Pesticide toxicity
A sign warning about potential pesticide exposure.
SpecialtyEmergency medicine, toxicology

Health effects of pesticides may be acute or delayed in those who are exposed.[1] Acute effects can include pesticide poisoning, which may be a medical emergency.[2] Strong evidence exists for other, long-term negative health outcomes from pesticide exposure including birth defects, fetal death,[3] neurodevelopmental disorder,[4] cancer, and neurologic illness including Parkinson's disease.[5] Toxicity of pesticides depend on the type of chemical, route of exposure, dosage, and timing of exposure.[5]

According to The Stockholm Convention on Persistent Organic Pollutants (2001), 9 of the 12 most dangerous and persistent chemicals were pesticides,[6][7] so many have now been withdrawn from use.

Route of exposure

People can be exposed to pesticides, which include insecticides, herbicides, fungicides, by a number of different routes including: occupation, in the home, at school, in the air, water, soil, and in food. Almost all humans are exposed to some level of pesticides.[5] For example, pesticide drift, may be a potentially significant source of exposure to the general public.[8] Exposure can occur via ingestion, inhalation, or contact with skin.[9] Some pesticides can remain in the environment for prolonged periods of time.

There are concerns that pesticides used to control pests on food crops are dangerous to people who consume those foods. Many food crops, including fruits and vegetables, contain pesticide residues even 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.[10] For example, most people in the United States still have detectable levels of dichlorodiphenyltrichloroethane (DDT), an insecticide, despite its ban in the US in 1972.[7] These concerns are one reason for the organic food movement. In California, 92% of farmworkers are Latino[11] and exposure to pesticides in majority-Latino counties of the state to pesticides is 906% higher than counties in which the Latino population is fewer than 24%. This has raised concerns over environmental justice.[12]

Because of the common use of pesticides in agriculture, the United Nations Codex Alimentarius Commission has recommended international standards for maximum residue limits (MRLs), for individual pesticides in food.[13] In the United States, levels of residues permitted to remain on foods are limited based on tolerance levels considered to be safe as established by the U.S. Environmental Protection Agency (EPA).[14] The EPA sets the permitted levels of pesticide residues based on the toxicity of the pesticide, 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 distributed.[15] Tolerance levels are obtained using scientific risk assessments that pesticide manufacturers are required to conduct—assessments include toxicological studies, exposure modeling and residue studies before a particular pesticide can be registered. However, the effects are tested a single pesticide at a time and there is little information on the possible synergistic effects of exposure to multiple pesticide traces in the air, food and water on human health.[16]

While pesticide use is commonly associated with agriculture, pesticides are also used as part of public health interventions to control vector-borne diseases (e.g. malaria and Dengue fever) and unwanted plants in the landscaping of parks and gardens.[5]

Mechanism of action

Pesticides are designed to kill living organisms and vary in their mechanisms of action, depending on their class. The major classes of pesticides are organochlorines (OCPs) or persistent organic pollutants (POPs), organophosphates, carbamates, phyrethroids, and triazines. While all pesticides have been shown to have effects on human health, OCPs are notable for significant risk for adverse effects as they dissolve in fatty tissues and can, thus, accumulate to harmful levels in these tissues. For example, some OCPs are structurally similar to estrogen and can mimic the effects of endogenous estrogen via binding to the estrogen receptors.[5] These pesticides exhibit their toxic effects by interfering with hormonal homeostasis, resulting in hormonal dysregulation. This promotes abnormal growth and development of reproductive tissues and can lead to cancer or harmful effects on reproductive health.[9] OCPs or POPs, which were used in agricultural practices in the 1950s, have now been banned in most countries. However, their breakdown products are persistent and can still be found in soil.[17]

Pesticides can also exert their adverse effects on human health by acting on cell receptors and ion channels, suppressing key signal pathways in cells, and by affecting DNA methylation and histone modifications, thus resulting in changes in gene expression and cellular function.[17]

Acute effects

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.[18] In China, an estimated half-million people are poisoned by pesticides each year, 500 of whom die.[19] Pyrethrins, insecticides commonly used in common bug killers, can cause a potentially deadly condition if breathed in.[20]

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, stomach, esophageal, and skin cancers.[7][21] This increased risk occurs with both residential and occupational exposures.[7] Increased rates of cancer have been found among farm workers who apply these chemicals.[22] Studies suggest an association between carbamate exposure and glioma and meningioma, glyphosate exposure and diffuse large B-cell lymphoma, as well as alachlor exposure and laryngeal cancer.[23] 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.[7][24] Exposure to insecticides within the home and herbicides outside is associated with blood cancers in children.[25] 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.[26]

The suggested molecular mechanism for association of pesticide exposure and cancer development is damage to genetic materials such as chromosomes, DNA, and histone proteins, or damage to cell organelles such as endoplasmic reticulum, mitochondria, endocrine networks, and nuclear receptors.[21]

Neurological

There is accumulating evidence of neurological effects secondary to pesticide exposure. Acute exposure to high levels of pesticides that affect the central nervous system can cause neurotoxicity, including cognitive and motor changes.[27][3] In-utero and early-childhood exposure to organophosphates can cause neurodevelopmental impairment,[3][28][29] in particular because some pesticides and their metabolites cross the placenta and fetal blood-brain-barrier, which has not fully developed in a fetus.[29] In addition, an accumulation of chronic exposure has been associated with an increased risk of developing neurodegenerative disease later in life.[3][28][21] There is strong evidence that chronic exposure to pesticides increases risk of developing Parkinson’s disease, potentially through direct toxic effects on dopaminergic neurons (which are depleted in Parkinson’s disease).[28] In addition, there is increasing evidence that chronic exposure increases risk of Alzheimer’s disease.[28][21] A review of multiple studies that looked at high pesticide exposure, mainly organophosphates, among agricultural workers further suggested neurological consequences for such exposures.[23] High pesticide exposure is associates with neurologic, neuropsychiatric, and neurodegenerative disorders among agricultural workers who apply the pesticides.[23][21] The reported disorders are: ADHD, depression, anxiety, dizziness, headaches and olfactory impairment (which was used as an early indicator for neurodegenerative disorders).[23]

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.[30][31] Comparable studies have not been done with newer pesticides that are replacing organophosphates.[32]

Reproductive effects

Many pesticides act as endocrine-disrupting chemicals (EDC) or substances that interfere with normal hormonal activity.[33] As of 2013, 101 pesticides have been listed as proven or possible endocrine disruptors. As such, high levels of and/or long-term exposure to pesticides can impact reproductive health and is associated with decreased fertility, increased rates of miscarriage, and changes in pattern of maturity. Specifically, triazines, organs-chlorine, and carbamate insecticides have anti-androgenic effects impacting males, resulting in the lack of development of male characteristics including decreases in testicular size, sperm production, and androgen production.[21] A number of pesticides including dibromochlorophane and 2,4-D has been associated with impaired fertility in males.[34] 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.[35] 

The effects of endocrine disruption is dependent on the timing of pesticide exposure (for example, during embryogenesis in early pregnancy or in infancy) as windows of varying susceptibility dictate disease manifestation.[33] Several studies suggest that higher levels of pesticides in the blood of the mother is associated with longer time to pregnancy and greater infertility rates. For example, in mothers and/or their partners who reported pesticide exposure, there was an increased risk of miscarriage with the strongest association with exposure during the first three weeks of pregnancy. This is perhaps linked to the possible negative impact of pesticides on oocyte development and fertilization. Similarly, studies evaluating the short-term impact of occupational exposure to a variety of pesticides on reproductive health suggest that pesticides can have deleterious effects on sperm—pesticide exposure, associated with decreased sperm motility, defects in sperm morphology and semen volume. However, the long-term impacts of pesticide exposure on spermatogenesis and fertility are unknown.[29]

Because some pesticides and their resulting metabolites can cross the placenta and, therefore, the blood-brain-barrier, they can also impact development of the fetus; strong evidence links pre- and post-natal exposures to pesticides to congenital disorders, including physical and/or mental disabilities, fetal death and altered fetal growth.[3][29][21] Perhaps the more widely known health effect of pesticides is the elevated rate of birth defects in areas in Vietnam sprayed with defoliant or Agent Orange, a 50:50 mixture of 2,4,5-T and 2,4-D, which has been associated with bad health and genetic effects in Malaya and Vietnam.[36][37][21] It was also found that offspring who were at some point exposed to pesticides had a low birth weight and had developmental defects.[38] Maternal exposure to pesticides has also been linked to higher incidence of hypospadias in the newborn, which is the abnormal opening of the urethra in males.[21]

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.[39] A significant association was found between exposure to pesticides and decreased lung function along with related airway symptoms.[23] Studies have suggested an association between exposure to pesticides and airway symptoms such as wheezing, cough, shortness of breath, runny nose, sore or irritation of throat, and difficulty breathing.[23][40] Decreased lung function was associated with occupational exposure to pesticides. Studies have suggested a correlation between inhibition of cholinesterase by pesticides like carbamate and organophosphate and reduction or impairment of lung function.[40] In addition, exposure to pesticides was also reported to be linked with obstructive and restrictive lung conditions. Specifically, organophosphate exposure was associated with lung function decline driven by a restrictive process.[40]

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.[41][42]

There is increasing evidence that possibly suggests increased risk of development of type 2 diabetes with exposure to pesticides and their metabolites.[9]

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.[43]

The American Medical Association recommend limiting exposure to pesticides.[44] They came to this conclusion due to the fact that surveillance systems currently in place are inadequate to determine problems related to exposure.[44] The utility of applicator certification and public notification programs are also of unknown value in their ability to prevent adverse outcomes.[44]

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.[45] According to one study, as many as 25 million workers in developing countries may suffer mild pesticide poisoning yearly.[46] Detectable levels of 50 different pesticides were found in the blood of a representative sample of the U.S. population.[7]

Research conflicts of interest

Concerns regarding conflict of interests regarding the research base have been raised for some research into toxicity of pesticides. For example, Richard Doll of the Imperial Cancer Research Fund in England was found to have undisclosed ties to industry funding.[47][48]

Other animals

A number of pesticides including the neonicotinoids clothianidin, dinotefuran, imidacloprid are toxic to bees.[49] Exposure to pesticides may be one of the contributory factors to colony collapse disorder.[50] 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.[51]

See also

References

  1. ↑ U.S. Environmental Protection Agency (August 30, 2007), Pesticides: Health and Safety. National Assessment of the Worker Protection Workshop #3.
  2. ↑ Eddleston M, Buckley NA, Eyer P, Dawson AH (February 2008). "Management of acute organophosphorus pesticide poisoning". Lancet. 371 (9612): 597–607. doi:10.1016/S0140-6736(07)61202-1. PMC 2493390. PMID 17706760.
  3. 1 2 3 4 5 6 7 8 9 Sanborn M, Kerr KJ, Sanin LH, Cole DC, Bassil KL, Vakil C (October 2007). "Non-cancer health effects of pesticides: systematic review and implications for family doctors". Canadian Family Physician. 53 (10): 1712–1720. PMC 2231436. PMID 17934035.
  4. ↑ Jurewicz J, Hanke W (2008). "Prenatal and childhood exposure to pesticides and neurobehavioral development: review of epidemiological studies". International Journal of Occupational Medicine and Environmental Health. 21 (2): 121–132. doi:10.2478/v10001-008-0014-z. PMID 18614459.
  5. 1 2 3 4 5 Kim KH, Kabir E, Jahan SA (January 2017). "Exposure to pesticides and the associated human health effects". The Science of the Total Environment. 575: 525–535. Bibcode:2017ScTEn.575..525K. doi:10.1016/j.scitotenv.2016.09.009. PMID 27614863.
  6. ↑ "What are POPs?". Pops.int. Archived from the original on 2014-04-16. Retrieved 2014-02-04.
  7. 1 2 3 4 5 6 Gilden RC, Huffling K, Sattler B (2010). "Pesticides and health risks". Journal of Obstetric, Gynecologic, and Neonatal Nursing (Review). 39 (1): 103–110. doi:10.1111/j.1552-6909.2009.01092.x. PMID 20409108.
  8. ↑ U.S. Environmental Protection Agency (December 1999), Spray drift of pesticides. Retrieved on September 15, 2007.
  9. 1 2 3 Yilmaz B, Terekeci H, Sandal S, Kelestimur F (March 2020). "Endocrine disrupting chemicals: exposure, effects on human health, mechanism of action, models for testing and strategies for prevention". Reviews in Endocrine & Metabolic Disorders. 21 (1): 127–147. doi:10.1007/s11154-019-09521-z. PMID 31792807. S2CID 208539785.
  10. ↑ Cornell University, College of Veterinary Medicine (March 1999), Consumer concerns about pesticides in food. Fact Sheet #24. Retrieved on 2007-10-25.
  11. ↑ "Farmworkers in California: A Brief Introduction" (PDF). CRB Short Subjects. October 2013.
  12. ↑ "Pesticide use in California remains at record high, new data show | Pesticide Action Network". www.panna.org. Retrieved 2022-12-30.
  13. ↑ Codex Alimentarius Commission Code of Ethics for International Trade in Food Archived 2012-02-29 at the Wayback Machine. CAC/RCP 20-1979 (Rev. 1-1985). Retrieved on 2007-10-25.
  14. ↑ 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.
  15. ↑ U.S. Environmental Protection Agency (July 24, 2007), Setting tolerances for pesticide residues in foods. epa.gov. Retrieved on September 15, 2007.
  16. ↑ Rabideau, Christine L. Multiple pesticide exposure: Immunotoxicty and oxidative stress 2001
  17. 1 2 Kalyabina VP, Esimbekova EN, Kopylova KV, Kratasyuk VA (2021). "Pesticides: formulants, distribution pathways and effects on human health - a review". Toxicology Reports. 8: 1179–1192. doi:10.1016/j.toxrep.2021.06.004. PMC 8193068. PMID 34150527.
  18. ↑ 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.
  19. ↑ 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.
  20. ↑ Medline Plus (May 17, 2006), Medical Encyclopedia: Insecticide. Retrieved on September 15, 2007.
  21. 1 2 3 4 5 6 7 8 9 Mostafalou S, Abdollahi M (April 2013). "Pesticides and human chronic diseases: evidences, mechanisms, and perspectives". Toxicology and Applied Pharmacology. 268 (2): 157–177. doi:10.1016/j.taap.2013.01.025. PMID 23402800. S2CID 8523721.
  22. ↑ McCauley LA, Anger WK, Keifer M, Langley R, Robson MG, Rohlman D (June 2006). "Studying health outcomes in farmworker populations exposed to pesticides". Environmental Health Perspectives. 114 (6): 953–960. doi:10.1289/ehp.8526. PMC 1480483. PMID 16760000. Archived from the original on 2007-09-27. Retrieved 2007-09-15.
  23. 1 2 3 4 5 6 Curl CL, Spivak M, Phinney R, Montrose L (March 2020). "Synthetic Pesticides and Health in Vulnerable Populations: Agricultural Workers". Current Environmental Health Reports. 7 (1): 13–29. doi:10.1007/s40572-020-00266-5. PMC 7035203. PMID 31960353.
  24. ↑ Van Maele-Fabry G, Lantin AC, Hoet P, Lison D (June 2010). "Childhood leukaemia and parental occupational exposure to pesticides: a systematic review and meta-analysis". Cancer Causes & Control. 21 (6): 787–809. doi:10.1007/s10552-010-9516-7. PMID 20467891. S2CID 36791309.
  25. ↑ Chen M, Chang CH, Tao L, Lu C (October 2015). "Residential Exposure to Pesticide During Childhood and Childhood Cancers: A Meta-Analysis". Pediatrics. 136 (4): 719–729. doi:10.1542/peds.2015-0006. PMID 26371195.
  26. ↑ Bassil KL, Vakil C, Sanborn M, Cole DC, Kaur JS, Kerr KJ (October 2007). "Cancer health effects of pesticides: systematic review". Canadian Family Physician. 53 (10): 1704–1711. PMC 2231435. PMID 17934034.
  27. ↑ Richardson JR, Fitsanakis V, Westerink RH, Kanthasamy AG (September 2019). "Neurotoxicity of pesticides". Acta Neuropathologica. 138 (3): 343–362. doi:10.1007/s00401-019-02033-9. PMC 6826260. PMID 31197504.
  28. 1 2 3 4 Rani L, Thapa K, Kanojia N, Sharma N, Singh S, Grewal AS, et al. (2021-02-10). "An extensive review on the consequences of chemical pesticides on human health and environment". Journal of Cleaner Production. 283: 124657. doi:10.1016/j.jclepro.2020.124657. ISSN 0959-6526. S2CID 225137646.
  29. 1 2 3 4 Fucic A, Duca RC, Galea KS, Maric T, Garcia K, Bloom MS, et al. (June 2021). "Reproductive Health Risks Associated with Occupational and Environmental Exposure to Pesticides". International Journal of Environmental Research and Public Health. 18 (12): 6576. doi:10.3390/ijerph18126576. PMC 8296378. PMID 34207279.
  30. ↑ Phillips ML (October 2006). "Registering skepticism: does the EPA's pesticide review protect children?". Environmental Health Perspectives. 114 (10): A592–A595. doi:10.1289/ehp.114-a592. PMC 1626397. PMID 17035127.
  31. ↑ 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 Archived 2006-10-05 at the Wayback Machine. The Oregonian, Mindfully.org Retrieved on 2007-10-10.
  32. ↑ Mascarelli A (August 2013). "Growing up with pesticides". Science. 341 (6147): 740–741. doi:10.1126/science.341.6147.740. PMID 23950529.
  33. 1 2 Zlatnik MG (July 2016). "Endocrine-Disrupting Chemicals and Reproductive Health". Journal of Midwifery & Women's Health. 61 (4): 442–455. doi:10.1111/jmwh.12500. PMC 6701840. PMID 27391253.
  34. ↑ Sheiner EK, Sheiner E, Hammel RD, Potashnik G, Carel R (April 2003). "Effect of occupational exposures on male fertility: literature review". Industrial Health. 41 (2): 55–62. doi:10.2486/indhealth.41.55. PMID 12725464.
  35. ↑ "Environmental Impacts on Reproductive Health: Pesticides". 29 August 2022.
  36. ↑ Ngo AD, Taylor R, Roberts CL, Nguyen TV (October 2006). "Association between Agent Orange and birth defects: systematic review and meta-analysis". International Journal of Epidemiology. 35 (5): 1220–1230. doi:10.1093/ije/dyl038. PMID 16543362.
  37. ↑ Ngo AD, Taylor R, Roberts CL (2010). "Paternal exposure to Agent Orange and spina bifida: a meta-analysis". European Journal of Epidemiology. 25 (1): 37–44. doi:10.1007/s10654-009-9401-4. PMID 19894129. S2CID 9066329.
  38. ↑ Bretveld RW, Thomas CM, Scheepers PT, Zielhuis GA, Roeleveld N (May 2006). "Pesticide exposure: the hormonal function of the female reproductive system disrupted?". Reproductive Biology and Endocrinology. 4 (1): 30. doi:10.1186/1477-7827-4-30. PMC 1524969. PMID 16737536.
  39. ↑ Doust E, Ayres JG, Devereux G, Dick F, Crawford JO, Cowie H, Dixon K (June 2014). "Is pesticide exposure a cause of obstructive airways disease?". European Respiratory Review. 23 (132): 180–192. doi:10.1183/09059180.00005113. PMC 9487561. PMID 24881073.
  40. 1 2 3 Ye M, Beach J, Martin JW, Senthilselvan A (November 2013). "Occupational pesticide exposures and respiratory health". International Journal of Environmental Research and Public Health. 10 (12): 6442–6471. doi:10.3390/ijerph10126442. PMC 3881124. PMID 24287863.
  41. ↑ Alavanja MC, Hoppin JA, Kamel F (2004). "Health effects of chronic pesticide exposure: cancer and neurotoxicity". Annual Review of Public Health. 25: 155–197. doi:10.1146/annurev.publhealth.25.101802.123020. PMID 15015917.
  42. ↑ Kamel F, Hoppin JA (June 2004). "Association of pesticide exposure with neurologic dysfunction and disease". Environmental Health Perspectives. 112 (9): 950–958. doi:10.1289/ehp.7135. PMC 1247187. PMID 15198914.
  43. ↑ Lockwood AH (December 2000). "Pesticides and parkinsonism: is there an etiological link?". Current Opinion in Neurology. 13 (6): 687–690. doi:10.1097/00019052-200012000-00013. PMID 11148671.
  44. 1 2 3 "Educational and informational strategies to reduce pesticide risks. Council on Scientific Affairs". Preventive Medicine. 26 (2): 191–200. 1997. doi:10.1006/pmed.1996.0122. PMID 9085387.
  45. ↑ Miller GT (2004), Sustaining the Earth, 6th edition. Thompson Learning, Inc. Pacific Grove, California. Chapter 9, Pages 211-216.
  46. ↑ Jeyaratnam J (1990). "Acute pesticide poisoning: a major global health problem". World Health Statistics Quarterly. Rapport Trimestriel de Statistiques Sanitaires Mondiales. 43 (3): 139–144. PMID 2238694.
  47. ↑ Hardell L, Walker MJ, Walhjalt B, Friedman LS, Richter ED (March 2007). "Secret ties to industry and conflicting interests in cancer research". American Journal of Industrial Medicine. 50 (3): 227–233. doi:10.1002/ajim.20357. PMID 17086516.
  48. ↑ Boseley S (8 December 2006). "Renowned cancer scientist was paid by chemical firm for 20 years". theguardian.com. Retrieved 21 January 2018.
  49. ↑ Decourtye A, Devillers J (2010). "Ecotoxicity of Neonicotinoid Insecticides to Bees". Insect Nicotinic Acetylcholine Receptors. Advances in Experimental Medicine and Biology. Vol. 683. pp. 85–95. doi:10.1007/978-1-4419-6445-8_8. ISBN 978-1-4419-6444-1. PMID 20737791.
  50. ↑ Myrna E. Watanabe‌ (May 2008). "Colony Collapse Disorder: Many Suspects, No Smoking Gun". BioScience. 58 (5): 384–388. doi:10.1641/B580503.
  51. ↑ "Wildlife & Pesticides - Corn".

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