DDT Profile

CAS No. 50-29-3
IARC Monograph Vol. 53, Suppl. 7, 1991 (Group 2A)
IARC Monograph Vol. 113, 2017(Group 2A)

DDT Profile


  • A banned insecticide and persistent organic pollutant
  • Associated cancers: Non-Hodgkin lymphoma, liver and testicular cancers (limited evidence)
  • Most important route of exposure: Diet
  • Primary source: DDT is persistent and present in the environment although it is no longer used in Canada
  • Occupational exposures: No longer a concern after DDT use was discontinued in Canada
  • Environmental exposures: Via meat, poultry, fish, and dairy consumption
  • Fast fact: Arctic communities are at higher risk of exposure because DDT accumulates in polar regions and in the high-fat foods consumed via a traditional diet

General Information

4,4′-Dichlorodiphenyltrichloroethane (DDT) is a white, crystalline insecticide.[1] First synthesized in 1874, DDT was not widely used until the 1940s. It has been used in forestry, agriculture, domestic settings, and warfare.[1] Although it was never produced in Canada and was banned in December 1990, DDT and its metabolites are present in our environment due to their persistent nature.[2] DDT is used in certain countries to combat malaria and in China in paints that impede the growth of barnacles and other marine

DDT is a persistent organic pollutant (POP), meaning that it is a chemically stable toxic substance that resists degradation.[4] It is considered “CEPA-toxic” under the Canadian Environmental Protection Act, and is able to bioaccumulate.[4] Environment Canada has targeted DDT and its metabolites for virtual elimination, with the goal of reducing releases to the environment to a level below which they cannot be detected.[5] Furthermore, Canada is a signatory to the Stockholm Convention, under which DDT is listed. The Stockholm Convention is a global treaty that aims to protect human health and the environment from persistent organic pollutants.[6]

In June 2015, the International Agency for Research on Cancer (IARC) classified DDT as Group 2A, probably carcinogenic to humans.[7] This classification was based on limited evidence of carcinogenicity in humans for non-Hodgkin lymphoma and cancers of the liver and testis reported in a number of studies published since 1992. There was sufficient evidence that DDT can cause cancer in laboratory animals and strong evidence that DDT affects several bodily mechanisms in humans. These effects include suppressing the immune system and increasing oxidative stress.[7]

Other non-cancer health effects are documented for DDT exposures. Acute oral exposures primarily target the central nervous system and can result in increased excitability, tremors, seizures, sweating, headache, nausea, vomiting, and dizziness.[8] Chronic oral exposures may change levels of liver enzymes in the blood, and may shorten lactation periods.[8] Long-term occupational exposure to DDT can result in chronic nervous system effects. These include a permanent decline in neurobehavioral functioning, such as paying verbal attention and synchronizing visual information with physical movement, as well as an increase in neuropsychological and psychiatric symptoms.[9]

Regulations and Guidelines

Occupational exposure limits (OEL) [10,11,12,13,14,15,16,17,18,19,20,21,22,23,24]

Canadian Jurisdictions OEL (mg/m3) Notes
Canada Labour Code 1 [TWA]
AB, BC, QC 1 [TWA]
MB, NB, NL, NS, PE 1 [TWA]
NT, NU, SK, YT 1
ON 1 [TWA]
Other Jurisdiction OEL (mg/m3) Notes
ACGIH 2020 TLV 1 [TWA]
mg/m3 = milligrams per cubic meter
stel = short term exposure limit (15 min. maximum)
TWA = time weighted average (8 hours)
ACGIH = American Conference of Governmental Industrial Hygienists
TLV = threshold limit value

Canadian environmental guidelines

Jurisdiction Limit Year
Health Canada’s Maximum Residue Limits (MRL) for Foods Food type:
Fish: 5 ppm
Meat, fat, cheese, milk: 1 ppm
Eggs, vegetables: 0.5 ppm
Health Canada’s Toxicological reference values and chemical-specific factors ADI = 10 µg/kg body weight/day 2007[26]
Guidelines for Canadian Drinking Water Quality Guidelines for DDT and its metabolites have been archived since levels that pose a risk to human health are no longer found in Canadian drinking water supplies. 2017[27]
Government of BC’s Contaminated Sites Regulation Sets soil standards for the protection of human health:
Agricultural and low density residential sites: 20 μg/g
Urban park and high density residential sites: 40 μg/g
Commercial sites: 150 μg/g
Industrial sites: 1,000 μg/gDrinking water: 0.45 μg/L**
WHO Drinking Water Guideline 0.001 mg/L* 2011[29]
ppm = part per million
ADI = acceptable daily intake
µg/g = micrograms per gram
MAC = maximum allowable concentration
µg/L = micrograms per litre
WHO = World Health Organization
* for DDT and its metabolites
** Standards are for the sum of DDT (2,4′ + 4,4″ isomers), DDD (2,4′ + 4,4″ isomers), and DDE(2,4′ + 4,4″ isomers)

Canadian designation

Agency Designation/Position Year
CEPA Schedule 1: DDT is considered toxic as defined in Section 64 1999[30]
Federal Toxic Substances Management Policy Track 1: Persistent and bioaccumulative substance; goal of virtual elimination 2010[31]
Canada-Ontario Agreement on Great Lakes Water Quality and Ecosystem Health Tier 1 chemical: targeted for virtual elimination 2014[32]
Health Canada DSL – low priority substance (already risk managed) 2006[33]
CCME Water Quality Guidelines Rank: High hazard; Potential human carcinogen 2008[34]
Stockholm Convention on POPs Annex B: Measures must be taken to restrict the production and use of DDT 2004[6]
CEPA = Canadian Environmental Protection Act
DSL = domestic substance list
CCME = Canadian Council of Ministers of the Environment

DDT was not included in other Canadian government guidelines, standards, or chemical listings reviewed.

Canadian legal status[35]

Most DDT uses were phased out in the mid 1970s. By 1985, the registration of all remaining pesticide uses of DDT was
discontinued.[36] Existing stocks could be sold, used, or disposed of until December 1990, after which selling or using DDT was strictly prohibited and all existing stocks were disposed of. Currently, the manufacture, use, sale, offer for sale, and import of DDT is prohibited at the federal level.[36]

Jurisdiction Legislation Notes

List of Pest Control Product Formulants and Contaminants of Health or Environmental Concern I/2005-114 

Pest Control Products Act, SC 2002, c 28

Prohibition of Certain Toxic Substances Regulations, 2012, SOR/2012-285

Canadian Environmental Protection Act, 1999, SC 1999, c 33

Identifies DDT as a contaminant of health or environmental concern

DDT not registered pesticide under the PCPA

Prohibits DDT manufacture, use, sale, offer for sale, or import

Lists DDT as a Schedule 1 Toxic Substance; intended for virtual elimination

AB, BC, MB, NB, NL, NS, NT, NU, PE, SK, YT Multiple titles Not included
ON General, O Reg 63/09 Prohibits use, handle, storage, display, disposal, sale, offer for sale, transfer or transport of DDT
QC Pesticides Management Code, CQLR c P-9.3, r 1 Prohibits the use of DDT

Main Uses

DDT was the first modern synthetic insecticide. It was initially used to control insect-borne diseases during World War II and to address mosquito-borne malaria.[1] In Canada, DDT was primarily used to control agricultural pests, including the codling moth on deciduous fruit, Colorado potato beetle, and European corn borer. It was also used to control forest pests, such as the gypsy moth and spruce budworm.[8] DDT was primarily applied using aerial and ground spraying techniques.[37] It was also used in domestic settings to control moths and lice.[8,37] While its use is banned in many regions, including North America and Europe,[1,6] DDT is still used agriculturally in some nations and is promoted in the World Health Organization’s efforts to eradicate malaria.[38]

Canadian Production and Trade

When used in Canada, DDT was imported from the United States, as it was never manufactured here.[37] Information about the amount of DDT used in Canada is difficult to find, however it is known that by the 1970s more than 1 million tonnes was used throughout North America.[39] In the United States alone, 600,000 tonnes had been applied domestically by the 1970s. In 1959, DDT usage in the United States peaked at 36,000 tonnes, and steadily declined to 5,400 tonnes in 1971.[40] Estimates show that a total of 1.8 million tonnes of DDT have been produced and applied in the world since 1940.[41]

Environmental Exposures Overview

Environmental Exposure

The primary route of exposure to DDT and its metabolites in the general population is through diet.[8] DDT levels in air and water are currently low, and exposure to DDT in drinking water is considered negligible. This is because DDT is not very soluble in water and because standard drinking water treatment methods are efficient.[8]

Most DDT exposure through diet occurs through consuming meat, poultry, fish, and dairy products. Vegetables are also a source. Leafy vegetables tend to contain more DDT than others due to greater surface area for DDT to deposit onto the plant surface. Breast milk may also act as a source of exposure for infants,[8] although levels appear to be dropping following DDT bans in many countries.[42]

The 1998 Canadian Total Diet Study analyzed foods in Whitehorse for average DDT and dichlorodiphenyldichloroethylene (DDE, a breakdown product of DDT) residue levels.[43] The study indicated that average residue levels in food are generally below 1 µg/L. Where a maximum residue limit (MRL) had been established, DDT and DDE levels were less than 1% of the MRL.[31,43]

Highest exposures generally occur through fish from the Great Lakes and the St. Lawrence River. The US Environmental Protection Agency’s Great Lakes Fish Monitoring program has monitored DDT levels in fish since 1970. As of 2000, DDT levels were below 1 ppm. This is the standard set by the Great Lakes Water Quality Agreement between the United States and Canada, which aims to restore and maintain the integrity of the Great Lakes Basin Ecosystem.[44] More recent studies found that DDT levels in fish from the Great Lakes remain below 1 ppm.[45,46] As concentrations in these bodies of water and fish decline, DDT intake in fish-eaters has also decreased.[31,47] Overall, DDT levels in all Ontario lakes are low enough that exposure via fish consumption is not a concern.[48]

DDT can travel far distances in the atmosphere as a result of emissions or volatilization. It may deposit on the earth with the rain or on its own, and re-volatilize back into the atmosphere several times. This process is called “The Grasshopper Effect”. Since DDT tends to re-volatilize at a much slower rate in cold conditions, it accumulates in the colder, polar regions of the globe. This process is called “global distillation”.[8] Members of Inuit communities residing in Nunavut have significantly higher DDT and DDE blood concentrations compared to residents of Southern Canada.[1] Northern populations are at increased risk of exposure compared to the general population due to global distillation and due to their traditional diet. The traditional diet tends to include foods that are high in fat, such as seal and whale, in which DDT is more likely to accumulate.[31] Even so, levels of DDT in Arctic biota have typically decreased by more than 5% a year from the early 1990s to 2011.[49]

Environmental Fate

DDT is broken down primarily into DDE and dichlorodiphenyldichloroethane (DDD).[8] DDT and its metabolites bind strongly to soil. As a result, DDT tends to remain in surface layers of soil and does not leach into groundwater. A portion of DDT and its metabolites are bioavailable to plants and soil invertebrates; in plants, uptake of DDT and its metabolites after they have volatilized into the air may be up to 6.8 times higher than uptake through roots.[8]

DDT and its metabolites are only slightly soluble in water and are highly soluble in lipids. In aquatic environments, DDT binds to sediments, which can then be ingested by organisms such as bottom feeders to bring DDT into the aquatic food chain. DDT rapidly biomagnifies up this food chain, resulting in higher levels at the top.[50] DDE is the metabolite that generally accumulates in humans.[31]

The half-life of DDT varies depending on the medium in which it is found. In air, DDT and its metabolites are quickly broken down by sunlight and have a half-life of approximately two days.[50] DDT in soil can break down in 2-15 years, with greater persistence in cooler temperatures and in soils with high pH.[8,50] In aquatic environments, DDT has a half-life of 150 years.[51] Volatilization of DDT and its metabolites may account for considerable losses from soil surfaces and water.[8]

Occupational Exposures Overview

Exposures can occur through dermal contact, and inhalation of dust or vapors in occupational settings.[8]

Because it is no longer produced or used in Canada, occupational exposure to DDT is not a concern. DDT remaining in historically-treated agricultural soils could volatilize into the air, resulting in exposures in those areas, but those exposures are relatively insignificant when compared to exposures during DDT production or formulation.[8,52]

CAREX Canada has not prioritized for exposure estimate development. This is because the likelihood of exposure in Canadian workers is very low.

Exposure Reduction

DDT use has been restricted and banned for decades in Canada, which has significantly decreased exposures in workplace and community environments. Exposure to DDT and DDE in northern Aboriginal communities tends to be higher compared to those in southern Canada due to the reliance on traditional foods and higher deposition rates in polar regions. The Arctic Monitoring and Assessment Program (AMAP)[53], the Inuit Tapiriit Kanatami (ITK)[54], and several studies have stated that the overall benefits of eating a traditional diet outweigh any exposure risks, such that food advisories are not recommended.[1,55,56,57] The ITK has emphasized that the benefits of breastfeeding for infants outweigh the potential risks of exposure.[58]

See the Resources tab for more information.


1. Aboriginal Affairs and Northern Development Canada. Persistent Organic Pollutants (POPs) Fact Sheet Series: DDT Dichlorodiphenyltrichloroethane(2010) (PDF)
2. Environment and Climate Change Canada. Dichlordiphenyltrichloroethane (2013)
3. Ricking M, Schwarzbauer J. “DDT isomers and metabolites in the environment: an overview.” Environ Chem Lett 2012;10:317-323.
4. Environment and Climate Change Canada. Research, wildlife and landscape science (2013)
6. Stockholm Convention. The POPs (2008)
7. International Agency for Research on Cancer (IARC). IARC Monographs, Volume 113 (2017) (PDF)
8. Agency for Toxic Substances and Disease Registry (ATSDR). Toxicological profile for DDT, DDE, and DDD (2002)
9. Van Wendel de Joode B, Wesseling C, Kromhout H, Monge P, Garcia M, Mergler D. “Chronic nervous-system effects of long-term occupational exposure to DDT.” The Lancet 2001;357:1014-1016.
15. Government of Newfoundland and Labrador. Regulation 5,12 Occupational Health and Safety Regulations (2018)
16. Government of the Northwest Territories. Occupational Health and Safety Regulations, R-039-2015 (2020) (PDF)
18. The Canadian Legal Information Institute (CanLII). Government of Nunavut’s Occupational Health and Safety Regulations, Nu Reg 003-2016 (2010)
20. Government of Prince Edward Island. Occupational Health and Safety Act Regulations Chapter 0-1 (2013) (PDF)
22. Government of Saskatchewan. The Occupational Health and Safety Regulations, 1996 (2016) (PDF)
23. The Canadian Legal Information Institute (CanLII). Yukon’s Occupational Health Regulations, O.I.C. 1986/164 (2020) (PDF)
24. Occupational Safety and Health Administration (OSHA). Annotated PELs (2020)
28. Government of British Columbia. Contaminated Sites Regulation B.C. Reg. 375/96 (2019)
30. Environment and Climate Change Canada. List of Toxic Substances Managed Under CEPA (Schedule 1) (1999)
34. Canadian Council of Ministers of the Environment (CCME). National Classification System for Contaminated Sites (2008) (PDF)
35. The Canadian Legal Information Institute (CanLII). The Canadian Legal Information Institute website
37. Canadian Council of Ministers of the Environment (CCME). Canadian soil quality guidelines for the protection of environmental and human health: DDT (1999)
38. World Health Organization (WHO). The use of DDT in malaria vector control (2011) (PDF)
40. US Environmental Protection Agency (EPA). DDT regulatory history: A brief survey (1975)
41. US Environmental Protection Agency (EPA). Persistent organic pollutants: A global issue, a global response (2009)
42. Smith, D. “Worldwide trends in DDT levels in human breast milk.” International Journal of Epidemiology 1999;28:179-188.
44. US Environmental Protection Agency (EPA). Great Lakes Monitoring – Fish indicators (2012)
45. Canadian Council of Ministers of the Environment (CCME). National Classification System for Contaminated Sites (2008) (PDF)
47. Dellinger JD, Moths MD, Dellinger MJ, Ripley MP. “Contaminant trends in freshwater fish from the Laurentian Great Lakes: A 20-year analysis.” Hum Ecol Risk Assess 2014;20:461-478.
48. Mahmood M, Bhavsar SP, Arhonditsis GB. “Examination of temporal DDT trends in Lake Erie fish communities using dynamic linear modeling.” Journal of Great Lakes Research 2013;39:437-448.
50. Ontario Ministry of the Environment. Guide to eating Ontario sport fish (2009)
52. Kurt-Karakus PB, Bidleman TF, Staebler RM, Jones KC. “Measurement of DDT fluxes from a historically treated agricultural soil in Canada.” Environ Sci and Technol 2006;40:4578-4585.
53. Agency for Toxic Substances and Disease Registry (ATSDR). ToxFAQs for DDT, DDE, and DDD (2002)
54. National Pesticide Information Centre. DDT (Technical fact sheet) (2000) (PDF)
55. Hansen, J.C. “Environmental contaminants and human health in the Arctic.” Toxicology Letters 2000;112-113:119-125.
57. Van Oostdam J, Donaldson SG, Feeley M, Arnold D, Ayotte P, Bondy G, Chan L, Dewaily E, Furgal CM, Kuhnlein H, Loring E, Muckle G, Myles E, Receveur O, Tracy B, Gill U, Kalhok S. “Human health implications of environmental contaminants in Arctic Canada: A review.” Sci Total Environ 2005;351-352:165-246.



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