E X T O X N E T
Extension Toxicology Network
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
Publication Date: 9/93
TRADE OR OTHER NAMES
Trade names for products containing napropamide include Devrinol and R-
7465. It may also be found in formulations with other pesticides such as
monolinuron, nitralin, simizine, trifluralin, tefurthrin and tebutam. It is
also compatible with many other herbicides and fungicides.
Napropamide is a selective systemic amide herbicide. The compound is
used against a number of annual grasses and broad-leaved weeds. Napropamide
is applied to fields containing vegetables, fruit trees and bushes, vines,
strawberries, sunflowers, tobacco, olives, mint, turf or other crops. The
compound is absorbed by the roots and works by inhibiting root development and
Napropamide is a General Use Pesticide.
Napropamide is a slightly toxic compound by the oral route. The signal
word CAUTION is required on the label of products containing the compound.
The oral LD50 of the technical product is nearly 5,000 mg/kg/day in rats (2, 3).
Toxic effects from acute exposure in rats included diarrhea, excessive
tearing and urination, depression, salivation, rapid weight loss, respiratory
changes, decreased blood pressure and fluid in their body cavity (2).
No studies have evaluated the acute toxicity of the technical product
(95% napropamide) through inhalation exposure. However, several inhalation
studies have been conducted for Devrinol 4F (43.2% napropamide). The
inhalation LC50 for this formulation is greater than 0.2 mg/l for four hours
of exposure in rats. This indicates that the compound is highly toxic by this
route of exposure. Acute toxicity of napropamide due to exposure through the
skin (dermal) is low. The LC50 values for dermal exposure in rats and rabbits
are greater than 5,000 mg/kg (2).
Rats fed napropamide at low doses (up to 30 mg/kg/day) for 13 weeks
produced no significant compound-related effects (5). At slightly higher
doses however, (40 mg/kg/day), for the same length of time, female rats
experienced a reduction in uterine weight. In a similar study in dogs (13
week feeding study), the males experienced a decrease in liver weight and in
body weight (4). Some blood chemistry changes were noted at the highest dose
tested (100 mg/kg). There were no tissue changes in either the rats or dogs.
One study conducted over three successive generations of rats produced
compound related effects in the fetal pups at the 100 mg/kg/day dose. The
effects were associated with a decrease in body weight gain (4). No
conclusions can be drawn from such a limited data base on the potential
reproductive harm to humans from chronic exposure to napropamide.
Three separate tests with rats have all produced different results
making any conclusion difficult to draw. One study indicated that the
compound had no dose related effects at amounts over 400 mg/kg/day in
pregnant rats or in their offspring. However, two other studies produced
incomplete formation of bone in the rats at doses as low as 25 mg/kg (2).
Neither study tested doses below this amount so the smallest dose that
produces this effect remains unevaluated.
Three separate tests on mutagenicity of the compound have all produced
negative (non-mutagenic) results (2). Tests were conducted on bacterial
cells and in mice.
Two tests, each conducted over two years, produced no cancer related
changes in either rats or mice. The highest dose in both of the studies was
100 mg/kg/day (2). In both cases the only effects noted were decreases in
body weight gains for both species.
Though numerous organ related adverse effects have been noted for acute
exposure to napropamide, few have been correlated with chronic exposure. Only
decreases in uterine weights and liver weights have been observed at low doses
in test animals. Acute exposure to napropamide has caused changes in lungs,
liver and intestines (2).
Fate in Humans and Animals
Elimination is very rapid following oral exposure to napropamide.
Generally, most (99%) of a single dose is excreted within four days. The
dose was not indicated in the reference.
Napropamide is practically non-toxic to game birds. The compound has
LC50 values ranging from nearly 7,200 ppm for the mallard duck to 56,000 ppm
for the bobwhite quail (5).
The compound is moderately toxic to freshwater fish. Its toxicity is
relatively consistent among different fish species. The LC50 for the
compound ranges from 9.4 to 13.3 mg/l in rainbow trout and ranges from 20
to 30 mg/l in bluegill sunfish (5). The LC50 in goldfish is less than 10
mg/l (3). Aquatic freshwater invertebrates (Daphnia magna) are only
moderately susceptible to napropamide. The LC50 for the compound to this
species is 14.3 mg/l. Tests with marine organisms indicate that the compound
is moderately toxic (pink shrimp and eastern oyster) to slightly toxic
(fiddler crab) to these species.
One study indicates that the compound is not likely to accumulate
appreciably in the tissue of fish. During a ten day exposure the compound had
accumulated to 50 times the water concentration in the edible portions of
the fish. Most of the accumulated amounts were eliminated within 24 hours
in a napropamide-free environment (6).
In soil, degradation of napropamide by microbes is slow. Breakdown by
the action of sunlight however, speeds the process and is an important avenue
of loss of the compound from soil (3). Field studies indicate that half of
the initially applied amount of the chemical is lost between 9 and 17 days in
sandy-loam soil. At higher application rates however, the compound
persisted longer in the soil (6). Other studies indicate that the
compound may persist for considerably longer periods of time (half-lives
up to 8 weeks) (3).
In water, the compound is broken down very quickly. The half-life for
napropamide may be as rapid as seven minutes. In water, the breakdown was
predominantly mediated by the action of sunlight (photolysis). No information
was found regarding the breakdown potential without the presence of sunlight
such as found in lake sediments or deeper in the water column of a lake.
As of 1988, napropamide was not found in the samples from 172 different
wells across the country (7). The EPA has stated that although the
potential for the compound has not been fully assessed, leaching to
groundwater is only likely at sites with highly permeable soils with low
organic content and in shallow, unconfined aquifers (6).
|NOEL (rat): ||30 mg/kg (body weight gain)
|RfD: ||0.01 mg/kg/day
|Common Name: ||napropamide
|CAS #: ||15299-99-7
|Chemical Name: ||N,N-Diethyl-2-(1-Naphthylenoxy)-Propanamide
|Chemical class: ||amide; napthalene
|Chemical Use: ||herbicide
|Solubility in water: ||73 mg at 20 degrees C
|Melting Point: ||74.8-75.5 degrees C
|Vapor pressure: ||0.53 mPa at 25 degrees C
Zeneca Ag Products
Wilmington, DE 19897
Review by Basic Manufacturer:
Comments solicited: June, 1993
The Farm Chemicals Handbook. 1992. Meister Publishing. Willoughby,
Devrinol. 1986. US Environmental Protection Agency. Tox Oneliners.
The Agrochemicals Handbook. 1991. The Royal Society of Chemistry.
Integrated Risk Information System (IRIS). National Library of
Medicine, MEDLARS. Napropamide. 4/30/93.
Napropamide. 1984. Environmental Effects Branch. US Environmental
Pesticide Environmental Fate One Line Summary for Napropamide.
Environmental Fate and Effects Division. Environmental Protection
Williams, W.M., P.W. Holden, D.W. Parsons, M.N. Lorber. 1988.
Pesticides in Groundwater Data Base. 1988 Interim report. US
Environmental Protection Agency. Office of Pesticide Programs.
Environmental Fate and Effects Division. Environmental Fate and Ground