Allergic rhinitis affects the quality of life of millions of people worldwide. Air pollution not only causes morbidity, but nearly 3 million people per year die from unhealthy indoor air exposure. Furthermore, allergic rhinitis and air pollution interact. This report summarizes the discussion of an International Expert Consensus on the management of allergic rhinitis aggravated by air pollution. The report begins with a review of indoor and outdoor air pollutants followed by epidemiologic evidence showing the impact of air pollution and climate change on the upper airway and allergic rhinitis. Mechanisms, particularly oxidative stress, potentially explaining the interactions between air pollution and allergic rhinitis are discussed. Treatment for the management of allergic rhinitis aggravated by air pollution primarily involves treating allergic rhinitis by guidelines and reducing exposure to pollutants. Fexofenadine a non-sedating oral antihistamine improves AR symptoms aggravated by air pollution. However, more efficacy studies on other pharmacological therapy of coexisting AR and air pollution are currently lacking.

Air pollution causes significant morbidity and mortality in patients with inflammatory airway diseases (IAD) such as allergic rhinitis (AR), chronic rhinosinusitis (CRS), asthma, and chronic obstructive pulmonary disease (COPD). Oxidative stress in patients with IAD can induce eosinophilic inflammation in the airways, augment atopic allergic sensitization, and increase susceptibility to infection. We reviewed emerging data depicting the involvement of oxidative stress in IAD patients. We evaluated biomarkers, outcome measures and immunopathological alterations across the airway mucosal barrier following exposure, particularly when accentuated by an infectious insult.

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Introduction: An increased number of otic capsule dehiscence (OCD) variants relying on the third window pathomechanism have been reported lately. Therefore, a characterization of the anatomical structures involved and an accurate radiological description of the third window (TW) interface location have become essential for improving the diagnosis and appropriate therapeutic modalities. The purpose of this article is to propose a classification based on clinical, anatomical, and radiological data of third mobile window abnormalities (TMWA) and to discuss the alleged pathomechanism in lesser-known clinical variants.Materials and Methods: The imaging records of 259 patients who underwent, over the last 6 years, a high-resolution CT (HRCT) of the petrosal bone for conductive hearing loss were analyzed retrospectively. Patients with degenerative, traumatic, or chronic infectious petrosal bone pathology were excluded. As cases with a clinical presentation similar to those of a TW syndrome have recently been described in the literature but without these being confirmed radiologically, we thought it necessary to be integrated in a separated branch of this classification as “CT - TMWA.” The same goes for certain intralabyrinthine pathologies also recently reported in the literature, which mimic to some extent the symptoms of a TW pathology. Therefore, we suggest to call them intralabyrinthine TW-like abnormalities.Results: Temporal bone HRCT and, in some cases, 3T MRI of 97 patients presenting symptomatic or pauci-symptomatic, single or multiple, unilateral or bilateral OCD were used to develop this classification. According to the topography and anatomical structures involved at the site of the interface of the TW, a third-type classification of OCD is proposed.Conclusions: A classification reuniting all types of TMWA as the one proposed in this article would allow for a better systematization and understanding of this complex pathology and possibly paves the way for innovative therapeutic approaches. To encompass all clinical and radiological variants of TMWA reported in the literature so far, TMWAs have been conventionally divided into two major subgroups: Extralabyrinthine (or “true” OCD with three subtypes) and Intralabyrinthine (in which an additional mobile window-like mechanism is highly suspected) or TMWA-like subtype. Along these subgroups, clinical forms of OCD with multiple localization (multiple OCD) and those that, despite the fact that they have obvious characteristics of OCD have a negative CT scan (or CT – TMWA), were also included.

Broader intra-cochlear current spread (ICCS) implies higher cochlear implant (CI) channel interactions. This study aimed to investigate the relationship between ICCS and speech intelligibility in experienced CI users. Using voltage matrices collected for impedance measurements, an individual exponential spread coefficient (ESC) was computed. Speech audiometry was performed to determine the intelligibility at 40 dB Sound Pressure Level (SPL) and the 50% speech reception threshold: I40 and SRT50 respectively. Correlations between ESC and either I40 or SRT50 were assessed. A total of 36 adults (mean age: 50 years) with more than 11 months (mean: 34 months) of CI experience were included. In the 21 subjects for whom all electrodes were active, ESC was moderately correlated with both I40 (r = −0.557, p = 0.009) and SRT50 (r = 0.569, p = 0.007). The results indicate that speech perception performance is negatively affected by the ICCS. Estimates of current spread at the closest vicinity of CI electrodes and prior to any activation of auditory neurons are indispensable to better characterize the relationship between CI stimulation and auditory perception in cochlear implantees.