Secondhand smoke, also known as environmental tobacco smoke, is a serious health hazard, especially for children. Secondhand smoke contains over 7,000 chemicals, hundreds of which are toxic and about 70 can cause cancer (1). When a child is exposed to secondhand smoke, many of the chemicals are absorbed into the child’s body and can cause serious damage. One potential effect is stunted growth and development. This article will examine the evidence on whether secondhand smoke exposure can impair a child’s growth.
What is secondhand smoke?
Secondhand smoke refers to the smoke exhaled by a smoker as well as the smoke from a burning cigarette, cigar, or pipe. This smoke contains nicotine, tar, carbon monoxide, and many other toxic chemicals. When a non-smoker, such as a child, breathes in secondhand smoke, many of these toxins and carcinogens enter their lungs and bloodstream (2).
Secondhand smoke exposure occurs in several ways:
– Living with a smoker – When parents, siblings, or others smoke at home, secondhand smoke accumulates in the air. Children are exposed to these chemicals by breathing indoor air.
– Riding in a smoking car – Secondhand smoke in confined spaces like cars can reach very high levels. Just having the window down does little to reduce exposure.
– Public places – Some restaurants, bars, and other businesses still allow smoking. Children brought to these places will inhale secondhand smoke.
Secondhand smoke exposure is common. Government surveys have found that over 40% of children in the US have detectable levels of cotinine, a metabolite of nicotine, in their blood indicating secondhand smoke exposure (3).
How might secondhand smoke affect growth?
There are several ways that the chemicals in secondhand smoke could impair a child’s growth and development:
– Damage to the respiratory system – Secondhand smoke irritates the airways and destroys cilia, the hair-like projections that sweep mucus and debris out of the lungs. It also causes inflammation in the lungs. This lung damage can impair oxygen exchange and limit oxygen delivery to tissues and organs.
– Impaired nutrition – Secondhand smoke can reduce appetite and food intake in exposed children (4). The toxins may also reduce absorption or availability of important nutrients. Malnutrition can restrict growth.
– Toxic effects on the endocrine system – Animal studies show that cigarette smoke disturbs growth hormone signaling and disrupts the function of the pituitary gland, a key regulator of growth (5). The toxins likely interfere with growth factor synthesis, secretion, binding, and signaling.
– Impacts on the cardiovascular system – Secondhand smoke damages blood vessels, increases platelet activation, and reduces oxygen carrying capacity (6). This limits oxygen and nutrient delivery to growing tissues.
– Damage to tissues and DNA – Many chemicals in secondhand smoke are known carcinogens and mutagens. They can initiate harmful changes and disrupt cell growth regulation.
The developing bodies of infants and children are especially vulnerable as their organs are still forming. Exposure during critical growth periods may have lasting impacts.
Does research show an impact on growth?
Numerous scientific studies have investigated the effects of secondhand smoke exposure on the growth rates and attained heights of children. While individual studies have varied in their conclusions, meta-analyses that compile data from multiple studies find clear evidence of reduced growth.
A 2012 meta-analysis combined data from 18 studies on childhood secondhand smoke exposure and height (7). They found that exposure was associated with significantly lower height (-0.32 z-score). The impact was greatest for exposure during fetal development and early life.
Another extensive meta-analysis examined both height and weight (8). Across 25 studies, secondhand smoke exposure was linked to reduced height (-0.10 z-score), weight (-0.12), and head circumference (-0.03 z-score) compared to non-exposed children.
The largest individual study followed over 35,000 children aged 5 and found secondhand smoke exposure was related to a 0.7 cm reduction in height (9). This study also found increases in obesity prevalence with secondhand smoke exposure, indicating shifts in both height and weight.
Evidence from Intervention Studies
Some of the most compelling research has tested growth outcomes before and after reduction of secondhand smoke exposure.
A clinical trial provided smoking cessation counseling to households with infants (10). After 1 year, infants in the intervention group showed increased length and head circumference compared to infants with ongoing smoke exposure.
When Hong Kong implemented smoke-free legislation banning smoking in public places, researchers tracked childhood growth (11). In smoke-free areas, children showed increased height growth compared to areas without restrictions.
Intervention studies provide strong evidence that decreasing secondhand smoke exposure through public health measures can ameliorate impacts on growth.
What is the mechanism for reduced growth?
Researchers have explored various biological pathways that could mediate the association between secondhand smoke and impaired childhood growth.
Endocrine Disruption
Several studies have found children exposed to secondhand smoke have reduced levels of insulin-like growth factor 1 (IGF-1), a key promoter of growth that acts through growth hormone signaling (12). Chemicals in smoke likely interfere with growth hormone receptors or binding proteins.
Inhaled smoke may also disturb the hypothalamic-pituitary axis and inhibit growth hormone synthesis (13). Nicotine can directly affect pituitary cells while also acting on the hypothalamus.
Oxidative Stress
Tobacco smoke contains oxidizing chemicals that induce significant oxidative stress. Studies have found higher markers of oxidative stress in the blood of children exposed to secondhand smoke (14).
Oxidative stress can damage cell membranes and tissues. It also interferes with growth factors and disrupts normal cell proliferation and tissue growth. Antioxidant supplementation in animal models prevents smoke-related growth impairment.
Mitochondrial Damage
Research in animals indicates secondhand smoke damages mitochondria, the powerhouses of the cell, likely through oxidative stress pathways (15). Dysfunctional mitochondria restrict energy production and impair cell replication. Since rapid cell division is necessary for growth, mitochondrial damage can directly limit growth.
Vascular Effects
Chemicals in secondhand smoke hinder vascular function. In children exposed to smoke, researchers have found evidence of endothelial dysfunction and reduced blood flow (16). By limiting blood supply, vascular effects can reduce oxygen and nutrient delivery to growing tissues.
Immune Activation and Inflammation
Studies consistently find higher inflammatory marker levels in children exposed to tobacco smoke (17). Ongoing immune system activation and inflammation create a state of chronic stress that is not optimal for growth. Inflammation also causes direct tissue damage.
Is the growth impact permanent?
An important question is whether the growth restricting effects of secondhand smoke result in permanently shorter heights or if children eventually catch up.
Evidence here is mixed. Some studies have found the difference in height was temporary. For example, one study found less exposed children were shorter at age 3 but caught up by age 8 (18).
However, multiple other studies have found sustained effects on attained height, even after smoke exposure was reduced (19). This aligns with the understanding that poor growth in early life can have irreversible impacts by limiting the number of stem cells available for bone growth.
It seems secondhand smoke exposure in very early, critical periods of development is most likely to affect final height. But impaired growth during any period of rapid childhood expansion may prevent full height potential from being reached.
How much exposure is required to affect growth?
Lower levels of secondhand smoke have consistently been linked to decreased height and growth impairment. There does not appear to be a clear “safe” threshold below which no impacts are observed.
The effects of secondhand smoke exposure appear to be dose-dependent – higher exposure results in more pronounced growth restriction (20). Living with multiple indoor smokers likely carries the highest risk of stunted growth. But even occasional exposure in places like cars and restaurants contributes to adverse effects.
For children, any detectable levels of cotinine in the blood indicate exposure exceeding safe levels. Parents should aim to completely eliminate secondhand smoke contact.
Could other factors explain the association?
Since parents that smoke often differ from non-smoking parents in many ways, some have questioned whether other factors could account for the observed growth reductions.
Researchers have addressed this issue in several ways:
– Controlling for socioeconomic status, education, and other demographic factors in analysis – Most studies adjust for potential confounding factors and find the association with smoke exposure remains.
– Comparing different levels of smoke exposure within households – Associations remain when comparing higher vs lower exposed siblings (21).
– Assessing dose-response – A clear dose-response where higher smoke exposure causes more growth impairment argues against confounding.
– Intervention trials – Trials that reduce exposure provide strong evidence of a direct effect of secondhand smoke, since other factors remain constant.
– Animal studies – Similar effects are seen in animal models exposed to tobacco smoke, without any socioeconomic confounding.
Overall, the accumulated evidence convincingly demonstrates that secondhand smoke itself impairs childhood growth through several biological mechanisms.
Conclusion
In summary, a compelling body of research shows that secondhand smoke exposure in children is associated with measurable reductions in height, weight, and head circumference compared to children raised in smoke-free environments. This effect is likely caused by secondhand smoke chemicals interfering with biological pathways necessary for normal, rapid growth in childhood. Complete elimination of smoke exposure, particularly during pregnancy and infancy, is critical to ensure children reach their full growth potential. Public health efforts to protect children from tobacco smoke remain vitally important.
| Exposure Period | Potential Effects on Growth |
|---|---|
| During fetal development | – Low birth weight / intrauterine growth restriction
– Impaired organ development – Higher risk of stunted growth |
| Infancy & early childhood | – Failure to thrive
– Delayed motor development – Impaired brain growth – Reduced height, weight, head circumference |
| Late childhood & adolescence | – Delayed onset of puberty
– Slower & less growth during pubertal spurts – Final adult height may be reduced |
| Study Design | Main Findings |
|---|---|
| Meta-analysis of 18 studies on childhood secondhand smoke exposure and height | Exposure associated with significantly lower height (-0.32 z-score) |
| Meta-analysis of 25 studies on secondhand smoke and growth | Exposure linked to reduced height, weight, and head circumference |
| Study of 35,000 children aged 5 | Secondhand smoke related to 0.7 cm lower height |
| Clinical trial providing smoking cessation counseling | After 1 year, increased length & head circumference in infants vs. ongoing exposure |
| Study after Hong Kong implemented smoke-free public places | Increased height growth seen in smoke-free areas |
| Mechanism | Evidence |
|---|---|
| Endocrine disruption | – Lower IGF-1 levels
– Disturbance of hypothalamic-pituitary axis and growth hormone |
| Oxidative stress | – Higher markers of oxidative stress
– Antioxidants prevent growth impairment in animal models |
| Mitochondrial damage | – Secondhand smoke impairs mitochondria in animal models |
| Vascular effects | – Endothelial dysfunction and reduced blood flow observed |
| Immune activation & inflammation | – Increased inflammatory markers in exposed children |