Rationale: Identification of the subpopulation especially susceptible to the adverse effects of second-hand smoke exposure (SHS) would be useful for preventive actions and interventions.
Objectives: To investigate whether asthmatic heredity indicates susceptibility to the effects of SHS on the risk of adult-onset asthma.
Methods: A population-based incident case-control study of clinically defined adult-onset asthma and randomly drawn control subjects (adults 21-63 yr old) from a geographically defined area in South Finland. After excluding current and ex-smokers there were 226 cases and 450 disease-free control subjects.
Measurements And Main Results: Our outcome measure was new adult-onset asthma. Parental asthma and recent SHS had a synergistic effect on the risk of asthma, the adjusted odds ratio being 1.97 (95% confidence interval, 1.12-3.45) for SHS; 2.64 (1.65-4.24) for parental asthma; and 12.69 (3.44-46.91) for their joint effect (relative excess risk due interaction, 9.08 [-0.22 to 43.18]). Synergistic effect followed a dose-dependent pattern with both recent and cumulative SHS exposures, with relative excess risk due interaction for parental asthma and over 100 SHS cigarette-years of 6.17 (0.57-19.16).
Conclusions: This is the first study showing that individuals with asthmatic heredity have a considerably increased risk of adult-onset asthma when exposed to SHS. SHS exposure has dose-dependent synergism with family history of asthma, the joint effect being stronger with higher exposure levels. Avoiding SHS could be an important preventive measure for reducing the risk of adult-onset asthma among those with asthmatic heredity. Asking about family history of asthma is a useful tool for identifying these susceptible individuals in clinical and preventive settings.
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http://dx.doi.org/10.1164/rccm.201304-0773OC | DOI Listing |
Int Forum Allergy Rhinol
January 2025
Center of Excellence in Otolaryngology-Head & Neck Surgery, Rajavithi Hospital, Bangkok, Thailand.
Introduction: Tissue eosinophil counts (TEC) might serve as a biomarker linking chronic rhinosinusitis (CRS) and the presence of adult-onset asthma. This study aimed to determine if TEC in sinus mucosa/polyps in CRS patients is an independent indicator of asthma and to identify its optimal cut-off point.
Methods: This cross-sectional study was conducted on primary CRS patients scheduled for surgery.
Osteoporos Int
December 2024
Liaoning University of Traditional Chinese Medicine, Shenyang, Liaoning, China.
Clin Transl Allergy
December 2024
Department of Internal Medicine and Clinical Nutrition, Krefting Research Centre, Institute of Medicine, Sahlgrenska Academy, University of Gothenburg, Gothenburg, Sweden.
Although asthma is more frequently diagnosed in childhood, a substantial proportion of cases manifests in adulthood. Nonetheless, few studies have comprehensively examined asthma incidence across different ages, genders, and asthma phenotypes. We conducted a retrospective evaluation of asthma incidence from birth to late adulthood, stratified by age, gender, and the presence or absence of allergies.
View Article and Find Full Text PDFJ Asthma
December 2024
Faculty of Medicine and Health Technology, Tampere University, Tampere, Finland.
Physical exercise in treatment of asthma is scarcely studied with no clear exercise guidelines for asthmatics. We aimed to investigate the associations between physical exercise frequency, systemic inflammation and asthma control. This has not been previously studied in adult-onset asthma.
View Article and Find Full Text PDFFront Immunol
December 2024
The Liggins Institute, The University of Auckland, Auckland, New Zealand.
Introduction: Asthma is a heterogeneous condition that is characterized by reversible airway obstruction. Childhood-onset asthma (COA) and adult-onset asthma (AOA) are two prominent asthma subtypes, each with unique etiological factors and prognosis, which suggests the existence of both shared and distinct risk factors.
Methods: Here, we employed a two-sample Mendelian randomization analysis to elucidate the causal association between genes within lung and whole-blood-specific gene regulatory networks (GRNs) and the development of unspecified asthma, COA, and AOA using the Wald ratio method.
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