Etiological factors and mechanism involved in relationships between pesticide exposure and cancer.
Professional as well as public exposure to pesticides raise cancer risk. Interaction with adjuvants and with other toxicants increases the actual risk. Endocrine disruption, procarcinogen activation by detoxification enzymes and intercellular communication impairment are involved in the carcinogenic processes. Organochlorine pesticides, including DDT, persist in human tissues for years, with correlated breast cancer incidence. One major point usually underestimated in risk evaluation is the individual variability in detoxification capabilities. Furthermore cellular sites of cancerisation are not necessarily identical to sites primarily exposed to toxicants. Post-diagnostic stress factors and iatrogenic effects of treatment concur to complication of the status of patients. The abnormal increase in the rates of cancer emergence denotes a failure in the application of the precautionary action principle.
Bounias
M
M
INRA-DSPE and University of Avignon, I.H.S., Unite de Biomathèmatique et Toxicologie, Domaine de Sagne-Soulier, F-07470 Le Lac d'Issarles, France.
D003577:Cytochrome P-450 Enzyme System / Q000235:genetics / Q000494:pharmacology; D020022:Genetic Predisposition to Disease; D005982:Glutathione Transferase; D006801:Humans; D009369:Neoplasms / Q000139:chemically induced*; D016273:Occupational Exposure; D010575:Pesticides / Q000506:poisoning*; D011110:Polymorphism, Genetic; D018570:Risk Assessment
D010575:Pesticides; D003577:Cytochrome P-450 Enzyme System; D005982:Glutathione Transferase