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New York Public Interest Research Group New York Coalition for Alternatives to Pesticides | ||||||||
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January, 2000 | ||||||||
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INTRODUCTION Last fall, the dual crises of West Nile encephalitis and widespread
pesticide spraying highlighted significant gaps in the preventative public
health infrastructure of many, if not all, of the affected municipalities
in the New York City region. During this winter hiatus, while state and
county budgets are being negotiated, it is time to step back and fully
evaluate the events of the fall in order to plan effectively and avoid
repeating them.
There is no foolproof means of preventing infectious disease outbreaks,
and their incidence will likely be exacerbated and entail more unfamiliar
illnesses as global warming and global travel increase microbe
circulation. We will always be at risk. But, when faced with similar
hazards, other communities across the country have found that it is
possible to keep them in check without the kind of wholesale pesticide
exposure spawned by this past fall's outbreak. In Houston, Los Angeles,
St. Louis, and other areas where mosquito-borne diseases erupt repeatedly,
widespread aerial spraying of pesticides that target adult mosquitoes
(known as adulticides) rarely if ever occurs. We have an example of the
elements of a comprehensive mosquito control program closer to home in
Suffolk County, but if the preventative measures it employs are not fully
financed and consistently followed regionwide, everyone remains at risk.
It is essential to implement preventative measures, not only because,
ideally, disease outbreaks should be avoided, rather than contained after
they have claimed lives, but also because the containment measure _
pesticide spraying _ entails risks of its own. Furthermore, over-reliance
on emergency applications of adulticides, as opposed to preventative
public health measures, is one of the factors implicated in the resurgence
of other mosquito-borne diseases, such as malaria and dengue fever, in
other parts of the world.1
The New York State Department of Health (DOH) has put forward an
overall game plan for addressing a potential disease outbreak in the
coming season. Although it contains many necessary elements, it omits
several others (outlined below under alternative mosquito control). Nor
does it contain any explicit provisions for follow-up analysis of last
year's events: the actual and possible course of the epidemic, whether or
not aerial spraying influenced that course, and the corollary public
health effects of pesticide exposure. With the greater perspective that
hindsight allows, the adverse effects of the pesticides used must be fully
examined and compared to the risks of the encephalitis for all affected
populations. The pesticides' actual efficacy in checking the threatened
epidemic must also be objectively evaluated.
West Nile encephalitis is not the only, or even the most dangerous,
mosquito-borne disease that looms on the horizon in this
region.2 But this moment represents an opportunity to look at
all aspects of the crisis in order to learn how best to prevent other
potential epidemics at least cost to our overall health and the
environment.
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PESTICIDE RISKS The pesticides chosen to combat West Nile encephalitis are not neutral agents, but entail their own entirely separate set of risks. The following briefly summarizes the characteristics of the three major pesticides used last fall for mosquito control.
Malathion. Malathion is an organophosphate insecticide that
works by interfering with an enzyme, cholinesterase, essential to normal
nervous system function in insects and humans alike. Although it is one of
the less acutely poisonous of this family of pesticides, exposure to
malathion nonetheless entails real toxicity concerns, including
respiratory distress, headaches, dizziness, and nausea.3 Like
all organophosphates, at high doses it can cause more serious
symptoms.4 For example, malathion was the second leading cause
of hospitalization for occupational pesticide poisoning in the United
States during the period 1977-1982.5 A recent study of acute
adverse effects from aerially applied malathion bait for medfly control in
Florida found 123 probable or possible cases tied to the spraying,
including respiratory, gastrointestinal, neurological effects, dermatitis,
and eye damage.6
Infants and children, whose immature nervous systems are vulnerable to
insult, and newborns, whose metabolisms are less capable of detoxifying
malathion, are more susceptible than adults to its toxic
effects.7 Organophosphate poisoning in children may also result
in a different set of symptoms than adults commonly experience, including
increased muscle tension and rigidity.8
Information on long-term, chronic effects is less abundant. Currently,
malathion has not yet been classified by the United States Environmental
Protection Agency (EPA) as to its carcinogenic potential, although a
decision on its classification is pending and likely in the early part of
2000.9 Over the years, reports in the epidemiological
literature have indicated that malathion may compromise the immune
system,10 cause reproductive harm,11 and cause
genetic mutations or interfere with normal cell replication.12
One study of aerially applied malathion for medfly control in California
found an association between malathion exposure during the second
trimester of pregnancy and the occurrence of gastrointestinal
abnormalities in infants.13
Being a broad spectrum insecticide, malathion kills other insects as
well as mosquitoes, including honeybees, to which it is highly toxic. It
is also highly toxic to many aquatic organisms and the aquatic stages of
amphibians.14
Resmethrin and d-phenothrin. Resmethrin and d-phenothrin (also
known as SumithrinŽ) are synthetic pyrethroid insecticides.15
Pyrethroids, like organophosphates, affect the nervous system, though they
do not inhibit cholinesterase. They are of relatively low acute toxicity,
although poisoning can occur and allergic responses have been
reported.16 There are also reports of persistent symptoms when
exposures occurred indoors.17
Like malathion, resmethrin and d-phenothrin have not yet been
classified with regard to carcinogenicity, although products that contain
these substances often include the synergist piperonyl butoxide (PBO),
which has been classified by the EPA as a possible human carcinogen, as
have several other pyrethroid insecticides.18 There are
indications that pyrethroids may interfere with the immune19
and endocrine systems.20 Other adverse chronic effects,
including effects on the liver and thyroid, have been reported in
toxicology testing of resmethrin.21
How these reports of possible chronic health problems of malathion,
resmethrin, and d-phenothrin may relate to the dose or frequency of
exposure encountered in last fall's spraying campaign is unknown and to
date, no cataloguing of adverse effects has been forthcoming from the
state or local health departments that would help with such an assessment.
It is also impossible to say how they may interact with the other
pesticides to which area residents are exposed. Data on such chemical
interactions are virtually nonexistent. | |||||
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BASICS OF ALTERNATIVE MOSQUITO CONTROL
Effective preventative mosquito control thus relies on a combination of
before-the-fact measures, including: ˇ Removal of
breeding habitat by reducing standing water wherever
possible.23 This is less effective with mosquitoes, including
some Culex species, which breed in confined or inaccessible water
sources such as storm drains.
ˇ The use of meteorological data to identify weather patterns known to
exacerbate specific vector-borne diseases (such as the prolonged drought
conditions followed by heavy rains that the New York City region
experienced last summer) and follow up with enhanced monitoring when such
conditions exist.24
ˇ Control of mosquito populations when they are in the larval and pupal
stages. There are a variety of non-toxic and least toxic methods of larval
control, such as applying Bacillus thuringiensis israelensis (BTI)
bacteria to stagnant waters, using Bacillus sphaericus in storm
sewers, and stocking isolated water bodies with mosquito-eating
fish.25 Certain fungal and zooplankton species that attack
mosquito larvae have been examined as potential control
measures26 and insect growth regulators are currently in use
(though these, by interfering with insect hormonal signals, may pose
endocrine system hazards beyond their intended use). Mechanical controls
in the larval and pupal stage include use of light vegetable-based oils to
smother egg rafts, and (as yet untested) controlled burns.27
Some of these products or techniques have effects on non-target species
and thus each use should be evaluated from this perspective.28
ˇ Trapping and monitoring mosquitoes to detect the presence of
mosquito-borne illnesses and their levels in the mosquito population.
Trapping can also localize those areas of greatest mosquito/disease
potential should a targeted response with least-toxic insecticides be
deemed necessary, instead of blanket spraying of wide areas. In addition
to monitoring, new traps are on the market, using carbon dioxide as a
lure, which are designed to control mosquito populations for areas of up
to an acre.
ˇ The use of sentinel birds to detect the presence of disease before it
reaches humans. For instance, chickens are commonly used bird hosts for
monitoring whether St. Louis encephalitis is present in the local bird
population. Like trapping and monitoring of mosquitoes, the use of
sentinels detects the presence of disease before it reaches human
populations and helps pinpoint the areas where it must be
controlled.29
The benefits of preventive control and monitoring are myriad. They
reduce the likelihood that a surprise outbreak will occur while minimizing
the use of hazardous pesticides. Harris County, Texas (Houston), which has
one of the most active St. Louis encephalitis programs in the country, has
not resorted to aerial spraying for years. Through effective monitoring,
its program can identify infected areas a month before any human comes
down with the virus, and thereby address potential outbreaks at the
source. This approach not only saves human lives, but also reduces
pesticide use and saves the county approximately one million dollars each
year.30
Examining the 1999 Outbreak and Response
No plans for a new mosquito season can be confidently accepted unless
they are based on a full and rigorous assessment of the events of last
fall. The following issues should be thoroughly examined by state and
county health departments, and results reported to the public:
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The observed adverse effects of spraying. A complete accounting of all adverse effects associated with this crisis, whether from the disease or the spraying, is essential in order to evaluate their relative risks. The Centers for Disease Control's (CDC) recent assessment of human poisoning incidents from malathion spraying for medfly control in Florida provides a precedent for assessing such effects ,31 as do at least two birth defect studies done in the wake of medfly spraying in California.32 Retrospective surveys of clinic and emergency room admissions, calls to poison control hotlines, private physician records, and birth defects registries can all be used to catalogue and assess the dimension, nature, and severity of adverse reactions for comparison to the toll (actual and potential) from encephalitis. Environmental impacts on non-target insect, bird, and aquatic species must also be assessed. The potential and actual size and virulence of the West Nile epidemic. The projected possible dimensions of the West Nile outbreak that caused state health authorities to recommend spraying must be fully disclosed. Messages from state and local authorities describing the low relative virulence and likelihood of contracting West Nile disease (apparently in order to quell public panic over the disease) directly conflicted with the dramatic remedy chosen _ widespread pesticide spraying. These disparate signals cannot be reconciled without a full accounting of the underlying assumptions of the potential epidemic by state and federal authorities. The size, severity, and relevance of other West Nile epidemics across the globe; mosquito population data and infection rate; local serological studies; and a catalogue of case outcomes, should all be compiled to both describe the assumptions made last fall when deciding on a course of action, and to verify the accuracy of those assumptions in light of what actually transpired.
Spraying efficacy. The state must examine the actual course of
the epidemic to determine whether spraying was truly effective in checking
it. Data now available indicate that the epidemic peaked in late August,
prior to the earliest spraying on September 3.33 The overall
effectiveness of the spraying should thus be assessed, but particularly
that spraying which occurred after cold weather had set in and mosquito
dormancy begun. Experience with other vector-borne diseases can serve as
models for making such judgements. For example, aerial and ground
adulticide spraying for control of Aedes aegypti, the mosquito
species responsible for spreading dengue fever, are widely acknowledged to
be ineffective at both controlling the mosquito population and influencing
the course of dengue epidemics.34 Though this may be due to
features of Aedes aegypti natural ecology not shared by all other
mosquito species, the fact that spraying programs of long standing were
ultimately found futile indicates that pesticide efficacy (not the simple
of efficacy of killing exposed mosquitoes but the broader efficacy of
controlling populations and curtailing disease) is an open question with
each new climate/mosquito/disease combination that arises. All potential
disease vectors (other mosquito species besides Culex pipiens may
have been involved) must be evaluated in this manner.
RECOMMENDATIONS DOH has released the outline of a
"collaborative" campaign with county health departments to tackle a
potential West Nile outbreak next spring.35 The plan focuses on
breeding site abatement, disease reporting, mosquito and bird/animal
surveillance, laboratory capacity and readiness _ all essential elements
of a successful plan. Missing however are a number of key steps referred
to above, most notably biological or least toxic larvaciding, that are
hallmarks of successful vector control programs across the country.
Breeding site reduction alone cannot accomplish larval population
reduction because many of the potential vector species breed in water
sources, such as storm drains, sewers, and wetlands, that by their nature
cannot be eliminated.
A comprehensive DOH plan, to be implemented in conjunction with the
counties, should include all of the following:
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| Long term mosquito monitoring and preventative control. When
spring arrives, a comprehensive mosquito control policy must be in place _
one which uses all of the various techniques outlined above and also
investigates newer, non-toxic adult mosquito trapping technology for
potential effectiveness. Avoiding the use of adulticides should be a
priority. Regardless of whether the West Nile virus reemerges this spring,
the state must maintain a constant vigilance for potential mosquito-borne
disease outbreaks, including those of a far more serious nature, such as
eastern equine encephalitis. Early detection and control is safer for
humans and the environment, because it minimizes the use of pesticides and
uses animal sentinels, not humans, as a surveillance tool. A preventative
approach is far less expensive and more effective than the after-the-fact
spraying resorted to last fall.
Coordination among state and local public health officials to
improve surveillance, control measures, and emergency response
planning. The state should work closely with counties, coordinating
and monitoring their varying responses with one another and those of
neighboring states, some of which have effective mosquito control
programs. The state should develop a regional plan for monitoring and
preventing disease outbreaks, and timely information and resource sharing
to implement such a plan. A working group of state and local health
officials has begun this task. Their meetings should be well-advertised,
open, and should provide timely documentation of their plans and
conclusions.
Funding for implementation. The State Legislature should ensure,
through the budget process, that adequate funding is provided to the State
Department of Health both for its own coordination efforts and for
reimbursement to the counties for monitoring and surveillance. To date
reimbursement levels to the counties for expensive monitoring,
surveillance, and larvaciding activities have not been clarified.
A vector control plan to guide the state in responding to future
arboviral disease outbreaks. These response guidelines should include
different response recommendations for each potential arbovirus keyed to
threshold levels of disease in sentinel birds and mosquitoes, mosquito
activity, and human cases. Full-scale aerial spraying response is not the
appropriate response to most disease situations and should not constitute
the first line of defense when arboviruses are detected. Other states,
such as California36 and Massachusetts have tiered systems for
responding to different disease potential indicators in sentinel,
mosquito, animal, and human populations.
Curtailment of other pesticide use. Both because of their
inherent hazards, and the risk of developing resistance and
cross-resistance in disease vector species,37 overall pesticide
use in New York State should be minimized. Purely aesthetic uses, such as
lawn and garden applications, should be eliminated. Other pesticide uses
for which ready alternatives exist, such as many interior structural
applications, should also be eliminated. The state should phase-out its
own use of most pesticides (as communities across the country, including
six New York State municipalities, have already begun doing) and should
actively support organic farming, through research and procurement
programs. Avoiding the use of adulticides should be one of the inherent
tenets of a vector control program. But in the extreme event that some
applications are necessary to prevent a serious disease outbreak, their
effectiveness as a control tool is potentially compromised by the
widespread, frivolous use of the pesticides that are the same as or
related to the agents of mosquito control, or which confer
cross-resistance to them.
CONCLUSION
The events of this past fall should serve as a wake-up call to state
and local officials to examine not only disease detection and response
readiness, but also pest and pesticide risks in general, in order to
devise preventative, less hazardous methods of dealing with them. We
should be proceeding forward with alternative means of preventing
outbreaks, and we should do so in tandem with a close examination of the
actual events of the fall in order to make more educated predictions of
and responses to any future disease occurrence.
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REFERENCES
1 Gubler, D.J. 1998. Resurgent Vector-Borne Diseases as a
Global Health Problem. Emerging Infectious Diseases. 4(3):442-450.
2 Deibel, R. et al. 1979. Arboviruses in New York State.
American Journal of Tropical Medicine. 28(3):577-582.
3 Reigart, J.R. and J.R. Roberts. 1999. Recognition and
Management of Pesticide Poisonings. United States Environmental
Protection Agency. EPA 735-R-98-003.
4 Ibid.
5 Blondell, J. 1997. Epidemiology of Pesticide Poisonings in
the United States, With Special Reference to Occupational Cases.
Occupational Medicine: State of the Art Reviews. 12(2) 209-221.
6 Morbidity and Mortality Weekly Report. 1999. Surveillance
for Acute Pesticide-Related Illness During the Medfly Eradication Program
_ Florida, 1998. Morbidity and Mortality Weekly Report. 48(44):
1015-1027.
7 National Research Council. 1993. Pesticides in the
Diets of Infants and Children. National Academy Press. Washington D.C.
8 Lifshitz, M. et al. 1999. Carbamate and organophosphate
poisoning in young children. Pediatric Emergency Care.
15(2):102-103. see also Wagner, S.L. and D.L. Orwick. 1994. Chronic
Organophosphate Exposure Associated with Transient Hypertonia in an
Infant. Pediatrics. 94(1):94-97.
9 Burnam. W.L. August 25, 1999 Memorandum. Office of
Pesticide Programs List of Chemicals Evaluated for Carcinogenic
Potential. United States Environmental Protection Agency.
10 Fan, A. 1998. 1998 Malathion Literature Review.
Memorandum from Anna M. Fan PhD, Chief, Pesticide And Environmental
Toxicology Section to Richard Kreutzer, M.D. Chief Environmental Health
Investigations Branch, Department of Health Services, California
Environmental Protection Agency. June 26, 1998. see also State of
California Department of Health Services. 1991. Health Risk Assessment
of Aerial Application of Malathion-Bait. Berkeley, CA. Desi, I. et al.
1978. Studies on the Immunosuppressive Effect of Organochlorine and
Organophosphoric Insecticides in Subacute Experiments. Journal of
Hygiene, Epidemiology, Microbiology, and Immunology. 1:115-122.
11 Contreras H.R. and E. Bustos-Obregon. 1999. Morphological
alterations in mouse testis by a single dose of
malathion. Journal of Experimental Zoology. 284(3):355-9. see also
Balasubramanian, K. et al. 1987. Effect of malathion on the testis of male
albino rats. Medical Science Research. 15:229-230. see also
Wyttenbach, C.R. and S.C. Thompson. 1985. The Effects of the
Organophosphate Insecticide Malathion on Very Young Chick Embryos:
Malformations Detected by Histological Examination. The American
Journal Of Anatomy. 174:187-202.
12 See State of California and Fan note 10 above. see also
Rupa, D.S. et al. 1991. Frequency of Sister-Chromatid Exchange in
Peripheral Lymphocytes of Male Pesticide Applicators. Environmental and
Molecular Mutagenesis. 18:136-138. see also New Jersey Department of
Health and Senior Services. 1997. Hazardous Substances Fact Sheet:
Malathion. Trenton, New Jersey.
13 Thomas, D.C. et al. 1992, Reproductive Outcomes in
Relation to Malathion Spraying in the San Francisco Bay Area, 1981-1982.
Epidemiology. 3:32-39.
14 Extension Toxicology Network. 1996. Pesticide
Information Profile: Malathion. Oregon State University.
15 Resmethrin is the active ingredient in ScourgeŽ, which
was ground-sprayed. D-phenothrin is the active ingredient in AnvilŽ, which
was aerially sprayed.
16 See Reigart and Roberts note 3 above. see also Extension
Toxicology Network note 14 above.
17 Muller-Mohnssen, H. 1999. Chronic sequelae and
irreversible injuries following acute pyrethroid intoxication.
Toxicology Letters. 197:161-175.
18 See National Research Council note 7 above.
19 Diel, F. et al. 1999. Pyrethroids and piperonyl _butoxide
affect human T-lymphocytes in vitro. Toxicology Letters. 107:65-74.
see also Stiller-Winkler, R. et al. 1999. Immunological parameters in
humans exposed to pesticides in the agricultural environment.
Toxicology Letters. 107:219-224.
20 Go, V. et al. 1999. Estrogenic Potential of Certain
Pyrethroid Compounds in the MCF-7 Human Breast Carcinoma Cell Line.
Environmental Health Perspectives. 107(3):173-177. Eil, C. and B.C.
Nisula. 1990. The Binding Properties of Pyrethroids to Human Skin
Fibroblast Androgen Receptors and to Sex Hormone Binding Globulin.
Journal of Steroid Biochemistry. 35(3/4):409-414.
21 Extension Toxicology Network. 1996. Pesticide
Information Profile: Resmethrin. Oregon State University.
22 Lenormand, T. et al. 1999. Tracking the evolution of
insecticide resistance in the mosquito Culex pipiens. Nature.
400:861-864. Sukontason, K. et al. 1998. Organophosphate and Pyrethroid
Susceptibilities of Culex Salinarius Adults from Texas and New
Jersey. Journal of the American Mosquito Control Association.
14(4):477-480. Bisset, J. et al. 1997. Cross-Resistance to Pyrethroid and
Organophosphorus Insecticides in the Southern House Mosquito (Diptera:
Culicidae) from Cuba. Journal of Medical Entomology. 34(2):244-246.
Wirth, M.C. and G. P. Georghiou. 1996. Organophosphate Resistance in
Culex Pipiens from Cyprus. Journal of the American Mosquito
Control Association. 12(1):112-118. Rawlins, S.C. and J.O. H. Wan.
1995. Resistance in Some Caribbean Populations of Aedes Aegypti to
Several Insecticides. Journal of the American Mosquito Control
Association. 11(1):59-65. Mekuria, Y. et al. 1994. Malathion
Resistance in Mosquitoes from Charleston and Georgetown Counties of
Coastal South Carolina. Journal of the American Mosquito Control
Association. 10(1)56-63.
23 Olkowski. W. et al. 1991. Common-Sense Pest
Control. The Taunton Press. Newtown, Connecticut.
24 Moore, C.G. et al. 1993. Guidelines for Arbovirus
Surveillance Programs in the United States. Centers for Disease
Control.
25 See Olkowski et al. note 23 above. see also Webb, C.E.
and R.C. Russell. 1999. Towards Management of Mosquitoes at Homebush Bay,
Sydney Australia I: Seasonal Activity and Relative Abundance of Adults of
Aedes Vigilax and Culex Sitiens, and Other Salt March
Species, 1993-94 Through 1997-98. Journal of the American Mosquito
Control Association. 15(2):242-249. see also Elias, M. et al. 1995.
Biological Control of Mosquito Larvae by Guppy Fish. Bangladesh Medical
Research Council Bulletin. 21(2):81-86.
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26 Mittal, P.K. et al. 1997. Laboratory Evaluation of the Biocontrol Potential of Mesocyclops thermocyclopoides (Copepoda: Cycolpidae) Against Mosquito Larvae. Southeast Asian Journal of Tropical Medicine and Public Health. 28(4):857-861. see also Serit, M.A. and H.H. Yap. 1984. Comparative Bioassays of Tolypocladium Cyclindrosporum Gams (California Strain) Against Four Species of Mosquitoes in Malaysia. Southeast Asian Journal of Tropical Medicine and Public Health. 15(3):331-233. 27 Janousek, T.E. and J.K. Olson. 1994. Effects of a Natural Marsh Fire on Larval Populations of Culex Salinarius in East Texas. Journal of the American Mosquito Control Association. 10(2):233-235. 28 See Olkowski et al. note 23 above. 29 See Moore et al. note 24 above. 30 Interview with Dr. Ray Parsons. Harris County (Texas) Mosquito Control Division. September 11, 1999. 31 See MMWR note 6 above. 32 See Thomas, D.C et al. note 13 above. see also Grether, J.K. et al. 1987. Exposure to Aerial Malathion Application and the Occurrence of Congenital Anomalies and Low Birthweight. American Journal of Public Health. 77(8):1009-1010. 33 Morbidity and Mortality Weekly Report. 1999. Update: West Nile Virus Encephalitis _ New York, 1999. Morbidity and Mortality Weekly Report. 48(41):944-946. Morbidity and Mortality Weekly Report. 1999. Outbreak of West Nile-Like Viral Encephalitis _ New York, 1999. Morbidity and Mortality Weekly Report. 48(38):845-849. 34 Castle, T. et al. 1999. Absence of impact of aerial malathion treatment on Aedes aegypti during a dengue outbreak in Kingston, Jamaica. Pan American Journal of Public Health. 5(2):100-104. Newton, E.A.C. and P. Reiter. 1992. A Model of the Transmission of Dengue Fever with an Evaluation of the Impact of Ultra-Low Volume (ULV) Insecticide Applications on Dengue Epidemics. American Journal of Tropical Medicine. 47(6):709-720. Perich, M.J. et al. 1990. Comparison of Ground and Aerial Ultra-Low Volume Applications of Malathion Against Aedes Aegypyti in Santo Domingo, Dominican Republic. Journal of the American Mosquito Control Association. 6(1):1-6. Gubler, D.J. 1989. Aedes Aegypti and Aedes Aegypti-Borne Disease Control in the 1990s: Top Down or Bottom Up. American Journal of Tropical Medicine. 40(6):571-578. 35 State of New York Department of Health. 1999. State Health Officials Target West Nile Virus. December 16, 1999 Press Release. 36 Reisen, W. et al. 1995. Interagency Guidelines for the Surveillance and Control of Selected Vector-Borne Pathogens in California. Mosquito and Vector Control Association of California. Elk Grove, CA. 37 See all references note 34 above. | ||||||||||||||||||
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