Determination of nicotine absorption from multiple tobacco products and nicotine gum.

Introduction: Snus is a smokeless tobacco product traditionally used in Scandinavia and available in pouched or loose forms. The objective of this study was to determine nicotine absorption for current pouched and loose snus products in comparison with a cigarette and an over-the-counter nicotine gum.

Methods: We conducted an open-label, randomized, 6-way, crossover study involving 20 healthy snus and cigarette users.

Smoking intensity before and after introduction of the public place smoking ban in Scotland.

A study was performed to determine whether cigarettes were smoked more intensely outside of public venues in Scotland, compared to indoors, after introduction of the public place smoking (PPS) ban. It was conducted in three waves: before the ban, immediately after and 6 months after introduction. The study included 322 regular smokers of four cigarette brand variants.

Cigarette smoke total particulate matter increases mucous secreting cell numbers in vitro: a potential model of goblet cell hyperplasia.

Cigarette smoking is associated with chronic obstructive pulmonary disease (COPD)--a term encompassing chronic lung inflammation, chronic bronchitis and emphysema. Goblet cell hyperplasia is a characteristic feature of the lung epithelium in COPD patients contributing to the overproduction of airway mucus, including mucin MUC5AC. Using an in vitro model of differentiated lung epithelium we have investigated morphological and cellular changes in response to interleukin (IL)-13 (2.

Patterns and behaviors of snus consumption in Sweden.

Introduction: Snus is an oral snuff consisting of moist finely ground tobacco which is available in a loose form or with portions of the tobacco sealed in small sachets termed "pouches." The product has a long history of use in Sweden. Currently, there is very little published information on levels of consumption and usage behaviors for snus in Sweden.

Agents associated with lung inflammation induce similar responses in NCI-H292 lung epithelial cells.

The aim of this study was to investigate an in vitro lung epithelial model for assessment of potential inhalation toxicity. The selected NCI-H292 lung carcinoma cell line is sensitive to cigarette smoke, responds in a similar manner to primary human lung epithelial cells and produces airway mucins. The following agents associated with inhalation toxicity were tested in the model: cigarette smoke total particulate matter, fly ash, bleomycin, lipopolysaccharide, vanadyl sulphate, diesel exhaust particles and carbon black.

Human bronchial epithelial cell transcriptome: gene expression changes following acute exposure to whole cigarette smoke in vitro.

Cigarette smoke is a complex mixture of more than 4,000 constituents. Its effects on cell biology are poorly understood, partly because whole smoke exposure in vitro is technically challenging. To investigate the effects of smoke on cell signaling and function, a three-dimensional air-liquid interface model of tracheobronchial epithelium, grown from primary human lung epithelial cells, was exposed to air or whole mainstream cigarette smoke for 1 h in a purpose-designed chamber.

Expression of genes involved in oxidative stress responses in airway epithelial cells of smokers with chronic obstructive pulmonary disease.

Rationale: The molecular mechanisms involved in airway oxidative stress responses reported in healthy smokers and in those with chronic obstructive pulmonary disease (COPD) are poorly understood.

Objectives: To assess the expression of genes involved in oxidative stress responses in the bronchial epithelium of smokers with or without COPD and in relation to disease severity.

Methods: Global gene expression was assessed in bronchial brushings in 38 subjects with COPD, 14 healthy nonsmokers, and 18 healthy smokers.

Exposure of bronchial epithelial cells to whole cigarette smoke: assessment of cellular responses.

Cigarette smoke is composed of approximately 5% particulate phase and 95% vapour phase by weight. However, routine in vitro toxicological testing of smoke normally only measures the activity of the particulate phase. This study describes a new system for exposing cells at an air-liquid interface to serial dilutions of gaseous smoke.

Increased expression of p21(waf) cyclin-dependent kinase inhibitor in asthmatic bronchial epithelium.

Because the asthmatic bronchial epithelium is characterized by widespread damage, we postulated that this is associated with expression of cell cycle inhibitors that control proliferation. Using bronchial biopsies, the epithelium was the major site of expression of the cyclin-dependent kinase inhibitor, p21(waf). Immunostaining usually occurred in the cytoplasm of columnar cells; however, in severe asthma, nuclear staining was also evident in the proliferative, basal cell compartment.

Asthmatic bronchial epithelium is more susceptible to oxidant-induced apoptosis.

Abnormal apoptotic mechanisms are associated with disease pathogenesis. Because the asthmatic bronchial epithelium is characteristically damaged with loss of columnar epithelial cells, we postulated that this is due to unscheduled apoptosis. Using an antibody directed toward the caspase cleavage product of poly(ADP-ribose) polymerase, immunohistochemistry applied to endobronchial biopsies showed higher levels of staining in the bronchial epithelium of subjects with asthma as compared with normal control subjects (% epithelial staining [median (range) = 10.

Autocrine ligands for the epidermal growth factor receptor mediate interleukin-8 release from bronchial epithelial cells in response to cigarette smoke.

Airway neutrophilia is a prominent feature of chronic obstructive pulmonary disease. As cigarette smoke (CS) and epidermal growth factor (EGF) both cause release of interleukin-8 (IL-8) from epithelial cells in vitro, we investigated whether autocrine ligands for the EGF receptor (EGFR) are involved in this proinflammatory response to CS. NCI-H292 or primary bronchial epithelial cells were cultured with or without cigarette smoke extract (CSE) or EGF for 6-48 h.

Cooperative effects of Th2 cytokines and allergen on normal and asthmatic bronchial epithelial cells.

In sensitized individuals, exposure to allergens such as Dermatophagoides pteronyssinus (Der p) causes Th2 polarization and release of cytokines, including IL-4 and IL-13. Because Der p extracts also have direct effects on epithelial cells, we hypothesized that allergen augments the effects of Th2 cytokines by promoting mediator release from the bronchial epithelium in allergic asthma. To test our hypothesis, primary bronchial epithelial cultures were grown from bronchial brushings of normal and atopic asthmatic subjects.