West Nile Virus is not a "deadly epidemic." Approximately 1 in 1000 mosquitoes in areas where WNV is endemic carry the virus, and only 1 in 300 people bitten by a WNV-carrying mosquito show any signs of sickness, and then usually only mild, flu-like symptoms. In 1999, out of a population of ten million in the New York City area, seven people died, all of whom were elderly (67-87 years) and/or immune compromised before they contracted WNV. Seven deaths in a population of over 10 million people is certainly tragic, but pales beside the number of deaths from many other diseases that are addressed less aggressively.

The chemicals under consideration for WNV mosquito control in Maine can cause one or more of the following: cancer, immune and nervous system disruption, vision loss, and reproductive and learning problems. Many are highly toxic to wildlife, particularly fish, bees, birds, and other non-target arthropods like lobsters. Long Island Sound lobstermen speculate that pesticide spraying and larvicide application for WNV mosquito control in New York are responsible for the 90% decline of their fishery. They have filed a $125 million lawsuit against the chemical's manufacturers.

Given available evidence on the low risk of WNV as a public health threat and the low efficacy and potential harm of a chemical response, it does not make sense to use pesticides to control mosquitoes that may carry WNV -- it may be do more harm than good.

The good news is that Maine has the opportunity to implement a WNV prevention program that will ensure that people, ecosystems, and the lobster fishery are not harmed by toxic chemicals. Intensive monitoring and surveillance for the virus, combined with on the ground educational efforts aimed at minimizing breeding and biting opportunities for mosquitoes are needed. Citizens should also be educated on the minimal risk WNV poses to their health. This approach will reduce the possibility of WNV infections in Maine -- to levels arguably better than a spray program could achieve -- while reassuring the public that government agencies are taking responsible action to address the problem. It will also guarantee that these same agencies are not creating an even worse public health problem and potential economic and ecological disaster by spreading toxic chemicals into the environment.

In researching the issue of West Nile Virus, one is struck by the lack of understanding of the public and decision makers about the risks that WNV actually poses to their health, and their acquiescence to spray programs. There is little consideration of the harm that the release of pesticides can do to human health and the environment. When people hear that a "deadly" virus from the "heart of Africa" is responsible for killing residents in their community they are understandably upset and want the government agencies and public officials to "do something!" Unfortunately, the first line of defense has been toxic chemicals. The reasons for this are complex. They are rooted in everything from our innate fear of disease to media-induced hysteria to many people's feeling that the government will make the right decisions when it comes to protecting their health and the environment when responding to and defining a public health "crisis."

The reality is that government agencies are seriously lacking all the information they need to make effective choices regarding the introduction of toxic chemicals into the environment. These chemicals are often tested only under ideal laboratory conditions, using mortality levels of lab animals to determine relative toxicities. As most toxicity tests are based on this "Lethal Concentration" (LC50: concentration required to kill 50% of the test organisms), or similar esoteric mathematical 'risk' criteria, the reality of the complex interactions of chemicals in the environment, are, for the most part, not even studied. These interactions include the way the chemicals react in other species, to light, heat, biological systems, how one acts synergistically with another in nature.

In the real world chemicals act in complex and insidious ways. They can act as hormone mimics, crippling an animal's ability to effectively court, mate, and have offspring. They can cause subtle behavioral and learning disabilities in developing children and fetuses, and initiate cancers that may not manifest themselves for decades.

Residents should not bear the burden of having to prove to government agencies and chemical companies that sprays and other toxics are harmful to human health and the environment. Chemical companies should prove that they are safe. Had this approach -- the precautionary principle -- been followed, we would not have the toxic legacies of lead in paint and gasoline, the pesticide DDT, DES and thalidomide for pregnant women, and a long list of other examples. All of these compounds were at one time widely distributed, or even recommended or mandated by government agencies. They are now banned because they were found to cause serious health and environmental problems.

Let's not make similar mistakes in the future.

The focus needs to be on why the spraying is even being considered in the first place: to reduce the incidence of West Nile Virus carrying mosquitoes, one would hope. Amazingly, there is no scientific evidence that demonstrates a decrease in human mortality from WNV after a spray program, or even a long-term reduction in the number of mosquitoes. Rates of kill for mosquitoes at over 80%, as claimed by New York officials during their spray campaign, are based on speculation: a kill rate of around 30% is probably more accurate according to other experts. It is estimated that for every 1,000,000 droplets of spray released to kill mosquitoes, only one droplet lands on a mosquito. It takes 2-3 droplets to kill the mosquito.

The purpose of this report is to empower the people and communities of Maine with the information they need to protect themselves from West Nile Virus while at the same time protecting themselves, their children, wildlife, and the lobster fishery from the potential harm a spray campaign could inflict.

The report examines the history and epidemiology of West Nile Virus, takes a hard look at the threats it poses and discusses the mosquitoes and animals that are involved in spreading the disease. It looks at how WNV has spread in the eastern US, what the response has been, and what Maine is doing about the situation. The chemical weapons used against the mosquitoes and how they behave in the environment and in human and animal bodies, and their effectiveness at killing mosquitoes and stopping the spread of WNV are examined in depth. Most importantly, we describe alternatives to toxic chemicals to control mosquitoes.

This report uses references from professional journals, newspaper accounts, personal interviews, government documents, and many other sources. In all cases when a fact is presented, a corresponding reference is used to back it up. When there is speculation -- on either side -- this is pointed out clearly. If you read the report online, many of the full-text references will be just a click away.

The Maine Environmental Policy Institute relies heavily on its web site to distribute information on this and other environmental issues. Consider the printed version of this report to be merely a snapshot of an evolving issue. West Nile Virus looks as though it's here to stay. You can stay on top of all the latest developments on our site at www.meepi.org. Please feel free to contact us with any questions or comments you might have.

William C. Sugg, III

Director, Maine Environmental Policy Institute and author of this report.

To receive additional copies of this report, send $10 per report, or $7 each if ordering more than ten copies to: MEPI, 126 2nd Street, POB 347, Hallowell, ME 04347. Price includes shipping. This is edition 1.0, release date 5/15/01.

The most important person to acknowledge in this paper is Rachel Carson. Her book Silent Spring is the wellspring from which this continuing work on pesticides flows. It was there she wrote forty years ago......

- Rachel Carson, Silent Spring, 1962.

I would like to thank the MEPI board of directors: Kevin Mattson, Tom Federle, Matt Scease, and Susie O'Keefe for their support and suggestions for this report. The reviewers of this report gave much helpful guidance and advice: Heather Spalding, Rob Baldwin, Mitchel Cohen, Sharon Tisher, RusselI Libby, Kathleen McGee, George Appell, Paul Donahue, Mitch Lansky, Will Everitt, and especially Kim DeFeo. I would like to give special thanks to George and Laura Appell and Elizabeth Spalding. Without their advice and generosity this report would not have been possible.

This report is based on work previously published in many different places. Some groups and resources stand out as being particularly valuable to anyone researching this issue, and to me in particular as sources of information, quotes, references, inspiration, and guidance: The No Spray Coalition of New York; Pesticide Action Network of North America; Extension Toxicology Network; Toxics Action Center; Environmental Risk Analysis Program (ERAP) of Cornell University Center for the Environment; and most of all Rachel Massey and Peter Montague of the Environmental Research Foundation.

Photo, graphic credits: If reading report online, click on graphic or photo to see credits.

West Nile virus (WNV) is a disease new to the Western Hemisphere. It appeared in New York City in 1999 and has now spread to animal populations in six other states from New Hampshire to North Carolina. Some municipal officials have responded to the disease by spraying entire neighborhoods and other areas with pesticides intended to kill the mosquitoes which transmit the virus.

See a map of human cases of West Nile Virus. See a map of avian cases of West Nile Virus.

Transmitted primarily by bird biting mosquitoes, WNV can also infect humans and other animals. See the transmission cycle of West Nile Virus, and life cycle of the mosquito. Most human infections with WNV go unnoticed or feel like an ordinary flu. Some cases lead to encephalitis (inflammation of the brain) or meningitis (inflammation of the membranes surrounding the brain and spinal cord) and can be fatal. The elderly and individuals with compromised immune systems may be particularly vulnerable to serious illness resulting from the virus.⁶⁴

A New York City Health Department survey of blood samples taken from people who lived in northern Queens, the epicenter of the 1999 outbreak, showed that 19 out of 677 tested positive for the virus. None of the 19 became seriously ill, and all either reported no symptoms or mild illness, such as a low-grade fever.⁷⁷

In 2000, WNV reappeared in New York City, and infected birds were found in upstate New York as well as New Jersey, Massachusetts, Rhode Island, New Hampshire, Connecticut, and Maryland.

Increasing international trade and travel create new opportunities for exchange of diseases quickly and effectively across regions. Paul Epstein of Harvard Medical School's Center for Health and the Global Environment argues that the spread of mosquito-borne diseases like WNV is also aided by several phenomena associated with climate change, including mild winters, hot summers, and drought.

According to Epstein, back-to-back weather extremes in 1998 and 1999 probably encouraged the proliferation of WNV and the mosquitoes that carry it. In a recent article in Scientific American he writes, "The mild winter of 1998-99 enabled many of the mosquitoes to survive into the spring, which arrived early. Drought in spring and summer concentrated nourishing organic matter in their breeding areas and simultaneously killed off mosquito predators, such as lacewings and ladybugs, that would otherwise have helped limit mosquito populations. Drought would also have led birds to congregate more, as they shared fewer and smaller watering holes, many of which were frequented, naturally, by mosquitoes." Later in the summer, heavy rain created new mosquito breeding opportunities. Higher temperatures also tend to increase mosquito activity. "Computer models indicate that many diseases will surge as the earth's atmosphere heats up, [and that] signs of predicted troubles have begun to appear," he writes in the article.^25a,64

For more information on the history, transmission, symptoms, and more on West Nile Virus, see the Question and Answer section.

It would be unfair to downplay the seriousness of a severe infection of West Nile Encephalitis. It is reported to be a painful disease that can be debilitating if not fatal. Fortunately, it is extremely unlikely that you or any member of your family will get sick and die from WNV, even in areas where it is endemic. While determining any one person's risk level is difficult, it is important to point out the range within which uncertainty exists. Some of the evidence available for understanding the risks of illness from the bite of a WNV-infected mosquito follows.

West Nile Virus was first identified in the United States during the summer of 1999 when a large number of birds were found dead in the New York City area. Out of a population of more than 7 million, 62 people -- or less than .0009% -- became ill with the virus, and 7 died (1 in 1 million). The median age of the people who became ill was 68 years. The seven who died ranged in age from 68 to 87 years of age. Of these seven, one had HIV and 3 were on immunosuppressive drugs for cancer.⁷⁷ By comparison, more than 2,000 New Yorkers died from the flu in 1999.¹⁴

In 2000, one 82-year-old man from Little Falls, N.J. died from WNV. The victim had an undisclosed pre-existing medical condition "that probably contributed to his death as well," said Dr. Eddy Bresnitz, a New Jersey epidemiologist and assistant Health commissioner.⁶⁶ The New York City Department of Health Bureau of Communicable Disease's Questions and Answers About West Nile Fever answers the risk question this way: "Q: If I live in an area where birds with West Nile Fever have been reported, and I am bitten by a mosquito, am I likely to get sick? A: No. Even in areas where mosquitoes do carry the virus, very few mosquitoes -- perhaps only one out of 1,000 -- are infected. The chances that any one bite will be from an infected mosquito are very small. Q: But if I am bitten by an infected mosquito, won't I get sick? A: Probably not. Even if you are bitten by an infected mosquito, your chances of developing illness are roughly one in 300."⁷⁸ From these statistics we can conclude that if 1 in 1000 mosquitoes in an area with WNV are carriers, and your chances of getting sick from a bite from an infected mosquito are 1 in 300, then a bite from 1 in 300,000 mosquitoes could make you ill.

A New York City Health Department survey of blood samples taken from people who lived in northern Queens, the epicenter of the 1999 outbreak, showed that 19 out of 677 tested positive for the virus. But none had become seriously ill, and all either reported no symptoms or mild illness, such as a low-grade fever. The survey concluded that between 1.2 percent to 4.1 percent (between 533 and 1,903 people) of the 46,000 residents in that three-square-mile area had been infected. Of the infected group, four people in the sample had non-specific aches, pains or fever.⁷⁷

WNV was first identified in the Boston area in July 2000 when a dead crow was found near Willow Pond. As of mid-November, a total of 448 birds had died in Massachusetts due to infection from the virus, and one horse had developed severe neurological disease. There were, however, no reported cases in Massachusetts of human infection.¹³ In a story about the psychological impact of the outbreak, the Boston Globe (8/20/00) put the risk of West Nile infection in perspective: "Based on current information on casualties, the odds of an American dying of this summer's most dreaded virus are roughly 1 in a million, the statistical cutoff point for saying something has almost no risk at all."¹⁴

Michael Gochfeld, Professor of Environmental and Community Medicine at the Robert Wood Johnson Medical School and School of Public Health writes: "In weighing the risks and benefits of mosquito control, we should consider the disease itself and the risk to the human population. The media always paired the words "lethal" or "deadly" with "West Nile" or "encephalitis," reinforcing in the public's mind the danger from the disease. But it would be equally appropriate to characterize West Nile Virus infection as "inapparent," "usually asymptomatic," or "occasionally serious." Seven deaths in a population of over 10 million people over a one month period is certainly tragic, but pales beside the number of deaths from many other diseases that are addressed less aggressively.³⁹

The only human epidemic of West Nile Virus infection that has been well-studied occurred in Romania in the late summer of 1996. The U.S. Centers for Disease Control and Prevention assisted in the evaluation and control of that epidemic and recently published a report in The Lancet, the leading British medical journal.¹⁰⁸

Webster's New World Dictionary defines 'epidemic' as "prevalent and spreading rapidly among many individuals in a community at the same time; widespread," and 'deadly' as "causing death or likely to cause death." As we have seen from the available data, West Nile Virus can hardly be considered a "deadly epidemic." So what's behind the big push to spray where the virus shows up? The Centers for Disease Control recommend spraying under certain circumstances in their guidelines for surveillance, prevention, and control of WNV.¹² Their mission is "To promote health and quality of life by preventing and controlling disease, injury, and disability." They tend to focus more on the disease agents, not the possible effects of the 'cure' -- spraying and larvicides -- on human health, ecosystems, and lobsters.

Certainly pesticide manufacturers and applicators stand to make millions of dollars by manufacturing and applying sprays for WNV mosquito control. A pesticide applicator in Maine has been reported as saying WNV mosquito control spraying "would be good for business."¹⁰⁴ Clarke Environmental Mosquito Management, Inc. was paid $650/hour per truck in a $4.6 million New York City contract.⁸¹ The company's recent bid to spray was in excess of $50 million over three years.⁴²

The only hard evidence available that pesticide applicators are behind efforts to increase public hysteria and thus the market for their products comes from the New York State Attorney General's Office. A Long Island landscaping company agreed to pay a fine and cease an advertising campaign that falsely claimed its spraying of homeowners' trees and shrubs would kill mosquitoes carrying the West Nile Virus. The action against Green Island Tree Spray Inc. of Huntington includes a fine of $35,000 and restitution to customers who hired the company based on its deceptive advertising. "This pesticides applicator cynically preyed upon peoples' fear of the West Nile virus for the sake of increased profit," said Attorney General Spitzer. "This action should serve as a warning to others who might contemplate similar schemes."

Spitzer's action against Green Island Tree Spray Inc. focused on solicitations mailed to homeowners in which the company emphasized the "very real threat of an Encephalitic Mosquito outbreak come this Spring and Summer" and offered to spray trees and shrubs with a product it described as "extremely effective" in killing mosquito eggs before they hatch. Mosquito eggs hatch in stagnant water, not in trees and shrubs. Green Island did not have the proper certification to engage in the business of controlling public health pests such as mosquitos and the product it was advertising could not legally be applied to control mosquitos.⁸⁰

The Maine Bureau of Health (BOH) has formed a 22-member, multi-agency West Nile Virus Working Group, headed by state epidemiologist Kathleen Gensheimer. It includes four subgroups: Pesticides and Spraying, Entomology, Avian Surveillance, and Clinical/Laboratory diagnostics. The group has organized a proactive course of study to provide the best information available about methods of surveillance for West Nile Virus (WNV) in mosquitoes, humans or birds, and factors to consider before a decision is made to spray.⁴⁵

Maine Board of Pesticide Control (BPC) toxicologist LeBelle Hicks is chair of the Pesticide/Spraying group. This group has reviewed the toxicity of the 10 pesticides used for mosquito control. The document they prepared was developed by BPC staff with input from both the Board's Medical Advisory and Environmental Risk Advisory Committees.⁶¹ The study provides conventional environmental and human risk assessment data for each should spraying be deemed essential to public health either by the state or a given municipality.⁴⁵

Hicks is compiling an information sheet for residents and a list of recommendations for municipalities. A draft of the municipal fact sheet released in February included the admonition that "chemical controls are not appropriate for WNV mosquito management in the absence of confirmed virus." The draft emphasized the use of nonchemical controls, like those outlined in this report. Municipalities are advised to contact appropriate state agencies for advice and technical assistance: Maine Forest Service for questions about mosquitoes; Board of Pesticide Control about pesticide risks and licensing; the Bureau of Health for Surveillance and WNV in humans; and the Department of Environmental Protection (DEP) for adding pesticides to water.⁴⁵

The Entomology subgroup, chaired by Dave Struble, State Entomologist for the Maine Forest Service, will assess mosquito populations of the five species of mosquitoes (of about 40 species that live in Maine) known at this time to be WNV vectors (transmitters of the disease). A thorough survey of mosquitoes in Maine has not been performed since 1950.¹⁰⁴ Paul Dearborn, who is with the Insect and Disease Lab of the state Department of Conservation, said two of these, Culex pippiens and Culex restuans are considered most important in Maine as possible vectors. They breed in stagnant water in containers such as old tires, dumpsters and bird baths. The plentiful salt marsh mosquito does not carry WNV. The Maine Forest Service has prepared detailed information on their web site about mosquitoes in Maine.⁶² If the summer does bring positive WNV identification in humans, birds or other animals, it will be necessary to know mosquito species distributions and densities to assess risk.⁴⁵

Avian surveillance will include a phone number (toll-free: 1-888-697-5846 or 207-287-5301) to report dead birds and will include pick up of bird specimens. Bird reporting and testing will be an important component of the State's efforts. A system for reporting human cases is also being devised to ensure that they are accurately diagnosed.⁴⁵ It would be helpful if all state agencies worked together to develop a statewide toll-free 'hotline' to act as a clearinghouse for all questions related to WNV.

It is not known at this time how many WNV infected dead birds, mosquitoes, and/or infected people would be required to elicit a chemical response recommendation from Maine state officials, what the spray radius would be, what chemicals would be used, etc. The Centers for Disease Control's guidelines for surveillance, prevention, and control of WNV for 2000 said: "Adult mosquitoes should be controlled within approximately a 2-mile radius around the area where a WNV positive dead bird or infected mosquitoes are found."^13a

The just released revised guidelines for 2001 are less aggressive when it comes to broadcast spraying of adulticides. They say: "Control activity should be initiated in response to evidence of virus transmission [to humans], as deemed necessary by local health departments."¹² As to the recommended spray radius, the revised guidelines leave it up to local officials as well: "There is no simple formula for determining how large an area to treat around a positive surveillance indicator or a suspected or confirmed human case of WN virus. Nor is there adequate information to guide decisions about the degree of vector population suppression that must be attained, or for how long this suppression must be maintained to reduce risk of disease."¹²

So while the CDC guidelines for 2000 recommended spraying within a 2-mile radius of even one confirmed positive bird, the 2001 guidelines only trigger a spray recommendation after human case(s) are identified, and the CDC defers the decision on the size of the spray radius to local officials. "There is no definitive formula this year," said Dr. Lyle Petersen of the CDC in a New York Daily News article. "You just have to look at the local situation." New York environmentalists had filed a lawsuit arguing that the 2-mile spray radius/1 dead bird criteria was overkill.^17a

Towns may elect to spray pesticides approved by the Board of Environmental Protection and Maine Board of Pesticides Control, but they must use all products according to label directions, use a licensed commercial applicator and follow current rules for notification as stated by the Board of Pesticides Control. If surface water or an outlet to surface water is involved, the town must obtain a permit from the DEP before spraying. If the BOH believes the number of dead birds or infected mosquitoes or human cases of WNV in a given area warrants declaring a public health emergency, all jurisdiction would revert to the BOH. Then the State would have the authority to spray a community if it did not do it itself. Dr. Dora Mills, the state Director of Public Health, who would be responsible for such a decision, emphasized she seriously doubted this would happen. She noted no other state has so far declared a public health emergency.⁴⁵

The Entomology subgroup chair Dave Struble posed the big question in an article in Working Waterfront this way: "Are we at a greater risk from the potential of getting the disease or from getting a response from what we do to keep the disease from occurring? "⁴⁵

The article says that Gensheimer insisted the State will do everything in its power to be rational and hopes municipalities will follow suit and use all available information to weigh health and environmental consequences. She urged Maine residents to instigate preventive cleanup measures before the mosquito season. "These," she observed, "do not cost anything, or take a lot of time or have any risk associated with them, and they can be very helpful." The Bureau of Health has said there will be a public forum to allow discussion on the State's preparations for West Nile Virus, but no date has been set.^45,104 Check http://www.meepi.org often for all the latest developments.

There are some consistent themes and results that arise from any governmental agency review, approval and subsequent environmental application of pesticides. When chemical company scientists come up with the latest pesticide, the evaluation process used to determine its 'safety' often does not take into account how the compound actually behaves in nature. Factors like synergistic effects with other chemicals, even those that the active ingredient is mixed with -- so called 'inerts' -- are not thoroughly evaluated.

The toxic effect on humans, particularly at risk populations like the elderly, children, and pregnant and nursing mothers, is not thoroughly examined. Studies of the long-term subtle effects on endocrine systems, behavior, intelligence, cancer, etc., are either not done or are inadequate. The chemical manufacturer usually does the testing and supplies the data. Rarely taken into consideration are effects on animals and ecosystems. For example, how will frogs, fish, birds, otters, etc., be affected if all arthropods -- so important in the food chain -- are wiped out from the pond they live in or near?

The chemical company then uses public relations and lobbying efforts to gain agency and public approval for the new pesticide. The compound is released into the environment and the unintended consequences begin. Sprayed broadly over fields, in neighborhoods, in wetlands, from planes and trucks, or dumped into sewers and bodies of water, its effects are seen in unpredicted and insidious ways. People become sick, others develop multiple chemical sensitivity disorder, some die. Lobsters, birds, bees and butterflies are found sick, dead, or exhibiting bizarre behaviors.

Then people fight back, and it's a tough fight. Because the compound has gone through such a "thorough scientific review process," and those fighting it are often not scientists, they are ridiculed, ignored, and told to be quiet. It can be years before a dangerous compound, once approved and even mandated for use by the government, is banned or certain uses of it restricted. Consider the examples of lead in paint and gasoline, DDT in pesticides, DES and thalidomide for pregnant women. On June 8, 2000 the EPA announced a ban on virtually all uses of Dursban (chlorpyrifos) in residential and commercial buildings. Diazinon, one of the most widely used pesticides in the United States, will be phased out of home and garden use by 2004 because of health concerns. Nearly 100 pesticides have been banned or severely restricted by the EPA since their introduction.¹¹⁰

The 'risk assessment' models used by the state to evaluate the chemicals, although they enjoy widespread use in the regulatory community, are inadequate in determining whether the introduction of these compounds into the environment will adversely affect humans, wildlife, and lobsters.

As Peter Montague of the Environmental Research Foundation points out in his criticism of risk assessment, "Current policies such as risk assessment and cost-benefit analysis give the benefit of the doubt to new products and technologies, which may later prove harmful. And when damage occurs, victims and their advocates have the nearly-impossible task of proving that a particular product or activity was responsible."⁷¹ In order to protect public health and the environment, our standard should be equivalent to that of the FDA's, where a product is considered harmful until it is proven safe.

The Wingspread Statement on the Precautionary Principle states: "When an activity raises threats of harm to the environment or human health, precautionary measures should be taken even if some cause and effect relationships are not fully established scientifically."^103a

The most common argument that activists will come across when pointing out some of the real dangers of the following compounds and their use for mosquito control will be the dose. The officials and applicators will assure the public that the levels of chemicals they will be exposed to will be so low, and so infrequently applied, that there will be no effect on the environment and human health, and/or that the compound's toxicities quickly degrade. This is not true for two reasons. First, many of these chemicals have significant to subtle negative health and environmental effects at extremely low levels. Secondly, they are never applied as planned. There will always be mistakes, spills, and oversprays: the compounds, although analyzed for safety and degradation characteristics under ideal laboratory conditions, will be applied by real people into the real world.

These compounds vary greatly in their toxicities, behavior in nature, and in their method of application. We review available information on these ten compounds, but it is important to keep in mind that these are the compounds that are under review at this time -- new ones can and will make the list. Stay up-to-date on this and all aspects of the WNV virus situation in Maine and the northeast at http://www.meepi.org.

Malathion is one of the most widely used organophosphate insecticides in the United States and throughout the world. Contributing to its popularity is malathion's relatively low acute mammalian toxicity. But like DDT and other pesticides that have been found to cause irreparable damage to human and environmental health, malathion may pose a greater risk than the product label would lead one to believe.

Shown to be mutagenic, a possible carcinogen, implicated in vision loss, reproductive and learning problems, immune system disruption and other negative health effects in human and animal studies, damaging to nontarget organisms, and containing highly toxic impurities, malathion has a legacy of serious problems.⁸⁴

Organophosphates, in the same chemical class as the nerve gas Sarin, act as neurotoxins, disrupting the nervous system by inhibiting the enzyme cholinesterase. High exposures can produce fatal poisoning.⁹⁷ In April 2000, a U.S. Environmental Protection Agency (EPA) committee reviewed a series of studies on mice and rats exposed to malathion. Based on this review, the committee concluded that there was "suggestive evidence of carcinogenicity."¹¹² For the moment malathion remains listed by EPA as "not classifiable" with regard to carcinogenicity.⁶⁴ Recent evidence suggests that organophosphates such as malathion can cause Non-Hodgkin's Lymphoma (NHL).^123,70

During a malaria mosquito eradication spray program in Pakistan in 1976, 2,800 people became poisoned from malathion and 5 died.³ Seven children with bone marrow disorders have been observed over the past 8 years by physicians at Travis Air Force Base Medical Center in California. The physicians believe the blood disorders, in all cases, were caused by organophosphate pesticides. All blood disorders occurred shortly after exposure to the pesticides DDVP/propoxur and malathion.⁹⁶

In laboratory animals, malathion exposure has caused stomach ulcers, testicular atrophy, chronic kidney disease,⁹⁸ increased liver and kidney weights, adverse gastrointestinal tract effects,⁹ and changes in the adrenal glands, liver, and blood sugar levels.^43,4 Use of malathion by farmers in Iowa and Minnesota has recently been linked to an increased risk of one type of NHL.¹⁰ Juvenile male rats exposed to daily doses of malathion had decreased numbers of sperm forming cells.^53,54 In sheep, malathion exposure of pregnant ewes resulted in an increase in aborted fetuses, still births, low birth weight babies. Longer duration and earlier initiation of malathion exposure resulted in more severe problems.¹⁰⁶

Between 1957 and 1971 Japanese school children experienced a tremendous increase in cases of myopia (nearsightedness), that correlated with the increased use of organophosphate insecticides, including malathion.⁴⁸ 98 percent of the children examined from Saku, an agricultural area where malathion was regularly applied, had reduced visual keenness. Other examples of what is now called 'Saku disease' in both children and adults were reported throughout Japan where organophosphate pesticides were applied. In California, a lawsuit is pending on behalf of a 15 year old boy who was declared legally blind after being outside while helicopters were spraying malathion. An ophthalmologist and a pesticide expert both agree that the boy may have Saku disease.⁵⁶

Eradication programs for pests such as mosquitoes and fruit flies expose thousands of people to malathion applied in aerial applications. This type of pesticide application often provokes complaints of allergic reactions and flu-like symptoms.^101,52,93 Impurities and byproducts present in malathion can further disrupt immune system function.^20,100 Immunosuppression may enhance susceptibility of mammalian systems to bacterial, viral, or parasitic infection or possible increased tumor formation.^99,84a

Ironically, use of these pesticides for WNV mosquito control could actually end up suppressing human and avian immune systems in the areas sprayed, putting each species at greater risk than before of spreading, contracting, and becoming seriously ill from WNV.

Malathion is lethal to beneficial insects, snails, microcrustaceans, fish, birds, amphibians, and soil microorganisms. Sublethal exposure of these species can cause a variety of behavioral and physiological abnormalities.⁸⁴

Naled (trade name Dibrom) is an organophosphate with many of the same characteristics and concerns as malathion. Naled can cause cholinesterase inhibition in humans: that is, it can overstimulate the nervous system causing nausea, dizziness, confusion, and at high exposures, can cause respiratory paralysis and death. One of the byproducts of degradation of Naled is dichlorvos, another registered organophosphate. This compound is of toxicological concern.¹¹⁵

Researchers at the Cornell University Program on Breast Cancer and Environmental Risk Factors in New York State review several studies on dichlorvos. In one study female mice that were fed high doses of dichlorvos over a long time had a higher frequency of stomach cancers than untreated mice. High doses of dichlorvos fed over two years caused an increase in the number of male rats that had pancreatic tumors and leukemia. A higher number of leukemia cases were reported in one study among male farmers who used dichlorvos for more than ten days per year, compared to those who had not used dichlorvos. A higher number of childhood brain cancer cases were reported among families that used dichlorvos than among families that did not.¹⁸

The pesticide trichlorfon is a common ingredient in the mosquito pesticide dibrom (naled). In one study, trichlorfon was found to cause a "severe reduction" in brain weight (and shape) in test animals exposed. The timing of exposure to the developing offspring appeared to be the key factor in determining neurological damage (known as the "critical brain growth period"). It occurred when the chemical was administered between 40-50 days gestation for the guinea pig which scientists say correlates with the brain growth spurt period for the animal.⁶⁸

Russian scientists studied the growth rates of fish called Bream (Abramis brama) after exposure to the dibrom/naled contaminant dichlorvos. The first major effect detected was a significant reduction in the growth rates of the fish. Researchers believe it may be due to the subtle neurotoxic actions of the pesticide and its effects upon the areas of the brain involved in feeding or food search mechanisms.⁴⁰

Naled is characterized as very highly toxic to bees and aquatic invertebrates. It is moderately to highly toxic to fish and slightly toxic to upland game birds and waterfowl.^29a There is potential for chronic risk from Naled to estuarine invertebrates.¹¹⁵

Temephos (Abate) is a nonsystemic organophosphate insecticide used to control mosquito, midge, and black fly larvae. It is used in lakes, ponds, and wetlands. It also may be used to control fleas on dogs and cats and to control lice on humans. The compound may also be found in mixed formulations with other insecticides including trichlorfon. As an organophosphate, it has many of the same concerns and characteristics as malathion and naled.

Symptoms of acute exposure are similar to other organophosphates and may include nausea, salivation, headache, loss of muscle coordination, and difficulty breathing.¹¹⁹ Temephos produces signs and symptoms typical of cholinesterase inhibition at moderate levels of exposure, but mortality does not occur unless very large doses of the compound are administered.^33,119 Temephos may greatly increase the observed toxicity of malathion when used in combination with it at very high doses.³³ The compound has the potential to cause significant toxic effects (depression of the activity of the enzyme cholinesterase in the blood and the brain) in mammals exposed over long periods of time.

Tests with various wildlife species indicate that the compound is highly toxic to some bird species. The compound is highly toxic to bees.^51,30a Temephos shows a wide range of toxicity to aquatic organisms, including salmon.⁴⁷ Freshwater aquatic invertebrates such as amphipods are very highly susceptible to temephos, as are some marine invertebrates.⁵⁰ Temephos is very highly toxic to saltwater species such as the pink shrimp,⁵⁰ and presumably to lobsters as well.

Temephos has the potential to accumulate in aquatic organisms. In one study, the bluegill sunfish accumulated 2300 times the concentration present in the water.¹¹⁹

Maine officials are considering the use of three synthetic pyrethroids; permethrin (Ambush, Pounce), sumithrin (Anvil) and resmethrin (Scourge) for use against adult mosquitoes. Pyrethrins are natural insecticides produced by certain species of the chrysanthemum plant. The natural pyrethrins are contact poisons which quickly penetrate the nerve system of the insect. A few minutes after application, the insect cannot move or fly away. But, a "knockdown dose" does not mean a killing dose. The natural pyrethrins are swiftly detoxified by enzymes in the insect. Thus, some pests will recover. To delay the enzyme action so a lethal dose is assured, organophosphates, carbamates, or synergists may be added to the pyrethrins (see inerts section).

Semisynthetic derivatives of the chrysanthemumic acids have been developed as insecticides. In general, the term "pyrethrins" refers to the natural insecticides derived from chrysanthemum flowers; "pyrethroids" are the synthetic chemicals, and "pyrethrum" is a general name covering both compounds.²⁹

Synthetic pyrethroid compounds vary in their toxicity as do the natural pyrethrins. Inhaling high levels of pyrethrum may bring about asthmatic breathing, sneezing, nasal stuffiness, headache, nausea, incoordination, tremors, convulsions, facial flushing and swelling, and burning and itching sensations. The most severe poisonings have been reported in infants.⁸⁵ Pyrethrin is extremely toxic to aquatic life, such as bluegill and lake trout while it is slightly toxic to bird species, such as mallards. Toxicity increases with higher water temperatures and acidity.²⁴ EPA is scheduled to re-evaluate the health effects of the pyrethroids in 2002.⁶⁴

A report in the New York Daily News (9/9/00) tells of a woman who was sprayed directly on the street in Manhattan with Anvil (sumithrin) and ended up in the emergency room after experiencing blurry vision, nausea, itching, coughing, choking and a swollen tongue. "I threw up three days in a row, I really thought I was going to die," said the unidentified woman. In the story, a New York City Health Department spokesperson says this incident was one of 200 complaints from people who called the city's pesticide hotline stating the spraying had made them sick.⁷

Pyrethroid insecticide poisoning can be of unexpectedly long duration. Pyrethroids can produce reflex hyperexcitability and fine tremor, salivation, hyperexcitability, choreoathetosis (involuntary movements), and seizures. Local effects are also seen: skin contamination producing numbness and tingling, and ingestion producing gastrointestinal irritation.⁹⁵

The Cornell University Program on Breast Cancer and Environmental Risk Factors in New York State lists over 125 journal studies on the health effects of pyrethroids on their web site.¹⁹

Links between pyrethroids and hormonal disruption^83a

Several studies indicate that pyrethroids disrupt the endocrine system by mimicking the effects of the hormone estrogen, which can cause breast cancer in women and lowered sperm counts in men. A Mount Sinai School of Medicine study examined four pyrethroid pesticides, including sumithrin. It concludes "Overall, our studies imply that each pyrethroid compound is unique in its ability to influence several cellular pathways. These findings suggest that pyrethroids should be considered to be hormone disruptors, and their potential to affect endocrine function in humans and wildlife should be investigated."³⁸

A study at the Roger Williams General Hospital of Brown University on pyrethroids concludes "Chronic exposure of humans or animals to pesticides containing these compounds may result in disturbances in endocrine effects."²³

A Cambridge University report issued in June 2000 by the Royal Society in England called for international cooperation to deal with the dangers posed by endocrine-disrupting chemicals, including pyrethroids, and recommends reducing human exposure to these chemicals.^4a

A report of pesticides and childhood brain cancers published in Environmental Health Perspectives revealed a strong relationship between brain cancers and pyrethroids used to kill fleas and ticks. The study concludes "The specific chemicals associated with children's brain cancers were pyrethrins and pyrethroids (which are synthetic pyrethrins, such as permethrin, tetramethrin, allethrin, resmethrin and fenvalerate) and chlorpyrifos (trade name: Dursban)."⁹¹

A study conducted by the Physiological Institute at Ludwig Maximilians University in Munich, Germany, found that although "a majority of complaints following an acute pyrethroid intoxication disappeared after the end of exposure," several effects were still seen in patients after more than two years. Among these long-term symptoms were " 1) cerebro-organic disorders (reduced intellectual performance with 20%-30% reduction of endurance during mental work, personality disorder), visual disturbances, dysacousia, tinnitus; 2) sensomotor-polyneuropathy, most frequently in the lower legs; 3) vegetative nervous disorders," including increased heat-sensitivity and reduced exercise tolerance due to circulatory disorder. The study concludes "Many of these patients exhibit pathological autoimmune diagnostical findings and developed autoimmune diseases."⁵⁹

A study conducted by the Department of Environmental Toxicology at Uppsala University in Sweden studying mice found that "low-dose exposure" to pyrethroids "resulted in irreversible changes in adult brain function in the mouse" when exposed during the growth period. This occurred at levels of exposure less than what was found to affect adult mice. The study also found "neonatal exposure to a low dose of a neurotoxic agent can lead to an increased susceptibility in adults to an agent having a similar neurotoxic action, resulting in additional behavioral disturbances and learning disabilities."²⁷

Northwestern University Medical School conducted a series of investigations at Northwestern's Department of Molecular Pharmacology and Biological Chemistry in Chicago, has found neurological damage from pyrethroids. One study, conducted by international expert Toshio Narahashi, finds nervous-system damage from pyrethroids to be comparable to DDT. This study found that "Detailed voltage clamp and patch clamp analyses have revealed that pyrethroids and DDT modify the sodium channel to remain open for an extended period of time." The results of this damage are "potent effects on the nervous system."⁷⁴

A separate study found that pyrethroids cause "membrane depolarization, repetitive discharges and synaptic disturbances leading to hyperexcitatory symptoms of poisoning in animals." This study found that only 1% "of sodium channel population is required to be modified by pyrethroids to produce severe hyperexcitatory symptoms."⁷⁵

A pesticide study conducted on rats concludes "exposure to organochlorine, organophosphorus, and pyrethroid insecticides for a relatively short time can suppress thyroid secretory activity in young adult rats." The study also said a decrease in body weight seen "suggests that pyrethroid insecticides can inhibit growth rate."²

The larvicide methoprene (Altosid) is considered to be a slightly to practically nontoxic compound in EPA human toxicity ratings, which as noted, do not include adequate testing for hormone disrupting potential, etc. However, its effects on wildlife and ecosystems -- especially lobsters -- could prove devastating. The compound is dumped into water bodies like sewers, wetlands, ditches, and ponds. Massachusetts authorities dumped Altosid briquets into 27,000 catch basins across Boston in the summer of 2000.⁷⁶ Use of methoprene is particularly worrying because it is being put forth as a completely harmless way to control mosquitoes, especially in communities that have shown resistance to being sprayed.

Methoprene is a compound which mimics the action of an insect growth regulation hormone. It is used as an insecticide because it interferes with the normal maturation process. In a normal life cycle, an insect goes from egg to larva, to pupa, and eventually to adult (see mosquito life cycle). Methoprene artificially stunts the insects' development, making it impossible for insects to mature to the adult stages, and thus preventing them from reproducing. To be effective, it is essential that this growth inhibitor be administered at the proper stage of the target pest's life cycle. Methoprene is not toxic to the pupal or adult stages. Treated larvae will pupate but adults do not hatch from the pupal stage.²⁸ This is especially important in the context of Maine's lobster fishery.

Methoprene is slightly toxic to birds.^51,124 Nonlethal effects that may affect survival of the birds did appear at acute oral doses of 500 mg/kg. These effects appeared as soon as 2 hours after treatment and persisted for up to 2 days and included slowness, reluctance to move, sitting, withdrawal, and incoordination.⁴⁷ These effects may decrease bird survival by making them temporarily more susceptible to predation or by affecting reproductive and parenting behaviors.

Methoprene is slightly to moderately toxic to fish.¹¹⁷ Methoprene residues may have a slight potential for bioconcentration in bluegill sunfish and crayfish.¹¹⁸ Methoprene is very highly toxic to some species of freshwater, estuarine, and marine invertebrates.^28,28a

Studies at the laboratory of researcher Charles McKenney have shown that methoprene, an insect JHA (juvenile hormone analogue) used in mosquito control, inhibits the metamorphic success of larval estuarine shrimp (Palaemonetes pugio) and crabs (Rhithropanopeus harrisii) with exposure to concentrations which proved lethal to insect pests, including salt marsh mosquitoes. Differential survival and developmental rates of larval shrimp and crabs indicate that certain larval stages are more sensitive to exposure than others.⁶⁷

Research into the toxic effects of methoprene and other mosquito control chemicals on lobsters is ongoing. The Lobster Institute at the University of Maine is working on such research projects, but have not yet completed or published their study results.¹⁰⁴ The $125 million putative class action lawsuit filed in New York by lobstermen against insecticide manufacturers for allegedly wiping out the lobster fishery there includes Zoecon Corp., the manufacturer of Altosid (methoprene).¹⁰⁷ It seems only prudent to prohibit the use of methoprene in Maine until more is known about its potential effects on the lobster fishery. Figures released by the National Marine Fisheries Service show that Maine lobstermen caught almost 57 million pounds of lobster worth more than $186 million in 2000.

Hans Laufer, a University of Connecticut professor emeritus, who has studied reproductive hormones in crustaceans for 20 years, has questioned the use of a larvicide that interferes with a mosquito's ability to molt. "In mosquitoes, it (methoprene) acts as an anti- hormone, and that's what's killing them,'' Laufer said. "It's doing exactly the same thing to lobsters, exactly the same."²¹

Use of methoprene is also a significant concern due to the effects of the retinoids that are formed when the compound breaks down after exposure to sunlight. Retinoids, a class of chemicals closely related to vitamin A, can cause birth defects in humans and may be contributing to the global epidemic of skeletal deformities in frogs.⁶⁴ Dr. David Gardiner, a research biologist at the University of California at Irvine, has been studying retinoids for at least a decade, and in recent years he has probed frog deformities. To him, retinoids are the obvious culprit in the mystery of the misshapen frogs because of the peculiar kind of limb deformities being observed. "There is no other known mechanism for this [besides retinoids]," Gardiner says. "Much of early development is controlled by retinoids," he says. "Our body [and the body of a frog] is completely dependent on them," he told a reporter.^60,72

Exposure to retinoids could also make frogs more susceptible to infectious diseases, Gardiner says: "The kinds of chemicals that would target development of limbs would target all organ systems," including the immune system. Frogs with abnormal legs would also very likely have abnormal immune systems. This could explain why some frogs are now suddenly falling victim to infectious agents that they resisted for millions of years.

Peter Montague, of the Environmental Research Foundation points out: "The pesticide regulators at U.S. Environmental Protection Agency have missed a key feature of a chemical (methoprene) whose safety they regulate. It shows once again that relying on risk assessment leads to bad public health decisions. EPA's risk assessments have routinely failed to evaluate the breakdown by-products of the pesticidal chemicals that the agency has deemed safe enough to allow as residues on our dinner plates. It also means that thousands of pesticides now in common use need to be re-tested to see if their breakdown by- products are dangerous to humans or other species."⁷²

Agnique MMF (monomolecular film) and Surface Oils

These compounds are applied as a film to water surfaces. Agnique reduces the surface tension of the water and makes it difficult for the larvae and pupae to attach. The film also blocks the breathing tubes of larvae and pupae causing them to drown (see diagram at right). Resting males and egg-laying females that come in contact with the film will also drown. Mosquito control begins minutes after application. Laboratory and field testing has shown the film to remain potent for 10 to 14 days on standing water.¹ Although there is no evidence that this compound is harmful to human health, it is certainly a significant alteration to an aquatic ecosystem if broadly applied to ponds and wetlands, as it will come into prolonged, intimate contact with invertebrates, fish, birds, frogs, otters, and other ecosystem inhabitants.

Oils, like films, are used to suffocate larvae, pupae, and emerging mosquitoes. They are derived from petroleum distillates and have the trade names Bonide and BVA2. The EPA admits that misapplied surface oils may be toxic to fish and other aquatic organisms.¹¹³ More research is needed on the effects Agnique MMF and other surface oil films may show at an ecosystem level.

BTi is a biological pesticide that contains naturally occurring soil bacteria in different strains that target specific insects. BT's are not known to be toxic to animals, birds, humans, fish or beneficial insects. BTi is required to have EPA warning and caution labels as is the requirement by law for any registered pesticide. BTi and variants, are widely used in organic farming. Some trade names are Aquabac, Teknar, and LarvX. Bacillus sphaericus (VectoLex) is another naturally occurring "biopesticide." It was registered in 1991 for use against mosquito larvae, who ingest the bacteria and die after the toxin in the bacteria disrupts their gut function.

Based on extensive testing, no harmful effects to the public are expected to occur when biopesticide products are applied according to label directions. Because there is the potential for skin and eye irritation, applicators are warned to avoid direct contact with the granules or a concentrated spray mix. Various tests revealed no expected harm to non-target organisms.¹¹¹

Although these compounds are not used in agriculture, related ones are approved for use in organic farming. It is unwise to broadcast these biopesticides widely. If their use is not limited, there is a chance that insects may develop immunity to these important pesticides, thereby limiting their effectiveness for mosquito control and for organic farmers.

More research needs to be done on the ecological effects of biopesticides. What non-target invertebrates that are important in the food chain are also affected by their use? How will a potential decrease in this part of the food chain affect fish and amphibians, and the birds and animals that feed on them?

There can be numerous "inert" ingredients in pesticides that are added to improve its storage, handling, application, and effectiveness. Many of these compounds are potentially harmful, or even more so than the active ingredient in the pesticide. Since the technical (chemically pure) grade of a pyrethroid is usually formulated (mixed with carriers, solvents, synergists, etc.) for use in commercial pest control, the toxicity of these other ingredients must be taken into consideration when assessing the toxicity of a formulated product. Researchers found a ten-fold difference in toxicity between formulations with the same active ingredient, but with different carriers, solvents, etc.⁷³ Some mixtures of Anvil are made up not only of 10% artificially manufactured Sumithrin but 10% piperonyl butoxide (PBO), a suspected carcinogen, and 80% "inert" ingredients such as polyethylbenzene, which is listed by the EPA as being "potentially toxic."⁸²

PBO is added to make the pyrethroids more effective. It acts by inhibiting naturally occurring enzymes that would otherwise degrade the insecticide. PBO breaks through the insect's defense, making the insecticide more powerful. PBO is suspected of being a carcinogen by the EPA's Office of Pesticide Programs. It is also listed as a suspected gastrointestinal or liver toxicant, and a suspected neurotoxicant, by the National Institute for Occupational Safety and Health's Registry of Toxic Effects of Chemical Substances. It has also been reported as a suspected reproductive toxicant.^49,83 There is also some evidence that PBO-pyrethroid mixes can affect the human immune system.²²

Polyethylbenzene (PEB), also known as heavy aromatic solvent naptha (petroleum), is widely used in pesticides. PEB is listed on the EPA Office of Pesticide Programs' Inert Pesticide Ingredients List No 2, which is a list of 64 substances the EPA "believes are potentially toxic and should be assessed for effects of concern. Many of these inert ingredients are structurally similar to chemicals known to be toxic; some have data suggesting a basis for concern about the toxicity of chemical." PEB is related to ethylbenzene, which is listed as a suspected reproductive toxicant and a suspected respiratory toxicant by the EPA. The white mineral oil, also known as hydrotreated light paraffinic petroleum distillate, is also listed on the EPA's Inert Pesticide Ingredients List No 2 of potentially toxic chemicals.⁸³

All of the aforementioned chemicals are designed to kill insects, many of which are responsible for pollinating wild and cultivated plants in Maine. The future of agriculture depends on pollinators. Insect pollination is a necessary step in the production of most fruits and vegetables we eat and in the regeneration of many forage crops utilized by livestock. Maine growers of apples, cherries, blueberries, cucumbers, pumpkins, and many other crops depend on insect pollinators -- both managed and wild -- to produce fertile seeds and full-bodied fruit. Recent surveys document that more than thirty genera of animals -- consisting of hundreds of species of floral visitors -- are required to pollinate the 100 or so crops that feed the world. Only 15% of these crops are serviced by domestic honey bees, while at least 80% are pollinated by wild bees and other wildlife.^47a

What percentage of the mosquito population in a sprayed area survives the spraying? This question, along with the question about the chances of getting sick from WNV (see risk factors), would seem the most important. If the chance of getting sick from WNV, even in areas where it is known to exist, approaches zero and the efficacy of spraying also approaches zero, what's the point of exposing our bodies, wildlife, and lobsters to toxic chemicals in the first place? "We need to address this, because if we're just spraying all over and not doing a damn bit of good, then this is a waste of time and money, and it's also a hazard," says Dr. David Pimentel, a professor of entomology at Cornell University and a longtime pesticide researcher.³¹

Most spraying efficacy studies are done under outdoor "lab" type conditions, often with caged mosquitoes placed a measured distance from spraying, and at differing pesticide potencies. As mosquitoes are mobile, and hide under leaves and in vegetation, and truck spraying only sprays people's front yards, extrapolating the efficacy numbers from these studies to actual spraying programs is questionable. Most places where mosquitoes would breed are in people's back yards, and there are many quasi-residential areas in southern Maine, those with lots greater than half an acre, for example.

Months after local governments throughout metropolitan New York began deploying spray trucks and helicopters to fight West Nile, health officials at all levels of government still have released only rough estimates, not specific data, about how effective spraying has been in killing disease-carrying mosquitoes."We agree that effectiveness is an important question, and we intend to answer it," said Dr. James Miller, West Nile coordinator for the New York City Health Department. Though they haven't released any data, Miller and other New York City officials estimate that in the city, mosquito counts after a spraying are "up to 85 percent" lower than they were beforehand. And Deputy Commissioner Carl Johnson of the state Department of Environmental Conservation, which regulates pesticide use around the state, said local governments have anecdotally reported "60 to 80 percent reductions" after spraying.³¹

Some mosquito-control experts from outside the region, however, are skeptical. "I find it hard to think that they could consistently get 85 percent control spraying in an environment with so many trees and houses and other obstructions," said Judy Hansen, a past president of the American Mosquito Control Association who has run the mosquito-control program in Cape May County, N.J., for 40 years.³¹ "The people in New York ought to be very cautious about saying they're getting 85 percent control," agreed Ray Parsons, who runs Houston's program and was a consultant to Rockland County this year. Trap experiments in residential areas in Florida, the state with the most extensive mosquito-control experience, generally show a reduction of about 30 percent after a spraying, "and that's also about what we get in Houston," Parsons said.³¹

In one study, it took 2-3 times more insecticide to kill 90% of the mosquitoes in residential settings versus open areas. Such a high saturation is not permitted under current labeling safety guidelines: they would have to be increased to allow the higher application rates necessary for 90% control of mosquitoes in residential and/or highly vegetated areas.³⁷

Spraying pesticides for mosquito control may be worse than ineffective, it may even make the West Nile Virus situation worse. There are several reasons for this. First, spraying can increase mosquito populations by killing off natural predators (fish, other arthropods, birds, etc.) of the mosquitoes and their larvae, thereby removing natural checks on population levels. A 1997 study looked at trends in populations of Culiseta melanura, the mosquito primarily responsible for transmitting eastern equine encephalitis (EEE) among birds. Over a period of eleven years, Cicero Swamp in central New York state was sprayed fifteen times with the insecticide Dibrom (naled). Instead of declining, the population of Culiseta melanura grew fifteen-fold during this period. The study suggests that the pesticides may have altered the ecological balance of the swamp, killing organisms whose presence would ordinarily help limit the mosquito population.^46,65

Second, as ecologist Garret Hardin puts it "every biocide selects for its own failure." This means that mosquitoes can and will become resistant to chemical efforts to destroy them. Overuse of pesticides may create resistant super-mosquitoes that require ever increasingly toxic chemicals to kill them.²⁵

Also, toxic chemicals may be leaving mosquitoes that are sprayed but not killed in an immuno-compromised state, thereby allowing them to accumulate and spread more WNV than healthy mosquitoes. "Every time a mosquito spray plane or truck sprays these proven genetically damaging pesticides over the area, they are very likely increasing the amount of subtle genetic damage in the mosquito population, and hence, increasing the number of mosquitoes with genetic flaws which could in theory, allow the encephalitis virus to take hold and grow more rapidly," speculates pesticide researcher Richard Pressinger.⁹² Walter Tabachnick, director of the Florida Medical Entomology Laboratory, disputes this theory: "To my knowledge there is no information that indicates sublethal doses influence movement (of WNV within a mosquito's body). This too seems unlikely to me to have any major role in mosquito biology and disease epidemiology."¹⁰⁴ Clearly, more research is needed on this question.

Dr. Ray Parsons, who heads the Harris County Mosquito Control Division in Houston, has observed that malathion may actually aggravate Culex, causing an increase in aggressive biting behavior for an hour or two after spraying.⁷⁹

Finally, the public living in sprayed areas may feel a false sense of security. If they feel that fewer WNV mosquitoes are around, they may be less likely to use other proven measures to prevent mosquito breeding on their property and bites to themselves.

Joseph Finke, a Long Island lobsterman for the past 20 years, recalls the day that death, not lobsters, came crawling out of his mesh wire traps. It was Sept. 20, 1999, four days after Hurricane Floyd dumped more than a foot of rain on Long Island. "Not in my worst nightmare could I ever have imagined that sight," said Finke, remembering the dead, dying or deformed lobsters that clogged his traps. Many area lobstermen, and a growing number of scientists, believe that New York City's use of pesticides in 1999 to combat the West Nile virus, along with huge runoffs from Hurricane Floyd, may have combined to trigger the lobster kill. More than 10 million lobsters, or 90% of the stock, are thought to have died in the western part of the Long Island Sound.¹⁰² Nick Crismale, president of the Connecticut Lobstermen's Association, said 150 lobstermen who fished in the western Long Island Sound lost their livelihoods. The remaining 1,150 who fish in the Sound have seen a dramatic reduction in their catch, some as much as 65 percent.⁴⁵

The pesticides used for mosquito control are designed to kill bugs, and lobsters are bugs, or more specifically, arthropods. They share many life characteristics and a common evolutionary history with insects. They both have chitinous external skeletons and develop and grow from larvae through a series of molts. Although there is clear evidence that lobsters and other aquatic arthropods are susceptible to pyrethroids,⁸ temephos,⁹⁰ and methoprene,^5,6,15,90,94 many public officials and some scientists have been unwilling to pin the devastation of the Long Island Sound lobster fishery on the 1999 spraying for West Nile Virus.

The lobstermen, however, are not holding back. They lay the blame for the loss of their $45 million fishery firmly on WNV spraying, and have filed a $125 million putative class action lawsuit against insecticide manufacturers.¹⁰⁷ Figures released by the National Marine Fisheries Service show that Maine lobstermen caught almost 57 million pounds of lobster worth more than $186 million in 2000.

"If it [pyrethroid insecticide] gets into the water, it will kill aquatic life," says pesticide expert Richard Bromilow of Britain's Institute of Arable Crops Research in Rothamsted. Robert Bayer of the Lobster Institute at the University of Maine agrees. "There's no smoking gun, but it's very likely insecticides [are the cause]."⁶³ Bayer is currently conducting experiments on the effects of methoprene and other pesticides on lobsters, but he has not yet completed or published study results.¹⁰⁴

Hans Laufer, a University of Connecticut professor emeritus, said he became alarmed after listening to lobstermen describe finding egg-bearing lobsters that had molted before their eggs hatched, in effect shedding their eggs along with their shells. Laufer, who has studied reproductive hormones in crustaceans for 20 years, questioned the use of one larvicide that interferes with a mosquito's ability to molt. Insects, Laufer said, are biologically related to lobsters. The larvicide, methoprene, is known to harm small crustaceans, Laufer said. It acts in a similar fashion as nonylphenols, disrupting endocrine hormones and interfering with reproduction. "In mosquitoes, it acts as an anti- hormone, and that's what's killing them," Laufer said. "It's doing exactly the same thing to lobsters, exactly the same."²¹

Even if the insecticides are not directly killing the lobsters, they triggered the population crash, say other investigators. Richard French of the University of Connecticut and his colleagues found no evidence of bacterial, viral or fungal disease. But they discovered a Paramoeba parasite in the nervous system of all the lobsters studied. "The insecticide probably lowered their immune system, allowing the infection to overwhelm the population," says French. However, he has yet to prove the parasite actually kills the lobsters. The EPA has now launched an investigation into the cause of the lobster crash. Scientists estimate it will take at least 10 years for the population to recover.⁶³

Carl Wilson, marine biologist and lobster scientist at the Maine Department of Marine Resources (DMR), said there is no question that non-target species like shrimp and shellfish are susceptible to very low concentrations of different pesticides. He emphasized that the harm clearly depends on the dosage. Considering Maine's extremely high number of mosquitoes, he and others wondered if spraying would be effective.⁴⁵ John Sowles, Director of Ecology at DMR, is also wary of spraying. "I am very concerned about initial overreaction at the expense of the environment," Sowles said in a recent interview for Working Waterfront. "If a massive spraying program to attack a perceived risk creates measurable problems in the environment, it could be like swerving to miss a squirrel and hitting a telephone pole."⁴⁵

Clearly, more research is needed on the effects that mosquito control pesticides might have on lobsters, particularly sublethal effects at low levels. If exceedingly low doses, even in the part per billion range, can cause behavioral, reproductive, and immune system impairments, the results for Maine's lobster industry, and indeed the ecology of the marine environment, could be disastrous. It would be irresponsible and shortsighted to introduce these chemicals onto land or water bodies without knowing the effects they might have on lobsters.

One very important aspect of WNV mosquito control operations that receives little attention in traditional risk assessment/cost benefit analysis by public agencies is the potential threat of litigation related to the broadcast of toxics. So far there are suits relating to personal injury of pesticide applicators, personal injury to residents and a class action suit for destruction of the Long Island lobster fishery. Other potential areas of litigation related to toxic mosquito control are: losses to agriculture from the demise of bees and other pollinators; loss of recreational and other commercial fisheries; and loss of organic certification from farms that are over sprayed. Towns in Maine, state agencies, pesticide applicators and manufacturers need to factor into their decision-making process that they can and will be sued for perhaps millions of dollars if they make the decision to use toxics to control WNV mosquitoes. Here we review some of the lawsuits that have been brought since control measures began in the Northeast in 1999.

A coalition of environmental groups sought an emergency order to halt the spraying of Anvil, a pesticide that had already been used in Central Park, across Staten Island and in parts of Queens and Brooklyn, in areas where WNV was found in birds and mosquitoes. The environmentalists, represented by the Pace Environmental Litigation Clinic at the Pace University School of Law in White Plains, filed a lawsuit contending that the spraying campaign violated environmental laws (No Spray Coalition Inc. v. New York City, S.D.N.Y., No. 00-5395, 9/25/00).⁸⁸

Five workers who sprayed pesticides for a city contractor last summer to kill mosquitoes carrying WNV have filed a complaint with the Occupational Safety and Health Administration, contending that improper training and prolonged exposure to the chemicals made them sick. In an affidavit, the men detailed how they were repeatedly saturated with the pesticide Anvil during their nightly spraying shifts, while driving or riding without protective clothing on the backs of trucks. The former sprayers and truck drivers also said they handled and loaded pesticides without training or supervision, contrary to state and federal regulations. In sworn affidavits and interviews with the New York Daily News, the men said they've been plagued by ailments including fatigue, severe headaches, difficulty breathing, loss of hair, nausea and even sexual dysfunction. The New York Environmental Law and Justice Project, is representing them in making the claim.⁸⁷

Kent Smith (right) was assigned to one of the company's three all-terrain vehicles and sent to spray Yankee and Shea stadiums and various golf courses and cemeteries. He sometimes worked 16 hours a day, and his skin was constantly drenched with the pesticide, he said. "They only had two respirators in the whole place and wanted us to share them," he said. "I refused and forced them to get me my own respirator. There wasn't even a place to wash up after you finished spraying. Just a fountain where you washed your hands," he said. While the men were paid $11 an hour, the city paid Clarke $650 an hour per truck. After investigating their claims, the federal Occupational Safety and Health Administration cited the firm for five serious safety violations and fined it $6,750.⁴¹

In the biggest suit so far, commercial fishermen who claim the dramatic decrease in their lobster harvest was caused by pesticides used against mosquitos to combat the West Nile virus filed a $125 million putative class action against the insecticide manufacturers in a federal district court Aug. 25, 2000 (Fox v. Cheminova Inc., E.D.N.Y., filed 8/25/00). The proposed class consists of lobstermen from New York and Connecticut operating in Long Island Sound "who sustained legally recognizable damages as a result of the contamination and death of lobsters ... caused by Defendants' negligence, strict products liability, and other fault," according to the complaint.¹⁰⁷

When and if cases of WNV show up in Maine, citizens will understandably want government officials to "DO SOMETHING!" to prevent them from being bitten by WNV carrying mosquitoes. In many ways this is the reason that spray programs happen in the first place, given that their efficacy is questionable. A massive spraying campaign runs the risk of giving residents a false sense of security, encouraging them to think they are less likely to be bitten after the spraying, and less likely to implement some of the control measures listed below.

Government officials, from the town to state and federal level, can make a proactive, effective, and also non-toxic response to WNV. Imagine a van driving through neighborhoods with knowledgeable technicians getting out at every house, doing an inspection for potential mosquito breeding pools, pointing out ineffective screens, showing residents grills, toys, tires, sagging gutters, etc., in their yard that might harbor larvae. Each property could receive a 'report card' and specific instructions on what to do to correct problems. The technicians could also hand out information about WNV, list hotlines and information resources, discuss repellents, biopesticides, and talk about the minuscule risk that diligent residents have from WNV illness. This sort of approach would be safer, would ensure residents that officials were engaged, and would arguably be cheaper and more effective than spraying.

Community level guidelines for safe and effective mosquito control⁶⁵

To avoid being bitten outdoors, wear hats, long sleeves and long pants in the evenings, when mosquitoes are most active.

Insect repellents

DEET should be avoided

Do not use DEET, especially on children! The U.S. Environmental Protection Agency (EPA) acknowledges fourteen cases in which individuals reported seizures associated with exposure to DEET. Twelve were children, three of whom died.¹¹⁶ DEET can also interact with other chemicals to produce severe toxic effects on the nervous system, and may have played a role in Gulf War Syndrome. Based on existing information about DEET's health effects, EPA determined in September 1998 that the labels on some DEET-containing products were misleading. Under EPA's new requirements, it is illegal to label DEET-containing products as designed for children or "safe for kids." However, EPA chose to allow a grace period of more than four years during which products with old labels can be sold,¹¹⁶ so stores can still sell products with misleading safety claims." Treat clothing, rather than skin, whenever possible, and wash off repellents with soap and water after returning indoors.⁶⁵

Bite Blocker^TM

Bite Blocker^TM is a plant-based repellent that was released in the United States in 1997. Bite Blocker combines soybean oil, geranium oil, and coconut oil in a formulation that has been available in Europe for several years. Studies conducted at the University of Guelph, Ontario, Canada, showed that this product gave more than 97% protection against Aedes mosquitoes under field conditions, even 3.5 hours after application. During the same period, a 6.65% DEET-based spray afforded 86% protection, and Avon Skin-So-Soft^TM citronella-based repellent gave only 40% protection. It is available from Gardens Alive, 5100 Schenley Place, Lawrenceburg, IN 47025.^32,35

Citronella repellents and candles are non-toxic and fairly effective

Studies show that citronella can be an effective repellent, but it provides shorter complete protection time than most DEET-based products. Frequent reapplication of the repellent can partially compensate for this.³²

Canadian researchers studied, under field conditions, the efficacy of three citronella-based products (lotion, milk and sunblock formulations (active ingredients: 10% oil of citronella and 5% terpene of citronella) to protect against biting mosquitoes. All of the repellents "reduced the number of mosquitoes biting by 95% over the 1st and 2nd 30 minutes after application."⁵⁷

The same group of researchers assessed the efficacy of 3% citronella candles and 5% citronella incense in protecting against mosquito bites under field conditions. "Although significantly fewer bites were received by subjects at positions with citronella candles and incense than at nontreated locations, the overall reduction in bites provided by the citronella candles and incense was only 42.3% and 24.2%, respectively."⁵⁸

The manufacturer of Natrapel citronella-based insect repellent (Tender Corp., Littleton, New Hampshire) has laboratory data showing that their 10% lotion reduced mosquito bites by 84% during a 4-minute test period.¹⁰⁵

Avon Skin-So-Soft^TM

This bath oil is more often mentioned in Maine for use as an 'unofficial' blackfly repellent, and received considerable national media attention several years ago when it was reported to be effective as a mosquito repellent. When tested under laboratory conditions against Aedes aegypti mosquitoes, this product was shown to be only mildly effective with a half-life of 30 minutes.¹⁰³

Electronic repellents don't work

The CDC and several other sources report that Vitamin B and "ultrasonic" devices are NOT effective in preventing mosquito bites.

Appendix: West Nile Virus, Mosquitoes, Pesticides:
Questions and Answers¹¹

Overview of West Nile Virus

Q. Where did West Nile virus come from?

A. West Nile virus has been commonly found in humans and birds and other vertebrates in Africa, Eastern Europe, West Asia, and the Middle East, but until 1999 had not previously been documented in the Western Hemisphere. It is not known from where the U.S. virus originated, but it is most closely related genetically to strains found in the Middle East.

Q. How long has West Nile virus been in the U.S.?

A. It is not known how long it has been in the U.S., but scientists believe the virus has probably been in the eastern U.S. since the early summer of 1999, possibly longer.

Q. How many cases of West Nile encephalitis in humans have occurred in the U.S. ?

A. In 1999, 62 cases of severe disease, including 7 deaths, occurred in the New York area. In 2000, 17 cases had been reported through September, including 1 death. No reliable estimates are available for the number of cases of West Nile encephalitis that occur worldwide.

Q. I understand West Nile virus was found in "overwintering" mosquitoes in the New York City area in early 2000. What does this mean?

A. One of the species of mosquitos found to carry West Nile virus is the Culex species which survive through the winter, or "overwinter," in the adult stage. That the virus survived along with the mosquitoes was documented by the widespread transmission during the summer of 2000.

Q. Do the findings indicate that West Nile virus is established in the Western Hemisphere?

A. It is too early to speculate about the permanent establishment of West Nile virus. Continued surveillance will assist in answering this question.

Q. Is the disease seasonal in its occurrence?

A. In the temperate zone of the world (i.e., between latitudes 23.5° and 66.5° north and south), West Nile encephalitis cases occur primarily in the late summer or early fall. In the southern climates where temperatures are milder, West Nile virus can be transmitted year round.

Q. What is West Nile encephalitis?

A. "Encephalitis" means an inflammation of the brain and can be caused by viruses and bacteria, including viruses transmitted by mosquitoes. West Nile encephalitis is an infection of the brain caused by West Nile virus, a flavivirus (a type of virus usually transmitted by arthropods) commonly found in Africa, West Asia, and the Middle East. It is closely related to St. Louis encephalitis virus found in the United States.

Transmission of West Nile Virus

Q. How do people get West Nile encephalitis?

A. By the bite of mosquitoes infected with West Nile virus. See diagram of Culex life cycle.

Q. What is the basic transmission cycle?

A. Mosquitoes become infected when they feed on infected birds, which may circulate the virus in their blood for a few days. Infected mosquitoes can then transmit West Nile virus to humans and animals while biting to take blood. The virus is located in the mosquito's salivary glands. During blood feeding, the virus may be injected into the animal or human, where it may multiply, possibly causing illness. See diagram.

Q. If I live in an area where birds or mosquitoes with West Nile virus have been reported and a mosquito bites me, am I likely to get sick?

A. No. Even in areas where mosquitoes do carry the virus, very few mosquitoes--much less than 1%--are infected. If the mosquito is infected, less than 1% of people who get bitten and become infected will get severely ill. The chances you will become severely ill from any one mosquito bite are extremely small. See risk section.

Q. Can you get West Nile encephalitis from another person?

A. No. West Nile encephalitis is NOT transmitted from person-to-person. For example, you cannot get West Nile virus from touching or kissing a person who has the disease, or from a health care worker who has treated someone with the disease.

Q. Is a woman's pregnancy at risk if she gets West Nile encephalitis?

A. There is no documented evidence that a pregnancy is at risk due to infection with West Nile virus.

Q. Besides mosquitoes, can you get West Nile virus directly from other insects or ticks?

A. Infected mosquitoes are the primary source for West Nile virus. Although ticks infected with West Nile virus have been found in Asia and Africa, their role in the transmission and maintenance of the virus is uncertain. However, there is no information to suggest that ticks played any role in the cases identified in the United States.

Q. How many types of animals have been found to be infected with West Nile virus?

A. Although the vast majority of infections have been identified in birds, through September 2000 CDC has received reports of WN virus infection in horses, cats, bats, chipmunks, skunks, squirrels, domestic rabbits, and raccoons.

Q. Can you get West Nile virus directly from birds?

A. There is no evidence that a person can get the virus from handling live or dead infected birds. However, persons should avoid bare-handed contact when handling any dead animals and use gloves or double plastic bags to place the carcass in a garbage can.

Q. Can I get infected with West Nile virus by caring for an infected horse?

A. West Nile virus is transmitted by infectious mosquitoes. There is no documented evidence of person-to-person or animal-to-person transmission of West Nile virus. Normal veterinary infection control precautions should be followed when caring for a horse suspected to have this or any viral infection.

Q. How does West Nile virus actually cause severe illness and death in humans?

A. Following transmission by an infected mosquito, West Nile virus multiplies in the person's blood system and crosses the blood-brain barrier to reach the brain. The virus interferes with normal central nervous system functioning and causes inflammation of brain tissue.

Q. What proportion of people with severe illness due to West Nile virus die?

A. Among those with severe illness due to West Nile virus, case-fatality rates range from 3% to 15% and are highest among the elderly. Less than 1% of those infected with West Nile virus will develop severe illness. See risk section.

Q. If a person contracts West Nile virus, does that person develop a natural immunity to future infection by the virus?

A. It is assumed that immunity will be lifelong; however, it may wane in later years.

Q. Is there a vaccine available for WNV?

A. No. Currently there is no vaccine for West Nile Virus. Peptide Therapeutics Group announced in August of 2000 that it had been awarded a Fast-Track Small Business Innovative Research grant by the US National Institutes of Health to develop a new vaccine to prevent West Nile virus disease. Dr. Thomas Monath, Vice President Research & Medical Affairs of Peptide, said: "The advantages of ChimeriVax vaccines include their high safety profile, ability to induce protection within a few days after a single dose, and long-lasting immunity without the need for booster doses. A ChimeriVax West Nile vaccine is therefore ideally suited for use in an impending epidemic, where rapid immunization is required."⁸⁶ It is not known how long it will take to develop a vaccine.

Q. Is there a treatment for WNV?

A. Currently, there's no treatment that will cure the disease. Doctors may recommend remedies to cope with the symptoms of mild cases. Severe cases of West Nile virus may require hospitalization, and treatment may include: Intravenous (IV) fluids; Respiratory support (help with breathing); Precautions to prevent other infections, such as urinary tract infections and pneumonia.¹²⁰ There may soon be a new treatment for WNV. Doctors at New York Hospital Queens will be testing the drug Intron-A this summer on patients diagnosed with the disease. "Intron-A is a cloned version of interferon, which is a protein in our body that fights viruses and stimulates the immune system," explains Dr. James Rahal, director of the Infectious Disease Section of New York Hospital Queens. Intron-A is already used to treat Hepatitis C, a virus in the same class as West Nile. Lab tests have shown that the drug is effective in wiping out the virus. But not everyone with West Nile will get Intron-A. "We're only going to use it on people who have developed encephalitis," says Rahal.⁵⁵

Symptoms of West Nile Virus

Q. Who is at risk for getting West Nile encephalitis?

A. All residents of areas where virus activity has been identified are at some risk of getting West Nile encephalitis; persons older than 50 years or with compromised immune systems have the highest risk of severe disease. See in depth discussion of risk factors.

Q. What are the symptoms of West Nile encephalitis?

A. Most infections are mild, and symptoms include fever, headache, and body aches, occasionally with skin rash and swollen lymph glands. More severe infection may be marked by headache, high fever, neck stiffness, stupor, disorientation, coma, tremors, convulsions, muscle weakness, paralysis, and, rarely, death.

Q. What is the incubation period in humans (i.e., time from infection to onset of disease symptoms) for West Nile encephalitis?

A. Usually 3 to 15 days.

Testing and Treating West Nile Encephalitis in Humans

Q. I think I have symptoms of West Nile virus. What should I do?

A. Contact your health care provider if you have concerns about your health. If you or your family members develop symptoms such as high fever, confusion, muscle weakness, and severe headaches, you should see your doctor immediately.

Q. I am a physician in Maine and believe I have a patient who may have WNV. What should I do?

A. Suspect WNV cases are reportable to the Maine Bureau of Health at 207-287-5301, Infectious Disease Epidemiology Section. This is the same office and number to which all reportable communicable diseases come. The BOH has requested that physicians report (and consider panarboviral serologic/CSF testing) on all cases of encephalitis and for aseptic meningitis in any individual age 15 or older.¹⁰⁴

Q. How do health care providers test for West Nile virus?

A. Your physician will first take a medical history to assess your risk for West Nile virus. People who live in or travel to areas where West Nile virus activity has been identified are at risk of getting West Nile encephalitis; persons older than 50 years of age have the highest risk of severe disease. If you are determined to be at high risk and have symptoms of West Nile encephalitis, your provider will draw a blood sample and send it to a commercial or public health laboratory for confirmation.

West Nile Virus and Birds

Q. Do birds infected with West Nile virus die or become ill?

A. In the 1999 New York area epidemic, there was a large die-off of American crows. Through September 2000, West Nile virus has been identified in at least 70 species of birds found dead in the United States. Most of these birds were identified through reporting of dead birds by the public.

Q. How can I report a sighting of a dead bird(s) in my area?

A. Contact the Maine Bureau of Health at 1-888-697-5846 or 207- 287-5301.

West Nile Virus and Dogs and Cats

Q. Can West Nile virus cause illness in dogs or cats?

A. There is a published report of West Nile virus isolated from a dog in southern Africa (Botswana) in 1982. West Nile virus has been isolated from several dead cats in 1999 and 2000. A serosurvey of dogs and cats in the epidemic area showed a low infection rate.

Q. Can infected dogs or cats be carriers (i.e., reservoirs) for West Nile virus and transmit the virus to humans?

A. West Nile virus is transmitted by infectious mosquitoes. There is no documented evidence of person-to-person, animal-to-animal, or animal-to-person transmission of West Nile virus. Veterinarians should take normal infection control precautions when caring for an animal suspected to have this or any viral infection.

Q. Can a dog or cat infected with West Nile virus infect other dogs or cats?

A. No. There is no documented evidence that West Nile virus is transmitted from animal to animal.

Q. How long can a dog or cat be infected with West Nile virus?

A. The answer is not known at this time.

Q. Should a dog or cat infected with West Nile virus be destroyed? What is the treatment for an animal infected with West Nile virus?

A. No. There is no reason to destroy an animal just because it has been infected with West Nile virus. Full recovery from the infection is likely. Treatment would be supportive and consistent with standard veterinary practices for animals infected with a viral agent.

West Nile Virus and Horses

Q. Has West Nile virus caused severe illness or death in horses?

A. Yes, while data suggest that most horses infected with West Nile virus recover, results of investigations indicate that West Nile virus has caused deaths in horses in both the 1999 outbreak and in 2000.

Q. How do the horses become infected with West Nile virus?

A. The same way humans become infected--by the bite of infectious mosquitoes. The virus is located in the mosquito's salivary glands. When mosquitoes bite or "feed" on the horse, the virus is injected into its blood system. The virus then multiplies and may cause illness. The mosquitoes become infected when they feed on infected birds or other animals.

Q. How does the virus cause severe illness or death in horses?

A. Following transmission by an infected mosquito, West Nile virus multiplies in the horse's blood system, crosses the blood brain barrier, and infects the brain. The virus interferes with normal central nervous system functioning and causes inflammation of the brain.

Q. Can I get infected with West Nile virus by caring for an infected horse?

A. West Nile virus is transmitted by infectious mosquitoes. There is no documented evidence of person-to-person or animal-to-person transmission of West Nile virus. Normal veterinary infection control precautions should be followed when caring for a horse suspected to have this or any viral infection.

Q. Can a horse infected with West Nile virus infect horses in neighboring stalls?

A. No. There is no documented evidence that West Nile virus is transmitted between horses. However, horses with suspected West Nile virus should be isolated from mosquito bites, if at all possible.

Q. My horse is vaccinated against eastern equine encephalitis (EEE), western equine encephalitis (WEE), and Venezuelan equine encephalitis (VEE). Will these vaccines protect my horse against West Nile virus infection?

A. No. EEE, WEE, and VEE belong to another family of viruses for which there is no cross-protection. There is no approved vaccine currently available for West Nile virus.

Q. How long will a horse infected with West Nile virus be infectious?

A. We do not know if an infected horse can be infectious (i.e., cause mosquitoes feeding on it to become infected). However, previously published data suggest that the virus is detectable in the blood for only a few days.

Q. What is the treatment for a horse infected with West Nile virus? Should it be destroyed?

A. There is no reason to destroy a horse just because it has been infected with West Nile virus. Data suggest that most horses recover from the infection. Treatment would be supportive and consistent with standard veterinary practices for animals infected with a viral agent.

Q. Where can I get more information on horses and West Nile virus?

A. Visit the USDA Web site Animal and Plant Inspection Service (APHIS).

West Nile Virus and Wild Game Hunters

Q. Are duck and other wild game hunters at risk for West Nile virus infection?

A. Because of their outdoor exposure, game hunters may be at risk if they become bitten by mosquitoes in areas with West Nile virus activity. The extent to which West Nile virus may be present in wild game is unknown. Surveillance studies are currently underway in collaboration with the U.S. Geological Survey (USGS) National Wildlife Health Center (in Madison, Wisconsin) and with state and local wildlife biologists and naturalists to answer this question.

Q. What should wild game hunters do to protect against West Nile virus infection?

A. Hunters should follow the usual precautions when handling wild animals. If they anticipate being exposed to mosquitoes, they should apply insect repellents to clothing and skin, according to label instructions, to prevent mosquito bites. Hunters should wear gloves when handling and cleaning animals to prevent blood exposure to bare hands and meat should be cooked thoroughly.

Q. Who should wild game hunters contact for information about the risk for West Nile virus infection in specific geographic areas?

A. Hunters should check with their local area department of wildlife and naturalist resources, state epidemiologist at the state health department (Maine Bureau of Health: 207-287-5301), or the U.S. Geological Survey (USGS) National Wildlife Health Center, Madison, WI, 608-270-2400 for information on local area risk.

Prevention of West Nile Virus and pesticide injury

Q. What pesticides are used to control WNV mosquitoes? What are their effects on human and environmental health?

A. See information on pesticides.

Q. What can I do if aerial or truck spraying of pesticides occurs near my house?¹⁷

1. Keep windows closed during and immediately after spraying. If possible, also turn off window air conditioners.

2. Stay inside and keep children and pets inside during spraying and until the next morning after spraying.

3. Bring in or cover portable outdoor furniture, toys, laundry, pet dishes and tools.

4. Cover larger outdoor items such as barbecue grills or sand boxes. Swing sets and items that can not be covered should be rinsed thoroughly after the spraying.

5. Cover ornamental fish ponds because pesticides are highly toxic to fish.

6. Cover vegetable gardens if you can with plastic sheeting; wash any exposed vegetables before storing, cooking or eating.

7. Remove shoes when entering the home after spraying because pesticides can be tracked indoors and remain toxic for months in synthetic carpet fibers. Pesticides used for mosquitos are most easily degraded in direct sunlight and are sheltered when inside where they do not degrade quickly.

8. Hose off window screens, door handles and hand railings after spraying occurs to avoid direct contact.

9. If you suffer symptoms such as dizziness, headache, nausea, vomiting, weakness, blurred vision, breathing difficulties, or irritation of the eyes, nose, lips, mouth or throat, see your doctor immediately.

Q. How can I protect myself and my family from pesticide exposure due to WNV spraying?

A. Call, write, and meet with officials in your local municipality and ask them not to spray!