The research in our lab centers around understanding relationships between socioeconomic status (SES) and physical health outcomes in childhood.  Across different social factors, one of the most consistent and robust findings is that individuals low in low socioeconomic status (SES) have poorer health than individuals high in SES. This relationship holds true whether health is measured as the prevalence rate of illness, the severity of illness, or the likelihood of mortality, and it is true for most types of diseases, as well as for many risk factors for diseases. This finding has been reported for many countries, including those with and those without universal health care. And it has been demonstrated across the life span, from childhood to older adulthood.

Our research explores the psychosocial and psychobiological pathways involved in these SES-health relationships.  Current projects include two major studies described below:

SES and Childhood Asthma

We have an ongoing longitudinal study that assesses children with asthma and a comparison group of children with no chronic illnesses.  Parents and children participate in a laboratory visit consisting of psychosocial and health interviews, health assessments (e.g., lung function, blood draw to measure immune markers), and a parent-child interaction task.  Children also collect measures at home of lung function, salivary cortisol, and keep diaries about asthma symptoms.  Families return every six months so that we can assess how changes in life circumstances affect biological profiles and clinical outcomes related to asthma.

Some of the most exciting findings from this study include:

• Low SES children with asthma were more likely to have a biological profile of greater stimulated production of inflammatory molecules (Th-2 cytokines) implicated in asthma.  Both chronic life stress and psychological appraisals of stress formed pathways between SES and cytokine production.  This study is one of the first to describe a psychobiological explanation for the linear relationship seen at the epidemiological level between SES and health in children.
   

• Children with asthma who experienced a major acute life event on top of having high chronic stress in their lives exhibited a 5.5-fold reduction in glucocorticoid receptor mRNA and a 9.5-fold reduction in b2-adrenergic receptor mRNA relative to children with asthma without comparable stressor exposure. These findings suggest that stressful experience diminishes expression of the glucocorticoid and b2-adrenergic receptor genes in children with asthma. Given that glucocorticoids and bronchodilators are often given as treatments for asthma, this study is important for suggesting a mechanism at the genomic level for why stress is associated with increased asthma morbidity.
   

• Conducting genome-wide transcriptional profiling on T lymphocytes, we found that children with asthma from a low SES background showed overexpression of genes regulating inflammatory processes, including those involved in chemokine activity, stress responses, and wound responses.  Bioinformatic analysis suggested that decreased activity of CREB and NF-Y, and increased NF-kB, transcriptional signaling mediated these effects.  These pathways are known to regulate catecholamine and inflammatory signaling in immune cells.  This study provides the first evidence in a clinical patient population that the larger social environment can affect processes at the genomic level.  Because these pathways are the primary targets of many asthma medications, these findings suggest that the larger social environment may alter molecular mechanisms that would have implications for the efficacy of asthma therapeutics.
   

• We explored how social factors at the neighborhood, peer, and family level relate to asthma, and the behavioral and biological pathways through which they operate.  Lower levels of family support were associated with greater symptoms and poorer pulmonary function via biological pathways.  In contrast, higher levels of neighborhood problems were associated with greater symptoms via behavioral pathways related to smoking.  Peer support was not associated with symptoms or pulmonary function.  These findings suggest that family factors affect youths’ asthma via physiological changes, whereas neighborhood factors help shape the health behaviors of youth with asthma.

Early Childhood SES and Biological Markers of Health

Childhood SES has been found to predict health outcomes later in adult life, including cardiovascular disease, stroke, stomach cancer, and infectious illness.  These findings remain even after controlling for the effects of adult SES, indicating that childhood SES is not merely serving as a proxy for the effects of adult, or current, SES on health.  These types of observations led to the ‘critical period’ hypothesis, the idea that exposure to certain environmental stimuli early in life programs biological systems in a way that affects physical health throughout the lifecourse.

To test this hypothesis, we conducted a study in which lifetime SES measures were obtained on a sample of healthy adolescent girls, and a sample of blood was drawn in adolescence to assess the expression of genes implicated in inflammatory responses.  Three findings emerged: (1) Years 2-3 of life were a critical period:  participants whose families were higher in SES during these years showed higher glucocorticoid receptor mRNA and lower Toll-like receptor 4 mRNA during adolescence, a profile that suggests better regulation of inflammatory responses. (2) These effects were not mediated through current economic circumstances, life stress, or health practices. (3) Changes in SES during later years were unable to “undo” these effects.  These findings suggest that unfavorable socioeconomic circumstances in the early years of life presage the expression of a pro-inflammatory phenotype in adolescence. To the extent that this proclivity towards inflammation persists over the lifespan, it could explain the heightened incidence of respiratory and cardiovascular disease in low-SES populations.

We have an ongoing study to further test these hypotheses by recruiting a sample of healthy adults that fall into one of 4 categories: L-L (low SES early in life, low SES currently), L-H (low SES early in life, high SES currently), H-L (high SES early in life, low SES currently), and H-H (high SES early in life, high SES currently).  By recruiting into these 4 groups, we can test whether early life SES truly represents a critical period for biological embedding.  If so, the L-L and L-H groups will be equivalent in terms of their biological profiles in adulthood, and will appear more biologically vulnerable than either the H-L or H-H groups.  In this study, we will also test molecular pathways for how early childhood SES gets embedded biologically.  We hypothesize that exposure to low SES during the first years of life, when patterns of immune responsivity are being established, can become embedded permanently through epigenetic modifications. Epigenetics refers to acquired changes in the activity of genes, which can persist over the lifespan, and are not the result of changes in DNA sequence. They involve biochemical modifications to the nucleotides that comprise DNA, or to histone proteins that package DNA within chromosomes.  We hypothesize that these modifications will facilitate activation of the genomic control pathways that orchestrate inflammation, and at the same time facilitate repression of the signaling cascades that normally function to counter-regulate it.

Chen, E., & Paterson, L. Q. (2006). Neighborhood, family, and subjective socioeconomic status: How do they relate to adolescent health? Health Psychology, 25, 704-714.

Griffin, M. J., & Chen, E. (2006).  Perceived control and immune and pulmonary outcomes in children with asthma.  Psychosomatic Medicine, 68, 493-499.

Miller, G.E., & Chen, E. (2006). Life stress and diminished expression of genes encoding the glucocorticoid receptor and b2-adrenergic receptor in children with asthma. Proceedings of the National Academy of Sciences of the United States of America, 103, 5496-5501.

Stetler, C., Chen, E., & Miller, G.E. (2006). Written disclosure of experiences with racial discrimination and antibody response to an influenza vaccine.  International Journal of Behavioral Medicine, 13, 60-68.

Bloomberg, G.R. & Chen, E. (2005).  The relationship of psychological stress with childhood asthma.  Immunology and Allergy Clinics of North America, 25, 83-105.

Chen, E., & Hanson, M.D. (2005).  Perceptions of threat: Understanding pathways between stress and health in adolescents.  Prevention Researcher, 12, 10-12.

Langer, D.A., Chen, E., & Luhmann, J. (2005). Attributions and coping in children’s pain experiences.  Journal of Pediatric Psychology, 30, 615-622.

Miller, G.E. & Chen, E. (Eds.) (2005).  Current Directions in Health Psychology.  Upper Saddle River, NJ:  Prentice Hall.

Murali, R. & Chen, E. (2005).  Exposure to violence and cardiovascular and neuroendocrine measures in adolescents.  Annals of Behavioral Medicine, 30, 155-163.

Chen, E. (2004). Why socioeconomic status affects the health of children: A psychosocial perspective. Current Directions in Psychological Science, 13, 112-115.

Chen, E., Cole, S. W., Kato, P. M. (2004). A review of empirically supported psychosocial interventions for sickle cell disease outcomes. Journal of Pediatric Psychology, 29, 197-209.

Chen, E., Langer, D., Raphaelson, Y., & Matthews, K. (2004). Socioeconomic status and health in adolescents: The role of stress interpretations. Child Development, 75, 1039-1052.

Chen, E., Bloomberg, G. R., Fisher, Jr., E. B., & Strunk, R. C. (2003). Predictors of repeat hospitalizations in children with asthma: The role of psychosocial and socio-environmental factors. Health Psychology, 22, 12-18.

Chen, E., Fisher, Jr., E. B., Bacharier, L. B., & Strunk, R. C. (2003). Socioeconomic status, stress, and immune markers in adolescents with asthma. Psychosomatic Medicine, 65, 984-992.

Chen, E. & Matthews, K. A. (2003). Development of the Cognitive Appraisal and Understanding of Social Events (CAUSE) Videos. Health Psychology, 22, 106-110.

Chen, E., Matthews, K. A., & Boyce, W. T. (2002). Socioeconomic differences in children’s health: How and why do these relationships change with age? Psychological Bulletin, 128, 295-329.

Chen, E., Matthews, K. A., Salomon, K., & Ewart, C. K. (2002). Cardiovascular reactivity during social and nonsocial stressors: Do children’s personal goals and expressive skills matter? Health Psychology, 21, 16-24.

Ewart, C. K., Jorgenson, R. S., Suchday, S., Chen, E., & Matthews, K. A. (2002). Measuring stress resilience and coping in vulnerable youth: The Social Competence Interview. Psychological Assessment, 14, 339-352.

Chen, E., & Matthews, K. A. (2001). Cognitive appraisal biases: An approach to understanding the relationship between socioeconomic status and cardiovascular reactivity in children. Annals of Behavioral Medicine, 23, 101-111.

Chen, E., Craske, M. G., Katz, E R., Schwartz, E, & Zeltzer, L. K. (2000). Pain-sensitive temperament: Does it predict procedural distress and response to psychological treatment among children with cancer? Journal of Pediatric Psychology, 25, 269-278.

Chen, E., Joseph, M. H., & Zeltzer, L.K. (2000). Behavioral and cognitive interventions in the treatment of pain. Pediatric Clinics of North America, 47, 513-525.

Chen, E., Zeltzer, L. K., Craske, M. G., & Katz, E. R. (2000). Alterations of memory in the reduction of children’s distress during repeated aversive medical procedures. Abstracted in Evidence-Based Mental Health, 3, 12.

Chen, E., Zeltzer, L. K., Craske, M. G., & Katz, E. R. (2000). Children’s memories for painful cancer treatment procedures: Implications for distress. Child Development, 71, 933-947.

Chen, E., & Matthews, K. A. (1999). Socioeconomic differences in social information processing and cardiovascular reactivity. Annals of the New York Academy of Sciences, 896, 417-419.

Chen, E., Zeltzer, L. K., Craske, M. G., & Katz, E. R. (1999). Alterations of memory in the reduction of children’s distress during repeated aversive medical procedures. Journal of Consulting and Clinical Psychology, 67, 481-490.

Chen, E., & Craske, M. G. (1998). Risk perception and interpretations of ambiguity related to anxiety during a stressful event. Cognitive Therapy and Research, 22, 137-148.

Chen, E., Zeltzer, L. K., Bentler, P. B., Byrne, J., Nicholson, H. S., Meadows, A. T., Mills, J. L., Haupt, R., Fears, T. R., & Robison, L. L. (1998). Pathways linking treatment intensity and psychosocial outcomes among adult survivors of childhood leukemia. Journal of Health Psychology, 3, 23-38.

Chen, E., Bush, J. P., Zeltzer, L. K. (1997). Psychologic issues in pediatric pain management. In: G. M. Aronoff, W. C. V. Parris, R. P. Pawl, & P. P. Raj (Eds.), Current Review of Pain: Vol. 1. Psychiatric Management of Pain (pp. 153-164). Philadelphia, PA: Current Science.

Zeltzer, L. K., Chen, E., Weiss, R., Guo, M. D., Byrne, J., Robison, L. L., Meadows, A. T., Mills, J. L., & Nicholson, H. S. (1997). A comparison of psychological outcomes in adult survivors of childhood acute lymphoblastic leukemia versus sibling controls: A cooperative Children’s Cancer Group and National Institutes of Health study. Journal of Clinical Oncology, 15, 547-556.

Zeltzer, L. K., Bush, J. P., Chen, E., & Riveral, A. (1997). A psychobiologic approach to pediatric pain: Part I. History, physiology, and assessment strategies. Current Problems in Pediatrics, 27, 225-253.

Zeltzer, L. K., Bush, J. P., Chen, E., & Riveral, A. (1997). A psychobiologic approach to pediatric pain: Part II. Prevention and treatment. Current Problems in Pediatrics, 27, 261-292.

Chen, E., Lewin, M. R., & Craske, M. G. (1996). Effects of state anxiety on selective processing of threatening information. Cognition and Emotion, 10, 225-240.

Maidenberg, E., Chen, E., Craske, M. , Bohn, P., & Bytstritsky, A. (1996). Specificity of attentional bias in panic disorder and social phobia. Journal of Anxiety Disorders, 10, 529-541.

Otto, M. W., McNally, R. J., Pollack, M. H., Chen, E., & Rosenbaum, J. F. (1994). Hemispheric laterality and memory bias for threat in anxiety disorders. Journal of Abnormal Psychology, 103, 828-831.

Otto, M. W., McNally, R. J., Pollack, M. H., Chen, E., & Rosenbaum, J. F. (1994). Hemispheric laterality and memory bias for threat in anxiety disorders. Journal of Abnormal Psychology, 103, 828-831.