Airway Mast Cells in a Rhesus Model of Childhood Allergic Airways Disease

Asthma is a leading cause of morbidity in children. Risk factors include chronic exposure to allergens and air pollution. While chronically activated mast cells contribute to the pathophysiology of asthma in part through their proteases such as chymase and tryptase, previous studies of airway mast cell abundance and distribution in asthmatics have been inconsistent. To determine whether repeated episodic exposures to environmental pollutants during postnatal lung development alter airway mast cell abundance and distribution, we exposed infant rhesus monkeys to a known human allergen, house dust mite antigen (HDMA), and/or a known environmental pollutant, ozone (O3), and quantitatively compared the abundance of tryptase- or chymase-positive mast cells in three airway levels. Mast cells are resident in multiple compartments of the airway wall in infant rhesus monkeys raised from birth in filtered air. Tryptase- and chymase-positive cells were most abundant in trachea and least in terminal bronchioles. The majority of tryptase-positive and almost all chymase-positive cells were in extracellular matrix and smooth muscle bundles. Chronic exposure to HDMA elevated the abundance of both tryptase- and chymase-positive cells in the trachea and intrapulmonary bronchi. Neither exposure to O3 nor HDMA + O3 increased mast cell accumulations in the airway wall. We conclude that during postnatal airway development (1) mast cells are a resident airway cell population even in the absence of toxic air contaminants; (2) aeroallergen exposure alters large airway mast cell distribution and abundance, increasing chymase-positive mast cells; and (3) this response is attenuated by exposure to oxidant air pollutants

Clinical Characterization of Children With Resistant Airflow Obstruction, a Multicenter Study

OBJECTIVE: To characterize a cohort of children with airflow limitation resistant to bronchodilator (BD) therapy. METHODS: Pulmonary function tests performed in children 6-17 years of age at 15 centers in a clinical research consortium were screened for resistant airflow limitation, defined as a post-BD FEV1 and/or an FEV1/FVC less than the lower limits of normal. Demographic and clinical data were analyzed for associations with pulmonary function. RESULTS: 582 children were identified. Median age was 13 years (IQR: 11, 16), 60% were males; 62% were Caucasian, 28% were African-American; 19% were obese; 32% were born prematurely and 21% exposed to second hand smoke. Pulmonary diagnoses included asthma (93%), prior significant pneumonia (28%), and bronchiectasis (5%). 65% reported allergic rhinitis, and 11% chronic sinusitis. Subjects without a history of asthma had significantly lower post-BD FEV1% predicted (p = 0.008). Subjects without allergic rhinitis had lower post-BD FEV1% predicted (p = 0.003). Children with allergic rhinitis, male sex, obesity and Black race had better pulmonary function post-BD. There was lower pulmonary function in children after age 11 years without a history of allergic rhinitis, as compared to those with a history of allergic rhinitis. CONCLUSIONS: The most prevalent diagnosis in children with BD-resistant airflow limitation is asthma. Allergic rhinitis and premature birth are common co-morbidities. Children without a history of asthma, as well as those with asthma but no allergic rhinitis, had lower pulmonary function. Children with BD-resistant airflow limitation may represent a sub-group of children with persistent obstruction and high risk for life-long airway disease

Effects of accessibility and environmental health risk on housing prices: a case of Salt Lake County, Utah

While transportation infrastructure can increase housing price by improving accessibility to opportunities, it generates environmental health risks, such as noise and air pollution, which may have negative effects on housing price. However, the combined effects of accessibility and environmental health risk on housing price have not been well examined in the literature, especially in the auto-oriented urban context of the United States. In this study, we use assessed housing value data and the hedonic model to examine the single-family housing market's reaction to accessibility and environment health risks in Salt Lake County, a growing metropolitan area in Utah experiencing significant air pollution. Three regression models are employed with the consideration of spatial effects: ordinary least squares (OLS), spatial lag regression (SLR), and hierarchical linear modeling (HLM, or multilevel modeling/MLM). By controlling for the influences of structural attributes and socioeconomic conditions, we find that the negative impacts (traffic noise and air pollution) of transportation systems on single-family housing prices are greater than the positive impact (accessibility). Single-family residents in Salt Lake County are willing to pay more to reduce environmental health risks than to get better accessibility. These findings are different from what have been found in some dense and compact urban areas in the literature. These findings suggest that people's willingness to pay for minimizing environmental health risks varies across different urban contexts

Smoking and Hormesis as Confounding Factors in Radiation Pulmonary Carcinogenesis

Confounding factors in radiation pulmonary carcinogenesis are passive and active cigarette smoke exposures and radiation hormesis. Significantly increased lung cancer risk from ionizing radiation at lung doses < 1 Gy is not observed in never smokers exposed to ionizing radiations. Residential radon is not a cause of lung cancer in never smokers and may protect against lung cancer in smokers. The risk of lung cancer found in many epi-demiological studies was less than the expected risk (hormetic effect) for nuclear weapons and power plant workers, shipyard workers, fluoroscopy patients, and inhabitants of high-dose background radiation. The protective effect was noted for low- and mixed high- and low-linear energy transfer (LET) radiations in both genders. Many studies showed a protection factor (PROFAC) > 0.40 (40% avoided) against the occurrence of lung cancer. The ubiquitous nature of the radiation hormesis response in cellular, animal, and epidemio-logical studies negates the healthy worker effect as an explanation for radiation hormesis. Low-dose radiation may stimulate DNA repair/apoptosis and immunity to suppress and eliminate cigarette-smoke-induced transformed cells in the lung, reducing lung cancer occurrence in smokers