To assess the maximum sound levels that may be experienced by young people in Canada from modern digital audio players, this study measured nine recent models of players and 20 earphones. Measurement methodology followed European standard BS EN 50332. Playback levels ranged from 101 to 107 dBA at maximum volume level. Estimated listener sound levels could vary from 79 to 125 dBA due to the following factors: (i) earphone seal against the ear, (ii) player output voltage, (iii) earphone sensitivity, and (iv) recorded music levels. There was a greater potential for high sound levels if intra-concha "earbud" earphones were used due to the effect of earphone seal. Simpler measurement techniques were explored as field test methods; the best results were obtained by sealing the microphone of a sound level meter to the earphone using a cupped hand and correcting for the free field response of the ear. Measurement of noise levels 0.25 m from the earphone showed that a bystander is unlikely to accurately judge listener sound levels.

Airway epithelial cells (AEC) exhibit a pro-inflammatory phenotype in patients with allergic asthma. We examined the effect of an allergic cytokine environment on the response of AEC to rhinovirus (RV), the most common trigger of acute exacerbations of asthma. Calu-3 cells, a well-differentiated human AEC line, were cultured with or without the T-helper type 2 cytokines interleukin (IL)-4 and IL-13, then stimulated with a toll-like receptor (TLR) 3 agonist (poly I:C, dsRNA) or a TLR7 agonist (imiquimod), or infected with RV 16. Expression of pro-inflammatory and antiviral mediators, and of viral pattern-recognition molecules, was assessed using nCounter assays, quantitative real-time PCR (qRT-PCR) and protein immunoassays. Both dsRNA and imiquimod stimulated expression of mRNA for whereas expression of several chemokines and antiviral response genes was induced only by dsRNA. Conversely, expression of other cytokines and growth factors was induced only by imiquimod. RV infection not only stimulated expression of the inflammation-related genes induced by dsRNA, but also of complement factor B and the novel pro-inflammatory cytokine IL-32. In the T helper type 2 (Th2) cytokine environment, several mediators exhibited significantly enhanced expression, whereas expression of interferons was either unchanged or enhanced. The allergic environment also increased expression of pattern-recognition receptors and of intercellular adhesion molecule 1, the cell surface receptor for RV. We conclude that Th2 cytokines promote increased production of pro-inflammatory mediators by AEC following infection with RV. Increased viral entry or enhanced signalling via pattern-recognition receptors could also contribute to the exaggerated inflammatory response to RV observed in allergic asthmatics.

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To assist the development of a precision scanning intensity standard for sound power determinations, this study investigated two accuracy estimation methods proposed by ISO Working Group 25. One method used the F4 sampling criterion from the precision grade discrete point intensity standard [ISO 9614-1:1993], adapted for the scanning intensity technique. The other method assumed that measurement accuracy was related to the difference between measurements using two different scanning paths. This method was a variation of the repeatability test from the engineering grade scanning intensity standard [ISO 9614-2:1996]. The study compared the estimated accuracy from each of the two methods to a third accuracy estimate, the difference between a sound power determination using the scanning intensity technique and a precision grade measurement using sound pressure [ISO 3745:1977]. All measurements were made under hemi-anechoic conditions and all intensity scannning was done manually. Results were obtained for the following three sound sources: a Bruel & Kjaer reference source, a vacuum cleaner, and a loudspeaker. The results suggested that both of the proposed methods can be of use in achieving precision grade accuracy.

Residual pressure intensity index measurements and performance evaluation of sound intensity probes and analyzers are discussed. The residual pressure intensity index was determined separately for the analyzers using identical electrical input signals, and for probe and analyzer combinations using identical sound-pressure inputs. Both FFT and digital frequency analyzers were examined in the investigations. The results show that the residual pressure intensity index depends on the input signal levels, and any phase compensation scheme should be considered in relation to these measurements. Performance of the probes was examined using a gating technique in a large enclosed space. The measured sound intensity levels using the sound intensity probe were compared with the levels derived from sound-pressure measurements from a single standard microphone. The results are in agreement with the predicted performance. Further discussions in the paper include the directivity of the probes and phase compensation schemes.