No full-text available
To read the full-text of this research,
you can request a copy directly from the authors.
Are There Harmful Effects Caused by the Silent Noise of Infrasound Produced by Windparks? An Experimental Approach
Background:
Human exposure to infrasound is increasing due to man-made factors, such as occupational conditions, wind farms and transportation. The concern among the public regarding the safety of infrasound exposure is growing.
Aims:
To evaluate whether exposure to infrasound interferes directly with human cardiac function and contributes to pathological processes.
Setting:
The University Hospital of Mainz, Germany.
Methods:
Human myocardial tissues, obtained from patients undergoing cardiac surgery, were prepared in small muscle samples and stimulated electrically in-vitro for a period of almost two hours under physiological conditions to induce continuous pulsatile contractions and simulating a working human heart. Two samples were obtained from each donor: one was subjected to infrasound for 60 min and the other served as a control. Their contraction forces (CF) and durations (CD) were measured before and after each testing period and their relative changes (CF% and CD%) were calculated and introduced in a multilinear regression model. The following three infrasound levels of exposure were used in this study: 100, 110 and 120 dBz.
Results:
The measured CF% corresponded negatively with the infrasound level measured in dBz (R2 = 0.631; P = 0.018). The decrease measured almost -11% at 110 dBz and -18% at 120 dBz, after correction for control. The CD on the other hand remained unchanged.
Conclusions:
Exposure to high levels of infrasound (more than 100 dBz) interferes with cardiac muscle contractile ability, as early as one hour after exposure. There are numerous additional studies which support this conclusion. These results should be taken into account when considering environmental regulations.
A narrative review of observational and experimental studies was conducted to assess the association between exposure to wind turbine sound and its components and health effects in the general population. Literature databases Scopus, Medline and Embase and additional bibliographic sources such as reference sections of key publications and journal databases were systematically searched for peer-reviewed studies published from 2009 to 2017. For the period until early 2015 only reviews were included, while for the period between January 2015 and January 2017 all relevant publications were screened. Ten reviews and 22 studies met the inclusion criteria. Most studies examined subjective annoyance as the primary outcome, indicating an association between exposure levels and the percentage highly annoyed. Sound from wind turbines leads to a higher percentage of highly annoyed when compared to other sound sources. Annoyance due to aspects, like shadow flicker, the visual (in) appropriateness in the landscape and blinking lights, can add to the noise annoyance. There is no evidence of a specific effect of the low-frequency component nor of infrasound. There are indications that the rhythmic pressure pulses on a building can lead to additional annoyance indoors. Personal characteristics such as noise sensitivity, privacy issues and social acceptance, benefits and attitudes, the local situation and the conditions of planning a wind farm also play a role in reported annoyance. Less data are available to evaluate the effects of wind turbines on sleep and long-term health effects. Sleep disturbance as well as other health effects in the vicinity of wind turbines was found to be related to annoyance, rather than directly to exposure.
Abstract Background Our study aimed to evaluate changes in the contractile behavior of human myocardium after exposure to caffeine and taurine, the main active ingredients of energy drinks (EDs), and to evaluate whether taurine exhibits any inotropic effect at all in the dosages commonly used in EDs. Methods Myocardial tissue was removed from the right atrial appendages of patients undergoing cardiac surgery and prepared to obtain specimens measuring 4 mm in length. A total of 92 specimens were exposed to electrical impulses at a frequency of 75 bpm for at least 40 min to elicit their maximum contractile force before measuring the isometric contractile force (ICF) and duration of contraction (CD). Following this, each specimen was treated with either taurine (group 1, n = 29), or caffeine (group 2, n = 31) or both (group 3, n = 32). After exposure, ICF and CD measuring were repeated. Post-treatment values were compared with pre-treatments values and indicated as percentages. Results Exposure to taurine did not alter the contraction behavior of the specimens. Exposure to caffeine, in contrast, led to a significant increase in ICF (118 ± 03%, p
Environmental factors can act as facilitators of chronic non-communicable diseases. Ambient noise and air pollution collectively outrank all other environmental risk factors in importance, contributing to over 75% of the disease and disability burden associated with known environmental risk factors. In the first part of this review, we discussed the global burden and epidemiologic evidence supporting the importance of these novel risk factors as facilitators of cardiometabolic disease. In this part, we will discuss pathophysiological mechanisms responsible for noise and air pollution-mediated effects. Akin to traditional cardiovascular risk factors, a considerable body of evidence suggests that these environmental agents induce low-grade inflammation, oxidative stress, vascular dysfunction, and autonomic nervous system imbalance, thereby facilitating the development of diseases such as hypertension and diabetes. Through their impact on traditional risk factors and via additional novel mechanisms, environmental risk factors may have much larger impact on cardiovascular events than currently appreciated. In the second part of this review, we discuss deficiencies and gaps in knowledge and opportunities for new research.
The paper reviews perception of low frequency noise (LFN) and the responses of people to LFN. Sometimes, when there are complaints of LFN and its effects, a specific noise cannot be measured. The possibilities are considered for development of enhanced sensitivity, for alternative (non-aural) receptors at very low frequencies and for false perceptions. The way in which we measure LFN may contribute to the problems.
The aim of the present study was to examine the effects of acute infrasound exposure on oxidative damage and investigate the underlying mechanisms in rat cardiomyocytes. Neonatal rat cardiomyocytes were cultured and exposed to infrasound for several days. In the study, the expression of CAT, GPx, SOD1, and SOD2 and their activities in rat cardiomyocytes in infrasound exposure groups were significantly decreased compared to those in the various time controls, along with significantly higher levels of O2 (-) and H2O2. Decreased cardiac cell viability was not observed in various time controls. A significant reduction in cardiac cell viability was observed in the infrasound group compared to the control, while significantly increased cardiac cell viability was observed in the infrasound exposure and rosiglitazone pretreatment group. Compared to the control, rosiglitazone significantly upregulated CAT, GPx, SOD1, and SOD2 expression and their activities in rat cardiomyocytes exposed to infrasound, while the levels of O2 (-) or H2O2 were significantly decreased. A potential link between a significant downregulation of PPAR-γ expression in rat cardiomyocytes in the infrasound group was compared to the control and infrasound-induced oxidative stress. These findings indicate that infrasound can induce oxidative damage in rat cardiomyocytes by inactivating PPAR-γ.
Noise is pervasive in everyday life and induces both auditory and non-auditory health effects. Systematic research of the effects of noise on the cardiovascular system has been carried out for more than 50 decades. Noise is a stressor that affects the autonomic nervous system and the endocrine system. Animal experiments, laboratory and field studies carried out on humans provide evidence that persistent exposure to environmental noise affects physiological endpoints, which in turn are adversely associated with cardiovascular diseases. These include hypertension, coronary heart disease, and stroke. New endpoints have been studied, including clinical states of metabolic syndrome such as diabetes mellitus. Chronic sleep disturbance is considered as an important mediator of the effects. Public health policies rely on quantitative risk assessment to set environmental quality standards and to regulate the noise exposure that is generated by environmental noise sources in the communities. Meta-analyses were carried out to derive exposure-response relationships between noise and cardiovascular health. Most of the epidemiological studies refer to road traffic and aircraft noise. No biologically determined threshold values can be determined. Cardiovascular effects due to noise and traffic-related air pollutants are largely independent of one another due to different biological mechanisms.
Low frequency noise, the frequency range from about 10 Hz to 200 Hz, has been recognised as a special environmental noise problem, particularly to sensitive people in their homes. Conventional methods of assessing annoyance, typically based on A-weighted equivalent level, are inadequate for low frequency noise and lead to incorrect decisions by regulatory authorities. There have been a large number of laboratory measurements of annoyance by low frequency noise, each with different spectra and levels, making comparisons difficult, but the main conclusions are that annoyance of low frequencies increases rapidly with level. Additionally the A-weighted level underestimates the effects of low frequency noises. There is a possibility of learned aversion to low frequency noise, leading to annoyance and stress which may receive unsympathetic treatment from regulatory authorities. In particular, problems of the Hum often remain unresolved. An approximate estimate is that about 2.5% of the population may have a low frequency threshold which is at least 12 dB more sensitive than the average threshold, corresponding to nearly 1,000,000 persons in the 50-59 year old age group in the EU-15 countries. This is the group which generates many complaints. Low frequency noise specific criteria have been introduced in some countries, but do not deal adequately with fluctuations. Validation of the criteria has been for a limited range of noises and subjects.
Background
Chronic exposure to industrial noise is known to affect biological systems, namely, by inducing fibrosis in the absence of inflammatory cells. In rat hearts exposed to this environmental hazard, we have previously found myocardial and perivascular fibrosis. The acoustic spectrum of industrial environments is particularly rich in high-intensity infrasound (<20 Hz), whose effects on the heart are unknown. We evaluated the morphological changes induced by IFS in rat coronaries in the presence and absence of dexamethasone.
Methods
Adult Wistar rats were divided into three groups: group A (GA)—IFS (<20 Hz, 120 dB)-exposed rats for 28 days treated with dexamethasone; group B (GB)—IFS-exposed rats; group C (GC)—age-matched controls. The midventricle was prepared for observation with an optical microscope using 100× magnification. Thirty-one arterial vessels were selected (GA 8, GB 10, GC 13). The vessel caliber, thickness of the wall, and perivascular dimensions were quantified using image J software. Mann–Whitney and Kruskal–Wallis tests were used to compare the groups for lumen-to-vessel wall (L/W) and vessel wall-to-perivascular tissue (W/P) ratios.
Results
IFS-exposed rats exhibited a prominent perivascular tissue. The median L/W and median W/P ratios were 0.54 and 0.48, 0.66 and 0.49, and 0.71 and 0.68, respectively, in GA, GB, and GC. The W/P ratio was significantly higher in GC compared with IFS-exposed animals (P=.001). The difference was significant between GC and GB (P=.008) but not between GC and GA.
Conclusion
IFS induces coronary perivascular fibrosis that differs under treatment with corticosteroid.
Aims:
Blood biochemistry may provide information on associations between road traffic noise, air pollution, and cardiovascular disease risk. We evaluated this in two large European cohorts (HUNT3, Lifelines).
Methods and results:
Road traffic noise exposure was modelled for 2009 using a simplified version of the Common Noise Assessment Methods in Europe (CNOSSOS-EU). Annual ambient air pollution (PM10, NO2) at residence was estimated for 2007 using a Land Use Regression model. The statistical platform DataSHIELD was used to pool data from 144 082 participants aged ≥20 years to enable individual-level analysis. Generalized linear models were fitted to assess cross-sectional associations between pollutants and high-sensitivity C-reactive protein (hsCRP), blood lipids and for (Lifelines only) fasting blood glucose, for samples taken during recruitment in 2006-2013. Pooling both cohorts, an inter-quartile range (IQR) higher day-time noise (5.1 dB(A)) was associated with 1.1% [95% confidence interval (95% CI: 0.02-2.2%)] higher hsCRP, 0.7% (95% CI: 0.3-1.1%) higher triglycerides, and 0.5% (95% CI: 0.3-0.7%) higher high-density lipoprotein (HDL); only the association with HDL was robust to adjustment for air pollution. An IQR higher PM10 (2.0 µg/m3) or NO2 (7.4 µg/m3) was associated with higher triglycerides (1.9%, 95% CI: 1.5-2.4% and 2.2%, 95% CI: 1.6-2.7%), independent of adjustment for noise. Additionally for NO2, a significant association with hsCRP (1.9%, 95% CI: 0.5-3.3%) was seen. In Lifelines, an IQR higher noise (4.2 dB(A)) and PM10 (2.4 µg/m3) was associated with 0.2% (95% CI: 0.1-0.3%) and 0.6% (95% CI: 0.4-0.7%) higher fasting glucose respectively, with both remaining robust to adjustment for air/noise pollution.
Conclusion:
Long-term exposures to road traffic noise and ambient air pollution were associated with blood biochemistry, providing a possible link between road traffic noise/air pollution and cardio-metabolic disease risk.
Traffic noise and air pollution together represent the two most important environmental risk factors in urbanized societies. The first of this two-part review discusses the epidemiologic evidence in support of the existence of an association between these risk factors with cardiovascular and metabolic disease. While independent effects of these risk factors have now clearly been shown, recent studies also suggest that the two exposures may interact with each other and with traditional risk factors such as hypertension and type 2 diabetes. From a societal and policy perspective, the health effects of both air pollution and traffic noise are observed for exposures well below the thresholds currently accepted as being safe. Current gaps in knowledge, effects of intervention and their impact on cardiovascular disease, will be discussed in the last section of this review. Increased awareness of the societal burden posed by these novel risk factors and acknowledgement in traditional risk factor guidelines may intensify the efforts required for effective legislation to reduce air pollution and noise.
A survey of complaints about infrasound and low frequency noise has been carried out. 198 persons reported their troubles in a questionnaire. Their verbal reports often described the sound as deep and humming or rumbling, as if coming from the distant idling engine of a truck or pump. Nearly all respondent's reported a sensory perception of a sound. In general they reported that they perceived the sound with their ears, but many mention also the perception of vibration, either in their body or in external objects. The sound disturbs and irritates during most activities, and many consider its mere presence as a torment to them. Many of the respondents reported secondary effects, such as insomnia, headache and palpitation, which they associated with the sound mainly because it occured at the same place as the sound. In a majority of the cases, only one or a few persons can hear the sound, but there are also examples, where it is claimed to be audible to everybody. Typically, measurements have shown that existing limits (and hearing thresholds) are not exceeded. The investigation leaves the key question: Are the troubles induced by an external sound or not, and if they are, which frequencies and levels are involved? The feasibility of a study of this is supported by the results.
The main aim of this paper is to present recent knowledge about the assessment and evaluation of low-frequency sounds (noise) and infrasound, close to the threshold of hearing, and identify their potential effect on human health and annoyance. Low-frequency noise generated by air flowing over a moving car with an open window was chosen as a typical scenario which can be subjectively assessed by people traveling by automobile. The principle of noise generated within the interior of the car and its effects on the comfort of the driver and passengers are analyzed at different velocities. An open window of a car at high velocity behaves as a source of specifically strong tonal low-frequency noise which is generally perceived as annoying. The interior noise generated by an open window of a passenger car was measured under different conditions: Driving on a highway and driving on a typical roadway. First, an octave-band analysis was used to assess the noise level and its impact on the driver's comfort. Second, a fast Fourier transform (FFT) analysis and one-third octave-band analysis were used for the detection of tonal low-frequency noise. Comparison between two different car makers was also done. Finally, the paper suggests some possibilities for scientifically assessing and evaluating low-frequency sounds in general, and some recommendations are introduced for scientific discussion, since sounds with strong low-frequency content (but not only strong) engender greater annoyance than is predicted by an A-weighted sound pressure level.
The main aim is to present the available updated knowledge regarding the potential health effects of standing waves generated by low frequency noise (LFN) from an open window in a moving car where the negative effects of LFN induced by heating components and/or heating, ventilation and air-conditioning are assessed. Furthermore, the assessment of noise in chosen enclosed spaces, such as rooms, offices, and classrooms, or other LFN sources and their effect on the human being were investigated. These types of noise are responsible for disturbance during relaxation, sleep, mental work, education, and concentration, which may reflect negatively on the comfort and health of the population and on the mental state of people such as scientific staff and students. The assessment points out the most exposed areas, and analyzes the conditions of standing wave generation in these rooms caused by outdoor and/or indoor sources. Measurements were made for three different enclosed spaces (office, flat, and passenger car) and sources (traffic specific noise at intersections, noise induced by pipe vibration, and aerodynamic noise) and their operating conditions. For the detection of LFN, the A-weighted sound pressure level and vibration were measured and a fast Fourier transform analysis was used. The LFN sources are specified and the direct effects on the human are reported. Finally, this paper suggests the possibilities for the assessment of LFN and some possible measures that can be taken to prevent or reduce them.
The Helmholtz resonator effect of a room with an open window or ventilation duct has been studied theoretically and experimentally. The effect results in a sound pressure buildup at infrasonic frequencies. For comparison, the frequencies of the standing-wave room resonances are above the infrasonic range for residential dwellings. The relations between the sound pressure inside a room and outside (environmental) sound pressure or vibration acceleration have been calculated for the third-octave frequency band incorporating the Helmholtz resonance frequency. The experiment on a small-scale model illustrated the Helmholtz resonator effect caused by environmental vibration.
1.
Die Hrgrenzen werden nicht durch die Schnittpunkte der die sog. Hrflche einschlieenden Kurven gebildet, sondern lediglich durch das im Bereich der nieder- bzw. hochfrequenten Schwingungen steile Ansteigen der Hrschwellen bestimmt.
2.
Bei gengend groer Schwingungsintensitt (etwa 1000 Bar) knnen noch pendeifrmige Schwingungen mit einer Frequenz von etwa 7 Hertz einen Hreindruck auslsen.
3.
Die Beziehung der unteren Hrgrenze zu Frequenz und Intensitt der Schwingungen wird in Kurvenform dargestellt.
4.
Durch den anscheinend asymptotischen Verlauf der Hrschwellenkurve bei Schwingungen niederer Frequenz ist nicht nur praktisch, sondern auch theoretisch eine untere Hrgrenze gegeben.
5.
Die Hrempfindung, die von Schwingungen unterhalb 18 Hertz ausgelst wird, hat einen diskontinuierlichen Charakter und geht oberhalb dieser Frequenz in eine kontinuierliche Hrempfindung — einen Ton — ber. Diese Verschmelzungsgrenze von einzelnen, getrennten Hrereignissen (Tonsten) zu einem kontinuierlichen Hreindruck bildet die untere Tongrenze, die unabhngig von der Reizintensitt bei allen Menschen bei etwa 18 Hertz liegt.
6.
Untere Hrgrenze und Tongrenze sind nicht identisch, sondern verdanken ihre Entstehung verschiedenen Ursachen.
7.
Das Vorhandensein einer unteren (wie oberen)Hrgrenze liegt in der Mechanik des Gehrorganes begrndet. Die untereTongrenze ist dagegen auf die Rezeptionstrgheit des Nervensystems (den Moment) zurckzufhren, wie eine Parallele mit der gleich groen Verschmelzungsgrenze von Reizen in anderen Sinnesgebieten (Tast- und Lichtreize) zeigt.
Sound pressure level measurements in cars travelling at motorway speeds have shown that in many cases the overall level is very high in relation to the dB(A) and octave band levels, suggesting that much of the sound energy is in the low frequency and infrasonic regions. These levels have been measured down to the octave centred on 2 Hz. Experiments to investigate the effects of infrasound on balance and psychological awareness are described. The results show that levels of infrasound measured in moving vehicles can produce symptoms of balance disturbance, including vertical nystagmus, in normal observers, and also have profound effects on psychological awareness of normal human observers. Possible mechanisms for these effects are discussed.
It has been reported that exposure to infrasound causes cardiac dysfunction. Allowing for the key role of apoptosis in the pathogenesis of cardiovascular diseases, the objective of this study was to investigate the apoptotic effects of infrasound. Cardiac myocytes cultured from neonatal rats were exposed to infrasound of 5 Hz at 130 dB. The apoptosis was determined by terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling. Also, the expression levels of a series of apoptosis-related proteins were detected. As a result, infrasound induced apoptosis of cultured rat cardiac myocytes in a time-dependant manner. The expression of proapoptotic proteins such as Bax, caspase-3, caspase-8, caspase-9, and FAS was significantly up-regulated, with concomitant down-regulated expression of antiapoptotic proteins such as Bcl-x, and the inhibitory apoptosis proteins family proteins including XIAP, cIAP-1, and cIAP-2. The expression of poly (ADP-ribose) polymerase and β-catenin, which are the substrate proteins of caspase-3, was significantly decreased. In conclusion, infrasound is an apoptotic inducer of cardiac myocytes.
Adult rats were used to identify the effects of infrasound on neurogenesis in the hippocampal dentate gyrus. After 7 consecutive days' exposure to infrasound of 16 Hz at 130 dB, immunostaining of 5-bromo-2'-deoxyuridine (BrdU) and doublecortin (DCX) was preformed. Compared with those in normal groups, the numbers of BrdU+ and DCX+/BrdU+ cells in the subgranular zone in infrasound groups were significantly decreased at 3, 6, 10 and 14 days and returned to normal at 18 days. The percentage of BrdU+ cells that were co-labeled with DCX showed no significant differences between the infrasound and normal groups. These data suggest that infrasound inhibits the cell proliferation in adult rat dentate gyrus but has no effects on early migration and differentiation of these newborn cells.
This study was designed to examine the effect of infrasound exposure (5 Hz at 130 dB) on whole-cell L-type Ca2+ currents (WLCC) in rat ventricular myocytes and the underlying mechanism(s) involved. Thirty-two adult Sprague-Dawley rats were randomly assigned to infrasound exposure and control groups. [Ca2+]i, WLCC, mRNA expression of the a1c subunit of L-type Ca2+ channels (LCC), and SERCA2 protein were examined on day 1, 7, and 14 after initiation of infrasound exposure. Fluo-3/AM fluorescence and the laser scanning confocal microscope techniques were used to measure [Ca2+]i in freshly isolated ventricular myocytes. The Ca2+ fluorescence intensity (FI), denoting [Ca2+]i in cardiomyocytes, was significantly elevated in a time-dependent manner in the exposure groups. There was a significant increase in WLCC in the 1-day group and a further significant increase in the 7- and 14-day groups. LCC mRNA expression measured by RT-PCR revealed a significant rise in the 1-day group and a significant additional rise in the 7- and 14-day groups compared with control group. SERCA2 expression was significantly upregulated in the 1-day group followed by an overt decrease in the 7- and 14-day groups. Prolonged exposure of infrasound altered WLCC in rat cardiomyocytes by shifting the steady-state inactivation curves to the right (more depolarized direction) without altering the slope and biophysical properties of I
Ca,L. Taken together, our data suggest that changes in [Ca2+]I levels as well as expression of LCC and SERCA2 may contribute to the infrasound exposure-elicited cardiac response.
The role that Ca(2+) plays in ventricular excitation contraction coupling is well defined and much is known about the marked differences in the spatiotemporal properties of the systolic Ca(2+) transient between atrial and ventricular myocytes. However, to date there has been no systematic appraisal of the Ca(2+) homeostatic mechanisms employed by atrial cells and how these compare to the ventricle. In the present study we sought to determine the fractional contributions made to the systolic Ca(2+) transient and the decay of [Ca(2+)](i) by the sarcoplasmic reticulum and sarcolemmal mechanisms. Experiments were performed on single myocytes isolated from the atria and ventricles of the rat. Intracellular Ca(2+) concentration, membrane currents, SR Ca(2+) content and cellular Ca(2+) buffering capacity were measured at 23 degrees C. Atrial cells had smaller systolic Ca(2+) transients (251+/-39 vs. 376+/-41 nmol x L(-1)) that decayed more rapidly (7.4+/-0.6 vs. 5.45+/-0.3 s(-1)). This was due primarily to an increased rate of SR mediated Ca(2+) uptake (k(SR), 6.88+/-0.6 vs. 4.57+/-0.3 s(-1)). SR Ca(2+) content was 289% greater and Ca(2+) buffering capacity was increased approximately 3-fold in atrial cells (B(max) 371.9+/-32.4 vs. 121.8+/-8 micromol x L(-1), all differences P<0.05). The fractional release of Ca(2+) from the SR was greater in atrial cells, although the gain of excitation contraction coupling was the same in both cell types. In summary our data demonstrate fundamental differences in Ca(2+) homeostasis between atrial and ventricular cells and we speculate that the increased SR Ca(2+) content may be significant in determining the increased prevalence of arrhythmias in the atria.
The paper identifies industrial sources of low-frequency acoustic oscillations and presents their hygienic evaluations for various branches of industry. It then analyzes results of a study, on a specially designed facility, into the effects on the body of oscillations having a frequency of 5 to 10 Hz and a sound pressure of 100 or 135 dB. In this study, electroencephalography, electrocardiography, rheoencephalography, seismocardiography, pneumography, and audiometry were used to detect early responses to low-frequency oscillations of the central nervous, cardiovascular, respiratory, and auditory systems. Morphologic changes were studied in muscles, internal organs, brain structures, and spiral organ of the cochlea to gain an insight into mechanisms of infrasound action on the body.
60 mature white male rats were used to study the effect of infrasound at a frequency of 8 and 16 Hz, sound pressure from 110 dB to 140 dB, on hepatocytes. The duration of exposure to the given factor was 5, 10, 15, 25 and 40 days, 3 hours daily. It was found out, that diffuse changes appearing in the liver parenchyma were of the mosaic character, and were observed both in individual hepatocytes and in a whole group of cells. The degree of manifestation of changes was to a larger degree associated with the duration of exposure to infrasound and the level of sound pressure, than with the frequency.
The Ca2+ sensitivity of cardiac myofibrillar force production can be decreased by acidosis or inorganic phosphate (P(i)) and increased by caffeine. To investigate whether the source of tissue influences the potency of these agents, we compared the actions of acidosis (change of pH from 7.0 to 6.2), P(i) and caffeine (both 20 mM) on force production of skinned cardiac muscles from adult ventricle, adult atrium and neonate ventricle of the rat. Maximum Ca(2+)-activated force was reduced by all three interventions and the responses of the different muscle types to a given intervention were similar. Acidosis reduced myofibrillar Ca2+ sensitivity by 1.09 and 1.04 pCa units in adult ventricle and atrium, respectively, and P(i) reduced it by 0.19 and 0.22 pCa units. However, each effect was only one-third as great in the neonate ventricle, which showed falls of 0.33 pCa units for acidosis and 0.06 for P(i). In contrast, caffeine raised the Ca2+ sensitivity by the same amount (approximately 0.4 pCa units) in all three muscle types. The differential effect between adult and neonate seen with both acidosis and P(i) suggests some similarity in the mechanisms by which these factors decrease Ca2+ sensitivity. In contrast, the equal effects of caffeine on neonate and adult suggests that caffeine acts by a completely different mechanism. The lower pH- and P(i)-sensitivity of the neonatal ventricle can help to explain why neonatal and adult myocardium exhibit differential force responses to ischaemia (or hypoxia alone).
To understand the factors underlying the functional differences between atrial and ventricular tissues, intrinsic properties of myofibrils and mitochondria of atrial skinned fibers were compared with those of fibers from adult or immature (1 and 2 weeks old) ventricular muscle. Isometric mechanical parameters were determined at various calcium concentrations in fibers treated with Triton X-100 to solubilize all cellular membranes. Maximal active tension and stiffness measured at pCa 4.5, as well as calcium sensitivity, were not different in adult atria and ventricles. Both force and stiffness increased in adult ventricles, while calcium sensitivity diminished in adult ventricles, compared with immature muscles. Myofibrillar contractile kinetics, assessed by the rate constant of tension fall following quick stretches, were similar in adult atria (79.7 +/- 6.9 s-1) and ventricles (72.4 +/- 6.8 s-1) and higher in adult atria and ventricles than in immature ventricles (24.1 +/- 2.3 s-1 in 1-week-old rats and 49.3 +/- 4.2 s-1 in 2-week-old rats). Sensitivity of rigor tension development to MgATP in the presence and in the absence of phosphocreatine was not markedly different in the different tissues. Mitochondrial function was assessed in saponin-skinned fibers. Tissue oxidative capacities, expressed as nmol O2.min-1.mg-1 fiber dry weight, were lower in immature ventricles and atria than in adult ventricles. Creatine failed to stimulate respiration in ventricles of young rats and in adult atria, whereas a 74 +/- 10% increase in respiration was observed in adult ventricles. Since mitochondrial creatine kinase was present in adult atria, this suggests an absence of coupling between oxidative phosphorylation and mitochondrial creatine kinase in this tissue. Thus, adult atrial tissue differs from neonatal ventricular tissue but it exhibits contractile properties similar to adult ventricular properties and differs from adult ventricle mainly in metabolic properties.
Many forms of industrial illness are thought to result from the effects of vibration on the human body. Prolonged exposure causes undue stress and discomfort. At the human whole-body resonant frequency there is maximum displacement between the organs and the skeletal structure and thus this is one frequency of vibration that should be minimized in the workplace and elsewhere. The vertical whole-body resonant frequencies of 113 fully-clothed standing humans were measured using a vibrating beam method, which imposed a very low acceleration magnitude at the subjects' feet. The overall range of resonant frequencies was found to be from 9 to 16 Hz and independent of mass, height and mass to height ratio. The mean values (+/-1 s.e.) were 12.2 +/- 0.1 Hz for males and 12.8 +/- 0.2 Hz for females with an overall mean population value of 12.3 +/- 0.1 Hz.
Exposure to high intensity, low frequency noise can cause whole-body vibration. Such exposures to airborne vibration can reach the limits of human tolerance and have been associated with physiological and pathological disorders. The objective of this study was to characterize human body vibration response during exposures to operational airborne vibration.
Triaxial body accelerations were collected at multiple anatomical sites with the subject located at selected crew positions during ground-based engine runup tests on several military tactical aircraft. The acceleration time histories were processed in one-third octave frequency bands and compared with the one-third octave band noise data.
The most significant finding was the occurrence of a resonance peak in the fore-and-aft (X) chest acceleration in the frequency bands between 63 and 100 Hz. Both the chest acceleration and associated noise level increased as the subject moved aft of the exhaust outlet, coinciding with the report of increasing chest vibration. A relatively linear relationship was found between the overall chest accelerations and noise levels between 5 and 250 Hz. An approach to developing combined noise and vibration exposure criteria was proposed.
The resonance observed in the upper torso strongly suggested that airborne vibration in the 60 to 100 Hz frequency band may be an important contributing factor in the generation of subjective symptoms and possibly physiological and pathological disorders. Additional field and laboratory studies are required to validate the relationship between the biodynamic responses, noise levels, and physiological and pathological consequences.
Intracellular [Ca2+] ([Ca2+]i) was imaged in atrial and ventricular rat myocytes by means of a high-speed Nipkow confocal microscope. Atrial myocytes with an absent t-tubule system on 8-di- ANEPPS staining showed an initial rise in Ca2+ at the periphery of the cell, which propagated to the interior of the cell. Ventricular myocytes showed a uniform rise in [Ca2+]i after electrical stimulation, consistent with a prominent t-tubular network. In atrial myocytes, there was a much shorter time between the peak of the [Ca2+]i transient and the peak contraction as compared to ventricular myocytes. A regional release of Ca2+ induced by an exposure of one end of the myocyte to caffeine with a rapid solution switcher resulted in a uniform propagation of Ca2+ down the length of the cell in atrial myocytes, but we found no propagation in ventricular myocytes. A staining with rhodamine 123 indicated a much greater density of mitochondria in ventricular myocytes than in atrial myocytes. Thus the atrial myocytes display a lack of "local control" of Ca2+ release, with propagation after the Ca2+ release at the periphery induced by stimulation or at one end of the cell induced by exposure to caffeine. Ventricular myocytes showed the presence of local control, as indicated by an absence of the propagation of a local caffeine-induced Ca2+ transient. We suggest that this finding, as well as a reduced delay between the peak of the [Ca2+]i transient and the peak shortening in atrial myocytes, could be due in part to reduced Ca2+ buffering provided by mitochondria in atrial myocytes as opposed to ventricular myocytes.
Recent interest in adverse effects of infrasound on organisms arises from health concerns. We assessed the association between infrasound exposure of 5 Hz at 130 dB and changes of cardiac ultrastructure and function in rats. Thirty-two Sprague-Dawley rats were randomized into control, 1, 7, and 14 days groups for 2 h of infrasound once daily according to planned schedules. Changes of cardiac ultrastructure, hemodynamics indices, intracellular Ca(2+) concentrations ([Ca(2+)](i)), and sarcoplasmic reticulum Ca(2+)-ATPase 2 (SERCA2) were detected. Heart rates in 1 day group were significantly increased compared with control group and no significant changes in other groups. Left ventricular systolic pressures were significantly increased with time. Left ventricular diastolic end pressure and maximum rising rates of left ventricular pressure (+dl/dt) were significantly increased in 7 and 14 days groups and not changed in 1 day group, compared with control group. Maximum dropping rates of left ventricular pressure (-dl/dt) were significantly decreased in 7 and 14 days groups and not changed in 1 day group, compared with control group. In heart cells, there were several swelled mitochondria in 1 day group, more swelled mitochondria in 7 days group, platelet aggregation in the intercellular substance in 14 days group. [Ca(2+)](i) were significantly increased with time. There was a significant increase in SERCA2 in 1 day group, while a significant decrease in 7 and 14 days groups, compared with control group. Infrasound of 5 Hz at 130 dB can damage cardiac ultrastructure and function. Changes of [Ca(2+)](i) and SERCA2 play an important role in the secondary cardiac damage.
Experimentelle Untersuchungen zum Einfluss von Infraschalldruck auf den Menschen
- K Wysocki
- K Schultz
- P Wieg
Wysocki K, Schultz K, Wieg P. Experimentelle Untersuchungen zum
Einfluss von Infraschalldruck auf den Menschen. Z ges Hyg
1980;26:436:440.
Low-frequency noise, infrasound and vibrations in the environment, Orientation no. 9 from the Danish Environmental Protection Agency")
- Miljøstyrelsen
Miljøstyrelsen, "Lavfrekvent støj, infralyd og vibrationer i eksternt
miljø (in Danish, trans: "Low-frequency noise, infrasound and
vibrations in the environment, Orientation no. 9 from the Danish
Environmental Protection Agency")", 1997, Orientering fra
Miljøstyrelsen nr. 9, 1-50, Miljøstyrelsen, Denmark.