- I'm sorry, but both of those statements saying the opposite are exaggerations. And I have to ask, how was the DDT situation about emotion and not science? The connection to weakened egg shells in birds of prey was pretty watertight from my understanding,
then you understand wrong, which makes my point, i think. to this day, there is no scientific link between DDT and the weakened egg shells. there are, however, some disease in birds that cause just such things. because of a nutty tree huggers book, millions died of malaria, while 1st worlders wept for birds.
so, how much proof? more than we have. any insecticide will kill bees. that does not mean that insecticides are causing CCD. CCD predates insecticides. bring me more.
Effects on wildlife and eggshell thinning
<DDT is toxic to a wide range of living organisms, including marine animals such as crayfish, daphnids, sea shrimp and many species of fish. It is less toxic to mammals, but may be moderately toxic to some amphibian species, especially in the larval stage. DDT, through its metabolite DDE, caused eggshell thinning and resulted in severe population declines in multiple North American and European bird of prey species. Eggshell thinning lowers the reproductive rate of certain bird species by causing egg breakage and embryo deaths. DDE related eggshell thinning is considered a major reason for the decline of the bald eagle, brown pelican, peregrine falcon, and osprey. However, different groups of birds vary greatly in their sensitivity to these chemicals. Birds of prey, waterfowl, and song birds are more susceptible to eggshell thinning than chickens and related species, and DDE appears to be more potent than DDT. Even in 2010, more than forty years after the U.S. ban, California condors which feed on sea lions at Big Sur which in turn feed in the Palos Verdes Shelf area of the Montrose Chemical Superfund site seemed to be having continued thin-shell problems. Scientists with the Ventana Wildlife Society and others are intensifying studies and remediations of the condors' problems.
The biological thinning mechanism is not entirely known, but there is strong evidence that p,p'-DDE inhibits calcium ATPase in the membrane of the shell gland and reduces the transport of calcium carbonate from blood into the eggshell gland. This results in a dose-dependent thickness reduction. There is also evidence that o,p'-DDT disrupts female reproductive tract development, impairing eggshell quality later. Multiple mechanisms may be at work, or different mechanisms may operate in different species. Some studies show that although DDE levels have fallen dramatically, eggshell thickness remains 10–12 percent thinner than before DDT was first used.>There were those weeping for birds, but we may be weeping for ourselves due to our playing fast and loose with these powerful chemicals -
DDT and DDE, like other organochlorines, have been shown to have xenoestrogenic activity, meaning they are chemically similar enough to estrogens to trigger hormonal responses in animals. This endocrine disrupting activity has been observed in mice and rat toxicological studies, and available epidemiological evidence indicates that these effects may be occurring in humans as a result of DDT exposure. The US Environmental Protection Agency states that DDT exposure damages the reproductive system and reduces reproductive success. These effects may cause developmental and reproductive toxicity:
A review article in The Lancet states, "research has shown that exposure to DDT at amounts that would be needed in malaria control might cause preterm birth and early weaning ... toxicological evidence shows endocrine-disrupting properties; human data also indicate possible disruption in semen quality, menstruation, gestational length, and duration of lactation."
Human epidemiological studies suggest that exposure is a risk factor for premature birth and low birth weight, and may harm a mother's ability to breast feed. Some 21st-century researchers argue that these effects may increase infant deaths, offsetting any anti-malarial benefits. A 2008 study, however, failed to confirm the association between exposure and difficulty breastfeeding.
Several recent studies demonstrate a link between in utero exposure to DDT or DDE and developmental neurotoxicity in humans. For example, a 2006 University of California, Berkeley study suggests that children exposed while in the womb have a greater chance of development problems, and other studies have found that even low levels of DDT or DDE in umbilical cord serum at birth are associated with decreased attention at infancy and decreased cognitive skills at 4 years of age. Similarly, Mexican researchers have linked first trimester DDE exposure to retarded psychomotor development.
Other studies document decreases in semen quality among men with high exposures (generally from IRS).
Studies generally find that high blood DDT or DDE levels do not increase time to pregnancy (TTP.) There is some evidence that the daughters of highly exposed women may have more difficulty getting pregnant (i.e. increased TTP).
DDT is associated with early pregnancy loss, a type of miscarriage. A prospective cohort study of Chinese textile workers found "a positive, monotonic, exposure-response association between preconception serum total DDT and the risk of subsequent early pregnancy losses." The median serum DDE level of study group was lower than that typically observed in women living in homes sprayed with DDT.
A Japanese study of congenital hypothyroidism concluded that in utero DDT exposure may affect thyroid hormone levels and "play an important role in the incidence and/or causation of cretinism." Other studies have also found that DDT or DDE interfere with proper thyroid function.