Explore the vast range of titles available.

Short-term exposure to air pollution has adverse effects among patients with asthma, but whether long-term exposure to air pollution is a cause of adult-onset asthma is unclear. We aimed to investigate the association between air pollution and adult onset asthma. Asthma incidence was prospectively assessed in six European cohorts. Exposures studied were annual average concentrations at home addresses for nitrogen oxides assessed for 23,704 participants (including 1,257 incident cases) and particulate matter (PM) assessed for 17,909 participants through ESCAPE land-use regression models and traffic exposure indicators. Meta-analyses of cohort-specific logistic regression on asthma incidence were performed. Models were adjusted for age, sex, overweight, education, and smoking and included city/area within each cohort as a random effect. In this longitudinal analysis, asthma incidence was positively, but not significantly, associated with all exposure metrics, except for PMcoarse. Positive associations of borderline significance were observed for nitrogen dioxide [adjusted odds ratio (OR) = 1.10; 95% CI: 0.99, 1.21 per 10 μg/m3; p = 0.10] and nitrogen oxides (adjusted OR = 1.04; 95% CI: 0.99, 1.08 per 20 μg/m3; p = 0.08). Nonsignificant positive associations were estimated for PM10 (adjusted OR = 1.04; 95% CI: 0.88, 1.23 per 10 μg/m3), PM2.5 (adjusted OR = 1.04; 95% CI: 0.88, 1.23 per 5 μg/m3), PM2.5absorbance (adjusted OR = 1.06; 95% CI: 0.95, 1.19 per 10-5/m), traffic load (adjusted OR = 1.10; 95% CI: 0.93, 1.30 per 4 million vehicles × meters/day on major roads in a 100-m buffer), and traffic intensity (adjusted OR = 1.10; 95% CI: 0.93, 1.30 per 5,000 vehicles/day on the nearest road). A nonsignificant negative association was estimated for PMcoarse (adjusted OR = 0.98; 95% CI: 0.87, 1.14 per 5 μg/m3). Results suggest a deleterious effect of ambient air pollution on asthma incidence in adults. Further research with improved personal-level exposure assessment (vs. residential exposure assessment only) and phenotypic characterization is needed.

Lipopolysaccharide (LPS) from Gram-negative bacteria has been one of the most studied pathogen-associated molecular patterns triggering rapid inflammatory reactions. However, evidence shows that not all LPS molecules are proinflammatory (“bad”), and that “good” LPS from gut commensal bacteria exert immunomodulatory actions. The Limulus amebocyte lysis test commonly used to quantify LPS in circulation, only targets “bad” LPS, when not inactivated by plasma components. Use of other methods showed healthy subjects featuring elevated levels of LPS (suggesting predominance of “good” or inactive LPS in circulation). This review aims to summarize the evidence supporting the higher abundance of “good” LPS coming from gut commensals of healthy individuals and their potential impact in human health.

Wastewater-based Epidemiology (WBE) was initially employed as a valuable tool for monitoring pathogens. Nowadays, WBE has expanded its original focus to the quantification of several “community-level metabolism” indicators to complement Public Health monitoring campaigns. Recently, wastewater isoprostanes have been suggested as biological indicators of oxidative stress and community anxiety levels during the COVID-19 pandemic. However, previous studies were lacking of concomitant quantifications linking isoprostanes in sewage with COVID-19 pandemic indicators. This study provides an application case to expand the application of a WBE approach for the investigation of community-wide oxidative stress levels and COVID-19 disease. We quantified the occurrence of three oxidative stress biomarkers in wastewater samples collected from two Italian cities (study sites A and B) from January to December 2022. Among the selected oxidative stress biomarkers, only 8-isoprostaglandin F2α (8-iso-PGF2α) and 5-iso Prostaglandin F2α-VI (5-iPF2α-VI) were detectable, while prostaglandin E2 (PGE2) was undetectable during the entire study period in both sites. The annual trend of 8-iso-PGF2α mass load and SARS-CoV-2 concentration in sewage was significantly and moderately cross-correlated, as a at study site A (Spearman’s rho = 0.62) and study site B (Spearman’s rho = 0.68). The same findings were confirmed for the cross-correlations including 8-iso-PGF2α concentrations instead of per capita mass load. A moderate and significant cross-correlation with the annual trend of monthly average daily COVID-19 cases (Spearman’s rho = 0.67) was observed for one study site and with a time lag = 1. Our findings support the hypothesis that human biomonitoring, via the quantification of oxidative stress biomarkers in sewage, can be effectively used to investigate the emerging field of the community-level metabolism.

Background Today, nanomaterials are broadly used in a wide range of industrial applications. Such large utilization and the limited knowledge on to the possible health effects have raised concerns about potential consequences on human health and safety, beyond the environmental burden. Given that inhalation is the main exposure route, workers exposed to nanomaterials might be at risk of occurrence of respiratory morbidity and/or reduced pulmonary function. However, epidemiological evidence regarding the association between cumulative exposure to nanomaterials and respiratory health is still scarce. This study focused on the association between cumulative exposure to nanomaterials and pulmonary function among 136 workers enrolled in the framework of the European multicentric NanoExplore project. Results Our findings suggest that, independently of lifelong tobacco smoking, ethnicity, age, sex, body mass index and physical activity habits, 10-year cumulative exposure to nanomaterials is associated to worse FEV 1 and FEF 25 − 75% , which might be consistent with the involvement of both large and small airway components and early signs of airflow obstruction. We further explored the hypothesis of a mediating effect via airway inflammation, assessed by interleukin (IL-)10, IL-1β and Tumor Necrosis Factor alpha (TNF-α), all quantified in the Exhaled Breath Condensate of workers. The mediation analysis results suggest that IL-10, TNF-α and their ratio (i.e., anti-pro inflammatory ratio) may fully mediate the negative association between cumulative exposure to nanomaterials and the FEV 1 /FVC ratio. This pattern was not observed for other pulmonary function parameters. Conclusions Safeguarding the respiratory health of workers exposed to nanomaterials should be of primary importance. The observed association between cumulative exposure to nanomaterials and worse pulmonary function parameters underscores the importance of implementing adequate protective measures in the nanocomposite sector. The mitigation of harmful exposures may ensure that workers can continue to contribute productively to their workplaces while preserving their respiratory health over time.

IntroductionObesity is a known risk factor for asthma. Although some evidence showed asthma causing obesity in children, the link between asthma and obesity has not been investigated in adults.MethodsWe used data from the European Community Respiratory Health Survey (ECRHS), a cohort study in 11 European countries and Australia in 3 waves between 1990 and 2014, at intervals of approximately 10 years. We considered two study periods: from ECRHS I (t) to ECRHS II (t+1), and from ECRHS II (t) to ECRHS III (t+1). We excluded obese (body mass index≥30 kg/m2) individuals at visit t. The relative risk (RR) of obesity at t+1 associated with asthma at t was estimated by multivariable modified Poisson regression (lag) with repeated measurements. Additionally, we examined the association of atopy and asthma medication on the development of obesity.ResultsWe included 7576 participants in the period ECRHS I-II (51.5% female, mean (SD) age of 34 (7) years) and 4976 in ECRHS II-III (51.3% female, 42 (8) years). 9% of participants became obese in ECRHS I-II and 15% in ECRHS II—III. The risk of developing obesity was higher among asthmatics than non-asthmatics (RR 1.22, 95% CI 1.07 to 1.38), and particularly higher among non-atopic than atopic (1.47; 1.17 to 1.86 vs 1.04; 0.86 to 1.27), those with longer disease duration (1.32; 1.10 to 1.59 in >20 years vs 1.12; 0.87 to 1.43 in ≤20 years) and those on oral corticosteroids (1.99; 1.26 to 3.15 vs 1.15; 1.03 to 1.28). Physical activity was not a mediator of this association.ConclusionThis is the first study showing that adult asthmatics have a higher risk of developing obesity than non-asthmatics, particularly those non-atopic, of longer disease duration or on oral corticosteroids.

Smoking is the main risk factor for most of the leading causes of death. Cessation is the single most important step that smokers can take to improve their health. With the aim of informing policy makers about decisions on future tobacco control strategies, we estimated time and age trends in smoking cessation in Europe between 1980 and 2010. Data on the smoking history of 50,228 lifetime smokers from 17 European countries were obtained from six large population-based studies included in the Ageing Lungs in European Cohorts (ALEC) consortium. Smoking cessation rates were assessed retrospectively, and age trends were estimated for three decades (1980-1989, 1990-1999, 2000-2010). The analyses were stratified by sex and region (North, East, South, West Europe). Overall, 21,735 subjects (43.3%) quit smoking over a total time-at-risk of 803,031 years. Cessation rates increased between 1980 and 2010 in young adults (16-40 years), especially females, from all the regions, and in older adults (41-60 years) from North Europe, while they were stable in older adults from East, South and West Europe. In the 2000s, the cessation rates for men and women combined were highest in North Europe (49.9 per 1,000/year) compared to the other regions (range: 26.5-32.7 per 1,000/year). A sharp peak in rates was observed for women around the age of 30, possibly as a consequence of pregnancy-related smoking cessation. In most regions, subjects who started smoking before the age of 16 were less likely to quit than those who started later. Our findings suggest an increasing awareness on the detrimental effects of smoking across Europe. However, East, South and West European countries are lagging behind North Europe, suggesting the need to intensify tobacco control strategies in these regions. Additional efforts should be made to keep young adolescents away from taking up smoking, as early initiation could make quitting more challenging during later life.

Background The relationship between diet, respiratory diseases and the mechanisms underlying their association are still poorly understood. In an adult sample, we investigated the associations between diet quality evaluated by two dietary scores (Italian Mediterranean Index (IMI), Modified Mediterranean Score (MDS)) and asthma and rhinitis prevalence. Additionally, total and differential white blood cells count, as inflammation indicators and two markers of oxidative stress, 8-iso-prostaglandin F 2α (8-isoprostane) and 8-oxo-dihydro-deoxyguanosine (8-OHdG), were measured. Methods A total of 1183 subjects (aged 20–84) in the frame of a population-based multi-case-control study were studied: 186 with current asthma (CA), 103 with past asthma (PA), 445 with rhinitis (RN) and 449 controls. Food intake was assessed by using the EPIC Food Frequency Questionnaire. 8-OHdG and 8-isoprostane were measured on spot urine and standardized by creatinine. Results A higher adherence to IMI was associated with a lower risk of CA (RRR: 0.50; 95%CI: 0.31;0.81; p  = 0.005), but not PA or RN. In CA a higher adherence to the Mediterranean diet (MD) was associated with a lower neutrophil percentage out of total leukocytes (p for trend = 0.022 and p  = 0.014 for IMI and MDS, respectively). Urinary 8-isoprostane was not associated with the MD adherence in any of the groups. In subjects with CA, those who were highly adherent according to MDS had higher 8-OH-dG urinary concentrations than non-adherents ( p  = 0.040) and in subjects with PA, they had lower 8-isoprostane than non-adherents ( p  = 0.026). Conclusions Our findings suggest that the MD might be a protecting factor for asthma, but not for rhinitis. The link between diet and asthma is probably the reduction in chronic inflammation, whereas oxidative stress does not seem to influence this relationship.

Background Air pollution can cause respiratory symptoms or exacerbate pre-existing respiratory diseases, especially in children. This study looked at the short-term association of air pollution concentrations with Emergency Room (ER) admissions for respiratory reasons in pediatric age (0–18 years). Methods Daily number of ER admissions in a children’s Hospital, concentrations of urban-background PM 2.5 , NO 2 , O 3 and total aeroallergens (Corylaceae, Cupressaceae, Gramineae, Urticaceae, Ambrosia, Betula) were collected in Turin, northwestern Italy, for the period 1/08/2008 to 31/12/2010 (883 days). The associations between exposures and ER admissions were estimated, at time lags between 0 and 5 days, using generalized linear Poisson regression models, adjusted for non-meteorological potential confounders. Results In the study period, 21,793 ER admissions were observed, mainly (81 %) for upper respiratory tract infections. Median air pollution concentrations were 22.0, 42.5, 34.1 μg/m 3 for urban-background PM 2.5 , NO 2 , and O 3 , respectively, and 2.9 grains/m 3 for aeroallergens. We found that ER admissions increased by 1.3 % (95 % CI: 0.3-2.2 %) five days after a 10 μg/m 3 increase in NO 2 , and by 0.7 % (95 % CI: 0.1-1.2 %) one day after a 10 grains/m 3 increase in aeroallergens, while they were not associated with PM 2.5 concentrations. ER admissions were negatively associated with O 3 and aeroallergen concentrations at some time lags, but these association shifted to the null when meteorological confounders were adjusted for in the models. Conclusions Overall, these findings confirm adverse short-term health effects of air pollution on the risk of ER admission in children and encourage a careful management of the urban environment to health protection.

To analyse the associations between chronic respiratory diseases and intakes of total flavonoids and their major subclasses (flavanones, anthocyanins, flavan-3-ols, flavonols, flavones, polymers and proanthocyanidins). Multi-case-control study. The analysis was conducted in the frame of the Genes Environment Interaction in Respiratory Diseases (GEIRD) study. The European Prospective Investigation into Cancer and Nutrition FFQ was used to ascertain dietary intake. Multinomial regression models adjusting for age, sex, centre, BMI, smoking habit, alcohol intake, education, total energy intake, vitamin C intake and total fruit intake were used to examine the associations between dietary exposures and the relative risk ratio (RRR) of being a case. Individuals (n 990) hierarchically defined as follows: cases with asthma (current, n 159; past, n 78), chronic bronchitis (n 47), rhinitis (allergic rhinitis, n 167; non-allergic rhinitis, n 142) and controls (n 97). An increase of 1 sd in flavanones was associated with a reduced risk of non-allergic rhinitis (adjusted RRR = 0·68, 95 % CI 0·47, 0·97); a similar result was found comparing the highest v. lowest quartile of flavanones intake (adjusted RRR = 0·24, 95 % CI 0·10, 0·59). Flavonoids contained in fruits and vegetables, especially flavanones, might reduce the risk of non-allergic rhinitis. No associations were found between other flavonoids and the considered outcomes.

Formaldehyde (FA) is a human carcinogen used as formalin in hospital laboratories. We evaluated its association with human chromosomal aberrations (CAs) and the risk/protective role played by several genetic polymorphisms in this relationship, on a cohort of 57 exposed pathologists vs 48 controls. All subjects were assessed for CAs on peripheral blood lymphocytes and genotyped for the most common cancer-associated gene polymorphisms which could be related with the genotoxic outcome: CYP1A1 exon 7 (A > G) , CYP1A1*2A (T > C) , CYP2C19*2 (G > A) , GSTT1 (Positive/Null), GSTM1 (Positive/null), GSTP1 (A > G) , XRCC1 (G399A) , XRCC1 (C194T) , XRCC1 (A280G) , XPD (A751C) , XPC exon 15 (A939C) , XPC exon 9 (C499T) , TNFα − 308 (G > A) , IL10 − 1082 (G > A) , IL10 − 819 (C > T) and IL6 − 174 (G > C) . Air-FA concentration was assessed through personal samplers. The comparison between pathologists and controls showed a significantly higher CAs frequency in pathologists. Significant positive correlations were found between CAs frequency and air-FA concentration while significant associations were found between variation in CAs frequency and the mutated allele for CYP1A1 exon 7 (A > G) , CYP2C19*2 (G > A) , GSTT1 -positive, GSTM1 -positive and XRCC1 (G399A) . Our study confirms the role of FA as genotoxicity inductor, even in workers chronically exposed to low air-FA levels and reveals the role played by some genetic polymorphisms in this association, highlighting the importance of individual susceptibility biomarkers assessment in occupational health studies.