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Pesticides constitute a heterogeneous category of chemicals specifically designed for preventing; destroying, repelling or mitigating any pest.1 the broad term of pesticides includes both herbicides and insecticides. Pesticide describes hundreds of synthetic and naturally occurring chemicals designed or naturally produced to deter insects and other agricultural pests, including weeds. Numerous groups of pesticides can be classified and can be grouped according to the target organisms (such as insecti-cides, fungicides and herbicides), chemical structure (such as organochlorine, organophosphorus, phenoxy acid herbicides, urea and pyrethroids), or type of health hazards produced 2. Six specific pesticides – captafol, ethylene dibromide, glyphosate, Malathion, diazinon and dichlorophenyltrichloroethane (DDT) – are classed as a probable cause of cancer (Group 2A). Seven pesticides: tetrachlorvinphos, parathion, metolachlor, pendimethalin, permethrin, trifluralin and 2, 4-dichlorophenoxyacetic acid (2, 4-D) have been classified as possible causes of cancer (Group 2B). The association between pesticide exposure and cancerogen¬esis is actually one of the main issues in occupational and environmental toxicology.
Many rural women have been driven into the plantation sector or into other forms of corporate cash cropping (such as floriculture) where their exposure to pesticides has increased dramatically. In some countries, women make up 85 percent or more of the pesticide applicators on commercial farms plantations, often working whilst pregnant or breastfeeding. There are estimated 30,000 women pesticide sprayers in Malaysia alone that spray pesticides, and frequently exposed to highly toxic ones like paraquat, on an average of 262 days per year. Eighty percent of the spraying is carried out with leaky hand-held equipment. An incentive of extra 50 cents per day is enough to encourage these impoverished women to spray. 3 still if they do not directly apply the pesticides, women work and raise their children in a toxic environment. They mix pesticides, weed while pesticides are being applied, wash out pesticide containers, or harvest pesticide-doused crops. They wash pesticide- soaked clothing and store pesticides in their homes. 4 Data collected from developing countries in various research shows that women’s exposure to pesticides is significantly higher than is formally recognized, and that pesticide poisonings are greatly underestimated. In 2014, 235,030 new cases of breast cancer were projected to be diagnosed in the U.S., making it the most common cancer diagnosis among women.5 Endogenous and exogenous estrogen exposure contribute to breast cancer development; factors such as younger age at menarche and use of postmenopausal estrogen and progestin are recognized to increase breast cancer risk. Endocrine-disrupting properties have been attributed to several environmental agents used for pest control, including pesticides like Atrazine, Di-chloro Di-phenyl Trichloro Ethane (DDT/DDE), Dieldrin and Aldrin, Hepatochlor, Endosulfan and Dichlorvos suggesting that exposure to pesticides could also influence breast cancer risk.6, 7, 8, 9.
Organochlorine pesticides such as 1, 1’-(2, 2, 2-trichloroethane-1, 1-diyl) bis (4-chlorobenzene) (DDT) have been used extensively as insecticides. DDT, a halogenated hydrocarbon, was introduced as an insecticide in the 1940s, and in 1972, the United States Environmental Protection Agency.DDT and its metabolite 1, 1’-(2, 2-dichloroethene-1, 1-diyl) bis (4-chlorobenzene) (DDE) are lipid soluble compounds that persist in the environment and bio accumulate in the body in adipose tissue at levels far higher than those in blood and breast milk, and therefore some researcher groups investigated whether exposure to these pesticides is associated with breast cancer risk in women10, 11, 12,13,14,15. Some findings suggested that environmental chemical contamination with organochlorine residues may be an important etiologic factor in breast cancer.
Organophosphorous pesticides have been used extensively to control mosquito plagues. Parathion (O, O-diethyl O-(4-nitrophenyl) phosphorothioate) and malathion (diethyl 2-[(dimethoxyphosphorothioyl) sulfanyl] butanedioate) that are extensively used to control a wide range of sucking and chewing pests of field crops, fruits and vegetables have many structural similarities with naturally occurring compounds, and their primary target of action in insects is the nervous system; they inhibit the release of the enzyme acetylcholinesterase at the synaptic junction. In rats parathion and Malathion were found to induce changes in the epithelium of mammary gland influencing the process of carcinogenesis and such alterations occurred at the level of nervous system by increasing the cholinergic stimulation. Mammary tumour incidence in the parathion-treated rats was 14.3% and in malathion-treated animals was 24.3%, and treating the animals with atropine (which acts to oppose the cholinergic effects of the organophosphates) allowed the milk ducts to develop more normally and prevented the mammary cancers. Parathion and Malathion induced malignant transformation of breast cells through genomic instability altering p53 and c-Ha-ras genes considered pivotal to cancer process. Parathion was able to induce malignant transformation of an immortalized human breast epithelial cell line MCF-10F, as indicated by increased cell proliferation, and it was found to be an initiator factor in the transformation process in breast cancer. Though high doses of organophosphorus insecticide chlorpyrifos (O, O-diethyl O-(3, 5, 6-trichloropyridin-2-yl) phosphorothioate) inhibited cell proliferation, low levels of this insecticide induced proliferation in MCF-7 cells. Combination of an environmental substance such as the pesticide Malathion and an endogenous substance such as estrogen can enhance the deleterious effects in human mammary glands inducing cancer, and atropine is able to diminish these effects.
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