Parathion

Description

After exposure to parathion ethyl, one case of a bullous contact dermatitis was reported.

Chemical properties

Pure parathion is a pale yellow liquid with a faint odor of garlic, while technical parathion is a deep brown to yellow liquid. It is sparingly soluble in water, but soluble in alcohols, aromatic hydrocarbons, esters, ethers, n-hexane, dichloromethane, 2-propanol, toluene,and ketones. Parathion is one of the most acutely toxic pesticides and the US EPA has classifi ed parathion as an RUP, meaning it should only be handled by qualifi ed, trained, and certifi ed workers. In January 1992, the US EPA announced the cancellation of parathion for all uses on fruit, nut, and vegetable crops. Parathion was used for the control of pests of fruits, nuts, and vegetable crops. The only uses retained are those on alfalfa, barley, corn, cotton, sorghum, soybeans, sunfl owers, and wheat. Further, to reduce exposure of agricultural workers, parathion may only be applied to these crops by commercially certifi ed aerial applicators and treated crops may not be harvested by hand. Parathion is a broad spectrum, organophosphate pesticide used to control many insects and mites.

Chemical properties

Parathion is a clear liquid when fresh; pale yellow to dark brown liquid with a garlic-like odor. Commercial formulations use carrier solvents that may change the physical properties shown.

Physical properties

Pale yellow to dark brown liquid with a garlic-like odor. Robeck et al. (1965) reported odor threshold concentrations of 3 and 36 ppm for technical and pure grades, respectively.

The Uses of Parathion

Parathion is an organophosphate insecticide used on cotton, rice and fruit trees.

The Uses of Parathion

Insecticide; acaricide.

The Uses of Parathion

Parathion is used to control sucking and chewing insects, mites and soil insects in a very wide range of crops.

Definition

ChEBI: Parathion is an organic thiophosphate, a C-nitro compound and an organothiophosphate insecticide. It has a role as an EC 3.1.1.7 (acetylcholinesterase) inhibitor, an EC 3.1.1.8 (cholinesterase) inhibitor, an acaricide, an agrochemical, an avicide and a mouse metabolite. It is functionally related to a 4-nitrophenol.

General Description

Light-yellow liquid, Parathion turn solid at 6° C, a deadly poison by all routes. Organic phosphate insecticide, acts as an inhibitor of cholinesterase.

General Description

Parathion, O,O-diethyl O-p-nitrophenylphosphorothioate (Thiophos), is a yellow liquid that is freelysoluble in aromatic hydrocarbons, ethers, ketones, esters,and alcohols but practically insoluble in water, petroleumether, kerosene, and the usual spray oils. It is decomposedat a pH above 7.5. Parathion is used as an agricultural insecticide.It is a relatively weak inhibitor of cholinesterase;however, enzymes present in liver microsomes and insecttissues convert parathion (pI50＜4) to paraoxon, a more potentinhibitor of cholinesterase (pI50＞8).64 Parathion is alsometabolized by liver microsomes to yield p-nitrophenol anddiethylphosphate; the latter is inactive as an irreversiblecholinesterase inhibitor.

Air & Water Reactions

Parathion is slightly soluble in water.

Reactivity Profile

Pure parathion is a pale yellow liquid with a faint odour of garlic, while the technical parathion is a deep brown to yellow liquid. It is sparingly soluble in water but soluble in alcohols, aromatic hydrocarbons, esters, ethers, n-hexane, dichloromethane, 2-propanol, toluene, and ketones.
Violent reaction when PARATHION is used as solvent to dissolve endrin. When heated to decomposition Parathion emits very toxic fumes of oxides of sulfur, phosphorus and nitrogen [Lewis, 3rd ed., 1993, p. 984].

Health Hazard

Highly toxic, may be fatal if inhaled, swallowed or absorbed through skin. 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.

Health Hazard

Parathion is highly toxic by all routes of exposure. Parathion, like all organophosphate pesticides, inhibits acetylcholinesterase and alters cholinergic synaptic transmission at neuroeffector junctions (muscarinic effects), at skeletal myoneural junctions, in autonomic ganglia (nicotinic effects), and in the CNS. Exposures to parathion cause symptoms of poisoning that include, but are not limited to, abdominal cramps, vomiting, diarrhea, pinpoint pupils, blurred vision, excessive sweating, salivation and lacrimation, wheezing, excessive tracheobronchial secretions, agitation, seizures, bradycardia or tachycardia, muscle twitching and weakness, and urinary bladder and fecal incontinence. Seizures are much more common in children than in adults. Severe exposures cause loss of consciousness, coma, excessive bronchial secretions, respiratory depression, cardiac irregularity, eventually leading to death. Occupational workers and the general public with health disorders and abnormalities, such as cardiovascular, liver or kidney diseases, glaucoma, or CNS, are at an increased risk of parathion poisoning. Further, high environmental temperatures enhance the severity of parathion poisoning.

Health Hazard

Extremely toxic; acetylcholinesterase inhibitor; toxic symptoms include nausea,vomiting, diarrhea, excessive salivation,lacrimation, constriction of the pupils, bronchoconstriction, convulsions, coma, and respiratory failure; metabolizes to paraoxon; oralLD50 value (rats): 2 mg/kg, LD50 value, skin(rats): 6.8 mg/kg RCRA Waste Number P089.

Fire Hazard

Combustible material: may burn but does not ignite readily. Containers may explode when heated. Runoff may pollute waterways. Substance may be transported in a molten form.

Agricultural Uses

Insecticide, Acaricide: The U.S. EPA announced in November, 2000, the cancellation of ethyl parathion immediately on seed corn and the eventual phase out for its use in other pesticide products by the end of 2000. By the end of October, 2003, the U.S. EPA phased out its use to control insects and mites on alfalfa, barley, corn, canola, sorghum, soybeans, sunflowers and wheat. Also used to control nuisance birds. Not listed for use in EU countries. Not registered for use in the U.S. There are 25 global suppliers.

Trade name

(There are 921 active and canceled/transferred labels registered with the U.S. EPA) ACC 3422®; ALKRON®[C]; ALLERON®; AMERICAN CYANAMID 3422®; APHAMITE®; ARALO®; B 404®; BAY E-605®; BAYER E-605®; BLADAN®; BLADAN F®; COMPOUND 3422®; COROTHION®; CORTHION®; COR-THION®; DANTHION®; DREXEL PARATHION 8E®; E 605®; E 605 F®; ECATOX®; EKATIN WF & WF ULV®; EKATOX®; ETHLON®; ETILON®; FIGHTER®; FOLIDOL®; FOLIDOL E®; FOLIDOL E-605®; FOLIDOL E&E 605®; FOLIDOL OIL®; FOSFERMO®; FOSFERNO®; FOSFEX®; FOSFIVE®; FOSOVA®; FOSTERN®; FOSTOX®; GEARPHOS®; GENITHION®; IDA SEIS-TRES 6-3®; KALPHOS®; KOLODUST®[C]; KYPTHION®; LETHALAIRE G-54®; LIROTHION®; MURFOS®; MURPHOS®; NIRAN®[C]; NIUIF 100®; NITROSTIGMINE®; NOURITHION®; NOVAFOS-M®; OLEOFOS 20®; OLEOPARATHENE®; OLEOPARATHION®; ORTHOPHOS®; PAC®; PACOL®; PARA-KILL®[C]; PARAMAR®; PARA-TOX®[C]; PANTHION®; PARADUST®; PARAPHOS®; PARAWET®; PENNCAP E®; PESTOX PLUS®; PETHION®; PHOSKIL®; PLEOPARAPHENE®; RHODIASOL®; RHODIATOX®; RHODIATROX®; SEIS-TRES 6-3®; SELEPHOS®; SOPRATHION®; STATHION®; SULPHOS®; SUPER RODIATOX®; T-47®; THIOMEX®; THIOPHOS®; THIOPHOS® 3422; TIOFOS®; TOX 47®; TOXOL®; VAPOPHOS®; VITREX®; WOPROPHOS®

Contact allergens

One case was reported of a bullous contact dermatitis due to ethylparathion.

Safety Profile

A deadly poison by all routes. Human systemic effects by ingestion: general anesthetic; pulmonary effects; and hdney, ureter, bladder effects, true cholinesterase changes. Experimental teratogenic and reproductive effects. Questionable carcinogen with experimental carcinogenic and tumorigenic data. Human mutation data reported. A cholinesterase inhibitor. Parathon, like the other organic phosphorus poisons, acts as an irreversible inhibitor of the enzyme cholinesterase and thus allows the accumulation of large amounts of acetylcholine. When a critical level of cholinesterase depletion is reached, grave symptoms appear. Whether death is actually caused entirely by cholinesterase depletion or by the disturbance of a number of enzymes is not yet known. Recovery is apparently complete if a poisoned animal or human has time to re-form a critical amount of cholinesterase. The organism exposed remains susceptible to relatively low dosages of parathion untd the chohnesterase has regenerated. Small doses at frequent intervals are, therefore, more or less additive. There is no indication that, when recovery from a given exposure is entirely complete, the exposed organism is prejudiced in any way. Combustible when exposed to heat or flame. Violent reaction with endrin. Highly dangerous; shock can shatter the container, releasing the contents A broad spectrum insecticide in agricultural applications. When heated to decomposition it emits highly toxic fumes of NOx, POx, and SOx.

Potential Exposure

A severely hazardous pesticide formulation. Those exposed include those engaged in manufacture,formulation and application of this broad spectrum insecticide. This material has also been used as a chemical warfare agent.

Carcinogenicity

In an animal bioassay a dose-related increase in the incidence of adrenal cortical adenomas (with a few carcinomas at this site as well) has been observed in one strain of rats in both sexes. The significance of these lesions in aged rats in unclear. Other bioassays in mice and rats had sufficient limitations, such that the IARC deemed them inadequate for evaluation and concluded that there are insufficient data to evaluate the carcinogenicity of parathion for animals and no data for humans.

Environmental Fate

Biological. Initial hydrolysis products include diethyl-O-thiophosphoric acid, p-nitrophenol (Sethunathan, 1973, 1973a; Munnecke and Hsieh, 1976; Sethunathan et al., 1977; Verschueren, 1983) and the biodegradation products p-aminoparathion and p-aminophenol (Sethunathan, 1973; Laplanche et al., 1981; Nelson, 1982). Mixed bacterial cultures were capable of growing on technical parathion as the sole carbon and energy source (Munnecke and Hsieh, 1976). Three oxidative pathways were reported. The primary degradative pathway is initial hydrolysis to yield p-nitrophenol and diethylthiophosphoric acid. The secondary pathway involves the formation of paraoxon (diethyl p-nitrophenyl phosphate)
which subsequently undergoes hydrolysis to yield p-nitrophenol and diethylphosphoric acid. The third degradative pathway involved reduction of parathion under low oxygen conditions to yield p-amino-parathion followed by hydrolysis to p-aminophenol and die
A Flavobacterium sp. (ATCC 27551), isolated from rice paddy water, degraded parathion to p-nitrophenol. The microbial hydrolysis half-life of this reaction was <1 hour (Sethunathan and Yoshida, 1973; Forrest, 1981). Sharmila et al. (1989) isolated a Baci
In both soils and water, chemical- and biological-mediated reactions transform parathion to paraoxon (Alexander, 1981). Parathion was reported to biologically hydrolyze to p-nitrophenol in different soils under flooded conditions (Sudhakar-Barik and Sethunathan, 1978; Ferris and Lichtenstein, 1980)
p-Nitrophenol, paraoxon and three unidentified metabolites were identified in a model ecosystem containing algae, Daphnia magna, fish, mosquito and snails (Yu and Sanborn, 1975)

Metabolic pathway

The structure of parathion is similar to those of methyl parathion (the dimethylphosphoryl analogue) and fenitrothion which has a 3-methyl group on the phenyl ring: consequently the environmental fate and pathways for biotransformation are similar. As the first commercial organophosphorus insecticide, many studies have been conducted on its mechanisms of activation and degradation in a very wide range of organisms. The following is necessarily a selection of only some of the results which have been used to illustrate the principles of its metabolism. The principal metabolic routes of degradation in all media are via de-esterification to give O,O-diethyl phosphorothioate and 4-nitrophenol and by de-ethylation to desethylparathion (a less important route). Activation to the toxic anticholinesterase metabolite paraoxon is also a major metabolic route in soil, plants and animals. Paraoxon is also formed photochemically in the environment; however, it is relatively quickly detoxified in animals and plants by esterase and base-catalysed hydrolysis to 4-nitrophenol and diethyl phosphate. A further detoxification mechanism, which is mainly important in the soil, and possibly in plants and in ruminants, is reduction of the 4nitro group to yield aminoparathion. 4-Nitrophenol is conjugated in plants as the glucoside, in insects as the glucoside and/or sulfate ester and in mammals as the glucuronide and the sulfate ester.

Metabolism

The principal degradation routes of parathion in animals, plants, and soil are dearylation and dealkylation to give O,O-diethyl hydrogen phosphorothioate, p-nitrophenol, and desethylparathion. Oxidative desulfuration also occurs to form the active methabolite paraoxon, which is quickly detoxified by hydrolysis. DT₅₀ in soil was 65 d.

Shipping

UN3278 Organophosphorus compound, liquid, toxic, n.o.s., Hazard Class: 6.1; Labels: 6.1-Poisonous materials, Technical Name Required, Potential Inhalation Hazard (Special Provision 5).UN2783 Organophosphorus pesticides, solid, toxic, Hazard Class: 6.1; Labels: 6.1-Poisonous materials. UN3018 Organophosphorus pesticides, liquid, toxic, Hazard Class: 6.1; Labels: 6.1- Poisonous materials.

Degradation

Parathion is hydrolysed very slowly in acidic media and more rapidly in alkaline solution. The DT₅₀, values at pH 4, 7 and 8 (22 °C) were 272,260 and 130 days, respectively. The compound isomerises on heating (>130 °C) via a thiono-thiolo rearrangement to O,S-diethyl O-(4- nitrophenyl) phosphorothioate (iso-parathion) (2) (PM).
Many photochemical experiments on parathion have demonstrated paraoxon (3) as a major product. When parathion was irradiated at 350 nm in the presence of oxygen with various dicarbonyl photosensitisers, it was oxidatively desulfurated to paraoxon (3). The singlet oxygen generator Rose Bengal did not catalyse this reaction so it was implied that the reaction was mediated via peroxy radicals rather than singlet oxygen (Buckland and Davidson, 1987). A potentially important photochemical reaction with respect to phosphorothioates is the photo-oxidation of aerosols generated as a result of spraying since such reactions will generate the generally more toxic oxon compounds in a medium which will be susceptible to spray drift away from the site of application. This was demonstrated by Woodrow ef al. (1978), who showed that the half-life of photo-oxidation of an aerosol generated from an EC formulation of paratfuon to paraoxon (3) was as short as 2 minutes under midday summer sunlight conditions. Other reports have demonstrated that many other photolysis products, apart from paraoxon, are formed. In aqueous THF or ethanol the major product of photolysis when irradiated at wavelengths between 254 and 350 nm was O,O,S-triethyl phosphorothioate (4). Lesser mounts of O,O,O-triethyl phosphorothioate (5) were produced and triethyl phosphate (6) was also formed via the photolysis of paraoxon (3). Minor photoproducts were 4-nitrophenol (7) and ethanethiol(8) (Grunwell and Erickson, 1973). Conversely, Mansour et al. (1983) reported that the main products of photolysis were paraoxon (3) and 4-nitrophenol (7). Other photoproducts identified from parathion were the thiono-thiolo rearranged products,O,s-diethyl O-(4- nitrophenyl) (2) and O,O-diethyl S-(4-nitrophenyl) phosphorothioate (9) (Joiner and Baetcke, 1974).
When parathion was irradiated in methanolic solution with either a xenon arc lamp or a medium pressure mercury arc lamp filtered to remove light of <280 nm the nature of the photoproducts was similar. Six photoproducts were identified and the reasons for the apparent discrepancy in other reports with respect to the main products of photodegredation were shown to be the kinetics whereby certain products were formed and subsequently degraded through their own photolysis. Compounds formed in the initial stages of photolysis were paraoxon (3) and O,O-diethyl O-phenyl phosphorothioate (10) (formed via loss of the 4-nitro group). 4-Nitrophenol (7), desethylparathion (11) and O,O,Striethyl phosphorothioate (4) were produced in the later stages of photodegradation after considerable decomposition of parathion had already occurred. These products were thus likely to be the products of secondary processes (see Scheme 1). The sixth photolysis product,O,O-diethyl S-methyl phosphorothioate (not shown in Scheme l), was demonstrated to be formed via the participation of the methanol solvent. Analysis of the photolysis products was by GC-MS and ¹H NMR spectroscopy (Mok et al., 1987).
In an investigation of the effect of plant cuticle components on the nature of parathion photolysis products, Schwack et al. (1994) incorporated methyl 12-hydroxystearate and parathion into thin films and analysed the products of photodegradation by HPLC separation and ¹H and ¹³C NMR and UV and IR spectroscopy. Under these conditions the major products of photolysis were azoparathion (12), azoxyparathion (13) and 2-hydroxyazoparathion (14). These dimeric products were formed via the self-condensation of nitroso (15), hydroxylamino (16) and aminoparathion (17) (not isolated in this experiment) generated by the sequential photoreduction of the 4-nitro group. Subsequent photolytic hydrolysis of (14) yielded O,O-diethyl 2,4’-dihydroxyazobenene-4-phosphorothioate (18) and 2,4,4’-trihydroxyazobenzene (19) (Scheme 1).

Toxicity evaluation

The acute oral LD₅₀ for rats is about 2 mg/kg. Inhalation LC50 (4 h) for rats is 0.03 mg/L air. NOEL (2 yr) for rats is 2 mg/kg diet (0.1 mg/kg/d). ADI is 4 μg/kg b.w.

Incompatibilities

Incompatible with oxidizers (chlorates, nitrates, peroxides, permanganates, perchlorates, chlorine, bromine, fluorine, etc.); contact may cause fires or explosions. Keep away from alkaline materials, strong bases, strong acids, oxoacids, epoxides. Strong oxidizers may cause release of toxic phosphorus oxides. Organophosphates, in the presence of strong reducing agents such as hydrides, may form highly toxic and flammable phosphine gas. Keep away from alkaline materials. Attacks some plastics, rubbers, and coatings. Rapidly hydrolyzed by alkalis.

Waste Disposal

Consult with environmental regulatory agencies for guidance on acceptable disposal practices. Generators of waste containing this contaminant (≥100 kg/mo) must conform with EPA regulations governing storage, transportation, treatment, and waste disposal. 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. One manufacturer recommends the use of a detergent in a 5% trisodium phosphate solution for parathion disposal and cleanup problems. For parathion disposal in general, however, the recommended method is incineration (816°C, 0.5 second minimum for primary combustion; 1204°C, 1.0 second for secondary combustion) with adequate scrubbing and ash disposal facilities.