Overkill: Why Pesticide Spraying for West Nile Virus in California ...

Pesticide WatchMatt Wilson, Toxics Action Center

Will Sugg, The Maine Environmental Policy InstituteJasmine Vasavada, Pesticide Watch

August 2003

OverkillWhy Pesticide Spraying forWest Nile Virus in CaliforniaMay Cause More HarmThan Good

Acknowledgments

The most important person to acknowl-edge in this paper is Rachel Carson. Herbook Silent Spring is the wellspring fromwhich this continuing work to protect thepublic from toxic pesticides flows.

This report is heavily indebted to ear-lier editions that described problems withpesticide spraying for West Nile Viruscontrol in Maine and Massachusetts. TheMaine Environmental Policy Instituteboard of directors (Kevin Mattson, TomFederle, Matt Scease, and Susie O’Keefe)supported the first edition, which ben-efited from the careful review of HeatherSpalding, Rob Baldwin, Mitchel Cohen,Sharon Tisher, RusselI Libby, KathleenMcGee, George and Laura Appell, PaulDonahue, Mitch Lansky, Will Everitt,Kim DeFeo, and Elizabeth Spalding.Without their advice and generosity thisreport would not have been possible.

Dr. David Ozonoff, Rachel Zegerius,Sue Phelan, Stephen Seymour, EllieGoldberg, Sarah Little, Monica Garlick,and Aimee Qui provided significant in-sights and review of the report’s Massa-chusetts edition.

Pesticide Watch gratefully acknowl-edges Gina Solomon, M.D., M.P.H.,Natural Resources Defense Council forher review and comments, Dave Hensonof the Occidental Arts and EcologyCenter for his insights, and Cornell

“We should no longer accept the counsel of

those who tell us that we must fill our world with

poisonous chemicals; we should look about and

see what other course is open to us.”

Rachel Carson, Silent Spring, 1962

University Professor David Pimentel forhelping navigate the scientific literature.Also, thanks are due to Tony Dutzik andBrad Heavner of the Frontier Group ofthe State PIRGs who provided keen edi-torial oversight.

Some groups and resources stand outas being particularly valuable to anyoneresearching this issue, and to us in par-ticular: the No Spray Coalition of NewYork; Northwest Coalition for Alterna-tives to Pesticides; Pesticide Action Net-work of North America; ExtensionToxicology Network; EnvironmentalRisk Analysis Program (ERAP) ofCornell University Center for the Envi-ronment; and Rachel Massey and PeterMontague of the Environmental Re-search Foundation.

In addition, we would like to acknowl-edge numerous scientists and public edu-cation staff at California mosquito andvector control agencies who pro-vided␣ timely, localized information aboutpreparations for West Nile Virus alreadyongoing in the state. In researching thisreport, we found that these men andwomen, on the front lines of protectingpublic health from West Nile Virus inCalifornia, are highly sensitized to therisks entailed by indiscriminate pesticidespraying, and are working hard to edu-cate and activate the public to help takepreventative measures before the virusarrives in the Golden State.

Thanks also to Harriet EcksteinGraphic Design.

This report was made possible by thegenerous support of Pesticide Watch’scitizen members. The recommendationsare those of Pesticide Watch, who alonebears responsibility for any factual errors.

© 2003 Pesticide Watch Pesticide Watch is a grassroots non-profit organization dedicated to turning the toxictide of pesticide use in California while pioneering new strategies for empowering communities to protect themselvesand their local environment from the hazards of pesticides.

Table of ContentsExecutive Summary 5

Introduction 7

Background 9Transmission of West Nile Virus 9The Westward Spread of West Nile Virus 10The Public Health Impact of West Nile Virus 10

Preparing for West Nile Virus in California 13West Nile Virus in California? 13California’s West Nile Virus Surveillance and Response Plan 15California’s Pesticide Spray Policy 18Federal Guidelines 18The Role of Local Agencies in Mosquito Control 19

Pesticide Spraying May Do More Harm Than Good 21Pesticide Spraying Is Not Proven Effective in Curbing Human Infection Rates 21Effectiveness of Spraying in Controlling Mosquito Populations Is Limited 22Pesticide Spraying Could Make West Nile Virus Worse 23Pesticides May Kill Off Natural Mosquito Predators 24Pesticides Can Make Animals More Susceptible to WNV Infection 25Pesticide Spraying May Reduce Participation in Other Important Public Health Measures 26Pesticide Spraying Entails Significant Risk of Public Exposure 26

Known Health and Environmental Impactsof Pesticides Approved for Use in California 27Pyrethroids 27Organophosphates 29Larvicides 34Biopesticides 36

Unknown Health Impacts of Mosquito Control Pesticides 38“Inert” Ingredients Escape Public Disclosure 38Pesticides Are Not Proven Safe 39

Balancing the Risks 41Principles for Safe, Effective Mosquito Control Measures on the State and Local Level 43Give Public Health, Not Pesticides, the Benefit of the Doubt 43To Protect Public Health, Prioritize Alternatives to Pesticide Spraying 43Steps Individuals Can Take 45

Appendix: California Mosquito Control Contacts 49

Endnotes 55

4 Overkill: Pesticide Spraying in California

Introduction 5

Executive Summary

S ince its emergence in New York Cityin 1999, West Nile Virus (WNV)has spread rapidly across the United

States. The disease, borne by wild birdsand transferred to humans by bird-bit-ing mosquitoes, is likely to reach Cali-fornia shortly. If and when WNV doesarrive, California communities must beprepared to respond in a manner that pre-vents harm to human health and the en-vironment. In doing so, California canand should avoid the massive pesticidespraying programs that have been trig-gered in other states at the first sign ofWest Nile Virus.

Broadcast pesticide spraying, by truckor aerial application, has not beenproven effective in curbing WNV:

• The Centers for Disease Control andPrevention have stated that groundand aerial spraying targeted at adultmosquitoes is one of the least effec-tive mosquito control techniques.

• Northeastern communities (Boston,NYC) that first responded to WNVwith massive spraying subsequentlyscaled back their use of adulticides,

prioritizing preventative measuresand establishing stricter criteria tolimit adulticide spraying.

• Despite three years of widespreadspraying to control WNV, no scien-tific studies have demonstrated thatsuch spraying has effectively reducedthe human risk of infection.

Spraying may cause more harm thangood:

• Pesticide spraying may actuallyincrease the number of mosquitoesby killing off insect predators such asdragonflies that feed on mosquitoesand their larvae.

• Pesticide spraying may increaseinfection rates by leading mosquitoesto develop resistance, live longer,exhibit more aggressive bitingbehavior, and become more suscep-tible to infection by WNV.

• Pesticide spraying may create a falsesense of security, diminishing publicparticipation in preventative publichealth measures that are necessaryto effectively reduce the risk of


contracting WNV. Such measuresinclude wearing protective clothingand helping reduce mosquito habitatby eliminating stagnant water thatserves as a breeding ground formosquitoes.

Pesticide spraying will expose humanbeings and nontarget organisms tochemicals known to affect humanhealth and the environment:

• For spraying to be effective at all, itmust be timed during the hourswhen the mosquitoes are most active(for most species, the early evening).However, these same times entail thegreatest risk of exposure to thegeneral population.

• The chance of any one individualbecoming seriously ill from exposureto West Nile may be significantlylower than an individual’s chance ofbecoming ill from pesticide exposure.For example, in 1999 there were 59known cases of meningitis due toWNV infection in New York City,and 187 individuals who reportedexperiencing illness after malathionexposure.

California’s current West Nile VirusResponse Plan is overly permissive ofdangerous and ineffective pesticidespraying:

• Current pesticides approved formosquito control in the state includeorganophosphates (malathion) and

pyrethroids (Pyrethrin, Sumethrin,Resmethrin) known to have serioushuman health impacts.

• Human health risk assessmentstudies, conducted to show thesepesticides are theoretically "safe" ifapplied correctly, routinely fail toaccount for errors in applicationrates and vulnerability of certainpopulations, such as infants and theelderly.

To ensure minimal environmental andhuman health impact, and maximumeffectiveness in mosquito control, thestate plan should be revised to:

• Include strict parameters limitingthe use of health-threateningpesticides.

• Include specific benchmarks to helppromote public outreach, communi-cation, and education activitiesessential for a preventative publichealth strategy.

In addition, local mosquito and vectorcontrol agencies, which will have signifi-cant decision-making power to chooseamong mosquito control options, shouldimmediately initiate a public process inwhich concerned community memberscan be involved in outreach and educa-tion about mosquito prevention activitiesas well as the establishment of strictlocal thresholds to reduce or eliminatethe use of pesticide sprays in mosquitocontrol.

Introduction 7

Introduction

If and when West Nile virus hits

the West Coast, officials are

prepared to pull out the big

guns. California mosquito

control, now quelling larvae

with environmentally

compatible hormones and

bacteria, would expand to

include air and ground spraying

with insecticides to kill adult

mosquitoes, a state health

official said.

Wall Street Journal Aug 13, 20021

The mosquito-borne West Nile Virushas traveled across the nation asfar as the Rockies and Washington

State, and is expected to eventually reachCalifornia. When it does, local leadersand mosquito vector control districts maybe sorely tempted to “pull out the bigguns,” supplementing normal mosquitocontrol programs with widespread aerialand ground spraying of toxic pesticides.Considering the toxicity of such pesti-cides to human beings, the ecologicaldamage they may cause, and their lack ofproven effectiveness in curbing WestNile, mounting such an offensive maypose a greater threat to public health thanthe West Nile Virus itself.

As the disease has spread rapidlythroughout the nation, states and munici-palities have been forced to scramble todevelop emergency control plans formosquitoes. Too often, this crisis man-agement has relied on spraying entireneighborhoods, fields, and water bodiesin an attempt to wipe out adult mosqui-toes.

Only after the initial crisis has subsidedhave health officials and local leaders


taken time and resources to develop ef-fective control plans emphasizing mos-quito surveillance, prevention, and publiceducation—and ensuring a response ap-propriate to the level of risk that WestNile Virus actually poses to most people.

Fortunately, California communitiesare in a unique position to avoid the over-kill that has characterized the responseto West Nile Virus in so many parts ofthe country. California has had time to ab-sorb the lessons from WNV control inthe northeastern and Gulf states. Further-more, California has a robust infrastruc-ture in place to prevent mosquito-bornediseases, several of which are endemic tothe Golden State.

More than 50 mosquito control dis-tricts have been established throughoutthe state, with budgets ranging from sev-eral hundred thousand to several milliondollars. These districts rely on guidelinesfrom the California Department ofHealth, which has designed a West Nile

Virus response plan focused on preven-tative measures that limit the need forpesticide spraying—prioritizing elementsof an ideal strategy to effectively controlmosquito populations while minimizingthe spraying of harmful (and largely in-effective) pesticides.

While the state plan includes guidanceabout how to determine when pesticidespraying is appropriate, local agencies areleft to decide when and where to do so.Ultimately, community leaders, healthexperts, and concerned citizens will needto work on the local level to ensure thatthe agencies, and the public, are notforced to make a false choice between“doing something” to stop WNV byspraying pesticides, or allowing West Nileto spread by not using pesticides. Rather,the true choice is between addressingWest Nile Virus with rational controlmeasures that have been proven effectiveor spraying pesticides that may do moreharm than good.

Background 9

Background

The 2002 WNV epidemic in the

U.S. was the largest arboviral

meningoencephalitis epidemic

documented in the Western Hemi-

sphere and the largest reported

WNME [West Nile Meningoen-

cephalitis] epidemic. Epizootic and

epidemic activity was most intense

in the central U.S., especially in the

Great Lakes region, and extended

to the West Coast [indicating]

complete transcontinental

movement of WNV within 3 years.

Centers for Disease Control, Morbidityand Mortality Weekly, December 20, 2002

Figure 1. West Nile Virus Transmission Cycle

Transmission of WNVMosquitoes transmit WNV to humansafter biting infected birds, the primaryhosts of WNV. In addition to humans,horses, bats, and other small mammalscan all serve as alternate hosts. There issome evidence that amphibians such asfrogs can host WNV as well.2 The WNVtransmission cycle is depicted in Figure 1.

WNV is in a family of arboviruses (ar-thropod-borne viruses). It is closely re-lated to Western Equine encephalitis andSt. Louis encephalitis, mosquito-bornediseases for which many states have alreadydeveloped mosquito control programs.


Indicates verified human disease case(s)Verified avian, animal, or mosquitoinfections during 2003

Figure 2. West Nile Virus in the United States asof July, 2003

The Westward Spreadof West Nile VirusWNV originated in Africa, from whichit spread to the Mediterranean, theMiddle East, and parts of Asia. In 1999,it emerged in the Western Hemispherefor the first time in New York City. In-fected wild birds carried the disease upand down the Eastern Seaboard, thenwestward through the Gulf States and upto the Rockies.4 By the end of 2002,WNV had been detected in 2,289 coun-ties in 44 states across the US, an increasefrom 359 counties in 27 states and Wash-ington, D.C. in 2001.5

Experts now believe WNV will neverbe eradicated from the United States butrather will become endemic throughoutthe country in areas where related ill-nesses such as Western Equine encepha-litis and St. Louis encephalitis are found.According to the Centers for DiseaseControl and Prevention (CDC), from1964 to 1998, there were 122 confirmedhuman St. Louis encephalitis cases inCalifornia.

Over the past three years, WNV hasdemonstrated its ability to adapt to dif-ferent types of mosquitoes — the vectorsthat transfer the virus from one host to

another — allowing WNV to thrive inIllinois’ long summer days as well as thehot, humid weather of Louisiana, Mis-sissippi and Texas.6 The map in Figure 2depicts states where infected birds, mos-quitoes, or animals have been discoveredas of July 2003.

The Public Health Impactof West Nile Virus

Rates of Human Infection by WNVAs the disease has spread across the coun-try, the number of people infected byWest Nile has also steadily increased.From 1999 to 2001, the CDC confirmed149 cases of human illness and 18 deathsattributed to WNV. Last year, as the dis-ease traveled to the Midwest and South,the number of laboratory-confirmedhuman infections grew to 4,156, includ-ing 284 deaths.7

In 2002, the Midwest was especiallyhard hit by WNV. A provisional analysisby the CDC estimated that 5 states ex-perienced 64% of the nation’s knownWNV illness in 2002: Illinois, Michigan,Ohio, Louisiana, and Indiana. The firstfour of these states, together with Texas,accounted for 67% of reported meningi-tis resulting from West Nile infection.8

The data show that WNV poses asmall but real risk to the general popula-tion. In New York State, where the dis-ease first emerged, studies showed thatless than one-tenth of one percent ofpeople bitten by infected mosquitoesevinced any symptoms of the disease, andeven fewer exhibited serious symptomssuch encephalitis or meningitis, in whichthe brain or its casing becomes inflamed.9

A Louisiana study found that in St.Tammany Parish, eight people in 100,000showed any WNV symptoms (also lessthan one-tenth of one percent), but of

Background 11

those, a significant number developedencephalitis, and the risk of death was 4in 1 million.10

In general, elderly and immuno-com-promised individuals face the greatest riskof serious illness associated with a WestNile infection. According to a CDCanalysis of WNV cases from Januarythrough November 2002, the median ageof WNV-infected people was 55 years,and the median age of people who expe-rienced meningitis was 59 years. Of the2,354 people with meningitis, 199, or 9%,died; in addition, 2 elderly people (morethan 80 years old) died of the normallyless-serious West Nile Fever. The medianage of those who died from West Nile-associated illness was 78 years.11

Many believe that these infection rateswill subside as West Nile Virus becomes“endemic” to the United States, and willbe characterized by low baseline infec-tion rates interrupted by sporadic out-breaks. In Africa, where West Nile Virushas been recognized for more than sixtyyears and where it is widespread, very fewhuman epidemics have been identified.The same has been observed in theUnited States with related infections,such as St. Louis encephalitis and East-ern equine encephalitis, where 30 or moreyears may pass between human outbreaks.

New York City’s Experience withWNV and Mosquito ControlIn the summer of 1999, a physician noteda cluster of patients in Queens, New YorkCity, who were thought to be infectedwith St. Louis encephalitis. This was laterdetermined to be WNV, the first knownemergence of the disease in the UnitedStates.12

City officials, lacking a robust mos-quito control plan, followed CDC rec-ommendations to embark on an aerialinsecticide spraying program. A $5 millionprogram of repeated aerial applications

of malathion, a pesticide related to chemi-cals developed for military use in WorldWar II, ensued. Some neighboring coun-ties sprayed heavily as well, some even inthe absence of confirmed human infec-tion. Other counties did not spray.

This emergency management measureoccurred with minimal assessment of therelative risks to human health associatedwith exposures to the sprayed insecticidesversus those of contracting WNV. In-deed, little was known about WNV orwhether the outbreak could be limitedgeographically by intensive aerial spraying.

During the first spray season, 187people reported health symptoms asso-ciated with malathion exposure to NewYork City’s Poison Control Center.13

In 2000, after significant public oppo-sition to aerial spraying and hundreds ofcomplaints from people reporting pesti-cide exposure, the NYC Health Depart-ment switched from its aerial campaignto largely ground-based spraying of An-vil, a pyrethroid.14 A private contractorhired by the city sprayed this pesticide(which consists of the active ingredientssumithrin and piperonyl butoxide) in atwo-mile radius around places whereWNV infections or infected dead birdswere reported.

By 2001, new data indicated that spray-ing should be further restricted to a one-mile radius, and even then only as a “lastresort.” Furthermore, city officialsswitched to an emphasis on prevention.“While last year we had a formulaic andsomewhat reflexive approach . . . this yearwe’re going to look very carefully to de-termine where the greatest risk to peopleis,” City Health Commissioner Dr. NealCohen told a New York Post reporter.15 Ina separate interview with the New YorkTimes, city officials stated: “To reduce thereliance on pesticides in the battle againstWest Nile virus, the city will use a moreconservative, concentrated approach tospraying this summer.”16


Infection Rates Case Study:A Closer Look at NYC

Surveys of blood samples taken from NewYorkers have revealed that many peopleinfected with the virus never evinced anysymptoms. A New York City Health De-partment survey of blood samples takenfrom people who lived in northernQueens, the epicenter of the 1999 out-break, showed that 19 out of 677 testedpositive for the virus, but none had be-come seriously ill, and all either reportedno symptoms or mild illness, such as alow-grade fever.

The survey’s statistical analysis con-cluded that between 1.2 percent and 4.1percent of the 46,000 residents (533 and1,903 people) in that three-square-milearea had probably been infected. Of theinfected group, four people in the sample

had non-specific aches, pains or fever.The others presented no symptoms.17

However, some people did become illfrom WNV, and some deaths were re-corded. Out of New York City’s popula-tion of more than 7 million, 62 people —or less than .0009% — became ill withthe virus, and 7 died (one in one million).

While this is a real and quantifiablepublic health impact that should not bedismissed, one must question whether thepesticide spraying campaign that NewYork City embarked upon was an appro-priate response to the West Nile threat.

A comparison of WNV infection ratesto rates of influenza in New York City in1999 can provide some context, reveal-ing that 2,474 individuals in New YorkCity died from influenza or pneumoniain 1999, representing 400 times the num-ber of WNV mortalities.18

Preparing for WNV in California 13

WNV in California?Given the rapid spread of WNV in thethree years since its introduction on theEast Coast, it is likely that WNV willarrive here this summer.

To date, no wild birds, sentinel chick-ens, or mosquito pools have testedpositive for WNV in California. Oneknown instance of human infection hasbeen documented. However, since theperson lived near Los Angeles Interna-tional Airport and no other tests haverevealed the presence of WNV, this in-fection is generally attributed to a bitefrom an infected mosquito that arrivedon board an airplane.

California is home to more than 40mosquito species. The state’s urban areas,coastal bays and wetlands, and the drain-age ditches and irrigation canals of theCentral Valley provide a range of potentialhabitats. Laboratory experiments haveindicated that several California speciesare likely to transmit West Nile Virus.

While mosquitoes are found in all partsof the state, officials have noted thatsouthern areas, such as the Imperial Val-ley and Riverside County, have been most

Preparing for WNV in California

We fully expect that, over time,

the virus will make it to the West

Coast. What the timing of it will

be is unknown at this time. It’s

unknown whether the virus

will make it to California or the

West Coast this year or next

year or the year after that. It’s

completely a matter of conjecture.

Dr. Peterson, Medical Epidemiologist,CDC Center for Infectious Diseases19


Figure 4: Culex pipiens, the housemosquito

Figure 3: A NASA-funded study mappedsatellite imagery of temperature andvegetation to help predict where WestNile virus will spread.

Phot

o: C

ourt

esy

of C

DC

Phot

o co

urte

sy o

f NA

SA

Culex pipiens, the “housemosquito”In residential and urban areas, the com-mon house mosquito, C. pipiens, is ex-pected to play a significant role as well.C. pipiens has been the primary WNVvector in much of the nation, and breedsin stagnant, standing fresh water. It canbe found in high concentrations atsewage treatment plants and often livesunderneath buildings, in storm drains,and in catch basins. It bites primarily inthe evening and after dark, and is not ac-tive in daylight. Because C. pipiens rarelytravels distances greater than a half mile,local efforts to eliminate breeding sitescan play a major role in controlling hu-man health impacts.

Ochlerotatus squamigerThe salt marsh mosquito, Ochlerotatussquamiger, inhabits coastal regions fromSonoma County down to the Baja pen-insula. Unlike Culex species, this mos-quito breeds in brackish tidal waters. Astrong flyer, it easily reaches nearby cit-ies during its early morning and late af-ternoon flights, and is considered asignificant nuisance in cities like SanFrancisco.24 Preliminary studies show itis not as readily infected with WNV asC. pipiens. However, it is of concern dueto its abundance and more aggressive bit-ing behavior.

vulnerable to other forms of mosquito-born encephalitis, and are therefore likelyto be most vulnerable to WNV as well.20

Culex tarsalis, the “encephalitismosquito”In the western United States, Culextarsalis is the primary carrier of WesternEquine encephalitis and St. Louis en-cephalitis, and is therefore expected to bea significant vector of WNV should itarrive in California. This mosquito,which bites mostly between sunset andmidnight, has been shown in laboratoryexperiments to readily become infectedby and transmit WNV.

C. tarsalis is especially abundant in theCentral Valley and coastal regions. It canlive in all but the most polluted waters,ranging from wetlands and salt marshesto puddles and containers. In most placesC. tarsalis is most active in the spring andfall, but in Southern California it is ac-tive all winter long.21 After years of in-tense efforts to keep this endemic speciesunder control, vast populations in theCentral Valley have become resistant tonearly all the common chemical insecti-cides.22

In populated areas, other species suchas Culex quinquefasciatus and Culex pipiensare also expected to play a significant rolein the transmission of WNV.23


“‘Carpet bombing, like what some states have done, would be our last resort,’ and only

‘if the powers that be agree that it’s necessary to protect human life.’”

Ted Toppin, Spokesperson, Mosquito and Vector Control Association of California, Boston Globe April 3, 200325

Mosquito Surveillance: Because mos-quitoes are the vectors of viruses like WestNile Virus, monitoring mosquitoes pro-vides a somewhat accurate estimate of theimmediacy of risks to humans. Mosquitoesare tested using fixed trap sites. Thesesites provide information regardingmosquito numbers, virus prevalence andestimation of WNV risk. More intensivemosquito trapping will be employed inresponse to increased virus activity in spe-cific areas.

Sentinel Chickens and Wild BirdSurveillance: WNV is fatal to birds, witha particularly high mortality rate inAmerican crows. Therefore, dead birdsare potential indicators of virus activityin an area, and bird reporting and testingwill be an important component ofCalifornia’s efforts. Approximately 200chicken flocks, known as “sentinel chickens,”are strategically placed throughout thestate and are tested routinely during themosquito season to detect evidence ofinfection from West Nile and other re-lated viruses.

In addition, the California AnimalHealth and Food Safety Laboratoryscreens dead wild birds and sends tissuesamples to UC-Davis and the Depart-ment of Health Services for testing.25

Equine Surveillance: Because manyhorses are vaccinated against virusesborne by mosquitoes, they are not theideal species to study to keep track of thespread of these viruses. Veterinarians arecontacted annually by DHS and theCalifornia Department of Agriculture(CDFA) to ensure that horses are vacci-nated and to describe diagnostic services

California’sWest Nile Virus Surveillanceand Response Plan

Following the West Nile outbreak inNew York in 1999, California leaders rec-ognized the need to update the state’smosquito control strategy to ensuredetection and prevention of the spreadof WNV.

The state plan was developed in a jointeffort of the California Department ofHealth Services (DHS), the Mosquitoand Vector Control Association of Cali-fornia (MVCAC), and the University ofCalifornia at Davis and Berkeley. It pro-vides guidelines for local agencies to usein responding to the WNV threat.

This plan, available on the Web atwestnile.ca.gov/CA_WNV, emphasizespublic education, prevention, and moni-toring as critical strategies to effectivelyreduce the risk of WNV while minimiz-ing the use of harmful pesticides. However,the plan does not rule out or set strictthresholds to limit the systematic broad-cast of pesticides to kill adult mosquitoes.

Mosquito Monitoring andSurveillanceMonitoring and surveillance are the firstline of defense against mosquito-borneillnesses. California’s mosquito controlplan includes an extensive monitoring andsurveillance network to ensure promptdetection and identification of WNV.Such surveillance can play a critical rolein helping towns and counties avoidunnecessary spraying. California’s sur-veillance plan includes the following:


Figure 5: Mosquitofish feed on mosquitolarvae

Biological ControlsBiological control entails the intentionaluse of natural predators or parasites tocontrol mosquito populations. Accordingto the state Surveillance and ResponsePlan, the most widely used biologicalcontrol agent in California is theMosquitofish, which can be releasedannually in rice fields, small ponds, andcanals.

In addition, Bti and Bacillus sphae-ricus, two microbial control agents, arerecommended for use in larval control.Since these biological agents are appliedto treat water bodies in a manner similarto chemical pesticides, they are discussedfurther in the following section on chemi-cal control.

Chemical ControlIn addition to physical and biological con-trol measures, the State Mosquito ControlPlan explicitly lists a range of pesticides“approved for use” in California. Thesepesticides include adulticides, usually pes-ticide sprays, which target adult mosqui-toes, and larvicides, generally liquids thatare applied to the pools of water wheremosquitoes breed. Many of these insec-ticides are chemicals known to have sig-nificant impacts on human health andother organisms in the environment. Apartial list of pesticides “approved” foruse in California can be found in Table 1.

that are available in the event of a sus-pected case of WNV or related diseases,such as western equine encephalitis.

Human Surveillance: Specimens fromclinical human cases of encephalitis willbe screened in order to determine thepossible cause of infection. In addition,hospitals will be contacted in the geo-graphic areas of increased virus activity.

EducationThe Mosquito-Borne Virus Surveillance& Response Plan notes the importanceof public education in teaching peoplehow to protect themselves, and others,from WNV. It refers to the importantrole of residents, farmers, and duck clubowners in eliminating standing water, andthe need for education of the medicalcommunity. The plan does not make spe-cific prescriptions of how such educationshould be conducted, however.

Mosquito Control MeasuresThere are three general kinds of mosquitocontrol articulated in California’s plan:environmental management, biologicalcontrol, and chemical control.

Environmental ManagementPhysical control measures discussed inthe California plan include water man-agement and vegetation management.These include measures that increase thewater disposal rate through evaporation,recirculation, or drainage, as well as re-stricting growth of vegetation to decreasehabitat availability for immature mosqui-toes. These measures can be considered“source reduction,” since they decreasethe number of breeding sites for mosqui-toes. According to the CDC, such mea-sures are the most effective andeconomical methods of providing long-term mosquito control in many habitats.26

Phot

o co

urte

sy o

f CD

C


Table 1: Pesticides Approved For Use In California Mosquito Control Larvicides

Larvicides

Bacillus thuringiensis israelensis(BTI: e.g. Vectobac, Teknar)

Bacillus sphaericus (e.g. Vectolex)

Methoprene (e.g. Altosid)

Diflurobenzamide (e.g. Dimilin)

Larviciding oils (e.g. Golden Bear 1111,BVA Chrysalin)

Monomolecular Films (e.g. AgniqueMMF)

Adulticides

Organophosphates:

a. Malathion (e.g. Fyfanon)

b. Naled (e.g. Dibrom, Trumpet EC)

Pyrethrins (natural pyrethrin products:e.g. Pyrenone Mosquito Spray, Pyrocide)

Pyrethroids (synthetic pyrethrin productscontaining resmethrin or permethrin:e.g. Scourge)

Use: Approved for most permanentand temporary bodies of water.



Use: Impounded tailwater, sewageeffluent, urban drains and catch basins.

Use: Ditches, dairy lagoons, floodwater.Effective against all stages, includingpupae.

Use: Most standing water includingcertain crops.

Use: May be applied by air or groundequipment over urban areas, somecrops including rice, wetlands.

Use: Air or ground application onfodder crops, swamps, floodwater,residential areas.

Use: Wetlands, floodwater, residentialareas, some crops.

Use: All non-crop areas includingwetlands and floodwater.

Note: Many Cx. tarsalis populations in the Central Valley are resistant to label organophosphateapplication rates.

The plan acknowledges that some pes-ticides, such as organophosphates, shouldbe used infrequently because of their im-pact on non-target organisms and theenvironment, but does not expressly

limit the use of these pesticides, beyondstating that adulticides in particular areused “when larval control is not possibleor has been used to the fullest extentpossible.”


California’s PesticideSpray PolicyThe California Surveillance and Re-sponse Plan identifies three levels ofmosquito control in response to threelevels of threat: normal season, emer-gency planning, and epidemic conditions.

The plan states that adulticide spraying“may be recommended” as an appropri-ate response in the “emergency planning”stage, as determined by the followingindicators:

• Snow pack and rainfall aboveaverage;

• Significant increase in adultmosquito populations;

• One or more WNV isolationsfrom mosquitoes;

• One to three chickens carryingthe virus antibodies per flock of10 birds;

• One or two equine cases;

• One human case statewide;

• Viral activity in small towns orsuburban area; and

• Evidence of recent infection inwild birds.

However, the plan does not set a strictthreshold that must be reached in a com-munity before a mosquito control districtcan decide to spray. In the absence of suchthresholds, California mosquito controldistricts may be vulnerable to politically-motivated calls for spraying, potentiallyresulting in unwarranted application ofhazardous pesticides. They do not haveto prove that there is a public healththreat to conduct widespread spraying.

Like the federal guidelines, the stateplan leaves this decision in the handsof local mosquito and vector controldistricts.

Federal GuidelinesOn the federal level, the Centers for Dis-ease Control and Prevention, Division ofVector-Borne Infectious Diseases, hasdeveloped West Nile Virus responseguidelines for individual states to use.27

These federal guidelines for surveil-lance, prevention, and control of WNVhave changed with time, raising thethreshold at which pesticide sprayingshould be considered and placing moreemphasis on preventative measures.

In 2000, for example, the guidelinesrecommended chemical control (pesti-cide spraying) of adult mosquitoes withinapproximately a 2-mile radius around thearea where a WNV-positive dead bird orinfected mosquitoes were found.28 By thefollowing year, however, the CDC hadremoved this direct recommendation ofbroadcast spraying of adulticides. Theguidelines now state, “Control activityshould be initiated in response to evi-dence of virus transmission [to humans],as deemed necessary by local health de-partments.”29

These revisions acknowledged the factthat there is no truly objective evidenceto determine when and if spraying shouldoccur. “There is no simple formula fordetermining how large an area to treataround a positive surveillance indicatoror a suspected or confirmed human caseof WNV. Nor is there adequate informa-tion to determine the degree of vectorpopulation suppression that must be at-tained, or for how long this suppressionmust be maintained to reduce risk of dis-ease.”

In the absence of scientific evidence tosupport a specific spray policy, the revisedfederal guidelines give state and localofficials significant flexibility in determin-ing how large an area to treat around apositive surveillance indicator or a sus-pected or confirmed human case ofWNV, or even whether to spray at all.


East Bay vector control districts already are doing their part.

Wednesday, a team of all-terrain vehicles sprayed a flooded

pasture in Bethel Island, while a helicopter dropped insecticide

pellets into blackberry thickets and other hard-to-reach areas.

News report on March 14, 2003 in Contra Costa Times30

Figure 6. Organizational Flow Chart of a Mosquito Control District(www.mosquitoes.org/PDF/Prog99.pdf:)

The Role of Local Agenciesin Mosquito ControlIn California, mosquito control is con-ducted by more than 70 local agencies.This includes 53 mosquito and vectorcontrol districts, servicing areas inhabitedby 80% of the state’s population, anddozens of environmental health andcounty health departments. In areas with-out defined vector-borne disease controlprograms, the California Department ofHealth Services provides oversight.

These local mosquito control districtshave significant leeway to decide to de-fer pesticide spraying even if “EmergencyConditions” specified by the state planare met. Conversely, these agencies havesignificant leeway to increase use ofchemical pesticides even before a knownthreat has emerged. Many of these districtsroutinely spray pesticides to control mos-quito populations, even in the absence ofan “emergency” situation.

Mosquito Control Districts operateunder Sections 2200-2398 of the Healthand Safety Code of California. They de-velop mosquito control plans based onguidelines developed by the CDC and theCalifornia Department of Health Ser-vices, which outline acceptable mosquito

control practices and pesticide usages.They also report pesticide use to theCounty Agricultural Commissioner eachmonth.

Mosquito control districts typicallycover half a dozen or more municipali-ties, and many have a county-wide juris-diction. They are governed by boards oftrustees comprised of representatives ap-pointed from each member city and thecounty at large. In most districts, theBoard of Trustees oversees the fiscal ad-ministration of the organization butleaves day-to-day operation and decision-making in the hands of the District Man-ager. (See Figure 6.) Funding is providedby a combination of property taxes andother special taxes authorized by localvoters. For a complete listing of Califor-nia Mosquito Control Districts and con-tact information, see Appendix A.

AdministrativeAssistant

DistrictManager

Support StaffEnvironmental Specialist

Equipment & Facilities SpecialistEntomological Specialist

Systems Specialist

Control StaffAssistant Mosquito Control Technician, Mosquito Control Technician, Vector Biologist

Board of TrusteesOne from each incorporated city and one from the County


Local districts have considerabledecision-making power in choosing touse, or refrain from using, pesticides. TheAlameda County Mosquito and VectorControl District (CMVCD) is particu-larly open about its decision-making pro-cess, which is outlined in the Control Planposted on its Web site.

In 2002, the Alameda CMVCD re-ported “regularly using” methoprene andlarvicides, and “occasionally using” theadulticides pyrethrins, resmethrin, andpermethrin. In fact, adulticides, totalingless than 1 ounce, were only applied ontwo occasions in that year.

The following is an excerpt from theircontrol plan, available on the web atwww.mosquitoes.org/PDF/Prog99.pdf:

The District uses a phased approachto pesticide treatments. In the choice ofmaterial to use District personnel willuse the material with the least impactto control larvae and as a last resort,localized adulticiding may be chosen.In general this progression of choiceswould be:

2Bti, Duplex (Bti + methoprene),Methoprene, Oil or Agnique, Pyre-throids

Decisions on where and when totreat are based on thresholds....Thesethresholds are meant to be guidelinessince each site is different and otherfactors play a role in the levels of

mosquitoes that can be tolerated. Someof these factors are as listed:

• The proximity of homes or heavyhuman use areas to the source.

• The age and distribution of theimmature mosquitoes in a source.

• The number of mosquito servicecalls attributed to the source fromprevious seasons.

• The expected weather conditionsand the season of the year.

• The accessibility to the source(including special restrictions).

• The pest or disease significance ofthe mosquito to be controlled inthe source.

• The size of the source (staff andequipment needs increase withsize).

• The sampling method used tocheck the source.

• The number of active sources andavailable personnel and equipment.

We surveyed Web sites of 20 mosquitocontrol districts, finding that controlplans are generally not posted on theirWeb sites. However, these plans are pub-lic information and should be availableupon request.

Pesticide Spraying 21

Pesticide Spraying May DoMore Harm Than Good

Pesticide SprayingNot Proven EffectiveIn Curbing HumanInfection RatesDoes spraying pesticides to kill mos-quitoes have a significant impact on thetransmission rates of the West Nile Virus?Does spraying prevent more illness thanunintended pesticide exposures cause?

Despite three years of potential data,in which pesticide spraying was used inan attempt to stop the spread of WNV,these are critical questions that have notbeen answered by scientific study. At themoment, given the relative lack of knowl-edge about WNV, the Centers for Dis-ease Control and Prevention are notconducting the statistical analysis neces-sary to identify the effect of insecticidespraying on infection rates in communi-ties throughout the country. In fact, fewstudies have even been conducted to an-swer a simpler question: How effective isspraying at killing targeted mosquitoes?

The average person thinks the

way you control mosquitoes is you

spray for them. That’s absolutely

not true. Spraying is a last, last

resort.

Dr. Wayne J. Crans, Director of MosquitoResearch and Control at Rutgers University,New York Times, Sept 8, 199931


Effectiveness of Spraying inControlling MosquitoPopulations is LimitedOne study conducted by the Connecti-cut Agricultural Experiment Station in2002 found that mosquito populationsdid not drop notably after trucks sprayedpesticides in the cities of Greenwich andStamford.33 However, very few studieshave been conducted to document theeffectiveness—or lack of effectiveness—of pesticide spraying in curbing mosquitopopulations under real-word conditions.

Most studies on the impact of pesti-cide spraying are performed under out-door “lab” type conditions. In suchstudies, caged mosquitoes are placed atmeasured distances from spraying, at dif-fering pesticide potencies. Some cage-trap experiments in residential areas haveshown a reduction in mosquito popula-tions of about 30 percent after a spraying.34

Such studies, however, may overesti-mate the effectiveness of spraying sincethey do not take into account the manyvariables that are involved in groundspraying. Real-world mosquitoes are nottrapped in one place. Rather, they canhide under leaves and in vegetation. As aresult, extrapolating the efficacy numbersfrom cage or trap studies to actual spray-ing programs is questionable.

“In order to work, the insecticide musthit the mosquito directly,” Cornell Uni-versity researcher Dr. David Pimentelreported in a November 2000 interviewwith Newsday. “But since spray trucks areonly fogging the street side of buildings,

I doubt that more than one-tenth of 1percent of the poison is actually hittingits target. And you have to put out a lotof material to get that one-tenth of apercent onto the mosquito.”35

In fact, scientists have estimated thatless than 0.0001% of ULV (Ultra LowVolume) pesticide sprays actually reachthe target insects.36 So for every dropletthat reaches a mosquito, hundreds ofthousands more droplets circulate point-lessly in the environment.37

The CDC has also noted that, “groundapplications are prone to skips and patchycoverage in areas where road coverage isnot adequate or in which the habitat con-tains significant barriers to spray dispersaland penetration.”38

In a 1998 study, it took two to threetimes more insecticide to kill 90% of themosquitoes in residential settings than ittook to kill 90% of the mosquitoes inopen areas. Spraying high enough levelsof insecticide to kill most of the mosqui-toes in residential areas would require vio-lating current labeling safety guidelines.39

Many factors decrease the effectivenessof pesticide spraying in urban areas. Forexample, the West Nile Virus AdvisoryGroup to Cambridge, MA has pointedout the following factors:

• Most mosquitoes prefer to bite birds,particularly birds at rest, of whichthere are few in the street andbuilding-front areas at the time thespray is applied.

• Mosquitoes may be located inroosting areas that are higher thanthe reach of the spray.

There’s not enough evidence that all this spraying has changed the dynamic of the

outbreak, and that’s in part because the studies really haven’t been done to find out.

Michael Hansen, the chief pesticide researcher at Consumers Union, which publishes Consumer Reports magazine,Newsday, November 7, 200032


You’re going to see a resistant strain of these insects. It’s like every time you get the sniffles,

you don’t use an antibiotic. We’re running out of those. You want to use the worst treatment

for the worst cases—you don’t want to use the extreme approach if the risk is not that high.

Sheldon Krimsky, Professor of Urban and Environmental Policy, Tufts University42

• Buildings and trees close to the streetmay block the spray from spreadingto reach mosquito habitat.

• Backyard roosting areas are noteffectively reached because closespacing of buildings limits penetra-tion beyond the buildings.

• The period that the spray is effectiveand airborne is of relatively shortduration.40

Furthermore, in many places mosqui-toes may already be resistant to pesticidesapplied at health-protective label rates.California’s Mosquito Control Plan notesthat mosquitoes in the Central Valleyhave now developed sufficient resistanceto organophosphates like malathion thatspraying at the levels permissible undercurrent labeling requirements is ineffec-tive.

Too often, agencies will assume a highrate of effectiveness from spraying that isnever backed up with experimental veri-fication. For example, Deputy Commis-sioner Carl Johnson of the New YorkState Department of EnvironmentalConservation, which regulates pesticideuse around the state, told reporters thatlocal governments had anecdotally re-ported “60 to 80 percent reductions” af-ter spraying.

Yet although New York City HealthDepartment researchers told reporters inNovember, 2000, that they were conduct-ing studies to determine the effectivenessof pesticide spraying in WNV control,such studies have not been released to the

public. As of June 6, 2003, a health de-partment official told Pesticide Watchthat the data were still being analyzed,and may be available to the public in fourto six weeks. Three weeks later, the sameofficial reported that the principal inves-tigator had resigned, delaying the study’srelease indefinitely.41

Pesticide Spraying CouldEven Make WNV WorseSpraying pesticides for mosquito controlmay be worse than ineffective—it mayeven make the West Nile virus situationworse, contributing to higher infection rates.

Pesticide spraying may buildresistance, leading to resurgenceof mosquito-borne diseaseEcologist Garret Hardin has stated that“every biocide selects for its own failure.”This means that mosquitoes can and willbecome resistant to chemical efforts todestroy them. Overuse of pesticides maycreate resistant super-mosquitoes thatrequire ever increasingly toxic chemicalsto kill them.43

Few studies have been conducted todocument the actual impact of aerial andground adulticide spraying for West NileVirus control on mosquito resistance.However, there is documentation thatspraying may have contributed to a glo-bal resurgence in mosquito-borne diseaseover the last twenty years. The year be-fore West Nile emerged in the United


Figure 7. Pesticide spraying can increase populations of harmful pests.

States, a CDC researcher, Dr. DuaneGubler, wrote that while the factors con-tributing to this resurgence are complex,“the technical problems of insecticide anddrug resistance, as well as too much em-phasis on insecticide sprays to kill adultmosquitoes, contributed greatly to theresurgence of diseases such as malaria anddengue.” Furthermore, according to Dr.Gubler, the lack of emphasis on preven-tative measures “and emphasis on high-tech solutions to disease control have ledmost physicians, health officials, and thepublic to rely on ‘magic bullets’ to curean illness or control an epidemic.”44

Such “magic bullet” spraying targetedat Aedes aegypti, the mosquito species re-sponsible for spreading dengue fever, hasbeen ineffective at both controlling themosquito population and influencing thecourse of dengue epidemics. Though thismay be due to features of Aedes aegyptinatural ecology not shared by all othermosquito species, the fact that sprayingprograms of long standing were ulti-mately found futile indicates that pesticide

efficacy (not the simple of efficacy of kill-ing exposed mosquitoes but the broaderefficacy of controlling populations andcurtailing disease) is an open question witheach new climate/mosquito species/dis-ease combination that arises.

Pesticides May Kill OffNatural Mosquito PredatorsSpraying can increase mosquito popula-tions by killing off natural predators (fish,other arthropods, birds, etc.) of the mos-quitoes and their larvae, thereby remov-ing natural checks on population levels.

A 1997 study looked at trends in popu-lations of a mosquito primarily respon-sible for transmitting eastern equineencephalitis (EEE) among birds. Over aperiod of eleven years, Cicero Swamp incentral New York State was sprayed fifteentimes with the insecticide Dibrom(naled). Instead of declining, the mos-quito population grew fifteen-fold during

Phot

o: C

ourt

esy

of C

DC


this period. The study suggests that thepesticides may have altered the ecologi-cal balance of the swamp, killing organ-isms whose presence would ordinarilyhelp limit the mosquito population.45

Other studies have shown that spray-ing malathion, another pesticide ap-proved for mosquito control inCalifornia, may have similar results. Forexample, in California in the early 80s,widespread aerial applications of mala-thion were used in attempts to eradicatethe Mediterranean Fruit Fly, an agricul-tural pest. An observed increase in thepopulation of another pest, Old BlackScale, was attributed to the effect of thepesticide spray on beneficial insects. InFlorida, where malathion was also usedin an attempt to control Medfly infesta-tions, the spraying did not kill mosquitolarvae but did kill the larvae of an impor-tant mosquito predator, the dragonfly.46

Populations of scale insects on citrustrees exploded following medfly eradica-tion sprays in California. This occurredbecause parasitoids that normally keepscale populations under control werekilled by the malathion spray.

Pesticides Can MakeAnimals More Susceptibleto WNV InfectionLow level chemical exposures to pesti-cides can decrease the quality of animals’immune system function, leading some tospeculate that wildlife with compromisedimmune systems may be more susceptibleto becoming infected by encephalitiswhen bitten by an infected mosquito.

This in turn would increase the num-bers of formerly healthy mosquitoesdeveloping encephalitis (since theirchance of biting encephalitis infectedwildlife has also increased), contributingto the spread of the illness.

Studies have shown that impurities andby-products present in malathion canfurther disrupt immune system func-tion.47 Immunosuppression may enhancesusceptibility of mammalian systems tobacterial, viral, or parasitic infection orpossible increased tumor formation.48

Use of these pesticides for WNV mos-quito control could actually end up sup-pressing human and avian immunesystems in the areas sprayed, putting eachspecies at greater risk than before ofspreading, contracting, and becomingseriously ill from WNV.

Another theory, still untested, is thatmosquitoes that are sprayed but not killedmay themselves experience genetic dam-age that would increase their infectionrates—by weakening a stomach barrierknown to play a role in preventing readyinfection by the virus, for example.

Pesticide researcher Richard Pres-singer advanced this theory to help explainobserved increases in rates of encephalitisinfection among sentinel chickens inFlorida counties over the past decade.“Every time a mosquito spray plane ortruck sprays these proven geneticallydamaging pesticides over the area, theyare very likely increasing the amount ofsubtle genetic damage in the mosquitopopulation, and hence, increasing thenumber of mosquitoes with genetic flawswhich could in theory, allow the en-cephalitis virus to take hold and grow morerapidly,” he surmised.49

Some scientists have disputed Pres-singer’s theory.50 Clearly, more researchis needed to explain the increasing infec-tion rates despite widespread pesticidespraying.

Another way spraying can contributeto increased infection rates is simply byaggravating biting behavior. In an inter-view with the New York Public InterestResearch Group, Dr. Ray Parsons, whoheads the Harris County Mosquito Con-trol Division in Houston, observed that


pesticides or other chemicals. Further-more, many pesticides continue to bewidely used, despite large volumes ofclinical and laboratory evidence that ex-posure to these pesticides can have se-vere, sometimes fatal, human healthimpacts.

The Centers for Disease Control havenoted, “For adult mosquito control, in-secticide must drift through the habitatin which mosquitoes are flying in orderto provide optimal control benefits.” Thiskind of drift inevitably entails exposureto human populations if spraying is con-ducted in urban areas. Furthermore, sincemost mosquitoes are active nocturnally,spraying must occur during the eveninghours, times of maximum exposure tothose living in residential areas, for thespraying to have the desired impact onthe targeted mosquitoes.

Although public notification effortssuch as television broadcasts or reverse911 calls may caution listeners to remainindoors during spraying, the time ofspraying at any one location can be diffi-cult to predict and many people cannotor choose not to remain indoors all dayon the announced day of spraying. Fur-thermore, it is not easy to keep these pes-ticides from entering people’s homes.Indeed, outdoor air pollutants tend to ac-cumulate at higher levels indoors thanout.

Widely used adulticides such asmalathion (an organophosphate) and thesynthetic pyrethroids sumithrin (Anvil)and resmithrin (Scourge) have significant,well-documented, human health impactsthat are discussed in the following pages.

malathion may actually aggravate Culex,causing an increase in aggressive bitingbehavior for an hour or two after spraying.51

Pesticide Spraying MayReduce Participation inOther Important PublicHealth MeasuresWhen cases of WNV show up in Cali-fornia, citizens may understandably wantgovernment officials to “do something”to prevent them from being bitten byWNV-carrying mosquitoes. A massivespraying campaign runs the risk of givingresidents a false sense of security, encour-aging them to think they are less likely tobe bitten after the spraying, and less likelyto implement non-toxic preventativemeasures.

Pesticide Spraying EntailsSignificant Risk of PublicExposureAerial and ground spraying of pesticidesin urban and residential areas is of par-ticular concern due to the heightenedrisks of exposure to the general population.Whenever these pesticides are broadcast,there are unintended impacts on humanhealth and the environment. Even pesti-cides with relatively low acute toxicity toadults may pose a significant threat toyoung children with immature nervoussystems, asthmatics, the elderly, and otherindividuals with unusual sensitivities to

Health & Environmental Impacts 27

Known Health and EnvironmentalImpacts of Pesticides

Approved for Use in California

Pyrethroids“Pyrethroids” are a class of chemicalsmodeled on natural insecticides derivedfrom chrysanthemum flowers, called“pyrethrins.”52 Synthetic pyrethroid com-pounds vary in their toxicity, as do thenatural pyrethrins.

Many health effects of pyrethroid ex-posure have been well documented. TheCornell University Program on BreastCancer and Environmental Risk Factorsin New York State lists over 125 journalstudies on the health effects of pyre-throids on its Web site.53

Acute pyrethroid insecticide poisoningcan result in tremors, salivation, hyper-excitability, choreoathetosis (involuntarymovements), and seizures, as well asnumbness and tingling in exposed bodyparts, and gastrointestinal irritation wheningested.54

Despite these known human healthimpacts, synthetic pyrethroids such asresmethrin (sold under the trade nameScourge), sumithrin (sold under the tradename Anvil), and permethrin (sold underthe trade names Ambush or Pounce) havebeen widely used in mosquito control.

New Yorkers exposed to sumithrinwhen the compound was sprayed tocontrol for WNV reported symptomstypical of pyrethrum inhalation, includ-ing asthmatic breathing, sneezing, nasalstuffiness, headache, nausea, poor coor-dination, tremors, convulsions, facialflushing and swelling, and burning anditching sensations. The most severepoisonings have been reported in in-fants.55

A report in the New York Daily Newstold the story of a woman who wassprayed directly on the street in Manhat-tan with sumithrin who ended up in theemergency room after experiencingblurry vision, nausea, itching, coughing,choking and a swollen tongue. “I threwup three days in a row, I really thought Iwas going to die,” said the unidentifiedwoman. In the story, a New York CityHealth Department spokesperson statedthat this incident was one of 200 com-plaints from people who called the city’spesticide hotline in 2000 reporting illnessdue to pesticide spraying.56

Inert ingredients are often added todelay the enzyme action in pyrethroids


so a lethal dose is assured. These inertsmay include toxic organophosphates, car-bamates, or other synergists. The inertsin resmetherin (sold under the trade nameScourge) include piperonyl butoxid andpetroleum distillates. Piperonyl butoxidehas been shown to cause liver tumors inrats and mice.16

Natural PyrethrinsNatural pyrethrins are contact poisonsthat quickly penetrate the nerve systemof the insect. A few minutes after appli-cation, the insect cannot move or fly away.Natural pyrethrins can be swiftly detoxi-fied by enzymes in the insect. Thus, somepests will recover.

Links between pyrethroids andhormonal disruptionNumerous studies have indicated thatpyrethroids disrupt the endocrine systemby mimicking the effects of the hormoneestrogen, which can cause breast cancerin women and lowered sperm counts inmen.57

A Mount Sinai School of Medicinestudy examined four pyrethroid pesti-cides, including sumithrin. It concludedthat pyrethroids “should be consideredto be hormone disruptors, and their po-tential to affect endocrine function inhumans and wildlife should be investi-gated.”58

A study at the Roger Williams Gen-eral Hospital of Brown University onpyrethroids concluded, “chronic expo-sure of humans or animals to pesticidescontaining these compounds may resultin disturbances in endocrine effects.”59

A Cambridge University report issuedin June 2000 by the Royal Society in En-gland called for international cooperationto deal with the dangers posed by endo-crine-disrupting chemicals, includingpyrethroids, and recommended reducinghuman exposure to these chemicals.60

Links between pyrethroids andchildhood brain cancersStudies have found nervous-system dam-age from pyrethroids to be comparableto damage from DDT.61

A report of pesticides and childhoodbrain cancers published in Environmen-tal Health Perspectives revealed a strongrelationship between brain cancers andpyrethroids used to kill fleas and ticks.The study concludes, “The specificchemicals associated with children’s braincancers were pyrethrins and pyrethroids(which are synthetic pyrethrins, such aspermethrin, tetramethrin, allethrin,resmethrin and fenvalerate) andchlorpyrifos (trade name: Dursban).”62

Links between pyrethroids andneurological damageA study conducted by the PhysiologicalInstitute at Ludwig Maximilians Univer-sity in Munich, Germany, found that neu-rological effects of pyrethroid poisoningwere still seen in patients after more thantwo years.

Among these long-term symptomswere:

1) reduced intellectual performancewith 20%-30% reduction ofendurance during mental work;

2) personality disorders;

3) visual disturbances and tinnitus(ringing in the ears);

4) sensomotor-polyneuropathy,most frequently in the lowerlegs;

5) increased heat-sensitivity andreduced exercise tolerance due tocirculatory disorders.63

This has been corroborated by Swedishlab studies showing that low-dose exposureto pyrethroids “resulted in irreversiblechanges in adult brain function in themouse” when exposed during


the growth period. This occurred at levelsof exposure less than what was found toaffect adult mice. The study also found“neonatal exposure to a low dose of aneurotoxic agent can lead to an increasedsusceptibility in adults to an agent hav-ing a similar neurotoxic action, resultingin additional behavioral disturbances andlearning disabilities.”64

Links between pyrethroidsand thyroid damageA pesticide study conducted on rats con-cludes, “[E]xposure to organochlorine,organophosphorus, and pyrethroid insec-ticides for a relatively short time can sup-press thyroid secretory activity in youngadult rats.” The study also said a decreasein body weight seen “suggests that pyre-throid insecticides can inhibit growthrate.”65 “We tested four frequently en-countered pyrethroids, fenvalerate,sumithrin, d-trans allethrin, and per-methrin, for estrogen and progesteroneagonist/antagonist activities. Throughthese hormonal pathways, exposure tocertain pyrethroids may contribute toreproductive dysfunction, developmentalimpairment, and cancer.”66

Wildlife impactsAll pyrethroids are extremely toxic tobeneficial insects, including bees. Theyare also extremely toxic to aquatic life,such as bluegill and lake trout, whileslightly toxic to bird species, such as mal-lards. Toxicity increases with higher wa-ter temperatures and acidity.67 EPAwarnings on the pesticide labels includerestrictions that prohibit the direct ap-plication of products to open water orwithin 100 feet of lakes, streams, riversor bays. Because most pyrethroids wereregistered with the EPA before 1984,when comprehensive health assessmentreviews were first required, EPA hasscheduled such a review of pyrethroidsfor 2004.68

Organophosphates

MalathionIn response to WNV, New York Cityembarked on a control program relyingon malathion, one of the most widelyused organophosphate insecticides in theUnited States and throughout the world.Eradication programs for pests such asmosquitoes and fruit flies have exposedthousands of people to malathion appliedin aerial applications, in many casesprovoking citizen complaints of allergicreactions and flu-like symptoms.69

Proponents of malathion use often re-fer to the chemical’s relatively low acutemammalian toxicity. But like DDT andother pesticides that have been found tocause irreparable damage to human andenvironmental health, malathion maypose a greater risk than the product labelwould lead one to believe.

Shown to be mutagenic; a possible car-cinogen; implicated in vision loss, repro-ductive and learning problems, immunesystem disruption and other negativehealth effects in human and animal stud-ies; damaging to non-target organisms;and containing highly toxic impurities,malathion has a legacy of serious problems.70

Acute Malathion PoisoningNumerous incidents of acute poisoninghave been documented for this widely-used pesticide. For example, in June 2001,the Glens Falls Post-Start reported that 37fourteen and fifteen year-old girls becameill at a softball game after being exposedto malathion, which was being applied toan area adjacent to the field.

Organophosphates such as malathionare in the same chemical class as the nervegas Sarin. These chemicals act as neuro-toxins, disrupting the nervous system byinhibiting the enzyme cholinesterase.High exposures can produce fatal poi-soning.71


Symptoms oflife-threateningpoisoning

ComaSeizuresIncontinenceRespiratory arrestPulmonary edemaLoss of reflexesFlaccid paralysis

Symptoms of moderateor severe poisoning

Tightness in chestDifficult breathingBradycardiaTachycardiaHypertensionHypotensionPallor/cyanosisAbdominal painDiarrheaAnorexiaTremor/AtaxiaFasciculationsLacrimationHeavy salivationProfuse sweatingBronchorrheaBlurred visionPinpoint pupilsPoor concentrationConfusion/delusionsMemory loss

Common early or mildsigns/symptoms

HeadacheNausea/VomitingDizzinessMuscle weaknessDrowsiness/lethargyAgitated/anxiety

Table 2: Symptoms of Organophosphate Insecticide Poisoning73

In laboratory animals, malathion ex-posure has caused stomach ulcers, testicu-lar atrophy, chronic kidney disease,increased liver and kidney weights, ad-verse gastrointestinal tract effects, andchanges in the adrenal glands, liver, andblood sugar levels.72

Table 2 lists symptoms of organophos-phate exposure compiled by the UnitedStates Environmental Protection Agency.

Link between malathion andblood disordersDuring a malaria mosquito eradicationspray program in Pakistan in 1976, 2,800people became poisoned from malathionand five died.79 Physicians at Travis AirForce Base Medical Center in Californiahave observed seven children with bone

marrow disorders over the past eightyears. The physicians believe organo-phosphate pesticides caused the blooddisorders in all cases. All blood disordersoccurred shortly after exposure to thepesticides DDVP/propoxur andmalathion.80

Malathion and reproductivedisordersJuvenile male rats exposed to daily dosesof malathion had decreased numbers ofsperm forming cells.81 In sheep,malathion exposure of pregnant ewes re-sulted in an increase in aborted fetuses,stillbirths, and low birth weight babies.Longer duration and earlier initiation ofmalathion exposure resulted in more se-vere problems.82


Case Study: Malathion Spraying to Control Medflies in California

D espite strong public opposition, malathion spraying was repeatedly (andultimately unsuccessfully) used in California from 1980 through the early1990s in an attempt to eradicate an agricultural pest called the Mediter-

ranean fruit fly, commonly known as the Medfly.An infestation of this pest, which can feed on and damage more than 200

species of fruit and vegetables, first appeared in California in 1975, but quicklysubsided. However, a bigger infestation in 1980 led the United States Depart-ment of Agriculture to order an unprecedented campaign of widespread aerialmalathion spraying. Citizen and local government opposition, including citycouncil resolutions, helped stave off the spraying for nearly a year, when thegovernor authorized an all-out aerial assault. From July 10, 1981, through Sep-tember 1982, more than 1,300 square miles of land were subjected to aerialspraying each week, resulting in several deaths due to accidental poisoning.74

Similar waves of infestation and aerial malathion spraying occurred despitepublic opposition throughout the 80s and early 90s. Often, the aerial sprayingoccurred in populated areas, exposing thousands of residents in Santa ClaraCounty in 1983 and 1984, and 1.6 million people in the Greater Los Angelesarea over a six-month period in 1989 and 1990.75

Dr. Jorge Mancillas, a neurobiologist at UCLA and profes-sor at the UCLA School of Medicine, calculated that during theLos Angeles spraying, a 50-pound child exposed to malathionon a surface equivalent to that of a dollar bill would have beensubjected to an exposure exceeding the EPA’s “acceptable dailyintake level.” Although in theory the spray levels were set lowenough to be “safe” (amounting to 1.4 milligrams per squarefoot) the actual rate of deposition of the chemical exceeded thepredicted rates by 40% or more, resulting in clearly unsafe expo-sure levels.

In 1990, Ventura County successfully filed an injunction toprevent malathion spraying, helping end the aerial campaign. In 1992, one studyof aerially applied malathion for Medfly control in California found an associa-tion between malathion exposure during the second trimester of pregnancy andthe occurrence of gastrointestinal abnormalities in infants.76 By that time, 10%of residents in affected areas refused to allow access to their backyards for spray-ing.77

After nearly a decade of repeated aerial bombardments, communities finallywon an end to the aerial spraying program, which was replaced by release ofsterile Medflies to prevent any introduced Medflies from mating successfully.According to a senior economic entomologist with the Medfly Prevention Re-lease Program based in Orange County, since the shift to a preventative sterilerelease program in 1996, “there has been only one minor infestation of Med-flies within the boundaries of the program.”78 After years of harmful spraying,the preventative approach turned out not only to be the least threatening topublic health, but also the most effective in controlling the pest.

“. . . a 50-pound child exposed

to malathion on a surface

equivalent to that of a dollar bill

would have been subjected to an

exposure exceeding the EPA’s

acceptable daily intake level.”


Malathion and vision disordersBetween 1957 and 1971, Japanese schoolchildren experienced a tremendous in-crease in cases of myopia (nearsighted-ness), which correlated with the increaseduse of organophosphate insecticides, in-cluding malathion.83 Reduced visualkeenness was discovered in 98 percent ofthe children examined from Saku, an ag-ricultural area where malathion was regu-larly applied. Other examples of what isnow called “Saku disease” in both chil-dren and adults were reported through-out Japan where organophosphatepesticides were applied.

In California, one incident involved a15-year-old boy who was declared legallyblind after being outside while helicop-ters were spraying malathion. An oph-thalmologist and a pesticide expert bothagreed that the boy may have Saku disease.84

Malathion and immunosuppressionImpurities and by-products present inmalathion can further disrupt immunesystem function.85 Immunosuppressionmay enhance susceptibility of mamma-lian systems to bacterial, viral, or para-sitic infection or possible increased tumorformation.86

Ironically, use of these pesticides forWNV mosquito control could actuallyend up suppressing human and avian im-mune systems in the areas sprayed, put-ting each species at greater risk thanbefore of spreading, contracting, and be-coming seriously ill from WNV.

Link between malathion and cancerIn April 2000, a U.S. Environmental Pro-tection Agency (EPA) committee re-viewed a series of studies on mice and ratsexposed to malathion. Based on this re-view, the committee concluded that therewas “suggestive evidence of carcinogenic-ity.”87 For the moment, malathion re-mains listed by EPA as “not classifiable”

with regard to carcinogenicity.88 However,recent evidence suggests that organo-phosphates such as malathion can causeNon-Hodgkin’s Lymphoma (NHL).89

Use of malathion by farmers in Iowa andMinnesota has recently been linked to anincreased risk of one type of NHL.90

Wildlife impactsMalathion is lethal to beneficial insects,snails, microcrustaceans, fish, birds, am-phibians, and soil microorganisms. Sub-lethal exposure of these species can causea variety of behavioral and physiologicalabnormalities.91

Naled and Related PesticidesNaled (trade name Dibrom) is an orga-nophosphate with many of the same char-acteristics and concerns as malathion.

Naled can cause cholinesterase inhi-bition in humans; that is, it can overstimu-late the nervous system causing nausea,dizziness, confusion, and at high expo-sures, can cause respiratory paralysis anddeath.

Dichlorvos: toxic byproduct of naledOne of the byproducts of degradation ofnaled is dichlorvos, another registeredorganophosphate.92 Researchers at theCornell University Program on BreastCancer and Environmental Risk Factorsin New York State prepared a fact sheetreviewing several studies on dichlorvos.They found the following:

• Female mice that were fed high dosesof dichlorvos over a long period oftime had a higher frequency ofstomach cancers than untreatedmice.

• High doses of dichlorvos fed overtwo years caused an increase in thenumber of male rats that hadpancreatic tumors and leukemia.


“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.”

• A higher number of leukemia caseswere reported in one study amongmale farmers who used dichlorvosfor more than ten days per year,compared to those who had notused dichlorvos.

• A higher number of childhood braincancer cases were reported amongfamilies that used dichlorvos thanamong families that did not.93

In addition, Russian researchers foundfish exposed to dichlorvos demonstratedslower growth rates. Researchers believeit may be due to the subtle neurotoxinactions of the pesticide and its effectsupon the areas of the brain involved infeeding or food search mechanisms.94

Trichlorfon: ingredient in naledThe pesticide trichlorfon is a commoningredient in the mosquito pesticideDibrom (naled). In one study, trichlor-fon was found to cause a “severe reduc-tion” in brain weight (and shape) in testanimals exposed. The timing of exposureto the developing offspring appeared tobe the key factor in determining neuro-logical damage (known as the “criticalbrain growth period”). It occurred whenthe chemical was administered between40-50 days gestation for the guinea pig,which scientists say, correlates with thebrain growth spurt period for the animal.95

Wildlife impactsNaled is characterized as very highly toxicto bees and aquatic invertebrates. It ismoderately to highly toxic to fish and

slightly toxic to upland game birds andwaterfowl.96 There is potential forchronic risk from naled to estuarine in-vertebrates.97

TemephosTemephos (Abate) is an organophosphateinsecticide used to control mosquito,midge, and black fly larvae. It is used inlakes, ponds, and wetlands. It also maybe used to control fleas on dogs and catsand to control lice on humans. The com-pound is sometimes found in mixed for-mulations with other insecticidesincluding trichlorfon. As an organophos-phate, it has many of the same concernsand characteristics as malathion andnaled.

Symptoms of acute exposure toTemephos are similar to other organo-phosphates and may include nausea, sali-vation, headache, loss of musclecoordination, and breathing difficulties.98

Some studies show that Temephos maygreatly increase the observed toxicity ofmalathion when used in combinationwith it at very high doses.99

Wildlife impactsTests with various wildlife species indi-cate that the compound is highly toxic tosome bird species. The compound is alsohighly toxic to bees.100 Temephos showsa wide range of toxicity to aquatic organ-isms, including salmon.101 Freshwateraquatic invertebrates such as amphipodsare very highly susceptible to temephos,as are some marine invertebrates.102

Temephos is very highly toxic to saltwater


species such as the pink shrimp, and pre-sumably to lobsters as well.

Temephos has the potential to accu-mulate in aquatic organisms. In one study,the bluegill sunfish accumulated 2,300times the concentration present in thewater.103

LarvicidesLarvicides applied to mosquito breedingpools are generally considered to havelesser impacts on public health thanadulticide sprays. For this reason, manymosquito and vector control programsrely on larviciding as the primary inter-vention strategy to limit mosquito popu-lations. Indiscriminate use of larvicides,however, may have harmful impacts onwildlife and contaminate drinking watersupplies.

MethopreneMethoprene is applied to water bodiessuch as sewers, wetlands, ditches, andponds for the purpose of killing mosquitolarvae. According to EPA human toxicityratings, the larvicide methoprene(Altosid) is considered to be practicallynontoxic to humans.104

Interrupting the normal life cycle ofan insect, methoprene prevents larvaefrom maturing to the adult stages, andthus prevents them from reproducing. Tobe effective, it is essential that this growthinhibitor be administered at the properstage of the target pest's life cycle.Methoprene is not toxic to the pupal oradult stages. Treated larvae will pupatebut adults do not hatch from the pupalstage.105

Methoprene may be the larvicide ofchoice in many mosquito control dis-tricts, due to the fact that one applica-tion remains effective for significantlylonger than a single application of bio-logical agents such as Bti, discussed in the

following section. This can reduce thelabor costs of ongoing larviciding bymore than fifty percent. Methoprenemimics the action of an insect growthregulation hormone. However, applica-tion of methoprene may have significantecological impacts.106

Wildlife impactsStudies have documented methoprene tobe slightly toxic to birds and slightly tomoderately toxic to fish.107 Methopreneresidues may have a slight potential forbioconcentration in bluegill sunfish andcrayfish.108 Methoprene is very highlytoxic to some species of freshwater, es-tuarine, and marine invertebrates.109

Methoprene harms shrimp develop-ment.110 Studies at the laboratory of re-searcher Charles McKenney have shownthat methoprene inhibits the metamor-phic success of larval estuarine shrimp andcrabs with exposure to concentrationsused in killing salt marsh mosquitoes.111

Methoprene and birth defectsin vertebratesSome researchers have hypothesized thatmethoprene may cause birth defects anddeformities that have been observed infrogs throughout the United States.112

The larvicide methoprene has beenlinked to frog deformities, particularlyextra limbs growing from various partsof a frog’s body or head.113 These defor-mities are thought to result from expo-sure to methoprene acid, a chemical thatis formed when methoprene breaks down.This byproduct may function as a retin-oid, a compound that stimulates genetranscription in vertebrates.114 Changesin exposure to retinoids during certaincritical stages can cause birth defects inall vertebrates, including humans, andmay be contributing to the global epi-demic of skeletal deformities in frogs.115

A recent controlled study published inAquatic Toxicology demonstrated that


Spraying to Kill Mosquitoes and Killing Lobsters Instead

I n 1999, immediately after Hurricane Floyd hit the eastern seaboard,lobstermen who fish in the Long Island Sound noticed a sharp decline in thelocal lobster population.By the following year, experts estimated that more than 10 million lobsters,

or 90% of the stock, had died off in the western part of the Long Island Sound.116

President Clinton declared the Sound a natural resource disaster area, and Con-gress appropriated $13.9 million for research and financial assistance to licensedlobstermen.117

The lobstermen, arguing that the lobster had survived pollutedrunoff in the past, believe that WNV spraying in the summer of1999 was the cause for the decimation of their fishery, and filed a$125 million putative class action lawsuit against insecticide manu-facturers.118

This hypothesis is potentially bolstered by studies that have docu-mented that exposure to pyrethroids used in mosquito control cankill lobsters and shrimp.119 Although shellfish appear very differentfrom mosquitoes, they share many life characteristics and a commonevolutionary history with insects. Insects, for example, an externalskeleton and development from a larval stage through a series of molts.

Some scientists, such as those studying the lobsters at the Univer-sity of Connecticut, have hypothesized that insecticides may havebeen indirectly responsible for the lobster die-off. For example, pes-ticide exposure may have lowered their immune system, allowing aparasitic infection to overwhelm the population.

The EPA has launched an investigation into the cause of the lobster crash.Scientists estimate it will take at least 10 years for the population to recover.Research is still being conducted to determine the effects that mosquito controlpesticides might have on lobsters, particularly sub-lethal effects at low levels. Iflobstermen are right and widespread use of mosquito control pesticides was re-sponsible for the crash in Long Island’s lobster population, California’s lobsterindustry could be similarly imperiled.120

California’s Lobster Industry

Recently, the California lobster harvest has rebounded to the highest levelsin over fifty years, totaling over 950,000 pounds. The economic value ofCalifornia’s fishing industry to the state is estimated at more than $800

million annually. The industry ranks among the top 5 seafood-producing statesin the U.S. (472 million pounds in 1999).121

It is not clear how the California lobster and shellfish industry could be dam-aged if pesticides are used more widely to control mosquito populations. How-ever, it would be irresponsible and shortsighted to introduce these chemicals ontoland or water bodies without knowing the effects they might have on lobsters.

“This hypothesis is

potentially bolstered

by studies that have

documented that

exposure to pyrethroids

used in mosquito

control can kill lobsters

and shrimp.”


Figure 8. Some researchers havehypothecized that methoprene maybreakdown into compounds that causedeformities in vertebrates.

BiopesticidesBiopesticides have emerged as importantalternatives to traditional chemical pes-ticides with fewer known human healthimpacts. However, they, too, should beused sparingly. Like traditional chemicalpesticides, significant research needs tobe done on the ecological effects ofbiopesticides. What non-target inverte-brates that are important in the foodchain are also affected by their use? Howwill a potential decrease in this part ofthe food chain affect fish and amphibians,and the birds and animals that feed onthem? Many unanswered questions makeit difficult to estimate the potential riskof biopesticide use.

Bacillus thurengiensis israelensis (Bti)and Bacillus sphaericusBti is a biological pesticide that containsnaturally occurring soil bacteria in dif-ferent strains that target specific insects.It is not known to be toxic to animals,birds, humans, fish or beneficial insects.Bti is required to have EPA warning andcaution labels, as is the requirement bylaw for any registered pesticide.123

Based on extensive testing, no harm-ful effects to the public are expected tooccur when biopesticide products areapplied according to label directions.Because there is the potential for skin andeye irritation, applicators are warned toavoid direct contact with the granules ora concentrated spray mix. Various testsrevealed no expected harm to non-targetorganisms.124

Biopesticides closely related to Bti arewidely used in organic farming. Sometrade names are Aquabac, Teknar, andLarvX. Bacillus sphaericus (VectoLex) isanother naturally occurring biopesticide.It was registered in 1991 for use againstmosquito larvae, which ingest the bacte-ria and die after the toxin in the bacteriadisrupts their gut function.

Phot

o: L

abor

ator

y of

Joe

Kie

seck

er, P

enn

Stat

e U

nive

rsity

frog embryos exposed to high concentra-tions of methoprene did not show anydevelopmental defects. However, thestudy found that methoprene can degradeinto other compounds that do cause de-velopmental toxicity at concentrationssignificantly higher than those expectedto result from proper application of thelarvicide.122

The U.S. Environmental ProtectionAgency risk assessment for methoprenedid not include an evaluation of its chemi-cal breakdown products, retinoids. Thisillustrates a common failure of theagency’s risk assessments, which do notevaluate the breakdown by-products of thechemical pesticides under consideration.


If Bti and variants are too widely used,insects may develop immunity to thesepesticides, thereby limiting their effec-tiveness for mosquito control and for useby organic farmers. The University ofCalifornia Working Group on OrganicFarming has estimated that this industryhas a value exceeding $225 million in thestate of California alone.125

The Threat to AgricultureAll of the aforementioned chemicals aredesigned to kill insects, many of whichare responsible for pollinating wild andcultivated plants in California. The fu-ture of agriculture depends on pollinators.Insect pollination is a necessary step inthe production of most fruits and veg-etables we eat and in the regenerationof many forage crops utilized by live-stock.

California growers of almonds, apples,and many other crops depend on insect

pollinators — both managed and wild —to produce fertile seeds and full-bodiedfruit. Recent surveys document that morethan thirty genera of animals — consist-ing of hundreds of species of floral visi-tors — are required to pollinate the 100or so crops that feed the world. Domes-tic honey bees service only 15% of thesecrops, while at least 80% are pollinatedby wild bees and other wildlife.126

Researchers have estimated severe rev-enue losses to both almond growers andhoney producers in California resultingfrom a pesticide-induced decline in thenumbers of pollinators where pollina-tion by honeybees alone is valued at over$14.6 billion.127

Organic crops are also at risk, shouldthe state choose the method of aerial orground spraying of pesticides. It is un-likely that sprayed farms will lose theircertified status, but sprayed crops andplant material may not be able to be mar-keted as ‘organically produced.’128


it to mean “harmless.” Since neither the fed-eral law nor the regulations define the term“inert” on the basis of toxicity, hazard or riskto humans, non-target species, or the envi-ronment, it should not be assumed that allinert ingredients are non-toxic.129

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 ingredientsmust be taken into consideration whenassessing the toxicity of a formulatedproduct. Researchers found a ten-folddifference in toxicity between formula-tions with the same active ingredient, butwith different carriers, solvents, etc.130

Some mixtures of Anvil are made upnot only of 10% artificially manufacturedSumithrin but 10% piperonyl butoxide(PBO), a suspected carcinogen, and 80%“inert” ingredients such as poly-ethylbenzene, which is listed by the EPAas being “potentially toxic.”131

PBO is added to make the pyrethroidsmore effective. It acts by inhibiting natu-rally occurring enzymes that would other-wise degrade the insecticide. PBO breaks

“Inert” Ingredients EscapePublic DisclosureThe true nature and health threat of apesticide is difficult to analyze, since manyof its ingredients may never be made public.

The Federal Insecticide, Fungicide,and Rodenticide Act (FIFRA), thenation’s primary pesticide control law,classifies pesticide ingredients into twocategories—active and inert. The activeingredients are those designed to kill pestswhile the inerts are added to make theactive ingredient more potent and easierto use. Inert ingredients can make up asignificant percentage of the material thatis actually sprayed. Yet these inerts, whichare often highly toxic, are often classifiedas “trade secrets” under law and are notlisted on the label. In September 1997, U.S.EPA issued a memo encouraging pesti-cide manufacturers to voluntarily substi-tute the term “inert ingredients,” with theterm “other ingredients,” noting that:

Many of these compounds are potentiallyharmful, even more so than the active ingre-dient in the pesticide. Many consumers aremisled by the term “inert ingredient”, believing

Unknown Health Impactsof Mosquito Control Pesticides

Unknown Health Risks 39

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.135

Peter Montague, Environmental Research Foundation

Although they may be off the publicradar screen, inert chemicals may havesignificant impacts on public health andthe environment.

Pesticides AreNot Proven SafeMany people assume that a pesticide issafe to use if it has been approved for useand is available on the store shelves attheir local hardware store. However,thousands of chemicals on the market lackadequate testing to demonstrate that theywill not harm human health or the envi-ronment.

Pesticides are routinely approved be-fore their health consequences have beenaccurately determined, as evinced by thefact that nearly 100 pesticides have beenbanned or severely restricted by the EPAsince their introduction.136 As recently asJune 8, 2000 the EPA announced a banon virtually all uses of Dursban (chlorpy-rifos) in residential and commercial build-ings. Diazinon, one of the most widelyused pesticides in the United States, willbe phased out of home and garden useby 2004 because of health concerns.

Yet it can be years or even generationsbefore a dangerous compound is bannedor its use restricted. Consider the ex-amples of lead in paint and gasoline,

through the insect’s defense, making theinsecticide more powerful. The EPA’sOffice of Pesticide Programs suspectsPBO of being a carcinogen. The NationalInstitute for Occupational Safety andHealth’s Registry of Toxic Effects ofChemical Substances lists it as a suspectedgastrointestinal or liver toxicant, and asuspected neurotoxicant. It has also beenreported as a suspected reproductive toxi-cant.132 In addition, there is some evi-dence that PBO-pyrethroid mixes canaffect the human immune system.133

Polyethylbenzene (PEB), a heavy aro-matic solvant also known as naphtha, iswidely used in pesticides. PEB is listed onthe 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 shouldbe assessed for effects of concern. Manyof these inert ingredients are structurallysimilar to chemicals known to be toxic;some have data suggesting a basis for con-cern about the toxicity of the chemical.”

PEB, for example, is related to ethyl-benzene, which is listed as a suspectedreproductive toxicant and a suspectedrespiratory toxicant by the EPA. Whitemineral oil, also known as hydro-treatedlight paraffinic petroleum distillate, isalso listed on the EPA’s Inert PesticideIngredients List No. 2 of potentially toxicchemicals.134


Risk assessments may be designed andconducted to prove that a pesticide sprayprogram is safe. Yet, significant uncertain-ties often underlie these assessments. Aworking group of the U.S. Environmen-tal Protection Agency identified thefollowing uncertainties in current knowl-edge which limit regulators’ “ability tomake decisive assessment conclusions andtake fully informed actions to prevent ormitigate pesticide problems:”

• What is the efficacy of spraying,especially ground spraying withoutaerial?

• What should agencies do whenpublic health comes head-to-headwith environmental risks?

• Communication of risk of diseasevs. risk of control.

• What are effects of multiplespraying (risks)?

• More measurements of (outdoor andindoor) pesticides via spraying.

• Is turning air-conditioning offeffective in reducing exposure; whatabout restarting?

• When is it safe to allow children andpets out after spraying?

• What are the results of environmen-tal spraying and implications to thelower end of food web/chain?137

Only rarely will risk assessments per-formed to justify proposed spraying pro-grams clearly delineate the aboveuncertainties.

DDT in pesticides, and DES and thali-domide for pregnant women.

This demonstrates a faulty system inwhich pesticides, not public health, aregiven the benefit of the doubt in regula-tory decision-making. The risk assess-ment models used by the state to evaluatethe chemicals, although they enjoy wide-spread use in the regulatory community,are often inadequate in determiningwhether the introduction of these com-pounds into the environment will ad-versely affect humans, wildlife, and entireecosystems.

In order to protect public health andthe environment, pesticides should besubjected to standards like those used bythe Food and Drug Administration, inwhich a product is considered harmfuluntil it is proven safe.

Risk assessments are used to demon-strate the relative safety of using a giventoxic chemical when exposure is limitedto a certain level. The officials and appli-cators will assure the public, based ontheir risk assessments, that the levels ofchemicals they will be exposed to will beso low, and so infrequently applied, thatthere will be no effect on the environ-ment and human health, or that thecompound’s toxicities quickly degrade.

These assessments may be unreliablefor a number of reasons. First, many ofthese chemicals may have significant tosubtle negative health and environmentaleffects at extremely low levels. Secondly,pesticides are never applied under idealconditions as planned. There will alwaysbe mistakes, spills, and oversprays. Thecompounds, although analyzed for safetyand degradation characteristics underideal laboratory conditions, will be ap-plied by real people in the real world.

Balancing the Risks 41

Balancing the Risks

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.

Dr. David Pimentel, Professor of Entomology,Cornell University, Newsday, November 7, 2000

As Michael Gochfeld, Professor of Envi-ronmental and Community Medicine atthe Robert Wood Johnson MedicalSchool and School of Public Health,Rutgers University has written:

In weighing the risks and benefits of mos-quito control, we should consider the diseaseitself and the risk to the human population.The media always paired the words “lethal”or “deadly” with “West Nile” or “encephali-tis,” reinforcing in the public’s mind the dan-ger from the disease. But it would be equallypropriate to characterize West Nile virus in-fection as “unapparent,” “usually asymptom-atic,” or “occasionally serious.” Seven deathsin a population of over 10 million people overa one month period is certainly tragic, butpales beside the number of deaths from manyother diseases that are addressed less aggres-sively.138

Dr. Gochfeld and other experts haveargued further that we have insufficientevidence to know how to control WNV-type diseases or how our control measuresmay affect them. Filling in these data gapswill be crucial in assessing the risktradeoffs essential to public health deci-sions in this area.139


Why the Push for Pesticide Spraying?

Considering the lack of evidence demonstrating the effectiveness of pesti-cide spraying, it may seem surprising at first that the vast majority of gov-ernment officials have responded to the emergence of West Nile Virus

with broadcast spraying programs.The push to spray comes from several very different sources: the urge to do

something highly visible to show that action is being taken to address the healththreat; momentum resulting from the fact that pesticide spraying has been thedominant approach to such problems for the past thirty or forty years; and theinfluence of pesticide manufacturers on local, state, and national decision-mak-ing processes.

In states lacking mosquito control plans when WNV first appeared, pesticidespraying provided a quick and easy solution to a very complicated and multifac-eted problem. Thinking they had to “do something,” most government officialsput their finger firmly on the pesticide trigger, picking the easiest and quickest,but not the safest, least costly, or most effective response to address the WNV.These officials could say that they had done “something,” highly visible to theaffected communities, even though their solution may have caused more harmthan good.

In states with more prevalent and long-standing mosquito control problems,the decision to spray may be based in years of precedent in which spraying hasbeen the main approach to mosquito control.

There is also big money to be made by spraying pesticides. Pesticide manufac-turers and applicators stand to profit from manufacturing and applying sprays forWNV mosquito control. In New York City, for example, Clarke EnvironmentalMosquito Management, Inc. was paid $650/hour per truck in a $4.6 million NewYork City contract.140 (The company’s bid for a three year contract to spray wasin excess of $50 million.141 This bid was rejected by the state, and Clarke was

recently fined $1 million for violating New York State’spesticide application laws.)

The corporations who manufacture the pesticides areoften the same entities funding research to document theeffectiveness of those same pesticides. Furthermore, theline between publicly-funded mosquito control and for-profit chemical companies is consistently blurred by “pub-lic/private partnerships.” For example, many pesticidecompanies have direct links to the California Mosquito andVector Control Association’s (MVCAC) website, and arecorporate sponsors or “members” of this governmental

agency. “Sustaining members” who made significant financial contributions toMVCAC in 2002 include large chemical pesticide manufacturers and distribu-tors, such as Aventis Chemical Corporation, Clarke Mosquito Control Products,Inc., Electramist, Inc., Fen-nimore Chemicals, Pigott & Associates, Inc., ValentBiosciences Corporation, Vopak USA, and Zoecon Professional Products.142

“. . . the line between publicly-

funded mosquito control and

for-profit chemical companies

is consistently blurred by

“public/private partnerships.”


In this sense, the state of knowledgeof WNV control is analogous to the stateof understanding of Medfly control inCalifornia in the mid 1980s (described onpage 31) when there was no clear-cuttechnical or scientific evidence to supporta program of ground spraying, aerialspraying, or the mass application of pes-ticides in any form. In the case of theMedfly infestations, pesticides were giventhe benefit of the doubt until exposedcommunities organized against the on-slaught. It took more than a decade ofineffective pesticide spraying before pre-ventative, nonchemical control programswere implemented in their place.

This time, communities can be pre-pared. In many parts of the country, theWest Nile Virus outbreak has been ac-companied by intensive media coverage,including daily or near-daily reports high-lighting each additional case discoveredin humans or birds. The impacts of pes-ticides on nontarget organisms rarelyhave been given comparable attention. Animportant first step may be actively work-ing with journalists in California to en-sure that media representations of WNVinclude clear discussion of the risks andknown impacts of pesticides, rather thansimply inflaming public fears of a newhealth threat.

Principles for Safe, EffectiveMosquito Control Measureson the State and Local Level 143

I. Give Public Health, Not Pesticides,the Benefit of the DoubtIn order to safeguard public health in thestate, a balanced approach to West NileVirus must weigh the threats posed bypesticide use to the general population

against the threat posed by West NileVirus. In the absence of evidence dem-onstrating that spraying helps limit trans-mission of the disease to humans,pesticide spraying should not be part ofthe WNV control plan.

1. Before any decision to use pesticides,community-specific assessments ofhealth and environmental hazards ofproposed products that take intoconsideration all pesticide ingredi-ents (including inerts) should beconducted, with full public input.

2. Reevaluate and eliminate sprayingconducted for nuisance reasons. Suchspraying generally relies on the samepotentially hazardous pesticides usedin WNV control. Furthermore,indiscriminate use of these pesticidesbuilds up resistance in mosquitopopulations, making targeted use fordisease control even less effective.

II. To Protect Public Health,Prioritize Alternatives ToPesticide SprayingPublic education and outreach, behav-ioral changes and preventative measuresthat reduce mosquito breeding habitatcan effectively minimize risk of WNVwhile reducing momentum for danger-ous pesticide spraying programs.

While public outreach and educationof this nature may be a significant part ofa mosquito control district’s strategies for

“An important first step may be to actively work

with journalists in California to ensure that media

representations of WNV include clear discussion of the

risks and known impacts of pesticides, rather than

simply inflaming public fears of a new health threat.”


Healthy Wetlands Help Control Mosquito Populations

L aboratory studies have shown that salt marsh mosquitoes are unlikely to bemajor vectors of West Nile Virus. However, they are among the mosquitoesmost commonly sprayed for nuisance reasons. Restoring degraded wetlands

can help limit both the public health threat and nuisance of mosquito popula-tions. For example, the Ora Loma Marsh in the San Francisco area was recentlyrestored for a number of sensitive species, including the endangered salt marsh

harvest mouse. According to a paper by Wes Maffei, the manager ofthe Napa County Mosquito Abatement District, the marsh design“was altered to improve tidal flow, thereby reducing the amount ofstagnant water in which mosquitoes thrive. Although it has only beena couple of years since the restoration occurred, mosquito breedinghas been markedly reduced and it is quite apparent that the health ofa degraded marsh is now returning.”145

On the flip-side, wetland restoration projects that lack adequatedesign controls and funding for ongoing maintenance may actuallyundermine attempts at effective mosquito control.

Open Marsh Water Management, or OMWM, was developed tocontrol mosquitoes by facilitating access of their natural fish predators to areason salt marsh where mosquitoes breed.146 Through a system of pools and pannesconnected by radial ditches, small fish that eat mosquito larvae can reach thelarvae during high tide, then retreat to sumps or reservoirs at low tide. RobertScheirer, a coordinator with the US Fish and Wildlife Service, has written that“This has been found to be an effective, long-term method of controlling mos-quito populations without using sprays.”147

“Restoring degraded

wetlands can help limit

both the public health

threat and nuisance of

mosquito populations.”

controlling mosquito populations, thestate plan does not lay out specific pa-rameters for it. Community leaders andactivists can work with district managersto ensure that mosquito control resourcesare focused on prevention and education,rather than chemical spraying response.

Focus on source reductionSource reduction encompasses a broadrange of activities. It can be as simple assteps taken by individuals where they live,such as turning over empty containers,removing used tires and cleaning raingutters and bird baths. Source reductionalso encompasses extensive regional wa-ter management projects conducted bymosquito control agencies or fish andwildlife officers. Comprehensive source

reduction activities can eliminate or sub-stantially reduce mosquito breeding andthe need for repeated applications of in-secticides in the affected habitat.

• Stock manmade ponds and otherappropriate bodies of water withmosquito-eating fish. In some cases,it may be appropriate to use bacteriallarvicides or mechanical controlssuch as vegetable-based oils thatsmother mosquito eggs floating onthe surface of the water (see larvicidesection).144

• Keep waterways clean so that fishand other mosquito predators cansurvive. Ensure vegetation is cleanedout of natural sloughs in marshyareas to keep water flowing, prevent-ing mosquito habitat from forming.


Involve and Engage the Community

• On a municipal or county level, setup a system for citizens to reportstanding water near their homes.148

• Educate the public about whatpeople can do at home to minimizemosquito exposure and eliminatebreeding sites through press releases,Web sites, school presentations,mailings, and distribution of bro-chures in public offices. Public healtheducation is a good investment ofresources and will pay off better thanquick-fix expenditures on chemicalsprays.

• Respect public requests not to spray,both on the individual and municipallevel.

• Hold public hearings that offercommunity members the opportu-nity for meaningful input into localmosquito control decisions involvingthe use of pesticides.

• Continuously evaluate the effective-ness of all mosquito control measures.

Steps Individuals Can Take1. Learn about local mosquito controlpolicies.Contact your mosquito control district toobtain a copy of their mosquito controlplan, including information about theirpolicies regarding pesticide use (what in-dicators will “trigger” spraying, how willthey notify the public of their intent tospray?)

Find out when there may be opportu-nities for public input (e.g. schedule ofmosquito control board meetings.)

2. Reduce standing water and othermosquito habitat.

• Get rid of any unnecessary items onyour property that can hold stagnant

water, such as old tires. If you use oldtires for farming or gardening, drillholes in them and empty themregularly.

• Empty water from buckets, toys, andcontainers, and store them in placeswhere they will not collect rain.

• Drill holes in the bottoms of recy-cling bins and any other containersthat must be kept outdoors.

• Drain the water from bird baths,fountains, wading pools, plant potsand drip trays twice a week. Callyour local mosquito control districtto learn whether stocking fountainsor ponds with mosquito fish mightbe appropriate.

• Check for other ways water may becollecting around your house, such aspuddles beneath air conditioners.

• Clean out your gutters and fix guttersthat sag or do not drain completely.Check for areas of standing water onflat roofs.

• If you have a swimming pool, out-door sauna, or hot tub, make surerainwater does not collect on thecover.

• Clear vegetation and trash from anydrains, culverts, ponds or streams onyour property so that water drainsproperly.

• Keep grass cut short and trim shrubsto minimize hiding places for adultmosquitoes.

• Eliminate standing water in yourbasement.

3. Report dead birds.Reports of dead birds can be made to theCalifornia Department of Health Ser-vices Surveillance program by calling(877) WNV-BIRD or by clicking the


Mosquito Sources

Ponds

Swimming pools

Tree holes

Plastic pools

Containers

Bird baths

Standing water

Watering troughs

Cooler drains

Street gutter or catch basins

Cesspool or septic tanks

Roof gutters

Irrigated lawns or fields

What to Do to Reduce Mosquitoes

Stock pond with Mosquitofish. Each fish can eat100 to 500 larvae per day. They play an importantrole in mosquito control in ponds, canals, irrigatedfields and some other freshwater sources. The fishlive two to three years; they are live-bearing andproduce 3 to 4 broods each year.Remove excess vegetation.

Keep water off cover.Maintain water quality at all times.

Fill hole with sand or mortar.

Drain water when not in use, or cover somosquitoes cannot lay eggs.

Empty water.Store in an inverted position.Dispose.Cover so mosquitoes cannot lay eggs.

Change water at least once a week.

Eliminate by draining.Fill in low areas.

Stock with fish, or change water weekly.

Prevent water from standing.

Keep litter and garden debris out of gutter.Do not over-water yard.

Seal and cover opening so mosquitoes can’tlay eggs.

Clean once a year to remove debris.

Avoid over-irrigation.Drain standing water.

Table 3. Checklist of Possible Mosquito Sources Around the Home149

“Report Dead Bird” link: westnile.ca.gov/Dead_Birds. Cal DHS willinitiate the pick up of bird specimens.

4. Mosquito-proof your house and body.

• To minimize the likelihood of beingbitten inside your house, make sure

window and door screens fit properlyand replace outdoor lights withyellow “bug lights.”

• To avoid being bitten outdoors, wearhats, long sleeves and long pants inthe evenings, when mosquitoes aremost active.


What You Should KnowAbout Personal Protectionand Insect RepellentsThe most effective method of personalprotection from mosquito bites is to avoidplaces where mosquito densities are highand to avoid being out-of-doors at timesof the day when mosquito activity is atits highest. Wearing protective clothingsuch as hats, long sleeves and pants canhelp limit exposure.

If you choose to use insect repellents,treat clothing, rather than skin, wheneverpossible, and wash off repellents with soapand water after returning indoors.150

DEETDEET has been demonstrated to be aneffective mosquito repellent. However,use of DEET may entail the risk of seri-ous side effects.

A recent study published in the NewEngland Journal of Medicine found aformulation containing 23.8 percentDEET offered complete protectionfrom mosquito bites for 5 hours, on av-erage, compared to a soybean-oil-basedrepellent (see Bite Blocker/Buzz-Offsection below), which protected againstmosquito bites for an average of 94.6minutes.151

More than 50 cases of serious toxic sideeffects experienced by people using theinsecticide DEET have been documentedin the medical literature. The U.S. En-vironmental Protection Agency (EPA)acknowledges fourteen cases in whichindividuals reported seizures associatedwith exposure to DEET.152 Twelve werechildren, three of whom died.

A press release from Duke UniversityMedical Center research pharmacologistMohamed Abou-Donia, Ph.D., whoseanimal studies have shown that DEEThas potential interactions in humans, ar-gues that “safe is better than sorry.”153

Dr. Abou-Donia recommended:

1. Never use insect repellents oninfants, and be wary of using themon children in general.

2. Never combine insecticides witheach other or use them with othermedications. Even so simple a drugas an antihistamine could interactwith DEET to cause toxic sideeffects.

Some state Bureaus of Health in theUSA and Health Canada do not recom-mend using DEET at all on infants and/or children under 2, and only 10% (or less)DEET preparations on kids 2-12. HealthCanada also recommends that adults notuse preparations with over 30% DEET,and will not register products with a higherconcentration than 30% after 2004.

Plant-Based Insect RepellentsUniversity of California Pest Manage-ment Guidelines note that plant oils suchas those from birch, bluestem grass, ge-ranium, pine, rosemary, spearmint, yar-row, lantana, and neem have been shownto be somewhat repellent to mosquitoes,but most are not available in commercialmosquito repellents.154

Two commercially available plant oil-based repellents are Bite Blocker andBuzz-Off.155 Studies published in the NewEngland Journal of Medicine have shownthat repellents containing oil of eucalyp-tus provided protection for an average oftwo hours, and a product containing soy-bean oil (Bite Blocker for Kids, HOMS)was effective for an average of 90 minutes.156

Citronella repellents and candles arenon-toxic and somewhat effectiveStudies show that citronella can be aneffective repellent, but it provides shortercomplete protection time than mostDEET-based products. Frequent reappli-cation of the repellent can partially com-pensate for this.157


State Department of Health, April 2003,downloaded on June 6, 2003)

1. Keep windows closed during andimmediately after spraying. Ifpossible, also turn off window airconditioners.

2. Stay inside and keep children andpets inside during spraying and untilthe next morning after spraying.Pregnant women should take specialprecautions to avoid exposure.

3. Bring in or cover portable outdoorfurniture, toys, laundry, pet dishesand tools.

4. Cover larger outdoor items such asbarbecue grills or sand boxes. Swingsets and items that cannot be coveredshould be rinsed thoroughly after thespraying.

5. Cover ornamental fish ponds becausepesticides are highly toxic to fish.

6. Cover vegetable gardens if you canwith plastic sheeting; wash anyexposed vegetables before storing,cooking or eating.

7. Remove shoes when entering thehome after spraying becausepesticides can be tracked indoors andremain toxic for months in syntheticcarpet fibers. Pesticides used formosquitoes are most easily degradedin direct sunlight and are shelteredwhen inside where they do notdegrade quickly.

8. Hose off window screens, doorhandles and hand railings after spray-ing occurs to avoid direct contact.

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

Canadian researchers studied, underfield conditions, the efficacy of three cit-ronella-based products (lotion, milk andsun block formulations (active ingredi-ents: 10% oil of citronella and 5% ter-pene of citronella) to protect againstbiting mosquitoes. All of the repellents“reduced the number of mosquitoes bit-ing by 95% over the 1st and 2nd 30 min-utes after application.”158

The same group of researchers as-sessed the efficacy of 3% citronellacandles and 5% citronella incense in pro-tecting against mosquito bites under fieldconditions. “Although significantly fewerbites were received by subjects at posi-tions with citronella candles and incensethan at nontreated locations, the overallreduction in bites provided by the cit-ronella candles and incense was only42.3% and 24.2%, respectively.”159

Avon Skin-So-Soft TM

When tested under laboratory conditionsagainst Aedes aegypti mosquitoes, thisproduct was shown to be mildly effective.However, with a half-life of 30 minutes,frequent reapplication is necessary tomaintain a protective layer of the oil onthe skin, which works by forming a bar-rier that insect mouthparts have difficultypenetrating.160

Mosquito trapsA range of devices are being marketedthat have been shown to trap and killmeasurable numbers of mosquitoes overa geographic range. Such traps may bean adjunct to other precautionary mea-sures, but homeowners should be awarethat depending upon their placement,such traps may attract more mosquitoesinto an area than they can catch.

If pesticide spraying occurs in yourcommunity, take precautions to limitexposure:(adapted from “Fight the Bite,” New York

Appendix 49

APPENDIX:California Mosquito Control Contacts

Public Interest Advocacy Organizations• Pesticide Watch at (213) 251-3690 ext. 308

• Environment California, at (415) 206-9185

• The Pesticide Action Network of NorthAmerica at (415) 981-1771

• Californians for Pesticide Reform at(888) CPR-4880 or (888) 277-4880

• Your local Mosquito and Vector ControlDistrict or Environmental Health Depart-ment. (See following table.)

Mosquito and Vector ControlAssociation of California: www.mvcac.org

California Department of Health Services/Vector-Borne Disease [email protected] orwww.dhs.cahwnet.gov/ps/dcdc/disb/disbindex.htm

The U.S. Environmental ProtectionAgency (EPA) Web site: www.epa.gov/pesticides/factsheets/skeeters.htm

California Mosquito Control Districtswww.mvcac.org/Download/map.pdf

Who do I contact if

I have more questions

about mosquito control

or pesticide use

in California?


California Mosquito Control Districts, available on the web at:www.mvcac.org/Download/map.pdf

Agency Contact InfoCoastal Region

Alameda County MAD 23187 Connecticut St., Hayward,-94545John R. Rusmisel510/783-7744 (510/783-3903)[email protected]

Alameda County VCSD 1131 Harbor Bay Parkway, Alameda, CA 94502William Pitcher

510/567-6800 (510/337-9137)[email protected]

Contra Costa MVCD 155 Mason Circle Concord, CA 94520Craig Downs925/685-9301 (925/685-0266)[email protected]

Marin-Sonoma MVCD 595 Helman Lane, Cotati, CA 94931 Jim Wanderscheid707/285-2200 (707/285-2210)[email protected]

Napa County MAD Post Office Box 10053, American Canyon, CA 94503Wesley A. Maffei707/553-9610 (707/553-9611)

No. Salinas Valley MAD 342 Airport Blvd., Salinas, CA 93905Peter B. Ghormley831/422-6438 (831/422-3337)[email protected]

San Mateo County MAD 1351 Rollins Road, Burlingame, CA 94010Robert Gay650/344-8592 (650/344-3843)[email protected]

Santa Clara County VCD 976 Lenzen Drive, San Jose, CA 95126Tim D. Mulligan408/792-5010 (408/298-6356)[email protected]

Santa Cruz County MVCD 640 Capitola Road, Santa Cruz, CA 95062Paul Binding831/454-2590 (831/464-9161)[email protected]

Solano County MAD 2950 Industrial Court, Fairfield, CA 94533Jon A. Blegen707/437-1116 (707/437-1187)[email protected]

Sacramento Valley Region

Burney Basin MAD Post Office Box 1049, Burney, CA 96013Michael S. Churney530/335-2133 (530/335-2663)[email protected]

Appendix 51

Butte County MVCD 5117 Larkin Road, Oroville, CA 95965James A. Camy530/533-6038 (530/534-9916)[email protected]

Colusa MAD Post Office Box 208, Colusa, CA 95932David B. Whitesell530/458-4966 (530/458-0818) [email protected]

Durham MAD Post Office Box 386, Durham, CA 95938Aaron A. Amator530/345-2875 (530/345-1792)

El Dorado Co. V.C.-CSA3 1170 Rufus Allen Road, S. Lake Tahoe, CA 96150Virginia Huber530/573-3450 (530/542-3364)[email protected]

Glenn County MVCD 165 Co. Rd. G, Willows, CA 95988Richard T. Ramsey 530/934-4025 (530/934-5971)

Lake County VCD Post Office Box 310, Lakeport, CA 95453Arthur Colwell, Ph.D.707/263-4770 (707/263-3653)[email protected]

Oroville MAD Post Office Box, CA 940, Oroville, CA 95965Jeff Cahn530/[email protected]

Pine Grove MAD Post Office Box 328, McArthur, CA 96056William Clark530/336-5740 (530/336-6866)

Placer MAD Post Office Box 216, Lincoln, CA 95648Charlie Dill916/435-2140 (916/435-8171)[email protected]

Sacramento-Yolo MVCD 8631 Bond Road, Elk Grove, CA 95624David Brown916/685-1022 (916/685-5464)[email protected]

Shasta MVCD Post Office Box 99033, Redding, CA 96099William C. Hazeleur530/365-3768 (530/365-0305)[email protected]

Sutter-Yuba MVCD Post Office Box 726, Yuba City, CA 95992Ronald L. McBride530/674-5456 (530/674-5534)[email protected]

Tehama County MVCD Post Office Box 1005, Red Bluff, CA 96080D. Andrew Cox530/527-1676 (530/527-3353)[email protected]

North San Joaquin Valley Region

East Side MAD 2000 Santa Fe Avenue, Modesto, CA 95357Claude L. Watson209/522-4098 (209/522-7841)[email protected]


Merced County MAD Post Office Box 909, Merced 95341Allan D. Inman209/722-1527 (209/722-3051)[email protected]

San Joaquin County MVCD 7759 S. Airport Way, Stockton 95206 John R. Stroh209/982-4675 (209/982-0120)[email protected]

Turlock MAD 4412 North Washington Road, Turlock 95380 Jerry M. Davis209/634-8331 (209/634-4103)[email protected]

South San Joaquin Valley Region

Coalinga-Huron MAD Post Office Box 447, Coalinga 93210Ralph Baiza559/935-3198

Consolidated MAD Post Office Box 278, Selma 93662Steve Mulligan559/896-1085 (559/896-6425)[email protected]

Delano MAD Post Office Box 220, Delano 93216Ralph T. Alls, Ph.D.661/725-3114 (661/725-3179) [email protected]

Delta VCD Post Office Box 310, Visalia 93279Michael W. Alburn559/732-8606 (559/732-7441) [email protected]

Fresno MVCD 2338 McKinley Ave, Fresno 93703David G. Farley559/268-6565 (559/268-8918)[email protected]

Fresno Westside MAD Post Office Box 125, Firebaugh 93622Elizabeth A. Cline559/659-2437 (559/659-2193)[email protected]

Kern MVCD 4705 Allen Road, Bakersfield 93312Robert A. Quiring661/589-2744 (661/589-4913)[email protected]

Kings MAD Post Office Box 907, Hanford 93232Lue Casey559/584-3326 (559/584-3310)[email protected]

Madera County MVCD 900 North Gateway Dr., Madera 93637Kevin Pinion559/674-6729 (559/674-6004)[email protected]

Tulare MAD Post Office Box 1476, Tulare 93275Marshall Norgaard559/686-6628 (559/686-2013)[email protected]

West Side MVCD Post Office Box 205, Taft 93268Don W. Black661/763-3510 (661/763-5793)[email protected]

Appendix 53

Southern California Region

Antelope Valley MVCD Post Office Box 1192, Lancaster, CA 93584Cei Kratz661/942-2917 (661/940-6367)[email protected]

Coachella Valley MVCD 43-420 Trader Place, Indio, CA 92201Donald E. Gomsi760/342-8287 (760/342-8110)[email protected]

Compton Creek MAD . 1224 So. Santa Fe Avenue, Compton, CA 90221Mitchel R. Weinbaum310/639-7375 (310/639-4768)

Greater L. A. County VCD 12545 Florence Avenue, Santa Fe Springs, CA 90670Jack Hazelrigg, Ph.D.562/944-9656 (562/944-7976)[email protected]

Long Beach -Vector Control Prog 2525 Grand Ave, Rm 220, Long Beach90815 Donald D. Cillay562/570-4132 (562/570-4038)[email protected]

Los Angeles Co. W. VCD 6750 Centinela Ave, Culver City, CA 90230Robert Saviskas310/915-7370 (310/915-9148)[email protected]

City of Moorpark/VC . 799 N. Moorpark Ave, Moorpark, CA 93020John Brand805/517-6267 (805/529-0267)[email protected]

Northwest MVCD 1966 Compton Avenue, Corona, CA 92881Major S. Dhillon, Ph.D.909/340-9792 (909/340-2515)[email protected]

Orange County VCD Post Office Box 87, Santa Ana, CA 92702Robert Sjogren, Ph.D.714/971-2421 (714/971-3940)[email protected]

Owens Valley MAP 207 W. South Street, Bishop, CA 93514Ernest Poncet760/873-7853 (760/873-3236)[email protected]

San Bernardino Co. VCP 2355 E. 5th Street, San Bernardino, CA 92410Joan Mulcare909/388-4600 (909/386-5148)[email protected]

San Gabriel Valley MVCD 1145 N. Azusa Canyon Rd, West Covina, CA 91790Steve A. West 626/814-9466 (626/337-5686)[email protected]

Santa Barbara Coastal VCD P.O. Box 1389, Summerland, CA 93067Mitchell J. Bernstein805/969-5050 (805/969-5643) [email protected]

West Valley MVCD 13355 Elliot Avenue, Chino, CA 91710Min-Lee Cheng, Ph.D.909/627-0931 (909/627-0553)[email protected]


1. Marilyn Chase and Ann Carnns, “RapidSpread of West Nile Virus Has Health Officialson Defensive,” Wall Street Journal, 13 August2002.2. Kostyukov MA et al., “Experimental infectionof Culex pipiens with West Nile virus by feedingon infected Rana ridibunda frogs and its subse-quent transmission,” Med Parazitol., 1986;6:76-8, as cited by VPIRG, “West Nile virus,Vermont, and Pesticides,” March 2001.3. California Department of Health ServicesBrochure, ‘West Nile Virus,” January 20, 2003.4. USGS, “West Nile Virus Maps 2002,” foundat cindi.usgs.gov/hazard/event/west_nile/west_nile.html5. Environmental Risk Analysis Program,Cornell University, “What’s Going on with theWest Nile Virus: Information, educationalmaterials, scientific resources about the disease,its prevention & control,” 13 March 2003.6. Seth Borenstein, “Science Tracks West NileVirus Mutating as it Creeps Across Nation,”Mercury News, 26 November 2002.7. CDC, “West Nile Virus 2002 Case Count,”reviewed 16 May 2003.8. CDC, “Provisional Surveillance Summary ofthe West Nile Virus Epidemic — United States,January—November 2002” MMWR Weekly,51(50); 1129-1133, 20 December 2002.9. Gochfeld, Michael, Professor of Environmental and Community Medicine, Robert WoodJohnson Medical School and School of PublicHealth, "Public Panic Over West Nile Virus,"American Butterflies, Summer 2000.

Endnotes

10. State of Louisiana Dept. of Health andHospitals, “Only Seven New West Nile VirusCases,” 24 October 2002.11. CDC, “Provisional Surveillance Summary ofthe West Nile Virus Epidemic — United States,January—November 2002” MMWR Weekly,51(50); 1129-1133, 20 December 2002.12. U.S. EPA, “Region/ORD Pesticides Work-shop Summary Report,” October 31 2000, 20.13. New York State Poison Control Network,“Annual Report, 1999 Data,” June 18, 2001,downloaded from www.health.state.ny.us/nysdoh/poisoncontrol/pdf 1999_annual_report.pdf on June 27, 2003.14. According to the Web site of a New Yorkpublic interest organization, the CitizensCampaign for the Environment, in 2000, 14people were hospitalized in New York State withWNV, but 100s of people reported to healthofficials adverse reactions from exposure toWNV pesticides. The DOH Pesticide Poison-ing Registry listed 14 cases of adverse pesticidereactions, in spite of very limited surveillance forsuch reactions. See www.citizenscampaign.org/campaigns/westnilevirus.htm.15. “W. Nile Tactics Shift Away From JustSpray,” New York Post, 4 May 2001,16. “City to Look Beyond Spraying for WestNile,” New York Times, 4 May 2001.17. New York City Department of Health,“West Nile Virus: A Briefing, City HealthInformation,” Vol. 19, No. 1, May 2000, pg. 2.18. New York City Department of Health,“Summary of Vital Statistics,” 1999.

Endnotes 55

19. Centers for Disease Control, “TelebriefingTranscript: West Nile Virus Activity Update,”22 August 2002.20. Guy Ashley, “East Bay getting in gear formosquitoes, West Nile,” Contra Costa Times, 14March 2003.21. Deanna McKinney, “Meeting the Challengeof West Nile Virus Without Poisons,” Journal ofPesticide Reform, Winter 2002.22. Marin/Sonoma Mosquito and VectorControl District, “Featured Mosquitoes”23. Goddard LB, Roth AE, Reisen WK, ScottTW, “Vector competence of California mosqui-toes for West Nile virus,” Emerg Infect Dis [serialonline] 200224. www.msmosquito.com/asquamig.html,downloaded 6/16/2003.25. Bobby Caina Calvan, “Calif. Readies for theWest Nile Virus,” Boston Globe, 3 April 2003, A2.26. Centers for Disease Control and Prevention,“Epidemic/epizootic West Nile Virus in theUnited States: Revised guidelines for surveil-lance, prevention, and control,” April 2001.27. To view the federal plan visit: www.cdc.gov.28. Centers for Disease Control, “Update: WestNile Virus Activity in the Eastern United States,2000,” CDC Morbidity and Mortality WeeklyReport, July 21, 2000, 49:28, www.cdc.gov/mmwr/preview/mmwrhtml/mm4928a3.htm29. Centers for Disease Control, “Epidemic/Epizootic West Nile Virus in the United States:Revised Guidelines for Surveillance, Prevention,and Control,” April 2001. On the web at.cdc.gov/ncidod/dvbid/westnile/resources/WNV-guidelines-apr-2001.pdf30. Guy Ashley, “East Bay getting in gear formosquitoes, West Nile,” Contra Costa Times, 14March 2003.31. Jodi Wilgoren, “New York MosquitoControl is Weak and Late, Experts Say,” NewYork Times, 8 September 1999, B1.32. Dan Fagin, “Doubts about Spraying —Some Experts Call it Ineffective Against WestNile Virus,” Newsday, 8 November 2000,downloaded 6/11/2003 at www.cfe.cornell.edu/risk/WNV-LArchive/11-8-00.html.33. Christine Woodside, “No Big Fall inMosquitoes After Communities Spray,” NewYork Times, 6 October 2002, 14CN.34. Dan Fagin, “Doubts about Spraying —Some Experts Call it Ineffective Against WestNile Virus,” Newsday, 8 November 2000.

35. Dan Fagin, “Doubts about Spraying —Some Experts Call it Ineffective Against WestNile Virus,” Newsday, 8 November 2000.36. David Pimentel, “Amounts of PesticidesReaching Target Pests: Environmental Impactsand Ethics,” Journal of Agricultural andEnvironmental Ethics Vol. 8, No. 1 (1995),pp. 17-29.37. Rachel Massey, “#710 West Nile Virus —Part 2,” Rachel’s Environment & Health News,26 October 2000.38. Centers for Disease Control, ”Epidemic/Epizootic West Nile Virus in the United States:Revised Guidelines for Surveillance, Prevention,and Control,” April 2001. On the web atwww.cdc.gov/ncidod/dvbid/westnile/resources/WNV-guidelines-apr-2001.pdf39. Gary Mount, “A Critical Review ofUltralow-Volume Aerosols of Insecticide,”Journal of the American Mosquito Control Associa-tion, 14(3):305-334, 1998.40. Cambridge West Nile Virus AdvisoryCommittee. “Addendum to Cambridge WNVResponse Plan,” June 2001, Cambridge, MA.41. Personal communication, Dr. WaheedBajwa, New York City Vector Control Program,June 25, 2003.42. Erin Callahan, “Untenable Choices,”Westchester Weekly, 2000, New Mass. Media Inc.43. Environmental Advocates, ”Toward SaferMosquito Control in New York State,” January2000. On the web at www.crisny.org/not-for-profit/nycap/mosquitopaper.htm44. Dr. Duane Gubler, “Resurgent Vector-BorneDiseases as a Global Health Problem,” EmergingInfectious Diseases 4:3, Centers for DiseaseControl, July 1998.45. Oliver Howard, “Impact of naled (Dibrom14) on the mosquito vectors of eastern equineencephalitis virus,” Journal of the Am MosquitoControl Assoc, Dec; 13(4):315-25, 1997.46. Jan Hollingsworth, “Fly War’s Legacy ofDoubt,” Tampa Tribune, p.1, 4 June 1998.47. Rodgers, K.E., M.L. Stern, and C.F. Ware,“Effects of subacute administration of O,S,S-trimethyl phosphorodithioate on cellular andhumoral immune response systems,” Toxicology54:183-195, 1989, 101; Russell-Manning, B.R.,1990, Malathion: The toxic time bomb, SanFrancisco, Greensward Press; Devons, B.H. et al.,1985, “O,O,S-trimethyl phosphorothioateeffects on immunocompetence,” Pestic. Biochem.Physiol, 24:251-259.


48. Rodgers, K.E., N. Leung, and C.F. Ware,1988, “Effects of acute administration of O,S,S-trimethyl phosphorodithioate on the generationof cellular and humoral immune responsesfollowing in vitro stimulation,” Toxicology51:241-253.49. Pressinger, Richard. “The Theory ShowingHow Pesticides Could Be Increasing theEncephalitis Risk,” downloaded from Chem-Toxwebsite on 11 June 2003, at www.chem-tox.com/brevard/encephalitis/.50. Sugg, William C. Maine EnvironmentalPolicy Institute. Personal communication.Includes correspondence, interviews, notes fromhearings attended, etc., in preparation of thisreport. Contact [email protected] or MEPI,POB 347, Hallowell, ME 04347 for details on aspecific reference.51. New York Public Interest Research Group,Interview with Dr. Ray Parsons. Harris County(Texas) Mosquito Control Division. September11, 1999. www.nypirg.org/mosquito.htm52. Extension Toxicology Network, CornellUniversity, “Pesticide Information Profiles,Pyrethrins And Pyrethroid,” available online atace.orst.edu/cgi-bin/mfs/01/pips/pyrethri.htm53. Cornell University Program on BreastCancer and Environmental Risk Factors,“Bibliography: Pyrethroids and the Risk ofBreast Cancer,” www.cfe.cornell.edu/bcerf/Bibliography/Pesticide/bib.pyrethroid.cfm54. Ray D.E. and P.J. Forshaw, “PyrethroidInsecticides: Poisoning Syndromes, Synergies,and Therapy,” Journal of Toxicology. ClinicalToxicology 38(2):95-101, 2000.55. Occupational Health Services, Inc. “Pyre-thrum.” Material Safety Data Sheet., 1 April1987. New York: OHS, Inc.56. Blood, Michael R. New York Daily News, 9/9/00. Artist: I’m A Victim Of Skeeter Spraying.www.nydailynews.com/2000-09-09/News_and_Views/City_Beat/a-79389.asp57. Following references on pyrethroidscompiled by No Spray Coalition in Medicalstudies indicating health hazards from pyre-throid pesticides fact sheet. www.nospray.org/pyrethroids.html58. Go, Vera, et al. Estrogenic Potential ofCertain Pyrethroid Compounds in the MCF-7Human Breast Carcinoma Cell Line, Environ-mental Health Perspectives, vol. 107, no. 3,March 1999, pages 173-177.

59. Eil, C., and Nisula, B. C., “The bindingproperties of pyrethroids to human skin fibro-blast androgen receptors and to sex hormonebinding globulin,” Journal of Steroid Biochemistry,March 1990, volume 35, issue 3-4, pages409-414.

60. Bateson, Patrick, et al, “Endocrine Disrupt-ing Chemicals (EDCs).,” London: The RoyalSociety, June 2000.

61. Narahashi, T. Nerve membrane ion channelsas the target site of environmental toxicants,Environmental Health Perspectives,71:25-9, April1987.

62. Pogoda, Janice M. and Susan Preston-Martin, “Household Pesticides and Risk ofPediatric Brain Tumors,” EnvironmentalHealth Perspectives,105:11, 1214-1220,November 1997.

63. Ludwig Maximilians University, Physiologi-cal Institute, “Toxicology Letters,” 1999 June30;107(1-3):161-76.

64. Eriksson, P. “Developmental neurotoxicity ofenvironmental agents in the neonate,”Neurotoxicology, 1997;18(3):719-26.

65. Akhtar, N., et al, “Insecticide-inducedchanges in secretory activity of the thyroid glandin rats,” Journal of Applied Toxicology, vol. 16, no.5, pages 397-400, 1996.

66. Garey, Joan, and Mary S. Wolff., “Estrogenicand Antiprohestagenic Activities of PyrethroidInsecticides,” Biochemical and Biophysical ResearchCommunications (3) 251:855-859., 1998.www.idealibrary.com/links/toc/bbrc/251/3/0

67. Elliot, M, et al, “ Metabolic Fate of PyrethrinI, Pyrethrin II, and Allethrin AdministeredOrally to Rats,” J. Agr. Food Chem. 20: 300-312,1972.

68. U.S. EPA “Synthetic Pyrethroids forMosquito Control,” www.epa.gov/pesticides/factsheets/pyrethroids4mosquitos.htm

69. Russell-Manning, B.R. 1990. Malathion:The toxic time bomb. San Francisco, CA:Greensward Press.

70. Northwest Coalition for Alternatives toPesticides (NCAP). Malathion InsecticideFactsheet. Journal of Pesticide Reform, Winter1992, Vol 12 #4.

71. Reigart, J. Routt and James R. Roberts,“Recognition and Management of PesticidePoisonings,” U.S. Environmental ProtectionAgency Office of Pesticide Programs, 1999.

Endnotes 57

72. Reuber, M.D, “Carcinogenicity and toxicityof malathion and malaoxon,” Environ. Res.37:119-153; California Department of Food andAgriculture. Medical Toxicology Branch,“Summary of toxicological data: Malathion,”Sacramento, CA, 30 July 1990; Balasubra-manian, K., et al., “Effect of malathionadministration on adrenal function in malealbino rats,” Med. Sci. Res. 18(4):129-130, 1990;Gowda, H., R.P. Uppal, B.D. Garg. 1983,“Effect of malathion on adrenal activity, liverglycogen, and blood glucose in rats,” Indian J.Med. Res. 78:847-851.

73. Jerome Blondell, Ph.D., and Monica Spann,M.P.H., U.S. EPA, “Review of MalathionIncident Reports,” August 18, 1998.

74. Erik Larsen, “A Close Watch on U.S.Borders to Keep the World’s Bugs Out,”Smithsonian, June 1987, p.110.

75. Dr. Jorge Mancillas, “How Malathion Kills,”Legislative Briefing on Malathion and MedflyIssues Testimony to the Monterey Park CityCouncil Chambers, 10 May 1995.

76. Thomas, D.C. et al. 1992. ReproductiveOutcomes in Relation to Malathion Spraying inthe San Francisco Bay Area, 1981-1982.Epidemiology, 3:32-39.

77. Anne Dawson, Sarah Hassenpflug, JamesSloan, and Izumi Yoshioka with the assistance ofAndrew Procassini, D.B.A., “California Agricul-tural Trade: Combating the Medfly Menace,”Center for Trade and Commercial Diplomacy,Monterey Institute of International Studies,Monterey, California, 1998.

78. Ray Sotero, “Newest Los Angeles Medflywas mated to a sterile male,” California FarmBureau Federation Ag Alert, May 12, 1999.

79. Aldridge, W.N. et al., “Malathion Not asSafe as Believed - 5 Die - 2,800 Poisoned,”Archives in Toxicology, 42:95-106, 1979.

80. Reeves, J.D. et al. “California ChildLeukemia & Aplastic Anemia after MalathionExposure,” The Lancet, pg.300, 8 August 1981.

81. Krause, W., “Influence of DDT, DDVP, andmalathion on FSH, LH and testosterone serumlevels and testosterone concentration in testes,”Bull. Environ. Contam. Toxicol. 18(2):231-242,1997; Krause, W., et al. “Damage tospermatogenesis in juvenile rat treated withDDVP and mala-thion,” Bull. Environ. Contam.Toxicol. 15(4):458-462, 1976.

82. Thathoo, A.K. and M.C. Prasad, “Gesta-tional disorders associated with malathiontoxicity in sheep,” Indian Vet. J., 65:379-382,1988.

83. Ishikawa, S. and M. Miyata., “Developmentof myopia following chronic organophosphatepesticide intoxication: An epidemiological andexperimental study,” in Merigan, W.H. and B.Weiss (eds.) Neurotoxicity of the visual system, NY:Raven Press, 1980.

84. Lindsay, A.E. “ Memo to Douglas D. Campt,director, U.S. EPA Office of Pesticide Programs:Section 18-USDA quarantine exemptions foruse of malathion and diazinon to eradicate exoticfruit fly species in Florida,” 16 October 1991.

85. Rodgers, K.E., M.L. Stern, and C.F. Ware,“Effects of subacute administration of O,S,S-trimethyl phosphorodithioate on cellular andhumoral immune response systems,” Toxicology,54:183-195, 1989

86. Rodgers, K.E., N. Leung, and C.F. Ware,“Effects of acute administration ofO,S,Strimethyl phosphorodithioate on thegeneration of cellular and humoral immuneresponses following in vitro stimulation,”Toxicology 51:241-253, 1988.

87. USEPA Cancer Assessment Review Com-mittee, Health Effects Division, Office ofPesticide Programs, “Cancer AssessmentDocument #2: Report of the 12-April-2000Meeting: Evaluation of the CarcinogenicPotential of Malathion.”

88. Massey, Rachel. Rachel’s Environment &Health News #709. “West Nile Virus — Part 1,”October 12, 2000. Environmental ResearchFoundation.

89. Montague, Peter. Rachel’s Environment &Health News, #562 – “The Causes Of LymphCancers,” September 04, 1997. EnvironmentalResearch Foundation.

90. Cantor, K.P. et al. 1992. “Pesticides andother risk factors for non-Hodgkin’s lymphomaamong men in Iowa and Minnesota,” Cancer Res.52:2447-2455.

91. Northwest Coalition for Alternatives toPesticides (NCAP), “Malathion InsecticideFactsheet,” Journal of Pesticide Reform, Winter1992, Vol 12 #4. www.pesticide.org/malathion.pdf

92. USEPA, Naled Summary, October 18, 1999,www.epa.gov/pesticides/op/naled/naledsum.htm


93. Cornell University Program on BreastCancer and Environmental Risk Factors,“Pesticides and Breast Cancer Risk: An Evalua-tion of Dichlorvos.”

94. Golovanova, I. L. et al, “Marine LifeDamaged by Pesticide Dibrom,” Fish Behavior.Proc. All-Union Science Conference, Nov 20-24, pg. 165, 1989.

95. Mehl, Anna et al. “The effect of trichlorfonand other organiphosphates on prenatal braindevelopment in the guinea pig,” NeurochemicalResearch, 19(5),569-574, 1994.

96. Extension Toxicology Network,”PesticideInformation Profiles, Naled,” ace.orst.edu/cgi-bin/mfs/01/pips/naled.htm.

97. US EPA, “Naled Summary,” October 18,1999,www.epa.gov/pesticides/op/naled/naledsum.htm

98. U.S. Public Health Service, “West Nile virusQ&A,” Hazardous Substance Data Bank.

99. Gallo, M. A. and Lawryk, N. J., “Organicphosphorus pesticides,” in Handbook of PesticideToxicology. Hayes, W. J., Jr. and Laws, E. R., Jr.,Eds. Academic Press, New York, NY, 1991.

100. Extension Toxicology Network, PesticideInformation Profiles, temephos.ace.ace.orst.edu/info/extoxnet/pips/temephos.htm

101. Ingram, Mrill, et al, “Reasons to ProtectThe Birds and the Bees: How an impendingpollination crisis threatens plants and the foodon your table,” Arizona Sonora Desert Museum.1998.

102. Johnson, W. W. and Finley, M. T., “Hand-book of Acute Toxicity of Chemicals to Fish andAquatic Invertebrates,” Resource Publication137. U.S. Department of Interior, Fish andWildlife Service, Washington, DC, 1980.

103. U.S. Public Health Service, “HazardousSubstance Data Bank,” Washington, DC,1995.5-9 120. University of Pennsylvania HealthSystem, West Nile virus Q&A.

104. USEPA. R.E.D. Facts: Methoprene. Officeof Pesticides and Toxic Substances, Washington,DC, 1991.10-158.

105. Extension Toxicology Network, A PesticideInformation Project of Cooperative ExtensionOffices of Cornell University, “PesticideInformation Profiles, methoprene.”

106. Hudson, R. H., et al. Handbook of Toxicityof Pesticides to Wildlife. Resource Publication

153. U.S. Department of Interior, Fish andWildlife Service, Washington, DC, 1984.5-16.107. USEPA. R.E.D. Facts: Methoprene. Officeof Pesticides and Toxic Substances, Washington,DC, 1991.10-158.108. USEPA. Guidance for the Reregistration ofPesticide Products Containing Methoprene asthe Active Ingredient. Office of PesticidePrograms, Washington, DC, 1982.10-156.109. Extension Toxicology Network, A PesticideInformation Project of Cooperative ExtensionOffices of Cornell University, et al. PesticideInformation Profiles, methoprene. ace.orst.edu/cgi-bin/mfs/01/pips/methopre.htm110. “Toxicity of methoprene to all states of thesalt marsh copepod, Apocyclops spartinus (Cyclo-poida),” J. Am. Mosq. Control Assoc. 4(4)520-523.111. McKenney, Charles L., Jr., “Developmentof Crustacean Larvae as Biomarkers of Endo-crine Disrupting Chemicals in the MarineEnvironment (Abstract),” American Society forTesting and Materials, 20-22 April 1998,Atlanta, GA, www.epa.gov/gbwebdev/ged/publica/keycb3.htm112. Maggie Fox, “Common chemical may be toblame for dead frogs.” Reuters wire serviceAugust 5, 1998; Peter Montague, “Rachel’sEnvironment & Health News, #623– AnotherPesticide Surprise,” November 5, 1998.Environmental Research Foundation, P.O. Box5036, Annapolis, MD 21403-7036.113. Montague, Peter. “Rachel’s Environment &Health News, #623 – Another Pesticide Surprise,”November 5, 1998. Environmental ResearchFoundation, P.O. Box 5036, Annapolis, MD21403-7036.114. Bryant, S.V. and Gardiner, D.M. (1992), “Reti-noic acid, local cell-cell interactions, and patternformation in vertebrate limbs,” Devel. Biol. 152:1-25.115. Maggie Fox, “Common chemical may be toblame for dead frogs.” Reuters wire serviceAugust 5, 1998; Montague, Peter, “Rachel’sEnvironment & Health News, #623 – AnotherPesticide Surprise,” November 5, 1998.Environmental Research Foundation, P.O. Box5036, Annapolis, MD 21403-7036.116. Saltonstall, Dave, “Lobsters Vanish andFishermen too, Fingers pointed at skeeter spray forL.I.’s dieoff,” New York Daily News, 6 August 2000.117. Laurie Nadel, “Mosquito Control:Weighing Cost Versus Benefits,” New YorkTimes, 11 August 2002, 14 LI1.

Endnotes 59

118. Toxics Law Daily, 9/14/00.119. Burridge, L. E., and Haya, K. (1997).”Le-thality of pyrethrins to larvae and postlarvae ofthe American lobster (Homarus americanus).,”Ecotoxicology and Environmental Safety 38, 150-154; Pinkney, A. E., et al., “Effects of themosquito larvicides temephos and methopreneon insect populations in experimental ponds,”.Environmental Toxicology and Chemistry,19(3):678-684. 2000; Reish, D.J. LeMay, J.A. ,and Asato, S.L. 1985, “The effect of BTI (H-4)and methoprene on two species of marineinvertebrates from southern California estuar-ies,” Bull. Soc. Vector. Ecol., 10(1):20-22; Chu,K.H., Wong, C,K. and Chuid, K.C. 1997,“Effects of the insect growth regulator (S)-methoprene on survival and reporodution of thedaphnia Moina macrocopa,” EnvironmentalPollution. 96(2):173-178; Bircher, S. and Ruber,E. 1988, “Toxicity of methoprene to all states ofthe salt marsh copepod, Apocyclops spartinus(Cyclopoida).,” J. Am. Mosq. Control Assoc.4(4)520-523; Betzer, D.P. and Sjogren, R.D.1986. Potential effects of altosid (Methoprene)briquet treatments on Eubranchipus bundyi(Anostraca: Chirocephalidae). J. Am. Mosq.Control Assoc. 2(2):226-227.120. Diane Martindale, “Lobsters are the firstvictims of New York’s pesticide frenzy,” NewScientist, 12 August 2000.121. ca-seafood.ucdavis.edu/csc_org/index.htm122. S Degitz et al, Aquatic Toxicology 64(2003) 97-105123. US EPA, Biopesticide Fact Sheet, Novem-ber 1999, www.epa.gov/pesticides/biopesticides/factsheets/fs128128e.htm124. Ibid.125. Organic Farming Workgroup, “Mission,”2001, groups.ucanr.org/organic/volunteer.htm126. Ingram, Mrill, et al., “Reasons to ProtectThe Birds and the Bees: How an impendingpollination crisis threatens plants and the foodon your table,” Arizona Sonora Desert Museum.1998. www.desertmuseum.org/fp/ten_reasons.html127. Siebert, J. W. 1980. Beekeeping, pollinationand externalities in California agriculture.American Journal of Agricultural Economics 62:165-171.128. Kittredge, Jack. Social Action Program,Northeast Organic Farming Association. Emailcorrespondence.

129. U.S. EPA, “Inert Ingredients in PesticideProducts,” on the web at www.epa.gov/opprd001/inerts/, last updated 6 January 2003.

130. Mueller-Beilschmidt, Doria. 1990. Toxicol-ogy and Environmental Fate of SyntheticPyrethroids. Journal of Pesticide Reform 10 (3).

131. No Spray Coalition. Press release. 1/25/01.

132. Jankovic, J., “A Screening Method forOccupational Reproductive Health Risk,”American Industrial Hygiene Association Journal.57: 641-649. 1996.

133. Diel, F. Et al., “Pyrethroids and piperonylbutoxide affect human T-lymphocytes in vitro.”Toxicology Letters, Vol. 107, Nos. 1-3, June 1999,pp. 65-74.

134. No Spray Coalition Technical Bulletin,10/24/00. P.O. Box 334, Peck Slip Station, New York,NY 10272-0334. www.nospray.org/technical.html

135. Montague, Peter, “Rachel’s Environment &Health News, #586 – The PrecautionaryPrinciple,” February 19, 1998. EnvironmentalResearch Foundation, P.O. Box 5036, Annapolis,MD 21403-7036. www.rachel.org/bulletin/bulletin.cfm?Issue_ID=532&bulletin_ID=48

136. United States Environmental ProtectionAgency (USEPA). EPA List of Pesticides Bannedand Severely Restricted in the U.S.www.epa.gov/oppfead1/international/piclist.htm

137. US EPA Office of Research and Develop-ment, “Region/ORD Pesticides WorkshopSummary Report,” 31 October 2000.

138. Gochfeld, Michael. Professor of Environ-mental and Community Medicine, RobertWood Johnson Medical School and School ofPublic Health. Public Panic over West NileVirus. American Butterflies. Summer, 2000.

139. Gochfeld, Michael. Professor of Environ-mental and Community Medicine, RobertWood Johnson Medical School and School ofPublic Health. Public Panic over West NileVirus. American Butterflies. Summer, 2000.

140. No Spray Coalition. Press release. 1/24/01. P.O.Box 334, Peck Slip Station, New York, NY 10272-0334. www.safe2use.com/ca-ipm/01-01-25a.htm

141. Juan Gonzalez, “Eye on Skeeter-SprayBid,” New York Daily News, 4/3/01.142. Mosquito and Vector Control Associationof California, “Proceedings and Papers of theSeventieth Annual Conference of the Mosquitoand Vector Control Association of California,”27 January 2002.


143. Massey, Rachel, “Rachel’s Environment &Health News #710. West Nile Virus — Part 2,”October 26, 2000. Environmental ResearchFoundation, P.O. Box 5036, Annapolis, MD21403-7036.

144. Environmental Advocates, “Toward SaferMosquito Control in New York State,” January2000. www.crisny.org/not-for-profit/nycap/mosquitopaper.htm

145. Wes Maffie, “San Francisco Bayshore’sMost Numerous Resident,” California Coastand Ocean, Winter 1998-1999.

146. For a nice overview of OMWM, seeChristopher Lesser’s “Open Marsh WaterManagement, A Source Reduction Techniquefor Mosquito Control.” Delaware MosquitoControl Section, on the web at www.dnrec.state.de.us/fw/mosquito Final%20Draft%202%20of%20omw marticleapril.pdf

147. Robert Scheirer, U.S. Fish and WildlifeService, “Wetlands Restoration and MosquitoControl,” Northeastern Mosquito ControlAssociation, December 1994.

148. For example, please see Erie County.Standing Water Monitoring Report Form.www.erie.gov/standing_water_form.phtml

149. Adapted from the Sacramento/YoloMosquito & Vector Control District.

150. Massey, Rachel, “Rachel’s Environment &Health News #710. West Nile Virus — Part 2,”October 26, 2000. Environmental ResearchFoundation, P.O. Box 5036, Annapolis, MD21403-7036.151. Fradin, Mark S., M.D., and John F. Day,Ph.D. “Comparative Efficacy of Insect Repel-lents against Mosquito Bites,” New England

Journal of Medicine, 347:13-18 July 4, 2002.152. USEPA Office of Prevention Pesticides,and Toxic Substances, “Reregistration EligibilityDecision. (RED): DEET,” EPA publication 738-R-98-010. www.epa.gov/oppsrrd1/REDs/0002red.pdf, September 1998.153. Abou-Donia, Mohamed, Ph.D., “DukePharmacologist Says Animal Studies on DEET’sBrain Effects Warrant Further Testing andCaution in Human Use,” Duke UniversityMedical Center, 1 May 2002.154. Bruce Eldridge, UC Davis, “Pest Notes:Mosquitoes,” February 1998.155. Available on the web at www.homs.com andwww.buzzoff.us156. Mark Fradin M.D. and John Day Ph.D.,“Comparative Efficacy of Insect RepellentsAgainst Mosquito Bites,” New England Journal ofMedicine 347:13-18, 4 July 2002.157. Mark Fradin M.D., “Mosquitoes andmosquito repellents: A clinician’s guide,” Annalsof Internal Medicine, 1 June 1998, 128:931-940.158. Lindsay, L.R., et al, “Field Evaluation ofthe Efficacy of Three Druide Reg. Citronella-Based Repellents to Protect Against AedesSpecies Mosquitoes in Ontario,” 1996.159. Lindsay, L.R., et al.,“Evaluation of theEfficacy of 3% Citronella Candles and 5%Citronella Incense for Protection Against FieldPopula-tions of Aedes Mosquitoes,” Journal ofthe American Mosquito Control Association 12 (2):293-294, 1996.160. Schreck CE, McGovern TP, “Repellentsand other personal protection strategies againstAedes albopictus,” J Am Mosq Control Assoc.,5:247-50, 1989.

Overkill: Why Pesticide Spraying for West Nile Virus in California ...

Documents