Validity of reported indicators of pesticide exposure and relevance for cytotoxic and genotoxic effects on buccal cells.

Higher rates of nuclear anomalies in buccal cells of coffee workers exposed to pesticides in comparison to their unexposed peers were detected in our field study. Here, we extend our findings by examining other exposure indicators in this sample. Occupational exposure of 38 exposed and 33 non-exposed farmworkers was assessed as exposure days in the last month (0-25 days) and as years of exposure (0-47 years). Genotoxic and cytotoxic markers in buccal cells were analysed following standard procedures for buccal micronucleus cytome assay. Both exposure markers were associated with a higher frequency of nuclear anomalies with odds ratios more than 1. After restricting the analysis to the exposed workers only, this association remained only with the marker of recent exposure. In a secondary analysis also environmental exposure defined as proximity of the home to the nearest sprayed field (distance <1000 m) was assessed. Proximity led to increased rates (with odds ratios more than 3) of genotoxic but not cytotoxic nuclear anomalies. Reported recent frequency and intensity of pesticide use and application are a valid exposure marker relevant for cytological pathologies in the buccal mucosa. The exposure metric for environmental exposure was rather crude and confounding by some unmeasured factor cannot be fully excluded. Nevertheless, simple exposure indicators that can even be obtained under rather difficult field conditions do provide health-relevant and valid information.

Targeting cardiac hypertrophy: toward a causal heart failure therapy.

Cardiac hypertrophy is commonly observed in conditions of increased hemodynamic or metabolic stress. This hypertrophy is not compensatory but rather reflects activation of maladaptive cellular processes that promote disease progression. Myocardial hypertrophy serves as a diagnostic and prognostic marker of cardiac remodeling, and underlying regulatory processes have provided effective therapeutic targets to slow disease progression and improve outcome. We review hypertrophic signaling pathways in cardiomyocytes and discuss established and novel targets for pharmacological intervention. New drugs in the pipeline include the third generation aldosterone antagonists (PF-03882845 and BAY94-8862) and biased angiotensin II receptor agonists. Furthermore, different approaches to stimulate cGMP-dependent protective signaling are currently evaluated in clinical trials, including the combination of the vasopeptidase neprilysin inhibitor and an angiotensin receptor blocker (ARNi). In an overview on cardiomyocyte hypertrophic signaling, we also highlight emerging experimental treatment concepts such as inhibition of Ca-mediated transcriptional regulation, adeno-associated viruses for sarcoplasmic/endoplasmic reticulum calcium ATPase (SERCA2a), PI3 kinase gene transfer and microRNA-based therapy. We conclude that antihypertrophic therapy extends beyond blocking the classical ß-adrenergic and renin-angiotensin-aldosterone system-dependent signaling cascades, although new therapies require clinical validation regarding outcome.

PKC-dependent coupling of calcium permeation through transient receptor potential canonical 3 (TRPC3) to calcineurin signaling in HL-1 myocytes.

Cardiac transient receptor potential canonical (TRPC) channels are crucial upstream components of Ca(2+)/calcineurin/nuclear factor of activated T cells (NFAT) signaling, thereby controlling cardiac transcriptional programs. The linkage between TRPC-mediated Ca(2+) signals and NFAT activity is still incompletely understood. TRPC conductances may govern calcineurin activity and NFAT translocation by supplying Ca(2+) either directly through the TRPC pore into a regulatory microdomain or indirectly via promotion of voltage-dependent Ca(2+) entry. Here, we show that a point mutation in the TRPC3 selectivity filter (E630Q), which disrupts Ca(2+) permeability but preserves monovalent permeation, abrogates agonist-induced NFAT signaling in HEK293 cells as well as in murine HL-1 atrial myocytes. The E630Q mutation fully retains the ability to convert phospholipase C-linked stimuli into L-type (Ca(V)1.2) channel-mediated Ca(2+) entry in HL-1 cells, thereby generating a dihydropyridine-sensitive Ca(2+) signal that is isolated from the NFAT pathway. Prevention of PKC-dependent modulation of TRPC3 by either inhibition of cellular kinase activity or mutation of a critical phosphorylation site in TRPC3 (T573A), which disrupts targeting of calcineurin into the channel complex, converts cardiac TRPC3-mediated Ca(2+) signaling into a transcriptionally silent mode. Thus, we demonstrate a dichotomy of TRPC-mediated Ca(2+) signaling in the heart constituting two distinct pathways that are differentially linked to gene transcription. Coupling of TRPC3 activity to NFAT translocation requires microdomain Ca(2+) signaling by PKC-modified TRPC3 complexes. Our results identify TRPC3 as a pivotal signaling gateway in Ca(2+)-dependent control of cardiac gene expression.

Microplastics: Omnipresent and an ongoing challenge for medical science.

Micro- and nanoplastics are omnipresent not only in the environment, but have also been detected in human body fluids and tissue. The subsequent commentary provides a perspective about potential risks for human health as well as resulting challenges for medical science.

Inhibition of Orai1-mediated Ca(2+) entry is a key mechanism of the antiproliferative action of sirolimus in human arterial smooth muscle.

Sirolimus (rapamycin) is used in drug-eluting stent strategies and proved clearly superior in this application compared with other immunomodulators such as pimecrolimus. The molecular basis of this action of sirolimus in the vascular system is still incompletely understood. Measurements of cell proliferation in human coronary artery smooth muscle cells (hCASM) demonstrated a higher antiproliferative activity of sirolimus compared with pimecrolimus. Although sirolimus lacks inhibitory effects on calcineurin, nuclear factor of activated T-cell activation in hCASM was suppressed to a similar extent by both drugs at 10 µM. Sirolimus, but not pimecrolimus, inhibited agonist-induced and store-operated Ca(2+) entry as well as cAMP response element binding protein (CREB) phosphorylation in human arterial smooth muscle, suggesting the existence of an as-yet unrecognized inhibitory effect of sirolimus on Ca(2+) signaling and Ca(2+)-dependent gene transcription. Electrophysiological experiments revealed that only sirolimus but not pimecrolimus significantly blocked the classical stromal interaction molecule/Orai-mediated, store-operated Ca(2+) current reconstituted in human embryonic kidney cells (HEK293). A link between Orai function and proliferation was confirmed by dominant-negative knockout of Orai in hCASM. Analysis of the effects of sirolimus on cell proliferation and CREB activation in an in vitro model of arterial intervention using human aorta corroborated the ability of sirolimus to suppress stent implantation-induced CREB activation in human arteries. We suggest inhibition of store-operated Ca(2+) entry based on Orai channels and the resulting suppression of Ca(2+) transcription coupling as a key mechanism underlying the antiproliferative activity of sirolimus in human arteries. This mechanism of action is specific for sirolimus and not a general feature of drugs interacting with FK506-binding proteins.

Determinants of exposure to acrylamide in European children and adults based on urinary biomarkers: results from the "European Human Biomonitoring Initiative" HBM4EU participating studies.

Little is known about exposure determinants of acrylamide (AA), a genotoxic food-processing contaminant, in Europe. We assessed determinants of AA exposure, measured by urinary mercapturic acids of AA (AAMA) and glycidamide (GAMA), its main metabolite, in 3157 children/adolescents and 1297 adults in the European Human Biomonitoring Initiative. Harmonized individual-level questionnaires data and quality assured measurements of AAMA and GAMA (urine collection: 2014-2021), the short-term validated biomarkers of AA exposure, were obtained from four studies (Italy, France, Germany, and Norway) in children/adolescents (age range: 3-18 years) and six studies (Portugal, Spain, France, Germany, Luxembourg, and Iceland) in adults (age range: 20-45 years). Multivariable-adjusted pooled quantile regressions were employed to assess median differences (ß coefficients) with 95% confidence intervals (95% CI) in AAMA and GAMA (µg/g creatinine) in relation to exposure determinants. Southern European studies had higher AAMA than Northern studies. In children/adolescents, we observed significant lower AA associated with high socioeconomic status (AAMA:ß = - 9.1 µg/g creatinine, 95% CI - 15.8, - 2.4; GAMA: ß = - 3.4 µg/g creatinine, 95% CI - 4.7, - 2.2), living in rural areas (AAMA:ß = - 4.7 µg/g creatinine, 95% CI - 8.6, - 0.8; GAMA:ß = - 1.1 µg/g creatinine, 95% CI - 1.9, - 0.4) and increasing age (AAMA:ß = - 1.9 µg/g creatinine, 95% CI - 2.4, - 1.4; GAMA:ß = - 0.7 µg/g creatinine, 95% CI - 0.8, - 0.6). In adults, higher AAMA was also associated with high consumption of fried potatoes whereas lower AAMA was associated with higher body-mass-index. Based on this large-scale study, several potential determinants of AA exposure were identified in children/adolescents and adults in European countries.

Mitochondrial Ca2+ uptake and not mitochondrial motility is required for STIM1-Orai1-dependent store-operated Ca2+ entry.

Store-operated Ca(2+) entry (SOCE) is established by formation of subplasmalemmal clusters of the endoplasmic reticulum (ER) protein, stromal interacting molecule 1 (STIM1) upon ER Ca(2+) depletion. Thereby, STIM1 couples to plasma membrane channels such as Orai1. Thus, a close proximity of ER domains to the plasma membrane is a prerequisite for SOCE activation, challenging the concept of local Ca(2+) buffering by mitochondria as being essential for SOCE. This study assesses the impact of mitochondrial Ca(2+) handling and motility on STIM1-Orai1-dependent SOCE. High-resolution microscopy showed only 10% of subplasmalemmal STIM1 clusters to be colocalized with mitochondria. Impairments of mitochondrial Ca(2+) handling by inhibition of mitochondrial Na(+)-Ca(2+) exchanger (NCX(mito)) or depolarization only partially suppressed Ca(2+) entry in cells overexpressing STIM1-Orai1. However, SOCE was completely abolished when both NCX(mito) was inhibited and the inner mitochondrial membrane was depolarized, in STIM1- and Orai1-overexpressing cells. Immobilization of mitochondria by expression of mAKAP-RFP-CAAX, a construct that physically links mitochondria to the plasma membrane, affected the Ca(2+) handling of the organelles but not the activity of SOCE. Our observations indicate that mitochondrial Ca(2+) uptake, including reversal of NCX(mito), is fundamental for STIM1-Orai1-dependent SOCE, whereas the proximity of mitochondria to STIM1-Orai1 SOCE units and their motility is not required.

COVID-19: Regional Differences in Austria.

In the turbulent year 2020, overshadowed by the global COVID-19 pandemic, Austria experienced multiple waves of increased case incidence. While governmental measures to curb the numbers were based on current knowledge of infection risk factors, a retrospective analysis of incidence and lethality at the district level revealed correlations of relative infection risk with socioeconomic, geographical, and behavioral population parameters. We identified unexpected correlations between political orientation and smoking behavior and COVID-19 infection risk and/or mortality. For example, a decrease in daily smokers by 2.3 percentage points would be associated with an increase in cumulative incidence by 10% in the adjusted model, and an increase in voters of the right-wing populist party by 1.6 percentage points with an increase in cumulative mortality by 10%. While these parameters are apparently only single elements of complex causal chains that finally lead to individual susceptibility and vulnerability levels, our findings might have identified ecological parameters that can be utilized to develop fine-tuned communications and measures in upcoming challenges of this and other pandemics.

Anti-Inflammatory Effects of Melatonin in Rats with Induced Type 2 Diabetes Mellitus.

INTRODUCTION: Insulin resistance is associated with a pro-inflammatory state increasing the risk for complications in patients with type 2 diabetes mellitus (T2DM). In addition to its chronobiotic effects, the pineal hormone melatonin is known to exert anti-inflammatory and antioxidant effects. Melatonin was also suggested to affect insulin secretion. The aim of this study was therefore to investigate the effect of melatonin on inflammation in diabetic rats and to study the possible involvement of the melatonin receptor, MT2. MATERIALS AND METHODS: Male Sprague Dawley rats were randomly divided into four experimental groups (n = 10 per group): (1) control, (2) streptozotocin/nicotinamide induced diabetes type 2 (T2DM), (3) T2DM treated with melatonin (500 µg/kg/day), and (4) T2DM treated with melatonin (500 µg/kg/day for 6 weeks) and the selective MT2 receptor antagonist luzindole (0.25 g/kg/day for 6 weeks). Blood samples were taken for biochemical parameters and various tissue samples (liver, adipose tissue, brain) were removed for immunohistochemistry (IHC), Western blot (WB), and Q-PCR analyses, respectively. RESULTS: Melatonin significantly reduced increased blood levels of liver transaminases (AST, ALT), blood urea nitrogen (BUN), triglyceride, very low-density lipoprotein (VLDL), and cholesterol in diabetic rats with luzindole treatment partly reversing this effect regarding the lipids. Furthermore, the liver and adipose tissues of T2DM rats treated with melatonin showed lower expression of the inflammatory markers IL-1ß, IL-6, TNF-α, and NF-κB as compared to the T2DM group without melatonin. The results also showed that the MT2 receptor is at least partly involved in the protective effects of melatonin. CONCLUSIONS: Our results suggest that melatonin exerts relevant anti-inflammatory effects on various tissues in type 2 diabetic rats.

Trends of Exposure to Acrylamide as Measured by Urinary Biomarkers Levels within the HBM4EU Biomonitoring Aligned Studies (2000-2021).

Acrylamide, a substance potentially carcinogenic in humans, represents a very prevalent contaminant in food and is also contained in tobacco smoke. Occupational exposure to higher concentrations of acrylamide was shown to induce neurotoxicity in humans. To minimize related risks for public health, it is vital to obtain data on the actual level of exposure in differently affected segments of the population. To achieve this aim, acrylamide has been added to the list of substances of concern to be investigated in the HBM4EU project, a European initiative to obtain biomonitoring data for a number of pollutants highly relevant for public health. This report summarizes the results obtained for acrylamide, with a focus on time-trends and recent exposure levels, obtained by HBM4EU as well as by associated studies in a total of seven European countries. Mean biomarker levels were compared by sampling year and time-trends were analyzed using linear regression models and an adequate statistical test. An increasing trend of acrylamide biomarker concentrations was found in children for the years 2014-2017, while in adults an overall increase in exposure was found to be not significant for the time period of observation (2000-2021). For smokers, represented by two studies and sampling for, over a total three years, no clear tendency was observed. In conclusion, samples from European countries indicate that average acrylamide exposure still exceeds suggested benchmark levels and may be of specific concern in children. More research is required to confirm trends of declining values observed in most recent years.

Time Trends of Acrylamide Exposure in Europe: Combined Analysis of Published Reports and Current HBM4EU Studies.

More than 20 years ago, acrylamide was added to the list of potential carcinogens found in many common dietary products and tobacco smoke. Consequently, human biomonitoring studies investigating exposure to acrylamide in the form of adducts in blood and metabolites in urine have been performed to obtain data on the actual burden in different populations of the world and in Europe. Recognizing the related health risk, the European Commission responded with measures to curb the acrylamide content in food products. In 2017, a trans-European human biomonitoring project (HBM4EU) was started with the aim to investigate exposure to several chemicals, including acrylamide. Here we set out to provide a combined analysis of previous and current European acrylamide biomonitoring study results by harmonizing and integrating different data sources, including HBM4EU aligned studies, with the aim to resolve overall and current time trends of acrylamide exposure in Europe. Data from 10 European countries were included in the analysis, comprising more than 5500 individual samples (3214 children and teenagers, 2293 adults). We utilized linear models as well as a non-linear fit and breakpoint analysis to investigate trends in temporal acrylamide exposure as well as descriptive statistics and statistical tests to validate findings. Our results indicate an overall increase in acrylamide exposure between the years 2001 and 2017. Studies with samples collected after 2018 focusing on adults do not indicate increasing exposure but show declining values. Regional differences appear to affect absolute values, but not the overall time-trend of exposure. As benchmark levels for acrylamide content in food have been adopted in Europe in 2018, our results may imply the effects of these measures, but only indicated for adults, as corresponding data are still missing for children.

Cell-cell contact formation governs Ca2+ signaling by TRPC4 in the vascular endothelium: evidence for a regulatory TRPC4-beta-catenin interaction.

TRPC4 is well recognized as a prominent cation channel in the vascular endothelium, but its contribution to agonist-induced endothelial Ca(2+) entry is still a matter of controversy. Here we report that the cellular targeting and Ca(2+) signaling function of TRPC4 is determined by the state of cell-cell adhesions during endothelial phenotype transitions. TRPC4 surface expression in human microvascular endothelial cells (HMEC-1) increased with the formation of cell-cell contacts. Epidermal growth factor recruited TRPC4 into the plasma membrane of proliferating cells but initiated retrieval of TRPC4 from the plasma membrane in quiescent, barrier-forming cells. Epidermal growth factor-induced Ca(2+) entry was strongly promoted by the formation of cell-cell contacts, and both siRNA and dominant negative knockdown experiments revealed that TRPC4 mediates stimulated Ca(2+) entry exclusively in proliferating clusters that form immature cell-cell contacts. TRPC4 co-precipitated with the junctional proteins beta-catenin and VE-cadherin. Analysis of cellular localization of fluorescent fusion proteins provided further evidence for recruitment of TRPC4 into junctional complexes. Analysis of TRPC4 function in the HEK293 expression system identified beta-catenin as a signaling molecule that enables cell-cell contact-dependent promotion of TRPC4 function. Our results place TRPC4 as a Ca(2+) entry channel that is regulated by cell-cell contact formation and interaction with beta-catenin. TRPC4 is suggested to serve stimulated Ca(2+) entry in a specific endothelial state during the transition from a proliferating to a quiescent phenotype. Thus, TRPC4 may adopt divergent, as yet unappreciated functions in endothelial Ca(2+) homeostasis and emerges as a potential key player in endothelial phenotype switching and tuning of cellular growth factor signaling.

COVID-19 and air pollution in Vienna-a time series approach.

We performed a time series analysis in Vienna, Austria, investigating the temporal association between daily air pollution (nitrogen dioxide, NO2 and particulate matter smaller than 10 µm, PM10) concentration and risk of coronavirus disease 2019 (COVID-19) infection and death. Data covering about 2 months (March-April 2020) were retrieved from public databases. Infection risk was defined as the ratio between infected and infectious. In a separate sensitivity analysis different models were applied to estimate the number of infectious people per day. The impact of air pollution was assessed through a linear regression on the natural logarithm of infection risk. Risk of COVID-19 mortality was estimated by Poisson regression. Both pollutants were positively correlated with the risk of infection with the coefficient for NO2 being 0.032 and for PM10 0.014. That association was significant for the irritant gas (p = 0.012) but not for particles (p = 0.22). Pollutants did not affect COVID-19-related mortality. The study findings might have wider implications on an interaction between air pollution and infectious agents.

Health Symptoms Related to Pesticide Use in Farmers and Laborers of Ecological and Conventional Banana Plantations in Ecuador.

Conventional banana farming is pesticide-intensive and leads to high exposure of farmworkers. Ecuador is the world's biggest exporter of bananas. In this field study in 5 communities in Ecuador, we recorded potentially pesticide-associated subjective health symptoms in farmworkers and compared pesticide users to workers in organic farming. With one exception, symptom rates were always higher in the pesticide-exposed group. Significance was reached in 8 out of 19 investigated symptoms with the highest odds ratios (and smallest p-values) for local irritation like skin and eye irritation (OR = 3.58, CI 1.10-11.71, and 4.10, CI 1.37-12.31, respectively) as well as systemic symptoms like dizziness (OR = 4.80, CI 1.55-14.87) and fatigue (OR = 4.96, CI 1.65-14.88). Moreover, gastrointestinal symptoms were reported more frequently by pesticide users: nausea (OR = 7.5, CI 1.77-31.77) and diarrhea (OR = 6.43, CI 1.06-30.00). The majority of farmworkers were not adequately protected from pesticide exposure. For example, only 3 of 31 farmworkers that had used pesticides recently reported using gloves and only 6 reported using masks during active spraying. Improved safety measures and a reduction in pesticide use are necessary to protect the health of banana farmworkers.

Correlative SEM-Raman microscopy to reveal nanoplastics in complex environments.

Nowadays "microplastics" (MPs) is an already well-known term and results of micro-sized particles found in consumer products or environments are regularly reported. However, studies of native MPs smaller than 1 µm, often referred to as nanoplastics (NPs), in analytically challenging environments are rare. In this study, a correlative approach between scanning electron microscopy and Raman microscopy is tested to meet the challenges of finding and identifying NPs in the 100 nm range in various environments, ranging from ideal (distilled water) to challenging (sea salt, human amniotic fluid). To test the viability of this approach in principle, standardized polystyrene beads (Ø 200 nm) are mixed into the various environments in different concentrations. Promising detection limits of 2 10-3 µg/L (distilled water), 20 µg/L (sea salt) and 200 µg/L (human amniotic fluid) are found. To test the approach in practices both sea salt and amniotic fluid are analysed for native NPs as well. Interestingly a nylon-NP was found in the amniotic fluid, maybe originating from the sampling device. However, the practical test reveals limitations, especially with regard to the reliable identification of unknown NPs by Raman microscopy, due to strong background signals from the environments. We conclude from this in combination with the excellent performance in distilled water that a combination of this approach with an advanced sample preparation technique would yield a powerful tool for the analysis of NPs in various environments.

Daylight Saving Time Transitions: Impact on Total Mortality.

In Europe and many countries worldwide, a half-yearly changing time scheme has been adopted with the aim of optimizing the use of natural daylight during working hours and saving energy. Because the expected net economic benefit was not achieved, the discussion about the optimal solution has been reopened with a shifted focus on social and health related consequences. We set out to produce evidence for this discussion and analysed the impact of daylight saving time on total mortality of a general population in a time series study on daily total mortality for the years 1970-2018 in the city of Vienna, Austria. Daily deaths were modelled by Poisson regression controlling for seasonal and long-term trend, same-day and 14-day average temperature, humidity, and day of week. During the week after the spring transition a significant increase in daily total mortality of about 3% per day was observed. This was not the case during the week after the fall transition. The increase in daily mortality as observed in the week after spring DST-transition is most likely causally linked to the change in time scheme.

More pesticides-less children?

A previously presented study investigated the impact of recent pesticide exposure on cytological signs of genotoxicity and on symptoms of intoxication in 71 male coffee workers in the Dominican Republic. An unexpected finding of this study was that conventional farming workers, among other symptoms, reported fewer children than controls working in organic farms without pesticide use. This study set out to investigate possible reasons for the latter difference. One statistical problem of this analysis is that the age of the workers is a strong predictor for the number of children and available data on the exposure determinants "duration of pesticide exposure" as well as "age at first pesticide exposure" are correlated with age. To correctly control statistics for these confounding parameters, different approaches to best control for age were explored. After careful elimination of the age-related confounding factors, a reduced number of children was still observed in exposed workers. The clearest effect is seen in those workers that reported first exposure before the age of 20 years. Socioeconomic factors could still confound that finding, but a direct effect of early life pesticide exposure is the most likely explanation of the observation.

Perfluoroctanoic acid (PFOA) enhances NOTCH-signaling in an angiogenesis model of placental trophoblast cells.

Exposure to perfluoroalkyl substances (PFAS) was found to be associated with several pathological endpoints, including high cholesterol levels, specific defective functions of the immune system and reduced birth weight. While environmental PFAS have been recognized as threats for public health, surprisingly little is known about the underlying mechanisms of toxicity. We hypothesized that some of the observed vascular and developmental effects of environmental PFAS may share a common molecular pathway. At elevated levels of exposure to PFAS, a reduction in mean birth weight of newborns has been observed in combination with a high incidence rate of preeclampsia. As both, preeclampsia and reduced birth weight are consequences of an inadequate placental vascularization, we hypothesized that the adaptation of placental vasculature may get compromised by PFAS. We analyzed pseudo-vascular network formation and protein expression in the HTR8/SVneo cell line, an embryonic trophoblast cell type that is able to form vessel-like vascular networks in 3D-matrices, similar to endothelial cells. PFOA (perfluoroctanoic acid), but not PFOS (perfuoroctanesulfonic acid), induced morphological changes in the vascular 3D-network structure, without indications of compromised cellular viability. Incubation with PFOA reduced cellular sprouting and elongated isolated stalks in pseudo-vascular networks, while a γ-secretase inhibitor BMS-906024 induced directional opposite effects. We found a PFOA-induced increase in NOTCH intracellular domain (NICD) abundance in HTR8/SVneo, indicating that PFOA enhances NOTCH-signaling in this cell type. Enhancement of NOTCH-pathway by PFOA may be a key to understand the mode of action of PFAS, as this pathway is critically involved in many confirmed physiological/toxicological symptoms associated with PFAS exposure.

Time Course of COVID-19 Cases in Austria.

COVID-19 is an infectious disease caused by a novel coronavirus, which first appeared in China in late 2019, and reached pandemic distribution in early 2020. The first major outbreak in Europe occurred in Northern Italy where it spread to neighboring countries, notably to Austria, where skiing resorts served as a main transmission hub. Soon, the Austrian government introduced strict measures to curb the spread of the virus. Using publicly available data, we assessed the efficiency of the governmental measures. We assumed an average incubation period of one week and an average duration of infectivity of 10 days. One week after the introduction of strict measures, the increase in daily new cases was reversed, and the reproduction number dropped. The crude estimates tended to overestimate the reproduction rate in the early phase. Publicly available data provide a first estimate about the effectiveness of public health measures. However, more data are needed for an unbiased assessment.

Air Pollution Is Associated with COVID-19 Incidence and Mortality in Vienna, Austria.

We determined the impact of air pollution on COVID-19-related mortality and reported-case incidence, analyzing the correlation of infection case numbers and outcomes with previous-year air pollution data from the populations of 23 Viennese districts. Time at risk started in a district when the first COVID-19 case was diagnosed. High exposure levels were defined as living in a district with an average (year 2019) concentration of nitrogen dioxide (NO2) and/or particulate matter (PM10) higher than the upper quartile (30 and 20 µg/m3, respectively) of all districts. The total population of the individual districts was followed until diagnosis of or death from COVID-19, or until 21 April 2020, whichever came first. Cox proportional hazard regression was performed after controlling for percentage of population aged 65 and more, percentage of foreigners and of persons with a university degree, unemployment rate, and population density. PM10 and NO2 were significantly and positively associated with the risk of a COVID-19 diagnosis (hazard ratio (HR) = 1.44 and 1.16, respectively). NO2 was also significantly associated with death from COVID-19 (HR = 1.72). Even within a single city, higher levels of air pollution are associated with an adverse impact on COVID-19 risk.