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IntroductionIndoor air pollution poses many challenges to the health professional. This booklet offers an overview of those challenges, focusing on acute conditions, with patterns that point to particular agents and suggestions for appropriate remedial action. The individual presenting with environmentally associated symptoms is apt to have been exposed to airborne substances originating not outdoors, but indoors. Studies from the United States and Europe show that persons in industrialized nations spend more than 90 percent of their time indoors1. For infants, the elderly, persons with chronic diseases, and most urban residents of any age, the proportion is probably higher. In addition, the concentrations of many pollutants indoors exceed those outdoors. The locations of highest concern are those involving prolonged, continuing exposure - that is, the home, school, and workplace. The lung is the most common site of injury by airborne pollutants. Acute effects, however, may also include non-respiratory signs and symptoms, which may depend upon toxicological characteristics of the substances and host-related factors. Heavy industry-related occupational hazards are generally regulated and likely to be dealt with by an on-site or company physician or other health personnel2. This booklet addresses the indoor air pollution problems that may be caused by contaminants encountered in the daily lives of persons in their homes and offices. These are the problems more likely to be encountered by the primary health care provider. Etiology can be difficult to establish because many signs and symptoms are nonspecific, making differential diagnosis a distinct challenge. Indeed, multiple pollutants may be involved. The challenge is further compounded by the similar manifestations of many of the pollutants and by the similarity of those effects, in turn, to those that may be associated with allergies, influenza, and the common cold. Many effects may also be associated, independently or in combination with, stress, work pressures, and seasonal discomforts. Because a few prominent aspects of indoor air pollution, notably environmental tobacco smoke and "sick building syndrome," have been brought to public attention, individuals may volunteer suggestions of a connection between respiratory or other symptoms and conditions in the home or, especially, the workplace. Such suggestions should be seriously considered and pursued, with the caution that such attention could also lead to inaccurate attribution of effects. Questions listed in the diagnostic leads sections will help determine the cause of the health problem. The probability of an etiological association increases if the individual can convincingly relate the disappearance or lessening of symptoms to being away from the home or workplace. How To Use This BookletThe health professional should use this booklet as a tool in diagnosing an individual's signs and symptoms that could be related to an indoor air pollution problem. The document is organized according to pollutant or pollutant group. Key signs and symptoms from exposure to the pollutant(s) are listed, with diagnostic leads to help determine the cause of the health problem. A quick reference summary of this information is included in this booklet. Remedial action is suggested, with comment providing more detailed information in each section. References for information included in each section are listed at the end of this document. It must be noted that some of the signs and symptoms noted in the text may occur only in association with significant exposures, and that effects of lower exposures may be milder and more vague, unfortunately underscoring the diagnostic challenge. Further, signs and symptoms in infants and children may be a typical (some such departures have been specifically noted). The reader is cautioned that this is not an all-inclusive reference, but a necessarily selective survey intended to suggest the scope of the problem. A detailed medical history is essential, and the diagnostic checklist may be helpful in this regard. Resolving the problem may sometimes require a multi-disciplinary approach, enlisting the advice and assistance of others outside the medical profession. The references cited throughout and the For Assistance and Additional Information section will provide the reader with additional information. Diagnostic Quick Reference
Particular Effects Seen in Infants and ChildrenEnvironmental Tobacco Smoke: frequent upper respiratory infections, otitis media; persistent middle-ear effusion; asthma onset, increased severity; recurrent pneumonia, bronchitis. Acute Lead Toxicity: irritability, abdominal pain, ataxia, seizures, loss of consciousness. Diagnostic ChecklistIt is vital that the individual and the health care professional comprise a cooperative diagnostic team in analyzing diurnal and other patterns that may provide clues to a complaint's link with indoor air pollution. A diary or log of symptoms correlated with time and place may prove helpful. If an association between symptoms and events or conditions in the home or workplace is not volunteered by the individual, answers to the following questions may be useful, together with the medical history. The health care professional can investigate further by matching the individual's signs and symptoms to those pollutants with which they may be associated, as detailed in the discussions of various pollutant categories.
NOTE: A more detailed exposure history form, developed by the U.S. Public Health Service's Agency for Toxic Substances and Disease Registry (ATSDR) in conjunction with the National Institute for Occupational Safety and Health, is available from: Allen Jansen, ATSDR, 1600 Clifton Road, N.E., Mail Drop E33, Atlanta, Georgia 30333, (404) 639-6205. Request "Case Studies in Environmental Medicine #26: Taking an Exposure History." Continuing Medical Education Credit is available in conjunction with this monograph.
Health Problems Related
To
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Relationship between carbon monoxide (CO) concentrations and
carboxyhemoglobin (COHb) levels in blood |
| % COHb in blood |
Effects Associated with this COHb Level |
|---|---|
| 80 | Deatha |
| 60 | Loss of consciousness; death if exposure continuesa |
| 40 | Confusion; collapse on exercisea |
| 30 | Headache; fatigue; impaired judgementa |
| 7-20 | Statistically significant decreased maximal oxygen consumption during strenuous exercise in healthy young menb |
| 5-17 | Statistically significant diminution of visual perception, manual dexterity, ability to learn, or performance in complex sensorimotor tasks (such as driving)b |
| 5-5.5 | Statistically significant decreased maximal oxygen consumption and exercise time during strenuous exercise in young healthy menb |
| Below 5 | No statistically significant vigilance decrements after exposure to COb |
| 2.9-4.5 | Statistically significant decreased exercise capacity (i.e., shortened duration of exercise before onset of pain) in patients with angina pectoris and increased duration of angina attacksb |
| 2.3-4.3 | Statistically significant decreased (about 3-7%) work time to exhaustion in exercising healthy menb |
SOURCE: aU.S. EPA (1979); bU.S. EPA (1985)
Nitrogen dioxide (NO) and sulfur dioxide (SO2) act mainly as irritants, affecting the mucosa of the eyes, nose, throat, and respiratory tract. Acute S02-related bronchial constriction may also occur in people with asthma or as a hypersensitivity reaction. Extremely high-dose exposure (as in a building fire) to N02 may result in pulmonary edema and diffuse lung injury. Continued exposure to high N02 levels can contribute to the development of acute or chronic bronchitis.
The relatively low water solubility of N02 results in minimal mucous membrane irritation of the upper airway. The principal site of toxicity is the lower respiratory tract. Recent studies indicate that low-level N02 exposure may cause increased bronchial reactivity in some asthmatics, decreased lung function in patients with chronic obstructive pulmonary disease, and an increased risk of respiratory infections, especially in young children.
The high water solubility of S02 causes it to be extremely irritating to the eyes and upper respiratory tract. Concentrations above six parts per million produce mucous membrane irritation. Epidemiologic studies indicate that chronic exposure to S02 is associated with increased respiratory symptoms and decrements in pulmonary function21. Clinical studies have found that some asthmatics respond with bronchoconstriction to even brief exposure to S02 levels as low as 0.4 parts per million22.
Provide adequate outdoor air ventilation to dilute human source aerosols.
Keep equipment water reservoirs clean and potable water systems adequately chlorinated, according to manufacturer instructions. Be sure there is no standing water in air conditioners. Maintain humidifiers and dehumidifiers according to manufacturer instructions.
Repair leaks and seepage. Thoroughly clean and dry water-damaged carpets and building materials within 24 hours of damage, or consider removal and replacement.
Keep relative humidity
below 50 percent. Use exhaust fans in bathrooms and kitchens, and vent
clothes
dryers to outside.
Control exposure to pets.
Vacuum carpets and upholstered furniture regularly. Note: While it is important to keep an area as dust-free as possible, cleaning activities often re-suspend fine particles during and immediately after the activity. Sensitive individuals should be cautioned to avoid such exposure, and have others perform the vacuuming, or use a commercially available HEPA (High Efficiency Particulate Air) filtered vacuum.
Cover mattresses. Wash bedding and soft toys frequently in water at a temperature above 130oF to kill dust mites.
Biological air pollutants are found to some degree in every home, school, and workplace. Sources include outdoor air and human occupants who shed viruses and bacteria, animal occupants (insects and other arthropods, mammals) that shed allergens, and indoor surfaces and water reservoirs where fungi and bacteria can grow, such as humidifiers23. A number of factors allow biological agents to grow and be released into the air. Especially important is high relative humidity, which encourages house dust mite populations to increase and allows fungal growth on damp surfaces. Mite and fungus contamination can be caused by flooding, continually damp carpet (which may occur when carpet is installed on poorly ventilated concrete floors), inadequate exhaust of bathrooms, or kitchen-generated moisture24. Appliances such as humidifiers, dehumidifiers, air conditioners, and drip pans under cooling coils (as in refrigerators), support the growth of bacteria and fungi.
Components of mechanical heating, ventilating, and air conditioning (HVAC) systems may also serve as reservoirs or sites of microbial amplification25. These include air intakes near potential sources of contamination such as standing water, organic debris or bird droppings, or integral parts of the mechanical system itself, such as various humidification systems, cooling coils, or condensate drain pans. Dust and debris may be deposited in the duct work or mixing boxes of the air handler.
Biological agents in indoor air are known to cause three types of human disease: infections, where pathogens invade human tissues; hypersensitivity diseases, where specific activation of the immune system causes disease; and toxicosis, where biologically produced chemical toxins cause direct toxic effects. In addition, exposure to conditions conducive to biological contamination (e.g., dampness, water damage) has been related to nonspecific upper and lower respiratory symptoms. Evidence is available that shows that some episodes of the group of nonspecific symptoms known as "sick building syndrome" may be related to microbial contamination in buildings26.
The transmission of airborne infectious diseases is increased where there is poor indoor air quality27,28. The rising incidence of tuberculosis is at least in part a problem associated with crowding and inadequate ventilation. Evidence is increasing that inadequate or inappropriately designed ventilation systems in health care settings or other crowded conditions with high-risk populations can increase the risk of exposure29.
The incidence of tuberculosis began to rise in the mid 1980s, after a steady decline. The 1989 increase of 4.7 percent to a total of 23,495 cases in the United States was the largest since national reporting of the disease began in 1953, and the number of cases has continued to increase each year30. Fresh air ventilation is an important factor in contagion control. Such procedures as sputum induction and collection, bronchoscopy, and aerosolized pentamidine treatments in persons who may be at risk for tuberculosis (e.g., AIDS patients) should be carried out in negative air pressure areas, with air exhausted directly to the outside and away from intake sources31. Unfortunately, many health care facilities are not so equipped. Properly installed and maintained ultraviolet irradiation, particularly of upper air levels in an indoor area, is also a useful means of disinfection32.
A disease associated with indoor air contamination is Legionnaires' Disease, a pneumonia that primarily attacks exposed people over 50 years old, especially those who are immune suppressed, smoke, or abuse alcohol. Exposure to especially virulent strains can also cause the disease in other susceptible populations. The case fatality rate is high, ranging from five to 25 percent. Erythromycin is the most effective treatment. The agent, Legionella pneumophila, has been found in association with cooling systems, whirlpool baths, humidifiers, food market vegetable misters, and other sources, including residential tap water33. This bacterium or a closely related strain also causes a self-limited (two- to five-day), flu-like illness without pneumonia, sometimes called Pontiac Fever, after a 1968 outbreak in that Michigan city.
A major concern associated with exposure to biological pollutants is allergic reactions, which range from rhinitis, nasal congestion, conjunctival inflammation, and urticaria to asthma. Notable triggers for these diseases are allergens derived from house dust mites; other arthropods, including cockroaches; pets (cats, dogs, birds, rodents); molds; and protein-containing furnishings, including feathers, kapok, etc. In occupational settings, more unusual allergens (e.g., bacterial enzymes, algae) have caused asthma epidemics. Probably most proteins of non-human origin can cause asthma in a subset of any appropriately exposed population34.
The role of mites as a source of house dust allergens has been known for 20 years34,35. It is now possible to measure mite allergens in the environment and IgE antibody levels in patients using readily available techniques and standardized protocols. Experts have proposed provisional standards for levels of mite allergens in dust that lead to sensitization and symptoms. A risk level where chronic exposure may cause sensitization is 2µg Der pI (Dermatophagoides pteronysinus allergen I) per gram of dust (or 100 mites /g or 0.6 mg guanine /g of dust). A risk level for acute asthma in mite-allergic individuals is 10µg (Der pI) of the allergen per gram of dust (or 500 mites /g of dust).
Controlling house dust mite infestation includes covering mattresses, hot washing of bedding, and removing carpet from bedrooms. For mite allergic individuals, it is recommended that home relative humidities be lower than 45 percent. Mites desiccate in drier air (absolute humidities below 7 kg.). Vacuum cleaning and use of acaricides can be effective short-term remedial strategies. One such acaracide, Acarosan, is registered with EPA to treat carpets, furniture, and beds for dust mites.
Another class of hypersensitivity disease is hypersensitivity pneumonitis, which may include humidifier fever. Hypersensitivity pneumonitis, also called allergic alveo-litis, is a granulomatous interstitial lung disease caused by exposure to airborne antigens. It may affect from one to five percent or more of a specialized population exposed to appropriate antigens (e.g., farmers and farmers' lung, pigeon breeders and pigeon breeders' disease)37. Continued antigen exposure may lead to end-stage pulmonary fibrosis. Hypersensitivity pneumonitis is frequently misdiagnosed as a pneumonia of infectious etiology. The prevalence of hypersensitivity pneumonitis in the general population is unknown.
Outbreaks of hypersensitivity pneumonitis in office buildings have been traced to air conditioning and humidification systems contaminated with bacteria and molds38. In the home, hypersensitivity pneumonitis is often caused by contaminated humidifiers or by pigeon or pet bird antigens. The period of sensitization before a reaction occurs may be as long as months or even years. Acute symptoms, which occur four to six hours postexposure and recur on challenge with the offending agent, include cough, dyspnea, chills, myalgia, fatigue, and high fever. Nodules and nonspecific infiltrates may be noted on chest films. The white blood cell count is elevated, as is specific IgG to the offending antigen. Hypersensitivity pneumonitis generally responds to corticosteroids or cessation of exposure (either keeping symptomatic people out of contaminated environments or removing the offering agents).
Humidifier fever is a disease of uncertain etiology39. It shares symptoms with hypersensitivity pneumonitis, but the high attack rate and short-term effects may indicate that toxins (e.g., bacterial endotoxins) are involved. Onset occurs a few hours after exposure. It is a flu-like illness marked by fever, headache, chills, myalgia, and malaise but without prominent pulmonary symptoms. It normally subsides within 24 hours without residual effects, and a physician is rarely consulted. Humidifier fever has been related to exposure to amoebae, bacteria, and fungi found in humidifier reservoirs, air conditioners, and aquaria. The attack rate within a workplace may be quite high, sometimes exceeding 25 percent.
Bacterial and fungal organisms can be emitted from impeller (cool mist) and ultrasonic humidifiers. Mesophilic fungi, thermophilic bacteria, and thermophilic actinomycetes -- all of which are associated with development of allergic responses -- have been isolated from humidifiers built into the forced-air heating system as well as separate console units. Airborne concentrations of microorganisms are noted during operation and might be quite high for individuals using ultrasonic or cool mist units. Drying and chemical disinfection with bleach or 3% hydrogen peroxide solution are effective remedial measures over a short period, but cannot be considered as reliable maintenance. Only rigorous, daily, and end-of-season cleaning regimens, coupled with disinfection, have been shown to be effective. Manual cleaning of contaminated reservoirs can cause exposure to allergens and pathogens.
Another class of agents that may cause disease related to indoor airborne exposure is the mycotoxins. These agents are fungal metabolites that have toxic effects ranging from short-term irritation to immunosuppression and cancer. Virtually all the information related to diseases caused by mycotoxins concerns ingestion of contaminated food40. However, mycotoxins are contained in some kinds of fungus spores, and these can enter the body through the respiratory tract. At least one case of neurotoxic symptoms possibly related to airborne mycotoxin exposure in a heavily contaminated environment has been reported41. Skin is another potential route of exposure to mycotoxins. Toxins of several fungi have caused cases of severe dermatosis. In view of the serious nature of the toxic effects reported for mycotoxins, exposure to mycotoxin-producing agents should be minimized.
Does the individual
reside in mobile home or new conventional home containing large amounts
of pressed wood
products?
Has individual recently acquired new pressed wood furniture?
Increase ventilation when using products that emit volatile organic compounds, and meet or exceed any label precautions. Do not store opened containers of unused paints and similar materials within home or office. See special note on pesticides.
Formaldehyde is one of the best known volatile organic compound (VOC) pollutants, and is one of the few indoor air pollutants that can be readily measured. Identify, and if possible, remove the source if formaldehyde is the potential cause of the problem. If not possible, reduce exposure: use polyurethane or other sealants on cabinets, paneling and other furnishings. To be effective, any such coating must cover all surfaces and edges and remain intact. Formaldehyde is also used in permanent press fabric and mattress ticking. Sensitive individuals may choose to avoid these products.
At room temperature, volatile organic compounds are emitted as gases from certain solids or liquids. VOCs include a variety of chemicals (e.g., formaldehyde, benzene, perchloroethylene), some of which may have short- and long-term effects. Concentrations of many VOCs are consistently higher indoors than outdoors. A study by the EPA, covering six communities in various parts of the United States, found indoor levels up to ten times higher than those outdoors -- even in locations with significant outdoor air pollution sources, such as petrochemical plants42.
A wide array of volatile organics are emitted by products used in home, office, school, and arts/crafts and hobby activities. These products, which number in the thousands, include:
Many of these items carry precautionary labels specifying risks and procedures for safe use; some do not. Signs and symptoms of VOC exposure may include eye and upper respiratory irritation, rhinitis, nasal congestion, rash, pruritus, headache, nausea, vomiting, dyspnea and, in the case of formaldehyde vapor, epistaxis.
Formaldehyde has been classified as a probable human carcinogen by the EPA45. Urea-formaldehyde foam insulation (UFFI), one source of formaldehyde used in home construction until the early 1980s, is now seldom installed, but formaldehyde-based resins are components of finishes, plywood, paneling, fiberboard, and particleboard, all widely employed in mobile and conventional home construction as building materials (sub flooring, paneling) and as components of furniture and cabinets, permanent press fabric, draperies, and mattress ticking.
Airborne formaldehyde acts as an irritant to the conjunctiva and upper and lower respiratory tract. Symptoms are temporary and, depends upon the level and length of exposure, may range from burning or tingling sensations in eyes, nose, and throat to chest tightness and wheezing. Acute, severe reactions to formaldehyde vapor -- which has a distinctive, pungent odor -- may be associated with hypersensitivity. It is estimated that 10 to 20 percent of the U.S. population, including asthmatics, may have hyper reactive airways which may make them more susceptible to formaldehyde's effects46.
Pesticides sold for household use, notably impregnated strips, and foggers or "bombs", which are technically classed as semi volatile organic compounds, include a variety of chemicals in various forms. Exposure to pesticides may cause harm if they are used improperly. However, exposure to pesticides via inhalation of spray mists may occur during normal use. Exposure can also occur via inhalation of vapors and contaminated dusts after use (particularly to children who may be in close contact with contaminated surfaces). Symptoms may include headache, dizziness, muscular weakness, and nausea. In addition, some pesticide active ingredients and inert components are considered possible human carcinogens. Label directions must be explicitly followed47.
Wet-mop and wipe furniture frequently to control lead dust. Have professional remove or encapsulate lead containing paint; individuals involved in this and other high exposure activities should use appropriate protective gear and work in well-ventilated areas. Do not burn painted or treated wood.
Most health professionals are aware of the threat of lead (Pb) toxicity, particularly its long term impact on children in the form of cognitive and developmental deficits which are often cumulative and subtle. Such deficits may persist into adulthood48. According to the American Academy of Pediatrics, an estimated three to four million children in the U.S. under age six have blood lead levels that could cause impaired development, and an additional 400,000 fetuses are at similar risk49.
Lead toxicity may alternatively present as acute illness. Signs and symptoms in children may include irritability, abdominal pain, emesis, marked ataxia, and seizures or loss of consciousness. In adults, diffuse complaints -- including headache, nausea, anorexia (and weight loss), constipation, fatigue, personality changes, and hearing loss -- coupled with exposure opportunity may lead to suspicion of lead poisoning.
Lead inhibits heme synthesis. Since interruption of that process produces protoporphyrin accumulation at the cellular level, the standard screening method is investigation of blood lead (PbB) levels which reveal recent exposure to lead. Acute symptomology in adults is often associated with PbB at levels of 40 g/ dl or higher. There is good evidence for adverse effects of lead in very young children at much lower levels.50,51 The Centers for Disease Control and Prevention has set 10 g/ dl as the level of concern52. Increased maternal Pb exposure has also been deemed significant in pregnancy, since an umbilical cord PbB of greater than 10 g/ dl has been correlated with early developmental deficits. If sufficiently high PbB levels are confirmed, chelation therapy may be indicated. Suspected low level lead contamination cannot be accurately identified by a erythrocyte protoporphyrin (EP) finger-stick test, but requires blood lead analysis.
Lead poisoning via ingestion has been most widely publicized, stressing the roles played by nibbling of flaking paint by infants and toddlers and by the use of lead-containing food ware (glass, and soldered metal-ceramic ware) by adults. Lead dust flaking or "chalking" off lead painted walls generated by friction surfaces is a major concern. Airborne lead, however, is also a worrisome source of toxicity. There is no skin absorption associated with inorganic lead.
Airborne lead outdoors, originating chiefly from gasoline additives, has been effectively controlled since the 1980s through regulation at the federal level. Much of this lead still remains in the soil near heavily trafficked highways and in urban areas, however, and can become airborne at times. It may enter dwellings via windows and doors, and contaminated soil can also be tracked inside.
Indoors, the chief source is paint. Lead levels in paints for interior use have been increasingly restricted since the 1950s, and many paints are now virtually lead free. But older housing and furniture may still be coated with leaded paint, sometimes surfacing only after layers of later, non-lead paint have flaked away or have been stripped away in the course of restoration or renovation. In these circumstances, lead dust and fumes can permeate the air breathed by both adults and children.
Additional sources of airborne lead include art and craft materials, from which lead is not banned, but the U.S. Consumer Product Safety Commission (CPSC) requires its presence to be declared on the product label if it is present in toxic amounts. Significant quantities are found in many paints and glazes, stained glass, as well as in some solder. Hazardous levels of atmospheric lead have been found at police and civilian firing ranges. Repair and cleaning of automobile radiators in inadequately ventilated premises can expose workers to perilous levels of airborne lead. The use of treated or painted wood in fireplaces or improperly vented wood stoves may release a variety of substances, including lead and other heavy metals, into the air.
While old paint has been the most publicized source of airborne heavy metal (i.e., lead), new paint has emerged as a concern as well. A 1990 report detailed elevated levels of mercury in persons exposed to interior latex (water-based) paint containing phenylmercuric acetate (PMA)53. PMA was a preservative that was used to prolong the product's shelf life.
Initial action by the U.S. Environmental Protection Agency resulted in the elimination of mercury compounds from indoor latex paints at the point of manufacture as of August 1990, with the requirement that paints containing mercury, including existing stocks originally designed for indoor use, be labeled or relabeled "For Exterior Use Only". As of September 1991, phenylmercuric acetate is forbidden in the manufacture of exterior latex paints as well. Latex paints containing hazardous levels of mercury may still remain on store shelves or in homes where they were left over after initial use, however.
An additional matter of concern, recently noted by the CPSC, is the sprinkling of mercury about the home by some ethnic/religious groups54. According to the CPSC, mercury for this purpose is purveyed by some herbal medicine or botanical shops to consumers unaware of the dangers of the substance.
Appropriate persons -- employer, building owner or manager, building investigation specialist, if necessary state and local government agency medical epidemiologists and other public health officials -- should undertake investigation and analysis of the implicated building, particularly the design and operation of HVAC systems, and correct contributing conditions. Persistence on the part of individual(s) and health care consultant(s) may be required to diagnose and remediate the building problems.
The term "sick building syndrome" (SBS), first employed in the 1970s, describes a situation in which reported symptoms among a population of building occupants can be temporally associated with their presence in that building. Typically, though not always, the structure is an office building.
Generally, a spectrum of specific and nonspecific complaints are involved. Typical complaints, in addition to the signs and symptoms already listed, may also include eye and/or nasopharyngeal irritation, rhinitis or nasal congestion, inability to concentrate, and general malaise-complaints suggestive of a host of common ailments, some ubiquitous and easily communicable. The key factors are commonality of symptoms and absence of symptoms among building occupants when the individuals are not in the building.
Sick building syndrome should be suspected when a substantial proportion of those spending extended time in a building (as in daily employment) report or experience acute on-site discomfort. If is important, however, to distinguish SBS from problems of building related illness. The latter term is reserved for situations in which signs and symptoms of diagnosable illness are identified and can be attributed directly to specific airborne building contaminants. Legionnaires' Disease and hypersensitivity pneumonitis, for example, are building related illnesses.
There has been extensive speculation about the cause or causes of SBS. Poor design, maintenance, and/or operation of the structure's ventilation system may be at fault55. The ventilation system itself can be a source of irritants. Interior redesign, such as the rearrangement of offices or installation of partitions, may also interfere with efficient functioning of such systems.
Another theory suggests that very low levels of specific pollutants, including some discussed in the preceding pages, may be present and may act synergistically, or at least in combination, to cause health effects. Humidity may also be a factor: while high relative humility may contribute to biological pollutant problems, an unusually low level -- below 20 or 30 percent -- may heighten the effects of mucosal irritants and may even prove irritating itself. Other contributing elements may include poor lighting and adverse ergonomic conditions, temperature extremes, noise, and psychological stresses that may have both individual and interpersonal impact.
The prevalence of the problem is unknown. A 1984 World Health Organization report suggested that as many as 30 percent of new and remodeled buildings worldwide may generate excessive complaints related to indoor air quality56. In a nationwide, random sampling of U.S. office workers, 24 percent perceived air quality problems in their work environments, and 20 percent believed their work performance was hampered thereby57.
When SBS is suspected, the individual physician or other health care provider may need to join forces with others (e.g., clinicians consulted by an individual's co-workers, as well as industrial hygienists and public health officials) to adequately investigate the problem and develop appropriate solutions.
Asbestos and radon are among the most publicized indoor air pollutants. Both are known human carcinogens. Their carcinogenic effects are not immediate but are evident only years, even decades, after prolonged exposure.
Once widely used in structural fireproofing, asbestos may be found predominantly in heating systems and acoustic insulation, in floor and ceiling tiles, and in shingles in many older houses. It was formerly used in such consumer products as fireplace gloves, ironing board covers, and certain hair dryers.
When asbestos-containing material is damaged or disintegrates with age, microscopic fibers may be dispersed into the air. Over as long as twenty, thirty, or more years, the presence of these fibers within the lungs may result in asbestosis (asbestos-caused fibrosis of the lung, seen as a result of heavy occupational exposure)58, lung cancer and pleural or peritoneal cancer, or mesothelioma59. For lung cancer, the effect of tobacco smoking in combination with asbestos exposure appears to be synergistic by approximately fivefold60. Occupational exposure may also be associated with increased risk of gastrointestinal malignancies. Attention should be focused on those populations with continual exposure and documented health effects, e.g. maintenance workers.
Products and materials containing asbestos are not necessarily so labeled. Construction professionals or state or local environmental agencies may inspect and analyze suspect materials. Manufacturers of particular products may also be able to supply information.
The risk of disease depends on exposure to airborne asbestos fibers. Average levels in buildings are low, and the risk to building occupants is therefore low.
Removal of asbestos is not always the best choice to reduce exposure. The EPA requires asbestos removal only in order to prevent significant public exposure and generally recommends an in-place management program when asbestos has been discovered and is in good condition61.
Radon is the second leading cause of lung cancer, following smoking. Radon is odorless, colorless, and tasteless. It is a naturally occurring radioactive gas resulting from the decay of radium, itself a decay product of uranium. Radon in turn breaks down into radon decay products, short-lived radionuclides. These decay products, either free or attached to airborne particles, are inhaled, and further decay can take place in the lungs before removal by clearance mechanisms.
It is the emission of high-energy alpha particles during the radon decay process that increases the risk of lung cancer. While the risk to underground miners has long been known, the potential danger of residential radon pollution has been widely recognized only since the late 1970s, with the documentation of high indoor levels.
When radon decay products are inhaled and deposited in the lungs, the alpha emissions penetrate the cells of the epithelium lining the lung. Energy deposited in these cells during irradiation is believed to initiate the process of carcinogenesis. The EPA, the National Cancer Institute, the Centers for Disease Control and Prevention, and others estimate that thousands of lung cancer deaths per year are attributable to radon, based on data from epidemiologic studies of thousands of underground miners and from animal studies. Lung cancer is presently the only commonly accepted disease risk associated with radon.
Tobacco smoke in combination with radon exposure has a synergistic effect. Smokers and former smokers are believed to be at especially high risk. Scientists estimate that the increased risk of lung cancer to smokers from radon exposure is ten to twenty times higher than to people who have never smoked.
The EPA estimates that as many as six million homes throughout the country have elevated levels of radon. Since 1988, EPA and the Office of the Surgeon General have recommended that homes below the third floor be tested for radon.
Short term testing is the quickest way to determine if a potential problem exists, taking from two to ninety days to complete. Low-cost radon test kits are available by mail order, in hardware stores, and through other retail outlets62.
Measurement devices should be state-certified or display the phrase, "Meets EPA Requirements". Trained contractors who meet EPA's requirements can also provide testing services. The most commonly used devices are charcoal canisters, electret ion detectors, alpha track detectors, and continuous monitors placed by contractors. Short term testing should be conducted in the lowest lived in area of the home, with the doors and windows shut. Long term testing can take up to a full year but is more likely to reflect the home's year round average radon level than short term testing. Alpha track detectors and electret ion detectors are the most common long-term testing devices.
Corrective steps include sealing foundation cracks and holes, and venting radon-laden air from beneath the foundation. Professional expertise should be sought for effective execution of these measures.
The subject of indoor air pollution is not without some controversy. Indoor air quality is an evolving issue; it is important to keep informed about continuing developments in this area. The following questions may be asked of physicians and other health professionals.
The diagnostic label of multiple chemical sensitivity (MCS) -- also referred to as "chemical hypersensitivity" or "environmental illness" -- is being applied increasingly, although definition of the phenomenon is elusive and its pathogenesis as a distinct entity is not confirmed. Multiple chemical sensitivity has become more widely known and increasingly controversial as more patients receive the label63.
Persons with the diagnostic label of multiple chemical sensitivity are said to suffer multi-system illness as a result of contact with, or proximity to, a spectrum of substances, including airborne agents. These may include both recognized pollutants discussed earlier (such as tobacco smoke, formaldehyde, et al.) and other pollutants ordinarily considered innocuous. Some who espouse the concept of MCS believe that it may explain such chronic conditions as some forms of arthritis and colitis, in addition to generally recognized types of hypersensitivity reactions.
Some practitioners believe that the condition has a purely psychological basis. One study63 reported a 65 percent incidence of current or past clinical depression, anxiety disorders, or somatoform disorders in subjects with this diagnosis compared with 28 percent in controls. Others, however, counter that the disorder itself may cause such problems64, since those affected are no longer able to lead a normal life, or that these conditions stem from effects on the nervous system65.
The current consensus is that in cases of claimed or suspected MCS, complaints should not be dismissed as psychogenic, and a thorough workup is essential. Primary care givers should determine that the individual does not have an underlying physiological problem and should consider the value of consultation with allergists and other specialists.
"Clinical ecology", while not a recognized conventional medical specialty, has drawn the attention of health care professionals as well as laypersons. The organization of c