Excess mortality due to COVID-19 in Germany Stang, Andreas; Standl, Fabian; Kowall, Bernd ...
Journal of infection/The Journal of infection,
11/2020, Letnik:
81, Številka:
5
Journal Article
Recenzirano
Odprti dostop
•The management of the SARS-Cov-2 pandemic in Germany was named a success story.•A statistically sound estimate of excess mortality has not been made for Germany.•The excess mortality during the ...first wave of the pandemic is 8071 cases.•After age adjustment, there were 4926 fewer deaths than expected.•Several factors explain the comparatively mild course of the pandemic in Germany.
The first wave of the SARS-CoV-2 pandemic in Germany lasted from week 10 to 23 in 2020. The aim is to provide estimates of excess mortality in Germany during this time.
We analyzed age-specific numbers of deaths per week from 2016 to week 26 in 2020. We used weekly mean numbers of deaths of 2016–2019 to estimate expected weekly numbers for 2020. We estimated standardized mortality ratios (SMR) and 95% confidence intervals.
During the first wave observed numbers of deaths were higher than expected for age groups 60–69, 80–89, and 90+. The age group 70–79 years did not show excess mortality. The net excess number of deaths for weeks 10–23 was +8,071. The overall SMR was 1•03 (95%CI 1•03–1•04). The largest increase occurred among people aged 80–89 and 90+ (SMR=1•08 and SMR=1•09). A sensitivity analysis that accounts for demographic changes revealed an overall SMR of 0•98 (95%CI 0•98–0•99) and a deficit of 4,926 deaths for week 10–23, 2020.
The excess mortality existed for two months. The favorable course of the first wave may be explained by a younger age at infection at the beginning of the pandemic, lower contact rates, and a more efficient pandemic management.
Background and purpose
Cross‐sectional studies showed an inverse association between serum 25‐hydroxyvitamin D (25OHD) and white matter hyperintensities (WMHs) whereas the few longitudinal studies ...did not. The association between baseline 25OHD and WMHs at 10‐year follow‐up in the Heinz Nixdorf Recall Study plus 1000BRAINS was investigated.
Methods
Data of 505 participants (49% women, 56.2 ± 6.6 years) with 25OHD at baseline (2000–2003) and WMH volume and grade of WMHs using the Fazekas classification at 10‐year follow‐up were analysed. The association between deseasonalized 25OHD and the base‐10 logarithm of WMH volume was evaluated by multiple linear regression, adjusted for age, sex, education, smoking, alcohol consumption, sports, diabetes mellitus, systolic blood pressure and total cholesterol. β‐estimators were transformed back (10β). Using multiple logistic regression, odds ratios (ORs) and 95% confidence intervals (95% CI) were calculated to evaluate the association between deseasonalized 25OHD and Fazekas grades (0, absence and 1, punctate foci vs. 2, beginning and 3, large confluence).
Results
Mean 25OHD was 17.0 ± 8.2 ng/ml, and mean deseasonalized 25OHD was 16.9 ± 7.5 ng/ml. Mean WMH volume was 16.6 ± 17.4 ml, range 1–132 ml. Most grade 2–3 WMHs were found to be periventricular (39% of the participants), parietal (32%) and frontal (31%) (temporal 6%, occipital 3%). The linear regression showed an inverse association between 25OHD and WMH volume. On average, a 25OHD increase of 1 ng/ml was associated with a reduced WMH volume by a factor of 0.99 (95% CI 0.98; 1.00) (fully adjusted). There was also some indication for an inverse association between 25OHD and extent of periventricular (OR 0.98 95% CI 0.96; 1.01), frontal (0.99 0.97; 1.02) and parietal (0.98 0.95; 1.00) WMHs according to the Fazekas classification.
Conclusions
Lower 25OHD may be a risk factor for the occurrence of WMHs.
The figure shows the results of univariate and multiple linear regression to investigate the association between deseasonalized baseline 25‐hydroxyvitamin D (25OHD) and white matter hyperintensities (WMHs) at 10‐year follow‐up in the Heinz Nixdorf Recall Study plus 1000BRAINS (LCL, lower confidence limit; UCL, upper confidence limit). In the fully adjusted model that included all participants, on average a 25OHD increase of 1 ng/ml was associated with a reduced WMH volume by a factor of 0.986 (95% CI 0.978; 0.995). In conclusion, a lower baseline 25OHD might be a weak risk factor for more pronounced WMHs 10 years later.
Background
Survivors of heritable retinoblastoma carry a high risk to develop second cancers. Eye‐preserving radiotherapy raises this risk, while the impact of chemotherapy remains less defined.
...Procedure
This population‐based study characterizes the impact of all treatment modalities on second cancers incidence and type after retinoblastoma treatment in Germany. Data on second cancer incidence in 648 patients with heritable retinoblastoma treated between 1940 and 2008 at the German national reference center for retinoblastoma were analyzed to identify associations with treatment.
Results
The cumulative incidence ratio (per 1,000 person years) of second cancers was 8.6 (95% confidence interval 7.0–10.4). Second cancer incidence was influenced by type of retinoblastoma treatment but not by the year of diagnosis or by sex. Radiotherapy and systemic chemotherapy increased the incidence of second cancers (by 3.0‐ and 1.8‐fold, respectively). While radiotherapy was specifically associated with second cancers arising within the periorbital region in the previously irradiated field, chemotherapy was the strongest risk factor for second cancers in other localizations. Soft tissue sarcomas and osteosarcomas were the most prevalent second cancers (standardized incidence ratio 179.35 compared to the German population).
Conclusions
Second cancers remain a major concern in heritable retinoblastoma survivors. Consistent with previous reports, radiotherapy increased second cancer incidence and influenced type and localization. However, chemotherapy was the strongest risk factor for second malignancies outside the periorbital region. Our results provide screening priorities during life‐long oncological follow‐up based on the curative therapy the patient has received and emphasize the need for less‐detrimental therapies for children with heritable retinoblastoma.
Mild cognitive impairment (MCI) describes the intermediate state between normal cognitive aging and dementia. Adverse effects of air pollution (AP) on cognitive functions have been proposed, but ...investigations of simultaneous exposure to noise are scarce.
We analyzed the cross-sectional associations of long-term exposure to AP and traffic noise with overall MCI and amnestic (aMCI) and nonamnestic (naMCI) MCI.
At the second examination of the population-based Heinz Nixdorf Recall study, cognitive assessment was completed in 4,086 participants who were 50-80 years old. Of these, 592 participants were diagnosed as having MCI (aMCI, n = 309; naMCI, n = 283) according to previously published criteria using five neuropsychological subtests. We assessed long-term residential concentrations for size-fractioned particulate matter (PM) and nitrogen oxides with land use regression, and for traffic noise weighted 24-hr (LDEN) and night-time (LNIGHT) means. Logistic regression models adjusted for individual risk factors were calculated to estimate the association of environmental exposures with MCI in single- and two-exposure models.
Most air pollutants and traffic noise were associated with overall MCI and aMCI. For example, an interquartile range increase in PM2.5 and a 10 A-weighted decibel dB(A) increase in LDEN were associated with overall MCI as follows odds ratio (95% confidence interval): 1.16 (1.05, 1.27) and 1.40 (1.03, 1.91), respectively, and with aMCI as follows: 1.22 (1.08, 1.38) and 1.53 (1.05, 2.24), respectively. In two-exposure models, AP and noise associations were attenuated e.g., for aMCI, PM2.5 1.13 (0.98, 1.30) and LDEN 1.46 (1.11, 1.92).
Long-term exposures to air pollution and traffic noise were positively associated with MCI, mainly with the amnestic subtype.
Tzivian L, Dlugaj M, Winkler A, Weinmayr G, Hennig F, Fuks KB, Vossoughi M, Schikowski T, Weimar C, Erbel R, Jöckel KH, Moebus S, Hoffmann B, on behalf of the Heinz Nixdorf Recall study Investigative Group. 2016. Long-term air pollution and traffic noise exposures and mild cognitive impairment in older adults: a cross-sectional analysis of the Heinz Nixdorf Recall Study. Environ Health Perspect 124:1361-1368; http://dx.doi.org/10.1289/ehp.1509824.
Celotno besedilo
Dostopno za:
CEKLJ, DOBA, IZUM, KILJ, NUK, OILJ, PILJ, PNG, SAZU, SIK, UILJ, UKNU, UL, UM, UPUK, VSZLJ
BackgroundIn several studies, exposure to fine particulate matter (PM) has been associated with inflammation, with inconsistent results. We used repeated measurements to examine the association of ...long-term fine and ultrafine particle exposure with several blood markers of inflammation and coagulation.MethodsWe used baseline (2000–2003) and follow-up (2006–2008) data from the Heinz Nixdorf Recall Study, a German population-based prospective cohort of 4814 participants. A chemistry transport model was applied to model daily surface concentrations of PM air pollutants (PM10, PM2.5) and particle number on a grid of 1 km2. Applying mixed regression models, we analysed associations of long-term (mean of 365 days prior to blood draw) particle exposure at each participant's residence with the level of high-sensitivity C reactive protein (hs-CRP), fibrinogen, platelet and white cell count (WCC), adjusting for short-term PM exposure (moving averages of 1–7 days), personal characteristics, season, ambient temperature (1–5 days), ozone and time trend.ResultsWe analysed 6488 observations: 3275 participants with baseline data and 3213 with follow-up data. An increase of 2.4 µg/m3 in long-term PM2.5 was associated with an adjusted increase of 5.4% (95% CI 0.6% to 10.5%) in hs-CRP and of 2.3% (95% CI 1.4% to 3.3%) in the platelet count. Fibrinogen and WCC were not associated with long-term particle exposure.ConclusionsIn this population-based cohort, we found associations of long-term exposure to PM with markers of inflammation (hs-CRP) and coagulation (platelets). This finding supports the hypothesis that inflammatory processes might contribute to chronic effects of air pollution on cardiovascular disease.
To assess the prevalence of acute mountain sickness (AMS) in 1370 mountaineers at four different altitudes in the Western Alps. We also examined the influence of potential risk factors and the ...knowledge about AMS on its prevalence. In this observational cross-sectional study AMS was assessed on the day of ascent by the Lake Louise score (LLS, cut-off greater than or equal to3, version 2018) and the AMS-Cerebral (AMS-C) score of the environmental symptom questionnaire (cut-off greater than or equal to0,70). The latter was also obtained in the next morning. Knowledge regarding AMS and high-altitude cerebral edema (HACE) and the potential risk factors for AMS were evaluated by questionnaires. On the day of ascent, the prevalence of AMS assessed by the LLS and AMS-C score was 5.8 and 3.9% at 2850 m, 2.1 and 3.1% at 3050 m, 14.8 and 10.1% at 3650 m, and 21.9 and 15% at 4559 m, respectively. The AMS prevalence increased overnight from 10.1 to 14.5% and from 15 to 25.2% at 3650 m and 4559 m, respectively, and was unchanged at 2850 m and 3050 m. A history of AMS, higher altitude, lower degree of pre-acclimatization, and younger age were identified as risk factors for developing AMS. Slow ascent was weakly associated with AMS prevalence, and sex and knowledge about AMS and HACE were indistinct. AMS is common at altitudes greater than or equal to 3650 m and better knowledge about AMS and HACE was not associated with less AMS in mountaineers with on average little knowledge.
Celotno besedilo
Dostopno za:
DOBA, IZUM, KILJ, NUK, PILJ, PNG, SAZU, SIK, UILJ, UKNU, UL, UM, UPUK
Background
White matter hyperintensities of presumed vascular origin (WMH) are frequent in cerebral magnetic resonance imaging of older people. They are promoted by vascular risk factors, especially ...hypertension, and are associated with cognitive deficits at the group level. It has been suggested that not only the severity, but also the location, of lesions might critically influence cognitive deficits and represent different pathologies.
Methods
In 560 participants (65.2 ± 7.5 years, 51.4% males) of the population‐based 1000BRAINS study, we analyzed the association of regional WMH using Fazekas scoring separately for cerebral lobes, with hypertension and cognition.
Results
WMH most often affected the frontal lobe (83.7% score >0), followed by the parietal (75.8%), temporal (32.7%), and occipital lobe (7.3%). Higher Fazekas scores in the frontal, parietal, and temporal lobe were associated with higher blood pressure and antihypertensive treatment in unadjusted ordinal regression models and in models adjusted for age, sex, and vascular risk factors (e.g., age‐ and sex‐adjusted odds ratio = 1.14, 95% confidence interval = 1.03–1.25 for the association of frontal lobe WMH Fazekas score with systolic blood pressure SBP per 10 mm Hg; 1.13 1.02–1.23 for the association of parietal lobe score with SBP; 1.72 1.19–2.48 for the association of temporal lobe score with antihypertensive medications). In linear regressions, higher frontal lobe scores were associated with lower performance in executive function and non‐verbal memory, and higher parietal lobe scores were associated with lower performance in executive function, verbal‐, and non‐verbal memory.
Conclusions
Hypertension promotes WMH in the frontal, parietal, and temporal lobe. WMH in the frontal and parietal lobe are associated with reduced executive function and memory.
Several studies have demonstrated the tremendous potential of using coronary artery calcium (CAC) in addition to traditional risk factors for coronary heart disease (CHD) risk prediction. However, to ...date, no risk score incorporating CAC has been developed.
The goal of this study was to derive and validate a novel risk score to estimate 10-year CHD risk using CAC and traditional risk factors.
Algorithm development was conducted in the MESA (Multi-Ethnic Study of Atherosclerosis), a prospective community-based cohort study of 6,814 participants age 45 to 84 years, who were free of clinical heart disease at baseline and followed for 10 years. MESA is sex balanced and included 39% non-Hispanic whites, 12% Chinese Americans, 28% African Americans, and 22% Hispanic Americans. External validation was conducted in the HNR (Heinz Nixdorf Recall Study) and the DHS (Dallas Heart Study).
Inclusion of CAC in the MESA risk score offered significant improvements in risk prediction (C-statistic 0.80 vs. 0.75; p < 0.0001). External validation in both the HNR and DHS studies provided evidence of very good discrimination and calibration. Harrell's C-statistic was 0.779 in HNR and 0.816 in DHS. Additionally, the difference in estimated 10-year risk between events and nonevents was approximately 8% to 9%, indicating excellent discrimination. Mean calibration, or calibration-in-the-large, was excellent for both studies, with average predicted 10-year risk within one-half of a percent of the observed event rate.
An accurate estimate of 10-year CHD risk can be obtained using traditional risk factors and CAC. The MESA risk score, which is available online on the MESA web site for easy use, can be used to aid clinicians when communicating risk to patients and when determining risk-based treatment strategies.
Traffic noise affects a large number of people, particularly in urbanized areas. Noise causes stress and annoyance, but less is known about the relationship between noise and depression.
We ...investigated the association of residential road traffic noise with depressive symptoms using 5-year follow-up data from a German population-based study.
We analyzed data from 3,300 participants in the Heinz Nixdorf Recall study who were between 45 and 75 years old and were without depressive symptoms at baseline (2000-2003). Depressive symptoms were defined based on the Center for Epidemiologic Studies Depression scale (CES-D) 15-item questionnaire (total score ≥ 17) and antidepressant medication intake. Road traffic noise was modeled according to European Parliament/Council Directive 2002/49/EC. High noise exposure was defined as annual mean 24-hr noise levels > 55 A-weighted decibels dB(A). Poisson regression with robust variance was used to estimate relative risks (RRs) a) adjusting for the potential confounders age, sex, socioeconomic status (SES), neighborhood-level SES, and traffic proximity; b) additionally adjusting for body mass index and smoking; and c) additionally adjusting for the potential confounders/intermediates comorbidities and insomnia.
Overall, 35.7% of the participants were exposed to high residential road traffic noise levels. At follow-up (mean = 5.1 years after baseline), 302 participants were classified as having high depressive symptoms, corresponding to an adjusted RR of 1.29 (95% CI: 1.03, 1.62; Model 1) for exposure to > 55 versus ≤ 55 dB(A). Adjustment for potential confounders/intermediates did not substantially alter the results. Associations were stronger among those who reported insomnia at baseline (RR = 1.62; 95% CI: 1.10, 2.59 vs. RR = 1.21; 95% CI: 0.94, 1.57) and appeared to be limited to those with ≤ 13 years of education (RR = 1.43; 95% CI: 1.10, 1.85 vs. 0.92; 95% CI: 0.56, 1.53 for > 13 years).
Our results suggest that exposure to residential road traffic noise increases the risk of depressive symptoms.
Orban E, McDonald K, Sutcliffe R, Hoffmann B, Fuks KB, Dragano N, Viehmann A, Erbel R, Jöckel KH, Pundt N, Moebus S. 2016. Residential road traffic noise and high depressive symptoms after five years of follow-up: results from the Heinz Nixdorf Recall Study. Environ Health Perspect 124:578-585; http://dx.doi.org/10.1289/ehp.1409400.
Celotno besedilo
Dostopno za:
CEKLJ, DOBA, IZUM, KILJ, NUK, OILJ, PILJ, PNG, SAZU, SIK, UILJ, UKNU, UL, UM, UPUK, VSZLJ
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