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Introduction
Environmental pollution has been a controversial topic and is at the heart of scientific driven research to address the associated public health impacts, in particular the global burden of disease. Scientists have highlighted that the concern was not simply the pollution of the environment, but also the effect that chemical pollutants are having on human and animal health (1, 2). Endocrine disrupting chemicals (EDCs) are ubiquitous in the environment and have the ability to interfere with, amongst others, hormonedependent physiological processes through the interaction with hormone receptors (3).
The potential of EDCs to disrupt normal hormone-dependent processes both pre- and post-natally in humans and wildlife is of great concern. The 2012 ‘State of the science of endocrine disrupting chemicals’ report (3) detailed various aspects of monitoring and investigation of possible solutions to reduce the adverse health effects caused by exposure to EDCs. Recently journal the Endocrinology devoted the October 2015 issue to ‘Prenatal Programming and Endocrinology’, discussing topics on developmental origins of health and disease and the fetal basis of adult disease (4). Numerous studies focused on the effects that both acute and chronic exposure to EDCs may have on humans and wildlife. These studies have shown that exposure to EDCs potentially impact growth and development of various bodily organs, bodily processes and fertility (5-12). Exposures to various EDCs have been reported to influence embryonic development, especially at the androgen-sensitive sex-determining programing windows during early gestation (13). Changes in endogenous hormone regulation during embryonic development may result in impaired functioning of bodily systems, such as the male urogenital system (14, 15). The impact of embryonic exposure may be identifiable at birth, as in the case of urogenital abnormalities, or later in adult life, such as testicular cancer in young men, or poor semen quality after puberty. However, effects manifesting in adulthood are difficult to attribute to pre- and postnatal developmental exposure without reliable exposure data occurring during either pre- or postnatal periods.
Known EDCs include various alkylphenols, dioxins and furans, pharmaceuticals,phthalates, phytoestrogens and polychlorinated biphenyls (PCBs) and organochlorine pesticides (3, 16). The use of pesticides has given humankind a weapon to fight both the onslaught of insect-derived crop damage and vector-borne diseases. The organochlorine pesticide 1,1,1-trichloro-2,2-bis(p-chlorophenyl)ethane (DDT) was successfully used across the world until its ban in most countries, including the United States of America (USA) in 1972, following reports of adverse health effects in wildlife (17). In South Africa (SA), the use of DDT was banned for agricultural use in 1976, but not for malaria vector control.
In the Limpopo Province, South Africa, DDT has been sprayed continually since the 1940s (7). In 2002 SA ratified the Stockholm Convention and is therefore permitted to use DDT for malaria vector control (18) through indoor residual spraying (IRS) programs (19). The major concern with IRS programs stem from incorrect storage, application and contamination of the surrounding areas (20) which poses a health concern for both animals and humans.
Technical-grade DDT consisting of 65–80% of the active insecticidal ingredient p,p′-DDT and 15–21% of the less insecticidal o,p′-DDT (17, 21) is used for IRS. The o,p’-DDT and to a lesser extent p,p′-DDT component, both have estrogenic properties (21). Dietary and environmental exposures to p,p′-DDT and its metabolites result in bio-accumulation of these chemicals in adipose tissue and serum in the human body (21-24). The DDT from the circulation is metabolized into 1,1-dichloro-2,2-bis(p-chlorophenyl)ethylene (p,p′-DDE) which is the persistent metabolite that bio-accumulates in fatty tissue. DDT and p,p′-DDE have the ability to cross the placenta with concentrations in cord blood being similar to concentrations in maternal blood (21). p,p′-DDE is a potent inhibitor of androgen binding to the androgen receptor (25), androgen-induced transcriptional activity and androgen action in males during development and in adulthood (26). This suggests that abnormalities in male sex development induced by p,p’-DDE may be mediated at the level of the androgen receptor (26).
CHAPTER 1: INTRODUCTION
1.1. Background
1.2. Problem statement
CHAPTER 2: LITERATURE REVIEW.
2.1. Male reproduction
2.2. Testes
2.3. Sertoli and Leydig cells
2.4. Spermatogenesis
2.5. Endocrine system
2.6. Endocrine disrupting chemicals
2.7. Environmental mixtures
2.8. Effects of EDC exposure
CHAPTER 3: AIM AND OBJECTIVES
CHAPTER 4: MATERIALS AND METHODS
CHAPTER 5: RESULTS
