what we do

At our secret headquarters in room A304 of the Levine Science Research Center on the Duke University campus in Durham, North Carolina, we use the nematode Caenorhabditis elegans, a versatile model organism, as well as cells in culture in experiments aimed at improving environmental health. Our efforts range from studying the effects of environmental stressors at the molecular and cellular level to effects on the organism as a whole. We have a special interest in mitochondria, and mitochondrial and nuclear DNA damage. By collaborating with other researchers, we also study environmental health in people, other model organisms, and ecosystems.

If you are unfamiliar with environmental toxicology, mitochondria and mitochondrial DNA, or C. elegans (“worms”) and would like a short introduction, click the links below.

why we do it

Science is really fascinating and fun. But there is another reason. Pollution is a major health problem, especially in parts of the world with less environmental protection. It is responsible for at least 9 million premature deaths per year, more than AIDS, tuberculosis, and malaria combined. Most of this results from chronic disease, which will increase as the world’s population lives longer. Such diseases (cancers, neurodegenerative diseases, etc.) are also influenced by genetics, but genetics alone explains only 15-30% of most chronic diseases.

how we do it

We have joined forces with other Duke ecoteams to battle eco-evil:

Including regional groups:


Here are some recent publications from our band of green crimefighters. For a full list, please go to Dr. Meyer’s Google Scholar profile (automatically updated), or his CV at his NSOE site (more or less regularly updated).

Early-life mitochondrial DNA damage results in lifelong deficits in energy production mediated by redox signaling in Caenorhabditis elegans. Redox Biology 2021.

Xenobiotic metabolism and transport in Caenorhabditis elegans. Journal of Toxicology and Environmental Health, Part B 2021.

Zebrafish CYP1A expression in transgenic Caenorhabditis elegans protects from exposures to benzo[a]pyrene and a complex polycyclic aromatic hydrocarbon mixture. Toxicology 2020.

Caenorhabditis elegans strain sensitivity to sodium arsenite exposure is varied based on age and outcome measured. microPublication Biology, 2019.

Genetic defects in mitochondrial dynamics in Caenorhabditis elegans impact ultraviolet C radiation- and 6-hydroxydopamine-induced neurodegeneration. International Journal of Molecular Sciences, 2019.

Predictors of mitochondrial DNA copy number and damage in a mercury-exposed rural Peruvian population near artisanal and small-scale gold mining: an exploratory study. Environmental and Molecular Mutagenesis, 2019.


Mitochondrial toxicity. Toxicological Sciences, 2018.

The high production volume fungicide pyraclostrobin induces triglyceride accumulation associated with mitochondrial dysfunction, and promotes adipocyte differentiation independent of PPARγ activation, in 3T3-L1 cells. Toxicology, 2018.

Mitochondrial fusion, fission, and mitochondrial toxicity. Toxicology, 2017.

Deficiencies in mitochondrial dynamics sensitize Caenorhabditis elegans to arsenite and other mitochondrial toxicants by reducing mitochondrial adaptability. Toxicology, 2017.

helpful resources

This page contains a variety of resources, intended especially for members of my own lab but also potentially useful to other scientists or people interested in science.

contact us

Feel free to contact us by the traditional means (or you can always just light the Worm Beacon).