Consequences of Exposure to Carcinogens Beginning During Developmental Life

Cesare Maltoni Cancer Research Center, European Ramazzini Foundation of Oncology and Environmental Sciences, Bologna, Italy.
Basic & Clinical Pharmacology & Toxicology (Impact Factor: 2.38). 03/2008; 102(2):118-24. DOI: 10.1111/j.1742-7843.2007.00200.x
Source: PubMed


The increased incidence of cancer over the last 50-60 years may be largely attributed to two factors: the ageing of the population and the diffusion of agents and situations presenting carcinogenic risks. Today, we have entered into a new era in which populations are ever-increasingly exposed to diffuse carcinogenic risks, present not only in the occupational, but also in the general environment. We must now also consider an additional factor in the carcinogenic process, that is, the age in which exposure to carcinogenic risks begins. Apart from the paradigmatic cases of diethylstilboestrol and ionizing radiation, the available epidemiological data concerning the adult consequences of developmental exposure to carcinogens is very limited. However, important data have been provided by long-term experimental carcinogenicity bioassays conducted using rodents. This paper reports a selection of studies conducted in the laboratories of the Cesare Maltoni Cancer Research Center of the European Ramazzini Foundation in which exposure to the chemical agents vinyl acetate monomer, ethyl alcohol and aspartame was started during developmental life and continued into adulthood. The results of these studies provide supporting evidence that lifespan exposure to carcinogenic agents beginning during developmental life produces an overall increase in the carcinogenic effects observed. Moreover, when comparing prenatal and postnatal exposure, the data demonstrate that the development of cancers may appear earlier in life.

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    • "However, the safety of their long-term ingestion, especially when starting from early development throughout life, has been questioned by a considerable number of studies [21] [22] [23] [24] [25]. Due to this, we aimed to review the available information about the impact of NNS exposure during the perigestational period on the later in life offspring's risk of developing diseases (in particular metabolic diseases), and to discuss the mechanisms involved in the potential fetal programming effects of NNS. "
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    • "Responses to some of these criticisms have already been provided in a number of our earlier works [Soffritti et al., 2007, 2008, 2010]. "
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