4,6-Dinitro-o-cresol

534-52-1

On dormant plants or on waste ground as an ovicide,
insecticide, and as a broad leaf herbicide. 
It is used as a
defoliant on actively growing plants and as a blossom thinner
and a preventer of alternate bearing fruit trees. 
It is also
used as a fungicide, acaricide, and in scab apple control.

Yellow prisms. 
In water: colourless aqueous solution turns
yellow when alkaline.

198.15

Dinitrophenols are stable at low pH, but decompose upon
ultraviolet radiation in alkaline solutions. -  
DNOC rapidly
forms water soluble ammonium, sodium, potassium, and calcium
salts. -  
Although it is slow, photolysis is the main process
of DNOC breakdown in an aqueous environment. 
Bacterial
breakdown may be very slow in water. 
DNOC does absorb on clay
and may hydrolyse during sorption (Sax 1986).

Biodegradation: adapted culture: 1 % removal after 48 hr
incubation (feed 207 mg/l).

Photolysis is thought to be the main route of degradation in an
aquatic environment. 
No half-life is given but the process is
described as slow. 
The time of disappearance in soil is from a
few weeks to 2 months (Sax 1986).

The half-life in man is 5.78 days (Sax 1986).

Most organisms reduce a NO2 grout to NH2. 
This process is most
significant in microorganisms and fish (Sax 1986).

Confirmed to be non-accumulative or low accumulative (Anon.
1987).

DNOC uncouples the oxidation of cytochrome B by flavoprotein
during oxidative phosphorylation in both animals and plants. 1
mg/m3 has resulted in central nervous system effects in humans. 
DNOC produces hyperpyrexia, hyperglycemia, glycouria, kidney
damage, cardiovascular changes and gastrointestinal tract
changes (Sax 1986).

Symptoms of poisoning include deep, rapid respiration,
sweating, thirst, heat sensation, motor weakness, collapse,
coma, and death. 
Rigor mortis occurs early. 
The poison action
is cumulative. 
Chronic poisoning symptoms include cataracts,
chest pain, dermatitis, dyspnea, fever, jaundice, nausea and
vomiting, flushing, weight loss, headache, diarrhea, kidney
damage, cardiovascular changes, gastrointestinal tract changes,
central nervous system effects, hyperpyrexia, hyperglycemia,
and glycosuria (Sax 1986).

Skin and eye irritation data:
skn, rbt, 105 mg, 9 D-I, mild;
eye, rbt, 20 mg, 24 hr, severe (Sax 1986).

Salmonella, T4 bacteriophage and two R III mutagens of the T4
bacteriophage did not produce mutations when treated with
dinitro-o-cresol. 
Escherichia coli did not produce mutagens but
there is evidence of DNA damage to proteus (Sax 1986).

Mutagen data:
mmo, sat, 0.050 ml/plate;
snr, omi, 10 mg/plate;
sln, dmg, orl, 0.250 mmol/l (Sax 1986).

Ivn-pgn, LDLO 7 mg/kg (Sax 1986).

NOEC, 0.32 mg/l, 100d, Xenopus laevis, mortality.

NOEC, 0.32 mg/l, 100d, Xenopus laevis, development.

NOEC, 0.32 mg/l, 100d, Xenopus laevis, growth.

(Slooff & Canton 1983)

NOEC, 10 mg/l, 25d, Culex pipiens, mortality.

NOEC, 10 mg/l, 25d, Culex pipiens, development.

(Slooff & Canton 1983)

Irrigable plants: as an herbicide, DNOC primarily produces
local root damage. 
The first effect in solution is to reduce
transpiration drastically. 
Dinitrophenols inhibit oxidative
phosphorylation. 
DNOC inhibits pollen tube growth, prevents
pollen generation, and injures the stigma so that it cannot
function (Sax 1986).

NOEC, 0.32 mg/l, 7d, Lemna minor, specific growth rate.

(Slooff & Canton 1983)

NOEC, 10 mg/l, 0.3d, Pseudomonas fluorescens, specific growth
rate.

NOEC, 3.2 mg/l, 4d, Microcystis aeruginosa, specific growth
rate. 
(Slooff & Canton 1983)

Toxicity threshold (cell multiplication inhibition test):
bacteria (Pseudomonas putida): 16 mg/l
(Bringmann & Kühn 1980a)

Adsorption of DNOC by clays is pH dependent. 
At pH 4.6 the
adsorption is > 99 % on illite and montmorillonite clays. 
No
adsorption at pH 7.3. 
Cultures of Arthrobacter simplex and
Pseudomonas sp. metabolize DNOC. 
A pseudomonad reduced DNOC by
progressive reduction and deamination. 
A. simplex degraded DNOC
by oxidative elimination of the two nitro groups. 
The two
pathways converge until ring cleavage and the fission products
were identical. 
Concentrations of 40 - 2000 ppm inhibit growth
of soil actinomycetes, bacteria and fungi. 
Only 40 ppm
inhibited Cytophaga sp. and Mucor sp.; > 400 ppm inhibits
Bacterium subtilis, B. mycoides, and Actinomyces sp. 
Effects on
numbers of soil fungi and bacteria is only transitory. 
At 25
ppm DNOC in soil inhibited nitrogen-fixing capacity for about 2
mos. -  
Soil treated with DNOC at 6 kg/ha showed increased
numbers of collembola and soil mites after 9 months after
initial toxicity. 
Though all population eventually increased,
folsoma were most susceptible to DNOC. 
Tullsergia were less
susceptible but hypogastrua thrived. 
The increase in population
is attributed to an increase on the bacteria,fungi, and nematode
population which is a food source for mites and springtails.

DNOC is harmless to carbid predators. -  
DNOC is toxic to
Lumbricus castaneus but harmless to Allolobophora caliginosa
(both earthworms). -  
The time for disapperance in soil is a few
weeks to two months. -  
Degradation takes place more quickly in
soils previously treated with DNOC than in other soils. 
Soil
with a previous DNOC treatment loses 90 % in 11 days. 
Soils
without a previous DNOC treatment loses 90 % in 15 days (Sax
1986).

LC50 0.00032 mg/l, 96 hr, Pteronarcys californica;
LD50 4.2 mg/l, 48 hr, Cloeon, dipterum nymph (Sax 1986).

NOEC, 0.32 mg/l, 21d, Hydra oligactis, specific growth rate.

NOEC, 1 mg/l, 40d, Lymnaea stagnalis, mortality.

NOEC, 0.032 mg/l, 40d, Lymnaea stagnalis, reproduction.

NOEC, 1 mg/l, 40d, Lymnaea stagnalis, hatching.

(Slooff & Canton 1983)

Toxicity threshold (cell multiplication inhibition test):
green algae (Scenedesmus quadricauda): 13 mg/l
protozoa (Entosiphon sulcatum): 5.4 mg/l
(Bringmann & Kühn 1980a)

0.001 ppm the proposed 1976 EPA water quality criteria set the
allowable level of DNOC at 0.001 mg/l to protect against fish
tainting (Sax 1986).