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EXT'OXNET PIP - DDT
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<br /> } maternal doses of 26 mg/kg/day DDT from gestation through lactation resulted in impaired learning
<br /> performance in maze tests (73). In a two-generational study of rats, 10 mg/kg/day resulted in abnormal tail
<br /> development (73). Epidemiological evidence regarding the occurance of teratogenic effects as a result of DDT
<br /> exposure are unavailable (73). It seems unlikely that teratogenic effects will occur in humans due to DDT at
<br /> likely exposure levels.
<br /> • Mutagenic Effects: The evidence for mutagenicity and genotoxicity is contradictory. In only 1 out of I 1
<br /> mutagenicity assays in various cell cultures and organisms did DDT show positive results (73). Results of in
<br /> vitro and in vivo genotoxocity assays for chromosomal aberrations indicated that DDT was genotoxic in 8 out
<br /> of 12 cases, and weakly genotoxic in 1 case (73). In humans, blood cell cultures of men occupationally
<br /> exposed to DDT showed an increase in chromosomal damage. In a.separate study, significant increases in
<br /> chromosomal damage were reported in workers who had direct and indirect occupational exposure to DDT
<br /> (73). Thus it appears that DDT may have the potential to cause genotoxic effects in humans, but does not
<br /> appear to be strongly mutagenic. It is unclear whether these effects may occur at exposure levels likely to be
<br /> encountered by most people.
<br /> • Carcinogenic Effects: The evidence regarding the carcinogenicity of DDT is equivocal. It has been shown to
<br /> cause increased tumor production (mainly in the liver and lung) in test animals such as rats, mice and hamsters
<br /> in some studies but not in others (73) In rats, liver tumors were induced in three separate studies at doses of
<br /> 12.5 mg/kg/day over periods of 78 weeks to Iife, and thyroid tumors were induced at doses of 85 mg/kg/day
<br /> over 78 weeks (73). In mice, lifetime doses of 0.4 mg/kg/day resulted in lung tumors in the second generation
<br /> and leukemia in the third generation; liver tumors were induced at oral doses of 0.26 mg/kg/day in two
<br /> separate studies over several generations. In hamsters, significant increases in adrenal gland tumors were seen
<br /> 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
<br /> (73). In other studies, however, no carcinogenic activity was observed in rats at doses less than 25 mg/kg/day;
<br /> no carcinogenic activity was seen in mice with at doses of 3-23 mg/kg/day over an unspecified period, and in
<br /> other hamster studies there have been no indications of carcinogenic effects (73). The available
<br /> epidemiological evidence regarding DDTOs carcinogenicity in humans, when taken as a whole, does not
<br /> suggest that DDT and its metabolites are carcinogenic in humans at likely dose levels (73). In several
<br /> epimiological studies, no significant associations were seen between DDT exposure and disease, but in one
<br /> other study, a weak association was observed (73, 80). In this Iatter study, which found a significant
<br /> association between long-term, high DDT exposures and pancreatic cancers in chemical workers, there were
<br /> questions raised as to the reliability of the medical records of a large proportion of the cancer cases (73,80).
<br /> . Organ Toxicity: Acute human exposure data and animal studies reveal that DDT can affect the nervous
<br /> system, liver, kidney (73). Increased tumor production in the liver and lung has been observed in test animals
<br /> (73). An association with pancreatic cancer was suggested in humans in one study (73, 80).
<br /> . Fate in Humans & Animals: DDT is very slowly transformed in animal systems (74). Initial degradates in
<br /> mammalian systems are 1,1-dichloro-2,2-bis(p-dichlorodiphenyl)ethylene (DDE) and 1,1-dichloro-2,2-bis(p-
<br /> chlorophenyl)ethane (DDD), which are very readily stored in fatty tissues (73). These compounds in turn are
<br /> ultimately transformed into bis(dichlorodiphenyl) acetic acid (DDA) via other metabolites at a very slow rate
<br /> (73). DDA, or conjugates of DDA, are readily excreted via the urine (73). Available data from analysis of
<br /> human blood and fat tissue samples collected in the early 1970s showed detectable levels in all samples, but a
<br /> downward trend in the levels over time (73). Later study of blood samples collected in the latter half of the C
<br /> 1970s showed that blood levels were declining further, but DDT or metabolites were still seen in a very high I
<br /> proportion of the samples (73). Levels of DDT or metabolites may occur in fatty tissues (e.g. fat cells, the
<br /> brain, etc.) at levels of up to several hundred times that seen in the blood (73). DDT or metabolites may also
<br /> be elminated via motherOs milk by lactating women (73).
<br /> ECOLOGICAL EFFECTS
<br /> . Effects on Birds: DDT may be slightly toxic to practically non-toxic to birds. Reported dietary LD50s range
<br /> from greater than 2,240 mg/kg in mallard, 841 mg/kg in Japanese quail and 1,334 mg/kg in pheasant (81).
<br /> Other reported dietary LD50s in such species as bobwhite quail, California quail, red-winged blackbird,
<br /> cardinal, house sparrow, blue jay, sandhill crane and clapper rail also indicate slight toxicity both in acute 5-
<br /> day trials and over longer periods of up to I00 days (82). In birds, exposure to DDT occurs mainly through the
<br /> food web through predation on aquatic and/or terrestrial species having body burdens of DDT, such as fish,
<br /> earthworms and other birds (82). There has been much concern over chronic exposure of bird species to DDT
<br /> and effects on reproduction, especially eggshell thinning and embryo deaths (82). The mechanisms of eggshell
<br /> thinning are not fully understood. It is thought that this may occur from the major metabolite, DDE, and that
<br /> predator species of birds are the most sensitive to these effects (82). Laboratory studies on bird reproduction
<br /> have demonstrated the potential of DDT and DDE to cause subtle effects on courtship behavior, delays in
<br /> pairing and egg laying and decreases in egg weight in ring doves and Bengalese finches (82). The implications
<br /> of these for long-term survival and reproduction of wild bird species is unclear. There is evidence that
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