PMEP Home Page --> Pesticide Active Ingredient Information --> EXTOXNET: The Extension Toxicology Network --> Metiram to Propoxur --> Napropamide

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 Assessment Program.

  Pesticide
Information
Profile
Napropamide

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.

INTRODUCTION

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 growth.

Napropamide is a General Use Pesticide.

TOXICOLOGICAL EFFECTS

ACUTE TOXICITY

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).

CHRONIC TOXICITY

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.

Reproductive Effects

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.

Teratogenic Effects

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.

Mutagenic Effects

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.

Carcinogenic Effects

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.

Organ Toxicity

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.

ECOLOGICAL EFFECTS

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).

ENVIRONMENTAL FATE

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).

Exposure Guidelines:

NOEL (rat): 30 mg/kg (body weight gain)
ADI: NA
TLV: NA
HA: NA
RfD: 0.01 mg/kg/day

Physical Properties:

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

BASIC MANUFACTURER

Zeneca Ag Products
Wilmington, DE 19897
Telephone: 800-759-4500

Review by Basic Manufacturer:

Comments solicited: June, 1993
Comments received:

REFERENCES

  1. The Farm Chemicals Handbook. 1992. Meister Publishing. Willoughby, OH.
  2. Devrinol. 1986. US Environmental Protection Agency. Tox Oneliners.
  3. The Agrochemicals Handbook. 1991. The Royal Society of Chemistry. Cambridge, England.
  4. Integrated Risk Information System (IRIS). National Library of Medicine, MEDLARS. Napropamide. 4/30/93.
  5. Napropamide. 1984. Environmental Effects Branch. US Environmental Protection Agency.
  6. Pesticide Environmental Fate One Line Summary for Napropamide. 1991. Environmental Fate and Effects Division. Environmental Protection Agency.
  7. 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 Water Branch.