The nose has an important role in filtering, warming, and humidifying inspired air before inhalation into the lungs. The nose also provides a resistance to both inspiration and expiration that is twice that of the open mouth. This increased resistance appears to have a number of physiological benefits. In a study of arterial oxygen levels (PaO₂) before and after jaw wiring, which forced patients to breathe continuously through their noses, PaO₂ increased by nearly 10 % (Swift et al. 1988). Nasal packing after nasal surgery forcing patients to breathe through their mouths is associated with a reduction in arterial O₂ saturation (Ogretmenoglu et al. 2002). At rest, end-tidal CO₂ levels in expired air, which are considered to be a reliable indirect measure of CO₂ levels in the arterial blood, increase with nasal breathing indicating that nasal breathing improves the efficiency of CO₂ excretion from the lungs (Tanaka et al. 1988). During exercise, nasal breathing reduces the fraction of expired oxygen (F_EO₂), indicating that on expiration the percentage of O₂ extracted from the air by the lungs is increased, and increases the fraction of expired carbon dioxide (F_ECO₂), indicating an increase in the percentage of expired air that is CO₂ (Morton et al. 1995). This equates to more efficient O₂ extraction and CO₂ excretion during exercise.

Explanations for these observations still remain largely hypothetical. Nasal breathing increases total lung volume (Swift et al. 1988). The corresponding increase in functional residual capacity (volume of air present in the lungs present after passive expiration) is thought to improve gas exchange leading to improved PaO₂. NO derived from the nose and sinuses might also improve ventilation-perfusion relationships in the lungs (Della Rocca and Coccia 2005). The nose also provides an inspiratory resistance forcing the diaphragm to contract against a resistance. On a long-term basis, this might also have an important role in maintaining diaphragmatic muscle strength, although the role of inspiratory muscle training in a range of lung diseases continues to be debated (Padula and Yeaw 2007; Gosselink et al. 2011). Regardless, nasal breathing appears important in aiding O₂ absorption and in facilitating CO₂ excretion in the lungs.

The breathing cycle is divided into inspiratory and expiratory phases. When the respiratory rate increases, the expiratory phase shortens. Nasal breathing slows the respiratory rate increasing the length of the expiratory phase (Ayoub et al. 1997). Increasing the expiratory phase of the respiratory cycle is known to increase the body’s relaxation response (Cappo and Holmes 1984). A number of ancient disciplines, such as yoga and tai chi, emphasize the importance of nasal breathing in relaxation and meditation.

Upper and lower airway inflammatory processes often coexist and share common pathogenic mechanisms (Selimoglu 2005; Hare et al. 2010; Marple 2010). Based on the predominant cell type, chronic rhinosinusitis (CRS) has been classified as being either eosinophilic or neutrophilic (Meltzer and Hamilos 2011). The eosinophilic group includes CRS with polyps, a subset of CRS without polyps, aspirin hypersensitivity, asthma and nasal polyps (Samter’s triad), and allergic fungal rhinosinusitis. Eosinophilic CRS and allergic rhinitis are associated with asthma (Marple 2010). Lower airway inflammation has also been classified according to the cell profile of induced sputum as being either eosinophilic or non-eosinophilic (Hargreave 2007). In asthma patients, eosinophils are the dominant inflammatory cells in middle meatal lavage (Ragab et al. 2005). In small airway disease patients, neutrophils are the dominant inflammatory cells in middle meatal lavage (Ragab et al. 2005).

Asthma and allergic rhinitis are strongly interrelated (Corren 1997; Krouse et al. 2007; Marple 2010). Corren reported nasal symptoms in 78 % of asthmatic patients and that 38 % of allergic and nonallergic rhinitis patients have asthma (Corren 1997). The severity of asthma symptoms correlates closely with rhinitis symptoms (Krouse et al. 2007). The presence of allergic rhinitis also increases the risk of subsequent asthma development nearly fourfold (Shaaban et al. 2008).

Asthma has also been associated with CRS. The prevalence of asthma is 20 % in CRS patients, which is higher than that seen in the general population (Jani and Hamilos 2005). Asthma severity also correlates with CRS disease severity, as determined by computed tomography (Bresciani et al. 2001). In patients having functional endoscopic sinus surgery, the asthma prevalence is 42 %, rising to 50 % in those with nasal polyps (Senior et al. 1999).

Neutrophilic inflammation is a feature of both chronic obstructive pulmonary disease (COPD) and bronchiectasis (Hargreave 2007). While tissue eosinophilia is an established feature of asthma, a neutrophilic picture can also be seen (Hargreave 2007). In COPD patients, inflammatory cells are found both in the sputum and in lung biopsy specimens (Hurst 2009). COPD patients commonly report nasal symptoms, the most common of which is rhinorrhea (Hurst et al. 2006). Nasal symptoms are also more common in COPD patients with chronic sputum production (Hurst et al. 2006). Nasal symptoms double the risk over 8 years of patients developing COPD (Nihlén et al. 2008). Increased levels of the neutrophil chemoattractant protein IL-8 are found in the upper airways of COPD patients, when compared to control subjects (Hurst et al. 2006). Upper airway IL-8 concentrations correlate with those in the lower airway, and the concentration at both sites is related to indexes of bacterial colonization (Hurst et al. 2006). Many bronchiectatic patients also have nasal and sinus disease. Most bronchiectasis patients (77 %) meet the diagnostic criteria for CRS with 25 % of bronchiectasis patients having nasal polyps. Bronchiectasis severity also correlates with CRS severity (Guilemany et al. 2009).

Nasobronchial reflexes have also been implicated in the interactions between the upper and lower respiratory airways. Mechanical or chemical stimulation of nasal, tracheal, and laryngeal receptors could produce sneezing, coughing, or bronchoconstriction, thus preventing deeper penetration of allergens or irritants into the airway (Sarin et al. 2006). Unilateral models of nasal provocation show that secretory responses can be measured in both nostrils (Sarin et al. 2006). The mechanism appears to be neural (Sarin et al. 2006).

When asthmatic patients exercise with their noses occluded, a 20 % decline in forced expiratory flow occurs, compared with less than a 5 % reduction among patients allowed to exercise while nose breathing (Shturman-Ellstein et al. 1978). Recent research has shown that bursts of cold air on the nasal mucosa increase nasal resistance. This effect was blocked by anesthetizing the nose or by inhaling atropine, an anticholinergic drug, before the provocation (Fontanari et al. 1996, 1997). Other researchers have not been able to confirm these results (Johansson et al. 2000). The existence of nasobronchial reflexes secondary to inflammatory exposure in the upper respiratory airway remains controversial (Sarin et al. 2006).

Evolutionary theory teaches that in primitive life forms, the olfactory brain was probably a layer of cells above the brain stem that registered a smell and then simply categorized it. New layers of the olfactory brain then developed into what was initially called the rhinencephalon (nose brain) or limbic system (Le Doux 2003). Our limbic system coordinates the stress “fight or flight” response. As part of this response, not only does the heart rate increase, but the respiratory rate also goes up; the limbic system is able to override normal pCO₂ homeostasis (Plum 1992). The physiological evidence suggests that fragrances such as rosemary and lavender may have direct effects on human memory and mood (Herz 2009). Fragrances such as lavender by influencing the limbic system and the stress response could potentially affect breathing patterns and rate. The pheromone androstadienone when applied to women’s nasovomerine organs slowed both their heart and breathing rates (Grosser et al. 2000).