Evidence map›Paper›PMID 27509177›Full record

ArticleOncotarget2016

Smoking, second-hand smoke exposure and smoking cessation in relation to leukocyte telomere length and mortality.

Wahyu Wulaningsih, Fidel Emmanuel C Serrano, Adi Utarini, Tetsuya Matsuguchi, Johnathan Watkins, PILAR Research Network

Abstract read
In one paragraph

Article in Oncotarget, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed, 2 pooled it
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

16 citing papers in PubMed, 2 syntheses or guidelines pooled it.

  1. Pooled it
  2. Pooled it
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  4. Review
  5. Article
  6. Race Differences in Telomere Length in Benign Prostate Biopsies and Subsequent Risk of Prostate Cancer.Cancer epidemiology, biomarkers & prevention : a publication of the American Association for Cancer Research, cosponsored by the American Society of Preventive Oncology · 2022
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  15. Why are there associations between telomere length and behaviour?Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2018
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  16. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

6 authors.

Wahyu WulaningsihDivision of Cancer Studies, King's College London, London, UK.
Fidel Emmanuel C SerranoNational Institute of Molecular Biology and Biotechnology, University of The Philippines Diliman, Diliman, Quezon City, Metro Manila, The Philippines.
Adi UtariniDepartment of Health Policy and Management, Faculty of Medicine, Universitas Gadjah Mada, Yogyakarta, Indonesia.
Tetsuya MatsuguchiDepartment of Biochemistry and Biophysics, University of California, San Francisco, CA, USA.
Johnathan WatkinsPILAR Research and Education, Cambridge, UK.
PILAR Research Network

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

objectivesTo investigate the link between smoking exposure, telomere length and mortality, with emphasis on second-hand smoke (SHS) exposure and the duration of smoking cessation.

resultsA total of 1,018 participants died during follow-up (mean: 10.3 years). A 50 base-pair decrease in LTL was shown among cotinine-confirmed current versus never smokers. The 90th quantile of LTL decreased with increasing cotinine among never smokers, indicating a role of SHS. Longer telomeres with smoking cessation were indicated but limited to a 3-16 year period of abstaining smoking. When assessing mortality, we observed a lower risk of all-cause death for the second quintile compared to the first among never smokers (HR: 0.67, 95% CI: 0.52-0.87), and a higher risk was found among current smokers (HR: 1.89, 1.19-2.92). MATERIALS AND

methodsWe studied 6,456 nationally representative U.S. respondents with mortality follow-up through to 31 December 2011. Smoking status was assessed by interviews and cotinine levels. Relative leukocyte telomere length (LTL) was quantified by polymerase chain reaction (PCR). Multivariable linear regression was performed to examine LTL by smoking exposure, adjusted for age, sex, race/ethnicity, socioeconomic status, education, body mass index, alcohol consumption, and physical activity. We further estimated the association of LTL with cotinine levels using quantile regression, and with smoking cessation dynamics. Cox regression was used to estimate mortality by smoking status and LTL.

conclusionOur findings indicated a complex association between smoking, telomere length, and mortality. LTL alterations with SHS and smoking cessation warrant further investigation for translation to public health measures.

Indexed as

Telomere HomeostasisAdultAgedAged, 80 and overAging, PrematureCigarette SmokingEnvironmental ExposureFemaleFollow-Up StudiesHumansLeukocytesMaleMiddle AgedSmoking CessationSurvival AnalysisTobacco Smoke PollutionTobacco Smoke Pollutionageingsecond-hand smoke exposuresmokingsmoking cessationtelomere

Identifiers

PMID27509177
PMCPMC5312393

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Registered trials

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.