title: Low-level environmental tobacco smoke exposure and inflammatory biomarkers in children with asthma.
abstract: OBJECTIVE
  The effects of low-level environmental tobacco smoke (ETS) exposure, on asthma control, lung function and inflammatory biomarkers in children with asthma have not been well studied. The objective of the study was to assess ETS exposure in school-age children with asthma whose parents either deny smoking or only smoke outside the home, and to assess the impact of low-level ETS exposure on asthma control, spirometry and inflammatory biomarkers.
  
  
  METHODS
  Forty patients age 8-18 years with well-controlled, mild-to-moderate persistent asthma treated with either inhaled corticosteroids (ICS) or montelukast were enrolled. Subjects completed an age-appropriate Asthma Control Test and a smoke exposure questionnaire, and exhaled nitric oxide (FeNO), spirometry, urinary cotinine and leukotriene E(4) (LTE(4)) were measured. ETS-exposed and unexposed groups were compared.
  
  
  RESULTS
  Only one parent reported smoking in the home, yet 28 (70%) subjects had urinary cotinine levels ≥1 ng/ml, suggesting ETS exposure. Seven subjects (18%) had FeNO levels >25parts per billion, six of whom were in the ETS-exposed group. In the ICS-treated subjects, but not in the montelukast-treated subjects, ETS exposure was associated with higher urinary LTE(4), p = 0.04, but had no effect on asthma control, forced expiratory volume in 1 s or FeNO.
  
  
  CONCLUSIONS
  A majority of school-age children with persistent asthma may be exposed to ETS, as measured by urinary cotinine, even if their parents insist they don't smoke in the home. Urinary LTE(4) was higher in the ETS-exposed children treated with ICS, but not in children treated with montelukast.
authors.affiliation: Division of Pulmonary & Critical Care and Sleep Medicine, Department of Medicine, Wayne State University , Detroit, MI , USA and.
authors.forename: Ramneet
authors.initials: R
authors.lastname: Gill
authors.forename: Sankaran
authors.initials: S
authors.lastname: Krishnan
authors.forename: A J
authors.initials: AJ
authors.lastname: Dozor
mesh_terms: D000085:Acetates / Q000627:therapeutic use; D000280:Administration, Inhalation; D000293:Adolescent; D000305:Adrenal Cortex Hormones / Q000627:therapeutic use; D018927:Anti-Asthmatic Agents / Q000627:therapeutic use; D001249:Asthma / Q000188:drug therapy / Q000209:etiology / Q000503:physiopathology*; D002648:Child; D015331:Cohort Studies; D003367:Cotinine / Q000652:urine*; D003521:Cyclopropanes; D004784:Environmental Monitoring / Q000379:methods; D005260:Female; D005500:Follow-Up Studies; D006801:Humans; D018836:Inflammation Mediators / Q000032:analysis / Q000378:metabolism*; D017999:Leukotriene E4 / Q000652:urine*; D008297:Male; D011446:Prospective Studies; D011804:Quinolines / Q000627:therapeutic use; D018570:Risk Assessment; D012720:Severity of Illness Index; D013147:Spirometry / Q000379:methods; D013440:Sulfides; D014028:Tobacco Smoke Pollution / Q000009:adverse effects*; D016896:Treatment Outcome
chemical_list: D000085:Acetates; D000305:Adrenal Cortex Hormones; D018927:Anti-Asthmatic Agents; D003521:Cyclopropanes; D018836:Inflammation Mediators; D011804:Quinolines; D013440:Sulfides; D014028:Tobacco Smoke Pollution; D017999:Leukotriene E4; D003367:Cotinine; C093875:montelukast