Airborne Respiratory Diseases and Mechanical Systems for ... · of outdoor air,4,5 probably be-cause most people, especially Americans and Europeans, spend over 90 percent of their

1Airborne transmission of respiratorydiseases in indoor environments re-mains a problem of indoor air quality

(IAQ) with few engineering alternativesand for which performance goals and de-sign parameters are unclear. The engineerwho attempts to deal with microbial IAQfinds that pertinent microbiological infor-mation exists in abundance but not in eas-ily digestible forms. This article summa-rizes the relevant literature of medicalmicrobiology and aerobiology in a mannerthat engineers may find useful and infor-mative and that will facilitate the designof HVAC systems intended to reduce thethreat. The general principles presentedhere can be applied to any indoor environ-ment, including office buildings, schools,residences, hospitals, and isolation wards.

Origin of respiratory diseasesThe first indoor environments, built by

man over half a million years ago, in-cluded caves with leather-draped interi-ors, fur-carpeted tents, and huts coveredwith animal hides. Microbial predators ex-isted from time immemorial, but trans-mission had always required direct con-tact because they could not tolerate thesunlight and temperature extremes out-doors. Man’s cozy new habitats made itpossible for these ancient parasites to sur-vive short airborne trips between hosts.

Animal husbandry seems to have re-sulted in a number of pathogens jumpingspecies and then becoming adapted to in-door transmission to the exclusion ofoutdoor transmission. These include rhi-noviruses, diptheria, TB, smallpox,measles, and influenza, which appear tohave come variously from horses, cows,dogs, pigs, and chickens. Most conta-gious human pathogens have evolved tosuch dependence on man’s habitats for

transmission that they lack any abilityto survive outdoors for long.1

In contrast, the non-contagiouspathogens, including the fungi, environ-mental bacteria, and some animalpathogens, have maintained the abilityto survive in the environment. Even so,direct sunlight is rapidly fatal to almostanything but spores.1

Classification of pathogensPathogens are any disease-causing mi-

croorganism, but the term applies to anymicrobial agent of respiratory irritation,including allergens or toxigenic fungi. Res-piratory pathogens fall into three majortaxonomic groups: viruses, bacteria, andfungi. The fungi and some bacteria, mostnotably the actinomycetes, form spores.Since spores are characteristically largerand more resistant to factors that will de-stroy viruses and bacteria, the engineermay find it more convenient to considerspores a definitive and separate category.

The single most important physicalcharacteristic by which to classify airbornepathogens is size since it directly impactsfiltration efficiency.2 Fig. 1 presents agraphic comparison of airborne respira-tory pathogens in which the spores, bacte-ria, and viruses can be observed to differ-entiate well, based on size alone. The leftaxis indicates the “average” or typical di-ameter or width. The areas of the circles donot represent the actual sizes of the mi-crobes, but each represents the diameterin proportion to one another. The span ofdiameters is seen to be almost four ordersof magnitude. Some microbes are oval orrod-shaped, and for these only, the smallerdimension is indicated.

34 HPAC Heating/Piping/AirConditioning July 1998

Airbornerespiratory

pathogens anddiseases inhealth care

facilities arenumerous

and dangerous.HVAC systems are critical in

controlling them.

By W. J. Kowalski, PE,Graduate Researcher, and

William Bahnfleth, PhD, PE,Assistant Professor,

The Pennsylvania StateUniversity, Architectural

Engineering Dept., University Park, Pa.

Airborne Respiratory Diseases and Mechanical Systems for

CONTROL OF MICROBES

1Superscript numerals indicate referenceslisted at end of article.

July 1998 HPAC Heating/Piping/AirConditioning 35

Perhaps the most important classifica-tion is that of communicable versus non-communicable, a distinction that has bothmedical and engineering relevance. Theterm communicable is synonymous withthe term contagious. Communicable dis-eases come mainly from humans, whilenon-communicable diseases hail mostlyfrom the environment. However, many mi-crobes that are endogenous to humans orare environmentally common may causeopportunistic infections in those whosehealth has been compromised. These occurprimarily as nosocomial, or hospital-ac-quired, infections. These three categoriesthen define all airborne pathogens:

● Communicable● Non-communicable● Primarily nosocomialTable 1 lists all respiratory

pathogens under these three cat-egories, along with major dis-eases, common sources, and aver-age diameters. In the columnidentifying microbial group, theterm actinomycetes refers only tothe spore-forming actinomycetes.Some general observations can bemade from these charts such asthe fact that most contagiouspathogens come from humans,most non-contagious pathogenscome from the environment, andmost primarily nosocomial infec-tions tend to be endogenous.These tables are not necessarilyinclusive since a number ofpathogens, such as E. coli, Bacil-lus subtilis, and some otherstrains of Legionella, can, on rareoccasions, cause respiratory dis-ease or allergic reactions.3 Theabbreviation “spp.” denotes thatinfections may be caused by morethan one species of the genera butdoes not imply that all species arepathogenic.

Table 1 lists only respiratorypathogens, although non-respira-tory pathogens can also be air-borne. Certain infections of theskin or eyes, nosocomial infectionsof open wounds and burns, andcontamination of medical equip-ment may occur by the airborneroute. Although these types of in-fections have not been well stud-ied, any pathogen that transmits

by the airborne route will be subject to thesame principles and removal processes de-scribed in this article.

Communicable diseasesTable 1 lists all the main respiratory dis-

eases that can transmit between humanhosts via the airborne route. Humans arethe natural reservoir for most contagiouspathogens but some notable exceptionsexist. Pneumonic plague and Arenavirusepidemics originate with rodents or othermammals.1 In regards to the mysteriousorigin of Influenza, humans apparentlyshare the function of natural reservoirwith birds and pigs, as strains of thisvirus periodically jump between species.3

C O N T R O L L I N G M I C R O B E S

Figure 1. Relative size of airborne respiratory pathogens.continued on page 37

Many contagious respiratory pathogensalso transmit by direct contact through theexchange of infectious droplets or particlescalled fomites.4 The eyes and nasal pas-sages are vulnerable to fomite transmis-sion. The predominance of these directroutes in comparison with the inhalationroute has not been well established but canbe very species-dependent.5 Infectivity isalso lost upon drying, and therefore handor surface contact may require the ex-change of moisture as well as an infectiousdose.1,6

Barely 20 pathogens account for theoverwhelming number of contagious respi-ratory infections. Table 2 lists the charac-teristics of these infections, while the typi-cal course of these infections is depicted inFig. 2. The infection rate refers to the frac-tion of those exposed to an infectious dosewho contract the disease. This type of in-formation can be useful to engineers at-tempting risk assessment or proceduralcontrol of infectious occupants or patients.Few infectious doses have been estab-lished, but for purposes of making rough orconservative estimations, as few as 1-10TB bacilli can be infectious for humans—while a total of 200 Rhinovirus virions maybe required to cause a cold.4

Most respiratory parasites induce theirhosts to aerosolize large quantities of infec-tious bioaerosols by nasopharyngeal irrita-tion, which causes coughing and sneez-ing.4,5 Consider the profiles of the particlesizes shown in Fig. 3. A single sneeze cangenerate a hundred thousand floatingbioaerosol particles, and many may con-tain viable microorganisms.7 A singlecough typically produces about one per-cent of this amount, but coughs occurabout 10 times more frequently thansneezes.7 Bioaerosols produced by talkingare negligible, but extended shouting andsinging can transmit infections.

Some limited data from Duguid7 isavailable in generation rates stating thatA TB infective can produce 1-249 bacilliper hr,8 while a person in the infectiousstage of a cold may produce 6200 dropletnuclei per hr containing viable virusesthat remain airborne longer than 10 min.In one measles epidemic, 5480 virionswere generated per hr.8

The dose received from an airborne con-centration of microbes could be considereda factor under engineering control since it

M I C R O B E S


continued from page 35

depends on the local air change rate anddegree of mixing as well as the generationrate. The successful transmission of an in-fection, however, depends on all of the fol-lowing factors:

● Susceptibility of the individual (immunity).

● Duration of exposure.● Concentration of infectious agent.● Virulence of infectious agent.● Breathing rate. ● Route of infection (inhalation, eyes,

nasopharynx, etc.).None of these factors is necessarily an

absolute determinant. Health and degreeof immunity can be as important as thedose received from prolonged exposure.

Computations of infectious airbornedoses can be fraught with uncertainty.Epidemiological studies on colds avoidthese problems by computing actual risks.Fig. 4 shows how duration and proximityto an infectious person can increase thelikelihood of infection, based on data fromLidwell’s studies of the common cold.9

These data suggest that there may be athreshold distance beyond which risk de-creases sharply. This risk may result fromlocal airborne concentrations but may alsoinclude the risk of contact with fomites.

Non-communicable diseasesThe list of non-communicable pathogens

in Table 1 includes all known that causerespiratory infections, allergic reactions,and toxic reactions. Included among thediseases are EAA and HP (see notes),



Figure 2. Genericcurve for duration of

symptoms of respira-tory infections

Figure 3. Profile of particle sizes produced by an infectious person. Based on data from Duguid et al 1945.

continued on page 40


which are sometimes associated with sickbuilding syndrome (SBS). Non-communi-cable infections are almost entirely due tofungal or actinomycete spores and envi-ronmental or agricultural bacteria.

Spores form the most important group ofnon-communicable diseases. Outdoorspore levels vary with season and climateand can reach very high levels when dry,windy conditions result in disturbance ofthe soil where fungi grow.Surprisingly, few cases of res-piratory infection have everbeen attributed to inhalationof outdoor air,4,5 probably be-cause most people, especiallyAmericans and Europeans,spend over 90 percent of theirtime indoors.10 A small pro-portion of actinomycete infec-tions have occurred outdoors

in agricultural facilities, although mosttend to occur inside barns and work-sheds.11,12

Indoor air spore levels can differ fromoutdoor air in both concentration and com-position of spores. In normal, dry build-ings, spore levels tend to be anywhere from10 to 100 percent of outdoor spore levels11

and are mostly less than 200 colony form-ing units (CFU) per cu meter. Problem-free, multi-story office buildings typicallyhave levels that are 10 to 31 percent of theoutdoor air11 levels. The composition offungal species indoors tends to reflect thatof the outdoors.13 Some fungal species,most notably Aspergillus and Penicillium,are often found to account for 80 percent ofindoor spores.10

Spores will germinate and grow in thepresence of moisture and nutrients13 in lo-cations such as basements, drain pans,and on refrigerator coils. As a result ofsuch growth, spores can be generated in-ternally in problem buildings, wet build-ings, and certain agricultural facilities at ahigh enough rate to cause indoor spore lev-els to exceed outdoor levels. If spore con-centrations indoors consistently exceed


Figure 5. Indoor spore levels by ventilation system type. From the

California Healthy Buildings Study.11

Figure 4. Risk of cold infection from

proximity. Risk at zerorepresents intimate

(husband-wife) contact. Estimated per data

from Lidwell.9



outdoor levels, the building can be inferredto contain an indoor amplifier.14

In the California Healthy BuildingsStudy,11 naturally ventilated, mechani-cally ventilated, and air conditioned build-ings all had lower indoor spore levels thanthe outdoors (Fig. 5).However, Fig. 5 mayreflect favorable localconditions since manystudies have measuredmuch higher levelsthan these in non-prob-lem buildings.

Table 3 lists the re-sults of various stud-ies that include mea-surements of outdoorspore levels and typi-cal, average, or repre-sentative indoor lev-els. These levels donot necessarily pose ahealth threat. Mea-surements and guide-lines vary almost aswidely as outdoor lev-els vary seasonallyand geographically.

Mic roorgan i smswill take advantage ofany opportunity to es-tablish themselvesand multiply in a newenvironment.4 Nichesfor microbial growthmay be created inad-vertently by engi-neered systems thatgenerate moisturesuch as humidifiers,evaporative air cool-ers, cooling coil drainpans, and condensa-tion on ductwork insu-lation. Amplificationmay result in airborneconcentrations abovethe outdoors10 and may reach unhealthylevels.13 Legionnaire’s Disease provides asentinel example of pathogenic microbialamplification by an engineered system.

Amplifying factors can be controlledthrough various means, including preven-tive design through humidity and mois-ture control. Some other first and secondline defensive measures include filtration,the removal of materials that provide nu-

trients, procedural cleaning and mainte-nance, and the use of biocidal equipment.

Table 4 identifies fungal pathogens thathave been found to grow indoors on vari-ous surfaces or in HVAC equipment.Unidentified multiple species (spp.) may

not necessarily be pathogenic. Many fac-tors may dictate which pathogens willgrow indoors such as climate, indoor mate-rials, degree of human occupancy, hygiene,and moisture levels.1,8

Table 5 identifies some pathogenic en-vironmental bacteria that have beenfound growing indoors or on HVACequipment. Occasionally, some conta-gious bacteria disemminated from hu-


mans can be found in water, equipment,or in dust, but these are transient occu-pants and unlikely to grow or survivelong outside of human hosts.1,5

Nosocomial infectionsAll respiratory pathogens are poten-

tially nosocomial, but those that occur al-most exclusively as nonsocomial infectionsare listed in Table 1 such as primarilynosocomia l r e sp i ra to ry pathogens.

The other common nosocomial infectionsare identified with a purple boxed N in thenotes column.

In intensive-care units, almost a third ofnosocomial infections are respiratory, butnot all of these are airborne since some aretransmitted by contact or by intrusivemedical equipment.15 Nosocomial infec-tions can also be airborne but non-respira-tory such as when common microbes likeStaphylococcus settle on open wounds,burns, or medical equipment.

Patients who succumb to nosocomial in-fections are often those whose natural de-fenses have been compromised either as aresult of disease, medication, injury, or by-passed by intrusive procedures. In cases ofimmune system deficiency, even a pa-tient’s own endogenous flora could causeinfection, while normally benign environ-mental microbes can become pathogenic.

The protection of patients from poten-tial pathogens requires the reduction ofmicrobial contaminants below normal orambient levels. This is usually accom-plished through the use of isolationrooms, HEPA filters, UVGI, and strict hy-giene procedures.15 In the health care en-vironment, particular attention must bepaid to the possibility of microbial growthindoors and in the air handling units,even if levels are not a threat to healthy

people. Low-level indoor microbial ampli-fication in health care settings may causebuilding-related illness (BRI) without ac-tually representing SBS.

Technically, nosocomial infections re-late to those who are hospitalized, buthealth care professionals themselves maybe at risk. The Center for Disease Con-trol(CDC) publishes guidelines for controlof infections15 among hospital employees,but appropriate engineering design andmaintenance can play a significant role inreducing the risks for medical profession-als as well as for patients.

Natural microbial decayVarious environmental factors destroy

airborne microbes.1 Direct sunlight con-tains lethal levels of ultraviolet radiation.Dehydration renders most microbes inac-tive, although many spores may surviveindefinitely. High temperatures will inac-tivate all pathogens, some more rapidlythan others. Freezing will destroy mostpathogens; except that some, especiallyspores, may be preserved. Oxygen slowlykills most airborne microorganismsthrough oxidation. Pollution levels that wetolerate our entire lives can be fatal to mi-croorganisms. Plate-out, or adsorption, oc-curs on all interior building surfaces, butthis removal rate tends to be negligible.

Each of these environmental processesreduces pathogen populations according tothe following general equation:1,6

N 4 N0 e-kt (1)where

N 4 population at time tN0 4 population at time t40k 4 rate constant for processe 4 2.718The resulting exponential decay curve is

known as a survival curve, or death curve.Often, a very small fraction of the micro-bial population, usually about 0.01 per-cent, resists chemical or physical inactiva-tion for extended periods of exposure.1,16

This relation applies additively to all re-duction processes—except that humiditylevels will influence the effects of other fac-tors such as ultraviolet germicidal irradia-tion (UVGI) and heat on a species-depen-dent basis. In the outdoors, sunlight,temperature extremes, and wind ensurethat non-spore microbial populations de-cay and disperse rapidly, generally withinminutes.1,16 In the indoors, these factors



are controlled for human comfort, result-ing in airborne microbes surviving longer,sometimes even days.1,4

After expulsion by sneezing or coughing,most large droplets will settle out of the airwithin a matter of minutes. Fig. 6 illus-trates this process and is based on fitteddata. Many of the micron-sized dropletswill rapidly evaporate to droplet nucleithat approach the size of the individual mi-crobe. Micron-sized particles can remainsuspended for hours and spread by diffu-sion or air currents.8

Airborne microbes lose viability overtime. In the absence of sunlight, the decayrates for each microbial group, based onrates measured in a variety of studies,16

are shown in Fig. 7. Curiously, bacteria de-cay faster in air than viruses apparentlybecause they depend more on moisture fortheir survival than do viruses.

Pathways and disseminationFig. 8 illustrates some distinctions be-

tween airborne pathogens in relation to a

typical air handling unit (AHU). Conta-gious viruses and bacteria come almost ex-clusively from humans, and they will ap-pear only in the return air. Spores andenvironmental bacteria may enter fromthe outdoors, but once growth (amplifica-tion) occurs indoors, they may appear inthe return air at higher levels than in theoutdoor air. Environmental bacteria arerarely pathogenic for healthy people(Table 1), but they may provide a nutrientsource for pathogenic fungi.

Spores can initially enter a building byvarious routes, including inlet air or infil-tration, or they may be brought in withbuilding materials, carpets, clothes, food,pets, or potting soil. In a normal, dry build-ing, the return air will have lower levels ofspores than the outdoor air,11,12 exceptwhen snow covers the ground and outdoorspore levels approach zero. When indooramplifiers are present, the return air couldbe expected to contain higher levels ofspores than the outdoor air, except duringdry, windy, summer conditions when out-door levels of spores can become very high.

Once spores germinate and growth oc-curs in an AHU or anywhere inside thebuilding, new spores may be generatedand appear in the return air. Filters mayintercept spores, but moisture may causethem to “grow through” the filter media.Cooling coils can have a pronounced filter-ing effect on spores,11,12 but the presence ofcondensation may also cause microbialgrowth and amplification10 downstream ofthe coils, negating the effect.

Boosting outside air flow may be an op-tion only if the ventilation system is notthe source of microbial contamination; inwhich case, increasing air flow may exac-erbate the problem.11 A fungus problemthat is not caused by the ventilation sys-tem, such as a leaky roof or wall, requiresseparate remedial action such as removingthe damaged material.l7

Engineered alternativesNatural decay mechanisms operate too

slowly inside most buildings to preventsecondary infections.16 Available engineer-ing alternatives include purging with out-side air, filtration, UVGI, and isolationthrough pressurization control. Each ofthese technologies has advantages andlimitations, but optimization for any appli-cation is always possible if the microbialIAQ goals are clearly specified.


Figure 6. Disappearance of

airborne sneezedroplets from room

air by size. Based on fitted, normalized data

from Duguid.7

Figure 7. Viability of airborne microbes indoors in absence of sunlight.Based on averages for each

microbial group. 1,16



Pressurization control is com-monly used in biohazard facilitiesand isolation rooms to prevent mi-gration of microbes from one areato another, but inherent costs andoperational instability at normalair flow rates limit feasibility forother applications.

Full outside air systems are oftenused in health care facilities and TBisolation rooms, subject to CDCguidelines.15 Fig. 9 shows the effectof full purge air flow on the reduc-tion of pathogens in a room with an initialconcentration of 100 microbe CFU per cumeter. Comparing this with Fig. 10 showsthe results of HEPA filtration at the samerecirculation flow rates. The results arepractically identical.

The use of HEPA recirculation, ofcourse, carries a lower total energy pen-alty2 in hot or cold climates. But in mild ordry climates, high percentages of outsideair can prove economical, especially in ap-plications involving evaporative coolers.Hospitals often have commitments to spe-cific guidelines, but other facilities may se-lect and size systems to suit their goals andbudgets.

HEPA filters, for example, are not theonly choice for controlling microbial IAQ.High or medium efficiency filters are capa-ble of removing airborne pathogens, espe-cially spores, without high operation or re-placement costs.2,16 Overall, particleremoval efficiency might be improved bylocating medium efficiency filters in the re-circulation loop vs. the outside air in-takes16 or even downstream of the coolingcoils. But, this choice will depend on eachindividual system’s operating parameters.

Combining purge air with HEPA fil-tration results in performance that is es-sentially additive, and cost optimizationbecomes straightforward. Energy con-sumption, replacement costs, and micro-bial IAQ goals will dictate the economicchoice for any particular installation.16

The performance of medium efficiencyfilters in combination with purge airflow is not directly additive but dependson the filter efficiency vs. particle sizecurves, the sizes of the pathogens of con-cern, and the system operating parame-ters.

UVGI can be an efficient method to usein the right applications such as control-ling microbial growth in cooling coils.18

The continuous exposure appears to in-hibit fungal growth and may kill thespores as well. In applications involvingthe disinfection of air streams, the effec-tiveness of UVGI depends on factors thatinclude air velocity, local air flow pat-terns, degree of maintenance, character-istic resistance of the microbes, and hu-midity.16 A single pass through a UVGIsystem may have a limited effect, but re-circulation, either through stand-aloneunits or ventilation systems, will result inmultiple exposures or chronic dosing.

Figure 8.Sources andpathways ofmicrobial contaminationin a typical airhandling unit.

Spores may be intercepted, germinate in moisture, and produce new spores

Mixing damper Filter Cooling coil

Supply air

Outside air may include spores and environmental bacteria

Return air may include viruses, bacteria, and internally generated spores

Figure 9. 100 percent outside air: effect of achon reduction of initial level of room microbial contamination.

Figure 10.HEPA filter recirculation:effect offlowrate (in ach) on thereduction ofinitial level of room microbial contamination.


Chronic dosing with UVGI can have amajor impact on airborne viruses andbacteria.16

A graphic comparison of the relative ef-fectiveness of the three main alterna-tives—outside air purge, filtration, andUVGI—is provided in Fig. 11 through 13.Fig. 11 shows the effect of 1 air changer perhr (ach) of outside air on reduction of roomair contaminant concentrations from aninitial value. Perfect mixing is assumed,along with 500 CFU per cu meter contami-nation of each microbial group initially,100 CFU per cu meter of spores in the out-side air, and no internal generation. Natu-ral decay rates from Fig. 7 are incorpo-rated in the model. The scenario of aninitially contaminated room may not be re-

alistic but provides dramatic differ-entiation of the effectiveness ofpathogen removal.

Fig. 12 shows the effect of anASHRAE medium efficiency filter(80 to 85 percent dust spot) to thesupply air of the model buildingwhile maintaining 1 ach of outsideair. The filter model describes filterefficiency vs. diameters in accor-dance with typical vendor perfor-mance curves.16 Spore levels indoorsare clearly reduced below outdoorambient levels. Some reduction ofbacteria and viruses can also benoted, but their removal is still dom-inated by the purging effect of theoutside air. The filter used in thisanalysis provides a baseline for com-parison. High efficiency filters, suchas the 90 to 95 percent filters used inhospitals,2 would result in evenhigher removal rates.

Fig. 13 shows the impact of aUVGI system with 25 mW (W=watt)per sq cm placed in the recirculationloop. The outside air is maintainedat 1 ach, but no filters are included.Spores are relatively unaffected bythe UVGI, but the viruses aremarkedly reduced. This model in-corporates chronic dosing effectsfrom recirculation with an exposureof 0.2 sec for each pass. The decayrate Equation 1 is applied withknown rate constants16 for a widecross-section of the microbial spe-cies listed in Table 1.

The unusual performance charac-teristics of each technology have

been highlighted in these examples. In-clusion of these characteristics in anyevaluation, along with the IAQ designgoals, ambient conditions, and internalgeneration rates, will dictate the choicesfor any given application—subject onlyto economic limitations.

Other alternativesVarious current or experimental tech-

nologies have the potential for reducingairborne disease transmission or indooramplification. Biocidal filters can limitor prevent fungal growth on the filtermedia. Electrostatic filters (i.e., electretsor electrically stimulated filters) areavailable but have not seen widespread



Figure 11. Effects of 25

percent outsideair (1 ach) on

indoor contami-nant levels.16

Outdoor sporelevel = 100 cfuper cu meter.

Figure 12. Effect of

ASHRAE filter,80 to 85 percent

efficiency on indoor

contaminant levels.16

Recirculation with 25 percent

outside air.

Figure 13. Effect of UVGI

on indoor contaminant levels.16 Re-

circulation with 25 percent

OA. UVGI powermW (W=watt)

per sq cm



use. Carbon adsorbers have pore sizestoo small to remove viruses, but they areeffective at removing VOCs produced bysome fungi and bacteria.

Other technologies currently under re-search include low-level ozonation, nega-tive air ionization, and photocatalytic ox-idation—a technology that may one dayresult in a type of light-powered, self-cleaning, microbial filter.

ConclusionsPerfect solutions to the problem of air-

borne disease transmission do not yet ex-ist, but the available technologies—out-side purge air, filtration, and UVGI—canbe successfully implemented when theircharacteristic effects are understood andthe goals clearly defined. Whether theapplication involves improvement of mi-crobial IAQ in an office building or mini-mizing the risk of infection in an operat-ing room, these technologies can beoptimized individually or in combinationfrom a cost or performance standpoint.

Finally, since microbes will never ignoreopportunities provided to them, appropri-ate design, regular surveillance, and main-tenance of these technologies in particular,and HVAC systems in general, should al-ways be proactive. HPAC

References1) Mitscherlich, E. and E. H. Marth. Micro-

bial Survival in the Environment. Berlin:Springer-Verlag, 1984.

2) Burroughs, H. E. “Filtration: An invest-ment in IAQ.” HPAC Aug. 1997: 55-65.

3) Freeman, B. A. ed. Burrows Textbook ofMicrobiology. Philadelphia: W. B. SaundersCo., 1985.

4) Ryan, K. J. ed. Sherris Medical Microbiol-ogy. Norwalk: Appleton & Lange, 1994.

5) Mandell, G. L. ed. Principles and Practiceof Infectious Diseases. New York: Wiley, 1985.

6) Hers, J. F. ed. Airborne Transmission andAirborne Infection. Proc. of VIth InternationalSymposium on Aerobiology. Technical Univer-sity at Enschede. The Netherlands: OosthoekPublishing Company, 1973.

7) Duguid, J. P. “The size and the duration ofair-carriage of respiratory droplets and droplet-nuclei.” Journal of Hygiene 54 (1945): 471-479.

8) Kundsin, R. B. Architectural design andindoor microbial pollution. Oxford Press, 1988.

9) Lidwell, O. M. and R. E. O. Williams. “Theepidemiology of the common cold.” Journal ofHygiene 59 (1961): 309-334.

10) Woods, J. E. ed. Healthy Buildings/IAQ’97. Proc. of ASHRAE Annual IAQ Conference.

Washington, DC, 1997.11) Godish, T. Sick Buildings: Definition, Di-

agnosis, and Mitigation. Boca Raton: LewisPublishers, 1995.

12) Samson, R. A., ed. Health Implications ofFungi in Indoor Environments. Amsterdam:Elsevier, 1994.

13) Burge, H. “Bioaerosols: Prevalence andhealth effects in the indoor environment.” Journal of Allerg. Clin. Immunol. May 1990:687-781.

14) Rao, C. Y. and H. A. Burge. “Review ofquantitative standards and guidelines for fungiin indoor air.” Journal of Air & Waste Manage-ment. Assoc. Sep. 1996: 899-908.

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16) Kowalski, W. J. “Technologies for control-ling respiratory disease transmission in indoorenvironments: Theoretical performance andeconomics.” Master’s Thesis. Ann Arbor: UMIDissertation Services, 1997.

17) Kemp, S. J., et al. “Filter collection effi-ciency and growth of microorganisms on filtersloaded with outdoor air.” ASHRAE Transac-tions Jan. 1995: 228.

18) Scheir, R. and F. B. Fencl. “Using UVCTechnology to Enhance IAQ.” HPAC Feb. 1996:28-29, 85, 87.

Bibliography1) Ahearn, D. G., et al. “Colonization by Cla-

dosporium spp. of painted metal surfaces asso-ciated with heating and air conditioning sys-tems.” Journal of Ind. Microbiol Aug. 1991:277-280.

2) Chang, J. C. S., K. K. Foarde and D. W.VanOsdell. “Assessment of fungal (Penicilliumchrysogenum) growth on three HVAC duct ma-terials.” Environment International Apr. 1996:425.

3) Flanningan, et al. Allergenic and toxigenicmicro-organisms in houses. Pathogens in theEnvironment. Oxford: Blackwell ScientificPublications, 1991.

4) Hyvarinen, et al. “Influence of cooling typeon airborne viable fungi.” Journal of AerosolScience 26.S1 (1995): s887-s888.

5) Macher, J. M. and J. R. Girman. “Multipli-cation of microorganisms in an evaporative aircooler and possible indoor air contamination.”Environment International 16 (1990): 203-211.

6) Price, D. L., et al. “Colonization of fiber-glass insulation used in heating, ventilation,and air conditioning systems.” Journal of Ind.Microbiol. 13 (1994): 154-158.

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Documents

Airborne Respiratory Diseases and Mechanical Systems for ... · of outdoor air,4,5 probably be-cause most people, especially Americans and Europeans, spend over 90 percent of their