DDT

Ina Keyser 10144383

ANA324 University of Pretoria 24 October 2012

1. DDT: A History and its Uses [1] Dichlorodiphenyltrichloroethane (DDT) is an organo-chlorinephosphate hydrophobic molecule, produced and used as a contact insecticide. In its industrially produced form, DDT is a tasteless and almost odourless white crystalline solid which is powdered and modified to a water-soluble dust to be sprayed over plants and water. In the past DDT was also transformed into aerosols for direct application to humans and animals. Commercial DDT is a mixture of several similar compounds: 77% DDT, 15% dichlorodiphenyldichloroethylene (DDE) and 8% dichlorodiphenyldichloroethane (DDD).

Figure 1: Chemical Structure of DDT

Figure 2: Farmer spraying dam with DDT

Figure 3: Soldier Sprayed with DDT

DDT was first synthesized in 1874. Its properties, however, were not discovered until 1939 by Swiss chemist Paul Hermann Mller, who was awarded the Nobel Prize in Physiology or Medicine in 1948: "for his discovery of the high efficiency of DDT as a contact poison against several arthropods. [3]. DDT was introduced to the world during the second part of World War II as a method to control malaria and typhus among civilians and troops. After the war, DDT was made available for use as an agricultural insecticide and mass production and use skyrocketed in USA, China and India [4].

Silent Spring, a book published in 1962 by American biologist Rachel Carson, catalogued the environmental impacts of the indiscriminate spraying of DDT in the US. Carson noted that the there was a massive increase in the incidence level of cancer, especially breast cancer, in areas where DDT was sprayed. It also became evident there was a decrease in biodiversity in wildlife and most notably in apex animals, such as birds of prey. The book resulted in an outcry from the scientific community as well as the general population and the large scale spraying of DDT in nature reserves and community neighbourhoods was banned in the US in 1972 [4].

In the following years worldwide controversy surfaced, due to the unpredicted, but visible negative effects of DDT. It was only in 2001, under the Stockholm Convention, that the use of DDT for agricultural use was globally banned [4]. The limited use of DDT in disease vector control is still permitted and continues to this day in some developing countries, such as in Africa. This however is remains controversial and other methods of disease prevention, e.g. malaria, is continually sought after [6, 7].

2. Mechanism of Action a. Soil, Water and Plants [6] DDT is a persistent organic pollutant that is readily absorbed by soil and sediments. Depending on the soil quality and condition, the average halflife of DDT ranges from 22 days to 30 years (reduced by counteracting with green algae extract). DDT and its metabolites (incl. isomeric forms) are degraded and removed from the soil by: runoff, volatilization, photolysis, and aerobic and anaerobic biodegradation by bacteria in the soil.

Due to the hydrophobic properties of DDT, it is absorbed by creatures and suspended particles in an aquatic ecosystem, e.g. fish, frogs, plants and other micro-organisms such as amoebas. Very little DDT remains dissolved in the water.

Plants are the only living organisms that are not affected by the chemical itself. However, DDT can accumulate in the amylose stores of plant material and be transferred to other organisms that feed on the plant.

b. Insects [7] Arthropods (or in laymans terms insects with an exoskeleton) absorb DDT through the gastro-intestinal tract (GIT) and respiratory and sensory organs in exoskeleton. DDT directly competes with neurotransmitters, such as acetylcholine (Ach), to bind to receptors of the post-synaptic neuron and stimulates sodium ion channels in the post-synaptic neuron to open. The central nervous system (CNS) as well as the peripheral nervous system (PNS) is compromised and results in spasms throughout the body. The spontaneously firing neurons cause irregular neural stimulation in vital organs, such as the heart, and leads to eventual death of the arthropod. Some insects with certain mutations in their sodium channel transcribing gene are resistant to DDT and DDT resistance is also conferred by upregulation of genes expressing cytochrome P450 in some insect species.

c. Animals and Humans [8] DDT is toxic to a wide range of living organisms, especially in: Marine animals, such as crayfish and many fish species; and Amphibians, such as frogs and salamanders during the larval phase.

It is less toxic in mammals, but can still have detrimental effects. DDT has lipophilic properties which mean that it is stored and accumulates in adipose tissue of animals and humans. It has as high potential to bioaccumulate through the food chain, causing a build-up of the chemical as one animal feeds on another that has been exposed to DDT. Apex

predators e.g. raptor birds, tend to present with a higher concentration of DDT than other animals that live in the same environment. In birds DDT and more so DDE, has been found to supress the reproductive systems of birds, resulting in eggshell thinning. These species have a decreased chance for survival in the wild and biodiversity tends to drop. In rats an LD50 of 113mg/kg has been proved [9], indicating that DDT may not be lethal in rats, but can still be toxic. The half-life in the human body ranges from 6 to ten years a very long time! The mechanism of action is described as: i. Direct Genotoxicity DDT and/or DDE diffuse through the cell membrane and enter the nucleus where the chemical starts to disrupt the DNA structure causing the DNA molecule to lose its double helix configuration. ii. Indirect Induction of Apoptotic Enzymes DDT and/DDE diffuse through the cell membrane and binds to apoptotic receptors in the cytosol, which activates the apoptosis enzyme cascade thus resulting in DNA degradation. iii. Endocrine disruptor DDT metabolite DDE acts as an anti-androgen and in some very rare cases, it has been proved that DDE may have mild-oestrogen activity. DDE disrupts the levels and relationships of the sex hormones which has devastating effects on the reproductive systems (both male and female) and reproduction. In men, due to irregularity in testosterone cycles, DDE may decrease semen quality; either due to the production of defective sperm or a decrease in the number of normal sperm produced. Menstrual cycles, in women, are altered in duration and frequency. Fluctuating oestrogen and progesterone levels (due to DDT exposure) can cause other syndromes and defects, e.g. cystic ovarian syndrome, which may render a woman infertile. In a pregnant woman, DDE may alter the gestational length as well as post-natal duration of lactation. Other endocrine associated diseases may also occur, e.g. cancer of the liver, pancreas (associated with Type II Diabetes), testicles, ovaries and breasts.

iv. Neurological Stimulant DDT directly competes with neurotransmitters, such as acetylcholine (Ach), to bind to receptors of the post-synaptic neuron and stimulates sodium ion channels in the post-synaptic neuron to open. The central nervous system (CNS) as well as the peripheral nervous system (PNS) is compromised and results in spasms throughout the body. The spontaneously firing of neurons of the parasympathetic and sympathetic nervous systems may cause irregular neural stimulation in vital organs, such as the heart and can manifest in cardiac arrhythmias Other associated neurological dysfunctions include Parkinsons disease and asthma.

3. DDT: Effects on Embryological Development Various detrimental effects of DDT and DDE on embryological development have been documented and researched. Studies conducted at the University of California suggest that in vitro exposure of mice and zebra fish may cause abnormal neural development or complete neurotoxicity in an embryo [13]. Less invasive studies conducted on humans, also at the University of California, confirmed that low levels of DDE in umbilical serum is associated with decreased attention and cognitive functions of the child at infancy. First trimester exposure to DDE may also result in retarded psychomotor development [9]. A Japanese study conducted on congenital hypo- and hyperthyroidism concluded that in utero DDT exposure may affect thyroid function, resulting in hypo/hyperthyroidism [10]. As a result, abnormal levels of T3 and T4 can increase the incidence and/or causation of cretinism. Research done by The Lancet has shown that exposure to DDT, at amounts similar to that which would be needed in malaria control, may cause [11]: preterm birth, low birth weight, early weaning, and shorten lactation and weaning which may result in malnutrition at infancy.

A Study done of Chinese textile workers in 1964, showed a 64% increase in miscarriages in pregnant workers (mostly in first trimester) who were exposed to DDT in factories [12].

4. Conclusion DDT is a toxic and environmentally harmful chemical with a lipophilic accumulative mechanism of action. It is bio-accumulative and may cause worsening effects at higher levels in the food chain (such as apex animals). The effects are hyper-toxic and in some cases, lethal in lower class animals, e.g. marine and aquatic organisms. In mammals the effects are less toxic, but still harmful. In humans DDT and its metabolites (e.g. DDE) especially affects the reproductive system of adults that leads to abnormal spermatogenesis (male) and oogenesis (female); miscarriage; premature birth and decreased post-natal lactation. When accumulated in the adipose tissue of the body, DDT may cause abnormal endocrine activity which is associated with cancer and decreased neurological functioning.

5. References 1. Toxicological Profile: for DDT, DDE, and DDE. Agency for Toxic Substances and Disease Registry, September 2002. 2. DDT and Its Derivatives. Geneva: World Health Organisation. 1989. p. 83. ISBN 92-4-154283-7. 3. NobelPrize.org: The Nobel Prize in Physiology of Medicine 1948 Accessed July 26, 2007. 4. Environmental Health Criteria 9: DDT and its derivatives, World Health Organization, 1979. 5. Lear, Linda (1997). Rachel Carson: Witness for Nature. New York: Henry Hoyten. 6. Larson, Kim (December 1, 2007). "Bad Blood". On Earth (Winter 2008). Retrieved 2008-06-05. 7. Moyers, Bill (2007-09-21), Rachel Carson and DDT, retrieved 2011-03-05 8. Stokstad E (June 2007). "Species conservation. Can the bald eagle still soar after it is delisted?. Science 316 (5832): 168990. doi:10.1126/science.316.5832.1689. PMID 17588911. 9. Geisz HN, Dickhut RM, Cochran MA, Fraser WR, Ducklow HW (2005). 10. Melting Glaciers: A Probable Source of DDT to the Antarctic Marine Ecosystem". Environ. Sci. Technol. ASAP: 3958. doi:10.1021/es702919n. Retrieved 2008-0507. 11. DAVID, DAVID (July 4, 2008) McIntosh residents file suit against Ciba. Archived from the original on 2010-11-18. Retrieved 2008-07-07. 12. Environmental Cleanup Site Information Database for Arkema (former Pennwalt) facility, Oregon DEQ, April 2009. 13. Rosemary, Rosemary (2008-01-27). Tests shed light on how pCBSA got into St. Louis water