Month: April 2017

Political Corruption of Science Revealed in New Book

kaykiser

Perverted Truth Exposed cover image

In Perverted Truth Exposed, Kay Kiser exposes areas of science that have been corrupted by progressive and atheist philosophies disguised as science, including  evolution, origin of life, cosmology, quantum physics and climate change.

The climate change debate presents a modern example of how the perversion of science is politically imposed to support an anti-God, anti-human progress agenda of Marxist control and power while silencing opposition through intimidation. Kiser also answers:

  • Did Darwin really steal his theory of evolution from Alfred Wallace?
  • Why did Wallace later abandon the theory as not having sufficient evidence?
  • If Hubble discovered the expanding universe leading to the Big Bang Theory, why did he continually try to convince others that their conclusion was wrong?
  • Is man-made carbon dioxide causing global warming or is it a trailing indicator of climate change in a system dominated by solar cycles, cloud cover, and ocean currents?

Available online from the following outlets in print and as an eBook.

The Truth about AIDS in Africa

kaykiser

The Truth about AIDS in Africa

The Claims: HIV/AIDS from unsafe heterosexual contact is rampant in Africa. Many children are left as orphans because both parents have died from AIDS.

The Truth:  While HIV/AIDS is undoubtedly present in Africa and other destitute areas, there are problems with its reported transmission, diagnosis and treatment.  HIV infections in the developed world occurs almost exclusively among homosexual males and IV drug users who share needles with infected people, and heterosexual transmission is rare.  In Africa, half of those diagnosed with HIV and HIV/AIDS are heterosexual women, so there must be other mitigating circumstances.  It is possible that actual infections are acquired through non-sterile injections in contraceptive clinics.  This could help to explain why HIV in Africa is diagnosed equally among men and heterosexual women.  It is very likely that HIV and HIV/AIDS are over diagnosed in Africa and other poverty stricken areas of the world with or without actual HIV testing.  Many cases of AIDS in Africa may have little or no connection to the HIV virus or indiscriminate sexual practices.  Those that are malnourished or have chronic diseases such as TB or malaria naturally have compromised immune systems, i.e. Acquired Immune Deficiency Syndrome, AIDS, from these conditions without carrying the actual Human Immunodeficiency Virus (HIV).

Because of poor healthcare facilities and abilities, HIV/AIDS may be diagnosed based on symptoms without HIV testing in many rural and isolated areas.  In other areas, where actual testing for HIV antibodies is done, a high incidence of false positives is likely to occur.  This is due to the poor specificity of the test and reaction with antibodies from other diseases and conditions.  Most of those diagnosed with HIV/AIDS, whether tested or untested for HIV, have been assumed to have full blown HIV/AIDS through disparate symptoms recognized by the UN WHO including fever, headache, rash, sore throat, swollen lymph nodes, weight loss, chronic diarrhea or cough, all of which can be caused by many common parasites or infectious diseases as well as severe illnesses such as malaria and tuberculosis (TB). UN WHO has named TB as a leading indicator of HIV/AIDS and lists TB as causing 2/3 of HIV/AIDS deaths. HIV/AIDS itself does not cause death; it opens the way for other diseases that kill people. Reporting TB deaths as HIV/AIDS deaths without confirmation of HIV bolsters the statistics, as does reporting orphans as AIDS orphans.  At this time it is impossible to know how prevalent over diagnosis is in Africa and other poor areas.

Over diagnosis of HIV and HIV/AIDS, when promoted by the international media, paints a picture of Africa that packs a triple whammy for AIDS advocates and international population control governmental and nongovernmental organizations. First, it excuses high death rates and failure to treat endemic diseases; secondly, it incentivizes HIV/AIDS research funding in developed countries by falsely declaring AIDS a heterosexual pandemic; thirdly it has the potential for vindicating population control programs in the minds of potential donors by creating a false picture of rampant immorality and promiscuity. As a bonus, it also encourages the use of condoms that furthers population control agendas.

HIV facts and questions:

HIV causes AIDS: Unlike those who deny that HIV causes AIDS or that it even exists, I do not deny that HIV causes AIDS or that HIV exists. I do question some of the current statistics, testing and treatment options.  Because it is politically incorrect to question the UN WHO recommended practices and conclusions, those who question the status quo will undoubtedly be accused of denialism by AIDS advocates in order to conflate, confuse, discredit and silence anyone daring to question the efficacy of the current testing and treatment methods, even when it might lead to better understanding and improved protocols.

Non-HIV AIDS:  TB, Malaria, dysentery and other serious chronic diseases cause a more common form of Acquired Immune Deficiency Syndrome, AIDS, that has no connection to HIV/AIDS or sexually indiscriminate behavior.   It is well known that anyone who is chronically ill and/ or malnourished naturally has a compromised immune system.  Other opportunistic diseases are easily acquired by persons whose immune systems are compromised. By labeling these non-HIV AIDS cases as HIV/AIDS, it can be an excuse for not treating the underlying conditions.

Unfortunately, for USAID, UN WHO and activist NGOs or agencies that provide aid to poor countries, because their emphasis is on required or coerced population control and not on treating disease, many clinics do not have the basic medicines, equipment or facilities to treat endemic diseases, but have store rooms filled with birth control drugs, condoms and other birth control and abortion materials and equipment. This is a human tragedy and a crime against humanity that must be stopped. It is unconscionable that Western aid not be heavily weighted toward supplying medicines and equipment for prevention and treatment of endemic diseases.

Recommendation: In both HIV/AIDS and non-HIV AIDS, treatment should always begin with addressing the presenting diseases and malnutrition. Once the patient is stabilized then HIV/AIDS treatment can begin, but only after further confirmation of the original diagnosis of HIV/AIDS.  HIV/AIDS treatment drugs further compromise the immune system so that treatment of weakened, disease ravaged patients and those with non-HIV AIDS using these drugs may do more harm than good.

International aid organizations should be encouraged or required to reverse their decades old practice of oversupplying population control materials and under-supplying needed medicines, facilities, equipment and supplies to treat endemic diseases.

Demographic Shift: HIV/AIDS in developed countries is confined almost exclusively among homosexual men and IV drug users who share needles with HIV infected people. The expected pandemic in developed countries never materialized. According to official statistics, Sub-Saharan Africa accounts for 2/3 of the HIV incidence in the world, with Southern Africa, (South Africa and Botswana), accounting for most of that. 15 to 25% of the South African population has been diagnosed with HIV or HIV/AIDS. More than half of the HIV positive people in South Africa are heterosexual women. Heterosexual contact is blamed for causing the spread of HIV, but in other countries heterosexual transmission is very rare. Unless the HIV virus has mutated, this theory of frequent heterosexual transmission cannot be valid and other mitigating factors must be considered.

Shared needles as a possible source:  One theory is that the reuse of hypodermic needles for injected birth control drugs is responsible for the spread of HIV, and, if true, could account for the higher incidence in women in Africa and other poor countries where injected birth control is required or advocated.  Injectable birth control drugs such as Depo Provera that must be reinjected every 3 months are sometimes administered in a clinic, but more often the drug and the syringes are given to patients for administration at home.  Because viruses do not live very long on surfaces outside the body, HIV could not be transferred unless an HIV infected person has used the needle just prior to reuse by a second person for birth control. This could only happen in a clinic where multiple women are injected one after another without proper sterilization of needles.

How are these in-home administered reused needles causing HIV/AIDS without an immediate HIV contamination source in each case? It is more likely that in-home injections with improperly sterilized needles would transfer opportunistic bacterial infections such as staph and strep.  The whole idea of giving hypodermic syringes to uneducated people is ludicrous; it is the worst of the birth control methods, and the best way to spread more disease and misery.  Poor women with little or no concept of microbial infective agents are unlikely to discard or destroy needles even if the package instructions say to discard after use.

Recommendation:  If this form of birth control must be injected every 3 months, it should only be done by a professional in a clinic with properly sterilized or disposable needles.  If birth control is desired, a better alternative would be insertion of an IUD, Intrauterine Device, which does not require regular follow up treatments.

Could Depo-Provera make women more susceptible to HIV infection? According to this theory, the active ingredient in Depo-Provera, (Depo-medroxyprogesterone acetate, aka DMPA), may chemically predispose at risk women to acquiring HIV through sexual contact with infected men, through thinning of vaginal epithelial cells and immunosuppression. Three recent meta-studies[1] show a statistically significant link between use of the drug and incidence of HIV in at risk women. The link to HIV transmission was not established statistically for use of either oral contraceptives or another injectable contraceptive drug, NET-EN, (norethisterone enanthate), in these studies.

Clinical Diagnosis without HIV testing: In rural poor areas of Africa HIV/AIDS may be diagnosed without HIV testing by the clinical indicators listed by WHO such as fever, headache, rash, sore throat, swollen lymph nodes, weight loss, chronic diarrhea or cough. These symptoms may also be caused by endemic diseases such as TB, malaria and other insect borne diseases, dysentery and other water borne diseases, parasites and malnutrition. WHO considers TB to be a leading indicator of HIV/AIDS. Some people diagnosed without HIV testing may instead have non-HIV AIDS caused by these endemic diseases.

Diagnosis with HIV testing: Clinical HIV tests detect antibodies to the virus, not the virus itself. HIV tests have a high incidence of false positives, so that retesting and other confirmation are needed after a positive test result. False positives of HIV testing may be the result of non-HIV AIDS caused by other diseases and pregnancy because the HIV tests are non-specific and may detect antibodies to other diseases or conditions.

Causes of False Positives:  HIV testing is not specific to HIV and is prone to false positives. It tests for antibodies to HIV, not the virus itself, but can also detect other antibodies present in chronic diseases or those acquired over a lifetime.  There are over 65 documented causes of false positives including TB, malaria, leprosy, hepatitis, Q fever, influenza or colds, herpes simplex, leishmaniosis, and Epstein Barr virus.  Pregnancy or prior pregnancies are among factors that can cause false positives due to presence of HLA (human leukocyte antigen). Is it time to question whether HIV testing, without thorough validation, is valid in parts of Africa where the population is routinely exposed to numerous diseases that leave a heavy load of antibodies in their blood?

Validation needed for HIV positives:  False positives are common so that, according to manufacturers’ instructions, positive tests must be retested in duplicate and then by another method to verify results, e.g. ELISA twice then Western Blot.  ELISA, Enzyme Linked ImmunoSorbent Assay, uses an antigen for the (in this case HIV) antibody bound to a solid surface and an enzyme that causes a color change when the target antibody attaches itself to the antigen.  Western Blot actually separates, by gel electrophoresis, each component in a mixture of antibodies bound to specific antigens. Medical testing protocols vary from country to country, so that the same test may be interpreted as positive or negative depending on the protocol. For example, UK does not use the Western Blot verification of duplicate ELISA tests, and different countries require from one to four Western Blot markers to verify and confirm a positive result.

South Africa uses duplicate ELISA only to verify positive HIV tests, resulting in 15-25% of the population testing positive, 60% of which are heterosexual women. South Africa also has a high rate of drug treatment for prevention of mother to child HIV transmission, which may mean that most HIV tests are conducted at gynecological clinics and obstetric hospitals on pregnant women. This is a problem since pregnancy is known to cause false positives. The incidence of HIV and AIDS in most of the other countries in Africa, and indeed the world, ranges from 0.1 to 5.0 percent of the population. South Africa’s 15 – 25% incidence needs a closer look. The fact that over half of these are heterosexual women is also problematic as described above.

Recommendation:  South Africans and Botswanans when first diagnosed with HIV or HIV/AIDS need to be retested using a more stringent verification protocol in the future. Unfortunately, the drugs used for treating HIV can cause false negatives, so retesting those already receiving therapy may be useless or at lease confusing.

Opportunistic Diseases: When people sicken and die with HIV/AIDS, it is not the HIV that kills them; it is other opportunistic infections that are able to invade and thrive because HIV has crippled the immune system. TB is the leading cause of death in Africa, with or without HIV/AIDS. A diagnosis of HIV/AIDS can be an excuse not to treat underlying endemic diseases.

Treatment Options:  HIV treatment drugs suppress the immune system further than the disease itself. Wouldn’t it make sense to treat the opportunistic diseases and malnutrition more aggressively first before suppressing the immune system further with AIDS treatment drugs?  In some areas of Africa, TB and HIV are treated simultaneously, which is a step in the right direction.

Orphans from AIDS? AIDS orphans are defined as anyone 15 years or younger who has lost, depending on the country, their mother, one parent or both parents to “AIDS related diseases.” South Africa includes people up to 18 years old.  WHO estimates that 70% of “AIDS orphans” have one living parent.  TB is the leading cause of death in Africa and the leading clinical indicator of the presence of AIDS.  Since many people in Africa live very short lives, with or without AIDS, how is this any different from the pattern of the past where lifespans are short and teenagers often are orphaned?

 

[1] References cited in Population Research Institute newsletter article: “While Admitting Risks, WHO Continues to Recommend Injectable Contraceptives for Women at High Risk of Contracting HIV” by Jonathan Abbamonte, April 20, 2017 as follows:

Brind J, Condly SJ, Mosher SW, Morse AR, Kimball J. Risk of HIV Infection in Depot-Medroxyprogesterone Acetate (DMPA) Users: A Systematic Review and Meta-analysis. Issues Law Med 2015; 30(2): 129-39.

Morrison CS, Chen PL, Kwok C, Baeten JM, Brown J, Crook AM, et al. Hormonal contraception and the risk of HIV acquisition: an individual participant data meta-analysis. PLoS Med 2015; 12(1): e1001778.

Ralph LJ, McCoy SI, Shiu K, Padian N. Hormonal contraceptive use and women’s risk of HIV acquisition: a meta-analysis of observational studies. Lancet Infect Dis. 2015; 15(2): 181-9.

 

Day of Reckoning for DDT Foes? NOT! Junkscience.com 2006

kaykiser

“…terrible toll in human lives (tens of millions dead — mostly pregnant women and children under the age of 5), illness (billions sickened) and poverty (more than $1 trillion dollars in lost GDP in sub-Saharan Africa alone) caused by the tragic, decades-long ban.”

Day of Reckoning for DDT Foes?  Reblog from Junkscience.com 2006

By Steven Milloy September 21, 2006, FoxNews.com

Last week’s announcement that the World Health Organization lifted its nearly 30-year ban on the insecticide DDT is perhaps the most promising development in global public health since… well, 1943 when DDT was first used to combat insect-borne diseases like typhus and malaria.

Overlooked in all the hoopla over the announcement, however, is the terrible toll in human lives (tens of millions dead — mostly pregnant women and children under the age of 5), illness (billions sickened) and poverty (more than $1 trillion dollars in lost GDP in sub-Saharan Africa alone) caused by the tragic, decades-long ban.

Much of this human catastrophe was preventable, so why did it happen? Who is responsible? Should the individuals and activist groups who caused the DDT ban be held accountable in some way?

Rachel Carson kicked-off DDT hysteria with her pseudo-scientific 1962 book, “Silent Spring.” Carson materially misrepresented DDT science in order to advance her anti-pesticide agenda. Today she is hailed as having launched the global environmental movement. A Pennsylvania state office building, Maryland elementary school, Pittsburgh bridge and a Maryland state park are named for her. The Smithsonian Institution commemorates her work against DDT. She was even honored with a 1981 U.S. postage stamp. Next year will be the 100th anniversary of her birth. Many celebrations are being planned.

It’s quite a tribute for someone who was so dead wrong. At the very least, her name should be removed from public property and there should be no government-sponsored honors of Carson.

The Audubon Society was a leader in the attack on DDT, including falsely accusing DDT defenders (who subsequently won a libel suit) of lying. Not wanting to jeopardize its non-profit tax status, the Audubon Society formed the Environmental Defense Fund (now simply known as Environmental Defense) in 1967 to spearhead its anti-DDT efforts. Today the National Audubon Society takes in more than $100 million per year and has assets worth more than $200 million. Environmental Defense takes in more than $65 million per year with a net worth exceeding $73 million.

In a February 25, 1971, media release, the president of the Sierra Club stated that his organization wanted “a ban, not just a curb” on DDT, “even in the tropical countries where DDT has kept malaria under control.” Today the Sierra Club rakes in more than $90 million per year and has more than $50 million in assets.

Business are often held liable and forced to pay monetary damages for defective products and false statements. Why shouldn’t the National Audubon Society, Environmental Defense, Sierra Club and other anti-DDT activist groups be held liable for the harm caused by their recklessly defective activism?

It was, of course, then-Environmental Protection Agency administrator William Ruckelshaus who actually banned DDT after ignoring an EPA administrative law judge’s ruling that there was no evidence indicating that DDT posed any sort of threat to human health or the environment. Ruckleshaus never attended any of the agency’s hearings on DDT. He didn’t read the hearing transcripts and refused to explain his decision.

None of this is surprising given that, in a May 22, 1971, speech before the Wisconsin Audubon Society, Ruckleshaus said that EPA procedures had been streamlined so that DDT could be banned. Ruckleshaus was also a member of — and wrote fundraising letters for — the EDF.

My note: This speech was before the seven months long EPA hearings before Judge Sweeney began in fall of 1971, so even though the hearings concluded DDT was not harmful to man or environment, Ruckelshaus  already had his mind made up.

The DDT ban solidified Ruckelshaus’ environmental credentials, which he has surfed to great success in business, including stints as CEO of Browning Ferris Industries and as a director of a number of other companies including Cummins Engine, Nordstrom, and Weyerhaeuser Company. Ruckelshaus currently is a principal in a Seattle, Wash., -based investment group called Madrona Venture Group.

Corporate wrongdoers — like WorldCom’s Bernie Ebbers and Tyco’s Dennis Kozlowski — were sentenced to prison for crimes against mere property. But what should the punishment be for government wrongdoers like Ruckleshaus who, apparently for the sake of his personal environmental interests, abused his power and affirmatively deprived billions of poor, helpless people of the only practical weapon against malaria?

Finally, there is the question of the World Health Organization itself. What’s the WHO been doing for all these years? There are no new facts on DDT — all the relevant science about DDT safety has been available since the 1960s. Moreover, the WHO’s strategy of mosquito bednets and malaria vaccine development has been a dismal failure. While the death toll in malarial regions has mounted, the WHO has been distracted by such dubious issues as whether cell phones and French fries cause cancer.

It’s a relief that the WHO has finally come to its senses, but on the other hand, the organization has done too little, too late. The ranks of the WHO’s leadership need to be purged of those who place the agenda of environmental elitists over the basic survival of the world’s needy.

In addition to the day of reckoning and societal rebuke that DDT-ban advocates should face, we should all learn from the DDT tragedy.

With the exception of Rachel Carson (who died in 1964), all of the groups and individuals above mentioned also promote global warming alarmism. If they and others could be so wrong about DDT, why should we trust them now? Should we really put the global economy and the welfare of billions at risk based on their track record?

Steven Milloy publishes JunkScience.com and CSRWatch.com. He is a junk science expert, an advocate of free enterprise and an adjunct scholar at the Competitive Enterprise Institute.

See “DDT: A Case Study in Scientific Fraud” by J. Gordon Edwards, PhD, 2004 at http://www.jpands.org/vol9no3/edwards.pdf

For more information see also my earlier blog – Bring back DDT – Save Africa and other impoverished areas

 

100 Things Your Should Know About DDT – Junkscience.com 1999

kaykiser

In case you still think DDT is evil, read this repost from Junkscience.com in 1999.

Bring back DDT to save Africa, India, etc. from Malaria, etc. Resistance claims are overblown. Repellancy is under emphasized. Health and Environmental dangers are demagogued, and long ago were proven untrue as reported below.

Also see my previous post “Bring back DDT – Save Africa and other impoverished areas.” containing more facts from a 2004 J. Gordon Edwards review article.

100 Things You Should Know About DDT

by J. Gordon Edwards and Steven Milloy July 26, 1999, JunkScience.com Recommended Reading by the New York Times

  1. Historical Background
  2. Advocacy against DDT
  3. EPA hearings
  4. Human exposure
  5. Cancer
  6. Egg shell thinning
  7. Bald eagles
  8. Peregrine falcons
  9. Brown pelicans
  10. Bird populations increase during DDT years
  11. Erroneous detection

1. HISTORICAL BACKGROUND. Discovered by accident, DDT became one of the greatest public health tools of the 20th century. Overuse harmed its efficacy — and made it politically unpopular.

  1. Dichloro-diphenyl-trichloroethane (DDT) was first synthesized, for no purpose, in 1874 by German chemist Othmar Zeidler. In 1939, Dr. Paul Müller independently produced DDT. Müller found that DDT quickly killed flies, aphids, mosquitoes, walking sticks and Colorado potato beetles. Müller and the Geigy corporation patented DDT in Switzerland (1940), England (1942) and U.S. (1943).
  2. The first large-scale use of DDT occurred in 1943 when 500 gallons of DDT were produced by Merck & Company and delivered to Italy to help squelch a rapidly spreading epidemic of louse-borne typhus. Later in 1943, the U.S. Army issued small tin boxes of 10 percent DDT dust to its soldiers around the world who used it to kill body lice, head lice and crab lice.
  3. Müller won the Nobel Prize in 1948 for his work on DDT.
  4. Peak usage occurred in 1962, when 80 million kilograms of DDT were used and 82 million kilograms produced.
  5. “In May 1955 the Eighth World Health Assembly adopted a Global Malaria Eradication Campaign based on the widespread use of DDT against mosquitos and of antimalarial drugs to treat malaria and to eliminate the parasite in humans. As a result of the Campaign, malaria was eradicated by 1967 from all developed countries where the disease was endemic and large areas of tropical Asia and Latin America were freed from the risk of infection. The Malaria Eradication Campaign was only launched in three countries of tropical Africa since it was not considered feasible in the others. Despite these achievements, improvements in the malaria situation could not be maintained indefinitely by time-limited, highly prescriptive and centralized programmes.” [Bull World Health Organ 1998;76(1):11-6]
  6. “To only a few chemicals does man owe as great a debt as to DDT… In little more than two decades, DDT has prevented 500 million human deaths, due to malaria, that otherwise would have been inevitable.” [National Academy of Sciences, Committee on Research in the Life Sciences of the Committee on Science and Public Policy. 1970. The Life Sciences; Recent Progress and Application to Human Affairs; The World of Biological Research; Requirements for the Future.]
  7. It is believed that [malaria] afflicts between 300 and 500 million every year, causing up to 2.7 million deaths, mainly among children under five years. [Africa News, January 27, 1999]
  8. Some mosquitoes became “resistant” to DDT. “There is persuasive evidence that antimalarial operations did not produce mosquito resistance to DDT. That crime, and in a very real sense it was a crime, can be laid to the intemperate and inappropriate use of DDT by farmers, espeially cotton growers. They used the insecticide at levels that would accelerate, if not actually induce, the selection of a resistant population of mosquitoes.” [Desowitz, RS. 1992. Malaria Capers, W.W. Norton & Company]
  9. “Resistance” may be a misleading term when discussing DDT and mosquitoes. While some mosquitoes develop biochemical/physiological mechanisms of resistance to the chemical, DDT also can provoke strong avoidance behavior in some mosquitoes so they spend less time in areas where DDT has been applied — this still reduces mosquito-human contact. “This avoidance behavior, exhibited when malaria vectors avoid insecticides by not entering or by rapidly exiting sprayed houses, should raise serious questions about the overall value of current physiological and biochemical resistance tests. The continued efficacy of DDT in Africa, India, Brazil, and Mexico, where 69% of all reported cases of malaria occur and where vectors are physiologically resistant to DDT (excluding Brazil), serves as one indicator that repellency is very important in preventing indoor transmission of malaria.” [See, e.g.,J Am Mosq Control Assoc 1998 Dec;14(4):410-20; and Am J Trop Med Hyg 1994;50(6 Suppl):21-34].
  10. ADVOCACY AGAINST DDT. DDT was demagogued out of use.

10.Rachel Carson sounded the initial alarm against DDT, but represented the science of DDT erroneously in her 1962 book Silent Spring. Carson wrote “Dr. DeWitt’s now classic experiments [on quail and pheasants] have now established the fact that exposure to DDT, even when doing no observable harm to the birds, may seriously affect reproduction. Quail into whose diet DDT was introduced throughout the breeding season survived and even produced normal numbers of fertile eggs. But few of the eggs hatched.” DeWitt’s 1956 article (in Journal of Agriculture and Food Chemistry) actually yielded a very different conclusion. Quail were fed 200 parts per million of DDT in all of their food throughout the breeding season. DeWitt reports that 80% of their eggs hatched, compared with the “control”” birds which hatched 83.9% of their eggs. Carson also omitted mention of DeWitt’s report that “control” pheasants hatched only 57 percent of their eggs, while those that were fed high levels of DDT in all of their food for an entire year hatched more than 80% of their eggs.

  1. Population control advocates blamed DDT for increasing third world population. In the 1960s, World Health Organization authorities believed there was no alternative to the overpopulation problem but to assure than up to 40 percent of the children in poor nations would die of malaria. As an official of the Agency for International Development stated, “Rather dead than alive and riotously reproducing.” [Desowitz, RS. 1992. Malaria Capers, W.W. Norton & Company]
  2. The environmental movement used DDT as a means to increase their power. Charles Wurster, chief scientist for the Environmental Defense Fund, commented, “If the environmentalists win on DDT, they will achieve a level of authority they have never had before.. In a sense, much more is at stake than DDT.”[Seattle Times, October 5, 1969]
  3. Science journals were biased against DDT. Philip Abelson, editor of Science informed Dr. Thomas Jukes that Science would never publish any article on DDT that was not antagonistic.
  4. William Ruckelshaus, the administrator of the U.S. Environmental Protection Agency who made the ultimate decision to ban DDT in 1972, was a member of the Environmental Defense Fund. Ruckelshaus solicited donations for EDF on his personal stationery that read “EDF’s scientists blew the whistle on DDT by showing it to be a cancer hazard, and three years later, when the dust had cleared, EDF had won.”
  5. But as an assistant attorney general, William Ruckelshaus stated on August 31, 1970 in a U.S. Court of Appeals that “DDT has an amazing an exemplary record of safe use, does not cause a toxic response in man or other animals, and is not harmful. Carcinogenic claims regarding DDT are unproven speculation.” But in a May 2, 1971 address to the Audubon Society, Ruckelshaus stated, “As a member of the Society, myself, I was highly suspicious of this compound, to put it mildly. But I was compelled by the facts to temper my emotions … because the best scientific evidence available did not warrant such a precipitate action. However, we in the EPA have streamlined our administrative procedures so we can now suspend registration of DDT and the other persistent pesticides at any time during the period of review.” Ruckelshaus later explained his ambivalence by stating that as assistant attorney general he was an advocate for the government, but as head of the EPA he was “a maker of policy.” [Barron’s, 10 November 1975]
  6. Environmental activists planned to defame scientists who defended DDT. In an uncontradicted deposition in a federal lawsuit, Victor Yannacone, a founder of the Environmental Defense Fund, testified that he attended a meeting in which Roland Clement of the Audubon Society and officials of the Environmental Defense Fund decided that University of California-Berkeley professor and DDT-supporter Thomas H. Jukes was to be muzzled by attacking his credibility. [21st Century, Spring 1992]

III. EPA HEARINGS. DDT was banned by an EPA administrator who ignored the decision of his own administrative law judge.

  1. Extensive hearings on DDT before an EPA administrative law judge occurred during 1971-1972. The EPA hearing examiner, Judge Edmund Sweeney, concluded that “DDT is not a carcinogenic hazard to man… DDT is not a mutagenic or teratogenic hazard to man… The use of DDT under the regulations involved here do not have a deleterious effect on freshwater fish, estuarine organisms, wild birds or other wildlife.” [Sweeney, EM. 1972. EPA Hearing Examiner’s recommendations and findings concerning DDT hearings, April 25, 1972 (40 CFR 164.32, 113 pages). Summarized in Barrons (May 1, 1972) and Oregonian (April 26, 1972)]
  2. Overruling the EPA hearing examiner, EPA administrator Ruckelshaus banned DDT in 1972. Ruckelshaus never attended a single hour of the seven months of EPA hearings on DDT. Ruckelshaus’ aides reported he did not even read the transcript of the EPA hearings on DDT. [Santa Ana Register, April 25, 1972]
  3. After reversing the EPA hearing examiner’s decision, Ruckelshaus refused to release materials upon which his ban was based. Ruckelshaus rebuffed USDA efforts to obtain those materials through the Freedom of Information Act, claiming that they were just “internal memos.” Scientists were therefore prevented from refuting the false allegations in the Ruckelshaus’ “Opinion and Order on DDT.”
  4. HUMAN EXPOSURE. Actual human exposures have always been far lower than the “acceptable” level.
  5. Human ingestion of DDT was estimated to average about 0.0026 milligrams per kilogram of body weight per day (mg/kg/day) about 0.18 milligrams per day. [Hayes, W. 1956. J Amer Medical Assn, Oct. 1956]
  6. In 1967, the daily average intake of DDT by 20 men with high occupational exposure was estimated to be 17.5 to 18 mg/man per day, as compared with an average of 0.04 mg/man per day for the general population. [IARC V.5, 1974].
  7. Dr. Alice Ottoboni, toxicologist for the state of California, estimated that the average American ingests between 0.0006 mg/kg/day and 0.0001 mg/kg/day of DDT. [Ottoboni, A. et al. California’s Health, August 1969 & May 1972]
  8. “In the United States, the average amount of DDT and DDE eaten daily in food in 1981 was 2.24 micrograms per day (ug/day) (0.000032 mg/kg/day), with root and leafy vegetables containing the highest amount. Meat, fish, and poultry also contain very low levels of these compounds.” [Agency for Toxic Substances and Disease Registry. 1989.Public Health Statement: DDT, DDE, and DDD]
  9. The World Health Organization set an acceptable daily intake of DDT for humans at 0.01 mg/kg/day.
  10. “Air samples in the United States have shown levels of DDT ranging from 0.00001 to 1.56 micrograms per cubic meter of air (ug/m3), depending on the location and year of sampling. Most reported samples were collected in the mid 1970s, and present levels are expected to be much lower. DDT and DDE have been reported in surface waters at levels of 0.001 micrograms per liter (ug/L), while DDD generally is not found in surface water. National soil testing programs in the early 1970s have reported levels in soil ranging from 0.18 to 5.86 parts per million (ppm).” [Agency for Toxic Substances and Disease Registry. 1989.Public Health Statement: DDT, DDE, and DDD]
  11. CANCER. DDT was alleged to be a liver carcinogen in Silent Spring and a breast carcinogen in Our Stolen Future.
  12. Feeding primates more than 33,000 times the average daily human exposure to DDT (as estimated in 1969 and 1972) was “inconclusive with respect to a carcinogenic effect of DDT in nonhuman primates.” [J Cancer Res Clin Oncol 1999;125(3-4):219-25]
  13. A nested case-control study was conducted to examine the association between serum concentrations of DDE and PCBs and the development of breast cancer up to 20 years later. Cases (n = 346) and controls (n = 346) were selected from cohorts of women who donated blood in 1974, 1989, or both, and were matched on age, race, menopausal status, and month and year of blood donation. “Even after 20 years of follow-up, exposure to relatively high concentrations of DDE or PCBs showed no evidence of contributing to an increased risk of breast cancer.” [Cancer Epidemiol Biomarkers Prev 1999 Jun;8(6):525-32]
  14. To prospectively evaluate relationships of organochlorine pesticides and PCBs with breast cancer, a case-control study nested in a cohort using the Columbia, Missouri Breast Cancer Serum Bank. Women donated blood in 1977- 87, and during up to 9.5 years follow-up, 105 donors who met the inclusion criteria for the current study were diagnosed with breast cancer. For each case, two controls matched on age and date of blood collection were selected. Five DDT analogs, 13 other organochlorine pesticides, and 27 PCBs were measured in serum. Results of this study do not support a role for organochlorine pesticides and PCBs in breast cancer etiology. [Cancer Causes Control 1999 Feb;10(1):1-11]
  15. A pooled analysis examined whether exposure to DDT was associated with the risk of non-Hodgkin’s lymphoma among male farmers. Data from three case-control studies from four midwestern states in the United States (Nebraska, Iowa, Minnesota, Kansas) were pooled to carry out analyses of 993 cases and 2918 controls. No strong consistent evidence was found for an association between exposure to DDT and risk of non-Hodgkin’s lymphoma. [Occup Environ Med 1998 Aug;55(8):522-7]
  16. “We measured plasma levels of DDE and PCBs prospectively among 240 women who gave a blood sample in 1989 or 1990 and who were subsequently given a diagnosis of breast cancer before June 1, 1992. We compared these levels with those measured in matched control women in whom breast cancer did not develop. Data on DDE were available for 236 pairs, and data on PCBs were available for 230 pairs. Our data do not support the hypothesis that exposure to [DDT] and PCBs increases the risk of breast cancer.” [N Engl J Med 1997;337:1253-8]
  17. “… weakly estrogenic organochlorine compounds such as PCBs, DDT, and DDE are not a cause of breast cancer.” [http://www.nejm.org/content/1997/0337/0018/1303.asp]
  18. To examine any possible links between exposure to DDE, the persistent metabolite of the pesticide dicophane (DDT), and breast cancer, 265 postmenopausal women with breast cancer and 341 controls matched for age and center were studied. Women with breast cancer had adipose DDE concentrations 9.2% lower than control women. No increased risk of breast cancer was found at higher concentrations. The odds ratio of breast cancer, adjusted for age and center, for the highest versus the lowest fourth of DDE distribution was 0.73 (95% confidence interval 0.44 to 1.21) and decreased to 0.48 (0.25 to 0.95; P for trend = 0.02) after adjustment for body mass index, age at first birth, and current alcohol drinking. Adjustment for other risk factors did not materially affect these estimates. This study does not support the hypothesis that DDE increases risk of breast cancer in postmenopausal women in Europe. [BMJ 1997 Jul 12;315(7100):81-5]
  19. No correlation at the population level can be demonstrated between exposures to DDT and the incidence of cancer at any site. It is concluded that DDT has had no significant impact on human cancer patterns and is unlikely to be an important carcinogen for man at previous exposure levels, within the statistical limitations of the data. [IARC Sci Publ 1985;(65):107-17]
  20. Syrian golden hamsters were fed for their lifespan a diet containing 0, 125, 250 and 500 parts per million (ppm) of DDT. The incidence of tumor bearing animals was 13% among control females and ranged between 11-20% in treated females. In control males 8% had tumors. The incidence of tumor bearing animals among treated males ranged between 17-28%. [Tumori 1982 Feb 28;68(1):5-10]
  21. None of 35 workers heavily exposed to DDT (600 times the average U.S. exposure for 9 to 19 years) developed cancer. [Laws, ER. 1967. Arch Env Health 15:766-775]
  22. Men who voluntarily ingested 35 mgs of DDT daily for nearly two years were carefully examined for years and “developed no adverse effects.” [Hayes, W. 1956. JAMA 162:890-897]
  23. DDT was found to reduce tumors in animals. [Laws, ER. 1971. Arch. Env Health, 23:181-184; McLean, AEM & EK McLean. 1967. Proc Nutr Soc 26;Okey, AB. 1972. Life Sciences 11:833-843;Sillinskas, KC & AB Okey. 1975. J Natl Cancer Inst 55:653- 657, 1975]
  24. Rodent tests for a carcinogenic effect of DDT, DDE and TDE produced equivocal results despite extremely high doses (642 ppm of DDT, 3,295 ppm of TDE and 839 ppm of DDE). [National Toxicology Program, TR-131 Bioassays of DDT, TDE, and p,p’-DDE for Possible Carcinogenicity (CAS No. 50-29-3, CAS No. 72-54-8, CAS No. 72-55-9)]
  25. EGG-SHELL THINNING. DDT was alleged to have thinned bird egg shells.
  26. Many experiments on caged-birds demonstrate that DDT and its metabolites (DDD and DDE) do not cause serious egg shell thinning, even at levels many hundreds of times greater than wild birds would ever accumulate. [Cecil, HC et al. 1971. Poultry Science 50: 656-659 (No effects of DDT or DDE, if adequate calcium is in diet); Chang, ES & ELR Stokstad. 1975. Poultry Science 54: 3-10 1975. (No effects of DDT on shells); Edwards, JG. 1971. Chem Eng News p. 6 & 59 (August 16, 1971) (Summary of egg shell- thinning and refutations presented revealing all data); Hazeltine, WE. 1974. Statement and affidavit, EPA Hearings on Tussock Moth Control, Portland Oregon, p. 9 (January 14, 1974); Jeffries, DJ. 1969. J Wildlife Management 32: 441-456 (Shells 7 percent thicker after two years on DDT diet); Robson, WA et al. 1976. Poultry Science 55:2222- 2227; Scott, ML et al. 1975. Poultry Science 54: 350-368 (Egg production, hatchability and shell quality depend on calcium, and are not effected by DDT and its metabolites); Spears, G & P. Waibel. 1972. Minn. Science 28(3):4-5; Tucker, RK & HA Haegele. 1970. Bull Environ Contam. Toxicol 5:191-194 (Neither egg weight nor shell thickness affected by 300 parts per million DDT in daily diet);Edwards, JG. 1973. Statement and affidavit, U.S. Senate Committee on Agriculture, 24 pages, October 24, 1973; Poult Sci 1979 Nov;58(6):1432-49 (“There was no correlation between concentrations of pesticides and egg shell thinning.”)]
  27. Experiments associating DDT with egg shell thinning involve doses much higher than would ever be encountered in the wild. [J Toxicol Environ Health 1977 Nov;3(4):699-704 (50 ppm for 6 months); Arch Environ Contam Toxicol 1978;7(3):359-67 (“acute” doses); Acta Pharmacol Toxicol (Copenh) 1982 Feb;50(2):121-9 (40 mg/kg/day for 45 days); Fed Proc 1977 May;36(6):1888-93 (“In well-controlled experiments using white leghorn chickens and Japanese quail, dietary PCBs, DDT and related compounds produced no detrimental effects on eggshell quality. … no detrimental effects on eggshell quality, egg production or hatchability were found with … DDT up to 100 ppm)]
  28. Laboratory egg shell thinning required massive doses of DDE far in excess of anything expected in nature, and massive laboratory doses produce much less thinning than is seen in many of the thin-shelled eggs collected in the wild. [Hazeltine, WE. 1974. Statement and affidavit, EPA Hearings on Tussock Moth Control, Portland Oregon, p. 9 (January 14, 1974)]
  29. Years of carefully controlled feeding experiments involving levels of DDT as high as present in most wild birds resulted in no tremors, mortality, thinning of egg shells nor reproductive interference. [Scott, ML et al. 1975. Poultry Science 54: 350-368 (Egg production, hatch ability and shell quality depend on calcium, and are not effected by DDT and its metabolites)]
  30. Egg shell thinning is not correlated with pesticide residues. [Krantz WC. 1970 (No correlation between shell-thinning and pesticide residues in eggs) Pesticide Monitoring J 4(3): 136-141; Postupalsky, S. 1971. Canadian Wildlife Service manuscript, April 8, 1971 (No correlation between shell-thinning and DDE in eggs of bald eagles and cormorants); Anon. 1970. Oregon State University Health Sciences Conference, Annual report, p. 94. (Lowest DDT residues associated with thinnest shells in Cooper’s hawk, sharp-shinned hawk and goshawk); Claus G and K Bolander. 1977. Ecological Sanity, David McKay Co., N.Y., p. 461. (Feeding thyreprotein causes hens to lay lighter eggs, with heavier, thicker shells)]<
  31. Among brown pelican egg shells examined there was no correlation between DDT residue and shell thickness. [Switzer, B. 1972. Consolidated EPA hearings, Transcript pp. 8212-8336; and Hazeltine, WE. 1972. Why pelican eggshells are thin. Nature 239: 410-412]
  32. Egg shells of red-tailed hawks were reported to be six percent thicker during years of heavy DDT usage than just before DDT use began. Golden eagle egg shells were 5 percent thicker than those produced before DDT use. [Hickey, JJ and DW Anderson. 1968. Science 162: 271-273]
  33. To the extent egg shell thinning occurred, many other substances and conditions could have been responsible.
  34. Oil has been associated with egg shell thinning. [Anon. National Wildlife Federation, Conservation News, pp. 6-10, October 15 1979. (Embryonic mortality from oil on feathers of adults birds) ; Hartung, R. 1965. J Wildlife Management 29:872-874 (Oil on eggs reduces hatch ability by 68 percent); Libby, EE. 1978. Fish, wildlife and oil. Ecolibrium 2(4):7-10; King, KA et al. 1979 Bull Environ Contam Tox 23:800-805 (Oil a probably cause of pelican mortality for six weeks after spill);Albers, PH. 1977. Fate and Effects of Petroleum Hydrocarbons in Marine Ecosystems, Pergamon Press, N.Y. (Chapters 15 & 16; Dieter, MP. 1977. Interagency Energy-Environment Research and Development Program Report, pp. 35-42 (5 microliters of oil on fertile egg kills 76 to 98 percent of embryos within; birds ingesting oil produce 70 percent to 100 percent less eggs than normal; offspring failed to develop normal flight feathers); Szaro, RC. 1977. Proc 42nd N Amer Wildlife Nat Resources Conference, pp. 375-376]
  35. Lead has been associated with egg shell thinning. [Bellrose, RC. 1959. Ill Nat Hist Survey Bull 27:235-288 (Lead poisoning in wildlife)]
  36. Mercury has been associated with egg shell thinning. [D’Itri, FM & PB Trost. 1970. International Conference on Mercury Contamination, Ann Arbor, September 30, 1070; Scott, JL et al. 1975. Effects of PCBs, DDT and mercury upon egg production, hatch ability and shell quality. Poultry Sci 54:3350-368; Stoewssand, GS et al.. 1971. Shell- thinning in quail fed mercuric chloride. Science 173:1030-1031; Tucker, RK. 1971. Utah Science June 1971:47-49 (Effects of many chemicals on shell thickness).; Tucker, RK & HA Haegle. 1970. Bull Environ Contamin Toxicol 5:191-194]
  37. Stress from noise, fear or excitement and disease are associated with egg shell thinning. [Scott, HM et al.. 1944. (Physiological stress thins shells) Poultry Science 23:446-453; Draper, MH & PE Lake. 1967. Effects of stress and defensive responses. In Environmental Control in Poultry Production, Oliver and Boyd, London; Reid, BL. 1971. (Effects of stress on laying birds) Farm Technology, Fall 1971; Sykes, AH. 1955 (Adrenaline excess inhibits shell formation) Poultry Science 34: 622-628]
  38. Older birds produce thinner shells. [Sunde, ML. 1971 (Older birds produce thinner shells) Farm Technology, Fall 1971]
  39. Normal egg shells become 5 percent thinner as developing embryos withdraw calcium for bone development. [Romanoff, AL and AJ Romanoff. 1967. Biochemistry of the Avian Embryo, Wiley & Sons, N.Y.; Simkiss, K. 1967. (Shells thinned by embryo development within) In Calcium in Reproductive Physiology, Reinhold, NY, pp 198-213]
  40. Larger birds tend to produce thicker-shelled eggs. [Asmundson, VS et al. 1943. (Relations between the parts of birds’ eggs) Auk 60:34-44]
  41. Dehydration is associated with thinner egg shells. [Tucker, RK and HA Haegle. 1970. (30 percent thinner shells formed after quail were kept from water for 36 hours) Bull Environ Contam Toxicol 5(3): 191-194]
  42. Temperature extremes are associated with thinner egg shells. [Romanoff, AL and AJ Romanoff, 1949. The Avian Egg, Wiley & Sons]
  43. Decreased illumination is associated with thinner egg shells. [Peakall, DB. 1970. (Shells not thinned even after illumination was abruptly reduced from 16 hours daily to 8 hours daily and high DDT dosage begun simultaneously) Science 168:592-594; Day, EJ. 1971. (Importance of even illumination on laying birds) Farm Technology, Fall 1971;Houser, EJ. 1962. Pacific Poultryman, August 1962; Morris, TR et al. 1964. (The most critical area of light duration is that between 16 hours and 8 hours daily) British Poultry Science 5: 133-147; Ward, P. 1972 (Physiological importance of photo period in bird experiments) Ibis 114: 275]
  44. Human and predator intrusion is associated with thinner egg shells. [Beatty, RG. 1973. The DDT Myth, John Day Co., N.Y. 201 pages; Anon. 1971. Hawk Chalk 10(3):47-57; Cade, TJ. 1960. Ecology of the peregrine and gyrfalcon populations in Alaska. Univ Calif Publ Zool 63(3): 151-290]
  45. Simple restraint interferes with the transport of calcium throughout the body of birds, preventing adequate calcium from reaching the shell gland and forming good shells. [Sykes, AH. 1955. Poultry Science 34:622-628]
  46. Uncovering eggs after parent birds are removed or frightened off exposes eggs to potentially fatal chilling, especially in northern or high altitude locations. [Cade, TJ. 1960. Ecology of the peregrine and gyrfalcon populations in Alaska. Uni Calif Publ Zool 63(3):151-290]
  47. Phosphorus deficiency is associated with thinner shells. [Crowley, TA et al. 1963. Poultry Science 54: 350-368]
  48. Calcium deficiency is associated with thinner shells.[Greely, F.. 196 (Effects of calcium deficiency) J Wildlife Management 70:149-153; Romanoff, AL and AJ Romanoff. 1949. The Avian Egg, Wiley & Sons; Scott, ML. 1975. Poultry Science 54:350-368; Taylor, TG. 1970. How and eggshell is formed. Scientific American 222:89-95; Tucker, RK and HA Tucker. 1970. Bull Environ Contamin Toxicol 5(3):1191-194]
  49. Egg shell deficiencies were attributed to DDT and DDE by U.S. Fish and Wildlife researchers even though the birds had been placed on low-calcium diets. [Bitman, J et al. 1969. Nature 224: 44-46; Bitman, J et al. 1970. Science 594-595.]
  50. Cutting illumination from 16 hours daily to 8 hours daily at the same time as DDT feeding began had no significant adverse effect on shell quality. Shell quality was only adversely impacted after large amounts of DDE were injected into birds. [Peakall, DB. 1970. Science 168:592-594]
  51. DDT was blamed for egg shell thinning even though a known egg shell thinner (dieldrin) was also added to the diet. [Porter, RD and SN Wiemeyer. 1969. Science 165: 199-200]
  52. No significant correlation between DDE and egg shell thinning in Canadian terns even though the eggs contained as much as 100 parts per million of DDE. [Switzer, BG et al. 1971. Can J Zool 49:69-73]

VII. BALD EAGLES. DDT was blamed for the decline in the bald eagle population.

  1. Bald eagles were reportedly threatened with extinction in 1921 — 25 years before widespread use of DDT. [Van Name, WG. 1921. Ecology 2:76]
  2. Alaska paid over $100,000 in bounties for 115,000 bald eagles between 1917 and 1942. [Anon. Science News Letter, July 3, 1943]
  3. The bald eagle had vanished from New England by 1937. [Bent, AC. 1937. Raptorial Birds of America. US National Museum Bull 167:321-349]
  4. After 15 years of heavy and widespread usage of DDT, Audubon Society ornithologists counted 25 percent more eagles per observer in 1960 than during the pre-DDT 1941 bird census. [Marvin, PH. 1964 Birds on the rise. Bull Entomol Soc Amer 10(3):184-186; Wurster, CF. 1969 Congressional Record S4599, May 5, 1969; Anon. 1942. The 42nd Annual Christmas Bird Census. Audubon Magazine 44:1-75 (Jan/Feb 1942; Cruickshank, AD (Editor). 1961. The 61st Annual Christmas Bird Census. Audubon Field Notes 15(2):84-300; White-Stevens, R.. 1972. Statistical analyses of Audubon Christmas Bird censuses. Letter to New York Times, August 15, 1972]
  5. No significant correlation between DDE residues and shell thickness was reported in a large series of bald eagle eggs. [Postupalsky, S. 1971. (DDE residues and shell thickness). Canadian Wildlife Service manuscript, April 8, 1971]
  6. Thickness of eggshells from Florida, Maine and Wisconsin was found to not be correlated with DDT residues.
Data from Krantz, WC. 1970. Pesticides Monitoring Journal 4(3):136-140.
State Thickness (mm) DDE residue (ppm)
Florida 0.50 About 10
Maine 0.53 About 22
Wisconsin 0.55 About 4
  1. U.S. Forest Service studies reported an increase in nesting bald eagle productivity (51 in 1964 to 107 in 1970). [U.S. Forest Service (Milwaukee, WI). 1970. Annual Report on Bald Eagle Status]
  2. U.S. Fish and Wildlife Service biologists fed large doses of DDT to captive bald eagles for 112 days and concluded that “DDT residues encountered by eagles in the environment would not adversely affect eagles or their eggs.” [Stickel, L. 1966. Bald eagle-pesticide relationships. Trans 31st N Amer Wildlife Conference, pp.190-200]
  3. Wildlife authorities attributed bald eagle population reductions to a “widespread loss of suitable habitat”, but noted that “illegal shooting continues to be the leading cause of direct mortality in both adult and immature bald eagles.” [Anon.. 1978. U.S. Fish and Wildlife Service, Endangered Species Tech Bull 3:8-9]
  4. Every bald eagle found dead in the U.S., between 1961-1977 (266 birds) was analyzed by U.S. Fish and Wildlife Service biologists who reported no adverse effects caused by DDT or its residues. [Reichel, WL. 1969. (Pesticide residues in 45 bald eagles found dead in the U.S. 1964-1965). Pesticides Monitoring J 3(3)142-144; Belisle, AA. 1972. (Pesticide residues and PCBs and mercury, in bald eagles found dead in the U.S. 1969-1970). Pesticides Monitoring J 6(3): 133-138; Cromartie, E. 1974. (Organochlorine pesticides and PCBs in 37 bald eagles found dead in the U.S. 1971-1972). Pesticides Monitoring J 9:11-14; Coon, NC. 1970. (Causes of bald eagle mortality in the US 1960-1065). Journal of Wildlife Diseases 6:72-76]
  5. U.S. Fish and Wildlife Service biologists linked high intake of mercury from contaminated fish with eagle reproductive problems. [Spann, JW, RG Heath, JF Kreitzer, LN Locke. 1972. (Lethal and reproductive effects of mercury on birds) Science 175:328- 331]
  6. Shooting, power line electrocution, collisions in flight and poisoning from eating ducks containing lead shot were ranked by the National Wildlife Federation as late as 1984 as the leading causes of eagle deaths. [Anon. 1984. National Wildlife Federation publication. (Eagle deaths)]

VIII. PEREGRINE FALCONS. DDT was blamed for the decline in the peregrine falcon population.

  1. The decline in the U.S. peregrine falcon population occurred long before the DDT years. [Hickey JJ. 1942. (Only 170 pairs of peregrines in eastern U.S. in 1940) Auk 59:176; Hickey JJ. 1971 Testimony at DDT hearings before EPA hearing examiner. (350 pre-DDT peregrines claimed in eastern U.S., with 28 of the females sterile); and Beebe FL. 1971. The Myth of the Vanishing Peregrine Falcon: A study in manipulation of public and official attitudes. Canadian Raptor Society Publication, 31 pages]
  2. Peregrine falcons were deemed undesirable in the early 20th century. Dr. William Hornaday of the New York Zoological Society referred to them as birds that “deserve death, but are so rare that we need not take them into account.” [Hornaday, WT. 1913. Our Vanishing Wild Life. New York Zoological Society, p. 226]
  3. Oologists amassed great collections of falcon eggs. [Peterson, RT. 1948. Birds Over American, Dodd Mead & Co., NY, pp 135-151; Rice, JN. 1969. In Peregrine Falcon Populations, Univ. Of Wisconsin Press, pp 155-164; Berger, DD. 1969. In Peregrine Falcon Populations, Univ. Of Wisconsin Press, pp 165-173]
  4. The decline in falcons along the Hudson River was attributed to falconers, egg collectors, pigeon fanciers and disturbance by construction workers and others. [Herbert, RA and KG Herbert. 1969. In Peregrine Falcon Populations, Univ. Of Wisconsin Press, pp 133- 154. (Also in Auk 82: 62-94)]
  5. The 1950’s and 1960’s saw continuing harassment trapping brooding birds in their nests, removing fat samples for analysis and operating time-lapse cameras beside the nests for extended periods of time), predation and habitat destruction. [Hazeltine, WE. 1972. Statement before Secretary of State’s Advisory Committee on United Nations Conference on the Human Environment, March 16, 1972; Enderson, JH and DD Berger. 1968. (Chlorinated hydrocarbons in peregrines from Northern Canada). Condor 70:149-153; Enderson, JH.. 1972. (Time lapse photography in peregrine nests) Living Bird 11: 113- 128; Risebrough, RW. 1970. (Organochlorines in peregrines and merlins migrating through Wisconsin). Canadian Field-Naturalist 84:247-253]
  6. Changes in climate (higher temperatures and decreasing precipitation) were blamed for the gradual disappearance of peregrines from the Rocky Mountains. [Nelson, MW. 1969. Peregrine Falcon Populations, pp 61-72]
  7. Falconers were blamed for decimating western populations. [Herman, S. 1969. Peregrine Falcon Populations, University of Wisconsin Press]
  8. During the 1960’s, peregrines in northern Canada were “reproducing normally,” even though they contained 30 times more DDT, DDD, and DDE than the midwestern peregrines that were allegedly extirpated by those chemicals. [Enderson, JH and DD Berger. 1968. (Chlorinated hydrocarbons in peregrines from Northern Canada) Condor 70:170-178]
  9. There was no decline in peregrine falcon pairs in Canada and Alaska between 1950 and 1967 despite the presence of DDT and DDE. [Fyfe, RW. 1959. Peregrine Falcon Populations, pp 101-114; and Fyfe, RW. 1968. Auk 85: 383-384]
  10. The peregrine with the very highest DDT residue (2,435 parts per million) was found feeding three healthy young. [Enderson, JH. 1968. (Pesticide residues in Alaska and Yukon Territory) Auk 85: 683]
  11. Shooting, egg collecting, falconry and disruption of nesting birds along the Yukon River and Colville River were reported to be the cause of the decline in peregrine falcon population. [Beebe, FL. 1971. The Myth of the Vanishing Peregrine Falcon: A study in manipulation of public and official attitudes. Canadian Raptor Society Publication, 31 pages; and Beebe, FL. 1975. Brit Columbia Provincial Museum Occas. Paper No. 17, pages 126-144]
  12. The decline in British peregrine falcons ended by 1966, though DDT was as abundant as ever. The Federal Advisory Committee on Pesticides concluded “There is no close correlation between the declines in populations of predatory birds, particularly the peregrine falcon and the sparrow hawk, and the use of DDT.” [Wilson report. 1969. Review of Organochlorine pesticides in Britain. Report by the Advisory Committee on toxic chemicals. Department of Education and Science]
  13. During 1940-1945, the British Air Ministry shot about 600 peregrines (half the pre-1939 level) to protect carrier pigeons.
  14. Peregrine falcon and sparrow hawk egg shells thinned in Britain prior to the use of DDT. [Redcliff, DH. 1967. Nature 215: 208-210; Redcliff, DH. 1970 J Applied Biology 7:67; and Redcliff, DH. 1967. Nature 215: 208-210]
  15. BROWN PELICANS. DDT was blamed for the decline in the brown pelican population.
  16. Brown pelicans declined in Texas from a high of 5,000 birds in 1918 to a low of 200 in 1941, three years before the presence of DDT. [Pearson TG. 1919. Review of reviews. Pp. 509-511 (May 1919); Pearson TG. 1934. Adventures in Bird Protection, Appleton- Century Co., p. 332; Pearson TG. 1934 (Discussion of 1918 survey) National Geographic pp. 299-302 (March 1934); Allen RG. 1935. Auk 52: p.199;]
  17. Disappearance of the brown pelicans from Texas was attributed to fisherman and hunters. Gustafson AF. 1939. Conservation in the United States, Comstock Publ. Co., Ithaca, NY. (Repeated in U.S. Fish and Wildlife Service Report No. 1, 1970)]
  18. Brown pelicans experienced no difficulty in reproducing during the DDT years. [See Banks, RC. 1966. Trans San Diego Soc Nat Hist 14:173-188; and Schreiber RW and RL DeLong. 1969. Audubon Field Notes 23:57-59]
  19. Brown pelicans did suffer reproductive problems following the 1969 Santa Barbara oil spill. Oil on eggs is a known cause of embryo death. [See e.g., National Wildlife Federation . 1979. Embryonic mortality from oil on feathers of adult birds. Conservation News, pp. 6-10 (October 15, 1979); Hartung, R. 1965. (Oil on eggs reduces hatch ability by 68 percent). J Wildlife Management 29: 872-874; King, KA 1979. (Oil a probable cause of pelican mortality for six weeks after spill). Bull Environ Contam. Toxicol 23:800-805; and Dieter, MP. 1977. (5 micro liters of oil on fertile egg kills 76 percent to 98 percent of embryos within. Interagency Energy-Environment Research and Development Program Report, pp 35-42]
  20. Among brown pelican egg shells examined (72 percent), there was no correlation between DDT residue and shell thickness. [Switzer, B. 1972. Consolidated EPA hearings, Transcript pp. 8212-8336; and Hazeltine, WE. 1972. Why pelican eggshells are thin. Nature 239: 410-412]
  21. An epidemic of Newcastle disease resulted in millions of birds put to death to eradicate the disease. [United Press International. “Newcastle disease epidemic in California (April 1972)] The epidemic among U.S. birds was caused by the migration of sick pelicans along the Mexican coast. [Hofstad MC. 1972. Diseases of Poultry. Iowa State Univ. Press]
  22. BIRD POPULATIONS INCREASE DURING DDT YEARS. Widespread declines in bird populations during the DDT years is a myth.
  23. In congressional testimony, Charles Wurster, a biologist for the Environmental Defense Fund, noted the abundance of birds during the DDT years, referring to “increasing numbers of pheasants, quail, doves, turkeys and other game species.” [Wurster, C.F. 1969 Congressional Record S4599, May 5, 1969]
  24. The Audubon Society’s annual bird census in 1960 reported that at least 26 kinds of birds became more numerous during 1941 – 1960. [See Anon. 1942. The 42nd annual Christmas bird census.” Audubon Magazine 44;1-75 (Jan/Feb 1942), and Cruicjshank, AD (editor) 1961. The 61st annual Christmas bird census. Audubon Field Notes 15(2); 84-300]
  25. Statistical analysis of the Audubon data bore out the perceived increases. [White-Stevens, R. 1972. Statistical analyses of Audubon Christmas bird censuses. Letter to New York Times, August 15, 1972]
  26. The white-tailed kite, a raptor, was “in very real danger of complete extirpation in the U.S.” in 1935, but “by the 1960’s, a very great population increase and range expansion had become apparent in California and the breeding range had extended through the Central American countries.” [Eisenmann, E. 1971. Range expansion and population increase of the White-tailed kite. American Birds 25(3):529-535]
  27. Great increases in most kinds of hawks during the DDT years were reported by the Hawk Mountain Sanctuary Association (Hawk Mountain, Pennsylvania). [Taylor, JW. Summaries of Hawk Mountain migrations of raptors, 1934 to 1970. In Hawk Mountain Sanctuary Association Newsletters]
  28. National forest studies from Wisconsin and Michigan reported an increase in nesting osprey productivity from 11 young in 1965 to 74 young in 1970. [U.S. Forest Service, Milwaukee. 1970. Annual report on osprey status in national forests in Wisconsin and Michigan]
  29. A study of fish-eaters at Funk Island (on the North Atlantic coast) reported that, despite diets contaminated with DDT, gannet and murres pairs increased by 1,500 percent and 10,000 percent from 1945 to the early 1970s. [Bruemmer, F. 1971. Animals Magazine, p.555, April]
  30. Herring gulls reportedly increased from 2,000 pairs in 1941 to 35,000 pairs in 1971. Ironically, the Massachusetts department of Natural resources permitted the Audubon Society to poison 30,000 of the pairs on Tern Island. The Audubon-ers preferred terns. Audubon Society scientist William Drury stated, “it’s kind of like weeding a garden.” [Graham, F. 1985. Audubon Magazine, p.17, January 1985]
  31. Some birds multiplied so well during the DDT years that they became pests:
  • 6 million blackbirds ruined Scotland Neck, North Carolina in 1970, polluting streams, depositing nine inches of droppings on the ground and killing the forest where they roosted at night. [Associated Press, March 18, 1970]
  • 77 million blackbirds roosted within 50 miles of Ft. Campbell, KY increasing the risk of histoplasmosis in humans. [Louisville Courier-Journal, December 1975.]
  • Ten million redwings were reported in a small area of northern Ohio. [Graham, F. 1971. Bye-bye blackbirds? Audubon Magazine, pp. 29-35, September]
  • The Virginia Department of Agriculture stated, “We can no longer tolerate the damage caused by the redwing … 15 million tons of grain are destroyed annually enough to feed 90 million people.” [Bulletin of the Virginia Department of Agriculture, May 1967]XI. ERRONEOUS DETECTION. Gas chromatography was universally used for pesticide analysis in the mid-1960’s. But it often failed to differentiate between DDT residues and other chemicals.109. DDT was mistaken for other organochlorines. [Glotfelty, DE.. 1970. Anal Chem 42:82-84 (Misidentifications of DDT resulted from interference by “pigment-related natural products in photosynthesic tissues.”); Hylin, JW. 1969. Residue Reviews 26:127 (“Organochlorine compounds in plants can cause interference in residue analyses “); Sims, JJ. 1977. Press release, June 15, 1977 (Certain marine algae produce halogen compounds that are detected by gas chromatography and may be misidentified as DDT metabolites);George JL and DEH Frear. 1966. Pesticides in the Antarctic. J Appld Ecology 3 (suppl): 155-167 (Antarctic samples of fish and birds widely touted as containing DDT residues likely contained PCBs instead that leached from the plastic containers they were stored in for 6 months prior to analysis)]111. The coating of aluminum foil used to wrap specimens, formalin, and sodium sulfate may also have contained PCBs or oils that might have interfered with analyses. [Risebrough, RW. 1971. Presentation to International Symposium on Identification and Measurement of Environmental Pollutants, Ottawa, Canada, June 15, 1971]
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  • 110. Laboratory fluorescent lights containing liquid PCBs and plastic tubing leaching PCBs erroneously led to PCBs misidentified as DDT or DDE. [Gustafson, CG. 1970. Environ Sci Technology 4(10):814-819; Lisk, DJ. 1970. Analysis of pesticide residues: methods and problems. Science 170:589-593; Anderson, DW et al. 1969. Can Field-Naturalist 83:91-112 (Samples reported in 1965 to be contaminated with DDT were acknowledged in 1969 to actually have been contaminated with PCBs. Faulty analytic methods were blamed); National Audubon Society, Research Dept. 1968. Brown Pelican Newsletter (Tavernier, Florida) No. 1, page 9 (The Audubon Society was aware of the problem of PCB interference in announcing its warning: “DO NOT BRING PLASTICS INTO CONTACT WITH THE SPECIMEN.”)]
  • 108. Gas chromatography detected DDT in samples of wildlife and soil collected before DDT was even produced. [Scott, ML et al. 1975. Poultry Science 54: 350-368 (“Many reports relating reproductive declines of wild birds (and body stores in those birds) to DDT and DDE were based on analytical procedures that did not distinguish between DDT and PCBs.”); Sherman, RW. 1973. Artifacts and mimics of DDT and other insecticides. J New York Entomol Soc 81:152-163 (Robin collected in 1938); Coon, FB. 1966. Electron capture gas chromatograph analyses of selected samples of authentic pre-DDT origin. Presented at the Conference of American Chemical Society in New York (Gibbon collected in 1935); Frazier, BE et al. 1970. Pesticides Monitoring J 4:67-70, 1970 (Soil collected in 1911); Bowman, MC et al. 1965. J Econ Entomology 58: 896-902 (Soil collected in 1940); Hom, W. 1974. Science 184:1197-1199 (1930-vintage Santa Barbara basin sediment)]
  • 107. The phenomena of increasing bird populations during the DDT years may be due, in part, to (1) fewer blood-sucking insects and reduced spread of avian diseases (avian malaria, rickettsial-pox, avian bronchitis, Newcastle disease, encephalitis, etc); (2) more seed and fruits available for birds to eat after plant-eating insects were decimated; and (3) Ingestion of DDT triggers hepatic enzymes that detoxify carcinogens such as aflatoxin.
    1. ERRONEOUS DETECTION. Gas chromatography was universally used for pesticide analysis in the mid-1960’s. But it often failed to differentiate between DDT residues and other chemicals.
    2. Gas chromatography detected DDT in samples of wildlife and soil collected before DDT was even produced. [Scott, ML et al. 1975. Poultry Science 54: 350-368 (“Many reports relating reproductive declines of wild birds (and body stores in those birds) to DDT and DDE were based on analytical procedures that did not distinguish between DDT and PCBs.”); Sherman, RW. 1973. Artifacts and mimics of DDT and other insecticides. J New York Entomol Soc 81:152-163 (Robin collected in 1938); Coon, FB. 1966. Electron capture gas chromatograph analyses of selected samples of authentic pre-DDT origin. Presented at the Conference of American Chemical Society in New York (Gibbon collected in 1935); Frazier, BE et al. 1970. Pesticides Monitoring J 4:67-70, 1970 (Soil collected in 1911); Bowman, MC et al. 1965. J Econ Entomology 58: 896-902 (Soil collected in 1940); Hom, W. 1974. Science 184:1197-1199 (1930-vintage Santa Barbara basin sediment)]
    3. DDT was mistaken for other organochlorines. [Glotfelty, DE.. 1970. Anal Chem 42:82-84 (Misidentifications of DDT resulted from interference by “pigment-related natural products in photosynthesic tissues.”); Hylin, JW. 1969. Residue Reviews 26:127 (“Organochlorine compounds in plants can cause interference in residue analyses “); Sims, JJ. 1977. Press release, June 15, 1977 (Certain marine algae produce halogen compounds that are detected by gas chromatography and may be misidentified as DDT metabolites);George JL and DEH Frear. 1966. Pesticides in the Antarctic. J Appld Ecology 3 (suppl): 155-167 (Antarctic samples of fish and birds widely touted as containing DDT residues likely contained PCBs instead that leached from the plastic containers they were stored in for 6 months prior to analysis)]
    4. Laboratory fluorescent lights containing liquid PCBs and plastic tubing leaching PCBs erroneously led to PCBs misidentified as DDT or DDE. [Gustafson, CG. 1970. Environ Sci Technology 4(10):814-819; Lisk, DJ. 1970. Analysis of pesticide residues: methods and problems. Science 170:589-593; Anderson, DW et al. 1969. Can Field-Naturalist 83:91-112 (Samples reported in 1965 to be contaminated with DDT were acknowledged in 1969 to actually have been contaminated with PCBs. Faulty analytic methods were blamed); National Audubon Society, Research Dept. 1968. Brown Pelican Newsletter (Tavernier, Florida) No. 1, page 9 (The Audubon Society was aware of the problem of PCB interference in announcing its warning: “DO NOT BRING PLASTICS INTO CONTACT WITH THE SPECIMEN.”)]
    5. The coating of aluminum foil used to wrap specimens, formalin, and sodium sulfate may also have contained PCBs or oils that might have interfered with analyses. [Risebrough, RW. 1971. Presentation to International Symposium on Identification and Measurement of Environmental Pollutants, Ottawa, Canada, June 15, 1971]
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