New study on Mancozeb

Mancozeb is non-systemic fungicide, Organic-Dithiocarbamate group. Foliar protection of many fruits, vegetables, nuts and field crops against a wide spectrum of fungal diseases including potato blight, leaf spots, scab on apples and pears, anthracnose and rust. 

For seed treatment of rice, cotton, potatoes,safflower, sorghum, peanuts, tomatoes, flax, and cereal grains.Mancozeb(CAS NO:8018-01-7) does not induce in fungi and is therefore an essential componentof alternating spray program or of mixed formulations with systemic and other fungicides.

Polyvalence: use on more than 70 crops for the control of 400 fungal diseases of which mildews, excoriosis, black-rot, red fire, alternaria, etc. Multi-site action: making it an ideal partner for recent mono-site molecules. 

Nutrient: correction of crop deficiencies in manganese and zinc.The worldwide use mancozeb(CAS NO:8018-01-7) without danger to the environment. Because mancozeb break down rapidly in the environment. It is not harmful to beneficial insects and natural pollinators. Hence it is a useful product in integrated pest management programs. Mancozeb is a contact fungicide which remains on the treated surface of the plant.

Mancozeb is a member of the ethylene bisdithiocarbamate (EBDC) group of fungicides that also includes the related active ingredient metiram, the only other registered EBDC. A third EBDC, maneb, is no longer registered for use. 

Mancozeb and metiram are metabolized to ethylenethiourea (ETU) in the body and both degrade to ETU in the environment. Therefore, EPA has considered the aggregate or combined risks from food, water and non-occupational exposure resulting from mancozeb alone and ETU from all sources (i.e., the other EBDC fungicides) for this action. EPA's assessment of exposures and risks associated with mancozeb and ETU follows.

Mancozeb is not acutely toxic via the oral, dermal or inhalation routes of exposure. Further, mancozeb is not a skin irritant nor is it a skin sensitizer, although it does cause mild eye irritation. The findings in multiple studies demonstrate that the thyroid is a target organ for mancozeb. 

Thyroid toxicity is manifested as alternations in thyroid hormones, increased thyroid weight, and microscopic thyroid lesions (mainly thyroid follicular cell hyperplasia). These effects are due to the ETU metabolite.

Mancozeb is rapidly absorbed and eliminated in the urine. In oral rat metabolism studies with radiolabeled mancozeb and other EBDCs, an average 7.5%in vivo metabolic conversion of EBDC to ETU occurred, on a weight-to-weight basis. 

Metabolism data indicate mancozeb does not bio-accumulate. Mancozeb has been tested in a series of in vitro and in vivo genotoxicity assays, which have shown that it exhibits weak genotoxic potential.

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