Rachel's Democracy & Health News #879
Thursday, November 2, 2006
From: Rachel's Democracy & Health News #879 ..........[This story printer-friendly]
November 2, 2006
WHAT GUIDES OUR WORK?
[Rachel's introduction: What are we doing and why are we doing it? Are we succeeding?]
By Peter Montague
Occasionally a reader will ask, "What guides your selection of stories for Rachel's News?" In this short series, we'll provide an answer.
Basically, the question is, What are we doing and why are we doing it? Are we succeeding?
Here at Rachel's News we hold a fundamentally conservative view of our role: this world came to us as gift from our forebears and we have an obligation to pass it along undiminished and undamaged.
Simple ideas guide our work
Our work springs from a simple, universal ethic -- every culture and every religion endorses the Golden Rule [1,2], which says, "Treat others the way you want to be treated." This tells us, first, to alleviate suffering. This, in turn, leads directly to human rights -- we all have a basic right to a life free of suffering, to the extent possible. The elements of such a life were laid out in the Universal Declaration of Human Rights, which the U.S. endorsed Dec. 10, 1948.
For us, the Golden Rule and the Universal Declaration together define justice. Justice is that which tends to manifest the Golden Rule and the Universal Declaration; injustice tends to manifest the opposite. It is unjust -- unfair and therefore unacceptable -- to impose suffering on others or to stand by and allow suffering to go unnoticed or unchecked. It is unjust -- unfair and unacceptable -- to deprive anyone of any human right as spelled out in 1948.
In recent years, science has confirmed what people have always known: human community is essential for human well-being. We humans evolved as social creatures[3,4] who cannot thrive when separated from our circle of family, friends, acquaintances, and animal companions. Social isolation makes us sick and leads to an early death. This is one reason why racism and white privilege are profoundly wrong. At a minimum, they create social isolation, which leads to illness and suffering, and so they are unjust and unacceptable.
Furthermore, when we damage nature we diminish our own -- and everyone's -- possibilities for a life as free as possible of suffering. When we create havoc via global warming or damage to the Earth's protective ozone layer, or when we pave over fertile farmland, or exterminate the fish of the sea or the birds of the air, we diminish everyone's possibilities for securing life, liberty and the pursuit of happiness (to quote the Declaration of Independence of 1776). To us, this is unjust and unacceptable.
Our dependence of all creatures
Science now confirms the wisdom of indigenous peoples, that we are all interdependent, all humans, all species. We humans are part of, and are supported by, a biological platform of enormous complexity, which we cannot understand, but which we know with absolute certainty nourishes and sustains us. Even a child can see that, without it. we are lost.
Because human rights and justice cannot be secured if our biological platform is shredded, we all have a right to intact natural and social environments -- environments that enable us to provide for ourselves the essentials of air, water, food, shelter and community (the basic prerequisites for "happiness"), which we all require to prevent suffering.
Furthermore, as Jeremy Bentham articulated in 1789, animals too have a right to live a life free of suffering to the extent possible. As Bentham said, the question is not whether they can reason, or whether they can talk. Their right to live free from torment hinges on the question, can they suffer? Their suffering stands on a moral plane with ours.
Because the biological platform, upon which we all depend, cannot be secured unless we are free to take action to protect it, human rights and justice are essential requirements for human survival.
The earth is our home and we have to take care of it, for the reason that we absolutely depend on it. To preserve our home without understanding all its billions of inter-related parts, we can aim to preserve every part of it. No part of creation can be presumed dispensable. We can say we know what's dispensable, but what if we're wrong? In recent years we came close to making the surface of the earth uninhabitable for humans because we failed to understand how DuPont's CFC chemicals were damaging the ozone layer. It was a close call. Our ignorance is vast. As Albert Einstein reportedly said, "We still do not know one-thousandth of one percent of what nature has revealed to us."
When flying blind, go cautiously
Whenever we set out to do anything that might harm any part of our home, we can move slowly, move cautiously, as we would when flying blind. Like any good pilot, we can constantly check for signs of trouble, and when any such signs are observed, we can take action to prevent further trouble. This is common sense and ancient wisdom. Look before you leap. A stitch in time saves nine. Prevention is better than cure, Erasmus told us.
We are all in this boat together and none of us has the right to endanger the ship. To do so is a deep and intolerable injustice to all.
Purpose of Government
From these principles, we understand the purpose of government. For example, the Declaration of Independence of 1776 tells us,
"We hold these truths to be self-evident, that all men are created equal, that they are endowed by their Creator with certain unalienable Rights, that among these are Life, Liberty and the pursuit of Happiness. That to secure these rights, Governments are instituted among Men, deriving their just powers from the consent of the governed..."
The purpose of government, then, is to secure human rights, including the right to enjoy intact natural and social environments without which we cannot have life, liberty or the pursuit of happiness. Put another way, the purpose of government is to protect and secure the things that we all depend upon and share in common, the air, water, soil, human language and accumulated knowledge, the genome, public health, reciprocal relationships of trust, and much more.
And finally any government becomes illegitimate when it fails to gain the consent of the governed. People have an inherent, unalienable right to participate in the decisions that affect their lives.
These, then, are the basic, conservative ideas that guide our choice of stories for Rachel's news. Now the plot thickens. More next time.
 As CrossRoadsMinistry.org says, racism is one group's individual race prejudice enforced by the misuse of power via systems and institutions.
 A shorthand version of the Universal Declaration is Franklin Roosevelt's "four freedoms," which he described this way: "In the future days which we seek to make secure, we look forward to a world founded upon four essential human freedoms. The first is freedom of speech and expression -- everywhere in the world. The second is freedom of every person to worship God in his own way -- everywhere in the world. The third is freedom from want, which, translated into world terms, means economic understandings which will secure to every nation a healthy peacetime life for its inhabitants -- everywhere in the world. The fourth is freedom from fear, which, translated into world terms, means a world-wide reduction of armaments to such a point and in such a thorough fashion that no nation will be in a position to commit an act of physical aggression against any neighbor -- anywhere in the world. That is no vision of a distant millennium, it is a definite basis for a world attainable in our own time and generation. That kind of world is the very antithesis of the so called 'new order' of tyranny which the dictators seek to create with the crash of a bomb. To that new order we oppose the greater conception -- the moral order. A good society is able to face schemes of world domination and foreign revolutions alike without fear.... Freedom means the supremacy of human rights everywhere. Our support goes to those who struggle to gain those rights and keep them."
 Einstein quoted in The Sun (June 2006), pg. 48.
From: Reuters Health ......................................[This story printer-friendly]
August 15, 2006
HARMFUL CHEMICALS MAY LEACH FROM SEPTIC SYSTEMS
[Rachel's introduction: Septic systems do not effectively remove hormone-disrupting chemicals, which can leach into groundwater.]
By Megan Rauscher
NEW YORK (Reuters Health) -- Septic systems may not remove natural hormone-disrupting chemicals -- like estrogen excreted in women's urine -- from wastewater before it gets into groundwater, which feeds many drinking water supplies, according to tests conducted in Cape Cod, Massachusetts.
In Cape Cod, more than 85 percent of residential and commercial properties use septic systems.
In a telephone interview, Dr. Chris Swartz said: "We did find both natural estrogen and alkyl phenols from detergents entering groundwater at concentrations very similar to concentrations that have been documented in the literature to show adverse reproductive effects in fish swimming in rivers downstream of wastewater treatment discharges."
Other chemicals detected in groundwater near the tested septic system include caffeine and detergent brightening compounds.
Swartz, senior scientist at the Silent Spring Institute in Newton, Massachusetts, said there is still "hot debate" in the Environmental Protection Agency and among scientists in general as to whether the concentrations of these and other chemicals that are being found in the environment have human health implications.
"The biggest concern is for prenatal exposures, because fetuses are exquisitely sensitive to any type of hormonal imbalances during their development," he explained.
Swartz hopes publication of his team's findings in the August 15 issue of Environmental Science and Technology will fuel dialogue among land use planners and policy makers about what septic systems are and are not removing.
"It's important to understand this if we are going to rely on septic systems," said Swartz.
Currently about 25 percent of US households and probably a larger amount globally, Swartz noted, use on-site septic systems for household waste treatment as opposed to public sewage treatment plants.
"And there is a US and global trend toward decentralized wastewater treatment," Swartz said.
Prior research on septic systems have dealt only with nutrients such as nitrogen and phosphorus that may leach from septic tanks, get into groundwater, and eventually make it to surface body waters that the groundwater feeds.
The current tests, Swartz said, clearly show that other chemicals, like natural estrogens, known to interfere with human hormonal regulation, are also getting away from septic system treatment. Future studies, he concludes, are needed to determine the extent and potential effects of drinking water contamination with hormone- disrupting chemicals and other potentially harmful chemicals.
SOURCE: Environmental and Science Technology August 15, 2006.
Copyright 1995-2006 Medicine Online Inc.
From: American Association for Cancer Research ............[This story printer-friendly]
June 1, 2005
ENVIRONMENTAL EXPOSURE TO TRAFFIC PAHS AND RISK OF BREAST CANCER
Peter Rogerson, Dominica Vito, Paola Muti, Maurizio Trevisan and Jo
[Rachel's introduction: A study links breast cancer to pollutants from automobile traffic, specifically polycyclic aromatic hydrocarbons (PAHs).]
By Jing Nie, Jan Beyea, Matthew Bonner, Daikwon Han, John Vena,
Peter Rogerson, Dominica Vito, Paola Muti, Maurizio Trevisan and Jo Freudenheim
Polycyclic aromatic hydrocarbons (PAHs) are an important component of air pollution and potential human carcinogens. While they have been shown to cause mammary cancer in animal studies, the association between PAH exposure and breast cancer risk is not well understood.
Traffic emissions are one of the major sources of PAH exposure in cities. Further, growing evidence suggests that there may be critical time periods of exposure in breast cancer initiation and development.
In this study, we examined the association between breast cancer risk and exposure to PAHs from traffic emissions estimated for each woman at menarche, at the time when she had her first pregnancy and birth, and at 20 and 10 years prior to interview, using data collected from the Western New York Exposures and Breast Cancer (WEB) study, a population based case control study in western New York.
All participants were women, aged 35-79, residents of Erie and Niagara Counties. Cases had incident, primary, histologically-confirmed breast cancer. Controls were randomly selected and frequency-matched to cases on age, race and county. In-person interviews were used to collect data on potential breast cancer risk factors including self-reported lifetime residential history. Traffic volumes on roads were obtained from historical records for the years from 1960-2002. Tailpipe emission data were based on previous reports, including measurements carried out in tunnels or on individual vehicles run in place on test beds.
A geographic model, developed by Dr. Beyea and colleagues from the Long Island Breast Cancer project, was used to reconstruct historical traffic PAHs, using BaP as a surrogate for total PAH exposure. Cruise emissions, cold engine emissions and intersection emissions were used to estimate total traffic PAH emissions.
Meteorological information was also utilized in the geographic dispersion model to assign PAH exposure at each residence. The model was validated using data collected from both Long Island and our study area.
We found evidence that higher exposure to traffic PAH emissions at menarche was associated with increased risk of premenopausal breast cancer (OR 2.07, 95% CI 0.91-4.72, p for trend 0.03) and emissions at the time of a woman's first birth was associated with postmenopausal breast cancer (OR 2.58, 95% CI 1.15-5.83, p for trend 0.19).
Both associations were limited to lifetime non-smokers. There was no association of traffic emissions with risk for any of the other time periods.
These findings provide evidence for both the potential importance of early exposures and the potential importance of an environmental agent in risk of breast cancer.
Copyright 2005 by the American Association for Cancer Research.
From: Environmental Health Perspectives ...................[This story printer-friendly]
November 1, 2006
FERTILE GROUNDS FOR INQUIRY
[Rachel's introduction: Are chemicals interfering with human reproduction? Approximately 12% of American couples experienced impaired fecundity in 2002. This is a 20% increase from the 6.1 million couples who reported an inability to have children in 1995.]
By Julia R. Barrett
In a world whose population exceeds 6.5 billion, declining human fertility might not seem to be a critical problem. After all, overpopulation has been a global concern for decades. Declining fertility rates in more advanced nations largely reflect the changing role of women and their rapidly growing presence in the workplace -- fertility declines may stem at least in part from the modern tendency to delay childbearing until later in life, when fertility naturally declines.
But this doesn't explain the fact that, according to a December 2005 report of the CDC's National Survey on Family Growth (NSFG), the fastest-growing segment of U.S. women with impaired fecundity (the capacity to conceive and carry a child to term) is those under 25. The rising incidence of fertility-impairing health factors such as obesity also likely plays animportant role. Clues from environmental exposure assessments, wildlife studies, and animal and human studies hint at additional factors: exposure to low-level environmental contaminants such as phthalates, polychlorinated biphenyls (PCBs), dioxins, pesticides, and other chemicals may be subtly undermining our ability to reproduce.
As recognized by the American Society of Reproductive Medicine, infertility is a biological disease that impairs a couple's ability to achieve a viable pregnancy. It can be caused by hormonal, ovarian, uterine, urological, and other medical factors. Known risk factors include advanced age, being over- or underweight, lack of exercise, smoking, alcohol and substance abuse, sexually transmitted diseases, and poor nutrition.
According to the American Society of Reproductive Medicine, a medical infertility cause can be identified, or perhaps only indefinitely suggested, in approximately 90% of cases and may be multifactorial in 25% of cases. Male factors include low sperm count and sperm abnormalities, such as altered morphology and low motility. Female factors stem from ovulation problems such as premature ovarian failure (early menopause), thyroid irregularities, polycystic ovarian syndrome, and fallopian tube obstruction.
Up to 10% of infertility cannot be explained medically. Fertility transcends the reproductive system, notes Louis Guillette, a professor of zoology at the University of Florida in Gainesville. "When you talk about infertility, you literally are talking about probably almost every system in the body -- infertility is an integrated signal of all these different systems," he explains. "Trying to tease out which system, or more than likely what multiple systems have been altered, leading to that phenomenon, is very tough work."
Infertility is generally defined as occurring when a couple cannot become pregnant after trying to conceive for at least one year (or six months if the woman is over age 35). According to the 2001 WHO report Current Practices and Controversies in Assisted Reproduction, at least 80 million people worldwide are estimated to be affected by infertility. Infertility rates range from less than 5% to greater than 30% depending on location and how infertility is defined, with higher rates associated with lack of medical care access. Based on the 2005 NSFG report, approximately 12% of American couples experienced impaired fecundity in 2002. This is a 20% increase from the 6.1 million couples who reported an inability to have children in 1995.
Her side. Female factors in infertility stem from ovulation problems, thyroid irregularities, polycystic ovarian syndrome, and fallopian tube obstruction. A trend among women to delay starting a family also has impacted fertility rates. image: Sebastian Kaulitzki/Shutterstock
Determining whether infertility is actually increasing is more complicated than these numbers imply, however. In a paper published in the September 2006 issue of Fertility and Sterility, David Guzick and Shanna Swan of the University of Rochester School of Medicine and Dentistry noted that "impaired fecundity" as defined by the NSFG implies a decrease in fertility, but the same study also showed that fertility, defined there as a married woman unable to become pregnant within 12 months, has increased.
The absence of definitive information can frustrate couples experiencing fertility problems as well as experts. "There seems to be more to it than can be explained from traditional understanding about impacts," says Joseph Isaacs, president and CEO of RESOLVE: The National Infertility Association. "As a patient advocacy group, we believe more research into environmental impacts is needed. We fear that future generations may be at risk because of exposures to toxic substances as early as in utero."
Foundations of Fertility
A person's reproductive potential begins shortly after his or her own conception. Based on the embryo's chromosomal inheritance, hormonal signals are created to direct the structure and function of the reproductive tract. Normal development depends upon a correct balance of androgen and estrogen signals being delivered at appropriate times.
Fetal development can be altered by external factors as demonstrated by the human experience with the synthetic estrogen diethylstilbestrol (DES), prescribed to prevent miscarriage between 1947 and 1971. The drug didn't affect mothers, and it didn't lower miscarriage incidence; in fact, it significantly increased it. It also induced changes in the developing reproductive tract of female offspring.
In the 15 April 1971 issue of the New England Journal of Medicine, it was reported that daughters with prenatal DES exposure had significantly increased incidence of vaginal cancer, which is normally quite rare and was virtually unknown in young women prior to DES. Later research revealed structural abnormalities of these women's reproductive tracts and effects in their male offspring including increased risk of cryptorchidism (undescended testes) and low sperm counts.
The study of endocrine disruptors has raised concerns about the reproductive effects of exposure to certain environmental compounds that affect the endocrine system via estrogenic, androgenic, antiandrogenic, and antithyroid mechanisms. One key report was a 12 September 1992 review in the British Medical Journal indicating significant declines in sperm counts in many countries between 1938 and 1990. The findings were controversial because the reviewed studies used inconsistent designs and methods. In November 1997, however, a review published in EHP by Swan and others confirmed the findings for males in the United States and indicated an even sharper decline among European men. Other studies have found declines for specific areas or no decline at all.
"I think the evidence across studies is mixed," says Russ Hauser, an associate professor of environmental and occupational epidemiology at Harvard School of Public Health. "Historical studies were not designed to explore this question. It wasn't that someone set out forty or fifty years ago to design a study to look at how semen quality is going to change over time." There are going to be limitations in the data because of that, he explains, so it's hard to determine whether there is a true temporal trend. "However," he adds, "the data suggest there are definite geographical differences between countries and regions within countries in semen quality."
According to Niels Skakkebaek of Rigshospitalet in Copenhagen and colleagues writing in the February 2006 issue of the International Journal of Andrology, comparisons of sperm quality among populations of European men have revealed that as many as 30% of young Danish men have low sperm count, and an additional 10% may be infertile. Denmark also has an unusually high rate of testicular cancer. Rates have been increasing in many countries over the last 50 years, but the Danish rate is noticeably higher; for example, four to five times higher than the Finnish rate.
This difference prompted researchers to also examine incidence of hypospadias (in which the urethra opens along the underside of the penis shaft rather than the tip) and cryptorchidism. Not only did both disorders occur more frequently in Danish boys compared with Finnish boys, but the Danish rates had risen in recent decades. These findings as a whole inspired Skakkebaek and colleagues to propose, in the May 2001 issue of Human Reproduction, an overarching disorder, testicular dysgenesis syndrome (TDS), in which perturbation of testis development in fetal life sets the stage for hypospadias, cryptorchidism, testicular cancer, and reduced sperm quality.
It's reasonable to suspect there might be a female corollary to TDS. "We have no really good reasons not to expect that women are as sensitive to environmental chemicals as the males are," says Jens Peter Bonde, a professor of occupational medicine at Arhus University Hospital in Copenhagen. He points out that it's easier to study male fertility because men can easily provide sperm samples. "That's one basic reason that there has been so much attention on the males, but from a biological point of view one would definitely expect that the female reproductive system might be vulnerable also," says Bonde.
According to Guillette, another stumbling block is the accepted, but unproven, dogma that an embryo will develop as a normal female barring any hormonal signals to become male. "It hasn't been an area where there have been substantial amounts of work done. There's certainly very good work, but not the same kind of huge body of literature that one sees about the developing testis and the male reproductive system," he says.
His side. Male infertility can arise from factors such as low sperm count and sperm abnormalities including altered morphology and low motility. Up to 10% of infertility cannot be explained medically. image: Christian Darkin/Shutterstock
One of the few epidemiologic studies to link low-level human exposure to an environmental contaminant with a specific end point was Swan and colleagues' investigation of prenatal phthalate exposure, published in the August 2005 issue of EHP. Their results suggested a subtle change in boys' development -- a shortening of the anogenital index (the distance between the anus and the scrotum, divided by weight) -- associated with prenatal exposure to several phthalates. This finding is not a predictor of future fertility and needs confirmation, but it is noteworthy as the first study to link verified prenatal exposure to a specific outcome.
Animal Findings to Human Concerns?
Consequences of disrupting the normal hormone milieu have also been observed in wildlife. Examining alligators in polluted lakes in northern Florida, Guillette's group has observed altered function of the ovaries and testes, smaller penis size, and abnormalities that extend to the thyroid gland, liver, and immune system. A robust body of literature details reproductive effects in fish, amphibians, and reptiles related to their exposure to endocrine disruptors. Evidence of these effects has also been seen in wild mammals such as polar bears and seals. Laboratory animal experiments have confirmed these wildlife findings, demonstrating that effects are not necessarily from steroid receptor disruption, however, but may, for example, be observed in altered synthesis and control of endogenous hormones.
The study of fertility also encompasses pregnancy, especially the early weeks following fertilization. Early pregnancy loss is normally quite high in humans, with an estimated 30% of pregnancies ending in miscarriage in the first six weeks. A frequent cause of miscarriage is aneuploidy, an incorrect number of chromosomes in the embryo, and mouse studies have shed some light on potential environmental contributors to this condition.
During a 1998 investigation of age-related aneuploidy rate increases, Patricia Hunt, a professor of molecular biosciences and a reproductive biologist at Washington State University, and her colleagues were amazed to see a sudden rate spike in their mouse colony. An investigation revealed correlation between damage to the plastic mouse cages and the chromosomal abnormality. Further scrutiny implicated bisphenol A (BPA), a suspected environmental estrogen used in plastics manufacture, as the potential causal agent. In a study published in the 1 April 2003 issue of Current Biology, the researchers replicated exposure experimentally and found that BPA derailed proper chromosome segregation during oocyte meiosis.
An extension of this research has been completed with amazing -- but not yet published -- results, and Hunt hopes that the line of inquiry can be extended to humans. "One of the things that my new research on BPA has made me wonder is whether or not there could be environmental effects that would change the frequency or in specific populations might cause noticeable differences in aneuploidy," she says.
Hunt says it's hard to know precise numbers of human aneuploidy cases. "We can't see the loss that occurs preimplantation, but we make an assumption that there's quite a bit, based on what we can see and what we think must happen," she says. But whether there's been an increase in aneuploidy over time cannot be known. "Human aneuploidy studies were done mostly in the 1970s and early 1980s," says Hunt. "Is this aneuploidy rate the same across all populations? To the best of our knowledge, it has been, at least in those previous studies. But is the rate the same as it was then? We wouldn't know. We wouldn't be able to see a dramatic increase in chromosomally abnormal spontaneous abortions, because those kinds of studies aren't currently under way."
The wild side. Animal and wildlife studies of reproductive health effects, including mouse aneuploidy data, may help inform knowledge of human effects. Although the reproductive system is highly conserved across species, differences in exposure, metabolism, and anatomy make direct interspecies comparisons impossible. image: Getty Images
Extending animal studies to human health is a challenge, though. Genetically, the reproductive system is highly conserved across species, making it likely that responses to inputs would be similar. But species differences in exposure, metabolism, and anatomy preclude making a direct comparison.
"Wildlife studies cannot be related to humans one to one," says Guillette. "If one's looking at the functioning of the ovary, or the functioning of the brain, and hormones, and even the genes that seem to be involved with the proliferation or the growth of the uterus or the development of an egg, for example, they're incredibly conserved." He explains that if problems are seen in these animals at a certain level, and researchers are able to identify mechanisms that are being disturbed leading to those abnormalities, then that raises possible concerns for humans, even if humans are exposed in a slightly different manner.
Geographic differences may suggest environmental exposures that need investigation, wrote Swan in a paper published in the February 2006 issue of Seminars in Reproductive Medicine. For example, in the first phase of the EPA-funded Study for Future Families, of' which Swan is the principal investigator, she and her colleagues saw significant reductions in sperm concentration, motility, and total motile sperm in men from Columbia, Missouri, compared with men in New York City, Minneapolis, and Los Angeles. In an in-depth follow-up study comparing variables between the Columbia and Minneapolis men, the researcher discovered that the Missouri group had had higher exposure to agricultural pesticides. Further, men with low sperm counts were more likely to have higher urine metabolite levels of the pesticides alachlor, atrazine, metolachlor, and diazinon.
Another geographically based study, INUENDO, investigates risks to human fertility from persistent environmental organochlorines. The European Commission project centers on Arctic populations including Swedish fishermen and the Inuit of North America and Greenland, whose exposure to persistent organic pollutants such as PCBs and DDT metabolites are among the highest in the world. "There are many indications from animal studies and from wildlife studies, but very few indications from human studies telling us whether we have a problem or not," says Bonde, who serves as coordinator of INUENDO.
"The basic idea [behind INUENDO] was to go to places in the world where we know that people have high level of exposures to substances that are suspected to cause these effects in fertility," says Bonde. "That's the reason we went to Greenland and to Sweden, where fishermen are known to have very high exposure levels; we have other populations that have lower levels of exposures, so we have contrasts of exposure." Results published in March 2006 in Human Reproduction suggested a longer time to pregnancy related to serum concentrations of PCB and DDE in mothers and fathers. Additional results published in the May 2006 EHP suggested an altered sex ratio of offspring (fewer boys than would otherwise be expected) related to PCB and DDE exposures.
Exploring multicompound exposures is yet another challenge in environmental epidemiology. "Individuals are exposed to many different phthalates, a variety of persistent and nonpersistent pesticides, different patterns of PCB congeners, as well as other chemicals," says Hauser. "How do we take all that information, based on the chemical assessment in urine or in blood, and use that to assign exposure for that individual to ten, or twelve, or many more different compounds?" he says. In the April 2005 issue of EHP, Hauser's group described evidence suggesting a relationship between PCBs and phthalates and human sperm motility, possibly due to PCBs' inhibiting a key enzyme in phthalate metabolism.
Genes themselves offer another platform for investigation. Hugh Taylor, director of the Yale Center for Research in Reproductive Biology, leads a team investigating the role of estrogen-regulated Hox genes that direct uterine development. The researchers initially focused on DES effects and discovered that the compound alters expression of the Hoxa10 gene in mice, affecting the tissue type that grows in the uterus, cervix, and vagina. Effects were triggered only with exposure during development, but not during adulthood, and later experiments revealed that the pesticide methoxychlor had similar effects.
"The important thing is that these agents really seem to imprint the expression pattern, even long after the agent is removed or there's no longer an exposure," says Taylor. "When we have a clear-cut animal model and know the genes that are affected, we can start to think about evaluating that exposure by looking for changes in the gene expression earlier and see if it has a significant effect rather than waiting a whole generation."
A view inside. Understanding that a person's reproductive health can be linked to the very earliest of exposures, possibly even paternal or maternal exposures prior to conception, points up the critical need to elucidate the health effects of environmental chemicals. image: geopaul/iStockphoto
This is a goal of research in epigenetics, the study of how genetic messages may be edited through methylation or other means without changing the actual DNA sequence. For example, Rebecca Sokol and colleagues at the University of Southern California are currently investigating whether DNA methylation in sperm might serve as a biomarker of environmental exposure and a means of assessing male fertility. Additionally, preliminary work at Washington State University and at the NIEHS indicates that an epigenetic event in one generation can "reprogram" the germline and affect later generations. In essence, the exposures of one's great-grandparents could still matter today.
Previous generations' exposures would be useful information to have, according to Hunt. "What we really need is data on generations ago, and we simply don't have that data," she says. "We have to wait a generation to see. We have to wait until... young exposed males grow up to the point where we can assess sperm counts."
This will require prospective studies to determine early exposures. "If you want to look at fertility -- and it's difficult to do -- you ideally would want to do a study in which you start assessing environmental exposures preconception," says Hauser. "You'd have to identify couples who are thinking of trying to conceive and try to understand their environmental exposures, and then follow them forward in time."
According to Alison Carlson, a senior fellow at The Collaborative on Health and the Environment (CHE) in Bolinas, California, another need is very basic: tracking the incidences of infertility and common known causes. "For us to try to make headway studying environmental influences on fertility, it's really hard when we don't have good baseline data," she says. "We don't know the real incidence and prevalence rates of premature ovarian failure and polycystic ovarian syndrome and lots of other end points that people study. We don't know what they are, so how can we study trends and the environmental contributions?" she asks.
A thorough exploration of environmental effects on fertility will require the expertise of demographers, epidemiologists, clinicians, biologists, wildlife researchers, geneticists, molecular biologists, exposure assessment specialists, toxicologists, and others -- and discussion requires someone "to set the table," says Carlson. A February 2005 workshop titled "Understanding Environmental Contaminants and Human Fertility Compromise: Science and Strategy" demonstrated multidisciplinary fervor for investigation, and a more in-depth conference, the "Summit on Environmental Challenges to Reproductive Health and Fertility," cosponsored by CHE and the University of California, San Francisco, is scheduled for 28-30 January 2007. "Reproduction is such a human, deep-seated, deeply psychically coded thing," says Carlson. "It's hard not to care about fertility compromise."
From: Tolerance.org .......................................[This story printer-friendly]
March 6, 2003
WHITE PRIVILEGE: SWIMMING IN RACIAL PREFERENCE
[Rachel's introduction: Without meaning to offend anyone, it seems like a good idea to unpack the true history of the U.S. Our institutions were created by Europeans who viewed it as their sacred obligation to dominate the "lesser races," meaning all non-whites. As a result, white people today enjoy unearned privilege and power that they may not even recognize.]
By Tim Wise
Ask a fish what water is and you'll get no answer.
Even if fish were capable of speech, they would likely have no explanation for the element they swim in every minute of every day of their lives. Water simply is. Fish take it for granted.
So too with this thing we hear so much about, "racial preference." While many whites seem to think the notion originated with affirmative action programs, intended to expand opportunities for historically marginalized people of color, racial preference actually has had a long and very white history.
Affirmative action for whites was embodied in the abolition of European indentured servitude, which left black (and occasionally indigenous) slaves as the only unfree labor in the colonies that would become the U.S.
Affirmative action for whites was the essence of the 1790 Naturalization Act, which allowed virtually any European immigrant to become a full citizen, even while blacks, Asians and American Indians could not.
Affirmative action for whites was the guiding principle of segregation, Asian exclusion laws, and the theft of half of Mexico for the fulfillment of Manifest Destiny.
In recent history, affirmative action for whites motivated racially restrictive housing policies that helped 15 million white families procure homes with FHA loans from the 1930s to the '60s, while people of color were mostly excluded from the same programs.
In other words, it is hardly an exaggeration to say that white America is the biggest collective recipient of racial preference in the history of the cosmos. It has skewed our laws, shaped our public policy and helped create the glaring inequalities with which we still live.
Income and inheritance
White families, on average, have a net worth that is 11 times the net worth of black families, according to a recent study; and this gap remains substantial even when only comparing families of like size, composition, education and income status.
A full-time black male worker in 2003 makes less in real dollar terms than similar white men were earning in 1967. Such realities are not merely indicative of the disadvantages faced by blacks, but indeed are evidence of the preferences afforded whites -- a demarcation of privilege that is the necessary flipside of discrimination.
Indeed, the value of preferences to whites over the years is so enormous that the current baby-boomer generation of whites is currently in the process of inheriting between $7 trillion and $10 trillion in assets from their parents and grandparents -- property handed down by those who were able to accumulate assets at a time when people of color by and large could not.
To place this in the proper perspective, we should note that this amount of money is more than all the outstanding mortgage debt, all the credit card debt, all the savings account assets, all the money in IRAs and 401k retirement plans, all the annual profits for U.S. manufacturers, and our entire merchandise trade deficit combined.
Yet few whites have ever thought of our position as resulting from racial preferences. Indeed, we pride ourselves on our hard work and ambition, as if somehow we invented the concepts.
As if we have worked harder than the folks who were forced to pick cotton and build levies for free; harder than the Latino immigrants who spend 10 hours a day in fields picking strawberries or tomatoes; harder than the (mostly) women of color who clean hotel rooms or change bedpans in hospitals, or the (mostly) men of color who collect our garbage.
We strike the pose of self-sufficiency while ignoring the advantages we have been afforded in every realm of activity: housing, education, employment, criminal justice, politics, banking and business.
We ignore the fact that at almost every turn, our hard work has been met with access to an opportunity structure denied to millions of others. Privilege, to us, is like water to the fish: invisible precisely because we cannot imagine life without it.
The point of points
It is that context that best explains the duplicity of President Bush's recent criticisms of affirmative action at the University of Michigan.
President Bush, himself a lifelong recipient of affirmative action -- the kind set aside for the mediocre rich -- recently proclaimed that the school's policies were examples of unfair racial preference.
Yet in doing so he not only showed a profound ignorance of the Michigan policy but also made clear the inability of yet another white person to grasp the magnitude of white privilege still in operation.
The President attacked Michigan's policy of awarding 20 points (on a 150-point evaluation scale) to undergraduate applicants who are members of underrepresented minorities (which at U of M means blacks, Latinos and American Indians). To many whites such a "preference" is blatantly discriminatory.
Bush failed to mention that greater numbers of points are awarded for other things that amount to preferences for whites to the exclusion of people of color.
For example, Michigan awards 20 points to any student from a low- income background, regardless of race. Since these points cannot be combined with those for minority status (in other words poor blacks don't get 40 points), in effect this is a preference for poor whites.
Then Michigan awards 16 points to students who hail from the Upper Peninsula of the state: a rural, largely isolated and almost completely white area.
Of course both preferences are fair, based as they are on the recognition that economic status and even geography (as with race) can have a profound effect on the quality of K-12 schooling that one receives, and that no one should be punished for things that are beyond their control.
But note that such preferences -- though disproportionately awarded to whites -- remain uncriticized, while preferences for people of color become the target for reactionary anger. Once again, white preference remains hidden because it is more subtle, more ingrained and isn't called white preference, even if that's the effect.
But that's not all. Ten points are awarded to students who attended top-notch high schools, and another eight points are given to students who took an especially demanding AP and honors curriculum.
As with points for those from the Upper Peninsula, these preferences may be race-neutral in theory, but in practice they are anything but.
Because of intense racial isolation (and Michigan's schools are the most segregated in America for blacks, according to research by the Harvard Civil Rights Project), students of color will rarely attend the "best" schools, and on average, schools serving mostly black and Latino students offer only a third as many AP and honors courses as schools serving mostly whites.
So even truly talented students of color will be unable to access those extra points simply because of where they live, their economic status and ultimately their race, which is intertwined with both.
Four more points are awarded to students who have a parent who attended the U of M: a kind of affirmative action with which the President is intimately familiar, and which almost exclusively goes to whites.
Ironically, while alumni preference could work toward the interest of diversity if combined with aggressive race-based affirmative action (by creating a larger number of black and brown alums), the rollback of the latter, combined with the almost guaranteed retention of the former, will only further perpetuate white preference.
So the U of M offers 20 "extra" points to the typical black, Latino or indigenous applicant, while offering various combinations worth up to 58 extra points for students who will almost all be white. But while the first of these are seen as examples of racial preferences, the second are not, hidden as they are behind the structure of social inequities that limit where people live, where they go to school, and the kinds of opportunities they have been afforded.
Undercurrents of privilege
White preferences, the result of the normal workings of a racist society, can remain out of sight and out of mind, while the power of the state is turned against the paltry preferences meant to offset them.
Very telling is the oft-heard comment by whites, "If I had only been black I would have gotten into my first-choice college."
Such a statement not only ignores the fact that whites are more likely than members of any other group -- even with affirmative action in place -- to get into their first-choice school, but it also presumes, as anti-racist activist Paul Marcus explains, "that if these whites were black, everything else about their life would have remained the same."
In other words, that it would have made no negative difference as to where they went to school, what their family income was, or anything else.
The ability to believe that being black would have made no difference (other than a beneficial one when it came time for college), and that being white has made no positive difference, is rooted in privilege itself. The privilege that allows one to not have:
** to think about race on a daily basis;
** one's intelligence questioned by best-selling books;
** to worry about being viewed as a "out of place" when driving, shopping, buying a home, or for that matter, attending the University of Michigan.
So long as those privileges remain firmly in place and the preferential treatment that flows from those privileges continues to work to the benefit of whites, all talk of ending affirmative action is not only premature but a slap in the face to those who have fought, and died, for equal opportunity.
Tim Wise is an antiracist activist, essayist and lecturer. This article was reprinted with permission from Alternet.
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