Heptenophos

250.62

250.62

245-737-0

DTXSID5042037

Light brown liquid... .

2919900090

44.8

2.32

1.28 g/cm³ @ Temp: 20 °C

<25 °C

64 °C @ Press: 0.075 Torr

2 °C

1.518

2200 mg l -1 (20 °C)

APPROX 4°C

6.5 x 10 -2 Pa (15 °C)

LD50 orally in rats: 96-117 mg/kg (Hewson)

...Odor typical of a phosphate ester.

144.04 Ų [M+H]+ [CCS Type: TW]

III

6.1(b)

3018

3

25-50/53-52/53-36-20/21/22-11

23-28-37-45-60-61-36/37-26

TB8545000

T,N,Xn,F

Hydrolysed in acidic and alkaline media.

P260-P273-P284-P301 + P310 + P330-P304 + P340 + P310-P403 + P233

H301-H312-H330-H410

|Danger|H301: Toxic if swallowed [Danger Acute toxicity, oral]|P264, P270, P273, P301+P310, P321, P330, P391, P405, and P501|H301 (100%): Toxic if swallowed [Danger Acute toxicity, oral]|P260, P264, P270, P271, P273, P280, P284, P301+P310, P302+P352, P304+P340, P310, P312, P320, P321, P322, P330, P363, P391, P403+P233, P405, and P501|Aggregated GHS information provided by 41 companies from 2 notifications to the ECHA C&L Inventory. Each notification may be associated with multiple companies.

If material on fire or involved in fire: Do not extinguish fire unless flow can be stopped. Use water in flooding quantities as fog. Solid streams of water may be ineffective. Cool all affected containers with flooding quantities of water. Apply water from as far a distance as possible. Use "alcohol" foam, dry chemical or carbon dioxide. /Organophosphorus pesticides, liquid, flammable, toxic; Organophosphorus pesticides, liquid, toxic/|If material on fire or involved in fire: Use water in flooding quantities as fog. Extinguish fire using agent suitable for type of surrounding fire. (Material itself does not burn or burns with difficulty.) /Organophosphorus pesticides, solid, toxic/

Environmental considerations: Air spill: Apply water spray or mist to knock down vapors. /Organophosphorus pesticides, liquid, flammable, toxic; Organophosphorus pesticides, liquid, toxic; Organophosphorus pesticides, solid, toxic/|Environmental considerations: Water spill: Use natural barriers or oil spill control booms to limit spill travel. Remove trapped material with suction hoses. /Organophosphorus pesticides, liquid, flammable, toxic; Organophosphorus pesticides, liquid, toxic; Organophosphorus pesticides, solid, toxic/|Environmental considerations: Land spill: Dig a pit, pond, lagoon, holding area to contain liquid or solid material. /SRP: If time permits, pits, ponds, lagoons, soak holes, or holding areas should be sealed with an impermeable flexible membrane liner./ Dike surface flow using soil, sand bags, foamed polyurethane, or foamed concrete. Absorb bulk liquid with fly ash, cement powder, or commercial sorbents. /Organophosphorus pesticides, liquid, flammable, toxic; Organophosphorus pesticides, liquid, toxic; Organophosphorus pesticides, solid, toxic/

If material not on fire and not involved in fire: Keep sparks, flames, and other sources of ignition away. Keep material out of water sources and sewers. /Organophosphorus pesticides, solid, toxic/|If material not on fire and not involved in fire: Keep sparks, flames, and other sources of ignition away. Keep material out of water sources and sewers. Build dikes to contain flow as necessary. Attempt to stop leak if without undue personnel hazard. Use water spray to knock-down vapors. /Organophosphorus pesticides, liquid, toxic/|If material not on fire and not involved in fire: Keep sparks, flames, and other sources of ignition away. Keep material out of water sources and sewers. Build dikes to contain flow as necessary. Use water spray to knock-down vapors. /Organophosphorus pesticides, liquid, flammable, toxic/|Personnel protection: Avoid breathing dusts, and fumes from burning material. Keep upwind. Avoid bodily contact with the material. Do not handle broken packages unless wearing appropriate personal protective equipment. Wash away any material which may have contacted the body with copious amounts of water or soap and water. /Organophosphorus pesticides, solid, toxic/|For more Preventive Measures (Complete) data for HEPTENOPHOS (8 total), please visit the HSDB record page.

/GUIDE 131: FLAMMABLE LIQUIDS-TOXIC/ Health: TOXIC; may be fatal if inhaled, ingested or absorbed through skin. Inhalation or contact with some of these materials will irritate or burn skin and eyes. Fire will produce irritating, corrosive and/or toxic gases. Vapors may cause dizziness or suffocation. Runoff from fire control or dilution water may cause pollution. /Organophosphorus pesticide, liquid, flammable, poisonous; Organophosphorus pesticide, liquid, flammable, toxic; Organophosphorus pesticide, liquid, poisonous, flammable; Organophosphorus pesticide, liquid, toxic, flammable/|/GUIDE 131: FLAMMABLE LIQUIDS-TOXIC/ Fire or Explosion: HIGHLY FLAMMABLE: Will be easily ignited by heat, sparks or flames. Vapors may form explosive mixtures with air. Vapors may travel to source of ignition and flash back. Most vapors are heavier than air. They will spread along ground and collect in low or confined areas (sewers, basements, tanks). Vapor explosion and poison hazard indoors, outdoors or in sewers. Those substances designated with a "P" may polymerize explosively when heated or involved in a fire. Runoff to sewer may create fire or explosion hazard. Containers may explode when heated. Many liquids are lighter than water. /Organophosphorus pesticide, liquid, flammable, poisonous; Organophosphorus pesticide, liquid, flammable, toxic; Organophosphorus pesticide, liquid, poisonous, flammable; Organophosphorus pesticide, liquid, toxic, flammable/|/GUIDE 131: FLAMMABLE LIQUIDS-TOXIC/ Public Safety: CALL Emergency Response Telephone Number ... . As an immediate precautionary measure, isolate spill or leak area for at least 50 meters (150 feet) in all directions. Keep unauthorized personnel away. Stay upwind. Keep out of low areas. Ventilate closed spaces before entering. /Organophosphorus pesticide, liquid, flammable, poisonous; Organophosphorus pesticide, liquid, flammable, toxic; Organophosphorus pesticide, liquid, poisonous, flammable; Organophosphorus pesticide, liquid, toxic, flammable/|/GUIDE 131: FLAMMABLE LIQUIDS-TOXIC/ Protective Clothing: Wear positive pressure self-contained breathing apparatus (SCBA). Wear chemical protective clothing that is specifically recommended by the manufacturer. It may provide little or no thermal protection. Structural firefighters' protective clothing provides limited protection in fire situations ONLY; it is not effective in spill situations where direct contact with the substance is possible. /Organophosphorus pesticide, liquid, flammable, poisonous; Organophosphorus pesticide, liquid, flammable, toxic; Organophosphorus pesticide, liquid, poisonous, flammable; Organophosphorus pesticide, liquid, toxic, flammable/|For more DOT Emergency Guidelines (Complete) data for HEPTENOPHOS (16 total), please visit the HSDB record page.

No person may /transport,/ offer or accept a hazardous material for transportation in commerce unless that person is registered in conformance ... and the hazardous material is properly classed, described, packaged, marked, labeled, and in condition for shipment as required or authorized by ... /the hazardous materials regulations (49 CFR 171-177)./|The International Air Transport Association (IATA) Dangerous Goods Regulations are published by the IATA Dangerous Goods Board pursuant to IATA Resolutions 618 and 619 and constitute a manual of industry carrier regulations to be followed by all IATA Member airlines when transporting hazardous materials.|The International Maritime Dangerous Goods Code lays down basic principles for transporting hazardous chemicals. Detailed recommendations for individual substances and a number of recommendations for good practice are included in the classes dealing with such substances. A general index of technical names has also been compiled. This index should always be consulted when attempting to locate the appropriate procedures to be used when shipping any substance or article.|Marine pollutant

Because different classes of enzymes may be inhibited, the effects of organophosphorus pesticide poisoning may be complex and potentially at least could involve interactions with drugs as well as with other pesticides or chemicals. Potentiation may also involve solvents or other components of formulated pesticides. Certain drugs such a phenothiazines, antihistamines, CNS depressants, barbiturates, xanthines (theophylline), aminoglycosides and parasympathomimetic agents are to be avoided because of increased toxicity. /Organophosphorus pesticides/

LD50 Rat oral 96-117 mg/kg|LD50 Rat dermal >2000 mg/kg|LD50 Mouse dermal 2 g/kg|LD50 Dog oral 500-1,000 mg/kg bw|LC50 Rat inhalation 0.95 mg/L air/4 hr

/PLANTS/ Non-phytotoxic when used as directed, except to some varieties of apple, sweet cherry, and rose.

Heptenophos' production may have resulted in its release to the environment through various waste streams; its use as an insecticide(1) will have resulted in its direct release to the environment(SRC).

TERRESTRIAL FATE: Based on a classification scheme(1), an estimated Koc value of 508(SRC), determined from a structure estimation method(2), indicates that heptenophos is expected to have low mobility in soil(SRC). Volatilization of heptenophos from moist soil surfaces is not expected to be an important fate process(SRC) given a Henry's Law constant of 1.69X10-7 atm-cu m/mole(SRC), derived from its vapor pressure, 1.28X10-3 mm Hg(3), and water solubility, 2,500 mg/l(4). Heptenophos is not expected to volatilize from dry soil surfaces(SRC) based upon a vapor pressure of 1.28X10-3 mm Hg(3). Heptenophos is rapidly degraded in soil with a field half-life of 1.4 days, depending on temperature and soil type(3). In active fresh field sandy loam soil and autoclaved soil, 22 % and 0%, respectively, of the applied (6-14C)-heptenophos was released as CO2 after 240 hours(5). Field and laboratory research indicate heptenophos has short persistence in soil; half-lives ranged from 1 to 25 hr(5).|AQUATIC FATE: Based on a classification scheme(1), an estimated Koc value of 508(SRC), determined from a structure estimation method(2), indicates that heptenophos is expected to adsorb to suspended solids and sediment(SRC). Volatilization from water surfaces is not expected(3) based upon a Henry's Law constant of 1.69X10-7 atm-cu m/mole(SRC), derived from its vapor pressure, 1.28X10-3 mm Hg(4), and water solubility, 2,500 mg/l(5). According to a classification scheme(6), an estimated BCF of 2.0(SRC), from its log Kow of 2.32(4) and a regression-derived equation(7), suggests the potential for bioconcentration in aquatic organisms is low(SRC). Heptenophos is hydrolyzed in acidic and alkaline media(4). A range of 3-23 days was reported for half-lives for hydrolysis for heptenophos; however, no experimental details were provided(8). Degradation in the water phase of a water sediment system was 27-77 hrs(4).|ATMOSPHERIC FATE: According to a model of gas/particle partitioning of semivolatile organic compounds in the atmosphere(1), heptenophos, which has a vapor pressure of 1.28X10-3 mm Hg at 25 °C(2), is expected to exist solely as a vapor in the ambient atmosphere. Vapor-phase heptenophos is degraded in the atmosphere by reaction with photochemically-produced hydroxyl radicals(SRC); the half-life for this reaction in air is estimated to be 4.4 hours(SRC), calculated from its rate constant of 8.7X10-11 cu cm/molecule-sec at 25 °C(SRC) that was derived using a structure estimation method(3). Heptenophos may absorb light with wavelengths >290 nm and may be expected to be susceptible to direct photolysis by sunlight(SRC).

The rate constant for the vapor-phase reaction of heptenophos with photochemically-produced hydroxyl radicals has been estimated as 8.7X10-11 cu cm/molecule-sec at 25 °C(SRC) using a structure estimation method(1). This corresponds to an atmospheric half-life of about 4.4 hours at an atmospheric concentration of 5X10+5 hydroxyl radicals per cu cm(1). Heptenophos is hydrolyzed in acidic and alkaline media(2). A range of 3-23 days was reported for half-lives for hydrolysis for heptenophos; however, no experimental details were provided(3). Heptenophos may absorb light with wavelengths >290 nm and may be expected to be susceptible to direct photolysis by sunlight(SRC).

An estimated BCF of 2.0 was calculated for heptenophos(SRC), using a log Kow of 2.32(1) and a regression-derived equation(2). According to a classification scheme(3), this BCF suggests the potential for bioconcentration in aquatic organisms is low.

Using a structure estimation method based on molecular connectivity indices(1), the Koc for heptenophos can be estimated to be 508(SRC). According to a classification scheme(2), this estimated Koc value suggests that heptenophos is expected to have low mobility in soil.

The Henry's Law constant for heptenophos is 1.69X10-7 atm-cu m/mole(SRC) derived from its vapor pressure, 1.28X10-3 mm Hg(1), and water solubility, 2,500 mg/l(2). This Henry's Law constant indicates that heptenophos is expected to be essentially nonvolatile from water surfaces(3). This Henry's Law constant indicates that volatilization from moist soil surfaces is not expected(SRC). Heptenophos is not expected to volatilize from dry soil surfaces(SRC) based upon its vapor pressure(1).

Heptenophos was not found in the Danish National Pesticide Monitoring Program 1995-1996 in selected food commodities(1). Heptenophos was detected in 1.2% of parsley samples at maximum and mean concentrations of 0.14 and 0.006 ppm, respectively, in a monitoring program of fresh vegetables, fruits, and other selected food items in Belgium 1991-1993(2).

Many of the organophosphorus insecticides are excreted in the milk ... /Organophosphorus insecticides/

Occupational exposure to heptenophos may have occurred through inhalation and dermal contact with this compound at workplaces where heptenophos was produced or used. Occupational exposure and general population exposure should be low or non-existent since heptenophos is no longer produced or used. (SRC)|Secondary exposure of children through contact with their parents' contaminated clothing can also occur. /Organophosphorus pesticides/

(Vet) Also effective against ectoparasites (fleas, lice, mites and ticks) of cattle, dogs, pigs, sheep and pets.

Pesticides designed to control insects that are harmful to man. The insects may be directly harmful, as those acting as disease vectors, or indirectly harmful, as destroyers of crops, food products, or textile fabrics. (See all compounds classified as Insecticides.)

In rats, following oral administration, 90% is excreted in the urine and 6% in the feces in metabolised form within 6 days.|Most organophosphorus pesticides are not ionized and are very lipophilic. Thus, inhaled or swallowed material will be easily taken up. /Organophosphorus Pesticides/|In rats, the /gastrointestinal/ uptake of most of the organophosphorus pesticides reviewed seems to be rapid and efficient under test conditions usually involving a dose well below the LD50. /Organophosphorus Pesticides/

Metabolism occurs principally by oxidation, hydrolysis by esterases, and by transfer of portions of the molecule to glutathione. Oxidation of organophosphorus insecticides may result in more or less toxic products. The glutathione transferase reactions produce products, that are, in most cases, of low toxicity. Hydrolytic and transferase reactions affect both thioates and their oxons. /Organophosphorus Pesticides/|It is well-known that active metabolites of most organophosphorus insecticides react covalently to some extent with tissue esterases other than AChE. Since few of these esterases appear vital to health, the binding reaction may be considered a detoxification process. Although the catalytic activity of these esterases is high, the actual quantity of such sites is comparatively small. Crude measurements using 32 P-labelled diisopropyl phosphorofluoridate (an agent reacting with most organophosphorus-sensitive esterases) suggest that 100-150 g bind/kg bw of an adult hen injected with about the LD50 dose. Binding was principally in liver and muscle. The quantity bound would not be expected to be much greater whatever the LD50 of an administered organophosphorus insecticide. Thus, it is a significant proportion of the total dose only for a very toxic compound such as paraoxon but not for compounds with much higher LD50s. However, the number of binding sites may, in some cases, be very significant compared with the quantity of circulating anticholinesterase oxon that has avoided other metabolic disposal processes. Molecules of oxon bound to these non-vital sites are prevented from attacking the vital sites such as AChE or NTE. Binding sites can therefore be considered an important second line of defence against intoxication. /Organophosphorus Pesticides/

Organophosphorus insecticides exert their acute effects in both insects and mammals by inhibiting acetylcholinesterase (AChE) in the nervous system with subsequent accumulation of toxic levels of acetylcholine (ACh), which is a neurotransmitter. In many cases, the organophosphorylated enzyme is fairly stable, so that recovery from intoxication may be slow. /Organophosphorus Pesticides/|The first essential step in the initiation of the delayed neuropathic effect of an organophosphate is phosphorylation of a target protein in the nervous system. The protein has esteratic enzyme activity. The phosphorylation, which was originally studied radiochemically, can be monitored conveniently as progressive inhibition of the activity of this enzyme, which is now referred to as Neuropathy Target Esterase (NTE or Neurotoxic Esterase)... . The second, and equally essential, step is the transformation of the phosphorylated NTE to a modified form: one of the remaining ester bonds of the inhibitor molecule attached to the NTE active site undergoes a biochemical cleavage leaving an ionized acidic residue bound to the protein: this residue is negatively charged and the reaction is referred to as "aging". Both inhibition and aging of inhibited NTE are essential to initiate neuropathy, but the role of the negative charge in the initiation of axonal degeneration is not known. The process of "aging" of inhibited NTE has some analogy with the better-known "aging" of inhibited AChE. However, the analogy does not last above the level of enzyme inhibition. Acute toxicity arises directly from the loss of catalytic activity of AChE, leading to accumulation of excess physiological substrate. Mere loss of catalytic activity of NTE (without aging) does not initiate neuropathy. There is no evidence of a deleterious accumulation of a physiological substrate for NTE or lack of hydrolysis products after inhibition in vivo, and the effect of the negative charge may be focused on some quite separate process. /Organophosphorus Pesticides/

Airway protection. Ensure that a clear airway exists. Intubate the patients and aspirate the secretions with a large-bore suction device if necessary. Administer oxygen by mechanically assisted pulmonary ventilation if respiration is depressed. Improve tissue oxygenation as much as possible before administering atropine, so as to minimize the risk of ventricular fibrillation. In severe poisonings, it may be necessary to support pulmonary ventilation mechanically for several days. /Organophosphate pesticides/|Atropine sulfate. Administer atropine sulfate intravenously, or intramuscularly if intravenous injection is not possible. Remember that atropine can be administered through an endotracheal tube if initial IV access if difficult to obtain. Depending on the severity of poisoning, doses of atropine ranging from very low to...high... . The objective of atropine antidotal therapy is to antagonize the effects of excessive concentrations of acetylcholine at end-organs having muscarinic receptors. Atropine does not reactivate the cholinesterase enzyme or accelerate disposition of organophosphate. Recrudescence of poisoning may occur if tissue concentrations of organophosphate remain high when the effect of atropine wears off. Atropine is effective against muscarinic manifestations, but it is ineffective against nicotinic actions, specifically muscle weakness and twitching, and respiratory depression. Despite the limitations, atropine is often a life-saving agent in organophosphate poisonings. Favorable response to a test dose of atropine can help differentiate poisoning by anticholinesterase agents from other conditions. However, lack of response, with no evidence of atropinization (atropine refractoriness) is typical of more severe poisonings. The adjunctive use of nebulized atropine has been reported to improve respiratory distress, decrease bronchial secretions, and increase oxygenation. ...Do not administer atropine or pralidoxime prophylactically to workers exposed to organophosphate pesticides. Prophylactic dosage with either atropine or pralidoxime may mask early signs and symptoms of organophosphate poisoning and thus allow the worker to continue exposure and possibly progress to more severe poisoning. Atropine itself may enhance the health hazards of the agricultural work setting: impaired heat loss due to reduced sweating and impaired ability to operate mechanical equipment due to blurred vision. This can be caused by mydriasis, one of the effects of atropine. /Organophosphate pesticides/|Glycopyrolate has been studied as an alternative to atropine and found to have similar outcomes using continuous infusion. Ampules of 7.5 mg of glycopyrolate were added to 200 ml of saline and this infusion was titrated to the desired effects of dry mucous membranes and heart rate above 60 beats/min. During this study, atropine was used as a bolus for a heart rate less than 60 beats/min. The other apparent advantage to this regimen was a decreased number of respiratory infections. This may represent an alternative when there is a concern for respiratory infection due to excessive and difficult to control secretions, and in the presence of altered level of consciousness where the distinction between atropine toxicity or relapse of organophosphate poisoning is unclear. /Organophosphate pesticides/|Pralidoxime. Before administration of pralidoxime, draw a blood sample (heparinized) for cholinesterase analysis (since pralidoxime tends to reverse the cholinesterase depression). Administration pralidoxime (Protopam, 2-PAM), a cholinesterase reactivator, in cases of severe poisoning by organophosphate pesticides in which respiratory depression, muscle weakness, and/or twitching are severe. When administered early (usually less than 48 hours after poisoning) pralidoxime relieves the nicotinic as well as the muscarinic effects of poisoning. Pralidoxime works by reactivating the cholinesterase and also by slowing the "aging" process of phosphorylated cholinesterase to a non-reactivatable form. ... Dosage of pralidoxime may be repeated in 1-2 hours, then at 10-12 hour intervals if needed. In very severe poisonings, dosage rates may be doubled. Repeated doses of pralidoxime are usually required. In cases that involve continuing absorption of organophosphate (as after ingestion of large amounts), or continuing transfer of highly lipophilic organophosphate from fat into blood, it may be necessary to continue administration of pralidoxime for several days beyond the 48 hour post-exposure interval usually cited as the limit of its effectiveness. ... Blood pressure should be monitored during administration because of the occasional occurrence of hypertensive crisis. Administration should be slowed or stopped if blood pressure rises to hazardous levels. Be prepared to assist pulmonary ventilation mechanically if respiration is depressed during or after pralidoxime administration. If intravenous injection is not possible, pralidoxime may be given by deep intramuscular injection. /Organophosphate pesticides/|For more Antidote and Emergency Treatment (Complete) data for HEPTENOPHOS (18 total), please visit the HSDB record page.

/SIGNS AND SYMPTOMS/ Although many epidemiological studies have been carried out, few controlled studies on man have been reported. It is generally recognized that there are behavioural and psychic changes during overt clinical poisoning by organophosphorus insecticides and that these may take several months to regress. However, there is no information to suggest that effects occur at exposure levels that do not either alter ChE levels or produce physical symptoms. ...Much /of the work on different aspects of behavior as affected by organophosphates/ was based on generalized complaints from workers occupationally exposed to many agricultural chemicals (and probably also to automobile fuels and lubricants and to alcohol). In summary, ...in human subjects sufficiently exposed to organophosphates to depress plasma- or erythrocyte-ChEs, some or all of the following behavioral variables might be impaired. In cognition: vigilance, information processing and psychomotor speed, and memory; in speech: both performance and perception; in psychic state: increased tendencies to depression, anxiety, and irritability; and in EEG records: a tendency to faster frequencies and higher voltages. /Organophosphorus pesticides/|/SIGNS AND SYMPTOMS/ Signs and symptoms of acute intoxication by organophosphorus insecticides include muscarinic, nicotinic, and central nervous system (CNS) manifestations. Symptoms may develop rapidly, or there may be a delay of several hours after exposure before they become evident. The delay tends to be longer in the case of more lipophilic compounds, which also require metabolic activation. Symptoms may increase in severity for more than one day and may last for several days. In severe cases, respiratory failure is a dominant effect. /Organophosphorus pesticides/|/SIGNS AND SYMPTOMS/ Respiratory and ocular symptoms are expected to appear first after exposure to airborne organophosphorus pesticides. /Organophosphorus pesticides/|/SIGNS AND SYMPTOMS/ The clinical picture of organophosphorus intoxication results from accumulation of ACh at nerve endings. ...The symptoms can be summarized in three groups as follows: (a) Muscarinic manifestations- increased bronchial secretion, excessive sweating, salivation, and lachrymation; pinpoint pupils, bronchoconstriction, abdominal cramps (vomiting and diarrhea); and bradycardia. (b) Nicotinic manifestations- fasciculation of fine muscles and, in more severe cases, of diaphragm and respiratory muscles; and tachycardia. (c) Central nervous system manifestations- headache, dizziness, restlessness, and anxiety; mental confusion, convulsions, and coma; and depression of the respiratory centre. All these symptoms can occur in different combinations and can vary in time of onset, sequence, and duration, depending on the chemical, dose, and route of exposure. Mild poisoning might include muscarinic and nicotinic signs only. Severe cases always show central nervous system involvement; the clinical picture is dominated by respiratory failure, sometimes leading to pulmonary edema, due to the combination of the above-mentioned symptoms. /Organophosphorus Pesticides/|For more Human Toxicity Excerpts (Complete) data for HEPTENOPHOS (7 total), please visit the HSDB record page.

heptenophos

Emulsifiable concentrate.|Selected tradenames: 'Hostaquick' (crop protection use) (Aventis); 'Ragadan' (veterinary use) (Intervet).|Mixtures: 'Decisquick' (+deltamethrin)|Technical grade is 93% pure.

The WHO Recommended Classification of Pesticides by Hazard identifies Heptenophos (technical grade) as Class IB: highly hazardous; Main Use: insecticide.

Agrochemicals -> Insecticides