Will a memorial to Chunky Monkey
consumers be next?
By Steven Milloy and Michael Gough
Copyright 2000 The Washington Times
April 30, 2000
James Zumwalt’s April 25 Commentary column, “Honoring all who died,” has noble intentions but lacks a factual basis. Mr. Zumwalt urges a memorial for Vietnam veterans who died as a result of Agent Orange exposure and suicides related to post-traumatic stress disorder.
No credible scientific evidence exists that Agent Orange has caused harm to human health. The Environmental Protection Agency’s (EPA) Science Advisory Board concluded that dioxin, the substance of concern in Agent Orange, has caused no health effects except for a skin disease seen at very high exposure levels.
Tests for dioxin in U.S. ground troops serving in areas sprayed by Agent Orange indicate there were no measurable exposures. There is no excess mortality among U.S. Air Force personnel who sprayed 90 percent of the Agent Orange and definitely were exposed.
The hype surrounding dioxin is best deflated by our recent study measuring the level of dioxin in a serving of Ben & Jerry’s ice cream at about 200 times the EPA’s so-called “safe” level. Ben & Jerry’s claims, “The only safe level of dioxin exposure is no exposure at all,” but no one is rushing to build a monument to consumers of Chunky Monkey.
Finally, there is no question that suicides have been elevated in combat veterans. A monument would be better dedicated to all combat veterans whose minds were so damaged that they took their own lives.
STEVEN MILLOY
Publisher
Junkscience.com
Potomac
MICHAEL GOUGH
Bethesda
Michael Gough was chairman (1990-95) of the Department of Health and Human Services’ advisory panel to the U.S. Air Force study of the effects of Agent Orange.
The Chunky-Monkey Study:
Malloy and Gough measured all the chemical costituents that could be classified as "Dioxins". Scientists use the term 'dioxin' to refer to a group of compounds that share certain similar chemical structures and biological characteristics.
Several hundred of these compounds exist and are members of three closely related families: the polychlorinated dibenzo-p-dioxins (PCDDs); the polychlorinated dibenzofurans (PCDFs or furans); and co-planar polychlorinated biphenyls (PCBs). Malloy and Gough counted any compound that fell in these groups. Not surprisingly all of the compounds found in Chunky Monkey were in the non-toxic group of these compounds. Something they also neglected to mention
Dioxins in General:
Most Dioxins are generated from natural sources such as bushfires, and most particularly volcanoes. Man made Dioxins are not deliberately produced, but are released into the environment as a result of combustion and other chemical processes. Human activities involving these processes include power generation and waste incineration, and the manufacture of metals and some chemicals. The amount of Dioxins that are man-made approach the amount produced by brush and forest fires. Volcanic action is the prime source of Dioxins in the environment.
Twenty-nine of these compounds are believed to be very harmful or toxic to humans and animals. For a given dioxin, furan or PCB it is both the number of chlorine atoms, and their position in the molecule, that determine their physical and chemical properties, as well as their toxicity. The most studied and most toxic PCDD is 2,3,7,8-tetrachlorodibenzo-p-dioxin (or TCDD).
To help measure the toxicity of dioxins and dioxins-like substances in the environment the concept of toxic equivalents (TEQs) has been developed. This concept allows the toxicity of a complex mixture to be estimated and expressed as a single number. TCDD is the most toxic dioxin and is assigned a weighting factor (or toxic equivalency factor, TEF) of 1; all other dioxins have a TEF of less than 1. Multiplication of the mass of a specific dioxin by its TEF yields the corresponding TCDD mass (or TEQ). The total toxicity of any mixture is then simply the sum of the individual dioxin TEQs.
TCDD Contamination of 'Agent Orange':
Again, the herbicidal organophosphates known as 2,4,D (2,4, dichlorophenoxyacetic acid) and 2,4,5,T (2,4,5 trichlorophenoxyacetic acid) were contaminated in the manufacturing process and produced TCDD (2,3,7,8-tetrachlorodibenzo-p-dioxin) among other Dioxins. These herbicides are still manufactured and used today, but in chemical processes which do not produce TCDD. Thus, while 2,4,D and 2,4,5,T are still made and used, you aren't going to get cancer from spraying Roundup around your fence or on your driveway.
Further; the Royal Australian Navy's study concluded that the steam flash-distillers of naval vessels off Vietnam not only concentrated the TCDD from runoff, it also converted non- or less toxic dioxin compounds into TCDD in the distilling process by adding chlorine atoms. The presence of chlorine or chlorine compounds (like say, sea water!) and a temperature range between 200-400°C provide the optimum conditions for the formation of TCDD.
As a personal example, I served on a World War II era Aircraft Carrier, the USS Intrepid. Day in and day out, Intrepid produced about 200,000 gallons of 'potable' water. Most of that water was used to power the ship, and to operate 2 steam catapults. Think about that, 200,000 gallons of water, every day, per 180 day deployment. And Intrepid was there from '64 to '69; you think she sucked up enough contaminated sea water to 'expose' those of us in her crew? And newer 4 catapult carriers produced a half-million gallons per day during flight operations.
Cancer and TCDD — The Mitochondrial Connection:
And, I just found this while researching this answer:
Elevated blood TCDD concentrations have been implicated in many cancers, skin rashes, and other health problems experienced by Vietnam veterans. Although TCDD is carcinogenic, it is not directly genotoxic. A report in the 8 January 2008 Proceedings of the National Academy of Sciences now demonstrates one of the ways that TCDD may promote cancer's growth and spread.
The new study describes a novel mechanism of TCDD action that focuses on the mitochondria: "We found that TCDD induces tumor cell proliferation and invasion by directly acting on mitochondrial transcription machinery and inducing mitochondrial respiratory stress," says principal investigator Narayan G. Avadhani, a biochemistry professor at the University of Pennsylvania. Such mitochondrial dysfunction inhibits apoptosis in malignant cells and increases the invasive potential of cancer. Mitochondrial dysfunction is also associated with conditions such as heart disease, diabetes, obesity, blindness, deafness, kidney disease, and neurodegenerative disorders, as well as with aging.
"[The respiratory stress-signaling] cascade culminates in the activation of a large number of nuclear genes that affect various cellular processes including cell metabolism, proliferation, and apoptosis," says lead author Gopa Biswas, a researcher in Avadhani's lab. "We have now established that TCDD alters cellular morphology and physiology through a similar mechanism."
It is generally accepted that adverse effects of TCDD result from its activation of the Ah receptor, with effects occurring at very low exposures. In the presence of TCDD, the Ah receptor has been shown to either induce or suppress the transcription of numerous genes that have been linked with cancer development via changes in tumor suppressor proteins, oncogenes, growth factors, and cell cycle proteins, among other factors.
Mitochondrial dysfunction may entail a more fundamental mechanism. It appears that TCDD-induced mitochondrial stress signaling in cancer cells is propagated in part through the Ah receptor but also acts through mechanisms that are independent of the Ah receptor, such as by inducing protein kinase C and extracellular signal–regulated kinases.
"Our findings show that at subtoxic levels of ten to fifty nanomolar, TCDD is sufficient to cause mitochondrial dysfunction and induce the signaling cascade," says Avadhani. "These results raise concerns over the adverse health implications of dioxins and PCBs even at very low levels."
In both animal and human studies (notably epidemiologic analyses of cancer rates following the 1976 industrial accident in Seveso, Italy), TCDD exposure has increased cancer incidence and mortality at all cancer sites rather than at a few specific sites. In 1997, the International Agency for Research on Cancer upgraded TCDD to a Group 1 human carcinogen on the basis of mechanistic data. Considering subsequent dose–response assessments for TCDD and cancer, Kyle Steenland, a professor of environmental and occupational health at Emory University, and colleagues argued in the September 2004 issue of EHP that "TCDD exposure levels close to those in the general population may be carcinogenic and argue for caution in setting the upper ranges of long-term permissible exposure to dioxins."
Not to mention blood, bone marrow, and lymphatic cancers like Chronic Lymphocytic Leukemia and other Non-Hodgkins Lymphomas.
Two of which I have.
Note: While CLL can run in familys, no one else in mine (3 siblings, 2 parents, 6 uncles/aunts, 4 grandparents with 10 siblings between them) have had any type of cancer.
People in my family die of falls, alcohol, or bad age. In their 80's or 90's...
I hope this primer on Agent Orange helps you understand why I'm so passionate on this subject.
P.S. Unrepentant, there's another bill you might want to check out: HR 6562 - The Agent Orange Equity Act of 2008. Another time sink I've been buried in. More about this shortly.