On December 27, Interior Secretary Dirk Kempthorne announced a proposal to list the polar bear as a threatened species under the Endangered Species Act
One study estimates that a third of the Earth's creatures will be condemned to extinction by 2050. Polar bears may not be extinct until 2040, but that doesn't mean we have 30 years to do nothing.
http://www.commondreams.org/views07/0108-23.htm
(this will speed it up)
The government approved the controlled spraying of DDT inside homes on Tuesday
http://www.alertnet.org/thenews/newsdesk/L05595221.htm
WHO Urges Use of DDT in Africa
http://www.washingtonpost.com/wp-dyn/co ... 01012.html
I could not imagine that the UN body, knowing the effects of the DDT compound which led to its global ban over 40 years ago, could change its stand on the chemical as if its formula had equally changed. DDT is still carcinogenious and persistent. It is on record that the standards of WHO have also been changing in recent years.
At one time in the recent past WHO openly apologised to the people of Uganda for having administered a bad anti-Polio vaccine. As a result of that error, a number children developed deformities on their bodies, rashes and irritations, while others died.
We should think twice before allowing the Government to apply DDT in our houses. If they did, I wonder whether the Queen of England and her entourage will taste Uganda's fish delicacies when they come here in November next year
excerpt.
http://www.globalenvision.org/library/1/1317/
Polar bears + DDT
EPA Targets DDT Contaminated Fish
http://www.californiafish.org/DDT.html
Mean concentrations of total DDT (t-DDT; DDT+DDD+DDE) in muscle fillet ranged from 60 ng/g (parts per billion) in yellow perch to 1,110 ng/g in lake whitefish. Carp had the second highest t-DDT concentrations in muscle (437 ng/g), followed by mountain whitefish (105 ng/g), and smallmouth bass (73 ng/g). PCBs, hexachlorobenzene (HCB), and DDMU, a further breakdown product of DDT, were detected at low concentrations (? 60 ng/g) in whole fish.
Results were compared to criteria for the protection of human health, wildlife, and aquatic life. t-DDT concentrations in all species exceed the level expected to result in a 10-6 excess cancer risk, by factors of 1.9 to 35. Levels of t-DDT in whole suckers exceed several criteria to protect piscivorous birds and mammals.
http://www.ecy.wa.gov/biblio/98337.html
TOXICOLOGICAL EFFECTS
* 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).
ECOLOGICAL EFFECTS
* Effects on Birds: DDT may be slightly toxic to practically non-toxic to birds. Reported dietary LD50s range from greater than 2,240 mg/kg in mallard, 841 mg/kg in Japanese quail and 1,334 mg/kg in pheasant (81). Other reported dietary LD50s in such species as bobwhite quail, California quail, red-winged blackbird, cardinal, house sparrow, blue jay, sandhill crane and clapper rail also indicate slight toxicity both in acute 5-day trials and over longer periods of up to 100 days (82). In birds, exposure to DDT occurs mainly through the food web through predation on aquatic and/or terrestrial species having body burdens of DDT, such as fish, earthworms and other birds (82). There has been much concern over chronic exposure of bird species to DDT and effects on reproduction, especially eggshell thinning and embryo deaths (82). The mechanisms of eggshell thinning are not fully understood. It is thought that this may occur from the major metabolite, DDE, and that predator species of birds are the most sensitive to these effects (82). Laboratory studies on bird reproduction have demonstrated the potential of DDT and DDE to cause subtle effects on courtship behavior, delays in pairing and egg laying and decreases in egg weight in ring doves and Bengalese finches (82). The implications of these for long-term survival and reproduction of wild bird species is unclear. There is evidence that synergism may be possible between DDTÕs metabolites and organophosphate (cholinesterase-inhibiting) pesticides to produce greater toxicity to the nervous system and higher mortality (82). Aroclor (polychlorinated biphenyls, or PCBs) may result in additive effects on eggshell thinning (82).
* Effects on Aquatic Species: DDT is very highly toxic to many aquatic invertebrate species. Reported 96-hour LC50s in various aquatic invertebrates (e.g., stoneflies, midges, crayfish, sow bugs) range from 0.18 ug/L to 7.0 ug/L, and 48-hour LC50s are 4.7 ug/L for daphnids and 15 ug/L for sea shrimp (55). Other reported 96-hour LC50s for various aquatic invertebrate species are from 1.8 ug/L to 54 ug/L (82). Early developmental stages are more susceptible than adults to DDTÕs effects (82). The reversibility of some effects, as well as the development of some resistance, may be possible in some aquatic invertebrates (55). DDT is very highly toxic to fish species as well. Reported 96-hour LC50s are less than 10 ug/L in coho salmon (4.0 ug/L), rainbow trout (8.7 ug/L), northern pike (2.7 ug/L), black bullhead (4.8 ug/L), bluegill sunfish (8.6 ug/L), largemouth bass (1.5 ug/L), and walleye (2.9 ug/L) (55). The reported 96-hour LC50s in fathead minnow and channel catfish are 21.5 ug/L and 12.2 ug/L respectively (55). Other reported 96-hour LC50s in largemouth bass and guppy were 1.5 ug/L and 56 ug/L respectively (82). Observed toxicity in coho and chinook salmon was greater in smaller fish than in larger (82). It is reported that DDT levels of 1 ng/L in Lake Michigan were sufficient to affect the hatching of coho salmon eggs (3). DDT may be moderately toxic to some amphibian species and larval stages are probably more susceptible than adults (81, 82). In addition to acute toxic effects, DDT may bioaccumulate significantly in fish and other aquatic species, leading to long-term exposure. This occurs mainly through uptake from sediment and water into aquatic flora and fauna, and also fish (82). Fish uptake of DDT from the water will be size-dependent with smaller fish taking up relatively more than larger fish (82). A half-time for elimination of DDT from rainbow trout was estimated to be 160 days (82). The reported bioconcentration factor for DDT is 1,000 to 1,000,000 in various aquatic species (83), and bioaccumulation may occur in some species at very low environmental concentrations (55). Bioaccumulation may also result in exposure to species which prey on fish or other aquatic organisms (e.g., birds of prey).
* Effects on Other Animals (Nontarget species): Earthworms are not susceptible to acute effects of DDT and its metabolites at levels higher than those likely to be found in the environment, but they may serve as an exposure source to species that feed on them (82). DDT is non-toxic to bees; the reported topical LD50 for DDT in honeybees is 27 ug/bee (82). Laboratory studies indicate that bats may be affected by DDT released from stored body fat during long migratory periods (82).
ENVIRONMENTAL FATE
* Breakdown in Soil and Groundwater: DDT is very highly persistent in the environment, with a reported half life of between 2-15 years (83, 84) and is immobile in most soils. Routes of loss and degradation include runoff, volatilization, photolysis and biodegradation (aerobic and anaerobic) (73). These processes generally occur only very slowly. Breakdown products in the soil environment are DDE and DDD, which are also highly persistent and have similar chemical and physical properties (82, 84). Due to its extremely low solubility in water, DDT will be retained to a greater degree by soils and soil fractions with higher proportions of soil organic matter (82). It may accumulate in the top soil layer in situations where heavy applications are (or were) made annually; e.g., for apples (72). Generally DDT is tightly sorbed by soil organic matter, but it (along with its metabolites) has been detected in many locations in soil and groundwater where it may be available to organisms (82, 83). This is probably due to its high persistence; although it is immobile or only very slightly mobile, over very long periods of time it may be able to eventually leach into groundwater, especially in soils with little soil organic matter. Residues at the surface of the soil are much more likely to be broken down or otherwise dissipated than those below several inches (3). Studies in Arizona have shown that volatilization losses may be significant and rapid in soils with very low organic matter content (desert soils) and high irradiance of sunlight, with volatilization losses reported as high as 50% in 5 months (85). In other soils (Hood River and Medford) this rate may be as low as 17-18% over 5 years (85). Volatilization loss will vary with the amount of DDT applied, proportion of soil organic matter, proximity to soil-air interface and the amount of sunlight (82).
* Breakdown of Chemical in Surface Water: DDT may reach surface waters primarily by runoff, atmospheric transport, drift, or by direct application (e.g. to control mosquito-borne malaria) (73). The reported half-life for DDT in the water environment is 56 days in lake water and approximately 28 days in river water (83). The main pathways for loss are volatilization, photodegradation, adsorption to water-borne particulates and sedimentation (73) Aquatic organisms, as noted above, also readily take up and store DDT and its metabolites. Field and laboratory studies in the United Kingdom demonstrated that very little breakdown of DDT occurred in estuary sediments over the course of 46 days (82). DDT has been widely detected in ambient surface water sampling in the United States at a median level of 1 ng/L (part per trillion) (73, 76).
* Breakdown of Chemical in Vegetation: DDT does not appear to be taken up or stored by plants to a great extent. It was not translocated into alfalfa or soybean plants, and only trace amounts of DDT or its metabolites were observed in carrots, radishes and turnips all grown in DDT-treated soils (82). Some accumulation was reported in grain, maize and riceplants, but little translocation occured and residues were located primarily in the roots (73).
http://extoxnet.orst.edu/pips/ddt.htm
Advisory Location: Yakima River
Nearest Community: Yakima
Chemicals of Concern: DDT, DDE
Species Affected: Large Scale and Bridgelip Sucker, Mountain Whitefish, Common Carp, Channel Catfish, and Northern Pikeminnow.
Issued by: Washington State Department of Health
Advisory Method: DDT in Bottom fish in Yakima River, pamphlet (pdf) and DDT pescados que Rio Yakima comen en el fondo del, pamphlet (pdf)
Recommendations: Anglers are recommended to limit their consumption of the above species to one meal per week and eat fish such as trout instead of bottom fish.
Contact: Washington State Department of Health, Office of Environmental Health Assessments, 1-877-485-7316
http://www.doh.wa.gov/ehp/oehas/EHA_fish_adv.htm
http://www.californiafish.org/DDT.html
Mean concentrations of total DDT (t-DDT; DDT+DDD+DDE) in muscle fillet ranged from 60 ng/g (parts per billion) in yellow perch to 1,110 ng/g in lake whitefish. Carp had the second highest t-DDT concentrations in muscle (437 ng/g), followed by mountain whitefish (105 ng/g), and smallmouth bass (73 ng/g). PCBs, hexachlorobenzene (HCB), and DDMU, a further breakdown product of DDT, were detected at low concentrations (? 60 ng/g) in whole fish.
Results were compared to criteria for the protection of human health, wildlife, and aquatic life. t-DDT concentrations in all species exceed the level expected to result in a 10-6 excess cancer risk, by factors of 1.9 to 35. Levels of t-DDT in whole suckers exceed several criteria to protect piscivorous birds and mammals.
http://www.ecy.wa.gov/biblio/98337.html
TOXICOLOGICAL EFFECTS
* 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).
ECOLOGICAL EFFECTS
* Effects on Birds: DDT may be slightly toxic to practically non-toxic to birds. Reported dietary LD50s range from greater than 2,240 mg/kg in mallard, 841 mg/kg in Japanese quail and 1,334 mg/kg in pheasant (81). Other reported dietary LD50s in such species as bobwhite quail, California quail, red-winged blackbird, cardinal, house sparrow, blue jay, sandhill crane and clapper rail also indicate slight toxicity both in acute 5-day trials and over longer periods of up to 100 days (82). In birds, exposure to DDT occurs mainly through the food web through predation on aquatic and/or terrestrial species having body burdens of DDT, such as fish, earthworms and other birds (82). There has been much concern over chronic exposure of bird species to DDT and effects on reproduction, especially eggshell thinning and embryo deaths (82). The mechanisms of eggshell thinning are not fully understood. It is thought that this may occur from the major metabolite, DDE, and that predator species of birds are the most sensitive to these effects (82). Laboratory studies on bird reproduction have demonstrated the potential of DDT and DDE to cause subtle effects on courtship behavior, delays in pairing and egg laying and decreases in egg weight in ring doves and Bengalese finches (82). The implications of these for long-term survival and reproduction of wild bird species is unclear. There is evidence that synergism may be possible between DDTÕs metabolites and organophosphate (cholinesterase-inhibiting) pesticides to produce greater toxicity to the nervous system and higher mortality (82). Aroclor (polychlorinated biphenyls, or PCBs) may result in additive effects on eggshell thinning (82).
* Effects on Aquatic Species: DDT is very highly toxic to many aquatic invertebrate species. Reported 96-hour LC50s in various aquatic invertebrates (e.g., stoneflies, midges, crayfish, sow bugs) range from 0.18 ug/L to 7.0 ug/L, and 48-hour LC50s are 4.7 ug/L for daphnids and 15 ug/L for sea shrimp (55). Other reported 96-hour LC50s for various aquatic invertebrate species are from 1.8 ug/L to 54 ug/L (82). Early developmental stages are more susceptible than adults to DDTÕs effects (82). The reversibility of some effects, as well as the development of some resistance, may be possible in some aquatic invertebrates (55). DDT is very highly toxic to fish species as well. Reported 96-hour LC50s are less than 10 ug/L in coho salmon (4.0 ug/L), rainbow trout (8.7 ug/L), northern pike (2.7 ug/L), black bullhead (4.8 ug/L), bluegill sunfish (8.6 ug/L), largemouth bass (1.5 ug/L), and walleye (2.9 ug/L) (55). The reported 96-hour LC50s in fathead minnow and channel catfish are 21.5 ug/L and 12.2 ug/L respectively (55). Other reported 96-hour LC50s in largemouth bass and guppy were 1.5 ug/L and 56 ug/L respectively (82). Observed toxicity in coho and chinook salmon was greater in smaller fish than in larger (82). It is reported that DDT levels of 1 ng/L in Lake Michigan were sufficient to affect the hatching of coho salmon eggs (3). DDT may be moderately toxic to some amphibian species and larval stages are probably more susceptible than adults (81, 82). In addition to acute toxic effects, DDT may bioaccumulate significantly in fish and other aquatic species, leading to long-term exposure. This occurs mainly through uptake from sediment and water into aquatic flora and fauna, and also fish (82). Fish uptake of DDT from the water will be size-dependent with smaller fish taking up relatively more than larger fish (82). A half-time for elimination of DDT from rainbow trout was estimated to be 160 days (82). The reported bioconcentration factor for DDT is 1,000 to 1,000,000 in various aquatic species (83), and bioaccumulation may occur in some species at very low environmental concentrations (55). Bioaccumulation may also result in exposure to species which prey on fish or other aquatic organisms (e.g., birds of prey).
* Effects on Other Animals (Nontarget species): Earthworms are not susceptible to acute effects of DDT and its metabolites at levels higher than those likely to be found in the environment, but they may serve as an exposure source to species that feed on them (82). DDT is non-toxic to bees; the reported topical LD50 for DDT in honeybees is 27 ug/bee (82). Laboratory studies indicate that bats may be affected by DDT released from stored body fat during long migratory periods (82).
ENVIRONMENTAL FATE
* Breakdown in Soil and Groundwater: DDT is very highly persistent in the environment, with a reported half life of between 2-15 years (83, 84) and is immobile in most soils. Routes of loss and degradation include runoff, volatilization, photolysis and biodegradation (aerobic and anaerobic) (73). These processes generally occur only very slowly. Breakdown products in the soil environment are DDE and DDD, which are also highly persistent and have similar chemical and physical properties (82, 84). Due to its extremely low solubility in water, DDT will be retained to a greater degree by soils and soil fractions with higher proportions of soil organic matter (82). It may accumulate in the top soil layer in situations where heavy applications are (or were) made annually; e.g., for apples (72). Generally DDT is tightly sorbed by soil organic matter, but it (along with its metabolites) has been detected in many locations in soil and groundwater where it may be available to organisms (82, 83). This is probably due to its high persistence; although it is immobile or only very slightly mobile, over very long periods of time it may be able to eventually leach into groundwater, especially in soils with little soil organic matter. Residues at the surface of the soil are much more likely to be broken down or otherwise dissipated than those below several inches (3). Studies in Arizona have shown that volatilization losses may be significant and rapid in soils with very low organic matter content (desert soils) and high irradiance of sunlight, with volatilization losses reported as high as 50% in 5 months (85). In other soils (Hood River and Medford) this rate may be as low as 17-18% over 5 years (85). Volatilization loss will vary with the amount of DDT applied, proportion of soil organic matter, proximity to soil-air interface and the amount of sunlight (82).
* Breakdown of Chemical in Surface Water: DDT may reach surface waters primarily by runoff, atmospheric transport, drift, or by direct application (e.g. to control mosquito-borne malaria) (73). The reported half-life for DDT in the water environment is 56 days in lake water and approximately 28 days in river water (83). The main pathways for loss are volatilization, photodegradation, adsorption to water-borne particulates and sedimentation (73) Aquatic organisms, as noted above, also readily take up and store DDT and its metabolites. Field and laboratory studies in the United Kingdom demonstrated that very little breakdown of DDT occurred in estuary sediments over the course of 46 days (82). DDT has been widely detected in ambient surface water sampling in the United States at a median level of 1 ng/L (part per trillion) (73, 76).
* Breakdown of Chemical in Vegetation: DDT does not appear to be taken up or stored by plants to a great extent. It was not translocated into alfalfa or soybean plants, and only trace amounts of DDT or its metabolites were observed in carrots, radishes and turnips all grown in DDT-treated soils (82). Some accumulation was reported in grain, maize and riceplants, but little translocation occured and residues were located primarily in the roots (73).
http://extoxnet.orst.edu/pips/ddt.htm
Advisory Location: Yakima River
Nearest Community: Yakima
Chemicals of Concern: DDT, DDE
Species Affected: Large Scale and Bridgelip Sucker, Mountain Whitefish, Common Carp, Channel Catfish, and Northern Pikeminnow.
Issued by: Washington State Department of Health
Advisory Method: DDT in Bottom fish in Yakima River, pamphlet (pdf) and DDT pescados que Rio Yakima comen en el fondo del, pamphlet (pdf)
Recommendations: Anglers are recommended to limit their consumption of the above species to one meal per week and eat fish such as trout instead of bottom fish.
Contact: Washington State Department of Health, Office of Environmental Health Assessments, 1-877-485-7316
http://www.doh.wa.gov/ehp/oehas/EHA_fish_adv.htm
we have entered a period of consequences
The potential worldwide catastrophe demands awareness and even fear. This issue will, in the next decade, be unavoidable for policy makers -- and the sooner this happens the better.
The choice is ours: create a storm of public opinion in the face of governmental lethargy or face the coming storm
excerpted
http://www.commondreams.org/views07/0109-33.htm
The potential worldwide catastrophe demands awareness and even fear. This issue will, in the next decade, be unavoidable for policy makers -- and the sooner this happens the better.
The choice is ours: create a storm of public opinion in the face of governmental lethargy or face the coming storm
excerpted
http://www.commondreams.org/views07/0109-33.htm
I remember frogs..
Atrazine
Even the lowest concentration used in his study (0.1 parts per billion) was able to feminise male frogs. Feminised males had smaller voice organs than normal and had ovary tissue in their testes. Although the ability of atrazine to impair sexual development had been documented before, this study observed effects at concentrations much lower than those observed previously and at concentrations routinely found in the US environment.
http://www.pan-uk.org/pestnews/Issue/pn58/pn58p19.htm
EPA Won't Restrict Toxic Herbicide Atrazine, Despite Health Threat
White House documents obtained by NRDC reveal that industry influenced the decision.
The EPA has decided not to limit one of the nation's most widely used weed-killers, a chemical that, according to several recent studies, threatens human health and the environment. The October 2003 decision -- which the EPA was required to make under a court-approved consent decree reached with NRDC in 2001 -- will allow Syngenta, the main manufacturer of atrazine, and other companies to continue to sell the chemical in the United States with no significant restrictions.
To determine whether industry played a role in shaping the EPA's decision, NRDC filed a series of Freedom of Information Act requests....
excerpt
http://www.nrdc.org/health/pesticides/natrazine.asp
On the basis of an estimated application rate of 1.4 lb/acre (pounds per acre) and about 25 percent of the basin in sorghum and corn, it was calculated that about 260,000 lb of atrazine were applied to crops in the Little Arkansas River Basin upstream from Sedgwick during 1995, 1996, and 1997. Of this 260,000 lb, about 1 percent or 2,600 lb were transported annually in surface runoff to the Little Arkansas River. Ninety percent of this runoff load occurred during a short period of time, generally from May through July, following application of herbicides. In fact, at the Halstead site, 90 percent of the atrazine load occurred during about 15 days each year. Similarly, at the Sedgwick site, 90 percent of the atrazine load occurred during about 40 days each year.
The mean atrazine concentration during this period of 15 or 40 days was between 5.2 and 13 µg/L at the Halstead site and between 3.7 and 14 µg/L at the Sedgwick site. The large discharge during 90 percent of the annual load transport possibly may be used as an indicator of when treatment for atrazine is necessary.
Data from this study have defined seasonal distribution of atrazine in the Little Arkansas River and have provided information related to timing and requirements for treatment of water withdrawn from the river for artificial recharge. During the growing season when discharge generally is large and water is available for artificial recharge, atrazine concentrations are also typically large. Therefore, water treatment prior to recharge may be important to prevent degradation of the Equus Beds aquifer by atrazine.
excerpt
http://ks.water.usgs.gov/Kansas/pubs/fa ... 74-98.html
The European Union recently banned atrazine because of pervasive drinking
water contamination. Instead of restricting or banning atrazine in the
United States, however, the EPA recently negotiated an agreement that only
requires Syngenta to monitor streams and drinking water supplies for
contamination. Under this deal, Syngenta will test fewer than 4 percent of
the streams identified by the EPA as being at highest risk for atrazine
contamination.
DDVP is one of a class of chemicals called organophosphates, which are
neurotoxins that were originally developed as chemical weapons during World
War II. DDVP causes permanent nervous system damage in young test animals,
and may cause related abnormalities in exposed infants and children.
Exposure to DDVP also can cause uncontrollable sweating, nausea, dizziness,
muscle tremors and even death. Despite the risks, EPA is privately
negotiating with DDVP's manufacturer Amvac to allow the company to continue
to sell this nerve poison for many home and agricultural uses.
excerpt
http://www.organicconsumers.org/Politic ... 022105.cfm
Atrazine
Even the lowest concentration used in his study (0.1 parts per billion) was able to feminise male frogs. Feminised males had smaller voice organs than normal and had ovary tissue in their testes. Although the ability of atrazine to impair sexual development had been documented before, this study observed effects at concentrations much lower than those observed previously and at concentrations routinely found in the US environment.
http://www.pan-uk.org/pestnews/Issue/pn58/pn58p19.htm
EPA Won't Restrict Toxic Herbicide Atrazine, Despite Health Threat
White House documents obtained by NRDC reveal that industry influenced the decision.
The EPA has decided not to limit one of the nation's most widely used weed-killers, a chemical that, according to several recent studies, threatens human health and the environment. The October 2003 decision -- which the EPA was required to make under a court-approved consent decree reached with NRDC in 2001 -- will allow Syngenta, the main manufacturer of atrazine, and other companies to continue to sell the chemical in the United States with no significant restrictions.
To determine whether industry played a role in shaping the EPA's decision, NRDC filed a series of Freedom of Information Act requests....
excerpt
http://www.nrdc.org/health/pesticides/natrazine.asp
On the basis of an estimated application rate of 1.4 lb/acre (pounds per acre) and about 25 percent of the basin in sorghum and corn, it was calculated that about 260,000 lb of atrazine were applied to crops in the Little Arkansas River Basin upstream from Sedgwick during 1995, 1996, and 1997. Of this 260,000 lb, about 1 percent or 2,600 lb were transported annually in surface runoff to the Little Arkansas River. Ninety percent of this runoff load occurred during a short period of time, generally from May through July, following application of herbicides. In fact, at the Halstead site, 90 percent of the atrazine load occurred during about 15 days each year. Similarly, at the Sedgwick site, 90 percent of the atrazine load occurred during about 40 days each year.
The mean atrazine concentration during this period of 15 or 40 days was between 5.2 and 13 µg/L at the Halstead site and between 3.7 and 14 µg/L at the Sedgwick site. The large discharge during 90 percent of the annual load transport possibly may be used as an indicator of when treatment for atrazine is necessary.
Data from this study have defined seasonal distribution of atrazine in the Little Arkansas River and have provided information related to timing and requirements for treatment of water withdrawn from the river for artificial recharge. During the growing season when discharge generally is large and water is available for artificial recharge, atrazine concentrations are also typically large. Therefore, water treatment prior to recharge may be important to prevent degradation of the Equus Beds aquifer by atrazine.
excerpt
http://ks.water.usgs.gov/Kansas/pubs/fa ... 74-98.html
The European Union recently banned atrazine because of pervasive drinking
water contamination. Instead of restricting or banning atrazine in the
United States, however, the EPA recently negotiated an agreement that only
requires Syngenta to monitor streams and drinking water supplies for
contamination. Under this deal, Syngenta will test fewer than 4 percent of
the streams identified by the EPA as being at highest risk for atrazine
contamination.
DDVP is one of a class of chemicals called organophosphates, which are
neurotoxins that were originally developed as chemical weapons during World
War II. DDVP causes permanent nervous system damage in young test animals,
and may cause related abnormalities in exposed infants and children.
Exposure to DDVP also can cause uncontrollable sweating, nausea, dizziness,
muscle tremors and even death. Despite the risks, EPA is privately
negotiating with DDVP's manufacturer Amvac to allow the company to continue
to sell this nerve poison for many home and agricultural uses.
excerpt
http://www.organicconsumers.org/Politic ... 022105.cfm
This vulture has had the same problem with small quantities of chemicals nearly wiping it out - hopefully it is not too late....
http://www.birdlife.org/news/news/2007/ ... tches.html
At least this is the first time round for the chemical and the lesson - unlike DDT.
Will we ever learn?
Best regards
Chris
http://www.birdlife.org/news/news/2007/ ... tches.html
At least this is the first time round for the chemical and the lesson - unlike DDT.
Will we ever learn?
Best regards
Chris
at the rate we're being dumbed down, not in Time. I hear that's what got the dinosaurs, They were just too stupid to survive.Will we ever learn?
child brain drain” taking place in Europe and around the world as a result of environmental mercury pollution
http://www.env-health.org/
Relaxing the Toxics Release Inventory rules is "just downright ignorant and stupid," said Michael Pops, who was active in the Phoenix Brick Yard fight. "It gives the polluters greater (weight) than protecting the citizenry."
An analysis of the 122,420 public comments the EPA received on the proposed change found that 99.97 percent opposed the softer rules, according to OMB Watch.
In July, the EPA's own scientific advisory board sent a letter to Administrator Stephen Johnson opposing the changes, stating that the new rule could "hinder the advances of environmental research used to protect public health and the environment."
In September, the EPA ignored the advice of its scientific advisory panel and adopted new air pollution standards below what the panel deemed necessary to protect public health.
Thirteen states and the District of Columbia have since sued the EPA over those standards.
excerpts
http://www.azcentral.com/arizonarepubli ... s1223.html