The Impact of Environmental Chronic and Toxic Stress on Asthma

Several factors have been associated with the development of asthma and asthma-related morbidity and mortality. Exposures in the environment such as allergens and air pollutants have traditionally been linked to the risk of asthma and asthma outcomes. More recent literature has identified chronic psychosocial stress as an additional environmental exposure to consider in relation to asthma. Adverse childhood events (ACEs) and chronic and toxic stress have been associated with chronic diseases such as cardiovascular disease, cancer, and chronic obstructive pulmonary disease. Chronic stress has also been shown to result in biological changes such as expression of immunologic genes, changes in expression of the beta-adrenergic (B2AR) and the glucocorticoid receptor (GR-α) genes, cytokine regulation, and alterations in the hypothalamic pituitary axis and cortisol levels which all may affect asthma pathophysiology and therapeutic response among patients exposed to chronic stress. Recent research has revealed associations between ACEs and chronic and toxic stress and asthma risk in pre-conception to early childhood as well as morbidity and response to asthma treatments among pediatric and adult age groups. As some populations are more significantly impacted by asthma such as racial and ethnic minority groups, the influence of psychosocial stress has also been explored as a potential factor responsible for observed disparities in asthma prevalence and outcomes among these groups which also experience higher rates of psychosocial stress. Racial discrimination has specifically been shown to affect asthma-related outcomes among minority groups. Interventions to address the impact of chronic and toxic stress such as yoga and meditation have been shown to improve asthma outcome measures. Chronic and toxic stress is an important environmental exposure to further consider as we continue to explore the differences in underlying asthma pathophysiology leading to various disease phenotypes among patients and clinical/therapeutic response to interventions and treatments.