No abstract

. (1969). Brit. J. industr. Med., 26,[59][60][61][62][63][64]. A method for determining the dermal toxicity of pesticides. A method is described for the measurement of the percutaneous LD50 of a pesticide, using the laboratory rat as a test animal. The results obtained by this method on a selection of pesticide chemicals are tabulated and discussed. The reproducibility of the method was validated by a collaborative study with five other laboratories.The importance of dermal absorption as the main route of entry in occupational poisoning by agricultural chemicals has been reviewed by Barnes (1959) and Hayes (1960). Their findings have been confirmed by several recent field studies in which the dermal exposure to pesticides during spraying operations was measured and found to be greater in most cases than exposure by other routes (Jegier, 1964a(Jegier, , 1964bSimpson, 1965;Simpson and Beck, 1965;Durham, 1965). Kay (1964), reviewing occupational poisoning by industrial and agricultural chemicals in California in 1960, found that percutaneous absorption was recorded as the probable route of entry in nearly 80 % of cases. Furthermore, Gaines (1960) has demonstrated that the incidence of occupational poisoning by various pesticides is more closely related to their acute dermal toxicities in animals than to their acute oral toxicities. Despite these observations, there is not yet any generally accepted method for testing the dermal toxicity of pesticides, and variations in technique between different laboratories often result in very different LD50 values being obtained for the same chemical. In animal tests made to compare hazards from different materials it is essential to know the relative acute oral and acute dermal toxicities on the same species, and to use standard techniques for determining these toxicities. This is particularly important for dermal toxicity since so many factors influence the dermal penetration rate.

No abstract

No clinical toxic effects or loss of condition were seen in any growing hen at any time during a feeding period of 15 weeks on diets containing 10, 50 and 250 p.p.m. of DDT, and no bird developed signs of poisoning during a subsequent partial-starvation period of 3 weeks. There were no differences between the test groups and controls (without DDT) in respect of food consumption or weight gain.A t the end of the 15-week feeding period, DDT, DDE and TDE (DDD) were found in the tissues in amounts roughly proportional to the dosage levels. The largest amounts were found in the fat, with lesser amounts in ovary, liver, muscle, brain and eggs. After three weeks on a reduced intake of control diet, DDT had disappeared from the liver and had slightly decreased in other tissues. There was a general trend towards decrease of TDE and increase of DDE in all tissues, but these changes were occurring very slowly.

Illness or death in a person who has recently used or had access to organophosphate insecticides—some of which are highly poisonous—may present a difficult problem in diagnosis. Post-mortem appearances are likely to be non-specific, and the gastric contents may not be helpful, especially if skin absorption or inhalation was the route of absorption. However, all organophosphate insecticides cause inactivation of the vital enzyme cholinesterase, which is present in the blood and tissues, and for which an accurate biochemical determination is possible. Is this inactivating effect on the enzyme persistent after death, or does the test become useless due to post-mortem changes? The investigation described in this report suggests that for at least one widely-used organophosphate, and probably for many others, the inactivation is persistent long after death, and that diagnosis of the probable cause of death may be possible for weeks afterwards, from the reduced enzyme content of the blood or tissues.