# Indoor Air Quality; Proposed Rule DEPARTMENT OF LABOR

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## Record

- **Collection:** Federal Register
- **Document type:** Uncategorized Document
- **Published:** April 5, 1994

## Text

SUMMARY: By this notice, the Occupational Safety and Health
Administration (OSHA) proposes to adopt standards addressing indoor air
quality in indoor work environments. The basis for this proposed action
is a preliminary determination that employees working in indoor work
environments face a significant risk of material impairment to their
health due to poor indoor air quality, and that compliance with the
provisions proposed in this notice will substantially reduce that risk.
The provisions of the standard are proposed to apply to all indoor
``nonindustrial work environments.'' In addition, all worksites, both
industrial and nonindustrial within OSHA's jurisdiction are covered
with respect to the proposed provisions addressing control of
environmental tobacco smoke. The proposal would require affected
employers to develop a written indoor air quality compliance plan and
implement that plan through actions such as inspection and maintenance
of building systems which influence indoor air quality.
Provisions under the standard also propose to require employers to
implement controls for specific contaminants and their sources such as
outdoor air contaminants, microbial contamination, maintenance and
cleaning chemicals, pesticides, and other hazardous chemicals within
indoor work environments. Designated smoking areas which are to be
separate, enclosed rooms exhausted directly to the outside are proposed
to be required in buildings where the smoking of tobacco products is
not prohibited. Specific provisions are also proposed to limit the
degradation of indoor air quality during the performance of renovation,
remodeling and similar activities. Provisions for information and
training of building system maintenance and operation workers and other
employees within the facility are also included in this notice.
Finally, proposed provisions in this notice address the
establishment, retention, availability, and transfer of records such as
inspection and maintenance records, records of written compliance
programs, and employee complaints of building-related illness.
The Agency invites the submission of written data, views and
comments on all regulatory provisions proposed in this notice, and on
all relevant issues pertinent to those provisions. OSHA is also
scheduling an informal public hearing where persons may orally submit
their views. It is noted here that subsequent Federal Register notices
may be published subsequent to this notice, if the public presents
views leading to a substantial change in focus or it is otherwise
determined to be appropriate.

DATES: Comments on the proposed standard must be postmarked by June 29,
1994. Notices of intention to appear must be postmarked by June 20,
1994. Testimony and evidence to be submitted at the hearing must be
postmarked by July 5, 1994. The hearing will commence at 9:30 a.m. on
July 12, 1994.

ADDRESSES: Comments are to be submitted in quadruplicate or 1 original
(hardcopy) and 1 disk (5\1/4\ or 3\1/2\) in WP 5.0, 5.1, 6.0 or Ascii
to: The Docket Office, Docket No. H-122, Room N-2625, U.S. Department
of Labor, 200 Constitution Avenue, NW., Washington, DC 20210, Telephone
No. (202) 219-7894. (Any information not contained on disk, e.g.,
studies, articles, etc., must be submitted in quadruplicate.)
Notices of intention to appear and testimony and evidence are to be
submitted in quadruplicate to: Mr. Tom Hall, Division of Consumer
Affairs, Occupational Safety and Health Administration, 200
Constitution Avenue, NW., room N3649, Washington, DC 20210; (202) 219-
8615.
The hearing will be held in the auditorium of the U.S. Department
of Labor, 200 Constitution Avenue, NW., Washington, DC.

FOR FURTHER INFORMATION CONTACT: Proposal: Mr. James F. Foster,
Director of Information and Consumer Affairs, Occupational Safety and
Health Administration, 200 Constitution Avenue, NW., room N3641,
Washington, DC 20210; (202) 219-8151.
Informal Hearing Information: Mr. Tom Hall, Division of Consumer
Affairs, Occupational Safety and Health Administration, 200
Constitution Avenue, NW., room N3649, Washington, DC 20210; (202) 219-
8615.

Table of Contents

I. Supplementary Information
A. Events Leading to This Action
II. Health Effects
A. Sick Building Syndrome
B. Building-Related Illness
1. Indoor Air Contaminants
2. Microbial Contaminants
C. Environmental Tobacco Smoke
1. Pharmacokinetics
(a) Absorption and Distribution
(b) Metabolism
2. Irritation
3. Pulmonary Effects
4. Cardiovascular Effects
(a) Thrombus Formation
(b) Vascular Wall Injury
(c) Possible Mechanisms of Effect
(d) Acute Heart Effects
(e) Chronic Heart Effects
5. Reproductive Effects
6. Cancer
(a) Evidence of Association
(b) Epidemiological and Experimental Studies
7. Genotoxicity
8. Conclusions
D. Case Reports
1. Sick Building Syndrome and Building-Related Illness
2. Environmental Tobacco Smoke
III. Exposure
A. Sources of Indoor Air Contaminants
B. Microbial Contamination
C. Exposure Studies
1. Low-level Contaminants
2. Bioaerosols
3. Environmental Tobacco Smoke
(a) Chemistry
(b) Human Activity Pattern Studies Used to Assess Workplace
Exposure
(c) Indoor Levels of Environmental Tobacco Smoke Constituents
(d) Levels of Respirable Suspended Particulates and Nicotine
Found in Field Studies
(e) Biomarkers of Environmental Tobacco Smoke Exposure
(f) Inadequacy of General Dilution Ventilation to Address
Environmental Tobacco Smoke Exposure Control
IV. Preliminary Quantitative Risk Assessment
A. Introduction
B. Review of Epidemiologic Studies and Published Risk Estimates
C. Data Sources
D. OSHA's Estimates of Risk-Environmental Tobacco Smoke Exposure
E. OSHA's Risk Estimates--Indoor Air Quality
F. Pharmacokinetic Modeling of Environmental Tobacco Smoke
Exposure
1. Considerations for Selection of a Biomarker for Environmental
Tobacco Smoke
2. Cardiovascular Effects
3. Carcinogenicity
4. Evaluation of Cotinine as a Biomarker for Environmental
Tobacco Smoke
5. Description of Pharmacokinetic Models for Nicotine and
Cotinine
6. Application of Pharmacokinetic Modeling for Environmental
Tobacco Smoke Exposure Estimation
7. Analysis of Uncertainty
(a) Physiological Parameters
(b) Distribution Parameters
(c) Kinetic Parameters
V. Significance of Risk
A. Environmental Tobacco Smoke
B. Indoor Air Quality
VI. Preliminary Regulatory Impact Analysis
A. Introduction
B. Industry Profile
1. Affected Industries
2. Indoor Contaminants-Sources
3. Controlling Indoor Air
4. Building Characteristics
5. Profile of Affected Buildings
6. Buildings with Indoor Air Problems
7. Number of Employees Affected
8. Environmental Tobacco Smoke
(a) Smoking Ordinances and Policies
(b) Number of Nonsmokers Working Indoors
C. Nonregulatory Alternatives
1. Introduction
2. Market Imperfections
3. Alternative Nonregulatory Options
(a) Tort Liability
(b) Workers' Compensation
4. Conclusion
D. Benefits
1. Indoor Air Quality
2. Environmental Tobacco Smoke
3. Cost Savings
(a) Worker Productivity
(b) Property Damage, Maintenance and Cleaning Costs
E. Technological Feasibility and Compliance Costs
1. Technological Feasibility
2. Compliance Costs
(a) Developing Indoor Air Quality Compliance Programs
(b) Indoor Air Quality Operation and Maintenance Program
(c) Training for HVAC Maintenance Workers and Informing
Employees About the Indoor Air Quality Standard
(d) Compliance with Related Standards
(e) Air Contaminant-Tobacco Smoke
(f) Air Quality During Renovation and Remodeling
F. Economic Impact and Regulatory Flexibility Analysis
1. Economic Feasibility
2. Regulatory Flexibility Analysis
3. Environmental Impact
VII. Summary and Explanation
A. Scope and Application: Paragraph (a)
B. Definitions: Paragraph (b)
C. Indoor Air Quality Compliance Program: Paragraph (c)
D. Compliance Program Implementation: Paragraph (d)
E. Controls for Specific Contaminant Sources: Paragraph (e)
F. Air Quality During Renovation and Remodeling: Paragraph (f)
G. Employee Information and Training: Paragraph (g)
H. Recordkeeping: Paragraph (h)
I. Dates: Paragraph (i)
J. Appendices: Paragraph (j)
K. Specific Issues
VIII. State-Plan Standards
IX. Federalism
X. Information Collection Requirements
XI. Public Participation
XII. List of Subjects in 29 CFR Parts 1910, 1915, 1926, and 1928
XIII. Authority and Signature
XIV. Part 1910, 1915, 1926, 1928--Proposed Occupational Safety and
Health Standards

Supplementary Information

A. Events Leading to This Action

Concern about the health hazards posed by occupational exposure to
environmental tobacco smoke (ETS) prompted three public interest groups
to petition the Agency in May 1987 for an Emergency Temporary Standard
under section 6(c) of the Occupational Safety and Health (OSH) Act, 29
U.S.C. 655(c). The American Public Health Association and Public
Citizen submitted a joint petition; Action on Smoking and Health (ASH)
also submitted a petition. The petitions requested the prohibition of
smoking in most indoor workplaces.
OSHA determined, that available data with respect to exposures were
insufficient to demonstrate the existence of a ``grave danger,'' within
the meaning of section 6(c) of the OSH Act, from workplace exposure to
ETS. OSHA denied the petitions in September 1989 but continued to
investigate regulatory options.
In October 1989 ASH filed suit in the U.S. Court of Appeals for the
District of Columbia Circuit for review of OSHA's denial of its
petition for an Emergency Temporary Standard. The court denied ASH's
petition for review in May 1991, finding that OSHA has reasonably
determined that it could not sufficiently quantify the workplace risk
associated with tobacco smoke to justify an Emergency Temporary
Standard.
OSHA issued on September 20, 1991, a Request for Information (RFI)
(56 FR 47892) on indoor air quality problems, in order to obtain
information necessary to determine whether it would be appropriate and
feasible to pursue regulatory action concerning Indoor Air Quality
(IAQ). Issues on which comments were requested in the RFI included
health effects attributable to poor IAQ, ventilation systems
performance, exposure assessment, and abatement methods. Information
concerning specific contaminants such as ETS and bioaerosols was also
requested.
In March 1992, the AFL-CIO petitioned OSHA to promulgate an overall
IAQ standard. OSHA responded in May 1992 that such a standard was under
consideration.
In response to the RFI, over 1,200 comments were submitted by
interested persons, groups, unions, and industries. Issues of
particular concern identified in the comments, in addition to health
effects considerations, include the lack of ventilation performance
standards; the lack of worker training on the operation and maintenance
of Heating Ventilation and Air Conditioning (HVAC) systems; the lack of
pollutant source control; and the lack of available technical guidance
on IAQ issues and control techniques.
Of the comments that specifically addressed the question of whether
OSHA should regulate IAQ, a majority (75%) indicate support for
regulation. Of those that commented on the need for regulation,
approximately 21% were explicitly in favor of a regulation on ETS, more
than 41% were in favor of an overall IAQ regulation, and approximately
13% were in favor of a combined IAQ regulation.
Numerous comments focused on the adverse health effects of tobacco
smoke and of general indoor air pollution. The health effects of
concern relevant to both tobacco smoke and indoor air pollutants ranged
from the acute irritant effects to cancer.
Comments submitted in response to the RFI indicated wide support
for a regulatory approach that would focus on the design, operation and
maintenance of building ventilation systems, source reduction
methodology, and worker information and training programs. Commenters
also recommended that provisions should require that employers receive
training about the regulation and the need for compliance, and that
their training regarding building HVAC maintenance and operation be
tailored to the level of complexity of the HVAC system and their
personal degree of involvement.
Many commenters particularly felt that regulation of IAQ was
necessary to eliminate exposures to ETS in the workplace. Commenters
urged the Agency to either ban smoking completely from the workplace or
allow smoking only in separately ventilated, designated smoking areas
that were separate from work areas.
OSHA believes that data submitted to the record, and other
evidence, support the conclusion that air contaminants and other air
quality factors can act to present a significant risk of material
impairment to employees working in indoor environments. Adverse health
effects associated with poor IAQ may include sensory irritation,
respiratory allergies, asthma, nosocomial infections, humidifier fever,
hypersensitivity pneumonitis, Legionnaires' disease, and the signs and
symptoms characteristic of exposure to chemical or biologic substances
such as carbon monoxide, formaldehyde, pesticides, endotoxins, or
mycotoxins.
The Agency believes that available data support proposing
regulation of IAQ, including exposure to ETS. Further stimulus for this
determination was provided by conclusions reached in a report published
in December, 1992 by the Environmental Protection Agency, addressing
hazards associated with exposure to ETS. In that study, Respiratory
Health Effects of Passive Smoking: Lung Cancer and Other Disorders [Ex.
4-311], EPA concluded that exposure to ETS presents an excess risk of
induction of cancer in humans. OSHA has submitted this proposed
standard to the U.S. Environmental Protection Agency which is reviewing
it in detail for purposes of submitting detailed comments to the
docket.
For the reasons noted above, and discussed in the following
sections, OSHA is proposing to address indoor air quality problems,
including exposure to ETS, as set forth in this notice.

II. Health Effects

Indoor air quality problems can occur in all types and ages of
buildings; in newly constructed buildings, in renovated or remodeled
buildings, and in old buildings. Problems in new, clean buildings are
rarely, if ever, related to microbial growth, since the physical
structures are new [Ex. 3-61]. Older buildings that have not been
adequately maintained and operated may have problems with bioaerosols
if parts of the building have been allowed to become reservoirs for
microbial growth. Also, if inadequate outside air is provided,
regardless of the age of the building, chemical and biological
contaminants will build up to levels that can cause health effects in
some workers. In addition, other physical factors such as lack of
windows, noise, and inadequate lighting, and ergonomic factors
involving uncomfortable furniture and intensive use of video display
units, etc., will cause discomfort in occupants that may be
inaccurately attributed to air quality.
Some information contained in the docket indicates that these
chronic health complaints are psychological, however, OSHA believes
that chronic health complaints related to poor indoor air quality are
unlikely to be due to mass psychogenic illness, even though a
psychological overlay is common. It is true that poor management,
boring work, poor lighting conditions, temperature variations, poor
ergonomic design, and noise may all lower the threshold for complaint.
Nevertheless, air quality complaints usually have some basis, although
they are often difficult to assess with specificity [Exs. 3-61C, 4-
144].
Indoor air quality problems are generally classified as Sick
Building Syndrome (SBS) or Building-related Illness (BRI). However, a
very important constituent of poor indoor air quality is ETS because of
the serious health effects that result from exposure. The following
discussion will first identify the health effects associated with SBS
and BRI. A discussion of the health effects associated with exposure to
ETS will follow.
It is important to note that OSHA considers these health effects to
be material impairments of health when the worker is clinically
diagnosed with a condition that is either caused or aggravated by poor
indoor air quality in the workplace. For example, in the formaldehyde
standard (29 CFR 1910.1048) [Ex. 4-107] OSHA determined that a
physician's diagnosis of irritation met the requirement of material
impairment of health. In addition, OSHA considers all the other health
effects discussed, which are more clinically severe than irritation, to
be material impairments of health as well.

A. Sick Building Syndrome

Typically, health effects caused by poor indoor air quality have
been categorized as SBS or BRI. In 1983, the World Health Organization
published a list of eight non-inclusive symptoms that characterize Sick
Building Syndrome [Ex. 4-325]. These include irritation of the eyes,
nose and throat; dry mucous membranes and skin; erythema; mental
fatigue and headache; respiratory infections and cough; hoarseness of
voice and wheezing; hypersensitivity reactions; and nausea and
dizziness. Generally, these conditions are not easily traced to a
specific substance, but are perceived as resulting from some
unidentified contaminant or combination of contaminants. Symptoms are
relieved when the employee leaves the building and may be reduced or
eliminated by modifying the ventilation system. Comments to the docket
indicate that such symptoms have been observed in and reported by
workers [Exs. 3-446, 4-87].
In some instances, outbreaks of SBS are identified with specific
pollutant exposures, but in general only general etiologic factors
related to building design, operation and maintenance can be identified
[Ex. 4-274]. In 1987, Woods et al. [Ex. 3-745] conducted a stratified
random telephone survey of 600 U.S. office workers across the national.
Twenty four percent reported that they were dissatisfied with the air
quality at the office; while 20% perceived their performance to be
hampered by poor indoor air quality. Women were nearly twice as likely
to report a productivity effect of poor indoor air quality than men
(28% versus 15%). Based on this, Woods et al. [Ex. 3-745] hypothesized
that 20% of U.S. office workers are exposed to indoor conditions which
manifest as SBS. In fact, complaints about SBS have become so numerous
that 37 out of 53 states and territories have designated a building
complaints investigation contact person [Ex. 4-310].
Breysse [Ex. 4-32] reported on symptoms associated with new
carpeting in a state office building, in order of prevalence: headache,
eye and throat irritation, nausea, dizziness, eye tearing, chest
tightness, diarrhea, cough, muscle aches, burning nose, fatigue, dark
urine, and rashes. Twenty out of 35 persons were affected. Air sampling
was conducted before and after carpet removal; a similar range of
aliphatic hydrocarbons was found after removal, but in much lower
concentrations. Many individuals who believe the building they work in
is implicated in SBS, have described similar effects. Symptoms usually
include one or more of the following: mucous membrane (eye, nose, or
throat) irritation, dry skin, headache, nausea, fatigue, and lethargy
[Ex. 4-293]. These symptoms are generally believed to result from
indoor air pollution. There is no secondary spread of symptoms to
others outside the building who are exposed to the occupants (unlike
the situation faced by many chemical and asbestos workers). Anderson
[Ex. 4-10] suggested the possible causes for SBS as related to
psychosocial, chemical, physical, or biological factors.
Anderson [Ex. 4-10] distinguished SBS symptoms as different from
mass psychogenic illness; although in general the causes of SBS are
unknown, he suggested that most SBS symptoms could be explained by
stimulation of sensory nerve fibers in the upper airways and the face
(referred to as common chemical sense). Because these fibers can
respond in only one way, SBS cases largely have the same symptoms
irrespective of the cause [Ex. 4-10].
It is now known that there is a variety of important health effects
from indoor air pollution. In addition to the indoor environmental
disease caused by infectious agents, carcinogens or toxins; the indoor
environment may create conditions that can produce skin and mucosal
allergy and hyperactivity reactions, sensory effects (odors and
irritations), airways effects (from both acute and chronic exposures),
neuropsychological effects, and psychosocial effects, especially due to
the lack of social support [Ex. 4-200].
Indoor air pollution may be caused by physical, chemical, or
microbiological agents, and is aggravated by poor ventilation. The
causation of SBS by indoor air pollution was first objectively
demonstrated in 1984 in a study of 62 Danish subjects suffering from
``indoor climate symptoms'' [Ex. 4-20]. These subjects reported
primarily eye and upper respiratory irritation, but were otherwise
healthy individuals, and did not suffer from asthma, allergy, or
bronchitis. The subjects were exposed to a mixture of 22 volatile
organic chemicals commonly found in the indoor environment at
concentrations of 0, 5, and 25 mg/m3. These concentrations
corresponded respectively to ``clean'' air, average polluted air in
Danish houses, and maximum polluted air in Danish houses. After
exposure, the Digit Span test was administered. The Digit Span test
consists of the subject being allowed to view a series of random digits
for a short period of time; the numbers are then covered up and the
subject asked to repeat the sequence backwards. This test is reported
to be sensitive to situational anxiety and alertness, and therefore a
measure of stress and ability to concentrate. Bach et al. found
significant declines in performance on the digit span test following
exposure to these low levels of volatile organic chemicals,
demonstrating objectively the existence of SBS [Ex. 4-20].
Molhave et al. [Ex. 4-228], in reporting on the same 62 subjects,
found that subjects exposed for 2\3/4\ hrs did not adapt, and that the
subjects reacted to irritation of the mucous membranes and not to odor
intensity. The exposure was doubled-blind, and neither the subjects nor
the testers knew the exposure.
Although these problems have been demonstrated to be real, they may
affect only a small percentage of building occupants. Also, there are
various degrees of problems which may occur. Some individuals who
experience relatively mild and treatable symptoms such as headache, may
be able to cope with the sick building environment for extended
periods, although suffering from increased stress. Other individuals,
more seriously affected, may find symptoms so severe that they may be
unable to be in the building for extended periods, or at all. Still
others may become temporarily or permanently disabled.
It has been suggested that SBS may not be one syndrome but a number
of sub-syndromes [Ex. 4-170]. This hypothesis suggests that the
symptoms particularly associated with chemical exposure include
fatigue; headache; dry and irritated eyes, nose, and throat; and
sometimes include nausea and dizziness. Those symptoms most related to
microbial exposures would result in itchy, congested, or runny nose;
itchy watery eyes; and sometimes include wheezing, tight chest, or flu-
like symptoms. The overlapping symptoms in each case are eye, nose, and
throat irritation, perhaps making the two sub-syndromes, chemical and
microbial, difficult to distinguish. Jones concludes that there is a
need for a treatment protocol as well as a diagnostic protocol, which,
in addition to describing corrective actions available in response to
different diagnostic findings, would also provide guidelines for the
design and implementation of follow-up studies of buildings and
individuals in order to assess treatment effectiveness [Ex. 3-170].
Randolph and Moss [Ex. 4-258] have written about a number of
problems ascribed to indoor air pollution in the chemically sensitive
patient. These problems include irritability from natural gas fumes,
allergy to dust from forced air ventilation systems, intoxication and
even hallucination from paint fumes. Randolph describes chemical
sensitivity to dry cleaning chemicals, and rug shampoo, and implicates
moldy carpets in producing allergenic substances. He also describes
joint pain, malaise, and fatigue due to pesticide exposure; and skin
rashes from exposure to plasticizers. Randolph further describes
intolerance to highly scented products such as deodorant soaps, toilet
deodorants, and disinfectants, especially pine-scented ones. Other
patients have reported reacting to strong perfumes and other cosmetics.
So-called air fresheners often prove to be particularly troublesome. He
also describes that some patients are sensitive to the odors from hot
plastic-coated wires in electronic equipment.
There is little data on the perceptions of victims of SBS. Shapiro
[Ex. 4-282] has complied a summary of 16 case-histories of SBS in the
victims' own words. It is useful to review these for insight into the
problems from the victims' point of view.
One episode that Shapiro [Ex. 4-282] reported on was in a building
occupied by a government agency. As a result of problems related to
carpeting and other suspected causes, five workers were reported to
have left the agency, 11 were relocated to alternative workspace or
worked at home, and 100 reported to the agency's medical officer that
they had SBS related problems. The range of self-reported symptoms
included a variety of moderate and acute respiratory problems;
headache; sore throat; burning of the eyes, lungs, and skin; rashes;
fatigue; laryngitis; clumsiness; disorientation; loss of balance;
nausea; numbness in extremities and face; and difficulty with mental
tasks.
The patient's reported that the diagnoses of the occupational
health physicians they visited included upper and lower respiratory
irritation, intoxication-type syndrome, occupational asthma, and
chronic hypersensitivity pneumonitis.
The central nervous system effects reported by many do not lend
themselves to ready diagnosis [Ex. 4-282]. Some of the lesser affected
individuals either saw no physician at all or saw a family doctor or
allergist who was not familiar with occupational or environmental
health [Ex. 4-282].
The Air Force Procedural Guide [Ex. 4-199] on dealing with SBS
takes a practical view: ``* * * in most cases the sick building
syndrome does not have a clearly understood etiology and many of the
SBS studies and investigations were inconclusive. The significance of
exposure that [what chemical or physical agent concentrations cause
symptoms] can be pathogenic remains unanswered, but the realities of
worker complaints and discomfort are valid reasons to seriously address
this problem.''
In summary, SBS is not a well-defined disease with well-defined
causes. It appears to be a reaction, at least in part due to
stimulation of the common chemical sense, to a variety of chemical,
physical or biological stimuli. Its victims display all or some of a
pattern of irritation of the mucous membranes, and the worst affected
individuals have neurological symptoms as well.

B. Building-Related Illness

Building-related illness (BRI) describes specific medical
conditions of known etiology which can often be documented by physical
signs and laboratory findings. Such illnesses include sensory
irritation when caused by known agents, respiratory allergies,
nosocomial infections, humidifier fever, hypersensitivity pneumonitis,
Legionnaires' disease, and the symptoms and signs characteristic of
exposure to chemical or biologic substances such as carbon monoxide,
formaldehyde, pesticides, endotoxins, or mycotoxins [Exs. 3-61, 4-144].
Some of these conditions are caused by exposure to bioaerosols
containing whole or parts of viruses, fungi, bacteria, or protozoans.
These illnesses are often potentially severe and, in contrast to SBS
complaints, are often traceable to a specific contaminant source, such
as mold infestation and/or microbial growth in cooling towers, air
handling systems, and water-damaged furnishings. Symptoms may or may
not disappear when the employee leaves the building. Susceptibility is
influenced by host factors, such as age and immune system status.
Mitigation of building-related illnesses requires identification and
removal of the source, especially in cases involving hypersensitivity
responses.
1. Indoor Air Contaminants
Comments submitted to the docket in response to the RFI and
contained in the literature indicate that specific substances or
classes of substances have been implicated as contributing to poor
indoor air quality problems. These substances, either alone or in
synergy, have produced health effects that OSHA believes can be
considered material impairment [Ex. 4-124]. In most cases, people
likely to be at risk have specific susceptibility.
But such susceptibility is common and adverse effects can arise
suddenly following exposure. The relevant effects can be categorized
into six categories: irritation, pulmonary, cardiovascular, nervous
system, reproductive, and cancer.
Common chemical sense or irritation perception is mediated through
receptors found not only throughout the nasal, pharyngeal, and
laryngeal areas of the respiratory system but also on the surface of
the eyes, specifically the conjunctiva and cornea [Ex. 4-239]. It is
partially through the stimulation of these receptors that exposed
persons perceive irritation. Many comments to the docket, from
citizens, researchers, and indoor air consultants, raised the issue
about the irritating effects related to known indoor air contaminants.
The air contaminants of concern include formaldehyde [Exs. 3-14, 3-32,
3-38, 3-188, 3-440a, 3-446, 3-575, 4-125, 4-144, 4-214], volatile
organic compounds (VOCs) [Exs. 3-32, 3-446, 3-500, 4-145, 4-243, 4-
320], ozone [Exs. 3-14, 4-42, 4-134, 4-236, 4-237], carpet-associated
chemicals [Exs. 3-25, 3-444D, 3-576, 4-144, 4-214], vehicle exhausts
[Exs. 3-6, 3-63, 3-206, 3-238, 3-360, 3-437, 3-444D, 3-631, 3-659],
combustion gases [Ex. 3-32], particulates [Exs. 3-32, 3-446, 3-500],
man-made mineral fibers (fiberglass, glasswool and rockwool) [Ex. 4-
33], and pesticides [Ex. 3-446]. The irritation effects present as
sensory irritation of the skin and upper airways, irritation of eye,
nose and throat, dry mucous membranes, erythema, headache, and abnormal
taste [Ex. 3-14, 4-33]. The pulmonary effects include upper and lower
respiratory tract effects such as rapid breathing, fatigue, increased
infection rate, broncho-constriction, pulmonary edema, asthma,
allergies and flu-like symptoms. Acute exposure to low level of air
contaminants results in primarily reversible effects, while chronic
exposure may result in pulmonary fibrosis that can result in
irreversible damage [Exs. 3-14, 4-33].
These health effects were associated, as reported in many comments
to the docket, with specific contaminants, including asbestos [Exs. 3-
38, 3-440A, 3-500], combustion gases [Exs. 3-14, 3-34, 3-440A, 3-446,
3-500], formaldehyde [Exs. 3-32, 3-38, 3-188, 3-440A, 4-124], ozone
[Exs. 4-42, 4-237], VOCs [Ex. 3-32], vehicular exhaust [Ex. 3-63], and
particulates [Exs. 3-32, 3-38, 3-440A, 3-500].
Individuals with underlying pulmonary disease, such as asthma, are
more susceptible than others to acute exposure to these indoor air
contaminants and experience coughing and wheezing at low levels of
exposure. Synergism may occur between chemical contaminants, such as
ozone and VOCs, in aggravating asthma [Ex. 4-33]. These affected
individuals may also be at increased risk of pulmonary infections due
to the synergistic effect between chemical and microbial contaminants
[Ex. 4-33].
Cardiovascular effects have also been associated with poor indoor
air quality. These effects are presented as headache, fatigue,
dizziness, aggravation of existing cardiovascular disease, and damage
to the heart. These effects are associated with exposure to combustion
gases such as carbon monoxide [Exs. 3-38, 3-440A], VOCs [Ex. 3-500],
and particulates [Ex. 3-500].
Nervous system effects have also been produced due to exposure to
poor indoor air quality. These effects include headache, blurred
vision, fatigue, malaise with nausea, ringing in the ears, impaired
judgement, and polyneuritis. These effects are associated with exposure
to carbon dioxide [Ex. 3-14], carbon monoxide [Exs. 3-32, 3-38, 3-446,
3-500], formaldehyde [Exs. 3-32, 3-38, 3-446, 3-500], and VOCs [Exs. 3-
32, 3-446, 3-500].
Relevant reproductive effects include menstrual irregularities and
birth defects and are associated with exposure to formaldehyde [Exs. 3-
446, 3-500] and VOCs [Exs. 3-446, 3-500].
The occurrence of cancer has also been attributed to exposures
associated with poor indoor air quality. In particular, cancer of the
lung, including mesothelioma, esophagus, stomach, and colon have been
associated with exposure to asbestos [Exs. 3-6, 3-14, 3-38, 3-188, 3-
440A, 3-500], radon [Exs. 3-35, 3-38, 3-188, 3-440A, 3-500], vehicular
exhausts [Exs. 3-84, 3-206, 3-360H], combustion gases [Ex. 3-500], VOCs
[Exs. 3-446, 3-500, 4-294], and particulates [Ex. 3-500].
2. Microbial Contamination
Building-related illnesses can result in serious illness and death.
Indoor transmission of disease caused by obligate pathogens (microbes
that require a living host) is common in indoor environments,
especially those that are overcrowded and inadequately ventilated [Ex.
4-33]. Diseases in this category include influenza, rhinovirus or
colds, and measles. Indoor transmission of disease caused by
opportunistic microorganisms usually affects compromised individuals,
those with existing conditions that make them more susceptible to
infection, such as pulmonary disease or immunodeficiency. Legionnaires'
disease, pulmonary tract infections, and humidifier fever are diseases
that fall into this category. Diseases that affect the immune system
include allergic reactions, as seen in antibody-mediated responses
(asthma and rhinitis) and interstitial lung disease, as seen in cell-
mediated reactions (hypersensitivity pneumonitis) [Ex. 4-33]. All of
these diseases produce substantial amounts of illness each year [Exs.
4-33, 4-41, 4-214].
In the U.S., Legionnaires' disease is considered to be a fairly
common, serious form of pneumonia. The Legionella bacterium is one of
the top three bacterial agents in the U.S. which causes sporadic
community-acquired pneumonia. Because of the difficulty in clinically
distinguishing this disease from other forms of pneumonia, many cases
go unreported. Although approximately 1,000 cases are reported to the
Centers for Disease Control and Prevention annually, it has been
estimated that over 25,000 cases of the illness actually occur. This
disease burden is estimated to result in over 5,000 to 7,000 deaths per
year [Ex. 4-41]. Brooks et al. [Ex. 4-33] reported that as many as
116,000 cases occur each year. Of these cases, it is estimated that
between 35,000 and 40,000 die. The attack rate for L. pneumophila
ranges from 0.1 to 5%. The case fatality rate ranges from 15 to 20%
[Ex. 4-214].
Two serious allergic or hypersensitivity diseases are asthma and
hypersensitivity pneumonitis (extrinsic allergic alveolitis). An
estimated 3% of the U.S. population suffers from asthma (approximately
9,000,000 people) [Ex. 4-41]. These individuals may be more susceptible
to bioaerosol contamination or chemical contamination of the indoor
environment.
Hypersensitivity pneumonitis is triggered by recurrent exposure to
microbials, fumes, vapors, and dusts [Ex. 4-33]. The lung interstitium,
terminal bronchioles, and alveoli react in an inflammatory process that
can organize into granulomas and progress to fibrosis. The symptoms of
acute episodes of this disease are malaise, fever, chills, cough and
dyspnea. The symptoms of chronic episodes are serious respiratory
symptoms such as progressive dyspnea. Chronic disease can lead to
irreversible pulmonary structural and functional changes [Ex. 4-33].
Approximately 15% (20,250) of 135,000 hospital admissions per year
that last an average of more than eight days are due to allergic
disease [Ex. 4-41]. Burge and Hodgson estimate that these
hospitalizations cost five million work days per year. The prevalence
of symptoms consistent with hypersensitivity pneumonitis, an
interstitial lung disease caused by organic dusts or by aerosols has
been examined in subpopulations at well-defined, increased risk, such
as farmers (0.1-32%) or pigeon breeders (0.1-21%) [Exs. 4-41, 4-214].
The only unbiased source of complaint rates in unselected office
workers are control buildings used in the study of hypersensitivity
pneumonitis in the U.S. Arnow et al. [Ex. 4-15] reported complaints
consistent with hypersensitivity pneumonitis in 1.2 percent and Gamble
et al. [Ex. 4-116] in 4 percent of these populations. Since no clinical
data are available, it is not known how these complaints are related to
actual disease, and it is unknown whether these complaints are
associated with lost work time, doctor visits or hospital admissions
[Ex. 4-41].
Humidifier fever, a less serious variant of hypersensitivity
pneumonitis, also is caused by exposure to microorganisms contained in
an aerosol. Attack rates in building epidemics have been as high as
75%, whereas complaint rates are usually 2-3% in nonepidemic situations
[Ex. 4-41]. Because of the similarity of the individual symptoms to
other diseases (fever, headache, polyuria, weight loss and joint pain),
it is often difficult to separate actual disease from complaints
related to the common cold in nonepidemic situations [Exs. 4-33, 4-41].
While rare, a workplace epidemic of humidifier fever can virtually shut
down an entire building, and only removal of the contamination will end
the epidemic [Exs. 4-41, 4-144, 4-214].
Microbial contamination of building structures, furnishings, and
HVAC system components contribute to poor indoor air quality problems,
especially those related to building-related illnesses. OSHA believes
that consequent health effects constitute material impairment of health
[Exs. 3-61, 4-41]. These can be categorized as irritation, pulmonary,
cardiovascular, nervous system, reproductive, and cancer effects.
Irritation effects, either from the physical presence of
bioaerosols or from exposure to VOCs released by biologicals, have been
demonstrated in susceptible workers [Ex. 3-32]. In addition, water
leakage on furnishings or within building components can result in the
proliferation of microorganisms that can release acutely irritating
substances into the air. Typically, where microorganisms are allowed to
grow, a moldy smell develops. This moldy smell is often associated with
microbial contamination and is a result of VOCs released during
microbial growth on environmental substrates [Ex. 4-41].
Pulmonary effects which have been associated with exposure to
bioaerosols include rhinitis, asthma, allergies, hypersensitivity
diseases, humidifier fever, spread of infections including colds,
viruses, and tuberculosis, and the occurrence of Legionnaire's disease
[Exs. 3-17, 3-32, 3-38, 3-61B, 3-188, 3-440A, 3-446, 3-500, 4-41, 4-
144, 4-214].
Building-related asthma has also recently been documented in office
workers [Exs. 3-61, 4-43] and some case reports show it to be
associated specifically with humidifier use. Biocides used in
humidification systems are suspected causes of office-associated asthma
[Ex. 4-103].
Cardiovascular effects manifested as chest pain, and nervous system
effects manifested as headache, blurred vision, and impaired judgment,
have occurred in susceptible people following exposure to bioaerosols
[Exs. 3-32, 3-446]. It has been suggested that these effects may be
caused by VOCs released by the microbiologicals, or they may be a
complication of related pulmonary effects.
The development of cancer in susceptible people is possible
following exposure to certain types of toxigenic fungi and mycotoxins.
However, the probability of such exposures occurring in workplaces
covered by this standard is probably limited. Mycotoxins (toxins
produced as secondary metabolites by many fungi) are among the most
carcinogenic of known substances, and are also acutely toxic. The
American Conference of Governmental and Industrial Hygienists wrote
``[t]he toxigenic fungi are common contaminants of stored grain and
other food products and have caused well-described outbreaks of acute
systemic toxicosis as well as specific organ carcinogenesis when such
food is consumed * * * It appears clear that massive contamination with
a highly toxigenic fungus strain of a site in which aerial dispersion
of metabolic products occurred would be necessary to induce acute
symptoms. However, considering the carcinogenicity of many fungal
toxins, an examination of the risks of chronic inhalation exposure
appears justified'' [Ex. 3-61].
In summary, most of the health effects associated with SBS and BRI
occur in indoor environments were concentrations of pollutants are much
less than the OSHA Permissible Exposure Levels (PELs) (29 CFR
1910.1000) [Ex. 4-3]. It is important to point out that the PELs are
chemical-specific standards that are not only based on health effects
but also on technological feasibility, cost restraints and a
``healthy'' worker exposed for a 40-hour work week. In the industrial
workplace, hazards are minimized by the use of administrative and
engineering controls and the use of personal protective equipment. The
nonindustrial environment, however, does not have these controls.
Ventilation systems are designed only to remove occupant-generated
contaminants, such as carbon dioxide and odors. These types of systems
were not designed to dilute multiple point sources of contaminants that
are typically found in nonindustrial workplaces (see section III).
Unless adequate ventilation and source controls are utilized and
adequately maintained, many of the chemical contaminants can
concentrate to levels that induce symptoms. The possibility exists that
synergistic effects occur. These effects occur not only between
substances to enhance their toxicity but also by lowering the
resistance to lung infection in susceptible persons.

C. Environmental Tobacco Smoke

ETS is composed of exhaled mainstream and sidestream smoke. The
chemical composition and exposure sources of ETS are described in the
Exposure section of this preamble (see Section III). The
pharmacokinetics of ETS have been widely studied and are described in
the following section.
A wide spectrum of health effects have been associated with
exposure to ETS. These effects include mucous membrane irritation,
decrease in respiratory system performance, adverse effects on the
cardiovascular system, reproductive effects, and cancer. The following
section also presents more detailed information on these health
effects.
1. Pharmacokinetics
Whether a chemical elicits toxicity or not depends not only on its
inherent potency and site specificity but also on how the human system
can metabolize and excrete that particular chemical. To produce health
effects, the constituents of ETS must be absorbed and must be present
in appropriate concentration at the sites of action. After absorption,
some of these contaminants are metabolized to less toxic metabolites
while some carcinogens are activated by metabolism in the body.
Available biomarkers of ETS, such as nicotine, clearly show that
nonsmoker exposure is of sufficient magnitude to be absorbed and to
result in measurable levels of these biomarkers. There is sufficient
evidence in the literature to indicate that several components of
sidestream smoke are rapidly absorbed and widely distributed within the
body. However, the extent of absorption, distribution, retention and
metabolism of these contaminants in the body depends upon various
physiological and pharmacokinetic parameters that are influenced by
gender, race, age and smoking habits of the exposed individuals. These
parameters and others may result in differences in susceptibility among
exposed subpopulations. Nicotine is one of the most widely studied
constituents of tobacco smoke. There have been numerous studies on the
pharmacokinetics of nicotine in both animals and man.
(a) Absorption and distribution. Absorption and distribution of
tobacco smoke constituents are usually measured by using surrogate
markers. A correlation between nicotine absorption and exposure to
tobacco smoke has between demonstrated, thus making nicotine an
appropriate marker for tobacco smoke in pharmacokinetic studies. The
steady state volume of distribution for nicotine is large indicating
that it is widely distributed within the body [Ex. 4-185]. Nicotine has
been shown to bind with plasma proteins which may interfere with
elimination and thereby prolong retention in the body. The studies in
the docket clearly indicate that nicotine and other constituents of
tobacco smoke are readily absorbed and distributed throughout the body
thereby increasing the potential of producing adverse effects at more
then one target site.
(b) Metabolism. Nicotine is rapidly eliminated, primarily via
metabolism and urinary excretion. The investigation of metabolism in
vivo and in vitro, has resulted in the identification of more than 20
metabolic products in the plasma and urine of humans and animals. The
principle metabolic pathways of nicotine appear to involve oxidation of
the pyrrolidine ring to yield nicotine-1'-N-oxide and cotinine, the
latter being the major metabolite and the precursor of many of the
metabolic products of nicotine. Some of the metabolites detected in the
urine of rats after intravenous administration in a study by Kyerematen
et al. [Ex. 4-185] are listed in Table II-1. In humans, cotinine is the
major degradation product of nicotine metabolism and has a serum half-
life of about 17 hours compared to two hours for the parent compound,
nicotine [Exs. 4-27, 4-253]. Trans-3'-hydroxycotinine in the free form
constitutes the largest single metabolite in smokers' urine accounting
for 35-40% of the urinary nicotine metabolite [Exs. 4-48, 4-241].
Smokers and nonsmokers differ in their metabolism of nicotine and
cotinine [Exs. 4-133, 4-184, 4-279]. The half-life values for urinary
elimination of nicotine and cotinine were found to be significantly
shorter in smokers than nonsmokers [Ex. 4-186]. Plasma nicotine
clearance was faster in smokers than in nonsmokers in this study. More
rapid elimination of nicotine and cotinine has been attributed to the
inductive effects of chronic cigarette smoking on the hepatic
metabolism of many xenobiotic agents. However, Benowitz et al. [Ex. 4-
29] were unable to confirm published research suggesting that smokers
metabolize nicotine and cotinine more rapidly than nonsmokers.
Variations in nicotine metabolism occur among individuals.
Variations also occur due to differences in gender and race [Exs. 4-26,
4-186, 4-314]. It has also been suggested that the metabolism of
nicotine between smokers and nonsmokers may differ. Male smokers have
been shown to metabolize nicotine faster than do female smokers after
intravenous infusion of nicotine and active smoking. However, this
difference was not observed by Benowitz and Jacob [Ex. 4-23] during a
study of daily intake of nicotine in smokers versus nonsmokers. The
metabolism of nicotine has also been studied in animals. Male rats (4
strains) were shown to metabolize nicotine faster than did females [Ex.
4-185].
In summary, the potential effect of nicotine, and other ETS
constituents in the body, is governed by interactions between several
physiological and pharmacokinetics parameters. These interactions may
lead to longer retention of toxic constituents, thus prolonging the
effects on the target organs resulting in tissue injury.
2. Irritation
Exposure to ETS is capable of inducing eye and upper respiratory
tract irritation. Common chemical sense or irritation perception is
mediated through receptors in the fifth, ninth, and tenth cranial
nerves. These receptors are found throughout the nasal, pharyngeal, and
laryngeal areas of the respiratory system and also on the surface of
the eyes [Ex. 4-239]. It is partially through the stimulation of these
receptors that exposed persons perceive irritation.

Table II-1.--Urinary Excretion of Nicotine and Metabolites in Male and Female Rats After Intravenous
Administration of [\14\C]Nicotine (0.5 mg/kg)
----------------------------------------------------------------------------------------------------------------
Male Female
---------------------------------------------------------------
Recovery of Recovery of
Metabolite administered t1/2 administered t1/2
radioactivity (Hr) radioactivity (Hr)
(percentage) (percentage)
----------------------------------------------------------------------------------------------------------------
Nicotine........................................ 10.8 plus-
minuse> 1.5 2.5 plus-
minuse> 0.4 \1\24.0 plus-
minuse> 4.6 \2\5.6 plus-
minuse> 0.5
Cotinine........................................ 9.3 plus-
minuse> 0.8 6.0 plus-
minuse> 0.6 \1\5.7 plus-
minuse> 0.7 \2\6.8 plus-
minuse> 0.8
Nicotine-N-oxide................................ 10.8 plus-
minuse> 0.9 1.6 plus-
minuse> 1.4 7.8 plus-
minuse> 1.4 2.6 plus-
minuse> 0.3
Cotinine-N-oxide................................ 8.5 plus-
minuse> 1.6 7.5 plus-
minuse> 0.8 \1\3.7 plus-
minuse> 1.0 6.8 plus-
minuse> 0.6
3-Pyridylacetic acid............................ 1.8 plus-
minuse> 0.3 5.8 plus-
minuse> 0.3 1.2 plus-
minuse> 0.2 \3\ND
3-(3-Pyridyl)--oxobutyric acid 2.7 plus-
minuse> 0.6 5.3 plus-
minuse> 0.9 2.4 plus-
minuse> 0.7 6.0 plus-
minuse> 0.6
3-Hydroxycotinine............................... 5.7 plus-
minuse> 0.5 6.7 plus-
minuse> 0.8 5.6 plus-
minuse> 1.5 9.9 plus-
minuse>1.5
-(3-Pyridyl)--
methylaminobutyric acid........................ 4.2 plus-
minuse> 0.6 5.9 plus-
minuse> 0.8 \1\1.4 plus-
minuse> 0.4 ND
Nornicotine..................................... 8.1 plus-
minuse> 0.9 4.1 plus-
minuse> 0.6 8.1 plus-
minuse> 1.8 \1\8.3 plus-
minuse>1.3
Demethylcotinine................................ 0.8 plus-
minuse> 0.1 ND -(3-Pyridyl)--oxo-N-
Methylbutramide................................ 1.8 plus-
minuse> 0.3 3.5 plus-
minuse> 0.6 \1\0.6 plus-
minuse> 0.3 ND
Isomethylnicotinium ion......................... 2.1 plus-
minuse> 4.5 plus-
minuse> 0.7 plus-
minuse> 0.4 9.8 plus-
minuse> 1.4 1.9 plus-
minuse> 0.6 10.0 plus-
minuse>1.6
---------------------------------------------------------------
Total....................................... 69.4 plus-
minuse> 3.0 .............. 65.0 plus-
minuse> 3.6 ..............
----------------------------------------------------------------------------------------------------------------
\1\0.01 0.05.
\2\p 0.01.
\3\ND, not determined; concentration too low to estimate t1/2 accurately.

The ability of tobacco smoke to elicit irritation may be enhanced
by low relative humidity and varies according to concentration [Ex. 4-
239]. Irritating components of ETS are contained in both the vapor
phase and the particulate phase (see Tables III-6 and III-7). These
effects have been studied in both experimental (e.g., animals studies;
clinical and chamber studies on humans) and field (e.g., surveys and
epidemiological studies) studies. The NRC report [Ex. 4-239] summarized
these studies and concluded that even though the specific components of
ETS that cause irritation were not identified, the overall effects were
eye and throat irritation and immunological responses. Weber [Ex. 4-
317] reported the results of a field study that included 44 workrooms
where smoking was taking place. Eye irritation was reported by 52 out
of 167 workers. Nonsmokers reacted more than smokers to the ETS; 36 of
the 52 workers who reported eye irritation at work were nonsmokers [Ex.
4-317]. Asano et al. [Ex. 4-18] reported significant eye irritation, as
measured by blinking rates, in both healthy smoking and nonsmoking
adults following exposure to ETS. Nonsmokers reported more eye
irritation than smokers did. Effects such as eye irritation and nasal
stuffiness were reported to OSHA in comments to the docket [Exs. 3-38,
3-58, 3-59, 3-188, 3-438D, 3-440A].
3. Pulmonary Effects
Much of the literature relevant to the association between non-
cancerous health effects and ETS has focused on children. Because
children are undergoing development and maturation, they are not
physiologically equivalent to adults exposed to the same conditions.
Therefore, findings in studies conducted with respect to ETS and
children may not be directly applicable to adults. However, a number of
studies have investigated the relationship between ETS and pulmonary
health effects in adults.
Studies which are restricted to adults vary by numerous factors,
such as the population studied, the measures used to estimate exposure
to ETS, and the physiologic and health outcomes examined. The studies
also varied in the consideration of potential confounders. A number of
studies have found relationships between ETS exposure and pulmonary
health effects. These studies have: (1) used pulmonary function tests,
which may be more sensitive than methods used in other studies, to
detect physiological changes occurring in the small airways of the
lungs (e.g., forced mid-expiratory flow rate (FEF25-75), and
forced end-expiratory flow rate (FEF75-85)); (2) studied older
populations with a longer history of exposure to ETS; (3) stratified
the level of ETS exposure with significant findings more likely to
occur in persons with higher exposures; and (4) more frequently found
significant changes in lung function in men, although adverse pulmonary
effects to ETS have also been shown in women. The following discussion
summarizes the results of these studies [Exs. 4-18, 4-37, 4-62, 4-148,
4-173, 4-176, 4-178, 4-180, 4-209, 4-210, 4-278, 4-295, 4-321].
Asano et al. [Ex. 4-18] demonstrated the acute physiologic changes
which occur as a result of exposure to ETS. Nonsmokers had more
pronounced changes in eye blinking rates (a measure of eye irritation),
expired carbon monoxide, increased heart rate and systolic blood
pressure.
Studies of ETS and chronic health effects in adults differ by how
they define ``never smokers'', ``exsmokers'', and how other various
levels of ETS exposure are defined, either in nominal, ordinal or
interval scales; and whether or not they take into account exposure
both in the workplace and at home. The potential for misclassification
bias occurs when ``nonsmokers'' are loosely defined and used as the
comparative group to passive smokers. Several studies considered the
confounding impact of environmental air pollution [Ex. 4-278], indoor
cooking fuels [Exs. 4-37, 4-62] or occupational exposures to dusts and
fumes [Exs. 4-176, 4-178, 4-209, 4-210, 4-321].
There have been fewer longitudinal studies [Exs. 4-148, 4-278, 4-
295] as compared to the majority which have been cross-sectional
studies. The duration of exposure, which is critical to producing a
measurable health effect, was quantified by number of years directly in
several studies [Exs. 4-37, 4-148, 4-173, 4-295, 4-321], or indirectly
by the age of the population under study [Exs. 4-176, 4-209, 4-210]. In
those studies which had carefully assessed for level of exposure and
had specified a duration of at least 10 years, significant pulmonary
function decrements were noted in both men and women [Exs. 4-37, 4-148,
4 176, 4-321]. Overall, changes in pulmonary indices are more likely to
occur in men than in women, however, several studies have documented
statistically significant physiological changes in pulmonary function
occurring in women [Exs. 4-37, 4-176, 4-178, 4-321].
Understanding the significance of findings is complicated because
studies used a variety of measures from spirometry. Although most
studies evaluated FVC (forced vital capacity) and FEV1 (forced
expiratory volume in one second), fewer studies have measured
FEF25-75 or FEF75-85 [Exs. 4-176, 4-180, 4-209, 4-210, 4-
321]. These later measures have been suggested as being more sensitive
to detecting changes in the small airways where effects of ETS are most
likely to occur [Exs. 4-46, 4-216, 4-230, 4-231]. However, there is no
clear consensus in the medical literature as to the routine clinical
use of FEF25-75 or FEF75-85, or their diagnostic value in
independently detecting small airway disease [Ex. 4-8].
Estimates of the decrement in FEV1 due to ETS exposure in
passive smokers as compared to never smokers, ranges from 80
milliliters (ml) [Ex. 4-148] to 190 ml [Ex. 4-37]. When this decrement
is expressed as a percent of FEV1, it has been estimated to be
5.7% in males, or 7.3% when these same subjects were matched for age
[Ex. 4-210]. As a means of comparison, the average loss in lung volume
per year due to aging alone is estimated to be 25 to 30 ml [Ex. 4-329].
The American Thoracic Society [Ex. 4-8] specifies that spirometry
equipment have a level of accuracy within 50 ml. Since pulmonary
function maneuvers are very effort dependent, intra-individual
variation between the three best efforts should be within 5% to be
acceptable. The importance of these spirometry criteria is emphasized
by the fact that the FEV1 may result in being 100 to 200 ml lower
than when a maximal effort is given by the subject. Furthermore, a
decrease of 15% must be achieved before certain pulmonary indices are
considered outside of normal limits. Given this perspective, although
changes in pulmonary function tests may truly occur as a result of
exposure to ETS over a number of years, the actual clinical impact may
not be apparent in the healthy, young individual. Older individuals and
those with preexisting pulmonary disease are more susceptible to the
pulmonary effects of exposure to ETS.
Outside of respiratory changes being documented through pulmonary
function testing, other symptoms have been found to be significantly
associated with ETS exposure. Hole et al. [Ex. 4-148] found a
significant increase in the prevalence of infected sputum, persistent
sputum, dyspnea and hypersecretion in passive smokers as compared to
controls. Furthermore, rates increased as those exposed were stratified
by level of exposure to passive smoke from low to high. Kauffmann et
al. [Ex. 4-178] noted a significant increased risk for dyspnea in
American (Odds Ratio (OR)=1.42) and French women (OR=1.43), and an
increased risk for wheeze in American women (OR=1.36). Schwartz and
Zeger [Ex. 4-278] found an increased risk for phlegm or sputum in a 3-
year longitudinal study (OR=1.41). This risk was raised to 1.76 when
asthmatics, who may be medicated, were excluded from the analysis.
As small airway disease progresses to chronic obstructive pulmonary
disease (COPD) (also referred to as chronic obstructive lung disease
(COLD)), the impact of ETS becomes more detectable. Kalandidi et al.
[Ex. 4-173] reported an adjusted odds ratio of 2.5 (90% Confidence
Interval (CI), 1.3 to 5.0) for Greek women never smokers exposed to
their husbands' tobacco smoke.
While there is a clear trend, and in several studies a
statistically significant finding of a demonstrated decrease in
pulmonary function indices, or an increase in respiratory symptoms in
passive smokers, the impairment nonsmokers suffer by the exposure may
not be immediately obvious. It is important to note that these findings
have been demonstrated in otherwise healthy individuals. Based upon the
finding of White and Froeb [Ex. 4-321], Fielding and Phenow [Ex. 4-102]
have described such changes as being equivalent to those found in light
smokers, who smoke from 1 to 10 cigarettes per day. Where a decrease of
100 to 200 ml of FVC or FEV1 may be clinically insignificant in
healthy persons, such a change may be significant for workers with
already impaired pulmonary function [Exs. 3-438D, 3-440A, 4-76, 4-182].
These changes may be the pivotal point at which a worker becomes unable
to continue to work.
Cellular effects on the pulmonary tissue have also been observed in
animals exposed to ETS during experimental studies. Several studies
reviewed by OSHA have demonstrated that chronic cigarette smoke
exposure produces an accumulation of alveolar macrophages (AM) (the
presence of AM indicates a body's response to environmental insults),
within the respiratory bronchioles of many animals species. This effect
is similar to that seen in human smokers [Exs. 4-31, 4-58, 4-109, 4-
110, 4-140, 4-147, 4-150, 4-179, 4-212, 4-249]. Increased elastase
secretion by alveolar macrophages from mice chronically exposed to
cigarette smoke has also been observed [Ex. 4-322].
Accumulation of polymorphonuclear leucocytes (PMNs) is also an
indication of the body's response to environmental insults. PMNs were
found in the alveolar septum of cigarette smoke-exposed hamsters,
similar to the PMNs observed in the lungs of human smokers [Ex. 4-204].
In contrast to the focal nature of the alveolar macrophages
accumulation, the accumulation of PMN is diffuse. Studies of PMN
leukocyte function have not been systematically evaluated in smoke-
exposed animals.
Other studies also show effects of ETS exposure at the cellular
level. For example, young lambs exposed to ETS for one month did not
develop detectable pulmonary system effects or alteration in lung
mechanics or airway responsiveness. However, the lambs did develop
inflammation of pulmonary cells [Ex. 4-290]. A cytotoxic effect of
tobacco smoke was also demonstrated by decreased intracellular
adenosine triphosphate (ATP) content in guinea pig alveolar macrophages
and lowered cell bacteriocidal activity in a study by Firlik [Ex. 4-
104]).
Exposure to tobacco smoke has been shown to increase the
permeability of the respiratory epithelial membrane to macromolecules.
Burns et al. [Ex. 4-45] have shown that exposure of guinea pigs to
tobacco smoke followed by fluorescein isothiocyanate-dextran (FITC-D,
molecular weight 10,000) increased the amount of intact FITC-D that
crossed the respiratory epithelium into the vascular space.
Transmission electron-microscopic studies showed that the FITC-D
diffused across damaged type I pneumocyte membranes and cytoplasm to
reach the basal lamina and entered the alveolar capillaries through the
endothelial junction. Damage to alveolar epithelium was more frequent
for the smoke-exposed animals than the room air-exposed animals.
Aryl hydrocarbon hydroxylase (AHH) participates in the activation
of various carcinogens, such as benzo(a)pyrene. This is one of the many
carcinogens found in ETS. Both mainstream and sidestream smoke are
capable of inducing pulmonary AHH activity. Gairola [Ex. 114] has
demonstrated the induction of pulmonary AHH activity in Sprague-Dawley
rats and male C57BL mice after exposure to either mainstream or
sidestream smoke from University of Kentucky Reference cigarettes (2R1)
for seven days per week for 16 weeks. However, no such induction was
noted in Hartley guinea-pigs under similar conditions, indicating a
species difference. The mainstream and the sidestream smoke were
equally effective in inducing the AHH activity.
There is consistent evidence that decrements in pulmonary function
and increases in respiratory symptoms occur in current smokers and in
exsmokers. However, in passive smokers these health effects are not as
easily demonstrated. The Environmental Protection Agency's December
1992 report, Respiratory Health Effects of Passive Smoking: Lung Cancer
and Other Disorders [Ex. 4-311], reviewed an abundance of evidence
showing persistent physiologic changes in children's respiratory
function and related health effects as a result of exposure to ETS.
Studies evaluating these same effects are not as plentiful in adults.
However, the EPA concluded, ``recent evidence suggests that passive
smoking has subtle but statistically significant effects on the
respiratory health of adults'' [Ex. 4-311].
The weight of the evidence shows that exposure to ETS results in
decreases in pulmonary function indices and increases in respiratory
symptoms in otherwise healthy men and women who are exposed to ETS for
periods of 10 or more years. The risk of developing COPD appears to be
increased in passive smokers with lifelong exposures to ETS. Whether
these changes impact upon respiratory function to a degree that
impairment occurs may be dependent upon the individual's pulmonary
status and overall health condition.
4. Cardiovascular Effects
A developing body of research indicates that the cardiovascular
effects of ETS exposure on the health of nonsmokers include acute
effects, such as exacerbation of angina, as well as chronic effects,
such as atherosclerosis [Exs. 4-123, 4-291, 4-330].
Cardiovascular diseases [Exs. 4-91, 4-136] such as myocardial
infarction [Ex. 4-12], sudden death, and arterial thrombosis occur more
frequently in cigarette smokers as opposed to nonsmokers [Exs. 4-86, 4-
233]. The same chemicals which produce these effects in active smokers
are present in ETS. These include nicotine, carbon monoxide, polycyclic
aromatic hydrocarbons (PAHs) and tobacco glycoproteins.
The following discussion on cardiovascular effects covers thrombus
formation, vascular wall injury and the possible mechanisms of these
effects in nonsmokers. Discussion of the acute and chronic health
effects follows.
(a) Thrombus Formation. Blood clots in the coronary arteries are an
important component of an acute myocardial infarction (MI). An
additional component of the acute MI is the presence of atherosclerotic
plaques in the walls of the coronary arteries. Platelets are involved
in both the acute formation of blood clots and the chronic formation of
atherosclerotic plaques.
There is evidence that ETS exposure can cause platelets to become
more easily activated thus predisposing the platelets to become
involved in forming clots and atherosclerotic plaques. For example,
evidence exists that demonstrates that the platelets of nonsmokers
exposed to ETS are more easily activated [Exs. 4-40, 4-80]. The study
by Burghuber [Exs. 4-40] demonstrates that the platelet activating
capabilities of ETS are more prominent in nonsmokers than in smokers.
The results of this study suggest that nonsmokers are at a greater risk
of blood clot formation secondary to ETS exposure than smokers.
Acute ETS exposure also results in an increased platelet
aggregation, which is an initial stage of the development of coronary
thrombosis or vasoconstriction. This vasoconstriction can lead to the
development of coronary atherosclerosis after chronic exposure [Exs. 4-
111, 4-123, 4-272]. Environmental smoke exposure also can increase
platelet-activating factor (PAF), platelet factor 4, beta-
thromboglobulin, and fibrinogen concentration which provides a marker
of its effect on coronary heart disease [Exs. 4-85, 4-157, 4-224].
(b) Vascular Wall Injury. Atherosclerotic plaque formation is a
complicated chronic process that can lead to constriction of the lumen
of the blood vessels, resulting in reduced blood supply to the
myocardial tissues. It is thought that an essential step in plaque
formation is injury to the endothelial lining of the arterial wall. ETS
has been implicated in causing injury to the endothelial cells which
line the arterial walls. This was demonstrated in the study by Davis et
al. [Ex. 4-80] which identified an increase in the number of
endothelial cell carcasses in the circulation of healthy people after
being exposed to ETS.
ETS has also been implicated in stimulating smooth muscle cell
proliferation and in altering blood lipids. Each of these can
contribute to plaque formation which leads to an increased
susceptibility to heart attacks.
(c) Possible Mechanisms of Effect. At least three mechanisms are
described in the literature by which ETS may place stress on the heart
by increasing myocardial oxygen demand, decreasing myocardial oxygen
supply or interfering with the cell's ability to utilize oxygen for
energy production.
One mechanism by which ETS may reduce oxygen supply is through the
formation of carboxyhemoglobin. Carboxyhemoglobin is formed when a
person is exposed to carbon monoxide, a component of ETS. The carbon
monoxide effectively competes with oxygen for the heme group of the
hemoglobin molecule in the red blood cell (RBC). In fact, carbon
monoxide has a much greater affinity for hemoglobin than does oxygen
and binds very strongly with hemoglobin making it unavailable for the
transport of oxygen. The heart muscle (myocardium) can experience
injury at the cellular level when the oxygen demanded by the heart
muscle exceeds the oxygen supplied by the blood. Therefore, the
formation of carboxyhemoglobin can decrease the ability of the blood to
deliver oxygen to the myocardium and can cause injury to the heart if
myocardial oxygen demand exceeds supply.
A number of studies have suggested that ETS exposure adversely
affects the myocardial oxygen supply-demand relationship; this would
predispose the heart to develop ischemia or exacerbate preexisting
ischemia. Direct or indirect exposure to tobacco smoke has been shown
to increase the hemodynamic determinants of myocardial oxygen demand
[Exs. 4-13, 4-242] at the same time that it potentially reduces both
myocardial oxygen supply and delivery by enhancing the development of
coronary atherosclerosis [Exs. 4-242, 4-323], causing coronary
vasoconstriction [Exs. 4-323, 4-324] and reducing the oxygen carrying
capacity of blood through increased carboxyhemoglobin levels [Ex. 4-
13]. As a result, fewer red blood cells are available to transport
oxygen to the body, and to the heart muscle itself. To compensate for
this reduced oxygen carrying capacity of the blood, the heart must work
harder, for example, by increasing the heart rate. This is an example
of one mechanism by which ETS may place even further stress on the
heart by increasing myocardial oxygen demand, precisely at a time when
the oxygen delivery capabilities of the blood are reduced.
A second mechanism by which ETS may increase myocardial oxygen
demand is via the direct effect of nicotine. The nicotine in ETS may
cause an increased resting heart rate and blood pressure in exposed
individuals.
One study examined the effects of ETS on healthy individuals during
exercise, and found that healthy individuals experienced fatigue at
lower work levels when exercising in the presence of ETS [Ex. 4-123].
The authors concluded that ETS exposure interfered with the heart
muscle cells' ability to utilize oxygen for energy production.
Consequently, ETS exposure may have an adverse impact on myocardial
metabolism and expose the heart muscle to an increased susceptibility
to injury. These mechanisms of cardiac stress and potential injury to
the heart are in agreement with accepted theories of cardiac injury.
(d) Acute Heart Effects. An acute effect of exposure to ETS is the
aggravation of existing heart conditions, such as angina. The National
Research Council (1986) reported, based on the effects of studies by
Anderson et al. [Ex. 4-9] and Aronow et al. [Exs. 4-14, 4-16, 4-17],
that angina patients are especially sensitive at carboxyhemoglobin
levels between 2 and 4%. Guerin et al. [Ex. 4-129] report that
physiologically adverse effects occur in humans at 2.5%
carboxyhemoglobin blood content. Cumulative carbon monoxide levels, due
to ETS that result in such an effect are not uncommon in work
environments [Ex. 4-129]. Acute exposure to ETS has been reported to
increase heart rate, elevate blood pressure, and increase
carboxyhemoglobin levels in both angina patients [Exs. 3-38, 4-222] and
in healthy subjects [Exs. 4-18, 4-217]. Acute exposure has also been
associated with slight changes in blood components thought to be
involved in the pathogenesis of atherosclerosis, such as endothelial
cell count, platelet aggregate ratio, and platelet sensitivity to
prostacyclin [Exs. 4-40, 4-80]. Many effects of ETS exposure, such as
ischemia, may be additionally aggravated by simultaneous exposure to
other compounds, such as solvents [Exs. 3-446, 4-99].
(e) Chronic Heart Effects. The occurrence of coronary heart disease
in ETS-exposed nonsmokers has been studied by various epidemiological
researchers [Exs. 4-85, 4-120, 4-122, 4-138, 4-139, 4-142, 4-148, 4-
154, 4-191, 4-277, 4-295]. Small, but statistically significant (at p
0.05), increases in coronary heart disease mortality [Exs.
4-85, 4-138, 4-139, 4-142, 4-277] indicate a modest impact of long-term
ETS tobacco smoke exposure on the cardiovascular health of nonsmokers.
The relative risks calculated in these studies ranged from 1.3 to 2.7.
The ability of ETS exposure to induce coronary heart disease has
also been studied in animals. Zhu et al. [Ex. 4-330] exposed rats to
ETS and showed a dose-related increase in myocardial infarct size and a
decrease in bleeding time. But there were no significant differences in
serum triglycerides, high density lipoprotein and cholesterol. This
study showed that air nicotine, carbon monoxide, and total particulate
concentrations increased with ETS exposure, and this increased exposure
led to a continuous increase in plasma carboxyhemoglobin, nicotine, and
cotinine levels in ETS-exposed rats. There was a positive relationship
between the infarct size and air nicotine, carbon monoxide, total
particulate concentrations and plasma carboxyhemoglobin, nicotine, and
cotinine levels. The average concentrations of air nicotine, carbon
monoxide and particulates, according to the authors, were 30-fold, 3-
fold and 10- fold higher, respectively, than in a heavy smoking
environment. The duration of exposure, however, was short compared to
even a rat's lifetime. Infarct size nearly doubled following only 180
hours of ETS exposure distributed over a six week period.
In the same study, the effect of ETS exposure on platelet function
and aortic and pulmonary artery atherosclerosis in New Zealand male
rabbits was demonstrated. The increase of atherosclerosis after
exposure to ETS was shown to be independent of changes in serum lipids
and exhibited a dose-response relationship in this study. Average air
nicotine, carbon monoxide and total particulate concentrations were
1,040 g/m\3\, 60.2 ppm and 32.8 mg/m\3\ for high dose group
and 30 g/m\3\, 18.8 ppm and 4.0 mg/m\3\ for low dose group and
g/m\3\, 3.1 ppm and 0.13 mg/m\3\ for the control group.
Atherosclerosis in this study was significantly increased in the high
dose group.
Olsen [Ex. 245] exposed rats daily to smoke from University of
Kentucky 2R1 Reference cigarettes for 10 minutes, 7 times a week for 4,
8 or 20 weeks. Sidestream (SS) smoke was collected by a moving column
of air spiked every minute with a puff of fresh mainstream (MS) smoke.
Rats were exposed to this SS smoke collected in a 2 L/min air flow
using a glass container placed over a burning cigarette. A fraction of
this air flow containing SS smoke was diluted with fresh room air and
continuously diverted to the rats as follows: 50%, 25% and 10% SS
smoke. Carboxyhemoglobin content for each treatment group was
determined immediately after the last smoke exposure and percent
carboxyhemoglobin for each group was found to be: 4 week exposure-
mainstream=7.2plus-minuss>1.2 and 25%
sidestream=11.8plus-minuss>0.7; 8 week exposure
mainstream=6.1plus-minuss>1.2 and 25%
sidestream=11.9plus-minuss>0.9; 20 week exposure
mainstream=8.3plus-minuss>0.9, 10%
sidestream=6.30plus-minuss>0.5, 25%
sidestream=10.8plus-minuss>0.8 and 50%
sidestream=18.3plus-minuss>1.2. This indicates a tobacco smoke-
related detrimental effect on blood components, thus increasing the
probability that coronary disease would develop over a longer exposure
period.
Research has shown that passive exposure to tobacco smoke damages
endothelial cells and increases the number of circulating anuclear
carcasses of endothelial cells [Ex. 4-80]. ETS appears to alter cardiac
cellular metabolism in such a way that renders the myocyte less capable
of producing adenosine triphosphate (ATP). Reduced oxidative
phosphorylation in cardiac mitochondrial fractions taken from rabbits
exposed to ETS has been demonstrated [Ex. 4-130]. Studies have
indicated that the reduction in mitochondrial respiration secondary to
ETS exposure is likely due to decreased cytochrome oxidase activity
[Exs. 4-130, 4-131].
Nicotine, a component of tobacco smoke, has been shown in in vitro
studies, to inhibit the release of prostacyclin, through inhibition of
cyclooxygenase, from the rings of rabbit or rat aorta. Nicotine could
also affect platelets by releasing catecholamines which lead to
increased thromboxane A2 [Ex. 4-25]. Passive smoke also increases blood
viscosity and hematocrit due to relative hypoxia induced by chronic
carbon monoxide exposure [Ex. 4-25]. Nicotine, contained in cigarette
smoke can lead to catecholamine release, which enhances platelet
adhesiveness and decreases the ventricular fibrillation threshold. This
threshold is also affected by carbon monoxide levels [Exs. 4-25, 4-
196]. Cigarette smoke also increases the lipolysis that increases
levels of plasma free fatty acids, which result in enhanced synthesis
of LDL [Ex. 4-234].
In conclusion, there are multiple pathways by which ETS may damage
the heart. ETS exposure has been demonstrated to both increase
myocardial oxygen demand and decrease myocardial oxygen supply. If
oxygen demand exceeds supply for a long enough period of time, then
myocardial cell injury or even cell death can occur. In addition, ETS
exposure may cause platelets to become less sensitive to the anti-
clotting regulatory substances in the blood and therefore increase the
tendency of the blood to clot. An increased tendency for the blood to
clot may lead to an increased susceptibility to heart attacks.
ETS exposure may also contribute to the chronic formation of
arterial wall plaques which are implicated in the event of an acute
myocardial infarction. The two mechanisms described by which ETS
exposure may stimulate plaque formation are endothelial cell injury and
increased platelet activation.
Different people will have different abilities to deal with the
increased stress on the heart and the increased tendency of the blood
to clot as a result of ETS exposure. For example, a young, otherwise
healthy individual may be able to tolerate short-term ETS exposure
without apparent difficulty, although asymptomatic arterial wall injury
may occur which can contribute to cardiac injury in the future.
However, an older person with pre-existing coronary artery disease and
therefore minimum cardiac reserve may not be able to tolerate short-
term ETS exposure, due to the increased stress on the heart.
5. Reproductive Effects
Data on the reproductive effects due to the exposure of nonsmoking
pregnant women to ETS has been presented in many studies [Exs. 3-438,
4-92, 4-132, 4-174, 4-208, 4-273, 4-285, 4-287, 4-299]. This is
important since many nonsmoking women continue to work throughout their
pregnancies. Pregnant women working in indoor environments without
tobacco smoking restrictions, as in restaurants, comprise one of the
most heavily ETS-exposed groups [Exs. 4-151, 4-287].
Low birthweight has also been shown to be associated with paternal
smoking, implying passive exposure to tobacco smoke by the nonsmoking
mother [Exs. 4-92, 4-273]. Passive exposure to tobacco smoke is
estimated to double the risk of low birthweight in a full-term baby
[Ex. 4-208]. Nonsmoking pregnant women who are exposed to ETS have been
reported to deliver neonates that range 24 to 120 grams lighter in
weight than those babies delivered by nonexposed pregnant women [Exs.
4-132, 4-174, 4-208, 4-273]. This relationship between passive smoking
and low birthweight remains statistically significant even after
accounting for mother's age, parity, social class, sex of baby, and
alcohol consumption. This effect is more apparent in neonates born to
actively smoking women who deliver babies that weigh, on average, 200
grams less than those of nonsmoking women [Ex. 4-101]. The reduction in
birthweight is clinically significant at the low end of the birthweight
distribution. These infants have higher perinatal mortality [Ex. 4-
239].
Other reproductive effects that have been ascribed to maternal ETS
exposure include miscarriage, an increase in congenital abnormalities
[Exs. 4-239, 4-299], and numerous other physiological effects [Ex. 4-
297]. It was reported that these effects may be part of a general
immunosuppressive condition associated with the occurrence of low
birthweight [Ex. 4-299]. This effect may predispose the baby to
respiratory tract infections.
The effects of environmental smoke exposure on the fetus may have
long-term sequelae into childhood and adulthood [Exs. 4-53, 4-181, 4-
213, 4-225, 4-239, 4-51, 4-297]. There is limited evidence which
suggests that growth retardation observed in the fetus is reflected in
the growing child as reductions in lung development [3-438]. This is
especially relevant if that child continues to be exposed to ETS
throughout childhood and into adulthood [Exs. 4-177, 4-297]. Prenatal
exposure to ETS and exposure to ETS as a child may also increase an
individual's cancer risk, perhaps by a factor of two (2) [Exs. 4-65, 4-
164, 4-252].
Experimental research on the adverse reproductive effects
associated with ETS exposure in animals is limited. However, one study
[Ex. 4-6] demonstrated such effects. Sciatic nerve tissue taken from
the offspring of ETS-exposed female mice revealed definite toxic
effects on the neonatal tissue [Ex. 4-6]. Pregnant female mice (C57BL/
KsJ) were exposed to low-tar cigarette smoke in a special smoking
chamber. Cigarette smoke was blown into the chamber for 4 minutes, 5
times daily, except on weekends when this was done 3 times daily. At 18
days of gestation, blood samples were taken and carbon monoxide levels
were measured. Ultrastructural abnormalities of fetal tissue revealed
swollen mitochondria with distorted cristae, some indication of
deformed mitochondria, darkened nuclei with condensations of nuclear
material, lamellar bodies, granules and myelin bodies similar to those
found in human toxicity studies. The blood samples from pregnant mice
revealed a mean carbon monoxide saturation in the hemoglobin of 9%
which is equivalent to that found in humans who actively smoke 10-20
cigarettes per day.
6. Cancer
Concern over the carcinogenic effects of ETS was expressed in many
comments submitted to the docket, such as Exs. 3-32, 3-35, 3-38, 3-207,
3-438, 3-440A, and 3-449. The results of epidemiological and
experimental studies indicate that exposure to ETS is causally
associated with cancer of the lung in chronically-exposed nonsmokers. A
discussion of this evidence follows.
(a) Evidence of Association.--The results of epidemiological
studies taken in the aggregate suggest that nonsmoker exposure to ETS
is causally-related to the development of lung cancer.
Evidence of specificity of effect is provided by active smoking
studies that report a causal association with lung cancer [Ex. 4-311].
It was therefore logical to examine nonsmokers with passive exposure to
tobacco smoke, since the chemicals found in passive smoke are
qualitatively similar to those in mainstream smoke. Active smoking
induces all four major histological types of human lung cancer--
squamous-cell carcinomas, small-cell carcinomas, large-cell carcinomas,
and adenocarcinomas [Ex. 4-311]. The results of lung cancer studies
that examined the variation in tumor cell type induced by ETS exposure
indicate that mostly adenocarcinomas and squamous cell carcinomas are
produced by ETS exposure. Some studies have reported an excess of
adenocarcinomas, while others have reported excesses in squamous cell
and small-cell carcinomas. From this information, it is apparent that
similar tumor cell types are induced by ETS exposure as are induced by
active smoking.
The unequivocal causal association between active tobacco smoking
and lung cancer in humans, as well as the corroborative evidence of the
carcinogenicity of tobacco smoke provided by animal bioassays and in
vitro studies and the chemical similarity between mainstream smoke and
ETS, clearly establish the plausibility that ETS is also a human lung
carcinogen (Table II-2). In addition, biomarker studies verify that ETS
exposure results in detectable uptake of tobacco constituents by
nonsmokers [Exs. 4-50, 4-311].

Table II-2.--43 Chemical Compounds Identified in Tobacco Smoke for
Which There is ``Sufficient Evidence'' of Carcinogenicity in Humans or
Animals [Ex. 4-160]

Acetaldehyde
Acylonitrile
Arsenic
Benz (a)anthracene
Benzene
Benzo (a)pyrene
Benzo(b)fluoranthene
Benzo (k)fluoranthene
Cadmium
Chromium VI
DDT
Dibenz(a,h)acridine
Dibenz(a,j)acridine
Dibenz(a,h)anthracene
Dibenzo (a,i)pyrene
Dibenzo (a,e)pyrene
Dibenzo (a,l)pyrene
Dibenzo (a,h)pyrene
Formaldehyde
Hydrazine
Lead
Nickel
N-nitrosodiethanolamine
N-nitrosodiethylamine
N'-nitrosodimethylamine
N'-nitrosonornicotine
N-nitrosopiperidine
N-nitrosodi-n-propylamine
N-nitrosopyrrolidine
N-nitrosodi-n-butylamine
ortho-toluidine
Styrene
Urethane
Vinyl chloride
1,1-dimethylhydrazine
2-nitropropane
2-napthylamine
4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone
4-aminobiphenyl
5-methylchrysene
7H-dibenzo(c,g)carbazole
Indeno (1,2,3,-cd)pryene

(b) Epidemiological and Experimental Studies. There are at least 32
epidemiological studies that have attempted to evaluate the
carcinogenic potential of ETS. OSHA analyzed these studies and
determined that 14 were positive for an association [Exs. 4-36, 4-65,
4-106, 4-119, 4-121, 4-142, 4-143, 4-153, 4-158, 4-187, 4-252, 4-275,
4-276, 4-292, 4-300], 5 were equivocal with a positive trend [Exs. 4-4,
4-47, 4-117, 4-122, 4-171], and 13 were equivocal [Exs. 4-35, 4-38, 4-
52, 4-118, 4-148, 4-164, 4-175, 4-183, 4-192, 4-283, 4-286, 4-296, 4-
326]. [See the Risk Assessment section for further discussion.]
OSHA considered the consistency of the association to determine if
the finding of the same exposure effect occurred in different
populations and different types of studies. The great number of
epidemiological studies available on ETS were conducted by different
researchers, on different populations, in various countries with
diverse study designs. This extensive amount of data increases
confidence that the associations seen between ETS exposure and the
development of lung cancer is externally consistent and is not due to
artifacts or a product of some unidentified, indirect factors unlikely
to be common to all of the studies. The fact that exposure to ETS is
common dilutes the risk estimates derived from these studies because
the comparison group has some exposure to ETS. A recent Centers for
Disease Control and Prevention (CDC) report [Ex. 4-50] found that 100%
of a subset of the National Health and Nutrition Evaluation Survey
(NHANES) III conducted by the National Center for Health Statistics had
detectable levels of cotinine in their bodies indicating that everyone
in the sample had detectable exposure to tobacco smoke [Ex. 4-50].
Cotinine is a metabolite of nicotine and is used as a surrogate of
exposure to tobacco smoke. This indicates that the cancer risk may
indeed be greater since the relationship in these studies has been more
exposed versus less exposed instead of exposed versus nonexposed.
Many potential sources of bias, such as publication bias (the
tendency of scientific journals to publish studies with positive
results), misclassification bias (smokers or former smokers claiming to
be nonsmokers), and recall bias (the reliance on self-reporting of both
personal smoking habits and exposure to others' tobacco smoke) can not
account for the elevation in risks seen in these various studies. Also,
the relative risks that were estimated from prospective study data are
similar to those estimated from case/control study data. Biases that
may be problematic to case-control studies are not a problem in
prospective studies. Since the results from both types of studies are
similar it is apparent that these biases are not important in the case-
control studies (e.g., misclassification bias and recall bias). This
information strengthens the confidence of a causal connection.
Animal studies have shown the carcinogenicity of cigarette smoke.
Limited existing data suggest that sidestream smoke may contain more
carcinogenic activity per milligram of cigarette smoke concentrate than
does mainstream smoke [Ex. 3-689D]. Currently, OSHA is aware of only a
few experimental inhalation studies with sidestream smoke or ETS
reported in the literature. A discussion of these studies follows.
Otto and Elmenhorst [Ex. 4-247] have shown that there are
carcinogenic constituents in the vapor phase of tobacco smoke. They
exposed C57B1 and BLH mice to the gas phase of cigarette mainstream
smoke of 12 cigarettes for 90 minutes daily over 27 months. The
particulate matter was removed by passing the smoke through a Cambridge
filter. The percentages of mice with lung adenomas were 5.5% and 32% in
the smoke-exposed C57B1 and BLH mice, as compared to 3.4% and 22% for
their respective controls. Leuchtenberger and Leuchtenberger [Ex. 4-
197] have also shown that the rate of tumors among mice exposed to the
gas phase was greater than animals exposed to the whole smoke.
Pulmonary adenomas and adenocarcinomas were induced in Snell's mice by
the gas phase but not by the whole smoke in this study. These studies
demonstrate that the carcinogenicity of tobacco smoke is not limited to
the particulate phase.
Studies have also reported hyperplasia and metaplasia in the
trachea and bronchi of mice exposed to cigarette smoke by the
inhalation route [Exs. 4-226, 4-327]. Four lung tumors and emphysema
were detected in 100 male and female C57B1 mice exposed, nose only, to
fresh mainstream smoke [Ex. 4-135].
Pulmonary squamous neoplasms were detected in female Wistar rats
exposed to a 1:5 smoke-to-air mixture for 15 seconds of every minute
during an 11 minute exposure twice a day, 5 days per week, for the
lifespan of the animals [Ex. 4-79]. Respiratory tumors were also
observed in Fischer-344 rats exposed, nose only, to a 1:10 smoke to air
mixture for approximately 30 seconds every minute, 7 hours per day, 5
days per week for 128 weeks [Ex. 4-77]. The incidence of laryngeal
leukoplakias in Syrian golden hamsters ranged from 11.3% for the
animals that received the low dose to 30.6% of those animals that
received the highest dose. These animals were exposed to a 1:7 smoke-
to-air mixture for 10 to 30 minutes, 5 days a week, nose only, for a
period of up to 52 weeks [Ex. 4-88]. Exposing hamsters twice a day, 5
days a week for up to 100 weeks resulted in almost 90% of the exposed
hamsters having hyperplastic or neoplastic changes in the larynx in a
study by Bernfeld et al. [Ex. 4-30]. Lung tumors have been reported in
beagle dogs exposed to the smoke from nonfilter cigarettes [Ex. 4-19].
However, no tumors were seen in rabbits exposed to cigarette smoke for
up to 5\1/2\ years [Ex. 4-149].
Sidestream condensates have also been shown to cause
carcinogenicity when implanted into female Osborne-Mendel rat lungs
[Ex. 4-127]. Cigarette smoke condensate fraction from sidestream smoke
was implanted at a dose level of one cigarette per animal in this
study.
Coggins et al. [Ex. 4-59] reported epithelial hyperplasia in the
nasal cavity of high-dosed rats exposed to environmental tobacco smoke.
They exposed Sprague-Dawley rats of both sexes, nose only, to ``aged
and diluted sidestream smoke'' (ADSS) at 0.1, 1 or 10 mg of
particulates per meter for 14 days and found ``slight to mild''
epithelial hyperplasia and inflammation in the most rostral part of the
nasal cavity in the 10 mg group only. They also found that these
changes were reversible if the animals were kept without further
exposure for an additional 14 days. No effects in the lung were
reported. Similar results of mild hyperplasia were also obtained when
male rats were exposed to the same concentrations for up to 13 weeks
[Ex. 4-60]. In this study the authors reported hypercellularity and the
thickening of the respiratory epithelium of the dorsal nasal conchae
and adjacent wall of the middle meatus.
Rats are obligatory nose-breathers, and the anatomy and physiology
of the respiratory tract and the biochemistry of the lung differ
between rodents and humans. Because of these distinctions, laboratory
animals and humans are likely to have different deposition and exposure
patterns for the various cigarette smoke components in the respiratory
system. For example, rodents have extensive and complex nasal
turbinates where significant particle deposition could occur,
decreasing exposure to the lung. These anatomical and physiological
differences, aside from the subchronic exposure, may partially account
for absence of any lung tumors in the study by Coggins et al.
The application of cigarette smoke condensate (CSC) to mouse skin
is a widely employed assay for the evaluation of carcinogenic
potential. CSC assays may not, however, reveal all of the carcinogenic
activity of actual cigarette smoke, because these condensates lack most
of the volatile and semi-volatile components of whole smoke. Benign
skin tumors and carcinomas were seen in Swiss-ICR mice exposed to
cigarette tar from the sidestream smoke of nonfilter cigarettes
suspended in acetone and applied to skin for 15 months [Ex. 4-327]. In
lifetime rat studies, intrapulmonary implants of mainstream smoke
condensate in a lipid vehicle caused a dose-dependent increase in the
incidence of lung carcinomas [Exs. 4-75, 4-289].
The polyamines contained in tobacco smoke, spermidine, spermine,
and their diamine precursor, putrescine, are believed to have an
essential role in cellular proliferation and differentiation. Formation
of putrescine from ornithine is catalyzed by ornithine decarboxylase
(ODC), the rate-limiting enzyme in polyamine biosynthesis. A
significant increase in lung and trachea ornithine decarboxylase
activity was observed by Olsen [Ex. 4-245] after an eight week exposure
of male Sprague-Dawley rats to MS smoke. All dilutions of SS smoke
exposure caused significant increase in trachea ODC activity but did
not influence the lung ODC activity.
Environmental tobacco smoke induced carcinogenicity is also
supported by a case-control study of lung cancer in pet dogs [Ex. 4-
259]. The study compared the incidence of lung cancer in pet dogs
exposed to their owners' smoking versus dogs whose owners did not
smoke. Dogs have a very low natural incidence of lung cancer. There was
an elevated risk of lung cancer (Relative Risk = 1.6) observed in pets
with smoking owners. However, the analysis was statistically
insignificant, perhaps in part due to small sample size.
7. Genotoxicity
Short-term mutagenicity tests have gained widespread acceptance as
an initial step in the identification of potential carcinogens.
Extensive use of these tests has come about because they are easy to
perform and are inexpensive and also because of the reported high
positive correlations between short-term mutagenicity tests and
carcinogenicity. It has been reported that 90 percent of the
carcinogens tested are mutagens and 90 percent of the noncarcinogens
are nonmutagens.
Several short-term bioassays have been performed to evaluate the
genotoxicity of cigarette smoke. While most of them have evaluated the
effect of cigarette smoke condensate, some have attempted to evaluate
either the gas phase or the whole smoke.
The most commonly employed assay for mutagenic activity employs
various strains of Salmonella typhimurium. Whole smoke as well as
cigarette smoke condensate of tobacco have been shown to be mutagenic
in Salmonella typhimurium strain TA 1538 [Ex. 4-21]. Sidestream smoke
was also found to be mutagenic in a system where the smoke was tested
directly on the bacterial plates [Ex. 4-246]. Sidestream smoke and
extracts of ETS collected from indoor air [Exs. 4-202, 4-5, 4-198, 4-
201, 4-203] also exhibited mutagenic activity in this bacterial strain.
Claxton et al. [Ex. 4-55] found that sidestream smoke accounted for
approximately 60% of the total S. typhimurium mutagenicity per
cigarette, 40% from the sidestream smoke particulates and 20% from the
semi-volatiles. The highly volatile fraction, from either mainstream or
sidestream smoke was not mutagenic.
Condensates from both mainstream [Exs. 4-89, 4-193] and sidestream
smoke [Ex. 4-90] have also been reported to have mutagenic activity.
Doolittle et al. [Ex. 4-89] demonstrated the genotoxicity of the
sidestream smoke from the Kentucky Reference cigarette (1R4F) by
employing several different assays. In their study, sidestream smoke
produced positive results in Salmonella typhimurium strains TA98,
TA100, TA1537, and TA1538 in the presence of S9 mix from aroclor-
induced rat liver but produced negative results in strain TA1535. They
also showed that sidestream smoke produced positive results in the
Chinese hamster ovary cells chromosomal aberration assay and in the
Chinese hamster ovary cell sister-chromatid exchange assay both with
and without metabolic activation. They demonstrated that the sidestream
smoke was weakly positive in inducing DNA repair in cultured rat
hepatocytes. However, sidestream smoke was nonmutagenic in the Chinese
hamster ovary cell-HGPRT assay both with and without metabolic
activation but it was found to be cytotoxic in this system.
In their further studies, Doolittle et al. [Ex. 4-90] observed
similar responses when they measured the genotoxic activity of
mainstream cigarette smoke condensate (CSC) from Kentucky reference
research cigarette (1R4F). As seen with sidestream smoke, CSC in this
study was mutagenic in Salmonella typhimurium strain TA98, TA100,
TA1537, and TA1538 in the presence of S9 mix but was negative in strain
TA1535. CSC was also positive in the Chinese hamster ovary (CHO) cells-
chromosomal aberration assay and in the CHO-sister-chromatid exchange
assay both with and without metabolic activation. CSC was weakly
positive in inducing DNA repair in cultured rat hepatocytes. However,
again as seen with sidestream smoke, CSC was nonmutagenic in the CHO-
HGPRT assay, with or without metabolic activation but was found to be
cytotoxic in this system. The results from these two studies appear to
indicate that sidestream smoke behaves very much like mainstream smoke
in these assays.
Mohtashamipur et al. [Ex. 4-227] demonstrated significant mutagenic
activity in the urine of rats exposed to sidestream smoke. In this
study, cigarettes were machine smoked under standardized laboratory
conditions and the sidestream smoke of two cigarettes was directed
through metabolism cages containing rats. The urine of these rats was
collected 24 hours prior to the SS exposure and 24 hours after the
onset of the exposure. The individual urine samples of all (10) rats
after exposure showed significantly higher activity for direct-acting
mutagens (in strain TA1538) than the urine samples of the same rats
before the exposure.
The formation of DNA adducts is widely accepted as an initial step
in the carcinogenesis process. The measurement of DNA adducts by the
\32\P-postlabeling assay has been used as a way to assess DNA damage
following exposure to cigarette smoke. Lee et al. [Ex. 4-194] exposed
Sprague-Dawley rats to 0.1, 1.0 and 10 mg total particulate matter/m\3\
of aged and diluted sidestream smoke (ADSS) for 6 hours per day for 14
consecutive days. They examined the DNA from lung, heart, larynx and
liver after 7 and 14 days of exposure and after 14 days of recovery.
They also examined alveolar macrophages for chromosomal aberrations.
Exposure related DNA adducts were found in the highest dose test.
However, no elevation in chromosomal aberrations was observed in
alveolar macrophages in this study. Similar results were also obtained
when animals were exposed to the same three concentrations for up to 90
days. DNA adducts were seen in lung, heart and larynx DNA of the
animals exposed to the highest concentration of ADSS [Ex. 4-195]. The
adduct levels were highest after 90 days of exposure and were
significantly reduced in all target tissues 90 days after cessation of
exposure. Again, chromosomal aberrations in alveolar macrophages were
not elevated in any group after 90 days of exposure. The authors
concluded that the concentration of DNA adducts formed in the lung
tissue did not increase linearly as the ADSS concentration was
increased from 1 to 10 mg.
Several short-term tests have been performed in eukaryotic systems.
A solution of the gas phase of mainstream cigarette smoke has been
shown to induce reciprocal mitotic recombination in Saccharomyces
cerevisiae D3 and petite mutants in an isolate of strain D3 [Ex. 4-
163]. Whole mainstream cigarette smoke induced mitotic gene conversion,
reverse mutation, and reciprocal mitotic recombination in strain D7 of
Saccharomyces cerevisiae [Ex. 4-113]. Transformation of mammalian cells
was induced in several cell systems using the cigarette smoke
condensate from mainstream cigarette smoke [Exs. 4-22, 4-161, 4-188, 4-
267, 4-268, 4-298].
Another in vitro assay that measures the number of sister-chromatid
exchanges (SCEs) induced has been employed widely to determine the
mutagenic activity of cigarette smoke. Valadand-Berrieu and Izard [Ex.
4-313] used a solution of the gas phase from cigarette mainstream smoke
and showed that this solution induced a significant dose-related
increase in sister-chromatid exchanges. Putman et al. [Ex. 4-257] have
also demonstrated dose-dependent increases in sister chromatid exchange
frequencies in bone-marrow cells of mice exposed to cigarette smoke for
2 weeks.
Review of the literature clearly demonstrates that MS smoke and ETS
exposure causes cancer in humans. These results are supported not only
by animal studies but also by studies that show SS smoke to be both
genotoxic and clastogenic.
8. Conclusions
The epidemiological and clinical studies, taken in aggregate,
indicate that exposure to environmental tobacco smoke may produce
mucous membrane irritation, pulmonary, cardiovascular, reproductive,
and carcinogenic effects in nonsmokers. Exposure to ETS may aggravate
existing pulmonary or cardiovascular disease in nonsmokers. In
addition, animal studies show that both mainstream and sidestream
tobacco smoke produce similar adverse effects.

D. Case Reports

1. Sick Building Syndrome and Building-Related Illness
Many case reports of material impairment of health due to
occupational exposure to poor IAQ have been reported to OSHA through
submission to the indoor air quality docket [H-122]. These adverse
health effects range from irritation effects to more severe, life-
threatening building-related illnesses, such as Legionnaire's disease,
and cancer.
Ford Motor Company responded in docket comment 3-447, that
``[p]resently, at Ford, we investigate an average of two IAQ complaints
per month which are predominantly classified as Sick Building Syndrome.
We have seen Building-Related Illness, but these incidents have been
rare and associated with specific contaminant episodes. The IAQ
complaints we generally investigate are characterized by general
malaise, headache, and flu-like symptoms that are said to disappear
when the occupants leave the building * * * Of the IAQ problems
investigated, about 20 percent can be attributed to PTS [passive
tobacco smoke]/ETS. Upper respiratory irritation or eye irritation
typically are associated with these complaints.'' Similar types of
health effects were reported to the agency in docket comments 3-1, 3-
22, 3-58, 3-142C, 3-367, 3-413, 3-529, 3-632, 3-634, 3-642, 3-659, and
3-698.
One comment [Ex. 3-433 reported that ``based upon approximately 30
IAQ investigations in a member company over the past two and one-half
years, the following adverse health effects have been reported in
office environments: eye, nose, and throat irritations; headaches,
nausea, dizziness, fatigue; cough, shortness of breath, chest
tightness. These so-called ``sick building syndrome (SBS)'' symptoms
often disappear when the person leaves the building environment. These
symptoms are usually subjective and non-specific, lacking a physician's
diagnosis of a definite illness.'' Others have reported [Ex. 3-377]
that ``as air flow and ventilation are cut back, our workers are
becoming sick. Many are exposed to contaminants or other harmful
substances; and, without ventilation, these sources linger and cause
nausea, skin irritations and other unhealthy symptoms of illness. In
severe cases, these contaminants and bacteria have been known to
contribute to upper respiratory infections.'' Comment 3-570 reported
similar health effects due to poor indoor air quality.
More serious health conditions have been reported ranging from
severe asthma to central nervous systems disorders. For example,
Comment 3-158 responded that ``I have developed a serious asthma
condition due to indoor air quality problems. Besides, three of the
remaining five employees at the branch office have been diagnosed with
chronic fatigue syndrome. In conversations with various health care
professionals, I have come to the conclusion that the diagnoses of
chronic fatigue syndrome were actually sick building syndrome. Of the
six employees at the branch office, four of the six are moderate to
heavy smokers. This does not take into consideration the other factors
that could be causing poor indoor air quality problems in the office.''
Comment 3-631 was a collection of reports from the workers in one
building that illustrate the poor conditions of a building that can
lead to serious health effects in workers. Health problems experienced
by workers in this building included chronic sinus infections;
headaches; fatigue; eye, nose and throat irritations; difficulty
breathing and congestion; allergies; and asthma. These health problems
seem to clear up when the workers were out of the building over a
weekend or a vacation.
The physical condition of this building was obviously in disrepair
since the commenters reported pails of stagnant water, collected from
leaks in the roof, were left in hallways. Water in ``[t]hese pails
ha[d] overflowed and run down the stairs. What [wa]s left in the pails
evaporate[d] leaving a gross residue of who knows what.'' The water
leaks from the roof caused mold infestation and water damage. Water
logged insulation hung in the ceiling out in a hallway. There was an
obvious lack of routine, sufficient cleaning. Dust and particulate
matter were visible in the air. The bathrooms were dirty. Smells of
sewer gas, mold, and diesel and other vehicular fumes permeated the
office space. Ventilation problems were evident since paint or varnish
fumes lingered whenever part of the inside physical structure of the
building was painted. Tar fumes were evident from constant patching of
the leaky roof. Insect infestation of the building was evident.
Pesticide fumes lingered whenever the building was spray[ed] for
roaches and steam bugs. Workers sighted cockroaches, silverfish, and
steam bugs near the coffee shop and on back stairs. The comment
continued that ``a sink faucet in the lunch room has been leaking for
years and water runs on the counter under the toaster and microwave.
The water heater had leaked for about 2 months before it was fixed. At
that time the carpet was soaked and water was running under the wall
into a supervisor's office. There is a moldy odor from this carpet and
the floor below.''
Cancer has also been reported to be associated with poor indoor air
quality. A courthouse in San Diego, California [Ex. 3-55], ``is
notorious for poor air quality and employee respiratory illness and
cancer.'' It was reported to OSHA that many long-term employees have
cancer (stomach and lung cancer), terminal lung disease, chronic ear
and throat infections, and bronchial problems'' [Exs. 3-585, 3-635, 3-
637, 3-68].
Comment 3-630 from a union reported that ``[a]fter surveying
thousands of workers across the country, SEIU compiled actual survey
responses that list adverse health effects caused by indoor air
pollution. These include headaches, nose congestion or irritation,
throat irritation, dry cough, dry or itchy skin, dizziness, nausea,
lethargy or fatigue, colds, asthma/wheezing, chest tightness, runny
nose/post nasal drip, eye or contact lens irritation, respiratory
difficulties. In addition, EPA estimates that pollutants found in
indoor air are responsible for 2,500 to 6,500 cancer deaths each year''
[refer to Ex. 3-630L].
These concerns are not just relevant to office workers but also to
maintenance and other nonindustrial workers that work in indoor
environments. For example, comment 3-347 responded that ``[i]n our
closed, indoor work environments, air quality is a very real health and
safety concern to professional painters. I have seen firsthand
otherwise healthy men and women pass out or get violently ill as a
result of being exposed to indoor air contaminants.'' Comment 3-412
responded ``[o]ur locals have encountered air-pollution problems
ranging from ink mist and photocopier emissions to asbestos and
microbial disease. The level of toxic chemical contaminants is often
alarmingly high in our darkrooms, and carbon-monoxide emissions from
trucks at newspaper loading docks frequently penetrate the ventilation
system. In 1985 microbial contamination from a water tower infected six
New York Times employees with Legionnaires' Disease and 34 others with
less serious respiratory infections.''
Operation engineers are also affected by poor indoor air quality.
Comment 3-452 responded that ``[t]his is particularly important for the
operation engineers who appear healthy and then suffer from respiratory
problems, much like allergic reactions, after working in a building
with poor ventilation.''
2. Environmental Tobacco Smoke
Many case reports of severe material impairment of health due to
occupational exposure to ETS have been reported to OSHA through
submission to the indoor air quality docket [H-122]. Information
contained in these comments indicate that adverse health effects in
workers due to environmental tobacco smoke exposure while at work range
from mucous membrane irritation (eye, nose, and throat effects) to more
severe, life-threatening conditions, such as status asthma, other
chronic lung diseases and heart diseases. For example, comment 3-309
responded [Regarding ETS exposure in a cafeteria], ``By the time I have
finished lunch my eyes are tearing, my nose is plugged, and I have a
headache'' as well as comment 3-315, ``I had fewer headaches and fewer
respiratory ailments; my chronic sore throat disappeared [after a
company-wide no smoking policy was implemented]''. Comment 3-22
responded ``[m]y patients find it hard to obtain smoke free workplaces.
I have seen patients who have suffered status asthma from workplace
smoking, patients who have had to quit their jobs because of ETS in the
workplace. Recently, one of my never smoking patients sustained vocal
cord lesions seen almost entirely in smokers.'' Comment 3-104 continued
that ``[p]assive tobacco smoke (PTS) is the principal indoor air
contaminant in my office building in Rockefeller Center. While smoking
is limited to `private offices', the smoke flows freely from these
private offices throughout the entire general office areas since the
smokers will not keep their doors closed, and even when they do, they
have to come out sometime. And, as soon as the door is opened, the
dense smoke accumulation within the office is diffused to all adjacent
work areas. Because office buildings have closed ventilation systems,
only a `smoke free' office policy can be effective. Half measures only
cause further stress, frustration and irritation to both smokers and
nonsmokers.'' Comment 3-289 responded that ``I have been exposed to
asbestos culminating in my getting asbestosis (plural plaque) of the
lungs. The combination of asbestos exposure plus second-hand smoke from
my smoking co-workers has posed and is currently posing a health risk
to me.''

III. Exposure

Contaminants which contribute to poor indoor air quality can be
attributed to both outside air and inside air. Outside air contaminants
can be introduced into a building through the ventilation intakes,
doors, building envelope, and windows. Outside air contaminants include
vehicular exhausts, industrial emissions, microbiologicals, and pollen.
Inside air contaminants are emitted from building materials and
furnishings, appliances, office equipment and supplies, biological
organisms, and of course, pollutants introduced by the building
occupants themselves. Inside air contaminants include tobacco smoke,
volatile organic compounds, combustion gases such as carbon monoxide,
and occupant-generated bioeffluents. The concentration of these
contaminants in buildings can increase if ventilation systems are
inadequately designed, maintained and operated or if strong local
contaminant sources are not controlled.

A. Sources of Indoor Air Contaminants

A wide variety of substances are emitted by building construction
materials and interior furnishings, appliances, office equipment, and
supplies, human activities, and biological agents. For example,
formaldehyde is emitted from various wood products, including particle
board, plywood, pressed-wood, paneling, some carpeting and backing,
some furniture and dyed materials, urea-formaldehyde insulating foam,
some cleaners and deodorizers, and from press textiles. Volatile
organic compounds, including alkanes, aromatic hydrocarbons, esters,
alcohols, aldehydes, and ketones are emitted from solvents and cleaning
compounds, paints, glues, caulks, and resins, spray propellants, fabric
softeners and deodorizers, unvented combustion sources, dry-cleaning
fluids, arts and crafts, some fabrics and furnishings, stored gasoline,
cooking, building and roofing materials, waxes and polishing compounds,
pens and markers, binders and plasticizers. Pesticides also contain a
variety of toxic organic compounds.
Building materials are point sources of emissions that include a
variety of VOCs (Table III-1). Some of these materials have been linked
to indoor air quality problems. The probability of a source emitting
contaminants is related to the age of the material. The newer the
material, the higher the potential for emitting contaminants. These
materials include adhesives, carpeting, caulks, glazing compounds, and
paints [Ex. 4-33]. These materials, as well as furnishings can act as a
sponge or sink in which VOCs are absorbed and then re-emitted later.
Appliances, office equipment, and supplies can emit VOCs and also
particulates [Ex. 4-33]. Table III-2 lists the many contaminants that
can be emitted from these point sources. There is an indirect
relationship between the age of the point source and the potential rate
of contaminant emission [Ex. 4-33].

Table III-1.--Emissions From Building Materials or Interior Furnishings
------------------------------------------------------------------------
Material Typical pollutants emitted
------------------------------------------------------------------------
Adhesives.......................... Alcohols.
Amines.
Benzene.
Decane.
Dimethylbenzene.
Formaldehyde.
Terpenes.
Toluene.
Xylenes.
Caulking Compounds................. Alcohols.
Alkanes.
Amines.
Benzene.
Diethylbenzene.
Formaldehyde.
Methylethylketone.
Xylenes.
Carpeting.......................... Alcohols.
Formaldehyde.
4-Methylethyl- benzene.
4-Phenylcyclohexene.
Styrene.
Ceiling Tiles...................... Formaldehyde.
Clipboard/Particle Board........... Alcohols.
Alkanes.
Amines.
Benzene.
3-Carene.
Formaldehyde.
Terpenes.
Toluene.
Floor and Wall Coverings........... Acetates.
Alcohols.
Alkanes.
Amines.
Benzenes.
Formaldehyde.
Methyl styrene.
Xylenes.
Paints, Stains & Varnishes......... Acetates.
Acrylates.
Alcohols.
Alkanes.
Amines.
Benzenes.
Formaldehyde.
Limonene.
Polyurethane.
Toluene.
------------------------------------------------------------------------

Table III-2.--Emissions From Appliances, Office Equipment and
Supplies\1\
Appliances......................... Carbon Monoxide.
Nitrogen Dioxide.
Sulfur Dioxide.
Polyaromatic hydrocarbons.
Carbonless Copy Paper.............. Chlorobiphenyl.
Cyclohexane.
Dibutylphthalate.
Formaldehyde.
Computers/Video Display Terminals.. n-Butanol.
2-Butanole.
2-Butoxyethanol.
Butyl-2-Methylpropyl phthalate.
Computer/Video Display Terminals... Caprolactam.
Cresol.
Diisooctyl phthalate.
Dodecamethyl cyclosiloxane.
2-Ethoxyethyl acetate.
Ethylbenzene.
Hexanedioic acid.
3-Methylene-2-pentanone.
Ozone.
Phenol.
Phosphoric Acid.
Toluene.
Xylene.
Duplicating Machines............... Ethanol.
Methanol.
1,1,1-Trichloroethane.
Trichloroethylene.
Electrophotographic Printers, Ammonia.
Photocopiers & Related Supplies. Benzaldehyde.
Benzene.
Butyl methacrylate.
Carbon black.
Cyclotrisiloxane.
Ethylbenzene.
Isopropanol.
Methylmethacrylate.
Nonanal.
Ozone.
Styrene.
Terpene.
Toluene.
1,1,1-Trichloroethane.
Trichloroethylene.
Xylenes.
Zinc stearate combustion Products.
Microfiche Developers/Blueprint Ammonia.
Machines.
Preprinted Paper Forms............. Acetaldehyde.
Acetic Acid.
Acetone.
Acrolein.
Benzaldehyde.
Butanal.
1,5-Dimethylcyclopentene.
2-Ethyl furan.
Heptane.
Hexamethyl cyclosiloxane.
Hexanal.
4-Hydroxy-4-methyl pentanone.
Isopropanol.
Paper dust.
Propionaldehyde.
1,1,1-Trichloroethane.
Typewriter Corrections Fluid....... Acetone.
1,1,1-Trichloroethane.
\1\Source: [Ex. 4-33]

Emissions from equipment, such as computers, will decrease over
time compared to emissions from equipment that continually use
chemicals. Emissions from such equipment (e.g., laser printers) that
use chemicals continually, will obtain a steady state concentration
dependent upon the chemicals used and frequency of equipment use.

B. Microbial Contamination

Three conditions must exist in buildings before microbial
contamination can occur: high humidity (over 60%), appropriate
temperatures (varies according to microbe), and appropriate growth
media [Exs. 3-61, 4-33]. These conditions are found in heating,
ventilating, and air conditioning (HVAC) systems. HVAC systems provide
multiple sites for microbes to grow (reservoir) and also the means to
disperse the microbes throughout the ventilated space. These reservoirs
of microbial growth, if allowed to proliferate unchecked, can lead to
indoor air quality problems once the microbes or microbe-related
products, such as endotoxins, are dispersed.
Building materials that have been soaked with water, such as
fiberglass insulation in air handlers, furnishings and fabrics, ceiling
tiles, and carpeting are excellent media for microbial growth.
Biological organisms, including fungal spores, bacteria, viruses,
pollens, and protozoa derived from mold growth have been identified in
humidifiers with stagnant water, water damaged surfaces and materials,
condensing coils and drip-pans in HVAC systems, drainage pans in
refrigerators, dirty heating coils, and are also associated with
mammals, arthopods and insects. Table III-3 gives examples of
biologicals found in indoor environments.
Various allergens have been associated with the development of
allergic rhinitis, asthma, or airway hyperresponsiveness (Table III-3)
[Ex. 4-33]. Many of these allergens are common to the nonindustrial
work environment. These include chemical volatiles and dusts,
arthropods, and dusts, particulates & fibers.

Table III-3.--Examples of Biologicals Found in Indoor Environments\1\
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Source: Frix Law Library, https://www.frixlaw.com/law-library/documents/fr%3A94-7619. Public record. Not legal advice.