NORBORMIDE Chemical Properties

Melting point:

190-198°

Boiling point:

598.31°C (rough estimate)

Density 

1.2065 (rough estimate)

refractive index 

1.7800 (estimate)

storage temp. 

Amber Vial, -20°C Freezer, Under inert atmosphere

solubility 

Chloroform (Slightly), Methanol (Slightly, Heated)

form 

Solid

color 

Crystals

Water Solubility 

60mg/L(room temperature)

Stability:

Light Sensitive

EPA Substance Registry System

Norbormide (991-42-4)

Safety Information

Hazard Codes 

Xn

Risk Statements 

22

RIDADR 

2588

HazardClass 

6.1(a)

PackingGroup 

I

Hazardous Substances Data

991-42-4(Hazardous Substances Data)

Toxicity

LD50 in rats (mg/kg): 5.3 orally; 0.65 i.v. (Roszkowski)

NORBORMIDE Usage And Synthesis

Description

Norbormide was first introduced on the market in 1964 as a selective raticide, but does not have a current registration for commercial use in the European Union or North America. Current use as a pesticide is minimal to nonexistent worldwide. This compound’s toxicity is highly specific for rats.

Chemical Properties

White solid. Insoluble in water; soluble in dilute acids.

Chemical Properties

Nonyl trichlorosilane is a clear fuming liquid. Irritating odor.

Uses

The only commercial use was as a rodenticide specifically for Rattus species. However, there have been some reports of this compound or its derivatives being investigated as a calcium channel blocker for use as a potential drug to treat human cardiovascular disease.

Uses

Norbormide is used as a rodenticide. It acts as a vasoconstrictor and calcium channel blocker, but is selectively toxic to rats and has relatively low toxicity to other species, due to a species specific action of opening the permeability transition pores in rat mitochondria.

Definition

A rodenticide specific for rats, supposedly nontoxic to other animals or to humans .

General Description

Colorless to off-white crystalline powder. Used as a selective rat poison.

Reactivity Profile

When heated to decomposition, NORBORMIDE emits toxic fumes of nitrogen oxides. Avoid alkalis. [EPA, 1998].

Hazard

Toxic by ingestion.

Health Hazard

Moderately to highly toxic to humans. Probable human lethal dose is 50 to 500 mg/kg, or 1 teaspoon to 1 pint for a 150 lb. person.

Fire Hazard

When heated to decomposition, NORBORMIDE emits toxic fumes of nitrogen oxides. Avoid alkalies.

Safety Profile

Poison by ingestion andintravenous routes. A rodenticide. When heated todecomposition it emits toxic fumes of NOx.

Potential Exposure

This material is used as a selective, fast acting rat poison.

Environmental Fate

Because of its use as a rodenticide, norbormide may have entered the environment, particularly as a soil contaminant. The vapor pressure for norbormide is estimated to be 4.3 ×10^-22 mmHg at 25 ℃, while Henry’s constant is 2.7 × 10^-23 atmm³ mol^-1. Therefore, volatilization from wet or dry soil is not likely to occur. If present in contaminated soil, norbormide may be transported in the air and undergo wet or dry deposition. Also, with a Koc of 2000, there would be some minor soil mobility. The high Koc coupled with a bioconcentration factor (BCF) of 290 predicts that norbormide contaminating aquatic systems would adsorb to suspended solids or sediments and would bioconcentrate.

Shipping

UN2588 Pesticides, solid, toxic, Hazard Class: 6.1; Labels: 6.1-Poisonous materials, Technical Name Required.

Toxicity evaluation

Norbormide causes an extreme and irreversible vasoconstriction in small arteries in rats following both systemic and local administration. However, large rat arteries (e.g., aorta), nonvascular rat smooth muscles (e.g., duodenum and trachea), and all smooth muscles from non-rat species do not constrict even at high concentrations/doses of norbormide. The massive peripheral vasoconstriction in small rat arteries subsequently reduces coronary blood flow rate, leading to cardiac arrhythmias and possible death. However, small artery vasoconstriction in vascular beds supplying other organs (e.g., brain, kidney, and liver) and subsequent severe ischemic damage are likely responsible for death in most cases. The norbormideinduced vasoconstriction is mediated by activation of phospholipase C/protein kinase C and calcium influx via L-type voltage-dependent calcium channels. In contrast, norbormideresistant arteries and smooth muscles exhibit inhibition of L-type voltage-dependent calcium channels and instead exhibit a mild relaxation response. A lethal dose of norbormide in rats (1 g kg-1) can also elevate the blood glucose level twofold with a decrease in both liver and muscle glycogen. Exposed animals became comatose within 30 min to 2 h after treatment. The hyperglycemic effect of this compound in rats is considered to be a secondary effect.

Incompatibilities

Compounds of the carboxyl group react with all bases, both inorganic and organic (i.e., amines) releasing substantial heat, water and a salt that may be harmful. Incompatible with arsenic compounds (releases hydrogen cyanide gas), diazo compounds, dithiocarbamates, isocyanates, mercaptans, nitrides, and sulfides (releasing heat, toxic and possibly flammable gases), thiosulfates and dithionites (releasing hydrogen sulfate and oxides of sulfur).

Waste Disposal

Small amounts may be treated with alkali, then landfilled. Large amounts should be incinerated . In accordance with 40CFR165, follow recommendations for the disposal of pesticides and pesticide containers. Must be disposed properly by following package label directions or by contacting your local or federal environmental control agency, or by contacting your regional EPA office.

NORBORMIDE(991-42-4)Related Product Information

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