To the Editor:
It is well documented that passive exposure to tobacco smoke (secondhand smoking) is a risk factor for cardiovascular disease.1 Plausible mechanisms include plaque formation on the arterial wall resulting in decreased blood flow.2 This disease process, plus other deleterious consequences of passive smoking—impaired lung and cognitive function3—may have implications for additional health outcomes, including physical capacity. In older adults, lower levels of indicators of physical capacity—walking speed, balance, and grip strength—appear to be linked to direct smoking,4 but the impact of passive smoking, particularly when quantified objectively, has, to our knowledge, yet to be examined longitudinally.
The English Longitudinal Study of Ageing (ELSA) is an ongoing, open, prospective cohort study of a representative sample of men and women who were aged ≥ 50 years at baseline (2002-2003) when living in private households in England.5 Ethical approval for data collection was provided by the London Multicentre Research Ethics Committee. Study members had earlier participated in data collection in the Health Survey for England6 (1998, 1999, 2001), from which they had been sampled, when salivary cotinine (ng/ml), a biomarker for recent exposure to secondhand smoke, was analyzed using a rapid liquid chromatography technique (hp5890; Hewlett Packard, Palo Alto, CA). With a rapid liquid chromatography technique. A total of 6511 participants (3369 women) had data on salivary cotinine. In order to focus on study members whose only exposure to cigarette smoke was apparently passive, we excluded from analyses 2,170 people who were self-declared current smokers plus 232 so-called deceivers who claimed to be ex-smokers or nonsmokers but had salivary cotinine concentrations that belied this status
At each of the six waves of data collection in ELSA, in their home respondents aged 60 years and over were asked to walk a distance of 8 feet (2.4 m) and back; speed was then calculated. During alternative waves, grip strength (kg) was assessed during six trials (three per hand) using a hand-held dynamometer with the average of the maximum value on each hand used in our analyses.
Lower body strength was based on the capacity to rise from a chair with arms across the chest to a full standing position on five occasions for persons
years (10 occasions for persons < 70 years). We evaluated static balance in three separate and progressively more difficult tests: in a feet side-by-side stand for 10 seconds (side-by-side stand); a preferred heel and toe side-by-side stand (semi-tandem) for 10 seconds; and a preferred heel in front of toe stand (full tandem) for 10 seconds if aged
years (30 seconds if aged < 70 years). Failure on each test was denoted by an inability to fully complete the protocol. Covariates were captured using standard protocols.
A greater exposure to passive smoking, as indexed by a higher salivary cotinine level, was associated with a lower performance on tests of both gait speed and grip strength (Table). These modest effects were seen at all waves of data collection. People with higher levels of salivary cotinine were also somewhat more likely to fail to complete the balance and chair rise tests. When we modeled trajectories in each of the four physical function measures, however, there was no consistent association with cotinine. With the inevitable loss to follow-up, we tested if data imputation had an impact on our positive results for gait speed, an outcome which had the greatest degree of missing data. The same pattern of association remained.
Our main finding was that, in nonsmokers, cotinine levels were modestly inversely related to performance on several tests of physical capacity. While our cotinine biomarker has the advantage of capturing all forms of exposure to passive smoking, some of which may be missed by self-report, a limitation is that its short half-life may mean it has less utility as an indicator of longer term patterns.
The English Longitudinal Study of Ageing was developed by a team of researchers based at University College London, the Institute for Fiscal Studies and the National Centre for Social Research, United Kingdom. Funding has been provided by the U.S. National Institute on Aging, and a consortium of U.K. government departments coordinated by the Economic and Social Research Council. G.D.B. is supported by the U.K. Medical Research Council and the U.S. National Institute on Aging.
G. David Batty, DSc
Paola Zaninotto, PhD
Department of Epidemiology & Public
University College London
London, United Kingdom
1. Batty GD, Gale CR, Jefferis B, et alPassive smoking assessed by salivary cotinine and self-report in relation to cause-specific mortality: 17-year follow-up of study participants in the UK Health and Lifestyle Survey. J Epidemiol Community Health. 2014;68:1200–1203.
2. Barnoya J, Glantz SACardiovascular effects of secondhand smoke: nearly as large as smoking. Circulation. 2005;111:2684–2698.
3. Llewellyn DJ, Lang IA, Langa KM, et alExposure to secondhand smoke and cognitive impairment in non-smokers: national cross sectional study with cotinine measurement. BMJ. 2009;338:b462.
4. North TL, Palmer TM, Lewis SJ, et alEffect of smoking on physical and cognitive capability in later life: a multicohort study using observational and genetic approaches. BMJ Open. 2015;5:e008393.
5. Steptoe A, Breeze E, Banks J, et alCohort profile: the English longitudinal study of ageing. Int J Epidemiol. 2013;42:1640–1648.
6. Mindell J, Biddulph JP, Hirani V, et alCohort profile: the health survey for England. Int J Epidemiol. 2012;41:1585–1593.