A new study published in the British Medical Journal (BMJ) concludes that secondhand smoke exposure is associated with decreased cognitive function among middle-age adults (see: Llewellyn DJ et al. Exposure to secondhand smoke and cognitive impairment in nonsmokers: national cross sectional study with cotinine measurement. BMJ 2009; 338:b462).
The manuscript reports the results of a cross-sectional study which correlates saliva cotinine levels and cognitive function scores on a battery of neuropsychological tests among a sample of 4809 adults ages 50 and older in the Health Survey for England and English Longitudinal Study of Ageing. Cognitive impairment was defined as performance in the lowest 10% of combined scores on the neuropsychological tests. The primary result of the study was that adults in the highest quartile of cotinine exposure were significantly more likely to have cognitive impairment.
The variables controlled for in the study included "age, sex, ethnicity, education (highest educational qualification), manual occupational class, fourths of net non-housing wealth (measured in pounds sterling), smoking history (never smokers, former smokers who stopped smoking less than 10 years ago, former smokers who stopped smoking 10 years or more ago), obesity (body mass index >29.9), alcohol consumption (g/day), physical inactivity (participating in sport or physical activity less than once a month), and depressive symptoms (more than three symptoms on the eight item version of the Center for Epidemiological Studies depression scale)."
The results of the study are summarized as follows: "Compared with the lowest fourth of cotinine concentration (0.0-0.1 ng/ml) the odds ratios (95% confidence intervals) for cognitive impairment in the second (0.2-0.3 ng/ml), third (0.4-0.7 ng/ml), and highest fourths (0.8-13.5 ng/ml) were 1.08 (0.78 to 1.48), 1.13 (0.81 to 1.56), and 1.44 (1.07 to 1.94; P for trend 0.02), after adjustment for a wide range of established risk factors for cognitive impairment. A similar pattern of associations was observed for never smokers and former smokers."
The article concludes: "our results provide new evidence to suggest that exposure to secondhand smoke may be associated with increased odds of cognitive impairment."
The newspaper coverage of the study reported that secondhand smoke is linked to dementia. For example, the headline of one article read: "Secondhand Smoke Linked to Dementia: Exposure May Increase Risk by 44%, Researchers Say." In this article, a study author is quoted as stating: "There is an association between cognitive function, which is often but not necessarily a precursor of dementia, and exposure to passive smoking. ... We know that active smoking is bad -- being a smoker is bad for your health and increases your risk of Alzheimer's. This study suggests that this is the same for passive smoking."
Also according to this article: "Maria Carrillo, director of medical and scientific relations for the Alzheimer's Association, said this study offers more evidence of the dangers of secondhand smoke and the risk for dementia. Smoking is already recognized as a risk factor for Alzheimer's, and the risk can be extended to exposure to secondhand smoke, she said. 'There are findings that secondhand smoke can be just as detrimental as smoking itself.'"
In another article, a study author was quoted as stating: "Our results suggest that inhaling other people's smoke may damage the brain, impair cognitive functions, such as memory, and make dementia more likely."
The Rest of the Story
The findings of this study are provocative, but in a cross-sectional study such as this one, they should not be viewed as conclusive. The problem is that people at the highest quartile of secondhand smoke exposure are very different in a number of ways from people at the lowest quartile of exposure and there are reasonable alternative explanations for why that subsample might be expected to have lower levels of cognitive function on neuropsychological tests.
Among the differences that one would expect between groups at the highest and lowest levels of secondhand smoke exposure that were not adequately controlled for in the study are baseline levels of cognitive function, parental smoking, parental education, social class, and marijuana and other drug use. It could be reasonably hypothesized that those with higher exposure to secondhand smoke are more likely to have had poorer baseline cognitive function, greater exposure to parental smoking, lower levels of parental education, lower social class, and increased drug use - all of which could serve as alternative explanations for the lower cognitive function observed in this cross-sectional study.
To derive conclusive evidence of a causal link between secondhand smoke and reduced cognitive function, one would have to conduct a longitudinal study, in which decreases in cognitive function over time were shown to occur among individuals with higher secondhand smoke exposure.
The problem here is not the study itself, but the way the researchers appear to have communicated their findings to the media. It appears that they gave the media a very strong impression that their study had concluded that secondhand smoke is a cause of cognitive dysfunction and dementia, when it really just identified an association which needs to be assessed in further studies - especially longitudinal ones.
In addition, it appears that the media were given the impression that these data suggest a link between secondhand smoke and dementia. But dementia was not studied at all - the link is between secondhand smoke and lower levels of cognitive function, which may have no relation at all to the risk of developing dementia.
The Alzheimer's Association also appears to have taken the finding too far, having concluded that there is a causal link between secondhand smoke and Alzheimer's disease.