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BACKGROUND: A few studies have reported associations between traffic-related air pollution exposure at schools and cognitive development. The role of PM components or sources other than traffic on cognitive development has been little explored. OBJECTIVES: We aimed to explore the role of PM sources in school air on cognitive development. METHODS: A cohort of 2,618 schoolchildren (average age, 8.5 years) belonging to 39 schools in Barcelona (Spain) was followed up for a year. Children completed computerized tests assessing working memory, superior working memory, and inattentiveness during four visits. Particulate matter ≤ 2.5 μm (PM[sub 2.5]) was measured during two 1-week campaigns in each school, both outdoors and in the classroom. Source apportionment resulted in nine sources: mineral, organic/textile/chalk, traffic, secondary sulfate and organics, secondary nitrate, road dust, metallurgy, sea spray, and heavy oil combustion. Differences in cognitive growth trajectories were assessed with mixed models with age-by-source interaction terms. RESULTS: An interquartile range increase in indoor traffic-related PM2 5 was associated with reductions in cognitive growth equivalent to 22% (95% CI: 2%, 42%) of the annual change in working memory, 30% (95% CI: 6%, 54%) of the annual change in superior working memory, and 11% (95% CI: 0%, 22%) of the annual change in the inattentiveness scale. None of the other PM[sub 2.5] sources was associated with adverse effects on cognitive development. CONCLUSIONS: Traffic was the only source of fine particles associated with a reduction in cognitive development. Reducing air pollution from traffic at primary schools may result in beneficial effects on cognition. CITATION: Basagafia X, Esnaola M, Rivas I, Amato F, Alvarez-Pedrerol M, Forns J, Lôpez-Vicente M, Pujol J, Nieuwenhuijsen M, Querol X, Sunyer J. 2016. Neurodevelopmental deceleration by urban fine particles from different emission sources: a longitudinal observational study. Environ Health Perspect 124:1630-1636; http://dx.doi.org/10.1289/EHP209 [ABSTRACT FROM AUTHOR]

Background:Knowledge on factors associated with mortality can help identify patients with COPD that might benefit from close monitoring and intervention. Arterial blood gases (ABGs) are related to mortality, but both arterial tension of oxygen (PaO2) and arterial tension of carbon dioxide (PaCO2) vary over time. The aim of our study was to investigate the association between repeatedly measured ABGs and mortality in men and women with COPD.Methods:A cohort of 419 Norwegian subjects with COPD, GOLD stage II-IV, aged 40–75, was followed up with up to seven ABGs, measured during stable phase for three years. Cox proportional hazard models were used to quantify the relationship between both single and repeatedly measured ABGs and all-cause mortality after five years, adjusting for age, sex, and the updated BODE index.Results:A total of 64 subjects died during follow-up. Mean initial arterial oxygen tension (standard deviation) was significantly higher in survivors compared to deceased, with PaO2(in kPa) 9.4 (1.1) versus 8.8 (1.2), p<0.001. Corresponding numbers for PaCO2were 5.3 (0.5) and 5.5 (0.7),p< 0.001. In analyses adjusting for age, sex, and the updated BODE index hazard ratios – HR(95% confidence intervals) - for all-cause mortality were 0.73 (0.55, 0.97) and 1.58 (0.90, 2.76) for repeated measures of PaO2and PaCO2, respectively.Conclusion:Both arterial oxygen and carbon dioxide tension were related to mortality in this study, and arterial oxygen tension added prognostic information to the updated BODE index in COPD. [ABSTRACT FROM PUBLISHER]

BackgroundHospital workers have been the most frequently and severely affected professional group during the COVID-19 pandemic, and have a big impact on transmission. In this context, innovative tools are required to measure the symptoms compatible with COVID-19, the spread of infection, and testing capabilities within hospitals in real time. ObjectiveWe aimed to develop and test an effective and user-friendly tool to identify and track symptoms compatible with COVID-19 in hospital workers. MethodsWe developed and pilot tested Hospital Epidemics Tracker (HEpiTracker), a newly designed app to track the spread of COVID-19 among hospital workers. Hospital staff in 9 hospital centers across 5 Spanish regions (Andalusia, Balearics, Catalonia, Galicia, and Madrid) were invited to download the app on their phones and to register their daily body temperature, COVID-19–compatible symptoms, and general health score, as well as any polymerase chain reaction and serological test results. ResultsA total of 477 hospital staff participated in the study between April 8 and June 2, 2020. Of note, both health-related (n=329) and non–health-related (n=148) professionals participated in the study; over two-thirds of participants (68.8%) were health workers (43.4% physicians and 25.4% nurses), while the proportion of non–health-related workers by center ranged from 40% to 85%. Most participants were female (n=323, 67.5%), with a mean age of 45.4 years (SD 10.6). Regarding smoking habits, 13.0% and 34.2% of participants were current or former smokers, respectively. The daily reporting of symptoms was highly variable across participating hospitals; although we observed a decline in adherence after an initial participation peak in some hospitals, other sites were characterized by low participation rates throughout the study period. ConclusionsHEpiTracker is an already available tool to monitor COVID-19 and other infectious diseases in hospital workers. This tool has already been tested in real conditions. HEpiTracker is available in Spanish, Portuguese, and English. It has the potential to become a customized asset to be used in future COVID-19 pandemic waves and other environments. Trial RegistrationClinicalTrials.gov NCT04326400; https://clinicaltrials.gov/ct2/show/NCT04326400

Background: Smoking is the primary cause of deterioration in forced expiratory volume (FEV1) and the development of chronic obstructive lung disease. This study assessed the independent association of smoking with respiratory symptoms and lung function in young adults who took part in the European Community Respiratory Health Survey (ECRHS-I). Methods: Cross-sectional multi-centre survey of a general population of young adults aged 20(44 years in the ECRHS(I conducted in five Spanish centres. Several groups were created in an exclusive and descendent manner from the subjects who completed the questionnaire in accordance with how they had answered the questions: asthma-related symptoms; chronic bronchitis symptoms; minor respiratory symptoms; chronic cough; and no respiratory symptoms. Among a subset of the population, forced spirometry tests were performed. Linear and logistical regression models were used to assess the relationship of smoking in the presence of symptoms and its impact on lung function, adjusted by other important variables. Results: The prevalence of respiratory symptoms was higher among smokers. After adjusting for geographical area, total IgE, age, sex, and FEV1, smoking was associated with an increased risk of chronic bronchitis and other respiratory symptoms. These risks increased with increasing number of cigarettes smoked per day. A deterioration of FEV1 and the FEV1/FVC ratio was also directly associated with the number of cigarettes smoked per day. Conclusion: Even among young adults, smoking confers a high risk of developing a number of respiratory symptoms and the deterioration of the ventilatory function. [ABSTRACT FROM AUTHOR]

Introduction: Epidemiological studies are highlighting the negative effects of the exposure to air pollution on children's neurodevelopment. However, most studies assessed children's neurodevelopment using neuropsychological tests or questionnaires. Using magnetic resonance imaging (MRI) to precisely measure global and region-specific brain development would provide details of brain morphology and connectivity. This would help us understand the observed cognitive and behavioral changes related to air pollution exposure. Moreover, most studies assessed only a few air pollutants. This project investigates whether air pollution exposure to many pollutants during pregnancy and childhood is associated with the morphology and connectivity of the brain in school-age children and pre-adolescents., Methods: We used data from the Generation R Study, a population-based birth cohort set up in Rotterdam, the Netherlands in 2002-2006 (n = 9,610). We used land-use regression (LUR) models to estimate the levels of 14 air pollutants at participant's homes during pregnancy and childhood: nitrogen oxides (NO x ), nitrogen dioxide (NO 2 ), particulate matter with aerodynamic diameter ≤10 μm (PM 10 ) or ≤2.5 μm (PM 2.5 ), PM between 10 μm and 2.5 μm (PM COARSE ), absorbance of the PM 2.5 fraction - a measure of soot (PM 2.5 absorbance), the composition of PM 2.5 such as polycyclic aromatic hydrocarbons (PAHs), organic carbon (OC), copper (Cu), iron (Fe), silicon (Si), zinc (Zn), and the oxidative potential of PM 2.5 evaluated using two acellular methods: dithiothreitol (OP DTT ) and electron spin resonance (OP ESR ). We performed MRI measurements of structural morphology (i.e., brain volumes, cortical thickness, and cortical surface area) using T 1 -weighted images in 6- to 10-year-old school-age children and 9- to 12-year-old pre-adolescents, structural connectivity (i.e., white matter microstructure) using diffusion tensor imaging (DTI) in pre-adolescents, and functional connectivity (i.e., connectivity score between brain areas) using resting-state functional MRI (rs-fMRI) in pre-adolescents. We assessed cognitive function using the Developmental Neuropsychological Assessment test (NEPSY-II) in school-age children. For each outcome, we ran regression analysis adjusted for several socioeconomic and lifestyle characteristics. We performed single-pollutant analyses followed by multipollutant analyses using the deletion/substitution/addition (DSA) approach., Results: The project has air pollution and brain MRI data for 783 school-age children and 3,857 pre-adolescents. First, exposure to air pollution during pregnancy or childhood was not associated with global brain volumes (e.g., total brain, cortical gray matter, and cortical white matter) in school-age children or pre-adolescents. However, higher pregnancy or childhood exposure to several air pollutants was associated with a smaller corpus callosum and hippocampus, and a larger amygdala, nucleus accumbens, and cerebellum in pre-adolescents, but not in school-age children. Second, higher exposure to several air pollutants during pregnancy was associated with a thinner cortex in various regions of the brain in both school-age children and pre-adolescents. Higher exposure to air pollution during childhood was also associated with a thinner cortex in a single region in pre-adolescents. A thinner cortex in two regions mediated the association between higher exposure to air pollution during pregnancy and an impaired inhibitory control in school-age children. Third, higher exposure to air pollution during childhood was associated with smaller cortical surface areas in various regions of the brain except in a region where we observed a larger cortical surface area in pre-adolescents. In relation to brain structural connectivity, higher exposure to air pollution during pregnancy and childhood was associated with an alteration in white matter microstructure in pre-adolescents. In relation to brain functional connectivity, a higher exposure to air pollution, mainly during pregnancy and early childhood, was associated with a higher brain functional connectivity among several brain regions in pre-adolescents. Overall, we identified several air pollutants associated with brain structural morphology, structural connectivity, and functional connectivity, such as NO x , NO 2 , PM of various size fractions (i.e., PM 10 , PM COARSE , and PM 2.5 ), PM 2.5 absorbance, PAHs, OC, three elemental components of PM 2.5 (i.e., Cu, Si, Zn), and the oxidative potential of PM 2.5., Conclusions: The results of this project suggest that exposure to air pollution during pregnancy and childhood play an adverse role in brain development. We observed this relationship even at levels of exposure that were below the European Union legislations. We acknowledge that identifying the independent effects of specific pollutants was particularly challenging. Most of our conclusions generally refer to traffic-related air pollutants. However, we did identify pollutants specifically originating from brake linings, tire wear, and tailpipe emissions from diesel combustion. The current direction toward innovative solutions for cleaner energy vehicles is a step in the right direction. However, our findings indicate that these measures might not be completely adequate to mitigate health problems attributable to traffic-related air pollution, as we also observed associations with markers of brake linings and tire wear., (© 2022 Health Effects Institute. All rights reserved.)

Background: In all societies, the burden and cost of allergic and chronic respiratory diseases are increasing rapidly. Most economies are struggling to deliver modern health care effectively. There is a need to support the transformation of the health care system into integrated care with organizational health literacy., Main Body: As an example for chronic disease care, MASK (Mobile Airways Sentinel NetworK), a new project of the ARIA (Allergic Rhinitis and its Impact on Asthma) initiative, and POLLAR (Impact of Air POLLution on Asthma and Rhinitis, EIT Health), in collaboration with professional and patient organizations in the field of allergy and airway diseases, are proposing real-life ICPs centred around the patient with rhinitis, and using mHealth to monitor environmental exposure. Three aspects of care pathways are being developed: (i) Patient participation, health literacy and self-care through technology-assisted "patient activation", (ii) Implementation of care pathways by pharmacists and (iii) Next-generation guidelines assessing the recommendations of GRADE guidelines in rhinitis and asthma using real-world evidence (RWE) obtained through mobile technology. The EU and global political agendas are of great importance in supporting the digital transformation of health and care, and MASK has been recognized by DG Santé as a Good Practice in the field of digitally-enabled, integrated, person-centred care., Conclusion: In 20 years, ARIA has considerably evolved from the first multimorbidity guideline in respiratory diseases to the digital transformation of health and care with a strong political involvement., Competing Interests: Competing interestsDr. Ansotegui reports personal fees from Mundipharma, Roxall, Sanofi, MSD, Faes Farma, Hikma, UCB, Astra Zeneca, outside the submitted work. Dr. Bosnic-Anticevich reports grants from TEVA, personal fees from TEVA, Boehringer Ingelheim, AstraZeneca, Sanofi, Mylan, outside the submitted work. Dr. Bousquet reports personal fees and others from Chiesi, Cipla, Hikma, Menarini, Mundipharma, Mylan, Novartis, Sanofi-Aventis, Takeda, Teva, Uriach, others from Kyomed, outside the submitted work. Dr. Boulet reports and Disclosure of potential conflicts of interest—last 3 years. Research grants for participation to multicentre studies, AstraZeneca, Boston Scientific, GlaxoSmithKline, Hoffman La Roche, Novartis, Ono Pharma, Sanofi, Takeda. Support for research projects introduced by the investigator AstraZeneca, Boehringer-Ingelheim, GlaxoSmithKline, Merck, Takeda. Consulting and advisory boards Astra Zeneca, Novartis, Methapharm. Royalties Co-author of “Up-To-Date” (occupational asthma). Nonprofit grants for production of educational materials AstraZeneca, Boehringer-Ingelheim, GlaxoSmithKline, Merck Frosst, Novartis. Conference fees AstraZeneca, GlaxoSmithKline, Merck, Novartis. Support for participation in conferences and meetings Novartis, Takeda. Other participations Past president and Member of the Canadian Thoracic Society Respiratory Guidelines Committee; Chair of the Board of Directors of the Global Initiative for Asthma (GINA). Chair of Global Initiative for Asthma (GINA) Guidelines Dissemination and Implementation Committee; Laval University Chair on Knowledge Transfer, Prevention and Education in Respiratory and Cardiovascular Health; Member of scientific committees for the American College of Chest Physicians, American Thoracic Society, European Respiratory Society and the World Allergy Organization; 1st Vice-President of the Global Asthma Organization “InterAsma”. Dr. Casale reports grants and non-financial support from Stallergenes, outside the submitted work. Dr. Cruz reports grants and personal fees from GlaxoSmithKline, personal fees from Boehrinher Ingelheim, AstraZeneca, Novartis, Merk, Sharp & Dohme, MEDA Pharma, EUROFARMA, Sanofi Aventis, outside the submitted work. Dr. Ebisawa reports personal fees from DBV Technologies, Mylan EPD maruho, Shionogi & CO., Ltd., Kyorin Pharmaceutical Co., Ltd., Thermofisher Diagnostics, Pfizer, Beyer, Nippon Chemifar, Takeda Pharmaceutical Co., Ltd., MSD, outside the submitted work. Dr. Ivancevich reports personal fees from Euro Farma Argentina, Faes Farma, non-financial support from Laboratorios Casasco, outside the submitted work. Dr. Haahtela reports personal fees from Mundipharma, Novartis, and Orion Pharma, outside the submitted work. Dr. Klimek reports grants and personal fees from ALK Abelló, Denmark, Novartis, Switzerland, Allergopharma, Germany, Bionorica, Germany, GSK, Great Britain, Lofarma, Italy, personal fees from MEDA, Sweden, Boehringer Ingelheim, Germany, grants from Biomay, Austria, HAL, Netherlands, LETI, Spain, Roxall, Germany, Bencard, Great Britain, outside the submitted work. V.KV has received payment for consultancy from GSK and for lectures from StallergensGreer, Berlin-CHemie and sponsorship from MYLAN for in the following professional training: ARIA masterclass in allergic rhinitis participation. Dr. Larenas Linnemann reports personal fees from GSK, Astrazeneca, MEDA, Boehringer Ingelheim, Novartis, Grunenthal, UCB, Amstrong, Siegfried, DBV Technologies, MSD, Pfizer., grants from Sanofi, Astrazeneca, Novartis, UCB, GSK, TEVA, Chiesi, Boehringer Ingelheim, outside the submitted work. Dr. Mösges reports personal fees from ALK, grants from ASIT biotech, Leti, BitopAG, Hulka, Ursapharm, Optima; personal fees from allergopharma, Nuvo, Meda, Friulchem, Hexal, Servier, Bayer, Johnson & Johnson, Klosterfrau, GSK, MSD, FAES, Stada, UCB, Allergy Therapeutics; grants and personal fees from Bencard, Stallergenes; grants, personal fees and non-financial support from Lofarma; non-financial support from Roxall, Atmos, Bionorica, Otonomy, Ferrero; personal fees and non-financial support from Novartis; Dr. Okamoto reports personal fees from Eizai Co., Ltd., Shionogi Co., Ltd., Torii Co., Ltd., GSK, MSD, Kyowa Co., Ltd., grants and personal fees from Kyorin Co., Ltd., Tiho Co., Ltd., grants from Yakuruto Co., Ltd., Yamada Bee Farm, outside the submitted work. Dr. Papadopoulos reports grants from Gerolymatos, personal fees from Hal Allergy B.V., Novartis Pharma AG, Menarini, Hal Allergy B.V., outside the submitted work. Dr. Pépin reports grants from AIR LIQUIDE FOUNDATION, AGIR à dom, ASTRA ZENECA, FISHER & PAYKEL, MUTUALIA, PHILIPS, RESMED, VITALAIRE, other from AGIR à dom, ASTRA ZENECA, BOEHRINGER INGELHEIM, JAZZ PHARMACEUTICAL, NIGHT BALANCE, PHILIPS, RESMED, SEFAM, outside the submitted work. Dr. Pfaar reports grants and personal fees from ALK-Abelló, Allergopharma Stallergenes Greer, HAL Allergy Holding B.V./HAL Allergie GmbH, Bencard Allergie GmbH/Allergy Therapeutics, Lofarma, grants from Biomay, ASIT Biotech Tools S.A, Laboratorios LETI/LETI Pharma, Anergis S.A., grants from Nuvo, Circassia, Glaxo Smith Kline, personal fees from Novartis Pharma, MEDA Pharma, Mobile Chamber Experts (a GA2LEN Partner), Pohl-Boskamp, Indoor Biotechnologies, grants from, outside the submitted work. Dr. Todo-Bom reports grants and personal fees from Novartis, Mundipharma, GSK Teva Pharma, personal fees from AstraZeneca, grants from Leti, outside the submitted work. Dr. Tsiligianni reports advisory boards from Boehringer Ingelheim and Novartis and a grant from GSK, outside the submitted work. Dr. Wallace reports and Indicates that she is the co-chair of the Joint Task Force on Practice Parameters, a task force composed of 12 members of the American Academy of Allergy, Asthma, and Immunology and the American College of Allergy, Asthma, and Immunology. Dr. Waserman reports other from CSL Behring, Shire, AstraZeneca,Teva, Meda, Merck, outside the submitted work. Dr. Zuberbier reports and Organizational affiliations: Commitee member: WHO-Initiative “Allergic Rhinitis and Its Impact on Asthma” (ARIA). Member of the Board: German Society for Allergy and Clinical Immunology (DGAKI). Head: European Centre for Allergy Research Foundation (ECARF). Secretary General: Global Allergy and Asthma European Network (GA2LEN). Member: Committee on Allergy Diagnosis and Molecular Allergology, World Allergy Organization (WAO).

Background: Harmonized data describing simultaneous exposure to a large number of environmental contaminants in-utero and during childhood is currently very limited., Objectives: To characterize concentrations of a large number of environmental contaminants in pregnant women from Europe and their children, based on chemical analysis of biological samples from mother-child pairs., Methods: We relied on the Early-Life Exposome project, HELIX, a collaborative project across six established population-based birth cohort studies in Europe. In 1301 subjects, biomarkers of exposure to 45 contaminants (i.e. organochlorine compounds, polybrominated diphenyl ethers, per- and polyfluoroalkyl substances, toxic and essential elements, phthalate metabolites, environmental phenols, organophosphate pesticide metabolites and cotinine) were measured in biological samples from children (6-12 years) and their mothers during pregnancy, using highly sensitive biomonitoring methods., Results: Most of the exposure biomarkers had high detection frequencies in mothers (35 out of 45 biomarkers with >90% detected) and children (33 out of 45 biomarkers with >90% detected). Concentrations were significantly different between cohorts for all compounds, and were generally higher in maternal compared to children samples. For most of the persistent compounds the correlations between maternal and child concentrations were moderate to high (Spearman Rho > 0.35), while for most non-persistent compounds correlations were considerably lower (Spearman Rho < 0.15). For mercury, PFOS and PFOA a considerable proportion of the samples of both mothers and their children exceeded the HBM I value established by The Human Biomonitoring Commission of the German Federal Environment Agency., Discussion: Although not based on a representative sample, our study suggests that children across Europe are exposed to a wide range of environmental contaminants in fetal life and childhood including many with potential adverse effects. For values exceeding the HBM I value identification of specific sources of exposure and reducing exposure in an adequate way is recommended. Considerable variability in this "chemical exposome" was seen between cohorts, showing that place of residence is a strong determinant of one's personal exposome. This extensive dataset comprising >100,000 concentrations of environmental contaminants in mother-child pairs forms a unique possibility for conducting epidemiological studies using an exposome approach., (Copyright © 2018 Elsevier Ltd. All rights reserved.)

Objective: We integratively assessed the effect of different indoor and outdoor environmental exposures early in life on respiratory and allergic health conditions among children from (sub-) urban areas., Methods: This study included children participating in four ongoing European birth cohorts located in three different geographical regions: INMA (Spain), LISAplus (Germany), GINIplus (Germany) and BAMSE (Sweden). Wheezing, bronchitis, asthma and allergic rhinitis throughout childhood were assessed using parental-completed questionnaires. We designed "environmental scores" corresponding to different indoor, green- and grey-related exposures (main analysis, a-priori-approach). Cohort-specific associations between these environmental scores and the respiratory health outcomes were assessed using random-effects meta-analyses. In addition, a factor analysis was performed based on the same exposure information used to develop the environmental scores (confirmatory analysis, data-driven-approach)., Results: A higher early exposure to the indoor environmental score increased the risk for wheezing and bronchitis within the first year of life (combined adjusted odds ratio: 1.20 [95% confidence interval: 1.13-1.27] and 1.28 [1.18-1.39], respectively). In contrast, there was an inverse association with allergic rhinitis between 6 and 8 years (0.85 [0.79-0.92]). There were no statistically significant associations for the outdoor related environmental scores in relation to any of the health outcomes tested. The factor analysis conducted confirmed these trends., Conclusion: Although a higher exposure to indoor related exposure through occupants was associated with an increased risk for wheezing and bronchitis within the 1st year, it might serve as a preventive mechanism against later childhood allergic respiratory outcomes in urbanized environments through enhanced shared contact with microbial agents., (Copyright © 2017 Elsevier Inc. All rights reserved.)

Asthma, rhinitis, and eczema are complex diseases with multiple genetic and environmental factors interlinked through IgE-associated and non-IgE-associated mechanisms. Mechanisms of the Development of ALLergy (MeDALL; EU FP7-CP-IP; project no: 261357; 2010-2015) studied the complex links of allergic diseases at the clinical and mechanistic levels by linking epidemiologic, clinical, and mechanistic research, including in vivo and in vitro models. MeDALL integrated 14 European birth cohorts, including 44,010 participants and 160 cohort follow-ups between pregnancy and age 20 years. Thirteen thousand children were prospectively followed after puberty by using a newly standardized MeDALL Core Questionnaire. A microarray developed for allergen molecules with increased IgE sensitivity was obtained for 3,292 children. Estimates of air pollution exposure from previous studies were available for 10,000 children. Omics data included those from historical genome-wide association studies (23,000 children) and DNA methylation (2,173), targeted multiplex biomarker (1,427), and transcriptomic (723) studies. Using classical epidemiology and machine-learning methods in 16,147 children aged 4 years and 11,080 children aged 8 years, MeDALL showed the multimorbidity of eczema, rhinitis, and asthma and estimated that only 38% of multimorbidity was attributable to IgE sensitization. MeDALL has proposed a new vision of multimorbidity independent of IgE sensitization, and has shown that monosensitization and polysensitization represent 2 distinct phenotypes. The translational component of MeDALL is shown by the identification of a novel allergic phenotype characterized by polysensitization and multimorbidity, which is associated with the frequency, persistence, and severity of allergic symptoms. The results of MeDALL will help integrate personalized, predictive, preventative, and participatory approaches in allergic diseases., (Copyright © 2016 American Academy of Allergy, Asthma & Immunology. Published by Elsevier Inc. All rights reserved.)

Introduction: Environmental exposures have been linked to length of gestation but the question as to during which weeks of gestation pregnancies are most susceptible still remains little explored. We estimated the effect of maximum apparent temperature and air pollution levels on risk of birth by week of gestation., Methods: We analyzed two cohorts of singleton live births in Rome (2001-2010) and Barcelona (2007-2012). Maximum apparent temperature (MAT), PM10, O3 and NO2 were analyzed in the warm period (1st April-31st October). Gestational week-specific hazard ratios of giving birth associated to a 1-unit increase in exposure were estimated fitting Cox regression models adjusted for seasonality, and demographic and clinical characteristics of the mother., Results: We observed 78,633 births (5.5% preterm) in Rome and 27,255 (4.5% preterm) in Barcelona. The highest hazard ratios for 1°C increase in MAT were in the 22nd-26th weeks of gestation, 1.071, (95% CI 1.052-1.091) in Rome and 1.071 (95% CI 1.036-1.106) in Barcelona, and decreased to 1.032 (95% CI 1.026-1.038) and 1.033 (95% CI 1.020-1.045) at the 36th week of gestation, respectively. Similar associations and trends were observed for PM10 and NO2 after adjusting for MAT. O3 showed similar trends but weaker associations., Conclusions: We found, consistently in Rome and Barcelona, an increased risk of delivery for a unit increase in MAT, PM10, NO2 and O3, especially in the second half of the second trimester, thus effectively increasing the risk of preterm and particularly early preterm birth. Results may help to increase awareness of these risks among public-health regulators and clinicians, leading to better preventive strategies., (Published by Elsevier Ltd.)

Although ambient particulate matter contributes to atherosclerosis in animal models, its role in atherogenesis in humans needs to be established. This article discusses concepts, study design, and choice of health outcomes to efficiently investigate the atherogenic role of ambient air pollution, with an emphasis on early preclinical biomarkers of atherosclerosis that are unaffected by short-term exposure to air pollution (eg, carotid intima-media thickness [CIMT] and functional performance of the vessel). Air pollution studies using these end points are summarized. The CIMT is currently the most frequently used outcome in this field (6 studies). The continuous nature of CIMT, the lack of short-term variation, its relationship to atherosclerotic changes in the artery wall, its predictive value for coronary heart disease, and the noninvasiveness of the assessment make it a useful candidate for cross-sectional and longitudinal studies investigating the role of air pollution in atherogenesis., (Copyright © 2011 Elsevier Inc. All rights reserved.)