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The ongoing COVID-19 pandemic is shaking the foundations of public health governance all over the world. Researchers are challenged by informing and supporting authorities on acquired knowledge and practical implications. This Editorial applies established theories of risk perception research to COVID-19 pandemic, and reflects on the role of risk perceptions in these unprecedented times, and specifically in the framework of the International Journal of Environmental Research and Public Health Special Issue “Research about risk perception in the Environmental Health domain”.

The adverse health effects of exposure to air pollutants, notably to particulate matter (PM), are well-known, as well as the association with measured or estimated concentration levels. The role of perception can be relevant in exploring effects and pollution control actions. The purpose of this study was to explore studies that analyse people’s perception, together with the measurement of air pollution, in order to elucidate the relationship between them. We conducted a systematic review in accordance with the Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) guidelines. In March 2020, PubMed, EMBASE, and Scopus databases were explored in an attempt to search for studies published from 2000 to 2020. The review included 38 studies, most of which were conducted in China (n = 13) and the United States (n = 11) and published over the last four years (n = 26). Three studies were multicenter investigations, while five articles were based on a national-level survey. The air quality (AQ) was assessed by monitoring stations (n = 24) or dispersion models (n = 7). Many studies were population questionnaire-based, air monitoring and time-series studies, and web-based investigations. A direct association between exposure and perception emerged in 20 studies. This systematic review has shown that most of the studies establish a relationship between risk perception measurement. A broad spectrum of concepts and notions related to perception also emerged, which is undoubtedly an indicator of the wealth of available knowledge and is promising for future research.

Breast cancer (BC) is a leading cause of global cancer-related mortality in women, necessitating accurate tumor classification for timely intervention. Molecular and histological factors, including PAM50 classification, estrogen receptor α (ERα), breast cancer type 1 susceptibility protein (BRCA1), progesterone receptor (PR), and HER2 expression, contribute to intricate BC subtyping. In this work, through a combination of bioinformatic and wet lab screenings, followed by classical signal transduction and cell proliferation methods, and employing multiple BC cell lines, we identified enhanced sensitivity of ERα-positive BC cell lines to ALK and MELK inhibitors, inducing ERα degradation and diminishing proliferation in specific BC subtypes. MELK inhibition attenuated ERα transcriptional activity, impeding E2-induced gene expression, and hampering proliferation in MCF-7 cells. Synergies between MELK inhibition with 4OH-tamoxifen (Tam) and ALK inhibition with HER2 inhibitors revealed potential therapeutic avenues for ERα-positive/PR-positive/HER2-negative and ERα-positive/PR-negative/HER2-positive tumors, respectively. Our findings propose MELK as a promising target for ERα-positive/PR-positive/HER2-negative BC and highlight ALK as a potential focus for ERα-positive/PR-negative/HER2-positive BC. The synergistic anti-proliferative effects of MELK with Tam and ALK with HER2 inhibitors underscore kinase inhibitors’ potential for selective treatment in diverse BC subtypes, paving the way for personalized and effective therapeutic strategies in BC management.

Background Atmospheric pollution has been recognized as the greatest environmental threat to human health. The population of the Venafro Valley, southern Italy, is exposed to emissions from a Waste-To-Energy (WTE) and a cement plant and potentially also to another WTE located in the neighboring region of Lazio; also, the vehicular atmospheric pollution situation is critical. In order to assess the environmental health risk of residents in eight municipalities of the Venafro Valley, a retrospective residential cohort study during 2006–2019 was carried out. Methods Four exposure classes were defined by natural-break method, using a dispersion map of nitrogen dioxides (chosen as proxy of industrial pollution). The association between the industrial pollution and cause-specific mortality/morbidity of the cohort was calculated using the Hazard Ratio (HR) through a multiple time-dependent and sex-specific Cox regression adjusting for age, proximity to main roads and socio-economic deprivation index. Results Results showed, for both sexes, mortality and morbidity excesses in the most exposed class for diseases of the circulatory system and some signals for respiratory diseases. Particularly, mortality excesses in both sexes in class 3 for diseases of the circulatory system [men: HR = 1.37 (1.04–1.79); women: HR = 1.27 (1.01–1.60)] and for cerebrovascular diseases [men: HR = 2.50 (1.44–4.35); women: HR = 1.41 (0.92–2.17)] were observed and confirmed by morbidity analyses. Mortality excesses for heart diseases for both sexes [men-class 3: HR = 1.32 (0.93–1.87); men-class 4: HR = 1.95 (0.99–3.85); women-class 3: HR = 1.49 (1.10–2.04)] and for acute respiratory diseases among women [HR = 2.31 (0.67-8.00)] were observed. Morbidity excesses in both sexes for ischemic heart diseases [men-class 3: HR = 1.24 (0.96–1.61); women-class 4: HR = 2.04 (1.04–4.02)] and in class 4 only among men for respiratory diseases [HR = 1.43 (0.88–2.31)] were also found. Conclusions The present study provides several not-negligible signals indicating mitigation actions and deserve further investigations. For future studies, the authors recommend enriching the exposure and lifestyle profile using tools such as questionnaires and human biomonitoring.

Lung cancer is the deadliest cancer type worldwide with ~ 1.8 million deaths per-year. Smoking accounts for ~ 85% of all cases, with a described joint effect with unhealthy diet in lung cancer risk increase. Public health policies to prevent carcinogens exposure, promote smoking cessation and advocacy for healthy nutrition, are therefore highly recommended. Here we have examined the benefits of the Mediterranean Diet (MedDiet) in protecting against some non-communicable diseases including lung cancer, highlighting the epidemiological and biomolecular aspects of MedDiet anti-inflammatory effect and its interaction with smoking habits closely linked to risk of lung cancer. Considering the high incidence and mortality rates of lung cancer, we discussed also about the global impact that a Planeterranean extension of the benefits of MedDiet could have on controlling lung cancer risk. We also debated the impact of personalized nutrition on lung cancer prevention, considering individual heterogeneity in response to diet plans as well as recent advancements on nutri-omics in lung cancer research, with a specific focus on the role of microRNAs (miRNAs) as a promising nutritional molecular hub for lung cancer prevention. We strongly believe that a deep understanding of the molecular link between food components and genetic/epigenetics factors can expand effective intervention strategies.

Arsenic is a human carcinogen with weak mutagenic properties that induces tumors through mechanisms not yet completely understood. People worldwide are exposed to arsenic-contaminated drinking water, and epidemiological studies showed a high percentage of lung, bladder, liver, and kidney cancer in these populations. Several mechanisms by which arsenical compounds induce tumorigenesis were proposed including genotoxic damage and chromosomal abnormalities. Over the past decade, a growing body of evidence indicated that epigenetic modifications have a role in arsenic-inducing adverse effects on human health. The main epigenetic mechanisms are DNA methylation in gene promoter regions that regulate gene expression, histone tail modifications that regulate the accessibility of transcriptional machinery to genes, and microRNA activity (noncoding RNA able to modulate mRNA translation). The “double capacity” of arsenic to induce mutations and epimutations could be the main cause of arsenic-induced carcinogenesis. The aim of this review is to better clarify the mechanisms of the initiation and/or the promotion of arsenic-induced carcinogenesis in order to understand the best way to perform an early diagnosis and a prompt prevention that is the key point for protecting arsenic-exposed population. Studies on arsenic-exposed population should be designed in order to examine more comprehensively the presence and consequences of these genetic/epigenetic alterations.

The outbreak of coronavirus disease 2019 (COVID-19), caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), has rapidly spread worldwide. A number of serious effects on various organs and systems have been reported in humans, and recently emerging evidence on the potential association between the infection and thyroid dysfunction are attracting attention from the scientific community. This editorial critically summarizes the main findings on this topic published so far and defines research lines according to the translational approach from the bench to the bed to epidemiological studies and back again, aimed at patient care and effective public health measures.

Study question What are the long term trends in the total (live births, fetal deaths, and terminations of pregnancy for fetal anomaly) and live birth prevalence of neural tube defects (NTD) in Europe, where many countries have issued recommendations for folic acid supplementation but a policy for mandatory folic acid fortification of food does not exist?Methods This was a population based, observational study using data on 11 353 cases of NTD not associated with chromosomal anomalies, including 4162 cases of anencephaly and 5776 cases of spina bifida from 28 EUROCAT (European Surveillance of Congenital Anomalies) registries covering approximately 12.5 million births in 19 countries between 1991 and 2011. The main outcome measures were total and live birth prevalence of NTD, as well as anencephaly and spina bifida, with time trends analysed using random effects Poisson regression models to account for heterogeneities across registries and splines to model non-linear time trends.Summary answer and limitations Overall, the pooled total prevalence of NTD during the study period was 9.1 per 10 000 births. Prevalence of NTD fluctuated slightly but without an obvious downward trend, with the final estimate of the pooled total prevalence of NTD in 2011 similar to that in 1991. Estimates from Poisson models that took registry heterogeneities into account showed an annual increase of 4% (prevalence ratio 1.04, 95% confidence interval 1.01 to 1.07) in 1995-99 and a decrease of 3% per year in 1999-2003 (0.97, 0.95 to 0.99), with stable rates thereafter. The trend patterns for anencephaly and spina bifida were similar, but neither anomaly decreased substantially over time. The live birth prevalence of NTD generally decreased, especially for anencephaly. Registration problems or other data artefacts cannot be excluded as a partial explanation of the observed trends (or lack thereof) in the prevalence of NTD.What this study adds In the absence of mandatory fortification, the prevalence of NTD has not decreased in Europe despite longstanding recommendations aimed at promoting peri-conceptional folic acid supplementation and existence of voluntary folic acid fortification.Funding, competing interests, data sharing The study was funded by the European Public Health Commission, EUROCAT Joint Action 2011-2013. HD and ML received support from the European Commission DG Sanco during the conduct of this study. No additional data available.

The integration of endocytic routes is critical to regulate receptor signaling. A nonclathrin endocytic (NCE) pathway of the epidermal growth factor receptor (EGFR) is activated at high ligand concentrations and targets receptors to degradation, attenuating signaling. Here we performed an unbiased molecular characterization of EGFR-NCE.We identified NCE-specific regulators, including the endoplasmic reticulum (ER)–resident protein reticulon 3 (RTN3) and a specific cargo, CD147. RTN3 was critical for EGFR/CD147-NCE, promoting the creation of plasma membrane (PM)–ER contact sites that were required for the formation and/or maturation of NCE invaginations. Ca2+ release at these sites, triggered by inositol 1,4,5-trisphosphate (IP₃)–dependent activation of ER Ca2+ channels, was needed for the completion of EGFR internalization. Thus, we identified a mechanism of EGFR endocytosis that relies on ER-PM contact sites and local Ca2+ signaling.

Neuroendocrine neoplasms (NENs) of the lung encompass neuroendocrine tumors (NETs) composed of typical (TC) and atypical (AC) carcinoids and full-fledged carcinomas (NECs) inclusive of large cell neuroendocrine carcinoma (LCNEC) and small cell carcinoma (SCLC). NETs and NECs are thought to represent distinct and separate lesions with neither molecular overlap nor common developmental continuum. Two perspectives were addressed regarding the morphologic and molecular classification of lung NENs: (i) a supervised approach by browsing the traditional classification, the relevant gene alterations, and their clinical implications; and (ii) an unsupervised approach, by reappraising neoplasms according to risk factors and natural history of disease to construct an interpretation model relied on biological data. We herein emphasize lights and shadows of the current classification of lung NENs and provide an alternative outlook on these tumors focused on what we currently know about the biological determinants and the natural history of disease.