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Published online before print December 24, 2007, 10.1097/PSY.0b013e318160687c
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Psychosomatic Medicine 70:160-169 (2008)
© 2008 American Psychosomatic Society

ORIGINAL ARTICLES

Violence Exposure, A Chronic Psychosocial Stressor, and Childhood Lung Function

Shakira Franco Suglia, MS,ScD, Louise Ryan, PhD, Francine Laden, ScD, Douglas W. Dockery, ScD and Rosalind J. Wright, MD,MPH

From the Department of Epidemiology (S.F.S., F.L., D.W.D.), Department of Environmental Health (S.F.S., F.L., D.W.D.), Department of Biostatistics (L.R.), and Department of Society (R.J.W.), Human Development and Health, Harvard School of Public Health, Boston, Massachusetts; and Channing Laboratory (R.J.W.), Brigham & Women’s Hospital, Boston, Massachusetts.

Address correspondence and reprint requests to Shakira Franco Suglia, Harvard School of Public Health, Department of Environmental Health, Landmark 415W, 401 Park Drive, Boston, MA 02215. E-mail: sfranco{at}hsph.harvard.edu


   ABSTRACT
TOP
 ABSTRACT
INTRODUCTION
 METHODS
 RESULTS
 DISCUSSION
 NOTES
 REFERENCES
 
Objective: Chronic psychosocial stressors, including violence, and neuropsychological and behavioral development in children as well as physiologic alterations that may lead to broader health effects.

Methods: We studied the relationship between violence and childhood lung function in a prospective birth cohort of 313 urban children (age range = 6–7 years). Mothers reported on their child’s lifetime exposure to community violence (ETV) and interparental conflict in the home (Conflict Tactics Scale (CTS)) within 1 year of the lung function assessment.

Results: In linear regression analyses, adjusting for maternal education, child’s age, race, birthweight, tobacco smoke exposure, and medical history, girls in the highest CTS verbal aggression tertile had a 5.5% (95% confidence interval (CI) = –9.6, –1.5) decrease in percent predicted forced expiratory volume (FEV1) and a 5.4% (95% CI = –9.7, –1.1) decrease in forced vital capacity (FVC) compared with girls in the lowest tertile. The CTS verbal aggression subscale was associated with lung function among boys in the same direction, albeit this was not statistically significant. Boys in the highest ETV tertile had a 3.4% (95% CI = –8.0, 1.1) lower FEV1 and 5.3% lower FVC (95% CI = –10.2, –0.4) compared with boys in the lowest tertile. The ETV score was not a significant predictor of girls’ lung function.

Conclusions: Interparental conflict, specifically verbal aggression, and ETV were associated with decreased childhood lung function independent of socioeconomic status, tobacco smoke exposure, birthweight, and respiratory illness history. Gender differences were noted based on the type of violence exposure, which may warrant further exploration.

Key Words: lung function • violence exposure • children

Abbreviations: ETV = exposure to violence; CTS = Conflict Tactic Scale; FEV1 = forced expiratory volume; FVC = forced vital capacity; FEF25%–75% = forced mid-expiratory flow rate; UTS = in utero tobacco smoke; SHS = second hand smoke.


   INTRODUCTION
TOP
 ABSTRACT
 INTRODUCTION
METHODS
 RESULTS
 DISCUSSION
 NOTES
 REFERENCES
 
Earlylife factors contributing to lung growth are of interest, given that childhood lung function is important to the development of chronic obstructive pulmonary disease (COPD) in later life (1). The public health implications are substantial as COPD is projected to be the fourth leading cause of death worldwide by the year 2020 (2). To date, longitudinal studies of the natural history of lung function have shown that a number of early life risk factors including asthma (3), active and passive smoking prenatally and during childhood (4,5), atopy (6), lower respiratory infections (7), and perinatal factors including birthweight, gestational age, and nutrition (8,9) are associated with reduced lung function over the life course. However, these factors account for a small proportion of the risk, suggesting that as yet unidentified risk factors deserve further exploration.

Overlapping research from a number of areas suggest that negative emotion and psychological stress influence respiratory processes and lung function, having both transient (10,11) and more long-term effects (12). These findings have been described in asthmatics and normal controls as well as both children and adults, albeit studies demonstrating more long-term effects have focused largely on adults.

The mind-body paradigm linking psychological stress and affective states to key physiological mechanisms (e.g., neuroendocrine and immune functioning, oxidative stress, autonomic response) and ultimately to disease expression provides a framework to explore plausible physiologic mechanisms through which psychological stress may operate to influence lung function (13). Factors known to induce chronic persistent inflammation (e.g., tobacco smoke exposure, asthma, air pollution, viral respiratory infections) are recognized risk factors for reduced lung function (14,15). Imbalance of physiologic processes that lead to chronic inflammation (e.g., hypothalamic-pituitary-adrenal (HPA) axis function, the proteases-antiproteases, the oxidants-antioxidants) can occur both in the face of these known risk factors (15) and under chronic stress (13). In humans, altered cortisol expression has been negatively associated with lung function (16). Chronic caregiver stress in the postpartum and early childhood periods have been associated with persistent wheeze in early childhood (17) as well as factors that may initiate or potentiate inflammation in the lung (e.g., immunoglobulin E (IgE) expression, enhanced nonspecific and allergen-specific lymphocyte proliferation, differential cytokine expression) (18,19). Both persistent wheeze and atopy have been linked to reduced lung function in childhood (20). Chronic psychological stress has also been linked to other risk factors that are associated with reduced lung function including asthma (13), respiratory infections (21,22), and smoking behaviors. Other studies have associated lung growth and development with broader social constructs known to be associated with increased psychosocial stress and more negative affect (e.g., lower socioeconomic status) (23–25).

Recent research considers exposure to violence, conceptualized as a specific chronic psychological stressor, as a major cause of childhood morbidity in urban communities, including respiratory outcomes (26). The notion that experiencing episodic violence leads to chronic psychological stress is grounded in trauma theory (27). In general, stressors are thought to influence the pathogenesis of disease by causing negative affective states (e.g., anxiety, depression, and posttraumatic stress disorder (PTSD)), which in turn exert direct effects on biological processes or behavioral patterns that influence disease risk (28). When environmental demands are perceived to be threatening and exceed one’s abilities to cope or when one feels that events are unpredictable or that one has no control, the individual experiences stress. Children and families living with violence are likely to view their world and their lives to be out of their control. Living in an unpredictable or uncontrollable environment associated with a chronic pervasive atmosphere of fear and perceived threat predisposes these populations to greater deleterious effects of stress (26,27). A growing body of research, conceptualizing violence exposure as a chronic psychosocial stressor, documents the adverse psychological, behavioral, and physiological consequences on children growing up in chronically violent neighborhoods and homes (26,29–32).

Frequency of experiencing and witnessing serious and lethal violence among inner-city youth are high, particularly among lower socioeconomic status (SES) urban communities in the United States (33). In addition, estimates of domestic violence against women and children indicate widespread exposure to violence in the home (34). Given this, research focused on understanding the possible broader pediatric health effects of growing up with violence is of great public health importance.

We examined the association between violence exposure, conceptualized as a chronic psychological stressor, and lung function among urban children adjusting for SES, in utero and second hand tobacco smoke (SHS) exposure, birthweight, and history of respiratory illness including asthma, allergies, and lower respiratory tract infections which may mediate this relationship.


   METHODS
TOP
 ABSTRACT
 INTRODUCTION
 METHODS
RESULTS
 DISCUSSION
 NOTES
 REFERENCES
 
Study Population
Participants were drawn from the Maternal-Infant Smoking Study of East Boston, a prospective cohort designed to study the effects of pre- and postnatal tobacco smoke exposure on childhood lung growth and development and respiratory health (4). Pregnant women receiving prenatal care (<20th week of gestation) at an urban community health center in Boston, Massachusetts, between March 1986 and October 1992 were eligible for enrollment. Women who did not speak English or Spanish, who did not plan to have pediatric follow-up at the clinic, or who were <18 years of age were excluded. One thousand women were eligible and enrolled, of whom 848 continued participation and delivered live-born infants. In 1996 to 1997, new study initiatives were implemented, including the assessment of social stressors, at which time 500 women and their children continued active follow-up. The Human Studies Committees at the Brigham & Women’s Hospital and the Beth Israel Deaconess Medical Center approved the study.

Violence Exposure Assessment
Violence exposure was ascertained using a modified version of the Survey of Children’s Exposure to Community Violence (ETV) (29). The ETV questionnaire gathers data on both direct victimization and witnessing violence as well as factors known to influence the impact of violence (e.g., familiarity with the perpetrator or victim, events occurring more than once, and events occurring at home). The survey measured lifetime exposure to specific events including hearing gunshots, and witnessing and/or experiencing shoving, hitting or punching, knife attacks, or shootings. Mothers were asked to report on their child’s lifetime exposure to violence. Among subjects continuing participation in 1996 to 1997, 412 mothers completed the violence assessment. Those who did not participate in the violence assessment were more likely to be non-Hispanic (52% nonresponders versus 45% responders) and current smokers (42% nonresponders versus 28% responders). In addition, 171 children who were at least 8 years of age reported on their own lifetime community violence exposure on the ETV questionnaire. Acceptable 2-week test-retest reliability in a random sample of mothers and their children has been demonstrated for the violence survey in this cohort (35).

Mothers also completed the Conflict Tactics Scale (CTS) Form R (36) designed to measure the extent to which their spouse or partner engaged in psychological and physical attacks against them in the past year. Internal consistency, test-retest reliability, and validity have been established for the CTS including the Spanish translation (37). The CTS was scored according to published guidelines—subscales were calculated for verbal aggression and physical violence (38). The verbal aggression subscale consisted of seven items (e.g., insulting or swearing at a partner, destroying a belonging, threatening to hit a partner). Minor physical violence consisted of three items (e.g., throwing something at a partner, pushing, or slapping). Severe physical violence included six items (e.g., did your partner kick, hit, choke, or beat you or use a knife or gun against you?). Participants indicated whether a behavior had occurred never, once, twice, 2 to 5, 6 to 10, 11 to 20, or >20 times in the past year. Subscales were calculated by converting the frequency categories to a 0 to 6 scale and summing the items within each of the three subscales. Among those reporting any of the major violence events (n = 91), nearly all (n = 83) also reported minor violence consistent with prior research (38). Because of the significant overlap between the minor and major violence subscales, these were combined into a composite scale for any physical violence. Scores on the CTS subscales ranged from 0 to 30 (mean ± standard deviation, 12.3 ± 7.8) on the verbal aggression subscale and from 0 to 39 (3.3 ± 6.1) on the physical violence subscale.

Lung Function Measures
Lung function was measured using a spirometer (P. K. Morgan, Andover, Massachusetts) when children were between the ages of 6 and 7 years, within 1 year of the violence assessment. Standing height without shoes was measured before spirometry. The lung function protocol was developed by an experienced pulmonologist and pediatric pulmonary function technologist. The children were not naïve to spirometry as they had been participating in lung function testing from the time they were 4 years old in anticipation of formal testing at age 6 to 7 years. A trained pulmonary function technologist instructed children during testing and monitored the flow-volume curve to ensure good effort. Maneuvers were repeated to obtain three acceptable curves; data from each technically acceptable effort were stored following established guidelines (39,40). Forced expiratory volume in 1 second (FEV1), forced vital capacity (FVC), and forced mid-expiratory flow rate (FEF25% –75%) were measured from the best acceptable blow (39).

Covariates
Demographic characteristics as well as smoking and medical history were ascertained through standardized questionnaires. Maternal education level was categorized as less than high school, high school graduate or technical school graduate, or some college. Low birthweight was defined as <2500 g.

At each clinic visit during pregnancy, mothers were asked about their smoking status and a urine specimen was obtained for determination of a creatinine-corrected cotinine (4). Mothers were classified as nonsmokers if they always reported not smoking and each of their urine cotinine levels were <200 ng/mg creatinine (4). If the report of nonsmoking by the mother was contradicted by the urine cotinine, the mother was classified as a current smoker for that interval. Maternal reported postnatal SHS exposure was assessed monthly through age 26 months, every 6 months between 26 months and 4 years, and annually thereafter. Children were considered to be exposed to SHS at each follow-up interval if the mother reported active smoking or smoking by any other person living in the household. Postnatal SHS was categorized as early only (occurring from birth to 25 months of age) and both early and late as there were few children (n = 20) in the late only category (≥26 months). Also, prenatal smoke exposure was highly correlated with postnatal SHS exposure (i.e., of 66 children exposed to in utero tobacco smoke, only one was not exposed to SHS after birth).

Information on respiratory illness history was ascertained using the standardized ATS-DLD-78-C questionnaire (41). History of childhood asthma was determined based on parental report of physician-diagnosed asthma. Mothers were also asked if their child was ever diagnosed with hay fever, eczema or if they received allergy shots up until the time that pulmonary function testing occurred. Presence of allergies was dichotomized as none, or one or more (eczema, hay fever, or allergy shots). In addition, they were asked whether the children had had a lower respiratory tract infection (croup, bronchitis, bronchiolitis, or pneumonia) on the monthly follow-up questionnaires administered from birth to the time the child was 2 years old. Lower respiratory infections were categorized as having had none, one to two, and three or more in that interval.

Statistical Analysis
Lung function measurements were available for 330 children who also had information on violence exposure. Among the children for whom violence exposure data were available, there were no significant differences between those who participated in the lung function tests and those who did not based on sociodemographics, medical history, tobacco smoke exposure, or violence exposure. Seventeen children were missing data on birthweight, mother’s education level, or in utero tobacco exposure, leaving 313 children for analyses.

We implemented Rasch modeling techniques to summarize responses to the community ETV questionnaire into a continuous score (35,42). The continuous ETV measurement was obtained by modeling the conditional probabilities of responding yes to each violence question, given the extremity of each question and the true, but unobserved, violence exposure level of each person. The model was generalized to account for salient features of each event (e.g., whether the event occurred once or more than once, whether the child knew the victims or perpetrators) (43) and to include both the mother and child’s report of events in a multi-informant model (44). The Rasch model produces two scores, one based on the parent’s responses to the violence survey, the other on the child’s responses to the survey. If a child is missing his or her self-report, the model predicts the Rasch score based on the existing correlation between the parent’s and child’s responses in the remainder of the cohort, so that all children have two scores. The final violence score is the average of the two Rasch scores. This is a desirable approach as children are unlikely to be able to recall events occurring during very early childhood at the same time that parents may be more likely to underreport events that occur when children are older and violence occurs outside of the parents’ supervision (45,46). As violence was assessed within 1 year of lung function testing, some subjects reported experiences that may have occurred after lung function was measured. For each item on the ETV asking about a particular event, subjects and their mothers were asked a follow-up question to report how old the child was when each reported event had occurred. Only those events reported before the lung function measurement were included in the Rasch model. In prior research, construct validity using Rasch modeling to summarize the multi-item survey of exposure to community violence demonstrates that the summary measure is moderately to strongly associated with aggressive behavior, delinquency, and psychological comorbidities (e.g., anxiety, depression) in a positive direction as expected (47,48). We previously reported the inverse relationship between sociodemographic factors and the Rasch ETV in this cohort (35), corroborating other research (46,48). As a further validity check, we assessed the relationship between the Rasch ETV scale and the parent-report version of the Checklist of Children’s Distress Symptoms (CCDS) (49), which had been administered contemporaneously with the violence assessment in this sample. The CCDS is a 24-item measure of children’s distress symptoms (including posttraumatic stress symptoms) occurring in the previous 6 months, with higher scores indicating greater distress. In these data, the continuous ETV measure was positively correlated with scores on the CCDS (Spearman r = .31, p < .0001).

Estimated effects of lung function are reported using percent predicted lung function (based on height, age, gender, and race/ethnicity) as the independent variable. To obtain the predicted lung function values for each child, we regressed the log-transformed lung function measures against log height, age, gender, and race/ethnicity. The effect of the violence measures on lung function was estimated using multiple linear regression adjusting for mother’s education level, child’s age, race/ethnicity, birthweight, pre- and postnatal smoking exposure. All models were stratified by gender. The Rasch community ETV measure and the CTS subscales were entered as continuous measures (per 1-SD change) and also considered tertiles to assess for a threshold effect or a dose-response relationship (50). To evaluate whether lower respiratory infections and having a history of asthma or allergies would attenuate the association between violence exposure and lung function, we conducted additional regressions further adjusting for these variables. Model assumptions were assessed using regression diagnostics. All analyses were conducted in SAS version 9.0 (SAS Institute, Cary, North Carolina).


   RESULTS
TOP
 ABSTRACT
 INTRODUCTION
 METHODS
 RESULTS
DISCUSSION
 NOTES
 REFERENCES
 
Fifty percent of the children were females, 51% Hispanic, 39% of the mothers had not completed high school, and 21% of the mothers smoked during pregnancy (Table 1). The average age for both boys and girls at the time of lung function testing was 6.2 ± 0.3. The lung function results for girls were FEV1 1.25 ± 0.20 L, FVC 1.35 ± 0.22 L, and FEF25% –75% 1.81 ± 0.40 L/sec and for boys were FEV1 1.31 ± 0.21 L, FVC 1.42 ± 0.25 L, and FEF25% –75% 1.84 ± 0.44 L/sec. There were no significant differences in the level of exposure on the violence scales when comparing boys and girls. Scores on the continuous scales comparing boys and girls, respectively, were 1.08 ± 0.09 versus 1.11 ± 1.1 on the ETV, 1.44 ± 1.0 versus 1.63 ± 0.9 on the CTS verbal aggression subscale, and 0.46 ± 0.9 versus 0.61 ± 1.1 on CTS physical violence subscale.


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  		TABLE 1. Mean and Standard Error of Mean Height-Adjusted Lung Function Outcomes by Demographic and Exposure Characteristics; Stratified by Gender

 


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  		TABLE 1. Continued

 
Unadjusted analyses are presented in Table 1. In multivariate models (Table 2), a 1-SD increase in the verbal aggression scale significantly predicted a 2.8% decrease (95% Confidence Interval (CI) = –4.6, –1.0) in FEV1 and a 2.4% decrease (95% CI = –4.0, –0.7) in FVC among girls. Girls exposed to tobacco smoke exposure in utero had a 6.4% (95% CI = –12.1, –0.7) decrease in FEV1; those exposed to early second hand smoke up to 25 months of age had a 7.0% decrease (95% CI = –13.1, –0.9); and those exposed to both early and late tobacco smoke postnatally had a 4.5% decrease (95% CI = –9.1, 0.04) in FEV1 compared with girls who were not exposed to tobacco smoke. Similar decreases were noted in FVC among girls. No significant associations were noted with tobacco smoke exposure among boys (data not shown).


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  		TABLE 2. Percent Predicted (95% Confidence Interval) Lung Function Measures Stratified by Gender: Adjusted Linear Regression Models

 

In multivariate analyses of the violence categorical variables, girls exposed to the highest tertile of verbal aggression had significantly lower FEV1 5.5% (95% CI = –9.6, –1.5; p for trend .007), and FVC 5.4% (95% CI = –9.7, –1.1; p for trend .01), compared with girls in the lowest tertile (Figure 1); girls in the highest tertile of physical violence exposure at home had also lower FEV1 4.0% (95% CI = –8.4, 0.4; p for trend .05) and FVC 2.6% (95% CI = –7.3, 2.2; p for trend .13). The ETV indicator was not significantly related to lung function among girls. Among boys, exposure to the highest tertile of the ETV scale compared with the lowest was associated with decreases in FEV1 3.4% (95% CI = –8.0, 1.1); p for trend 0.14) and FVC 5.3% (95% CI = –10.2, –0.4; p for trend .03) (Figure 2). Higher scores on the verbal aggression CTS subscale were also associated with reduced lung function in boys although these associations did not reach statistical significance. Boys in the 2nd tertile of physical violence exposure had lower FEV1 –4.0% (95% CI = –8.7, 0.7) and FVC –5.0% (95% CI = –10.1, 0.1) compared with boys in the lowest category; however, boys in the highest tertile had a higher FEV1 3.3% (95% CI = –2.1, 8.7) and FVC 2.1% (95% CI = –3.8, 7.9) than boys in the lowest category of exposure. No significant associations between FEF25%–75% and the verbal aggression, physical violence CTS subscale, or ETV were found.


Figure 15
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  		Figure 1. Girls percent predicted (95% confidence interval) lung function measures: adjusted linear regression models. FEV1 p for trend: verbal aggression p = .007; ETV p = .73; physical violence p = .05. FVC p for trend: verbal aggression p = .01; ETV p = .55; physical violence p = .13. Each multivariate model is adjusted for race/ethnicity, birthweight, age, tobacco smoke exposure, and maternal education. Ver = verbal aggression tertiles; ETV = Exposure to Violence Scale tertiles; Phys = physical violence scale tertiles; tertiles are ranked from 1 = lowest level of exposure to 3 = highest level of exposure.

 

Figure 25
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  		Figure 2. Boys percent predicted (95% confidence interval) lung function measures: adjusted linear regression models. FEV1 p for trend: verbal aggression p = .41; ETV p = .14; physical violence p = .89. FVC p for trend: verbal aggression p = .11; ETV p = .03; physical violence p = .62. Each multivariate model is adjusted for race/ethnicity, birthweight, age, tobacco smoke exposure, and maternal education. Ver = verbal aggression tertiles; ETV = Exposure to Violence Scale tertiles; Phys = Physical violence scale tertiles; tertiles are ranked from 1 = lowest level of exposure to 3 = highest level of exposure.

 

On further adjustment for asthma diagnosis, lower respiratory infections, or presence of allergies, the associations previously seen between the violence indicators and lung function did not change. To confirm that the associations seen were not due to the tertile categorization of the violence variables, we repeated these analyses categorizing the violence variables by the median split and quartiles; the associations remained qualitatively similar.

We further explored two additional models: a) jointly modeling the verbal aggression scale and the ETV scale, and b) jointly modeling the ETV scale and the physical violence scale. The independent significant associations noted when examining the verbal aggression scale remained statistically significant even after inclusion of the community ETV scale in the model. The effect estimates seen when independently examining the ETV scale and the physical violence scale did not change after inclusion of these two variables together in the model. Due to concerns with collinearity, we did not include all three measures in one model as the verbal and physical violence scales were highly correlated (r = .65, p < .0001).


   DISCUSSION
TOP
 ABSTRACT
 INTRODUCTION
 METHODS
 RESULTS
 DISCUSSION
NOTES
 REFERENCES
 
In this urban cohort, maternal report of community violence and parental conflict in the home were significantly associated with early childhood lung function even after adjusting for tobacco smoke exposure, race/ethnicity, birthweight, socioeconomic status, and relevant respiratory health factors including, asthma, allergies, and respiratory infections. Gender differences were observed suggesting differential effects of the type of violence exposure on lung function in that, among girls, indicators of parental conflict in the home had the greatest effect whereas, among boys, the community violence exposure seemed to have the stronger influence.

The observed reductions in childhood lung function in relationship to violence exposure measures were of comparable magnitude to effect estimates reported for prenatal tobacco smoke exposure and postnatal environmental tobacco smoke exposure both in our data and from other studies (51,52). In the 24 Cities Study, Cunningham et al. reported a 1.3% decrease in FEV1, 0.2% decrease in FVC, and 4.9% decrease in FEF25%–75% among children who were exposed to prenatal tobacco smoke exposure compared with those who were not exposed. Among children exposed to postnatal tobacco smoke, a decrease of 0.1% FEV1, 0.1% increase in FVC, and a 0.6% decrease in FEF25%–75% were reported compared with children not exposed (52).

A number of pathways can be considered when linking violence and lung function. Violence exposure has increasingly been conceptualized as a chronic social stressor (26). Psychological stress has been associated with the activation of the sympathetic and adrenomedullary (SAM) system and the HPA axis (13). Negative emotional responses disturb the regulation of the HPA axis and the SAM systems; that is, in the face of stress, physiological systems may operate at higher or lower levels than during normal homeostasis. The disturbed balance of these systems is relevant to disease. Immune, metabolic, and neural defensive biological responses important for the short-term response to stress may produce long-term damage if not checked and eventually terminated (53). Disturbed regulation of both the HPA axis and the SAM system related to chronic stress suggests that immune function, which is modulated by these systems, may also be dysregulated; this may have implications for respiratory processes including lung growth and development (13). Overlapping research in other studies has demonstrated that exposure to violence is associated with disrupted cortisol response in children (32,54). Finally, altered cortisol expression has been found to be negatively associated with lung function in adults, albeit this has not been studied in children (16).

Additionally, chronic stress may operate through pathways that have been hypothesized for other environmental toxicants influencing lung function (13). For example, tobacco smoke contains a number of compounds with oxidative potential (55). Spiteri et al. (56) proposed that differences in host detoxification provide the basis for either resolution or progression of inflammation in atopic individuals after exposure to an environmental trigger, such as allergens or air pollutants. This hypothesis may be extended to other environmental factors, such as psychological stress, that may augment oxidative toxicity and increase airway inflammation. Some studies suggest that psychological stress augments oxidative toxicity. Emotionally stressed rats have increased levels of 8-deoxy-hydroxy-guanosine (8-OhdG), a commonly used biomarker of oxidative stress (57). Similarly, staying awake all night increased the levels of thiobarbituric acid reactive substances (an indicator of lipid peroxidation) in humans (58). It is plausible that chronic stress may enhance airway inflammation through similar mechanisms to influence lung function.

Possible explanations for the observed gender differences based on type of violence exposure may be grounded in child development research, suggesting that factors may modify the impact of violence events occurring at home and in the community differently for boys and girls. Gender differences in psychological distress associated with marital or family discord have been demonstrated. Specifically, evidence suggests that girls possess a greater propensity than boys to become directly involved in parental conflict situations (59). Girls may be more susceptible than boys to adverse effects of family conflict, in part, because girls are more sensitive to affective cues and the states of others or because of identification with their mother, who is commonly the one being abused. Other research finds that aggressive responses to stressors, including community violence exposure, are more common among boys than among girls, which may lead to a more direct impact of community violence among boys (60). Boys are more likely to confront violent situations alone and with aggression whereas girls are more likely to respond with greater depressive symptomatology and seek out support in addressing problems (61). Such differential behavioral and psychological responding based on gender may also translate into varied disruption of underlying physiological stress pathways (e.g., HPA axis, nervous system reactivity) that, in turn, may have varied influence on physical health outcomes.

Moreover, the effects of violence exposure on health outcomes may also be mediated through the influence of violence on emotional development. In overlapping research, early life caregiving experiences and trauma exposures have been shown to influence childhood emotional understanding and expression (62,63) with some studies showing differential gender effects (64). Children exposed to violence and neglect in their environment have been found to express higher levels of negative emotion (anxiety, depressive mood, anger, hostility, and irritability) and more adverse stress reactivity (65,66). Negative emotion, in turn, has been linked to impaired lung function in both cross-sectional (67) and longitudinal analyses (12) whereas positive emotion seems to be protective (68).

It is also the case that methodological issues could partially explain the observed differences, in that boys may be more likely (relative to girls) to report experiences of violence; however, we found no difference in mean levels of violence scores based on gender in these analyses. We also noted more robust associations among girls than boys, particularly when continuous exposure indicators were utilized. Girl’s lung function was associated with conflict in the home, which was measured over the past year; boy’s lung function was associated with neighborhood violence, which was measured over the lifetime. It is possible there is less accurate recall among lifetime measures of exposures, leading to more random error which could lead to weaker associations. The observed U-shape relationship between witnessing physical violence at home and lung function among boys was unexpected. Although this is possibly a spurious association, existing literature has documented inverted U-shaped associations between stress and task performance consistent with Yerkes-Dodson (1908) model of stress and learning (69,70). However, it is difficult to conclude that higher levels of violence exposure lead to better lung function in this case. If such a relationship holds in future research, it will likely be more informative to also explore other characteristics of individuals showing enhanced functioning in the setting of violence exposure (e.g., resiliency factors, stress buffers, emotion regulation).

The present findings may be relevant to other empirical studies demonstrating an inverse association between childhood social status indicators and pulmonary function. Childhood SES predicted both baseline lung function and rates of decline among young adults in the Coronary Artery (Disease) Risk Development in (Young) Adults study (24) as well as in older women in the British Women’s Heart and Health Study (25), when controlling for current SES, childhood tobacco smoke exposure, and childhood asthma. Poor housing and neighborhoods are associated with increased exposure to environmental factors that may affect lung growth and development (e.g., chronic dampness, vermin, cockroaches, tobacco smoke, air pollution) (71,72). Marginalized populations of lower SES disproportionately exposed to these physical environmental toxicants may also experience elevated psychosocial stressors, such as violence exposure (26). Differential exposure to life stressors including violence may partially explain socioeconomic disparities in health (73) and thus warrants further attention.

We acknowledge a number of strengths and weaknesses in these analyses. The rigorous protocol used to assess lung function is a particular strength in this cohort. We were able to control for a number of covariates that have been associated with both violence exposure and lung function in prior studies (i.e., SES, race/ethnicity, and tobacco smoke exposure) as well as prenatal factors and child health indicators (i.e., birthweight, history of asthma, and/or allergies, respiratory infections). The use of cotinine validation of in utero tobacco exposure is an additional strength. However, it is possible that the observed associations may be due to unmeasured confounding by home characteristics or other exposures, which may affect children’s lung function and be associated with violence exposure, given that both may disproportionately affect lower-income urban populations (e.g., air pollution). The availability of both child self-report of violence exposure as well as parents’ report for their children can be seen as a strength, given that we were trying to examine the relationship between violence experienced before lung function assessment at a young age (approximately 6 to 7 years). Children are unlikely to recall very early life experiences with violence whereas parents may be more accurate reporters for the early preschool years. Although the concordance between parent-child reporting of violence exposure has been shown to be moderate, with parents consistently underreporting (35), the discordance increases as children get older and are no longer under direct parental supervision, particularly in the preadolescent years (i.e., ≥12 years) (45). Thus, discordance in reporting for earlier events, as in this analysis, is less of a concern.

Although we account for various forms of home and community violence exposure, we do not have information on sexual violence or more direct measures of child abuse and neglect potentially underestimating violence exposure. Moreover, if children were exposed to other violent events between the time of the initial assessment and the lung function measurements (as the violence could have been assessed up to 1 year before lung function testing), there may be misclassification of our sample based on violence exposure which would be expected to drive the results toward the null. Studies that both expand on the measure of different violence exposure types and ascertain exposure at specific critical periods of development may offer further insight into the characteristics of violence exposure that most affects lung development. Other considerations for future directions based on these findings include the assessment of emotion dysregulation and affective states as well as neuroendocrine biomarkers of purported stress pathways that may be mediating these effects. It will also be important to examine whether the effects of exposure to violence in early childhood and lung function hold as these children age into adolescence and early adulthood.

Chronic psychosocial stressors, including violence, have been linked to neuropsychological and behavioral development in children as well as physiologic alterations that may lead to broader health effects. However, the effects of violence exposure on children’s respiratory health are largely unknown. This study demonstrates a relationship between higher-level violence exposure, both at home and in the community, on childhood lung function, which was independent of tobacco smoke exposure, childhood SES, and respiratory illness history. Understanding early childhood risk factors that contribute to lung function growth and decline and may be amenable to prevention and intervention is an important area of research, given the relationship between childhood lung function and later development of chronic obstructive pulmonary disease (74). Studies, such as ours, may inform new interventions. Moreover, further exploration of specific environmental stressors, such as violence that disproportionately burdens lower-income populations, may also help to explain socioeconomic disparities in lung function.


   NOTES
TOP
 ABSTRACT
 INTRODUCTION
 METHODS
 RESULTS
 DISCUSSION
 NOTES
REFERENCES
 
Data collection for this study was funded by Grant K08 HL 04187 and a Deborah Monroe Noonan Foundation Grant. During preparation of this manuscript, Shakira Franco Suglia was supported by Grants F31 HD049317 and T32 ES007142; Rosalind J. Wright was supported by Grants R01 ES10932 and U01 HL072494.

Received for publication February 19, 2007; revision received September 18, 2007.

DOI:10.1097/PSY.0b013e318160687c


   REFERENCES
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 ABSTRACT
 INTRODUCTION
 METHODS
 RESULTS
 DISCUSSION
 NOTES
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Maternal Intimate Partner Violence and Increased Asthma Incidence in Children: Buffering Effects of Supportive Caregiving
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