Panel members would testify as courtappointed experts at relevant hearings and advise Spector on what scientific evidence is admissible. At least a month before the judge begins hearings on the value of breast implant claims, Dow Corning proposes the panel would submit a report on its views of whether implants cause disease. The report and the panel's testimony would then be admitted as evidence in the hearings. Marc Reisch
Comet's radiance linked to carbon monoxide Hazleton: views of evidence differ ing also says it will argue that, based upon the scientific evidence, the value of disease claims against it should be set at zero. However, Dow Corning has nearly $2 billion in insurance coverage in place to cover breast implant claims. Plaintiffs' attorneys oppose Dow Coming's motion. Diana Pendleton, an attorney with Waite, Schneider, Bayless & Chasley in Cincinnati, says Dow Coming's motion is "a marketing ploy" intended to improve the firm's public image. "I think it has almost no chance of success," she says. The selection of a scientific advisory panel "has never been done before in any bankruptcy case." Dow Corning counters that judges have appointed experts in civil cases and argues that federal rules allow courtappointed experts in bankruptcy cases. In its filing with the court, Dow Coming says the reason for its request is "a well-founded fear" among scientists and others that the "judicial system with its exclusive reliance on partisan 'experts' is ill-equipped to deal with difficult . . . mass-tort litigation" in which complex scientific issues are involved. Dow Corning says panel experts should be "well-respected" medical doctors or other scientists with expertise in rheumatology and neurology. To ensure the panel's impartiality, Dow Corning recommends the judge ask the National Academy of Sciences (NAS) in Washington, D.C., for help in selecting experts. An NAS source says a request from Spector for help in selecting a panel of experts would be unusual. Moreover, NAS would want to be sure its participation would benefit the public and not be used as a protective screen for any of the disputants.
The startling brilliance of the distant, recently discovered comet Hale-Bopp may be caused by great jets of carbon monoxide streaming from its nucleus at a rate of more than 1 ton per second. Typically, a comet must pass near the sun for its cloudy coma to become bright, as chunks of the ice that compose much of the nucleus sublimate into a streaming, gassy cloak. But Hale-Bopp is still more than six times the distance of Earth from the sun—too far away for water to sublimate—leading astronomers to believe that much more volatile substances must be escaping. "For a comet to be active this far from the sun seems to suggest we have to be dealing with substances more volatile than water, and CO is perhaps as good as any," says comet expert Brian G. Marsden, associate director of planetary sciences at the Harvard-Smithsonian Center for Astrophysics in Cambridge, Mass. With radio telescope technology made possible only in the past six to eight years, astronomers David C. Jewitt and Matthew Senay at the Institute for Astronomy in Honolulu, and Henry Matthews at the Joint Astronomy Center in Hilo, Hawaii, searched for a spectroscopic fingerprint of CO in Hale-Bopp. The comet's coma, they confirm, is chock full of it [Science, 271,1110 (1996)]. The CO from Hale-Bopp is streaming out in well-defined jets from vents perhaps a few kilometers in diameter, they observe. Other substances may be outgassing as well, such as carbon dioxide or other volatile compounds of carbon, nitrogen, oxygen, and hydrogen. Astronomers will be searching for the signatures of those compounds in the coming year. Hale-Bopp, which was discovered
only last year, is expected to put on quite a show when it passes near Earth in April 1997. According to recent calculations by scientists at Ireland's Armagh Observatory, Hale-Bopp has traversed at least one huge orbit that has lasted more than 4,000 years. The famous Halley's comet, by contrast, appears to contain only about 5% volatile molecules, and most may have outgassed millennia ago. But HaleBopp may be a comet still rich in its original materials. "One reason why people are all jumpy about Hale-Bopp is that it looks like it's relatively chemically primitive," Jewitt says. The only prior detection of cometary CO has been in comet Schwassmann Wachmann 1, which displays a bright coma even when far from the sun. "There's not a big history of comets like this," Jewitt adds. As Hale-Bopp approaches the sun, astronomers will be avidly searching for a possible transition from a CO coma to one made largely of water. Because Hale-Bopp has already been past the sun at least once, and still retained its volatile molecules, the chances of it petering out are small, scientists say. "All indications are that this is a tremendous comet," says Marsden. "We've never had anything like it before— persisting in being this bright." Elizabeth Wilson
NRC report downplays concern about chemicals The great majority of naturally occurring and synthetic chemicals found in food for humans are present at such low levels that they are unlikely to pose an appreciable risk of cancer, even those known to have carcinogenic potential in bioassays and animal studies. So concludes a National Research Council (NRC) panel, the Committee on Comparative Toxicology of Naturally Occurring Carcinogens. Furthermore, the committee says, too many calories and too much fat or alcohol pose a greater cancer threat than such chemicals. And the panel notes that certain chemicals in the diet act as anticarcinogens. The committee, convened in 1993 upon the recommendation of NRC's Board on Environmental Studies & Toxicology, estimates that the number of FEBRUARY 26,1996 C&EN 7
naturally occurring chemicals present in the food supply is enormous, probably exceeding 1 million. The number of synthetic chemicals present in the human diet is far smaller. However, not much data are available on the carcinogenic potential of either naturally occurring or synthetic chemicals. The committee worked with information that was available, collecting and analyzing data on more than 200 carcinogens, 65 of which occur naturally in the food supply. "What people have to realize is that foods in diets are chemicals/7 says committee member Samuel M. Cohen, professor and chairman of the department of pathology and microbiology at the University of Nebraska Medical Center, Omaha. This report corroborates what has been observed in other studies during the past five years. That is, he says, "that whether a chemical is man-made or God-made, it is still a chemical and the body handles it in similar ways. All the evidence we could find was that, for a given class of chemical, whether natural or synthetic, it behaves the same. The range of potencies was the same, the body handled it similarly. To the body, it doesn't matter—a chemical is a chemical." The report also finds that much more research needs to be conducted before, as committee chairman Ronald W. Estabrook concludes, "We can speak with greater certainty about the role of chemicals in the diet as contributors to the burden of cancer in the human population." Estabrook is Virginia Lazenby O'Hara Professor of Chemistry and chairman of the department of biochemistry at the University of Texas Southwestern Medical Center, Dallas. Arthur Whitmore, a spokesman for the Food & Drug Administration's Center for Food Safety & Nutrition, welcomes the report's cautions against drawing conclusions about the carcinogenic potential in humans of chemicals, including food additives, based solely on animal bioassays. He praises the report's recognition that a number of compounds are both carcinogens and anticarcinogens. Whitmore speculates that the report "may get some real policy play in this discussion about what to do with the Delaney clause," which is now taking place on Capitol Hill. The Delaney clause, part of the Food, Drug & Cosmetic Act of 1958, prohibits the addition to processed food of any chemical shown to be a carcinogen. Copies of the 417-page report, "Car8
FEBRUARY 26,1996 C&EN
cinogens and Anticarcinogens in the Human Diet: A Comparison of Naturally Occurring and Synthetic Substances," are available from the National Academy Press for $44.95 (prepaid) plus shipping and handling by calling (202) 334-3313 or (800) 624-6242. Janice Long
Non-Smoker (male, 42 years)
Smoking lowers level of key brain enzyme Cigarette smokers have a 40% lower concentration of monoamine oxidase in their brains than either nonsmokers or former smokers, researchers at Brookhaven National Laboratory, Upton, N.Y., have shown. The enzyme plays a key role in the metabolism of dopamine, a neurotransmitter that regulates movement and is implicated in the addictive effect of drugs. The Brookhaven group believes the reduction in monoamine oxidase amplifies the addictive effect of nicotine and explains why smokers have a lower risk of developing Parkinson's disease. Earlier research had indicated that levels of monoamine oxidase in blood platelets are low in smokers, but return to normal when people stop smoking. Led by organic chemist Joanna S. Fowler, the Brookhaven team set out to measure the concentration of the enzyme in the brain [Nature, 379, 733 (1996)]. They used positron emission tomography to image monoamine oxidase in the brains
Fowler: led Brookhaven team
Smoker (male, 44 years) In vivo PET images of brain slices in smoker and nonsmoker show smoker's brain has lower levels of monoamine oxidase—concentration ranges from high (orange) to low (purple). of volunteers who had been given intravenous injections of [nC]L-deprenyl. That drug, used to treat Parkinson's disease, binds to monoamine oxidase. Nicotine causes neurons to release excess dopamine, which binds to receptors on other neurons and sets up the reinforcing effect that leads to addiction. When monoamine oxidase is deficient, dopamine levels build up. Such a scenario would augment the addictive effect. of nicotine, the researchers suggest. Thus, they say, drugs that inhibit monoamine oxidase might help smokers kick the habit. One such drug, the antidepressant moclobemide, is being tested in highly dependent smokers. The Brookhaven group also offers an explanation for how low levels of monoamine oxidase could lessen the risk of developing Parkinson's disease, which is caused by a loss of dopamineproducing neurons. A decrease in the enzyme would be accompanied by a decrease in hydrogen peroxide, a byproduct of oxidation reactions that is a source of reactive species that can damage neurons. This may be one of the ways L-deprenyl delays progression of Parkinson's disease, the group says. Exactly how cigarette smoke inhibits monoamine oxidase is not yet known. But in a commentary in the same issue of Nature, psychiatrist Alexander H. Glassman of Columbia University and psychopharmacologist George F. Koob of Scripps Research Institute, La Jolla, Calif., say the Brookhaven work opens "a new vista on the biological effects of cigarette smoking." Mairin Brennan
