ABSTRACT Background: Asthma is a chronic lung disease that inflames and narrows the airways. This results in recurrent episodes of coughing, wheezing, shortness of breath, and chest tightness. Although the causes of asthma are poorly understood, genetic and environmental factors have been implicated in the development and exacerbation of the disease. Among environmental risk factors, cigarette smoke is a well-known risk factor to trigger asthma symptoms. Exposure to secondhand smoke irritates the airways and may trigger an attack in adults with asthma. Smoke-free laws and regulations in the United States differ by state. The enforcement of smoke-free legislation has been related to asthma rates as it has been shown that they lead to a sustained drop in emergency hospital admission for asthma among adults. These laws and regulations are also necessary in reducing smoking rate and secondhand smoke exposure. Objective: The purpose of this thesis is to examine the association between tobacco smoke rates and asthma status among adults at the national and state levels and to evaluate the effects of state smoke-free laws and regulations on tobacco smoking rate among adults with asthma. Methods: The Centers for Disease Control and Prevention’s 2009–2010 Behavioral Risk Factor Surveillance System data was used for the analyses. SAS-callable SUDAAN (version 10.0.0, RTI International, NC) was utilized to account for the complex sampling design of the BRFSS, and sample weights were used to produce estimates that were generalizable to the state and U.S. adult population. In addition to calculating descriptive statistics, chi-square tests and multivariate logistic regression were used to test for group differences and association between variables of interest. State level smoking rates were ranked to identify states that are in the lower and upper 20th percentiles and compare them with states’ smoke-free laws and regulation status. Results were considered significantly different if 95% confidence intervals (CIs) did not overlap or if statistical testing at p<0.05 was applicable. Results: Asthma prevalence rates are higher among adults that smoke cigarettes (10.5%, [aPR] =1.2) compared to non-smokers (7.8%, [aPR] =1.0). Of the 869,519 adult respondents in the survey, 8.5% reported having asthma. Nearly one-fifth (17.2%) of adults without asthma smoked cigarettes, while (21.7 %) of adults with asthma smoked. Females (10.5%) had higher asthma prevalence rates than males (6.4%). Black persons (10.0%), persons of American Indian (13.0%) descent had higher, and those of Hispanic (6.7%) descent had lower asthma rates than white persons (8.6%). Adults with a high school education or less (9.1%) had higher asthma rates than those with an education level that was equivalent to a 4 year college or more (7.3%) , and those with low income (<$15,000) had higher rates (13.3%) than those with high income (6.8%). Percentage of male (23.4%) and females (20.7%) with asthma who smoke are higher than those that do not smoke (19.3% and 15.1%, respectively). Asthma prevalence rates and smoking rates vary by geographic location. Smoking rates among adults with asthma was highest in the South (LA, AL, SC, TN, OK, MS, AR, WV, KY) and a couple of Midwest states (OH, IN,). Evaluating the association between the 2008 State of Tobacco Control Report and smoking rate among adults with asthma by state showed a statistically significant relationship between smoking rate among adults with asthma and smoke-free policy and regulation at the state and national level. On average, states with the lowest smoking rate among persons with asthma (smoking rates less than 20th percentile) had significantly higher smoke-free policy grades (mean grade [sd]=7.2 [1.99]) than states with a high smoking rate (smoking rate of 80th percentile or more) (mean grade [sd]=2.0 [2.00]) (p-value < 0.00001). Conclusion: Although most U.S. state smoke-free policies and regulations are relatively new, it is evident that these laws are effective in promoting cessation among adults and reducing nonsmokers’ exposure to secondhand smoke. The study found that smoke-free laws may improve health by lowering asthma prevalence and smoking rates among adult smokers. Also, these policies in turn protect non-smokers from the harmful health effects of secondhand smoke.

In verschiedenen Studien konnte eine Korrelation im Auftreten von Übergewicht bzw. Adipositas und Asthma bronchiale sowohl bei Erwachsenen als auch bei Kindern festgestellt werden. Als Hintergrund für diesen Zusammenhang werden aktuell verschiedene Theorien, die die biochemischen, genetischen und Lebensstil-abhängigen Ursachen betrachten, diskutiert. In dieser Arbeit wurden die Ursachen für Übergewicht und Asthma sowie der Zusammenhang zwischen beiden Erkrankungen innerhalb der LISA-Studie untersucht. Hierbei handelt es sich um eine prospektive Geburtskohortenstudie, wobei insgesamt 3097 Neugeborene zwischen 1997-1999 aus 4 verschiedenen deutschen Städten rekrutiert worden sind. In regelmäßigen zeitlichen Abständen wurden mittels standardiesierten Fragebögen Daten zu Lebensbedingungen und Gesundheitszustand der Kinder erhoben. Als statistische Methode wurden vorwiegend logistische Modelle erstellt, sodass Odds Ratios in einem multivariaten Zusammenhang angegeben werden konnten. Ergebnisse: Als signifikante Risikofaktoren für Übergewicht im Alter von 5 Jahren stellten sich heraus: Mütterliches Übergewicht (OR: 2,05; KI:1,22-3,46), väterliches Übergewicht (OR: 1,77; KI: 1,02-3,06). Rauchen der Mutter im 1. Trimenon der Schwangerschaft (OR: 2,10; KI: 1,16-3,80). Geburtsgewicht des Kindes > 90. Perzentile (OR: 2,80; KI: 1,63-4,80). Niedriger Bildungsstand der Eltern (OR: 3,41; KI: 2,04-5,71), Zeitdauer,die pro Tag vor einem Bildschirm verbracht wird, > 1 Stunde (OR: 2,12; KI: 1,23-3,65). Für die Entwicklung eines Asthma bronchiale bis zum 6. Lebensjahre wirkten in der LISA-Studie folgende Faktoren als signifikante Einflüsse: eine positive Familienanamnese (OR: 4,57; KI: 2,69 – 7,77), ein männliches Geschlecht ( OR: 1,70; KI: 1,02 – 2,83), Rauchen während der Schwangerschaft ( OR: 2,05; KI: 1,04 – 4,02), Wohnen an einer Haupstraße bis zum 6. Lebensmonat (OR:1,72; KI:1,02 – 2,95) sowie das Renovieren der Wohnung während der Schwangerschaft und im 1. Lebensmonat (OR: 2,13; KI: 1,03 – 4,39). Anhand unserer Daten konnte insgesamt eher geschlossen werden, dass bei dem besprochenen Zusammenhang Übergewicht bzw. Adipositas den Risikofaktor für Asthma bronchiale darstellen. Bei der Untersuchung im logistischen Modell waren hierbei ein sehr hoher Geburts-BMI (OR: 2,06; KI: 0,95 – 4,47) und Übergewicht im Alter von 5 Jahren (OR: 2,26, KI: 0,93 – 5,50) in der Tendenz als Risikofaktor zu sehen. Für Adipositas mit 5 Jahren konnte auch im logistischen Modell ein signifikanter Einfluss auf die Entwicklung eines Asthma bronchiale gesehen werden (OR: 6,48; KI: 1,91 – 21,96 )

Thesis (Ph. D.)--University of Missouri--Columbia, 2001. / "December 2001." Typescript. Vita. Includes bibliographical references (leaves 111-120). Also available on the Internet.

Source: Masters Abstracts International, Volume: 47-06, page: 3545. Adviser: Benjamin S. Bradshaw. Includes bibliographical references.

Includes bibliographical references.

Asthma is a complex, chronic disorder of the airways that is characterized by underlying inflammation, airflow obstruction, and bronchial hyperresponsiveness. Asthma symptoms can be frightening and can have an effect on the emotional functioning Quality of Life (QOL) of school-aged children who have asthma. The purpose of this exploratory, descriptive, cross-sectional, correlational study was to explore the influence of factors identified in the literature on school-aged children’s emotional responses to asthma. Guiding this study was a theoretical model that proposed that the impact of chronic illness severity on QOL is potentially mediated by both resource and barrier factors. The population of interest was 85 school-aged children (ages 6-12) and parents of children who have asthma that were recruited from participants already enrolled in year 4 of the Asthma in Central Texas (ACT) study (R01NR007770, Sharon D. Horner, P.I.) at The University of Texas at Austin. Significant inverse correlations were found between asthma related child emotional functioning QOL and each of the following variables: asthma severity, r = -.30, p < .01; child internalizing behaviors, r = -.26, p < .05, and child externalizing behaviors, r = -.43, p < .001. Significant inverse relationships were found between caregiver emotional functioning QOL and each of the following variables: asthma severity, r = -.39, p < .001; child internalizing behaviors, r = -.22, p < .05 and child externalizing behaviors, r = -.25, p < .05. Multiple regression analysis revealed that asthma severity and child externalizing problems accounted for 26% of the variance in child emotional functioning QOL. No moderators or mediators were identified. Findings from this study imply that externalizing problem behaviors of school-aged children may be a predictor of their negative feelings about their asthma. Nursing educators should consider including the emotional impact of asthma on children in nursing curriculums as this may ultimately influence health care providers to more skillfully address this important issue in both assessment and intervention settings. / text

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Background: Asthma exacerbations are a leading cause of school absenteeism and time lost from work, affecting the quality of life (QOL) of children with asthma and their caregivers. Objective: The objective of this study was to determine the relationship between measures of asthma severity and the QOL of children with asthma and their caregivers living in rural Saskatchewan. Methods: Data for this research was previously collected in 2005-2007 using a case-control study design. Children were recruited for the case control study following a cross-sectional school based survey of children aged 6-18 years. Cases with physician-diagnosed asthma (n=77) were then selected to examine associations between asthma severity and QOL, with respiratory information collected from a home visit, clinic visit and two-week home monitoring of diurnal peak flow variability (DPV). During the clinic visit, children underwent spirometry and completed the Pediatric Asthma QOL Questionnaire (PAQLQ). During the home visit, parents completed the Child Health Questionnaire (CHQ-PF50) and the Pediatric Asthma Caregiver QOL Questionnaire (PACQLQ) and were given instructions on how to complete the two-week diurnal peak flow home monitoring. Higher mean scores on measures of QOL questionnaires indicated better QOL. Asthma severity was measured by Forced Vital Capacity (FVC), Forced Expiratory Volume in one Second (FEV1), and mean DPV. Linear regression was used to assess the association between the three QOL measures and measures of asthma severity (mean diurnal peak flow variability and percent predicted lung function adjusting for smoking, parental education and asthma medication use in the last 12 months). Results: The lowest QOL score on the PAQLQ completed by the children was being bothered by physical activity (mean = 5.8, standard deviation = 1.19) whereas the lowest mean score on the PACQLQ completed by parents was feeling helpless or frightened (mean = 6.1, standard deviation = 1.28). No significant relationships were found between QOL scales. When the PACQLQ and the PAQLQ were stratified by age groups, parents reported higher mean scores for children in the 13-17 age group (p = 0.01) on the total score of the PACQLQ and activity and emotional subscales (p = 0.003 and 0.03, respectively). No significant correlations were found between spirometry measurements and the three QOL measures. Significant negative correlations were found between mean DPV and the mean PAQLQ Total Score. In a post hoc analysis, examining minimum morning peak flow expressed as percent recent best and QOL, significant positive correlations were found between the minimum morning peak flow measurements and the mean PAQLQ Total Score and Activity subscale. Conclusions: While findings from this study suggest that the CHQ-PF50 could be used to assess emotional aspects of QOL in children with asthma, overall, it may not be a useful tool in assessing the QOL of children with asthma. Peak flow may be a better measure of asthma severity than spirometry when assessing QOL for children with asthma and their parents.

No description available.

Several genes are associated with an increased susceptibility to respiratory diseases, including asthma, which may be exacerbated by ambient air pollution. These genes include the Gluthathione-S-Transferase family (GSTM1 and GST1l) and the NAD(P)H quinone oxidoreductase (NQO1). This, the first genetic epidemiological study conducted in Sub-Saharan Africa had 2 main objectives: I) to evaluate whether the above genotypes confer susceptibility to asthma and related phenotypes; and 2) to investigate if polymorphisms in these genes known to modulate the response to or protect from epithelial oxidative damage modify pulmonary response to ambient air pollutants. A total of 369 schoolchildren from seven primary schools in a heavily industrialized region of south Durban and a demographically similar area in north Durban, Kwa-Zulu Natal, South Africa during the period May 2004 - October 2005, participated in the study. DNA was extracted from whole blood using the GENTRA Puregene kit. Genotyping for the GSTM1 (null vs present genotype) was done using multiplex PCR while the GSTP1 (I1e105Val; AA>AG/GG) and the NQO1(Pro/Ser; CC>CT/TT) genotypes were determined using real time PCR and Taqman probes (Applied Biosystems). Persistent asthma and asthma of "any severity" was determined by questionnaires based on the ATS and BRMC questionnaires. Positive atopy was determined by at least one positive skin test reaction to the seven allergens tested. Other health assessments included spirometry, methacholine challenge testing and four cycles of three-week serial peak flow measurements. Acute respiratory measures included within day variability in FEV1 and PF and the lowest valid values on a given day. SO2. NO2, NO and PM10 were measured over a year using ultraviolet fluorescence, gas-phase chemiluminescence and gravimetric methods respectively. STATA (version 9, College Station, TX, USA) was used for data analysis. Multiple logistic models and Pearson's chi-squared tests were used to evaluate the association between asthma, BHR, atopy and genotype. Covariate-adjusted generalised estimating equations (GEE) with lags of 1-5 days were used to evaluate genotype effect modification of exposure-response. The GSTM1 gene deletion (GSTM1null) was detected in 28.9% of the study population while the distribution of GSTP1 AG/GG and the NQO1 CT/IT polymorphisms were 64.9% and 36.0% respectively. Multiple regression with the adjustment for relevant covariates indicated that individuals carrying one or more copies of the GSTP 1 minor allele had a statistically significant risk for persistent asthma. GSTM1 and NQO1 genotypes showed no significant association with any of the respiratory outcomes tested. However, we found a protective effect for those individuals carrying the GSTM1null genotype and at least one Ser allele (NQO1 CT/TT) for persistent asthma and marked BHR (OR = 0.7, Cl: 0.3-1.5 and OR= 0.3, Cl: 0.0-1.9 respectively). This protective effect is consistent with the role of NQO1 in metabolic activation. Children from the south schools had almost twice the risk of persistent asthma (OR=2.0, Cl: 1.2-3.2, p<.005) and 3 times the risk of BHR (OR=3.5, Cl: 1.4-8.4, p<.005) than those from the schools in the north. Based on symptoms, 20.4% of children from the random sample had persistent asthma and 10.3% had marked BHR (PC20< 2mg/ml). The GEE model results were consistent with modification of air pollutant-pulmonary function relationships by oxidative stress associated genotypes. Statistically significant gene*environment interactions with NO2, NO, and PM10 using FEV1 and PEF outcomes in the expected direction were more frequent for GSTP1 AA and NQO1 CC genotypes (interaction p-values <0.05). There were very few gene*environment interactions for SO2 and any of the 3 SNPs tested. The most striking finding in our study was that pollutant exposure, especially oxides of nitrogen and PM10, even at levels below the recommended limits of South African guidelines, is associated with poorer lung function and that this association is significantly modified by an individual's genotype, particularly the GSTMlnull, GSTPIAA and NQOICC genotypes. Children with the GSTMlnull GSTPI AG/GG, GSTPI AG/GG NQOI CC and GSTMlpos NQOICC gene-gene combinations showed a significant interaction with NO2, NO, and PM10 with decrement in lung function measures. The increased risk to air pollution conferred by the GSTPI and GSTMl genotypes may have clinical and public health importance because this variant is common in most populations. The findings suggest that the risk of developing respiratory symptoms is increased when genetic susceptibility is included with environmental exposures. Our models suggest significant gene*environment interactions i.e the response to the level of air pollutants, as indicated by variability in pulmonary function measures, is modified by genotype. The heightened allergic airway response may be a consequence of a decreased capacity to mount an effective cytoprotective response to oxidative stress. Studying genes may inform us about the biology of asthma which may lead to new therapies or preventative strategies. This study supports the importance of further investigation on these and other genotype variants involved in oxidative stress and respiratory phenotypes in larger cohorts. / Thesis (Ph.D.)-University of KwaZulu-Natal, Durban, 2008.