Dinitrophenol,dry or wetted with less than 15% water,by mass Chemical Properties

Melting point:

86°C

Boiling point:

318.03°C (rough estimate)

Density 

1.6800

refractive index 

1.4738 (estimate)

EPA Substance Registry System

Dinitrophenol (25550-58-7)

Safety Information

RIDADR 

0076

HazardClass 

1.1D

PackingGroup 

II

Hazardous Substances Data

25550-58-7(Hazardous Substances Data)

Dinitrophenol,dry or wetted with less than 15% water,by mass Usage And Synthesis

Description

Dinitrophenol (DNP) was first introduced in the United States in 1933 as a treatment for obesity but was removed from the market in 1938 due to several fatalities and occurrences of cataracts.

Uses

DNPs are used as fungicides, herbicides, or insecticides. The fungicidal, herbicidal, or insecticidal properties depend on minor differences in the chemical structures of the different DNP compounds, and several DNP compounds have more than one pesticidal use. The pesticidal use of one DNP, Dinoseb, was eliminated in the United States in 1986. While there has been a cancellation of all United States registrations for the fungicide/miticide Dinocap, it still has agricultural uses worldwide. DNPs have also been used in the production of dyes, explosives, and photographic developing fluids.

Definition

ChEBI: 2,3-dinitrophenol is a dinitrophenol.

General Description

A yellow colored liquid dissolved in an organic solvent. The flammability of the solution depends on the solvent. Dinitrophenol itself is combustible though Dinitrophenol,dry or wetted with less than 15% water,by mass may require some effort to ignite. Toxic by skin absorption and inhalation. Prolonged exposure to fire or heat may result in the spontaneous decomposition and heating with a resultant explosion. Produces toxic oxides of nitrogen during combustion.

Air & Water Reactions

Slightly soluble in water.

Reactivity Profile

DINITROPHENOL SOLUTION serves as a slight to strong oxidizing agent. If mixed with reducing agents, including hydrides, sulfides and nitrides, may begin a vigorous reaction that culminates in a detonation. May explode in the presence of a base such as sodium hydroxide or potassium hydroxide. Severe explosion hazard when dry.

Health Hazard

TOXIC; inhalation, ingestion or skin contact with material may cause severe injury or death. Contact with molten substance may cause severe burns to skin and eyes. Avoid any skin contact. Effects of contact or inhalation may be delayed. Fire may produce irritating, corrosive and/or toxic gases. Runoff from fire control or dilution water may be corrosive and/or toxic and cause pollution.

Fire Hazard

Combustible material: may burn but does not ignite readily. When heated, vapors may form explosive mixtures with air: indoors, outdoors and sewers explosion hazards. Contact with metals may evolve flammable hydrogen gas. Containers may explode when heated. Runoff may pollute waterways. Substance may be transported in a molten form.

Safety Profile

Poison by ingestion and subcutaneous routes. An explosive and flammable solid. When heated to decomposition it emits toxic fumes of NOx. See also NITRO COMPOUNDS of AROMATIC HYDROCARBONS.

Environmental Fate

The uses of DNPs indicate that they may be released into the environment. DNPs are expected to have moderate to high mobility in soil based on an estimated Koc value of 460. Mobility will be particularly evident in moist soils, since DNPs will exist primarily as anions. If released into water, DNPs will largely remain in solution and not adsorb significantly to particulate matter or sediment. Volatilization of DNPs from soil or water is not expected to be a significant fate process due to Henry’s law constants ranging from 2.8 ×10^-8 to 8.6 × 10^-8 m³ atm mol^-1. DNPs are not known to undergo hydrolysis in the environment, although photolysis may be an important abiotic degradation process. Log Kow values ranging from 1.37 to 1.75 and bioconcentration factors of <6.6 in fish suggest that accumulation in aquatic organisms is low.

Toxicity evaluation

DNPs act as uncouplers of oxidative phosphorylation; these compounds reduce the electrochemical (proton) gradient necessary for oxidative phosphorylation by releasing phenolic protons in the mitochondrial matrix. The energy produced due to oxidation is not utilized for the synthesis of ATP but elevates body temperature, which can lead to fatal hyperpyrexia. Oxygen consumption, body temperature, breathing rate, and heart rate are increased following exposure to toxic levels of DNPs. Permeability of mitochondrial membranes to hydrogen ions was found to be increased with the failure of conversion of ADP to ATP. Inefficient circulation and respiration cannot meet the increased metabolic demand, resulting in anoxia and acidosis. Fat serves as an alternative fuel for metabolism. Weight loss occurs as a result of inhibition of lipogenesis from pyruvate and lactate following exposure to DNPs.