Simpler methods of assessing respiratory function and their application in infancy

The need to develop and evaluate simple non-invasive tests to measure respiratory function in wheezy infants, in order to investigate the physiological basis of lung disease and move towards a more rational basis for the treatment of airway disease in infancy was well recognised at the inception of this work. The main aims of this thesis were: to evaluate simpler methods of assessment of lung function such as the tidal breathing parameter tPTEF:tE, passive respiratory mechanics using the Single Breath technique and the rapid thoraco-abdominal compression technique (RTC) by comparison with established "gold standard" techniques, and: to address applications of such assessments, when comparing respiratory function in survivors of each limb of the Collaborative ECMO trial. tPTEF:tE and specific airway conductance were measured in healthy infants and those with recurrent wheezing and it was found that both parameters were significantly lower in the wheezy compared to the healthy group. There was a significant although weak association between these variables in infants, irrespective of prior wheezing status, which was also confirmed in the ECMO Respiratory Follow-up population. Although a variable relationship between respiratory and airway resistance was found, both were significantly higher in infants with prior wheeze. Measurements obtained using the Single Breath technique had a relatively high failure rate. Inter observer variability was compared within and between two specialised infant lung function testing centres and a strategy developed for performing and analysing infant respiratory function tests to facilitate future similar trials. A collaborative approach to trials with infant respiratory function as an outcome measure appears feasible, providing close attention is paid to study design. Airway function was compared in survivors of the Collaborative ECMO trial. Respiratory function outcomes in those managed conventionally suggested that the larger proportion of these infants receiving respiratory medication and reporting respiratory symptoms may be attributed to subtle impairment of small airway function, relative to those assigned to ECMO. These findings probably reflected differences in neonatal management, since initial disease severity and background characteristics were similar in both groups

Effects of air pollution and the introduction of the London Low Emission Zone on the prevalence of respiratory and allergic symptoms in schoolchildren in East London: a sequential cross-sectional study

The adverse effects of traffic-related air pollution on children’s respiratory health have been widely reported, but few studies have evaluated the impact of traffic-control policies designed to reduce urban air pollution. We assessed associations between traffic-related air pollutants and respiratory/allergic symptoms amongst 8–9 year-old schoolchildren living within the London Low Emission Zone (LEZ). Information on respiratory/allergic symptoms was obtained using a parent-completed questionnaire and linked to modelled annual air pollutant concentrations based on the residential address of each child, using a multivariable mixed effects logistic regression analysis. Exposure to traffic-related air pollutants was associated with current rhinitis: NOx (OR 1.01, 95% CI 1.00–1.02), NO2 (1.03, 1.00–1.06), PM10 (1.16, 1.04–1.28) and PM2.5 (1.38, 1.08–1.78), all per μg/m3 of pollutant, but not with other respiratory/allergic symptoms. The LEZ did not reduce ambient air pollution levels, or affect the prevalence of respiratory/allergic symptoms over the period studied. These data confirm the previous association between traffic-related air pollutant exposures and symptoms of current rhinitis. Importantly, the London LEZ has not significantly improved air quality within the city, or the respiratory health of the resident population in its first three years of operation. This highlights the need for more robust measures to reduce traffic emissions

Induction and Mentoring of Beginning Researchers at Academic Colleges of Education in Israel

Obesity affects ethnic minority groups disproportionately, especially in the pediatric population. However, little is known about the impact of obesity on health-related quality of life (HRQoL) in children and adolescents from mixed-ethnic samples. The purpose of this study was to: 1) measure HRQoL in a mixed-ethnic clinical sample of obese children and adolescents, 2) compare HRQoL assessments in obese participants and healthy controls, and 3) compare HRQoL in obese children and adolescents according to their pubertal status

Annual mean levels of air pollutants at residential address, by year and averaged across study period, μg/m³.

<p>Values are mean ± SD (range);</p><p>* air pollution data were not available for two participants (one in each of Years 1 and 2 of the study) because their residential addresses were outside the Greater London area</p><p>Annual mean levels of air pollutants at residential address, by year and averaged across study period, μg/m³.</p

Odds ratios for associations of potentially confounding variables with prevalence of current respiratory/allergic symptoms.

<p>Data shown as odds ratio (OR) for unit increase in variable unless otherwise stated, with 95% confidence intervals in brackets; ORs adjusted for all variables shown in table; ETS exposure = positive urinary cotinine:creatinine ratio (CCR ≥ 30ng/mg);</p><p>* p<0.05</p><p>**p<0.01</p><p>Odds ratios for associations of potentially confounding variables with prevalence of current respiratory/allergic symptoms.</p

Prevalence of current respiratory/allergic symptoms among all children, and by sex and ethnicity.

<p>Percentages are for rows, except for first column which reads vertically (e.g. 49.9% of all respondents were male; 14.1% of males have current wheeze); percentages may not add to 100.0 due to rounding</p><p>Prevalence of current respiratory/allergic symptoms among all children, and by sex and ethnicity.</p

Exposure to air pollution as a risk factor for current and lifetime respiratory/allergic symptoms.

<p>Adjusted associations between air pollutants and the prevalence of current and lifetime respiratory/allergic symptoms. Odds ratios adjusted for age, sex, BMI, socio-economic deprivation (IMD score), ETS exposure and year of study, with a random effect for school. Single-pollutant models were calculated for each air pollutant. Odds ratios are for unit increase in pollutant, in μg/m³. Current symptoms defined as within the last 12 months; lifetime conditions defined as ‘having ever had’ asthma, hay fever or eczema. Vertical dotted line indicates null (OR = 1). Horizontal lines indicate 95% confidence intervals of odds ratios. * p<0.05, **p<0.01</p

Odds ratios for associations of potentially confounding variables with prevalence of lifetime (ever having had) asthma, hay fever and eczema.

<p>Data shown as odds ratio (OR) for unit increase in variable unless otherwise stated, with 95% confidence intervals in brackets; ORs adjusted for all variables shown in table; ETS exposure = positive urinary cotinine:creatinine ratio (CCR ≥ 30ng/mg);</p><p>* p<0.05</p><p>**p<0.01</p><p>Odds ratios for associations of potentially confounding variables with prevalence of lifetime (ever having had) asthma, hay fever and eczema.</p

Carbon in airway macrophages from children with asthma

BACKGROUND: Airway macrophage (AM) phagocytosis is impaired in severe asthma. Prostaglandin (PG) E2 and D2 are increased in severe asthma and suppress AM phagocytic function in vitro. In this study, we sought evidence for PG-mediated impairment of phagocytosis of inhalable carbonaceous particulate matter (PM) by AM in children with severe asthma compared with mild asthmatics and healthy controls. METHODS: AM were obtained from children with asthma and healthy controls using induced sputum. AM carbon area (μm(2)) was assessed by image analysis. In a subgroup of asthmatics, urinary PGE2 and PGD2 metabolites were measured by high-performance liquid chromatography, and PM exposure at the home address was modelled. Phagocytosis of PM by human monocyte-derived macrophages and rat AM was assessed in vitro by image analysis. RESULTS: AM carbon was 51% lower in children with moderate-to-severe asthma (n=36) compared with mild asthmatics (n=12, p<0.01) and healthy controls (n=47, p<0.01). There was no association between modelled PM exposure and AM carbon in 33 asthmatics who had a urine sample, but there was an inverse association between AM carbon and urinary metabolites of PGE2 and D2 (n=33, rs=-0.40, p<0.05, and rs=-0.44, p<0.01). PGE2 10(-6) M, but not PGD2 10(-6) M, suppressed phagocytosis of PM10 by human macrophages in vitro (p<0.05 vs control). PGE2 10(-6) M also suppressed phagocytosis of PM10 by rat AM in vitro (p<0.01 vs control). CONCLUSIONS: Phagocytosis of inhaled carbonaceous PM by AMs is impaired in severe asthma. PGE2 may contribute to impaired AM phagocytic function in severe asthma