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The Use of DDT in the United States - Essay Example

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The paper "The Use of DDT in the United States" highlights that reduction of vector-breeding habitats and heightened socioeconomic development with better hygiene and sanitation facilities can help get rid of malaria for good, thus eliminating the need to use DDT altogether…
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The Use of DDT in the United States
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Toxicology data would be that pertaining to the carcinogeni teratogeni and mutageni . The main toxicity to humans has to do more with the solvent rather than the DDT itself. 10 mg/kg is the single oral dose of DDT required to cause illness in some but not all subjects though there is chance of vomiting. (Hayes & Laws, 1991) . Convulsions are known to have taken place when the dosage level was 16 mg/kg or greater and no proper treatment had been taken. (Hseih, 1954). Amounts to the tune of 285 mg/kg are known to have been ingested without causing any harm. (Hayes & Laws, 1991). “Estimated lethal dose for man is 500 mg/kg and in kerosene solution it’s 150 mg/kg. Woodward et al. (1944) have stated the accepted acute mean lethal dose in rats as 250 mg/kg and Gosselin et al. (1984) has mentioned that the same amount would also be fatal for human beings. Baselt (1982) has stated that DDT is comparatively alright with a lethal dose of 30 g in an adult. “Exposure to an aerosol mist containing 80 mg DDT in a room of 113 m3 on five consecutive days for two hours two times a day showed no evidence of toxic effects”. (DDT, 1990) Studies have also revealed that the young are at no greater risk than adults. The four phases of the disposition of a toxic compound to estimate its toxicity are absorption through membranes in a system, the distribution throughout the system, the excretion and elimination from the system and finally, the metabolic fate of the chemical. Absorption happens from the gastrointestinal tract and through inhalation. DDT can also be taken in by intact skin in oily solution. DDT gets distributed in the body and primarily affects the central nervous system causing irritability. Violent agitations might also take place but is less common than with other organ chlorine pesticides. DDT tends to get accumulated in fatty tissues along with metabolites DDD and DDE. It also gets converted to DDA and dispatched through urine. Breathing in fine DDT aerosol or dust can cause problems for the nose, throat and eyes (Hayes & Laws, 1991). Formulations of DDT dissolved in a solvent is also known to cause temporary dermatitis. In most cases, the effect is attributable to the solvent and not DDT itself. Increased urinary excretion of the more polar metabolites is generally compensated for by increased steroid biosynthesis (Gosselin et al. , 1984). ). The effects of DDT on the respiratory system are only minor compared to the effects that it has on the nervous system. Heightened salivation has been observed in persons who consumed DDT-infested food (Hayes & Laws, 1991). Apart from vomiting, the gastrointestinal system is hardly affected in cases of extreme poisoning and Renal damage has also been observed in people to some extent. Types of Exposure and Responses associated with DDT: Food is the primary way in which the population gets exposed to DDT. And “due to its low biodegradability and high lyophilise properties, small amounts of DDT are found to have accumulated in adipose tissue. DDT tends to get stored to a lesser extent in other tissue and this amount is proportional to their neutral fat content.”(Data Sheet on Pesticides, 1976, 2.2) Almost 5000 tonnes of DDT is used every year for the control of vector-borne diseases, primarily for malaria and visceral leishmaniasis control. DDT is acknowledged as a persistent organic pollutant(POP). It gets stored in the fatty tissue of animals and humans, makes its way up the food chain and is found in high concentrations in human breast milk(biomagnification). Populations in areas close to countries which make use of DDT and in temperate regions can be indirectly affected by long-range atmospheric transport so that DDT may contaminate environments far from where it is used. Large exposures can result in vomiting. “The earliest symptoms include par aesthesia of the tongue, dizziness, tremors and vomiting. It is generally believed that long exposure to DDT and its main metabolic product DDE (dichlo-rodiphenyldichloroehtylene) can lead to deterioration of semen quality, early pregnancy loss, preterm birth, decreased lactation, fertility loss, leukaemia, neuro-developmental deficits, diabetes, breast cancer and urogenital birth defects. Studies on animals have shown neurotoxin, carcinogenic, immunologic and reproductive effects of DDT and DDE. DDT also affects shrimps, fish and wild birds.” (Vanessa et.al) “Paraesthesia of the tongue, lips and face are also symptoms arising from long-term exposure to DDT. The patient suffers dizziness, and objective disturbance equilibrium, and ataxia. Person will also suffer from headaches, feel lethargic and throat might also become sore.”(Data Sheet on Pesticides, 1976, 4.4) When the eyes are exposed to DDT, ocular irritation might occur. “Intravenous administration in animals can also result in ventricular fibrillation and death. This could infer similar implications for human beings also”. (DDT, 1990) Some risks of lymphoma, leukaemia, pancreatic cancer and breast cancer has been seen in humans exposed to DDT. Studies have also revealed a link between administration and lymphoma, respiratory cancer, liver cancer and estrogenic effects on mammary tissue. A human study has brought to light a not so strong relationship between DDT levels in core blood and low birth weight. IARC (1991) has conducted a study in which chromosomal irregularities were seen to have taken place in the peripheral lymphocytes of workers with increased plasma DDT levels. However, similar studies on bone-marrow cells of rodents have not led to the same findings. DDT is also seen to play truant with the metabolism and function of steroid hormones. Cardiac arrhythmias have been linked with death as a result of DDT poisoning in certain species of laboratory animals, but chances of something similar happening with human beings is less. Heart action may be affected and tachycardia may occur in cases of extreme poisoning. (Hayes & Laws, 1991). Exposure to DDT is also known to affect the eyes. Chronic superficial punctuate keratitis is one such complication that arises from long exposure to DDT dust. Dryness of throat is known to occur from the inhalation of DDT. In extreme cases of poisoning, haemoglobin levels are seen to fall and slight leukocytosis without any fixed deviation in the differential white count have been observed. DDT is also known to lead to depression though there is no conclusive proof to this effect. “Despite the increased exposure of the entire population of the world and the heavy occupational exposure of a great number, the only reported poisoning cases were owing to intentional or accidental ingestion.” (Data Sheet on Pesticides, 1976, 2.2.6) There are some alternatives to the use of DDT few of which include indoor residential spraying with pyrethroids or impregnated mosquito nets. (Vanessa et al.) But then, even these alternatives are known to inflict some damage because even they are after all chemicals, albeit of a different kind! It is common knowledge that reduction of vector-breeding habitats and heightened socioeconomic development with better hygiene and sanitation facilities can help get rid of malaria for good, thus eliminating the need to use DDT altogether. May counties have done away with the use of DDT, instead choosing to employ environmental management strategies and biological control for controlling malaria. In light of these facts, I think that the WHO should disallow the spraying of DDT for malaria-eradication purposes. References DDT. Dr Nida Besbelli Poison Centre. February 1990 http://www.inchem.org/documents/pds/pds/pest21_e.htm Laumann Vanessa, Brechelt Andrea, Gomero Luis, Bejarano Fernando, RAAA, RAPAM, Haffmans Susan. Phasing in Alternatives to DDT. Dec 2009. Gosselin RE, Smith RP & Hodge HC (1984) Clinical toxicology of commercial products, Williams & Wilkins, Baltimore 134-136 pp. Hayes WJ (Jr) & Laws ER (Jr) (eds) (1991) Handbook of pesticide toxicology, Academic Press, Inc. 743-780 pp. IARC (1991) IARC Monograph: Occupational Exposures in Insecticide Application and Some Pesticides. Vol. 53 179-248 pp. Hsieh HC (1954) DDT intoxication in a family of southern Taiwan. Arch. Ind. Hyg. Occup. Med. 10:3 44-346. Data Sheet on Pesticides, 1976 http://www.inchem.org/documents/pds/pds/pest21_e.htm Read More
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