EPA
HUD
United States
Environmental Protection
Agency
United States
Department of Housing
and Urban Development
Environmental Monitoring and Support Laboratory
Office of Research and Development
U.S. Environmental Protection Agency
Research Triangle Park, North Carolina 27711
Office of Policy Development and Research
Office of Housing and Urban Development
Washington. D.C. 20410
fcPA 600/7-78-027
March 1978
SURVEY OF INDOOR AIR
QUALITY HEALTH CRITERIA
AND STANDARDS
Interagency
Energy-Environment
Research and Development
Program Report
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RESEARCH REPORTING SERIES
Research reports of the Office of Research and Development, U.S. Environmental
Protection Agency, have been grouped into nine series. These nine broad cate-
gories were established to facilitate further development and application of en-
vironmental technology. Elimination of traditional grouping was consciously
planned to foster technology transfer and a maximum interface in related fields.
The nine series are:
1. Environmental Health Effects Research
2. Environmental Protection Technology
3. Ecological Research
4. Environmental Monitoring
5. Socioeconomic Environmental Studies
6. Scientific and Technical Assessment Reports (STAR)
7. Interagency Energy-Environment Research and Development
8. "Special" Reports
9. Miscellaneous Reports
This report has been assigned to the INTERAGENCY ENERGY-ENVIRONMENT
RESEARCH AND DEVELOPMENT series. Reports in this series result from the
effort funded under the 17-agency Federal Energy/Environment Research and
Development Program. These studies relate to EPA's mission to protect the public
health and welfare from adverse effects of pollutants associated with energy sys-
tems. The goal of the Program is to assure the rapid development of domestic
energy supplies in an environmentally-compatible manner by providing the nec-
essary environmental data and control technology. Investigations include analy-
ses of the transport of energy-related pollutants and their health and ecological
effects; assessments of, and development of, control technologies for energy
systems; and integrated assessments of a wide range of energy-related environ-
mental issues.
This document is available to the public through the National Technical Informa-
tion Service, Springfield, Virginia 22161.
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SURVEY OF INDOOR AIR QUALITY HEALTH CRITERIA
AND STANDARDS
by
James E. McFadden
J. Howard Beard, III
Demetrios J. Moschandreas
GEOMET, Incorporated
15 Firstfield Road
Gaithersburg, Maryland 20760
EPA Contract Number 68-02-2294
Steven M. Bromberg
Lnvironmental Monitoring and Support Laboratory
Environmental Research Center
U.S. Environmental Protection Agency
Research Triangle Park, N.C. 27711
Prepared for
Office of Policy Development and Research
U.S. Department of Housing and Urban Development
Washington, D.C. 20410
ENVIRONMENTAL MONITORING AND SUPPORT LABORATORY
OFFICE OF RESEARCH AND DEVELOPMENT
U.S. ENVIRONMENTAL PROTECTION AGENCY
RESEARCH TRIANGLE PARK, N.C. 27711
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DISCLAIMER
This report has been reviewed by the Environmental Monitoring and Support
Laboratory, U.S. Environmental Protection Agency, and approved for publication.
Approval does not signify that the contents necessarily reflect the views and
policies of the U.S. Environmental Protection Agency, nor does mention of trade
names or commercial products constitute endorsement or recommendation for use.
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CONTENTS
Figures iv
Tables v
1. Executive Summary 1
2. Indoor Air Quality Health Criteria 6
3. Indoor Air Quality Standards. . . 10
Introduction .10
Background for Standard Setting 12
Ambient Air Quality Standards 16
Workplace Air Quality Standards 17
Air Quality Standards for a Totally Enclosed
Environment - The Submarine Atmosphere 20
An Indoor Air Quality Standard - ASHRAE 62-73 24
Energy Conservation in New Building Design -
ASHRAE Standard 90-75 31
Indoor Air Quality Standard for Ozone. 34
4. Design Level and Emission Indoor Air Standards 35
Introduction . ; 35
Design-Level Standards . .36
ASA Standard A53.1 .36
ASHRAE Standard 62-73 37
ASHRAE Standard.90-75 37
Emission Standards 45
Building Codes . . .46
5. Indoor Air Quality Standards Abroad 51
Introduction 51
Maximum Allowable Indoor Air Quality
Standards Abroad 51
Design-Level Indoor Air Quality
Standards Abroad 53
Indoor Air Quality Emission
Standards Abroad 58
6. Bibliography. . . 60
Appendices
A. Health Criteria for Indoor Air Pollution 65
B. U.S. Department of Labor, Occupational Safety. . . . 126
and Health Administration, Air Quality Standards
for Workroom Air
C. Canadian Provinces and Foreign Coutries Queried
in the Search for Indoor Air Quality Standards . . 133
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FIGURES
Number
1
A-l
A-2
A-3
A-4
A-5
Diagram of definitions ,
Reference data for effects of sulfur dioxide exposures. .
Reference data for effects of carbon monoxide exposures .
Reference data for effects of nitrogen dioxide exposures.
Reference data for health effects of photochemical
oxidant exposure ,
Reference data for health effects of particulate
exposures .
. .25
. .66
. .77
. .79
.85
101
-TV-
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TABLES
Number Page
1 National Ambient Air Quality Standards. 18
2 Maximum Allowable Contaminant Concentrations for
Ventilation Air 25
3 Air Quality Standards for Ventilation Air, Ambient
Air, and Workplace Air 28
4 Comparative Air Quality Standards 29
5 Comparison of Typical Minimum Mechanical Ventilation
Requirements Between the ASHRAE Standard 62-73
and the ASA Standard A53.1 38
6 ASHRAE 62-73 Ventilation Requirements . .39
7 General Pressure Relationships and Ventilation
of Certain Hospital Areas 43
8 Pressure Relationships and Ventilation of
Medical Facilities 44
9 Statewide Building Code Programs - Application and
Type of Codes Adopted 48
A-l Best Judgment Estimates of Pollutant Thresholds for
Sulfur Oxides and Suspended Particulates .71
A-2 Effects of Controlled Ozone Exposure on Adult Males 87
A-3 Illustrative Health Information on Some Household
Solvents and Cleaners 90
A-4 Illustrative Summary Information on Selected Pesticides . . .98
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SECTION 1
EXECUTIVE SUMMARY
In recent years the national need to conserve energy resources has
resulted in a major thrust toward energy conservation measures in the
design and use of buildings. Concurrently, there has been an increasing
concern with the impact of air pollution upon the health of the American
people, and an awareness that air pollution within residential and other
nonworkplace buildings may be as important a health factor as outdoor
"ambient" air pollution. These two concerns are brought together in a
recognition that measures to conserve energy within buildings, through
the introduction of new energy transfer systems and the reduction of
building ventilation rates, will result in changes in the indoor air
quality characteristics of buildings. These changes may affect air
quality either adversely or beneficially.
The U.S. Department of Housing and Urban Development (HUD) is con-
cerned with ensuring that the American public has an opportunity to
obtain satisfactory housing and suitable living environments. As a result
of this concern, it is HUD's intention that HUD-assisted housing projects
provide environments meeting national clean air standards promulgated by
EPA (wherever these are applicable) and that where no standards now apply
(as in indoor environments), design guidance be provided which will pro-
mote healthful, desirable residential air environments. For this reason
HUD is now concerned with the availability, use and utility of existing
indoor air quality standards. HUD's Office of Research and Policy Develop-
ment has joined with EPA in requesting GEOMET, Incorporated, under EPA
Contract Number 68-02-2294, to undertake a survey of indoor air quality
standards. This report is the result.
Indoor Air Quality Standards may be classified into three types:
(1) maximum allowable air quality standards, (2) design-level standards,
and (3) emissions standards. Each type may be a guideline, a rule or
regulation, or a standard with the force of law.
Maximum allowable air quality standards are those which specify a
numerical limiting value for a contaminant as an amount of concentration
per unit volume (i.e., parts per million by volume) or on a weight to unit
volume basis. Care must be taken in comparing standards for the same con-
taminant published by different authorities, since they may have different
purposes (i.e., protection of the entire population versus protection of
workers), different averaging times (e.g., eight hours versus annual aver-
age) and different methods for measuring. Acceptable contaminant levels
may be specified at times in units other than on a volume or weight to
unit volume basis; an example being the Threshold Limit Value for asbestos
(i.e., five fibers greater than five microns in length per cubic centi-
meter). Maximum allowable air quality standards are discussed in depth
in Section 3.
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Design-level standards are those standards which specify a numerical
value for the volume of air required to be used in air circulation or
ventilation air. In such standards the term "ventilation" should be
defined by the authority promulgating the standards, since it may include
both natural and mechanical ventilation and fresh or recirculated air.
Typically design-level standards specify the volume of air required for
venti.lation as a rate per human occupant, floor space area, or volume
(e.g., cubic feet per minute (cfm) per person, cfm per square foot of
floor area, or air changes per hour). Design-level standards are discus-
sed in more detail in Section 4.
Emission standards are those standards that specify a numerical limit-
ing value for the amount of contaminant which may be emitted from a source
or sources. Such standards may specify this limiting numerical value as a
rate (micrograms of ozone per second) or as a concentration accompanied by
locations for measurement and the volume of the test room in which the sample
is taken. Emission standards are also discussed in Section 4.
The purpose of all three types of indoor air quality standards is to
safeguard the health, safety and well-being of inhabitants within the indoor
environment. However, indoor air quality standards for nonworkplace environ-
ments have more often been developed to ensure the occupants' comfort than
their safety; in effect an assumption has been made that indoor exposure to
air pollutants outside the workplace is of minor concern. But with more
knowledge being obtained on the health effects of exposures due to the lower
pollutant concentrations which may characterize indoor residential environ-
ments, more concern is being placed on the quality of all indoor air. Dis-
cussions in this document attempt to define and explain the standards used
to control the quality of nonworkplace indoor air.
Because all air pollution regulation is undertaken primarily to safe-
guard human health (with other aspects of welfare - including the integrity
of building materials under air pollution stress - being secondary consider-
ations), it is necessary to know what the critical relations are between air
pollution exposure and human health. Specific dose-response data must be
scrutinized to determine the appropriate pollutant levels at which signifi-
cant increases in adverse human health effects begin to occur. The critical
relationships between air pollution exposures and adverse human health effects
are summarized, for five criteria pollutants (S02, CO, NCL, TSP, and
Photochemical Oxidants), in Figures A-l through A-5 in Appendix A.
The authors of this document strongly recommend that the readers study
Appendix A, "Health Criteria for Indoor Air Pollution," for a discussion of
the health effects for both criteria and noncriteria pollutants. The pic-
torial summaries, Figures A-l through A-5, are useful for obtaining an over-
view of the potential health risks involved with various pollutant exposures.
However, these figures can be misinterpreted and misleading if not associated
with the appropriate background information supplied in Appendix A.
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The Air Quality Criteria Documents, published by the Department of
Health, Education, and Welfare (HEW), and the Documentation of Threshold
Limit Values for Substances in Workroom Air, published by the American
Conference of Governmental Industrial Hygienists (ACGIH), include obser-
vations of health effects based on toxicological studies with animals and
epidemiological investigations of humans. To promulgate standards based
on this information, dose-response curves must be developed and adequate
safety margins must be incorporated. Safety margins have been incorpor-
ated into the Threshold Limit Values (TLVs) issued by the ACGIH (although
these are not quantified in the TLV documentation). With these safety
margins the TLVs are representative of allowable pollutant levels to
which workers may be exposed day after day without suffering adverse health
effects. The TLVs have been adopted by the Occupational Safety and Health
Administration (OSHA) as acceptable industrial workplace standards and are
enforced under Federal law.
The TLVs, as published by ACGIH, are applicable to the industrial or
laboratory worker who is carefully screened to ensure his health status
prior to exposure episodes but are not necessarily acceptable exposure
levels for the general public, which contains individuals highly susceptible
to particular pollutants. To ensure the safety of these sensitive individ-
uals the American Society of Heating, Refrigerating and Air Conditioning
Engineers (ASHRAE), in its Ventilation Standards 62-73 and 90-75, has typi-
cally specified that air used for ventilation purposes in the indoor environ-
ment must not contain contaminants at concentrations greater than one-tenth
the TLV.
The ASHRAE Standards 62-73 and 90-75 are presently applicable only to
buildings with newly installed forced ventilation systems. Their enforce-
ment relies upon control of design measures prior to the system installation,
and is largely a matter of good engineering practice rather than legal
enforcement by governmental jurisdictions.
The U.S. Department of Health, Education, and Welfare's Food and Drug
Administration (FDA) has recently issued a maximum allowable indoor air
quality standard for ozone. This standard considers any device that pro-
duces ozone, either by design or as a byproduct, to be unacceptable if it
causes the accumulation of ozone in excess of 0.05 parts per million by
volume of air in the atmosphere of enclosed spaces intended to be occupied
by people for extended periods of time (e.g., houses, apartments, hospitals,
and offices).
The indoor air standard for ozone established by FDA (0.05 ppm) is lower
than the ACGIH's TLV level (0.10 ppm) and the EPA's National Ambient Air
Quality Standard (NAAQS) (0.08 ppm). It is important to realize that the
FDA standard protects individuals exposed for extended periods of time with-
out sufficient recovery intervals whereas the ACGIH and EPA standards assume
maximum 8-hour and 1-hour averaging times. The low FDA standard attempts to
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include a margin of safety that will protect sensitive individuals exposed for
extensive periods.
In countries other than the United States there are few maximum allowable
indoor air quality standards for the nonworkplace indoor environment. Many
countries assume that the standards they have developed for outdoor ambient or
workplace air quality can be applied directly to the indoor environment. How-
ever, Sweden has recently developed a maximum allowable indoor air quality
standard using studies which measured the emissions of formaldehydes generated
by particle boards in enclosed indoor environments. Sweden designated 0.40 mg/
m3 of formaldehyde as a maximum'acceptable nonworkplace indoor air quality
standard.
Based upon the same research on indoor formaldehyde levels, Denmark has
decided to control levels of formaldehyde in the indoor air through the devel-
opment of an emission standard. The particle board industry has been required
to use lower concentrations of formaldehydes in its products as means for
reducing emissions in the indoor environment.
The Canadian Standards Association (CSA) has also developed an emission
standard to protect individuals in enclosed residential environments, the
CSA standard designated 0.04 ppm as the maximum level of ozone which can be
produced by devices for household use. This standard is similar to the Ameri-
can ozone standard developed by FDA.
Integrated research into the occurrence and significance of nonworkplace
indoor air pollution is only just beginning. Researchers in many disciplines
are studying indoor environments to identify the sources, and concentrations
of indoor air pollutants. Much remains to be learned but many species of
potentially hazardous air pollution have been identified in the indoor
environment.
Existing ambient standards in the United States and abroad are based upon
health effects studies of human responses to the levels of air pollutant con-
centrations and exposures which may be experienced by healthy people. The most
susceptible populations, the young, the old and those with a history of respir-
atory and cardiovascular illness, spend much time indoors in residential (or
institutional) environments. Data on indoor air pollutant exposures experienced
by such people are scarce. Standards controlling the acceptable levels of air
quality to which these individuals can be exposed are even more scarce.
A major conclusion has been reached by the authors of this study: There
has been no scientific effort to establish air pollution standards specifically
for the indoor, nonworkplace environment.
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Several characteristics of the indoor environment identify its distinct
nature from the ambient outdoor environment: (1) occupants of the indoor
environment may be exposed to low-level pollutant concentrations for exten-
sive periods of time, such an exposure can lead to long-term adverse effects;
(2) under certain conditions indoor concentrations of some criteria pollu-
tants can reach peaks that violate the ambient air quality standards while
the outdoor levels do not violate these standards; and (3) often the residen-
tial environment has pollutant levels lower than outdoors, i.e., the dwelling
cell shields its occupants from high ambient pollutant levels.
Given the distinct nature of the indoor environment and the lack of
relevant studies, the following sequential steps are recommended:
e Further field studies of nonworkplace indoor air pollution
levels should be undertaken.
9 Epidemiological studies of the nonworkplace environment
should be undertaken to identify relationships between
indoor pollution levels and health effects.
e Based upon the epidemiological studies, the need for and
feasibility of establishing indoor air quality standards
should be assessed.
The characterization of the indoor air pollution problem (the first
step in the above seqence) is underway. As one major element of this
effort an on-going EPA-HUD-GEOMET project is identifying and quantifying
indoor pollution levels in residences. Preliminary results from the field
monitoring indicate incidents of high indoor concentrations of some poten-
tially hazardous pollutants and persistent low background levels of others.
The need for epidemiological studies (the middle step of the recommended
sequence) and for careful consideration of possible indoor residential air
pollution standards (the last step of our procedure) is therefore apparent.
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SECTION 2
INDOOR AIR QUALITY HEALTH CRITERIA
Air quality criteria are expressions of the scientific knowledge of
the relationship between various concentrations of pollutants in the air
and their adverse effects on man and his environment. Air quality criteria
documents have been issued by EPA and its predecessor organizations to
assist states in developing air quality standards. To develop these stan-
dards the criteria needed to be descriptive; that is, they described health
effects observed to occur when the ambient air levels of a pollutant reached
or exceeded a specific figure for a specific time period (USHEW 1969).
Air quality standards on the other hand are prescriptive. They pre-
scribe pollutant exposures which a political jurisdiction determines
should not be exceeded in a specified geographic area under specified
circumstances, and are used as one of several factors in designing legally
enforceable pollutant emission standards (USHEW 1969).
The air quality criteria documents were written pursuant to authority
delegated to the Commissioner of the National A1r Pollution Control Admin-
istration in accordance with Section 107 bl of the Clean A1r Act of 1967
(42 U.S.C. 1857 - 2bl). The Clean Air Act of 1970 set forth regulations
prescribing national primary and secondary ambient air quality standards
as Part 410 of 42 CFR. The Act, as amended, required promulgation of
national standards for six air pollutants on the basis of available data
set forth 1n air quality criteria documents. The Administrator of the
then newly created Environmental Protection Agency was required to make
judgements as to the proper Interpretation of presently available data
as described in the criteria documents and to establish national primary
standards which would include an adequate margin of safety to protect human
health.
The authors of the criteria documents relied upon the best available
knowledge of the effects of air pollutants on human health. They used
research data which included epldemiological studies, observed industrial
responses to pollutant exposures, observed human responses in a laboratory
or chamber environment, and animal studies. The criteria documents did
not differentiate between an exposure to air pollutants within or outside
buildings. As noted, the research studies described in the criteria docu-
ments were conducted and observed in both indoor and outdoor environments.
Studies of workers described in the criteria documents report the
results of observing human responses to isolated chemical exposures emit-
ted in industrial situations. The result of such observations may not be
wholly relevant to human health effects in ambient or indoor air pollution
conditions. Exposures of industrial workers are often at a high level
of concentration, and sometimes over a long period of time, but seldom
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is the exposure documented in terms of the concentration of the pol-
lutant or the time period of exposure. Further, the exposures and
the resulting health effects are experienced by active adults whose
general health is sufficiently good to permit them to work 1n these
environments. It cannot be concluded that the health responses of
Industrial workers can be used to set health criteria for the air pollu-
tant exposure of a general population in indoor, nonworkplace environ-
ments, which includes the elderly, Infirm and young children. An addi-
tional factor is that those individuals who are sensitive to pollutant
exposures, such as those with cardiorespiratory disease are either not
selected for employment or are lost to employment. Hence these indoor
studies included in the criteria documents which are concerned with
occupational exposures to pollutants were seldom useful in defining the
effects of exposures to low concentrations of a pollutant by groups of
sensitive individuals.
Studies conducted in the laboratory take place in an artifically con-
structed indoor environment, where volunteers are exposed to known concen-
trations of a selected pollutant for a specific period of time. Such studies
are not ususally described as indoor studies in the criteria documents. The
differentiation between the location of air pollution exposure as indoor or
outdoor is made here because the existing standards for air pollution con-
centrations apply only to the workplaces and outdoor environments. Further
discussion of the standards for indoor and outdoor environments follows in
Section 3.
Threshold Limit Values (TLVs) for chemical contaminants refer to
airborne concentrations of substances and represent conditions under
which it is believed that nearly all workers may be repeatedly exposed to
day after day without adverse effects (ACGIH 1975). Criteria for the
TLVs are published in the Documentation of the Threshold Limit Values for
Substances in Workroom Air and are based upon Industrial studies, human
and animal chamber studies, and combinations of all three (ACGIH 1971,
1975).
The recommendations for TLVs included in the documentation includes
a margin of safety, although It is not quantified. It is important to
note, however, that the definition for Threshold Limit Values applies to
"nearly all workers" and therefore may exclude individuals who may be
sensitive to particular chemical contaminant exposures. Additionally
because the TLVs are expressed as seven or eight hour time-weighted
averages, based in part on observations of workers in industrial settings
where the average workday 1s seven or eight hours, exposures to given
chemical contaminants are not continuous. There is a long recovery time,
16 hours or more, in each typical day. Nonworkplace indoor exposures,
on the other hand, may be continuous without adequate recovery, particu-
larly among sensitive subpopulations of the very young, elderly, and
Infirm who may be exposed almost continually to indoor air pollution in
homes and Institutions.
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Though the TLVs as promulgated by the American Conference of Govern-
mental Industrial Hygienists did not have the force of law, the TLVs for
airborne contaminants for 1970 were incorporated almost without exception
into law on May 29, 1971 (Federal Register 37(202). 1971). The TLVs thus
became criteria for standards enforced under Federal regulations by the
Occupational Safety and Health Administration (OSHA). Also incorporated
into law on that day were the American National Standards published by the
American National Standards Institute under their Z37 series of standards
which included 18 chemical contaminants (ANSI 1976).
The United States Department of Health, Education, and Welfare's
National Institute of Occupational Safety and Health (NIOSH) was given the
authority to publish criteria and recommend occupational health standards
under the Occupational Safety and Health Act of 1970. Since 1970, some
56 criteria documents for pollutants have been published. OSHA uses such.'
criteria documents as a basis for promulgating new standards for chemical
contaminants or for revising those which have been previously published.
Again, however, the sources of studies used for the OSHA standards, and the
uses for which the standards are intended, are not that of the general
public.
Objectives in setting nonworkplace indoor air quality standards
will be similar to those of the National Ambient A1r Quality Standards:
to protect the public health with an adequate margin of safety. Criteria
for Indoor air quality standards should therefore rely on studies similar
to those in the air quality criteria documents: epidemiological studies
for the general public including studies of susceptible subpopulations,
Industrial studies, human and animal chamber studies, and other informa-
tion which defines the lowest thresholds for adverse health effects. The
special conditions of nonworkplace indoor environments, with respect to
populations, pollutants and exposures, must receive special consideration.
Criteria for recommended occupational standards, including the
documentation of the Threshold Limit Values for substances in workroom
air, are of use in providing information concerning toxlcological effects
to healthy individuals from pcllutant exposures, especially exposure to
pollutants for which there 1s no other Information concerning their
effects on the general population. But, as has been noted, the existing
observational data on short-term, Indoor concentrations of a limited
number of air pollutants, and probable resulting exposures, are Inade-
quate as a basis for definitive conclusions about the magnitude of the
health problems which may exist as a result of Indoor air pollution.
Comparisons of the limited, available indoor air quality data with results
of research into the health effects of ambient pollutants, and with
research into health effects of air pollution in some industrial workplace
contexts, have confirmed that Indoor air pollution 1n nonworkplace envi-
ronments does reach levels at which human exposures, resulting in adverse
health impacts, may occur. The evidence for this, as reported in the
scientific literature, is discussed at length, for major pollutants, 1n
Appendix A of this report.
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The scope of the health effects section of GEOMET's earlier report
under Contract 68-02-2294, The Status of Indoor A1r Pollution Research -
1976, was defined at its outset as a comprehensive review of the state-
of-the-art, described in published literature and unpublished ongoing
research, the knowledge of the health effects of those indoor air pollu-
tants for which studies of Indoor concentrations and behavior .have been
made. Subgroups of populations which have demonstrated increased sensi-
tivity to those pollutants, and evidence for additive, synergistic or
antagonistic properties of the pollutants with respect to health status,
were described. The extent of available information was evaluated, and
areas of current research and research gaps identified. Findings from
the review were incorporated into an overall appraisal of the potential
impact of indoor air pollution, with a relative ranking of the hazards
from different indoor air pollutants.
Section 8.0 of the earlier report dealt extensively with the health
effects of indoor air pollutants as reported in past and current research
through October 1976. The health effects section, with minor modifica-
tions, has been reproduced as Appendix A of this report. Essentially, it
provides a set of preliminary criteria for recommended indoor air standards.
The review appearing in Appendix A is presented under the following head-
ings:
• Sulfur oxides
0 Carbon monoxide
• Carbon dioxide
o Nitrogen oxides
• Photochemical oxidants
e Organic pollutants
• Particulates
• A1r pollution and lung cancer
« Susceptibility of population subgroups
• Interactive pollutant effects.
The reader 1s cautioned that few 1f any of the indoor air pollution
health effects reported in the literature surveyed in Appendix A are
based upon thorough epidem1olog1cal studies which have addressed the
problem of Identifying human health effects of indoor air pollutants in
typical, residential or Institutional indoor environments. The reported
health effects are generally to be ascribed to Indoor air pollution only
by inference from studies made either in other contexts or in contexts
in which the role played by nonworkplace indoor air pollution was not
clearly segregated from the effects of outdoor or workplace air pollution.
Further ep1demiolog1cal studies specifically addressing the nonwork-
place indoor air pollution problem, leading to health criteria specifically
applicable to nonworkplace Indoor air pollution, are now being conducted
or planned by the Environmental Protection Agency.
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Section 3
INDOOR AIR QUALITY STANDARDS
INTRODUCTION
Although "criteria" may be considered standards (i.e., the words are
synonyms), the meaning of "criteria" in air pollution control terminology
has evolved to become the foundation or basis for standards. Therefore, a
description of the health effects of air pollution may form criteria for an
air quality standard. To the extent that the standard must be concerned with
other air pollution effects, e.g., upon materials or upon visibility, studies
of these effects are also required. For indoor air pollution in residential
contexts, however, we are concerned almost entirely with potential adverse
impacts upon human health.
The scope of the present survey includes a review of "indoor air quality
health criteria." Because of the size of the information assembled on the
health effects of various air pollutants, we have included this material
in Appendix A, "Health Criteria for Indoor Air Pollution."
Air quality standards must be understandable, measurable, enforceable
and fair. Indoor air pollution standards should prescribe maximum allowable
limits which are below those levels at which human health effects have been
observed by an adequate margin of safety, giving due consideration to the
exposures and dosages likely in indoor residential contexts. Jackson and
Newill (1974) point out the difficulties in selecting adequate margins of
safety and the philosophical viewpoints associated with determining the
required levels of environmental protection.
One viewpoint discussed is the zero tolerance, or no risk approach,
which states that no health risk is acceptable when dealing with any toxic
substance in the environment. The U.S. Congress has adopted this particular
approach for dealing with carcinogenic materials in foods and drugs under the
Delaney Clause.
Another approach used in applying safety margins 1s the threshold or
no-permlsslble-adverse-health-effects approach. This approach was used as
the basis for the Clean A1r Act to establish primary ambient air quality
standards which set exposure limits at levels where no adverse health effects
would be measured.
A final approach used to establish safety margins is the socially
acceptable risk approach. This approach has been used to determine some
industrial exposure standards and most recently was the basis for the U.S.
Environmental Protection Agency's proposed benzidine effluent guideline.
This approach poses many difficult questions concerning the statistical/
mathematical point of view as well as the moral/ethical considerations.
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One method of obtaining data to develop adequate safety margins is
through toxicological studies which use animals and tissue cultures to
demonstrate biological responses to various pollutant or chemical exposures.
An intrinsic problem with such studies is that the effects measured from the
various levels of pollutant exposures usually are evaluated only in healthy
animals. Jackson and Newill (1974) notes that the problem of extrapolating
data from laboratory animal studies to the human subject is particularly
difficult, especially when attempting to use this data to estimate a "threshold"
level for adverse human response. The U.S. Department of Health, Education,
and Welfare through the Food and Drug Administration (FDA) used this technique
to develop safety margins for food additives. Regulations issued under the
Federal Food, Drug, and Cosmetic Act as Part 121, Food and Drug Standards, of
Title 21 of the Code of Federal Regulations (1969) in section .121.5, "Safety
Factors to be Considered," states that
"...the following safety factors will be applied in
determining whether the proposed use of a food additive
will be safe: Except where evidence is submitted which
justifies use of a different safety factor, a safety
factor in applying animal experimentation data to man
of 100 to 1, will be used; that is, a food additive for
use by man will not be granted a tolerance that will
exceed 1/100th of the maximum amount demonstrated to be
without harm to experimental animals."
The FDA used a 1:10 safety margin in food and drug testing to determine
safe doses for humans from the lowest dose for which a significant response
is observed in mice or rats. Another 1:10 safety margin is then added to
protect sensitive individuals. This method has been suggested for determining
safe exposures to air contaminant concentrations and in fact has been used in
part in the TLV documentation. That is, once a dose-response curve for mice
and rats has been determined, a safety margin one-tenth that of the lowest
threshold for a dose-response on humans is incorporated. This 1:10 safety
margin is used for healthy individuals in applications such as workroom air,
for spacecraft and for submarines. Another 1:10 safety margin would be
incorporated to ensure the safety of sensitive individuals for applications
such as the outside air or nonworkplace indoor air.
Both the Air Quality Criteria documents and the Documentation of the
Threshold Limit Values for Substances in Workroom Air include observations
not only from animal studies but from epidemiological investigations of air
pollution health effects to determine the dose-response of humans. Epidemiol-
ogy or population studies provide information on the effects of pollution
exposure on populations in a real-world situation and eliminates the problems
of extrapolating results from one species to another. Another advantage is
that studies can be performed on the most vulnerable population groups, not
just the healthy individuals. If such studies include observations of sub-
populations of workers, usually classified as healthy populations, a rule of
of thumb might be to include a 1:10 safety margin from the lowest observed dose-
response to protect sensitive individuals. If, however, the subpopulations
studied are sensitive individuals, less of a safety margin may be required.
-11-
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Jackson and Newill (1974) point out that there are certain key limi-
tations with epidemiclogical studies. The quantification of the exposure
profile for each individual 1s very difficult to determine. Often one cannot
obtain any dose-response curves from this Information. These studies deal
with a multiplicity of covarlates, making isolation of a single variable
virtually impossible.
The National Ambient Air Quality Standards, developed from the Air
Quality Criteria documents, has incorporated Information obtained from
epldemiological studies. Since the criteria and epidemiological studies
used to establish the human dose-response curve observed sensitive Indi-
viduals, the margins of safety used in developing the NAAQS for CO is less
than 1:10. A 1:5.5 TLV margin of safety has been used based on the effects
of CO exposure on susceptible individuals (e.g., individuals with anemia,
cardiovascular disease and abnormal metabolic states).
Additionally, however, 1t is important to recognize that the ACGIH and
NIOSH documentation is not solely based upon "animal studies plus a safety
margin." Since epidemiological Information and observations of individual
exposures are also used as documentation, many of the maximum allowable
concentration limits should adequately protect all "individuals." A Threshold
Limit Value (TLV) divided by 10 could in many cases be "overkill," especially
for TLVs that already incorporate substantial safety margins. Epstein (1974)
discussed the adequacy of safety margins by contrasting general environmental
standards to occupational standards. He notes the3current occupational
standards on lead developed by the ACGIH, 150 ug/m , which are considered
safe levels for healthy workers, are in contrast with proposed general
environmental standards in California which are 100-fold lower.
The air quality standards must be understandable, enforceable, measur-
able and fair. Architects and engineers who design the heating and ventilat-
ing systems must understand the principles involved, and requirements imposed
by these standards. In addition, the building inspectors who are charged
with enforcing the standard must see that available instruments can measure
the required concentrations, and that the state-of-the-art of the air pollu-
tion control technology provides the vehicle for obtaining the air quality
standards. Finally the air quality standards must be fair; energy considera-
tions and economic factors must also be considered along with the health
parameters which constitute the principal input in the generation of these
standards.
To better evaluate the utility and veracity of these standards, it is
important to place their formulation into historical context.
BACKGROUND FOR STANDARD SETTING
One of the early theories on ventilation was that put forth by Max von
Pettenkofer in 1863 (Brauer and Kuehner 1969). Based on the premise that
certain toxic morbific substances excreted by the body produce a vitiated
atmosphere, he used the concentration of carbon dioxide present in the
atmosphere as an index of the amount of anthropotoxin present. Since the
-12-
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average individual produced 0.6 cubic feet of carbon dioxide per hour in
expired breath, and selecting twice the normal carbon dioxide in the air as
the upper limit where 0.3 percent is the normal amount, the ventilation
required is calculated directly,
(0.0006°160.003)60 = 30 cfm per Person'
By 1925, 25 states had ventilation rates for schools written into their
laws based upon this theory, which was accepted and supported by the American
Society of Heating and Ventilating Engineers when they were founded in
1894 (Brauer and Kuehner 1969). Thus the first minimum acceptable indoor air
quality standard was for carbon dioxide at 0.06 percent or 600 ppm which
was hence the basis for the most widely accepted design level air quality
standard of 30 cfm per person.
At about this same time, physiologists were studying the effects
of close and crowded conditions on man and proved that the discomfort and
faintness which occurred under such circumstances were due to the failure
of the body to lose sufficient heat and not to any chemical changes in
the air (Baetjer 1965). The work by LeBlanc, Hermans, Flugge and others
(Brauer and Kuehner 1969), showed that undesirable effects of air in occupied
rooms and the sensation of uncomfortable conditions had a physical basis due
to temperature and humidity excesses (i.e., reduced temperature and humidity
or increased air velocity in unventilated rooms). Carbon dioxide was thereby
shown to be not harmful in the concentrations normally encountered in expired
air (Rush 1926).
Requirements for thermal comfort became fairly well established by
Houghton and Yaglou (1923) concurrent with the development of more reli-
able and automatic mechanical heating systems. During this period it was
found that the air quality of the air in occupied spaces was not satisfactory
to occupants because odors were still present. In 1935 Lehmberg et al.
suggested that the intensity of body odor in occupied rooms could be taken as
a satisfactory index of minimum ventilation requirements. Later in 1935
Houghton et al. showed that when the air change drops below 11 cfm per
person, individuals entering a classroom in search of odors often found the
occupants' odor noticeable. In studies published in 1936 by Yaglou et al.
and in 1937 by Yaglou and Witheridge, it was noticed that perceived room odor
level was not only a function of ventilation rate, body surface area and
whether entering a room or being an occupant, but was also related to the
time since the last bath and the cleanliness of clothing (sodoeconomic
status) as well as excessive room temperatures, average volume occupied by
individuals in a room and air distribution in the room (Brauer and Kuehner
1969).
-13-
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The American Standards Association (ASA) developed ventilation standards
as part of ASA Standard A53.1, "Light and Ventilation." This standard, dated
May 23, 1946, was based on 100 percent outdoor air with adequate temperature
control and particulate filtration. With "adequate particulate filtration"
unquantified, these standards were primarily design-level indoor air quality
standards and will be discussed in Section 4.
The Committee on Atmospheric Comfort of the American Public Health
Association (Yaglou et al. 1950) recommended not less than 15 cubic feet
per minute per person for persons doing light work and not less than 20
cubic feet per minute for persons engaged in heavy work. This air supply
probably will be effective in removing tobacco smoke (Baetjer 1965).
Yaglou (1956) investigated the ventilation rates required to reduce
cigarette smoke to an acceptable level. Data from Yaglou's tests were used
to define recommended outside air supplies of 35 to 40 cfm per smoker to
remove objectionable odors of fresh cigarette smoke.
In 1965 the American Society of Heating, Refrigerating and Air Condition-
ing Engineers, Inc. (ASHRAE) was invited to participate in the revision and
updating of A53.1, "Light and Ventilation." The American Standards Association
invited the Illuminating Engineers Society to revise and update those portions
of the standard dealing with light while an ASHRAE Project Committee was
assigned responsibility for the Mechanical Ventilation Section. When ASA
became reorganized (now American National Standards Institute (ANSI)) and its
procedures were changed, the A53 committee became inactive. The ASHRAE
Standards Committee advised the Project Committee (62P) to continue its
efforts and develop an ASHRAE Standard. The 62P Committee, after nine
drafts and an extensive review and comparison of existing ventilation codes,
published the standard in late 1973, although the maximum allowable concentra-
tion specifications were made in 1969.
National Ambient Air Quality Standards which apply to that portion
of the atmosphere, exclusive of buildings, to which the general public
has access were published in the Federal Register on April 30, 1971. States
were given the task of adopting and submitting implementation plans for
meeting levels of air quality at least as stringent as these standards (no
later than January 30, 1972) as well as deadlines for doing so (usually July
1975 or July 1977). These standards, therefore, have behind them the force
of law and are enforced by the respective states. The Environmental Protection
Agency (EPA) was empowered with the right to enforce the National Ambient
Air Quality Standards should the states for any reason fail to comply with
the NAAQS by the deadlines.
The Occupational Safety and Health Administration (OSHA) of the U.S.
Department of Labor has also published air quality standards in the Federal
Register (1971). These standards apply to workroom air in the sense that
they were promulgated to protect the health of "employees." The standards
also protect the employees working outdoors but do not apply to the general
public.
-14-
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Therefore, if EPA standards apply to the outdoor environment and OSHA
standards to the protection of "workroom" air, who then would be respon-
sible for the air quality of the "nonworkplace" indoor environment? It
is the responsibility of the engineers and architects who are designing the
Cheating and ventilation systems and the appropriate authorities who approve
the building permits to consider the indoor air quality. The standards to
which the engineers, designers, and authorities must comply are those of good
engineering practice only. However, some of the model codes, such as the
National Building Code (1976), have adopted from ASHRAE Standard 62-73 the
maximum allowable contaminant concentrations for intake air used in the
ventilation systems.
Designers and builders must comply with the building codes in force in
the location where they desire to construct. Building permits are reviewed by
local authorities for compliance with the many regulations written to insure
the safety and health of the occupants. These regulations attempt to cover
all building elements including construction materials, electrical systems,
plumbing systems, stairways, and of course the ventilation system. Of primary
concern and a predominant theme in building codes is the safety of occupants
from fire.
Since building codes are written and enforced by state and local authorities
a wide variation exists in their uniformity. Agencies in charge of regulating
local building codes will often only adopt portions from several of the basic
model building codes or develop one of their own which will serve their
present requirements. Both the National Bureau of Standards and indepen-
dent trade institutions such as the American Society for Testing of Materials
(ASTM) have provided universal standards for construction materials. Although
electrical codes vary somewhat among state and municipal building codes, the
National Electrical Code published by the National Fire Protection Association,
is incorporated in its entirety in most building codes or electrical codes.
Ventilation codes usually do not specify maximum allowable concentration
limits for ventilation or supply air. We are aware of only those specified in
ASHRAE 62-73 which by itself is not a code with the .force of law. Most
ventilation codes specify design-level indoor air quality standards and are
discussed in Section 4 in more depth.
Nonworkroom indoor air quality is apparently not regulated by any
of the Federal Government's departments or agencies with the exception of
design standards for mechanical ventilation under the Hill-Burton Act for
the construction of hospitals which are to be funded by the U.S. Department
of Health, Education, and Welfare. One of the problems involved in the
establishment of nonworkplace indoor air quality standards is the identi-
fication of the responsible agency within the Federal Government.
This is not to say that there are no indoor air quality standards
in the United States with the force of law which protect the public from
-15-
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exposures to contaminants in schools, public buildings, apartments or other
nonworkplace indoor environments. There are simply no Federal standards
for such places and no state standards enforced by the state health or
labor departments or associated authorities of which we are aware. States
and municipalities which do have indoor air quality standards with the force
of law for these spaces are those jurisdictions which have incorporated
the standards suggested by the 62P Committee of the American Society of
Heating, Refrigerating and Air Conditioning Engineers in late 1973. These
standards, or guidelines, (ASHRAE Standard 62-73, Standards for Natural and
Mechanical Ventilation) have only most recently been incorporated into several
of the model building codes used by the states and municipalities to devise
their own building codes and/or to update those portions of the building codes
which require revision.
In this section of our report we shall discuss the ambient air quality
standards, the air quality standards which apply to the workplace, and those
air quality standards which are presently in existence or proposed which
apply to the nonworkplace indoor spaces.
AMBIENT AIR QUALITY STANDARDS
It is important to discuss the ambient air quality standards since
those indoor air quality standards presently in existence are in part based
on at least portions of these standards. Additionally, it is important
to place the establishment of these standards into historical perspective
and compare them with indoor standards which apply to the workplace and
those that apply to spaces other than the workplace.
The National Ambient Air Quality Standards were proposed for adoption as
National Primary and Secondary Ambient Air Quality Standards, of Title 42 of
the Code of Federal Regulations. Part 410 (42 CFR) which deals with public
health^The Standards were proposed on January 30, 1971 (36 F.R. 1502) and
March 26, 1971 (36 F.R. 5867). Part 410 of Title 42 was added to Chapter IV,
"Environmental Protection Agency" (which was less than one year old at the
time). After extensive review and public comment a new Part 410 was added to
Chapter IV, Title 42, Code of Federal Regulations on April 30, 1971.
Although scientific knowledge of the health and welfare hazards of the
pollutants was recognized to be imperfect, the Administrator of the EPA was
required to assemble and appraise the best information available, as set
forth in the air quality criteria documents, and to establish national
primary standards which include an adequate margin of safety to protect the
public health. Thus, in addition to the standards, the studies and reports
described and summarized in the air quality criteria documents were available
for public criticism. For instance, the proposed standard for photochemical
oxidants for one hour was 125 yg/m based upon evidence of the impairment
of athletic performance reported by Wayne et al. (1967) when ozone levels were
-16-
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in range of 0.15 and 0.3 ppm. Serious questions were raised about the validity
of these data and particularly on the line of regression drawn to show the
lower threshold for adverse effects. When the new Part 410 of 42 CFR was
promulgated, an hourly photochemical oxidant standard higher than that pre-
viously proposed, was established based on the Schoettlin and Landau (1961)
study published in the Air Quality Criteria for Photochemical Oxidants (USHEW
1970). Since this study demonstrated.,adverse health effects associated with
one-hour averages of ozone of 200 ug/m , the new standard was promulgated
at 160 ug/m one-hour maximum, providing a 20 percent safety margin. Table 1
lists the National Primary and Secondary Ambient Air Quality Standards and
the reference methods for sampling and analyzing the respective pollutants.
WORKPLACE AIR QUALITY STANDARDS
Air quality standards for workroom air in the United States were first
promulgated by the U.S. Labor Department's Occupational Safety and Health
Administration (OSHA) May 29, 1971 under paragraph 1910.93 "Air Contaminants"
(gases, vapors, fumes, dust and mists) of Subpart G - "Occupational Health and
Environmental Control" (Federal Register 1971). OSHA had been given the
authority to publish and enforce occupational air quality standards by the
Williams-Steiger Occupational Safety Act of 1970 (84 Stat. of Title 29 -
"Labor, Code of Federal Regulations ).
The regulations specified that:
"Exposures by inhalation, ingestion, skin absorption, or
contact to any material or substance (1) at a concentration
above those specified in the 'Threshold Limit Values of
Airborne Contaminants for 1970' of the American Conference
of Governmental Industrial Hygienists, listed in Table G-l,
except for the American National Standards listed in
Table G-2 of this Section and except for values of mineral
dusts listed in Table G-3 of this Section, and (2) concentra-
tions above those specified in Tables G-l, G-2, and G-3 of
this Section, shall be avoided, or protective equipment
shall be provided and used."
On June 27, 1974 and again on May 28, 1975 the Section 1910.43 "Air
Contaminants" was changed to 1910.1000 and placed under subpart Z. This
new designation was made so that subsequent contaminants could be added to
the list in a more logical numerical scheme. Appendix B of this report
includes Tables Z-l, Z-2, and Z-3 of subpart Z, as published on July 1,
1976. Table Z-l included TLVs for airborne contaminants published by ACGIH
in 1970. Table Z-2 included 8-hour time weighted average "limits" for 18
contaminants and acceptable ceiling concentrations for 3 contaminants
-17-
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TABLE 1. NATIONAL AMBIENT AIR QUALITY STANDARDS
Pollutant
S°2
Particulale
Matter
Carbon
Monoxide
Photochemical
Ox id ants
Hydrocarbons
(measured and
corrected for
methane)
NO
Averaging
Time
Annual
Arithmetic
Mean
24-hour maxtt
3 -hour maxtf
Annual
Geometric
Mean
24-hour max ft
8-hour max tt
1-hour max tt
1 -hour max tt
3-hour maxtT
(6-9 AM)
Annual
Arithmetic
Mean
Primary
Standard*
3
80 p g/m'
(0.03 ppm)
365)ig/nf
(0.14 ppm)
3
75pg/m
^
260 p g/m
10, 000 p g/m
(9 ppm)
^
40, 000 p g/m
(35 ppm)
160|i g/m
(0.08 ppm)
3
160p g/m
(0.24 ppm)
3
lOOpg/m
Secondary
Standard**
3
(0.02 ppm)
2(>0p g/m
(0. 10 ppm)
J, 300 p g/m
(0.50 ppm)
3
60 p g/m
3
150yg/m
(Same as Prim:iry)
(Same as Primary)
(Same as Primary)
(Same as Primary)
Reference
Method***
Pararosnniline .
Hi-Volume
Sampler
Non-Dispensive
Infrared
Spectrometry
(NDIR)
Chemi lumines-
cence
Flame lonization
Jacobs-Hocheiser
* With an adequate margin of safety, to protect public health
** To protect public welfare
**•* Reference method: The reference method is the method of sampling and analyzing for an air
pollutant as described in the Appendix of 36 FR 8187. An equivalent method
is approved if it can be demonstrated to have a consistent relationship to the
reference method.
t Challenged and no longer a standard
ft Not to be exceeded more than once a year
-18-
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published by the American National Standards Institute, and Table Z-3, also
published by ACGIH, comprised limits for mineral dusts such as quartz and
coal dust. Previous to their inclusion within these tables, both the TLV
and the American National Standards were described as National Voluntary
Consensus Standards. They were published by ACGIH and ANSI respectively,
without the force of law and therefore might be defined as guidelines.
Threshold Limit Values are reviewed yearly but those published in 1970
(Table Z-l) were used by OSHA. The National Institute of Occupational Safety
and Health Administration was given authority to publish criteria for recom-
mended OSHA standards by the Williams-Steiger Occupational Safety and Health
Act. They may therefore recommend revision of any of the substances listed
in the three tables or propose standards for OSHA regulation for substances
not so included. Although ACGIH reviews its TLV on an annual basis and may
revise or propose additions or changes, they only become an established
Federal standard if recommended by NIOSH and promulgated by OSHA. NIOSH has
published criteria for a recommended standard for some 56 substances since
1970. The most recent revision was published in Title 29 CFR Part 1910.1000
as of July 1, 1976 by OSHA.
A discussion of the utility and veracity of these NIOSH standards
as they apply to nonworkplace indoor air quality standards follows in Section
4. It is important to note here, however, that Threshold Limit Values for
chemical contaminants refer to airborne concentrations of substances and
represent conditions under which it is believed that nearly all workers may
be repeatedly exposed day after day without adverse effects. Although not
quantified as such, a safety margin is incorporated into the Threshold Limit
Value for any of the substances to insure no adverse effects. Though TLVs
are, in several cases, an order of magnitude higher than Ambient Air Quality
Standards, there is no information that demonstrates that the health of the
workers exposed to these higher concentrations is in danger. Part of the
discrepancy lies in the criteria used for each standard, a question which is
discussed in Appendix A. For instance, the Ambient Air Quality Standards for
both S02 and particulate matter were based upon epidemiological studies
where persons were exposed to relatively high concentrations of both pollutants.
The TLV for S02 is based on evidence of adverse effects to SO^ alone.
There is no TLV for particulate matter as such. Further, the Ambient Air
Quality Standards for hydrocarbons were promulgated as a guide for states to
use in devising implementation plans to achieve the oxldant standard. The
3-hour concentration (6-9 AM) maximum of 160 ug/m was used so as to
coincide with the one-hour standard for oxldants of 160 wg/m based upon
evidence that there is a 1 to 1 ratio between hydrocarbon concentrations and
subsequent formation of the secondary pollutant, oxldants. Concentrations of
nonmethane hydrocarbons at this level were not shown to directly affect the
public health in the air quality criteria document for hydrocarbons (USHEW
1970). There is no Threshold Limit Value for hydrocarbons since individual
hydrocarbons are assigned TLVs.
-19-
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AIR QUALITY STANDARDS FOR A TOTALLY ENCLOSED ENVIRONMENT - THE SUBMARINE
ATMOSPHERE
Submarine air has been studied by scientists at the Naval Research
Laboratory and other Naval laboratories. As indicated in the Navy publica-
tion NAVSEA 0938-011-4010, the submarine atmosphere differs from the ambient
atmosphere in two major aspects: (1) it possesses a greater variability
in oxygen and carbon dioxide content, and (2) it displays a wide range of
organic and inorganic contaminants including gases, vapors and aerosols.
Almost all air pollutants have some effect on the submarine personnel,
the extent of the adverse effect depends on three factors:
• Length of exposure
• Concentration
• Chemical considerations such as solubility in body
fluids and tissue proliferation.
The following text and two tables are quoted from the Navy publication
NAVSEA 0938-011-4010:
"3.1.2 (U) Atmosphere Constituents Limits. Criteria have been developed
for establishing safe limits of contaminants. The limits shown in Table 3-6
and Table 3-7 represent the lowest value of the concentrations:
a. Required to avoid explosive or combustible mixtures.
b. Required to avoid toxicological hazard, including
those of decomposition products formed by passage of the
contaminant through the CO-HL burner or other equipment.
c. Required to minimize corrosion of equipment and
machinery.
d. Obtainable with current air purification equipment and
proper control over contamination sources.
In regard to the toxicological limits (Table 3-6 and Table
3-7), it should be understood that they do not represent fine
lines between safe and unsafe conditions. They represent the
best available information regarding the maximum concentrations
to which personnel may be exposed for the period indicated
without adverse effects. Thus, they are the limits within which
the body is able to compensate for small changes by healing or
is able to engage in a process of detoxification without signi-
ficant effect. To the maximum extent possible, it is incumbent
upon operating personnel to decrease contaminant concentration
levels by proper housekeeping, equipment maintenance, and control
over materials brought onboard. It is probable that unusual heat
or a high level of physical activity will contribute to reduced
-20-
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" Table 3-6. (U) Limits and Measuring
Methods for Atmospheric Constituents in Nuclear Submarines
(Limits are in PPM Unless Otherwise. Noted.) (U)
Compound
1. Acetone (NOTE .1)
2. Ammonia
3. Benzene
A. C;;rlu>n Dioxide
(NOTES 2, 3)
5. Carbon Monoxide
6. Chlorine
7. Hydrocarbons
(n) Total Aromatics
(Less Benzene)
(b) Total Aliphatics
(Less Methane)
8. Hydrogen
(NOTE /»)
9. Hydrogen Chloride
(Hydrochloric Acid)
LO. Methane (NOTE 5)
11. Methyl Chloroform
(1,1,1 Trichloro-
ethane) Note 6
12. Monoethanolamine
(MFA)
90-Day
Limit
300
25
1.0
3
3 mg/m'
6.1 mm Hg
0.8%
6.1 Torr
15
11.5 Milli-
torr
0.1
10 mg/m
3
60 mg/m
10,000
n
7.6 Torr
1.0
13,000
2.5
0.5
1
24-Hour
Limit
2000
50 :.
100
: 3
300 mg/m
7.6 mm Hg
1%
I
7.6 Torr
200
152.6
i
Millitorr
1.0
*
*
10,000
1%
7.6 Torr
4.0
13,000
10
3.0
1-Hour
Emergency
Limit
6000
400
•t:
v'c
19 inm Hg
?. 1/2%
19 Torr
200
152.6
Millitorr
3.0
*
*
10,000
1%
7.6 Torr
10
13,000
25
50
Measuring
Method
T
T
THA
C, P
C, T
T
THA
C
T
THA
THA
T
-21-
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Table 3-6. (U) Limits and Tfoasuririp,
Jlethods for Atmospho:ric Constituents in Nuclear Submarines
(Limits are in PPM Un.lnss Otherwise Noted.) (Continued) (U)
13.
14.
15.
16.
17.
18.
19.
20.
Compound
Oxygen (NOTE 7)
Ozone (NOTE 8)
Refrigerant R-ll
(Trichloromono Fluoro-
Ethane)
Refrigerant R-12
(Dichlorotetra Fluoro-
Methans) (NOTE 6)
Refrigerant R-114
(Dichlorotetra Fluoro-
Kethane) (NOTE 6)
Sulfur Dioxide
Toluene
Vinylidena Chloride
90-Day
Limit
140-160
inm Hg
not ex-
ceeding
2 IX by
volume
140-160
Torr
0.02
5
3.8 Milli-
torr
200
152 Milli-
torr
200
152 Milli-
torr
1.0
50
2.0
24-Hour
Limit
140-160
mm Hg
not ex-
ceeding
21% by
volume
140-160
Torr
0.1
20
15.2 Milli-
torr
1000
760 Milli-
torr
1000
760 Milli-
torr
5.0
100
10
1-Hour
Emergency
Limit
140-220
mm Hg
not ex-
ceeding
30% by
volume
140-160
Torr
1.0
50
38 Milli-
torr
2000
1520
Millitorr
2000
1520
Millitorr
10
200
25
Me a.
M<
C, P
T
THA, C
THA, C
THA, C
T
X
THA
Method
T
P
*L:lmit hiis not baen established
}CEY: THA - Tof.nl Hydrocarbon Analyzer (See 6.8)
C - Central System (See 6.2-6.7)
- Detector Tubes (See 6.9.2)
- Portable Analytical Equipment (See 6.9)
Values iire set at 1/4 of the explosive limit of 2.55.
The 90-day limit for carbon dioxide is an average reading. Levels are
not to exceed a maximum of 1 percent, tactical situation permitting.
The 90-day limit for Trident and later class submarines is 0.5 percent
maximum.
NOTE 1:
NOTE 2:
DOTE 3:
NOTE 4: During battery charges, the hydrogen limit shown above may be exceeded
as discussed in Chapter 9623, NAVSHIPS Technical Manual 0901-623-0003.
-22-
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"Table 3-7. (U) Limits for Atmospheric
Constituents in Nuclear :Submarines Without Measuring Methods
(Limits are in PPM Unless Otherwise Noted.)
Compound
1. Acetylene (Note 1)
2. Acrolein
3. Arsine
4. Ethanol
5. Ethylcne (Note 2)
6. Formaldehyde
7. Hydrogen Fluoride
(Hydrofluoric Acid)
S. Isopropanol
9. Mercury
10. ' Methanol
11. Nitrogen Dioxide
12. Stibine
90-Day
Limit
6000
:o.i
0.01
100
6000
•0.5
0.1
50
3
0.01 mg/m
10
0.5
0.01
24-Hour
Limit
6000
0.1
.1
500
6000
1
1.0
200
. 20 mg/m
200
1.0
0.05
1-Hour
Emergency Limit
6000
0.2
1.0
1000
6000
3
8
400
*
1000
10
1.0
*Limit has not been established.
NOTE 1: Values are set at approximately 1/4 lower explosive limit of 2-1 /
percent. This compound is explosive.
NOTE 2: Values are set at 1/4 of the lower explosive limit of 2.75."
-23-
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human tolerance. Further, the levels are determined individually,
and effects of combinations of contaminants (synergistic effects),
if any, are not accounted for."
AN INDOOR AIR QUALITY STANDARD - ASHRAE STANDARD 62-73
The purpose and scope of ASHRAE Standard 62-73 is to define "...venti-
lation requirements for spaces intended for human occupancy and specify
minimum and recommended ventilation air quantities for the preservation
of the occupant's health, safety and well being." In Section 2.0 of the
Standard, "Definitions," ventilation air is defined as "...that portion of
supply air which comes from outside (outdoors) plus any recirculated air that
has been treated to maintain the desired quality of air within the designated
space." Ventilation, on the other hand, is "...the process of supplying
ventilation air to any space by natural or mechanical means." In Section
3.1, acceptable ventilation air quality is numerically quantified with a
table of maximum allowable contaminant concentration (limits). Additionally,
the Standard states in Section 3.3 that "...air shall be considered unaccept-
able for ventilation use 1n accordance with this standard if it contains any
contaminant in a concentration greater than one-tenth the Threshold Limit
Value (TLV) currently accepted by the American Conference of Governmental
Industrial Hygienists." Table 2, taken from ASHRAE Standard 62-73, is shown
following with ASHRAE's diagram of definitions (Figure 1).
Section 4.0 of ASHRAE Standard 62-73 describes general requirements
for ventilating systems including the requirement that outdoor air inlets
shall be located to minimize or eliminate possible contamination. Additionally,
"this standard assumes that contaminants from concentrated sources which can
be a potential hazard or nuisance (heat, smoke, fumes, etc.) are collected as
close to the source by exhaust systems separate from the space ventilating
system."
Section 5.0 of the Standard describes the requirements for air ventil-
ation quality, the amounts of recirculation permissible and the minimum
design level air quantity. Because of its importance and to avoid any
misinterpretation we reproduce this section on the following page.
-24-
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TABLE 2 . MAXIMUM ALLOWABLE CONTAMINANT CONCENTRATIONS FOR
VENTILATION AIR (From ASHRAE Standard 62-73)
Contaminant
Annual Average
(Arithmetic Mean)
Mg/m3
Short-Term Level
(Not to be exceeded
More than once a Year) Mg/m3
Particulates 60* 150*
Sulfur Oxides 80 400
Carbon Monoxide 20.000 30,000
PhotochemtcalOxidant 100 500
Hydrocarbons (not
including methane) 1,800 4,000
Nitrogen Oxides 200 500
Odor Essentially Unobjectionable**
Averaging
Period (hr)
24
24
8
1
3
24
•Federal criteria for U.S. by 1975.
"Judged unobjectionable by 60% of a panel of 10 untrained subjects.
IMPILTMATION
EXFILTRATION
ALTERNATE
AIA CLEANER
LOCATION CL
OUTOOOM_ 1 1
AIM .1 1
L_J
r
i
r
L
w
AIM
CANI
B
^VCNTILATIN*
AIA
ALTERNATE
,— AIM aEANER >
/ LOCATION \
1 r
_J L.
1
T
1
> Jt
) /
SUPfliT
CONOITIONCO
WACI
RBTURH
'
.
——EXHAUST
T
— . — — RECIMCULATEO — " '
Figure '1. Diagram of definitions.
-25-
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"Section 5.0. RECIRCULATION
"The requirements for ventilation quantities given in Section 6.0 arc for
10096 outdoor air when die outdoor air meets the specifications for air quality given
in Section 3.0. Except for areas where reclrculatdon is prohibited by other codes or
standards having precedence, the outdoor air requirements may be reduced to 33% of
the specified required ventilation air quantity if adequate temperature control is pro-
vided, in addition to filtering equipment, so that the maximum allowable concen-
tration of particulates entering the space is less than that specified in Table [_2j. If,
in addition, high efficient adsorption or other odor and gas removal equipment is
employed, so that the air entering the space has been purified to meet the require-
ments of Sections 3.1 and 3.3, the outdoor air requirement may be reduced to 15%
of the specified required ventilation air quantity. In no case shall the outdoor air
quantity be less than 5 cfm per person. "
In reviewing the definition of ventilation air and the requirements
for determinations of acceptable ventilation air quality, one can readily see
that the portion of indoor air quality for which Sections 3.1 (Table 2) and
3.3 (TLV/10) apply is that of ventilation air. By consulting the diagram of
definitions and reviewing the definition for ventilating air, it would appear
that only recirculated air (and outside air) which has been treated to maintain
the desired quality of air within the designated space is applicable but other
recirculated air which could be of lower quality yet higher volume does not
apply. However, the requirements for recirculation state that outdoor air may
be reduced to 33 percent of the design levels specified in Section 6.0 of the
Standard when "...adequate temperature control is provided, in addition to
filtering equipment, so that the minimum allowable concentration of particulates
entering the space is less than that specified" in Table 2.
It would appear therefore that this requirement for a minimum allowable
concentration of particulates "entering the space" is made applicable to
supply air. Again in the next sentence the application of gas absorption or
other odor and gas removal equipment employed to meet the requirements of
Sections 3.1 (Table 2) and 3.3 (TLV/10) to insure that the "...air entering
the space has been purified to meet the requirements..." applies to supply
air.
The question we are trying to resolve here is if both outside
and inside air quality is protected by the standards, since indoor sources
of contamination such as tobacco smoke and gas appliance emissions which
are emitted in the "conditioned space" may be recirculated into supply
air without adequate filtration. Section 5.0, by specifying particulate and
gas control to insure that air "entering the space" meets the requirements
of 3.1 and 3.3, insures that the quality of air indoors must also comply.
-26-
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Section 6.0 of the ASHRAE 62-73 Standard, "Ventilation Requirements,"
is discussed in more detail in Section 4.0 of this report, Design Level
Indoor Air Quality Standards.
Table 3 is a comparison of Table 2 (from ASHRAE Standard 62-73), the
National Ambient Air Quality Standards, TLVs, and recommendations for OSHA
standards by NIOSH.
Because of the importance of ASHRAE Standard 62-73 as being the first,
if not the only, standard which incorporates "...a quantitative defini-
tion of 'acceptable outdoor' air and specifies conditions under which the
amount of outdoor air may be reduced, thereby taking advantage of advance-
ments in air cleaning technology...," we shall examine the maximum allowable
contaminant concentration (limits) in more depth.
Contaminants listed in Table 2, except for odors, are the same as
those for which the EPA promulgated ambient air quality. As discussed
in our Section 2 the purpose for the standards and the criteria to be
used for the Standard would be similar (i.e., air quality levels to protect
the public health including susceptible subpopulations). It is also important
to recognize the time frame in which ASHRAE developed these quantitative
definitions since research on the health effects of air pollution concentra-
tions continuously provides new information to be used as criteria for
standards.
The ASHRAE Committee 62P was activated in 1966 and worked to develop
this standard through nine drafts until it was published in late 1973. Its
first drafts had no quantitative definition such as Table 2 or the TLV/10
but the concensus of ASHRAE members invited to comment on the drafts was
that the quantitative definition of air quality should be incorporated. By
examining each draft, it can be determined at what point these specifications
became incorporated. The TLV was added as part of Table 2 but later became
Section 3.3 of the ASHRAE Standard with a separate paragraph describing its
application. At first only the TLV was included but in later drafts the
TLV/10 was used. The TLV is designed to protect a worker directly exposed
to the pollutant as an incident of his work, in situations where protection
and control are normally feasible. The TLVs are probably typically too
high for the safety of the general public which may be exposed over long
periods of time with no possibility of protection. Where a TLV would be
extremely high, the TLV/10 may be unnecessarily low. Arthur D. Little,
Inc. (1975) discusses ASHRAE 62-73 in an impact assessment of a subsequent
standard which incorporates 62-73. Arthur D. Little, Inc. compared the
standards in Table 2 from ASHRAE 62-73 with the National Ambient Air
Quality Standards. This comparison, shown in Table 4, included the TLV/10
values for the various contaminants listed in ASHRAE 62-73. Although the
ASHRAE 62-73 Standard did not specify the application of TLV/10 to all
contaminants "except those specified 1n Table [2]," such an application
should be implied or else Table 2 from ASHRAE 62-73 would be meaningless.
Additionally, the TLV/10 values for the contaminants were included by the
-27-
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TABLE 3. AIR QUALITY STANDARDS FOR VENTILATION AIR, AMBIENT AIR, AND WORKPLACE AIR
Pollutant
Sulfur
Dioxide
Paniculate
Matter
Carton
Monoxide
Photochemical
Oxldana
Non- Methane
Hydra eubonl
Nitrogen
Dioxide
Averaging
Time
Annul!
Arithmetic
Mean
24-Hour
8- Hour
3-Hour
Annual
Geometric
Mean
24-Hour
Annual
Arithmetic
8-Hour
1-Hour
Annual
Arithmetic
Mean
8-Hour
1-Hour
Annual
Arithmetic
8-Hour
3-Hour
Annual
Arithmetic
Mean
24-Hour
8-Hour
A SHRAE Standard
62-73 Table 1
80pg/m3 (0.03 ppm)
400 fig/ m3 (0.13 ppm)
60/ig/m3
(Annual arithmetic
mean)
ISOpg/m3
20,OOC/ig/m3
(17.S ppm)
30,000 fig/m3
(26 ppm)
lOOfig/m3
(0.05 ppm)
SOOpg/m*
(0.2Sppm)
1800 jig/m3
(2. 73 ppm)
4000 pg/tn3
(6. 1 ppm)
200pg/m3
(0.11 ppm)
SOOug/m3
(0.27 ppm)
National Anbtont
Primary
80 fit/ m3 (0.03 ppm)
365/ig/m3 (0.14 ppm)
7Sjjg/m3
260pg/m3
10,000(ig/m3
(9 ppm)
40,000^g/m3
(JSppm)
160jig/m3
(0.08 ppm)
160 ftg/m3
(0.24 ppm)
100(lg/m3
(0.05 ppm)
Secondary
1300 (ig/m3
(0.3 ppm)
«0j4g/m3
ISOjig/m3
Same OB
Prlmuy
Sam* at
Primary
Same u
Primary
Sana ai
Primary
Same a>
Primary
WodcpUce
TLV
13000 (ig/m3
(S ppm)
SS.OOOpg/m3
(50 ppm)
200|ig/m3
(0.10 ppm)
360,000
( 100 ppm-hexane)
9000 Mg/m3
(S.O ppm)
N1OSH
Recommended
5600 (jg/m3
(2 ppm)
40, 000 MS/™3
(33 ppm)
-28-
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TABLE 4. COMPARATIVE AIR QUALITY STANDARDS
Pollutant
Participate
matter n
Sulfur dioxide
Carbon
monoxide
Photochemical
oxidants^
Nonmethane
hydrocarbons
Nitrogen
dioxide
Odor
Averaging Time
Annual geo-
metric mean
24 hr
Annual arith-
metic mean
24 hr
3 hr
8 hr
1 hr
1 hr
3 hr
Annual arith-
metic mean
-
ASHRAE Standard 62-73
Table I TLV/10
60 Pg/m3
150 pg/m3 10,000 pg/m3
80 VJg/m3
400 pg/m3 1,300 pg/m3
(0.5 ppm)
30,000 pg/m3 5,600 pg/m3
(5 ppm)
500 Pg/ir3 20 pg/m3
(0.01 ppm)
4,000 Pg/m3 3fc,000 pg/m3
(10 ppm Hexane)
200 Pg/m3 1,000 Pg/m3
(0.5 ppm)
c
National Ambient8
Primary Secondary
75 Pg/m3 60 Pg/m3
260 Pg/m3 150 Pg/m3
80 Pg/m3
(0.03 ppm)
365 Pg/m-4
(0.14 ppm)
1,300 Pg/m3
(0.5 ppm)
10,000 Pg/m3 Same as
(9 ppm) primary
40,000 Pg/m3
(35 ppm)
160 Pg/m3 Same as
(0.08 ppm) primary
160 pg/m3 Same as
(0.044 ppm primary
hexane)
100 Pg/m3 Same as
(0.05 ppm) primary
^National Primary Standards: the levels of air quality necessary, with an
adequate margin of safety, to protect the public health.
National Secondary Standards: the levels of air quality necessary to
protect the public welfare from any known or anticipated adverse effects
of a pollutant .
National standards other than those based on annual arithmetic means or
annual geometric means are not to be exceeded more than once per year
(Federal Register 1971, and 1973).
indoor oxidant limits proposed by FDA and Canadian Standards Association are
0.05 ppm (100 pg/m3) and 0.04 ppm (80 pg/m3), respectively (Mueller, et al., 1973),
Odor judged unobjectionable; by a panel of 10 untrained subjects.
Source: Arthur D. Little, Inc.
-29-
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Arthur 0. Little, Inc. in comparison to annual, 24-hour, 3-hour, and
1-hour averaging times. Since the TLVs are 7-8 hour time-weighted averages,
it would seem that the TLV/10 would also be applicable for this averaging
time or at least is compared with other contaminants a similar averaging
time. We are not confident in our assessment of this application, however,
since the TLV/10 specification in Section 3.3 of ASHRAE 62-73 makes no
mention of an averaging time. Although, since this section does mention
that the TLVs are accepted by the ACGIH one may assume 8-hour time-weighted
averages. ';
Arthur D. Little, Inc.'s tabular display of the TLV/10 for contamin-
ants and Table 2 from 62-73, served to demonstrate that for some contaminants
this specification can be unnecessarily low. For example, the TLV for
carbon dioxide is 5000 ppm. The ACGIH documentation of this TLV reports
studies showing symptoms at 10 times this level (50,000 ppm) and reports on
incidence whereby submarine personnel exposed continuously to 3 percent
(30,000 ppm) carbon dioxide showed only slight effects. The TLV of 5000
ppm (0.5 percent) w?s chosen because it appeared "...to provide a reasonably
good margin of safety for an 8-hour daily exposure, provided ordinary
amounts of oxygen are inhaled. Under these conditions no significant signs
of oxygen deficiency should appear" (ACGIH 1971). Although it would appear
from this documentation that a substantial safety margin has been built
into the TLV, ASHRAE added an additional and quite substantial safety
margin by using the TLV by 10 formula. This standard of 500 ppm is higher
than the C02 content of clean ambient air, which ranges between approxi-
mately 310 to 330 ppm (Seinfeld 1975), but the standard is quite commonly
exceeded in downtown metropolitan areas and in occupied indoor spaces.
By reviewing Table 2 and comparing the values with other standards
for the same averaging time, one can see several unique features as compared
with the National Ambient Air Quality Standards. The ambient air quality
standards are based on health criteria which may show long- and short-term
effects of the same pollutant. The National Ambient Air Quality Standards
reflect this criteria by having for some contaminants both short-term stan-
dards (1, 3, 8, and 24-hour maximums) to protect against acute health effects
and annual standards to protect the public from chronic effects.
There is no annual National Ambient Air Quality Standard for 03
or CO partly because there was no valid data in the criteria documents
for these two pollutants to show long-term chronic effects. Additionally,
0., is a seasonal pollutant with concentrations near zero in the winter
but quite variable during the warmer months as a function of precursor
emissions, solar radiation (and time of day) and stagnant meteorological
conditions. Annual average maximum allowable carbon monoxide and ozone
standards listed in Table 2 from ASAHRAE 62-73 appear to be without dis-
cernible health criteria although the Air Quality Criteria documents for
both pollutants are listed in the References of the Standard.
-30-
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Neither standard, however, is unreasonable. The annual exposure
to 20,000 pg/m (17.5 ppm) of carbon monoxide is equivalent to approxi-
mately 2.5-3.5 percent COHb (Forbes 1972). The standard of 100 ug/m
(0.05 ppm) for photochemical oxidants, although low, on a short-term
basis is not so easily comparable in terms of an annual average.
The short-term standards in Table 2 from ASHRAE 62-73 for both pollu-
tants, CO and 0,, are more than twice that of the National Ambient Air Quality
Standards and would not appear to adequately protect the public health. For
example the 1-hour ASHRAE Standard 1s 500 yg/m3 (0.25 ppm) for 03 but the
threshold for eye irritation, as discussed in Appendix A of this report,
begins at about 200 ppm. The ASHRAE 8-hour standard of 30,000 yg/m3 (26 ppm)
for CO represents a potential COHb level to those exposed at more than 4 per-
cent (Forbes 1972). This level does not represent a significant health risk
but 1t represents twice the COHb level (2 percent) for which the national
1-hour and 8-hour standards are based. Recent recommendations by the Ad Hoc
Committee on Carbon Monoxide Poisoning and the National Academy of Sciences
recommend 15 ppm as a nonworkplace indoor air quality standard, both organi-
zations using a carboxyhemoglobln limit of 2.6 percent (Forbes 1972, National
Academy of Sciences 1972). The ASHRAE maximum allowable concentration (lim-
its) for sulfur dioxide and partlculate are comparable to the National Ambient
A1r Quality Standards.
ENERGY CONSERVATION IN NEW BUILDING DESIGN - ASHRAE STANDARD 90-75
As the title of the Standard implies, the American Society of Heating,
Refrigerating and Air Conditioning Engineers developed a standard for
effective energy utilization that applies to the selection of building and
systems components for new building design.
In Section 5.0 of the Standard, "Heating, Ventilation and Air Condition-
ing (HVAC)," systems, the requirements are as follows:
"Ventilation air shall conform to ASHRAE Standard 62-73
'Natural and Mechanical Ventilation.'
"The minimum column value for each type of occupancy shall
be used for design. The ventilation quantities tabulated in
Section 6.0 of ASHRAE Standard 62-73 are for 100 percent out-
door air ventilating systems. Section 5.0 of ASHRAE Standard
62-73 permits a reduction to 33 percent of the specified mini-
mum outdoor air requirement for recirculating HVAC systems."
-31-
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Hence, Standard 90-75 did not alter the ventilation air require-
ments of Standard 62-73 but incorporated them into the Standard. The
difference between the Standards is found in the interpretation of the
columns in Section 6.0 of Standard 62-73 which specify required ventilation
air, cubic feet per minute per human occupant. In Section 6.0 of Standard
62-73 two columns are shown for required ventilation air, one is for
minimum ventilation air and the second is a range of values for recommended
ventilation air. Of course the "minimum" ventilation air is less than the
"recommended" values. In formulating ASHRAE 90-75, the project committee
chose to conform to the least ventilation air quantity in order to conserve
energy by limiting the number of air exchanges that usually necessarily
would require higher heating and cooling loads.
Although the above principally pertains to design-level air quality
standards, discussed herein in Section 4, the opening statement that
"... ventilation air shall conform to ASHRAE Standard 62-73 'Natural and
Mechanical Ventilation1..." implies that sections of Standard 62-73 which
designate the quality of the ventilation air (i.e., Sections 3.1 with Table
2 and Section 3.3, 10 percent of the TLV) would be included.
Additionally, Section 5.6 of ASHRAE 90-75 requires cooling with
outdoor air under certain conditions. However, cooling with outside air is
not required when "...the quality of the outdoor air (as defined in Table [2]
of ASHRAE Standard 62-73) is so poor as to require extensive treatment of
the air," (ASHRAE 1975).
It can readily be seen that ASHRAE 62-73 and indirectly 90-75, designate
maximum allowable air quality pollutant standards. Although both standards
are guidelines, they have been incorporated into two of the four proprietary
building codes which are used either in entirety or in part of many state
and municipal building codes.
The effects of incorporating ASHRAE Standards 62-73 and 90-75 are
confusing since it is not readily discernible if indoor air or air in
the "conditioned space" is adequately protected by Section 3.1 (Table 2)
and 3.3 (10 percent of TLV) of ASHRAE 62-73 which applies to "ventilation
air." As discussed in the previous section concerning ASHRAE 62-73,
Section 5.0 of the Standard allows recirculation if air "entering the
space" complies with Sections 3.1 and 3.3. This section would imply
application of the requirements to "supply air." Again, however, the air
from the conditioned space where people breathe and indoor air pollution
sources are often exhausted (i.e., tobacco smoke) is seemingly left to be
diluted by ventilation air. This air, used for ventilation purposes, then
is a combination of outdoor and recirculated air and the mixture must meet
or exceed the quality limits stated in Sections 3.1 and 3.3 of ASHRAE
62-73.
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The impact of 90-75 however is obvious in stipulating that the "minimum1
ventilation requirements will be used for design purposes. Seemingly these
reductions will decrease contamination from outdoor sources but increase
contamination from indoor sources.
The Arthur D. Little, Inc. report on the impact of ASHRAE Standard
90-75 interprets the standards as the above. Additionally the authors
report:
"Existing information on indoor air pollution levels
suggests that the most adverse effect of the proposed
reductions in ventilation and infiltration will be exposure
of nonsmokers to higher particulate (and possible CO) con-
centrations due to tobacco smoking. As discussed in the
previous section, particulate concentrations in several
conventional smoking places have been reported to be at
least 1.5 to 5 times higher than the ambient air quality
standard of 75 wg/m . At lower ventilation and infiltra-
tion rates, the particulate concentrations will be increased
by roughly proportional amounts, as follows:
Approximate
. Average Reduction Increase in
of Ventilation and Pollution
Infiltration Level
Single-Family Residence 3.5 4
Multi -family Low-Rise 45 82
Office 40 67
Retail Store 34 52
School 45 82
"In view of the high present concentrations of
cigarette smoke particulates these increases would appear
to be excessive, and that smoking spaces in public build-
ings should be ventilated at ASHRAE 62-73 recommended
rates rather than the minimum rates. ADL believes that
reduced infiltration will lead to greater demand for sep-
arate smoking and nonsmoking zones in public buildings and
corresponding needs for different ventilation approaches."
(Arthur D. Little, Inc. 1975)
Model state and municipal building codes are discussed in more depth
in the next section.
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INDOOR AIR QUALITY STANDARD FOR OZONE
The only indoor nonworkplace standard promulgated by the U.S. Federal
Government has been issued by the Department of Health, Education, and
Welfare's Food and Drug Administration. The ozone standard for indoor
environments in houses, apartments, hospitals, and offices is 0.05 parts
per million by volume of air. The following paragraph from Title 21 of the
Code of Federal Regulations section 801.415, 1972, "Maximum Acceptable Level
of Ozone," describes that any device will be considered adulterated or mis-
branded if,
"...it generates ozone at a level in excess of 0.05 parts
per million by volume of air circulating through the device
or causes an accumulation of ozone in excess of 0.05 parts
per million by volume of air (when measured under standard
conditions at 25°C (77°F) and 760 millimeters of mercury) in
the atmosphere of enclosed space intended to be occupied by
people for extended periods of time, e.g., houses, apartments,
hospitals, and offices. This applies to any such device,
whether portable or permanent or part of any system, which
generates ozone by design or as an inadvertent or incidental
product.
It is important to note that this standard is not only a maximum
allowable indoor air quality standard but also an emission standard and
will be discussed as such in Section 4 of this document.
The Threshold Limit Value (TLV) established the American Conference of
Governmental Industrial Hygienists (1976) for ozone on an 8-hour time
weighted average is 0.10 ppm. The National Ambient Air Quality Standard
for ozone is 0.08 ppm maximum 1-hour concentration not to be exceeded more
than once per year. The FDA ozone standard of 0.05 ppm for enclosed indoor
environments is lower than the other ozone standards and allows for a 50
percent safety margin or TLV/2 over the ACGIH's standard. This is to
protect sensitive individuals exposed in the indoor environment for extended
periods of time which may be 24-hours or greater.
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SECTION 4
DESIGN LEVEL AND EMISSION
INDOOR AIR STANDARDS
INTRODUCTION
Adequate control of indoor air quality must be accomplished through
the ventilation of air from the space exposed to pollutant concentrations.
The amount of ventilated air required to maintain levels safe for human
occupancy depends on the total volumetric air flow or breathing rate of
the building. This is not only dependent upon the air flow 1n the build-
ing's HVAC system but also reflects rates of infiltration and .exf11tra-
tion.
At one time it was considered quite acceptable to replenish indoor
air with fresh outdoor air. However, with the decreasing quality of out-
door air and an increasing knowledge of acceptable levels of pollutants, -
cleansing of the air became a necessity for certain indoor functions.
Control of acceptable pollution levels on the indoor environment must be
accomplished through the development of guidelines and standards. The
limited number of existing enforceable standards was previously discussed
in Section 3. Application .of these standards will be discussed in this
section on design levels and em-lsslon standards.
Before our discussion of design levels, a distinction must bs made
between the difference in design levels and maximum allowable limits
of indoor air quality. Maximum allowable limits are measurable quantities
that are established to provide health, safety and well-being to human
occupancy through legal enforcement of standards and regulations. These
allowable limits are often established with the,use of Threshold Limit
Values (TLV). With respect to indoor air quality and pollutant exposure
episodes indoors the majority of work has been on the Industrial work-
place. The increased knowledge of health effects associated with a4r
pollutant concentrations has made us aware of the potential hazardous
levels occurring in industrial workplace exposures. Development and
enforcement of maximum allowable limits has been based on the 7- or 8-hour
workday exposure. The Occupational Safety and Health Administration has
been responsible for the development and enforcement of the guidelines
and standards regulating the workplace atmosphere.
Design levels are typically based on minimum acceptable airflow or
air exchange to maintain indoor air quality. The distinction between
maximum allowable and minimum acceptable is made dependent on the use
of the standards. Maximum allowable refers to a quantitative figure based
on acceptable maximum pollutant concentration levels. The term minimum
allowable- refers to the design level standards used by building Inspectors,
engineers, architects and manufacturers. In the case of a ventilation sys-
tem, the minimum allowable would be the minimum volumetric airflow the HVAC
-35-
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system is required to produce to maintain the maximum allowable limits of
indoor pollutants.
Design levels are not established solely on maximum allowable limits
of indoor pollutants or minimum volume of airflow to maintain these pollu-
tant concentrations. Design levels also take into consideration several
factors dealing with the comfort of the occupants' space. These comfort
factors consist of heating, coolitig and humidification of the space. Design
levels, which are usually incorporated into building codes as minimum accept-
able limits, are used to control the occupied indoor space in order to main-
tain an acceptable comfort level for the occupant as well as ensure minimum
safety and health requirements.
DESIGN-LEVEL STANDARDS
Design-level standards, as previously noted, are used to control
interior spaces to ensure they meet health, safety and comfort standards,
acceptable to the occupants. Incorporation of design-level standards /
into the physical building is accomplished through the use of building/
codes. Building codes are developed to establish the building ventilation
requirements used to control the quality of air in occupied spaces. For
our discussion of design-level standards we will look specifically at
standards dealing with the minimum acceptable limits for indoor air
quality.
Design-level standards are used by engineers, architects and manu-
facturers in the design of building ventilation systems. To make these
standards compatible to the building Industry they are written in ventil-
ation requirements as a volumetric flow of air. Units commonly used in
the design level standards are cfm/person, cfm/sq.ft., cfm/cu.ft. or air
changes per hour. These units of measurements will vary from standard
to standard, however, the most common units used are ones of volumetric
rates per person because of their sensitivity to population density.
ASA STANDARD A53.1
The American Standard Association (now known as the American National
Standards Institute) was one of the first organizations to attempt to
develop a national standard for ventilation requirements. The ASA
Standard A53.1 was developed 1n 1946 at which time 1t was generally accept-
able to control Indoor air quality by replenishment with fresh outdoor
air. At this time Indoor air quality was based largely on odor control.
With the advancements 1n filtration technology and with effective
recirculatlon units produced in later years, a reduction in typical mini-
mum ventilation requirements began to appear in ventilation standards.
As an example of these allowable ventilation reductions the typical mini-
mum mechanical ventilation rates specified in the 1946 ASA Standard A53.1
-36-
-------
are compared to the ASHRAE Standard 62-73 in Table 5 (Woods 1975). The
importance in the revision of these standards shows how treatment of
recirculated air can result in less expensive filtration cost and less
energy consumption without compromising the health, safety or well-betng
of the occupant.
ASHRAE STANDARD 62-73
The purpose of ASHRAE 62-73 is to define ventilation requirements
for spaces Intended for human occupancy and specify minimum and recom-
mended air quantities for the preservation of the occupants' health,
safety, and well-being. As a design standard for engineers and architects
ASHRAE 62-73 is useful because it provides the ventilation rates in vol-
umetric flow per person (cfm per person) required to maintain the oxygen,
carbon dioxide and other air quality levels in the space under considera-
tion.
Section 6.0 of ASHRAE 62-73 defines minimum and recommended ventila-
tion requirements for residential dwellings as well as commercial,
industrial, agricultural, institutional, and organizational establishments.
Table 6 shows the required minimum and recommended ventilation air in cfm
per person for residential, institutional and organizational building
ventilation systems. Ventilation air in this table is defined in
ASHRAE 62-73 as "...that portion of supply air which comes from outside
(outdoors) plus any recirculated air that has been treated to maintain
the desired quality of air within a designated space." For a discussion
of unacceptable outside air for ventilation use see Section 3 of this
report.
ASHRAE 62-73 provides the designer with minimum and recommended levels
of ventilation. This allows the designer to select different quality
levels in recognition of the need to provide choices of environmental
performance for different classes of projects. The designer 1s encouraged
to use his experience and judgment in the application of this standard as
long as the minimum requirements are satisfied.
ASHRAE STANDARD 90-75
Stanford Research Institute (1972) reported that the control of
building heating and cooling loads requires nearly 20 percent of the
energy consumed 1n the United States. With an increased awareness of
limited sources of fuel and the recent experiences of the energy crisis,
ASHRAE responded in 1975 with Its Standard 90-75 titled "Energy Conserva-
tion in New Building Design." In Section 5.0, "Heating, Ventilating and
Air Conditioning Systems" under subsection 5.3.2 "Design Parameters,"
ASHRAE 90-75 describes ventilation requirements as follows:
"5.3.2.3 Ventilation. Ventilation air shall conform
to ASHRAE Standard 62-73 'Natural and Mechanical
Ventilation.1
-37-
-------
TABLE 5. COMPARISON OF TYPICAL MINIMUM MECHANICA L VENTILATION REQUIREMENTS BETWEEN THE ASHRAE
STANDARD 62-73 (1973) AND THE ASA STANDARD A53. 1 - 1946^'
Occupied
Space
Retail Sales
Theaters
Office Space
Exhibit Halls
Dining Areas
Classrooms
Hospitals -
Patient Rooms
Wards
Operating Rooms
Laboratories
Animal Rooms
ASHRAE Standard 62-73
(1973)
Estimated Persons/, -v
1000 ft2 Floor Area^ ;
30
150
10
70
5
50
15
20
—
50
20
Minimum
Ventilation
Air
(cfm/person)
5
5
5
5
5
5
5
5
7(4)
5
13.3
Equivalent
Air Change
Per Hour (3)
1.1
5.6
0.4
2.8
0.2
1.9
0.6
0.8
1.9
1.9
ASA Standard A53.1
(1946)
Minimum
Ventilation
Air
(cfm/fO
1.5
1.5
0.5
1.5
Not Covered
1.5
1.0
1.0
2.0
2.0
Not Covered
Equivalent
Air Change
Per Hour (3)
11.2
11.2
3.8
11.2
11.2
7.5
7.5
15
15
CO
00
I
Notes: 1. Based on 100 percent outdoor air with adequate temperature control and particulate
filtration.
2. Use only when design occupancy is not known.
3. Based on 8 ft (2.4 m) ceiling height.
4. Special Codes or Requirements may determine ventilation rate.
-------
TABLE 6. .ASHRAE 62-73 VENTILATION REQUIREMENTS
Estimated
persons/
1000 sq
ft floor
area. Use
only when
design oc-
cupancy U
not kaowo
Required ventilation sir,
cable feet per minute per
human occupant, (whan the
number is bracketed, refer
to the notes).
W^miim
4.1. RESIDENTIAL
(FrtiBta dwelling places.
si
Single Unit Dwdliafs
General Lfrint Areas, Bedrooms
Kitchen
Baths, Toilet Rooms
Bosements, Utility Rooms
Mottrplo Unit Dwefflmja
General Uvimj Areas, Bedrooms
Kitchen
Baths, Toilet Rooms
Basements, Utility ROODS
Garagce
Mobile ROOMS
•InettIM esfMitp tot UmrmUMrt u*&
**v4tai pot MI ft o/ HOOT Mvfe
keji* cr mulnpie units)
5
. . —
—
—
7
— .
- •
— • •
—
7
5
20
20
5
5
20
20
5
(0.75)
5
&5. INSTITUTIONAL
Schools
Classrooms
Multiple Us* Rooms
Laboratories
Ctaft Shops, Vocational
Training Shops
Mudo, Rehearsal Rooms
Audttodums
Gymsasmms
Libmies
Common Rooms, Lounges
Offices
Lavatories
Locker Rooms
Iiiiirshinv>int Pining Halli
Conidon
Utility Rooms
Dormitory Btdrootnt
50
70
30
30
70
150
70
20
70
10
100
20
100
50
3
•jft
^8p*«lii< eeoonteMt ooatrol ijrtutM may b« raqulnd
10
10
10
10
10
5
20
7
10
7
15
(30)
15
5
7
1
Recommended
7-10
30-50
30-50
5
7-10
30-50
30-50
7-10
(1.0H1.3)
7-10
10-15
10-15
10-15
10-15
15-20
5-Ttt
25-30
10-12
10-15
10-15
20-25
(40X50)
14.20
1 J*AW
20-25
7-10
Comments
•
a
•
•
••
•
•
••
(Continued)
-39-
-------
TABLE 6. ASHRAE 62-73 VENTILATION REQUIREMENTS (Continued)
Hospitals, Mussing and Cosvateacea* HOOKS
Foyers
Hallways
Single, Dual Bedrooms
Wards
Food Sorrics Centers
Opwattos Rooms, Delivery
Rooms
Ready Rooms, Recovery Rooms
Ampbiiheacns
Physical Therapy Areas
Autopsy Rooms
Incinerator Service Areas
50
50
15
20
20
—
_
100
20
10
—
20
20
10
10
35
20
15
10
15
30
5
25-30
25-30
15-20
15-20
35
1 ^m ^»
_ «•
15-20
20-25
40-50
7-10
•
«
••
•Speefal reqetHHSsae or codm mar detonates raqiafaumann
"•SposioJ oo&enst tr&aaa rwpUtad
Laboratories (Ughs-duty,
now hnmtaal)
Laboratories (Chemical)
Laboratories (Hoary-duty)
Laboratories (Radioisotops,
Chemically and Biologically
Toxic)
Machine Shops
Darkrooms, Spectsoscopy Rooms
AnimdRooEK}
50
50
50
50
50
50
20
A
""S pastel roqiUwoseoffi or aodM mar dmnnntoo nqulrMMOta
MQitary and Narol Installations
Barracks
Toilets/Washrooms
Shower Rooms
Drill HaBa
Ready Rooms, MP Stations
Indoor Target Ranges
•Fteoraraa bantod flftaiQ lino oalr
Biiuenuoo
Exhibit Hallo
Workrooms
Warehouses
Pifeono (S£K) dso CsrraaadBns,
LfiMEffios, AppJfenbte
JajJnggjtal Areas)
Cofi Blocks
Eating Hallo
Guard Stations
Votenjcsry Hospitsls
Kanneto, Stalls
Operating Rooms
Reception Rooms
20
100
100
70
40
70
70
10
5
20
70
40
20
20
30
15
15
15
15
15
10
40
7
15
10
15
7
20
7
10
5
7
15
7
25
25
10
20-25
20-25
20-25
20-25
20-25
15-20
45-50
10-15
20-25
15-20
20-25
10-15
• 25-30
10-15
15-20
7-10
10-15
20-25
10-15
30-35
30-35
15-20
•
•
•
•
..
*
•
*
(Continued)
-40-
-------
TABLE 6. ASHRAE 62-73 VENTILATION REQUIREMENTS (Concluded)
Estimated
persons/
100 sq
ft floor
wee. Use
only when
design oc-
not known
Required ventilation air,
cub*r feet per minute per
human occepant, (when the
number b bracketed, refer
to the notas).
Minimum
6.6. ORGANIZATIONAL
Churches, Temples
(See theaters, schools
and offices)
Upslwive Chambers
Committee Rooms and Conference
Rooms
Foyers, Corridoa
Offices
Press Lounges
Press/Radlo/TV Booths
Public Rest Rooms
Private Rest Rooms
(For Food Service, Utilities,
etc. sea Ho tab)
Police and Fire Stations
(Sen Prisons and Military
Surrrrd Shelters
—
70
70
50
10
20
20
20
_
•Spadad nqofeMMMi or ee
-------
"The ml til n mm column value for c;ich type of occu-
pancy shall be used for design. Tlie ventilation i|uanti-
ties tabulated in Section 6 of ASHRAE Standard 62-73
are for 100 percent outdoor air ventilating systems. Sec-
tion 5 of ASHRAE Standard 62-73 permits a reduction to
33 percent of the specified minimum outdoor air require-
ment for recirculating HVAC systems.
"EXCEPTIONS. If outdoor air quantities other than those
shown in ASHRAE Standard 62-73 are used or required
because of special occupancy or process requirements, source
control of air contamination, or conflicting codes, the
required outdoor air quantities shall be used as the basis of
calculating the heating and/or cooling design loads. "
It is important to note that ASHRAE Standard 90-75 uses the require-
ments established by ASHRAE Standard 62-73. However, in ASHRAE 90-75 it
is suggested that the minimum ventilation rates rather than the recom-
mended be used for design purposes. This complies with energy conserva-
tion measures to reducr to a minimum the fuel consumption required to
heat or cool ventilation air.
Section 5.7, "Mechanical Ventilation," of ASHRAE 90-75 states that
"Each mechanical ventilation system (supply and/or exhaust) shall be
equipped with a readily accessible means for either shut-off or volume
reduction and shut-off when ventilation is not required." This design
parameter will have an effect on the manufacturers of ventilation equip-
ment as well as construction and building engineers installing HVAC
systems. As state or local authorities adopt ASHRAE Standard 90-75
manufacturers and designers must incorporate systems that will enable
cut-off and reduction, switches to be readily accessible to the occupants.
Design Level Ventilation Standards for Hospitals and Medical Facilities
General Standards of Construction and Equipment for Hospital and
Medical Facilities issued by the U.S. Department of Health, Education,
and Welfare in 1969 was streamlined and revised to include only the mini-
mum requirements in a 1975 HEW publication "Minimum Requirements of
Construction and Equipment for Hospital and Medical Facilities" whose
name reflects that change. Additionally, however, ventilation require-
ments for various hospital areas have been changed and for the most part
are reduced (in air changes per hour) to enhance energy conservation.
Tables 7 and 8 list the pressure relationships and ventilation
requirements for hospitals and medical facilities. Filter efficiencies
are required to be average atmospheric dust spot efficiencies tested
in accordance with ASHRAE Standard 52-68 (1968). These ventilation rates
specify design requirements for adequate particulate control, but there
are no gas absorption equipment requirements. Presumably the use of
laboratory hoods would minimize indoor contamination, however outdoor
gaseous pollutants could enter into the makeup ventilation air and be
-42-
-------
TABLE 7. GENERAL PRESSURE RELATIONSHIPS AND VENTILATION
OF CERTAIN HOSPITAL AREAS
Minimum Minlfnum
Prcuiue Air Changes r0^] /u, A" Atr
Area Relationship Of Outdoor Changes per Exhaujtwl
Designation to Adjacent All per Hour .. ? \jL, Directly to
Areas Supplied to . ' n_lL. Outdoon
Room
Operating Koom
Emergency Operating Kouin
Emergency Examination and Treatment Room
Delivery Room
Nursery L'nit
Recovery Room
Intensive Care
Patient Room
Patient Room Corridor
l.iol.ition Room
Isolation Room-Alcove or Anteroom
Examination Room
Medication Room
Pharmacy
Treatment Room
X-ray, Fluoroscopy Room
X-ray. Treatment Room
Physical Therapy and Hydrotherapy
.Soiled Workroom or Soiled Holding
Clean Workroom or Clean Holding
Autopsy
Darkroom
Nonrefrigerated Body Holding Room
Toilet Room
Bedpan Room
Bathroom
Jantion' Closet
Sterilizer Equipment Room
Linen and Trash Chute Rooms
Laboratory, General'
Laboratory, Media Transfer*
Food Preparation Centers
Ware washing
Dietary Day Storage
Laundry, General
Soiled Linen Sorting and Storage
Clean Linen Storage
Anesthesia Storage'
Central Medical and Surgical Supply
Soiled or Decontamination Room
Clean Workroom
Unsterile Supply Storage
P
P
E
P
P
P
P
E
E
E
E
E
P
P
E
N
E
N
N
P
N
N
N
N
N
N
N
N
N
N
P
E
N
E
E
N
P
E
N
P
E
5
5
2
5
5
2
2
2
2
2
2
2
2
2
2
2
2
2
2
2
2
2
Optional
Optional
Optional
Optional
Optional
Optional
Optional
2
2
2
Optional
Optional
2
Optional
2
Optional
2
2
2
25
25
6
12
12
6
6
2
4
6
10
6
4
4
6
6
6
6
10
4
12
10
10
10
10
10
10
10
10
6
4
10
10
2
10
10
2
8
6
4
2
Optional
Optional
Optional
Optional
Optional
Optional
Optional
Optional
Optional
Yes
Yes
Optional
Optional
Optional
Optional
Yes
Optional
Optional
Yes
Optional
Yes
Yes
Yes
Yes
Yes
Yes
Yes
Yes
Yes
Optional
Optional
Ye*
Yes
Optional
Yes
Yes
Optional
Yes
Yes
Optional
Optional
Recfacalated
within
Room Units
No4
No*
Optional
No4
No4
No4
No4-5
Optional
Optional
No5
No*
Optional
Optional
Optional
No4
No
Optional
Optional
No
Optional
No
No
No
No
No
No
No
No
No
Optional
No4
No
No
No
No
No
Optional
No
No
Optional
Optional
P = Positive
N = Negative
E = Equal
'See sections 7.30.D (2Xk), 7.30.0(2X1), and 7.30.D (2Xm) for additional requirements.
2Sce section 7.30.D (2Xk) for additional requirements.
^See section 7.30.D (2Xo) for additional requirement*.
4Reciruilaling room units meeting the filtering requirement for sensitive areas in section 7.30.D (2Xg) may be used.
5Se«-section 7.30.0 (2X0.
(HEW publication No. HRA 76-4000)
-43-
-------
TABLE 8. PRESSURE RELATIONSHIPS AND VENTILATION OF MEDICAL FACILITIES
Rehabilitation Areas
PRESSURE
RELATIONSHIP TO
*RiA Of MON ATKJN ADJACENT AREAS
Ontal Operalury
Patient Ri>om
Patient Aiea Corridor
Occupational Therapy
Physical Therapy and Hydrotherlpy
Speech and Hearing Unit
Soiled Workroom and Soiled Holding
Clean Workroom and Clean Holding
Activities of Daily Living
X-ray Diagnostic
Trealmenl Room
Laboratory
Dark Room
Toilet Room and Locker Roomi
Bedpan Room
Bathroom
Janitor*) Closet
Stenli/er Equipment Room
Linen and Trash Chute Koomt
Food Piepjration Center
W-irewjNhing Room
Personal Care Room
Dietary Day Storage
Laundry. General
Soiled Linen Sorting and Storage
Clean Linen Storage
P f,.»l,.r N ' Nruli.r t < K
N
H
t
N
N
t
N
P
t
N
t
N
N
N
N
N
N
N
N
t
N
N
k
t
N
P
,u.l
•Nmrrulllinif mom Ural* inrHittK ihr riltrnnl rrqiiiirmrnli titr
Long- Term Care Facilities
Patient Room
Patient Area Corridor
Elimination and Trealmenl Room
Physical Therapy
Occupational Therapy
Soiled Workroom or Soiled Holding
Clean Workroom or Clean Holding
Toilet Room
Bathroom
Janitors' Cloiel(i)
Slerilner Equipment Room
Linen 4nd Trash Chute Roomi
Food Preparation Center
WarewBjning Room
Dietary Day Storage
Liundry, General
Soiled Linen Sorting and Storage
Clean Linen Storage
P • Po.l>» N • Mr,*,,. t
Outpatient Facilities
Dentil Room
Tmtnwnl Room
Laboratory, Genital'
X-ray and Film Proctuiflg
Clean Workroom or Clran Holding
Soiled Workroom or Soiled Holding
Wailing Room
Corridors
Eaiminltion Room
Observation
Janitors' Closet
va* S.-M-.
iwim KAMI
P ' PiMitin •> • >«,•»•' t • EquJ
•s««.0on.-,M.D,W).~irii012),).r«^
•rrtrrulttn
Other than
E
E
E
N
N
N
P
N
N
N
N
N
F.
N
E
t
N
P
"fqud
iiiofuf m
N
E
N
N
P
N
E
E
E
N
N
N
N
pmnieritt.
MINIMI M AIR CHANCE]
OF OUTDOOR AIR
PER HOUR
SUPPLIED TO ROOM
,
2
2
;
2
:
2
2
2
Optional
Optional
Opllonal
Optional
Optional
Optional
2
Optional
2
Optional
Optional
MINIMUM TOTAL - .
AIRCHAMiEI ALLAIREXHAUStCD '
PER HOI' R DIRECTLY TO
STPPIIED TO ROOM
h
2
4
ft
ft
2
10
4
4
ft
ft
ft
in
10
10
ID
10
10
10
IU
10
N
10
10
OLTDOOR]
Optional
Optional
Optional
Optional
Optional
Optional
Yes
Optional
Optional
Optional
Optional
Optional
Yes
Yes
Yes
Yes
Yes
Yes
Yei
Yes
Yes
Optional
Optional
\c<
Optional
REC1RC1JLATED
WITHIN AREA
Nor
Oplionil
Optionil
Optional
Oplionil
Oplionil
No
Optional
Opfonal
Optional
No'
Oplionil
No
No
No
No
No
No
No
No
No •
Yes
No
No
No
Oplionil
1 "Hint urn 'I'm- l»*i»*. III.W.IH i»'llm.> hr ,.-J
Chronic Disease
2
Optiorul
Opllonal
Opllonal
Optional ;
Opllonal
1
Optional
Optional
2
Optional
2
1
1
2
2
2
2
2
2
2
':
Optional
Option!
Opuorul
Hospitals
2
4
6
6
6
10
4
10
10
10
10
10
10
10
2
10
10
2
6
6
6
6
4
10
6
6
6
6
10
10
10
Optional
Optional
Optiorul
Optional
Optional
Yei
Oplionil
Yes
Yes
Yes
Yes
Yes
Yes
Yes
Yes
Yts
Yts
Optionil
Yts
Optional
Optional
Yes
Optional
YM
Optional
Optional
Oplionil
Yei
Yo
Yn
Yts
Optional
Optional
Optional
Oplionil
Optional
No
Optional
No
No
No
No
No
No
No
No
No
No
Optional
-44-
(HEW publication No. HRA 76-4000)
-------
supplied to all of the indoor spaces. For a detailed description of
ventilation system design requirements for hospitals and medical facili-
ties, readers should consult the "Minimum Requirements of Construction
and Equipment for Hospital and Medical Facilities," DHEW Publication
No. (HRA) 76-4000.
EMISSION STANDARDS
Emission standards are those standards that specify a numerically
limiting value on the amount of contaminant which may be emitted from a
source or sources. Several of these standards exist for the industrial
work environment to control the levels of pollutant concentrations the
worker may be exposed to. Such standards put regulations on industrial
indoor emissions by two means; one is to define limits that designate the
levels of pollutants which particular processes can emit during their
operations, and the other is to put a limit on the pollutant concentra-
tions that can be attained in the ambient indoor atmosphere.
Emission standards for nonworkplace indoor air quality control are
almost nonexistent. A few guidelines are followed by the manufacturers
to ensure that operation of their equipment will not be hazardous to the
occupants, but there are few Federal standards existing to control levels
of pollutants emitted into the nonworkplace Indoor environment.
An Ozone Emission Standard"
In the Federal Register, June 27, 1972, the U.S. Department of
Health, Education, and Welfare's Food and Drug Administration published
a proposed standard to control ozone generators and other devices emitting
ozone. This standard later was incorporated into Title 21 CFR, section
801.415, 1972, "Maximum Acceptable Levels of Ozone." This particular stan-
dard has previously been discussed as a maximum allowable indoor air quality
standard, however, it is also important to note that this standard includes
an emission standard which, regulates the amount of ozone any device can pro-
duce. A portion of this standard states that any device will be considered
in violation of the standard 1f it is used
"...in such a manner that it generates ozone at
a level in excess of 0.05 parts per million by
volume of air circulating through the device
...of an enclosed space Intended to be occupied
by people for extended periods of time, e.g.,
houses, apartments, hospitals, and offices."
Clearly, this standard places a numerically limiting value on the
amount of ozone which may be emitted by any ozone generating device. The
purpose of this standard is to prevent ozone exposures from occurring at
levels which could be hazardous to the inhabitants of nonworkplace
Indoor environments. In many mechanical ventilation systems there are
-45-
-------
a number of devices, used to treat indoor air for odors and particulate
pollutants, which inadvertantly produce various quantities of ozone.
The American Society of Heating, Refrigerating and Air Conditioning
Engineers, Inc. recommended that the maximum concentration of ozone in an
air conditioning and ventilating system be 0.05 parts per million in
occupied areas, such as homes and hospitals, where people may be exposed
continuously for up to 24 hours a day (Federal Register 1972). This
recommendation led to the development of the Food and Drug Adminitra-
tion's proposed ozone standard.
BUILDING CODES
The control of indoor air quality is accomplished through the ventila-
tion of air to and from the Indoor space. Control of ventilation rates
for various building types 1s accomplished with regulations established by
building codes. Building codes are considered legal documents controlled
by local and state authorities. They have the force of law and violators
are subject to legal penalties.
Building codes exist in vast numbers across the international scale.
Arthur D. Little, Inc. (1975) points out that in the United States alone
there are approximately 8,000 building codes and regulations. To compli-
cate the problem there exists a lack of uniformity of codes between state
jurisdictions and even more so between local jurisdictions. The need
for greater uniformity in building codes is evident but development of
codes at the national level is nonexistent.
Attempts have been made to create greater uniformity in codes.
Several groups concerned with the building codes have developed model
codes as examples for local and state jurisdictions to follow. The four
model codes in existence today are discussed below.
Model Codes
Attempts to standardize building codes occurred through the develop-
ment of model codes. Model codes allow local jurisdictions to adopt
building codes and standards rather than attempting to create a locally
written code. Adoption of a model code can be obtained through selection
of all or part of any of the four model codes in use today.
1. Basic Building Code (BBC) -
The Basic Building Code was developed 1n 1950 by the Building
Officials and Code Administrators International (BOCA). Use of
this model code is found predominantly in the Mid-West and the
northeastern United States. In respect to Its regulation on
ventilation rates and Indoor air quality, this code has adopted
the ASHRAE Standard 90-75 and ASHRAE Standard 62-73.
-46-
-------
2. Southern Building Code (SBC) -
The Southern Building Code Congress International devel-
oped and issued the SBC model code in 1945. This code is in
use mainly throughout the southern U.S. Regulation of indoor
air quality is achieved with their standard on mechanical ven-
tilation. This standard states that "where ventilation is pro-
vided by mechanical means, fresh air in sufficient quantity to
maintain healthful conditions shall be provided to meet the
requirements of all state laws."
3. National Building Code (NBC) -
This model code was developed by the Engineering and Safety
Service for the American Insurance Association in 1905. This
code has adopted the ventilation requirements from ASHRAE Standard
62-73 but is used primarily as a fire code. General use is in the
northern and eastern states.
4. Uniform Building Code (UBC) -
This code, developed in 1927 by the International Con-
ference of Building Officials, is used primarily in the Moun-
tain, Pacific, and Midwestern states. They are currently
reviewing and updating the sections for ventilation requirements.
Statewide adoption of all or any part of these four model codes is
compiled in the following table obtained from the Office of Housing and
Building Technology at the National Bureau of Standards (1976).
From Table 9 one can see that not all states have adopted the same
model codes. Of the model codes that have been adopted the Basic Build-
ing Code and the Uniform Building Code are most frequently used. Arthur
D. Little, Inc. (1975) notes that the Federal Government, viewing code
variation as a major deterrent to Industrialized building, and therefore,
adding unnecessarily to building cost, is pushing communities, or pre-
ferably states, to adopt one of the model codes with as little modifica-
tion as possible. This is being accomplished through agencies such as
the Department of Housing and Urban Development, the National Bureau of
Standards, and the National Conference of States on Building Codes and
Standards.
A state's decision to adopt a building code is not often easy. The
model codes are not sufficiently different from one another, except for
the National Building Code which is primarily only for fire regulations.
For example, the Office of Housing for the State of Virginia made several
extensive reviews of the three main model codes before they could select
the appropriate one for their state. Recently they adopted as a statewide
code the Basic Building Code for the two following reasons:
-47-
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TABLE 9. STATEWIDE BUILDING CODE PROGRAMS - APPLICATION AND TYPE OF CODES ADOPTED
00
I
A
ST
AL
AK
AZ
AJt
CT
r'L
GA
KI
ID
IL
n
TA
'fS
KY
LA.
1C
HA
1C
1:1
K:
iiv
in
IIP
o:-:
OR
PA
RI
t«n
CD
TX
UT
VT
VA
VA
V.V
HI
HY
. B
APPLICATION
HAN KIN KAX VOL
X X
X X
XXX
X X
XI
X X
X X
' x<
X X
x»
XX X
X X
X> X X
X X
X ' X X
x x x'
XXX
X X
XX X
XXX
XXV
X X
X X
c
LOCAL
YES ST NO
x x'
* X
X X
X X
X X
X X
X X
X X
X X
X X
X X
X X
xt x
X X
X X
X X
7
X X
X X
D
TECHNICAL BASIS (
K3CEL CCCE
BBC UBC SBC KBC
X
X
x
x-
x'
I
X
X
X
X
1
X •
X
x'
I-
X
X
X
I1
x* •
X
y CODE
AWM>
YES NO
X
X
X
X
X
X
X
X
X
X
X
X
X
X
X
X
X
X
X
X
X
STHE
SEP INC
X
xs
X
I
X
X
X
X
ED
YEAR
1970
1973
WY3
1971
1975
1973
1973
197T
1970
197S
1975
1973
1973
1973
1975
1970
1973
1973
1975
1973'
1975
EXPLANATION OP OOUM4 HEALINGS
COL. EXPLANATION
A STANDARD TWO LETTER ABBREVIATION REPRESENTING
T5S 50 STATES
B PREEWTION STATUS OP CCCE. PREEMPTION PEATIRES OP THE "TF
HAY INCUSE:
"MAN" - MANDATORY THCUGHDUT STATE
"HUT1 - KAWWOTY KDHHM THCUGHXn1 STATE
"MAX" - HAIlDATDRr HAXDW THHDUatWT 3TATE
"VOL" - COEE IS VOLU/TAHY ONLY
c Airaewnf c* LOCAL JURisiicnotE TO WBJD STATEWIDE CODE
•YES" - CCtE HAY BE AfGSED BY LOCAL JURISDICTIOKS
"ST" - UJCAL AMMMMTS MOST HAVE SZATE APPREVAL
"NO" - LOCAL AttJOCNES DO NOT NEED STATE APPROVAL
D TEONIQIL BASIS DPOS HUGH STAHHTDE COEE IS ESMBLISHED
"BBC" - BASIC BUHADC OCCE (EOCA)
"IBC" - IHIK») BDILDT« CODE (ICBO)
"SBC" - STMIDARD BUILDDB CODE (SBCC)
"NBC" - HATICIIAL BUnXtDE CODE (AInsA)
AMEffltNT STATUS (ff BASD ON MODEL COEE):
• "YES" - HEEL OOIZ ADOPTED WIB1 TEOMCAL AfBOTSfTS
"NO" - MODEL CODE ADOPTED HTfHJOT TEOffHCAL AKBtt!-B?rS
STjYTg Wll'im CCCE:
"SEP" - COEE PK*UX)ATED AS SEPARATE EOCUe.T
"INC* - SttSE WffTTEH rrff, OR RBaTUXZQN THE REQUIJOEnS
OP UHIC9 ARE INCLUDED AS PART OF TIE STATE BUUDINQ
OCCE.
EOrrJCH CP ADQPin))OOEE3:
•ED YEAR" - EDTTICM YEAR Of COTE, K3EEL OR STATE WROTE!
CUE INDICATED
-------
1. They felt the training program being offered by BOCA was
best suited to adequately prepare their building inspect-
ors for the implementation of the new code.
2. The BBC, as a performance code, was more oriented to the
use of new technologies and materials. This would allow
designers of projects in the State to be more innovative
in the projects.
These are only the feelings of the State of Virginia. Another state
at the same time could use similar reasons to select one of the other
model codes. The important point to note is that the states are looking
for performance codes. That is, in theory, any material can be used as
long as it meets the standard of performance set up for it. This charac-
teristic of model codes makes them easily adoptable because they ar« less
dependent on material resources or climatic conditions in the particular
geographical area adopting the code.
Building Code Enforcement
The Federal Government has very little participation in building
code development but does however Influence code requirements to some
extent by their own acceptance of standards and specifications. Often
Federal specifications are adopted as reference standards in building
codes. But these reference standards, although created from Federal
specifications, are not enforceable by the Federal Government.
Enforcement of building codes is left to the governing body of the
particular jurisdiction which adopts the code. Either the state or any
local governing body, depending on the nature of the adopting agency,
has the power to enforce the codes adopted. In either case there exist
problems with code enforcement.
Arthur D. Little, Inc. (1975) points out that experience with state
codes has shown that, because of resource limitations, enforcement of
state codes is weak. Substantial financial resources are the main
requirement, together with the commitment by state code officials to use
these monies for the recruitment, effective training and deployment of
sufficient manpower to do an adequate job of enforcement. But how much
manpower is sufficient and how much money would be required, especially
for the residential sector, remains an unanswered question.
Even with sufficient manpower and effective training a problem still
exists with effective field enforcement. Enforcement at the design level
is easily handled with design inspections and the issuing of building
permits. Compliance of design with the local authorities building code
is a requirement for building permit approval. Field inspections on the
other hand are accomplished with on-site inspections by officials of the
local authority before occupancy permits are granted. These inspections
-49-
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are performed during the construction stage to ensure compliance with
the already approved building specifications. If necessary penalties are
imposed during the construction stage and mandatory compliance with the
approved design specifications are enforced.
With respect to indoor air quality, building code enforcement has
been negligible to compliance with indoor air quality requirements,
partly because of the lack of sufficient standards. Enforcement of codes
that have adopted ASHRAE Standards 90-75 or 62-73, which'have established
allowable limits for indoor air, still show a failure to'"comply-with the
standards of the code.
Arthur D. Little, Inc. (1975) points out some of the problems in
complying with indoor air quality standards. The perspective performance
approach of ASHRAE 90-75 includes air quality requirements only by
reference to ASHRAE 62-73. These requirements could be overlooked by
designers or even by inspectors. Those who study the requirements thor-
oughly might not comply adequately because the requirements are confusing,
controversial, and possibly not feasible. Feasibility Issues noted by
Arthur D. Little, Inc. are as follows:
© Purification of Recirculated Air - The technical feasibility
of purifying recirculated air as specified in ASHRAE 62-73
has been demonstrated for particulate pollutants, but not
for all gaseous pollutants (especially long-term operation
and maintenance). The economics of achieving the latter
are also uncertain.
o Air Quality Monitoring - Sampling and analysis of ventilation
air as required by ASHRAE 62-73 where there is "reasonable
expectation that air quality is unacceptable." In many
cases, however, methods of sampling and analysis are either
not specified, not sensitive enough, or possibly too costly.
To ensure that compliance to building code standards on indoor air
quality is occurring, an additional step in the building inspection
procedures must be performed. Inspection of a building in stagnant state
just after construction will not give an accurate picture of the levels
of indoor pollutants. A follow-up inspection at a sufficient length of
time after the building operation has obtained a "normal" state should
be performed to ensure that building ventilation is in compliance with
standards. However, this poses another problem with enforcement. How
will enforcement be carried out for a building already in operation?
It would be economically unfeasible to tear down and replace equipment.
Also, imposing penalties would be unfair since the specifications
originally approved were the criteria the building was to meet.
Solution to problems of enforcement often rests on the development
of the standards themselves. Building code standards must be practical
in order that enforcement and compliance can be effectively handled but
they must also be receptive to the occupants to ensure their health,
safety and well-being.
-50-
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SECTION 5
INDOOR AIR QUALITY STANDARDS ABROAD
INTRODUCTION
The most widely used indoor air quality standard in the United States
is the one incorporated in the American Society of Heating, Refrigerating
and Air Conditioning Engineers (ASHRAE) Standard 62-73. In an effort
to determine whether other indoor air quality standards were in use in
other countries, we queried environmental officials 1n some 50 countries
and provinces abroad, as listed in Appendix C. An assembly of numerical
air quality management standards of the world, including the United States,
by Martin and Stern (1974) is referenced in the bibliography. Tables
provided by Martin and Stern list emission standards, air quality stan-
dards and point of impingement on ground-level standards. The World
Environmental Directory (1975) was used for the names and addresses of
organizations abroad which were contacted by GEOMET, with the added pro-
vision that queries were also addressed to all those countries listed
by Martin and Stern as having air quality management standards.
MAXIMUM ALLOWABLE INDOOR AIR QUALITY STANDARDS ABROAD
In their response to us, environmental officials 1n Australia,
Denmark, France, Hong Kong, Israel, Japan, Mexico, Poland, Singapore,
South Africa, Sweden, Yugoslavia, and several Canadian Provinces stated
that no indoor air quality standards for nonworkplace air exist or are
proposed for use in their countries. However, the majority of the
responses did note that their countries had developed standards for out-
side ambient air pollutants and many others associated.with occupational
exposures. Several officials commented that they felt these standards,
established to protect the safety of employees in the workplace as well
as the general public, would be applicable to residential Indoor envir-
onment should circumstances arise that require the establishment of
Indoor air quality standards.
The Canadian Approach
The Canadian Department of Fisheries and the Environment, which is
responsible for the Canadian Clean Air Act, has jurisdiction over ambient
outdoor air quality, but the-£Stabl1shment of occupational and indoor
air standards is delegated largely to the Canadian provinces. With;
the Clean A1r Act the federal government has the authority to set National
Air Quality Objectives at three levels: "Desirable," "Acceptable," and
"Tolerable." Dr. V. C. Armstrong (1977) with the Canadian Department of
Health and Welfare, Environmental Standards Division notes that "These
levels are not legally enforceable standards. Provisions under the Clean
Air Act exist to set enforceable National Emission Standards where there
is a significant danger to health."
-51-
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Part IV of the Canada Labour Code does however give the federal
government some power to control health hazards associated with work-
places falling under federal jurisdiction, but this covers only about
750,000 workers (Armstrong 1977). Other Canadian workers are protected
under standards adopted by the provincial authorities. The occupational
standards used by the federal government and provinces are the Threshold
Limit Values published by the American Conference of Governmental Indus-
trial Hygienists. However, the Canadian Government and most provinces
have no minimum acceptable, nonoccupational, indoor air quality stan-
dards.
South Africa's Best Practicable Means Approach
The Republic of South Africa informed us that a committee function-
ing under the auspices of the National Environmental Programme of the
Council for Scientific and Industrial Research (CSIR), Pretoria, was
recently established to deal with indoor environmental problems. CSIR is
mostly concerned with research on the Indoor environment with regard to
thermal, acoustic, and lighting aspects and does not really deal with
Indoor air pollution. There are no fixed standards laid down for indoor
air pollution in nonindustrial environments in South Africa. It is
generally considered that the quality of the air indoors must be fairly
s1m1liar to that outdoors, especially in a country like South Africa
which uses natural ventilation as a rule. However, the Department of
Health's Chief A1r Pollution Control Officer, who 1s responsible for
outdoor air pollution, uses the best practicable means approach, follow-
ing the British model, to set acceptable levels of outdoor ambient air
quality.
Japan's Environmental Codes
The Environmental Agency of Japan responded to the indoor air quality
survey by stating they had no appropriate information concerning nonwork-
place indoor air pollution regulations. However, the National Technical
Information Service (1974) published two abstracts of Japanese documents
which described "1974 Japanese building environment codes." The two
environmental codes, as translated in the abstracts, specified standards
for dusts (0.15 yg/m3), carbon monoxide (less than 10 ppm) and carbon
dioxide (less than 1000 ppm). Averaging times for these pollutants were
not included in the abstracts though both abstracts mention that the
code includes a list of maximum allowable concentration "limits" for
50 toxic substances.
Sweden's Formadelhyde Standard
Dr. Ib Anderson et al. (1974) from the Institute of Hygiene, Univer-
sity of Aarhus in Denmark, monitored 23 single-family Danish homes to
determine the formaIdehude content of the indoor atmospheres. They
suspected that the formaldehyde-urea glue used in the manufacturing of
particle board was releasing formaldehydes into the living environments.
Measured formaldehyde concentrations in the indoor atmosphere of the homes
-52-
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averaged 0.62 inii/ni air- with a range from 0.08 to 2.24 mg/ni air. Con-
centrations in two rooms were higher than the permitted upper values
for workroom air (1.2 mg/m3) and in 17 rooms the values were higher than
a calculated value for long-term exposure (0.04 mg/m3). All the measured.,
values were higher than the recommended values for outdoor air (0.03 mg/m ).
From this research Dr. Anderson and his colleagues (1977) suggested a
threshold limit value for formaldehyde in dwellings at 0.04 mg/m3. Recently,
Sweden has adopted this value as a. maximum allowable indoor air quality
standard. Prior to this, the Swedish standard had been 3 mg/m3, the same
as the TLV used by the ACGIH. Denmark has used this same research to
develop an indoor air quality emissions standard which will be discussed
later in this section.
DESIGN-LEVEL INDOOR AIR QUALITY STANDARDS ABROAD
Responses that we have received show that there are few countries with
standards to regulate the quality of indoor air. Some countries, however,
responded positively to our request with regulations for design-level
standards. These regulations exist in building codes and attempt to con-
trol indoor air quality through minimum levels of ventilation rates.
Scotland Ventilation Requirements
The Scottish Development Department of Scotland, sent us the Build-
ing Standards Regulation 1971 (Scotland Consolidation) in response to
our letter. The definition used in this document for mechanical ventila-
tion is "a system of ventilation operated by a power driven mechanism which
causes a change of air between any part of the interior of a building and
the external air." This standard establishes requirements for which fresh
outdoor air must be supplied by the mechanical ventilation system to the
occupied indoor space. However, they note a concern for energy conserva-
tion by. urging the use of natural ventilation. From the regulation they
point out that:
"1) Every house, whether or not it forms only part of a building,
shall be so constructed as to have at least two external walls,
being either -
a) on opposite sides of the house, or
b) adjacent to each other, so, that the
relevant area in the house, or if the house
contains more than one story, 1n each story,
shall not be less than one-third of the floor
area of the house, or of that story.
"2) In each of these walls there shall be a window or ventilator
from an apartment, kitchen, passage, stairway or landing to
the external air, such window or ventilator having an opening
area of 0.1 square metre.
-53-
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"3) Nothing in this regulation shall apply to a house in which
there is installed a system of mechanical ventilation which -
a) will provide a supply of fresh air 1n each
apartment in the house and in the kitchen
b) is so designed that air is fed directly into
any part of the house from any kitchen,
bathroom or water closet, and
c) is designed so as to be capable of continuous
operation."
Ventilation Requirements of the Institution of Heating and
Ventilating Engineers of London, England
The Chartered Institution of Building Services (formerly, The
Institution of Heating and Ventilating Engineers) of London, England
sent us a document entitled IHVE Guide B2 - Ventilation and Air Condi-
tioning Requirements 1976. This document discusses the need for venti- ;
lation by establishing three main functions of a ventilating system,
which are:
a) provision of a continuous supply of oxygen for breathing
b) removal of products of respiration and occupation
c) removal of artificial contaminants produced within the
ventilated space by process work, cooking, etc.
Design-level standards for minimum and recommended ventilation rates
are presented as either outdoor air supply rates or as a number of air
changes per hour for building type. The ventilation requirement for out-
door air supply in the IHVE Guide is as follows:
"...the necessary outdoor air supply per person need be only
1.0 litre/s to prevent the C02 produced by respiration from
increasing the C02 concentration in the space beyond the
threshold limit value. However, the minimum outdoor air
supply required to dilute the odours created by occupation
to an acceptable level is a more significant factor as
illustrated in Table B2.1.
"In instances where rooms or enclosures are to be provided
with a supply of outdoor air by means of an air conditioning
system, the rates should be as listed in Table B2.4."
-54-
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'Table B2.I. Minimum ventilation rates where density of
occupation Is known.
Air ipacti
per person
(m')
3
6
9
12
Outdoor air fuppljr per pnsoo
(Urre/«)
Minimum
11-3
7-1
5-2
4-0
Recommended minima
Smoking not Smoking
permitted permitted
17-0 22-6
10-7 14-2
7-8 10-4
6-0 8-0
The statutory minimum volume per person in factories and
offices is 11-5 m3. The corresponding minimum outdoor air
supply is 4-27 litre/s per person.
' Table B2.4. Recommended outdoor air supply rates for
air condition-id spaces.
Typo of »pace
Factories*t
Offices (open plan)
Shops, department stores
and supermarkets
Theatres*
Dance Halls*
Hotel bedroomst
Laboratories!
Offices (private)
Residences (average)
Restaurants (cafeteria)tt
Cocktail bars
Conference rooms
(average)
Residences (luxury)
Restaurants (dining
rooms)!
Board rooms, executive
offices and conference
rooms
Corridors
Kitchens (domestic)!
Kitchens (restaurant)!
Toilets*
Smoking
None
Some
Some
Some
Some
Heavy
Some
Heavy
Heavy
Some
Heavy
Some
Heavy
Heavy
Very
heavy
Outdoor air iiipply
(litre/i)
Recom-
mended
Per
penoa
8
12
18
25
Minimum
(Tike greater ol two)
Per Per m1
penoa floor area
08
1-3
5
3-0
1-7
8 KJ
12 ~
18 6-0
A per capita basis is . Q.Q
not appropriate to these jo-O
spaces. ,0.0
Notts:
* See statutory requirements and local bye-laws.
t Rate of extract may be over-riding factor.
J Where queueing occurs in the space, the seating capacity
may not be the appropriate total occupancy.
1 For hospital wards, operating theatres see Department of
Health and Social Security Building Notes.
2 The outdoor air supply rates given take account of the
likely density of occupation and the type and amount of
smoking." .
-55-
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Some of the ventilation rates given as air changes per hour for
various building types from the IHVE Guide are shown in Table B2.2.
"Table B2. 2. Mechanical ventilation rates for various types of building
Room or building
Boilerhouses and engine rooms
Banking halls
Bathrooms, Internal
Canteens
Cinemas
Dance halls
Dining and banqueting halls,
restaurants
Garages, public (parking)
repair shops
Kitchens, hotel and industrial
Laboratories
Laundries
Recommended
air change rates*
(h-1)
15-30
6
6t
8-12 f
6-10 +
10-12 *
10-15 *
6t minimum
lOt minimum
20-60 t
4-6
10-15
Room or building
Lavatories and toilets, internal
Libraries, public book stacks
Offices, internal
Sculleries and wash-ups, large scale
Smoking rooms
Swimming baths: bath hall
changing areas
Theatres
Recommended
air change rates*
(h-1)
6-8 t
3-4*
4-6*
10-15 t
10-15
10
6-10 *
Notes:
* The recommended air change rates do not apply in cases of warm-air heating, when the rate may be
dictated by the heat requirements of the building or room.
T Refers to extract ventilation.
* The supply air at the recommended rate will not necessarily be all outdoor air; the required quantity
of outdoor air must be checked against the number of occupants at a desirable rate per person."
The standards used by Scotland and England are design-level standards
for the ventilation of indoor air. They attempt to improve indoor air
quality through the introduction of outdoor air. However, these standards
lack quantitative values for the quality of the outdoor air being used as
the supply air in the ventilation system. They do attempt to classify
the supply air qualitatively through language such as "fresh outdoor air."
This sort of qualitative standard may be sufficient 1f the main concern
for the indoor environment is to supply oxygen and reduce odors. If
concerns are more for the health and safety of the occupant then quantita-
tive standards must be used to regulate the pollutant concentrations in
the supply air of ventilating systems.
-56-
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Denmark's Ventilation Requirements
Dr. Andersen (1977) of the Institute of Hygiene, University of Aarhus
in Denmark, notes that "By demonstrations of the high indoor concentra-
tions of several airborne pollutants we have been able to change a new
law, where the natural ventilation in buildings was set to a maximum of
0.3 air changes per hour. The reason for this low air change was energy
conservation consideration." This particular standard apparently estab-
lishes a maximum allowable limit for air leakage within a single struc-
ture.
Canadian National Building Code
The 1975 National Building Code of Canada under Section 3.6, Health
Requirements, has developed a design-level standard to limit the maximum
concentration of carbon monoxide in enclosed storage garages. The code
adopted the American Conference of Governmental Industrial Hygienists1
(ACGIH) recommended maximum allowable concentration for carbon monoxide.
Under Subsection 3.6.3.4, "Ventilation," the standard states,
"(l)...An enclosed storage garage and repair areas in a garage
shall have a mechanical ventilation system designed to limit
the maximum concentration of carbon monoxide at any time to
not more than 100 parts per million parts of air for periods
longer than one hour with a maximum concentration at any time
of not more than 400 parts of carbon monoxide per million parts
of air when measured between 3 ft (0.9 m) and 4 ft (1.2 m from
the floor.
"(2) The requirements in Sentence (1) is considered to be
met by a system designed to provide a continuous supply of
fresh air at a rate equal to at least 0.75 cu ft of air
per^minute for each square foot of floor area.
"(3) Mechanical ventilation systems provided in accordance
with Sentence (1) shall include automatic ventilating fan
control by means of 'approved1 carbon monoxide monitoring
devices, or by other 'approved' means located so as to pro-
vide full protection for the occupancy."
This standard is not one that attempts to place restrictions on auto
manufacturers but places the burden on manufacturers of mechanical ventila-
tion systems. Mechanical ventilation systems must be developed that will
incorporate carbon monoxide monitoring devices and ensure automatic oper-
ation to regulate the levels of CO within the maximum allowable limits.
-57-
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Winnipeg Carbon Monoxide Standard
The Department of Mines, Resources and Environmental Management of
the Province of Manitoba supplied us with information on the city of
Winnipeg Building By-Law No. 740/74. Winnipeg's building code has adopted
the same requirements for maximum allowable concentrations of carbon mon-
oxide in enclosed garages as published in the 1975 National. Building Code.
As before, the maximum allowable concentration for carbon monoxide is the
same as the threshold limit values published by the American Conference of
Governmental Industrial Hygienists.
INDOOR AIR QUALITY EMISSION STANDARDS ABROAD
Canadian Standards Associations Ozone Standard
Electrical Bulletin No. 750B published by the Canadian Standards
Association in 1970 was designed to regulate the control of ozone emis-
sions in the air of enclosed spaces used by people. This standard restricts
manufacturers from marketing devices that produce ozone in concentrations
greater than that described in the standard below.
"1) Devices for houshold use shall not produce a concentration of ozone exceeding 0.04 parts
per million (by volume) when tested according to the procedure described below.
The test room shall be approximately 7 feet by 7 feet by 7 feet, without windows but
with a conventional door frame 6 feet 6 inches high, 32 inches wide, set in a frame with
a gap around the door of approximately 1/8 inch nt top nnd sides and 1/4 inch at the
bottom. The device shall be placed centrally within 6 inches of the wall opposite the
door and about 30 Inches above the floor. The device shall be operated from a 125 volt,
60 cycle source If the unit Is Intended for use on a nominal 120 volt system or 250 volts
if the unit is intended for use on a nominal 240 volt system. If the output is adjustable
it shall be set for maximum output. The emission of ozone shall be monitored over a
7 hour period to determine the sustained concentration. Measurements shall be made
at a point 30 inches above the floor midway between the device and the opposite wall.
To measure the concentration a "Drager" multi-gas detector and ozone detector tubes
marked "0. 05/a ozone" will be used.
"2) All devices producing a concentration greater than that described in (1) above shall
be deemed to be for industrial and other supervised usages. "
It is important to note that this standard attempts to regulate the
maximum ozone concentration for the indoor space of nonworkplace environ-
ments. Although not establishing a quantitative value for maximum allow-
able indoor concentrations, this standard does specify limits on the
levels of ozone which can be produced under controlled laboratory situa-
tions. The Canadian Standards Association has developed an emission
standard, if with which manufacturers of ozone-producing devices comply,
will protect the health of inhabitants in enclosed indoor environments.
-58-
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Denmark Formaldehyde Emission Standard
As discussed previously in Section 5.2 Dr. Ib Andersen et al. (1974)
performed an extensive monitoring program to determine the level of for-
maldehydes in single-family Danish homes. From their investigations it
was found that levels exceeded what was generally accepted as safe occupa-
tional exposure levels as we-1-1'as calculated values-for long term exposures.
From their research Sweden adopted a maximum allowable indoor concentra-
tion standard. Based on conclusions from the same study Denmark decided
to control formaldehyde levels in indoor environments with the development
of an emission standard. In the same communication Dr. Andersen (1977)
noted that "...we in Denmark have forced industry to decrease the formal-
dehyde concentration in chipboard." By reduction of formaldehyde concen-
trations in chipboard, Denmark hopes to achieve a healthy, safe indoor
environment in Danish dwellings.
-59-
-------
SECTION 6
BIBLIOGRAPHY
American Conference of Governmental Industrial Hygienists. 1971.
Threshold Ltmtt Values of Airborne Contaminants. Cincinnati: American
Conference of Governmental Industrial Hygienists.
American Conference of Governmental Industrial Hygienists. 1975. TLV's
for Chemical Substances and Physical Agents in the Workroom Environment
with Iritended Changes for 1975. Cincinnati: American of Government
Industrial Hygienists.
American Conference of Governmental Industrial Hygienists. 1976.
'Documentation of the Threshold Limit Values for Substances in Workroom
Air, 3rd ed., 3rd printing.Cincinnati:American Conference of
Governmental Industrial Hygienists.
American Insurance Association. 1976. The National Building Code - 1976
Edition. New York, New York.
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APPENDIX A
HEALTH CRITERIA FOR INDOOR AIR POLLUTION
This Appendix describes the results of a literature search and
appraisal of the health effects of the commonly occurring indoor air pol-
lutants, as reported in the scientific literature, with a particular
effort to identify those health effects relevant to the levels of pollu-
tant concentrations and exposure which might be expected in residential
and other nonworkplace indoor environments. Most of the applicable stud-
ies have dealt with ambient and workplace air pollution; we have neces-
sarily drawn heavily upon these peripherally relevant studies for lack
of work specifically directed to the indoor residential context.
The health effects of air pollutants are discussed under the follow-
ing headings.
1. Sulfur Oxides
2. Carbon Monoxides
3. Carbon Dioxides
4. Nitrogen Oxides
5. Photochemical Oxidants
6. Organic Pollutants
7. Particulates
8. Air Pollution and Cancer
9. Susceptibility of Population Subgroups to Indoor Air Pollution
10. Interactive Air Pollution Effects.
Finally, there is attached a bibliography of research into indoor
air pollution health effects.
SULFUR DIOXIDES
The principal sulfur oxide of interest in health effects studies has
been sulfur dioxide (SOp) but sulfate ion (SO.), occurring as a component
of sulfuric acid or its salts (sulfates), has also been extensively stud-
ied. Sulfur dioxide may be converted to sulfate ion (among other reac-
tions) in chemical transformations which can take place in ambient air or
on surfaces with which SOp comes into contact.
The considerable body of research reviewed as background for setting
a National Ambient Air Quality Standard for SOp linked ambient concen-
trations with human effects ranging from reduced respiratory function to
increased mortality from a variety of causes (Stern et al. 1973). Research
used as reference data in defining the SOp standards is summarized in
Figure A-l. In Figure A-l, the vertical scale at the left shows levels
of ambient SOp concentration, over annual or 24-hour exposure periods,
with which the corresponding health effects were associated. Because the
adverse effects demonstrated in these studies were considered to represent
-65-
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ug/mj ppro
6000
5000
4000 -
3000 -
2000
1SOO
1000 -
900
<300
700
«00
300 -
300 -
200
ISO
100
90
80
70
60
50
40
5000 ng/m3 (Z ppm) NIOSH Roaommondad SOj randud
2.00 In woriooom all (U. S. HEW 1974)
4000 ug/m3 (1.34 ppm) Maximum daily SOJ concentration la Oacomtaor 1952
London unag apicods w/4SOOu g/m3 nnoka.
A bant 4000 enc«m death! (Wllklan 19S4)
-1.U3
0. SO 1500 ug/m3 SO2 (24-hi average) w/6 Coh. Ingeaiod Morality (Groanbarg et aL 1962)
-0.40
0.30
'0.20
•0. IS
0.10
0.09
O.OS
-0.07
0.00
-O.OS
-0.04
-0.03
-0.02
71SU g/m3 SOj (24-hr moan) w/730u g/m3 rmoka. lacranod Dally D«ath Raw (Uwit«r 1963)
715 ^ 2/n)3 502 (24-or moon) w/panicuiflt<»Sh*ni RlM ia IUa»ti fat TTtoM w/BroBchitij (Canow at %!• 1968)
SO] (24-B? raonn) tr/400ug/m' onoka. SymotBini Won«n tot Oaoolc Broacfaldi PMltnB
(Uwtox 19S8)
SOOus/n*3 SOj (24-hr mean) w/ tow partculnto. Incraimd MorHilHy Rate (B«M»t «c »L 1967)
300-500 us/ns3 SO2 (26-Kt nicflB) w/10w putlcaiflto. IncruQMtl HoiPiBii Emifilff^i fl
36S u g/m1 SO; - MAAQS far SO; (24-hr majdmnm)
from WotK (8mm «t »L 1967)
10S-26S
SO2 (oanual mooa) w
imoko. Incroaj<^R<»a|gtpaTy SVTPOTOIM and
Inn Plnnm /Ba*rf'" at tt 1966)
120 u g/m3 SO? (annual moaal w/ 100 ug/m3 nnoke. Incraamd Praqu«ncv and Saverltv of '.
Ropignonr PiaoM in School Children
111 u g/m3 SO2 (
at al. 1967)
l moan) w/160 ug/m3 imoko. Increnad MortaUtr (torn Bronehltl» and Um« Otncar
(Wlckaa and Buck, 1964)
80 ua/m3 SO 2 - NAAQS for SO2 (anmul uitnmodc main)
FlguTOA-1. Roforonea data far offoeo of rolfur dloxido axpotun*.
-66-
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the possible combined effects of sulfur oxides and particulate matter,
Figure A-l also shows parenthetically the corresponding levels of smoke,
coefficient of haze (Coh), or particulates measured in these studies. The
studies reviewed in the preparation of the NAAQS criteria for SCL, dis-
cussed below, clearly indicated the hazard of both peak and long-term
exposures to SCL when it is accompanied by elevated concentrations of par-
ticulate matter. However, the role of SO- alone in causing adverse effects
at the NAAQS levels was not established.
Figure A-l displays the health effects of SO,, concentrations sum-
marized in the conclusion of the Air Quality Criteria for Sulfur Oxides
(USHEW 1969). The source of the data used in this summary is cited and
shown in parentheses. It can be seen from Figure A-l that the 24-hour
maximum National Ambient Air Quality Standard for sulfur dioxide was prin-
cipally based upon the extensive work of Brasser et al. (1967). Brasser
et al. reviewed in detail seven air pollution episodes in London and Rot-
terdam. Here, a 24-hour mean concentration of 500 yg/m S0? lasted for
three to four days leading to increases in total mortality Tn the number
of hospital admissions for respiratory tract irritation, especially in
older persons, and in job absenteeism. Brasser et al. point out:
"From investigations at Rotterdam, indications have
been obtained that there exists a positive association with
the total mortality if the value of 500 yg/m per 24 hours is
surpassed for a few days. Perhaps this effect begins to be
active at lower concentrations already present. There is a
faint indication that this will happen somewhere between 300
and 500 yg SO,, per 24 hours."
Although the particulate levels in Rotterdam are historically low,
there were no measurements of particulates taken during the Rotterdam epi-
sode studied by Brasser et al. Joosting (1967), however, has character-
ized the ratio of these particulates to S0? concentrations in Rotterdam
as from 1:3 to 1:4.
Recognizing the importance of knowing more precisely the Rotterdam
particulate levels during this episode the U.S. Environmental Protection
Agency used a statistical estimating technique to predict that the three
to four day levels were between 125 and 166 ug/m and the three to four
day average S02 concentrations were 288 yg/m (Neuberger and Radford 1974).
Dr. K. Biersteker (1977) of the Department of Environmental Health and
Tropical Health with the Agricultural University in the Netherlands inter-
prets the findings from the Rotterdam data differently. He notes that the
original report of the Rotterdam study was his doctoral thesis published
in 1966. From his analysis Dr. Biersteker concluded that:
"There was only a statistically significant effect on
hospital admissions for elderly persons during the December
1962 air pollution episode, during which SOp levels (24 hours)
-67-
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were 500+ yg/m for 3 days. The black soot concentrations reached a
level of 500 yg/m on the worst of the 3 days in December (24 hrs.
avg.)."
London fog episodes during the 1950's and early 1960's have been studied
and reviewed by numerous authors (Brasser et al. 1967, Martin and Bradley
1960, Lawther 1963, Joosting 1967, Gore and Shaddick 1958, Burgess and
Shaddick 1959). Generally the high concentrations of S02 were accompanied
by high concentrations of smoke and soot. Lawther's (1958) analysis of the
mortality studies during the 1958-1959 London episodes places the mortality
"effect" at about 715 yg/m for SOp and 750 yg/m for smoke. Joosting
(1967) reports, however, significant correlations between maximum sulfur -
dioxide concentrations and death and disease at a range of 400 to 500 g/m
SOp accompanied with high soot concentration. Martin's (1964) review of
the same episode showed similar S02 concentrations and health effect data
as that of Joosting (1967) including SO,, concentrations ranging upward from
about 400 g/m accompanied by smoke concentrations upwind from 500 g/m .
Specific types of morbidity reported, in general, point to the accentuation
of symptoms of those with chronic lung diseases particularly those with
bronchitis.
Studies of episodes in the United States have demonstrated similar
findings insofar as identifying the populations most susceptible to high
concentrations of S02 and their effects. Carnow et al. (1968) studied
over 500 patients with respiratory disease in Chicago during the winter
of 1966-1967 and found a marked increase in the rate of illness for patients
exposed to 24-hour average S02 concentrations of 715 yg/m or more.
Additionally for patients over 55 years of age with severe chronic bronchitis,
a significant association was found between the level of pollution and per-
cent of person-days of illness. Unfortunately, however, there were no
measures of particulate nor any information concerning the patients' occu-
pational or smoking histories or socioeconomic variable which could pos-
sibly modify the results of the study.
Greenberg et al. (1962) and McCarrol and Bradley (1966) reviewed pol-
lutant concentrations and excess mortality and morbidity during several
episodes in New York City. Greenberg et al. (1962) observed that both
mortality and morbidity reported as clinic visits for upper respiratory
infections and cardiac illness, increased in relation to increases in S02
concentrations and smoke, as measured by the coefficient of haze. During
a severe episode during the Thanksgiving weekend, November 23*25, 1966,
the 24-hour S02 concentrations were 1460, 1344, and 1175 yg/m on
each of the three days. Associated smoke was in excess of 6 Coh units.
Similar to data reported in London, high particulate concentrations
were reported accompanying high S0? concentrations in the various studies
reviewed by NAPCA (USHEW 1969) which were conducted in New York City and
elsewhere in the United States. However, the sulfur dioxide and partic-
ulate concentrations for which a more definite relationship to mortality
-68-
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and morbidity were associated was higher than those in London and Rotter-
dam. As criteria for a short-term standard, the concentrations of SCL of
300 to 500 ug/m associated with increased hospital admissions of older
persons for irritations of the upper respiratory tract, and absenteeism
from work were of great significance to determining a threshold on a
short-term or 24-hour basis.
The association of longer term sulfur dioxide concentrations with
various forms of respiratory morbidity led to the setting of the annual
S02 standard of 80 ug/m • Of particular importance is the extensive
work in Genoa, Italy by Petrilli and his coworkers. Petrilli et al. (1966)
showed an increase in the prevalence of chronic cough, sputum production, and
upper respiratory tract infections among nonsmoking housewives above 65 years
of age. The study also showed a significant correlation between the annual
mean of sulfur dioxide levels and chronic bronchitis. Of particular signifi-
cance was the differences in respiratory disease between areas with an annual
SOp mean concentration of 105 ug/m and one of 80 ug/m .
The thresholds for irritant effects of S02 and sulfuric acid have
been reported as 1600-2600 ug/m and 600-850 ug/m , respectively by
Bushtueva (USHEW 1969). Administration of the two agents together produced
these changes at a substantially lower threshold and Bushtueva considered the
effects of the combinations to be additive. Other stidies reviewed by NAPCA
(USHEW 1969) indicated that measurable respiratory function changes occurred
at levels over 3000 ug/m (1.2 ppm) for SOp and over 350 ug/m for sulfuric
acid mist, with associated exposure times of 30 and 15 minutes, respectively.
NAPCA considered that several important toxicological findings were derived
from their review:
• Sulfuric acid aerosol is a considerably more potent irri-
tant than S0? with effects more pronounced at particle
sizes of 3 uMMD or less and particle sizes of less than
1 uMMD were more effective at lower doses.
• Sulfuric acid mist is considerably more irritative than
dry sulfate particles, indicating a more pronounced effect
under conditions of high humidity.
© While SOj is absorbed in the upper respiratory passages
and significant protection is provided by nose-breathing,
80 percent or more (by weight) of ambient suspended sul-
fates may be less than 2 uMMD in diameter and penetrate
deeply into the respiratory system.
o SOp inhibits respiratory clearance through reduced ciliary
action and mucus removal, but at very high concentrations.
® The effects of sulfur oxides are, for the most part,
related to irritation of the respiratory system.
The apparent minimal effects of S02 at usual ambient levels, the potency
of sulfates and sulfuric acid, and the interaction of S0? and particulates
relate to a number of unresolved issues.
-69-
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In many epidemiological studies where SO,, has shown significant
association with health effects, correlations with participate concentra-
tions (variously measured as particulates, smoke or soiling) have been
found. A number of investigations have reported a direct association
between the concentration of suspended sulfates and the health effects
(Winkelstein et al. 1968; Zeidberg et al. 1964, 1967; Hagstrom et al.
1967; Sprey and Takacs 1974).
Studies by Sprey and Takacs (1974) are interesting in that while
there is no evidence of an increase in the incidence of carcinoma associ-
ated with exposure to concentrations of S02 alone, there was an increase
in mortality from cancer of various types frespiratory, gastrointestinal,
urologic) when elevated SCL concentrations were associated with elevated
sulfate levels. Winkelstefn and Gay (1971) found a graded positive asso-
ciation between suspended particulates and cirrhosis of the liver. Some
correlation of SOp with mortality from respiratory and cardiovascular
disease was present but strongest associations were found when elevated
particulate or soiling levels were also present. The Sprey and Takacs
(1974) data revealed a positive correlation between mortality from arterio-
sclerotic heart disease, and neoplasms of the respiratory and gastrointestinal
tracts, with increased sulfate levels. Winkelstein et al. (1968) using
sulfur oxides as the pollution measure, found a positive association between
sulfation and chronic respiratory disease mortality.
While the results of these studies were not consistent among age,
sex and socioeconomic groups, and other factors could have been involved
(smoking habits were not measured), presumptive evidence is offered on
several points.
1. Sulfates are involved in disease production beyond the cardio-
pulmonary system, perhaps by reaction of S02 with metals or other
particulates.
2. Although respiratory system cancer was found, primary bron-
chiogenic cancer was not. This may be due to the high solubility of
the sulfates, and their rapid clearance to the blood, lymph, and
gastrointestinal compartments. This is consistent with findings of
the prominent effects of sulfur oxides occurring in the higher res-
piratory passages.
3. While S0? may serve as a proxy measure, direct sulfate mea-
surement seems a more appropriate indicator of the potential hazard
involved.
Early studies by Schimmel and Greenberg (1972) and Buechley et al.
(1973) demonstrated an increased daily mortality in the New York metro-
politan region with the higher than usual S0? levels. However, Schimmel
and Greenberg concluded that 80 percent of tne excess was attributable to
smoke and only 20 percent to SO,. In a recent revaluation of their data,
Schimmel and Murawski (1975) ana Buechley (1975) reached the conclusion that
SO- was a proxy for some other factor. Schimmel and Murawski (1975)
-70-
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indicate the data suggest "that S02 is not only serving as an indicator of
air quality but also that S02 is not an injurious pollutant, at least at
the ambient levels encountered in New York City in the late 1960's - namely,
average levels of 525 ug/m and peak levels of 1575 ug/m ."
Finklea and his colleagues (USEPA 1974) analyzed data from CHESS and
presented evidence that adverse respiratory effects in the human are asso-
ciated with sulfates, independent of S02 and other suspended particulates.
In the case of asthma attacks, response to sulfate levels varied with tem-
perature - the attack rate substantially increasing at lower sulfate levels
when the temperature was above 50°F. For the series of responses analyzed
in these studies, "best judgement" estimates of combined pollutant thresh-
olds were made for adverse effects of long- and short-term exposures.
These are included in Table A-l. The authors consider that suspended sul-
fates have been identified as a pollutant of present concern but that there
are many unresolved issues pertinent to establishing standards and control
measures. These include better understanding of the environmental reac-
tions and chemical makeup of sulfates and the biological response to sul-
fates (USEPA 1974).
TABLE A-l. BEST JUDGMENT ESTIMATES OF POLLUTANT THRESHOLDS FOR SULFUR
OXIDES AND SUSPENDED PARTICULATES (USEPA 1974)
Leaa-Tm^ EKieti (Aaaoal Ara^io. up/m3)
• laentud pnviUnea of etaiaole braachitlj
la ^iJMitt
• laowMd lowo tMplxamy dlMtu la
• locruud fnquaacy of icuc* ropiruoiy
Hltiitr la »««»tii..
• DwrmMd luaf taaeOm of ehildxu
Sbatt-Torm Ufora (2Hlll'i J'R/'ffl3,1
• AggrrrutOB of eadlapulataaaiy
(ymptnau la •Id*rt7
• Agftiruioo of uthBU
SO,
95
95
100
200
>3«S
1SO-2SO
Tout
Pudculatt*
100
102
131
too
10.100
70
Siop«ad«d
SuUuu
IS
IS
IS
13
S-10
3-10
In addition to the potentiating effect of S02 in air that also con-
tains significant concentrations of particulates fsulfates, nitrates, heavy
metals, etc.) there is evidence that other factors, such as the relative
humidity, have an influence on the functional effects of SOp (Davies 1961).
Guinea pigs were exposed .to 1 ppm of sulfur dioxide and 1 ug/m of sodium
chloride aerosol. At low humidity (< 40 percent), the aerosolwas a crys-
tal and at high humidity (> 80 percent), a droplet. Increased flow resist-
ance and decreased pulmonary compliance were only noted at high relative
humidity.
-71-
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It is postulated that the highly soluble SCL was absorbed into the
droplets prior to inhalation, with the secondary formation of sulfurous
acid and a lowering of pH. It is not clear whether the described changes
in respiratory mechanics were related to: the acidity; the hydrogen sul-
fite (HSOZ), the sulfite ion (SOp, or to transport of SCL to
lower airways by the aerosol.
It is of interest at this point to note that the Threshold Limit
Value (TLV) established for SCL by the American Conference of Govern-
mental Industrial Hygienists (T976) is at the high level of 5 parts per
million (ppm), approximately 13,000 ug/m . Studies with human.subjects
cited in the Documentation of Threshold Limit Values (1971) indicate the
following effects of S0? with increasing concentration:
3-5 ppm - Noticable odor
8-12 ppm - Irritation of the mucous membranes, i.e., nose,
eyes, etc.
13 ppm - Increased airway resistance
150 ppm - Increased incidence of respiratory disease,
hospitalization, deaths from all causes, etc.
These are considerably higher thresholds than those reported in the NAPCA
data. TLVs are established for use in industrial contexts and are not
necessarily applicable to the nonworkplace environment in which exposures
may be of much greater duration and in which particularly susceptible popu-
lations of children, ill and elderly people may be found. The principal
reasons for this discrepancy may lie in the sources of health effects data
examined by the two groups. Epidemiological data examined by NAPCA was
exlusively studies of the effects of concentrations of sulfur dioxide in
conjuction with high concentrations of particulate. However, the ACGIH
committee concerned itself more with the toxlcological effects of S02
concentrations above. One study cited by the ACGIH committee was observa-
tions made by the Michigan Division of Occupational Health where definite
symptoms of discomfort and upper respiratory irritation among working popu-
lations was associated with exposures to 10 ppm S0?. The symptoms disap-
peared at 5 ppm S02 (ACGIH 1971).
Wolff et al. (1975) subjected healthy humans to concentrations to 5 ppm
of S02 and found a slight decrease in the maximal midexpiratory flow rate
but no significant effect on mucociliary clearance.
The TLV of sulfuric acid is 1 yg/m3 (ACGIH 1976) since above this
level it causes respiratory irritation and over prolonged periods, dental
injury. In a study by Admur et al. (1952) in which normal human subjects
were exposed to the inhalation of sulfuric acid mist for 5-15 minutes,
concentrations below 1 ug/m could3not be detected by odor, taste or irri- 3
tation. A concentration of 3 mg/m was noticed by most subjects, and 5 mg/m
resulted in irritation of the respiratory tract. Raule (1954) noted that
workers chronically exposed to H2$0. may show lesions of the skin,
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tracheobronchitis, stomatitis, conjuctivitis and gastritis. There is also
evidence that chronic exposure causes corrosion of dental enamel.
Concern with adverse effects of sulfate aerosols is strengthened
by results of studies by Admur and Corn (1963) and Davies (1961) which
revealed a significant increase in pulmonary airflow resistance in guinea
pigs exposed to sulfuric acid droplets and particles of zinc ammonium sul-
fate, zinc sulfate, and ammonium sulfate.
In the light of the various reports of concentration levels at which
sulfur dioxide is associated with adverse health effects, it is appropri-
ate to recapitulate here some of the evidence for the existence of ele-
vated SCL concentrations in indoor, nonworkplace environments. The highest
24-hour s09 concentrations found indoors have been on the order of 850
ug/nT (Weatherly 1966) and 1300 ug/nr (Kruglikova and Efimova 1958)
found in Moscow and^London, respectively. In Cincinnati indoor concentrations
as high as 500 ug/m were reported (Shepard et al. 1960). In studies
conducted in Hartford, Connecticut, seasonal averages of SOx concentrations
were found as high as 182 yg/m (Yocum, Cote and Clink 19697. Information
on indoor sulfate and sulfuric acid concentrations in nonindustrial envi-
ronments is not yet available. Though S02 concentrations have been shown
to be lower indoors than outdoors, the mechanism for SOp depletion may
be a cause for concern since the process involves the oxidation of SOp to
sulfates with potential hydration to form acid mists.
In summary, the combination of atmospheric sulfur oxide, its conver-
sion products, and suspended particulates, appears to present a clear
health hazard at commonly realized ambient levels, although the role of
sulfur dioxide alone has not been clearly established except at signifi-
cantly higher concentrations. If recent work is correct, sulfates pre-
sent a greater health hazard than S02. There is evidence that chronic
exposure to sulfates may produce serious extrapulmonary effects, particularly
neoplasms in the body systems involved in clearance.
Sulfates which tend toward micron- and submicron-sized aerosols may
be important indoor pollutants. While S02 is reactive and may pose an
indoor problem, it tends to disappear quite rapidly (Cox and Penkett 1972).
Suspended sulfates may remain at levels more equal to outside ambient lev-
els and therefore present a more persistent hazard. Further research is
indicated on the issues of chemical composition and concentration of indoor
sulfates, and the human clearance of sulfates.
CARBON MONOXIDE
Carbon monoxide (CO) has been the most extensively studied of all
pollutants in terms of toxicologlcal aspects and this research seems to
be continuing to a greater degree than for any other pollutant. The major
aspect of the present interest is 1n effects on the cardiovascular sys-
tem and the brain. Because the characteristics of CO health effects are
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so generally known, only a brief summary of salient points will be included
here.
While in some respects CO concentrations indoors are similar to those
of SOp, there is an important difference. CO is relatively unreactive
and decays slowly, compared with SOp. Since it is also generated!ndoors
(from gas-fired appliances, leaky fnrnaces and chimneys, and from attached
garages), it is an extremely important indoor pollutant.
Carbon monoxide is rapidly lethal at concentrations over 1000 ppm,
when the blood carboxyhemoglobin (COHb) exceeds 50 percent. It exerts
its effect by binding more strongly to hemoglobin than oxygen and interfering
with oxygen delivery both by displacing oxygen and making oxygen delibery in
the tissues more difficult. Because the heart and brain have high metabolic
needs and limited blood flow, they are most at risk if oxygen delivery is
compromised by carbon monoxide. The effects of concentrations of carbon
monoxide on the brain have been studied using psychological or behavioral
tests to determine the lowest level of carboxyhemoglobin at which central
nervous system effects become measurable. Once an appropriate threshold level
for the percent of COHb is determined, mathematical techniques exist to
convert this concentration of COHb to 1- and 8-hour ambient concentrations in
air required to produce it, as was done in criteria documents for carbon
monoxide and the setting of carbon monoxide standards (Neuberger and Radford
1974).
3
The TLV for carbon monoxide is 50 ppm (approximately 55 mg/m ) (ACGIH
1976). The inhalation of carbon monoxide, a colorless, odorless gas of
specific gravity similar to that of air, causes asphyxiation (anoxia hyp-
oxia) by forming metastable chemical compounds, primarily with hemoglobin
and secondarily, with other biochemical constituents which in a complex
manner reduces the availability of oxygen for other cellular systems of the
body. The resulting physiologic effect is similar to, but in some respects
more serious, than a simple lack of oxygen caused by a reduced partial
pressure in inspired air.
The equilibrium concentration of carbon monoxide with the hemoglobin
of the blood is substantially complete for individuals at work in 6 to 8
hours (ACGIH 1976). When the air contains 100 ppm of CO, the blood at
equilibrium will contain 18-20 percent of carboxyhemoglobin (COHb); if air
has 50 ppm CO, blood will have 8-10 percent COHb; for air of 25-30 ppm CO,
there will be a 4-5 percent COHb.
The effect of carbon monoxide exposure on man is enhanced by factors
such as heavy labor, high environmental temperature, and increasing alti-
tude (above 2000 feet). Susceptibility is greatest in the aged, the very
young, those with cardiac or chronic respiratory disease, and with preg-
nancy (Handbook of Medical Physiology 1961). However, some individuals,
particularly cigarette smokers, have an increased tolerance of CO. The
latter may tolerate COHb values of 5-10 percent (with its appreciable
chemical effect) as compared to nonexposed adults.
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Approximate relationships between ambient CO concentrations, the
percent of COHb in the blood, and the resultant symptoms are as follows
(USHEW 1972, Forbes 1972):
COHb Concentrations -
Atmospheric CO (ppm) (Percent) Principal Symptoms
10-30 2.5-5 Encroachment on
functional reserve
of heart and brain
50 7-8 Slight heachache in
some
100 12-15 Moderate headache
and dizziness
250 25 Severe headache and
dizziness
500 45 Nausea, headache,
possible collapse
1,000 50-60 Coma
10,000 95 Death
An ad hoc committee, established in 1972 by the Bureau of Community
Environmental Management, reviewed the effects of CO on human health with
the specific objective of developing recommendations for residential stan-
dards. They concluded that continuous exposure should not exceed 15 ppm
(resulting in about 2.6 percent COHb at equilibrium in nonsmokers). This
level was considered to allow for both the higher CO concentration toler-
ance of smokers and the increased susceptibility of cardiac patients. Con-
sidering the ambient standard to be 9 ppm for 8 hours, indoor concentrations
should not be allowed to raise the baseline air content by more than 6 ppm.
For comparison, 15 ppm has also been proposed as the short-term public limit
by the National Academy of Sciences for a 4 to 5 hour exposure, 3 to 4 days
per month (USEPA 1972, NationalResearch Council 1972).
Stewart (1974) recently reviewed evidence pertaining to the effects of
low CO concentrations on man. CO is eliminated nearly completely by the
lungs. In healthy, sedentary adults at sea level the biological half life is
4 to 5 hours; this time increases with altitude. Increased blood flow, to
compensate for oxygen reduction, is noted at 1-5 percent COHb and may be
significant for those with substantially impaired cardiac reserve. Reduction
in exercise tolerance is noted in normal individuals, and less exertion is
required to produce anginal pain in cardiacs at 5-9 percent COHb. Above this
level of COHb, definite symptoms and neurological changes are observed and
increased mortality in those with severe cardiac disease is possible. For
reference, exposure of a sedentary adult with normal physiology and under
standard conditions of 50 ppm CO for 5 hours would raise COHb to about 5
percent.
A study of the possible correlation of ambient CO concentrations and
the incidence of myocardial infarction and sudden death in Baltimore (Kuller
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et al. 1975) did not support other evidence that CO exposure was a major
factor. The risk of sudden death was higher in smokers than nonsmokers, and
those who had formerly resided in high ambient CO areas had higher post-mortem
COHb levels. The authors postulated that there may be a time lag between ah
increase in ambient CO concentrations and its deleterious effect in the
human. Kuller et al. (1974) did not find marked differences in post-mortem
COHb levels in individuals with and without acute coronary lesions, nor were
COHb levels related to the degree of coronary stenosis. Radford and Weisfeldt
(1975) studied hospital admissions for chest pain and concluded that the
clinical source and severity of infarction among smokers was consistent with
both an arute and a chronic effect of CO exposure. However, other constituents
of cigarette smoke may be of equal or greater importance. Both the Kuller
and Radford reports emphasized the difficulty in establishing the independent
roles of environmental CO and smoking in any study of the low-level effects
of CO. While neurological and cardiac lesions have been attributed to
chronic CO exposure by some, the majority of investigators have not reported
such pathological changes.
Figure A-2 shows the relations between concentration levels of CO and
associated health effects as shown in the summary of the air quality cri-
teria document for carbon monoxide (USHEW 1970). For reference, various
existing and proposed standards for carbon monoxide are also shown.
The special hazards of carbon monoxide in indoor environments are
widely known. Studies have shown indoor concentrations of carbon mon-
oxide at potentially hazardous levels to be a frequent occurrence. The
impact of tobacco smoke on indoor CO levels has been often cited (Bridge
and Corn 1972, Stewart 1974, Russel et al. 1973, Harke 1970, Arnow et al.
1974). Internal combustion engines as sources of indoor CO produced symp-
toms of drowsiness, headache and nausea in school children which led teams
of investigators to monitor for carbon monoxide in school buses and ice-
skating rinks (Johnson et al. 1975, Koch 1976). Radford (1973) reported
1 percent of the sample of 302 old houses in Baltimore as having carbon
monoxide levels greater than 50 ppm, attributed to faulty indoor combus-
tion sources. Biersteker et al. (1965) and Yocom et al. (1970) found sim-
ilar faulty combustion sources in a small percent of the samples surveyed.
These findings are of particular concern if extrapolated to a large popu-
lation using stoves, heating systems and space heaters of which even a
small percentage is faulty.
CARBON DIOXIDE
Carbon dioxide, while not normally considered a hazardous constituent
of the air (with a normal ambient concentration above 325 ppm (Seinfeld
1975)), under certain unusual circumstances can be present in the indoor
environment in asphyxiating concentrations. There have been a number of
instances reported, usually occupational in nature, where C02 has caused
fatalities. The normal symptoms of excessive COp exposure as reported by
Hamilton and Hardy (1974) are attributable to oxygen deprivation. These
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CO
mg/m3 ppm
200
150
_ 200 (High concentrations 30-120 sec) Physiological stress on heart patients.
5% COHb (Ayres et al. 1969}
150
100
90
80
70
60
50
40
30
20
IS
10
100 115
20
15
10
— mg/m (100 ppm) (Introduced intermittently through a face mask)
Impairment in performance of some psyehomotor tests. 5% COHb (Schulte 1963)
90
30
70
60
50 TLV for CO (7-8 hr) 55 mg/m3 (50 ppm) (nonsmokers for 90 min) impairment
of time interval discrimination about 2.5% COHb (Beard and Wertheim 1967)
40
NAAQS for CO (1 hr) (40 mg/m3) 35 ppm NIOSH recommendation tor OSHA
standard 40% COHb in excess of 5%
35 mg/m (30 ppm) (nonsmokers 8-12 hrs) Equilibrium value of 5% COHb.
80% is reached in 4 hrs or 4% COHb. Verifies formulas used for estimating
equilibrium values of COHb after exposure to Low concentrations of CO (Smith 1968)
(17 mg/m3) 15 ppm recommended limit for community residents by ad hoc committee
on carbon monoxide poisoning associated with 2.6% COHb (USEPA 1972)
(17.3 mg/m3) 15 ppm NAS/NRC Committee on toxicology recommended short-term
public exposure limit for 4-5 hrs, 3-4 Jays/month.
(12-17 mg/m ) 10-15 ppm exposure of 8 or more hours produces a 2.0-2.5% COHb in
nonsmokers (USHEW 1970)
(10 mg/m3) 9 ppm NAAQS for CO (8 hrs)
1.15 mg/m3 CO = 1 ppm (vol)
Figure A-2. Reference data.for effects of carbon monoxide exposures.
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authors also state that "unconsciousness and death do not occur unless
oxygen is as low as 5 percent - unless the victim makes strenuous exer-
tion, in which case death may come while there is still 8 percent oxygen."
Carbon dioxide has been reported to be a " weak narcotic at 30,000 ppm
...at 50,000 ppm, a 30-minute exposure produces signs of intoxication,
and at 70,000 to 100,000 ppm, unconsciousness in a few minutes." The
Threshold Limit Value (TLV) has been set at 5,000 ppm for an 8-hour expo-
sure (ACGIH 1976). The personnel of a submarine experienced chronic
fatigue when COp levels reached 3 to 15 percent (30,000 to 150,000 ppm)
for several weeKs (LaVerne et al. 1973). In the same report, LaVerne and
coworkers state that C0~ is easily "eliminated from the body and brain
by reflex hyperventilatfon within seconds after treatment, thereby pre-
venting cumulative toxic side effects."
Carbon dioxide has been used in varying concentrations for many dif-
ferent therapeutic reasons for almost 50 years. COp is a cerebrovascu-
lar dilator and respiratory stimulant and has been used in the fields of
pediatrics and geriatrics as well as for the treatment of narcotic addic-
tion and alcoholism (Hamilton and Hardy 1974).
The normal ambient concentration of COp is approximately 325 ppm.
Ishido (1965) has found indoor concentrations of COp ranging from 1 to 10
times the outdoor concentration. Therefore the COp comprised from 0.03
to 0.32 percent (300 to 3200 ppm) of the indoor air. Although these con-
centrations are not as high as the TLV of 5,000 ppm, the potential expo-
sure could be for longer periods of time than the 8 hours that the TLVs
are based upon. Therefore, as stated by LaVerne et al., "it appears that
COp inhalation, whether therapeutic or nontherapeutic can be as safe or
as dangerous as the conditions created in each specific situation."
NITROGEN OXIDES
The pollutants of concern among the nitrogen oxides are nitrogen diox-
ide (NOp), nitric oxide (NO) and nitric acid and acid salts (nitrates).
Nitric oxide (NO) peak ambient levels are not generally considered to pre-
sent a direct health hazard; the greatest toxic potential of NO at these
concentrations is related to its tendency to undergo oxidation to nitro-
gen dioxide (USHEW 1971). The evidence for respiratory disease associated
with NOp is cited below. Nitrogen oxide reaction products have been asso-
ciated with equipment corrosion but biological effects are generally not
well-researched. As contrasted with sulfates, nitrates appear to have a
more uniform particle size distribution and the proportion available as
respirable aerosols (< 3.5u ) may be smaller (Stern et al. 1973).
Few toxicological or epidemiological studies of atmospheric nitrogen
oxides are available. Figure A-3 indicates the parameters used to estab-
lish the National Ambient Air Quality Standards by NAPCA (USHEW 1971).
The original study reported reduced respiratory function in children, and
increased respiratory illness among families, in the high NOp area (Shy
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NO,
Ug/m-
ppm
(2 hr at 20,200-94,000 Ug/m3)
tissue changes in lungs, heart, kidney,
etc. - Monkeys
5000 -
(3 wks) polycythemia - Rats, Monkeys - - 2.0
(Life) epithelial changes - Rats
(1 hi) changes lung collagen - Rabbits, 2000
(Life) bronchiolar hypertrophy - Rats
1000 - - 0.5
(4 hr) changes in lung mast cells - Rats
alveolar distension Mice
(4 hr/day) changes lung collagen - 500 -
Rabbits
(10 min) increased airway resistance
1.0
(21-48 hr) visible leaf damage in sensitive
vegetation
(35 days) naval orange leaf abcission
- 0.4
- 0.3
I- 0.2
Human olfactory threshold
200 + 0.1 (2-3 yrs) increased respiratory disease
(2-3 yrs) increased bronchitis in children
100 -1- NAAOS (annual average) 100 Pg/m3 (0.05 ppm)
Figure A-3. Reference data for effects of nitrogen dioxide exposure
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et al. (1970a). Because the originial aerometric data were considered
unreliable, N0? data for the previous year were used in a subsequent
analysis by Shy et al. (1973) providing similar results at slightly different
concentrations. Subsequent studies of the same Chattanooga areas were
conducted by Pearlman et al „ (1971) and Chapman et al. (1973). Pearlman and
coworkers (1971) reported an increased incidence of bronchitis among school
children in the defined high and intermediate NCL areas after two and three
years of residence. No significant difference was found in the incidence of
croup or pneumonia, or in reported hospitalization for lower respiratory
tract illness. Chapman and coworkers (1973) found no association between
current or past pollution levels and the prevalence of chronic respiratory
disease among parents of high school students residing in the three areas.
The original study of Shy and his associates was criticized by Warner
and Stevens (1973) because no attempt was made to control for acid mists,
which were probably present in significanct concentrations. Pearlman et
al. (1971) in their retrospective study found that for the intermediate and
high N02 areas, suspended nitrates ranged from 2.6 to 5.8 ug/m (24-hour
mean over a six-month period). It is interesting to note that bronchitis
prevalence was not related linearly to any of the pollutant measures, and
that there could have been different contributions of pollutants in the
various residential areas.
From a review of (unpublished) data produced in subsequent epidemic-
logical studies of Chattanooga, Riggan (1976) has proposed that "repeated
short-term exposures of 228-815 ug/m N02 may contribute to excess risk of
acute respiratory disease in the absence of excessive long-term exposures."
He points to the work of Coffin and Gardner (1972) in which rates were
challenged with bacilli after varying NCL exposures. This study showed
that in short-term exposure to NCL, the concentration employed has a much
greater influence than the duration of the exposure, for equivalent expo-
sures (i.e., for equal products of concentration and time). Other work
(Coffin et al. 1975, Gardner et al. 1971) using an infectivity model in
experimental animals, indicates that exposure to NCu and CL may decrease
resistance to respiratory infection via destructive action on pulmonary
alveolar macrophages - i.e., reduction in number, in phagocytic competence,
in viability and enzymatic function. However, since the effect of a single
dose of an oxidant on the macrophages is known to last approximately 24
hours (until they are replaced), the authors suggest that additional fac-
tors which enhance pulmonary infectivity are present - particularly with
intermittent exposure to NCL.
French (1975) after reviewing published and unpublished data from the
Chattanooga studies, concludes that the findings suggest:
1. Exposure to prolonged levels of nitrogen dioxide, ranging from
113 to 395 ug/m , in combination with short-term exposures of 301 to 1203
yg/m may contribute to excess risk of acute respiratory disease and the
residual effects from this exposure may last for as long as four years.
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2. Repeated short-term exposures of 228 to 815 yg/m may contribute
to excess risk of acute respiratory disease in the absence of excessive
long-term exposures.
3. Prior high short-term and long-term exposures to NOp, coupled
with continuous excessive shortrterm exposures, might trigger the onset
of chronic respiratory disease symptoms.
Riggan (1976) has developed a protocol for the prospective study of
acute respiratory disease and its variation related to peak hourly and
daily exposures of NOp and other pollutants. The study will be con-
ducted in several locations in the Los Angeles basin to provide controls
and a variety of pollutant combinations, including oxidants and sulfur
oxides. Data collection was scheduled to begin in late 1976, with a pre-
liminary report expected by February 1978.
The TLV established for N02 by the American Conference of Governmental
Industrial Hygienists is 5 ppm fapproximately 9 mg/m ) (ACGIH 1976). This
ceiling was to some extent established to minimize the risk of acccelerating
lung tumor development.
The TLV for nitric acid is 2 ppm (approximately 5 mg/m ) (ACGIH 1976).
in practice HNCk is usually found in conjunction with nitrogen dioxide.
According to Fafrhall (1957) continued exposure to the vapor mist of nitric
acid may result in chronic bronchitis and more severe exposure, to chemical
pneumonitis. It may also erode the dental enamel (Lynch and Bell 1947).
Two recent studies which suggest a statistical association between
mortality and exposure to nitrogen oxides have been identified. Sprey
and Takacs (1974) in analyzing data for 42 cities, found a strong asso-
ciation between NOp and median disease-specific mortality rates for hyper-
tensive and arteriosclerotic heart disease, and for lung cancer. There
was a fairly linear relationship for each cause of death for NOp levels,
increasing from 0.03 to 0.8 ppm. Analysis of pooled variables and of
independent age groups, subsequently showed arteriosclerotic heart disease
to be associated with an interrelationship of NOp and ambient sulfate
levels. (Because of the strong involvement of smoking in pulmonary car-
cinogenesis, discussion of air pollution and lung cancer is considered
in more detail later.) In a similar type of investigation, Lave and Ses-
kin (1976) have reported an association between nitric oxide (NO) levels
and daily mortality in Chicago (Hershaft et al. 1976).
Much about the mechanisms and degree of nitrogen oxide effects is
not well understood. Although apparently less acutely toxic than ozone,
NOp is considered to have more similarities with 03 than S02 in terms
of biological actions. Avaido and Salem (1968) point out tnat S02 and
S03 are believed to exert their primary effects on airways while NOp and
03 exert their primary effects on pulmonary capillaries. A difference in
solubility is possible one reason, with the relatively insoluble N09 and
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0- able to penetrate deeply Into the lung without appreciable loss 1n
Inspired concentration. Stoklnger and Coffin (1968) have listed a number of
apparent analogies and dissimilarities in actions of NOp and CL. Among
differences cited are the high threshold of acute lung response, the relatively
low toxicity, and the short-acting tolerance of NOp. Most animal studies
and observations on human responses to peak exposures have been at concentra-
tions far exceeding typical ambient levels. It is understood that chamber
experiments are now being conducted by EPA which will include NOp alone and
in combinations with other major pollutants. With the limited epidemiological
research, little information is available on sensitivity differentials
presumably those groups mentioned for SOp would also be sensitive to NOp.
It has been reported that nitrogen oxides can result 1n increased methefnoglobin
so that anemics may be more susceptible. This effect may be due to the
formation of organic nitrates (obtained by combining the NCL group with an
organic radical )which are transformed into nitrates in the Dody. This
promotes the formation of methemoglobin.*
Seinfeld (1975) his stated that NOp is transformed in the lungs to
nitrosamines, some of which are suspected human carcinogens. Johnson
(1972) has suggested that nitrous oxide (N^O), if metabolized, could pro-
vide the nitrating source for nitrosamine formation in gastric juice or
other acid substances in the body. He points out that there are many sec-
ondary amines in our diet (e.g., proline) and in tobacco smoke (e.g., pyr-
rol i dine), of which some nitrosamine forms have been shown to be potent
carcinogens in various animal systems. Johnson hypothesizes that this
mechanism may be the causative agent in excess cancer mortality among anes-
thesiologists.
The hazard to human health from nitrogen oxides in indoor air may be
assessed in the light of reported indoor concentrations. Peak one-hour
average concentrations of NOp have been found in kitchens during gas
appliance operations to range between 450 and 950 ug/m (Eaton et al.
1973, Elkins et al. 1974, Hollowell et al. 1976). Peak concentrations of
N09 less than one hour in duration, have been reported as high as 1900
ug/m (1 ppm) (Eaton et al. 1973) and 2800 yg/nT (1.5 ppm) (Hollowell et
al. 1976). These values cannot be readily compared with the criteria which
established the National Ambient Air Quality Standard (NAAQS) for NOp since
the reference data were concerned with chronic respiratory illnesses!
These indoor NOp data, however, may be compared with recent conclusions
regarding short-term NOp exposures reported by Riggan (1976) and French
(1975). On reviewing tne earlier NO, health effects criteria, principally
the Chattanooga study, the authors or those studies report that repeated
short-term exposures to NOp contribute to an excess risk of acute respir-
atory disease 1n the absence of excessive long-term exposure. Riggan^pro-
posed a range of short-term exposures to NOp between 228 and 815 vg/m .
The range of high one-hour average NOp concentrations reported in kitchens
* Occupational Health and Safety, International Labor Office, Geneva, Switzerland, 1972.
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where gas-fired appliances are in operation, as summarized above, are
within this range of potential risk to acute respiratory disease. Although
a survey by the American Gas Institute does not lend support to this rela-
tionship, the AGI investigators did not monitor N02 in the homes where
the survey was conducted.
Two studies have compared the incidence of reported respiratory ill-
ness in households cooking with gas and electricity. Eaton et al. (1973)
found an association with the use of gas stoves but Keller et al. (1975)
could determine no significant difference among households. Further field
studies to determine short-term NCL exposure and effects are required
particularly in homes using gas-fired appliances. Additionally, nitric
acid, nitrate, and nitrosamine concentrations should be monitored. Studies
of the blood level concentrations of methemoglobin of residents of homes
with and without gas-fired appliances is also indicated.
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PHOTOCHEMICAL OXIDANTS
This section covers oxidants (excepting NC^) that result from photo-
chemical atmospheric reactions and their precursor gaseous hydrocarbons.
The principal individual compounds in this class of primary interest as
potential hazards to human health at ambient levels are:
o Ozone ((L)
o Peroxyacetyl nitrates - peroxyacetyl nitrate (PAN)
and peroxybenzoyl nitrate (PBzN)
o Aldenhydes - formaldehyde (HCHO) and acrolein
(CH2:CHCHO).
Ozone and PAN are secondary pollutants in the ambient air, typically
arising from interactions of automobile-generated hydrocarbons and NO
emissions in the presence of sunlight. Ozone does not usually originate
in significant quantities in indoor environments. Ozone and PAN are
highly reactive and, like SO^ do not persist in high concentrations
indoors even when outdoor concentrations are high, because of rapid decay
through absorption on indoor surfaces.
Many other organic conversion compounds are known or are hypothesized
to exist in polluted air (e.g., organic peroxides, ketones) but not at
concentrations for which effects on man have been documented. Similarly,
many individual hydrocarb ons have been identified in polluted air which
are biologically active but human responses have not been found below
concentrations of several hundred ppm. The precursor ambient gaseous
hydrocarbons are considered important only as an index of potential photo-
chemical conversion (USHEW 1970). However, before these low-concentration
pollutants are dismissed, two points concerning their toxicity should be
made. First, the hazard from possible cumulative effects of repeated
exposures at ambient levels is unknown. It has been demonstrated that
repeated sublethal doses (one-fifth LDrQ) of hydrogen peroxide can result
in a cumulative effect and eventually death in experimental animals
(Stokinger and Coffin 1968). Second, many of these chemicals or their
homologs are components of household and industrial products which are
used in concentrations within the toxic range. Hazards from vapors and
aerosols generated by the use of such agents will be taken up in subse-
quent sections.
Ozone has been found to be the major component of observed ambient
levels of the photochemical oxidants and therefore is used as the standard
in the measurement of total oxidants. For this reason, oxidants and
ozone are frequently used interchangeably in exposure-response studies,
although varying concentration of other oxidants with different biological
actions may be present. The national standard for ambient ozone and oxi-
dants' is the same.
Figure A-4 presents the data base used in development of air quality
criteria for ozone and oxidants by NAPCA (USHEW 1970). Because of its
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Oxtdant
20 jig/m' Ozone • 0.01 ppm (vol)
(Daily maximum) respiratory problems
(Peak rallies) eye Irritation
(1 hr) Impaired athlete performance
(4 hr) Vegetation damage
n1) Ozone
4000 (2 hr) Reduced VC, severe cough, In-
ability to concentrate
3000
- 2000
(2 hr) Impaired diffusion capacity (DLCO)
— 1000 (3 hr/day) Changes in pulmonary (unction
- 800
— 600 (8 hr) Respiratory irritation and chest
constriction
— 400
(8 hr) Small decrements In VC, FRC,
TLV (8-hr) 200 u»/mj
— 200 ( 1 hr) Uciwud tirwty raiiuac*
NAAQS (or photochemical oxidaao, IMug/m1
>- 100
-80
- 60 (8 hr) Vegetation damage
(1 hr) Crocking of'stretched rubber, odor
"- 40 detection In 5 m in
Figure A-4. Reference data for health effects of photochemical oxidant exposure.
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relative toxicity, the one-hour standard for oxidants is about one-fourth
that of $62 and one-third of the California standard for N02 (0.25 ppm,
one hour). The standard was based in part on evidence reported by Schoettlin
and Landau (1961) where increased asthma attacks in some asthmatic subjects
were reported when estimated hourly average concentrations of photochemical
oxidant reached 200 yg/m3 (0.10 ppm). Sterling et al. (1969) found a signi-
ficant correlation between the concentration of ambient oxidants and hospi-
tal admissions for cardiovascular and respiratory conditions. However,
they also noted similar strong associations for 502, NO?, and particulate
matter. Data analyzed by Wayne and Wehrle (1969) showed no significant
association between oxidant levels and school absenteeism due to respira-
tory illness.
According to Griswald et al. (1957) ozone exposures for two hours at
an average concentration of 1.5 ppm Oo resulted in a 20 percent reduction
of the timed vital capacity. In addition to its more serious effects,
air concentrations of ozone in excess of a few tenths ppm cause headache
and dryness of mucous membranes in exposed individuals (Wilska 1951).
After review of the research and industrial health experience up to 1964
(Stokinger 1965), it was pointed out that 03 is radiomimetic and thus with
continuous exposure (eight hours daily) to concentrations not acutely
injurious per se, may be associated with premature aging and a shortened
life span.
Hammer et al. (1965) compared the daily percent of nursing students
reporting each of several symptoms with the daily maximum concentration of
oxidants. Patterns for several of the symptoms, particularly eye discom-
fort, conformed with oxidant levels. Further analysis of the symptom data
by Hammer and his coworkers (1974) showed that incidence could not be
attributed to carbon monoxide, nitrogen dioxide, or elevated temperature.
The investigators developed oxidant thresholds for several symptoms:
eye discomfort (0.15 ppm); cough (0.26 ppm); chest discomfort (0.30 ppm);
and headache (0.50 ppm). A TLV for ozone established by the American
Conference of Governmental Industrial Hygienists (1976) is 0.1 ppm (approxi-
mately 200 yg/m3).
Symptoms at various oxidant concentrations can be compared with
results found in chamber studies. As a recent example, Hackney et al.
(1975) conducted a series of experiments with adult male volunteers who
were subjected to short-duration (two and four hours) exposures to various
levels of ozone. While the findings are too complex to cover fully,
selected results are summarized in Table A-2.
Reactive (sensitive) subjects, as defined by history or testing,
developed such severe symptoms after exposure to 60 pphm for four hours,
that subsequent exposure was shortened to two hours, even though normal
subjects reported few symptoms. At 37 pphm (two hours), symptoms in
some reactive subjects were more severe than at 50 pphm (two hours),
but respiratory system changes were less marked. Normal subjects
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exhibited few important symptoms or signs at any level, for either time
duration, or with various pollutant mixes. Oxidative blood changes were
found in reactive subjects at 37 and 50 pphm, and increased erythrocyte
fragility at 50 pphm. The decrements in pulmonary function at 37 pphm
(two hours) are similar to those reported by Bates et al. (1972) and
Hazucha et al. (1973, 1974). PAN has been reported to approach eye irri-
tation threshold at a concentration of 0.05 ppm in 12 minutes and an
increased oxygen uptake (during exercise) resulted at a concentration of
0.3 ppm (Stokinger and Coffin 1968). Formaldehyde is known to induce
hypersensitivity and to depress ciliary activity. The irritation threshold
of mucous membranes for formaldehyde has been reported to be between 0.01
and 1.0 ppm; for acrolein as low as 0.25 ppm. As these agents are not
consistently proportional to ozone it may be suitable to investigate their
irritant properties separately under ambient conditions. No information
was identified on long-term, low concentration effects of these agents.
TABLE A-2. EFFECTS OF. CONTROLLED OZONE EXPOSURE ON ADULT MALES (HACKNEY ET AL. 1975)
Croup
#1- Normal
#2 - Reactive
#3 > Normal
Reactive
#4 - On* Normal,
Five Reactive
£5 - Mixed
One Reactive
O3 (pphm)
30-SO
25
37
SO
50
25**
37
Duration
(Hours)
4
2
2
4-»2
2
2
2
Respiratory
Physiology
Few changes
One measure
Mild
Marked
Few or none
Marked (2nd
day)
Few or son*
None impor-
tant
Marked
Symptoms
Few
Nona
Sever*
Marked
Few or none
Marked
None
Marked
Blood
Biochemistry
NR
NR
•
Oxidative chaegea
Erythrocyta fra-
gility
Few or none
Oxidative change*
Oxidative changes
*03, O3 + NO2 and 03 + NOz + CO
** 03 +• NO2 * CO
NR Not Repotted
A survey of the origins and consequences of atmospheric pollution by
vapor-phase organic pollutants published in 1976 by the National Research
Council notes that the photochemical reaction products of organic pollu-
tants present potential hazards of mutagenicity as well as the unfavorable
health effects of ozone, lachrymaters such as PAN and PBzN, and the alde-
hydes (NRC 1976).
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The hazard to human health from ozone in indoor concentrations may be
assessed by comparing the results of these health effect studies to the.
levels of ozone which researchers have reported inside buildings. Indoor
one hour ozone and oxidant concentrations have been reported to range as
high as 300 to 500 yg/nH (14-16 pphm) in a surgical intensive care unit
(Thompson 1971). The buildings where ozone or oxidant values were reported
in this range were reasonably well ventilated. Inside ozone or oxidant
values in residential buildings and schools were between 50 to 80 percent
of those found outdoors (Shair and Heitner 1974, Thompson 1971, Thompson
et al. 1973). In comparison with ozone criteria associated with adverse
health effects (Figure A-4), these values are in excess of those associ-
ated with eye irritation and increased airway resistance. However, the
relative indoor-outdoor relationship indicates that significant pollution
for ambient levels may be achieved in air conditioned buildings.
Further investigation of the effects of ozone and other oxidants is
indicated in the following areas:
• The synergistic health effects of oxidants in the
presence of particulates, sulfates, and nitrates
o The long-term effects on those chronically exposed
to typical ambient levels.
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ORGANIC POLLUTANTS
The term "organic pollutants" as used here refers principally to
the diverse class of manufacturers of organic chemicals which may enter
the air (1) in the vapor or liquid phase of aerosol spray operation,
(2) through vaporization from the surface of liquid solvents, fuels,
household cleaners and similar products, or (3) as a residual dust from
pesticide use. Organic pollutants also include complex aldehydes which
may arise from cooking operations. The term "organic pollutants" in
this context does not include the photochemical oxidahts which have been
considered earlier, nor does it include the biological and allergenic
materials which have not been examined in this report.
These nonphotochemical organic air pollutants do not fit neatly
into categories of gases and particulates. They may occur in both phases,
even simultaneously in the case of aerosol sprays. As particulates they
may be in the form of liquid droplets in an aerosol or as solid particles
for some pesticides.
Organics are contained in a wide variety of products used in homes,
offices, and schools. They may be present in either the active ingredients
or the propel 1 ants of packaged aerosol sprays, as well as being used directly
in liquid applications. Many of them contain chlorine, bromine, or fluorine,
forming a general class known as halogenated hydrocarbons. These substances
in general can cause liver and respiratory system pathology and are neuro-
toxic. Several (carbon tetrachloride, trichlorethylene, chloroform, vinyl
chloride) have produced cancer in animals. The degree of toxicity of the
organics varies considerably. The discussion of health effects of organic
pollutants may be somewhat arbitrarily considered under headings of solvents
and fuels, aerosol propellants, and pesticides and combination of pollutants.
Solvents and Fuels
One of the major sources of exposure to toxic chemicals in indoor
spaces is through the endless variety of products used as fuels, cleaners,
paint and paint products, laundry products and hobby materials. Other
than their use as fuels (propane, butane, gasoline, kerosene, etc.), most
of these chemicals are used directly as solvents (degreasers, paint removers)
or are solvent components of compounds (paint thinners, kitchen and bathroom
cleaners, plastic and rubber cements). Many are in gaseous form; many others
volatize readily or are used as sprays. Little information pertinent to
evaluation of human hazards in nonindustrial exposure situations are available,
so that we must turn to studies made for workplace settings.
Table A-3 lists health-related information for a number of chemicals
commonly found in domestic products to illustrate the variation in type,
toxicity, and dose-response data. Threshold Limit Values (TLVs) given are
recommendations for 8-hour average time weighted exposure for healthy adults
assuming a 40-hour work week. Therefore, the TLVs are only crude proxy
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TABLE A-3. ILLUSTRATIVE HEALTH INFORMATION ON SOME HOUSEHOLD SOLVENTS AND CLEANERS
Compound
Use
TLV*
Exposure-Response Data*
i
vo
o
Methylene chloride
Perchloretliylene
VMCP Naplitha
Benzol (benzene)
Toluol (toluene)
Xylol (xylene)
Methanol
Acetone
Ethyl ether
Sodium hydroxide
Ammonia
Turpentine
Paint remover
Cleaning fluid
Paint thinner
Lacquer and
cement
solvents
Shellac and
varnish thinner
Lacquer
solvent
Lacquer, wax,
plastic solvent
Drain cleaner
Window
cleaner
Palndng
200 ppm (720 mg/ni3)
100 ppm (670 mg/m3)
200 ppm (90O mg/m3)
10 ppm (30 rng/ra3)-Skin
200 ppm (260 mg/m3)-Skin
1000 ppm (2400 mg/m3)
400 ppm (1200 mg/m3)
2 mg/m3
25 ppm (18 mg/m3)
100 ppm (560 mg/m3)
180-200 ppm per day results in increment of 4.5 percent COHb.
Narcosis above 4,000 ppm. Brain damage reported from repeated
peaks above 500 ppm.
10O ppm for 7 hours produced narcotic effect, headache, mild eye
and respiratory irritation. Marked narcotic effect above 200 ppm
for 3 hours.
Multiple hydrocarbon content (TLV based in nonane, xylene).
Myelotoxicant. Skin absorption can produce chronic poisoning.
Headache, nausea, narcosis above 200 ppm. May contain benzene
200 ppm irritating. CI, neurological and vascular effects reported
in workers. May contain 6-15 percent ethyl benzene.
No worker Injury at average 160-780 ppm. Repeated exposure above
3,000 ppm may result in cumulative body concentration.
Minor eye and nose irritation above 2500 ppm.
Nasal irritation above 200 ppm. No worker injury demonstrated from
regular exposure of 500-1000 ppm. Chronic effects noted after long-
term exposure.
Upper respiratory Irritant at 2 mg/m'.
Rat ciliary motion stopped at 3 ppm. Detection at 1-5 ppm. Eye
and nasal irritation at 20-25 ppm.
Respiratory Irritation at 75 ppm. Marked irritation and nausea occur
above 75O ppm for several hours.
* TLV's and Response Data from Documentation of the Threshold Limit Values (1974)
-------
guidelines at best for household exposures and perhaps several times higher
than a "safe" level, particularly when children and more susceptible persons
are involved. The exposure-response data given is the information available
concerning the lowest concentrations at which human effects were observed.
Most of these studies are on short-term exposures and acute effects. Data
on long-term exposure is seldom found.
Many of the chemicals in this section fall into a number of groups which
have common exposure characteristics and toxic properties.. The review that
follows was drawn primarily from Hamilton and Hardy (1974).
Saturated Aliphatic Hydrocarbons - Of interest in this group are the
gases methane, propane and butane, and liquids from pentanes (Cg) through
C,g compounds. Methane, the principal component of natural gas, is bio-
logically inert. In general the series from propane (C.J through the
octanes (Cg) show increasingly strong narcotic properties, although the
thresholds are very high. Sources of vapors from compounds containing
liquid hydrocarbons in the series from pentane through octane are mixtures
such as petroleum ether, benzine, petroleum naphtha, gasoline, mineral
spirits, Stoddard solvent and varsol - which are commonly found in house-
hold use. The vapors are moderately irritating and have narcotic effects
typical of heptane or octane. However, these mixtures may contain other
chemicals such as benzene which are of much greater significance toxico-
Icgically.
Aromatic Hydrocarbons - The important chemicals here are benzene,
toluene and xylene, which are used as plastic and rubber solvents. Many
hydrocarbon mixtures, and in particular coal- and petroleum-derived solvents,
may contain unknown quantities of benzene. Besides the central nervous
system depression usual to hydrocarbons, benzene exposure can result in
chronic poisoning with insidious onset, resulting in aplastic anemia and
possibly leukemia. Toluene and the xylenes are less toxic and similar in
their effects, which are primarily narcotic. Lethal cardiac arrhythmias
have resulted in "glue sniffers." There is some evidence that toluene also
may be a myelotoxicant after chronic exposure but a causal association has
not been established.
Chlorinated Hydrocarbons - This group includes most of the solvents
routinely encountered in cleaning and painting products. Toxic levels
vary considerably. Two of these agents, carbon tetrachloride and chloro-
form, have been identified as carcinogens in laboratory animals. Toxic
manifestations reported for the various chlorinated hydrocarbons have
included eye and respiratory irritation, neurasthenia, cardiac irregular-
ities, and liver damage. The extreme volatility of these compounds permits
rapid achievement of significant concentrations within a short time.
Absorbed dose varies with metabolism. For example, most, like tetrachloro-
ethylene, are exhaled unchanged. Methylene chloride however is almost
completely metabolized to carbon monoxide, a unique and dangerous char-
acteristic (Stokinger and Coffin 1968).
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Other Solvent Compounds - Other chemicals of interest are the alcohols,
ketones and ethers, esters, aitds.arvd caustics. Methane! is a•yuxevp&ao^t'Qf
lacquer thinners and canned heating preparations (sterno). Eye and res-
piratory irritation may result from exposure to vapors but systemic intox-
ication is unlikely without accidental ingestion. Ketones and ethers are
common lacquer solvents. Acetone is the most frequently encountered.
Others-of this group are more irritating, but severe complaints have
occurred only at a very high occupational level. Bischloromelthylether
(BCME) has been established as a human carcinogen but is unlikely to be
found outside of industrial settings or laboratories. Aliphatic esters,
primarily ethyl acetate and butyl acetate, are used as lacquer thinners.
Vapors are irritative but other significant toxicological effects have not
been established. Several types of acids and caustics may be found in the
home: sulfuric, nitric, and hydrochloric acids, sodium hydroxide, ammonia.
Except for nitrous fumes from exposure of nitric acid to air, or deliberate
creation of aerosols through spraying, most of these products are likely to
produce only minor irritative effects in their usual applications.
In recent years the dose-response characteristics of many common sol-
vents have been undergoing revaluation, using improved biological monitor-
ing techniques (USHEW 1976). It has been found that measures of exhaled
breath concentration and metabolites in blood and urine have correlated -v.H
much better with biological response tests than air concentrations. These
investigations have led to establishment of standards on a firm metabolic
basis.
Stewart (1974) has confirmed the metabolism of methylene chloride to
carbon monoxide and he has developed the correlation of ambient concen-
trations of CH2C12 with COHb levels in those exposed. Halse* indicated \*
that this Winconsfn group has now tested 10 solvents, and they and others
have found that only the dihalomethanes are CO converters. In testing the
usual standard levels with human volunteers, they have not Identified any
factor which would indicate a need to change the recommendations for
acceptable concentrations.
Aerosol Propel!ants
The three essential components of aerosol sprays are the propel 1 ant,
the solvent, and the active ingredient. Each might prove hazardous to
health. The most common propel!ants are fluorochlorohydrocarbons bearing
the trade name Freon.** Freon 12, the most common of the group, is a gas
at room temperature, is relatively inert and has a high vapor pressure that
provides the propel 1 ant force. We know little concerning the range of
exposure to aerosol sprays that might occur with their use in relatively
confined (indoor) space (Frank 1975). The use of these propellants varies
from hand nebulizers (i.e., by asthmatics), to hair sprays, to other purposes
* Personal communication.
*'* Freon is a trademark of E. I. DuPont de Nemours and Co.
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Fluorocarbons In high concentrations have been reported to affect
both the respiratory and cardiovascular systems. Taylor and Harris (1970)
noted that a mixture of Freon 12 and Freon 114 Induced sinus brachycardla
and atroventHcular block 1n experimental animals. The arrhythmias were
more readily elicited and more severe 1f anoxemla was present. Often-these
effects are noted only when high concentrations of flurorcarbons and other
substances are combined (Clark and Tlnston 1972). Harris and Kilen (1971)
in further studies reported that Freon 12 affected the contractility of
myocardial muscle fibers. An Increase in mortality from asthma in children
and young adults 1n England and Wales during the last decade has been
attributed to the Introduction of hand nebulizers (Frank 1975). One
hypothesis is that the hypoxemla (and hypercarboxemla) of the underlying
asthma, in combination with the inhaled fluorocarbon and adrenogenic drugs,
led to fatal cardiac arrhythmias. Trochinowitz et al. (1974) found that
industrial halocarbons posed no greater risk in persons who had recovered
from myocardial infarcts than in normal individuals.
Morgan et al. (1972) used radioactive tracer techniques to study
retention of Freon in human volunteers. Mean retentions of these sub-
stances were:
• Freon 11 - 23.0 percent (+_ 2.2)
e Freon 12 - 10.3 percent (+ 2.2)
e Freon 113 - 19.8 percent T± 0.9)
• Freon 114 - 12.3 percent (+.4.1)
Indicating that much of the vapor was exhaled without being absorbed. After
30 minutes the fraction retained in the lungs ranges from 10 percent for
Freon 114 to 23 percent for Freon 11. Only a small fraction was present in
the blood at 5 minutes. The authors concluded that because of low liquid
solubility, absorption is quite slow and more than half the material is
exhaled immediately.
Foltz and Fuest (1975) conducted mutation studies with Drosophila
Malanogaster exposed to four fluorinated hydrocarbons. They found signifi-
cantly increased mutation rates 1n the F2 generation, including two tumors
not previously reported in deviant genotypes. The contribution of anoxia
to mutations was not determined. Vozovaza (1974) used dichloroethane in
mutagenic and hetrogenic studies of rats. Although concentrations did not
produce observable toxlcity, reduced fertility, reduced birth-weight and
an increased still-birth rate were detected. Increased perinatal mortality
was seen in second generation Utters from the exposed males.
Pesticides
The term pesticide is used here in a generltftnanner and includes the
wide variety of chemicals used as Insecticides, miticides, fungicides,
rodenticides, and herbicides. Many of these chemicals can be obtained in
a number of forms (powders, dusts, liquids) for application and used for
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multiple purposes. Frequently they are combined in proprietary preparations.
When considering the relative toxldty of each chemical, one must review
the following points:*
o The lethal dose in animals
o The method of use (solid, liquid spray, dust)
o The route of human absorption (ingestion, skin absorption,
inhalation)
o The vehicle in which the pesticide 1s applied - the diluent
itself may be toxic or may influence the rate of absorption
o The formulation - many pesticides contain nonpesticide
ingredients which may enhance toxicity, combinations of
pesticides may act in synergistic or antagonistic fashion
relative to human toxicity.
The individual chemicals and combinations are far too numerous to discuss
separately here but important characteristics of each class can be
described.
The following summary of pertinent aspects of major classes of pesticides
is drawn from Hamilton and Hardy (1974).
Orqanophpsphorous Compounds - The mechanism of toxic action of these
compounds 1s based on their inactlvatlon of acethylcholinesterase. The
natural substrate (AcCh) of this enzyme is a primary neurohumoral trans-
mitter substance. Because of certain structural similarities, the organo-
phosphorous compounds undergo changes analogous to the natural substrate.
However, the bond to the enzyme is abnormally stable so that the phos-
phorylated enzyme loses its normal function as an AcCH esterase, causing
first increased function and finally decreased function, with greater
AcCH accumulation.
The consequences are primarily disturbances of the central and auto-
nomic nervous systems. Systemic responses produce initial symptons such
as anorexia, nausea and sweating. Eventually the respiratory muscles may
be impaired. Studies of workers with chronic exposures have shown neuro-
logical deficits (memory defects, delayed reaction times) without obvious
clinical signs of intoxication.
There is wide variation in mammalian toxicity shown by this group.
Certain sulfur-substituted compounds require metabolic oxidation before
toxicity develops (e.g., parathlon), while others (e.g., TEPP, Phosdrin,
DDVP) do not require such modification and are direct Inhibitors of AcCH.
The latter generally are more toxic and show more rapid onset of systematic
symptoms. Recent evidence (Wood 1974) indicates that parathlon and related
compounds are rnore_ toxl£ when inhaled than by skin absorption. Also, the
toxidty of parathlon may be potentiated by ultraviolet and visible
irradiation.
Occupational Health and Safety, International Labour Office, Geneva, Switzerland, 1972.
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Chlorinated Hydrocarbon Insecticides - The mechanism of action in
mammals or insects is not clearly understood. It is apparent that these
materials are neurological poisons, and severity of symptoms appears to
be directly related to the concentration in nervous tissues. Signs of
central nervous system stimulation from slight exposures include headache,
anorexia, nausea and irritability. Increasing exposure produces weakness,
paresthesias, tremors and muscle fibrillation. Seizures or coma may occur
after high levels of absorption. Long-term, low-level exposures produce
the clinical picture of acute response to intense single exposures after
sufficient dose.
Compounds in this category can be absorbed through ingestion, through
inhalation, and most through the skin. Dieldrin can be absorbed through
the skin in a dry state, the others must be in solution. There are two
particular health concerns with the chlorinated hydrocarbons. First, the
material absorbed is stored in fatty tissue. It has been noted that the
total amount stored in the fat of an experimental animal may be greater
than the amount necessary for a single fatal dose. Although the stored
material is probably biologically inactive, there is a question of the
potential danger from release of the pesticide during periods of rapid
weight loss. The second concern is the carcinogendtic potential of
these compounds. Those identified so far as possible human carcirfl&gens
are aldrln, dleldrin and DDT. 'Because of these concerns, use of DDT .
has been banned in the U.S. and others are being withdrawn or limited in
application. However, pesticides in the same chemical and toxicity cate-
gories remain in common use.
Persistence of the chlorinated hydrocarbons over time at effective
levels aids their insecticidal properties but consequently poses a health
hazard. Davies and his associates (1975) studied DDT concentrations in
an area where no aerial spraying had been done but where this insecticide
was used extensively for domestic pests. They concluded that contamination
of house dust was primarily responsible, for the human serum residues found.
Comparison of exterior soil and interior dust revealed contrasts in
concentrations of 8.4 ppm outdoors and 129.1 ppm inside.
Inhalation of contaminated house dust may be one important source of
uptake. Another source consists of the continuous vapors from sprayed
insecticides or from solid forms such as Shell's No-Pest Strip (DDVP).
Although the long-term consequences of such exposures have not been demon-
strated as adverse, many scientists feel that the use of these products
is imprudent. Although we have not obtained the detailed results, we
understand that Savage has recently shown that heavy application of
chloridane and similar chemicals for termite control can result in sig-
nificant levels Inside the home five years after the spraying. Thus
substantial indoor exposure does not necessarily depend on direct house-
hold use of these pollutants.
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Other Pesticide Compounds - The two categories described above
probably are the most important in terms of potential health consequences.
However, many other toxic compounds are in general use. Carbamates are
growing more popular because of their effectiveness and relatively low
order of mammalian toxicity. These chemicals are also cholinesterase
inhibitors but the reaction is rapidly reversible when exposure ceases.
Most aerosol "bombs" for home use contain esters of the biological
pyrethrum. Other biological derivatives used are rotenone and nicotine.
Pyrethrum and rotenone may cause skin sensitivation but systemic intox-
ication is not of concern. Nicotine however, is a potent neurotoxic agent
which may be absorbed from skin, lungs or GI tract.
There are a considerable number of other chemicals which may be of
importance as indoor pollutants because of applications on foliage and
soil around indoor spaces. These include those for mites and other plant
pests, fungicides, soil fumigants, and herbicides. Among those of note
are:
Chlorbenzilate and Chlorbenside - These miticides resemble
the chlorinated hydrocarbons and have similar effects.
Dithiocarbomates^ - Foliage fungicidal sprays which may cause
eye and nasal irritation but are not considered to have
important systemic toxicity.
Organomercury compounds - Aryl mercury compounds, the less
toxic of this group, are more likely to be used as
domestic fungicides. Mercury is a neurotoxic poison
and can cause active dermatitis.
Phthalimides - Frequently found in home garden fungicides,
they have not been shown to be a significant hazard.
Dim'trophenols - These are used in different formulations as
herbicides, fungicides, miticides and insecticides.
Action in man is based upon interference with temperature
control mechanisms. Members of this group used for
domestic applications are less toxic systemically but are
eye and airway irritants.
Chlorphenoxy group - This group includes the well-known herbicides
2,4-D and 2,4,5-T. Skin absorption is'slight and toxicity
by oral or inhalation routes has not been a reported health
problem.
General statements in attempting to evaluate pesticides as an indoor
pollutant hazard are made difficult by the variety of formulations, bio-
logical actions and toxicity levels associated with the many products in
use. Some of the aspects pertinent to exposure have been pointed out:
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persistence in house dust, vaporization, transformation through oxidation
to a more toxic substance.' To illustrate the diversity of pesticides,
Table A-4 summarizes some relevant data on selected chemicals. Exposure
response data was obtained primarily from the Documentation of the Thresh-
old Limit Values for Substances in Workroom Air (ACGIH 1976) and Hayes (1963)
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TABUE A-4. ILLUSTRATIVE SUMMARY INFORMATION ON SELECTED PESTICIDES
Compound
^lACUOp^OfpfjUJO,^
Pare talon
Arinpho»-ni ethyl
(CudtlOD)
Dlcfalomi (DDVP,
Vepona)
Mol.thlon
ChlO"1nif\d HvdnoftHMn
Und.no Mn)
10 mo/rn1
(lldn)
Sraa/m3
5 mg/nt'
S mB/m^
0.5 mQ/m3
0.2 mg/ra1
(iMa)
5 mg/m3
0. OS mg/m'
(«Mn)
0. 25 mg/m Bl
AS
Toxiclty
LDjO ruln °ral 3"I! °>g/kgf
daimal 0-21 mg/Kg
LD5Q rao o«al 11-13 mg/kg,
durmal 220 mg/kg
LDSO "W oal 54-80 mo/kg,
domtl 73-107 mo/kg
LDSOna anl 1000.1375
mg/kg dannal 4400 rag/
kg
LOjO m« oral at-91 mg/kg,
donnal 900- 1000 mg/kg
U>so ma onl M mg/kg,
domnl 6O-M mg/kg
LDsO n« 00.1 100- 1«2 mo/
kg, dotmal 193-130 mg/kg
LDjo B8 onl ud domal,
eOOOmg/kg
IClO rao on' "° ft/^Si
dontial 4000 mg/kg
LDjo ma onl 820 mg/kg
LD50 rate oral 1BOO mg/kg
Lathal I. V. dora In mbbltn
22 mg/kg
U>30ioO 11 mg/kg
LCjo no oml 12. 5 g/kg
10 mg/nj9 lattaal QD mica
Rxpotura-Rogponn Data
Pncoolog plane 0. 1-0. 6 mj/m3 daciouod mtrma anlTtty
IntuUdan OTxldty grootoi tfatm by ddn abtDtptfoo
A cmcoli (mln, don) highly haocdna
1. 7 mg/m* Ui «nutmlmt (is dlanry lataka) pndacnd no etfoct
mna
RolatKaly low domal tDidclty pvobabty accouats tot good tafoty
toooM
0. 14-0. SI mg/m' tot 30 minuet/ hoa let 10 hooa orot 14 doyo
piHinnioo no ouiyiuo du^ULUton 1 ng/nr' tot 7-S AOUJD
pmdnccd 20-23 pareooi ptcamn ouymo dopnraSon
M. 8 ng/m* 1 hour for 50 dayi oadacod no maytno tympueu at
ttcnlfloim chugoi. Modcmtn uHtntton to com and oya
Cammalnmor (Uudano) of BHC axhlbto gtouas eaidty bta
rolmlvaly rapid oxcrodon. Coaoicc ifarmoddi tayuitod tea vapa*.
ToaidB/ nrlao among upodo 0. 19 mg/m> eanataiaa to
653 dnyo vitb no ottoca In nut, 0. 7 mg/m) imago long-toai
fopostod ojcpoouro produced mloln>ai paefaolagy to no. Tocmttenl
BHC ptDdacod lymptonu tn man at onl dota oi Undaao tolcmtod
for 14 dayo
Moutollto o( aldrln with dmilAi chnnctratalca. Undianlvod dtolMn
readily abcorbod mnugh ddn, In con «jt with DDT. Ropoatad
oxponm OM cumulailv* tDxtdty and ratldunl nniunft-mdncod
Injury may preto Air daoa aabltahad on bnda of analogy m
Undone
Action dmilar to aldrino, chtotdana. Dotmal ttixleitir to «an ed-
mntod46 gta Ungb doo, 1.2 jm/duy muWplo anBoana
350 mj/ mat/ day dlomry doio over 2 yoon pndoctd no fymnomu,
700 mg/man/day ptodueod no dmo (hango No InhnlotleB
dan touud
Dlatair lovola IB ran) of 225 mg/kg/ day without dgnlflooat ettoct
Compound quickly motatollnd. Inhakdon of honoo oqoin-
lotol 100mg/dav(10mg/m2) In rao psidncad no groo vlttMa
Injtar. No akin natation for TLV
14 mg/m' par 10 almrau oral 31 dayi produced only illjht tuaj
imtaflon la KB, dop. No ildn notation tor TLV
Rao ourvrvod clowd with eoOmatod 500 mg/m' tor 4 boos. Slmlhu
ottoea tt> intabrao, but man anlc. Uttla cKpodonco data. No
ilda aondati (01 TLV
Iidtatton of noao at 0. 3 mg/m', matkod Irrttadcm to nom and oy«
abovo 1 mg/m3. Skin abcorpiion major factor In mportnd urrcao
oflooo
Human aoa-fatal Intoxication abovo 2.5 mg/m'. Cumalatlva btood
lavolg and tortc aflocta aftnr ropcatod axpocuro
Low moor acnto corfolty but much hlghar chronic roilclty. 9000
mg/kg on lab anlmalfl causod iHght ikln Itricatfon. Accoptabla
dally Intake tor man enlmatad aa 0. 1 mg/kg/ day. No ikln
notation for TLV
0.01-0. 1 mg/m' with hlghar paaki did not reveal conllnant
rynaptoma of Hg poteomng. However, curront oompoutidj conttdend
more «nlo,TLV It 0.05 (or othor noo-ilkyl Hg compotnub
TLV band In potential AS2Oj at dutt contrlgudon to anaolcal
dermatldj. No Inhaladon dan oa AS In duaa or aoludoa ipmy
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PARTICULATES
Particulates are a subset of the larger class of aerosols, an aerosol
being defined as a colloid system in which liquid or solid particles are
dispersed in a continuous gaseous medium. Aerosols are ubiquitous in man's
environment. They include primary particulate matter (pollen, dust, soot,
fibers) emitted from natural or anthropogenic sources and suspended in
ambient air, and they include secondary particulate matter (sulfates, nitrates,
some hydrocarbons) which are formed in the atmosphere by gaseous reactions
involving S02, N02 and oxidants. Aerosols also include the large class of
diverse materials packaged under pressure to be dispersed by a gaseous pro-
pellant (a class including deodorants, paints, hair sprays, etc.). Particle
sizes of aerosols range from that of aggregations of a few molecules to
visible dust and vapor.
The mix in these aerosols includes substances that are inert and others
that are biochemically and biologically active. The gas components of aero-
sols range from those harmless to man in appreciable quantities to those
extremely hazardous in relatively small concentrations. These chemical
substances may not be detectable by any of the senses, may not produce sig-
nificant early physiological effects (to warn of their presence before
serious injury) and may not produce clinically recognizable pathology until
many years after exposure. These facts, and the continuing introduction of
new materials in our environment from changing technology, make evaluation
of hazards extremely difficult and complex.
Brain and Valberg (1974) have described the results of studies on
respiratory aerosol retention, employing a model developed by a Task Group
of the International Commission on Radiological Protection (ICRP). Three
distinct physical mechanisms are involved in deposition of particles:
inertial impaction, sedimentation, and Brownian motion. The relative
significance of these mechanisms depends on the anatomy of the respiratory
tract, the effective aerodynamic diameters of the particles, and the pat-
tern of breathing. The important anatomic pulmonary changes, such as
diminished lung volume, are associated with aging and with various types
of respiratory disease. Particle aerodynamic characteristics are a func-
tion of particle size, shape, and density. Breathing patterns change as
a result of exertion, existing pulmonary disease and various biochemical
stimuli.
Clearance of inspired substances is a complex process including direct
expiration, transport by cilia and mucus to the pharynx where the material
is swallowed, and absorption into the blood stream. Metabolism and excre-
tion from the blood, gastrointestinal and urinary tract are related to the
chemical properties of the individual substances involved. The inspired
material may physically or biochemically affect clearance mechanisms, and
metabolites may induce pathology before clearance or be deposited in body
tissues where the potential for long-term action is realized. Results from
the model developed by the ICRP demonstrated that variations in effective
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particle size and solubility can greatly alter retention and exposure in
some respiratory compartments (Brain and Valberg 1974).
Another recent study deserving citation here is an analysis of trace
element retention in the human respiratory system using proton-induced
X-ray emission techniques. Desaedeleer and Winchester (1975) measured
the respiratory retention of lead halide and chalk dust sized by cascade
impactor with stages ranging from 0.25-4 \im. For both substances, minimum
deposition was well under 50 percent with particles in the region of 0.5 ym
diameter, and deposition was well over 50 percent for both smaller arid
larger particles. Retention results were consistent with those found using
the ICRP model and with those reported by other investigators: minimal
retention of particles in a size range of about 0.3-1.0 pm, with larger
particles captured in the naso-pharynx compartment and smaller particles
lodging primarily in the pulmonary compartment.
The health hazards for several classes of particulates and other
aerosols are discussed below, grouped under the following headings:
© Total suspended particulates
o Tobacco smoke
o Trace metals and minerals.
These categories do not embrace the whole range of possible aerosols -
biological pathogens and allergens have been excluded, for instance, because
of time constraints in the literature review - and they are not mutually
exclusive categories. They have been selected as areas of special interest
to researchers.
The organic compounds which enter the indoor air as components of ,
aerosol sprays will not be discussed under this section. They appeared pre-
viously.
Total Suspended Particulates
The standard method of measuring the particulate content of outdoor air
has been to weigh the total amount of particulate matter of all kinds retained
on a filter paper through which ambient air has been forced by a high volume
air pump for a 24-hour period. The only characteristic of the particulate
matter so identified is its weight per unit volume of air passed through the
filter. The wide availability of these measurements of total suspended par-
ticulate (TSP), usually expressed in terms of 24-hour average ambient concen-
trations in micrograms per cubic meter, has led to the use of this measure ,
of particulate concentration in epidemiological studies. Another measure of
TSP, the soiling index, has also been used.
Sized analyses of ambient particulate matter, which separate particles
into size ranges, are available for research studies of the smaller, respi-
rable fractions of particulate. This type of particulate analysis is not
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routinely available from air quality monitoring systems established by
states and cities. It is usually available only in special research
contexts, such as EPA's Community Health Air Monitoring Program and
other pollutant monitoring projects especially established for health
studies.
Total suspended ambient particulates as a group have been.implicated
in a variety of pulmonary and extrapulmonary health effects. Their pres-
ence and interaction with irritant gases were discussed earlier. Figure A-5
shows the data base for the National Ambient Air Quality Standards criteria
used by NAPCA (USHEW 1969); it; includes in parentheses the concomitant con-
centrations of S02 found in these studies.
TSP
700 •—
600
300
400
300
200
100
80
70
60
(SO2 715 yg/m3, 24 hr) Increased illness, excess deaths
(SC*2 630 yg/m', 24 hr) worsening symptoms bronchitis
(SC>2) 250
^, 24 hr) increased absenteeism
(70% RH, small particles) reduced visibility
(SC>2 120 pg/m3, annual) increased respiratory disease
Direct sunlight reduced; (sulfatlon 30 mg/cm^ /month
annual geometric) increased deaths likely
_ (Sulfatlon 30 mg/cm2 /month, annual geometric) increased
deaths possible,
(Other pollutants, .annual geometric) public concern
(SC>2, H2O, annual geometric) increased metal corrosion
Figure A-5. Reference data for health effects of particulate exposures.
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Cohen et al. (1972) studied the incidence of asthma attacks asso-
ciated with pollution from a coal-fueled power plant. Sulfur dioxide,
soiling index, total suspended particulates, suspended sulfates and sus-
pended nitrates were each found, by individual analysis, to explain a
significant variation in attack rate. However, (low) temperature and
any one of these pollutant measures, when taken together (multivariate
analysis), eliminated the significant contribution of the others. Tempera-
ture alone appeared to be the most significant variable. It was concluded
that temperature and pollutant concentrations had a greater relative effect
when the temperature was above freezing. This is consistent with the poten-
tiation of pollutant toxicity by higher temperatures reported by a number
of investigators.
Sultz et al. (1970) found a close association between the continuing
exposure to air pollution (defined by TSP level) and the severity of asthma
and eczema in children. Jacobs and Langdoc (1972) reported an excess of
cardiovascular deaths among residents of a highly polluted industrial area
(with a variety of particulate pollutants), when compared with cleaner areas,
Lewis and Coughlin (1973) studied the acid-insoluble soot contents of
male lung samples obtained at autopsy. A mean concentration of total soot
for both lungs of 1.7 g was estimated. A statistically significant correla-
tion was found between age and the quantity of soot accumulated, but no
association emerged when correction for occupational history and smoking
habits was made. Thirteen patients dying with mention of a cerebrovascular
accident had accumulated significantly greater quantities of lung soot than
the rest of the study population.
Stephenson et al. exposed dogs to wood smoke for various lengths of
time and studied the alteration in pulmonary function which occurred. The
pulmonary dysfunction consisted of an early progressive increase in the
alveolar-arterial P0£ gradient and a decrease in compliance. As exposure
was prolonged, the respiratory effects were followed by cardiovascular and
neural dysfunction. In those animals which survived, the authors noted a
decreased resistance to bacterial infection. They did not separate the
effects of specific constituents of the smoke (heat, CO, aldehydes, other
particulates).
As an indication of the hazard from TSP in indoor environments it
should be noted that TSP concentrations for one hour have been found in
indoor air as high as 462 yg/m3 (Jacobs et al. 1962) and 539 yg/m3
(Goldwater et al. 1961). Elliot and Rowe (1975) observed peak concentra-
tions of 620 yg/m3. Penkala and DeOliyeira (1975), among other investi-
gators, have found that cigarette smoking will increase indoor air TSP
concentrations to above the NAAQS ambient standards of 260 yg/m3 for a
24-hour average. Since the ambient air standard for particulate is based
in part on the health effects of particulate as measured by high-volume
samplers, comparisons of indoor particulate concentrations with ambient
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standards should take into account the size and hence weight, or particu-
late which enters these samplers. Since tobacco smoke parti oil ate is con-
siderably smaller in size (approximately 1 ym mean aerodynamic cut size)
a significantly larger number of these smaller, and hence lighter particles
would be required to reach concentrations as high as the ambient air stan-
dard. Further discussion of the health effects associated with tobacco
smoke appears next.
In general, the data on suspended particulates suggest that the quan-
tity, composition, size, and interaction of the particulates with pollutant
gases, must be taken into account when evaluating their health hazards.
Tobacco Smoke
Tobacco smoke has been shown to increase the risk of cancer, cardio-
vascular and other diseases, and to act in a synergistic manner with other
chemicals in carcinogenesis. These hazards have been extensively studied
from the point of view of their impact upon the smoker. The primary inter-
est in tobacco smoke in this literature review is, however, in its impact
as an indoor air pollutant affecting the health of the bystander.
Extensive reviews of tobacco smoke and its averse effects on human
health have been provided by Kilburn (1974) and by Schmeltz, Hoffman and
Wynder (1975). Kilburn points out that the pyrolysis of tobacco yields
over a thousand products, and she considers that the contents of tobacco
and smoke condensates are much too complex "to achieve the idea of relating
biological effects to single chemical components." Nevertheless, smoke
gases and particulates are of interest as composite pollutants, and indi-
vidual components may constitute a hazard in themselves if they reach suffi-
cient concentration from tobacco smoke alone, or in combination with multiple
sources.
Schmeltz et al. (1975) found no data suggesting that the passive
inhalation of tobacco smoke by nonsmokers increases the risk of developing
cancer. However, his review cites three studies in which there was an
increased incidence of actute respiratory ailments in children and infants
in homes where the parents smoke. Griffin (1975) notes that these studies
are suspect because of the statistical interference caused by increased
respiratory infections among the smokers themselves. However, Griffin
cites a further study in which parents' symptoms are controlled and the
increased risk of respiratory illness remains. Other effects cited by
Schmeltz are eye irritation and chronic respiratory symptoms (in persons
particularly sensitive to smoke), and elevated COHb and nicotine levels.
Tobacco smoke has the potential for causing a wide spectrum of adverse
health effects, since smoke contains carcinogens and cocarcindgens, cilio-
toxins and other agents implicated as contributing to an increased incidence
of cardiovascular disease and emphysema. Cigarette smoke has been impli-
cated as a source of cadmium in human tissue. Accidental exposure to cad-
mium fumes can cause acute lung damage of the severe central-lobular
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emphysema type. Hayes et al. (1976) exposed rats to a polydispersed
aerosol of O.OOBin cadmium chloride for two hours. They rioted a one-hour
peak of malate dehydrogenase activity (which may indicate specific mito-
chondrial injury) and after two hours, type II cell proliferation and
elevation of glucose-6-phosphate dehydrogenase. They concluded that
more than one mechanism (effect) may be operating.
Most interest in tobacco smoke has been confined to CO as the major
hazard although more recently it is recognized as an indicator of smokers
pollution as well as a hazard in itself. Schmeltz cites a number of
studies which indicate that those more susceptible to oxygen deprivation,
such as cardiacs and anemics, may develop dangerously elevated COHb levels
from passive inhalation (Schmeltz et al., 1975). The controversy sur-
rounding the hazards of indoor tobacco smoke concerns whether these persons
should ever be exposed to such concentrations, produced by others.
An important concern with tobacco smoke is the possible adverse effects
following chronic, low-level exposure to tobacco's separate components.
Nicotine is the most prominent in terms of volunhand has been found in
indoor air in concentrations as high as 10.3 'pg/nr. Others of particular
interest are N0«, the several existing nitrosamines, and its possible con-
version in the air or body to other known carcinogenic nitrosamines.
Trace Metals and Minerals
The respiratory intake of lead has been of concern because of wide-
spread generation from automotive sources. Research relative to the
problem of atmospheric lead was reviewed by a committee of the National
Academy of Sciences (NRC 1972). They concluded that, at present ambient
levels, lead inspiration did not represent a clear-cut significant problem,
but that further research was required on acceptable body burden and to
its potential long-term effects.
The TLV established for lead by the American Conference of Govern-
mental Hygienists for lead is 200 yg/m3 (ACGIH 1976). The work of Shapiro
et al. (1975) gives some hint of the importance of lead as a pollutant in
the urban society. The authors examined the teeth from seven Egyptian
mummies and teeth from mofern nonindustrialized Indians from the Lacandon
Forest in Mexico. These two groups had similar and low concentrations of
lead in their teeth. A comparison with teeth from a modern, industrialized,
U.S. population, revealed a 45 fold increase in the latter group's dental
lead concentration.
Inspired lead is absorbed by the pulmonary bloodstream. The degree
of absorption is related in main to the proportion of lead dust particles
less than 5 urn in size and to the individual's minute volume. Increased
workload therefore results in higher lead absorption.* More than 90 percent
Occupational Health and Safety, International Labour Office, Geneva, Switzerland, 1972.
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of the lead in the bloodstream will be held by the erythrocytes but lead
has a preference for bone and accumulates in bony tissue. Thus the lead
effects on the hemopoietic system include a decreased hemoglobin content,
a decreased number of erythrocytes and an increased number of reticulo-
cytes.
The chief early symptoms of lead poisoning are nonspecific and include
diminished physical fitness, fatigue, sleep disturbance, headache, aching .
bones and muscles, and digestive upset including anorwxia. As severity of
poisoning ensues the disease will manifest itself in increased signs and
symptoms particularly involving the gastrointestinal tract and the peri-
pheral and central nervous system.
Except in patients with anemia, the first clearly defined signs of
lead poisoning usually do not occur at a blood lead concentration lower
than 80 gg/100g of whole blood. However, certain chemical changes can be
demonstrated at levels below 40 ug/100g and possible subtle effects on
health and behavior are postulated. Two categories of people may be sub-
ject to exceptional risk: workers exposed to unusually high ambient con-
centrations associated with their employment, and infants and young children
exposed to lead in street dust. The latter group can probably ingest and
inspire sufficient lead to increase body burdens above a safe level. On
the basis of available epidemiological evidence, it was not possible to
attribute any increase in blood lead concentration to ambient Iead3air
pollution exposure below a mean concentration of about 2 or 3 ug/m - only
small groups of people have been identified as being exposed to higher
ambient concentrations than these. A special case of exposure, studied
by Bridboard (1973) concerns the burning of candles with lead-core wicks.
Concentrations were observed to reach 20 ug/m3 in an indoor home environ-
ment.
Kopple et al. (1976) have reported on a series of metabolic studies
designed to evaluate the relative contributions of inspired and dietary
lead to body burden. Using three techniques to calculate inspired lead
intake when breathing normal urban air was estimated as high as 18 +_ 3 \ig
per day, suggesting that a person can incorporate a substantial quantity
of lead from inhalation of the ambient urban atmosphere. The authors
point out that despite the relationship shown with body burden usual
ambient lead levels have not been established as a health hazard.
Bogen et al. (1975), in studying exposure of New York City residents
to lead, concluded that inhalation was the principal source of stable lead
intake. In a study of occupationally exposed persons, Johnson et al. (1974)
found that lead and cadmium content of excreta, blood and hair were corre-
lated with airborne levels of these metals, but zinc, manganese and copper
were not. Angle and Mclntire (1975) compared blood lead levels of urban
and suburban children of various ages. Urban children had higher levels,
the difference decreasing in the older age groups. No significant differ-
ence was found between urban and suburban sites in the lead content of
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air, house dust, milk or water, or in available paint chips. Increased
blood lead levels for urba n children were correlated with lead in urban
dust fall, yard soil and boot trays. Yard dirt and blood lead levels were
associated with residential proximity to traffic. Although all blood
levels were less than 40 ug, enzyme studies supported evidence for decreased
red blood cell survival at the levels found in urban children.
Excessive levels of aluminum from air conditioner deterioration have
been noted as a potential indoor hazard. Hamilton and Hardy (1974) in
reviewing studies on this metal, cite reported cases of interstitial pneu-
monia, pulmonary fibrosis, severe aluminum pneumoconiosis, and emphysema
from industrial exposures. Effects are apparently limited to respiratory
damage and severity is dependent on dose and particle size. Many of the
reports on the pulmonary effects of aluminum are from the aluminum abra-
sives (Alo03) industry where a progressive, non-nodular interstitial
fibrosis (shaver's Disease) has been noted among workers.* Since exposure
in all cases was not only to aluminum oxide but also to silicon dioxide
and ion fumes, the role of aluminum as the etiologic agent of Shaver's
Disease remains unclear. In the U.S., aluminum is considered nontoxic^
and regulated as a nuisance dust, with exposure limitations of 15 mg/m .
As inhaled aluminum reaching the lung appears to remain there, the effects
of a cumulative burden must be considered.
In reference to hazards from air conditioning it is interesting to note,
although biological contaminants have not been treated in this review, the
work of Banasznk et al. (1970) who repeated four cases of hypersensitive
pneumonities among workers in the same office that was eventually traced to
contamination of the air conditioning system with a thermophilic actino-
mycete. Since that time four additional cases have been encountered, three
of which were verified as due to this group of agents in home air condi-
tioners or furnace humidifiers.
Many other toxic trace metals are found in urban air but do not appear
to obtain sufficient concentrations to be of concern, unless there is an
unusual local source. The use of platinum and palladium in automotive cata-
lytic converters has raised the question of their importance in ambient air
and studies are underway to assess concentrations, body burden and toxicity
(Johnson et al. 1976, Holbrook 1976). Hamilton and Hardy (1974) indicate
toxic reactions to palladium were only produced in animals after injection
and there are no current reports of ill effects in workers. Platinum has
resulted in dermatitis and asthma in workers with occupational exposures.
Asbestos and talc have been associated with neoplasms in persons
exposed to occupational concentrations, and asbestos with nonoccupational
exposures (Selikoff et al. 1976).
Occupational Health and Safety, International Labour Office, Geneva, Swit/erland, 1972.
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Asbestos is a broad term embracing a number of fibrous mineral sili-
cates that differ in chemical composition. The three types of greatest
commercial importance are chrysotile, a hydrated magnesium silicate;
crocidolite, a sodium iron silicate; amosite, an iron magnesium silicate;
Chrysotile is the most widely used. The TLV asbestos is 5 fibers per
milliliter longer than 5 urn (ACGIH 1976).
The hazardous effects of exposure to asbestos of industrial workers
have been demonstrated repeatedly since the 1920's. The clinical conse-
quences are generally considered to be of three types:
1. A potentially disabling pneumoconiosis characterized by a
"restrictive" pulmonary functional pattern with reduced total lung capa-
city, lowered vital capacity without evidence of airway obstruction,
reduced compliance and impaired transfer factor for carbon monoxide.*
2. Bronchogenic carcinoma (Selikoff 1976). Enterline (1976) in
a discussion of the methodologic difficulty of precisely relating expo-
sure to asbestos and carcinoma, states that while most agree that there
is an excess of the disease in exposed persons, the magnitude of the e
excess related to exposure is not clear. Many believe (Shettigara and
Morgan 1975)* that there is clearly a greater risk of cancer of the
upper respiratory tract in asbestos workers who also smoke.
3. Mesothelioma, a diffuse carcinoma which invades the pleura
and sometimes the peritoneum.
Nicholson et al. reported measurements of asbestos fiber concentra-
tions of between 100 and 5000 yg/m^ in the air of homes of asbestos workers,
Additionally, 500 fibers/ml, were observed in a building which uses a
rotary asbestos heat exchanger. Other important potential sources of
asbestos dust in the home are the use of insulation and fireproofing
materials in standard construction. Brake lining wear also introduces
asbestos fibers into ambient air. Selikoff (1976) cites several reports
which confirm the deposition of these fibers in the lungs of the general
population; he and his colleagues examined relatives living in homes of
amosite asbestos workers and found asbestos-related pathology in 38.6
percent of the first 210 persons studied. Selikoff reports that data are
now becoming available that will permit relating the degree of asbestos
exposure to lung burden.
Occurrences of nonoccupational risk from asbestos dust have been
reported from Britain and France; a few cases of mesothelioma have
occurred in persons who were living near a source of asbestos dust or who
were exposed at home, from dusty clothes brought back from work (Tomson
et al. 1963).
Occupational Health and Safety, International Labour Office, Geneva, Switzerland, 1972.
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An important finding in the production of tumors by asbestos has been
made by Stanton (1973). Upon comparing the effects of various structural
forms of asbestos, fiberglass and aluminum oxide in rats, he found that
carcinogenicity was related primarily to the fibrous structure rather than
to physiochemical properties. Fibers below 2.5 m in diameter and 10-80 m
in length were particularly carcinogenic.
Consumer talc products have been indicated as potential hazards because
of increased cancer risk among talc workers and because many talc minerals
contain asbestos fibers. Stanton and Wrench (1972) have reported the develop-
ment of an experimental mesothelioma with several varieties of fine fibrous
glass. Selikoff (1976) concludes that while there is no convincing evidence
of cancer risk from inorganic dust (other than asbestos), there are still
too few studies on the potential risk, particularly at levels to which the
general population may be exposed.
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AIR POLLUTION AND LUNG CANCER
The role of atmospheric pollution in primary cancer of the lung is
the subject of continuing controversy. One principal class of causal
agents of interest is the polynuclear aromatic hydrocarbons (PAH), many
of which are known animal carcinogens. Evidence for the relation of PAH
to lung cancer is based on their production of cancer in animals, their
presence in tobacco smoke, and the strong statistical association of smok-
ing with increased lung cancer in man. In addition to the argument that
this apparently logical sequence of observations does not constitute unequiv-
ocal proof, the controversy stems from difficulty in separating the individ-
ual contribution of more usual atmospheric pollutants from those related to
smoking and to occupational exposures.
Research on particulate polycyclic organic matter (POM) was subjected
to intensive review by a committee established by ,the National Research
Council of the National Academy of Sciences (1972). It was concluded that
there is an "urban factor" in the pathogenesis of lung cancer in man and
that benzo(a)pyrene (BAP) could be used as an indicator molecule implying
the presence of polycyclic organic carcinogens. However, the NAS committee
believed that these substances had not been shown to be teratogenic, and the
presence of hydrocarbon mutagenesis and carcinogenesis had not been proven
to be closely related.
Carnow and Meier (1973), in a statistical study relating BAP to lung
cancer in the U.S. and 19 other countries, estimated that an increase of
1 ug/1000 m3 in concentration of BAP was associated with a 5 percent increase
in lung cancer mortality. (These data were used as the basis for the Academy's
recommendation for a working exposure-response hypothesis.)
Hirayama (1976) has reported on a series of epidemiological studies of
lung cancer in Japan. In one prospective study the data indicated that the
risk of lung cancer increases 10 fold if atmospheric contamination is added
to cigarette smoking. Sterling (1975) published a critical reassessment of
smoking and lung cancer, suggesting that the evidence was weaker than popularly
viewed and citing many studies which evaluated the important contribution of
occupational and other atmospheric pollutants. Subsequent rebuttals were made
by Weiss (1975), Higgins (1976), and Bross (1976). Some of the material ,
related to the discussion in these papers concerned trends in respiratory
cancer mortality reported by Higgins (1974).
The increased risk of lung cancer associated with cigarette smoking
is accepted by most of the scientific community, although the particular
constituents responsible have not been completely established. Polycyclic
aromatic hydrocarbons (including BAP) in the smoke are considered a primary
candidate. These compounds are highly carcinogenic in animals and recognized
as a cause of occupational skin and cervical cancers (NRC 1972). Implication
of PAH in inhalation carcinogenesis has been reported for gas workers and men
working at coke ovens, and workers heavily exposed to printing ink (NRC 1972).
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Most evidence for a role of other air pollutants in lung and upper respiratory
cancer has also involvetL-occupational exposures, e.g., radon daughters, asbes-
tos, haloethers, nickel, and chromium. Although the high exposure levels con-
cerned would seem to make many of these factors inapplicable to the nonindus-
trial indoor environment, evidence is accumulating on nonworkplace risk of
respiratory cancer.
Blot and Franmoni (1975) have reviewed data on arsenical air pollution
and lung cancer. They cite studies indicating an excessive risk in smelter
and pesticide workers. These data led to an analysis of lung cancer mortality
patterns in communities with arsenic-emitting smelters which suggested an
increased incidence of lung cancer in residents of these areas. Selikoff (1976)
cites work of his own associates, and others, which indicates significant
asbestos levels and increased mesotheliomas in families of asbestos workers
and residents of areas near asbestos industries.
The report of an association of respiratory cancer and sulfur compounds
by Winkelstein et al. (1968) was discussed earlier. In this regard, S02;has
been demonstrated as a cofactor in carcinogenesis with BAP (NRC 1972) and with
arsenic (Blot and Franmoni 1975). This work provides further evidence of the
hazard posed by sulfur oxide-particulate combinations.
SUSCEPTIBILITY OF POPULATION SUBGROUPS TO INDOOR AIR POLLUTION
Consideration of those population groups particularly susceptible to
pollutants requires that certain facts be borne in mind:
e There is a wide variation in the susceptibility of
different'persons to air pollution
@ Preexisting or underlying disease conditions augment
the stresses added by air pollution
© Under some conditions, some types of air pollution
cause structural damage and persistent disease in
well persons.
The primary population groups most effected by air pollutants are those
which have underlying disease of the organ systems involved in the absorp-
tion, clearance and deposition of the polluting agent.
By far the most seriously affected population is that with pulmonary
disease - such as chronic obstructive pulmonary disease, bronchitis or emphy-
sema - since the most frequent route of absorption of air pollutants- is via
the respiratory tract. This is evident from studies of the effects of severe
episodes of air pollution, such as that which occurred in London in 1952.
There was a dramatic increase in the mortality of those with chronic lung
disease at that time. Lawther (1958) and Glasser et al. (1967) have presented
evidence that during less severe episodes of air pollution (in London and New
York) in many patients severe chronic respiratory disease is aggrevated.
Individuals with pulmonary emphysema have some degree of decreased dynamic
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compliance, increased airflow resistence, ventilation/perfusion abnormalities,
etc. Many of these patients often have a reduced arterial oxygen saturation,
usually with a concomitant increase in PC02 (Bates and Christie 1971). Thus
it is evident why their fragile physiologic situation is adversely effected
by air pollutants of various types such as S02, NOX, and CO.
Asthmatics are patients with a disease characterized by intermittent
bronchoconstriction and increased viscosity of bronchial mucus. There is
evidence that many common pollutants, including inert dust (DuBois and Dautre-
baude 1958), tobacco smoke and S02 (Nadel et al. 1965) cause bronchoconstric-
tion and thus tend to aggravate the preexisting condition.
Patients with low cardiac reserve due to chronic cardiovascular disease,
or with elevated COHb levels, can be jeopardized by high ambient CO levels.
Other groups, such as those with anemia or cirrhosis of the liver, will suffer
deleterious effects from agents which react with the hemopoitic (CO) or.hepatic
(carbon tetrachloride) systems.
The older-aged population appears to be more susceptible to the adverse
effects of air pollution. The extent to which this phenomenon is related to
the increased incidence of cardiopulmonary disease in this age group, or to
other factors related to the aging process and increased infirmity, is not
totally clear.
Douglas and Waller (1969) followed 5,000 children from birth to age 16
and studies the incidence of morbidity from respiratory disease. They found
a clear-cut association between an increased rate of lower respiratory tract
infection and the degree of air pollution in their environment. Other studies,
for example, the work of Lunn et al. (1967) in Britain, have confirmed this
relationship. Children also seem more affected by other pollutants, such as
lead. To some degree this observation may be related to absorption routes
such as paint chip ingestion, less likely to occur in adults. Although the
factors in lead intake and balance are not well established, children or
workers who may already have a high blood level could possibly achieve clini-
cally important burdens from respiration of ambient concentrations.
Further work appears warranted on the effects of air pollution on those
persons with preexisting depression, hypersensitivity states of various types,
and collagen disease (Burch 1974).
INTERACTIVE POLLUTANT EFFECTS
The interactive effects of combinations of pollutants have been noted
by many investigators and have been discussed in this literature review in
the reporting of research into the health effects of individual pollutants.
In summary it may be said that the synergistic action of particulates and
S02 seems to be well established. Some evidence is available implying a
similar action between particulates, N02, and oxidants. Hackney et al. (1975)
found no significant differences in human volunteers exposed to 03 and
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combinations of 03, N02, and CO, although these experiments could not be
considered adequate. The studies available suggest an additive or syner-
gistic effect on lung cancer of exposures of POM from smoking, occupational
pollutants, and ambient pollutants.
Several studies have investigated the contributions (individual and in
combination with pollutants) of temperature and humidity. The CHESS studies
and others have been cited which imply that the ambient pollutants contribute
more to aggravation of respiratory disease at higher temperatures. PAN
appears to be more potent at higher temperatures. In a review by Green (1975)
of studies on the effects of indoor humidity, it was concluded that increasing
the relative humidity of occupied spaces from 20 to 50 percent reduces the
relative incidence of respiratory conditions among school children.
Burch (1974) and Randolph (1970) have been concerned with the exposure
to myriad chemical substances in the home. From his clinical observations,
Burch feels it is evident that home pollutants play a role in autoimmune, col-
lagen, and cardiovascular diseases. Randolph reviewed the ecological basis
for mental illness and describes a comprehensive environmental control approach
to managing mental problems. He presents a lengthy case listing in which sen-
sitivity to a wide variety of agents in the patient's home was involved.
Randolph describes the often subtle progression to chronic symptoms. The
extent of substances to which hypersensitivity may occur is illustrated by
cases reported by Randolph:
t> Gas appliances (many cases)
e Hair spray
Perfumed toilet paper
Plastic furniture arid curtains
Chlordane for termite control
Noise from electric applicance motors
Petroleum distillate for house dust control
Many pesticides, insecticides
© Refrigerants (probably a Freon)
e Foam rubber and hydrocarbon vapors
e Textiles
<3> Cresote, adhesives, bleaches, ammonia, mothballs, and
such miscellaneous household products. >,
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444-51.
Shapiro, I.M., et al. 1975. "The Lead Content of Teeth." Arch. Environ.
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Shephard, R.J., M.E. Turner, G.C.R. Carey, and J.J. Phair. 1960. "Corre-
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-121-
-------
Shy, C.M., V. Hasselbald, R. Burton, C.J. Nelson, and A.A. Cohen. 1973.
"Air Pollution Effects on Ventilatdry Function of U.S. School Children."
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-122-
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-123-
-------
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-124-
-------
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in
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-125-
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Appendix B
U.S. DEPARTMENT OF LABOR, OCCUPATIONAL SAFETY AND HEALTH
ADMINISTRATION, AIR QUALITY STANDARDS FOR WORKROOM AIR
Title 29—Labor
Subpart Z—Toxic and Hazardous
Substances
SOURCE: 39 PR 23S02, June 27, 1974, unless
otherwise noted. Recleslgnated at 40 • FR
27073, May 28, 1975.
§ 19J0.1000 Air coutnminanla.
An employee's exposure to any mate-
rial listed in table Z-l. Z-2, or Z-3 of
this section shall be limited in accord-
ance with the requirements of the follow-
ing paragraphs of this section.
. (a) Table Z-l:
(1) Materials with names preceded by .
"C"—Ceiling Values. An employee's ex-
posure to any material in table. Z-l, tha
name of which is preceded by a "C" (e.g..
C Boron trifluoride), shall at. no time
exceed the celling value given for that
material in the table, . . ,•..-.'
(2) Other , materials—8-hour time
weighted averages. An employee's expo-,
sure to any material In'table zVl, .tlid
name of which is not preceded by "C", in
any 8-hour work shift of a 40-hour work
week, shall not exceed ;the 8-hour, time
weighted average given for that material
in the table!, \
(b) Table Z-2: ,•:•..•:-'• ;
(1) 8-hour time weighted averdges. An
employee's exposure to any material
listed in table Z-2, in any 8-hour, work
shift of a 40-hour work week, shall not
exceed the 8-hour time Weighted average
limit given for that material in the 'table. <,
(2) Acceptable ceiling concentrations'.,
An employee's exposure to a; material
listed in table Z-2 shall not exceed at
any time during an 8-hour shift the ac-;'
ceptable ceiling concentration limit given
for the material in the table, except for
a time period, and up to a concentration •
not exceeding the maximum duration
and concentration allowed in the column
under "acceptable maximum peak above
the acceptable ceiling concentration for
an 8-hour shift".
(3) Example. During an 8-hour work
shift, an employee may be exposed to a
concentration of Benzene above 25 p.p.m-
(but never above 50 p.p.m:) only for »
•maximum period of 10 minutes. Such ex-.
posure must be compensated by expo-
sures to conccntratioas less than H> .
p.p.m. so that the cumulative exposure ;
for the entire 8-hour work shift docs not
exceed a weighted average of 10 p.p.m. '.
(c) Table Z^3: An employee's expoj-
sure to any material listed In table Z-3,
In any 8-hour work shift of a 40-hour
-126-
-------
Chapter XVII — Occupational Safety and. Health Admin.
§ 1910.1000
work week, shall not exceed'the 8-hour
time weighted average limit given for
that material In the table.
(d) Computation formulae:
(1X1) The cumulative exposure for an
8-hour work shift shall be computed as
follows :
a
Where:
S Is the equivalent exposure for tho work-
Ing shift.
O la tho concentration during any period
of time r whore the concentration remains
constant.
T IB the duration In hours of the exposure
at tho concentration O.
The value of E shall not exceed the 8-
hour time weighted average limit in table
Z-l. Z-2, or z-3 for the material
Involved.
(11) To Illustrate the formula pre-
scribed In subdivision (1) of this subpara-
graph, note that Isoamyl acetate has an
8-hour time weighted average limit of
100 p.pm. (table Z-l). Assume that an
employee Is subject to the following;
exposure: . . .
Two hours exposure at 180 p.p.m.
Two hours oxponure at 78 p.p.m.
Four hours exposure at 60 p.p.m.
Substituting this Information. In the
formula, we have ' •• •> •
3x100-1-2x75-1-4X50 ' '
~81.2Sp.pjn.
0 ' -
Since 81.25 p.p.m. is less than 100 p.p.m.,
the fl-hour tlmo weighted average;limit,
the exposure Is acceptable.. :
(2) (1) In case ot :i mixture of air con-
taminants &n employer shall compute the
equivalent exposure as follows:,,
C, O, C,
Em=—+—+ . . . '
.. • • v L. .-.. L"".v•'->., ..
Where:
Em 13 tho equivalent .exposure for the •
mixture. •
C Is tho concentration of a particular con-
taminant. , • \'..\ . . :., '
L Is tho exposure limit for that cpntaml-
nnnt, from tnblo Z-l, Z-2. or Z-3,; ,-..':.• . ;
Tlie viiluc of Em Hlmll not exceed unity
d). ' : • ,;- • •.','•'.
(11) To llluntrato the formula pro-
scribed In subdivision (1) of tills s.ub-
parngraph. consider tho following
exposures: ' ..'. '••:'-; 1: ; '•• •/•' X-: ; .'•
Material
Actual con-
centration
of 8-hour
eiposure
8-hoor time
weighted
average
eiposure
limit
Acetone (Tnhlp Z-l) MOp.p.m... l.OOOp.p.m.'•
2-nutanono (Tnhlo Z-l)... 4fi p.p.m 200 p.p.in.
Toluene (Tnble Z-2) 40 p.p.tn 200 p.p.m.
Substituting In the formula, we have:
600 46 10 ."'• .
E. = 4 +—
1,000 200 200
E» = 0.600 + 0.226 + 0.200
Em-0.036
Since E» Is less than unity '!), the expo-
sure combination is within acceptable
limits.
(e) To achieve compliance with para-
graph (a) through (d) of this section,
administrative or engineering controls
must first be determined and Imple-
mented whenever1 feasible. When such
controls are not feasible to achieve full
compliance, protective equipment Or any
other protective measures shall be used
to keep the exposure of employees to air
contaminants within the limits pre-
scribed In this section. Any equipment
and/or technical measures used for this
purpose must be approved for each par-
ticular use by. a competent industrial
'.hyglenlst or other technically qualified
person. Whenever respirators are used,
their use shall comply with 8 1910:134.
T.MIL19 £ 1 .'
• 8nh.ani.ai -
Aci't'il'lpl.vdll'
Aorion*1 . .. .-'.'.
Aci'innll.illn
Arciylrni- dlchlorlde, sro 1, 2-
nlrlllomrlliylrno
Aornl-'ln
'•Acrylninl'li"— Rkln '
Aoi'ylonltillo— Skin" ;.-.
AlMrln Nkln • •
Allvl nlcolml— Bkln '
p.p.m." .
2on
10
it
1,001)
1
0. I '
20
2
1
mg.lM* »
3f',n
°i( -.
2. 41^1 '
7(1
14
•"• 0.8'
4.1 .,
0.25
^
•vrldlno .'..
"*Ainnioiilu..
Atntnunluni!>.iltaiiinln(Aii)-
inniM. ..;..:..... - --
n-A in y 1 fU'fJt.nl n >.. "
BFC-Ainylnrrtnto -1'
••Aiillliw Skin..:..'
••An.:;l'llnp (o. ii-lsomnrs)— Rkln..:.b.
Antimony und compounds .
OuSh) .....i
' dca fnotuotee at eud of table.
as .
BO
100
128 : '•
B
•
' •' '..,' .
. 2 .
3r» '
15 - .
• 52/i
dm .
• in
an .
-i ' • Olfl
-127-
-------
§1910.1000
TIHe 29 — Labor
TAiu,B Z--1 — Continued
Bubstnnco' : .
ANTU (alplin nnphthyl ' • .
IhloUl'rii).... . . .: . .^ .......
Awnlo nud compounds (03 As).
.AiRliin ;..: :.:
jUliiplios-intilhyl— Sklii ..;.
Uui'liim (solnblii compounds)!-.
n-DruioiuliioiiiVmio CJuluond..
Mouzoyl luToxlilo .'-
HiMiT.vl chlnrltln ;.:...
1 Iiliiliimyl. sco DIpliMiyl ..
IIIsplH'tiol A, Eto Dlglyclrtyl
Union oxlrt> - ;.;...'-
C, Moron trlduorlde
Hronilmi '......'
liroinotonrt— Skin.. ...... I'.1....
Uulnilliiuo (1, S-biitudleiie)....,
Duiiinoihlol, sot; flulyl WIT- '
2-Ilntoiy ollmiiol (Butyl Cel-
Inflol vi') --Skin. -...'..: --
lluiyl ncctiUo (n-butyl acetate).
sou- Hulyl itcutatn ,...
torl-liutyl uciaale... :..;.:
Butyl alcohol.. : ^
tdrt-IIulyl uicoboi :.'.' 1
t> Hiilylumlnn-Hkln..:..
C ti'il.lluiylcliromule (ae
CrOi)--Skln
. n-Hiitylglyi'ldvl other (DQK). .
• Hulyl mrrruptun. '
n-lort-Uulvltolnoiio
(laViiiin nrjiynutu ..fc....:
Cnriinryl (Huvlu®)...... ~
(."nrboii lilm'k . ....
Ciiihnn mnimxlrlo
C.hliinbin,,- Pklll
Cliliirliiuli'il I'lininlirnt— Slrln...
f'hlni limtMl dlplionyl o>ld«
•Chlipilno
ChlnrliindlnxllUt
(' ( -bloi'liii) trlduorkle
O Ulilaraiii'i'tiililiiliydo
p-Clilnrimrolm'honone
(nlinnaoylchlorldo) ' -.'..
CluorobiMiKonfi (inonochloro-
b.'iizono)
o-Clilnroboniyllden"
niuloiionltrlle (OCBM).......
Chlorobrotnomothane..:.
2-Cliloro-1.3-bulndleno, sat
Chloroprcno
Cliliirndlphenyl (42 percent •
Chlorine) 3kln..._ .'.:..
Chlurodlpbonyl (64 percent
Clilorlno)— Skin...- •-..
Eplcblorbydrln
2-Chlnroet)mnol, see Etbylone
Chlaroothylciio, sou Vinyl
clilurlde
C Oblnrolorm (trlchloro-
I'Chluro-l'iiltropropnno
Chlnropreno (2^bloro-l,8-
butudlenoJ-Kkin
Chromium, sol. chromic,
Mutul aiul liisol. salts.
P*;UVV;,'
:;::?pt
:!i,;: '.".".i*
,i»,r i :-.,\
..< . •-:::•
^ - , - ....
1
;.-'., 0.1,.;: '
•1,000 •:,,'•:
200
; BO
200 .. .
200 '•
• 100
100
ft ,
(10 !
• 10.
lo ••"
a •'.
0,000
•• • 60
.:}.....:.:-.
1 !'•
0.1
- 0.1,
aw '
''. 78' "
' 0.08
300
, 'i
80
.20
OL 1
26
nilr./M1 '
: ' •• • s
>' '. O.3..
!; "• ,0.6.-
i-1.-,.,, '!?•'•
;4-|8u
"'V?1^
';.- •'.'•
•'•-" Ifl >
,*''•* 'i 3. ' I-
• , a-?(,'
, 2,200 ,• ,
. j.. . .
690
240
.710 .
' 980 . .
960.
800. .
460
800'
. IB. . .'
0.1
i270
,36
80 '
1
8
.••v.. i • •
., 8.8 .
9,000 .
, 0.8 ..
' 0./1 '
• 0. 8 '.
8
0.8
., .0.4
3 <
I .'•
. . 860 ••
>i.oro'
' .• i-,.
, 0.8
240
• 100 •
0.7
M
Sec (onliiDii'snt end of table. . , !-
• •;' • Bubstiince "•:'. . •. • ... p.pjn.'-.'
/•i '" , '• •• ' ' ," '' ^
' ' ''CouMar pitch Volatile (bun.1 '/ '••
.-,' tone anlnblu traction) dathra- . .,
i 'i! cen«'Dal3. pnennnthrono, ,
'• acrldino, cUryaeno, pyrouo. . , ...
.. Cobalt, niotalfumouiiddust.^ .:.
Copper tumo.';i:. '.....'.. L;
." : l5ustsan(iMlsU.'::.ir.:;,.J. :.:
, Cotton dust (row) :'.i'.: j'..1. . .-.
1 ! Orcsol (all Isomors)— 6'kln.....
'- Cuincne— Bkln'.. .•:•...'...;...:. '. •
. OyanWo (as CNJ— Bkln-i.-.y1. .-•-
"' • Cyclohoxane.....'.'^. i...'.1. .^...
.. .Cyolobiuanbl.JV-. -'•---•--••-'-- '
Oyclohoxanone.v.-i.. :.-...;.-.
".' 'Cyololioxene.-.:*.:.. •,. '
. . • Dyclopentodlcno . . i .• . . ^ .'. 1 . : .
• '. 2,4-1) .'.'..\ .;:...:: :
DDT Skin
UDVPjooo Dlchlorvos. . ; - • .
necaborone— Skin. ...... .;:....
Dometon®— Skin :
. Dlhcetono alcohol (4-hydroiy- .
4-mothyl-2-po.ntanono)
• l,2-dl(imlnootlmi)p, BOD • :
Dlazoinothane.^ ..'. .•-.'.' •'
Plbimiuo -,...:..^ '
. Dlbutylphthalnto. :
C o-D(chli>robonr.(mn. ....... '....
. n-IMchlorobcnzMie.
Ulclilnrmlldiioruini'tlinno I
l1:H)lcl]lnro-i.6.dlmi.,thyl
hvilnnlnln
l.l-Ok'hloroctlmno
1.2-DlcbloroothTlene. ..'..'...'...• '
C Plcliloiuclliyl Ml, or -Skin... .:
DIobloroninMiune. sco .
Dlchlnrnmnnofluorouiottiane... 1
C l.l-1)lcliloro-l-nltro«tlinno
l,2-l>lcliloroprnpaue, too
Dlchiorotiitrnlliniroatliane...... 1
nicblorvoo (DDVJ1)— Skin :
ninthylumlnx
Dlethylainlno ethanol— Bkln. ..
Dinuorodlbromomethane
C ntglyoldyl ether (DOE)
DlhyUroiyboiueae, ceo
Dllsobutyl ketone
Dllsopropylnmlno— Bkln
Dlinethoiymethnne, seo
Mothylol
, Dlmothylainlno
Dlmrthylamlnoboniene, see
Dimcthylunl]ino(N-dlmcthyl-
anlline)-Skln..
Dimethyl l,2-dlbromo-2>dl-
ohloroelbyl phosphate.
(Dlbrom) :
Dlniathylfurninnildo— Skin
2,6-Dlmolhyllirptanone, sue
1,1-Dlmotbylhydnalno— Skin...
Dlmetbylphthalate
Dlmothylsullato— Skin
Skin 1
No,' foutnnd'B lit end of table.
'" ;i •'• '
..;.;:y:
:."6"""
"'W': ,-
BOO'*.
, 60 ;,'- -
8,00 -;
76 .
0. 03 .
«o • : ,
0.2 .
- ! 0. 1 ' ' -
60 ••'••"'
'76
000 -' »
100 ; '
200 ; ',
16 '• .-;
; "
000 ,
10
000
10
100
at
60
6
10
10
8
10
0.6 .
1
rng./MO '.
. M '
•'•• i!.'/'1' ''A
• •, .0.1
'•'"" 'I:'"
^;:.';;.22 "
(•'.'' 246.''-
•''£•'• 3
• )j050''.- :
• i7,' Z0fl.'';.i;
. '^OlA* , •
'•" 200 .,.. •
1 ,. .
'v O.|.
i' 240 .••1.;
•• o7i
ji ... P* i '•
, • •! •' sno -"
'.,4,660 '..',..
'• ' •
t '•: ttJ1.
.... '400.
"I 700
.' 90'
4,200
•• CO •
.7,000
• 1
0 26
7» '.
60 •
800
18
290
20.
36
18 .
26
-3
80 •
1
6
6
1
-128-
-------
Chapter XVII—Occupational Safety and Health Admin.
§1910.1000
/?-!—iCoptlhuod-
,. . TADtn
• .•!•'•• : .iBubstnneoi ;. • ;.^
1 . •". ' ' . • ••'''-,.''
ninltro-o-trcaal— Bkln.. ... ::;i..-
Dlnltrotoluono— Skin. :.„!..-.
Dloiimo (Dlethylcno dloilde)--
Kkln.-i .'...::':.:i.:.i.;1Ji
Diphcnyl: ::. ;,..i:..:.
Dlplii'iivlmnthane dllsocyanate
(sno Mi'thylcno blsphenyl..
Isocyanntc (MPI).-.
, nipronylme glycol methyl .
cihrr'-Skln..
DI-sPc, ootyl phtlmliito (I)l-i-
Epichlorhydrlri-Skln '....
ErN--Bkin ' ' ,~'
1,2-Epoxypropano, seo ..
rropyli'nooxlde. „..; —
2,3-Epo»y-l-propimol, aeo
.Ulyoldol..;-. „.;.•..:.
Klliiiuetlilol, ecu Ethyluier- .
• rnpun .'.... -.1 :...
2-K.lliniytlhnnol— Bkln ;;.'.;
•J-l'-.thoxypthylcicelruo (Cello-
1 ' pylvo nci'ttito)— 8kln.i j.'.. —
Elhyl iicryluto- Bkln. .: ..'.
Klliyl alcohol (etbiuiol).. ......
Kihylainlno.. •-.
.Ethyl joc-aruyl kntone (8-
mnlhyl-3-heptiuiOno) — .,-...
Ethyl.bontcno." '
Kihvl 1 bromide
Klliyl butyl kctono (8-
Klliyl chloride
Klhyl ether :.: ,
Elhyl formate;... ... — .::
O Klhyl inorcaptan...-.
Klhyl nllloate :.'. :-.
.Kthylono chlorohydrln— Bkln. .
Kthylcncdlanitno
EtbvliMio dlbromldc, soe L2-
Dlbroruoothane
Elhylcne dlchlortde, soe 1,2-
1 JJlchloroethane '
C Ethyleno slycol dlnltrate ,
and/or Nllroglycerln— Bkln.:.
Ethvluno plycol inonomethyl
cdlosolve acotato. ...:..:
Ethylcne linlne— Bkln
Ethyleno oildo —
Ethylldlne chloride, aeo 1,1- ,
N-Kthylmorphollne— Bkln......
Koi'bam .' :-'.
Fifrnwunadlum dusti
Fluoride (oa F) : '.
• Fluorotrlchloromothane •-
Formic acid :....
Furfuryl alcohol ' :
(Jlycldol (2,3-Epoiy-l-
Olvrol monoothyl ether, see..
• Qnihlnn ®p seo Ailnphos-
Hrpuchlor— Skin
llcpinnc (n-ltpptmie)
Hexiirhloroothane — Skin
llt'xiichloronnphihnlono — Skin..
Ilftann (n-heianu)
lloion- (Mpthyl Isolmtyl
Uriiiiie).:. .:
Bro-lloiyl irctnte
i^m^v.^^;.:; ^
:•'.. - -
i. . : • -;
•
!;'.V ^ a.
•j •, I- . . .
. .' '• •'-. V
. 1 ........
ibo".
:.........
"" "l ','•
. - -
..........
. - 3
• zoo,.-.
' -:ioo
. : 400 '
.. 28
1,000 .
10
28
100 .
200
80
1.000
• 400
.100.
- •• 10...
100
'••:•.• 10.'-.
- . ' .
i'.-'':^l- '••'','' ;
- : ';.'!'.'*t.-,-i;. '.
•' V.vJ!'.-1:1 .;,';'•.•
...^:'..',; J.i_J -
-."-',"''' i'obo-Vi." '.
. ~ "*' • • , .••'',
• • .:•..,• 5 '-. '
• ' ' 0 1 '"
:•;...: 1» ' i •: '
.: ... ;•. a6'lj'
' ,' . • ' • .;.l' -'V' .
-.!".?;••::'">••/•
'. • . • •
- •• "4 •';•,•;'••.
•:!• • .740 ./ .
. .''-MO .• , •
. i, 4oa '•
. 100 .•; ' .
.'..'• 1.000- .
'•"' ;. .' 18 :•
':' '. Vl30'.,V " '
: . i 438 ••;;•...•
•'. 8BO .'•.-
• <> 330 -
3,600 '-,
1,200
- ' 300, ••••.
..-. ...28.;.:
: : '. 860-:
: 10 . ' '
1 . -n •••':••
'•>,'.
:..i.....
'.'.,' ..,'.: 1;. .•
...'.• 1 .
,; '• 90 . •
. . - 94 .
:. . 16
.: . i
.:. ''• 2.8
:. 0.2
8,600
9
;• •' • 20 ;,
200
160
0.6
0.6
2,000
. 10
0.2
1,800
410
410
300
Nee footnote nt end of tuble.
;. ' . ..i , .'•'-': -, • -. •.. '•. t . .'• .-.' ;... , ...
Hydrritirio—-HVIiHL '' ,'..^'.'j,',i
Hydroitoii brpinldo..;,1:...^:1.::.' »'.
C HyoroKuh chloride...'.'...-.::.
Hydrogen cyanide- Skin.. '^.. '.
', Hydrogen peroild.0 (00%).;...- .
Hy droiten'solenlde.:.: . J, .'. ._fi . . •'
Hydroqulnoni)......' „,.:.:,..>
O lodlno :.'j.....:..'i:uL. •!•
Iron oildofumo.: ,y^:..;.
'Isoiinjylacotnto.......-.:w.':..;. •.
Isoamyl olcoliol... i-V.i;,^
Isobntyl uootato.......:..^;..',:, . . .
.Isophorone : -.• ':...!.. •.
Isopropyl ocolate ;.-.';.:.:.. ;:
Isopn.pyUlwihol.....;..^,;...:
tsopropyliuiilno :. 1 •
•Isopropylethor.:.,::.,...iiJ:1.4j' •-
IsoprOpy] glycldyl ethoi (1QE}:.M :;
Ketone..... ...,...-;^.., v.
Llndiino-Bltln .'.;.•.[.:::....
Lithium hydildq.;.. .-..:. -j,..::....
L.P.O. (llqulilod petroleum1 'V.
UOS) .-.j: j.:.' '1,
Mnnnoalum oxide fumo.;.: — ... ..
Malnthlon-Skln .'A'...
Mulelo auhydrldo J.....J..
'O ManiTQiioso ' ' » **>^
MOHltyl oiidn -.-. i'-.-Wii .•,.'.
Mothnnethtol, see Molbyl !:.'.":., •'.
roercapton .'.;'.'......
Mothoxychlor .;
2-Mothoxyethunol, coo Metbyl ..'.
Methyl acotote... ;:.-..:..•
Methyl orotyleno (propyno) - . . . 1,
Methyl acotyleno-propadlene' '
mlrture (MAPI1). .:...,:...'.: 1,
Methyl aoryloto-Skln....-,i
MethylaKdlmothojy ruethone).. 1.
Methyl alcohol (motUunoU...... '
Methylnmlno .'.' •....,:..
Methyl amy) alcohol, see
Methyl tsobuty 1 ourblnol.... '.-
Methyl (n-amyl) kotone (2- '
Heptanone).: ...i.i;. .
C Mothvl bromide— Skin. ...:..
Methyl butyl ketone, seo 2-
Heianono
Melhyl cellosolve— Skin
Melbyl cellosolve acetate— Skin
Mothyl chloroform
Mothylcyclohexano...
Motbvlcyclohcxanol
o-Mothylcyclohexanone — Bkln..
Metbyl ethyl ketone (MEK),
see 2-Butanone
Methyl (ornmte
Mothyl lodldo-Bkln :....
Mothyl Isobutyl carblnol— Bkln.
Mothyl Isobutyl ketone, BOO
Iloxone ^: .:
Mothvl (socyanote— Skin
O Methyl inorcnptnn-
Mothvl mul.hacrylato
Mothyl propyl ketone, seo 2-
I'onlanunn
C a Mulhyl styrene
C Muthylone blunhonyl
. Isouynimtc (MU1)
MolybdRiium:
Soluble compounds
1 ii30liiblo compounds '.
Mono methyl ftiillliio- Skin
C Mmiomothylhydrattno—
Skin
Mnriihollnn— Skin
Naphtha (coullar)
Naphthalene
See footnotes nt end of tnblo.
' ': V ', * •• '
'lij '..' :'.
<••»•-. • ..
8 . :. .
w*
:'•'*•• -':.';.
. 0.1 :
ioo':'"X:'
100 „•:;•; •.:
160; ."••'
26 .,'-...-
280 ' -..,.
400 v •..'•.•
•', 8 T.'i '.. :
J50D '.'V'-., .
:; as' r...'
000,..,. •.;
1
6f 28 'V
.•'•'». '
?*".:•''"'
j^ •
200 . .:
ooo :
OOO'/:':.
10V
000 '.-'
200 •.,. ; '
.10. '••
100 • .
20
36 •
- 28 .-,-
880 .
600
100
100 •••;
100 .
A
23
' ft 02 '
10
100
100
0.02
2
0.2
20
100
10
' • '•'•
.',;' ,.:,.1,'3 ;' . '.''. .
i •' Jfi-. • ,',' . , ,'
'•''i:' 1.4.. '-'i1'*.']
,: ,.. 0. 2. ' ^
: ' .. ' 2 -^ - . .
;; ', 1 ' '.."- -•
'::,m .:•'.'.>'•
;'. 880 .•'•• "...•'• '
1 :- 800 '.' ' •
'•/•..HO/:.'.1 '' -.•
: .'jflBO- . '' ;.
!.'•.- 980^ ';, ' / '-'
,. .- '12' '[ , • ;
,/2, loo.' r1:-,. ,.
.- .240 :•:•!;•.'•'"
H''I -a'9 •• .. •••
v . '. a 6'. •• . '
-•;. ,0.028 :
: i.Boo.-7'.-, ' '..
" 16--' '. '
.;-U8::'
••:•:>, I.':.' • '
.'. •-• :8 . u
'.. -. 100: •• .
'.'. .'.18 '.
" •''",'
010 !•• ;. '
' • 1, 680 .. ' .-.'
' 1.800... "
:. ,3.r> . .
;.3,IOO:
'.' ' 12. .. .
• 40S '
' '80
80
..-120
1,000.
, 2,000
. -.. 470
;.!4«o . .
250
28
100
a 06
20
410
480
0.2- •
8 '
18
• y
0.38
70
• 400
60
-129-
-------
§ 1910.1000
Title 29—Labor
TABLD 3-1—Continued
TABLE Z-l—Continued
:i. . '•• Substance
NlcUol carbdnyK . :
Nickel, metal and soluble •
ompds, us Nl....-
Nltiitlno-Skln...,-. '
.NHrluncid.'... .:, • •
Mtilooildo..
p-Nltroanlllne--8kln:
Nltiobunv.oMo-Slcln
p-Nltnx'.lilornboiiiona-r-SUn
Nltroothuoo...
Nllrogon illnildiil
NllrO||iMi trtllciorldo :
Nil romel linne •
2-NIUopu)piuio. . --- -;
Nliniliiliioiio -Skin
Nitron IcMdnniiuthaiio, >ee
Chloroplrrln
Oiaut-hlormiiiphlliHlono 'Skill...
•' (r.tuiio
•Oil HiJst, mineral
Osmium letruxiitfl,
Oinllenrlil
Oxygon dltluoi-lde. -.'
Ozii'in
Pnramiat — Shin
Pnratmon— Skin
Pimtuchloronaphthnlono— dkln .
•Ponlaiio
2-poiitanonfl
Pnrcliloromeihyl mercaptau
Purchlory I fluoride
Petroleum distillates (naphtha).
Phcmol— Hkin
p-Phnnylmin dlamlne— Skin
Pheiiylothor (vniwr)
Phimyl uther-hlphonyl
Mixture (vnpor)
Phonylethylmiii, urn Stvreno
Phenyl glyc.ldyl ether (PUE). ..
Pheiiylhydratlne -Skin
Phosdrln (Mevlnphos Oj) )—
Skin
PhoiKnne (carbonyl chloride)...
Phnsphliip
Phosphoric ai-ld
Phosphorus (yellow)
Phosphorus trichloride
1'liTlcncld- Skin...
PiviU © (2-Plvnly 1-1.3- .
Indoiidloiin)
I't
Pnipantyl alcohol— Skin
Propane
n-l'ropyl acotiito
Propyl ulciihol
n- Pi opyl nl trate
Propylnne rtlchlorlde
Propyle.no oslde .'
Pyrcthrum
Pyrldlno
Qulnono
UDX— Skin
Khodlum, Metal fume and
dusts, as Un
Soluble Balls
Rotenone (commercial)
p.p.ro.v. ' i
'0.001
-2 ' •
1 • • ' i
i - .;
100
3
in
as '
100
25 •
29
8
600
O.OS
(HI
0.009
1.000
200
o.« •
3
too
9
1
1
10
9
0.1
0.3
0.8
2
1
l.ono
'JCO
200
III
7»
0
100
9
ai
n njl
ng./M» • •
6.007
'' ''' 1
•• , a 9
,• 30' :
,. ,fl .
-••' -'.I- .,
31 Ov
.• . u
,, 2H
2
' • 2^0 '
90.
. • 91)
i 30
0.1
2,391)
•9
0.009
1
ai
1 0.3
: 0. 6
an
• • o 01
; o. 8
09
,700
. ' 0.8
13.9
2, oin
in
0.1
I
7
60
y2
0.1
0.4
0.4
1
0.1
1
1
8
12
• ai
ai
0.002
"i.'soo""
840
600
111)
3W
MO
6
19
0.4
1.9
ai
0.001
10
6
n A
. - ' .. . '. Substance f. •'„• • :. I
. Silver, motal oiid soluble com-
pounds :...' — ...;...
Sodium Guoroncntuto (1080)— ' .
Skin
Sodium hydroxide..
Btiblno....
•Htoddard solvent
Htrychubie
Sulfur dloildn.. i
fiulinr hniufluorlde ;
tjulfuilc iicld .';.•...„
Sulfur inoiiuchloi'lde
Sulfur prntufluorlde.
Sulfliryl Iliiorliin.. ::
2.4.BT
Tftntnluni
TKDP-Skln
Tellurium.. : '.
Tolluiluin hninfluorlde
•I'KPl'— Kklii
C 'rerphoiiyly
l,l,1.2-Tntiachloru-2,V!-dllluoro-
othnno
l,l,' •
0.01
. a 09
2
0.9
2,950
0.15
. 13
8,000 '
1
0
0.25
20
10
8
0.2
0.1
0.2
0.06
8
4, 170
4,170
38
i , Z
0.078
6 DO
a 07
3
8
1.8
0.1
6
2
0.1
0.14
22
9
46
1.1
9
800
7,000
100
6.100
1.8
0.1
3
(60
0.09
0.8
ai
Set: footnotes ut end of table.
Seo footnotes at end of table.
-130-
-------
Chapter XVII—Occupational Safety and Health Admin.
§ 1910.1000
: TABLE Z-\—Continued .
I TABLB: Z-t-^Conttnued
•'•'.. .Substance;, .
Vluyl toluene
Warfarin.....::.;:.,...,
Xylono(xylol).........:
.Xylldlne— SUn...-v...
•I<)7n Ailtminn '''.'.
-.•;• . • ]+&^2w$$';:f$f' ': :®&&"»yM^ 1ww$l;:'«
....:.'. '.'.'-•'lOB / <;•'••. ''\(JIM''^.«'.: ''Vttrtum1.::^^;.^^::^:;!:;^......^.. ,
A ..;..-.' *">M •• .. Zlno chloride fumo......»...... .......,...-, .
....:;. ' 100 ••••-, 'i 438 -. i Zinc oxide fume..... lr. .....:.... ;..:"....;;
....... :ft ..-.Bar. Zirconium compounto(aaZr)... '...........
(6-/M»f; '.
'.^';i';.'-'':"
•M'-S." ••
,;,.->-•' O ' / ':, .
. Tana of vapor or ROB per million parts o( contarhl-:•
Dated air by volume at 28° O. and 760 mm. Hg pressure.
* Approximate milligrams of paniculate par cubic
motor ol air. : • . . .
. (No footnote1 "c" Is used to avoid confusion with
celling value notations.)
.
0.02, p.p.m., or personal protection may be necessary .
to avoid headache. ' ~ •,.••,.'/;.'••.,.• ','<>?[ •
• As sampled by method thqt does not collect vapor.
/ For control ol general room air, Biologic monitoring
Is essential tor personnel control. . '' . "-',''. ' '•
TABU Z-2
Material
•-.v: .••.-•!•.: • >-'':- ...,.
8-hour time >coeptable
weighted • celllna '
Acceptable maximum peak above
the acceptable colling concentra-
tion for an 8-hour sain. "..'."
•'••-'••' ' ' '••' . •;.. '•'.'
nenzone ^237.4-1989) : . ........':
Oerylllum and beryllium compounds
. (237.30-1970). ; • \ • , •• .
Oadniluiu fume(Z37.H970). .' ...
CoJmluin dust (Z37.5-1070)...;.., •.:...
Oarbou teirauhlorlde (237.17-1907)111!""^
Etliylenadlbromlde(Z3T.31-1970)
llthylone (llchlorlde (237.21-1969)
Formaldehyde (237.16-1967) . ......„;.....
Hyilrosuu fluoride (7.37.28-1909)....
Fluoride us dust (Z37. 28-1000) . . ...
1W19). • ... • .••... i
MetliylclUorldo(Z37.18-1909)..:... :..
Mctliylene ohlorldo (737J-I909):.:
Styrono (Z87.I5-1UOO) . .... .. . .i
Trlcliloroothyloiie(Z37.19-10C7J....:
Totrnchloroetliylone (237.22-1987)
Toluona (Z37.12-10H7) :..... ...
llydr<4;(ir.iiumde(Z37.2-19«8)
Meriniry (787.8-1071) . .. .
• Chroiiiio iir.ld und oliromatea (Z37.7-1971)
pywoge
^ IQp.pjn. ..'...
•0.1rag./M'.....
O.Smg./M«.....
•20p.p.1:p.. —
10 p.p.m
20. p.p.m..
60p.pjn
ap.p.ro-.....-
0 2 012 /M1
100p.pjn
800 p.p.m
001m(T./M'
100 p.pjn.'....
.....do.........
SOOp.pJD
S'mg'/Mi
.. O.Oiug./M>....L..
.. 80 p.p.m. .-.
,. 28 p. pjn.. .......
.. Mp.p.ml..
... lOOp.p.m ...
.. 8 p.p.m
200 p.p.m.. ...
1,000 p.p.m
0.04mg./M« . ...
200p.rxm
do.....
...;.do.....,~. ....
300 p.p.m
20 p.p.m
IrogJlOM'
Concentration
M • •_•: ;
2ftug.VM* •• . ' •
.' . '• . '•
200 p. p.m. !".....
obp-p.m":: — ..
10 p.p;m.. ......
SOOp.pjn.
9,000 p.p.m. ....
600p.p.m.
800 p.p.m. .....:
.....do :..
500 p.p.m
80 p.p.m
'..duration .: • - ',:'••'.
10 minutes. ' '
SOmlnutee. '
' i ' -'.'• • • ' ''.''•'
.•;''i"bo. .;- ",, ••.. . . ' ;• .
8 minutes In
any 4 hours.
S minutes; '. • •
' fl minutes In" . -' '
: any 3 hours. :
30 rn|nutes. ; ,; . . ;;.
•:. - ' . ' ' -
8 minutes In . ' ;
any 3 hours. ;•
8 minutes In ; :•
any 2 hours.
(minutes In
any 8 hoars.
6 minutes In i
any 2 hours.
t minutes ID
any 8 hour*. . .
10 minutes. . •
10 minutes once
only If no
. other measur-
able exposure
occurs. • , •
-131-
-------
§ 1910.1001
! ' Subttance . . 'Mppc(» . > Wg/Mi
.aiilc'n: .' ".•';••'.••''•
Crystalline: :
. Quartf (rosp|rnble).
: • %HlOi+« . . %6IOi-f3
Quartt (total du.it)......'..; :...... 8flrng/M»
%8lOi-f« ..
'
Cil.iiohnJllo: UTO M the
vuliin imloutuUHl from tho
count or III.IHS fbrumlno (or
quurU.
TrMyuillo: U«u H Oin valutt
I (nun tho for-
,,
Aniorpliou>, Including natural
Killantn On" thtn 1% cry»-
lalllno elllco): '
Tata(non«3bu»to»-fornD)... :
Tolo(nbrouB). U«e oaboitoa • .• •
limit . ••". • ;
Tnupollto (uo tole, flbrotu) .
. PorUunitromnni..,.-. M .
Clraplillo (inltuml)....- 16
Ooitl dust (ri'3plr»me traction ...
Itva than 6% BlOi).. 3.4ulg/M"
or
For more than 6% BIOj...' lOmg/M"
Inort or Nnlsunci' Dust:
KasplrfiWo fraction... IB
Total dust M ISmg/M"
Nora: Cuiivrrelon footers—
mppcfXSi 3»ml|lloii panlolos per cubic meter •
. -.ourtloKo per c.o.
• Million] of purttclei ixr cubic Coot of nlr, bcued on
Iroiitnger wimples oounUd by llght-flc
.
iMroinitaia of oryitiullno silltu In ihn tormuln
In tlio pmuiint dttermlnoil from alr-burnn :;>unrilo3, n-
c\M>t In IbnM InatuiiouM In vrblch othor nioihods haro buun •
sbuwn (o bu uppllcabla.
i At doMJinlnmJ by tho moinbrniio flltor nittbod M
4HUXuha»o ooDtnuil roannlflcutkiii.
• ItDlh I'onornlrAtlon and uarrnnt qunrti tor th) eppll-
cnilnn of Hi U limit am to heoiiterinlnnl bom tlir fraction
pallid a tttiH^hH'lor wllh thn fdllowliift churnclorlstlcs:
•OantulpUig < 1% qtuirti; If > i%i4uurtt, tue quarts
Illllll.
Arnulyrmnili' dliunotor I'orront poking
(milt iluiully splinru) wlector
•I 00
2.6 71
3.6 U>
6.0 an
10 . o
'l"be ineiisiiroramts under this note rotor to tho USD oj
an AVX; Instrument.C' tho rosiilrnbl" fntctlun of roiil
(luHtlirtutKrinlncU wllh oMRE iliiillKiiroooirospoiitlliil
tn Unit of 2.4 Mj/M' In i ho tnbln for >'oi>l MIIBI Iv 4.1 M«/M«.
|39 PH 23602. June 27. 1074. Krdu.Hliincttcd
unit runondecl at 10 PR 2:1073. Muy ^0, 1976 J
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Appendix C
CANADIAN PROVINCES AND FOREIGN COUNTRIES QUERIED IN
THE SEARCH FOR INDOOR AIR QUALITY STANDARDS
Country
Arc'tulnu
Argentina
AU.B.IU
Austra llu
UutralU
\uftrulia
AustrU
Department
Secretarial of Natural
Resources and Human
Environment
Argentina Association A sal nit •
Air Pollution
Dept. of Environment and
Conservation
Mlnlitry of Coruervarion
State Pollution Control Cum minion
National Health .ind Medical
Research Commission
Health and Environment Protection
Dept.
Standards
Indoor Oeilcn •
Reply None Air level E mittimus Com menu
\ * Industrial Standard*
X A
Industrial and outflde
x x ambient standard*
XX ,
B«ilRlum Mlnlrtry of Public Health and
Environment
Brail! '
Bulgaria
C Jtudu
C.inada
C.mvdj
CaniuU
Cjnada
Canada, Manitoba
C.inada
Canada
Newfoundland
C madu
Canada, Prince
Edward Iltand
Canada
0,,a.U
Canada
China, Republic of
Ministry of Interior
Ministry of Forestry and Environment
Council of Resources and
Environment Mini teen
Dept. of the Environment
Environment Canada
A Iberta Dept. of the Environment
Britain Columbia Pollution
Control Branch
Dept. of Mine*, Resources end
Environment Management
New Brunswick Dept. ofFUherlea
and Environment
Canadian Standard! Association
Dept. of Tourtim
Ontario Ministry of the Environment
Environmental Control Commlaion
Montreal Air Purification and Food
Inspection Dept.
Quebec Environmental Protection
Services
Saskatchewan Dept. of the
Environment
Ministry of the Interior
X X
X X
x xx UseACCIH
Co Standard
-
UseACCIH
x xx Co Standard
x x
x x Standard for Oj
PCDduclai Device)
x x Outdoor ambieat standard*
X X
XX
-133-
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Country
Colombia
Cieclw ilovaki a
Denmark
Denmark
France
France
France
Fedora! Republic
of Cermanv
Federal RepuMIc
o ( C «rm a n \'
Finland
Creece •
Creece
Creece
Hunt; Konc
Indoor Deiign
Department Reply None Air Level Emtatoni Commenti
National Unlvenlty of Colombia
Czech Technical Environmental
Control
Init. of Hyp;. U. of Aortal x • x
Mlnlitry of Environmental Protection x x
National Intomtadon Office on
Environment*! Problems
Protection of Nature and Environment x x
International Association of Medicine
ind Biology of Environment x x
Bavarian Scale Ministry for Countryride
Development and Environment x x
Mlnlnry or Agriculture
jnd Environment x x
Division of Environmental Protection,
Mlalstry c( Interior
Ministry of F nergv
"K. E. P. E. ," ProgramminR and
Economic Research Center
Committee for the Protection of
Atmosphere from Pollution
Labour Dept. x x
Huim^rv Eorvoi Lorand University, Faculty
of Natural Sciences
India
hull*
[ran
IreUnd
.'Israel
Israel
Italy
Japan
Japan
Malta
Mexico
Mexico
Sutherland!
New Zealand
National Committee on Environmental
Planolnfi and Coordination
A 11 India Institute of Hygiene and
Public Health
Mlnlnry of Health
Foreit and Wildlife Service
Environmental Protection Service x x i**««»i»rficwii MUM dim
Central Laboratory for Prevention of
Air Pollution and Radiation Haiardi
Centre of Initiative! for the Tutelage
and Rehabilitation of the Environment
Environ men ta 1 A gency x x
Environmental Improvement Team
Malta Human Environment Council
Secretariat for Health and Welfare
Subiecretary of Environmental
Improvement _ x . x
Sufafdellng International Zaken
Commlttion for the Environmeat
NVn\ J> Norwegian Injtltuto (or Air Retouch
Phtllpptnei
IMl.md
Manila Health Dept.
Ntlnlstry of Resourcoi and Cnvlranmontal ^_^
Protection x x
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-------
Country
department
Standards
Indoor Design
Reply None Air Level Emissions Comments
RomuniJ Dlrectia Ue Posta a Munlclplului
Bucurud
SI,,™**
South Africa
Spain
Sweden
Sweden
SwitTerUml
Ministry of Environment Air Pollution
Unit
Dept. of Planning and Environment
Dept. Contra La Contamlnaclon
Acmosfertua Del Aquntaralento Oe
Madrid
National Board of Environmental
Protection
Scandinavian School of Public Health
Kedenl Air Quality Commission
X X
X X
XX
t'niiiiij A oo eld don fur Protection of Nature
• nj ihe Environment
I'urkev
U.S.S.R.
United Kingdom
U.K. , England
U.K., England
U.K., England
Venezuela
Yugoslavia
Auocliidoti for tlte Conservation of
Nature and Natural Resources
Institute of Sute and Uw •
Clean All Council for Scotland
Dept, of the Environment
Royal Commission on Environmental
Pollution
Institute of Heating and Ventilating
Engineers
Ministry of Agriculture
Committee for Chemical Engineering
Yugoslav Society for Clean Atr
* ^rTVTjr^'*"*"
x x Minimum ventilation
rates for supply of fresh
outdoor air
X X
X X
x x Minimum ventilation
rates for supply of fresh
outdoor air
X X
-135-
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TECHNICAL REPORT DATA
(Please read Inductions on the reverse before completing)
i .
4.
7.
REPORT NO. 2
EPA-600/7-78-027
TITLE AND SUBTITLE
SURVEY OF INDOOR AIR QUALITY HEALTH CRITERIA AND STANDARDS
AUTHOR(S)
James E. McFadden, J. Howard Beard, III, Demetrios J. Moschandreas
9. PERFORMING ORGANIZATION NAME AND ADDRESS
CEOMET, Incorporated
15 Firstfield Road
Gaithersburg, Maryland 20760
12
15
16
17.
a.
. SPONSORING AGENCY NAME AND ADDRESS
U.S. Environmental Protection Agency
Research Triangle Park, North Carolina 27711
U.S. Department of Housing and Urban Development
Washington, D. C.
SUPPLEMENTARY NOTES
3. RECIPIENT'S ACCESSIOWNO.
5. REPORT DATE
August 1977
6. PERFORMING ORGANIZATION CODE
8. PERFORMING ORGANIZATION REPORT NO.
GEOMET Report Number EF-595
10. PROGRAM ELEMENT NO.
11. CONTRACT/GRANT NO.
Contract Number 68-02-2294
13. TYPE OF REPORT AND PERIOD COVERED
14. SPONSORING AGENCY CODE
EPA-ORD
ABSTRACT
This report is a survey of the state-of-the-art of the scientific studies on indoor air quality criteria and standards.
The principal subject is the Indoor nonworkplace environment. Indoor air quality standards are classified into three
types: (1) maximum allowable air quality standards; (2) design-level standards; and (3) emission standards. Each type
may be a guideline, a rule or regulation or a standard with force of law. Both American and foreign efforts to issue
standards in each of the types are discussed. The existing indoor air pollution standards and the health criteria docu-
ments on which they are based are enumerated. The major conclusion reached is that there has been no scientific
effort to establish air pollution standards specifically for the indoor nonworkplace environment.
KEY WORDS AND DOCUMENT ANALYSIS
DESCRIPTORS
Indoor nonworkplace environment
Air pollution
Criteria pollutants
Threshold Limit Values
Health Criteria Documents
Ambient Air Pollution Standards
18
DISTRIBUTION STATEMENT
RELEASE TO PUBLIC
h. IDENTIFIERS/OPEN ENDED TERMS
19. SECURITY CLASS (This Report)
UNCLASSIFIED
20. SECURITY CLASS (This page)
UNCLASSIFIED
c. COSATl Field/Group
21. NO. OF PAGES
136
22. PRICE
EPA Form 2220-1 (9-73)
136
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