title: Lower FEV1 in non-COPD, nonasthmatic subjects: association with smoking, annual decline in FEV1, total IgE levels, and TSLP genotypes.
abstract: Few studies have investigated the significance of decreased FEV(1) in non-COPD, nonasthmatic healthy subjects. We hypothesized that a lower FEV(1) in these subjects is a potential marker of an increased susceptibility to obstructive lung disease such as asthma and COPD. This was a cross-sectional analysis of 1505 Japanese adults. We divided the population of healthy adults with no respiratory diseases whose FEV(1)/FVC ratio was ≥ 70% (n = 1369) into 2 groups according to their prebronchodilator FEV(1) (% predicted) measurements: < 80% (n = 217) and ≥ 80% (n = 1152). We compared clinical data - including gender, age, smoking habits, total IgE levels, and annual decline of FEV(1) - between these 2 groups. In addition, as our group recently found that TSLP variants are associated with asthma and reduced lung function, we assessed whether TSLP single nucleotide polymorphisms (SNPs) were associated with baseline lung function in non-COPD, nonasthmatic healthy subjects (n = 1368). Although about half of the subjects with lower FEV(1) had never smoked, smoking was the main risk factor for the decreased FEV(1) in non-COPD, nonasthmatic subjects. However, the subjects with lower FEV(1) had a significantly higher annual decline in FEV(1) independent of smoking status. Airflow obstruction was associated with increased levels of total serum IgE (P = 0.029) and with 2 functional TSLP SNPs (corrected P = 0.027-0.058 for FEV(1)% predicted, corrected P = 0.015-0.033 for FEV(1)/FVC). This study highlights the importance of early recognition of a decreased FEV(1) in healthy subjects without evident pulmonary diseases because it predicts a rapid decline in FEV(1) irrespective of smoking status. Our series of studies identified TSLP variants as a potential susceptibility locus to asthma and to lower lung function in non-COPD, nonasthmatic healthy subjects, which may support the contention that genetic determinants of lung function influence susceptibility to asthma.
authors.affiliation: Division of Respiratory Medicine, Institute of Clinical Medicine, University of Tsukuba, Ibaraki, Japan.
authors.forename: Hironori
authors.initials: H
authors.lastname: Masuko
authors.forename: Tohru
authors.initials: T
authors.lastname: Sakamoto
authors.forename: Yoshiko
authors.initials: Y
authors.lastname: Kaneko
authors.forename: Hiroaki
authors.initials: H
authors.lastname: Iijima
authors.forename: Takashi
authors.initials: T
authors.lastname: Naito
authors.forename: Emiko
authors.initials: E
authors.lastname: Noguchi
authors.forename: Tomomitsu
authors.initials: T
authors.lastname: Hirota
authors.forename: Mayumi
authors.initials: M
authors.lastname: Tamari
authors.forename: Nobuyuki
authors.initials: N
authors.lastname: Hizawa
mesh_terms: D000328:Adult; D000368:Aged; D001249:Asthma / Q000209:etiology* / Q000235:genetics / Q000276:immunology / Q000503:physiopathology; D016009:Chi-Square Distribution; D003430:Cross-Sectional Studies; D016207:Cytokines / Q000235:genetics*; D005541:Forced Expiratory Volume; D005838:Genotype; D006801:Humans; D007073:Immunoglobulin E / Q000097:blood*; D007564:Japan; D016014:Linear Models; D008168:Lung / Q000503:physiopathology*; D008875:Middle Aged; D010641:Phenotype; D020641:Polymorphism, Single Nucleotide; D029424:Pulmonary Disease, Chronic Obstructive / Q000209:etiology* / Q000235:genetics / Q000276:immunology / Q000503:physiopathology; D012189:Retrospective Studies; D018570:Risk Assessment; D012307:Risk Factors; D012907:Smoking / Q000009:adverse effects* / Q000235:genetics / Q000276:immunology / Q000503:physiopathology; D013997:Time Factors; D014797:Vital Capacity; D055815:Young Adult; D000094632:Thymic Stromal Lymphopoietin
chemical_list: D016207:Cytokines; D007073:Immunoglobulin E; D000094632:Thymic Stromal Lymphopoietin