Citizens for Safe Drinking Water, a San Diego, California, group opposed to fluoridation as a means of preventing tooth decay, is trying to repeal the state's 1995 mandatory fluoridation law by gathering enough signatures to place an initiative before the voters. David Kennedy, a biochemist and part-time dentist in San Diego who is also president of the 4,000-member organization, points to studies concluding that fluoridation causes health problems and doesn't reduce tooth decay.
Among Kennedy's supporters is EPA chemist William Hirzy, who is backing the initiative in his capacity as an officer in the National Federation of Federal Employees. Arrayed against Kennedy and others opposed to fluoridation are scientists who claim fluoridated water is beneficial and nontoxic.
The practice of adding fluoride to tap water began in 1945. In the United States today, the tap water for approximately 134 million people has fluoride added to it, according to the CDC, and about 10 million people drink water that naturally contains the chemical. The reported optimal amount of fluoride is between 0.7 and 1.2 parts per million. A 1991 Public Health Service report credited community water fluoridation as being responsible for 20-40% fewer dental cavities compared with nonfluoridated areas.
Unsafe smiles? A California-based group is pushing to repeal mandatory fluoridation laws, citing health concerns.
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Though fluoride can be directly applied to teeth or used in mouth rinses, community water fluoridation is "a remarkably efficient way of controlling dental caries at the community level," says Lawrence Furman, a dentist and scientist at the National Institute of Dental Research. "Fluoridated water reaches everybody, that's why we need it," argues epidemiologist Brian Burt of the University of Michigan in Ann Arbor. But making fluoride so ubiquitous bothers opponents. Kennedy cites a number of studies that conclude that drinking fluoridated water is responsible for increased hip fractures. Some research indicates that fluoride may build up in bones over a lifetime and make them brittle, leaving the elderly particularly at risk for fractures. Other studies, however, have not supported this conclusion.
But studies on both sides of the issue have flaws, says Thomas Reeves, a fluoridation engineer at the CDC. For instance, a 10-year study reported in the 12 August 1992 issue of the Journal of the American Medical Association compared the incidence of hip fractures in residents of a fluoridated locality with the incidence in two nonfluoridated localities. The researchers concluded there was a link between water fluoridation and the fractures. The conclusion, Reeves says, is flawed for 3 of the 10 years because fluoride was not actually added to water in the so-called fluoridated locality. Furthermore, the studies show only slight differences in either direction, he said, adding that the CDC's official position is that more research is needed. But some say that the most compelling weakness of the JAMA study is the fact that it is an ecologic study, in which the characteristics of the group as a whole, rather than those of the individual constituents of the group, were studied, conceivably leading to the derivation of inaccurate inferences.
Fluoridation opponents point to an even more dire alleged consequence of fluoridating water--osteosarcoma, a form of bone cancer. They cite studies done in New Jersey as linking fluoridated water with this rare cancer in the United States. But Burt argues those analyses are statistically faulty. And the most recent animal studies performed by the National Toxicology Program failed to find a link.
Another point of contention raised by fluoridation opponents is dental fluorosis, the mottling of teeth that can result from drinking water containing fluoride from multiple sources. While Kennedy argues that dental fluorosis is a marker for serious internal problems caused by fluoride, Reeves, Furman, and other fluoride proponents disagree and state that the mild dental fluorosis that can occur from drinking fluoridated water is often detectable only by trained dentists. Reeves does acknowledge that, because fluoridated water is used in many products that people eat and drink, the incidence of dental fluorosis has been increasing. "We're seeing [dental fluorosis in] 7, 8, and 10% [of the population]," says Reeves. "A certain percent of the population may be getting too much."
Some scientists, says Reeves, suspect the high fluoride content of many toothpastes is a major reason for dental fluorosis. There is some discussion among fluoride specialists, he says, of lowering the dose in toothpastes aimed at young children for this reason, and also because some scientists worry that young children who swallow fluoride toothpaste may become ill.
The opposite concern--that children are getting too little fluoride--has also surfaced. A number of dental specialists fear the increased consumption of nonfluoridated bottled water may lead to increases in dental cavities. But there are currently no data to support this contention. Meanwhile, the debate over fluoridation of water continues.
Scientists recently had a bright idea about how to screen for environmental toxins. Researchers at the University of California at Davis have developed a bioassay system to detect polyhalogenated aromatic hydrocarbons such as dioxins in environmental samples. Dubbed the CALUX (for chemically activated luciferase gene expression) system, the assay is based on recombinant cell lines into which researchers have inserted the firefly luciferase gene. When exposed to dioxin-like compounds, the recombinant cells luminesce.
The glow gives it away. A new assay uses the firefly luciferase reporter gene, which luminesces in the presence of the Ah receptor, to test for the presence of dioxins in environmental samples.
Photo credit: Michael Dension
Polyhalogenated aromatic hydrocarbons are a diverse group of compounds that are widespread in the environment. Exposure to these compounds can lead to carcinogenesis, liver toxicity, birth defects, damage to the immune system, skin lesions, and even death. "Given the ubiquitous presence of these toxic compounds in the environment, there is a need for a rapid, inexpensive screening assay to monitor toxic output at a given site, to detect the presence of these chemicals in individuals who work in such environments, and to test sites in which these chemicals are believed to be deposited," says Michael Denison, professor of environmental toxicology at the University of California at Davis and one of the assay's inventors.
Denison and his colleagues have studied human, rat, guinea pig, hamster, and mouse cells, and are currently experimenting with a fish cell line. Testing is carried out by placing the environmental specimen in a test plate with the recombinant cells. The cells contain the luciferase reporter gene, which is linked to a DNA sequence called a dioxin-responsive element (DRE). The DRE is the binding site for the dioxin-activated aryl hydrocarbon receptor (AhR), a cell protein that mediates the toxic effects of dioxins. When the cells are exposed to dioxin-like compounds present in environmental samples, the AhR is activated and stimulates expression of the luciferase gene via the DRE. Luciferase can be easily measured because it emits light.
EPA regulations require an assay of the concentration of individual dioxin-like compounds in an environmental sample using high-resolution gas chromatography coupled with high-resolution mass spectrometry. Results for the individual compounds are then multiplied by a toxic equivalency factor to arrive at the total toxic equivalency for the mixture of toxins. This is a slow, cumbersome, and expensive process. The CALUX system detects the presence of such chemicals, but does not indicate which individual chemical or combination is present. Still, it is a rapid and inexpensive screening method, Denison explains.
"This [system] is a natural progression from the current bioassay," says Denison. "The previous bioassay, [using] the H4IIE wild-type cells, lacks much of the selectivity and sensitivity that the CALUX system has. An advantage or our system is that luciferase reporter activity is unaffected by chemicals that are known to inhibit activity in the H4IIE assay."
The bioassay is so promising that it is now the object of a commercial enterprise. George Clark, president of Xenobiotic Detection Systems, Inc. in Durham, North Carolina, is marketing the assay to environmental researchers. "Currently we're offering analyses of blood, serum, milk, water, or sediment in parts per trillion of 2,3,7,8-tetrachlorodibenzo-p-dioxin equivalents. We're seeking regulatory approval for our assay as a screening method that can be confirmed by gas chromatography-mass spectrometry, which should provide significant savings in the analysis of the toxicity of this class of compounds," Clark says.
The bioassay is not a test that can currently be run in the field, but specimens can be collected, frozen, and forwarded to the laboratory for assay. "However," says Clark, "we're developing a mobile laboratory that can be parked at the site of investigation in areas that require a large number of tests."
"The strong point of this assay is its speed and potential as a screening method," according to Scott Masten, a fellow in the Environmental Toxicology Program at the NIEHS who is familiar with the assay. "Using the chromatograph-spectrometer method you could assay perhaps two dozen specimens in a week. This bioassay can screen a hundred specimens in a week and only those that show activity, that luminesce, need to be run through the chromatograph and spectrometer. The bioassay will be even faster if it is automated, which can be done. The major disadvantage of the CALUX method is the problem with specificity. It measures total dioxin-like activity in the specimen without indicating which chemicals are present. The active sample still must be analyzed by chromatograph and spectrometer, but even so, the bioassay is around 20% the cost of the chromatograph-spectrometer."
In case-control studies in which a researcher is trying to determine how genetics and environmental exposure interact to cause illness, the job of being a control is not very appealing. Controls must fill out questionnaires that will determine if they have been exposed to the environmental agent, supply tissue samples for the genetic analysis (which normally involves a needle prick), and perhaps suffer the anxiety of questions raised by the genetic analysis itself, including how they will be affected if the analysis shows a genetic susceptibility to illness. For study subjects that have a disease, there is at least the hope that the research will lead to a new treatment for their ailment, but for the healthy control even this comfort is missing. It is not unusual for many controls to quit in the middle of a study on genetic susceptibility to environmental exposures. Sometimes so many quit that the study loses its validity.
However, according to two NIEHS research statisticians, in most studies of this type, the effect of the gene-exposure interaction can be found without using a control group. David Umbach and Clarice Weinberg report in the 15 August 1997 issue of Statistics in Medicine that if two assumptions can be made--that the disease or condition under investigation is rare in the general population and that the exposure of interest and the genetic condition are not statistically related--mathematical analysis of the gene-exposure interaction can progress with no data from controls at all.
The drawback to this method is that without data on the exposure history or on the genetic makeup of a control group, only the combined effect of the susceptible genotype and the exposure can be found. Neither the effect of the exposure alone nor of the genotype alone can be assessed.
Since it is less difficult (and less expensive) to convince a group of controls to fill out a questionnaire on exposure than it is to collect blood samples and perform genetic analysis, Umbach and Weinberg propose a research method in which a control group is used but not asked to supply tissue samples. This method should erase most of the anxiety for controls, while allowing the effect of the gene-exposure interaction, as well as the effect of the exposure alone, to be evaluated.
Ouchless experiments. A new statistical method means that some gene-environment studies can now be done without subjects having to provide blood samples.
For example, in a study of how smoking and a particular gene interact to cause lung cancer, if the assumption of random occurrence of the gene among smokers and nonsmokers can be made, the combined effect of the gene and smoking could be found without using a control group. However, what Weinberg and Umbach propose is that a control group be used, but only to fill out questionnaires about their smoking histories. This would allow the researchers to also analyze what effect smoking alone has on the incidence of lung cancer. The major drawback of this method is that it could not be used to determine the effect of the genotype alone, independent of smoking, as this would require collecting genetic information from the control group.
However, even in studies in which uncovering the lone genotype effect is important, Umbach and Weinberg report that researchers can still save controls some anxiety. This is because, even though the genotype of controls is necessary to find the genotype effect, it is not necessary to link those genotypes to specific exposures or, hence, to the individuals that supplied them. Genetic information can be collected from a control anonymously, without so much as a number to link the data to a specific individual or exposure history. The important information for determining the genotype effect, according to Umbach and Weinberg, is the total number of genetically susceptible controls. Umbach and Weinberg suggest that when statistical software is being employed that requires the exposure and genotype of each individual to be entered separately, researchers can simply pair genotypes and exposures randomly without harming the validity of the study.
However, both methods of analysis described by the NIEHS researchers--using no genetic data from controls and using only anonymous data--rely on the crucial assumption that the susceptible genotype and the exposure vary independently in the population. Neither analysis allows the validity of this assumption to be checked. The researchers say that in most cases, though, such a genotype-exposure relationship would not be expected, and, indeed, the independence of exposure and genetics is often assumed in studies of this type.
Still, there are cases where Umbach and Weinberg's method would not work. For example, this method could not be used to study how a gene that gives rise to skin color interacts with lifetime exposure to sunlight to cause skin cancer because it is probable that people with the variant of the gene that leads to very fair skin would avoid exposure to sunlight more than other people would. Thus, the exposure of interest would be linked to the genetic condition, and a central assumption of Umbach and Weinberg's method would be violated.
To show that there are many practical applications for their method of analysis, however, the authors present a reanalysis of a study of how maternal smoking and genetic predisposition of infants interact to cause cleft palates in newborns. In the original study, blood samples from all the control infants were available, but Umbach and Weinberg show that similar results could have been obtained without these samples.
In cases like these, the ability to take fewer blood samples could lower the cost and time involved in the research project while easing the anxieties of the control subjects, ensuring their continued cooperation and the ability of researchers to get at the important questions on gene-environment interactions.
Health concerns have led many developed countries in recent years to phase out the use of asbestos. But demand for these fibrous minerals has surged in the developing world, and the asbestos industry continues to flourish in nations such as China, Brazil, and Zimbabwe. This has raised concern among many public health experts who claim that all forms of asbestos are deadly, and that the risk is particularly pronounced in poorer countries where government infrastructures may not be sufficient to protect worker health. On the other side of the debate, multinational asbestos corporations and industry groups claim that the primary type of asbestos used today, chrysotile asbestos, presents no appreciable health risk when used properly and that reports of exploitation of asbestos workers in developing countries are highly exaggerated.
One such report, published in the April-June 1997 issue of the International Journal of Occupational and Environmental Health (IJOEH), describes a "silent epidemic of asbestos-related diseases" among workers in Brazil, which is the world's fifth largest producer and consumer of asbestos products. Much of the asbestos mining and production in Brazil is controlled by multinational corporations, and the authors of the article, Fernanda Giannasi of the Brazilian Labor Ministry and Annie Thébaud-Mony of the French National Institute for Health and Medical Research, claim that these companies have routinely exposed workers to asbestos while ignoring the lung disease and premature death caused by such exposures.
As an example, the authors describe an investigation into the health of Brazilians who had been employed at an asbestos cement plant in the city of Osasco that is owned by the Swiss-based Eternit Corporation. According to the reports of the company medical director at the Osasco plant, the diseases commonly associated with inhaling asbestos were rarely seen among workers during the plant's 50 years of operation. However, after the plant closed in the early 1990s, workers began to report illnesses to a local health agency. Of the first 12 workers seen at one clinic, four were diagnosed with asbestosis, a scarring of the lungs caused by inhalation of asbestos fibers, seven others had pleural plaques (calcification of the thin membranes that line the chest cavity), and one died four months later with peritoneal cancer. Some scientists say all of these illnesses are attributable to asbestos exposure. Though the authors report that efforts to locate more workers were hindered by Eternit, 421 former Osasco workers were eventually examined. In an unpublished follow-up to the IJOEH paper, Giannasi reports that 57.5% of these people had diseases that could be related to inhalation of asbestos dust, including asbestosis, asthma, peritoneal plaques, lung cancer, and reduced respiratory capacity.
This high incidence of morbidity, the authors conclude, is evidence that asbestos fibers simply cannot be used safely. "The world's experience with the industrial use of asbestos leads to the conclusion that the only way to ensure an end to asbestos-related disease is to ban [asbestos]," Giannasi and Thébaud-Mony write. "This approach, which has been taken in Sweden and other developed countries, is even more necessary in developing countries, where stringent regulation and enforcement are not a viable alternative to the ban."
However, industry-supported groups such as Canada's Asbestos Institute claim that calls for an outright ban on asbestos are overzealous because only certain varieties of the fiber present a real danger and these varieties are rarely used now. "Ninety percent of the asbestos used in the world right now is chrysotile," says Scott Houston, director general of the Asbestos Institute. "Chrysotile asbestos does not present a public health risk, and as for occupational exposures, if the levels of exposure during manufacture are controlled using very basic industrial ventilation technology--and these technologies are available in every country--there is really no excess risk there either." The Montréal-based institute is supported by a consortium of asbestos companies and the governments of Canada and Québec; Canada is the world's second leading producer of chrysotile asbestos after Russia.
Asbestos industry representatives say that reports of rampant health problems in Brazilian asbestos workers are either exaggerated or isolated problems, not representative of the whole industry there. "I visited a factory in Brazil," says Houston, "and it was an extraordinarily clean operation. . . . The asbestos mines there probably have the best industrial hygiene of any mines in Brazil . . . There are some problems in the small- and medium-sized business sectors, and we realize that, and are actively trying to clean those problems up." To address isolated abuses in developing countries where government enforcement may be lax, Houston says the Asbestos Institute supports a policy of "responsible use," in which the asbestos mines would agree to stop fiber sales to industries that do not meet certain safety standards and allow government inspections.
However, many public health advocates say that industry measures cannot possibly go far enough to protect worker health. "There is every reason to believe that a very low dose of asbestos can cause cancer," says Joseph LaDou, editor-in-chief of the IJOEH. That, says LaDou, is reason enough for stopping the use of asbestos completely.
A safeguard . . . sort of. A Brazilian asbestos worker fails to use even the minimal protection of his mask.
Photo credit: Fermanda Giannasi |
Houston asserts, however, that if asbestos was banned, the materials used to replace it may not be any safer. The primary use of asbestos fiber today is to increase the tensile strength of cement products, and, Houston says, research has been done on replacing asbestos in cement with other fibers. "A lot of research has been done on cellulose fiber, for example," he says, "and what was found is that these fibers are very bio-persistent and more dangerous than asbestos. That is why it's a bad idea for people to make hasty substitution decisions. You have to be very prudent or it is likely that you will end up replacing asbestos with something more dangerous." This argument has been accepted by both the World Health Organization (WHO), which supports continued controlled use of chrysotile asbestos, and the U.S. Fifth Circuit Court of Appeals, which overturned an EPA-proposed ban of asbestos in 1989.
Barry Castleman, an independent environmental consultant who has spent the last 25 years studying asbestos and public health in the United States, calls the idea that other dangerous fibers would replace asbestos absurd. "The main uses of asbestos cement are in pipes and in construction materials like cement-asbestos shingles," Castleman says. "It is not necessary to replace the fibers in the cement [for these uses]. There are other materials completely different from cement that can be used. . . . For example, there is plastic pipe for transporting water; there is clay pipe, cast-iron pipe."
Though the EPA's ban on asbestos was overturned, Castleman reports, U.S. companies have still managed to find asbestos substitutes. "Industry is still phasing out asbestos because of fear of liability suits," he says. Castleman says this changeover, combined with asbestos bans in many European countries, has led to an intense effort on the part of industry groups to promote asbestos use in other parts of the world. "The asbestos industry is really fighting for its life right now with the European market disappearing and distributors in the United States leery of selling the stuff," he says. "Asbestos companies can't afford to lose markets in the developing world."
To prevent this from happening, Giannasi and Thébaud-Mony claim that the asbestos industry has begun a practice of sending its representatives to developing countries such as Brazil to pose as independent experts, vouching that asbestos is safe. Such tactics, the authors claim, were instrumental in preventing an asbestos ban from being implemented in Brazil in 1993.
In addition, Castleman says, industry groups have kept organizations such as the WHO and the International Labor Organization (ILO) from denouncing asbestos by using similar tactics. For example, he says that the International Fiber Safety Group has tried to influence ILO policy under the guise that the group is composed of impartial health experts, when in fact it is a spin-off of the Asbestos Institute, formed for the purpose of gathering support for the asbestos industry. LaDou makes similar accusations against the International Commission of Occupational Health. "When we looked at where the WHO and [the] ILO were getting their information, we found that most of it was coming from the International Commission on Occupational Health . . . a group made up of virtually all consultants to the Asbestos Institute of Canada," LaDou says.
Houston defends the actions of the Asbestos Institute, saying that neither the organization nor its consultants have misrepresented themselves. Rather, he says, the institute has simply worked with international organizations like the ILO and the WHO to establish guidelines for the safe use of asbestos and to provide training for asbestos workers in developing countries.
Houston says that public health advocates in the developed world are overreacting to the use of asbestos in developing countries because of their past experiences with the more dangerous amphibole form of asbestos. "For many years, amphibole asbestos was used in those countries, especially in the construction and shipbuilding industries, with very little regulation, and that has led to a terrible legacy of disease," Houston says. However, he asserts that the chrysotile asbestos used in asbestos cement does not present the same health problems, and in fact represents a valuable resource for the developing world.
But many public health advocates in both developed and developing nations point to reports like the one by Giannasi and Thébaud-Mony as evidence that the use of asbestos is continuing to cause death and disease around the world. "As long as asbestos continues to be used, it's going to be a problem," says Castleman.
One of the reasons often cited by world leaders for refusing to take direct actions to curb global warming is that we know too little about the problem. For instance, they argue, we don't know how fast the planet is warming, what the effects of the warming will be, or even exactly where all the excess atmospheric carbon dioxide is coming from. Leaders often say that in the face of such uncertainty, it would be imprudent to burden people with new laws and regulations. These issues are expected to be the topic of heated debate at the International Climate Summit to be held in Kyoto, Japan, in December. One key issue to be addressed at that meeting is the importance of protecting the earth's rain forests as a means of stopping global warming. Rain forests are particularly dense in biomass--and, therefore, carbon--and the routine burning of these forests in many countries releases carbon dioxide and destroys an important terrestrial carbon sink. However, the role of rain forest destruction has remained largely unknown in the global warming equation because tracking and quantifying the destruction has been a nearly impossible task.
Now, however, a joint project of NASA, the University of Maryland, and the University of New Hampshire is, quite literally, painting a clearer picture of rain forest destruction. Researchers with the Landsat Pathfinder's Humid Tropical Forest Inventory Project are using satellite images of the earth to construct maps that accurately portray land use and vegetation density across the great rain forests of the Amazon, Southeast Asia, and Africa for several recent time periods. The data gathered by this effort will function like a CAT scan of the earth, allowing scientists to pinpoint where the destruction of rain forests is occurring the fastest so that remediation efforts can be concentrated on these areas.
A site on the World Wide Web has been constructed by the Institute for the Study of Earth, Oceans, and Space at the University of New Hampshire to share the information gathered by the project. The satellite data are compiled by the institute, analyzed, and edited before being plotted on a map of the rain forest. Though the group can discern land use in areas smaller than a square kilometer from the satellite images, the data are aggregated into 16-km squares for distribution over the Internet. Maps of deforestation, regrowth, and forest density for entire rain forests are compiled by color coding and plotting these squares, and the maps can be viewed on the project's Internet site by following the Data Products and Results link from the home page, which is located at http://pathfinder-www.sr.unh.edu/pathfinder1/.
Original satellite images of the areas being studied can also be viewed on the site by following the Satellite Image Browser link on the home page. Through this link, users can find the satellite pictures of the area they want to view either by using interactive maps or by selecting the area from lists of cities and geographical features. To better illustrate how the rain forests have changed in the past few decades, the site also provides several maps that are animated to show the transformation of the land. These maps, which can be found through the Morphs link, available through the Multimedia link on the home page, vividly show how logging roads, dams, and expanding populations can devastate huge sections of forest in a short amount of time. Also under the Multimedia link is a collection of media kits that provide a succinct introduction to the project.
The General Information link on the home page leads to more detailed accounts of the project. Explanations of how data are gathered, processed, analyzed, and checked are available via the Project Overview link. The full texts of some of the scientific papers that have been generated by the project are available under the Published Papers link, while news articles that utilized Landsat data and project reports can be accessed by the Reports, Miscellaneous link.
These papers and reports, as well as the ongoing research, will make it easier to eliminate some of the unknowns from the global warming equation. And the Landsat Pathfinder World Wide Web site will allow new findings to be quickly disseminated to scientists, leaders, and policy makers around the world--even in Kyoto.
Last Update: November 7, 1997