Carbophos poisoning

In summer, repair and construction work is often carried out. The substances used are quite dangerous and have toxic properties. These substances are especially dangerous for children, since their metabolism is much faster, and accordingly, the symptoms of pathology develop much faster.

In medical practice, we increasingly encounter diagnoses such as organophosphorus poisoning. First of all, let's figure out what this abbreviation is. The decoding is quite simple - organophosphorus substances. Also, a synonym is often encountered - FOS (organophosphorus compound). This is a group of substances that are most often used as an insecticide, pesticide. It is worth noting that this includes a large number of substances, including malathion.

Pesticide poisoning most often occurs in the summer, when various works are carried out on the garden plot, the harvest and vegetation are processed. Acute poisoning develops quickly, sharply. The main symptoms are the development of signs of intoxication.

In case of poisoning, there is no time to wait, so you need to call an ambulance. When calling an ambulance, you should inform the dispatcher in advance about the case of poisoning. This can make the doctor's job easier: he will immediately take with him an antidote, everything necessary to provide assistance. This will reduce the risk of complications.

There are certain principles of treatment and diagnostics of poisoning. First, it is necessary to carry out treatment (provide emergency care). Only after the person is already safe and his condition is stable, it is necessary to proceed to diagnostics. At the initial stage, before providing emergency care, diagnostics should be minimized, and it comes down to the fact that first it is necessary to at least approximately identify the area of damage, determine those organs and systems that have been subjected to the greatest pathology. This will allow the most effective support of vital functions, and will also allow to determine the picture of the pathology, on the basis of which further treatment will be selected. An antidote may be required, which will simply neutralize the poison and remove it from the body.

After the body has stabilized, the most effective methods of instrumental diagnostics are selected in accordance with the suspected pathologies.

Epidemiology

Acute pesticide poisoning is now an important cause of morbidity and mortality worldwide (Jeyaratnam 1990). According to World Health Organization (WHO) estimates published in 1990, approximately 3 million cases of poisoning occur annually.[ 1 ]

Organophosphorus pesticide poisoning is a major clinical problem in rural areas of the developing world, causing approximately 200,000 deaths each year. [ 2 ] About 99% of these deaths occur in developing countries.

According to statistics, about 15% of poisonings with malathion are caused by household methods. These are private works using this substance, its storage at home. About 65% of poisonings are industrial poisonings that occur in connection with the professional activities of workers. About 15% are children and animals, incapacitated persons who are poisoned accidentally. The remaining 5% are poisonings with the purpose of committing murder or suicide.

Of all poisonings, approximately 69% are acute poisonings, the remaining 31% are chronic poisonings. In the absence of treatment and failure to provide emergency care, 98% of poisonings end in death. If emergency care is provided in a timely manner, approximately 15-30% of poisoning cases end in death. [ 3 ]

Causes carbophos poisoning

There are many reasons for poisoning. Poisoning can occur accidentally or intentionally. Most poisonings occur accidentally: during prolonged contact with toxic substances, during work in a production or garden plot, during repairs or construction, when cultivating gardens and vegetable gardens.

In addition, poisoning occurs with people who, due to their professional duties, are forced to contact with malathion and other similar substances. This often happens in production, in laboratories. This happens both due to a malfunction of the working equipment, and due to carelessness, negligence, or irresponsibility of workers. A frequent cause is non-compliance with the rules of work, or operating conditions of equipment, the absence of an exhaust hood or its faulty condition, an unventilated room.

Poisoning often occurs in children, as they have a natural, innate curiosity and desire to learn. Having found something new, they will certainly try it. Banal inattention and absent-mindedness can cause poisoning. For example, if you store a product without a label, or with food products, you can confuse the substances, which will lead to poisoning.

If we talk about intentional cases of poisoning, they happen rarely. However, there are such cases, mainly with the purpose of committing suicide or murder.

Risk factors

Risk factors include the need to be in contact with malathion: whether it is periodic contact arising due to the need to carry out certain work, or constant, long-term contact, which leads to the development of chronic poisoning. The risk group includes people of various professions that are associated with the need to use various toxic substances, including malathion. Also at risk are small children, animals, the elderly, people with mental disorders. Personality disorders, disorders of consciousness, memory, psychosis, neurosis, neuropsychiatric disorders.

Pathogenesis

Exposure to organophosphate pesticides can occur through inhalation, ingestion, or skin contact. Crops that agricultural workers encounter may also include organophosphates such as apples, celery, bell peppers, peaches, strawberries, nectarines, grapes, spinach, lettuce, cucumbers, blueberries, and potatoes.

Organophosphorus pesticides inhibit esterase enzymes, particularly acetylcholinesterase (EC 3.1.1.7) in synapses and on red blood cell membranes, and butyrylcholinesterase (EC 3.1.1.8) in plasma. Although acute inhibition of butyrylcholinesterase does not appear to cause clinical manifestations, inhibition of acetylcholinesterase results in accumulation of acetylcholine and excessive stimulation of acetylcholine receptors at synapses of the autonomic nervous system, CNS, and neuromuscular junctions. The subsequent autonomic, CNS, and neuromuscular features of organophosphorus poisoning are well known.

Clinical features due to excessive stimulation of muscarinic acetylcholine receptors in the parasympathetic system:

• bronchospasm;
• bronchorrhea;
• miosis;
• lacrimation;
• urination;
• diarrhea;
• hypotension;
• bradycardia;
• vomit;
• salivation.

Clinical features due to overstimulation of nicotinic acetylcholine receptors in the sympathetic system:

• tachycardia;
• mydriasis;
• hypertension;
• sweating.

Clinical features due to excessive stimulation of nicotinic and muscarinic acetylcholine receptors in the CNS:

• confusion;
• agitation;
• coma;
• breathing disorder.

Clinical features due to overstimulation of nicotinic acetylcholine receptors at the neuromuscular junction:

• muscle weakness;
• paralysis;
• fasciculations.

The basis of poisoning with malathion is the development of the intoxication process. Toxic substances enter the body in one of the known ways - through the respiratory tract, through the gastrointestinal tract, or through the mucous membranes and skin. It is worth noting that the pathogenesis depends on which route of penetration of the substance, what amount of the substance has penetrated the body, and how long ago the substance entered the body.

When penetrating through the respiratory tract, the mucous membranes are burned, toxins further penetrate into the respiratory cells and tissues, swelling and irritation develop on the mucous membranes of the upper and lower respiratory tract. The main substance accumulates in the alveoli. They are also absorbed there, absorbed through the cell membranes. The substance is absorbed and then enters the blood, where the main toxic effect occurs.

When penetrating through the gastrointestinal tract, a chemical burn of the esophagus and stomach develops. The main absorption occurs through the walls of the large intestine, then through the walls of the small intestine. After absorption, the substance enters the blood, and then has a toxic effect there.

The substance is transported in the blood, then it enters the liver, where a number of transformations occur, it is neutralized. It is the process of processing the substance by the liver that determines the further course of poisoning. A number of transformations occur in the immune system, kidneys, and liver.

Symptoms carbophos poisoning

The main symptoms of poisoning with malathion are nausea, vomiting, dizziness, loss of consciousness, diarrhea. Later, if emergency assistance is not provided, the condition worsens. Sharp pain in the stomach, profuse vomiting, bleeding appear. A person may lose consciousness, his body temperature rises or falls sharply, the pulse slows down, the pressure decreases. Cardiac arrhythmia, suffocation, cough, clouding of consciousness, hallucinations and delirium appear. Later, signs of liver and kidney damage, dyspeptic syndromes join. As the condition worsens, liver or kidney failure, heart failure develops. Pulmonary or cerebral edema may develop. Multiple organ failure gradually develops, which ends in death. [ 4 ]

The first signs are a general deterioration in health, in which a person experiences a slight tremor in the body, and the extremities become sweaty and cold. Gradually, the body temperature rises, weakness develops, appetite decreases, the person is unable to concentrate, and his or her performance capacity sharply decreases. Cold sweat appears, the heartbeat and breathing quicken. Individual reactions develop - blood pressure may either increase or decrease. If a person is prone to allergic reactions, an allergic reaction, anaphylactic shock, or an asthma attack develops. The victim needs emergency care. [ 5 ]

Poisoning with malathion through the skin

Poisoning with malathion can also occur through the skin. In this case, the toxic substance is absorbed through the skin surface with further transport throughout the body through the blood. This route of penetration of the substance into the blood is called the transdermal barrier. The main manifestation is damage to the surface layers of the skin, the development of a chemical burn. It is necessary to stop the effect of the toxic substance on the body as quickly as possible with further emergency care. To do this, immediately wash the affected area with water, then wipe the affected area with a fatty substance (oil, fatty cream, glycerin). [ 6 ], [ 7 ]

The victim is then taken to the hospital as quickly as possible, where further diagnostics and treatment are performed. Diagnostics is based on determining the typical picture of poisoning, which is characteristic of this type of poisoning. The main analysis for any type of poisoning is traditionally considered to be a toxicological study and a biochemical blood test. Then other tests are carried out. Usually, standard tests are prescribed - clinical blood, urine, feces. This allows you to assess the general direction of the pathological process, to identify the range of damage that has arisen due to the effect of the poison on the body. [ 8 ]

The following indicates poisoning with malathion:

• high eosinophil levels;
• the appearance of mast cells in the blood;
• increased ESR level;
• high bilirubin levels;
• the presence of leukocytes or a large amount of protein in the urine;

An accurate clinical picture of the pathology with a detailed description of symptoms and early signs of the pathology is also important. Based on the diagnosis, a basic assumption can be made regarding the cause of the poisoning, on the basis of which further treatment will be prescribed. Therefore, when the first signs of poisoning or malaise appear, you need to see a doctor as soon as possible.

Organophosphorus pesticide poisoning

When working with organophosphorus pesticides, severe intoxication of the body can occur, in which the toxin enters the body. It can enter the bloodstream in various ways. This can happen through the skin (transdermal barrier), or through the respiratory tract, or through the digestive tract. A typical picture of poisoning develops, which is practically no different from other types of poisoning. [ 9 ]

The first signs of poisoning are a sharp deterioration in the general condition of the body, deterioration of health, dizziness, shortness of breath, suffocation. Nausea, vomiting, and diarrhea gradually appear. Convulsive syndrome, abdominal pain, accompanied by delirium, clouding of consciousness, and sometimes hallucinations may develop. As the symptoms develop, the condition worsens, weakness, cold sweat, and trembling in the body develop.

Urgent assistance is required, and it is also necessary to urgently call an ambulance, which will provide professional assistance and, if necessary, take you to the hospital for further hospitalization and treatment.

It is necessary to take into account that there are specific diagnostic features in case of poisoning with malathion. The patient is first given emergency care, and diagnostics are carried out later, after the threat to life has passed. This is quite easy to explain: the poison can act covertly, asymptomatically. Remote consequences are also possible, which will appear much later. But the changes occur at an early stage, and they can be promptly identified and eliminated.

It is important to conduct a toxicological study, since toxins are contained in human biological fluids. Biochemical analysis shows what changes have occurred in the body under the influence of toxins. If it is impossible to conduct a toxicological or biochemical analysis, a regular clinical blood test is carried out. The clinic will indicate an inflammatory, infectious, or allergic process. The blood formula can suggest the cause of the pathology. [ 10 ]

To clarify the data, various laboratory research methods can be used, including: allergy tests, analysis of total and specific immunoglobulin E, analysis of histamine levels, analysis of toxins, a detailed immunogram, rheumatic tests, analysis of C-reactive protein levels, analysis of CIC levels, etc.

Chronic pesticide poisoning

Chronic pesticide poisoning involves the body being exposed to a toxic substance for a fairly long period of time. It is usually observed in people who, due to their professional activities, are forced to work with pesticides. They are exposed to them for a long period of time, systematically and regularly. Poisoning can occur slowly, with symptoms gradually becoming more pronounced and the severity of intoxication increasing. [ 11 ]

When the first signs of poisoning appear, it is necessary to provide first aid to the victim and call an ambulance. The ambulance doctor will provide emergency care, make a diagnosis, and hospitalize. To make a diagnosis, it is important to describe all the symptoms in as much detail as possible to the arriving doctor, and say what substances you had to deal with. It is important to understand that the doctor needs as much information as possible about what substances the victim came into contact with, how the reaction to poisoning developed (this will allow you to quickly navigate the situation, make a diagnosis, and provide the necessary assistance). Treatment consists primarily in providing first aid correctly and quickly to the victim. Only after first aid has been provided and it has been established that the patient's life is not in danger, can you move on to further treatment.

Metaphos poisoning

Metaphos poisoning is indicated by the development of a clinical picture typical of intoxication. A mainly muscular reaction develops: convulsions appear, breathing is impaired, involuntary stool, vomiting, rapid heartbeat and urination appear. A comatose state is possible if left untreated.

What needs to be done when symptoms of poisoning appear is to neutralize the poison and stop its effect on the body. If it is known exactly what substance the victim was poisoned with, an antidote should be administered as soon as possible. The antidote to metaphos is atropine (administered intramuscularly or intravenously in an amount of 0.5-1 ml). The mechanism of action is that atropine has a relaxing effect on blood vessels and smooth muscles. Further treatment is carried out in a hospital. Hospitalization is recommended, even if the patient feels well.
After first aid has been provided and the condition has stabilized, detoxification therapy is carried out (sorbents are administered), and concomitant symptomatic therapy with the use of medications is also carried out. During therapy, it is recommended to administer vitamin complexes, minerals, glucose, Ringer's solution, and other supporting substances to the body. Restorative therapy is an equally important stage of complex treatment. During this time, it is important to follow a dietary diet (table No. 1). Symptomatic treatment and prevention are carried out. Often poisoning is accompanied by vitamin deficiency, and vitamin therapy is prescribed accordingly. Sometimes hormone therapy and antibiotic therapy are required. At this stage, there is also a need for physiotherapeutic methods. Inhalations, thermal procedures, some electrical procedures, UF, and administration of drugs using electrophoresis may be required.

Complications and consequences

The consequences of poisoning are unfavorable, complications almost always occur. First of all, poisoning has a negative effect on the state of the circulatory system. The nervous and cardiovascular systems also suffer. Immunity is significantly reduced. The kidneys and liver suffer, since these are the main organs that participate in the metabolism of toxins, participate in the removal and neutralization of toxic substances.

Death from cardiac causes in malathion poisoning occurs either due to arrhythmias,[ 12 ] or severe and refractory hypotension, leading to cardiac arrest.[ 13 ] Although shock is mainly vasodilatory,[ 14 ],[ 15 ] peripheral endocardial ischemia with cardiogenic shock and death has also been reported with malathion poisoning.[ 16 ] Autopsies of patients who died from subsequent organophosphorus poisonings have shown pericarditis, atrial thrombus, and right ventricular hypertrophy and dilation. Infarction, interstitial edema, interstitial inflammation, thrombi, and myocarditis were histological findings.[ 17 ]

Metabolic complications such as hyperglycemia, glycosuria [ 18 ] and diabetic ketoacidosis [ 19 ] have been described.

Respiratory failure occurs in 24-66% of patients.[ 20 ] The severity of poisoning was the main determinant of respiratory failure.[ 21 ] Other factors contributing to respiratory failure include pneumonia, cardiovascular collapse, acute pulmonary edema,[ 22 ] and acute respiratory distress syndrome.

Coma occurs in 17-29% of patients and may last from several hours to several days.[ 23 ] Poisoning may also manifest as a brainstem stroke.[ 24 ]

Diagnostics carbophos poisoning

The basis for diagnosing poisoning with malathion, as with any other chemical substance, is, first of all, determining the typical picture of poisoning, which is characteristic of this type of poisoning. This requires the patient's medical history and an accurate clinical picture of the pathology with a detailed description of symptoms, early signs of pathology. It is on this basis that one can make a basic assumption regarding the cause of poisoning, on the basis of which further treatment will be prescribed. The sooner the diagnosis is made, the greater the chances of a favorable outcome. Therefore, when the first signs of poisoning or malaise appear, you need to see a doctor as soon as possible.

In case of poisoning, there is no time to wait, so you need to call an ambulance. It is in your interests to describe all the symptoms to the arriving doctor in as much detail as possible, and tell him what substances you had to deal with. This will give him the opportunity to quickly get his bearings in the current situation, make a diagnosis, and provide the necessary assistance. It is even better, when calling an ambulance, to inform the dispatcher in advance about everything that happened, perhaps the doctor will immediately assume poisoning and take with him an antidote, everything necessary to provide assistance. There is a chance to provide the patient with more effective assistance with minimal complications and risks.

Features of diagnostics - the patient is first given emergency care, and diagnostics are carried out later. The poison may act covertly, or have remote consequences that will appear much later. But this does not mean that changes in the body have not already occurred at the early stages, and they cannot be detected during diagnostic measures.

Tests

The diagnosis of organophosphate poisoning should ideally be confirmed by assaying plasma butyrylcholinesterase activity (or whole blood acetylcholinesterase). However, such assay results are rarely available in time to influence clinical decisions. Their value is to guide clinical trials; understanding their limitations is important for interpreting studies of individual pesticides and specific interventions.

Studies show that erythrocyte acetylcholinesterase is a good marker of synaptic function and atropine requirements in patients poisoned by organophosphates and therefore probably a good marker of severity.[ 25 ]

The main analysis for any type of poisoning is traditionally considered to be a toxicological study and a biochemical blood test. These are express methods that allow you to quickly and effectively assess the situation. Toxicology shows what toxins are contained in human biological fluids, and a biochemical analysis shows what changes have occurred in the body under the influence of these toxins, what measures should be taken first to provide first aid.

Then, other tests are carried out, without which it is impossible to assess the condition of the body. Usually, standard tests are prescribed - clinical blood, urine, and feces tests. This allows you to assess the general direction of the pathological process, to identify the range of damage that has arisen due to the effect of the poison on the body. A regular blood test can be very informative (it will indicate an inflammatory, infectious, or allergic process). Based on the blood formula, you can assume the cause of the pathology - bacterial or viral pathology. You can also roughly assume in which organ system the main pathological process occurs, what its severity is; whether the processes that occur in the body are reversible, or the damage to tissues and organs has already become irreversible.

Direct indication of acute poisoning is a high level of eosinophils, the appearance of mast cells in the blood, and an increase in the ESR level. Similarly, a high level of bilirubin indicates liver pathology. The higher the bilirubin level, the more severe the pathological process. Also, the presence of leukocytes or a large amount of protein in the urine indicates the development of an inflammatory process in the kidneys. Based on these general data, it is possible to determine the course of further diagnostics. This will eliminate a large number of unnecessary, uninformative tests and, at the same time, will reduce the period of time spent on diagnostics, significantly increasing the effectiveness of the diagnostic measures themselves.

To clarify the data, various laboratory research methods can be used:

• allergy tests;
• analysis of total and specific immunoglobulin E;
• histamine level test;
• toxin analysis;
• detailed immunogram;
• rheumatic tests;
• C-reactive protein test
• analysis and determination of the level of CIC – circulating immune complexes and many other studies.

Instrumental diagnostics

It is important to understand that first it is necessary to at least approximately identify the area of damage, determine those organs and systems that have been subjected to the greatest pathology. After that, the most effective methods of instrumental diagnostics are selected, adequate to the current situation.

In many ways, the choice of method depends on the route of poison penetration into the body. Thus, malathion, entering the body through the digestive tract, can cause corresponding pathologies of the digestive tract and associated organs and systems. If such injury or the development of any gastrointestinal disease is suspected, gastroscopy, radiography, ultrasound, colonoscopy may be required.

When acetone vapors enter through the respiratory tract, injuries and diseases of the respiratory system develop. In this case, the following research methods can be used:

• spirogram,
• radiograph,
• functional tests,
• fluorographic examination.

Almost universal research methods, which are used regardless of the route by which the poison entered the body, are various methods of research of the cardiovascular, nervous, musculoskeletal systems, since they are most exposed to the poison. They are used:

• electrocardiogram,
• angiography,
• ultrasound of the heart,
• magnetic resonance imaging and computed tomography.

Differential diagnosis

The main differential diagnosis is carbamate poisoning, which is clinically indistinguishable.

Differential diagnostics is based on the need to clearly distinguish between the symptoms of several similar pathologies and conditions that have similar manifestations and to make the most accurate diagnosis. In particular, in case of poisoning, it is important to accurately determine the substance, or at least a group of substances, that caused the poisoning. Further treatment, its effectiveness, and sometimes even the patient's life directly depend on this.

So, when a doctor tries to make a differential diagnosis, he usually already has several presumptive diagnoses that match the symptoms. At this stage, it is important to carefully study the anamnesis and analyze the available data. The patient is required to describe his condition and subjective sensations to the doctor in as much detail as possible, which is an important diagnostic indicator. At the early stages of diagnosis, a standard examination is carried out: the doctor first interviews the patient, collects general information about him, anamnesis of life. Then the doctor conducts a mandatory collection of anamnesis of the disease, on the basis of which he can judge the features of the course of poisoning. It is on the basis of the anamnesis data that the doctor can predict the further development and outcome of poisoning. The results of existing laboratory and instrumental research methods are taken into account. It is also necessary to know whether any treatment was carried out, what its effectiveness is, what other measures were taken. On this basis, further treatment can be developed and the final diagnosis is made.

Treatment carbophos poisoning

Treatment of poisoning with karbofos consists primarily of correct and prompt first aid to the victim. It is on this that life depends first of all, and the patient's health second.

Prevention

Prevention - follow the rules for working with malathion. Especially if there are children in the house, since their body is more sensitive to the effects of any toxins. Do not leave acetone unattended, since children can drink it out of curiosity. Do not leave it with food products.

Forecast

Factors affecting the outcome of organophosphorus pesticide poisoning:

• Toxicity: Toxicity is usually assessed according to the oral LD50 in rats. This scale is able to differentiate approximately between safe and very toxic pesticides. However, after poisoning with organophosphates with approximately the same toxicity in animals, large differences in toxicity in humans have been found and this classification does not take into account the effects of treatment. [ 26 ], [ 27 ]
• Impurities: WHO toxicity classification evaluates fresh pesticide from approved manufacturers. Storing pesticides in hot conditions can lead to chemical reactions with toxic by-products. Such a process was blamed for the deaths of pesticide sprayers using malathion in Pakistan in the late 1970s [ 28 ], [ 29 ], and has also been noted with both diazinon and dimethoate. [ 30 ], [ 31 ]
• Composition: The toxicity of a pesticide will vary depending on its composition, which varies depending on the organophosphate and where it is produced. For example, malathion is available as an 80% solution at street pesticide stands in Burma, but as a 3% powder in Sri Lanka.
• Alkyl subgroups: Most pesticides have either two methyl groups attached via oxygen atoms to the phosphate (dimethyl organophosphorus) or two ethyl groups (diethyl organophosphates). AChE aging occurs much more rapidly in dimethyl poisoning than in diethyl poisoning, so to be effective, oximes must be given quickly to patients with dimethyl poisoning. Some pesticides have unusual structures, with another alkyl group (e.g., the propyl in profenofos) attached to the phosphate group via a sulfur atom. These organophosphorus pesticides age AChE even more rapidly, and oximes are probably not effective.
• Necessity for activation. Many compounds are inactive thioates (with a sulfur double bond attached to a phosphorus atom) and must be desulfurized to form the active oxon via cytochrome P450 enzymes in the gut wall and liver. P450 3A4 appears to be the most active enzyme when the organof is present in high concentrations, as occurs after poisoning.[ 32 ]
• Rate of AChE activation and inhibition. The rate of activation of thioate organophosphates varies between pesticides.[ 33 ] There are also large differences in the rate of acetylcholinesterase inhibition between organophosphorus pesticide oxons.
• Duration of effect - lipid solubility and half-life. Some lipid-soluble thioate organophosphate pesticides (eg, fenthion) distribute extensively into fat stores after absorption. This appears to reduce the peak blood concentration of the organophosphate, and early cholinergic effects are usually minor. Subsequent slow redistribution and activation produce recurrent cholinergic effects lasting days to weeks. Peripheral respiratory failure is common with these organophosphates, probably due to ongoing acetylcholinesterase inhibition. Senescence only begins after acetylcholinesterase inhibition, so oximes could theoretically be useful for many days in such patients. In contrast, other organophosphates (eg, dichlorvos) do not require activation, are lipid insoluble, and may have a much more rapid onset of action and shorter duration of activity. Fat solubility is estimated by Kow (log octanol/water ratio): less than 1 0 = insoluble in fat; more than 4 0 = very fat soluble.[ 34 ]

The above factors have important implications for the rapidity of onset of organophosphate poisoning after ingestion. Ingestion of the organophosphate oxon, which rapidly inhibits acetylcholinesterase, will result in early clinical signs and respiratory arrest before reaching hospital, increasing the risk of hypoxic brain injury and aspiration. The conversion of the thioate organophosphate parathion to paraoxon is so rapid that patients may become unconscious within 20 minutes. Clinical signs after poisoning with other thioate organophosphates, such as dimethoate and fenthion, occur later, giving the patient more time to be transported to hospital.

If you provide first aid to the patient in a timely manner, neutralize the toxin, give the victim an antidote, and then carry out the necessary treatment, the prognosis will be favorable. Poisoning with malathion ends in death only if first aid is not provided in a timely manner.