Cyanazine in the Brid River

Dr Alison Bleaney
THE presence of cyanazine in the lower reaches of the Brid River in January 2009- even at 0.13ppb – is another indication of the apparent disregard by the Tasmanian Government for the health and safety of water users.

The USA prohibited the use of cyanazine in 2002; it is an endocrine disruptor, an immunotoxic, a developmental and reproductive toxin, a possible human carcinogen and a groundwater contaminant.

Quote from a recent article reviewed by Environmental Health Perspectives – cited below:
The herbicide cyanazine is a synthetic s-triazine (along with atrazine and
simazine) that has been widely used to control broadleaf weeds and grasses in agricultural crops. It is applied as a preemergent herbicide once during the growing season to control weeds in corn, sorghum, cotton, barley, wheat, oil rape seed, sugar cane, and potatoes. (In Tasamnaia it is used for potatoes peas and onions.)

In the 1990s, cyanazine ranked as the fifth most commonly used herbicide in the United States, with an estimated 32 million pounds applied annually [U.S. Environmental Protection Agency (EPA) 2004]. Human exposure to cyanazine occurs in farming and pesticide manufacturing and through contaminated groundwater (Barbash et al. 2001; Ritter 1990) and agricultural runoff (Hansen et al. 2001). The most common application methods for cyanazine are in solution by ground boom or as a pellet, with the most common route of exposure to humans being dermal. There is little evidence to suggest that applicators are exposed to cyanazine via inhalation with recommended methods of use (U.S. EPA 1994).

The U.S. EPA classified cyanazine as a restricted use pesticide based on the detection of cyanazine in ground and surface water (i.e., restricted use pesticides may only be used by pesticide applicators certified by the state authorities), and as a Group C, possible human carcinogen based on the increased incidence of mammary tumors in rats from dietary cyanazine exposure of 25 or 50 ppm (Bogdanffy MS, unpublished data) and the possible mutagenic effect of cyanazine in mice lymphoma cells (Jannasch M, Sawin V, unpublished data). The manufacturer proposed to gradually phase out cyanazine production and use in the United States by 1999. The U.S. EPA Office of Pesticide Programs cancelled cyanazine product registrations and prohibited the sale and use of existing stocks of cyanazine after 30 September 2002 (U.S. EPA 1996). Although cyanazine is banned in the United States, it is still used in various African nations (e.g., South Africa, Niger), Asia and the Pacific Region (e.g., Australia, India, New Zealand, the Philippines), Europe (e.g., Hungary, Portugal, United Kingdom), Central Asia, Canada, and South America (Pesticide Action Network 2004).

Despite its worldwide use, studies on the health effects from cyanazine exposure specifically have been limited and results have been mixed. Studies suggest that cyanazine could be mutagenic (Jannasch M, Sawin V, unpublished
data) and induce marginal DNA damage in vivo in mouse leukocytes administered high doses intraperitoneally (Tennant et al. 2001), but others showed no effects in human lymphocytes and rat bone marrow (Hrelia et al.
1994). Cyanazine exposure was associated with the formation of mammary-gland tumors in Sprague-Dawley rats (Bogdanffy MS, unpublished data); mechanism of action studies suggest that tumor formation is mediated through a prolactin mechanism thought to be of low relevance to the development of human breast cancer (Bogdanffy et al. 2000). However, a new study suggests that prolactin may play a larger role in the development of human breast cancer, more than previously thought (Harvey 2005).

http://www.ehponline.org/members/2006/8997/8997.html