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avermectin (Agri-Mek, Affirm) E X T O X N E T EXTENSION TOXICOLOGY

                          E  X  T  O  X  N  E  T

A Pesticide Information Project of Cooperative Extension Offices of
CornellUniversity, 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.



     Also known as Avermectin B1 and MK-936.  Trade names include Affirm, 
Agri-Mek, Avid, Dynamec, Vertimec and Zephyr.


     Abamectin is a mixture of avermectins containing > 80% avermectin B1a 
and < 20% avermectin B1b (1).  These two components, B1a and B1b have very 
similar biological and toxicological properties (5).  The avermectins are 
insecticidal or anthelmintic compounds derived from the soil bacterium 
Streptomyces avermitilis (2).  Abamectin is a natural fermentation product 
of this bacterium (5).  Abamectin is used to control insect and mite pests 
of a range of agronomic, fruit, vegetable and ornamental crops, and it is 
used by homeowners for control of fire ants (5).  Doses of 50 to 200 ug/kg 
of ivermectin, a similar member of the avermectin family of comounds, is 
widely used to treat humans in the World Health Organization onchocerciasis 
(river blindness) program (2, 8).



     Abamectin is a highly toxic material, however most formulated products 
containing abamectin are of low toxicity to mammals (5, 7).  Emulsifiable 
concentrate formulations may cause moderate eye irritation and mild skin 
irritation (1).  Symptoms of poisoning observed in laboratory animals 
include pupil dilation, vomiting, convulsions and/or tremors, and coma (5).
     Abamectin acts on insects by interfering with neural and neuromuscular 
transmission.  It acts on a specific type of synapse located only within 
the brain and is protected by the blood-brain barrier.  However, at very 
high doses, the mammalian blood-brain barrier can be penetrated, causing 
symptoms of CNS depression such as incoordination, tremors, lethargy, 
excitation and pupil dilation.  Very high doses have caused death from 
respiratory failure (2).
     Abamectin is not readily absorbed through skin.  Tests with monkeys 
show that less than 1% of dermally applied abamectin was absorbed into the 
bloodstream through the skin (5).  Abamectin does not cause allergic skin 
reactions (7).
     The amount of a chemical that is lethal to one-half (50%) of 
experimental animals fed the material is referred to as its acute oral 
lethal dose fifty, or LD50.  The oral LD50 for abamectin in rats is 11 
mg/kg, and in mice range from 14 (5) to > 80 mg/kg (7).  The dermal LD50 
for technical abamectin on rats and rabbits is > 330 mg/kg (4).  The oral 
LD50 for the product Affirm 0.011% Fire Ant Bait in rats is > 5,000 mg/kg, 
and its dermal LD50 on rabbits is > 2,000 mg/kg (1).  The oral LD50 for the 
1.8% w/v Abamectin EC product in rats is 300 mg/kg, and the dermal LD50 for 
this product on rabbits is > 2,000 mg/kg (8).


     In a 1-year study with dogs given oral doses of 0, 0.25, 0.5, or 1 
mg/kg/day, there were no changes in tissue at any dose level.  However, 
some dogs at the 0.5 and 1 mg/kg/day levels had pupillary dilation, weight 
loss, lethargy, tremors and recumbency.  The NOEL for this study was 0.25 
mg/kg/day (5, 8).  Similar results were seen in a 2-year study with rats 
fed 0, 0.75, 1.5, or 2 mg/kg/day.  No changes in the nervous or muscular 
systems were observed, but rats in all the dosage levels exhibited body 
weight gains significantly higher than the controls.  A few individuals in 
the high dose group exhibited tremors (5).
     When mice were fed 8 mg/kg/day, the highest dose tested, for 94 weeks, 
the males developed dermatitis and changes in blood formation in the 
spleen, while females exhibited tremors and weight loss (7).

Reproductive Effects

     In rats, the pup toxicity NOEL was 0.12 mg/kg/day.  At 0.40 mg/kg/day, 
there were increased stillbirths, decreased pup viability, decreased 
lactation, and decreased pup weights (7).

Teratogenic Effects

     Abamectin has produced cleft palate in the offspring of treated mice 
and rabbits, but only at doses that were also toxic to the mothers (5).  
There were no birth defects in the offspring of rats given up to 1 
mg/kg/day (7).

Mutagenic Effects

     Abamectin is not mutagenic.  The microbial mutagenesis and 
mutagenicity tests in live mice were negative.  One test on rat liver cell 
cultures was positive (7).

Carcinogenic Effects

     Abamectin was not carcinogenic in rats or mice fed the maximum 
tolerated doses.  The rats were fed dietary doses of 0.75, 1.5, or 2 
mg/kg/day for 24 months, and the mice were fed 2, 4 or 8 mg/kg/day for 22 
months (5).

Fate in Humans and Animals

     Tests with laboratory animals show that ingested avermectin B1a is 
absorbed into the bloodstream by mammals and that it is rapidly eliminated 
from the body within 2 days via the feces (7, 8).  Rats given single oral 
doses of radio-labeled avermectin B1a excreted most of the dose (69 to 82%) 
unchanged in the feces.  The half-life of avermectin B1a residues in rat 
tissues averaged 1.2 days (4).  Similarly, when monkeys were given a single 
intravenous injection of avermectin B1a, more than 90% of the dose was 
excreted in the feces within 7 days of the dosing (5, 8).  Lactating goats 
given daily oral doses for 10 days excreted 89% of the administered 
avermectin, mainly in the feces.  Less than 1% was recovered in the urine 


Effects on Birds

     Abamectin is relatively non-toxic to birds (7).  The LD50 for 
abamectin in Bobwhite quail is 2,000 mg/kg.  When exposed to abamectin in 
their feed for 5 days, the LC50 for bobwhite quail was 3,102 ppm, and for 
mallard ducks was 383 ppm.  There were no adverse effects on reproduction 
when mallard ducks were fed dietary doses of 3, 6 or 12 ppm for 18 weeks 

Effects on Aquatic Organisms

     Abamectin is highly toxic to fish and aquatic invertebrates (7).  Its 
96-hour LC50 in rainbow trout is 3.2 ppb, 9.6 ppb in bluegill sunfish, 15 
ppb in sheepshead minnow, 24 ppb in channel catfish, and 42 ppb in carp.  
Its 48-hour LC50 in Daphnia magna, a small freshwater crustacean, is 0.34 
ppb.  The 96-hour LC50 for abamectin in pink shrimp (Panaeus duorarum) is 
1.6 ppb, 0.022 ppb in mysid shrimp, 430 ppb in eastern oysters, and 153 ppb 
in blue crab (6).
     While the above LC50 values are quite low, indicating a high level of 
toxicity to aquatic organisms, actual concentrations of abamectin in 
surface waters (fresh water) adjacent to treated areas are expected to be 
low.  Application rates of 0.025 pounds of abamectin per acre (the highest 
recommended rate) should result in concentrations no higher than 26 parts 
per trillion in adjacent surface waters one day after the application.  
Rapid photodegradation and adsorption to sediments should produce even 
lower concentrations within days.  The degradation products of abamectin 
are less toxic to aquatic organisms than abamectin itself (6).
     Abamectin did not bioaccumulate in bluegill sunfish exposed to 0.099 
ppb for 28 days in a flow-through tank.  On day 28, the concentration of 
residues in the fish was 6.8 ppb, but this rapidly decreased to 0.32 ppb by 
day 42.  The BCF value calculated from this study is 52, indicating that 
abamectin does not accumulate or persist in fish (6).

Effects on Other Animals (Nontarget species)

     Abamectin is highly toxic to bees, with a 24-hour contact LC50 of 
0.002 ug/bee and an oral LD50 of 0.009 ug/bee.  Rapid degradation of 
abamectin will reduce the risk of bee deaths.  Citrus and alfalfa foliage 
was not toxic to bees 24 to 48 hours after treatment with abamectin (6).
     The 28-day LC50 for abamectin in earthworms is 28 ppm.  Earthworms 
will not be adversely affected by use of abamectin at recommended 
application rates.


Breakdown of Chemical in Soil and Groundwater

     Because abamectin is nearly insoluble in water and has a strong 
tendency to bind to soil particles, it is therefore immobile in soil and 
unlikely to leach or contaminate groundwater (6, 7).  Compounds produced by 
the degradation of abamectin are also immobile and unlikely to contaminate 
groundwater (6).
     Abamectin is rapidly degraded in soil.  At the soil surface, it is 
subject to rapid photodegradation, with half-lives of 8 and 21 hours (6) or 
1 day (7) reported.  When applied to the soil surface and not shaded, its 
soil half-life was about 1 week.  Under dark, aerobic conditions,  the soil 
half-life was 2 weeks to 2 months (7).  The half-life for avermectin B1a in 
fine sandy loam, clay and construction grade sand was 20 to 47 days.  Loss 
of abamectin from these soils is thought to be due to microbial degradation 
because abamectin remained undegraded in sterile soil.  The rate of 
degradation was significantly decreased under anaerobic conditions (6).

Breakdown of Chemical in Surface Water

     Abamectin is rapidly degraded in water.  After an initial 
distribution, its half-life in artificial pond water was 4 days.  Its half-
life in pond sediment was 2 to 4 weeks (6).  It undergoes rapid 
photodegradation, with a half-life of 12 hours in water (6, 7).  When 
tested at pH levels common to surface and groundwater (pH 5, 7, and 9), 
abamectin did not hydrolyze (6).

Breakdown of Chemical in Vegetation

     Plants do not absorb abamectin from the soil (6).  Abamectin is 
subject to rapid degradation when present as a thin film, as on treated 
leaf surfaces.  Under laboratory conditions and in the presence of light, 
its half-life as a thin film was 4 to 6 hours (6).


     Abamectin is a white to yellowish crystalline powder (4).  It poses a 
slight fire hazard if exposed to heat or flame, and a fire and explosion 
hazard in the presence of strong oxidizers.  It may burn but will not 
readily ignite.  Avoid contact with strong oxidizers, excessive heat, 
sparks or open flame.  Thermal decomposition may release toxic oxides of 
carbon (3).  Workers handling abamectin should wear goggles to prevent eye 
contact and protective clothing to prevent prolonged skin contact (3).

Exposure Guidelines:

     No occupational exposure limits have been established for abamectin by 

Physical Properties:

CAS #:  Avermectin B1a - 65195-55-3; Avermectin B1b - 65195-56-4

Chemical name:  avermectin B1a

Chemical Class/Use:  avermectin acaricide/insecticide; macrocyclic lactone 
disaccharide isolated from the soil bacterium Streptomyces avermitilis.

Density:  1.16 at 21 degrees C (7)

H20 solubility:  practically insoluble; 7.8 ppb (6)

Solubility in other solvents:  soluble in acetone, methanol, isopropanol 
and toluene (4, 8)

Melting point:  155-157 degrees C (4)

Vapor pressure:  negligible (4); 1.5 x 10 to the minus 9 torr (7)

Koc:  4,000 (6)

Merck & Co., Inc.
Agvet Div.
P.O. Box 2000
Rahway, NJ  07065
Telephone:  908-855-4277

Review by Basic Manufacturer:
Comments solicited:  April, 1993
Comments received:  July, 1993


(1)   Meister, R.T. (ed.).  1992.  Farm Chemicals Handbook '92.  Meister 
Publishing Company, Willoughby, OH.

(2)   Hayes, W.J. and E.R. Laws (eds.).  1990.  Handbook of Pesticide 
Toxicology, Classes of Pesticides, Vol. 3.  Academic Press, Inc., NY.

(3)   Occupational Health Services, Inc.  1992 (Nov. 17).  MSDS for 
Avermectin B1a.  OHS Inc., Secaucus, NJ.

(4)   Thongsinthusak, T., et. al.  June 5, 1990.  HS 1567: Estimation of 
exposure of persons in California to pesticide products that contain 
abamectin.  California Dept. of Food and Agriculture, Div. of Pest 
Management, Environmental Protection and Worker Safety, Worker Health and 
Safety Branch, Sacramento, CA.

(5)   Lankas, G.R and L.R. Gordon.  Toxicology in W.C. Campbell (ed.).  
1989.  Ivermectin and Abamectin.  Springer-Verlag, NY.

(6)   Wislocki, P.G., et al.  Environmental Aspects of Abamectin Use in 
Crop Protection  in  W.C. Campbell (ed.).  1989.  Ivermectin and Abamectin.  
Springer-Verlag, NY.

(7)   U.S. Environmental Protection Agency.  July 20, 1990.  Pesticide Fact 
Sheet Number 89.2: Avermectin B1.  US EPA, Office of Pesticide Programs, 
Registration Div., Washington, DC.

(8)   Review by Merck Research Laboratories.  May 23, 1993.

     This PIP is part of the EXTOXNET Pesticide Information Notebook.  For 
more information, contact the Pesticide Management Education Program, 
Cornell University, 5123 Comstock Hall, Ithaca, N.Y.  14853-0901.

DISCLAIMER:  The information in this profile does not in any way replace or 
supersede the information on the pesticide product label/ing or other 
regulatory requirements.  Please refer to the pesticide product label/ing.