Lipoprotein and oxygen transport alterations in passive smoking preadolescent children. The MCV Twin Study.

Moskowitz, William B.; Mosteller, Michael; Schieken, Richard M.; Bossano, R; Hewitt, John K.; Bodurtha, Joann; Segrest, Jere P.

doi:10.1161/01.cir.81.2.586

Cited by 72 publications

(30 citation statements)

References 18 publications

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“…• Altered lipid profiles and endothelium effects in adolescents and young adults [236][237][238] • Asthma 232,239…”

Section: Effects On the Adult Of Childhood Shs Exposurementioning

confidence: 99%

Secondhand and Prenatal Tobacco Smoke Exposure

Best¹

2009

Pediatrics

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Secondhand tobacco smoke (SHS) exposure of children and their families causes significant morbidity and mortality. In their personal and professional roles, pediatricians have many opportunities to advocate for elimination of SHS exposure of children, to counsel tobacco users to quit, and to counsel children never to start. This report discusses the harms of tobacco use and SHS exposure, the extent and costs of tobacco use and SHS exposure, and the evidence that supports counseling and other clinical interventions in the cycle of tobacco use. Recommendations for future research, policy, and clinical practice change are discussed. To improve understanding and provide support for these activities, the harms of SHS exposure are discussed, effective ways to eliminate or reduce SHS exposure are presented, and policies that support a smoke-free environment are outlined.

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“…• Altered lipid profiles and endothelium effects in adolescents and young adults [236][237][238] • Asthma 232,239…”

Section: Effects On the Adult Of Childhood Shs Exposurementioning

confidence: 99%

Secondhand and Prenatal Tobacco Smoke Exposure

Best¹

2009

Pediatrics

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“…Exposure to tobacco smoke may lead to alterations in serum lipid profile, especially to decrease in HDL cholesterol, in children 14,15 and adolescents. 16,17 In adults, heavy workplace exposure to tobacco smoke has been demonstrated to have an adverse influence on serum lipids.…”

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confidence: 99%

Arterial Intima-Media Thickness, Endothelial Function, and Apolipoproteins in Adolescents Frequently Exposed to Tobacco Smoke

Kallio

Jokinen

Saarinen

et al. 2010

Circ: Cardiovascular Quality and Outcomes

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Background-Exposure to tobacco smoke is associated with markers of preclinical atherosclerosis in adults, but its effect on arterial structure in adolescents is unknown. Methods and Results-Healthy 13-year-old adolescents from the atherosclerosis prevention trial STRIP were studied.Maximum carotid and aortic intima-media thickness and brachial artery flow-mediated dilation were measured in 494 adolescents using high-resolution ultrasound. Serum lipid, lipoprotein, and apolipoprotein (Apo) A-I and B concentrations were determined using standard methods. Exposure to tobacco smoke was measured annually between ages 8 and 13 years using serum cotinine concentrations, analyzed with gas chromatography. To define longitudinal exposure, cotinine values of children having serum cotinine measured 2 to 6 times during follow-up were averaged and divided into tertiles (exposure groups): low (nϭ160), intermediate (nϭ171), and high (nϭ163 1 Passive smoking has been associated with attenuated endothelium-dependent dilation in young healthy adults. 2,3 We have previously shown in 11-year-old healthy children that tobacco smoke exposure is associated with endothelial dysfunction measured by flowmediated dilation (FMD) of the brachial artery. 4 In addition, both past and current passive smoking has been related with increased carotid intima-media thickness (cIMT) in adults. [5][6][7] Moreover, tobacco smoke exposure in pregnancy has recently been associated with increased aortic intima-media thickness (aIMT) in neonates 8 and increased cIMT in young adulthood. 9 Conventional cardiovascular risk factors have been related to early structural vascular wall changes in childhood, 10 -12 and exposure to cardiovascular risk factors in adolescence predicts increased adult cIMT. 13 However, none of the previous studies has examined the impact of exposure to tobacco smoke on IMT in healthy children or adolescents.Exposure to tobacco smoke may lead to alterations in serum lipid profile, especially to decrease in HDL cholesterol, in children 14,15 and adolescents. 16,17 In adults, heavy workplace exposure to tobacco smoke has been demonstrated to have an adverse influence on serum lipids. 18,19 Recently, it was indicated that maternal smoking in pregnancy is associ- 21 Exposure to tobacco smoke as indicated by objective measurement, serum cotinine concentration, has been frequently determined in school-aged children. The aim of the present study was to examine the effects of frequent exposure to tobacco smoke on vascular wall structure, endothelial function, and serum lipid profile in healthy 13-year-old adolescents. WHAT IS KNOWN• Exposure to environmental tobacco smoke is related to increased carotid intima-media thickness in adults, but this association has not been studied in children.• Exposure to environmental tobacco smoke may lead to alterations in serum lipid profile, but there are no data on the relations of tobacco smoke exposure and apolipoprotein levels in children. WHAT THE STUDY ADDS• This study shows that frequent exposure ...

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“…We have previously shown (22) that passive-smoking preadolescent boys had lower levels of HDL2 cholesterol, which were related to the number of cigarettes smoked daily by the parents of the boys. The lowest HDL2 cholesterol levels were found in boys exposed to the highest number of cigarettes smoked by their mothers.…”

Section: Discussionmentioning

confidence: 90%

“…We have previously shown (22) that in families with adult smokers, the DPG level in the children correlated directly with the serum thiocyanate level and the total number of cigarettes smoked by the parents. DPG levels in preadolescent boys increased in a dose-dependent relationship with the amount of passive cigarette-smoke exposure.…”

Section: Discussionmentioning

confidence: 94%

Univariate Genetic Analysis of Oxygen Transport Regulation in Children: The Medical College of Virginia Twin Study

et al. 1993

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ABSTRACT. We investigated the relative contributions of genetic, individual environmental, and shared environmental effects on 2,3-diphosphoglycerate (DPG) regulation in preadolescent children. In a population of 165 early pubescent boy and girl twin pairs (11.4 y old), of whom 63 were passive smokers, we asked: 1 ) Are there differences in the control of DPG levels between early pubertal boys and girls? 2) If present, are these differences influenced by exposure to passive cigarette smoke? Non-passive-smoking boys and girls had similar DPG levels. With exposure to passive smoke, DPG levels increased in boys ( p = 0.02) but not in girls. Analysis of variance on DPG demonstrated a parental smoking effect ( p = 0.008) and suggested an interactive effect between parental smoking and sex of the child (p = 0.08). Univariate genetic analyses suggested that genes operated at different magnitudes in boys (9%) and girls (39%) in explaining a significant portion of the variance in DPG. The magnitude of shared environmental influences was greater in boys (62%) than in girls (34%), whereas individual environmental effects were similar in boys (29%) and girls (26%). Early pubertal boys differ from girls in their regulation of DPG. Environmental stressors such as passive cigarette smoke may elicit different responses in males and females, even at an early age. The use of path analysis may provide important insights into the mechanisms and interactions of genetic and environmental effects that underly the childhood antecedents of atherosclerotic heart disease. (Pediatr Res 33: [645][646][647][648] 1993) Abbreviations DPG, 2,3-diphosphoglycerate Systemic oxygen transport is accomplished using many integrated, self-regulated organ systems. Essential components of this system include pulmonary gas exchange, blood flow, Hb concentration, and Hb affinity for oxygen (1). Organic phosphates within the red cell decrease the oxygen affinity of Hb. The most important quantitatively is DPG. The mechanism of the DPG effect on oxygen affinity involves binding of DPG to the two beta chains in the central cavity of deoxy Hb, forcing a conformational shift that drives oxygen off. Oxyhemoglobin (as well as carboxyhemoglobin) binds DPG poorly because of a stereochemically smaller central cavity created by changes in the quarternary structure of Hb with oxygenation (2). An increase in red-cell DPG compensates for an impairment in oxygen supply to tissue and is proportional to the increase in deoxyhemoglobin concentration.Considerable variation in DPG levels, Hb levels, and oxygen affinity occurs in the normal population. A negative correlation has been observed between Hb levels and the levels of DPG in normal people (3, 4). Measurement of red-cell DPG levels has been used as a "functional biopsy" of the adequacy of tissue oxygenation (5). Whereas the correlation between DPG and Hb level may not be causal, feedback mechanisms appear to regulate them in tandem. Therefore, DPG may function as a monitor for environmental influences on systemic ...

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Lipoprotein and oxygen transport alterations in passive smoking preadolescent children. The MCV Twin Study.

Cited by 72 publications

References 18 publications

Secondhand and Prenatal Tobacco Smoke Exposure

Secondhand and Prenatal Tobacco Smoke Exposure

Arterial Intima-Media Thickness, Endothelial Function, and Apolipoproteins in Adolescents Frequently Exposed to Tobacco Smoke

Univariate Genetic Analysis of Oxygen Transport Regulation in Children: The Medical College of Virginia Twin Study

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