SWEHSC Environmental Health Sciences Pilot Program Award 2025
We have recently announced the pilot programs we will be funding for 2025. We are looking forward to collaborating with these researchers to further environmental health science. Please see the summaries of the funded pilot projects below.
Occupational Chemical Exposures among Breastfeeding Nurses in the Postnatal Period – Jessica Rainbow, PhD
Hospital environments expose nurses to a wide range of cleaning chemicals, raising concerns about their potential impact on breastfeeding and infant health. The pilot project Occupational Chemical Exposures among Breastfeeding Nurses in the Postnatal Period, led by Principal Investigator Jessica Rainbow, PhD, and supported by Leslie Farland, ScD, through the Bio5/Udall Center Faculty Fellowship, explores whether occupational chemical exposure affects the breast milk of nurses during the postnatal period. The team will analyze levels of quaternary ammonium compounds (QACs) and per- and polyfluoroalkyl substances (PFAS) in breast milk from both nurses and non-nurses on work and non-workdays, using mass spectrometry to detect differences in exposure. These findings determine whether workplace exposures contribute to increased chemical levels in breast milk, with potential implications for maternal and infant health.
This project builds on Rainbow’s nationally recognized research on nurse well-being, including work on occupational fatigue, presenteeism, and nursing workforce policy. Prior studies have shown that nearly 90% of nurses report exposure to cleaning chemicals during pregnancy, and most continue breastfeeding after returning to work. With few existing data on chemical exposures in lactating nurses, this study fills a critical gap while supporting future NIEHS R21 funding proposals to protect the health of nurses and their infants. The findings will also inform evidence-based workplace safety recommendations in healthcare settings.
Effects of Pesticide Exposure on Early Recognition of Coccidioides – Dr. Daniel Powell
Coccidioidomycosis (Valley fever) is a serious fungal infection caused by Coccidioides, a soil-dwelling fungus endemic to Arizona’s “Valley fever corridor” between Tucson and Phoenix. Individuals in dirt-disturbing professions like farming, landscaping, and construction are at higher risk—not only due to exposure to fungal spores but also because of regular contact with pesticides known to alter immune function. This pilot project, led by Dr. Daniel Powell, determines how pesticide exposure impacts the body’s initial immune recognition of Coccidioides, a critical step in preventing severe or disseminated disease. The research focuses on the innate immune receptor Dectin-1, which is key to recognizing the fungus and triggering a protective response.
To explore these effects, Powell’s team examines immune responses in two key lung cell types—hematopoietic and epithelial cells—using advanced techniques like fungal binding assays, cytokine analysis, and single-cell RNA sequencing. Special attention is prioritized with the commonly used pyrethroid pesticide zeta-cypermethrin, which tests for its impact on fungal detection and immune signaling. By comparing genetically susceptible and resistant mouse models, the study uncovers pesticide-induced vulnerabilities in antifungal defenses. Findings from this pilot will lay the foundation for future NIH-funded studies involving human populations and broader pesticide classes, to improve health outcomes for at-risk workers and guide safer agricultural practices.
Modeling Human Relevant Wildfire Smoke-Induced Reproductive Toxicity in Mice – Zelieann Craig, PhD
This pilot project, led by Zelieann Craig, PhD, investigates the reproductive toxicity of wildfire smoke exposure using a mouse model, addressing a growing public health concern linked to climate change. Motivated by reports of increased reproductive issues among firefighters—including miscarriage, preterm birth, abnormal sperm morphology, and decreased fertility—this study aims to identify the chemical constituents of wood smoke that are absorbed and distributed to reproductive organs. Using a controlled inhalation exposure system and untargeted mass spectrometry, the research characterizes the chemical profiles in smoke, serum, urine, and male and female mice reproductive tissues. The study also explores whether cytochrome P450-dependent hepatic metabolism modulates these reproductive effects by comparing outcomes in wild-type mice versus liver-Cpr-null (LCN) mice, which lack hepatic microsomal P450 activity.
This research builds on promising preliminary findings where wood smoke exposure in mice replicated gonadal toxicities similar to those observed in firefighters. The study leverages the unique capabilities of the Southwest Environmental Health Sciences Center (SWEHSC) Inhalation Exposure Resource and the Analytical and Biological Mass Spectrometry (ABMS) Facility to provide critical mechanistic insights into how smoke-derived chemicals may impair reproductive function. By establishing chemical distribution patterns and assessing the role of liver metabolism in mediating toxicity, the project aims to generate foundational data for a future NIEHS grant application. Ultimately, this research will inform potential interventions and public health guidelines to mitigate the reproductive risks of wildfire smoke exposure, both in occupational settings and in the general population.
PFAS-Induced Hypertension and Kidney Injury – Jing (Jason) Wu, PhD
Led by Jing (Jason) Wu, PhD, this research project investigates the potential causal relationship between PFAS (per- and polyfluoroalkyl substances) exposure, hypertension (HTN), and kidney injury, conditions that significantly contribute to morbidity and mortality in the United States. PFAS are persistent environmental toxins detected in the plasma of over 98% of Americans and a significant portion of U.S. drinking water samples. Given their long half-life and renal excretion, PFAS exposure is believed to affect both renal endothelial and epithelial cells, leading to HTN and kidney dysfunction. However, the causal mechanisms underlying these associations remain poorly understood. This project addresses this gap by examining how PFAS exposure promotes HTN and kidney injury through specific biological pathways, including PPARγ-dependent Arginase1-mediated endothelial dysfunction and epithelial sodium channel (ENaC)-mediated sodium reabsorption. It will also explore how pre-existing chronic kidney disease (CKD) may exacerbate these effects due to impaired PFAS clearance.
The research focuses on four PFAS species commonly found in human serum, examining their effects on blood pressure and kidney function in intact and CKD mouse models chronically exposed to PFAS in drinking water. Wu’s team will investigate how PFAS exposure alters renal microvascular function, sodium reabsorption, and how renal dysfunction influences PFAS clearance. The project will generate new insights into PFAS-induced kidney toxicity and its role in the development of HTN and CKD. The outcomes of this study are expected to significantly advance our understanding of PFAS’s role in renal health, paving the way for future R01 funding and further investigation into PFAS-related diseases.