1

ALDICARB INTOXICATION IN DOGS

Deborah K Glaum DVM

DMP 806

Environmental Toxicology

Kansas State University

Spring 2012

2 INTRODUCTION

Although not immune to their effects, the early hunter-gather

societies were generally not concerned with pests. It was only with the

adoption of the agrarian lifestyle when pest control became

important; the increased density of human and animal populations, as

well as the cultivation and storage of crops, created an environment

where pests could thrive. Even in ancient times, mankind sought ways

to control pests.

The Fertile Crescent, also known as the “Cradle of Civilization,”

produced some of the earliest documentation of the use of pesticides.

As early as 2500 BC, Sumerians were using sulfur to control mites and

insects; 3 sulfur was also mentioned by Greek poet Homer around 1000

BC. Chinese writings from 1200 BC told of using mercury and arsenic

for the control of body lice. The burning of bitumen was

recommended by Roman writer Cato in 200 BC as a method of

controlling insects in vineyards. 4

Centuries later, arsenic mixed with honey was described as an

effective method for controlling ants in the 1600’s. 3 With the

increasing production of crops in America, farmers in the 19th century

found themselves using products such as sulfur, nicotine sulfate,

acetoarsenite and calcium arsenite to control insects. 4 Pyrethroids

derived from the plant genus Chrysanthemum have also been used for

centuries to control insects and lice.5

The modern age of pesticides began in the 20th century with the

discovery of DDT’s effectiveness in controlling a wide variety of insects,

not only those of agricultural importance but also for those who

spread human diseases. The development of organochlorines, like DDT

were important in World War 2 because of the limited accessibility of

pyrethroids and the necessity to protect large numbers of military

personnel in tropical climates. 6 Organophosphates became widely

studied in Germany in the 1930’s as their neurotoxic properties made

them not only good pesticides but also chemical warfare agents.

Americans took this knowledge and produced products like parathion

and malathion. 7 Carbamates, an organic compound created in the

production of urea, is a neurotoxin like the organophosphates

although not generally as toxic. 8,9 Pesticide use increased greatly

during the mid-twentieth century because they were effective and

helped to greatly increase crop yields by minimizing loss to pests, plus

they were easy and inexpensive to mass produce.

Pest

Fungus, insect, nematode,

rodent, weed, or other form

of terrestrial or aquatic life

form that is injurious to

human or farm animal

health, or interferes with

economic activities such as

agriculture and logging. 1

BusinessDictionary.com

Pesticide

A pesticide is generally a

chemical or biological agent

(such as a virus, bacterium,

antimicrobial or disinfectant)

that through its effect

deters, incapacitates, kills

or otherwise discourages

pests. 2

Wikipedia

3 Pesticide legislation began in the United States in 1910 with the

Federal Insecticide Act (FIA) and regulated the use of properly labeled

and unadulterated products. 10 To address the increased production in

synthetic pesticides as well as address health and ecologic hazards, the

Federal Insecticide, Fungicide and Rodenticide Act was passed in 1947.

In 1972 regulatory control over pesticides was transferred from the

Department of Agriculture to the newly created Environmental

Protection Agency (USEPA). FIRPA has since undergone two major

revisions: one in 1988 to require re-registration of pesticides registered

prior to 1984, and it was further amended in 1996 by the Food Quality

Protection Act. 10

HAZARD IDENTIFICATION

Aldicarb is a carbamate insecticide. It was owned and produced by

Union Carbide, but through several industrial acquisitions is now

manufactured by Bayer Crop Science. It is the active ingredient in

Bayer’s Temik, which is labeled for professional use only on restricted

crops. Aldicarb is sometimes referred to as a “hot” carbamate due to

its quick onset of clinical signs. Aldicarb is sold in Mexico and Latin

America under the name “Tres Pasitos” as a rodenticide and roach

killer; it has been brought illegally into the United States. The name

“Tres Pasitos” (three little steps), or “Two Steps” as it is sometimes

known by, is thought to refer to the number of steps an animal will

take after ingesting the product. 11, 12

SCOPE OF ASSESSMENT

Because of its effective and rapid kill, aldicarb is sometimes used as

bait for killing vermin; it is not unusual for dogs and scavengers to be

poisoned by consuming the bait or carcasses. Additionally, aldicarb has

been used intentionally to poison domestic and wild animals. Although

it may be unusual to see, aldicarb intoxication of dogs has been well

documented. Furthermore, aldicarb has been well studied under

laboratory conditions in dogs.

PHYSICAL AND CHEMICAL PROPERTIES OF ALDICARB

Aldicarb is a white crystalline solid. It is heat sensitive and unstable

under normal conditions. Unlike other carbamates, it is extremely toxic

by oral and dermal routes, by liquids and emulsions. Due to this and its

instability, it is distributed in granular form. It is not corrosive to

plastic or metals. 13, 14 Aldicarb is quickly oxidized and hydrolyzed;

aldicarb sulfoxide and aldicarb sulfone are the byproducts of oxidation

and are commonly tested for along with aldicarb. 15

Aldicarb

Proprietary Name

Temik

Chemical Class

N-Methyl Carbamate

CAS Number

116-06-03

Molecular Formula

C7H14N2O2S

Molecular Weight

190.26

Octanol/Water Partition

Log Kow = 1.13

Soil Sorption Coefficient

Koc = 8-37, high to very high mobility in soil

Formulation

Granular, 5-15% aldicarb

28, 35

4 Aldicarb is very water soluble and highly mobile in sandy and loam soils. Its half-life varies greatly

(anywhere from one day to several months) depending upon pH, moisture levels, and degradation by

bacteria and sunlight. Because of this instability, aldicarb and its metabolites are more likely to be found

in ground water than in surface water. It is not at this point considered a bioaccumulator. 14

MECHANISM OF TOXICITY

Acetylcholine (ACh) is a neurochemical present in the synaptic space between nerve cells. It relays

signals from the pre-synaptic membrane to the post-synaptic membrane and has both neurotransmitter

and neuromodulator functions. Under normal conditions, the acetylcholinesterase (AChE) enzymes are

present on the post-synaptic membrane and terminate the transmission. As a carbamate, aldicarb binds

with AChE and allows ACh to accumulate in the synapse. This results in over-stimulation of the nerves.

With carbamates this binding is only temporary (unlike with organophosphates), but long enough for

clinical signs to appear and possibly even lead to death. 16 Clinical signs include increased secretions of

eyes, mouth and respiratory tract, gastrointestinal distress due to hypermotility, respiratory depression

and bradycardia. Hypoxia mainly due to respiratory paralysis is the usual cause of death. 17

Aldicarb is readily absorbed through the gut; it is easily absorbed through the skin if combined with oil

or organic solvents. Elimination occurs rapidly (hours to days), mainly through urine excretion but also

Acetylcholinesterase Mechanism of Action and Inhibition

Wikipedia 36

5 through feces, lactation and a very small amount through expiration. Aldicarb metabolism appears to be

consistent throughout most animal species that have been studied and is considered highly toxic for

most mammalian species. 18

IN VIVO STUDIES

Laboratory studies have been conducted with individual and combination exposure to aldicarb and its

metabolites. The toxicant was generally delivered in bolus form or as part of the diet. One study looked

at smoke inhalation of aldicarb-treated tobacco to assess possible toxicity via inhalation. Dogs in these

studies have been observed for clinical signs of intoxication (tremors, vomiting, decreased food intake

and changes in body weight). AChE levels in plasma and red blood cells were measured as that is the

best indicator of toxicity. Post-mortem examination was routinely done and included gross and

microscopic pathology. The following is a summary of the early aldicarb studies conducted in dogs: 18

Summary report for United Kingdom Ministry of Agriculture, Fisheries and Food 18

USEPA Integrated Risk Information System 19

Clinical signs of aldicarb intoxication were only noticed in dogs given the very highest doses.

Measurement of plasma AChE was done usually 24-48 hours after the last exposure. Since aldicarb is

metabolized and excreted so rapidly, these tests would not have accurately expressed AChE inhibition

during the period of toxicity; due to this, these NOAEL’s are no longer considered adequate for

regulatory purposes. Studies done more recently have used methods designed to maximize detection of

AChE levels, resulting in a NOAEL of 0.2-0.3mg/kg/d. 18

Summary of Aldicarb Toxicity Studies

Study Subjects/Groups Toxicant Dosage * Length NOAEL

Weil & Carpenter, 1973 2 beagle/sex aldicarb 0, 0.2, 0.3, 0.7 7 d >0.07

Weil & Carpenter, 1974c 4 beagles/sex aldicarb 0, 0.2, 0.3, 0.7 100 d 0.3 mg/kg/d

Weil & Carpenter 1966c 3 beagles/sex aldicarb 0, 0.025, 0.05, 0.1 5d/wk x 2yrs 0.1 mg/kg/d

Hamada 1985 1 dog/sex aldicarb 0, 1, 3, 10, 30, 100 ppm 14 d

Hamada 1987b 1 dog/sex aldicarb 0, 0.1, 0.3, 1, 3, 10 ppm 14 d 0.096 mg/kg/d

Hamada 1991 6 beagles/sex aldicarb 0, 0.35, 0.7, 2 ppm 5wks 0.2 mg/kg/d

Hamada 1988 5 beagles/sex aldicarb 0, 1, 2, 5, 10 ppm 52 wks 0.027 mg/kg/d

Weil & Carpenter 1968b 3 beagles/sex aldicarb sulfoxide 0, 0.0625, 0.125, 0.25, 0.5 5d/wk x 3mos 0.25 mg/kg/d

Weil & Carpenter 1968c 3 dogs/sex aldicarb sulfone 0, 0.2, 0.6, 1.8, 5.4 5d/wk x 90d 5.4 mg/kg/d

Hamada 1985a 1 dog/sex aldicarb sulfone 0, 3, 10, 30, 100, 300 ppm 2 wks

Hamada 1987a 6 beagles/sex aldicarb sulfone 0, 5, 25, 100 ppm 1 yr 0.54 mg/kg/d

* Doses were in mg/kg/d unless otherwise noted.

6 In some of the original studies, there were gross changes noted: decreased body weight, as well as

decreased testicular size and increased adrenal size in males. Extended exposure at low levels does not

cause apparent disease; even the LD50 bolus dose, when given daily as part of the dogs’ diets, was not

lethal and caused only minor disease. 18 Because aldicarb is apparently metabolized the same in all

laboratory animals, following reproductive studies, carcinogenic studies and immunotoxic studies in rats

and mice it has been determined that there are no chronic effects of aldicarb exposure and it is not a

teratogen, carcinogen or immunotoxin. 14, 18

AGRICULTURAL AND ENVIRONMENTAL STUDIES

Because of its ability to move in soil, concerns have been raised over the potential of aldicarb to

contaminate drinking water sources. In 2005, Bayer Crop Science tested 1,673 drinking wells. These

wells were located in 9 different areas of the United States where aldicarb was widely used, and within

300m of fields that had been treated at least once between 2002 and 2005. Only 10 of those wells

tested were positive for residue using gas chromatography, and levels were between 1.0 and 2.9

micrograms/Litre. The USEPA Health Advisory Limit at that time was 10 micrograms/Litre. Bayer

concluded that using aldicarb according to label instructions was adequate at preventing potable well

contamination. 20

A 2002 study looked for the presence of aldicarb in water in canals draining citrus groves in southern

Florida. Application of aldicarb was permitted between January 1 and April 30 in Florida. 457 water

samples were collected between mid-May, 2001 and mid-August, 2002. Aldicarb, A. sulfoxide and A.

sulfone were detected in 20 samples, with concentrations ranging from <0.16 to 4.97 ng ml (-1). 21

The half-life for aldicarb in pond water is between 5 to 10 days. Aldicarb is considered moderately toxic

to fish and exhibits little bioaccumulation. 24 Recently, USEPA published an aquatic risk assessment of

aldicarb as part of a re-registration process. Using models, they looked at 30 years of peak pond residue

levels of aldicarb and its metabolites in areas where the pesticide had been used for a variety of crops.

Taking the risk curves into account along with incident reports, they concluded that exposure risk to

freshwater fish and invertebrates is minor. 23

In the past, aldicarb was commonly applied to many crops, including sugar beets, potatoes, onions,

cotton, beans, strawberries and citrus fruits. 22 Although most cases of human intoxication occur in

agricultural workers where the pesticide is being applied, aldicarb has been identified as the culprit in

several pesticide food poisoning events. Outbreaks related to contaminated cucumbers and

watermelons in the United States and Canada were reported in the 1970’s and 1980’s. 18 Incorrect

storage and labeling was blamed for an accidental food poisoning incident that occurred in Louisiana in

1998. Aldicarb had been stored in a container labeled “black pepper” and was mistakenly added to a

cabbage salad and caused illness in 14 people. 27 In 2007 the US Food and Drug Administration (FDA)

issued a recall for fresh ginger imported from China to northern California after aldicarb sulfoxide

residues were detected in the California Department of Public Health monitoring program. 25 In 2010, in

response to continued USEPA concerns, Bayer Crop Science agreed to voluntarily phase out production

of its product Temik; its use in potatoes and citrus was immediately stopped with a total phase out

required by 2015. 26

7 EXPOSURE ASSESSMENT

It is estimated that 80% of aldicarb intoxications in food animals are related to improper storage and

handling. Pesticide containers may be mislabeled and be inadvertently added to feedstuffs or the

pesticide could be transported in vehicles prior to carrying feed. Additionally, large animals may become

intoxicated when grazing on pastures or croplands that are excessively or recently treated with the

pesticide. 15

Accidental exposure in dogs and cats is usually related to miscalculation or misapplication of the product

to the wrong species. Pesticides are routinely labeled for use in healthy adult animals, and those who

are sick or stressed may suffer ill effects. Aldicarb has also been used to maliciously poison pets,

especially dogs that are more likely to ingest adulterated food material. 15

Dogs can be accidently exposed when they eat poisoned bait intended to kill wild predators like coyotes

and foxes. There are sites on the internet where information on product (Temik) as well as dosage (8

tiny granules) is published for creating bait. 35 Unfortunately, without the evidence of bait it may be very

difficult to determine exactly how much aldicarb was ingested and whatever was ingested will be readily

absorbed. Due to rapid onset and progression of signs, a clinician may need to make a presumptive

diagnosis of carbamate toxicity rather than wait for laboratory confirmation.

CLINICAL SIGNS OF ALDICARB INTOXICATION

Carbamates work by interfering with the enzyme acetylcholinesterase (AChE) and permitting

acetylcholine (ACh) to accumulate in the synapse between nerves. Decreased levels of AChE permit

increased transmission of nerve impulses. Since aldicarb is readily and quickly distributed throughout

the body (thus the term “hot” carbamate), clinical signs are related to the organ systems where ACh is a

neurotransmitter. Signs include:

Skeletal muscle and motor neurons – twitching, tremors, ataxia, weakness and paralysis,

Gastrointestinal – increased salivation, nausea, hypermotility and diarrhea,

Respiratory – increased bronchial secretions, bronchial constriction and dyspnea,

Cardiac – bradycardia and hypoxia,

Ocular – increased lacrimation and miosis,

Urinary – increased micturition, and

Central Nervous System – seizure activity and centrally mediated respiratory. 15

TREATMENT OF ALDICARB INTOXICATION

If exposure to this pesticide is known and very recent (which is seldom the case in dog poisonings),

emesis may be induced and activated charcoal can be given to prevent absorption. Atropine sulfate is

given at higher than anesthetic levels to reverse and decrease the severity of signs. Anti-convulsive

medications like diazepam are used for seizure control; diphenhydramine and methocarbamol are used

to control skeletal muscle signs. Systemic acidosis can be treated with intravenous sodium bicarbonate

or respiratory ventilation. Supportive care, especially for respiratory depression, is very important.

Although the onset of aldicarb toxicity is very fast and the signs can be quite severe, the neurologic

8 effects and signs of toxicity are reversible and complete recovery can happen in a period of hours or a

few days. 29

LITERATURE REVIEW OF ALDICARB POISONING IN DOGS

In 2011, the Veterinary Emergency and Critical Care Society produced a retrospective, observational

study of aldicarb poisoning in 15 dogs. These were dogs that were owned by clients and presented to an

urban referral hospital. Eleven of the dogs were admitted to the hospital and 10 survived. This study

found that treatment of aldicarb toxicity was very effective and that the average patient was discharged

within one day. 29

The Veterinary Diagnostic and Investigational Laboratory at the University of Georgia’s College of

Veterinary Medicine released the results of a decade-long retrospective study in 1999. From 1988

through 1998, 162 cases of aldicarb intoxication were positively identified; although there were several

domestic species involved, dogs represented the largest numbers of cases. From examination of

stomach contents, it appeared that most cases were malicious and that the toxin had been given with

bait in the form of hamburger, hotdogs and ham. At that time aldicarb was widely used as a pesticide on

crops in Georgia, with its accessibility making it more likely to be used as the agent of poisoning. 30

Aldicarb was implicated in a string of poisoning incidents in the Yellowstone and Salmon National Park

regions of the United States in 2004 and 2005. Dog cases included some that were visiting the parks and

wildlife regions and others that were residents of the area. In addition to the dogs, investigators found a

dead wolf, fox, coyote and three magpies. Forensic evidence showed that the aldicarb granules had

been mixed with elk meat and used as bait, presumably to kill wolves. Further evidence led to the arrest

of a vocal anti-wolf activist; he was convicted under the Endangered Species Protection Act and

sentenced to 6 days in jail and banned from public lands for 2 years. 31

Reports out of South Africa note that not only has aldicarb been used for malicious poisoning, but that

there has been criminal activity associated with it as well. Aldicarb was available be purchased through

illegal channels as a rat poison. There were many cases where family dogs were poisoned days before

the family’s residence was robbed; presumably this was done in order to allow the perpetrators easier

access to the building. In Gauteng province in 2003 there were a reported 97 victims, nearly all dogs.

Another criminal activity where aldicarb has been used was the adulteration of watering holes by

wildlife poachers. 32, 33

Aldicarb is frequently the choice when trying to control feral dogs and other wild canids. The state of

South Carolina reports 6 to 12 poisoning cases each year.34 Bayer’s Temik is the pesticide most

commonly reported to have been used. Three prized hunting dogs were killed in 2009 by a man trying to

keep coyotes away from his horses. In 2010 a Hampton County man pleaded guilty to tainting

hamburger meat with aldicarb resulting in the deaths, not only of the foxes he intended to kill, but also a

pet dog and cat and several vultures. He told authorities he got the idea off of the internet and then

stole the pesticide from a nearby farm. A small community of mobile homes lost 4 dogs to aldicarb

poisoning after the manager of a local turkey hunt operation put out meat bait to kill feral dogs. In Lee

County in 2011 three hunting dogs were poisoned and died after consuming meat mixed with aldicarb.

Their owners were exposed to the pesticide while trying to help their dogs had to be decontaminated at

a local hospital; one 13 year old boy was ill and hospitalized overnight. 34,35

9 RISK CHARACTERIZATION

The risk for aldicarb intoxication must be broken down into likely and possible scenarios. Potential

exposure to aldicarb, when used as a pesticide following proper label instructions, would occur mainly

through ingestion. Sources of the pesticide would include contaminated surface or ground water or food

produced from meat, vegetables, fruits or grains containing residue. Due to the studies cited above, it

seems that intoxication via water is unlikely. Exposure due to food contamination is not likely because

most pet food processing would break down the pesticide. Dermal exposure could be possible if dogs

were allowed access to recently treated land (hunting dogs or herding dogs), but again is not likely.

The most likely scenarios for aldicarb poisoning in dogs continues to be from ingestion of adulterated

meat, whether as collateral damage from trying to control wildlife or due to malicious intention to kill

the pet. Wherever aldicarb is in use or is available through illegal channels, it will be used by people as a

poison, and must be on the list of rule-outs for dogs exhibiting signs of toxicity.

RISK MANAGEMENT

The most obvious step to decrease canine exposure to aldicarb has already been taken by Bayer Crop

Science with their decision to voluntarily discontinue production of Temik. Despite educational materials

provided by Bayer and agricultural extension services, and in the face of regulations regarding access

and handling, there has been a willingness to obtain and use this product illegally. Steps that may need

to be taken in the future may include:

Discovery and promotion of pesticides that only affect the pests they are targeting (like Insect

Growth Regulators),

Development of ways to produce and distribute pesticides in such a manner where they cannot

be removed from their original and labeled packaging,

Enact regulations requiring that individuals who handle pesticides have been trained in their

proper use and are certified,

Increased enforcement of laws aimed at illegal importation of pesticides and off-label use, and

Improved communication with the public about the proper uses and dangers of pesticides.

CONCLUSION AND COMMENTS

There are several lessons to be learned by looking at the history and uses of aldicarb.

First, there is a wide range of reactions to the use of pesticides. Since the book “Silent Spring” was

published in the 1960’s, there was attention to the harmful and long-term effects on humans and the

environment. This led to the banning of DDT and many other insecticides. 2 While this caution is

necessary and commendable, one consequence is the increase in vector-borne diseases like malaria.

There is a need for pesticides and regulatory agencies to look at all sides of public health issues in

decision-making processes. There needs to be a balancing act between efforts made in research and

development of new pesticides and protection of human and non-human health and the environment.

At the other end of the spectrum is a distinct casualness in the way many people approach pesticides,

similar to how many view antibiotics. One need only walk into a local discount store to find shelves full

of all manner of products for humans and pets. Internet-based pet supply and pharmaceutical

10 companies make a large profit on pesticides. Flea, tick and heartworm products, that have until recently

been sold only by prescription from veterinarians, will soon be sold over-the-counter or by human

pharmacies. Unfortunately, most pet owners do not understand information given on product packaging

which can lead to inappropriate handling and usage. Retail and pharmaceutical sales persons are not

trained but are often in the position of giving advice to pet owners. This situation will increase the

likelihood that there will be pets poisoned by misuse; furthermore resistance in insects and nematodes

is of increasing concern.

Although aldicarb intoxication by ingestion of pet food products is very unlikely, there are increasing

numbers of products imported into the United States from other countries. The United States has

effectively banned aldicarb from being used in domestic products, and although they can exert some

pressure on WTO trading partners, there must be increased vigilance in monitoring items from non-

compliant countries.

Lastly, the internet is providing access to knowledge and products, and this has been and will be a

problem. The question becomes: Who is responsible for monitoring the internet? There will need to be

coordination and cooperation between industry, government and law enforcement agencies for any

efforts to be effective. Veterinarians and the animal health industry continues to play a vital role in

educating pet owners and the public in general to the proper uses, benefits and hazards that pesticides

play in our lives.

11 REFERENCES

1 BusinessDictionary.com. 2012. “Pest.” Accessed April, 2012 from:

http://www.businessdictionary.com/definition/pest.html

2 Wikipedia. 2012. “Pesticide.” Accessed April, 2012 from: http://en.wikipedia.org/wiki/Pesticide

3 New World Encyclopedia. 2008. “Pesticide.” Accessed April, 2012 from:

http://www.newworldencyclopedia.org/entry/Pesticide

4 http://www.alternative-agriproducts.com/a_brief_history_of_pesticides.php

5 Wikipedia. 2012. “Pyrethrum.” Accessed April, 2012 from: http://en.wikipedia.org/wiki/Pyrethrum

6 Wikipedia. 2012. “DDT.” Accessed April, 2012 from: http://en.wikipedia.org/wiki/DDT

7 Wikipedia. 2012. “Organophosphate.” Accessed April, 2012 from:

http://en.wikipedia.org/wiki/Organophosphate

8 Wikipedia. 2012. “Carbamate.” Accessed April, 2012 from: http://en.wikipedia.org/wiki/Carbamate

9 Wikipedia. 2012. “Pesticide.” Accessed April, 2012 from: http://en.wikipedia.org/wiki/Pesticide

10 Wikipedia. 2012. “Federal Insecticide, Fungicide, and Rodenticide Act.” Accessed April, 2012 from:

http://en.wikipedia.org/wiki/Federal_Insecticide,_Fungicide,_and_Rodenticide_Act

11 Medpedia. 2010. “Aldicarb.” Accessed April, 2012 from: http://wiki.medpedia.com/Aldicarb

12 Health24. 2005. “Temik: killer on the loose.” Accessed April, 2012 from:

http://www.health24.com/news/poisoning/1-939%2C31989.asp

13 http://pmep.cce.cornell.edu/profiles/insect-mite/abamectin-

bufencarb/aldicarb/aldicarb_cfs_0688.html

14 Cornell University Pesticide Management Education Program. 1988. “Aldicarb (Temik) – Chemical

Fact Sheet 6/88.” Accessed April, 2012 from: http://pmep.cce.cornell.edu/profiles/extoxnet/24d-

captan/aldicarb-ext.html

15 US Department of Health and Human Services National Toxicology Program. 2012. Accessed April,

2012 from: http://ntp-server.niehs.nih.gov/index.cfm?objectid=E87C9440-BDB5-82F8-

F133FEACE9329208

16 Wikipedia. 2012. “Acetylcholine.” Accessed April, 2012 from:

http://en.wikipedia.org/wiki/Acetylcholine

17 Beasley, V. 1999. “Toxicants that Affect the Autonomic Nervous System.” Veterinary Toxicology. Aug

9, 1999. Accessed April, 2012 from:

http://www.ivis.org/advances/Beasley/Cpt2G/chapter_frm.asp?LA=1

18 International Programme on Chemical Safety. 2012. “Aldicarb.” Accessed April, 2012 from:

http://www.inchem.org/documents/jmpr/jmpmono/v92pr03.htm

12 19 US Environmental Protection Agency Integrated Risk Information System. 2012. “Aldicarb.” Accessed

April, 2012 from: http://www.epa.gov/ncea/iris/subst/0003.htm

20 Jones, R.L., and R. Allen. 2007. “Summary of potable well monitoring conducted for aldicarb and its

metabolites in the United States in 2005.” Environmental Toxicology and Chemistry. 2007, Jul;

26(7):1355-60. Accessed April, 2012 from: http://toxnet.nlm.nih.gov/

21 Wilson, P.C., J.F. Foos, and R.L. Jones. 2005. “Pulsed losses and degradation of aldicarb in a South

Florida agricultural watershed.” Archives of Environmental Contamination and Toxicology. 2005, Jan;

48(1):24-31. Accessed April, 2012 from: http://toxnet.nlm.nih.gov/

22 Medpedia. 2010. “Aldicarb.” Accessed April, 2012 from: http://wiki.medpedia.com/Aldicarb

23 Moore, Dwayne R.J., R. Teed, Sara Rodney, Ryan Thompson, and David Fischer. 2010. “Refined avian

risk assessment for aldicarb in the United States.” Integrated Environmental Assessment and

Management. 2010, Jan; 6(1):83-101. Accessed April, 2012 from:

http://www.vin.com/members/cms/document/default.aspx?objecttypeid=2&template=articleview

&redirect=1&objectid=1760462

24 Oregon State University Extension Toxicology Network. 1996. “Aldicarb.” Accessed April, 2012 from:

http://extoxnet.orst.edu/pips/aldicarb.htm

25 Nixon, Melissa. 2007. “Recall: Ginger From China Contaminated With Pesticide Aldicarb Sulfoxide;

Symptoms Of Poisoning.” The Veterinary Information Network Message Board, 07/30/07. Accessed

April, 2012 from:

http://www.vin.com/Members/boards/discussionviewer.aspx?FirstMsg=1&LastMsg=20&DocumentI

d=3567253

26 US Environmental Protection Agency Pesticides: Reregistration. 2010. “Agreement to Terminate All

Uses of Aldicarb.” Accessed April, 2012 from:

http://www.epa.gov/oppsrrd1/REDs/factsheets/aldicarb_fs.html

27 Morbidity and Mortality Weekly Report. 1999. “Aldicarb as a Cause of Food Poisoning – Louisiana

1998.” April, 1999. 48(13):269-271. Accessed April, 2012 from:

http://www.cdc.gov/mmwr/preview/mmwrhtml/00056877.htm

28 Pesticide Action Network. 2010. “Aldicarb.” Accessed April, 2012 from:

http://www.pesticideinfo.org/Detail_Chemical.jsp?Rec_Id=PC35144http://www.vin.com/members/

cms/document/default.aspx?objecttypeid=2&template=articleview&redirect=1&objectid=1759687

29 Frazier, K., G. Hullinger, M. Hines, A. Liggett, and L. Sangster. 1999. “162 cases of aldicarb

intoxication in Georgia domestic animals from 1998-1998.” Veterinary Human Toxicology. Aug 1999;

13

41(4):233-235. Accessed April, 2012 from:

http://www.vin.com/members/cms/document/default.aspx?objecttypeid=2&template=articleview

&redirect=1&objectid=205019

30 Tolme, Paul. 2009. “Wildlife CSI: Inside the Case of the Poisoned Meatballs.” Popular Mechanics. Oct

1, 2009. Accessed April, 2012 from:

http://www.popularmechanics.com/science/earth/4231025.html

31 Health24. 2005. “Temik: killer on the loose.” Accessed April, 2012 from:

http://www.health24.com/news/poisoning/1-939%2C31989.asp

32 Servamus Safety and Security Magazine. 2007. “Chemical Crime Calls For Management.” Accessed

April, 2012 from:

http://www.servamus.co.za/index.php?option=com_content&task=view&id=26&Itemid=9

33 Holleman, Joey. 2012. “Poisoning cases illustrate dangers of pesticide misuse.” The State. Jan 03,

2012. Accessed April, 2012 from: http://www.thestate.com/2012/01/03/2098924/poisoning-cases-

illustrate-dangers.html

34 Bayou Bucks Hunting Community. 2012. “Can you poison Hogs?” Accessed April, 2012 from:

http://www.bayoubucks.com/forum/archive/index.php/t-28414.html

35 US Environmental Protection Agency, 2012. “Technical Factsheet on: Aldicarb and Metabolites.:

Accessed April, 2012 from: http://www.epa.gov/safewater/pdfs/factsheets/soc/tech/aldicarb.pdf

36 Wikipedia. 2012. “Acetylcholinesterase.” Accessed April, 2012 from:

http://en.wikipedia.org/wiki/Acetylcholinesterase