Aerosols and Dentistry – The science and its Limitations

By Dominic O’Hooley





“An inefficient virus kills its host. A clever virus stays with it.”

James Ephraim Lovelock

Any opinion piece on this, by the above premise, rather inefficient virus, is at best, a document that may provide some pause for thought, a rough guide perhaps, to how we as dental professionals; scientifically trained individuals to a fault but mostly baffled by information overload, can at least understand what we know to be true, what we know we don’t know, and perhaps, give direction to our thought processes as we pass the first peak of this awful virus, and head towards practicing dentistry again.

In this case, I have taken the lazy man’s road. Rather than an overarching treatise on SARS-CoV-2 and its impact on dentistry, I have chosen to discuss specifics regarding aerosols. I have elected to try and cut through some of the nonsense I have been reading and give objectivity where I can do so.

I want to highlight areas where I feel the cart is before the horse. Our absolutely understandable urgency to find workable solutions is clouding our judgement, with rash purchases of expensive equipment on one level, but a misplaced sense of complacency, perhaps brought about by the promise of said equipment, at a far more dangerous level for both us and our patients.


Dental Aerosols – What are they anyway?

I am not here to patronise you all. I am well aware that many readers will be better qualified than me to broach the fine scientific details of this massive subject. What I am going to do is start with two premises;

An aerosol is a colloidal suspension of particles dispersed in air or a gas.

Dental aerosols are not one entity, but three at least.

So, we should all reflect on the widely used term, Aerosol Generating Procedure (AGP), and prepare to challenge its misuse within the current crisis as a rather arbitrary marker flag placed to provide a sense of relative safety on one side, and danger on the other.

A good proxy measure for being alive is the production of aerosols. Every breath we take, our tidal breathing whilst sitting in a chair, the deeper, higher frequency respirations seen during exercise, sex, pain or fear. Aerosols. (F.Wurie, 2013)

Respiratory secretions ciliated up from our lung bases, the postnasal drip, harrumphed into the mouth to mix with saliva prior to being ejected as, guess what? Aerosol. Well, respiratory secretion droplets of various dimensions that desiccate in contact with air to form tiny dried droplet nuclei that float free, aerosolized and able to remain in the air for hours, to disperse widely before coming to rest, potentially as fomites. (G.N.Sze To, 2009) (X. Xie, 2007)

So, we produce respiratory secretion aerosols with every breath we take. Even more so when we talk, with a direct relationship to volume and relative frequency we use, deeper sounds producing more. During tidal respiration through the nose, we still produce these aerosols. (J.W. Tang, 2014)

When we cough or sneeze, both droplet quantity, size range and velocity are increased massively. Some studies suggest that aerosol can be measured 8 metres away from the sneezing subject immediately after the sneeze, with the aerosol then dispersing widely using air currents to follow a complex dispersal path that even the latest computer modelling struggles to depict. (Bourouiba, 2020)

Both us; dental professionals, our patients and everybody within the surgery are producing this respiratory secretion aerosol all the time. We can call this aerosol Type 1 for now.

Type 2 is what we all probably have in our mind’s eye when we think of AGP. The fine mist from our high-speed turbine, the 3inOne with both air and water buttons depressed, the haze surrounding the tip of the cavitron.  This is usually a clean water combination of droplets and aerosol. It may contain antimicrobials primarily to reduce biofilms within waterlines, but at the current time, discussion points for providing a dose directly to the source of the problem. Hypochlorous acid (HOCL) appears to be emerging as an early front runner in this race. (R.M. Madden, 1969) (M.J. O’Donnell, 2011)

Type 3 is what I have tentatively called “mixed aerosols”. When our clean or antimicrobial water spray with its high velocity droplets of various sizes and associated aerosol impacts on the oral commissure. The pooled saliva, moist complex surface of the tongue, the teeth and sometimes, the hard-walled cavity. The other fluids inherent in the mouth, gingival crevicular fluid, blood and respiratory secretions too. The salivary glands, shown to harbour virus with its subsequent presence in saliva has been shown. For GCF, no current study exists as yet. (C. Zemouri, 2017)

We then can add pulverised biofilm, enamel and dentine, restorative materials and sometimes, lubricating oil from an over lubricated handpiece.  This complex and very variable set of circumstances create various outcomes. Spatter of mixed constituent and mixed size droplets either directly caught or ejected by the spinning vortex of a rotating bur or reflected of the surface of a tooth or wall of a cavity. Droplets disturbed from pooled fluids in the mouth by perturbation by the clean water droplets ejected by the handpiece or scaler tip. And aerosol, as droplets desiccate to form droplet nuclei, or the Venturi effect of the air jets/ possible laminar air flows created by the instruments. (J.R. Grundy, 1967)

I told you it was complex. I’m afraid that even this grossly simplified version continues to ramp up the complexity.


Let’s Talk about High Volume Aspiration (HVA)

We are all familiar with using HVA when we are doing a wide variety of procedures on patients. Using the ideal of four-handed dentistry, from a dentists point of view, a dental nurse who instinctively places the aspirator to both tissue-retract and keeps the operating field free of excess moisture, optimising visibility. From the dental nurse’s point of view, learning the idiosyncrasies of the dentist of DCP they are working with, the subconscious establishment of behavioural pattern optimisation to achieve a state of flow, that ideal of tightly focussed art meeting science, where the perception of time seems to recede into the background and this four-handed dental beast does its thing. (B.L. Finkbeiner, 2000)

And we all instinctively know two things; If the dental aerosol/aspiration interface is poorly controlled, it makes dental artistry more like a Jackson Pollock than a Piet Mondrian. (R. Taylor, 2004)

We also can see that even when we are working together in perfect harmony, our face shield tells us the story of our inability to control that droplet and aerosol miasma entirely. (Roberge, 2016)

Studies using high speed video or UV visible dyes can help us quantify this imperfect system that we routinely operate. It is telling to see video of the halo of mist billowing vertically above the clearly defined vapour trail shooting down the tip of the aspirator. How this mist then disperses widely, including directly into the facial zone of the operator. (C.L. Fogh, 1999)

No scientific study has compared violent expiratory events like coughing, sneezing or choking (what can be termed, ballistic droplet events), with mechanically created dental aerosol. Many scientific studies create aerosols using standardised nebulisers and keep them optimally dispersed using technical apparatus such as Goldberg drums. This type of experimental standardisation is obviously necessary when trying to provide statistically measurable results. The trouble is, these laboratory experiments bear almost no relation to our daily dental surgery-based experiences. (S. Asadi N. B., 2020)

To cut to the chase, there is logically no doubt that HVA aspiration removes a majority of aerosol and moisture from both the clinical field and our faces. This is obviously a “good thing”.  What interests me is methods we can use to increase that majority.

Once we have ensured our aspiration system is working as well as it can be, so, we have ensured it has been serviced properly, that we have cleaned the filters as recommended for the volume and types of dental procedures we do, that our aspirator tips are smooth bored

and not partially occluded my debris. Then, we can possibly look at adaptations to enlarge the orifice of the aspirator.

Without blowing both our minds with a detailed technical discussion on conductance, flow resistance, pressure differentials, Knudsen flow and orifice related choked flow; I do want you to reflect on the flow resistance that occurs as our created dental aerosol enters and travels down the aspirator tubing. This is partly the friction between the gas and the pipe walls (explaining the need for a smooth bore), but also the friction between the gas/aerosol particles. (A.N. Kucherov, 1991)

It thus seems intuitive to me, that a wider bore, will have lower flow resistance, as long as the pressure differential between the aspirator motor vacuum, and the orifice of the aspirator/external environment is maintained.

Several companies have attempted to address this, by providing either ready made or 3D printer ready, adaptors for our existing HVA, with far larger surface area orifices, but at the same time, a gradual specific reduction in bore volume to optimise gas flow. No formal scientific studies exist at the current time to quantify the degree improvement in aerosol clearance percentage provided by these adaptors. (S.K. Harrell, 1996)

A further method that can be used to remove dentally created aerosol is the External Oral Suction apparatus, of which many different systems are commercially available. Often presented as a wheeled unit with a universally hinged rigid tube with large orifice that can be positioned in front of the patients mouth, but far enough away to allow access for the dental team, these can contain HEPA filters UV light sources and plasma filtration to provide a cleaned air discharge. The noise, reduction in access and cost have prevented these becoming mainstream prior to the current COVID 19 crisis.

Before I go any further, let us go back to what I talked about at the beginning of this essay. Let’s think about rash purchases of expensive dental equipment, and how these can be actioned with the highest of patient focussed intentions, whilst actually, on occasion, really just providing us, the purchaser, with assuagement of our guilt, as we try to reconcile the financial necessity of going back to work, with the concern that by doing so, we are putting our patients, our staff and ourselves at risk.

I would suggest that we contemplate deeply, whether impetuous purchases of the latest safety focussed solution, really has any benefit at all, or perhaps only for the commercially opportune company, selling us the kit?


Do we have evidence that dental aerosols transmit SARS-CoV-2?

Direct, unequivocal evidence of primary transmission via dental aerosol to dental providers? No. None.

Direct, unequivocal evidence of primary transmission from the respiratory secretion tidal breathing aerosol of the dental providers to the patient? No. None.

Do we have evidence of transfer to dentally created bioaerosols to hard surfaces and floor within the dental surgery? Well, we have proxy measures that suggest it. We have viral RNA that can be quantified. What we don’t currently have is evidence of viable virions, the individual virus particles that have the same size and shape profiles as pre-aerosolised virus under electron microscopy, and thus seem likely to be viable still. (A.C. Fears, 2020)

Do we have direct, unequivocal evidence of aerosolized SARS-COV-2 being the primary infective source for any outbreak worldwide? No.

Hold on. Really?

Well, it isn’t easy to prove this. Respiratory viruses are usually droplet and fomite spread. Some viruses can also aerosolise and primarily infect that way it seems, measles being a good example. Now, measles is regarded as highly infectious and we know that 90% of non-immune people in close proximity to a measles infected person will become infected. We also know that measles virions remain viable (appearance wise) within aerosol. So, it’s a supposition based on the available evidence. For measles, the available evidence leads us to the conclusion that aerosolised viable virus is a primary infective vector. (R.D. de Vries, 2012)

Do we have direct, unequivocal evidence of excess infection rate, when compared to the general population, for dentists and dental care professionals anywhere on the world? No.

What about in the UK? No. (C. Heneghan, 2020)

Hold on again! We closed up shop before the end of March in most cases. This was before the community spread phase of the UK COVID 19 epidemic. Well. Let’s think back to the serological testing for actual infections at that time. It was hospital based for referred or self-referred symptomatic individuals. Testing of self-isolating symptomatic people wasn’t happening. The unknown cohort of asymptomatic people were not being tested either. (M.S. Razai, 2020)

So, could we have all been exposed to asymptomatic/pre-symptomatic patients before close down? Yes.

Could patients have been exposed to asymptomatic/ pre-symptomatic dental providers before close down? Yes.

Can we make firm decisions on the future direction for dentistry using the above limited data?

Well. This is where things get particularly complicated. If you like black and white answers, stop reading now.


Let’s look at Super Spreader Events

Looking at Super Spreader Events (SSE) is an inexact science.  You may be aware of the term – Super Spreader. One way to look at these unfortunate individuals is as follows: About 20% of a given population contribute to 80% plus of the transmission potential of a given pathogen. In this case, SARS-CoV-2. You will have read about them in the media. An SSE is an event where a large infection cluster develops due to interactions at that event. It is assumed that individual Super Spreaders may play a part here but may not either. The term SSE is really more about the high frequency and specificity of infections from one geographical site, at one chronological time. (R.A. Stein, 2011)

What is clear to me from my reading around this topic is the following. These Super Spreader Events have common characteristics; no social distancing, lots of close face to face

speaking often with raised voices, personal familiarity between the group leading to intimate contact such as hugging and lip/cheek kissing, religious events, birthday parties, weddings, funerals, business networking events and alcohol fuelled parties. They are all inside.

But really interestingly, the events not associated with SSEs are revealing to me. Going to the cinema, travelling by train, tube, bus or coach and music events such as the opera. The millions of open cubicle office spaces, call centres and airplanes where people are packed close together. There are no verified reports of SSEs from these situations, but there is a disputed report of an SSE at a Seoul, South Korea call centre. This appears to be related to members of the Shincheonji Church of Jesus, and the large number of confounding factors make it difficult to ascertain whether it is now regarded as an SSE at the call centre or not. If, we take an SSE as a microcosm of real life, a kind of magnified and condensed reality which can highlight much wider realities in a far wider population, then SSEs can be viewed as very revealing indeed. (S.Y. Park, 2020)

So, what do they reveal to me?

These events and situations do not involve lots of intimate, social distance ignoring face to face talking with the spreading of large ballistic droplets of respiratory secretion and oral fluid from one person to another. Many of the situations involve limited talking, or lots of talking in the case of call centres, but not into the face of another person. These events ignore social class, ignore travel status, ignore whether inside or outside. (J. Kay, 2020)

But what has this got to do with dentistry?

Well, on the surface, quite a lot. We are inside, we are up close and personal with our patients, our mouths inches from theirs.

But let’s think about it a little bit more.

We tend to speak but we tend to use the hushed tones of the surgery. Our mouths are covered with surgical masks and possibly full-face shields (not when using a microscope or wearing loupes) when we are practicing dentistry and then we tend to have professional social distance from our patients when we are not. (Washburn, 1960)

Not one SSE has been reported from a dental surgery worldwide.

If you give credence to the concept of the SSE, you might consider that the common factor is sharing droplets and not distributing aerosols.


So, what about returning to dentistry?

At the time of writing, no evidence worldwide has been presented to show that dentists or dental care professionals have an excess rate of infection with SARS-CoV-2.

No evidence has been presented of excess infection rate, or SSE generated at a dental surgery.

The current developing consensus regarding using FPP3 valve respirators ignores the fact that the expired air is not filtered at all. So, if aerosol from tidal breathing is a primary vector of infection, and asymptomatic/pre-symptomatic infected people shed virus, then the FPP3 will not prevent respiratory secretion aerosol being emitted onto patients. In addition, the FPP3 mask has no data suggesting improved efficacy compared to FPP2. It is clear they are uncomfortable during extended wearing and it has been shown that extended wearing leads to fomites developing at the angles of the mandible, due to constant adjustment via contaminated hands. (N.F. Phin, 2009)

As this is an opinion piece, I am going to give my opinion.

My opinion is that we as dentists and DCPS, have effectively risk mitigated for infective risk for many years. The paucity of evidence of direct primary infective risk of SARS-CoV-2 from either tidal breathing aerosol, dental generated mixed aerosol, or residual room-based aerosol suggests to me that ballistic droplet and fomite spread are the primary vectors of infection.

This means that normal surgical masking with regular changes between all patients, the use of full face shields where possible, or adapted loupes/microscope interfaces where not, careful decontamination between patients and our existing level of universal precautions, are in my view, sufficient to allow appropriate risk mitigation as we contemplate a timely return to dentistry.

Careful pre-screening of our patients, the rigorous adherence to risk profiling based on age, co-morbidities and our universal precautions, will in my opinion, allow a risk mitigated return to dental service provision with the associated reduction in avoidable dental morbidity.

This virus is with us for the long term. It is facile to imagine that it will suddenly go away. We must therefore be coolly rigorous in our dispassionate and non-emotive analysis of the risks and benefits of any major decision we make.

For me, the transfer of that decision-making process to outside the wet-fingered majority of our profession, would have to fulfil a clear position of unambiguous science-based theorising, being proven to be true. It is clear that is currently not the situation at all.

As dental professionals, not one of us want to put our patients at risk of harm. We should not conflate that noble aim, with a passive acceptance of the poor, arbitrary and confused guidance that we have received to date.

Our patients deserve so much more than this, and so we must engage with the science. We must have the courage to put our heads above the parapet. I will be doing so.


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