Chemical flea programs-

What your Veterinarian may or may not know and what the manufacturers do know and keep from you! This information applies to all chemical flea programs including Capstar, frontline, bio spot, program and advantage. At the end of the first article, you will find information on Capstar.


Should you use Chemical Pesticide Flea Control for your pets? If it kills the insects, you can be assured that it will eventually kill your pets! Quick run down of what Veterinarians and Pet shops have told you: So safe it can be touched by babies, so safe it can be applied without gloves, so safe it can be used without any side-effects, Sits inside a fatty layer of skin on the back of the neck, great for animals allergic to fleas.

#1. Please read the following and then you decide if this is safe enough to let babies touch it.
#2. Would you really want to apply this without gloves? It has carcinogens in it and it is classified as a type 2 agent by the EPA.
#3.Some of the side effects caused by all chemical flea products. 2 animals were near death and one animal was on CAPSTAR for only 48 hours and is now suffering from neuromuscular problems! It also breaks down the immune system causing auto-immune disorders.
#4.The back of the neck is the pathway to the blood stream. It is an excellant way to get medications into an animal when they are refusing it by mouth.
#5. How can it be great for animals that are allergic to fleas, when the fleas have to bite the animal to die? Do you really want something on your animal that kills things?

Below you will find an independant study done by the following Universities.

A Pesticide Information Project of Cooperative Extension Offices of Cornell University, Michigan State University, Oregon State University, and University of California at Davis. Major support and funding was provided by the USDA/Extension Service/National Agricultural Pesticide Impact Assessment Program.

Pesticide
Information
Profile Imidacloprid

TRADE OR OTHER NAMES
Imidacloprid is found in a variety of commercial insecticides. The products Admire, Condifor, Advantage, Gaucho, Premier, Premise, Provado, and Marathon all contain imidacloprid as the active ingredient (1).

REGULATORY STATUS
Imidacloprid is a General Use Pesticide, and is classified by EPA as both a toxicity class II and class III agent, and must be labeled with the signal word "Warning" or "Caution" (1). There are tolerances for residues of imidacloprid and its metabolites on food/feed additives ranging from 0.02 ppm in eggs, to 3.0 ppm in hops (2).

INTRODUCTION
Imidacloprid is a systemic, chloro-nicotinyl insecticide used for the control of sucking insects including fleas, rice hoppers, aphids, thrips, whiteflies, termites, turf insects, soil insects and some beetles. It is most commonly used on rice, cereal, maize, potatoes, vegetables, sugar beets, fruit, cotton, hops and turf, and is especially systemic when used as a seed or soil treatment. The chemical works by interfering with the transmission of stimuli in the insect nervous system. Specifically, it causes a blockage in a type of neuronal pathway (nicotinergic) that is more abundant in insects than in warm-blooded animals (making the chemical selectively more toxic to insects than warm-blooded animals). This blockage leads to the accumulation of acetylcholine, an important neurotransmitter, resulting in the insect's paralysis, and eventually death. It is effective on contact and via stomach action (3). Imidacloprid based insecticide formulations are available as dustable powder, flea preparations, granular, seed dressing (flowable slurry concentrate), soluble concentrate, suspension concentrate, and wettable powder (1). Typical application rates range from 0.05 - 0.125 pounds/acre. These application rates are considerably lower than older, traditionally used insecticides. It is considered phytotoxic. (4).

TOXICOLOGICAL EFFECTS
ACUTE TOXICITY
Imidacloprid is moderately toxic. The oral dose of technical grade imidacloprid that resulted in mortality to half of the test animals (LD50) is 450 mg/kg body weight in rats (1), and 131 mg/kg in mice (3). The 24-hour dermal LD50 in rats is >5,000 mg/kg. It is considered irritating to eyes and skin (rabbits), and sensitizing to skin (guinea pigs) (3). Some granular formulations may contain clays as inert ingredients that act as eye irritants. In acute inhalation toxicity tests with rats, the airborne concentration of imidacloprid that resulted in mortality to half of the test organisms (LC50) is > 69 mg/meters cubed air in the form of an aerosol, and >5323 mg/meters cubed air in the form of dust. These values represent the maximum attainable airborne concentrations (3).

Signs and Symptoms of Poisoning
Symptoms, including fatigue, twitching, cramps, and muscle weakness including the muscles necessary for breathing (5).

CHRONIC TOXICITY
A 2-year feeding study in rats fed up to 1,800 ppm resulted in a No Observable Effect Level (NOEL) of 100 ppm (5.7 mg/kg body weight in males and 7.6 mg/kg in females). Adverse effects included decreased body weight gain in females at 300 ppm, and increased thyroid lesions in males at 300 ppm and females at 900 ppm. A 1-year feeding study in dogs fed up to 2,500 ppm resulted in a NOEL of 1,250 ppm (41 mg/kg). Adverse effects included increased cholesterol levels in the blood, and stress to the liver (measured by elevated liver cytochrome p-450 levels) (6).

Reproductive Effects
A three generation reproduction study in rats fed up to 700 ppm imidacloprid resulted in a NOEL of 100 ppm (equivalent to 8 mg/kg/day) based on decreased pup body weight observed at the 250 ppm dose level (6).

Teratogenic Effects
A developmental toxicity study in rats given doses up to 100 ppm by gavage on days 6 to 16 of gestation resulted in a NOEL of 30 mg/kg/day (based on skeletal abnormalities observed at the next highest dose tested of 100 ppm) (4). In a developmental toxicity study with rabbits given doses of imidacloprid by gavage during days 6 through 19 of gestation, resulted in a NOEL of 24 mg/kg/day based on decreased body weight and skeletal abnormalities observed at 72 mg/kg/day (highest dose tested) (6).

Mutagenic Effects
Imidacloprid may be mutagenic. In a battery of 23 laboratory mutagenicity assays, imidacloprid tested positive for causing changes in chromosomes in human lymphocytes, as well as testing positive for genotoxicity in Chinese hamster ovary cells (6).

Carcinogenic Effects
Imidacloprid is considered to be a carcinogenic risk, and is thus categorized by EPA as a "Group E" carcinogen (evidence of carcinogenicity for humans). There were carcinogenic effects in rats fed up to 1,800 ppm imidacloprid (2).

Organ Toxicity
In short-term feeding studies in rats, there were thyroid lesions associated with very high doses of imidacloprid (6).

Fate in Humans and Animals
Imidacloprid is quickly and almost completely absorbed from the gastrointestinal tract, and eliminated via urine and feces (70-80% and 20-30%, respectively, of the 96% of the parent compound administered within 48 hours). The most important metabolic steps include the degradation to 6-chloronicotinic acid, a compound that acts on the nervous system as described above. This compound may be conjugated with glycine and eliminated, or reduced to guanidine (3). Most people don't wear gloves when administering Advantage assuming it is 100% safe!!!

ECOLOGICAL EFFECTS

Effects on Birds

Imidacloprid is toxic to upland game birds. The LD50 is 152 mg/kg for bobwhite quail, and 31 mg/kg in Japanese quail (1, 3). In studies with red- winged blackbirds and brown-headed cowbirds, it was observed that birds learned to avoid imidacloprid treated seeds after experiencing transitory gastrointestinal distress (retching) and ataxia (loss of coordination). It was concluded that the risk of dietary exposure to birds via treated seeds was minimal. Based on these studies, imidacloprid appears to have potential as a bird repellent seed treatment (7, 8).

Effects on Aquatic Organisms
Products containing imidacloprid may be very toxic to aquatic invertebrates.( 3)

Effects on Other Animals (Nontarget species)
Imidacloprid is highly toxic to bees if used as a foliar application, especially during flowering. (3).

ENVIRONMENTAL FATE

Breakdown of Chemical in Soil and Groundwater
The half-life of imidacloprid in soil is 48-190 days, depending on the amount of ground cover (it breaks down faster in soils with plant ground cover than in fallow soils) (9). Organic material aging may also affect the breakdown rate of imidacloprid. Plots treated with cow manure and allowed to age before sowing showed longer persistence of imidacloprid in soils than in plots where the manure was more recently applied, and not allowed to age (10). Imidacloprid is degraded stepwise to the primary metabolite 6-chloronicotinic acid, which eventually breaks down into carbon dioxide (11). There is generally not a high risk of groundwater contamination with imidacloprid if used as directed. The chemical is moderately soluble, and has moderate binding affinity to organic materials in soils. However, there is a potential for the compound to move through sensitive soil types including porous, gravelly, or cobbly soils, depending on irrigation practices (12).

Breakdown of Chemical in Surface Water
The half-life in water is much greater than 31 days at pH 5, 7 and 9. No other information was found. Breakdown of Chemical in Vegetation

Imidacloprid penetrates the plant, and moves from the stem to the tips of the plant. It has been tested in a variety of application and crop types, and is metabolized following the same pathways. The most important steps were loss of the nitro group, hydroxylation at the imidazolidine ring, hydrolysis to 6- chloronicotinic acid and formation of conjugates (3).


BASIC MANUFACTURER
Bayer Products
P. O. Box 4913
Kansas City, MO 64120 Review by Basic Manufacturer:

Comments solicited: May and October, 1995
Comments received: not received

REFERENCES
Meister, R.T. (ed.). 1995. Farm Chemicals Handbook '95. Meister Publishing Company. Willoughby, OH.
U.S. Environmental Protection Agency. 1995. Imidacloprid; Pesticide Tolerance and Raw Agricultural commodities. 40 CFR Part 180 Section 472.
Kidd, H. and D. James (eds.). 1994. Agrochemicals Handbook. Third Edition. Royal Society of Chemistry. Cambridge, England.
Pike, K.S., G.L. Reed, G.T. Graf and D. Allison. 1993. Compatibility of Imidacloprid with Fungicides as a Seed-Treatment Control of Russian Wheat Aphid (Homoptera: Aphidae) and Effect on Germination, Growth, and Yield of Wheat Barley. J.Econ.Entomol. 86(2): 586-593.
Doull, J., C.D. Klassen, and M.O. Amdur (eds.). 1991. Cassarett and Doull's Toxicology. The Basic Science of Poisons. Fourth Edition. Pergamon Press, Elmsford, NY.
Federal Register. Imidacloprid; Pesticide Tolerances. July 5, 1995. 60(128): 34943-24945.
Avery, M.L., D.G. Decker and D.L. Fischer. 1994. Cage and Flight Pen Evaluation of Avian Repellancy and Hazard Associated with Imidacloprid-Treated Rice Seed. Crop Protection 13(7): 535-540.
Avery, M.L., D. Decker, D.L. Fischer and T.R. Stafford. 1993. Responses of Captive Blackbirds to a New Seed Treatment. J. Wildl. Manage. 57(3): 652-656.
Scholz, K., and M. Spiteller. 1992. Influence of Groundcover on the Degradation of 14C-Imidacloprid in Soil. Brighton Crop Protection Conference. Pests and Diseases. pp. 883-888.
Rouchard, J., F. Gustin and A. Wauters. 1994. Soil Organic Matter Aging and its Effect on Insecticide Imidacloprid Soil Biodegradation in Sugar Beet Crop. Toxicol. Environ. Chem. 45(3-4): 149-155.
Hellpointer, E. 1994. Degradation and Translocation of Imidacloprid (NTN 33893) Under Field Conditions on a Lysimeter. Miles Report No. 106426, pp. 1-71. Miles Inc., Agricultural Division, PO Box 4913, Kansas City, MO.
Jenkins, J.J. 1994. Use of Imidacloprid for Aphid Control on Apples in Oregon. Potential for Ground and Surface Water Contamination. Department of Agricultural Chemistry. Oregon State University, Corvallis, OR.
Placke, F.J. and E. Weber. 1993. Method of Determining Imidacloprid Residues in Plant Materials. Pflanzenschutz-Nachrichten Bayer. 46(2): 109-182.

What Veterinarians and manufacturers (Bayer) say of product!!!!
Nitenpyram (Capstar)

Nitenpyram (Capstar) is approved in dogs and cats to kill fleas.

Mode of Action: Nitenpyram interferes with the nerve conduction system of insects, blocking the nerve receptors.
Use:
Nitenpyram is approved for use in dogs and cats over 4 weeks of age and 2
pounds of bodyweight. Nitenpyram starts killing adult fleas that are on the
pet within 30 minutes. The peak effect after administering the medication is about 3 hours for the dog and 4 hours for the cat. It will be very useful in certain circumstances such as prior to surgery, boarding, or grooming. It will also help prevent pets from bringing fleas home from shows, trials, or trips to the park. The pet could be given the pill before leaving for the park or before heading home from a distant show. Any fleas on the pet will be dead within several hours.

What the Scientists say:
Nicotinoids include acetamiprid (Mospilan(r)), thiamethoxam (Actara(r),
Platinum(r)), and nitenpyram (CapStar and Bestguard(r)). All are
pursuing U.S. registration.
Mode of action--The nicotinoids act on the central nervous system of insects
and mammals, causing irreversible blockage of postsynaptic nicotinergic
acetylcholine receptors.

Nicotine is extracted by several methods from tobacco, and is effective
against most all types of insect pests, but is used particularly for aphids
and caterpillars--soft bodied insects. Nicotine is an alkaloid, a chemical
class of heterocyclic compounds containing nitrogen and having prominent
physiological properties. Other well-known alkaloids that are not insecticides are caffeine (coffee, tea), quinine (cinchona bark), morphine (opium poppy), cocaine (coca leaves), ricinine (a poison in castor oil beans), strychnine (Strychnos nux vomica), coniine (spotted hemlock, the poison used by Socrates), and, finally LSD (a hallucigen from the ergot
fungus attacking grain).

Mode of action--Nicotine action is one of the first, classic modes of action
identified by pharmacologists. Drugs that act similarly to nicotine are said
to have a nicotinic response. Nicotine mimics acetylcholine (ACh) at the
neuromuscular (nerve/muscle) junction in mammals, and results in twitching,
convulsions, and death, all in rapid order. In insects the same action is
observed, but only in the central nervous system ganglia.