Vaccination at 6 months of age followed by routine revaccination is recommended when exposure of infants to measles is likely. Dade County, Florida, began this early two-dose schedule during a large epidemic in 1986-1987 (i.e., 22% of cases occurred in infants aged 6-11 months). This schedule was continued routinely in high-risk areas. The effect of an early two-dose schedule on measles prevention in the county was examined by comparing measles vaccination coverage and epidemiology before (1985-1987) and after (1988-1996) the schedule became routine. To assess serologic response, seroprevalence of measles antibody among children aged 4-6 years in 1995 was examined. To evaluate vaccine effectiveness, a case-control study was conducted among preschool-aged children. Among those aged 2 years, vaccination coverage with > or =1 dose increased from 75% to 94% in 1996. The number of annual cases declined, and endemic measles transmission reportedly ended after 1993. Seroprevalence of plaque reduction neutralization antibody (titer > 1:120) among those receiving vaccination according to an early two-dose schedule and a single dose at age > or =12 months was 94% (95% confidence interval: 89, 98) and 98% (95% confidence interval: 95, 100). In these groups, vaccine effectiveness was comparably high. Early two-dose measles vaccination is associated with improved coverage and a comparably high level of humoral immunity and clinical protection as a single dose at age > or =12 months. This strategy can be useful in areas at high risk for measles among infants.

A measles epidemic occurred in Romania with 32,915 cases and 21 deaths reported between November 1996 and June 1998, despite high vaccination coverage since the early 1980s. Most cases were unvaccinated children aged <2 years and vaccinated school-aged children. A case-control study among preschool children and a cohort study among primary-school children were conducted to estimate effectiveness of Romanian-produced measles vaccine, and to evaluate age at vaccination and waning immunity as risk factors for vaccine failure. Both studies indicated that measles vaccine was highly effective. One dose reduced the risk for measles by 89% (95% confidence interval (CI) 85, 91); two doses reduced the risk by 96% (95% CI 92, 98). Children vaccinated at <1 year of age were not at increased risk for measles compared with children vaccinated at > or =1 year. Waning immunity was not identified as a risk factor since vaccine effectiveness was similar for children vaccinated 6-8, 9-11, and 12-14 years in the past. Because specific groups were not at risk for vaccine failure, an immunization campaign that targets all school-aged children who lack two doses may be an effective strategy for preventing outbreaks. A mass campaign followed by increased first-dose coverage should provide the population immunity required to interrupt indigenous measles virus transmission in Romania.

LEARNING OUTCOME: To describe ethnic and gender differences in serum cholesteryl ester fatty acids in young adults.

BACKGROUND:Epidemiologic surveys from different parts of the developed world are showing increases in asthma prevalence; the causes are not known.OBJECTIVE:To describe trends in prevalence of childhood asthma measured across serial cross-sectional surveys of the school age population of Bogalusa, Louisiana.METHODS:The Bogalusa Heart Study is a long-term epidemiologic study of risk factors for cardiovascular disease in children in a stable, semirural, biracial community. Part of the examination includes a parent-completed health history questionnaire. The item, "Does your child have or has your child had in the past...asthma?" was included in the 1983-5, 1987-8, and 1992-4 surveys. Data analysis was restricted to subjects aged 5 to 17 years.RESULTS:Three thousand two hundred seventy-six subjects participated in 1983-5, 3256 in 1987-8, and 3128 in 1992-4. Reported asthma prevalence increased from 9.2% to 15.9% between 1983-5 and 1992-4. Maternal smoking was associated with asthma in all three surveys. Young age and African American ethnicity were associated with asthma only in the 1992-4 survey.CONCLUSIONS:The prevalence of asthma among the school age population of Bogalusa, Louisiana increased by 73% between the 1983-5 and the 1992-4 surveys. Whether the increase in asthma prevalence represents an increase in disease presence or an increase in disease recognition cannot be determined from these data.

PURPOSE: Cross-sectional and longitudinal associations of serum lipids and lipoproteins with oral contraceptive (OC) use were examined among white and black women aged 18-27 years in 1985-86 and 1988-1991 in the Bogalusa Heart Study, a study of cardiovascular disease in a Southern community.METHODS: Analyses of covariance.RESULTS: In 1985-1986, white OC users had significantly (p < 0.05) higher adjusted mean total and low density lipoprotein (LDL) cholesterols, and lower high density lipoprotein (HDL) cholesterol compared with nonusers; black OC users had higher triglycerides and LDL cholesterol, and lower HDL cholesterol. In 1988-1991, white OC users bad higher total cholesterol, triglycerides, and LDL cholesterol, while black OC users had higher triglycerides. OC use was unrelated to mean HDL cholesterol levels in 1988-1991; however, a lower percentage of white OC users than nonusers in 1988-1991 had HDL cholesterol levels < 35 mg/dl. Longitudinally, white OC nonusers at baseline who used OCs at follow up had significant increases from baseline levels in total cholesterol, triglycerides, and very low density lipoprotein (VLDL) and LDL cholesterols; black women showed an increase only in LDL cholesterol. White women who stopped using OCs by follow-up had a decrease in VLDL and LDL cholesterols, and an increase in HDL cholesterol. White OC users at both exams also had a significant increase in HDL cholesterol, whereas women who began using OCs by follow-up did not.CONCLUSIONS: The unfavorable lipid profile associated with OC use was not apparent upon discontinued use. Lack of an adverse effect of OC use on HDL cholesterol at follow-up may be the result of changing formulations, and requires further examination. (C) 1997 Elsevier Science Inc.

Background Mortality from coronary heart disease is relatively low in Japan compared with other developed countries and has remained low despite an increasing standard of living and an apparent increase in mean plasma cholesterol concentration in adults over the past three decades. Important differences in childhood plasma lipoprotein profile might contribute to some of the difference in coronary heart disease mortality seen between Japan and both Australia and North America. Methods and Results Plasma HDL cholesterol and total cholesterol were surveyed in representative populations of schoolchildren in Australia, Japan, and Bogalusa, La. The mean concentration of plasma HDL cholesterol (but not total cholesterol) was higher for Japanese schoolchildren than for Australian or US schoolchildren ( P <.001). In addition, the difference in plasma HDL cholesterol between the ages of 8 to 10 years and 12 to 15 years was much greater for Australian (boys, 15.2%; girls, 2.6%) and US (boys, 9.1%; girls, 2.7%) children than for their Japanese counterparts (boys, 4.2%; girls, 1.9%). An examination of potential explanatory factors revealed little difference in body mass index between samples, higher physical activity levels for the Japanese compared with the Australians, and substantial differences in dietary intake between Japanese and Australian schoolchildren. Conclusions The relatively high ratio of plasma HDL cholesterol to total cholesterol in Japanese schoolchildren and the relatively small negative difference of plasma HDL cholesterol with age may help to explain why the coronary heart disease mortality rate in Japan is low compared with that in other developed countries.

The hypothesis that birth weight predicts blood pressure inversely at age 7 through 11 years was examined in 1,446 white children and black children in Washington Parish, Louisiana. Two data sets of the Bogalusa Heart Study were merged: 1) newborn cohort participants (n = 233), initially examined at birth, 1973-1974, and reexamined in 1984-1985 at ages 9 through 11 years; and 2) subjects examined at ages 7 through 11 years in 1987-1988 (n = 1,213) whose birth weight was collected from birth certificates in 1991. The prevalence ratios for being in the race-, sex-, and age-specific upper decile of diastolic blood pressure in children born with low birth weight (< 2,500 g) versus those with birth weight > or = 2,500 g were 0.85 (95% confidence interval 0.28-2.56) for white boys, 2.66 (95% confidence interval 1.24-5.70, p < 0.05) for black boys, 1.38 (95% confidence interval 0.63-3.03) for white girls, and 1.05 (95% confidence interval 0.40-2.75) for black girls. For systolic blood pressure, the corresponding prevalence ratio for each race-sex group did not differ from one. When the analyses were restricted to full-term births, prevalence ratios in any race-sex group did not differ from one for systolic and diastolic blood pressure. In multiple linear regression analyses, the concurrently determined Quetelet index (p < 0.001) was a much stronger correlate of systolic and diastolic blood pressure after appropriate adjustment than was birth weight (p > 0.05). From this study, there is some evidence that low birth weight may determine a risk for subsequent high blood pressure in black boys in the age group 7 through 11 years, but the inconsistency of the results for other race-sex groups was unexpected and remains unexplained, if the underlying hypothesis is true.

Cigarette smoking among adolescents continues to be a major public health problem in the United States. Smoking trends from 1976–1977 to 1992–1994 were examined in the Bogalusa Heart Study, an investigation of cardiovascular disease risk factors among black and white, male and female adolescents in a semirural town in the southern United States. Age-race-sex specific χ2 tests for trends over five survey periods were conducted. In almost every age group, black boys and girls were less likely to be current smokers or to have ever smoked or tried cigarettes, as compared with white boys and girls, respectively (P < 0.01). Within age groups, few significant trends in smoking status from 1976–1977 through 1992–1994 were observed among white boys and girls. Among black males and females, however, sharp decreases were observed among all age groups in the prevalence of having ever smoked or tried cigarettes (P = 0.0001) and among the older age groups in the prevalence of being a current smoker (P = 0.0001). Thus, substantial declines in the prevalence of smoking were observed among black children but not among white children. Further research is required to understand why these ethnic differences in smoking occurred so that public health programs may target further the smoking behaviors in children.

The structural gene locus for apolipoprotein E (apo E) is polymorphic. The relative apo E allele frequencies and the influence of this polymorphism on serum lipoprotein concentrations were studied in 8- to 17-year-old black (n = 444) and white (n = 446) children from the community of Bogalusa, LA. The frequencies of the e2, e3, and e4 alleles for white males/females were 0.027/0.024, 0.849/0.823, and 0.124/0.153, respectively; corresponding values for black males/females were 0.087/0.074, 0.713/0.721, and 0.20/0.205, respectively. Apo E phenotype distributions and allele frequencies showed a significant race difference, but no sex difference. Significant differences among apo E phenotypes were noted for total cholesterol, low-density lipoprotein cholesterol (LDL-C), and apo B in both races; significant effects were noted for high-density lipoprotein cholesterol (HDL-C) and apo A-I in black children, but not in white children. Among white children, the average excess of the apo e2 allele showed lower LDL-C (-12.5 mg/dL) and apo B (-15.8 mg/dL) concentrations, while the average excess of the apo e4 allele showed higher LDL-C (7.0 mg/dL) and apo B (7.5 mg/dL) concentrations. Black children showed a similar trend for these variables, but to a lesser degree; in addition, the average excess of apo e2 allele showed higher HDL-C (12.8 mg/dL) and apo A-I (8.3 mg/dL) concentrations in this racial group. It is noteworthy that the association of apo E polymorphism with serum lipoprotein concentrations noted in adults can be seen already in children.

The Heart Smart Family Health Promotion Program is a multidisciplinary, school-based program for cardiovascular risk reduction among high-risk children and their families. As a program that includes young adults at high risk, it is adaptable to a clinical practice. Nineteen fourth and fifth graders were selected as probands for elevated risk factors after a general screening to identify families for an intervention program. Twenty-three parents participated in a 12-week program focused on eating, exercise, and smoking behavior changes enhanced by behavicral support strategies. Weekly sessions were held in the auditorium/cafeteria of the elementary school and consisted of orientation and presentations, cardiovascular (CV) screening with medical feedback, activities, self-monitoring, counseling, and contingency contracting. Information gathered before and after the program included medical history, CV health knowledge and relevant behavior, blood pressure, serum lipid and lipoprotein values, anthropometric measurements, and urine electrolyte excretion. Both children and parents showed positive changes in eating habits and physical activity and significant changes in knowledge and blood pressure levels, while the children halted their weight gain. We believe this multidisciplinary, behavior-oriented, school-based program can be an effective cardiovascular risk intervention adaptable for a clinical office practice.

Annals of the New York Academy of SciencesVolume 623, Issue 1 p. 16-25 Autopsy Studies in United States Children and Adolescentsa Relationship of Risk Factors to Atherosclerotic Lesions WILLIAM P. NEWMAN III, WILLIAM P. NEWMAN III Department of Pathology Louisiana State University School of Medicine 1901 Perdido Street New Orleans, Louisiana 70112-1393Search for more papers by this authorWENDY WATTIGNEY, WENDY WATTIGNEY Department of Medicine Louisiana State University School of Medicine 1901 Perdido Street New Orleans, Louisiana 70112-1393Search for more papers by this authorGERALD S. BERENSON, GERALD S. BERENSON Department of Medicine Louisiana State University School of Medicine 1901 Perdido Street New Orleans, Louisiana 70112-1393Search for more papers by this author WILLIAM P. NEWMAN III, WILLIAM P. NEWMAN III Department of Pathology Louisiana State University School of Medicine 1901 Perdido Street New Orleans, Louisiana 70112-1393Search for more papers by this authorWENDY WATTIGNEY, WENDY WATTIGNEY Department of Medicine Louisiana State University School of Medicine 1901 Perdido Street New Orleans, Louisiana 70112-1393Search for more papers by this authorGERALD S. BERENSON, GERALD S. BERENSON Department of Medicine Louisiana State University School of Medicine 1901 Perdido Street New Orleans, Louisiana 70112-1393Search for more papers by this author First published: April 1991 https://doi.org/10.1111/j.1749-6632.1991.tb43715.xCitations: 81 a Supported in part by Grants No. HL 08974, HL 38844, and HL 33746 from the National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, Maryland. AboutPDF ToolsRequest permissionExport citationAdd to favoritesTrack citation ShareShare Give accessShare full text accessShare full-text accessPlease review our Terms and Conditions of Use and check box below to share full-text version of article.I have read and accept the Wiley Online Library Terms and Conditions of UseShareable LinkUse the link below to share a full-text version of this article with your friends and colleagues. Learn more.Copy URL Share a linkShare onEmailFacebookTwitterLinkedInRedditWechat References 1 Holan, R. L., H. C. Mcgill, Jr., J. P. Strong & J. C. Geer. 1958. The natural history of atherosclerosis; the early aortic lesions as seen in New Orleans in the middle of the 20th century. Am. J. Pathol. 34: 209–235. 2 Strong, J. P. & H. C. Mcgill, Jr. 1962. The natural history of coronary atherosclerosis. Am. J. Pathol. 40: 37–49. 3 Strong, J. P. & H. C. Mcgill, Jr. 1969. The pediatric aspects of atherosclerosis. J. Atheroscler. Res. 9: 251–265. 4 Enos, W. F., R. H. Holmes & J. Beyer. 1953. Coronary disease among United States soldiers killed in action in Korea: preliminary report. J. Am. Med. Assoc. 152: 1090–1093. 5 Virmani, R., M. Robinowitz, et al . 1987. Coronary artery atherosclerosis revisited in Korean War combat casualties. Arch. Pathol. Lab. Med. 111: 972–976. 6 Mcnamara, J. J., M. A. Molot, J. F. Stremple & R. T. Cutting. 1971. Coronary artery disease in combat casualties in Vietnam. J. Am. Med. Assoc. 216: 1185–1187. 7 Solberg, L. A. & J. P. Strong. 1983. Risk factors and atherosclerotic lesions. A review of autopsy studies. Arteriosclerosis 3: 187–198. 8 1984. Lipid Research Clinics Program. The Lipid Research Clinics Coronary Primary Prevention Trial results. I. Reduction in incidence of coronary heart disease. JAMA 251: 351–364. 9 1984. Lipid Research Clinics Program. The Lipid Research Clinics Coronary Primary Prevention Trial results. II. The relationship of reduction in incidence of coronary heart disease to cholesterol lowering. JAMA 251: 365–374. 10 Newman, W. P., III, D. S. Freedman, A. W. Voors, et al . 1986. Relation of serum lipoproteins and systolic blood pressure to early atherosclerosis. The Bogalusa Heart Study. N. Engl. J. Med. 314: 138–144. 11 Freedman, D. S., W. P. Newman III, R. E. Tracy, et al . 1988. Black-white differences in aortic fatty streaks in adolescence and early adulthood: the Bogalusa Heart Study, Circulation 77: 856–864. 12 Berenson, G. S., C. A. Mcmahan, A. W. Voors, et al . 1980. Cardiovascular risk factors in children: the early natural history of atherosclerosis and essential hypertension. Oxford University Press. New York , NY . 13 Srinivasan, S. R. & G. S. Berenson. 1983. Serum lipoproteins and methods for study. In CRC Handbook of Electrophoresis, Lipoprotein Methodology and Human Studies. L. A. Lewis, Ed. 3: 185–204. CRC Press. Boca Raton , Fla. 14 Frerichs, R. R., S. R. Srinivasan, L. S. Webber & G. S. Berenson. 1976. Serum cholesterol and triglyceride levels in 3,446 children from a biracial community: the Bogalusa Heart Study. Circulation 54: 302–309. 15 Srinivasan, S. R., R. R. Frerichs, L. S. Webber & G. S. Berenson. 1976. Serum lipoprotein profile in children from a biracial community: the Bogalusa Heart Study. Circulation 54: 309–318. 16 Sprecher, D. L., E. J. Schaefer, K. M. Kent, et al . 1984. Cardiovascular features of homozygous familial hypercholesterolemia: analysis of 16 patients. Am. J. Cardiol. 54: 20–30. 17 Mcgill, H. C., Jr., J. C. Geer & J. P. Strong. 1963. Natural history of human atherosclerotic lesions. In Atherosclerosis and Its Origin. M. Sandler & G. H. Bourne, Eds.: 39–65. Academic Press. New York , N.Y. 18 Newman, W. P., III & J. P. Strong. 1978. Natural history, geographic pathology, and pediatric aspects of atherosclerosis. In Atherosclerosis: Its Pediatric Aspects. W. B. Strong, Ed.: 15–40. Grune & Stratton. New York , N.Y. 19 Montenegro, M. R. & D. A. Eggen. 1968. Topography of atherosclerosis in the coronary arteries. Lab. Invest. 18: 586–593. 20 Mcgill, H. C., Jr. 1968. Fatty streaks in the coronary arteries and aorta. Lab. Invest. 18: 560–564. 21 Stary, H. C. 1989. Evolution and progression of atherosclerotic lesions in coronary arteries of children and young adults. Arteriosclerosis 9(Suppl. 1): I-19–I-32. 22 Mcgill, H. C., Jr. 1984. Persistent problems in the pathogenesis of atherosclerosis. Arteriosclerosis 4: 443–451. 23 Rhoads, G. G., W. C. Black Welder, G. N. Stemmermann, et al . 1978. Coronary risk factors and autopsy findings in Japanese-American men. Lab. Invest. 38: 304–311. 24 Kannel, W. B., P. Sorlie, F. Brand, et al . 1980. Epidemiology of coronary atherosclerosis: postmortem vs. clinical risk factor correlations: the Framingham Study. In Atherosclerosis V: Proceedings of the Fifth International Symposium. A. M. Gotto, L. C. Smith & B. Allen, Eds.: 54–56. Springer-Verlag. New York , N.Y. 25 Sternby, N. H. 1980. Atherosclerosis, smoking and other risk factors. In Atherosclerosis V: Proceedings of the Fifth International Symposium. A. M. Gotto, L. C. Smith & B. Allen, Eds.: 67–70. Springer-Verlag. New York , N.Y. 26 Holme, I., S. C. Enger, A. Helgeland, et al . 1981. Risk factors and raised atherosclerotic lesions in coronary and cerebral arteries: statistical analysis from the Oslo study. Arteriosclerosis 1: 250–256. 27 Sorlie, P. D., M. R. Garcia-Palmieri, M. I. Castillo-Staab, et al . 1981. The relation of antemortem factors to atherosclerosis at autopsy: the Puerto Rico Heart Health Program. Am. J. Pathol. 103: 345–352. 28 Okumiya, N., K. Tanaka, K. Ueda, et al . 1985. Coronary atherosclerosis and antecedent risk factors: pathologic and epidemiologic study in Hisayama, Japan. Am. J. Cardiol. 56: 62–66. Citing Literature Volume623, Issue1Hyperlipidemia in Childhood and the Development of AtherosclerosisApril 1991Pages 16-25 ReferencesRelatedInformation

Methods. Serum lipoprotein profiles in 4,231 individuals, ages 5–26 years, were studied cross-sectionally in a biracial community to describe the race- and gender-specific changes from adolescence into young adulthood.

Arterionephrosclerosis is diagnosed at autopsy by assessing the severity and extent of certain structural features in the renal cortical arteries seen in tissue sections. These features are characterized by fibrotic intimal thickening and medial shrinkage, a progressive change from the youthful muscular pattern to the elderly sclerotic pattern. Intimal fibrosis can be quantified by expressing intimal thickness as a percentage of the arterial outer diameter (% OD). The magnitude of arterionephrosclerosis, found by averaging the measures of intimal fibrosis seen in a kidney, can be calculated from age and mean blood pressure, using a standard prediction function. This function is a quantitative statement of a fundamentally important principle: just as blood pressure is a continuous variable that can range from low to high levels, arterionephrosclerosis is also a continuous variable that can take any degree of abnormality of arterial structure from minimal to maximal. Furthermore, a correspondence exists between the two quantities so that each can be calculated from the other. In this study, a correlation of 0.966 was found between the observed and the calculated magnitudes of arterionephrosclerosis over 10-year age groups from 25 to 34 years to 65 to 74 years, using group average data within age groups. For individuals, however, the correlations between observed and calculated magnitudes of arterionephrosclerosis were about 0.6 in a former study of elderly subjects and about 0.1 in the subjects aged 6 to 27 years in this study. The average growth rate of arterionephrosclerosis was found to be about 0.25 %OD per year from ages 15 to 54 years, and about 0.13 %OD per year from ages 55 to 70 years; the growth rate did not increase in the oldest age groups when blood pressure averaged higher than blood pressure in more youthful subjects. These and other findings are consistent with the view that the reason a correlation exists between blood pressure and arterionephrosclerosis could be because the magnitude of arterionephrosclerosis is one of the determinants that sets the level of blood pressure. From this perspective, each individual can be viewed as having other determinants of blood pressure, methodologic or biologic, which add to or subtract from the values set by age and arterionephrosclerosis. When subjects are pooled into groups, so that individual determinants balance out, the group average levels of mean blood pressure could be interpreted as reflecting little other than the magnitude of arterionephrosclerosis at each specific age.

The distributions of serum creatinine levels and their relationship with selected anthropometric and cardiovascular risk variables have been described in 3983 children and young adults, aged 5 to 26 years, obtained from a biracial population, Bogalusa, Louisiana. For both blacks and whites serum creatinine levels increased slowly with age, until 11 years of age when a steeper increase occurred to around 19 years of age. Before this age there was a significant age by sex interaction (p less than 0.0001) in the distributions of serum creatinine. After the age of 19 years mean serum creatinine levels were significantly higher in black men than in white men (1.16 mg/dl vs 1.09 mg/dl, p less than 0.0005) and in black women than in white women (0.87 mg/dl vs 0.84 mg/dl, p less than 0.08). Creatinine levels were also significantly higher in men than in women (1.11 mg/dl vs 0.85 mg/dl, p less than 0.0001). Creatinine clearance, estimated from an equation using serum creatine, age, and weight, showed a steady increase until 13 years of age when a maximum range of 120 to 140 ml/min was reached. By the age of 19 years the clearance had declined to a relatively constant range of 100 to 120 ml/min. Black men had the highest correlation of serum creatinine concentration with height, weight, and lean body mass after adjusting for age. White men had the highest correlation of serum creatinine concentration with uric acid. Diastolic blood pressure becomes an important determinant of creatinine levels by the age of 11 years. The race-sex differences in serum creatinine levels in children and young adults are likely related to body mass.