Secondary Logo

Institutional members access full text with Ovid®

Share this article on:

Tobacco smoke as a risk factor for meningococcal disease

FISCHER, MARC MD; HEDBERG, KATRINA MD, MPH; CARDOSI, PAUL MD; PLIKAYTIS, BRIAN D. MS; HOESLY, FREDERICK C. MD, MPH; STEINGART, KAREN R. MD, MPH; BELL, THOMAS A. MD,MPH; FLEMING, DAVID W. MD; WENGER, JAY D. MD; PERKINS, BRADLEY A. MD

The Pediatric Infectious Disease Journal: October 1997 - Volume 16 - Issue 10 - p 979-983
Original Studies

Background. Since 1992 the US Pacific Northwest has experienced a substantial increase in the incidence of serogroup B meningococcal disease. The current meningococcal polysaccharide vaccine is poorly immunogenic in young children and does not protect against N. meningitidis serogroup B. Defining alternative approaches to the prevention and control of meningococcal disease is of considerable public health importance.

Methods. We performed a case-control study comparing 129 patients in Oregon and southwest Washington with 274 age- and area-matched controls. We used conditional logistic regression analysis to determine which exposures remained associated with disease after adjusting for other risk factors and confounders and calculated the proportion of disease attributable to modifiable exposures.

Results. After adjustment for all other significant exposures identified, having a mother who smokes was the strongest independent risk factor for invasive meningococcal disease in children <18 years of age [odds ratio (OR), 3.8; 95% confidence interval (CI) 1.6 to 8.9)], with 37% (CI 15 to 65) of all cases in this age group potentially attributable to maternal smoking. Adult patients were more likely than controls to have a chronic underlying illness (OR 10.8, CI 2.7 to 43.3), passive tobacco smoke exposure (OR 2.5, CI 0.9 to 6.9) and to smoke tobacco (OR 2.4, CI 0.9 to 6.6). Dose-response effects were seen for passive smoke exposure and risk of disease in all age groups.

Conclusion. Tobacco smoke exposure independently increases the risk of developing meningococcal disease.

From the Childhood and Respiratory Diseases Branch, Division of Bacterial and Mycotic Diseases, National Center for Infectious Diseases, Centers for Disease Control and Prevention, Atlanta, GA (MF, BDP, JDW, BAP); Oregon Health Division, Portland, OR (KH, PC, FCH, DWF); Southwest Washington Health District, Vancouver, WA (KRS); and Cowlitz County Health Department, Longview, WA (TAB).

Accepted for publication July 11, 1997.

Presented in part at the 10th International Pathogenic Neisseria Conference, Baltimore, MD, September 8 to 13, 1996.

Address for reprints: Bradley A. Perkins, M.D., Meningitis and Special Pathogens Branch, National Center for Infectious Diseases, Centers for Disease Control and Prevention, MS C-09, 1600 Clifton Rd. N.E., Atlanta, GA 30333. Fax 404-639-3970; E-mail bap4@cdc.gov.

© Williams & Wilkins 1997. All Rights Reserved.