Accounting
for Natural Variability in Airborne Pathogen Risk Estimation
Basic Background
Much
has been made of the anthrax
attacks of 2001. There’s
just something sensationalistic about an airborne “nasty thing” that
could kill a large number of people that the media just loves to scare people
with (exhibit two – the SARS
hoopla).
My
cynicism aside, there is a non-negligible risk that somewhere down the line,
something nasty will be put into the atmosphere – either intentionally or
accidentally. It has happened
before on a fairly large scale (e.g. the accidental anthrax
leak in Sverdlovsk in 1979), and to think that it will never happen again
is just naïve. Too many unstable
people have access to too many nasty things.
In
addition to preparing and informing the general populus regarding what should be
done in the event of an airborne threat, as scientists we are in the
position to make another contribution – estimating the severity of an
airborne pathogen release to get realistic infection estimates into the hands
of the “deciders”.
So what’s the Problem?
Let us say you are put into a room
with 100 particles of some nasty airborne thing “X”. What are your chances of getting
infected?
Well, that depends on a number of
things including (but probably not limited to):
1.
What is your personal tolerance to
nasty thing X?
2.
How long are you in the room?
3.
How quickly are you breathing?
4.
How deeply are you breathing?
5.
Are you moving around? (How does that affect how many of the
100 particles stay in the air and how often you rebreathe the “same air”
you already inhaled?)
6.
What’s the ventilation in the
room like?
7.
Will nasty thing X hurt you if it
gets caught in your throat, or does it have to make its way to your lungs to be
a threat?
To determine your personal risk, we’ve
got to ballpark all of these things.
Some of these are easier than others; some are nearly impossible to
guess accurately, but we have to try anyway.
The problem gets even uglier when
you remove the borders of the room and include complicated geometry (e.g.
buildings), flow patterns near the surface of the earth (e.g. winds), and a
bunch of other people with a bunch of different personal tolerances.
What is Dr. Larsen doing to try and Solve the Problem?
There are “standard ways”
of estimating each of the 7 items in the list above. Some of the ways are reasonable, some
are obviously extreme oversimplifications made because there doesn’t seem
to be a reasonable way to handle the problem more realistically. There are some cases, however, where
improvements could be made in a way that isn’t too impossible.
For example, items 2,3,4, and 5
combine to help determine the “expected dose” of an individual in
the room. If you are in the room
for T seconds, you take B breaths per second, your average breath contains a
volume V of new air, the volume of the room is S, and by moving around you don’t
change too many things, then your “expected dose” would be equal
to:
D = 100*T*B*V/S
(The 100 because we said there were
100 particles of X in the room).
However, if you are in the room for 2 seconds, it is highly doubtful you
received EXACTLY 200*B*V/S particles.
D is just the MEAN expected dose.
There is a distribution around this value.
Some people actually take into
account that the actual received dose is not exactly D. HOWEVER, in every published case that I
have found, when the actual received dose is not assumed to always be equal to
D, they assume that the particles – at the very least – are distributed
perfectly randomly. (If you are reading these research pages
in order, you’re probably getting sick of that link. Maybe you can see the recurring theme in
the research).
Even if you ignore all of the other
work I and other scientists have done on the clustering of airborne
particulates, it hardly seems reasonable to assume that the particles
associated with an intentional release of an airborne pathogen would be equally
distributed through a volume. You’d
expect that all the particles were likely released from a point and not
necessarily mixed perfectly throughout the volume. Consequently, the implications of that
false assumption of perfect randomness should be fleshed out to come up with a
more reasonable estimate of infection risk.
Unfortunately, this is not easy
because issue number 1 in the above section is rather difficult to handle in an
accurate way. There are some cases
(e.g. Q-fever, Tuberculosis, or roto-virus) where relationship 1 may be very
simple – a dose of 1 particle means infection. These pathogens may be the best way to
start examining the problem due to the simplicity of the so-called “dose-response
relationship”.
Currently, Dr. Larsen is attempting
to use the current assumptions regarding number 1 above for individuals and
populations, combined with more realistic methods of examining the true dose
variability likely experienced by a population to come up with more reliable
risk estimates.
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