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 launched a $2 million effort last week to find
out why Lake Erie's central basin is running out of oxygen.
This 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 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 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
"It's a real cause for concern," said 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 as a barrier
to the colder, denser bottom water.
"The cold bottom layer is essentially isolated from
the atmosphere," said 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, Ohio, 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 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," Rockwell
said. While a few testing stations in the central basin
often show anoxic conditions by late August, some stations
showed depleted oxygen in early August last year. 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,
Ciborowski said. 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 ultraviolet 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
Researchers also will 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
Ciborowski. "If it's all zebra mussels, we're in trouble.
I don't know how you would control zebra mussels."