Annotated bibliography on vital and health statistics.

  • United States. Office of Health Statistics Analysis.
Date:
1970
Catalogue details

Licence: Public Domain Mark

Credit: Annotated bibliography on vital and health statistics. Source: Wellcome Collection.

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    84 palate, clubfoot, craniospinal, and external uretheral 6,800 cases with a single anomaly, 838 with 2, 549 with anomalies. Continued surveillance of human as well as animal malformations are planned. 3 tables. 5 refer- Spina bifida in Liverpool. Develop Med Child Neurol 7:258-68, Jun 65. Incidence of spina bifida (including cranium bifidum) in Liverpool, England, 1960-63, was 3.5 per 1,000 total births. There was an excess of winter births over sum- mer. The sex ratio was 1.2 females to 1 male and this rence of spina bifida was not related to the length of the preceding fallow period. When mothers of spina bifida were compared with controls, the cases showed: an excess of primiparas; a higher proportion 20-24 years of age; a two-fold increase in incidence of abortion or stillbirth immediately before the birth of the index in- fant; an increase in the number of malformed children preceding the index birth; and a higher incidence of threatened abortions and hydramnios. (AEd) STARK, C.R., MANTEL, N. Effects of maternal age and birth order on the risk of mongolism and leukemia. J Nat Cancer Inst. 37:687-98, Nov 66. Maternal age and birth order effects on the risk of mongolism and leukemia were determined for children born in Michigan, 1950-1964. There was a striking asso- order did not.independently affect the risk of mongo- lism. Both maternal age and birth order independently affected the risk of death from leukemia, the risk of death from leukemia decreasing with advancing birth order and increasing with advancing maternal age. Except for the older maternal age groups, these trends age and birth order on death due to all causes. This contrast suggests maternal age and birth order may be closely associated with the etiological agents of child- hood leukemia. 6 tables. 34 references. (AA) STARK, C. R., MANTEL, N. Lack of seasonal-or-temporal-spatial clustering of Down’s syndrome births in Michigan. Amer J Epidem 86:199-213, Jul 67. Data from 2,431 Down’s syndrome births, 1950-1964, in Michigan were used to detect temporal-spatial clustering. It is concluded that Down’s syndrome is caused by a factor (or factors) randomly distributed in time and space. The strong association between Down’s syndrome etiology, risk and advancing maternal (or paternal) age, and other epidemiologic and cytogenetic findings led to the characterization of Down’s syndrome etiology as some event (or group of events) with a stable temporal- spatial distribution which irreversibly alters the probabil- ity of an error in the disposition of G-group chromo- somal material during meiosis or in the young zygote. It is speculated that if meiosis can be shown to become less precise with advancing age, as shown for mitosis, the search for cause of Down’s syndrome may be furthered on physiologic or environmental factors likely to have a direct effect on meiosis. 6 tables. 21 references. Appendix, with equations. (AEd) STEVENSON, A.C., JOHNSTON, H.A.,STEWART, M.L.P. of consecutive births in 24 countries. centers in 16 countries. Among 421,781 pregnancies, incidence of malformations was 12.7 per 1,000 hospital could be coded for every live birth and stillbirth over 28 weeks gestation. Data include number of single and mul- tiple births, by sex, malformation, maternal age, and survival for each center. Separate chapters discuss major malformations including Down’s syndrome, neural tube defects, congenital heart disease, and cleft lip and/or palate. 42 tables. 52 references. (Ed) STROLLER, A., COLLMANN,R. D. Area relationship between incidences of infectious hepa- titis and of the births of children with Down’s syndrome nine months later. A highly significant and consistent area difference in the incidence of infectious hepatitis for the eastern and western divisions of metropolitan Melbourne, 1953/4 to 1956/7, has been demonstrated. For each of these years, there was a tendency for annual incidences of Down’s syndrome to follow the pattern of infectious hepatitis in being greater in the east than in the west, but differences for the former only reached statistical significance (P <0.01) in the year 1956, the peak year for the inci- dence of both. However, the difference for the overall 4- year period was significant (P <0.01) for both diseases. As a by-product of this study, the inverse correlation be- tween the annual incidence of infectious hepatitis and population density has been confirmed, and it is postu- lated that this relates to poorer sanitation which could be involved in the etiology of Down’s syndrome. 1 STOLLER, A., COLLMANN, R. D. Patterns of occurrence of births in Victoria, Australia, producing Down’s syndrome (mongolism) and congenital anomalies of the central nervous system: A 21-year pro- spective and retrospective survey. Med J Aust 1:1-4, 2 Jan 65. Study of the occurrence of mongolism, hydrocephaly, spina bifida, and anencephaly has produceda predicted pattern of concordant peaking for mongolism and hydro- cephaly, and a continuance of the patterns for the other anomalies. The incidence rates obtained by these surveys are: (1) mongolism, 1.45 per 1,000 live births (State of Victoria, 1942-1957), (2) anencephaly, live and still- births, 0.72 per 1,000 total births (three large Mel- bourne maternity hospitals, 1942-1962), (3) spina bifida, 0.59 (determined as for anencephaly), (4) hydrocephaly, 0.65 (determined as for anencephaly). The evidence for an infective etiology in a high proportion of cases of mongolism and hydrocephaly is presented. Suggestion are given for biological investigation of the hypothesis that mongolism, hydrocephaly, and perhaps other con- genital anomalies are due to interaction between virus and aging ovum at or around the time of conception. 1 table. 2 figures. references. (AEd)