Childrens Affect Expression and Frontal EEG Asymmetry:Transactional Associations with MothersDepressive Symptoms

Erika E. Forbes & Daniel S. Shaw & Jennifer S. Silk &Xin Feng & Jeffrey F. Cohn & Nathan A. Fox &Maria Kovacs

Published online: 13 September 2007# Springer Science+Business Media, LLC 2007

Abstract Although parents and children are thought toinfluence one anothers affect and behavior, few studieshave examined the direction of effects from children toparents, particularly with respect to parental psychopathol-ogy. We tested the hypothesis that childrens affectivecharacteristics are associated with the course of mothersdepressive symptoms. Childrens affect expression wasobserved during a series of motherchild interaction tasks,and childrens resting frontal electroencephalogram (EEG)asymmetry was assessed in a psychophysiology laboratory.Mothers depressive symptoms were assessed at two timepoints, approximately one year apart, at the motherchildinteraction visits. Depressive symptoms increased over timefor mothers with a history of childhood-onset depressionwhose children exhibited right frontal EEG asymmetry.

Depressive symptoms were associated with high childnegative affect at both time points for mothers whosechildren exhibited right frontal EEG asymmetry. Cross-lagged models with a subset of participants provided someevidence of both parent-to-child and child-to-parent direc-tions of effects. Findings suggest that akin to otherinterpersonal stressors, childrens affective characteristicsmay contribute to maternal depressive symptoms.

Keywords Maternal depression . Child effects .

Negative affect . Frontal EEG asymmetry

Investigations of families with a depressed parent haveprimarily focused on the effect of parental depression on childoutcomes (Beardslee et al. 1998; Downey and Coyne 1990)and difficulties in interpersonal functioning (Cummingsand Davies 1994). It is widely acknowledged that childcharacteristics can influence child development by elicitingspecific parental behavior, which in turn influences subse-quent child behavior (Bell and Harper 1977; Grusec andLytton 1988; Scarr and McCartney 1983). In addition,because affect can be regulated by others as well as oneself,children can also influence parents behavior by serving asregulators of their parents affect (Cole et al. 2004; Eisenbergand Spinrad 2004). However, very few studies haveexamined whether child attributes are associated with thecourse of parental psychopathology. The current studysought to advance our understanding of child effects inrelation to parental psychopathology by investigating thelongitudinal effects of childrens affective attributes inrelation to maternal depressive symptomatology.

The transactional perspective emphasizes the reciprocalinterplay of parent and child influences on outcomes overtime (Bell and Harper 1977; Field 1994; Grusec and Lytton1988; Sameroff and Chandler 1975). Bells (1968) seminal

J Abnorm Child Psychol (2008) 36:207221DOI 10.1007/s10802-007-9171-y

E. E. Forbes (*)WPICLoeffler 319, Department of Psychiatry,University of Pittsburgh,3811 OHara Street,Pittsburgh, PA 15213, USAe-mail: forbese@upmc.edu

D. S. Shaw : J. F. CohnDepartment of Psychology,University of Pittsburgh,Sennott Square, 210 South Bouquet Street,Pittsburgh, PA 15260, USA

N. A. FoxUniversity of Maryland,College Park, MD, USA

J. S. Silk :X. Feng :M. KovacsDepartment of Psychiatry,University of Pittsburgh,3811 OHara Street,Pittsburgh, PA 15213, USA

paper argued that many parent effects findings in thesocialization literature could be re-interpreted as supportingchild effects on parents behavior. Over the past twodecades, greater emphasis has been paid to reciprocalinfluences in outcomes such as early child psychopathology(Eisenberg et al. 2001; Sanson et al. 1991). Indeed, the fieldof affect regulation has addressed the importance ofviewing affect as regulated by others (e.g., Cole et al.2004).

Child effects on parental depression are hypothesizedto occur because depression appears to be highlyinfluenced by the interpersonal context (Hammen 2003).From an evolutionary perspective, the basis of depressedmood is interpersonal, with increases in depressed moodpostulated to follow changes in social functioning (Allenand Badcock 2003). From a stressful life events perspec-tive, interpersonal stressors contribute importantly to theonset and maintenance of depression in women inparticular (Hammen 2003). Depressive episodes are likelyto occur in conjunction with events such as family conflictand strained parentchild interactions (Hammen 2003),and interpersonal stress has been found to mediatechanges in womens depressive symptoms over time(Davila et al. 1995). These findings suggest that thequality of the motherchild relationship is a potentialinfluence on the course of maternal depressive symptoms.

One domain of childrens behavior may be particularlysalient in relation to the course of maternal depressivesymptoms: Childrens affective characteristics, includingthe expression and regulation of positive and negativeaffect. Symptoms of maternal depression may be particu-larly sensitive to individual differences in childrens affectregulation because depression is considered to involvefundamental affect regulation difficulties (Gross and Muoz1995). Indeed, disruption of affect is thought to be acommon and important feature in families of depressedindividuals (Sheeber et al. 2001; Silk et al. 2006). Whiletypical mothers might become affectively dysregulated inresponse to their childrens negative affect, mothers withdepression might be especially vulnerable, experiencinglonger and more intense negative affect in response to theexpression of child negative affect. This vulnerability toaffective dysregulation in mothers with depression couldoccur as a result of tendencies toward high trait levels ofnegative affect (Kendler et al. 1993); genetic predispositionto affective reactivity (Caspi et al. 2003); physiologicalcharacteristics, including greater response to negativeaffective stimuli in brain regions such as the amygdala(Surguladze et al. 2005); or cognitive processes such asrumination about negative affect (Nolen-Hoeksema 2000)and beliefs of low parenting self-efficacy (Teti and Gelfand1991). Furthermore, the impact of childrens dysregulatedaffect expression on mothers mood may be cumulative,

with mothers becoming increasingly sensitized to itspresence over time.

Affect regulation in mothers and children may beespecially compromised when mothers have a history ofchildhood-onset depression (COD). This subtype of depres-sion tends to be chronic, severe, and familial (Harringtonet al. 1990; Kovacs et al. 1997; Kovacs et al. 1984b;Newman et al. 1996; Weissman et al. 1999). Furthermore,COD is associated with impairments in the development ofaffect regulation and social relationship skills (Goodyer et al.1997; Kovacs and Goldston 1991). These impairments maycreate vulnerability to interpersonal stressors in adulthood,which may then trigger future depressive episodes. Motherswith a history of COD are especially likely to developparentchild interaction patterns characterized by high levelsof negative affect, low levels of positive affect, and mutuallydysregulated affect (Shaw et al. 2006).

The risk for depressive symptoms in the context of achallenging motherchild relationship may not be a staticrisk, as childrens affective characteristics could predictchange in mothers symptoms over time. Interactions with atroublesome child could exert a mounting pressure onmothersjust as enduring a high-conflict marriage, dan-gerous neighborhood, or interpersonally antagonistic workatmosphere couldand mothers symptoms could increasewith exposure to this pressure. Mothers symptoms may beespecially vulnerable during periods of their childrensdevelopment in which affect regulation skills are typicallydeveloping. The preschool and early school-age periods areworthy of focus because they are periods at which cognitiveand affective skills supporting affect regulation generallyimprove (Kopp 1982; Posner and Rothbart 1998). If childrenin this age range show only modest competence or littleprogress in regulating affect, their mothers depressivesymptoms may be maintained or even exacerbated.

In considering the pathways by which childrensaffective characteristics may increase or contribute tomothers depressive symptoms, we focus on affectivebehavior and affective physiology. In the behavioraldomain, there are several possible mechanisms by whichchildrens affective characteristics can contribute to moth-ers depressive symptoms. Childrens affective characteristicsmay elicit increases in mothers affective distress throughreinforcement and punishment (Patterson 1982). A child whoexhibits high rates of negative affect could serve as anegative reinforcer for her mothers sadness, social with-drawal, and helplessness (Shaw et al. in press; Shaw et al.2006), and depressed mothers dysphoric affect caneffectively suppress their childrens aggressive behavior(Hops et al. 1987). Also, based on models of affectregulation that emphasize the role of others in regulatingaffect expression (Cole et al. 2004; Eisenberg and Spinrad2004), children high in negative affect or low in positive

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affect may be less likely to contribute adaptively tomothers own affect regulation. Although little researchhas been conducted on the role of children in helping toregulate parents emotions, reciprocal effects have beenfound in research involving adultadult (Gottman 1998;Levenson et al. 1994) and parentchild relationships (Coleet al. 2003). For example, when children experience andexpress intense or persistent negative affect, they may beless able to help their parent regulate affect through meanssuch as distracting, offering comfort, and expressingpositive affect.

Both behavioral and physiological components of childaffectivity could be associated with mothers depressivesymptoms. As noted above, behavioral components, espe-cially childrens behavior during motherchild interactions,provide a window into childrens typical behavior in thefamily context. But physiological components offer anotherperspective that may provide additional, complementaryinformation on affective tendencies. Although physiologi-cal components are valuable for investigating childrensaffective characteristics, they have rarely been examined inrelation to maternal affective symptoms.

Resting frontal electroencephalogram (EEG) asymmetryis an especially promising index of physiologically basedaffective tendencies. Frontal EEG asymmetry reflectsunderlying disposition to approach or withdraw fromappealing or aversive stimuli (Davidson et al. 2000a; Fox1991). Left frontal EEG asymmetry is thought to indexapproach-related dispositional tendencies, while right front-al EEG asymmetry is thought to index withdrawal-relatedtendencies (Davidson 2004; Fox 1994). Right frontal EEGasymmetry is hypothesized to be a risk factor for depression(Davidson 1994; Tomarken and Keener 1998) and has beenobserved in children who are behaviorally inhibited or shy(e.g., Fox et al. 2001).

In addition to its association with depression, childrenright frontal EEG asymmetry at rest is thought to influencebehaviors such as expression of fear and anxiety, activewithdrawal from challenges, social withdrawal, and failureto pursue rewarding experiences (Fox 1994). Generally,right frontal EEG asymmetry is conceptualized as reflectingchildrens tendencies to pull themselves away from sit-uations involving threat. These tendencies could contributeto motherchild interactions that mothers experience asaversive or unrewarding. If negative affect between mothersand children becomes mutually expressed, leading toreciprocal negative affect and interpersonal withdrawal,mothers might be more likely to maintain depressivesymptoms such as persistent low mood, helplessness,worthlessness, and hopelessness. Right frontal EEG asym-metry in children could thus predict mothers depressionover time via its behavioral manifestations. In addition,right frontal EEG asymmetry in children could capture

aspects of childrens affectivity that are independent ofthose measured in typical laboratory paradigms of affectivebehavior and, thus, could predict mothers symptoms incombination with other forms of child negative affectivity.Accordingly, we hypothesized that childrens right frontalEEG asymmetry, possibly in combination with factors suchas maternal history of depression and childrens expressionsof affect during motherchild interaction, would be associ-ated with mothers depressive symptoms.

Goals of the Current Study

The current study applied a child effects perspective (Bell1968) to the longitudinal course of mothers depressivesymptoms. Specifically, we examined associations betweenbehavioral and physiological markers of childrens affectand the course of mothers depressive symptoms over oneyear. Some of the mothers in the sample had a history ofCOD, while others had no history of serious psychopathol-ogy. We predicted that both behavioral and physiologicalmarkers of childrens affect would be associated withmothers depressive symptoms over time. Our hypothesiswas that mothers of children who exhibit high negativeaffect, right frontal EEG asymmetry, or a combination ofthe two would exhibit higher overall depressive symptomsthan mothers whose children exhibit lower levels of thesemarkers. In addition, we examined whether mothershistory of COD interacted with childrens affective charac-teristics (i.e., high negative affect or right frontal EEGasymmetry) to predict mothers depressive symptomsoverall or change in symptoms over time. Finally, weconducted exploratory cross-lagged models to considerwhether child effects were a plausible explanation ofobserved relations between childrens affective character-istics and mothers depressive symptoms.

Method

Participants

Participants were 74 children and their mothers from 61families who were participating in a longitudinal programproject on affect regulation in families with a parent historyof COD. Of the 74 children, 44 had a maternal history ofCOD. All offspring in the COD group in the target agerange were assessed (31 families total, with a range of 14children per family); as a result, nine families contributedmore than one child. One child per control family wasassessed. The effect of including multiple siblings fromsome families in the COD group was accounted for

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statistically by using random effects modeling to control forshared variance among siblings. A total of 40 dyads hadchild frontal EEG asymmetry data from both time points;60 had child affective behavior data from both time points;and 34 families had both types of data from both timepoints.

Families were recruited either through prior researchstudies or community advertisements. A subgroup of theCOD mothers (n=17) had participated in a longitudinal,naturalistic follow-up study of COD during childhood(Kovacs et al. 1984a). The remaining mothers in the CODgroup (n=14) were recruited from the community duringadulthood. Mothers in both COD subgroups had docu-mented histories of childhood-onset mood disorders. Moth-ers in the two COD subgroups did not differ in depressivesymptoms at either time point or in lifetime comorbiddisorders. In the control group, families (n=30) wererecruited by accessing individuals who had participated instudies during their childhood or adolescence as normalcontrols, soliciting participation using the Cole directoryof households in neighborhoods comparable in socioeco-nomic status to the COD group, and advertising in thegeneral community or through special community pro-grams. For adults in the control group, criteria forparticipation in the program project included a lifetimehistory free of major psychiatric disorder. All adultparticipants were required to be free of major systemicmedical disorders.

Families in the current study were selected from thelarger program project sample if five criteria were met: (1)the adult participant was a woman with children; (2)children were in the age range of 39 years; (3) childrenhad been assessed in both the psychophysiology study andthe motherchild interaction study; (4) children hadcomplete resting EEG data from the psychophysiologyassessment; and (5) mothers had completed symptomquestionnaires in the motherchild interaction study at theinitial assessment and again one year after the childsparticipation in the psychophysiology and motherchildinteraction studies. The age range of 39 years was selectedbecause of the increasing acquisition of affect regulationskills during this period and the inclusion of this age rangein similar studies (e.g., Cole 1986). For program projectfamilies with children age 39 years who completed themotherchild interaction study at time 1, 63% of childrenreturned for another assessment one year later. Of those,76% also completed the psychophysiology study at time 1.

As shown in Table 1, children of mothers in the CODand control groups did not differ in age, ethnicity, orhandedness, although the control group contained a greaterproportion of EuropeanAmerican children than did theCOD group (X2=4.01, p

this subgroup was evaluated using the SCID. The subgroupcontaining the remaining mothers in the COD group wasdiagnosed with COD based on psychiatric and/or researchdocumentation dating from childhood. In addition, thissubgroup was administered the SCID at the time of entryinto the study to confirm the presence of childhood mooddisorder and to assess current disorders.

Design, Procedure, and Data Quantification

Laboratory Visits At both time points, participants visitedtwo laboratories: a psychophysiology laboratory, in whichchild resting EEG was recorded; and a parentchildinteraction laboratory, in which motherchild interactionwas observed. Participants completed affect-eliciting tasksin both laboratories. The visits to the two laboratoriesoccurred within 2 months of each other for 88% of theparticipants, with 6 months as the greatest lag between thevisits. After the physiology assessment, children wereadministered an 11-item behavioral version of the Edin-burgh Handedness Inventory (Oldfield 1971) adapted forchildren. During the motherchild interaction assessments,mothers completed questionnaires about their currentdepressive and anxiety symptoms. At time 2, approximatelyone year later, the psychophysiology and motherchildbehavior assessments were repeated.

Childrens Affective Behavior Mothers and children en-gaged in a series of 45 tasks lasting 25 min designed toelicit (1) both positive and negative affect in children and(2) comparable levels of affect for children varying indevelopmental status. For example, at age 3, tasks involveda dinosaur puzzle; Etch-a-Sketch (fine-motor drawingboard), stack-n-pop (motor and balance), and toss-a-cross(gross motor and handeye coordination) games; andexposure to a wiggle ball (a ball with flashing lights thatemits shrill sounds). At age 5, tasks included HungryHungry Hippos (a competitive game involving fine motorskills and speed), Marble Works (a building task usingmarbles), a naming game (e.g., name things that fly), ashape sorter task, and a tractor treader (a large wheel thatturns when a child crawls while inside it). At least one taskwithin each group was selected to provide a provocative orfrightening element (e.g., wiggle ball at age 3). Because thetasks were designed to elicit similar amounts of positiveand negative affect across the age range of children in thestudy, we did not expect to find age effects on behavior.

Childrens affective behavior was subsequently coded fromvideotapes. The following behaviors were coded within 10-sintervals: positive affect, negative affect, disruptiveness, taskinvolvement, and task uninvolvement. Additionally, codersrated the following behaviors on four-point global scales afterviewing all tasks: positivity toward mother, negative affect

toward mother, involvement with tasks, involvement withmother, appropriate affect, inhibition, and sociability. Allcoders were blind to the group status of participants. Kappasfor coder reliability ranged between 0.590.76, with a mean of0.65. These levels are consistent with established reliabilityexpectations for observational codes (Mitchell 1979).

Behavioral data were reduced using principal compo-nents analysis with varimax rotation, which resulted in atwo-factor solution. The two factors that emerged explained53% of the variance and corresponded to task engagementand affect expression.1 The affect expression factorexplained 16.5% of the variance (eigenvalue=1.97, internalconsistency alpha=0.60) and involved low negative affect(loading=0.60), low negative affect toward mother(0.47), high positive affect toward mother (0.67), highsociability (0.79), and high appropriate affect (0.73). Basedon our hypotheses and the literature on children at risk fordepression, we included the affect expression factor inhypothesis tests. At low levels, this factor representsfrequent expression of negative affect; at high levels, thefactor represents frequent expression of positive affect.Because the factor includes sociability and appropriateaffect, high levels are likely to reflect the suitability ofaffect expression for the social context. The inclusion ofboth negative affect and positive affect in this empiricallyderived factor is consistent with research indicating that thebalance of positive and negative affect is related to humanflourishing, which represents optimal mental health(Fredrickson and Losada 2005), and that positive andnegative affect are somewhat related (e.g., Watson 2000).

Frontal EEG Asymmetry Childrens EEG was recordedduring six 30-s resting segments, during which children satquietly and alternately looked at a small model spaceshipand closed their eyes. EEG was recorded with an electrodecap (Electro-Cap International) placed according to stan-dard landmarks. The following sites were included forchildren: mid-frontal (F3, F4), lateral frontal (F7, F8),central (C3, C4), anterior temporal (T7, T8), mid-parietal(P3, P4), and occipital (O1, O2).

On-line recordings were referenced to the vertex (Cz),then re-referenced to a whole-head average. The signal wasamplified with a gain of 5,000 and bandpass filtered at 1100 Hz. Data were digitized on-line at a sampling rate of512 Hz per channel. Electrode impedances were below 5 k,and impedances for homologous sites were within 0.5 k.Vertical and horizontal electrooculogram (EOG) data were

1 We have previously used the term affect regulation for this factorbecause we conceptualize it as a proxy, in some ways, for appropriateaffect regulation in a social context. Upon reconsideration of theconstruct captured by this combination of behaviors in this behavioralparadigm, we have decided that affect expression is a more appropriateterm.

J Abnorm Child Psychol (2008) 36:207221 211211

used to identify and manually remove eye movementartifact. Artifact rejection was conducted by two trainedcoders who were blind to group status. Coders visuallyinspected data from EOG and EEG channels for the entireresting period and manually removed data from epochs thatincluded blinks, eye movements, or motor activity. EOG wasrecorded using tin cup electrodes; vertical EOG electrodeswere placed on the suborbital and supraorbital areas aroundthe right eye, and horizontal EOG electrodes were placed onthe left and right outer canthi.

The EEG signal was quantified with discrete Fouriertransformation (DFT) using a Hanning window 1-s wideand with 50% overlap. Prior to DFT computation, the meanvoltage was subtracted from each data point to eliminateany influence of DC offset. Power (in units of picowattOhms or squared microvolts) was computed for 1-Hzfrequency bins for frequencies between 1 and 30 Hz. Thefrequency range of interest was the alpha band, which isputatively inversely related to brain activation (Pfurtschelleret al. 1996). Based on an examination of each participantsEEG activity in single-Hz bins, as well as previous develop-mental findings (Marshall et al. 2002), the alpha range wasdefined as 710 Hz for 3- to 5-year-olds and 811 Hz for 6-to 9-year-olds. Alpha power values (in picowattOhms orsquared microvolts) for each electrode site were weighted bythe number of artifact-free epochs in each segment andaveraged across segments. Average values were subjected toa natural-logarithm transformation to normalize distributions(Gasser et al. 1982). Following a widely used approach(Davidson et al. 2000b), asymmetry scores were computedas the difference of transformed power scores for midfrontalleads (lnF4lnF3). Positive scores reflect greater relative leftfrontal activity, and negative scores reflect greater relativeright frontal activity.

Mothers Symptoms Mothers current depressive and anxietysymptoms were measured using the Beck DepressionInventory (BDI; Beck et al. 1988a) and the Beck AnxietyInventory (BAI; Beck et al. 1988b), respectively. Thesequestionnaires are reliable and valid self-report measures ofdepressive and anxiety symptoms. Each questionnaire con-tains 21 items, with four possible responses per item. Internalconsistency for the entire set of items was high for both theBDI and the BAI (Cronbachs =0.92 for each).

Data Analysis

Hypotheses were tested using repeated measures randomeffects models, which allow modeling of within-familysimilarity (across siblings) and within-mother similarity(across time) and which have important advantages overtraditional models that assume independence of cases.

Random effects models adjust the degrees of freedom foreach factor to accommodate the presence of both fixed andrandom factors in the model.

Mothers level of depressive symptoms was the depen-dent variable. COD group, child frontal EEG asymmetry,and child affect expression were fixed effects. Family andmother were random effects. The family effect could bemodeled only for the COD group, since siblings werepresent in this group but not the control group. Time was awithin-subjects factor. Rather than consider time 1 depressivesymptoms an independent variable and time 2 depressivesymptoms the dependent variable, we included time as anindependent variable in a repeated-measures analysis. Wecould then test whether depressive symptoms changed withtime and whether the relation between child characteristicsand maternal depression varied with time (i.e., time interactedwith other fixed effects). The compound symmetry covariancestructure was used.

We computed a random effects model with only maineffects, then a full model with both main and interactioneffects. As the emphasis of the full-model analyses was onfactors related to change in mothers symptoms, hypothesistesting was focused on two- and three-way interactions thatincluded time (e.g., time X COD X frontal EEG asymmetry).

Level of anxiety symptoms at time 1 was included as acovariate, allowing us to examine an index of maternaldepression that is somewhat pure and independent ofanxiety. Because depressive symptoms and anxious symp-toms tend to be strongly correlated (r=0.78, p

confidence intervals that correspond to conditional valuesof the moderator.

Finally, in an attempt to examine whether findings mightreflect a direction of effects from children to mothers (inaddition to effects from mothers to children), we conductedexploratory cross-lagged path analysis models using datafrom both time points. Because only a subset of cases hadchild data from both time points (e.g., 40 for frontal EEGasymmetry), limiting our power to detect effects with largemodels, we conducted separate models for child frontalEEG asymmetry and child affect expression, with the childvariable and maternal depressive symptoms included atboth time points. Within each model, child and mothereffects were estimated simultaneously, accounting for theautoregressive relations between child and mother measuresat two time points and the relations with COD group.

Preliminary Findings

Preliminary random effects regression models examined theeffects of child age, gender, ethnicity, or family SES onchild physiology, child affect expression, and motherssymptoms of depression. None of these characteristics wasrelated to the variables of interest. In addition, results of thefull model for depressive symptoms did not differ when weincluded ethnicity (defined as EuropeanAmerican or non-EuropeanAmerican), when left-handed participants wereremoved from EEG-related analyses, or when child age wasincluded as a covariate. Thus, these variables weresubsequently excluded from the main analyses. Further-more, the pattern of findings did not differ when modelswere computed with child age as a factor or when siblingswere excluded from the analyses. Models with significantfrontal EEG asymmetry effects were re-computed withparietal rather than frontal asymmetry, confirming thateffects were specific to the frontal region.

Bivariate correlation analyses indicated that age, maternalhistory of COD, child affect expression, and child frontalEEG asymmetry were uncorrelated (rs=0.01 to 0.14, ps>0.14; Spearmans rho=0.01 to 0.07, ps>0.10 for correla-tions with COD group). Maternal history of COD wasmoderately correlated with depressive symptoms and anx-iety symptoms (Spearmans rho=0.60 p

depressive symptoms is depicted in Fig. 1a. To examinethis interaction, the sample was split by COD group, andrandom effects regression models were conducted for eachgroup. The time X frontal EEG asymmetry interaction wassignificant within the COD group, F(1, 41.92)=9.21, p /JPEG2000ColorACSImageDict > /JPEG2000ColorImageDict > /AntiAliasGrayImages false /DownsampleGrayImages true /GrayImageDownsampleType /Bicubic /GrayImageResolution 150 /GrayImageDepth -1 /GrayImageDownsampleThreshold 1.50000 /EncodeGrayImages true /GrayImageFilter /DCTEncode /AutoFilterGrayImages true /GrayImageAutoFilterStrategy /JPEG /GrayACSImageDict > /GrayImageDict > /JPEG2000GrayACSImageDict > /JPEG2000GrayImageDict > /AntiAliasMonoImages false /DownsampleMonoImages true /MonoImageDownsampleType /Bicubic /MonoImageResolution 600 /MonoImageDepth -1 /MonoImageDownsampleThreshold 1.50000 /EncodeMonoImages true /MonoImageFilter /CCITTFaxEncode /MonoImageDict > /AllowPSXObjects false /PDFX1aCheck false /PDFX3Check false /PDFXCompliantPDFOnly false /PDFXNoTrimBoxError true /PDFXTrimBoxToMediaBoxOffset [ 0.00000 0.00000 0.00000 0.00000 ] /PDFXSetBleedBoxToMediaBox true /PDFXBleedBoxToTrimBoxOffset [ 0.00000 0.00000 0.00000 0.00000 ] /PDFXOutputIntentProfile (None) /PDFXOutputCondition () /PDFXRegistryName (http://www.color.org?) /PDFXTrapped /False

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