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ObjectiveUsing a summary measure of health inequalities, this study evaluated the distribution of adverse birth outcomes (ABO) and related maternal risk factors across area-level socioeconomic status (SES) gradients in urban and rural Alberta, Canada.DesignCross-sectional study using a validated perinatal clinical registry and an area-level SES.SettingThe study was conducted in Alberta, Canada. Data about ABO and related maternal risk factors were obtained from the Alberta Perinatal Health Program between 2006 and 2012. An area-level SES index derived from census data (2006) was linked to the postal code at delivery.ParticipantsWomen (n=3 30 957) having singleton live births with gestational age ≥22 weeks.Primary and secondary outcome measuresWe estimated concentration indexes to assess inequalities across SES gradients in both rural and urban areas (CIdxR and CIdxU, respectively) for spontaneous preterm birth (PTB), small for gestational age (SGA), large for gestational age (LGA), gestational hypertension, gestational diabetes, smoking and substance use during pregnancy and pre-pregnancy weight >91 kg.ResultsThe highest health inequalities disfavouring low SES groups were identified for substance abuse and smoking in rural areas (CIdxR−0.38 and −0.23, respectively). Medium inequalities were identified for LGA (CIdxR−0.08), pre-pregnancy weight >91 kg (CIdxR−0.07), substance use (CIdxU−0.15), smoking (CIdxU−0.14), gestational diabetes (CIdxU−0.10) and SGA (CIdxU−0.07). Low inequalities were identified for PTB (CIdxR−0.05; CIdxU−0.05) and gestational diabetes (CIdxR−0.04). Inequalities disfavouring high SES groups were identified for gestational hypertension (CIdxR+0.04), SGA (CIdxR+0.03) and LGA (CIdxU+0.03).ConclusionsABO and related maternal risk factors were unequally distributed across the socioeconomic gradient in urban–rural settings, with the greatest concentrations in lower SES groups of rural areas. Future research is needed on underlying mechanisms driving SES gradients in perinatal health across the rural–urban spectrum.

Urban air pollution is a serious worldwide problem due to its impact on human health. In the past 60 years, growing evidence established a correlation between exposure to air pollutants and the developing of severe respiratory diseases. Recently particulate matter (PM) is drawing more public attention to various aspects including historical backgrounds, physicochemical characteristics, and its pathological role. Therefore, this review is focused on these aspects. The most famous air pollution disaster happened in London on December 1952; it has been calculated that more than 4,000 deaths occurred during this event. Air pollution is a complex mix of gases and particles. Gaseous pollutants disseminate deeply into the alveoli, allowing its diffusion through the blood-air barrier to several organs. Meanwhile, PM is a mix of solid or liquid particles suspended in the air. PM is deposited at different levels of the respiratory tract, depending on its size: coarse particles (PM10) in upper airways and fine particles (PM2.5) can be accumulated in the lung parenchyma, inducing several respiratory diseases. Additionally to size, the composition of PM has been associated with different toxicological outcomes on clinical and epidemiological, as well as in vivo and in vitro animal and human studies. PM can be constituted by organic, inorganic, and biological compounds. All these compounds are capable of modifying several biological activities, including alterations in cytokine production, coagulation factors balance, pulmonary function, respiratory symptoms, and cardiac function. It can also generate different modifications during its passage through the airways, like inflammatory cells recruitment, with the release of cytokines and reactive oxygen species (ROS). These inflammatory mediators can activate different pathways, such as MAP kinases, NF-κB, and Stat-1, or induce DNA adducts. All these alterations can mediate obstructive or restrictive respiratory diseases like asthma, COPD, pulmonary fibrosis, and even cancer. In 2013, outdoor air pollution was classified as Group 1 by IARC based on all research studies data about air pollution effects. Therefore, it is important to understand how PM composition can generate several pulmonary pathologies.

In cold temperatures, vehicles idle more, have high cold-start emissions including greenhouse gases, and have less effective exhaust filtration systems, which can cause up to ten-fold more harmful vehicular emissions. Only a few vehicle technologies have been tested for emissions below −7 °C (20 °F). Four-hundred-million people living in cities with sub-zero temperatures may be impacted. We conducted a scoping review to identify the existing knowledge about air-pollution-related health outcomes in a cold climate, and pinpoint any research gaps. Of 1019 papers identified, 76 were selected for review. The papers described short-term health impacts associated with air pollutants. However, most papers removed the possible direct effect of temperature on pollution and health by adjusting for temperature. Only eight papers formally explored the modifying effect of temperatures. Five studies identified how extreme cold and warm temperatures aggravated mortality/morbidity associated with ozone, particles, and carbon-monoxide. The other three found no health associations with tested pollutants and temperature. Additionally, in most papers, emissions could not be attributed solely to traffic. In conclusion, evidence on the relationship between cold temperatures, traffic-related pollution, and related health outcomes is lacking. Therefore, targeted research is required to guide vehicle regulations, assess extreme weather-related risks in the context of climate change, and inform public health interventions.

Exposure to air pollution particulate matter (PM) and tuberculosis (TB) are two of the leading global public health challenges affecting low and middle income countries. An estimated 4.26 million premature deaths are attributable to household air pollution and an additional 4.1 million to outdoor air pollution annually. Mycobacterium tuberculosis (M.tb) infects a large proportion of the world's population with the risk for TB development increasing during immunosuppressing conditions. There is strong evidence that such immunosuppressive conditions develop during household air pollution exposure, which increases rates of TB development. Exposure to urban air pollution has been shown to alter the outcome of TB therapy. Here we examined whether in vitro exposure to urban air pollution PM alters human immune responses to M.tb. PM2.5 and PM10 (aerodynamic diameters <2.5μm, <10μm) were collected monthly from rainy, cold-dry and warm-dry seasons in Iztapalapa, a highly populated TB-endemic municipality of Mexico City with elevated outdoor air pollution levels. We evaluated the effects of seasonality and size of PM on cytotoxicity and antimycobacterial host immunity in human peripheral blood mononuclear cells (PBMC) from interferon gamma (IFN-γ) release assay (IGRA)+ and IGRA- healthy study subjects. PM10 from cold-dry and warm-dry seasons induced the highest cytotoxicity in PBMC. With the exception of PM2.5 from the cold-dry season, pre-exposure to all seasonal PM reduced M.tb phagocytosis by PBMC. Furthermore, M.tb-induced IFN-γ production was suppressed in PM2.5 and PM10-pre-exposed PBMC from IGRA+ subjects. This observation coincides with the reduced expression of M.tb-induced T-bet, a transcription factor regulating IFN-γ expression in T cells. Pre-exposure to PM10 compared to PM2.5 led to greater loss of M.tb growth control. Exposure to PM2.5 and PM10 collected in different seasons differentially impairs M.tb-induced human host immunity, suggesting biological mechanisms underlying altered M.tb infection and TB treatment outcomes during air pollution exposures.

Exposure to urban air pollution, specifically particulate matter (PM), has been shown to modify the immune response to Mycobacterium tuberculosis (Mtb) infection in the human lung. In this study, bronchoalveolar cells (BACs) from healthy adult residents of Mexico City were pre-exposed to PM2.5 and then infected with Mtb to examine the gene expression of early innate Th1/Th2 responses. The results showed that PM2.5 exposure induced pro-inflammatory cytokines and suppressed Th2-related genes in a dose-dependent manner. PM2.5 pre-exposure also reduced the expression of several genes involved in the immune response to Mtb, including Th1 markers and cytokines. Furthermore, PM2.5 exposure impaired the production of IFNa, a key cytokine in the immune response to Mtb. The study suggests that PM2.5 exposure can impair the early host immune response to Mtb infection, leading to an increased susceptibility to tuberculosis. These findings highlight the importance of reducing air pollution for global tuberculosis control efforts.

RationaleAssociations between urban (outdoor) airborne particulate matter (PM) exposure and TB and potential biological mechanisms are poorly explored.ObjectivesTo examine whether in vivo exposure to urban outdoor PM in Mexico City and in vitro exposure to urban outdoor PM2.5 (< 2.5 µm median aerodynamic diameter) alters human host immune cell responses to Mycobacterium tuberculosis.MethodsCellular toxicity (flow cytometry, proliferation assay (MTS assay)), M. tuberculosis and PM2.5 phagocytosis (microscopy), cytokine-producing cells (Enzyme-linked immune absorbent spot (ELISPOT)), and signalling pathway markers (western blot) were examined in bronchoalveolar cells (BAC) and peripheral blood mononuclear cells (PBMC) from healthy, non-smoking, residents of Mexico City (n=35; 13 female, 22 male). In vivo-acquired PM burden in alveolar macrophages (AM) was measured by digital image analysis.Measurements and main resultsIn vitro exposure of AM to PM2.5 did not affect M. tuberculosis phagocytosis. High in vivo-acquired AM PM burden reduced constitutive, M. tuberculosis and PM-induced interleukin-1β production in freshly isolated BAC but not in autologous PBMC while it reduced constitutive production of tumour necrosis factor-alpha in both BAC and PBMC. Further, PM burden was positively correlated with constitutive, PM, M. tuberculosis and purified protein derivative (PPD)-induced interferon gamma (IFN-γ) in BAC, and negatively correlated with PPD-induced IFN-γ in PBMC.ConclusionsInhalation exposure to urban air pollution PM impairs important components of the protective human lung and systemic immune response against M. tuberculosis. PM load in AM is correlated with altered M. tuberculosis-induced cytokine production in the lung and systemic compartments. Chronic PM exposure with high constitutive expression of proinflammatory cytokines results in relative cellular unresponsiveness.

Background Exposure to particulate matter (PM) is associated with an adverse intrauterine environment, which can promote adult cardiovascular disease (CVD) risk. Ultrafine particles (UFP) (small size and large surface area/mass ratio) are systemically distributed, induce inflammation and oxidative stress, and have been associated with vascular endothelial dysfunction and arterial vasoconstriction, increasing hypertension risk. Placental stress and alterations in methylation of promoter regions of renin-angiotensin system (RAS)-related elements could be involved in UFP exposure-related programming of hypertension. We investigated whether in utero UFP exposure promotes placental stress by inflammation and oxidative stress, alterations in hydroxysteroid dehydrogenase 11b-type 2 (HSD11B2) and programming of RAS-related elements, and result in altered blood pressure in adult offspring. UFP were collected from ambient air using an aerosol concentrator and physicochemically characterized. Pregnant C57BL/6J p un / p un female mice were exposed to collected UFP (400 μg/kg accumulated dose) by intratracheal instillation and compared to control (nonexposed) and sterile H 2 O (vehicle) exposed mice. Embryo reabsorption and placental stress by measurement of the uterus, placental and fetal weights, dam serum and fetal cortisol, placental HSD11B2 DNA methylation and protein levels, were evaluated. Polycyclic aromatic hydrocarbon (PAH) biotransformation (CYP1A1 and NQO1 (NAD(P)H dehydrogenase (quinone)1)) enzymes, inflammation and oxidative stress in placentas and fetuses were measured. Postnatal day (PND) 50 in male offspring blood pressure was measured. Methylation and protein expression of (RAS)-related elements, angiotensin II receptor type 1 (AT 1 R) and angiotensin I-converting enzyme (ACE) in fetuses and lungs of PND 50 male offspring were also assessed. Results In utero UFP exposure induced placental stress as indicated by an increase in embryo reabsorption, decreases in the uterus, placental, and fetal weights, and HSD11B2 hypermethylation and protein downregulation. In utero UFP exposure induced increases in the PAH-biotransforming enzymes, intrauterine oxidative damage and inflammation and stimulated programming and activation of AT 1 R and ACE, which resulted in increased blood pressure in the PND 50 male offspring. Conclusions In utero UFP exposure promotes placental stress through inflammation and oxidative stress, and programs RAS-related elements that result in altered blood pressure in the offspring. Exposure to UFP during fetal development could influence susceptibility to CVD in adulthood.

Air pollution in developing countries is a growing concern. It is associated with urbanization and social and economic structures. The understanding of how social factors can influence the perception and the potential impact of air pollution have not been addressed sufficiently. This paper addresses the social vulnerability and exposure to PM10 association and its influence on the air quality perception of residents in Mexicali, a Mexico–US border city. This study used individual variables and population census data, as well as statistical and spatial analyses. A cluster of socially vulnerable populations with high exposure to coarse particulate matter (PM10) was found in the city’s peripheral areas. The spatial distribution of the local perception of air quality varied by the exposure zones of the estimated PM10 concentrations. Respondents living in very high exposure areas perceive air quality as “poor,” contrarily to a worse perception in areas of intermediate and lower exposure to PM10. Proximity to stationary sources of pollution was associated with a poor perception of air quality. Results also indicate that low household income and poor air quality perceived at the place of residence negatively influences the perceived changes in the air quality over time. The knowledge of chronic health effects related to air pollution was scarce in the sampled population, especially in the areas with very high exposure and high social vulnerability. These findings can serve as a support in local air quality management.

Background Data measuring airborne pollutants, public health and environmental factors are increasingly being stored and merged. These big datasets offer great potential, but also challenge traditional epidemiological methods. This has motivated the exploration of alternative methods to make predictions, find patterns and extract information. To this end, data mining and machine learning algorithms are increasingly being applied to air pollution epidemiology. Methods We conducted a systematic literature review on the application of data mining and machine learning methods in air pollution epidemiology. We carried out our search process in PubMed, the MEDLINE database and Google Scholar. Research articles applying data mining and machine learning methods to air pollution epidemiology were queried and reviewed. Results Our search queries resulted in 400 research articles. Our fine-grained analysis employed our inclusion/exclusion criteria to reduce the results to 47 articles, which we separate into three primary areas of interest: 1) source apportionment; 2) forecasting/prediction of air pollution/quality or exposure; and 3) generating hypotheses. Early applications had a preference for artificial neural networks. In more recent work, decision trees, support vector machines, k-means clustering and the APRIORI algorithm have been widely applied. Our survey shows that the majority of the research has been conducted in Europe, China and the USA, and that data mining is becoming an increasingly common tool in environmental health. For potential new directions, we have identified that deep learning and geo-spacial pattern mining are two burgeoning areas of data mining that have good potential for future applications in air pollution epidemiology. Conclusions We carried out a systematic review identifying the current trends, challenges and new directions to explore in the application of data mining methods to air pollution epidemiology. This work shows that data mining is increasingly being applied in air pollution epidemiology. The potential to support air pollution epidemiology continues to grow with advancements in data mining related to temporal and geo-spacial mining, and deep learning. This is further supported by new sensors and storage mediums that enable larger, better quality data. This suggests that many more fruitful applications can be expected in the future.

Background: In the rapidly shifting Canadian climate, an ageing population, and increased migration, a greater understanding of how local climate and air pollution hazards impact older adults and immigrant populations will be necessary for mitigating and adapting to adverse health impacts. Objectives: To explore the reported health impacts of climate change and air pollution exposures in older adults and immigrant people living in Canada, identify known factors influencing risk and resilience in these populations and gaps in the literature. Methods: We searched for research focused on older adults and immigrants living in Canada, published from 2010 onward, where the primary exposures were related to climate or air pollution. We extracted data on setting, exposures, health outcomes, and other relevant contextual factors. Results and Discussion: We identified 52 eligible studies, most focused in Ontario and Quebec. Older people in Canada experience health risks due to climate and air pollution exposures. The extent of the risk depends on multiple factors. We found little information about the climate- and air pollution-related health impacts experienced by immigrant communities. Conclusions: Further research about climate- and air pollution-related exposures, health, and which factors promote or reduce resiliency in Canada’s older adults and immigrant communities is necessary.