Thomas and Mark question this DOE strategy. To support fuel cells, the existing gasoline infrastructure could require alterations, Thomas said, explaining that the cells may require a special, low-sulfur grade of gasoline. That could require a "lot of investment" at gas stations, including new pumps and new tanks, he said. Borroni-Bird acknowledged that DaimlerChrysler is using California's reduced Slllflir 23.S formulation as the fuel for its POX "Cramming gasoline into a fuel cell vehicle compromises its true environmental promise," charged Mark, who called methanol the second best option. While all of the fuel-cell vehicle fueling options would emit dra-
matically less pollution, only a vehicle powered directly by hydrogen would be a true zeroemissions vehicle. The direct hydrogen fuel-cell method would also result in lower greenhouse gas emissions, according to research by Mark Delucchi, a research scientist at the University of California at Davis's Institute of Transportation Studies. Also, gasoline would produce higher emissions than either direct hydrogen or methanol, according to DTI research. For all its potential virtues, hydrogen is hobbled by public perception, which is still colored by the Hindenburg explosion. "Hydrogen has a bad rap—it's much safer than people think," BorroniBird said. "A compressed hydro-
gen tank on board a vehicle would be far safer than anything available today, particularly gasoline tanks," Thomas said. At least two hydrogen storage options are technically and economically feasible today, he said. "From a societal viewpoint, you're going to have to make investments" to render fuel-cell technology a viable option, summarized Thomas. "If we go down either the methanol or the gasoline route, we could be postponing the time when we get to a really sustainable energy system for the transportation sector." Borroni-Bird agreed, but stressed that "it really comes down to trying to convince the oil industry and the general customer."–KELLYN S. BETTS
New test advances understanding of fish-killing algae Although scientists are far from understanding what drives blooms of the toxic alga Pfi.esteria piscicida, major breakthroughs have been made in detecting the dinoflagellate at fish kills. A new test promises to speed decisions to close waters where Pflesteria has bloomed, said state officials. Parke Rublee, biology professor at the University of North Carolina, announced at an EPA conference in January that his new genetic probe "verifies the suspicion that Pflesteria is widespread in estuaries along the East Coast." Despite the probe's inability to distinguish between toxic and nontoxic forms of the alga, its development "will save time and money and help protect public health," said Liz Kalinowski, spokesperson for the Maryland Department of Natural Resources (DNR). Because the test is inexpensive and fast state officials can now respond more quickly to outbreaks by closing off access to affected water she explained Discovered in 1991 by Joann Burkholder, a botany professor at North Carolina State University, Pflesteria is an ambush predator that has killed billions of fish and sickened people in outbreaks in North Carolina and Maryland
Mistaken identity? Open, bleeding sores on menhaden could be caused by either a fungus or Pfiesteria. (Courtesy Vicki Blazer, U.S. Geological Survey)
{ES&T, ,198, 32(1), 26A-30A). It has a complex lifecycle with 24 different forms, most of them nontoxic. It can react swiftly to dense populations of fish, typically menhaden, by changing its form and releasing a toxin that creates bleeding lesions, disorientation, and death. Because of its complexity and ability to rapidly revert to a nontoxic form, monitoring and identification of Pflesteria in the field has been cumbersome and expensive, Rublee said. Electron microscopy and fish toxicity tests to detect Pflesteria in water samples can take as long as four weeks and cost $1500, he said. Rublee's new test for the alga costs $25 and requires two days
to process. Known as a polymerase chain reaction (PCR), it utilizes a primer—a short piece of DNA unique to Pflesteria piscicida. When exposed to complementary fragments of Pflesteria DNA from a water sample, the primer manufactures millions of copies of a protein that researchers can identify with gel electrophoresis, a common method for identifying DNA and protein molecules. In late July,tinePCR probe verified the presence of Pflesteria in the Neuse River at the only fish kill of the summer. Rublee's lab also found Pflesteria in samples of coastal water from Delaware to Georgia. Rublee emphasized that "the probes confirm whether Pflesteria is present or not, but can't determine if it is in a toxic or nontoxic form." He concluded that "the probe won't be really effective until it can be used with a probe for the toxin." The state of Maryland will be using Rublee's probes in monitoring efforts this summer, Kalinowski said. But the state will continue to rely on the presence of fish lesions as an indicator of toxic Pflesteria, despite new studies concluding that such lesions may have other causes.
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Researchers have just published a consensus document that concludes that "lesions are not a very good indicator of whether or not there is a Pfiesteria risk," said Don Boesch, president of the University of Maryland Center for Environmental Science. Vicki Blazer, a fish pathologist with the U.S. Geological Survey, explained at the EPA conference that nearly all the fish she examined from areas in Maryland, with and without fish kills, had deep fungal infections in their lesions. Closer investigation of the lesions revealed that they were more than one week old. On the other hand, lesions caused by Pfiesteria toxins develop within several hours and are characterized by rapid cell death and inflammation. "What we can't rule out," said Blazer, "is that low levels of the toxin could be damaging fish skin and allowing the fungus to invade." Alternatively, fish with established fungal infections and
open bleeding sores may be stimulating Pfiesteria to bloom in its toxic form, she said. In any case, lesions remain the only visible sign of toxic Pfiesteria, said Burkholder. "We have used lesions very successfully to indicate the presence of Pfiesteria," she said. But she emphasized that they must be used only in conjunction with other conditions such as dense populations of fish and calm, poorly flushed, brackish water. Even with the advances in identifying Pfiesteria, scientists were stumped by the dinoflagellate's no-show in 1998 after delivering a series of fish kills to Maryland and North Carolina in 1997. Rob Magnien, director of tidewater ecosystem assessment with the Maryland DNR, has floated a hypothesis that outbreaks result from the right combination of nutrient enrichment and dense populations of Pfiesteria and menhaden. This "recipe" is favored by warm, poorly flushed estuaries,
according to Magnien. For instance, in the lower reaches of Maryland's Pocomoke River in 1997, large algal blooms provided food for Pfiesteria, while low dissolved oxygen upstream concentrated menhaden in the same area, Magnien said. But the heavy rainfall in the first half of 1998 may have altered the timing and location of algal blooms, which prevented toxic outbreaks of Pfiesteria. Despite uncertainties about the mechanisms that control the growth of Pfiesteria, emerging evidence continues to strengthen the link between nutrient pollution and toxic outbreaks, Burkholder said. She and her colleagues have demonstrated that Pfiesteria can directly consume organic forms of nitrogen such as urea, commonly found in poultry manure. These results indicate that initiatives such as EPA's draft strategy to reduce pollution from animal feeding operations "are on the right track " she concluded. JANET PELLEY
EPA draft almost doubles safe dose of perchlorate in water Perchlorate concentrations of less than 32 parts per billion (ppb) are safe for human consumption in drinking water, based on a new reference dose recommended in a draft EPA toxicological report released in January. The reference dose is almost double the value of EPA's current provisional reference dose, which California has used to set a cleanup action level, triggering the closure of several drinking water sources. EPA began this study of perchlorate in May 1997 after California regulators found low levels of the rocket fuel ingredient in drinking water {ES&T 1998, 32(9), 210A) The state has shut down a number of drinking water supplies and set a provisional action level of 18 ppb based on EPA's current reference dose. Nevada and Utah have also set the same provisional action level. Perchlorate affects the thyroid by inhibiting the uptake of iodine, which it uses to produce hor-
Perchlorate manufacturers and users are located in all but six states—Hawaii, Maine, Vermont Connecticut, and Rhode Island. In California, most of the perchlorate detections were found near rocket fuel plants. (Source: EPA)
mones. In the past, doctors prescribed relatively high doses of potassium perchlorate to treat patients with hyperactive thyroids, and the current provisional reference dose was based on such
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data. Today, potential health concerns related to this hormone disruption include carcinogenic, neurodevelopmental, developmental, reproductive, and immunotoxic effects.
