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Indoor Allergens: Assessing and Controlling Adverse Health Effects 2 Magnitude and Dimensions of Sensitization and Disease Caused by Indoor Allergens The magnitude and dimensions of a disease or its antecedents can be measured and described in several ways (Table 2-1). The prevalence of a disease, for example, is a measure of its frequency in a population at some specified point in time. The incidence of a disease is the number of new cases of the disease that occur during a specified period of time. Exploration of disease incidence can focus public health attention on critical time periods in the development of disease. For example, the observation that allergy often develops by age 5 suggests that interventions are needed for infants and young children. Incidence and prevalence rates can be determined for the entire population, or they can be specified by gender, age, ethnic group, socioeconomic class, geographical region, or time of year. The increased mortality from asthma among African Americans (Sly, 1988; NHLBI, 1991), for instance, has focused attention on the disease in this segment of the population. Community-based epidemiological studies and national health surveys provide the best available estimates of the overall prevalence of immunologic sensitization and of specific diseases. Disease severity—a measure of the impact of a disease on a patient's life, the intensity of medical care required, and the ultimate outcome—is another indicator of the magnitude and dimensions of a particular disease. Measures of disease severity are often derived from national mortality data and hospital discharge statistics. They are used to evaluate the effectiveness of therapeutic regimens, environmental control strategies, and educational and behavior modification self-management programs.
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Indoor Allergens: Assessing and Controlling Adverse Health Effects TABLE 2-1 How Diseases Can Be Measured Question Appropriate Measure How many people have asthma sometime in their life? Cumulative prevalence How many people have asthma in the United States today? Current prevalence How many people get asthma when they are children? Age-specific incidence rates Do children have more asthma than adults? Comparison of prevalence rates for specific age ranges Does allergy have a role in asthma? Comparison of the probability of developing asthma among people with and without skin test reactivity What proportion of asthma is attributable to allergy? Attributable fraction What proportion of asthma in children is attributable to house dust mite exposure? Attributable fraction Generally speaking, mild disease causes symptoms but only intermittently requires medication and infrequently alters life activities. Moderately severe disease may require regular physician visits, regular medication, and lost time from work or school. Severe illness may require admission to an intensive care unit, to a regular medical floor, or to a hospital emergency room (in decreasing order of intensity). In the case of allergic disease, death occurs relatively infrequently. Other measures that can be used to indicate the magnitude and dimensions of a particular disease (such as allergy) include quality of life, trends over time, and economic and psychosocial impact. This chapter uses these and other measures to discuss the magnitude and dimensions of two aspects of allergic disease: sensitization and the specific allergic diseases themselves. Immunologic sensitization is important because it is an indicator of the population at greatest risk of developing allergic disease. The remainder of this chapter discusses the public health significance of immunologic sensitization and allergic disease in these terms. IMMUNOLOGIC SENSITIZATION Allergic disease develops through a series of steps that are becoming more clearly understood (Figure 2-1). As described briefly in Chapter 1, allergic disease occurs when a genetically predisposed or susceptible individual is exposed to an allergen and becomes immunologically sensitized. The occurrence of different types of sensitization can be ascertained by skin
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Indoor Allergens: Assessing and Controlling Adverse Health Effects FIGURE 2-1 Development of allergic disease, illustrated schematically. A genetically susceptible individual is exposed to an allergen and becomes immunologically sensitized. At this stage the person is asymptomatic, but the sensitization may be detected by skin tests or laboratory tests. Over time, a proportion of sensitized individuals will develop one of a group of allergic diseases. Exposure to allergen is understood to be a major factor at each stage of the pathogenesis of these diseases. tests, serologic measurements, or tests of cell function. In the early stages of sensitization, people who are sensitized have not developed symptoms of disease. The magnitude of this group within the population is of interest, however, because it reflects the proportion of the population at greatest risk of developing allergic disease. Additional exposure to the sensitizing allergen leads to the development of an allergic reaction (disease) that can be mild, moderate, or severe, depending on the amount of exposure. Exposure to other substances that might irritate the respiratory tract (e.g., environmental tobacco smoke) can serve to promote the development of allergic reactions and disease. Skin testing has been the primary diagnostic tool for allergy for over 100 years. Skin test reactivity (i.e., a positive skin test, also known as atopy) indicates that an individual has been immunologically sensitized and now has specific immunoglobulin E (IgE) antibody against one or more common allergens. The presence of skin test reactivity indicates an increased risk for one of several diseases including allergic rhinitis and asthma, but at the time skin test reactivity is detected, disease may or may not be present. Table 2-2 shows results from several studies that measured sensitization
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Indoor Allergens: Assessing and Controlling Adverse Health Effects prevalence in various populations. The results indicate a range from a low of 20 percent to a high of 51 percent in different studies. It is estimated that about 40 percent of people in the United States have been immunologically sensitized as indicated by skin test reactivity to a panel of currently available allergens. The recent International Consensus Report (NHLBI, 1992) claims that about 30 percent of all populations are skin test positive. Early childhood is a common time for sensitization. Barbee and others (1987) showed that 22 percent of a cohort of children less than 5 years old had skin test reactivity to one or more allergens. During an 8-year follow-up, the prevalence increased to 44 percent. Gergen and coworkers showed that 18 percent of Caucasian and 28 percent of African American children showed skin test reactivity when tested between the ages of 6 and 11 (Gergen et al., 1987). In a cohort of genetically susceptible children, 20 percent developed skin test reactivity by age 5; another 20 percent became reactive between ages 5 and 11 (Sporik et al., 1990). Skin test reactivity increases in prevalence until age 20–45 and then decreases (Figure 2-2; Barbee et al., 1976, 1987; Gergen et al., 1987). In most studies, skin test reactivity is similar for both sexes, although men have more total IgE (Barbee et al., 1976; Burrows et al., 1980; Klink et al., 1990). Although immunologic sensitization is generally stable over time, small seasonal variations have been observed (Peat et al., 1987). Prevalence rates of sensitization also increase somewhat with the use of a greater number of allergens during testing (Barbee et al., 1987). Table 2-3 and Figure 2-3 show estimates of the prevalence of sensitization in certain population samples to specific allergens as determined by skin test reactivity. Among Australian schoolchildren, for example, sensitization to house dust mite was shown to be most common, followed by grass and weeds, animal danders, and molds (Peat et al., 1987). Similar rates of sensitization have recently been found in middle-class American children. The prevalence of cockroach allergy shown in Figure 2-3 may well be higher in selected populations, such as among residents in cities in which cockroach infestations are widespread. A study of patients visiting an emergency room in Virginia showed that 5 percent of nonasthmatics were sensitized to cockroaches, compared to 33 percent of asthmatics (Pollart et al., 1989). Fifty-four percent of patients referred to a Kansas City clinic for possible allergic disease were sensitized to cockroach allergen (Hulett and Dockhorn, 1979). Risk Factors In keeping with a public health approach to prevention and control of allergic disease and the need to improve the understanding of the etiology,
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Indoor Allergens: Assessing and Controlling Adverse Health Effects TABLE 2-2 Partial Listing of Published Data on the Prevalence of Skin Test Reactivity Source Population %a Notes United States Barbee et al., 1987 Community sample (N = 1,333; Arizona) 39 51 Ages 8–60 Rates with retesting 8 years later Gergen et al., 1987 Nationwide sample (N = 16,204; NHANESb) 20.2 Some people with disease were excluded; the skin test flare was used as the response Freidhoff et al., 1981 Workplace study (N = 174; Maryland) 24 Lower rates are seen in other workplace studies Barbee et al., 1976 Community sample (N = 3,012; Arizona) 34 Ages 5–55 Hagy and Settipane, 1969 College freshmen (N = 1,243) 30.9 Henderson, 1993 (personal communication 1-26-93) Schoolchildren (N = 225; North Carolina) 40
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Indoor Allergens: Assessing and Controlling Adverse Health Effects Other countries D. Charpin et al., 1991 Schoolchildren (N = 933; France) 25 Methodologic differences probably account for the lower rates in this study Sears et al., 1989 Birth cohort; (N = 714; New Zealand 45.8 Peat et al., 1987 Schoolchildren (N = 2,363; Australia) 39 Chan-Yeung et al., 1985 Adult workers (Canada) 22 Lower rates are seen in other workplaces Cockroft et al., 1984 Canadians 35 Haahtela et al., 1980 Teenagers (N = 708; Finland) 49 Woolcock et al., 1978 Australia Community sample (N = 188) 39 New Guinea natives (N = 317) 49 a Percentage of population with skin test reactivity. b NHANES, National Health and Nutrition Examination Survey.
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Indoor Allergens: Assessing and Controlling Adverse Health Effects FIGURE 2-2 Changes in skin test reactivity with age. By age 5, approximately 20 percent of children will be sensitized to common aeroallergens. Skin test reactivity increases with age until ages 25–34 and then declines. Source: Barbee et al., 1987. it is important to identify potential risk factors associated with allergic disease. Risk factors are biological, environmental, and behavioral characteristics that are causally associated with health-related conditions (Lalonde, 1974; Last, 1986). Heredity, for example, is an important biological risk factor in the development of immunologic sensitization and allergy. Infants of parents with allergic disease develop positive skin tests at higher rates than infants in population-based studies. Skin prick test reactivity during the first year of life has been reported as ranging between 30 and 70 percent of at-risk infants—i.e., those who have one or both parents with allergic disease (Zeiger, 1988). In general, if one parent has allergies and the other does not, then the chances are one in three that each of their children will have allergies. If both parents have allergies, it is much more likely (seven in ten) that each of their children will have some manifestation of allergic disease. Exposure to allergens is an example of an environmental risk factor related to the prevalence of sensitization. Household exposure to elevated levels of dust mite allergen (see Chapter 3) in infancy, for example, has been associated by age 5 with an increased prevalence of positive dust mite skin tests and an increased concentration of dust mite IgE antibody (Zeiger, 1988). Another example is found among people living at high altitudes in Briançon, France, where significantly lower rates of sensitization to house
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Indoor Allergens: Assessing and Controlling Adverse Health Effects TABLE 2-3 Partial Listing of Published Prevalence Data on Sensitization (per 100 population) to Some of the Common Aeroallergens Source Population House Dust Mite Grasses and/or Weed Pollen Animal Danders Molds Notes Barbee et al., 1976 Community (N = 3,101; United States) ND 17–24 NDa 8 Crude house dust: 9b Peat et al., 1987 Schoolchildren (N = 2,363; Australia) 19–31 18–29 20–25 10–20 Sears et al., 1989 Birth cohort to age 13 (N = 714; New Zealand) 30.1 32.5 13.3 D. Charpin et al., 1988a Adults (France) Marseille (N = 4,008; low altitude) 44.5 Briançon (N = 1,055; high altitude) 10 D. Charpin et al., 1991 Schoolchildren (France) Martigues (N = 693; low altitude) 16.7 8.5 5.6 Briançon (N = 240; high altitude) 4.1 21.7 3.3 Henderson, 1992 (personal communication) Schoolchildren (North Carolina) 27 Pending Pending Godfrey and Griffiths, 1976 Schoolchildren (N = 303; Southampton, England) 26 24 a ND, no data. b Crude house dust is a skin test reagent that contains unpredictable amounts of antigens such as dust mite, animal dander, and molds. Its use has been largely replaced by purified allergen extracts.
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Indoor Allergens: Assessing and Controlling Adverse Health Effects FIGURE 2-3 Estimated prevalence of skin test reactivity to selected aeroallergens among schoolchildren. The presence of skin test reactivity indicates that the child has been sensitized to that aeroallergen by an IgE mechanism. Henderson found lower rates of skin test reactivity to animal danders and molds in their population. (Table 2-3 shows results from additional epidemiological studies.) Sources: Henderson, 1993; Peat et al., 1987; Sears et al., 1989. dust mite occur than in comparison populations at lower altitudes (Martigues for children and Marseilles for adults) (D. Charpin et al., 1988a, 1991; Vervloet et al., 1979). Analyses of house dust from Briançon found lower levels of house dust mite compared with the levels in dust from low-altitude homes (see Table 2-3). In addition, Sporik and colleagues (1990) demonstrated a trend toward an increasing degree of sensitization among children at age 11 with greater dust mite exposure at age 1. Chapter 6 analyzes these and other studies and suggests that there may be an exposure-response relationship between dust mite exposure and the prevalence of skin test reactivity (sensitization). Exposure to environmental tobacco smoke is another example of an environmental risk factor in that it appears to be associated with increased skin test reactivity in children (Burrows and Martinez, 1989) and a twofold increase in serum IgE in infants (Zeiger, 1988). Zeiger also discussed the possible effects of exposure to ingestants and microbial agents on the risk
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Indoor Allergens: Assessing and Controlling Adverse Health Effects of sensitization. Animal studies have shown an increased rate of new IgE sensitization when allergen exposure is interspersed with ozone, nitrogen dioxide, or sulfur dioxide inhalation (Matsumura, 1970a–c; Riedel et al., 1988; Sheppard, 1988b). Diesel fumes have also been shown to act as an adjuvant for IgE sensitization (Muranaka et al., 1986). The effect of active smoking—a possible behavioral risk factor—on the prevalence of skin test reactivity in adults is uncertain, given the existence of conflicting data. Barbee and colleagues (1987) found lower rates of skin test reactivity among current smokers than either nonsmokers or ex-smokers; ex-smokers had higher rates of skin test reactivity than nonsmokers. The study team interpreted this finding as demonstrating a self-selection process; that is, smokers with skin test reactivity would stop smoking. In contrast, Gergen and coworkers (1987) did not find a relationship between skin test reactivity and smoking status. Other Types of Sensitization Immunologic sensitization may also occur through non-IgE mechanisms. Specific IgG in the serum, for example, is a marker of sensitization to allergens known to cause hypersensitivity pneumonitis. Tests of lymphocyte proliferation can indicate sensitization through cellular immune mechanisms (see Chapter 4). Exposure to allergens in the workplace may result in immunologic sensitization and occupational disease. Table 2-4 lists agents that are associated with causing asthma in occupational settings. The prevalence of sensitization among workers ranges from less than 10 percent for some agents to as much as 80 percent for platinum. Exposures may occur in an industrial or office setting. Although many of the protein allergens have long been recognized, a lengthening list of newly recognized allergenic chemicals is developing (see Chapter 3). The prevalence of exposure and sensitization to defined, reactive, allergenic chemicals has led to a relatively new but growing category of chemical allergens. Most of these chemicals were initially developed for use in specific industrial processes, but their commercially useful reactive properties often make them react with human proteins as well, a feature that is thought to contribute to their allergenicity. As with other allergens, immunologic sensitization to these chemicals may occur in the absence of symptoms of allergic disease. DISEASES Although some people remain asymptomatic despite being immunologically sensitized, many develop one of several diseases including asthma,
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Indoor Allergens: Assessing and Controlling Adverse Health Effects TABLE 2-4 Selected Agents Causing Asthma in Selected Occupations Occupation or Occupational Field Agent Animal-related Laboratory animal workers, veterinarians Dander, urine proteins Food processing Shellfish, egg proteins, pancreatic enzymes, papain, amylase Dairy farmers Storage mites Poultry farmers Poultry mites, droppings, feathers Granary workers Storage mites, aspergillus, indoor ragweed, grass pollen Research workers Locusts Fish food manufacturing Midges Detergent manufacturing Bacillus subtilis enzymes Silk workers Silkworm moths and larvae Plant proteins Bakers Flour Food processing Coffee bean dust, meat tenderizer (papain), tea Farmers Soybean dust Shipping workers Grain dust (molds, insects, grain) Laxative manufacturing Ispaghula, psyllium Sawmill workers, carpenters Wood dust (western red cedar, oak, mahogany, zebrawood, redwood, Lebanon cedar, African maple, eastern white cedar) Electric soldering Colophony (pine resin) Cotton textile workers Cotton dust Nurses Psyllium, latex Inorganic chemicals Refining Platinum salts Plating Nickel salts Diamond polishing Cobalt salts Stainless steel welding Chromium salts Manufacturing Aluminum fluoride Beauty shop Persulfate Refinery workers Vanadium Welding Stainless steel fumes Organic chemicals Manufacturing Antibiotics, piperazine, methyldopa, salbutanol, cimetidine Hospital workers Disinfectants (sulfathiazole, chloramine, formaldehyde, psyllium, glutaraldehyde) Anesthesiology Enflurane Poultry workers Aprolium Fur dyeing Paraphenylene diamine Rubber processing Formaldehyde, ethylenediamine, phthalic anhydride
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Indoor Allergens: Assessing and Controlling Adverse Health Effects HYPERSENSITIVITY PNEUMONITIS Hypersensitivity pneumonitis is a specific immunologic lung disease characterized by inflammation of the lung parenchyma. The causative agents are numerous and diverse, and the immune pathogenesis includes formation of specific IgG antibody and formation of lung granulomas. The clinical spectrum is also diverse and ranges from recurrent, acute flu-like illnesses to a gradually increasing breathlessness. Hypersensitivity pneumonitis sometimes occurs in sporadic outbreaks, for example, when a building's ventilation system becomes contaminated. Diagnosis is often difficult because it requires a high index of suspicion, and the appropriate laboratory studies (i.e., precipitins) are sometimes unfamiliar to many physicians (see Chapter 5). Table 2-7 lists various causes of hypersensitivity pneumonitis that have been reported in nonindustrial indoor environments. Prevalence No prevalence rates are available for the general population. Clinical assessments of the type recommended by Solomon (1990) have not been utilized to obtain rate estimates or population impacts. Disease Severity In 1977, it was estimated that 2,000 hospitalizations occurred in the United States in which hypersensitivity pneumonitis was the primary (50 percent) or secondary (50 percent) diagnosis. Treatment consists of corticosteroid therapy and removal from exposure. Failure to institute these measures can result in disease or disability resulting from irreversible fibrosis and respiratory failure (EPA, 1991b). Risk Factors Indoor Environment Exposure to allergenic bioaerosols in residential or commercial heating, ventilation, and air-conditioning (HVAC) systems can cause hypersensitivity pneumonitis. Causative agents include thermophilic actinomycetes, Aspergillus species, Aureobasidium species, and other proteins. Occupation/Hobby The risk of hypersensitivity pneumonitis increases markedly with exposure to allergens through hobbies and occupations, ranging from 0.5 to 10 percent of exposed populations. For example, the prevalence of hypersensitivity pneumonitis among pigeon breeders ranges from 6 to 15 percent (NIAID, 1979). Farmer's lung, a hypersensitivity pneumonitis that usually arises from exposure to thermophilic actinomycetes, probably occurs in 3–4 percent of exposed populations, with estimates ranging from 0.5 to 10 percent of farmers (NHLBI, 1982; NIAID, 1979). Occurrences among
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Indoor Allergens: Assessing and Controlling Adverse Health Effects TABLE 2-7 Hypersensitivity Pneumonitis in Indoor Environments Disease Source of Antigen Probable Allergen Familial hypersensitivity pneumonitis Contaminated wood dust in walls Bacillus subtilis Humidifier lung Contaminated humidifiers, dehumidifiers, air conditioners Thermophilic actinomycetes: Micropolyspora faeni, T. candidus, T. vulgaris, Penicillium spp., Cephalosporium spp. Amebae: Naegleria gruberi and Acanthamoeba castellani Cephalosporium hypersensitivity pneumonitis Contaminated basement (sewage) Cephalosporium spp. Pigeon breeder's disease Pigeon droppings Altered pigeon serum Laboratory worker's hypersensitivity pneumonitis Rat fur Male rat urine Summer type hypersensitivity pneumonitis House dust Trichosporon cutaneum SOURCES: Fink, 1988; Lopez and Salvaggio, 1988; Rose, 1992.
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Indoor Allergens: Assessing and Controlling Adverse Health Effects farmers have decreased markedly with changes in methods of harvesting and baling hay. Other occupations also present opportunities for development of hypersensitivity pneumonitis. Office workers are estimated to develop hypersensitivity pneumonitis at rates of from 1.2 to 4 percent (EPA, 1991b). Banaszak and colleagues (1970) reported that 15 percent of workers in one office displayed pulmonary disease from thermophilic actinomycetes; their exposure had occurred through a contaminated air-conditioning system. Sauna takers disease (caused by Aureobasidium pullulans) occurs infrequently. However, lifeguards at an indoor swimming pool reportedly experienced an extremely high rate of attack of a hypersensitivity pneumonitis-like condition; the causative agent of the disease remains unidentified (Rose and King, 1992). Climate/Season In Japan, 74 percent of the cases of hypersensitivity pneumonitis reported by hospitals (a total of 835 cases) were associated with predominantly hot, humid climates and occurred in the summer. These cases were attributed to Trichosporon cutaneum on the basis of detection of antibody in the blood. Immunologic Sensitization In some studies, up to 20 percent of exposed populations will have IgG against the allergen in their serum. Because more than 90 percent of affected individuals will have a specific antibody, these individuals are thought to constitute a subset of the exposed population who are at increased risk of developing the disease. These general figures, however, may vary markedly across individual circumstances. HUMIDIFIER FEVER Humidifier fever is an illness with influenza-like symptoms that develops shortly after exposure to aerosols from microbiologically contaminated humidifiers. Recovery can occur within days, even with continuing exposure. It often recurs on the first day of reexposure following a period of no exposure. Inhalation challenge with extracts from contaminated water can produce symptoms of humidifier fever, but the causative agent is still unknown. Experimental exposure of symptomatic workers to humidifier allergens can induce headache, rhinitis, and lethargy as well as asthma and alveolitis; similar exposure does not cause symptoms in previously unexposed individuals. These findings have led to a presumption that a specific immunologic mechanism is operative. A World Health Organization report, for example, listed endotoxin as the leading suspect (WHO, 1990). Finnegan and others (1987) identified allergens of amebae in contaminated humidifiers but failed to correlate their presence with humidifier fever or with work-related
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Indoor Allergens: Assessing and Controlling Adverse Health Effects symptoms in a group of 25 workers with humidifier fever and 90 workmate controls. Prevalence In general, published estimates are only educated guesses. The U.S. Environmental Protection Agency (EPA, 1991b) states that epidemics in the workplace are rare but that when they do occur, ''attack rates are high (30–75 percent)." Based on symptoms, Finnegan and coworkers (1984) estimated a rate of occurrence of 2–3 percent in Great Britain in office buildings with mechanical ventilation. Prevalence rates in the home, however, have not been evaluated (EPA, 1991b). Common Diseases Possibly Related to Allergy There are several syndromes in which a role for indoor allergens is possible or suspected but largely undefined. These include chronic sinusitis and bronchitis, sick building syndrome and other nonspecific syndromes, and acute respiratory illnesses. SINUSITIS Sinusitis is defined as inflammation of the sinuses, which are four pairs of hollow structures that surround the nasal cavity. Chronic sinusitis is defined by physicians as persistent inflammation of the mucosa of the sinuses lasting for more than 3 months (Slavin, 1989). Symptoms may include facial pressure, nasal stuffiness, hyposmia, prurulent nasal secretions, sore throat, fetid breath, and malaise. Coughing and wheezing occasionally occur. Prevalence and Severity Sinusitis is an important cause of morbidity (Slavin, 1989). In 1981, statistics from the U.S. Department of Health and Human Services indicated that 31 million people had chronic sinusitis; data from the National Center for Health Statistics (NCHS, 1986) are similar (13.9 percent, more than 30 million people). Sinusitis is thus more prevalent than arthritis (27 million) and hypertension (25.5 million). In Great Britain, the Department of Health and Social Security estimates that a half million working days are lost in that country each year due to sinusitis (Slavin, 1989). In 1975, the rate of physician-confirmed sinusitis in Tucson adults was reported to be 29.4 percent (Lebowitz et al., 1975). The difference between this rate and the figures listed above does not reflect decreasing prevalence over time but rather variable case definitions.
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Indoor Allergens: Assessing and Controlling Adverse Health Effects Risk Factors Age The prevalence of chronic sinusitis varies with age. According to estimates from the National Center for Health Statistics, it occurs in 6 percent of people under age 18, 16.4 percent of those between ages 18 and 44, 18.5 percent of those age 45–64, and 15.4 percent of those over age 65 (NCHS, 1986). A similar age pattern was reported in Tucson (Lebowitz et al., 1975). Allergy Allergic rhinitis is considered a common risk factor for both acute and chronic sinusitis (Slavin, 1989), but the proportion of chronic sinusitis for which it is the dominant factor is unknown. The NHANES data, analyzed by Gergen and Turkeltaub (1992), did not show a relationship between reported sinusitis and skin test reactivity. Nonallergic factors that predispose an individual to sinusitis are upper respiratory infection, overuse of topical decongestants, hypertrophied adenoids, deviated nasal septum, nasal polys, nasal tumors, foreign bodies, cigarette smoke, swimming and diving, barotrauma, and dental extractions. Immunodeficiency syndromes, cystic fibrosis, bronchiectasis, and the immotile cilia syndrome can also be associated with chronic sinusitis. CHRONIC BRONCHITIS Chronic bronchitis is commonly defined by clinicians as a chronic productive cough, without a medically discernible cause, that is present more than half the time for 2 years (Snider, 1988). Epidemiologists define chronic bronchitis more precisely as a cough productive of phlegm for a total of 3 months per year for at least 2 years in a patient in whom other causes of chronic cough have been excluded (e.g., infection with Mycobacterium tuberculosis, carcinoma of the lung, chronic congestive heart failure; Snider, 1988). The major risk factor for chronic bronchitis is cigarette smoking. The prevalence of chronic bronchitis among nonsmokers rises from age 15 to 60, increasing from 7 to 18 percent; prevalence among smokers rises from 40 to 82 percent (Snider, 1988). Figure 2-10 illustrates the overlap between asthma, chronic bronchitis, and emphysema (Snider, 1988). Asthma, by definition, is characterized by reversible airflow obstruction, although a few patients may develop unremitting airflow obstruction. Patients with chronic bronchitis may have partially reversible airflow obstruction (Snider, 1988). The term chronic obstructive pulmonary disease (COPD) is often used by doctors when adult patients have evidence of one or more of three diseases: chronic bronchitis, emphysema, and asthma. The nonproportional Venn diagram in Figure 2-10 shows subsets of patients with chronic bronchitis, emphysema, and asthma in three overlapping
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Indoor Allergens: Assessing and Controlling Adverse Health Effects FIGURE 2-10 Relationship between asthma, chronic bronchitis, emphysema, and allergy. Numbers refer to subsets described in text. Source: Snider, 1988. circles. Subsets of patients lying within the rectangle have obstruction of their airways. Patients with asthma, subset 9, are defined as having completely reversible airways obstruction and lie entirely within the rectangle; their diagnosis is unequivocal. Patients in subsets 6 and 7 have reversible airways obstruction with chronic productive cough or emphysema, respectively. Patients in subset 8 have features of all three disorders. It may be difficult to be certain whether patients in subsets 6 and 8 indeed have asthma or whether they have developed bronchial hyperreactivity as a complication of chronic bronchitis or emphysema; the history helps. Patients in subset 3 have chronic productive cough with airways obstruction but no emphysema; it is not known how large this subset is, since data from epidemiologic studies using the computer tomography scan, the most sensitive in vivo imaging technique for diagnosing or excluding emphysema, are not available. It is much easier to identify in the chest radiography patients with emphysema who do not have chronic bronchitis (subset 4). Most patients in subsets 1 and 2 do not have airways obstruction as determined by the FEV1 (forced expiratory volume exhaled in 1 second) but have clinical or radiographic features of chronic bronchitis or emphysema, respectively. Because COPD, when defined as a process, does not have airways obstruction as a defining characteristic, and because pure asthma is not included in the term COPD, patient subsets 1–8 are included within the area outlined by the shaded band that denotes COPD (Snider, 1988).
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Indoor Allergens: Assessing and Controlling Adverse Health Effects There is a recognized association between bronchial hyperresponsiveness, atopy (skin test reactivity), and COPD. Studies have demonstrated that the risk of bronchial hyperresponsiveness is related to skin test reactivity (Cockroft et al., 1984; Lebowitz et al., 1991, Peat et al., 1987; Sears et al., 1989). The index rises with the number of positive skin tests and the magnitude of the skin test reaction to each allergen. Therefore, an individual with many strongly positive skin tests to many allergens is much more likely to show bronchial hyperresponsiveness than an individual with no skin test reactivity. The association between atopy, bronchial hyperresponsiveness, and COPD may be explained by three alternative models (Sparrow et al., 1988). First, cigarette smoke may cause inflammation and mucosal damage, resulting in three unrelated by-products: atopy, bronchial hyperresponsiveness, and COPD. Second, when a person has atopy and therefore bronchial hyperresponsiveness, exposure to cigarette smoke leads to COPD. Third, cigarette smoke, atopy, and bronchial hyperresponsiveness are independent factors that contribute to the development of COPD. SICK BUILDING SYNDROME Sick building syndrome (also known as tight building syndrome, closed building syndrome, and new building syndrome) is a term given to nonspecific building-related illness. Figure 2-11 shows the relationship between these and other diseases and conditions that may occur in indoor environments and the general approach to their evaluation and management. Sick building syndrome describes a constellation of symptoms including mucosal irritation, fatigue, headache, and occasionally, lower respiratory symptoms and nausea. Patients or workers report that symptoms increase with the amount of time spent in certain buildings and tend to improve when they leave that building. Symptom prevalence rates associated with indoor environments vary tremendously, from less than 5 percent to as much as 50 percent. For the majority of cases of sick building syndrome, the cause is unknown. A contribution by allergy has been considered unlikely since atopy or specific sensitivity to indoor allergens often is not found. Nevertheless, people with allergic disease frequently are the individuals who are most affected when an indoor air quality problem is occurring. A definitive conclusion that indoor allergens are not related to sick building syndrome awaits further study, particularly with respect to fungal allergens. SPECIFIC BUILDING-RELATED ILLNESS Specific building-related illness is defined as illness caused by identifiable toxic, infectious, or allergenic agents, which can be detected by appropriate
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Indoor Allergens: Assessing and Controlling Adverse Health Effects FIGURE 2-11 Approach to the evaluation of symptoms occurring in indoor environments. clinical laboratory tests in patients or by identification of the source in the building (Samet, 1990). Hypersensitivity pneumonitis, humidifier fever (see above), and infection with Legionella species are included in this category of illness. Prevalence rates for specific syndromes are largely unknown and estimates vary tremendously among buildings. Some researchers believe that there is a set of nonspecific symptoms that are distinguishable, that are different from the other conditions described above, and that are due to indoor allergens (Burge, 1990). Fungus-related
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Indoor Allergens: Assessing and Controlling Adverse Health Effects illnesses, for example, have been identified or suggested in some instances (Anderson and Korsgaard, 1986; Finnegan et al., 1984; Morey, 1988). Further information can be obtained from a review and an editorial by Kreiss (1988, 1990). ACUTE RESPIRATORY ILLNESSES Assessments of disease magnitude often depend on a subject's recalling the occurrence of a disease and recognizing its relationship to allergy. For example, questionnaires will ask, "Have you had hay fever?" For an affirmative answer, the subject must recognize that his or her recurrent nasal symptoms are in fact due to an allergic nasal condition. Diary studies, that ask subjects to record symptoms on a daily basis, are another way of assessing the burden of respiratory symptoms in the population. In general, they suggest that respiratory symptoms are quite common, more so than recall studies would indicate. In a diary study of Manhattan (New York) residents, it was determined that the rates of symptoms were much greater when diaries were used than when subjects were asked to recall their health status over the past several years (Lebowitz et al., 1972a,b). The study of 1,707 residents assessed respiratory symptoms for 1,168 person-years of observation. One or more symptoms occurred at least one-quarter of the time among 22 percent of subjects in the study and at least half the time among 6.5 percent. The symptoms that were most often reported included common cold and rhinitis (8 percent of all person-days each), cough (5 percent), headache (2.45 percent), eye irritation (1.8 percent), and chest whistling/wheezing (0.77 percent). The investigator in this study has speculated that reported colds and other infections could have been mislabeled and that an unknown portion of these symptoms could be attributable to allergic diseases. Data from the NHIS (NCHS, 1986) indicate that in 1985 there were 87.1 acute respiratory conditions per 100 persons. Of these, 46.4 percent were categorized as influenza, 35 percent as common colds, and 11.7 percent as other acute respiratory illnesses. The remainder were labeled as acute bronchitis (3 percent), pneumonia (1 percent), and other (2 percent). CONCLUSIONS AND RECOMMENDATIONS As outlined in this chapter, allergic disease constitutes a substantial public health problem in the United States. Data on its exact magnitude and dimensions, however, are incomplete, or lacking, in many cases. Better data regarding the incidence, prevalence, attributable fraction, and cost of allergic diseases are essential to the development of effective programs of prevention and control. Accurate determinations of the magnitude and dimensions
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Indoor Allergens: Assessing and Controlling Adverse Health Effects of sensitization and disease caused by regional and local indoor allergens would be useful in this regard. The following recommendations for research and data collection will be useful in accurately determining the magnitude and dimensions of sensitization and disease caused by indoor allergens. Research Agenda Item: Determine prevalence rates of sensitization, allergic diseases, and respiratory morbidity caused by regionally and locally relevant indoor allergens and assess the contributions of different allergens to these conditions. Socioeconomic status seems to contribute to asthma prevalence rates and to indices of disease severity. Similarly, several studies have reported racial differences in the prevalence and severity of asthma in the United States, but such results are inconsistent. In order that these differentials can be translated into effectively targeted public health interventions, additional research is needed to clarify these relationships. Research Agenda Item: Conduct studies to clarify the relationships that exist between socio- economic status, race, and cultural environment and the incidence, prevalence, severity, and mortality associated with allergic disease including asthma. The annual costs (direct and indirect) associated with asthma have been estimated at more than $6.2 billion—an increase of 39 percent since 1985. The size of these costs and the trend towards even greater costs argue for careful attention not only to the effects of allergy in causing asthma but also to the litany of other conditions that are more commonly thought to be associated with "allergies." Accurate assessments of the costs associated with asthma and other allergic diseases would be useful in the development of health policy initiatives and the implementation of appropriate and cost effective interventions. Research Agenda Item: Determine the economic impact of asthma and other allergic diseases. Allergic disease occurs when a genetically predisposed or susceptible individual is exposed to an allergen and becomes immunologically sensitized. In the early stages of sensitization, people who are sensitized have not developed symptoms of disease. The magnitude of this group within the population is of interest, however, because it reflects the proportion of the population at greatest risk of developing allergic disease. Additional exposure to the sensitizing allergen leads to the development of an allergic reaction (disease) that can be mild, moderate, or severe, depending on the amount of exposure. The relationship between exposure, sensitization, and disease, and the
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Indoor Allergens: Assessing and Controlling Adverse Health Effects potential for a threshold level of exposure below which the risk of sensitization is reduced, is of critical importance in the prevention and control of allergic disease. Epidemiological data would be useful in determining these relationships and in developing and evaluating public health and medical intervention strategies. Research Agenda Item: Conduct appropriate epidemiological studies of exposure-response relationships of important defined indoor allergens that induce sensitization in humans. Such studies should include a focus on identifying threshold exposures. Indoor allergens are associated with a wide variety of particles in a broad size range, only some of which are microscopically identifiable, culturable, or detectable with existing immunoassays. Evaluation of indoor allergens requires both air and source sampling, and several different analytical techniques (including microscopy, culture, and immunoassays) must be used to characterize even the well-known allergens. Because of the complexity of the assessment problem, indoor allergens, with a few exceptions, have not been identified and studied. Research Agenda Item: Encourage and conduct additional research to identify and characterize indoor allergens. The new information should be used to advise patients about avoiding specific allergenic agents.
Representative terms from entire chapter: