Review articles

By Ms. Marziyeh Amizadeh , Mr. Ghasem Askari Saryazdi
Corresponding Author Ms. Marziyeh Amizadeh
University of Tabriz, - Iran (Islamic Republic of)
Submitting Author Ms. Marziye Amizadeh
Other Authors Mr. Ghasem Askari Saryazdi
University of Tabriz, - Iran (Islamic Republic of)


Endosulfan, Organochlorin pesticide, Human, Acute toxicity, Chronic toxicity, Health risk

Amizadeh M, Askari Saryazdi G. Effects of Endosulfan on Human Health. WebmedCentral TOXICOLOGY 2011;2(12):WMC002617
doi: 10.9754/journal.wmc.2011.002617

This is an open-access article distributed under the terms of the Creative Commons Attribution License(CC-BY), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
Submitted on: 12 Dec 2011 09:59:18 AM GMT
Published on: 13 Dec 2011 03:34:33 PM GMT


Endosulfan is an organochlorine insecticide and acaracide used to control a broad range of insect and arthropod pests on a wide variety of crops in many agrosystems. Endosulfan is readily absorbed by humans via the stomach, lungs and through the skin. It can cause acute and chronic toxicity. Laboratory assays suggested more susceptibility of female than males to the lethal effects of endosulfan. Central nervous system is the main target in endosulfan toxicity. Endosulfan is a neurotoxin, haematoxin, genotoxin and nephrotoxin. Laboratory studies have also shown that there are potential carcinogenic effects. Toxicity of this insecticide on reproductive organs was confirmed. Endosulfan has been linked to congenital physical disorders, mental disabilities and deaths in farm workers and communities across the globe. Symptoms of poisoning include headaches, dizziness, nausea, vomiting, mental confusion, convulsions, hyperactivity, seizures, coma and respiratory depression, in severe cases resulting in death.


Endosulfan (6, 7, 8, 9, 10, 10-hexachloro-1, 5, 5a, 6, 9, 9a-hexahydro-6, 9-methano-2, 4, 3-benzodioxathiepin-3-oxide) is a broad-spectrum organochlorine insecticide and acaricide for control of agricultur pests on a variety of field, fruit, and vegetable crops. Endosulfan active ingredient is mixture of two isomers α and β, in the ratio of approximately 70% and 30% respectively (Saiyed et al. 2003). Endosulfan residue has been identified in a variety of environmental media (air, surface water, ground water, soil and sediment) and its metabolites have been reported in human and domestic animals milk (Nag and Raikwar, 2008, Campoy et al. 2001), fruit and vegetable (Mitchell, 1976; Pokharkar and Dethe, 1981). The most likely way for people to be exposed to endosulfan is eating the contaminated food with it. Exposure to endosulfan may occur by breathing, eating, or drinking the substance, or by skin contact (Anonymous, 1002; 2000).
In mammals, commercial endosulfan is transformed into more water soluble metabolites, mostly endosulfan sulfate, followed by ether and diol metabolites. All of these metabolites are bioaccumulated in the adipose tissue, depending on their lipophilicity (Cerilo et al. 2005).
Toxicity studies of endosulfan have been conducted in animals. These studies are carried out to identify the target organs of toxicity and possible spectrum of effects. The effects of any chemical substance are determined by the dose, duration and the time of exposure. There is a close similarity between the spectrum of health effects observed in the human population exposed to endosulfan and those described in animal studies. It has been demonstrated that much lower doses of toxicants may result in adverse health effects manifesting as functional or organic disorders in later life if the exposure takes place during the early developmental phase (Anonymous, 2002). Several cases of poisoning have been reported in work place where men have exposed to endosulfan over long periods (Paul and Balasubramaniam, 1997).
In chronic studies, endosulfan was used in oral test by corn oil (Gupta and Gupta, 1977), peanut oil (Gupta, 1978) or as a suspension in water with tragacanth powder (Paul et al., 1992; 1993; 1994). For acute intraperitoneal injection, alcohol or peanut oil was used (Gupta, 1976; Gupta and Gupta, 1977).


Endosulfan acute toxicity
As in the cases of most other pesticides, endosulfan can cause acute toxicity in animals and human beings due to over exposure (Anonymous, 2002). Acute oral toxicity is higher than dermal toxicity (silva and gammon, 2009). Endosulfan poisoning can be suspected in the presence of primary central nervous system manifestations including seizures, with or without clinical or laboratory evidence of other organs dysfunction such as liver failure (Karatas et al., 2006). Symptoms of poisoning include death, clinical signs, irritation of stomach and small intestine, congestion of kidneys, lungs and adrenals, reddening of small intestine, neurotoxicity, erythema, atonia, desquamation, hemorrhagic lung, granular livers, irritation of large intestine, congested kidneys,  nausea, vomiting, seizures and dizziness (Karatas et al. 2006; Silva, 2007).
Endosulfan chronic toxicity
The sub-acute and chronic toxicity studies of endosulfan in animals suggest that the kidneys, liver, immune system, and testes are the main target organs (Paul and Balasubramaniam, 1997). Long term exposure is linked to immunosuppression, neurological disorders, congenital birth defects, chromosomal abnormalities, mental retardation, impaired learning and memory loss (Silva, 2007).
Histopathological changes were observed in liver, kidney and muscles of rats when exposed to a mixture of endosulfan various intervals. The examinations revealed hepatotoxic, nephrotoxic and muscular necrotic effects in pesticides exposed rats (Benjamin et al. 2006; Kurutas et al. 2006).  Endosulfan alters the activities of some enzymes such as lactic dehydrogenase, glucose-6-phosphate dehydrogenase and alkaline phosphatase, and decreases mitochondrial energy production in mice (Kurutas et al., 2006; Tietz, 1999).
There are some indications that endosulfan can have adverse effects on the immune system at low levels of exposure (Anonymous, 2000). There is mounting evidence that organochlorine compounds can act as hormones. Endosulfan may also be a part of the cause for the disease in the quality of semen, an increase in testicular and prostate cancer, an increase in defects in male sex organs, and increases incidence of breast cancer which has been observed in the last fifty years (Saiyed et al. 2003; Chitra et al., 2001; Singh and Pandey, 1990; Sinha et al., 1995; Soto et al., 2008).
Neurological effects of endosulfan
Neurotoxicity of endosulfan is the primary effect observed both acutely and chronically in both humans and animals. Documented human data have shown the central nervous system to be the major target of endosulfan action (Silva, 2007; Anonymous, 2000). Neurotoxicity of endosulfan has been studied experimentally in tissue cultures (Sunol et al., 2008; Wozniak et al., 2005), invertebrates (Ghiasuddin and Matsumura, 1982; Chen et al., 2006; Bloomquist, 1993) and vertebrates including mammals (Brunelli et al., 2009; Ballesteros et al., 2009; Paul et al., 1992; Cabaleiro et al., 2008; Banerjee and Hussain, 1986).
The mechanism of neurotoxicity of endosulfan appears to be dominated by its capacity to inhibit non-competitively the GABA-A type of receptors (Cole and Casida, 1986; Chen et al., 2006), although other targets are believed to exist (Sunol et al., 2008; Paul et al., 1994; Vale et al., 2003). Scremin et al. (2011) suggested that endosulfan induced a large increase of cortical evoked potentials amplitudes at doses that did not elicit convulsions. These responses could be used as a non-invasive diagnostic tool to detect low-level endosulfan intoxication in humans.  Exposure has also been linked to conditions such as cerebral palsy, epilepsy and it may increase the risk of Parkinson’s disease (Stoytcheva, 2011).
Toxicity on reproductive system
In recent years, there has been growing concern about toxicity of a number of chemicals, including pesticides, on the male reproductive system (Murray et al. 2001; Sharpe, 2001). Reported effects of endosulfan on the male reproductive system in experimental animals have been variable, depending on species, age at exposure, dose, duration of exposure, and study end points (saiyed et al. 2003). When adult rats were exposed to endosulfan for 10 weeks (5day per week), reduction in intratesticular spermatid counts, sperm abnormalities, and changes in the marker enzymes of testicular activities, such as lactate dehydrogenase, sorbitol dehydrogenase, γ-glutamyl transpeptidase, and glucose-6-phosphate dehydrogenase were shown providing further evidence of effects on spermatogenesis (Khan and Sinha 1996; Sinha et al. 1995). Exposure of younger animals (3 weeks old) showed marked depletion of spermatid count as well as decreased daily sperm production at a dose of 2.5 mg/kg/day (Sinha et al. 1997). More recent studies have shown that exposure of pregnant rats to endosulfan at 1 mg/kg/day from day 12 through parturition leads to decreased spermatogenesis in offspring (Sinha et al. 2001).
Saiyed et al. (2003) undertook a study to examine the relationship between environmental endosulfan exposure and reproductive development in male children and adolescents. The study parameters included recording of clinical history, physical examination, sexual maturity rating (SMR) (including pubic hair, testes and penis) and estimation of serum levels of testosterone, luteinizing hormone (LH), follicle-stimulating hormone, and endosulfan residues. Their study results, after controlling for age, showed significantly lower SMR scores and serum testosterone levels and higher levels of serum LH in the study group compared with controls.
Oral administration of the pesticides endosulfan, methyl parathion and mancozeb inhibits compensatory ovarian hypertrophy, decreases the number of healthy follicles, increases the number of atretic follicles, and affects the oestrous cycle in rats (Asmathbanu and Kaliwal, 1997; Dhondup and Kaliwal, 1997; Mahadevaswami et al., 2000). Azarnia et al. (2008) were assessed the effects of endosulfan on ovary structures of 50-day-old BALB/C mice. The endosulfan induced decrease of ovarian size in mice was associated with a decrease in healthy ovarian follicles and corpora lutea, and increased number of atretic follicles. Whether this endosulfan effect is due to a direct effect on the ovary or an indirect effect on the hypothalamus or pituitary, or to a desensitization of the ovary to gonadotropins, cannot be ascertained from this study.
Estrogenic Effects of endosulfan
Several xenobiotic such as polychlorinated biphenyls, chlordecone, and methoxychlor were shown to be estrogenic in animal models (Soto et al. 1994); however, their lower estrogenic potency was interpreted as having none or weaker deleterious effects on humans exposed through the food chain. Occupational exposure to chlordecone, on the other hand, resulted in overt estrogenicity manifested as oligospermia and sterility (Guzelian, 1982).
The estrogenic activity of xenobiotic was assessed by 1) determining the relative proliferative potency (RPP); this is the ratio between the minimal concentration of estradiol needed for maximal cell yield at 6 days and the dose of the test compound to achieve a comparable proliferative effect, and 2) measuring the relative proliferative effect (RPE); this is 100x the ratio between the highest cell yield obtained with the chemical and with estradiol (Soto et al. 1994).
Soto et al. (1994) were used “in culture” bioassay to assess the strogenicity of endusolfan insecticide. The E-screen test (that measures the proliferative effect of estrogens on their target cells) uses human breast strogen-sensitive MCF7 cells and compares the yield achieved after 6 days of culture in medium supplement with 5% charcoal-dextran stripped human serum in the presence (positive control) or absence (negative control) of estradiol and with diverse concentration of xenobiotic suspected of being estrogenic. Their results showed that technical grade endosulfan and α and β endosulfan isomers were estrogenic at concentrations of 10-25 µM. Higher concentrations were cytotoxic.
Sex-related difference in the toxicities of endosulfan
Acute toxicity studies have indicated that female rats are more highly susceptible than males to the lethal effects of endosulfan (Gaines, 1969; Gupta, 1976). Liver injury that occurred after chronic oral exposure to endosulfan was more marked in female rats in comparison to males (Paul et al., 1995). A slow metabolism of the insecticide in females as compared to male rats accounted for these findings. In support of this suggestion, blood and tissue residue levels of endosulfan were significantly higher in female rats when compared to that in males (Dikshith et al., 1988). Male rats responded more than females to the locomotor stimulating action of chronic endosulfan (2 mg/kg for 90 days) treatment (Paul et al., 1995). A metabolic factor may account for this finding too, if the metabolite endosulfan sulphate is responsible for locomotor stimulation as a result of its greater neurotoxic property than the parent compound (Dorough et al., 1978) and if biotransformation of endosulfan occurs at a much faster rate in males in comparison to females (Paul and Balasubramaniam, 1997).
Genotoxicity of endosulfan
Earlier studies on the genotoxicity of endosulfan have yielded inconsistent results (Pednekar et al., 1987; Scarpato et al., 1996; Chaudhuri et al., 1999; Falck et al., 1999). Bajpayee et al. (2006) in their study, endosulfan and its metabolites were assayed for their ability to induce DNA damage in Chinese hamster ovary (CHO) cells and human lymphocytes. The compounds produced statistically significant (P < 0.01), concentration-dependent (0.25–10 lM) increases in DNA damage in both CHO cells and human lymphocytes. Endosulfan lactone caused the most DNA damage in CHO cells, while the isomeric mixture of endosulfan produced the greatest response in lymphocytes. The results indicate that exposure to sublethal doses of endosulfan and its metabolites induce DNA damage and mutation.
Lu et al. (2000) in their study examined the genotoxicity of α- and β-endosulfan in vitro with a HepG2 cell line. they used sister chromatid exchanges (SCE), micronuclei (MN), and DNA strand breaks as detected by single-cell gel electrophoresis (SCG) assays as biomarkers to judge the genotoxicity of α- and β-endosulfan at concentrations from 1×10-12 M to 1×10-3 M. After treating HepG2 cells for 48 h with β-endosulfan, SCE showed a significant increase at concentrations from 1×10-7 M to 1×10-5 M, and MN showed a significant increase at concentrations from 5×10-5 M to 1×10-3 M. α-Endosulfan failed to show significant effect in both the SCE and MN assays. After treating HepG2 cells with α- or β-endosulfan for l h, DNA strand breaks were significantly induced by α-endosulfan at concentrations from 2×10-4 M to 1×10-3 M, and by, β-endosulfn at 1×10-3 M. The results of this study suggest that both α- and β-endosulfan are genotoxic to HepG2 cells and that the genotoxicity of β-endosulfan seems stronger than that of α-endosulfan.
Neurobehavioral effects of endosulfan
Results of receptor binding and biochemical studies have shown that endosulfan has a potential to alter the activities of central cholinergic, dopaminergic and serotonergic mechanisms. Thus considerable interest has been generated in investigating a correlation between endosulfan-induced behavioral aberrations and changes in neurotransmitter activities (Paul and Balasubramaniam, 1997). Endosulfan after chronic exposure at low dose levels produced circling movement (Anand et al., 1985) and stimulation of motor activity in rats (Anand et al., 1985; Paul et al., 1993b; 1994b; 1995). An involvement of dopaminergic mechanism accounted for endosulfan induced hypermotor activity and circling movement, since these effects were suppressed by the antidopaminergic drug chlorpromazine (Anand et al., 1985).
Bioaccumulation of endosulfan in fatty tissues
Endosulfan stores easily within the fatty tissues of living organisms. Cerrillo et al. (2005) in their study investigated the presence of α-endosulfan, β-endosulfan, and its metabolites in fatty and non-fatty tissues and fluids from women in reproductive age and children in Southern Spain. The highest concentration of commercial α-endosulfan and β-endosulfan was found in adipose tissue, with a mean value of 17.72 ng/g lipids, followed by human milk, with a mean value of 11.38 ng/mL milk. These findings support the lipophilicity of these chemicals and their elimination by milk secretion. The concentration in the placenta homogenate was similar to that in the blood from the umbilical cord (7.74 and 6.11 ng/mL, respectively) and reflected their lower fat content. Endosulfan diol and endosulfan sulfate were more frequently found in placenta homogenate, with a mean concentration of 12.56 and 3.57 ng/mL, respectively, and in blood from umbilical cord, at 13.23 and 2.82 ng/mL, respectively.
Botella et al. (2004) determined and compared the levels of 15 organochlorine pesticides in the adipose tissue and blood of 200 women living in Southern Spain. Endosulfan was found in both adipose tissue and serum samples. Among endosulfan metabolites, endosulfan-ether was the most predominant compound in both adipose tissue (68%) and serum (86%) samples.
Their results suggested that exposure from mother to child is a common event, both in utero and via breastfeeding, due to the high frequency of exposure of women in reproductive age (Cerrillo, 2005).


Endosulfan is a highly toxic chemical and poisonous to most living organisms. The United States Environmental Protection Agency classifies it as ‘highly hazardous. It has been responsible for hundreds of deaths worldwide, and significant short and long-term human health impacts. Endosulfan kills indiscriminately and is devastating to the environment, contaminating soils, air and water, and damaging mammals and other animals. Endosulfan’s ability for long-range environmental transport, together with its adverse effects supports the need for concerted international action. To date, 62 countries have already voluntarily banned the use of endosulfan.
Endosulfan has killed, and will continue to kill and maim if it continues to be legal. National prohibitions on use, together with inclusion under the Stockholm Convention will ensure endosulfan’s eradication from global use and an opportunity to protect people and their shared environment from this deadly chemical.


1. Anand M, Mehrotra S, Gopal K, Sur RN, Chandra SV. Role of neurotransmitters in endosulfan-induced aggressive behavior in normal and lesioned rats.Toxicology Letters, 1985; 24: 79-84.
2. Anonymous. NIOSH (national institute for occupational safety and health, USA). 1992; NIOSH, Atlanta, GA, USA.
3. Anonymous. Toxicological profile for endosulfan. U. S. Department of health and human services. Public health service. Agency for toxic substances and disease registry. 2000; 323 pages.
4. Anonymous. Final report of the investigation of unusual illnesses allegedly produced by endosulfan exposure in padre village of Kasargod district (N.Kerala). National Institute of occupational Health (Indian Council of Medical Research). 2002; 98 pages.
5. Asmathbanu I, Kaliwal BB. Temporal effect of methyl parathion on ovarian compensatory hypertrophy, follicular dynamics and estrous cycle in hemicastrated albino rats. Journal of Basic and Clinical Physiology and Pharmacology, 1997; 8: 237− 254.
6. Azarnia M, Koochesfahani HM, Rajabi M, Tahamtani Y, Tamadon A. Histological examination of endosulfan effects on follicular development of BALB/C mice. Bulgarian Journal of Veterinary Medicine, 2008; 12: 33−41.
7. Bajpayee M, Pandey A, Zaidi S, Musarrat J, Parmar D, Mathur N, Seth P, Dhawan A. DNA damage and mutagenicity induced by endosulfanand and its metabolites. Environmental and Molecular Mutagenesis, 2006; 47: 682-692.
8. Ballesteros ML, Durando PE, Nores ML, Diaz MP, Bistoni MA, Wunderlin DA. Endosulfan induces changes in spontaneous swimming activity and acetylcholinesterase activity of Jenynsiamultidentata (Anablepidae, Cyprinodontiformes). Environmental Pollution, 2009; 157:1573–1580.
9. Banerjee BD, Hussain QZ. Effect of sub-chronic endosulfan exposure on humoral and cell-mediated immune responses in albino rats. Archives of Toxicology, 1986; 59: 279–284.
10. Benjamin N, Kushwah A, Sharma RK, Katiyar AK.Histopathological changes in liver, kidney and muscles of pesticides exposed malnourished and diabetic rats. Indian Journal of Experimental Biology, 2006; 44: 228-232.
11. Bloomquist JR. Toxicology, mode of action and target site-mediated resistance to insecticides acting on chloride channels. Comparative Biochemistry and Physiology, 1993; 106: 301–314.
12. Botella B, Crespo J, Rivas A, Cerrillo I,  Olea-Serrano M, Olea N. 2004. Exposure of women to organochlorine pesticides in Southern Spain. Environmental Research, 2004; 96: 34–40.
13. Brunelli E, Bernabo I, Berg C, Lundstedt-Enkel K, Bonacci A, Tripepi S. Environmentally relevant concentrations of endosulfan impair development, metamorphosis and behaviour in Bufobufo tadpoles. Aquatic Toxicology, 2009; 91: 135–142.
14. Cabaleiro T, Caride A, Romero A, Lafuente A. Effects of in utero and lactational exposure to endosulfan in prefrontal cortex of male rats. Toxicology Letters, 2008; 176: 58–67.
15. Campoy C, Jimenez M, Olea-Serrano MF, Moreno-Frias M, Canabate F, Olea N, Bayes R, Molina-Font JA. Analysis of organochlorine pesticides in human milk: preliminary results. Early Human Development, 2001; 65: 183–190.
16. Cerrillo I, Granada A, Lopez-Espinosa MJ, Olmos B, Jimenez M, Cano A, Olea N, Olea-Serrano MF. Endosulfan and its metabolites in fertile women, placenta, cord blood, and human milk. Environmental Research, 2005; 98: 233–239.
17. Chaudhuri K, Selvaraj S, Pal AK. Studies on the genotoxicity of endosulfan in bacterial systems. Mutation Research, 1999; 439: 63–67.
18. Chen L, Durkin KA, Casida JE. Structural model for gamma-aminobutyric acid receptor noncompetitive antagonist binding: widely diverse structures fit the same site. Proceedings of the National Academy of Sciences of the United States of America, 2006; 103: 5185–5190.
19. Chitra KC, Sujatha R, Latchoumycandane C, Mathur PP. Effect of lindane on antioxidant enzymes in epididymis and epididymal sperm of adult rats. Asian Journal of Andrology, 2001; 3: 205-208.
20. Cole LM, Casida JE. Polychlorocycloalkane insecticide-induced convulsions in mice in relation to disruption of the GABA-regulated chloride ionophore. Life Sciences, 1986; 39: 1855–1862.
21. Dhondup P, Kaliwal BB. Inhibition of ovarian compensatory hypertrophy by the administration of methyl parathion in hemicastrated albino rats. Reproductive Toxicology, 1997; 11: 77−84.
22. Dikshith TSS, Raizada RB, Kumar SN, Srivastava MK, Kaushal RA, Singh RP, Gupta KP. Effect of repeated dermal application of endosulfan to rats. Veterinary & Human Toxicology, 1988; 30: 219-224.
23. Dourough HW, Huntanen K, Marshall TC, Bryant HE. Fate of endosulfan in rats and toxicological considerations of apolar metabolites. Pesticide Biochemistry and Physiology, 1978; 8: 241-252.
24. Falck GC, Hirvonen A, Scarpato R, Saarikoski ST, Migliore L, Norppa H. Micronuclei in blood lymphocytes and genetic polymorphism for GSTM1, GSTT1 and NAT2 in pesticide-exposed greenhouse workers. Mutation Research, 1999; 441: 225–237.
25. Gaines TB. Acute toxicity of pesticides. Toxicology and Applied Pharmacology, 1969; 14: 515-534.
26. Ghiasuddin SM, Matsumura F. Inhibition of gamma-aminobutyric acid (GABA)-induced chloride uptake by gamma-BHC and heptachlor epoxide. Comparative Biochemistry and Physiology, 1982; 73C: 141–144.
27. Gupta PK. Endosulfan-induced neurotoxicity in rats and mice.Bulletin of Environmental Contamination and Toxicology, 1976; 15: 708-713.
28. Gupta PK. Distribution of endosulfan in plasma and brain after repeated oral administration to rats. Toxicology, 1978; 9: 371-377.
29. Gupta PK, Gupta RC. Effect of endosulfan pretreatment on organ weights and on pentobarbital hypnosis in rats. Toxicology, 1977; 7: 283–288.
30. Guzelian PS. Comparative toxicology of chlordecone (kepone) in humans and experimental animals. Annual Review of Pharmacology and Toxicology, 1982;  22: 89-113.
31. Karatas AD, Aygun D, Baydin A. Characteristics of endosulfan poisoning: a study of 23 cases. Singapore Medical Journal, 2006; 47: 1030-1032.
32. Khan PK, Sinha SP. Ameliorating effect of vitamin C on murine sperm toxicity induced by three pesticides (endosulfan, phosphamidon and mancozeb). Mutagenesis, 1996; 11:33–36.
33. Kurutas EB, Doran F, C?ral?k H. The effect of endosulfan on lactic dehydrogenase enzyme system in liver of Musmusculus: a histochemical study. European Journal of General Medicine, 2006; 3: 148-151.
34. Lu Y, Morimoto K, Takeshita T, Takeuchi T, Saito T. Genotoxic effects of α-endosulfan and β-endosulfan on human HepG2 cells. Environmental Health Perspectives, 2000; 108: 559-561.
35. Mahadevaswami MP, Jadaramkunti UC, HiremathMB,Kaliwal BB. Effect of mancozeb on ovarian compensatory hypertrophy and biochemical constituents in hemicastrated albino rat. Reproductive Toxicology, 2000; 14: 127−134.
36. Mitchell LR. Collaborative study of the determination of endosulfan, endosulfan sulfate, tetrasul, and tetradifon residues in fresh fruits and vegetables. Journal of the Association of Official Analytical Chemists, 1976; 59: 209−212.
37. Murray TJ, Lea RG, Abramovich D R, Haites NE, Fowler PA. Endocrine disrupting chemicals: effects on human male reproductive health. Early Pregnancy, 2001; 5: 80–112.
38. Nag SK, Raikwar MK. Organochlorine pesticide residues in bovine milk. Bulletin of Environmental Contamination and Toxicology,  2008; 80: 5–9.
39. Paul V, Balasubramaniam E. Effects of single and repeated administration of endosulfan on behavior and its interaction with centrally acting drugs in experimental animals: a mini review. Environmental Toxicology and Pharmacology, 1997; 3: 151–157.
40. Paul V, Balasubramaniam E, Jayakumar AR, Kazi M. A sex-related difference in the neurobehavioral and hepatic effects following chronic endosulfan treatment in rats.European Journal of Pharmacology.Environmental Toxicology and Pharmacology Section, 1995; 293: 355-360.
41. Paul V, Balasubramaniam E, Kazi M. The neurobehavioural toxicity of endosulfan in rats: a serotonergic involvement in learning impairment. European Journal of Pharmacology, 1994; 270: 1–7.
42. Paul V, Balasubramaniam E, Muthu P, Krishna-moorthy MS. Evidence for a hazardous interaction between ethanol and the insecticide endosulfan in rats. Pharmacology and Toxicology, 1992; 70: 268-270.
43. Paul V, Kazi M, Balasubramaniam E, Sheela S. Effect of chronic endosulfan treatment on pharmacological actions of diazepam in rats. Bulletin of Environmental Contamination and Toxicology, 1993; 51: 18-23.
44. Pednekar MD, Gandhi SR, Netrawali MS. Evaluation of mutagenic activities of endosulfan, malathione and permethrin, before and after metabolic activation in the Ames Salmonella test. Bull Environ ContamToxicol, 1987; 38: 925–933.
45. Pokharkar DS, Dethe MD. Gas liquid chromatographic studies on residues of endosulfan on chilli fruits. Journal of Environmental Science and Health. Part B, Pesticides, Food Contaminants, and Agricultural Wastes, 1981; B16: 439−451.
46. Saiyed H, Dewan A, Bhatnagar V, Shenoy U, Shenoy R, Rajmohan H, Patel K, Kashyap R, Kulkarni P, Rajan B, Lakkad B. Effect of endosulfan on male reproductive development. Environmental Health Perspectives,  2003; 111: 1958- 1962.
47. Scarpato R, Migliore L, Angotzi G, Fedi A, Miligi L, Loprieno N. Cytogenetic monitoring of a group of Italian floriculturists: No evidence of DNA damage related to pesticide exposure. Mutation Research, 1996; 367: 73–82.
48. Scremin OU, ChialvoDR, Lavarello S, Berra HH, Lucero MA. The environmental pollutant endosulfan disrupts cerebral cortical function at low doses. NeuroToxicology, 2011; 32: 31-37.
49. Sharpe RM. Hormones and testis development and the possible adverse effects of environmental chemicals. Toxicology Letters, 2001; 120: 221–232.
50. Silva MH. Endosulfan risk characterization document. Medical toxicology and worker health and safety branches department of pesticide regulation California environmental protection. 2007; Available from:
51. Silva MH, Gammon D. An assessment of the developmental, reproductive and neurotoxicity of endosulfan. Birth Defects Research Part B: Developmental and Reproductive Toxicology, 2009; 86: 1-28.
52. Singh SK, Pandey RS. Effect of sub-chronic endosulfan exposures on plasma gonadotrophins, testosterone, testicular testosterone and enzymes of androgen biosynthesis in rat. Indian Journal of Experimental Biology, 1990; 28: 953-956.
53. Sinha N, Adhikari N, Saxena DK. Effect of endosulfan during fetal gonadal differentiation on spermatogenesis in rats. Environmental Toxicology and Pharmacology, 2001; 10: 29–32.
54. Sinha N, Narayan R, Saxena DK. Effect of endosulfan on the testis of growing rats. Bulletin of Environmental Contamination and Toxicology, 1997; 58: 79–86.
55. Sinha N, Narayan R, Shanker R, Saxena DK. Endosulfan induced biochemical changes in the testis of rats. Veterinary & Human Toxicology, 1995; 37: 547–549.
56. Soto AM, Chung kL, Sonnenschein C. The pesticides endosulfan, toxaphene, and dieldrin have estrogenic effects on human estrogen-sensitive cells. Environmental Health Perspectives, 1994; 102: 380-383.
57. Stoytcheva, M. (Ed). Pesticide-The impacts of pesticide exposure. 2011. 446 pages.
58. Sunol C, Babot Z, Fonfria E, Galofre M, Garcia D, Herrera N, Iraola S, Vendrell I. Studies with neuronal cells: from basic studies of mechanisms of neurotoxicity to the prediction of chemical toxicity. Toxicol In Vitro, 2008; 22:1350–1355.
59. Tietz W. Fundamentals of Clinical Chemistry (Eds. CA. Burtis and ER.Ashwood) W.B. Saunders Comp. Philadelphia, London, Toronto, Montreal, Sydney, Tokyo, 1999; pp:803-804.
60. Vale C, Fonfria E, Bujons J, Messeguer A, Rodriguez-Farre E, Sunol C. The organochlorine pesticides gamma-hexachlorocyclohexane (lindane), alpha-endosulfan and dieldrin differentially interact with GABA(A) and glycine-gated chloride channels in primary cultures of cerebellar granule cells. Neuroscience, 2003; 117: 397–403.
61. Wozniak AL, Bulayeva NN, Watson CS. Xenoestrogens at picomolar to nanomolar concentrations trigger membrane estrogen receptor-alpha-mediated Ca2+ fluxes and prolactin release in GH3/B6 pituitary tumor cells. Environmental Health Perspectives, 2005; 113: 431–439.

Source(s) of Funding


Competing Interests



This article has been downloaded from WebmedCentral. With our unique author driven post publication peer review, contents posted on this web portal do not undergo any prepublication peer or editorial review. It is completely the responsibility of the authors to ensure not only scientific and ethical standards of the manuscript but also its grammatical accuracy. Authors must ensure that they obtain all the necessary permissions before submitting any information that requires obtaining a consent or approval from a third party. Authors should also ensure not to submit any information which they do not have the copyright of or of which they have transferred the copyrights to a third party.
Contents on WebmedCentral are purely for biomedical researchers and scientists. They are not meant to cater to the needs of an individual patient. The web portal or any content(s) therein is neither designed to support, nor replace, the relationship that exists between a patient/site visitor and his/her physician. Your use of the WebmedCentral site and its contents is entirely at your own risk. We do not take any responsibility for any harm that you may suffer or inflict on a third person by following the contents of this website.

3 reviews posted so far

Effects Of Endosulfan On Human Health Review
Posted by Dr. Marie Bourgeois on 17 Mar 2012 02:24:59 PM GMT

Could have been better.
Posted by Prof. Prasunpriya Nayak on 31 Dec 2011 02:56:43 PM GMT

Effects of endosulfan on human health
Posted by Dr. Prateek Rastogi on 30 Dec 2011 07:44:26 AM GMT

1 comment posted so far

Please use this functionality to flag objectionable, inappropriate, inaccurate, and offensive content to WebmedCentral Team and the authors.


Author Comments
0 comments posted so far


What is article Popularity?

Article popularity is calculated by considering the scores: age of the article
Popularity = (P - 1) / (T + 2)^1.5
P : points is the sum of individual scores, which includes article Views, Downloads, Reviews, Comments and their weightage

Scores   Weightage
Views Points X 1
Download Points X 2
Comment Points X 5
Review Points X 10
Points= sum(Views Points + Download Points + Comment Points + Review Points)
T : time since submission in hours.
P is subtracted by 1 to negate submitter's vote.
Age factor is (time since submission in hours plus two) to the power of 1.5.factor.

How Article Quality Works?

For each article Authors/Readers, Reviewers and WMC Editors can review/rate the articles. These ratings are used to determine Feedback Scores.

In most cases, article receive ratings in the range of 0 to 10. We calculate average of all the ratings and consider it as article quality.

Quality=Average(Authors/Readers Ratings + Reviewers Ratings + WMC Editor Ratings)