Document zoVBkrB8DEy7byjD0ekBvQLJg
Dioxin Package
March 1993 Price: $10.00
Environmental Research Foundation P.O. Box 5036
Annapolis, MD 21403-7036 Telephone: (410) 263-1584
Fax: (410) 263-8944
Printed on recycled paper
THICT
ENVIRONMENTAL RESEARCH FOUNDATION
Environmental Research Foundation (ERF) provides technical assistance to grass-roots, environmental groups working to strengthen democracy at the local level-. E R F 's projects are designed to sustain a democratic movement of grass-roots groups, to curtail abuses of toxic and radioactive materials and to advocate reduction of the use of hazardous materials. O ur weekly newsletter, R achel's Hazardous Waste News and our on-line com puter database RACHEL (Remote Access Chemical Hazards Electronic Library) provide timely informa tion to citizens.
Contact E R F (P.O. Box 5036, Annapolis, M D 21403-7036, phone: 410-263-1584, fax: 410263-8944) to receive a free four-issue trial subscription to Rachel's H azardous Waste News, to learn about the RACHEL database, or to get more information about ERF.
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ENVIRONMENTAL
RESEARCH FOUNDATION
P.O. Box 5036 Annapolis, MD 21403-7036 Telephone (410) 263-1584
Econet: erf
Internet: erf@igc.apc.org
Fax (410) 263-8944
O ur D IO X IN package includes the following:
Incineration and Dioxin
"Will New 'Mass B u m ' Incinerators Produce Any A ir Pollution T hat T hreatens to H arm H um an Health?" from Rachel's H azardous Waste News #31
"Part 4: Scientists Study H ow 'Mass Bum* Incinerators Produce Dioxin, but Public's Fears M ay N ot Disappear" from Rachel's H azardous Waste News # 4 5
"Incineration o f Infectious Waste" from Rachel's H azardous Waste N ew s # 8 2
"Medical Incinerators Em it D angerous M etals and Dioxin, New Study Says" from Rachel's Hazardous Waste News #179
"All H azardous W aste Incinerators Fail to M eet E P A Regulations, E P A Says" from Rachel's H azardous Waste News #280
"Jacksonville" from Rachel's H azardous Waste N ews #311
"New EPA M em o Says All Hazardous W aste Incinerators Fail to M eet Regulations" from Rachel's H azardous Waste News #312
"Cement and Kiln D ust Contain Dioxins" from Rachel's H azardous Waste News #314
"A Sea of Troubles Engulfc Incineration" from Rachel's H azardous Waste News #325
Studies on Dioxin
"Study of Dioxin-Exposed Hum ans Reveals Cancer, Birth Defects, Liver and Cardiovascular Damage" from Rachel's H azardous Waste News # 7 3
"Dangers of Dioxin Exposures: A bsorption Through the Skin" from Rachel's H azardous Waste News #120
"Dioxin--Part 1; Dioxins and Cancer: Fraudulent Studies" from Rachel's Hazardous Waste News #171
"D ioxin-Part 2; Gauging the Toxicity of Dioxin" from Rachel's H azardous Waste News #173
"D ioxin-Part 3; New Evidence that Dioxin Causes H um an Cancers and O th er Diseases" from Rachel's H azardous Waste News #175
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"Report Links H erbicide Exposure to Illnesses A m ong Vietnam Vets" from Rachel's Hazardous Waste News #212 "D ioxin-Part 4; New Study Links Dioxin to H um an Cancer" from Rachel's Hazardous Waste News #219 "The W ingspread S ta te m e n t-P a rt 1; Chemicals in Environm ent Affect Sexual D evelopm ent in Wildlife. A nd Humans?" from Rachel's Hazardous Waste News #263 "The W ingspread S ta te m e n t-P a rt 2; M ajor Challenge to 'Business as U sual'" from Rachel's Hazardous Waste News #264 "Young M ale Rats are 'Demasculinized* and 'Fem inized' by Low Doses o f Dioxin" from Rachel's H azardous Waste News #290 Reassessment of Dioxin "A Tale of Science and Industry" from Rachel's H azardous Waste News #248 "Dioxin D an g ers-W h at's Going On?" from Rachel's H azardous Waste News #249 "EPA's Dioxin R eassessm ent-P art 1; New Picture o f Dioxin's Toxicity Emerges" from Rachel's H azardous Waste News #269 "EPA's Dioxin R eassessm ent--P art 2; Dioxin Dam ages H um an Im m une System" from Rachel's H azardous Waste News #270 "Dioxin Detoxification Campaign Exposed" from Rachel's Hazardous Waste News #275 "Waste Wars: T he Army O pens a New Front" from Rachel's H azardous Waste N ews #283 "The N .Y. Tim es Detoxifies Dioxin (Again)" from Rachel's H azardous Waste News #310
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Tncineration and Dioxin
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Reprint of:
RACHEL'S HAZARDOUS WASTE NEWS # 3 1
Providing news and resources to the Movement for Environmental Justice --June 29, 1987
WILL NEW 'MASS BURN' INCINERATORS PRODUCE ANY AIR POLLUTION THAT THREATENS TO HARM HUMAN HEALTH?
Are there valid reasons for people to be worried about air pollution from garbage incinerators? The incineration of garbage (often called "mass bum," "resource recovery" or "waste-to- energy") seems to produce the family of toxic chemicals known as dioxins. The dioxins are partly released from the smoke stack of the incinerator, and they are partly retained in the ash, which is eventually sent to a landfill. No one seems to dispute that burning garbage produces dioxins. People argue about the amount of dioxins produced, and they argue about which particular components of garbage cause the production of dioxins. But no one seems to argue that you can bum garbage without producing dioxins. Given that mass bum produces dioxins, whenever someone proposes a mass bum incinerator for garbage, we need to ask ourselves whether dioxins are really dangerous to humans. No one seems to doubt that dioxins are harmful to animals. The only unsettled question seems to be whether dio xins are harmful to humans. Writing in the Journal o f the American MedicalAssociation April 18,1986 (pgs. 2031-2038) a team of doctors and scientists reported on their study of 154 humans who had been exposed to dioxins during a two-year period (and their study of a control group of 155 people who had not been exposed to dioxins). The exposed group had lived for two years in a trailer park where dioxins had been mixed with waste oil and sprayed on roads to suppress dust. The doctors reported no differences in the medical histories o f the exposed and non-exposed groups; physical exams showed no differences; studies of blood and urine chemistry showed no differences; neurologic tests showed no differences. Yet the doctors reported that protective cells in the immune systems of the dioxin-exposed humans were reduced in number or impaired, not operating at peak levels, compared to.the immune systems of the unexposed control group. The results were expressed in terms of impaired liver function, and in terms of impaired T-cell characteristics. It is the immune system in humans that fights off disease, so an impaired immune system would expose a person to risk of disease from non dioxin-related causes. For a free reprint of the medical article, write to Dr. Richard E. Hoffman, MD, Division of Environmental Hazards and Health Effects, Center for Environmental Health, Centers for Disease Control, U.S. Department of Health and Human Services, Atlanta, GA 30333; or phone (404) 3293311 and ask for Dr. Hoffman. Request a copy of "Health Effects of Long-term Exposure to 2,3,7,8Tetrachlorodibenzo-p-Dioxin."
*
The Califomia'AIr Resources Board (the state agency concerned with air pollution) in 1986 asked a Scientific Review Panel on Toxic Air Contaminants to look at available evidence on dioxins. Dr. Emil M. Mrak, Chancellor Emeritus of the University of California at Davis, on May 23, 1986, submitted the findings of the Scientific Review Panel, which he chaired. The report says, in part, "Dioxins are potent toxins and are known carcinogens and/or promoters of carcinogenesis in animals. Dioxins... are potential carcinogens or promoters of carcinogenesis in humans. The current and planned waste-to-energy facilities in California will provide a high potential for emissions of dioxins into air in the state. An exposure level [at] which no significant health effects will occur cannot be identified. For these reasons, we agree that dioxins should be listed by the ARB [Air Resources Board] as toxic air contaminants with no determined threshold below which adverse health effects will not occur."
The report goes on to say, "Dioxins and dibenzofurans are stable, lipophilic [fat-soluble] compounds that may be expected to accumulate up the food chain. Thus, airborne dioxins emitted during combustion may contribute to dioxin intake by humans not only via inhalation but by other routes such as ingestion of food. Assessment of dioxin intake only via inhalation may thus underestimate total intake.
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"Given that tissue levels of these compounds [in humans] are measurable, we expect measurable levels in air, and we feel that the expense involved in obtaining baseline data [on dioxins in air] is small compared to the potential risk. Monitoring of ambient dioxin levels should be commenced before any waste-to-energy facilities go on line....
"Since there is good evidence that dioxins can enhance the action of other carcinogens, the potential for the harmful interaction of dioxins with other environmental toxins could be important and must not be forgotten or underestimated when considering research reports on the actions of dioxins alone." *
The two-page report, "Findings of the Scientific Review Panel on the R eport on Chlorinated Dioxins and Dibenzofiirans as Adopted at the April 16,1986 Meeting" is available from Mr. William Lockett, California Air Resources Board, P.O. Box 2815, Sacramento, CA 95812; phone (916) 3228168; or from Dr. Emil Mrak, Chancellor Emeritus, University of California at Davis, Davis, CA 95616; phone (916) 752-2442.
NEW STUDY SHOWS HOW ONE TOWN CAN RECYCLE AND CUT LANDFILL USE 70%
The town of East Hampton, New York, hired Barry Commoner's Center for the Biology of Natural Systems (CBNS) to devise a plan for handling the town's garbage without using an incinerator. The town has 15,000 winter time residents but it swells with tourists during summer. The resulting report recommends a combination o f recycling and composting that would reduce by 70% the amount of garbage going to the landfill. G et A n Intensive Trash Separation and Recycling System for the Town o f East Hampton for $10 from CBNS, Queens College, Flushing, NY 11367; phone (718) 670-4182. [Dated announcement omitted from this reprint.]
Reprint o f R achels Hazardous Waste News #J1 R achels Hazardous Waste News (ISSN 1065-4623) is published weekly by Environmental Research Foundation (ERF), P.O. Box 5036, Annapolis, MD 21403-7036; Telephone (410) 263-1584; Fax (410) 263-8944; Econet: erf; Internet: erf@igc.apc.oig. Editor Peter Montague, Ph.D.; Associate editor Maria B. Pellerano; Research Assistant: Andrea K. Feameyhough. Subscription rates: $25 per year for individuals and citizen groups; $80 for professionals and government agencies; $15 for students and seniors with ID; $400 for businesses; in Canada and Mexico, add $6.00; in all other countries, add $11.00. All payments in U.S. funds drawn on U.S. banks. Visa & Mastercard accepted. RacheVs Hazardous Waste News is not copyrighted; we encourage reprinting so long as you send us a copy. Printed on 100% recycled paper.
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Reprint of:
RACHEL'S HAZARDOUS WASTE NEWS # 4 5
Providing news and resources to the Movement for Environmental Justice --October 5,1987
Part 4: SCIENTISTS STUDY HOW 'MASS BURN'INCINERATORS PRODUCE DIOXIN, BUT PUBLIC'S FEARS MAY NOT DISAPPEAR
W hen municipal garbage goes into a "mass bum" incinerator, one of the products that
goes out the smokestack (or is trapped by a filter and ends up in an ash landfill) is the
family of chemicals called dioxins. N o one disputes th at dioxins are produced by m ass bum
incineration, but scientists .disagree on where the dioxins come from.
Ju st a few years ago, m any scientists w ere saying th a t the dioxins was produced by low-
tem perature com bustion (less than, say, 1400 degrees Fahrenheit). They advocated th at
incinerators should be designed to bum hotter to "bum up" the dioxins or perhaps n o t ever
create the dioxins a t all. O thers scientists w ere saying th at dioxins was produced by the
burning of pvc plastic and if we would just keep the pvc out of the waste stream, all would
be well.
D r. Barry Com m oner had a different idea. H e thought that dioxins was being created
inside the smokestack itself, after the smoke left the combustion cham ber of the incinerator.
If h e w as right, running th e firebox h o tte r w ouldn't p rev en t th e form ation o f dioxins. H e
did some experiments, w rote up his results, and then began advocating his ideas. H e's a
persuasive speaker and a tough opponent in a debate. H is effective argum ents angered his
opponents and they began to call him a charlatan and a "pseudo-scientist."
R ecently, new research has confirm ed D r. C om m oner's original ideas. In th e Journal o f
Chrom atography, Vol. 389 (1987), pgs. 127-137 and in Science Vol. 237 (A ugust 14, 1987),
pgs. 754-756, Canadian scientists report that they have found a m ajor m echanism for
creating dioxins in waste combustion: the fly ash (the particles th at m ake up th e sm oke in
the-sm okestack) acts as a catalyst (a chemical prom oter) and causes the form ation of
dioxins. They reported experiments in which they created dioxins with chlorine-containing
wastes b u t they also reported creation of dioxins from non-chlorinated com pounds. Science
News (Aug. 22,1987, pgs. 118-119) quoted one of these researchers saying, "We found th at
[fly ash] is in d eed a very strong catalyst which causes dioxins to form from alm ost anything."
They are now hard at work trying to m anipulate the composition of garbage to minimize
the production of certain types of fly ash catalysts, especially those containing m etals.
Figm ents in printing inks, for example, contain m etals th at may produce fly ash th at
produces dioxins. They think that getting the m etal out of garbage m ight substantially
reduce dioxin production.
Still other recent research throws additional light on the "dioxin from mass burn"
problem . Experim ents a t an incinerator in Pittsfield, M assachusetts w ere aimed at
discovering relationships between combustion conditions, garbage constitu
ents, and dioxin production. The report, Results of the Combustion and Emissions
Research Project at the Vicon Incinerator Facility in Pittsfield, M assachusetts appeared in
June, 1987. Som e of its m ore interesting conclusions were:
** T h e re is n o evidence th a t th e am o u n t o f PV C plastic in th e garbage affects th e
am ount of dioxin produced (pg. 10-4);
** W e t garbage produces m o re dioxins th an d rier garbage (pg. 10-4);
** T h e re is n o consistent relationship betw een th e am o u n t o f dioxin in the raw garbage
and the am ount of dioxin in the smoke stack gases (pg. 10-5);
** T h e re is a relationship betw een the am ount of carbon monoxide in th e sm okestack
gas and th e am ount of dioxin (pgs. 10-1, 10-5); "However," the rep o rt says, "one m ust be
cautioned th at the specific relationships betw een operating tem perature, carbon monoxide
levels, and levels of [dioxins] found during this study cannot necessarily be generalized to
other incinerators, particularly of a different design."
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** T h e location o f m easuring devices in th e in cin erato r affects how m uch dioxin is found (pg. 10-1).
W hat can we conclude from all this? A uthors of the Pittsfield study say future research should focus on the effects of facility design and operation (especially carbon monoxide levels, operating tem perature, and air pollution control systems) on the production of dioxins, instead of focusing on characteristics of the garbage.
On the other hand, the Canadian researchers believe that m anipulating the contents of the garbage is the key to discouraging dioxin production.
From th e citizen's perspective, faced w ith a m achine th a t will b e in o p eratio n fo r 20 to 30 years, during which tim e the chemical contents of A m erican garbage are likely to change dramatically (if the last 20 or 30 years are any indication), trying to m anipulate the contents of the garbage seem s complicated, untrustw orthy and doom ed to fail. N o governm ent authority will ever be able to control the contents of the stream of garbage entering a mass burn incinerator.
O n the other hand, trying to find and m aintain the exact operating conditions that minimize dioxin form ation (a narrow range of tem peratures, for example, and 100 ppm of carbon monoxide in the stack) seems equally hopeless. G arbage incinerators are n o t going to be ru n u n d e r laboratory conditions by chemists. T hey're going to b e ru n by garbage companies who have dem onstrated tim e and tim e again th at they'll cut any corner necessary to m ake a buck. T he garbage industry, including the incineration industry, is dom inated by organized crime or by people who com peted with organized crime and won o u t These are not the kind of people to whom you want to entrust an enormous, complex and dangerous machine, the careful operation of which will dramatically affect public health and safety.
In any case, knowing w hat minimizes dioxin production under controlled conditions cannot ease th e public's fear th a t m ass b u m will po llu te th e air. T h e fly ash researchers writing in Science noted th a t "more than 600 organic com pounds" have been identified on incinerator fly ash. T h a t's 600 m o re th a n th e public w ants to b re a th e o r dum p in to th e local landfill. D ioxin is simply N o. 601 on th e public's list o f unw anted p o llu tan ts from m ass bum.
T he Pittsfield study is N Y SER D A R eport 87-16, available from D epartm ent of Communications, N Y State Energy R& D Authority, Two Rockefeller Plaza, Albany, NY 12223; phone (518) 465-6251.
[Dated announcem ent om itted horn this reprint]
Reprint o f Rachel's Hazardous Waste News # 4 5 Rachel's Hazardous Waste News (ISSN 1065-4623) is published weekly by Environmental Research Foundation (ERF), P.O. Box 5036, Annapolis, M D 21403-7036; Telephone (410) 263-1584; Fax (410) 263-8944; Econet: erf; Internet: eif@igc.apc.org. E ditor Peter Montague, Ph.D.; Associate editor Maria B. Pellerano; Research Assistant: Andrea K. Fearneyhough. Subscription rates: $25 per year for individuals and citizen groups; $80 for professionals and government agencies; $15 for students and seniors with ID; $400 for businesses; in Canada and Mexico, add $6.00; in all other countries, add $11.00. All payments in U.S. funds drawn on U.S. banks. Visa & Mastercard accepted. Rachel's Hazardous Waste N ews is not copyrighted; we encourage reprinting so long as you send us a copy. Printed on 100% recycled paper.
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Reprint oft
rachel's HAZARDOUS WASTE NEWS # 8 2
Providing news and resources to the Movement for Environmental Justice --June 20,1988
INCINERATION OF INFECTIOUS WASTE
In 1985, th e re w ere 6872 hospitals in th e U .S. w ith 1.3 m illion beds. If beds a re occupied 70% of th e tim e and each occupied bed creates 13 p o unds o f w aste p e r day, U .S. hospitals produce 2.2 million tons of waste p er year. A n estim ated 15% of this is infectious waste containing hum an anatomical waste, plus garments, gauze pads, diapers, catheters, and so forth. B ut the infectious 15% cannot be segregated from the non-infectious, so it all gets mixed together, creating a larger mass that m ust all be considered infectious.
A n estim ated 90% o f all hospitals ru n their own incinerators; this m eans about 6,200 neighborhoods are im pacted by such m achines. From the viewpoint of people living near hospitals, there are five item s of concern: (1) the emission of bacteria or viruses that m ight m ake people sick; (2) th e emission of low m olecular weight organic m olecules (trichloroeth ylene [a suspected carcinogen], and tetrachloroethylene, am ong others); (3) the emission of high m olecular weight organic molecules, (so-called "products of incom plete combustion," benzopyrenes, PCBs, polynuclear arom atic hydrocarbons and other polycyclic organic m atter, m uch of which is carcinogenic); (4) the emission of toxic particles small enough for a person to breathe deep into their lungs; (5) and the emission of dioxins and furans.
The U.S. Environm ental Protection Agency (EPA) recently released a report com pleted under contract by the R adian Corporation. T he aim was to gather w hat is known about pollution from hospital incinerators. The authors searched the scientific literature, and interviewed many knowledgeable experts: staff of regulatory agencies (EPA, state and local), the Am erican H ospital Association, and incinerator vendors.
O f the estim ated 6200 hospital incinerators in use, perhaps 1200 are large incinerators (burning m ore than 400 pounds per hour or 400 tons per year) and 5000 are smaller. H ospital incinerators fall into three types: rotary kiln, excess air and starved air. By far the com m onest (especially am ong units installed during th e last 15 years) is starved a ir (also called "controlled air," "two-stage" and "modular"). Excess air incinerators (also called "pyrolitic incinerators," and "multi-chamber incinerators") come in two types: large units, which are generally "in-line," and sm aller units, which are generally "retort" types.
R adian could find no air emissions data for small excess-air incinerators, the kind that serve perhaps 75% or m ore of th nation's hospitals. Therefore, the rem ainder of this article describes air emissions from large controUed-air incinerators.
Even am ong these few incinerators, the lack of data is shocking. L et's look a t the five categories m entioned above.
B acteria a n d ^viruses. Y ou m ight think emission of disease-causing organisms (pathogens) from hospital incinerators would be the subject of intense scrutiny. N ot so. The R adian corporation could find only two studies in the scientific literature. O ne study found twice as many bacteria leaving an incinerator smoke stack as w ere found in norm al outdoor air (though the results w ere not statistically significant; in other words, they may have occurred by chance). The second study showed that, in a two-chamber incinerator, the tem perature in the first cham ber has to be 1400 degrees F ahrenheit and in the second cham ber had to be 1600 deg. F. to guarantee sterilization of bacteria and viruses. (M any incinerators are not designed to exceed 1400 deg. in their secondary chamber, so presumably do n o t effectively sterilize wastes they burn.) That ends the discussion of bacteria and viruses in th e R adian study. T h e en tire section on pathogens takes up 14 lines o f text in a 151-page report.
Low m olecular weight organic com pounds: R adian says, "One large data gap in the current hospital waste incinerator emissions data base is for lower m olecular weight organic compounds." End of discussion.
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Products of incomplete combustion, benzopyrene. PCBs and other carcinogenic organic molecules: These pollutants are "important," says Radian, but are n o t included in the study "due to lack of emissions data."
Tinv toxic particles: A micron is a m illionth of a m eter (and a m eter is about a yard). If you b re a th e particles (soot) in th e size ran g e o f 2 to 10 m icrons in diam eter, they are filtered out by the respiratory system (nose, esophagus, etc.) and are moved into the mouth, then swallowed. Particles smaller than 2 microns are considered "respirable" because they can enter the deep lungs. The smallest particles (1 m icron or less) enter the deepest part of the lung, the alveoli, the 3 million little sacs th at pass oxygen into the blood and let carbon dioxide pass back o u t Particles that enter the alveoli may eventually be removed by natural cleansing mechanisms, or they may lodge there, contributing a grey color to the normally-pink lungs, or they may actually pass into the blood stream and go someplace else in the body.
As luck would have it,, th e respirable particles from an incinerator contain m ore than their fair share of toxic m aterials, especially toxic m etals and the often-carcinogenic polycyclic organic molecules. T he small particles have a larger surface area in relation to their bulk than do larger particles. (A physicist would say small particles have a larger surface-to-volume ratio.) T he relatively large surface area of the smallest particles attracts toxic heavy m etals during combustion. Thus, respirable particles end up loaded (Radian says "enriched") with lead, arsenic, cadmium, chrom ium and other dangerous metals. (R adian presents no data on enrichm ent by polycyclic organics, unfortunately.) Thus the particles th a t reach deepest into the lungs are the m ost toxic. Typical hospital incinerators em it 1.5 to 36 pounds of particles p e r to n o f w aste incinerated. (Incidentally, b acteria and viruses have diam eters ranging from 0.4 microns down to 0.02 microns, so they are definitely respirable.)
Dioxins and furans: The R adian study describes in detail the combustion conditions under which dioxins and furans will be formed. They conclude that the prim aiy cham ber of a hospital incinerator is perfect for m anufacturing dioxins and furans, and th at safety depends upon the secondary cham ber completely destroying the dioxins by m aintaining ideal combustion conditions. They conclude that the average am ount of total dioxins em itted from a 1000 pound-per-hour hospital incinerator operating 2000 hours per year would be 3.7 grams of dioxin per y ear.' (There are 28 grams in an ounce.) This may not sound like much, bu t dioxin is considered extremely toxic, so it may be a lot, depending on w here it goes once it is released into your neighborhood.
C onclusion: T h e n atio n 's prim ary m edical care institutions a re alm ost all operating incinerators w ithout knowing w hat they are doing, literally. T he data are simply not available. W hat data there are, on respirable particles and dioxins, indicate the need for very tight air pollution control, which is n o t provided un d er federal law, n o r un d er m ost state laws. In short, hospital incineration of infectious wastes is a scandal.
T o g et your free copy of R ad ian 's H ospital Waste C om bustion Study, D ata G athering Phase, F inal DrqfjtM eport, w rite R ay M orrison, P o llu tan t A ssessm ent B ranch, Office of A ir Quality Planning and Standards, EPA, R esearch Triangle, N C 27711; phone (919) 541-5332.
Reprint o f Rachel's Hazardous Waste News # 8 2
Rachel's Hazardous Waste News (ISSN 1065-4623) is published weekly by Environmental Research Foundation (ERF),
P.O. Box 5036, Annapolis, M D 21403-7036; Telephone (410) 263-1584; Fax (410) 263-8944; Econet: erf; Internet:
erf@igc.apc.org. E ditor Peter Montague, Ph.D.; Associate editor Maria B. Pellerano; Research Assistant: Andrea
K. Feameyhough. Subscription rates: $25 per year for individuals and citizen groups; $80 for professionals and
government agencies; $15 for students and seniors with ID; $400 for businesses; in Canada and Mexico, add $6.00;
in all other countries, add $11.00. All payments in U.S. funds drawn on U.S. banks. Visa & Mastercard accepted.
Rachel's H azardous Waste News is not copyrighted; we encourage reprinting so long as you send us a copy. Printed
on 100% recycled paper.
Q O O ll
Reprint of:
RACHEL'S HAZARDOUS WASTE NEWS # 1 7 9
Providing news and resources to the Movement for Environmental Justice --May 2,1990
MEDICAL INCINERATORS EMIT DANGEROUS METALS AND DIOXIN, NEW STUDY SAYS
Medical waste incinerators are a major source of toxic air emissions, especially dioxin and
cadmium, according to a lengthy study just released by the California Air Resources Board
(CARB), a state agency. [Page numbers in our text (below) refer to pages in this new study,
which is cited in our next-to-last paragraph.] T he study says the public health risks from
breathing these emissions are unacceptably high. O n M ay 23, the CA RB will propose new air
pollution controls on California's medical incinerators; CARB predicts the new rules will force
129 of the state's 142 incinerators to cease operation because compliance will be too costly.
Dioxin
T he CA RB studied dioxin in 1986 and declared it "highly toxic" in experim ental animals.
Toxic effects in animals include severe weight loss, liver necrosis [death of tissue] and hypertro
phy [enlargement], skin lesions, immunosuppression, reproductive toxicity, teratogenesis [birth
defects], carcinogenesis [cancer] and death. T he CARB concluded that dioxin is an animal
carcinogen and a "potential human carcinogen." They also reported that both acute (short-term)
and chronic (long-term) exposure to dioxin has caused liver damage in humans (pg. 10).
Cadmium
Chronic exposure to cadmium, a toxic metal, causes a wide range o f adverse effects in
humans, including "cardiovascular [heart, arteries], endocrine [hormone], hepatic [liver], bone,
hematological [blood], immunological [immune system], respiratory [lung], renal [kidney],
reproductive and teratogenic [birth defect] effects." Furtherm ore, "There is strong evidence o f
an association betw een cadmium exposure and an increased risk o f respiratory [lung] cancer,"
says the CARB report (pg. 18).
California has 142 medical waste incinerators operating today. Together, they bum 20,050
tons of wastes p er year, so they are not large. (For example, a big municipal waste incinerator
bum s this m uch waste every 10 days.) M edical waste includes paper, cardboard, plastic, rubber,
food wastes, cans, bottles, animal carcasses, sharps [hypodermic needles, scalpels, etc.],
chemotherapy wastes, diapers, bandages, solvents, and pathological wastes [body parts, bed pan
residues, and so forth]. Medical waste also contains metals such as lead, cadmium, mercury, and
zinc; it can also contain low-level radioactivity (pg. 34).
D espite th eir relatively small size, California's 142 medwaste incinerators em it substantial
quantities o f dioxins and cadmium: 16 grams o f dioxin each year (pg. 31) and 30 to 40 pounds
of cadmium (pg. 33) each year.
To gather emissions data, the CARB monitored eight medwaste incinerators. The report
notes that, "Although the emissions tests were not conducted for compliance purposes, we
observed that many of the facilities tested could not meet the particulate limitations in their
permits. In addition, the hydrochloric acid emissions were elevated...." (pg. 48)
The eight emissions tests revealed many other air contaminants emitted by one or m ore of
the incinerators. H ere is a list of pollutants em itted, followed by the num ber (1 to 8) of
incinerators, out of 8 tested, found to be emitting each pollutant: arsenic (7); ammonia fl);
benzene (8); brom odichlorom ethane(2); cadmium (8); carbon tetrachloride (6); chromium (7);
chlorodibromomethane(3); chloroform (4); cumene (5); l,2-dibromoethane(5); dichloromethane
(6) ; dichloroethane (3); dioxins and furans (8); ethyl benzene (7); lead (8); mercury (5);
mesitylene(7); nickel (3); particulate m atter (8); naphthalene (5); tetrachloroethane(4); toluene
(7) ; trichloroethane (3); 1,1,1-trichloroethane (6); trichloroethylene (6); trichlorom ethane (5);
vinyl chloride (2); xylenes (7) (pg. 51).
The CA RB study indicates th at it will cost from $383,000 to $479,000 to put best available
control air pollution control technology (BACT) (a spray dryer [also called a dry scrubber] and
baghouse filter) on an existing large, regional medwaste incinerators (pg. 115), o f which Cali
fornia has 12.
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According to the CA RB's data, small medwaste incinerators serving an individual institution will not be able to afford to install air pollution equipm ent that would allow continued operation o f the incinerator after the new dioxin and cadmium regulations become effective this summer. For these 129 incinerators, the available alternatives include (a) shut down and use a large, regional medwaste incinerator; (b) shut down and use off-site steam sterilization; (c) shut down and use onsite steam sterilization.
Steam sterilization (also called autoclaving) means heating the wastes in a metal chamber by filling the cham ber with saturated steam and holding the tem perature at 250 Fahrenheit for 30 minutes. It effectively sterilizes wastes, killing viruses and bacteria. The wastes then go to a landfill. O f these three options, the cheapest is onsite sterilization; this option would increase medwaste disposal costs 10 cents per pound, and would increase patient costs 16 cents per hospital bed per day, com pared to present costs of onsite incineration. The use of offsite, regional incineration would increase disposal costs 16 cents per pound and would increase aver age patient costs 41 cents p er bed per day. O nsite steam sterilization would increase disposal costs 16 cents p er pound and would increase patient costs 42 cents per bed p er day. Thus, shutting down its incinerator and sending wastes out for regional steam sterilization is the cheapest way for a hospital to come into compliance with the proposed California air regulations for cadmium and dioxin (pg. 118).
A different study of medical wastes, by members o f the Civil Engineering D epartm ent of University of California at Davis (cited below in our last paragraph), points out that, in a typical hospital, infectious waste makes up only about 15% of the total waste stream. Infectious waste by itself will bum , but the volume is usually not sufficient to allow heat recovery. Therefore, the decision to install an incinerator for infectious waste encourages the burning of other non-infectious wastes. In effect, a medwaste incinerator is a municipal solid w aste incinerator with 15% of the waste being infectious.
There are, however, a few differences between municipal wastes and infectious wastes. Plastics make up 5% to 7% of municipal waste, but 14% to 30% of infectious waste. Because plastics are the m ajor sources of cadmium and lead, medical waste incinerators emit m ore of these toxic metals, per pound o f burned waste, than do municipal incinerators.
Lead is present as a pigm ent and as a stiffening and strengthening agent in many plastic items, especially those m ade of PVC (polyvinyl chloride). F or example, the red bags themselves, in which "red bag" medical wastes are packaged, is colored red by a lead compound. L ead is also present in yellow bags for collecting soiled linens, yellow bedpans, and yellow tops of urine containers. In plastics, a bright color (yellow, orange, red, purple) is often an indication o f a toxic metal (cadmium or lead).
The Davis researchers didn't say so, but hospitals could refuse to purchase m edical supplies m ade with toxic metals, thus m inim izing problem s.
G et: D R A F T Technical Support D ocum ent to Proposed D ioxins and C adm ium ControlM easure fo r M edical Waste Incinerators (Sacramento, CA: A ir Resources B oard [1102 Q St., P.O . Box 2815, Sacramento, CA 95812], 1990. Phone Inform ation Officer Jerry M artin at (916) 322-2990. This docum ent is about 500 pages long, contains a great deal o f useful inform ation on medical waste incineration, and is free while supplies last.
Also get: D.Cr Hickman, D.P.Y. Chang, and H . Glasser, "Cadmium, and Lead in Bio-Medical Waste Incinerators," a paper presented at the 82nd Annual Meeting of the A ir and Waste Management Association at Anaheim, CA, June 25-30,1989; available free from Dan Chang, D epartm ent of Civil Engineering, Mail ID # 1855, University of California at Davis, Davis, CA 95616.
Reprint o f Rachel's Hazardous Waste News #179 Rachel's Hazardous Waste News (ISSN 1065-4623) is published weekly by Environmental Research Foundation (ERF), P.O. Box 5036, Annapolis, M D 21403-7036; Telephone (410) 263-1584; Fax (410) 263-8944; Econet: erf; Internet: erf@igc.apc.org. Editor: Peter Montague, Ph.D.; Associate editor Maria B. Pellerano; Research Assistant: Andrea K. Feameyhough. Subscription rates: $25 per year for individuals and citizen groups; $80 for professionals and government agencies; $15 for students and seniors with ID; $400 for businesses; in Canada and Mexico, add $6.00; in all other countries, add $11.00. All payments in U.S. funds drawn on U.S. banks. Visa & Mastercard accepted. Rachel's Hazardous Waste News is not copyrighted; we encourage reprinting so long as you send us a copy. Printed on 100% recycled paper.
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Reprint ol
RACHEL'S HAZARDOUS WASTE NEWS #280
Providing news and resources to the Movement for Environmental Justice --April 7,1992
ALL HAZARDOUS WASTE INCINERATORS FAIL TO MEET EPA REGULATIONS, EPA SAYS
Hazardous waste incinerators, and the web o f regulations intended to make them operate safely, have come under withering criticism from government scientists, private researchers, and the Wall Street Journal during the last 60 days. Officials o f EPA (U.S. Environmental Protection Agency) and private research scientists now admit that hazardous waste incinerators emit hundreds of times more dioxins and other toxic air pollutants than is allowed by EPA regulations, and the Journal revealed a record of malfunctions, including explosions and major releases of toxins, that incinerator operators have tried to cover up and that regulatory officials seem powerless to understand, much less curtail.
Scientists employed by U.S. EPA (Environmental Protection Agency) admitted last month that modem hazardous waste incinerators simply cannot comply with existing federal regulations because they cannot destroy all chemicals with 99.99% destruction/removal efficiency (DRE), which is the efficiency required by federal law. Federal law further requires that certain wastes o f "special concern" such as dioxins, furans, and PCBs must be destroyed with 99.9999% DRE. EPA scientists said last month that they have known since at least 1985 that hazardous waste incinerators could not meet any of these regulatory requirements.
The story broke when Pat Costner, a chemist and research director for Greenpeace, published an independent analysis of dioxin emissions from the Jacksonville, Arkansas incinerator.1 The Jacksonville incinerator has begun burning 16.5 million pounds o f herbicides (2,4,5-T and 2,4-D) left over from the Vietnam war. These wastes are known to be contaminated with total dioxins and furans at concentrations ranging from to 3 to 40 parts per million (ppm).
Costner's analysis revealed that the Jacksonville incinerator was only achieving 99.96% destruction of the dioxins entering the incinerator, thus emitting 400 times more dioxin into the community than the law allows. An official with the Arkansas Department of Pollution Control and Ecology (DPC&E) acknowledged in telephone interviews that Costner's calculations are correct. H e also said the department had no intention of shutting down the incinerator despite its continuing emissions of dioxin directly into a residential community. H e said the department did not know what the total dioxin emissions into the population of Jacksonville would be, but, he said, no matter what the total may be, it is safe.
The Jacksonville incinerator is a key demonstration project, established with the cooperation of EPA Administrator William Reilly and Arkansas Governor Bill Clinton to show that dioxin-contain ing wastes can be incinerated in a residential neighborhood over the objections of the community.2 In a city-wide referendum in March, 1986, the people of Jacksonville voted two-to-one (1383 to 656) to stop the project but government officials simply ignored the vote and have overridden all objections ever since. Costner's analysis clearly showed that residents of Jacksonville are being exposed to levels of dioxin contamination that exceed federal health and safety standards by a wide margin. This is the first systematic dioxin experiment on humans using a residential population. Previous dioxin exposures of humans have occurred during industrial accidents and in the industrial manufacture of chemical-biological warfare agents. Dioxin is now known to cause cancer in humans and to disrupt normal growth and development of fetuses and infants at low levels of exposure.3
About 100 waste sites in the U.S. contain substantial quantities o f dioxin,4 and the U.S. has stockpiles containing billions of pounds of chemical-biological warfare (CBW) agents the govern ment has said it wants to incinerate. If the Jacksonville dioxin experiment can be maintained despite ethical and public health objections, government agencies will be able to claim they have a green light to incinerate just about anything just about anywhere.
However the Jacksonville experiment has brought to light information that could derail the entire U.S. incineration program. In preparing her analysis of dioxin exposure of the Jacksonville populace, Costner uncovered a government study showing that tests in 1984-85 by private research ers, under contract to EPA, revealed that hazardous waste incinerators cannot be expected to achieve 99.9999 percent destruction of wastes that occur in concentrations lower than 10,000 parts
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per million, and cannot be expected to achieve 99.99 percent destruction of wastes that occur in concentrations lower than 1000 ppm. EPA published the 1985 data in 1989.5
When this information came to light, a news reporter from the Arkansas Democrat-Gazette, Sandy Davis, interviewed Bob Hall, chief of the EPA's Combustion Research Branch in Research Triangle, North Carolina, and he confirmed what the EPA report had shown. "The fact is that you run into problems with your D R E [destruction/removal efficiency] when a low concentration of wastes is fed into the incinerator," Hall said. "Our data clearly shows that," he said. Davis asked Hall why EPA hasn't changed its regulations since it knows existing incinerators cannot comply with the regulations. Hall said, "I don't know why that hasn't been changed. It's a regulatory issue. I'm in research."6
Costner uncovered a second EPA report,7published in 1984 but never widely circulated, showing that, among eight major hazardous waste incinerators studied, none could achieve 99.99% DRE. Sandy Davis interviewed the author of that report, Drew Trenholm o f the Midwest Research Institute in Research Triangle, North Carolina, who said incinerators simply cannot achieve the D R E required by federal law. "The trend is very strong in the data that this is the case," Trenholm told Davis.
At public hearings over the past decade, dozens of EPA officials have stated for the record that incinerators can achieve the legally-required DREs, in what appears to be a coverup of public health information of astonishing proportions.
Many of the most dangerous toxins such as dioxins, furans, and PCBs occur in wastes at low concentrations. If low-concentration chemicals cannot be destroyed effectively, this means all sludge incinerators, all contaminated-soil burners, and all wood-treatment-waste incinerators will fail to meet federal regulations and will emit illegal quantities o f potent toxins into surrounding air.
Ongoing failure to achieve the required destruction efficiencies is not all that plagues incinerators. Wall Street Journal reporter Jeff Bailey pointed out March 20 that federal, state and local regulatory officials pay close attention to hazardous waste incinerators but they can't be everywhere at the same time and they often learn about accidents, explosions and violations from tips phoned to them anonymously by insiders.8 For example, Chem Waste, the nation's largest haz ardous waste hauler, is not considered a fly-by-night operator. According to Joan Bernstein, vicepresident for environmental policy and ethical standards at Chem Waste, "Environmental com pliance is what drives this company." If this is true, then Chem Waste's ongoing record of acci dents, explosions, leaks, releases and coverups involving their incinerators must mean that even the wealthiest companies that have written down their best intentions on a piece o f paper still cannot operate hazardous waste incinerators in a fashion that any reasonable person would call safe.
[To be continued.]
[1] Pat Costner, The Incineration o f Dioxin in Jacksonville, Arkansas: A Review o f Trial Bums and Related A ir Monitoring at Vertac Site Contractors Incinerator, Jacksonville, AR (Washington, DC: Greenpeace Toxics Campaign, January 29,1992). [2] Stephanie Arfoanel and others, T oxic Nightmare on Main Street," Family Circle August 14,1990, pgs. 77-80,120-128. [3] Karen F. Schmidt, "Puzzling Over a Poison; On. closer inspection, the ubiquitous pollutant dioxin appears more dangerous than ever," U.S. News & World Report April 6, 1992, pgs. 60-61. [4] Peter A. Johnson and others, Dioxin Treatment Technologies: Background Paper [OTA-BP-O-93] (Washington, DC: U.S. Government Printing Office, 1991). 80 pages. $4.00 from U.S. Government Printing Office, P.O. Box 371954, Pittsburgh, PA 15250-7954 or phone your order to (202) 783-3238. [5] John C. Kramlich and others, Experimental Investigation o f Critical Fundamental Issues in Hazardous Waste Incineration (Springfield, VA: National Technical Information Service [NTIS], September, 1989.) This is EPA document No. EPA/600/2-89/048 available from NTIS for $26.00; phone (800) 553-6847 and request NTIS document No. PB90-108507. [6] Sandy Davis, "Incinerator can't do job, engineer says," Arkansas Democrat-Gazette March 14, 1992, pgs, 1A, 15A. [7] A. Trenholm and others, Performance Evaluation o fFull-Scale Hazardous Waste Incinerators. Vol. I. Executive Summary. [EPA/600/2-84/181A]. (Washington, DC: U.S. Environmental Protection Agency, 1984). Available from NTIS as document No. PB 85-129500. $17.00. Phone 800/553-6847. [8] Jeff Bailey, "Concerns Mount Over Operating Methods Of Plants That Incinerate Toxic Waste," Wall Street Journal March 20, 1992, pgs. B l, B5.
Reprint o f R achels Hazardous Waste News #280 Rachels Hazardous Waste News (ISSN 1065-4623) is published weekly by Environmental Research Foundation (ERF), P.O. Box 5036, Annapolis, M D 21403-7036; Telephone (410) 263-1584; Fax (410) 263-8944; Econet: erf; Internet: erf@igc.apc.org. Editor Peter Montague, Ph.D.; Associate editor: Maria B. Pellerano; Research Assistant: Andrea K. Fearneyhough. Subscription rates: $25 per year for individuals and citizen groups; $80 for professionals and government agencies; $15 for students and seniors with ID; $400 for businesses; in Canada and Mexico, add $6.00; in all other countries, add $11.00. All payments in U.S. funds drawn on U.S. banks. Visa & Mastercard accepted. R achels Hazardous Waste News is not copyrighted; we encourage reprinting so long as you send us a copy. Printed on 100% recycled paper.
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Reprint of:
RACHEL'S HAZARDOUS WASTE NEWS #311
Providing news and resources to the Movement for Environmental Justice --November 12, 1992
JACKSONVILLE
On Tuesday, October 27, one week before his election as President of the United States, Governor Bill Clinton of Arkansas gave the final order to start burning dioxin in an incinerator in a residential area of Jacksonville, Arkansas, a community of 29,000 people 15 miles northeast of Little Rock. The incinerator was built in the residential neighborhood with state funds for the purpose of burning 30,000 barrels of mixed hazardous wastes abandoned in Jacksonville by a company called Vertac Chemical, which manufactured pesticides and herbicides there from 1948 to 1986.
The New York Times (Nov. 2, 1992, pg. B ll) reported that the Governor made the decision himself to start the bum: "Mr. Clinton, who has overseen the investigation and cleanup at Vertac most of the last 13 years, gave final approval on Tuesday to a plan to bum the chemical wastes in an incinerator...." The Times said (Oct. 28, 1992, pg. A14), "No other environmental issue in Arkansas has so dominated the public debate during Gov. Bill Clinton's 12 years in the Governor's Mansion as the chemical contamination in Jacksonville and what to do about it."
Over the years the Vertac site was used for manufacture of DDT, aldrin, dieldrin, toxaphene and the chemical warfare defoliants 2,4-D, Silvex, 2,4,5-T, and Agent Orange. In 1979 state and federal investigators discovered dioxin on the Vertac property and in the soil and water several hundred yards from the site. Official surveys subsequently found dioxin from the plant in Jacksonville's central city park, making its oncepopular swimming and fishing lake off limits to the public.
Almost immediately, citizens began pressing for a thorough, safe cleanup of the Vertac site. In what has now become a familiar story, state and federal authorities delayed cleanup. According to the New York Times, "Since 1979... Vertac's toxic wastes and what to do about them have been the source of considerable strife in the community and have dominated the attention of Gov. Bill Clinton and his environmental advisers." (Oct. 30, 1992, pg. A 16.)
In 1986, Vertac declared bankruptcy and willed its 93-acre site to the people of Arkansas. Vertac's executives abruptly left town and have never been successfully traced. The New York Times said, "Vertac abandoned the plant leaving behind roughly 30,000 barrels of chemical wastes, along with acres of contaminated soil, tanks filled with toxic materials, and miles of poisonous piping. The EPA [U.S. Environmental Protection Agency] considers the site one of the country's worst hazardous waste sites, not only because of [the] extent of the contamination but also because the plant is only a few blocks from a day care center, a hospital, and hundreds of houses." (Oct. 28, 1992, pg. A14.)
By 1989 state and federal officials had made firm plans to build an incinerator in a residential neighbor hood of Jacksonville to burn some 22 million pounds of Vertac's dioxin-laced wastes.
On at least two occasions a majority of the citizens of Jacksonville expressed, through referendums and public meetings, that they did not want the incinerator built. Many local people considered it a dirty, dangerous way to "get rid o f the wastes. They pointed out that cleanup teams had already packed the 30,000 barrels in special drums, which were not an immediate threat. The real threat was the wastes already released into the community, the ground and the groundwater. Incinerating the 30,000 barrels would be a cosmetic gesture that did not address the residual problems. State and federal officials ignored these expressions of sentiment and forged ahead with their plan to burn the visible evidence, to make Jacksonville look clean again. Tlie real cleanup of soil and water would have to wait for a later time.
In 1990, Marco Kaltofen, a chemical engineer with the National Toxics Campaign presented Governor Clinton with a White Paper outlining alternatives to incineration, including chemical destruction (dechlorina tion), and above-ground storage in steel-reinforced concrete buildings.1 Subsequently in 1991 the U.S. Office of Technology Assessment (an arm of Congress) released a report called Dioxin Treatment Technologies, in which they reported the successful destruction of dioxin-containing wastes by chemical dechlorination processes. Chemical dechlorination occurs inside a closed container, releasing nothing to the surrounding environment. Jacksonville has two other Superfund dumps besides the Vertac site, and OTA reported that a chemical dechlorination technology called BCD had been shown to successfully detoxify soils from these other sites. "Test results confirmed that BCD is a candidate technology for the cleanup of halo-carbon-contaminated liquids and soils in an environmentally acceptable manner (closed system)," OTA said.2 The term "halo-carbon" in this case referred specifically to 2,4,-D, Silvex, 2,4,5-T, and dioxins, which were successfully destroyed by the BCD process. The U.S. Navy has selected BCD technology to clean up its contaminated sites, and has built a BCD decontamination machine which is in use now to clean up PCB-contaminated soils in Stockton, California. State and federal officials in Arkansas turned a blind eye to these alternative technologies.
At public meetings throughout 1989 and 1990 -som e of which we attended-state and federal environmental officials insisted repeatedly that the Vertac site incinerator would emit zero dioxin into the
coons
surrounding community. A trial burn was conducted during October, 1991. State and federal officials examined the data and de
clared the incinerator a resounding success. But Greenpeace chemist Pat Costner analyzed the trial bum data and published her own analysis, showing that the incinerator had not achieved the required 99.9999% destruction of the wastes, but had in fact achieved only 99.96% destruction. This meant that the incinerator was releasing 400 times as much dioxin as the regulations intended.
State and federal officials studied Costner's analysis and subsequently admitted that she was right. Costner then calculated that the incinerator would release somewhere between 150 and 800 grams of dioxin into the community during the two-year burn. Is this a lot of dioxin? EPA has established a "safe" level of dioxin as 0.000001 micrograms of dioxin per kilogram of body weight per day. If you ate this much dioxin every day for a lifetime and retained it all in your body, you would accumulate a body burden of 1.79 micrograms of dioxin. (A microgram is a millionth of a gram, and there are 28 grams in an ounce.) So we'll call 1.79 micrograms an "EPA safe" dose.
If we say, somewhat arbitrarily, that 10 times this amount represents an "EPA unsafe" dose, we can calculate that the Vertac incinerator will emit somewhere between 8 million and 45 million "EPA unsafe" doses of dioxin into the community of Jacksonville during the two-year burn. State and federal officials say the proposed burn does not violate any state or federal laws and thus should be allowed to proceed. One Arkansas health department official excused the dumping of 150 to 800 grams of dioxin into the community saying, "You have to appreciate how much dioxin there is in this community already." Pat Costner points out that this will be the largest intentional release of dioxin that has ever been executed.
Officials of the Arkansas Health Department say they had nothing to do with choosing incineration to get rid of the Vertac wastes. However, they have made careful plans to take advantage of the experiment by gathering data about dioxin levels in human tissues in Jacksonville residents before and after the bum. The pre-burn study of dioxin in blood and urine of Jacksonville residents will be released some time during the next month or so. After the experimental burn is over, new samples will be taken and comparisons will be made to see what levels of toxins (if any) have lodged in the tissues of the human subjects of the Jacksonville dioxin experiment. "I can say without fear of contradiction, we will have the best database on (dioxin in tissues of] the general population of the U.S. that has ever been developed," Dr. Morris Kranmer, principal investigator of the study, told us. No long-term follow up of health effects in the community has been planned.
Despite massive pressure from national environmental groups and local community organizations, one week before the election, Bill Clinton gave the final order to begin the Jacksonville dioxin burn experiment. The New York Times noted, "Unfavorable publicity about the Vertac project contributed to Mr. Clinton's reputation as a leader with a less than sterling environmental record, his aides said. 'He's been beaten up pretty badly over this,' said Kenneth L. Smith, Mr. Clinton's top environmental advisor." (Nov. 2, 1992, pg. B ll.)
The Times went on: "The Vertac project has become typical of toxic waste cleanups around the country in which costs escalate amid interminable delays caused by Federal rules aimed at gaining public trust. Mr. Smith said the Governor believed that unless changes were made in the rules and the public began to accept some degree of risk, fewer toxic-waste cleanup projects could proceed or ever larger sums of money would be siphoned from the Government's budget for all environmental programs."
No sooner had the Governor given the go-ahead than a coalition of five organizations-including the Washington-based Government Accountability Project-sued in court to stop the experiment. Judge Stephen M. Reasoner ruled October 29 that the experimental burn could go ahead for three days, during which the state must test the incinerator's ability to destroy dioxin with 99.9999% efficiency. If anything less than 99.9999% is achieved, "the Court orders that the burning be stopped immediately," said Judge Stephen M. Reasoner.
The experimental burn occurred over the weekend, but by that time Governor Clinton's attention had been swept up by other matters, namely a nation to which he has solemnly promised that things will now
be different.
[1] Marco Kaltofen and Sanford J. Lewis, A While Paper on the Feasibility of Alternatives to Incineration of Wastes at the Vertac Site in Jacksonville, Arkansas (Boston: National Toxics Campaign Fund, October 27, 1990). [2] U.S. Congress, Office of Technology Assessment, Dioxin Treatment Technologies-Background Paper [OTA-BP-O-93] (Washington, D.C: U.S. Government Printing Office, November, 1991).
Reprint of Rachel's Hazardous Waste News #311
Rachel's Hazardous Waste News (ISSN 1065-4623) is published weekly by Environmental Research Foundation (ERF),
P.O. Box 5036, Annapolis, MD 21403-7036; Telephone (410) 263-1584; Fax (410) 263-8944; Econet: erf; Internet:
erf@igc.apc.org. Editor: Peter Montague, Ph.D.; Associate editor: Maria B. Pellerano; Research Assistant: Andrea
K. Feameyhough. Subscription rates: $25 per year for individuals and citizen groups; $80 for professionals and
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RACHEL'S HAZARDOUS WASTE NEWS # 3 1 2
Providing news and resources to the Movement for Environmental Justice --November 18,1992
NEW EPA MEMO SAYS ALL HAZARDOUS WASTE INCINERATORS FAIL TO MEET REGULATIONS
An internal memo sent to all 10 regional offices of EPA [U.S. Environmental Protection Agency] by Sylvia Lowrance, EPA Director of Solid Waste, confirms that hazardous waste incinerators cannot meet EPA requirements for near-total destruction o f hazardous wastes. (See RH W N #280.)
EPA's incinerator regulations require 99.99 percent destruction of all hazardous wastes and 99.9999 percent destruction of especially-hazardous wastes such as PCBs and dioxins. The Lowrance memo dated Sept. 22,1992, and interviews with Sonya Sasseville o f Ms. Lowrance's staff, confirm that the agency possessed scientific information as early as 1984 showing that hazardous waste incin erators cannot destroy some of the most dangerous wastes as completely as the regulations require.
EPA possessed this information but chose to ignore it when hazardous waste incinerator regula tions were established for dioxin in 1985.
These new revelations cast doubt on the safety o f all hazardous waste incinerators, and could conceivably lead to charges of criminal wrongdoing by some EPA officials. The agency has been touting incineration as "safe" for more than a decade. When asked, agency officials define "safe" as "in compliance with all regulations." In sum, the agency established regulations in 1985 knowing no incinerator could comply, and now the agency's own logic forces the conclusion that no hazardous waste incinerator can be operated safely. It would appear to expose the agency to liability claims by anyone believing they have been harmed by incinerator emissions.
EPA's acknowledgement of its malfeasance surfaced during an incinerator battle in Jacksonville, Arkansas. For the past decade Arkansas Governor Bill Clinton and the citizens of Jacksonville, have been battling each other over the Governor's plan to bum dioxin-contaminated chemical warfare , agents in a residential neighborhood of Jacksonville. (See RH W N #311.) EPA officials in Region 6 (Dallas, Texas) supported the Governor's plan.
The Jacksonville wastes contain an estimated 75 pounds (34 kilograms) of pure dioxin, a poison that kills laboratory animals such as guinea pigs exposed to only a few micrograms, making it one of the most powerful poisons ever found. From 1988 onward, federal and state environmental officials in Jacksonville said publicly on numerous occasions that an incinerator could destroy dioxin with 99.9999 percent efficiency, thus eliminating all health threats to the surrounding community. The Lowrance memo makes it clear that Region 6 EPA officials were either lying or were kept ignorant by officials at EPA headquarters in Washington who knew the truth.
EPA's regulatory failure was discovered when an independent researcher, chemist Pat Costner of Greenpeace, analyzed government data, from the Jacksonville incinerator as it was being tested before startup. In early 1992, Costner analyzed government data collected during an October, 1991, trial bum in Jacksonville. H er analysis revealed that instead of 99.9999 percent ("six nines") destruction, the Jacksonville incinerator had achieved only 99.96 percent destruction o f dioxin. Federal and state officials confirmed her analysis. At that rate the Jacksonville incinerator would release 400 times as much dioxin as the regulations say it should.
How the R egulations W ork
EPA's hazardous waste regulations require the owner/operator of a new incinerator to select several POHCs (principal organic hazardous constituents)-chemicals to be destroyed. The selected POHCs must be harder to bum than dioxin. The POHCs are "surrogates" for dioxin-they "stand for" dioxin or "represent" dioxin during the test. During a "trial bum," the POHC surrogates are fed into the incinerator in nearly pure form under ideal laboratory conditions, and the incinerator's ability to destroy them is measured. If a destruction/removal efficiency (DRE) of 99.9999 percent is achieved with the POHCs, then EPA allows the owner/operator to assume that 99.9999 percent of dioxin will also have been destroyed. It is this assumption that EPA has known since 1984 is false.
The trial bum procedure was followed precisely in the Jacksonville case, with one exception. The owner/operator inadvertently burned some actual dioxin along with the POHCs during the trial bum and dutifully reported the D R E for the POHCs, but did not analyze the data to establish a DRE
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for dioxin. Costner did the calculation for dioxin and revealed that dioxin was not destroyed with an efficiency anywhere near six nines.
Since Region 6 officials had been promising for several years that the Jacksonville incinerator would destroy dioxin with six nines efficiency, Costner's analysis made them look like fools o r liars or both. Region 6 called headquarters for guidance and on September 22, Sylvia Lowrance sent out a memo telling regional EPA offices how to handle this embarrassing situation.
The Lowrance memo says, in part, T h e low dioxin D R E in this recent [Jacksonville] case was consistent with our current body of incinerator performance data, which show a very clear trend of decreasing D R E for hazardous constituents with decreasing incoming concentration o f the constituents in the waste feed. (That is, the lower the constituent concentration in the waste, the lower the DRE.) The data show that a properly operating incinerator, which reached 99.99% D RE (four nines) on higher concentrations of POHCs, will often achieve less than four nines when the concentration of a POHC (principal organic hazardous constituent) in the waste is less than 1000 ppm [parts per million]. At this time we have not established a definitive scientific explanation for this phenomenon," the memo says.
The Lowrance memo goes on to point out that, in establishing regulations for incineration of dioxin-contaminated wastes, in 1985, EPA relied on risk assessments in which the agency assumed that 99.9999 percent destruction was routinely achieved. "For this reason, the risk assessment calculations performed in the course of the rulemaking may not be representative in some cases," the Lowrance memo says. In sum, the entire superstructure o f regulations created for dioxin incineration in 1985 was based on assumptions that the agency knew at the time were false. Indeed, in an internal EPA memo dated October 24, 1985, Robert A. Olexsey, who was at the time an employee of EPA's Hazardous Waste Environmental Research Laboratory, wrote "We have a problem with the 'surrogate POHC* approach for the determination o f the dioxin destruction efficiency. In our incinerator and boiler field tests, we found a consistent relationship.... In essence, across the entire test program, POHC DRE increased with increasing POHC concentration in the feed. If this relationship holds for dioxin (we see no reason why it would not), reporting the D R E for the dioxin material as being identical to that of the higher concentration surrogate will result in overstating the D R E for the dioxin waste." Olexsey went on to recommend that dioxin itself be measured during incinerator tests, to check the efficiency of destruction, rather than testing a POHC and assuming that it revealed something about dioxin. Olexsey's advice was not followed.
During 1984-1985, John C. Kramlich of the Energy and Environmental Research Corporation (Irvine, Cal.) completed a contract study for EPA, analyzing the failure of hazardous waste incinerators to destroy wastes. EPA did not publish the Kramlich study until 1989. Kramlich wrote, "[Our] results indicate that current technology has difficulty meeting the licensing regulations when the waste represents less than 1000 ppm [parts per million] o f the feed stream. This finding has significance with respect to waste streams contaminated by low concentrations o f extremely hazardous materials (e.g. dioxin or chlorophenol contaminated pesticides)."1
EPA's data reveal that all incinerators fail in the same way, but the public health hazard seems especially great at sites burning wood-preservative wastes, pesticides, PCBs, pulp and paper mill sludges, or dioxins. All contaminated-soil incinerators, all Superfund cleanup incinerators, and all of the Army's proposed chemical weapons incinerators are also cast into doubt by EPA's recent admissions. Furthermore, all of the agency's risk assessments and rulemakings regarding hazardous waste incinerators are now known to have been based on false assumptions. In short, the entire regulatory structureIntended to guarantee the protection of public health and safety from hazardous waste incinerators has now been thrown into grave question.
[1] John C. Kramlich and others, ExperimentalInvestigation o f CriticalFundamentalIssues in Hazardous Waste Incineration (Springfield, VA: National Technical Information Service [NUS], September, 1989.) H iis is EPA document No. EPA/600/2-89/048 available from NTTS for $26.00; phone (800) 553-6847 and request NTIS document No. PB90-108507. See pgs. 5-1,5-2.
[Dated announcement omitted from this reprint.]
Reprint o f RacheVs Hazardous Waste News 41312 Rachel's Hazardous Waste News (ISSN 1065-4623) is published weekly by Environmental Research Foundation (ERF), P.O. Box 5036, Annapolis, MD 21403-7036; Telephone (410) 263-1584; Fax (410) 263-8944; Econet: erf; Internet: erf@igc.apc.org. Editor Peter Montague, Ph.D.; Associate editor: Maria B. Pellerano; Research Assistant: Andrea K. Feameyhough. Subscription rates: 325 per year for individuals and citizen groups; $80 for professionals and government agencies; $15 for students and seniors with ID; $400 for businesses; in Canada and Mexico, add $6.00; in all other countries, add $11.00. A ll payments in U.S. funds drawn on U.S. banks. Visa & Mastercard accepted. Rachel's H azardous Waste News is not copyrighted; we encourage reprinting so long as you send us a copy. Printed on 100% recycled paper.
000119
Reprint of:
RACHEL'S HAZARDOUS WASTE NEWS # 3 1 4
Providing news and resources to the Movement for Environmental Justice --December 2,1992
CEMENT AND KILN DUST CONTAIN DIOXINS
During routine preparation of a Report to Congress on Cement Kilns, the U.S. Environmental Protection Agency (EPA) has learned that cement and cement kiln dust contain dioxins and furans (both of which are powerful poisons in animals and humans), according to a briefing document dated October 8,1992, prepared by EPA staff for EPA's Director o f Solid Waste, Sylvia Lowrance. The October briering document also says 20 percent of the cement kiln dust that EPA tested contains the non-natural radioactive elements plutonium-238, plutonium-239and cesium-137. Dioxins are the most powerful carcinogens (cancer-causing agents) ever tested in laboratory animals; plutonium is the most potent carcinogen in humans ever discovered.
Cement is a principal component of pipe often used to distribute drinking water in many American cities. Cement kiln dust is a byproduct of cement manufacture and is routinely given o r sold to farmers as a soil treatment, or is discarded into pits or is piled on the ground near cement kilns in an uncontrolled fashion. According to Bill Schoenbom, an EPA staff member working on the Report to Congress, about 6 million tons of kiln dust is disposed of each year by cement kilns, 5.1 million tons of it buried on-site, and 900,000 tons of it shipped off-site for use in stabilizing other wastes (such as sewage sludge) or as a soil additive on farms. Cement kiln dust has previously been reported to con taminate groundwater with the toxic metals lead and chromium,1but until now no one has reported dioxins, furans, plutonium or cesium-137 in cement or cement kiln dust.
The Report to Congress is required by the federal Resource Conservation and Recovery Act (RCRA), the nation's basic hazardous waste law. Like mine wastes, cement kiln dust was initially exempt from RCRA because it is a high-volume waste presumed to be low in toxicity. Cement clinker (that is to say, cement itself) is exempt from RCRA because it is a product, not a waste. Section 8002(o) of RCRA required EPA to study cement kiln dust and to write a report for Congress on its findings. For several years, EPA dragged its feet preparing the report. Then Environmental Defense Fund (EDF) brought' a lawsuit, and now EPA is under a court order to finish the report by April, 1993.
In the course of preparing the Report to Congress, EPA randomly selected 15 cement manufacturing plants (called kilns) for sampling, out of the 114 such plants presently operating in the U.S. O f the 15 plants sampled, eight bum hazardous waste as fuel and seven do not. In recent years, cement kiln operators have increasingly been using hazardous waste as fuel, to reduce fuel costs and thus increase profitability. The practice has proved controversial. (See RHW N # 174 and # 243.) Opponents of the practice say they fear cement will become contaminated with industrial poisons. Cement is a key raw material in concrete pipe for water delivery systems, and in concrete block and other concrete materials used in construction of private homes, commercial dwellings, public buildings, bridges and highways. Seventy to 80 million tons of cement are produced in the U.S. each year, depending on market demand.
Sam pling R esults
EPA took 15 samples of "clinker'' (the product of a kiln, from which cement is made), plus 28 samples of dust (the unwanted byproduct of a kiln). All samples were analyzed for metals, chloride, cyanide, fluoride, total sulfate, total organic carbon, moisture content, and radioactive elements.
Samples from six kilns (4 burning hazardous waste, 2 not burning hazardous waste) were tested for dioxins and furans, volatile organic compounds, semivolatile organic compounds, and pesticides. All chemical analyses were completed by EPA's National Air and Radiation Environmental Laboratory (NAREL) in Alabama.
Dioxins and furans were detected in all samples of "clinker" and all samples of kiln dust analyzed for these compounds. The October briefing document says that the dioxin molecule known as 2,3,7,8TCDD, the most potent poison in the dioxin family, was only identified in samples from kilns burning hazardous waste. Other dioxins were found in samples from kilns not burning hazardous waste, but no 2,3,7,8-TCDD. However, the October briefing document says it is not possible to generalize these differences to the entire 114 operating cement kilns.
Samples of cement kiln "clinker" did not contain pesticides or semivolatile organics. Clinker was not analyzed for volatile organics. On the other hand, cement kiln dust contained amounts o f the volatile organics benzene and acetonitrile that exceeded RCRA limits "in a number of the samples of
000120hazardous waste burners" but not in samples from kilns not burning hazardous wastes. The dust from
one kiln not burning hazardous waste proved to be high in methylene chloride, according to the October briefing document.
These findings lend support to the view that burning hazardous waste in a cement kiln increases the amount and potency of toxins in the resulting cement kiln dust and perhaps in the cement itself.
At three kilns (2 burning hazardous waste, one not burning hazardous waste) levels of naturallyoccurring radioactive radium-226 exceeded the cleanup standard for uranium mine and mill wastes (the standard being 5 picoCuries per gram). Cesium-137, a non-natural radioactive element, was present in the dust of 26 percent of the kilns tested (4 out of 15)--one hazardous waste burner and three non-hazardous waste burners. Plutonium-238 and plutomum-239 were detected in kiln dust samples from 3 of the 15 kilns tested. Each of these 3 facilities is "located near a D O E [U.S. Depart ment of Energy] nuclear weapons production/testing facility," according to EPA's October briefing document. Plutonium and cesium-137 do not occur in nature but are created by nuclear bomb explosions and in nuclear power reactors.
A second EPA briefing document dated November24,1992, contains additional information about the problem of potent toxins being found in cement and in cement kiln dust. The document is titled "OSW Office Briefing on Cement Kiln Dust Risk Screening" and it contains a summary of a risk assessment that is being conducted by the EPA's Communications and Budget Division within the Regulatory Analysis Branch, Office of Solid Waste.
The Novemberbriefing document outlines two risk assessment scenarios: one in which cement dust blows off-site and affects a person living 750 feet from an active waste pile, and a second in which an individual is presumed to be living on top of an abandoned waste pile. No risk assessment was reported for the case of a farmer growing crops in soil to which cement kiln dust has been added.
Furthermore, no risk assessment is reported for the dioxins and furans measured in cement clinker, which it to say, in cement itself.
Based on the two risk assessment scenarios, the November briefing document describes amounts of toxins in cement kiln dust that appear to be acceptable, which is to say will only give cancer to one in 100,000 individuals so exposed. The November document lists 22 instances in which one or more EPA tests of cement kiln dust exceeded the criteria developed in the risk assessments. Criteria that are exceeded by one or more samples include: 2,3,7,8-TCDD,total dioxins, total dioxins and furans, total hexachloro dioxins, arsenic, beryllium, cadmium, chromium, lead, and thallium, plus the following radioactive elements: bismuth-214, cesium-137, potassium-40, lead-212, lead-214, radium-226, radium- 228 and thorium-227.
The purpose of the risk assessments reported in the November document is to help EPA decide whether the agency needs to regulate cement kiln dust as a legally hazardous waste or not. Declaring cement kiln dust a legally hazardous waste would greatly increase the cost of waste disposal for some cement kilns, and thus might reduce the profitability of some kilns.
EPA employee Hugh Kaufinan has previously charged that the agency has been "accommodating the regulated cement kiln hazardous waste incineration industry with nonexistent, or at best loose, regulation..."2
Now that EPA has found dioxins in cement clinker, and dioxins and radioactive elements in cement kiln dust, the agency will likely come under considerable pressure to regulate all cement kiln wastes as hazardous wastes.
For their part, citizens seem likely to start asking themselves anew whether kilns can be good neighbors.
[1] Jeffrey D. Smith, "Cement Kilns 1991," E l Digest (August, 1991), pgs. 20-32. [2] Kaufinan made his charge in a letter to EPA chief William Reilly dated Dec. 7,1990; on February 21,1991, cement kilns burning hazardous waste became regulated under the so-called "BIF" (boiler and industrial furnace) regulations, which can be found in the Federal Register February 21,1991, pgs. 7134-7240. See also Federal Register July 17,1991, pgs. 32688-32692; August 27, 1991, pgs. 42504-42517; September 5,1991, pgs. 43874-43877; and August 25,1992, pgs. 3855838566.
[Dated announcement omitted from this reprint.]
Reprint o f R achel's Hazardous Waste News #314
Rachel's Hazardous Waste News (ISSN 1065-4623) is published weekly by Environmental Research Foundation (ERF),
P.O. Box 5036, Annapolis, MD 21403-7036; Telephone (410) 263-1584; Fax (410) 263-8944; Econet: erf; Internet:
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000121
Reprint of:
RACHEL'S HAZARDOUS WASTE NEWS #325
Providing news and resources to the Movement for Environmental Justice -- February 17, 1993
A SEA OF TROUBLES ENGULFS INCINERATION
The incineration industry has suffered a series of major setbacks in recent weeks. The federal govern ment's showcase dioxin-burning incinerator in Jacksonville, Arkansas~to which Bill Clinton personally gave a green light one week before he was elected President (see RH W N # 3 1 1 )-was shut down last week by a federal judge. Lawyers for EPA (U.S. Environmental Protection Agency) admitted to U.S. District Judge Stephen Reasoner in Little Rock that the Jacksonville incinerator could not destroy 99.9999% of the dioxin fed into it, as is required by EPA regulations, whereupon the judge ordered the plant shut.
It was a stunning victory for Greenpeace chemist Pat Costner, who had been the first to reveal that incinerators could not achieve 99.9999% destruction (see RH W N #312 and #280), and for local activist-citi zens like Sharon Golgan in Jacksonville who had fought the incinerator proposal for at least six years.
The nation's other showcase incinerator-built by Waste Technologies Industries (WTI) on the banks of the Ohio River in East Liverpool, Ohio-was fighting for its life in federal court in Cleveland earlier this week. Local citizens there have been opposing the WTI incinerator proposal for 12 years. EPA's Region 5 ofGce in Chicago and Ohio state officials bent the rules, and even broke a few, to give WTI a permit to start burning wastes (see RH W N #287). The state of West Virginia, local citizens, and Greenpeace filed a lawsuit January 13 asking a federal judge to prevent WTI from conducting a "test burn."1 As soon as a test bum is completed, the WTI incinerator can begin commercial operation for up to a year while EPA evaluates the test results. (Vice-President A1 Gore said December 7, 1992, that he and Mr. Clinton would stop WTI from proceeding until a study was completed of all health issues, and all legal issues surrounding EPA's issuance of a permit [see RH W N # 3 i5 ]-b u t it now appears that Mr. Gore has changed his mind.) Federal Judge Ann Aldrich in Cleveland issued a temporary restraining order against WTI January 15 and set February 16 as the day she would decide whether to issue a preliminary injunction, which would prevent WTI from conducting the trial burn until a full court trial could be held.2
As we go to press, it is not clear how this phase of the battle will come out. However, secret EPA docu ments that came to light during in court have raised serious health questions about every incinerator in the country, including solid waste incinerators.
Background At issue in every instance is dioxin, which is created as an unwanted byproduct of incineration (and as a byproduct of other industrial processes, such as pulp and paper manufacture, and the manufacture of some pesticides). In April, 1991, EPA began a major "scientific reassessment" of dioxin and discovered that effects of dioxin can be observed in human cells at the levels of exposure now present in the environment. In other words, there's already sufficient dioxin in the environment to produce observable effects in humans. The Clinton/Gore administration knows this is a problem because a December, 1992, briefing document prepared by the EPA Transition Team says, "This [EPA's dioxin reassessment] is likely to be an extremely controversial document as there are new findings indicating adverse reproductive effects at existing environmental levels." A Secret Risk Assessment and a Leaked Memo EPA's position throughout the 1980s has been that incineration is safe, even though every incinerator is known to produce dioxin. To "prove" the safety of incinerators, EPA has used a technique called "risk asses sment." A risk assessment estimates the amount of dioxin being released, estimates various pathways it might travel through the environment, and calculates the resulting exposures of humans. Finally, a risk assessment estimates the health effects resulting from the calculated exposures. In the case of dioxin, over the years EPA's "standard" risk assessment has assumed that airborne dioxin only enters humans through their lungs. Dioxin that falls to the ground and is then incorporated into the food chain and eaten has always been ignored in EPA risk assessments. However, the EPA's team of scientists conducting the official "reassessment" of dioxin's toxicity published a draft report last summer called, Estimating Exposure to Dioxin-like Compounds in which they clearly stated that a proper risk assessment for an incinerator must include all routes of exposure for dioxin, not merely via the lungs.3 It is well known that dioxins accumulate in the food chain, and that meat, milk and fish are the major sources of dioxin exposure for humans.4 When Greenpeace researcher Joe Thornton did his own risk assessment on the WTI incinerator, using the technique recommended in EPA's draft report, including dioxins in beef and milk, he found that WTI posed risks 10000 times higher than EPA had calculated. To counter Thornton, EPA did its own food-chain risk assessment, which was not released to the public, but which came to light in court.5 The EPA's secret risk assessment concludes that dioxin from WTI is 1000 times more dangerous than the "ofGcial" published EPA risk assessment says it is. Leaving aside the serious ethical issue of EPA refusing to publish important health and safety information about WTI, an internal memo from Richard Guimond, acting chief of EPA's OfGce of Solid Waste and
C 001Z 2
Emergency Response, dated January 22,1993, leaked to Greenpeace, says, "There are very serious implica tions associated with adopting risk assessment procedures based on indirect exposure routes for air em ission sources."6 Translation: if food-chain exposures are now to be counted in incinerator risk assessm ents, many incinerators will be found to be unacceptably dangerous.
T he new understanding o f dioxin-that it's already present in the environment at levels that affect humans-plus the inclusion o f food-chain exposures in risk assessments, plus the failure o f incinerators to achieve the destruction efficiencies required by regulations~all seem to add up to a mushrooming debacle for the incin eration industry.
What are the alternatives to incineration? Jacksonville holds the key EPA scientists have known since 1985 that incinerators cannot achieve 99.9999% efficiency in destroying wastes present in low concentrations (seeR H W N # 2 8 0 and # 3 1 2 .), but EPA officials have stated at hundreds o f public presentations since 1985 that 99.9999% could be achieved. Lying to the public carries no penalty, but tying to a judge is a different matter. A t the hearing in Little Rock February 12, E P A was represented by U.S. Justice Departm ent lawyer R on Spritzer. Judge Reasoner said to Spritzer, "Indulge m e for a m o m en t If I asked you to prove that you could achieve a six 9 D R E [99.9999% destruction and removal efficiency] on dioxin, could you physically produce technological data that shows that?" "No sir, w e could not," said Mr. Spritzer.7 That damaging admission was sufficient for the judge. H e ordered the plant shut. EPA is considering appealing the judge's verdict, but they do not appear to have a strong case. In all likelihood, the Jacksonville incinerator is shut for good. T he Jacksonville incinerator w as in considerable trouble even before Judge R easoner's decision. O n Jan uary 22, an Arkansas state official revealed that the incinerator was producing a larger volum e o f hazardous waste than it was destroying. The machine had been set up in a residential neighborhood o f Jacksonville to "destroy" 30,000 drums o f hazardous liquids left over from a defunct chemical factory that had m ade chemical warfare agents on the site for many years (most recently, herbicides for Vietnam). Local citizens had recom m ended moving the waste out of town by rail, or simply building a concrete mausoleum on the site to contain the waste safety until som eone found a way to detoxify i t But Arkansas and federal E PA ofGcials insisted that incineration was the safest, cheapest solution to the problem. They convinced then-Govem or Bill Clinton to put up $10.7 million o f state money to build and operate the incinerator. A t the end o f a year's burning, 9,600 drums o f waste had been "destroyed" by the Jacksonville incinerator, but in the process the incinerator had created 12,000 drums o f salt and another 1730 drums o f ash (13,730 drums total) for a net gain o f 43% in the volume of waste. Furthermore, the salt and the ash are so laced with dioxin that they are legally a "hazardous waste" and thus cannot be taken o ff the site. "We did not anticipate this," said D o u g Szenher, a spokesperson for the Arkansas state department o f Pol lution Control and Ecology. "The w hole idea was that the salt and ash was to have been de-listed [declared non-hazardous] and taken to a landfill site. It just didn't work out that way," he said.8 So after spending $7 million burning chemicals fruitlessly for a year, EPA is now spending $400,000 to build a 30,000-square-foot building on the site, to store the hazardous salt and ash until som eone can Ggure out how to detoxify it. So far as w e know, this is the first above-ground mausoleum built to store hazardous waste. (See RH W N # 2 6 0 .) In Jacksonville, above-ground concrete storage will soon be a real, demonstrated alternative to incineration.
[1] Greenwire staff, "WTI Incinerator Foes File Suit in Effort to Block Test," Greenwire Vol. 2 No. 171 (January 14,1993). Greenwire is "the daily executive briefing on the environment" available on-line; phone (703) 237-5130. [2] Greenwire staff, "Incinerator:WTI Counterswith Suit of its Own," Greenwire Vol. 2 No. 172 (January 15,1993). Greenwire is "the daily executive briefing on the environment" available on-line; phone (703) 237-5130. [3] U.S. Environmental Protection Agency, Estimating Exposure to Dioxin-Like Compounds [EPA/600I6-88J005B] Workshop Review Draft (Washington, D .C: U.S. Environmental Protection Agency, August, 1992). [4] U.S. Environmental Protection Agency, cited above, Appendix B. [5] Memo from William Farland, director o f EPA's Office of Health and Environmental Assessment, to Brian Grant, U.S. Department o f Justice, "WTI Screening Level Analysis," dated Feb. 8, 1993, attaching a 21-page risk assessment called "Screening Level Analysis o f Impacts From WTI Facility," dated Feb. 5,1993. [6] Memo from Richard Guimond, Acting Assistant Administrator, Office o f Solid Waste and Emergency response, to EPA Administrator Carol Browner, "WIT Incinerator Issues," dated January 22,1993.2 pgs. [7] Sandy Davis, "Judge Halts Dioxin Bum at Vertac "Arkansas Democrat Gazette February 13,1993, pgs. 1A, 13A [8] Sandy Davis, "At vertac, more waste rolls out than Arkansas Democrat Gazette January 24,1993, pg. 12A
Reprint o f RacheVs Hazardous Waste News #325 Rachel's Hazardous Waste News (ISSN 1065-4623) is published weekly by Environmental Research Foundation (ERF), P.O. Box 5036, Annapolis, MD 21403-7036; Telephone (410) 263-1584; Fax (410) 263-8944; Econet: erf; Internet: erf@igc.apc.org. Editor; Peter Montague, Ph.D.; Associate editor Maria B. Pellerano; Research Assistant: Andrea K. Feameyhough. Subscription rates: $25 per year for individuals and citizen groups; $80 for professionals and government agencies; $15 for students and seniors with ID; $400 for businesses; in Canada and Mexico, add $6.00; in all other countries, add $11.00. All payments in U.S. funds drawn on U.S. banks. Visa & Mastercard accepted. Rachel's Hazardous Waste News is not copyrighted; we encourage reprinting so long as you send us a copy. Printed on 100% recycled paper.
000123
Studies on Dioxin
C001Z4
Reprint of:
RACHEL'S HAZARDOUS WASTE NEWS # 7 3
Providing news and resources to the Movement for Environmental Justice --April 18, 1988
STUDY OF DIOXIN-EXPOSED HUMANS REVEALS CANCER, BIRTH DEFECTS, LIVER AND CARDIOVASCULAR DAMAGE
A new study of Vietnam veterans, conducted by A ir Force physicians, links dioxin exposure to increases in cancer, birth defects, psychological damage, liver damage, cardiovascular deterioration, and degeneration of the endocrine system, The new work stops short of saying dioxin exposures caused the observable health dam age am ong dioxinexposed vets, b u t it explicitly reverses the conclusions of a 1984 A ir Force study which said dioxin exposures had been shown to be harmless.
T he study is continuing, and will begin using sensitive new blood tests to determ ine past exposures to dioxin; future study may be able to pin down, or rule out, direct causal effects. In the m eantim e, advocates of mass burn incinerators and other dioxin-producing facilities can no longer claim lack of evidence that dioxin harm s humans. T here is now tangible cause for concern about serious effects of dioxin on humans.
T h e new w ork is p a rt of th e A ir F o rce's ongoing study o f V ietnam v eteran s w ho partici pated in O peration Ranch H and, which was a military program spraying herbicides on the jungles o f V ietnam from 1961 to 1972, to defoliate and thus eradicate V iet Cong hiding places. In m anufacture, the herbicides (Agents Orange, Pink, G reen and Purple) were contam inated w ith dioxin (33 ppm to 66 ppm [parts p er million]).
T h e study com pares two groups of V ietnam v eteran s--one group o f 1045 R an ch H ands who definitely had dioxin exposures and another group of 773 veterans not known to have been exposed to dioxin. In addition, 2708 wives and form er wives of veterans in the two groups participated in the study.
Tlie study team first reviewed m ore than 400 published articles on the effects of dioxin on animals and hum ans; from this they derived a profile of 190 different health effects th at m ight be expected to be related to dioxin exposure. They examined the 1818 study participants for these 190 health effects.
Cancer The study found that 4.59% of the R anch H ands have some kind of cancer, compared to 2.33% of th e unexposed group. iThus the overall risk of cancer am ong the dioxin-exposed group is doubled (risk increased by a factor of 1.97). T he greatest risk increase is for skin cancers (w here th e risk is increased by a factor of 2.6), w hereas th e risk of "systemic cancers" (non-skin cancers) is increased by a facto r o f 1.2; in o th er words, th e dioxinexposed group has a 20% greater chance of getting a non-skin cancer.
B irth Defects Analyzing for birth defects, the study looked at children bom before the Vietnam experience and children born after Vietnam . Prior to Vietnam, the dioxin-exposed group had born 85% as many children with birth defects as the non-exposed group; after Vietnam, the exposed group bore 139% as many children with birth defects. The earlier A ir Force study had said birth defects am ong dioxin-exposed families w ere limited to "minor skin lesions" b u t the new study reverses that conclusion; 32 children with severe defects were b o m to fam ilies in the exposed group, vs. 18 in th e non-exposed group. T he to ta l num ber of birth defects in the two groups was: 80 with defects o u t of 917 total births in th e exposed group vs. 48 with defects out of 744 total births in the non-exposed group.
0001^5
Psychological Damage Psychological testing revealed significant increases in fatigue, anger, anxiety, and isolation among the dioxin-exposed group compared to the non-exposed group.
Liver Functions The new study looked at nine chemical measures of liver function and in three categories the dioxin-exposed group showed reduced liver functions, com pared to the non-exposed group. In addition, am ong th e exposed group, 16 showed enlarged livers, vs. six am ong th e non-exposed group. F u rth erm o re, 13 am ong th e exposed group h ad a verifiable m edical history of liver disorder other than hepatitis, jaundice, or cirrhosis, vs. only two w ith such histories among the non-exposed group.
Cardiovascular system H eart disease rates and heart attack rates did not differ am ong the two groups. H ow ever, during physical exam ination, 10 d ifferent h e a rt pulse m easu rem en ts w ere taken in the extremities (e.g., the ankle), and statistically significant abnorm alities w ere found in one or m ore pulses in 12.8% of the exposed group vs. 9.4% of the non-exposed group. Abnorm al pulses in the extremities are evidence of blood circulation problems.
Endocrine system T he endocrine system is a body control system composed of a group of glands that m aintain a stable internal environm ent by producing chemical regulatory substances called horm ones. G lands that participate in the endocrine system include the pituitary, thyroid, parathyroid and adrenal glands, as well as the pancreas, ovaries and testicles. T he new study looked at five chemical m easures of endocrine system functions. In three of the five measures, the dioxin-exposed group showed abnorm al functioning of the endocrine system, com pared to the non-exposed group. Functioning of the endocrine system reduces with age, but the new study showed that, among the dioxin-exposed group, functioning of the endocrine system is being reduced m uch faster than am ong the non-exposed group. T hus th e new study shows th at, in six o u t of 11 areas o f suspected dioxin effects, exposed Vietnam veterans have health problem s in greater proportion than the com parison group. The Ranch H and Study (formally known as the Air Force H ealth Study [AFHS]) began in 1979 and is continuing. T h e m ost recen t publication, reviewed above, is: R ichard A. A lbanese, United States A ir Force Personnel and Exposure to H erbicide Orange, Interim R eport fo r Period M arch 1984 - February 1988 (U nited States A ir Force: B rooks A ir F orce Base, TX, Feb., 1988). T he study is 34 pages long; it is available from D r. A lbanese, U SA F School of Aerospace M edicine, H um an Systems Division (AFSC), Brooks A ir Force Base, TX 78235-5301; phone (512) 536-3884. O ur thanks to L aura Petrou, legislative assistant to U.S. Senator Thom as Daschle (South D akota) who m ade the study available to us. Ms. Petrou can be reached at (202) 224-2321.
[Dated announcem ent omitted from this reprint.]
Reprint o f Rachel's Hazardous Waste News # 7 3 Rachel's Hazardous Waste News (ISSN 1065-4623) is published weekly by Environmental Research Foundation (ERF), P.O. Box 5036, Annapolis, M D 21403-7036; Telephone (410) 263-1584; Fax (410) 263-8944; Econet: erf; Internet: erf@igc.apc.org. Editor: Peter Montague, Ph.D.; Associate editor: Maria B. Pellerano; Research Assistant: Andrea K. Feameyhough. Subscription rates: $25 per year for individuals and citizen groups; $80 for professionals and government agencies; $15 for students and seniors with ID; $400 for businesses; in Canada and Mexico, add $6.00; in all other countries, add $11.00. All payments in U.S. funds drawn on U.S. banks. Visa & Mastercard accepted. R achel's Hazardous Waste News is not copyrighted; we encourage reprinting so long as you send us a copy. Printed on 100% recycled paper.
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RACHEL'S HAZARDOUS WASTE NEWS # 1 2 0
Providing news and resources to the Movement for Environmental Justice --March 14,1989
DANGERS OF DIOXIN EXPOSURES: ABSORPTION THROUGH THE SKIN
Traditionally, people concerned about the toxicity of chemicals have mainly w orried about the m outh and lungs as a m eans of entry into the hum an body. Now new evidence suggests th at absorption through the skin may be an im portant way for some chemicals to enter the body. In addition, the skin of babies may allow m ore toxics to pass through it than the skin of older humans.
Researchers at the N ational Institute of Environm ental H ealth Sciences studied the absorption of dioxins and furans in mice and rats. They discovered several new aspects of chemical absorption by the skin: (1) the skin presents a m ore effective barrier against some chemicals than against others; (2) mice absorb a greater percent of dioxin when lower doses are adm inistered than when higher doses are administered; (3) young adult rats absorbed a greater percentage of the administered dose than did middle-aged rats.
In the past, the theoiy has been th a t the skin (which has a to tal area o f 1.3 square m eters in the adult hum an) has served as a passive barrier to chemicals. Now it is apparent th at the skin is very active in metabolizing (biologically altering) chemicals and th at these metabolic processes affect the way the body absorbs (or does not absorb) a particular chemical. Sweat glands, sebaceous glands (which produce oils), and hair follicles can all contribute to the way chemicals are absorbed through the skin.
Chemicals adm inistered at low doses are m ore effectively absorbed through the skin than are chem icals adm inistered a t high doses. M ice receiving 0.3 m icrogram s o f dioxin p er kilogram of body weight absorbed 40% of the dose; mice receiving 32 to 320 micrograms of dioxin per kilogram of body weight absorbed less than 20% of the dose. This may be im portant for hum an exposures, which usually occur a t low doses over long periods rather than in high doses over short periods.
T hree m onth old rats (young adults) absorbed 16% of dioxin applied to their skin; ninem onth-old rats (middle-aged) absorbed less than 5% of a similar dose.
Linda Bim baum , who directed the research, says that her work shows th at acute toxicity from skin exposure to dioxins and furans is "unlikely." C hronic (long-term ) toxicity is a different m atter: T h a t's w here "you're going to have th e p o ten tial to build up a body burden" of the toxic chemicals, she says. H er w ork with young rats also concerns her because there is evidence th at the skin of hum an babies is much m ore perm eable than skin of adults.
The im portance of this work for grass roots activists seems to be this: if som eone is going to expose your community to small amounts of dioxins and furans for a long time, ask them to please consider absorption through the skin, and especially so in the case of babies and chdren. Any risk assessments that have been done w ithout considering skin absorption should be redone in light of the new findings.
G et: David Brewster and others, "Comparative D erm al A bsorption of 2,3,7,8-Tetrachlorodibenzo-p-dioxin and T h ree Polychlorinated D ibenzofurans." Toxicology and A pplied Pharm acology, Vol. 97 (January, 1989), pgs. 156-166. R ep rin ts a re free from: L in d a S. Birnbaum , Systemic Toxicology Branch, N ational Institute of Environm ental H ealth Sciences, Research Triangle, N orth Carolina 27709; phone (919) 541-3212. Ask Ms. Birnbaum for a copy of her unpublished paper on absorption of dioxins by young rats, which she presented at a meeting of the Society of Toxicology in A tlanta, GA, the week of Feb. 27, 1989.
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NIOSH ISSUES CANCER ALERT FOR DIESEL EXHAUST FUMES
O ne reason why people often oppose a new facility is increased truck traffic. Trucks are big and noisy and subject to accidents, and w hen accidents occur involving trucks, th e re 's a high likelihood of fatalities.
However, the federal governm ent has recently concluded officially that there is another good reason to be concerned about increased truck traffic in your neighborhood: five separate studies in the last 3 years have shown that diesel exhaust certainly causes cancer in laboratory animals, and two studies of railroad workers show th at it causes cancer in humans as well. A s a result of this determ ination, the N ational Institute for Occupational Safety and H ealth (N IO SH ) has issued a special publication, Carcinogenic E ffects o f Exposure to D iesel Exhaust, offering this recom m endation: "As p ru d en t public health policy, employers should assess the conditions under which workers may be exposed to diesel exhaust and reduce exposures to th e lowest feasible limits." Citizens m ay reasonably ask: if NIO SH believes workers should not be exposed to diesel exhaust because of the cancer hazard, can health officials in other parts of governm ent believe th at the general public should continue to be exposed to diesel exhaust? Taken in this light, risk assessments that discuss only the traffic hazards associated with a facility are missing the m ajor point: diesel trucks can evidently kill innocent people even if no traffic accidents occur.
D iesel engines are m ore efficient than gasoline engines; they produce m ore horsepower per gallon of fuel, and they use a less-refined (thus cheaper and m ore plentiful) fuel. W hen diesel fuel b u m s in an engine's com bustion cham ber, th e resulting exhaust contains gases and particles (soot). T he gases include nitric oxide, nitrogen dioxide, oxides of sulfur, and hydrocarbons (e.g., ethylene, formaldehyde, m ethane, benzene, phenol, 1,3-butadiene, acrolein, and polynuclear arom atic hydrocarbons [PAHs], several of which are known carcinogens). O f the particles in diesel exhaust, 95% are less than 1 micron in diam eter and thus they are respirable, which is to say they are easily taken into the deepest portions of the hum an lung w here they may lodge forever. T he core of each particle is m ade up of pure carbon, bu t as m any as 18,000 different chemicals from the gaseous portion of the exhaust may be adsorbed (attached) onto the carbon core, and thus diesel exhaust can carry a whole host of exotic, toxic and carcinogenic chemicals into the deepest portions of your lung-dow n in the region where the transfer of gas occurs to put oxygen into your blood stream and to take carbon dioxide o u t
A s recently as 1986, N IO SH concluded th a t diesel exhaust did no t cause cancer in laboratory animals. However, in the period 1986-1988, five long-term anim al studies, and two epidemiologic studies of humans, all concluded that exposure to diesel exhaust causes lung cancer. As a result, N IO SH reversed itself and in August, 1988, issued a special "current intelligence bulletin" to get the word out that diesel fumes are dangerous. N IO SH estim ates th a t 1.35 m illion A m erican w orkers are routinely exposed to diesel exhausts.
G et: Carcinogenic E ffects ofE xposure to D ieselE xhaust [C urrent Intelligence Bulletin 50; D H H S (N IO SH ) Publication No. 88-116]. Cincinnati, OH: Division of Standards D evelopm ent and Technology Transfer, N IO SH , R o b ert A. T aft L aboratories [4676 C olum bia Parkway, C incinnati, O H 45226], A ugust, 1988; p h o n e (513) 533-8287. It's 30 pages and free.
Reprint o f R achel's Hazardous Waste News # 1 2 0
Rachel's Hazardous Waste News (ISSN 1065-4623) is published weekly by Environmental Research Foundation (ERF),
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RACHEL'S HAZARDOUS WASTE NEWS #171
Providing news and resources to the Movement for Environmental Justice --March 7,1990
Dioxin-Part 1 DIOXINS AND CANCER: FRAUDULENT STUDIES
F o r years, industry scientists have been claiming th e re 's n o evidence th a t dioxins cause cancer in hum ans. Now there is m ounting evidence that such claims rely heavily on studies that are fraudulent Two companies recently accused of producing fraudulent dioxin-andhealth data are M onsanto and BASF.
M onsanto A scientist with U.S. Environm ental Protection Agency (EPA ) says M onsanto falsified data in im portant studies that M onsanto used to support its claim th at dioxin does not cause cancer in hum ans. D r. C ate Jenkins, a chem ist in E P A 's O ffice o f Solid W aste and Em ergency Response, says E PA itself relied upon M onsanto's fraudulent data in setting health standards fo r dioxin, and Jenkins has asked th e E P A 's Science A dvisory B o ard to reo p en th e m a tte r of E P A 's dioxin standards, to tak e a fresh look a t available d ata.1 Two im portant sources of dioxins in the environm ent are old chemical dumps and the incineration of m unicipal solid wastes,2 which is why E PA is concerned about allowable levels of hum an exposures to dioxin. BASF T h e British technical journal, N ew Scientist, says, "A new analysis by a W est G erm an epidemiologist may have established the first clearcut evidence of a direct link between exposure to dioxins and cancer in humans. Friedem ann Rohleder, an independent specialist, has produced a report detailing an unexpectedly high incidence of cancer am ong w orkers exposed to dioxins during an industrial accident at a chemicals p lant in 1953.3 41T he plant, o p erated by th e W est G erm an com pany BA SF, m ad e trichlorophenol. R ohleder claims the company presented the data in a way that disguised the cancers," says N ew Scientist. Background Each of these claims of fraud relates to an industrial accident in which workers were exposed to dioxins; follow-up medical studies funded by the responsible com panies have been published in m ainstream scientific journals, claiming to show that no excess cancers have occurred in the dioxin-exposed workers. In fact, excess cancers have occurred, but it appears that the data have been m anipulated to hide the facts. The M onsanto Case In 1949, an explosion occurred at a M onsanto chemical factoiy in N itro, W est Virginia; as a result, many workers in the plant were exposed to the herbicide 2,4,5-T, which was contam inated with dioxin. (This herbicide was later the principal com ponent of Agent Orange, the chemical defoliant used by the U.S. in V iet Nam .) In subsequent years, two M onsanto scientists, J.A. Zack and R. W. Gaffey, studied the exposed workers, comparing their health against the health of a similar group of workers who w ere not exposed to dioxin or 2,4,5-T.4 According to court documents attached to the EPA memo,"Zack and Gaffey deliberately and knowingly om itted 5 deaths from the exposed group and took four workers who had been exposed and p u t these workers in the unexposed group, serving, of course, to decrease the death rate in the exposed group and increase the death rate in the unexposed group." O ther studies of this same accident were also fraudulent, according to the same court docum ents, including a study by R .R . Suskind published in th e Journal o f the Am erican M edical A ssociation. "This published study of th e w orkers exposed in the 1949 accident reported only 14 cancers in the exposed group and 6 in th e unexposed group (a sm aller cohort). H ow ever, th e m edical records produced [by M onsanto] to the Pli f [ / 2 9
conclusively prove gross miscalculations and omissions... there were 28 cancers in the group that had been exposed to dioxins in 1949 as opposed to only 2 cancers in the unexposed group." Mr. Suskind published two other reports6,7 on the same accident, using his same data, to reach the conclusion that dioxin does not cause cancer.
The BASF Case On the night of November 17, 1953, a runaway chemical reaction spewed dioxincontaminated chemicals over workers and community residents of two small German cities, Mannheim and Ludwigshafen. Subsequently, an epidemiological study was used to deny workers any compensation for ailments they claimed they suffered as a result of exposure. In keeping with German law, the workers retained their own expert to review the data. Their expert, Friedemann Rohleder, received the data from the German government but found, to his surprise, that all the data actually came from the BASF company itself. He analyzed the data and found that some workers suffering from chloracne, which is universally acknowledged to be evidence of high exposure to dioxin, had been placed in the low-exposure or non-exposed group. He found evidence of "diluting" the exposed group with 20 plant supervisory staff who, Rohleder believes, were not exposed. When Rohleder omitted the 20 supervisory staff, his analysis revealed statistically significant increases in two groups of cancers: cancers of the respiratory organs (lungs, trachea, etc.), and cancers of the digestive tract. "This analysis adds further evidence to an association between dioxin exposure and human malignancy," Rohleder told New Scientist. [To be continued.]
[1] Cate Jenkins, "Memo to Raymond Loehr: Newly Revealed Fraud by Monsanto in an Epidemiological Study Used by EPA to Assess Human health Effects from Dioxins," dated February 23,1990. Jenkins is a chemist with the Waste CharacterizationBranch(OS 332), Characterization and Assessment Division, U.S. EPA 401 M St., SW, Washington, DC 20460. Loehr is Chairperson of the Executive Committee of the Science Advisory Board (A-101), Office of the Administrator, U.S. EPA 401 M St., SW, Washington, DC 20460. The Jenkins memo has attached to it 25 pages of a brief filed in Case No. 5-88-0420, in the Appellate Court of Illinois, Fifth District by attorneys suing Monsanto on behalf of plaintiffs who say they were harmed when a Norfolk and Western railroad tank car derailed, spilling 19,000 gallons of a Monsanto chemical called "OCP-crude" into the community of Sturgeon, Missouri the night of January 10, 1979. Chief attorney for the plaintiffs is Rex Carr, 412 Missouri Avenue, East St. Louis, IL 62201; phone (618) 274-0434. Our thanks to Margo Blackwell, People Against the Incinerator (PATI), Bloomington, Indiana, and to EPA official William Sanjour, both of whom independently sent us the information about Monsanto. We can mail copies of the Jenkins memo and attachments (28 pages) for $14.00, which covers our actual costs of photocopying, handling and mailing. [2] Oak Ridge National Laboratory. Toxicological Profile for 2,3,7,8-Tetrachlorodibenzo-p-dioxin[ATSDR/TP-88/23,` PB89-214522] (Springfield, VA: National Technical Information Service, June, 1989), pg. 22, identifies dumps and incinerators as "the important sources of 2,3,7,8-TCDDexposure to the general population." This is the Agency for Toxic Substances and Disease Registry [ATSDR] toxicological profile for dioxin (See RUWN #169.) [3] Stephanie Wanchinksi, "New Analysis links dioxin to cancer," New Scientist October 28, 1989, pg. 24. Thanks to Paul Connett of Work on Waste USA, we have a copy of Friedemann Rohleder's paper, which he presented in late September at a dioxin conference in Toronto, Ontario; Rohleder's paper is entitled "Dioxins and Cancer MortalityReanalysis of the BASF Cohort." We can mail you the 14-page Rohleder paper for $7.00, or you can request a copy directly from the author; Friedemann Rohleder, Friedrich - Hebei Str. 13, 1712 Weme, West Germany. [4] Zack, J.A., and W. R. Gaffey, "A Mortality Study Of Workers Employed At The Monsanto Company Plant In Nitro, West Virginia," Environmental Science Research, Vol. 26 (1983), pgs. 575-591. [5] R.R. Suskind, and V.S. Hertzberg, "Human Health Effects Of 2,4,5-T And Its Toxic Contaminants,"/ou/7ia/ o f the American Medical Association, Vol. 251, No. 18 (1984), pgs. 2372-2380. [6] R.R. Suskind, "Chloracne, The Hallmark Of Dioxin Intoxication,'"ScandinavianJournal o f Work, Environmentand Health, Vol. 11, No. 3 (1985), pgs. 165-171. [7] R.R. Suskind, "Long-Term Health Effects Of Exposure To 2,4,5-T And/Or Its Contaminants," Chemosphere, Vol. 12, No. 4-5 (1983), pg. 769.
Reprint of Rachel's Hazardous Waste News #171 Rachel's Hazardous Waste News (ISSN 1065-4623) is published weekly by Environmental Research Foundation (ERF), P.O. Box 5036, Annapolis, MD 21403-7036; Telephone (410) 263-1584; Fax (410) 263-8944; Econct: erf; Internet: erf@igc.apc.org. Editor; Peter Montague, Ph.D.; Associate editor: Maria B. Pellcrano; Research Assistant; Andrea K. Feameyhough. Subscription rates; $25 per year for individuals and citizen groups; $80 for professionals and government agencies; $15 for students and seniors with ID; $400 for businesses; in Canada and Mexico, add $6.00; in all other countries, add $11.00. All payments in U.S. funds drawn on U.S. banks. Visa & Mastercard accepted. Rachel's Hazardous Waste News is not copyrighted; we encourage reprinting so long as you send us a copy. Pnnted on 100% recycled paper.
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RACHEL'S HAZARDOUS WASTE NEWS #173
Providing news and resources to the Movement for Environmental Justice --March 21,1990
Dioxin-Part 2 GAUGING THE TOXICITY OF DIOXIN
[Continuing our series on dioxin. Page numbers in parentheses refer to the ATSDR (the federal Agency for Toxic Substances and Disease Registry) Toxicological Profile for dioxin, cited in our last paragraph, below.]
It has become fashionable to pooh-pooh dioxin. We believe there are two reasons why this is occurring. First, some scientists have been publishing studies indicating that humans exposed to dioxin do not have an increased risk of cancer. As we saw in RH W N #171, some o f the most im portant of these studies have now been exposed as fraudulent. The second reason is that dioxin is so toxic that it is difficult to express its potency in normal terms; therefore the media frequently print scary claims without offering much evidence, leading some people to conclude (incorrectly) that there isn't much substance to any_ claims about the extreme toxicity o f dioxin.
In this series, we hope to lay the groundwork for an understanding o f dioxin, to help people put dioxin into perspective. Some of what follows may seem a bit more technical than you are ac customed to reading in this newsletter; but stick with it, and you'll see why we have taken this approach.
The scientific and medical evidence presented by ATSDR forces us to conclude that dioxin de serves our greatest respect. It seems to be one o f the two or three most toxic chemicals ever discovered, and it is produced as a byproduct of several different industrial processes. For years, industry has been dumping dioxin into the environment in large quantities without paying attention to the consequences. This does not mean there have been no consequences; it just means no one has made any systematic effort to tally them up.
Dioxin is a family of chemicals (75 in all) that does not occur naturally, nor is it intentionally manufactured by any industry (pg. 1). The most toxic dioxin is called 2,3,7,8-TCDD. Dioxins are produced as byproducts of the manufacture of some herbicides (for example, 2,4,5-T), wood preservatives made from trichlorophenols, and some germicides (for example, hexachlorophene). Dioxins are also produced by the manufacture of pulp and paper, by the combustion o f wood in the presence of chlorine, by fires involving chlorinated benzenes and biphenyls (e.g., PCBs), by the exhaust of automobiles burning leaded fbel, and by municipal solid waste incinerators.
ATSDR says, "2,3,7,8-TCDD is highly toxic to all laboratory animals tested...." (pg. 11). Even the most conservative of toxicologists says, "TCDD has been called the most toxic synthetic chemical known to man. If its acute toxicity to the guinea pig, and even the rat and mouse, is the criterion, the statement is probably correct.... TCDD is unquestionably a chemical o f supreme toxicity to experimental animals. Moreover, severe chronic effects from low dosages have also been demonstrated in experimental animals. Therefore, the concern about its effects on human health and the environment is understandable."1
In cases of high exposure of humans through industrial accidents, 2,3,7,8-TCDD causes a severe acne (called chloracne) which is not just a skin ailment; chloracne is a systemic disease that is more disfiguring than teenage acne and its effects last for years (in some cases, decades) after exposure (pgs. 3, 39).
There is "suggestive evidence" that 2,3,7,8-TCDD causes liver damage in humans (pgs. 3,52-53). It definitely causes severe liver damage in animals.
In animals, 2,3,7,8-TCDD is toxic to the immune system; such effects have not been proven in humans (pgs. 3, 40, 54-56). In animals, 2,3,7,8-TCDD causes reproductive disorders, including spontaneous abortions. Monkeys are particularly sensitive to reproductive effects from exposure to 2,3,7,8-TCDD. Such effects have not been proven in humans (pgs. 3, 17, 58-59). In animals, dioxin causes genetic damage (pgs. 60-61).
Both the U.S. Environmental Protection Agency (EPA) and the International Agency for Research on Cancer (IARC) have concluded that dioxin is a "probable human carcinogen" (pgs. 7, 61-68, 94). As we saw in RH W N #171, scientists within EPA have asked that this question be reviewed again because some of the key studies o f dioxin and cancer were fraudulent, and EPA has relied on these fraudulent studies to set current standards.
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How can we judge the toxicity of dioxin (or o f any chemical, for that matter)? One way is to look at the standards that have been set by regulatory agencies.
In the case of dioxin, HPA has calculated a "safe" dose, taking into consideration dioxin's ability to cause cancer. The "safe" dose is expressed in extremely small units: femtograms. There are 28 grams in an ounce, and one femtogram is 0.000,000,000,000,001 grams, or one quadrillionth of a gram, or 10*15 grams.
EPA believes that ingesting (eating) 6.4 femtograms (6.4 x 10 15 grams) o f 2,3,7,8-TCDD per kilogram of body weight per day would cause cancer in one in a million people so exposed (pg. 95). Since an average adult weighs 62 kilograms or 137 pounds (average men weigh 70 kilograms [154 pounds] and average women weigh 55 kg [120 pounds]), the EPA is saying that 397 femtograms of 2,3,7,8-TCDD consumed in food each day would kill one-in-a-million humans so exposed. Over a year's time, 397 femtograms per day add up to 145,000 femtograms; over a 70-year lifetime, this would add up to 10.1 million femtograms, so 10.1 million femtograms (or 0.01 micrograms) is the maximum amount you could safely get into your body during your entire lifetime, EPA believes.
How can we express this in terms that people can grasp? Let's compare it to one'single aspirin tablet. One aspirin tablet weighs 5 grains (or 325 milli grams, or 325 trillion femtograms), so to express one "safe" lifetime dose of 2,3,7,8-TCDD, you would take a single aspirin tablet and divide it into 32 million (actually 32,172,218) minuscule pieces. Then one of those tiny pieces would represent one "safe" lifetime dose o f 2,3,7,8-TCDD. Another comparison: A single grain of table salt weighs approximately 0.1 milligrams or 100 billion femtograms, so to get an amount of table salt that weighs the same amount as one "safe" lifetime dose of 2,3,7,8-TCDD, you would divide a single grain o f table salt into 9,900 microscopic pieces. One of those tiny pieces would represent a "safe" lifetime dose o f dioxin. The U.S. Food and Drug Administration (FDA) has its own way of calculating the same one-ina-million cancer risk and they believe the EPA has overestimated the hazard by a factor of 10. In other words, FD A believes you could represent a "safe" dose of 2,3,7,8-TCDD by dividing a single grain of table salt into 990 pieces, with one of those pieces representing a safe lifetime dose. The federal Centers for Disease Control (CDC) in Atlanta has done its own calculation, concluding that the cancer hazard from dioxin is about half-way between the EPA's estimate and the FDA's esti mate. EPA says 6.4 femtograms per kilogram of bodyweight per day is the safe dose; CDC says the correct number is 27.6; FD A says it's 57.2 (pg. 95). No m atter which agency does the calculation, there's no escaping the fact that dioxin is considered supremely toxic. One other way to understand the toxicity of dioxin is to compare the dioxin "reference dose" established by EPA to the "reference dose" they have set for other common toxic materials. The "reference dose" is the highest amount they believe you could eat regularly without incurring any disease (not considering cancer). The reference dose for dioxin is 0.000,000,001 milligrams per kilogram of body weight per day (mg/kgMay) (pg. 94); the reference dose for the toxic metal cadmium5 is 0.001 mg/kg/day and the "reference dose" for the toxic metal arsenic3 is the same as for cadmium. Thus we can see that EPA considers dioxin in food 1,000,000 times (one million times) more toxic than cadmium or arsenic, not counting the cancer hazard from dioxin. Yes, dioxin is toxic, no doubt about it.
[1] Fred H. Tschirley, "Dioxin," Scientific American Vol. 254 (February, 1986), pg. 34. [2] Agency for Toxic Substances and Disease Registry, Toxicological Profile for Cadmium (Springfield, VA: National Technical Information Service [NTIS], 5285 Port Royal Rd., Springfield, VA 22161; phone (703) 487-4650), pg. 76.;NTIS number PB89-194476. $21.95. [3] Agency for Toxic Substances and Disease Registry, Toxicological ProfileforArsenic (Springfield, VA: National Technical Information Service [NTIS], 5285 Port Royal Rd., Springfield, VA 22161; phone (703) 487-4650), pg. 92.; NTIS number PB89-185706. $21.95.
Get: Agency for Toxic Substances and Disease Registry, Toxicological Profile for 2,3,7,8-Tetrachlorodibenzo-p-Dioxin (Springfield, VA: National Technical Information Service [NTIS], 5285 Port Royal Rd., Springfield, VA 22161; phone (703) 487-4650); NTIS number PB89-214522. $21.95.
Reprint o f Rachel's Hazardous Waste News #175
Rachel's Hazardous Waste News (ISSN 1065-4623) is published weekly by Environmental Research Foundation (ERF),
P.O. Box 5036, Annapolis, MD 21403-7036; Telephone (410) 263-1584; Fax (410) 263-8944; Econet: erf; Internet:
erf@igc.apc.org. Editor Peter Montague, Ph.D.; Associate editor Maria B. Pellerano; Research Assistant: Andrea
K. Feameyhough. Subscription rates: $25 per year for individuals and citizen groups; $80 for professionals and
government agencies; $15 for students and seniors with ID; $400 for businesses; in Canada and Mexico, add $6.00;
in all other countries, add $11,00, A ll payments in U.S. funds drawn on U.S. banks. Visa & Mastercard accepted.
Rachel's H azardous Waste News is not copyrighted; we encourage reprinting so long as you send us a copy. Printed
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Reprint of:
RACHEL'S H A Z A R D O U S W A ST E N E W S # 1 7 5
Providing news and resources to the Movement for Environmental Justice --April 4, 1990
Dioxin-Part 3 NEW EVIDENCE THAT DIOXIN CAUSES HUMAN CANCERS AND OTHER DISEASES
Two recent studies, published in 1988 and 1989, have indicated a connection between exposure to dioxin and development of cancers in humans. Earlier studies had shown little evidence linking cancers to dioxins, but these earlier studies have now been challenged by U.S. government officials as fraudulent. (See RHWN # 171.) One of the recent studies also reveals a connection between dioxin exposure and a variety of non-cancer health effects, including heart attacks (among men), and digestive diseases, cirrhosis of the liver, gall bladder and biliary tract diseases, and genitourinary diseases (among women).
Seveso, Italy On July 10, 1976, an industrial disaster occurred at a chemical plant operated by the phar maceutical giant, Hoffman-La Roche, in the town of Meda, Italy. A visible chemical cloud containing dioxin (2,3,7,8-TCDD and other dioxins) spread over several square miles of populated countryside; most heavily hit was the community of Seveso. More than 200,000 peo ple aged 20 to 74 lived in towns near the accident. Nearly 31,000 people aged 20 to 74 lived in zones contaminated to some degree by the accident and about 200 individuals had such high exposures that they developed chloracne, an acne condition known to be caused by exposure to dioxins. A team of Italian physicians and researchers has been studying health conditions, including death certificates, of 30,703 people aged 20 to 74 living in areas termed "exposed," comparing people's experience there against a larger population of 167,391 individuals aged 20 to 74 living nearby in non-exposed areas. A recent report in iht American Journal of Epidemiology1reveals several elevated disease rates among the exposed group. The report covers the decade 1976 to 1986, which is a short period in which to find cancer occurrences. All cancers exhibit a "latency period" (or delay period) between the time a cancercausing exposure occurs and a cancer actually develops; the latency period varies from 7 to 40 or 50 years. Thus a study of cancers occurring 10 years after an exposure to cancer-causing chemicals could only reveal the earliest evidence of cancers and should be understood to be preliminary in nature. The results of the study are reported for people living in three areas, labeled zones A, B and R. Zone A is closest to the accident site and zone R extends several miles distant; zone B is between the two. The assumption is that people's exposure varied with distance from the accident. In zone A women had elevated cancers of the gall bladder and biliary tract. They also had elevated occurrences of circulatory diseases and of chronic rheumatic heart disease. Men in zone A had elevated occurrence of cerebrovascular disease (such as stroke). In zone B, men had elevated melanomas (serious skin cancers) and cancers of the lining of the chest cavity (pleura); women in zone B had elevated incidence of soft tissue sarcomas. In zone R, men had elevated incidence of cancers of the lining of the chest cavity (pleura), and they had increased incidence of all blood diseases, and of cerebrovascular disease; women in zone R had increased incidence of cancer of the uterus, as well as hypertensive vascular disease. The results reported above are averages for the entire decade. In the case of cancers, which would only begin to occur after a latency period, the time-period of interest is the second five years of the decade, and, accordingly, the Italian researchers reported results for each half of the decade. During the second half of the decade: In zone A there were no elevated cancer levels. In zone B, men showed elevated incidence of cancers of the lung, cancers of the lining of the chest cavity (pleura), serious skin cancers (melanoma), Hodgkin's disease (cancer of the lymph nodes), and leukemia. In zone B, women showed increased incidence of soft tissue sarcomas and of the thyroid gland. In zone R, men showed elevated incidence of leukemia, and women
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showed elevated incidence of cancer o f the brain. It is perhaps relevant to note th at two previous studies have implicated brain cancer with exposure to dioxins in weed killers.2,3
This study of the people exposed to dioxin during the Seveso accident does not prove that dioxin exposure caused the cancers or the other serious ailments from which these people suffer in abnormally high numbers (mainly diseases of the heart, blood, and arteries). Nevertheless, this study confirms that it is definitely misleading and untrue when anyone says there is "no evidence" of cancer or o th er serious diseases among hum ans exposed to dioxins. (In addition, an earlier U.S. government study has shown that Vietnam veterans exposed to Agent Orange [a weed killer contam inated with dioxin] suffer from elevated incidence of cancers, liver damage, cardiovascular deterioration, and degeneration o f the endocrine system.
S ce R H W N # 7 3 .)
Sweden Phenoxyacetic acids (for example, the weed killers known as 2,4,5-T and 2,4-D) are almost always contam inated with dioxins during manufacture. D uring the late 1970s, Swedish researchers studied workers who had been exposed to phenoxyacetic acids and found increased incidence of soft tissue sarcomas (rare cancers o f the connective tissues).4,3 D uring the mid'80s, several additional studies confirmed the relationship betw een soft tissue sarcomas and exposure to phenoxy herbicides, while other studies failed to confirm such a relationship. Now a new study has once again shown a three-fold increase in soft tissue sarcomas among workers exposed to phenoxy herbicides.6 This is the tenth study that we know o f showing a positive relationship betw een exposure to phenoxy herbicides and soft tissue sarcom as.7 Five studies have failed to confirm such a relationship.8 How can one m ake sense out of conflicting reports, w hen 10 studies show that certain chemicals cause cancer and 5 studies show that those same chemicals do not cause cancer? How can the public know what policies make sense to pursue? In our experience, people who make money manufacturing, or using, such chemicals prefer to argue that "we just don't know," and "until all the facts are in, we should not m ake any changes." U nfortunately, all the facts will never be in. People, including consumers buying phenoxy herbicides at the lawn-care store and politicians making laws, will always have to make decisions based on incomplete information. From our viewpoint, the key question is this: Is it m ore im portant to protect people and the environment from damage, or to protect chemicals from regulation, control and outright bans?
[1] Pier Alberto Bertazzi and others, "Ten-year Mortality Study o f the Population Involved in the Seveso Incident in 1976,"American Journal o f Epidem iology, Voi. 129 (1989), pgs. 1187-1200. [2] A. Bair and others, "Lung Cancer and Other Causes o f Death Among Licensed Pesticide Applicators," Journal o f the N ational Cancer Institute Voi. 71 (1983), pgs. 31-37. [3] D . Coggon and others, "Mortality o f Workers Exposed to 2-methyl-4-chlorophenoxy-aceticacid." Scandinavian Journal o f Work, Environment and Health Voi. 12 (1986), pgs. 448-454. [4] Olav Axelson and others, "Herbicide Exposure and Cancer Mortality," Scandinavian Journal o f Work, Environment and Health Voi. 6 (1980), pgs. 73-79. [5] Lennart Harde11and others, "MalignantLymphoma and Exposure to Chemicals, Especially OrganicSolvents,Chlorophenols, and Phenoxy Acids: A Case-Control Study." British Journal o f Cancer Voi. 43 (1981), pgs. 169-176. [6] Lennart Hardell and others, "The Association Between Soft Tissue Sarcomas and Exposure to Phenoxyacetic A cid s-A New Case-referent Study," Cancer Voi, 62 ( 1988), pgs. 652-656. [7] Nine o f the studies are listed in footnotes 1 through 9 o f the Hardell study we cited in our footnote 6 (above), and the tenth study is the Hardell study itself cited in our footnote 6 (above). [8] The five studies are listed in footnotes 10 through 14 o f the Hardell study we cited in our footnote 6 (above).
Reprint o f Rachel's Hazardous Waste News #775
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RACHEL'S HAZARDOUS WASTE NEWS #212
Providing news and resources to the Movement for Environmental Justice --December 19,1990
REPORT LINKS HERBICIDE EXPOSURE TO ILLNESSES AMONG VIETNAM VETS
For m ore than a decade Vietnam veterans have sought compensation for illnesses they believe were caused by their wartim e exposure to herbicides, which w ere used heavily during the war to defoliate the jungle, to reduce available cover for enemy troops. U.S. soldiers and airmen who prepared, handled or sprayed the herbicides, and ground troops who were doused, have been routinely denied compensation by the federal D epartm ent of V eterans Affairs (VA) because the V A has taken the position th at there is not enough scientific evi dence linking herbicide exposure to disease.
Now an independent scientific review sponsored by the A m erican Legion, the Vietnam V eterans of America, and the N ational V eterans Legal Services Project has concluded that there is a "significant statistical association" betw een exposure to chemical herbicides and several serious illnesses. According to the April, 1990, report of the A gent O range Scientific Task Force, there is "a significant statistical association" betw een exposure to the herbicide A g en t O range and various cancers (non-H odgkin's lym phom a and soft tissue sarcomas), serious skin disorders (chloracne), and liver disorders. T he Task Force said, "The aggregate interpretation of several sound studies showing a statistically significant as sociation for each of these conditions m akes this conclusion inescapable." A gent O range was the m ilitaiy code nam e for the chemical herbicide used m ost often in Vietnam to defoliate the jungle. A gent O range was a chlorinated phenoxy herbicide m ade up o f two common weed killers, 2,4,5-T and 2,4-D, both of which are routinely contam inated with dioxins during m anufacture. Anyone exposed to A gent O range is presum ed to have been exposed to dioxins.
"When a scientist says there is a "significant statistical association" betw een one event (such as exposure to an herbicide) and another event (such as the onset of illness), he or site m eans it is veiy unlikely that the two events occurred together by random chance; it is m uch m ore likely th at the two events occurred together for a reason. (W hat is m eant by "very unlikely" differs from study to study; often "very unlikely" m eans there is less than a 5% probability that the observed relationship occurred by random chance; som etim es "very unlikely" m eans there was less than a 1% probability that the observed relationship occurred by random chance. In each individual study, the author decides which definition of "very unlikely" he or she will use.)
T he 1990 re p o rt is based on a review of 285 different published studies of hum an exposure to phenoxy herbicides and/or dioxins, all appearing in scientific journals from 1978 onward. T he 285 studies are listed on pages 49-75 of the 1990 report; the list provides a unique resource for anyone seeking additional information on phenoxy herbicide effects on humans. The V A does not allow consideration of animal studies, so only hum an data were evaluated for the 1990 report. However, to m ake the point th at animal studies are universally recognized as valid evidence for hum an cancer risk, the 1990 report contains an appendix in which various scientists and governm ent agencies are quoted saying th at anim al studies provide valid evidence for those trying to understand hum an cancers in relation to chem ical exposures. This appendix (pgs. 42-48 of the 1990 report) is a unique resource for citizens trying to m ake the case that animal studies should be heeded in public policy decisions involving hum an exposure to chemicals.
T he 1990 report concludes further that three additional health effects "are a t least as likely as not" to be associated w ith exposure to phenoxy herbicides: H odgkin's disease (a cancerous enlargem ent of the lymph nodes, spleen, and general lymphoid tissues, which usually appears first in the neck), neurologic effects, and reproductive and developm ental disorders.
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The observed reproductive and developmental disorders include (a) low sperm count among Vietnam vets compared to a control group of non-Vietnam veterans; (b) increased incidence of spontaneous abortion among wives of V ietnam vets; (c) increased incidence of birth defects in children of Vietnam vets, including skin defects, nerve defects, heart defects, kidney defects, and oral clefts (cleft lip and cleft palate).
The conclusion th at these illnesses are "at least as ukely as not" to occur from Agent O range exposure is im p o rtan t w ithin th e V A because th e V A 's rules for com pensation require a finding th at a disease is "as likely as not" to occur from a chemical exposure before that disease becomes compensable.
The report concludes further that there is "sound scientific evidence of an association with exposure to agent orange, but the evidence does not reach the level of form al statistical significance for the following additional effects:" cancers of the kidney, testicles, stomach, prostate, colon, hepatobiliary tract (liver and related systems), brain, and blood-forming cells (leukemia); psychosocial effects; im m une system disorders; gastrointestinal ulcers; and altered lipid m etabolism (the body's ability to digest and han d le fats and som e oils).
A uthors of the report (the A gent Orange Scientific Task Force) are seven prom inent independent scientists and physicians: R ichard W. Clapp, Barry Com m oner, John D. Constable, Sam uel S. Epstein, P eter C. K ahn, Jam es R . Olson, and D avid M . Ozonoff.
This is an im portant report because the issue of com pensation for V ietnam vets is merely the tip of an enorm ous iceberg. T he com ponents of agent orange (2,4,5-T and 2,4-D) are both still widely used in the U nited States for clearing rights of way beneath power lines and along highways; rain then carries the chemicals into w ater supplies. M any homeowners use these chemicals (knowingly or not) to kill lawn "pests" (broad-leaf plants such as crab grass and dandelions). Farm ers use them extensively for weed control. Thus exposure to these chemicals is very widespread am ong the A m erican people.
Since the 1990 report appeared (in April), the V A has reversed itself and declared that soft tissue sarcom as and non-H odgkin's lym phom as in V ietnam vets a re com pensable. T h e V A 's A dvisory C om m ittee on E nvironm ental H azards continues to study th e relationship of other diseases to A gent O range exposures among vets.
G et: H um an H ealth E ffects A ssociated W ith Exposure to H erbicides A n d jO r Their A ssociated C ontam inants - Chlorinated D ioxins (W ashington, D C : N ational V eterans Legal Services Project [2001 S Street, NW , W ashington, D C 20009-1125; phone 202/265-8305], April, 1990); 41 pages, plus 33 pages of useful appendices; $10.00 plus $3.00 shipping.
[Dated announcem ent omitted from this reprint.]
Reprint o f Rachel's H azardous Waste News #212
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RACHEL'S HAZARDOUS WASTE NEWS # 2 1 9
Providing news and resources to the Movement for Environmental Justice --February 6,1991
Dioxin-Part 4 NEW STUDY LINKS DIOXIN TO HUMAN CANCER
A new study published last m onth provides fresh evidence that dioxin [TCDD] causes cancer in humans. Dioxin is n o t a commercial product but is created as an unw anted byproduct of many industrial processes; significant quantities of dioxin are released from the smoke stacks (and the ash landfills) of incinerators that burn chlorine-containing item s-such as medical wastes (RH W N #179), sewage sludge, and municipal solid wastes. O nce it is released into the environm ent dioxin persists for a very long time, enters food chains, and accumulates; when hum ans eat dioxin-contaminated food, such as m ilk or fish, the hum ans themselves accum ulate dioxin in their blood and fatty tissues.1
Scientists have known since the mid-1960s th at dioxin is an extremely powerful prom oter of cancer in laboratoiy animals, b ut industry researchers have recently been claiming that hum ans somehow are exempt from the dioxin danger. T he question of dioxin's hazard to hum ans took on real urgency in the early '80s when 15,000 veterans sued D ow chem ical and other producers of A gent O range (a dioxin-contaminated herbicide widely used to defoliate the jungle in V ietnam from 1962 to 1971); the vets sought m oney dam ages for health effects (cancer, defective offspring, and so forth) they said they w ere experiencing. Lawyers for the Vietnam vets offered documentary evidence that Dow chemists convened a private m eeting of their com petitors in 1965 to share new inform ation th at im purities [dioxins] in the herbicide 2,4,5-T (principal com ponent of A gent O range) caused severe liver dam age in rabbits. According to court records, a chemist at Hercules Powder Company who attended the private D ow m eeting in 1965, received a phone call from a D ow executive who "warned him to keep the findings away from the federal government," according to a reporter for N ature, th e B ritish science jo u rn a l.2 If this is tru e, it w ould n o t b e th e first tim e, n o r th e last, that m oney has influenced the outcomes, and the uses, of scientific studies.
In any case, as a result of these lawsuits, during the 1980s the question of dioxin's effects on humans became subject of bitter controversy-with enormous sums of money riding on the outcom e of the debate. As th e 1980s drew to a close and it becam e known th a t all incinerators create and release dioxin into the local environment, industry felt enorm ous pressure to "prove" that dioxin was harm less to humans. From 1980 onward, industry researchers published several studies of dioxin-exposed workers, claiming to show th at they suffered no m ore cancer than the general public. Last year, however, evidence began to accumulate indicating that the industry-funded studies of dioxin dangers to hum ans w ere badly flawed or-were simply fraudulent (see R H W N #171, #173, #775).
The latest study is not by industry researchers but by D r. Marilyn Fingerhut of the federal N ational Institute for Occupational Safety and H ealth (NIOSH); Fingerhut looked at the health of 5172 w orkers at 12 chemical plants th at m anufacture (or form erly m anu factured) products contam inated w ith dioxin such as th e herbicides 2,4,5-T, Silvex, R on n el, Erbon, and pentachlorophenol (which has also been used as a fungicide, algicide, and wood preservative for telephone poles and pilings), and the bacterial cleansing agent, hexachlorop h e n e -u n til the 1970s, a leading bactericide in hospitals.
O f the 5172 exposed workers (all of whom were m ale), 1520 m et two key conditions: they had been exposed for at least a year, and their exposure had begun at least 20 years previously. T h e onset of cancer is always delayed by 7 to 40 years (or m ore) betw een the time of initial exposure and the tim e disease appears; therefore, the "latency" period of at least 20 years is im portant in studying cancer that may be related to a particular chem ical exposure. This group ("cohort," to use the language of m edical researchers) had nine times (900% ) th e norm al am ount of soft tissue sarcom a--m alignant cancer o f th e soft connective tissues. T he sam e group also had 42% m ore cancers of the respiratory tract (trachea,
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bronchus and lung) than would be expected among males in the general public; by various means, D r. Fingerhut examined and tried to eliminate the possibility that tobacco smoking explained the increase in respiratory cancers.
Among the entire cohort of 5172 men, the occurrence of all cancers was significantly increased, by 15%; in the high-exposure group o f 1520 m en, the "all cancers combined" increase was even m o re pronounced --46% ; fu rth erm o re "all cancers combined" w ere increased am ong w orkers a t nine o f th e 12 plants studied. Even w hen cancers o f th e respiratory tract were omitted in an attem pt to eliminate smoking as a possible the cause, "all cancers combined" was increased among the 5172 and even m ore so am ong th e highexposure 1520.
Dr. Fingerhut says correctly that her results do not prove that dioxin causes cancer in exposed workers. The workers she studied w ere exposed to many other chemicals, in addition to dioxin, on the job, and these other chemicals could explain the cancer increases she observed.
Nevertheless, the Fingerhut study m akes it ever m ore difficult for the purveyors of dioxin-creating machines (such as incinerators for solid waste, hazardous waste, or sewage sludge) to claim that their dioxin emissions are negligible or harmless. Because dioxin accumulates in the food chain, even small am ounts can build up to significant levels as time passes.
A n editorial in the N ew England Journal o f M edicine tried to shed light on the m eaning of th e F in g erh u t study th e day it ap p eared .3 T h e well-known C anadian biostatistician, Jo h n Bailar, wrote, "This evidence is short of proof, as the authors explain, but it m ust be taken seriously as a flag of a probable hum an risk. If one accepts the best estim ate of excess risk given h ere (3 deaths observed am ong the 1520 w orkers m inus 0.3 expected deaths equals 2.7), the lifetim e risk of death from T C D D -related soft-tissue sarcom a is already approaching 2 per 1000 workers, and it may increase with additional follow-up study. This estim ate falls in a range that is widely considered unacceptable for occupational hazards, and it is far in excess of th e usual limits for lifetim e risk to th e public o f 1 p e r 100,000 or 1 per million.
"Despite th e problem s, which Fingerhut et al. carefully note, this w ork is a m odel o f its kind. O ccupational cohort studies are inherently difficult and uncertain, and we are likely to wait a long tim e for appreciably better or broader evidence of the effects of TC D D [dioxin] on hum an health....
"The hypothesis that low exposures [to dioxin] are entirely safe is distinctly less tenable now than before," D r. Bailar said.
[1] Bengt-Goran Svensson and others, "Exposure to Dioxins and Dibenzofurans Through the Consumption of Fish." New England Journal o f Medicine Vol. 324 (Jan. 3, 1991), pgs. 8-12. [2] Peter David, "Dioxin-When was the Danger Known?" Nature Vol. 303 (May 12, 1983), pg. 104. [3] John C. Bailar III, "How Dangerous is Dioxin?" New England Journal o f Medicine Vol. 324 (Jan. 24,1991), pgs. 260262.
And get: Marilyn A. Fingerhut and others, "Cancer Mortality in Workers Exposed to 2^,7,8-TetrachIorodibenzo-pdioxin," New Englandloumal o f Medicine Vol. 324 (Jan. 24,1991), pgs. 212-218. Reprints free from Dr. Fingerhut at: Industrywide Studies Branch, Division of Surveillance, National Institute for Occupational Safety and Health, Centers for Disease Control, 4676 Columbia Parkway, Cincinnati, OH 45226.
A more complete report of this research is available under the title Mortality Among U.S. Workers Employed in the Production of Chemicals Contaminated with 2,3,7,8-Tetrachlorodibenzo-p-diccn (TCDD). Springfield, VA: National Technical Information Service (NTIS), Dec., 1990. Available from NTIS, 5285 Port Royal Rd., Springfield, VA 22161; phone (703) 487-4650); NTIS number PB9 F125971. $15.00 + shipping.
Reprint o f Rachel's Hazardous Waste News #219 RachePs Hazardous Waste News (ISSN 1065-4623) is published weekly by Environmental Research Foundation (ERF), P.O. Box 5036, Annapolis, MD 21403-7036; Telephone (410) 263-1584; Fax (410) 263-8944; Econet: erf; Internet: erf@igc.apc.org. Editor: Peter Montague, Ph.D.; Associate editor Maria B. Pellerano; Research Assistant: Andrea K. Feameyhough. Subscription rates: 525 per year for individuals and citizen groups; $80 for professionals and government agencies; $15 for students and seniors with ID; $400 for businesses; in Canada and Mexico, add $6.00; in all other countries, add $11.00. All payments in U.S. funds drawn on U.S. banks. Visa & Mastercard accepted. RachePs Hazardous Waste News is not copyrighted; we encourage reprinting so long as you send us a copy. Printed on 100% recycled paper.
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RACHEL'S HAZARDOUS WASTE NEWS #263
Providing news and resources to the Movement for Environmental Justice --December 11,1991
The Wingspread Statement-Part 1 CHEMICALS IN ENVIRONMENT AFFECT SEXUAL DEVELOPMENT IN WILDLIFE. AND HUMANS?
Gradually during recent years a new body o f knowledge has developed showing that som e chemicals in food and w ater can m im ic horm ones and disrupt the developm ent o f living things like Osh, birds, and mammals, including their sexual developm ent.
In som e cases, the effects on wildlife have been dramatic. For example, m ale herring gulls on Lake Ontario, exposed to D D T and other organochlorine com pounds, developed fem ale sex organs. Fem ale-
fem ale pairing has b een observed in herring gulls o n L ake M ichigan and o n Santa Barbara Island, Cali
fornia. B ecause humans share the sam e basic mechanisms o f growth and developm ent as wildlife, an increasing number o f scientists has becom e concerned that humans may already be affected without recog nizing it.
In July o f this year an international group o f 21 scientists m et at W ingspread in Racine, W isconsin to assess what is known about these matters. They have now released a "consensus statem ent" containing information and opinions about the nature and possible causes o f these problems. T he five-page statem ent is called "Chemically Induced Alterations in Sexual D evelopm ent: T he W ildlife/Hum an Connec tion."
Background H o rm on es are produced by th e endocrine system --a bodily system consisting o f specialized cells, tissues, and organs that create and secrete (usually into the blood) organic chem icals called horm ones, which then regulate other kinds o f cells in the body. Particular horm ones only affect particular cells that contain "receptors" for those horm ones. A small am ount o f a horm one attaches to a "receptor site" and the hor m one-receptor pair then initiates a cascade o f chem ical changes, often with major and far-reaching conse quences. T he en d ocrin e system shares with the nervous system the job o f adjusting th e body's response to a changing external environment. The nervous system copes with environmental changes on an immediate basis, whereas the endocrine system copes with environmental changes on a sustaining basis. For example, w h en th e bocfy g ets cold, th e nervous system causes shivering, w hich raises th e body's tem perature. But each month it is the endocrine system that starts the human fem ale menstrual cycle. In a developing fetus, it is the endocrine system that regulates cell division and organ differentiation. The endocrine system regulates pattern and timing o f bird migration and o f hibernation in mammals. Exam ples o f endo crine glands in humans include the adrenal gland, pancreas, thyroid, pituitary, ovaries and testes. The scientists gathered at W ingspread last July focused on the sex h orm on es-th e androgens that make m ales look and act like m ales and the estrogens that make fem ales look and act like females. The W ingspread Statem ent begins, "Many com pounds introduced into the environment by human activity are capable o f disrupting the endocrine system o f animals, including fish, w ildlife, and humans. The consequences o f such disruption can be profound because o f the crucial role horm ones play in controlling develop m en t...." "The following-consensus was reached by participants at the workshop. "1. W e are certain o f the follow ing: "A large number o f man-made chem icals that have been released into the environment, as well as a few natural ones, have the potential to disrupt the endocrine system o f animals, including humans. A m ong these are the persistent, bioaccumulative, organohalogen com pounds that include som e pesticides (fungicides, herbicides, and insecticides) and industrial chemicals, other synthetic products, and som e m etals.1 "Many wildlife populations are already affected by these com pounds. T he im pacts include thyroid dys function [im paired or abnormal functioning] in birds and fish; d ecreased fertility in birds, fish, shellfish, and mammals; decreased hatching success in birds, fish and turtles; gross birth deform ities in birds, fish and turtles; m etabolic abnormalities [impaired or abnormal use o f energy, manufacture o f tissue, or handling o f resulting wastes] in birds, fish, and mammals; behavioral abnorm alities in birds; dem asculinization and feminization in male fish, birds, and mammals; defem inization and masculinization o f fem ale fish and birds; and com prom ised [impaired] immune system s in birds and mammals. "The patterns o f effects vary among species and am ong com pounds. Four general points can nonethe less be made: (1) the chem icals o f concern may have entirely different effects on the embryo, fetus, or perinatal [m eaning "near th e tim e o f birth," from the 28th w eek o f pregnancy through the first w eek o f life, in humans] organism than on the adult; (2) the effects are m ost often m anifested in offspring, not
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in the exposed parent; (3) the timing of exposure in the developing organism is crucial in determining its character and future potential; and (4) although critical exposure occurs during embryonic development [from conception through the end of the second month of pregnancy], obvious manifestations [effects] may not occur until maturity.
"Laboratory studies corroborate the abnormal sexual development observed in the field and provide biological mechanisms to explain the observations in wildlife.
"Humans have been affected by compounds of this nature, too. The effects of DES (diethylstilbesterol), a synthetic therapeutic agent, like many of the compounds mentioned [in footnote 1] are estro genic [meaning they act like estrogen, a family of female sex hormones]. Daughters bom to mothers who took DES now suffer increased rates of clear cell adenocarcinoma [cancer], various genital tract abnormalities, abnormal pregnancies, and some changes in immune responses. Both sons and daughters exposed in utero [while in the uterus] experience congenital anomalies of their reproductive system and reduced fertility. The effects seen in in utero DES-exposed humans parallel those found in contaminated wildlife and laboratory animals, suggesting that humans may be at risk to those same environmental hazards as wildlife."
The Wingspread Statement goes on: "2. We estimate with confidence that: "Some of the developmental impairments reported in humans today are seen in adult offspring of parents exposed to synthetic hormone disruptors (agonists and antagonists) released in the environment. The concentrations of a number of synthetic hormone agonists and antagonists measured in the U.S. human population today are well within the range and dosages at which effects are seen in wildlife popula tions. {An agonist is a chemical that is not a hormone but mimics a natural hormone; an antagonist interferes with a natural hormone.] In fact, experimental results [in animals] are being seen at the low end of current environmental concentrations [in humans]. "Unless the environmental load of synthetic hormone disruptors is abated and controlled, large scale dysfunction at the population level is possible. The scope and potential hazard to wildlife and humans are great because of the probability of repeated and/or constant exposure to numerous synthetic chemicals that are known to be endocrine disruptors...." "3. Current models predict that: "... Both exogenous (external source) and endogenous (internal source) androgens (male hormones) and estrogens (female hormones) can alter the development of brain function. "Any perturbation [disturbance] of the endocrine system of a developing organism may alter the devel opment of that organism: typically these effects are irreversible. For example, many sex-related charac teristics are determined hormonally during a window of time in the early stages of development, and can be influenced by small changes in hormone balance. Evidence suggests that sex-related characteristics, once imprinted, may be irreversible." The Wingspread statement then gives three reasons why these predictions are subject to "many uncer tainties:" (1) effects of exposure of humans are not well understood, especially exposure of embryos; (2) data on reproductive problems in wildlife exist but data on behavior changes are not so readily available; (3) the potency of many synthetic [human-created] estrogenic chemicals is not well known. The British publisher, Elsevier Applied Science, will publish a book on this subject by next fall. Until then, the best source of information is Theodora E. Colbom and others, Great Lakes GreatLegacy? avail able for $20.00 (plus $2.00 shipping) from: World Wildlife Fund, P.O. Box 4866, Hampden Post Office, Baltimore, MD 21211; phone (301) 516-6951. For $3.00 plus stamped, self-addressed envelope, we can send you the Wingspread statement itself. [More on this subject coming soon.]
[1] A footnote on page 1 o f the Wingspread Statement says, "Chemicals known to disrupt the endocrine system include: DDT and its degradation products, DEHP (di(2-ethylhexyl)phthalate), dicofol, HCB (hexachlorobenzene), kelthane, kepone, lindane and other hexachlorocyclohexane congeners, methoxychlor, octachlorostyrene, synthetic pyrethroids, triazine herbicides, EBDC fungicides, certain PCB congeners, 2,3,7,8-TCDD and other dioxins, 2,3,7,8-TCDF and other furans, cadmium, lead, mercury, tributyltin and other organo-tin compounds, alkyl phenols (non-biodegradable detergents and anti-oxidants present in modified polystyrene and PVCs), styrene dimers and trimers, soy products, and laboratory animal and pet food products."
Reprint o f Rachel's Hazardous Waste News #263 RacheVs Hazardous Waste News (ISSN 1065-4623) is published weekly by Environmental ResearchFoundation (ERF), P.O. Box 5036, Annapolis, MD 21403-7036; Telephone (410) 263-1584; Fax (410) 263-8944; Econet: erf; Internet: erf@igc.apc.oig. Editor: Peter Montague, Ph.D.; Associate editor Maria B. Pellerano; Research Assistant: Andrea K. Fearneyhough. Subscription rates: $25 per year for individuals and citizen groups; $80 for professionals and government agencies; $15 for students and seniors with ID; $400 for businesses; in Canada and Mexico, add $6.00; in all other countries, add $11.00. All payments in U.S. funds drawn on U.S. banks. Visa & Mastercard accepted. Rachel's H azardous Waste News is not copyrighted; we encourage reprinting so long as you send us a copy. Printed on 100% recycled paper.
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RACHEL'S HAZARDOUS WASTE NEWS # 2 6 4
Providing news and resources to the Movement for Environmental Justice -- December 18, 1991
The Wingspread Statement-Part 2 MAJOR CHALLENGE TO "BUSINESS AS USUAL"
A n international group of 21 scientists1m et at W ingspread in Racine, W isconsin in July, 1991 to discuss evidence that chemicals in the environment are causing changes in the sexual development o f wildlife and conceivably in humans as well. (See R H W N #263.) The group produced a five-page "consensus statement."
Sexual developm ent in wildlife, as in humans, is controlled by the endocrine system, a group of organs, tissues and cells that secrete hormones; the hormones interact with other cells, initiating chemical/biological reactions with far-reaching consequences. M ale hormones are called androgens; female hormones are called estrogens.
It is now known that some chemicals disrupt the endocrine system. T he W ingspread statem ent identifies the following: "Chemicals known to disrupt the endocrine system include: D D T and its degradation products [D D E and DDD], D EH P (di(2-ethyIhexyl)phthalate),dicofol, HCB (hexachlorobenzene), kelthane, kepone, lindane and other hexachlorocyclohexane con geners [forms], methoxychlor, octachlorostyrene, synthetic pyrethroids, triazine herbicides, EBDC fungicides, certain PCB congeners [forms], 2,3,7,8-TCDD and other dioxins, 2,3,7,8TCDF and other furans, cadmium, lead, mercury, tributyltin and other organo-tin compounds, alkyl phenols (non-biodegradable detergents and anti-oxidants present in modified polystyrene and PVCs), styrene dimers and trimers, soy products, and laboratory animal and pet food pro ducts."
In animals, and in humans, sexual characteristics are established at a particular point during development in the womb or egg. For example, D r. Theodora Colbom of the W orld Wildlife Fund (Washington, DC) points out that a single dose of dioxin, administered to a pregnant rat at day 15 of the pregnancy-near the tim e when gender is established--results in demasculinization and feminization of male offspring.2
Samples of herring gulls from Lake O ntario collected in 1975 and 1976 showed cellular and anatomical changes in embryos and in newly hatched chicks that caused feminization o f male chicks and overdevelopment of female reproductive organs. Elevated concentrations of D D E [a break down by product of DDT] and other residues were found in eggs from the same population. To test whether these sexual problems might be linked to the presence of the DDT, laboratory experiments were conducted in which W estern gull eggs were injected with concentrations of D D T similar to those found in the G reat Lakes environment. M ale chicks became feminized, developing ovarian tissue and oviducts.3
W hat is becoming clear is that the older picture of chemical toxicity underestim ates the num ber and kinds of effects that chemicals can have in fish, birds, and mammals. F or decades, U.S. regulatory officials have focused their attention almost exclusively on cancer. Meanwhile, many of the chemicals that have been dumped into the environment, and are now coursing through food chains, cause many other detrimental effects besides cancer.
For example pesticides such as DDE, dieldrin, lindane, mirex, toxaphene, and PCBs, block communication between cells. Normal metabolism [energy use] and development of a cell may be disrupted because movement of nutrients, electrolytes, and horm ones in arid out o f a cell is blocked by the presence of these poisons.4
Furans, benzo[a]pyrene, 2,3,7,8-TCDD [dioxin], D D E , dieldrin, HCB [hexachlorobenzene], lindane [beta-HCH], mirex, toxaphene, and PCBs induce enzyme activity. [Enzymes are large protein molecules that prom ote chemical activity in the body, the presence of particular enzymes makes possible particular chemical reactions that would not otherwise be possible.] W hen the enzyme activity is induced, norm al products of the endocrine horm onal system can be released into the bloodstream. This can disrupt the role of steroid hormones, affecting growth and sexual m aturation.4
The structure of D D T and D D E are, themselves, quite similar to estrogens and thus ma 0
mimic female hormones. In addition, D D E induces enzymes that break down male hormones. U nder different circumstances, dioxin acts like an estrogen, or it may act as an anti-estrogen (what causes the same chemical to have opposite effects is not understood).4
A t one Superfund site where data are available, humans are experiencing abnormalities of sexual development. At the Brio site south of Houston, Texas, where a housing development was built atop a chemical dump, girls 4 to 5 years old have developed pubic hair and enlarged breasts. One child (now four years old) was bom without any genital organs; chromosome tests revealed that this is a male child, though he has a birth canal. This information, and other data about abnorm al sexual developm ent o f children at the Brio site, is contained in a unique database of information that resulted from a health survey of the community by a local group (H ELP) and by the Environm ental H ealth N etw ork (E H N ) in Harvey, Louisiana.5 Such surveys--providing an unusually valuable source of information about health problems near chemical dumps--are underw ay in several Superfund communities, looking for patterns o f prob lems, including the kinds the W ingspread statem ent warns of.
The Wingspread statement presents a major new challenge to advocates of "business as usual." The participants in the conference represent 17 different Helds o f scientific inquiry. They have many thousands of data points on which they have based their conclusions. If they are right, we are all being exposed, on a daily basis, to chemicals that threaten out reproductive health, and the health of our offspring.
Because hormones and horm one disrupters do their work at extremely low concentrations, the only "safe" dose of an endocrine-system disrupter is zero. Thus any new sources o f these chemicals should be aggressively discouraged while we figure out how to minimize exposure to the quantities o f these chemicals already in the environment.
[1] Participants in the Wingspread meeting included the following individuals (whose institutional affiliations are given for identification purposes only): Dr. Howard A. Bern, Professor o f Integrative Biology (emeritus) and Research Endocrinologist, University of California-Berkeley, Dr. Phyllis Blair, Professor o f Immunology, University o f CaliforniaBerkeley; Sophie Brasseur, Marine Biologist, Research Institute for Nature Management, Texel, The Netherlands; Dr. Thee Colbom, Senior Fellow, World Wildlife Fund, Washington, DC; Dr. Gerald R. Cunha, Developmental Biologist, University o f Califomia-San Francisco; Dr. William Davis, Research Ecologist, Environmental Research Laboratory, U.S. Environmental Protection Agency, Sabine Island, FL; Dr. Klaus D. Dohier, Director, Research, Development & Production, Pharma BissendorfPeptide GmbH, Hannover, Germany; Glen Fox, Contaminants Evaluator, National Wildlife Research Center, Environment Canada, Quebec, Canada; Dr. Michael Fry, Research Faculty, Department o f Avian Sciences, University o f Califomia-Davis; Dr. Earl Gray, Section Chief, Developmental and Reproductive Toxicology Divi sion, Health Effects Research Laboratory, U.S. Environmental Protection Agency, Research Triangle Park, N Q Dr. Richard Green, Professor o f Psychiatry in Residence, School o f Medicine, University o f Califomia-Los Angeles; Dr. Melissa Hines, Assistant Professor in Residence, School o f Medicine, University o f Califomia-Los Angeles; Timothy J. Kubiak, U.S. Fish and Wildlife Service, East Lansing, MI; Dr. John McLachlan, Director, Division of Intramural Research, National Institute of Environmental Health Sciences, Research Triangle Park, N Q Dr. J.P. Myers, Director, W. Alton Jones Foundation, Charlottesville, VA; Dr. Richard E. Peterson, Professor o f Toxicology and Pharmacology, School o f Pharmacy, University o f Wisconsin-Madison; Dr. PJ.H. Reijnders, Head, Section o f Marine Mammology, Research Institute for Nature Management, Texel, The Netherlands; Dr. Ana Soto, Associate Professor, Tufts University School of Medicine, Boston, MA; Dr. Glen Van Der Kraak; Assistant Professor, University o f Guelph, Ontario, Canada; Dr. Frederick vom Saal, Professor, Division o f Biological Sciences, University o f Missouri-Columbia; Dr. Pat Whitten, Assistant Professor, Department o f Anthropology, Emory University, Atlanta, GA. [2] David J. Hanson, "Dioxin Toxicity: New Studies Prompt Debate, Regulatory Action," C&EN [Chemical & Engineering News] August 12,1991,'pg. 13. [3] Theodora E. Colbom and others, Great Lakes Great Legacy? (Washington, DC: Conservation Foundation, 1990), pg. 139. [4] Theodora E. Colbom and others, cited above, pg. 142. [5] For more information about the Brio site, contact HELP: 10904 Scarsdale Boulevard, M263, Houston, TX 77089; phone (713) 992-1867. For advice about health surveys, contact Linda King, Environmental Health Network, P.O. Box 1628, Harvey, LA 70058; phone (504) 362-6574.
Reprint o f Rachel's Hazardous Waste News # 264
Rachels Hazardous Waste News (ISSN 1065-4623) is published weekly by Environmental Research Foundation (ERF), P.O. Box 5036, Annapolis, MD 21403-7036; Telephone (410) 263-1584; Fax (410) 263-8944; Econet: erf; Internet:
erf@igc.apc.oig. Editor Peter Montague, Ph.D.; Associate editor: Maria B. Pellerano; Research Assistant: Andrea K. Feameyhough. Subscription rates: $25 per year for individuals and citizen groups; $80 for government agencies;
$15 for students and seniors with ID; $400 for businesses and professionals; in Canada and Mexico, add $6.00; in all other countries, add $11.00. All payments in U.S. funds drawn on U.S. banks. Visa & Mastercard accepted. RacheVs Hazardous Waste News is not copyrighted; we encourage reprinting so long as you send us a copy. Printed
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RACHEL'S H A Z A R D O U S W A ST E N E W S # 2 9 0
Providing news and resources to the Movement for Environmental Justice --June 17, 1992
YOUNG MALE RATS ARE 'DEMASCUUNIZED' AND 'FEMINIZED' BY LOW DOSES OF DIOXIN
Three new studies by researchers at University of Wisconsin reveal that very low doses of dioxin alter the sexual development of young male rats, causing demasculinization and feminization.1,23
Dr. Linda S. Birnbaum, a scientist with U.S. EPA [Environmental Protection Agency] calls the new studies "highly significant."4 Birnbaum is one of the chief scientists conducting the EPA's formal reass essment of the toxicity of dioxin (see RHWN #269, #276, #275). As we reported earlier {RHW N #279), many scientists, including Birnbaum, now consider dioxin an "environmental hormone." The new Wisconsin studies support that view.
The Wisconsin researchers, led by Dr. Richard E. Peterson, showed that dioxin interferes with the sexual development of male rats exposed to dioxin before, and shortly after, birth. Pregnant female rats were given a single oral dose of dioxin on the 15th day of pregnancy; their male offspring showed reduced levels of male hormones in their blood and a variety of sexual aberrations that stayed with them as they matured. The young males are demasculinized and feminized by doses of dioxin too low to cause any measurable toxicity in the mother rat. The sexual changes in the young males are both physiological and behavioral, and last into adulthood.
Dioxin passes through the placenta and enters the fetus, so the rat fetuses received part of the mother's dose almost immediately. After birth, the baby rats continued to receive a small dose of dioxin through their mother's milk. Peterson says the baby rats received the bulk of their dose through milk. In rats and humans both, females rid their bodies of dioxin chiefly by excreting it in their milk. Dioxin is soluble in fats and oils, and milk is high in fat.
Dioxin is the common name for a family of 75 toxins, the most potent of which is TCDD [2,3,7,8tetrachlorodibenzo-p-dioxin]. The Wisconsin researchers used TCDD in their experiments.
Dioxin is not made intentionally for any industrial purpose, but is produced as a byproduct of the com bustion of chlorine-containing wastes, the bleaching of paper, and the manufacture of some pesticides. The burning of municipal solid waste, and of many hazardous wastes, releases dioxin into the environment, as does paper manufacture. Government officials responsible for the quality of the environment in the Great Lakes have called for a phase-out of chlorine, to reduce dioxin levels in wildlife and humans around the Lakes. (See RH W N #284.)
In the Wisconsin experiments, young males whose mothers were given as little as 0.064 micrograms of dioxin per kilogram of body weight showed consistently reduced levels of male hormones, plus a variety of physical and behavioral changes, including:
--reduced testosterone levels and probably a reduced response to testosterone. Testosterone is a powerful hormone controlling various aspects of sexual development in males.
--smaller accessory sex organs, including smaller testicles; --slower sexual maturation; --distinctly feminine-style regulation of one hormone related to testosterone production; -greater willingness to assume a receptive-female posture when approached by a sexually stimulated male. These effects "strongly suggest, though do not conclusively prove, that TCDD impairs sexual differ entiation in the CNS [central nervous system]," according to Peterson and co-workers. They go on to say that, "The present study provides the first evidence that TCDD impairs sexual differentiation of the CNS." Sexual differentiation-the full development of a female instead of a male, or vice vcrsa-is affected by hor mones circulating in the blood before and after birth. Furthermore, these studies "strongly suggest" that "the demasculinization and feminization caused by in utero and lactational TCDD exposure are irreversible," the Wisconsin researchers say. in utero means "in the womb" and lactational means "from milk." Other effects revealed by these studies include: -E ven the lowest dose tested (0.064 micrograms of dioxin per kilogram of the mother's body weight), yielded consistent reductions in a male offspring's daily sperm production. -T h e developing male reproductive system is more sensitive to the effects of this hormone-like toxicant [dioxin] that any other organ or organ-system studied. --the unborn or newborn is about 100 times more sensitive to dioxin than the sexually mature animal. What do these studies mean for humans? The Wisconsin researchers speculate, "Thus the findings from this study raise the possibility that TCDD could potentially affect sexually dimorphic behavior in man if exposure were to occur during fetal dcvelop-
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ment." "Sexually dimorphic behavior" refers to the bodily and behavioral differences betw een men and
women. Peterson and co-workers point out that male rats typically inseminate a female rat with up to 10 times
as many sperm as are typically needed to ensure impregnation. Humans, by contrast, typically release only about as m any sperm as w ould b e required for fertilization. "As a result," Peterson and his co-workers write, human reductions in sperm production "similar in magnitude to that in rats would be expected to reduce fertility in man." In other words, rats can continue to reproduce despite a reduction in sperm count because they produce an excess of sperm, but humans do not produce excess sperm so a reduction in human sperm count would likely reduce humans' ability to reproduce.5
"The real question is how general these effects are," Birnbaum says. H er E P A lab will repeat the Peterson studies with another strain o f rats and eventually other species. A nd if these effects occur in another species? "I w ould get very concerned [about the potential human-health implications]," Birnbaum told Science N ew s reporter Janet Raloff.
A t a public hearing on E P A 's dioxin reassessment at E P A headquarters in W ashington April 28, a representative o f the American Paper Institute argued that only the study o f humans can reveal anything meaningful about humans. Birnbaum responded somewhat testily, spelling out a dozen ways in which
studies o f rats and m ice reveal useful information about dioxin's potential effects on humans. June 10 at a Congressional hearing on dioxin in W ashington, Assistant U .S. Surgeon General Barry L.
Johnson, announced that a new study by the National Institute for Occupational Safety and Health (NIO SH ) has found that workers exposed to high levels o f dioxin have abnormally low levels o f testosterone (male hormone) in their blood streams.6 This finding is consistent with the rat studies o f Peterson and co workers. W e have learned that this new N IO SH study was presented at a scientific m eeting on June 10, but N IO SH sources have so far not released details o f the new stutfy to the general public.
A t the Congressional hearing June 10, under questioning from Representative T ed W eiss (D -N Y ), Barry
Johnson said that if it were faced with the Times Beach, Missouri, situation today, the U.S. Public Health Service would do exactly what it did 10 years ago, which is to evacuate people from their homes.' H e said the Times Beach evacuation was the appropriate response and would be repeated under similar circum stances today. Another official o f U.S. Public Health Service, Vernon L. Houk, made headlines 14 months ago saying if h e had the decision to make over again, he would not evacuate people from Times Beach.
Tim es Beach is a town near St. Louis where an unscrupulous waste hauler spread dioxin-contaminated oil
around as a dust suppressant in the 1970s. Horses and other animals becam e sick and died, and the Public Health Service evacuated the town in the early 1980s.
During the Congressional hearing D r. H ouk's views were further contradicted by the testimony o f Dr.
Marilyn Fingerhut o f NIOSH, who studied the health of 5172 workers exposed to dioxin on the job. (See R H W N # 2 2 9 .) Dr. Houk made headlines a year ago when he said that, if dioxin causes cancer in humans at all, it is only "a weak carcinogen." (S ee R H W N # 2 4 9 .) D r. Fingerhut contradicted this view, reporting that, among workers who had been exposed to dioxin for at least a year at least 20 years ago, there was 46% more cancer than among average U.S. males. During the hearing, Representative W eiss characterized Dr. H ouk's views o n dioxin as "quirky" and "cockamamie."
[1] Thomas A. Mably and others, "In Utero and Lactational Exposure of Male Rats to 2,3,7,8-Tetrachlorodibenzo-p-dioxin. 1. Effects on Androgenic Status." Toxicology and Applied Pharmacology Vol. 114 (May, 1992), pgs. 97-107. [2] Thomas A. Mably and others, "In Utero and Lactational Exposure of Male Rats to 23,7,8-Tetrachlorodibenzo-p-dioxin. 2. Effects on Sexual Behavior and the Regulation of Luteinizing Hormone Secretion in Adulthood." Toxicology and Applied Pharmacology Vol. 114 (May, 1992), pgs. 108-117. [3] Thomas A. Mably and others, 7n Utero and Lactational Exposure of Male Rats to 2,3,7,8-TetrachIorodibenzo-/Mlioxin. 3. Effects on Spermatogenesis and Reproductive Capability." Toxicology and Applied Pharmacology Vol. 114 (May, 1992), pgs. 118-126. [4] J. Raloff, "Perinatal dioxin feminizes male rats," Science News Vol. 141 (May 30, 1992), pg. 359. [5] In unrelated studies, Congress's Office of Technology Assessment (OTA) reported several years ago that Americans in their prime reproductive years (ages 20 to 24) have experienced an increase in infertility in recent years. See "Repro ductive Dysfunction in the Population," in U.S. Congress, Office of Technology Assessment, Reproductive Health Hazards in the Workplace [OTA-BA-266] (Washington, DC: U.S. Government Printing Office, 1985), pgs. 341-364. At the time of this 1985 OTA report, low doses of dioxin were not known to interfere with reproductive systems of rats or humans. [6] Barry L Johnson, "Testimony... Before the Subcommittee on Human Resources and Intergovernmental Relations, Com mittee on Government Operations, House of Representatives, June 10, 1992," pg. 8. Johnson is Assistant U.S. Surgeon General with the U.S. Public Health Service.
Reprint of RacheVs Hazardous Waste News #290
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Reassessment of Dioxin
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RACHEL'S H A Z A R D O U S W A ST E N E W S # 2 4 8
Providing news and resources to the Movement for Environmental Justice - August 28, 1991
A TALE OF SCIENCE AND INDUSTRY
For the last several years two debates have been swirling around the notorious chemical dioxin. One debate has engaged real scientists in the question, How dangerous is dioxin to humans and to wildlife? The second debate has occurred within industries that release dioxin into the environment and so will be directly affected by the outcome of the science debate.
According to Chemistry & Industry magazine (Feb. 18, 1991, pg. 112) the chlor-alkali industry (which produces chlorine, the use of which by many other industries creates dioxin) "has taken an active interest in the course of the scientific debate." In fact, the Chlorine Institute-a trade association-is coordinating a "public outreach program" to "capitalise [sic] on the outcome of a recent Banbury conference on dioxin."
Could such a "public outreach program" have any effect? The New York Times took a most unusual step August 15, 1991, when it announced on page one that the U.S. Environmental Protection Agency (EPA) was beginning a year-long review to develop "a new formal opinion on the risks of dioxin." The Times often reports that studies have been completed, but it rarely reports that studies have been begun. Furthermore, Science magazine had reported May 17, 1991 (pg. 911) that "(EPA) administrator William Reilly has launched a major new effort to reassess the toxicity" of dioxin-so the Times's August 15th news was three months old.
In the Times's August 15th story, EPA Administrator Reilly not only announced that his agency was undertaking a year-long review of dioxin toxicity, he also took the unusual step of suggesting to the Times how the study would come out: "I don't want to prejudge the issue, but we are seeing new information on dioxin that suggests a lower risk assessment for dioxin should be applied," Mr. Reilly told the Times.
The next day the Times ran an editorial praising federal officials for "sensibly considering new evidence that could lead to relaxation of the current strict and costly regulatory standards [for dioxin]." And three days later the Times ran a second front-page story which began, "Dioxin, once thought of as the most toxic chemical known, does not deserve that reputation, according to many scientists." The Times did not name any of the "many scien tists."
What "new information" about dioxin has EPA Administrator Reilly found? According to Science May 17th, the "new information" is a "description [given to Mr. Reilly by two EPA scientists] of a meeting last November at the Banbury Center at Cold Spring Harbor Laboratory that Reilly says made the most compelling case for change [in EPA standards for dioxin]."
Science had written its own description of the Banbury Conference Feb. 8, 1991 (pg. 624): Science said 38 dioxin researchers from the U.S. and Europe met at Banbury and "reached an agreement that surprised almost everyone." Science went on to say, "And this unlikely agreement on how dioxin works at the molecular level-and some hurried calculations scribbled on a blackboard--could force a dramatic change in how the federal government assesses the risk of this and similar carcinogens [cancer-causing chemicals]."
However, two weeks later--February 22, \9 9 \--Science reported something quite different about the Banbury meeting ("Flap Erupts Over Dioxin Meeting," pg. 866), revealing that the meeting had been sponsored by the Chlorine Institute and that the Institute had hired a public relations firm to circulate a summary of the meeting claiming a "consensus" had been reached when in fact nothing of the kind had happened. For example, one letter, from a PR firm to the North Carolina Environmental Management Commission, said, "The Banbury Conference was organized for the express purpose of developing a scientific
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consensus concerning a biological basis for risk assessment.... They w ere able to achieve consensus."
However, independent scientists who had attended the Banbury m eeting dispute this view. F or example, according to Science, D r. Ellen Silbergeld of the University of M aryland and "a num ber of other participants" at the conference felt "manipulated and misused." Silbergeld sent a le tte r to th e B anbury C en ter's d irecto r saying, "I am in fact ra th e r astounded by such a product from a Banbury Conference.... The press releases and state m ents imply that a m ajor focus of the conference was a discussion of the regulatory risk assessments th at have been applied to dioxins; this was not the focus of this meeting." "I did not expect to be m anipulated by industry and governm ent spokespeople (who are not dioxin researchers, incidentally) to be m ade into a supporter of their political views on dioxin and risk assessment," Silbergeld said.
A ccording to Science, the C hlorine Institute initiated the B anbury C onference and paid for h alf of i t Science quoted T h e C hlorine In stitu te's h e ad o f com m unications, saying th e Institute believed the meeting could be "beneficial to our interests, particularly our interest in the paper industry." T he use of chlorine in industrial processes often leads to the creation of dioxin as a by-product; the paper industry is under great pressure to reduce its dioxin emissions. F o r exam ple, th e new sletter E nvironm ent W eek re p o rte d Feb. 14, 1991:
A $1 m illion punitive dam ages aw ard by a M ississippi jury last O ctober against Georgia Pacific [paper com pany] fo r alleged dioxin pollution o f the L e a f River has touched o ff a stam pede o f sim ilar suits against paper m ills in M ississippi\ Tennessee and several other states. The legal actions, w hich involve thousands o fp la in tiffs and billions o f dollars in dam age claim s against m ajor paper com panies, have begun to resemble the avalanche o f legal problem s that h it the asbestos industry in the 1980s.
E n o rm o u s dioxin liabilities d o n 't stop with th e p a p e r industry. O n July 10, 1991, a M issouri jury aw arded $1.5 m illion to the family of Alvin J. O verm ann, a St. Louis trucker who died of cancer; his workplace had been contam inated by dioxin. Several hundred similar lawsuits are pending in the M issouri courts now as a result of the contam ination of the town of Times Beach.
W hy m ight the N ew York Tim es participate in a public relations campaign to prom ote the view th at dioxin is less dangerous than previously believed? Jam es Ledbetter, a m edia colum nist fo r N ew Y ork's Village Voice said A ug. 27 (pg. 8) said, "For som e reason, A ugust is dioxin revisionism m onth.... O nce again, the chemical industry is trying to bam boozle federal regulators and the public, with the eager cooperation of the m ainstream press," he said, citing th e Tim es. L e d b e tte r suggested th a t p erh ap s th e Tim es's "industrial-strength enthusiasm over elim inating 'strict and costly' standards can be traced to th e fact th a t th e New Y ork Tim es Company has an 80 per cent interest in a M aine paper mill, and a 49 per cen t in terest in th ree C anadian p a p er mills. Indeed, on A ugust 12, ju st fo u r days before [the Tim er's] editorial ran, two groups of C anadian Indians filed suit against K im berly C lark and the Tim es Company for $1.3 billion (C anadian), charging th a t one of the mills has polluted th ree rivers with dioxin and other toxins," L edbetter said.
[Dated announcem ent om itted from this reprint.]
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RACHEL'S HAZARDOUS WASTE NEWS #249
Providing news and resources to the Movement for Environmental Justice --September 4,1991
DIOXIN DANGERS-WHAT'S GOING ON?
The recent flap in the press over dioxin can all be traced back to a single government scientist who announced in April that he believes dioxin is less able to cause cancer in humans, and is therefore less dangerous, than he believed 10 years ago. In late April, V ernon N. Houk, a 62-year-old government worker, was keynote speaker at a University of Missouri conference sponsored by Syntex, a company that was being sued in a M issouri court by the family of a truck driver who had died of cancer and who had worked for years in a truck terminal that was contaminated with dioxin. Syntex faces another 350 dioxin lawsuits from individuals who lived at Times Beach, Missouri--a town the U.S. government bought out when they found it was heavily contam inated with dioxin, 10 years ago. D uring his speech in April, D r. H ouk dropped a bombshell: he said he believed he himself had m ade a mistake 10 years ago when he urged the federal government to evacuate 2200 residents from Times Beach. In August, the New York Tim es turned D r. H ouk's reassessment into two front-page stories and an editorial, the main message o f which was, "Many scientists now believe dioxin isn't as bad as we thought." A t least 26 other newspapers in the U.S. and Canada jum ped on the bandwagon.
As the summer wore on, Dr. Houk himself went even further. In August he was quoted in the Seattle (W ashington) Tim es (August 18, pg. B3) saying he believed the pulp and paper in dustry in the northwestern U.S. "has reduced dioxin levels enough to protect public health." H e said this was his personal view, not a government opinion. As we saw last week (RH W N #248), the paper industry is facing so many dioxin lawsuits that it is now being com pared to the asbestos industry. In a story devoted to Dr. H ouk himself, the N ew York Times noted that he is now being praised and acclaimed (the Times said "lionized") by industrial companies th a t produce dioxin as a waste product, because they say he has put an end to the "dioxin scare."
D r. H ouk's views on the dangers o f dioxin reflect the narrow public health perspectives o f the federal government. Standards for exposure to a chemical are generally based on the chemical's ability to cause cancer, and not on its ability to cause other health problems. O n this basis, D r.,H ouk justifies his change o f heart: "If [dioxin's] a carcinogen, it's a very weak carcinogen and Federal policy needs to reflect that," D r. H ouk says.
In actual fact there is much new scientific evidence indicating th at dioxin is m ore dangerous than anyone knew 10 years ago. R ecent evidence (summarized in a long article in the New . York Tim es May 15,1991 [pg. C4], and in Chemical & Engineering News August 12,1991 [pgs. 7-14]) reveals that dioxin has many toxic effects on wildlife and humans besides its ability to cause cancer. In-one species of animal or another, dioxin causes wasting syndrome [progressive weight loss leading to death]; atrophy of the thymus (a blood-forming organ important in the immune system); atrophy o f the spleen (another blood-forming organ important in the immune system); atrophy of the testicles; enlargement, deterioration and death of liver tissue; hyper plasia (excessive cell growth) in the urinary tract and bile ducts; birth defects; and suppression o f the immune system. In addition, its ability to cause cancer in laboratory animals, wildlife and humans is now a m atter of record (see R H W N #219.)
The present understanding of dioxin is that it functions like a steroid hormone. Steroid hormones are powerful chemicals that enter cells, bind to a "receptor" (a protein), form a "complex" th at then attaches to the cell's chromosomes where it directly encounters the genetic m aterial, turning on and off chemical switches that may then affect distant parts o f the bocfy in various important ways. It is not unusual for very small am ounts o f a steroid horm one to have major effects on the body.
In animal studies, dioxin is still the most potent poison ever seen. F o r example, it kills hamsters at one 64-thousandth of the fatal dose of sodium cyanide. The hamsters die of "wasting syndrome"-they lose weight and die. In rainbow trout, northern pike, and salmon, one-tenth of a part p er trillion of dioxin in w ater causes growth retardation o f young fish. The
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U.S. Fish and Wildlife Service calls dioxin "the most toxic synthetic compound ever tested under laboratory conditions."1 N o new evidence has changed any of this. Back when Dr. H ouk was recommending that people be evacuated from Times Beach, in 1981, the danger did not seem remote or theoretical. Seventy-five horses in the town had died. Dogs, rodents, chickens, cats and birds had died. N o new evidence has been found in the past 10 years to change anyone's estimate of dioxin's toxicity to these species.
In rhesus monkeys, as little as 25 parts per trillion in the diet causes increased passivity and measurable reductions in the ability to learn.2
"With laboratory animals, it seemed as if dioxin caused just about any effect you can think of," says D r. Steven Safe, a toxicologist at Texas A & M University. "You nam e it, it did it, and at extremely low doses,!' he says. D r. Safe says the mystery o f dioxin has largely been solved by confirmation th at TC D D [dioxin] and other toxic agents interact directly with genetic material [the chromosomes that, taken together, comprise the DNA molecule], the way hor mones do. It is not unusual for a horm one to have different effects and different potencies in different species o f animals. This does not make dioxin any less toxic--it merely makes it better-understood.
Chem ical & Engineering News says, "One o f the m ost significant realizations o f the past few years is that TC D D [dioxin] cannot be considered by itself... that there are a num ber o f dioxin like compounds that can all have toxic effects." Dioxins, dibenzofurans, PCBs, and some halogenated naphthalenes all mimic hormones; therefore scientists now believe they can all cause the range o f toxic effects attributed to dioxin. This is not good news for anyone because dioxin alone may account for 7 ppt [parts per trillion] in the blood of average Americans but when these related compounds are taken into consideration, the average American- may be carrying 100 ppt o f dioxin equivalents in his o r h er blood stream. The meaning o f these levels of contamination will become clearer in the next few years.
Even now, far-reaching effects in fish and birds in the G reat Lakes are observable at 35 to 65 ppt. Philip M . Cook at the U.S. Environmental Protection Agency laboratory in Duluth, MN, says he believes G reat Lakes fish are failing to reproduce already because o f the dioxin burden they carry.
Researchers observing wildlife in the G reat Lakes are seeing hermaphroditic offspring of birds-for example, male birds with partially developed female sex organs. They are seeing female-female bonding behavior. These potent dioxin-family toxins seem to act like, or interfere with, normal sex hormones like estrogen, producing "chemically castrated" males, and sexually-confused females.
Linda S. Bim baum , director of the Environm ental Toxicology Division o f the E P A 's Environm ental H ealth Effects R esearch Laboratory has overall responsibility for the EPA 's year-long reassessment of dioxin's toxicity (see R H W N #248). Unlike V em on H ouk, for whom "the issue is mostly decided" already (says Chemical & Engineering News), D r. Bim baum believes when all the evidence has been evaulated, E P A may not change its regulatory num ber for dioxin much. The num ber was initially established because of a great fear of dioxin as a carcinogen. Now a whole new set of toxic properties o f dioxin, and dioxin-like chemicals, have become apparent, even as the carcinogenicity question has assumed less importance.
[1] Ronard Eisler, Dioxin Hazards to Fish, Wildlife, and Invertebrates: A Synoptic Review. [Biological Report 85(1.8); ContaminantHazard Reviews Report No. 8}. Laurel, Maryland: U.S. Department of the Interior, Fish and Wildlife Service, Patuxent Wildlife Research Center, May, 1986. [2] R. Bowman and others. "Behavioral Effects in Monkeys Exposed to 2,3,7,8-TCDD Transmitted Maternally During Gestation and for Four Months of Nursing," Chemosphere Vol. 18 (1989), pg. 235.
[Dated announcement omitted from this reprint.]
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Providing news and resources to the Movement for Environmental Justice --January 22, 1992
EPA's Dioxin Reassessment-Part 1 NEW PICTURE OF DIOXIN'S TOXICITY EMERGES
U.S. Environmental Protection Agency [EPA] is pressing ahead with its "reassessment" o f the toxicity o f dioxin, aiming to produce a draft report by June. It has been widely rumored in news papers that EPA 's reassessment will downgrade the dangers o f dioxin. But in fact it now appears that EPA may conclude in June that dioxin is at least as toxic as the agency now assumes it to be~ and it's even possible the agency will declare dioxin more toxic, not less.
EPA officials announced in April 1991 that "new scientific evidence" showed dioxin may be less dangerous than the agency had said back in 1985 when it first set stringent standards for dioxin exposure to humans. Based on the "new evidence" it was time to reassess the dangers o f dioxin, agency chief William Reilly announced in April. Then, as the year-long reassessment got under way, Mr. Reilly jumped the gun and told the New York Times August 15 (pg. 1) what the conclusions of his agency's study would be: "We are now seeing new information on dioxin that suggests a lower risk assessment for dioxin should be applied." The Times ran the story on page one.
We have since learned that the whole idea of reassessing the toxicity o f dioxin originated with executives o f four major paper companies who visited Mr. Reilly's office January 23rd, 1991, and that Mr. Reilly's August statement to the New York Times reflected the paper industry's agenda, not the views of EPA scientists. At an EPA public hearing on dioxin in Washington November 15, Greenpeace and Alder-Hill Associates o f Tidewater, Oregon [(503) 528-7151], released leaked documents including a January 25th, 1991, letter from the four paper company chief executive offi cers (John A. Georges, International Paper; T. Marshall Hahn, Jr., Georgia-Pacific Corp.; Furman C. Moseley, Simpson Paper; and Andrew C. Sigler, Champion International) thanking Mr. Reilly forliis receptiveness to their ideas January 23: "We were also encouraged by what we perceived as your willingness to move expeditiously to re-examine the potency o f dioxin and chloroform in light of the important new information that has been submitted with respect to those chemicals."
In their discussions with Mr. Reilly Jan. 23, these executives browbeat EPA for "failure to act on the emerging health science." They claimed there is now a "prevailing view that low-level dioxin exposures do not pose a serious health threat." "Despite this new reality," they said in their January 25 letter, "EPA has taken no tangible or timely steps to revisit its health criteria for dioxin, and has even failed to tem per the Agency's zeal in acting on the worst risk estimates...." As a direct result of these EPA failures, the executives told Mr. Reilly, the paper industry is belea guered by "public fears about risk associated with dioxin which bears no relationship to scientific evidence. A consequence of this atmosphere is that our companies are now the subject o f ground less class action toxic tort suits seeking billions o f dollars in damages."
In other words, it's entirely EPA 's fault that the paper industry has now begun to resemble the asbestos industry--overwhelmed by lawsuits by citizens claiming harm from exposure. In no uncertain terms, these paper company executives told Mr. Reilly how important it was that his agency play down the toxicity o f dioxin in public statements: "Reasoned public statements can help calm the needless public alarm that has, in turn, stimulated the proliferation of unjustified.legal action against so many companies in our industry," the paper company officials said.
In August Mr. Reilly met the paper industry's need for "reasoned public statements" and the New York Times put it on page one: "U.S Officials Say Dangers o f Dioxin W ere Exaggerated." At least 26 other major American newspapers picked up this story, and it is now "common knowledge" that dioxin is not as dangerous as officials used to think. William Reilly himself says so.
Meanwhile EPA 's scientific staff was pursuing a very different line o f reasoning. They had con cluded that dioxin not only causes cancer in humans, but also that it interferes with human health in a broad range of ways. EPA scientists are now referring to dioxin as an "environmental hor mone."
Based on concern about dioxin's potency as a carcinogen, EPA in 1985 established a very strin gent allowable intake of dioxin for humans: 0.006 picograms (or 0.000000006 micrograms) per kilo-
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gram of body weight per day. Since the "average" person is assumed to weigh 70 kilograms (154 pounds), this "average" person is allowed to eat no more than 0.006 x 70 = 0.42 picograms of dioxin each day. One microgram (pg) is one-millionth o f one gram; a picogram (pg) is a millionth o f a microgram, or a trillionth o f a gram. There are 28 grams in an ounce.
Unfortunately, because of widespread dioxin contamination o f the food chain by the paper in dustry and other sources, the average American eats dioxin in daily quantities ranging from 3 to 50 picograms, thus exceeding the EPA 's "safe" dose o f 0.42 picograms by anywhere from seven-fold to 120-fold, depending on whose data you accept regarding dioxin contamination o f our food supply. [1, pgs. 94-95.].
H ere is the basic problem: if the EPA 's stringent 1985 standard is warranted, then the dioxin in our food supply represents a major failure o f public health protection. Naturally, therefore, it is in the interests of EPA itself--which does not want to look like a failure-am i o f the dioxin dum pers in the paper industiy (and others)-w ho do not want to look like thoughtless poisoners~to find "new" evidence making dioxin appear less potent. Unfortunately, all the new evidence seems to be pointing in the other direction.
Dioxin is never produced intentionally; dioxin serves no useful purpose and, so far as anyone knows, there are no benefits from dioxin in your body, only risks. Nevertheless, dioxin is created in major quantities as a byproduct: from chlorine bleaching o f pulp and paper, from manufacture of certain herbicides (e.g., 2,4,5-T), from manufacture of many plastics (e.g., PVC), from manufac ture of many chlorinated hydrocarbon chemicals, and from incineration of municipal solid wastes.
At the heart of the dioxin problem is chlorine. Chlorine is a highly reactive chemical (it tries to hook ontp anything it touches, to form a new chlorinated molecule). Because it is so reactive, chlorine almost never occurs in a free state in nature; it is all bound up in the very stable molecule known as sodium chloride, or table salt.
Starting at the turn of this century Dow Chemical, and later other firms, began producing free chlorine as they split salt to get sodium, which they sold commercially as sodium hydroxide (caustic soda). Then they began to invent uses (to create markets) for all the waste chlorine, and thus the chemistry of "chlorinated hydrocarbons" was developed. Unfortunately, chlorinated hydrocarbons-- solvents, pesticides, plastics, and a host o f other chemicals-have turned out to be uniquely persistent, uniquely able to accumulate in food chains, and uniquely toxic in fish, birds and mam mals, like humans.
Now, with EPA 's dioxin reassessment chugging along, a new body o f knowledge about the toxicity of dioxin is developing rapidly. A review article in Science News (Vol. 141, January 11, 1992, pgs. 24-27) summarizes current understanding o f dioxin's toxicity--and there is nothing in the new picture that would be comforting to the paper industry o r to its fellow dioxin polluters in chemicals, plastics, pesticides or solid waste incineration.
Dioxin has always baffled toxicologists because it produces different effects in different species, and different effects within the same species at various doses. But the new science o f dioxin is beginning to explain these mysteries by viewing dioxin as a hormone. Hormones are chemical messengers that travel throughout the body turning on and off various chemical switches. H or mones need only be present in tiny quantities to set off a cascade o f major changes in bodily sys tems, changes not limited to cancer.
Linda B im baum -a key member of EPA 's team reassessing dioxin-told Science News, "If you think of TCD D lis 'a hormone, it makes it easier to understand these veiy big differences [in dioxin's behavior]."
[Continued next week.]
[1] Agency for Toixic Substances and Disease Registry, Toxicological Profile for 2,3,7,8-Tetrachlorodibenzo-p-diadn [ATSDR/IP-88/23] (Springfield, VA: National Technical Information Service [NTIS], 1989); available from NTIS [phone (703) 487-4650] as publication number PB89-214522.
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Providing news and resources to the Movement for Environmental Justice - January 29,1992
EPA's Dioxin Reassessment-Part 2 DIOXIN DAMAGES HUMAN IMMUNE SYSTEM
U.S. Environmental Protection Agency [EPA] is presently reassessing the dangers of dioxin, one of the most toxic chemicals ever tested on laboratory animals. As a result of animal tests, EPA has declared only exceedingly small amounts of dioxin "safe" for the human food supply. Americans eat food routinely containing roughly 10 to 100 times more dioxin than EPA considers safe. [See RHW N #269.]
No one makes dioxin intentionally, but many industries create dioxin as a byproduct o f their main activity. Industries that emit dioxin into the environment (paper, plastics, chemicals, and solid waste incinerators) are being sued for their emissions by citizens claiming harm from exposure, and one industry-paper--faces billions of dollars in lawsuits.
Partly to please the paper industry, and partly because there were new scientific findings worth considering, EPA chief William Reilly announced a year-long dioxin reassessment to begin in April, 1991.
Now, nine months into the year-long process, EPA scientists responsible for parts of the reassess ment have begun talking openly about new findings that make dioxin seem as bad as, or worse than, EPA used to think.
For two decades dioxin has baffled toxicologists. They are used to seeing cancer-causing chemicals that predominantly cause cancer in one organ or another-like asbestos, which chiefly affects the lungs, or benzene, which chiefly affects the blood-forming cells, causing leukemia. But dioxin seems to cause cancer in many organs, raising the general level o f cancer in a population without causing a huge increase in any one type of cancer. In addition, dioxin causes certain toxic effects in one species and other effects in another species. Likewise, dioxin at low doses causes one kind o f illness, and at higher doses it causes different illnesses. Only recently have EPA scientists concluded that this puzzling pattern occurs because dioxin acts like an "environmental hormone." Hormones are potent natural chemicals that send messages via the bloodstream, turning on and off chemical switches throughout the body, creating an array of effects in different organs. Dioxin behaves this way. Hormones are present in the body in tiny amounts, yet they can trigger huge changes in various bodily systems. For example, it is hormones that trigger the different stages of growth in a fetus, and that cause young humans to go through puberty.
New Information EPA chief William Reilly was right--there is new information about dioxin. But it won't be reas suring to the paper industry. On the contrary, two studies of workers exposed to dioxin, published during the past year, have shown unmistakable increases in cancers o f several types. A study of 5172 American workers revealed a cancer rate 46% above the norm.1 Likewise, a study o f 1583 German workers revealed a-cancer rate 39% above the norm; among German workers 20 years on the job, the rate was 82% above the norm, and among the most heavily exposed Germans workers, the cancer rate was three times the norm.2 Notably, among female German workers, the risk of breast cancer was doubled. Whereas a year ago one might have argued whether dioxin had ever been shown to cause cancer in humans, now such arguments are only voiced by the kind of people who say it still isn't proven that cigarettes cause lung cancer. Linda Bimbaum, one of the scientists conducting EPA's reassessment o f dioxin, says these two stu dies have convinced her that dioxin causes cancer in humans, at least at relatively high exposures. But, she told Science News (January 11, 1992, pgs. 24-27.), she has an even greater concern about dioxin: "I'm very concerned that much lower exposure to dioxin may result in adverse health effects that are very subtle and difficult to detect." She was talking about dioxin's impact on the immune system. The immune system is an exceedingly complex network of organs, cells, and chemical secretions (hormones) that react to preserve health in the face of a vast array of hostile microorganisms and toxi cants that our bodies encounter every day. The immune system fights against common colds, influ enza, and the body's own cells that go haywire and start to multiply uncontrollably (a definition of can cer). A degraded immune system leaves the body less able to defend itself against hostile forces in the natural environment. Dioxin attacks the immune system.
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EPA's dioxin reassessment will "focus much greater attention on toxicological data revealing TCDD's [dioxin's] reproductive, developmental, and immunotoxic effects," says Science News. Immunotoxic means toxic to the immune system. Furthermore, "This document [EPA's draft reassessment][ will also establish TCDD as the first pollutant to be regulated on the basis of toxicity observed at the cellular level."
This is one reason why the dioxin controversy is being followed so carefully by industry and by en vironmentalists. It promises to set precedents in the way chemicals are regulated in the future. In the past, chemicals were considered harmless if they caused no "clinical" damage (damage your family doctor might detect). Now, with the dioxin reassessment, evidence of chemical changes inside in dividual cells is being considered important to a person's well being.
"So far, studies in mice suggest that dioxin's immunotoxic punch occurs in extremely low doses and may well be more important than cancer in determining dioxin's primary health risk," says Bimbaum."
To study TCDD's toxicity to the immune system, researchers use mice, whose immune systems mo del those of humans. For example, EPA researchers have measured how well TCDD-treated mice withstand the influenza virus. Mice pre-treated with TCDD readily die after exposure to a quantity of virus that rarely kills healthy mice.
Naturally, it would be very difficult to detect such effects in people. If people exposed to unusually high levels of dioxin, say from a solid waste incinerator, had damaged immune systems and consequen tly experienced various illnesses, no one might ever suspect dioxin as a cause.
People might question whether some of dioxin's low-level effects represent real harm to people, but "...few people will contend that suppression of the immune system is not an adverse health effect," Bimbaum told Science News.
Unlike hormones, which remain in the body only a few hours, dioxin has a half-life in the body of seven years. At the end of one half-life, half the initial dioxin remains. What this means is that dioxin has, relatively, a very long half-life in the body, unlike the hormones that it mimics, so it stays around to play havoc with the body's chemical systems year after year. "Thus one TCDD [dioxin] molecule can continuously disrupt normal cell physiology," says Science News, citing work by well-known dioxin researcher Thomas A. Gasiewicz at the University of Rochester (NY) Medical School. EPA's Bimbaum, and Michael Holsapple, a well-known dioxin researcher at the Medical College of Virginia, say studies of humans at Times Beach, Missouri, and of Vietnam veterans, were essentially bungled. Holsapple says, "If I were to take mice and iask the same [research] questions that are routinely asked of the populations of Times Beach or in the Ranch Hand study [of Vietnam vets exposed to dioxincontaminated herbicide], I would come up with a very nebulous picture [of dioxin's immunotoxicity]," says'Holsapple. "But when we ask different questions [in mice], we can certainly show very strong effects on the immune response," he says.
Is there a threshold for dioxin's damage to the human body? Is there a level o f dioxin below which no effects can be observed? George Lucier o f the National Institute of Environmental Health Scien ces in Research Triangle, North Carolina, has been asking this question in his laboratory. His data show no evidence of any threshold. "My data might not prove that a threshold doesn't exist," he told Science News, "but there's also no evidence of any thresholds." In other words, any amount o f dioxin does some damage, according to Lucier's findings. This means the only safe amount is zero.
This conclusion is not what the paper industry wanted to hear when its executives urged William Reilly to initiate EPA's dioxin reassessment. As the reassessment reaches its draft stages early this summer, we'll have new measures of the potency not only of dioxin, but also of industry's muscle in a contest with unwelcome scientific conclusions.
For all of us, much is riding on the outcome.
[1] Marilyn Fingerhut and others, "Cancer Mortality in Workers Exposed to 2,3,7,8-tetrachlorodibenzo-p-dioxin,T,Are>v England Journal o f Medicine Vol. 324 (1991), pgs. 212-218. [2] A . Manz and others, "CancerMortality Among Workers in Chemical Plant ContaminatedWith Dioxin," The Lancet Vol. 338 (October 19,1991), pgs. 959-964.
Reprint o f Rachel's Hazardous Waste News #270 RacheVs Hazardous Waste News (ISSN 1065-4623) is published weekly by Environmental Research Foundation (ERF), P.O. Box 5036, Annapolis, MD 21403-7036; Telephone (410) 263-1584; Fax (410) 263-8944; Econet: erf; Internet:
erf@igc.apc.org. Editor Peter Montague, Ph.D.; Associate editor Maria B. Pellerano; Research Assistant: Andrea K. Feameyhough. Subscription rates: $25 per year for individuals and citizen groups; $80 for government agencies; $15 for students and seniors with ID; $400 for businesses and professionals; in Canada and Mexico, add $6.00; in
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RACHEL'S H A Z A R D O U S W A ST E N E W S # 2 7 5
Providing news and resources to the Movement for Environmental Justice --March 4, 1992
DIOXIN DETOXIFICATION CAMPAIGN EXPOSED
A remarkable front-page story in the Wall Street Journal February 20 confirmed that the paper and chlorine industries have waged a successful two-year campaign to bamboozle the nation's media about the toxicity of dioxin, and that U.S. Environmental Protection (EPA) fell for it too.
The point of the campaign was to salvage the paper industry, which uses 15% of all the chemical industry's chlorine output, and which is facing billions of dollars in lawsuits brought by citizens clai ming damages from dioxin released from paper mills.
TheJournal's story ("HowTwo Industries Created a Fresh Spin on the Dioxin Debate") by Chica go-based staffer Jeff Bailey, describes a bald-faced campaign by the American Paper Institute (API) and the Chlorine Institute to "revisit" the scientific evidence that dioxin is a potent carcinogen.
The Journal says, "The paper industry scored its first major public-relations success in 1990, when paper companies arranged to challenge the findings of the most influential dioxin study ever done. That study, reported in 1978 by Richard Kociba, a Dow Chemical Co. pathologist, was done on 485 white rats, whose food was spiked with dioxin. Dr. Kociba found a strong link to cancer: a daily dose of billionths of a gram led to tumors."
To counteract the Kociba study, API hired five pathologists and brought them to a Maryland Lab in March, 1990, where for two days they reviewed Dr. Kociba's rat slides under a microscope. The pathologists voted on each slide-were they looking at a cancer tumor or at a "benign" tumor? At the end of the two days, they had voted for 50% fewer cancer tumors than Dr. Kociba had observed 12 years earlier. Robert A. Squire, the pathologist who oversaw the recount, told theJournal, 'There was't much unanimity. This was an uncertain finding."
Nevertheless API managed to ignore the uncertainties. Based on its "new evidence" that dioxin is less potent than previously believed, API wrote stem letters to the Food and Drug Administration (FDA), to President Bush's science adviser, and to William Reilly, chief of EPA. API told EPA, "All of the Agency's analyses are now out of date in light of the significant new evidence showing that the risks of dioxin has been overstated."
The Journal does not say so, but almost immediately the API's publicity machine began cranking out the "news" that dioxin was no longer considered very dangerous. May 31,1990 the Washington Post (pg. A3) surprised the world with the headline, "Scientists Temper Views on Cancer-Causing Potential of Dioxin." The story, by Malcolm Gladwell, said, "Dioxin-the chemical that forced the evacuation of Love Canal, sparked a wave of lawsuits over Agent Orange and became notorious as the most potent carcinogen ever tested-may be far less dangerous than previously imagined, according to new scientific evidence." Gladwell went on, "Enough experts have joined the revisionist chorus that some scientists consider a softening of the government's stance toward the chemical inevitable." Gladwell's "chorus"consisted of quotations from four scientists. Gladwell neglected to mention that three of them were consultants paid by the paper industry.
With the Washington Post on board, the "detoxify dioxin" campaign was rolling. The Journal goes on: "Next the Chlorine Institute... arranged to bring three dozen of the world's foremost experts on dioxin to a conference at the Banbury Center [on Long Island in October, 1990]."TheJournal continues, "Also present was George L. Carlo, a scientist but not widely regarded as a dioxin expert...." "Carlo is not a scientist with a long history of dioxin credentials," Dr. George Lucier of the National Institutes of Environmental Health Sciences told the Journal. The Journal goes on: "Why was Carlo there? Though described as a 'conference participant' by the Chlorine Institute, he was actually the industry's $150-an-hour observer. Based on his account, the institute would later circulate reports that the scientists had reached an important consensus...." Carlo's account, which the Chlorine Institute immediately circulated widely to journalists and to state regulatory officials, said that the scientists at Banbury had reached consensus that dioxin does no harm until a certain threshold of exposure is reached. In other words, Carlo claimed-and the Chlorine Institute sent out press statements claiming-that the Banbury meeting had reached agree ment that there is some amount of dioxin that is safe. The Journal continues, 'The institute's stat ement, however, didn'taccurately reflect what had happened at the conference....AChlorine Institute official concedes its representations about the conference were a 'botched publicity effort.' The in stitute now agrees there was no conference consensus on whether a dioxin threshold exists."
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However, before the world had a chance to learn that the Chlorine Institute was playing fast and loose with the facts, the Institute's disinformation about Banbury was fed to William Reilly, chief of EPA, who fell for it. Citing the Banbury "consensus,11in early 1991 Reilly ordered his scientific staff to officially "reassess" the toxicity of dioxin.
The paper industry got help from other friends in high places. In May, 1991, a highly-placed fed eral health official just three years shy o f retirement announced that dioxin was much less toxic than previously believed. Dr. Vernon Houk, Director of the Center for Environmental Health and Injury Control, announced that he believed dioxin was only "a weak carcinogen." H ouk's statements formed the "news hook" that allowed the New York Times to climb on board with its own page-one story August 15, 1991: "U.S. Officials Say Dangers of Dioxin W ere Exaggerated." W ith the Post, the Times, Houk and Reilly all speaking with one voice, the "detoxify dioxin" campaign was clearly succeeding.
But with the publication of the Wall Street Journal's story Feb. 20, the campaign has come unra veled. The scientist in charge of EPA 's reassessment, Peter Preuss, is quoted in the Journal saying that Vernon H ouk's statements "misled" the public about the dangers o f dioxin. O ther scientists on EPA 's reassessment team sy dioxin seems to be just the tip of a nasty iceberg-that other chemicals in the environment seem to share dioxin's ability to interfere with the human reproductive and immune systems. If we all carry dioxin in our bodies at an average o f 7 ppt [parts per trillion], when you add furans and PCBs [polychlorinated biphenyls], our average body burden o f "dioxin equivalents" may be as high as 100 ppt.1 This is not good news. A nd it means that any additional dioxins or furans added to the environment would worsen a situation that it already unacceptable from a public health perspective. Knowing this, anyone who intentionally emits dioxins into the environment seems like a logical target for a barrage o f lawsuits.
It is now clear that dioxin lawsuits can devastate an industry. F or example, the Wall StreetJournal reported February 7,1992 (pg. A5), that the Georgia-Pacific C o .-a major paper producer-recently lost two dioxin lawsuits in which juries awarded $4.2 million to residents living downstream o f its paper mill on the Leaf River in New Augusta, Mississippi. Georgia-Pacific has been named in 159 additional lawsuits filed by 8209 plaintiffs who claim they suffered emotional harm after eating fish contaminated with dioxins from the Georgia-Pacific Plant. Furtherm ore, according to the Journal, Georgia-Pacific's insurance carriers say their policies don't cover damages in lawsuits like these. Georgia-Pacific has now sued A etna Life & Casualty and seven other insurance companies in Mississippi federal court asking a judge to force the insurance carriers to pay. No m atter how that lawsuit comes out, someone is likely to have to pay tens, o r perhaps hundreds, o f millions o f dollarsand this represents the problems of only one mill owned by one company.
As the Journal commented, "Other paper companies are likely taking note o f Georgia-Pacific's setbacks. International Paper Co. and Champion International Corp. are among those who faced similar suits." Likely they are.
O ther industries are also likely watching the paper's industry's dioxin troubles proliferate. F or example, cement kilns don't produce dioxin in substantial amounts until they start burning hazardous waste as a fuel, which many kilns have recently started doing. It is interesting to note reports that George Carlo has recently been hired as a consultant by a trade association representing the cement kiln industry. When will dioxin lawsuits against cement kilns and against municipal solid waste incinerators be gin? And how big will the jury awards be in these cases? When your community is deciding whe ther to install a solid waste incinerator,2o r whether to tolerate a cement kiln seeking permission to bum hazardous waste, ask your community leaders, "Have you been reading the Wall Street Journal lately?"
[1] David J. Hanson, "Dioxin Toxicity: New Studies Prompt Debate, Regulatory Action," C&EN [Chemical & Engineering News] Aug. 12, 1991, pgs. 7-14. [2] A good discussion o f dioxin emissions from solid waste incinerators appears in Donald J. Lisk, "Environmental'Impli cations o f Incineration o f Municipal Solid Waste and Ash Disposal," Science o f the Total Environment Vol. 74 (1988), pgs. 39-66, and in the articles Lisk cites in his footnotes.
Reprint o f RacheVs Hazardous Waste News # 275 Rachel's Hazardous Waste News (ISSN 1065-4623) is published weekly by Environmental Research Foundation (ERF),P.O. Box 5036, Annapolis, MD 21403-7036; Telephone (410) 263-1584; Fax (410) 263-8944; Econet: erf; Internet: erf@igc.apc.org. Editor: Peter Montague, Ph.D.; Associate editor: Maria B. Pellerano; Research Assistant: Andrea K. Feameyhough. Subscription rates: $25 per year for individuals and citizen groups; $80 for professionals and government agencies; $15 for students and seniors with ID; $400 for businesses; in Canada and Mexico, add $6.00; in all other countries, add $11.00. All payments in U.S. funds drawn on U.S. banks. Visa & Mastercard accepted. Rachel's Hazardous Waste News is not copyrighted; we encourage reprinting so long as you send us a copy. Printed on 100% recycled paper.
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Reprint of:
RACHEL'S HAZARDOUS WASTE NEWS #283
Providing news and resources to the Movement for Environmental Justice ~ April 29,1992
WASTE WARS: THE ARMY OPENS A NEW FRONT
Here's the emerging picture of hazardous waste disposal in the U.S.: Citizens have blocked construction of all new hazardous waste dumps. There are no new dumps on the drawingboards. EPA [U.S. Environmental ProtectionAgency] is aggressivelypromotinghazardous waste incin erators because the alternative-waste avoidance and pollution prevention--would inconvenience the generators of hazardous waste. Rather than inconvenience anyone with power and connections, EPA is promoting incinerators. It's really that simple. Industry likes incinerators because liability for toxic waste disappears when the waste enters the incinerator. From the Superfund dump-cleanup program where they're spending billions defending themselves against lawsuits, industry knows the liabilityproblem is serious. Incinerators solve this problem because after chemicals pass through an incinerator, there are no labels left on the barrels to identify responsible parties. Most of the waste goes up the smoke stack and can't be traced. The incineratorcompany--notthe original waste generatorbears responsibilityfor the toxic ash, but in the scheme of things incinerator companies are relatively small and can declare bankruptcy when their ash dumps begin to leak, a few decades from now. EPA will then put the ash dumps on the Superfund list, and the taxpayer will bear all the costs. It's a practical system and it should work. The only hitch is that citizens are blocking the siting of new incinerators. So EPA is cooperating with the U.S. Army and the Department of Energy (DOE) to solve this problem. The Department of Energy has an nounced plans to site a huge, privately-owned incinerator on the Hanford Reservation in Washington state. DOE has produced plutonium for A-bombs at Hanford for 40 years. DOE will deflect public outrage about siting the privately-owned incinerator, and Chem Waste will run it, despite Chem Waste's embarrassing record of failure running incinerators (see RHWN #280 and #281). For its part, the Army has announced plans to site eight huge chemical-waste incinerators at Aberdeen, Maryland; Richmond, Kentucky; Anniston, Alabama; Pine Bluff, Arkansas; Pueblo, Colo.; Newport, Indiana; Tooele, Utah; and Umatilla, Oregon. The Army's stated goal is to bum up old chemical warfare weapons that now aren't needed. At a public hearing at Aberdeen three weeks ago, the Army said with a straight face it will spend $500 million building the incinerator, use it for 14 months to destroy mustard gas and then dismantle it, never burning any other defense wastes or civilian wastes. Local people don't believe it, and they fear military incinerators would be as dangerous as civilian incinerators. But let's be fair. Maybe the private incinerator companies have bungled the job merely because they are careless and cut comers to increase profits. The army would have no such motives and could perhaps be relied upon to do a better job. What do we know about Army experience running incinerators? The military has already built and operated a modern, state-of-the-art incinerator specifically designed to destroy left-over chemical warfare weapons. To avoid a hassle with local citizens, they built the incinerator on an island in the South Paciflc-Johnston Atoll. Environmentalists and local native people opposed the facility but that did not deter the Army. During the period July 16, 1990 through February 27, 1991, the Army fed 7490 M55 rockets containing 75,000 pounds of the nerve agent GB (also known as Sarin), into the Johnston Atoll Chemical Disposal System (JACADS). GB is among the most powerful nerve poisons ever developed. The operation of the JACADS incineratorwas evaluated by MITRE Corporation (McLean, Virginia) under contract to the Army. T h e MITRE report has been scrutinized by chemist Pat Costner, research director for Greenpeace. Her paper, "Chemical Weapons Demilitarization and Disposal; The Army's Experience at Johnston Atoll Chemical Disposal System," contains valuable data and insights into what we can expect from the Army's path-breaking chemical-weapons incineration program.1 Here are facts Costner gleaned from the book-length MITRE report: ** During the period of operation, the JACADS incinerator functioned for 500 hours but during the same period it experienced 929 hours of down-time because of malfunctions. The "mean (average) time between failures" throughout the period was 5.6 hours. M During the 500-hour operating period when agent GB was being burned, the network of monitors for detecting GB releases triggered776 major process alarms, an average of 22 per day. Major process alarms are "those that are so important that agent or spent decontamination] processing is stopped," according to the MITRE report. A high level of carbon monoxide (CO) in smoke-stack gases is an indication of poor burning. Of the 776 major process alarms that occurred, "the majority" were for high carbon monoxide in the stack gas--a dead give away that the incinerator was experiencing "upsets." During upset conditions, an incinerator emits large quantities of pollutants into the environment. The EPA Science Advisory Board says, "Even relatively short-term operation of incinerators in upset conditions can greatly increase the total incinerator-emitted loadings [pollution emissions] to the environment." Accordingto the MITRE report, the JACADS incineratorsuffered 90 burner lockouts and 40 fuel flow shut-
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downs during the GB-burning campaign, further evidence o f upsets. A s Costner said in her report, "In other words, the [incinerator] operated in a continuous upset condition during the G B campaign."
On 32 occasions the JACADS incinerator released GB nerve agent into corridors frequented by workers. Furthermore, during 500 hours o f incineration, the JACADS workforce accumulated 1944 hours o f lost-time accidents., In other words, every hour o f operation was accompanied by 3.9 hours o f injury-related lost-time among the workers. Costner documents other serious problems with the Army's JA C A D S incinerator as well.
This is not good news. It m eans the Army's 8 proposed state-side incinerators will do no better-perhaps considerably w orse--than civilian hazardous waste incinerators, which are poor indeed.
Inside their furnaces, incinerators destroy som e chemicals, but in the process they create many new toxic by products that did not exist before, all o f which they emit into the environment partly via the sm oke stack and partly via the ash, which is buried temporarily in a landfill until it leaks out. Am ong the most toxic o f those chemicals are dioxins and furans. On January 27,1992, EPA staff presented their latest Endings about dioxins and furans to E P A chief William Reilly. RH W N has obtained a set o f 24 acetate transparencies prepared by EPA staff for chief Reilly. They contain important new information about dioxin:
E PA 's transparency 17 says: R ecent scientific results and conclusions: * D ioxin does cause cancer in humans. * Cancer m ay n o t be the m ost sensitive toxic response resulting from dioxin exposure. Im m unotaxicity and reproductive effects appear to occur a t body burdens that are approxim ately 100 tim es low er than those associated with cancer. * R ecent data indicate that there m ay n o t be a threshold fo r certain responses to dioxin. However, the im plications fo r specific risk assessm ents, such as fo r cancer, are n o t yet clear. * R ecent evidence has strengthened the conclusion that the sensitivity o f hum ans is sim ilar to that o f experim ental anim als (cancer, im m unotaxicity, A h receptor binding, etc.). E P A 's transparency 18 says: N ew science and conclusions......continued. * Current exposure levels to dioxin and related com pounds appear to p la ce peo p le a t o r near the body burden when sensitive responses m ay occur, especially fo r subpopulations a t high-end exposure, e.g., nursing infants, recreational and subsistence anglers. * Continuing research into the risk from dioxin expo-sure should result in a continuing process o f reassessm ent as new data becom e available and are incorporated into a new, m ore flexible m o d el * O R D [EPA's Office o f R esearch and Developm ent] scientists have reached the tentative conclusion that dioxin exposure m ay have been responsible fo r the decline o f L ake Trout in L ake O ntario as a result o f the reproductive toxicity o f dioxin. L et's review briefly what E P A has said here: One. Dioxin causes cancer in humans, but cancer is not the most sensitive indicator o f damage from dioxin; damage to the immune system, and reproductive damage, are the m ost sensitive indicators. Two. Animals and humans are about equally sensitive to damage from dioxin. Three. The amount o f dioxin presently in our food ("current exposure levels," E P A calls it) puts humans at or near the body-burden o f dioxin at which "sensitive responses" [immune system damage, and damage to the reproductive system] may occur. T hose at greatest risk are infants who drink their mother's breast milk, or people who eat more-than-average amounts o f fish because fish accumulate these poisons in their tissues. Four. In fact, it appears that because fish accumulate these poisons in the fat tissues o f their bodies, and because Osh eggs have a high fat content and therefore a high dioxin content, Lake Trout in the Great Lakes are not able to thrive. Evidently humans are not the only species endangered by dioxin. T he logical conclusion from E P A 's data is that Americans cannot afford to increase the amount o f dioxins and furans in their bodies-they are already at or near the levels where immune system damage and reproduc tive system damage occurs, especially babies. Thus all plans to build new incinerators in the U .S. stand in direct conflict with public"health priorities. New incinerators (and uses o f chlorine) should be banned, old ones phased out.
[1] Pat Costner, "Chemical Weapons Demilitarization and Disposal: The Army's Experience at Johnston Atoll Chemical Disposal System." (Washington, DC: Greenpeace, April 11,1922). Available for $5.00 from Greenpeace, 1436 U St., NW, Washington,DC 20009. Telephone (202) 462-1177 and ask for Sanjay.
There's a growing network of activists fighting all 9 of the Army's proposed Incinerators; contact: Craig Williams, Kentuclqr Environmental Foundation, P.O. Box 467, Berea, KY 40403; phone (606) 986-7565.
Reprint o f Rachel's Hazardous Waste News #283 RacheVs Hazardous Waste News (ISSN 1065-4623) is published weekly by Environmental Research Foundation (ERF), P.O. Box 5036, Annapolis, MD 21403-7036; Telephone (410) 263-1584; Fax (410) 263-8944; Econet: erf; Internet: erf@igc.apc.org. Editor Peter Montague, Ph.D.; Associate editor Maria B. Pellerano; Research Assistant: Andrea K. Feameyhough. Subscription rates: $25 per year for individuals and citizen groups; $80 for professionals and government agencies; $15 for students and seniors with ID; $400 for businesses; in Canada and Mexico, add $6.00; in all other countries, add $11.00. All payments in U.S. funds drawn on U.S, banks. Visa & Mastercard accepted. Rachel's Hazardous Waste News is not copyrighted; we encourage reprinting so long as you send us a copy. Printed on 100% recycled paper.
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Reprint of:
RACHEL'S HAZARDOUS WASTE NEWS #310
Providing news and resources to the Movement for Environmental Justice -- November 4, 1992
THE N.Y. TIMES DETOXIFIES DIOXIN (AGAIN)
During August and September U.S. Environmental Protection Agency (EPA) released drafts of 8 chapters of its long-awaited report on the dangers of dioxin. The agency then promptly convened a 4-day meeting of independent scientists September 22-25 to review and discuss the drafts.
The day after the meeting ended, th e N ew Y ork Tim es reported (Sept. 26,1992, pg. 9) that "An inde pendent panel of scientists concluded today that dioxin was not a large-scale cancer threat except to people exposed to unusually high levels of the toxic compound in chemical factories and from accidents."
The Time? said, "The panel based its conclusions about the effects of dioxin on human health largely on four studies...."
The Tim es story said, "...the risk to average Americans exposed to dioxin, principally by eating beef, dairy products, chicken and fish, is lower than previously believed."
The Tim es reported that, "The risks, said several panelists, are largely confined to chemical workers and people exposed to high levels of dioxin from industrial accidents. They said the levels of dioxin ordinarily found in the environment had not been shown to be dangerous to people."
The T im es went on, "Scientists have known for a long time that laboratory animals are apparently much more sensitive to the dioxin molecule than people for reasons that are not well understood, and newer studies have shown that trout, salmon, and some species of birds also are very sensitive."
The Tim es concluded, "In separate interviews, several panelists said today that they did not consider the levels of dioxin in most Americans, about 5 parts per trillion in fat, to be an important health hazard."
In sum, the Afew Y ork Tim es led its readers to believe that a panel of independent scientists reviewed four studies and concluded, apparently by consensus, that dioxin is only a danger to the health of heavilyexposed chemical workers and victims of rare accidents, and even for them the only danger is cancer; that existing levels of dioxin in the environment are not dangerous to.people; that the risks of dioxin are lower than previously believed; that laboratory animals and some wildlife may be at risk but this has little to do with humans because humans--for reasons unknown--seem to be uniquely unaffected by low doses of dioxin.
The Tim es put this comforting story on the wire and many U.S. newspapers picked it up. The result was a nation-wide press blitz saying dioxin is basically harmless to humans. For example, the D etroit N ew s reprinted.the T im es story, then capped it off Sept. 29 with an editorial,"The End of Dioxin Hys teria?" which concluded, "But the fact that dioxin has turned out to be something of a non-issue where humans are concerned suggests the religious zeal with which some environmentalists are trying to close down the chemical industry deserves to be greeted with extreme skepticism."
Is this the last word on dioxin? It's not a threat to human health; levels found in the environment today are of little concern; the risks used to seem worse than they seem today; and the risks are limited to cancer among chemical factory employees. Is that what EPA spent 18 months and untold millions of dollars to find out?
It seems not. Other reporters and participants in the four-day meeting-including top EPA officials who called the meeting--came away with views and information almost 180 degrees out of sync with what the N ew York Tim es reported. On October 9, Erich W. Bretthauer, EPA's Assistant Administrator for Research and Development, sent a memo to EPA chief William Reilly giving Reilly his own views on what EPA has learned so far about dioxin. In-his memo, Bretthauer made seven points, each of which was either contradicted, or missed entirely, by the Tim es:
1. To understand the risks of dioxin, we should consider a broad range of health effects, not just cancer, Bretthauer told Reilly.
2. Dioxin has been observed to cause certain non-cancer effects in animals by disrupting the body's endocrine system (glands and tissues that control bodily functions via chemical messengers called hormones). These endrocrine effects include reproduction, behavior of offspring, and changes in the immune system. "Some data suggest that these effects may be occurring in people at body burden levels that can result from exposures at, or near, current background," Bretthauer told Reilly. In other words, the amount of dioxin already present in the environment, and in the bodies of Americans, is at, or close to, levels that, in animals, cause hormone shifts, reproductive disorders, changes in behavior, and immune system damage.
3. Recent studies indicate that dioxin causes cancer in humans; these studies need to be evaluated further and then EPA needs to form a new official position about the cancer hazard to humans.
4. Additional compounds besides dioxin (for example, some types of PCBs) have dioxin-h^ygfects
and should be included in EPA's reassessment of the hazards of dioxin. 5. There is insufficient data to develop a model that will allow us to predict the cancer hazards to hu
mans from low-level exposure to dioxin. During the next 3 to 5 months, government studies may provide the needed data.
6. The available data seem to indicate that dioxin will cause cancer in humans in proportion to the exposure-high doses will cause many cancers, lower doses will cause fewer cancers, and the only dose that is risk-free is zero. In other words, the so-called "linear hypothesis" of cancer causation appears to hold true in the case of dioxin, though this is not certain.
7. Risks from existing background levels of dioxin in the general population need to be "carefully considered."
The W all S treet Journal (Oct. 16, 1992, pg. B9) summarized Bretthauer's memo this way: "Data re viewed by an independent scientific panel suggest that the danger from dioxin may be broader and more serious than previously thought, according to an internal Environmental Protection Agency memo."
The business journal, E nvironm ent R eporter [R] (Oct. 2,1992, pg. 1504), offered its own coverage of the Sept. 22-25 meeting. The basis of /?'s story was an interview with William H. Farland, director of the EPA Office of Health and Environmental Assessment, the man in charge of the EPA's reassessment of dioxin. Farland summarized the four-day meeting by saying dioxin is "a major health threat," and that the draft report on dioxin is "unlikely to ease public concern over dioxin."
Farland said that "scientists at the recent meeting reported a host of non-carcinogenic effects at very low dose levels-near background levels-as well as the ability to cause cancer in humans at high doses," E n viron m en t R eporter said.
In sum, EPA's scientific reassessment of dioxin-which is based on several thousand studies of dioxinisn't over yet, but so far the scientific evidence is showing dioxin to be a worse problem than formerly believed. The reassessment was initiated by EPA chief Reilly 18 months ago in response to complaints by the paper and chlorine industries, who charged that EPA's regulation of dioxin was too strict because low doses of dioxin are harmless. These industries argued that there is a "threshold," an amount of dioxin below'which no effects will occur. EPA's scientific reassessment of dioxin has, so far, substantiated EPA's original view of dioxin, that it is a potent toxin for which there is no observable threshold. Furthermore, the reassessment has added a host of new concerns, which were discussed at length during the four-day meeting-concerns about disruption of the reproductive system, harm to the immune system, and behavioral changes in offspring of dioxin-exposed parents.
The really big news from the meeting was the revelation that these endrocrine-system effects in ani mals are observable at body burdens similar to the body burdens in Americans today. If this view is upheld in the next few weeks as scientists continue to review the available data, it will mean that any addition of dioxin to the environment will be adding to an already-unacceptable situation. This would provide a scientific foundation for a demand that "zero discharge" be adopted as the basis for control of dioxin. William Farland nearly said as much in his interview with E R : "We have to be very cautious about any additions of dioxin to the environment. We must be very concerned about these high background levels of dioxin and what they may mean for human health."
Industries that emit dioxin into the environment-paper producers, waste incinerators, metal smelters, and herbicide producers and users-are feeling tremendous pressure to curtail emissions, and the pressure seems likely to increase.
Newspapers, of course, are dependent upon paper for their existence and they have a material interest in keeping paper prices low. According to the W all Street Journal, the paper industry has already spent over a billion dollars trying to control dioxin.
The iVew Y ork lim e s , which has a history of odd reporting on dioxin (see R H W N # 2 4 8 , # 2 4 9 , #275), received at least three letters to the editor complaining about its misleading coverage of the September meeting-two of them from scientists who participated in the meeting and who objected strongly to the Tim es's reporting. The Tim es also received a letter from a consultant to the incineration industry who said it was "comforting" to learn that the dioxin found now in the bodies of Americans is "less toxic than previously assumed." The Tim es did not print either of the letters from the scientists but did print the letter from the incineration consultant, who argued that automobiles are the leading source of dioxin. This point of view, which is no doubt comforting to the incineration industry, and to the paper and newspaper industries, is almost certainly wrong. We will provide more details next week.
Reprint o f Rachel's Hazardous Waste News #310 Rachel's Hazardous Waste News (ISSN 1065-4623) is published weekly by Environmental Research Foundation (ERF),
P.O. Box 5036, Annapolis, MD 21403-7036; Telephone (410) 263-1584; Fax (410) 263-8944; Econet: erf; Internet: erf@igc.apc.org. Editor: Peter Montague, Ph.D.; Associate editor Maria B. Pellerano; Research Assistant: Andrea K. Feameyhough. Subscription rates: $25 per year for individuals and citizen groups; $80 for professionals and government agencies; $15 for students and seniors with ID; $400 for businesses; in Canada and Mexico, add $6.00; in all other countries, add $11.00. All payments in U.S. funds drawn on U.S. banks. Visa & Mastercard accepted.
Rachel's Hazardous Waste News is not copyrighted; we encourage reprinting so long as you send us a copy. Printed on 100% recycled paper.
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