HICNet Medical News Digest Tue, 11 Apr 1995 Volume 08 : Issue 14 Today's Topics: [MMWR Apr 7] National Alcohol Awareness Month - April 1995 [MMWR] Trends in Fetal Alcohol Syndrome [MMWR] Birth Cert. as a source of information [MMWR] Use of Internation Class. of Diseases... [MMWR] Sociodemographic and Behavioral Characteristics... [MMWR] Licensure of Varicella Vaccine, Live [MMWR] NIOSH Alert: Request for Assistance... [MMWR] Monthly Immunization Report CancerNet Update for April 1995 How Cells Recognize Onslaught of Toxic Chemicals Chimpanzee Vaccine Model Protects Against HIV-1 Infection +------------------------------------------------+ ! ! ! Health Info-Com Network ! ! Medical Newsletter ! +------------------------------------------------+ Editor: David Dodell, D.M.D. 10250 North 92nd Street, Suite 210, Scottsdale, Arizona 85258-4599 USA Telephone +1 (602) 860-1121 FAX +1 (602) 451-1165 Internet: mednews@stat.com Bitnet: ATW1H@ASUACAD Mosaic WWW *Asia/Pacific: http://biomed.nus.sg/MEDNEWS/welcome.html *Americas: http://cancer.med.upenn.edu:3000/ *Europe: http://www.dmu.ac.uk/ln/MEDNEWS/ Compilation Copyright 1995 by David Dodell, D.M.D. All rights Reserved. License is hereby granted to republish on electronic media for which no fees are charged, so long as the text of this copyright notice and license are attached intact to any and all republished portion or portions. The Health Info-Com Network Newsletter is distributed biweekly. Articles on a medical nature are welcomed. If you have an article, please contact the editor for information on how to submit it. If you are interested in joining the automated distribution system, please contact the editor. Associate Editors: E. Loren Buhle, Jr. Ph.D. Dept. of Radiation Oncology, Univ of Pennsylvania Tom Whalen, M.D., Robert Wood Johnson Medical School at Camden Douglas B. Hanson, Ph.D., Forsyth Dental Center, Boston, MA Lawrence Lee Miller, B.S. Biological Sciences, UCI Dr K C Lun, National University Hospital, Singapore W. Scott Erdley, MS, RN, SUNY@UB School of Nursing Jack E. Cross, B.S Health Care Admin, 882 Medical Trng Grp, USAF Albert Shar, Ph.D. CIO, Associate Prof, Univ of Penn School of Medicine Stephen Cristol, M.D. MPH, Dept of Ophthalmology, Emory Univ, Atlanta, GA Subscription Requests = mednews@stat.com anonymous ftp = vm1.nodak.edu; directory HICNEWS FAX Delivery = Contact Editor for information ---------------------------------------------------------------------- To: hicnews National Alcohol Awareness Month -- April 1995 April is National Alcohol Awareness Month. Maternal alcohol consumption during pregnancy is one of the most common preventable causes of birth defects and childhood disabilities. Varying levels of fetal alcohol exposure result in a spectrum of alcohol-related disabling conditions, including fetal alcohol syndrome (FAS) (with its characteristic physical features) and cognitive and behavioral problems. National health objectives for the year 2000 include reducing the incidence of FAS to no more than 0.12 cases per 1000 live births (i.e., 1.2 cases per 10,000 live births) and increasing abstinence from alcohol drinking by pregnant women by 20% (objectives 14.4 and 14.10) (1). Although adverse health effects associated with fetal exposure to alcohol are preventable, effective intervention strategies are still being developed. An important step toward developing these strategies is improving the understanding of the occurrence and epidemiology of FAS, including determination of population subgroups at increased risk for this condition. This issue of MMWR includes four articles related to maternal alcohol consumption during pregnancy and its effects on exposed offspring. Reference 1. Public Health Service. Healthy people 2000: national health promotion and disease prevention objectives--full report, with commentary. Washington, DC: US Department of Health and Human Services, Public Health Service, 1991; DHHS publication no. (PHS)91-50212. ------------------------------ To: hicnews Update: Trends in Fetal Alcohol Syndrome -- United States, 1979-1993 Fetal alcohol syndrome (FAS) is characterized by a variety of physical and behavioral traits that result from maternal alcohol consumption during pregnancy. Features of FAS include prenatal or postnatal growth deficiency, characteristic abnormal facial features, and central nervous system deficits (1). Based on data from the national Birth Defects Monitoring Program (BDMP) (2), the rate of reported cases of FAS identified among newborns in the United States during 1979- 1992 increased approximately fourfold (2). This report updates data characterizing the occurrence of FAS through 1993, the latest complete year of data reporting for BDMP. BDMP data are abstracted from hospital discharge data of newborns provided voluntarily by nonfederal, short-term stay hospitals. FAS cases were identified based on coded hospital discharge diagnoses (International Classification of Diseases, Ninth Revision, Clinical Modification [ICD-9- CM], code 760.71, "Noxious influences affecting fetus via placenta or breast milk, specifically alcohol; includes fetal alcohol syndrome"). However, this code is not specific for FAS and may reflect maternal alcohol consumption during pregnancy or other adverse effects of alcohol on the fetus. During 1993, the BDMP monitored data on approximately 5% of all births, compared with approximately 30% in 1979. In 1993, FAS was reported in 126 of 188,905 newborns (rate: 6.7 per 10,000) (Figure 1). Overall, during 1979-1993, FAS was reported in 2032 of 9,434,560 newborns (overall rate: 2.2 per 10,000 births). The rate for 1993 was more than sixfold higher than that for 1979 (1.0 per 10,000 births). Reported by: Birth Defects and Genetic Diseases Br, Div of Birth Defects and Developmental Disabilities, National Center for Environmental Health, CDC. Editorial Note: Although the cause of FAS--alcohol consumption during pregnancy-- is preventable, the findings in this report suggest an increasing frequency of this problem. This increase may reflect a true increase in the number of infants with FAS--the most severe expression of in utero alcohol damage to the fetus--or an increase in the awareness and diagnosis by primary-care clinicians of FAS in newborns. Although ICD-9-CM code 760.71 is not specific for FAS, it has been used in this analysis because it may reflect a maternal history of alcohol consumption during pregnancy; the diagnosis or suspicion of FAS or its less severe manifestation (fetal alcohol effect); or other alcohol-related birth abnormalities. After the newborn period, this code also may be assigned to children for whom diminished cognitive function or behavioral problems are believed to be associated with maternal alcohol consumption during pregnancy-- particularly in older children in whom developmental and neurobehavioral abnormalities are more readily diagnosed. Studies are under way to better characterize the magnitude of FAS, particularly among population subgroups at increased risk for alcohol consumption during pregnancy and for having an infant with FAS. These studies may enable public health officials to more effectively target FAS prevention and alcohol consumption intervention efforts. References 1. Sokol RJ, Clarren SK. Guidelines for use of terminology describing the impact of prenatal alcohol on the offspring. Alcohol Clin Exp Res 1989;13:597- 8. 2. CDC. Fetal alcohol syndrome--United States, 1979-1992. MMWR 1993;42:339-41. ------------------------------ To: hicnews Birth Certificates as a Source for Fetal Alcohol Syndrome Case Ascertainment -- Georgia, 1989-1992 Fetal alcohol syndrome (FAS) is a major cause of preventable mental retardation (1). The development and evaluation of programs for preventing FAS may be enhanced by timely and reliable estimates of the occurrence of this complex birth defect. In 1989, birth certificates were standardized nationally to include check-boxes for reporting FAS and other congenital abnormalities (2). These changes were implemented to improve the potential usefulness of birth certificates for timely and systematic population-based ascertainment of FAS and other abnormal conditions of the newborn (3). To assess the usefulness of birth certificates for surveillance of FAS, the Division of Public Health, Georgia Department of Human Resources (DPH-GDHR), compared information about congenital anomalies from birth certificates to data collected by CDC's Metropolitan Atlanta Congenital Defects Program (MACDP) during 1989- 1992. This report summarizes the results of the assessment of FAS. MACDP is a population-based birth defects registry that identifies children with birth defects diagnosed during the neonatal and infant periods (4). MACDP uses multiple sources (including birth certificates) for identifying birth defect cases and reviews medical and laboratory records of identified cases for verifying case status. Since 1968, MACDP has collected data on approximately 26,000 infants with major congenital anomalies from among nearly 775,000 live-born infants in the five-county area of metropolitan Atlanta. For this study, MACDP was considered the standard for FAS case identification because of its multiple-source case ascertainment, including maternal and infant medical record review within the hospital of birth during the newborn period. Birth certificates were compared with the MACDP registry for sensitivity and predictive value positive (PVP). Potential cases identified by birth certificates were considered true positives if they were registered as FAS in the MACDP registry; potential cases were considered false positives if FAS was noted on the birth certificates but not in the MACDP. Each false-positive case then underwent medical record review to determine whether it had been missed by MACDP. To determine whether personnel completing birth certificates could have used medical record review to determine an infant's FAS status, the date of diagnosis reported in the MACDP file was compared with the date of birth. If the diagnosis was recorded within 2 days of birth, it was assumed that this information was available to the person completing the birth certificate for inclusion on the birth certificate. For infants included in MACDP with FAS, 86% had FAS diagnosed on the date of birth and 94% within 2 days of birth. From 1989 through 1992, MACDP identified 35 FAS cases (overall rate: 2.3 per 10,000 births). FAS was noted on the birth certificates of 14 infants. Four of the 14 were true positives, and the other 10 were false positives. The sensitivity of the birth certificates was 11% (four of 35); the PVP was 29% (four of 14). False positives accounted for 71% of cases reported through birth certificates. Birth certificates recorded any maternal alcohol consumption during pregnancy for only five of the 10 false positives, while medical record review of the false positives indicated a specific maternal history of alcohol consumption for only three. Reported by: MP Mathis, PhD, Office of Perinatal Epidemiology, Epidemiology and Prevention Br; M Lavoie, MA, Center for Health Information; C Hadley, MN, Family Health Br; K Toomey, MD, State Epidemiologist, Div of Public Health, Georgia Dept of Human Resources. Birth Defects and Genetic Diseases Br, and Fetal Alcohol Syndrome Prevention Section, Developmental Disabilities Br, Div of Birth Defects and Developmental Disabilities, National Center for Environmental Health, CDC. Editorial Note: The findings in this report indicate that birth certificates alone are a poor source for FAS case surveillance. In Georgia, birth certificates underreported FAS cases as well as incorrectly identified FAS cases. These findings underscore the need for improving the quality of diagnostic information for FAS on birth certificates. For 86% of MACDP-enrolled FAS cases, the information used to verify FAS status was recorded on the day of birth, suggesting that correct information about FAS status could be obtained and recorded on birth certificates if personnel completing the vital record routinely reviewed diagnoses contained in birth charts. The high rate (71%) of false positives reported on birth certificates in this report represents an over-reporting of FAS without indication of physical findings from medical records to substantiate the report. Maternal history of alcohol consumption during pregnancy may be considered sufficient evidence by some health professionals for a diagnosis of FAS on the birth certificate. However, FAS is a complex birth syndrome with specific physical and developmental findings; maternal alcohol consumption during pregnancy is essential but not sufficient for a diagnosis of FAS. In the United States, birth defects are the leading cause of infant mortality (5), emphasizing the necessity of accurate information on birth defects for public health assessment. To improve the usefulness of birth certificates for birth defects surveillance and other public health needs, however, the quality of birth certificate data will need to be improved. The data for more accurate diagnosis and reporting of FAS and other abnormal conditions of the newborn often are available from the medical record, and consultation of these records before completion of the birth certificate may improve the quality and utility of birth certificate data. Pediatricians should be enlisted to provide information about the conditions of the newborn while obstetricians continue to provide information about conditions of the mother (6). In addition, birthing hospitals should consider developing more specific protocols for completing birth certificates and instituting a formal process for evaluating the accuracy of reporting birth certificate information. References 1. Abel EL, Sokol RJ. Incidence of fetal alcohol syndrome and economic impact of FAS-related anomalies. Drug Alcohol Depend 1987;19:51-70. 2. Freedman MA, Gay GA, Brockert JE, et al. The 1989 revisions of the US Standard Certificates of Live Birth and Death and the US Standard Report of Fetal Death. Am J Public Health 1988;78:168-72. 3. Taffel SM, Ventura SJ, Gay GA. Revised U.S. Certificate of Birth: new opportunities for research on birth outcome. Birth 1989;16:188-93. 4. Lynberg MC, Edmonds LD. Surveillance of birth defects. In: Halperin W, Baker EL, Monson RR, eds. Public Health Surveillance. New York: Van Norstand Reinhold, 1992. 5. CDC. Contribution of birth defects to infant mortality--United States, 1986. MMWR 1989;38:633-5. 6. Hexter AC, Harris JA. Bias in congenital malformations information from the birth certificate. Teratology 1991;44:177-80. ------------------------------ To: hicnews Use of International Classification of Diseases Coding to Identify Fetal Alcohol Syndrome -- Indian Health Service Facilities, 1981-1992 Fetal alcohol syndrome (FAS) is one of the leading causes of preventable birth defects and developmental disabilities in the United States (1). Since 1979, surveillance systems for estimating and tracking FAS have categorized cases using International Classification of Diseases, Ninth Revision, Clinical Modification (ICD-9-CM), code 760.71 (2). This code comprises noxious influences affecting the fetus or newborn through placenta or breast milk, specifically alcohol, and includes FAS. Because the code is not specific for FAS and may reflect maternal alcohol consumption during pregnancy or other adverse effects of alcohol on the fetus, CDC assessed the usefulness of this code in ascertaining FAS cases by reviewing medical records for 1981- 1993 from the Aberdeen Area* Indian Health Service (IHS) and IHS contract facilities in eight of the 19 tribal or American Indian communities in the area. This report summarizes the findings of the analysis. During June-July 1993, IHS medical records with the diagnostic code 760.71 were abstracted. Data were collected from records of persons who were inpatients during 1981-1991 and from the records of outpatients during August 1, 1989-July 12, 1993. A case of FAS was defined as documentation of the following five criteria in a person's medical records: 1) prenatal alcohol exposure or maternal history of alcohol consumption, 2) FAS diagnosed or noted as a suspected diagnosis by a physician, 3) one or more facial features characteristic of FAS, 4) growth deficiency (i.e., prenatal or postnatal height or weight less than or equal to 10th percentile for age), and 5) central nervous system (CNS) impairment (3). Maternal medical records were not reviewed in this study. During 1981-1992, a total of 19,000 infants were born in the Aberdeen area. During 1981-1992, medical records of 251 persons had the diagnostic code 760.71; 60 (24%) persons met all five criteria for FAS (Table 1). Of the 60 persons with FAS, the mean age was 8 years (range: birth-31 years); 58% were male. Of the 60 case-patients, 52 (87%) were born during 1981-1992; based on the 19,000 deliveries during 1981-1992, the rate of FAS was 2.7 per 1000 live births during this period. The most common facial features documented in the medical records of the 60 case-patients were long and flat philtrum (60%); low nasal bridge (52%), short palpebral fissures (42%); thin upper lip (30%); and midface hypoplasia (28%). The most common CNS impairments were microcephaly (45%), developmental delay (45%), speech or language delay (40%), delayed gross motor development (32%), hyperactivity (30%), seizures (25%), delayed fine motor development úÿ úÿ(Continued from last message) (23%), and attention deficit disorder (20%). Of the 57 cases for which data were available, low birthweight ( less than 2500 g [ less than 5 lbs, 8 oz]) was documented in 21 (37%). Of the 47 cases for which data were available, 16 (34%) were small for gestational age (i.e., birthweight less than or equal to 10th percentile for gestational age). For 41 (68%) of the 60 cases, postnatal growth deficiency had been documented in the medical records. Based on the review of records, dysmorphologists had independently examined 18 (30%) of the 60 case-patients and diagnosed FAS in 14 of these persons. Of the 191 persons whose medical records included the diagnostic code 760.71 but who did not meet all five criteria of the study case definition, one or more of the clinical signs of FAS were present in 168 (88%). A dysmorphologist had diagnosed FAS in 15 of these persons. For 23 persons whose medical records included the diagnostic code 760.71, none of the typical physical findings associated with in utero exposure to alcohol were documented in their records. Reported by: T Welty, MD, LR Canfield, K Selva, Aberdeen Area Indian Health Svc, Rapid City, South Dakota. Fetal Alcohol Syndrome Prevention Section, Developmental Disabilities Br, Div of Birth Defects and Developmental Disabilities, National Center for Environmental Health, CDC. Editorial Note: The rate of FAS for American Indians is higher than for other racial/ethnic groups in the United States (4). The estimated rate of FAS for American Indians in the Aberdeen area during 1981-1992 (2.7 per 1000 live births) was similar to the rate reported for Alaskan Natives during 1978- 1991 (2.1) (3). Population-based screening studies during 1980-1982 documented rates of FAS for American Indians as 1.4 per 1000 live births for Navajo, 2.0 for Pueblo, and 9.8 for American Indians of the Southwest plains (5). The rate of FAS in the IHS study was substantially lower than that estimated by a prospective follow-up study of American Indian children in whom FAS was diagnosed by dysmorphologists (8.5) (6). The variability in rates in these studies may reflect the use of different diagnostic criteria or case- finding methodologies or real differences in rates for the population subgroups. The findings in this report indicate that only a small proportion of medical records in the IHS study coded 760.71 represented cases that met the rigorous case definition for FAS. However, the code can be useful in assessing the rate of adverse effects of maternal alcohol consumption during pregnancy. In this study, 76% of the persons with medical records coded 760.71 did not meet the diagnostic criteria for FAS; however, most (79%) had substantial developmental and behavioral problems that could be related to maternal alcohol consumption during pregnancy. The findings that high proportions of these persons had growth deficiencies, CNS impairment, or documented maternal alcohol consumption during pregnancy suggest that the ICD-9-CM code 760.71 may be a marker for problems in children associated with in utero exposure to alcohol. The finding that maternal alcohol consumption was not documented in the medical records of 30% of patients may reflect failure to record this information or failure to ask the mother about alcohol consumption during pregnancy. Because surveillance systems using ICD-9-CM code 760.71 lack specificity for monitoring FAS, calculation of accurate population estimates of FAS is complex and difficult. However, use of these surveillance systems should be continued because of the importance of measuring the overall adverse effects of in utero exposure to alcohol. Approaches to enhance surveillance for adverse effects of maternal alcohol consumption on the fetus should be expanded to include multiple data sources, such as hospital discharge data from the newborn period (similar to data used by CDC's Birth Defects Monitoring Program) and insurance claims data for clinic visits. Use of Medicaid and other insurance claims may be an inexpensive method of monitoring FAS and other outcomes related to maternal alcohol consumption during pregnancy in the general population and in patients with documented in utero exposure to alcohol. Accurate surveillance data will help target screening and prevention efforts to those women whose children are at greatest risk for adverse sequelae from in utero alcohol exposure. References 1. Streissguth AP. A long-term perspective of FAS. Alcohol Health Res World 1994;18:74-81. 2. Cordero JF, Floyd RL, Martin ML, Davis M, Hymbaugh K. Tracking the prevalence of FAS. Alcohol Health Res World 1994;18:82-5. 3. CDC. Linking multiple data sources in fetal alcohol syndrome surveillance-- Alaska. MMWR 1994;42:312-4. 4. Chavez GF, Cordero JF, Becerra JE. Leading major congenital malformations among minority groups in the United States, 1981-1986. In: CDC surveillance summaries (July). MMWR 1988;37(no. SS-3):17-24. 5. May AM, Hymbaugh DJ, Aase JM, Samet JM. Epidemiology of fetal alcohol syndrome among American Indians of the Southwest. Soc Biol 1983;30:374- 87. 6. Duimstra C, Johnson D, Kutsch C, et al. Alcohol syndrome surveillance pilot project in American Indian communities in the northern plains. Public Health Rep 1993;108:225-9. * Iowa, Nebraska, North Dakota, and South Dakota (1990 total American Indian population: 84,280). ------------------------------ To: hicnews Sociodemographic and Behavioral Characteristics Associated with Alcohol Consumption During Pregnancy -- United States, 1988 Identification of women at risk for consuming alcohol during pregnancy is critical to the design of interventions for reducing the adverse effects of alcohol on both women and their children. This report uses data from the 1988 National Maternal and Infant Health Survey (NMIHS)--the most recent vital records survey for which a population-based sample of this size was available--conducted by CDC's National Center for Health Statistics to analyze characteristics of women who drink alcohol during pregnancy. The NMIHS was a mail survey of a stratified systematic sample of 13,417 women who had a live-born infant during 1988 (1); data from the survey became available in 1991. A total of 9953 (74%) responded. Maternal characteristics analyzed included age, race/ethnicity, education, household income, marital status, parity, smoking status, prenatal care, and alcohol drinking patterns during the 3 months before respondents learned of their pregnancy and during their pregnancy (i.e., prenatal drinkers)*. Data were further analyzed for women who reported having had six or more drinks per week during their pregnancy (i.e., frequent drinkers). The sample data were weighted to reflect general population estimates, and standard errors were calculated using SUDAAN (2). Overall, 45.4% of the respondents reported drinking alcohol during the 3 months before they learned of their pregnancy, 20.7% reported drinking alcohol after they learned of their pregnancy, 16.8% reported drinking three or fewer drinks per month during pregnancy, and 0.6% reported having had six or more drinks per week during pregnancy. The likelihood of any reported prenatal drinking increased directly with age through age group 30-34 years (Table 1). The race/ethnicity-specific proportion of prenatal drinkers was highest among white, non-Hispanic women (25.4% [95% confidence interval (CI)=23.9%-27.0%]). The likelihood of prenatal drinking was higher among women with greater than or equal to 16 years of education (30.8% [95% CI=28.3%-33.2%]) than among women in other educational groups and higher among women with annual household incomes of greater than or equal to $40,000 (29.1% [95% CI=26.5%-31.7%]) compared with women in other income groups. Prenatal drinking was reported by 38.2% (95% CI=33.5%- 42.9%) of women who smoked greater than 10 cigarettes a day and by 17.2% (95% CI=16.0%-18.4%) of women who were nonsmokers. Frequent prenatal drinking was more prevalent among women aged greater than or equal to 35 years (1.4% [95% CI=0.2%-2.5%]) than among younger women (Table 1). The race/ethnicity-specific proportion of frequent drinkers was higher among all racial/ethnic groups other than white. The likelihood of frequent drinking was higher among women with annual household incomes less than or equal to $10,000 (1.3% [95% CI=0.7%-1.9%]). The proportion of frequent drinkers increased as smoking level increased, and was more than three times higher among women receiving no prenatal care than among those who received prenatal care (2.2% [95% CI=0.9%-3.6%] compared with 0.6% [95% CI=0.4%- 0.8%]). Reported by: Fetal Alcohol Syndrome Prevention Section, Developmental Disabilities Br, Div of Birth Defects and Developmental Disabilities, National Center for Environmental Health; Followback Survey Br, Div of Vital Statistics, National Center for Health Statistics, CDC. Editorial Note: An advisory both for women who are pregnant and for those trying to become pregnant not to drink alcohol was issued by the U.S. Surgeon General in 1981 (3) and was reiterated in 1990 by the Secretary of Health and Human Services (4). Although only a small proportion of the population surveyed reported frequent drinking during pregnancy, analyses of risk factors suggest these women have some different sociodemographic characteristics than those of all women who drink during pregnancy; however, the number of frequent drinkers in the survey was small, producing unstable population estimates that require further evaluation. The findings in this report are consistent with selected findings in previous studies (5,6) and can assist in targeting programs for the prevention of maternal alcohol consumption during pregnancy. The findings in this report are subject to at least three limitations. First, alcohol drinking was self-reported and could not be verified. Disclosure of prenatal alcohol consumption may have been underreported because of increasing awareness of the dangers of alcohol consumption during pregnancy (7). Second, NMIHS data do not include a question about "binge" drinking (i.e., consuming five or more drinks on any one occasion), which has been associated with neurodevelopmental deficits (8). Third, drinking patterns may have changed since these data were collected. Analyses of more recent data from CDC's Behavioral Risk Factor Surveillance System may provide information about recent trends in maternal alcohol consumption during pregnancy. The high prevalence of alcohol drinking by women during pregnancy in 1988 (21%) underscores the need to sustain efforts by public health agencies and health-care providers to advise women against drinking if they are trying to become pregnant or are likely to become pregnant. Although in this study frequent alcohol drinkers were a small proportion of all women who consumed alcohol during pregnancy, they are at greater risk than infrequent drinkers for delivering infants with alcohol-related disorders (9,10). Although previous studies documented adverse fetal effects of prenatal alcohol at relatively high thresholds, more recent studies have found adverse physical and neurobehavioral effects at lower exposure levels. Population-based surveys that oversample women with characteristics described in this and other studies may assist in better defining women who drink alcohol frequently during pregnancy because they may account for a disproportionately larger number of children affected by in utero alcohol exposure. References 1. NCHS. National Maternal and Infant Health Survey [Machine-readable public-use data tape]. Hyattsville, Maryland: US Department of Health and Human Services, Public Health Service, CDC, 1988. 2. Shah BV. Software for survey data analysis (SUDAAN) version 5.5 [Software documentation]. Research Triangle Park, North Carolina: Research Triangle Institute, 1991. 3. Office of the U.S. Surgeon General. Surgeon General's advisory on alcohol and pregnancy. FDA Drug Bulletin 1981;11:9-10. 4. US Department of Agriculture/US Department of Health and Human Services. Nutrition and your health: dietary guidelines for Americans. 3rd ed. Washington, DC: US Department of Agriculture/US Department of Health and Human Services, 1990:25-6. 5. Streissguth AP, Grant TM, Barr HM, et al. Cocaine and the use of alcohol and other drugs during pregnancy. Am J Obstet Gynecol 1991;164:1239-43. 6. Serdula M, Williamson D, Kendrick J, Anda RF, Byers T. Trends in alcohol consumption by pregnant women, 1985 through 1988. JAMA 1991;265:876-9. 7. Dufour MC, Williams GD, Campbell KE, Aitken SS. Knowledge of FAS and the risks of heavy drinking during pregnancy, 1985-1990. Alcohol Health Res World 1994:18;86-92. 8. Streissguth AP, Bookstein FL, Sampson PD, Barr HM. Neurobehavioral effects of prenatal alcohol, part III: PLS analyses of neuropsychologic tests. Neurotoxicol Teratol 1989;11:493-507. 9. Day NL, Richardson GA, Geva D, Robles N. Alcohol, marijuana, and tobacco: effects of prenatal exposure on offspring growth and morphology at age six. Alcohol Clin Exp Res 1994;18:786-94. 10. Jacobson JL, Jacobson SW. Prenatal alcohol exposure and neurobehavioral development: where is the threshold? Alcohol Health Res World 1994;18:30- 6. * Women who responded yes to "Did you drink any alcoholic beverages during the 12 months before your delivery?" were asked "How many drinks did you have on average during the 3 months before you found out you were pregnant?" and "How many drinks did you have on average after you found out you were pregnant?" One drink was defined as 12 oz of beer, 4 oz of wine, or 1 1/2 oz of liquor. ------------------------------ To: hicnews Licensure of Varicella Virus Vaccine, Live On March 17, 1995, the Food and Drug Administration licensed Varicella Virus Vaccine, Live (VARIVAX [registered symbol]), manufactured and distributed by Merck and Co., Inc., (Rahway, New Jersey). This vaccine has been licensed for use in persons aged greater than or equal to 12 months. The recommended dose for susceptible children aged 12 months-12 years is one 0.5 mL dose administered subcutaneously. The recommended dosage for susceptible adolescents aged greater than or equal to 13 years and adults is two 0.5 mL doses of vaccine 4-8 weeks apart. The recommendations of the Advisory Committee on Immunization Practices on the use of varicella vaccine will be published. Reported by: Center for Biologics Evaluation and Research, Food and Drug Administration. National Immunization Program, CDC. ------------------------------ To: hicnews NIOSH Alert: Request for Assistance in Preventing Injuries and Deaths of Loggers CDC's National Institute for Occupational Safety and Health (NIOSH) periodically issues alerts on workplace hazards that have caused death, serious injury, or illness to workers. One such alert, Request for Assistance in Preventing Injuries and Deaths of Loggers (1), was recently published and is available to the public.* This alert warns workers in the logging industry that they are at high risk for injury and death if they do not use proper safety procedures and equipment. The National Traumatic Occupational Fatalities Surveillance System indicates that during 1980-1989, approximately 6400 U.S. workers died each year from traumatic injuries in the workplace. During this time, an estimated 1492 of these deaths occurred in the logging industry, where the average annual fatality rate is more than 23 times that for all U.S. workers (164 deaths per 100,000 workers, compared with seven per 100,000). Most of these logging-associated deaths occurred in four occupational groups: logging (e.g., fellers, limbers, buckers, and choker setters), truck drivers, general laborers, and material machine operators. In addition, the Bureau of Labor Statistics reported in 1992 that logging had a workplace injury rate of more than 14,000 injuries per 100,000 full-time workers, compared with 8000 per 100,000 for the total private sector. The alert describes six fatal incidents that involved workers in the logging industry during October 1991-May 1993 and provides recommendations for workers and employers to prevent logging-related deaths and injuries. Reference 1. NIOSH. Request for assistance in preventing injuries and deaths of loggers. Cincinnati: US Department of Health and Human Services, Public Health Service, CDC, 1994; DHHS publication no. (NIOSH)94-101. * Single copies of this document are available without charge from the Publications Office, Division of Standards Development and Technology Transfer, NIOSH, CDC, Mailstop C-13, 4676 Columbia Parkway, Cincinnati, OH 45226- 1998; telephone (800) 356-4674 ([513] 533-8328 for persons outside the United States); fax (513) 533-8573. ------------------------------ To: hicnews 1995 Institute: Frontiers in Laboratory Practice Research CDC is sponsoring the 1995 Institute, "Frontiers in Laboratory Practice Research," in Atlanta, October 1-3. The Institute will include research strategies and methods for addressing major issues in laboratory practice. Abstracts for poster presentations will be accepted until July 28 in the following areas: Personnel, Proficiency Testing, Quality Assurance, Detection of Problems Affecting Patient Outcome, Establishing Analytical Performance Goals, Measuring the Impact of Change on Laboratory Testing, Laboratory-Focused Health Systems Research, and Establishing Medically Relevant Performance Goals for the Laboratory. The registration deadline is September 1. Registration and abstract submission information are available from the Meeting Manager, Division of Laboratory Systems, Public Health Practice Program Office, CDC, Mailstop G-23, 4770 Buford Highway, Atlanta, GA, 30341- 3724; telephone (404) 488-7680. ------------------------------ To: hicnews +----------------------------------------------+ | NATIONAL INSTITUTE | | C A N C E R | | INTERNATIONAL INFORMATION | | C E N T E R | +----------------------------------------------+ | CancerNet@icicb.nci.nih.gov | +-------------------------------+ Changes to CancerNet, April 1995 CancerNet was updated on April 3, 1995. PDQ Statements -------------- The following PDQ statements were added or updated in CancerNet with the April update (see the file Monthly PDQ Changes -- cn-405001 for detailed information on the changes in each statement). New Statements: None Changed Statements: Changed treatment statements for physicians: Adult Acute Lymphocytic Leukemia (cn-101024) Adult Liver Cancer (cn-101195) Adult Non-Hodgkin's Lymphoma (cn-100066) Adult Soft Tissue Sarcoma (cn-100921) Anal Cancer (cn-100022) úÿ úÿ(Continued from last message) Bladder Cancer (cn-101206) Breast Cancer (cn-100013) Carcinoma of Unknown Primary (cn-103331) Childhood Non-Hodgkin's Lymphoma (cn-100915) Childhood Rhabdomyosarcoma (cn-100759) Childhood Soft Tissue Sarcoma (Non-Rhabdomyosarcoma) (cn-103085) Colon Cancer (cn-100008) Cutaneous T-cell Lymphoma (cn-100098) Esophageal Cancer (cn-100089) Gastric Cancer (cn-100025) Intraocular Melanoma (cn-101279) Liver metastases (cn-103856) Malignant pleural effusion (cn-103861) Nasopharyngeal Cancer (cn-101402) Nonsmall Cell Lung Cancer (cn-100039) Oropharyngeal Cancer (cn-101521) Ovarian Epithelial Cancer (cn-100950) Pancreatic Cancer (exocrine) (cn-100046) Plasma Cell Neoplasm (cn-100281) Rectal Cancer (cn-100076) Retinoblastoma (cn-100993) Testicular Cancer (cn-101121) Wilms' Tumor (cn-100719) Changed treatment statements for patients: Adult Acute Lymphocytic Leukemia (cn-201024) Adult Liver Cancer (cn-201195) Adult Non-Hodgkin's Lymphoma (cn-200066) Anal Cancer (cn-200022) Bladder Cancer (cn-201206) Breast Cancer (cn-200013) Childhood Non-Hodgkin's Lymphoma(cn-200915) Intraocular Melanoma (cn-201279) Ovarian Epithelial Cancer (cn-200950) Plasma Cell Neoplasm (cn-200281) Changed supportive care statements: Nutrition (cn-304467) Changed cancer screening and prevention statements: Prevention of Aerodigestive Tract Cancer (head & neck, esophagus, lung) (cn-305233) Prevention of Cervical Cancer (cn-304734) Prevention of Ovarian Cancer (cn-305375) Cancer Screening Overview (cn-303092) Screening for Breast Cancer (cn-304723) Screening for Cervical Cancer (cn-304728) Screening for Colorectal Cancer (cn-304726) Screening for Gastric Cancer (cn-304880) Screening for Oral Cancer (cn-304725) Screening for Ovarian Cancer (cn-305145) Screening for Prostate Cancer (cn-304727) Screening for Skin Cancer (cn-304724) Screening for Testicular Cancer (cn-304729) Changed drug information statements: None. Changed other PDQ information: None. Changed CancerNet News and NCI Publication Information: ------------------------------------------------------- The following news bulletins were added: Retraction of Annotations in NSABP Citations (cn-400078) [This bulletin was added in a Special Update on March 9, 1995.] Women and Cancer (cn-400079) NIH Awarded Broad Gene Therapy Patent (cn-400080) NCI Surgical Oncology Branch Trials (cn-400081) The following news bulletins were changed: NCI High Priority Clinical Trials (cn-400007) FDA's Mammography Quality Standards Act Takes Effect (cn-400075) No news bulletins were deleted. No NCI publications were changed. NCI Fact Sheets --------------- There were no new fact sheets added. The following fact sheets were changed: Fertility Drugs as a Risk Factor for Ovarian Cancer (cn-600036) Environmental Tobacco Smoke (cn-600039) Oral Contraceptives and Cancer Risk (cn-600313) Results of Community Effort to Enhance Cigarette Smokers Quit Rates (cn-600344) Q & A on Community Intervention Trial for Smoking Cessation (COMMIT) (cn-600345) Q & A About Breast Calcifications (cn-600519) Surge in Prostate Cancer Incidence Rates Due to More PSA Testing (cn- 600614) CANCERLIT Citations and Abstracts: ---------------------------------- No new CANCERLIT citation and abstract topics were added. The CANCERLIT citations and abstracts for April will be available on April 10, 1995. Instructions: To request the CancerNet Instructions and Contents List, send a mail message, and in the body of the message, enter HELP. Address the mail message to: cancernet@icicb.nci.nih.gov To request the modified statements, follow the above directions, and in the body of the mail message, enter the statement code. When requesting more than one statement, enter each code on a separate line. CancerNet statements are also available in Spanish. To request the Instructions and Contents List in Spanish, enter SPANISH in the body of the mail message. If you would like to request the statements in Spanish, substitute the prefix "cs-" in front of the number (e.g., cs-100022) to receive the statement on anal cancer in Spanish . All of the physician and patient statements are available in Spanish. News items that are available in Spanish have a # next to the statement title. Although both the English and Spanish are updated at the same time each month, the Spanish statements do not reflect the changes made in the English statements until the following month to allow time for translation . If you are interested in requesting CancerNet statements or news articles in Spanish, it is suggested that you request an updated Contents List. If you are redistributing the PDQ information you retrieve from CancerNet to others at your location, or are interested in redistributing the information from CancerNet, request the news article, Redistribution of Cancernet (cn-400030) , to find out about conditions that apply when redistributing the information. This article also has information on other sites providing access to CancerNet information. Please send comments or questions to: Cheryl Burg NCI International Cancer Information Center Internet: cheryl@icicb.nci.nih.gov ------------------------------ To: hicnews How Cells Recognize Onslaught of Toxic Chemicals Science News from Rehovot, Israel Research from The Weizman Institute of Science May 1994 No 31 Although our bodies are constantly bombarded by small amounts of toxic and cancer-inducing chemicals, sophisticated protective mechanisms operate to break down and neutralize these poisons. However, the powerful drugs used to treat cancer and other illnesses can also be destroyed by these natural detoxification processes. Long-time investigator of detoxification biochemistry Prof. Violet Daniel (Dept. of Biochemistry) and her graduate students Svetlana Bergelson and Ron Pinkus have recently answered a key question in this area and explained how various drugs and toxic compounds trigger the enhanced production of the same group of detoxification proteins. This improved understanding of a cell's chemical defense mechanism may enable pharmaceutical manufacturers to design new chemotherapeutic drugs that can circumvent natural detoxification, as well as allow biomedical researchers to find ways of strengthening detoxification in individuals exposed to poisons. In explaining the triggering of cell chemoprotection mechanisms, the Institute researchers base their theory on the fact that, aside from any specific toxic effects in cells, all hazardous materials studied by the Weizmann and other groups are also capable of inducing oxidative stress. When toxic substances enter cells, this oxidative stress can be produced either by a direct oxidation of natural cell components by the poison or by its being transformed by natural metabolic processes to compounds with high oxidation capabilities. Daniel now believes that since so many different kinds of chemicals lead to a similar shift in a cell's oxidative status (known by scientists as its oxidation-reduction balance), it is this situation that signals cells to turn on their chemoprotective mechanisms and is responsible for signaling the activation of genes controlling poison detoxification. Turning to the genetic mechanisms operating to activate production of chemoprotective enzymes, the Daniel team discovered that some of the toxic materials studied induce the enhanced expression of the fos and jun genes, which in turn leads to the production of transcription factor AP-1, a well-known genetic control protein. The Weizmann workers therefore sought to determine a possible role for AP-1 in turning on detoxification biochemistry. Examining the genes for several major enzymes involved in chemoprotection, including glutathione S-transferase and quinone reductase, they found that these genes contain special regions that can bind AP-1. This strongly indicated that the AP-1 produced in response to chemicals and the resultant oxidative stress was indeed responsible for induction of the poison-dismantling enzymes. Quite intriguingly, fos and jun are also proto-oncogenes - genes sometimes involved in cancerous changes - that participate in the regulation of cell growth, proliferation, and differentiation. Because of this, the finding that fos and jun take part in the normal defense against carcinogenic and other materials is extremely significant. It could be, notes Prof. Daniel, that when carcinogenic chemicals enter the body from time to time in small quantities, the chemoprotective defenses are alerted, the materials are destroyed, and the system returns to its normal basic state. However, when carcinogens are present in larger amounts, the oncogenes work overtime to produce AP-1. As a result, the cell can enter a continually proliferating, malignant state. In fact, AP-1 is known to stimulate, in addition to chemoprotective enzymes, proteins involved in cell replication. One drug demonstrating the connection between chemoprotection and cancer is phenobarbital, a common anticonvulsant and sedative. While there is no evidence that this drug is carcinogenic when taken by humans in low doses, when administered to mice and in large doses, phenobarbital is a co-factor that potentiates the initiation of cancer by other materials. As has been determined by the Daniel team, this pharmaceutical indeed stimulates the production of AP- 1. Knowledge of the body's poison defense mechanisms that is now coming to the fore is beginning to change the way scientists view the question of environmental carcinogens. "What we are now thinking," says Daniel, "is that the level of exposure to a carcinogen or co-carcinogen is critical for its ability to produce cancer. At low levels, the natural protective mechanisms can adequately take care of it. There is, therefore, no reason to strive for zero exposure to these materials. That would be, in any case, impossible since we are - as is now widely recognized - constantly exposed to a wide assortment of potentially cancer causing substances, and even organically grown fruits and vegetables will often contain carcinogens as part of their natural biochemical complements." Prof. Daniel holds the Bee Wiggs Chair of Molecular Biology at the Weizmann Institute of Science. ------------------------------ To: hicnews N E W S R E L E A S E *************************** National Institutes of Health National Institute of Allergies and Infectious Diseases February 1, 1995 Chimpanzee Vaccine Model Protects Against HIV-1 Infection Chimpanzees inoculated with one HIV-1 strain can resist later infection with a different strain, according to scientists from the National Institutes of Health (NIH) and two other institutions. Successful protection, their experiments show, depends on the infectiousness of the first strain. Unlike humans, chimpanzees infected with HIV-1 fail to develop disease. The scientists reasoned that an initial HIV infection might act like a weakened live-virus vaccine such as the Sabin polio vaccine. "In this study, the first infection simulated the effect of a successful attenuated HIV-1 vaccine," says Riri Shibata, Ph.D., the study's lead author. "The virus induced protective immunity against a subsequent HIV-1 infection. Scientists now have a model system that can help develop an attenuated HIV-1 vaccine for humans." Dr. Shibata, a Fogarty visiting associate with the National Institute of Allergy and Infectious Diseases (NIAID), part of NIH, plans to present the study data on Wednesday, Feb. 1 at the Second National Conference on Human Retroviruses and Related Infections in Washington, D. C. For their study, they used two chimpanzees infected three and seven years earlier, respectively, with the laboratory-grown HIV- 1 strain IIIB. They tried to superinfect the animals by exposing them to multiple high doses of HIV-1-DH-12, a strain recently isolated from an AIDS patient and known to thrive in chimpanzee cells. In September 1993, the scientists injected one animal with a dose of DH-12 known to induce infection in a chimpanzee. In the ensuing four and a half months, they used a technique called polymerase chain reaction (PCR), which can detect minute amounts of virus, to determine if the DH-12 virus successfully infected the chimpanzee. Repeated PCR tests consistently found evidence of IIIB but not of DH-12, suggesting that the animal was protected from the DH-12 challenge. In January 1994, the investigators gave the first chimpanzee a second DH-12 dose 10 times larger than the first. They also gave the same larger dose of DH-12 to the second IIIB-infected chimpanzee. Multiple PCR tests and virus isolations in both animals over the next four months were positive for IIIB but always negative for DH-12. In May 1994, the researchers exposed the second chimpanzee to another dose of DH-12 100 times larger than the first. They also took 10 milliliters (about two teaspoonsful) of blood from a third chimpanzee experimentally infected with DH-12 four months earlier and injected it into the first IIIB-infected chimpanzee to mimic the type of exposure that occurs to an intravenous drug user. To date, both IIIB-infected chimpanzees show no evidence of DH-12 infection by either PCR or virus isolation techniques, Dr. Shibata plans to report. Before the study, in both animals the scientists could detect neutralizing antibodies against the IIIB strain but not against the DH- 12 strain, suggesting that cell-mediated immunity was responsible for the protection observed. This finding will be investigated further to delineate what component(s) of the immune system may be responsible for resistance to infection. To evaluate how potent an attenuated vaccine must be to protect an animal from a subsequent HIV-1 infection, the scientists recently challenged two more chimpanzees inoculated earlier with SF2, a different HIV-1 strain. SF2 also does not induce disease in chimpanzees but is much weaker than IIIB, generating only very low levels of virus in infected animals. In September 1994, the scientists inoculated each of the two SF2-infected chimpanzees with a low-dose of DH-12. In contrast to the experiments with the IIIB-infected animals, the two SF2-infected animals became infected with DH-12 within four weeks of exposure. However, they had 35- to 50-fold less DH-12 in their blood than did an unvaccinated chimpanzee exposed to DH-12. These studies show that chimpanzees can be protected from a subsequent challenge with HIV-1, provided the animals are first immunized with a potent attenuated live-virus vaccine. Experiments in progress will ascertain how the extent of virus attenuation correlates with resistance to subsequent HIV infection. Dr. Shibata works as a microbiologist in NIAID's Laboratory of Molecular Microbiology, headed by Malcolm A. Martin, M.D., senior author on the study. Study collaborators include Christine Broscius, B.S., of NIAID in Bethesda, Md.; Patrice Frost, D.V.M., and Zimra Israel, Ph.D., of the Coulston Foundation in Almagordo, N.M.; Thomas Matthews, Ph.D., of Duke University in Durham, N.C.; and Larry O. Arthur, Ph.D., of the National Cancer Institute facility in Frederick, Md. NIAID supports investigators and scientific studies at universities, medical schools, hospitals and research institutions in the United States and abroad aimed at preventing, diagnosing and treating such illnesses as AIDS, tuberculosis and asthma as well as allergies. NIH is an agency of the U.S. Public Health Service, part of the U.S. Department of Health and Human Services. ------------------------------ End of HICNet Medical News Digest V08 Issue #14 ********************************************* --- Editor, HICNet Medical Newsletter Internet: david@stat.com FAX: +1 (602) 451-6135