4685-14-7

ChEBI: An organic cation that consists of 4,4'-bipyridine bearing two N-methyl substituents loctated at the 1and 1'-positions.

Those engaged in manufacture, formulation and application of this herbicide. Classified for restricted use: limited to use by a certified applicator, or those under applicator’s direct supervision.

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, or bentonite clay in water, or activated charcoal in water; and induce vomiting. Do not make an unconscious person vomit. Medical observation is recommended for 24
48 hours after breathing overexposure, as pulmonary edema may be delayed. As first aid for pulmonary edema, a doctor or authorized paramedic may consider administering a drug or other inhalation therapy. Obtain authorization and/or further instructions from the local hospital for performance of other invasive procedures. Rush to a health care facility.

UN2781 Bipyridilium pesticide, solid, toxic, Hazard Class: 6.1; Labels: 6.1-Poisonous materials.

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 (hydrolysis), alkylarylsulfonate wetting agents. Corrosive to metals. Decomposes in presence of ultraviolet (UV) light. Decomposes in heat (see physical properties, above) and in the presence of UV light, producing nitrogen oxides, hydrogen chloride.

Paraquat is a yellow solid with a faint, ammonia-like odor.

Paraquat is rapidly inactivated in soil. It is also inactivated by anionic surfactants. Therefore an effective and environmentally safe disposal method would be to mix the product with ordinary household detergent and bury the mixture in clay soil. 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. 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.

Herbicide

It can cause contact and phototoxic contact dermatitis, acne, and leucoderma, mainly in agrieultural workers.

Paraquat is synthesized by the direct quaternization of 4,4 -bipyridyl with chloromethane under pressure (1,9). Diquat is synthesized by reaction of 2,2 -bipridyl with di-n-propyl amine.

Paraquat is produced in several countries by coupling pyridine in the presence of sodium in anhydrous ammonia and quaternizing the resulting 4,4-bipyridyl with methyl chloride. The only impurity permitted is the 4,40-bipyridyl at a maximum level of 0.25% of the paraquat content. It is formulated for commercial use in various concentrations and mixtures. In the United States, paraquat is sold in watersoluble concentrates at 1.5–2.5 lb/gal.

Paraquat salts show moderate to high acutetoxicity among species, the oral LD50 values ranging between 25 and 300 mg/kg.The LD50 values in dogs, cats, guinea pigs,and rats are 25, 35, 30, and 100 mg/kg,respectively, for the sulfate salts. The toxicsymptoms from ingestion and inhalationof dusts include headache, nausea, vomiting, diarrhea, ulceration, dyspnea, and lunginjury. Single exposure to paraquat aerosols 3–5 mm in diameter at 1 mg/m³ concentration for 6 hours caused death to rats (ACGIH 1986). Inhalation of nonrespirable size dustscaused intense irritation and nose bleeding.Repeated exposures can lead to severe pulmonary edema and fibrosis. The dusts are anirritant to the respiratory tract.
Dey and associates (1990) investigatedparaquat pharmacokinetics in rats, using asubcutaneous toxic low dose (72 mmol/kg)of [¹⁴CH3] paraquat, which would producelung disease but no renal damage. Paraquatwas rapidly absorbed. Peak blood concentrations were 58 nmol/mL at 20 minutes,while its peak concentrations in the lungand kidney were 65 and 359 nmol/g, respectively, at 40 minutes. About 85% of dosewas eliminated in the urine by 7 days. Of theremaining radioactivity, 79% remained in thebody and 21% remained in the lung, causing progressive lung disease. Excretion ofthe retained amount was slow and prolonged.Chui and coworkers (1988) investigated thetoxicokinetics of paraquat and the effects ofdifferent routes of administration. A singledose of 11.4 mg/kg of [¹⁴CH3 ]paraquat wasadministered in rats by intravenous, intragastric, dermal, and pulmonary (exposure byaqueous or liquid aerosols) routes. The majorexcretion routes were urine and feces.
The radioactivity absorbed into thesystemic circulation of the rat was about27.5, 23.8, 8.5, and 1.5 nmol for inhalationthrough a tracheal cannula, nose-only expo-sure, intragastric injection, and dermalabsorption, respectively. The bulk of theherbicide administered by the inhalation anddermal routes remained at the sites of theadministration.
In humans, cardiovascular collapse result-ing from acute paraquat poisoning is asso-ciated with the distribution phase; the lateoccurrence of death-related pulmonary fibro-sis is associated with the elimination phase(Houze et al. 1990). Toxicokinetics studiesconducted by these investigators in acutehuman poisoning cases indicated a concen-tration of paraquat in blood that had a mean distribution half-life of 5 hours and a meaneliminationhalf-lifeof84 hours,respectively.It was excreted in the urine. It was retainedin the muscle for several weeks after poi-soning. Electron microscopy studies (TEMand SEM) on the lungs obtained from adog after 7 days of intravenous administra-tion of paraquat (12 mg/kg) indicate detach-ment of alveolar epithelial cells and alve-olar macrophage, which plays a significantrole in paraquat-induced pulmonary fibrosis(Hampson and Pond 1988). Administrationof paraquat to adult rat pulmonary alveolarmacrophages in primary culture caused celldeaththatwasdependentonthedoseandtime.The cell death was potentiated by hyperoxia(95% O) and extracellular production of anactive oxygen species, the superoxide anionradical (Wong and Stevens 1985). Althoughdiquat can enter the cells to a greater extent,than can paraquat, the latter is about twice aspotent as diquat (Wong and Stevens 1986).
Paraquat is a urinary metabolite of 4,48-bipyridyl when the latter is administeredintraperitoneally to guinea pigs. Godin andCrooks (1989) detected 2.9% N-methyl-4,48-bipyridinium ion in the urine of animalstreated with 4,48-bipyridyl, thus indicat-ing the formation of such toxic metabolitesthrough the N-methylation pathway.
Certain substances have been reported topotentiate the toxicity of paraquat. Theseinclude transition metal ions such as copper(Kohen and Chevion 1985) and ethanol (Kuoand Nanikawa 1990). Blood paraquat lev-els showed significant elevation in rabbits,and the mortality rates increased when theanimals were orally administered paraquatcombined with ethanol in amounts of 2.0and 3.8 g/kg. Continuous breathing of highoxygen concentrations 12–24 hours afteradministration of paraquat caused severe andextensive pulmonary lesions and interstitialfibrosis (Selman et al. 1985). On the otherhand, a reverse sequence of treatment—inhalation of high oxygen concentrations followed by paraquat administration—causedno mortality and pulmonary lesions.
The effect of light on toxicity of paraquathas been reported (Barabas et al. 1986). A72-hour exposure to illumination increasedthe lethality of paraquat in mice. Changesin the activity of the enzymes, catalase, superoxide dismutase, and glutathione peroxidase,were also noted after exposure to light.
Antidote actions of a few substancesagainst paraquat toxicity have been reported.These include several sodium sugar sulfates,including dextran sulfate, cellulose sulfate,chondroitin sulfate, sucrose sulfate, and glu-cose sulfate (Tsuchiya et al. 1989; Ukai et al.1987). Sugar sulfates 2000 mg/kg, givenorally immediately after paraquat ingestion (200 mg/kg), protected mice againstthe acute toxicity of the herbicide. Thiols,cystein, d-penicillamine, and GSH were found to protect mice against a LD50 dose of paraquat(Szabo et al. 1986). The protecting actionof these compounds decreased in the ordernoted above.

Herbicide, Defoliant, Desiccant: Paraquat is a quaternary nitrogen herbicide widely used for broadleaf weed control. It is a quick-acting, nonselective compound, that destroys green plant tissue on contact and by translocation within the plant. It has been employed for killing marijuana in the U.S. and in Mexico. It is also used as a crop desiccant and defoliant, and as an aquatic herbicide. It is used in many formulations with other herbicides, e. g., simazine and diquat. Paraquat dichloride is registered for the control of weeds and grasses in agricultural and non-agricultural areas. It is used as a preplant or pre-emergence herbicide on vegetables, grains, cotton, grasses, sugarcane, peanuts, potatoes, and on areas for tree plantation establishment. Paraquat is applied as a directed spray post-emergence herbicide around fruit crops, vegetables, trees, vines, grains, soybeans, and sugarcane. It is used for dormant season applications on clover and other legumes, and for chemical fallow. It is also used as a desiccant or harvest aid on cotton, dry beans, soybeans, potatoes, sunflowers, sugarcane and as a post-harvest desiccant on tomatoes. It is applied to pine trees to induce resin soaking. Paraquat dichloride is also used on non-crop areas such as public airports, electric transformer stations and around commercial buildings to control weeds. Not approved for use in EU countries. A U.S. EPA restricted Use Pesticide (RUP).

HERBICIDE®[C]; CRISQUAT®; CYCLONE®; DEXTRONE®; DEXTRONE-X®; ESGRAM®; GAMIXEL®; GOLDQUAT 276®; GRAMOXONE®; GRAMOXONE D®; GRAMOXONE DICHLORIDE®; GRAMOXONE S®; GRAMOXONE W®; HERBIKILL®; HERBOXONE®; OK 622®; ORTHO PARAQUAT CL®[C]; PARA-COL®; PARAMINE®; PARAQUAT CL®[C]; PARAQUAT DICHLORIDE BIPYRIDYLNIUM HERBICIDE®; PATHCLEAR®; PILLARQUAT®; PILLARXONE®; PP148®; PRELUDE®[C]; STARFIRE®; SUREFIRE®; SWEEP®; TERRAKLENE®; TOTACOL®; TOXER TOTAL®; UNIQUAT®; WEEDOL®

Broad-spectrum, non-residual activity with contact and some desiccant action. Photosystem I (electron transport) inhibitor.

Several carcinogenicity studies have been conducted on paraquat by the oral route. In a 2-year feeding study at doses as high as 75 mg/kg in mice, and a drinking water study at doses as high as 2.6 mg/L of water in rats, no evidence of tumorigenicity was seen. Similar negative results were reported for diquat in a 2-year feeding study (Hayes, 1991) in rats at dose levels up to 720 mg/kg and in a 2-year drinking water study in mice at doses of 2–4 mg/kg.

Because paraquat and diquat are positively charged ions, they are very quickly and tightly bound to negatively charged clay particles in the soil, rendering them totally inactive (1). Thus, these herbicides have no soil activity.
Plants do not actively metabolize either paraquat or diquat (31); however, substantial photodegradation does occur on the leaf surface. Isonicotinic acid and methylamine hydrochloride are the decomposition products most often noted from paraquat (1). With diquat, the decomposition products included the pyrazinium salt, picolinamide, and picolinic acid (1). Photodegradation of diquat was greater than that of paraquat at equal irradiances (1–3).

Paraquat is most active in rapidly respiring tissue and in the presence of oxygen, it is not surprising that most of the damage in mammalian systems is associated with lung tissue. Symptoms such as fibrosis and hemorrhage of the lungs are often detected after paraquat poisoning.

Herbicide