Background Air pollution and obstructive sleep apnea (OSA) are both linked with cardiovascular co-morbidities and share similar pathophysiological mechanisms. A causal association between the two has been postulated. However, the results of the studies on this topic are conflicting mainly because of the lack of adjustment for important confounders such as seasonality and temperature. We aimed to evaluate if such an association exists in a highly polluted area like Lombardy region (Italy) when accounting for all confounders. Methods Data of adult patients seen at the Sleep Disorder Centre in Milan from 2010 to 2020 were analysed and the main polygraphic data were retrieved. Air pollutant concentrations of the following pollutants NO 2 , O 3 , PM 2.5 , and PM 10 were collected through monitoring stations. Results A total of 3493 patients were included: males (2358, 67.5%) mean age 60.1 (SD = 14.3) years, BMI 29.2 (6.2) kg/m 2 , mean AHI 16.5 (18.1) events/h. After adjusting for all confounders, in the multivariable analysis, the only associations that remained significant were long-term exposure to O 3 with indexes of OSA severity (AHI and ODI) but only in spring. Furthermore, a positive association was seen between long-term exposure to PM 10 and ODI but in springtime only. Conclusion The findings of the current study does not support an association between fine particulate matter and OSA severity.

Osteoarthritis is a degenerative disease of the joint, affecting over 30 million people in the US1. A key characteristic of OA is chondrocyte hypertrophy, characterized by chondrocyte changes to a more rounded and osteoblastic phenotype, characterized by increased IL-6 and IL-8 secretion2. While there are no cures for OA, treatments focus on mitigating pain and inflammation, the two main symptoms of OA. However, the analgesics, NSAIDS and corticosteroids commonly used, do not target regeneration and have negative side effects. Local anesthetics (LA) can be used as a pain management alternative but are usually short lasting and therefore, not suited for chronic conditions such as OA. Our engineered sustained release local anesthetic construct successfully delivers bupivacaine for an extended period of time3-5. This study is designed to evaluate the effect of the LA system on chondrocytes in an inflammatory OA-like environment.Chondrocytes were cultured with bolus, liposomal, or construct LA and either untreated or treated with TNF-α and IL-1α for 24 hrs, 48 hrs, or 96 hrs. Chondrocyte viability, interleukin-8 (IL-8), interleukin-6 (IL-6), collagenase activity and proteoglycan deposition were assessed.In the presence of the engineered construct, the chondrocytes retained viability and regenerative function. Moreover, the construct allowed for higher initial doses to be used, which promoted more regeneration and decreased inflammation without compromising cellular viability.The construct promotes a less hypertrophic chondrocyte environment while promoting a more anti-inflammatory environment. These two factors are consistent with a less OA progressive environment when using the engineered construct, compared to bolus LA.

Air source heat pumps (ASHPs) have worldwide applications due to their superior performance in energy saving and environmental friendliness. Two challenges of frosting and fouling for outdoor coils of ASHPs were of attention individually. This study investigated the effect of PM2.5 air pollution on the frosting process of the outdoor evaporator of ASHPs. The system performance and frosting characteristics of ASHPs with different environmental parameters were measured experimentally. The results showed that PM2.5 could significantly promote the frosting process when the concentration was greater than 146 μg/m3. Under the condition of severe pollution, both the experimental data and evaporator surface images reflected the shortening of the frost column generation period and frost layer growth period. On the theoretical basis of the three periods of the frosting process, the frost layer growth period was further divided into transition period and frost thickening period. At the same time, in order to quantitatively analyze the difference of frosting rate between severe pollution condition and no pollution condition, frosting rate ratio (FRR) was defined to reflect the influence of PM2.5 on frosting in different periods. Based on the analysis of the experimental results under different temperature and humidity conditions, it was considered that the frosting zone could be divided into two regions. In the Region I where the moisture content of the air was very low, the effect of PM2.5 on the frosting was weakened, and the FRR was positively correlated with the moisture content of the air. While in Region II with a relatively high moisture content of air, the FRR was positively correlated with the mass ratio of PM2.5 to moisture.

Acta Psychiatrica ScandinavicaVolume 140, Issue 4 p. 382-384 Research Letter The role of clock genes in perinatal depression: the light in the darkness M. Buoli, Corresponding Author massimiliano.buoli@unimi.it orcid.org/0000-0003-3359-3191 Department of Psychiatry, University of Milan, Fondazione IRCCS Ca' Granda Ospedale Maggiore Policlinico, Milan, ItalySearch for more papers by this authorS. Grassi, Department of Psychiatry, University of Milan, Fondazione IRCCS Ca' Granda Ospedale Maggiore Policlinico, Milan, ItalySearch for more papers by this authorS. Iodice, EPIGET-Epidemiology, Epigenetics and Toxicology Lab-Department of Clinical Sciences and Community Health, University of Milan, Milan, ItalySearch for more papers by this authorG. S. Carnevali, Department of Psychiatry, University of Milan, Fondazione IRCCS Ca' Granda Ospedale Maggiore Policlinico, Milan, ItalySearch for more papers by this authorC. M. Esposito, Department of Psychiatry, University of Milan, Fondazione IRCCS Ca' Granda Ospedale Maggiore Policlinico, Milan, ItalySearch for more papers by this authorL. Tarantini, EPIGET-Epidemiology, Epigenetics and Toxicology Lab-Department of Clinical Sciences and Community Health, University of Milan, Milan, ItalySearch for more papers by this authorJ. L. Barkin, Department of Community Medicine, Mercer University School of Medicine, Macon, GA, USASearch for more papers by this authorV. Bollati, EPIGET-Epidemiology, Epigenetics and Toxicology Lab-Department of Clinical Sciences and Community Health, University of Milan, Milan, ItalySearch for more papers by this author M. Buoli, Corresponding Author massimiliano.buoli@unimi.it orcid.org/0000-0003-3359-3191 Department of Psychiatry, University of Milan, Fondazione IRCCS Ca' Granda Ospedale Maggiore Policlinico, Milan, ItalySearch for more papers by this authorS. Grassi, Department of Psychiatry, University of Milan, Fondazione IRCCS Ca' Granda Ospedale Maggiore Policlinico, Milan, ItalySearch for more papers by this authorS. Iodice, EPIGET-Epidemiology, Epigenetics and Toxicology Lab-Department of Clinical Sciences and Community Health, University of Milan, Milan, ItalySearch for more papers by this authorG. S. Carnevali, Department of Psychiatry, University of Milan, Fondazione IRCCS Ca' Granda Ospedale Maggiore Policlinico, Milan, ItalySearch for more papers by this authorC. M. Esposito, Department of Psychiatry, University of Milan, Fondazione IRCCS Ca' Granda Ospedale Maggiore Policlinico, Milan, ItalySearch for more papers by this authorL. Tarantini, EPIGET-Epidemiology, Epigenetics and Toxicology Lab-Department of Clinical Sciences and Community Health, University of Milan, Milan, ItalySearch for more papers by this authorJ. L. Barkin, Department of Community Medicine, Mercer University School of Medicine, Macon, GA, USASearch for more papers by this authorV. Bollati, EPIGET-Epidemiology, Epigenetics and Toxicology Lab-Department of Clinical Sciences and Community Health, University of Milan, Milan, ItalySearch for more papers by this author First published: 10 August 2019 https://doi.org/10.1111/acps.13084Citations: 8Read the full textAboutPDF ToolsRequest permissionExport citationAdd to favoritesTrack citation ShareShare Give accessShare full text accessShare full-text accessPlease review our Terms and Conditions of Use and check box below to share full-text version of article.I have read and accept the Wiley Online Library Terms and Conditions of UseShareable LinkUse the link below to share a full-text version of this article with your friends and colleagues. Learn more.Copy URL Share a linkShare onEmailFacebookTwitterLinked InRedditWechat No abstract is available for this article.Citing Literature Volume140, Issue4October 2019Pages 382-384 RelatedInformation

BackgroundRaynaud’s phenomenon (RP) is the most frequent manifestation of patients with systemic sclerosis (SSc) and it is responsible for significant morbidity. RP has been ranked by patients with SSc as the second most disturbing related-disease symptom.1 It’s well known that RP, defined as episodic digital ischemia characterised by pain, numbness and digital colour changes, is provoked by environmental factors such as cold temperature and smoking exposure.2 No data are available on the impact of particular matter (PM) exposure on SSc-RP severity.ObjectivesOur aim was to evaluate the association between PM with aerodynamic diameter ≤10 µm (PM10) and SSc-RP severity.MethodsWe applied multivariable continuous ordinal regression model to evaluate the association between short-term exposure to PM10 and a measure of RP severity (in terms of number and duration of RP attacks, numbness, pain, burning and tingling) as measured by a Visual Analogue Scale (VAS). The model was then adjusted by sex, intravenous prostacyclin therapy (alprostar or iloprost), SSc subtype, general health (GH) VAS and season. Daily PM10 concentrations, from monitoring stations measured by Regional Environmental Protection Agency (ARPA Lombardia), were used to assign short-term exposure (mean of the 3 days preceding the evaluation) to each study subjects at his/her area of residence.ResultsWe enrolled 87 consecutive patients with SSc-RP from September 2016 to February 2017. 88.5% were female, mean age was 61 years, median time from diagnosis was 14 years (q1-q3: 7–21 years), and 10% had diffuse cutaneous SSc. The median VAS severity was 5 mm (q1-q3: 2–7 mm). 43.7% were treated with prostacyclin therapy. The model, performed as described above, estimated that for each 10 μg/m3 increase in PM10 there is a worsening of 40% in RP VAS severity (OR 10 μg/m3=1.40; 95% CI: 1.12–1.74).ConclusionsTo our knowledge a correlation between SSc-RP and air pollution as assessed by PM10 has never been published before. There is increasing evidence that a number of environmental factors are fundamental in the development and course of SSc.3 These results support the need to perform exposome epidemiology studies, next to genomics, to fully reveal the underlying mechanisms of diseases.References[1] Bassel M, et al. Frequency and impact of symptoms experienced by patients with systemic sclerosis: results from a Canadian National Survey. Rheumatology2011. [2] Fardoun MM, et al. Raynaud’s phenomenon: a brief review of the underlying mechanisms. Front Pharmacol2016. [3] Borghini A, et al. Environmental pollution by benzene and PM10 and clinical manifestations of systemic sclerosis: a correlation study. Int J Environ Res Public Health2017.AcknowledgementsWe thank Regional Environmental Protection Agency (ARPA Lombardia) for providing air pollution data.Disclosure of InterestNone declared

Introduction In Italy about 45% of people aged ≥18 years are overweight/obese and might thus be more susceptible to the adverse health effects of air pollution exposure. Particulate matter ≤10 µm (PM10) represents a common pollutant of living and working environments and has been associated with increased risk of cardiovascular diseases (CVD) and hypercoagulability. Extracellular vesicles (EV) might play an important role in PM-related CVD, as they can travel in body fluids and transfer miRNAs between cells. We investigated whether PM10 exposure is associated with changes in fibrinogen levels, EV release, and EV-miRNA content in a large sample of overweight/obese adults. Methods EV concentrations were quantified by nanoparticle tracking analysis and flow cytometry. To identify altered levels of EV-miRNAs, we profiled miRNAs of 883 subjects by the QuantStudio 12K Flex Real Time PCR System. The top 40 EV-miRNAs were validated through custom miRNA plates. Statistical analyses included multiple linear regressions, mediation analysis and bioinformatics analysis. Results In a sample of 1630 overweight/obese subjects from the SPHERE ( S usceptibility to P article H ealth E ffects, mi R NAs and E xosomes) study, short-term exposure to PM10 was associated with increased release of EVs, especially those from monocyte/macrophage components (CD14+) and platelets (CD61+). Nine EV-miRNAs (let-7c-5p; miR-106a-5p; miR-143–3 p; miR-185–5 p; miR-218–5 p; miR-331–3 p; miR-642–5 p; miR-652–3 p; miR-99b-5p) were downregulated in response to PM10 exposure and exhibited putative roles in CVD. Five of these nine EV-miRNAs were mediators in the positive association between PM10 exposure and fibrinogen levels. Conclusions Our study sheds some light on the potential mechanisms underlying the adverse cardiovascular health effects of air pollution exposure. Our results were obtained in a hypersusceptible population and thus strengthen the relevance of health promotion interventions for both the general public and the working population, as they might be particularly feasible in the workplace.

Growing evidences have shown that particulate matter (PM) exposures during pregnancy are associated with impaired fetal development and adverse birth outcomes, possibly as a result of an exaggerated systemic oxidative stress and inflammation. Telomere length (TL) is strongly linked to biological age and is impacted by oxidative stress. We hypothesized that PM exposure during different time windows in the first trimester of pregnancy influences both mitochondrial DNA copy number (mtDNAcn), an established biomarker for oxidative stress, and TL. Maternal blood TL and mtDNAcn were analysed in 199 healthy pregnant women recruited at the 11th week of pregnancy by quantitative polymerase chain reaction. We also examined whether maternal mtDNAcn and TL were associated with fetal growth outcomes measured at the end of the first trimester of pregnancy (fetal heart rate, FHR; crown-rump length, CRL; and nuchal translucency, NT) and at delivery (birth weight, length, head circumference). The possible modifying effect of prepregnancy maternal body mass index was evaluated. PM 10 exposure during the first pregnancy trimester was associated with an increased maternal mtDNAcn and a reduced TL. As regards ultrasound fetal outcomes, both FHR and CRL were positively associated with PM 2.5 , whereas the association with FHR was confirmed only when examining PM 10 exposure. PM 10 was also associated with a reduced birth weight. While no association was found between mtDNAcn and CRL, we found a negative relationship between mtDNAcn and fetal CRL only in overweight women, whereas normal-weight women exhibited a positive, albeit nonsignificant, association. As abnormalities of growth in utero have been associated with postnatal childhood and adulthood onset diseases and as PM is a widespread pollutant relevant to the large majority of the human population and obesity a rising risk factor, our results, if confirmed in a larger population, might represent an important contribution towards the development of more targeted public health strategies.

Epidemiological studies suggest a link between chromium (Cr) status and cardiovascular disease. Increased urinary excretion of Cr was reported in subjects with diabetes compared with non-diabetic controls and those with non-diabetic insulin resistance. Epigenetic alterations have been linked to the presence of Cr, and microRNA (miRNA) expression has been implicated in the pathogenesis of metabolic diseases and cardiovascular diseases (CVDs). We investigated the association between Cr excretion and miRNA expression in leukocytes from obese subjects. We also examined the relationship between altered miRNA expression and selected clinical parameters to further investigate mechanisms linking Cr to metabolic diseases and CVDs. We analyzed urinary Cr in 90 Italian subjects using inductively coupled plasma-mass spectrometry. Peripheral blood miRNA levels were screened with TaqMan Low-Density Array Human MicroRNA A. Cr level-associated expression of miRNAs was detected with multivariate regression analyses, and the top 10 candidate miRNAs were selected for validation. We also used multivariate regression analyses to assess possible associations between validated miRNAs and glycated hemoglobin (A1c) and blood pressure (BP). The validated miRNAs were further investigated by functional analysis with Ingenuity Pathway Analysis software. Urinary Cr levels (mean: 0.35 μg/l; s.d.=0.24) ranged from 0.05 to 1.27 μg/l. In the screening phase, 43 miRNAs were negatively associated with Cr. Of the top 10 miRNAs selected for validation, nine (miR-451, miR-301, miR-15b, miR-21, miR-26a, miR-362-3p, miR-182, miR-183 and miR-486-3p) were downregulated in association with Cr (P-false discovery rate (FDR)<0.10). miR-451 expression was associated with A1c (β=–0.06; P=0.0416), whereas miR-486-3p expression was associated both with diastolic (β=2.1; P=0.004) and systolic BP (β=3.3; P=0.003). These results indicate that miR-451 and miR-486-3p are involved in the link between Cr levels and metabolic diseases and CVDs.