192 ALCOHOL HEALTH & RESEARCH WORLDPregnant alcoholic women riskthe health of their offspring inmultiple ways: (1) Exposure toalcohol during gestation may lead tofetal alcohol syndrome (FAS) or fetalalcohol effects; (2) the physical conse-quences of alcoholism in the mother(e.g., falls or malnutrition) may inde-pendently affect the developing fetus;(3) genetic vulnerability to alcoholismin the fetus may increase the effects ofprenatal exposure; and (4) the lifestyleof an alcoholic parent may lead tonegative consequences for the fetus,the pregnancy, and the developingchild. This article addresses the firstof these issuesthe effects of expo-sure to alcohol during gestationindetail. However, any or all of theother issues listed (i.e., concomitantgenetic background and the physicaland lifestyle deficits that accompanyalcoholism) may exacerbate the adverseeffects of prenatal alcohol exposure.As a teratogen, alcohol is capableof directly inducing developmentalabnormalities in a fetus. Alcohol useduring pregnancy is one of the mostcommon known causes of preventablebirth defects, and its results can persistas long-term deficits in physical andcognitive growth and development. The dangers of fetal alcohol expo-sure, initially identified in the late1960s, are entirely preventable if wom-en abstain from drinking during preg-nancy. Given this fact, in 1981 the U.S.Surgeon General issued the first healthadvisory recommending that womenwho are pregnant or planning a pregnan-cy should not drink alcohol, and thisadvisory was repeated in 1990 and 1995.FAS DEFINITION AND DIAGNOSISAt the extreme end of the spectrum ofprenatal exposure effects, FAS is aclinical diagnosis applied to childrenwho have been exposed to alcoholduring gestation and exhibit deficits ingrowth, physical structure (i.e., mor-phology), and the central nervous sys-tem (CNS). To meet the clinical casedefinition, the child must have symp-toms in each of the following threeThe Effects of Prenatal Alcohol Exposure CYNTHIA LARKBY, M.S.W., AND NANCY DAY, PH.D, M.P.H.Exposuretoalcoholduringgestationcancausepersistentabnormalitiesinphysicalandcognitivedevelopment.Childrenwhomeettheclinicaldefinitionoffetalalcoholsyndrome(FAS)aresmallfortheirage,exhibitcharacteristicfacialanomalies,anddemonstratedeficitsincentralnervoussystemdevelopment.Alcoholeffectsinchildrenwithprenatalexposure,butnotFAS,aresimilar,althoughofsmallermagnitudeandnotnecessarilypresentinallthreesystems.Thedegreetowhichapersonisaffectedbyprenatalalcoholexposuredependsontheamount,timing,anddurationofthemothersalcoholconsumptionduringpregnancyaswellasmaternalcharacteristics(e.g.,ageandcomorbidpsychiatricdisorders)andenvironmentalfactors(e.g.,socioeconomicstatusandfamilyproblems).Someexposure-relatedeffects,suchasgrowthdeficits,aredirectlyrelatedtotheamountofalcoholconsumed,however,sothatevenasmallamountofalcoholmayaffectchilddevelopment. Therefore, the best policy continues to be abstinence during pregnancy.KEY WORDS:gestation;prenatalalcoholexposure;fetalalcoholeffects;fetalalcoholsyndrome;teratogens;congenitalanomaly;fetaldevelopment;disorderdefinition;epidemiology;amountofAODuse;growthretardation;morphology;CNSfunction;mentalretardation; cognitive development; demographic characteristics; psychosocial environment;literature reviewCYNTHIA LARKBY, M.S.W., is a doctoralcandidate and NANCY DAY, M.P.H.,PH.D., is a professor of psychiatry,epidemiology, and pediatrics and direc-tor of the Program in Epidemiology atWestern Psychiatric Institute andClinic, University of Pittsburgh Schoolof Medicine, Pittsburgh, Pennsylvania.categories: (1) growth deficiency inboth the prenatal and postnatal periods;(2) abnormalities in facial and skullstructure, including small eye openings(i.e., short palpebral fissures), alter-ations in nose and forehead structure, anabsent or elongated groove between theupper lip and nose (i.e., philtrum), a thinupper lip, a flattened midface, and un-derdevelopment of the upper or lowerjaw; and (3) CNS deficits, such as men-tal retardation and behavioral problems(Sokol and Clarren 1989). Of thesesymptoms, the facial abnormalities arethe most characteristic of FAS, whereasthe CNS anomalies have the most signif-icant effect on overall development.Separately, each of these features isdefined as an alcohol-related birth defect(ARBD) or a fetal alcohol effect.The features associated with FASmay change with age, complicating thediagnosis. Before age 2, CNS dysfunc-tion is difficult to assess, and the clas-sic facial abnormalities (see figure)may not be clearly evident. At olderages, growth deficits are offset by theadolescent growth spurt as well asnormal changes in facial length andwidth associated with maturation.Because of these changes, growthdeficits and facial features become lessapparent after puberty, and withoutprepubertal photographs and reliablegrowth records, FAS may be difficultto diagnose in adolescents or adults.Accurately assessing fetal alcoholexposure may prove even more difficult.To obtain correct information regardingthe quantity of alcohol consumed as wellas the timing and duration of alcohol useduring pregnancy, clinicians and re-searchers need reliable methods to deter-mine alcohol exposure. Althoughbiological tests are available to measurethe amount of alcohol consumed, thesetests reflect use over a very short timeperiod and do not allow estimates of thepattern or duration of use to be made. Ingeneral, clinicians and researchers relyon the mothers self-report of alcoholuse. Self-reports may be inaccurate,however, because social pressures, fearof being labeled, and anxiety aboutlosing custody of her child may lead awoman to underreport her alcohol con-sumption during pregnancy. Problemsrecalling the frequency and quantity ofalcohol consumed also can lead to erro-neous estimates. In the absence of anaccurate report, clinicians and caretak-ers, such as foster and adoptive parents,will not know whether or to what extentthe child was exposed to alcohol duringgestation. Therefore, both clinicians andresearchers must establish trust andrapport with all pregnant women toenable them to report their alcohol useboth honestly and accurately.Because of the difficulty in reliablyascertaining fetal alcohol exposure, acommittee convened by the Institute ofMedicine to study FAS recently re-viewed the diagnostic criteria currentlyin use and recommended revisions. Thecommittee members proposed a diag-nostic classification system with fivecategories: (1) FAS with confirmedmaternal alcohol exposure, (2) FASwithout confirmed maternal alcoholexposure, (3) partial FAS with con-firmed maternal alcohol exposure, (4)ARBD with a history of maternal alco-hol exposure, and (5) alcohol-relatedneurodevelopmental disorder (ARND)with a history of maternal alcohol expo-sure (Stratton et al. 1996). The last twocategories are used for offspring whohave morphologic and neurologic alco-hol-related effects, respectively, with-out the full features of FAS, and theymay co-occur in the same individual. FAS EPIDEMIOLOGYAlcoholism and Alcohol UseAmong WomenIn a nationwide household surveyconducted in 1992, 4.08 percent of thewomen who were interviewed met thecriteria1for alcohol abuse and/or de-VOL. 21, NO. 3, 1997 193Effects of Prenatal Alcohol ExposureFacial features particularly characteristic of a child with fetal alcohol syndrome(FAS). Discriminating features (i.e., those considered definitive signs of FAS) areshown on the left side of the illustration; characteristics listed on the right side areassociated with FAS but are not sufficient to determine the presence of thesyndrome. Microencephaly (small head circumference) is not a facial feature per se,but a central nervous system characteristic. (Palpebral fissures = eye openings;philtrum = groove between nose and upper lip; epicanthal folds = skin folds coveringinner corner of the eye; micrognathia = abnormal smallness of the jaws. )SOURCE: Streissguth and Little 1994.DiscriminatingFeaturesAssociatedFeaturesShort palpebralfissuresFlat midfaceShort noseIndistinct philtrumThin upper lipEpicanthal foldsLow nasal bridgeMinor ear anomaliesMicrognathia1The criteria used in this study corresponded tothe criteria for alcohol abuse and dependencelisted in the American Psychiatric Associa-tions Diagnostic and Statistical Manual ofMental Disorders, Fourth Edition. In general,the terms alcoholic and alcoholism, as usedin this article, encompass both diagnoses. pendence within the 12 months pre-ceding the survey (Grant et al. 1994).The highest prevalence rates for alco-hol abuse and/or dependence werefound among women of childbearingage (9.84 percent for women ages 18to 29 and 3.98 percent for womenages 30 to 44).Women who are alcoholic typicallyexperience several other problems,including comorbid medical or psy-chiatric disorders (e.g., depression)and social problems (e.g., unstablemarriages; spouses with drinkingproblems; and child-care responsibili-ties, often as single mothers). Thismultiplicity of problems complicatesthe pregnancy of an alcoholic woman,because her fetus is exposed not onlyto the teratogenic effects of alcohol,but also to the negative effects of theother factors that coexist in her life.By comparing birth outcomes in uppermiddle class and lower class alcoholicmothers, Bingol and colleagues (1987)showed that economic or lifestylefactors play a role in the rate of FAS.They found that, although the intakeof absolute alcohol was equivalent inthe two groups, 2.7 percent of theupper middle class mothers had achild with FAS, compared with 40.5percent of the lower class mothers.The problem of alcohol exposureduring pregnancy is not limited toalcoholic women, however. A majori-ty of women drink, as evidenced by anational household survey (Hilton1991) in which 64 percent of thewomen surveyed were drinkers (i.e.,drank at least once a year), 4 percentreported daily drinking, 6 percentdrank five or more drinks on occasionat least weekly, and 1 percent reporteddrinking enough to feel drunk at leastweekly. Age, race, social class, andoccupation all predicted drinkingpatterns among women. For example,younger women were most likely todrink, and white women drank morethan their black or Hispanic counter-parts. Drinkers had a higher educationlevel and income than nondrinkersand were more likely to work full timeoutside the home. These same fourcharacteristics also described womenwho were heavy drinkers.2Despite the fact that womens drinkingrates have remained relatively constantsince the 1960s (Hilton 1991), the rateof drinking during pregnancy appearsto be increasing. For example, theBehavioral Risk Factor SurveillanceSystem reported that among pregnantwomen, the rate of drinking increasedfrom 12.4 percent in 1991 to 16.3 percent in 1995 and that the rate offrequent drinking3was four times higherin 1995 than in 1991, increasing from0.8 percent in 1991 to 3.5 percent in1995 (Centers for Disease Control andPrevention 1997). Prevalence of FASAbel and Sokol (1987) estimated thatapproximately 6 percent of the off-spring of alcoholic women have FAS,although for offspring born after anFAS sibling, the risk is very high (70percent) (Abel 1988). The high proba-bility that all subsequent offspringwill be affected after an initial casemeans that some consequence ofchronic alcoholism in addition toalcohol exposure must lead to thehigher rate of FAS among offspringborn later. Even in the absence of full-blown FAS, babies of alcoholic wom-en have a higher rate of the separatecharacteristics of FAS.Among the general population, anational surveillance program knownas the Birth Defects MonitoringProgram reported a rate of 5.2 FAScases per 10,000 live births (Corderoet al. 1994). Similarly, in a recentsummary of findings from prospectivestudies, Abel and Sokol (1991) esti-mated the overall rate of FAS to be3.3 cases per 10,000 live births. Therate of FAS is likely to be consider-ably underestimated, however, be-cause of the difficulty in making thediagnosis and the reluctance of clini-cians to label children and mothers.For example, Little and colleagues(1990) studied the outcomes of 40pregnancies of 38 women whosealcohol abuse was noted in their medi-cal records. Although one-half of the34 liveborn infants demonstrated poorpostnatal growth and developmentand 6 neonates met the diagnosticcriteria for FAS, none of the infantswas diagnosed as having FAS.RELATIONSHIP OF EXPOSUREAND EFFECTSFetal development is a sequential,multistaged process. To determine theeffects of prenatal exposure on childdevelopment, factors such as the tim-ing, dose, and pattern of alcohol expo-sure must be considered, becausegrowth, morphologic abnormalities,and CNS deficits occur at differentpoints during gestation. Major mor-phologic abnormalities result fromexposure early in pregnancy, growthis most affected by late exposure, andCNS deficits occur throughout gesta-tion. Thus, offspring who are exposedto alcohol throughout pregnancy willnot have the same outcome as off-spring who are exposed only duringearly pregnancy or only at specifictimes during pregnancy.Identifying the nature of the rela-tionships between prenatal alcoholexposure and outcome is also impor-tant for research and clinical reasons.Exposure to a toxin may affect fetaloutcome in two ways: The effect maybe directly related to the amount ofexposure (i.e., a linear relationship),or exposure may be problematic onlyabove a certain level (i.e., a thresholdrelationship). A linear relationshipbetween alcohol exposure and childdevelopment means that no safelevel of drinking during pregnancyexists, because even a small amountof alcohol could produce an effect. Incontrast, the threshold model impliesthat a safe level of drinking doesexist, below which negative effects donot occur. Data from studies to datedemonstrate that the relationship be-tween alcohol exposure and outcome194 ALCOHOL HEALTH & RESEARCH WORLD2In this study, heavy drinkers were defined aspeople who consumed eight or more drinks perday as often as three times per week.3Frequent drinking was defined in this studyas consuming seven or more drinks per week or five or more drinks on an occasion in thepast month.varies depending on the type of out-come under consideration, however.For example, reports from the animal(Schenker et al. 1990) and humanliterature (Sampson et al. 1989; Gold-schmidt et al. 1996) support a thresh-old relationship between prenatalalcohol exposure and CNS develop-ment, whereas the data on physicalgrowth indicate that the effect of ges-tational exposure to alcohol is linear(Day et al. 1994). Therefore, no safelevel of consumption exists, and thebest policy for women continues to beabstinence during pregnancy to avoidany negative effects on their offspring.SPECIFIC EFFECTS OF PRENATALEXPOSUREPeople with FAS demonstrate growthdeficits, morphologic abnormalities,mental retardation, and behavioraldifficulties. In a systematic followupstudy, Streissguth and colleagues(1991) examined 61 subjects identi-fied as having FAS or fetal alcoholeffects to determine adolescent andadult manifestations of the syndrome.The study results give an overview ofthe long-term impact of prenatal alco-hol exposure. At adolescence andadulthood, the subjects were short instature and small in head circumfer-ence; they also exhibited a high rate ofabnormal facial features, althoughthese characteristics were not as pro-nounced as they had been at youngerages. The subjects IQ scores rangedfrom 20 to 105 with a mean of 68. Sixpercent of the subjects took regularschool classes, but the remainder ofthe study participants were unable toachieve this schooling level or main-tain regular outside employment. Inaddition, the subjects demonstratedpoor concentration and attention; aninability to live independently inadulthood; stubbornness; social with-drawal; and conduct problems, suchas lying, cheating, and stealing. Theircharacteristics and long-term outcomepredict the expected outcome forpeople who were prenatally exposedto alcohol but do not have the fullsyndrome. At lower levels of expo-sure, a subset of fetal alcohol effects,rather than the full extent of FASfeatures, is most likely to occur.The following sections describe theeffects of prenatal alcohol exposure ongrowth, morphology, and CNS devel-opment in turn. Many of the examplesare taken from the Maternal HealthPractices and Child Development(MHPCD) project, a longitudinalstudy of the long-term effects of pre-natal alcohol exposure. In this study,researchers recruited adult women intheir fourth month of pregnancy froma prenatal clinic. All women whoconsumed an average of three or moredrinks per week during their firsttrimester, plus a random sample ofone-third of the women who drankalcohol less often, were selected asstudy subjects. In general, alcohol useduring pregnancy was light to moder-ate among the women participating inthe study, although subjects who rep-resented the entire spectrum of usewere included in the sample.Growth DeficitsChildren with FAS are small for theirage (Streissguth et al. 1991)indeed,such smallness is one of the criteriafor diagnosis, although growth deficitsalso are found among children whowere exposed to alcohol during preg-nancy but do not fulfill the full criteriafor FAS. As noted previously, howev-er, growth retardation is somewhatameliorated at puberty. In the MHPCDproject, these growth deficits are sym-metrical, affecting height, weight, andhead circumference to the same de-gree, and remain significant throughage 10. The relationship betweenprenatal exposure and growth deficitsis linear (i.e., the greater the prenatalalcohol exposure, the more pronouncedthe effect on postnatal growth). Smithand colleagues (1986) also found thatthe duration of exposure, in additionto amount, affected birth weight. Postnatal environment and mater-nal characteristics influence the rela-tionship between prenatal alcoholexposure and growth, however.Whereas studies of disadvantagedpopulations (Coles et al. 1991; Day etal. 1994; Jacobson et al. 1994b;Russell 1991) have found that prenatalalcohol exposure continues to affectgrowth at followup, studies of moreadvantaged cohorts (Barr et al. 1984;Fried and OConnell 1987; OConnoret al. 1986) have found that growthdeficits are not maintained as thechildren get older. Another study(Jacobson et al. 1994a) found thatalcohol exposure was associated withdecreased birth weight, length, andhead circumference, although onlyamong infants of women over age 30.Thus, postnatal environment andmaternal characteristics apparentlyexacerbate the effects of prenatalalcohol exposure. Morphologic AbnormalitiesAnother criterion of FAS is the pres-ence of the specific group of facialanomalies mentioned previously (i.e.,short palpebral fissures, a flattenednasal bridge, an absent or elongatedphiltrum, and a thin upper lip). Fromembryological studies, investigatorsknow that these morphologic abnor-malities occur when the midline of theface is formed during the firsttrimester. A significant correlationbetween first-trimester alcohol expo-sure and the rate of these physicalanomalies was found in the MHPCDproject (Day et al. 1990). As noted inother studies of FAS, however, therelationship between prenatal alcoholexposure and the characteristic facialfeatures associated with FAS dimin-ished as the children matured. CNS DeficitsBoth animal and human studies havedemonstrated that brain structures,including the hippocampus, frontallobes, corpus callosum, and basalganglia, are important sites of alco-hols action on the fetal brain (Clarrenet al. 1978; Coulter et al. 1993; Mat-tson et al. 1992, 1996b; Pfeiffer et al.1979; Riley et al. 1995; Shapiro et al.1984; Wisniewski et al. 1983). Indeed,researchers have documented anoma-lies of brain structure and functionamong children with FAS. EvidenceVOL. 21, NO. 3, 1997 195Effects of Prenatal Alcohol Exposureof CNS deficits in FAS children alsoappears in their tendency to have de-layed motor and speech developmentand speech and hearing impairments(Steinhausen et al. 1982; Church andGerkin 1988). In prenatally exposedchildren who do not have FAS, re-searchers have identified neurologiceffects at birth that reflect abnormali-ties in sleep patterns (Scher et al.1988) and in the newborns ability torespond and adapt, as measured by theBrazelton Neonatal BehavioralAssessment Scale (Coles et al. 1985;Streissguth et al. 1983).One way to gauge CNS functioningis to use neuropsychological measuresdesigned to assess brain functioning.Using such measures, Mattson andcolleagues (1996a) found that 5- to16-year-old children with FAS hadsignificant verbal learning and memo-ry deficits. Similarly, Kodituwakkuand colleagues (1995) reported mem-ory deficits in 13-year-old childrenwith FAS, and Coles and colleagues(1997) found that children with FAShad deficits in problem-solving, infor-mation processing and storage, andvisual and spatial skills. The neuropsychological findingsare similar for children who were ex-posed to alcohol during gestation butdo not have FAS. Jacobson and col-leagues (1993) reported that prenatallyexposed 13-month-old infants wereslower or less efficient at informationprocessing. Such deficits apparentlypersist: In a study by Streissguth andcolleagues (1994), 14-year-old childrenwho had been prenatally exposed toalcohol had difficulty performing tasksthat required processing information inorder to make complex decisions.Researchers also have found that pre-natally exposed children have particu-lar difficulty in mathematical tasks(Kopera-Frye et al. 1996). In anotherstudy, Coles and colleagues (1991)compared the cognitive performance ofchildren whose mothers drank an aver-age of 11.8 ounces of absolute alcohol(i.e., approximately 24 drinks) perweek throughout pregnancy and chil-dren whose mothers stopped drinkingin the second trimester or did not drinkat all during pregnancy. The resear-chers found that the children exposedthroughout gestation performed morepoorly than children in the other twogroups, exhibiting deficits in short-term memory and encoding (i.e., se-quential processing) and overall mentalprocessing at an average age of 5 yearsand 10 months.People with FAS often are mental-ly retarded, although the degree ofdeficit varies (Landesman-Dwyer1982; Streissguth et al. 1991). Streiss-guth and colleagues (1996) reportedthat the IQ scores of FAS patientsranged from 29 (severely retarded) to120 (high average). Like other exposure-related effects, the impact of prenatalalcohol exposure on cognitive devel-opment demonstrates a continuum.Although study results are not com-pletely consistent, alcohol exposure isrelated to decreased cognitive abilitieseven at lower levels of exposure. Forexample, Streissguth and colleagues(1989a) reported that the daily con-sumption of 112 ounces of absolutealcohol (i.e., approximately threedrinks) was associated with an aver-age decrease of 5 points in the childsIQ score at age 4. At age 712, childrenexposed to more than 1 ounce of abso-lute alcohol (i.e., approximately twodrinks) per day scored an average of 7IQ points lower compared with chil-dren not exposed to this amount(Streissguth et al. 1990).People with FAS commonly exhib-it behavioral problems as well (Ma-jewski 1978a; Majewski 1978b;Olegard et al. 1979; Shaywitz et al.1980; Steinhausen et al. 1982; Streiss-guth et al. 1991). These problems caninclude poor concentration and atten-tion, lack of independent living skills,stubbornness, and social withdrawal.In addition, children with FAS exhibithigher rates of conduct problems (e.g.,lying, cheating, and stealing). Streiss-guth (1993) reported that as childrenwith FAS mature, they demonstratepoor socialization and communicationskills and commonly experience prob-lems with alcohol and drug abuse andantisocial behavior.Behavior problems also have beenreported among offspring prenatallyexposed to alcohol but without FAS.In one study, 4-year-old childrenwhose mothers drank one to fivedrinks per day during pregnancy wereless attentive and more active whenobserved in the home, compared withchildren of control mothers who drankless (Landesman-Dwyer 1982). At age712, the children were less attentiveand took a longer time to react to astimulus on a Continuous PerformanceTask (Streissguth et al. 1986). In chil-dren ages 7 (Streissguth et al. 1989b)and 14 (Streissguth et al. 1994), re-searchers demonstrated the effects ofprenatal exposure to alcohol on bothattention and memory. These effectswere linear (i.e., the extent of theeffect was directly correlated with theamount of alcohol exposure), implyingthat no safe threshold of alcoholexposure exists.In the MHPCD project, mothersand teachers described children ages3, 6, and 10 who were prenatallyexposed to alcohol as showing in-creased activity and poorer attention,as well as social problems, anxiety,and depression (Day 1997). Brownand colleagues (1991) noted that chil-dren who had been exposed to alcoholthroughout pregnancy showed deficitsin their ability to sustain attention, andtheir teachers reported that they hadproblems with both attention andbehavior in school.Clinical studies provide furtherevidence of the neurobehavioral con-sequences of prenatal alcohol expo-sure. Such studies have reported thatpeople with FAS experience trouble inschool and maintaining jobs, a likelycompound of their lower IQ scores,neuropsychological deficits, and be-havior problems. Even among chil-dren and adults who do not have FAS,lower academic achievement is signif-icantly related to prenatal alcoholexposure (Coles et al. 1991; Streiss-guth et al. 1990). An analysis of theoutcomes among 6-year-olds in theMHPCD project, for example, demon-strated effects of second-trimesteralcohol exposure on reading, spelling,196 ALCOHOL HEALTH & RESEARCH WORLDand mathematics skills (Goldschmidtet al. 1996). Coles and colleagues(1991) also found that children whowere exposed in early pregnancyperformed more poorly in mathemat-ics and reading than their peers whohad not been exposed.SUMMARY AND CONCLUSIONSIn summary, cases of FAS are charac-terized by abnormalities in growth,morphology, and CNS development.Among exposed offspring who do nothave FAS, deficits are seen in thesame pattern, although they may be ofsmaller magnitude and do not affectall three systems in each person.Therefore, the effects of prenatalalcohol exposure range over a contin-uum from fully developed FAS to themilder constellation of fetal alcoholeffects.Studies show that the effects ofprenatal alcohol exposure can be influ-enced by maternal characteristics, suchas age and comorbid psychiatric disor-ders, or by factors in the postnatalenvironment such as socioeconomicstatus and family problems. Thus, theinteraction between a vulnerable childand a disadvantaged environmentcompounds the negative outcomes.There is a pressing need to under-stand the broad picture of the com-bined effects of alcohol exposure,poverty, and lifestyle on the develop-ing fetus. Each of these risk factorsfor poor pregnancy outcome must beconsidered in evaluating the effects ofprenatal alcohol use, because it isunclear whether alcohol effects occurindependently or in interaction withrisk factors such as an impoverishedsocial environment. Given that alcohol is a teratogen,an appropriate goal would be to elimi-nate drinking during pregnancy. Thismeans finding effective methods tohelp women who are alcoholic abstainduring pregnancy and to motivateother drinking women to abstain fromlevels of alcohol consumption thatwould be insignificant outside ofpregnancy. 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