scholarly journals Environmental radiofrequency radiation at the Järntorget Square in Stockholm Old Town, Sweden in May, 2018 compared with results on brain and heart tumour risks in rats exposed to 1.8 GHz base station environmental emissions

2018 ◽  
Author(s):  
LENNART HARDELL ◽  
MICHAEL CARLBERG ◽  
LENA K. HEDENDAHL ◽  
TARMO KOPPEL ◽  
MIKKO AHONEN
Keyword(s):  
Epidemiological Studies ◽  
Mean Value ◽  
Base Station ◽  
Female Rats ◽  
Male Rats ◽  
International Agency ◽  
Malignant Schwannoma ◽  
Environmental Radiation ◽  
Carcinogenicity Study ◽  
Increased Risk

Radiofrequency (RF) radiation in the frequency range 30 kHz to 300 GHz was evaluated in 2011 by the International Agency for Research on Cancer (IARC) at WHO to be a 'possible human carcinogen' Group 2B. The conclusion was based on human epidemiological studies on an increased risk of glioma and acoustic neuroma. In previous measurement studies, we found high environmental RF radiation levels at certain public places and also in an apartment in Stockholm, Sweden. One such place was the Järntorget square in the Stockholm Old Town. The EME Spy exposimeter was used for these studies. We have now conducted a field spatial distribution measurement with a radiofrequency broadband analyser. The maximum E-field topped at 11.6 V/m at the centre of the square, where the antenna was focused. Järntorget's mean value was 5.2 V/m, median 5.0 V/m, range 1.2-11.6 V/m. Of interest is that this level can be compared to a lifespan carcinogenicity study on rats exposed to 1.8 GHz GSM environmental radiation performed at the Ramazzini Institute (RI) in Italy. A statistically significant increase in the incidence of malignant schwannoma in the heart was found in male rats at the highest dose, 50 V/m. In treated female rats at the highest dose, the incidence of malignant glial tumours was increased, although this was not statistically significant. On the whole, the findings of this study showed that RF radiation levels at one square, Järntorget, in Sweden, were only one order of magnitude lower than those showing an increased incidence of tumours in the RI animal study. An increased cancer risk cannot be excluded for those working in the proximity of Järntorget for longer time periods.

scholarly journals Environmental radiofrequency radiation at the Järntorget Square in Stockholm Old Town, Sweden in May, 2018 compared with results on brain and heart tumour risks in rats exposed to 1.8 GHz base station environmental emissions

2018 ◽  
pp. 47-54 ◽  
Author(s):  
Lennart Hardell ◽  
Michael Carlberg ◽  
Lena K. Hedendahl ◽  
Tarmo Koppel ◽  
Mikko Ahonen
Keyword(s):  
Epidemiological Studies ◽  
Mean Value ◽  
Base Station ◽  
Female Rats ◽  
Male Rats ◽  
International Agency ◽  
Malignant Schwannoma ◽  
Environmental Radiation ◽  
Carcinogenicity Study ◽  
Increased Risk

Radiofrequency (RF) radiation in the frequency range 30 kHz to 300 GHz was evaluated in 2011 by the International Agency for Research on Cancer (IARC) at WHO to be a 'possible human carcinogen' Group 2B. The conclusion was based on human epidemiological studies on an increased risk of glioma and acoustic neuroma. In previous measurement studies, we found high environmental RF radiation levels at certain public places and also in an apartment in Stockholm, Sweden. One such place was the Järntorget square in the Stockholm Old Town. The EME Spy exposimeter was used for these studies. We have now conducted a field spatial distribution measurement with a radiofrequency broadband analyser. The maximum E-field topped at 11.6 V/m at the centre of the square, where the antenna was focused. Järntorget's mean value was 5.2 V/m, median 5.0 V/m, range 1.2-11.6 V/m. Of interest is that this level can be compared to a lifespan carcinogenicity study on rats exposed to 1.8 GHz GSM environmental radiation performed at the Ramazzini Institute (RI) in Italy. A statistically significant increase in the incidence of malignant schwannoma in the heart was found in male rats at the highest dose, 50 V/m. In treated female rats at the highest dose, the incidence of malignant glial tumours was increased, although this was not statistically significant. On the whole, the findings of this study showed that RF radiation levels at one square, Järntorget, in Sweden, were only one order of magnitude lower than those showing an increased incidence of tumours in the RI animal study. An increased cancer risk cannot be excluded for those working in the proximity of Järntorget for longer time periods.

scholarly journals Kidney Injury Caused by Preeclamptic Pregnancy Recovers Postpartum in a Transgenic Rat Model

2021 ◽  
Vol 22 (7) ◽  
pp. 3762
Author(s):  
Sarah M. Kedziora ◽  
Kristin Kräker ◽  
Lajos Markó ◽  
Julia Binder ◽  
Meryam Sugulle ◽  
...  
Keyword(s):  
Rat Model ◽  
Renal Damage ◽  
Kidney Injury ◽  
Tissue Growth ◽  
Female Rats ◽  
Male Rats ◽  
Renal Diseases ◽  
Transgenic Rat ◽  
Increased Risk ◽  
Before And After

Preeclampsia (PE) is characterized by the onset of hypertension (≥140/90 mmHg) and presence of proteinuria (>300 mg/L/24 h urine) or other maternal organ dysfunctions. During human PE, renal injuries have been observed. Some studies suggest that women with PE diagnosis have an increased risk to develop renal diseases later in life. However, in human studies PE as a single cause of this development cannot be investigated. Here, we aimed to investigate the effect of PE on postpartum renal damage in an established transgenic PE rat model. Female rats harboring the human-angiotensinogen gene develop a preeclamptic phenotype after mating with male rats harboring the human-renin gene, but are normotensive before and after pregnancy. During pregnancy PE rats developed mild tubular and glomerular changes assessed by histologic analysis, increased gene expression of renal damage markers such as kidney injury marker 1 and connective-tissue growth factor, and albuminuria compared to female wild-type rats (WT). However, four weeks postpartum, most PE-related renal pathologies were absent, including albuminuria and elevated biomarker expression. Only mild enlargement of the glomerular tuft could be detected. Overall, the glomerular and tubular function were affected during pregnancy in the transgenic PE rat. However, almost all these pathologies observed during PE recovered postpartum.

scholarly journals Electromagnetic Fields, Oxidative Stress, and Neurodegeneration

2012 ◽  
Vol 2012 ◽  
pp. 1-16 ◽  
Author(s):  
Claudia Consales ◽  
Caterina Merla ◽  
Carmela Marino ◽  
Barbara Benassi
Keyword(s):  
Oxidative Stress ◽  
Electromagnetic Fields ◽  
Childhood Leukemia ◽  
Low Frequency ◽  
Epidemiological Studies ◽  
Data Uncertainty ◽  
International Agency ◽  
Neuroprotective Effects ◽  
Great Debate ◽  
Increased Risk

Electromagnetic fields (EMFs) originating both from both natural and manmade sources permeate our environment. As people are continuously exposed to EMFs in everyday life, it is a matter of great debate whether they can be harmful to human health. On the basis of two decades of epidemiological studies, an increased risk for childhood leukemia associated with Extremely Low Frequency fields has been consistently assessed, inducing the International Agency for Research on Cancer to insert them in the 2B section of carcinogens in 2001. EMFs interaction with biological systems may cause oxidative stress under certain circumstances. Since free radicals are essential for brain physiological processes and pathological degeneration, research focusing on the possible influence of the EMFs-driven oxidative stress is still in progress, especially in the light of recent studies suggesting that EMFs may contribute to the etiology of neurodegenerative disorders. This review synthesizes the emerging evidences about this topic, highlighting the wide data uncertainty that still characterizes the EMFs effect on oxidative stress modulation, as both pro-oxidant and neuroprotective effects have been documented. Care should be taken to avoid methodological limitations and to determine the patho-physiological relevance of any alteration found in EMFs-exposed biological system.

Induction of micronuclei in rat bone marrow after chronic exposure to lead acetate trihydrate

2008 ◽  
Vol 24 (9) ◽  
pp. 587-593 ◽  
Author(s):  
MA Alghazal ◽  
I Šutiaková ◽  
N Kovalkovičová ◽  
J Legáth ◽  
M Falis ◽  
...  
Keyword(s):  
Bone Marrow ◽  
Lead Acetate ◽  
Mean Value ◽  
Female Rats ◽  
Male Rats ◽  
Control Group ◽  
Lead Acetate Trihydrate ◽  
Tukey Test ◽  
Acetate Trihydrate ◽  
Polychromatic Erythrocytes

Lead increasingly contributes to pollution of the environment and may play a role in the development of adverse effects in the human and animal body. Data concerning its mutagenic, clastogenic, and carcinogenic properties have been conflicting. In this study, we evaluated the frequency of micronuclei in bone marrow erythrocytes of rats treated with lead acetate trihydrate. Outbred Wistar rats were exposed to a daily dose of 100 mg/L drinking water for 125 days. The mean value of the total number of micronuclei observed in polychromatic erythrocytes of female rats was significantly higher than that found in the control group (13.375 ± 2.722 against 9.625 ± 3.204 micronuclei/1000 cells; P = 0.024 in ANOVA). In exposed female animals, no significant reduction of the ratio of polychromatic to normochromatic erythrocytes was observed (0.990 ± 0.228 against 1.208 ± 0.195; P = 0.060 in ANOVA). The effects of lead acetate trihydrate in male rats are both cytotoxic and genotoxic because of a decrease in ratio of polychromatic to normochromatic erythrocytes (0.715 ± 0.431 against 1.343 ± 0.306; P = 0.023, ANOVA followed by Tukey test) and an increase in frequency of micronucleated polychromatic erythrocytes (24.167 ± 7.859 against 4.0 ± 4.528 micronuclei/1000 cells; P ≤ 0.001, ANOVA followed by Tukey test), respectively.

scholarly journals Organ-selective growth in the offspring of protein-restricted mothers

1996 ◽  
Vol 76 (4) ◽  
pp. 591-603 ◽  
Author(s):  
Mina Desai ◽  
Nigel J. Crowther ◽  
Alan Lucas ◽  
C. Nicholas Hales
Keyword(s):  
G Protein ◽  
Infant Development ◽  
Relative Weight ◽  
Epidemiological Studies ◽  
The Body ◽  
Female Rats ◽  
Male Rats ◽  
Critical Periods ◽  
Long Term Effects ◽  
Muscle Weight

Recent epidemiological studies in people whose birth weights were recorded many years ago suggest links between impaired growth during early life and the development of diseases, including diabetes, much later in life. The long-term effects of retarded early growth are proposed to result from malnutrition at critical periods of fetal or infant development leading to reduction in the growth of organs and permanent changes in their metabolism or structure, or both. In order to investigate this, a rat model was established which involved feeding either a diet containing 200 g protein/kg or an isoenergetic diet containing 80 g protein/kg to pregnant and lactating rats. In addition, cross-fostering techniques were employed which allowed a separate evaluation of the prenatal or the postnatal periods. The offspring were studied at 21 d of age or were weaned onto a normal laboratory chow and studied at 11 months of age. The 80g protein/kg diet during pregnancy did not affect the overall reproductive performance although more subtle differences were evident. Permanent growth retardation was evident in offspring subjected to maternal protein restriction during the postnatal period. At 21 d of age the offspring of protein-restricted mothers exhibited selective changes in organ growth: compared with the body weight, the lung and brain experienced a smaller decrease in weight; the heart, kidney and thymus decreased proportionately; whereas, the pancreas, spleen, muscle and liver showed a greater reduction in weight. In older animals the muscle weight was lower in the male rats and the relative weight ofpancreas was increased in the female rats.

Intergenerational consequences of fetal programming by in utero exposure to glucocorticoids in rats

2005 ◽  
Vol 288 (1) ◽  
pp. R34-R38 ◽  
Author(s):  
Amanda J. Drake ◽  
Brian R. Walker ◽  
Jonathan R. Seckl
Keyword(s):  
Cardiovascular Risk ◽  
Birth Weight ◽  
Low Birth Weight ◽  
Fetal Programming ◽  
First Generation ◽  
Epidemiological Studies ◽  
Female Rats ◽  
Male Rats ◽  
Fetal Life ◽  
Gluconeogenic Enzyme

Epidemiological studies linking low birth weight and subsequent cardiometabolic disease have given rise to the hypothesis that events in fetal life permanently program subsequent cardiovascular risk. The effects of fetal programming may not be limited to the first-generation offspring. We have explored intergenerational effects in the dexamethasone-programmed rat, a model in which fetal exposure to excess glucocorticoid results in low birth weight with subsequent adult hyperinsulinemia and hyperglycemia underpinned by increased activity of the key hepatic gluconeogenic enzyme, phospho enolpyruvate carboxykinase (PEPCK). We found that the male offspring of female rats that had been exposed prenatally to dexamethasone, but were not manipulated in their own pregnancy, also had reduced birth weight (5.66 ± 0.06 vs. 6.12 ± 0.06 g, P < 0.001), glucose intolerance, and elevated hepatic PEPCK activity (5.7 ± 0.6 vs. 3.3 ± 0.2 nmol·min−1·mg protein−1, P < 0.001). These effects resolved in a third generation. Similar intergenerational programming was observed in offspring of male rats exposed prenatally to dexamethasone mated with control females. The persistence of such programming effects through several generations, transmitted by either maternal or paternal lines, indicates the potential importance of epigenetic factors in the intergenerational inheritance of the “programming phenotype” and provides a basis for the inherited association between low birth weight and cardiovascular risk factors.

scholarly journals Injury threshold of oral contact with hot foods and method for its sensory evaluation

2018 ◽  
Author(s):  
Dirk W. Lachenmeier ◽  
Walter Lachenmeier
Keyword(s):  
Contact Time ◽  
Food Product ◽  
Epidemiological Studies ◽  
Contact Temperature ◽  
International Agency ◽  
Threshold Values ◽  
Test Technique ◽  
Risk Of Injury ◽  
Increased Risk ◽  
Risk Of Cancer

Epidemiological studies indicate an increased risk of cancer from the consumption of very hot foods and beverages. The International Agency for Research on Cancer (IARC) has already recommended threshold values for the maximum drinking temperature of very hot beverages. The contact time and the contact temperature are decisive for the risk of injury when hot media come into contact with human skin. However, measuring the contact temperature is not easily possible in practice. In the present study, a numerical simulation based on the solution of the heat conduction equation was initially used to investigate whether and for what period of time a constant contact temperature is to be expected under oral conditions. For small circular 3-cm food samples (e.g., cooked potatoes) with 2.5 mm thickness in contact with the tongue, the simulation results in a constant contact temperature of 10 s before cooling. With a thickness of 0.5 mm, the contact temperature is only maintained 1 s. Hot beverages, which spread as a thin film and thereby increase their surface area, can therefore be consumed at higher temperatures than solid foods. Furthermore, a simple test technique with a "measuring spoon" was developed. A hot sample is placed on the tongue. Orientating measurements were used to determine which contact temperature was considered to be just comfortable for any period &gt; 10 s and for which period of less than 10 s it was still just bearable. The contact temperature, which was still perceived as tolerable for periods &gt; 10 s, was 46.5 &deg;C. The time spans for the higher contact temperature 48 &deg;C were between 2 and 4 s and for 49 &deg;C between 1 and 2 s. The course of the contact temperatures determined in the experiment over time allows to calculate the corresponding threshold values of consumption temperatures for various foods. Consumption temperatures of about 56 &deg;C for potatoes and 60 &deg;C for cheese are still perceived as tolerable. In view of the fact that the contact temperature is obviously the determining factor for the risk of injury from burns in the oral cavity in addition to the contact time, it makes sense to reference threshold values to the contact temperature rather than to the surface or consumption temperature of a food product, which is current customary practice. If this contact temperature is defined as a threshold value, the surface or consumption temperature for any other food can be calculated.

scholarly journals Transient neonatal exposure to hyperoxia, an experimental model of preterm birth, leads to skeletal muscle atrophy and fiber type switching

2021 ◽  
Author(s):  
Alyson Deprez ◽  
Zakaria Orfi ◽  
Alexandra Radu ◽  
Ying He ◽  
Daniela Ravizzoni Dartora ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Preterm Birth ◽  
Exercise Capacity ◽  
Skeletal Muscles ◽  
Fiber Type ◽  
Female Rats ◽  
Male Rats ◽  
Antioxidant Defenses ◽  
Increased Risk ◽  
And Function

Individuals born preterm show reduced exercise capacity and increased risk for pulmonary and cardiovascular diseases, but the impact of preterm birth on skeletal muscle, an inherently critical part of cardiorespiratory fitness, remains unknown. We evaluated the impacts of preterm birth-related conditions on the development, growth, and function of skeletal muscle using a recognized preclinical rodent model in which newborn rats are exposed to 80% oxygen from day 3 to 10 of life. We analyzed different hindlimb muscles of male and female rats at 10 days (neonatal), 4 weeks (juvenile) and 16 weeks (young adults). Neonatal high oxygen exposure increased the generation of reactive oxygen species and the signs of inflammation in skeletal muscles, which was associated with muscle fiber atrophy, fiber type shifting (reduced proportion of type I slow fibers and increased proportion of type IIb fast-fatigable fibers), and impairment in muscle function. These effects were maintained until adulthood. Fast-twitch muscles were more vulnerable to the effects of hyperoxia than slow-twitch muscles. Male rats, which expressed lower antioxidant defenses, were more susceptible than females to oxygen-induced myopathy. Overall, preterm birth-related conditions have long-lasting effects on the composition, morphology, and function of skeletal muscles; and these effects are sex-specific. Oxygen-induced changes in skeletal muscles could contribute to the reduced exercise capacity and to increased risk of diseases of preterm born individuals.

scholarly journals Development of health-based exposure limits for radiofrequency radiation from wireless devices using a benchmark dose approach

2021 ◽  
Vol 20 (1) ◽  
Author(s):  
Uloma Igara Uche ◽  
Olga V. Naidenko
Keyword(s):  
Biological Tissues ◽  
Female Rats ◽  
Male Rats ◽  
Whole Body ◽  
Exposure Limits ◽  
Radiofrequency Radiation ◽  
Incidence Data ◽  
Increased Risk ◽  
Code Division Multiple ◽  
Benchmark Dose Approach

Abstract Background Epidemiological studies and research on laboratory animals link radiofrequency radiation (RFR) with impacts on the heart, brain, and other organs. Data from the large-scale animal studies conducted by the U.S. National Toxicology Program (NTP) and the Ramazzini Institute support the need for updated health-based guidelines for general population RFR exposure. Objectives The development of RFR exposure limits expressed in whole-body Specific Absorption Rate (SAR), a metric of RFR energy absorbed by biological tissues. Methods Using frequentist and Bayesian averaging modeling of non-neoplastic lesion incidence data from the NTP study, we calculated the benchmark doses (BMD) that elicited a 10% response above background (BMD10) and the lower confidence limits on the BMD at 10% extra risk (BMDL10). Incidence data for individual neoplasms and combined tumor incidence were modeled for 5% and 10% response above background. Results Cardiomyopathy and increased risk of neoplasms in male rats were the most sensitive health outcomes following RFR exposures at 900 MHz frequency with Code Division Multiple Access (CDMA) and Global System for Mobile Communications (GSM) modulations. BMDL10 for all sites cardiomyopathy in male rats following 19 weeks of exposure, calculated with Bayesian model averaging, corresponded to 0.27–0.42 W/kg whole-body SAR for CDMA and 0.20–0.29 W/kg for GSM modulation. BMDL10 for right ventricle cardiomyopathy in female rats following 2 years of exposure corresponded to 2.7–5.16 W/kg whole-body SAR for CDMA and 1.91–2.18 W/kg for GSM modulation. For multi-site tumor modeling using the multistage cancer model with a 5% extra risk, BMDL5 in male rats corresponded to 0.31 W/kg for CDMA and 0.21 W/kg for GSM modulation. Conclusion BMDL10 range of 0.2—0.4 W/kg for all sites cardiomyopathy in male rats was selected as a point of departure. Applying two ten-fold safety factors for interspecies and intraspecies variability, we derived a whole-body SAR limit of 2 to 4 mW/kg, an exposure level that is 20–40-fold lower than the legally permissible level of 0.08 W/kg for whole-body SAR under the current U.S. regulations. Use of an additional ten-fold children’s health safety factor points to a whole-body SAR limit of 0.2–0.4 mW/kg for young children.

scholarly journals Ethylene Oxide: Cancer Evidence Integration and Dose–Response Implications

Dose-Response ◽  
2019 ◽  
Vol 17 (4) ◽  
pp. 155932581988831 ◽  
Author(s):  
Melissa J. Vincent ◽  
Jordan S. Kozal ◽  
William J. Thompson ◽  
Andrew Maier ◽  
G. Scott Dotson ◽  
...  
Keyword(s):  
Ethylene Oxide ◽  
Dose Response ◽  
The United States ◽  
Epidemiological Studies ◽  
International Agency ◽  
Breast Cancers ◽  
Early Effect ◽  
Human Carcinogen ◽  
Increased Risk ◽  
Toxicological Studies

The International Agency for Research on Cancer (IARC) and the United States Environmental Protection Agency (USEPA) classified ethylene oxide (EtO) as a known human carcinogen. Critically, both noted that the epidemiological evidence based on lymphoid and breast cancers was “limited,” but that the evidence in animal studies was “sufficient” and “extensive” (respectively) and that EtO is genotoxic. The USEPA derived one of the highest published inhalation unit risk (IUR) values (3 × 10−3 per [µg/m3 EtO]), based on results from 2 epidemiological studies. We performed focused reviews of the epidemiological and toxicological evidence on the carcinogenicity of EtO and considered the USEPA’s reliance on a genotoxic mode of action to establish EtO’s carcinogenicity and to determine likely dose–response patterns. Higher quality epidemiological studies demonstrated no increased risk of breast cancers or lymphohematopoietic malignancies (LHM). Similarly, toxicological studies and studies of early effect biomarkers in animals and humans provided no strong indication that EtO causes LHM or mammary cancers. Ultimately, animal data are inadequate to define the actual dose–response shape or predict tumor response at very low doses with any confidence. We conclude that the IARC and USEPA classification of EtO as a known human carcinogen overstates the underlying evidence and that the IUR derived by USEPA grossly overestimates risk.

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