DDT (1,1,1-trichloro-di-(4-chlorophenyl) ethane)
(endorsed 2011)
Guideline
Based on human health concerns, DDT in drinking water should not exceed 0.009 mg/L.
Related chemicals
DDT (CAS 50-29-3(p.p’)/CAS 789-02-6 (o.p’)) belongs to the organochlorine class of chemicals and is classified as a persistant organic pollutant (POP). Other POPs that were previously used as pesticides include aldrin, dieldrin and heptachlor (Tomlin 2006).
Human risk statement
With good water quality management practices, the exposure of the general population is expected to be well below levels that may cause health concerns.
If present as a contaminant in drinking water, DDT would not be a health concern unless the concentration exceeded 0.009 mg/L. Minor excursions above this level would need to occur over a significant period to be a health concern, as the health-based guideline is based on long-term effects.
With good water quality management practices, pesticides should not be detected in source waters used for drinking water supplies. Persistent detection of pesticides may indicate inappropriate use or accidental spillage, and investigation is required in line with established procedures in the risk management plan for the particular water source.
General description
Uses: DDT is a contact insecticide used in some parts of the world for the control of insects, including those carrying diseases that are infectious to humans such as malaria.
There are no registered products that contain DDT in Australia, but de-registered compounds may still be detected in water.
Exposure sources: DDT persists in the environment as a result of previous use as an insecticide. The general public may be exposed to low levels of DDT through residues in food and/or contaminated source waters.
Typical values in Australian drinking water
Since banning in the 1980s, DDT has not been commonly reported in Australian drinking waters. Evidence suggests that the concentrations of DDT in Australian rivers have progressively declined, as indicated by water in the Brisbane River, which consistently fell from maximum concentrations of about 1.7 µg/L in 1972-1973 to not detectable in 1986-1987 (Connell et al. 2001).
Treatment of drinking water
DDT can be effectively removed from drinking waters by activated carbon treatment (Thacker et al. 1997, Ormad et al. 2008). Flocculation-coagulation can also be effective under suitable conditions (Ormad et al. 2008).
Measurement
DDT can be measured in drinking water using gas chromatography with electron caption detection (WHO 2004). The limit of detection for this technique is 0.01 µg/L.
History of the health values
The current tolerable daily intake (TDI) for DDT is 0.002 mg per kg bodyweight (mg/kg bw), based on a no-observed-effect level (NOEL) of 0.25 mg/kg bw/day from an epidemiological study. The NOEL is based on the absence of toxicological effects at this dose. The TDI incorporates a safety factor of 100, comprising 10 for intraspecies variation and 10 to take into account the uncertainty due to lack of detail in the study. The TDI was established in 2003.
When DDT was used previously, the ADI was 0.02 mg/kg bw based on a NOEL of 0.25 mg/kg bw/day from the same epidemiological study. The ADI was not maintained, as DDT is no longer used in agricultural practice.
The previous health value was 0.02 mg/L (NHMRC and NRMMC 2004).
Health considerations
Metabolism: DDT is absorbed moderately well via the gastrointestinal tract in rats, and absorption is enhanced in the presence of fat. DDT and its metabolite DDE accumulate and are stored in adipose tissue and in organs containing large amounts of fat. DDT is also able to cross the placental barrier in rats and rabbits and accumulate in the foetus. It is excreted mainly unchanged in the faeces, with some excretion of the metabolite DDE occurring in urine and bile. DDT and its metabolites are also excreted in the milk of lactating animals. DDT residues have been found in human breastmilk.
Acute effects: DDT has moderate acute oral toxicity in mice, rats, guinea pigs and rabbits. Data are not available on its potential dermal toxicity or skin sensitisation.
Short-term effects: A short-term oral study in rabbits reported liver and kidney damage, and increased mortality, at 50 mg/kg bw/day. A 1-year oral study in monkeys reported hyperglycaemia, liver enlargement and hepatitis at 0.2 mg/kg bw/day. A 21-month oral study in human volunteers at 0.5 mg/kg bw/day of DDT did not produce any obvious signs of toxicity.
Long-term effects: Long-term oral studies were conducted in mice, rats, guinea pigs, dogs and monkeys. The liver was the main target organ of toxicity, with mice and rats showing particular sensitivity. In mice, there were increased benign and malignant liver tumours at dose levels above 3 mg/kg bw/day. In rats, there was hypertrophy, formation of lipospheres and cell proliferation at 0.25 mg/kg bw/day, and benign hepatocellular tumours at 12.5 mg/kg bw/day. In dogs, jaundice and haemorrhagic symptoms were reported at 50 mg/kg bw/day. In monkeys, loss of appetite, decreased bodyweight gain and convulsions were reported at 55 mg/kg bw/day.
In an epidemiological study of workers exposed to 0.25 mg/kg bw/day for 25 years, there was no association between adverse health outcomes and exposure to DDT. The NOEL of 0.25 mg/kg bw/day from this study is the basis for the current TDI. Two other epidemiological studies reported an association between the incidence of liver and pancreatic cancer and exposure to DDT, however, there were significant confounding factors in these studies.
Carcinogenicity: Long-term dietary studies in mice and rats reported evidence of liver cancer following exposure to DDT. In lifetime studies in hamsters and monkeys, there was no evidence of cancer from exposure to DDT. Epidemiological studies in humans produced only limited evidence of liver and pancreatic cancers following exposure to DDT.
Genotoxicity: DDT is not considered to be genotoxic, based on in vitro and in vivo short-term studies.
Reproductive and developmental effects: A 2- and 3-generation reproduction study in rats and dogs respectively did not produce evidence of adverse effects on reproductive parameters at 10 mg/kg bw. Developmental studies in mice and rabbits have produced conflicting results but the weight of evidence indicates no effects on foetal development, except at high dose levels, well in excess of the likely level of human exposure.
Poisons Schedule: DDT is included in Appendix C of the Standard for the Uniform Scheduling of Medicines and Poisons No.1, 2010 (the Poisons Standard)(DoHA 2010). This appendix is for ‘Substances, other than those included in schedule 9, of such danger to health as to warrant prohibition of sale, supply and use’. Current versions of the Poisons Standard should be consulted for further information.
Derivation of the health-based guideline
The health-based guideline of 0.009 mg/L for DDT was determined as follows:
where:
0.25 mg/kg bw/day is the NOEL based on a 25-year study in humans.
70 kg is taken as the average weight of an adult.
0.1 is a proportionality factor based on the assumption that 10% of the
TDI will arise from the consumption of drinking water.
2 L/day is the estimated maximum amount of water consumed by an adult.
100 is the safety factor applied to the NOEL derived from animal studies. This safety factor incorporates a factor of 10 for intraspecies variation and 10 for the uncertainty arising from the lack of detail in the epidemiological study.
The World Health Organization has a health-based guideline value of 0.001 mg/L for DDT (WHO 2004).
References
NOTE: The toxicological information used in developing this fact sheet is from reports and data held by the Department of Health, Office of Chemical Safety.
Connell DW, Miller G, Anderson S (2001). Chlorohydrocarbon pesticides in the Australian marine environment after banning in the period from the 1970s to 1980s. In: 3rd International Conference on Marine Pollution and Ecotoxicology, Pergamon-Elsevier Science Ltd, Hong Kong, Peoples Republic of China, pp 78-83.
DoHA (2010) The Poisons Standard; Schedule 1-Standard for the Uniform Scheduling of Medicines and Poisons, Department of Health and Ageing, Commonwealth of Australia, Canberra.
NHMRC (National Health and Medical Research Council), NRMMC (Natural Resources Management Ministerial Council) (2004). Australian Drinking Water Guidelines. National Water Quality Management Strategy, Paper 6. NHMRC and NRMMC.
Ormad MP, Miguel N, Claver A, Matesanz JM, Ovelleiro JL (2008). Pesticides removal in the process of drinking water production. Chemosphere, 71(1):97-106.
Thacker NP, Vaidya MV, Sipani M, Kalra A (1997). Removal technology for pesticide contaminants in potable water. Journal of Environmental Science and Health Part B – Pesticides, Food Contaminants and Agricultural Wastes, 32(4):483-496.
Tomlin CD (ed) (2006). The Pesticide Manual: a world compendium, 14th Edition, British Crop Production Council, UK.
WHO (World Health Organization) (2004). Guidelines for Drinking-water Quality. 3rd Edition, WHO, Geneva, Switzerland.
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