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      Aerosol emission and superemission during human speech increase with voice loudness

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          Abstract

          Mechanistic hypotheses about airborne infectious disease transmission have traditionally emphasized the role of coughing and sneezing, which are dramatic expiratory events that yield both easily visible droplets and large quantities of particles too small to see by eye. Nonetheless, it has long been known that normal speech also yields large quantities of particles that are too small to see by eye, but are large enough to carry a variety of communicable respiratory pathogens. Here we show that the rate of particle emission during normal human speech is positively correlated with the loudness (amplitude) of vocalization, ranging from approximately 1 to 50 particles per second (0.06 to 3 particles per cm 3) for low to high amplitudes, regardless of the language spoken (English, Spanish, Mandarin, or Arabic). Furthermore, a small fraction of individuals behaves as “speech superemitters,” consistently releasing an order of magnitude more particles than their peers. Our data demonstrate that the phenomenon of speech superemission cannot be fully explained either by the phonic structures or the amplitude of the speech. These results suggest that other unknown physiological factors, varying dramatically among individuals, could affect the probability of respiratory infectious disease transmission, and also help explain the existence of superspreaders who are disproportionately responsible for outbreaks of airborne infectious disease.

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          Most cited references52

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          Superspreading and the effect of individual variation on disease emergence

          Coughs and sneezes... From Typhoid Mary to SARS, it has long been known that some people spread disease more than others. But for diseases transmitted via casual contact, contagiousness arises from a plethora of social and physiological factors, so epidemiologists have tended to rely on population averages to assess a disease's potential to spread. A new analysis of outbreak data shows that individual differences in infectiousness exert powerful influences on the epidemiology of ten deadly diseases. SARS and measles (and perhaps avian influenza) show strong tendencies towards ‘superspreading events’ that can ignite explosive epidemics — but this same volatility makes outbreaks more likely to fizzle out. Smallpox and pneumonic plague, two potential bioterrorism agents, show steadier growth but still differ markedly from the traditional average-based view. These findings are relevant to how emerging diseases are detected and controlled. Supplementary information The online version of this article (doi:10.1038/nature04153) contains supplementary material, which is available to authorized users.
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            Avian flu: influenza virus receptors in the human airway.

            Although more than 100 people have been infected by H5N1 influenza A viruses, human-to-human transmission is rare. What are the molecular barriers limiting human-to-human transmission? Here we demonstrate an anatomical difference in the distribution in the human airway of the different binding molecules preferred by the avian and human influenza viruses. The respective molecules are sialic acid linked to galactose by an alpha-2,3 linkage (SAalpha2,3Gal) and by an alpha-2,6 linkage (SAalpha2,6Gal). Our findings may provide a rational explanation for why H5N1 viruses at present rarely infect and spread between humans although they can replicate efficiently in the lungs.
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              Size distribution and sites of origin of droplets expelled from the human respiratory tract during expiratory activities

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                Author and article information

                Contributors
                wdristenpart@ucdavis.edu
                Journal
                Sci Rep
                Sci Rep
                Scientific Reports
                Nature Publishing Group UK (London )
                2045-2322
                20 February 2019
                20 February 2019
                2019
                : 9
                : 2348
                Affiliations
                [1 ]ISNI 0000 0004 1936 9684, GRID grid.27860.3b, Department of Chemical Engineering, , University of California Davis, 1 Shields Ave, ; Davis, CA 95616 USA
                [2 ]ISNI 0000 0004 1936 9684, GRID grid.27860.3b, Department of Mechanical and Aerospace Engineering, , University of California Davis, 1 Shields Ave, ; Davis, CA 95616 USA
                [3 ]ISNI 0000 0004 1936 9684, GRID grid.27860.3b, Air Quality Research Center, , University of California Davis, 1 Shields Ave, ; Davis, CA 95616 USA
                [4 ]ISNI 0000 0004 1936 9684, GRID grid.27860.3b, Department of Civil and Environmental Engineering, , University of California Davis, 1 Shields Ave, ; Davis, CA 95616 USA
                [5 ]ISNI 0000 0004 1936 9684, GRID grid.27860.3b, Department of Land, Air and Water Resources, , University of California Davis, 1 Shields Ave, ; Davis, CA, 95616 USA
                [6 ]ISNI 0000 0004 1936 9684, GRID grid.27860.3b, Department of Linguistics, , University of California Davis, 1 Shields Ave, ; Davis, CA 95616 USA
                [7 ]ISNI 0000 0001 0670 2351, GRID grid.59734.3c, Department of Medicine, Div. of Infectious Diseases, , Icahn School of Medicine at Mount Sinai, 1 Gustave Levy Place, ; New York, NY 10029 USA
                [8 ]ISNI 0000 0001 0670 2351, GRID grid.59734.3c, Department of Microbiology, , Icahn School of Medicine at Mount Sinai, 1 Gustave Levy Place, ; New York, NY 10029 USA
                Article
                38808
                10.1038/s41598-019-38808-z
                6382806
                30787335
                14c8de01-9214-4f80-8675-1bd38aaa32c3
                © The Author(s) 2019

                Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/.

                History
                : 14 June 2018
                : 10 January 2019
                Funding
                Funded by: FundRef https://doi.org/10.13039/100006492, Division of Intramural Research, National Institute of Allergy and Infectious Diseases (Division of Intramural Research of the NIAID);
                Award ID: R01 AI110703
                Award ID: R01 AI110703
                Award ID: R01 AI110703
                Award ID: R01 AI110703
                Award ID: R01 AI110703
                Award ID: R01 AI110703
                Award Recipient :
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