A Pesticide Information Project of Cooperative Extension Offices of Cornell University, Michigan State University, Oregon State University, and University of California at Davis. Major support and funding was provided by the USDA/Extension Service/National Agricultural Pesticide Impact Assessment Program.
It is available in several different forms: aerosols, dustable powders, emulsifiable concentrates, granules and wettable powders (1, 2). It is reported to be compatible with many other pesticides and incompatible with alkaline substances (1). Many insect pests may have developed resistance to DDT (1).
Unless otherwise specified, the toxicological, environmental effects and environmental fate and chemistry data presented here refer to the technical product DDT. Technical grade DDT is actually a mixture of three isomers of DDT, principally the p,p'-DDT isomer (ca. 85%), with the o,p'-DDT and o,o'-DDT isomers typically present in much lesser amounts (3).
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 (3). 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 (3). 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 (3).
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 (1-3), 1000 in guinea pigs (3) and 300 in rabbits (3). It is not readily absorbed through the skin unless it is in solution (3).
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 (3).
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 (3, 6). 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 (3).
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 (3). In many cases lower doses produced subtle changes in liver cell physiology, and in some cases higher doses produced more severe effects (3). In mice doses of 8.33 mg/kg/day over 28 days caused increased liver weight and increased liver enzyme activity (3). 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 (3).
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 (3). Kidney damage was also seen in rats at doses of 10 mg/kg/day over 27 months (3).
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 (3). No immune system effects were observed in mice at doses of 6.5 mg/kg/day for 3-12 weeks (3).
Dose levels at which effects were observed in test animals are very much higher than those which may be typically encountered by humans (4). 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 (5). 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 (3). 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 (3). 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 (3). Persons eating fish contaminated with DDT or metabolites may also be exposed via bioaccumulation of the compound in fish (3).
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 (3). 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 (3).
Available epidemiological evidence from two studies does not indicate that reproductive effects have occurred in humans as a result of DDT exposure (3). No associations between maternal blood levels of DDT and miscarriage nor premature rupture of fetal membranes were observed in two separate studies (3, 7, 8). 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 (9).
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 (3). 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.
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 (3).
The available epidemiological evidence regarding DDT's carcinogenicity in humans, when taken as a whole, does not suggest that DDT and its metabolites are carcinogenic in humans at likely dose levels (3). In several epimiological studies, no significant associations were seen between DDT exposure and disease, but in one other study, a weak association was observed (3, 10). 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 (3, 10).
DDT is very slowly transformed in animal systems (4). 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 (3). These compounds in turn are ultimately transformed into bis(dichlorodiphenyl) acetic acid (DDA) via other metabolites at a very slow rate (3). DDA, or conjugates of DDA, are readily excreted via the urine (3).
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 (3). 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 (3). 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 (3). DDT or metabolites may also be elminated via mother's milk by lactating women (3).
There has been much concern over chronic exposure of bird species to DDT and effects on reproduction, especially eggshell thinning and embryo deaths (12). 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 (12). 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 (12). 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 DDT's metabolites and organophosphate (cholinesterase-inhibiting) pesticides to produce greater toxicity to the nervous system and higher mortality (12). Aroclor (polychlorinated biphenyls, or PCBs) may result in additive effects on eggshell thinning (12).
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) (13). The reported 96-hour LC50s in fathead minnow and channel catfish are 21.5 ug/L and 12.2 ug/L respectively (13). Other reported 96-hour LC50s in largemouth bass and guppy were 1.5 ug/L and 56 ug/L respectively (12). Observed toxicity in coho and chinook salmon was greater in smaller fish than in larger (12). It is reported that DDT levels of 1 ng/L in Lake Michigan were sufficient to affect the hatching of coho salmon eggs (14). DDT may be moderately toxic to some amphibian species and larval stages are probably more susceptible than adults (11, 12).
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 (12). Fish uptake of DDT from the water will be size-dependent with smaller fish taking up relatively more than larger fish (12). A half- time for elimination of DDT from rainbow trout was estimated to be 160 days (12).
The reported bioconcentration factor for DDT is 1,000 to 1,000,000 in various aquatic species (15), and bioaccumulation may occur in some species at very low environmental concentrations (13). Bioaccumulation may also result in exposure to species which prey on fish or other aquatic organisms (e.g., birds of prey).
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 (12). DDT is non-toxic to bees; the reported topical LD50 for DDT in honeybees is 27 ug/bee (12). Laboratory studies indicate that bats may be affected by DDT released from stored body fat during long migratory periods (12).
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 (12). It may accumulate in the top soil layer in situations where heavy applications are (or were) made annually; e.g., for apples (2). 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 (12, 15). 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 (14). 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 (17). In other soils (Hood River and Medford) this rate may be as low as 17- 18% over 5 years (17). 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 (12).
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) (3, 6).
|ADI:||0.02 mg/kg/d (3)|
|RfD:||0.0005 mg/kg/day (3)|
|PEL:||1 mg/meters cubed (8-hour) (3) Chemical Name: 1,1,1- trichloro-2,2-bis(4-chlorophenyl) ethane (1)|
|Molecular Weight:||354.51 (1)|
|Water solubility:||< 1 mg/L @ 20 degrees C (1)|
|Solubility in other solvents:||cyclohexanone v.s., dioxane v.s., benzene v.s., xylene v.s., trichloroethylene v.s., dichloromethane v.s., acetone v.s., chloroform v.s., diethyl ether v.s., ethanol s. and methanol s. (1).|
|Melting Point:||108.5-109 degrees C (1)|
|Vapor Pressure:||0.025 mPa @ 25 degrees C (1)|
|Partition Coefficient (octanol/water):||100,000 (16)|
|Adsorption Coefficient:||245,000 (16)|