As a biologist and toxicologist, I take exception to the new toxics strategy based wholly on “chemical” contaminant reduction that is currently being pushed in the Bay Program.

I think we need to make a top priority change, and that we must begin by closely examining the organisms we are concerned with and proceeding from there to determine the sources of impacts on their health. Just as with human health problems, we need to search for malfunctions in Bay organisms (such as tumors, sterility, population changes) and then focus on their potential causes before assigning or eliminating toxics as a cause.

It is easier and less expensive to establish the role and regulation of toxics by beginning with specific biological problems and using recognized toxicological methods developed in the medical field and elsewhere. This approach has the added benefit and credit of solving publicly recognized concerns.

You may recall the first industrial contaminant to be considered of major importance and impact to the Chesapeake Bay system was thermal pollution from power plants. Thermal pollution was extensively studied and subsequently regulated. It is nonchemical.

Other relevant examples are the environmental endocrine disrupters DDT and TBT — the first chemicals to be regulated worldwide because they cause effects such as eggshell thinning, the loss of bird populations, and imposex (the development of male characteristics in a female) and sterility in mollusks.

Bird populations were extensively researched before the cause of the problem was found to be the unsuspected DDT, now regulated.

TBT, now banned, was found to cause imposex long before the technology to find the trace levels in the environment was developed.

Endocrine disrupters can be effective at levels (hormonal concentrations) below detection in the environment. Our knowledge of environmental endocrine disrupters, which have broad impacts that include the masculinization of fish populations, almost always begins with the discovery of the biological effects followed by the research to find the unsuspected contaminant.

We have too many new chemicals entering the environment each year to draw up any regulations based on already known “chemical contaminants.”

The whole “chemical contaminants” approach completely misses synergism or the interaction between components in the Bay, such as the chemical complexation and detoxification of toxics in the salt but not fresh water portions of the Bay ecosystem. Some of these interactions are significant in the fresh but not the buffered salt water of the Bay ecosystem in that they pump nutrients and toxicants out of the sediment, such as episodes of anoxia, which affects the sorptive hydroxides in marine and estuarine sediments, or the effects of pH changes, which cause the release of phosphates from freshwater sediments.

In addition, much of the sediment toxics data, though only a few years old, is no longer relevant because of sedimentation and burial — changes have been recorded within one month.

Only relying on the detection of known “chemical contaminants” to protect the environment is an approach that has long been abandoned by scientists as well as the EPA.

I think it unfortunate that the 2000 strategy does not take this into account. If the 2000 strategy could redirect just a portion of its resources towards determining the role of toxic materials in biological changes in Chesapeake Bay populations, I think it would have much greater productivity and effect.

Harriette Phelps
Biological & Environmental Sciences Department
University of the District of Columbia