Childhood passive smoking, race, and coronary artery disease risk: the MCV Twin Study. Medical College of Virginia.

Abstract

Children with long-term exposure to passive cigarette smoke may be at elevated risk for the development of premature coronary artery disease (CAD). To examine how CAD risk factors, exposure to passive smoking, sex, and race are related in pubertal children and to determine if there is an identifiable childhood risk profile (i.e., does passive smoking interact with other coronary risk factors to increase the risk of developing premature CAD). Cohort analytic study. The Medical College of Virginia (MCV) Twin Study, Richmond, Va. Randomly selected twins from 408 11-year-old twin pairs recruited from nearby schools. Data collection occurred at 18-month intervals on family and health histories, smoking and alcohol consumption, blood pressure, anthropometrics, and biochemical assays. Data from cohorts of 11-year-olds studied through age 15 years were analyzed by repeated-measures analyses of variance using a mixed modeling approach. Models for high-density lipoprotein cholesterol (HDL-C) included race, sex, passive smoking status, weight, systolic and diastolic blood pressures, and all interactions. Passive smoke exposure was greater in white families than in black families. Levels of HDL-C and HDL2-C (HDL subfraction 2 cholesterol) were lower in white children than in black children (visit 1: HDL-C, mean +/- SD, 1.21+/-0.26 vs. 1.31+/-0.26 mmol/L [47.0+/-10.1 vs. 50.6+/-10.1 mg/dL], P< or =.01; HDL2, mean +/- SD, 0.31+/-0.18 vs. 0.41+/-0.19 mmol/L [12.3+/-7.0 vs. 15.9+/-7.4 mg/dL], P< or =.001). Children with a family history of cardiovascular disease had differences in HDL-C levels related to race that were worsened by exposure to cigarette smoke. In these children, HDL-C level was lower in those exposed to passive smoking (visit 1: 1.18+/-0.23 vs. 1.25+/-0.23 mmol/L [45.6+/-9 vs. 48.2+/-9 mg/dL] and visit 4: 0.98+/-0.10 vs. 1.19+/-0.18 mmol/L [37.8+/-4 vs. 46.0+/-7 mg/dL]; P<.001), with white children having lower HDL-C levels than black children (visit 1: 1.12+/-0.21 vs. 1.36+/-0.23 mmol/L [43.2+/-8 vs. 52.7+/-9 mg/ dL] and visit 4: 0.97+/-0.31 vs. 1.01+/-0.31 mmol/L [37.6+/-12 vs. 39.0+/-12 mg/dL]; P = .004). In white families, as weight increased, boys exposed to passive smoking showed the greatest decrease in HDL-C level (P<.01 for weight by sex and passive smoking interaction). Risk factors for CAD, such as blood pressure, interacted with HDL-C and these relationships varied by race and sex. Pubertal children with long-term passive cigarette smoke exposure have lower HDL-C levels. Racial differences in HDL-C levels are related to passive smoke exposure. In children with a family history of cardiovascular disease, interactions exist between passive smoking, HDL-C level, and blood pressure that differ by sex and race. White males exposed to passive smoking who have a family history of cardiovascular disease and higher weights and diastolic blood pressures may be at special risk for premature CAD.