Superfund Research Program
Persistent Mitochondrial and Epigenetic Effects of Early Life Toxicant Exposure
Project Leader: Joel N. Meyer
Co-Investigators: Susan K. Murphy, Theodore A. Slotkin (Duke University Medical Center)
Grant Number: P42ES010356
Funding Period: 2017-2022
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Progress Reports
The project's research highlights three findings. First, people are exposed to many pollutants that decrease the function of mitochondria, the parts of cells that produce energy. In the nematode model organism C. elegans, researchers found that exposure to one such chemical, the pesticide rotenone, results in changes in energy metabolism that permitted survival, but also made the animals more sensitive to another stressor (Gonzalez-Hunt 2020). This information is important because it helps the research team understand how pollutants that affect mitochondria could affect sensitivity to other stressors, whether chemical or non-chemical. Second, people are often exposed to pollutants called polycyclic aromatic hydrocarbons (PAHs), which are common at Superfund sites but also in air pollution and elsewhere. PAHs can be metabolized (altered chemically) to forms that are more or less toxic; the more toxic metabolites are important in human diseases including cancers. The research team found that one of the enzymes suspected of producing these more toxic forms, cytochrome P4501A, instead acts to produce less-toxic forms (Harris 2020). This information will be helpful in understanding how PAH exposures affect human health. Finally, in a collaborative effort, the team also built new tools for manipulating and imaging these near-microscopic animals (Zhang 2020). These efforts will facilitate future toxicological studies with this alternate model, which permits faster and more economical analysis of chemical toxicity compared to traditional mammalian models.