During recent years, numerous newspaper and magazine articles have suggested that humans may be at risk because small amounts of well known environmental contaminants, such as dioxin, PCBs and DDT, can affect hormone levels. Hormones are produced by the endocrine system as regulators of biological function in target organs. Because hormones play a critical role in early development, toxicological effects on the endocrine system often have an impact on the reproductive system. The term endocrine disruptor is used to describe chemicals that can mimic hormones and may either enhance or counteract their effects.
It has been suggested that these hormone changes can, in turn, lead to a variety of health problems including cancer, decreased fertility, and abnormalities in newborns. Evidence provided to support these claims of human and wildlife harm is largely from laboratory studies in which large doses are fed to test animals, usually rats or mice, and field studies of wildlife species that have been exposed to the chemicals mentioned above. In laboratory studies, high doses are required to give weak hormone activity. These doses are not likely to be encountered in the environment.
However the process of bioaccumulation can result in top-level predators such as humans to have contaminants at levels many million times greater than the environmental background levels (Guilette 1994). In field studies, toxicity caused by endocrine disruption has been associated with the presence of certain pollutants. Findings from such studies include: reproductive disruption in starfish due to PCBs, bird eggshell thinning due to DDT, reproductive failure in mink, small penises in alligators due to DDT and dicofol (Guillette 1994, Colburn et al 1996).
In addition, a variety of reproductive problems in many other species are claimed to be associated with environmental contamination although the specific causative agents have not been determined. One recent discovery that complicates the situation is that there are many naturally occurring “phytoestrogens”, or chemicals of plant origin that exhibit weak estrogenic properties. Pesticides that behave like the female hormone estrogens can have serious effects on reproductive success and function on animal exposed to them.
Reproductive success or fitness is defined by having live reproductively capable offspring that go on to reproduce. Many estrogenic chemicals have been shown to cause the foetuses of exposed animals to be reproductively incapable. Fry and Toone (1986) found when they inject fertilised seabird eggs with DDT and its metabolites. The male chicks produced have varying degrees of intersexuality depending on dosage, reproductive system with both male and female structures. The female chicks had a partial to full developed right oviducts, instead of just left functional structures.
In the area where the eggs were collected, there was multiple female-female pairing and low hatchability of eggs. Males exposed as embryos to estrogenic pesticides showed decreased to no sexual behaviour. (Fry and Toone, 1981) Louis Guillette noticed that male alligators from Lake Apopka in Florida have vestigial penis, follicle-like testis and elevated estrogens/testosterone ratios and the female hatchings ovaries were producing multiple egg follicles and eggs with several nuclei (Luoma, 1995, Guillette et al. , 1995) The females also had above normal estrogens levels.
When he and his colleagues did a similar injection study with DDT and DDE, they produced results similar to those found in the field. The reduction in penis length and the abnormal gonads made the hatchlings reproductively incapable. Both the bird and alligator studies were prompted by the contamination of large water bodies by organochlorins and the low breeding success of the animals living and feeding in these areas. Of particular interest are those chemicals, which mimic the female hormone of estrogen, which is thought to promote breast cancer (Montague 1991).
Publicity about these possible effects is being used to support demands for tighter emission controls and for drastic changes in the use of industrial chemicals and pesticides. A dramatic example is the proposal to phase out the chemical industrys use of chlorine as a raw material (Montague 1991). One of the most significant examples of synthetic estrogens having possible toxic effect was exhibited through the use of diethylstilboestrol or DES. DES was used extensively as a growth stimulant in cattle, however, as early as the 1950 it was also being used a clinical drug for the prevention of miscarriages in women (McLachlan and Arnold, 1996).
Several researchers have used the exposure of human foetuses to DES as a model for the prenatal effects of estrogens on development. This exogenous estrogen effects both male and female foetuses. In adulthood it was discovered that men had increase incidences of testicular cancer, low sperm counts and semen volume. (Sharpe and Skakkebaek, 1993, Newbold, 1995) Females foetuses can have structural malformations of the cervix, oviducts, uterus and vagina as well as anatomical masculinisation.
In adolescence and early adulthood, a number of reproductive cancers can appear as well as an inability to become pregnant or high incidence of abnormal pregnancies. DES was the first documented example of a human transplacental carcinogen, being administered to the mother that caused cancer in the daughter (McLachlan and Arnold, 1996). The effects seen in in-utero DES-exposed humans parallel those found in contaminated wildlife and laboratory animals, suggesting that humans may be at risk to those same environmental hazards as wildlife.
Thus many studies directed at wildlife may well be applicable to the well being of mankind (Montague 1991). If foetuses are exposed to estrogenic chemicals early in life, studies have shown that a number of reproductive abnormalities can develop. Sons born to mothers that ate foods contaminated with polyhalogenated compounds have underside penises and testicular malformations (Begley and Glick, 1994). In utero exposure of male rats to hormonally active dioxin causes a decrease in the anogenital distance, delayed testicular descent and reduced seminal vesical weights (Mably et al. 992) They also exhibited feminine behaviours when estrogen-primed and had decreased sperm counts.
The mothers of the exposed rats were given a single dose of dioxin in the fifteen-day of gestation. This study shows that there is a small window for sexual development because if the rats are exposes after the fifteenth day, they do not elicit the same abnormalities. Female foetuses were born with urogenital defects: absence of vaginal openings and cleft clitoris. (Mably et al. , 1992) Because pregnant woman use their fat stores during pregnancy, the foetus absorbs the pesticides that are mobilised.
A study of pesticide content in maternal blood, umbilical-cord blood and placental from stillborn and live-born infants showed that percentage of total DDT and aldrin in the specimen was significantly greater in the stillborn infants (Saxena et al. , 1983). The researchers suggest that the high pesticide concentration contributed to the death of the infants. Estrogenic pesticides can have detrimental reproductive effects on adult animals. Chronic exposure of rhesus monkeys to dioxin causes a dosage-dependent increase in the severity and occurrence of endometriosis (Kamrin Unknown).
The pain and ovarian cysts make the monkey incapable to breed. Similar conditions can be found in six million women (Montague 1991). In another study, kepone was administered to sexually active rats just before ovulation and after ovulation (Brown et al. , 1991). In both cases, the rats showed a rapid decrease in pre-copulatory and receptivity behaviours. Ovulation was also suppressed. In a study by Bradlow and his colleagues (1995), they found that organochlorins pesticides increase the breakdown of estrogens into 16u-Hydroxyestrone, which cause uncontrolled cell proliferation.
This cell proliferation is one of the leading cause of pesticide induce breast and endometrial cancers. Adult males also can suffer from the accumulation of pesticides in their diet and bodies. An investigation into the reproductive performance of man exposed to pesticides in the work showed that there was significant decrease frequency of live births and stillbirths, neonatal deaths and congenital defects in the children of exposed man compared to control group. (Rupa et al. , 1991) The men also have decreased fertility and increased incidence of abnormal sperm and dead sperm.
In birds, organochlorins accumulation causes eggshell thinning by inhibition of calcium ATPase as well as decreased incubation attentiveness, territorial defence and impairment of chick- rearing behaviours (Fry, 1995). All this deficiency causes a reduction in the reproductive fitness of the birds. The detrimental effects of endocrine disruptors and particularly estrogenic mimics on the reproductive fitness can be seen at all developmental stages of an animals life. The most dramatic effects occur while the animal is in utero and before puberty while the tissues are maturing and differentiating.
Many of the damaging effect of endocrine disruptors on the reproductive and development processes of an organisms may not be evident until the animal reaches puberty, a time when sex hormones levels increase and formally dormant cells become active. Due to this factor it is difficult for researchers to study the direct effect of many of these chemicals. The fact that responses of animal subjects and humans alike to these chemicals parallel each other indicates that this problem will have far reaching and devastating consequences.
