Organochlorine pesticide exposure in mothers and neural tube defects in offsprings

Kalra, Swati; Dewan, Pooja; Batra, Prerna; Sharma, T.; Tyagi, Vipin; Banerjee, Basu Dev

doi:10.1016/j.reprotox.2016.09.005

Cited by 37 publications

(23 citation statements)

References 22 publications

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“…The significance of maternal or paternal environmental/occupational exposure was debated. Maternal exposure to OCs such as endosulfan, DDT and dichlorodiphenyldichloroethylene (DDE) was linked to fetal NTDs (Kalra et al, 2016), with mothers delivering affected neonates reported to have 11.3 times greater chances of been exposed to DDE levels above median concentration of controls. Other risk factors are maternal residential proximity to pesticide application, parental pesticide exposure prior/during a periconceptual period of three months and co-exposure (Brender et al, 2010; Makelarski et al, 2014; Wang et al, 2014).…”

Section: Neural Tube Defectsmentioning

confidence: 99%

Association of pesticide exposure with human congenital abnormalities

Kalliora

Mamoulakis

Vasilopoulos

et al. 2018

Toxicology and Applied Pharmacology

102

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Human pesticide exposure can occur both occupationally and environmentally during manufacture and after the application of indoor and outdoor pesticides, as well as through consumption via residues in food and water. There is evidence from experimental studies that numerous pesticides, either in isolation or in combination, act as endocrine disruptors, neurodevelopmental toxicants, immunotoxicants, and carcinogens. We reviewed the international literature on this subject for the years between 1990 and 2017. The studies were considered in this review through MEDLINE and WHO resources. Out of the n = 1817 studies identified, n = 94 were reviewed because they fulfilled criteria of validity and addressed associations of interest. Epidemiological studies have provided limited evidence linking pre- and post-natal exposure to pesticides with cancers in childhood, neurological deficits, fetal death, intrauterine growth restriction, preterm birth, and congenital abnormalities (CAs). In this review, the potential association between pesticide exposure and the appearance of some human CAs (including among others musculoskeletal abnormalities; neural tube defects; urogenital and cardiovascular abnormalities) was investigated. A trend towards a positive association between environmental or occupational exposure to some pesticides and some CAs was detected, but this association remains to be substantiated. Main limitations of the review include inadequate exposure assessment and limited sample size. Adequately powered studies with precise exposure assessments such as biomonitoring, are warranted to clarify with certainty the potential association between pesticide exposure and human CAs.

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Section: Neural Tube Defectsmentioning

confidence: 99%

Association of pesticide exposure with human congenital abnormalities

Kalliora

Mamoulakis

Vasilopoulos

et al. 2018

Toxicology and Applied Pharmacology

102

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“…Differences in study design and exposure assessment accuracy, which relies on self-reporting, are thought to underlie the different study outcomes, along with limited cohort sizes and complex exposure mixtures ( Kalliora et al, 2018 ). Maternal exposure to endosulfan, DDT, and dichlorodiphenyldichloroethylene (DDE) has been positively associated with an increased risk for NTDs in exposed offspring ( Kalra et al, 2016 ). Women who have been exposed to these compounds are at an 11-fold increased risk of having an NTD affected pregnancy compared to unexposed control mothers ( Kalra et al, 2016 ).…”

Section: Clinical Findings and Epidemiologymentioning

confidence: 99%

“…Maternal exposure to endosulfan, DDT, and dichlorodiphenyldichloroethylene (DDE) has been positively associated with an increased risk for NTDs in exposed offspring ( Kalra et al, 2016 ). Women who have been exposed to these compounds are at an 11-fold increased risk of having an NTD affected pregnancy compared to unexposed control mothers ( Kalra et al, 2016 ). Clearly, there is much more work to be done with respect to the suspected or confirmed teratogenicity of many agriculturally significant pesticides.…”

Section: Clinical Findings and Epidemiologymentioning

confidence: 99%

Gene Environment Interactions in the Etiology of Neural Tube Defects

et al. 2021

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Human structural congenital malformations are the leading cause of infant mortality in the United States. Estimates from the United States Center for Disease Control and Prevention (CDC) determine that close to 3% of all United States newborns present with birth defects; the worldwide estimate approaches 6% of infants presenting with congenital anomalies. The scientific community has recognized for decades that the majority of birth defects have undetermined etiologies, although we propose that environmental agents interacting with inherited susceptibility genes are the major contributing factors. Neural tube defects (NTDs) are among the most prevalent human birth defects and as such, these malformations will be the primary focus of this review. NTDs result from failures in embryonic central nervous system development and are classified by their anatomical locations. Defects in the posterior portion of the neural tube are referred to as meningomyeloceles (spina bifida), while the more anterior defects are differentiated as anencephaly, encephalocele, or iniencephaly. Craniorachischisis involves a failure of the neural folds to elevate and thus disrupt the entire length of the neural tube. Worldwide NTDs have a prevalence of approximately 18.6 per 10,000 live births. It is widely believed that genetic factors are responsible for some 70% of NTDs, while the intrauterine environment tips the balance toward neurulation failure in at risk individuals. Despite aggressive educational campaigns to inform the public about folic acid supplementation and the benefits of providing mandatory folic acid food fortification in the United States, NTDs still affect up to 2,300 United States births annually and some 166,000 spina bifida patients currently live in the United States, more than half of whom are now adults. Within the context of this review, we will consider the role of maternal nutritional status (deficiency states involving B vitamins and one carbon analytes) and the potential modifiers of NTD risk beyond folic acid. There are several well-established human teratogens that contribute to the population burden of NTDs, including: industrial waste and pollutants [e.g., arsenic, pesticides, and polycyclic aromatic hydrocarbons (PAHs)], pharmaceuticals (e.g., anti-epileptic medications), and maternal hyperthermia during the first trimester. Animal models for these teratogens are described with attention focused on valproic acid (VPA; Depakote). Genetic interrogation of model systems involving VPA will be used as a model approach to discerning susceptibility factors that define the gene-environment interactions contributing to the etiology of NTDs.

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“…Though OCPs have been banned in several countries for more than three decades, they are still found in soil, water, air, foods and in human blood serum and breast milk. [7][8][9] Endosulfan is a pesticide used in growing Theobroma cacao L plant. The pesticide which is represented chemically as 6,7,8,9,10,10-Hexachloro-1,5,5a,6,9,9ahexahydro-6,9-methano-2,3,4-benzo(e)dioxathiepin-3oxide is an OCP POP as well as a prohibited pesticide.…”

Section: Introductionmentioning

confidence: 99%

“…Though OCPs have been banned in several countries for more than three decades, they are still found in soil, water, air, foods and in human blood serum and breast milk. 7–9…”

Section: Introductionmentioning

confidence: 99%

GC-MS fragmentation patterns of sprayed endosulfan and its sulphate metabolite in samples of Theobroma cacao L from a field kinetic study

Vaikosen

Gibson

Davidson

et al. 2018

Eur J Mass Spectrom (Chichester)

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Most environmental analytical methods for the determination of organochlorine pesticides (OCPs) are multi-residual with other organic compounds co-extracted and co-eluted. This has been observed in GC spectra using classical detectors like electron-capture detector (ECD) even after appropriate clean-up. This limitation could be resolved by using GC-MS methods which are more specific and selective. Thus, a commercial-grade endosulfan treated Theobroma cacao plantation was sampled. Representative samples comprising leaves, stem bark and pulp were obtained between 0.5 h and 60 days after treatment. Samples were analyzed for residual parent endosulfan ( α- and β-isomers) as well as the metabolite endosulfan sulphate using an ion trap GC-MS. The retention times and chromatogram peaks obtained for various endosulfan were identified and compared with reference standards, and confirmed with National Institute of Standards and Technology library. Results showed that the molecular ion at m/z 407 was exhibited by α- and β-endosulfan, representing the parent molecular ion M+• ([C9H6Cl6SO3]+•). The α-isomer was more thermally stable, hence exhibited more relative abundance. Other predominant peaks were 339, 307, 277, 265, 243, 241, 207, 195, 160, 159, 99 and 75 m/z. The peak at m/z 159 was the base molecular ion. For endosulfan sulphate, the peak at m/z 422 corresponded to parent molecular ion (M+•), while m/z 424 was due to isotopic pattern characteristic of the chlorine atom. The peaks at 387, 357, 289, 272, 229, 206, 170, and 120 m/z were characteristic for the sulphate metabolite. The m/z peak at 272 was the base molecular ion, while m/z 143 may be due to metabolite diol and lactone. These results showed that the various endosulfan species can be identified and confirmed simultaneously using a GC-MS.

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Organochlorine pesticide exposure in mothers and neural tube defects in offsprings

Cited by 37 publications

References 22 publications

Association of pesticide exposure with human congenital abnormalities

Association of pesticide exposure with human congenital abnormalities

Gene Environment Interactions in the Etiology of Neural Tube Defects

GC-MS fragmentation patterns of sprayed endosulfan and its sulphate metabolite in samples of Theobroma cacao L from a field kinetic study

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