Simazine was introduced in 1957 as a systemic herbicide for use on grasses and weeds in food crops, especially maize, and for general weed control. It is available in many types of formulation, including wettable powders, granules, concentrates, suspensions and liquids. Exposure can occur during its production and application and via contamination of ground- and surface water.
Exposure could also occur through consumption of foods containing residues. Simazine residues were not detected in large-scale surveys of food products in Canada and the USA.
No data on the genetic and related effects of simazine in humans were available to the Working Group.
Simazine did not induce micronucleus formation in mice. It induced a small increase in the frequency of sister chromatid exchange in human cells in vitro but not in rodent cells. Simazine did not induce genetic damage in any other tests, except in plants where chromosomal aberrations were induced and in Drosophila melanogaster where dominant lethal effects and gene mutation were induced.
There is inadequate evidence in humans for the carcinogenicity of simazine.
There is inadequate evidence in experimental animals for the carcinogenicity of simazine.
Simazine is not classifiable as to its carcinogenicity to humans (Group 3).