In March, he and his colleagues reported that almost all the tomcod in the Hudson share the same mutation in a gene called AHR2. PCBs must first bind to the protein encoded by AHR2 to cause damage. The Hudson River mutation makes it difficult for PCBs to grab onto the receptor, shielding the fish from the chemical’s harm.

The AHR2 mutation is entirely missing from tomcod that live in northern New England and Canada. A small percentage of tomcod in Long Island and Connecticut carry the mutation. Dr. Wirgin and his colleagues concluded that once PCBs entered the Hudson, the mutant gene spread quickly.

“When these chemicals first starting getting released, if you had the normal form of the gene, you probably weren’t going to make it,” Dr. Wirgin said.

Evolution has also run in the opposite direction as government agencies cleaned up some of the pollution around New York. In 1989, Jeffrey Levinton of Stony Brook University and his colleagues discovered that a population of mud-dwelling worms in the Hudson had evolved resistance to cadmium. They lived in a place called Foundry Cove near a battery factory near West Point. Dr. Levinton and his colleagues found that the worms produced huge amounts of a protein that binds cadmium and prevents it from doing harm.

In the early 1990s, the federal Environmental Protection Agency hauled away most of the cadmium-laced sediment from Foundry Cove. Over nine generations, the Foundry Cove worm populations became vulnerable again. This shift occurred, Dr. Levinton and his colleagues reported last year, as worms from less contaminated parts of the river moved in. They are interbreeding with the resident worms, and the resistant mutations are becoming rarer.

Bacteria Adapt, Too

Today, scientists can scan the entire genomes of New York’s animals and plants to look for evolutionary changes. Last month, Mr. Harris presented new data on white-footed mice at the annual meeting of the Society for the Study of Evolution. Mr. Harris and his colleagues have identified mutations in more than 1,000 genes that are present in all New York City mice, but missing from mice in Harriman State Park, 45 miles north of the city.

The scientists are investigating whether these mutations have helped the mice adapt to life in New York City. Clues that some of them do are found in the functions of the mutated genes. Many of the genes are involved in fighting bacteria, while others are for reproduction and still others for coping with stress from exposure to chemicals. It’s possible that these new mutations are spreading independently in each of the parks in the city.