It was reported that the alligator population of Lake Apopka in northern Florida was declining, presumably because of lack of success in reproduction. The male animals were found to have abnormal testes, low testosterone levels, and small phalli (penises). The female alligators had abnormalities too and high levels of oestrogen. It is believed that high levels of organochlorine compounds, resulting from a spillage of the pesticide difocol, were responsible. The difocol was contaminated with DDE, a breakdown product of DDT, which may have affected the level of the sex hormones. Apparently such effects can be produced in alligators by treating them with DDE.
What of the effects in humans? While there is evidence, some of it controversial, that changes have occurred in the reproductive systems of humans in various countries throughout the world over the last fifty years or so, ascribing these changes to particular chemicals, or even to chemicals at all, has been difficult. There has been an increase in testicular cancer as well as breast cancer since i945, particularly in certain countries. Data from studies of populations in some countries, for example Finland, have indicated that sperm counts and the quality of the sperm in males have declined over the same time period, but by no means all studies have found this and some have found the reverse. In some places there has been an apparent increase in disorders of the male reproductive system such as hypospadia (a defect of the penis) and cryptorchidism (undescended testicles).
There is, however, one example of a chemical known to have caused adverse effects in both males and females. The chemical is the synthetic oestrogen diethylstilboestrol. This was used in the i950s to prevent miscarriages until its use was stopped in the early 1970s. Women were given the drug during pregnancy. However, the effects did not occur in the women who took the drug but in their offspring. In a significant proportion of girls born to women who had used the drug there was dysfunction of the reproductive organs, disruption of the menstrual cycle, and abnormal pregnancies. A few of the girls developed vaginal cancer but not until they had reached puberty. In boys born to the women who had taken the drug there was an increased incidence of cryptorchidism and a small penis. There was also some evidence of a decrease in sperm count and ability of the sperm to move. These effects and testicular cancer have been reproduced in experimental animals treated with diethylstilboestrol. Diethylstilboestrol has been used as a growth promoter in cattle and so residues in food may exist; the chemical and its breakdown products could also potentially appear in river water.
The oestrogen ethynyloestradiol is, as we saw earlier, known to be present in sewage treatment plant effluents and could potentially appear in drinking water. It has apparently been detected in drinking water in the UK but the data have been questioned. Even if it were present, it is not known whether the concentrations would be high enough to affect human males.
As we have seen, there are many other chemicals capable of causing these effects, although they are generally very much less potent that the natural oestrogens and the synthetic oestrogens used in the contraceptive pill. Mixtures of these chemicals, which includes natural substances from plants, pesticides, and industrial chemicals, may be more potent than the individual components. This phenomenon is called synergy (see p. 35) and is currently an area of intense scientific interest, as is the subject of endocrine disruptors.
Effects on the male reproductive system can also be produced by substances that interfere with male hormones, so-called anti-androgens. DDE is one such chemical, but attempts to correlate DDE levels in human breast fat tissue with the incidence of breast cancer have produced equivocal results. Dioxin shows significant anti-oestrogenic activity, but after the accident at Seveso a decreased incidence of breast cancer was observed in those who had been exposed.
Although all the synthetic chemicals and natural chemicals considered here have weak oestrogenic activity compared to natural oestrogens, there are several ways in which chemicals can affect hormones, and combinations of chemicals could be more potent than expected. Although there is little indication of this at present, future research may resolve the issue.
In conclusion, there is no doubt that the effects of endocrine disruptors can be reproduced in experimental animals. However, the effects in animals after environmental exposure, and in which levels were measured, have been detected mostly when contamination was relatively high and in most other cases evidence for a causal link is weak.
For humans, except for cases where high levels of exposure have occurred (for example, in the therapeutic use of diethylstilboestrol), the data is inconsistent and inconclusive. Information on levels of exposure is lacking and there is no firm evidence for a link between low level exposure and adverse health outcomes in the human population. For all the adverse health outcomes the evidence of association with environmental exposure to endocrine disruptors is weak (except in the case of minor effects on thyroid hormones, where evidence is moderate). In some cases, such as changes in sperm count, a possible connection is scientifically plausible. Further evidence is needed, and especially evidence that links actual exposure levels in humans to effects.8
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