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<\/div>\nAbstract<\/span><\/strong><\/em><\/p>\n Masks and respirators do not work. There have been extensive randomized controlled trial (RCT) studies, and meta-analysis reviews of RCT studies, which all show that\u00a0masks and respirators do not work to prevent respiratory influenza-like illnesses, or respiratory illnesses believed to be transmitted by droplets and aerosol particles<\/span>.<\/em><\/p>\n Furthermore, the relevant known physics and biology, which I review, are such that masks and respirators should not work.<\/p>\n It would be a paradox if masks and respirators worked, given what we know about viral respiratory diseases:\u00a0The main transmission path is long-residence-time aerosol particles (< 2.5 \u03bcm), which are too fine to be blocked, and the minimum-infective-dose is smaller than one aerosol particle.<\/strong><\/p>\n The present paper about masks illustrates\u00a0the degree to which governments, the mainstream media, and institutional propagandists can decide to operate in a science vacuum,<\/strong>\u00a0or select only incomplete science that serves their interests. Such recklessness is also certainly the case with the current global lockdown of over 1 billion people, an unprecedented experiment in medical and political history.<\/p>\n Conclusion regarding masks that do not work<\/span><\/strong><\/p>\n No RCT study with verified outcome shows a benefit for HCW or community members in households to wearing a mask or respirator.\u00a0There is no such study. There are no exceptions.\u00a0<\/strong>Likewise,\u00a0<\/strong>no study exists that shows a benefit from a broad policy to wear masks in public\u00a0<\/span>(more on this below).<\/p>\n Furthermore, if there were any benefit to wearing a mask, because of the blocking power against droplets and aerosol particles, then there should be more benefit from wearing a respirator (N95) compared to a surgical mask,\u00a0yet several large meta-analyses, and all the RCT, prove that there is no such relative benefit<\/strong>.\u00a0Masks and respirators do not work<\/span>.<\/p>\n Precautionary Principle turned on its head with masks<\/span><\/strong><\/p>\n In light of the medical research, therefore, it is difficult to understand why public-health authorities are not consistently adamant about this established scientific result, since the distributed psychological, economic and environmental harm from a broad recommendation to wear masks is significant, not to mention the unknown potential harm from concentration and distribution of pathogens on and from used masks.<\/p>\n In this case, public authorities would be turning the precautionary principle on its head (see below).<\/p>\n Physics and Biology of Viral Respiratory Disease, and why masks do not work<\/span><\/strong><\/p>\n In order to understand why masks cannot possibly work, we must review established knowledge about viral respiratory diseases, the mechanism of seasonal variation of excess deaths from pneumonia and influenza, the aerosol mechanism of infectious disease transmission, the physics and chemistry of aerosols, and the mechanism of the so-called minimum-infective-dose.<\/p>\n In addition to pandemics that can occur anytime, in the temperate latitudes there is an extra burden of respiratory-disease mortality that is seasonal, and which is caused by viruses. For example, see the review of influenza by Paules and Subbarao (2017).\u00a0This has been known for a long time, and the seasonal pattern is exceedingly regular<\/strong>.<\/p>\n For example, see Figure 1 of Viboud (2010), which has \u201cWeekly time series of the ratio of deaths from pneumonia and influenza to all deaths, based on the 122 cities surveillance in the US (blue line). The red line represents the expected baseline ratio in the absence of influenza activity,\u201d here:<\/p>\n The seasonality of the phenomenon was largely not understood until a decade ago. Until recently, it was debated whether the pattern arose primarily because of seasonal change in virulence of the pathogens, or because of seasonal change in susceptibility of the host (such as from dry air causing tissue irritation, or diminished daylight causing vitamin deficiency or hormonal stress). For example, see Dowell (2001).<\/p>\n In a landmark study, Shaman et al. (2010) showed that\u00a0the seasonal pattern of extra respiratory-disease mortality can be explained quantitatively on the sole basis of absolute humidity, and its direct controlling impact on transmission of airborne pathogens<\/strong>.<\/p>\n Lowen et al. (2007) demonstrated the phenomenon of humidity-dependent airborne-virus virulence in actual disease transmission between guinea pigs, and discussed potential underlying mechanisms for the measured controlling effect of humidity.<\/p>\n The underlying mechanism is that the pathogen-laden aerosol particles or droplets are neutralized within a half-life that monotonically and significantly decreases with increasing ambient humidity. This is based on the seminal work of Harper (1961). Harper experimentally showed that\u00a0viral-pathogen-carrying droplets were inactivated within shorter and shorter times, as ambient humidity was increased<\/strong>.<\/p>\n Harper argued that the viruses themselves were made inoperative by the humidity (\u201cviable decay\u201d), however, he admitted that the effect could be from humidity-enhanced physical removal or sedimentation of the droplets (\u201cphysical loss\u201d): \u201cAerosol viabilities reported in this paper are based on the ratio of virus titre to radioactive count in suspension and cloud samples, and can be criticized on the ground that test and tracer materials were not physically identical.\u201d<\/p>\n The latter (\u201cphysical loss\u201d) seems more plausible to me, since humidity would have a universal physical effect of causing particle \/ droplet growth and sedimentation, and all tested viral pathogens have essentially the same humidity-driven \u201cdecay\u201d. Furthermore, it is difficult to understand how a virion (of all virus types) in a droplet would be molecularly or structurally attacked or damaged by an increase in ambient humidity. A \u201cvirion\u201d is the complete, infective form of a virus outside a host cell, with a core of RNA or DNA and a capsid. The actual mechanism of such humidity-driven intra-droplet \u201cviable decay\u201d of a virion has not been explained or studied.<\/p>\n In any case, the explanation and model of\u00a0Shaman et al<\/strong>. (2010) is not dependant on the particular mechanism of the humidity-driven decay of virions in aerosol \/ droplets. Shaman\u2019s quantitatively demonstrated model of seasonal regional viral epidemiology is valid for either mechanism (or combination of mechanisms), whether \u201cviable decay\u201d or \u201cphysical loss\u201d.<\/p>\n The breakthrough achieved by Shaman et al. is not merely some academic point. Rather,\u00a0it has profound health-policy implications, which have been entirely ignored or overlooked in the current coronavirus pandemic.<\/strong><\/p>\n In particular, Shaman\u2019s work necessarily implies that, rather than being a fixed number (dependent solely on the spatial-temporal structure of social interactions in a completely susceptible population, and on the viral strain),\u00a0the epidemic\u2019s basic reproduction number (R0) is highly or predominantly dependent on ambient absolute humidity<\/strong>.<\/p>\n For a definition of R0, see HealthKnowlege-UK (2020): R0 is \u201cthe average number of secondary infections produced by a typical case of an infection in a population where everyone is susceptible.\u201d The average R0 for influenza is said to be 1.28 (1.19-1.37); see the comprehensive review by Biggerstaff et al. (2014).<\/p>\n In fact, Shaman et al. showed that R0 must be understood to seasonally vary between humid-summer values of just larger than \u201c1\u201d and dry-winter values typically as large as \u201c4\u201d (for example, see their Table 2). In other words,\u00a0the seasonal infectious viral respiratory diseases that plague temperate latitudes every year go from being intrinsically mildly contagious to virulently contagious, due simply to the bio-physical mode of transmission controlled by atmospheric humidity, irrespective of any other consideration<\/strong>.<\/p>\n Therefore,\u00a0all the epidemiological mathematical modelling of the benefits of mediating policies (such as social distancing), which assumes humidity-independent R0 values, has a large likelihood of being of little value, on this basis alone<\/strong>. For studies about modelling and regarding mediation effects on the effective reproduction number, see Coburn (2009) and Tracht (2010).<\/p>\n To put it simply,\u00a0the \u201csecond wave\u201d of an epidemic is not a consequence of human sin regarding mask wearing and hand shaking<\/strong>. Rather,\u00a0t<\/span>he \u201csecond wave\u201d is an inescapable consequence of an air-dryness-driven many-fold increase in disease contagiousness, in a population that has not yet attained immunity<\/span>.<\/p>\n If my view of the mechanism is correct (i.e., \u201cphysical loss\u201d), then Shaman\u2019s work further necessarily implies that\u00a0the dryness-driven high transmissibility (large R0) arises from small aerosol particles fluidly suspended in the air; as opposed to large droplets that are quickly gravitationally removed from the air.<\/strong><\/p>\n Such small aerosol particles fluidly suspended in air, of biological origin,\u00a0are of every variety and are everywhere<\/strong>, including down to virion-sizes (Despres, 2012). It is not entirely unlikely that\u00a0viruses can thereby be physically transported over inter-continental distances<\/strong>\u00a0(e.g., Hammond, 1989).<\/p>\n More to the point, indoor airborne virus concentrations have been shown to exist (in day-care facilities, health centres, and onboard airplanes) primarily as aerosol particles of diameters smaller than 2.5 \u03bcm, such as in the work of Yang et al. (2011):Such small particles (< 2.5 \u03bcm) are part of air fluidity, are not subject to gravitational sedimentation, and would not be stopped by long-range inertial impact.\u00a0This means that the slightest (even momentary) facial misfit of a mask or respirator renders the design filtration norm of the mask or respirator entirely irrelevant<\/span>. In any case,\u00a0the filtration material itself of N95 (average pore size ~0.3\u22120.5 \u03bcm) does not block virion penetration, not to mention surgical masks<\/strong>. For example, see Balazy et al. (2006).<\/p>\n Mask stoppage efficiency and host inhalation are only half of the equation, however, because the minimal infective dose (MID) must also be considered. For example, if a large number of pathogen-laden particles must be delivered to the lung within a certain time for the illness to take hold, then partial blocking by any mask or cloth can be enough to make a significant difference.<\/p>\n On the other hand, if the MID is amply surpassed by the virions carried in a single aerosol particle able to evade mask-capture, then the mask is of no practical utility, which is the case.<\/p>\n Yezli and Otter<\/strong>\u00a0(2011), in their review of the MID, point out relevant features:<\/p>\n For further background:<\/p>\n All of this to say that:\u00a0if anything gets through (and it always does, irrespective of the mask), then you are going to be infected<\/strong>.\u00a0Masks cannot possibly work<\/span>. It is not surprising, therefore, that\u00a0no bias-free study has ever found a benefit from wearing a mask or respirator in this application<\/strong>.<\/p>\n Therefore, the studies that show partial stopping power of masks, or that show that masks can capture many large droplets produced by a sneezing or coughing mask-wearer, in light of the above-described features of the problem, are irrelevant. For example, see such studies as these: Leung (2020), Davies (2013), Lai (2012), and Sande (2008).<\/p>\n Why there can never be an empirical test of a nationwide mask-wearing policy<\/span><\/strong><\/p>\n As mentioned above, no study exists that shows a benefit from a broad policy to wear masks in public. There is good reason for this. It would be impossible to obtain unambiguous and bias-free results:<\/p>\n Unknown aspects of mask-wearing<\/span><\/strong><\/p>\n Many potential harms may arise from broad public policies to wear masks, and the following unanswered questions arise:<\/p>\n Conclusion<\/span><\/strong><\/p>\n By making mask-wearing recommendations and policies for the general public, or by expressly condoning the practice,\u00a0governments have both ignored the scientific evidence and done the opposite of following the precautionary principle<\/strong>.<\/p>\n In an absence of knowledge, governments should not make policies that have a hypothetical potential to cause harm.\u00a0The government has an onus barrier before it instigates a broad social-engineering intervention, or allows corporations to exploit fear-based sentiments.<\/strong><\/p>\n Furthermore, individuals should know that\u00a0there is no known benefit arising from wearing a mask in a viral respiratory illness epidemic<\/strong>, and that scientific studies have shown that any benefit must be residually small, compared to other and determinative factors.<\/p>\n Otherwise, what is the point of publicly-funded science?<\/span><\/p>\n The present paper about masks illustrates the degree to which\u00a0governments, the mainstream media, and institutional propagandists can decide to operate in a science vacuum, or select only incomplete science that serves their interests<\/strong>. Such recklessness is also certainly the case with the current global lockdown of over 1 billion people, an unprecedented experiment in medical and political history.<\/p>\n *<\/p>\n Note to readers: please click the share buttons above or below. Forward this article to your email lists. Crosspost on your blog site, internet forums. etc.<\/p>\n Dr. Dennis Rancourt<\/strong>\u00a0is Ph.D from University of Toronto (1984), and is a former professor of physics at the University of Ottawa.<\/em><\/p>\n Sources<\/strong><\/p>\n![\"mortality](\"https:\/\/www.sott.net\/image\/s28\/569688\/large\/Mortality_rate_chart.jpg\" "\\"Click")
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