The mechanism by which DDT acts is to disturb the function of nerves in the insect. Nerves in both insects and humans work by allowing an electric current to move down them. This action potential, as it is called, depends on the movement of two metal ions, sodium and potassium, across the membrane of the nerve, and involves channels for the sodium being opened very briefly. DDT interacts with the sodium channel in the insect nerve and retards its closure. This means that the flow of sodium and hence the electric current is prolonged and there may be several impulses instead of just one. The function of the nerves thus becomes uncontrolled. This effect of DDT seems to be reversible.
It seems that insects are more susceptible than mammals, for two reasons. The first is that insect nerves are more susceptible to the DDT. The second is that mammals have a more well-developed system of detoxication than insects and so remove it more effectively. Naturally, at high doses DDT will cause toxic effects in humans, due to effects on nerve function, but these effects are reversible.
As well as the direct and lethal effects of DDT on animals such as birds, there are also indirect and more subtle effects. For example, the decline in the numbers of predatory birds in the UK and USA, such as the peregrine falcon and the kestrel, was not necessarily due to lethal effects on the birds themselves but due to effects on their reproductive process. One such effect of DDT is to alter the production of eggs, in particular the eggshells. During the 1960s the eggs of birds such as the peregrine falcon and pelican were found to have thinner shells and were therefore liable to break, a phenomenon which had started in the i940s. This was later found to correlate with the level of DDE, a breakdown product of DDT, in the egg. It is believed to be due to the effect of DDE on the disposition of calcium in the shell gland which is involved in the production of the eggshell. Other organochlorine compounds may also cause this effect but it seems that birds vary significantly in their sensitivity; the raptors and fish-eating birds being the most sensitive. However, recently the role of DDE in the decline in numbers of raptor birds, such as the California Condor, has been questioned.2
More recently, it has been found that substances such as DDT and other organochlorine compounds can have other effects on wildlife, again affecting the reproductive process and leading to reproductive failure, but also causing deformities in reproductive organs. This effect, now called endocrine disruption, was first noticed in fish in rivers in the USA and the UK where there may be many causes (see pp. i3i-6). One of the most celebrated cases was in Lake Apopka in Florida. The population of alligators in this lake was found to be in decline and there seemed to be poor reproductive success among the animals. Both male and female animals had abnormalities in their reproductive organs. It was then found that there were very high levels of the DDT breakdown product/metabolite DDE in the lake. This was due to spillage of a related pesticide called dicofol, which was contaminated with DDE. The latter substance has been found to be capable of causing these effects under experimental conditions. DDE is now known to affect levels of the male hormone testosterone (it is known as anti-androgenic) rather than increasing the amount of female hormone (known as an oestrogenic effect). One of the effects of such endocrine disruptor chemicals is believed to be a reduction in sperm count as a result of early changes in the testicles. As there is some evidence that human sperm counts and fertility are declining (although some studies have shown an increase in sperm counts), it has been suggested that such substances as organochlorine compounds (for example, DDT) may be responsible. However, there is no direct evidence for this in humans. This will be discussed further in Chapter 5.
The real problem with DDT is its persistence in the environment and its accumulation in certain animals. It is degraded only slowly in soil and in some of the animals exposed to it. It may take between five and twenty-five years for the soil to lose 95 per cent of the DDT. Thus over the years of its use it accumulated in the environment, and certainly in wildlife there is a problem of continued exposure to the substance at levels higher than might be expected from the environment level.
Although DDT localizes in fat where it is probably relatively harmless, release from this fat when it is broken down in an animal's body to provide energy can release enough DDT to cause toxicity in susceptible species, for example in bats. As bats are insectivorous, they can accumulate DDT from their prey, which will become localized in their fat tissue. In the southern USA it was found that bats were dying during their migratory flights, when their fat was mobilized for energy, hence releasing DDT into the blood, which then caused toxic, in some cases lethal, effects.
What of its potential toxicity to humans? There have been no documented deaths and no established cases of illness in which DDT is the causal agent but it is still detectable in the environment and in some food. Because the levels of such substances in food are monitored and we have efficient detoxication systems, and because DDT tends to be stored in fat, it is likely that the potential toxicity is minimal.
What does the DDT story illustrate and what lessons can be learnt about the use of chemicals? When DDT was first used it was not only very effective but apparently also relatively harmless. This led to it being used in excessive quantities (the 'more is better' fallacy). The inevitable consequence was the death of wildlife and a public outcry which crystallized around the book Silent Spring. This was predicated partly on the fear, 'If it does this to birds, what is it doing to us?' DDT is designed to be especially toxic to insects, and other species such as birds are more sensitive than mammals such as humans. The development of a new technique for the detection of DDT which was extremely sensitive allowed traces to be found in many things such as breast milk and food as well as wildlife. It became easy to point the finger at DDT because many birds and other animals had detectable levels of the chemical. But just because a chemical is detectable in an animal does not mean that it causes either death or ill health or that the level is hazardous.
This story also serves to remind us that it is dangerous to assume that when problems don't appear immediately there is no problem. When the technique became available for the sensitive measurement of DDT it was found to be accumulating in the environment. And it has been only relatively recently that the effects on reproductive systems have been detected. This shows that it is necessary to have both the right tools and the inclination to detect potential problems.
It is possible to use chemicals such as DDT effectively and responsibly, as has been illustrated, and this particular substance has been of enormous benefit to humans. A little more care and respect for the chemical when it was introduced would have improved the risk-benefit balance. The example of DDT again illustrates that recognition of the principle of Paracelsus is vital in the use of chemicals, especially those intended as pesticides. We know also that the relationship between the dose and the effect is different in insects and in other species. Therefore using less DDT would still have been effective but have caused little, if any, harm to other species.
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