 |
|
|
 |
Indoor Air Pollution |
 |
|---|---|---|
|
|
|
|
|
|
Indoor Air Pollution |
|
|---|---|---|
|
Consumer Product Safety Commssion, |
| Signs and Symptoms | Environmental Tobacco Smoke | Other Combustion Products | Biological Pollutants | Volatile Organics | Heavy Metals | Sick Building Syndrome |
|---|---|---|---|---|---|---|
| RESPIRATORY | ||||||
| Rhinitis, nasal congestion | YES | YES | YES | YES | NO | YES |
| Epistaxis | NO | NO | NO | YES1 | NO | NO |
| Pharyngitis, cough | YES | YES | YES | YES | NO | YES |
| Wheezing, worsening asthma | YES | YES | NO | YES | NO | YES |
| Dyspnea | YES2 | NO | YES | NO | NO | YES |
| Severe lung disease | NO | NO | NO | NO | NO | YES3 |
| OTHER | ||||||
| Conjunctival irritation | YES | YES | YES | YES | NO | YES |
| Headache or dizziness | YES | YES | YES | YES | YES | YES |
| Lethargy, fatigue, malaise | NO | YES4 | YES5 | YES | YES | YES |
| Nausea, vomiting, anorexia | NO | YES4 | YES | YES | YES | NO |
| Cognitive impairment, personality change | NO | YES4 | NO | YES | YES | YES |
| Rashes | NO | NO | YES | YES | YES | NO |
| Fever, chills | NO | NO | YES6 | NO | YES | NO |
| Tachycardia | NO | YES4 | NO | NO | YES | NO |
| Retinal hemorrhage | NO | YES4 | NO | NO | NO | NO |
| Myalgia | NO | NO | NO | YES5 | NO | YES |
| Hearing loss | NO | NO | NO | YES | NO | NO |
Environmental 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.
It 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.
 | When did the [symptom or complaint] begin? |
| Does the [symptom or complaint] exist all the time, or does it come and
go? That is, is it associated with times of day, days of the week, or seasons
of the year? |
| (If so) Are you usually in a particular place at those times? |
| Does the problem abate or cease, either immediately or gradually, when you
leave there? Does it recur when you return? |
| What is your work? Have you recently changed employers or assignments, or
has your employer recently changed location? |
| (If not) Has the place where you work been redecorated or refurnished, or
have you recently started working with new or different materials or
equipment? (These may include pesticides, cleaning products, craft supplies,
et al.) |
| What is the smoking policy at your workplace? Are you exposed to
environmental tobacco smoke at work, school, home, etc.? |
| Describe your work area. |
| Have you recently changed your place of residence? |
| (If not) Have you made any recent changes in, or additions to, your
home? |
| Have you, or has anyone else in your family, recently started a new hobby
or other activity? |
| Have you recently acquired a new pet? |
| Does anyone else in your home have a similar problem? How about anyone
with whom you work? (An affirmative reply may suggest either a common source
or a communicable condition.) |
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.
Return to the Table of Contents
| rhinitis/pharyngitis, nasal congestion, persistent cough |
| conjunctival irritation |
| headache |
| wheezing (bronchial constriction) |
| exacerbation of chronic respiratory conditions |
| asthma onset |
| increased severity of, or difficulty in controlling, asthma |
| frequent upper respiratory infections and/or episodes of otitis media |
| persistent middle-ear effusion |
| snoring |
| repeated pneumonia, bronchitis |
| Is individual exposed to environmental tobacco smoke on a regular basis? |
| Test urine of infants and small children for cotinine, a biomarker for nicotine |
While improved general ventilation of indoor spaces may decrease the odor of environmental tobacco smoke (ETS), health risks cannot be eliminated by generally accepted ventilation methods. Research has led to the conclusion that total removal of tobacco smoke - a complex mixture of gaseous and particulate components - through general ventilation is not feasible.3
The most effective solution is to eliminate all smoking from the individual's environment, either through smoking prohibitions or by restricting smoking to properly designed smoking rooms. These rooms should be separately ventilated to the outside.4
Some higher efficiency air cleaning systems, under select conditions, can remove some tobacco smoke particles. Most air cleaners, including the popular desk-top models, however, cannot remove the gaseous pollutants from this source. And while some air cleaners are designed to remove specific gaseous pollutants, none is expected to remove all of them and should not be relied upon to do so. (For further comment, see Questions That May Be Asked - Can Other Air Cleaners Help?)
Environmental tobacco smoke is a major source of indoor air contaminants. The ubiquitous nature of ETS in indoor environments indicates that some unintentional inhalation of ETS by nonsmokers is unavoidable. Environmental tobacco smoke is a dynamic, complex mixture of more than 4,000 chemicals found in both vapor and particle phases. Many of these chemicals are known toxic or carcinogenic agents. Nonsmoker exposure to ETS-related toxic and carcinogenic substances will occur in indoor spaces where there is smoking.
All the compounds found in "mainstream" smoke, the smoke inhaled by the active smoker, are also found in "sidestream" smoke, the emission from the burning end of the cigarette, cigar, or pipe. ETS consists of both sidestream smoke and exhaled mainstream smoke. Inhalation of ETS is often termed "secondhand smoking", "passive smoking", or "involuntary smoking."
The role of exposure to tobacco smoke via active smoking as a cause of lung and other cancers, emphysema and other chronic obstructive pulmonary diseases, and cardiovascular and other diseases in adults has been firmly established.5,6,7 Smokers, however, are not the only ones affected.
The U.S. Environmental Protection Agency (EPA) has classified ETS as a known human (Group A) carcinogen and estimates that it is responsible for approximately 3,000 lung cancer deaths per year among nonsmokers in the United States.8 The U.S. Surgeon General, the National Research Council, and the National Institute for Occupational Safety and Health also concluded that passive smoking can cause lung cancer in otherwise healthy adults who never smoked.9,10,11
Children's lungs are even more susceptible to harmful effects from ETS. In infants and young children up to three years, exposure to ETS causes an approximate doubling in the incidence of pneumonia, bronchitis, and bronchiolitis. There is also strong evidence of increased middle ear effusion, reduced lung function, and reduced lung growth. Several recent studies link ETS with increased incidence and prevalence of asthma and increased severity of asthmatic symptoms in children of mothers who smoke heavily. These respiratory illnesses in childhood may very well contribute to the small but significant lung function reductions associated with exposure to ETS in adults. The adverse health effects of ETS, especially in children, correlate with the amount of smoking in the home and are often more prevalent when both parents smoke.12
The connection of children's symptoms with ETS may not be immediately evident to the clinician and may become apparent only after careful questioning. Measurement of biochemical markers such as cotinine (a metabolic nicotine derivative) in body fluids (ordinarily urine) can provide evidence of a child's exposure to ETS.13
The impact of maternal smoking on fetal development has also been well documented. Maternal smoking is also associated with increased incidence of Sudden Infant Death Syndrome, although it has not been determined to what extent this increase is due to in utero versus postnatal (lactational and ETS) exposure.14
Airborne particulate matter contained in ETS has been associated with impaired breathing, lung diseases, aggravation of existing respiratory and cardiovascular disease, changes to the body's immune system, and lowered defenses against inhaled particles.15 For direct ETS exposure, measurable annoyance, irritation, and adverse health effects have been demonstrated in nonsmokers, children and spouses in particular, who spend significant time in the presence of smokers.16,17 Acute cardiovascular effects of ETS include increased heart rate, blood pressure, blood carboxyhemoglobin; and related reduction in exercise capacity in those with stable angina and in healthy people. Studies have also found increased incidence of nonfatal heart disease among nonsmokers exposed to ETS, and it is thought likely that ETS increases the risk of peripheral vascular disease, as well.18
Return to the Table of Contents
| dizziness or headache |
| confusion |
| nausea/emesis |
| fatigue |
| tachycardia |
| eye and upper respiratory tract irritation |
| wheezing/bronchial constriction |
| persistent cough |
| elevated blood carboxyhemoglobin levels |
| increased frequency of angina in persons with coronary heart disease |
| What types of combustion equipment are present, including gas furnaces or water heaters, stoves, unvented gas or kerosene space heaters, clothes dryers, fireplaces? Are vented appliances properly vented to the outside? |
| Are household members exhibiting influenza-like symptoms during the heating season? Are they complaining of nausea, watery eyes, coughing, headaches? |
| Is a gas oven or range used as a home heating source? |
| Is the individual aware of odor when a heat source is in use? |
| Is heating equipment in disrepair or misused? When was it last professionally inspected? |
| Does structure have an attached or underground garage where motor vehicles may idle? |
| Is charcoal being burned indoors in a hibachi, grill, or fireplace? |
Periodic professional inspection and maintenance of installed equipment such as furnaces, water heaters, and clothes dryers are recommended. Such equipment should be vented directly to the outdoors. Fireplace and wood or coal stove flues should be regularly cleaned and inspected before each heating season. Kitchen exhaust fans should be exhausted to outside. Vented appliances should be used whenever possible. Charcoal should never be burned inside. Individuals potentially exposed to combustion sources should consider installing carbon monoxide detectors that meet the requirements of Underwriters Laboratory (UL) Standard 2034. No detector is 100% reliable, and some individuals may experience health problems at levels of carbon monoxide below the detection sensitivity of these devices.
Aside from environmental tobacco smoke, the major combustion pollutants that may be present at harmful levels in the home or workplace stem chiefly from malfunctioning heating devices, or inappropriate, inefficient use of such devices. Incidents are largely seasonal. Another source may be motor vehicle emissions due, for example, to proximity to a garage (or a loading dock located near air intake vents).
A variety of particulates, acting as additional irritants or, in some cases, carcinogens, may also be released in the course of combustion. Although faulty venting in office buildings and other nonresidential structures has resulted in combustion product problems, most cases involve the home or non-work-related consumer activity. Among possible sources of contaminants: gas ranges that are malfunctioning or used as heat sources; improperly flued or vented fireplaces, furnaces, wood or coal stoves, gas water heaters and gas clothes dryers; and unvented or otherwise improperly used kerosene or gas space heaters.
The gaseous pollutants from combustion sources include some identified as prominent atmospheric pollutants -- carbon monoxide (CO), nitrogen dioxide (NO2), and sulfur dioxide (SO2).
Carbon monoxide is an asphyxiant. An accumulation of this odorless, colorless gas may result in a varied constellation of symptoms deriving from the compound's affinity for and combination with hemoglobin, forming carboxyhemoglobin (COHb) and disrupting oxygen transport. The elderly, the fetus, and persons with cardiovascular and pulmonary diseases are particularly sensitive to elevated CO levels. Methylene chloride, found in some common household products, such as paint strippers, can be metabolized to form carbon monoxide which combines with hemoglobin to form COHb. The following chart shows the relationship between CO concentrations and COHb levels in blood.
Tissues with the highest oxygen needs -- myocardium, brain, and exercising muscle -- are the first affected. Symptoms may mimic influenza and include fatigue, headache, dizziness, nausea and vomiting, cognitive impairment, and tachycardia. Retinal hemorrhage on funduscopic examination is an important diagnostic sign19, but COHb must be present before this finding can be made, and the diagnosis is not exclusive. Studies involving controlled exposure have also shown that CO exposure shortens time to the onset of angina in exercising individuals with ischemic heart disease and decreases exercise tolerance in those with chronic obstructive pulmonary disease (COPD)20.
Note: Since CO poisoning can mimic influenza, the health care provider should be suspicious when an entire family exhibits such symptoms at the start of the heating season and symptoms persist with medical treatment and time.
 |
| Relationship between carbon
monoxide (CO) concentrations and carboxyhemoglobin (COHb) levels in
blood Predicted COHb levels resulting from 1- and 8-hour exposures to carbon monoxide at rest (10 l/min) and with light exercise (20 l/min) are based on the Coburn-Foster-Kane equation using the following assumed parameters for nonsmoking adults: altitude = 0 ft; initial COHb level = 0.5%; Haldane constant = 218; blood volume = 5.5 l; hemoglobin level = 15 g/100ml; lung diffusivity = 30 ml/torr/min; endogenous rate = 0.007 ml/min. Source: Raub, J.A. and Grant, L.D. 1989. "Critical health issues associated with review of the scientific criteria for carbon monoxide." Presented at the 82nd Annual Meeting of the Air Waste Management Association. June 25-30. Anaheim, CA. Paper No. 89.54.1, Used with permission. |
| % COHb in blood | Effects Assocated 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.
Return to the Table of Contents
| recognized infectious disease |
| exacerbation of asthma |
| rhinitis |
| conjunctival inflammation |
| recurrent fever |
| malaise |
| dyspnea |
| chest tightness |
| cough |
| Is the case related to the workplace, home, or other location? (Note: It is difficult to associate a single case of any infectious disease with a specific site of exposure.) |
| Does the location have a reservoir or disseminator of biologicals that may logically lead to exposure? |
| Is the relative humidity in the home or workplace consistently above 50 percent? |
| Are humidifiers or other water-spray systems in use? How often are they cleaned? Are they cleaned appropriately? |
| Has there been flooding or leaks? |
| Is there evidence of mold growth (visible growth or odors)? |
| Are organic materials handled in the workplace? |
| Is carpet installed on unventilated concrete (e.g., slab on grade) floors? |
| Are there pets in the home? |
| Are there problems with cockroaches or rodents? |
| Is adequate outdoor air being provided? |
| Is the relative humidity in the home or workplace above 50 percent or below 30 percent? |
| Are humidifiers or other water-spray systems in use? |
| Is there evidence of mold growth (visible growth or odors)? |
| Are bacterial odors present (fishy or locker-room smells)? |
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 immunosuppressed, 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.
Return to the Table of Contents
| conjunctival irritation |
| nose, throat discomfort |
| headache |
| allergic skin reaction |
| dyspnea |
| declines in serum cholinesterase levels |
| nausea, emesis |
| epistaxis (formaldehyde) |
| fatigue |
| dizziness |
| 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? |
| Does the individual's job or avocational pursuit include clerical, craft, graphics, or photographic materials? |
| Are chemical cleaners used extensively in the home, school, or workplace? |
| Has remodeling recently been done in home, school or workplace? |
| Has individual recently used pesticides, paints, or solvents? |
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:
| personal items such as scents and hair sprays; |
| household products such as finishes, rug and oven cleaners, paints and lacquers (and their thinners), paint strippers, pesticides (see below); |
| dry-cleaning fluids; |
| building materials and home furnishings; |
| office equipment such as some copiers and printers; |
| office products such as correction fluids and carbonless copy paper43,44; |
| graphics and craft materials including glues and adhesives, permanent markers, and photographic solutions. |
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 (subflooring, 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 hyperreactive 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 semivolatile 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.
Return to the Table of Contents
| gastrointestinal discomfort/constipation/anorexia/nausea |
| fatigue, weakness |
| personality changes |
| headache |
| hearing loss |
| tremor, lack of coordination |
| irritability |
| abdominal pain |
| ataxia |
| seizures/ loss of consciousness |
| (chronic) learning deficits |
| hyperactivity, reduced attention span |
| muscle cramps or tremors |
| headache |
| tachycardia |
| intermittent fever |
| acrodynia |
| personality change |
| neurological dysfunction |
| Does the family reside in old or restored housing? |
| Has renovation work been conducted in the home, workplace, school, or day care facility? |
| Is the home located near a busy highway or industrial area? |
| Does the individual work with lead materials such as solder or automobile radiators? |
| Does the child have sibling, friend, or classmate recently diagnosed with lead poisoning? |
| Has the individual engaged in art, craft, or workshop pursuits? |
| Does the individual regularly handle firearms? |
| Has the home interior recently been painted with latex paint that may contain mercury? |
| Does the individual use mercury in religious or cultural activities? |
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 foodware (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 h
