Something is wrong in Lake Erie.
For 30 years, scientists thought they knew how to manage the pollution that all but killed the lake in the 1960s.
Now, no one is sure how to mount a rescue.
In what one scientist calls the second battle for the environment of Lake Erie, researchers in the United States and Canada yesterday launched a $2 million effort to find out why Lake Erie's central basin is running out of oxygen. For the summer, the U.S. Environmental Protection Agency research vessel Lake Guardian will study puzzling changes on the lake.
If oxygen depletion in Lake Erie persists, the results could be massive fish kills and damage to the walleye fishery, toxic algae blooms, smelly, bad-tasting drinking water, and mucky, putrid beaches, said Dr. Gerald Matisoff, the Case Western Reserve University geologist who helped organize the research effort.
“It's like going back to the bad old days when Lake Erie was dead,'' said Glenn Warren, an aquatic biologist at the U.S. EPA's Great Lakes National Program Office in Chicago.
In the 1960s, it was pollution, pure and simple, that choked the life out of the lake. As a result, a gargantuan multimillion dollar effort over many years finally limited phosphorus pollution. Phosphorus was the chief culprit in the strangling process.
But there are signs that the problem is no longer so simple.
“It's a real cause for concern,'' said Dr. Jan Ciborowski, a biology professor at the University of Windsor, one of 30 researchers attacking the issue. “It means our billions of dollars spent on sewage treatment - we're losing ground on that. It's a much more serious problem, and requires a much more complicated solution.''
“This is the beginning of the second environmental war in Lake Erie,'' said David Rockwell, a senior scientist at the U.S. EPA's Great Lakes office. “The brakes we thought we had on the system aren't working anymore.''
Until recently, the death knell of lakes played out like this: Phosphorus dumping rose. Phosphorus fertilized algae. Algae grew.
But, what's born must die. As massive algae blooms faded and fell to the bottom, their decay took up oxygen. Anoxia - or the lack of dissolved oxygen, the stuff that fish breathe - resulted.
None of this is an issue in Lake Erie's shallow 1,200-square-mile western basin. But in the deeper central and eastern basins, summer warms the surface water, which acts a barrier to the colder, denser, bottom water.
“The cold bottom layer is essentially isolated from the atmosphere,'' said Dr. Paul Bertram, an environmental scientist with the Great Lakes National Program Office.
In the eastern basin, the oxygen remains adequate for life, simply because the basin is deeper. The 2,400-square-mile eastern basin has an average depth of 82 feet.
But the 6,300-square-mile central basin is in a reverse “Goldilocks” position - everything is just wrong. The central basin, at about 60 feet deep, isn't deep enough to absorb the increasing decay rates of algae, and it's not shallow enough to avoid the isolation of the bottom layer in the first place. The central basin extends from Sandusky to Erie, Pa.
What bewilders scientists this time is that low-oxygen, high-phosphorus conditions are not accompanied by a corresponding algae bloom. Such a bloom would account for the low oxygen.
Further, it appears that phosphorus dumping has been relatively flat in recent years, which should have kept oxygen levels high.
“That's very peculiar,'' said Dr. Ciborowski. “Where's that phosphorus coming from? And why do we have no algae, yet lots of phosphorus? So something is wrong.''
“Last year we had the most rapid depletion of oxygen in the central basin that we monitored since 1983,'' Mr. Rockwell said. While a few testing stations in the central basin often show anoxic conditions by late August, last year, some stations showed depleted oxygen in early August. By late August, oxygen was down all over the central basin.
The question is, why. Research this summer will focus on three central hypotheses for Lake Erie's troubles, said Dr. Ciborowski. It may surprise no one that two of the theories put the European invader, the zebra mussel, and its cousin, the quagga mussel, in the equation.
One hypothesis suggests that atmospheric ozone depletion may allow more ultra violet light to reach deeper into Lake Erie. This may warm more of the lake, reducing the depth of the cool bottom level in the central basin. Thus allowing quicker oxygen depletion.
A second hypothesis revolves around the lack of algae blooms despite the high phosphorus levels. The ideas here explore whether mussels eat the algae before it can proliferate, or whether ultraviolet light inhibits algae blooms. Another theory suggests that petroleum in the water, in the form of polycyclic aromatic hydrocarbons, may damage algae production.
Researchers will also look at whether something other than phosphorus limits algae growth. For instance, lack of available iron may keep algae levels low no matter how much phosphorus fertilizes the lake.
Finally, the culprit may be mussel feces. One hypothesis suggests that as the feces and something called pseudo feces - essentially matter the mussels spit out. decays, it takes up oxygen, and contributes to anoxia.
No matter which theory - or which part of which theory - proves accurate, it appears that the source of Lake Erie's trouble is entirely different from what it was 30 years ago.
“We're talking about changes in the way things are going on inside the lake rather than external changes,'' said Dr. Ciborowski. “If it's all zebra mussels, we're in trouble. I don't know how you would control zebra mussels.''