Description of Use in Document

While the data provide useful information for characterization of the potential effects of malathion exposure on the adrenal gland and its associated components, it is unclear how they impact survival or reproduction of the whole organism. Also, there is uncertainty with regards to the impurity profile relative to current standards.

Rishi, S. and B.D. Garg. 1993. Effect of malathion on immune response to T-dependent and T-independent antigen in chicken. Indian Journal of Poultry Science. 28 (3), pp. 208-216.

6-8 week old white leg-horned chicken were randomly divided into four groups containing 40-45 birds. Group I birds received 22.6 mg/kg malathion; Group II birds received 45.2 mg/kg malathion; and Group III birds received 90.4 mg/kg malathion. Doses were given daily in groundnut oil for 10 or 20 days. Control birds (Group C) were given 1 mg groundnut oil per bird for 10 or 20 days. After 10 days of treatment, 6-8 birds from each group were given 1 ml of 1% SRBC i.v. as T-dependent antigen and 6-8 birds from each group were given 1 ml of 1% LPS in complete Freund’s adjuvant as T-independent antigen. After 8 days of antigen administration blood was collected from each bird daily up to day 14. Blood samples were also taken 20 days after pesticide administration. The total antibody titre to SRBC antigen was determined. The ME-resistant (IgG) and ME-sensitive (IgM) antibodies titres were also determined. In addition, the effect of malathion on cell-mediated immunity was determined using h ypersensitivity reaction assay to 2,4-dinitrochlorobenzene (DNCB) and phytohemagglutinin-P (PHA-P). 7 days after antigen administration 4 birds from each group were injected in one wing web with 0.1 ml of 1 mg/ml of PHA-P in PBS solution or 0.1 ml of 1% DBCB solution in acetone water (4:1) was applied. The opposite wing web, which served as a solvent control. The difference in wing thickness was measured.

Based on the results of this study, the authors suggest that malathion has an immunostimulatory effect at lower does and immunosuppressive effect at higher doses.

While the data provide useful information for characterization of the potential immune effects of malathion exposure it is unclear how they impact survival or reproduction of the whole organism. For the antibody portion of the test, data from the study is only presented in figures and as a % difference from the control. Raw data is not available to confirm statistical differences. For the wing response portion of the test data is only presented as an increase or decrease from the control. The form of the test material (formulation product vs. technical; source; purity) is not described.

Sodhi, S., A. Sharma, A.P.S. Brar, R.S. Brar. 2008. Effect of α tocopherol and selenium on antioxidant status, lipid peroxidation and hepatopathy induced by malathion in chicks. Pesticide Biochemistry and Physiology. 90 (2008), pp. 82-86.

Day old broiler chicks (n=45) were acclimatized for 7 days, vaccinated against New Castle disease and an infections bursal disease. They were supplied with food and water ad libitum. At one week of age chicks were divided randomly into three groups of 15 chicks each. The chicks in group I were given 10 mg/kg bw of malathion orally each day for 60 days. The chicks in group II were given the same dose of malathion plus α tocopherol and selenium combination (α tocopherol 150 IU/kg feed and selenium 0.1 mg/kg feed), daily for 60 days. The chicks in group III were the controls. Blood samples were collected from 5 chicks in each group by cardiac puncture at 20 day intervals. Various biochemical measures, including plasma lipid peroxidation (table 1), erythrocytic glutathione peroxidase activity (table 2) and plasma vitamin E concentration (table 3), were measured. At the end of the study, five chicks from each group were sacrificed and liver was collected for histopathological studies.

Based on limitations below

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  While the biochemical and histopathological data provide useful information for characterization of the potential cellular effects of chronic malathion exposure it is unclear how they impact survival or reproduction of the whole organism. The raw information supporting the histophathological findings, including the number of chicks with moderate to severe cellular damage in the Group I chicks and the number of chicks with severe histopathological changes, are not available. Without this information it is not possible to compare the effects observed in the treatment and control groups or fully understand the scope of the damage.
  
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  Additionally, the purity or form (e.g., technical grade or formulation) of the malathion used were not reported.
  

Giri, S., G.D., Sharma, A. Giri, and S.B. Prasad. 2002. Genotoxic effects of malathion in chick in vivo micronucleus assay. Cytologia. 67, pp. 53-59.

5-7 day old chicks (Gallus domesticus) were obtained from Arambagh Hatcheries Ltd, Guwahati, India and housed in wooden cages. Birds were provided food and water ad libitum. Healthy animals (30-32g, both sexes) were randomly assigned to one of the following study groups:

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  Group 1 (n=4) served as the control. Two birds were exposed to saline via an intraperitoneal injection (i.p) and two birds were exposed via post oral gavage (p.o).
  
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  Group 2 (n= 6) received 2.0 mg/kg mitomycin C via i.p.
  
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  Group 3 (n= 3) received 2.0 mg/kgmitomycin C via o.p.
  
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  Group 4 (n=6) received 2.5 mg/kg malathion via i.p.
  
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  Group 5 (n= 6) received 5 mg/kg malathion via i.p.
  
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  Group 6 (n= 6) received 10 mg/kg malathion via i.p.
  
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  Group 7 (n=3) received 2 mg/kg malathion via i.p. for 5 consecutive days at 24 h intervals
  
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  Group 8 (n= 3) received 2 mg/kg malathion via p.o. for 5 consecutive days at 24 h intervals.
  
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  Group 9 (n=3) received 2.5 mg/kg malathion via o.p.
  
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  Group 10 (n= 6) received 5 mg/kg malathion via o.p.
  
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  Group 11 (n= 6) received 10 mg/kg malathion via o.p.
  

In peripheral blood cells, acute exposure to malathion significantly increased the incidence of MN for the intraperitoneal injection exposure route only. Chicks exposed via post oral gavage were not significantly different from controls.