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The Latest Hormone Science
[In this series, we have been reviewing studies published during the past two years in ENVIRONMENTAL HEALTH PERSPECTIVES, a peer-reviewed journal published by the U.S. National Institutes of Health. Our purpose has been to discover whether mainstream scientists believe that industrial chemicals, released into the environment, can interfere with the hormones of wildlife and humans, leading to widepsread harm. It is abundantly clear that they do. To keep abreast of the torrent of new studies of hormone disruption appearing in dozens of journals, check in regularly at https://www.ourstolenfuture.org.
Now the question becomes, "What does all this information about hormone disruption mean?" One person eminently qualified to comment on that question is Dr. J.P. Myers, a zoologist and co-author (with Theo Colborn and Dianne Dumanoski) of OUR STOLEN FUTURE, the book that pushed "hormone disruption" to the top of the international environment-and-health agenda. The following essay first appeared in the February, 2002, issue of OUR PLANET, the journal of environmental sustainability published by the United Nations Environment Program.
Disrupting Life's Messages
by John Peterson Myers*
A revolution in scientific understanding of the impacts of contamination on health is under way. As it unfolds, it is likely dramatically to alter our understanding of the consequences of pollutants for human well-being, and to require fundamental changes in how chemicals are regulated. The revolution arises from scientific discoveries which establish that many chemicals both from the natural world and synthesized in laboratories interfere with the natural chemical messaging systems that direct the biological development of plants and animals, including humans.
Virtually all biological development is under the control of various chemical messaging systems that convey instructions from the genes to their targets, thereby directing development. Hormones, neurotransmitters and growth factors, among others, are key elements of these message systems. Their successful transmission of genetic instructions is vital to normal healthy development, as they control almost if not every aspect of the process from what sex a baby will become to how many fingers it will have, to whether its brain is capable of intelligent reasoning or whether its immune system will be able to resist disease.
Science has now established that a wide array of chemicals can disrupt these genetically based messages without damaging the genes themselves. Much attention has focused on disruption of hormonal signalling, which has become known as endocrine disruption.
The roots of research in this arena go back to the 1930s, but it has burgeoned in the last ten years because of very significant investments of funds by European, Japanese and North American governments. New results are published virtually every week. These new findings are rich in detail, fascinating in what they reveal about biological mechanisms, and sometimes breathtaking in their implications.
For example, a study published in July 2001 by the United States Centers for Disease Control reported a strong relationship between DDT contamination in mothers and the likelihood of pre-term birth of their infants.[1] Using biological samples stored since the 1960s, the authors report that their findings indicate that the United States experienced an epidemic of pre-term birth during the hey-day of DDT use, and that this persistent pollutant may have caused up to 15 per cent of infant mortality in America during that period.
Several important broad trends in the pattern of research findings can be identified from the thousands of studies on endocrine disruption published since the early 1990s.
First, the research confirms that contamination by hormonally active compounds is globally ubiquitous. No one is unexposed, even in the womb. The same is true for most, if not all living organisms, especially those higher in ecological food chains and thus consuming foods in which the contaminants have become concentrated by bioaccumulation. Contamination is partly so widespread because of the global redistribution of pollutants transported through air and water. The inadvertent but pervasive inclusion of hormonally active compounds in consumer products such as many cosmetics and plastics also contributes.
Empirical confirmation
Second, effects of exposure can be observed at levels dramatically lower than those thought relevant to health a decade ago. Scientists are measuring the endocrine-disruption impacts of contaminants like arsenic, dioxin and bisphenol A (a basic component of polycarbonate plastic) in the low parts-per-billion. This was unmeasurable two decades ago (scientific instruments simply were not that accurate) and highly controversial until recent review and empirical confirmation.
Third, the findings indicate that virtually all chemical messaging systems are vulnerable, in principle, to message disruption. Work in this area focused for decades on interference with oestrogen. As the focus has expanded to other hormones, one or more disrupting contaminants have been discovered for every system studied carefully, including the thyroid system (crucial for brain development), the retinoid system (involved in very basic control of development), and the glucocorticoids (important for metabolism and tumour suppression, among other things). In the summer of 2001, new results reinforced this trend dramatically, with a report that the ecological symbiosis between leguminaceous plants like beans and the bacteria responsible for nitrogen fixation is vulnerable to disruption by contaminants.[2] This symbiosis, mediated by chemical communication between the plant and the bacteria, is a vital component of the global nitrogen cycle.
Fourth, the health effects of concern have expanded dramatically beyond those of the traditional focus for toxicology. Laboratory studies unequivocally demonstrate effects on disease resistance, cognitive function and fertility resulting from low-level exposures.
These findings should be of deep concern to people, organizations and agencies focused on human economic development and equity. It is clear, for example, that background levels of contamination can make children less resistant to infectious agents. Further research in this area may force a radical reassessment of the toll of contamination, as this implies that many deaths and diseases would have been avoided had contaminants not reduced resistance.
Similarly, the research suggests that widespread exposure to neurologically active contaminants as might occur, for example, in agricultural areas in the developing world with intensive pesticide use may lead to community-wide erosion of cognitive abilities. In a world in which information is a key economic currency, this contamination burden could consign those affected to the economic margins forever. \tab\b Conceptual shifts
These emerging trends are forcing toxicologists toward several conceptual shifts that will lead to fundamental changes in the ways that chemicals are managed. The most important of these involves a change in the way that toxicologists think about what is relevant to human health.
Traditional toxicology focuses on damage, such as cell death, mutations, cancer or genotoxicity. Message disruption can cause these, but the effects may also be of a very different, but equally important, nature. Most challenging to traditional toxicology, message disruption does not work by overwhelming the body's (or the cell's) defences. It works by hijacking the developmental process, adding to or subtracting from the body's own control mechanisms at remarkably low levels of exposure. By subtly (or blatantly) altering the path of development, message disruption leads the victim to a different future. The difference may be small, as in the loss of a few IQ points, or it may be large, as in a completely dysfunctional immune system.
Toxicology has focused traditionally on the impact of high levels of exposure on small numbers of people. This new approach requires considering widespread, low-level exposures experienced by many people -- exposure levels that many had come to write-off as "background" and, by implication, irrelevant.
Taken together, these new scientific findings add to growing pressure to change the basic rules of chemical regulation. Once again, we have been blind-sided. Our ability to synthesize chemicals got far ahead of our scientific understanding of their impacts.
Traditional risk assessment allowed them to be commercialized and distributed, causing pervasive contamination. Risk assessment's partner in developing protective standards, epidemiology, by definition works only after an epidemic. Even then, its tools are remarkably insensitive in studies of the effects of endocrine disruption, and strongly biased toward negative results even when there are real effects.
The answer, still imperfect, lies in implementing precautionary measures that impose far more stringent requirements on old and new products alike. As the Swedish Chemicals Policy Committee has recognized, certain attributes should be knock-out criteria.[3] Persistent bioaccumulative compounds, for example should be eliminated from use even without demonstrating toxicological risk. Endocrine-disrupting materials should be removed from consumer products and their environmental release should be phased out. More generally, the demonstration of potentially harmful biological impacts in laboratory studies should reverse the burden of proof in developing regulations from one in which harm must be demonstrated before a product is withdrawn, to an approach where safety is ensured beyond reasonable doubt before widespread deployment is allowed. These steps will help ensure that the benefits we all enjoy from modern chemistry do not come back to haunt us.
THE LATEST HORMONE SCIENCE, PT. 3
In this series we are asking whether mainstream scientists still believe that industrial chemicals released into the environment can interfere with hormones in wildlife and humans, causing widespread harm. The NEW YORK TIMES in August said most scientists don't. (See RACHEL'S #750, #751.) We have tried to answer the question by examining the most recent 24 monthly issues of ENVIRONMENTAL HEALTH PERSPECTIVES (EHP), a peer-reviewed journal published by the federal National Institutes of Health.
In RACHEL'S #751 we reported on seven studies linking hormone-disrupting chemicals to human illnesses. This week, we continue reporting on human studies, then turn to animal studies (wildlife and laboratory animals).
** Background (meaning "normal" or everyday) exposure of healthy Dutch pre-school children to PCBs and dioxins (potent hormone-disrupting chemicals) via breast feeding is related to a diminished number of immune system cells and increased middle ear infections, coughing, and chest congestion, persisting at least to the age of 42 months. Previously, immune system damage had been observed in laboratory animals exposed to PCBs and dioxins in their diet. (Dioxins are extremely toxic chemicals created as by-products of many industrial processes, such as incinerators, where chlorine combines with carbon at high temperatures. PCBs are dioxin-like industrial chemicals manufactured by Monsanto between 1929 and 1976 and now found almost everywhere on the planet.
An earlier study of Inuit children had found an increase in otitis media (ear infections) among those exposed to hormone-disrupting chlorinated chemicals through their mother's milk. The Inuit live in the extreme northern part of the planet, about as far away from industrial sources as anyone can get, but many organochlorine chemicals march steadily northward as time passes because cool weather "distills" them out of the atmosphere.
The authors of the Dutch study point out that the proper response to their findings would be to reduce the discharge of hormone-disrupting chemicals into the environment, not curtail breast feeding.
** A pilot study of 29 men in Massachusetts showed an association between levels of PCBs and DDE in their blood and reduced sperm count, reduced sperm motility (ability to move), and sperm shape. (DDE is a breakdown byproduct of the pesticide DDT.) Based on the findings of the pilot study, a larger study has begun.
In 1992, an analysis of 62 published studies reported that American men today produce only half as much sperm as their grandfather's did. In 1997, a re-analysis of the original 62 studies, using a different statistical technique, confirmed the finding -- 50% average sperm loss among U.S. and Eur\- opean/Australian men, 1938-1990, though no evident decline among non-Western males. Within the U.S., regional variations occur, but the average decline is 50% nationwide.
Now a third analysis has been published, which includes an additional 47 English-language studies, and extends the time-period slightly, from 1934 to 1996. The basic finding remains unchanged: a 50% reduction in sperm count among U.S. and European/Australian men but not among non-Western men.
** A new study shows that the common plasticizer, DEHP [Di(2-ethylhexyl) phthalate], blocks the normal action of male sex hormone (androgen) and disrupts the normal growth of penis, testicles, prostate, and semen tubes (seminal vesicles) in male rats. (A plasticizer is a chemical added to hard plastics, such as vinyl or PVC, to make them soft.) Furthermore, DEHP caused malformed penises and caused male rats to lose interest in female rats. The authors report that, at lower doses than were used in this study, DEHP diminished the size of rats' testicles. The authors conclude, "These results imply that the acceptable daily intake for DEHP is only 3 micrograms of DEHP per kilogram of body weight per day." They report that typical exposure to DEHP in the U.S. ranges from 4 micrograms to 30 micrograms per kilogram of body weight per day. Thus typical human exposures in the U.S. far exceed the level of DEHP thought to be safe. The authors also point out that DEHP may produce additive effects when combined with other chemicals that behave in a similar manner.
** Diesel exhaust is a complex mixture of hydrocarbons and metals. In young rats, exposure to diesel exhaust has been shown to reduce the levels of certain hormones in the blood and to diminish the production of sperm. A new study exposed 90 female rats (72 pregnant, 18 not pregnant) to diesel exhaust for 13 days (from day 7 to day 20 of pregnancy). In the offspring of the pregnant rats, the development of testicles, ovaries and the thymus gland (an important part of the immune system in mammals) was "delayed and disturbed," the authors say. They go on, "Our study provides evidence for the first time that inhalation of diesel exhaust during pregnancy masculinizes fetuses through accumulation of testosterone in mother rats." The authors wonder what effects diesel exhaust might have on the immune system in later life. Immune disorders such as asthma and diabetes are rapidly increasing in industrialized nations.
** Hypospadias is arrested development of the penis, and it occurs in about 1 out of every 125 live male births in the U.S. With hypospadias, the normal opening of the penis occurs not at the tip but on the underside, sometimes as far back as the scrotum. In the most extreme cases, hypospadias can make it difficult to tell whether a newborn is a boy or a girl. The problem can only be corrected surgically. The cause of hypospadias is unknown.
The important discovery in 1995, that some environmental chemicals act as anti-androgens,[1] meaning they disrupt the normal function of male sex hormones, has led researchers to ask whether environmental anti-androgens may contribute to the occurrence of hypospadias.
Four pesticides (or pesticide breakdown byproducts) are now classified as anti-androgens: DDE (a breakdown byproduct of DDT), Vinclozolin, Procymidone, and Linuron. In addition, two phthalates, widely used in plastics and personal care products -- DBP [dibutyl phthalate] and DEHP [Di(2-ethylhexyl) phthalate] -- are anti-androgens. And dioxin and PCBs have anti-androgenic properties. These eight chemicals have all been shown to cause hypospadias in laboratory animals.
Hypospadias and other genital abnormalities were recently reported in mink and river otters on the Columbia River, and among populations of black bears and polar bears. With the exception of the black bears, which were not monitored for chemicals, all the abnormal animals had elevated levels of organochlorine chemicals in their bodies.
** Although chlorinated chemical discharges from pulp (paper) mills have decreased substantially during the past decade with the adoption of nonchlorine bleaching systems (especially outside the U.S.), harmful effects on fish downstream are still regularly observed, including depression of hormone levels in blood, delayed maturation, smaller gonad size, and confusion of sexual characteristics -- for example, females developing an elongated anal fin that is characteristic of males. This study took advantage of a "natural experiment\rdblquote -- a pulp mill closed for a period of time, then started up again. Researchers examined the ratio of male to female eels hatched in waters below pulp mills that were operating, then when the mills closed temporarily. While the mill was operating, the sex ratio was significantly altered (only 42% males instead of the usual 50%) but returned to normal when the mill temporarily closed.
** The salmon populations of the northwestern U.S. have been declining for decades, some to the point where they have already gone extinct; others are listed as endangered. This study examined female salmon on the Hanford Reach of the Columbia River and found that an astonishing 84% of them had a genetic marker that is normally only found in male salmon. The long-term effect of this sex reversal would be to reduce the number of females in each successive generation, eventually driving the species to extinction. The researchers do not know what has caused the sex shift in such a large proportion of wild salmon on the Columbia River. They point out that some pesticides (atrazine, carbofuran, lindane, methyl parathion, and dieldrin) are known to behave like estrogen in rainbow trout and are present in the Columbia River, though at levels considered too low to create this problem. Thus the mystery remains unsolved.
** Among male tadpoles exposed to dibutyl phthalate (DBP) at low levels, about 7% of the males developed ovaries, thus confirming previous studies showing that DBP is a hormone disrupter. DBP is widely used in PVC pipe. The authors conclude that DBP is "an environmentally dangerous hormone" that disrupts the development of testicles in male animals. EHP Vol. 108, No. 12 (December 2000), pgs. 1189-1193.
** A survey of bullfrogs and green frogs in New Hampshire found deformed frogs at 13 of 16 sites that were checked. Examination of hormone levels in deformed and normal frogs revealed that normal frogs have 3 times as much male sex hormone (androgen) in their blood, compared to the deformed frogs. Normal frogs also had three times as much of a hormone called gonadotropin-releasing hormone (GnRH) which is produced by the brain. This study suggests that hormone-disrupting chemicals may be one of multiple causes that are producing malformed frogs, and declines in frog populations, at many locations around the world. EHP Vol. 108, No. 11 (November 2000), pgs. 1085-1090.
From this brief examination of one peer-reviewed journal over the past two years, the conclusion seems inescapable that industrial chemicals in the environment can and do interfere with the hormones of wildlife and humans, causing widespread harm. Furthermore, it is clear that large numbers of scientists agree that this is so because they are spending their lives researching these problems instead of pursuing more lucrative opportunities. Unfortunately, the full extent of these problems remains unknown, and unknowable, for practical reasons that will become clear.
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