
 
 
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
 
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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
 



(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)
 



(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
 

