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Uses and environmental levels

DDT is no longer used in developed countries, though it is used in various parts of the developing world, particularly for mosquito control, but also in general agriculture. The UNEP Persistent Organic Pollutants negotiations currently underway are discussing a full or partial phase out of DDT (the UNEP site is here). The main area of controversy is the use of DDT for mosquito control - WWF are very involved in this debate.

Commercial DDT comprises several isomers, the main one (75-80%) being p, p'-DDT:

DDT is metabolised in the body to DDE, and both these compounds persist in the body fat. Because of the banning of DDT use, body fat concentrations in the USA have reduced from 15 mg/kg in 1955 to less than 5 mg/kg in 1980 - though this is still pretty high (IEH, 1995).


Wildlife effects

Many hormone-related wildlife effects have been ascribed to DDT, including thinning of eggshells, damage to male reproductive ability and behavioural changes, for more details see the following references (amongst many others): Colborn (1995), LeBlanc (1995).

Effects on oestrogen metabolism in women

Oestradiol is metabolised (broken down) by two pathways in women, one via 16alpha-hydroxyoestrone (16aOHE) and the other via 2-hydroxyoestrone (2-OHE) (Bradlow et al., 1995). Research has found that high levels of 16aOHE relative to 2-OHE lead to a higher risk of breast cancer, possibly because 16aOHE is itself an oestrogen. Conversely, high levels of 2-OHE relative to 16aOHE reduce the risk of breast cancer, as 2-OHE is only a weak oestrogen.

The ratio of these two chemicals isn't fixed, and can be altered by exercise (more exercise, more 2-OHE) and fat in diet (less fat, more 2-OHE). Additionally certain chemicals affect the balance: indole-3-carbinol, present in vegetables such as cabbage and broccoli, also increases the level of 2-OHE, and so may reduce the chance of breast cancer. However, it has been found that exposure of human breast cell cultures to DDT, DDE, atrazine, chlordecone, lindane and endosulfan leads to increased levels of 16aOHE - potentially leading to an increased risk of breast cancer (Bradlow et al., 1995). Atrazine is already known to cause breast cancer in rats (ENDS, 1995).

Some research has found that the concentration of p, p'-DDE is higher in women with breast cancer than in women without breast cancer, and other research has suggested that hormone-responsive breast cancer (but not hormone-unresponsive breast cancer) may be strongly associated with high levels of DDE in adipose tissue (fat) and plasma (IEH, 1995). These results suggest that the more DDE present in a woman's body, the higher the chance of developing breast cancer. A variety of studies have suggested a link between exposure to organochlorines a breast cancer (Wolff, 1995).

Oestrogenic effects

Oestrogenic chlorinated pesticides, using MCF-7 breast cancer cells (the E-SCREEN assay) include: several isomers of DDT ,including o,p'-DDT and p,p'-DDT, Dieldrin, Chlordecone, Endosulfan, Methoxychlor and Toxaphene (Soto et al., 1995). Most of these chemicals were oestrogenic at 10 micromolar, but a mixture of 10 oestrogenic organochlorines at 1 micromolar led to a similar response, showing that the effects are additive.

Workers exposed to high levels of the pesticide chlordecone suffer decreased sperm motility and abnormal sperm (IEH, 1995).

Anti-androgenic effects

One of the most significant new findings to have been published in the field of oestrogenic toxicity published in June 1995 (Kelce et al., 1995). This work revealed that the DDT metabolite p, p'-DDE was capable of blocking the action of androgens (the male hormones) in male rats. As the authors report:

"the major and persistent DDT metabolite, p, p'-DDE, has little ability to bind the oestrogen receptor, but inhibits androgen binding to the androgen receptor, androgen-induced transcriptional activity, and androgen action in developing, pubertal and adult male rats. The results suggest that abnormalities in male sex development induced by p, p'-DDE and related environmental chemicals may be mediated at the level of the androgen receptor" (Kelce et al., 1995)

- or in other words, the p, p'-DDE switches off all the 'maleness' signals in these rats

A significant point about these results is that oestradiol normally has the same effect - this is just another way in which this chemical, and potentially other oestrogens, is imitating oestradiol. The concentrations of DDE at which effects were observed were as low as 0.2 micromolar, or 63.6 ppb, which is lower than the 140 ppb found in people living in DDT-treated dwellings (Kelce et al., 1995). Male alligators in Lake Apopka in Florida contain high levels of p, p'-DDE and have abnormally small penises and other reproductive disorders (Sharpe, 1995). It is also known that p, p'-DDE can cross the placenta to the developing foetus, leading the authors to conclude:

"The above reports suggest that p, p'-DDE crosses the placenta to the developing human foetus and can reach levels known to inhibit human androgen receptor transcriptional activity in vitro and to induce antiandrogenic effects in rats in vivo. Taken together, these results suggest that the reported increased incidence of developmental male reproductive system abnormalities in wildlife and humans may reflect antiandrogenic activity of the persistent DDT metabolite, p, p'-DDE " (Kelce et al., 1995)

For more information on the effects of organochlorine pesticides on male reproductive health, there is a large review by Toppari et al (1996).

This page was last updated in October 1999
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Bradlow, H. L., Davis, D. L., Lin, G., Sepkovic, D. and Tiwari, R. 1995. Effects of pesticides on the ratio of 16alpha/2-hydroxyestrone: A biologic marker of breast cancer risk. Environ. Health Persp. 103: 147-150.

Colborn, T. 1995. Pesticides - How research has succeeded and failed to translate science into policy: Endocrinological effects on wildlife. Environmental Health Perspectives Supplements 103 (Suppl 6): 81-86.

ENDS 1995. Pesticides in drinking water linked to breast cancer. ENDS Report 241: 8-9.

IEH 1995. Environmental oestrogens: Consequences to human health and wildlife. Institute for Environment and Health, University of Leicester, Leicester, UK

Kelce, W. R., Stone, C. R., Laws, S. C., Gray, L. E., Kemppainen, J. A. and Wilson, E. M. 1995. Persistent DDT metabolite p, p'-DDE is a potent androgen receptor antagonist. Nature 375: 581-585.

LeBlanc, G. A. 1995. Are environmental sentinels signalling? Environ. Health Persp. 103: 888-890.

Maynard, R. 1995. Sperm alert. Living Earth 188: 8-9.

Sharpe, R. M. 1995. Another DDT connection. Nature 375: 538-539.

Soto, A. M., Sonnenschein, C., Chung, K. L., Fernandez, M. F., Olea, N. and Serrano, F. O. 1995. The E-SCREEN assay as a tool to identify estrogens: An update on estrogenic environmental pollutants. Environ. Health Persp. 103 (Suppl. 7): 113-122.

Toppari, J., Larsen, J. C., Christiansen, P., Giwercman, A., Grandjean, P., Guillette, L. J., Jégou, B., Jensen, T. K., Jouannet, P., Keiding, N., Leffers, H., McLachlan, J. A., Meyer, O., Müller, J., Rajpert-De Meyts, E., Scheike, T., Sharpe, R., Sumpter, J. and Skakkebaek, N. E. 1996. Male reproductive health and environmental xenoestrogens. Environ. Health Persp. 104 Suppl. 4: 741-803.

Wolff, M. S. 1995. Pesticides - How research has succeeded and failed in informing policy: DDT and the link with breast cancer. Environmental Health Perspectives Supplements 103 (Suppl 6): 87-91.

URL: http://website.lineone.net/~mwarhurst/ddt.html