Good asthma control is the main goal of long-term asthma treatment. According to the Global Initiative for Asthma (GINA) guidelines (www.ginasthma.com), medical professionals assess asthma control based on specific questions regarding asthma symptoms and by spirometry measuring forced expiratory volume in 1 second (FEV(1)). Patients trained in early self-detection of asthma exacerbations use a symptom-based questionnaire, such as the Asthma Control Test (ACT) [Nathan RA, Sorkness CA, Kosinski M, et al. Development of the Asthma Control Test. A survey for assessing asthma control. J Allergy Clin Immunol 2004; 113:59-64]. However, some patients may prefer harder indicators, like peak flow values, when considering how to act within their regular asthma self-management plan.

OBJECTIVES: Monitoring of FEV(1) at home could be an even more valuable alternative to recording peak flow values. The inexpensive handheld pocket spirometer "Piko-1®" offers the opportunity to monitor and store consecutive FEV(1) values. This study assesses the accuracy of the Piko-1 device.

METHODS: Twenty volunteers tested 20 Piko-1 devices over five consecutive days. All results were compared to daily FEV(1) values, as measured by a calibrated reference spirometer.

RESULTS: Overall, the accuracy was acceptable, although Piko-1 tended to underestimate FEV(1) in the lower range. Moreover, there was no evidence of major heterogeneity between Piko-1 devices.

CONCLUSION: The Piko-1 FEV(1) measurements are sufficiently accurate to start a clinical trial to compare the detection of asthma exacerbations with this device and based on asthma symptoms alone.

Traffic related air pollutants from diesel engine exhaust are found in fine and ultrafine particulates. The Cincinnati Childrens Allergy and Air Pollution Birth Cohort Study was initiated to determine if early exposure to these pollutants increased risk for development of early atopic sensitization and allergic respiratory disease phenotypes in children.

MATERIALS AND METHODS: Over 700 infants born to at least one atopic parent were recruited to participate in a birth cohort study. Participants received annual medical evaluations and skin testing to two foods and 15 aeroallergens from ages 1-4 and again at age seven. Indoor home assessments were conducted at age one. Outdoor traffic related air pollutant exposure was estimated using proximity and land use regression (LUR) modeling. Clinical outcomes were based upon case definitions for wheezing at ages one and three and allergic rhinitis at age three.

RESULTS: At age 1 exposure to stop and go traffic was associated with wheezing during infancy and recurrent wheezing was twice more likely among African-American infants. Exposure to high levels of elemental carbon attributable to traffic (ECAT) estimated with a LUR model predicted recurrent wheezing at age 1 as well as multiple wheezing phenotypes at age 3. Exposure to high levels of endotoxin combined with multiple dogs during the first year reduced risk for recurrent wheezing during the first year of life. Early sensitization to tree pollen aeroallergens in foods (egg white, milk) in infancy increased likelihood of allergic rhinitis during age 3.

CONCLUSION: High exposure to traffic related air pollutants represent independent risk factors for wheezing during infancy and early childhood. Further studies are needed to explore long-term effects of traffic exposure on development of asthma in childhood. Scientific significance. Reduction and mitigation of exposure to traffic related air pollutants could reduce risk of respiratory illnesses during childhood.

COPD (Chronic Obstructive Pulmonary Disease) is an important lung and airway disease which affects the lives of around 200 million people worldwide with an increasing incidence particularly in developing countries.

The pathogenesis of COPD is based on the innate and adaptive inflammatory immune response to the inhalation of toxic particles and gases. Although cigarette smoking is the primary cause of this inflammation, many other environmental and occupational exposures contribute to the pathology of COPD.

The immune inflammatory changes associated with COPD are linked to a tissue repair and remodeling process that increases mucus production and causes emphysematous destruction of the gas-exchanging surface of the lung. The inflamed airways of COPD patients contain several inflammatory cells including neutrophils, macrophages, T lymphocytes, and dendritic cells (DCs). Little is known about the relative contribution of DCs in the pathogenesis of COPD. However the number of DCs is changed in smokers and COPD patients and cigarette smoke (CS) induces the release of chemokines from DCs that play a role in the pathogenesis of COPD.

In this review paper, an overview is presented on the role of DCs and their mediators in the pathogenesis of COPD. The activation of DCs and their signaling in response to CS will also be highlighted and discussed.