The following studies find that increased MTBE levels in gasoline beginning in 1995 correlate with increased incidence of neurological disease in humans and animals. Studies show that MTBE may generate methyl nitrite, which is a strong neurotoxin (170 LC50), and MTBE might actually increase ozone levels in photochemical smog, though purported to decrease ozone. Ozone is one of the most neurotoxic substances in photochemical smog, having been shown in animal studies to cause extra-pulmonary damage. Barenque, et al found nerve damage in rats exposed to 1 ppm ozone for 4 hours. Cholinesterase inhibition occurred in rats exposed for 1 hour at 0.1ppm ozone. The EPA states that acute dysfunction can occur at levels below 0.08ppm, and levels far over 0.10ppm can occur during NYS summers. Ozone serves as an indicator of photochemical smog levels. Smog contains many highly neurotoxic chemicals in addition to ozone. See toxicology notes.
Contents Abstract of Previous study by Peter Joseph, Ph.D. Philadelphia: DOH Data, 1993-1996: MTBE and Human Neurological Diseases Chart 1: Insomnia Annual 1993-1996 Chart 2: Malaise and Fatigue Annual 1993-1996 Chart 3: Cardiac Dysrythmia Annual 1993-1996 Present study (A), by Jim West. NYC Region: DEC Data, 1992-1998: MTBE and Animal Neurological Disease Chart1: NYSDEC Intake Log: Neurological Disease Entries (narrow interpretation) Annual 1992-1998 Chart2: NYSDEC Intake Log: Neurological Disease Entries (narrow interpretation) Annual, Monthly Chart3: NYSDEC Intake Log: Neurological Disease Entries (broad interpretation) Annual 1992-1998 Changing Air Neurotoxics Present study (B) by Jim West. NYC Region: CDC/EPA Data, Summer 1999: Human West Nile Virus Seropositives vs Ozone Chart 1: EPA Ozone Station Monitor at College Point, Queens (full Y-axis) Daily 1999 Chart 2: EPA Ozone Station Monitor at College Point, Queens (reduced Y-axis) Daily 1999 Conclusion
Previous Study: Abstract
Philadelphia: MTBE and Human Neurological Disease
Dr. Peter M. Joseph (University of Pennsylvania), in his "Changes In Disease Rates In Philadelphia Following The Introduction Of Oxygenated Gasoline" (1997), presented data demonstrating a rise in neurological disease in Philadelphia, which correlates with the increased presence of MTBE in gasoline in 1995. Three of his charts are presented below. He briefly explains the history and some aspects of the chemistry.
"While methyl tertiary butyl ether (MTBE) has been used as an octane enhancer in the USA since 1979, the quantities used were later substantially increased in certain areas where it is used as an oxygenate in concentrations of 11-15% by volume. Ever since the winter oxygenated gasoline (WOG) program was initiated (1989-90) many citizens have complained of uncomfortable symptoms and illnesses that they associate with its use. When the reformulated gasoline (RFG) program was introduced even further in January 1995, again more citizen complaints arose."
"...I present new data on increases in purely neurological conditions in Philadelphia, as well as argue that the unknown MDT may be the indirect result of the production of methoxy radicals from MTBE pyrolysis. I especially emphasize the possible importance of methyl nitrite (CH3ONO) and hydro-peroxy radicals (HO2) [in smog production]." [bolding added]
Dr. Joseph presents several charts, three of which are reproduced exactly from his report, below
Dr. Joseph gives credit to, among others, "Mr. Warner Tillack of the Philadelphia Department of Health for providing the statistical data..." Dr. Joseph's studies and contact information are online.
Present Study (A)
MTBE and Animal Neurological Disease in NYC Region (1992-1998)
The increased presence of MTBE, beginning in 1995, evidently correlates with increased animal death In New York State. The following three charts were derived from the New York State Department Of Environmental Conservation's intake log book at the Wildlife Pathology Unit, from the years 1992 to 1998.
Only intake entries were included where their (brief) description of physiology and symptoms could possibly be interpreted as related to ozone related disease (neurological, respiratory) and whose location was the NYC region. These are examples of intake log entries accepted for this study.
Examples of descriptions are:
"Found with upper resp. infection"
"Emaciated, dehydrated, joints"
"Unable to stand, gasping, convulsions"
"Found walking, would not fly, insensible, had seizures during transport, DOA"
"Convulsions, uncontrolled vocalizations, head lolling, suggested toxosis"
"Found on the ground, convulsions, death possible poisoning"
"Found weak, thin"
Using these parameters, only one such case (in February) occurred outside of the time frame of the high ozone season (May through August) which usually peaks in mid-July, being temperature dependent.
Ward B. Stone, the wildlife pathologist, who has extensive experience (over 30 years) in New York State, remarked that the habits of people in the NYC region is such that they generally do not report bird deaths.
It appears from Stone's remark that it would require exceptional numbers of deaths before the urban New Yorkers would have reported any bird deaths from the NYC region. Significant reporting did begin during 1995, when MTBE concentrations were substantially increased in gasoline. Additionally, there are questions regarding refinery dumping of chemicals into gasoline.
The June/July occurrences of bird deaths are similar to the timing of most of the bird deaths in 1999, according to witnesses and some media articles. The unique feature of 1999 is the huge numbers. Approximately 3,000 to 6,000 crow deaths were reported to the NYSDOH according to EIDTEXT.DOC (NYSDOH). Dr. Charos, a Bayside (Queens) veterinarian who worked at the epidemic's epicenter, stated that most of the crow deaths in 1999 began in June, peaked in July, with crow deaths during the publicized WNV epidemic, being the result of that publicity, and not in his opinion, due to WNV. Two other media articles (New Yorker and NandoTimes/Associated Press online) refer to tremendous numbers of crow deaths beginning in June.
Yet, the official epidemiology omits the June/July crow deaths as "unconfirmed". Virtually all news media and scientific magazines omit entirely any mention of the June/July crow deaths, giving the distinct impression that crows began dying in August. According to my interviews, it seems clear that the NYC office of the NYSDEC became aware of crow deaths in early August, and the NYSDEC's Wildlife Pathology Unit received crows only from August onward, with the earliest "Date Found" being August 10, 1999, 2 days before the first human case.
The following chart includes all deaths that could in any way be ascribed to or influenced by ozone/smog. Examples of such descriptions accepted for this study include, unavailable details, possible misdiagnosis, erratic behavior, inability to defend or escape, such as:
"Found dead, no details."
"Presumed lead poisoned."
"Attacked by crows, membrane torn on "
Note: All 6 charts, in all 3 studies presented above, show very much the same pattern from 1993 to 1996.
All of the preceding graphs correlate increasing disease with the implementation of MTBE in gasoline in 1995.
Ozone 1999: Record-High
In the following graph, ozone shows a lesser correlation with neurological diseases. Ozone levels have been fairly constant since 1993, with the exception of 1999.
The extreme ozone levels of 1999 correspond with the advent of the WNV epidemic. High ozone also indicates high levels of other neurotoxic smog components such as MTBE byproducts.
The New York Times (8/1/99) described record-high ozone exceedances as the highest since the late-1980s.
"ALBANY, July 31 -- As New Yorkers endure one of the hottest summers on record, they are also suffering a curse that compounds their lethargy and sense of ill-being: the worst smog in more than a decade. Levels of ozone, a toxic chemical that burns the lungs, stings the eyes and can dim vistas with a brown haze, are the highest since the late 1980's, records kept by the State Department of Environmental Conservation show, and as usual, the worst of it has blanketed New York City and its suburbs."
The following graph was generated from an NYSDEC graph which ended at 1997. It was brought up to date with online data.
A more comprehensive graph should be done, based on the also hazardous NOx and particulate matter components, which may be a byproduct of MTBE. If equal weight is given to each of the data lines (Max1, Max2, and exceedances), it is possible that year 1999 represented the highest level of air neurotoxins in the history of New York State. Exceedances only, also gives us this possibility. Maximums (Max1+Max2) only , also gives this possibility. Air neurotoxins include: ozone, MTBE, MTBE byproducts (methyl nitrite, formaldehyde, methyl alcohol), aromatic nitros, carbon dioxide, and particulate matter (aerosols of sulfides and nitrogen oxide compounds).
If one adds in the purported toxic effects of MTBE, then 1999 is easily the most polluted year in the history of New York State.
In the New York City region, 1999 was a year of intense, novel air neurotoxics and unprecedented bird death. A ban on MTBE had been recommended in July, 1999, refinery dumping laws were dependent on voluntary compliance, and an EPA "no-action memo" was in effect.
Changing Air Pollution
A ban or phase-out of MTBE was recommended clearly at the conclusion of the UC Davis study in November, 1998, and then after a series of discussions held by an EPA Blue Ribbon Panel beginning in January 1999, that panel recommended in July 1999, a phase-out and ban of MTBE, just after the peak of record-level ozone. The critics of MTBE have long held that MTBE actually increases ozone.
Refinery gasoline formulations are proprietary, so it is not publicly known what impact the UC Davis study may have had on these formulations, or how the approaching ban may have affected formulations in terms of the petroleum industry's legal and economic risk assessments. What effect did the impending ban have on strategies regarding EPA regulations, excess MTBE inventory, refinery dumping of MTBE, benzene and other toxic chemicals, and quickly changing prices of gasoline components?
New York City has long endured one of the highest levels of air neurotoxics in the nation. The epidemic occurred primarily in a small area within the city (northern Queens). This area suffers very high air pollution, being very close to La Guardia Airport, SE Bronx, many expressways, and an industrial park, and 1999 was the summer of record-high air neurotoxics.
The first media reports of widespread bird death in NYC were reported during the summers of 1997, 1998 and 1999. They were estimated to have been caused by purposeful poisonings (the NYSDEC has no capability to determine death by air neurotoxins). A similar story of mass pigeon death was reported by the NYT (1/9/99) in Beijing, China. That NYT article stated that New Yorkers consider pigeons to be "rats with wings" and that their deaths would be a "blessing".
Ozone Maps of 7/14/99
The following two ozone maps were downloaded from the EPA AIRNOW archives. The first was downloaded February 19, 2000 and the second was downloaded on July 12, 2000. However, they are both for the same date, 7/14/99:
The map on the left bears a striking resemblance to the WNV epidemic center, 100 square miles of unhealthy red-coded ground-level ozone over Bergen County, Bronx, upper Manhattan, and northern Queens. The map on the right is a grossly revised version of the same map.
Such revisions are now common throughout the archived AIRNOW maps for the summer of 1999. The EPA website does not explain this or announce this, according to my search. On July 19, 2000, I inquired an incredulous EPA representative, and after several minutes managed to convey that the maps had indeed been changed. I was told that that the issue was incredible, unknown, would be researched (he would "call Albany"), and that I would receive a reply soon. A week later, July 25th, I received a reasonable explanation.
In fact, the maps are generated again after the end of the year, using the
actual, final data that the states send to EPA's data base. The original maps
are based on preliminary data.
The final maps can be different due to corrections of the original data or
additional data that did was not available in real-time.
Thanks for your question.
Since the EPA Region #2 representative, a person of substantial position, was initially unaware of the issue, I suspect that the maps are not usually revised to such an extent. Possibly the "EPA maps" (Region #2, includes New York City) are grossly revised directly by the NYSDEC in Albany without informing the EPA, unless there is an EPA office is in Albany that reworks New York City data without informing EPA Region #2. This is another area of research. I do know that the NYSDEC headquarters is in Albany.
The phrase "after the end of the year" is interesting. I downloaded the different versions on 2/19/00 and 7/12/00.
How did the new "final data" convey that there was actually no ozone pollution in the Bronx on 7/14/99? What data had initially indicated that there was high pollution in the Bronx? I immediately requested a more detailed explanation (how, when) and have received no response.
The EPA explained that the various state DEC's collect the raw data and send it to Atlanta. The data is evaluated and sent to the EPA after 90 days, and in 3 month blocks. The delay could take as much as 6 months at the most. It was 7 months after July, 1999 for my first download, and 12 months later for my second download.
The maps are generated by software which interpolates linear data fed from many monitor stations. Since the EPA can completely revise, months later, without explanation, medium red (or orange) to green, skipping the intermediary level of yellow, in an often polluted area (Bronx) with 14 monitors in NYC and others in Jersey, it appears that the changes are not the result of a slight mollification of the software calculations. Until the EPA gives further explanation, and in view of the political sensitivity obviously surrounding the entire epidemic, I can reasonably assume that data from several New York City monitors in Bergen County, the SE Bronx, and northern Queens was largely dropped from the latter map versions.
Compare both versions of AIRNOW maps for summer of 1999.
Ozone Levels And Human WNV Seropositives
The average daily ozone level for the summer of 1999 is presented in the graph below.
Ozone is one of the most dangerous toxins in smog, capable of destroying nerves, as demonstrated by animal lab experiments at only 1ppm ozone for 4 hours.
"Ozone is the strongest oxidizing gas in air pollution... Brain tissue is highly susceptible to oxidative stress -- Colin-Barenque L., et al., 1999
Ozone was not 1ppm in New York City, however, it was at high sustained levels for the entire summer.
"Worst Ozone Levels in a Decade... the city and its suburbs are... experiencing the worst smog in more than a decade. Levels of ozone are the highest since the late 1980's, records kept by the State Department of Environmental Conservation show. The state has already exceeded the Federal standard for ozone pollution more times this year than it did in each of the last seven years." - NYT, 8/1/99
In College Point, the average round-the-clock monthly ozone exposure during June, July, and August was 0.026ppm for 2184 hours with peaks over 0.100ppm. And ozone was just one of many neurotoxins present, acting synergistically.
The WNV encephalitis was fatal to some elderly persons who were described by NYSDOH epidemiologist Dr. Marcelle Layton as active, healthy, outdoors types, before the epidemic.
"The only common thread was they spent time outdoors in their backyards." -- Dr. Marcelle Layton, The New York Times, 9/9/99
While Joseph, Colin-Barenque, and others describe ozone as a neurotoxin, common literature (medical and popular) always describe ozone as a respiratory irritant, and potentially fatal, with accumulative effects:
"'Years of exposure can do serious damage,' Mr. Iwanowicz said. 'It impairs the ability to fight off infection, in kids especially, and it can aggravate the trouble that heart and lung patients already have breathing, which can be fatal.'" -- The New York Times, 8/1/99
During high ozone levels, the EPA advises the very young and elderly to stay indoors and avoid strenuous activity.
Perhaps the elderly are more susceptible because they are less able to repair tissue between the spikes, during the low ozone levels. During the epidemic, these elderly fatalities were said to have had "minor health problems" but by May, 2000, NYCDOH reported (CHI, Vol 19, No.1), "One patient was infected with HIV but had not been diagnosed with AIDS; 3 patients were receiving immunosuppressant drugs for cancer." The birds that died in 1999 were almost entirely young birds, according to NYSDEC records and the Bayside veterinarian, Dr. Charos.
College Point was at the epicenter, which is a highly polluted area containing 5 expressways. The area is downwind from an industrial park, the NYC sewage treatment plant, the La Guardia Airport, the highly polluted industrial zone of SE Bronx (one of the highest levels of air pollution in the U.S.), and two major bridges. MTBE, the most prevalent neurotoxin in the world, is now being phased out for its poisonous characteristics. It has contributed to an unprecedented smog of record-level air neurotoxics in ways not entirely understood and insufficiently studied.
Two Ozone Charts
Fundamentally, neurotoxins have five important aspects:
|1)||Lethal dosage (LD50, or LC50)|
|2)||Duration of exposure. A poison can be strong or weak, however, it has accumulative effects.|
|3)||Age factor. The very young are often 3 to 30 times more susceptible to a given neurotoxin -- with some poisons, as much as several hundreds of times more susceptible. This is because they have a higher metabolism, i.e., absorb more toxins from air, water and food, and because they have an undeveloped myelin sheathing over their nerves structure, i.e., is little protection from poisons that target the nervous system, like ozone. The elderly can be susceptible due to their diminished physical abilities, reduced ability to recover from accumulative stress.|
|4)||Species susceptibility. This can vary to up to a factor of several thousand, although there is often a similarity between similar species.|
|5)||Individual susceptibility. Commonly, individuals in a poisoned group react in a highly varied manner to poisoning. Thus, toxicity is measured for a given chemical in terms of LD50, the lethal dosage required to bring about the death of 50% of a group of test animals.|
The third aspect (age) could be seen in the death of thousands of crows. It is little known that the avian death involved mostly young crows, which are very active, inexperienced, and have not achieved the prime, safe territories. Avian death was the most prominent aspect of the epidemic in terms of mortality. Birds are often more sensitive to poisons, perhaps because their mobility has allowed them to evolve without adapting to toxic environments in terms of tissue and metabolism responses.
Dosage aspects (items one and two, above) are represented in the chart below in terms of potential effect. The blue line is the daily average values of ozone and the red line is the 21-day average of the blue line. The red line represents accumulative exposure. This is important because industry is often trying to optimize and balance emissions vs health, so the aspects of accumulative exposure should have a primary role in this assessment. In general, long-term exposure characteristics of poisons are not known very well, and are not studied much, perhaps because their impact is more subtle and more negative towards industry.
The blue columns represent the small WNV epidemic in terms of antibody seropositves from the day of onset, with Y-values set at 0.010=10 people.
Increasing the focus: In the following graph, 7-day moving average is employed and the Y-axis for antibody seropositives is set at 0.024=10 persons:
A critic may say many things also correlated with the neurological disease epidemic in NYC 1999. No doubt this is true, but the other things were not sustained, record-high levels of neurotoxins.
The Miner's Canary
The "miner's canary" saved the lives of miners who brought these birds with them into potentially toxic atmospheres. Because birds are highly sensitive to air neurotoxics, their death gave miners a warning, and time to escape.
If miners believed the cause of death for their canaries was an encephalitis arbovirus, then miners could also die of such an "arbovirus infection", leaving the owner's of the mine with no liability. Modern PCR technology can always detect a virus, such as the ubiquitous herpesvirus, which causes "the most frequently fatal encephalitide."(ref) Birds carry herpesviruses, so isn't herpesvirus also an arbovirus?
If New Yorkers believed the unprecedented cause of death for thousands of crows was an arbovirus, then New Yorkers died and suffered disease as the result of this viral infection, and industry has no liability. The current disease definition opens the door to increased, regulated emissions.
A Few Questions
Why was toxicology entirely omitted from WNV epidemiology?
In an area of 17 million people (tristate area of the epidemic), where there are many greater health priorities, why did the death of 7 elderly persons (sometimes stated as 6 because WNV was not stated as found in one of the NYC "5" during Lipkin's analysis) during the regular annual season for encephalitis bring about such a dramatic, mobilized response? 3 of these elderly persons were on immunosuppressive drugs for cancer, one was HIV positive (AZT chemotherapy?), and another had a quadruple by-pass surgery.
Why did a mild virus (WNV), not known to kill birds, suddenly cause the greatest epidemic bird death ever in New York State? Or anywhere else in history? If WNV-naive birds is the answer, then why to date, has the epidemic of massive avian death not spread beyond the original New York City region?
Why was there only a search for a virus? The search yielded a PCR identification of a virus, but no quantitative data regarding virus concentration in tissue. The virus did not exist in quantity sufficient to isolate in a purified form. So how can it be known to have existed in sufficient quantity (i.e., at a threshold level) to have brought about disease? Virus lethality for WNV has been demonstrated by intracranial injection in lab animals, a too severe and artificial method for proof of disease causation.
Ozone can be clearly demonstrated to cause encephalitis by normal exposure portals into the test animal. How can the role of the virus be viable when toxicology has not been considered?
Note that I have not included the "400 pigeons", found in several different boroughs of New York City from 1997 forward. Avitrol was suspected for many of these deaths. Diagnosing death from pesticide residues is a difficult judgment call. If these pigeons had been included in the above graphs, the indictment of MTBE herein would be even more clear.