Benutzer:JonskiC/Gesundheitliche Auswirkungen von Pestiziden

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Health effects of pesticides may be acute or delayed in those who are exposed.[1] A 2007 systematic review found that "most studies on non-Hodgkin lymphoma and leukemia showed positive associations with pesticide exposure" and thus concluded that cosmetic use of pesticides should be decreased.[2] Strong evidence also exists for other negative outcomes from pesticide exposure including neurological problems, birth defects, fetal death,[3] and neurodevelopmental disorder.[4]

According to The Stockholm Convention on Persistent Organic Pollutants, 9 of the 12 most dangerous and persistent chemicals are pesticides.[5][6]

Acute effects

Vorlage:Main article Acute health problems may occur in workers that handle pesticides, such as abdominal pain, dizziness, headaches, nausea, vomiting, as well as skin and eye problems.[7] In China, an estimated half million people are poisoned by pesticides each year, 500 of whom die.[8] Pyrethrins, insecticides commonly used in common bug killers, can cause a potentially deadly condition if breathed in.[9]

Long-term effects

Cancer

Many studies have examined the effects of pesticide exposure on the risk of cancer. Associations have been found with: leukemia, lymphoma, brain, kidney, breast, prostate, pancreas, liver, lung, and skin cancers.[6] This increased risk occurs with both residential and occupational exposures.[6] Increased rates of cancer have been found among farm workers who apply these chemicals.[10] A mother's occupational exposure to pesticides during pregnancy is associated with an increases in her child's risk of leukemia, Wilms' tumor, and brain cancer.[6][11] Exposure to insecticides within the home and herbicides outside is associated with blood cancers in children.[12]

Neurological

Evidence links pesticide exposure to worsened neurological outcomes.[3]

The United States Environmental Protection Agency finished a 10-year review of the organophosphate pesticides following the 1996 Food Quality Protection Act, but did little to account for developmental neurotoxic effects, drawing strong criticism from within the agency and from outside researchers.[13][14] Comparable studies have not been done with newer pesticides that are replacing organophosphates.[15]

Reproductive effects

Strong evidence links pesticide exposure to birth defects, fetal death and altered fetal growth.[3] Agent Orange, a 50:50 mixture of 2,4,5-T and 2,4-D, has been associated with bad health and genetic effects in Malaya and Vietnam.[16][17] It was also found that offspring that were at some point exposed to pesticides had a low birth weight and had developmental defects.[18]

Fertility

A number of pesticides including dibromochlorophane and 2,4-D has been associated with impaired fertility in males.[19] Pesticide exposure resulted in reduced fertility in males, genetic alterations in sperm, a reduced number of sperm, damage to germinal epithelium and altered hormone function.[20]

Other

Some studies have found increased risks of dermatitis in those exposed.[3]

Additionally, studies have indicated that pesticide exposure is associated with long-term respiratory problems.[21] Summaries of peer-reviewed research have examined the link between pesticide exposure and neurologic outcomes and cancer, perhaps the two most significant things resulting in organophosphate-exposed workers.[22][23]

According to researchers from the National Institutes of Health (NIH), licensed pesticide applicators who used chlorinated pesticides on more than 100 days in their lifetime were at greater risk of diabetes. One study found that associations between specific pesticides and incident diabetes ranged from a 20 percent to a 200 percent increase in risk. New cases of diabetes were reported by 3.4 percent of those in the lowest pesticide use category compared with 4.6 percent of those in the highest category. Risks were greater when users of specific pesticides were compared with applicators who never applied that chemical.[24][25]

Route of exposure

People can be exposed to pesticides by a number of different routes including: occupation, in the home, at school and in their food.

There are concerns that pesticides used to control pests on food crops are dangerous to people who consume those foods. These concerns are one reason for the organic food movement. Many food crops, including fruits and vegetables, contain pesticide residues after being washed or peeled. Chemicals that are no longer used but that are resistant to breakdown for long periods may remain in soil and water and thus in food.[26]

The United Nations Codex Alimentarius Commission has recommended international standards for maximum residue limits (MRLs), for individual pesticides in food.[27]

In the EU, MRLs are set by DG-SANCO.

In the United States, levels of residues that remain on foods are limited to tolerance levels that are established by the U.S. Environmental Protection Agency and are considered safe.[28] The EPA sets the tolerances based on the toxicity of the pesticide and its breakdown products, the amount and frequency of pesticide application, and how much of the pesticide (i.e., the residue) remains in or on food by the time it is marketed and prepared.[29] Tolerance levels are obtained using scientific risk assessments that pesticide manufacturers are required to produce by conducting toxicological studies, exposure modeling and residue studies before a particular pesticide can be registered, however, the effects are tested for single pesticides, and there is little information on possible synergistic effects of exposure to multiple pesticide traces in the air, food and water.[30]

Strawberries and tomatoes are the two crops with the most intensive use of soil fumigants. They are particularly vulnerable to several type of diseases, insects, mites, and parasitic worms. In 2003, in California alone, 3.7 million pounds (1,700 metric tons) of metham sodium were used on tomatoes. In recent years other farmers have demonstrated that it is possible to produce strawberries and tomatoes without the use of harmful chemicals and in a cost-effective way.[31]

Exposure routes other than consuming food that contains residues, in particular pesticide drift, are potentially significant to the general public.[32]

Some pesticides can remain in the environment for prolonged periods of time. For example, most people in the United States still have detectable levels of DDT in their bodies even though it was banned in the US in 1972.[6]

Prevention

Pesticides exposure cannot be studied in placebo controlled trials as this would be unethical.[3] A definitive cause effect relationship therefore cannot be established.[3] Consistent evidence can and has been gathered through other study designs.[3] The precautionary principle is thus frequently used in environmental law such that absolute proof is not required before efforts to decrease exposure to potential toxins are enacted.[33]

The American Medical Association recommend limiting exposure to pesticides.[34] They came to this conclusion due to the fact that surveillance systems currently in place are inadequate to determine problems related to exposure.[34] The utility of applicator certification and public notification programs are also of unknown value in their ability to prevent adverse outcomes.[34]

Epidemiology

The World Health Organization and the UN Environment Programme estimate that each year, 3 million workers in agriculture in the developing world experience severe poisoning from pesticides, about 18,000 of whom die.[35] According to one study, as many as 25 million workers in developing countries may suffer mild pesticide poisoning yearly.[36] Detectable levels of 50 different pesticides were found in the blood of a representative sample of the U.S. population.[6]

Society and culture

Concerns regarding conflict of interests regarding the research base have been raised. A number of researchers involved with pesticides have been found to have undisclosed ties to industry including: Richard Doll or the Imperial Cancer Research Fund in England and Hans-Olov Adami of the Karolinska Institute in Sweden.[37]

Other animals

System-search.svg⧼Seealso⧽Lua-Fehler in package.lua, Zeile 80: module 'strict' not foundPesticide toxicity to bees.

A number of pesticides including clothianidin, dinotefuran, imidacloprid are toxic to bees.[38] Exposure to pesticides may be one of the contributory factors to colony collapse disorder.[39] A study in North Carolina indicated that more than 30 percent of the quail tested were made sick by one aerial insecticide application. Once sick, wild birds may neglect their young, abandon their nests, and become more susceptible to predators or disease.[40]

See also

References

Vorlage:Reflist

Vorlage:Pesticides Vorlage:Health effects of food, drink and lifestyle

Category:Health effects by subject Category:Pesticides

  1. ↑ U.S. Environmental Protection Agency (August 30, 2007), Pesticides: Health and Safety. National Assessment of the Worker Protection Workshop #3.
  2. ↑ Cancer health effects of pesticides: systematic review. In: Can Fam Physician. 53, Nr. 10, October 2007, S. 1704–11. PMID 17934034. PMC 2231435 (freier Volltext).
  3. ↑ a b c d e f g Non-cancer health effects of pesticides: systematic review and implications for family doctors. In: Can Fam Physician. 53, Nr. 10, October 2007, S. 1712–20. PMID 17934035. PMC 2231436 (freier Volltext).
  4. ↑ Prenatal and childhood exposure to pesticides and neurobehavioral development: review of epidemiological studies. In: Int J Occup Med Environ Health. 21, Nr. 2, 2008, S. 121–32. doi:10.2478/v10001-008-0014-z. PMID 18614459.
  5. ↑ What are POPs?. Pops.int. Abgerufen am 4. Februar 2014.
  6. ↑ a b c d e f Pesticides and health risks. In: J Obstet Gynecol Neonatal Nurs. 39, Nr. 1, 2010, S. 103–10. doi:10.1111/j.1552-6909.2009.01092.x. PMID 20409108.
  7. ↑ Ecobichon DJ. 1996. Toxic effects of pesticides. In: Casarett and Doull's Toxicology: The Basic Science of Poisons (Klaassen CD, Doull J, eds). 5th ed. New York:MacMillan, 643–689.
  8. ↑ Lawrence, Dune (February 13, 2007), Chinese develop taste for organic food: Higher cost no barrier to safer eating. Bloomberg News, International Herald Tribune Retrieved on 2007-10-25.
  9. ↑ Medline Plus (May 17, 2006), Medical Encyclopedia: Insecticide. Retrieved on September 15, 2007.
  10. ↑ Studying health outcomes in farmworker populations exposed to pesticides. In: Environmental Health Perspectives. 114, Nr. 3, 2006, S. 953–960. doi:10.1289/ehp.8526. Abgerufen am 15. September 2007.
  11. ↑ Childhood leukaemia and parental occupational exposure to pesticides: a systematic review and meta-analysis. In: Cancer Causes Control. 21, Nr. 6, June 2010, S. 787–809. doi:10.1007/s10552-010-9516-7. PMID 20467891.
  12. ↑ M Chen, CH Chang, L Tao, C Lu: Residential Exposure to Pesticide During Childhood and Childhood Cancers: A Meta-Analysis.. In: Pediatrics. 136, Nr. 4, October 2015, S. 719–29. doi:10.1542/peds.2015-0006. PMID 26371195.
  13. ↑ Phillips ML: Registering skepticism: does the EPA's pesticide review protect children?. In: ENVIRONMENTAL HEALTH PERSPECTIVES. 114, Nr. 10, 2006, S. A592–A595. doi:10.1289/ehp.114-a592. PMID 17035127. PMC 1626397 (freier Volltext).
  14. ↑ Pulaski A (May 26, 2006), EPA workers blast agency's rulings on deadly pesticides: Letter sent to EPA administrator Stephen L. Johnson by unions representing 9,000 EPA scientists. The Oregonian, Mindfully.org Retrieved on 2007-10-10.
  15. ↑ A. Mascarelli: Growing Up with Pesticides. In: Science. 341, Nr. 6147, 2013, S. 740–741. doi:10.1126/science.341.6147.740.
  16. ↑ Association between Agent Orange and birth defects: systematic review and meta-analysis. In: Int J Epidemiol. 35, Nr. 5, October 2006, S. 1220–30. doi:10.1093/ije/dyl038. PMID 16543362.
  17. ↑ Paternal exposure to Agent Orange and spina bifida: a meta-analysis. In: Eur. J. Epidemiol.. 25, Nr. 1, 2010, S. 37–44. doi:10.1007/s10654-009-9401-4. PMID 19894129.
  18. ↑ Pesticide exposure: the hormonal function of the female reproductive system disrupted?. In: Reproductive Biology and Endocrinology. 4, Nr. 1, 2006, ISSN 1477-7827, S. 30. doi:10.1186/1477-7827-4-30. PMID 16737536. PMC 1524969 (freier Volltext).
  19. ↑ Effect of occupational exposures on male fertility: literature review. In: Ind Health. 41, Nr. 2, April 2003, S. 55–62. doi:10.2486/indhealth.41.55. PMID 12725464.
  20. ↑ Environmental Impacts on Reproductive Health: Pesticides.
  21. ↑ E Doust, JG Ayres, G Devereux, F Dick, JO Crawford, H Cowie, K Dixon: Is pesticide exposure a cause of obstructive airways disease?. In: European respiratory review : an official journal of the European Respiratory Society. 23, Nr. 132, June 2014, S. 180–92. doi:10.1183/09059180.00005113. PMID 24881073.
  22. ↑ Health effects of chronic pesticide exposure: cancer and neurotoxicity. In: Annu Rev Public Health. 25, 2004, S. 155–97. doi:10.1146/annurev.publhealth.25.101802.123020. PMID 15015917.
  23. ↑ Association of pesticide exposure with neurologic dysfunction and disease. In: Environ. Health Perspect.. 112, Nr. 9, June 2004, S. 950–8. doi:10.1289/ehp.7135. PMID 15198914. PMC 1247187 (freier Volltext).
  24. ↑ Incident diabetes and pesticide exposure among licensed pesticide applicators: Agricultural Health Study, 1993–2003. In: Am J Epidemiol.. 167, Nr. 10, May 2008, S. 235–46.. doi:10.1093/aje/kwn028. PMID 18343878. PMC 2832308 (freier Volltext).
  25. ↑ Newswise: Long-term Pesticide Exposure May Increase Risk of Diabetes Retrieved on June 4, 2008.
  26. ↑ Cornell University, College of Veterinary Medicine (March 1999), Consumer concerns about pesticides in food. Fact Sheet #24. Retrieved on 2007-10-25.
  27. ↑ Codex Alimentarius Commission Code of Ethics for International Trade in Food. CAC/RCP 20-1979 (Rev. 1-1985). Retrieved on 2007-10-25.
  28. ↑ U.S. Environmental Protection Agency (March 27, 2007), Pesticides and food: What the pesticide residue limits are on food. epa.gov. Retrieved on September 15, 2007.
  29. ↑ U.S. Environmental Protection Agency (July 24, 2007), Setting tolerances for pesticide residues in foods. epa.gov. Retrieved on September 15, 2007.
  30. ↑ Rabideau, Christine L. Multiple pesticide exposure: Immunotoxicty and oxidative tress 2001
  31. ↑ Levine, Marvin J.: Pesticides: A Toxic Time Bomb in our Midst. Praeger Publishers, 2007, ISBN 978-0-275-99127-2, S. 213–214.
  32. ↑ U.S. Environmental Protection Agency (December 1999), Spray drift of pesticides. Retrieved on September 15, 2007.
  33. ↑ Lockwood AH: Pesticides and parkinsonism: is there an etiological link?. In: Curr. Opin. Neurol.. 13, Nr. 6, December 2000, S. 687–90. doi:10.1097/00019052-200012000-00013. PMID 11148671.
  34. ↑ a b c Educational and informational strategies to reduce pesticide risks. Council on Scientific Affairs. In: Prev Med. 26, Nr. 2, 1997, S. 191–200. doi:10.1006/pmed.1996.0122. PMID 9085387.
  35. ↑ Miller GT (2004), Sustaining the Earth, 6th edition. Thompson Learning, Inc. Pacific Grove, California. Chapter 9, Pages 211-216.
  36. ↑ Jeyaratnam J: Acute pesticide poisoning: a major global health problem. In: World Health Stat Q. 43, Nr. 3, 1990, S. 139–44. PMID 2238694.
  37. ↑ Secret ties to industry and conflicting interests in cancer research. In: Am. J. Ind. Med.. 50, Nr. 3, March 2007, S. 227–33. doi:10.1002/ajim.20357. PMID 17086516.
  38. ↑ Ecotoxicity of neonicotinoid insecticides to bees. In: Adv. Exp. Med. Biol.. 683, 2010, S. 85–95. doi:10.1007/978-1-4419-6445-8_8. PMID 20737791.
  39. ↑ Myrna E. Watanabe‌: Colony Collapse Disorder: Many Suspects, No Smoking Gun. In: BioScience. 58, Nr. 5, May 2008, S. 384–388. doi:10.1641/B580503.
  40. ↑ Wildlife & Pesticides - Corn.
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