Passive smoke and dementia
“Inhaling second-hand smoke could increase the risk of developing dementia,” The Daily Telegraph has reported, saying new research has found that non-smokers with higher levels of a smoking-related chemical in their saliva were at “44% greater risk of early memory problems”. The Daily Mail has claimed that the same group had a 44% increased risk of developing Alzheimer’s disease.
It is already established that smokers are at greater risk of dementia, but the study in question is the first to consider the effects of passive smoking. Researchers looked at data on over 5,000 non-smokers aged over 50 and measured their levels of cotinine, which is produced when the body breaks down nicotine. They found higher cotinine levels were associated with poorer cognitive ability.
It should be noted that the study assessed degree of cognitive impairment, not a diagnosis of dementia, or in particular the Alzheimer’s disease suggested by the Daily Mail. A diagnosis of Alzheimer’s requires that specific medical criteria be met.
While the design of this study means it cannot prove that passive smoking has caused individuals to have poorer cognitive ability, it does have many strengths and will undoubtedly lead to more research into this highly significant area of public health.
Where did the story come from?
This research was conducted by Dr David Llewellyn and colleagues from the University of Cambridge, the Institute of Public Health, Cambridge, Peninsula Medical School, Exeter, the University of Michigan and the Veterans Affairs Center for Practice Management and Outcomes Research, Michigan.
The research was funded by the US National Institute on Aging and some departments of the UK government. Some of the researchers are supported by grants from academic, charity and government departments across the US and the UK. The study was published in the peer-reviewed_ British Medical Journal._
What kind of scientific study was this?
This was a cross-sectional study describing the association between exposure to second-hand smoke and cognitive impairment in people aged 50 and above.
This study used data from people who had participated in the 1998, 1999 and 2001 waves of the Health Survey for England (HSE) as well as the English Longitudinal Study of Ageing. The HSE is an annual survey of a random sample of people living in England. The English Longitudinal Study of Ageing draws on those participating in the HSE, but only includes adults who were aged over 50 years in 2002.
Through the HSE, saliva samples were collected from 73% of participants in 1998, 70% in 2001 and 8% in 1999. Levels of the chemical cotinine in the saliva are a good indicator of recent exposure to second-hand smoke. Cotinine is made in the body when nicotine is metabolised. The researchers used the data available on those non-smokers who had saliva samples available, a total of 4,809 people.
Cognitive impairment had been assessed in the English Longitudinal Study of Ageing using tests that determined attention, memory, numeracy, verbal fluency and processing speed, and through questionnaires. Cognitive impairment was defined as the lowest 10% of overall scores.
The researchers used statistical analysis methods to determine whether there was any relationship between passive smoking and cognitive impairment. They took into account other factors that may have been affecting cognitive health including age, sex, ethnicity, occupation, education, smoking history, obesity, alcohol consumption, physical activity and depression.
In another analysis, they also looked at the effects of medical conditions believed to be associated with smoke inhalation (diabetes, cardiovascular disease, stroke, high blood pressure). Those who were former smokers and those who had never smoked were analysed separately.
What were the results of the study?
The study found that people with high levels of salivary cotinine were 1.44 times more likely to be cognitively impaired (95% CI 1.07 to 1.94) than those who were exposed to little or no second-hand smoke.
The authors say there was some evidence that increasing doses of exposure meant an increased risk of cognitive impairment.
When they looked at former smokers and those who had never smoked separately, they found that the effect of smoking exposure was greater in these never-smokers, who were 1.7 times more likely to be cognitively impaired if they had high salivary cotinine compared with people with no exposure. Former smokers were 1.32 times more likely to be cognitively impaired, though this result was not statistically significant.
What interpretations did the researchers draw from these results?
Researchers conclude that high levels of salivary cotinine in non-smoking adults may be associated with increased risk of cognitive impairment.
What does the NHS Knowledge Service make of this study?
This cross-sectional analysis of population-level data was well conducted, and is representative of the English population.
The researchers have made adjustments to account for non-response in order to ensure that their results can be generalised to the population in England. The researchers have also taken into account a large number of factors that may be linked to cognitive impairment, and, when adjusting for these factors, found the relationship between high salivary cotinine and cognitive impairment remains.
It is important to note that this study assessed degree of cognitive impairment, not a diagnosis of dementia. In particular, this study does not identify a link between passive smoking and Alzheimer’s disease (as incorrectly headlined by the Daily Mail ). Alzheimer’s is a specific diagnosis characterised by impairments of memory, recognition (of people, objects and places), normal daily functioning and language, and requires that no other cause for the dementia can be identified.
As this was a cross-sectional study it cannot prove causation (that exposure to second-hand smoke caused any observed cognitive impairment). The primary reason for this is that there is no way of knowing whether exposure to second-hand smoke preceded or followed development of cognitive impairment.
This is a particularly relevant issue as this study used cotinine levels as a marker of exposure to second-hand smoke. This is only useful for measuring the participants’ recent exposure to tobacco smoke, as cotinine only stays in the body for about a week. The accompanying editorial article, and indeed the researchers themselves, raise this as a problem of the study.
However, while causation cannot be established through this particular study, the association in question has important public health implications, and a finding of this type warrants further investigation. Studies will need to do more to establish whether this is a causal link, or whether there are other factors linked to both second-hand smoke and cognitive impairment that should be the focus of interventions.
