Passive smoking and cognitive impairment

Exposure to secondhand smoke is an established cause of coronary heart disease, lung cancer, and premature death.1 Mounting evidence also links such exposure to airway disease, including asthma, chronic obstructive pulmonary disease, and impaired lung function.2‐4 On the basis of knowledge about these and other serious health effects, North America, Europe, and Australia have introduced smoke‐free legislation. None the less, millions of people are still exposed to secondhand smoke in public places in many parts of the world. Globally, passive smoking is responsible for a substan‐ tial burden of disease, disability, and mortality. In this context, the linked study by Llewellyn and colleagues (doi:10.1136/bmj.b462) adds cognitive impairment to the list of adverse health effects related to secondhand smoke.5 Although the serious negative health effects of expo‐ sure to secondhand smoke are established, we still have much to learn about the full spectrum of effects.1 In particular, we have only just begun to understand how it affects cognitive development and function over the life span. Emerging evidence suggests that parental smoking may impair cognitive development in children.6 Later in life, secondhand smoke may cause cardiovascular disease and stroke, which are themselves linked to cognitive decline.7 8 Until now, however, the suspicion that passive smoking is bad for the adult brain has not been scientifically confirmed. Llewellyn and colleagues found that higher con‐ centrations of salivary cotinine were associated with a significantly greater risk of cognitive impairment after controlling for past smoking history and other poten‐ tial confounding variables.5 They found evidence of an exposure‐response gradient between cotinine con‐ centration and cognitive impairment, which increases the likelihood that the association is a causal one. The study had many important strengths includ‐ ing population based sampling, use of an objective biomarker of secondhand smoke, the definition of cognitive impairment being based on neuropsycho‐ logical testing, and careful control of confounding. The main limitation, which the authors acknowledged, is that salivary cotinine measurement reflects exposure over a short time period (two to three days). Because cognitive impairment develops over many years, the ideal metric to measure exposure would be one that captures cumulative lifetime exposure. Unfortu‐ nately, no existing biomarkers measure exposure to secondhand smoke for longer than several months. Although recent exposure probably correlates with longer term exposure, studies that examine the lon‐ gitudinal effect of self reported lifetime exposure on cognitive impairment would strengthen the evidence of a causal association. Consequently, this study raises the strong possibility that secondhand smoke causes cognitive decline, but further research is needed to establish a causal effect. If secondhand smoke is a known cause of serious disease and shortened life span, why are these lat‐ est findings about its effect on cognitive impairment important? Uncovering a link between passive smok‐ ing and dementia—the most severe form of cognitive impairment—could have important benefits for public health. Dementia has terrible consequences for qual‐ ity of life, is greatly feared, and is not easy to prevent. Consequently, publicising the link between second‐ hand smoke and dementia may resonate powerfully with the public and increase awareness of the harms of passive smoking. Greater public awareness would eventually translate into political action aimed at passing smoke‐free legislation in regions of the world where public smoking is still permitted. Llewellyn and colleagues’ study contains another important public health message, that smokers may also be harmed by passive smoking. Their results strongly suggested that exposure to secondhand smoke was associated with cognitive impairment in former smokers. This observation supports a recent study showing that smokers and non‐smokers had a decreased risk of acute coronary syndrome after Scot‐ land’s smoking ban.9 Moreover, studies of bartend‐ ers, who are exposed to high amounts of secondhand smoke, have found that their respiratory health rap‐ idly improved after their workplaces became smoke free, regardless of whether they were smokers or non‐smokers.10‐12 Taken together, these data challenge the conventional wisdom that the effects of passive smoking are overwhelmed by those of active smoking. They imply that secondhand smoke has deleterious health effects on smokers, and that smokers would also benefit from smoke‐free legislation. We are nearing the close of the first decade of the 21st century. Excitement and optimism have been generated by groundbreaking science aimed at decod‐ ing the human genome and uncovering the molecu‐ lar mechanisms of disease. But millions of people continue to die worldwide from passive smoking. In addition to technologically sophisticated science, we should not forget the “low tech” intervention of clear‐ ing the air we breathe. m Ar k th o m As