Judith Groner

Pediatric Precursors of Adult Cardiovascular Disease: Noninvasive Assessment of Early Vascular Changes in Children and Adolescents

BACKGROUND. Until recently, our understanding of the childhood antecedents of adult cardiovascular disease was limited mainly to autopsy studies and pathologic findings in teens and young adults who died from accidental causes. Recent advances in the understanding of atherosclerosis and new technologies allowing detection of early events have made it possible to observe anatomic and physiologic evidence of cardiovascular disease in young adults and children. OBJECTIVES. The goal of this article was to introduce pediatricians to new methods for noninvasive measurement of cardiovascular disease and its precursors, to describe the potential application of these techniques in detecting childhood precursors of adult cardiovascular disease, and to summarize knowledge gained from this approach. METHODS. We conducted a computerized search of peer-reviewed articles listed in PubMed and Medline from 1980 to April 2006. We reviewed 63 and 84 articles from the adult and pediatric literature, respectively. RESULTS. Reviewing the research on childhood antecedents of adult cardiovascular disease is sobering. Vascular alterations in anatomy, physiology, mechanical properties, and proinflammatory and prothrombotic changes are present from a very early age of childhood and are associated with the risk factors common in adult cardiovascular disease. At the same time, this body of research supports the concept that the vascular impairment from childhood may improve over time with appropriate intervention. CONCLUSIONS. The measurement tools and concepts described in this article offer diagnostic and therapeutic opportunities for collaboration between clinical pediatricians and pediatric researchers. These partnerships will enable pediatricians to contribute in an effort to reduce the burdens of cardiovascular disease to individuals, families, and society.

Protecting Children From Tobacco, Nicotine, and Tobacco Smoke.

This technical report serves to provide the evidence base for the American Academy of Pediatrics’ policy statements “Clinical Practice Policy to Protect Children From Tobacco, Nicotine, and Tobacco Smoke” and “Public Policy to Protect Children From Tobacco, Nicotine, and Tobacco Smoke.” Tobacco use and involuntary exposure are major preventable causes of morbidity and premature mortality in adults and children. Tobacco dependence almost always starts in childhood or adolescence. Electronic nicotine delivery systems are rapidly gaining popularity among youth, and their significant harms are being documented. In utero tobacco smoke exposure, in addition to increasing the risk of preterm birth, low birth weight, stillbirth, placental abruption, and sudden infant death, has been found to increase the risk of obesity and neurodevelopmental disorders. Actions by pediatricians can help to reduce children’s risk of developing tobacco dependence and reduce children’s involuntary tobacco smoke exposure. Public policy actions to protect children from tobacco are essential to reduce the toll that the tobacco epidemic takes on our children.

Staying smoke free: An intervention to prevent postpartum relapse

This pilot study evaluated the effectiveness of a nurse-delivered home-visiting program during the postpartum period that included a low-intensity smoking relapse-prevention intervention. A prospective two-group design was used. Participants were women who had quit smoking during their pregnancy. They were invited to participate during postpartum hospitalization on a university hospital postpartum ward. A brief intervention during postpartum hospitalization, a home visit, and two follow-up phone calls over a 1- to 2-month period were compared with a routine home visit without any prescribed focus on tobacco use. The main outcome was biochemically verified smoking abstinence at 3 and 6 months postenrollment. Abstinence was defined as a salivary cotinine level of 14 ng/ml or less. At 3 months postenrollment, 26.4% of the intervention group were classified as abstinent, compared with 12.4% of the comparison group (OR = 2.4, 95% CI = 1.16-4.98). At 6 months, the proportion of the intervention group categorized as abstinent was 21.5%, compared with 10.2% of comparison group participants (OR = 2.5, 95% CI = 1.13-5.71). Greater than three times as many in the intervention group remained abstinent at both times (18.2%), compared with the comparison group (5.2%; OR = 2.4, 95% CI = 1.16-4.93). The effectiveness of this brief, low-cost, and potentially replicable intervention in improving the rate of persistent postpartum smoke-free status for women who quit smoking during pregnancy is encouraging. A randomized trial of the approach is warranted.

Smoke constituent exposure and smoking topography of adolescent daily cigarette smokers

Adolescent smoking prevalence is a major health concern, with 24.4% reporting smoking in the past 30 days and 15.8% considered daily smokers. The purpose of this study was to characterize biobehavioral nicotine dependence, smoke constituent exposure and smoking topography in adolescent daily smokers. Relationships among biological markers of nicotine dependence (nicotine boost, carbon monoxide [CO] boost and cotinine levels) with existing self-report measures (modified Fagerström Tolerance Questionnaire [mFTQ] and the motivations for smoking scale) were examined. Gender differences were characterized. Fifty adolescents 13-18 years old were recruited for the study, 50% female. CO, plasma nicotine levels pre- and postcigarette, cotinine, and smoking topography were measured during a smoking bout with participants usual cigarette. Average CO boost, pre- to postcigarette was 7.2 + 3.6 ppm, baseline cotinine level averaged 224.0 +/- 169.6 ng/ml and nicotine boost averaged 23.4 +/- 21.7 ng/ml. Mean puffs per cigarette was 14.2 +/- 6.3. Males had significantly higher total puff volumes, but similar smoke constituent exposure to females, and higher handling of cigarettes as smoking motive. In regression analysis, 35% of variance in tobacco use, as indicated by baseline cotinine concentration, was explained by maximum puff duration, postcigarette CO level, and nicotine dependence, as measured by the mFTQ. Results indicated adolescents had considerable smoke constituent exposure and nicotine dependence suggesting the importance of appropriate smoking cessation treatment.

Clinical Practice Policy to Protect Children From Tobacco, Nicotine, and Tobacco Smoke.

Tobacco dependence starts in childhood. Tobacco exposure of children is common and causes illness and premature death in children and adults, with adverse effects starting in the womb. There is no safe level of tobacco smoke exposure. Pediatricians should screen for use of tobacco and other nicotine delivery devices and provide anticipatory guidance to prevent smoking initiation and reduce tobacco smoke exposure. Pediatricians need to be aware of the different nicotine delivery systems marketed and available. Parents and caregivers are important sources of children’s tobacco smoke exposure. Because tobacco dependence is a severe addiction, to protect children’s health, caregiver tobacco dependence treatment should be offered or referral for treatment should be provided (such as referral to the national smoker’s quitline at 1-800-QUIT-NOW). If the source of tobacco exposure cannot be eliminated, counseling about reducing exposure to children should be provided. Health care delivery systems should facilitate the effective prevention, identification, and treatment of tobacco dependence in children and adolescents, their parents, and other caregivers. Health care facilities should protect children from tobacco smoke exposure and tobacco promotion. Tobacco dependence prevention and treatment should be part of medical education, with knowledge assessed as part of board certification examinations.

Public Policy to Protect Children From Tobacco, Nicotine, and Tobacco Smoke.

Tobacco use and tobacco smoke exposure are among the most important health threats to children, adolescents, and adults. There is no safe level of tobacco smoke exposure. The developing brains of children and adolescents are particularly vulnerable to the development of tobacco and nicotine dependence. Tobacco is unique among consumer products in that it causes disease and death when used exactly as intended. Tobacco continues to be heavily promoted to children and young adults. Flavored and alternative tobacco products, including little cigars, chewing tobacco, and electronic nicotine delivery systems are gaining popularity among youth. This statement describes important evidence-based public policy actions that, when implemented, will reduce tobacco product use and tobacco smoke exposure among youth and, by doing so, improve the health of children and young adults.

Active and passive tobacco smoke exposure: A comparison of maternal and child hair cotinine levels

The objective of this study was to compare tobacco smoke exposure in mothers and their healthy children less than 3 years old using hair cotinine (HC) levels as an objective long-term measure of exposure. Hair samples were obtained from mother/child pairs recruited from the Columbus Childrens Hospital Primary Care Center, and were analyzed by radioimmunoassay to compare HC levels. Mothers were both self-reported smokers and nonsmokers. Contributing and confounding variables were assessed based on questionnaires completed by participants. Exclusion criteria for children were prematurity and presence of chronic cardiopulmonary disease. Hair samples and questionnaires were obtained from 104 mother/child pairs. Child and maternal HC levels were correlated for both self-reported maternal smokers (R2 = .13, p < .013) and self-reported maternal nonsmokers (R2 = .54, p < 001). Child HC levels were higher than maternal HC levels (1.18 ng/mg vs. .78 ng/mg, p < .001). Children of nonsmokers had higher HC levels than their mothers (.77 ng/mg vs. .35 ng/mg, p < .001), while HC levels of smokers and their children were no different (1.91 ng/mg vs. 1.92 ng/mg, p = .978). The relationship between child and maternal HC did not differ by child age, gender, or race. In conclusion, environmental tobacco smoke exposure in young children as reflected by HC is higher than expected based on prior studies of biomarkers and passive tobacco smoke exposure in adult nonsmokers.

Secondhand Smoke Exposure and Endothelial Stress in Children and Adolescents

OBJECTIVE Links between secondhand smoke exposure and cardiovascular disease in adults are well established. Little is known about the impact of this exposure on cardiovascular status during childhood. The purpose of this study was to investigate relationships between secondhand smoke exposure in children and adolescents and cardiovascular disease risk--systemic inflammation, endothelial stress, and endothelial repair. METHODS A total of 145 subjects, aged 9 to 18 years, were studied. Tobacco smoke exposure was determined by hair nicotine level. Cardiovascular risk was assessed by markers of systemic inflammation (C-reactive protein [CRP] and adiponectin); by soluble intercellular adhesion molecule 1 (s-ICAM1), which measures endothelial activation after surface vascular injury; and by endothelial repair. This was measured by prevalence of endothelial progenitor cells (EPCs), which are bone marrow-derived cells that home preferentially to sites of vascular damage. RESULTS Hair nicotine was directly correlated with s-ICAM1 (r = 0.4090, P < .0001) and negatively correlated with EPC prevalence (r = -0.2002, P = .0195). There was no relationship between hair nicotine and CRP, and a trend toward a weak relationship with adiponectin. Hair nicotine and body mass index were independent variables in a multivariate model predicting s-ICAM1; hair nicotine was the only significant variable in a model predicting EPC prevalence. CONCLUSIONS Secondhand smoke exposure during childhood and adolescence is detrimental to vascular health because s-ICAM1 is a marker for endothelial activation and stress after vascular surface injury, and EPCs contribute to vascular repair. The fact that body mass index is also a factor in the model predicting s-ICAM1 is concerning, in that 2 risk factors may both contribute to endothelial stress.

Process evaluation of a nurse-delivered smoking relapse prevention program for new mothers.

The objective of this study1 is to evaluate the feasibility, recall, and acceptability of an evidence-based intervention using home-health nurses to provide smoking relapse prevention skills to new mothers. The design of this study is process evaluation. Setting and participants include women who had delivered a normal newborn at a university hospital, who quit smoking during pregnancy, were smoke free for 7 days, and had saliva cotinine of less than or equal to 14 nanogram/ml. The intervention is a multicomponent cognitive-behavioral intervention, including inpatient contact, a home-health visit, and 2 follow-up phone calls. Results are as follows: 121 participants enrolled, and the intervention was implemented in 78 home visits. Nurses discussed tobacco issues for an average of 12.0 min. Almost all participants recalled the home visit; nearly two thirds recalled discussing tobacco use. Only 4% reported negative feelings toward discussing tobacco issues. In 87% of home visits, nurses implemented all 5 intervention components with self-reported nonsmokers. The conclusion is as follows: A nurse-delivered smoking relapse prevention intervention for new mothers was feasible and acceptable.

Oxidative Stress in Youth and Adolescents With Elevated Body Mass Index Exposed to Secondhand Smoke.

INTRODUCTION Our objective was to investigate the relationships between secondhand smoke (SHS) exposure and oxidative stress in a group of youth and adolescents with elevated body mass index. METHODS Participants in this cross sectional study were healthy nonsmoking youth and adolescents ages 9 to 18 years old. Three-quarters of the participants were either overweight or obese. SHS exposure was determined by survey and hair nicotine level. Markers of oxidation were total antioxidant capacity and protein malondialdehyde adducts (MDA). RESULTS Ninety subjects were studied; adequate hair samples were available for 86. The mean hair nicotine level was 0.75ng/mg, the median was 0.58ng/mg and the range was 0.09-2.88ng/mg. There was a significant relationship between MDA and the three survey questions regarding smoke exposure ([mother smokes, r = 0.29, P = .006], [smoker lives in the home, r = 0.31, P = .004], and [number of smokers in the home, r = 0.36, P = .002]). There was a significant positive relationship between log-hair nicotine and MDA (Pearson r = 0.233, P = .031), which remained significant after controlling for age, sex, race, and method of insurance. No relationship was found between log-hair nicotine and total antioxidant capacity. However, there was a significant relationship between number of smokers in the home (r = 0.24, P = .042) and total antioxidant capacity. CONCLUSIONS We have demonstrated a significant positive relationship hair nicotine level and MDA in a group of youth with a high proportion of overweight/obese subjects. IMPLICATIONS We have shown a significant relationship between objectively measured SHS exposure and one marker of oxidative stress in a sample of youth and adolescents with a high proportion of overweight/obese subjects, and who were nonsmokers with relatively low tobacco exposure. This finding remains significant after controlling for age, sex, race, and type of medical insurance. Since the cardiovascular effects of SHS exposure are related to oxidative stress, this finding adds to our knowledge that the sequence of deleterious effects of tobacco exposure on the cardiovascular system begins long before clinical disease is evident.