[afro-nets] Two Articles on Mosquito Control

[Zaher Farag <zaherefarag@yahoo.com>]

Two Articles on Mosquito Control
--------------------------------

Dear Sir:

I have noted questions and answers regarding mosquito control
among your readers. I offer two articles below which have ap-
peared here that may be of assistance. While the articles them-
selves may not offer anything new to your readers the resources
cited and the people involved may prove to be of great assis-
tance to your readers.

Sincerely,
Z. E. Farag, Ph.D.
mailto:zaherefarag@yahoo.com


--
Human Exposure to Mosquito-Control Pesticides - Mississippi,
North Carolina and Virginia, 2002 and 2003

Public health officials weigh the risk for mosquito-borne dis-
eases against the risk for human exposure to pesticides sprayed
to control mosquitoes (1). Response to outbreaks of mosquito-
borne diseases has focused on vector control through habitat re-
duction and application of pesticides that kill mosquito larvae.
However, in certain situations, public health officials control
adult mosquito populations by spraying ultra-low volume (ULV)
(<3 fluid ounces per acre [oz/acre]) mosquito-control (MC) pes-
ticides, such as naled, permethrin, and d-phenothrin. These ULV
applications generate aerosols of fine droplets of pesticides
that stay aloft and kill mosquitoes on contact while minimizing
the risk for exposure to persons, wildlife, and the environment
(2). This report summarizes the results of studies in Missis-
sippi, North Carolina, and Virginia that assessed human exposure
to ULV naled, permethrin, and d-phenothrin used in emergency,
large-scale MC activities. The findings indicated ULV applica-
tion in MC activities did not result in substantial pesticide
exposure to humans; however, public health interventions should
focus on the reduction of home and workplace exposure to pesti-
cides.

Mississippi, 2002

The 2002 West Nile virus (WNV) epidemic in Mississippi prompted
an increase in MC activities, including application of ULV per-
methrin by truck-mounted foggers (Figure). Because of concerns
about potential health effects from pesticides, the Mississippi
Department of Health and CDC assessed whether MC activities in-
creased individual urine pesticide metabolite concentrations.
During September 8--19, 2002, investigators selected a geo-
graphically-random sample of 125 persons by using maps of two
regions where public health officials applied MC pesticides and
67 persons from two control regions. Each participant completed
a questionnaire describing home and occupational use of pesti-
cides and provided a spot urine sample for analysis of pesticide
metabolites 1--4 days after MC (i.e., within 5 half-lives). By
using a cross-sectional design, investigators compared urine
pesticide metabolite concentrations of exposed and unexposed
study participants. Exposure to permethrin was verified by
cross-referencing the global positioning systems location of
participants with local MC spray routes. Permethrin was applied
in MC regions at a concentration of 0.032 oz/acre.

Urine samples were analyzed at CDC by using tandem mass spec-
trometry (3). Urinary metabolite concentrations of 3-
phenoxybenzoic acid (3pba), a metabolite of synthetic pyrethroid
pesticides such as permethrin, did not differ significantly be-
tween MC and non-MC regions (geometric mean [GM] = 1.25 µg/L
versus 1.13 µg/L, respectively). Although 3pba concentrations
did not differ between participants who used pesticides at home
or at work and those who did not, participants who used pesti-
cides on pets (n = 17) had significantly higher (p = 0.02) mean
3pba concentrations than those who did not (n = 174) (4.27 µg/L
versus 1.07 µg/L, respectively). These findings indicated that
local MC activities did not lead to increased pesticide metabo-
lite concentrations in the urine of participants.

North Carolina, 2003

Hurricane Isabel made landfall in North Carolina on September
18, 2003. Because of ensuing rains and flooding, mosquito popu-
lations were expected to surge. To control mosquitoes and pre-
vent transmission of WNV and other arboviruses, the North Caro-
lina Department of Environmental and Natural Resources (NCDENR)
sprayed ULV naled and permethrin.

The North Carolina Department of Health and Human Services,
NCDENR, and CDC conducted a prospective exposure assessment of
ULV spraying of pesticides. Investigators recruited 90 persons
from a random sample of census blocks (that accounted for the
population density) marked for spraying. Participants then com-
pleted a pre-spray questionnaire about household and occupa-
tional exposure to pesticides and provided urine samples to
quantify concentrations of pesticide metabolites. On September
30, aircraft in North Carolina sprayed ULV naled at 0.7 oz/acre.
In addition, trucks sprayed ULV permethrin (Biomist 30+30®) at
0.0014 lbs/acre. Eighteen hours after aerial spraying (approxi-
mately one half-life), each participant completed a post-spray
questionnaire about household and occupational exposure to pes-
ticides and provided a second urine sample. Urine samples were
analyzed at CDC by using tandem mass spectrometry (3).

Of the 90 persons recruited to participate in this exposure as-
sessment, 75 (83%) provided pre-spray and post-spray question-
naires and urine samples. The concentrations of all pre- and
post-spray pesticide metabolites measured in participant urine
samples were low (Table). Dimethylphosphate (DMP), a metabolite
of organophosphate pesticides such as naled, was detected in 46%
of pre-spray and 49% of post-spray urine samples (limit of de-
tection [LOD] = 0.5 µg/L). The GM 3pba concentration from post-
spray urine sampled was 0.2 µg/L. Generalized estimating equa-
tions (GEE) indicated no statistically significant differences
in the urine concentrations of naled and permethrin metabolites
before and after spraying. Participants who ate fresh fruits or
vegetables <3 days before completing the pre-spray (n = 58) or
post-spray (n = 37) questionnaires had significantly higher
urine concentrations of dimethylthiophosphate than participants
who did not pre-spray (n = 16) or post-spray (n = 37) (pre-
spray: 3.2 µg/L versus 1.4 µg/L; GEE p = 0.02) (post-spray: 3.3
µg/L versus 1.2 µg/L; GEE p = 0.01). Two participants who worked
on farms and/or handled pesticides had significantly higher
urine concentrations of nonspecific organophosphorus pesticide
metabolites (e.g., dimethyldithiophosphate, diethylthiophos-
phate, and diethylphosphate) than participants who did not work
on farms (n = 73) or handle pesticides (n = 72).

Virginia, 2003

To control mosquitoes and prevent transmission of arboviruses
after Hurricane Isabel, the Virginia Department of Health (VDH)
decided to spray ULV naled and d-phenothrin. VDH and CDC as-
sessed exposure to ULV spraying of pesticides by randomly se-
lecting 95 residents of high population-density census blocks
marked for spraying. Participants then completed pre-spray ques-
tionnaires about household and occupational exposure to pesti-
cides and provided urine samples to quantify concentrations of
pesticide metabolites.

On September 30, aircraft sprayed ULV naled at 0.5 oz/acre while
trucks sprayed ULV of d-phenothrin (Anvil 10+10®) at 0.0036
lbs/acre. Eighteen hours after spraying (approximately one half-
life), each participant completed a post-spray questionnaire
about household and occupational exposure to pesticides and pro-
vided a second urine sample. Urine samples were analyzed at CDC
by using tandem mass spectrometry (3).

Of the 95 persons recruited for the assessment, 83 (87%) pro-
vided pre-spray and post-spray exposure questionnaires and urine
samples. The concentrations of all pesticide metabolites meas-
ured in participants' urine samples were low (Table). DMP was
detected in 42% of pre-spray and 48% of post-spray urine samples
(LOD = 0.5 µg/L). The geometric mean 3pba concentration from
post-spray urine samples was 0.6 µg/L. GEEs indicated no overall
difference in the urine concentrations of naled and d-phenothrin
metabolites before and after spraying.

Reported by: M Currier, MD, Univ of Mississippi Medical Center;
M McNeill, MD, Mississippi Dept of Health. D Campbell, MD, North
Carolina Dept of Health and Human Svcs; N Newton, PhD, North
Carolina Dept of Environment and Natural Resources. JS Marr, MD,
E Perry, MD, SW Berg, MD, Virginia Dept of Health. DB Barr, PhD,
Div of Laboratory Sciences, GE Luber, PhD, SM Kieszak, MA, HS
Rogers, PhD, LC Backer, PhD, MG Belson, MD, C Rubin, DVM, Div of
Environmental Hazards and Health Effects, National Center for
Environmental Health; E Azziz-Baumgartner, MD, ZH Duprey, DVM,
EIS officers, CDC.

Editorial Note:

Although ULV applications of naled and synthetic pyrethroids
have a low toxicity to humans, occupational studies suggest that
excessive exposure to these pesticides can cause serious health
effects (4). Prolonged exposure to high concentrations of naled
and synthetic pyrethroids can cause dermatitis, reactive airway
disease, gastrointestinal distress, central nervous system de-
pression, paralysis, and death (5). Exposure often results from
use of these pesticides in food production, treatment of wool,
wood products, and pest-control efforts; however, few studies
have quantitated the level of human exposure to MC pesticides in
nonoccupational settings (6).

The studies described in this report represent the first efforts
to quantitate human exposure to MC pesticides during large-scale
MC activities. Two of these studies used a prospective crossover
design that compared urine metabolite concentrations after ULV
spraying of pesticides with baseline concentrations. Use of sen-
sitive analytic methods in these studies indicated that the
urine pesticide metabolite concentrations measured were low
(parts per billion). The concentration of urine metabolites in
these studies are comparable with those measured in the general
population (6,7). In addition, these three studies did not indi-
cate an overall increase of pesticide metabolite concentrations
in the urine of participants after spraying during MC activi-
ties. The concentrations of naled, permethrin, and d-phenothrin
during emergency ULV applications might be too low to cause im-
portant human exposure.

In certain participants, investigators found an association be-
tween home and/or work application of pesticides and pesticide
metabolite concentrations. The concentrations in participants
who had histories of exposure were within the range of the gen-
eral U.S. population (8). These findings are consistent with oc-
cupational studies in which prolonged exposure to pesticides
through several hours of work in plant nurseries and greenhouses
was associated with low but measurable concentrations of urine
pesticide metabolites (9). These findings also are compatible
with a prospective study that quantitated higher 3pba concentra-
tions in the urine of pest-control operators 1 day after spray-
ing pyrethroids (10).

The findings in this report are subject to at least three limi-
tations. First, although naled, permethrin, and d-phenothrin re-
main in the environment for a short period (e.g., naled has a 1-
day half-life), CDC did not conduct environmental sampling to
confirm the presence of pesticide on the ground after spraying.
Second, the study did not quantify the effects of synergists
such as piperonyl butoxide in Anvil 10+10®, which help increase
the efficacy of synthetic pyrethroids. Finally, the use of self-
reported questionnaire data limits the ability to quantify ac-
tual home or occupational pesticide exposure.

Aerial spraying with ULV naled and truck-mounted spraying with
permethrin/d-phenothrin were not associated with an increase in
urine pesticide metabolite concentrations among residents of
these rural, suburban, and urban communities. These findings
suggest that ULV application of naled, permethrin, and d-
phenothrin is safe to humans as part of integrated vector con-
trol. The findings are noteworthy because ULV applications of
pesticides that kill adult mosquitoes are an important tool in
the public health response to WNV. Future studies should address
the long-term safety of low-concentration exposure to naled and
synthetic pyrethroid applications. In addition, public health
interventions might be needed to reduce home and workplace expo-
sure to pesticides.

References
1. Roche JP. Print media coverage of risk-risk tradeoffs associ-
ated with West Nile encephalitis and pesticide spraying. J Urban
Health 2002; 79:482--90.
2. US Environmental Protection Agency. Health and safety spe-
cific chemicals regulatory actions. Washington, DC: Office of
Pesticide Programs; 2002. Available at
http://www.epa.gov/pesticides/factsheets/pesticides4mosquitos.htm.
3. Olsson AO, Baker SE, Nguyen JV, et al. A liquid chromatogra-
phy--tandem mass spectrometry multiresidue method for quantifi-
cation of specific metabolites of organophosphorus pesticides,
synthetic pyrethroids, selected herbicides, and DEET in human
urine. Anal Chem 2004;76:2453--61.
4. Edmundson WF, Davies JE. Occupational dermatitis from naled:
a clinical report. Arch Environ Health 1967;15:89--91.
5. Mick DL, Gartin TD, Long KR. A case report: occupational ex-
posure to the insecticide naled. J Iowa Med Soc 1970;LX:395--6.
6. Heudorf U, Angerer J. Metabolites of pyrethroid insecticides
in urine specimens: current exposure in an urban population in
Germany. Environ Health Perspect 2001;109:213--7.
7. CDC. Second national report on human exposure to environ-
mental chemicals. Atlanta, GA: US Department of Health and Human
Services, CDC; 2003. Available at http://www.cdc.gov/exposurereport.
8. Barr DB, Bravo R, Weerasekera G, et al. Concentrations of
dialkyl phosphate metabolites of organophosphorus pesticides in
the U.S. population. Environ Health Perspect 2004;112:186--200.
9. Kolmodin-Hedman B, Swensson A, Åkerblom M. Occupational expo-
sure to some synthetic pyrethroids (permethrin and fenvalerate).
Arch Toxicol 1982;50:27--33.
10. Leng G, Ranft U, Sugiri D, Hadnagy W, Berger-Preiss E, Idel
H. Pyrethroids used indoors---biological monitoring of exposure
to pyrethroids following an indoor pest control operation. Int J
Hyg Environ Health 2003;206:85--92.

Acknowledgments

The findings in this report are based, in part, on contributions
by W Rayburn, Albemarle Regional Health Svcs, Elizabeth City; J
Engel, North Carolina Dept of Health and Human Svcs; M Tolliver,
North Carolina Dept of Environment and Natural Resources. Z
Kazzi, Office of Director, Agency for Toxic Substances and Dis-
ease Registry. K Johnson, C Sanchez, A Holmes, R Sabogal, M
Patel, A Funk, C Bell, S Young, A Greiling, D Burmeister, Div of
Environmental Hazards and Health Effects, C Dodson, Div of Labo-
ratory Sciences, J Mason, E Hansen, J Shughart, Div of Emergency
and Environmental Health Svcs, National Center for Environmental
Health; A Hedley, Div of Health Examination Statistics, National
Center for Health Statistics; G Shaughnessy, G Han, A Terra-
nella, Epidemiology Program Office, CDC.


--
If Malaria's the Problem, DDT's Not the Only Answer

By May Berenbaum
Post
Sunday, June 5, 2005; B03

In the pantheon of poisons, DDT occupies a special place. It's
the only pesticide celebrated with a Nobel Prize: Swiss chemist
Paul Mueller won in 1948 for having discovered its insecticidal
properties. But it's also the only pesticide condemned in pop
song lyrics -- Joni Mitchell's famous "Hey, farmer, farmer put
away your DDT now" -- for damaging the environment. Banned in
the United States more than 30 years ago, it remains America's
best known toxic substance. Like some sort of rap star, it's
known just by its initials; it's the Notorious B.I.G. of pesti-
cides.

Now DDT is making headlines again. Many African governments are
calling for access to the pesticide, believing that it's their
best hope against malaria, a disease that infects more than 300
million people worldwide a year and kills at least 3 million, a
large proportion of them children. And this has raised a contro-
versy of Solomonic dimensions, pitting environmentalists against
advocates of DDT use.

The dispute between them centers on whether the potential bene-
fits of reducing malaria transmission outweigh the potential
risks to the environment. But the problem isn't that simple.
This is a dispute in which science should play a significant
role, but what science tells us is that DDT is neither the ulti-
mate pesticide nor the ultimate poison, and that the lessons of
the past are being ignored in today's discussion.

The United Nations Environment Program has identified DDT as a
persistent organic pollutant that can cause environmental harm
and lists it as one of a "dirty dozen" whose use is scheduled
for worldwide reduction or elimination. But some DDT advocates
have resorted to anti-environmentalist drama to make their case
for its use in Africa.

They have accused environmental activists of having "blood on
their hands" and causing more than 50 million "needless deaths"
by enforcing DDT bans in developing nations. In his best-selling
anti-environmentalist novel "State of Fear," Michael Crichton
writes that a ban on using DDT to control malaria "has killed
more people than Hitler."

Such statements make good copy, but in reality, chemicals do not
wear white hats or black hats, and scientists know that there
really are no miracles. Malaria is caused by a protozoan para-
site that is transmitted by mosquitoes. For decades, there have
been two major strategies for curbing the disease: killing the
infectious agent or killing the carrier. Reliably killing the
protozoan has proved difficult; many older drugs are no longer
effective, new ones are prohibitively expensive, and delivering
and administering drugs to the susceptible populace presents
daunting challenges. Killing the carrier has long been an at-
tractive alternative.

And DDT has been an astonishingly effective killer of mosqui-
toes. DDT (which stands for the far less catchy dichloro-
diphenyl-richloroethane) is a synthetic chemical that didn't ex-
ist anywhere on the planet until it was cooked up for no par-
ticular purpose in a German laboratory in 1874. Decades later,
in 1939, Mueller pulled it off a shelf and tested it, along with
many other synthetic substances, for its ability to kill in-
sects. DDT distinguished itself both by its amazing efficacy and
its breadth of action -- by interfering with nervous system
function, it proved deadly to almost anything with six, or even
eight, legs. And it was dirt-cheap compared to other chemicals
in use -- it could be quickly and easily synthesized in chemical
laboratories from inexpensive ingredients.

Soon after its insecticidal properties were discovered, DDT was
put to use combating wartime insect-borne diseases that have be-
deviled troops mobilized around the world for centuries. It
stemmed a louse-borne typhus outbreak in Italy and prevented
mosquito-borne diseases in the Pacific theater, including ma-
laria and yellow fever, to almost miraculous effect. This mili-
tary success emboldened governments around the world to use DDT
after World War II to try to eradicate the longtime scourge of
malaria. And in many parts of the world, malaria deaths dropped
precipitously. This spectacular success is why many people are
calling for the use of DDT specifically for malaria control.

At the same time that malaria deaths were dropping in some
places, however, the environmental persistence of DDT was creat-
ing major problems for wildlife, as famously documented in Ra-
chel Carson's classic 1962 book, "Silent Spring." By 1972, the
pesticide had become the "poster poison" for fat-soluble chemi-
cals that accumulate in food chains and cause extensive collat-
eral damage to wildlife (including charismatic predators such as
songbirds and raptors), and a total ban on the use of DDT went
into effect in the United States.

What people aren't remembering about the history of DDT is that,
in Many places, it failed to eradicate malaria not because of
environmentalist restrictions on its use but because it simply
stopped working. Insects have a phenomenal capacity to adapt to
new poisons; anything that kills a large proportion of a popula-
tion ends up changing the insects' genetic composition so as to
favor those few individuals that manage to survive due to random
mutation. In the continued presence of the insecticide, suscep-
tible populations can be rapidly replaced by resistant ones.
Though widespread use of DDT didn't begin until WWII, there were
resistant houseflies in Europe by 1947, and by 1949, DDT-
resistant mosquitoes were documented on two continents.

By 1972, when the U.S. DDT ban went into effect, 19 species of
mosquitoes capable of transmitting malaria, including some in
Africa, were resistant to DDT. Genes for DDT resistance can per-
sist in populations for decades. Spraying DDT on the interior
walls of houses the form of chemical use advocated as the solu-
tion to Africa's malaria problem -- led to the evolution of re-
sistance 40 years ago and will almost certainly lead to it again
in many places unless resistance monitoring and management
strategies are put into place.

In fact, pockets of resistance to DDT in some mosquito species
in Africa are already well documented. There are strains of mos-
quitoes that can metabolize DDT into harmless byproducts and
mosquitoes whose nervous systems are immune to DDT. There are
even mosquitoes who avoid the toxic effects of DDT by resting
between meals not on the interior walls of houses, where chemi-
cals are sprayed, but on the exterior walls, where they don't
encounter the chemical at all.

The truth is that DDT is neither superhero nor supervillain --
it's Just a tool. And if entomologists have learned anything in
the last half-century of dealing with the million-plus species
of insects in the world, it's that there is no such thing as an
all-purpose weapon when it comes to pest management. DDT may be
useful in controlling malaria in some places in Africa, but it's
essential to determine whether target populations are resistant;
if they are, then no amount of DDT will be effective.

We have new means of determining whether populations are geneti-
cally prone to developing resistance. DDT advocates are right to
suggest that DDT may be useful as a precision instrument under
some circumstances, particularly considering that environmental
contamination in Africa may be less of a problem than it has
been in temperate ecosystems because the chemical can degrade
faster due to higher temperatures, moisture levels and microbial
activity. Moreover, resistance evolves due to random mutation,
so there are, by chance, malaria-carrying mosquito species in
Africa that remain susceptible to DDT despite more than two dec-
ades of exposure to the chemical.

But environmentalists are right to worry that the unwise use of
DDT, particularly where it is likely to be ineffective, may
cause environmental harm without any benefit. In 2000, I chaired
a National Research Council committee that published a study ti-
tled "The Future Role of Pesticides in U.S. Agriculture." Our
principal recommendation is germane to discussions of malaria
management: "There is no justification for completely abandoning
chemicals per se as components in the defensive toolbox used for
managing pests. The committee recommends maintaining a diversity
of tools for maximizing flexibility, precision, and stability of
pest management."

Overselling a chemical's capacity to solve a problem can do ir-
retrievable harm not only by raising false hopes but by delaying
the use of more effective long-term methods. So let's drop the
hyperbole and overblown rhetoric -- it's not what Africa needs.
What's needed is a recognition of the problem's complexity and a
willingness to use every available weapon to fight disease in an
informed and rational way.

Author's e-mail: maybe@uiuc.edu
May Berenbaum is head of the department of entomology at the
University of Illinois, Urbana-Champaign.