Building-Related Disease

CHAPTER 54
BUILDING-RELATED DISEASES
Michael Hodgson, M.D., M.P.H.
U.S. Department of Veterans Affairs Occupational Health Program Veterans Health Administration Washington, DC
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Building-related diseases (BRD) may be classified, among other ways, by mechanisms of disease, as is traditional in medical texts; by presenting symptoms, as is useful in the diagnosis and treatment of patients; or by source and etiologic agent, which are useful approaches in engineering and regulatory strategies. Some redundancy will occur in all three classification systems. This chapter will present diseases according to the first categorization (see Table 54.1). Users of this text should remember the distinction between the sick-building syndrome (SBS) and what is often called building-related illness (BRI). The latter represent clearly recognized clinical conditions with operational criteria (i.e., medical conditions for which wide agreement exists on how to make a diagnosis). Even for these, though, there may be disagreement on individual diagnoses, on best treatment strategies (as even national consensus guidelines may fail to address adequately specific occupational or environmental health aspects of treatment strategies such as removal from work or the importance of exposure control), and on the true cause. On the other hand, the SBS remains a term without operational criteria. Although the epidemiology of building-related complaints has been described since the mid-1980s (Finnegan 1984, Kreiss and Hodgson 1984, Mendell 1993) and dose-response relationships have been recognized for over 10 years (Hodgson et al. 1991), few studies have examined the mechanism of symptoms in an epidemiologic context. Such attempts for eye and nasal symptoms will be described later. Nevertheless, Jaakola (1998) suggests that the term SBS currently represents a construct for discussion purposes only. As the mechanisms for the various symptoms, from odor and irritation through headaches and allergies, are clarified, researchers will characterize the nature and severity of the underlying conditions and support the use of diagnostic tests in the clinical diagnosis of individuals. Individual components of what is now labeled SBS may become building-related illnesses.
54.1 Copyright 2001 by The McGraw-Hill Companies Retrieved from: www.knovel.com
54.2 TABLE 54.1 Disease Categories Disease Rhinitis, sinusitis Symptoms
ASSESSING IAQ
Mechanisms Allergy (IgE)
Diagnostic Criteria Eosinophilic granulocytes in nasal secretions Specific changes on nasal provocation symptoms

Irritation None described Allergic fungal sinusitis Stuffy nose, postnasal drip, headache Allergy (IgE), other? Asthma (airways disease) Coughing, wheezing, shortness of breath, chest tightness Allergy (IgE, IgG) CT-scan evidence of inflammation, eosinophilic mucous, fungal hyphae visible on staining Airways hyper-reactivity (more
than 15 percent change in FEV1)
Stuffy or runny nose; postnasal drip; sinus congestion; nosebleeds
Reversibility of obstruction with bronchodilators
Hypersensitivity pneumonitis
Cough, shortness of breath, muscle aches, feverishness
Pharmacologic irritant Type IV allergy (cellmediated immunity)
See above, history of exposure during onset of asthma Granulomas on biopsy, reversible restrictive changes, (DLCO, TLC, CXR), CT scan, thin-section CT scan
Organic dust toxic Cough, shortness of syndrome (inhalabreath, muscle aches. tion fevers) feverishness Contact dermatitis Dry, itching, scaling, (allergic) red skin Irritant contact dermatitis Contact urticaria testing Conjunctivitis (allergic) Dry itching or weeping skin Red, irritated skin, hives Eye irritation, dryness, tearing
Endotoxin response DLCO, TLC, spirometry, (macrophage white blood cell receptor based effect) count elevations Type IV skin allergy Inspection, skin biopsy, patch testing Irritation Inspection, skin biopsy
Type I allergy
Inspection, RAST or skin price
Type I allergy
Inspection, RAST or skin prick testing, tear-film break-up time, conjunctival staining Inspection, tear film break-up time
Conjunctivitis (irritant) CNS toxicity
Eye irritation, dryness, tearing
Irritation
Headaches, cognitive impairment
Carbon monoxide VOCs
Heat, noise
Elevated carboxyhemoglobin (COhgb) Abnormal neuropsychological tests Calculated heat indices outside range; noise levels above comfort range
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54.3
TABLE 54.1 Disease Categories Diagnostic tests Nasal secretions; eosinophiles CT scan for chronic inflammatory changes Acoustic rhinometry Rhinomanometry (anterior and posterior Linkage strategies IgE-based: RAST or skin prick tests; nasal challenge symptom patterns Causes Sensitizers in the workplace (allergens) including molds, carbonless copy paper, photoactive processes (toners), and secondary exposures, e.g., cat dander brought to work on clothing; pesticides (OPs, pyrethrin) Irritant exposures, including cleaning agents, volatile organic compounds, dust, molds and bacteria, low relative humidity Bioaerosols at work

None described Symptom patterns Surgical tissue for eosinophilic staining in mucous, fungal bodies Recurrences at work, same organisms in workplace Physical examination Spirometry with bronchodilators Methacholine challenge Substance specific challenge See above As above Granulomas, restrictive changes in lung function in a convincing clinical setting Bronchial lavage, DLCO, TLC, spirometry, white blood cell count elevations related to work Inspection, skin biopsy, patch testing Temporal relationship of lung function decrements at work (PEFR, spirometry) Immunologic tests (skin prick tests, RAST tests) As above Clinical history Physiologic linkage (acute disease: reversible patterns) Immunologic linkage: IgG exposure only; lymphocyte transformation to specific antigens Temporal pattern and exposure documentation Molds and thermotolerant bacteria related to moisture Gram negative bacteria, molds, polymers in thermal degradation Patch testing, temporal pattern Clinical history, lactic acid application (stinger test) Clinical history, RAST test Temporal pattern Punctate conjunctivitis, shortened tear film break-up time, RAST or skin prick testing, cobblestoning on physical examination Inspection, tear film break-up time Temporal pattern; RAST or skin prick test Clinical impression Office products Molds, sensitizers Clinical impression Neuropsychological tests, COhgb levels COhgb 3% in nonsmokers, 8% in smokers Abnormal neuropsychological tests None Abnormal neuropsychological tests Clinical impression Irritants (VOCs, dust, low relative humidity), failure to blink at VDUs Fossil fuel sources: Home attached garages, backdrafting appliances, barbecues; commercial/public buildingsentrained exhaust, indoor CO sources Imbalance between local VOC source and exhaust ventilation Inadequate control strategies Copyright 2001 by The McGraw-Hill Companies Retrieved from: www.knovel.com
As allergic rhinitis irritant exposures, including cleaning agents, volatile organic compounds, dust, molds and bacteria, low relative humidity
Formaldehyde, molds, laser toners, Behenic acid (photoactive process) Office products, VOC based
54.4
ASSESSING IAQ
TABLE 54.1 Disease Categories (Continued) Disease Legionnaires disease Symptoms Coughing, phlegm production, fevers Mechanisms Legionella exposure, susceptible host Diagnostic criteria Four-fold rise in antibody titers, culture of same Legionella strain from source as from tissue, epidemiologic clustering Isolation of organisms, positive skin test with typical chest x-ray pattern

Tuberculosis Coughing, phlegm production, fevers, weight loss Infection with Mycobacterium tuberculosis
FEV1 forced expiratory volume in the first second, PCR polymerase chain reaction-based lab test, RAST radioallergosorbent test, DLCO single breath carbon monoxide diffusing capacity, TLC total lung capacity, CXR chest x ray, and PERF = peak expiratory flow rate..
54.1 GENERAL APPROACHES
Diseases related to indoor environments are treated no differently than are conditions potentially related to other environmental and occupational exposures (see Table 54.2). The basic approach includes the following steps:
G G G G
Document disease Document exposure Define linkage (or exclusion) criteria Develop a management plan
For reasons described below, this approach has not been as successful in indoor environments as elsewhere, and the scientific basis for this approach is often still missing.
Document Disease
Physicians and other health care providers make a diagnosis of a condition based primarily on symptoms. Over 75 percent of conditions encountered in primary care need no further documentation (Peterson 1992). In fact, for many there is little objective evidence on an individual basis. In the setting of lawsuits and workers compensation proceedings, physicians are often asked to provide evidence. It is therefore important to seek objective signs on physical examination and measurements of abnormal organ function in laboratory testing, which can often be found. Even then, a few patients with symptoms will have evidence of some physiologic or immunologic process without meeting a set of diagnostic criteria for any specific condition. At times, even in symptomatic patients, tests are negative. That all tests may have false negative results is a fundamental truth, defined in the relationships of sensitivity, specificity, and predictive value. As a test identifies a greater proportion of individuals correctly as having a specific outcome, it also identifies more individuals without those characteristics. As tests are more precise, and identify fewer false positive results, more individuals with the condition are missed. In the absence of economic conflicts, physicians feel very comfortable ignoring unexpected and unlikely results. In the setting of workers compensation proceedings and litigation, where economic outcomes are implicit, physicians are often at a loss to explain their reasonable approaches. Elsewhere, evidence-based medicine seeks
54.5
TABLE 54.1 (Continued) Diagnostic tests Fourfold rise in antibody titers, culture from human samples, epidemiology Linkage strategies Same organisms from putative source and from patient, clinical pattern PCR similarity between organism from patient and from source Causes Aerosol dispersion, aspiration

PCR similarity between organism from patient and from source
consensus from a broad range of published literature to establish diagnostic and treatment guidelines. Such literature is often still missing for diseases related to indoor environments, as it is for much of occupational and environmental disease. This chapter will focus primarily on the management of building-related diseases and provide evidence where we recognize it.
Document Exposure
The discipline of industrial hygiene grew out of physicians needs to understand the exposures that made their patients sick and of engineers need to evaluate the control strategies underlying engineering processes. Since the early part of this century, a major goal in the field has been the definition of limits, criteria levels below which no adverse health effects were likely to occur. Setting such limits had as a consequence the development of evaluation methods, later also used for enforcement. Table 54.2 represents a compilation of exposure levels commonly used for the traditional occupational environment, for ambient environmental conditions, and for indoor environments. For building-related diseases, the exposures remain poorly defined for three reasons. First, the specific pertinent component remains unknown for many agents. Therefore, in hypersensitivity pneumonitis, it is unclear whether to measure for fungi with viable samplers (using culturable agents as the outcome), spore traps (using visible spores), immunological testing (in the absence of knowing which antigen), or biological assays such as endotoxin (which may trigger existing diseases without being the true cause). Second, even for diseases as clearly linked to environments with physiologic testing as hypersensitivity pneumonitis and asthma, the correct analytical methods are unclear. Because it is unclear whether only culturable (viable) particles are important for sensitization to fungal agents, and which components of other antigens, such as dust mites, are important, the appropriate analytical methods are unclear. Third, the best sampling approaches remain undefined. The exposures required for sensitization (duration, intensity, specific agent, and cofactors) or triggering of attacks are generally unknown, despite universal beliefs about the importance of dose-response relationships. Similar considerations arise for the spectrum of volatile organic compounds, for noise and vibration, and for other exposures in the indoor environment. For this reason, traditional industrial hygiene approaches (identification of the primary pollutant of concern, quantitative assessment, and comparison with a criterion level) have uniformly been unsuccessful in solving problems in the indoor environment. The evolution of building sciences
TABLE 54.2
Comparison of Guidelines and Standards Pertinent to Indoor Environmentsa Canadian (ref. C-23)
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WHO/Europe (ref. C-27) NAAQS/EPA (ref. C-9) SMAC NIOSH REL (ref. C-30) (ref. C-29) OSHA (ref. C-12)
0.081 ppm [30 m] 0.016 ppm 0.1 ppm [15 m] 0.75 ppm 2 ppm [15 m]
ACGIH (ref. C-1)

0.3 ppm [C]
MAK (ref. C-2)

0.5 ppm 1 ppm [5 m]
Formaldehyde
0.1 ppm [L] b 0.05 ppm [L]
Carbon dioxide
3,500 ppm [L]
5,000 ppm 10,000 ppm 5,000 ppm 5,000 ppm 30,000 ppm [15 m] 30,000 ppm [15 m] 30,000 ppm [15 m] 10,000 ppm [1 h]
Carbon monoxide
11 ppm [8 h] 25 ppm [1 h]
87 ppm [15 m] 52 ppm [30 m] 26 ppm [1 h] 8.7 ppm [8 h]
9 ppmg g 35 ppm [1 h]
50 ppm 200 ppm [C] 1500 [C]
35 ppm 200 ppm [5 m]
25 ppm
30 ppm 60 ppm [30 m]
Nitrogen dioxide
0.05 ppm 0.25 ppm [1 h]
0.2 ppm [1 h] 0.08 ppm [24 h]
0.05 ppm [1 y]
1 ppm [15 m]
1 ppm [15 m]
3 ppm 5 ppm [15 m]
5 ppm 10 ppm [5 m]
Ozone
0.12 ppm [1 h]
0.080.1 ppm [1 h] 0.050.06 ppm [8 h]
0.12 ppm [1 h] 0.08 ppm [8 h]
0.1 ppm [C]
0.1 ppm 0.3 ppm [15 m]
0.05 ppm 0.2 ppm [15 m]
0.1 ppm 0.2 ppm [5 m]
e Particles
0.1 mg/m3 [1 h]
5 mg/m3
3 mg/m3
2.5 MMADd e Particles
0.040 mg/m3 [L]
0.05 mg/m3 [1 y]
10 mg/m3
10 MMADd e Total particles
g 0.15 mg/m3 [24 h]
15 g/m3
Sulfur dioxide
0.38 ppm [5 m] 0.019 ppm
0.19 ppm [10 m] 0.13 ppm [1 h]
0.03 ppm [1 y] g 0.14 ppm [24 h]
2 ppm 5 ppm [15 m]
2 ppm 5 ppm [15 m]
2 ppm 5 ppm [15 m]
2 ppm 4 ppm [5 m]
Lead
Minimize exposure
0.51.0 g/m3 [1 y]
1.5 g/m3 [3 months]
0.1 mg/m3 [10 h] 0.05 mg/m3
0.05 mg/m3
0.1 mg/m3 1 mg/m3 [30 m]
Radon
2.7 pCi/L [1 y]
f 4 pCi/L [L]
2 ppm
4 ppm [5 m]
This table was prepared with Hal Levin for an appendix of Standard 62 (Ventilation for Acceptable Air Quality) and Guideline Project Committee 10 within the standards development process at the American Society of Heating, Refrigerating and Air-Conditioning Engineers. [ ] Numbers in brackets refer to either a ceiling or to averaging times of less than or greater to 8 hours (m minutes, h hours, y year, C ceiling, L long-term). Where no time is specified, the averaging time is 8 hours. a The values summarized in this table include the following:
G G
Canadian. Recommended maximum exposures for residences developed in 1987 by a committee of Provincial members convened by the federal government to establish consensus, guidelinetype levels. A revised version is being considered. These were not designed to be enforceable. They were designed explicitly for the residential environment. WHO/Europe. Environmental (nonindustrial) guidelines developed in 1987 by the WHO Office for Europe (Denmark). NAAQS. Criteria for outdoor air developed under the Clean Air Act by the U.S. EPA. The guidelines must, by law, be reviewed every 5 years, although this does not always occur. These levels are ostensibly selected to protect most sensitive individuals. Exposure level may vary by duration of exposure. Sensory irritation was not a consideration in establishing levels. NIOSH. Recommended maximum exposures for industrial environments developed by NIOSH (Centers for Disease Control). NIOSH criteria documents contain both a review of the literature and a recommended exposure guideline. Sensory irritation was not a consideration in establishing levels. These are not enforceable and not reviewed regularly. These levels are not selected to protect most sensitive individuals. OSHA. Enforceable maximum exposures for industrial environments developed by OSHA (U.S. Department of Labor) through a standard setting process. Once a standard has been set, levels can be changed only through reopening the rule-making process. These levels are not selected to protect most sensitive individuals. Sensory irritation was not a consideration in establishing levels. ACGIH. Recommended maximum exposures for industrial environments developed by ACGIHs Threshold Limit Values Committee. The committee reviews the scientific literature and recommends exposure guidelines. The assumptions are for usual working conditions, 40-hour weeks, and single exposures. These levels are not selected to protect most sensitive individuals. Sensory irritation was not a primary consideration in establishing levels. MAK. Recommended maximum exposures for industrial environments developed by the Deutsche Forschungs Gemeinschaft, a German institution akin to the National Academy of Sciences and Institutes of Health, without regulatory powers. Levels are set on a regular basis, with annual reviews and periodic republication of criteria levels. These levels are enforceable in Germany. These levels are not selected to protect most sensitive individuals. Sensory irritation was not a consideration in establishing levels. SMAC. Spacecraft Maximal Allowable Concentrations were developed by a Committee of Toxicology convened by the National Academy of Sciences. They were developed for prolonged exposure periods with consideration of continuous (24 hours per day) exposure. The Committee Report was funded by NASA. The four major questions to be considered in relying on the data from this table are as follows: Does the standard aim to prevent the effect of concern in the setting in which it is being used? Does the standard recognize the presence of susceptible groups or address the normal population? Are interactions between various contaminants of concern considered? Are the assumptions and conditions set forth by the standard met (such as 8-hour day, 40-hour workweek)?
G G G G
At times, the selection of a specific target level is best made by a team with wide experience in toxicology, industrial hygiene, and exposure assessment. level of .05 ppm because of its carcinogenic effects. Total aldehydes limited to 1 ppm. As one example, readers should consider the applicability of carbon monoxide concentrations. The concentrations considered acceptable for nonindustrial, as opposed to industrial occupational, exposure are substantially lower. This is due to the recognition that individuals with preexisting heart disease may develop exacerbation of heart disease at levels below 15 ppm. d MMAD mass median aerodynamic diameter in microns (micrometers). Less than 2.5 m are considered respirable; less than 10 m are considered inhalable. e Nuisance particles not otherwise classified, not known to contain significant amounts of asbestos, lead, crystalline silica, known carcinogens, or other particles known to cause significant adverse health effects. f The U.S. EPA has promulgated a guideline value of 4-pCi/L indoor concentration. This is not a regulatory value but an action level where mitigation is recommended if the value is exceeded in long-term tests. g Not to be exceeded more than once per year.
b Target c
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TABLE 54.2
Comparison of Guidelines and Standards Pertinent to Indoor Environmentsa
Continued
54.8
ASSESSING IAQ
has led to the need to review building plans, initial design and construction logs, commissioning strategies, operations and maintenance logs, and renovation work in an attempt to identify likely sources associated with the outcome of concern.

Linkage Linkage between diseases and exposures may occur on the basis of three theoretical considerations (Brennan 1987). The presence of all three is most convincing, but lesser evidence suffices for most purposes. Epidemiology. Epidemiologic linkage criteria are widely recognized (Bradford Hill 1965). Nevertheless, they presuppose that adequate numbers of epidemiologic investigations have been completed, using the outcome of interest as an endpoint, and that these measured the pertinent exposures. Such epidemiologic evidence exists to support the association of nonspecific symptoms such as headaches or mucosal irritation with large office buildings or with formaldehyde offgassing from ureaformaldehyde foam insulation. It generally does not support more serious conditions such as asthma or hypersensitivity pneumonitis. Toxicology. Linkage based on toxicologic considerations assumes the presence of research generally conducted on animals, usually with markers of exposure and effect. Most toxicologic documentation relies on some marker of exposure or effect, validated on an individual level, which exists only for infectious disease, carbon monoxide, and some pesticides. These allow treating physicians to document the same effects and markers in humans. For some rare phenomena, such as headaches associated with carbon monoxide poisoning, pesticide poisoning after misapplication, or hemorrhagic pneumonitis after exposure to Stachybotrys chartarum and Aspergillus versicolor, at least some mechanistic evidence exists, either in animal or in human studies. Other effects, such as formaldehyde causing irritation, are easily recognized. Still, in individual cases, linkage is difficult. Clinical Models. Finally, in the absence of generalizable evidence, clinical findings may be quite persuasive. The use of lung function tests to document worsening of disease in a specific environment, such as is possible in asthma, may be quite persuasive to physicians even though professionals from other disciplines may fail to understand the significance of such results. Such approaches have been used for unusual conditions for which no other linkage strategies are available. Clinical Practice: The Sentinel Events Model. A fundamental belief of practitioners of occupational and environmental medicine is that single cases of disease related to an exposure represent sentinels, markers for an exposure, an exposed group that requires followup, and a cause that may be remediated. The sentinel health events mode of practice is fundamental to the good practice occupational and environmental medicine. Failure to seek further cases of disease in this setting is considered inappropriate practice. As discussed under exposure assessment, once dose-response relationships and sampling strategies have been defined clearly for specific exposures, practitioners may use measured levels to develop knowledge of causal relationships. In the built environment, practitioners must rely on checklists, understanding of complex systems and their design and operations problems, and maintenance failures to interpret symptoms and diseases. Often, this leads to outbreak investigation approaches of screening for similar disease in a population, comparison of symptom or disease rates in a control population, and attempts to approximate exposure differences or surrogates for likely mechanisms of disease.
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54.9
Management Plans Standard medical treatment exists for many of the diseases attributed to indoor environments. Infections such as tuberculosis or Legionnaires disease must be treated with antibiotics. Asthma usually requires medical treatment with anti-inflammatory agents. Mucosal irritation may benefit from local treatment. In parallel to medical treatment (i.e., of the affected individual), treatment involves some considerations of exposure control, either through removal from work or through workplace intervention (Bracker 1999). Decisions to remove individuals from further exposure are appropriate to support symptomatic improvement, to prevent acute attacks of a disease, and to prevent long-term progression of disease. The medical and scientific literature suggests that the psychological components of disease are as important in clinical improvement, rehabilitation, and return to work as objective measures of organ function. A first major step for all health care providers is then the negotiation with patients about disease for clinical improvement. The usual steps in a sometimes complicated dance are as follows:
G G G G G

Showing respect Educating the patients Negotiating around differing sets of beliefs Defining obstacles Agreement on a plan In the absence of these steps it is unlikely that, at least in subjectively severe cases, patients will improve dramatically, even if their objective evidence of disease resolves. The first step is often simply the expression of sympathy and the willingness to listen to the patients story. Cutting off the story line, interrupting the patient early on, and downplaying the severity of the problem are likely to impede a strong relationship. After completing the more traditional medical activities (history taking, physical examination, lab testing, obtaining a diagnosis), physicians must educate patients. During such discussions, the knowledge of exposures, systems, dose-response relationships, causal relationships, and the limits of knowledge and uncertainty must be addressed. Often patients will have read widely and sometimes have belief systems that differ from the traditional scientific approaches of physicians. When conflicts in belief systems cannot be resolved, providers and patients must negotiate a strategy to move forward despite these beliefs. This may identify obstacles that may be resolved in the course of discussions with other involved parties. The implementation of environmental solutions to indoor environmental problems may require participation of additional parties: landlords, building owners or managers, maintenance contractors, cleaning personnel, school boards, and other groups with little familiarity with health considerations. Each of these may have a personal and differing set of beliefs that requires a process similar to the one outlined above. Developing a management plan requires disseminating information appropriately, developing consensus (or defining the level by which a solution may be forced), and documenting the benefits of solutions. In general, communication strategies that avoid laying blame, that offer solutions, and that suggest mutual ownership of the problem are most helpful. Obtaining as much certainty about the actual cause of disease as possible, for example through dynamic physiologic testing, allows health professionals far greater certainty in their initial contacts with employers, building owners, and other nonmedical personnel. Such greater certainty appears to be associated with the greater likelihood of persuading those parties of the severity of the problem, of the credibility of the professionals involved, and of the likelihood of successful intervention.
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ASSESSING IAQ
54.2 LUNG DISEASE TESTING

Several tests may be used for lung disease. These include spirometry, which measures the amount of air exhaled in timed volumes. Forced vital capacity (FVC) is the total amount of air breathed out, and forced expiratory volume in the first second (FEV1) is the timed volume after 1 second. Their ratio (FEV1/FVC ratio) represents a better indicator of airways obstruction (asthma, chronic obstructive pulmonary disease), that is, blockage in breathing out, than the FEV1 alone. A flow-volume loop measures forced in- and expiratory maneuvers and can distinguish an obstruction in the chest (e.g., asthma) from upper airways obstruction (e.g., laryngeal spasm associated with hoarseness and laryngitis). Lung diffusing capacity (DLCO), measured in several different ways, can document the decreased ability of the circulation to transport oxygen efficiently and is most commonly used as an indicator of oxygen diffusion across the lungs. Static lung volumes, total lung capacity (TLC), and functional residual capacity (FRC) are taken as evidence of reduction in the amount of air in the lung, as occurs in diffuse inflammation and stiffening of the lung tissues. Measured values are compared with a set of normal values, obtained from large groups of individuals (of which there are approximately 20 different sets), taking into account gender, age, height, and, sometimes, ethnic derivation because of anthropomorphometric differences. For all of these, common clinical usage holds that results of less than 80 percent of that predicted represent likely clinical abnormalities. As results approach 70 percent of that predicted, that certainty grows. Decreases in FVC, DLCO, TLC, and FRC are used as indicators of the restrictive lung disorders; decreases in FEV1 with a preserved FVC or FEV1/FVC ratios are taken as evidence of obstructive disease. Dynamic comparison of such tests may be undertaken in the laboratory or in the field. Provocation with nonspecific irritants, such as methacholine, may document airways hyperreactivity (twitchiness), usually considered evidence of asthma. Specific provocation with immunologically active agents, such as bioaerosols, may be used to document asthma or hypersensitivity pneumonitis, although such undertakings are often quite expensive. This assumes one has identified the correct antigens. Similarly, evaluation of lung function before and after exposures at work, whether on a single day, single week, or several weeks, is useful to document associations when no specific agent has been identified, purified, and characterized.

54.3 INTERSTITIAL LUNG DISORDERS
The interstitial lung diseases (ILDs) occur at a prevalence rate of about 70 per 1,000,000 persons and an incidence of 30/1,000,000 person years (Coultas 1994). Less than 3 percent of these represent hypersensitivity pneumonitis (HP), the disease most clearly associated with moisture and mold and widely acknowledged as the most likely disease to be building related when it occurs. Approximately 5 percent of these represent other work-related ILDs, such as asbestosis and silicosis, 5 percent represent sarcoidosis, and the remaining 80 percent represent diseases with recognized clinical characteristics but unknown causes. Hypersensitivity Pneumonitis Since the report of Fink (1971), hypersensitivity pneumonitis has been recognized as a consequence of contaminated ventilation systems. Outbreaks are associated with moisture in
54.11

Diagnostic Strategies/Linkage. After an initial history and physical examination, appropriate tests may suggest the presence of disease. Physicians are then left with the question of how to link disease to exposure. This often occurs through temporal linkage. A first step may be to evaluate individuals ability to return to work with a trial of removal and reexposure because this may show work-related decrements. Individuals may demonstrate major improvement in lung function even when tests are within the normal range when exposure ceases, so following tests dynamically over time appears useful. The presence of potential sources at work or at home makes this more likely (Table 54.3). Some authors find antibody testing useful despite old scientific literature documenting its frequent futility.
large buildings (Anonymous 1984) and with moisture in the home (Kreiss and Hodgson 1984). Population-based data suggest that between 1 and 4 percent of randomly selected office workers describe symptoms consistent with hypersensitivity pneumonitis, also consistent with organic dust toxic syndrome (ODTS, discussed later). The disease occurs on the basis of cell-mediated immunity, although several other components such as cytotoxicity may play a role. The disease may present in two different temporal patterns and varying degrees of severity. It may present acutely, with feverishness, chills, muscle aches, and chest symptoms of coughing and shortness of breath, often resembling an infectious pneumonia. This pattern generally leads to the recognition of a specific exposure. On the other hand, patients may present with insidious onset of fatigue and some shortness of breath without coughing. As the disease grows more severe, patients generally feel more ill. Cases have been documented with lung biopsy after patients simply felt very tired and nauseous, with chest symptoms arising only on strenuous exercise (Rose et al. 1998). Such disease is almost always completely reversible. On the other hand, patients may present with an acute pneumonia requiring hospitalization in intensive care units and may undergo biopsy, documenting characteristic lesions. Repeated episodes, and persisting exposure, are associated with worse prognosis, including with long-term persisting decreases in lung function. Once fibrosis is evident on chest x ray, full recovery is unlikely. Differing clinical traditions held that all patients with interstitial lung disease require a biopsy, if only for the determination of prognosis, whereas others have felt comfortable with clinical tests alone. With the spread of managed care, biopsies appear to be undertaken less frequently. This controversy has increased as more recent outbreaks have identified disease earlier on biopsy without any objective evidence of disease on usual clinical tests. The usual clinical tests include spirometry, lung volumes, and lung diffusing capacity for documentation of physiologic abnormalities; chest x rays (CXR), gallium scanning, and thin section (high resolution) computerized tomography for imaging (HRCT); and bronchioalveolar lavage (BAL) and lung biopsies for documentation of anatomic characteristics and inflammatory markers. The characteristic physiologic abnormalities include decreased FVC, DLCO, TLV, and FRC. Early on, patients may have evidence of abnormalities only on exercise testing (treadmill). When disease is clinically severe, almost all patients will show abnormalities. When disease is identified early, before irreversible scarring has occurred, such tests are often still normal. Characteristic abnormal results on imaging include diffuse uptake on gallium scanning, ground glass appearance on HRCT, and alveolar and interstitial changes on CXR. HP is increasingly recognized without abnormal CXRs (Hodgson 1989, Lynch et al. 1992, Rose et al. 1998), HRCTs (Lynch et al. 1992, Rose 1998), or gallium scans (Lynch et al. 1992). Transbronchial biopsy remains the gold standard of diagnosis, but up to 10 forceps bites may be needed for an identification rate of over 90 percent. Antibody testing (IgG) is often undertaken but has been shown to have very little utility (Burrell and Rylander 1981) in the diagnosis of disease although it is often considered a reasonable marker of exposure.
54.12
ASSESSING IAQ
TABLE 54.3 Causes of Hypersensitivity Pneumonitis HVAC systems Leaf mold contaminating inlet filters Contamination of filters Contamination of mixing plenum Standing water in drain pans with contamination Contamination of water reservoirs used for humidification

Building envelope Roof leaks (membranes, flashing) Below-grade moisture incursion Wall penetration
Prognosis and Surveillance. Often, patients have been unable to return to work (or their home) even after intervention that appeared successful based on disappearance of visible bioaerosols. It remains unclear whether more rigorous cleaning would solve such problems or whether buildings have some ecological characteristics that lead to the persistence of antigens. Few data have attempted to follow actual exposures, symptoms, and recurrence in buildings. At times patients have been able to return to the offending location. No long-term studies document that this may occur without deleterious consequences. It is therefore worth implementing a formal surveillance program in an attempt to document recurrence persistence of recovery. In general, symptoms are likely to recur if patients disease recurs. Greater reliance should be placed on symptoms than on objective testing, particularly as diffusing capacities and lung volumes tend to be far more variable than spirometric indexes. Long-term disability evaluation follows standard clinical practice. In general, exercise testing is the most suitable objective test for the documentation of residual abnormalities.
Other Forms of ILD
Increasing evidence suggests that other forms of interstitial lung disease may be associated with work in buildings. For each there is anecdotal evidence, either in case reports or in outbreaks of disease. Only for asbestosis is there planned, generalizable research.
Asbestosis. Cases of asbestos-related interstitial lung disease (i.e., asbestosis) are associated with work indoors for electricians, plumbers, carpenters, and other building trades. These exposures are no different than for similar occupations working outside of public access buildings. Teachers and other building occupants, such as children, who have no sustained contact with disturbed asbestos are usually not considered at risk. Two recent reports suggest that there may be very rare exceptions to this rule (Anderson et al. 1991, Lilienfeld 1991). The diagnosis of asbestosis is made on the basis of long-standing (i.e., usually years of daily exposure) exposure to asbestos and evidence of interstitial lung disease on radiographic studies. Although lung biopsy will show characteristic asbestos bodies or provide fiber counts indicating substantial exposure, these are usually considered unnecessary. Sarcoidosis. In general, sarcoidosis is thought likely to have some identifiable etiology (Newman et al. 1996). Evidence of moisture in basements (musty odor or floods) or mold
54.13
growing on bathroom walls is associated with sarcoidosis (Ortiz 2000). Recent reports of HP, initially diagnosed as pulmonary sarcoidosis (Thorn 1997, Forst 1994) have suggested, as have prior studies, some difficulties distinguishing these sarcoidosis from hypersensitivity pneumonitis in clinical practice. Usual Interstitial Pneumonitis. Usual interstitial pneumonitis (Mullen et al. 1998) may be associated with moisture in basements. Additional case-control studies have suggested that ILDs are associated with exposure to a range of bioaerosols, including wood, grains and hay, and farm animals (Iwai 1992, Scott 1991, Baumgartner 2000). At least one case report of nonspecific interstitial pneumonitis, distinct from HP, associated with a myopathy and antibody responses similar to HP, has been attributed to Aspergillus exposure (Lonneux et al. 1995).

Organic Dust Toxic Syndrome. Some evidence exists that office workers may develop yet another form of interstitial pulmonary response, possibly more frequently than commonly assumed, called an organic dust toxic syndrome, the same disease as humidifier fever. Beginning with C. A. C. Pickerings search for humidifiers as a cause of symptoms among office workers (Finnegan 1984), excess rates of chest tightness and flulike illness have been seen in buildings with humidification (Finnegan et al. 1984), HVAC systems with water (Burge et al. 1987), and buildings with moisture problems (Sieber 1997). Data from a Dutch study of office workers suggested a tripling of symptom rates associated with a tenfold increase in airborne endotoxin concentrations (Teuuw and Vandenbroucke 1994). A reanalysis of several older data sets (Apter et al. 1997) suggested that a symptom cluster of chest tightness, difficulty breathing, and flulike illness was distinct from those of mucosal irritation, central nervous system symptoms, and skin irritation. Although this syndrome is considered benign and self-limited, there is some evidence for impairment of lung function after long-term exposure or more severe illness (Milton 1966, 1996, 1997).
54.4 ALLERGIC AIRWAYS AND UPPER AIRWAYS DISEASE

Asthma
Between 5 and 8 percent of the U.S. population have asthma. In adults, about 20 per 100,000 persons will develop new onset asthma from their workplace (Milton 1998) and at present approximately 15 percent of these (between 0.5 and 1 percent of the U.S population) are thought to have occupational asthma (Venables and Chan-Yeung 1997). According to reports to the Health Departments in Michigan and Massachusetts (Kreiss 1999), where occupational asthma is a reportable disease, about 20 percent of workrelated asthma reported in the last years appear related to buildings relying on SENSOR criteria (Matte et al. 1990). Only one outbreak of building-related asthma has been described (Hofman et al. 1993). Jajoski et al. (1999) suggest that approximately 10 percent of work-related asthma reported to state departments of health in 19921993 was attributed to office buildings. More recently, substantially greater proportions appear to be building related (Gassert et al. 1998). Nevertheless, in support, in a recent series of NIOSH building investigations, chest symptoms appeared related to specific aspects of buildings operations including moisture and dirt and debris in the ventilation system (Sieber et al. 1996). This suggests that building-related asthma may in fact be much more common than recognized.
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Allergic Rhinitis Twenty to 30 percent of the U.S. population has complaints of a stuffy or runny nose, approximately half thought to be allergic rhinitis and some proportion of these are chronic irritation. Although the disease is clearly recognizable, no good linkage strategies have been developed for clinical use. Such symptoms among office workers are meanwhile thought to reflect both allergy and simple mucosal irritation. Few data allow estimation of a specific fraction due to either. Menzies et al. (1998) suggested that only 1 percent of nasal symptoms represented an allergic response to the work environment, although in general 20 to 30 percent of office workers describe regular nasal symptoms, and of these half appear at least temporally work related (Malkin et al. 1998). Studies of the upper respiratory tract suggest that at least some measures of effect, including cells in nasal lavage fluid, physiologic changes in the nose, and biopsy evidence (Koren et al. 1992, Ohm et al. 1993, Ohm and Juto 1993, Willes et al. 1992, Mlhave et al. 1993), are present when sought with sophisticated techniques. Similarly, challenges with specific substances are well known and widely accepted as accurate, although they are rarely performed and not widely available clinically. Individuals with atopic rhinitis often describe mucosal irritation in the office environment. It is clear that they experience irritation at lower levels of exposure than do nonatopics in controlled clinical trials (Kjaergard et al. 1985). In addition, their irritation thresholds may be substantially lower (Shusterman et al. 1998) even when they are not acutely ill. Whether this results from residual inflammation or represents some intrinsic characteristic of atopy remains unclear. The direct medical costs for allergic rhinitis are estimated at $1.8 billion (Malone et al. 1997). People with allergic rhinitis may lose several days of work per year or, for the period
Because linkage strategies for asthma are well developed, such reports can be rigorously evaluated. In addition to a careful history, the primary linkage rests on documentation of temporal relationships. Initial onset or recurrence of asthma after beginning work in a building, or exacerbation of previously stable asthma, may lead to suspicion of work relatedness. Linkage relies on examination of lung function at and away from work. Although peak expiratory flow rates are relatively easy to collect, they are often thought to produce insensitive (high rates of false-negative tests) results. Spirometry is the preferred technique but is often difficult to collect because of accessibility primarily through physicians offices. Commercially available portable diarying spirometers have recently become available and facilitate the collection of longitudinal data before, during, and after work to identify patterns of exacerbation at work and improvement over weekends. Although changes of 15 percent are considered diagnostic of asthma in laboratory settings, many physicians pursue further diagnostic testing with decrements of greater than 5 percent in the course of a day. The standard calculations for population attributable risk (or etiologic fraction) suggest that the population-attributable risk of asthma ranges from 13 to 26 percent for moisture in buildings, including homes and work places. Lost work time does not enter into such calculations. In fact, very few cases of occupational asthma related to buildings are recognized as such. Nevertheless, a Swedish study of office workers (Toren et al. 1991) suggested that those cases die more frequently of asthma than does the general population. Premature mortality costs are also not covered in direct medical benefits. Nevertheless, a follow-up study did not confirm this elevation. That means that of the $4 billion to $6 billion in annual medical costs, about $.52 billion to $1.56 billion of direct medical costs may be related to buildings. See Chapter 4 for a more complete discussion of indoor air quality health cost.
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Allergic Fungal Sinusitis Allergic fungal sinusitis is a third form of nasal disease that is at least potentially related to indoor environmental exposures. The frequency is at present unclear. Diagnosis is made through documentation of mucosal thickening on CT scan or other primary diagnostic procedures, the documentation of eosinophilic mucin in sinus drainage or biopsy material, and the presence of fungal organisms in those same materials (deShazo et al. 1997). Although the syndrome has been defined, no cases have been documented in the scientific literature as occurring because of exposures in the built environment. It is unclear whether fungal species present in the indoor environment are more likely to cause such disease or whether exposure in the workplace is any more likely to cause such disease than exposures elsewhere. The organisms associated with such disease, primarily Aspergillus species, are thought to occur more frequently where moisture problems occur indoors.
when they are symptomatic, have decreased productivity. Recent data suggest that at least some of this lost productivity may result from the choice of medications (Cockburn et al. 1999). Under the assumption that half of these cases are associated with work, based on questionnaire surveys, and under the assumption that these are associated with moisture indicators, population-attributable risks suggest an etiologic fraction of less than 6 percent for the workplace. At present, no specific diagnostic techniques have been described to link such disease to the workplace. It is possible to use the techniques outlined above to document changes at work, although the implementation of such studies is likely to be difficult for some techniques. One recent attempt to use acoustic rhinometry raised the question of allergies to cockroaches and molds being risk factors for work-related decrements in nasal function (Apter et al. 1997). Striking in that study was the rarity with which subjects who described work-related nasal symptoms actually described changes in nasal symptoms on a Monday at work.
54.5 MUCOSAL IRRITATION
The presence of symptoms alone is often unpersuasive as the basis for economic decisions, both in the clinical and the regulatory setting. The term nonspecific symptoms has been used to refer to such symptoms, implying the lack of specific mechanisms. This fails to acknowledge the distinction between irritant and allergically induced symptoms. In clinical settings, markers used in the diagnosis of mucosal irritation include decreased tear film break-up time, as an indicators of dry eyes, and punctate conjunctivitis, documented with lissamine green or fluorescein staining. In addition, in epidemiologic studies, fat foam thickness or canthal foam represent markers of susceptibility, markers of chronic effects, or mechanisms of disease that remain unclear. If these markers do not represent acute effects, they cannot be used in clinical linkage strategies. Punctate conjunctivitis, documented with lissamine green or fluorescein staining, represents an acute effect. Irritation is discussed in Chaps. 17, 25, and 26. Eye irritation is a common complaint among office workers and is thought to be by some the primary driver for interest in office worker complaints. The studies on mucosal irritation over the last 15 years by two groups of investigators are meanwhile well known. The work by Cain and colleagues (Cain 1996) has documented the predictable effects of volatile organic compounds on the irritant receptor in the eyes and nose. Complex mixtures of such agents are likely to cause more symptoms than are individual agents at low levels. Quantitative structure activity relationships suggest a predictable, dose-dependent
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54.6 HEADACHE
Headaches are a common complaint among office workers, often associated with subjective loss of productivity (Schwartz et al. 1997, 1998). Although attribution to buildings is a common approach, it is generally not a successful intervention for individuals, and a substantial proportion of headaches are attributed to the indoor environment without adequate characterization. Formal diagnostic approaches exist to identify the causes of headaches (ISSH 1993). Possible indoor environmental triggers and subsequent attribution to specific sources may lead to specific recommendations. On the other hand, identification of nonwork-related factors and appropriate interventions are equally important. Because headaches represent such a frequent cause of decreased work productivity, some employers have implemented workplace headache programs with some success (Schneider et al. 1999).
effect (Abraham 1996), at least for nonreactive, or relatively inert, compounds. This suggests that mucosal symptoms among office workers may represent simple irritation by commonly encountered volatile organic compounds. Work by Franck, Kjaergard, Skov, and Mlhave (Kjaergard 1992) suggests that complaints of eye irritation are measured reliably by different questionnaires, that there are physiologic indicators of eye irritation, and that at the very least subjects with those markers are at greater risk of eye irritation than subjects without. A primary hypothesis of this group of investigators is that volatile organic compounds indoors may change the physical characteristics of tear fluid and allow irritants to reach the mucosal surface in greater concentrations. See Chaps. 17 and 25. The work by Cain and colleagues (Cain 1996) has shed more light on the consideration that mucosal symptoms may represent simple irritation by commonly encountered volatile organic compounds. Individual agents are therefore clearly shown to have an irritant threshold, usually two to four orders of magnitude below established criteria such as Permissible Exposure Levels (PELs) set by the Occupational Safety and Health Administration, the American Conference of Governmental Industrial Hygienists, or other standard setting bodies. (See Chap. 20.) Diagnostic steps may include examination of the eyes using a slit lamp and the instillation of staining materials to determine dry eyes and punctate conjunctivitis. Limited clinical interventions are possible. A first important step is the explanation of the mechanism by which such symptoms arise. Second, the use of artificial tears often provides symptomatic relief. Finally, some limited evidence suggests that better cleaning, with lowering of particle levels, and humidification, especially where humidity levels are below 30 percent, may be helpful. Where bioaerosol contamination has been identified, remediation is appropriate.
54.7 INFECTIONS
Much interest in infections indoors has developed because of concerns that these might be transmitted through ventilation systems. These include human-source infections, such as tuberculosis, pneumococcal pneumonias, and viruses; infections emanating from building systems, such as Legionnaires disease from cooling towers or potable water systems; and infections from other sources such as animal research facilities. Outbreaks of tuberculosis in hospital settings are well known. Such ventilation-systemassociated clusters have also been reported for office workers (Nardell et al. 1991) and attributed to dysfunctional ventilation systems in jails (Steenland 1997, Cooper-Arnold et
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54.8 DERMATITIS
Contact is recognized as a common problem among office workers. This ranges from allergic contact urticaria, sometimes with asthma (Marx 1981, 1984), to skin irritation from dryness. A recent review suggests, nevertheless, that most of these symptoms actually represent simple mucosal irritation rather than allergy. Rare cases of vasculitis (palpable purpura) have been associated with photoactive copy paper (Tencati 1983). Recent interest has focused on whether low relative humidity is associated either with irritation alone or in combination with irritant exposures, such as volatile organic compounds. Close scrutiny of chamber studies shows that they clearly document mucosal irritation at levels below 20 percent (Andersen 1974). More recently, field studies have suggested that mucosal irritation increases as relative humidity drops below 35 percent (Nordstrom 1994).
al. 1999). Outbreaks of animal-source diseases, such as Q-fever or histoplasmosis from pigeon droppings, have been attributed to entrainment into ventilation systems (Kreiss and Hodgson 1984). At least one outbreak of pneumococcal pneumonia has been attributed to crowding in jails (Hoge et al. 1994), although this was thought due to person-to-person transmission. Similarly, viral epidemics of highly contagious agents such as chicken pox and measles have occurred through dissemination through ventilation systems. More interest has arisen recently about whether common respiratory tract viruses, primarily rhinoviruses, are likely to cause excess preventable respiratory tract disease among office workers that may be reduced by changes in ventilation rates (Fisk and Rosenfeld 1997), although they do not distinguish between the viruses that may and those that may not be transmitted through droplet aerosols. Older literature supported hand-to-hand transmission through secretions and suggested both experimentally and in-field studies that this was a more effective form of transmission than the airborne route (Gwaltney 1988, 1989). At the same time, experimental evidence suggested that droplet transmission might in fact contribute to the burden of disease (Dick et al. 1987). Because of the known associations with emotional states and fomite transmission, the importance of this mode A field study in barracks appeared to support this hypothesis although no data on ventilation or air exchange rates was available (Brundage et al. 1988). Even if disease is transmitted through droplets, reduction in frequency through general dilution ventilation may not come cheaply because of the inefficiency of general dilution ventilation in reducing local exposures (Nardell et al. 1991), nor may it intervene on the disease burden associated with emotional states.
54.9 MISCELLANEOUS DISORDERS
The built environment is put to many uses, so it is impossible to predict all of the potential exposures and diseases that may occur. Mixed-use buildings are those with work processes that are not just restricted to traditional office work. Printing shops, auto body shops, and dry-cleaning establishments may contribute to the levels of volatile organic compounds in offices. Garages, loading docks, and fossil-fuel-powered floor buffers may contribute to carbon monoxide levels. Other processes indoors may lead to problems. Organophosphate poisoning has been attributed to entrained organophosphates (Hodgson 1987); such events may be more frequent than commonly assumed (Muldoon 1993). Emissions from architectural blueprint
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ASSESSING IAQ

Work Stress Consistently, in cross-sectional studies, measures of work stress are associated with indoor environmental symptoms (Mendell 1993). This is true whether questionnaires simply asked ratings of work stressfulness or used formal validated work stress questionnaires. The scientific community generally agrees that work stress must be viewed as an effect modifier. That is, it may make the perception of irritation worse, but it will not lead to the perception of irritation without the presence of irritants. This does stand in contrast to some work in experimental psychology that suggests symptoms may arise without underlying causes but simply from expectation. In a case-control study, Eriksson (1996) suggested that control over work was the single most important factor. In any case, work stress is amenable to intervention. Two component models of work stress argue that only job demands and the control over work are important in workers perception of stress. Three component models include personality style and characteristics as components. The first implies an organizational analysis and identification of possible intervention strategies focused solely on the workplace factor. This would imply the need for management training in better supervisory practices. The second argues for the importance of scrutiny of the individual person, the environment, and the fit of the two. Solutions would then include focusing on the individual, including reeducation, personal stress management techniques, and coping skills. A more sophisticated view of work stress that argues that educating both workers and management about building needs and appropriate behaviors is appropriate risk communication, stress management, and good worker education practice. Such education could then focus on management and worker styles, address the recognized limitations of the current complex systems in the office, and lead to changed expectations. See Chap. 55 for more detail. A lesson may also be learned from the world of hazardous waste sites, community outrage, and public health. The needs of communities, their perception of pollutedness, and their intellectual dependency on regulatory agencies, outside exports, the media, and other forces beyond their control lead to major distress on their part. Over the last several years, a set of guidelines has evolved to help such communities recover. These include listening to the concerns of the affected individuals, respecting their sense of priorities and importance, and developing agendas that respect both the publics and professionals perceptions of needed action.
machines have been associated with palpable purpura, a form of blood vessel allergy (Tencati 1981). Carbonless copy paper has been associated with contact urticaria and asthma (Marx 1986), although the majority of complaints attributed to this exposure are considered to represent simple mucosal irritation (NIOSH 1999). Equally important, physical conditions indoors may lead to comfort problems. The combination of high indoor temperatures and low water consumption among teachers has been associated with mild heat illness presenting as headaches and fatigue. Transmitted vibration from mechanical building systems has been associated with headaches, dizziness, and irritability (Hodgson 1987). When strong suspicion arises about potential building relatedness of complaints, very thoughtful approaches may be required to identify true causal connections.
54.10 THE RESIDENTIAL ENVIRONMENT
The residential environment poses a broad set of hazards to adults and children, ranging from safety hazards with resulting injuries through planned emissions of pollutants, such
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54.11 CONCLUSIONS
Buildings provide shelter from the elements. Nevertheless, inadequate attention to building systems, in their design, operation, and maintenance, may induce a broad range of diseases. Many of these are widely recognized as diseases but often not clearly attributed to the true source, so disease progresses. Only cooperation between engineers, industrial hygienists, and health care providers allows the identification and remediation of problems and the maintenance of a healthy environment.
as oxides of nitrogen and carbon monoxide from cooking and heating appliances through problems generated in construction, operations, and maintenance of homes. Over the last 10 years, the residential environment has been recognized as a contributor to two primary health effects that are directly attributable to the home, distinct from the injuries and acute pesticide poisoning associated with homes. These conditions include respiratory tract disease associated with moisture and bioaerosols and carbon monoxide poisoning. This chapter will not deal with the more recent literature on combustion products and childrens asthma, including oxides of nitrogen. Nevertheless, the use of unvented space heaters appears to pose a similar risk for asthma. The literature on environmental tobacco smoke and asthma will not be recapitulated. Beginning in 1988, Strachan suggested that home dampness is associated with respiratory tract symptoms. After an initial review of published studies in 1991 (Spengler 1992) suggesting a consistent though small increase, subsequent reviews (Cooper-Arnold 1997) have suggested that this effect is consistent. Dales et al. (1998) have recently identified not only respiratory tract symptoms but also white cell activation. Measures of association are stronger in studies with better measures of exposure. It remains unclear whether this effect is mediated solely through known antigens, such as dust mites, fungal allergens such as Aspergillus and Penicillium, or also from nonspecific bioaerosol mass. The prevalence of moisture problems is controversial, although some groups have identified a substantial number of houses as potential contributors to disease (Nevalainen et al. 1998). Lawton et al. (1998) have suggested that moisture flow through houses is the single best predictor of the total bioaerosol load. A recent Institute of Medicine publication emphasizes the importance of moisture and the building envelope for at least childrens asthma. Residential carbon monoxide poisoning has become common. Series of investigations suggest that problems arise from improper venting of fossil fuel appliances or from entrainment of carbon monoxide. Retrofitting homes with increased insulation, such as through the use of plastic sheathing over windows, construction of basement enclosures around furnaces and boilers, and simply increased envelope tightness (Pandian et al. 1993, Conibear et al. 1996) may contribute to the problem. Entrainment has been attributed primarily to garages and migration through doors and from the use of charcoal grills (Liu et al. 1992). A final important cause is the use of small appliances in enclosed space. Even the use of adequate ventilation according to manufacturers recommendations may be inadequate to prevent CO poisoning. A recent study (Earnest et al. 1997) documented that air exchange rates are simply inadequate indoors even with dedicated ventilation.
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CHAPTER 54

Co py rig hte dM ate ria l

54.2 TABLE 54.1 Disease Categories Disease Rhinitis, sinusitis Symptoms

Mechanisms Allergy (IgE)

Co py rig hte dM ate ria l

Stuffy or runny nose; postnasal drip; sinus congestion; nosebleeds

Reversibility of obstruction with bronchodilators

Cough, shortness of breath, muscle aches, feverishness

Pharmacologic irritant Type IV allergy (cellmediated immunity)

Inspection, RAST or skin price

Conjunctivitis (irritant) CNS toxicity

Eye irritation, dryness, tearing

Headaches, cognitive impairment

Carbon monoxide VOCs

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Co py rig hte dM ate ria l

54.1 GENERAL APPROACHES

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py rig hte dM ate ri

ACGIH (ref. C-1)

MAK (ref. C-2)

0.1 ppm [L] b 0.05 ppm [L]

3,500 ppm [L]

87 ppm [15 m] 52 ppm [30 m] 26 ppm [1 h] 8.7 ppm [8 h]

50 ppm 200 ppm [C] 1500 [C]

35 ppm 200 ppm [5 m]

30 ppm 60 ppm [30 m]

0.05 ppm 0.25 ppm [1 h]

0.2 ppm [1 h] 0.08 ppm [24 h]

3 ppm 5 ppm [15 m]

0.080.1 ppm [1 h] 0.050.06 ppm [8 h]

0.12 ppm [1 h] 0.08 ppm [8 h]

0.1 ppm [C]

0.1 ppm 0.3 ppm [15 m]

0.05 ppm 0.2 ppm [15 m]

0.1 ppm 0.2 ppm [5 m]

2.5 MMADd e Particles

0.040 mg/m3 [L]

10 MMADd e Total particles

g 0.15 mg/m3 [24 h]

0.38 ppm [5 m] 0.019 ppm

0.19 ppm [10 m] 0.13 ppm [1 h]

0.03 ppm [1 y] g 0.14 ppm [24 h]

2 ppm 5 ppm [15 m]

2 ppm 5 ppm [15 m]

2 ppm 5 ppm [15 m]

1.5 g/m3 [3 months]

0.1 mg/m3 [10 h] 0.05 mg/m3

0.1 mg/m3 1 mg/m3 [30 m]

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py rig hte dM ate ri

Comparison of Guidelines and Standards Pertinent to Indoor Environmentsa

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