Discussion
This is the first study to demonstrate that young children whose mothers smoked both tobacco and cannabis were more likely to have higher urine cotinine than children whose mothers only smoked tobacco. Importantly, this significant positive association was evident when adjusting for the effects of potential confounds. This study included a sample of mothers recruited from safety net WIC clinics in low-income communities—a high-risk population that bears elevated burdens related to tobacco use and child exposure. Thus, these results underscore the importance of public health efforts to dispel myths about the minimal risks associated with cannabis use and secondhand cannabis exposure, to improve education about the considerable health consequences of co-exposure and to test behavioural intervention strategies that facilitate caregiver efforts to mitigate those exposures and resulting peadiatric health consequences.
To bolster such efforts, additional research is needed to improve our understanding of the degree to which co-exposure elevates tobacco-related toxicant levels in children. For example, prospective research could include other disease risk biomarkers along with cotinine (eg, urinary metabolites of tobacco-related volatile organic compounds, 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanol (NNAL), malondialdehyde (MDA), epithelial-mesenchymal transition (EMT) markers) to examine other potential additive risks associated with co-exposure.47 Future research is also necessary to understand mechanism(s) through which co-exposure elevates child cotinine and, potentially, other tobacco-related toxicants. Based on evidence among adult co-users,49 50 the inhibitory effects of cannabis and its constituents on multiple nicotine metabolism pathways are a primary suspect to examine. Other plausible factors could relate to the acute and long-term cognitive function impairments that accompany cannabis use58 (eg, response time, time perception, executive function). For example, people who smoke tobacco and cannabis may be less aware of the amount of time their children are playing in areas where tobacco smoking occurs. In addition, cannabis use could affect caregivers’ decision-making around prohibiting others from smoking around their children, whether undermining motivation to limit TSE or inhibiting assertiveness to overcome social pressure to ignore such rules.
Social and behavioural factors could also interact with environmental conditions in contributing to levels of co-exposure. Because TSE and co-exposure are most likely to occur within children’s residential milieu,1159,61 further examination of co-exposure levels and their effects on child health should focus on the social and behavioural contexts within children’s home environments. Residential third-hand smoke is one such context that could exacerbate the negative consequences of co-exposure. Third-hand tobacco smoke is known to elevate children’s cotinine levels,41 as it contains nicotine, carcinogens and other tobacco toxicants that are absorbed on hard surfaces (eg, floors, clutter), dust and fabrics—then remitted into the air even months after visible secondhand tobacco smoke has cleared the environment. Behaviours that result in greater residential clutter and dust are linked to higher thirdhand smoke62,65; and amotivation, fatigue and disorganisation (symptoms of cannabis use disorder and depression) could undermine caregivers’ ability to maintain a tidy home.66 Given the emerging evidence that co-users are more likely to experience depression symptoms than people who smoke tobacco only,67 68 the link between depressive symptoms and environmental factors that might elevate third-hand smoke risk among co-users is relevant to explore.
Strengths and limitations
The observed maternal co-smoking—child urinary cotinine association in this study appears to be robust despite the reliance on a gross measure of cannabis smoking in the past week. Primary strengths of the study include bioverified child tobacco exposure as the dependent variable and the focus on a high-risk population with elevated rates and associated risks of tobacco and cannabis smoking and child exposures. Limitations consistent with secondary analyses include a non-experimental design with cross-sectional data that is subject to internal validity threats and a defined participant sample that was not representative of a broader range of caregivers who smoke tobacco and cannabis. In addition, the assessment of cannabis smoking in the home did not capture others’ cannabis smoking in the home and did not include biomarkers of cannabis smoking (both beyond the scope of the parent trial). Importantly, future prospective research is needed and can provide more detailed assessment of adult residents’ cannabis use and child exposure to fill these gaps.
Conclusion
Compared with children of people who smoke tobacco only, children of people who smoke tobacco and cannabis in this study had higher urinary levels of the primary nicotine metabolite, cotinine. Concerns about the consequences of children’s cannabis smoke exposure are increasing,31 32 40 69 as it contains the psychoactive THC16 35 as well as higher concentrations of toxicants also found in tobacco smoke (eg, ammonia, nitrogen oxides, hydrogen cyanide).35 69 Co-exposed children not only suffer potential additive consequences of cannabis and tobacco smoke exposures, but may also sustain higher blood levels of nicotine, its metabolites and other tobacco toxicants relative to children only exposed to tobacco smoke.
Children’s secondhand cannabis and tobacco exposures frequently intersect within broader family and structural contexts, yet cannabis-related risks remain less fully integrated into paediatric and public health frameworks. Addressing these gaps is critical for advancing developmentally informed and equity-oriented approaches to child and family well-being.
Results from this study elevate the public health significance of addressing the rising rates of co-smoking of tobacco and cannabis and children’s co-exposure. Moreover, future research is needed to gain a better understanding of potential mechanisms that explain the co-exposure—child cotinine association.
Footnotes
Footnote Group
Data availability statement
Data are available upon reasonable request.
References
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Associated Data
Data Availability Statement
Data are available upon reasonable request.