No description available.

No description available.

Chapter II describes results from 197 rural households that were sampled over five continuous days for indoor and outdoor PM10, PM2.5, and endotoxin. Geometric mean indoor concentrations of PM10 and PM2.5 (21.2 πg m-3, 12.2 πg m-3) were larger than outdoor concentrations (19.6 πg m-3, 8.2 πg m-3; p =0.072, p<0.001). While geometric mean endotoxin levels were almost six times larger in outdoor air compared to indoor (1.47 EU m-3, 0.23 EU m-3; p <0.001). Airborne PM10 and endotoxin concentrations in a rural county were elevated compared to those previously reported in certain urban areas. Furthermore, during the harvest season, concentrations of endotoxin in ambient air approached levels that have been shown to cause decreased respiratory function in occupational workers. Chapter III evaluated the effectiveness of using Radiello passive monitors to measure hydrogen sulfide (H2S) in close proximity (<40 m) to a medium sized CAFO. A total of eight passive H2S monitors were deployed 7-14 days around a swine confinement for seven months. Additionally, a separate laboratory study was carried out to determine the monitor's H2S uptake rate. Concentrations of H2S measured near the confinement were varied and ranged from 0.6 to 95 ppb depending on the sampling period and proximity to the lagoon .The uptake rate provided by the supplier (0.096 ng ppb-1 min-1) was significantly larger (p=0.002) than the rate determined experimentally (0.062 ng ppb-1 min-1). In Chapter IV we evaluated the association between residential proximity to swine operations and childhood asthma. A metric was created to determine children's relative environmental exposure to swine CAFOs which incorporated facility size and distance and direction of the CAFO to the home. When controlling for six significant asthma risk factors, children with a larger relative environmental exposure to CAFOs had a significantly increased risk of physician-diagnosed asthma (OR=1.20, p=0.009). In stratified analysis that adjusted for a respiratory infection before the age of two years, the association between relative exposure and childhood asthma was significantly increased in children with a respiratory infection (OR=1.45, p=0.001) but not in children free from respiratory infection (OR=1.12, p=0.355).

Asthma is a chronic inflammatory lung disease characterized by recurrent wheezing, coughing and difficulties in breathing. Asthma affects 25.7 million people in the USA including 8 million children. Asthma is often associated with early-life exposure to environmental insults. However, mechanisms that link early-life insults to persistent airway dysfunction are unknown. Our previous studies in mice showed that early-life allergen exposure increases the levels of neurotrophin 4 (NT4) causing airway smooth muscle (ASM) hyper innervation and persistent airway hyper reactivity (AHR). I show that early-life allergen exposure selectively increases cholinergic innervation. Notably, cholinergic nerves release acetylcholine, a potent airway constrictor that signals through the M3 receptor in ASM. Building upon these findings, my thesis encompasses two components. Firstly, how is NT4 expression aberrantly up regulated following early-life allergen exposure? Secondly, what is the effect of enhanced cholinergic innervation on the neonatal ASM? I find that NT4 is selectively expressed by ASM and mast cells in mice, nonhuman primates and humans. We show in mice that while NT4 expression in ASM remains unchanged upon allergen exposure, mast cells expand in number and degranulate to release NT4 thereby increasing NT4 levels in the lung. Adoptive transfer of wild-type mast cells, but not NT4-/- mast cells restores ASM innervation and AHR in KitW-sh/W-sh mice following early-life insults. In an infant primate model of asthma, the increased ASM innervation is also associated with the expansion and degranulation of mast cells. Therefore, pulmonary mast cells are a key source of aberrant NT4 expression following early-life insults in both mice and possibly primates. Next, I speculated that an increased cholinergic output in the neonatal lung might lead to persistent AHR. Using recurrent methacholine exposure and M3 receptor blocker, 4-DAMP, I show that enhanced cholinergic signaling in neonatal mice leads to persistent AHR without inflammation. In contrast, methacholine exposure in adult mice has no prolonged effects on airway reactivity. Together, my findings support a model in which deregulated neural activities following early-life insults cause persistent ASM hyper contractility. Thus, early-life interventions to block mast cell degranulation and the cholinergic pathway may benefit children with recurrent wheezing. / 2016-12-15T00:00:00Z

Despite advancements in asthma treatment and diagnosis, asthma still remains the number 1 cause for hospitalizations in school-aged children. This usability study aimed to develop a child-friendly interactive narrative, Okay with Asthma v2.0, based on the Biopsychosocial Family Model using feedback from children. This fun and kid-friendly program encourages children to manage their own asthma with the help of peers, families, communities, and health care services. With these support structures, children can identify and avoid triggers, monitor their asthma, manage their condition with medications based on an action plan, and learn to live happily with asthma.

Despite advancements in asthma treatment and diagnosis, asthma still remains the number 1 cause for hospitalizations in school-aged children. This usability study aimed to develop a child-friendly interactive narrative, Okay with Asthma v2.0, based on the Biopsychosocial Family Model using feedback from children. This fun and kid-friendly program encourages children to manage their own asthma with the help of peers, families, communities, and health care services. With these support structures, children can identify and avoid triggers, monitor their asthma, manage their condition with medications based on an action plan, and learn to live happily with asthma.

Les objectifs de cette thèse est d'examiner l'hypothèses selon laquelle les caractéristiques psychologiques constituent modificateur de la relation entre l'exposition aux polluants atmosphériques et l'asthme infantile. A cet effet, nous avons utilisé les données de l'Etude des 6 villes avec dessein transversale, et l'étude de cohorte mère-enfant de type longitudinale EDEN (Étude sur les Déterminants pré et postnatalsdu développement de la santé l'ENfant) pour examiner cette hypothèse.Les données ont montré qu'à la fois les polluants atmosphériques mesurés subjectivement et les polluants atmosphériques mesurés objectivement étaient associés à l'asthme infantile. Les analyses sur les relations entre les facteurs psychologiques et de l'asthme infantile ont montré une association entre les problèmes comportementaux et la prévalence de l'asthme et de l'eczéma, l'asthme sévère et l'apparition de l'asthme précoce dans l'Etude des 6 villes et la dépression pendant la grossesse était associée au developpement de la rhino-conjonctivite allergique au cours des 5 premières années de vie chez les enfants de l'étude EDEN. La prise en compte des interactions entre les polluants de l'air et les facteurs psychologiques ont montré que les relations entre les polluants de l'air et l'asthme infantile étaient modifiées par les facteurs psychologiques. En conclusion, nos résultats fournissent de nouvelles données sur les relations entre les polluants atmosphériques mesurés subjectivement et objectivement et/ou des facteurs psychologiques (problèmes comportementaux et de dépression maternelle pendant la grossesse) et l'asthme infantile, ce qui suggère de considérer les enfants ayant des problèmes psychologiques comme une population sensible aux effets néfastes des polluants atmosphériques et de prendre en compte ces ces facteurs simultanément dans le paradigme de la prévention de l'asthme infantile . / The purposes of this thesis are to examine the hypothesis according to which psychological features are a modifier of the relation between exposure to air pollution and childhood asthma. To this extent, we used the data from the cross-sectional French 6 Cities Study and the longitudinal EDEN (Study of pre- and post-natal determinants of children?s growth and development) mother-child cohort study to examine the hypothesis. The data show that both subjectively and objectively measured air pollutants were related to childhood asthma. The analyses on the relationships between psychological factors and childhood asthma and allergies yielded that children with behavioral problems had a higher odds ratio in relation to prevalences of asthma and eczema, asthma severity and early asthma onset in the French 6 Cities study and maternal depression during pregnancy was associated with the development of allergic rhinoconjunctivitis in the first 5 years of life in children of the EDEN mother-child cohort study. Taking into account the interactions between air pollutants and psychological factors, results showed that the relationships between air pollutants and childhood asthma were modified by psychological factors. In conclusion, our results add new evidence on the relationships between subjectively and objectively measured air pollutants and/or psychological factors (behavioral problems and maternal depression during pregnancy) and childhood asthma and imply to consider children with psychological problems as a population susceptible to the detrimental effects of air pollutants and take into account these factors simultaneously into the paradigm of childhood asthma prevention.

Childhood asthma is one of the most common chronic diseases worldwide, including in South Africa. There has been substantial evidence on the role of air pollution in asthma exacerbation but limited research on the role of climate change and how the interaction between climate change and air pollution is affecting childhood asthma, specifically in low and middle-income countries (LMICs). Temperature changes can be used as an effect of climate change to investigate the association between climate change, air pollution and childhood asthma. This study, therefore, used a case study approach aimed at examining the interaction between air pollution and temperature in exacerbating childhood asthma focusing on clinical data obtained from Red Cross War Memorial Children's Hospital, air quality data (City of Cape Town) and temperature data (South African Weather Services) for Cape Town, South Africa for three study years (2009, 2014 and 2019). The protocol (Part A) of the mini dissertation describes childhood asthma literature globally and in LMICs and specifically in South Africa. It also discusses the increasing incidences and prevalence of the disease and possible causes such as air pollution and climate change. Furthermore, it discusses the vulnerability of children to the exposure of interest, being air pollution (PM2.5, PM10, NO2 and O3) and climate change (i.e., temperature). Subsequently, the development of air quality standards is discussed, specifically concerning whether they consider the specific children's vulnerability to exposures. The protocol then describes the study population and methodologies for conducting this study. The journal ready article (Part B) presents the findings of the study. Spearman's correlation was used to measure the degree of association between temperature variables and air pollutants. The results indicated that diurnal temperature was associated with PM2.5 (r=0.579: p< 0.01) and PM10 (r=0.505: p< 0.01). A Poisson regression analysis was applied to evaluate the relationship between asthma exacerbation with air pollutants and temperature variables. In a univariate analysis there was a statistically significant relationship between asthma exacerbation and diurnal temperature for 2019, IRR=0.98 (95% CI,0.97 – 0.99) p< 0.05, maximum temperature 2014, IRR=0.99(95% CI, 0.98 - 1.00) p< 0.05 and for 2019, IRR=0.98(95% CI, 0.97 - 0.99) p< 0.01, average temperature 2014, IRR=0.99(95% CI, 0.98 - 1.00) p< 0.05 and for 2019, IRR=0.98(95% CI, 0.97 - 0.99) p< 0.01. Using a multivariate analysis there v of 110 was no significant relationship between childhood asthma exacerbation and air pollutants (PM10, NO2 and O3) except for PM2.5 IRR=0.12(95% CI, 0.01 - 0.81) p< 0.05. Diurnal temperature statistically significant childhood asthma predictor for 2009, IRR=1.02(95% CI, 1.00 - 1.05) p< 0.05 and for 2014, IRR=0.97(95% CI, 0.96 - 0.99) p< 0.01. Temperature increase, therefore, seems to be related to asthma exacerbation. More research is needed on the relationship between diurnal temperature, childhood asthma, and air pollutants to inform adaptation strategies. The findings of this study are important for the development of climate change and health adaptation and prevention strategies in South Africa, particularly in relation to heat adaptation. These findings are also relevant for the development of air quality guidelines and guidelines to address children, as the most vulnerable population to environmental health exposures. The appendices (Part C) present the analyses that were not included in the protocol (Part A) and article (Part B). These also include documents relating to the study such as ethics approval and permission to conduct research by different entities.

No description available.

Background: Asthma Link is a program that aims to increase adherence to inhaled corticosteroids among children with persistent asthma by delivering evidence-based school-supervised therapy. This program, which leverages existing infrastructure, improves asthma outcomes in children from low-income, minority families. Our aim was to elicit the perspectives of school nurses who supervise preventive medication administration. Methods: Semi-structured qualitative interviews were conducted with 12 school nurses participating in Asthma Link. Thematic analysis was used to identify themes related to barriers and facilitators to preventive medication delivery. Results: Barriers described by school nurses included communication challenges with families and providers, inconsistent supplies of the preventive medicine at school, and the perception by some families and nurses that preventive therapy should be provided at home. Facilitators included the ease of incorporating preventive medication delivery into morning routines, recognizing the positive impacts on children from families with limited resources, feeling part of the preventive health care team, and being well-positioned to engage families in preventive asthma care. Conclusions: To facilitate Asthma Link adoption, it is critical to incorporate school nurse feedback in the program’s protocol refinement. School-supervised asthma therapy programs are advised to engage school nurses in the opportunity to provide preventive care, streamline communication, and address social and logistical challenges which may impede families from bringing medication to school.