IN March, the Campaign for Safe Cosmetics reported finding formaldehyde and 1,4-dioxane, a trace contaminant of some chemicals used in cosmetics, detergents and shampoos, in 55 children's personal-care products.
However, the model performed well for established LRI factors, suggesting that the findings for formaldehyde exposure were likewise valid.
Of interest, Zhang et al. (2010) equate their reported findings with formaldehyde as being similar to those produced by benzene or therapy-related AML.
These results additionally support the finding that formaldehyde inhibits fungal PCR.
Among the hypothetical causes of these findings was exposure to formaldehyde, a toxic, irritant and possibly carcinogenic substance.
Measurements of height and width of nuclei (Fig. 5c) revealed a slight swelling upon formaldehyde fixation, in agreement with earlier findings (Solovei et al. 2002).
Recent reports of no exogenously derived CD2-formaldehyde-DNA adducts in the bone marrow or lymphocytes (Lu et al., 2010a; Moeller et al., 2011) also challenges the likelihood that formaldehyde was the cause of the findings reported by Zhang et al. (2010).
The animal studies generally reported neither hematotoxicity nor leukemia associated with formaldehyde exposure, and although a few human study findings are consistent with hematotoxicity, they are inconsistent with other study findings and plagued by possible confounding.
More recently, a National Academy of Sciences report summarized the available controlled clinical studies evaluating the irritant effects of formaldehyde in asthmatic and non-asthmatic individuals, finding no differences in sensitivity between the two groups (NAS/NRC, 2007).
Despite these findings, three modes of action for formaldehyde leukemogenesis have been hypothesized by Zhang (2009, 2010a) and are also discussed in US EPA's recent draft toxicological profile for formaldehyde (US EPA, 2010).
