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“Introduction The chlorinated hydrocarbons dieldrin and aldrin were widely used as pesticides in agriculture from the 1950s up to the early 1970s (WHO
1989). Later, their use became more and more restricted to specific applications, such as termite control. They were withdrawn from the market for almost all uses in the USA in 1974 and subsequently in other countries. In 1987, production ceased in the last remaining dieldrin and aldrin producing plant at the Royal Dutch/Shell refinery in Pernis, The Netherlands (de Jong 1991). Dieldrin and aldrin are readily absorbed following inhalation, ingestion or skin contact. In the occupational setting, the latter is thought to be the most important route of exposure. After uptake, find more aldrin Prostatic acid phosphatase is rapidly converted to dieldrin, mainly by the P-450 system in the liver. Dieldrin can be stored in adipose tissue Since 1962, results from animal studies (Davis and Fitzhugh 1962) have spurred concerns that dieldrin and aldrin may be human carcinogens as well. The EPA published a report on the assessment of the human cancer risk of dieldrin and aldrin in 1987 (EPA 1987). In this report, dieldrin and aldrin were classified
as probable human carcinogens. This classification was mainly based on evidence of hepatocarcinogenesis in mice. The International Agency for Research on Cancer classified the evidence for carcinogenicity in humans as inadequate and animal carcinogenicity as limited (IARC 1987). However, since the EPA assessment of human cancer risk, there is accumulating evidence which has called into question the value of mouse liver tumors as a reliable predictor of carcinogenic potential in humans. Dieldrin-induced oxidative stress or its sequelae apparently buy NVP-BEZ235 result in modulation of gene expression that favors expansion of initiated mouse, but not rat, liver cells; thus, dieldrin acts as a nongenotoxic promoter/accelerator of background liver tumorigenesis in the mouse (Stevenson et al. 1999). Recent animal studies provide a possible explanation for the specific mouse hepatocarcinogenity of aldrin/dieldrin (Stevenson et al. 1999, 1995; Kolaja et al. 1996). More recently, Kamendulis et al.