AAN: Second-hand Smoke Can Add to Dementia Risk

BOSTON, May 1 -- Long-term exposure to second-hand smoke may be a risk factor for dementia in the presence of subclinical carotid artery disease, said investigators here.

In a subset of patients in the Cardiovascular Health Study, those who had a subclinical carotid stenosis and lived with a smoker for 30 years or more had a 2.5-fold greater risk for dementia than those free of cigarette smoke exposure, found statistician Thaddeus Haight, M.A., of the University of California at Berkeley.

In contrast, second-hand smoke exposure in the absence of carotid disease was not a significant risk factor for dementia, reported Haight at the American Academy of Neurology meeting

The findings did not meet the test of statistical significance, but pointed to second-hand or passive smoking as a possible additive risk factor for dementia.

"It's actually quite plausible that second-hand smoke, given its effects on the cardiovascular system, can affect the risk of dementia indirectly through the clinical cardiovascular disease pathway," he said. "But what's less well known is whether there are actually direct effects that may be neurotoxic effects with respect to people's cerebral functioning, and the neurotoxic effects of second-hand smoke with respect to some neurodegenerative process."

It's also not known whether passive smoking has an effect on dementia through subclinical processes, he said.

He and colleagues looked at cumulative exposure to second-hand smoke among 985 men and women who were never active smokers. There were 728 women and 257 men from the ages of 66 to 92 years, most of them in the 70- to 74-year age range.

The participants had no previous history of cardiovascular disease (myocardial infarction, angioplasty, angina pectoris, coronary artery bypass, claudication, stroke and/or transient ischemic attack), and had no prior diagnosis of dementia.

There were indications in some patients, however, of subclinical cerebrovascular disease, measured by initimal thickness of cerebral vessels on MRI, and on carotid ultrasound findings, Haight said.

Of these patients, 495 reported second-hand smoke exposure, defined as living fulltime with a smoker, for a mean 27.9 years, range one to 80 years. Some 50% of the patients had no second-hand smoke exposure, 25% had low exposure, defined as one to 30 years of living with a smoker, and 25% had high second-hand smoke exposure (more than 30 years cohabitation with a smoker).

The authors used marginal structural Cox proportional hazards models to calculate the causal relative hazard of clinical cardiovascular disease with respect to dementia over seven years.

They examined the effects within strata of age, age-adjusted SHS, and separately for cerebral vascular disease (infarct less than 3 mm, infarct 3mm or greater, or white grade matter disease) and carotid artery disease (25% or greater stenosis, or more than 80 percentile common or internal wall thickness).

During the study, 10% of the patients developed clinical cardiovascular disease, and 15% developed dementia.

"What we found was that second-hand smoke in and of itself did not independently contribute to incidence of dementia," Haight said. "But what we did see was that among those people with subclinical cardiovascular disease, based on carotid artery ultrasound, that there was in fact some suggestion of an interaction in the group with the highest levels of second-hand smoke exposure and abnormal carotid ultrasound findings, and incident dementia."

The relative hazard for dementia was 2.5 among those patients with subclinical cardiovascular disease and at least three decades of exposure to someone else's smoke, and 1.5 for those with cardiovascular risk factors but lower exposure (one to 30 years), compared with patients with no subclinical disease and no second-hand smoke exposure.

The associations between second hand smoke and dementia did not, however, meet the statistical significance level of P