Racism as a public health issue in environmental health disparities and environmental justice: working toward solutions.

BACKGROUND: Environmental health research in the US has shown that racial and ethnic minorities and members of low-socioeconomic groups, are disproportionately burdened by harmful environmental exposures, in their homes, workplace, and neighborhood environments that impact their overall health and well-being. Systemic racism is a fundamental cause of these disproportionate exposures and associated health effects. To invigorate and inform current efforts on environmental justice and to raise awareness of environmental racism, the National Institute of Environmental Health Sciences (NIEHS) hosted a workshop where community leaders, academic researchers, and NIEHS staff shared perspectives and discussed ways to inform future work to address health disparities. OBJECTIVES: To share best practices learned and experienced in partnerships between academic researchers and communities that are addressing environmental racism across the US; and to outline critical needs and future actions for NIEHS, other federal agencies, and anyone who is interested in conducting or funding research that addresses environmental racism and advances health equity for all communities. DISCUSSION: Through this workshop with community leaders and researchers funded by NIEHS, we learned that partnerships between academics and communities hold great promise for addressing environmental racism; however, there are still profound obstacles. To overcome these barriers, translation of research into plain language and health-protective interventions is needed. Structural changes are also needed in current funding mechanisms and training programs across federal agencies. We also learned the importance of leveraging advances in technology to develop creative solutions that can protect public health.

Responding to Disasters: Training Can Overcome Issues in Disaster Response.

Training can assist in overcoming gaps in disaster response. The National Institute of Environmental Health Sciences (NIEHS) Worker Training Program (WTP) funds a network of nonprofit organizations, or grantees, that deliver peer-reviewed safety and health training curricula to workers across a variety of occupational sectors. Grantees' experiences providing training for recovery workers after numerous disasters show the following issues need to be addressed to better protect the safety and health of recovery workers: (1) regulations and guidance documents not sufficient to protect workers; (2) protecting responders' health and safety which is a core value; (3) improving communication between responders and communities to assist in decision-making and guiding safety and health planning; (4) partnerships critical for disaster response; and (5) greater attention to protecting communities disproportionately affected by disasters. This article provides insight into addressing these recurring issues and utilizes them as part of a continuous quality improvement process for disaster responders that may help to reduce responder injuries, illness, and death during future disasters.

Government Program Celebrates 25 Years of Commitment to Environmental Justice Movement.

For over 25 years, the National Institute of Environmental Health Sciences (NIEHS) Environmental Career Worker Training Program (ECWTP) has advanced principles of environmental justice by funding nonprofit organizations, or grantees, to deliver health, safety, and job training for individuals from disadvantaged communities. This article provides a brief background of the environmental justice movement and examines the efforts of grantees to demonstrate how the ECWTP model can serve as a pathway for advancing environmental justice in disadvantaged and underserved communities.

Metabolomic and Gene Expression Profiles Exhibit Modular Genetic and Dietary Structure Linking Metabolic Syndrome Phenotypes in Drosophila.

Genetic and environmental factors influence complex disease in humans, such as metabolic syndrome, and Drosophila melanogaster serves as an excellent model in which to test these factors experimentally. Here we explore the modularity of endophenotypes with an in-depth reanalysis of a previous study by Reed et al. (2014), where we raised 20 wild-type genetic lines of Drosophila larvae on four diets and measured gross phenotypes of body weight, total sugar, and total triglycerides, as well as the endophenotypes of metabolomic and whole-genome expression profiles. We then perform new gene expression experiments to test for conservation of phenotype-expression correlations across different diets and populations. We find that transcript levels correlated with gross phenotypes were enriched for puparial adhesion, metamorphosis, and central energy metabolism functions. The specific metabolites L-DOPA and N-arachidonoyl dopamine make physiological links between the gross phenotypes across diets, whereas leucine and isoleucine thus exhibit genotype-by-diet interactions. Between diets, we find low conservation of the endophenotypes that correlate with the gross phenotypes. Through the follow-up expression study, we found that transcript-trait correlations are well conserved across populations raised on a familiar diet, but on a novel diet, the transcript-trait correlations are no longer conserved. Thus, physiological canalization of metabolic phenotypes breaks down in a novel environment exposing cryptic variation. We cannot predict the physiological basis of disease in a perturbing environment from profiles observed in the ancestral environment. This study demonstrates that variation for disease traits within a population is acquired through a multitude of physiological mechanisms, some of which transcend genetic and environmental influences, and others that are specific to an individual's genetic and environmental context.

Genotype-by-diet interactions drive metabolic phenotype variation in Drosophila melanogaster.

The rising prevalence of complex disease suggests that alterations to the human environment are increasing the proportion of individuals who exceed a threshold of liability. This might be due either to a global shift in the population mean of underlying contributing traits, or to increased variance of such underlying endophenotypes (such as body weight). To contrast these quantitative genetic mechanisms with respect to weight gain, we have quantified the effect of dietary perturbation on metabolic traits in 146 inbred lines of Drosophila melanogaster and show that genotype-by-diet interactions are pervasive. For several metabolic traits, genotype-by-diet interactions account for far more variance (between 12 and 17%) than diet alone (1-2%), and in some cases have as large an effect as genetics alone (11-23%). Substantial dew point effects were also observed. Larval foraging behavior was found to be a quantitative trait exhibiting significant genetic variation for path length (P = 0.0004). Metabolic and fitness traits exhibited a complex correlation structure, and there was evidence of selection minimizing weight under laboratory conditions. In addition, a high fat diet significantly increases population variance in metabolic phenotypes, suggesting decreased robustness in the face of dietary perturbation. Changes in metabolic trait mean and variance in response to diet indicates that shifts in both population mean and variance in underlying traits could contribute to increases in complex disease.