RELATIONSHIP OF UPPER AIRWAY DISEASE TO TOBACCO SMOKING AND ALLERGIC MARKERS - A COHORT STUDY OF MEN FOLLOWED UP FOR 5 YEARS

Citation
I. Annesimaesano et al., RELATIONSHIP OF UPPER AIRWAY DISEASE TO TOBACCO SMOKING AND ALLERGIC MARKERS - A COHORT STUDY OF MEN FOLLOWED UP FOR 5 YEARS, International archives of allergy and immunology, 114(2), 1997, pp. 193-201
Citations number
33
Categorie Soggetti
Allergy,Immunology
ISSN journal
10182438
Volume
114
Issue
2
Year of publication
1997
Pages
193 - 201
Database
ISI
SICI code
1018-2438(1997)114:2<193:ROUADT>2.0.ZU;2-#
Abstract
Data derived from a cohort study of 191 men, seen 5 years apart, were used to investigate the involvement in allergic as well as in nonaller gic upper airway disease (UAD) of two risk factors, immediate hypersen sitivity and tobacco smoking, the roles of which have been well establ ished in lower airway disease. At both surveys, UAD and smoking habits were assessed by an extended version of the BMRC/ECSC questionnaire. UAD consisted of usual or chronic rhinitis, seasonal allergic rhinitis and perceived nasal hyperresponsiveness (PNHR) to tobacco smoke, cold air or exercise. Immediate hypersensitivity was determined either in vivo (skin prick test, SPT, positivity) or in vitro (total IgE). UAD p revalence and smoking habits did not vary significantly over 5 years. On the contrary, SPT positivity increased significantly between the tw o surveys. At both surveys, SPT positivity for common aeroallergens (g rass pollens overall) was significantly related to seasonal allergic r hinitis but not to usual or chronic rhinitis and to PNHR. Similarly, t he total IgE level was increased in seasonal allergic rhinitis, but ne ver significantly. Current smoking was always a habit significantly mo re frequent in men reporting chronic rhinitis (odds ratios of 5.3 and 4.9 in 1985 and 1990, respectively). The relationship was of the dose- response type: the more the subjects smoked, the more they reported ch ronic rhinitis. In contrast, seasonal allergic rhinitis was more assoc iated with exsmoking, either in 1985 or in 1990. These results were co nfirmed longitudinally and after exclusion of asthmatics. Further inve stigations are needed to support the hypothesis raised by our data acc ording to which immediate hypersensitivity, as assessed by SPT positiv ity for common aeroallergens, and tobacco smoking might intervene alte rnatively in UAD, probably because of the 'healthy smoker effect'.