Academic literature on the topic 'Personnal exposure to atmospheric air pollution'

Prior studies suggest brick workers in Nepal may be chronically exposed to hazardous levels of fine particulate matter (PM2.5) from ambient, occupational, and household sources. However, findings from these studies were based on stationary monitoring data, and thus may not reflect a worker’s individual exposures. In this study, we used RTI International’s MicroPEMs to collect 24 h PM2.5 personal breathing zone (PBZ) samples among brick workers (n = 48) to estimate daily exposures from ambient, occupational, and household air pollution sources. Participants were sampled from five job categories at one kiln. The geometric mean (GM) PM2.5 exposure across all participants was 116 µg/m3 (95% confidence interval [CI]: 94.03, 143.42). Job category was significantly (p < 0.001) associated with PBZ PM2.5 concentrations. There were significant pairwise differences in geometric mean (GM) PBZ PM2.5 concentrations among workers in administration (GM: 47.92, 95% CI: 29.81, 77.03 µg/m3) vs. firemen (GM: 163.46, 95 CI: 108.36, 246.58 µg/m3, p = 0.003), administration vs. green brick hand molder (GM: 163.35, 95% CI: 122.15, 218.46 µg/m3, p < 0.001), administration vs. top loader (GM: 158.94, 95% CI: 102.42, 246.66 µg/m3, p = 0.005), firemen vs. green brick machine molder (GM: 73.18, 95% CI: 51.54, 103.90 µg/m3, p = 0.03), and green brick hand molder vs. green brick machine molder (p = 0.008). Temporal exposure trends suggested workers had chronic exposure to hazardous levels of PM2.5 with little to no recovery period during non-working hours. Multi-faceted interventions should focus on the control of ambient and household air pollution and tailored job-specific exposure controls.

Abstract. The inaccurate quantification of personal exposure to air pollution introduces error and bias in health estimations, severely limiting causal inference in epidemiological research worldwide. Rapid advancements in affordable, miniaturised air pollution sensor technologies offer the potential to address this limitation by capturing the high variability of personal exposure during daily life in large-scale studies with unprecedented spatial and temporal resolution. However, concerns remain regarding the suitability of novel sensing technologies for scientific and policy purposes. In this paper we characterise the performance of a portable personal air quality monitor (PAM) that integrates multiple miniaturised sensors for nitrogen oxides (NOx), carbon monoxide (CO), ozone (O3) and particulate matter (PM) measurements along with temperature, relative humidity, acceleration, noise and GPS sensors. Overall, the air pollution sensors showed high reproducibility (mean R‾2=0.93, min–max: 0.80–1.00) and excellent agreement with standard instrumentation (mean R‾2=0.82, min–max: 0.54–0.99) in outdoor, indoor and commuting microenvironments across seasons and different geographical settings. An important outcome of this study is that the error of the PAM is significantly smaller than the error introduced when estimating personal exposure based on sparsely distributed outdoor fixed monitoring stations. Hence, novel sensing technologies such as the ones demonstrated here can revolutionise health studies by providing highly resolved reliable exposure metrics at a large scale to investigate the underlying mechanisms of the effects of air pollution on health.

Occupational exposures in on-campus healthcare settings have increasingly been investigated, while the sector of home healthcare typically receives less focus. This study explored work stress exposure and air pollution’s effects on home healthcare workers through the collection of multiple salivary cortisol samples per day, the completion of stress diaries, and the use of low-cost personal air monitors. This study was designed to identify the physiological responses to various types of stress, as well as the impact of air pollution on the home healthcare workforce. Due to the sample size and duration, the data showed that neither the stress levels recorded in the diaries (p = 0.754), nor the air pollution data (with only VOC and PM1 having Pearson correlation coefficients of >0.25), exhibited a significant association with the cortisol levels. The air sensor data were inconsistent with previously published indoor air pollutant literature. Forty percent of events reported by participants were identified as high stressor (level 6–10) events. One participant in this study accounted for 18% of these high-stress events. The most common emotional responses to these stressor events included feelings of frustration, irritation, anger, and fury, which together comprised 22.4% of the reactions. Future work should include studies with a larger sample size, a more robust air quality monitor, and a longer study duration to improve the power to detect potential associations. Although previous studies have indicated that home healthcare workers experience workplace stress and exposure to multiple air pollutants, this study did not detect a consistent relationship between these exposures and the physiological stress response.

Abstract. Beijing, as a representative megacity in China, is experiencing some of the most severe air pollution episodes in the world, and its fast urbanization has led to substantial urban and peri-urban disparities in both health status and air quality. Uncertainties remain regarding the possible causal links between individual air pollutants and health outcomes, with spatial comparative investigations of these links lacking, particularly in developing megacities. In light of this challenge, Effects of AIR pollution on cardiopuLmonary disEaSe in urban and peri-urban reSidents in Beijing (AIRLESS) was initiated, with the aim of addressing the complex issue of relating multi-pollutant exposure to cardiopulmonary outcomes. This paper presents the novel methodological framework employed in the project, namely (1) the deployment of two panel studies from established cohorts in urban and peri-urban Beijing, with different exposure settings regarding pollution levels and diverse sources; (2) the collection of detailed measurements and biomarkers of participants from a nested case (hypertensive) and control (healthy) study setting; (3) the assessment of indoor and personal exposure to multiple gaseous pollutants and particulate matter at unprecedented spatial and temporal resolution with validated novel sensor technologies; (4) the assessment of ambient air pollution levels in a large-scale field campaign, particularly the chemical composition of particulate matter. Preliminary results showed that there is a large difference between ambient and personal air pollution levels, and the differences varied between seasons and locations. These large differences were reflected on the different health responses between the two panels.

In this work, a 2-D gridded air pollution map with a high resolution of 50 × 50 m2 was proposed to help the exposure assessment studies focusing on the association between air pollutants and their health effects. To establish a reliable air pollution map in a 2 × 2 km2 urban area, a mobile monitoring procedure and a data process were developed. Among the various vehicle-related air pollutants, the particle-bound polycyclic aromatic hydrocarbon (pPAH) was chosen as a sensitive indicator. The average pPAH concentration on major roads (293.1 ng/m3) was found to be 35 times higher than that at a background location (8.4 ng/m3). Based on the cell-based pPAH concentrations, the 50 × 50 m2 cells in the air pollution map were categorized into five pollution levels. The higher air pollution levels were generally shown by the cells close to the major traffic emission points. The proposed map can be used to make various policies regarding land use and traffic flow control in urban areas. Estimation of the personal exposure level to air pollutants is possible at a reliable location using the highly resolved 2-D gridded air pollution map in exposure assessment studies.

In humans, studies based on Developmental Origins of Health and Disease (DOHaD) concept and targeting short half-lived chemicals, including many endocrine disruptors, generally assessed exposures from spot biospecimens. Effects of early-life exposure to atmospheric pollutants were reported, based on outdoor air pollution levels. For both exposure families, exposure misclassification is expected from these designs: for non-persistent chemicals, because a spot biospecimen is unlikely to capture exposure over windows longer than a few days; for air pollutants, because indoor levels are ignored. We developed a couple-child cohort relying on deep phenotyping and extended personal exposure assessment aiming to better characterize the effects of components of the exposome, including air pollutants and non-persistent endocrine disruptors, on child health and development. Pregnant women were included in SEPAGES couple-child cohort (Grenoble area) from 2014 to 2017. Maternal and children exposure to air pollutants was repeatedly assessed by personal monitors. DNA, RNA, serum, plasma, placenta, cord blood, meconium, child and mother stools, living cells, milk, hair and repeated urine samples were collected. A total of 484 pregnant women were recruited, with excellent compliance to the repeated urine sampling protocol (median, 43 urine samples per woman during pregnancy). The main health outcomes are child respiratory health using early objective measures, growth and neurodevelopment. Compared to former studies, the accuracy of assessment of non-persistent exposures is expected to be strongly improved in this new type of birth cohort tailored for the exposome concept, with deep phenotyping and extended exposure characterization. By targeting weaknesses in exposure assessment of the current approaches of cohorts on effects of early life environmental exposures with strong temporal variations, and relying on a rich biobank to provide insight on the underlying biological pathways whereby exposures affect health, this design is expected to provide deeper understanding of the interplay between the Exposome and child development and health.

Low-cost personal exposure monitors (PEMs) to measure personal exposure to air pollution are potentially promising tools for health research. However, their adoption requires robust validation. This study evaluated the performance of twenty-one Plume Lab Flow2s (PLFs) by comparing its air pollutant measurements, particulate matter with a diameter of 2.5 μm or less (PM2.5), 10 μm or less (PM10), and nitrogen dioxide (NO2), against several high-quality air pollution monitors under field conditions (at indoor, outdoor, and roadside locations). Correlation and regression analysis were used to evaluate measurements obtained by different PLFs against reference instrumentation. For all measured pollutants, the overall correlation coefficient between the PLFs and the reference instruments was often weak (r < 0.4). Moderate correlation was observed for one PLF unit at the indoor location and two units at the roadside location when measuring PM2.5, but not for PM10 and NO2 concentration. During periods of particularly higher pollution, 11 PLF tools showed stronger regression results (R2 values > 0.5) with one-hour and 9 PLF units with one-minute time interval. Results show that the PLF cannot be used robustly to determine high and low exposure to poor air. Therefore, the use of PLFs in research studies should be approached with caution if data quality is important to the research outputs.

Biomass burning for home energy use is a major environmental health concern. Improved cooking technologies could generate environmental health benefits, yet prior results regarding reduced personal exposure to air pollution are mixed. In this study, two improved stove types were distributed over four study groups in Northern Ghana. Participants wore real-time carbon monoxide (CO) monitors to measure the effect of the intervention on personal exposures. Relative to the control group (those using traditional stoves), there was a 30.3% reduction in CO exposures in the group given two Philips forced draft stoves (p = 0.08), 10.5% reduction in the group given two Gyapa stoves (locally made rocket stoves) (p = 0.62), and 10.2% reduction in the group given one of each (p = 0.61). Overall, CO exposure for participants was low given the prevalence of cooking over traditional three-stone fires, with 8.2% of daily samples exceeding WHO Tier-1 standards. We present quantification methods and performance of duplicate monitors. We analyzed the relationship between personal carbonaceous particulate matter less than 2.5 microns (PM2.5) and CO exposure for the dataset that included both measurements, finding a weak relationship likely due to the diversity of identified air pollution sources in the region and behavior variability.

La pollution de l’air contribue à dégrader la qualité de vie et à réduire l’espérance de vie des populations. L’organisation mondiale de la santé estime que la pollution de l’air est responsable de 7 millions de morts par an dans le monde. Elle participe à aggraver les maladies respiratoires, cause des cancers du poumon et des crises cardiaques. La pollution de l’air a donc des conséquences sanitaires importantes sur la vie humaine et la biodiversité. Ces dernières années, des progrès considérables ont été réalisés dans le domaine des microcontrôleurs et des modules de télécommunications. Ces derniers sont de plus efficients énergétiquement, performants, abordables, accessibles et sont responsables de l’émergence des objets connectés. Parallèlement, les récents développements des microsystèmes électromécaniques et des capteurs électrochimiques ont permis la miniaturisation des technologies permettant de mesurer de nombreux paramètres environnementaux dont la qualité de l’air. Ces avancées technologiques ont ainsi permis la conception et la production dans un cadre académique de capteurs de la qualité de l’air, portatifs, connectés, autonomes et en capacité de réaliser des acquisitions à une fréquence temporelle élevée. Jusqu’à récemment, l’un des majeurs freins à la compréhension de l’impact de la pollution de l’air sur la santé fut l’impossibilité de connaître l’exposition réelle des individus durant leur vie quotidienne ; la pollution de l’air est complexe et varie en fonction des habitudes, des activités et environnements empruntés par les individus. Ces capteurs portatifs de la qualité de l’air permettent donc de lever entièrement ce frein ainsi qu’un nombre important de contraintes. Ils sont conçus pour être utilisables en mobilité, sur de longues périodes et produisent des données granulaires, immédiatement disponibles, décrivant l’exposition à la pollution de l’air du porteur. Bien que les modules de mesure embarqués dans ces capteurs ne soient aujourd’hui pas aussi performants que les instruments de références ou la télédétection, lorsqu’il s’agit d’évaluer l’exposition individuelle à la pollution de l’air, parce qu'ils sont au plus proche des individus, ils permettent d’obtenir l’information la plus fidèle et constituent donc un outil indispensable pour l’avenir de la recherche épidémiologique. Dans ce contexte, nous avons participé au développement et à l’amélioration de deux capteurs de la qualité de l’air ; le CANARIN II et le CANARIN nano. Le CANARIN II est un capteur connecté communiquant par Wi-Fi, qui rapporte les concentrations de particules de diamètre 10, 2.5 et 1 micromètre, ainsi que les paramètres environnementaux de température, humidité et pression, chaque minute et les rend disponible en temps réel. Le CANARIN nano est, quant à lui, un capteur de plus petite taille, possédant les mêmes capacités que le CANARIN II, tout en faisant additionnellement l’acquisition des composés organiques volatils. Il est en capacité de fonctionner de manière autonome, puisque communiquant par réseau cellulaire. Deux types de résultats ont été obtenus avec les capteurs CANARIN ; d’une part, des résultats produits à partir de leur utilisation dans des conditions de vie réelle, d'autre part, des résultats en lien avec l'interprétation et la compréhension des mesures produites par les capteurs de particules dont les CANARINs sont équipés. Ces deux capteurs furent ainsi tous deux exploités par deux projets de recherche, au sein desquels nous avons accompagné le déploiement de plusieurs flottes de capteurs hétérogènes et réalisé l’analyse des données acquises. [...]
Air pollution contributes to the degradation of the quality of life and the reduction of life expectancy of the populations. The World Health Organization estimates that air pollution is responsible for 7 million deaths per year worldwide. It contributes to the aggravation of respiratory diseases, causes lung cancer and heart attacks. Air pollution has therefore significant health consequences on human life and biodiversity. Over the last few years, considerable progress has been made in the field of microcontrollers and telecommunications modules. These are more energy efficient, powerful, affordable, accessible, and are responsible for the growth of connected objects. In the meantime, the recent development of microelectromechanical systems and electrochemical sensors has allowed the miniaturization of technologies measuring many environmental parameters including air quality. These technological breakthroughs have enabled the design and production in an academic environment, of portable, connected, autonomous air quality sensors capable of performing acquisitions at a high temporal frequency. Until recently, one of the major obstacles to understanding the impact of air pollution on human health was the inability to track the real exposure of individuals during their daily lives; air pollution is complex, and varies according to the habits, activities and environments in which individuals spend their lives. Portable air quality sensors completely remove this obstacle as well as a number of other important constraints. These are designed to be used in mobility, over long periods of time, and produce immediately available granular data, which describes the exposure to air pollution of the person wearing it. Although the measurement modules embedded in these sensors are not currently as reliable as reference tools or remote sensing, when it comes to assessing individual exposure to air pollution, because they are as close as possible to the wearer, they provide the most accurate information, and are therefore an indispensable tool for the future of epidemiological research. In this context, we have been involved in the development and improvement of two air quality sensors; the CANARIN II and the CANARIN nano. The CANARIN II is a connected sensor communicating via Wi-Fi, which reports the concentration of 10, 2.5 and 1 micrometer diameter particles, as well as the environmental parameters of temperature, humidity, and pressure, every minute, making them available in real time. The CANARIN nano is a smaller sensor with the same capabilities of the CANARIN II, while additionally sensing volatile organic compounds levels. The CANARIN nano is able to operate autonomously, as it communicates through the cellular network. Two types of results have been obtained with the CANARIN sensors; on one hand, results produced from their use in real life conditions, and on the other hand, results related to the interpretation and understanding of the measurements produced by the particle sensors. These two sensors were both used in two research projects, in which we have helped deploy several heterogeneous sensor fleets and analyzed the acquired data. Firstly, in the POLLUSCOPE project funded by the French National Research Agency, where 86 volunteers from the general population wore a set of air pollution sensors for a total of 101 weeks, 35 of which the volunteers were also equipped with health sensors. Secondly, in the POLLAR project, where 43 subjects underwent polysomnography and then wore one CANARIN sensor for 10 days, thus allowing for the first time to explore the link between sleep apnea and particulate matter exposure. [...]

Increasing vehicle dependence in the United States has resulted in substantial emissions of traffic-related air pollutants that contribute to the deterioration of urban air quality. Exposure to urban air pollutants trigger a number of public health concerns, including the potential of inequality of exposures and health effects among population subgroups. To better understand the impact of traffic-related pollutants on air quality, exposure, and exposure inequality, modeling methods that can appropriately characterize the spatiotemporally resolved concentration distributions of traffic-related pollutants need to be improved. These modeling methods can then be used to investigate the impacts of urban design and transportation management choices on air quality, pollution exposures, and related inequality. This work will address these needs with three objectives: 1) to improve modeling methods for investigating interactions between city and transportation design choices and air pollution exposures, 2) to characterize current exposures and the social distribution of exposures to traffic-related air pollutants for the case study area of Hillsborough County, Florida, and 3) to determine expected impacts of urban design and transportation management choices on air quality, air pollution exposures, and exposure inequality. To achieve these objectives, the impacts of a small-scale transportation management project, specifically the '95 Express' high occupancy toll lane project, on pollutant emissions and nearby air quality was investigated. Next, a modeling method capable of characterizing spatiotemporally resolved pollutant emissions, concentrations, and exposures was developed and applied to estimate the impact of traffic-related pollutants on exposure and exposure inequalities among several population subgroups in Hillsborough County, Florida. Finally, using these results as baseline, the impacts of sprawl and compact urban forms, as well as vehicle fleet electrification, on air quality, pollution exposure, and exposure inequality were explored. Major findings include slightly higher pollutant emissions, with the exception of hydrocarbons, due to the managed lane project. Results also show that ambient concentration contributions from on-road mobile sources are disproportionate to their emissions. Additionally, processes not captured by the CALPUFF model, such as atmospheric formation, contribute substantially to ambient concentration levels of the secondary pollutants such as acetaldehyde and formaldehyde. Exposure inequalities for NOx, 1,3-butadiene, and benzene air pollution were found for black, Hispanic, and low income (annual household income less than $20,000) subgroups at both short-term and long-term temporal scales, which is consistent with previous findings. Exposure disparities among the subgroups are complex, and sometimes reversed for acetaldehyde and formaldehyde, due primarily to their distinct concentration distributions. Compact urban form was found to result in lower average NOx and benzene concentrations, but higher exposure for all pollutants except for NOx when compared to sprawl urban form. Evidence suggests that exposure inequalities differ between sprawl and compact urban forms, and also differ by pollutants, but are generally consistent at both short and long-term temporal scales. In addition, vehicle fleet electrification was found to result in generally lower average pollutant concentrations and exposures, except for NOx. However, the elimination of on-road mobile source emissions does not substantially reduce exposure inequality. Results and findings from this work can be applied to assist transportation infrastructure and urban planning. In addition, method developed here can be applied elsewhere for better characterization of air pollution concentrations, exposure and related inequalities.

Air pollution is one of the leading environmental problems of the 21st century, and the rise of global urbanization has increasingly exacerbated air pollution’s public health impact. Existing epidemiologic studies have tackled the relationship between air pollution and health from a variety of perspectives, but many areas of research remain lacking, including studies originating from developing countries, the assessment of exposure windows and sensitivity of modeling choices, and a better understanding of the climate change impacts on air pollution and health. In this dissertation, I address all of the issues mentioned above. Chapter 1 formally introduces the topics of this dissertation and summarizes background information on several major air pollutants. It then provides an overview of existing research on air pollution epidemiology and describes key knowledge gaps. In Chapter 2, we conduct a systematic review of the scientific literature for data on fine particulate matter (PM2.5) in China, where historical PM2.5 data are not widely available prior to 2013. Using the 574 PM2.5 measurements we identified from the literature, we detected differences in PM2.5 levels across both geographic and economic regions of China. In Chapter 3, we investigate the associations between short- and intermediate-term exposure of nitrogen dioxide (NO2) and mortality in 42 counties in China from 2013 to 2015, and find evidence of significant associations up to seven days prior to exposure. In Chapter 4, we investigate the association between PM2.5 and hospitalizations in New York State using five separate exposure datasets from 2002 to 2012. We find that despite some fluctuations in effect estimates, the majority of models yielded consistently significantly harmful associations. In Chapter 5, we utilize a global chemistry-climate model to project ozone levels in 2050 under a variety of emissions scenarios and quantify the mortality impact associated with changes in ozone concentrations between 2015 and 2050 according to each scenario. We find that under climate change alone and adherence to current legislation, ozone-related deaths would increase. However, under a best-case scenario of maximum technologically feasible reductions in emissions, over 300,000 premature deaths related to ozone can be avoided. Finally, Chapter 6 summarizes the findings of this dissertation and discusses potential directions in future research. While much work remains to be done, this dissertation work takes an important step forward in closing existing knowledge gaps in the field of air pollution epidemiology. More importantly, we hope that our work sends a strong public health message on the importance of continuing research on air pollution and health.

Chapter 1. Background: Asthma is the most common chronic childhood disease and is characterized by recurrent airway obstruction, bronchial hyper-responsiveness, and airway inflammation. Asthma is the leading cause of childhood hospitalization and school absenteeism in the United States. The associations between adverse respiratory effects and exposure to indoor nitrogen dioxide (NO2) and other byproducts of combustion such as particulate matter (PM) in particular ultrafine particulates (UFP), Ozone (O3) and Sulfur Dioxide (SO2), have been the focus of many epidemiological studies in recent years. Indoor exposure to NO2 and other pollutants from combustion may increase the risk of acute and chronic respiratory disease, reduce lung function, initiate and exacerbate asthma in children. The levels of exposure to NO2 indoors are of public health concern because children spend nearly 70% of their time indoors at home. According to the 2010 US Census report, approximately 39% of US households use natural gas for cooking, and the primary source of residential NO2 is a gas-fuel cooking appliance. Indoor levels of NO2 where NO2 sources are present can be much higher than outdoors, where the primary source of NO2 is vehicular traffic. Epidemiological studies in developed countries suggest that gas stoves used for cooking and/or heat are associated with an increased risk of asthma and respiratory symptoms in children. While there are numerous, epidemiological studies supporting an association between increased NO2 levels and gas stoves and asthma symptom severity in children, there are other studies that have examined the relationship in homes that did not observe significant associations. A better understanding of how NO2 and other indoor environmental (e.g., environmental tobacco smoke (ETS), allergens) exposures contribute to asthma morbidity in inner city preschool children will allow interventions to more effectively designed and implemented. To date, there are conflicting results on the role of exposure to indoor NO2 and its association with new-onset asthma in young inner-city children. The recent studies assessing the effects of indoor NO2 on asthma morbidity were limited to inner-city children, largely older, who were diagnosed with asthma. A gap in knowledge remains regarding the role indoor NO2 plays on the development of asthma in children not previously diagnosed. The scientific and public health rationale for conducting this dissertation was to describe the association of exposure to indoor NO2 and primary sources with the initiation and exacerbation of asthma symptoms among pre-school children with and without diagnosed asthma. The data analyzed in the current research come from a larger study of Endotoxin, Obesity, and Asthma (EOA) in the New York City Head Start Program, funded in the summer of 2002. The primary research objective of that study was to identify modifiable risk factors associated with asthma and asthma persistence among preschool children from low-income families living in select New York City neighborhoods with high pediatric asthma hospitalization rates. We conducted a cross-sectional analysis of data collected from the study questionnaire and home visit sampling at study enrollment. The analyses were performed in two phases: the first phases used data collected at study enrollment and the second phase used data collected 12-months after study baseline. Henceforth, the dissertation will refer to the first analyses as the baseline study and the second as the follow-up study. The research evaluated the association of NO2 exposure with asthma status among New York City Head Start children with and without asthma at study enrollment and with respiratory symptoms among children with asthma at 12-month follow-up. Chapter 2. Baseline Study: We conducted a cross-sectional analysis of data collected from the study questionnaire and home visit sampling at study enrollment. Specifically, the research sought to evaluate the association of NO2 exposure with asthma status among New York City Head Start children with and without asthma at study enrollment and with respiratory symptoms among children with asthma at enrollment. A total of 503 children were included in the baseline study. A total of 105 children (20.9%) met the criteria for both asthma and allergy, and 67 (13.3%) met the criteria for asthma alone. Girls made up 51.7% and boys, 48.3% of the 503 study participants. Descriptive analyses suggested that asthma/allergy status was associated with: male gender, non-Mexican ethnicity/national origin, presence of a smoker in the child’s home, number of smokers in the child’s home, self-reported parental history of asthma, mother’s education level and sensitization to one or more of the four allergens. Logistic regression models were used to investigate the magnitude and direction (as well as trend) of the association between childhood asthma and indoor NO2 sources in the child’s home. Chapter 3. Follow-up Study: Our follow-up study involved the analysis of the 12-month follow-up data from the study of Endotoxin, Obesity, and Asthma in the New York City Head Start Program funded in the summer of 2002. We focused on assessing the magnitude and direction of the associations of exposure to indoor NO2 levels (based on baseline NO2 measurements) with children’s asthma status and with symptom severity among asthmatics at 1-year follow-up. For the follow-up study, we categorized children by whether their asthma status had changed since baseline. Descriptive analyses were performed looking at key characteristics by “change in asthma status.” Children’s asthma status at baseline and at follow-up, were based on responses to the questionnaire. We analyzed indoor NO2 level measurements at baseline in relation to asthma outcomes on follow-up. We did not have enough data on NO2 levels at follow-up to analyze them in relation to asthma status on follow-up. Unless the family had relocated since baseline and/or reported changes since baseline in the use of gas appliances or the number of smokers in the home, we assumed that baseline NO2 levels in the participating children’s homes were reasonable proxies for current exposures. We looked at the number of children who moved since baseline and whether the move (for example, looking at gas stove status, age of new building) may have impacted indoor NO2 levels. Of the 503 children who were included in the baseline analyses, 47.3% had data on asthma status on follow-up. A total of 238 children (111 male, 127 female) were grouped into the four mutually exclusive outcome categories: 122 (51.3%) did not have asthma at baseline or on follow-up, 34 (14.3%) had asthma on follow-up but not at baseline, 65 (27.3%) had asthma at baseline but not on follow-up, and 17 (7.1%) had asthma at baseline and on follow-up. The mean age at 1-year follow-up was 59.5 months (6.95), and neither age nor gender was associated with asthma. The distribution of ethnicity/national origin among the 238 children remained the same as at baseline; no one ethnicity group experienced disproportionate loss to follow-up, and asthma status remained associated with non-Mexican ethnicity/national origin, although 44.1% with new-onset asthma were of Mexican background. Asthma was also associated with self-reported parental history of asthma and allergy in children, but nearly 80% of children with new-onset asthma had no such parental history of asthma. More parents of children with new-onset (35.3%) or persistent asthma (23.5%) than of other children reported making efforts to reduce risk factors or triggers for asthma exacerbations in the past 12 months. Chapter 4. Dissertation Conclusion : The primary objective of the dissertation research was the examination of the relationship between asthma and asthma severity and exposure to gas cooking and residential NO2. In both our baseline and 12-month follow-up studies, exposure to indoor NO2 was represented by the baseline measurement of NO2 and the NO2 surrogate, gas stove. Asthma status of children was based on parental responses on the questionnaire regarding asthma symptoms and urgent care visits due to respiratory distress over the course of each 12-month period prior to the conducting study questionnaires. For both studies, we did not find an association between exposure to NO2 levels at baseline and asthma status or severity. Our findings contradict the results of most recent studies of both NO2 levels and residential sources of NO2 and their effects on asthma symptoms in very young children. However, it remains difficult to compare our results we those of previous published studies because those studies primarily focused on children who were diagnosed with asthma, whereas our research included preschool aged children with and without asthma. Based on our findings and the fact they conflict with other epidemiological studies, of which there were also conflicting results, we feel that the relationship between asthma symptoms and NO2 exposures remains ambiguous. The lack of consistent results of epidemiological research raises questions that should be the focus of future epidemiological studies. What are the roles of co-pollutants and co-risk factors? Does NO2 work alone or in concert with other indoor pollutants? There exists a real lack of understanding on the possible synergistic effects of exposure to NO2 and other combustion byproducts. Important to furthering our knowledge of the role of exposure to indoor NO2 and asthma is determining whether NO2 acts as a surrogate for co-pollutants that are considered risk factors for asthma and other respiratory conditions. Another focus of future indoor pollution studies should be the development of effective methods and technologies for measuring the constituents of the complex mixture of pollutants in indoor air; these methods and technologies can then be applied in personal monitoring of exposure to indoor pollutants in epidemiological studies that would help to determine with much more accuracy the effects of individual indoor pollutants on asthma and other respiratory symptoms. This knowledge would help in the development of more effective public health and environment policies towards reducing the burden of childhood asthma.

The air that we breathe remains a growing problem, with environmental air pollution generated by traffic, industry, and households continuing to be a serious public health issue. Increasing industrialization and the rapid expansion of urban environments across society mean that, for many, exposure to pollutants is unavoidable. Recent estimates suggest that air pollution is responsible for between 3 and 7 million deaths worldwide per year accompanied by high levels of morbidity (3.1% of global disability-adjusted life years) and associated economic risks (£16 billion per year in the United Kingdom alone). A recent report placed both indoor and outdoor air pollution within the top ten risk factors for all-cause disease, greater than that caused by risk factors such as sedentary lifestyle or high cholesterol. Importantly, the majority of deaths are caused by cardiovascular-related disease. This chapter provides an overview of how air pollution can have multiple detrimental effects on cardiovascular health.

Atmospheric pollution is a well-known environmental hazard, especially in developing countries where millions of people are exposed to airborne pollutant levels above safety standards. Accordingly, several epidemiological and animal studies confirmed its role in respiratory and cardiovascular pathologies and identified a strong link between ambient air pollution exposure and adverse health outcomes such as hospitalization and mortality. More recently, the potential deleterious effect of air pollution inhalation on the central nervous system was also investigated and mounting evidence supports a link between air pollution exposure and neurodegenerative pathologies, especially Alzheimer’s disease (AD). The focus of this review is to highlight the possible link between ozone air pollution exposure and AD incidence. This review’s approach will go from observational and epidemiological facts to the proposal of molecular mechanisms. First, epidemiological and postmortem human study data concerning residents of ozone-severely polluted megacities will be presented and discussed. Then, the more particular role of ozone air pollution in AD pathology will be described and evidenced by toxicological studies in rat or mouse with ozone pollution exposure only. The experimental paradigms used to reproduce in rodent the human exposure to ozone air pollution will be described. Finally, current insights into the molecular mechanisms through which ozone inhalation can affect the brain and play a role in AD development or progression will be recapitulated.

An air quality monitoring network (AQMN) is a basic piece of environmental management due to that it satisfies the major role in monitoring of environment emissions, in special relevance to target air pollutants. An adequate installation would lead to support high efficiency of the network. Therefore, AQMN pre-layout should be considered as an essential factor in regarding with the location of fixed measurement stations within AQMN, as the minimum number of sampling points. Nevertheless, once AQMN has been already installed, and given that the spatial air pollutants pattern can vary along time, an assessment of the AQMN design would be addressed in order to identify the presence of potential redundant fixed monitoring stations. This approach would let to improve the AQMN performance, reduce maintenance costs of the network and consolidate the investment on those more efficient fixed stations. The chapter includes aspects relative to air pollutants measured by networks, their representativeness, limitations, importance, and the future needs. It ponders the need of re-assessment of the AQMN layout for assuring (i) a right evaluation of the human being exposure to atmospheric pollutants and controlling the environmental emissions into the atmosphere and (ii) an adequate performance of the network along time.

Urban air pollution has become a salient environmental issue in many Asian countries due to their rapid industrial development, urbanization, and motorization. Human-induced air pollution has been and continues to be considered a major environmental and public health issue. Its severity lies in the fact that high levels of pollutants are produced in environments where damage to human to concentration, duration of exposure health and welfare is more likely. This potential is what makes anthropogenic air pollution an important concern. Extreme air pollution episodes were reported for the Meuse Valley, Belgium, in 1930; Donora, PA, and the Monongehela River Valley in 1948; and London in 1952. These episodes are significant in that they provided solid scientific documentation that exposure to elevated ambient pollutant levels can cause acute illness and even death. The most devastating events contributed to important efforts to control ambient air pollution. The International Agency for Research on Cancer (IARC) assessment concluded that outdoor air pollution is carcinogenic to humans, with the particulate matter component of air pollution mostly associated with increasing cancer incidence especially lung cancer. Pollutant effects typically occur in some target organs. These can be straightforward; i.e. pollutants come into close contact with the affected organ. Such is the case for eye and respiratory irritation. Effects may be indirect. For example, Pollutants can enter the bloodstream from the lungs or gastrointestinal system through the respiratory route. Effects may then be distant from the immediate organ of contact. A target organ can have no immediate and intimate contact with atmospheric contaminants. The primary organs or target organs are the eyes and the respiratory and cardiovascular systems.

It has long been known that atmospheric pollutants can be hazardous to human health and ecosystems. This includes effects from episodic peak levels as well as the long-term exposure to relatively moderate concentration enhancements. Environmental issues related to air pollution include acidification, mostly by the strong acids from sulphur and nitrogen oxides, eutrophication by the deposition of reactive nitrogen compounds, the reduction of air quality by photo-oxidants and particulate matter, and the radiative forcing of climate by increasing greenhouse gases and by aerosol particles. Many air pollutants are photochemically formed within the atmosphere from emissions by traffic, energy generation, industry, the burning of wastes, and forest fires. The Mediterranean basin in summer is largely cloudfree, and the relatively intense solar radiation promotes the photochemical formation of ozone (O3) and peroxyacetyl nitrate (PAN); O3 being health hazardous at levels in excess of about 100 μg/m3. Ozone is formed in the lower atmosphere as a by-product in the oxidation of reactive carbon compounds such as carbon monoxide (CO) and non-methane volatile organic compounds (NMVOC), catalysed by nitrogen oxides (NOx ≡ NO + NO2). In summer, notably the period from June to August, transport pathways of air pollution near the earth’s surface are typically dominated by northerly winds, carrying photo-oxidants and aerosol particles from Europe into the Mediterranean basin. Aerosol particles with a diameter of less than ∼10 μm (PM10) can have adverse health effects at a concentration of about 30 μg/m3 or higher. The fine mode particles (<2 μm diameter) are mostly composed of sulphates, nitrates, and particulate organic matter, whereas the coarse mode particles (≥2 μm) often contain substantial amounts of sea salt, Saharan dust (Chapter 14), and other mineral components. The aerosols can form widespread hazes that scatter and absorb solar radiation, thus reducing downward energy transfer and surface heating. Increased aerosol scattering causes a negative radiative forcing of climate (cooling tendency), to be weighted against the positive radiative forcing (warming tendency) by increasing greenhouse gases such as carbon dioxide (CO2), methane (CH4), nitrous oxide (N2O), halocarbons, and tropospheric ozone (IPCC 2001).

Background: Air pollution has been consistently linked with dementia and cognitive decline. However, it is unclear whether risk is accumulated through long-term exposure or whether there are sensitive/critical periods. A key barrier to clarifying this relationship is the dearth of historical air pollution data. Objective: To demonstrate the feasibility of modelling historical air pollution data and using them in epidemiological models. Methods: Using the EMEP4UK atmospheric chemistry transport model, we modelled historical fine particulate matter (PM2.5) concentrations for the years 1935, 1950, 1970, 1980, and 1990 and combined these with contemporary modelled data from 2001 to estimate life course exposure in 572 participants in the Lothian Birth Cohort 1936 with lifetime residential history recorded. Linear regression and latent growth models were constructed using cognitive ability (IQ) measured by the Moray House Test at the ages of 11, 70, 76, and 79 years to explore the effects of historical air pollution exposure. Covariates included sex, IQ at age 11 years, social class, and smoking. Results: Higher air pollution modelled for 1935 (when participants would have been in utero) was associated with worse change in IQ from age 11–70 years (β = −0.006, SE = 0.002, p = 0.03) but not cognitive trajectories from age 70–79 years (p > 0.05). There was no support for other critical/sensitive periods of exposure or an accumulation of risk (all p > 0.05). Conclusion: The life course paradigm is essential in understanding cognitive decline and this is the first study to examine life course air pollution exposure in relation to cognitive health.