Children respond to what is happening around them. It is helpful that children are resilient, but their resilience should not be interpreted as conferring them with a kevlar physiology that protects them from the impact of stress as a response to what is happening around them. Preliminary results from on-going studies suggest that the stress caused by environmental exposure to violence is significantly linked to both poorer lung function in children and asthma exacerbations. There is some speculation about plausible stress mechanisms that might be responsible for this.
[The] effects of acute stress on airway functioning may be largely mediated through the autonomic nervous system, whereas chronic stress may lead to alterations in the immune system.(Laube et al. 2003; pg. 617).
There is some support for this observation. Although the immunological response is not well understood, researchers report different emotional responses that may be classified as stress responses with distinctive immunological implications. For example, Niaura et al. (2000) report that stress-related hostility can induce an imbalance between sympathetic and parasympathetic nervous system activity, adversely affecting cardiovascular, endocrine and neuroendocrine function. Hashiro and Okumura (1998) report that anxiety may affect immune function as measured by changed levels of immune markers and decreases in natural killer (NK) cell activity: however, Miller et al. (1999) report that negative emotions such as anger and cynical hostility are linked to an increase in NK activity.
Researchers such as Kemeny and Taylor take the challenge further. Kemeny (2003) argues that different stressors elicit qualitatively distinct emotional and physiological responses (the integrated specificity model). For example, Kemeny reports that appraisals of threat (vs. challenge), uncontrollability and negative social evaluation can be shown “to provoke specific psychobiological responses” (pg 124). Taylor (2000, 2002) claims that until 1995 research into the fight-or-flight response was primarily conducted with males; females constituted 17% of the participants, and the findings therefore concealed important gender differences. Taylor argues for the existence of a predominantly female tend-and-befriend response that may be linked both to female responsiveness to oxytocin and the traditionally nurturing nature that can characterise female relationships. These challenges need further investigation and validation and explicit application to asthma research. However, they do lend some support to the notion that it may be useful to distinguish emotional arousal and stress, and that within the arena of stress there are different behavioural opportunities and responses that carry different immunological consequences.
For people with asthma, it seems as if there may be different immunological consequences to responding with anti-social behaviours such as hostility and aggression, rather than co-operation and conciliation. Similarly, there may be different consequences for environmental exposure to hostility and aggression that results in fear or helplessness. It is possible that allostatic load
is a useful explanation for the frequently-observed time-lag response to sensitivity to allergens, or delayed asthma exacerbations following an emotional trigger or a negative stressful event. The concept of allostatic load suggests that a challenge is perceived as stressful and triggers the release of adrenal steroids and catecholamines that promote the movement of immune cells to organs and tissues (such as those lining the airways) where they are recruited to fight a challenge: they also impact the production of cytokines and chemokines. Although there may be short-term advantages to these responses, chronic over-activity of these mediators produces allostatic load with immunosuppressive consequences when these hormones are secreted chronically (as may occur with long-term stressors) or are not shut-off efficiently. There is an optimal balance of these mediators that provides a healthy, functional balance within the competitively-regulated immune system: the absence of adequate levels of glucocorticoids and catecholamines allows other immune mediators to be over-abundant and increases the risk of inflammatory responses and disorders such as asthma.
As an interesting reflection on the above, there are preliminary studies that point towards poorer lung function in children who are exposed to parental fighting at home and violence in the community or in school. Wright and her colleagues (Suglia et al, 2006) report that:
Verbal aggression in the home and community violence were significantly associated with lower lung function in children even after controlling for tobacco exposure, race, birth-weight, markers of socioeconomic status and self-reported asthma diagnosis.
The study was carried out by the same lead researcher who reported that optimism is linked to higher levels of optimism in old men
. The children's study evaluated a prospective cohort of 330 children who have been followed since early gestation as part of a study on smoking in pregnancy and early childhood. The researchers say that they were careful to control for other relevant factors such as socioeconomic status, pre- and postnatal tobacco exposure etc. that are known to affect lung function. Controlling for these factors means that they are confident that their results are a reflection of the impact of stress related to exposure to violence.
The investigators collected maternal reports and various rating scales to assess the level of parental conflict and violence in the home, as well as community exposure to violence. Children older than eight were asked to self-assess their exposure to violence. Two of the outcome measures collected by the researchers were forced expiratory volume at one second (FEV1) and forced vital capacity.
The researchers findings have yet to be verified by the peer-review process, but their initial report is that verbal aggression was associated with a significant decrease both in FEV1 (P<0.05)>same or higher magnitude as those reported for postnatal and prenatal tobacco smoke exposure on lung function. These findings are bolstered by a separate study that investigated the impact of exposure to violence at school on children with asthma.
Riekert and her colleagues evaluated a sample of 1704 highschool students with asthma (Otsuki et al. 2006). The researchers say that they were careful to control for relevant factors such as age, gender, ethnicity, or urban vs. suburban setting of the school attended etc. They report that their findings indicate that adolescents with asthma who were exposed to violence in school were more likely to report having had at least one asthma exacerbation during the past year (p<.001). The researchers claim that:
[t]he present findings highlight the need for attention to the roles of violence exposure in daily social contexts in asthma morbidity among adolescents.
These findings have yet to be peer-reviewed but they are interesting. When the study is published, it would be useful to learn if the level of violence was classified according to intensity, or differentiated as verbal or physical. From the viewpoint of immunological response, it would be helpful to learn how many of the children had been prescribed preventer medication and were using it during the time of the study. As is necessary with such studies, the researchers relied upon self-reported recall of asthma exacerbations. The researcher acknowledge that the mechanism for such an association between exposure to violence at school and asthma exacerbations is not understood.
Both of the above studies report interesting preliminary results that await validation by peer-review. It would be useful to know if the researchers have collected any data on the children's responses to environmental violence: e.g., if they respond with helplessness or aggression. Future studies might investigate appropriate biomedical markers for stress that might illuminate the immunological consequences of different responses to exposure to environmental violence.
However, the key point for public health policy and for adults who care for children is that both verbal and physical aggression can have significant negative effects on the lung function of children and adolescents, whether it takes place in the home, at school, or in the community. Research may eventually show that the toxic impact of environmental exposure to verbal and physical aggression is as great as that of environmental exposure to tobacco smoke
Hashiro, M. & Okumura, M. (1998). The relationship between the psychological and immunological state in patients with atopic dermatitis. Jnl. of Dermatol. Sci. 16 (3): 231-235.
Kemeny, M.E. (2003). The psychobiology of stress. Current Directions in Psychological Science 12 (4): 124-129.
Laube, B.L., Curbow, B.A., Fitzgerald, S.D. & Spratt, K. (2003). Early pulmonary response to allergen is attenuated during acute emotional stress in females with asthma. European Respiratory Jnl. 22: 613-618.
Miller, G.E., Dopp, J.M., Myers, H.F., Stevens, S.Y. & Fahey, J.L. (1999). Psychological predictors of natural killer cell mobilization during marital conflict. Health Psychol. 18 (3): 262-271.
Niaura, R., Banks, S.M., Ward, K., Stoney, C.M., Spiro, A. III, Aldwin, C.M. Landsberg, L. & Weiss, S.T. (2000). Hostility and the metabolic syndrome in older men: The Normative Aging Study. Psychosomatic Medicine 62, 7-16.
Otsuki, M., Kalesan, B., Rand, C.S. & Riekert, K.A. (2006). School Violence Exposure and Asthma Exacerbations in Adolescents, [ATS Publication Page: A236]
Suglia, S.F., Ryan, L., Dockery, D.& Wright, R.J. (2006). Interparental Conflict and Community Violence Exposure as Indicators of Chronic Stress in Relation to Childhood Pulmonary Function. [ATS Publication Page: A237]
Taylor, S.E., Klein, L.C., Lewis, B.P., Gruenewald, T.L., Gurung, R.A.R. & Updegraff, J.A. (2000). Biobehavioral responses to stress in females: Tend-and-befriend, not fight-or-flight. Psychological Review 107, 441-449.
Taylor, S.E. (2002). The Tending Instinct: How Nurturing is Essential to Who We Are and How We Live. New York: Henry Holt.