We all worry about the population explosion--
but we don't worry about it at the right time.
Arthur Hoppe, attributed
Topics in this issue's forum:
Sixteen pesticides have been detected in eight brand-name baby foods, according to a study by the Environmental Working Group and the National Campaign for Pesticide Policy Reform, two public interest groups based in Washington, DC.
In their study, the EWG and the NCPPR collected a random sampling of 76 jars of baby food from grocery store shelves in Denver, Philadelphia, and San Francisco. The group chose fruits and vegetables babies most commonly eat during their first year of life. Of these, 53% harbored traces of one pesticide, and 18% had two or more pesticides. Plums contained the highest amounts at 46 parts per billion and peaches contained 29 parts per billion. Pears had the highest number of multiple pesticides overall (five).
Baby beware. Samples of common baby foods from Denver, Philadelphia, and San Francisco revealed that 53% had traces of one pesticide and 18% had two or more pesticides.Joseph Tart
The report,
Pesticides in Baby Food, was published in July by the EWG and the Tides Foundation (available on the World Wide Web at:
http://www.ewg.org) and indicates that all levels of pesticides found were below federal standards. While these standards are set with safety considerations for infants, children, and other sensitive populations, the actual risk assessments are based on an average adult. According to the EWG, the concern is that pesticides are not currently "tested for safety in the way babies are exposed to them," and that babies and young children "react differently than adults to many drugs and toxic substances."
These findings are consistent with the conclusions of a five-year investigation by the National Academy of Sciences, published in 1993 in the report Pesticides in the Diets of Infants and Children, which suggests that federal standards embodied in the Delaney Clause may not adequately account for the special vulnerability of infants and growing children to chemical substances. Nor do these standards account for the total doses of pesticides that babies receive from many other sources, including fresh produce, drinking water, possibly breast milk, or from the additive effects of these pesticides.
Some groups believe government standards are outdated and should be strengthened to provide broader protection to children. Other groups agree that federal standards are flawed, but see them as antiquated for other reasons. Scientists can measure one-billionth of the amount of a chemical now, for example, as compared with the 1950s when standards were set.
For almost four decades, the Delaney Clause, which bans the use of food additives shown to cause cancer in people or animals, has provided at least some measure of protection to the public food supply. The clause was passed in 1958 as an amendment to the Food, Drug and Cosmetic Act. However, this law is being challenged as obsolete. The current debate centers on whether Delaney should be repealed and, if so, what should take its place. Two bills are currently pending that would revise legislation governing food safety. HR 1627 would relax regulations by repealing the Delaney Clause and amending the Federal Insecticide, Fungicide and Rodenticide Act by bringing the separate standards for pesticide products under one umbrella. This bill calls for the EPA to apply a negligible risk standard to both raw and processed foods. HR 1771 also allows a negligible risk standard, but would require the EPA to determine whether a pesticide causes cancer, damages developing neurological, immune, or reproductive systems, or has other serious, adverse health effects in children before the agency could set tolerance levels. The bill would also require warning labels on foods that have been sprayed with a known or probable carcinogen.
Philip Landrigan, professor of pediatrics at the Mount Sinai School of Medicine in New York City, and chair of the committee that prepared the 1993 NAS report, believes the pesticide regulatory system in the United States is flawed because of its approach for setting food tolerances. Instead of being based on health considerations, says Landrigan, they are based on field trials conducted by pesticide manufacturers and are "a balancing process in which health considerations are weighed against economic factors and agricultural practices." Landrigan believes that HR 1627 is inconsistent with the recommendations of the NAS report because it "will perpetuate the current inadequately controlled exposure of children to pesticides in their diets."
Richard Wiles, vice president for research of the EWG, argues that Congress is moving toward weakening what he sees as already weak laws governing food safety for kids. For example, in describing the EWG study, he notes that a fungicide called iprodione was found in more samples and at higher levels than any other pesticide. EPA studies identify it as a probable human carcinogen, yet it slips through the regulatory cracks in the Delaney Clause. Language within the clause prohibits any amount of a cancer-causing pesticide "that concentrates during food processing." Iprodione levels do not concentrate in baby foods; thus, it passes the safety test. "There are no standards out there that are specifically designed to protect infants from pesticides in their diet, or from the environment in general," says Wiles.
Physicians for Social Responsibility, another Washington-based group, has also studied these issues. Beyond Delaney--Preventing Exposures to Hazardous Pesticides, a 1995 report by the group, updates the NAS study. The group supports the recommendations of the NAS, and likewise favors stronger regulations to safeguard young children from exposures to toxic chemicals.
Joseph Schwartz, associate director for policy of Physicians for Social Responsibility, says the debate over the Delaney Clause is important because it's time to begin phasing out the most unsafe pesticides on the market and provide the right kinds of incentives for safer biological alternatives. "We are looking for an opportunity to influence pesticide legislation reform, so five or ten or twenty years from now, farmers are not limited to the same pesticides their parents and grandparents were using," he says. "We can do better than that."
The agricultural community believes it is doing better than that. Will Carpenter, former vice president and general manager of Monsanto Agricultural Company, says that advances in biotechnology, coupled with integrated pest management strategies, are allowing great strides in reducing pesticide usage. "Within 5 to 10 years, the two biggest uses of insecticides in this country will drop precipitously," he says. "This is due to our ability to genetically vaccinate cotton and corn plants with a gene from a disease microbe. The insect eats the plant leaves, gets sick, and stops feeding." Carpenter continues, "Also, farmers are shifting to no-till/conservation tillage in greatly increasing numbers. This practice reduces soil erosion to 1% of what it once was, so pesticides stay in the soil on site, where they belong, instead of running into our reservoirs."
Meanwhile, the worldwide agricultural industry shoulders the responsibility of providing an adequate supply of food for millions of people in the world each day. Carpenter says pesticides are necessary if these goals are to be met. Carpenter opposes strict government regulations--especially when they are as old as Delaney. "I like to think we can do without them," he says.
At present, the Delaney Clause stands while alternative legislation is stalled at various stages in Congress. Whatever decision Congress reaches regarding the Delaney Clause, most participants in the debate agree that the major objective must continue to be protection of public health, especially children's health.
Researchers in Sweden have isolated a substance from human milk that destroys cancer cells while leaving healthy cells unaffected. The research, published in the August 15 issue of the
Proceedings of the National Academy of Sciences, may stimulate a new approach to developing antitumor drugs and suggests that breastfeeding may play yet another important role in infant health.
The discovery grew out of a serendipitous observation made by Anders Håkansson, a graduate student in clinical immunology at Lund University in Sweden. Håkansson originally set out to study how milk affects the attachment of pathogenic bacteria to lung cells, an important step in the disease process. Like many investigators, he used malignant, or transformed, lung cells in his experiment because these can be cultured more easily in vitro than normal cells. When the malignant cells were exposed to milk, the cells died. This observation stimulated further research by Håkansson and collaborators at Lund University and at the Karolinska Institute in Stockholm.
The investigators isolated the active component of milk, the common milk protein lactalbumin. For reasons not understood, the cytotoxic effect was not produced by single protein molecules but by aggregates of two or more molecules, called multimeric lactalbumin (MAL). Research on other cell types demonstrated that the effect of MAL was selective--in addition to tumor cells, lymphoid and embryonic cells were also killed, while mature normal cells of lung epithelium and solid organs were left unharmed. Moreover, the investigators noted that the antitumor property of human milk is not shared by bovine milk, which lacks the ability to form aggregates of the protein.
Although animal experiments using MAL are planned, Håkansson emphasizes that MAL is not a cancer cure. "We don't know anything about the in vivo effects of the protein, or if this will work as an anticancer drug," he said. In fact, Håkansson feels the real significance of his observation may be another line of research it has stimulated--the elucidation of the mechanism by which MAL destroys tumor cells.
The researchers found that MAL destroys tumor cells by inducing the process of apoptosis, the sequence of genetically programmed steps by which cells self-destruct. Apoptosis can occur naturally at the end of a cell's life or when a cell is diseased and "sacrifices itself" to prevent the spread of disease. In many diseases, however, the mechanism that initiates apoptosis malfunctions. "In about 50% of tumors, the cancer cells cannot undergo apoptosis," Håkansson observes. "The cells have inactivated the pathway [for apoptosis], so they live longer than they're supposed to. This is a mechanism of cancer. The interesting part of this study is that we can perhaps get past this inactivation and still induce apoptosis in these cells," he said.
"This is a unique observation that could have good potential in the design of new antitumor agents," comments Kathryn Rich, assistant professor of pathology and ophthalmology at the University of Southern California, whose research focuses on apoptosis in neurons. One of the goals of apoptosis research, Rich observes, is to "use this normal physiological process as a weapon against the cancer cell." Unraveling the apoptotic pathways in cancer cells could lead to design of antitumor agents that would switch on apoptosis, thereby killing cancer cells. An important finding of the Swedish study, Rich adds, is the selectivity of MAL's effects. "Most other external agents tend to kill both normal and tumor cells. Understanding why tumor cells are sensitive [to MAL] and why normal gut epithelial cells are resistant . . . could be very promising."
According to Charles Isaacs, director of the Laboratory of Protein Chemistry at the New York State Institute for Basic Research, the new study is also important because it suggests that breastfeeding plays a previously unrecognized role in infant development. He notes that while it has long been known that human milk provides excellent nutrition and protection against infection, a possible role in regulating cell growth has been hypothesized but never demonstrated. "This study suggests that yes, maybe some of the baby's cells can be affected because there are compounds in milk that induce apoptosis," Isaacs said. "It's possible that MAL has an effect on cells in the baby's gastrointestinal tract and also on the baby's own lymphocytes." Cautioning that further testing is needed to see if the same effects can be observed in vivo, Isaccs adds that the study could stimulate research to find other substances in milk that regulate cell growth.
Why would milk contain a substance that destroys tumor cells? The answer is uncertain, but may lie in another of MAL's effects--it destroys not only tumor cells, but immature cells as well. Håkansson speculates that this selective cytotoxicity may play a role in controlling populations of maturing cells in the infant's gastrointestinal tract. Controlling the growth of immature cells may, in fact, be the primary function of MAL, and its effects on tumor cells may be secondary. Håkansson notes, "Cancer cells also have a very immature cell phenotype, so [that may be the reason] they are also affected." He adds, "It is not strange that milk has effects other than just nutrition. We see now that it has some control over cell proliferation and cell death."
Two groups of scientists have independently identified an important trigger in apoptosis, the complex sequence of events that causes cells to self-destruct. The finding raises the possibility of developing drugs that could selectively induce or inhibit apoptosis.
The trigger, a protease, or enzyme that cleaves other proteins, was recently identified by Donald W. Nicholson at the Merck Frosst Centre for Therapeutic Research in Quebec, Muneesh Tewari at the University of Michigan Medical School, and their collaborators. In the July 6 issue of Nature, Nicholson and colleagues named the protease apopain. In the June 2 issue of Cell, Tewari's group named it "Yama" after the Hindu god of death.
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Yama. University of Michigan researchers named the new-found apoptosis enzyme after the Hindu god of death. |
The authors believe Yama/apopain is a crucial component of the mammalian cell-death pathway. "It is something that we suspect will be activated in a variety of different instances of apoptosis," Tewari said.
Apoptosis is a sequential, programmed series of steps by which cells destroy themselves. Some scientists suggest that inappropriate apoptosis may be responsible for damage seen in autoimmune disorders, immune deficiencies, Alzheimer's, Huntington's and Parkinson's diseases, cancers, stroke, and heart attack.
The recent discovery was made using mammalian systems. It underscores the similarities between apoptosis in the nematode worm, Caenorhabditis elegans (which has provided much of our understanding about apoptosis) and mammals. In the nematode, apoptosis is controlled by sets of genes including ced-3 and ced-9. Expression of ced-3 is required for cell death to occur. Expression of ced-9 blocks cell death. The ced-9 gene is homologous to a set of mammalian oncogenes.
Mammals also have a set of genes that function like the nematode's ced-3 gene. One such gene encodes an enzyme called ICE, interleukin-1ß converting enzyme. ICE is implicated in some forms of apoptosis but is not the trigger for all forms of mammalian apoptosis. Scientists concluded that a different, unidentified enzyme played that role. Both Tewari's and Nicholson's groups identified this enzyme as CPP32ß, a previously uncharacterized protein related to ICE, which they named Yama/apopain. As apoptosis begins, enzymes, including one called PARP [poly(ADP-ribose) polymerase], are cleaved into smaller fragments. PARP maintains and repairs DNA. The researchers used PARP cleavage to identify Yama/apopain.
"I am sort of surprised that this discovery hasn't received more coverage in the scientific lay press. It really is a pivotal finding," said Tewari's co-author Vishva M. Dixit of the University of Michigan Medical School. "It allows for the first time a toe in the door of mammalian cell death. We can enlarge on the knowledge and identify the other components. I think the entire story, the essential components of the pathway, will probably fall in place the next couple of years."
Gloria Preston, an apoptosis researcher at the NIEHS, notes that this is an important finding because proteolytic cleavage does appear to play a role in apoptosis. "Apparently, other proteases exist that have some similarity to Yama/apopain, and whether this particular protease is pivotal to the process is not clear. At this time it is difficult to determine what cleavage events are essential and what ones are merely part of the degradation process."
Yama/apopain does appear to be the key protease in the apoptosis studied in the mammalian osteosarcoma cells described by Nicholson et al., according to Shai Shahan, who studies apoptosis in nematodes at MIT. But since Yama/apopain is part of a family of proteases, it is possible there is redundancy. More than one protease might be responsible for triggering cell death in a given cell. Also, one protease might be responsible for activating cell death in a given tissue and another protease of the same class will activate it in yet another tissue, Shahan said.
That would please pharmaceutical companies. The question from a pharmaceutical point of view is whether or not there are certain proteases that are present in only certain cells. "I guess the ideal thing would be if in a neurodegenerative disease there were an ICE homologue or close relative that caused cell death. If one could identify a specific inhibitor, we would be able to prevent cell death," said Douglas K. Miller, senior investigator at the Merck Research Laboratories in New Jersey, and a co-author of the Cell paper. In applying the finding to cancer therapy, however, it would be necessary to induce, not inhibit, apoptosis under controlled conditions.
While Dixit and colleagues are now concentrating on identifying the enzyme that activates Yama, the Merck researchers are concentrating on characterizing the five other mammalian homologues of ICE. They will then look at them to see if they are associated at all with disease, Miller said.
Intense summer heat waves could kill thousands more people each year in New York, St. Louis, and other U.S. cities, epidemics of infectious diseases could continue sweeping into temperate climates from the tropics, and numbers of skin cancers will probably rise in mid-latitude regions of North America, Europe, and Australia, all during the next century. These impacts of climate change were predicted by experts at the Conference on Human Health and Global Climate Change, September 11-12, at the National Academy of Sciences in Washington, DC.
Until recently, scientists and policymakers had primarily focused on how the earth's physical systems would be affected by global warming, examining the potential for increased sea level rises and bigger hurricanes. But the Intergovernmental Panel on Climate Change, in a forthcoming update of its 1990 study, will for the first time include a chapter on the possible human health effects of climate change. In turn, Vice President Al Gore asked the Office of Science and Technology Policy and the Council on Environmental Quality to organize a conference on this theme. Co-sponsored by the National Science and Technology Council and the Institute of Medicine, the conference gathered a diverse group of experts from academia, government, and nongovernmental organizations. Conference participants discussed how climate change might damage human health, then made recommendations for improving global health surveillance systems, research, education of health professionals, and international cooperation.
In industrialized nations, the greatest impacts of climate change probably will be experienced through heat waves. Global warming of 1°-3°C would probably increase the frequency of intensely hot days in temperate regions, resulting in several thousand extra deaths annually due to heat stress in the United States, said Laurence S. Kalkstein of the Center for Climatic Research at the University of Delaware. More than 500 Chicagoans died during a July 1995 heat wave, a type of disaster that could occur more often in the future. "Living in heat-trapping brick tenements with black-tar roofs, many poor, elderly, or frail residents of New York, Chicago, and other cities will be unable to adjust to a warming climate," said Kalkstein.
Faced with hotter summers, those who can afford air conditioning will use it more frequently, resulting in more air pollution, predicted Joel Schwartz, epidemiologist at the Harvard University School of Public Health. Fine particulates from power plants, he noted, are clearly associated with hospital emissions for respiratory disease and heart disease. "Power plants are the biggest source of air pollution concentrations along the East Coast, and we think this pollution will get worse."
Over the next 50 years, depletion of stratospheric ozone is expected to lead to greater numbers of skin cancers, especially among fair-skinned people in temperate climates, where the ozone layer is thinner. Although the ozone layer will reach its lowest level around the year 2000, it will gradually thicken because of international regulations on the use of chlorofluorocarbons and other chlorine-containing chemicals. But skin cancers usually do not appear until decades after exposure. "Even under the Montreal Protocol, the numbers of nonmelanoma skin cancers will be about 25% higher in 2050 than in 1980 in mid-latitude cities such as Vancouver, Paris, and Prague," said Margaret Kripke, an immunologist with the M.D. Anderson Cancer Center in Houston. "Melanoma will also increase, but nobody knows by how much."
A warming planet will continue to bring more extreme and erratic weather, with greater incidence of droughts, floods, and hurricanes, which in turn will increase rates of death, injury, and infectious diseases due to proliferations of pests, experts said. For example, during each of the past five years, El Niño, an ocean warming system, has spread very warm, wet spells around the world. As a result, the mosquitoes that carry malaria, yellow fever, and dengue have moved into some temperate climates and higher altitudes, infecting people who lack immunity to these diseases, said Paul Epstein, specialist in tropical public health at Harvard University. Other major diseases likely to spread with global warming are cholera, filariasis, and sleeping sickness.
An uncertain future. Manufacturing and deforestation contribute to climate change effects such as global warming and spread of disease. (Ebola: Frederick A. Murphy, Aedes aegypti: Leonard Munstermann.)
Joseph Tart
Deforestation and urbanization in some developing countries contribute to this dangerous mix. As tropical forests are cut down for timber and agriculture, people are more likely to come into contact with previously remote disease carriers. Meanwhile, growing numbers of poor in developing nations are leaving rural areas for burgeoning, unsanitary cities, which are "veritable incubators for disease," said J. Brian Atwood, administrator for the U.S. Agency for International Development. The recent outbreak of the Ebola virus in Africa is an example of the movement of a very rare disease from a rural area into a city, where it could spread rapidly.
To address these issues, health professionals in the field must be better trained to monitor and report emerging diseases. "Local health-care workers need training to increase their sensitivity to new health problems, and they need to know who to tell about the problems," said William Bancroft, director of the Military Infectious Disease Research Program at the Army Medical Research and Materiel Command. A global network for disease surveillance exists informally, but it must be strengthed, with improved links to health professionals. "Health-care workers need to know how to get into the surveillance system so they can get a response," Bancroft added.
Vulnerable populations, including children, elderly people, and those in transitional areas where disease epidemics could spread, should be targets of an improved global surveillance system. Vulnerable people must be better educated about growing health risks, with access to vaccines and information about their exposure.
The United States has taken an international leadership role in disease surveillance, control, and research, a role that should be continued, said conference participants. "We're going to lead the situation," said Bancroft. "No other nation can do what we're suggesting ought to be done." But the nation's current funding for research on infectious diseases, other than AIDS and tuberculosis, is limited. Now the United States must better support the work of epidemiologists, laboratory scientists, entomologists, behavioral scientists, public health experts, and others so they can find new solutions for emerging disease threats, according to conference speakers. Conference participants also agreed that more bridges should be built between environmental science and the public health communities. In particular, physicians and other health professionals need improved environmental science education.
Finally, pilot research projects should study El Niño as a possible signal that we are entering a new climate pattern. "We should look at El Niño as an analogy for climate change," Epstein said. "El Niño, as a warming event in the ocean and atmosphere, gives us an idea of what future warming events might be like. [The current] El Niño has persisted for five years in a row, yet no El Niño has persisted for more than three years. So studying El Niño can help us understand the trends and variability of climate, and the effects that climate changes can have on disease carriers such as mosquitoes."
EHPnet
Recent reports in both the scientific and the popular press have focused attention on the potential hazards of radon exposure in homes. In the June 7 issue of the Journal of the National Cancer Institute, Jay Lubin and colleagues published an extensive analysis of 11 studies of radon-exposed mine workers that demonstrates that radon exposure in homes may account for as many as 14,400 lung cancer deaths per year. A research article in this issue of EHP suggests that EPA figures may overestimate radon risks by failing to account for residential mobility (see p. 1144).
The Radon Home Page (http://sedwww.cr.usgs.gov:8080/radon/radonhome.html), created by the United States Geological Survey (USGS), part of the Department of the Interior, provides information for citizens and scientists on basic and applied research on geology and geochemistry of radon in rocks, soils, and water.
Radon gas results from the natural breakdown of uranium in soil, rock, and water. Although levels of radon vary from place to place, high levels of indoor radon are found in every state. People may feel especially vulnerable to radon exposure because humans are unable, via their own senses, to detect radon. The Radon Home Page provides a means of becoming better educated about radon and of learning how to reduce potential radon risks. In addition to basic information on radon in the geologic environment, the site provides a link to The Citizen's Guide to Radon and other consumer publications on radon from the EPA, as well as a list of radon-related publications.
The Radon Home Page contains a hyperlink to two maps describing radon potential by state and by EPA region. More detailed information may be obtained from USGS geologic radon potential books (which can be ordered from the USGS or obtained from a local library). These reports describe the geology, soils, radioactivity, generalized housing construction characteristics, and other relevant information, and include discussions of the geologic factors controlling radon potential in each state. The site also describes the High Radon Homes Project, which is a cooperative effort of the USGS, the EPA, the Department of Energy, and Lawrence Berkeley National Laboratory that aims to develop a model for identifying the proportion of homes in an area where occupants are suffering high exposures (occupant exposures exceed the occupational radiation limit of 20 picocuries per liter) to radon decay products. Information from this project will be used to convey information to the public on high radon areas, assist homeowners in testing and remediation, develop procedures and codes for new construction, and confirm scientific investigations in high radon areas. Such information, coupled with epidemiologic studies, may also be useful in determining the cancer risk associated with high residential exposures to radon.
For research scientists, The Radon Home Page includes a section on basic and applied geographic radon research. Hyperlinks in this section take the user to abstracts of current work in fault and shear zones in the eastern United States, glacial deposits of the upper Midwest, and terrestrial gamma radioactivity of the contiguous United States.
In a move to prevent Republican lawmakers from weakening environmental laws through amendments tacked onto the budget bills, President Clinton signed an executive order August 8 requiring companies that contract with the federal government to report their releases of toxic chemicals.
The impetus for the order was 1 of 18 amendments to the House appropriations bill for the EPA. This rider would prohibit the EPA from requiring manufacturing plants to report new data to the Toxics Release Inventory (TRI) of the 1986 Emergency Planning and Community Right-to-Know Act for any reason not already in the law. The TRI contains emission reports of 23,000 companies on 651 chemicals. EPA Administrator Carol Browner said that the rider "essentially limits my ability to guarantee that the people of this country will know about toxic chemicals in their communities."
Although the executive order applies only to those firms doing business with the federal government and would not exempt any company already reporting to the TRI, it would effectively limit the EPA's proposed toxic use inventory--a system that would include not only toxic emissions, but also toxic chemicals entering a plant's process. Many industry groups, including chemical manufacturers, already question the effectiveness of the TRI and are lobbying against the new inventory.
And there may be some evidence to support industry claims that TRI data do not provide the most relevant information in terms of risk from chemical exposures. Researcher Reid Lea and colleagues at the University of New Orleans developed a system for weighing the risk of toxic exposure to humans and the environment and used it to analyze TRI data for Louisiana. They found that the amount of a chemical released into the environment does not necessarily correlate with the extent of the danger it poses. In their paper, "Comparative Risk Analysis of TRI Data as an Environmental Indicator--A Louisiana Case Study," presented at the Air & Waste Management Association's 88th Annual Meeting, the researchers wrote, "The traditional method of analyzing the TRI data fails to address the true concerns about chemical emission to the environment."
What's News to You?
Environmental Health Perspectives welcomes topic suggestions for upcoming "Environews" articles. Send suggestions to: News Editor, Environmental Health Perspectives, National Institutes of Environmental Health Sciences, PO Box 12233, 111 Alexander Drive, Research Triangle Park, NC 27709 USA. Fax: (919) 541-0273 or E-mail: thigpen_k@niehs. nih.gov.
Last Update: November 27, 1995