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 while among boys, the community violence exposure seemed to have the stronger influence.
The observed reductions in childhood lung function in relation 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
). In the Six cities studies, 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 to those 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%
was reported compared to 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 hypothalamic-pituitary-adrenocortical (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. It is the disturbed balance of these systems that 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 and 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
). And 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. There are studies to 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 posses 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 while 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 impact childhood emotional understanding and expression (62
) 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
). Negative emotion, in turn, has been linked to impaired lung function in both cross-sectional (67
) and longitudinal analyses (12
) while 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. While 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
). 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 (CARDIA) 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
). 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. socioeconomic status, 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 impact 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 prior to lung function assessment at a young age (approximately 6 to 7 years). Children are unlikely to recall very early life experiences with violence while parents may be more accurate reporters for the early preschool years. While 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 and older) (45
). Thus, discordance in reporting for earlier events as in this analysis is less of a concern.
While 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 one year prior to 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 impact 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 socioeconomic status 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 burden lower income populations, may also help to explain socioeconomic disparities in lung function.