Review Article

Effect of Pesticides Exposure on Human Health and Reproductive Life

Sushil Kumar Upadhyay*

Department of Biotechnology, Maharishi Markandeshwar (Deemed to be University), India

Submission:July 22, 2019; Published:August 20, 2019

*Corresponding author:Sushil Kumar Upadhyay, Department of Biotechnology, Maharishi Markandeshwar (Deemed to be University), Mullana Ambala (Haryana), India

How to cite this article:Sushil Kumar Upadhyay. Effect of Pesticides Exposure on Human Health and Reproductive Life. J Complement Med Alt Healthcare. 2019; 10(2): 555782. DOI:10.19080/JCMAH.2019.10.555782

Abstract

The current study demonstrates the importance of exposure of man-made extrinsic factors, chemicals, pesticides on the human health, reproductive life, and patterns of conception and context of pregnancy in India. Significantly higher levels of pesticides with endocrine disrupting potential in cases indicate the possible role of these compounds as one of the causes of pregnancy loss in exposed female. Possibly, increased pesticide level appears to indicate increased levels of oxidative damage that has been associated with possible cause of recurrent miscarriage (RM), it may reflect indirect evidence of toxicity rather than direct cause. Further epidemiological studies with larger cross-sectional population need to be performed to clearly elucidate the role of endocrine disruption, polymorphism in metabolic susceptibility genes and genetic environmental interaction in association with reproductive life. This might be helpful in identifying subpopulation/individuals at higher risk.

Introduction

Introduction Pregnancy is a complex, heterogenous, biological phenomenon in which the embryo develops into a fetus within the female uterus. The entire process is a vital immunological paradox, where the semiallogeneic fetus survives by evading maternal immune recognition and is delivered after the completion of the gestational period. However, due to various etiological factors, the growing embryo that is unable to survive is expelled from the pregnant mother at different gestational ages and this is referred to as pregnancy loss or abortion. Based on the incidence of sporadic pregnancy loss, the incidence of recurrent pregnancy loss should be approximately 1 in 300 pregnancies. During the last several decades there have been widespread uses of potent substances that, although effective in their intended use, have also been suspected of being harmful to female reproductive health. Prolong exposure of mixture of environmental contaminants that may adversely affect health of human [1]. According to WHO conception loss occurs in 10 to 15% of all gestation cases, out of which 1-2% are recurrent [2,3].

Pesticides Exposure Perspective to Health and Reproductive Life

Multifactorial etiology of recurrent pregnancy loss is among the most studied, yet unresolved issue in modern gynecology [4]. Humans have a great risk of exposure of environmental chemicals or pesticides (organochlorines and organophosphate) through several pathways (ingestion, respiration, skin contact) used in agricultural settings, public health and individual households [5]. Organochlorine pesticides (OCps) are a structurally heterogeneous class of organic compounds composed primarily of carbon, hydrogen and several chlorine atoms per molecule. It bio-magnify through the food chain and due to slow biodegradation, it accumulate in the body and can remain in the body mainly the adipose tissues, from which it leads in to the bloodstream and finally secreted into breast milk as the main elimination pathway in mammals [6-8].

Organophosphate pesticides (OPPs) are a generic term to include all the insecticides containing phosphorus. They are all derived from phosphoric acid and are generally the most toxic of all pesticides to vertebrate animals [5,9]. Nervous system is the primary target of OPPs [10,11]. The long-term earlier epidemiologic studies revealed its linkage to higher risk of cancer development [5]. The consequences of such exposures on human health are complex and still poorly understood, making risk assessment of any toxic effects of chemical mixtures on human health uneasy [12]. Acute professional exposure to pesticides provided data showing a correlation with several human pathologies, including hepatotoxicity, immunotoxicity, increased risk of mainly hematopoietic, brain and cancers [13-15] neuro-degenerative diseases such as Parkinson’s disease [16,17], deficiencies in cerebral development or immunity [18] and reproductive defects [19].

Fundamental Concept of Pesticides Invasion

Pesticide residues are commonly present in food that is grown through intensive industrial farming Sutton [20], food products [21-24], as mixtures or cocktails [25] and individual components [26]. Farmed animals can also accumulate pesticides in the fat and muscles of the animals, some can also be found in the brain, liver, lungs and other offal from contaminated feed and from veterinary pesticide application [27,28]. Household exposure to pesticides is more and more described as a significant risk [29] but the most important source of contamination for the consumer remains food and cocktails of pesticides ingested every day. Moreover, over 25% of fruits, vegetables, and cereals are known to contain detectable residues of at least two pesticides and more than 300 different pesticides are known to contaminate food products [30]. The families of farmers living in agricultural areas may also have a slightly higher than average exposure to pesticides than other people [31]. This is particularly of concern for infants and children because they may be more vulnerable to the toxic effects of some pesticides than adults [32]. When pregnant women and nursing mothers are exposed to pesticides, their children may also be exposed [33,34].

Mechanism of Pesticides Toxicity

Several mechanisms of pesticide toxicity have been proposed, the most important appears to be oxidative stress which are induced by free radicals. Experimental investigations as well as clinical and epidemiological findings have provided evidence supporting the role of reactive oxygen metabolites or free radicals such as singlet oxygen, superoxide anions, hydrogen peroxide and hydroxyl radical in the etiology of recurrent pregnancy loss [35]. The toxicity of chemical raid on human oxidative stress is largely unknown, particularly how mixtures of pesticides by-products affect human toxicity. Restricting analyses to more homogeneous endpoints are important in characterizing human toxicity of pesticides, organophosphate [10,36-39]. The concentrations of a pesticide (chlorpyrifos) in umbilical cord blood were negatively associated with birth weight and length of infants born to low-income minority mothers in New York City before the year 2001 [40]. Another study reported that in utero revelation of organophosphate pesticides associated with adverse birth outcomes and neural development [41]. The yesteryears investigations by earlier workers have suggested that exposure to pesticides at work whilst pregnancy may lead to miscarriage or preterm birth, but the evidence is as yet inconclusive [41-46]. Therefore, the aim of the present literature survey and study to provide and outline for invasion, exposure, and pesticides levels and its effects to induced oxidative stress and their correlation with health, reproductive life and their consequences to sustainability and mankind.

Acknowledgement

Author is grateful to Head of Biotechnology, Maharishi Markandeshwar (Deemed to be University), Mullana-Ambala for continuous encouragement during compilation of the findings.

Conflicts of Interest

The author claims no conflicts of interest because nonfinancial support was received from any government, nongovernment agency or organization to conduct this research work.

References

1. Yolton K, Xu Y, Sucharew H, Succop P, Altaye M, et al. (2013) Impact of low-level gestational exposure to organophosphate pesticides on neurobehavior in early infancy: a prospective study. Env Hlth 12(1): 79.
2. Baek KH, Lee EJ, Kim YS (2007) Recurrent pregnancy loss: the key potential mechanisms. Trends Mol Med13(7): 310-317.
3. Branch DW, Gibson M, Silver RM (2010) Clinical practice. Recurrent miscarriage. N Engl J Med 363(18): 1740-1747.
4. Jaslow CR, Carney JL, Kutteh WH (2010) Diagnostic factors identified in 1020 women with two verses three or more pregnancy loss. Fertile Steril 93(4): 1234-1243.
5. George J, Shukla Y (2011) Pesticides and cancer: Insights into toxic proteomic-based findings. J Proteom 74(12): 2713-2722.
6. Tutudaki M, Tsakalof AK, Tsatsakis AM (2003) Hair analysis used to assess chronic exposure to the organophosphate diazinon: a model study with rabbits. Human Exp Toxicol 22(3): 159-164.
7. Perera FP, Rauh V, Whyatt RM, Tang D, Tsai WY, et al. (2005) A summary of recent findings on birth outcomes and developmental effects of prenatal ETS, PAH, and pesticide exposures. Neurotoxicol 26(4): 573-587.
8. Tsang HL, Wu S, Leung CKM, Tao S, Wong MH (2011) Body burden of POPs of Hong Kong residents, based on human milk, maternal and cord serum. Env Int 37(1): 142-151.
9. Gupta RC (2006) Toxicology of Organophosphate & Carbamate Compound. Elsevier Acad Press.
10. Li M, Chang PA, Li YX, Li W, Wu YJ (2003) Effects of organophosphates on cell proliferation and 45Ca uptake of neuroblastoma SH-SY5Y cells. Zhonghua Lao Dong Wei Sheng Zhi Ye Bing Za Zhi 21(3): 200-202.
11. Costa LG (2006) Current issues in organophosphate toxicology. Clin a Chim Acta 366(1-2): 1-13.
12. PAN (Pesticide Action Network) (2006) Pesticide action data base-regulation.
13. Purdue MP, Hoppin JA, Blair A, Dosemeci M, Alavanja MC (2007) Occupational exposure to organochlorine insecticides and cancer incidence in the agricultural health study. Int J Cancer 120(3): 642-649.
14. Mahajan R, Blair A, Lynch CF, Schroeder P, Hoppin JA, et al. (2006) Fonofos exposure and cancer incidence in the agricultural health study. Env Hlth Persp 114(12): 1838-1842.
15. Ruder AM, Waters MA, Carreón T, Butler MA, Davis King KE, et al. (2006) Brain Cancer Collaborative Study Group The Upper Midwest Health Study: a case-control study of primary intracranial gliomas in farm and rural residents. J Agric Saf Hlth 12(4): 255-274.
16. Alavanja MC, Hoppin JA, Kamel F (2004) Health effects of chronic pesticide exposure: cancer and neurotoxicity. Annu Rev Pbl Hlth 25: 155-197.
17. Chade AR, Kasten M, Tanner CM (2006) Nongenetic causes of Parkinson’s disease. J Neural Transm Suppl 70: 147-151.
18. Colosio C, Birindelli S, Corsini E, Galli CL, Maroni M (2005) Low level exposure to chemicals and immune system. Toxicol Appl Pharmacol 207(2): 320-328.
19. Nicolopoulou P, Stamanti P (2001) The impact of endocrine disrupters on the female reproductive system. Hum Reprod Update 7(3): 323-330.
20. Sutton P, Perron J, Giudice LC, Woodruff TJ (2011) Pesticides Matter. A primer for reproductive health physicians. Prog Reprod Hlth Env Univ California.
21. Wilkowska A, Biziuk M (2011) Determination of pesticide residues in food matrices using the QuEChERS methodology. Food Chem 125(3): 803-812.
22. Lozowicka B, Jankowska M, Kaczyński P (2012) Pesticide residues in Brassica vegetables and exposure assessment of consumers. Food Contl 25(2): 561-575.
23. Li W, Tai L, Liu J, Gai G, Ding G (2014) Monitoring of pesticide residues levels in fresh vegetable from Hei bei Province, North China. Env Monit Assess 186(10): 6341-6349.
24. Yuan Y, Chen C, Zheng C, Wang X, Yang G, et al. (2014) Residue of chlorpyrifos and cypermethrin in vegetables and probabilistic exposure assessment for consumers in Zhejiang Province, China. Food Contrl 36(1): 63-68.
25. Fenik J, Tankiewicz M, Biziuk, M. (2011). Properties and determination of pesticides in fruits and vegetables. Trends Anal Chem 30(6): 814-826.
26. Reffstrup TK, Larsen JL, Meyer O (2010) Risk assessment of mixtures of pesticides: Current approaches and future strategies. Reg Toxicol Pharmacol 56(2): 174-192.
27. Schenck FJ, Donoghue DJ (2000) Determination of organochlorine and organophosphorus pesticide residues in eggs using a solid phase extraction clean-up. J Agri Food Chem 48(12): 6412-6415.
28. LeDoux M (2011) Analytical methods applied to the determination of pesticide residues in foods of animal origin: A review of the past two decades. J Chromato 1218(8): 1021-1036.
29. Abadi Korek I, Stark B, Zaizov R, Shaham J (2006) Parental occupational exposure and the risk of acute lymphoblastic leukemia in offspring in Israel. J Occup Environ Med 48(2): 165-174.
30. Weselak M, Arbuckle TE, Wigle DT, Krewski D (2007) In utero pesticide exposure and childhood morbidity. Env Res 103(3): 79-86
31. Naeher LP, Tulve NS, Egeghy PP, Barr DB, Adetona O, et al. (2010) Organophosphorus and pyrethroid insecticide urinary metabolite concentrations in young children living in a southeastern United States city. Sci Totl Env 408(5): 1145-1153.
32. Arcury TA, Grzywacz JG, Barr DB, Tapia J, Chen H, et al. (2007) Pesticide urinary metabolite levels of children in eastern North Carolina farmworker households. Env Hlth Persp 115(8): 1254-1260.
33. Weiss B (2000) Vulnerability of children and the developing brain to neurotoxic hazards. Env Hlth Persp 108: 375-381.
34. Holland N, Furlong C, Bastaki M, Richter R, Bradman A, et al. (2006) Paraoxonase polymorphisms, haplotypes, and enzyme activity in Latino mothers and newborns. Env Hlth Persp114(7): 985-991.
35. Kumar V, Singh S, Yadav CS, Ahmed RS, Gupta S, et al. (2010) CYP1A1 and CYP3A4 polymorphic variations in Delhi population of Northern India. Env Toxicol Pharmacol 29(2): 126-130.
36. Furlong CE (2007) Genetic variability in the cytochrome P450-paraoxonase 1 (PON1) pathway for detoxication of organophosphorus compounds. J Biochem Mol Toxicol 21(4): 197-205.
37. Richter RJ, Jarvik GP, Furlong CE (2009) Paraoxonase 1 PON1) status and substrate hydrolysis. Toxicol Appl Pharmacol 235(1): 1-9.
38. Tsatsakis AM, Androutsopoulos VP, Zafiropoulos A, Babatsikou F, Alegakis T, et al. (2011) Associations of xenobiotic metabolizing enzyme genotypes PON1Q192R, PON1L55M and CYP1A12A MspI with pathological symptoms of a rural population in south Greece. Xenobiot 41(10): 914-925.
39. Tsatsakis AM, Zafiropoulos A, Tzatzarakis MN, Tzanakakis GN, Kafatos A (2009) Relation of PON1 and CYP1A1 genetic polymorphisms to clinical findings in a cross-sectional study of a Greek rural population professionally exposed to pesticides. Toxicol Lett 186(1): 66-72.
40. Whyatt RM, Rauh V, Barr DB (2004) Prenatal insecticide exposures and birth weight and length among an urban minority cohort. Env Hlth Persp112(10): 1125-1132.
41. Huen K, Bradman A, Harley K, Yousefi P, Barr DB, et al. (2012) Organophosphate pesticide levels in blood and urine of women and newborns living in an agricultural community. Env Res 117: 8-16.
42. Gladen BC, Shkiryak Nyzhnyk ZA, Chyslovska N, Zadorozhnaja TD, Little RE (2003) Persistent organochlorine compounds and birth weight. Ann Epidemiol 13(3): 151-157.
43. Karmaus W, Zhu X (2004) Maternal concentration of polychlorinated biphenyls and dichlorodiphenyl dichlorethylene and birth weight in Michigan fish eaters, a cohort study. Env Hlth 3(1): 1-9.
44. Pathak R, Ahmed RS, Tripathi AK, Guleria K, Sharma CS, et al. (2009) Maternal and cord blood levels of organochlorine pesticides: association with preterm labour. Clin Biochem 42(7-8): 746-749.
45. Pathak R, Mustafa M, Ahmed RS, Tripathi AK, Guleria K, et al. (2010) Association between recurrent miscarriages and organochlorine pesticide levels. Clin Biochem 43(1-2): 131-135.
46. Sharma A, Gill JPS, Bedi JS, Pooni PA (2014) Monitoring of Pesticide Residues in Human Breast Milk from Punjab, India and Its Correlation with Health Associated Parameters. Bull Env Conta Toxicol 93(4): 465-471.