Pesticide poisoning

Introduction to pesticide poisoning Pesticide poisoning means that in the process of exposure to pesticides, the amount of pesticides entering the body exceeds the maximum tolerated amount of normal people, causing the normal physiological functions of human beings to be affected, causing physiological disorders and pathological changes of the body, showing a series of clinical symptoms of poisoning. . basic knowledge The proportion of diseases: farmers, deliberate suicides, pesticide manufacturing workers are more common, the incidence rate is about 0.01%, more common in organophosphate poisoning Susceptible people: Pesticide factory pesticide discharge, packing workers, maintenance workers; pesticide preparation during the busy season, application of pesticides. Mode of infection: non-infectious Complications: pulmonary edema, brain edema, sudden death

Causes of pesticide poisoning

Mistaken (30%):

Abuse of pesticides (30%):

Pesticide food poisoning (30%):

Oral pesticide poisoning (10%):

Productive poisoning (20%):

Pesticide poisoning prevention

(1) Prevention of pesticide pollution and poisoning

The main reasons for the high incidence of pesticide poisoning in China are: backward production process, lax storage, improper preparation, arbitrary abuse, poor operation and poor protection. Therefore, the main points of prevention are:

1. Reform the pesticide production process, especially the discharge, and the packaging is automated or semi-automated.

2. Strict implementation of pesticide safety regulations

(1) Dispensing, special tools and containers for seed dressing, and the concentration should be properly prepared to prevent pollution of the environment;

(2) Observe the safety operation procedures when spraying, and the spraying tools should be kept and repaired by special personnel to prevent blockage and leakage;

(3) Rational use of pesticides, highly toxic pesticides shall not be used for food crops and fruit trees to control pests at maturity, pesticides for food crops or fruit trees shall be strictly prescribed, and pesticides shall not be abused.

3. Pesticide is professionally managed and strictly kept to prevent abuse.

4. Strengthen personal protection and raise the awareness of self-care for the population.

(2) Contact poisoning screening

1. For high-risk groups of pesticide poisoning, such as pesticide discharge, packing workers, and maintenance workers in pesticide factories; pesticide preparation in the busy season, pesticide application personnel, blood cholinesterase as a screening index, and regular pesticide poisoning screening.

2. For patients with acute poisoning such as dichlorvos, trichlorfon, malathion, etc., after the symptoms of acute poisoning disappear, screening with neuro-electromyography, early detection of delayed peripheral neuropathy.

Pesticide poisoning complications Complications pulmonary edema cerebral edema

Acute organophosphorus pesticide poisoning has a high mortality rate, and death has two peaks:

1, early rescue due to severe inhibition of cholinesterase, pulmonary edema, cerebral edema and respiratory and circulatory failure;

2, the emergence of "rebound" in the late stage of rescue, mostly due to incomplete gastric lavage or atropine withdrawal prematurely caused, sudden death in the recovery period, the reasons are not fully clear, and some due to complications or heart toxic damage, Therefore, the focus of control is on detoxification and detoxification.

Symptoms of pesticide poisoning Common symptoms brain cells appear nutrition... irritability, nausea, poisoning, severe allergic dermatitis, abdominal pain, sensory dysfunction, central nervous system inhibitor...

1. Observed subjects: mild muscarinic, nicotinic or central nervous system symptoms, and whole blood cholinesterase activity is not less than 70%; or no obvious clinical manifestations of poisoning, and whole blood choline The esterase activity is below 705.

2, acute mild poisoning: short-term exposure to a larger amount of organophosphorus pesticides, dizziness, headache, nausea, vomiting, sweating, chest tightness, blurred vision, weakness and other symptoms within 24 hours, the pupil may shrink, whole blood Cholinesterase activity is generally between 50% and 70%.

3, acute moderate poisoning: In addition to the above symptoms, muscle tremor, pupil diminution, mild dyspnea, salivation, abdominal pain, diarrhea, gait sputum, clear or blurred consciousness, whole blood cholinesterase The activity is generally between 30% and 50%.

4, acute severe poisoning: In addition to the above symptoms, and one of the following conditions, can be diagnosed as severe poisoning: (1) pulmonary edema; (2) coma; (3) respiratory paralysis; (4) cerebral edema, whole blood Cholinesterase activity is generally below 30%.

5, delayed neuropathy: 2 to 3 weeks after the onset of acute severe poisoning symptoms, some cases may appear sensation, motor-type peripheral neuropathy, neuro-electromyography showed neurogenic damage.

Clinical manifestations:

1, acute poisoning

Clinical manifestations can be divided into three categories:

(1) muscarinic symptoms: early can appear, mainly manifested by loss of appetite, nausea, vomiting, abdominal pain, diarrhea, salivation, excessive sweating, blurred vision, dilated pupils, increased secretion of respiratory tract, pulmonary edema in severe cases.

(2) nicotinic-like symptoms: when the condition worsens, the whole body is tight, the speech is unclear, the chest, upper limbs, face and neck and even the whole body muscle tremor, chest pressure, heart rate, blood pressure, severe respiratory paralysis.

(3) central nervous system symptoms: dizziness, headache, fatigue, irritability, ataxia, coma in severe cases, convulsions, often endangered by respiratory center or respiratory muscle paralysis.

(4) Delayed neuropathy: Generally, 8 to 14 days after the symptom of acute poisoning is relieved, sensory disturbance occurs, and then the lower extremity is weak until the distal extremity is flaccid paralysis. In severe cases, the upper limb may be involved, mostly bilateral.

2, chronic poisoning

More common in pesticide factory workers, the outstanding performance is neurasthenic syndrome and cholinesterase activity decreased, and some organophosphorus pesticides can cause bronchial asthma, atopic dermatitis and contact dermatitis.

Pesticide poisoning inspection

Combined with the reduction of whole blood cholinesterase activity, reference to the working environment and skin pollution detection, urine metabolite determination, poisoning caused by food contamination, reference to residual food or gastric lavage fluid testing and population epidemiology, comprehensive analysis. Determination of chE activity: ChE activity decreased to 70% of the normal value is clinically significant. Dropping below 50% means more serious, and oral administration of vomit or stomach contents for toxic identification has a definite diagnosis.

Diagnosis and identification of pesticide poisoning

Acute poisoning according to the time of exposure to a large amount of organic phosphorus, clinical manifestations combined with reduced blood cholinesterase activity, occupational poisoning reference working environment and skin pollution detection, urine metabolite determination, food contamination caused by poisoning reference remaining food or gastric lavage fluid detection And population epidemiology, comprehensive analysis, exclusion of other diseases before they can be diagnosed.

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