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Sick-building syndrome and building-related illness.

Significant health problems linked to very poor indoor air quality are more prevalent than anyone could have predicted. Infectious disease specialists, as a result, search for more effective ways to diagnose and treat such threatening diseases.

Not long ago, a nurse working at a hospital experienced a series of asthma attacks that flared up whenever she worked on the bone marrow transplant unit. Another nurse and a patient aide assigned to the same unit suffered from symptoms including a constant runny nose, itchy eyes, chest tightness, and wheezing. All three complained to their supervisor about a dank, musty smell that seemed to characterize their ward, but their complaints fell on deaf ears.

About the same time, a 6-year-old patient on the transplant unit developed a fever, progressive pneumonitis, and died suddenly. An autopsy revealed many tissues were infected with mycelia, which upon culture revealed Aspergillus fumigatus.

The hospital's chief of infectious diseases found the two nurses and patient aide had elevated eosinophil counts, immediate skin reactivity to Aspergillus antigen, and elevated IgE levels. They were diagnosed with allergic bronchopulmonary aspergillosis caused by hypersensitivity due to the organisms.

An extensive environmental investigation of the hospital found the air filters on the bone marrow transplant unit were completely clogged with a greenish-black material, which upon culture demonstrated the presence of A. fumigatus. Air sampling showed 826 colony-forming units (CFU) per m3 of the same organism, an extremely high concentration for a hospital that typically should show less than 1 CFU per m3 of the specific organism isolated. The clogged filter, examined using bulk sampling, showed an elevated concentration of 1.5 x [10.sup.6] A. fumigatus CFU/gram of the filter material. As a result of these findings, the hospital's entire Heat Ventilation and Air Conditioning (HVAC) system in the bone marrow transplant wing was renovated immediately.

The above scenario is a perfect example of a building-related illness, which now has become commonplace in our era of energy efficiency and delayed preventive maintenance due to cost containment. This article focuses on the role played by microorganisms due to sick-building syndrome and building-related illness.


One of the major global public health concerns of the 20th century is pollution. In simple terms, pollution can be defined as "contamination of the environmental air with substances - items that have adverse effects on human health." With the onset of the energy crisis in the 1970s, buildings (commercial, nonresidential, and residential) in advanced countries were constructed to be energy efficient with less air exchange between them and their surroundings. Among the problems that arose in such buildings as a result of this energy-efficient mind-set were the following: retention of higher temperatures, higher humidity levels, decreased ventilation, and increased odor retention.

The advent of higher temperatures and increased humidity levels in buildings gave birth to the proliferation of microorganisms in indoor environments. Additionally, certain synthetic materials used to construct the buildings, as well as some furnishings, were found to produce volatile organic compounds, all of which have adverse effects on human health. These two factors have created indoor air pollution (IAP), which is used interchangeably with the term "indoor air quality" (IAQ).


Indoor air pollution has led to use of the terms "sick-building syndrome" (SBS) and "building-related illness" (BRI). SBS usually implies the existence of persistent, non-specific symptoms (e.g., eye, nose, and throat irritation; fatigue; headaches) that occur in more than 25% of a building's occupants and that dissipate once these inhabitants leave the building (see Figure 1).[1] For the most part, diagnosing SBS is based on the exclusion of other diseases.

In marked contrast, BRI refers to clinically diagnosed disease(s) in building occupants that result from exposure to indoor air pollutants (see Figure 2). These conditions are relatively well documented and have defined diagnostic criteria, recognizable causes, and defined treatments. Typically individuals suffering from a BRI require prolonged recovery times after leaving the suspected environment, and successful remediation or mitigation requires elimination of exposure to the causative agents.


Most urban residents spend about 90% of their time indoors, yet the air inside our homes, office buildings, schools, and shopping malls is not necessarily any cleaner than outdoor polluted air. In fact, in some cases, it can be worse. During the past few years, the U.S. Environmental Protection Agency (EPA), armed with input from the Centers for Disease Control and Prevention (CDC), has consistently ranked IAQ among the top five environmental risks to public health.[2]

A reasonable lay definition of IAQ is how indoor air affects the health and well-being of those individuals who are exposed to it. A more technical definition relates to how well indoor air satisfies three very basic requirements for human occupancy: 1) Thermal acceptability, 2) Maintenance of normal concentration of respiratory gases, and 3) Dilution as well as removal of contaminants and pollutants to a level below health or odor discomfort thresholds.

Certainly, there is an epidemic of indoor air pollution and its related human health effects. What's to blame for this epidemic? Among the contaminants are these:

* Combustion products

* Chemicals and chemical solutions

* Respirable particulates

* Respiratory products

* Radionuclides

* Microbiological agents (indoor bioaerosols).

Recently it has been suggested the above contaminants might be responsible for a wide variety of complaints, including SBS and BRI. Researchers suggest approximately 50% of these complaints may be attributed to microbiological agents.

Current interest in the health effects of indoor air pollutants has placed the primary focus on characterizing indoor bioaerosols with the goal of discovering a cause for on-going disease or discomfort. Bioaerosols also are studied to make connections between specific health effects (e.g., house dust mite allergens and asthma) and to increase understanding of these emerging microorganisms and their products, as well as understanding of the ecology and physiology of the source of the organism and the fate of the airborne effluents.


To make buildings more energy efficient in the 1970s, they were sealed and HVAC systems designed to recirculate rather than replenish indoor air. Such drastic measures resulted in the retention of indoor pollutants. For example, outdoor pollutants such as bacteria, fungi, and pollen can enter a building through open windows, ventilation system air intakes, water-damaged roofs, drainage leaks from septic systems, and cracks in building walls, floors, and ceilings. Other contributing factors include chemical emissions from carpeting, furnishings, and cleaning products that become concentrated in tightly sealed buildings with poor ventilation.

While ventilation systems are meant to bring in clean, filtered outdoor air that, in turn, flushes out and exhausts used indoor air, such systems fail to do so, either because of poor design or poor maintenance. In the hospital setting, the juncture of aesthetics and energy efficiency fostered sharp increases in airborne microbial levels within buildings. Due to the incidence of infection in hospitals, it is vital the medical community provide safer environments for an increasing population of traumatized, immunosuppressed patients.


Because the respiratory system is a portal of entry for human pathogens and pollutants, synergistic effect should be expected. Indoor air contains many microorganisms that can cause infectious disease, allergy, and mucosal and skin irritation. In fact, infectious disease is more readily transmitted indoors than outdoors. It also should be noted that respiratory infections account for about 60% of all community-acquired illnesses.[3]

Airborne infections are caused by two types of organisms: 1) obligate pathogens,[1] organisms that require a living host to survive, and 2) opportunistic pathogens, organisms found in normal flora of the body or environment that cause disease under unusual conditions (see Figure 3).[1,4,5]

Obligate pathogens. Airborne transmission of obligate pathogens such as influenza, measles, rubella, chicken pox, the Hantavirus, rhinovirus, streptococcal pneumonia, and tuberculosis infection are enhanced in crowded and poorly ventilated indoor environments.[6] Infectious agents that spread from person to person via indoor air can have a significant impact on worker absenteeism, productivity, and morale.

Airborne transmission of fungi responsible for systemic mycotic infections such as blastomycosis, coccidiomycosis, and histoplasmosis has been demonstrated both in healthy and compromised hosts. While fungi involved in these diseases primarily are encountered outdoors, they also can be concentrated in indoor niches and may, indeed, cause BRI.

Opportunistic pathogens. Opportunistic microbes infect individuals with preexisting health problems, such as mechanical/physiological pulmonary disorders, primary congenital immunodeficiencies, and secondary immunodeficiencies (e.g., HIV or drug-induced immunosuppression). Some opportunistic infections in compromised hosts appear to be dose-dependent; therefore, reducing microbial content in indoor air will decrease disease occurrence.

Some agents that cause opportunistic infections have been found in environmental niches that permit microbial preservation and, in some cases, amplification. While HVAC systems are well-known for their ability to support microbial growth, even unexpected environmental niches such as water storage systems have microbial lives of their own. One of the best known opportunistic pathogens associated with indoor air is Legionella pneumophila.

Environmental isolates of this bacteria come from air conditioning units, cooling towers, evaporation condensers, streams, tap water from shower heads, and drinking water. As many as 25,000 sporadic and epidemic Legionella infections occur annually (see Figure 4).[7]

Additional opportunistic pathogens - for instance, A. fumigatus - when found in indoor environments, can cause aspergillosis in immunocompromised hosts. Specialized indoor environments such as pools and hot tubs or equipment such as vaporizers and humidifiers also may serve as protective reservoirs for opportunistic pathogens, such as Pseudomonas sp., Acanthamoeba sp., Naegleria sp., Flavobacterium sp., Cephalosporium sp., Aureobasidium sp., Bacillus sp., and Thermophilic actinomycetes.

The ubiquitous distribution of opportunistic pathogens in indoor air and the rising number of immunocompromised persons in the general population present a new dilemma. Clearly, immunocompromised people are at significant risk wherever groups of people gather.


Endotoxins are composed of lipopolysaccharides (LPS) from the outer membrane of Gram-negative bacteria. They are released by disruption of the cell membrane either during cell lysis or by budding of the membrane during an active growth phase. Lipid A, the lipid portion of LPS, is responsible for characteristic toxicity of endotoxins. Because of their ubiquitous nature, bacterial endotoxins, commonly found in various environments, contribute to BRI.

Recently, several epidemiologic and experimental studies have focused on the health effects of airborne-endotoxin exposure in both occupational and nonoccupational environments. Endotoxins are believed to play an important role in the development of organic-dust - related diseases in exposed workers.[8] These high levels are found in varied environments such as cotton mills, agricultural workplaces, biosludge plants, machining operations, laboratories, homes, hospitals, and swimming pools. The highest reported levels (2-27 [[micro]gram]/m3 or 20-270 EU/m3) are associated with wastewater treatment and recirculating industrial wastewater spray. Endotoxins also are found in the mist of ultrasonic and cool-mist humidifiers.

Exposure to concentrations of airborne endotoxins ([greater than]2 [[micro]gram]/m3) can cause acute fever, lung-function alterations, respiratory complaints (chest tightness, cough, shortness of breath, wheezing), mucosal irritation, dry throat, skin irritation, and rash. Chronic endotoxin exposure may lead to chronically decreased pulmonary function, byssinosis, and chronic bronchitis. Esoteric clinical tests have demonstrated increases of IL-1, IL-6, and TNFa without specific recognition by antibody or T-cell receptors in workers with farmer's lung, a form of hypersensitivity pneumonitis. Additionally, endotoxins can promote B-lymphocytes isotype switching to IgE production in the presence of IL-4.[9] Neutrophils and basophils exposed to endotoxins are primed for increased inflammatory response.

Air sample methods can be controlled using cellulose or polyvinyl chloride (PVC) filter cassettes or a glass impinger at a flow rate of two liters per minute for 15 minutes. The analytical method to detect endotoxins can be performed using the ELISA Limulus amebocyte lysate test.


Fungi are eukaryotic microorganisms with cells containing one or more organized nuclei as well as other membrane-bound organelles. These organisms are uni- or multicellular and reproduce mainly by spores. Many fungi exist as long chains of cells called hyphae, which often are packed into masses of mycelium. Most fungi produce spores that are disseminated through the air.

In indoor environments, the predominant mode of reproduction is asexual. Most fungi related to IAQ, especially those associated with disease, belong to the Dikaryomycetes family (characterized by a binucleate multicellular stage preceding nuclear fission). As fungi grow, they produce metabolic by-products that may affect IAP.

Water is the key factor in determining whether saprophytic fungi will be found in a given indoor environment. Almost any material containing carbon provides a substrate for fungal growth, which will not occur if water is not present.

Common indoor fungi from the genera Aspergillus, Penicillium, and Fusarium produce mycotoxins. A subset of these mycotoxins, Aflatoxins, are potent liver and systemic toxins. Another subset is called trichothecenes, which are produced by molds including Fusarium, Trichothecium, and Trichoderma.

The best-known opportunistic fungal pathogen is A. fumigatus. This pathogen produces toxicoses and allergies, grows in mucoid secretion in the human respiratory tract, and invades living tissue. It is ubiquitous in that it occupies both natural and man-made environments where significant heating occurs (30 [degrees] C-45 [degrees] C). A. fumigatus can be recovered from the air of hospital wards, and outbreaks in susceptible patients have been associated with heavily colonized hospital-air ventilation systems. Aspergillus outbreaks have been known to occur during hospital renovation projects.

Although Aspergillus is universally present in the environment, it causes disease in few individuals. Life-threatening acute infection usually is linked to immunocompromised patients. Aspergillus infections of a more chronic and indolent nature typically are seen in people with less debilitating underlying diseases (asthma, chronic bronchitis, sarcoidosis). Acquisition of Aspergillus is exclusively via inhalation of airborne spores, not person-to-person transmission.


A clinical epidemiological study was conducted in 1993 to investigate health problems of several employees who worked in the early 1980s in the basement and subbasement areas of a remodeled office building. Over the years, flooding caused by drain-water backup occurred periodically. Air quality testing and microbial sampling revealed significant contamination of sheet rock walls, air handling insulation, and paper products by S. atra at a concentration [greater than][10.sup.5] cfu/g.

Samples contained the potent protein synthesis inhibitor Satratoxin H, a member of the Trichothecene mycotoxin group that causes immunosuppression. S. atra has been shown to have adverse effects on the central nervous system, eyes, skin, and upper and lower respiratory tract, and to cause excessive chronic fatigue. Clinical laboratory tests include the IgE-antibody assay, T and B lymphocytes and complement function, immunoglobulins, and angiotesin 1.

Eckardt Johanning, M.D., who practices occupational medicine at Mount Sinai Medical Center in New York, demonstrated that mycotoxins from workers exposed to high levels of Satratoxin in buildings contaminated with Stachybotrys can cause pathogenic effects.[10] In one instance involving S. atra contamination of homes in Cleveland Ohio, the CDC and the Cleveland Department of Health now speculate that fungus may be responsible for the cluster of acute pulmonary hemorrhage cases that occurred between 1993 and the present. To date, six of 35 infants from these homes have died.[11,12]

In adults, research literature suggests mycotoxin from Stachybotrys has been associated with immune suppression, bleeding, and adverse reproductive effects. S. atra, which grows as a slimy mold, sometimes is found during indoor air investigations, after water damage to materials containing cellulose (wood, wallpaper). Clearly more research is needed to understand this human illness. Still, it is important that any occupied environment known to be contaminated with this toxin-producing organism be considered a potential health hazard.


Hypersensitivity reactions can best be portrayed as exaggerated immune responses to foreign organic or inorganic substance (antigens). Allergic reactions are highly individualized. In other words, exposure conditions that elicit an allergic response in certain people may have no effect on other similarly exposed individuals.

Multiple factors influence human capacity to mount an allergic response, the most common being genetic makeup. Much of our understanding about allergies comes from studying human reaction to natural antigens such as pollen, fungi, bacteria, house dust, and animal dander. Examples of allergies key to indoor air considerations include both antibody-mediated (asthma and rhinitis) and cell-mediated (hypersensitivity pneumonitis) types of hypersensitivity.

Asthma, allergic rhinitis, and common allergies are attributed to indoor air pollutants. An estimated 40 million Americans suffer from some type of allergic disease.[13] In the work setting, these diseases are a frequent cause of low productivity and absenteeism.

During the past two decades, there also has been an alarming trend of increasing asthma mortality in the general population. These reactions are learned immune regimens; that is, previous exposure to an antigen always precedes an allergic response. Responses are produced as a result of an abnormal release of a potent vasoactive substance such as histamine, heparin, serotonin, esterase, prostaglands, and leukotrienes following interaction of allergen with specialized host cells, such as mast cells and basophils.[14] These biologically active substances can cause two phenomena within the host:

1. Smooth muscle contraction in nasal passages, dilation of small blood vessels, and continued inflammatory factor release in nasal tissue, resulting in itchy eyes and nasal irritation/congestion (rhinitis)

2. Immediate and/or delayed smooth muscle contraction in pulmonary bronchi, resulting in a reversible narrowing of the airways (asthma).

Exposure to soluble high-molecular-weight antigens such as peptides, proteins, glycoprotein, and polysaccharides can lead to allergies such as asthma and rhinitis. When combined with a suitable protein carrier, however, even low-molecular-weight chemicals and metals can elicit an allergic response.


If a building is suspected of having IAQ problems, it must be determined whether the problems are due to the presence of unusual amounts of microorganisms (bacteria and fungi). To confirm the presence or absence of microorganisms, various specimens must be collected from the building and subjected to scientific investigation. Specimen collection for scientific investigation is broadly defined as sampling.

Before any sampling can be done, a visual walk through of the building must be performed. Investigators look for signs (water damage, excess humidity) that may promote microbial growth and/or the presence of bacterial or fungal growth. Next, investigators may interview the occupants of the building to document symptoms that might have arisen due to specific IAQ problems.

At this point, an investigator may choose any or a combination of the following sampling protocols: a) air sampling, b) bulk sampling, c) swab (wipe) sampling, d) micro-vac sampling, and/or e) water sampling.

Air sampling. One particular protocol practiced by staff at Pure Earth Environmental Laboratory uses six plates of microbiological media. The collection is done with an impactor type sampler such as an Andersen N-6 (Graseby and Anderson, Atlanta, Ga.) Contaminated air is pulled through 400 injection holes by a vacuum pump and the suspended bacteria and fungi are impacted directly onto a standard agar plate containing various selective media. Samples are taken both at indoor and outdoor sites to establish an indoor/outdoor ratio that can be compared to the indoor site of concern. Plate numbers, type of media, sampling times (length of time plates are exposed in the sampler), incubation temperatures, and microbial groups being characterized on the plates are shown in Figure 5.

Quantitation of bacteria and fungi in air for this protocol requires that the sampler be calibrated each time by a Dry CAL DC-1 HC flow calibration (Domark Instrument Inc., Riverdale, N.J.) at 50 mL-50 L/min to provide an accurate measurement of the amount of air sampled per minute. After an appropriate incubation period (5-10 days for fungi, 48-96 hours for bacteria), all plates are evaluated to determine the number of organisms per cubic meter of air and to select predominant microbial taxa for identification.

In addition to air sampling, source sampling protocol is used to locate as well as to confirm suspected microbial growth in any buildings thought to have IAQ problems. Samples are collected from suspected materials for identification and enumeration, utilizing any of the following techniques described below:

Bulk sampling. Bulk samples damaged by water (carpeting, ceiling tiles, insulation materials) can be tested for microbial growth and identification. Typically only a portion of the sample is weighed.

Weighed materials (0.1-5 gm) are immersed in test tubes with 10 mL of sterile distilled water or PBS and allowed to sit at room temperature for 5 minutes. Then the suspension is vortexed vigorously for 1 minute. Depending on the turbidity of the suspension, a serial dilution may be necessary by transferring 1 mL of suspension into a new test tube containing 9 mL of sterile distilled water.

Culture plates are inoculated with 0.1 mL of the suspension, then spread with a sterile "hockey stick" and incubated at an appropriate temperature. The number of sets of plates used to culture each sample depends on the dilution factor used to plate each sample.

Swab (wipe) sampling. Each wipe sample is cut about 1 cm above the swab with a sterile pair of scissors, and the swab is immersed in a test tube containing 10 mL of sterile distilled water. The suspension is kept at room temperature for 5 minutes and vortexed vigorously for 1 minute. Depending on the turbidity of the suspension, a serial dilution may be necessary. The method of serial dilution is similar to that described for bulk sampling. If the area wiped is not accurately measured, the result is expressed as "CFU/wipe." The same media plates and incubation conditions are used for the swab samples.

Micro-vac sampling. Filter cassettes with a vacuum source (air pumps with flow rates of 2-12 LPM) can be used to suck and remove dust or suspected microbial growth from hard or soft surfaces for analysis. These surfaces include carpeting, fleecy facades, chairs, metal air ducts, and fiberglass lining. Filter cassettes should be clean and sterile and filter pore size 0.20-0.45 [[micro]meter]. If fungi are the primary interest of analysis, a filter pore size of 0.45-0.80 [[micro]meter] can be used. A micro-vac sample should have either enough weight (0.5-1 gram) or a known area (4-16 square inch) for proper result presentations in CFU/gram or CFU/square inch. Laboratorians then can process and analyze the specimen for fungi, bacteria, and microbial by-products.

Water sampling. Water is the primary source of bacteria, yeasts, and some notorious microorganisms, such as Legionella. Water can be collected and submitted to a lab for many microbiological analyses. A sample of 100-1,000 mL may be necessary depending on the type of analysis being done. Usually water samples are evaluated for total aerobic plate counts, yeast and mold (fungi), L. pneumophila, total coliform, fecal coliform, endotoxins, and others as deemed necessary.


A practical implication of IAQ problems is cost, which while not easily determined, is viewed by many as second only to the human health impact. IAQ control directly affects the energy consumption of a building, with up to 60% of U.S. total building energy consumption spent on conditioning and distributing indoor air.[2] Cost estimates exceed $80 million annually. The economics of this issue can be divided into direct medical costs and lost worker productivity costs.

The percentage of the population exposed to IAP develop health problems that require medical attention. Costs include physician office visits, emergency room fees, hospital care, surgical fees, and medication. Preliminary estimates contained in the EPA draft to Congress on IAP show the U.S. spends more than 1.5 billion annually on direct medical costs attributable to the health effects of IAP. Current estimates for lost earnings due to IAQ-related illness is approximately $5 million annually. Productivity loss per employee attributable to IAQ currently is estimated to be 3% (14 minutes/day) and 0.6 hours of added sick days annually. If these estimates are applied to the U.S. white-collar labor force, the costs are on the order of $10 billion annually. A recent survey of realistic costs associated with IAQ and productivity suggests the cost of absenteeism is about eight times greater than the money saved by reducing energy costs.[3]


It is essential that knowledge gained from IAQ research be applied to solve health-related problems. Without adequate understanding of IAQ problems, lasting solutions will be hard to come by.

Determining the health effects associated with indoor air pollutants is a demanding responsibility. Merely attempting to understand who is exposed to what has become a challenging task. Total exposure and dosage data for most indoor air contaminants is sparse, and additional re-search is needed to correlate IAQ testing to the clinical patient. While many health effects that are attributed to indoor air pollutants remain controversial, it is clear that indoor air pollutants do cause clinically relevant diseases. Due to the magnitude of potential exposure, public concern over the health risks associated with indoor air pollutants is not likely to diminish in the foreseeable future.

Figure 1 Symptoms commonly associated with sick-building syndrome

Eye, nose, and/or throat irritation Headaches Fatigue Nausea Nose bleeds Nasal congestion Difficulty in breathing Dry skin Irritability Flu-like symptoms
Figure 2
Examples of building-related illnesses

Disease Cause

Pontiac Fever Legionella sp. (bacteria)
An acute, self-limited, febrile,
nonpneumonic illness with an
incubation period of 36 hours.
Attack rate: 90%-100%.

Legionnaire's Disease Legionella pneumophila
Life-threatening bronchopneumonia (bacteria)
with an incubation period of
2-10 days.
Attack rate: 5%-10%.

Hypersensitivity Pneumonitis Fungi, bacteria, organic
Acute extrinsic allergic alveolitis. dust, organic chemicals,
Chronic form may have aerosolized protein, etc.
characteristics of an interstitial
fibrotic pneumonitis. Genetics
may influence attack rate.

Humidifier Fever Fungi, bacteria,
A type of hypersensitivity protozoa, microbial
pneumonitis characterized endotoxins, mycotoxins,
by an acute febrile attack arthropods
accompanied by malaise, cough,
and dyspnea. Chronic form is
called humidifier lung. Genetics
may influence attack rate.

Figure 3 Examples of infectious diseases transmitted via indoor air

Obligate pathogens


Anthrax Brucellosis Streptococcal pneumonia Tuberculosis


Common cold Chicken pox (Varicella) Influenza Measles Rubella Hantavirus


Blastomycosis Coccidioidomycosis Histoplasmosis

Opportunistic pathogens


Legionnaire's Disease Pontiac Fever Legionella sp. Pseudomonas sp.


Herpes I & II Shingles (Zoster)


Cryptosporidiosis Pneumocystis pneumonia


Aspergillosis Cryptococcosis Candida sp. Mucormycosis Phycomycosis

Figure 4 Typical genera of microorganisms isolated from indoor air and water


Alternaria Aspergillus Candida Cephalosporium Cladosporium Fusarium Penicillium Streptomyces Stachybotrys


Bacillus Cornynebacterium Legionella Micrococcus Pseudomonas Staphylococcus Thermoactinomyces


Naegleria Acanthamoeba Giardia



1. Brooks BO, Davis WF. Understanding Indoor Air Quality. Boca Raton, Fla: CRC Press; 1992: 53-75.

2. Burge H, Platt-Mills T. Indoor Biological Pollutants. U.S. Environmental Protection Agency. January 1992. EPA 600-8-91-202.

3. Feeley J. Impact of indoor air pathogens of human health. Indoor Air and Human Health. Boca Raton, Fla: Lewis Publishers; 1985: 183-187.

4. Burge H. Indoor air and infectious disease. Occup Med State Art Rev. 1989; 4: 713-721.

5. Burge H, Hodgson M. Health risks of indoor pollutants. ASHRAE. July 1988; 34-38.

6. Houk V. Spread of tuberculosis via recirculated air in a naval vessel. Ann NY Acad Sci. 1980; 353: 10-24.

7. Davis G, Winn W. Legionnaires disease: Respiratory infection caused by Legionella bacteria. Clin Chest Med. 1987; 8: 419-439.

8. Gammage RB, Berven BA, eds. Indoor Air and Human Health (2nd ed.) Boca Raton, Fla,: Lewis Publishers; 1996: (Chap 11); 179-89.

9. Snapper CM, Pecanha LM, Levine AD, Mond JJ. IgE class switching is critically dependent upon the nature of the B cell activator in addition to the presence of IL-4. J Immunol. 1991; 147: 1163-1170.

10. Johanning E., Morey P, Jarvis BB. Clinical Epidemiological Investigation of Health Effects Caused by Stachybotrys atra Building Contamination. Proceedings on Indoor Air. 1993; 1: 225-230.

11. Centers for Disease Control and Prevention. Acute pulmonary hemorrhage/hemosiderosis among infants - Cleveland. MMWR. January 1993-November 1994; 43: 881-883.

12. American Industrial Hygiene Conference: Bioaerosol Sampling: Why, How, and What Does it Mean? (Lecture Tapes). Washington, DC: May 1996.

13. Slavin E. Allergic and immunological disorders. J Allergic Clin Immunol. 1989; 84: 1059-1061.

14. Brodsky FM, Gaugliard LE. The cell biology of antigen processing and presentation. Annu Rev Immunol. 1991; 9: 707.

Theodore J. Passon Jr. is president and laboratory director of Pure Earth Environmental Laboratory Inc. in Pennsauken, N.J.; laboratory director at Monroe Laboratory in Williamstown, N.J.; and technical consultant for Laboratory Corporation of America in Audubon, N.J. James W. Brown, a member of MLO's Editorial Advisory Board, is assistant commissioner of health for the New Jersey State Department of Health in Trenton, N.J. Seth Mante is technical supervisor at Pure Earth Environmental Laboratory Inc.
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Title Annotation:New and Emerging Pathogens, part 6
Author:Passon, Theodore J., Jr.; Brown, James W.; Mante, Seth
Publication:Medical Laboratory Observer
Date:Jul 1, 1996
Previous Article:How to solve problems using the labor-management partnership.
Next Article:Flowcharting in the lab.

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