Epidemic Of Avian Die-Off
Not Explained By West Nile Virus
Only 7.7% WNV Positive
This is an analysis of an article by Marian Gail Brown in the Connecticut Post, 9/18/00, below. The article reveals at least three things of interest:
1) WNV bird death was 7.7% as of mid-September, 2000, after most of the dead birds were reported. [This was determined and reported as 13% later.]
2) To explain this low percentage for such an overly dramatized "West Nile epidemic", pesticide residues have been promoted as a primary suspect. This is a continuation of a theory that has been in vogue for decades. This theory was also greatly diminished later, in The New York Times, November 27, 2000, and replaced with a microbial causation theory. The Audubon Society has been, in year 2001, promoting the (banned) pesticide residues theory for the bird deaths.
3) The pesticide residue causation theory is brought back strongly in AP 6/3/01, describing 1/5 of tested birds in terms of pesticide residues, largely in terms of banned pesticides.
Before I continue, I first must deflate the idea that the massive avian die-off is not new, just a mere byproduct of increased bird death reporting, driven by media hype regarding the West Nile virus. This concept has been promoted by the NYCDOH press department to explain the inconsistencies in the WNV paradigm.
My studies conclude that media motivated the public to report dead birds and that massive numbers of dead birds were available to be reported. Media did not begin reporting until after the public began taking notice on its own. The massive deaths of thousands of birds clearly began in 1999. Unusual but lesser smaller numbers of mass bird deaths began to be reported in the New York City region as early as 1995. Media hype became interactive with the publics reporting of dead birds and various increased epidemics in the New York City region.
Update: The percentage of WNV-positive birds is quite different according to a poster at The International West Nile Virus Conference, in April 5-7, 2001. The poster was entitled "West Nile Virus In Birds And Mosquitoes In New York State In 2000", and was put together by several state agencies:
The percentage positive birds was 35% for the entire state, 51% (n=1,502) for the epicenter, and 23% (n=l,901) outside the epicenter."
This is quite different than 7.7%.
So here is an analysis that shows that agencies have greatly skewed the reporting of data since 9/18/2000, with the resulting higher WNV percentages.
As of 9/10/00, approximately 90% of the summer's massive bird death had already occurred, according to the Staten Island Wildlife Refuge Intake Log. So where did all the dead birds come from after 9/18/00, that could have allowed the percent to change? I need to check to see if the "Date Found" was moved forward, and birds delivered to DEC pathology late, by some bureaucratic error.
It is clear that media hype did not determine the number of reported bird deaths, because by August 4th, the Staten Island (the epidemic epicenter) Borough President Guy Molinari was quoted by the NYCDOH as saying that over 500 reports of dead birds had been received by his phone operators. Yet, adjacent boroughs had few or none reported by that date.
|Par||Text (The Connecticut Post, 9/18/00)||Comments|
|--||Banned Pesticides Found In Dead Birds||Title.|
|a||Some birds initially suspected of carrying West Nile virus in Connecticut are laced with insecticides and DDT byproducts, a pesticide the federal government banned about 30 years ago.||Old phenomena used to explain the new, massive avian die-off.|
|b||Whether or not the level of DDT or diazinon, a common pesticide used to protect lawns from insect infestation, killed them remains to be seen.||Disclaimer.|
|c||"We are finding pesticides in these birds that were applied 30 and 40 years ago. They stay in the ground for decades," said John Anderson, director of the Connecticut Agricultural Experiment Station.||This thesis (ground poisons) was the original thesis of the NYSDEC, which was announced in 1999, right up until the WNV paradigm took over with hyper-drama. Also see ToxicSentinel and ToxAbort.|
|d||Initial research by Anderson and his colleagues, Walter Krol and Mary Jane Mattina, both analytical chemists, show high concentrations of the banned and licensed pesticides.||See other quotes by Anderson (see Anderson1, Anderson2). What does "high concentrations" mean? Numbers? Relative to what?|
|e||"They have significant pesticides in their systems," Anderson said.||"Significant"?|
|f||The birds, most of which are not crows, were submitted by health directors in lower Fairfield County anxious to see whether the West Nile virus killed them.|
|g||"I'm surprised at the variety and quantity of the pesticides we are finding. None of the birds had any signs of resmethrin in its system. Right now, this research is a sideline of ours," Anderson said. "We still have so many, many birds to test [for West Nile] that it may be a while before we can concentrate on what else may be killing birds."||How much of the older, organochlorine pesticides? Compared to when? See Footnote 1.|
|h||So far, 6,949 dead birds have been reported throughout Connecticut since the state asked the public to report them. Only a fraction of those birds ultimately were suitable for testing. Altogether, 279 were infected by and ultimately died from West Nile fever.|
|i||"Those are the number of avian deaths that people have reported so far," Greenwich Health Director Caroline Baisely said. "In the backcountry part of Greenwich, where people have 5 acres of property or more, who knows how many of these birds are out there. Perhaps these dead birds are just the tip of something much bigger killing birds. We really don't know."||<=="...something much bigger killing birds."|
|j||In conference calls between state officials, both the Ag Station and the University of Connecticut indicated a desire to continue studying the avian mortalities, said Department of Environmental Protection Commissioner Arthur J. Rocque Jr.|
|k||The discussions are still in the "preliminary stage" right now, Rocque said. "Beyond the public health threat, there are issues about our scientific knowledge of [avian] disease that they feel should be explored."|
|l||Meredith Sampson, who has nurtured sick and wounded birds back to health for Wild Wings Wildlife Rehabilitation Center in Stamford and Greenwich, has watched the avian death toll mount with increasing alarm and frustration.||These areas are close to New York City, within the area of extremely high ozone concentration, and Connecticut's own considerable pollution sources.|
|m||A sharp-shinned hawk now in Sampson's care arrived with a fracture to a bone equivalent to that of a human's collarbone. Whether the break is the result of an accident, chronic disease or other illness, she has no idea.||Neurological disease produces dis-coordination.|
|n||The calls that come into Sampson's office are constant and persistent.|
|o||"They'll say 'I see this bird out there that's really sick looking, can you come get it?' " she said.|
|p||Given all of the bird carcasses sitting in refrigerators at the University of Connecticut's Pathobiology Lab and at the Ag Station, Sampson says it makes sense to examine what's killing the birds besides West Nile virus.||Finally, examine other causes.|
|q||"They should check for other viruses, other possibilities, such as pesticide poisoning and other illnesses," Sampson said. "Putting aside the crows, looking at song birds and other birds of prey, I think it's still too high a die-off."||Prevalent new neurotoxins are taboo?|
|r||To put the known avian fatalities in perspective, Stamford - a hotbed for avian West Nile cases this year - logged 620 dead bird reports. The cause of death is unknown for most of those birds. Greenwich and Westport had 471 and 212, respectively. To the east, Fairfield had 357. Milford reported finding 339 dead birds.||A recent (9/18/00) flyer put out by NYCDOH states that birds should be reported and then thrown in the trash. The city will not pick them up unless it requests to do so.|
|s||Nationally, avian surveillance has identified 1,471 West Nile-infected birds from 70 counties in six states, including Connecticut, New York, New Jersey, Massachusetts, Rhode Island and New Hampshire.|
|t||New York State alone found more than 15,000 birds dead for unknown reasons. Seven thousand of those birds were ultimately tested by the state's Department of Environmental Conservation. West Nile killed 536 of those birds. What killed the rest is an ongoing focus of wildlife pathologist Ward Stone's research.||"15,000" appears to be for "this year" (see paragraph r). The percent of WNV-positives calculates to 7.7%. This is consistent with the percent (6%) of birds tested positive for WNV in Staten Island by mid-summer. See PR000804 and ts000804.|
|u||While West Nile testing is a priority, Stone says his department has to be selective.||Avian toxicology was Stone's priority before the summer of 1999.|
|v||"I don't want to lose the opportunity when I have these birds in hand to determine what they've died of," Stone said.||WNV became a priority after the summer of 1999, with Mr. Stone.|
|w||Once West Nile is ruled out, wildlife pathologists in New York are examining their birds for Type E botulism, avian pox, influenza and a host of other diseases, some of which can be transmitted to people.||It is a toxicological axiom that responses to poisoning from individual to individual, within a specie, are extremely varied. There is also a great variety of response from specie to specie.|
|x||"There are so many animals coming in that I don't think any state will have the money needed to pursue all of these diagnostic avenues," Stone said. "What's out there now in terms of federal funds is not enough by far to cover the huge number of birds and mammals coming in with suspected West Nile cases."||This conforms with Stone's statement to me that he had no present or foreseeable capability to test for air toxins as causative, due to funding.|
|y||Nicholas Komar, a research biologist at the CDC's Arbovirus Diseases Branch in Fort Collins, Colo., believes avian mortality research would have value.||Komar also called Dr. Charos of Bayside in 1999 to inform him of the West Nile paradigm after Charos was quoted in The New York Times stating that it appeared that the crows had been poisoned.|
|z||"From a scientific point of view, if there is a lot of bird mortality, our society should want to know what's causing those bird deaths," Komar said. "Right now, the researchers are using their resources to document the West Nile virus."|
|aa||Nevertheless, Komar conceded that, if some new disease is attacking migratory birds, it might take some time to identify it unless there was an epidemic caseload or a corresponding human health threat.||"Conceded", did Komar (whose apparent job is to handle public inquiries) not want to release the cat out of the bag? Did he want to limit speculation re non-WNV factors?|
|ab||At the U.S. Geological Survey's National Wildlife Health Center in Madison, Wis., scientists have analyzed about 13,000 dead birds this year from 25 states.|
|ac||"There have been a lot that are West Nile-negative, and we could probably guess at what's killing them. But that wouldn't prove anything," said Bob McLean, director of the U.S. Geological Survey.||"A lot" is 92%. A more appropriate phrase is "most", or "almost all". Here the WNV paradigm fails Koch's Postulates (that the germ must be found in all of the epidemic cases). Isn't a guess necessary before the procedure of proof? "...we could guess... but that wouldn't prove anything..."|
|ad||"We have the capability to determine the cause of this mortality. We could learn what's killing these birds - whether it's pesticide poisoning, Type E avian botulism or something else," he said.||McLean appears to have focused entirely upon germ theory.|
|ae||"If you know some of the causes of this mortality, you can make recommendations to avoid certain pesticides, some agriculture products and maybe assist in changing the situation for the better."||The avian die-off and the "West Nile Epidemic" are new phenomena, yet only ancient data is being utilized. MTBE is not a well known. Dr. Stone had not heard of this most prevalent toxin when I interviewed him in April of 1999. Most environmentalists are not even aware of MTBE or the capability of air toxins to be neurotoxic.|
Another View of Pesticide Residues
A/C Filters and Chlordane
Here is some data regarding pesticides, for perspective: A resident of Huntington, Long Island, Donna Reilly, had her A/C filters and lawn soil analyzed by Toxicology International, Inc., in Virginia, by Dr. Robert Simon.
Window A/C filter, Foam, Changed Before Summer 1999; Collected October 2, 2000 Sample Item Pesticide Parts Per Million (Weight) Heptachlor 8.119 Gamma-chlordane 2.468 Alpha-chlordane 2.039 Total of various chlordane = 14.329ppm Transnachlor 1.703 Resmethrin 1.976 Sumethrin Not detected above level of detection (1.000ppm)
Soil, Surface, At Corner of House, Rear, SE Corner Sample Item Pesticide Parts Per Million (Weight) Heptachlor 0.080 Gamma-chlordane 0.105 Alpha-chlordane 0.110 Total of various chlordane = 0.324ppm Transnachlor 0.029 Resmethrin 0.220 Sumethrin Not detected above level of detection (1.000ppm)
Short Term Exposure Dosage
Chlordane is similar or less lethal than DDT, according to a comparison of various figures in Hayes and Laws, page 78. The only bird study I could find was for a chicken, where the LD50 was 65ppm. Chlordane was restricted by 1976, 5 years after DDT was banned. Chlordane is less pervasive in the environment than DDT according to B. E. Sample et al (1995).
Sustained Dosage Of Chlordane
In June/July of 1996 and 1997, the all-time record for chlordane-caused bird death (estimated 600-800) was reported as occurring in Scotch Plains, New Jersey, according to Stansley and Roscoe (FWS) in "Chlordane Poisoning of Birds in New Jersey, USA", Environmental Toxicology and Chemistry, 1999. Scotch Plains is exposed to dense vehicular emissions and is not far from Newark Airport and New Jersey oil refineries. The bird deaths occurred one year after MTBE levels were raised by government mandate. The reports states that the bird death could have been pervasive in the region. Chlordane residues were found, but not compared with residues in other birds that were living in the area. The levels of chlordane residues found in the brain tissue of the birds were very similar to the levels found in the A/C filter on Long Island, around 14ppm, as seen in the table, above, indicating that chlordane can be ubiquitous at those levels, in the Tri-state region.
Since chlordane was restricted and banned not long after DDT, and we are not seeing DDT epidemics in birds, then is "chlordane" (an imprecise mix of chlorinated hydrocarbons) actually oil refinery air pollution arising from the use of chlorine in refinery processes?
Where are the chlordane-caused bird epidemics elsewhere, away from high densities of petrochemical industry? Scotch Plains, NJ, is in the thick of it -- very close to the nation's highest density of "West Nile virus" bird-death epidemics, noted in 2000 and 2001 when NJ got around to counting WNV positive humans, birds and mosquitoes.
The standard used for evaluating the residues as causative for death is from a report by Stickel et al in 1978, which is widely quoted in other writings on bird death. I'm critical of that report and have reviewed it. Stansley and Roscoe describe Stickel, "In a laboratory study, Stickel et al established diagnostic criteria on the basis of brain residues of chlordane metabolites associated with lethal poisoning." I was questioning the phrase, "associated with lethal poisoning"; how was chlordane associated? In the same way that Stansley and Roscoe are associating chlordane? Or with laboratory induced death by chlordane? If so what were the rates of administration of chlordane?
I've hence looked at Stickel's two landmark studies, 1978(1) and 1983(2), and found:
1) Stickel's method of using residues to indicate chlordane causative is analogous to the belief that one can determine the amperage history of an electronic circuit by referring only to a residual capacitance in one component of the circuit, which has had various unknown durations of exposure to an unknown voltage and current and said residual capacitance measured after an unknown duration following shut-off of the circuit from its power supply. There are too many variables to allow a firm diagnoses of pesticide residue causations. The usage of chlordane in the foundations of houses to kill termites, and the Stickel study, creates an effective diversion from other more direct forms of air pollution.
2) Stickel, et al noticed was that there were two kinds of birds found at the end of their dosage testing: Dead birds and live birds. There was a big difference between the two. The dead birds had chlordane residues and the live birds had comparatively very low levels. That fact forms a major point of critique of the Stickel study. Stickel et al acknowledge that the dying bird begins to fast, losing the ability to use its organs. This in turn releases into the blood stream chlordane (and other pollutants) stored in the fatty tissue, thus accelerating the death of the bird. Air pollution could bring about this critical illness, the trigger, the release of stored pesticides. Pesticides generally are stored relatively safely in the fatty tissue of animals.
Stansley et al referred to the probable nutrient source of chlordane as June beetles, in which had been found 0.8ppm chlordane according to other studies in other areas. That source of chlordane was not confirmed. Also, 0.8ppm is far below the dietary dosage required to cause adverse effects of any kind, according to a recent listing of NOAEL and LOAEL data, found in "Toxicological Benchmarks for Wildlife", by B. E. Sample, et al, for the Department of Energy, 1996:
Animal Studied: Red-Winged Blackbird
NOAEL = "No Observed Adverse Effects Level"
LOAEL = "Lowest Observed Adverse Effects Level"
mg/kg/d = milligram/kilogram/diet weight
While 26% and 24% mortality was observed among birds on diets containing 50 and 100 mg/kg Chlordane, no adverse effects were observed among the 10 mg/kg dose group. Because the study considered exposure over 84 days, the 10 mg/kg dose was considered to be a chronic NOAEL. The 50 mg/kg dose was considered to be a chronic LOAEL.
Final NOAEL: 2.14 mg/kg/d
Final LOAEL: 10.7 mg/kg/d
Thus, regarding the Scotch Plains bird deaths, chlordane dosages were not sufficient to have caused this mass bird death, and chlordane seems to be ubiquitous at the brain tissue levels cited by Stansley et al.
I posit that these bird deaths are a multi-toxics event, with air toxics being the overwhelming trigger factor. The NJ chlordane birds stayed on their roosts and died there. Consider the principle of Avitrol (bird control pesticide), which is to cause a small percentage of bird deaths in order to scare away the flock from its roost. But, I posit, if air toxics were the cause, then the flock would have no escape, and would die at the roost area. Any movement, any breath, would cause greater poisoning to the bird.
The chlordane residue theory conflicts with studies which found lowering chlordane levels and rising reproduction rates in bald eagles. The chlordane phase-out began in 1976 and it was banned in 1988, with levels of chlordane substantially decreasing every year in the environment, according to a study re eagle egg shell thickness and organochlorines in the environment, Weimeyer et al, "Environmental Contaminants in Bald Eagle Eggs, 1980-84", Environmental Contamination and Toxicology, 1993.
The Stansley report encompassed several species, with widely differing dietary habits, from House Sparrow to Cooper's Hawk, although the primary bird was Grackle, and European Starlings. The Grackle is a iridescent black bird, similar to a crow.
With the advent of the "West Nile virus" epidemic of bird death in 1999, the NYC bird death was initially thought also to be due to "chemicals in the ground", according to the NYSDEC. A report was about to be released, officiating this belief, but then not released when the WNV paradigm acquired a sudden dominance by federal governmental edict (CDC), on September 3, 1999..
Assuming that chlordane is equal to or less than DDT (data is more available), consider this in terms of DDT:
Donna Reilly's filter concentration of chlordane is about 0.13 of the LD50 for chlordane.
Her filter concentration of chlordane is 60 (multiple) of the long-term susceptibility found for DDT.
Her soil concentration of chlordane is 0.002 of the LD50 for DDT.
Her soil concentration of chlordane is 1.35 (multiple) of the long-term susceptibility found for DDT.
The filter has more chlordane than resmethrin, and higher pesticide concentrations than the soil. How does chlordane, a banned pesticide, get into the filter, at these high levels? The reason is that chlordane has been in a phase-out mode, and allowed for termite usage around homes. It apparently vaporizes and accumulates in the filter material, to which it may have an affinity.
West Nile Epidemic
While the pesticide concentrations are disturbing, the issue of existing chlordane pollution has been an issue for many years, and was negated by the NYSDEC on November 22, 2000, according to The New York Times interview of Ward Stone. The West Nile epidemic is a new phenomena. Air neurotoxins are a better thesis because the bird death coincides with the high ozone season of 1999 and the annual summer high ozone levels. The presence of organochlorines in the air of the New York region is the link required for the confirmation of the Middlesex study regarding encephalitis and spontaneous virus proliferation caused by trace amounts of organochlorines in the presence of ether, aromatics petroleum products, aromatic nitros, and pure oxygen. This data deserves more study.
Footnotes 1) Stickel, et al, "Chlordane in Birds: A Study of Lethal Residues and Loss Rates" (1978) 2) Stickel, et al, "Oxychlordane, HCS-3260, and NonAChlor in Birds: Lethal Residues and Loss Rates" (1983)