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Investigations on the genotoxicity of formaldehyde in human cells in culture: Repair of DNA-protein crosslinks and identification of a 'threshold' dose for carcinogenic activity

Project

Food and consumer protection

This project contributes to the research aim 'Food and consumer protection'. Which funding institutions are active for this aim? What are the sub-aims? Take a look:
Food and consumer protection


Project code: BfR-PRS-02-1329-038
Contract period: 01.06.2007 - 31.12.2008
Purpose of research: Basic research

Formaldehyde (FA) is industrially produced in huge amounts throughout the world (> 20 tons p.a.). This compound is used in a wide range of consumer-related products such as apparel, furniture, cosmetics, tobacco products, disinfectants and so forth. On the other hand, FA is also transiently produced during endogenous metabolism (C1 cycle). Currently, FA is classified by regulatory bodies as a 'possible carcinogen'. In 2004, however, the IARC (WHO) notified that FA shall be considered as a 'human carcinogen'. This re-classification would trigger that all future handling of FA needs to be confined to closed systems/cycles. At the same time, preparations may not contain more than 0.1% of this compound (upper limit). In November 2004 and March 2006, the Federal Institute for Risk Assessment suggested a 'practical threshold value' (0.1 ppm) based on the lowest level of FA necessary for sensory perception by olfactory receptors located in the nose and throat. According to the data available it seems unlikely that exposure to levels below 0.1 ppm would entail any considerable carcinogenic risk. In animal experiments in vivo FA affects the mucous membranes of the nasopharyngeal tract by inducing DNA-protein crosslinks (DPX) and elevated cell proliferation rates. Both mechanisms together might be responsible for the generation of neoplastic tissue. At levels higher than 0.3 ppm FA in the breathing air, the formation of some small amounts of DPX already can be detected. However, levels of > 2 ppm are necessary to induce significant increases in DPX levels and cell proliferation rates. At present there is no clear picture about the role of FA-induced DPX. It is unclear whether they represent a pre-mutagenic lesion itself, how much DPX can be removed by endogenous DNA repair and which DNA repair pathway/factors are involved in fixing DPX damage. Insights into the pathogenetic value of low levels of DPX is the prerequisite, however, to better understand their role in FA-induced carcinogenesis. At the same time it would help to define a threshold value for this partly endogenous compound beneath which any carcinogenic risk can be deemed nearly impossible.

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Subjects

Framework programme

BMEL Frameworkprogramme 2002

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