Meli'sa S. Crawford

Assistant Professor
Foran Hall, Room 304
848-932-6389
melisa.crawford@rutgers.edu

Curriculum Vitae (243k PDF)

Research Statement

My research goals are to study the intersectionality and exposome of food production and human health. We can determine the largest factors that intersect in this vicious food pollution cycle by starting with issues that directly impact human health and affect food quality. There are few systematic studies that trace how pollutants enter and propagate through an organism’s physiological system and fewer still that track the individual and possible synergetic effects of direct and food-related effects on health outcomes. I propose to develop a systematic approach to track the effects and synergy of direct and food-based exposure to pollutants of rising concern, especially those impactful to underserved people, through controlled multi-omics, multi-organ studies of responses leading to development of metabolic diseases. Basing our work on public health data about pollutant concentrations and exposures and changes in food quality associated therein, we will utilize animal model systems that will allow us to gain actionable insight into the mechanisms by which exposures cascade into disease and ultimately lead to possible interventions that could aid in ameliorating these effects.

Air Pollution and Gastrointestinal Disease Risks: It is well known that gut dysbiosis, noted as alterations of the normal gut flora, is one of the contributing factors to the pathogenesis of GI disorders and metabolic syndrome (MetS). Epidemiological, and clinical studies have shown that exposure to particulate matter from ambient air pollution is associated with GI cancers, inflammatory bowel disease incidence, non-specific abdominal pain and significant reduction in gut microbial diversity. With increasing evidence that air pollution can significantly alter gastrointestinal physiology and promote gastrointestinal disease, my lab will examine this understudied environmental factor as well as other agricultural pollutants that have been recognized as contributors to obesity and metabolic syndrome. More specifically, we plan to elucidate the physiological mechanisms by which air pollutants can promote the development of metabolic syndrome through altered inter-organ communication, impaired intestinal epithelial integrity, and reduced gut microbial diversity.

Inter-organ communication in the development of MetS and intestinal disorders: Studies have reported that poor air quality can have severe impacts on crop development (e.g., damaged stomata) and can reduce the nutritional value of food. Access to safe and nutritious food is key to sustaining life and promoting good health. There is increasing evidence that chronic exposure to environmental pollutants (persistent organic pollutants (POPs) and PM) via diet may promote the development of obesity, type 2 diabetes and gastrointestinal diseases in humans. Although chronic gut inflammation has been explicitly associated with the development of obesity, there is little evidence about how exposure to air pollutants promotes intestinal inflammation and the subsequent development of MetS symptoms. Thus, I propose to investigate the functional properties of ingested pollutants on inter-organ crosstalk, the development of chronic intestinal inflammation and the progression of MetS symptoms.

How agricultural pollutants in food exacerbate disease in a genetically susceptible model: Obesity and metabolic disease are traditionally linked with many cardiometabolic risk factors such as insulin resistance, type 2 diabetes, and non-alcoholic fatty liver disease. Although lowering body weight has been an effective treatment for alleviating several metabolic complications, prevention remains the greatest challenge. Among different factors contributing to the regulation of energy balance, maintaining gut barrier integrity and the microbiome has received increasing attention. Important contributors to the onset of metabolic disease and obesity are genetic predispositions which have been well-established in twin and family studies. In obese humans, glucocorticoids play a prominent role in the occurrence of metabolic syndrome. Moreover, human and animal studies have revealed that metabolic syndrome and obesity are associated with the overexpression of the glucocorticoid-activating enzyme 11ß-hydroxysteroid dehydrogenase (11ß-HSD; type 1 and 2) in the liver visceral adipose tissue and the colon. Additionally, exposure to specific pollutants is correlated with an increased risk of type 2 diabetes, altered basal metabolism, adipose deposition, craving and/or satiety mechanisms, inflammation, and oxidative stress among those with higher adiposity. Therefore, I propose the hypothesis that consumption of agricultural pollutants in food will exacerbate MetS and gastrointestinal complications in mice selectively overexpressing the glucocorticoid-activating enzyme 11-ß hydroxysteroid dehydrogenase type 1 (11-ß HSD-1) in adipose tissue.

Experience

Education

*Applied and accepted into the School of Life Sciences (ASU) Biology, Ph.D. program