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Pesticide poisoning

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A pesticide poisoning occurs when chemicals intended to control a pest affect non-target organisms such as humans, wildlife, or bees.

Exposure

The most common exposure scenarios for pesticide-poisoning cases are accidental or suicidal poisonings, occupational exposure, by-stander exposure to off-target drift, and the general public who are exposed through environmental contamination.[1]

Accidental and suicidal poisonings

Self-poisoning with agricultural pesticides represents a major hidden public health problem. It is one of the most common forms of self-injury in the Global South. The World Health Organization estimates that 300,000 people die from self-harm each year in the Asia-Pacific region alone.[2] Most cases of intentional pesticide poisoning appear to be impulsive acts undertaken during stressful events, and the availability of pesticides strongly influences the incidence of self poisoning.

Occupational exposure

Pesticide poisoning is an important occupational health issue because pesticides are used in a large number of industries, which puts many different categories of workers at risk. Extensive use puts agricultural workers in particular at increased risk for pesticide illnesses.[3][4][5] Workers in other industries are at risk for exposure as well.[4][5] For example, commercial availability of pesticides in stores puts retail workers at risk for exposure and illness when they handle pesticide products.[6] The ubiquity of pesticides puts emergency responders such as fire-fighters and police officers at risk, because they are often the first responders to emergency events and may be unaware of the presence of a poisoning hazard.[7] The process of aircraft disinsection, in which pesticides are used on inbound international flights for insect and disease control, can also make flight attendants sick.[8][9]

Different job functions can lead to different levels of exposure.[1] Most occupational exposures are caused by absorption through exposed skin such as the face, hands, forearms, neck, and chest. This exposure is sometimes enhanced by inhalation in settings including spraying operations in greenhouses and other closed environments, tractor cabs, and the operation of rotary fan mist sprayers.[10]

Pathophysiology

Organochlorines

The organochlorine pesticides, like DDT, aldrin, and dieldrin are extremely persistent and accumulate in fatty tissue. Through the process of bioaccumulation (lower amounts in the environment get magnified sequentially up the food chain), large amounts of organochlorines can accumulate in top species like humans. There is substantial evidence to suggest that DDT, and its metabolite DDE, act as endocrine disruptors, interfering with hormonal function of estrogen, testosterone, and other steroid hormones.

Anticholinesterase compounds

Certain organophosphates have long been known to cause a delayed-onset toxicity to nerve cells, which is often irreversible. Several studies have shown persistent deficits in cognitive function in workers chronically exposed to pesticides.[11] Newer evidence suggests that these pesticides may cause developmental neurotoxicity at much lower doses and without depression of plasma cholinesterase levels.

Diagnosis

Most pesticide-related illnesses have signs and symptoms that are similar to common medical conditions, so a complete and detailed environmental and occupational history is essential for correctly diagnosing a pesticide poisoning. A few additional screening questions about the patient's work and home environment, in addition to a typical health questionnaire, can indicate whether there was a potential pesticide poisoning.[12]

If one is regularly using carbamate and organophosphate pesticides, it is important to obtain a baseline cholinesterase test. Cholinesterase is an important enzyme of the nervous system, and these chemical groups kill pests and potentially injure or kill humans by inhibiting cholinesterase. If one has had a baseline test and later suspects a poisoning, one can identify the extent of the problem by comparison of the current cholinesterase level with the baseline level.

Prevention

Accidental poisonings can be avoided by proper labeling and storage of containers. When handling or applying pesticides, exposure can be significantly reduced by protecting certain parts of the body where the skin shows increased absorption, such as the scrotal region, underarms, face, scalp, and hands.[13] Using chemical-resistant gloves has been shown to reduce contamination by 33-86%.[14]

Treatment

Specific treatments for acute pesticide poisoning are often dependent on the pesticide or class of pesticide responsible for the poisoining. However, there are basic management techniques that are applicable to most acute poisonings, including skin decontamination, airway protection, gastrointestinal decontamination, and seizure treatment.[12]

Decontamination of the skin is performed while other life-saving measures are taking place. Clothing is removed, the patient is showered with soap and water, and the hair is shampooed to remove chemicals from the skin and hair. The eyes are flushed with water for 10-15 minutes. The patient is intubated and oxygen administered, if necessary. In more severe cases, pulmonary ventilation must sometimes be supported mechanically.[15] Seizures are typically managed with lorazepam, phenytoin and phenobarbitol, or diazepam (particularly for organochlorine poisonings).[12]

Gastric lavage is not recommended to be used routinely in pesticide poisoning management, as clinical benefit has not been confirmed in controlled studies; it is indicated only when the patient has ingested a potentially life-threatening amount of poison and presents within 60 minutes of ingestion.[16] An orogastric tube is inserted and the stomach is flushed with saline to try to remove the poison. If the patient is neurologically impaired, a cuffed endotracheal tube inserted beforehand for airway protection.[12] Studies of poison recovery at 60 minutes have shown recovery of 8%-32%.[17][18] However, there is also evidence that lavage may flush the material into the small intestine, increasing absorption.[19] Lavage is contra-indicated in cases of hydrocarbon ingestion.[12]

Activated charcoal is sometimes administered as it has been shown to be successful with some pesticides. Studies have shown that it can reduce the amount absorbed if given withint 60 minutes,[20] though there is not enough data to determine if it is effective if time from ingestion is prolonged. Syrup of ipecac is no longer recommended for most pesticide poisonings.[21]

Epidemiology

Acute pesticide poisoning is a large-scale problem, especially in developing countries.

"Most estimates concerning the extent of acute pesticide poisoning have been based on data from hospital admissions which would include only the more serious cases. The latest estimate by a WHO task group indicates that there may be 1 million serious unintentional poisonings each year and in addition 2 million people hospitalized for suicide attempts with pesticides. This necessarily reflects only a fraction of the real problem. On the basis of a survey of self-reported minor poisoning carried out in the Asian region, it is estimated that there could be as many as 25 million agricultural workers in the developing world suffering an episode of poisoning each year."[22]

Estimating the numbers of chronic poisonings worldwide is even more difficult.

Poisoning of other non-target organisms (wildlife, bees)

An obvious side effect of using a chemical meant to kill is that one is likely to kill more than just the desired organism. Contact with a sprayed plant or "weed" can have an effect upon local wildlife, most notably insects.

Society and culture

Rachel Carson's Silent Spring brought about the first major wave of public concern over the chronic effects of pesticides.

References

  1. ^ a b Ecobichon (2001) pp. 767
  2. ^ WHO. The impact of pesticides on health: preventing intentional and unintentional deaths from pesticide poisoning. 2004: http://www.who.int/mental_health/prevention/suicide/en/PesticidesHealth2.pdf
  3. ^ Attention: This template ({{cite pmid}}) is deprecated. To cite the publication identified by PMID 12749629 , please use {{cite journal}} with |pmid=12749629 instead.
  4. ^ a b Attention: This template ({{cite doi}}) is deprecated. To cite the publication identified by doi:10.1002/ajim.20623, please use {{cite journal}} (if it was published in a bona fide academic journal, otherwise {{cite report}} with |doi=10.1002/ajim.20623 instead.
  5. ^ a b Attention: This template ({{cite doi}}) is deprecated. To cite the publication identified by doi:10.1002/ajim.10309, please use {{cite journal}} (if it was published in a bona fide academic journal, otherwise {{cite report}} with |doi=10.1002/ajim.10309 instead.
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  8. ^ WHO. World Health Organization Communicable Disease Control, Prevention and Eradication Pesticide Evaluation Scheme (WHOPES) & Protection of the Human Environment Programme on Chemical Safety (PCS). 2005. Safety of pyrethroids for public health use. Geneva: WHO. WHO/CDS/WHOPES/GCDPP/2005.10 WHO/PCS/RA/2005.1.
  9. ^ Attention: This template ({{cite doi}}) is deprecated. To cite the publication identified by doi:10.1002/ajim.20452, please use {{cite journal}} (if it was published in a bona fide academic journal, otherwise {{cite report}} with |doi=10.1002/ajim.20452 instead.
  10. ^ Ecobichon (2001) pp. 768
  11. ^ Attention: This template ({{cite pmid}}) is deprecated. To cite the publication identified by PMID 12505280, please use {{cite journal}} with |pmid=12505280 instead.
  12. ^ a b c d e Reigart, J.R. and Roberts, J.R. (1999). Recognition and Management of Pesticide Poisonings. Washtington, DC: Environmental Protection Agency.{{cite book}}: CS1 maint: multiple names: authors list (link)
  13. ^ Feldman RJ, Maiback HI: Percutaneous pentration of some pesticides and herbicides in man. Toxicol Appl Pharmacol 28: 126-132.
  14. ^ Bonsall (1985), pp 13-133.
  15. ^ Specific pesticides have special considerations with regard to respiratory support. In anticholinesterase poisoning, adequate tissue oxygenation is essential before administering atropine. In paraquat and diquat poisoining, however, oxygen is contraindicated.
  16. ^ Attention: This template ({{cite pmid}}) is deprecated. To cite the publication identified by PMID 9482426, please use {{cite journal}} with |pmid=9482426 instead.
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  19. ^ Attention: This template ({{cite pmid}}) is deprecated. To cite the publication identified by PMID 1674963, please use {{cite journal}} with |pmid=1674963 instead.
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  21. ^ Attention: This template ({{cite pmid}}) is deprecated. To cite the publication identified by PMID 9482425, please use {{cite journal}} with |pmid=9482425 instead.
  22. ^ Attention: This template ({{cite pmid}}) is deprecated. To cite the publication identified by PMID 2238694, please use {{cite journal}} with |pmid=2238694 instead.

Cited texts

  • Bonsal, J.L. (1985). "Measurement of occupational exposure to pesticides". In Turnbull, G.S. (ed.). Occupational Hazards of Pesticide use. London: Taylor & Francis. ISBN 0850663253.
  • Ecobichon, D.J. (2001). "Toxic effects of pesticides". In Klaassen, C.D. (ed.). Casarett and Doull's Toxicology: The Basic Science of Poisons, 6th edition. McGraw-Hill Professional. ISBN 0071347216.
  • Rang, H.P. (2003). Pharmacology. Edinburgh: Churchill Livingstone. ISBN 0443071454.


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