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2 EPIDEMIOLOGY OF ALCOHOL-RELATED PROBLEMS Alcohol use has been associated with a wide range of physical and social problems including disease, accidental and intentional violence, homelessness, unemployment, and marital discord. Awareness of the variety and magnitude of alcohol-related problems has led prevention research to move from a primary focus on severe problems of alcohol dependence toward the identification of multiple and interdependent mechanisms that underlie risks for specific problems. This can eventually lead to more effective approaches to early identification and preventive intervention. For some problems (e.g., cirrhosis), the causal role of alcohol is well understood. In many other cases, however, little is known about the nature and extent of alcohol's contribution to problem outcomes. For example, many studies demonstrate that victims of trauma had a history of alcohol abuse or were exposed to alcohol when injury occurred; yet the process of developing effective interventions is constrained because the mechanisms through which alcohol use causes traumatic events are not thoroughly understood. Moreover, the inability to identify the specific risk attributable to alcohol use for such events as automobile crashes limits the ability to design evaluations for interventions. In the sections that follow, the committee summarizes current knowledge about the epidemiology of a number of alcohol-related problems and identifies some of the gaps to be addressed in future research. The reader should note that this discussion is not meant to be comprehensive because many of these areas were discussed in the earlier report (IOM, 1987 see Chapters 3 and 10~. Rather, as noted in the report's introduction, this chapter aims to update the earlier information or, in some cases, to augment the previous discussion of a topic with information that has recently become available. INJURIES Injuries are a leading cause of morbidity and mortality in the United States and the most frequent cause of death among children, adolescents, and young adults. Automobile crashes are the single largest cause of death involving alcohol and perhaps the most studied. In 1987 there were 41,435 fatal crashes nationwide. It is well documented that as many as 50 percent of fatal car crashes involve alcohol, resulting in more than 20,000 fatalities annually (Zobeck, 1986; NIAAA, 1987~. People under the age of 25 are at particular risk for alcohol-related crashes. In 1984, 16 to 24 year aids constituted 20 percent of the population but accounted for 35 percent of drinking driver deaths (Zobeck, 1986~. Alcohol also has a demonstrated association with the risk of injury from falls (Honkanen et al., 1983; Hingson and Howland, 1987a) and drowning (Howland and Hingson, 1988~. Although estimates vary, evidence indicates that about half of all fire and burn deaths are associated with alcohol use, and from 25 to 50 percent of drowning may be the result of drinking. Alcohol may contribute to injury in a number of ways. Drinking impairs judgment and therefore may result in incautious exposure to inherently dangerous situations (e.g., reckless -31

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driving). Alcohol also impairs information processing and physical coordination, and can reduce an individual's ability to deal with threatening circumstances that are not necessarily attributable to his or her own actions. Finally, alcohol affects certain physiological functions (e.g., blood coagulation) and may contribute to the severity or outcome of an injury. Methodological Problems in Studying Alcohol-Related Injuries Determining the causal role of alcohol in traumatic events presents methodological difficulties. Investigations of the association between drinking and injury fall into four basic categories. Type I studies are descriptive and report alcohol exposure in a series of events (e.g., emergency room cases, coroner series, insurance-reported deaths). These studies provide no comparison groups and therefore no estimate of the risk associated with exposure. Type II studies compare the incidence of injury among populations being treated for alcohol abuse with the incidence among standard populations. Type III studies compare the frequency of the presence of alcohol in injury victims with the frequency of alcohol among cases of illness or death owing to natural causes. Type IV studies compare exposure to alcohol among injury victims with alcohol exposure among comparable, uninjured persons who are selected when they appear at the site of the injury at the same time of day as the injury occurred but at a later, predetermined time (e.g., one week later). Although there is a sizable literature on the contribution of alcohol to injuries, inferences about causal linkage must be approached with caution. For example, Type I studies determine the frequency of exposure among victims but not among nonvictims. Let us assume that a study finds that 30 percent of cases of injury from a violent event are positive for alcohol. Without knowledge of alcohol exposure among a comparable group of noninjured persons, it is difficult to determine the extent to which alcohol contributed to the injuries, if at all. Thus, Type I studies provide only part of the evidence needed to establish causality. Unfortunately, these studies are often presented as proof of the alcohol-injury relationship. Type I! studies often provide evidence that individuals who abuse alcohol are more likely to experience injuries than the general population. In this case, the general population provides the comparison group missing from Type I studies. These outcomes may be confounded, however, because we cannot assume that alcohol abusers-- except for their drinking habits and their propensity for injury--are in all ways like the general population. For instance, persons who chronically abuse alcohol may have individual characteristics that both increase their likelihood of substance abuse and increase their likelihood of experiencing violence. Alcohol abuse may be associated with lower socioeconomic status, which in turn may be associated with living conditions (poor housing or poor neighborhoods) in which the likelihood of unintentional or intentional violence is greater than the living conditions of the general public, regardless of the victim's exposure to alcohol. Here, an association between alcohol abuse and injury may be spurious because both are caused by a third factor (i.e., economic status). Type III studies use as controls those who died or accessed medical treatment because of illness as opposed to injury. Yet differences between the injured and the ill may be biased because ill persons may be less apt to consume alcohol than the general population. If this were so, the apparent association between alcohol and injury would be inflated. -32

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Type IV studies provide the most persuasive evidence of the alcohol-injury linkage. By comparing the frequency of exposure among cases to that of controls (matched in terms of demographics and the circumstances under which the injury took place), the kinds of bias associated with studies of Type I, II, or III are reduced. Unfortunately, Type IV studies are rarely conducted, owing in part to their logistical difficulties. Nevertheless, some Type IV studies have been conducted and have helped to establish a causal association between alcohol and vehicular injury. One problem in the study of the relationship between drinking and injury is the difficulty of determining with any degree of certainty the specific events or alcohol exposure involved in a given case. Event ascertainment is apt to be relatively complete for coroner studies (although this statement assumes that most victims of violence are located). However, in some jurisdictions, testing for alcohol at an autopsy is done at the coroner's discretion that is, when the coroner has reason to believe that alcohol contributed to the injury. If the only cases studied are those for which alcohol testing has been performed, it is possible that a disproportionate number of cases will be positive simply because only cases in which alcohol involvement was suspected were included. This bias would overestimate the alcohol-injury association. Similarly, in studies of emergency room patients, submitting to a test for alcohol is at the discretion of the victim. If a refusal to take the test was associated with alcohol exposure among injury cases (injuries often raise questions of responsibility for the event) but was less associated with alcohol among noninjured controls, the association between alcohol and injury would be understated. Another confounding factor is that inebriated persons may be less likely to seek medical attention for injuries, or more likely to delay seeking treatment, than injured persons who have not been drinking. In the first instance, alcohol-associated injuries would not be counted; in the second, some alcohol-related injuries would be incorrectly counted as no exposure to alcohol because the alcohol had been metabolized in the time during which treatment was delayed. In either case, the alcohol-inju~y association would again be understated. Ascertaining both event and alcohol exposure is a particular problem in studies of intentional violence in which the object of the study is alcohol exposure among perpetrators. First, the perpetrator is often never apprehended and therefore cannot be tested for alcohol. Alternatively, apprehension may take time, during which the alcohol that was present. at the event has been metabolized. On the other hand, inebriated criminals may be more likely to be caught, or to be caught quickly, because of impairments in judgment or mobility or because of other alcohol-related behaviors that draw attention to them. Thus, studies that show an association between intentional injury (e.g., assault or homicide) and alcohol exposure may actually be measuring the effect of alcohol on apprehension rather than an association between alcohol and the propensity for criminal violence. There are also other methodological problems in studies to determine alcohol-injury association. For example, few studies of this kind are conducted "blind. More often than not, the observers are aware of the intent of the study and may unwittingly distort information. Moreover, the consistency of research results may vary greatly depending on how or if alcohol exposure is personalized. Some studies base exposure on self-reports, whereas others define measured exposure (breathalyser readings or blood alcohol levels) differently Positive may mean a trace of alcohol or exposure beyond a specified level). -33

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Finally, few studies document carefully the temporal sequence of events, a lack that is important for several reasons. First, alcohol may have been ingested after the event (to Steady nerves or "kill the pains) but before observation. Second, the length of time between exposure and observation will affect the level of exposure because alcohol is metabolized relatively quickly. Third, in cases of fatality, decomposition generates alcohols through fermentation. Sophisticated techniques are required to distinguish between these alcohols and ingested alcohols. It may be concluded from the above discussion that, although it appears that alcohol consumption is causally related to excess numbers of injuries, any demonstration of the magnitude of that relationship presents very difficult methodological problems. Such difficulties include the determination of appropriate "cases," measurement of the extent of alcohol exposure, determination of the temporal sequence of exposure and incident, and distinguishing between the effect of alcohol on the likelihood of apprehension and its effects on the propensity to cause injury. The sections below present selected recent studies on the association between exposure to alcohol and the occurrence of various kinds of injuries. Vehicular Injuries Traffic crashes are the leading cause of death in the age group 1-34 years (Ross, 1982~. From 1980 to 1985, fatal crashes declined 13 percent nationwide, from 45,284 in 1980 to 39,168 in 1985; in 1986, however, they increased 5 percent, to 41,062; and in 1987 they increased 6 percent to 41,435. Alcohol is unquestionably a major contributor to these crashes. In 1986, 23,987 traffic deaths, 52 percent of the total, involved a driver or pedestrian who had been drinking; 16,728, or 36 percent of the total involved someone with a blood alcohol level above 0.10 percent (Fell and Klein, 1986~. Many of the victims of drunk driving crashes were not drinking at the time of the events, and more than one-third of alcohol-related vehicular deaths were persons other than drinking drivers (i.e., passengers, other drivers, or pedestrians). There is evidence that individuals who are at risk for drunk driving are also at risk for other behaviors that contribute to vehicular injury. For example, a survey of young (aged 18-25) New England drivers showed that 54 percent of drivers who reported driving in the last month after drinking four or more drinks also drove after marijuana use; only 11 percent of drivers who had not driven in the last month after drinking drove after marijuana use LEE < .001) (Hingson and Howland, 1987b). In this study, only 1 percent of drivers who reported driving in the last month after drinking four or more drinks always wore seat belts; in comparison, 13 percent of drivers who had not driven in the last month after drinking always wore seat belts LED < .001~. Almost half (45 percent) of drivers who reported driving in the last month after four or more drinks reported speeding (at least 20 miles per hour over the limit) in the past week; 21 percent of drivers who had not driven in the last month after drinking reported speeding during the past week LEE < .001~. Of drivers who reported driving in the last month after four or more drinks, 38 percent reported running at least one red light in the past week; this was true for only 14 percent of drivers who had not driven after drinking in the last month. -34

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Falls Each year, approximately 13,000 deaths in the United States are attributed to falls. Only motor vehicle crashes and firearms surpass falls as causes of fatal injuries (Baker, O'Neill, and Karpf, 1984~. Laboratory studies have demonstrated several mechanisms by which alcohol could contribute to falls. For example, studies using the Romberg test (a technique used to study the neuromuscular effects of alcohol, which measures the ability to stand upright without swaying) have found that all individuals who were tested exhibited a significant amount of swaying at blood alcohol concentrations (BACs) greater than 100 mg/dl (milligrams per deciliter) or 0.1 gram percent; however, many were affected at much lower levels (Perrine, 1973~. Other studies have shown that persons with BACs above 100 mg/dl have lowered divided attention performance, reduced visual acuity (Perrine, 1973), and reduced adaptation to brightness and glare (Adams and Brown, 1975~. Moreover, alcohol is known to affect judgment and thus increase risk-taking behavior according to the National Highway Traffic Safety Administration (NHISA, 1985~. In related research, Smart (1969) has shown that chronic alcohol abusers experience higher than expected rates of vehicular injuries even when sober. This finding suggests that either some unidentified factor (e.g., personality) contributes to both accidents and alcohol abuse or that chronic abuse has long-term neurological or physiological effects that increase a person's risk of injury. On the basis of clinical observation, Summerskill and Kelly (1963), for example, have suggested that alcohol abuse contributes to osteoporosis. Thus, some sober alcoholics may fall as a result of spontaneous fractures. Hingson and Howland (1987a) reviewed the English language literature on the alcohol-fall relationship. Twenty-one studies conducted in eight countries between 1950 and 1985 were identified. Most were Type I studies, reporting on the frequency of alcohol exposure among fall victims. Among these studies, the percentage of fatal falls involving alcohol ranged from 20 to 77 percent. The percentage of falls treated in emergency rooms (people alive on arrivals ranged from 17 to 53 percent. Type II studies comparing the incidence of falls among treated alcoholics with the incidence among a standard population (adjusted for age, sex, and nationality) reported ratios (observed to expected rates of fatal falls) from 2.9 to 16. Type III studies comparing alcohol exposure among fall victims with alcohol exposure among cases of illness or death resulting from natural causes reported that fall victims were from 2.5 to 10 times more likely to have been drinking than nontrauma comparison cases. There has been one casecontrol (i.e., Type IV) study of alcohol and falls (Honkanen et al., 1983~. This study compared blood alcohol content (and other variables) among fall victims who were treated in emergency rooms with controls who were selected by visiting each accident site at the same time of day exactly one week after each event: 53 percent of patients injured in accidental falls in the evening in Helsinki--and 15 percent of time-, site-, and sex-matched control pedestrians--were alcohol involved. The relative risk (on a scale of 1.0 at zero BAC) did not increase at BACs less than 50 mg per 100 milliliters (ml) was about 3 at BACs of 50-100 mg/100 ml, about 10 at BACs of 100-150 mg/100 ml, and about 60 at BACs of 160 mg/100 ml or higher. The authors of this definitive study concluded that the risk at BACs above 100 mg/100 ml was so high that practically all cases -35

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with such BACs can be considered to have been caused by alcohol. Drownings In the United States, drowning ranks third among causes of accidental death (Baker, O'Neill, and Karpf, 1984~. Approximately 7,200 Americans drown each year in a variety of settings (oceans, inland waters, bathtubs, swimming pools) and under a variety of circumstances (swimming, fishing, boating, diving, driving). Several observations suggest that alcohol contributes to some of these drownings. For example, drowning are much more apt to involve powerboats than sailboats (Dietz and Baker, 1974), and powerboats involve speed and require skills that are similar to those required for driving. Because it is well documented that drinking increases the risk of vehicular injury, it is reasonable to suppose that alcohol also contributes to powerboat accidents. Similarly, because there is substantial evidence that alcohol contributes to falls, it is likely that alcohol contributes to drownings that result from falls into the water (from shore, boats, or Pierson --, rat - ~~~ ~~~~~~~ ~~~~' ~~ ~~~~ ~-~~~~' preservers (just as drunk drivers are less likely to wear safety belts). In addition. persons who drink mav be less likely to wear life Alcohol may also contribute to drowning in somewhat less direct ways. For example, it creates a sensation of warmth and may lead some swimmers to remain in the water too long and develop hypothermia. There is evidence that when the chest and abdomen are exposed to cold water, breathlessness and severe hyperventilation often result (Keatings and Evans, 1961~. These reactions could limit a person's ability to swim or cause him or her to inhale water as a result of uncontrolled breathing. In addition, immersion in cold water increases venous pressure and pulse, and could lead to cardiovascular collapse through ventricular fibrillation (Giersten, 1970~. The Coast Guard has conducted tests demonstrating that environmental ~stressors" (e.g., sun, wind, glare, vibrations, wave motion associated with water activities) may work synergistically with alcohol in degrading an individual's performance (Wright, 1985~. Alcohol may also increase the risk of caloric labyrinthitis, an inner ear disturbance associated with sudden temperature drop. It has been suggested that this condition may cause a person who is unexpectedly submerged to become disoriented and swim down rather than up (Transportation Research Board, 1985~. Alcohol may retard laryngospasm when water is aspirated; it may also weaken the diving response or inhibit the body's response to increasing asphyxial blood-gas exchanges, or both (Gooden, 1984~. Alcohol may heighten depression or anxiety in some individuals, thereby contributing to suicides by drowning. Finally, sober persons may drown as a result of the actions taken by others who are under the influence of alcohol. A number of Type I studies of the frequency of alcohol exposure among drowning victims have been reported. The best of these suggest that 29 to 47 percent of the victims were exposed to alcohol (Howland and Hingson, 1988~. Wailer (1972) conducted a careful Type III study of nonhighway injury fatalities in Sacramento: 17 submersion deaths were included, of which 5 (29 percent) were positive for alcohol on autopsy. In the study, Wailer matched injury fatalities with fatalities from nontraumatic cases. Of the matched controls, 67 (18 percent) of 371 were positive for alcohol. Thus, drowning victims were almost twice as likely as controls to have been drinking. --or -36

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Fires and Burns Fires and burns rank fourth among the causes of unintentional deaths in the United States. About 6,000 deaths annually are attributed to fires and burns (Baker, O'Neill, and Karpf, 1984) (this figure excludes approximately 500 deaths that result from vehicular and plane crash fires): 75 percent of fire and burn fatalities result from conflagrations, of which 85 percent are house fires (National Safety Council, 1984), and half of all house Ores are blamed on cigarettes (Birly and Clarke, 1981~. Drinking may thus contribute directly to fires when, for example, a victim becomes unconscious while smoking. Intoxication may also exert indirect effects by preventing a victim from hearing or correctly interpreting alarms of fires caused by others. Similarly, excessive alcohol consumption may impair the ability to escape from a fire once it has started. Alcohol may contribute to fire and burn injuries in other ways. By decreasing a person's cognitive or neurological skills (e.g., balance), alcohol may also decrease his or her avoidance of inherently dangerous situations or cause burns as a result of falls into or against hot objects. There is some evidence that alcohol works synergistically with toxic gases, such as carbon monoxide, in accelerating behavioral incapacitation (Mitchell, Packham, and Fitzgerald, 1978~. Finally, several studies suggest that hepatic dysfunction from chronic alcohol abuse decreases the probability of surviving serious burns (Rittenbury et al., 1965; Crikelair et al., 1968~. A number of studies (Type I) indicate the percentage of fire and burn victims who have been exposed to alcohol. Of these, the most reliable studies report that between 37 and 64 percent of fire or burn casualties had been drinking (Howland and Hingson, 1987~. Ho Type II studies provide estimates of risk for fire deaths among treated alcoholics in comparison with members of standard populations. One of these (Schmidt and deLint, 1972) found that alcoholics were almost 10 times more likely to die in fires than were members of a standard population of comparable age and sex. Another (Combs-Orme et al., 1983) found that male alcoholics were 9.2 times more likely to die in fires. For women, the risk for alcoholics was 9.8 times that of the comparable population. In a similar study, Stephens (1985) compared alcohol exposure among burn victims treated in an emergency room with alcohol exposure in patients presenting with illness. She reported that victims of fires and burns were 2.75 times more likely than patients who were ill to have been drinking. A review of the literature on the role of alcohol in fire and burn deaths (Howland and Hingson, 1987) suggests that nearly half of those who die in fires are legally drunk at the time of their deaths. This observation is based on the relatively consistent results among 10 studies with complete blood alcohol testing. Although inferences about the causal role of alcohol in fire and burn injuries require some measure of exposure among noninjured persons, it seems clear that substantially less than 50 percent of the general population is intoxicated at any give time. Accordingly, there is convincing evidence that drinking is a risk factor in fire deaths. -37

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CRIME Studies indicate that alcohol is sometimes used by both the perpetrators and the victims of crimes immediately before the crime is committed. Alcohol is involved least in incidents of fraud, forgery, and embezzlement; it is most involved in homicides and assaults. In cases of violent crime (e.g., robbery, rape, homicide), the offender is more likely to have been drinking if the victim has been drinking. This association is stronger if the crime involves friends or acquaintances. For cases in which the crime occurs between strangers, the victim is more likely to have been drinking (Room, 1983~. In property crimes, alcohol is most often involved in unprofessional and unplanned crimes, and most often in incidents in which there are multiple perpetrators (Cordelia, 1985~. SUICIDE Suicide is one of the 10 leading causes of death in the United States for persons aged 34-54. Epically, some alcohol use is indicated in 35 percent of fatal suicides; 23 percent are intoxicated at the time of death (Roizen, 1982; U.S. Department of Health and Human Services, 1984; Abel and Zeidinberg, 1985~. Reviews of follow-up studies of alcoholics show suicide rates of 8-21 percent (Kendall, 1983; Berglund, 1984~. Yet many questions about the relationship between alcohol and suicide remain unanswered. There have been no studies comparing alcohol involvement among suicide attempters with alcohol involvement among suicide completers. Nor have studies assessed whether those committing suicide are more likely to drink than persons of comparable age, sex, and socioeconomic status (SES) who do not commit suicide. If, as seems likely, alcohol contributes to suicide, several questions come to mind. Is suicide attempted in part because the attempters are intoxicated and their judgment is impaired? Interviews with attempters could explore that question. Does chronic alcohol ingestion result in anxiety and depression that prompt suicidal thinking or in behavioral problems that socially isolate the potential suicide victim and reinforce a sense of guilt or worthlessness? It would be particularly useful to compare persons who are successfully treated for alcohol problems with those who are not successfully treated to see the extent to which the former may have lower subsequent suicide rates. CHILD ABUSE There is a widespread impression among direct service workers, which in turn is conveyed to the general public by the mass media, that child abuse and neglect are strongly associated with alcoholism and alcohol abuse. Literature reviews of this topic, however, indicate that research about possible associations between alcohol and child abuse has yielded contradictory findings (El-Guebaly and Offord, 1977; Epstein, Cameron, and Room, 1977; Hamilton and Collins, 1981; Orme and Rimmer, 1981~. It is certainly plausible that alcohol use could contribute to child abuse in that alcohol inhibits mechanisms that normally control aggressive, hostile, or violent impulses (Bennett, Buss, and Carpenter, 1975~. Alcohol use may also crowd out interpersonal relationships as a means of satisfying emotional need, and this could lead to child neglect. Alternatively, nonalcoholic parents -38

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or care givers with alcoholic spouses may be preoccupied with a spouse's drinking and exhaust energy that would otherwise be available for nurturing children. On the other hand, several researchers have observed that some drinkers become pacified by alcohol (Coleman and Strauss, 1983~. Unfortunately, there are no studies in the literature of interviewers who are blinded to the abuser status of those being interviewed. Without blinding, both interviewer and respondent bias may affect the interview results; either one might use alcohol to explain behavior that would have occurred even without it. Moreover, accurate measurements of drinking at the time of abuse are rarely, if ever, recorded. Only a few studies have included control groups of child abusers and nonabusers. Five reports found no association between alcohol use and child abuse (Steele and Polloch, 1968; Smith, Hanson, and Nobel, 1973; Ellwood, 1980; Herman and Hirschman, 1981; Emslie and Rosenfeld, 1983~. Four studies noted histories of alcohol abuse among child abusers (Bryant et al., 1963; Baldwin and Oliver, 1975; Rada, 1976; Ellwood, 1980), but this pattern was not significantly different from histories of alcohol use among nonabusers. Four other reports found alcohol abuse to be more pervasive among parents who abused children (Kaplan et al., 1983; Tarter et al., 1984; Famularo et al., 1986; Salzinger et al., 1986~. These studies would seem to indicate that research on the association between alcohol and child abuse warrants focused attention and more rigorous investigation by using blinded interviewers, quantification of alcohol consumption, and more designs that use non-child abuser control groups. SEXUALLY TRANSMITlED DISEASES Since the AIDS epidemic began, more than 90,000 cases of AIDS have been reported, nearly one-half of whom have died. Alcohol may play a role in HIV infection either by reducing the likelihood that people will employ safer sex practices or by increasing the likelihood that persons who are offered intravenous (IV) drugs will accept those drugs and share needles when injecting. In an exploratory study of a sample of homosexual and bisexual men in San Francisco that was drawn from bathhouses, gay bars, and newspaper advertising, Stall (1986) reported that, after drinking or psychoactive drug use, the men in the study were more likely to engage in sex than when they had not been drinking. A low response rate (37 percent) and the nature of the sampling strategy preclude generalizing these findings to other gay men who are less open about their sexual orientation. Yet despite these caveats, the results of the study suggest other questions that warrant investigation--for example, whether these findings apply to the entire male population or whether the heterosexual population is more likely to engage in unprotected sex after drinking. Studies of the mechanism by which alcohol may influence such activity are also warranted. Are persons more uninhibited after drinking and less concerned about the risks of exposure to HIV or the consequences of infection? Does drinking make people less likely to inquire about partners' possibly risky behaviors? Do heavy drinkers underestimate their susceptibility to HIV or the consequences of HIV infection? Do they believe that condoms reduce sexual pleasure and performance? Do they believe condoms are effective in reducing transmission? Do they perceive greater obstacles to the use of condoms (e.g., cost, embarrassment) than persons who do not drink? -39

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If an association between alcohol and HIV risk behavior becomes apparent, then educational programs that highlight the relationship of HIV to alcohol use and outline HIV risks to drinkers should be tested to see if they alter either drinking behavior or HIV risk-taking behavior after drinking. EARLY SEXUAL ACTIVITY AND ADOLESCENT PREGNANCY Various studies have shown a clustering of the variables of early sexual behavior in adolescents and early onset of the use of alcohol and tobacco (Jessor and Jessor, 1975; Jessor, 1983~. Although a causal link from alcohol use to early sexual behavior has not been proven in these studies, the disinhibitory effects of alcohol and the expectancies associated with alcohol use could lead to a causal link. Further research might clarify this issue. FETAL ALCOHOL SYNDROME AND FETAL ALCOHOL EELL;CTS Fetal alcohol syndrome (FAS), which was identified in the 1970s by researchers at the University of Washington, is a cluster of permanent physical deformities and mental retardation that results from drinking during pregnancy. There are approximately 1 to 3 FAS babies for every 1,000 live births resulting from alcohol misuse; among known alcoholic mothers, this rate increases to a range of 23 to 29 for every 1,000 live births (Hanson, Streissguth, and Smith, 1978; Sokol, Miller, and Reed, 1980; Rosett et al., 1983~. Incidences as high as 19.5 for 1,000 live births have been reported among some Plains tribes of Native Americans (May et al., 1987~. Although the full spectrum of FAS-related birth defects occurs almost exclusively among alcoholic mothers, there has been no threshold level identified below which drinking during pregnancy could be considered safe. Lower levels of drinking during pregnancy result in more subtle birth defects that are more often neurobehavioral rather than physical (Hanson, Streissguth, and Smith, 1978; Sokol, Miller, and Reed, 1980; Rosett et al., 1983~. Because women who drink heavily during pregnancy are also more likely to smoke cigarettes and to take psychoactive drugs during pregnancy, any deleterious effects of alcohol on the developing fetus may be superimposed on the adverse consequences of those other habits. Studies of special strains of inbred mice and limited studies in humans suggest that genetic determinants in the mother probably influence maternal alcohol metabolism (Chernoff, 1980~. In mice, the occurrence of malformations depends not only on the amount of ethanol consumed but also on the rate of alcohol metabolism. Preliminary studies of women showed that there is a tendency for blood alcohol and acetaldehyde levels to be higher in the first two hours after ingestion of a standard ethanol dose among women who had given birth to infants with FAS than in women in a control group (Cooper, 1984~. These results do not provide definitive evidence that a metabolic marker for susceptibility to this syndrome can be identified. Rather, they suggest that specific genetic differences may some day be useful in identifying high-risk mothers. Meanwhile, combinations of alcohol ingestion with one or more other factors (e.g., parity, socioeconomic status, -40

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smoking, marital status, abuse of recreational drugs, deficient placental function) can be used to target the population of mothers at highest risk for FAS and to implement intensive programs designed to prevent this birth defect. Babies who manifest the full range of FAS physical anomalies and mental retardation are readily recognized by physicians who are aware of the syndrome. However, some children may exhibit only mild growth deficiency and learning disabilities as indicators of prenatal alcohol exposure. These kinds of abnormalities are termed fetal alcohol effects (FAE). Thus, estimates of the frequency of deleterious prenatal alcohol exposure probably will have to be revised upward if clinicians can agree on the findings that should be designated as indicators of mild FAS (or FAE). Several kinds of information are needed to develop prevention programs to reduce the frequency of FAS. Efforts should be mounted to develop epidemiological data for FAE. Research needs to further delineate the range of fetal problems that constitute this syndrome and identifier the factors that place mothers at greatest risk of having babies with FAS. Further investigations should be undertaken of the bases for ethnic differences in the incidences of FAS and FAE. The Anti-Drug Abuse Act of 1988 mandates that, as of November 18, 1989, warning labels be placed on all bottles and cans containing spirits. The warning labels will advise women not to drink alcoholic beverages during pregnancy because of the risk of ensuing birth defects. Attitudes concerning FAS and FAE should be assessed both before and after this law goes into effect. Prospective studies are also needed to delineate the characteristic profile of high-risk mothers, especially those whose babies are affected by relatively small amounts of alcohol. In these women, genetic factors may play an important role in the susceptibility of the fetus to the toxic effects of alcohol. REFERENCES Abel, E. L., and R. Zeidinberg. Age, alcohol, and violent death: A postmortem study. J. Stud. Alcohol 46:228-231, 1985. Adams, ~ J., and B. Brown. Alcohol prolongs the time course of glare recovery. Nature 257:481-483, 1975. Baker, S. P., B. O Neill, and R. Karpf. The Injury Fact Book. Lexington, MA: Lexington Books, 1984. Bako, G., W. C. MacKenzie, and E. S. O. Smith. The effect of legislated lowering of the drinking age on fatal highway accidents among young drivers in Alberta, 1970-1972. Can. J. Public Health 67:161-163, 1976. Baldwin, J. A, and J. E. Oliver. Epidemiology and family characteristics of severely abused children. Br. J. Prev. Soc. Med. 29:205-221, 1975. -41

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Bennett, R. M., ~ H. Buss, and J. ~ Carpenter. Alcohol and human physical aggression. Q. J. Stud. Alcohol 30~4~:870-876, 1969. Berglund, M. Suicide in alcoholism. Arch. Gen. Psych. 41:~-891, 1984. Birky, M. M., and F. B. Clarke. Inhalation of toxic products from fires. Bull. N.Y. Acad. Med. 57:997-1013, 1981. Bonnie, R. J. Regulating conditions of alcohol availability: Possible effects on highway safety. J. Stud. Alcohol, Suppl. No. 10:129-143, 1985. Brown, D. B., and S. Maghsoodloo. A study of alcohol involvement in young driver accidents with the lowering of the legal age of drinking in Alabama. Accid. Anal. Prev. 13:319-332, 1981. Bryant, J. D., A. Billingsley, G. ~ Kerry, and W. K Leafman. Physical abuse of children. Child Welfare 42:125-130, 1963. Chernoff, G. F. The fetal alcohol syndrome in mice: An animal model. Teratology 22:71-75, 1980. Coate, D., and M. Grossman. Effects of Alcoholic Beverage Prices and Legal Drinking Ages on Youth Alcohol Use. Cambridge, MA: National Bureau of Economic Research, 1986. Coleman, D. H., and M. ~ Strauss. Alcohol abuse and family violence. In E. Gottheil, ed. Alcohol, Drug Abuse and Aggression. Springfield, IL: Charles C. Thomas, 1983. Combs-Orme, T., J. R. Taylor, E. B. Scott et al. Violent deaths among alcoholics. J. Stud. Alcohol 44:938-949, 1983. Cook, P. J. The effect of liquor taxes on drinking, cirrhosis and auto accidents. Pp. 255-285 in M. Moore, and D. Gerstein, eds. Alcohol and Public Policy: Beyond the Shadow of Prohibition. Washington, DC: National Academy Press, 1981. Cook, P. J., and G. Tauchen. The effect of minimum drinking age legislation on youthful auto fatalities, 1970-1977. J. Legal Studies 13:169-191, 1984. Cooper, J. R. Maternal alcohol metabolism in fetal alcohol syndrome. Clin. Res. 32:113A, 1984. Cordelia, ~ Alcohol and property crime: Exploring the causal nexus. J. Stud. Alcohol 46:161-171, 1985. Also in NIAAA (1987~. Crikelair, G. F., F. C. Symonds, R. N. Ollstein et al. Burn causation: Its many sides. J. Trauma 8:572-582, 1968. Dietz, P. E., and S. P. Baker. Drowning epidemiology and prevention. Am. J. Public Health 64:303-312, 1974. -42

OCR for page 31
El-Guebaly, N., and D. R. Afford. The offspring of alcoholics: A critical review. Am. J. Psych. 134:357-365, 1977. Ellwood, L. Effects of alcoholism as a family illness on child behavior and development. MilitaIy Med. 145~3~:188-192, 1980. Emslie, G. S., and ~ Rosenfeld. Incest reported by children and adolescents hospitalized for severe psychiatric problems. Am. J. Psych. 140~6~:708-711, 1983. Epstein, T., T. Cameron, and R. Room. Alcohol and family abuse. In M. Aarens et al. Alcohol Casualties and Crime. Special report prepared for NIAAA by the Social Research Group, Univer~sitr of California, Berkeley, 1977. Famularo, R., K Stone, R. Barnum, and T. Wharton. Alcoholism and severe child maltreatment. Am. J. Orthopsych. 56~3~:481-485, 1986. Fell, J. C., and T. Klein. The nature of the reduction in alcohol in U.S. fatal crashes. Society of Automotive Engineers Technical Paper Series 860038. Presented at the Society of Automotive Engineers Conference, Detroit, 1986. Giersten, J. C. Drowning while under the influence of alcohol. Med. Sci. Law 10:216-219, 1970. Gooden, B. Drowning and alcohol. Med. J. Aust. 141:478, 1984. Hamilton, D. J., and J. J. Collins. The role of alcohol in wife beating and child abuse: A review of the literature. In J. J. Collins, ed. Drinking and Crime. New York: Guilford Press, 1981. Hanson, J. W., ~ P. Streissguth, and D. W. Smith. The effects of moderate alcohol consumption during pregnancy on fetal growth and morphogenesis. J. Pediatrics 92: 457-460, 1978. Herman, J.,~and L. Hirschman. Families at risk for father-daughter incest. Am. J. Psych. 100:762-770, 1981. Hingson, R., and J. Howland. Alcohol as a risk factor for injury or death resulting from accidental falls: A review of the literature. J. Stud. Alcohol 48:212-219, 1987a. Hingson, R., and J. Howland. Prevention of drunk driving crashes involving young drivers: An overview of legislative countermeasures. Pp. 337-348 in T. Benjamin, ed. Young Drivers Impaired by Alcohol and Drugs. Royal Society of Medicine International Congress and Symposium Series No. 116. London: Royal Society of Medicine, 1987b. Honkanen, R., L. Ertama, P. Kuosmanen et al. The role of alcohol in accidental falls. J. Stud. Alcohol 44:231-245, 1983. Howland, J., and R. Hingson. Alcohol as a risk factor for injuries or death due to fires and burns: Review of the literature. Public Health Rep. 102:475-483, 1987. -43

OCR for page 31
Howland, J., and R. Hingson.- Alcohol as a risk factor for drowning: A review of the literature, 1950-1985. Accid. Anal. Prev. 20:19-25, 1988. Institute of Medicine. Causes and Consequences of Alcohol Problems: An Agenda for Research. Washington, DC: National Academy Press, 1987. Jessor, R. Adolescent problem drinking: Psychosocial aspects and developmental outcomes. Paper presented at the Alcohol Research Seminar held as part of the international ceremony designating the NIAAA as a Collaborative Center of the World Health Organization, Washington, DC, November 2, 1983. Jessor, R., and S. Jessor. Adolescent development and the onset of drinking: A longitudinal study. J. Stud. Alcohol 36:27-51, 1975. Kaplan, S. J., D. Pelcovitz, S. Salzinger, and D. Ganeles. Psychopathology of parents of abused and neglected children and adolescents. I. Am. Acad. Child Psych. 22~3~:238-244, 1983. Keatings, W. R., and M. Evans. The respiratory and cardiovascular response to immersion in cold and warm water. Q. J. Exp. Physiol. 46:83-94, 1961. Kendall, R. E. Alcohol and suicide. Substance and Alcohol ActionsIMisuse 4:121-127, 1983. May, P. A, K S. Hymbaugh, J. H. Aase, and J. H. Samet. Epidemiology of fetal alcohol syndrome among American Indians of the southwest. In Alcohol and Health: Sixth Special Report to the U.S. Congress from the Secretary of Health and Human Services. Washington, DC: NIAAA, January 1987. Mitchell, D. S., S. C. Packham, and W. E. Fitzgerald. Effects of ethanol and carbon monoxide on two measures of behavioral incapacitation of rats. Proc. West. Pharmacol. Soc. 21:427-431, 1978. National Highway Traffic Safety Administration. Alcohol and Highway Safety 1984: A Review of the State of the Art. DOT HS 806-569. Washington, DC: NHTSA, 1985. National Institute on Alcohol Abuse and Alcoholism. Sixth Special Report to the U.S. Congress on Alcohol and Health. DHHS Publ. No. (ADM) 87-1519. Rockville, MD: NIAAA' 1987. National Safety Council. Accident Facts. Chicago: National Safety Council, 1984. Orme, R. C., and J. Rimmer. Alcoholism and child abuse: A review. J. Stud. Alcohol 42:273-287, 1981. Perrine, M. W. Alcohol influences on drinking-related behavior: A critical review of laboratory studies of neurophysiological, neuromuscular and sensory activity. J. Safety Res. 5:165-184, 1973. Rada, R. T. Alcoholism and the child molester. Ann. N.Y. Acad. Sci. 273:492-496, 1976. -44

OCR for page 31
Rittenbu~y, M. S., F. H. Schmidt, R. W. Maddox et al. Factors significantly affecting mortality in burn patients. J. Trauma 5:587-600, 1965. Roiz en, J. Estimating alcohol~involvement in several events. In National Institute on Alcohol Abuse and Alcoholism. Alcohol Consumption and Related Problems. Alcohol and Health Monograph No. 1. DHHS Publ. (ADM) 82-1190. Washington, DC: Government Printing Office, 1982. Room, R. Alcohol and crime: Behavioral aspects. In S. H. Kadish, ed. Encyclopedia of Cnme and Justice, vol. 1. New York: Free Press, 1983. Also in NIAAA (1987~. Rosett, J. L., L. Weiner, ~ Lee, et al. Patterns of alcohol consumption and fetal development. Obstetrics and Gynecology 61:539-546, 1983. Ross, H. L. Deterring the Drinking Driver: Legal Policy and Social Control. Lexington, MA: DC Heath and Co., 1982. Salzinger, S., C. Samit, R. Krieger et al. A controlled study of the life events of mothers of maltreated children in suburban families. J. Am. Acad. Child Psych. 25~3~:419-426, 1986. Schmidt, W., and J. deLint. Causes of death of alcoholics. Q. J. Stud. Alcohol 33:171-185, 1972. Smart, R. G. Are alcoholics' accidents due solely to heavy drinking? J. Safety Res. 1:170-173, 1969. Smith, S. M., R. Hanson, and S. Nobel. Parents of battered babies: A controlled study. Br. Med. J. 3:17-32, 1973. Sokol, R. J., S. I. Miller, and G. Reed. Alcohol abuse during pregnancy: An epidemiologic study. Alcoholism Clin. Exp. Res. 4:135-145, 1980. Stall, R. D. A comparison of alcohol and drug use patterns of homosexual and heterosexual men: Working paper. Berkeley, CA: Alcohol Research Group, 1986. Steele, B., and C. Polloch. A psychiatric study of parents who abuse infants and small children. In R. E. Heifer and C. H. Kempe, eds. The Battered Child. Chicago: University of Chicago Press, 1968. Stephens, C. J. A study of alcohol use and injuries among emergency room patients. San Francisco: Medical Research Institute of San Francisco, 1985. Summerskill, W. H. J., and P. J. Kelly. Osteoporosis with fractures in anicteric cirrhosis: Observations supplemented by micro- radiographic evaluation of bone. Mayo Clin. Proc. 38:162-174, 1963. Tarter, R. E., ~ M. Hegedus, G. Goldstein et al. Adolescent sons of alcoholics: Neurological and personality characteristics. Alcoholism Clin. Exp. Res. 8:216-222, 1984. -45

OCR for page 31
Transportation Research Board. Proceedings of the Workshop on Alcohol-Related Accidents in Recreational Boating. Washington, DC: National Academy Press, 1986. U.S. Department of Health and Human Services. Fifth Special Report to the U.S Congress on Alcohol and Health. DHHS Publ. No. (ADM) 84-1291. Washington, DC: Government Printing Office, 1984. Wailer; J. A. Non-highway injury fatalities. I. The role of alcohol and problem drinking, drugs and medical impairment. J. Chron. Dis. 25:33-A5, 1972. Wright, S. J. SOS: Alcohol, drugs and boating. Alcohol Health Res. World 9:28-33, 1985. Zobeck, T. Trends in Alcohol-Related Fatal Traffic Accidents, United States: 1977-1984. Surveillance Report No. 1. Washington, DC: U.S. Department of Health and Human Services, 1986. -46