Particulate matter (PM) air pollution is one of the major causes of death worldwide, with demonstrated adverse effects from both short-term and long-term exposure. Most of the epidemiological studies have been conducted in cities because of the lack of reliable spatiotemporal estimates of particles exposure in nonurban settings. The objective of this study is to estimate daily PM10 (PM < 10 μm), fine (PM < 2.5 μm, PM2.5) and coarse particles (PM between 2.5 and 10 μm, PM2.5-10) at 1-km2 grid for 2013-2015 using a machine learning approach, the Random Forest (RF). Separate RF models were defined to: predict PM2.5 and PM2.5-10 concentrations in monitors where only PM10 data were available (stage 1); impute missing satellite Aerosol Optical Depth (AOD) data using estimates from atmospheric ensemble models (stage 2); establish a relationship between measured PM and satellite, land use and meteorological parameters (stage 3); predict stage 3 model over each 1-km2 grid cell of Italy (stage 4); and improve stage 3 predictions by using small-scale predictors computed at the monitor locations or within a small buffer (stage 5). Our models were able to capture most of PM variability, with mean cross-validation (CV) R2 of 0.75 and 0.80 (stage 3) and 0.84 and 0.86 (stage 5) for PM10 and PM2.5, respectively. Model fitting was less optimal for PM2.5-10, in summer months and in southern Italy. Finally, predictions were equally good in capturing annual and daily PM variability, therefore they can be used as reliable exposure estimates for investigating long-term and short-term health effects.

Chronic obstructive pulmonary disease (COPD) is the fifth cause of morbidity and mortality in the developed world and represents a substantial economic and social burden. Patients experience a progressive deterioration up to end-stage COPD, characterised by very severe airflow limitation, severely limited and declining performance status with chronic respiratory failure, advanced age, multiple comorbidities and severe systemic manifestations/complications.COPD is frequently underdiagnosed and under-treated. Today, COPD develops earlier in life and is less gender specific. Tobacco smoking is the major risk factor for COPD, followed by occupation and air pollution. Severe deficiency for α₁-antitrypsin is rare; several phenotypes are being associated with elevated risk for COPD in the presence of risk factor exposure. Any patient presenting with cough, sputum production or dyspnoea should be assessed by standardised spirometry. Continued exposure to noxious agents promotes a more rapid decline in lung function and increases the risk for repeated exacerbations, eventually leading to end-stage disease.Without major efforts in prevention, there will be an increasing proportion of end-stage patients who can live longer through long-term oxygen therapy and assisted ventilation, but with elevated suffering and huge costs. Smoking prevention and smoking cessation are the most important epidemiological measurements to counteract chronic obstructive pulmonary disease epidemics.

Background: Noncommunicable diseases (NCDs) and chronic respiratory diseases (CRDs) are the main causes of mortality and morbidity worldwide. Methods: The main evidences about the NCDs and CRDs burden and related risk factors, from updated international reports and results of original researches, were collected and described in this review. Results: Most recent evidence is available from the Global Burden of Diseases Study (GBD) 2017 reports. There were 3.2 million deaths due to chronic obstructive pulmonary disease (COPD) and 495,000 deaths due to asthma. COPD was the seventh leading cause of years of life lost (YLLs). Overall, prevalent cases of CRDs were 545 million: about 50% for COPD and 50% for asthma. Incident cases of CRDs were 62 million, mostly due to asthma (69%) and COPD (29%). COPD accounted for 81.6 million disability-adjusted life years, asthma for 22.8 million. COPD prevalence of 9.1% has been found in a recent general population sample of North-Eastern Italy, while in Central Italy a 25-year follow-up of a general population sample has shown an increased prevalence of COPD and asthma up to 6.8% and 7.8%, respectively. In Central Italy, a COPD incidence of 8% and an asthma incidence of 3.2% have been found in adult subjects at an 18-year follow-up. Among the risk factors, a relevant role is played by smoking and high body mass index for asthma, while smoking, particulate matter pollution, ambient ozone pollution, occupational exposure to particulate matter, gases and fumes, as well as second-hand smoke, play an important role for COPD. Forecasting the YLLs by 2040 indicates a rising toll from several NCDs due to population growth and aging, with COPD expected to reach the fourth leading cause. Conclusions: Several recent studies and international reports highlighted the huge global health burden of CRDs and other major NCDs, pointing out the need for implementing international collaborations to fight this epidemic trend.

Asthma, rhinitis, and atopic dermatitis (AD) are interrelated clinical phenotypes that partly overlap in the human interactome. The concept of “one‐airway‐one‐disease,” coined over 20 years ago, is a simplistic approach of the links between upper‐ and lower‐airway allergic diseases. With new data, it is time to reassess the concept. This article reviews (i) the clinical observations that led to Allergic Rhinitis and its Impact on Asthma (ARIA), (ii) new insights into polysensitization and multimorbidity, (iii) advances in mHealth for novel phenotype definitions, (iv) confirmation in canonical epidemiologic studies, (v) genomic findings, (vi) treatment approaches, and (vii) novel concepts on the onset of rhinitis and multimorbidity. One recent concept, bringing together upper‐ and lower‐airway allergic diseases with skin, gut, and neuropsychiatric multimorbidities, is the “Epithelial Barrier Hypothesis.” This review determined that the “one‐airway‐one‐disease” concept does not always hold true and that several phenotypes of disease can be defined. These phenotypes include an extreme “allergic” (asthma) phenotype combining asthma, rhinitis, and conjunctivitis. Rhinitis alone and rhinitis and asthma multimorbidity represent two distinct diseases with the following differences: (i) genomic and transcriptomic background (Toll‐Like Receptors and IL‐17 for rhinitis alone as a local disease; IL‐33 and IL‐5 for allergic and non‐allergic multimorbidity as a systemic disease), (ii) allergen sensitization patterns (mono‐ or pauci‐sensitization versus polysensitization), (iii) severity of symptoms, and (iv) treatment response. In conclusion, rhinitis alone (local disease) and rhinitis with asthma multimorbidity (systemic disease) should be considered as two distinct diseases, possibly modulated by the microbiome, and may be a model for understanding the epidemics of chronic and autoimmune diseases.

Aims:To report on the relation between home mould and/or dampness exposure and respiratory disorders in a large sample of children and adolescents in Italy, accounting for age at time of exposure.Methods:20 016 children (mean age 7 years) and 13 266 adolescents (mean age 13 years) completed questionnaires on indoor exposures and respiratory symptoms/diseases. Statistical analyses were adjusted for sex, age, questionnaire’s compiler, area of residence, season of interview, parental educational status, family history of asthma, rhinitis, eczema, chronic obstructive pulmonary disease, presence of gas water heaters, passive smoking, pets, and active smoking (only for adolescents). Population attributable risk % (PAR) was also computed.Results:Asthma was more strongly related to only early than to only current exposure, both in children (OR 1.80, 95% CI 1.41 to 2.30) and adolescents (OR 1.89, 95% CI 1.38 to 2.59). The same result was found for rhino-conjunctivitis (OR 1.46, 95% CI 1.17 to 1.82), in children, and for wheeze among adolescents (OR 1.56, 95% CI 1.15 to 2.11). In children, wheeze (OR 1.98, 95% CI 1.47 to 2.66) and eczema (OR 1.44, 95% CI 1.09 to 1.91) were more strongly related to mould/dampness when exposed both early and currently; the same occurred in adolescents for rhino-conjunctivitis (1.78, 95% CI 1.30 to 2.45). Although persistent cough/phlegm was significantly related to mould/dampness exposure in children, regardless of exposure timing, no significant association between mould/dampness exposure and eczema or cough/phlegm was found among adolescents. PAR estimates were higher for only early than only current exposures. Avoiding early only exposure would abate wheeze by 6%, asthma or cough/phlegm by 7%, rhino-conjunctivitis in children by 4%, and in adolescents, asthma by 6%, and wheeze by 4%.Conclusions:Respiratory disorders such as wheeze and asthma can often be explained by exposure to home mould/dampness, especially early in life. The association seems more evident in children than in adolescents. These findings may suggest the need for environmental prevention strategies.