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Inhalation therapy has an ancient history and has been recognized as the most effective and safe way of delivering pharmaceutical compounds directly to the airways for the treatment of respiratory diseases. Nowadays, a great variety of devices exist; nebulizers, soft mist inhalers (SMIs), pressurized Metered Dose Inhalers (pMDIs) and single-or multi-dose Dry Powder Inhalers (DPIs). The choice for the optimal device is patient-specific and depends on the advantages and disadvantages of each device category, and the patients' age and capacity to use them correctly. Factors that determine therapeutic success, apart from the previously mentioned, are: the physician-patient relationship, the patient's opinion, willingness, and preferences for certain medical devices, and proper training on device use. Various sources of evidence indicate that frequent change of devices is associated with treatment failure and should be avoided in order to achieve good therapeutic outcomes. The most frequently used types of inhalation devices for management of chronic and acute obstructive respiratory diseases are the pMDIs. Despite having some environmental footprint and requiring a good technique by the users to achieve reliable therapeutic effects, these devices are essential tools for primary care physicians and pulmonologists. In the COVID-19 era, and despite diametrically opposed opinions on the appropriateness of using nebulizers, most experts recommend against their use in order to reduce the potential risk of spreading the SARS-CoV-2 virus. If required, most experts recommend the use of pMDI via a spacer, except for life threatening exacerbations. The ongoing research, to improve the underlying technologies of these devices, introduce environmentally friendlier propellants and combine these devices with modern applications of telemedicine and artificial intelligence, creates new pathways for the continuous utilization of these inhalation devices in everyday clinical practice.

INTRODUCTION Tobacco use in any form leads to mortality and morbidity of millions of people every year, not only tobacco users but also non-users by inhaling secondhand tobacco smoke. The objective of this study was to assess predictors of cigarette and shisha use in urban and urban slum communities in Accra, Ghana. METHODS A cross-sectional study design was employed, using a quantitative data collection technique over two months, May to June 2017. Logistic regression was used to study the association between demographic characteristics of respondents and cigarette/shisha use, and data were analyzed in STATA.

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BACKGROUND: Several aspects of the inflammatory response to a single insult, i.e., exposure to 2 ppm of ozone (O(3)) for 3 h or 6 h, are less pronounced in surfactant protein A deficient (SP-A -/-) mice (KO) than in wild type mice (WT). It was hypothesized that a mild insult, specifically low doses of lipopolysaccharide (LPS), would adversely affect host defense and differentially potentiate O(3)-induced injury in WT and KO mice. METHODS: WT and KO mice were treated with different doses of LPS or LPS (2 ng) + O(3) (2 ppm) or filtered air (FA) for 3 h, then sacrificed 4 h following exposure (O(3), FA) or 20 h after LPS treatment alone. Several endpoints of inflammation were measured in bronchoalveolar lavage (BAL). RESULTS: 1) At 20 h after LPS treatment alone, both WT and KO mice exhibited signs of inflammation, but with differences in the macrophage inflammatory protein 2 (MIP-2) response pattern, total cells (at 0.5 ng LPS) and basal levels of oxidized protein and phospholipids; 2) After LPS + O(3), KO compared to WT showed decrease in polymorphonuclear leukocytes (PMNs) and MIP-2 and increase in phospholipids, and after LPS + FA an increase in total cells; 3) WT after LPS + FA showed an increase in SP-A with no further increase after LPS + O(3), and an increase in oxidized SP-A dimer following O(3) or LPS + O(3). CONCLUSIONS: LPS treatment has negative effects on inflammation endpoints in mouse BAL long after exposure and renders KO mice less capable of responding to a second insult. LPS and O(3) affect SP-A, quantitatively and qualitatively, respectively.