The volume and type of traffic and exposure to air pollution have been found to be associated with respiratory health, but few studies have considered the interaction with socioeconomic status at the household level. We investigated the relationships of respiratory health related to traffic type, traffic volume, and air pollution, stratifying by socioeconomic status, based on household income and education, in 3591 schoolchildren in Windsor, Canada. Interquartile range changes in traffic exposure and pollutant levels were linked to respiratory symptoms and objective measures of lung function using generalised linear models for three levels of income and education. In 95% of the relationships among all cases, the odds ratios for reported respiratory symptoms (a decrease in measured lung function), based on an interquartile range change in traffic exposure or pollutant, were greater in the lower income/education groups than the higher, although the odds ratios were in most cases not significant. However, in up to 62% of the cases, the differences between high and low socioeconomic groups were statistically significant, thus indicating socioeconomic status (SES) as a significant effect modifier. Our findings indicate that children from lower socioeconomic households have a higher risk of specific respiratory health problems (chest congestion, wheezing) due to traffic volume and air pollution exposure.

We investigated the associations between exposure to polycyclic aromatic hydrocarbons (PAHs) and selected respiratory physiologic measures in cycles 2 and 3 of the Canadian Health Measures Survey, a nationally representative population sample. Using generalized linear mixed models, we tested the association between selected PAH metabolites and 1-second forced expiratory volume (FEV), forced vital capacity (FVC), and the ratio between the two (FEV/FVC) in 3531 people from 6 to 79 years of age. An interquartile change in urinary PAH metabolite was associated with significant decrements in FEV and FVC for eight PAHs, 2-hydroxynapthalene, 1-, and 2-hydroxyphenanthrene, 2-, 3-, and 9-hydroxyfluorene and 3- and 4-hydroxyphenanthrene. Exposure to PAH may negatively affect lung function in the Canadian population.

Background: Major depressive disorder (MDD) is a debilitating mental illness that has been linked to increases in markers of inflammation, as well as to changes in brain functional and structural connectivity, particularly between the insula and the subgenual anterior cingulate cortex (sgACC). In this study, we directly related inflammation and dysconnectivity in treatment-resistant MDD by concurrently measuring the following: microglial activity with [ 18 F]N-2-(fluoroethoxyl)benzyl-N-(4phenoxypyridin-3-yl)acetamide ([ 18 F]FEPPA) positron emission tomography (PET); the severity of MDD; and functional or structural connectivity among insula or sgACC nodes. Methods: Twelve patients with treatment-resistant MDD (8 female, 4 male; mean age ± standard deviation 54.9 ± 4.5 years and 23 healthy controls (11 female, 12 male; 60.3 ± 8.5 years) completed a hybrid [ 18 F]FEPPA PET and MRI acquisition. From these, we extracted relative standardized uptake values for [ 18 F]FEPPA activity and Pearson r-to-z scores representing functional connectivity from our regions of interest. We extracted diffusion tensor imaging metrics from the cingulum bundle, a key white matter bundle in MDD. We performed regressions to relate microglial activity with functional connectivity, structural connectivity and scores on the 17-item Hamilton Depression Rating Scale. Results: We found significantly increased [ 18 F]FEPPA uptake in the left sgACC in patients with treatment-resistant MDD compared to healthy controls. Patients with MDD also had a reduction in connectivity between the sgACC and the insula. The [ 18 F]FEPPA uptake in the left sgACC was significantly related to functional connectivity with the insula, and to the structural connectivity of the cingulum bundle.[ 18 F]FEPPA uptake also predicted scores on the Hamilton Depression Rating Scale. Limitations: A relatively small sample size, lack of functional task data and concomitant medication use may have affected our findings. Conclusion: We present preliminary evidence linking a network-level dysfunction relevant to the pathophysiology of depression and related to increased microglial activity in MDD.