CRIMINAL JUSTICE AND BEHAVIOR, Vol. 41, No. 4, April, 2014, 400 –416.

DOI: 10.1177/0093854813508554

© 2013 International Association for Correctional and Forensic Psychology

400

The PersisTence of neighborhood disadvanTage

an experimental investigation of alcohol and Later Physical aggression

VOLkAN TOPALLIGeorgia State University

PETER R. GIANCOLAUniversity of Kentucky

RALPH E. TARTERUniversity of Pittsburgh

MONICA SwAHNGeorgia State University

MICHELLE M. MARTELUniversity of Kentucky

AARON J. GODLASkICentre College

k. TODD MCCOUNUniversity of Kentucky

This research examined the combined impact of alcohol and previous experience growing up in a disadvantaged neigh-borhood on aggression in a laboratory setting. Participants were 505 young adult social drinkers between 21 and 35 years of age who completed a retrospective measure of neighborhood disadvantage and then participated in an experi-mental procedure, where they either consumed an alcohol or placebo beverage. They were subsequently tested on a laboratory aggression task in which they were provoked by receiving electric shocks from a fictitious opponent under the guise of a competitive reaction-time task. Aggression was operationalized as shock intensities and durations admin-istered, in retaliation, by the participants to their fictitious opponent. Acute alcohol intoxication significantly increased aggression for those who grew up in disadvantaged neighborhoods. Thus, our investigation supports Sampson’s notions of “legacies of neighborhood inequality” with important implications for the etiology and prevention of violence in real-world settings.

Keywords: alcohol; aggression; violence; neighborhood disadvantage

auThors’ noTe: This research was supported by Grant R01-AA-11691 from the National Institute on Alcohol Abuse and Alcoholism and by the National Center for Research Resources awarded to Dr. Peter R. Giancola. Address correspondence to Volkan Topalli, PhD, Department of Criminal Justice & Criminology, The Andrew Young School of Policy Studies, 1225 Urban Life Building, Atlanta GA 30302; e-mail: vtopalli@gsu.edu.

508554 CJBXXX10.1177/0093854813508554Criminal Justice and BehaviorTopalli et al. / disadvantaged neighborhoods, alcohol, aggressionresearch-article2004

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It is well documented that violence is a critical public health problem in the United States (Haegerich & Dahlberg, 2011). In fact, homicide is the second leading cause of death

among youth and the third leading cause of death among young adults in the United States (Centers for Disease Control and Prevention, National Center for Injury Prevention and Control, 2007), and violence and associated aggression result in huge societal financial costs (Foster, Jones, & The Conduct Problems Prevention Research Group, 2005). Although there are a number of risk factors associated with violence and aggression, two particularly important and well-examined culprits are acute alcohol intoxication (Dembo et al., 1997; Foster, Vaughan, Foster, & Califano, 2003; Swahn, Bossarte, & Sullivent, 2008) and the social context of growing up in a disadvantaged neighborhood (Aisenberg, 2008; Fabio, Tu, Loeber, & Cohen, 2011; Sampson, 2012). what remains unclear is whether these two fac-tors exert additive or interactive effects on aggression and violence, and more importantly whether such effects are persistent over time.

Observational studies of youths and adults have documented that acute alcohol con-sumption patterns contribute to violence (Stafstrom, 2007; Swahn, Bossarte, west, & Topalli, 2010; Swahn & Donovan, 2005, 2006) and that alcohol has an independent explan-atory role in such violence (wells, Graham, Speechley, & koval, 2006; wells, Mihic, Tremblay, Graham, & Demers, 2008). Most studies investigating this relation have reported that individual and contextual factors enhance risk for alcohol-related violence (see Fagan, 1990) with the most frequently reported risk factors being dispositional aggressivity, alco-hol expectancies, a heavy drinking history, poor executive brain functioning, hostile attri-butional biases, gender, blood alcohol concentration limb effects, alcohol type and dose, social pressure, low empathy, and provocation (for reviews, see Giancola, Josephs, Parrott, & Duke, 2010). These findings, in aggregate, point to the fact that aggression is not simply a manifestation of the pharmacological actions of alcohol.

In addition, substantial literature establishes that growing up in a disadvantaged neigh-borhood has adverse effects on mental and physical health and psychological adjustment as documented on a range of outcomes (Evans, 2004; Hackman & Farah, 2009; Leventhal & Brooks-Gunn, 2011; McLoyd, 1998). In particular, community context and disadvantage are strongly linked to violent crime (Elliott et al., 1996; Sampson, Morenoff, & Gannon-Rowley, 2002). One explanation for this association is that neighborhood disadvantage may indoctrinate a set of cultural beliefs favorable to the use of violence in social situations (Anderson, 1990; 1999; Shover, 1996). Furthermore, recent work by Sampson has demon-strated a persistent effect of neighborhood disadvantage, wherein it not only influences the attitudes and behaviors of youth contemporaneously but also after they have grown up and/or moved away from their community of origin (see Sampson, 2012, 2013).

Overall, findings suggesting the facilitation of aggressive responding when under the influence of alcohol and when one has grown up in a disadvantaged social context begs the question of whether these two factors additively or interactively contribute to violence and aggression in youth and later when they have matured. Certainly, alcohol consumption and neighborhood disadvantage are not unrelated. A higher number of retail alcohol outlets and a higher proportion of problem drinkers are located in socioeconomically disadvantaged neighborhoods (Britt, Carlin, Toomey, & wagenaar, 2005; Livingston, Chikritzhs, & Room, 2007). Moreover, a proneness to social deviancy and affiliation with peers who have low adherence to societal mores and laws—as often found in disadvantaged neighborhoods—promote alcohol use, as well as the propensity for other risky and violent behavior (Snyder, Reid, & Patterson, 2003). Not surprisingly, survey and observational studies reveal a strong

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association between alcohol and violence in poor neighborhoods (Britt et al., 2005; Livingston et al., 2007). However, in the absence of laboratory investigations, it is not possible to ascer-tain whether the associations between alcohol consumption, neighborhood disadvantage, and violence are merely manifestations of the conflation of higher rates of alcohol consump-tion in the context of a childhood experience in a disadvantaged neighborhood. Moreover, there has been no research on whether the putative added effects of these factors persist into adulthood. This represents a significant gap in the extant literature. It is further intriguing that community disadvantage has not yet been incorporated in experimental research to better understand how the childhood neighborhood environment might impact associations between alcohol use and violent and aggressive behavior later in life.

Accordingly, this investigation examined the relationship between acute alcohol intoxi-cation and aggression in a controlled laboratory setting with incorporation of information about participants’ past childhood experience living in a disadvantaged neighborhood. Our methodological strategy was partially motivated by Sampson’s (2013) opposition to, “. . . the usual strategy in criminology to study current neighborhood conditions while control-ling for characteristics such as family supervision, achievement, and employment that instead may be outcomes of past neighborhood deprivation” (p. 12). we hypothesized that the childhood experience of growing up in a disadvantaged neighborhood would moderate the relation between alcohol use and physical aggression during adulthood. Confirmation of this hypothesis has potentially important criminal justice and social policy ramifications by shedding new insights on associations between risk factors for violence, as stringently tested using experimental design, as well as facilitating identification of individuals that might be particularly vulnerable for engaging in violence while under the influence of alcohol.

MeThod

ParTiciPanTs

Participants were 505 (244 men and 261 women) healthy social drinkers (defined below) between 21 and 35 years of age (M = 23.09; SD = 2.92) recruited from the greater Lexington, kentucky area through newspaper advertisements and fliers. Participants were ≈87% Caucasian, ≈10% African American, ≈1.0% Hispanic, and ≈ 2.0% Other, which is consis-tent with the local area’s ethnic composition. Ninety-two percent of the participants were never married and the sample had an average of 16 years of education. The sample also had a mean annual household income (i.e., including support from parents) of approximately US$61,000. The study was reviewed and approved by the university institutional review board.

Social drinking was defined by consuming at least 3 to 4 drinks per occasion at least twice a month.1 Respondents were initially screened by telephone. Individuals reporting any past or present drug- or alcohol-related problems, serious head injuries, learning dis-abilities, or serious psychiatric symptomatology were excluded from participation.2 Individuals reporting abstinence from alcohol use or a condition in which alcohol con-sumption is medically contraindicated were also not allowed to participate in the study. Respondents were screened for alcohol use problems using the Short Michigan Alcoholism Screening Test (SMAST; Selzer, Vinokur, & van Rooijen, 1975). Any person scoring an “8” or more on the SMAST was excluded from participation. Anyone with a positive breath alcohol concentration (BrAC) test or with a positive urine pregnancy/drug result

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(i.e., cocaine, marijuana, morphine, amphetamines, benzodiazepines, and barbiturates) was also excluded.

Following the telephone screening interview, persons eligible for participation were scheduled for an appointment to come to the laboratory. They were told to refrain from drinking alcohol 24 hr prior to testing, to avoid drinking caffeinated beverages the day of the study, to refrain from using recreational drugs from the time of the telephone interview, and to refrain from eating 1 hr prior to testing (given that participants did not begin drinking until 3 hr into the experiment, the standard 4-hr fast used in most alcohol studies was observed). Due to hormonal variations associated with menstruation that may affect aggres-sive responding (Volavka, 1995), women were not tested between 1 week before menstrua-tion and the beginning of menstruation. They were told that the investigation concerned the effects of alcohol and personality on reaction-time in a competitive situation. Participants received US$75 at the completion of the study as compensation.

Measures

Quality of childhood neighborhood scale

Participants completed the Neighborhood Scale (Loeber, Farrington, Stouthamer-Loeber, & Van kammen, 1998), a 17-item inventory scored on a 3-point Likert-type metric that assessed the quality of neighborhood in which participants resided during their elementary, middle, and high school years. Typical items consisted of “Vandalism, buildings and per-sonal belongings broken and torn up,” “Prostitution,” “Assaults and muggings,” peddling or fencing of stolen goods,” and so on. The measure has been show to exhibit excellent predictive validity with regard to violence in children and adolescents (Loeber, Farrington, Stouthamer-Loeber, & white, 2008). In the current study, items were averaged to create a composite with lower scores indicating more disadvantaged neighborhoods. This measure had an alpha coefficient of .98 in the present investigation.

beverage administration

Men and women were essentially evenly split between the beverage groups. Due to gen-der differences in body fat composition and alcohol metabolism (watson, watson, & Batt, 1981), men and women received different alcohol doses. Men received 1 g/kg of 95% alco-hol USP mixed at a 1:5 ratio with Tropicana orange juice, whereas women received 0.90 g/kg of alcohol. Beverages were poured into the requisite number of glasses in equal quanti-ties. The dosing procedure was also calculated for the placebo group; however, they received an isovolemic beverage consisting of only orange juice (i.e., the missing alcohol portion was replaced with orange juice). Four ml of alcohol were added to each placebo beverage and 4 ml were layered onto the juice in each glass for a total of 8 ml of alcohol in each glass. Immediately prior to serving the placebo beverages, the rims of the glasses were sprayed with alcohol. All participants were given 20 min to consume their beverages and were not given any information regarding what to expect from their beverages. However, during the informed consent process, they were told that they would consume the equivalent of about 3 to 4 mixed drinks. To ensure that participants would be accustomed to the dose of alcohol administered in our experiment, we excluded anyone who did not consume at least 3 to 4 drinks per occasion at least twice a month. No participant experienced any adverse effects due to alcohol consumption. In addition to our alcohol and placebo groups, we could have

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used a sober control group, in which participants know that they are not consuming alcohol. However, sober and placebo groups do not generally differ on aggression (Bushman & Cooper, 1990; Chermack & Giancola, 1997; Ito, Miller, & Pollock, 1996). Thus, in recogni-tion of this research, we employed only an alcohol and a placebo group. This choice of groups is ideal for studying the effects of alcohol on aggression while controlling for the belief that alcohol has been consumed (see also Martin, Earleywine, Finn, & Young, 1990).

Breath alcohol concentration (BrAC) levels were measured using the Alco-Sensor IV breath analyzer (Intoximeters Inc., St. Louis, Missouri) on entry at the laboratory and before and after the aggression task. Because the aggression-potentiating effects of alcohol are more likely to occur on the ascending limb of the BrAC curve, and because a BrAC of at least 0.08% is effective in eliciting aggression, participants in the alcohol group began the aggression task (described below) at an approximate BrAC of 0.09% (see Giancola & Zeichner, 1997). To enhance the effectiveness of the placebo manipulation, participants in the placebo group began the aggression task approximately 2 min following beverage con-sumption (e.g., Martin & Sayette, 1993). Just prior to beginning the aggression task, partici-pants rated how drunk they felt (0 = not drunk at all to 11 = more drunk than I have ever been), how impaired they were (0 = no impairment to 10 = strong impairment), and whether they believed they had consumed alcohol (no or yes). Right after completing the aggression task, participants again answered the same questions about their alcohol consumption. Finally, they were debriefed, and those who received alcohol remained in the laboratory until their BrAC dropped to 0.04%.

aggression Task

A modified version of the Taylor Aggression Paradigm (TAP; Taylor, 1967) was used to measure aggression. This task places participants in a situation where they are led to believe that electric shocks are received from, and administered to, a fictitious opponent during a supposed competitive reaction-time task. Participants were seated at a table in a small room. On the table facing the participant were a computer screen and a keyboard. white adhesive labels marked “1” through “10” were attached to the number keys running across the top of the keyboard. The labels “low,” “medium,” and “high” were placed above keys “1,” “5,” and “10,” respectively, to indicate the subjective levels of shock corresponding to the num-ber keys. The keyboard and monitor were connected to a computer located in an adjacent control room out of the participant’s view.

Participants were informed that shortly after the words “Get Ready” appeared on the computer screen, the words “Press the Spacebar” would appear at which time they had to press, and hold down, the spacebar. Following this, the words “Release the Spacebar” would appear at which time they had to lift their fingers off of the spacebar as quickly as possible. A “win” was signaled by the words “You won. You Get to Give a Shock” and a “loss” was signaled by the words “You Lost. You Get a Shock.” Participants were told that they had a choice of 10 different shock intensities to administer at the end of each winning trial for a duration of their choosing. Following a losing trial, they received 1 of 10 shock intensities that lasted 1 s. Participants viewed the shocks they selected and received on a “volt meter” and by the illumination of 1 of 10 “shock lights,” ranging from 1 (low) to 10 (high), on the computer screen. The entire TAP procedure consisted of 34 trials and shock intensities were administered to participants in an essentially random pattern with no more than three consecutive wins or losses. The trials were interspersed by 5-s intervals. The

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initiation of trials, administration of shocks to the participants, and the recording of their responses were controlled by a computer. The experimenters, other electronic equipment, and the computer that controlled the task were located in an adjacent control room out of the participants’ view. To ensure safety and to protect the integrity of the study, the experi-menter secretly viewed and heard the participant through a hidden video camera and micro-phone throughout the procedure.

Physical aggression was operationalized as the combined mean responses for shock intensity (“1” through “10”) and shock duration (in milliseconds) across all trials of the TAP. The score was calculated by transforming each corresponding shock intensity and duration value into z scores and then summing them. This was done to increase the reliabil-ity of indices inasmuch as a meta-analytic investigation demonstrated that shock intensity and duration are significantly related to one another and are considered to be part of a more general construct of aggression (Carlson, Marcus-Newhall, & Miller, 1989). For this rea-son, more recent studies using the TAP, and its modified versions, have adopted, and suc-cessfully used, similar combinatory techniques involving shock intensity and duration (Carnagey & Anderson, 2005; Parrott & Zeichner, 2001; ward et al., 2008). The TAP has been repeatedly shown to be a safe and valid measure of aggressive behavior for men and women (Anderson & Bushman, 1997; Giancola & Chermack, 1998; Hoaken & Pihl, 2000).

TaP validity issues

There has been discussion regarding whether laboratory measures of aggression general-ize to “real-world” violence. First, it is key to recognize that the goal of this investigation is to assess how theory-based hypotheses explain the alcohol–aggression relation. Thus, the use of the TAP is appropriate given that

. . . the primary goal of most laboratory research is the development of theories designed to explain underlying processes and mechanisms. Furthermore, it is these theoretical principles that one wishes to generalize, not the specific characteristics of the sample, setting, manipulation, or measure. (Anderson & Bushman, 1997, p. 22; see also Mook, 1983)

Second, research indicates that the TAP does indeed generalize to “real-world” vio-lence: (1) The TAP and its modified versions have successfully differentiated violent from nonviolent prison inmates (reviewed in Giancola & Chermack, 1998); (2) studies show positive relations between shock selections and self-report measures of physical assault, behavioral hostility, and outwardly directed anger (Giancola & Parrott, 2008; Hammock & Richardson, 1992); (3) our own data demonstrate that TAP responses are related to self-reports of (a) physical fights, (b) felonies, (c) deliberately hitting others, (d) cruelty to animals, and (e) breaking objects out of anger (Phillips & Giancola, 2009); in addition, many of our participants also yell vulgar names at their opponent and/or give them “the finger” during the task; (4) responses on the TAP are not related to nonviolent constructs such as guilt, suspicion, resentment, inwardly directed anger (Giancola & Zeichner, 1995), helping, and competition (Bernstein, Richardson, & Hammock, 1987); and (5) finally, it is difficult to dispute that within the ethical limits of the laboratory, participants control an actual weapon (i.e., the TAP) that can be used to inflict violence (i.e., painful electric shocks) on another person.

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resuLTs

ManiPuLaTion checks

Placebo checks

All participants in the placebo group indicated that they believed that they drank alcohol. with regard to the question how drunk they felt, persons in the alcohol group reported mean pre- and posttask ratings of 4.72 and 5.09 (scale range = 0-11) and those in the placebo group reported mean pre- and posttask ratings of 1.75 and 1.92, respectively, pretask rat-ings: t(501) = −20.64 p < .05; posttask ratings: t(503) = −20.00, p < .05. with regard to the question about whether the alcohol they drank caused any impairment, individuals in the alcohol group reported an average rating of 5.6 and those in the placebo group reported an average rating of 2.1, t(508) = −19.42, p < .05 (scale range = 0-10), indicating that persons in the placebo group did in fact believe that they consumed alcohol. Given the alcohol dose used in this investigation, it is impossible to expect that subjective feelings of intoxication can be equated between the alcohol and placebo groups, especially when dealing with expe-rienced drinkers. As such, it has astutely been pointed out by Martin and Sayette (1993) that the success of a placebo manipulation simply reflects that persons believed that they con-sumed alcohol which is, in and of itself, enough to activate any potential alcohol expectancy effects (Vogel-Sprott & Fillmore, 1999). Thus, according to this well-accepted guideline in the alcohol administration research literature, our placebo manipulation was indeed effective.

brac Levels

All participants tested in this study had BrACs of 0% on entering the laboratory. Individuals in the alcohol group had a mean BrAC of 0.095% (SD = 0.011) just before beginning the aggression task and a mean BrAC of 0.105% (SD = 0.015) immediately after the task. Persons given the placebo had a mean BrAC of 0.015% (SD = 0.011) just before the aggression task and a mean BrAC of 0.007% (SD = 0.007) immediately after the task. There were no gender differences in mean BrACs either before (men = .094%; women = .096%) or after (men = .102%; women = .107%) the task.

aggression Task checks

To verify the success of the aggression task deception, participants were administered a posttask interview in which they were asked a number of questions about their subjective perceptions of their opponent, such as whether she or he tried hard to win, whether they thought the task was a good measure of reaction-time, and how well they believed they performed on the task. The deception manipulation appeared successful. Many participants called their partner vulgar and profane names or gave their partner the “middle finger” dur-ing the task. Previous research has shown that this task provides a valid and reliable labora-tory measure of aggression (e.g., Giancola & Parrott, 2008). In approximately 20 years of conducting such research, the lead author has found that it was extremely rare (<1%) that participants admitted to being aware of the underlying purpose of the experiments. This statement is supported by empirical data from a recent meta-analytic analysis demonstrat-ing that people are generally incapable of correctly judging deception in research studies.

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Moreover, a seminal article by Berkowitz and Donnerstein (1982) noted that “there is not as much awareness of the research hypothesis in many experiments as the critics have claimed” (p. 250).

regression anaLyses

The chief aim of this investigation was to determine whether growing up in a disadvan-taged neighborhood would moderate the alcohol–aggression relation (i.e., act as a risk fac-tor). To reduce multicollinearity, we standardized the neighborhood variable (Aiken & west, 1991). Beverage (1 = alcohol, 0 = placebo) and gender (1 = male, 0 = female) were dummy coded. Analyses were conducted using three-step hierarchical regression models, with aggression scores as the dependent variable. All three main effects (beverage group, gender, and neighborhood) were entered into the models in the first step, followed by two-way inter-actions in the second step, and then the three-way interaction in the third step. we calculated the interaction terms by multiplying the pertinent first-order variables. we interpreted sig-nificant interaction terms by plotting the simple regression slopes and testing to determine whether they differed significantly from zero (Aiken & west, 1991; Friedrich, 1992).

aggression daTa

The first step of the model containing only the main effects was significant, F(3, 501) = 31.02, p < .001; R2 = .16. These analyses revealed that alcohol significantly increased aggression compared with placebo (b = −.38, p < .001), that men were significantly more aggressive than women (b = −.64, p < .001), and that the higher the level of childhood neighborhood disadvantage, the higher the level of participant aggression (b = .26, p < .001). The second step of model was also significant, F(6, 498) = 19.60, p < .001; R2 = .19. Here, the Neighborhood × Beverage (b = −.40, p < .001) was the only significant two-way effect (see Figure 1). The increment in R2 from Step 1 for the Neighborhood × Beverage interac-tion was .034 (F for change = 7.03, p < .001). when this interaction was probed, it revealed a positive relation between childhood neighborhood disadvantage and aggression in the alcohol group (simple slope b = .51, t = 6.75, p < .001), but no significant effect in the pla-cebo group (simple slope b = .12, t = 1.69, p = ns). The three-way interaction in the full third-step model was not significant and thus not further probed (see Aiken & west, 1991).

discussion

Although childhood neighborhood context and alcohol use have been associated with increased incidence of aggression, this is, to our knowledge, the first investigation to exam-ine their interactive effects on later behavior using an experimental paradigm. Results of this study of healthy young adult social drinkers demonstrated that childhood experience with neighborhood disadvantage moderates the current relation between alcohol’s effects on aggression. Specifically, growing up in a more disadvantaged neighborhood is associ-ated with higher levels of aggressive behavior, specifically while under the influence of alcohol.

These current findings are in line with extant research that has demonstrated a strong link between concentrated levels of urban disadvantage and a variety of social ills including, most notably, crime and violence (Evans, 2004; Hackman & Farah, 2009; Leventhal & Brooks-Gunn, 2011; McLoyd, 1998). It is important to note that the geographical distribution

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of violence is not random, but concentrated in disadvantaged neighborhoods (see below). Disadvantaged neighborhoods typically exhibit specific structural deficits (e.g., poverty, residential mobility, poor infrastructure, lack of social services, high unemployment) and unique cultural attributes (norms, beliefs, and values sympathetic to criminality and vio-lence; Markowitz, 2003; Sampson et al., 2002; wilson, 1987). These structural deficits and related cultural elements serve as the core components of disadvantage and contribute to a sense of social disorganization (Shaw & Mckay, 1942) among disadvantaged inhabitants.3 These are places where communities and parents are thwarted from adopting shared proso-cial values, cannot exert control over the criminally prone, and are unable to engage in effective community-level problem solving.

The structural and cultural roots of social disorganization have two interrelated effects. First, they act as risk factors by encouraging youth to interact with those who have adopted streetwise cultural beliefs encouraging violence (most often, delinquent peers; Snyder et al., 2003). Such beliefs are seen as advantageous in neighborhoods where financial and social success is not achievable through conventional means (e.g., attending school or finding work; see Anderson, 1999; wolfgang & Ferracuti, 1969). However, they hinder youth from establishing bonds to prosocial others such as parents, teachers, and other adult role models. These bonds serve as protective factors, encouraging youth to adopt cautious, planful behavior, and demonstrate self-control skills that they can maintain into adulthood and which they can access to implement conflict resolution strategies other than aggression and violence (Gottfredson & Hirschi, 1990; Hirschi, 1969; Pratt & Cullen, 2000; Sampson & Laub, 1990). Thus, neighborhood disadvantage decreases the availability of social capital that adults need to socialize youth, and this, in turn, reduces the extent to which youth can

Figure 1: Plot of Regression Slopes Depicting the Relation Between the Quality of Neighborhood in Which One Grew Up and Physical Aggression for Participants Who Consumed an Alcohol or a Placebo Beverage

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exhibit, and possibly even believe in, self-control (Teasdale & Silver, 2009). This premise is particularly relevant to the current study as alcohol also has widely been found to dimin-ish self-control, particularly when it comes to risky behaviors like violence (Fillmore & Vogel-Sprott, 2000; Haggård-Grann, Hallqvist, Långström, & Möller, 2005; Hoaken, Assaad, & Pihl, 1998).

Second, there is evidence from the developmental literature that early beliefs related to self-control and deviance persist into adulthood (Asendorpf, Denissen, & van Aken, 2008; Caspi, Moffitt, Newman, & Silva, 1996; Huesmann, Eron, Lefkowitz, & walder, 1984; Moffitt, 1993). More recently, Robert Sampson has advanced the hypothesis that the impact of neighborhood disadvantage goes beyond its contemporaneous effects on youth living in such environs (and which have been exhaustively investigated). Rather, he argues that the most important effects of neighborhood disadvantage are those that persist into adulthood, even when individuals have moved away from their original community. Sampson’s 2012 address to the American Society of Criminology makes specific reference to “legacies of inequality” as the causal mechanism for findings from a previous study of verbal ability and IQ, which used data from the Project on Healthy Development in Chicago Neighborhoods (PHDCN),

A major dimension of the legacy issue concerns neighborhood effects on individuals that develop over time. In research from the PHCDN, we found that childhood exposure to severely disadvantaged communities was linked to diminished verbal ability later in childhood, a lasting effect that continues even after moving out of the neighborhood . . . This is a lagged effect of context, one that has implications for how we understand the legacy of neighborhood effects. (Sampson, 2013; see also Elliott et al., 1996; Fagan & Davies, 2004; Hackman & Farah, 2009; McNulty, Bellair, & watts, 2013; Morenoff, Sampson, & Raudenbush, 2006; Sampson, Sharkey, & Raudenbush, 2008, p. 11)

For the most part, such persistent effects have to do with racial and socioeconomic inequality, but they are not restricted to cognitive-developmental effects, nor are they lim-ited to childhood. Our study, measuring effects of prior disadvantage with adults in a labo-ratory setting, fits within Sampson’s framework. Furthermore, it suggests an additive effect of alcohol, which, as previously mentioned, is more commonly available in disadvantaged neighborhoods.

In fact, the availability is not trivial here. Prior research has found a profusion of alcohol distribution outlets within disadvantaged neighborhoods and has linked this with increased levels of violence (see Britt et al., 2005; Livingston et al., 2007). More importantly to the current work, Anderson (1999) and others (see, for example, Hunt & Laidler, 2001; Vigil & Long, 1990; white, Hansell, & Brick, 1993) have described the central role that alcohol consumption plays in the lives of young people living in disadvantaged neighborhoods, particularly young men who are prone to offending and violence. Therefore, it is logical to assume that combining the structural and cultural characteristics associated with disadvan-taged neighborhoods that link alcohol consumption to antisocial behavior with an increased availability of alcohol would further augment the expression of aggression and violence.

Confirming these notions, Zhang, welte, and wieczorek (2002) found that aggression-related alcohol expectancies significantly increased drinking prior to offending, holding con-stant the effect of daily drinking patterns. Assuming such expectancies accrue culturally, this implies that offenders may consciously consume alcohol in anticipation of engaging in

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violence (and would also ex ante be unmotivated to regulate the effects of their consumption on their contemplated and enacted violence). They also determined that daily drinking pat-terns had an independent effect on drinking before offending. This finding is in line with the above-mentioned research on the relation between alcohol outlet distribution patterns and violence, which has as its underlying assumption that increased availability drives drinking patterns and subsequent violence (see also Quigley & Leonard, 2006; McMurran, 2007).

It is also likely that such effects are recursive. In keeping with a number of Sampson’s notions, Pridemore and Grubesic (2012) found that the relation between alcohol outlet den-sity and neighborhood violence rates is moderated by social organization (i.e., the weaker community bonds are, the stronger the relationship between alcohol outlets and say, assault). In disadvantaged neighborhoods, if consuming alcohol is viewed as a necessary and appro-priate antecedent to aggressive behavior, this may, in turn, encourage future alcohol con-sumption. The maintenance of this relation would be strengthened by the increased availability of alcohol made possible by the ubiquity of alcohol distribution outlets (see Resko et al., 2010). Once established, this pattern of alcohol consumption and aggression among young people is likely to have long-term effects on their ability to moderate their aggression when consuming alcohol as adults later in life, even when they no longer live in disadvantaged neighborhoods. Our findings more specifically demonstrate that attitudes and behaviors regarding the use and control of aggression and violence learned earlier in life by those who have experienced neighborhood disadvantage persist into adulthood and manifest themselves in situations where provocation has occurred, particularly when one is intoxicated, thus supporting an additive effect of these factors on violence as well as Sampson’s notions regarding the “persistence of inequality.”

This suggests that interventions for aggression and violence in adults should take into account the combined effects of prior history with neighborhood disadvantage, as well as current access to and use of alcohol. From a prevention perspective, this also means identi-fying youth who are at risk of linking alcohol to violence so that such attitudes do not become ingrained as they mature to adulthood. This requires a multipronged approach where individual-level variables (including exposure to deviance in the peer group, weak social bonds, aggression-related alcohol expectancies, etc.) are combined with neighborhood-level cultural variables (such as proalcohol and proviolence values), and structural indi-cators (poverty, lack of social services, presence and availability of alcohol, etc.) to identify at-risk individuals and to suggest important intervention targets for these individuals.

Several important limitations should be considered when interpreting these findings. Our data support previous research that examines the outcomes and disparities associated with community disadvantage and confirm that community disadvantage exacerbates the link between alcohol use and violence. In addition, they raise important questions for future violence-prevention research. It will be imperative to replicate these findings in experimen-tal as well as observational, and field studies, as well as longitudinal study designs begin-ning in childhood. It is particularly important to use more comprehensive, multifactored measures of prior history of neighborhood disadvantage in future research. Connecting neighborhood disadvantage to differential patterns of behavior is important in and of itself (as demonstrated in the current work; see also Attar, Guerra, & Tolan, 1994). However, neighborhood disadvantage is correlated with a variety of other potentially causal factors for aggression later in life—such as subcultural beliefs (see, for example, wright & Fagan, 2013) and social support (see, for example, koenen, Tendulkar, Dunn, Buka, & Subramanian,

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2012). Using more precise and comprehensive measure of neighborhood disadvantage that includes such variables would allow us to determine the extent to which observed effects are due solely to neighborhood disadvantage, other correlated factors, or both. The same is true for those factors that are caused by prior history with neighborhood disadvantage and may manifest themselves in current behavior. For example, we mentioned previously Sampson’s finding that earlier neighborhood disadvantage was associated with later deficits in verbal ability and IQ. But, these factors have their own independent association with aggression (for verbal ability, see, for example, Camp, 1977; Forrest, Eatough, & Shevlin, 2005; Muñoz, Frick, kimonis, & Aucoin, 2008; for IQ, see, for example, Diamond, Morris, & Barnes, 2012; Huesmann, Eron, & Yarmel,1987) therefore it is difficult to know whether they are serving as mediators of the neighborhood disadvantage effect or as independent causal factors. In effect, as our study does not include such measures, questions remain as to whether our observations may be due to more complex meditational or moderational processes; certainly a fertile ground for future work. Finally, future studies should examine the role of community disadvantage in alcohol-related violence in other populations and also determine if other forms of childhood disadvantage may exacerbate future risk for alcohol-related violence.

Moreover, the results underscore the need to better assess the underlying conceptual framework for when and how alcohol may facilitate the expression of violence within indi-viduals and violence as a potential coping skill or expected response to stressful conditions. we have outlined some possibilities above, but more focused efforts are clearly warranted. Specifically, it is important to distinguish whether the observed effect results from people with a history of disadvantage not being able to control their violent tendencies while under the influence of alcohol, or does this effect accrue from alcohol triggering positive attitudes toward violence, entrenched earlier in life? Relatedly, it is critical to determine the specific mechanism through which earlier experience with neighborhood disadvantage effects aggressive responding later in life. One possibility is that the effect accrues from the indi-vidual’s adoption of proaggressive beliefs (i.e., a socialization model; see kliewer et al., 2006; Loeber & Hay, 1997; Snyder & Patterson, 1995). Another is that aggressive respond-ing in the alcohol condition is a stress-induced response to prior experience with disadvan-tage (see, for example, Brody et al., 2003; Sheidow, Henry, Tolan, & Strachan, 2013). If anything, determining such a distinction will help us better understand whether there is a gender-based component to the phenomenon because males and females are now to respond differently (see Giancola et al., 2009; McLoyd et al., 2009). On a larger scale, this research points to the potential need for public health policies and intervention efforts that recognize and account for the moderating impact that prior neighborhood disadvantage may have on the relation between alcohol (as well as a host of other potential factors) and violence. Identifying those factors that may buffer or neutralize such moderating effects may have serious implications for the prevention of crime, violence, and other risky behaviors.

The study of risk factors associated with violence is of critical importance given the costs associated with alcohol-related violent crime and injuries (Levy, Stewart, & wilbur, 1999) and also because the development of effective intervention strategies has been hindered by the limited information on the risk factors for alcohol-related violent behavior. The National Research Council published a report nearly two decades ago, urging researchers to investi-gate individual differences that distinguish people who behave violently while drinking from those who do not (Reiss & Roth, 1994). Unfortunately, relatively few studies with

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412 CRIMINAL JUSTICE AND BEHAVIOR

public health significance have addressed this specific issue. Our study makes a unique contribution to explaining the association between alcohol and aggression with implica-tions for the sociological and criminological frameworks for violence prevention that has been adopted in public health.

noTes

1. This cutoff criterion was used to ensure that participants would not have an aversive physical reaction to the alcohol dose that we planned to administer (i.e., vomiting, etc.). In many cases, participants typically drank more than that amount. This threshold was selected as merely a safeguard for participant drinking and possible negative physical reactions to alcohol.

2. Beyond any confounding effect, the inclusion of such individuals would incur, there are serious ethical reasons for excluding such individuals from research of this nature. For example, it would be unethical to expose individuals with a his-tory of alcohol abuse to research where they would have to consume alcohol, potentially interfering with their current or past efforts at rehabilitation and recovery.

3. Although race was not a variable of direct interest in the current article, Sampson and wilson (1995) identified the underlying mechanism for social disorganization as the logical outcome of racial disparity. In explaining the overrepresenta-tion of African Americans as victims and offenders in violent crime they hypothesized that community-level patterns of racial inequality produce social isolation and physical clustering of the truly disadvantaged. This leads to structural barriers and cultural adaptations that undermine social organization and thereby foster crime. Thus, whites and Blacks are equally suscep-tible to community-level causes of violence, but African Americans are disproportionately vulnerable to these effects because racial segregation overexposes minorities to these criminogenic factors (also known as the “racial invariance” hypothesis).

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volkan Topalli, PhD, is an associate professor of criminal justice and criminology at Georgia State University in the Andrew Young School of Policy Studies. His research and teaching interests are in the areas of offender decision-making and street violence. His recent publications have appeared in such journals as Criminology, Justice Quarterly, Criminal Justice & Behavior, and the British Journal of Criminology, with funding from such agencies as the National Science Foundation, the National Institute of Justice, and the National Institutes of Health.

Peter r. giancola, PhD, is a professor of psychology at the University of kentucky and is the principal investigator of the National Institute on Alcohol Abuse and Alcoholism (NIAAA)–funded director of the alcohol and violence laboratory where the data for this study were collected. His research focuses on the experimental investigation of the effect of alcohol on

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aggression. He is the author of more than 100 articles and has received significant funding from such agencies as the National Institute on Drug Abuse, the NIAAA, and the National Institute of Mental Health.

ralph e. Tarter, PhD, is a professor of pharmaceutical sciences, psychiatry, and psychology at the University of Pittsburgh. He is the director of the Center for Education and Drug Abuse Research (CEDAR). His research focuses on the developmental origins and pathways to addiction.

Monica swahn, PhD, is a professor of epidemiology in the School of Public Health at Georgia State University, where she conducts research on primarily violence and injuries in United States as well as internationally. She is particularly interested in the link between alcohol use and interpersonal as well as self-directed violence among youth and young adults.

Michelle M. Martel, PhD, is an assistant professor at the University of kentucky who conducts research on etiology and assessment of attention deficit hyperactivity disorder (ADHD) and associated disruptive behavior problems. She earned her PhD in clinical psychology at Michigan State University and is a licensed clinical psychologist in kentucky.

aaron J. godlaski, PhD, is an assistant professor of psychology and behavioral neuroscience at Centre College in Danville, kentucky. His research focuses on personality and neuropsychological risk factors for alcohol-related aggression. He was involved in the grant organization, data collection, and theory development of this and previous related projects.

k. Todd Mccoun, DO, is an assistant professor and attending anesthesiologist at the University of kentucky Chandler Medical Center. He is board certified by the American Board of Anesthesiology.

at GEORGIA STATE UNIVERSITY on January 28, 2015cjb.sagepub.comDownloaded from All in-text references underlined in blue are linked to publications on ResearchGate, letting you access and read them immediately.