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Great Lakes Article:

Damage From Acid Rain Pollution Is Far Worse Than Previously Believed

Daily Science Magazine
07/18/2002

Amid the recent hoopla over the EPA and Bush administration's plans to make it easy for power plants, oil refineries and chemical factories (major sources of acid rain nationwide) to expand without installing new pollution controls and the Senate's consideration of Clean Power Act, there's an important new wrinkle to the story.

A new study revealed that acid rain's damage to America's forests may be much more widespread than previously believed. It may actually create conditions in trees similar to compromised immune systems in humans, establishing a vulnerably with grave potential implications.

"As with immune-compromised humans, plants may appear and function as if they were healthy, until exposed to even a routine stress or disease, then experience declines far more exaggerated than expected," says Donald DeHayes, Dean and Professor in the School of Natural Resources at The University of Vermont. DeHayes co-authored a study in the most recent issue of the journal "Ecosystem Health" released in June at an international conference on Ecosystem and Human Health in Washington, DC, which was attended by about 1000 environmental scientists and policy makers.

Up to now, acid rain has been associated with the decline of forests in certain specific locations. DeHayes and colleagues, UVM senior researcher Gary Hawley and USDA Forest Service scientist and UVM adjunct faculty Paul Schaberg previously documented the mechanism through which acid rain depletes calcium and weakens high elevation red spruce trees, making them more vulnerable to winter freezing injury.

Their new work shows that this mechanism is also applicable to other tree species, including balsam fir, white pine, and eastern hemlock. Because calcium is a critical ingredient in the plant's stress response system, acid rain's depletion of cellular calcium may suppress the capacity of trees to survive environmental stresses.

This connection between calcium deficiency and environmental stress exposure are common components in the declines of several tree species, including red spruce, sugar maple, and flowering dogwood. Their "immune response" hypothesis provides an overarching explanation of how acid rain ultimately threatens forests. The findings are especially relevant now because a growing assortment of human influences -- climate change, pollutants, and new pests and diseases, are burdening our forests.

"If extensive, the decline of individual species would radiate through plant communities," says DeHayes. "It would alter the competition and survival of populations, perhaps even species, including animals at higher levels of the forest food chains." DeHayes points out those calcium deficiencies in plants are passed on to herbivores, altering their nutrition. For instance, birds eating calcium- deficient plant material might have less calcium for egg production. Insects could experience weaker exoskeletons. Mammals could have weaker bones or change in the quantity or quality of milk production. The problems continue through the ecosystem and into economic system.

Ironically, the research was funded through the US Environmental Protection Agency (EPA) with long-term support of Vermont Sen. James Jeffords (I-VT).

"This important new research shows the insidious harm that acid rain is causing to our trees and wildlife," says Jeffords. We know how to stop acid rain, but have not had the will to do so." Jeffords, chairman of the Environment and Public Works Committee, is legislating for the Clean Power Act, which he co-authored and introduced in March 2001.

### For more information on Donald DeHayes: http://www.uvm.edu/~uvmpr/experts/?Page=experts.php&ID;=ddehayes

Here's the abstract: http://www.blackwell-synergy.com/servlet/useragent?func=synergy&synergyAction;=showAbstract&doi;=10.1046/j.1526-0992.2001.01046.x

Here's the full research text: http://www.blackwell-synergy.com/servlet/useragent?func=synergy&synergyAction;=showFullText&doi;=10.1046/j.1526-0992.2001.01046.x

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