- December 9 – UK authorities confirmed 2 cases of anaphylaxis after vaccination
- December 18*, 2020 – CDC has identified 6 case reports of anaphylaxis following Pfizer-BioNTech vaccine meeting Brighton Collaboration criteria for anaphylaxis
- Persons with anaphylaxis following COVID-19 vaccination should not receive additional doses of COVID-19 vaccine
Scientists in Italy have identified a sample of the novel coronavirus collected from a young boy late last year that they say is genetically identical to the earliest strain isolated in the Chinese city of Wuhan almost a year ago.
The sample was collected on December 5, 2019 in Milan from a boy who was first thought to have contracted measles, according to the researchers from the University of Milan.
It was a “100 per cent match” of a genome segment of the first Sars-CoV-2 viral strain collected from a seafood market worker in Wuhan on December 26, they said.
“These findings, in agreement with other evidence of early Covid-19 spread in Europe, advance the beginning of the outbreak to late autumn 2019,” said the team led by Professor Elisabetta Tanzi.
We identified severe acute respiratory syndrome coronavirus 2 RNA in an oropharyngeal swab specimen collected from a child with suspected measles in early December 2019, ≈3 months before the first identified coronavirus disease case in Italy. This finding expands our knowledge on timing and mapping of novel coronavirus transmission pathways.
The recommendation to wear surgical masks to supplement other public health measures did not reduce the SARS-CoV-2 infection rate among wearers by more than 50% in a community with modest infection rates, some degree of social distancing, and uncommon general mask use. The data were compatible with lesser degrees of self-protection.
The harmful consequences of public health choices should be explicitly considered and transparently reported to limit their damage, say Itai Bavli and colleagues
The SARS-CoV-2 pandemic has posed an unprecedented challenge for governments. Questions regarding the most effective interventions to reduce the spread of the virus—for example, more testing, requirements to wear face masks, and stricter and longer lockdowns—become widely discussed in the popular and scientific press, informed largely by models that aimed to predict the health benefits of proposed interventions. Central to all these studies is recognition that inaction, or delayed action, will put millions of people unnecessarily at risk of serious illness or death.
However, interventions to limit the spread of the coronavirus also carry negative health effects, which have yet to be considered systematically. Despite increasing evidence on the unintended, adverse effects of public health interventions such as social distancing and lockdown measures, there are few signs that policy decisions are being informed by a serious assessment and weighing of their harms on health. Instead, much of the discussion has become politicised, especially in the US, where President Trump’s provocative statements sparked debates along party lines about the necessity for policies to control covid-19. This politicisation, often fuelled by misinformation, has distracted from a much needed dispassionate discussion on the harms and benefits of potential public health measures against covid-19.
In the interest of public debate, we allow visitors to share opinions, experiences and research that may be of value to others. This is a visitor contribution from our Discussions page.
The views expressed are those of the individual posters themselves. Please read our Comments and contributions disclaimer.
- Credentials: Megan Mansell is a former district education director over special populations integration, serving students who are profoundly disabled, immunocompromised, undocumented, autistic, and behaviorally challenged; she also has a background in hazardous environs PPE applications. She is experienced in writing and monitoring protocol implementation for immunocompromised public sector access under full ADA/OSHA/IDEA compliance.
- E-mail: [email protected]
- Twitter: @mamasaurusMeg
A Rational Reopening Guide
A framework for operating any facility or business during COVID
The United States already has a body of law that requires making accommodations for persons with disabilities; if we start from the premise that Americans should be able to determine the level of risk they’re willing to take, all of those concepts can be extended to provide accommodations to anyone who is concerned about exposure to COVID, whether because they are vulnerable or because they live with someone who is vulnerable.
The first step is to ask everyone whether or not they consider themselves immunocompromised (IC). This can include people who themselves are immunocompromised or who live with someone who is immunocompromised. Allowing people to identify whether or not they consider themselves immunocompromised allows us to create reasonable accommodations for accessing the public sector. Some people cannot mask, and others prefer not to, but we can still allow them to safely access shared spaces if we know how many individuals are truly in need of accommodation.
Those who cannot or prefer not to mask should be free to assess their own risk, especially for a contagion with a 99.6% recovery rate.
If we ask everyone to identify the population they belong to, it all falls into place.
Read the full article on Rational Ground.
Note: This article, published on 5 February 2010, originally appeared in Forbes. It was removed sometime in mid October 2020 with no explanation.
While you can find a capture at archive.org, we have saved a copy here to protect against censorship and for easy sharing.
The World Health Organization has suddenly gone from crying “The sky is falling!” like a cackling Chicken Little to squealing like a stuck pig. The reason: charges that the agency deliberately fomented swine flu hysteria. “The world is going through a real pandemic. The description of it as a fake is wrong and irresponsible,” the agency claims on its Web site. A WHO spokesman declined to specify who or what gave this “description,” but the primary accuser is hard to ignore.
The Parliamentary Assembly of the Council of Europe (PACE), a human rights watchdog, is publicly investigating the WHO’s motives in declaring a pandemic. Indeed, the chairman of its influential health committee, epidemiologist Wolfgang Wodarg, has declared that the “false pandemic” is “one of the greatest medicine scandals of the century.”
Even within the agency, the director of the WHO Collaborating Center for Epidemiology in Munster, Germany, Dr. Ulrich Kiel, has essentially labeled the pandemic a hoax. “We are witnessing a gigantic misallocation of resources [$18 billion so far] in terms of public health,” he said.
They’re right. This wasn’t merely overcautiousness or simple misjudgment. The pandemic declaration and all the Klaxon-ringing since reflect sheer dishonesty motivated not by medical concerns but political ones.
Unquestionably, swine flu has proved to be vastly milder than ordinary seasonal flu. It kills at a third to a tenth the rate, according to U.S. Centers for Disease Control and Prevention estimates. Data from other countries like France and Japan indicate it’s far tamer than that.
Indeed, judging by what we’ve seen in New Zealand and Australia (where the epidemics have ended), and by what we’re seeing elsewhere in the world, we’ll have considerably fewer flu deaths this season than normal. That’s because swine flu muscles aside seasonal flu, acting as a sort of inoculation against the far deadlier strain.
Did the WHO have any indicators of this mildness when it declared the pandemic in June?
Absolutely, as I wrote at the time. We were then fully 11 weeks into the outbreak and swine flu had only killed 144 people worldwide–the same number who die of seasonal flu worldwide every few hours. (An estimated 250,000 to 500,000 per year by the WHO’s own numbers.) The mildest pandemics of the 20th century killed at least a million people.
But how could the organization declare a pandemic when its own official definition required “simultaneous epidemics worldwide with enormous numbers of deaths and illness.” Severity–that is, the number of deaths–is crucial, because every year flu causes “a global spread of disease.”
Easy. In May, in what it admitted was a direct response to the outbreak of swine flu the month before, WHO promulgated a new definition matched to swine flu that simply eliminated severity as a factor. You could now have a pandemic with zero deaths.
Under fire, the organization is boldly lying about the change, to which anybody with an Internet connection can attest. In a mid-January virtual conference WHO swine flu chief Keiji Fukuda stated: “Did WHO change its definition of a pandemic? The answer is no: WHO did not change its definition.” Two weeks later at a PACE conference he insisted: “Having severe deaths has never been part of the WHO definition.”
They did it; but why?
In part, it was CYA for the WHO. The agency was losing credibility over the refusal of avian flu H5N1 to go pandemic and kill as many as 150 million people worldwide, as its “flu czar” had predicted in 2005.
Around the world nations heeded the warnings and spent vast sums developing vaccines and making other preparations. So when swine flu conveniently trotted in, the WHO essentially crossed out “avian,” inserted “swine,” and WHO Director-General Margaret Chan arrogantly boasted, “The world can now reap the benefits of investments over the last five years in pandemic preparedness.”
But there’s more than bureaucratic self-interest at work here. Bizarrely enough, the WHO has also exploited its phony pandemic to push a hard left political agenda.
In a September speech WHO Director-General Chan said “ministers of health” should take advantage of the “devastating impact” swine flu will have on poorer nations to get out the message that “changes in the functioning of the global economy” are needed to “distribute wealth on the basis of” values “like community, solidarity, equity and social justice.” She further declared it should be used as a weapon against “international policies and systems that govern financial markets, economies, commerce, trade and foreign affairs.”
Chan’s dream now lies in tatters. All the WHO has done, says PACE’s Wodart, is to destroy “much of the credibility that they should have, which is invaluable to us if there’s a future scare that might turn out to be a killer on a large scale.”
Michael Fumento is director of the nonprofit Independent Journalism Project, where he specializes in health and science issues. He may be reached at [email protected]
The CDC has long maintained that the coronavirus is transmitted through droplets spread among people in close proximity to one another. On Friday, it updated its guidelines, adding that the virus also spreads through “respiratory droplets or small particles, such as those in aerosols, produced when an infected person coughs, sneezes, sings, talks, or breathes,” adding that this is the main vector of infection.
The guidance no longer says COVID-19 can be spread through the air, and the agency said it will update the language once its review process “has been completed.”
But where did this one percent figure come from? You may find this hard to believe, but this figure emerged by mistake. A pretty major thing to make a mistake about, but that’s what happened.
In order to understand what happened, you have to understand the difference between two medical terms that sound the same – but are completely different. [IFR and CFR.]
CFR will always be far higher than the IFR. With influenza, the CFR is around ten times as high as the IFR. Covid seems to have a similar proportion.
Now, clearly, you do not want to get these figures mixed up. By doing so you would either wildly overestimate, or wildly underestimate, the impact of Covid. But mix these figures up, they did.
…we’ve had all the deaths we were ever going to get. And which also means that lockdown achieved, almost precisely nothing with regard to Covid. No deaths were prevented.
Last weekend the CDC drastically downgraded the number of COVID deaths and noted that in truth less than 10,000 died of the virus.
The media is in love with the idea that 200,000 Americans have died of COVID-19, but last weekend the CDC drastically downgraded the number of deaths and noted that in truth less than 10,000 died solely of the virus.
As it turns out, the Centers for Disease Control and Prevention (CDC) website recently reported that very few died solely of the virus. Out of the 161,392 deaths in the CDC data, just six percent (9,700) were attributed to the coronavirus alone. In all the rest of the deaths, COVID was either only one contributor to death or was merely present in the system at the end.
The Centers for Disease Control and Prevention is no longer recommending testing for everyone who’s been exposed to Covid-19, saying people who don’t have symptoms “do not necessarily need a test.”
The CDC has quietly revised its guidance on coronavirus testing to say that people without symptoms who were exposed to an infected person might not need to be screened.
The agency previously recommended testing for anyone with a “recent known or suspected exposure” to the virus even if they did not have symptoms.
The CDC’s previous guidance cited “the potential for asymptomatic and pre-symptomatic transmission” as a reason why people without symptoms who were exposed to the virus be “quickly identified and tested.”
More than 180,000 Americans have died of coronavirus as of Monday
The CDC’s latest fatality data shows that COVID-19 was listed as the sole cause of death for just 6% of those killed by the virus
94% of fatalities were in people who also suffered at least one chronic health condition, such as high blood pressure, diabetes, obesity or heart disease
On average, people who died of coronavirus had 2.6 additional underlying health conditions
A positive test result shows you may have antibodies from an infection with the virus that causes COVID-19. However, there is a chance a positive result means that you have antibodies from an infection with a virus from the same family of viruses (called coronaviruses), such as the one that causes the common cold.
Regardless of whether you test positive or negative, the results do not confirm whether or not you are able to spread the virus that causes COVID-19.
Persons who are diagnosed with influenza…should remain at home until the fever is resolved for 24 hours…and the cough is resolving to avoid exposing other members of the public. If such symptomatic persons cannot stay home during the acute phase of their illness, consideration should be given to having them wear a mask in public places when they may have close contact with other persons.
No recommendation can be made at this time for mask use in the community by asymptomatic persons, including those at high risk for complications, to prevent exposure to influenza viruses.
From January 21 through February 23, 2020, public health agencies detected 14 U.S. cases of coronavirus disease 2019 (COVID-19), all related to travel from China (1,2). The first nontravel–related U.S. case was confirmed on February 26 in a California resident who had become ill on February 13 (3). Two days later, on February 28, a second nontravel–related case was confirmed in the state of Washington (4,5). Examination of four lines of evidence provides insight into the timing of introduction and early transmission of SARS-CoV-2, the virus that causes COVID-19, into the United States before the detection of these two cases. First, syndromic surveillance based on emergency department records from counties affected early by the pandemic did not show an increase in visits for COVID-19–like illness before February 28. Second, retrospective SARS-CoV-2 testing of approximately 11,000 respiratory specimens from several U.S. locations beginning January 1 identified no positive results before February 20. Third, analysis of viral RNA sequences from early cases suggested that a single lineage of virus imported directly or indirectly from China began circulating in the United States between January 18 and February 9, followed by several SARS-CoV-2 importations from Europe. Finally, the occurrence of three cases, one in a California resident who died on February 6, a second in another resident of the same county who died February 17, and a third in an unidentified passenger or crew member aboard a Pacific cruise ship that left San Francisco on February 11, confirms cryptic circulation of the virus by early February. These data indicate that sustained, community transmission had begun before detection of the first two nontravel–related U.S. cases, likely resulting from the importation of a single lineage of virus from China in late January or early February, followed by several importations from Europe. The widespread emergence of COVID-19 throughout the United States after February highlights the importance of robust public health systems to respond rapidly to emerging infectious threats.
There were 3 influenza pandemics in the 20th century, and there has been 1 so far in the 21st century. Local, national, and international health authorities regularly update their plans for mitigating the next influenza pandemic in light of the latest available evidence on the effectiveness of various control measures in reducing transmission. Here, we review the evidence base on the effectiveness of nonpharmaceutical personal protective measures and environmental hygiene measures in nonhealthcare settings and discuss their potential inclusion in pandemic plans. Although mechanistic studies support the potential effect of hand hygiene or face masks, evidence from 14 randomized controlled trials of these measures did not support a substantial effect on transmission of laboratory-confirmed influenza. We similarly found limited evidence on the effectiveness of improved hygiene and environmental cleaning. We identified several major knowledge gaps requiring further research, most fundamentally an improved characterization of the modes of person-to-person transmission.
Note: This article, published on 16 October 2016, originally appeared in the Oral Health website. It was removed sometime after the end of June 2020 with no explanation other than, it being ‘no longer relevant in our current climate.’
The science behind face masks has not changed considerably in the past few months so we can only guess about what ‘no longer relevant’ means.
While you can find a capture at archive.org, we have saved a copy here to protect against censorship and for easy sharing.
Yesterday’s Scientific Dogma is Today’s Discarded Fable
The above quotation is ascribed to Justice Archie Campbell author of Canada’s SARS Commission Final Report. 1 It is a stark reminder that scientific knowledge is constantly changing as new discoveries contradict established beliefs. For at least three decades a face mask has been deemed an essential component of the personal protective equipment worn by dental personnel. A current article, “Face Mask Performance: Are You Protected” gives the impression that masks are capable of providing an acceptable level of protection from airborne pathogens. 2 Studies of recent diseases such as Severe Acute Respiratory Syndrome (SARS), Middle Eastern Respiratory Syndrome (MERS) and the Ebola Crisis combined with those of seasonal influenza and drug resistant tuberculosis have promoted a better understanding of how respiratory diseases are transmitted. Concurrently, with this appreciation, there have been a number of clinical investigations into the efficacy of protective devices such as face masks. This article will describe how the findings of such studies lead to a rethinking of the benefits of wearing a mask during the practice of dentistry. It will begin by describing new concepts relating to infection control especially personal protective equipment (PPE).
Trends in Infection Control
For the past three decades there has been minimal opposition to what have become seemingly established and accepted infection control recommendations. In 2009, infection control specialist Dr. D. Diekema questioned the validity of these by asking what actual, front-line hospital-based infection control experiences were available to such authoritative organization as the Centers for Disease Control and Prevention (CDC), the Occupational Safety and Health Association (OSHA) and the National Institute for Occupational Safety and Health (NIOSH). 3 In the same year, while commenting on guidelines for face masks, Dr. M. Rupp of the Society for Healthcare Epidemiology of America noted that some of the practices relating to infection control that have been in place for decades, ”haven’t been subjected to the same strenuous investigation that, for instance, a new medicine might be subjected.” 4 He opined that perhaps it is the relative cheapness and apparent safety of face masks that has prevented them from undergoing the extensive studies that should be required for any quality improvement device. 4 More recently, Dr. R. MacIntyre, a prolific investigator of face masks, has forcefully stated that the historical reliance on theoretical assumptions for recommending PPEs should be replaced by rigorously acquired clinical data. 5 She noted that most studies on face masks have been based on laboratory simulated tests which quite simply have limited clinical applicability as they cannot account for such human factors as compliance, coughing and talking. 5
Covering the nose and mouth for infection control started in the early 1900s when the German physician Carl Flugge discovered that exhaled droplets could transmit tuberculosis. 4 The science regarding the aerosol transmission of infectious diseases has, for years, been based on what is now appreciated to be “very outmoded research and an overly simplistic interpretation of the data.” 6 Modern studies are employing sensitive instruments and interpretative techniques to better understand the size and distribution of potentially infectious aerosol particles. 6 Such knowledge is paramount to appreciating the limitations of face masks. Nevertheless, it is the historical understanding of droplet and airborne transmission that has driven the longstanding and continuing tradition of mask wearing among health professionals. In 2014, the nursing profession was implored to “stop using practice interventions that are based on tradition” but instead adopt protocols that are based on critical evaluations of the available evidence. 7
A December 2015 article in the National Post seems to ascribe to Dr. Gardam, Director of Infection Prevention and Control, Toronto University Health Network the quote, “I need to choose which stupid, arbitrary infection control rules I’m going to push.” 8 In a communication with the author, Dr. Gardam explained that this was not a personal belief but that it did reflect the views of some infection control practitioners. In her 2014 article, “Germs and the Pseudoscience of Quality Improvement”, Dr. K Sibert, an anaesthetist with an interest in infection control, is of the opinion that many infection control rules are indeed arbitrary, not justified by the available evidence or subjected to controlled follow-up studies, but are devised, often under pressure, to give the appearance of doing something. 9
The above illustrate the developing concerns that many infection control measures have been adopted with minimal supporting evidence. To address this fault, the authors of a 2007 New England Journal of Medicine (NEJM) article eloquently argue that all safety and quality improvement recommendations must be subjected to the same rigorous testing as would any new clinical intervention. 10 Dr. R. MacIntyre, a proponent of this trend in infection control, has used her research findings to boldly state that, “it would not seem justifiable to ask healthcare workers to wear surgical masks.” 4 To understand this conclusion it is necessary to appreciate the current concepts relating to airborne transmissions.
Early studies of airborne transmissions were hampered by the fact that the investigators were not able to detect small particles (less than 5 microns) near an infectious person. 6 Thus, they assumed that it was the exposure of the face, eyes and nose to large particles (greater than 5 microns) or “droplets” that transmitted the respiratory condition to a person in close proximity to the host. 6 This became known as “droplet infection”, and 5 microns or greater became established as the size of large particles and the traditional belief that such particles could, in theory, be trapped by a face mask. 5 The early researchers concluded that since only large particles were detected near an infectious person any small particles would be transmitted via air currents, dispersed over long distances, remain infective over time and might be inhaled by persons who never had any close contact with the host. 11 This became known as “airborne transmission” against which a face mask would be of little use. 5
Through the use of highly sensitive instruments it is now appreciated that the aerosols transmitted from the respiratory tract due to coughing, sneezing, talking, exhalation and certain medical and dental procedures produce respiratory particles that range from the very small (less than 5 microns) to the very large (greater than a 100 microns) and that all of these particles are capable of being inhaled by persons close to the source. 6, 11 This means that respiratory aerosols potentially contain bacteria averaging in size from 1-10 microns and viruses ranging in size from 0.004 to 0.1 microns. 12 It is also acknowledged that upon their emission large “droplets” will undergo evaporation producing a concentration of readily inhalable small particles surrounding the aerosol source. 6
The historical terms “droplet infection” and “airborne transmission” defined the routes of infection based on particle size. Current knowledge suggests that these are redundant descriptions since aerosols contain a wide distribution of particle sizes and that they ought to be replaced by the term, “aerosol transmissible.” 4, 5 Aerosol transmission has been defined as “person –to – person transmission of pathogens through air by means of inhalation of infectious particles.” 26 In addition, it is appreciated that the physics associated with the production of the aerosols imparts energy to microbial suspensions facilitating their inhalation. 11
Traditionally face masks have been recommended to protect the mouth and nose from the “droplet” route of infection, presumably because they will prevent the inhalation of relatively large particles. 11 Their efficacy must be re-examined in light of the fact that aerosols contain particles many times smaller than 5 microns. Prior to this examination, it is pertinent to review the defence mechanism of the respiratory tract.
Respiratory System Defences
Comprehensive details on the defence mechanisms of the respiratory tract will not be discussed. Instead readers are reminded that; coughing, sneezing, nasal hairs, respiratory tract cilia, mucous producing lining cells and the phagocytic activity of alveolar macrophages provide protection against inhaled foreign bodies including fungi, bacteria and viruses. 13 Indeed, the pathogen laden aerosols produced by everyday talking and eating would have the potential to cause significant disease if it were not for these effective respiratory tract defences.
These defences contradict the recently published belief that dentally produced aerosols, “enter unprotected bronchioles and alveoli.” 2 A pertinent demonstration of the respiratory tract’s ability to resist disease is the finding that- compared to controls- dentists had significantly elevated levels of antibodies to influenza A and B and the respiratory syncytial virus. 14 Thus, while dentists had greater than normal exposure to these aerosol transmissible pathogens, their potential to cause disease was resisted by respiratory immunologic responses. Interestingly, the wearing of masks and eye glasses did not lessen the production of antibodies, thus reducing their significance as personal protective barriers. 14 Another example of the effectiveness of respiratory defences is that although exposed to more aerosol transmissible pathogens than the general population, Tokyo dentists have a significantly lower risk of dying from pneumonia and bronchitis. 15 The ability of a face mask to prevent the infectious risk potentially inherent in sprays of blood and saliva reaching the wearers mouth and nose is questionable since, before the advent of mask use, dentists were no more likely to die of infectious diseases than the general population. 16
The respiratory tract has efficient defence mechanisms. Unless face masks have the ability to either enhance or lessen the need for such natural defences, their use as protection against airborne pathogens must be questioned.
History: Cloth or cotton gauze masks have been used since the late 19th century to protect sterile fields from spit and mucous generated by the wearer. 5,17,18 A secondary function was to protect the mouth and nose of the wearer from the sprays and splashes of blood and body fluids created during surgery. 17 As noted above, in the early 20th century masks were used to trap infectious “droplets” expelled by the wearer thus possibly reducing disease transmission to others. 18 Since the mid-20th century until to-day, face masks have been increasingly used for entirely the opposite function: that is to prevent the wearer from inhaling respiratory pathogens. 5,20,21 Indeed, most current dental infection control recommendations insist that a face mask be worn, “as a key component of personal protection against airborne pathogens”. 2
Literature reviews have confirmed that wearing a mask during surgery has no impact whatsoever on wound infection rates during clean surgery. 22,23,24,25,26 A recent 2014 report states categorically that no clinical trials have ever shown that wearing a mask prevents contamination of surgical sites. 26 With their original purpose being highly questionable it should be no surprise that the ability of face masks to act as respiratory protective devices is now the subject of intense scrutiny. 27 Appreciating the reasons for this, requires an understanding of the structure, fit and filtering capacity of face masks.
Structure and Fit: Disposable face masks usually consist of three to four layers of flat non-woven mats of fine fibres separated by one or two polypropylene barrier layers which act as filters capable of trapping material greater than 1 micron in diameter. 18,24,28 Masks are placed over the nose and mouth and secured by straps usually placed behind the head and neck. 21 No matter how well a mask conforms to the shape of a person’s face, it is not designed to create an air tight seal around the face. Masks will always fit fairly loosely with considerable gaps along the cheeks, around the bridge of the nose and along the bottom edge of the mask below the chin. 21 These gaps do not provide adequate protection as they permit the passage of air and aerosols when the wearer inhales. 11,17 It is important to appreciate that if masks contained filters capable of trapping viruses, the peripheral gaps around the masks would continue to permit the inhalation of unfiltered air and aerosols. 11
Filtering Capacity: The filters in masks do not act as sieves by trapping particles greater than a specific size while allowing smaller particles to pass through. 18 Instead the dynamics of aerosolized particles and their molecular attraction to filter fibres are such that at a certain range of sizes both large and small particles will penetrate through a face mask. 18 Accordingly, it should be no surprise that a study of eight brands of face masks found that they did not filter out 20-100% of particles varying in size from 0.1 to 4.0 microns. 21 Another investigation showed penetration ranges from 5-100% when masks were challenged with relatively large 1.0 micron particles. 29 A further study found that masks were incapable of filtering out 80-85% of particles varying in size from 0.3 to 2.0 microns. 30 A 2008 investigation identified the poor filtering performance of dental masks. 27 It should be concluded from these and similar studies that the filter material of face masks does not retain or filter out viruses or other submicron particles. 11,31 When this understanding is combined with the poor fit of masks, it is readily appreciated that neither the filter performance nor the facial fit characteristics of face masks qualify them as being devices which protect against respiratory infections. 27 Despite this determination the performance of masks against certain criteria has been used to justify their effectiveness.2 Accordingly, it is appropriate to review the limitations of these performance standards.
Performance Standards: Face masks are not subject to any regulations. 11 The USA Federal Food and Drug Administration (FDA) classifies face masks as Class II devices. To obtain the necessary approval to sell masks all that a manufacturer need do is satisfy the FDA that any new device is substantially the same as any mask currently available for sale. 21 As ironically noted by the Occupational Health and Safety Agency for Healthcare in BC, “There is no specific requirement to prove that the existing masks are effective and there is no standard test or set of data required supporting the assertion of equivalence. Nor does the FDA conduct or sponsor testing of surgical masks.” 21 Although the FDA recommends two filter efficiency tests; particulate filtration efficiency (PFE) and bacterial filtration efficiency (BFE) it does not stipulate a minimum level of filter performance for these tests. 27 The PFE test is a basis for comparing the efficiency of face masks when exposed to aerosol particle sizes between 0.1 and 5.0 microns. The test does not assess the effectiveness of a mask in preventing the ingress of potentially harmful particles nor can it be used to characterize the protective nature of a mask. 32 The BFE test is a measure of a mask’s ability to provide protection from large particles expelled by the wearer. It does not provide an assessment of a mask’s ability to protect the wearer. 17 Although these tests are conducted under the auspices of the American Society of Testing and Materials (ASTM) and often produce filtration efficiencies in the range of 95-98 %, they are not a measure of a masks ability to protect against respiratory pathogens. Failure to appreciate the limitations of these tests combined with a reliance on the high filtration efficiencies reported by the manufacturers has, according to Healthcare in BC, “created an environment in which health care workers think they are more protected than they actually are.” 21 For dental personnel the protection sought is mainly from treatment induced aerosols.
For approximately 40 years it has been known that dental restorative and especially ultrasonic scaling procedures produce aerosols containing not only blood and saliva but potentially pathogenic organisms. 33 The source of these organisms could be the oral cavities of patients and/or dental unit water lines. 34 Assessing the source and pathogenicity of these organisms has proven elusive as it is extremely difficult to culture bacteria especially anaerobes and viruses from dental aerosols. 34 Although there is no substantiated proof that dental aerosols are an infection control risk, it is a reasonable assumption that if pathogenic microbes are present at the treatment site they will become aerosolized and prone to inhalation by the clinician which a face mask will not prevent. As shown by the study of UK dentists, the inhalation resulted in the formation of appropriate antibodies to respiratory pathogens without overt signs and symptoms of respiratory distress. 14 This occurred whether masks were or were not worn. In a 2008 article, Dr. S. Harrel, of the Baylor College of Dentistry, is of the opinion that because there is a lack of epidemiologically detectable disease from the use of ultrasonic scalers, dental aerosols appear to have a low potential for transmitting disease but should not be ignored as a risk for disease transmission. 34 The most effective measures for reducing disease transmission from dental aerosols are pre-procedural rinses with mouthwashes such as chlorhexidine, large diameter high volume evacuators, and rubber dam whenever possible. 33 Face masks are not useful for this purpose, and Dr. Harrel believes that dental personnel have placed too great a reliance on their efficacy. 34 Perhaps this has occurred because dental regulatory agencies have failed to appreciate the increasing evidence on face mask inadequacies.
Between 2004 and 2016 at least a dozen research or review articles have been published on the inadequacies of face masks. 5,6,11,17,19,20,21,25,26,27,28,31 All agree that the poor facial fit and limited filtration characteristics of face masks make them unable to prevent the wearer inhaling airborne particles. In their well-referenced 2011 article on respiratory protection for healthcare workers, Drs. Harriman and Brosseau conclude that, “facemasks will not protect against the inhalation of aerosols.” 11 Following their 2015 literature review, Dr. Zhou and colleagues stated, “There is a lack of substantiated evidence to support claims that facemasks protect either patient or surgeon from infectious contamination.” 25 In the same year Dr. R. MacIntyre noted that randomized controlled trials of facemasks failed to prove their efficacy. 5 In August 2016 responding to a question on the protection from facemasks the Canadian Centre for Occupational Health and Safety replied:
- The filter material of surgical masks does not retain or filter out submicron particles;
- Surgical masks are not designed to eliminate air leakage around the edges;
- Surgical masks do not protect the wearer from inhaling small particles that can remain airborne for long periods of time. 31
In 2015, Dr. Leonie Walker, Principal Researcher of the New Zealand Nurses Organization succinctly described- within a historical context – the inadequacies of facemasks, “Health care workers have long relied heavily on surgical masks to provide protection against influenza and other infections. Yet there are no convincing scientific data that support the effectiveness of masks for respiratory protection. The masks we use are not designed for such purposes, and when tested, they have proved to vary widely in filtration capability, allowing penetration of aerosol particles ranging from four to 90%.” 35
Face masks do not satisfy the criteria for effectiveness as described by Drs. Landefeld and Shojania in their NEJM article, “The Tension between Needing to Improve Care and Knowing How to Do It. 10 The authors declare that, “…recommending or mandating the widespread adoption of interventions to improve quality or safety requires rigorous testing to determine whether, how, and where the intervention is effective…” They stress the critical nature of this concept because, “…a number of widely promulgated interventions are likely to be wholly ineffective, even if they do not harm patients.” 10 A significant inadequacy of face masks is that they were mandated as an intervention based on an assumption rather than on appropriate testing.
The primary reason for mandating the wearing of face masks is to protect dental personnel from airborne pathogens. This review has established that face masks are incapable of providing such a level of protection. Unless the Centers for Disease Control and Prevention, national and provincial dental associations and regulatory agencies publically admit this fact, they will be guilty of perpetuating a myth which will be a disservice to the dental profession and its patients. It would be beneficial if, as a consequence of the review, all present infection control recommendations were subjected to the same rigorous testing as any new clinical intervention. Professional associations and governing bodies must ensure the clinical efficacy of quality improvement procedures prior to them being mandated. It is heartening to know that such a trend is gaining a momentum which might reveal the inadequacies of other long held dental infection control assumptions. Surely, the hallmark of a mature profession is one which permits new evidence to trump established beliefs. In 1910, Dr. C. Chapin, a public health pioneer, summarized this idea by stating, “We should not be ashamed to change our methods; rather, we should be ashamed not to do so.” 36 Until this occurs, as this review has revealed, dentists have nothing to fear by unmasking. OH
Oral Health welcomes this original article.
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US CDC that antibody tests for Covid-19 may be wrong up to half of the time.
The CDC now warns antibody testing is not accurate enough for it to be used for any policy-making decisions, as even with high test specificity, ‘less than half of those testing positive will truly have antibodies’.
There is currently a high level of inaccuracy in the testing, however, caused by how uncommon the virus is within the population.
This is a screenshot and excerpt from the CDC page updated 13 April 2020.
The virus is thought to spread mainly from person-to-person.
- Between people who are in close contact with one another (within about 6 feet).
- Through respiratory droplets produced when an infected person coughs, sneezes, or talks.
- These droplets can land in the mouths or noses of people who are nearby or possibly be inhaled into the lungs.
- COVID-19 may be spread by people who are not showing symptoms.
The virus spreads easily between people
How easily a virus spreads from person-to-person can vary. Some viruses are highly contagious, like measles, while other viruses do not spread as easily. Another factor is whether the spread is sustained, which means it goes from person-to-person without stopping.
The virus that causes COVID-19 is spreading very easily and sustainably between people. Information from the ongoing COVID-19 pandemic suggest that this virus is spreading more efficiently than influenza, but not as efficiently as measles, which is highly contagious.
The virus does not spread easily in other ways
COVID-19 is a new disease and we are still learning about how it spreads. It may be possible for COVID-19 to spread in other ways, but these are not thought to be the main ways the virus spreads.
- From touching surfaces or objects. It may be possible that a person can get COVID-19 by touching a surface or object that has the virus on it and then touching their own mouth, nose, or possibly their eyes. This is not thought to be the main way the virus spreads, but we are still learning more about this virus.
- From animals to people. At this time, the risk of COVID-19 spreading from animals to people is considered to be low. Learn about COVID-19 and pets and other animals.
- From people to animals. It appears that the virus that causes COVID-19 can spread from people to animals in some situations. CDC is aware of a small number of pets worldwide, including cats and dogs, reported to be infected with the virus that causes COVID-19, mostly after close contact with people with COVID-19. Learn what you should do if you have pets.