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, nanomaterials, or C. elegans (“worms”), click the links below for brief introductions.

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).

Strengths and limitations of morphological and behavioral analyses in detecting dopaminergic deficiency in Caenorhabditis elegans. Neurotoxicology, 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.

Toxicological implications of mitochondrial CYP2E1 localization. Toxicology Research, 2017.

Effects of methyl and inorganic mercury exposure on genome homeostasis and mitochondrial function in Caenorhabditis elegans. DNA Repair, 2017.