Chronic Toxicity of DDT and Related Compounds

The large-scale use of DDT as an insecticide entailed the release of large amounts into the environment, where it and its degradation products persist for decades. These compounds are so volatile that, like PCBs, they were spread worldwide in small amounts by the global winds. Yet while the use of DDT was increasing, it was noted that there was a decrease in many species, especially those at the end of food chains, on earth. These included especially eagles, hawks, and falcons, birds that feed mainly on fish.

Correlations were observed between the decreasing number of young hatched and the amounts of DDT and its degradation products in the eggs that did not hatch. A greater number of broken eggs than usual were found in the nests, and all the eggs, both whole and broken, had thinner shells than normal. In addition, the adults tended to mate later than usual in the summer, giving their progeny less time to mature before winter arrived. Thus fewer of the immature adults survived to have offspring the following summer.

All these factors resulted in a precipitous drop in the populations of these fish-eating birds. The presence of both DDT and its degradation products and PCBs in the eggs that did not hatch suggested that both chloroorganics may have been responsible for the collapse of the populations of these birds. In the United States, the manufacture and use of DDT was stopped in 1972, and the manufacture of PCBs was halted in 1977. Within 10 years after the DDT ban, there was a marked increase in the number of young hatched by the affected birds and a corresponding decrease in the amounts of DDT and its degradation products in the eggs that did not hatch. In addition, there was a corresponding increase in the thickness of the egg shells. During this time period there was no change in the levels of PCBs in the eggs, suggesting that DDT and its derivatives were responsible for the initial decrease in these bird populations. Independent studies have shown that low concentrations of PCBs have little effect on the thickness of avian eggshells.

There are two proposals to explain the connection between eggshell thickness, mating behavior, and the DDT. In one theory the connector is the monooxygenase enzyme cytochrome P-450. As noted in Section 8.5, high levels of liver cytochrome P-450 are induced by some chlorinated organics, levels that remain high if the chloroorganics are heavily chlorinated and thus difficult to oxidize. DDT residues induce cytochrome P-450 isozymes, structurally different P-450s which have similar catalytic activity and cause changes in the level of the steroid hormone estradiol, which controls mating behavior.

The production of eggshells is also influenced by estradiol. The shell of an egg is not formed until the last day before laying. About 60% of the calcium needed to form the egg is obtained from the bird's food intake, and the remainder comes from calcium stored in bones. Since the level of calcium deposited in the bones is regulated by levels of estradiol in the blood, a low level of estradiol results in a low level of stored calcium. The absence of stored calcium could be a significant factor in egg survival, since a 20% decrease in shell thickness results in extensive egg breakage. A 20% decrease in shell thickness is correlated with as little as 25 ppm DDT or its breakdown products observed in the egg.

In addition, it has been observed that some pesticides inhibit the formation of eggshells even in the presence of an adequate supply of calcium. Presumably these pesticides interfere with the enzyme carbonic anhydrase, which is responsible for the conversion of carbon dioxide to carbonate. The latter is required to combine with calcium to form the calcium carbonate of the shell. It has been established that DDE interferes with the formation of the shell in this way.

The connector between DDT, DDE, and thin eggshell and delayed mating of birds in the second proposal is the induction of hyperthyroidism in birds. This proposal has been questioned by Moriarity.5 It has been observed that when

5F. Moriarity, ed., Organochlorine Insecticides: Persistent Organic Pollutants. Academic Press, New York, 1975.

these chemicals are administered to some strains of birds, there is a doubling of the size of the thyroid gland. Increased metabolism, pulse, and heart size are indicative of hyperthyroidism. Studies on birds with hyperthyroidism have shown that they delay mating, and lay lighter eggs with thinner shells. Male birds with hyperthyroidism have significantly lower fertility than those that do not. It is not clear at the time of writing if either of these proposals is correct or whether there is yet another explanation for the biological effects of DDT and its degradation products on fowl.

After DDT was banned, its levels in the environment slowly decreased over a 10-year period (the half-life of pure DDT is about 10 years, but its degradation products last much longer), and consequently its levels in fish and the animals that consumed the fish also decreased, and the steroidal hormonal balance gradually swung back closer to the pre-DDT levels. The result of the ban is that most of the eagles, hawks, pelicans, and falcons in the lower 48 states of the United States have returned to close to their pre-DDT levels either naturally or, in the case of some eagles, with the help of their reintroduction from Alaska and Canada (Figure 8-5). Another example is the dramatic

1966 1968 1970 1972 1974 1976 1978 1980 Year

FIGURE 8-5 Summary of average annual bald eagle reproduction and DDE residues in addled (spoiled) eggs in north western Ontario, 1966-1981. Dashed lines indicate weighted mean concentrations of DDE residues in clutches before (94 ppm) and after (29 ppm) the ban of DDT. Means for the 16-year period are 57 ppm DDE (weighted mean) and 0.82 young per breeding area. Redrawn with permission from James W. Grier, Science, 218 1232-1236. Copyright © 1982 American Association for the Advancement of Science.

1966 1968 1970 1972 1974 1976 1978 1980 Year

FIGURE 8-5 Summary of average annual bald eagle reproduction and DDE residues in addled (spoiled) eggs in north western Ontario, 1966-1981. Dashed lines indicate weighted mean concentrations of DDE residues in clutches before (94 ppm) and after (29 ppm) the ban of DDT. Means for the 16-year period are 57 ppm DDE (weighted mean) and 0.82 young per breeding area. Redrawn with permission from James W. Grier, Science, 218 1232-1236. Copyright © 1982 American Association for the Advancement of Science.

TABLE 8-3

Brown Pelican Breeding in Coastal Southern California (U.S.) and Northern Baja California (Mexico) and the Content of DDT and Its Breakdown Products in Anchovies and Pelican Eggs

DDE, DDT, and DDD"2

TABLE 8-3

Brown Pelican Breeding in Coastal Southern California (U.S.) and Northern Baja California (Mexico) and the Content of DDT and Its Breakdown Products in Anchovies and Pelican Eggs

DDE, DDT, and DDD"2

Anchovies

Pelican eggs

Year

Nests built

Young fledged

(ppm, fresh wet weight)"

(ppm, lipid mass)c

1969

1125

4

4.27

1055

1970

727

5

1.40

1971

650

42

1.34

1972

511

207

1.12

>221

1973

597

134

0.29

183

1974

1286

1185

0.15

97

"About 95% DDE.

A major food for the brown pelican.

c Addled and broken eggs.

Source: Adapted from D. W. Anderson, R. W. Risebrough, L. A. Woods, Jr., L. R. Deweese, and W. G. Edgecomb, Brown pelican: Improved reproduction of the southern California coast, Science, 190, 806-808 (1975).

"About 95% DDE.

A major food for the brown pelican.

c Addled and broken eggs.

Source: Adapted from D. W. Anderson, R. W. Risebrough, L. A. Woods, Jr., L. R. Deweese, and W. G. Edgecomb, Brown pelican: Improved reproduction of the southern California coast, Science, 190, 806-808 (1975).

increase in the successful hatching of the brown pelican after 1970, when effluent from a DDT manufacturing facility in Los Angles was diverted from the Pacific Ocean to a landfill (Table 8-3).

Although the manufacture and use of DDT has been banned in Europe and North America, it is still used in large amounts in India, Africa, the Middle East, Southeast Asia, and Central and South America. One of its major uses is for the control of the anopheles mosquito, which transmits malaria to humans. The total DDT use in developing countries at the turn of the century was comparable to that used in the developed countries in the 1960s. The volatility and stability of DDT and its degradation products, which have an approximate half-life of 60 years in temperate climates, suggests that these compounds will continue to be an environmental problem for many more years unless all the nations of the world decide to ban the manufacture and use of the pesticide.

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