Asthma is the most common cause of hospitalization in children in the U.S. other than infections, and cities such as Detroit have troublingly high asthma mortality rates. So-called risky families-characterized by conflict, neglect, and lacking in emotional warmth and support-place children in jeopardy for asthma, and lay the groundwork for various chronic illnesses throughout life. However, little is known about the pathways through which risky family environments get under the skin to exert their deleterious effects on health. Formulating a clear picture of everyday risky family behaviors and their effects on childhood asthma morbidity and biological mediators (e.g., epigenetic changes and gene expression) is essential for developing effective interventions targeted at improving health outcomes of children from risky families. The proposed research will take a multi-method biopsychosocial approach to the study of childhood asthma by investigating the links between everyday family behaviors and asthma morbidity in a sample of 180 youth aged 10-15 in Detroit, MI, in three waves of data collection over a 2-year period. The study will incorporate a novel naturalistic observation technology called the Electronically Activated Recorder (EAR), as well as well-validated parent- and child-reports of family functioning, clinical interviews, biological measures and clinical asthma evaluations. This project will test whether risky family behaviors assessed by the EAR (measuring conflict, neglect, lack of emotional warmth and support)-above and beyond traditional measures of family functioning-are longitudinally associated with greater asthma morbidity (e.g., symptom severity, ER visits, and pulmonary function) and with an increase in asthma morbidity (e.g., progression to more severe asthma diagnosis) over the three-wave, 2-year follow-up period. We will test biological mediators of these effects, including greater cortisol output in daily life, glucocorticoid receptor (GCR) gene expression, and methylation of GCR CpG promoter sites. Finally, we will test whether the links between risky family behaviors in daily life and asthma morbidity are mediated by avoidant coping behaviors and by poor asthma management behaviors (e.g., poorer asthma control medication adherence and poorer asthma trigger avoidance). Isolating specific biological and psychological processes in families that potentially contribute to, or buffer, asthma morbidity will foster future bench to bedside translation of key findings from this project into novel and developmentally sensitive interventions to reduce asthma morbidity, and will also inform and improve family interventions that are currently being tested by our team with NHLBI funding. Finally, the findings from this study will be used to inform how to more accurately assess family interactions and stress with new technology and biomarkers to better capture potential mechanisms of behavior change in family intervention research.