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oai:open-archive.highwire.org:amjepid:137/6/5892015-05-11HighWireOUPamjepid:137:6
Mother-to-Child Transmission of Human Immunodeficiency Virus Type 1 (HIV-1) and Its Determinants: A Cohort Study in Kigali, Rwanda
Lepage, Philippe
de Perre, Philippe Van
Msellati, Philippe
Hitimana, Déo-Gratias
Simonon, Arlette
Goethem, Christiaan Van
Mukamabano, Barbara
Karita, Etienne
Stevens, Anne-Maria
Mathieu, Guy
Salamon, Roger
Dabis, François
ORIGINAL CONTRIBUTIONS
The authors report the results of the first 2 years of follow–up of a prospective cohort study on the mother–to–child transmission of human immunodeficiency virus type 1 (HIV–1) and its determinants which started in November 1988 in Kigali, Rwanda. The study sample consists of 218 newborns of 215 HIV–1 seropositive women matched to 218 newborns of 216 HIV–1 seronegative women of the same age and parity. They were followed every 2 weeks during the first 2 years of follow–up. HIV–1 antibodies were detected by enzyme–linked immunoadsorbent assay and Western blot at 3–month intervals. Two methods of calculating the mother–to–child transmission rate were used: method 1 combines the information provided by the persistence of HIV–1 antibodies at 15 months of age in children born to HIV seropositive mothers and the excess mortality in this group compared with the cohort of children born to HIV seronegative mothers; method 2 is a case–by–case evaluation of all the children born to HIV seropositive mothers. A logistic regression model was used to study the determinants of transmission. The probability of survival at 24 months of age was 81% (95% confidence interval (Cl) 75–86) in children born to seropositive mothers, compared with 95% (95% Cl 92–98) in children born to seronegative mothers (<it>p</it> < 0.001). The mother–to–child transmission rate calculated with method 1 was 25.7% (95% Cl 18.8–32.5). With method 2, the medium estimate was 24.7%. In the multivariate analysis, a CD4/CD8 ratio <0.5 was the only maternal factor statistically associated with an increased risk of mother–to–child transmission of HIV–1 (odds ratio=2.9, 95% Cl 1.2–7.2). The authors' findings present evidence for a higher mother–to–child transmission rate of HIV–1 in children born in Rwanda than in industrialized countries. <it>Am J Epidemiol</it> 1993;137:589–99.
Oxford University Press
1993-03-15 00:00:00.0
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Copyright (C) 1993, Oxford University Press
oai:open-archive.highwire.org:amjepid:137/6/6002015-05-11HighWireOUPamjepid:137:6
Comparison of Voluntary and Blinded Human Immunodeficiency Virus Type 1 (HIV-1) Seroprevalence Surveys in a High Prevalence Sexually Transmitted Disease Clinic Population
Schwarcz, Sandra K.
Bolan, Gail A.
Kellogg, Tim A.
Kohn, Robert
Lemp, George F.
ORIGINAL CONTRIBUTIONS
To compare the seroprevalence of and risk factors for human immunodeficiency virus infection (HIV) among patients attending a public sexually transmitted disease clinic, the authors conducted both voluntary and blinded seroprevalence surveys between June 1989 and August 1990. For the voluntary survey, every twenty–fifth patient attending the clinic for a new problem was invited to receive anonymous testing for HIV antibody. For the blinded survey, sera obtained for syphilis serologies from 2,297 (86%) of the 2,682 patients attending the clinic for a new problem were tested for HIV antibody after all personal identifiers were removed. Of the 946 eligible patients, 631 (66.7%) agreed to participate in the voluntary survey. Black men were significantly less likely to participate than other men and women (<it>p</it> < 0.0001). The prevalence of HIV antibody was 25% greater in the blinded survey than in the voluntary survey (15.2% and 11.4%, respectively, <it>p</it> < 0.05). This difference was due primarily to black homosexual/bisexual men, who had a 12.7–fold greater risk of HIV infection in the blinded survey than in the voluntary survey. These results suggest that blinded seroprevalence surveys may provide a better prevalence estimate of HIV infection than voluntary surveys. The greater risk for HIV infection observed among homosexual and bisexual black men, who were tested only in the blinded serosurvey, suggests that efforts to increase voluntary testing for HIV infection in this group should be developed. <it>Am J Epidemiol</it> 1993;137:600–8
Oxford University Press
1993-03-15 00:00:00.0
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oai:open-archive.highwire.org:amjepid:137/6/6092015-05-11HighWireOUPamjepid:137:6
Leukemia in Telephone Linemen
Matanoski, Genevieve M.
Elliott, Elizabeth A.
Breysse, Patrick N.
Lynberg, Michele C.
ORIGINAL CONTRIBUTIONS
This case–control study examines potential associations between telephone linework and the occurrence of leukemia except chronic lymphocytic leukemia in a primarily retired population of American Telephone and Telegraph Company (AT&T) workers. Cases died between 1975 and 1980. Exposure is defined both by job title and, for workers with complete job histories, by a lifetime exposure score based on industrial hygiene personal monitoring measurements of line and nonline jobs. When the time–weighted average mean for each job is accumulated into a lifetime exposure score, workers with scores above the median for the population show an excess of leukemia 2.5 times higher than workers below the median (95% confidence interval (Cl) 0.7–8.6). Those individuals with long duration of employment in jobs with intermittent peak exposures may be at higher risk of leukemia than those with a constant exposure level. Analyses that allow for a latent period suggest the risk is associated with exposures that occurred 10 or more years before death. Workers with peak exposure scores above the median have odds ratios of 2.4 (95% Cl 0.7–9.0) and 6.6 (95% Cl 0.7–58) for latent periods of 10 and 15 years, respectively. The data suggest an increasing risk with increasing exposure (p for trend=0.05) when cumulated scores are based on peak exposure scores. Peak exposures tended to occur in cable splicing work and in old telephone switching offices. The numbers in this study are small and observed differences may be due to chance. <it>Am J Epidemiol</it> 1993;137:609–19.
Oxford University Press
1993-03-15 00:00:00.0
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oai:open-archive.highwire.org:amjepid:137/6/6202015-05-11HighWireOUPamjepid:137:6
Parental Smoking and Risk of Childhood Brain Tumors
Gold, Ellen B.
Leviton, Alan
Lopez, Ricardo
Gilles, Floyd H.
Hedley-Whyte, Tessa
Kolonel, Laurence N.
Lyon, Joseph L.
Swanson, G. Marie
Weiss, Noel S.
West, Dee
Aschenbrener, Carol
Austin, Donald F.
ORIGINAL CONTRIBUTIONS
Data from a large, population–based, case–control study were analyzed to assess the role of parental smoking in childhood brain tumors. Parents of 361 cases, newly diagnosed between January 1, 1977 and December 31, 1981 and ascertained from eight Surveillance, Epidemiology, and End Results (SEER) program registries, and 1,083 controls had been interviewed. No significant differences in risks were found to be associated with maternal or paternal smoking at any time (odds ratio (OR)=0.92 for mothers and 1.06 for fathers), during the year of birth of the child (which included both the prenatal and postnatal periods) (ORs = 0.84 for <1 pack/day and 1.0 for ≥1 pack/day for mothers, and 0.68 for<1 pack/day and 1.07 for >1 pack/day for fathers), or 2 years before the child was born, i.e., the pre–conception period (ORs=0.75 for <1 pack/day and 1.01 for>1 pack/day for mothers, and 0.90 for <1 pack/day and 1.15 for>1 pack/day for fathers). Mothers were also specifically asked if they smoked during the pregnancy, and no association was found compared with never smokers (OR=1.08,95% confidence interval (Cl) 0.80–1.45) or for ever-smokers who continued to smoke during pregnancy compared with those who stopped smoking during pregnancy (OR=1.15, 95% Cl 0.75–1.78). Finally, no significant increase in risk of brain tumors was found for the child's passive exposure to parental smoking during the period from birth to diagnosis of the brain tumor in the case. The lack of an effect of parental smoking was observed for both the major histologic types and locations of brain tumors. These findings and those from earlier studies provide no support for the hypothesis that parental cigarette smoking influences the risk of brain tumors in children. <it>Am J Epidemiol</it> 1993;137:620–8.
Oxford University Press
1993-03-15 00:00:00.0
TEXT
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oai:open-archive.highwire.org:amjepid:137/6/6292015-05-11HighWireOUPamjepid:137:6
Risk of Childhood Cancer for Infants with Birth Defects: I. A Record-Linkage Study, Atlanta, Georgia, 1968-1988
Mili, Fatima
Khoury, Muin J.
Flanders, W. Dana
Greenberg, Raymond S.
ORIGINAL CONTRIBUTIONS
To evaluate the risk of childhood cancer among infants with serious birth defects, the authors linked records of the population–based registry of the Georgia Center for Cancer Statistics for 1975 to 1988 with records of the population–based Metropolitan Atlanta Congenital Defects Program for 1968 to 1987. During the study period, birth defects were diagnosed in 19,373 infants younger than 1 year of age, and cancer was diagnosed in 400 children younger than 15 years of age. The observed number of children with a defect who developed cancer was compared with the number expected on the basis of the cancer registry rates. Of the 19,373 children with birth defects, 31 developed cancer (standardized incidence ratio (SIR)=2.2, 95% confidence interval (Cl) 1.5–3.2). Two associations were found: of 532 children with Down's syndrome (trisomy 21), three developed acute leukemia (SIR=50.8, 95% Cl 10.5–148.5) while of 746 children with pyloric stenosis, four developed cancer (SIR=7.5, 95% Cl 2.0–19.3). These data show that children with selected birth defects are at increased risk for specific childhood cancers. Such record-linkage can reveal new associations, which can in turn help researchers understand underlying mechanisms common to teratogenesis and carcinogenesis. <it>Am J Epidemiol</it> 1993;137:629–38.
Oxford University Press
1993-03-15 00:00:00.0
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oai:open-archive.highwire.org:amjepid:137/6/6392015-05-11HighWireOUPamjepid:137:6
Risk of Childhood Cancer for Infants with Birth Defects: II. A Record-Linkage Study, Iowa, 1983-1989
Mili, Fatima
Lynch, Charles F.
Khoury, Muin J.
Flanders, W. Data
Edmonds, Larry D.
ORIGINAL CONTRIBUTIONS
To attempt to confirm associations found in a companion study in Atlanta, Georgia between Down's syndrome and acute leukemia and between pyloric stenosis and childhood cancer, the authors used the State Health Registry of Iowa to link the records of infants and children with cancer for 1983 to 1989 with the records of infants with birth defects for 1983 to 1988. During the study period, birth defects were diagnosed in 10,891 infants younger than 1 year of age, and cancer was diagnosed in 396 children younger than 8 years of age. The authors compared the observed number of children with a defect who developed cancer with the number expected on the basis of the cancer registry rates. Of the 10,891 children with birth defects, 16 developed cancer (standardized incidence ratio (SIR)=2.0, 95% confidence interval (Cl) 1.2–3.3). Of 251 children with Down's syndrome (trisomy 21), two developed leukemia (SIR=32.1,95% Cl 3.9–116.0). None of the infants with cancer had pyloric stenosis (SIR=0.0, 95% Cl 0.0–6.7). The results of this study supported the association found in the Atlanta study between Down's syndrome and leukemia, but did not support the association found there between pyloric stenosis and childhood cancer. This study, however, had a shorter follow–up period and a smaller number of subjects than the Atlanta study. <it>Am J Epidemiol</it> 1993;137:639–44.
Oxford University Press
1993-03-15 00:00:00.0
TEXT
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oai:open-archive.highwire.org:amjepid:137/6/6452015-05-11HighWireOUPamjepid:137:6
Blood Pressure and Industrial Lead Exposure
Maheswaran, Ravi
Gill, Jaswinder Singh
Beevers, D. Gareth
ORIGINAL CONTRIBUTIONS
The association between environmental lead exposure and raised blood pressure remains controversial. This association was examined in a cross-sectional study in 1981 on 809 male workers who were occupationally exposed to lead in a factory manufacturing car lead accumulator batteries in Birmingham, United Kingdom. Lead exposure was assessed by blood lead levels, blood zinc protoporphyrin levels, and years of industrial exposure to lead. The geometric mean blood lead level was 31.6 μg/dl with minimum and maximum values of 0 μg/dl and 98 μg/dl, respectively. Unadjusted systolic blood pressure rose with increasing blood lead levels (analysis of variance, <it>F</it>=3.3, <it>p</it> <0.05) from 127 mmHg (95% confidence interval (Cl) 123.5–130.5) in men with blood lead levels less than 21 μg/dl to 133 mmHg (95% Cl 128.7–137.3) in men with levels exceeding 50 μg/dl. Following adjustment for the confounding effects of age, body mass index, and alcohol consumption, however, the effect of blood lead on systolic pressure was diminished (analysis of variance, <it>F</it>=1.3, not significant) to 129 mmHg and 132 mmHg in the respective categories. There was no association between diastolic blood pressure and blood lead. Zinc protoporphyrin levels and years of industrial lead exposure did not raise adjusted systolic or diastolic pressure. In conclusion, subject to the limitations inherent in a cross-sectional survey, the findings are consistent with a weak effect of industrial lead exposure on systolic blood pressure, within the range of exposures observed in this study. <it>Am J Epidemiol</it> 1993;137:645–53.
Oxford University Press
1993-03-15 00:00:00.0
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oai:open-archive.highwire.org:amjepid:137/6/6542015-05-11HighWireOUPamjepid:137:6
A Comparison of Prospective and Retrospective Responses on Sudden Infant Death Syndrome by Case and Control Mothers
Gibbons, Laura E.
Ponsonby, Anne-Louise
Dwyer, Terence
ORIGINAL CONTRIBUTIONS
Based on information from two studies of sudden infant death syndrome (SIDS) from 1988–1991 in Tasmania, Australia, prospective and retrospective maternal responses to an identical set of questions were compared for 27 cases and 25 controls. There was good agreement on demographic factors, maternal obstetric history, parental smoking, and infant feeding practices. Reported changes in sleep habits were slightly greater for cases, and further work is needed to determine if this reflects recall bias or real changes during early infant life. Case mother reports regarding family history of disease and infant bedding were more discrepant, suggesting recall bias and supporting prospective collection of this information. <it>Am J Epidemiol</it> 1993;137:654–9.
Oxford University Press
1993-03-15 00:00:00.0
TEXT
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Copyright (C) 1993, Oxford University Press
oai:open-archive.highwire.org:amjepid:137/6/6602015-05-11HighWireOUPamjepid:137:6
Representative and Misrepresentative Associations of Birth Defects in Livebirths: Conditions under which Relative Risks Greater than Unity in Livebirths Necessarily Imply Relative Risks Greater than Unity in All Conceptuses
Hook, Ernest B.
Regal, Ronald R.
ORIGINAL CONTRIBUTIONS
One may express the relative risk of defect in all conceptuses, <it>r</it><inf>def</inf>, as a function of the relative risk of defect in livebirths, <it>r</it><inf>def,lb,</inf> and in embryonic and fetal deaths, <it>r</it><inf>def,efd,</inf> as <it>r</it><inf>def</inf>=C<inf>lb</inf><it>r</it><inf>def.lb</inf>+<it>C</it><inf>efd</inf><it>r</it><inf>def.efd,</inf> where <it>C</it><inf>lb</inf> and <it>C</it><inf>efd</inf> are coefficients defined in terms of conceptus and defect viability and lethality. If the relative risk of birth defect in livebirths, <it>r</it><inf>def,lb,</inf> is greater than unity, but the relative risk of defect in all conceptuses, <it>r</it><inf>def,</inf> is equal to or less than unity (or the reverse pattern holds), then the relative risk of defects in livebirths may be said to be “distorting” or “misrepresentative” because it does not reflect the nature of the association in all conceptuses. The authors define and present an explicit expression for a boundary upon the relative risk of defect in livebirths. If the relative risk of defect in livebirths is (validly) greater than this boundary value, then the relative risk in all conceptuses must be greater than unity and the observed relative risk of defect in births is “representative” and not distorting. The authors show that the boundary value is equal to 1/<it>C</it><inf>lb,</inf> where <it>C</it><inf>lb</inf> is a simple function of the lethality of all unexposed conceptuses, the lethality of unexposed conceptuses with defect, and the relative risk of any embryonic and fetal death. Tables of the boundary relative risk for various values of these variables are presented. Over a very wide range of reference variables, a (valid) relative risk of defect in livebirths of 3.5 or greater implies a positive association with defect in all (recognized) conceptuses in the population studied. <it>Am J Epidemiol</it> 1993;137:660–75.
Oxford University Press
1993-03-15 00:00:00.0
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oai:open-archive.highwire.org:amjepid:137/6/6762015-05-11HighWireOUPamjepid:137:6
Sample Size and Power Determination for a Binary Outcome and an Ordinal Exposure when Logistic Regression Analysis Is Planned
Bull, S. B.
ORIGINAL CONTRIBUTIONS
General methods of sample size determination for logistic regression analyses are now available, but these will often require substantial information for their application. The author presents methods useful in the special case of a binary outcome and a three–level quantitative exposure, which includes application to a three–level ordinal exposure for a specified scaling. The computationally simple methods were developed in planning an investigation of the prognostic value of multidrug resistance gene (<it>mdr1</it>) expression in sarcoma. Because logistic regression was planned for the analysis, calculations were based on the ability to detect a linear trend in the log odds of tumor response to chemotherapy associated with increases in the level of <it>mdr1</it> expression from negative to low positive to high positive. Closed form expressions were used to assess sensitivity to the ordinal scaling and the distribution of the <it>mdr1</it> levels, and to the assumption of a linear trend in the log odds versus a linear trend in the proportions. <it>Am J Epidemiol</it> 1993;137:676–84.
Oxford University Press
1993-03-15 00:00:00.0
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Copyright (C) 1993, Oxford University Press
oai:open-archive.highwire.org:amjepid:137/6/6852015-05-11HighWireOUPamjepid:137:6
BOOK REVIEWS
Noah, Norman D.
BOOK REVIEWS
Oxford University Press
1993-03-15 00:00:00.0
TEXT
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http://aje.oxfordjournals.org/cgi/content/short/137/6/685
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oai:open-archive.highwire.org:amjepid:137/6/6872015-05-11HighWireOUPamjepid:137:6
BOOK REVIEWS
Rona, R. J.
BOOK REVIEWS
Oxford University Press
1993-03-15 00:00:00.0
TEXT
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http://aje.oxfordjournals.org/cgi/content/short/137/6/687
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Copyright (C) 1993, Oxford University Press
oai:open-archive.highwire.org:amjepid:137/6/6882015-05-11HighWireOUPamjepid:137:6
BOOKS RECEIVED
BOOKS RECEIVED
Oxford University Press
1993-03-15 00:00:00.0
TEXT
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http://aje.oxfordjournals.org/cgi/content/short/137/6/688
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Copyright (C) 1993, Oxford University Press