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).
