Secondhand Smoke Raises Stroke Risk

Pauline Anderson

July 13, 2015

Exposure to secondhand smoke (SHS) raises the risk for stroke by about 30%, which is independent of demographic characteristics, socioeconomic factors, smoking history, Framingham Stroke risk factors, and C-reactive protein (CRP) concentration, new research showed.

These findings "add to the body of evidence supporting stricter smoking regulations," said the authors, who noted that SHS is concerning as 18% of the US adult population smokes.

The study, led by Angela Malek, PhD, Department of Public Health Sciences, Medical University of South Carolina, Charleston, was published online June 16 in the American Journal of Preventive Medicine.

The overall stroke analysis included 21,743 participants in the Reasons for Geographic and Racial Differences in Stroke (REGARDS) study, a national, population-based longitudinal study investigating cardiovascular disease and mortality among white and African American adults aged 45 years and older.

Current smokers were excluded from the analysis. SHS exposure was assessed by duration and frequency. Exposure to SHS was defined as more than 1 hour per week in close contact with a smoker (anything less was deemed as not exposed).

Almost a quarter (23%) of study participants reported SHS exposure in the past year and 77% reported no SHS exposure. Those reporting exposure were significantly younger and more likely to be white, to be female, and to have lower education levels than those without exposure.

History of cardiovascular disease, atrial fibrillation, left ventricular hypertrophy, Framingham Stroke Risk Score, and region of residence (Stroke Belt vs non–Stroke Belt) did not differ significantly between the exposed and nonexposed groups.

Of the 5081 participants reporting SHS exposure, 53% were former smokers. About 44% of those without SHS exposure were former smokers.

During an average follow-up of 5.6 years, there were 428 stroke events: 352 ischemic strokes, 50 hemorrhagic strokes, and 26 strokes of unknown subtype.

In unadjusted models, the risk for stroke did not differ significantly between those exposed to SHS and those without exposure. However, after adjustment for demographic and socioeconomic status (SES) covariates, SHS exposure was associated with increased risk for stroke (hazard ratio [HR], 1.31; 95% confidence interval [CI], 1.03 - 1.65) among nonsmoking participants.

Further adjustment did not change the HRs meaningfully, although after adjustment for lifestyle factors, statistical significance was lost.

The stroke subtype analyses included 21,717 participants. After adjustment for demographic and SES covariates, the HR for ischemic stroke was 1.29 (95% CI, 1.00 - 1.68).

There was no association between SHS exposure and hemorrhagic stroke.

Although these findings are consistent with results of some previous studies, other research did not find associations between SHS exposure and stroke. According to the authors, earlier studies were limited in that they were prospective, varied in adjustment for potential confounders, had inconsistent definitions of stroke and SHS exposure, had differing measurement and sources of SHS exposure, used inconsistent assessment of stroke subtypes, and were underpowered by inadequate sample size.

Limitations of the current study are that it lacked cotinine measures to validate SHS exposure and used self-reports to classify prevalent stroke and transient ischemic attack. In addition, statistical power to examine the risk for SHS exposure by stroke subtype may have been limited. The null findings for an association between exposure and hemorrhagic stroke may be due to the small numbers of such strokes.

The authors have disclosed no relevant financial relationships.

Am J Prev Med. Published online June 16, 2015. Abstract

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