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In the general population, such exposures are likely to be a consequence of the lifestyle choices of the parents, with exposure to tobacco smoke one of the most pervasive and easily documented. Previous studies attempting to establish a direct link between active smoking and levels of somatic mutation have largely discounted the effects of passive or secondary exposure, and have produced contradictory results.<\/jats:p><\/jats:sec><jats:sec><jats:title>Methods<\/jats:title><jats:p>Data from three studies of possible smoking effects on<jats:italic>in utero<\/jats:italic>mutagenesis at the<jats:italic>HPRT<\/jats:italic>locus were compiled and reanalyzed, alone and in combination. Where possible, passive exposure to environmental tobacco smoke was considered as a separate category of exposure, rather than being included in the non-smoking controls. Molecular spectra from these studies were reanalyzed after adjustment for reported mutation frequencies from the individual studies and the entire data set.<\/jats:p><\/jats:sec><jats:sec><jats:title>Results<\/jats:title><jats:p>A series of related studies on mutation at the X-linked<jats:italic>HPRT<\/jats:italic>locus in human newborn cord blood samples has led to the novel conclusion that only passive maternal exposure to tobacco mutagens has a significant effect on the developing baby. We performed a pooled analysis of the complete data from these studies, at the levels of both induced mutation frequency and the resulting mutational spectrum.<\/jats:p><\/jats:sec><jats:sec><jats:title>Conclusion<\/jats:title><jats:p>Our analysis reveals a more commonsensical, yet no less cautionary result: both active maternal smoking and secondary maternal exposure produce quantitatively and qualitatively indistinguishable increases in fetal<jats:italic>HPRT<\/jats:italic>mutation. Further, it appears that this effect is not perceptibly ameliorated if the mother adjusts her behavior (<jats:italic>i.e<\/jats:italic>. stops smoking) when pregnancy is confirmed, although this conclusion may also be affected by continued passive exposure.<\/jats:p><\/jats:sec>","DOI":"10.1186\/1471-2431-5-20","type":"journal-article","created":{"date-parts":[[2005,6,29]],"date-time":"2005-06-29T18:13:49Z","timestamp":1120068829000},"update-policy":"http:\/\/dx.doi.org\/10.1007\/springer_crossmark_policy","source":"Crossref","is-referenced-by-count":16,"title":["Qualitatively and quantitatively similar effects of active and passive maternal tobacco smoke exposure on in utero mutagenesis at the HPRT locus"],"prefix":"10.1186","volume":"5","author":[{"given":"Stephen G","family":"Grant","sequence":"first","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"297","published-online":{"date-parts":[[2005,6,29]]},"reference":[{"key":"73_CR1","doi-asserted-by":"publisher","first-page":"1979","DOI":"10.1093\/carcin\/23.12.1979","volume":"23","author":"DH Phillips","year":"2002","unstructured":"Phillips DH: Smoking-related DNA and protein adducts in human tissues. 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