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Passive Smoking and Lung Disease Workup

  • Author: Timothy D Murphy, MD; Chief Editor: Girish D Sharma, MD, FCCP, FAAP  more...
 
Updated: Jun 07, 2016
 

Laboratory Studies

See the list below:

  • The diagnosis of passive smoking exposure (secondhand smoke) is primarily obtained by history.
  • Urinary cotinine levels have limitations and widely vary between individuals. As many as 50% of nonsmokers may show urinary cotinine, demonstrating the ubiquity of the exposure.
    • Levels are generally low and are less than 1% of those found in smokers.
    • Cotinine is a biomarker of environmental tobacco smoke (ETS) exposure but may not be related to the adverse effect under study.
    • Cotinine may not be specific for ETS exposure because dietary nicotine (eg, eggplant, green pepper, tea, tomato) may elevate cotinine levels.
    • Salivary or serum levels may also be measured.
  • Outside of a clinical history, questionnaires are the most common method to attempt to quantitate ETS exposure, but these can be limited by a lack of understanding of the questionnaire, bias, faulty memory, or intentional alteration of answers.
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Other Tests

See the list below:

  • Measuring hair cotinine levels in children exposed to ETS may prove a more sensitive biomarker of exposure.
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Histologic Findings

Kim et al investigated the relationship between exposure to secondhand smoke and lung cancer by histologic type on the basis of pooled data from 18 case-control studies in the International Lung Cancer Consortium.[13] Their data included those for 2,504 never-smoker case patients and 7,276 never-smoker control individuals; and 10,184 ever-smoker case patients and 7,176 ever-smoker control individuals. The researchers used multivariable logistic regression, adjusted for age, sex, race/ethnicity, smoking status, and pack-years of smoking. Among never-smokers, the odds ratios (ORs) comparing those ever exposed to secondhand smoke with those never exposed were 1.31 for all histologic types combined, 1.26 for adenocarcinoma, 1.41 for squamous cell carcinoma, 1.48 for large-cell lung cancer, and 3.09 for small-cell lung cancer. The estimated association with secondhand smoke exposure was greater for small-cell lung cancer than for non–small-cell lung cancers (OR, 2.11). The investigators concluded that the association with secondhand smoke is stronger for small-cell lung cancer than for cancers of other histologic types.[13]

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Contributor Information and Disclosures
Author

Timothy D Murphy, MD Consulting and Attending Staff, Pediatric Pulmonary and Sleep Medicine, Mary Bridge Children's Hospital

Timothy D Murphy, MD is a member of the following medical societies: American Thoracic Society, American Academy of Sleep Medicine

Disclosure: Nothing to disclose.

Specialty Editor Board

Mary L Windle, PharmD Adjunct Associate Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Nothing to disclose.

Chief Editor

Girish D Sharma, MD, FCCP, FAAP Professor of Pediatrics, Rush Medical College; Director, Section of Pediatric Pulmonology and Rush Cystic Fibrosis Center, Rush Children's Hospital, Rush University Medical Center

Girish D Sharma, MD, FCCP, FAAP is a member of the following medical societies: American Academy of Pediatrics, American College of Chest Physicians, American Thoracic Society, Royal College of Physicians of Ireland

Disclosure: Nothing to disclose.

Acknowledgements

Heidi Connolly, MD Associate Professor of Pediatrics and Psychiatry, University of Rochester School of Medicine and Dentistry; Director, Pediatric Sleep Medicine Services, Strong Sleep Disorders Center

Heidi Connolly, MD is a member of the following medical societies: American Academy of Pediatrics, American Thoracic Society, and Society of Critical Care Medicine

Disclosure: Nothing to disclose.

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