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Associations of smoking indicators and cotinine levels with telomere length: National Health and Nutrition Examination Survey

The influence of smoking exposure on telomere length with a focus on the impact of race has rarely been discussed. We performed a cross sectional analysis into the associations of smoking indicators with leukocyte telomere length (LTL) by race among 5864 nationally representative sample of US adults...

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Autores principales: Khan, Rumana J., Gebreab, Samson Y., Gaye, Amadou, Crespo, Pia R., Xu, Ruihua, Davis, Sharon K.
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Elsevier 2019
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6536775/
https://www.ncbi.nlm.nih.gov/pubmed/31193582
http://dx.doi.org/10.1016/j.pmedr.2019.100895
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author Khan, Rumana J.
Gebreab, Samson Y.
Gaye, Amadou
Crespo, Pia R.
Xu, Ruihua
Davis, Sharon K.
author_facet Khan, Rumana J.
Gebreab, Samson Y.
Gaye, Amadou
Crespo, Pia R.
Xu, Ruihua
Davis, Sharon K.
author_sort Khan, Rumana J.
collection PubMed
description The influence of smoking exposure on telomere length with a focus on the impact of race has rarely been discussed. We performed a cross sectional analysis into the associations of smoking indicators with leukocyte telomere length (LTL) by race among 5864 nationally representative sample of US adults (≥20 years). Data from 1999 to 2002 National Health and Nutrition Examination Survey was used for the analysis. Smoking indicators were assessed by interviews and serum cotinine levels. LTL was quantified by polymerase chain reaction. Multiple linear regressions were used to assess the association with adjustment for covariates, sample weights and design effects separately for Whites, Blacks and Mexican Americans. The intensity of smoking, measured by the average number of cigarettes consumed per day, was negatively associated with LTL among Whites (β: −3.87, 95% CI: −5.98 to −1.21) and among Blacks (β: −15.46, 95% CI: −29.79 to −2.12) participants. Compared with cotinine level < 0.05 ng/ml, cotinine level ≥3 ng/ml was associated with shorter LTL (β: −77.92, 95% CI = −143.05 to −11.70) among Whites, but not among Blacks. We found increased number of cigarette consumption to be associated with shorter LTL in both Blacks and Whites, indicating that the impact of smoking on life-shortening diseases could partly be explained by telomere biology. Increased cotinine concentration however, was associated with shorter LTL only among Whites, not among Blacks. This differential relationship that we observed may have implications in interpreting cotinine as an objective biomarker of smoking exposure across races and warrant additional prospective investigation.
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spelling pubmed-65367752019-05-30 Associations of smoking indicators and cotinine levels with telomere length: National Health and Nutrition Examination Survey Khan, Rumana J. Gebreab, Samson Y. Gaye, Amadou Crespo, Pia R. Xu, Ruihua Davis, Sharon K. Prev Med Rep Regular Article The influence of smoking exposure on telomere length with a focus on the impact of race has rarely been discussed. We performed a cross sectional analysis into the associations of smoking indicators with leukocyte telomere length (LTL) by race among 5864 nationally representative sample of US adults (≥20 years). Data from 1999 to 2002 National Health and Nutrition Examination Survey was used for the analysis. Smoking indicators were assessed by interviews and serum cotinine levels. LTL was quantified by polymerase chain reaction. Multiple linear regressions were used to assess the association with adjustment for covariates, sample weights and design effects separately for Whites, Blacks and Mexican Americans. The intensity of smoking, measured by the average number of cigarettes consumed per day, was negatively associated with LTL among Whites (β: −3.87, 95% CI: −5.98 to −1.21) and among Blacks (β: −15.46, 95% CI: −29.79 to −2.12) participants. Compared with cotinine level < 0.05 ng/ml, cotinine level ≥3 ng/ml was associated with shorter LTL (β: −77.92, 95% CI = −143.05 to −11.70) among Whites, but not among Blacks. We found increased number of cigarette consumption to be associated with shorter LTL in both Blacks and Whites, indicating that the impact of smoking on life-shortening diseases could partly be explained by telomere biology. Increased cotinine concentration however, was associated with shorter LTL only among Whites, not among Blacks. This differential relationship that we observed may have implications in interpreting cotinine as an objective biomarker of smoking exposure across races and warrant additional prospective investigation. Elsevier 2019-05-17 /pmc/articles/PMC6536775/ /pubmed/31193582 http://dx.doi.org/10.1016/j.pmedr.2019.100895 Text en © 2019 The Authors http://creativecommons.org/licenses/by-nc-nd/4.0/ This is an open access article under the CC BY-NC-ND license (http://creativecommons.org/licenses/by-nc-nd/4.0/).
spellingShingle Regular Article
Khan, Rumana J.
Gebreab, Samson Y.
Gaye, Amadou
Crespo, Pia R.
Xu, Ruihua
Davis, Sharon K.
Associations of smoking indicators and cotinine levels with telomere length: National Health and Nutrition Examination Survey
title Associations of smoking indicators and cotinine levels with telomere length: National Health and Nutrition Examination Survey
title_full Associations of smoking indicators and cotinine levels with telomere length: National Health and Nutrition Examination Survey
title_fullStr Associations of smoking indicators and cotinine levels with telomere length: National Health and Nutrition Examination Survey
title_full_unstemmed Associations of smoking indicators and cotinine levels with telomere length: National Health and Nutrition Examination Survey
title_short Associations of smoking indicators and cotinine levels with telomere length: National Health and Nutrition Examination Survey
title_sort associations of smoking indicators and cotinine levels with telomere length: national health and nutrition examination survey
topic Regular Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6536775/
https://www.ncbi.nlm.nih.gov/pubmed/31193582
http://dx.doi.org/10.1016/j.pmedr.2019.100895
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