Resource Documents: VAD (13 items)
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Author: Supremo Tribunal de Justiça
Wind turbine #2 is at a distance of 321.83 m from the house and 182.36 m from the stables; wind turbine #3 at 539.92 m and 439.64 m, respectively; wind turbine #4 at 579.86 m and 565.50 m; and wind turbine #1 at 642.08 m and 503 m.
Before November 2006, Quinta was a quiet and peaceful place, with little human presence in the surrounding area, and limited human presence at the site itself – only birds, vegetation, and trees. Before November 2006, the plaintiffs never reported the existence of insomnia, difficulty sleeping, or sleep disturbances. After the start of operation of wind turbines 1, 2, 3 and 4, the plaintiffs have reported the existence of insomnia, sleep difficulties, and sleep disturbances. … After the commissioning of the wind turbines, the 1st plaintiff had complaints of mood changes, fatigue, headache, and hypersensitivity to noise. The remaining members of the household had similar but less severe complaints. …
The right to rest, tranquility and sleep are aspects of the right to humane treatment (Article 25, para. 1 of the Constitution of the Republic of Portugal), which is part of established fundamental rights, the collection of rights, freedoms, and guarantees. These personhood rights are well protected against any unlawful interference, not necessarily in blame for an offense in intent to harm the victim, but in the offense itself.
The right to rest is offended even though the activity of operating the wind farm in question has been officially authorized. The fact that noise regulations are respected does not mean that it is allowed to affect the rights to rest and health. The wrongfulness, in this perspective, obviates measurement of the noise level by legal standards: The illegality of a noisy behavior that harms the rest, tranquility, and sleep of others is precisely the fact that unjustifiably and beyond socially tolerable limits is injurious to the rights integrated in the bundle of rights, freedoms, and guarantees.
Indeed, “the consecration of a maximum sound level of noise just means that the administration can not authorize the installation of equipment or grant licensing of activities that do not respect that ceiling, and disregard of this limit is considered a violation of a regulatory ordinance.” That is, “the General Regulation on Noise only have effects within the administrative activity and in scope, and may not interfere with the protection of personhood rights of the people, whose protection is not exhausted in the noise limit established in this law.”
Collision of Rights
On one side is the right to rest, person, absolute, inviolable, and enrolled in the framework of rights and freedoms …
On the other side, according to the position of the defendant, are constitutionally protected community values, particularly the achievement of the public interest, the unquestioned value of wind turbines as a source of clean energy and that the defendant represents a clean energy industry and thus a defender of the environment. …
Having been established that the 1st plaintiff lives and works full time at Quinta, the 2nd plaintiff is domestic (ie working from home), the social life of the family is passed at Quinta, and the two minor children study at Quinta outside school hours, this means that exposure to noise occurs not only at night but also during the day, causing sleep problems at night but constituting disturbed living throughout the day, caused by the noises and flashing shadows as a result of the activity of the wind turbines, physical and mental wear on the plaintiffs’ persons throughout the day.
For this reason, the decision to suspend the wind turbines only from dusk to dawn is unacceptable. … In fact, although not proven that the noise is less in the day day than during the night, if the wind turbines are not turned off, it is clear that the violation of personhood rights is also observed during the daytime, causing anxiety and physical and psychological distress in the whole family.
For this reason, a clear prevalence of personhood rights requires the suspension/removal of all the wind turbines in question. …
For these reasons, in dismissal of the defendant’s case, and the partial granting of the plaintiffs’, it is ordered that the defendant:
a) Suspend the total operation of wind turbine nos. 1, 2, 3, and 4 of the wind farm in the daytime and nighttime, and that the defendant, therefore, remove them.
b) Pay the plaintiffs as compensation the sum of thirty thousand euros.
Lisboa, 30 de Maio de 2013
Granja da Fonseca (Relator)
Ana Paula Boularot
Reply to: How the factoid of wind turbines causing ‘vibroacoustic disease’ came to be ‘irrefutably demonstrated’
Author: Alves-Pereira, Mariana; and Castelo Branco, Nuno
As lead researchers in vibroacoustic disease (VAD), we have been made aware of the article by Chapman et al. in which our work was greatly misrepresented and misunderstood. Correction and clarification are, therefore, required.
Chapman et al. reference a 2007 paper discussing Public health and the importance of low frequency noise (LFN), in which the LFN content of a ‘Grain Terminal home’ and a ‘Wind Turbine home’ are discussed. The grain terminal (GT) case, originally presented in 2004, was first-authored by our cardiologist, and the Wind Turbine (WT) case was first presented in 2007, with a follow-up in 2010. We stand behind the statements published in these papers.
Both families solicited our help. We did not select or procure either case, and we provided our services pro bono. Until then, our experience with LFN-induced pathology had been mostly within occupational exposures, not environmental or residential exposures.
It is not our intention herein to replicate the results of the above-mentioned studies, but some data is required to clarify to the issues at hand.
Some acoustical considerations
The owner of the WT-home paid an independent accredited firm for the acoustical measurements, and provided our team with the numerical information for further analyses. No commercial, financial or professional agreements (contractual or otherwise) existed between this firm and the VAD research team. Figure 1 shows acoustical data compiled by VAD researchers.
As seen in Figure 1, levels of LFN are clearly increased in the bedroom when WT are in operation.
Chapman et al. claimed our work was “of abject methodological quality” (p.247) because “The noise measuring equipment used to measure infrasound in the two houses was different” (p.246). However, in that paper, Alves-Pereira et al., being fully aware of that technical limitation, wrote: “In a perfect world, designed for the most efficient and accurate scientific studies, all noise assessments ought to be conducted with the same equipment and with the same procedures. This is not feasible. So, despite on-site and factory calibrations, a legitimate question will always remain: can the differences between the ILFN levels in the [GT and WT] homes (…) be due to differences in the noise measuring equipment and procedures alone? Despite this legitimate question, these data are sufficient to warrant precautionary measures”.
Some clinical considerations
Another criticism emerged because we “took no account of inattention and lack of energy in school children being common” (p.247).
Upon being contacted by these two families, VAD Team researchers provided non-invasive VAD screening tests. The rationale for these specific tests would require significant self-citation.
The 10-year-old residing since gestation in the GT-home disclosed “the most severe cardiovascular condition”, scoring the highest values in mitral valve leaflet thickening and pericardial thickening. These echo-imaging findings had only previously been seen in older LFN-exposed workers, and were entirely unexpected in a 10-year-old child.
Furthermore, this child had “suffered from asthma until the age of 1 year. At 5–8 months of age, he was medicated for reflux, and then again until he was 1 year old. At 8 months he suffered pneumonia. After the age of 1, he began to develop repeated ear infections that were not responsive to antibiotics. At age 3 he underwent ear surgery. At the age of 5, at school, he suddenly lost his vision, and was taken to the hospital where the EEG revealed a late onset epileptic seizure. Nose bleeds without an apparent cause used to be frequent, but have subsided with age. There is no history of rheumatic fever, radiation or asbestos exposure.” (In: Alves-Pereira et al., citing Araújo et al.)
In the WT-case, Evoked Potentials provided to the 12-year-old boy, disclosed “asymmetries in the right and left nerve conduction times, and the right I-V interlatency value was at the threshold of normal values (4.44ms). The endogenous evoked potential P300 recording occurred at 352ms (normal: 300ms)”. Taken alone, these values are not relevant, but after a two-month vacation away from the WT home, the child disclosed significant improvement: 322ms.
Neurophysiological tests were provided to this child because four months after WT began operation, the parents received a letter from the child’s teacher voicing “concern for the growing difficulties of an otherwise outstanding student, (…) it seems that [the child] has lost interest, makes a lesser effort, as if he were permanently tired. In Physical Education, an abnormal amount of tiredness is also observed. Is [the child] leading a healthy life? Does he sleep sufficient hours during the night?’”
These objective medical tests and clinical histories, disclosing morphological and brain potential changes, go well beyond the scope of “common” lack of energy in school children, as Chapman et al. suggest.
Some biological considerations
The fundamental histological feature found both in LFN-exposed patients and LFN-exposed laboratory animals was also observed in the horses raised on the WT-home property: thickening of vascular walls due to proliferation of extra-cellular matrices in the absence of an inflammatory process. To fully comprehend the rationale and the highly significant implications of these results, a large amount of self-citation would now be required.
Understanding the pathophysiology of LFN-induced diseases requires knowledge on cellular tensegrity architecture that goes beyond the classical models of general physiopathology.[8,9] Mechanotransduction cellular signaling, a relatively new concept, becomes of paramount importance because it is a major target of the LFN agent. In the absence of this new cellular model, the nature of the biological response prompted by LFN exposure cannot be fully understood.
Given the complexity of this subject, difficulty in recognising the significance of our scientific findings reported over the past three decades is entirely understandable.
Unfortunately, the vast majority of studies concerning health impacts of WT on neighbouring residents do not yet provide an adequate quantification of the physical agent of disease, and are based on highly subjective questionnaires lacking clinical corroboration on relevant endpoints. This is flagrantly perpetuated by the Wind Turbine Health Impact Study, as prepared for the State of Massachusetts. In our ongoing investigations, we have repeatedly pointed out the inadequacy of questionnaires as a valid measure of health effect, a position shared by the Strategic Health Impact Assessment on Wind Energy Development, as prepared for the State of Oregon.
We reiterate that LFN-contaminated homes are a significant public health concern, and substantial health deterioration can be observed in humans and animals dwelling without respite in LFN-rich environments. (Disclaimer: this statement cannot and should not be construed as an argument against the implementation of wind turbines.)
On 30 May 2013, the Supreme Court of Justice in Portugal decided upon the removal of the four WT, initially erected in 2006.
School of Economic Sciences and Organizations, Universidade Lusófona, Portugal
Nuno A. A. Castelo Branco
Principal Investigator, VAD Project
Australian and New Zealand Journal of Public Health 2014 vol. 38 no. 2 pp. 191-192.
1. Chapman S, St George A. How the factoid of wind turbines causing “vibroacoustic disease” came to be “irrefutably demonstrated”. Aust NZ J Public Health 2013; 37:244-9.
2. Alves-Pereira M, Castelo Branco NAA. Public health and noise exposure: the importance of low frequency noise. Proceedings of the Inter-Noise 2007 Conference ; 2007 Aug 28-31; Istanbul, Turkey. [link]
3. Araujo A, Alves-Pereira M, Joanaz de Melo J, Castelo Branco NAA. Vibroacoustic disease in a ten-year-old male. Proceedings of the Internoise 2004 Conference; 2004 Aug 22-25; Prague, Czech Republic
4. Alves-Pereira M, Castelo Branco NAA. In-home wind turbine noise is conducive to vibroacoustic disease. Proceedings of the 2nd International Meet Wind Turbine Noise; 2007 Sep 20-21; Lyon, France. [link]
5. Castelo Branco NAA, Costa e Curto T, Mendes Jorge L, Cavaco Faísca J, Amaral Dias L, Oliveira P, et al. Family with wind turbines in close proximity to home: follow-up of the case presented in 2007. Proceedings of the 14th International Meet Low Frequency Noise Vibration Control; 2010 Jun 9-11; Aalborg, Denmark.
6. Marciniak W, Rodriguez E, Olsowska K, Botvin I, Araujo A, Pais F, et al. Echocardiography in 485 aeronautical workers exposed to different noise environments. Aviat Space Environ Med. 1999;70 Suppl 3:A46-53.
7. Ingberg DE. Cellular tensegrity: defining new rules of biological design that governs the cytoskeleton. J Cell Sci. 1993;104:613-27.
8. Stamenovic D, Fredberg JJ, Wang N, Butler JP, Ingber DE. A microstructural approach to cytoskeletal mechanics based on tensegrity. J Theoretical Biol 1996; 181: 125-136.
9. Wang N, Butler JP, Ingber DE. Mechanotransduction across the cell surface and through the cytoskeleton. Science 1993; 260: 1124-27.
10. Alves-Pereira M, Castelo Branco NAA. Vibroacoustic disease: Biological effects of infrasound and low frequency noise explained by mechanotransduction cellular signaling. Prog Biophy Molec Biol 2007; 93: 256-79. [link]
11. Executive Office of Energy and Environmental Affairs. Wind Turbine Health Impact Study: Report of Independent Expert Panel [Internet]. Boston (MA): Commonwealth of Massachusetts EEA; 2012 [cited 2014 Jan 15]. Available from: http://www.mass.gov/eea/docs/dep/energy/wind/turbine-impact-study.pdf
12. Alves-Pereira M. Review of Wind Turbine Health Impact Study: Report of Independent Expert Panel [Internet]. Boston (MA): Massachusetts Department of Environmental Protection, Massachusetts Department of Public Health; 2012 [cited 2014 Jan 15]. Available from: //docs.wind-watch.org/MassDEP-wind-health-2-Alves_Pereira.pdf
13. Oregon Health Authority. Strategic Health Impact Assessment on Wind Energy Development in Oregon [Internet]. Portland (OR): Government of Oregon Public Health Division; 2013 [cited 2014 Jan 15]. Available from: http://public.health.oregon.gov/HealthyEnvironments/TrackingAssessment/HealthImpactAssessment/Documents/Wnd%20Energy%20HIA/Wind%20HIA_Final.pdf
14. Supreme Court of Justice (Portugal). Decision No. 2209/08.0TBTVD.L1.S1. Relevant Case Law in the Field of Environment in 2009 – Supreme Administrative Court, 22nd September, 2009, Judgement 161/05.2TBVLG.S1, Sector: Noise [Internet]. [cited 2014 Jan 15]. Available from: http://www.dgsi.pt/jstj.nsf/954f0ce6ad9dd8b980256b5f003fa814/4559d6d733d1589780257b7b004d464b?OpenDocument [link]
Download original document: “Reply to: How the factoid of wind turbines causing ‘vibroacoustic disease’ came to be ‘irrefutably demonstrated’”
Author: Alves-Pereira, Mariana; Joanaz de Melo, João; and Castelo Branco, Nuno
BACKGROUND: Vibroacoustic disease (VAD) is a systemic pathology caused by excessive exposure to low frequency noise (LFN). Until 1987, it was thought that the pathological effects of excessive LFN exposure were limited to the realm of cognitive and neurological disturbances. After the autopsy findings in a deceased VAD patient, it became clear that LFN impinges on the entire body, particularly the cardio-respiratory systems. In 1992, rodents were exposed to LFN, and the respiratory tract was studied through scanning and transmission electron microscopy. Pericardial, tracheal and lung fragments, removed with informed consent from VAD patients, have also been studied with light and electron microscopy. This report summarizes what is known to date on the tissue and cellular response to LFN exposure.
- TUBULIN-BASED STRUCTURES: Cilia are tubulin-based and exist in normal pericardia as well as in the respiratory tract. In VAD patients, pericardial cilia cease to exist, while tracheal and bronchial cilia are distributed in abnormal arrangements. In LFN-exposed rodents, respiratory tract cilia appear sheared, clipped or shaggy.
- ACTIN-BASED STRUCTURES: Cochlear cilia are actin-based structures, as are brush-cell microvilli that protrude into the respiratory tract airway. In LFN-exposed rodents, both structures appear fused. Actin filaments are also a fundamental element of the cellular cytoskeleton. In VAD patients’ pericardia, cytoskeletal deformations may be a consequence of LFN-induced changes of the actin filaments.
- BIOTENSEGRITY HYPOTHESIS: One of the most consistent findings in almost all human and rodent tissue fragments is the abnormal proliferation of collagen and elastin. It is hypothesized that the principles of biotensegrity structures may contribute to the explanation of tissue and cellular responses to LFN exposure.
For the past 24 years, the effects of low frequency noise (LFN) (<500 Hz, including infrasound) exposure have been the object of intense scientific inquiry. Vibroacoustic disease (VAD) is a whole-body pathology caused by excessive exposure to LFN, either due to occupational sources or environmental sources. The response of biological tissue to LFN has drawn great interest, particularly given the significant structural, or morphological, changes of the exposed organs, tissues and cells.
In 1987, an autopsy was performed on a deceased VAD patient, as specifically bequeathed by the patient in his will. Until then, it was thought that LFN-induced pathology was restricted to the realm of neuropathophysiology. Autopsy findings disclosed, among several other extraordinary features, widespread thickening of blood vessel walls, and abnormally thickened cardiac structures, namely valves and pericardium. Fibrosis (collagen proliferation) was also identified in the lungs.
In 1992, Wistar rats began to be used as animal models for VAD. Rodents were exposed to LFN, and fragments of different sections of the respiratory tract were studied with electron microscopy. In 1996, the first pericardial fragments were taken from fully informed VAD patients who were undergoing cardiac surgery (for other reasons). Since then, 12 VAD patients have provided pericardial fragments for our study. Similarly, several other VAD patients have provided fragments of respiratory tract tissue (epithelia) through biopsy (conducted for other reasons). All these tissue samples were examined with electron microscopy.
The goal of this report is to contribute to the characterisation of the biomechanical response of tissue to the presence of excessive LFN, drawing upon the data collected from the microscopy studies. …
LFN induces tissue reorganization and neo-formation. One of the underlying purposes may be the need to maintain structural integrity in a viscoelastic environment undergoing LFN-induced vibratory propagation.
Actin-based structures seem to have a tendency to fuse. Indeed, microvilli fusion (as seen in the brush cell) will alter the kinetic properties of the structure. Cochlear cilia, for example, are supposed to vibrate freely against the upper tectorial membrane, when an acoustical pressure wave is transduced along the basal membrane. This movement is what relays the acoustical signal to the brain. However, in LFN-exposed rats, cilia are fused together, as well as with the upper tectorial membrane. Hence, when the basal membrane attempts to transduce the acoustical signal, instead of freely vibrating, cochlear cilia, now a non-vibrating structure, will be pulled. If something similar occurs in the cochlear cilia of LFN-exposed humans, then perhaps discomfort might be felt. Discomfort that may be closely associated with the concept of annoyance.
The destruction of ciliary fields is dramatic, and might be related to its structural specificities. The cilium is anchored to the cellular cortex through an actin-based network located within the cytoskeleton directly under the plasma membrane. Given the response of other actin-based structures, namely brush cell microvilli as well as cochlear stereocilia, it is not unreasonable to hypothesize that perhaps the actin filaments that compose the cytoskeleton might also be reacting to LFN exposure. Corroborating this notion are transmission electron microscopy images showing intact internal ciliary structures. Yet, strands of apparently sheared cilia appear lying horizontally on the epithelial surface, and ciliary fields are depleted.
The response of the pericardium to LFN certainly appears to be an adaptation response. This does not exclude the loss of functional capabilities, for example, not a single cilium was found in mesothelial cells. Despite the dramatic alterations of the pericardia, heart function is normal and no diastolic dysfunction exists in VAD patients. It would seem that this newly formed loose tissue layer, rich in vessels and adipose tissue, with numerous elastic components, plays a very important role, possibly of a pneumatic and logistic nature, in maintaining normal function of the heart in these patients.
The ruptured cellular membranes seen in the pericardial mesothelial layer are very unusual. Cellular debris is seen in all layers of the pericardium. This sort of cellular death is not related to the normal, programmed, or apoptotic, cellular death. In VAD patients’ pericardia, cellular death seems to be associated with mechanical processes and stresses. The fact that the cellular debris is being spewed into the pericardial sac may be a contributing factor to the development of auto-immune diseases in VAD patients.
It would seem that in the presence of LFN, living tissue responds by reinforcing its structural integrity. This is strongly suggested by the thickening observed in blood vessel walls, as well as in alveoli walls.
In conclusion, while biochemical and molecular signalling play fundamental roles in tissue re-organization, given the nature of the mechanical insult perpetrated by LFN, mechanically-induced signalling must also be greatly implicated.
João Joanaz de Melo
New University of Lisbon, DCEA-FCT, Caparica (mariana.pereira/oninet.pt)
Maria Cristina Marques
Dept. Physiology, School of Pharmacology, University of Lisbon, Portugal
Nuno A. A. Castelo Branco
Center for Human Performance, Alverca, Portugal (n.cbranco/netcabo.pt)
Presented at the 11th International Meeting on Low Frequency Noise and Vibration and Its Control, Maastricht, The Netherlands, 30 August to 1 September 2004
Download original document: “Vibroacoustic Disease – The Response of Biological Tissue to Low-Frequency Noise”
Author: Alves-Pereira, Mariana; Castelo Branco, Nuno; et al.
On the Impact of Infrasound and Low Frequency Noise on Public Health – Two Cases of Residential Exposure
Abstract: Noise exposure is known to cause hearing loss and a variety of disturbances, such as annoyance, hypertension and loss of sleep. It is generally accepted that these situations are caused by the acoustical events processed by the auditory system. However, there are acoustical events that are not necessarily processed by the auditory system, but that nevertheless cause harm. Infrasound and low frequency noise (ILFN, <500Hz) are acoustical phenomena that can impact the human body causing irreversible organic damage to the organism, but that do not cause classical hearing impairment. Acoustical environments are normally composed of all types of acoustical events: those that are processed by the auditory system, and those that are not. It is generally assumed that acoustical phenomena not captured by the human auditory system are not harmful. This is reflected by current noise assessment procedures that merely require the quantification of the acoustical phenomena that are audible to human hearing (hence the dBA unit). Thus, studies investigating the effects ofnoise exposure on public health that do not take into account the entire spectrum of acoustical energy are misleading and may, in fact, be scientifically unsound. Two cases of in-home ILFN are described. …
Case Report 2: Family R. lives on a horse- and bull-breeding farm, located in a zoned, rural agricultural area, 1 hour north of Lisbon. Family R. consists of mother, father, 12-year-old son, and 8-year-old daughter. In November 2006, 4 wind turbines (2MW each) were installed around Family R.’s farm, at approximately 322m, 540m, 580m and 643m from the residential home. The distance to the stables is less than to the residential house. …
The wind turbines installed around Family R.’s home began operation in November 2006. In March 2007, the parents received a letter from the school inquiring about the reason for the sharp decrease in the memory and attention skills of the 12-year-old child, and the overwhelming tiredness he exhibited during physical education classes. The school questioned the parents if the boy was getting enough hours of sleep during the night.
The entire family has already received the typical vibroacoustic disease diagnostic tests, including echocardiograms which did not disclose any significant thickening of cardiovascular structures. Tissue fragments have been removed from the farm animals that have been scheduled for slaughter, and will be submitted to the light and electron microscopy analyses that this team usually conducts on ILFN-exposed tissue fragments. These procedures will be repeated every 6 months, and follow-up reports will ensue.
Revista Lusófona de Ciencias e Tecnologias da Saúde, 2007; (4) 2: 186-200
Direcção de Radiologia da Escola Superior de Saúde Ribeiro Sanches, Lisboa, Portugal.
Departamento de Ciencias da Saúde, Universidade Lusófona, Lisboa, Portugal.
Nuno A. A. Castelo Branco
Centro de Performance Humana, Alverca, Portugal.
Download original document: “On the Impact of Infrasound and Low Frequency Noise on Public Health – Two Cases of Residential Exposure”
Baixar documento original: “Sobre o Impacto de Infrasons e Ruído de Baixa Frequência na Saúde Pública – Dois Casos de Exposição Residencial”
Family with Wind Turbines in Close Proximity to Home: Follow-Up of the Case Presented in 2007
In 2007, at the 2nd International Conference on Wind Turbine (WT) Noise, held in Lyon, France, low frequency noise (<500 Hz, LFN)–induced pathology, consistent with vibroacoustic disease (VAD), was shown to be emerging in the R. Family, exposed to residential LFN generated by 4 WTs installed in close proximity (300-700 m) to their home. Herein, a follow-up is provided.
The wife and 2 children no longer reside within that home. Mr. R., however, must remain to care for the thoroughbred Lusitanian horses and bulls that he trains and breeds for bullfights. In addition to the continued deterioration of Mr. R’s health and well-being, his financial situation is aggravated by the condition now appearing in his horses during the first year of life. Between 2000 and 2006, 13 healthy thoroughbred Lusitanian horses were born and raised on Mr. R’s property. All horses (N=4) born or raised after 2007 developed asymmetric flexural limb deformities. WTs began operations in November 2006. No other changes (constructions, industries, etc) were introduced into the area during this time.
Tissue analyses of the defected tendons were performed and revealed the classical features of LFN-induced biological responses: thickening of blood vessel walls due to proliferation of collagen in the absence of an inflammatory process.
14th International Meeting on Low Frequency Noise and Vibration and Its Control, Aalborg, Denmark, 9-11 June 2010
Nuno A. A. Castelo Branco
Luis Amaral Dias
Centro da Performance Humana, Alverca, Portugal
Teresa Costa e Curto
João Pedro da Costa Pereira
Sociedade Hípica Portuguesa, Campo Grande, Lisboa, Portugal
Luisa Mendes Jorge
Júlio Cavaco Faísca
Faculty of Veterinary Medicine, Universidade Técnica de Lisboa, Lisbon, Portugal
José Martins dos Santos
Instituto Superior de Ciências da Saúde Egas Moniz, CiiEM, Almada, Portugal
Universidade Lusófona–ERISA, Lisboa, Portugal