Malaoxon

EYES: First check the victim for contact lenses and remove if present. Flush victim's eyes with water or normal saline solution for 20 to 30 minutes while simultaneously calling a hospital or poison control center. Do not put any ointments, oils, or medication in the victim's eyes without specific instructions from a physician. IMMEDIATELY transport the victim after flushing eyes to a hospital even if no symptoms (such as redness or irritation) develop.

Biological Exposure Indices (BEI) [ACGIH] - Acetylcholinesterase activity in red blood cells = 70% of individual's baseline; Butylcholinesterase activity in serum or plasma = 60% of individual's baseline; Sample at end of shift; [TLVs and BEIs]

If material on fire or involved in fire: Do not extinguish fire unless flow can be stopped or safely confined. 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, carbon dioxide or dry chemical. /Organophosphorus pesticides, liquid, NOS/

If material on fire or involved in fire: Extinguish fire using agent suitable for type of surrounding fire. (Material itself does not burn or burns with difficulty.) Use water in flooding quantities as fog. Use "alcohol" foam, carbon dioxide or dry chemical. /Organophosphorus pesticides, solid, NOS/

Rooms used for storage only should be soundly constructed & fitted with secure locks. Floors should be kept clear & pesticides clearly identified. If repacking is carried out in storage rooms, adequate light should be available; floors should be impervious & sound ... . /Pesticides/

Pesticides containers must be provided with labels indicating the degree of toxicity of the product they contain. The labels must not only give a short description of how to use the prepn, but also state basic precautions to be taken when applying it. /Organophosphorus pesticides/

Pesticides of any degree of toxicity should be transported in containers which are clearly labelled, leak-proof, and not easily damaged. They should never be transported /or stored/ beside, or above any type of food, and all spillages should be immediately reported. /Pesticides/

SMALL SPILLS AND LEAKAGE: If you spill this chemical, FIRST REMOVE ALL SOURCES OF IGNITION. Then, use absorbent paper to pick up all liquid spill material. Your contaminated clothing and absorbent paper should be sealed in a vapor-tight plastic bag for eventual disposal. Solvent wash all contaminated surfaces with 60-70% ethanol followed by washing with a soap and water solution. Do not reenter the contaminated area until the Safety Officer (or other responsible person) has verified that the area has been properly cleaned.

SRP: At the time of review, criteria for land treatment or burial (sanitary landfill) disposal practices are subject to significant revision. Prior to implementing land disposal of waste residue (including waste sludge), consult with environmental regulatory agencies for guidance on acceptable disposal practices.

All organic pesticides, whether of botanical or synthetic origin, can be destroyed by incineration. /Organic pesticides/

Manufacturers or formulators of very large amounts of pesticides may find it advantageous to build incinerators adequate to destroy all organic pesticides and equipped with scrubbers to remove acid wastes. /Organic pesticides/

In some situations where personnel may become accidently contaminated ... it is necessary to provide shower bath in addition to the usual washing facilities. Special arrangements for cleaning clothing & overalls may be necessary ... /Pesticides/

Special aircraft should preferably be used for spraying or dusting toxic organophosphorus pesticides. ... aerial spraying or dusting gives rise to clouds which spread over larger surfaces than clouds produced by ground application. Aerial spraying should therefore be carried out on windless days only. Residential areas, water supply sources, etc must be avoided. ... When aircraft approaches, signalmen /guiding the aircraft/ should leave the windward side. ... The local population should be informed about the site & time of aerial pesticide treatment. Access of unauthorized persons & especially children to the area to be treated must be ... forbidden. Warning signs should be placed at the limits of the area. Ground spraying must be carried out with compressed-air spraying equipment towed by tractors with closed cabs. /Organophosphorus pesticides/

Small packages of pesticides are preferable for individual application in order to limit the quantities to be weighed & metered. A special vessel with long stirring rod for dilution & suspension of the poison must be available in order to reduce manual handling to a minimum. The strict observance of hygiene rules--no smoking & no food intake during work. Thorough washing with soap after work, changing protective clothing before going home--is of utmost importance. /Organophosphorus pesticides/

Containers ... should be cleaned with a suspension of bleaching powder in water or with other alkaline soln after soaking for 24 hr and then be rinsed with hot water. /Organophosphorus pesticides/

For more Preventive Measures (Complete) data for MALAOXON (10 total), please visit the HSDB record page.

MINIMUM PROTECTIVE CLOTHING: If Tyvek-type disposable protective clothing is not worn during handling of this chemical, wear disposable Tyvek-type sleeves taped to your gloves.

Respiratory protection (supplied-air respirator with full facepiece or self-contained breathing apparatus) should be available where these compounds are manufactured or used and should be worn in case of emergency and overexposure. /Phosphorus compounds/

WORKERS HANDLING AND APPLYING ORGANOPHOSPHATE PESTICIDES (OPP) MUST ... BE GIVEN PERSONAL PROTECTIVE EQUIPMENT COMPRISING OVERALLS MADE OF A TIGHT FABRIC OR POLYVINYL CHLORIDE, GLOVES, AND RUBBER BOOTS. THEY MUST WEAR A RESPIRATOR WITH AN ACTIVATED-CARBON GAS FILTER CARTRIDGE AFFORDING PROTECTION FOR A DETERMINED NUMBER OF WORKING HOURS. THE EYES SHOULD BE PROTECTED BY GOGGLES. THE SIGNALMEN FOR AERIAL DUSTING OPERATIONS SHOULD BE EQUIPPED WITH A HAT AND CAPE MADE OF POLYVINYL CHLORIDE OR A FABRIC IMPREGNATED WITH A WATER REPELLENT. /PESTICIDES, ORGANOPHOSPHORUS/

If the compound has been ingested, rapid gastric lavage should be performed using 5% sodium bicarbonate. For skin contact, the skin should be washed with soap and water. If the compound has entered the eyes, they should be washed with large quantities of isotonic saline or water. In serious cases, atropine and/or pralidoxime should be administered. Anti-cholinergic drugs work to counteract the effects of excess acetylcholine and reactivate AChE. Atropine can be used as an antidote in conjunction with pralidoxime or other pyridinium oximes (such as trimedoxime or obidoxime), though the use of '-oximes' has been found to be of no benefit, or possibly harmful, in at least two meta-analyses. Atropine is a muscarinic antagonist, and thus blocks the action of acetylcholine peripherally.

TOXICITY OF MALATHION IS POTENTIATED BY O-ETHYL O-PARA-NITROPHENYL PHENYLPHOSPHOROTHIOATE, TRI-O-TOLYLPHOSPHATE, & SOME OTHER ORGANOPHOSPHORUS CMPD. IT IS POSTULATED THAT THIS POTENTIATION RESULTS FROM THE INHIBITION OF CARBOXYLESTERASE OR ALIESTERASE ENZYMES RESPONSIBLE FOR DEGRADATION OF MALATHION IN MAMMALS. PRESUMABLY, THIS MECHANISM WOULD LEAD TO INCR FORMATION OF MALAOXON, THE ACTIVATION PRODUCT, BECAUSE THE ENZYMES RESPONSIBLE FOR DEGRADATION OF MALAOXON WOULD BE INHIBITED.

Pretreatment of rats with chloramphenicol (100 mg/kg, ip) 30 min prior to a single oral LD50 dose of malathion at 340 mg/kg completely protected against malathion induced inhibition of cholinesterase. It appears that the inhibition of malathion toxicity by chloramphenicol pretreatment is attributable to inhibition by chloramphenicol of the metabolic activation of malathion to malaoxon.

Some phenothiazines may antagonize & some may potentiate the toxic anticholinesterase effects of ... /organophosphorus insecticides/. /Organophosphate cholinesterase inhibitors/

In long term therapy, adrenocorticoids antagonize the antiglaucoma effects of anticholinesterases (incr ocular pressure). ... Anticholinergics antagonize the miotic (antiglaucoma) & other muscarinic effects of anticholinesterases on the autonomic & central nervous systems. Tricyclic antidepressants (anticholinergic effects) antagonize the antiglaucoma (miotic) effects of anticholinesterases in glaucoma. ... Antihistamines with anticholinergic effects antagonize the miotic (antiglaucoma) & CNS effects of anticholinesterases. Anticholinesterases potentiate tranquilizing & behavioral changes induced by antihistamines. The actions of anticholinesterase agents on autonomic effector cells, & to some extent those on CNS, are antagonized by atropine, an antidote of choice. Barbiturates are potentiated by anticholinesterases. ... Dexpanthenol potentiates the effects of anticholinesterases. Fluorophosphate insecticides potentiate the effects of other anticholinesterases. /Anticholinesterases/

For more Interactions (Complete) data for MALAOXON (6 total), please visit the HSDB record page.

Acute exposure to cholinesterase inhibitors can cause a cholinergic crisis characterized by severe nausea/vomiting, salivation, sweating, bradycardia, hypotension, collapse, and convulsions. Increasing muscle weakness is a possibility and may result in death if respiratory muscles are involved. Accumulation of ACh at motor nerves causes overstimulation of nicotinic expression at the neuromuscular junction. When this occurs symptoms such as muscle weakness, fatigue, muscle cramps, fasciculation, and paralysis can be seen. When there is an accumulation of ACh at autonomic ganglia this causes overstimulation of nicotinic expression in the sympathetic system. Symptoms associated with this are hypertension, and hypoglycemia. Overstimulation of nicotinic acetylcholine receptors in the central nervous system, due to accumulation of ACh, results in anxiety, headache, convulsions, ataxia, depression of respiration and circulation, tremor, general weakness, and potentially coma. When there is expression of muscarinic overstimulation due to excess acetylcholine at muscarinic acetylcholine receptors symptoms of visual disturbances, tightness in chest, wheezing due to bronchoconstriction, increased bronchial secretions, increased salivation, lacrimation, sweating, peristalsis, and urination can occur. Certain reproductive effects in fertility, growth, and development for males and females have been linked specifically to organophosphate pesticide exposure. Most of the research on reproductive effects has been conducted on farmers working with pesticides and insecticdes in rural areas. In females menstrual cycle disturbances, longer pregnancies, spontaneous abortions, stillbirths, and some developmental effects in offspring have been linked to organophosphate pesticide exposure. Prenatal exposure has been linked to impaired fetal growth and development. Neurotoxic effects have also been linked to poisoning with OP pesticides causing four neurotoxic effects in humans: cholinergic syndrome, intermediate syndrome, organophosphate-induced delayed polyneuropathy (OPIDP), and chronic organophosphate-induced neuropsychiatric disorder (COPIND). These syndromes result after acute and chronic exposure to OP pesticides.

TERRESTRIAL FATE: Based on a classification scheme(1), an estimated Koc value of 46(SRC), determined from an estimated log Kow of 0.52(2,SRC) and a regression-derived equation(3), indicates that malaoxon is expected to have very high mobility in soil(SRC). Volatilization of malaoxon from moist soil surfaces is not expected to be an important fate process(SRC) given an estimated Henry's Law constant of 1.8X10-12 atm-cu m/mole(SRC), using a fragment constant estimation method(4). Malaoxon is not expected to volatilize from dry soil surfaces(SRC) based upon an estimated vapor pressure of 1X10-4 mm Hg(5), determined from a fragment constant method(5). If released to soil, malaoxon can be expected to undergo hydrolysis. The half-lives for hydrolysis in sterile soil have been determined to be 7.5, 5.1, and 3.9 days at a pH of 6.2, 7.2, and 8.2, respectively(6).

AQUATIC FATE: Based on a classification scheme(1), an estimated Koc value of 46(SRC), determined from an estimated log Kow of 0.52(2,SRC) and a regression-derived equation(3), indicates that malaoxon is not expected to adsorb to suspended solids and sediment in water(SRC). Volatilization from water surfaces is not expected(3) based upon an estimated Henry's Law constant of 1.8X10-12 atm-cu m/mole(SRC), developed using a fragment constant estimation method(4). According to a classification scheme(5), an estimated BCF of 3.2(SRC), from an estimated log Kow(2) and a regression-derived equation(6), suggests the potential for bioconcentration in aquatic organisms is low.

ATMOSPHERIC FATE: According to a model of gas/particle partitioning of semivolatile organic compounds in the atmosphere(1), malaoxon, which has an estimated vapor pressure of 1X10-4 mm Hg at 25 °C(2), is expected to exist solely in the vapor phase. Vapor-phase malaoxon 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 16 hr(SRC), calculated from its estimated rate constant of 24X10-12 cu cm/molecule-sec at 25 °C determined using a structure estimation method(3).

Malaoxon is a cholinesterase or acetylcholinesterase (AChE) inhibitor. A cholinesterase inhibitor (or 'anticholinesterase') suppresses the action of acetylcholinesterase. Because of its essential function, chemicals that interfere with the action of acetylcholinesterase are potent neurotoxins, causing excessive salivation and eye-watering in low doses, followed by muscle spasms and ultimately death. Nerve gases and many substances used in insecticides have been shown to act by binding a serine in the active site of acetylcholine esterase, inhibiting the enzyme completely. Acetylcholine esterase breaks down the neurotransmitter acetylcholine, which is released at nerve and muscle junctions, in order to allow the muscle or organ to relax. The result of acetylcholine esterase inhibition is that acetylcholine builds up and continues to act so that any nerve impulses are continually transmitted and muscle contractions do not stop. Among the most common acetylcholinesterase inhibitors are phosphorus-based compounds, which are designed to bind to the active site of the enzyme. The structural requirements are a phosphorus atom bearing two lipophilic groups, a leaving group (such as a halide or thiocyanate), and a terminal oxygen.

Symptoms of low dose exposure include excessive salivation and eye-watering. Acute dose symptoms include severe nausea/vomiting, salivation, sweating, bradycardia, hypotension, collapse, and convulsions. Increasing muscle weakness is a possibility and may result in death if respiratory muscles are involved. Hypertension, hypoglycemia, anxiety, headache, tremor and ataxia may also result.

The following link will take the user to the National Toxicology Program (NTP) Test Agent Search Results page, which tabulates all of the "Standard Toxicology & Carcinogenesis Studies", "Developmental Studies", and "Genetic Toxicity Studies" performed with this chemical. Clicking on the "Testing Status" link will take the user to the status (i.e., in review, in progress, in preparation, on test, completed, etc.) and results of all the studies that the NTP has done on this chemical. [http://ntp-apps.niehs.nih.gov/ntp_tox/index.cfm?fuseaction=ntpsearch.searchresults&searchterm=1634-78-2]

The assessment of exposure to the organophosphate pesticides, bromophos and dicrotophos can be accomplished through measurement of these compounds in the blood. However. since organophosphate pesticides are rapidly cleared from the blood, it is difficult to be able to detect the pesticides in blood unless very large quantities have been absorbed. This test may be useful for identification of the compound in cases of severe exposure, although documented tests for measurement of specific organophosphate pesticides in blood are very limited. Whole Blood Reference Ranges: Normal - none detected; Exposed - not established; Toxic -not established. Serum or Plasma Reference Ranges: Normal - not established; Exposed - not established; Toxic - not established. Urine Reference Ranges: Normal - not established; Exposed - not established; Toxic - not established. /Organophosphate pesticides/

Respiratory Symptom Questionnaires: Questionnaires have been published by the American Thoracic Society and the British Medical Research Council. These questionnaires have been found to be useful in identification of people with chronic bronchitis, however pulmonary function tests such as FEV1 (see pulmonary function test section) have been found to be better predictors of chronic airflow obstruction. /Organophosphate pesticides/

Chest Radiography: This test is widely used for assessing pulmonary disease. Chest radiography been found to be useful for detection of early lung cancer in asymptomatic people, especially for detection of peripheral tumors such as adenocarcinomas. However, even though OSHA mandates this test for exposure to some toxicants such as asbestos, there are conflicting views on its efficacy in detection of pulmonary disease. /Organophosphate pesticides/

Pulmonary Function Tests: The tests that have been found to be practical for population monitoring include: Spirometry and expiratory flow-volume curves; Determination of lung volumes; Diffusing capacity for carbon monoxide; Single-breath nitrogen washout; Inhalation challenge tests; Serial measurements of peak expiratory flow; Exercise testing. /Organophosphate pesticides/

For more Medical Surveillance (Complete) data for MALAOXON (8 total), please visit the HSDB record page.

The Koc of malaoxon is estimated as 46(SRC), using an estimated log Kow of 0.52(1,SRC) and a regression-derived equation(2). According to a classification scheme(3), this estimated Koc value suggests that malaoxon is expected to have very high mobility in soil.

TOXICITY OF MALATHION IS PROBABLY DUE TO ITS OXIDATION TO MALAOXON, WHICH IS SOME 1000 TIMES MORE ACTIVE THAN MALATHION AS AN ANTI-CHOLINESTERASE.

Cholinergic toxicity of organophosphate insecticides is regarded as the principle health hazard associated with both human and animal exposures. Recent studies indicate that these pesticides may have important effects on both the immune and hematopoietic systems. In the present study, human bone marrow cells were exposed in vitro to paraoxon and malaoxon (the primary metabolites of parathion and malathion). These compounds produced dose-dependent depression of colony formation by erythrocyte burst-forming units-erythroid and colony-forming units-erythroid and granulocyte-macrophage progenitors (colony-forming units-granulocyte-macrophage). Colony-forming units-erythroid colony formation was reduced 15%-57%, by both paraoxon and malaoxon, in the range of 10-8-10-5 M. No effects were seen at 10-9 and 10-10 M. Colony formation by burst-forming units-erythroid was reduced 15%-75%, at 10-9-10-5 M organophosphate, then returned to normal at 10-10 M organophosphate. In comparison to colony-forming units-erythroid, burst-forming units-erythroid appeared to be more sensitive to the suppressive action of organophosphates. Numbers of colony-forming units-granulocyte-macrophage colonies were reduced 16%-59% in the range of 10-9-10-5 M organophosphate, then returned to normal at 10-10 M organophosphates. Choline chloride added to marrow cultures (final concentration, 10 mM) enhanced colony-forming units-granulocyte-macrophage colony formation at all concentrations of paraoxon and malaoxon.

All the organophosphorus insecticides have a cumulative effect by progressive inhibition of cholinesterase ... /Organophosphorus insecticides/

The symptoms of chronic poisoning due to organophosphorus pesticides include headache, weakness, feeling of heaviness in head, decline of memory, quick onset of fatigue, disturbed sleep, loss of appetite, & loss of orientation. Psychic disorders, nystagmus, trembling of the hands & other nervous system disorders can be observed in certain cases. Sometimes neuritis, paresis & paralysis develop. /Organophosphorus pesticides/

For more Human Toxicity Excerpts (Complete) data for MALAOXON (19 total), please visit the HSDB record page.

A biological, chemical, or photolytic modification of Malathion (insecticide); An impurity and main oxidation product of Malathion; Not commercially produced in the US; [HSDB]

Farming (Pesticides) [Category: Industry]

/SRP/: Malaoxon is a biochemical or photolytic product of malathion.

AS SUBSTRATE IN DECARBOXYLATION REACTION FOR CONVENIENT IN VITRO TESTS FOR ACTIVITY OF CERTAIN MICROSOMAL ENZYMES. /FROM TABLE/

NOT PRODUCED COMMERCIALLY IN USA

Malaoxon is ... results from the chemical modification of malathion, an insecticide.

Malaoxon is ... results from the photolytic modification of malathion, an insecticide.

Malaoxon is ... results from the biological modification of malathion, an insecticide.