|
Indoor Air Pollution |
Disclaimer
Co-sponsored
by: The American Lung Assoc. (ALA),
The Environmental Protection Agency (EPA),
The Consumer Product Safety Commission (CPSC),
and the American Medical Association (AMA)
U.S. Govt. Printing Office Pub. No.
1994-523-217/81322 1994
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Indoor 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.
The 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.
|
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 |
- Associated especially with
formaldehyde.
- In asthma.
- Hypersensitivity pneumonitis,
Legionnaires' Disease.
- Particularly associated with high CO
levels.
- Hypersensitivity pneumonitis,
humidifier fever.
- With marked hypersensitivity reactions
and Legionnaires' Disease.
Particular Effects Seen
in Infants and Children
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.
Key Signs/Symptoms in Adults
...
- rhinitis/pharyngitis, nasal congestion,
persistent cough
- conjunctiva irritation
- headache
- wheezing (bronchial constriction)
- exacerbation of chronic respiratory
conditions
... and in Infants and
Children
- 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
Diagnostic Leads
- Is individual exposed to environmental
tobacco smoke on a regular basis?
- Test urine of infants and small
children for cotinine, a biomarker for nicotine
Remedial Action
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?)
Comment
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 "side stream" smoke, the emission from the burning end of the
cigarette, cigar, or pipe. ETS consists of both side stream 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 (lactation 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
Health Problems Caused By
OTHER COMBUSTION PRODUCTS
(Stoves, Space Heaters, Furnaces, Fireplaces)
Key Signs/Symptoms
- 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
Diagnostic Leads
-
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?
Remedial Action
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.
Comment
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. |
Carboxyhemoglobin levels
and related health effects
|
%
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.
Key Signs/Symptoms
- recognized infectious disease
- exacerbation of asthma
- rhinitis
- conjunctiva inflammation
- recurrent fever
- malaise
- dyspnea
- chest tightness
- cough
Diagnostic Leads
Infectious disease:
- 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 biological that may logically lead to exposure?
Hypersensitivity disease:
- 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?
Toxicities and/or
irritation:
- 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)?
Remedial Action
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.
Comment
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.
Health Problems Caused By
VOLATILE ORGANIC COMPOUNDS
(Formaldehyde, Pesticides, Solvents, Cleaning Agents)
Key Signs/Symptoms
- conjunctiva irritation
- nose, throat discomfort
- headache
- allergic skin reaction
- dyspnea
- declines in serum cholinesterase levels
- nausea, emesis
- epistaxis (formaldehyde)
- fatigue
- dizziness
Diagnostic Leads
Remedial Action
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.
Comment
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 (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.
Key Signs/Symptoms of
Lead Poisoning in Adults...
- gastrointestinal
discomfort/constipation/anorexia/nausea
- fatigue, weakness
- personality changes
- headache
- hearing loss
- tremor, lack of coordination
... and in Infants and Small
Children
- irritability
- abdominal pain
- ataxia
- seizures/ loss of consciousness
- (chronic) learning deficits
- hyperactivity, reduced attention span
Key Signs/Symptoms of
Mercury Poisoning
- muscle cramps or tremors
- headache
- tachycardia
- intermittent fever
- acrodynia
- personality change
- neurological dysfunction
Diagnostic Leads
- 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?
Remedial Action
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.
Comment
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.
Key Signs/Symptoms
- lethargy or fatigue
- headache, dizziness, nausea
- irritation of mucous membranes
- sensitivity to odors
Diagnostic Leads
- Are problems temporally related to time
spent in a particular building or part of a building?
- Do symptoms resolve when the individual
is not in the building?
- Do symptoms recur seasonally (heating,
cooling)?
- Have co-workers, peers noted similar
complaints?
Remedial Action
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.
Comment
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
clinical ecologists-physicians who treat individuals believed to be
suffering from "total allergy" or "multiple chemical sensitivity" -- was
founded as the Society for Clinical Ecology and is now known as the
American Academy of Environmental Medicine. Its ranks have attracted
allergists and physicians from other traditional medical specialties66.
Ion generators act by
charging the particles in a room so that they are attracted to walls,
floors, tabletops, draperies, occupants, etc. Abrasion can result in these
particles being resuspended into the air. In some cases these devices
contain a collector to attract the charged particles back to the unit.
While ion generators may remove small particles (e.g., those in tobacco
smoke) from the indoor air, they do not remove gases or odors, and may be
relatively ineffective in removing large particles such as pollen and
house dust allergens. Although some have suggested that these devices
provide a benefit by rectifying a hypothesized ion imbalance, no
controlled studies have confirmed this effect.
Ozone, a lung irritant, is
produced indirectly by ion generators and some other electronic air
cleaners and directly by ozone generators. While indirect ozone production
is of concern, there is even greater concern with the direct, and
purposeful introduction of a lung irritant into indoor air. There is no
difference, despite some marketers' claims, between ozone in smog outdoors
and ozone produced by these devices. Under certain use conditions ion
generators and other
ozone generating air cleaners can produce levels of this lung irritant
significantly above levels thought harmful to human health. A small
percentage of air cleaners that claim a health benefit may be regulated by
FDA as a medical device. The Food and Drug Administration has set a limit
of 0.05 parts per million of ozone for medical devices. Although ozone can
be used in reducing odors and pollutants in unoccupied spaces (such as
removing smoke odors from homes involved in fires) the levels needed to
achieve this are above those generally thought to be safe for humans.
Ion generators and
ozone generators are types of air cleaners; others include mechanical
filter air cleaners, electronic air cleaners (e.g., electrostatic
precipitators), and hybrid air cleaners utilizing two or more techniques.
Generally speaking, existing air cleaners are not appropriate single
solutions to indoor air quality problems, but can be useful as an adjunct
to effective source control and adequate ventilation. Air cleaning alone
cannot adequately remove all pollutants typically found in indoor air.
The value of any air
cleaner depends upon a number of factors, including its basic efficiency,
proper selection for the type of pollutant to be removed, proper
installation in relation to the space, and faithful maintenance.
Drawbacks, varying with type, may include inadequate pollutant removal,
re-dispersement of pollutants, deceptive masking rather than removal,
generation of ozone, and unacceptable noise levels.
[At the time of this
publication,] the EPA and CPSC had not taken a position either for or
against the use of these devices in the home67. For more
information on ozone generators, read the recently released fact sheet:
Ozone Generators That Are Sold As Air Cleaners. The purpose of
this document (which is only available via this web site) is to provide
accurate information regarding the use of ozone-generating devices in
indoor occupied spaces. This information is based on the most credible
scientific evidence currently available.
As awareness of the
importance of indoor air quality grows, more people are looking at duct
cleaning as a way to solve indoor air quality problems. Individuals
considering having ducts cleaned should determine that contaminated ducts
are the cause of their health problems. Even when contaminants are found
in ducts, the source may lie elsewhere, and cleaning ducts may not
permanently solve the problem. The duct cleaning industry is expanding to
meet demand, using extensive advertising to encourage people to use their
services.
Individuals who employ
such services should verify that the service provider takes steps to
protect individuals from exposure to dislodged pollutants and chemicals
used during the cleaning process. Such steps may range from using HEPA
filtration on cleaning equipment, providing respirators for workers, and
occupants vacating the premises during cleaning.
Update: EPA
has recently released the document "Should
You Have the Air Ducts in Your Home Cleaned," EPA-402-K-97-002, ISBN
0-16-042730-4, October 1997. You can click on the hyperlinked title or you
can order a copy of the document from IAQ INFO at 1-800-438-431 (local
(703) 356-4020).
Like many other household
products and furnishings, new carpet can be a source of chemical
emissions. Carpet emits volatile organic compounds, as do products that
accompany carpet installation such as adhesives and padding. Some people
report symptoms such as eye, nose and throat irritation; headaches; skin
irritations; shortness of breath or cough; and fatigue, which they may
associate with new carpet installation. Carpet can also act as a "sink"
for chemical and biological pollutants including pesticides, dust mites,
and fungi.
Individuals purchasing new
carpet should ask retailers for information to help them select lower
emitting carpet, cushion, and adhesives. Before new carpet is installed,
they should ask the retailer to unroll and air out the carpet in a clean,
well-ventilated area. They should consider leaving the premises during and
immediately after carpet installation or schedule the installation when
the space is unoccupied. Opening doors and windows and increasing the
amount of fresh air indoors will reduce exposure to most chemicals
released from newly installed carpet. During and after installation in a
home, use of window fans and room air conditioners to exhaust fumes to the
outdoors is recommended. Ventilation systems should be in proper working
order, and should be operated during installation, and for 48 to 72 hours
after the new carpet is installed.
Individuals should request
that the installer follow the Carpet and Rug Institute's installation
guidelines68. If new carpet has an objectionable odor, they
should contact their carpet retailer. Finally, carpet owners should follow
the manufacturer's instructions for proper carpet maintenance.
Recent reports in the
media and promotions by the decorative houseplant industry characterize
plants as "nature's clean air machine", claiming that National Aeronautics
and Space Administration (NASA) research shows plants remove indoor air
pollutants. While it is true that plants remove carbon dioxide from the
air, and the ability of plants to remove certain other pollutants from
water is the basis for some pollution control methods, the ability of
plants to control indoor air pollution is less well established. Most
research to date used small chambers without any air exchange which makes
extrapolation to real world environments extremely uncertain. The only
available study of the use of plants to control indoor air pollutants in
an actual building could not determine any benefit from the use of plants69.
As a practical means of pollution control, the plant removal mechanisms
appear to be inconsequential compared to common ventilation and air
exchange rates. In other words, the ability of plants to actually improve
indoor air quality is limited in comparison with provision of adequate
ventilation.
While decorative foliage
plants may be aesthetically pleasing, it should be noted that over damp
planter soil conditions may actually promote growth of unhealthy
microorganisms.
For assistance and
guidance in dealing with known or suspected adverse effects of indoor air
pollution, contact the U.S. Environmental Protection Agency Indoor Air
Quality Information Clearinghouse [IAQ INFO] (1-800-438-4318), EPA
regional offices, and state and local departments of health and
environmental quality, and your local
American Lung Association (1-800-LUNG-USA).
For information on
particular product hazards, contact the
U.S. Consumer Product Safety Commission
(1-800-638-CPSC). Individual manufacturers, as well as trade associations,
may also supply pertinent information.
For information about
regulation of specific pollutants, call the EPA Toxic Substances Control
Act (TSCA) Assistance Information Service (202-554-1404).
For information relating
to occupational exposures, contact the Occupational Safety and Health
Administration (202-523-6091) or the National Institute of Occupational
Safety and Health (1-800-35-NIOSH).
For information on lead,
contact the National Lead Information Center (1-800-LEAD FYI). For
information on pesticides, contact the National Pesticides
Telecommunications Network (1-800-858-PEST).
Many sources of
information are listed in the references for each chapter of this
document. The following publications may also be useful to the health
professional and to the patient.
GENERAL INFORMATION ON
INDOOR AIR POLLUTION
For the health
professional:
- American Lung Association. "Health
Effects and Sources of Indoor Air Pollution, Parts I and II". 1989.
Publication No. 0857C.
- American Thoracic Society.
"Environmental Controls and Lung Disease". American Review of
Respiratory Disease. 1990. 142: 915-939.
- Gammage, R.B., Kaye, S.V. Indoor Air
and Human Health. Lewis Publishers, Inc. Chelsea, MI.
- Gergan, Pj., Weiss, K.B. "The
Increasing Problem of Asthma in the United States". American Review
of Respiratory Disease. 1992. 146(4): 823-824.
- Gold, D.R. "Indoor Air Pollution".
Clinics in Chest Medicine. June 1992. 13(2):215-229.
- Samet, J.M., Spengler,J.D., eds.
Indoor Air Pollution - A Health Perspective.
Johns Hopkins
University Press. Baltimore, MD. 1991.
- Turiel, I. Indoor Air Quality and
Human Health. 1985. Stanford University Press. Stanford, CA.
- U.S. Environmental Protection Agency.
"Building Air Quality: A Guide for Building Owners and Facility
Managers". U.S. Government Printing Office. Washington, D.C.
EPA-055-000-00390-4. December 1991.
- U.S. Environmental Protection Agency.
"EPA Indoor Environmental Quality Survey". 1992. OMB No. 2060-0244.
- U.S. Environmental Protection Agency,
U.S. Public Health Service, National Environmental Health Association.
"Introduction to Indoor Air Quality: A Self-Paced Learning Module".
EPA-400-3-91-002. July 1991.
- U.S. Environmental Protection Agency.
The Total Exposure Assessment Methodology (TEAM) Study; Project Summary.
1987. EPA-600-56-87-002.
- Wadden, R.A., Scheff, P.A. Indoor
Air Pollution - Characterization, Prediction, and Control. 1983.
John Wiley and Sons, Inc. New York, NY.
For the patient (may be
helpful to the professional as well):
- American Lung Association. "Air
Pollution In Your Home?". 1990. Publication No. 1001C.
- American Lung Association. "Home Indoor
Air Quality Checklist". 1992. Publication No. 0679C.
- American Lung Association. "Indoor Air
Pollution Fact Sheet - Household Products". 1990. Publication No. 1187C.
- U.S. Environmental Protection Agency,
U.S. Consumer Product Safety Commission.
" The Inside Story: A Guide To Indoor Air Quality". 1993.
EPA-402-R-93-013.
- U.S. Environmental Protection Agency.
"Targeting Indoor Air Pollution -- EPA's Approach and Progress".
September 1992. EPA-400-R-92-012.
ENVIRONMENTAL TOBACCO SMOKE
(ETS)
For the health
professional:
- Bascom, R., Kulle T., Kagey-Sobotka A.,
Proud, D. "Upper Respiratory Tract Environmental Tobacco Smoke
Sensitivity". American Review of Respiratory Disease. 1991.
143:1304-1311.
- International Cancer Information
Center. "Selected Abstracts on Environmental Tobacco Smoke and Cancer".
National Cancer Institute. Oncology Reviews series. October 1989.
For the patient (may be
helpful to the professional as well):
COMBUSTION PRODUCTS
For the patient (may be
helpful to the professional as well):
CARBON MONOXIDE (CO)
the health professional:
- Chaitman, B.R., Dahms, T.E., Byers, S.,
Carroll, L.W., Younis, L.T., Wiens, R.D. "Carbon Monoxide Exposure of
Subjects With Documented Cardiac Arrhythmias". Health Effects Institute
Research Report No. 52. 1992.
- U.S. Consumer Product Safety
Commission.
"The Senseless Killer". 1993. GPO Publication No. 1993-0-356-764.
- Kirkpatrick, J.N. "Occult Carbon
Monoxide Poisoning". Western Journal of Medicine. 1987-147:52-56.
ANIMAL DANDER, MOLDS, DUST
MITES, OTHER BIOLOGICALS
For the health
professional:
- Burge, Harriet A. "Indoor Air and
Infectious Disease". In: Cone, J.E., Hodgson, Mj. Problem Buildings:
Building-Associated Illness and the Sick Building Syndrome. State of the
Art Reviews in Occupational Medicine. 1989. 4(4): 713-721.
- Burge, Harriet A. "Toxigenic Potential
of Indoor Microbial Aerosols". In: Sandhu, S.S., MeMarini, D.M., Mass,
Mj., Moore, M.M., Mumford, J.L. Short-Term Bioassays in the Analysis
of Complex Environmental Mixtures. V. Plenum Publishing, Inc.
1987:391-721.
- Gallup, J., Kozak, P., Cummins, L.,
Gillman, S. 1987. "Indoor Mold Spore Exposure: Characteristics of 127
Homes in Southern California with Endogenous Mold Problems",
Experintia Suppl. 51: 139-142.
- Health Department Victoria. 1989.
"Guidelines for Control of Legionnaire's Disease". Health Department
Victoria. Melbourne, Australia.
- Morey, P.H., Feeley, J.C. Sr.,
Otten,J.A. "Biological Contaminants In Indoor Environments". STP 1071,
Philadelphia: ASTM, 1990.
- Platts-Mills, T.A.E., de Weck, A.L.
1989. "Dust Mite Allergens and Asthma - A Worldwide Problem
(International Workshop)". Journal Allergy Clinical Immunology.
83: 416-427.
- Pope, A.M., Patterson, R., Burge,
Harriet A. "Indoor Allergens: Assessing and Controlling Adverse Health
Effects. 1993. National Academy Press.
For the patient (may be
helpful to the professional as well):
- American Lung Association. "Indoor Air
Pollution Fact Sheet - Biological Agents". 1991. Publication No. 1186C.
- National Institutes of Health, National
Institute of Allergy and Infectious Diseases. "Something in the Air:
Airborne Allergens". March 1993. NIH Publication No. 93-493.
- U.S. Consumer Product Safety
Commission, American Lung Association,.
"Biological
Pollutants In Your Home". 1990. ALA Publication No. 3715C.
- U.S. Consumer Product Safety
Commission, "News from CPSC - Portable Humidifiers Need Regular Cleaning
During Winter Months". January 1992. Release No. 92-48.
- U.S. Environmental Protection Agency.
"Indoor Air Fact Sheet: Use and Care of Home Humidifiers".
February
1991.
TUBERCULOSIS
For the health
professional:
- "Diagnostic Standards and
Classification of Tuberculosis".
American Review of Respiratory Disease. 1990-142:725-35.
- "Prevention and Control of Tuberculosis
Among Homeless Persons: Recommendations of the Advisory Committee for
Elimination of Tuberculosis". Morbidity and Mortality Weekly Report.
Centers for Disease Control and Prevention. 1992. 41 (No. RR-5):13-23.
- "Prevention and Control of Tuberculosis
in Facilities Providing Long-Term Care to the Elderly: Recommendations
of the Advisory Committee for Elimination of Tuberculosis.
- Morbidity and Mortality Weekly Report.
Centers for Disease Control and Prevention. 1990-39 (No. RR-IO): 7-20.
- "Prevention and Control of Tuberculosis
in U.S. Communities with At-Risk Minority Populations: Recommendations
of the Advisory Committee for Elimination of Tuberculosis". Morbidity
and Mortality Weekly Report. Centers for Disease Control and Prevention.
1992. 41 (No. RR-5):1-12.
- "Screening for Tuberculosis and
Tuberculosis Infection In High-Risk Populations: Recommendations of the
Advisory Committee for the Elimination of Tuberculosis". Morbidity and
Mortality Weekly Report. Centers for Disease Control and Prevention.
1990-39 (No. RR-8): 1-7.
- "The Use of Preventive Therapy for
Tuberculosis Infection in the United States: Recommendations of the
Advisory Committee for Elimination of Tuberculosis". Morbidity and
Mortality Weekly Report. Centers for Disease Control and Prevention.
1990-39 (No. RR-8): 8-12.
- "Tuberculosis Among Foreign-Born
Persons Entering the United States: Recommendations of the Advisory
Committee for Elimination of Tuberculosis". Morbidity and Mortality
Weekly Report. Centers for Disease Control and Prevention. 1990-39
(No.R-18): 1-21.
- "Tuberculosis and Human
Immunodeficiency Virus Infection: Recommendations of the Advisory
Committee for Elimination of Tuberculosis". Morbidity and Mortality
Weekly Report. Centers for Disease Control and Prevention. 1989.38(14):
236-238, 243-250.
For the patient (may be
helpful to the professional as well):
- American Lung Association. "Facts About
The TB Skin Test". 1992. Publication No. 0178. (Spanish version,
Publication No. 0177).
- American Lung Association. "Facts About
Tuberculosis". 1991. Publication No. 1091.
VOLATILE ORGANIC COMPOUNDS (VOCs)
For the health
professional:
- Harving, H., Dahl, R., Molhave, L.
"Lung Function and Bronchial Activity in Asthmatics During Exposure to
Volatile Organic Compounds". American Review of Respiratory Disease.
143:751-754.
- Molhave, L., Bach, B., Pederson, O.F.
1986. "Human Reactions to Low Concentrations of Volatile Organic
Compounds" Environmental International. 12:157-176.
- Norback, D. et al. 1990. "Volatile
Organic Compounds, Respirable Dust, and Personal Factors Related to the
Prevalence and Incidence of the Sick Building Syndrome in Primary
Schools". Brit. J. Ind. Med. 47:733-774.
- Otto, D.A. et al. 1990.
"Neurobehavioral and Sensory Irritant Effects of Controlled Exposure to
a Complex Mixture of Volatile Organic Compounds". Neurotox. and
Texatol. 12:1-4.
- U.S. Environmental Protection Agency.
Nonoccupational Pesticide Exposure Study (NOPES); Project Summary.
Publication No. IAQ-0028.
FORMALDEHYDE
For the patient (may be
helpful to the professional as well):
- American Lung Association. "Indoor Air
Pollution Fact Sheet - Formaldehyde". 1989. Publication No. 1184C.
- U.S. Consumer Product Safety
Commission. "An
Update On Formaldehyde". October 1990.
SICK BUILDING SYNDROME (SBS)
For the health
professional:
- Berney, B.W., Light, E.N., Bennett, A.C.
"Medical Evaluation of 'Building Related' Symptoms". Proceedings of the
Seventh Annual Hazardous Materials Management Conference International.
1989.
- Burge, S. et al. 1987. "Sick Building
Syndrome: A Study of 4373 Office Workers". Ann. Occupational Hygiene.
31: 493-504.
- Finnegan, M.J. et al. 1984. "The Sick
Building Syndrome Prevalence Studies". Brit. Medical Journal.
289: 1573-1575.
- Hedge, A. "Work-Related Illness In
Offices: A Proposed Model of the Sick Building Syndrome". Env. Int.
15: 143-158.
- Hodgson, V.S. et al. 1986. "The Sick
Building Syndrome". In: Proceedings of the Third International
Conference on Indoor Air Quality and Climate, Vol. 6. Evaluations and
Conclusions for Health Sciences and Technology, pp. 87-97. Swedish
Council for Building Research. Stockholm, Sweden.
- Kreiss, K. 1989. "The Epidemiology of
Building-Related Complaints and Illness". 572-592. In: Problem
Buildings: Building-Associated Illness and the Sick Building Syndrome.
Cone, J. E., Hodgson, M.E., eds. Hanley and Belfus, Inc., Philadelphia.
- Mendell, M.J., Smith, A.H. "Consistent
Pattern of Elevated Symptoms in Air-Conditioned Office Buildings: A
Reanalysis of Epidemiologic Studies". American Journal of Public
Health. 80: 1193-1199.
- McCunney, R.J. "The Role of Building
Construction and Ventilation in Indoor Air Pollution". New York State
Journal of Medicine. April 1987. pp. 203-209.
- Molina, C. et al. 1989. "Sick Building
Syndrome - A Practical Guide". Report No. 4. Commission of the European
Communities. Brussels, Luxembourg.
- Norback, D. et al. 1990. "Indoor Air
Quality and Personal Factors Related to the Sick Building Syndrome".
Scan. J. Work Environmental Health. 16: 121-128.
- Norback, D. et al. 1990. "Volatile
Organic Compounds, Respirable Dust, and Personal Factors Related to the
Prevalence and Incidence of the Sick Building Syndrome in Primary
Schools". Brit J Ind. Med.. 47: 733-774.
- Seitz, T.A. 1989. "NIOSH Indoor Air
Quality Investigations 1971-1988". 163-171. In: The Practitioners
Approach to Indoor Air Quality Investigations. Proc. Indoor Air Quality
International Symposium. Weedes, D.M., Gammage, R.B., eds. American
Industrial Hygiene Association, Akron, Ohio.
- Skov, P. et al. 1990. "Influence of
Indoor Air Climate on the Sick Building Syndrome in an Office
Environment". Scandinavian Journal Work Environmental Health. 16:
363-371.
- Skov, P. et al. 1989. "Influence of
Personal Characteristics, Job Related Factors and Psychological Factors
on the Sick Building Syndrome". Scandinavian Journal Work
Environmental Health. 15: 286-295.
- Skov, P. et al. 1987. "The Sick
Building Syndrome in the Office Environment: The Danish Town Hall
Study". Env. Int. 13: 334-349.
- Stenberg, B. 1989. "Skin Complaints in
Buildings with Indoor Climate Problems". Env. Int. 15: 81-84.
- Sterling, T.D. et al. 1983. "Building
Illness in the White Collar Workplace". International Journal of
Health Services. 13:277-287.
- U.S. Environmental Protection Agency.
"Indoor Air Quality and Work Environment Study". EPA-21-M-3004. June
1991.
For the patient (may be
helpful to the professional as well):
ASBESTOS
For the patient (may be
helpful to the professional as well):
- American Lung Association. "Indoor Air
Pollution Fact Sheet - Asbestos". 1991. Publication No. 1188C.
RADON
For the health
professional:
- American Medical Association and U.S.
Environmental Protection Agency.
"Radon: The Health Threat with a Simple Solution. A Physician's Guide".
AMA. EPA-402-K-93-008. 1993.
- Fabrikant, J. I. "Shelter and Indoor
Air in the Twenty-First Century - Radon, Smoking and Lung Cancer Risks".
Environmental Health Perspectives. 1990. 86:275-280.
- National Academy of Sciences.
Comparative Dosimetry of Radon in Mines -and Homes. National Academy
Press. Washington, D.C. 1991.
- National Research Council, Committee on
the Biological Effects of Ionizing Radiation. "Health Risks of Radon and
Other Internally Deposited Alpha-Emitters". BIER IV. Washington,
DC: National Academy Press, 1988.
- Nero, A.V., Jr. "Radon and Its Decay
Products in Indoor Air: An Overview". In: Nazaroff, W.W., Nero, A.V.,
Jr., eds. Radon and Its Decay Products In Indoor Air. New York:
John Wiley and Sons Inc. 1988:1-53.
- Roscoe, R.J. et al. "Lung Cancer
Mortality Among Non-Smoking Uranium Miners Exposed to Radon Daughters".
Journal of the American Medical Association. 262(5): 629-633. 1989.
- Samet, J.M. "Radon and Lung Cancer".
JNCI. 1989. 81: 745-757.
- Samet,J.M., Stolwijk J., Rose, S.L.
"Summary: International Workshop on Residential Radon Epidemiology".
Health Phys. 1991. 60: 223-227.
- U.S. Department of Health and Human
Services, Public Health Service, Agency for Toxic Substances and Disease
Registry, Radon Toxicity. 1992.
- U.S. Environmental Protection Agency.
National Residential Radon Survey: Summary Report. EPA-402-R-91-0111.
1992.
- U.S. Environmental Protection Agency.
Technical Support Document for the 1992 Citizens Guide to Radon. 1992.
For the patient (may be
helpful to the professional as well):
- American Lung Association. "Indoor Air
Pollution Fact Sheet - Radon". 1992. Publication No. 1183C.
- American Lung Association. "Facts About
Radon: The Health Risk Indoors". Publication No. 0174C.
- U.S. Environmental Protection Agency.
"A Citizens Guide to Radon (second edition)". EPA-402-K-02-001.
1992.
MULTIPLE CHEMICAL
SENSITIVITY (MCS)
For the health
professional:
- Ashford, N.A., Miller C.S. 1991.
Chemical Exposures. Low Levels and High Stakes. Van Nostrand
Reinhold, New York.
- Bell, Iris R. "Neuropsychiatric Aspects
of Sensitivity to Low Level Chemicals: A Neural Sensitization Model".
Conference on Low Level Exposure to Chemicals and Neurobiologic
Sensitivity, Agency for Toxic Substances and Diseases Registry,
Baltimore, MD, April 6-7, 1994. To be printed in Journal of Toxicity
and Public Health.
- Brooks, B.D. and Davis, W.F. 1991.
Understanding Indoor Air Quality. CRC Press. Boca Raton.
- Cullen, M.R. 1987. "The Worker with
Multiple Chemical Sensitivities: An Overview", In: Workers With
Multiple Chemical Sensitivity, State of Art Rev. Occup. Med.
2:669-681.
- Heilman, B. "Multiple Chemical
Sensitivity". Chemical & Engineering News. July 22, 1992.
- Miller, Claudia S. "Chemical
Sensitivity: History and Phenomenology". Conference on Low Level
Exposure to Chemicals and Neurobiologic Sensitivity, Agency for Toxic
Substances and Diseases Registry, Baltimore, MD, April 6-7, 1994. To be
printed in Journal of Toxicity and Public Health.
- Terr, A. "Clinical Ecology". Annals
of Internal Medicine. III(2): 168-178.
- U.S. National Research Council.
"Biologic Markers in Immunotoxicology". 1992. National Academy Press.
Washington, DC.
- U.S. National Research Council.
"Multiple Chemical Sensitivities - Addendum to Biologic Markers in
Immunotoxicology". 1992. National Academy Press. Washington, D.C.
AIR CLEANERS
For the patient (may be
helpful to the professional as well):
CARPET
- American Lung Association. "Indoor Air
Pollution Fact Sheet - Carpet". 1992. Publication No. 1189.
- U.S. Consumer Product Safety
Commission. "Tips for Purchasing and Installing New Carpet" Fact Sheet.
October 1992.
- U.S. Environmental Protection Agency.
"Carpet and Indoor Air Quality" Fact Sheet. October 1992.
- U.S. Environmental Protection Agency,
Office of Air and Radiation. Report to Congress on Indoor Air Quality,
Volume II: Assessment and Control of Indoor Air Pollution, pp. I, 4-14.
EPA 400-1-89-001C, 1989.
- The U.S. Environmental Protection
Agency sets and enforces air quality standards only for ambient air. The
Toxic Substances Control Act (TSCA) grants EPA broad authority to
control chemical substances and mixtures that present an unreasonable
risk of injury to health and environment. The Federal Insecticide,
Fungicide, and Rodenticide Act (FIFRA) authorizes EPA to control
pesticide exposures by requiring that any pesticide be registered with
EPA before it may be sold, distributed, or used in this country. The
Safe Drinking Water Act authorizes EPA to set and enforce standards for
contaminants in public water systems. EPA has set several standards for
volatile organic compounds that can enter the air through volatilization
from water used in a residence or other building. As to the indoor air
in workplaces, two Federal agencies have defined roles concerning
exposure to (usually single) substances. The National Institute for
Occupational Safety and Health and Human Services (NIOSH), part of the
Department of Health and Human Services, reviews scientific information,
suggests exposure limitations, and recommends measures to protect
workers' health. The Occupational Safety and Health Administration (OSHA),
part of the Department of Labor, sets and enforces workplace standards.
The U.S. Consumer Product Safety Commission (CPSC) regulates consumer
products which may release indoor air pollutants. In the United States
there are no Federal Standards that have been developed specifically for
indoor air contaminants in non-occupational environments. There are,
however, some source emission standards that specify maximum rates at
which contaminants can be released from a source.
- Leaderer, B.P., Cain, WS., Isseroff,
R., Berglund, L.G. "Ventilation Requirements in Buildings II". Atmos.
Environ. 18:99-106.
See also: Repace, J.L. and Lowrey, A.H. "An indoor air quality
standard for ambient tobacco smoke based on carcinogenic risk." New
York State Journal of Medicine 1985; 85:381-83.
- American Society of heating,
Refrigeration and Air-conditioning Engineers. Ventilation for
Acceptable Air Quality; ASHRAE Standard 62-1989.
- International Agency for Research on
Cancer. IARC Monographs on the Evaluation of the Carcinogenic Risk of
Chemicals to Man, Vol. 38: Tobacco Smoking. World Health
Organization, 1986.
- U.S. Department of Health and Human
Services. Reducing the Health Consequences of Smoking: 25 Years of
Progress, A Report of the Surgeon General. DHHS Publication No.
(CDC) 89-84". 1989.
- U.S. Department of Health and Human
Services. The Health Benefits of Smoking Cessation, A Report of the
Surgeon General. DHHS Publication No. (CDC) 90-8416. 1990.
- U.S. Environmental Protection Agency,
Office of Air and Radiation and Office of Research and Development.
Respiratory Health Effects of Passive Smoking: Lung Cancer and Other
Disorders. EPA 600-6-90-006F. 1992.
- U.S. Department of Health and Human
Services. The Health Consequences of Involuntary Smoking, A Report of
the Surgeon General. DHHS Publication No. (PHS) 87-8398. 1986.
- National Research Council,
Environmental Tobacco Smoke: Measuring Exposures and Assessing Health
Effects. National Academy Press. 1986.
- National Institute for Occupational
Safety and Health. Environmental Tobacco Smoke in the Workplace: Lung
Cancer and Other Health Effects. U.S. Department of Health and Human
Services, Current Intelligence Bulletin 54. 1991.
- U.S. Environmental Protection Agency.
Respiratory Health Effects of Passive Smoking: Lung Cancer and Other
Disorders.
- U.S. Environmental Protection Agency.
Respiratory Health Effects of Passive Smoking. Lung Cancer and Other
Disorders.
- U.S. Environmental Protection Agency.
Respiratory Health Effects of Passive Smoking: Lung Cancer and Other
Disorders.
- Pope,C.A. III, Schwartz,j. and Ransom,
MR. "Daily Mortality and PM 10 Pollution in Utah, Salt Lake, and Cache
Valleys". Archives of Environmental Health 1992: 46:90-96.
- U.S. Department of Health and Human
Services. The Health Consequences of Involuntary Smoking, A Report of
the Surgeon General.
- National Research Council.
Environmental Tobacco Smoke: Measuring Exposures and Assessing Health
Effects.
- American Heart Association Council on
Cardiopulmonary and Critical Care. "Environmental Tobacco Smoke and
Cardiovascular Disease." Circulation 1992; 86:1-4.
- Samet, J.M., Marbury, Marian C., and
Spengler, J.D. "Health Effects and Sources of Indoor Air Pollution, Part
I." American Review of Respiratory Disease 1987; 136:1486-1508.
- American Thoracic Society. "Report of
the ATS Workshop on Environmental Controls and Lung Disease, Santa Fe,
New Mexico, March 24-26, 1988." American Review of Respiratory
Disease 1990; 142:915-39.
- Lipsett, M. "Oxides of Nitrogen and
Sulfur." Hazardous Materials Technology 1992; 000:964-69.
- U.S. Environmental Protection Agency.
"Review of the National Ambient Air Quality Standards for Sulfur Oxides:
Updated Assessment of Scientific and Technical Information; Supplement
to the 1986 Staff Paper Addendum (July 1993)."
- Burge, Harriet A. and Feely, J.C.
"Indoor Air Pollution and Infectious Diseases." In: Samet, J.M. and
Spengler, J.D. eds., Indoor Air Pollution, A Health Perspective
(Baltimore MD: Johns Hopkins University Press, 1991), pp. 273-84.
- Brunekreeff, B., Dockery, D.W. et al.
"Home Dampness and Respiratory Morbidity in Children." American
Review of Respiratory Disease 1989; 140:1363-67.
- Berstein, R.S., Sorenson, W.G. et al.
"Exposures to Respirable Airborne Penicillium from a Contaminated
Ventilation System: Clinical, Environmental, and Epidemiological
Aspects." American Industrial Hygiene Association Journal 1983;
44:161-69.
- Burge, Harriet A. "Bioaerosols:
Prevalence and Health Effects in the Indoor Environment." Journal of
Allergy and Clinical Immunology 1990; 86:687-704.
- Burge, Harriet A. "Risks Associated
With Indoor Infectious Aerosols." Toxicology and Industrial Health
1990; 6:263-73.
- Brundage,J.F., Scott, R. et al.
"Building-Associated Risk of Febrile Acute Respiratory Disease in Army
trainees." Journal of the American Medical Association 1988;
259:2108-12.
- Nolan, C.M., Elarth, A.M. et al. "An
Outbreak of Tuberculosis in a Shelter for Homeless Men: A Description of
Its Evolution and Control." American Review of Respiratory Disease
1991; 143:257-61.
- American Lung Association. Lung
Disease Data 1993. Publication No. 0456, 1993.
- Centers for Disease Control and
American Thoracic Society. Core Curriculum on Tuberculosis.
Second Edition, 1991.
- Nardell, E.A., Keegan, Joann et al.
"Airborne Infection: Theoretical Limits of Protection Achievable By
Building Ventilation." American Review of Respiratory Disease
1991; 144:302-06.
- Lee, T.C., Stout, Janet E. and Yu, V.L.
"Factors Predisposing to Legionella pneumophila Colonization in
Residential Water Systems." Archives of Environmental Health
1988; 43:59-62.
- Weissman, D.N. and Schuyler, M.R.
"Biological Agents and Allergic Diseases." In: Samet, J.M. and Spengler,
J.D. eds., Indoor Air Pollution, A Health Perspective (Baltimore
MD: Johns Hopkins University Press, 1991), pp. 285-305.
- Arlian, L.G. "Biology and Ecology of
House Dust Mite, Dermatophagoldes spp. and Euroglyphus spp."
Immunology and Allergy Clinics of North America 1989;9:339-56.
- Platts-Mills, T.A. E. and Chapman, M.D.
"Dust Mites: Immunology, Allergic Disease, and Environmental Control."
Journal of Allergy and Clinical Immunology 1987; 80:755-75.
- FinkJ.N." Hypersensitivity Pneumonitis."
In: Middleton, E., Reed, C.E. and Ellis, E.F. eds., Allergy
Principles and Practice (St. Louis: C.V. Mosby, 19xx), pp.
1085-1100.
- Fink J.N. "Hypersensitivity Pneumonitis."
In: Middleton, E., Reed, C.E. and Ellis, E.F. eds., Allergy
Principles and Practice (St. Louis: C.V. Mosby, 19xx), pp.
1085-1100.
- Burge, Harriet A., Solomon,W.R. and
Boise, J.R. "Microbial Prevalence in Domestic Humidifiers." Applied
and Environmental Microbiology 1980; 39:840-44.
- Baxter, C.S., Wey, H.E. and Burg, W.R.
"A Prospective Analysis of the Potential Risk Associated with Inhalation
of Aflatoxin-Contaminated Grain dusts." Food and Cosmetics Toxicology
1981; 19:763-69.
- Croft, W.A.,Jarvia, B.B. Yatawara, C.S.
1986. Airborne outbreak of trichothecene toxicosis. Atmosph. Environ.
20:549-552. See also Baxter, C.S. Wey, H.E., Burg, W. E. 1981. A
prospective analysis of the potential risk associated with inhalation of
aflatoxin-contaminated grain dusts. Food Cosmet Toxicol. 19:763-769.
- U.S. Environmental Protection Agency,
Office of Acid Deposition, Environmental Monitoring and Quality
Assurance. Project Summary: The Total Exposure Assessment Methodology
(TEAM) Study. EPA-600-S6-87-002, 1987.
- Marks, J.G., Jr. Traudein, J.J. et al.
"Contact Urticaria and Airway Obstruction From Carbonless Copy Paper."
Journal of the American Medical Association 1984; 252:1038-40.
- LaMarte, F.P., Merchant, J.A. and
Casale, T.B. "Acute Systemic Reactions to Carbonless Copy Paper
Associated With Histamine Release." Journal of the American Medical
Association 1988; 260:242-43.
- U.S. Environmental Protection Agency,
Office of Air and Radiation. Report to Congress on Indoor Air
Quality, Volume II: Assessment and Control of Indoor Air Pollution,
pp. I, 4-14. EPA-400-I-89-001C, 1989.
- U.S. Environmental Protection Agency,
U.S. Public Health Service, and National Environmental Health
Association. Introduction to Indoor Air Quality: A Reference Manual,
p. 87. EPA-400-3-91-003, 1991.
- U.S. Environmental Protection Agency
Office of Research and Development. Final Report: Nonoccupational
Pesticide Exposure Study (NOPES), p. 60. EPA-600-3-90-003, 1990.
- Needleman, H.L. Schell, A. et al. "The
Long-Term Effects of Exposure to Low Doses of Lead in Childhood: An
11-Year Follow-up Report." The New England Journal of Medicine
1990; 322:83-88.
- American Academy of Pediatrics. "Lead
Poisoning: Next Focus of Environmental Action." Statement issued January
1991.
- Bellinger, D., Sloman, J. et al.
"Low-Level Lead Exposure and Children's Cognitive Function in the
Preschool Years." Pediatrics 1991; 87:219-27.
- "Lower "Threshold of Concern" for
Children's Lead Levels". FDA Consumer, December 1991. p.6.
- Centers for Disease Control.
"Preventing Lead Poisoning in Young Children". October 1991.
- Agocs, Mary M., Etzel, Ruth A. et al.
"Mercury Exposure from Latex Interior Paint." The New England Journal
of Medicine. 1990; 323:1096-11011.
- Consumer Product Safety Commission.
Safety Alert: Mercury Vapors.
- A professional group, the American
Society of Heating, Refrigerating, and Air-conditioning Engineers (ASHRAE),
has established standards of ventilation for the achievement of
acceptable indoor air quality. These criteria do not have the force of
law, are typically invoked only for new or renovated construction, and
even when met do not assure comfortable and healthy air quality under
all conditions and in all circumstances.
- U.S. Environmental Protection Agency,
Office of Air and Radiation.
Indoor Air Facts
No. 4: Sick Building Syndrome, revised, 1991.
- Kreiss, Kathleen. "The Sick Building
Syndrome: Where Is the Epidemiologic Basis? "American Journal of
Public Health 1990; 80:1172-73.
- The first death attributed to
occupational asbestos exposure occurred in 1924; the details were
recently recounted: Selikoff, I.J. and Greenberg, M. "A Landmark Case in
Asbestosis." Journal of the American Medical Association 1991;
265:898-901.
- For a detailed discussion of
asbestos-related pulmonary disease, see: Rom, W.N., Travis, W.D. and
Brody, A.R. "Cellular and Molecular Basis of the Asbestos-related
Diseases." American Review of Respiratory Disease 1991;
143:408-22.
- U.S. Environmental Protection Agency,
Office of Research and Development. Airborne Asbestos Health Assessment
Update. EPA-600-8-84-003F. June 1986.
- "Asbestos in Your Home", American Lung
Association, U.S. Consumer Product Safety Commission, U.S. Environmental
Protection Agency. September 1990. ALA Publication No. 3716.
- See Samet, J.M., Marbury, Marian C. and
Spengler, J.D. "Health Effects and Sources of Indoor Air Pollution, Part
II." American Review of Respiratory Disease 1988; 137:221-42.
This continuation of the overview cited earlier provides a table of
commercial sources of testing equipment for sampling and monitoring
levels of a variety of indoor air pollutants, including radon.
- Black, D.W. Rathe, Ann and Goldstein,
Rise B. "Environmental Illness: A Controlled Study of 26 Subjects With
'20th Century Disease." Journal of the American Medical Association
1990; 264:3166-70.
- Fiedler, N., Maccia, C., Mpen, H.
"Evaluation of Chemically Sensitive Patients". Journal of
Occupational Medicine. 1992. 34:529-538.
- Heuser, G., Wojdani, A., Heuser, S.
"Diagnostic Markers of Multiple Chemical Sensitivity". Multiple
Chemical Sensitivities: Addendum to Biologic Markers in Immunotoxicology.
1992. pp. 117-138. National Research Council. National Academy Press.
Washington D.C.
- See Ducataman et al. "What is
Environmental Medicine?" Journal of Occupational Medicine 1990;
32: 1130-32. Also see American College of Physicians Health and Public
Policy Committee. "Occupational and Environmental Medicine: The
Internist's's Role". Annals of Internal Medicine 1990; 113:974-82.
- For further specifics, see: U.S.
Environmental Protection Agency, Office of Air and Radiation.
Residential Air Cleaning Devices - A Summary of Available Information.
EPA-400-1-90-002,1990.
- Residential Carpet Installation
Standard. The Carpet and Rug Institute. First Edition. 1990. CRI
Publication No. 105-1990.
- National Aeronautics and Space
Administration. Interior Landscape Plants for Indoor Air Pollution
Abatement. September 15, 1989.
Last Revised: April 7, 1998
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