Background: Air pollution contributes to an estimated six million deaths per year. Epidemiological and experimental studies show an association between air pollutant exposure and respiratory allergy. Objective:We aimed to write a narrative review of the epidemiology of air pollution-related respiratory-related allergic disorders (including asthma and allergic rhinitis) and the effects of air pollutants -with an emphasis on the particulate matter -on respiratory allergy-related health.Methods: PubMed Medline was searched, and representative epidemiologic and controlled-exposure studies were selected by using terms for air pollutants, particulate matter, and respiratory allergy including asthma and allergic rhinitis.Results: Epidemiological studies showed methodologic heterogeneity, including variability in study populations, geographical regions, types and sources of pollutants, methods for exposure estimation, approaches to controlling for confounding, and case definitions. This heterogeneity affected measures of association between studies. There is strong evidence to support an association between exposure to particulate matter and asthmatic exacerbations. Although data are inconclusive, several studies suggest exposure to particulate matter contributes to the development of asthma, allergic sensitization, and allergic rhinitis. Experimental studies, such as controlled-exposure studies, support a causal association between particulate matter and adverse health effects.Conclusions: Particulate matter exposure can exacerbate pre-existing asthma and may contribute to developing asthma, allergic rhinitis, and aeroallergen sensitization. Short-term and long-term strategies are needed to reduce disease severity and prevent new-onset disease development. Additional research is needed to identify effective avoidance strategies and therapeutic approaches.

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Background Ventilator-associated pneumonia (VAP) is a common nocosomial infection in intensive care unit (ICU). Local microbiological surveillance of pathogens and resistance patterns for early-onset VAP (EOVAP) and late-onset VAP (LOVAP) will help to choose appropriate empiric antibiotics. Objective To compare the multi-drug resistant (MDR) pathogens, treatment outcomes, and factors associated with hospital mortality of VAP. Method A cross-sectional study between 1 January 2015 and 31 December 2017 at Srinagarind hospital, Khon Kaen University was conducted. The demographic data, causative pathogens, hospital length of stay (LOS), ICU LOS, mechanical ventilator (MV) days, and hospital mortality were retrospectively reviewed. Results One hundred and ninety patients were enrolled; 42 patients (22%) were EOVAP and 148 patients (78%) were LOVAP. Acinetobacter baumannii was the most common pathogen in both groups (50% EOVAP vs 52.7% LOVAP). MDR pathogens were significant greater in LOVAP (81.8%) than EOVAP (61.9%) (p = 0.007). The EOVAP had a significantly better ICU LOS [median (interquartile range, IQR) 20.0 (11.0, 30.0) vs. 26.5 (17.0, 43.0) days], hospital LOS [median (IQR) 26.5 (15.0, 44.0) vs. 35.5 (24.0, 56.0) days] shorter MV days [median (IQR) 14.0 (10.0, 29.0) vs. 23.0 (14.0, 35.5) days] and lower hospital mortality (16.7% vs 35.1%) than LOVAP (p < 0.05). The factor associated with hospital mortality was having simplified acute physiology (SAP) II score ≥ 40 with an adjusted odds ratio (aOR) of 2.22 [95% confidence interval (CI), 1.08–4.54, p = 0.02]. Conclusion LOVAP had significantly higher MDR pathogens, MV days, ICU LOS, hospital LOS and hospital mortality than EOVAP. A broad-spectrum antibiotic to cover MDR pathogens should be considered in LOVAP. The factor associated with hospital mortality of VAP was a SAPII score ≥ 40.

BackgroundOn high-resolution computed tomography (HRCT), pulmonary artery (PA) dimensions may hint at the presence of pulmonary hypertension. We aimed to determine how accurately various measures of the PA, as viewed on HRCT, predict right heart catheterisation (RHC)-confirmed pulmonary hypertension.MethodsWe retrospectively reviewed patients who had HRCT and RHC between 2010 and 2018. Analyses considered respiratory cycle, pulmonary hypertension diagnostic criteria, time between HRCT and RHC, and subgroup analysis in interstitial lung disease (ILD) and chronic obstructive pulmonary disease (COPD).ResultsOf 620 patients, 375 had pulmonary hypertension. For pulmonary hypertension (defined as mean PA pressure (mPAP) ≥25 mmHg) and from HRCT performed within 60 days of RHC, main PA diameter (MPAD) ≥29 mm had a sensitivity, specificity, positive predictive value (PPV) and negative predictive value (NPV) of 88%, 42%, 0.70 and 0.70, respectively, while ratio of the diameter of the PA to the diameter of the ascending aorta (PA:Ao) ≥1.0 showed 53%, 85%, 0.84 and 0.54, respectively. In general, results were similar when the interval between HRCT and RHC varied from 7 to 60 days and when measured on expiratory images. In ILD, the sensitivity of MPAD was higher; in COPD, the specificity of PA:Ao was higher. There was moderately positive correlation between mPAP and inspiratory MPAD, PA:Ao, right PA diameter (RPAD), left PA diameter (LPAD) and (RPAD+LPAD)/2 (r=0.48, 0.51, 0.34, 0.34 and 0.36, respectively), whereas there was weak negative correlation between mPAP and PA angle (r= −0.24).ConclusionsFindings on HRCT may assist in the diagnosis of RHC-confirmed pulmonary hypertension. MPAD ≥29 mm had high sensitivity and PA:Ao ≥1.0 had high specificity. Compared with the entire cohort, MPAD had greater sensitivity in ILD and PA:Ao had higher specificity in COPD.