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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 (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 representative of a greater complex of air pollution, not necessarily as the causative agent. It is possible 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. 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 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:

West Nile Database: Reported Dead Animal Count
	Severe-17 Nonattainment Counties			Other Counties
WNV positive	117	47.6% of tested dead animals		2	2.2% of tested dead animals
Negative	108			91
Pending	166			36
Total Tested	225			93
Total 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, “ New Hypotheses for MTBE Combustion Products", 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: