BackgroundWe previously reported an association between infant wheezing and residence < 100 m from stop-and-go bus and truck traffic. The use of a proximity model, however, may lead to exposure misclassification.ObjectiveResults obtained from a land use regression (LUR) model of exposure to truck and bus traffic are compared with those obtained with a proximity model. The estimates derived from the LUR model were then related to infant wheezing.MethodsWe derived a marker of diesel combustion—elemental carbon attributable to traffic sources (ECAT)—from ambient monitoring results of particulate matter with aerodynamic diameter < 2.5 μm. We developed a multiple regression model with ECAT as the outcome variable. Variables included in the model were locations of major roads, bus routes, truck traffic count, and elevation. Model parameter estimates were applied to estimate individual ECAT levels at infants’ homes.ResultsThe levels of estimated ECAT at the monitoring stations ranged from 0.20 to 1.02 μg/m3. A LUR model of exposure with a coefficient of determination (R2) of 0.75 was applied to infants’ homes. The mean (± SD) ambient exposure of ECAT for infants previously categorized as unexposed, exposed to stop-and-go traffic, or exposed to moving traffic was 0.32 ± 0.06, 0.42 ± 0.14, and 0.49 ± 0.14 μg/m3, respectively. Levels of ECAT from 0.30 to 0.90 μg/m3 were significantly associated with infant wheezing.ConclusionsThe LUR model resulted in a range of ECAT individually derived for all infants’ homes that may reduce the exposure misclassification that can arise from a proximity model.

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In recent years, ergonomics practices have increasingly relied upon the knowledge derived from epidemiological studies. In this regard, there is limited research devoted to the exclusive evaluation of the methodological qualities of ergonomics epidemiological studies. The aim of this study was to develop and test a general purpose 'epidemiological appraisal instrument' (EAI) for evaluating the methodological quality of existing or new ergonomic epidemiological studies using a critical appraisal system rooted in epidemiological principles. A pilot EAI version was developed and tested by a team of epidemiologists/physicians/biostatisticians, with the team leader being both epidemiologist and ergonomist. The pilot version was further tested with regard to other raters with/without a background in epidemiology, biostatistics and ergonomics. A revised version was evaluated for criterion validity and reliability. An assessor with a basic background in epidemiology and biostatistics would be able to correctly respond on four out of five questions, provided that subject matter expertise is obtained on specific items. This may improve with the article's quality. Training may have an effect upon assessors with virtually no background in epidemiology/biostatistics, but with a background in ergonomics. In this latter case, the inter-rater degree of agreement is largely above 90% and assessors can resolve their differences in a subsequent round. The EAI proved to be a valid and reliable appraisal instrument that may be used in various applications, such as systematic reviews and meta-analyses.

Background Exposure to traffic pollution particulate matter, predominantly diesel exhaust particles (DEP), increases risk for asthma and asthma exacerbation, however the underlying mechanisms remain poorly understood. Objective To examine the impact of DEP exposure on the generation and persistence of allergen-specific memory T-cells in asthma and translate these findings by determining the impact of early DEP exposure on the prevalence of allergic asthma in children. Methods The impact of DEP on HDM-specific memory responses was determined using an asthma model. Data from children enrolled in the Cincinnati Childhood Allergy and Air Pollution Study (CCAAPS) birth cohort were analyzed to determine the impact of the DEP exposure on asthma outcomes. Results DEP co-exposure with HDM resulted in persistent Th2/Th17 CD127+ effector/memory cells in the lungs, spleen and lymph nodes of adult and neonatal mice. After 7 weeks of rest, a single exposure to HDM resulted in airway hyperresponsiveness and increased levels of Th2 cytokines in only mice that had been previously exposed to both HDM and DEP versus HDM alone. Based on these data, we examined whether DEP exposure was similarly associated increased asthma prevalence in children in the presence or absence of allergen exposure/sensitization in the CCAAPS birth cohort. Early life exposure to high DEP was associated with significantly increased asthma prevalence among allergic children, but not among non-allergic children. Conclusion These findings suggest that DEP exposure results in accumulation of allergen specific Th2/Th17 cells in the lungs, potentiating secondary allergen recall responses and promoting the development of allergic asthma.