pesticides specially designed to kill rodents, pose particular risks for
accidental poisoning for several reasons. Since they have been designed to
kill mammals, they are also toxic to humans. Because rodents usually share
human environments, use of rodenticides poses an inherent risk of exposure
to people, particularly children and their pets, as well as other
non-target species. In addition, as rodents have developed resistance to
these chemicals, there continues to be a need to develop new and
potentially more toxic rodenticides.[i]
Environmental Protection Agency (EPA) recognizes that rodenticides are
acutely toxic to humans. EPA completed, in 1998, a reassessment of a
cluster of rodenticides. The agency calculates a margin of exposure (MOE)
for each pesticide as part of its reregistration eligibility decisions (REDs).
Mathematically, it is the ratio of human exposure to the level that had no
adverse effect on laboratory animals. Generally, EPA considers a MOE of
100 or above to be protective of the public’s health.[ii]
A MOE equal to or less than one means that human exposure equals the
adverse dose level. EPA calculated that rodenticide MOEs, when these
poisons are ingested, are less than one.[iii]
This means that every person exposed to rodenticides is ingesting enough
to cause illness.
can be broken down into three categories, baits, tracking powders and
fumigants. Both baits and tracking powders are rodent poisons in the
traditional sense, they must be eaten to kill the pest. Baits are designed
to attract the rodent to a feeding station. Baits can be used both in the
field and in and around buildings. Tracking powders are placed along
rodent runways in and around buildings, picked up by the fur as the animal
passes by, and then ingested during grooming. Fumigants are poisonous
gasses, designed to kill rodents in their burrows.
baits and tracking powders are the type of rodenticides that are most
often encountered by homeowners with a rodent problem. There are two types
of rodent poisons generally available – acute poisons (also known as
single feed baits) and chronic poisons (multiple feed baits).[iv]
Acute poisons are extremely dangerous to pets and children, as one
encounter can make them very sick or kill them.[v]
feed baits are the most commonly used type of rodent poisons. Typically
these poisons act as anti-coagulants, literally causing the victim to
bleed to death internally. The fact that these poisons must be made
available to the pest animal over time makes them very hazardous as
children, pets and other non-target animals have an extended opportunity
to get into them. The Environmental Protection Agency (EPA) recognizes
that anti-coagulant rodenticides, when used as directed, are responsible
for a high number of human incidents and accidental exposures each year[vi]
(more on that below). Current labels for rat and mouse baits used outdoors
require that baits be applied in protective, tamper proof bait stations or
placed in areas inaccessible to non-target wildlife.[vii]
are two classes of anti-coagulant type rodent poisons, the courmarins and
the indandiones. Courmarins include some very common rodent poisons such
as warfarin, bromadiolone, and courmafuryl. Indandiones include the rodent
poisons diphacionone and chlorophacinone.[viii]
of these classes of toxic materials work by blocking vitamin K-dependent
synthesis of the blood clotting substance prothrombin, which predisposes
the animal to widespread internal bleeding. Animals suffering from
exposure to anti-coagulant rodenticides suffer from the following list of
immediate toxic effects: nosebleeds, bleeding gums, blood in urine and
feces; bruises due to ruptured blood vessels; and skin damage.[ix]
to these poisons also has long-term health effects. The courmarin,
warfarin, for example, has been shown to cause paralysis due to cerebral
and is teratogenic[xi]
(causes birth defects). Long-term exposure to the indandione, diphacinone
causes nerve[xii], heart, liver, and kidney
damage as well as damage to skeletal muscles.[xiii]
known as vitamin D3, cholecalciferol has a unique mode of action. It is
metabolized by the body into its active form, which increases the
absorption of calcium and phosphorus from the gut, resulting in very high
serum levels of calcium.[xiv]
The prolonged hypercalcemia is delayed in onset and insidious in
progression, leading ultimately to the death of the victim.[xv]
is a neurotoxin, unlike the other rodent poisons. The poison affects the
body’s ability to control muscle contraction through uncoupling
oxidative phosphorylation. It can cause swelling of the brain, spinal
column and nerves, leading to a loss of the myelin nerve sheath and
ultimately to a reduction of nerve impulses and death.[xvi]
Immediate effects of exposure to bromethalin include skin and eye
irritation, weakness in legs,
loss of tactile sensation, and death by respiratory arrest.[xvii]
zinc phosphide is ingested, it reacts with water and stomach juices to
release phosphine gas, which can enter the blood stream and affect the
lungs, liver, kidneys, heart and central nervous system. It is easily
absorbed through skin or inhaled from fumes. With repeated exposure, it
accumulates in the body to dangerous levels.[xviii]
and symptoms of mild zinc phosphide poisoning include diarrhea and stomach
pains. In more severe cases, nausea, vomiting, chest tightness,
excitement, coldness, unconsciousness, coma and death can occur from
pulmonary edema and liver damage.
is no antidote for zinc phosphide poisoning. It is a slow-acting material,
which gives the victim time to get medical help.[xix]
causes violent convulsions because of its direct action on the central
nervous system, chiefly the spinal cord. The onset of symptoms begins
usually within 15 to 20 minutes of ingestion. A lethal dose of this
natural toxin is as little as 15 mg in children.[xx]
effects of exposure are irritation to the upper respiratory tract and
skin, vomiting, convulsions, hyperthermia, and death due to respiratory or
Victims of strychnine poisoning should be placed in a warm dark room in
order to reduce the stimuli that can trigger convulsions. Medical help
should be brought to the victim rather than transporting the victim to the
medical center because movement will trigger convulsions.[xxii]
are used to kill rodents in their burrows. As a result, homeowners are
much less likely to encounter the use of these chemicals but they are
worthy of mention. The two most commonly used gasses to kill rodents are
phosphine gas and methyl bromide.
in a variety of forms including aluminum phosphide and magnesium phosphide,
phosphine gas is extremely toxic. Accordingly, EPA has placed chemicals
that produce phosphine gas in toxicity category I, the highest toxicity
aluminum phosphide is dropped into a rodent burrow it reacts with moisture
to form phosphine gas. The signs and symptoms of exposure to phosphine gas
are described above under zinc phosphide.
bromide has also been placed in EPA’s toxicity category I. EPA has also
expressed concern over methyl bromide’s potential to destroy ozone.[xxiv]
As a result, methyl bromide is scheduled to be phased out by 2005,[xxv]
although there is political pressure to extend or reopen the phase out.
Long-term exposure studies have found that methyl bromide is a mutagen,
and neurotoxin that causes liver and kidney damage.[xxvi]
Rodenticide Risk to
Humans and Pets
rank second in the number of human exposures each year compared with the
three other major categories of pesticides for which data is collected by
the American Association of Poison Control Centers (AAPCC) (see table 1).
According to AAPCC’s latest numbers, 20,300 people were exposed to
rodenticides in 1998. As mentioned above, anti-coagulant poisonings make
up the vast majority of cases with 17,724 (87% of total) reported cases.
Young children are the most common victims of exposure to rodenticides,
17,608 cases of exposure (87%) were children under six years of age; that
is over seven times higher than the other two age groups (6-19, >19)
combined. Tragically, five people died as a result of their exposure to
rodenticides in 1998.
1. Demographic Profile of Exposures to Rodenticides in 1998.
Litovit, T.L., et al. 1999. 1998 Annual Report of the American Association
of Poison Control Centers Toxic Exposure Surveillance System. American
Journal of Emergency Medicine. Vol. 17, no. 5. <http://www.aapcc.org/1998.htm>
and non-target wildlife also fall victim to exposure to rodenticides.
Exposure to these animals can occur as a result of either feeding on the
bait or eating rodents that have been killed by rodenticides.
Toxicologists calculate the dose of poisons that will kill 50% of the
animals that are exposed; this measurement is called an LD50. It takes as
little as 0.16 ounces of zinc phosphide to kill a 10 lb. dog (see table
2). Rodent poisons should be used only as a last resort. If poisons are
used, homeowners need to practice extreme caution when choosing to control
rodents in this way.
2. Ounces of Rodenticide Bait LD50s for Pets.
1998. Rodenticide Risk to Dogs and Cats. Techletter: For Pest Control
Technicians. Vol. 4, no. 23.
dealing with a rodent problem need to consider all of the alternative,
nontoxic approaches to rodent control. Contact Beyond Pesticides/NCAMP to
find out more about nontoxic approaches to rodent control.
[i] Fishel, F. and P. Andre, 1999. “Pesticide Poisoning Symptoms and First Aid.” University of Missouri Agricultural Engineering. <http://muextension.missouri.edu/xplor/agguides/agengin/g01915.htm>
[ii] Environmental Protection Agency. 1998. R.E.D. Facts: Rodenticide Cluster. EPA-738-F-98-004. pps. 3-4 <http://www.epa.gov/oppsrrd1/REDs/factsheets/2100fact.pdf>
[iv] Simon, L. and W. Quarles, 1996. Integrated Rat Management, Common Sense Pest Control, Vol. 12, no. 1, ppgs. 5- 15, citing Meehan, A.P. 1984. Rats and Mice: Their Biology and Control. Rentokil, East Grinstead, West Sussex, United Kingdom.
[vi] Environmental Protection Agency. 1998. Reregistration Eligibility Decision: Rodenticide Cluster.
[vii] Environmental Protection Agency. 1998. R.E.D. Facts: Rodenticide Cluster. EPA-738-F-98-004. p. 2. <http://www.epa.gov/oppsrrd1/REDs/factsheets/2100fact.pdf>
[viii] Rachel Carson Council. 1992. Basic Guide to Pesticides: Their Characteristics and Hazards. Taylor & Francis, Washington, DC.
[xi] Extension Toxicology Network (ETN). 1995. “Warfarin.” Pesticide Information Profiles. <http://ace.orst.edu/cgi-bin/mfs/01/pips/warfarin.htm>
[xii] Rachel Carson Council. 1992. Basic Guide to Pesticides: Their Characteristics and Hazards.
[xiii] Extension Toxicology Network (ETN). 1995. “Diphacinone.” Pesticide Information Profiles. <http://ace.orst.edu/cgi-bin/mfs/01/pips/diphacin.htm>
[xiv] Craigmill, A. 1998. Veterinary Toxicology Notes: Hazards of New Rodenticides to Pets. UC Davis Env. Tox. Newsletter, Vol. 8, no. 2. <http://ace.orst.edu/cgi-bin/mfs/01/newsletters/n82_88.htm>
[xvi] Rachel Carson Council. 1992. Basic Guide to Pesticides: Their Characteristics and Hazards.
[xviii] Schulze, L.D., et al. 1997. “Signs and Symptoms of Pesticide Poisoning.” University of Nebraska Cooperative Extension EC97-2505-A. < http://www.ianr.unl.edu/pubs/pesticides/ec2505.htm>
[xx] Fishel, F. and P. Andre, 1999.
[xxi] Rachel Carson Council. 1992. Basic Guide to Pesticides: Their Characteristics and Hazards.
[xxii] Schulze, L.D., et al. 1997. “Signs and Symptoms of Pesticide Poisoning.”
[xxiii] Extension Toxicology Network (ETN). “Aluminum Phosphide.” Pesticide Information Profiles. <http://ace.orst.edu/cgi-bin/mfs/01/pips/alumphos.htm>
[xxiv] Extension Toxicology Network (ETN). 1996. “Methyl bromide: Bromomethane.” Pesticide Information Profiles. < http://ace.orst.edu/cgi-bin/mfs/01/pips/methylbr.htm>
[xxv] U.S. EPA Methyl Bromide Phase Out Web Site. < http://www.epa.gov/spdpublc/mbr/>
[xxvi] Rachel Carson Council. 1992. Basic Guide to Pesticides: Their Characteristics and Hazards.