Evidence map›Paper›PMID 33542031›Full record

ArticleJournal of epidemiology and community health2021

Biomarker-assessed passive smoking in relation to cause-specific mortality: pooled data from 12 prospective cohort studies comprising 36 584 individuals.

Elisabeth Kvaavik, Aage Tverdal, G David Batty

Abstract read
In one paragraph

Article in Journal of epidemiology and community health, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
–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

2 citing papers in PubMed.

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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

3 authors.

Elisabeth KvaavikDepartment of Alcohol, Tobacco and Drugs, Norwegian Institute of Public Health, Oslo, Norway Elisabeth.Kvaavik@fhi.no.ORCID 0000-0003-4570-0265
Aage TverdalNorwegian Institute of Public Health, Oslo, Norway.ORCID 0000-0002-2909-5678
G David BattyDepartment of Epidemiology and Public Health, University College London, London, UK.ORCID 0000-0003-1822-5753

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

aimsWhile investigators have typically quantified the health risk of passive (secondhand) smoking by using self-reported data, these are liable to measurement error. By pooling data across studies, we examined the prospective relation of a biochemical assessment of passive smoking, salivary cotinine, with mortality from a range of causes.

methodsWe combined data from 12 cohort studies from England and Scotland initiated between 1998 and 2008. A total of 36 584 men and women aged 16-85 years of age reported that they were non-smoking at baseline, provided baseline salivary cotinine and consented to mortality record linkage.

resultsA mean of 8.1 years of mortality follow-up of 36 584 non-smokers (16 792 men and 19 792 women) gave rise to 2367 deaths (775 from cardiovascular disease, 779 from all cancers and 289 from smoking-related cancers). After controlling for a range of covariates, a 10 ng/mL increase in salivary cotinine was related to an elevated risk of total (HRs; 95% CI) (1.46; 1.16 to 1.83), cardiovascular disease (1.41; 0.96 to 2.09), cancer (1.49; 1.00 to 2.22) and smoking-related cancer mortality (2.92; 1.77 to 4.83).

conclusionsAssessed biomedically, passive smoking was a risk factor for a range of health outcomes known to be causally linked to active smoking.

Indexed as

Tobacco Smoke PollutionBiomarkersCause of DeathCotinineFemaleHumansMaleProspective StudiesBiomarkersCotinineTobacco Smoke Pollutionmeasurementmortalitypassive smoking

Identifiers

PMID33542031
PMCPMC8292572

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