Printer Friendly

Fetal alcohol spectrum disorders: understanding the effects of prenatal alcohol exposure and supporting students.


Maternal alcohol consumption during pregnancy is known to adversely affect the developing fetus, resulting in a broad range of negative, lifelong developmental outcomes. (1-4) Fetal alcohol spectrum disorders (FASD) is a term referring the range of outcomes and disabilities that can occur when an individual is exposed to alcohol prenatally. (5) Given that FASD affect a large number of children in this country, 9.1 per 1000 live births, (6) it is imperative that education, health, and all professionals in schools understand the disabilities associated with prenatal alcohol exposure and are aware of strategies to support students in meeting academic, social, emotional, and behavioral goals of school. This article addresses the diagnosis of fetal alcohol syndrome (FAS) and other alcohol-related conditions, describes the cognitive, social, emotional, and behavioral characteristics of individuals with FASD, and introduces intervention strategies that are helpful in supporting individuals with FASD in schools.

The negative impact of alcohol on the developing fetus was recognized over 30 years ago. (7) Early observations and documentation of the characteristics of children exposed prenatally to alcohol are quite consistent with how the full syndrome of FAS is defined today. The diagnostic criteria for the full syndrome of FAS are relatively straightforward and have been recently clarified and updated by a diverse group of professionals, clinicians, and scientists. (8) Diagnostic criteria include facial dysmorphia, growth deficiency, and central nervous system (CNS) abnormalities, which may include small head circumference, neurological problems, cognitive/developmental deficits, and behavioral/emotional problems. (8) Facial dysmorphia refers to a characteristic pattern of facial features that include a smooth philtrum, thin upper lip, and small eyes. The philtrum is the vertical ridge between the nose and upper lip. Alcohol exposure during prenatal development affects the natural development of the philtrum, eyes, and lip as well as negatively affects brain development. (8) The CNS abnormalities or brain damage can range from severe structural abnormalities in the corpus callosum or basal ganglia (9) to mild cognitive deficits. (10) As described below, neurocognitive deficits, academic challenges, and emotional and behavioral concerns are commonly associated with FAS. (10-13) May and Gossage (14) estimate the prevalence rates for FAS from .5 to 2.0 cases per 1000 births.

While the diagnostic criteria for FAS are relatively straightforward, the diagnosis or identification of other FASD conditions is more complicated. Because not all individuals exposed prenatally to alcohol display the characteristic pattern of facial features, many do not meet the full criteria for FAS. However, they often demonstrate the cognitive, social, emotional, and behavioral difficulties associated with the teratogenic effects of alcohol on the brain. That is, the cognitive and behavioral effects of prenatal exposure can occur independently of the characteristic facial features. The term fetal alcohol spectrum disorders was coined to encompass the range of disabilities associated with prenatal alcohol exposure. (5) This umbrella term includes medical diagnoses such as fetal alcohol syndrome (FAS) and alcohol-related neurodevelopmental disorder (ARND) as well as older terms such as fetal alcohol effects and newer terms (eg, neurobehavioral disorder, alcohol exposed). For example, multiple diagnoses such as partial FAS with confirmed maternal alcohol exposure and ARND were identified within the Institute of Medicine's (IOM) diagnostic framework, which was published in 1996. According to the IOM criteria, (15) the diagnosis of partial FAS can be made when there is confirmation of substantial exposure to alcohol prenatally, some evidence of facial features, and at least one of the following: growth deficiency, CNS neurodevelopmental abnormalities, or a complex pattern of behavioral and cognitive abnormalities. Likewise, the diagnosis of ARND would be used when a patient presents with a confirmed history of prenatal alcohol exposure in addition to CNS abnormalities (decreased head size, structural abnormalities, neurological hard or soft signs) or a complex pattern of behavior or cognitive abnormalities that are inconsistent with developmental level and cannot be explained by familial background or environment. (15) At this point in time, the criteria for diagnoses such as ARND are not as objectively defined or generally accepted as the criteria for FAS. The prevalence of ARND and disabilities that are potentially related to prenatal alcohol exposure greatly exceeds estimates of FAS. In fact, Sampson et al (6) estimate that the combined rate for FAS and ARND at 9.1 per 1000 births, suggesting that the severe consequences of prenatal alcohol exposure affect a much larger number of children in this country than are affected by FAS.


Cognitive and Academic Decits

Prenatal alcohol exposure clearly causes brain damage, and the neuropsychological consequences are immense. In fact, prenatal alcohol exposure is one of the leading causes of mental retardation (MR) in the Western world. (16) In addition to deficits in basic cognitive functioning, consequences include difficulties in planning, organization, and attention; failure to learn from consequences; and memory deficits. (1,2,11,17,18) For some, speech/language, visuospatial functioning, and spatial memory are also adversely affected by prenatal alcohol exposure. (19) Deficits in verbal learning, specifically the encoding process, have also been linked to FASD. (20)

While some level of cognitive deficit characterizes most individuals with FASD, most individuals do not have MR. Furthermore, even for those who do meet full criteria for FAS, the range of IQ scores is quite large. Mattson and Riley (10) reviewed many studies on children with a diagnosis of FAS or alcohol exposure. The overall mean IQ for individuals with FAS in case studies was 65.73 (range 20-120). The mean score for studies on groups of children with FAS or alcohol exposure was 72.26 (range 47.4-98.2). Streissguth et al (3) studied a group of individuals with histories of prenatal alcohol exposure ranging in age from 6-51 years. They reported a mean IQ score of 79 (borderline MR) for 178 individuals with FAS. They also reported an average IQ of 90 (range 49-142) for individuals prenatally exposed to alcohol but not meeting criteria for FAS. This reflects the great variability in which prenatal alcohol exposure can affect the CNS and highlights the fact that some individuals without the facial dysmorphology required for a diagnosis of FAS may suffer from significant intellectual deficits. Mattson and Riley (10) (285), "... high levels of prenatal alcohol exposure are related to an increased risk for deficits in intellectual functioning and these deficits can occur in children without all of the physical features required for a diagnosis of FAS."

As noted above, most children with FASD do not have MR. However, an IQ score in the low-average or even average range does not preclude the presence of debilitating neurocognitive deficits or mental health problems. In the presence of average cognitive ability, other neurocognitive deficits are often not identified through traditional cognitive testing. The unfortunate but common consequence is that many children with prenatal alcohol exposure will not qualify for spedal education services on the basis of basic psychological testing. More spedalized, neuropsychological testing is often necessary to document deficits in executive functioning (EF) that affect a child's ability to function successfully in a school setting.

Individuals with FASD who perform in the average range on traditional IQ tests often show significant deficits on tasks that specifically challenge the executive functions of the brain. (12) EF includes the cognitive skills involved in planning, sequencing, appropriate use of feedback in response selection, set shifting, cognitive flexibility, ability to inhibit, concept formation, and reasoning. (1,21) Research studies have demonstrated deficits in EF in samples of full-FAS and non-FAS, alcohol-exposed individuals in comparison with controls. (1,18) Interestingly, individuals with full FAS demonstrate EF deficits similar to those of alcohol-exposed individuals without a FAS diagnosis. (220 The deficits in EF (planning, organization, attention) directly translate into dysfunctional behavior and problems with daily functioning. In fact, Kodituwakku et al (22) found a predictive relationship between neuropsychological measures of EF and behavioral problems in alcohol-exposed children.

Individuals with FASD often demonstrate a lack of inhibition, impulsivity, poor judgment, and great difficulty learning from consequences. (4,22,23) The concrete thinking style of alcohol-exposed individuals reflects a lack of cognitive flexibility and is sometimes expressed through an inability to generalize rules and difficulty in social interactions. Social cues are often misread as a result of the misinterpretation of a joke or sarcastic comment. For example, the child with FASD may not stop what he is doing in response to a directive by a peer to "cut it out!" Many parents also report difficulties with holding multiple directions in mind and carrying them through. For example, a task such as pick up your shoes, put your book bag away, and set the table for dinner may be problematic.

Academic achievement and learning are also negatively affected by prenatal alcohol exposure. Exposure to alcohol in the first and second trimesters has been associated with lower overall academic achievement. Specifically, lower reading scores were predicated by second trimester binge drinking. (24) The literature also suggests difficulties with spatial and verbal memory and learning. (4,10) Furthermore, Streissguth and her colleagues noted academic deficits in phonological processing and arithmetic. (4,17) Finally, difficulties with attention and impulsivity that are strongly associated with prenatal alcohol exposure will further affect a child's ability to learn in the classroom.

Emotional and Behavioral Issues

In addition to the neurocognitive effects, prenatal alcohol exposure is associated with serious mental health problems including debilitating emotional and behavioral disorders and substance abuse problems. Streissguth et al (3) reported that mental health problems were present in 94% of their sample of children and adults with prenatal alcohol exposure. Children with prenatal alcohol exposure present with a complex diagnostic picture and a wide variety of psychological symptoms including hyperactivity, emotional disorders, sleep disorders, behavior problems (aggression, inappropriate sexual behavior, delinquency, self-injury), social skill deficits, and abnormal habits and stereotypes. (25-27) Individuals with FASD carry a broad range of psychiatric diagnoses. O'Connor et al (13) report psychiatric diagnoses in 87% of a sample of 5-13 year olds with prenatal alcohol exposure. Hyperactivity and attention problems are some of the most frequently reported symptoms associated with prenatal alcohol exposure and have been examined thoroughly in the research literature. (18,26,28) Reported diagnoses include attention deficit hyperactivity disorder (ADHD), depression, oppositional defiant disorder, conduct disorder, anxiety disorders, obsessive compulsive disorder, and bipolar disorder. (13,25) Significant deficits in social behavior including aggression and inappropriate sexual behavior are also associated with prenatal alcohol exposure. (29) Children affected by prenatal alcohol exposure also suffer from internalizing symptoms such as low self-esteem, social isolation, and mood disorders. (13,25) Studies on adaptive behavior and social skills of children with prenatal alcohol exposure have documented deficits in these areas as well. (27,29-31)

One protective factor for individuals with FASD identified by Streissguth et al (3) is early diagnosis and intervention. They discovered that children who were diagnosed by the age of 6 were less likely to suffer many secondary disabilities. Diagnosis is the first of many steps in helping families and children cope with this disability. Accurate diagnosis will help family members and professionals design appropriate services and help community members understand sometimes perplexing behaviors. (3) The importance of providing appropriate psychological, medical, educational, and developmental services for children with prenatal alcohol effects cannot be overstated. Early diagnosis and intervention is key in helping children with FASD function and cope with the severe neuropsychological, social, and emotional disabilities they experience.


Children with prenatal alcohol exposure struggle with cognitive, academic and social, emotional, and behavioral challenges. These challenges are particularly evident in the school setting and negatively affect children's ability to learn and function successfully in the school environment. Regular education teachers, special education providers, school psychologists, school counselors, speech/language pathologists, occupational therapists, other specialists, support staff, and administrators are called upon to support children with FASD in schools so that they experience academic and social success. Once identified, the child with FASD will require unique interventions that address his/her brain differences affecting academic, emotional, and behavioral functioning.

Effective interventions must consider the interplay between behavioral symptoms and the neuropsychological effects of prenatal alcohol exposure. As noted above, EF deficits are directly linked to challenging behaviors. (22,32) Instead of viewing a child's difficulties as behavior problems as a result of the child being "defiant," "lazy," "intentional," or "manipulative," these behaviors should be viewed as symptoms of underlying neurocognitive deficits in EF. Interventions

will then focus on using a variety of strategies to teach the child new skills and to utilize extensive environmental modifications to support the use of new skills. The use of basic behavioral principles such as positive reinforcement and natural consequences will only be effective if EF limitations have been addressed. (32)

To support children with FASD to function effectively in the classroom, intervention plans will call upon strategies and ideas from literature in Positive Behavior Support (PBS) programming, (33) cognitive-behavioral therapy, and interventions for child behavior disorders such as ADHD. (34) Watson and Westby (32) have proposed interventions that draw from many of these approaches and specifically address EF deficits in children exposed to alcohol and other drugs. For example, they recommend the use of visual cues and schedules, teaching of self-directed speech and problem solving, social skills training, role play, cognitive modeling and coaching to support EF difficulties in the areas of nonverbal memory, internalization of self-directed speech or verbal working memory, self-regulation of mood, motivation, and level of arousal and problem solving. (32) Likewise, the PBS approach is particularly valuable. As described by Bambara and Kern, (33) the PBS model focuses on identifying specific problem behaviors, the environmental and/or setting events that contribute to the problem behaviors, and understanding the function or communicative intent of the problem behaviors. Interventions are focused on changing antecedent and setting events and teaching more appropriate and functional behaviors. A collaborative team approach that includes all service providers and educators as well as the individual's family and the individual himself/herself is used to develop and implement the PBS plan.

In designing interventions, children with FASD need opportunities to learn and build skills that will help them regulate their emotions and behaviors as well as environmental modifications that increase the likelihood of adaptive behaviors. Interventions to support emotional and behavioral regulation must focus on modifying the environment and providing structure and consistency in daily routines and rules. The use of detailed visual schedules and a detailed visual presentation of rules that cue appropriate behavior are recommended. Children with prenatal alcohol exposure will respond best to concrete rules that specify the appropriate or desired behavior. Displaying these rules with visual prompts such as a picture of the child engaging in the desired behavior will assist with understanding and behavioral follow-through. Visual prompts must be positioned in close proximity to the child, such as on his/her desk.

Successful interventions will need to balance the use of environmental modifications, immediate and meaningful positive and negative consequences for behaviors, and opportunities to teach children skills to monitor and modify their behavior. Environmental modifications with visual prompts might involve placing a sign, made by the child, on a door to remind him that he/she is not permitted in that room or a stop sign to remind the child not to leave the room. It is important for teachers, parents, and other school professionals to be aware of how aspects of the environment that may not be obvious may affect a child's behavior in school. Reductions of distractions through the use of study carrels or headphones are examples of environmental modifications that can be used in schools. The positioning of a child's desk away from a particular distraction (such as a door, peer, air-conditioning unit) or near to a stimulus that helps with attention (teacher, peer) may be helpful.

Immediate feedback for both positive and negative behaviors will be helpful in reducing challenging behaviors and teaching more appropriate behaviors. Positive feedback and praise are imperative for reinforcing desired behaviors. Caregivers and teachers must make an effort to "catch'em being good" and reward children for positive behaviors quite frequently. The child's team of professionals and caregivers can identify a limited number of target behaviors and provide frequent monitoring and reinforcement for appropriate behavior. Initially, the reinforcement may need to be provided in very small (1 minute) time increments. When considering how and whether to provide feedback for negative behaviors, caregivers and educators will want to first consider how the environment could be modified to assist the child in engaging in an alternative behavior and what skills the child may need to learn to engage in the alternative behavior. If negative consequences are to be administered, they must be administered immediately after the negative behavior occurs and must be designed with care not to inadvertently reinforce the negative behavior through escape or avoidance of undesirable activities. (33)

A lack of understanding abstract concepts such as time and cause and effect often leads to challenging behaviors. Difficulties understanding cause and effect relationships can be addressed through concrete examples using pictures and stories to illustrate abstract relationships. For example, the relationship between cleaning up toys, completing an assignment, or raising one's hand before talking and receiving a reward could be illustrated visually. The use of concrete prompts such as timers and stopwatches can help children understand concepts related to time and waiting. Multiple warnings (verbal, visual) that specify an amount of time before a transition and transitional objects will assist with time concepts and transition difficulties. Verbal signals and visual schedules help the child to feel more comfortable in moving from one activity to the next. Transitional objects further assist with increasing predictability for the child by providing a different type of signal for what is coming next.

Children with FASD need to learn new skills to effectively manage their behavior and emotions. The use of cognitive-behavioral strategies, such as social skills training, emotion identification, coping skills, anger management, and self-talk, may be helpful for children with FASD. However, many of the children will require ongoing environmental modifications and support to be able to use such strategies. The concept of the "external brain" has been suggested by Dr. Sterling Clarren (35) to reflect the need for parents, caregivers, and teachers to act as an "external brain," providing ongoing support in the areas of EF and emotional and behavioral control. This support may come in the form of environmental modifications, making abstract rules more concrete, teaching individuals to ask for help, and providing ongoing supervision and prompts for self-monitoring. While many individuals with prenatal alcohol exposure will need some level of support throughout their lives, more research is needed to develop intervention programs for children in the early childhood years that teach them strategies to improve self-regulation and emotional and behavioral control that will generalize as they grow older.


In summary, prenatal alcohol exposure has significant adverse effects on cognitive, emotional, and behavioral functioning. Not all children with FASD will carry a formal diagnosis of FAS. However, the brain damage associated with prenatal exposure may occur independently of physical characteristics. Children with FASD are at risk for difficulties in school related to challenges in academics, EF, attention, social skills, and behavioral control. Early diagnosis and intervention is key in helping children with FASD succeed in a school setting. All service providers, school professionals, and family members must work as a team to develop unique interventions that take into account the child's brain differences that are associated with prenatal alcohol exposure. Effective interventions will include environmental modifications and supports, positive feedback for appropriate behaviors, and opportunities to learn new skills.


(1.) Mattson SN, Goodman AM, Caine C, Delis DC, Riley EP. Executive functioning in children with heavy prenatal alcohol exposure. Alcohol Clin Exp Res. 1999;23(11):1808-1815.

(2.) Mattson SN, Schoenfeld AM, Riley EP. Teratogenic effects of alcohol on brain and behavior. Alcohol Res Health. 2001;25(3): 185-191.

(3.) Streissguth A, Barr H, Kogan J, Bookstein F. Understanding the Occurrence of Secondary Disabilities in Clients With Fetal Alcohol Syndrome (FAS) and Fetal Alcohol Effects (FAE): Final Report for Center for Disease Control & Prevention. Seattle: University of Washington; 1996.

(4.) Streissguth AP, Barr HM, Bookstein FL, Sampson PD, Olson HC. The long-term neurocognitive consequences of prenatal alcohol exposure: a 14-year study. Psychol Sci. 1999;10(3):186-190.

(5.) Substance Abuse & Mental Health Administration (SAMHSA) Fetal Alcohol Spectrum Disorders (FASD) Center for Excellence. What You Need to Know: Understanding Fetal Alcohol Spectrum Disorders: Getting a Diagnosis. Rockville, Md: Center for Substance Abuse Treatment, Substance Abuse and Mental Health Services Administration; 2005.

(6.) Sampson PD, Streissguth AP, Bookstein FL, et al. Incidence of fetal alcohol syndrome and prevalence of alcohol-related neurodevelopment disorder. Teratology. 1997;56(5):317-326.

(7.) Jones KL, Smith DW, Ulleland CN, Streissguth P. Pattern of malformation in offspring of chronic alcoholic mothers. Lancet. 1973;1 (7815):1267-1271.

(8.) Bertrand J, Floyd RL, Weber MK, et al. Fetal Alcohol Syndrome: Guidelines for Referral and Diagnosis. Atlanta, Ga: Centers for Disease Control and Prevention; 2004.

(9.) Sowell ER, Mattson SN, Thompson PM, Jernigan TL, Riley EP, Toga AW. Mapping callosal morphology and cognitive correlates: effects of heavy prenatal alcohol exposure. Neurology. 2001;57(2):235-244.

(10.) Mattson SN, Riley EP. A review of the neurobehavioral deficits in children with fetal alcohol syndrome or prenatal exposure to alcohol. Alcohol Clin Exp Res. 1998;22(2):279-294.

(11.) Olson HC, Feldman JJ, Streissguth AP, Sampson PD, Bookstein FL. Neuropsychologicai deficits in adolescents with fetal alcohol syndrome: clinical findings. Alcohol Clin Exp Res. 1998;22(9):1998-2012.

(12.) Kerns K, Don A, Mateer CA, Streissguth AP. Cognitive deficits in nonretarded adults with fetal alcohol syndrome. J Learn Disabil. 1997;30(6):685-693.

(13.) O'Connor M J, Shah B, Whaley S, Cronin P, Gunderson B, Graham J. Psychiatric illness in a clinical sample of children with prenatal alcohol exposure. Am J Drug Alcohol Abuse. 2002;28(4):743-754.

(14.) May PA, Gossage JP. Estimating the prevalence of fetal alcohol syndrome: a summary. Alcohol Res Health. 2001;25(3):159-167.

(15.) Stratton K, Howe C, Battaglia F, eds. Fetal Alcohol Syndrome: Diagnosis, Epidemiology, Prevention, and Treatment. Institute of Medicine, Washington, DC: National Academy Press; 1996.

(16.) Abel EL, Sokol RJ. Incidence of fetal alcohol syndrome and economic impact of FAS-related anomalies. Drug Alcohol Depend. 1987; 19(1):51-70.

(17.) Olson HC, Streissguth AP, Sampson PD, Barr HM, Bookstein FL, Thiede K. Association of prenatal alcohol exposure with behavioral and learning problems in early adolescence. J Am Acad Child Adolesc Psychiatry. 1997;36(9):1187-1194.

(18.) Kodituwakku PW, Handmaker NS, Cutler SK, Weathersby EK, Handmaker SD. Specific impairments in self-regulation in children exposed to alcohol prenatally. Alcohol Clin Exp Res. 1995;19(6):1558-1564.

(19.) Uecker A, Nadel L. Spatial but not object memory impairments in children with fetal alcohol syndrome. Am J Ment Retard. 1998;103(1):12-18.

(20.) Mattson SN, Riley EP, Dells DC, Stern C, Jones KL. Verbal learning and memory in children with fetal alcohol syndrome. Alcohol Clin Exp Res. 1996;20(5):810-816.

(21.) Kodituwakku PW, Kalberg W, May PA. The effects of prenatal alcohol exposure on executive functioning. Alcohol Res Health. 2001;25(3):192-198.

(22.) Kodituwakku PW, May PA, Clericuzio CL, Weers D. Emotion-related learning in individuals prenatally exposed to alcohol: an investigation of the relation between set shifting, extinction of responses, and behavior. Neuropsychologia. 2001;39(7): 699-708.

(23.) Olson HC, Morse B, Huffine C. Development and psychopathology: fetal alcohol syndrome and related conditions. Semin Clin Neuropsychiatry. 1998;3(4):262-284.

(24.) Goldschmidt L, Richardson GA, Cornelius MD, Day NL. Prenatal marijuana and alcohol exposure and academic achievement at age 10. Neurotoxicol Teratol. 2004;26(4):521-532.

(25.) Burd L, Klug MG, Martsolf JT, Kerbeshian J. Fetal alcohol syndrome: neuropsychiatric phenomics. Neurotoxicol Teratol. 2003;25(6):697-705.

(26.) Mattson SN, Riley EP. Parent ratings of behavior in children with heavy prenatal alcohol exposure and IQ-matched controls. Alcohol Clin Exp Res. 2000;24(2):226-231.

(27.) Steinhausen H. Psychopathology and cognitive functioning in children with fetal alcohol syndrome. In: Spohr H, Steinhausen H, eds. Alcohol, Pregnancy, and the Developing Child. Cambridge: Cambridge University Press; 1996:227-248.

(28.) Coles CD, Platzman KA, Raskind-Hood CL, Brown RT, Falek A, Smith IE. A comparison of children affected by prenatal alcohol exposure and attention deficit, hyperactivity disorder. Alcohol Clin Exp Res. 1997;21(1):150-161.

(29.) Kelly S J, Day N, Streissguth AP. Effects of prenatal alcohol exposure on social behavior in humans and other species. Neurotoxicol Teratol. 2000;22(2): 143-149.

(30.) Thomas SE, Kelly S J, Mattson SN, Riley EP. Comparison of social abilities of children with fetal alcohol syndrome to those of children with similar IQ scores and normal controls. Alcohol Clin Exp Res. 1998;22(2):528-533.

(31.) Whaley SE, O'Connor MJ, Gunderson B. Comparison of the adaptive functioning of children prenatally exposed to alcohol to a nonexposed clinical sample. Alcohol Clin Exp Res. 2001;25(7):1018-1024.

(32.) Watson SMR, Westby CE. Strategies for addressing the executive function impairments of students prenatally exposed to alcohol and other drugs. Commun Disord Q. 2003;24(4): 194-204.

(33.) Bambara LM, Kern L, eds. Individualized Supports for Students with Problem Behaviors. New York, NY: Guildford Press; 2005.

(34.) Barkley RA. Attention-Deficit Hyperactivity Disorder: A Handbook for Diagnosis and Treatment. 2nd ed. New York, NY: Guilford Press; 1998.

(35.) Doctor S. Creating an "external brain": supporting a mother and child with FAS. In: Kleinfeld J, ed. Fantastic Antone Grows Up. Fairbanks: University of Alaska Press; 2000:115-126.

Visiting Assistant Professor, (, Department of Psychology, Miami University, Oxford, OH 45056.

Address correspondence to: Jennifer H. Green, (, Department of Psychology, Miami University, Oxford, OH 45056.
COPYRIGHT 2007 American School Health Association
No portion of this article can be reproduced without the express written permission from the copyright holder.
Copyright 2007 Gale, Cengage Learning. All rights reserved.

Article Details
Printer friendly Cite/link Email Feedback
Author:Green, Jennifer H.
Publication:Journal of School Health
Geographic Code:1USA
Date:Mar 1, 2007
Previous Article:Pregnant teenagers and teenage mothers: how much they really know about the risks to children's health associated with smoking during and after...
Next Article:Academic performance and substance use: findings from a state survey of public high school students.

Terms of use | Privacy policy | Copyright © 2018 Farlex, Inc. | Feedback | For webmasters