Second hand smoke and COPD : : lessons from animal studies / / topic editors, Adelheid Kratzer, Laima Taraseviciene-Stewart and Michael Borchers.

• Author: Laima Taraseviciene-Stewart
• TeilnehmendeR: Kratzer, Adelheid,; Taraseviciene-Stewart, Laima,; Borchers, Michael,
• Place / Publishing House: [Lausanne, Switzerland] : : Frontiers Media SA,, 2014.
• Year of Publication: 2015; 2014
• Language: English
• Series: Frontiers Research Topics,
• Physical Description: 1 online resource (91 pages).
• Bibliography: Includes bibliographical references.
• ISSN: 1664-8714
• Hierarchical level: Monograph
• Statement of Responsibility: topic editors, Adelheid Kratzer, Laima Taraseviciene-Stewart and Michael Borchers.

Cigarette smoke exposure is the key initiator of chronic inflammation, alveolar destruction, and the loss of alveolar blood vessels that lead to the development of chronic obstructive pulmonary disease (COPD) which is comprised of emphysema and chronic bronchitis. Exposure to secondhand smoke (SHS) is the major risk factor for non-smokers to develop emphysema. While the first-hand smoke is directly inhaled by smokers, passive smoking occurs when non-smokers are involuntary exposed to environmental tobacco smoke also known as second hand smoke (SHS). SHS is a mixture of 2 forms of smoke that come from burning tobacco: side stream smoke (smoke that comes from the end of a lit cigarette, pipe, or cigar) and mainstream smoke (smoke that is exhaled by a smoker). These two types of smoke have basically the same composition, however in SHS many toxic components are more concentrated than in first-hand smoke, therefore more hazardous for people’s health. Several pathological events have been implicated in the development of SHS-induced COPD, but many aspects of this pathology remain poorly understood halting the development of new advanced treatments for this detrimental disease. In this respect we have welcomed leading investigators in the field to share their research findings and provide their thoughts regarding the mechanisms of the SHS exposure-induced immune responses and inflammatory mechanisms of lung destruction in SHS-induced COPD and related comorbidities.