DDT and its Effects on the Environment

DDT and its effect on the environment
Name
Institution

DDT and its effect on the environment
Introduction
Chemical compounds have become an important part of modern life owing to their use in industrial, agricultural and home environments. In fact, there are used for many functions to include artificial fibers, varnish, glue, cosmetics, paints, petrol, fertilizers, pesticides, medicine, nutritional additives and so on.1 Despite their value and importance for different values, chemical compounds have been reported to cause (or are implicated in causing) both environmental and health complications when released onto the environment. Examples of these complications include depletion of the ozone layer, acute poisoning, disruption of the endocrine system and cancer. Overall, these chemicals are known to contaminate environmental media that includes land, food, water, and air. This knowledge makes it evident that safety regarding chemical compounds is a challenge owing to their potential for causing harm.1
Internationally, the potential for chemical compounds to harm the environment when released is acknowledged and led to concerted efforts to avoid such scenarios as reflected in Chapter 19 of Agenda 21 concerning environmental protection. The document presents sound management strategies in the form of education programs, capacity to address emergencies, and ability to treat poisoning cases as well as rehabilitate contamination. In addition, it offers capacity for enforcement and implementation, establishes risks policies, interprets information, conducts risk assessment, and collects information for dissemination.

2 Other than Agenda 21, manufacture, storage and use of potentially harmful chemicals is managed by legally enforceable and ratified mechanisms that include the Vienna Convention, Basle Convention, and Rotterdam Convention.3 The present analysis acknowledges the need for controlling environmental exposure to harmful chemical compounds by exploring the potential of Dichlorodiphenyltrichloroethane (DDT) to cause harm and the need for concerted efforts in managing that harm.
Background information on DDT
First synthesized in 1874 by Othman Zeidler and reintroduced for public use in 1939 by Paul Muller, DDT is an insecticide (particularly organochlorine insecticide) that is typically used to control vectors for malaria and typhus. In fact, this was prominently use during the Second World War by Allied troops to control bubonic plague, body lice, typhus and malaria infections. Historical infection data for that time indicates that malaria infections fell from approximately half a million in 1946 to almost no new infections four years later.4 Following its successful use as an insecticide at the war front, the chemical compound was speedily adapted for agricultural use as an insecticide, and also for industrial use in controlling pests within buildings. This saw approximately 1.3 billion pounds of the chemical used for the next 30 years. As such, DDT was prominently used in the first half of the 20th century owing to its long half-life within the environment thereby allowing it to remain useful long after application, relative inexpensiveness to produce, and effectiveness. It is important to note that later evidence would reveal that DDT was actually harmful to the environment and insects developed resistance with the USA and Sweden taking decisive action to discontinue its use by initiating bans in 1972 and 1973 respectively. Currently, DDT use is heavily regulated across the world and presented in wettable powders, granules, emulsifiable concentrates, dustable powders, and aerosols. Besides that, it is presented in combination with other pesticides, although it is not compatible with alkaline substances.5,6
DDT’s potential to harm the environment was first documented by Rachel Carson (an American scientist) in 1962. She noted that the long-term use of the chemical compound as a pesticide made the environment uninhabitable by other organisms. In fact, she reported that birds suddenly died following the indiscriminate use of DDT as a spray in their environment. She reported her findings in a book titled ‘Silent Spring’. Rachel’s research findings shifted the public view on pesticides use by validating the concern for potentiality of negative effects on the environment. The book acts as the evidence base that informed the DDT ban by USA. More recent research studies have shown that DDT has a high persistence in the environment with a half-life of approximately 26 years.7 In addition, it has low solubility in water thereby allowing it to accumulate in fatty tissue of animals that come into contact with it. Owing to the extensive use of DDT during the mid 20th century, its tendency to travel over long distance uses the atmosphere, and chemical properties, DDT has now become widely distributed even in areas where it was never used to include the poles where its presence can be detected in the tissues of polar bears, birds, and fishes.7
Despite the ban on DDT use by most countries, there are some countries that have no legislation regarding DDT use. This means that there are countries where DDT is still routinely used. In addition, there are countries that have placed partial bans on DDT use, as seen in the case of USA where DDT manufacture is still ongoing and use is accepted for addressing public health emergencies that involve insects as vectors to include mosquitoes and body lice.8
DDT’s chemical properties
DDT has a molecular weight of 354.51. It is only slightly soluble in water at a rate of less than 1 milligram for every liter of water at a temperature of 20oC. Other than water, it is soluble in other chemical compounds and solvents that include methanol, ethanol, diethyl ether, chloroform, acetone, dichloromethane, trichloroethylene, xylene, benzene, dioxane, and cyclohexanone. The compound had a melting point of 108.75oC, a vapor pressure of 0.025 mPa at a temperature of 25oC. It has an absorption coefficient of 245,000, and partition coefficient (octanol/water) of 100,000.9
DDT’s environmental fate
Chemical Breakdown in vegetation
Unlike other organisms, plants only store the chemical for very short periods of time since they don’t take up much of it as seen in the case of turnips, radishes, and carrots that only report trace amounts when they are planted in soil treated with DDT. Very little accumulation has been reported in rice, maize and other grain plants, with the majority of the residues located in the plant roots.10 Still, there are cases when no translocation has been reported, particularly in the case of legumes to include soybean and alfalfa plants. This makes it clear that DDT has little to no effect on plants since accumulation and translocation is either minimal or does not occur at all.10
Chemical breakdown in surface water
DDT has been reported to reach surface water through the direct application (when controlling for water-borne disease vectors), drifts, transportation through the atmosphere, and runoff. This is not a significant source of concern since it has a half-life of 28 days in running water such as rivers and streams, and a half-life of 56 days in stagnant water such as lakes, dams, and ponds. Loss occurs at a fast rate through sedimentation, water-borne particulates adsorption, photodegradation, and volatilization. Despite having a very short half-life in water, DDT is still a source of concern for the organisms living in the water since aquatic organisms have been reported to readily take up and store the chemical along with its metabolites.8
Chemical breakdown in groundwater and soil
As earlier indicated, DDT persists for long periods of time in the environment, with a half-life of 26 years. In addition, it is immobilized when applied to soils, with its degradation and loss only occurring through respiration by microorganisms (biodegradation), photolysis, volatilization, and run off. Even when broken into dichlorodiphenyldichloroethane (DDD) and dichlorodiphenyldichloroethylene (DDE) as its metabolic products, DDT still remains very dangerous since these products have physical and chemical properties that match the properties of DDT.11 Owing to its low solubility in water, soil retains a lot of DDT especially in its organic matter. This means that it easily accumulates in the topsoil where it was applied, and the organisms that come into contact with the DDT died and rotted. By and large, soil organic matter tightly sorbs DDT, although some of it leaches to other areas where it ends up contaminating the ground water and becomes available to other organisms. That is despite the fact that it is only slightly mobile since it has a long half-life and makes use of that time to leach through the soil. DDT breakdown in soil occurs at a faster rate on the surface with that rate reducing with increasing depth into the soil. Also, it is notable that vitalization losses are less significant in soils rich in organic matter although exposure to sunlight increases those losses. In fact, 50% losses in 150 days have been reported in desert environments with high exposure to sunlight and low organic content while soils rich in organic content and away from direct sunlight have reported 17% losses occurring over a period of five years. As such, DDT breakdown in soil and ground water is dependent on exposure to sunlight, proximity to the surface, organic matter proportions and amount of DDT.11
DDT effects on the ecology
DDT has been reported to have little to no effect on avian life forms. In this case, DDT exposure typically occurs through the food chain when terrestrial and aquatic species feed on other organisms such as earthworms and fish with the DDT in their systems. Pheasants have reported DDT proportions of 1,334 mg/kg, Japanese quail reported 841 mg/kg, and mallard reported 2,240 mg/kg to imply that while DDT may not be directly dangerous to bird, it is dangerous other organisms that feed on the birds. In addition, DDT has been reported to result in death of embryos, thinning of eggshells, and compromised reproduction. It causes the death of embryos and eggshells thinking through DDE as a metabolite.12 Regarding reproduction, it decreases the weight of eggs, delays egg laying, delays pairing bird couples, and reduces courtship behavior. These effects have long-term implication for the survival and reproduction of birds. It must be noted that DDT can combine with other chemical compounds to have a direct effect on birds. This is seen in the case of cholinesterase-inhibiting pesticides (such as organophosphate) combining with DDT metabolites to increasing avian mortality by affecting the nervous system, and combinations with polychlorinated biphenyls such as arocolor to increase eggshell thinning.12,13
DDT has a profound effect on aquatic invertebrate organisms since it is toxic to them. Susceptibility decreases with increase in age to imply that younger invertebrates are more susceptible to the toxic effects of DDT than their older counterparts. In addition to having an immediate effect, DDT bioaccumulates in this organisms to result in long-term exposure. This is mainly seen when feeding occurs from contaminated aquatic fauna and flora, as well as sediments. Also, smaller sized fish accumulate large amounts of DDT owing to their larger surface area to volume ratio.14
DDT has been reported to have no effect on other non-target, other than them being bioaccumulation and exposure sources for other organisms. An example of this is seen in the case of earthworms that do not experience the acute effects of DDT and its metabolites owing to their unique body systems, but it is able to accumulate the compound and its metabolites and passes it on to other organisms in the food web. In addition to earthworms, DDT is not toxic to bees, with the LD50 being 27 ug/bee.15
DDT effect on vertebrate animals
DDT has an effect on the vertebrate animals, particularly the kidneys, lungs, liver and nerves. In this case, it causes the production of tumors in lungs and the liver. In this case, it is very slowly degraded in the body, initially presented as DDD and DDE before being stored in the fatty tissues. Next, they are converted into 2,2-bis(4-chlorophenyl)-acetic acid (DDA) and its conjugates that are then excreted in urine via the kidneys. DDT has also been linked to cancer occurrence when exposure occurs at high doses over long periods of time. In this case, evidence shows that it increases the production of tumors in the lungs and kidneys of vertebrate animals. This linked has been linked to genotoxicity and mutagenicity whereby exposure to DDT causes chromosomal damage.16,17,18
In addition, DDT has chronic effect on the immune system, kidneys, liver, and nervous system. It affects the kidneys by causing damage to the adrenal glands. It affects the liver by increasing the liver enzyme activity and weight, and changing the liver physiology. The effects on the nervous system have been noted to include loss of equilibrium, changes to cellular chemistry of the nerve cells, and tremors. It affects the immune system by reducing antibody formation.18
It is important to note that DDT is only slightly toxic to vertebrate animals when ingested through the oral route, although the toxicity may vary significantly depending on its formulation. It is readily absorbed through the gastrointestinal tract, with absorption levels noted to increase in direct proportion to the presence and amount of fat tissue. Once ingested, the chemical compound reduces thyroid function, increases the amounts of liver-produced enzymes, and alters the central nervous system’s cellular chemistry.17 Also, it produces paralysis of the hind leg, convulsions, and alters neurological development. Dermal application of DDT is typically non-toxic since it is not readily absorbed through the skin unless it is administered in solution form. Inhalation minimal toxic effect since the chemical compound is trapped by the mucosal secretions and cleared through the cilia-mediated tracheobronchial secretion clearance system found on the surface of gas exchange sacs in the lungs.17
DDT entrance into the body can cause immediate effects in the form of convulsions and tremors, excitability, malaise, disturbed gait, eyes, nose and throat irritation, elevated liver enzymes activity, diarrhea, and nausea. While adults can tolerate DDT when ingested, children report fatal poisoning outcomes when exposed to the same doses.16
DDT’s chemical properties allow it to accumulate in fatty tissues of animals, with that accumulation not associated with any toxic effects. Once in the body, the DDT is broken down into DDE, DDD and DDA that is then released into the nervous system and liver where it affects functions. It is then excreted from the body in breast milk, feces, urine and perspiration.17 Since DDT can be stored in fats, it has the capacity to accumulate in the body and it then transferred to other organisms in the food chain through feeding mechanisms when animals in the lower sections of the food chain feed the animals in the upper sections of the same chain. This cumulative effect continues until it reaches the primary predator at the topmost part of the chain who ends up receiving the highest dose and experiencing the most adverse effects.17
Overall, DDT presents different toxicity categories. Higher toxicity is reported for dermal application, with moderate toxicity reported for inhalation and high toxicity reported for oral application. Also, it is highly corrosive in large doses (see Table 1).19,20
Table SEQ Table * ARABIC 1. Toxicity categories based on mode of application and contact area for single dose application19,20
Toxicity level
Very low Low Moderate High
Advice Caution Caution Warning Danger
Application at LD50/LC50a Dermal More than 5,000 mg/kg Between 2,000 and 5,000 mg/kg Between 200 and 2,000 mg/kg Less than 200 mg/kg
Inhalation More than 20 mg/l Between 2 and 20 mg/l Between 0.2 and 2 mg/l Less than 0.2 mg/l
Oral More than 5,000 mg/kg Between 500 and 5,000 mg/kg Between 50 and 500 mg/kg Less than 50 mg/kg
Effects Skin Slight or mild irritation at 72 hours Moderate irritation occurs at 72 hours Severe irritation occurs at 72 hours Corrosive
Eye No irritation Irritation reverse within one week Irritation persists for more than one week Corrosive
a : LD50 refers to the lethal dose while LC50 refers to the lethal concentration as common measures of toxicity, which can cause death in at least half of the exposed organisms for single dose application.
Conclusion
One must accept that chemicals are important compounds for use in homes and industries. In addition, one must acknowledge that they present a contamination and pollution problem for the environment. This awareness has informed the development of legally enforceable and ratified mechanisms to facilitate environmental protection. DDT is an example of a chemical that was extensively used as a pesticide but whose use has since been discontinued owing to its harmful effects on the environment. In fact, DDT is noted for being retained in the environment for long periods of time where it flows through the food chain to cause toxic effects on living cells to include the chronic effect on the immune system, kidneys, liver, and nervous systems such as the formation of tumors and cancer occurrence. Also, it is noted that oral ingestion presents higher toxicity levels, to be followed by inhalation with dermal contact having the least toxicity. In this respect, DDT is a chemical compound that causes toxic effects on the environment but is applicable as an insecticide.

References
1. Whitacre, D. Reviews of Environmental Contamination and Toxicology; Springer: Berlin, 2009; pp. 4-5.
2. United Nations. Agenda 21: United Nations Conference on Environment & Development, Rio de Janerio, Brazil, 3 to 14 June 1992; Author; New York, NY, 1992; p. 226. <https://sustainabledevelopment.un.org/content/documents/Agenda21.pdf>
3. Baylis, J.; Smith, S.; Owen, P. The Globalization of World Politics: An introduction to international relations; Oxford University Press; Oxford, 2013; pp. 343-345.
4. Hoff, G.; Davis, J. Noninfectious diseases of wildlife; Iowa State University Press: Ames, IA, 1982; p. 38.
5. Gerlach, S. Marine Pollution: Diagnosis and therapy; Springer: Berlin, 2013, pp. 167-168.
6. Roberts, J. Organic Agriculture: Protecting our food supply or chasing imaginary risks? Twenty-First Century Books: Minneapolis, MN, 2012, pp. 62-63.
7. Sideris, L.; Moore, K. Rachel Carson: Legacy and Challenge; State University of New York: Albany, NY, 2008, pp. 196-199.
8. Friis, R. Essentials of Environmental Health; Jones & Bartlett Publishers: Burlington, MA, 2012, pp. 161-162.
9. Mackay, D.; Shiu, W; Ma, K. Illustrated Handbook of Physical-Chemical Properties and Environmental Fate for Organic Chemicals: Pesticide chemicals; Lewis Publishers: New York, NY, 1997, pp. 391-392.
10. Raven, P.; Berg, L.; Hassenzahl, D. Environment. John Wiley & Sons: Hoboken, NJ, 2012, p. 464.
11. Cockerham, L.; Shane, B. Basic Environmental Toxicology; CRC Press: Boca Raton, FL, 2000, pp. 192-194.
12. Goudie, A. The Human Impact on the Natural Environment, 5th ed.; The MIT Press: Cambridge, MA, 2000, p. 123.
13. Freedman, B. Environmental Ecology: The impacts of pollution and other stresses on ecosystem structure and function; Academic Press, Inc.: San Diego, CA, 2013, p. 195.
14. Sabljic, A. Environmental and Ecological Chemistry: Encyclopedia of life support systems; Eolss Publishers: Oxford, 2009, pp. 156-157.
15. Booth, D. The Environmental Consequences of Growth: Steady-State Economics as an alternative to ecological decline; Routledge, London, 2006, pp. 97-98.
16. Kirk, K. Biochemistry of the Elemental Halogens and Inorganic Halides. Plenum Books: New York, NY, 2012, pp. 254-256.
17. Walker, C.; Sibly, R.; Peakall, D. Principles of Ecotoxicology, 2nd ed.; CRC Press: Boca Raton, FL, 2009, pp. 95-96.
18. Walker, C.; Organic Pollutants: An ecotoxicological perspective, 2nd ed.; CRC Press: Boca Raton, FL, 2009, pp. 104-105.
19. Singh, D. Pesticide Chemistry and Toxicology; Bentham Science Publishers: Sharjah, UAE, 2012, pp. 50-52.
20. Vallero, D. Environmental Biotechnology: A biosystems approach; Academic Press: London, 2010, p. 653.