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Abstract

Despite significant declines in population smoking rates and effective policies to ban smoking in public places, environmental exposure to nicotine remains prevalent among children. Environmental smoke exposure affects children's respiratory, immune, and metabolic health but is also implicated in children's cognitive and behavioral development. Nicotine's chemical properties mimic naturally occurring chemicals in the brain. When nicotine is present during brain development (prenatally through the first five years of life), it alters developmental processes that affect systems involved in cognitive control, impulsivity, and sensitivity to rewarding substances, increasing risks for obesity. Because nicotine is the specific toxin underlying these outcomes, vaping is unlikely to be a safer alternative. Given the rise in vaping among young adults generally, and pregnant women specifically, this exposure represents a public health concern that warrants additional attention. Policies including modernized public health messaging and routine screening could reduce children's inadvertent exposure.

Keywords

smoking children’s health vaping second hand smoke brain development

Nicotine exposure in infancy and early childhood has lasting effects on brain development leading to lower cognitive control, greater impulsivity, and an increased risk for obesity.

Key Points

As many as 36% of children are exposed to nicotine, and exposure levels in infants can reach doses comparable to that of active smokers.

Infants can absorb nicotine residue from surfaces including toys, carpet, or adults’ skin and clothing, even if smoking does not take place around the infant.

Nicotine mimics naturally occurring chemicals in the brain, and its presence during brain development has lasting implications for cognitive and behavioral outcomes.

Increases in vaping among young adults and pregnant women suggest a coming increase in children's exposure to nicotine's neurotoxic effects.

Changes to public health practice including modernization of public health messaging coupled with routine screening could significantly reduce children's environmental exposure, with subsequent benefits for children's physical and behavioral health across the lifespan.

Policy changes related to licensing of childcare settings and rental properties have additional potential benefits, particularly among those most socioeconomically vulnerable to risks of smoke exposure.

Policy and public health messaging throughout the last several decades have successfully reduced the prevalence of smoking from 42% to 13% of adults (CDC, 2022). However, this still translates to over 30 million adults, and smoking remains the leading preventable cause of adult morbidity and mortality (CDC, 2022). Beyond the impact on the smoker's health, smoke exposure has substantial implications for children's health, requiring a policy approach to smoking that reflects the potential for collateral harm. Research demonstrates that policies such as bans on smoking in public places and taxes levied on cigarette products are effective in reducing children's exposure to smoke, with consequent reductions in outcomes such as infant mortality, preterm birth, low birth weight, and hospital admissions for asthma (Been et al., 2014; Been & Sheikh, 2018). This paper examines the extent to which nicotine continues to represent an environmental toxin, the range of adverse developmental consequences of exposure in children, and opportunities to enact policies and practices that further protect children's health.

Prevalence of Nicotine as an Environmental Toxin

Nicotine Use Is on the Rise, Particularly Among Young Adults

Despite steady and sustained declines in cigarette smoking over the past few decades, tobacco products remain popular among a subset of the population. Furthermore, the popularity of electronic cigarettes (i.e., vaping) among young adults (ages 18–24) is initiating a new generation into nicotine addiction, reversing antismoking trends previously observed in this age group. The perception of vaping as healthier than cigarette smoking, as well as the easy concealability of vaping, facilitates more frequent use and a consequent tendency toward a higher level of nicotine addiction (Gubner et al., 2016). Over 25% of young people report having ever used an e-cigarette, and stress related to the COVID-19 pandemic may contribute to further increases in vaping (Clendennen et al., 2021; Villarroel et al., 2020). Similar trends are also being observed among pregnant women, which is a particularly grave public health concern given the known implications for fetal health (McGrath-Morrow et al., 2020).

Risk for Exposure Lingers Long After the Cigarette is Put Out

Awareness of the risks of secondhand smoke prompts some individuals to change their smoking behavior, for instance, making a concerted effort not to smoke in the presence of children. However, aerosolized nicotine settles onto surfaces, where it remains for an extended period (sometimes referred to as thirdhand smoke). This allows nicotine to transfer into environments even where smoking is actively prohibited (Bush & Goniewicz, 2015; Matt et al., 2011; Matt et al., 2014). For instance, even if a parent goes outside to smoke, they return with nicotine residue on their skin, hair, and clothing, which is quickly transferred to the child when they are held or played with. Grandparents, visiting adults, and childcare providers could be consistent sources of exposure even if the child resides in a nonsmoking household. Furthermore, young children spend more time on the floor where carpeted surfaces can retain residue that persists after vacuuming. Studies have shown that nicotine residue can remain high in housing (Matt et al., 2011) and vehicles (Matt et al., 2008) previously occupied by a smoker, or transmitted through shared ventilation and common hallways in dense-occupancy spaces such as apartment buildings (Khachatoorian et al., 2019; Matt et al., 2014). As such, individuals may be unaware of the presence or extent of exposure in their environment. Indeed epidemiological data from the National Health and Nutrition Study (NHANES) indicate that ∼36% of children (ages 3 to 17 years) have evidence of environmental tobacco exposure (Brody et al., 2019).

Unintended Exposure can Reach High Levels

Exposure is measured by the amount of cotinine, the metabolic byproduct of nicotine, present in bodily fluid (blood, urine, and saliva). For many years, the prevailing belief was that environmental exposure resulted in blood cotinine concentrations below 10 µg and that active smoking was needed to reach values higher than that. However, more recent evidence questions this assumption. A study of over 1,100 infants ∼6 months of age found that as many as 15% had cotinine values in excess of this threshold, with some levels reaching over 500 µg (Gatzke-Kopp et al., 2019). A previous study examining women seeking prenatal care in public clinics serving low-income families found that 73% of the pregnant women who denied smoking had levels of urinary cotinine consistent with active smoking (Webb et al., 2003). Although the authors interpreted this discrepancy between self-report and a biological index of exposure to reflect mothers’ propensity for concealing or misrepresenting their cigarette use, increasing evidence indicates that individuals may in fact accumulate substantial exposure through environmental sources.

Outcomes Associated With Developmental Exposure

Developmental Consequences of Nicotine Exposure Include Every Major Physiological System

Nicotine is a known teratogen—a substance that disrupts normal fetal development. Consequences of prolonged exposure include reduced fetal growth, compromised immunity, respiratory impairment, and disrupted metabolic function (Gibbs et al., 2016; Goel et al., 2004; Kharrazi et al., 2004; McGrath-Morrow et al., 2020; Somm et al., 2009). Experimental studies in animals and observational studies in humans confirm that passive maternal exposure (e.g., secondhand) carries the same risks for fetal development as active maternal smoking (Eskenazi et al., 1995; Goel et al. 2004; Grant, 2005; Kharrazi et al., 2004). Nicotine is the primary teratogenic agent responsible for these outcomes, meaning that vaping does not offer protection despite the removal of other toxicants present in cigarettes.

The Most Sensitive Physiological System to Developmental Exposure to Nicotine is the Brain

While much attention focuses on the effects of nicotine for fetal growth and risk for respiratory problems, nicotine poses a particularly pronounced threat to brain development (Slotkin, 1998) because it possesses very similar molecular properties to acetylcholine, a naturally occurring neurotransmitter. In the adult brain, acetylcholine is involved in functions such as learning and memory formation; it interacts with systems related to reward and pleasure, contributing to the reasons users are attracted to nicotine. However, during brain development, acetylcholine plays an important role in the growth and differentiation of brain cells (Heath & Picciotto, 2009; Slotkin, 1998; Wessler & Kirkpatrick, 2008). Because nicotine acts like acetylcholine, its presence during this time affects these developmental processes. Exposure is associated with altered expression of thousands of genes, reductions in the number of brain cells in certain regions, and changes in the functional activity of the brain into adulthood (Chen et al., 2005; Keller et al., 2018; Lee et al., 2016).

Developmental Exposure is Associated With Increased Risk for Children's Behavior Problems

Several decades of research document an association between maternal smoking during pregnancy and children's behavior problems, including attention-deficit/hyperactivity disorder (ADHD), aggression, and delinquency (Button et al., 2005; Orlebeke et al., 1999; Wakschlag et al., 1997). Some researchers have argued that these associations are not a function of nicotine exposure per se, but rather that women who smoke during pregnancy are more likely to have these antisocial characteristics themselves, which may be directly passed to the child (Wakschlag et al., 2002). However, research demonstrates that the dose-dependent association between maternal smoking and child behavior problems persists when controlling for maternal characteristics and extends to exposure that is not based on the mother, such as mother's secondhand exposure (Gatzke-Kopp & Beauchaine, 2007) and children's postnatal exposure (Gatzke-Kopp et al., 2020; Leung et al., 2015).

The association between developmental exposure to nicotine and children's behavior problems is consistent with the regions of the brain that are most sensitive to nicotine's effects. Developmental exposure to nicotine results in lower numbers of brain cells in the prefrontal cortex, a region associated with cognitive processing and higher-order thinking (Chen et al., 2005). Exposed animals demonstrate impairments in cognitive skills such as working memory (McCarthy et al., 2022). Brain cells are also altered in a region called the striatum, which is responsible for how the brain responds to rewards (Chen et al., 2005). Developmental research indicates that exposure to nicotine during gestation and lactation results in more impulsive decision-making that favors immediacy of rewards and that the effects remain evident into adolescence (Lee et al., 2016). Indeed, prenatal nicotine exposure is considered a valid rodent model for studying ADHD (Kantak, 2022). Furthermore, developmental exposure has lasting effects on how brain cells respond to nicotine if exposed again during adolescence, making individuals exposed early in life more susceptible to developing an addiction to nicotine of their own, as well as increasing risk for other drugs of abuse (Kane et al., 2004).

The Neurobehavioral Effects of Nicotine Exposure may Also Increase Risk for Childhood Obesity

In part due to nicotine's ability to suppress appetite, maternal consumption is associated with lower pregnancy weight gain and lower infant birth weight. However, offspring exposed prenatally to nicotine are more likely to be overweight or obese later in childhood and adulthood (Jaakkola et al., 2021). Children classified with low birth weight are particularly susceptible to rapid weight gain in infancy and cascading risks for obesity across time (Ino, 2010). Moreover, secondhand nicotine exposure in childhood appears to confer similar risks on overweight status and obesity—one study found that children's overweight status related to environmental smoke exposure regardless of whether the exposure occurred prenatally, within the first year of life, within the 5th year of life, or any combination thereof (Raum et al., 2011). Thirdhand exposure via breast milk and surface contact has also related to excess body weight in animal models (Miranda et al., 2020), and insulin resistance has been observed among children exposed to environmental nicotine (Thiering et al., 2011). Thus, regardless of the type, nicotine exposure appears to strongly predict body weight and metabolic functioning across development.

Physiological mechanisms explaining weight gain as a result of prenatal and childhood nicotine exposure are not well understood. Obesity is a multiply determined outcome, and conditions such as nutritional environment (Nadhiroh et al., 2020), physical activity, family routines (Ino, 2010), and even regional differences in air pollution (McConnell et al., 2015) either exacerbate or protect against the development of obesity among children exposed to nicotine. Most likely, the effects of nicotine on brain systems related to reward sensitivity drive food preferences toward higher concentrations of sugar and fat. Animal models indicate that alterations in dopamine systems induced by low-dose nicotine exposure are associated with greater sensitivity and motivation for sugar in offspring (Lacy et al., 2012). In studies with humans, children with ADHD have less healthy diets, with research suggesting that high-sugar diets do not precede the onset of ADHD but are more likely a correlate of the condition (Del-Ponte et al., 2019). Findings from studies with preschool children show that those children higher in reward sensitivity work harder for a food reward, have a higher body mass index, and consume more food when given unlimited access (Rollins et al., 2014). Thus, children exposed to nicotine may show a preference for foods with artificially enhanced reward properties, such as large amounts of added sugar, and fail to find natural levels of sweetness, such as present in fruits, sufficiently rewarding. In addition to preferences for less healthy foods, ADHD has also been associated with deficits in regulating consumption amounts. Self-regulatory skills protect children against excessive weight gain (Francis & Susman, 2009), and research indicates a linear association between the severity of ADHD symptoms and children's overconsumption of food (Wilhelm et al., 2011). In summary, nicotine exposure is associated with increased motivation for reward and decreased cognitive regulatory control, which manifests as impulsivity. This trait increases children's vulnerability for behavior problems, as well as abuse of rewarding substances which can include drugs or food.

Policy Insights

Evidence regarding the health consequences of environmental smoke exposure for children is conclusive, and data demonstrate that children's exposure may reach higher levels than previously appreciated. In addition, research indicates that risks from developmental exposure (from conception through the first 5 years of life) extend beyond the highly publicized effects on prematurity and infant mortality to include altered cognitive and behavioral characteristics that may not become evident until later in childhood and persist throughout the lifespan. Given this evidence, policies that are effective in reducing this exposure have the potential to reap enormous benefits in reduced healthcare expenditures and improved educational outcomes.

This is especially important given the evidence that environmental nicotine exposure is a health inequity that disproportionately affects socioeconomically vulnerable individuals (Brody et al., 2019). At a time when bans on public smoking resulted in significant reductions in secondhand smoke exposure, decreases were the lowest among individuals who were Black, rented (versus owned) their housing, and lived below the poverty line (Homa et al., 2015). This is due, at least in part, to inequities in public protection from exposure. Less educated and low-income individuals are less likely to be covered by tobacco-free laws (Huang et al., 2015), and smoke-free policies are less likely to be enacted or enforced in rural areas (Buettner-Schmidt et al., 2019). In urban settings, individuals living below the poverty line are more likely to live in high-density housing with shared ventilation and common areas that distribute smoke exposure (Matt et al., 2011). Communities with higher residential segregation by race are also more likely to be exposed to not just environmental nicotine but also other pollutants that have compounding detrimental effects on development, like asbestos, lead pipes, industrial and vehicle exhaust, and waste treatment plants (Lee et al., 2022; White & Borrell, 2011). Here we identified three different mechanisms by which reductions in exposure can be pursued, specifically, (a) public health messaging, (b) policies enacted by regulatory agencies, and (c) clinical practices to identify and serve affected individuals.

Public Health Messaging

The Surgeon General first utilized mandated black-box warnings indicating the risks smoking has for a developing fetus in the 1980s, in an effort to discourage smoking by pregnant women. However, this messaging is limited in several important ways. Firstly, messaging primarily targets the mother's smoking behavior rather than her smoke exposure. Fathers may consider restrictions that come with pregnancy (such as drinking alcohol) as only necessary for the mother and are often a source of secondhand smoke exposure for the mother even when she refrains from smoking (Eiden et al., 2011). Secondly, the majority of messaging targets physical health outcomes that are often associated with the most extreme consequences of exposure. This may lead parents to a false sense of security if their child appeared healthy at birth or does not appear to have any respiratory problems. However, many of the physiological effects of nicotine are not visibly apparent or may not materialize until much later (such as vulnerability to addiction). Given the unique sensitivity of the brain to the presence of nicotine during neurodevelopment, parents should be educated on the risks that exposure may have for cognitive and behavioral function later in childhood and adolescence.

Thirdly, messaging is often focused on fetal outcomes (e.g., low birth weight, premature birth), which may lead women to believe that smoking is only problematic during pregnancy. Among women who successfully quit smoking during pregnancy, relapse rates in the year after delivering are high (Tong et al. 2013). Even within clinical smoking cessation programs that were able to achieve a 97% quit rate during pregnancy, fewer than half of the mothers remained abstinent 1 year later (Meernik & Goldstein, 2015). This suggests that mothers may not consider infancy to be as vulnerable of a developmental period as pregnancy. However, the rapid and extensive brain development occurring over the first several years of life results in an ongoing sensitivity of the brain to environmental nicotine. Furthermore, the messaging that does focus on risks for children's health is often limited to respiratory conditions (e.g., sudden infant death syndrome and asthma). This emphasis may lead parents to believe that only the secondhand smoke presents a risk, limiting their efforts to mitigate thirdhand exposure.

Finally, increasing research has begun to demonstrate that fathers’ toxin exposure may have consequences for spermatogenesis. For example, rat models have shown that paternal nicotine consumption relates to offspring hyperactivity and impaired learning even when the offspring themselves have had no exposure to nicotine (Hawkey et al., 2019), suggesting that effects may be related to changes in sperm composition (Soubry, 2018). Emerging evidence in humans also reports an association between fathers’ smoking and children's preadolescent smoking in one study, demonstrating potential transgenerational effects of smoking propensity, although this trend may be coupled with other social and economic risk factors (Northstone et al., 2014). Given the breadth of these concerns, black-box warning about the effect of smoking, including vaping, on children's health should not be limited to mothers.

Policies of Regulatory Agencies

Bans on smoking in public places have significantly reduced incidence of preterm birth, as well as hospital admissions for asthma (Been et al., 2014), highlighting exactly how policy decisions directly translate into children's health outcomes. However, these actions affect only some routes of exposure. Additional policies could further reduce inadvertent exposure, specifically targeting places where children spend the most time: home and childcare settings. High-density housing—with open windows, doors opening into common spaces, and shared ventilation—poses risks for greater secondhand and thirdhand exposure among nonsmokers. This is likely to contribute to the health disparities of exposure among individuals with lower socioeconomic resources (Homa et al., 2015). In addition, smoke residue can remain on surfaces long after the smoker vacates the premises, increasing the risks for families renting a home that was previously occupied by a smoker. Policies aimed at housing standards for rental properties could protect more vulnerable, lower-income families. Such policies could include ventilation systems that do not redistribute air, specific cleaning requirements between occupants, and prohibition of smoking in the perimeter of the building.

Similarly, licensing requirements for childcare centers could examine employee policies to eliminate any unintentional exposure within the childcare setting, particularly for home daycares. Research indicates that children who attended a high-quality childcare (where smoking is not permitted) had lower levels of cotinine than children who were cared for at home, suggesting that time outside of the home is beneficial for reducing accumulated exposure (Gatzke-Kopp et al., 2019). Licensing for childcare settings could prohibit smoking in buildings where children will spend time (even if the children are not present at the time of smoking). Employers in these settings should also clearly delineate rules for employees who take smoke breaks, to ensure that they do not bring smoke residue back into the childcare setting through their clothing, hair, or skin. Subsidies for childcare services provided to low-income individuals should be predicated on attendance at a smoke-free facility.

An additional emerging area of research investigates the health benefits of green space, which comprise publicly accessible, open areas with natural “green” elements, such as vegetation. In addition to broad benefits to overall well-being (Engemann et al., 2019), green space is associated with a lower prevalence of smoking (Martin et al., 2020). In places with more green space, children may be exposed to less secondhand and thirdhand smoke (Mahabee-Gittens et al., 2022). Although the exact mechanisms are unclear, a recent study of approximately five million individuals in urban California found that those who lived in closest proximity to existing green space and residential green cover paid an average of $374 less in annual healthcare costs relative to individuals with less access (Van Den Eeden et al., 2022).

Clinical Practices

The profound impact of lead exposure on cognitive development resulted in significant changes in environmental policy (e.g., removal of lead from everyday products such as paint and gasoline), as well as directly influencing best practices in maternal and pediatric medicine. Specifically, the recognition that lead exposure could occur without individuals’ awareness led to the routine use of screening for lead during pediatric well visits. Following that model, routine assessment of cotinine exposure during pregnancy and early childhood would be a powerful public health practice. Directly assessing exposure by measuring cotinine is a better predictor of exposure among pregnant women (Eiden et al., 2011), as well as a better predictor of child health outcomes (Howrylak et al., 2014), than reliance on parental report of smoking. Cotinine can be readily detected in dried blood spot, saliva, and urine, making it easy and minimally invasive to assess (Jacobsen et al., 2022). Providing parents feedback on exposure is an effective way to influence their actions. In one study, a standard screening of urinary cotinine of children in the 4th grade found that 27% of the children whose parents did not smoke tested positive for environmental exposure. This screening thus helps parents identify unrecognized and modifiable sources of exposure. This screening was also used to identify children with high exposure levels, whose parents were provided with educational pamphlets on smoking cessation. At a 1 year follow-up, over half of these children no longer tested positive for exposure, and parental reports indicated that several parents succeeded in quitting smoking, while others made significant changes to their habits (Ino et al., 2006). Providing feedback to families regarding their child's exposure may be more effective in motivating meaningful environmental and behavioral changes than general education. Given the healthcare costs of the acute and chronic conditions that smoke exposure increases children's susceptibility for (e.g., asthma), early screening would likely be extremely cost effective over time.

Summary

Developmental neuroscience research consistently indicates how early environmental nicotine exposure, whether direct, secondhand, or thirdhand, has serious implications for physical and psychological development. Policies such as imposing taxes on tobacco products and prohibiting public smoking have played a crucial role in reducing smoking rates in the United States, with measurable impact on children's health outcomes. Unfortunately, children continue to experience significant rates and doses of exposure, and this burden is greater among more socially vulnerable groups. The costs of such exposure include diminished physical health, academic underperformance, increased risk for substance abuse, and obesity, all of which pose significant costs to individuals and society. Opportunities to further reduce this exposure appear in revising and expanding public health education, providing routine screening to help parents recognize exposure, and enacting policies that protect children in housing and childcare settings.

Footnotes

Declaration of Conflicting Interests

The author(s) declared no potential conflicts of interest with respect to the research, authorship, and/or publication of this article.

Funding

The author(s) received no financial support for the research, authorship, and/or publication of this article.

ORCID iD

Lisa M. Gatzke-Kopp

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Nicotine as an Environmental Toxin: Implications for Children's Health

Abstract

Keywords

Tweet

Key Points

Prevalence of Nicotine as an Environmental Toxin

Nicotine Use Is on the Rise, Particularly Among Young Adults

Risk for Exposure Lingers Long After the Cigarette is Put Out

Unintended Exposure can Reach High Levels

Outcomes Associated With Developmental Exposure

Developmental Consequences of Nicotine Exposure Include Every Major Physiological System

The Most Sensitive Physiological System to Developmental Exposure to Nicotine is the Brain

Developmental Exposure is Associated With Increased Risk for Children's Behavior Problems

The Neurobehavioral Effects of Nicotine Exposure may Also Increase Risk for Childhood Obesity

Policy Insights

Public Health Messaging

Policies of Regulatory Agencies

Clinical Practices

Summary

Footnotes

Declaration of Conflicting Interests

Funding

ORCID iD

References