HPLC and GC/MS determination of 4-aminobiphenyl haemoglobin adducts in fetuses exposed to the tobacco smoke carcinogen in utero

Pinorini-Godly, Maria T.; Myers, Steven R.

doi:10.1016/0300-483x(95)03263-f

Cited by 31 publications

(16 citation statements)

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“…With the exception of m-toluidine, all other amines have been classi®ed as carcinogens (Sabbioni and Richter 1999). The adduct levels of 4-ABP were in the same concentration range as the levels reported in children from New York (Tang et al 1999) and in adult nonsmokers (Bartsch et al 1990;Bryant et al 1987;Falter et al 1994;Hammond et al 1993, Pinorini-Godly andMyers 1996;Rielmann et al 1995). Adducts from monocyclic aromatic amines have been determined for the ®rst time in children.…”

Section: Discussionsupporting

confidence: 51%

Haemoglobin adducts from aromatic amines in children in relation to area of residence and exposure to environmental tobacco smoke

Richter¹,

Rösler²,

Scherer

et al. 2001

International Archives of Occupational and Environmental Health

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Section: Discussionsupporting

confidence: 51%

Haemoglobin adducts from aromatic amines in children in relation to area of residence and exposure to environmental tobacco smoke

Richter¹,

Rösler²,

Scherer

et al. 2001

International Archives of Occupational and Environmental Health

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“…Many proven carcinogens are present in tobacco and tobacco smoke (Hecht, 1999;Hoffmann and Hoffmann, 1997). Tobacco-related compounds have also been detected in human placenta, fetal blood, urine of offspring and in breast milk of smoking mothers (Perlman and Dannenberg, 1942;Everson et al, 1986Everson et al, , 1988Woodward et al, 1986;Hansen et al, 1992;Myers et al, 1996;Pinorini-Godly and Myers, 1996;Arnould et al, 1997;Daube et al, 1997).Previous case -control studies have tended to show weak associations between maternal cigarette smoking during pregnancy and childhood cancers (IARC, 1986;Severson et al, 1993;Tredaniel et al, 1994;Sorahan et al, 1995Sorahan et al, , 1997a Sorahan et al, , b, 2001Klebanoff et al, 1996;Shu et al, 1996). There is somewhat stronger and more consistent evidence for a paternal preconceptional effect, although relative risks in most case -control studies are only just above one (Severson et al, 1993;Shu et al, 1996;Ji et al, 1997;Sorahan et al, 1997b;.…”

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confidence: 99%

mentioning

confidence: 99%

Parental smoking and childhood cancer: results from the United Kingdom Childhood Cancer Study

2003

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There are strong a priori reasons for considering parental smoking behaviour as a risk factor for childhood cancer but case -control studies have found relative risks of mostly only just above one. To investigate this further, self-reported smoking habits in parents of 3838 children with cancer and 7629 control children included in the United Kingdom Childhood Cancer Study (UKCCS) were analysed. Separate analyses were performed for four major groups (leukaemia, lymphoma, central nervous system tumours and other solid tumours) and more detailed diagnostic subgroups by logistic regression. In the four major groups, after adjustment for parental age and deprivation there were nonsignificant trends of increasing risk with number of cigarettes smoked for paternal preconception smoking and nonsignificant trends of decreasing risk for maternal preconception smoking (all P-values for trend 40.05). Among the diagnostic subgroups, a statistically significant increased risk of developing hepatoblastoma was found in children whose mothers smoked preconceptionally (OR ¼ 2.68, P ¼ 0.02) and strongest (relative to neither parent smoking) for both parents smoking (OR ¼ 4.74, P ¼ 0.003). This could be a chance result arising from multiple subgroup analysis. Statistically significant negative trends were found for maternal smoking during pregnancy for all diagnoses together (Po0.001) and for most individual groups, but there was evidence of under-reporting of smoking by case mothers. In conclusion, the UKCCS does not provide significant evidence that parental smoking is a risk factor for any of the major groups of childhood cancers. There are strong a priori reasons for considering parental smoking behaviour as a risk factor for childhood cancer. Many proven carcinogens are present in tobacco and tobacco smoke (Hecht, 1999;Hoffmann and Hoffmann, 1997). Tobacco-related compounds have also been detected in human placenta, fetal blood, urine of offspring and in breast milk of smoking mothers (Perlman and Dannenberg, 1942;Everson et al, 1986Everson et al, , 1988Woodward et al, 1986;Hansen et al, 1992;Myers et al, 1996;Pinorini-Godly and Myers, 1996;Arnould et al, 1997;Daube et al, 1997).Previous case -control studies have tended to show weak associations between maternal cigarette smoking during pregnancy and childhood cancers (IARC, 1986;Severson et al, 1993;Tredaniel et al, 1994;Sorahan et al, 1995Sorahan et al, , 1997a Sorahan et al, , b, 2001Klebanoff et al, 1996;Shu et al, 1996). There is somewhat stronger and more consistent evidence for a paternal preconceptional effect, although relative risks in most case -control studies are only just above one (Severson et al, 1993;Shu et al, 1996;Ji et al, 1997;Sorahan et al, 1997b;. This effect has been attributed to germ-cell mutations during spermatogenesis caused by tobacco products (Wyrobeck, 1993;Wyrobek and Adler, 1996;Woodall and Ames, 1997). Relevant studies are reviewed by Thornton and Lee (1998).The United Kingdom Childhood Cancer Study (UKCCS) is a nationwide population-based...

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“…Some of the metabolic intermediates known to be produced by phase I xenobiotic metabolism are active oxygen species and DNA or protein binding adducts [Meyer 1996]. While it has been suggested that harmful oxygen species and adducts can interfere with normal fetal development, the role of these compounds in the pathogenesis of clubfoot is unknown [Izzotti et al 2003; Pasanen 1999; Pinorini-Godly and Myers 1996]. Our results suggest that an increase in harmful metabolic intermediates could contribute to abnormal foot development or rotation of the foot.…”

Section: Discussionmentioning

confidence: 83%

Smoking, the xenobiotic pathway, and clubfoot

Sommer¹,

Blanton²,

Weymouth³

et al. 2010

Birth Defects Research

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Idiopathic clubfoot is a common orthopedic birth defect that affects approximately 135,000 newborns worldwide. It is characterized by equinus, varus and adductus deformities of the ankle and foot. While numerous studies suggest a multifactorial etiology, the specific genetic and environmental components have yet to be delineated. Maternal smoking during pregnancy is the only common environmental factor consistently shown to increase the risk for clubfoot. Moreover, a positive family history of clubfoot, in conjunction with maternal smoking, increases the risk twenty-fold. These findings suggest that genetic variation in smoking metabolism (xenobiotic) genes may increase susceptibility to clubfoot. Based on this reasoning, we interrogated eight candidate genes (CYP1A1, CYP1A2, CYP1B1, CYP2A6, EPHX1, NAT2, GSTM1 and GSTT1), chosen based on their involvement in xenobiotic metabolism. Twenty-two SNPs and two null alleles in these genes were genotyped in a dataset composed of nonHispanic white and Hispanic multiplex and simplex families. Only rs1048943/CYP1A1 had significantly altered transmission in the aggregate and multiplex NHW datasets (p=0.003 and p=0.009, respectively). Perturbation of CYP1A1 can cause an increase in harmful, adduct forming metabolic intermediates. A significant interaction between EPHX1 and NAT2 was also found (p=0.007). Importantly, for CYP1A2, significant maternal (p=0.03; RR=1.24; 95% CI: 1.04–1.44) and fetal (p=0.01; RR=1.33; 95% CI: 1.13–1.54) genotypic effects were identified, suggesting that both maternal and fetal genotypes can negatively impact limb development. No association was found between maternal smoking status and variation in xenobiotic metabolism genes. Together, these results suggest that xenobiotic metabolism genes are unlikely to play a major role in clubfoot, however, perturbation of this pathway may still play a contributory role.

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HPLC and GC/MS determination of 4-aminobiphenyl haemoglobin adducts in fetuses exposed to the tobacco smoke carcinogen in utero

Cited by 31 publications

References 10 publications

Haemoglobin adducts from aromatic amines in children in relation to area of residence and exposure to environmental tobacco smoke

Haemoglobin adducts from aromatic amines in children in relation to area of residence and exposure to environmental tobacco smoke

Parental smoking and childhood cancer: results from the United Kingdom Childhood Cancer Study

Smoking, the xenobiotic pathway, and clubfoot

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