Environment Hormone Mimics - Assignment Example

College: Environmental Hormone Mimics Introduction Environmental hormone mimics are synthetic chemicals that get depositedin the environment due to industrial activity and which disrupt the production, transport, receptor binding, action, or elimination of the body’s natural hormones that are responsible for normal development, fertility, behavior, and maintenance of homeostasis. They interfere with the hormone (endocrine) system in animals including humans. Therefore, they are also known as hormone disruptors since they disrupt the normal functional of hormones. The hormonal disruptions caused by environmental hormone mimics are suspected or known to induce a variety of pathological conditions in humans. They may result in developmental disorders such as birth defects and cancerous tumors. Scientists and medical experts have established that environmental hormone mimics cause cognitive and brain developmental problems, such as severe attention deficit disorder and learning disabilities. They can also cause physical deformations of various parts of the body such as limbs, and can cause sexual, developmental problems including the feminization of males or producing of masculine characteristics in females (Colborn, Saal & Soto, 1993). The Role of Hormones Hormones control most of the human body’s functions. They range from the maintenance of body heat, to growth and reproduction. For example, the pituitary and adrenal glands each secrete several hormones. Once released, these hormones travel to their target cells through the blood, where they bind to their receptors in a ‘lock and key’ fashion. Their binding triggers intracellular machinery, which brings about the desired response from the cell. Although hormones are quite large and complex molecules, they interact with their receptors in a rather simple way which simpler chemicals can emulate. However, only the hormone can elicit the normal response that result from binding to its receptors. The mimicking molecules only bind to the receptors, but do not trigger the desired response associated with the hormone. Thus, it prevents the hormone from binding to the receptor and elicits an undesired response. Some hormone mimics act by latching onto the hormone receptor and triggering a spurious response which may send associated body functions into overdrive. Consequently, the essential body function the hormone mediates alters in an adverse way. Ultimately, pathological states result which interfere with the life of the affected person or may even be lethal. The first of such hormone mimics to be identified had a tendency to interfere with the female hormone estrogens. However, researchers have now established that this is just one example of numerous hormone mimicking chemicals that are present in the environment, but have their origin in industrial processes (Clark, Watson & Upchurch, 2007). Overview Various classes of chemicals function as environmental hormone mimics. They include pesticides, drugs, and consumer products, compounds used in the plastic industry, pollutants, industrial by-products, and some botanical chemicals that have a natural origin. Some of these chemicals are pervasive and get widely dispersed in both the built and natural environments and may accumulate in biological systems. Some of them are persistent organic pollutants (POP’s), which can be carried long distances by water or wind to virtually all regions around the world. They especially portray a tendency to accumulate near the North Pole, as a result of cold conditions and weather patterns. However, some environmental hormone mimics last for only short periods in the environment or human body because various processes rapidly degrade them into environmentally compatible components (Colborn, Saal & Soto, 1993). The issue of environmental hormone mimics has not been around for long. Since these chemicals originate from industrial processes, they began to become serious toxins to humans and wildlife following increased mass production of manufactured goods in the mid-twentieth century. For the first time, synthetic chemicals became fundamental components of the numerous consumer and producer products that were now available to people and organizations. They were useful as refrigerants, pesticides, and cosmetics among numerous other uses. As a result, contamination of the environment by these chemicals, many of which are not biologically degradable or are extremely resistant to biological degrading mechanisms, increased considerably. As they accumulate in the environment, organisms at the bottom of food chains in the ecosystem consume them; and they begin to accumulate in organisms higher up the food chains. In addition, some organisms high up in the food chains consumer them directly , for example, through the drinking of contaminated water. Previously, research concerning potential harmful effects of synthetic chemicals to humans focused almost entirely on cancer. This is because cancer has been a serious threat to public health for the last few decades, whereas endocrine disorders have not. Furthermore, the link with cancer seemed more likely than the link with endocrine disorders because humans require only minor exposure to carcinogenic agents to develop cancer, whereas people thought endocrine disorders required significant exposure to large amounts of environmental hormone mimics before developing. Since, these chemicals occurred in low concentrations in the environment, the first alternative seemed more likely than the second. However, environmental scientists maintained that these chemicals could be causing serious endocrine disorders, but public health officials ignored them, preferring to allocate limited funds to areas of public health research that had the largest impact on safeguarding the health of the public (Trankina & Gough, 2007). In the late 1980s, a scientist by the name of Theo Colborn was undertaking a research study about the effects of industrial pollution in the region of the Great Lakes. The observations that she made enabled her to make crucial links between environmental hormone mimics and various developmental abnormalities, which were prevalent in the region at the time. Her interest spurred; and she began to review related works of other researchers and identified striking parallels between them. Colborn made contact with some of these researchers, and they began to coordinate their studies. This concerted effort eventually established the common hypothesis that all the endocrine disorders they observed in their subjects resulted from abnormal estrogen activity. Further studies identified more than 50 synthetic chemical compounds as the causative agents, which mimic the action of estrogenic hormones that mediate female sexual development and a host of other biological functions, or disrupt the normal functioning of this powerful hormone. These efforts were corroborated further by a large scale European study which suggested that the sperm counts of male Europeans had decreased by a staggering 50 percent in the past five decades, and that the rates of testicular cancer had increased three-fold. This study finally heightened concern that these chemical environment contaminants may cause serious health effects in humans. Later in the decade, some scientists claimed that there might be a relationship between cancer of the breast and these disruptors (Trankina & Gough, 2007). Research Providing Strong Evidence on Humans Scientific studies conducted in the last two decades have established a link between environmental hormone mimics and three crucial areas of human disease and abnormalities. These are declines in male sperm count, cancer, and a number of neurological disorders including neurobehavioral and cognitive effects. In the last 50 years, the density and quality of sperm in the general male population in industrialized regions of the world has undergone a downward trend. These studies are not conclusive because of lack of consistent patterns within each region. Nevertheless, they are something to go by because they portray striking parallelism in their results. Still, many reproductive toxicologists maintain that supporting evidence from studies carried out on animals justify the link between environmental hormone mimics. Researchers have uncovered quite strong evidence linking environmental hormone mimics to cancer. It is a common fact that estrogens induce the growth of certain types of cancer cells. Longer lifetime exposure to natural estrogen due to late menopause increases the risk of breast cancer among women. Low prevalence of cancer among women whose ovaries have been removed and those who have undergone tile procedures further provides strong evidence there is a link between high levels of estrogen and breast cancer (Clark, Watson & Upchurch, 2007). The most convincing evidence providing a link to environmental hormone mimics and adverse health effects in humans come from studies focusing on abnormalities involving the nervous system. Of particular not are polychrolinated biphenyls (PCBs), which are mainly useful as coolants in industrial plants and lubricants. Studies conducted on children in the Great Lakes region, where there is high consumption of fish, indicate that these children have a higher prevalence of neurodevelopment and neurological abnormalities. The fish in these lakes have a high concentration of PCBs, which leaks into the water from industrial plants in the area. Mothers who consumed fish excessively while pregnant exposed their developing fetus to these chemicals which eventually resulted in the aforementioned disorders. The neurological disorders exhibited by these children included abnormally low scores on intelligence tests and delayed neuromuscular development. In addition, quite a significant number of these children portrayed symptoms of disturbances in the proper functioning of thyroid hormones. Thus, researchers made the connection that these thyroid disturbances may be the cause of the neurodevelopment disorders because they are necessary for prenatal neurological growth and development. Even minor disturbances in the balance between these hormones may adversely impair cognitive development. The adverse effects of PCB exposure to the health of humans became confirmed when two incidents of contaminated cooking oil in Taiwan (Yu-Cheng disease, 1979) and Japan (Yusho disease), left thousands of residents poisoned due to PCB exposure. This led to the worldwide ban of its use in 1977. Some recent studies suggest that PCB increases the risk of childhood obesity when exposure occurs prenatally, and may elevate the risk of diabetes (Trankina & Gough, 2007). Polybrominated diphenyl ethers (PBDEs) are synthetic chemicals that have a structure similar to that of PCBs. Therefore, their neurotoxic effects are largely similar to those brought about by PCBs. PBDEs are mainly components of flame retardants that form part of the plastic cases of computers and televisions, electronics, lighting, carpets, clothing, bedding, foam cushions, car components, and various other textiles. Just like PCBs, PBDEs have the potential of inducing imbalance of thyroid hormones and cause various developmental and neurological deficits. These include learning disabilities and low intelligence. Studies conducted with rodents suggest that even brief PBDE exposure disrupts normal thyroid hormone regulation. Bisphenol A (BPA) is another known environmental hormone mimic. It is common in plastic food containers, plastic bottles, dental materials, and the lining of metallic food and infant formula cans. Studies conducted on laboratory animals indicate that low level exposure can lead to increased rates of diabetes, prostate and mammary cancer, reproductive problems, decreased sperm count, neurological problems, obesity, and early puberty. Prenatal development stages appear to be most vulnerable to its effects. The safety level of BPA previously determined by regulatory bodies is now under question or review because of new evidence provided by scientific studies. A study conducted in the U.S., to investigate the number of harmful chemicals pregnant women get exposed to, established that 96% of pregnant women have BPA in their system (Colborn, Saal & Soto, 1993). Phthalates are a class of compounds that are abundant in plastics that have chlorinated compounds as one of the essential components. Their main role in plastics is to serve as softening agents. However, the resin binds them loosely, making it relatively easy for them to leach off and leak into the environment. Di-(2-ethylexyl)-phthalate (DEHP) is put to extensive use in the plastic industry and causes reproductive deficiencies in females when exposed to it on an occupational capacity. According to the U.S. Center for Disease Control, beauty products including cosmetics and perfumes may be the chief source of this contamination because their volatile components are mainly phthalate-based compounds. Dichlorodiphenyltrichloroethane (DDT) is a pesticide and insecticide that found widespread use throughout the world to control various pests and insects that transmit diseases such as malaria, dysentery, epidemic typhus, and typhoid fever. Therefore, DDT was widely used to exterminate insects such as mosquitoes, lice, and houseflies, which are the carriers of these diseases. DDT also found extensive use as a pesticide in agriculture in the years after World War II, but its use in this capacity has now been banned in most countries. Studies conducted more than sixty years ago established that DDT disrupts normal reproductive development. Other studies conducted recently suggest that DDT interferes with proper development of female organs of reproduction, adversely affecting their maturation and proper functioning. Other studies indicate that a considerable decrease in male infertility could be due to exposure to DDT. More recently, researchers suggested that in utero exposure to DDT may elevate a child’s risk of developing childhood obesity. Despite these possible side effects of DDT exposure, the chemical still finds use as an anti-malarial insecticide in many regions of South East Asia and Africa, albeit in limited quantities (Clark, Watson & Upchurch, 2007). Research Providing Strong Evidence on Wildlife Researchers have carried out numerous studies to determine whether there a link exists between exposure of wildlife to environmental hormone mimics and certain reproductive and developmental abnormalities. One of these studies involved alligators inhabiting water bodies in Florida. Researchers observed that these alligators produced fewer eggs than normal and some of them had severe genital abnormalities. As a result, the populations of these alligators were in a steady decline. Chemical analysis of the water bodies inhabited by these alligators indicated that chemicals such as toxaphene, DDE, and dicofol, all of which originate from pesticides, heavily pooluted the environment. Many of the products that result from the breakdown of these chemicals are antiandrogenic in nature and, therefore, wreck havoc to the sex hormone systems of male alligators (Guillette et al, 1994). Another study carried out on animals involved sea mollusks. Scientists observed an unusual sex developmental abnormality in these creatures known as imposex’ whereby females developed sex organs normally associated with males. Studies indicated that antifouling boat paints containing tributyl tin (TBT) occurred in high concentrations, in the environment of these mollusks, whereas further studies suggested that TBT causes disruptions in the systems that are responsible for synthesizing sex hormones. Researchers have also identified cases of imposex in the UK involving fish living in rivers that flow near sewage treatment plants. Researchers found significant levels of synthetic estrogenic substances, including nonylphenol (a component of detergents) and ethinylestradiol (the main component of contraceptive pills), and natural estradiol from human wastes in the effluents released from the sewage treatment plants (Purdom & Hardiman, 2004). Several species of birds living in the Great Lakes region of the U.S. have also been affected by environmental hormone mimics. In particular, these chemicals have adversely affected the sex ratios of western gulls. Fundamental evidence obtained by toxicologists is the thinning of egg shells of certain bird species on exposure to DDE, a metabolite of DDT. Although the evidence linking environmental hormone mimics to various abnormalities in wildlife is much stronger than that linking suspected human abnormalities to these chemicals, uncertainties still exist regarding the mechanism through which they achieve this (Trankina & Gough, 2007). Level of Threat of Environmental Hormone Mimics to Public Health Although numerous scientific studies are making links between various environmental hormone mimics and adverse health effects in humans, the evidence that they provide is not strong enough to indicate that these synthetic chemicals pose a grave threat to public health. The studies, which suggested that environmental hormone mimics may be responsible for up to a 50 percent decline in male sperm counts in European males over the past four or five decades, took place only in France, Denmark, Belgium, and the United Kingdom. These studies established that this decline began roughly the same time when environmental hormone mimics began to become widespread in the environment. However, other studies undertaken in the U.S. and a number of other countries including Finland failed to register a decline in sperm count. In fact, some of them have reported an increase in sperm counts. These contrasting results leave researchers uncertain about whether, in the first place, there has been a decrease in sperm counts, in some western countries, and second, whether the effects of environmental hormone mimics are responsible for such a decline (Soto & Sonnenschein, 1996). Similarly, uncertainties mar the issue of whether exposure to environmental hormone mimics could be interfering with the ratio of male to female births in humans. Studies conducted on certain species of animals such as turtles, alligators and gulls, suggest that exposure to certain pesticides can interfere with this ratio in these species resulting in a decrease in the number of male births. However, only isolated studies conducted on humans suggest that environmental hormone mimics exposure can affect the proportion of male and female births. One study conducted in Denmark suggested a slight decline in male births between 1951 and 1995 while another suggested a similar decline in Netherlands between 1950 and 1994. Other studies undertaken in the U.S. and other European countries contradict these results. Thus, there are a lot of uncertainties regarding whether environmental hormone mimics can affect the birth ratio of males to females. Studies linking environmental hormone mimics with breast, prostate, and testicular cancer, are contradicted by other studies, which suggest otherwise. There is also the possibility that increase in rates of these cancers could be due to improved screening techniques and increased awareness leading to earlier diagnosis. In addition, the phenomenon of aging populations in western countries could be a contributing factor. For example, some studies suggest that farmers exposed to certain herbicides and pesticides have an elevated risk of developing testicular or prostate cancer. However, other studies indicate that this increased risk could be due to other chemicals other than environmental hormone mimics, whereas others suggest that no link exists. The only conclusive evidence of adverse health effects of environmental hormone mimics on humans stems from research concerning neurological and neurodevelopment abnormalities in children. However, the cases confirming this trend were not widespread and, therefore, the negative effects of these chemicals on normal neurological and neurodevelopment functions has not raised enough level of concern to elicit a serious response from public health authorities (Soto & Sonnenschein, 1996). Conclusion Environmental hormone mimics are indeed accumulating in the environment and are causing significant rates of abnormalities in wildlife. However, these rates are too low to attract enough attention that could elicit a desired response from the public and the authorities that could reverse the trend. The number of animal species affected by these chemicals in a negative manner, although significant, is too small to suggest that they pose a serious menace to the health of wildlife. Environmental hormone mimics accumulating in the biosphere are finding their way into humans through food chains. However, studies investigating the adverse effects of these chemicals on human health are not conclusive since some of them establish a link between the two while others do not. Therefore, additional studies have to be conducted and coordinated at the global level so as to determine whether these synthetic chemicals are indeed responsible for causing adverse health effects in humans. References Clark, J. H., Watson, C., & Upchurch, S. (2007). “Estrogen Action in Normal and Abnormal Cell Growth”. Estrogens in the Environment 105 (7), 53 – 67. Colborn, T., Saal F. S. & Soto A. M. (1993). “Developmental Effects of Endocrine-disrupting Chemicals in Wildlife and Humans”. Environmental Health Perspectives 101 (30), 378 – 384. Fry, D. M. (1997). “Sex Ratio Skew and Breeding Patterns of Gulls: Demographic and Toxicological Considerations”. Studies in Avian Biology 10 (15), 26 – 43. Guillette, L. J. et al. (1994). “Developmental Abnormalities of the Gonad and Abnormal Sex Hormone Concentrations in Juvenile Alligators from Contaminated and Control Lakes in Florida”. Environmental Health Perspectives 102 (36), 680 – 688. Purdom, C. E., Hardiman, P. A. & Bye V. J. (2004). “Estrogenic Effects from Sewage Treatmemt Works”. Chemical Ecology 8 (16) 275 – 285. Soto, A. M. & Sonnenschein, C. (1996). “Environmental Sex Hormone Agonists and Antagonists”. Comments on Toxicology 5 (42), 329 – 346. Trankina, M. & Gough, M. (2007). Do Environmental Hormone Mimics Pose a Potentially Serious Health Threat? Environmental Issues. Retrieved 26 Nov 2012, from http://highered.mcgraw-hill.com/sites/dl/free/0076667771/657007/Easton_TS_Environmental_Issues_15e_0073514519_TOC.pdf Read More