Endocrine-disrupting chemicals (EDCs) are substances in the environment that interfere with hormone (endocrine) systems to cause developmental, reproductive, immunological and neurological disorders including cancer, obesity, diabetes and a host of other illnesses.
U.S. regulatory, and traditional toxicological and medical science have been slow to recognize the environmental health hazards posed by EDCs in part because this class of chemicals operates at such low levels and with such complex causal mechanisms that reductive and mathematically linear risk models proceeding from the assumption that “the dose makes the poison” have been ill-suited to comprehend the messy realities of multiple chemical exposures and time-dependent dose response.
Increasingly, toxicologists and now even the American Medical Association, are poised to take up the public health paradigm challenge posed by EDCs. In the latest issue of Environmental Health Perspectives Linda Birnbaum, Director of the National Institute of Environmental Health Sciences, presents a summary of recent research that together refute the commonly held notion that ‘the dose makes the poison’.
Birnbaum explains how a growing number of studies show that many environmental toxicants can have significant consequences, including dysfunction and disease at very low-level exposures. Many of these low-dose studies (including with the pesticides hexachlorobenzene and atrazine) demonstrate that “the timing of exposure is critical to the outcome and that exposures during early life stages (fetal, infant, and pubertal) are particularly important. This recognition of critical windows of vulnerability not only demonstrates the developmental basis of disease but also that the timing, as well as the dose, makes the poison.” In addition, the effects of environmental toxins on the human hormone system, for example, are frequently non-linear such that “high doses may not be appropriate to predict the safety of low doses when hormonally active or modulating compounds are studied.” Birnbaum describes this body of research as responsible for disruptive “paradigm shifts in our understanding of the relationship between environmental toxicants and disease.”
Syngenta – the manufacturer of atrazine – was incorrect in a recent newsletter when trying to put small exposures into context using the analogy of Time and downplay the adverse effects of endocrine disrupting chemicals.
Noted international campaigner and recognised expert on the effects of endocrine disrupting chemicals that interfer with hormonal processes, Dr Theo Colborn set the record straight. She compared chemicals biologically active at 1 part per trillion [i.e. 1 part in 1,000,000,000,000 parts] to one second in 3,169 centuries!
Questions for the AMA and Ms Giddings
What stance does the Australian Medical Association and the Tasmania branch of the Australian Medical Association take on this area?
What is their comment on the American Medical Association’s statement?
What position does the Public Health Association of Australia take on preventing human exposure to endocrine disrupting chemicals?
Why have we not heard from these medical bodies after the remarkable Endocrine Society Statement in June 2009?
Why have we not heard from the national pesticide regulator (Australian Pesticides and Veterinary Medicine Authority) on this issue, let alone the local Tasmanian state authorities responsible for chemical use and public health – DPIPWE and DHHS?
Is Minister Giddings really confident that there are no studies showing that atrazine and related triazines when used in the environment can adversely affect humans?
Why then are the international experts in this field so sure that there are?
Both positions cannot be correct. What are the regulators really doing to protect our children and grandchildren from exposure to these chemicals?
There are several v important points in the article, below:
· reliance on old toxicological testing with no testing on human cells – this science has been available for many years – is insufficient to adequately protect human health.
· studies have shown an increased risk of NH lymphoma and Parkinsons and yet there has been no change to registration or use and these pesticides continue to be in waterways, drinking waters, and food with no evidence of a precautionary stance on behalf of our regulators or public health.
· 2,4-D is a volatile chemical and drift is a major problem. It should never be applied by aerial spraying and yet it continues to be applied by spraying.
· ‘metabolic consequences of short- and long-term exposures of humans to phenoxy-herbicides are unknown’ and yet we are all chronically exposed to these herbicides wherever they are used and wherever these herbicides drift or move to. It is not correct to state that a small amount of these pesticides will not harm you. Even with the manifestly inadequate DPIPWE pesticide monitoring programme, 12 of Tasmania’s 55 rivers have been found to have been polluted with these herbicides in the last 4 years; the Duck River alone has had 16 episodes recorded by DPIW, and the George River 5. There are no water treatment plants in Tasmania that remove these herbicides.
This is a disgraceful state of affairs.
APVMA and States and Territories should immediately take preventative action and stop use of these phenoxy herbicides.
Dr Alison Bleaney
Common Herbicides Block Important Nutrient Sensor in Humans
(Beyond Pesticides, October 15, 2009) New research from the Monell Center and the Mount Sinai School of Medicine reveals that phenoxy herbicides block T1R3, a nutrient-sensing taste receptor found in the pancreas and intestines of humans. These commonly used herbicides were not previously known to act on the T1R3 receptor, nor has any animal testing revealed any indication of this. The specific effects are unique to humans; thus, phenoxy herbicides may have adverse metabolic effects in humans that would have gone undetected in studies on rodents.
The T1R3 receptor is a critical component of both the sweet taste receptor and the umami (amino acid) taste receptor. First identified on the tongue, emerging evidence indicates that T1R3 and related taste receptors also are located on hormone-producing cells in the intestine and pancreas. These internal taste receptors detect nutrients in the gut and trigger the release of hormones involved in the regulation of glucose homeostasis and energy metabolism.
“Compounds that either activate or block T1R3 receptors could have significant metabolic effects, potentially influencing diseases such as obesity, type II diabetes and metabolic syndrome,” noted Monell geneticist and study leader Bedrich Mosinger, M.D., Ph.D.
The study, co-authored by Emeline Maillet from the Department of Neuroscience at Mount Sinai School of Medicine and co-author Robert Margolskee of Monell, and published online in the Journal of Medicinal Chemistry, tests the ability of two classes of chemical compounds to block the T1R3 receptor. Lipid lowering fibrate drugs used to treat high blood cholesterol; and phenoxy herbicides used in agriculture and in lawn care to control broad-leaf weeds. These two chemical compounds were selected based on their strong structural similarity to lactisole, a sweet taste inhibitor that exerts its taste effects by blocking T1R3.
Study researchers used an in vitro preparation to find that both classes of compounds, -phenoxy herbicides, along with fibrates, potently blocked activation of the human sweet taste receptor, acting at micromolar concentrations to inhibit binding of sugars to the T1R3 component of the receptor.
Additional testing revealed that the inhibitory effect of both fibrates and phenoxy herbicides on the T1R3 receptor is specific to humans. That is, the ability of these compounds to block the receptor did not generalize across species to the rodent form of the receptor.
Popular phenoxy herbicides include MCPA, Mecoprop (MCPB), and 2,4-D, one of the most extensively used herbicides in the world. According to the U.S. Environmental Protection Agency’s (EPA) Pesticide Industry and Usage Report, 2,4-D is the most commonly used pesticide in the nonagricultural sector and the fifth most commonly used pesticide in the nonagricultural sector in the U.S. It is a selective herbicide, used to kill broadleaf weeds with little to harm to grass crops. It is a plant growth regulator and mimics the natural plant growth hormone.
Phenoxy herbicides have been linked to a host of adverse human impacts, as well as water contamination and toxicity to aquatic organisms. Previous studies have shown that exposure to MCPA can more than double one’s risk of developing non-Hodgkin lymphoma (NHL). Another study published last month found that occupational 2,4-D exposure almost triples the risk of Parkinson’s disease compared to those reporting no exposure to the agent.
It is important to note that the implications of this study, as suggested by Dr. Mosinger, highlight the significance of testing chemicals intended for human use on human tissues, because these tests did not have the same results on lab rats. “The metabolic consequences of short- and long-term exposures of humans to phenoxy-herbicides are unknown. This is because most safety tests were done using animals, which have T1R3 receptors that are insensitive to these compounds,” he said.
Dr. Mosinger points out that little is known about how T1R3 blockade affects hormone levels and metabolism. “Given the number of compounds used in agriculture, medicine and the food industry that may affect human T1R3 and related receptors, more work is needed to identify the health-related effects of exposure to these compounds,” he said.
These highly toxic chemicals can be replaced by cost-competitive and effective management practices widely used in organic agriculture and lawn care. For information on ways to manage weeds without the use of phenoxy-herbicides, please refer to Beyond Pesticides’ Lawns and Landscapes page.
Source: Science Daily