Chesapeake dead zones return to life

JOHNS HOPKINS AND U. MARYLAND (US) — Reducing the flow of fertilizers, animal waste, and other pollutants into the Chesapeake Bay is shrinking oxygen-depleted “dead zones” in America’s largest estuary, a new study finds.

Researchers discovered that the size of mid- to late-summer dead zones, where plants and water animals cannot live, leveled off in deep channels of the bay during the 1980s and has been declining ever since.

The timing is important; in the 1980s, the multistate-federal Chesapeake Bay Program started a concerted effort to cut nutrient pollution in the bay. The goal was to restore water quality and the health of the bay.


The study, published in the November issue of Estuaries and Coasts, was conducted by researchers from Johns Hopkins University and the University of Maryland.

“I was really excited by these results because they point to improvement in the health of the Chesapeake Bay,” says lead author Rebecca R. Murphy, a doctoral student in the geography and environmental engineering department at Johns Hopkins. “We now have evidence that cutting back on the nutrient pollutants pouring into the bay can make a difference. I think that’s really significant.”

Don Boesch, president of the University of Maryland Center for Environmental Science, agrees. “This study shows that our regional efforts to limit nutrient pollution may be producing results,” he says. “Continuing nutrient reduction remains critically important for achieving bay restoration goals.”

The Chesapeake Bay is the nation’s largest estuary, a body of water where fresh and salt water mix. Located in Maryland and Virginia, the bay drains about 64,000 square miles in six states and Washington, D.C. According to the Chesapeake Bay Program, the bay is about 200 miles long, has roughly 4,480 square miles of surface area and supports more than 3,600 species of plants, fish and other animals.

But the bay’s health deteriorated during much of the 20th century, contributing to a drop in fish and shellfish populations. Environmental experts blamed this largely on a surge of nutrients entering the bay from sources such as farm fertilizer, animal waste, water treatment discharge, and atmospheric deposition.

Heavy spring rains typically flush the nutrient chemicals, primarily nitrogen and phosphorus, into the Susquehanna River, the Chesapeake’s source, and other waters that empty into it. In the bay, the nutrients promote the prolific growth of algae.

When the algae die, their remains sink to the bottom, where they are consumed by bacteria. As they dine on algae, the bacteria utilize dissolved oxygen in the water. This leads to a condition called hypoxia, or depletion of oxygen. As this process continues through the spring and summer, the lack of oxygen turns vast stretches of the Chesapeake into dead zones. Hypoxia sometimes results in fish kills.

To find out whether these dead zones were expanding or diminishing, the Johns Hopkins and Maryland researchers retrieved and analyzed bay water quality records from the past 60 years. They determined that the size of the dead zone in mid-to-late summer has decreased steadily since the late 1980s and that the duration—how long the dead zone persists each summer—is closely linked each year to the amount of nutrients entering the bay.

The onset of the improving trend coincides with the launch of state and federal efforts to reduce algae-feeding pollutants in the bay. For example, farmers were encouraged to plant natural barriers between their fields and streams and to take other steps to keep fertilizer out of waterways that feed the Chesapeake.

Also, water treatment plants began to pull more pollutants from their discharge, and air pollution control measures curbed the movement of nitrogen from the atmosphere into the bay.

“By looking at existing data, we have been able to link decreasing hypoxia to a reduction in the nutrient load in the bay,” says study co-author Michael Kemp, an ecologist with the University of Maryland’s Horn Point Laboratory. “The overall extent and duration of mid-to-late summer hypoxia are decreasing.”

Another part of the study looked at a trend that has troubled some bay watchers. In recent years, Chesapeake researchers have seen a spike in dead zones not in mid-to-late summer, but earlier in the season. They feared that meant that keeping more nutrients out of the bay was not improving its health.

But the new study found that the early summer jump in dead zones was influenced by climate forces, not by the runoff of pollutants.

Fresh water entering the bay from rivers forms a layer on top of more dense salt water from the ocean. The two layers don’t easily mix, so when air near the surface adds oxygen to the top layer, it doesn’t reach the deeper salt water. Without oxygen at these lower depths, marine animals cannot live, and a dead zone is formed.

“Rebecca discovered that the increase in these early summer dead zones is because of changes in climate forces like wind, sea levels and the salinity of the water. It was not because the efforts to keep pollutants out of the bay were ineffective,” says William P. Ball, a professor of environmental engineering at Johns Hopkins. Ball, a co-author of the new study, is Murphy’s advisor.

“We believe,” Ball adds, “that without those efforts to rein in the pollutants, the dead zone conditions in June and early July would have been even worse.”

The study was supported by funding from the National Science Foundation and the National Oceanic and Atmospheric Administration.

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