William C. Sugg, III, Director, Maine Environmental Policy Institute

Matthew L. Wilson, Director, Toxics Action Center

Published July, 2001

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. Forty years ago she wrote,

For the first edition of this report, which was written specifically for Maine (see Maine version of the report), we would like to thank the MEEPI 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.

For the second edition of the report, we would like to thank Rachel Zegerius for her Massachusetts specific research and writing. We would also like to thank Dr. David Ozonoff, Sue Phelan, Stephen Seymour, Ellie Goldberg, Sarah Little, Monica Garlick, and Aimee Qui for their input and review of the report.

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 us in particular as sources of information, quotations, references, inspiration, and guidance: The No Spray Coalition of New York; Northwest Coalition for Alternatives to Pesticides; Pesticide Action Network of North America; Extension Toxicology Network; Environmental Risk Analysis Program (ERAP) of Cornell University Center for the Environment; and Rachel Massey and Peter Montague of the Environmental Research Foundation.

The current policies by state and municipal officials in the Commonwealth that allow and encourage the spraying of toxic pesticides to combat the West Nile virus (WNv) are both dangerous and ineffective.

Spraying toxic pesticides to combat WNv, may cause more harm than good, exposing the population to a new public health threat through exposure to toxic chemicals. In fact, spraying may even have the paradoxical effect of increasing the mosquito population by affecting its predators.

The toxic pesticides proposed for spraying are harmful to human health, wildlife, and ecosystems. Children and the elderly are most susceptible to the effects of toxic pesticides. In both laboratory studies and occupational settings, the toxic pesticides being used for WNv mosquito control in Massachusetts have been known to cause short- and long-term respiratory problems, immune and nervous system disruption, cancer, and reproductive and learning disorders.

Adulticiding, or the spraying to kill adult mosquitoes, has not been proven effective. The Centers for Disease Control and Prevention state that ground and aerial spraying is usually the least effective mosquito control technique.¹²

In addition to exposing the public to toxic pesticides, spraying leaves communities with a false sense of security making them less likely to use effective, non-toxic control measures. Long-term spraying may actually increase the number of mosquitoes by destroying predators that feed on mosquito larvae and adults. Additionally, mosquitoes that are sprayed, but not killed, by the pesticides may become resistant, live longer, become more aggressive biters, and have increased prevalence of WNv within their bodies.

While the effects of West Nile virus on people can be serious, it is far from what some have called a "deadly epidemic". Seven people in New York City contracted West Nile virus in the year 2000 and eventually died. By comparison, 2,000 New York residents died from influenza in 2000.

The good news is that Massachusetts has the opportunity to implement a WNv prevention program that will ensure that people, ecosystems, and wildlife are not harmed by toxic chemicals. Monitoring and surveillance for the virus, combined with on the ground educational efforts aimed at minimizing breeding and biting opportunities for mosquitoes are needed. This approach may reduce the rate of WNv infections in Massachusetts to levels arguably better than a spray program could achieve.

West Nile Virus in the Northeastern United States:

An Introduction

West Nile virus (WNv) is a disease new to the Western Hemisphere. It appeared in New York City in 1999 and has since spread to animal populations in eleven states, including the District of Colombia, from New Hampshire to North Carolina. Many municipal officials have responded to the disease by spraying entire neighborhoods, fields, and water bodies with pesticides intended to kill mosquitoes that 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 of WNv go unnoticed or illicit ordinary flu-like symptoms. 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. So far this year in Massachusetts, 150 birds have been tested for the virus, none of which have tested positive. For weekly updates on surveillance reports and State Laboratory testing results visit the Massachusetts Department of Public Health website at: www.state.ma.us/dph/wnv/wnv1.htm.

Response to WNv involves input and regulation from a variety of governmental agencies. The Centers for Disease Control and Prevention (CDC), Division of Vector-Borne Infectious Diseases, are responsible for the development and modification of federal surveillance and response tactics, to be used as guidelines by individual states. To view the federal plan visit: www.cdc.gov.

The CDC will receive weekly updates from towns, detailing significant information about WNv.

The CDC guidelines for surveillance, prevention, and control of WNv for 2000 stated: "Adult mosquitoes should be chemically controlled within approximately a 2-mile radius around the area where a WNv positive dead bird or infected mosquitoes are found."^13a

The Massachusetts Department of Public Health (MDPH) has devised a surveillance and response plan, which recommends methods to be used by municipalities. ^63a

The Commonwealth’s surveillance plan includes the modification of the Arbovirus Surveillance Program (ASP), originally initiated in 1957. This past winter, MDPH convened four workgroups to revise the ASP and promote collaborative efforts between municipal health departments in order to address the threats of WNv. The purpose of the ASP is to test birds, mosquitoes, horses, and humans in order to detect disease or infection with the virus. The revised ASP sets comprehensive and flexible guidelines in five areas:

• Mosquito surveillance is at the core of the ASP. Because mosquitoes are the vectors of viruses like West Nile Encephalitis, monitoring mosquitoes provides a somewhat accurate estimate of the immediacy of risks to humans. Mosquitoes are tested using fixed trap sites established in Boston, Brookline, Cambridge, Newton, Middleboro, and areas of southeastern and western Massachusetts. These sites provide information regarding mosquito numbers, virus prevalence and estimation of WNV risk. More intensive mosquito trapping will be employed in response to increased virus activity in specific areas.
• Avian surveillance will focus on testing dead birds, and possibly live birds, throughout the summer to detect virus transmission between birds and mosquitoes. WNv is fatal to birds, with a particularly high mortality rate in American crows. Therefore, dead birds are potential indicators of virus activity in an area. Reports of dead birds can be made to the State Laboratory Institute (866-627-7968 or 866-MASS-WNv) and will initiate the pick up of bird specimens. Bird reporting and testing will be an important component of the Commonwealth's efforts.
• Equine surveillance will also take place at the State Laboratory Institute, testing horses that are suspect of infection. Random animal blood samples may also be tested.
• Specimens from clinical human cases of encephalitis will be screened in order to determine the possible cause of infection. In addition, hospitals will be contacted in the geographic areas of increased virus activity.
• Also included in the surveillance plan is the need for timely communication. Laboratory reports defining virus activity will be released to the media and public daily, via a web site. Laboratory confirmation of a human case of the virus will be communicated first to the health physician, and subsequently to the patient. Routine media advisories will be given by MDPH in the case of risk of human infection.

To view the entire MDPH Surveillance and Response Plan visit http://www.state.ma.us/dph/wnv/SandR.PDF.

Many Massachusetts municipalities contract with one of the County Mosquito Control Districts to conduct local surveillance and implement pesticide applications in the individual municipalities. The Control Districts have their own policies, which are primarily derived from the Commonwealth’s plan.

The decision to spray a particular community is in the hands of the local Board of Health. Most often Boards of Health defer to the Commonwealth’s plan, which is implemented by the Control Districts. Yet, municipalities do have the authority to halt or restrict spraying operations. For example, the cities of Boston and Cambridge will only consider pesticide spraying upon laboratory confirmation of a human infection. ¹⁶,^9b

Decisions are made on a town-by-town and case-by-case basis, in order to accommodate the needs and wants of the residents. However, in the case of a public health emergency, state and federal agencies can assume jurisdiction and override town decisions.

Three main chemicals were used against mosquitoes in public health situations last year in the state of Massachusetts.

• Scourge, a synthetic pyrethroid containing resmethrin was used, and is proposed to be used again this year, to kill adult mosquitoes. Scourge consists of resmethrin, piperonyl butoxide, and petroleum distillates.
• To kill larvae the state has used Bacillus thurengiensis israelensis (Bti), naturally occurring bacteria that is toxic to mosquito larvae.
• Another larvicide used is methoprene (Altosid), an arthropod growth inhibitor.

Other chemicals under review for use in killing adult mosquitoes in New England include two organophosphates; malathion and naled, and two other synthetic pyrethroids; permethrin (Ambush, Pounce) and sumithrin (Anvil).

To kill larvae, some New England states are considering the use of temephos (Abate), another organophosphate, and Bacillus sphaericusm another natural-occurring bacteria. A soapy oil called Agnique MMF (100% Poly (Oxy-1, 2-Ethanedilyl), Alpha-Isooctyl Decyl-Omega-Hydroxy) may be applied as a film to water surfaces in order to suffocate larvae in other New England states.⁶¹

The Federal Insecticide, Fungicide, and Rodenticide Act (FIFRA), the nation’s primary pesticide control law, classifies pesticide ingredients into two categories – active and inert. The active ingredients are those which are designed to kill pests while the inerts are added to make the active ingredient more potent and easier to use. Inert ingredients can make up a significant percentage of the material that is actually sprayed. Yet these inerts, which are often highly toxic, are often classified as "trade secrets" under law and are not listed on the label. The true nature and health threat of the petsicide are difficult to analyze.

Last year the synthetic pyrethroid resmethrin (Scourge) was used by many municipalities to control adult mosquito populations. It consists of the active ingredient resmetherin, and the inerts, piperonyl butoxide and petroleum distillates. The inerts do not kill the insects, but increase the potency of the resmetherin.

Other New England states are considering the use of two other synthetic pyrethroids, permethrin (Ambush, Pounce) and sumithrin (Anvil). Pyrethrins are natural insecticides produced by certain species of the chrysanthemum plant. The natural pyrethrins are contact poisons that 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 equal an exterminating 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, organo-phosphates, carbamates, or synergists may be added to the pyrethrins (see inerts section). The inert in Scourge, piperonyl butoxide, has been shown to cause liver tumors in rats and mice.¹⁶

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 The 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, and 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 "We tested four frequently encountered pyrethroids, fenvalerate, sumithrin, d-trans allethrin, and permethrin, for estrogen and progesterone agonist/antagonist activities. Through these hormonal pathways, exposure to certain pyrethroids may contribute to reproductive dysfunction, developmental impairment, and cancer."³⁶

The larvicide methoprene (Altosid) is considered to be a slightly to practically nontoxic compound in EPA human toxicity ratings, which do not include adequate testing for hormone disrupting potential. 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 for the purpose of killing mosquito larvae. Massachusetts authorities are dumping Altosid briquettes into 27,000 catch basins across Boston this summer.⁷⁶ Use of methoprene is particularly alarming, because it is being characterized as a harmless measure of controling mosquitoes, especially in communities that have shown resistance to being sprayed.

Methoprene is a compound that 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

Methoprene is slightly toxic to birds.^51,124 Non-lethal 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

Methoprene is believed to have a significant impact on lobsters. 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 A $125 million putative class action lawsuit has been filed in New York by lobstermen against insecticide manufacturers for allegedly wiping out the lobster fishery.¹⁰⁷

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".^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 chemical pesticides 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

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, which 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 use by 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?

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 non-target 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

In June of 2001, the Glens Falls Post-Star reported that 37 fourteen and fifteen year-old girls became ill at a softball game after being exposed to malathion, which was being applied to an area adjacent to the field. (See news story)

During a malaria mosquito eradication spray program in Pakistan in 1976, 2,800 people became poisoned from malathion and 5 died.³ Physicians at Travis Air Force Base Medical Center in California have observed seven children with bone marrow disorders over the past 8 years. The physicians believe organophosphate pesticides caused the blood disorders, in all cases. 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, stillbirths, and 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), which 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 by-products 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 over stimulate 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 period of 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 neurotoxin 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 non-systemic 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 also 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

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. 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 to determine the effects that Agnique MMF and other surface oil films may have at an ecosystem level.

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, 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. The EPA’s Office of Pesticide Programs suspects PBO of being a carcinogen. The National Institute for Occupational Safety and Health’s Registry of Toxic Effects of Chemical Substances also lists it as a suspected gastrointestinal or liver toxicant, and a suspected neurotoxicant. 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 naphtha (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 hydro treated 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 Massachusetts. 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. Massachusetts' 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. Domestic honey bees service only 15% of these crops, while at least 80% are pollinated by wild bees and other wildlife.^47a Organic crops are also at risk, should the state chose the method of aerial or ground spraying of pesticides. It is unlikely that sprayed farms will lose their certified status, but sprayed crops and plant material may not be able to be marketed as 'organically produced'. ^51a

Pesticides Risk Assessments: An Inexact Science

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.

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 entire ecosystems.

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.

"Comparative risk assessment (CRA) is chiefly a means for increasing the political power of 'experts' and reducing the political power of the general public. The experts will decide what is important and what is safe, and will be allowed to impose their views on the public. But CRA is not an objective, scientific enterprise; it is distinctly a political process. CRA 'experts' have no more legitimate claim to authority or power than anyone else in society. Using CRA will inevitably lead to new environmental injustices, as the voices of the public are excluded from the debate, and the 'experts' -- many of them the same people who created major environmental problems we now face -- make more bad decisions in a political vacuum."⁶⁹

Montague puts forth a model based on the Precautionary Principle,⁷¹ which says in summary:

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 the real dangers of pesticides 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 over sprays. The compounds, although analyzed for safety and degradation characteristics under ideal laboratory conditions, will be applied by real people in the real world.

What percentage of the mosquito population in a sprayed area is killed by the pesticide? This question seems the most important, but we face a lack of knowledge regarding the answer. If the efficacy of spraying approaches zero, what's the point of exposing our bodies, ecosystems, and wildlife 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 at measured distances from spraying, at differing pesticide potencies. The tests do not take into account the many variables that are involved in ground spraying. As mosquitoes are mobile, and hide under leaves and in vegetation, extrapolating the efficacy numbers from these studies to actual spraying programs is questionable.

"In order to work, the insecticide must hit the mosquito directly," says Dr. Pimentel. "But since spray trucks are only fogging the street side of buildings, I doubt that more than one-tenth of 1 percent of the poison is actually hitting its target. And you have to put out a lot of material to get that one-tenth of a percent onto the mosquito."³¹ Other scientists have estimated that less than 0.0001% of ULV (Ultra Low Volume) pesticide sprays actually reach the target insects.⁸⁹ So for every droplet that reaches a mosquito, hundreds of thousands more droplets circulate pointlessly in the environment.⁶⁵

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

The Cambridge, MA WNv Advisory Committee points out that the truck-based pesticide application methods that were used in Massachusetts may prove ineffective for a variety of reasons.^9a They point out the following factors that impact the effectiveness of pesticide spraying in urban areas:

• The most prevalent local bridge-vector mosquitoes prefer birds, particularly birds at rest, of which there are few in the street and building-front areas at the time the spray is applied
• Roosting areas may be higher than the reach of the spray
• Buildings close to the street restrict the lateral spread of the spray
• Backyard roosting areas are not effectively reached because close spacing of buildings limits penetration beyond the buildings
• The period that the spray is effective and airborne is of relatively short duration

The CDC agrees that, "ground applications are prone to skips and patchy coverage in areas where road coverage is not adequate or in which the habitat contains significant barriers to spray dispersal and penetration."¹² In a 1998 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.³⁷

It would be unfair to downplay the seriousness of a severe infection of West Nile Encephalitis. A severe infection can prove painfully debilitating, or even fatal. Fortunately, it is extremely unlikely that someone 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.

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

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

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 publics mind the danger from the disease. But it would be equally appropriate to characterize West Nile virus infection as "unapparent," "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

In that epidemic an estimated 94,000 people were infected by the virus, of which about 400 developed clinically apparent encephalitis confirmed by virological studies. Fifteen of those people, most over the age of 65, died. In Africa, where West Nile virus has been recognized for more than sixty years and where it is widespread, there have been very few human epidemics. It is important to note though that the lack of identifying these epidemics in Africa may be due to the incapacity of the medical infrastructure that exists there. However, West Nile virus infection is characterized by its sporadic outbreak in humans, even in areas where it is endemic in birds. This is likewise true of related infections, such as St. Louis encephalitis and Eastern equine encephalitis, where 30 or more years may pass between human outbreaks. In addition, our actual knowledge of the dynamics of arboviral diseases is deficient, to say the least. We have insufficient evidence to know how to control these diseases or how our control measures may affect them. Knowledge of these numbers is crucial in assessing the risk-risk tradeoffs essential to public health decisions in this area.³⁹

What's behind the big push by the vast majority of government officials to spray toxic pesticides when the West Nile virus appears? When the public heard of a potentially fatal virus being spread by mosquitoes, they looked to federal, state and local officials for solutions. Last year, when the West Nile virus came to Massachusetts, most government officials were caught off guard and were unprepared. They had not developed a plan on how to effectively address the issue. Pesticide spraying provided a quick and easy solution to a very complicated and multifaceted problem. Thinking they had to "do something", most government officials put their finger firmly on the pesticide trigger, picking the easiest and quickest, but not the safest or most effective response to address the WNv. These officials could say that they had done "something", even though their solution may have caused more harm than good.

There is also money to be made by spraying pesticides. Pesticide manufacturers and applicators stand to profit from 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 bid to spray was in excess of $50 million over three years.⁴² This bid was rejected by the state, and Clarke was recently fined $1 million for violating New York State's pesticide application laws.^7a

In New York, a Long Island landscaping company agreed to pay a fine and cease an advertising campaign falsely claiming that 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 New York Attorney General Spitzer. "This action should serve as a warning to others who might contemplate similar schemes."

Spraying pesticides for mosquito control may be worse than ineffective, it may even make the West Nile virus situation worse. 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

Thirdly, 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 sub-lethal 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.

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, which 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

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

"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

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

Clearly, more research is needed on the effects that mosquito control pesticides might have on lobsters, particularly sub lethal 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 Massachusetts' 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. To date 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. Municipalities in Massachusetts, state agencies, pesticide applicators and manufacturers need to factor into their decision-making process that they may be sued for millions of dollars if they make the decision to use toxic pesticides to control WNv mosquitoes. A number of lawsuits have been brought since pesticide spraying for WNv 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 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 mosquitoes 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 cases of WNv show up in Massachusetts, citizens will understandably want government officials to "DO SOMETHING!" to prevent them from being bitten by WNv carrying mosquitoes. 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 non-toxic preventative measures.

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 relative 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 control ⁶⁵

• Stop pesticide spraying conducted to control mosquito populations not because of public health threats, but for nuisance reasons. Many of the same pesticides are used in "nuisance spraying" that are used to control WNv and have harmful effects on pubic health, ecosystems and wildlife.
• Do not use "adulticides," or pesticides meant to kill adult mosquitoes.
• Make sure that people in Massachusetts understand that the common salt marsh mosquitoes do not carry West Nile virus. (Species: Aedes cantator and A. sollicitans)
• Focus on controlling mosquitoes in their immature forms: eggs, larvae, or pupae (see mosquito life cycle). Stock ponds and other bodies of water with mosquito-eating fish, and keep waterways clean so that fish and other mosquito predators can survive. In some cases, it is appropriate to use bacterial larvicides or mechanical controls such as vegetable-based oils that smother mosquito eggs floating on the surface of the water (see larvicide section).²⁵ Mechanical control of adults may be an option as well. Traps exist that may attract and kill mosquitoes over areas of up to an acre. The Mosquito Magnet mimics a large mammal by emitting a plume of carbon dioxide, heat and moisture.²⁵
• On a municipal or county level, set up a system for citizens to report standing water near their homes.²⁶
• Establish monitoring programs to pinpoint where mosquito-borne diseases are occurring. Monitoring can rely both on trapping mosquitoes and on "sentinel birds," such as chickens, tested regularly for signs of infection.²⁵
• Continuously evaluate the effectiveness of all mosquito control measures.
• Make sure the public knows what people can do at home to minimize mosquito exposure and eliminate breeding sites. Public health education is a good investment of resources and will pay off better than quick-fix expenditures on chemical sprays.

Some characteristics of Culex mosquitoes: a WNv carrier¹⁷

• Culex mosquitoes bite primarily in the hours between sunset (dusk), evening, and until the early morning (dawn). They are not highly active during full daylight.
• Culex breed in stagnant, standing fresh water. One of the most concentrated sites found with Culex were sewage treatment plants.
• Culex hide in tall grass and brush near inhabited locations, such as homes and other buildings. They are not the mosquitoes most often found in areas like the beach or salt marshes.
• Culex bite birds and other warm-blooded animals as well as humans as do many other types of mosquitoes. The primary host for WNv is birds. Mosquitoes spread the virus from birds to humans.
• Culex are a mosquito of modest size that produce a bite less severe than other, better-known mosquitoes such as the salt marsh mosquito.
• Culex do not tend to fly long distances (less than 1/2 mile) from their home base so keeping breeding down near your house will provide direct benefits.

Steps you can take around the house ¹¹⁴,⁶⁵

• Get rid of any unnecessary items on your property that can hold stagnant water, such as old tires. If you use old tires for farming or gardening, drill holes in them and empty them regularly.
• Empty water from buckets, toys, and containers, and store them in places where they will not collect rain.
• Make sure your dry-docked boats' drain is open so as not to collect rainwater and/or make sure that the cover is tight and has no standing water pockets. Keep your canoes and kayaks stored upside-down.
• Drill holes in the bottoms of recycling bins and any other containers that must be kept outdoors.
• Drain the water from birdbaths, fountains, wading pools, plant pots and drip trays twice a week.
• Check for other ways water may be collecting around your house, such as puddles beneath air conditioners.
• Clean out your gutters and fix gutters that sag or do not drain completely. Check for areas of standing water on flat roofs.
• If you have a swimming pool, outdoor sauna, or hot tub, make sure rainwater does not collect on the cover.
• Clear vegetation and trash from any drains, culverts, ponds or streams on your property so that water drains properly.
• Keep grass cut short and trim shrubs to minimize hiding places for adult mosquitoes.
• Eliminate standing water in your basement.
• To minimize the likelihood of being bitten inside your house, make sure window and door screens fit properly and replace outdoor lights with yellow "bug lights."
• To avoid being bitten outdoors, wear hats, long sleeves and long pants in the evenings, when mosquitoes are most active.

Insect repellents

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

Bite BlockerTM

Bite BlockerTM 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-SoftTM citronella-based repellent gave only 40% protection. It is available from Gardens Alive, 5100 Schenley Place, Lawrenceburg, IN 47025.³²,³⁵

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 sun block 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 for use as an 'unofficial' black fly 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

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

Appendix

Questions and Answers

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.

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.

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.

A. One of the species of mosquitoes 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.

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

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.

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

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

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 one mosquito bite are extremely small.

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.

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

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.

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.

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

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.

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.

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.

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

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.

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

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.

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.

A. Usually 3 to 15 days.

Testing and Treating West Nile Encephalitis in Humans

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.

A. Suspect WNv cases are reportable to the Massachusetts Department of Public Health's Division of Epidemiology and Immunization at 617-983-6800.

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

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.

A. Contact the Massachusetts Bureau of Health at 617-624-6000 or contact the WNv hotline at 866-627-7968.

West Nile virus and Dogs and 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.

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.

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

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.

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 cannot 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 mosquitoes 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.

 

 References, Bibliography, Notes