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Carbendazim
50%SC  80%WG  50%WP

INTRODUCTION

 

Carbendazim controls of Septoria, Fusarium, Erysiphe and Pseudocercosporella in cereals; Sclerotinia, Alternaria and Cylindrosporium in oilseed rape; Cercospora and Erysiphe in sugar beet; Uncinula and Botrytis in grapes; Cladosporium and Botrytis in tomatoes; Venturia and Podosphaera in pome fruit and Monilia and Sclerotinia in stone fruit. Application rates vary from 120-600 g/ha, depending on crop. A seed treatment (0.6-0.8 g/kg) will control Tilletia, Ustilago, Fusarium and Septoria in cereals, and Rhizoctonia in cotton. Also shows activity against storage diseases of fruit as a dip (0.3-0.5 g/l). 

 

Formulation types SC; WG; WP;

 

Acute toxicity


Carbendazim is classified by the World Health Organisation (WHO) as ‘unlikely to present hazard in normal use’. The acute oral LD50 (dose at which half the sample is dead) for rats is >15000 mg/kg and >2500 mg/kg for dogs. On the basis of the analysis of rat, dog and rabbit studies, the UK Advisory Committee of Pesticides (ACP) evaluation concluded that Carbendazim is of low toxicity to rodent and non-rodent species via the oral, dermal, inhalational and intraperitoneal routes’. 


The primary source of Carbendazim exposure for the public at large is dietary intake; this is discussed further below. For agricultural workers, occupational exposure during manufacture or use is considered to be within acceptable levels. The International Programme for Chemical Safety (IPCS) do not indicate that there is a danger of exposure to Carbendazim during its production and use in agriculture. As workers are most likely to suffer exposure through skin contact or inhalation, risk can be controlled by the use of protective clothing and the use of a dust mask is recommended.

 

Chronic effects


Research on mice showed increased tumours in two out of three studies. However, in reviewing other data, the Scientific Committee on Plants showed there was no DNA-reactive effect so they concluded ‘these mouse liver tumours could not be interpreted as predicting a carcinogenic hazard to humans’. This conclusion was also reached by the ACP evaluation of Carbendazim in 1992.



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