Simazine toxicity

McCann, J.A. and R.K. Hitch (1980). Simazine toxicity to fingerling striped bass. Prog. Fish Cult., 42 180-181. 

Until recently, the NRA has not participated during the approval process in assessing the potential environmental impact of pesticides. However, the NRA does supply monitoring data to MAFF and HSE for pesticide reviews. These occur once a pesticide has been approved for use for a certain length of time, or when further information is needed on an approved pesticide. In supplying these data, the NRA comments on any areas of concern. This contributed to the 1993 ban on the use of atrazine and simazine on non-cropped land. In January 1995 the NRA s National Centre for Toxic and Persistent Substances (TAPS) was made advisor to the DoF, on the potential impact on the aquatic environment of... 

Ureides (e.g., diuron, linuron) and triazines (e.g., atrazine, simazine, ametryne) all act as inhibitors of photosynthesis and are applied to soil (see Figure 14.1 for structures). They are toxic to seedling weeds, which they can absorb from the soil. Some of them (e.g., simazine) have very low water solubility and, consequently, are persistent and relatively immobile in soil (see Chapter 4, Section 4.3, which also mentions the question of depth selection when these soil-acting herbicides are used for selective weed control). 

Thus it is significant that for such si/m-triazine herbicides as simazine, atrazine, etc., the health and hygiene MPC (toxicity to warm-blooded animals, including humans) and phytotoxic MPC (toxicity to plants) differ by more than an order of magnitude 0.2-0.5 mg/kg for warm-blooded animals, and 0.01 mg/ kg for plants [89]. Warm-blooded animals and arthropods have a difference in sensitivity to many pyretroids that can reach tens of thousands of times [90]. 

Chlorophyll production inhibited more-than-additive toxicity observed in combination with simazine and malathion (Torres and O Flaherty 1976)... 

Kulshrestha, G., N.T. Yaduraju, and V.S. Mani. 1982. The relative toxicity of the s-triazine herbicides atrazine and simazine to crops. Jour. Environ. Sci. Health B17 341-354. 

Jain, Kiran. Technical Data on Some Chemicals, HOBr Generation Using Sodium Bromide and Chlorine, Toxicity Assessments, Simazine, Chlorine Dioxide. Various technical papers, USA, 1993. 

Distinct differences in cells with regard to the presence or absence of target structures or metabolic processes also offer opportunities for selectivity. Herbicides such as phenylureas, simazine, and so on, block the Hill reaction in chloroplasts, thereby killing plants without harm to animals. This is not always the case because paraquat, which blocks photosynthetic reactions in plants, is a pulmonary toxicant in mammals, due apparently to analogous free-radical reactions (see Figure 18.4) involving enzymes different from those involved in photosynthesis. 

In the United States, approval of new herbicides depended not only on performance and toxicity data, but also on a clear picture of eventual crop and soil residues. The Geigy Analytical Department began immediately to develop a reliable residue method for simazine and other triazines. Working methods for residues in plants and soil were available by the end of 1956. 

Worker and environmental safety Atrazine and simazine are safe to apply according to the directions on the label. Nontarget safety margins are good because atrazine is nonvolatile and has low specific activity. In addition, avian, mammalian, and aquatic toxicities are low. Relative safety to nontarget plant species is a positive characteristic that is not always found in alternative products. 

Hauswirth, J.W. and L.T. Wetzel (1998). Toxicity characteristics of the 2-chlorotriazines, atrazine and simazine. In L.G. Ballantine, J.E. McFarland, and D.S. Hackett, eds., Triazine Herbicides Risk Assessment. Symposium Series 683. Washington, DC American Chemical Society, pp. 370-383. 

Figure 28.3 Distributions of acute toxicity values (LC- and EC-50s)a for simazine and terbutryn to aquatic plants and aquatic animals. a EC50 = effective concentration causing a specified effect in 50% of the tested population. LC50 = lethal concentration causing death in 50% of the population tested.

The doses from exposure are characterized by distributions. For each possible dose level, these distributions quantify the probability that an individual in a specified population or subpopulation will receive that dose level as a result of exposure to atrazine and simazine through drinking water ingestion, dietary consumption, herbicide handling, or a combination of these potential exposure routes. For chronic toxic endpoints, the traditional (default) dose metric summarizing a lifetime of exposure is the lifetime average daily dose (LADD). Distributions of LADDs have been determined, and the corresponding distributions of the MOEs are presented herein. 

Exposure assessments characterize the water, diet, and herbicide handling exposure pathways for atrazine and simazine (Sielken et al, 1996, 1998). For each exposure pathway, the chemical-specific doses (mg/kg/day) from each relevant route (ingestion, inhalation, and dermal) are summed. The total chemical-specific dose for each exposure pathway is characterized separately, and then these doses are aggregated by summing over the multiple exposure pathways. The pathway-specific and aggregate assessments are performed separately for atrazine and simazine. In addition, because atrazine and simazine are assumed to have a common mechanism of toxicity, a cumulative exposure assessment is performed combining the doses of atrazine and simazine. 

Because Equation (31.4) is mathematically equivalent to either Equation (31.5) or (31.6) (shown below), the formula for MOEatrazine simazine in Equation (31.4) is of the proper form - namely, a benchmark dose corresponding to a known amount of toxicity, divided by a cumulative dose from exposure that reflects the relative toxicity of the cumulated chemicals. 

McCormick, G.C. (1988). Simazine Technical Combined Chronic Toxicity/Oncogenicity Study in Rats. Submitted to USEPA. 

Toxicity The acute oral toxicity of simazine for rats is more than 15,380 mg/kg, and the acute dermal LD50 in rabbits is 10,200 mg/kg. It demonstrated moderate primary skin and eye irritation effects in rabbits. The acute inhalation LC50 to rats is greater than 5 mg/L. Reports have indicated that simazine caused no serious effects in humans except minor skin rashes in some cases. Similarly, it caused no long-term effects in humans.5,36... 

The development of toxic symptoms on plants treated with pure electron transport inhibitors, such as simazine, diuron, and the uracils, can be prevented if the plants are supplied exogenously with a respirable carbohydrate (2). This observation suggests that the glycolytic or the mitochondrial system can provide sufficient energy to prevent the appearance of phyto-... 

Bipyridyl herbicides include alachlor, amitrole, atrazine, bromacil, bromoxynil, butylate, cyanazine, dalapon, dicamba, diuron, linuron, fluometuron, hexazinone, molinate, metolachlor, oryzalin, pendimethalin pronamide, propanil, propazine, simazine, terbacil, triallate, and triclopyr. In addition to these herbicides, the most common bipyridyls are diquat and paraquat. Paraquat is more toxic than diquat and produces chronic abnormal cell growth in the lungs, cornea and lens of the eye, nasal mucosa, skin, and fingernails. Diquat affects the eye lens and intestinal tract lining, but does not usually produce the frequently fatal lung changes characteristic of paraquat. 

The US Environmental Protection Agency (EPA) has determined that propazine belongs to a group of other triazines (including atrazine, simazine, and some related metabolites) that act through a common mechanism of toxicity based on ability to suppress the pituitary luteinizing hormone (LH) surge and elicit effects on reproductive function and development. 

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