Hannah M. C. Schreier

Chronic Traffic-Related Air Pollution and Stress Interact to Predict Biologic and Clinical Outcomes in Asthma

Background Previous research has documented effects of both physical and social environmental exposures on childhood asthma. However, few studies have considered how these two environments might interact to affect asthma. Objective This study aimed to test interactions between chronic exposure to traffic-related air pollution and chronic family stress in predicting biologic and clinical outcomes in children with asthma. Method Children with asthma (n = 73, 9–18 years of age) were interviewed about life stress, and asthma-relevant inflammatory markers [cytokine production, immunoglobulin E (IgE), eosinophil counts] were measured. Parents reported on children’s symptoms. Children completed daily diaries of symptoms and peak expiratory flow rate (PEFR) measures at baseline and 6 months later. Exposure to traffic-related air pollution was assessed using a land use regression model for nitrogen dioxide concentrations. Results NO2 by stress interactions were found for interleukin-5 (β for interaction term = −0.31, p = 0.02), IgE (interaction β = −0.29, p = 0.02), and eosinophil counts (interaction β = −0.24, p = 0.04). These interactions showed that higher chronic stress was associated with heightened inflammatory profiles as pollution levels decreased. Longitudinally, NO2 by stress interactions emerged for daily diary symptoms (interaction β = −0.28, p = 0.02), parent-reported symptoms (interaction β = −0.25, p = 0.07), and PEFR (interaction β = 0.30, p = 0.03). These interactions indicated that higher chronic stress was associated with increases over time in symptoms and decreases over time in PEFR as pollution levels decreased. Conclusions The physical and social environments interacted in predicting both biologic and clinical outcomes in children with asthma, suggesting that when pollution exposure is more modest, vulnerability to asthma exacerbations may be heightened in children with higher chronic stress.

Socioeconomic Status and the Health of Youth: A Multilevel, Multidomain Approach to Conceptualizing Pathways.

Previous research has clearly established associations between low socioeconomic status (SES) and poor youth physical health outcomes. This article provides an overview of the main pathways through which low SES environments come to influence youth health. We focus on 2 prevalent chronic health problems in youth today, asthma and obesity. We review and propose a model that encompasses (a) multiple levels of influence, including the neighborhood, family and person level; (b) both social and physical domains in the environment; and finally (c) dynamic relationships between these factors. A synthesis of existing research and our proposed model draw attention to the notion of adverse physical and social exposures in youths neighborhood environments altering family characteristics and youth psychosocial and behavioral profiles, thereby increasing youths risk for health problems. We also note the importance of acknowledging reciprocal influences across levels and domains (e.g., between family and child) that create self-perpetuating patterns of influence that further accentuate the impact of these factors on youth health. Finally, we document that factors across levels can interact (e.g., environmental pollution levels with child stress) to create unique, synergistic effects on youth health. Our model stresses the importance of evaluating influences on youths physical health not in isolation but in the context of the broader social and physical environments in which youth live. Understanding the complex relationships between the factors that link low SES to youths long-term health trajectories is necessary for the creation and implementation of successful interventions and policies to ultimately reduce health disparities.

Resilience in low-socioeconomic-status children with asthma: adaptations to stress.

BACKGROUND Low socioeconomic status (SES) is a strong predictor of many health problems, including asthma impairment; however, little is understood about why some patients defy this trend by exhibiting good asthma control despite living in adverse environments. OBJECTIVE This study sought to test whether a psychological characteristic, the shift-and-persist strategy (dealing with stressors by reframing them more positively while at the same time persisting in optimistic thoughts about the future), protects low-SES children with asthma. METHODS One hundred twenty-one children aged 9 to 18 years with a physicians diagnosis of asthma were recruited from medical practices and community advertisements (mean age, 12.6 years; 67% male; 61% white). Shift-and-persist scores and asthma inflammation (eosinophil counts and stimulated IL-4 cytokine production) were assessed at baseline, and asthma impairment (daily diary measures of rescue inhaler use and school absences) and daily peak flow were monitored at baseline and at a 6-month follow-up. RESULTS Children who came from low-SES backgrounds but who engaged in shift-and-persist strategies displayed less asthma inflammation at baseline (β = 0.19, P < .05), as well as less asthma impairment (reduced rescue inhaler use and fewer school absences; β = 0.32, P < .01) prospectively at the 6-month follow-up period. In contrast, shift-and-persist strategies were not beneficial among high-SES children with asthma. CONCLUSION An approach that focuses on the psychological qualities that low-SES children develop to adapt to stressors might represent a practical and effective starting point for reducing health disparities. Moreover, the approaches that are effective in low-SES communities might be different from those that are optimal in a high-SES context.

Longitudinal Relationships Between Family Routines and Biological Profiles Among Youth With Asthma

OBJECTIVE To investigate whether longitudinal trajectories of inflammatory markers of asthma can be predicted by levels of family routines in youth with asthma. DESIGN Family routines were assessed through parent questionnaires and peripheral blood samples obtained from youth every 6 months throughout the 18-month study period. Longitudinal relationships were evaluated using hierarchical linear modeling. MAIN OUTCOME MEASURES Mitogen-stimulated production of cytokines implicated in asthma, specifically IL-4, IL-5, and IL-13. RESULTS Youth with more family routines in their home environment showed decreases in IL-13 (but not IL-4 or IL-5) over the course of the study period. In turn, within-person analyses indicated that at times when stimulated production of IL-13 was high, asthma symptoms were also high, pointing to the clinical relevance of changes in IL-13 over time. A variety of child and parent psychosocial as well as child behavioral characteristics could not explain these effects. However, medication use eliminated the relationship between family routines and stimulated production of IL-13. CONCLUSION Our study suggests that family routines predict asthma outcomes at the biological level, possibly through influencing medication use. Considering daily family behaviors when treating asthma may help improve both biological and clinical profiles in youth with asthma.

Maternal sensitivity and infant autonomic and endocrine stress responses

BACKGROUND Early environmental exposures may help shape the development of the autonomic nervous system (ANS) and hypothalamic-pituitary-adrenal (HPA) axis, influencing vulnerability for health problems across the lifespan. Little is known about the role of maternal sensitivity in influencing the development of the ANS in early life. AIMS To examine associations among maternal sensitivity and infant behavioral distress and ANS and HPA axis reactivity to the Repeated Still-Face Paradigm (SFP-R), a dyadic stress task. STUDY DESIGN Observational repeated measures study. SUBJECTS Thirty-five urban, sociodemographically diverse mothers and their 6-month-old infants. OUTCOME MEASURES Changes in infant affective distress, heart rate, respiratory sinus arrhythmia (RSA), and T-wave amplitude (TWA) across episodes of the SFP-R were assessed. A measure of cortisol output (area under the curve) in the hour following cessation of the SFP-R was also obtained. RESULTS Greater maternal insensitivity was associated with greater infant sympathetic activation (TWA) during periods of stress and tended to be associated with greater cortisol output following the SFP-R. There was also evidence for greater affective distress and less parasympathetic activation (RSA) during the SFP-R among infants of predominantly insensitive mothers. CONCLUSIONS Caregiving quality in early life may influence the responsiveness of the sympathetic and parasympathetic branches of the ANS as well as the HPA axis. Consideration of the ANS and HPA axis systems together provides a fuller representation of adaptive versus maladaptive stress responses. The findings highlight the importance of supporting high quality caregiving in the early years of life, which is likely to promote later health.

Family chaos and adolescent inflammatory profiles: the moderating role of socioeconomic status.

Objective To test whether family chaos influences adolescents’ inflammatory profiles and whether adolescents from low socioeconomic status (SES) environments are at higher risk for experiencing adverse inflammatory profiles from living in chaotic family environments. Methods A total of 244 families with an adolescent aged 13 to 16 years participated. Parents completed measures of family SES and family chaos. Both systemic inflammation and stimulated proinflammatory cytokine production in response to bacterial challenge were assessed in adolescents. Results Our results suggest that SES moderates the detrimental effect of family chaos on systemic inflammation and interleukin-6 (B = −0.010, standard error [SE] = 0.004, p = .026), but not C-reactive protein (B = 0.009, SE = 0.006, p = .11), and on stimulated proinflammatory cytokine production (B = −0.098, SE = 0.044, p = .026) in adolescents, such that a chaotic family environment is positively associated with greater systemic inflammation and greater stimulated proinflammatory cytokine production in adolescents as family SES declines. Conclusions These findings indicate that living in chaotic family environments places youth who may be vulnerable based on socioeconomic factors at a potentially higher risk for inflammation-related diseases.

Childhood abuse is associated with increased hair cortisol levels among urban pregnant women

Background Hypothalamic–pituitary–adrenal (HPA) axis activity is known to be altered following events such as childhood abuse. However, despite potential adverse consequences for the offspring of women who have experienced abuse, very little is known about altered HPA axis activity during pregnancy. Methods During pregnancy, 180 women from diverse racial/ethnic backgrounds reported on their exposure to emotional, physical and/or sexual abuse before the age of 11, and general post-traumatic stress symptoms (ie, not limited to childhood years or abuse experiences). Around delivery, they provided hair samples for the assessment of cortisol levels during pregnancy. Hair cortisol was assessed for each pregnancy trimester. The effect of childhood abuse on hair cortisol was assessed using mixed-effects analyses of covariance models allowing for within-subject correlated observations, and were first performed in the entire sample and subsequently stratified by race/ethnicity. Results Controlling for post-traumatic stress symptoms, hair cortisol levels varied by history of child abuse, F(2,166)=3.66, p=0.028. Childhood physical and/or sexual abuse was associated with greater hair cortisol levels, t(166)=2.65, p=0.009, compared with no history of abuse. Because childhood rates of abuse and hair cortisol levels varied by race/ethnicity, analyses were stratified by race/ethnicity. The associations between history of abuse and cortisol levels were only significant among black women, F(2,23)=5.37, p=0.012. Conclusions Childhood abuse, especially physical and/or sexual abuse, is associated with differences in cortisol production during pregnancy, particularly among black women. Future research should investigate how these differences impact physical and mental health outcomes among offspring of affected women.

Lifetime exposure to traumatic and other stressful life events and hair cortisol in a multi-racial/ethnic sample of pregnant women

Abstract We examined whether lifetime exposure to stressful and traumatic events alters hypothalamic-pituitary-adrenal (HPA) axis functioning, as indexed by hair cortisol, regardless of associated psychopathology, among pregnant women of different racial/ethnic backgrounds. 180 women provided hair samples for measurement of integrated cortisol levels throughout pregnancy and information regarding their lifetime exposure to stressful and traumatic life events. Results indicate that increased lifetime exposure to traumatic events was associated with significantly greater hair cortisol over the course of pregnancy. Similarly, greater lifetime exposure to stressful and traumatic events weighted by reported negative impact (over the previous 12 months) was associated with significantly greater hair cortisol during pregnancy. All analyses controlled for maternal age, education, body mass index (BMI), use of inhaled corticosteroids, race/ethnicity, and post-traumatic stress disorder (PTSD) and depressive symptoms. Following stratification by race/ethnicity, associations between stressful and traumatic life events and hair cortisol were found among Black women only. This is the first study to consider associations between lifetime stress exposures and hair cortisol in a sociodemographically diverse sample of pregnant women. Increased exposure to stressful and traumatic events, independent of PTSD and depressive symptoms, was associated with higher cortisol production, particularly in Black women. Future research should investigate the influence of such increased cortisol exposure on developmental outcomes among offspring.

Prospective Associations between Coping and Health among Youth with Asthma.

The present study evaluated whether primary and secondary coping would predict longitudinal asthma-related clinical outcomes, such as peak expiratory flow rate (PEFR) and self-reported school absenteeism, rescue inhaler use, and asthma-related physician contacts, in youth with asthma. The 62 youth (68% males) had an average age of 12.6 +/- 2.73 years and were primarily of European origin. Coping and asthma outcomes were obtained by youth self-report at baseline and over a 12-month follow-up period. Greater secondary coping at baseline was related to greater increases in PEFR and a greater likelihood of physician contact over the following year. Greater primary coping at baseline was related to greater likelihood of rescue inhaler use, school absenteeism, and physician contact over the following year. In contrast, asthma measures at baseline did not predict changes in coping over the following year. These patterns suggest that youth who engage in secondary coping accept and adapt to their asthma in ways that improve pulmonary function over time. Youth who engage in primary coping may be more likely to communicate asthma problems to others, and such communication perhaps leads to increases in behaviors meant to address these problems.

Stress and food allergy: mechanistic considerations.

Recent years have seen a marked increase in food allergy prevalence among children, particularly in Western countries, that cannot be explained by genetic factors alone. This has resulted in an increased effort to identify environmental risk factors underlying food allergies and to understand how these factors may be modified through interventions. Food allergy is an immune-mediated adverse reaction to food. Consequently, considerations of candidate risk factors have begun to focus on environmental influences that perturb the healthy development of the emerging immune system during critical periods of development (eg, prenatally and during early childhood), particularly in the gut. Given that psychosocial stress is known to play an important role in other allergic and inflammatory diseases, such as asthma, its potential role in food allergy is a growing area of research. However, research to date has largely focused on animal studies. This review synthesizes relevant animal research and epidemiological data, providing proof of concept for moderating influences of psychological stress on food allergy outcomes in humans. Pathways that may underlie associations between psychosocial stress and the expression of food allergy are discussed.