The medical literature has emphasized that aspiration of gastric contents or oral bacteria is a common cause of aspiration pneumonia. Swallowing disorders have been implicated in this disease but not studied at the time that aspiration pneumonia was diagnosed. A significant difference was found in the incidence of videofluoroscopically confirmed oropharyngeal swallowing problems in a group of patients diagnosed with aspiration pneumonia (AP) when compared with patients with nonaspiration pneumonia (NAP). Six of the 9 patients in the AP group aspirated during the videofluoroscopic evaluation and 2 others were considered to be at risk for aspiration. None of the 7 NAP patients demonstrated swallowing problems or aspiration. A significant difference in oral transit time also occurred between the two groups. Liquid was found to have a significantly faster oral transit time than paste or a cookie. Pharyngeal transit times were not found to be significantly different. Although there were only a small number of patients who met the criteria for this pilot study, a strong association was found between swallowing dysfunction and aspiration pneumonia.

SummaryBackgroundLow emission zones (LEZ) are an increasingly common, but unevaluated, intervention aimed at improving urban air quality and public health. We investigated the impact of London's LEZ on air quality and children's respiratory health.MethodsWe did a sequential annual cross-sectional study of 2164 children aged 8–9 years attending primary schools between 2009–10 and 2013–14 in central London, UK, following the introduction of London's LEZ in February, 2008. We examined the association between modelled pollutant exposures of nitrogen oxides (including nitrogen dioxide [NO2]) and particulate matter with a diameter of less than 2·5 μm (PM2·5) and less than 10 μm (PM10) and lung function: postbronchodilator forced expiratory volume in 1 s (FEV1, primary outcome), forced vital capacity (FVC), and respiratory or allergic symptoms. We assigned annual exposures by each child's home and school address, as well as spatially resolved estimates for the 3 h (0600–0900 h), 24 h, and 7 days before each child's assessment, to isolate long-term from short-term effects.FindingsThe percentage of children living at addresses exceeding the EU limit value for annual NO2 (40 μg/m3) fell from 99% (444/450) in 2009 to 34% (150/441) in 2013. Over this period, we identified a reduction in NO2 at both roadside (median −1·35 μg/m3 per year; 95% CI −2·09 to −0·61; p=0·0004) and background locations (−0·97; −1·56 to −0·38; p=0·0013), but not for PM10. The effect on PM2·5 was equivocal. We found no association between postbronchodilator FEV1 and annual residential pollutant attributions. By contrast, FVC was inversely correlated with annual NO2 (−0·0023 L/μg per m3; −0·0044 to −0·0002; p=0·033) and PM10 (−0·0090 L/μg per m3; −0·0175 to −0·0005; p=0·038).InterpretationWithin London's LEZ, a smaller lung volume in children was associated with higher annual air pollutant exposures. We found no evidence of a reduction in the proportion of children with small lungs over this period, despite small improvements in air quality in highly polluted urban areas during the implementation of London's LEZ. Interventions that deliver larger reductions in emissions might yield improvements in children's health.FundingNational Institute for Health Research Biomedical Research Centre at Guy's and St Thomas' National Health Service (NHS) Foundation Trust and King's College London, NHS Hackney, Lee Him donation, and Felicity Wilde Charitable Trust.

Recently, we reported that dyspnea on exertion is strongly associated with an increased oxygen cost of breathing in otherwise healthy obese women; the mechanism of dyspnea on exertion in obese men is unknown. Obese men underwent measurements of body composition, fat distribution, pulmonary function, steady state and maximal graded cycle ergometry, and oxygen cost of breathing. Nine men (34±8yr, 35±4 BMI) with ratings of perceived breathlessness of ≤ 2 during cycling, and ten men (36±9yr, 38±5 BMI) with ratings of perceived breathlessness ≥ 4 were studied (ratings of perceived breathlessness: 1.8±0.4 vs. 4.7±0.8, respectively; p<0.0001). Groups had only minor differences in fat distribution, pulmonary function, and steady state exercise. There was no association between ratings of perceived breathlessness and oxygen cost of breathing; but ratings of perceived breathlessness was strongly correlated with ratings of perceived exertion (RPE, rho=0.87, p<0.0001). The differences in exercise intensity, ventilatory demand, cardiovascular conditioning and/or the quality of respiratory sensation did not appear to play a role in the development of dyspnea on exertion. The mechanism of dyspnea on exertion in obese men seems unrelated to the oxygen cost of breathing.

-Exertional dyspnea limits exercise in some mitochondrial myopathy (MM) patients, but the clinical features of this syndrome are poorly defined, and its underlying mechanism is unknown. We evaluated ventilation and arterial blood gases during cycle exercise and recovery in five MM patients with exertional dyspnea and genetically defined mitochondrial defects, and in four control subjects (C). Patient ventilation was normal at rest. During exercise, MM patients had low V O2peak (28 Ϯ 9% of predicted) and exaggerated systemic O 2 delivery relative to O2 utilization (i.e., a hyperkinetic circulation). High perceived breathing effort in patients was associated with exaggerated ventilation relative to metabolic rate with high V E/V O2peak, (MM ϭ 104 Ϯ 18; C ϭ 42 Ϯ 8, P Յ 0.001), and V E/V CO2peak, (MM ϭ 54 Ϯ 9; C ϭ 34 Ϯ 7, P Յ 0.01); a steeper slope of increase in ⌬V E/⌬V CO2 (MM ϭ 50.0 Ϯ 6.9; C ϭ 32.2 Ϯ 6.6, P Յ 0.01); and elevated peak respiratory exchange ratio (RER), (MM ϭ 1.95 Ϯ 0.31, C ϭ 1.25 Ϯ 0.03, P Յ 0.01). Arterial lactate was higher in MM patients, and evidence for ventilatory compensation to metabolic acidosis included lower Pa CO 2 and standard bicarbonate. However, during 5 min of recovery, despite a further fall in arterial pH and lactate elevation, ventilation in MM rapidly normalized. These data indicate that exertional dyspnea in MM is attributable to mitochondrial defects that severely impair muscle oxidative phosphorylation and result in a hyperkinetic circulation in exercise. Exaggerated exercise ventilation is indicated by markedly elevated V E/V O2, V E/V CO2, and RER. While lactic acidosis likely contributes to exercise hyperventilation, the fact that ventilation normalizes during recovery from exercise despite increasing metabolic acidosis strongly indicates that additional, exercise-specific mechanisms are responsible for this distinctive pattern of exercise ventilation.hyperventilation; lactic acidosis; metaboreflex; exercise; oxidative phosphorylation EXERTIONAL DYSPNEA WAS FIRST described as a symptom that limited exercise in mitochondrial myopathy (MM) in patients with a familial disorder studied by Linderholm and coworkers in the 1960s (36, 38), a disease now recognized to be attributable to a mutation in the iron-sulfur cluster scaffold (ISCU) gene (40, 42) and associated with deficiency of multiple iron-sulfur proteins, including succinate dehydrogenase and aconitase (20,21). Exertional dyspnea has since been described as a dominant feature of exercise intolerance in other mitochondrial myopathies that severely restrict muscle oxidative phosphorylation (3a, 22). Moreover, mitochondrial disease has been suggested to be an underrecognized cause of unexplained exertional dyspnea (16,25), although, these reports lacked genetic confirmation and, in most cases, did not include biochemical assessment to indicate the presence and severity of the putative mitochondrial defect (16). To better define the physiological manifestations of exertional dyspnea in mitochondrial myopathy, we have evalu...

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.

The non-pharmacological breathlessness management programme appears to offer a wide range of benefits to patients, including improving functional capacity, coping strategies and self-control. Such benefits are most likely to be due to a combination of breathing control, activity management and the therapist qualities.

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Telomere length increased with increasing annual exposure to NO (model coefficient 0.003, [0.001, 0.005], p<0.001), NO (0.009 [0.004, 0.015], p<0.001), PM (0.041, [0.020, 0.063], p<0.001) and PM (0.096, [0.044, 0.149], p<0.001). There was no association with environmental tobacco smoke. Telomere length was increased in children reporting black ethnicity (22% [95% CI 10%, 36%], p<0.001) CONCLUSIONS: Pollution exposure is associated with longer telomeres in children and genetic ancestry is an important determinant of telomere length. Further studies should investigate both short and long-term associations between pollutant exposure and telomeres in childhood and assess underlying mechanisms.