991-42-4

Rodenticide.

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

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

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.

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

Toxic by ingestion.

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

If this chemical gets into the eyes, remove any contact lenses at once and irrigate immediately for at least 15 minutes, occasionally lifting upper and lower lids. Seek medical attention immediately. If this chemical contacts the skin, remove contaminated clothing and wash immediately with soap and water. Seek medical attention immediately. If this chemical has been inhaled, remove from exposure, begin rescue breathing (using universal precautions, including resuscitation mask) if breathing has stopped and CPR if heart action has stopped. Transfer promptly to a medical facility. When this chemical has been swallowed, get medical attention. Give large quantities of water and induce vomiting. Do not make an unconscious person vomit.

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

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).

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.

Nonyl trichlorosilane is a clear fuming liquid. Irritating odor.

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

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.

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

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.

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.