1. Carson got into the thing only after 15 years of studies trying to sound the alarm from the U.S. Fish and Wildlife Service, the U.S. Forest Service, and others. The Forest Service stopped using DDT in 1958 because of its ecosystem destruction, a full year before Carson even started writing in earnest.
The shadow was on the land. Carson merely opened our eyes to it.
The truth is:
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.
Ed Darrell wrote:
Were it true that the ban on spraying DDT on cotton in Texas allowed malaria to spread in Africa (and I can't believe anyone is that map challenged), the annual death rate from malaria has run at or under a million people a year since EPA acted in 1972. That's 38 years. 38 times one million would be 38 million deaths worldwide. 60 million is an inflated figure in any case.
The US Ban on DDT helped spread the way for the World Health Organization to back off from their 1955 goal of using DDT to bring Malaria under control in the third world, like it already had been in the developed nations.
The World Health Organization disagrees with the "under 1 million" and calls it "at least one million". Africa News in 1999 put the estimate at 2.7 million per year for the continent of Africa. I simply guestimated between 1 million and 2.7 million and rounded down to get to 60 million. But obviously the difference between an "overinflated 60 million" and an "accurate and factual 38 million" isn't any problem, because after all, we are only talking about dark skinned people here, it isn't like they are really human or anything.
Ed Darrell said:
3. Mosquitoes don't migrate from Texas to Africa. Can you explain, please, how not using DDT in Texas causes a rise in malaria in Africa?
See above you simpering sub-monkey moron. Also there was never a "rise" in African malaria, just never a reduction. That place can be a real hell hole.
The truth is that even DDT resistant mosquitoes will avoid areas sprayed with DDT, which is why the WHO has issued a statement as recently as 2006 that supports the use of DDT in Africa. Evidently it's ok for the WHO to eradicate smallpox, but not use DDT to eradicate malaria according to the environmental elite who don't live in crushing poverty.
It's assholes like Ed Darrell that are all for condemning children to blindness because Golden Rice is a genetically engineered crop, and therefore it's ok for the EU to refuse to trade with countries that grow gene modified foodstuffs.
Ed Darrell said:
4. DDT resistance and immunity arose in African mosquitoes in the early 1960s. By 1965, most populations of mosquito that carried malaria and could be assaulted by spraying, were resistant or immune to DDT (see Malcolm Gladwell's profile of malaria-fighter Fred Soper; see Socrates Litsios's Tomorrow of Malaria; see Jonathan Weiner's The Beak of the Finch, a story of evolution in our time.
If DDT didn't work against mosquitoes, as Rachel Carson had predicted in 1962, how is it you blame her for anything? She wasn't the one who overused and abused DDT.
Once again, see above you mouth breathing simian. DDT is useful even against resistant mosquitoes. You don't have to kill all the malaria in the world, just stop the infection in humans.
Ed Darrell said:
5. Check with Audubon. Peregrine falcon populations did not increase during DDT's peak use years. DDT instead made the birds unable to reproduce, and pushed them to the brink of extinction. There are dozens of studies on this point, all of which deny precisely your claim. Peregrines came off the endangered species list, because the decline of residual DDT in their tissues stopped making their eggs and chicks unviable.
The truth is: Up through the 1960s, it was known as a "duck hawk" and regarded as a "bounty bird," a nuisance predator subject to indiscriminate shooting across the West. Overhunting is a much more rational explanation for the decline of Peregrine Falcons than DDT, especially when you look at the data that Rachel Carson so glibly misrepresented.
A Finnish study on historical bounty payment records found this: The ‘golden age’ of bounty schemes from 1898 to the 1920s contributed to local extinctions of both mammalian and avian species.
And what does the Audubon society say about raptor populations during DDT use?
In actuality, however, declines in bird populations either had occurred before DDT was present or had occured years after DDT’s use. A comparison of the annual Audubon Christmas Bird Counts between 1941 (pre-DDT) and 1960 (after DDT’s use had waned) reveals that at least 26 different kinds of birds became more numerous during those decades, the period of greatest DDT usage. The Audubon counts document an overall increase in birds seen per observer from 1941 to 1960, and statistical analyses of the Audubon data confirm the perceived increases. For example, only 197 bald eagles were documented in 194111; the number had increased to 891 in 1960.12
At Hawk Mountain, Pennsylvania, teams of ornithologists made daily counts of migrating raptors for over 40 years. The counts—published annually by the Hawk Mountain Sanctuary Association—reveal great increases in most kinds of hawks during the DDT years. The osprey counts increased as follows: in 1946, 191; in 1956, 288; in 1967, 457; and in 1972, 630.13 In 1942 Dr. Joseph Hickey—who in 1968 would blame DDT for bird population decline—reported that 70 per-cent of the eastern osprey population had been killed by pole traps around fish hatcheries.14 That same year, before DDT came into use, Hickey noted a decline in the population of peregrine falcons.15
Ed Darrell said:
6. Carson's sources showed that chicks either did not hatch, or could not survive to fledging, when the parents got dosed with DDT. No one fully understood the mechanism -- the research all showed bird death. It is misleading to say the research didn't show eggshell thinning, because that wasn't being researched.
See the truth of the Dewitt experiment, which means read my first response again.
Ed Darrell said:
7. Subsequent research fully and completely established that eggshell thinning is caused by DDT and its daughter products, and that this meant eggs laid by bald eagles, brown pelicans, peregrine falcons and osprey, could not survive.
And obviously you can show me the mechanism of action? Oh wait, it is "still unknown". And as I have already linked, hunting for bounty or anti-predation efforts is the more likely culprit for raptor decline.
8. Please explain this: Malaria death rates today are less than half what they were when DDT use was at its peak.
Is the rest of your research so sloppy as that?
My research isn't sloppy you koolaid drinking zombie, there is a huge effort at education, treated sleeping net distribution, limited indoor spraying efforts going on in Africa. But none of it is as effective as DDT was in the developed world.
30 comments:
Regarding "nuisance birds". Makes sense to me.
I was fishing on the Limpopo and saw a kid shoot a fish eagle with a probable .223 because he was fishing and it took a fish when he wasn't catching anything. Probably out of spite. Kid wasn't very environmentally friendly, but there isn't much of anybody on that continent that is except the people that run hunting farms and game reserves.
Get DeWitt's study. You've been sold a bill of goods. Carson quoted it correctly -- your source has misled, and thereby betrayed you.
http://timpanogos.wordpress.com/2007/11/08/100-things-about-ddt-dissecting-10/
Saying, for example:
[QUOTE]Did you catch that? Milloy claims Carson was wrong because hatch rates of the DDT-fed group were close to the hatch rates of the control group. This is called “quote mining.” Milloy omits the very next three sentences including a direct quote from Dr. DeWitt:
“But few of the eggs hatched. “Many embryos appeared to develop normally during the early stages of incubation, but died during the hatching period,” Dr. DeWitt said. Of those that did hatch, more than half died within 5 days.
That changes the point a bit, doesn’t it?[END QUOTE]
Why would you trust a source that tells you such outstanding falsehoods?
(When you go to that post, be sure to read the comments by Joshua Buhs.)
Get the original research and read it for yourself. Don't rely on the words of others, even me.
Odd.
You claim, And what does the Audubon society say about raptor populations during DDT use?
But then you quote the pro-smoking group.
Can you find the Audubon Society's statement that says what you claim?
If you do, you'll be the first.
Check your sources. Ronald Reagan was right in this case: Trust, but verify. You've not verified, and so you've been misled.
In well-controlled experiments using white leghorn chickens and Japanese quail, dietary polychlorinated biphenyls (PCBs), DDT and related compounds produced no detrimental effects on eggshell quality. A drastic reduction in hatchability of chicks occurred with 10-20 ppm PCBs, but no detrimental effects on eggshell quality, egg production or hatchability were found with 0.5 and 1.0 ppm PCBs, or DDT up to 100 ppm. Dietary PCBs potentiated a vitamin E-selenium deficiency in the chick, increased exudative diathesis, and decreased plasma glutathione peroxidase levels. Dietary PCBs induced hepatic microsomal benzopyrine hydroxylase. Dietary levles of 100 or 200 ppm inorganic mercury as HgSO4 or HgCl2 had little effect on egg production, hatchability, shell quality, morbidity and mortality. Methylmercury chloride, however, at levels providing 10 or 20 mg Hg/kg of diet, severely affected all of these parameters. Even though the present experiments demonstrate that neither DDT nor PCBs has any effect on eggshell quality in chickens and Japanese quail, they may cause thinning of eggshells in other species. Controlled experiments are lacking. Eagles, ospreys and pelicans all consume fish which in many areas of the world are known to contain methyl mercury. The thinning of eggshells in the species in the wild may have been due, at least in part, to environmental contamination with methylmercury rather than DDT, DDE or PCBs, as has been claimed.
From http://www.ncbi.nlm.nih.gov/pubmed/404195
A toxicity Evaluation of DDT and dieldrin was conducted using Japanese Quail. The effects of feeding DDT (5 and 50 ppm of diet) and dieldrin (0.1 and 1.0 ppm of diet) in this four generation study (parental, F1, F2 and F3) were examined in terms of growth, viability, and/or reproduction of offspring. Ten groups (including controls and replicates of groups) contained 21 birds/group for the parental generation, and 21-35 chicks for each respective generation study. At 50 ppm DDT, a marginal decrease in egg hatch-ability of F2 generation was evidenced; the decrease appeared related to a slight decrease in fertility rather than egg production or hatchability of fertile eggs. Data accumulated from all other experimental groups were within the expected range and were comparable to control data.
From http://www.ncbi.nlm.nih.gov/pubmed/573680
p,p' -DDT and p,p' -DDE were investigated for effects on egg production and eggshell thickness in Japanese quail. p,p' -DDT was examined for effects on hatchability and fertility. DDE was tested at 0, 2, 10, 40, and 200 ppm in the diet. No evidence suggested that DDE affected number of eggs laid, egg weight, or eggshell thickness at any level of DDE tested. DDT was tested at 1,2.5, 10 and 40 ppm in the diet. In one experiment, quail fed DDT at 40 ppm and caged in male-female pairs broke more eggs than quail caged similarly but fed lower amounts of DDT or than quail fed an equal amount of DDT but caged alone. DDT did not detectably reduce eggshell thickness, number of eggs laid, fertility, or hatchability. However, paired quail laid fewer eggs than did single quail in two experiments and laid eggs with thinner shells in one experiment.
From http://www.ncbi.nlm.nih.gov/pubmed/1268339
Considering that Rachel Carson contributed mortality to eggshell thinning, and therefore a lack of hatching, my source did not mislead me.
Since I do not have access to Dewitt's original published works at my current computer I'll take your word on chick mortality.
Considering that Rachel Carson contributed mortality to eggshell thinning, and therefore a lack of hatching, my source did not mislead me.
No, she didn't. Rachel Carson died in 1964. Eggshell thinning wasn't observed for another five years or so, and the first solid research showing DDT and its daughter products caused it didn't hit until well after 1975.
Carson didn't claim eggshell thinning killed the birds because she didn't know it, could not have known it.
Once again, you have a source telling you whoppers, making stuff up that is geographically impossible, impossible on the calendar, impossible chemically, or just flat out wrong.
But don't take my word for it. Check the sources. Check the sources.
You can start here, but check the sources.
Ed, what brings you back here after all this time? Either link to a primary source or shut the hell up.
Simply linking to your blog is not going to convince anyone that you are an unbiased source of scientific information that should guide public policy.
Oh, and you are still an idiot.
Clearly playing the idiot for thinking you might want to pursue the facts, yes.
If you find errors on my blog, let me know. I've been collecting studies on claims for some time. You might find what you want there.
Ed, you keep coming back seemingly at random and asking me to visit your site and read your conclusions.
Let me put this clear, unless you have some original research that you have conducted, or are linking to original research, you are wasting everybody's time.
The key to being a good scientist is to not look at the data and dismiss everything you don't want to. I can't dismiss how lead is handled differently in the metabolisms of Turkey Vultures and California Condors. I can't dismiss how some research shows a connection between DDT and chick mortality (however if you want to bring those studies up we can look at their methodology and see if it sound or not).
What I can do is point out primary research that is freely available online. Like I have before. In this very comment thread.
And BTW, I just finished off the last of my chemoprophylaxis for malaria last week. Glad I can travel the world and not have to worry about the diseases the locals get.
Not much original research by me, except into the history and law. I just have the facts. You quote the hoaxed claims about DeWitt's research. I quote his real research. You cite the hoax claims about malaria and DDT, I point out the real stuff (malaria deaths are at the lowest point in human history today -- there was no massive upsurge in malaria when WHO cut back on DDT; WHO didn't stop fighting malaria, just used better tools).
You don't want to look at research that contradicts your a priori decision, whether it's online (not a lot of good stuff available that way, but most of it contradicts your claims), or not available online.
Your prophyllaxis did not include DDT, of course. When the chips are down, you use the science, too, regardless your other biases.
Ed, do you even know how to use PubMed to search through original research? I mean, do you have any scientific training at all? Do you know anything about biochemistry, statistical analysis, or biology?
One of us here is linking to research (that would be me), and the other is self referencing his blog (that would be you). I don't know about you, but when I read some provocative article about "Scientists claim X" I want to get to the bottom of the research and find out:
What was the experiment? Was it well designed, did it confirm or deny a hypothesis? What were the controls, what was the statistical analysis, and what is the confidence interval? These things are important.
Your chronicles on DDT are links to nothing but press releases and propaganda articles that support your unwavering opinion.
I mean seriously, "George Clooney's Malaria: DDT didn't cure it" is a real piece of work. DDT has never been a cure for malaria, but it has been a way to break the transmission cycle between species.
And saying DDT didn't stop me from getting malaria, the doxycycline and primoquine are much more expensive than residential spraying of DDT. Because I was exposed to malaria, one of our interpreters got it.
Come on Ed, you can do better. Or maybe you can't, and that is just sad.
I'm linking to my blog because it has the quotes directly from Dr. DeWitt's paper which directly refute your claims. Unfortunately the full paper is no longer available for free on the internet.
Do you know what it means to misquote the researcher, and to say things contrary to the researcher's findings? Yes, I have years of research experience (I'm not strong in statistics, but good enough), and I have years of experience in the law, and years of experience correcting errors of those who make up stuff about research.
Have you read Dr. DeWitt's papers? Did you notice that on my blog is one of the writers who spent time with DeWitt, and who wrote a book about the research, and who quotes DeWitt, and who confirms that DeWitt's work was well represented by Rachel Carson, and misrepresented by Dr. Edwards and Steven Milloy?
Accuracy counts, much more than patronizing.
J Toxicol Environ Health B Crit Rev. 2010 Oct;13(7-8):579-603.
North American osprey populations and contaminants: historic and contemporary perspectives.
Henny CJ, Grove RA, Kaiser JL, Johnson BL.
Source
U.S. Geological Survey, Forest and Rangeland Ecosystem Science Center, Corvallis, Oregon 97331, USA. hennyc@usgs.gov
Abstract
Osprey (Pandion haliaetus) populations were adversely affected by DDT and perhaps other contaminants in the United States and elsewhere. Reduced productivity, eggshell thinning, and high DDE concentrations in eggs were the signs associated with declining osprey populations in the 1950s, 1960s, and 1970s. The species was one of the first studied on a large scale to bring contaminant issues into focus. Although few quantitative population data were available prior to the 1960s, many osprey populations in North America were studied during the 1960s and 1970s with much learned about basic life history and biology. This article reviews the historical and current effects of contaminants on regional osprey populations. Breeding populations in many regions of North America showed post-DDT-era (1972) population increases of varying magnitudes, with many populations now appearing to stabilize at much higher numbers than initially reported in the 1970s and 1980s. However, the magnitude of regional population increases in the United States between 1981 (first Nationwide Survey, ∼8,000 pairs), when some recovery had already occurred, 1994 (second survey, ∼14,200), and 2001 (third survey, ∼16,000-19,000), or any other years, is likely not a simple response to the release from earlier contaminant effects, but a response to multi-factorial effects. This indirect "contaminant effects" measurement comparing changes (i.e., recovery) in post-DDT-era population numbers over time is probably confounded by changing human attitudes toward birds of prey (shooting, destroying nests, etc.), changing habitats, changing fish populations, and perhaps competition from other species. The species' adaptation to newly created reservoirs and its increasing use of artificial nesting structures (power poles, nesting platforms, cell towers, channel markers, offshore duck blinds, etc.) are two important factors. The timing of the initial use of artificial nesting structures, which replaced declining numbers of suitable trees at many locations, varied regionally (much later in the western United States and Mexico). Because of the increasing use of artificial nesting structures, there may be more ospreys nesting in North America now than ever before. Now, with the impact of most legacy organic contaminants (DDT, other organochlorine [OC] pesticides, polychlorinated biphenyls [PCB], polychlorinated dibenzo-p-dioxins [PCDD], polychlorinated dibenzofurans (PCDF]) greatly reduced or eliminated, and some osprey populations showing evidence of stabilizing, the species was proposed as a Worldwide Sentinel Species for evaluating emerging contaminants. Several emerging contaminants are already being studied, such as polybrominated diphenyl ethers (PBDE) and perfluorinated acids and sulfonate compounds (PFC). The many advantages for continued contaminant investigations using the osprey include a good understanding of its biology and ecology, its known distribution and abundance, and its ability to habituate to humans and their activities, which permits nesting in some of the potentially most contaminated environments. It is a top predator in most ecosystems, and its nests are relatively easy to locate and study with little researcher impact on reproductive success.
PMID:
21170810
[PubMed - indexed for MEDLINE]
Environ Pollut. 2009 Jul;157(7):2184-8. Epub 2009 Apr 7.
Organchlorine content and shell thickness in brown booby (Sula leucogaster) eggs in the Gulf of California and the southern Pacific coast of Mexico.
Mellink E, Riojas-López ME, Luévano-Esparza J.
Source
Departamento de Biología de la Conservación, Centro de Investigación Científica y de Educación Superior de Ensenada, B.C. Carretera Tijuana-Ensenada Km. 107, 22860 Ensenada, B.C., México. emellink@cicese.mx
Abstract
We determined egg concentrations of organochlorines and thickness of eggshells from brown boobies at eight colonies ranging from the northern Gulf of California to southern Mexico. The only common residue was that of DDE, which was found in almost all eggs. DDE content apparently reflected pre-1990 DDT use in nearby agricultural areas and, at one site, intensive mosquito control for high-end tourism development. There were no inter-colony differences in eggshell thickness, and variation in this variable likely reflected individual bird characteristics and/or individual feeding source. This variable was not a good proxy to DDE exposure of brown boobies, under current DDE levels in the brown booby trophic chain. In the northern Gulf of California, eggshell thickness has recovered to pre-DDT conditions. Our data indicate that the Gulf of California and southwestern coast of Mexico have a healthy near-shore marine environment, as far as organochlorines are concerned.
PMID:
19356832
[PubMed - indexed for MEDLINE]
Sci Total Environ. 2006 Feb 15;355(1-3):127-34.
A long-term increase in eggshell thickness of Greenlandic Peregrine Falcons Falco peregrinus tundrius.
Falk K, Møller S, Mattox WG.
Source
Teglstrupvej 6a, DK-2100 Copenhagen, Denmark. kf@vandrefalk.dk
Abstract
Thickness of eggshell fragments and whole eggs from the Peregrine Falcon Falco peregrinus collected in South and West Greenland between 1972 and 2003 was measured and compared to shell thickness of pre-DDT eggs, also collected in Greenland. Linear regression yields a significant increase in the average thickness of eggshells over the period of 0.19% per year, corresponding to a change in eggshell thinning from 13.9% in 1972 to 7.8% in 2003. Backwards extrapolation of the data, suggests that the Greenlandic Peregrine population probably was never critically affected by DDT-induced eggshell thinning. By sampling eggshell fragments in many nests the spatial and temporal sample distribution was enlarged, allowing the detection of a significant long-term decrease in pollutant-induced eggshell thinning--a trend that could not have been identified if only the rarer whole, addled eggs had been sampled.
PMID:
15885749
[PubMed - indexed for MEDLINE]
See here:
http://www.ncbi.nlm.nih.gov/pubmed/15885749
Environ Pollut. 1997;95(1):67-74.
Clarification of effects of DDE on shell thickness, size, mass, and shape of avian eggs.
Blus LJ, Wiemeyer SN, Bunck CM.
Source
National Biological Service, Forest and Rangeland Ecosystem Science Center, Northwest Research Station, 3080 SE Clearwater Drive, Corvallis, OR 97333, USA.
Abstract
Moriarty et al. (1986) used field data to conclude that DDE decreased the size or altered the shape of avian eggs; therefore, they postulated that decreased eggshell thickness was a secondary effect because, as a general rule, thickness and egg size are positively correlated. To further test this relationship, the present authors analyzed data from eggs of captive American kestrels. Falco sparverius given DDT- or DDE-contaminated or clean diets and from wild brown pelicans Pelecanus occidentalis collected both before (pre-1946) and after (post-1945) DDT was introduced into the environment. Pertinent data from other field and laboratory studies were also summarized. DDE was not related to and did not affect size, mass, or shape of eggs of the brown pelican or American kestrel; but the relationship of DDE to eggshell thinning held true. Size and shape of eggs of brown pelicans from the post-1945 era and those of kestrels, on DDT-contaminated diets showed some significant, but inconsistent, changes compared to brown pelican data from the pre-1946 era or kestrels on clean diets. In contrast, nearly all samples of eggs of experimental kestrels given DDT-contaminated diets and those of wild brown pelicans from the post-1945 era exhibited significant eggshell thinning. Pertinent experimental studies with other sensitive avian species indicated no effects of DDE on the size or shape of eggs, even though the high dietary concentrations caused extreme eggshell thinning and mortality of some adult mallards (Anas platyrhynchos) in one study. These findings essentially controvert the argument that decreased eggshell thickness is a secondary effect resulting from the primary effect of DDE-induced changes in the size or shape of eggs.
PMID:
15093475
[PubMed]
See here:
http://www.ncbi.nlm.nih.gov/pubmed/15093475
Ok Ed, let me explain Dewitt's method for his 1955 experiment. If you are talking about Dewitt's later experiments then I'll look at those later.
Dewitt was testing for tissue holding of DDT and toxicity. This is "pure research" in terms of identifying how a molecule is metabolized or not. This means he fed his birds enough DDT to reach LD50, or half of them died. LD stands for "Lethal Dose." Every substance has an LD associated with it, even table salt.
So after killing off enough of the birds, the survivors hatched eggs that were not statistically different from control groups. However, since those chicks came from a stock that had at least an LD50 dose of DDT in them, it makes sense that they would have a higher mortality rate.
As someone who is looking at science, we need to ask the following question. Based on the evidence, does feeding a population of birds an LD50 level of a substance give us meaningful data on chick mortality? The answer is no.
Obviously it would be impossible for an adult bird to ingest an LD50 level of DDT in the wild, even with "biomagnification" acting to concentrate DDT and daughter compounds in birds. I have found no research where even the suggestion of an LD50 concentration could be reached in the wild. If you find some I would like to know about it.
Now, since you can't get an LD50 dose, there must be some "dose/response" curve that gets defined. Such as at X ppm only 10% increase in mortality, at 2X ppm 20% and so forth and so on. There is no "dose response" curve for DDT that I can find. In medicine the ratio of the minimum dose required for a clinical effect and the LD50 is the "therapeutic index" and this is how MD's figure out how much to medicine to write on a prescription. With poisons/toxins it works the same way, as "the dose makes the poison."
So, was Dewitt's experiment a well designed experiment? To answer Dewitt's original questions about lethality and tissue holding, yes. To answer questions about chick mortality and establishing a dose/response curve, no.
Think about it this way, if you poisoned 100 women with a substance, and 50% survived to give birth to a population of sickly babies who died at a rate higher than a healthy control group, would that tell you anything useful?
J Toxicol Environ Health B Crit Rev. 2010 Oct;13(7-8):579-603.
North American osprey populations and contaminants: historic and contemporary perspectives.
Henny CJ, Grove RA, Kaiser JL, Johnson BL.
Source
Errors, "correlation not linked to causation" and "begs the question" in that it presupposes DDT is the cause of bird population decline along with other unspecified "pollutants." This is a not research, it is a history report. This says, "this is what happened over time, while this other event happened over time." See how the lack of pirates is causing global warming.
Second article. This one doesn't support your position at all.
Organchlorine content and shell thickness in brown booby (Sula leucogaster) eggs in the Gulf of California and the southern Pacific coast of Mexico.
This is a better source but here is what you linked, There were no inter-colony differences in eggshell thickness, and variation in this variable likely reflected individual bird characteristics and/or individual feeding source.
So you linked to research that doesn't prove the point you are trying to make. Measurable levels of DDE having no measurable effect on egg shell thickness.
Third article, Sci Total Environ. 2006 Feb 15;355(1-3):127-34.
A long-term increase in eggshell thickness of Greenlandic Peregrine Falcons Falco peregrinus tundrius.
Falk K, Møller S, Mattox WG.
No control group, multiple confounding factors, begs the question. Do you expect tree rings to be the same every year? Do you expect egg shells to be the same every year? There are multiple causes of eggshell thinning, and without eliminating confounding factors such as seasonal variation and the banning of leaded gasoline it is interesting correlation with small statistical differences.
Fourth study: Clarification of effects of DDE on shell thickness, size, mass, and shape of avian eggs.
Blus LJ, Wiemeyer SN, Bunck CM.
So far it is the only one that backs up your point. The hypothesis is clear, does DDE affect egg size? The answer was no, but egg shell thinning was observed. However it does not establish a link between shell thickness and mortality and I don't have access to the full text to see significance.
You should have argued this with me this time last year when I had daily access to a research library.
Darrel you need to read, "Studying a Study and Testing a Test" http://www.amazon.com/Studying-Study-Testing-Test-Pediatrics/dp/0781745764 to help identify what is helpful as opposed to what is interesting but not useful.
Fascinating to me that you can tell the references of a study without having read the study, and that with the same level of absence of information, you can claim the authors of the study got their conclusions wrong and no one in the peer review process caught the error.
I should have realized that since you rely on a bogus, hoax claim about DeWitt's studies, without your ever having read his work in the first place.
Confess: Did you ever read Rachel Carson, either?
Ed, I'm sorry, I couldn't get through "Silent Spring" but I might give it another shot. Maybe I can disconnect the logic circuit and think with my heart for long enough to choke it down this time.
Since you don't have access to the full text any more than I do (since I am no longer in school) it will take me a bit more time to request the full text through a library with a journal subscription. Based solely on the abstracts that were available (which is largely all that journalists ever see as well) you got my analysis. And you are welcome.
Seriously Ed, you need to read "Studying a Study and Testing a Test" to begin to understand that not all research is good research. Not all experiments are well designed, and the pressure on researchers to publish SOMETHING is intense (it is publish or perish after all).
I've reviewed plenty of DDT related research that is available on pubmed and have come to the conclusion that DDT alone could not cause a "Silent Spring" as written by Carson. I do believe that a combination of any organochloride, lead phosphate anti knock agents in gasoline, and methylated mercury in the environment will cause toxicity in the animals. I also believe based on the research that different species will be affected differently and metabolise toxins with better or worse efficiency (exmples of California Condors and Lead verses Turkey Vultures and Lead, and West Highland Terriers and Copper verses other breeds and Copper).
You are falling into the trap of "proof through assertion" instead of trying to point me to a "dose response" curve and associating that with chick mortality. In science when there isn't a clear, smoking gun, proof, people interpret data to support a preconcieved bias. I'm not saying I am not biased. I'm saying that based on the evidence currently available DDT I do not believe an outright ban is scientifically supportable.
I know that uncertainty isn't pleasant to most people, but it is extremely important to scientists. Since you have such strong convictions without a hint of doubt I can only classify you as "faith based" and hope that you'll eventually abandon your logical fallacy of "proof through rigorous assertion." But I won't hold my breath.
See human health effects here:
http://www.atsdr.cdc.gov/PHS/PHS.asp?id=79&tid=20
Ed, this is directly quoted from the FAQ you linked (although I did bold some facts for emphasis),
All uses of DDT were banned by EPA in 1972, except in cases of public health emergencies. DDT was banned because the chemical was building up in the environment and possibly hurting wildlife. Also, some cancer tests in laboratory animals showed positive results. Although DDT is no longer used in the United States, federal regulations still control the amounts of DDT allowed in food and water.
Even the CDC isn't sure that there were effects on wildlife.
And remember what I wrote about something called an "LD50"? Anything that has an LD50 is going to be a toxic substance, from aspirin to DEET to commercial insecticides.
And speaking of insecticides...
Did you know there are several thousand cases of nerve agent poisoning in the US every year? Mainly from improper handling of OP pesticides. http://emedicine.medscape.com/article/167726-overview Funny how the "safe and approved" organophosphate insecticides we still have are more lethal as acetocholinesterase inhibitors than organochlorides such as DDT.
But as long as it is people dieing and not birds, you don't care, do you Ed?
The whole point of environmental protection is to save human lives -- but if you can score a political point with your buddies, you don't care, right? Birds are, almost literally, the canaries in the mine. The stuff kills birds, it most likely kills humans -- that's true almost across the spectrum (a few organic poisonous berries being excepted -- they sicken humans, but not birds who ingest them; go figure).
You keep harping on human lives, but you ignore the fact that human deaths to malaria are in steady decline -- almost a direct correlation between reduced DDT use and reduced human deaths to malaria. This reduction in deaths is largely without DDT, but with DDT use in those few places it still works and can be done (we hope) without injuring people more than malaria. From peak DDT use in 1959 and 1960, with deaths at 4 million a year and malaria infections at 500 million a year, hard work by health care officials cut deaths by more than 75%, to under 900,000 in 2008, and infections by 50%, to 250 million. That's more impressive when we consider the total number of people on Earth doubled in the same time.
Worried about humans? Stop thinking DDT will save them. It won't, often can't.
But the evidence mounts that even trace amounts of DDT do serious damage to people; see the Pine River Statement, for example.
ATSDR did an addendum to their toxic registry entry specifically on human health. We can say DDT isn't a powerful problem in human health, but we can say that only because doses are low due to restrictions on use. Wherever humans have elevated levels of DDT and its daughter products in their blood, we find the stuff implicated in liver and pancreatic cancers, and especially in any diseases of reproductive hormones. DDT won't kill your kids, but it will shrink your boys' testes and swell their mammaries, and swell the mammaries and cause premature menses in your girls. Their children will have increased incidence of breast and reproduction deformities and cancers.
But, to you, they are only kids, right? Maybe they'll grow out of it by the time they're 75, right?
Boy Ed, do you really want me to quote the people in the environmental movement leadership who have lobbied for human population control?
The environmental movement is NOT about "saving lives." Paul Ehlrich writes "The Population Bomb" in 1968 and DDT is banned by 1972? Really you see no connection here? Reducing human impact on "Gaia" has always been the agenda, never "saving lives" you sanctimonious simpleton.
The continuing decline of malaria deaths? Really? http://www.telegraph.co.uk/health/healthnews/9058283/Malaria-death-toll-far-higher-than-previously-thought.html
Have you ever stepped a foot into a third world hellhole? Why is it that we in the US don't deal with Malaria? Oh yeah, DDT. You know if there were an outbreak of malaria in the US it wouldn't be long before DDT were called again to help contain the outbreak.
But you want to deny the brown peoples the same access to malaria control options. Isn't that kind of racist?
Boy Ed, do you really want me to quote the people in the environmental movement leadership who have lobbied for human population control?
Why? It's a much shorter list than you think -- hint: Ehrlich isn't on it.
The article in The Telegraph does not deny the continuing decline in malaria deaths. It says the total is not so low as WHO counts, but at 1.2 million, that's still almost a 75% reduction from the 4 million in 1959 and 1960, at peak DDT use.
No one is seriously contesting the decline in total infections.
If one reads the article carefully, one notes that it does not blame a lack of DDT for difficulties in eradicating the disease, but rather the growth of resistance of the malaria parasites themselves to the pharmaceuticals used to treat the diseases. This is important. DDT is not a cure for malaria, but a way to temporarily knock down the populations of mosquitoes that spread the disease. In the WHO malaria eradication campaign, the plan was to cure every human of malaria so that when the mosquito population comes roaring back -- and it always does -- there would be no pool of infected humans from whom the mosquitoes could catch the disease. When that happens, killing mosquitoes is superfluous, because they cannot spread a disease they cannot catch.
It's not a lack of DDT causing problems now, but lack of effective pharmaceuticals in some places.
That lack of pharmaceuticals may have slowed, but has not stopped, the decline of malaria, and the steady progress toward wiping it out as a human affliction.
Darrel, Erlich equated the human race with unchecked cancer eating up the worlds resources.
Ever since then rabid environmentalists have advocated for "population control" to stave of everything from food shortages to "global warming." Google it if you don't believe me.
You need to get a refund on whoever taught you statistics if you extrapolate from the 1960s to now and claim "progess!" 4 million cases of malaria to 1.2 million cases now sounds like progress until you see that the "rate of progress" has been largely unchanged since I started giving any thought to malaria in the late 1990s.
A flat trend line is not trending towards a solution. Seriously Ed, how many nations lifted themselves out of poverty since the 1960s? Look up Hans Rosling's TED talk from 2007 to look at the economic progress (which is a good indicator of how well a country can deal with malaria).
Malaria deaths continue to trend down -- there has been a 13% reduction since 2000. Figures from WHO's annual report on malaria here: http://www.who.int/malaria/world_malaria_report_2011/burdenestimatesbriefing2011.pdf
Thanks Ed, why don't you correlate that data against rising incomes and increased WHO expenditures?
Otherwise you are just doing your normal "drive by posting" technique which is a banned activity on most webforums I frequent.
And finally did you actually read the report you linked to?
The estimates of the number of deaths outside Africa are also similar to those published in WMR
2010 but those for the WHO African Region are substantially different. This is for two reasons:
(i) A downward revision of the total number of child deaths occurring globally made by the
UN Inter-agency Group for Child Mortality Estimation (1).
(ii) Changes in the assignment in cause of death made by the Child Health Epidemiology
Reference Group (CHERG), that affected the proportion of deaths attributed to malaria,
particularly at the beginning of the last decade.
These methodological changes resulted in an overall lowering of the number of malaria deaths in
the African Region of approximately 11% for 2009 and larger percentages in earlier years. A
notable feature of the new estimates is that the number of deaths estimated to occur in the African
Region rose from 682,000 in 2000 to 748,000 in 2004, in line with population growth, before
they began to come down owing to a scale up of control activities. This pattern is consistent with
changes in the estimated number of cases.
While the number of deaths rose between 2000
What the report is saying isn't that the number of deaths is down, but how they assign cause of death has changed. This is called "changing the measuring stick" method of bullshitting the public in order to show some progress.
Total malaria deaths in the peak DDT years of 1959 and 1960 numbered 4 million. Today, you and I quibble about whether it's closer to 800,000 or 700,000.
Take the higher number. Assume counting has been in error -- that still gives us a reduction of greater than 75% in total malaria deaths, and it still confirms the trend to decreasing malaria deaths.
It's still progress.
You resent that I occasionally drop by to correct another error? In medicine, and most other sciences, when the overwhelming evidence runs against a claim, and it becomes clear that a claim is bogus (like the claim that DDT was wrongly banned from the U.S., or that the U.S. ban on DDT somehow increased malaria in Africa), there is a retraction printed.
You may note the errors any time, or retract the erroneous claims. I'd be happy to let this entire thread slip into the mists of Internet Past -- once the errors are gone and no innocent children are at risk of harm from the errors.
Ed,
You call it "correction" but all I see is "revision of estimation." You link to a paper that says "Malaria deaths are down because we choose to attribute some of those deaths to something other than malaria" and expect me to uncritically accept a "change the yardstick" approach to problem solving?
Why don't you read these?
http://www.newscientist.com/article/dn21424-malaria-may-kill-far-more-people-than-we-thought.html
http://globalhealth.kff.org/Daily-Reports/2010/October/21/GH-102110-India-Malaria-Study.aspx
http://www.cghr.org/index.php/2010/10/controversial-malaria-mortality-results-from-the-million-death-study-published-in-the-lancet/
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