Conservatives were the original "Conservationists". My definition is that conservationists would like to preserve the Earth for the people. Whereas the enviromentalists worship the earth as an end unto itself. They'd preffer a burned forrest to one that has been thinned so it won't burn.
As for DDT, the absence of it kills millions of people a year from malaria. The original "Silent Spring" author, who has a chain of parks named after her in Maine, should be scorned as a modern day Adolf Hitler, capable of killing far more humans than the old National Socialist could even dream of.
As for the harm of DDT vs. birds, there was apparently only one scientific study on that, which was not designed to test DDTs affect on birds eggs (only on its direct toxicity to the birds). The methodology was fatally flawed (because of the testing technology, they fed the test birds a different feed than the control group), and the bottom line is, DDT doesn't harm either humans, or birds eggs.
DDT just kills bugs. Which in the end, is enough to get the earth worshiping environmentalists to hate it.
Acute Toxicity: DDT is moderately to slightly toxic to studied mammalian species via the oral route. Reported oral LD50s range from 113 to 800 mg/kg in rats (79,73); 150-300 mg/kg in mice (79); 300 mg/kg in guinea pigs (73); 400 mg/kg in rabbits (73) ; 500-750 mg/kg in dogs (79) and greater than 1,000 mg/kg in sheep and goats (79). Toxicity will vary according to formulation (79). DDT is readily absorbed through the gastrointestinal tract, with increased absorption in the presence of fats (73). One-time administration of DDT to rats at doses of 50 mg/kg led to decreased thyroid function and a single dose of 150 mg/kg led to increased blood levels of liver-produced enzymes and changes in the cellular chemistry in the central nervous system of monkeys (73). Single doses of 50-160 mg/kg produced tremors in rats, and single doses of 160 mg/kg produced hind leg paralysis in guinea pigs (73). Mice suffered convulsions following a one-time oral dose of 200 mg/kg. Single administrations of low doses to developing 10-day old mice are reported to have caused subtle effects on their neurological development (73). DDT is slightly to practically non-toxic to test animals via the dermal route, with reported dermal LD50s of 2,500-3,000 mg/kg in female rats (79, 73), 1000 in guinea pigs (73) and 300 in rabbits (73). It is not readily absorbed through the skin unless it is in solution (73). It is thought that inhalation exposure to DDT will not result in significant absorption through the lung alveoli (tiny gas-exchange sacs) but rather that it is probably trapped in mucous secretions and swallowed by exposed individuals following the tracheo-bronchial clearance of secretions by the cilia (73). Acute effects likely in humans due to low to moderate exposure may include nausea, diarrhea, increased liver enzyme activity, irritation (of the eyes, nose or throat), disturbed gait, malaise and excitability; at higher doses, tremors and convulsions are possible (73, 76). While adults appear to tolerate moderate to high ingested doses of up to 280 mg/kg, a case of fatal poisoning was seen in a child who ingested one ounce of a 5% DDT:kerosene solution (73).
Chronic Toxicity: DDT has caused chronic effects on the nervous system, liver, kidneys,and immune systems in experimental animals (73, 74). Effects on the nervous system observed in test animals include: tremors in rats at doses of 16-32 mg/kg/day over 26 weeks; tremors in mice at doses of 6.5-13mg/kg/day over 80-140 weeks; changes in cellular chemistry in the central nervous system of monkeys at doses of 10 mg/kg/day over 100 days, and loss of equilibrium in monkeys at doses of 50 mg/kg/day for up to 6 months (73). The main effect on the liver seen in animal studies was localized liver damage. This effect was seen in rats given 3.75 mg/kg/day over 36 weeks, rats exposed to 5 mg/kg/day over 2 years and dogs at doses of 80 mg/kg/day over the course of 39 months (73). In many cases lower doses produced subtle changes in liver cell physiology, and in some cases higher doses produced more severe effects (73). In mice doses of 8.33 mg/kg/day over 28 days caused increased liver weight and increased liver enzyme activity (73). Liver enzymes are commonly involved in detoxification of foreign compounds, so it is unclear whether increased liver enzyme activity in itself would constitute an adverse effect. In some species (monkeys and hamsters), doses as high as 8-20 mg/kg/day caused no observed adverse effects over exposure periods as long as 3.5-7 years (73). Kidney effects observed in animal studies include adrenal gland hemorrhage in dogs at doses of 138.5 mg/kg/day over 10 days and adrenal gland damage at 50 mg/kg day over 150 days in dogs (73). Kidney damage was also seen in rats at doses of 10 mg/kg/day over 27 months (73). Immunological effects observed in test animals include: reduced antibody formation in mice following administration of 13 mg/kg/day for 3-12 weeks and reduced levels of immune cells in rats at doses of 1 mg/kg/day (73). No immune system effects were observed in mice at doses of 6.5 mg/kg/day for 3-12 weeks (73). Dose levels at which effects were observed in test animals are very much higher than those which may be typically encountered by humans (74). The most significant source of exposure to individuals in the United States is occupational, occurring only to those who work or worked in the production or formulation of DDT products for export (75). Analysis of U. S. market basket surveys showed approximately a 30-fold decrease in detected levels of DDT and metabolites in foodstuffs from 1969-1974, and another threefold drop from 1975-1981, with a final estimated daily dose of approximately 0.002 mg/person/day (73). Based on a standard 70-kg person, this results in a daily intake of approximately 0.00003 mg/kg/day. Due to the persistence of DDT and its metabolites in the environment, very low levels may continue to be detected in foodstuffs grown in some areas of prior use (73). It has been suggested that, depending on patterns of international DDT use and trade, it is possible that dietary exposure levels may actually increase over time (73). Persons eating fish contaminated with DDT or metabolites may also be exposed via bioaccumulation of the compound in fish (73). Even though current dietary levels are quite low, past and current exposures may result in measurable body burdens due to its persistence in the body (73). More information on the metabolism and storage of DDT and its metabolites in mammalian systems is provided below (Fate in Humans and Animals). Adverse effects on the liver, kidney and immune system due to DDT exposure have not been demonstrated in humans in any of the studies which have been conducted to date (73).
Reproductive Effects: There is evidence that DDT causes reproductive effects in test animals. No reproductive effects were observed in rats at doses of 38 mg/kg/day administered at days 15-19 of gestation (73). In another study in rats, oral doses of 7.5 mg/kg/day for 36 weeks resulted in sterility (73). In rabbits, doses of 1 mg/kg/day administered on gestation days 4-7 resulted in decreased fetal weights and 10 mg/kg/day on days 7-9 of gestation resulted in increased resorptions (73). In mice, doses of 1.67 mg/kg/day resulted in decreased embryo implantation and irregularities in the estrus cycle over 28 weeks (73). It is thought that many of these observed effects may be the result of disruptions in the endocrine (hormonal) system (73). Available epidemiological evidence from two studies does not indicate that reproductive effects have occurred in humans as a result of DDT exposure (73). No associations between maternal blood levels of DDT and miscarriage nor premature rupture of fetal membranes were observed in two separate studies (73, 77, 78). One study did report a significant association between maternal DDT blood levels and miscarriage, but the presence of other organochlorine chemicals (e.g., PCBs) in maternal blood which may have accounted for the effect make it impossible to attribute the effect to DDT and its metabolites (79).
Teratogenic Effects: There is evidence that DDT causes teratogenic effects in test animals as well. In mice, maternal doses of 26 mg/kg/day DDT from gestation through lactation resulted in impaired learning performance in maze tests (73). In a two-generational study of rats, 10 mg/kg/day resulted in abnormal tail development (73). Epidemiological evidence regarding the occurance of teratogenic effects as a result of DDT exposure are unavailable (73). It seems unlikely that teratogenic effects will occur in humans due to DDT at likely exposure levels.
Mutagenic Effects: The evidence for mutagenicity and genotoxicity is contradictory. In only 1 out of 11 mutagenicity assays in various cell cultures and organisms did DDT show positive results (73). Results of in vitro and in vivo genotoxocity assays for chromosomal aberrations indicated that DDT was genotoxic in 8 out of 12 cases, and weakly genotoxic in 1 case (73). In humans, blood cell cultures of men occupationally exposed to DDT showed an increase in chromosomal damage. In a separate study, significant increases in chromosomal damage were reported in workers who had direct and indirect occupational exposure to DDT (73). Thus it appears that DDT may have the potential to cause genotoxic effects in humans, but does not appear to be strongly mutagenic. It is unclear whether these effects may occur at exposure levels likely to be encountered by most people.
Carcinogenic Effects: The evidence regarding the carcinogenicity of DDT is equivocal. It has been shown to cause increased tumor production (mainly in the liver and lung) in test animals such as rats, mice and hamsters in some studies but not in others (73) In rats, liver tumors were induced in three separate studies at doses of 12.5 mg/kg/day over periods of 78 weeks to life, and thyroid tumors were induced at doses of 85 mg/kg/day over 78 weeks (73). In mice, lifetime doses of 0.4 mg/kg/day resulted in lung tumors in the second generation and leukemia in the third generation; liver tumors were induced at oral doses of 0.26 mg/kg/day in two separate studies over several generations. In hamsters, significant increases in adrenal gland tumors were seen at doses of 83 mg/kg/day in females (but not males) , and in males (but not females) at doses of 40 mg/kg/day (73). In other studies, however, no carcinogenic activity was observed in rats at doses less than 25 mg/kg/day; no carcinogenic activity was seen in mice with at doses of 3-23 mg/kg/day over an unspecified period, and in other hamster studies there have been no indications of carcinogenic effects (73). The available epidemiological evidence regarding DDTÕs carcinogenicity in humans, when taken as a whole, does not suggest that DDT and its metabolites are carcinogenic in humans at likely dose levels (73). In several epimiological studies, no significant associations were seen between DDT exposure and disease, but in one other study, a weak association was observed (73, 80). In this latter study, which found a significant association between long-term, high DDT exposures and pancreatic cancers in chemical workers, there were questions raised as to the reliability of the medical records of a large proportion of the cancer cases (73,80).
Organ Toxicity: Acute human exposure data and animal studies reveal that DDT can affect the nervous system, liver, kidney (73). Increased tumor production in the liver and lung has been observed in test animals (73). An association with pancreatic cancer was suggested in humans in one study (73, 80).
Fate in Humans & Animals: DDT is very slowly transformed in animal systems (74). Initial degradates in mammalian systems are 1,1-dichloro-2,2-bis(p-dichlorodiphenyl)ethylene (DDE) and 1,1-dichloro-2,2-bis(p-chlorophenyl)ethane (DDD), which are very readily stored in fatty tissues (73). These compounds in turn are ultimately transformed into bis(dichlorodiphenyl) acetic acid (DDA) via other metabolites at a very slow rate (73). DDA, or conjugates of DDA, are readily excreted via the urine (73). Available data from analysis of human blood and fat tissue samples collected in the early 1970s showed detectable levels in all samples, but a downward trend in the levels over time (73). Later study of blood samples collected in the latter half of the 1970s showed that blood levels were declining further, but DDT or metabolites were still seen in a very high proportion of the samples (73). Levels of DDT or metabolites may occur in fatty tissues (e.g. fat cells, the brain, etc.) at levels of up to several hundred times that seen in the blood (73). DDT or metabolites may also be elminated via motherÕs milk by lactating women (73).
In other words, not particularly dangerous compared to dying of all kinds of rotton equatorial diseases. Just don't eat it.