Are biomarkers the best indicators of toxicant exposure in the environment?

Using genes known to be turned on or off after an animal is exposed to chemical pollutants can be one way of quantifying the effects of exposure.

Think about any environmental release: oil spills like the Exxon Valdez in Alaska or Deepwater Horizons in the Gulf of Mexico; accidental releases such as the EPA spill in the Animas River in Colorado; unintended runoff from agricultural pesticide use; antibiotics and personal care products in remediated waste water. How do we figure out the scale, scope, and reach of these events?

Governments and local agencies primarily assess the impact of the spill or release by first quantifying the volume of the spill and determining how long the chemical will stay in the environment.

  • Does it degrade in sunlight?
  • Is it biometabolized by microbes?
  • If in water, what is the rate of flow and volume of the body of water?

The second step is often to assess whether a spill has immediate human health (or economic) impacts.

  • Is a release of industrial chemicals upstream of drinking water intake?
  • Will globs of black crude oil wash up on the beaches of popular vacation spots?
  • Is this near a large population center?

After these immediate concerns are addressed, plans for remediation and future prevention are usually developed and public interest in the problem wanes. What is often forgotten, overlooked, or ignored is the ecological impact of spills and accidental releases. This is not to say that this is always ignored, but often there is less public interest and funding to really understand the real impacts on our environment.

What needs to happen next are thorough environmental and ecosystem assessments. For example, aquatic organisms from different partitions of the food web need to be collected and assayed for evidence of exposure. In many fish, there are known genetic biomarkers, such as aryl hydrocarbon receptor or cytochrome P450, that can be measured to determine if these fish are impacted by exposure.

From “Air Pollution – New Developments” (2011) by Francisco Arenas-Huertero, Elisa Apatiga-Vega, Gabriela Miguel-Perez, David Villeda-Cuevas, and Jimen Trillo-Tinoco.

The weakness of this approach is that each animal and plant may have a different response to exposure. Therefore it is paramount to use species controls or well-studied animal systems for this type of assessment. Despite this potential weakness, this is one of the strongest in situ molecular assays for chemical exposure, as long as we interpret results carefully and appropriately. Molecular approaches provide early indicators of chemical exposure, and understanding the mechanisms behind how toxicants interact in the body can help us avoid later, larger negative impacts such as effects on reproduction, organ failure, or fatality.


One great example of this is the effect of DDT (an organochlorine insecticide) on egg shell thickness in raptors. Osprey of the Chesapeake Bay were hit hard in the 70s. Their numbers dwindled down to 1,500 pairs, but with the removal of DDT from the market numbers have slowly rebounded. Now there are 10,000 pairs and egg-shell thinning is no longer the major issue that it once was.


Unfortunately, chicks near the most polluted areas of Chesapeake Bay have molecular markers in their blood that indicate they are still being exposed to harmful contaminants. Brood pairs near the most polluted areas have lower success rates at raising chicks to adults. Since it’s a smaller population-localized to a small area-it doesn’t affect the entire osprey community, but is a valuable piece of information for managers to use for remediation and efforts to control releases of chemicals into the environment. This highlights the important fact that molecular markers of exposure can be used for early indicators of biological and population effects on animals within diverse environments.

A love affair: Me, myself, and my research

I am a PhD student in the Brown Lab at Portland State University. I study genomic structural variation, specifically copy number variation. Copy number variation is when there is more or less than the “normal” biallelic frequency of a region of DNA. Often times this is manifested as deletion or duplication of a gene.


The prototypical example of copy number variation is human salivary amylase. Salivary amylase is found in mammalian saliva and helps break starch down into sugar. The salivary amylase gene is present in different population at 2-16 copies. Increased copies of the gene results in a higher level of salivary amylase protein. And human populations with historically high starch diets have higher copies of the salivary amylase gene. Check out Perry, et al. (2007) for more details.


I utilize zebrafish as a model for my research. We know that different strains of zebrafish have differing loads of copy numbers variants (see Brown 2012) and that when exposed to the environmental pollutant polychlorinated biphenyl (PCB), these strains have differing susceptibilities as larvae (see Waits and Nebert 2011).

I have shown that adults have differing expression levels of RNA expression for two known biomarkers of PCB exposure: aryl hydrocarbon receptor 2 (AHR2) and cytochrome P450 subtype 1A (CYP1A). And my next step is too look at ALL the genes that are expressed following PCB exposure. If you want to know more, just send me a message. I love to talk about my research!