“Racism as a public health issue” APS racism series: at the intersection of equity, science, and social justice

The social unrest of the past several months highlights the importance of ensuring that science and fact-based objectivity align with the public discourse. A deepening body of literature makes clear the historical association of bias, discrimination, and injustice on Black, indigenous, and people of color (BIPOC) and the deleterious impact experiences of racism can have on healthy child development. This commentary surfaces recent and rooted evidence defining racism as a public health issue.

Among the ineluctable effects of racism are poverty and social marginalization. There has been a longstanding interest in the potential link between the chronic stress that accompanies poverty and marginalization and the poor health outcomes observed in populations that have been most subject to racism.¹ Only now, with advances in cell biology and epigenetics, have we begun to understand the underlying biology through which stress contributes to these outcomes.² A detailed review of this subject in not within the scope of this commentary; however, two recent examples from the literature are illustrative of the underlying biologic stressors that add support to the idea that racism is, in fact, a public health problem. Hong and colleagues investigated the effects of in utero stress on the adult immune system in an animal model.³ Prenatal stress was predictably associated with disruption of the hypothalamic–pituitary axis but more surprising was the effect on the immune system. These authors observed reduced survival and function in CD8+ T cells, a population of cells that is important in combatting viral and bacterial infections and also in suppressing tumors and autoimmunity. The reduced function of CD8+ T cells was mediated epigenetically, as demonstrated in chromatin accessibility experiments. In another study, Dias et al. demonstrated that stress-induced epigenetic effects can be transmitted intergenerationally, even when the stress-producing stimulus is no longer present.⁴ In this mouse model, the stress-inducing stimulus was preceded by a specific odor. The F1 generation of the stressed mice (that had not been exposed to either the odor or the stressful stimulus) demonstrated the same fear in response to the odor as did the F0 mice (i.e., those exposed to the odor and stress). Furthermore, the brains of the F1 mice demonstrated significant aberrations in the organization of the regions of the brain that regulate smell, as well as, altered DNA methylation of relevant genes. The F2 generation of these mice showed similar anatomy, behavior, and epigenetic changes. These two studies are illustrative of the degree to which we are beginning to understand the underlying biology of chronic stress, including the stresses that accompany racism and social marginalization. The Dias study in particular is a reminder that the biological effects of historically mediated trauma such as slavery and the forced removal of Native Americans may linger even in individuals who have seemingly escaped the more toxic environments to which their ancestors were exposed.

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