WNV Positive Wildlife And MTBE
Analysis of NYSDEC Pathology Unit's
West Nile Virus Database 1999 (pub. 2/3/00)

Abstract

In the New York City region, a public health disaster was recognized during the summer of 1999. That recurring seasonal phenomena is referred to as the “West Nile Virus Epidemic” and a virus was said to have caused the human illness, disease, and unprecedented wildlife mortality.

This study analyzes the NYSDEC Wildlife Pathology Unit’s “West Nile Virus Database” (1999) in terms of air pollution, ozone, MTBE protocols, animals reported, WNV-negatives, and WNV-positives.

The 62 counties of New York State are defined, for the purpose of this study, within three categories of air pollution: A) Severe counties (9) are the original EPA "Severe-17" counties. B) Moderate counties (10) are those originally designated by EPA as “Moderate NA”, plus the county of Albany and its surrounding counties that experience dense metropolitan traffic. Less polluted counties (43) are the remaining counties. (see map)

Findings: WNV-positive animal mortality correlated precisely with EPA county-by-county categories that affect gasoline formulations with MTBE (methyl ethyl butyl ether). MTBE is a poisonous gasoline additive that has been undergoing a phase-out and ban as recommended by the EPA on July 31, 1999, at the height of arguably the highest incidence of bird mortality in the history of the U.S.

The WNV-positive percentage of tested animals in the severe counties was 24 times greater than in the moderate counties plus less polluted counties.

No animal tested positive for WNV in the less polluted counties.

The method of analysis in this study is independent of population density, county area, county reporting capability, and the interplay of public media.

See graphic summary.

 

Summer of 1999

During the summer of 1999, an epidemic of animal mortality occurred in the tri-state area, which included thousands of birds, rodents, reptiles, and even some horses and humans. For example, Millicent Eidson, D.V.M. (NYSDOH) wrote, “...more than 17,000 dead bird sightings (not laboratory tested) were reported to the NYSDOH... with approximately a third of these sightings being crows.” (“vetltr.htm”, 5/19/2000, NYSDOH online). Yet, most of the epidemic was clearly overlooked by medical officials and by the public media until after the apex of the 1999 epidemic. Media images and medical reports placed the beginning of massive bird mortality and the first arrival of WNV at early August, 1999, and dramatized a causative relation to West Nile virus. The birds were said to play a role in the natural transmission cycle (bird, mosquito, human) of the virus. Later, with relatively little publicity, the various agencies have stated that extensive bird mortality began in June and associated these also with the WNV epidemic.

Before September 1999, Ward B. Stone, the wildlife pathologist for the New York State Department Of Conservation ("NYSDEC"), frequently diagnosed New York City's rising levels of reported bird mortality (from 1997 onward) as purposeful pesticide poisoning by individual, unknown "culprits". He also cited generally, pesticide residues.

Having acquired nine NYSDEC bird autopsies (six from 1998, three from 2000), I found that the toxicology reports can contradict the diagnoses of causation by pesticides. Four organophosphate and carbamate pesticide poisonings had "no pesticides" in the toxicology reports (findings based upon low cholinesterase levels); three suspected Avitrol (bird-control pesticide) poisonings had none, minimal, and positive (not quantified) Avitrol in their toxicology reports; one starvation (with lung damage) occurred during the high smog season in Staten Island; and only one (bromadolione poisoning) of the nine autopsies found substantial residues. My review of the work of other avian pathologists confirms that it is preferable to have quantified pesticide residues, yet common and acceptable to diagnose carbamate or organophosphate pesticide poisoning, utilizing only the test results for low cholinesterase levels.

Ward Stone told me that he does not order air toxicology tests and that it "would never happen" because of funding limitations. Furthermore, brain tissue is completely allocated for virus and conventional toxicology. Dr. Haliburton, an avian toxicologist in Amarillo, Texas, stated that he knew of no one who does avian air toxicology. Both Dr. Haliburton and Dr. Tracey McNamara, the pathologist at the Bronx Zoo, stated that air toxicology was not done because of a lack of interest and funding.

Having recently reviewed many additional NYSDEC Avitrol diagnoses, it is clear that Avitrol has been a major toxic burden on birds, however, in those cases where the presence of Avitrol is minimal or positive (non-quantified), is that enough to warrant Avitrol the sole cause of death, when air pollution is not investigated?

According to a study by Gordon, et al (Arch. Env. Health, 1981), ozone (said to be a major component of air pollution) can also inhibit CHe: "[Parathion (6.0 mg/kg) caused an inhibition of cholinesterase activity in guinea pig lung and diaphragm similar to that caused by pre-exposure to 0.8 ppm O3 for 1 hr." It is reasonable to assume that the actual complex of air pollution would more effectively inhibit CHe. Other studies show that air pollution can disrupt endocrine hormone levels. The EPA AirNow website states, "…air pollution can cause… damage to the body's immune, neurological, reproductive, and respiratory systems." Certainly, birds are not exempt from these hazards.

The NYSDEC follows established diagnostic protocols within stringent economic limitations. In effect, this serves to minimize considerations for air pollution and to make the most of pesticide residues, heavy metal residues, findings of cholinesterase inhibition and clinical observations. If all pesticide residue diagnoses were accepted uncritically, they would (in year 2000) account for 20% of wildlife death, and WNV, 13% (Michael Gormley, Associated Press 6/3/2001). Various causes such as blunt impact, heavy metal residues, and to a large degree, microbial infection, account for the remaining cases.

On September 3, 1999, Mayor Giuliani announced a St. Louis virus epidemic and the commencement of aerial pesticide spraying for mosquitoes carrying viruses. On September 5, an article in The New York Times stated that NYSDEC autopsies were about to be released to the public with the presumption of "pesticides in the soil and vegetation", the pesticide residue theory. Those diagnoses were not released, however, as they were held back when the West Nile Virus epidemic became an overwhelmingly dramatic and dominant theme, according to Joe Pane, a biologist with the New York City regional DEC. NYSDEC bird tissue samples were then sent to the CDC and other laboratories for virus analysis with the presumption of WNV encephalitis. The results were published in the NYSDEC’s West Nile Virus Database. These intricate events could not be found in the official timelines.

Several avian experts, including the veterinarian Dr. Charos, had assumed initially (NYT 8/22/99) that the crows (the most obvious dead bird) were dying from poisoning because crows often scavenge for food and therefore should be among the last species to succumb to microbes, not the first.

Media drama was likely a strong interactive factor in the vastly increased reporting of dead birds during September and October of 1999. Most of the bird mortality actually occurred in June, July (peak), and August, before the publicity of September according to the observations of the Bayside veterinarian Dr. Charos (interview). Dr. Charos, who worked at the epicenter of 1999, felt that most bird reporting from September onward was the result of publicity. Though frequently interviewed, virtually all media ignored his June observations.

Note the reproduction of the NYSDEC WNV database summary by locale.

Environmental Analysis

Ward Stone commented (10/11/2000) about toxicology, air pollution maps and ozone/WNV timelines that he had received:

"There is a correlation of dead birds in New York City with certain levels of air pollutants. However, there also probably are correlations with numbers of tourists, bus visits, human attendance in city parks, and numbers of other things. It is just a correlation and not causation. The birds are dying from West Nile Virus, trauma, exposure (e.g. fledglings and young birds in cold rain) and pesticides (not the pesticides used by government in mosquito control), and other infectious and parasitic diseases."

Stone acknowledges the correlation between ozone levels and bird mortality, but states this is a mere correlation. Apparently he felt that bias factors existed, such as human population densities, media interplay, and county reporting capabilities that render the correlation insufficient as evidence. The following method of analysis of the NYSDEC database alleviates such concerns.

The NYSDEC database contains 520 animals (almost entirely birds) that had been submitted to the CDC for WNV testing.

Analysis of that database demonstrates that the WNV-positive percent of tested, reported birds varied from county to county according to the levels of industrial ozone and EPA categories that affect the formulated levels of MTBE in gasoline.

In addition to the toxic hazards of MTBE itself, critics state that MTBE creates toxic byproducts, the results of engine combustion: formaldehyde, formic acid, isobutylene, and methyl nitrite. Peter Joseph, Ph.D., in his "New Hypotheses for MTBE Combustion Products” (1999) writes that methyl nitrite studies reveal an LC50 of 170ppm at 4 hours of exposure, and also that,

"The clinical data presented here suggest that some kinds of air pollution can have affects quite different from what is commonly assumed. It is of course known that various chemicals (gas phase or particulate) can be respiratory irritants, and that these can act via direct attack on the respiratory epithelium. However, the three symptoms documented here do not relate to any reaction with respiratory epithelium, but rather with the nervous system. This is not unexpected for MeONO [methyl nitrite]..."

Although officials claim that MTBE is a good thing for the air environment, critics claim that it actually raises ozone levels and increases photochemical smog. Ozone, at ground level is considered by the EPA to be a potentially fatal health hazard. In addition to the effects of ozone on cholinesterase levels, Colin-Barenque, et al, found that 1ppm ozone for 4 hours can produce damage to the olfactory bulb. Clemmons, et al, found reduction of endocrine hormone levels at 1ppm ozone exposure for 24 hours. Ozone in air pollution has been found as high as 0.5ppm in Southern California (Mehlman, et al, Env. Res, v42, 1987). In the New York City region, ozone levels can frequently exceed 0.1ppm during the summer.

There are significant differences in ozone levels utilized in the animal studies and ozone levels found in the air of industrial environments (with the exception of the cholinesterase study). Therefore, pending further study, ozone is viewed herein as a biomarker for toxicity, that is, as representative of a greater complex of air pollution, and not necessarily the causative agent. It is possible and perhaps likely that the greatest health hazards are not so much photochemical or ozone related but simply the result of direct exposure to a variety of emissions that are more prevalent in the afternoon heat when warm emissions cannot be efficiently convected away. Ozone is used by the atmosphere to clear pollution, and likewise, white blood cells generate ozone to clear foreign matter from the blood stream.  Lab studies of ozone employ ozone levels that are above natural levels.

It is well accepted that the concentration of ground level ozone is usually directly proportional to temperature and sunlight, the result of dissociation of O2 and emission compounds such as nitrogen dioxide. A look of the WNV data finds that during the so-called WNV epidemics, dead birds are often found near areas of high emissions: bridge outlets, expressways, airport take-off lanes, and oil refineries. Human casualties (some of which are WNV positive) were first discovered August 1999 in these areas during periods of high temperatures, still winds, and high emissions.

In the NYC region, summer of 1999, EPA ozone exceedances were the worst in decades. MTBE was set for phase-out and ban in many states, the procedure being set in motion by an EPA blue ribbon panel in late July, 1999. By April 2000, President Clinton called for a ban of MTBE.

The terminology and policy of the oxygenate programs are very confusing, arcane, and MTBE usage can only indirectly be determined. Two terms, which apply to the New York City region, need to be recognized. Effectively: 1) "RFG" (reformulated gasoline) means approximately 11% MTBE in gasoline, year-round. 2) "Oxygenated RFG" means approximately 15% MTBE in gasoline during the winter months (November thru February).

United States, 1999: MTBE

According to the following oxygenated fuels sales map, within the entire United States, the New York City region was unique. Only certain New York counties were mandated for both RFG (year-round) and oxygenated RFG (winter):

This partial image (NE US only) is from www.oxybusters.org [defunct] which printed
the full map from "Oxy-Fuel News", a private letter for industry.

New York State: Reformulated Gasoline Program Areas

The following is an EPA list ("rfgarea" document, April 5, 1999) by county, of the tri-state area, regarding Clean Air Act Required Areas:

Reformulated Gasoline Program Areas, April 5, 1999
NEW YORK - Northern New Jersey - Long Island - Connecticut area, NY-NJ-CT
Connecticut
Fairfield County	CT
Litchfield County, (partial)	CT
New Jersey
Bergen County	NJ
Essex County	NJ
Hudson County	NJ
Hunterdon County	NJ
Middlesex County	NJ
Monmouth County	NJ
Morris County	NJ
Ocean County	NJ
Passaic County	NJ
Somerset County	NJ
Sussex County	NJ
Union County	NJ
New York City Region
Bronx County	NY
Kings County	NY
Nassau County	NY
New York County	NY
Orange County	NY
Putnam	NY
Queens County	NY
Richmond County	NY
Rockland County	NY
Suffolk County	NY
Westchester County	NY

"Opt-In" (voluntary) counties were Dutchess, and Essex (partial). "Opt-Out" counties were Albany, Greene, Montgomery, Rennsselaer, Saratoga, and Schenectady.

From this list, the following color-coded NYS counties map is generated, which shows the 11 New York State counties. Yellow colored counties in this map are "Severe-17" counties, i.e., EPA non-attainment counties, all under the same EPA fuel rulings. The national sales map and the EPA regional map are similar to this map of NYS counties. Thus, it is apparent that these 11 counties are both RFG (year-round) and oxygenated RFG (winter).

(County map modified to reduce file size.) Counties colored yellow per EPA list ("rfgarea").

 

According to NYSDOT Environmental Procedures Manual (June, 1999), RFG is also required in Dutchess,

"Currently in New York State, reformulated gasoline is required in the New York City metropolitan area as well as in Dutchess, Putnam and Orange counties. Some upstate areas were initially "opted in" but have since been "opted out" of the program."

NYSDEC WNV/County Database (Altered To Include MTBE Data)

In the NYSDEC database, most of the animals (96%) were birds. 96.5% were found during 1999.

The "RFG" counties (in yellow) reported 117 WNV-positives, while the other counties reported only 2 WNV-positives. (See summary for percentages).

The analysis table (above) refers to EPA policy. Gasoline formulations are proprietary and thus actual MTBE levels and evidence of dumping are difficult if not impossible to directly ascertain. Therefore, it is suggested that while viewing the table, that the liabilities of MTBE implementation be understood according to EPA categories that influence actual oil refinery processes and output, in the following order: Severe-17, Moderate-NA, Opt-In, Opt-Out, none.

Orange and Putnam Counties: Abberative

Two counties are abberative regarding the otherwise consistent correlations found in the table, that is, Orange and Putnam counties reported dead animals, but none tested positive for WNV.

This can be understood with the following EPA map (year 1999), which shows the 2 counties as exceptions. These counties had been categorized as moderate, though some Orange townships remain with the larger Severe-17 categorization (in yellow). According to the EPA, Orange and Putnam must still comply with Severe-17 regulations in terms of oxygenation compliance; there is supposed to be no difference among the 3 states per the following map:

An EPA map of categories that affect
MTBE implementation in gasoline

 

However, returning for a close look at Oxy-Fuel News' national MTBE sales map, it shows New Jersey, Orange and possibly Putnam as excluded from the category "RFG and oxygenated RFG". An EPA source replied to my inquiry that Oxy-Fuel News is probably in error. Another EPA source minimized his commentary by stating that the national map was not clear enough, nevertheless, by superimposing the two maps (below), it can be seen that the cartographer for Oxy-Fuel News left much of the CMSA (“Consolidated Metropolitan Statistical Area”) out of the sales route for "RFG and Oxygenated RFG". Perhaps, in spite of EPA allowances, high levels of MTBE in gasoline, in an area that contains oil refineries, would be just too much.

The net result is that the national MTBE sales map just happens to conform to the 1999 WNV epidemic boundaries.

What was the Oxy-Fuel News data source? To date, no reply after several requests.

Dutchess County: Abberative

The EPA document "rfgarea.doc" states that Dutchess County is an "Opt-In, voluntary" county.

EPA's M. Moltzen responded:

"In New York, wintertime oxygenated gasoline and RFG was/is required in the following counties: Suffolk, Nassau, Queens, Kings, Richmond, New York, Bronx, Rockland, Westchester, Orange and Putnam."

"RFG but never oxygenated gasoline was and is required in Dutchess County."

EPA's T. Litterdale responded:

"Unfortunately EPA is the only organization with the details and they haven't published them. But, there shouldn't be a significant difference in product formulations across the 3 States in the NYC metro area."

"The only authoritative source for who is currently covered and when is provided by the EPA. Maps and lists from other sources will likely not agree because areas are added or taken away after they are published and mistakes are made when the EPA's list is copied/transformed." [...]

"The EPA does make one error when it lists Dutchess Co. as part of the Essex nonattainment area in the RFG opt-in list. Dutchess Co. is in the separate Poughkeepsie nonattainment area."

The Poughkeepsie nonattainment area inclusion also applied to northern Orange and Putnam.

Summary

Within the U.S., 1999, massive reported bird death occurred almost entirely in New York State, and according to National Atlas maps (2000), near urban areas near oil refineries, air ports, and high road densities.

1)	Those animals testing WNV positive occurred almost entirely in counties categorized as Severe-17 Nonattainment, a category that effects gasoline formulations in terms of higher levels of MTBE:

NYSDEC West Nile Database (Year 1999)
	Severe-17 Nonattainment Counties			Moderate and Other Counties
WNV-Positive Test Results	117	52% of test results (pos+neg)		2	2.2% of test results (pos+neg)
WNV-Negative Test Results	108			91
Total WNV Test Results	225			93
Pending WNV Test Results	166			36
Total Animals Reported	391			129

 

2)	Of the 62 New York counties, tested dead animals in the 9 "Severe-17" counties were 24 times more likely to be WNV-positive, in terms of percent WNV-positive of tested animals, i.e., 52/2.2 = 24.

 

3)	Some counties reported substantial animal deaths, which, however, were WNV-negative. These counties have been categorized as Severe-17 Moderate, or Opt-In, or were merely near a confluence of vehicular traffic:

Graphic Summary of 62 NYS Counties

3 categories, representing vehicular fuel air pollution, are shown:

Severe Counties (9)	The original EPA “Severe-17 NonAttainment”, and/or near oil refineries. MTBE (year-round). (marked "S" in chart above)
Moderate Counties (10)	Previously EPA “Moderate NA”, adjacent “Severe 17”, high auto traffic, or adjacent high auto traffic. Possibly MTBE. (Marked "m" in chart above)
Other Counties (43)	Other counties (lower levels of automobile or oil refinery air pollution). Conventional gasoline. Possibly MTBE (not year-round).

 

Year 2000: Brief Analysis

There is much to be said about the summer of 2000, for example:

The NYSDOH WNV Bulletin of 11/24/00 stated:

"West Nile Virus is throughout New York State... Positive Mosquitoes: 11 counties..."

With one exception, these were the same 11 counties where WNV-positive birds were found in 1999. Note that 1999 was more severe in terms of human illness and that there was no recognition of bird mortality until mid-August. Mosquito pool analysis did not exist in NYS in 1999. Mosquitoes are less mobile than birds and therefore are a more specific measure of local conditions. The patterns of bird mortality were also geographically similar when 1999 is compared with 2000, though WNV appeared to spread out from the NYC epicenter in 2000, with earlier publicity and testing.

What could be more mobile than an infectious mosquito/bird virus? Why did the disease maintain a similar geographical pattern from year to year?

ANSWER/POSTULATE:  WNV has already been well established for millennia, as a symbiont, an endogenous “virus”, manifesting its identifiable genetic structure as an adaptive, cellular response to environmental poisoning.

Discussion

Note in the preceding bar graphs that: 1) WNV-positives percentages correlate only with areas of severe air pollution which are also areas where MTBE is implemented. 2) Bird mortality (WNV-negative) correlates with areas designated “moderate NA”, and not originally designated for MTBE. 3) The absence of bird mortality correlates with low levels of automobile air pollution and no MTBE designations.

The table analysis does not distinguish well between extreme air pollution and extreme air pollution with MTBE because they both occur in the same counties, i.e., MTBE is required where air pollution exists. Thus, in these tables alone, there is much to implicate air pollution and little to directly implicate MTBE. A perusal of the table “Substantial Dead Animals, But WNV Negative” and the superimposed maps possibly bear evidence for MTBE as a differential factor.

Yet, the table analysis does work very well in conjunction with other evidence to implicate MTBE as causal for the "WNV epidemic", or as stated in purely environmental terminology, for bringing air pollution to a sufficient level to cause a genetic biomarker for air pollution (WNV) to manifest itself in tissue.

The other evidence is: 1) The air toxicity of MTBE and its combustion byproducts as understood by the critics of MTBE. 3) The previously described timeline of increasing incidence of pre-1999 bird mortality in the New York City region, which correlates with MTBE. 4) The emerging epidemics of human disease and emerging medical policy (non-environmental), which correlate with the legislated increases of MTBE in 1995. These are: a) 1994, CDC launched an Emerging Diseases program. b) 1995, President Clinton established the Emerging Infectious Diseases Task Force. c) 1996, various Asthma Task Forces established. d) 1992-1996, epidemic of diseases with neurological conditions, which correlate with the MTBE timeline in Philadelphia (Dr. Peter Joseph, “Changes in Disease Rates In Philadelphia Following The Introduction of Oxygenated Gasoline", 1997, Univ. of Penn.). 5) EPA’s recommendation to ban MTBE at the height of the wildlife epidemic in the summer of 1999. 6) The Summers-Smith sparrow population study in England (page 19).

The list of contradictions in the official epidemiology is endless. It is strange that the CDC implicated WNV, a mild virus that had not previously been known to kill birds, as causative for the tremendous bird mortality in NYS without first studying the obvious environmental factors. The summer of 1999 was a period of record-low mosquito populations and record-high air pollution, yet the epidemiology assumed a mosquito-borne arbovirus and the environmental toxicology was omitted. WNV has little species limitation, except that it is limited to air-breathing species, from horse to sparrow.

In every WNV epidemic, worldwide, there appears to be one environmental commonality: an urban area near oil refineries, dense vehicular traffic, and optionally, steel and aluminum mills (Haifa, Volgograd, Bucharest, and NYC region).

The official explanation for the NYC region is that the virus was new to the West (though never previously tested for) and avian immune systems were unprepared. Yet, if so, then an even more massive disease epidemic should explode throughout the U.S., emanating from New York City. A year later (8/4/2000) The New York Times announced this lack of explosion as paradoxical, according to expert opinion. The WNV disease phenomenon remains only in areas of dense vehicular traffic, and in industrial regions where WNV is hunted. WNV has thus failed the epidemiological law known as Farr’s Law, which requires that an epidemic develop exponentially.

The only novelties capable of bringing forth the emerging media stories regarding high human and animal mortality and morbidity are severe air pollution with MTBE and its byproducts, and the novelty of testing for West Nile virus in the U.S. It is possible that the many mortalities (among the elderly for instance) that have previously occurred every summer in highly polluted cities could be termed WNV disease -- if WNV had been tested for in those cases.

WNV does not satisfy the first of Koch’s Postulates because serum testing has found WNV equally infrequent in both symptomatic and asymptomatic cases. During the summer of 1999, 2.6% of the general population at the epicenter (northern Queens) tested positive for WNV (see NYCDOH online), and during the fall of 2000, a NYCDOH survey of hospitals re persons symptomatic for WNV disease also found WNV-positives in 2.6% of the cases.

Note that the northern Queens epicenter is under the take-off lanes of LaGuardia Airport, and surrounded by expressways and two bridge entrances. The Staten Island epicenter is downwind from NJ oil refineries.

Massive bird death has actually not been that novel in the tri-state region. Ever since 1995 (advent of year-round MTBE), reports of bird mortality had been increasing, with record-high episodes of bird mortality occurring each summer. Using pesticide residues in brain tissue as a basis for evaluation, diagnoses attributed a variety of chemical residues for each episode of bird mortality, such as chlordane, Avitrol, organophosphates, and carbamates. Examples: 1) In the summers of 1996 and 1997 in Scotch Plains, NJ, there occurred the largest “chlordane poisoning” of birds in U.S. history. However, oil refineries, high traffic, and Newark Airport lanes are near Scotch Plains. 2) Massive Brant geese die-off occurred in Long Island in 1996, and was attributed to pesticides, though severe air pollution occurs often in that area. 3) Another area of high air pollution, the Forsyth Wilderness Refuge, hosted at the end of the year 2000, massive Brant geese mortality, over 2,000 dead. Witnesses stated that geese fell dead from the sky. Though the Forsyth website is dedicated largely to the threats of air pollution to its animal and plant populations, the geese mortality were finally attributed to “an unknown pathogen”. Chemical causation had been initially “ruled out” before proceeding with testing for microbes. See press release, US Fish and Wildlife Service, 11/22/00.

Widespread bird epidemics of similar species (small, active birds, like canaries) correlating with MTBE implementation are found in both New York State and Britain, before 1999:

NYSDEC WPU Annual Report for 1995/1996:

“An outbreak of an eye infection caused by Mycoplasma gallisepticum in house finches is causing death in these birds statewide. This disease is poorly understood…”

NYSDEC WPU Annual Report for 1996/1997:

“…a 37% increase over FY 95/96… require additional funding… Live and dead house finches with an infectious conjunctivitis caused by the bacterium Mycoplasm gallisepticum continued to be submitted throughout the year...”

A leading expert on sparrow populations, Dr. Denis Summers-Smith, a chemical consultant and former senior scientific consultant to the ICI, and a member of the British Trust For Ornithology, is described in The Independent:

"For a start, he now believes that road traffic pollution is at the bottom of the sparrow mystery. He does so because of a remarkable discovery he has made after spending this summer analysing all the available sparrow population data: British sparrow populations have indeed collapsed in big cities - but not in small towns. […] Two substances associated with unleaded petrol in particular, he feels, deserve urgent investigation - MTBE (methyl tertiary butyl ether), an additive, and benzene, a by-product of the refining. […] While he calculates the drop in cities such as London or Glasgow is of the order of 95 per cent, in small towns such as Crewkerne in Somerset or Guisborough in Cleveland the numbers have stayed virtually the same. […]"

"Only road traffic pollution, he says, would be of a different order in cities, where a very much larger number of vehicles are present, often with engines idling, pumping out fumes." See Michael McCarthy, 'Lead-free petrol may be villain in mystery of demise of the world's most familiar bird', The Independent, 9/11/00

The following graph (“Fig. 2”) accompanied a speech given by Summers-Smith, “What Is Happening To Our Garden House Sparrows?”, 11/29/00. It conforms to the MTBE timeline where, describing European MTBE, Summers-Smith states, “Fig 2a... a significant change that occurred at that time was the introduction of unleaded petrol.” The European experience conforms to the U.S. MTBE timeline: 1979 (intro), 1992 (winter), 1995 (year-round):

The Summers-Smith study has spawned further European studies into the relation between MTBE and sparrow populations.

The Summers-Smith study is somewhat similar to the present study, yet they are entirely independent of each other. My MTBE/WNV study began at the end of 1999.  I was alerted to the Summer-Smith study on 3/24/01 by Diane Atkins, an MTBE critic.

Findings of massive bird mortality as a sentinel event for air toxics were also utilized in the work of Dr. Jay Gould, Low Level Radiation, High Level Deceit (www.radiation.org), where this correlated with radioactive air pollution. See an online excerpt and commentary.

Virology

WNV virology is tenuous. The clear avoidance of environmental toxicology has created suspicions regarding the validity of the virus paradigm and the motivations leading to its acceptance. This avoidance has been incredibly dramatic and heavy handed, with fearful visions of WNV disease pervading the New York media.

Several animal studies from the early part of the 20th century to the present have found that dilute injections of poisons can cause disease with a concurrent proliferation of viruses, and that poisons can even initiate transmissible viral disease in laboratory studies (see Albert Fischer; Alexis Carrel). Virus presence can be interpreted as a real-time genetic adaptation to a toxic environment, a cellular response. See the contemporary writings of Eleni Oleopulos (Perth University) and Mark Ptashne, molecular biologist (New York).

In other studies, researchers David Crowe, Lynn Gannett and myself have more thoroughly reviewed the problematic nature of proofs for WNV causation. Essentially, WNV has not been isolated. The crucial word, “isolate”, however, has been re-defined to mean “mixture” in order to accommodate the known and unknown tissue components in the co-culture. The filtrate utilizes a filter about 6 times the size of what is claimed to be WNV. Three WNV virologists (Lanciotti, Hubálek, Anderson) have stated that WNV has never been seen separate from tissue components. Thus, WNV cannot satisfy the basic rules of epidemiology, i.e., Koch’s Postulates.

The criticism of WNV virology follows a line similar to the well-established criticism of the HIV=AIDS paradigm by Eleopulos, Duesberg, Mullis, Lanka, and others, because neither WNV nor HIV can actually be isolated. According to dendographs that trace the molecular evolution of viruses, WNV is even more removed from the classical, isolatable virus (such as is thought to be the character of poliovirus) than HIV. Proof of causation has not moved beyond mere association.

WNV virologists have not yet settled on a visual description of WNV. Diameters of supposed WNV (from EM photographs) range widely, from 35nm to 60nm (Anderson, et al, CAES; Lanciotti, et al, CDC Ft. Collins; Harrick, et al, Pasteur Institute, CDC/DVBID/WNV). This is an impossible mass variation of over 500%.

All studies that claim to use WNV are then invalid due to neglect of the fundamentals. Injections of tissue extracts have long been known to cause disease during animal experiments, with or without a virus being present.

A USGS press release, 10/25/2000, describes an unusual study where complete mortality occurred among WNV inoculated crows that were kept in a room with non-inoculated crows. All of the non-inoculated crows also died except for one. The USGS ignored requests for the actual study, and eventually responded saying that it has never been published. One of the authors denied even knowing the agency or source of the study immediately after referring to the study during a discussion. I’ve not been able to find any details beyond a vague abstract. The study contradicts previous knowledge of West Nile virus, which describes WNV as a mild virus that does not kill birds (The New York Times, 9/29/1999). Apparently the USGS study has not been independently confirmed. The USGS study is often described at medical conferences and apparently sets a standard. It is well known that impure tissue filtrates cause disease in animal studies, and also, that disease can be caused by toxic contamination of biocontaminant rooms.

The difficulties associated with politically expedient virus theories are not new. In Britain, latter 1950s, during a period of about 6 years, thousands of birds died of encephalitis. This was particularly noticed in the severe population loss of the peregrine falcon. Foxes also began to similarly die in large numbers, to the chagrin of hunters who felt that their culture might become extinct. After years of political and scientific argument and investigation, it was finally determined that the epidemic was due to agricultural seed coatings of Dieldrin (organochlorine pesticide, more toxic than DDT). Seed eating birds, such as pigeons, had eaten this seed and become weak and unstable. If they did not die of the effects of their poisoning, then they were easily preyed upon by falcons and foxes that also died of encephalitis. A more gradual demise of the falcons also occurred through the weakening and thinning of their eggshells. Continual searches for encephalitis viruses, and claims of having found them causative, interfered effectively with the toxicology. Eventually, however, over the years, these claims subsided as Dieldrin causality became exceedingly obvious. See: John Sheail, Pesticides and Nature Conservation, 1985, Oxford.

In Japan, another mysterious encephalitis epidemic (during the 1950s) continued for a decade because the cure was sidetracked by virus research. SMON (Sub Acute Myelo Optical Neuropathy) took the lives of thousands -- before claims of a SMON virus were finally pushed aside by evidence, which pointed to the toxic pharmaceutical, Clioquinol, which had been utilized to treat gastro-intestinal disease. Lawsuits ensued and some compensations allowed. See Peter Duesberg’s Inventing The AIDS Virus.

The history of Clioquinol goes back at least to the late nineteenth century antibiotic named Enteroform. It bears a similarity to organochlorine pesticides in its chemical structure, having 5 chlorine atoms per molecule, like DDT. Clioquinol is manufactured by Ciba-Geigy (now Novartis), the developer of DDT for pesticide usage.

Conclusion

The present study indicates that air pollution with MTBE and its byproducts are toxic enough to justify the warnings of anti-MTBE groups (see www.oxybusters.com [defunct]). Recent studies have shown in a general way that smog is very dangerous to humans (see www.epa.gov/airnow). The EPA characterizes this danger for physically active children who breathe large quantities of air per body weight, and it brings special attention to the premature deaths of elderly persons, advising them to stay indoors and not to exercise. The present study, however, indicates that such dangers are not so general, but are probably a very tangible factor with regard to an infinite variety of diseases, amongst humans, animals, and plant life. There is even an ongoing epidemic of diseases of trees in New York City.

In November 1998, UC Davis released research that was heavily negative against MTBE with respects to water, ground, and air. Beginning January 1999, the EPA Blue Ribbon Panel convened in 6 meetings, extending to June 1999. In late-July the panel announced its recommendation to ban MTBE. Apparently, a voluntary phase-out has since been underway, accompanied by legislation that promises to ban MTBE (by 2004 in NYS).

Oil refinery dumping is another aspect of air pollution to consider. MTBE, and the ban of MTBE, may have opened up legal ways to rationalize increased dumping (of benzene, wastes, or excess MTBE inventory). The issues of dumping are difficult to ascertain because the EPA rules gasoline formulations proprietary. The EPA has issued a crucial statement about its inability to regulate dumping:

"The downstream segment of the petroleum industry is largely staffed by principled individuals interested in complying with the spirit of the regulations in a cost-effective manner. We believe the regulations and the subsequent interpretation of the regulations through the Q&A process have become overly complex in a misguided effort to eliminate highly unlikely scenarios that might include some immaterial increase in emissions. Those who choose to cheat will always find a way to do so. An attempt to close every conceivable loophole will limit the flexibility of well-meaning companies to respond efficiently and maintain the viability of our industry. It is vital to all of us that these regulations not be allowed to limit the creativity of our industry and the efficiency of the market place." -- "TM&C/KPMG RFG/Anti-Dumping Workshop: Questions and Comments for Panel Discussion" (EPA document date: 5/17/1995).

Note in the foregoing excerpt that the "downstream segment" is mentioned but not the "upstream segment".

Traditionally, bird behavior has served as an indicator of environmental quality. Birds are truly "miner's canaries" – reliable air assay tests. They should continue to serve us in that capacity without an inversion of our perceptions by a virus paradigm. A study of the NYSDEC tables can bring the public, medical, and environmental sectors towards an awareness of air pollution that was previously unavailable. Wildlife data is vital to the public, yet there is a movement to officially close public access to this data, according to Ward Stone. Since that interview in April, 2000, wildlife data has been placed under a system of restricted access, HIN.

It has been said that a lack of funding prevents the inclusion of air toxicology in bird diagnoses. Because of the importance of proper bird diagnoses to human epidemiology one obvious solution would be to increase funding.

Another solution would be to develop methods that are within the scope of existing protocols, previously discussed.

Accordingly, five criteria are suggested that could serve as a basis for economically viable diagnostic procedures to detect the affect of air pollution: 1) Evidence of CHe inhibition in the lung tissue; 2) The ratio of CHe inhibition in the lung versus CHe inhibition in organs farther from the lung; 3) The absence of pesticides or other toxics; 4) General or specific evidence of high air pollution at the death scene, as determined from DEC air monitor data, witnesses, and other environmental indicators; 5) Evidence of genetic biomarkers for toxic stress. It is apparent that WNV is such a biomarker. According to microbiologist, Howard Urnovitz, there are laboratories that perform these analyses within the context of toxicological diseases, utilizing serum and PCR testing. Such applications have contributed to the toxicological epidemiology of Gulf War Syndrome.

Finally, the basic diagnostic format should be restructured with regard to humans and animals. A multi-factor system is suggested, such as a spreadsheet that includes air pollution toxicology and allows microbes to be designated by degree as causative and/or resultant.

Epilogue

One of the more positive results of this study is an article by ABCNEWS investigative journalist Nicholas Regush, entitled “Virus Or Environment”, 8/29/01, which can be located online in the archives of his regularly featured column, “Second Opinion” (www.abcnews.com). Therein are confirmations of this study’s findings voiced by prominent West Nile virus scientists, in their terms:

‘"Because we don't have the resources, we're missing the opportunity to look at many different factors that may be going on with West Nile," he [Robert Maclean] said. As director of the Wisconsin-based National Wildlife Health Center of the U.S. Geological Survey, McLean...’

‘Dr. Ian Lipkin of Columbia University, who has played an important role in identifying the genetics of the West Nile virus... He too believes that an understanding of disease comes from probing the relationship between environmental factors, including viruses and toxic substances, and the genetic endowment of individuals. [para] To Lipkin, it makes perfect sense to want to know more about how, say, "an unhealthy environment might break down immunity in both birds and humans and make them more susceptible to viral infection. It's worthy to pursue this."’

‘"We don't order those tests because there are no funds to do that kind of work," he [Ward Stone, NYSDEC Wildlife Pathologist] said. [para] In fact, Stone couldn't recall anyone in his line of work doing air toxicology tests on birds.’

‘"We don't have a purified form of the virus," said Robert McLean matter-of-factly. "Cellular material could interact with the virus to enhance the replication of viral particles." [para] What McLean left unsaid was the possibility that the cellular material itself could be sufficiently toxic to cause damage to tissue, with or without the virus.’

‘Sean Ahearn, director of Hunter College's Center for the Analysis and Research of Spatial Information, offers another perspective. "I think it is extremely important to factor in air pollution and even MTBE because they may harm the immune system and make it easier for an infection to take hold." [para] Ahearn and his colleagues run a computer project for the City of New York that uses a sophisticated formula to chart clusters of dead birds across the city. Still in its testing phase, it is helping the city to link non-random dead bird clusters to pools of mosquitoes that show signs of the West Nile virus and then to possibly predict where human infection has a high probability of occurring. [para] "The next phase of the project will be to factor in the ecological context, things like air quality and weather," Ahearn said. "I think this is the only logical way to go."’