Carcinogenic, Reproductive and Development, and Neurobehavioral Effects of Pesticides

Published: 2021-09-15 01:55:10
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Category: Plants, Illness

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Different types of epidemiological studies have been carried out to understand the relationship between exposure to pesticides and cancer. These pesticides can enable the cancer process by either nongenotoxic mechanisms such as promotion, peroxisme proliferation, and hormone imbalance, or by affecting carcinogenic process in a different ways, both by changing the genomeUS-Environmental Protection Agency categorized the carcinogenic potential of a chemical based on their overall evidence weights. The categories are as follows: Group A (Human Carcinogen), Group B (Probable Human Carcinogen), Group C (Possible Human Carcinogen), Group D (Not Classified as to Human Carcinogenicity), and Group E (Evidence of Non-carcinogenicity for Humans). Epidemiological studies also found that breast fat and serum lipids of women with breast cancer contain significantly higher levels of some chlorinated hydrocarbons compared with non-cancer control.
Therefore, tests for estrogenicity is an essential screening tool to know the hazardous health effects of new and existing pesticides. So, cancer risk assessment wants to know how the occurrence of events increases and to pinpoint the occurrence of low probability events at low doses over long periods of time. Also, different compounds of halogenated hydrocarbons occupy gap functional intercellular communication (GJIC) in normal human breast epithelial cells (HBEC) when given as a single compound or as mixtures where they can alter the post-translational level, have tumor-promoting potential in human breast tissue and exert some human health effects if they meet all the conditions to inhibit GJIC. OPs react with biological molecules by means of phosphorylation of serine hydrolases and of alkylation of macromolecules, DNA which are considered to account for the acute cholinergic toxicity and initiation of the carcinogenic process, respectively. When the rate of phosphorylation is substantially higher than the rate of alkylation, in vivo genotoxic effects are unlikely to occur because effective doses cannot be achieved due to acute toxicity. Diazinon and dichlorvos meet these criteria, where the rate of phosphorylation of AChE being much faster than that of alkylation.Potential non-cancer health outcomes that may be influenced by an agent in the environment, particularly pesticides, include dangerous effects on the nervous, renal, respiratory and reproductive systems of both men and women. The mammalian development toxicity is defined as the adverse effects caused or evident during in utero development. The development toxicity includes adverse effects on the developing organism that may have been as a result of exposure of either parent before conception, of the mother during prenatal development, or postnatal to the time of sexual maturation. Embryo is the most vulnerable to the initiation of major birth defects between 3 weeks and 2 months of gestation, the critical period of organogensis. The exposure to toxic chemicals during the first 2 weeks results to fetal death, while exposure after organogensis is more likely to retard growth and functional deficits. Also, the pesticide used by appliers and exposure of the general population of the crop-growing region of Western Minnesota are associated with increased birth anomalies. It is now known that numerous endocrine disrupting pesticides from different chemical groups have been released into the environment in large quantity since world war II and exert their action as agonistic and antagonistic receptor binding, and affect hormone synthesis, storage, release, transport, and clearance.
The similarities between mammalian and insect nervous system, makes the insecticides to have effect on human being as they are designed to attack the insect nervous system they are also capable of producing acute and chronic neurotoxic effects in mammals. People exposed occupationally to relatively high levels of insecticides were diagnosed with both acute and chronic alterations in sensory, motor, autonomic, cognitive, and behavioral functions. These neurobehavioral effects and chemical-induced changes in behavior may be a relatively sensitive indicator of nervous dysfunction and can be used in neurotoxicology for neurotoxicity risk assessment. Organochlorine insecticides have effects on motor, sensory, or cognitive function that are detectable using functional indicators of neurotoxicity to assess neurotoxicity risk.
A number of OPs cause neurotoxicity, characterized as central- peripheral distal axonopathy. This syndrome commonly known as organophosphate induced delayed polyneuropathy (OPIDP), is totally independent of inhibition of AChE and is delayed as symptoms appear after 2-3 weeks. The mechanism of initiation of OPIDP involves the phosphorylation of a protein in the nervous system called neuropathy target esterase (NTE) and the aging of the phosphoryl enzyme complex (Johnson, 1982). The inhibition of NTE activity in human lymphocytes has been shown to predict the onset of OPIDP in a patient poisoned with chlorpyrifos. Preliminary studies in Central America suggested that mild or subclinical cases of OPIDP after severe cholinergic poisoning with methamidophos may be much more common than previously suspected. In humans, OPIDP also has been reported to occur after poisoning with merphos, mipafox, leptophos, trichlorphon and trichlornate. One of the reasons for toxicology and risk assessment is to determine, through experiments with animals and documentation of adverse effects following accidental exposure of human, safe limits of exposure to toxic chemicals. Since new pesticides are being released into the environment, it is essential to use rapid and sensitive toxicological screening procedures for these and already existing pesticides.
Once behavioral neurotoxic effects have been identified, it is important to improve the understanding of the mechanism of neurotoxicity at the neurochemical, neurophysiological, cellular, and molecular levels of analysis. Neurotoxicity risk assessment can be improved by a more complete understanding of the interrelationships between the various levels of nervous system. Neurobehavioral toxicology contributes directly to this issue by systemically assessing the threshold and magnitude of exposure beyond which normal processes are significantly affected.

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