Previous Finette study on HPRT

The effects of maternal cigarette smoke exposure on somatic mutant frequencies at the hprt locus in healthy newborns.

AUTHOR: Finette BA; Poseno T; Vacek PM; Albertini RJ

AUTHOR AFFILIATION: Department of Pediatrics, University of Vermont, Burlington 05401, USA.

SOURCE: Mutat Res 1997 Jun 9;377(1):115-23

CITATION IDS: PMID: 9219586 UI: 97363261

We utilized the hprt T-cell cloning assay to prospectively determined the somatic mutant frequency at the hprt locus of fetal T-lymphocytes exposed in utero to maternal active and passive cigarette smoke. In addition, a maternal questionnaire was administered to evaluate a number of social and medical parameters that may effect hprt mutant frequency. Newborn cord blood plasma cotinine levels were determined on all subjects to compare in utero tobacco metabolite levels with maternal smoking histories. A total of 63 newborns were enrolled and placed into four groups: Group I (n = 21), newborns whose mothers had no history of active or passive cigarette exposure during the pregnancy; Group II (n = 12), newborns whose mothers actively smoked cigarettes throughout the pregnancy; Group III (n = 8), newborns whose mothers actively smoked cigarettes during first trimester only; and Group IV (n = 22), newborns whose mothers were exposed only to passive cigarette smoke. Our analysis showed no statistically significant difference in hprt mutation frequency between any of the four groups. A significant increase in plasma cord blood cotinine was detected in Group II, newborns whose mothers were active cigarette smokers throughout the pregnancy. Our data indicate that exposure to active and passive maternal cigarette smoke in utero does not result in a significant increase in somatic mutant frequency as determined by the hprt T-cell cloning assay.

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