General Description
Clear colorless or faintly yellow slightly viscous liquid. Faint pleasant odor.
Reactivity Profile
N,N-DIETHYL-M-TOLUAMIDE(134-62-3) is incompatible with strong acids, strong bases and strong oxidizing agents. N,N-DIETHYL-M-TOLUAMIDE(134-62-3) hydrolyzes slowly in the presence of water. N,N-DIETHYL-M-TOLUAMIDE(134-62-3) has a solvent effect on most plastics, paints, and varnishes. N,N-DIETHYL-M-TOLUAMIDE(134-62-3) is also incompatible with rayon, acetate or dynel clothing.
Air & Water Reactions
This chemical is sensitive to prolonged exposure to moisture. Insoluble in water.
Fire Hazard
This chemical is combustible.
Description
DEET was first developed and patented by the US Army in
1946. It was approved for general public use by the US Environmental
Protection Agency (EPA) in 1957 and was reregistered
in 1998. It has been estimated that more than
1.8 million kg (～4 million pounds) of DEET are used in the
United States every year in more than 225 registered products.
DEET is often sold and used in lotions or sprays with concentrations
up to 100%. However, the Center for Disease Control
recommends only 30–50% DEET to reduce the incidence of
vector-borne disease transmission. Registered products must
contain at least 95% of the meta-isomer, but small amounts of
the more toxic ortho-isomer and the less toxic para-isomer are
permitted.
History
Formulations registered for direct human application contain from 4% to 100% DEET.
DEET was developed as a joint effort by the Department of Defense and U.S. Department of
Agriculture (USDA). After examining hundreds of compounds for their repellent capabilities
in the 1940s, DEET was selected and patented by the U.S. Army in 1946.the USDA did not
announce DEET’s discovery until 1954, and it was registered for public use in 1957. DEET
is prepared from m-toluoyl chloride and diethylamine in benzene or ether.
Definition
ChEBI: A monocarboxylic acid amide resulting from the formal condensation of the carboxy group of m-toluic acid with the nitrogen of diethylamine. It is the most widely used insect repellent worldwide.
Indications
DEET is an organic liquid that is an excellent mosquito repellent; stronger
preparations of DEET are also effective against stable flies, although little protection
is provided against ticks. Commercial preparations are available in aerosol,
cream, or lotion form and vary in concentration from 6% to 100%. Because
DEET is absorbed into the bloodstream, it should be applied sparingly. Lesser
concentrations of DEET should be used whenever possible, with additional applications
to the skin if needed. Reports of a toxic encephalopathy and brief
seizures have been documented in children after overzealous use. Less serious
neurologic side effects include confusion, irritability, and insomnia. Contact dermatitis
has been observed with preparations containing higher concentrations of
DEET.
Use preparations with <20% DEET in children. Avoid mucous membranes,
broken skin, and hands of children, because they are often in contact with the
mouth. Spray clothing instead of skin whenever possible, but avoid contact
with rayon, acetate, or spandex, because these materials may be damaged by
DEET.
Environmental Fate
Historically, it was thought that DEET worked via blocking of
insect olfactory receptors and that DEET masked the target to
the insect senses so the insect would not detect a food source.
Instead, however, recent evidence indicates that the odor of
DEET is what acts as the true repellent. A specific type of an
olfactory receptor neuron in the antennal sensilla of mosquitoes
was identified, and this neuron is activated by DEET. This
activity is responsible for the properties that give DEET its
repellent ability.
DEET is also toxic to the central nervous system(CNS). DEET
acts as an inhibitor to the enzyme acetylcholinesterase which is
required for the proper functioning of the human nervous
system, other vertebrates, and insects. The enzyme acetylcholinesterase
hydrolyzes acetylcholine, which is important to
muscle control. When this process is inhibited, acetylcholine
builds up in the synaptic cleft and causes neuromuscular paralysis
and death by asphyxiation.
Toxicity evaluation
Little information is available on the environmental fate of
DEET. DEET is stable to hydrolysis at environmental pH levels.
The initial belief was that DEET was not likely to enter aquatic
ecosystems because it was first registered for indoor use. It has
been shown in several studies, however, that DEET is found in
many waterways in the United States and around the world,such as groundwater, open water, sewage (influent and
effluent), surface water, and septic waste in concentrations
ranging from 30 ng l-1 to 13 μg l-1. A major source of introduction
to aquatic environments is via sewage following
washing and excretion by humans. The potential for DEET to
be transported through soil is unknown. Although, some
studies have shown that purification of water containing low
concentrations of DEET using a combination of sand filtration,
activated sludge treatment, and ozonation has a removal efficiency
less than 69% (ozonation being the most efficient step).
Sand filtration alone was inefficient, notably due to DEET’s
hydrophilic nature (Kow < 3). This evidence suggests that DEET
may not be retained in soil and other organic matter, but travels
with groundwater into larger bodies of water, and more
extreme measures than this must be taken to remove DEET
from natural and domestic waters. On the other hand, one
study noted that DEET ‘has an estimated Koc value of 536,
indicating potential for sorption to suspended solids and
sediment.’
