Maternal Nrf2 and gluthathione-S-transferase polymorphisms do not modify associations of prenatal tobacco smoke exposure with asthma and lung function in school-aged children
Maternal Nrf2 and gluthathione-S-transferase polymorphisms do not modify associations of prenatal tobacco smoke exposure with asthma and lung function in school-aged children
Background: Maternal smoking during pregnancy has detrimental effects on the respiratory health of infants and children. Polymorphisms of antioxidant genes including glutathione-S-transferases (GSTs) have been proposed as candidates for asthma and reduced lung function in children.
Methods: Women enrolled in the Avon Longitudinal Study of Parents and Children reported smoking habits during pregnancy. Asthma status in their children was established at age 7.5 years from parental reports and lung function was measured by spirometry at age 8.5 years. Maternal and child DNA were genotyped for deletions of GSTM1 and GSTT1 and functional polymorphisms of GSTP1 and Nrf2 genes. Associations of prenatal tobacco smoke exposure with asthma and lung function in children were stratified by maternal genotype.
Results: In 6606 children, maternal smoking during pregnancy was negatively associated with maximal mid expiratory flow (FEF25-75) (?0.05 SD units, 95% CI ?0.07 to ?0.03, p<0.001). There was little evidence for interactions between maternal smoking and any maternal genotype considered on children's asthma or lung function. Maternal smoking was associated with reduced childhood FEF25-75 only in mother-child pairs (n=1227) with both copies of GSTM1 deleted (?0.08 SD units, 95% CI ?0.14 to ?0.02, p=0.01) or (n=2313) at least one copy of GSTT1 present (?0.05 SD units, 95% CI ?0.09 to 0, p=0.03).
Conclusion: This study confirms a detrimental effect of intrauterine tobacco smoke exposure on childhood lung function but no strong evidence of modification by maternal genotype for important antioxidant genes. Adverse effects of fetal exposure to tobacco smoke on the respiratory health of children may be mediated by pathways other than oxidative stress.
897-902
Henderson, A.J.
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Newson, R.B.
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Rose-Zerilli, M.
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Ring, S.M.
5e4d0ad4-a323-40d0-8164-371041a3bd3e
Holloway, J.W.
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Shaheen, S.O.
ae8e3194-c8a7-4f38-a71f-32da3ad0ea21
October 2010
Henderson, A.J.
fed528f9-ccf9-4aca-85b8-e6d7da9cc8c3
Newson, R.B.
9c74a68e-2716-49cc-88bb-5f64312d6c13
Rose-Zerilli, M.
08b3afa4-dbc2-4c0d-a852-2a9f33431199
Ring, S.M.
5e4d0ad4-a323-40d0-8164-371041a3bd3e
Holloway, J.W.
4bbd77e6-c095-445d-a36b-a50a72f6fe1a
Shaheen, S.O.
ae8e3194-c8a7-4f38-a71f-32da3ad0ea21
Henderson, A.J., Newson, R.B., Rose-Zerilli, M., Ring, S.M., Holloway, J.W. and Shaheen, S.O.
(2010)
Maternal Nrf2 and gluthathione-S-transferase polymorphisms do not modify associations of prenatal tobacco smoke exposure with asthma and lung function in school-aged children.
Thorax, 65 (10), .
(doi:10.1136/thx.2009.125856).
Abstract
Background: Maternal smoking during pregnancy has detrimental effects on the respiratory health of infants and children. Polymorphisms of antioxidant genes including glutathione-S-transferases (GSTs) have been proposed as candidates for asthma and reduced lung function in children.
Methods: Women enrolled in the Avon Longitudinal Study of Parents and Children reported smoking habits during pregnancy. Asthma status in their children was established at age 7.5 years from parental reports and lung function was measured by spirometry at age 8.5 years. Maternal and child DNA were genotyped for deletions of GSTM1 and GSTT1 and functional polymorphisms of GSTP1 and Nrf2 genes. Associations of prenatal tobacco smoke exposure with asthma and lung function in children were stratified by maternal genotype.
Results: In 6606 children, maternal smoking during pregnancy was negatively associated with maximal mid expiratory flow (FEF25-75) (?0.05 SD units, 95% CI ?0.07 to ?0.03, p<0.001). There was little evidence for interactions between maternal smoking and any maternal genotype considered on children's asthma or lung function. Maternal smoking was associated with reduced childhood FEF25-75 only in mother-child pairs (n=1227) with both copies of GSTM1 deleted (?0.08 SD units, 95% CI ?0.14 to ?0.02, p=0.01) or (n=2313) at least one copy of GSTT1 present (?0.05 SD units, 95% CI ?0.09 to 0, p=0.03).
Conclusion: This study confirms a detrimental effect of intrauterine tobacco smoke exposure on childhood lung function but no strong evidence of modification by maternal genotype for important antioxidant genes. Adverse effects of fetal exposure to tobacco smoke on the respiratory health of children may be mediated by pathways other than oxidative stress.
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Accepted/In Press date: 30 August 2010
Published date: October 2010
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Local EPrints ID: 163053
URI: http://eprints.soton.ac.uk/id/eprint/163053
ISSN: 0040-6376
PURE UUID: 14a5d1d1-1840-4085-a386-8b738a8ca10f
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Date deposited: 02 Sep 2010 13:44
Last modified: 14 Mar 2024 02:56
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Author:
A.J. Henderson
Author:
R.B. Newson
Author:
S.M. Ring
Author:
S.O. Shaheen
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