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| | 1,1'-ジメチル-4,4'-ビピリジニウム 製品概要 |
| 化学名: | 1,1'-ジメチル-4,4'-ビピリジニウム | | 英語化学名: | Paraquat | | 别名: | Paraquat, inhalable;Paraquat, respirable;Paraquat aqueous solution;N，N′-dimethyl-4，4′-dipyridyl;1，1'-dimethyl-4,4'-bipyridylium ion;Pectone;Pillarzone;20% PARAQUAT AQUA | | CAS番号: | 4685-14-7 | | 分子式: | C12H14N2+2 | | 分子量: | 186.25 | | EINECS: | 225-141-7 | | カテゴリ情報: | Pesticide & intermediate | | Mol File: | 4685-14-7.mol |  |
| | 1,1'-ジメチル-4,4'-ビピリジニウム 物理性質 |
| 融点 | 300 °C (decomp) | | 沸点 | 310.75°C (rough estimate) | | 比重(密度) | 0.9748 (rough estimate) | | 屈折率 | 1.5600 (estimate) | | 外見 | Yellow solid | | 色 | Off-white Powder | | EPAの化学物質情報 | Paraquat (4685-14-7) |
| | 1,1'-ジメチル-4,4'-ビピリジニウム Usage And Synthesis |
| 農薬用途 | 除草剤 | | 説明 | Paraquat is a quaternary ammonium compound with
herbicide properties, as diquat. It is contained in
Cekuquat or Dipril. | | 化学的特性 | Paraquat is a yellow solid with a faint,
ammonia-like odor. | | 使用 | It can cause contact and phototoxic
contact dermatitis, acne, and leucoderma, mainly
in agrieultural workers. | | 使用 | Herbicide | | 製造方法 | 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. | | 調製方法 | 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. | | 定義 | ChEBI: An organic cation that consists of 4,4'-bipyridine bearing two N-methyl substituents loctated at the 1- and 1'-positions. | | 健康ハザード | 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. | | 农业用途 | 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). | | 製品名 | 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® | | 接触アレルゲン | Paraquat is a quaternary ammonium compound with herbicide
properties, as diquat. It is contained in Cekuquat? or
Dipril?. It can cause contact and phototoxic contact dermatitis,
acne, and leukoderma mainly in agricultural workers. | | 安全性プロファイル | Poison by ingestion and intraperitoneal routes. Mutation data reported. Human systemic effects: changes in structure or function of esophagus, darrhea, edema, fibrosis of lung, fibrosis, focal (pneumoconiosis), hemorrhage, jaundice, renal damage, renal function tests depressed, respiratory depression, ulceration or bleedmg from stomach, vomiting. Death from anoxia may result. When heated to decomposition it emits toxic fumes of NOx. See also PARAQUAT DICHLOFUDE | | 職業ばく露 | 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. | | 発がん性 | 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. | | 代謝 | 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). | | 輸送方法 | UN2781 Bipyridilium pesticide, solid, toxic,
Hazard Class: 6.1; Labels: 6.1-Poisonous materials. | | Toxicity evaluation | 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. | | 不和合性 | 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. | | 廃棄物の処理 | 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. |
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