Cardiovascular Consequences of Childhood Secondhand Tobacco Smoke Exposure: Prevailing Evidence, Burden, and Racial and Socioeconomic Disparities: A Scientific Statement From the American Heart Association

Abstract

Background: Although public health programs have led to a substantial decrease in the prevalence of tobacco smoking, the adverse health effects of tobacco smoke exposure are by no means a thing of the past. In the United States, 4 of 10 school-aged children and 1 of 3 adolescents are involuntarily exposed to secondhand tobacco smoke (SHS), with children of minority ethnic backgrounds and those living in low-socioeconomic-status households being disproportionately affected (68% and 43%, respectively). Children are particularly vulnerable, with little control over home and social environment, and lack the understanding, agency, and ability to avoid SHS exposure on their own volition; they also have physiological or behavioral characteristics that render them especially susceptible to effects of SHS. Side-stream smoke (the smoke emanating from the burning end of the cigarette), a major component of SHS, contains a higher concentration of some toxins than mainstream smoke (inhaled by the smoker directly), making SHS potentially as dangerous as or even more dangerous than direct smoking. Compelling animal and human evidence shows that SHS exposure during childhood is detrimental to arterial function and structure, resulting in premature atherosclerosis and its cardiovascular consequences. Childhood SHS exposure is also related to impaired cardiac autonomic function and changes in heart rate variability. In addition, childhood SHS exposure is associated with clustering of cardiometabolic risk factors such as obesity, dyslipidemia, and insulin resistance. Individualized interventions to reduce childhood exposure to SHS are shown to be at least modestly effective, as are broader-based policy initiatives such as community smoking bans and increased taxation.

Purpose: The purpose of this statement is to summarize the available evidence on the cardiovascular health consequences of childhood SHS exposure; this will support ongoing efforts to further reduce and eliminate SHS exposure in this vulnerable population. This statement reviews relevant data from epidemiological studies, laboratory-based experiments, and controlled behavioral trials concerning SHS and cardiovascular disease risk in children. Information on the effects of SHS exposure on the cardiovascular system in animal and pediatric studies, including vascular disruption and platelet activation, oxidation and inflammation, endothelial dysfunction, increased vascular stiffness, changes in vascular structure, and autonomic dysfunction, is examined.

Conclusions: The epidemiological, observational, and experimental evidence accumulated to date demonstrates the detrimental cardiovascular consequences of SHS exposure in children.

Implications: Increased awareness of the adverse, lifetime cardiovascular consequences of childhood SHS may facilitate the development of innovative individual, family-centered, and community health interventions to reduce and ideally eliminate SHS exposure in the vulnerable pediatric population. This evidence calls for a robust public health policy that embraces zero tolerance of childhood SHS exposure.

Keywords: AHA Scientific Statement; atherosclerosis; blood vessels; child; tobacco smoke pollution.

Figure 1

Trends in SHS exposure among non-smoking children and adolescents in US. Data compiled from NHANES periodic survey data^{, ,} Solid line: children aged 3–11 years; Dashed line: adolescents aged 12–19 years

Figure 2

Figure 2A and 2B. Prevalence and estimated source of SHS exposure in non-smoking A) children aged 3–11 years and B) adolescents aged 12–19 years by NHANES study years. Data for these figures were compiled using NHANES periodic survey data. Overall SHS exposure is presented as NHANES estimated prevalence of SHS exposure by age group ^, . To then estimate home-specific exposure, the proportion of non-smoking children or adolescents living with a smoker at home^, was multiplied by the proportion of these children (98%) with detectable cotinine levels ^, ; the remainder of SHS exposure was assumed to be not in the home. Black indicates no SHS exposure (inside or outside of the home), light gray indicates SHS exposure in the home, and dark gray indicates SHS exposure outside of the home.

Figure 2

Figure 2A and 2B. Prevalence and estimated source of SHS exposure in non-smoking A) children aged 3–11 years and B) adolescents aged 12–19 years by NHANES study years. Data for these figures were compiled using NHANES periodic survey data. Overall SHS exposure is presented as NHANES estimated prevalence of SHS exposure by age group ^, . To then estimate home-specific exposure, the proportion of non-smoking children or adolescents living with a smoker at home^, was multiplied by the proportion of these children (98%) with detectable cotinine levels ^, ; the remainder of SHS exposure was assumed to be not in the home. Black indicates no SHS exposure (inside or outside of the home), light gray indicates SHS exposure in the home, and dark gray indicates SHS exposure outside of the home.

Figure 3

Decline in SHS exposure prevalence from NHANES 1999–2000 to 2011–2012 by race

Figure 4

NHANES 2011–2012 SHS exposure prevalence by age and race

Figure 5

Mainstream and side stream smoke

Figure 6

Peak FMD of brachial artery in 11-year-old children according to cotinine group. Values are mean ± SEM. Kallio K, Jokinen E, Raitakari OT, Hamalainen M, Siltala M, Volanen I, Kaitosaari T, Viikari J, Ronnemaa T, Simell O. Tobacco smoke exposure is associated with attenuated endothelial function in 11-year-old healthy children. Circulation. 2007;115:3205–3212

Figure 7

Maximum cIMT (black circles) and maximum aIMT (black squares) in healthy 13-year-old adolescents according to longitudinal tobacco smoke exposure levels. Number of adolescents in exposure groups: cIMT: low (n=160), intermediate (n=171), high (n=163); aIMT: low (n=159), intermediate (n=167), high (n=161). Values are mean ± SEM cIMT – carotid artery intima media thickness aIMT – aortic intima media thickness Kallio K, Jokinen E, Saarinen M, Hamalainen M, Volanen I, Kaitosaari T, Ronnemaa T, Viikari J, Raitakari OT, Simell O. Arterial intima-media thickness, endothelial function, and apolipoproteins in adolescents frequently exposed to tobacco smoke. Circulation. Cardiovascular quality and outcomes. 2010;3:196–203

Figure 8

Aortic distensibility in children exposed to second hand tobacco smoke Kallio K, Jokinen E, Hamalainen M, Saarinen M, Volanen I, Kaitosaari T, Viikari J, Ronnemaa T, Simell O, Raitakari OT. Decreased aortic elasticity in healthy 11-year-old children exposed to tobacco smoke. Pediatrics. 2009;123:e267–273