arsanilicacid

This chemical does not meet GHS hazard criteria for 2.2% (1 of 45) of reports.

H301 (97.8%): Toxic if swallowed [Danger Acute toxicity, oral]

H331 (97.8%): Toxic if inhaled [Danger Acute toxicity, inhalation]

H400 (88.9%): Very toxic to aquatic life [Warning Hazardous to the aquatic environment, acute hazard]

H410 (97.8%): Very toxic to aquatic life with long lasting effects [Warning Hazardous to the aquatic environment, long-term hazard]

P261, P264, P270, P271, P273, P301+P316, P304+P340, P316, P321, P330, P391, P403+P233, P405, and P501 (click each P-code to see the statement)

Aggregated GHS information provided per 45 reports by companies from 5 notifications to the ECHA C&L Inventory. Each notification may be associated with multiple companies.

Reported as not meeting GHS hazard criteria per 1 of 45 reports by companies.

There are 4 notifications provided by 44 of 45 reports by companies with hazard statement code(s).

Information may vary between notifications depending on impurities, additives, and other factors. The percentage value in parenthesis indicates the notified classification ratio from companies that provide hazard codes. Only hazard codes with percentage values above 10% are shown. For more detailed information, please visit ECHA C&L website.

0.5 [mg/m3], as As

Acute Oral: 0.005 mg/kg/day (L134)

Chronic Oral: 0.0003 mg/kg/day (L134)

Chronic Inhalation: 0.01 mg/m3 (L134)

A time limited tolerance is established for residues of the plant growth regulator arsanilic acid [(4-aminophenyl) arsonic acid], in or on the following food commodities in connection with the use of the pesticide under section 5 experimental use permit. The tolerance will expire on the date specified in the following: grapefruit, 2 ppm (not to exceed 0.7 ppm total arsenic), expiration/revocation date: 2/28/01.

Tolerances for total residues of combined arsenic (calculated as As) in food are established as follows: (a) In edible tissues & in eggs of chickens & turkeys: 0.5 ppm in uncooked muscle tissue; 2 ppm in uncooked edible by-products; & 0.5 ppm in eggs. (b) In edible tissues of swine: 2 ppm in uncooked liver & kidney; 0.5 ppm in uncooked muscle tissue & by-products other than liver & kidney. /Arsenic/

White solid; [Hawley] Powder; [MSDSonline]

Needles from water or alcohol

Crystalline powder

Practically odorless

Slightly sol in cold water, alcohol, acetic acid; sol in hot water, amyl alcohol, soln of alkali carbonates; moderately sol in concn mineral acids; insol in acetone; insol in benzene, chloroform, ether, moderately dil mineral acids

>32.6 [ug/mL] (The mean of the results at pH 7.4)

1.9571 @ 10 °C

1880000000.0 [mmHg]

WHEN HEATED TO DECOMP ... EMITS HIGHLY TOXIC FUMES OF /ARSENIC AND NITROGEN OXIDES/.

139.0 Ų [M-H]- [CCS Type: DT; Buffer gas: N2; Ionization: ESI-; Dataset: TOXCAST; Source Identifier: DTXSID8035138]

144.9 Ų [M+Na]+ [CCS Type: DT; Buffer gas: N2; Ionization: ESI+; Dataset: TOXCAST; Source Identifier: DTXSID8035138]

130.9 Ų [M+H]+ [CCS Type: DT; Buffer gas: N2; Ionization: ESI+; Dataset: TOXCAST; Source Identifier: DTXSID8035138]

133.2 Ų [M+H]+ [CCS Type: TW; Method: calibrated with polyalanine and drug standards]

Metals -> Arsenic Compounds, Organic

Carcinogens

...ON CONTACT WITH ACID OR ACID FUMES, IT EMITS HIGHLY TOXIC FUMES OF /ARSENIC & NITROGEN OXIDE/.

Arsenic and its metabolites disrupt ATP production through several mechanisms. At the level of the citric acid cycle, arsenic inhibits pyruvate dehydrogenase and by competing with phosphate it uncouples oxidative phosphorylation, thus inhibiting energy-linked reduction of NAD+, mitochondrial respiration, and ATP synthesis. Hydrogen peroxide production is also increased, which might form reactive oxygen species and oxidative stress. Arsenic's carcinogenicity is influenced by the arsenical binding of tubulin, which results in aneuploidy, polyploidy and mitotic arrests. The binding of other arsenic protein targets may also cause altered DNA repair enzyme activity, altered DNA methylation patterns and cell proliferation. (T1, A17)

3, not classifiable as to its carcinogenicity to humans. (L135)

Arsenic poisoning can lead to death from multi-system organ failure, probably from necrotic cell death, not apoptosis. Arsenic is also a known carcinogen, especially in skin, liver, bladder and lung cancers. (T1, L20)

Oral (L2) ; inhalation (L2); dermal (L2)

Exposure to lower levels of arsenic can cause nausea and vomiting, decreased production of red and white blood cells, abnormal heart rhythm, damage to blood vessels, and a sensation of “pins and needles” in hands and feet. Breathing high levels of inorganic arsenic can give you a sore throat or irritated lungs. Arsenic also affects the brain, causing neurological disturbances such as headaches, confusion, and drowsiness. (A1)

Occupational hepatotoxin - Secondary hepatotoxins: the potential for toxic effect in the occupational setting is based on cases of poisoning by human ingestion or animal experimentation.

LD50: 248 mg/kg (Intraperitoneal, Mouse) (T14)

LD50: 100 mg/kg (Intravenous, Mouse) (T14)

LD50 Rat oral >1000 mg/kg

LD50 Mouse ip 248 mg/kg

LD50 Mouse iv 100 mg/kg

Arsenic poisoning can be treated by chelation therapy, using chelating agents such as dimercaprol, EDTA or DMSA. Charcoal tablets may also be used for less severe cases. In addition, maintaining a diet high in sulfur helps eliminate arsenic from the body. (L20)

... The effects of cadmium (50 mg/kg diet) & lead (200 mg/kg) on the toxicity of arsenic administered to rats as sodium arsenate or arsanilic acid in the food (50 mg As/kg diet) /was examined/. The efficiency of food utilization was more reduced by the combination of arsenic & cadmium than by each metal alone. The combination of arsenic & cadmium also caused a greater decr in serum alkaline phosphatase levels than either metal alone. Additive effects of arsenic & lead in coproporphyrin excretion were also noted. Increased uroporphyrin excretion in rats was reported ..., when lead cadmium & arsenic were combined compared with excretion levels following exposure to arsenic alone.

ARSANILIC ACID...CONSUMPTION DOES NOT GIVE RISE TO POISONING...IN MAN...

SIMILAR TO OTHER /ANTISYPHILITIC/ DERIVATIVES OF ARSANILIC ACID, /ACETARSOL/... CAUSED OPTIC NEURITIS & OPTIC ATROPHY...GREATEST DANGER...IV INJECTION... VISION FIELDS CONTRACTED & VISION...POOR IN DIM ILLUMINATION. IN ONE...CASE, RETROLOBULAR NEURITIS WITH CENTRAL SCOTOMA FOR COLORS...AFTER 20 DAYS TREATMENT... /ACETARSOL/

HIGHLY TOXIC.

Complaints of keratosis were roughly two-fold higher than unexposed controls in female packaging workers exposed to arsanilic acid at an avg concn of 0.05 mg As/m3 and in male manufacturing workers exposed to an avg concn of 0.13 mg As/m3 in a chemical factory ... .

ARSANILIC ACID FED TO PIGS IS STORED IN TISSUES IN FORM THAT IS METABOLICALLY INERT, & ITS CONSUMPTION DOES NOT GIVE RISE TO POISONING IN LAB ANIMALS...

TURKEYS & SWINE ARE MORE SUSCEPTIBLE TO TOXIC EFFECTS THAN CHICKEN. CAUSES SLIGHT INCR IN BLOOD CLOTTING TIME IN POULTRY & SWINE. THERAPEUTIC LEVEL GIVEN TO SWINE FOR PERIODS LONGER THAN RECOMMENDED HAS CAUSED BLINDNESS.

ARSANILIC ACID FED TO PIGS FOR WK @ 15 TIMES RECOMMENDED LEVEL INDUCED TOXIC SYMPTOMS...BUT EVEN 8000 PPM WAS NOT FATAL...TOXICITY OF ARSANILIC ACID INCR IF WATER INTAKE RESTRICTED. INCORPORATED INTO RATIONS @ RATE OF 2000 OR 4000 PPM IT CAUSED CONVULSIONS IN LAMBS.

...CHRONIC POISONING...PIGS...WITH ARSANILIC ACID SHOWED PROGRESSIVE BLINDNESS, ATAXIA & PARESIS... POST MORTEM APPEARANCES...IN PIGS POISONED WITH ARSANILIC ACID THE URINARY BLADDER MAY BE GROSSLY DISTENDED.

For more Non-Human Toxicity Excerpts (Complete) data for ARSANILIC ACID (6 total), please visit the HSDB record page.