Indoor Pollutants
(U.S.) National Research Council
Washington, DC
Prepared for
Environmental Protection Agency
Washington, DC
Mar 82
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Indoor Pollutants
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Committee on Indoor Pollutants
Board on Toxicology and Environmental Health Hazards
Assembly of Life Sciences
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TECHNICAL REPORT DATA
fPlcuit md ImDvclions on the rrvtrst ttfore completing)
1. REPORT NO. 2.
EPA-600/6-B2-001 ORD Report
3. RECIPIENT'S ACCESSION NO.
fNt 1 8056 13
4. TITLE AND SUBTITLE
INDOOR POLLUTANTS
5. REPORT DATE
MnrrN
S. PERFORMING ORGANIZATION CODE
EPA-600/00
7. AUTHOR(S)
Committee on Indoor Pollutants-National Academy of
Srlpnro
S. PERFORMING ORGANIZATION REPORT NO.
9. PERFORMING ORGANIZATION NAME AND ADDRESS
Committe on Indoor Pollutants-National Acadeuiy of
Science
10. PROGRAM ELEMENT NO.
11. CONTRACT/GRANT NO.
12. SPONSORING AGENCY NAME ANO AOORESS
Science Advisory Board
Office of Research and Development
U.S. EPA
WasMnofnn T1 C
13. TYPE OP REPORT ANO PERIOD COVERED
14. SPONSORING AGENCY CODE
IB. SUPPLEMENTARY NOTES
18. ABSTRACT
This report is intended to characterize the quality of the indoor environment—
primarily with respect to airborne pollutants, although others are discussed—
and to determine the potential adverse health effects of indoor pollutants. The
charge was to "view, compile, and appraise the available knowledge. The Committee
has also identified the research needed for abatement of indoor pollution "Indoor1
to »hich°t™e e°'lr™ts ln school,, public buildings, and ,paces
ScSS from considers»—¦ -
17. KEY WORDS ANO DOCUMENT ANALYSIS
a. OESCRIPTORS
b. IOENTI PIERS/OPEN ENOED TERMS
c. COSATi Field/Group
19. DISTRIBUTION STATEMENT
19. SECURITY CLASS (Thit Report)
21. NO. OF PAGES
sss
SC. SECURITY CLASS (ThUpagt)
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EPA Form 2229*1 (9-73)
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INDOOR POLLUTANTS
COMMITTEE ON INDOOR POLLUTANTS
BOARD ON TOXICOLOGY AMD ENVIRONMENTAL HEALTH HAZARDS
ASSEMBLY OF LIFE SCIENCES
NATIONAL RESEARCH COUNCIL
NATIONAL ACADEMY PRESS
WASHINGTON, D.C. 1981
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NOTICEi The ptoj«ct that ia the subject of this report was approved
by the Governing Board oE the National Research Council, whose members
are drawn from the councils of the National Academy of Eclences, the
National Academy of Engineering, and the Institute of Hedicine. The
members of the committee responsible for the report were chosen for
their special competences and with regard for appropriate balance.
This report has been reviewed by a group other than the authors
according to procedures approved by a Report Review Committee
consisting of members of the National Academy of Sciences, the
Nati6nal Academy of Engineering, and the Institute of Hedicine.
The National Research Council was established by the National
Academy of Sciences in 1916 to associate the broad community cf
science and technology with the Academy's purposes of furthering
knowledge and of advising the federal governmerit. The Council
operates in accordance with general policies determined by the Academy
under the authority of its Congressional charter of 1863, which
establishes the Academy as a private, nonprofit, self-governing
membership corporation. The Council has become the principal
operating agency of both the National Academy of Sciences and the
National Academy of Engineering in the conduct of their services to
the government- the public, and the scientific and engineering
communities. It is administered jointly by both Academies and the
Institute of Medicine. The National Academy of Engineering an
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COMMITTEE OH INDOOR POLLUTANTS
JOHN D. SPENGLER, Harvard School of Public Health, Boston,
Massachusetts, Chairman
MICHAEL D. LEBOWITZ, University qf Arizona Medical Center* Tucson,
Arizona, Cochairman
RONALD W. HART, National Center for Toxicological Research, Jefferson,
Arkansas
CRAIG D. HOLLOWELL, University of California, Berkeley, California
MORTON lippmann, New York' University Medical Center, New York, New York
DEMETRIOS J. MOSCHANDREAS, GEOMET Technologies, Inc., Gaithersburg,
Maryland
JAN A. J. STOLHIJK, Yale University School of Medicine, New Haven,
Connecticut
DAVID L. SWIFT, The Johns Hopkins University, Baltimore, Maryland
JAMES E. HOODS, JR., Iowa State University, Amen, Iowa
JAMES A. FRAZIER, National Research Council, Washington, D.C.,
Staff Officer
NORMAN GROSSBLATT, National Research Council, Washington, D.C., Editor
LESLYE B. GIESE, National Research Council, Washington, D.C.,
Research Assistant
JEAN E. PERRIN, National Research Council, Washington, D.C., Secretary
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C0OTR3BUT0RS TO the report oh ihdoor pollutants
jambs BERK, University of California* Berkeley, California
WILLIAM F. BRANDOM, University of Denver, Denver, Colorado
DAVID H. BURNS, University Hospital, San Diego, California
BENJAMIN BURROWS, Arizona Health Sciences Center, Tucson, Arizona
WILLIAM CAIN, Yale University School cC Medicine, New Haven, Connecticut
ROY R. CRAWFORD, Iowa State University, Ames, Iowa
CHARLES W. DEHNIGER, Stanley Consultants, Inc., Muscatine, Iowa
DOUGLAS DOCKERY, Harvard School of Public Health, Boston, Massachusetts
NURTAN ESMSN, University of Pittsburgh, Pittsburgh, Pennsylvania
HUGH EVANS, New York university Medical Center, New York, New York
ARTHUR FRANK, Mount Sinai School of Medicine, New York, New York
RALPH F. GOLDMAN, Institute of Environmental Repeatch, U.S. Army,
Natick,, Massachusetts
JACK D. HACKNEY, Rancho Los Amigos Hospital, Downey, California
CHARLES M. HUNT, National Bureau of Standards, Washington, D.C.
GEORGE JAKAB, The Johns Hopkins University, Baltimore, Maryland
JOHN E. JANSSEN, Honeywell, Inc., St. Paul, Minnesota
EDOARDO A. B. MALDONADO, Iowa State University, Ames, Iowa
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PRESTON £. McNALL, National Bureau of Standards* Washington, o.C.
BRIAN MOKLER, Lovelace Biomedical and Environmental Research
Institute, Albuquerque, New Mexico
GERALDINE M. MONTAG, Iowa State University, AmeB, Iowa
ANISONY NERO, University of California, Berkeley, California
ANTHONY NEWMAN-TAYLOR, Bronpton Hospital, London, England
WAYNE OTT, Stenzord University, Stanford, California
GARY L. REYNOLDS, Iowa State University, Ames, Iowa
RICHARD RILEY, Petersham, Massachusetts
GEORGE ROYAL, American Institute of Architects, Washington, D.C.
ROBERT N. SAWYER, Yale University Health Services, New Haven, Connecticut
FREDRICK H« SHAIR, California Institute of Technology, Pasadena, California
DONALD SIBBERT, GEOMET Technologies, Inc., Pomona, California
SAMUEL SILBERSTEIN, National Bureau of Standards, Washington, D.C.
WILLIAM R. SOLOMON, University of Michigan Hospital, Ann Arbor, Michigan
JAMES STEBBINGS, JR., Los Alamos Science Laboratory, Los Alamos, New Mexico
THEODOR D. STERLING, Simon Fraser University, Burnaby, British Columbia,
Canada
JAMBS E. TROSKO, Michigan State University, East Lansing, Michigan
MCDONALD E. WRENN, University of Utah, Salt Lake City, Utah
JOHN YCCUM, TRC Corporation of New England, Wethersfield, Connecticut
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BOARD ON TOXrCQLOCX AND ENVIRONMENTAL HEALTH HAZARDS
RONALD E3TABROOK, University of Texas Medical School/ Dallas, Texas,
Chairman
PHILIP LANDRXGAN, National Institute of Occupational Safety and
Health# Cincinnati, Ohio, V*.ce-Chalrman
THEODORE CAIRNS, Greenville# Delaware
VICTOR COHN, George Washington University Medicil Center, Washington, D.C.
JOHN W. DRAKE, National Institute for Environmental Health Sciences,
Research Triangle Park, North Carolina
A. MSRICK FREEMAN, Bowdoin College, Brunswick, Maine
RICHARD HALL, McCormick 6 Company, Hunt Valley, Maryland
RONALD W. HART, National Center for To*icological Research# Jefferson#
Arkansas
MICHAEL LIEBERMAN, Washington university School of Medicine# St. Louis#
Missouri
BRIAN MacMAHON, Harvard School of Public Health, Boston, Massachusetts
RICHARD MERRILL, University of Virginia Law School, Charlottesville,
Virginia
ROBERT A. NEAL, Chemical Industry Institute of Toxicology, Research
Triangle Park, North Carolina
IAN NISBET, Chemical Associates, Washington, D.C.
CHARLES R. SCHUSTER# JR., University of Chicago, Chicago, Illinois
GERALD KOGAN, Massachusetts Institute of Technology, Cambridge,
Massachusetts
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Ex Otficlo Members
EDWARD BRESNICK, University of Vermont, Arlington, Vermont
DAVID CLAYSON, Eppley institute for Cancer Research, Omaha, Nebraska
JAMES F. CROW, University of Wisconsin, Madison, Wisconsin
JOHN OOUI.L, University of Kansas Medical Center, Kansas City, Kansas
ROGER 0. McCLELIAN, Lovelace Biomedical and Environmental Research
Institute, Albuquerque, New Mexico
ROBERT MENZER, University of Maryland, College Park, Maryland
ROBERT MILLER, National Cancer Institute, Bethesda, Maryland
SHELDON MURPHY, University of Texas, Houston, Texas
NORTON NELSON, New York University Medical Center, New York, New York
JOHN ~. SPENGLER, Harvard School of Public Health, Boston,
Massachusetts
JAMES L. WHITTENBERGER, Harvard School of Public Health, Boston,
Massachusetts
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ACKNOWLEDGMENTS
This document Is a result o£ individual and coordinated efforts of
the members of the Committee on Indoor Pollutants and the contributors
selected to prepare various sections of the report.
Ors. John D. Spengler and Michael D. Lebowitz, Chairman and
Cochairman of the Committee, prepared Chapters I, II, and III, on the
basis of material submitted by the other members. Drs. Craig D.
Kollowell and Demetrios J. Moschandreas coordinated the preparation of
Chapters IV, V, and VI. Chapter VII was written under the direction of
Drs. Lebowitz, Morton Lippmann and David L. Swift. Drs. Lebowitz and
James 8. Hoods, Jr., collaborated in the preparation of Chapter VIII,
and Dr. Moods prepared Chapter IX and Appendix B. Appendix A was
compiled by Dr. Hollowell.
The whole manuscript was organized, reviewed, and approved by the
full Committee.
A special acknowledgment should be paid to Dr. Ronald W. Bart, who
chaired the Committee in its formative period and contributed
thereafter as a member.
Particular thanks should be extended to Dr. woods, who hosted a
subcommittee at Iowa State University to coordinate the material in
s&veral chapters.
For providing resource material and other information, we note our
gratitude to Dr. Joseph F. Cuba,* Director of Research at the American
Society of Heating, Refrigerating and Air-conditioning Engineers, inc.;
Mr. Harry Thompson at the U.S. Department of Commerce; Mrs. Nancy
Naismith at the Office of Technology Assessment; and Mr. James L.
Repace and Dr. Robert J. M. Horton of the Environmental Protection
Agency.
Assistance wi*s given also by the staff of the Committee on
Toxicology, National Research Council; the National Agricultural
Library; the National Library of Medicine; and the George Washington
University Library. Other persons assisted in many ways; our
appreciation is -extended to those not specifically mentioned.
'Deceased.
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Dr. Alan P. Carlin was the project officer for the Environmental
Protection Agency.
The staff officer foe the Committee on Indoor pollutants was Mr.
Janes A. Frazier, who acknowledges the generous assistance of Mrs. Jean
B. Perrin, secretary. The bibliographic references were verified and
prepared for publication by Mrs. Leslye B. Giese. Typing was done by
the Manuscript Processing Unit of the National Academy of Sciences#
coordinated.by, Miss Estelle Miller. The entire report was edited by
Mr. Norman Grossblatt.
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CONTENTS
EXECUTIVE SUMMARY
Scope of the Report ...... ES-2
Organization of the Report . . . , ES-4
Principal Findings on Specific Pollutants and Classes of Pollutants ES-5
Radon, ES-5
Formaldehyde, ES-6
Asbestos and Other Fibers, ES-6
Tobacco Smoke, ES-7
Indoor Combustion, ES-8
Microorganisms and Allergens, ES-9
Moisture, ES-9
Responsibilities . ES-9
Conclusions ES-10
Recommendations . . . ES-13
I INTRODUCTION
II SUMMARY AND CONCLUSIONS
Characterization of Indoor Air Pollution . . II-l
Radioactivity, II-l
Aldehydes, I1-2
Consumer Products, II-2
Asbestos and Other Fibers, 11-2
Indoor Combustion, II-3
Smoking, I1-4
Odors, II-5
Other Chemical Pollutants, 11-5
Airborne Microorganisms and Allergens, II-6
Monitoring and Modeling of Indoor Pollution . . . . . . . 11-7
Factors That Affect Exposure to Indoor Pollution 11-7
Health Effects of Indoor Pollution ................ II-8
Involuntary Smoking, II-9
Radon and Radon Progeny, II-9
Asbestos and Other Fibers, 11-10
Formaldehyde, 11-11
Indoor Combustion, II-12
Indoor Contagion, 11-13
Effects of Indoor Pollution on Human Welfare 11-13
Socioeconomic Status, 11-13
Productivity, 11-14
Soiling and Corrosion 11-14
Discomfort, 11-14
Control of Indoor Pollution 11-14
Control Strategies, 11-14
Codes and Standards, 11-13
Air Diffusion Control, 11-15
Indoor Environmental Control Sysreas, 11-15
Air-Cleaning Equipment, 11-16
Cost Effectiveness, 11-16
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Ill RECOMMENDATIONS
Radon
Formaldehyde ........
Tobacco Smoke . . . . ,
Asbestos and Asbeatlform Fibers ......
Combustion ........
Consumer Products
Aeropathogens and Allergens
Ventilation Standards and Control Strategies
Exposure Studies
Education ..... ..
11-3
11-4
II-5
11-6
II-6
II-8
II-9
II-9
11-10
11-11
IV SOURCES AND CHARACTERIZATION OF INDOOR POLLUTION
Radioactivity
1V-2
Introduction, IV-2
Sources of Radionuclides and Radiation, IV-7
Indoor Concentrations and Radiation Fluxes, IV-14
Control Techniques, IV-18
Research Needs, IV-20
Formaldehyde and Other Organic Substances IV-26
Formaldehyde, IV-27
Other Organic Substances, IV-37
Consumer Products IV-44
Aerosol-Producing Products, IV-46
Particles Produced as a Byproduct, IV-47
Products and Activities Assoctated with Evaporation or
Sublimation, IV-48
Some Mechanisms of Biomedical Effects, IV-50
Summary and Conclusions, IV-51
Asbestos IV-55
Definition of Asbestos, IV-55
Important Characteristics of Asbestiform Mineral Fibers, IV-55
Asbestos Production and Application, IV-56
Asbestos Contamination of the Environment, IV-57
Environmental Sampling for Asbestos, IV-58
Asbestos Air Data, IV-61
Standards, IV-65
Regulations, IV-67
Control of Contamination Potential, 1^68
Summary, IV-68
Fib roue- Glass . IV-7 2
Definition, IV-73
Concern over Potential Adverse Health Effects, IV-74
Importance of Characteristics of Fibrous Glass, IV-73
Analysis, IV-75
Standards, IV-73
Control, IV-76
Combustion Sources ................... IV-78
Residential Buildings, IV-79
Commercial Buildings, IV-91
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Tobacco Smoke IV-93
Background, IV-94
Contaminants in Smoke, XV-99
Indoor Concentrations of Particles and Vapors from
Cigarette Smoke, IV-100
Conclusions, IV-108
Odors IV-112
Sources, IV-113
Measurement of Odor, IV-119
Odor Control, IV-130
Research Needs, 1V-138
Temperature and Humidity .............. IV-147
Heat Exchange with the Indoor Atmosphere, IV-148
Physiologic Responses to the Thermal Environment, IV-154
Health Consequences of Extremes of Temperature and
Humidity, IV-157
Characterization of Additional Physical Indoor Pollutants IV-158
Sound and Noise, 1V-159
Radiofrequency and Microwave Radiation, IV-162
Far-Infrared and Infrared Radiation, IV-164
Visible Radiation, IV-166
Ultraviolet Radiation, IV-167
Summary, IV-167
V FACTORS THAT INFLUENCE EXPOSURE TO INDOOR AIR POLLUTANTS
Human Activities ............... V-2
Geographic and Local Variations V-7
Geographic Variations in Indoor Air Quality, V-10
Urban, Suburban, and Neighborhood Variations in Indoor
Air Quality, V-16
Variations in Indoor Air Quality in Buildings, V-21
Building Factors V-23
Site Characteristics, V-25
Occupancy, V-25
Design, V-26
Operations, V-28
Summary and Recommendations, V-28
VI MONITORING AND MODELING OF INDOOR AIR POLLUTION
Fixed-Station Sampling and Monitoring VI-1
Continuous Monitoring, VI-2
Integrated Sampling, VI-4
Grab Sampling, VI-5
Monitoring of Ventilation Rate, VI-6
Personal Monitors VI-7
Personal Sampling Devices, VI-8
Use of Personal Monitors in Exposure Studies, VI-11
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Modeling of Indoor Air Quality VI-19
Multicompartment Models, VI-21
Two-Compartment Models, VI-22
Single-Compartment Models, VI-24
Summary and Conclusions, VI-27
Estimation of Total Exposure to Air Pollution VI-28
VII HEALTH EFFECTS OF INDOOR POLLUTION
Introduction VII-1
Radon and Radon Progeny VII-6
Review of Dose and Exposure Calculations, VII-7
Biologic Effects, VII-8
Summary and Conclusions, VII-16
Formaldehyde and Other Organic Substances ............... VII-21
Effects of Tormaldehyde in Animals, VII-21
Effects of Formaldehyde in Humans, VII-22
Effects of Other Organic Substances, VII-31
Fibrous Building Materials VII-38
Specific Health Effects, VII-39
Laboratory Evidence of Health Effects, VII-4i
Epidemiology and Occupational Exposure,> VII-42
Nonoccupational Exposure, VII-44
Combustion Products VII-49
Carbon Monoxide, VII-50
Nitrogen Oxides, VII-52
Summary of Recent Epidemiologic Studies of Indoor Pollution
with Special Reference to N0X Exposure, VII-58
Involuntary Smoking * VI1-63
Absorption of Smoke Constituents, VTI-64
Effects on Healthy Persons, VII-67
Effects on Special Populations, VII-71
Conclusions, VI1-76
Indoor Airborne Contagion VI1-81
Assessing Indoor Biogenic Pollutants, VII-82
Evidence of Indoor Airborne Infection, VII-83
Importance of Airborne Contagion, VII-86
Prevention of Indoor Airborne Contagion, VII-87
Allergic Reactions in the Indoor Environment VII-93
Allergic Reactions on the Skin, VII-94
Allergic Reactions in the Respiratory Tract, VII-94
Factors Than Determine Allergic Reactions in the Respiratory
Tract, VII-98
Allergic Lung Diseases and Their Causal Allergens, VII-100
VIII EFFECTS OF INDOOR POLLUTON ON HUMAN WELFARE
Relationships between Socioeconomic Status and Indoor Pollution .... VIII-1
Human Discomfort ... VIII-3
Maiodors, VII1-4
Noise, VIII-5
Temperature, VIII-6
Interrelationships of Environmental Factors, VIII-12
Summary, VIII-12
Recommendations, VII1-13
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Decreased Productivity . VIII-13
Definition of "Productivity," VIII-14
Productivity in Industrial Environments, VIII-14
Productivity In Nonlndustrlal Environments, VIII-18
Soiling, Corrosion, Maintenance, and Housekeeping ... VIII-19
Particle Deposition, VII7.-19
Moisture and Fungal Growth, VIII-22
Gaseous Pollutants, VIII-22
Effects of Tight Construction, VIII-23
Effects on Maintenance for Corrosion and Deterioration, VIII-23
Effects on Housekeeping, VHI-25
Method of Treatment, VIII-26
Recommendations, VIII-26
IX CONTROL OF INDOOR POLLUTION
Ventilation Codes and Standards IX-2
Background, IX-3
Implementation of Codes and Standards, 1X-7
Summary, IX-14
Recommendations, TX-16
Air Diffusion Control IX-16
Air Diffusion Equipment, IX-16
Air Diffusion Criteria, IX-17
Conclusions, IX-22
Recommendations, IX-22
Air Cleaning Equipment IX-22
Location of Indoor-Air Cleaners, IX-23
Types of Air-Cleaners, IX-23
Summary, T.X-40
Strategies for Control of Indoor Pollution IX-39
APPENDIX A: AIR-QUALITY STANDARDS
APPENDIX B: ESTIMATING THE IMPACT OF RESIDENTIAL ENERGY-CONSERVATION
MEASURES ON AIR QUALITY: A HYPOTHETICAL CASE
Hypothetical Case Study B-l
Existing Conditions, B-2
Case Analysis, B-2
Summary B-20
Recommendations B-20
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EXECUTIVE SUMMARY
Many people spend large amounts of each day indoors—in many
cases, 80-90%—in a house, an automobile, a waiting room, an office or
other workplace, or a confined space accessible to the general public,
such as a store or a restaurant. It has been shown that indoor
exposure to environmental pollutants can be substantial. Although
there is little epidemiologic evidence on the health effects of indoor
pollutants, indoor concentrations of some pollutants that already have
primary ambient-air quality standards exceed those standards. Indoor
exposure has been largely overlooked in research on the health effects
of environmental pollutants, but it can constitute an important
fraction of the total exposure to many pollutants.
Indoor pollution in residences, public building, and offices is
created for the most part by the occupants' activities and their use
of appliances, power equipment, and chemicals, by wear and tear and
outgassing of some structural or decorative materials, by thermal
factors, and by the intrusion of outdoor pollutants.
In some cases, the outdoor pollutants that penetrate to the
indoors may represent the most important pollutant stress on human
health and welfare, and such effects have been addressed at length in
reports of previous National Research Council committees. This report
is focused primarily on the indoor air contaminants that are liberated
indoors. When they attain high concentrations, they may cause
nuisances, irritation of sensitive tissues, illness, and death from
acute as well as chronic exposures. Some pollutant sources—such as
cigarette-smoking—have been recognized for a long time, but their
importance has only recently been evaluated. Others arise from new
products or from old products in new uses, such as building materials,
pesticides, and insulation. A number of sources are of concern only
in the indoor environment, e.g., cooking, use of consumer products,
space-heating devices, and floor and wall coverings. The expanded use
of wood and coal for residential space-heating, of home hobby and
craft products, and of products that liberate organic substances is a
potential contributor to the contamination of indoor environments.
Infectious microbes and allergenic agents can grow indoors or be
transmitted into indoor environments.
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Ventilation alone (whether natural or forced) may not be
sufficient to dilute indoor pollution to an acceptable point. Natural
ventilation may be inappropriate because it i« variable and generally
not controllable in a precise way for many indoor settings. Exclusive
dependence on forced ventilation is inappropriate because it is not
universally available; moreover, introduction of untreated outdoor air
may not always be desirable. Also, natural ventilation and forced
ventilation may have substantial energy penalties, owing to heating
and cooling losses. The adoption of energy-saving proposals to reduce
ventilation rates could aggravate problems lr. indoor air quality,
create >iew problems, and perhaps be generally detrimental to health
and property, unless appropriate pollution-control measures are also
taken.
Public-health laws are broad enough to permit evaluation and, when
required, control of indoor environments. The public expects a safe
and healthful outdoor environment, and the same expectation applies to
public indoor environments. The regulatory authority to control
contaminant sources, to set or recommend building codes, and to
support or conduct research on or monitoring of indoor contaminants
rests with diverse federal, state, and local government units, but no
specific government unit has been directly charged with the
responsibility for protecting the quality of indoor environments.
For all the reasons stated above, the present quality of the
indoor environment and how this quality may change are matters of
immediate and great concern.
SCOPE OF THE REPORT
This report was prepared, at the request of the Environmental
Protection Agency (EPA), by the Committee on Indoor Pollutants, which
was appointed by the National Research Council in the Board on
Toxicology and Environmental Health Hazards, Assembly of Life
Sciences. It is intended to characterize the quality of the indoor
environment—primarily with respect to airborne pollutants, although
others are discussed--and to determine the potential adverse health
effects of indoor pollutants. The charge was to review, compile, and
appraise the available knowledge. The Committee has also identified
the research needed for abatement of indoor pollution. "Indoor"
refers to the environments in homes, schools, public buildings, and
similar spaces to which the public has access; industrial working
environments, however, are excluded from consideration here.
It is beyond the scope of this report to list all the pollutants
found Indoors that are hazardous to human health. The examples given
make it plain that humans are exposed to a variety of potentially
hazardous indoor pollutants from diverse sources. It is hoped that
this report will encourage researchers to broaden the list of
hazardous indoor pollutants and to characterize the hazards, so that
the general public and those responsible for pollution control and
abatement can be informed.
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Throughout this report, pollutants are mentioned without
discussion of thalr health effects. This does not constitute an
oversight on the part of the Committee, but cathec reflects a decision
that the discussion here be adequate to show that there are indoor
pollutants that cause adverse health effects in humans. The reader's
attention is directed to Chapter III, which offers so&e
recommendations for further health research with respect to these
pollutants, for further exposure studies, and for public education
about effective ways of reducing exposure to many contaminants
encountered Indoors. The Committee on Indoor Pollutants and its
contributors prepared concise reviews of such physical aspects as
sources and concentrations and of such biologic aspects as the
physiologic and toxicologic effects of a variety of contaminants
encountered indoors. In addition, the effects of those contaminants
that bear on human well-being in a more general way, such as soiling
and corrosion, and the available means of controlling the presence of
the contaminants are discussed in some detail. The report attempts to
focus personal, corporate, and government attention on present and
potential problems related to indoor contaminants.
The Committee notes that documentation of excessive indoor air
pollution should not in itself be considered sufficient reason to
relax standards for ambient air. The barriers between indoor air and
outdoor air are not absolute, and ambient air contributes to indoor
air. Furthermore, outdoor and indoor air pollutants may interact
chemically and physiologically. The Committee recognizes the
complexity of human exposures that have multiple sources. "Hie
development of effective and efficient strategies for mitigating
hazardous contamination requires improved understanding of responses
to exposure and of pollutant interactions.
The Committee has not attempted to sec priorities for research on
or regulation or control of indoor pollutants. Nor has it attempted
to develop risk analyses for these pollutants. The order in which
contaminants are presented in this report does not constitute a
ranking of importance by the members of the Committee.
To set priorities for differentiating among indoor contaminants
and to establish objectives for research and control programs, there
must be a system for comparison. The dimensions of this system
include the numbers of people exposed, the severity of exposures, and
the consequences of the exposures. To be comprehensive, the system
must also deal with ecalogic and material damage, loss of
productivity, degradation of artifacts, and othet kinds of impact not
related to health. Priorities could be derived from a ranking of
these variables for pollutants of interest, but proper risk analysis
would require measurement of exposures by population subgroups and
weighting of exposure-response relationships by impoetance of outcome.
Th*s Committee unanimously agreed that establishing firm priorities
for research on indoor pollutants that ranks one contaminant as more
important than another is premature. In most instances, we do not
appreciate the extent of population exposures. Available reports on
indoor air pollutants contain almost no data on the incidence of
disease or even annoyance related to changes in pollutant
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concentrations. Nevertheless/ the Committee has made judgments based
on its interpretation of reported concentrations) of prevalence ot
sources, and of evidence of effects on health and welfare. The
Committee offers guidance for research, development, and educational
programs by specifying current gaps In information and scientific and
engineering deficiencies. Priorities within these programs will have
to depend on the extent of federal and private funding; the Comaittee
believes that the determination of such priorities is urgent.
OBGAHI2ATIOH OP THE REPORT
The introduction, sunrcary and conclusions, and recommendations of
the Committee are in Chapters 1, II, and III, respectively. This
material is based on both the body of the report and Committee
deliberations. Some conclusions and recommendations were derived from
consideration of the documented information in specific sections of
the report and the substantiating discussions therein. OtherB, based
on Committee consensus, were formulated from a more comprehensive
perspective or the subject of indoor pollutants.
After the introduction, summary and. conclusions, and
recommendations in Chapters I, II, and III, the treatment of indoor
pollutants is presented in threi primary chapters and three secondary
chapters. The three primary chapters are Chapter IV, on the sources
and characterisation of indoor pollution; Chapter VII, on the health
effects; and Chapter IX, on the control of indoor pollutants. They
are the most voluminous chapters and respond most directly to the
Committee's charge to review and appraise the available knowledge on
indoor air pollution. The other chapters—Chapter v, on factors that
influence indoor pollution; Chapter VI, on the measurement of indoor
pollution and exposures; and Chapter VIII, on other non-health-related
effects—offer important additional information. They elaborate on
material presented in the primary chapters, and they introduce factual
and conceptual material that the Committee feels essential for
evaluating indoor pollution comprehensively.
Chapter IV, on the sources and characterization of indoor
pollution, covers radon and its decay products, formaldehyde, and other
organic substances, asbestos and fibrous glass, combustion products,
tobacco smoke, consumer products, cdors, temperature and humidity, and
other pollutants not specifically treated. The objective of the
chapter, as of Chapter VII (on health effects), Is not a global
treatment of every possible hazard encountered indoors, but lather a
selective treatment. The chief critetion for selection is direct or
circumstantial evidence that a contaminant causes or is reasonably
likely to cause human stress, illness, or material damage indoors.
Chapter V, on factors that influence indoor pollution, expands on
the physical characterization of indoor pollutions in Chapter IV.
Aspects of geography, building design, and human activity that lead to
variations in ventilation rates an
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Chapter VI, on the measurement and monitoring of indoor pollution,
and exposure, reviews the design and components of indoor and personal
monitors, mathematical models for estimating indoor pollutant
concentrations, and methods of estimating total personal exposure.
Chapter VII, on the health effects of indoor pollution, relates
the current understanding of the toxicologic and physiologic effects
of specific contaminants that are found at high enough concentrations
and in a broad enough range of indoor environments to constitute an
actual or reasonably likely challenge to the occupants of those
environments. In some cases, as in Chapter IV, the discussion is
structured by source, such as involuntary smoking or indoor combustion
products; the health effects may be attributable to specific
components of a mixture of gases and particles, or it may be
attributable to the general, mixed exposure. The chapter also
considers indoor airborne contagion and allergens.
Chapter VIII, on the effects of indoor pollution on human welfare,
covers a number of items related to comfort, productivity, and
material protection in indoor environments.
Chapter IX, on the control of indoor pollution, emphasizes the
engineering aspects of air-conditioning and indoor air-cleaning.
Ventilation codes and standards are reviewed, and mechanical systems
for conditioning and cleaning air are described. The chapter
discusses strategies for controlling contaminants to maintain
acceptable indoor air quality in general. Some pollutants, because of
their sources or their physical and chemical properties, cannot be
treated with conventional control systems, and strategies for
controlling these pollutants are described specifically.
Appendix A lists national primary ambient-a,ir quality standards
and occupational-health standards (for the industrial environment)
established for the United States. In addition, it lists indoor-air
pollution standards and guidelines of several foreign countries.
Ventilation standards for dwellings are also listed. This appendix is
not exhaustive with respect to relevant pollution or ventilation
standards, but it does offer a point of reference for some of the more
commonly used standards.
Appendix B presents an example of the interactions among energy
conservation, comfort, and indoor eir pollution in a residence. This
simulation exercise illustrates the tradeoffs among energy-cost
savings, retrofit costs, and thermal comfort under the constraints of
maintaining various hypothetical conditions of indoor air quality in a
particular kind of single-family residence.
PRINCIPAL FINDINGS ON SPECIFIC POLLOTANTS AND
CLASSES OF POIiLUTANTS
RADON
Radon ar\d its alpha-emitting decay products contribute a major
portion of the biologically significant dose associated with natural
background radiation. Many natural substances contain radium, a
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precursor of radon gas. Soil, construction materials/ and groundwater
are the major sources of indoor radon. Indoor radon concentrations
are often an order of magnitude greater than outdoor concentrations.
The dose-response relationships for alpha-emitting radionuclides are
not sufficiently well accepted to allow quantitation of the health
risk associated with measured indoor concentrations, and surveys of
radiation in homes are very limited. Expansion of the data base on
the variation of indoor radon exposure with time and location is a
necessary prerequisite for assignment of a health risk to indoor
radon. In theory, techniques for controlling radon exposure are
available; but they need development and evaluation before they can be
applied economically on a large scale. The effectiveness of several
contaminant control strategies* other than ventilation/ has not been
demonstrated in practice. Codes for new construction may be necessary,
to prevent the occurrence of high radon concentrations in modern or
refurbished dwellings. In any event, prudent judgment concerning
reduced ventilation in residences must be based on a better
understanding of radiation exposures in present houses.
FORMALDEHYDE
The major indoor sources of formaldehyde have been identified.
Aldehydes and other organic substances emanate from outgassing of
urea-formaldehyde foam insulationf particleboard, plywood/ fabrics/
and/ to a lesser extent/ cigarettes and indoor combustion sources.
The high surface-to-volume ratio of particleboard and plywood used as
building materials in mobile homes, as well as lower air-exchange
rates, causes the high measured formaldehyde concentrations.
Formaldehyde can cause skin, eye, and throat irritation in occupants.
Moreover, potential health problems associated with formaldehyde
exposures are readily identified in acute cases when concentrations
are high and tolerance is low. In addition co irritation, respiratory
disorders and allergies have been associated with high formaldehyde
concentrations. There is evidence of a decreased threshold of
sensitivity with prolonged exposure. Recent studies have indicated
that exposure of rats and mice to formaldehyde produces nasal cancer.
Owing to the ubiquitous and increasing use of resins and solvente in
building materials and furnishings/ indoor formaldehyde concentrations
have increased. Abatement technology is available, although at times
expensive; new and less expensive techniques are being developed. The
Committee is especially concerned with long-term and essentially
continuous indoor exposures to low concentrations of formaldehyde.
ASBESTOS AMP OTHER FIBERS
The health hazard posed by indoor exposure to asbetos has been
perceived as a problem by virtue of the presence of asbestos fibers in
insulating and decorative materials. Abrasion, mechanical vibration,
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or deliberate disruption of asbestos-containing surfaces can result in
increased fiber concentrations in the indoor environment. There have
been a small number of studies in which fiber counts have been
documented in association with normal building use. Extrapolation
from what we currently understand about the exposure-response
relationships for &Bbestos fibers to the very low concentrations
reported in indoor spaces, such as school8, suggests a small health
risk under conditions of normal use. However, deliberate modification
of surfaces to reuove asbestos from buildings may create a risk of
exposure of occupants and workers. Buildings in which asbestos
exposure is likely to occur can be identified. The risk of exposure
from dislodged fibers can be reduced by containment. The occurrence
of mesothelioma (a specific form of cancer believed to result only
from the inhalation of asbestos fibers) may provide a very sensitive
indicator of the exposure of the general population, ltome exposure to
asbestos due to aging, cracking, or physical disruption of insulated
pipes or asbestos-containing ceiling tiles and spackling compounds may
be greater than public exposures in schools, which have received the
most attention. HOroes built before 1950 in northern climates are more
likely to have pipes insulated with asbestos plaster. Given the very
common use of asbestos in homes, schools,and other buildings, there is
a need for further assessment to identify structures where actual
asbestos exposure constitutes substantial risk to humans.
The extent of exposure of the general public to asbestos fibers
has not been assessed} however, the occurrence of mesothelioma should
be carefully monitored in the general population. Man-made fibers
have produced skin irritation, but have not otherwise been
demonstrated convincingly as hazardous to health. Epidemiologic and
toxicologic investigation of synthetic fibers should continue. On the
basis of present knowledge* synthetic fibers in the indoor environment
should not cause undue concern.
TOBACCO SMOKE
Virtually every member of our society is exposed to tobacco
smoke: 33% of the population smokes, and the rest are exposed to the
smoke released by others. The constituents of tobacco smoke are well
documented as hazardous, the prevalence of population exposures is
very high, and there is an increased incidence of respiratory tract
symptoms and functional decrements in children residing in homeB with
smokers, compared with those in homes without smokers. These
considerations and recent evidence of increased lung-cancer rates
among nonsmoking women living with smoking husbands have led us to
conclude that indoor exposure to tobacco smoke has adverse effects.
Coughing, headache, nausea, and irritation of eyes, noser and throat
are among the reported symptoms. Although many studies have measured
various components of tobacco smoke indoors, total exposure has not
been determined. Passive exposure to tobacco smoke may constitute an
important exposure to respirable particles, such gaseous compounds as
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acrolein and formaldehyde* benzo[a]pyrene* nnd various trace metals.
Reduced ventilation increases concentrations of tobacco smoke. As an
energy-conserving compromise/ smoking could be restricted to zones
that are well ventilated. Public policy should clearly articulate
that involuntary exposure to tobacco smoke has adverse health effects
and ought to be minimized or avoided where possible. Under this
framework* the prohibition or restriction of smoking in public
buildings* offices* etc.* is a control option to be considered with
ventilation and air-cloaning.
INDOOR COMBUSTION
When fuel combustion occurs indoors—e.g.* for heating, cooking*
and power machinery, including automobiles—it giveq rise to increased
concentrations of gases and particles. Unventcd gas cooking is
probably responsible for a large portion of nitrogen dioxide exposures
in our population. In many homes, chronic exposures to nitrogen
dioxide indoors may exceed established national ambient-air quality
standards. Shorter-term 1-h average concentrations indoors often
exceed the highest hourly concentrations measured outdoors. The
concentrations of nitrogen dioxide and carbon monoxide in residences
have not been fully documented. However* some studies have shown an
association between gas cooking and the impairment of lung function in
children. Gas cooking appliances are also sources of carbon monoxide*
carbon dioxide, formaldehyde* hydrogen cyanide, sulfate particles,
organic particulate matter, and organic vapors. The problem of
chronic or even peak exposures to combustion products indoors will be
accentuated with decreased ventilation and the increased use of
portable space-heaters, wood- and coal-burning stoves, and indoor
venting of gas dryers. Carbon monoxide, nitrogen oxides, and
particles from automobile exhaust can produce increased concentrations
in office buildings and public areas. Concentrations exceeding 1-h
carbon monoxida national ambient-air quality standards (NAAQS) by a
factor of 2-4 have been reported in several ice-skating rinks that use
gasoline-powered ice resurfacing machinery. Office buildings and
apartment buildings with attached or underground garages can also have
sustained high concentrations of carbon monoxide indoors. Because
both carbon monoxide and nitrogen dioxide are odorless at typical
concentrations, the presence of increased and possibly hazardous
concentrations may go undetected.
Although confirmation is necessary, the available evidence
suggests that important population exposures to nitrogen dioxide and
carbon monoxide can occur indoors and may constitute a sufficient
threat to the general public health to justify remedial action.
Reducing exposure to those gases is relatively straightforward.
Source removal or direct venting of combustion sources should be
considered.
Efforts to conserve energy present other potential problems
indoors. Effective energy-conservation measures can result in an
overcapacity o£ existing heating equipment. Operation of such
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equipment at low load factors may decrease ite overall combustion
efficiency and increase emission of the products of combustion.
MICROORGANISMS AND ALLERGENS
Microorganisms are present in the indoor environment and are
associated with human activity and the presence of domestic animals*
The microorganisms include bacteria, viruses, and fungi. Many
microorganisms—such as spores, molds, and fungi--multiply in the
presence of increased humidity. Xt is possible that reduced
ventilation and the increased use of untreated recirculating air could
increase the concentrations of microorganisms. Many of these
microorganisms can produce infection, disease, or allergic reactions.
Respiratory viruses and bacteria can be transmitted from person to
person in buildings and confined spaces. Certainly, respiratory
infections are an important cause of morbidity that results in last
earnings and discomfort. It is reasonable to assume that some of the
incidence of respiratory disease results from airborne transmission,
but it is not at all clear what effect ventilation, air-conditioning,
or air-cleaning will have on incidence. If the main transmission is
between persons In contact with or close to each other, the mechanism
and efficiency of disease transfer will be relatively insensitive to
ventilation rates and other operating conditions of the air handling
systems. However, to the extent that infectious and allergenic
microorganisms remain viable and airborne, substantial reduction in
ventilation rates will tend to increase concentrations and most likely
the probability of infection and allergy.
MOISTURE
Hater vapor in confined spaces is a product of metabolic and
respiratory processes, as well as of indoor combustion and evaporation
from clothes and dish-washing and bathroom functions. Condensation of
water indoors has been shown to increase corrosive effects of absorbed
gases. Decreases in ventilation tend to increase the indoor relative
humidity during the heating seasons. Excess water vapor adsorbs or
condenses on drier or colder surfaces, and that gives rise to
Increased deterioration or corrosion of building materials,
furnishings, decorations, artwork, and other artifacts. Increased
relative humidity may also promote the growth of molds, algae, and
fungi. Thus, humidity control may become an important component of
reduced-ventilation strategies. Some energy penalty may result that
should be considered in relation to the energy savings that may be
obtained through reduced ventilation.
RESPONSIBILITIES
The quality of the indoor environment is not the responsibility
exclusively of any individual or government body. Even a single home
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built in isolation (away feoo outdoor sources of contaminants) has the
potential to be contaminated by its occupants# soil* outgaasing from
piped-vater use, building materials, cooking# space-heating# consumer
products) pesticides# molds# and fungi. Responsibility for the indoor
environment is on four levelst individuals} product manufacturers?
building designers#, contractors# and owners) and government.
Most sources of contamination are associated with human activity.
Individuals also exercise some control over contamination sources and
ventilation. Hence# the individual can directly affect hia or her own
exposure# as well as the exposure of those with whom the indoor space
is shared. This is also true# to a lesser extent# in the
nonindustrlal workplace and in public buildings.
Building owners and operators are responsible for maintaining the
indoor environment and ensuring that at least minimal ventilation
standards are being met. It should be noted that there is little or
no enforcement of ventilation standards# once building plans are
approved. Architects# engineers# and contractors should treat Indoor
environmental quality as a design objective. There are many
opportunities in building design to separate people from the sources
of contamination or to remove the sources entirely.
Manufacturers have the responsibility to warn the consumer
adequately of the potential hazards of products. As evidence qn
specific contaminants—such as formaldehyde and nitrogen dioxide from
gas stoves—becotces available# less harmful substituted can be
considered, and results of research on the control of the sources can
be made available.
Government shares the responsibility to -insure that the indoor
environments to which the public has access are healthful. Clearly#
in the assessment of indoor concentrations# in instrument development#
and in the control of health-directed research on indoor pollutants#
government can serve the public interest. Government can establish
ordinances (regulations) to protect the general public from nuisances,
contamination# or direct health damaget such ordinances may include
performance standards related to building materials and ventilation
codes for public and private buildings. In the same vein# government
can require product certification in the case of known or potential
hazards. Furthermore# government can establish concentration
standards or source-control specifications. Radon# a naturally
occurring substance, is a clear example of contaminants that yould
require government attention# as opposed to that of industry or the
Individual.
CONCLUSIONS
Definitive conclusions on the character of indoor air are
prevented by the lack of systematic studies. The available data base
has been generated by a series of pilot studies and does not fully
characterize the variety of pollutants, indoor environments, and
occupancy conditions. Furthermore, the implementation of
energy-conservation measures and the introduction of new building
materials have intensified the problem of indoor air contamination.
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Studies explicitly addressing both long-teem and episodic events
have not been undertaken. Episodic release of contaminants in the
indoor environment may be rare* but can lead to short-term high
contaminant concentrations/ which must be considered (in addition to
long-term low concentrations) in assessing *he overall health risk of
indoor contaminants.
Measurement of indoor contaminants necessitate* a sampling
protocol that considers the spatial and temporal profile of several
pollutants, as well as air diffusion and ventilation characteristics.
In addition« measurement techniques for assessing indoor
concentrations have to tceet more rigorous requirements, particularly
with regard to sensitivity and interferences. Unfortunately, many of
the instruments required to characterize long-term and short-term
indoor pollutant concentrations do not exist.
Prom a practical viewpoint, it would be desirable to determine the
emission rate of an indoor pollutant by simple physical measurements
and to infer the dose received by a human inhabiting the indoor space.
But several intervening steps must be evaluated that involve degrees
of uncertainty ranging from good estimates to total ignorance. The
first process to be considered is the transport by diffusion and
convection; transport is influenced initially by the fluid motion of
the air near the source and throughout the indoor space. These modes
of transport depend on a nu>nber of factors and are usually spatially
and temporally variable. They lead to a concentration profile of the
contaminant as a function of position and time. Measuring such
profiles is virtually impossible, so the usual approach is to use
mathematical modals of dispersion. The human receptor is not
stationary. Therefore, to obtain an exposure history, the spatial
history of the receptor should be specified or estimated. Inexact
knowledge of this function introduces a further degree of
uncertainty. Dose to the receptor is related to exposure through
deposition functions that express the fraction of the exposure that is
available to reach specific receptor sites and produce effects. These
deposition functions are themselves functions of several variables
that are usually poorly specified or unknown. Thus, several layers of
uncertainty are embedded between emission rate and receptor dose.
Indoor air pollutants generated or released indoors typically
occur in concentrations and mixtures that are often episodic and
generally vary over a wide range of time and from one space to
another. As a result, human exposures are difficult to assess for
individuals or groups. If, in addition, the adverse health effects
are subtle, and especially if they are delayed, associations between
indoor air pollutants and disease or premature mortality are unlikely
to be discovered or demonstrated without a specific and substantial
effort. Thus, efforts to improve indoor air quality most likely will
have, to be guided by information on the adverse health effects of
pollutants demonstrated and studied in other settings, such as the
occupational environment.
For a limited number of air contaminants that can be found in
residential and public buildings, there is direct and circumstantial
evidence that human exposures are largo enough and common enough to
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account for substantial morbidity and premature mortality. These
include radon progeny, sidestrearn tobacco smoke# formaldehyde/ carbon
monoxide# nitrogen dioxide, aeropathogens, and aeroallergens.
Howevert our knowledge of the extent of the exposures and of the
exposure-response relationships is inadequate to permit measurement or
even estimation of the resulting mortality and morbidity.
Furthermore* the kinds of health effects and the latent periods
between exposures and effects are quite varied. For example, they
extend from acute intoxication from carbon monoxide and formaldehyde
to cancer that appears long after exposure to radon decay products and
asbestos.
In evaluating health risks, it is reasonable to compare indoor
exposure with ambient air-quality standards for pollutants for which
there are such standards (carbon monoxide, sulfur dioxide, nitrogen
dioxidei ozone, lead, and total suspended particles). Depending on
how the standards were developed, however, they may or may not
consider exposure of the most sensitive population groups (the ill or
infirm or the very young). In addition, the composition o£
particulate matter indoors, the potential synergistic interaction of
gaseous and particulate matter, and the time characteristics of
exposures can differ widely between the indoors and the ambient
environment. Hence, for some pollutants, the ambient air-quality
standards may actually underestimate the health risks.
Current knowledge would permit the establishment of defensible
indoor-air quality standards for only a few, if any, contaminants. In
any case, the establishment of such standards would not necessarily
lead to rational or enforceable controls beyond ventilation codes for
dilution. Economical and reliable techniques for sampling and
analyzing the airborne contaminants of interest at very low
concentrations have not been developed; nor have methods been
developed to relate spot samples from specific locations to integrated
doses.
We conclude that the best approach to the reduction of health
damage from exposure to indoor contaminants is to reduce the
population exposure to those contaminants. Control strategies for
some pollutants would target the high-exposure groups. For other
pollutants, lowering the population-weighted mean exposure would, by
best estimates, reduce the health hazards.
Because of the diversity of indoor pollutants and their sources
and because of the unpredictability of the distribution of such
pollutants over time and in different buildings, efforts to improve
indoor air quality should concentrate on reducing the number and
strength of the sources by substitution of other materials.
Control strategies based on the specifications of source control
are preferred, whenever feasible, because they are generally the most
dependable, with respect to their, extent and reliability of exposure
reduction. That suggests that reducing exposure through source
control or removal or through material substitution must be tempered
by che practical realities of existing sources, which might not be
easy to eliminate, and by the unknown long-term toxicity of substitute
materials. When those strategies cannot achieve the desired degree of
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control at reasonable cost, they can be supplemented or replaced by
other engineering controls, such as dilution ventilation or
air-cleaning. However, it should be recognized that the concentration
reduction achieved through dilution may be less than that achievable
with source control or air-cleaning, whereas the effectiveness of
air-cleaning devices usually depends on frequent and effective
application of maintenance procedures.
The specific source controls appropriate to each kind of
contaminant can be expected to vary. For example, local exhaust
control is most appropriate for nitrogen dioxide and carbon monoxide
from gas ranges, the sealing of walls and floors for radon control,
prohibition for asbestos-containing products, and specifications for
care of furniture, drapery, ard carpeting materials prepared with
formaldehyde-containing substances.
Air-conditioning systems are generally designed to provide for all
or most of the thermal environmental requirements (i.e., heating,
cooling, and ventilating) of the occupied space. In the design of
these systems, it is necessary to select components that will meet thq
particular requirements, such as heating coils or furnaces to meet
winter design temperatures, evaporator coils and condensing units to
meet summer design temperatures and humidities, and air-cleaners or
ventilation air-flow rates to meet the air-quality requirements of the
occupied space. The functional requirements of the space (i.e.,
residential, office, cheater, etc.) also impose constraints on the
type of system that might be selected. Because of the wide variety of
functional requirements of indoor environments and the other
constraints on design, a vast variety of control systems are used.
For instance, lighting and acoustic requirements can influence the
size cind location of the air-conditioning system, the location of air
supply and return devices, and air velocities in the air distribution
system. Available information suggests that this trend will continue.
Although the requirements may be described discretely and sane
performance specifications are available for components of the system,
the effectiveness of the system as a whole, including its impact on
indoor air quality, must be evaluated. Unfortunately, very few data
are available to indicate whether these systems, under actual loads,
perform in accordance with their designs.
RECOMMENDATIONS
1. A staged assessment of the exposures of the general population to
indoor pollutants and of the effects of such exposures on health and
welfare should be conducted by the federal government in both
residential and office buildings. Federal agencies with substantial
interests in definition of the indoor exposures—i.e., the
Environmental Protection Agency, the Department of Energy, the
Consumer Product Safety Commission, the National Institute for
Occupational Safety and Health, the Centers for Disease Control, the
National Institute of Environmental Health Sciences, the Food and Drug
Administration, the National Center for Toxicological Research, the
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Department of Hpusing and Urban Development, etc.--should participate
in the formulation of the study objectives and protocols and should
provide technical assistance and financial support, as appropriate and
feasible. Congress should enunciate clearly its interest in healthful
and safe indoor environments.
2. Monitoring protocols and properly designed monitoring instruments
must be developed to satisfy the special requirements involved in
investigating the indoor environment.
3. The indoor pollutants that should receive the initial major focus
in investigation of sources, concentrations, dispersion, and removal
are radon and its progeny, tobacco smoke, formaldehyde, nitrogen
dioxide, carbon monoxide, pesticides, water vapor, carbon dioxide, and
airborne contagion, including allergens.
4. The health effects that should receive the initial major focus in
investigation are respiratory-infection rates and respiratory
mechanical function in relation to nitrogen dioxide, tobacco-smoke,
and airborne-contagion exposuresi respiratory-tract irritation and
potential carcinogenic effects in relation to formaldehyde, tobacco
smoke, asbestos, and alpha-emitting radon decay products; and acute
intoxication, blood carboxyhemoglobin, and cardiovascular-disease
aggravation in relation to carbon monoxide and nitrogen dioxide
exposures.
5. The low-level acute and chronic complaints of malaise, headache,
stuffinessr and eye and throat irritation that are reported with
increasing frequency in large buildings deserve careful study.
6. The welfare and behavioral effects that should receive the initial
major focus in investigation are material damage from mold formation
in relation to relative humidity; corrosion and surface deterioration
in relation to nitrogen dioxide, sulfur dioxide, and water vapor;
fabric fading and deterioration in relation to solar radiation in
combination with nitrogen dioxide, sulfur dioxide, house dust, and
water vapor; soiling due to tobacco smoke; and the lowering of work
productivity due to indoor air pollution and associated discomfort.
7. Responsibility for conducting a well-coordinated investigation of
the influence of.building design and operational factors on the
concentrations of pollutants in both residential and commercial
facilities should rest with the federal government, assisted by the
appropriate professional and scientific organizations.
8. The building factors that should receive the initial major focus
in Investigation are as follows:
a. The effects of reducing infiltration rates in existing
buildings on combustion efficiency of space-heating equipment and on
increases in relative humidity and concentrations of indoor-generated
air pollutants and airborne contagion.
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b. The effects of materials of construction and furnishings on
indocr-pollutant content—specifically, there should be systematic
evaluations of outgassing and surface attrition of particleboard and
plywood (for formaldehyde and other organic substances)t of wall and
floor coverings and fabrics (for organic substances); of masonry
products (for radon and dust)i of wallboard, plaster, and spackling
compounds (for dust and fibers); and of the materials used for heat
storage in dry solar systems (for radon, dust, surface molds, etc.).
c. The differences in air distribution, diffusion, mixing, etc.,
associated with the use of different climate-control systems, such as
forced-air, baseboard, and radiant floor or ceiling systems.
d. The effectiveness of air-cleaning systems in capturing
pollutants in recirculating air—specifically, this will require
in-place testing of systems, rather than test-stand evaluation of
components, and the effectiveness of a variety of commonly used
systems should be evaluated for radon and radon progeny, formaldehyde
and solvent vapors, and cigarette smoke.
9. The potential for consumer products to contaminate the indoor
environment needs to be evaluated. Hazardous components of these
pcoducts must be identified and tested. Adequate labeling, warning
users of hazards associated with product use and misuse in enclosed
spaces, should be required. Testing in homes is needed to assess the
extent of contamination, allergic reactions, and other health effects
of pesticides, residues, and consumer products.
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I
INTRODUCTION
This report was prepared, at the request of the Environmental
Protection Agency (EPA), by the Committee on Indoor Pollutants, which
was appointed by the National Research Council in the Board on
Toxicology and Environmental Health Hazards, Assembly of Li-'.e
Sciences. It is intended to characterize the quality of the indoor
environment, primarily with respect.to airborne pollutants, and to
determine the potential adverse health effects of indoor pollutants.
The charge was to review, compile, and appraise the available
knowledge. The Committee has also identified the research needed for
abatement of indoor pollution. "Indoor" refers to the environments
inside homes, schools, public buildings, and similar spaces to which
the public has access; industrial working environments, however, are
excluded from consideration here.
It is beyond the scope of this report to list all the pollutants
found indoors that are hazardous to human health. The examples given
make it plain that humans are exposed to a variety of potentially
hazardous indoor pollutants from diverse sources. It is hoped that
this report will encourage researchers to broaden the list of
hazardous indoor pollutants and to characterize the hazards, so that
the general.public and those responsible for pollution control and
abatement can be informed.
Throughout this report, pollutants are mentioned without
discussion of their health effects. This does not constitute an
oversight on the part of the Committee, but rather reflects a decision
that.the discussion here be adequate to show that there are indoor
pollutants that cause adverse health effects in humans. The reader's
attention is directed to Chapter III, which offers some
recooimeiidations for further health research with respect to these
pollutants, for further exposure studies, and for public education
about effective ways of reducing exposure to many contaminants
encountered indoors.
Attention has recently been drawn to the problems of specific
pollutants that originate indoors, e.g., formaldehyde released from
urea-formaldehyde foam insulation and from urea-formaldehyde resins
used to bind laminated-wood products, asbestos in building materials.
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and radon and its progeny. Efforts to reduse Infiltration of outdoor
air for energy conservation have heightened the interest in indoor
pollution. It is hoped that this report will be useful to the
Administrator- of EPA and other agencies, and individuals in considering
indoor environments, as a source of exposure of members of the general
public to hazardous pollutants. Some of the same pollutants; of
course, are now regulated as pollutants in the outdoor atmosphere and
in the workplace (see the lists of air-quality standards in Appendix
A).
The Committee's report outlines the scope of the problems
regarding indoor pollutants and discusses their sources, their effects
on human health and welfare (human comfort, productivity, soiling, and
corrosion), the technologies available for their control or abatement,
and concerns about ,the effects of energy-conservation strategies on
the indoor concentrations of pollutants. It approaches the subjiect of
indoor pollution from three viewpoints
Physical factors, such as indoor-pollutant sources and
concentrations and population exposures to those pollutants.
* Biomedical evidence on the effects of several pollutants
found in the indoor environment.
• Engineering, air-handling and -cleaning systems, &nd other
control options for reducing indoor exposures to pollutants.
The report reviews current understanding of these subjects,
assesses the quantity and quality of available information, and offers
recommendations for additional studies where appropriate.
Because of the raultidisciplinury and complex nature of the indoor
pollution question, this document could not possibly treat all
pertinent subjects. One important exclusion from the assessment is
the indoor industrial environment. It is recognized that many of the
pollutants found in areas to which the public has access are also
common to industrial settings, often in higher concentrations. The
Committee chose to consider only indoor environments to which the
general population has access; these include residences, public
facilities, recreational facilities, vehicles and
transportation-related buildings, educational facilities, and many
work settings. Examples of workplaces to which the public has access
and in which the public may be compromised by indoor pollution include
service stations, automobile showrooms with attached maintenance
areas, banks, offices, and buildings with multiple uses.
This document reviews the informationywi the health and welfare
effects of selected indoor pollutants, with emphasis on air
pollutants. It includes a critical appraisal of reported measurement
and exposure 9tudies, but it does not attempt a quantitative
assessment of exposure to the hazardous pollutants in the indoor
environment, because in mo'jt cases current methods are inadequate for
that.
There is no discussion here of the legal, social, or economic
implications of regulating the indoor environment in public buildings
or homes. Sociopolitical controls of pollution are quite complex and
beyond the scope of this document.
1-2
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Throughout the Committee's deliberations, and reflected in its
conclusions and recommendations, were the following questions:
• Do indoor pollution exposures adversely affect the health,
welfare, productivity, or sense of well-being of the population or any
portion of the population?
• Does the indoor environment constitute an important component
of exposure to pollutants?
• Are some groups or individuals at risk by virtue of,high
indoor concentrations of air pollutants or by virtue of susceptibility?
• What is known about the relative magnitudes of Indoor and
outdoor pollutant concentrations? Are the sources, ventilation rates,
and reaction and removal factors that influence the indoor-outdoor
relationships sufficiently well known to predict Indoor concentrations
and prescribe controls?
• What control strategies are effective for reducing population
exposures to specific indoor pollutants?
° Will future changes in housing materials, products,
ventilation codes, and activity patterns adversely affect health and
welfare through changes in indoor exposures to air pollution?
It is very important that health and welfare problems related to
indoor pollution be clearly differentiated from perceived problems or
pseudoproblems. This requires measurements that are both accurate and
sufficiently representative to identify or estimate the population at
risk. And it requires that health research provide reasonable
assurance that current or projected exposures can cause unacceptable
effects in a portion of th«: population. Only when these two
components are present can prudent judgments on recommended
concentrations and ccntrol strategies be made.
Efforts to improve the public health and protect the public from
hazardous airborne pollutants have been directed primarily toward
improving the ambient and industrial environments. Improvements in
outdoor (ambient) air have been achieved fundamentally through source
control or removal; dilution by tall stacks and source relocation are
not considered control strategies. In the indoor industrial
environment, however, ventilation or dilution with outdoor air has
usually proved to be the most cost-effective way of reducing worker
exposure.
The indoor concentrations of airborne contaminants depend on five
factors: the generation rate (for indoor-generated pollutants) or the
ambient concentration (for outdoor-generated pollutants), the volume
of the indoor environment, the air-exchange rate, the mixing
efficiency of the indoor space, and the decay (removal) rates of the
pollutants.
Until recently, the air in most buildings has been controlled for
comfort and odor considerations, not for contaminants. Depending on
heating, cooling, and humidity requirements for the indoor
environment, the natural or forced infiltration of outdoor air to
displace "conditioned" indoor air may entail a considerable energy
penalty. Diluting the indoor air with outdoor air reduces
1-3
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concentrations of airborne pollutants generated by indoor sources,
such as building materials, appliances, and tobacco-smoking. But
outdoor air can also introduce pollutants of outdoor origin, and these
pollutants may react with surfaces or other indoor contaminants.
Conversely, reducing air exchange without compensating with
air-clcaning will result in increased concentrations of contaminants
that are generated indoors.
The current growing interest in the quality of the indoor
environment is in part a result of efforts to reduce ventilation for
energy conservation. In the United States, an estimated 20-50% of
energy consumed is for space-heating and -cooling. In many buildings,
the energy used to move and condition ventilating air can be as much
as 90% of the total energy demand. Buildings lose energy by
conduction and radiation through windows, walls, and ceilings and by
exchange of indoor conditioned air with unconditioned outdoor air.
Reducing ventilation in residential and commercial buildings can be a
cost-effective way to achieve energy conservation. However, it is
reasonable to expect concentrations of contaminants generated by
building occupants, equipment, appliances, and materials to increase
when ventilation is reduced. Predicting the results of ventilation
changes is limited in some cases by lack of knowledge of the nature
and behavior of contaminant sources, of the existing concentrations of
pollutants, and of their chemical and physical reactions and removal
rates. Even for current situations, the significance of tho potential
indoor-pollucion problem is undefined for many pollutants, because the
populations at possible risk have not been identified and the
physiologic, behavioral, or welfare effects of various degrees of
exposure have not been determined.
Although there is considerable mass-media coverage of the quality
of indoor environments, the concern for indoor pollution in the
nonindustrial setting is- not new. Some countries have tried to
regulate pollutants in nonindustrial environments (see Appendix A).
Asbestos-fiber contamination in homes and schools has been monitored
and in some cases contained or removed. Ozone generation by office
copying machines has been regulated. Minimal acceptable ventilation
rates for smoke and odor control are incorporated into municipal and
state building codes. Several countries have set standards for.
residential or public lacilities to limit exposures to formaldehyde,
carbon dioxide, and radon. There have been surveys, but not
systematic evaluation, of indoor pollutant concentrations in a variety
of locations. The indoor environment has become an issue for the
public, government, scientific groups, and corporations because of
three phenomena: energy-conservation efforts, which may exacerbate an
indoor-pollution problem; the realization that little is known on the
hazards of many compounds that are commonly found indoors and
outdoors, including consumer products and fuels in common use (note,
for example, the resurgence in residential wood- and coal-burning);
and the evaluation of pollutant hazards by federal agencies, which
have begun to recognize the need to understand the total exposure.
For a large proportion of the population, normal activity occurs
disproportionately indoors. In a consideration of integrated
1-4
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pollutant exposures, indoor concentrations are relevant. Between 80%
and 90% of an average person's day or year is spent in enclosed
areas. On the average, people spend approximately 16 hours/day in
their homes. And a rather consistent 1-2 hour/day is spent in
transit. Thus, for at least some pollutants, the indoor
concentrations are the most important, with respect to potential
health effects ot material damage.
The time-integrated exposure is perhaps important in determining
chronic effects, such as corrosion. But the short-term peak or
transient pollutant exposures may be more important, causing or
contributing to both acute and chronic effects. Using the average
amount of time a person is outdoors or indoors or the time-averaged
concentrations may be misleading, if the concern is for peak-exposure
effects. Peak exposures may ?ccur indoors or outdoors. They may be
encountered only during specific activities or in locations occupied
only infrequently. In fact, ghor't-term peak concentrations may
contribute only a small proportion of a pecson's total time-integrated
exposure. Both time-integrated concentrations and short-term,
transient high concentrations must be considered, whether they occur
indoors or outdoors.
Although the indoor and outdoor environments have not been
sufficiently assessed to characterize all pollutant constituents
comprehensively, it is useful to categorize indoor pollutants into
three groups. Table 1-1 groups pollutants by source. Those in the
first group are principally of outdoor origin) thus, their
concentrations are generally higher outdoors. This group includes
sulfur dioxide; ozone; many elemental, inorganic, and organic species
of particles; pollen; and some organic vapors. They are encountered
indoors primarily because they are carried in with infiltrating air.
Some may be carried indoors' on surfaces. Once inside, particles can
be resuspended, or organic substances may volatilize because
temperatures and partial pressures are different. The higher indoor
surface-to-volume ratios increase the removal rates of many of these
pollutants.
Pollutants in the second group have both indoor and outdoor
sources. Generally considered as belonging to this class are
pollutants produced during combustion, such as carbon dioxide, carbon
monoxide, nitrogen oxides, and some components of suspended
particulate matter (primarily fine particles—diameter less than
3.0 m). Because of the limited indoor mixing volume and longer
residence times, concentrations of these and other combustion products
often exceed outdoor concentrations. This group also includes organic
vapors from solvents that can be used outdoors, as well as indoors.
Biologic materials, such as fungal spores, have both indoor and
outdoor sources. Fibers, including asbestos fibers, have indoor and
outdoor sources. Serpentine rock, brake linings, and industrial
facilities contribute asbestos fibers to the outdoor air. Insulation,
fireproofing, and decorative materials used indoors may contain
asbestos. Similarly, water vapor, sound, and nonionizing radiation
can be considered to belong to this group.
1-5
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Pollutants
TABLE 1-1
Typical Sources of Some Pollutants Grouped by Origin
Sources
Group 1—Sources predominantly outdoor:
Sulfur oxides (gases, particles) Fuel combustion, smelters
Ozone
Pollens
Lead, manganese
Calcium, chlorine, silicon,
cadmium
Organic substances
Photochemical reactions
Trees, grass, weeds, plants
Automobiles
Suspension of soils or industrial emission
Petrochemical solvents, natural sources,
vaporization of unburned fuels
Group II—Sources both indoor and outdoor:
Nitric oxide, nitrogen dioxide
Carbon monoxide
Carbon dioxide
Particles
Uater vapor
Organic substances
Spores
Group III—Sources predominantly indoor
Radon
Formaldehyde
Fuel-burning
Fuel-burning
Metabolic activity, combustion
Resuspenslon, condensation of vapors and
combustion products
Biologic activity, combustion, evapora-
tion
Volatilization, combustion, paint, meta-
bolic action, pesticides, insecticides,
fungicides
Fungi, molds
Asbestos, mineral, and syn-
thetic fibers
Organic substances
Ammonia
Polycycllc hydrocarbons,
arsenic, nicotine,
acrolein, etc*
Mercury
Aerosols
Viable organisms
Allergens
Building construction materials (concrete,
stone), water
Particleboard, Insulation, furnishings,
tobacco smoke
Fire-retardant, acoustic, thermal, or
electric insulation
Adhesives, solvents, cooking, cosmetics,
solvents
Metabolic activity, cleaning products
Tobacco smoke
Fungicides, in paints, spills in dental-
care facilities or laboratories,
thermometer breakage
Consumer products
infections
House dust, animal dander
1-6
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The third group of pollutant!! contains those whose sources are
predominantly Indoor. To this third group we may add pollutants whose
concentrations are high enough only indoors to warrant concern for
their effects. These pollutants are either generated by the occupants
or associated with building materials, appliances, machines, consumer
products, or art and craft materials. They include radon,
formaldehyde, other organic substances from a variety of materials,
asbestos and other fibers, odors, molds, and the numerous cbmpounds
identified in tobacco smoke.
Greater attention recently has been drawn to the third group of
indoor pollutants. There have been reports of complaints about
formaldehyde indoors after application of urea-formaldehyde foam
insulation and particleboard and the installation of furnishings.
Higher' formaldehyde concentrations in European homes were reported in
the early seventies. Radon, and its progeny have been found in high
concentrations in homes built on land reclaimed from phosphate mining
and in other areas. Building materials, concrete, granite, and
groundwater enriched in uranium are the apparent sources of radon. A
plaster-resin material containing 10-30% asbestos has been used for
fireproofing, acoustics, and, in some cases, decorative purposes.
Asbestos concentrations above U.S. occupational concentrations
occasionally have been found indoors.
The three general groups of contaminants found indoors are listed
in Table 1-1. Those in groups II and III are the prime focus of this
report. Chapter IV discusses their sources and concentrations, and
Chapter V, factors that affect indoor concentrations and personal
exposures. The current understanding is reported with an illustrative
but not exhaustive review of pertinent related work. Those two
chapters discuss the relationships araon^ sources, personal activity
patterns, building factors, and ventilation that influence indoor
concentrations and individual pollutant exposure. Temperature, light,
and especially relative humidity also help to determine
concentrations, chemical activity, and effects. Measurement of these
effects to the point of predicting the camifications of altering
ventilation or introducing new products is not possible for all
pollutants of interest, and in many cases the measurements have not
bieen made. For other pollutants, the data will not be available until
instruments are developed. For still others, the sources may be
known, but their prevalence and distribution in buildings are not
known.
Table 1-2 summarizes some typical pollutant concentrations found
in the indoor environment and compares them with outdoor
concentrations. An indoor-to-outdoor ratio, greater than 1 does not
imply that hazardous concentrations occur indoors. This table shows
that high concentrations of some pollutants have been reported in a
variety of buildings that are commonly used during normal daily
activities.
Water vapor is not reported in Table 1-2 as a contaminant, but it
is very important in the indoor environment. At low relative
humidities, odors, particles, and such vapors as acrolein may be more
irritating. Higher relative humidities favor mold and mite growth,
1-7
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TABLE 1-2
Sources, Possible Concentrations, and Indoor-to-Outdoor
Concentration Ratios of Some Indoor Pollutants
Pollutant
Sources of
Indoor Pollution
Possible Indoor
Concentration4
Carbon monoxide
Respirable
particles
Combustion equip- 100 ppm
ment, engines,
faulty heating
system
Organic vapors
Nitrogen dioxide
Stoves, fire-
places, cigar-
ettes, conden-
sation. of
volatiles,
aerosol sprays,
resuspension,
cooking
Combustion,
solvents, resin
products, pesti-
cides, aeroeol
sprays
Combustion, gas
stoves, water
heaters, dryers,
cigarettes,
engines
Total suspended
particles with-
out smoking
Sulfate
Formaldehyde
Radon and
progeny
100-500 p g/m
NA
<5
Sulfur dioxide Heating system 20 ug/m
Combustion, re-
suspension,
heating; system
Matches, gas
stoves
Insulation, pto-
duct binders,
particleboard
Building
materials,
groundwater, soil
100 ug/m
5 pg/m3
0.05-1.0 ppm
I/O Con-
centration
Ratio
»1
»1
>1
200-1,000 y g/m »1
<1
1
<1
>1
0.1-30 nCi/m3 »1
Location
Skating rinks,,
offices, homes,
cars, shops
Homes, offices,
cars, public
facilities, bars,
restaurants
Homes, restau-
rants, public
facilities,
offices, hospitals
Homes, skating
rinks
Removal inside
Homes, offices,
transportation,
restaurants
Removal inside
Homes, offices
Homes, buildings
1-8
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Table 1-2 (coned)
Pollutant
Asbestos
Sources of Possible Indoor
Indoor Pollution Concentration8
Flreprooflng
<1 flber/cc
I/O Con-
centration
Ratio
Location
Homes, schools,
offices
Mineral and
synthetic fibers
Products,
cloth, rugs,
vallboard
NA
Homes, schools,
offices
Carbon dioxide
Combustion,
humans, pets
3,000 ppm
»1
Homes, schools,
officer
Viable organ-
Isms
Humans, pets,
rodents, Insects,
plants, fungi,
humidifiers, air
conditioners
NA
>1
Homes, hospitals,
schools, offices,
public facilities
Ozone
Electric arcing, 20 ppb
UV light sources 200 ppb
<1
>1
Airplanes
Offices
aCoricentrations listed are only Illustrative of those reported Indoors. Both higher
and lower concentrations have been measured. No averaging times are given. NA,
not appropriate to list a concentration.
1-9
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greater formaldenyde release from particleboard, and deterioration o£
many materials.
Exposure of some members oC the population to many o£ these
pollutants may be determined by the frequency and duration of
activities that place then in particular buildings. Hence, knowing
use and activity patterns o£ the population and how these patterns
change with age, sex, socioeconomic status, race^ and geographic
region is important, if we are to assess the population exposure to
pollutants.
Seven classes of environmental factors with indoor sources have
been identified as having substantial known or reasonably likely
effects on human health: sidestream cigarette smoke, radon and radon
progeny, mineral and vitreous fibers, formaldehyde, products of indoor
combustion, agents of contagion and allergy, and extremes of
temperature and humidity.
Chapter VII presents the evidence on health effects of the seven
classes of indoor environmental factors. The seven classes were
identified as particularly relevant to indoor exposures of the general
population. For other cohtaminants that may represent special
concerns for particular indoor locations—such as exposures to organic
compounds found in pesticides, cleaning products, varnishes, or craft
and hobby products—the reader is referred to the literature developed
by the National Institute of Occupational Safety and Health, the
Environmental Protection Agency (Office of Toxic Substances), the
Consumer Product Safety commission, the Food and Drug Administration,
and the National Center for Toxicological Research. In the case of
other compounds that may be in products found in homes or
institutional buildings, not enough is known about their
concentrations or their effects to evaluate their health effects.
Although this report does not recommend specific standards for the
indoor environment, it discusses standards that have already been
established for the outdoor, .indoor working, and indoor public
environments. It is clear that there is a divergence of opinion in
the national and international health and regulatory communities as to
what constitutes a safe exposure to contaminants and which
contaminants are hazardous. Comparison with reported indoor
concentrations makes it evident that—by some established ambient,
occupational, or indoor standards—current exposures to some
contaminants indoors could constitute a health risk to occupants.
A full risk assessment of these pollutants that would identify the
population exposed and assign a health-damage function aimed at
determining current and projected.health consequences of indoor
pollution has not been attempted. In many instances, the review of
health-effects literature on specific pollutants produces conclusions
that are similar. At higher concentrations, these pollutants have
known carcinogenic, allergenic, respiratory, or other physiologic
effects. However, except for some contaminants that cause irritation,
the evidence' of direct or important health damage at reported
concentrations is not well established. The evidence in some
cases—as in passive smoking and the use of gas appliances—is a
statistical association between a health response and the source. For
1-10
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other indoor contaminants, such as radon and asbestos, the direct
health effects have been demonstrated in experimental animals and in
occupational studies. And for still others, such as formaldehyde,
information is from experimental conditions and anecdotal reports of
complaints. That these noncriteria pollutants do or will cause harm
through current or projected exposures of the general public has not
been demonstrated by epidemiologic studies. Indeed, direct evidence
from epidemiologic studies may not be forthcoming) epidemiologic
studies would be compromised from the outset by uncertainties in
indoor pollution concentrations and personal exposure. Nevertheless,
if there is consistency of toxicologic and occupational evidence of
the harmful nature of specific pollutants at the reported indoor
concentrations, then there is reason for serious concern.
In the absence of a confirmed dose-response relationship, careful
judgment is required. We should cautiously consider secondary
consequences of conservation strategies to the indoor environment.
Some pollutants may exert effects only at concentrations above a
threshold; others may have no threshold. There may be synergism
between pollutants or between pollutants and temperature, humidity, or
disease organisms. Some pollutants may manifest effects subtly in
behavioral changes. Others may have long latent periods between
exposure and effects. In view of the uncertainty in the myriad
potential outcomes, one fundamental relationship is clear: if, either
deliberately or inadvertently, we systematically modify indoor
environments by reducing ventilation or by increasing sources of
indoor contaminants without ameliorating efforts, we will be
increasing the population exposure to pollutants of indoor origin.
A review of indoor pollutant concentrations and possible health
significance would not be complete without a discussion of the
implications of these exposures for epidemiologic studies of
ambient-air pollution. Several substances generated indoors are
present in both indoor and outdoor air, including carbon monoxide,
nitric oxide, nitrogen dioxide, and particulate matter. Recent
investigations have confirmed that personal exposures to nitrogen
dioxide and respirable particles are not well represented by ambient
measurements if there are substantial indoor sources. For pollutants
of outdoor origin, the evidence indicates that personal and Indoor
exposures are less severe than outdoor exposures.
These observations have implications for epidemiologic studies
attempting to establish a relationship between ambient concentrations
and health responses. Air-pollution epidemiology attempts to
establish a statistical relationship between the dependent health
variable and the independent variable of pollution exposure,
correcting for other influential variables, such as age, sex, smoking,
occupation, and socioeconomic factors. The air-pollution exposure
most often chosen is derived from ambient monitoring appropriate to
the study population. Leaving aside the question of spatial
representation, consider the potential misclassification of exposure
that may result from indoor pollution. Depending on study design and
pollutant investigated, the results could overestimate, underestimate,
or simply incorrectly estimate the relationship between air-pollution
1-11
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exposure and health. Table 1-3 illustrates by examples the potential
bias imposed by indoor air pollution. The effects on the study can
reflect a systematic bias or a random bias in exposure. Regardless of
whether the pollutant is primarily outdoor or both indoor and outdoor
in origin, the effects of a random misclassification of population
exposure are the same. Zt tends to reduce the statistical power of
the association.
The imprecision in air-pollution health-effects data may be due in
part to indoor air-pollution concentrations. Indoor air-pollution
exposures may sufficiently complicate epidemiologic Investigations of
the effects of outdoor pollutants so that assessments of indoor
exposures, and thus larger study populations, will be needed to
discacn effects.
In Chapter VIII, the objective is to discuss the welfare effects
of contaminants in existing enclosures of all general types and the
impact o.? energy-conservation measures on indoor environmental
quality. The effects on human comfort and productivity are presented
in separate sections, and the effects of contaminants causing soiling
in another section. Chapter IX discusses some of the relevant
ventilation codes and standards. (Appendix A lists national primary
ambient-air quality standards and occupationalrsafety and -health
standards.} The effects of air-cleaning equipment and air diffusion
control are also in separate sections, followed by a general
discussion on the strategies used for control of indoor pollutants.
In an effort to exemplify this complex interaction of choices.
Appendix B presents some hypothetical assumptions for a residence.
1-12
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TABLE 1-3
Possible Consequences of Indoor Air Pollution in Epidemiology
Type of Pollution
Outdoor pollutant—indoor
concentration lower than
outdoor; air-conditioning
causes further reduction
(ozone, sulfur dioxide)
Source of Bias
Result of Bias
Systematic bias—air-
conditioned homes not
uniformly distributed
Random bias—distribu-
bution of air-condi-
tioned homes not known
Indoor pollutant—indoor
concentration higher than
outdoor (nitrogen dioxide,
respirable particles)
Systematic bias—gas-
cooking homes not
randomly distributed
Overstated relationship: if studied
(polluted) population has no air-
conditioning, this overstates
relationship between outdoor pol-
lutant and health effect
Understated relationship: if studied
(polluted) population has more air-
conditioning than other population,
relationship between pollutant and
health effects will be understated
Underestimated relationship:,
effect of pollutant on health
will be understated because
unknown number of people have
reduced exposure
Increased error of estimate
Overstated relationship: if
gas-cooking homes are found
mostly in studied (polluted) area,
this will overstate effect of out-
door pollutant
Incorrect relationship: if
different pollutants are
studied and outcome health
variable is Influenced by
indoor pollutant concentra-
tions, effect may be understated
or not detected and attributed
to wrong pollutant
Increased power: If distribu-
tion of indoor air pollution
sources or ventilation factors
are known, analysis is strati-
fied by exposure and statistical
power to measure effects nay
increase
Understated relationship: if
gas-cooking homes are found
mostly in clean area, effect of
outdoor concentration will be
understated
1-13
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TABLE 1-3 (continued)
Type of Pollutant
Source of Bias
Result of Bias
Random bias: gas-cook'
ing home8 and those
with cigarette-smokers
randomly distributed
among populations
studied
Understated relationship:
effect of outdoor pollutant
may be understated if indoor
concentration dominates ex-
posure and exerts an effect
Increased statistical power:
If distribution of smokers
or gas stoves is known and
study is large enough, stat-
istical power to discern
effects may Increase
1-14
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II
SUMMARY AND CONCLUSIONS
CHARACTERIZATION OP INDOOR AIR POLLUTION
The air quality of the indoor environment has been characterized in
a limited number of pilot studies. Because of the large variety of
distinct indoor environments—single and multifamily residences,
offices, hospitals, restaurants, schools, recreational facilities,
transportation facilities, etc.--there is a major difficulty in
characterizing "the indoor air environment." Moreover, even within one
indoor environment differences in structure, in the operation and
strength of emission sources, and in human activities add to the
complexity of characterizing air quality. The available data, mostly
from the residential environment, amply demonstrate the diversity of
characteristics of indoor air and help in identifying subjects that
warrant further research.
RADIOACTIVITY (pp. IV-2--IV-26)
The data base on sources and source strengths of indoor radon is
just beginning to be established. Initial attention focused on
building materials and groundwater. Recent evidence from regional
studies in the United States points to ground soils (under buildings)
as perhaps the major source of radon. Only a small number of buildings
in the United States have been measured for radon and radon progeny.
Indoor concentrations are affected by various factors, including
ventilation rate, deposition of radon progeny on indoor surfaces, and
interactions of radon progeny with fine particles from various sources
(e.g., tobacco smoke and house dust).
Data from several studies indicate that indoor radon-222
concentrations vary by at least two orders of magnitude, with average
values of about 1 nCi/ra3. Such a large range is not surprising,
inasmuch as the studies included various types of buildings, building
materials, underlying materials, and ventilation rates and used many
different measurement techniques. Radon progeny concentrations are
often given as potential alpha-energy concentrations (PAEC), expressed
Il-l
-------
in working levels (WL). Limited measurements indicate that typical
average radon progeny concentrations in residential buildings range
from 0.004 to 0.02 WL in some houses. Concentrations are much higher
indoors than outdoors.
ALDEHYDES (pp. IV-27--IV-44)
Aldehyde concentrations are almost always higher indoors than
outdoors. Formaldehyde is the most important aldehyde. Sources of
aldehydes include building materials (particleboard and plywood),
urea-formaldehyde (UF) insulation, and, to a lesser extent, combustion
appliances, tobacco smoke, and other consumer products. Variations in
indoor aldehyde concentrations are not well understood, and emanation
rates from the various sources are not well quantified. Owing to the
time spent inside residences (including mobile homes), offices# and
other indoor environments, human exposures to indoor formaldehyde are
markedly higher than exposures to outdoor formaldehyde.
Typical indoor formaldehyde concentrations in buildings with
products containing urea-formaldehyde resins range between 0.05 and 0.3
ppm, although in some unusual instances concentrations of a few parts
per million have been measured in houses with UF foam insulation. In
residences with sources of high rates of emission of formaldehyde-
containing products, the concentrations typically range from 0.01 to 1
ppm.
CONSUMER PRODUCTS (pp. IV-44—IV-55)
Many consumer products may emit gaseous and particulate
contaminants into the indoor environment during their use or even
during storage. Most of the chemicals in these gases and particles may
be known or can be identified, but the chemical products resulting from
mixtures and interactions of them are not known. Likely exposures and
durations are poorly understood, even for cases in which the products
are used as directed. Willful abuse of aerosols or careless use of
solvents in enclosed spaces have resulted in acute and delayed
disorders and in death. The carcinogenicity of some compounds, such as
benzene and vinyl chloride, has led to voluntary removal from consumer
products, but many chemicals with potentially toxic effects are still
in wide use. The use of insecticides, pesticides, and herbicides is
widespread. Even when applied outdoors, some compounds have been
measured indoors and have persisted over a considerable time.
ASBESTOS AND OTHER FIBERS (pp. IV-55—IV-72)
Asbestos is a widespread component of the structural environment in
schools, homes, and private and other public buildings. Its release in
the indoor environment depends on the cohesiveness of the
asbestos-containing material and the intensity of the disturbing
II-2
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force. Most contamination is episodic, activity-related, and local.
Fiber counts and mass concentrations of fibers have been measured and
shown to exceed those outdoors, and on occasion they may approximate
the occupational limit of 2 fibers per cubic centimeter. Fortunately,
during normal use, buildings containing asbestos have not shown indoor
fiber counts higher than ou'cdoor counts. Current data are very limited
and apply mostly to schools and a few office buildings, but it appears
that the general public exposure to asbestos fibers is exceedingly low
in public buildings. A systematic and comprehensive survey of indoor'
asbestos fiber contamination is needed and will require reliable,
portable, and continuous monitors. Asbestos control technologies have
been applied in various indoor environments. Asbestos removal requires
a complex protocol to be carefully applied, because the very activity
of removal may cause severe asbestos contamination.
INDOOR COMBUSTION (pp. IV-78—IV-112)
(Invented combustion appliances, especially gas stoves, are iaajor
sources of indoor air pollution. Although emission rates from a small
number of gas stoves have been determined for several pollutants, the
data base is very limited. Indoor concentrations of carbon monoxide
and nitrogen dioxide associated with incomplete combustion have been
observed to exceed current ambient-air quality standards. Carbon
dioxide emission from unvented combustion appliances may build up to
concentrations in the range of occupational air quality standards.
Local exhaust ventilation appears to be the most effective control
strategy for reducing pollutants from combustion. Improved combustion
efficiency and source elimination (i.e., adsorbers or a change to the
use of electric ranges) are two additional control approaches.
Residential wood and coal stoves are also potential sources of indoor
contamination. Attached and underground garages can contribute to
indoor carbon monoxide, nitrogen dioxide, and particle concentrations.
Carbon Monoxide
Indoor carbon monoxide concentrations are often higher than
corresponding outdoor concentrations. High indoor concentrations may
be attributed to emission from such sources as gas cooking facilities,
attached garages, faulty furnaces, and cigarette-smoking. Typical
average indoor carbon monoxide concentrations in residences vary
between 0.5 and 5 ppm; observed peak values reach 25 ppm. In public
buildings, the indoor concentrations are usually lower than observed
residential concentrations, except under conditions of. exceptionally
heavy smoking, as in bars, or in office buildings with underground
garages and improperly designed or malfunctioning HVAC systems.
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Carbon Dioxide
The indoor-to-cutdoor ratio is greater than 1 for at least 90% o£
the total monitored hours. Hourly indoor carbon dioxide concentrations
often exceed 2,000 pptn. Observed typical outdoor carbon dioxide
concentrations are approximately 40C ppm. The principal sources of
indoor carbon dioxide are the metabolic activity of occupants and
unvented combustion appliances.
Nitrogen Oxides
Emission from cooking appliances and emission from unvented heaters
are the principal contributors of oxides of nitrogen in the indoor
environment- The range of observed hourly indoor (residential) nitric
oxide concentrations is 30-300 ppb, with a maximum of about 500 ppb.
Indoor hourly concentrations of nitrogen dioxide vary between 50 and
500 ppb; indoor peaks of 700 ppb have been measured. Typical weekly
indoor concentrations of nitrogen dioxide range from 20 to 100 ppb.
The upper values in all the ranges just noted are associated with
unvented gas appliances.
SMOKING (pp. IV-93—IV-112)
Passive exposure of many nonsmokers to the contaminants in tobacco
smoke occurs repeatedly. The indoor concentrations of tobacco-smoke
compounds that have other sources exceed the concentrations found
outdoors. For many people, the main or sole exposure to numerous
gaseous and particulate compounds results from passive exposure to
tobacco smoke. Children of smoking parents are among the largest
identifiable groups in this category. For the most part, however, the
specific contribution of tobacco combustion products to personal
exposures has not been documented. Most nonchamber measurements have
been of the survey type; many have measured a single component of smoke
without reference to outdoor concentrations, ventilation, or air
dispersion.
Smoking is the major source of indoor particles, but other human
activities (e.g., cooking and vacuum cleaning) also contribute indoor
particles. Particulate matter has variable composition, and the data
base indicates that there are no constant ratios of indoor to outdoor
concentrations. The ratio of observed daily indoor concentrations of
total suspended particles (TSP) to corresponding outdoor TSP
concentrations varies from 0.3 to 4. Residences occupied by families
with pre-school-age children and smokers often have higher indoor than
outdoor concentrations. The TSP 24-h ambient-air quality standard,
which must not be exceeded more than once a year, is 260 ug/m^.
The typical range of observed indoor residential 24-h TSP
concentrations is 30-100 vq/m*, with an observed maximum of 600
ig/m3.
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Concentrations of fine particles (diameter, less than 2.5 un)
range from 10 to more than 260 wg/m3 for a 24-h sample. The higher
concentrations are almost always associated with smoking.
Concentrations in bars, offices* and cars with smoking can be higher
than 500 wg/m3.
ODORS {pp. IV-112--IV-147)
Odors arising from occupants and their activities figure in
indoor-air quality issues predominantly on the basis of comfort, rather
than health. Such routine indoor activities as cooking, smoking,
bathroom use, and maintenance give rise to odors that are often
disagreeable and in some cases offensive. To a varying degree, almost
all building materials and furnishings are sources of odor. The
determination of odor attributes—such as intensity, character
(pleasantness/unpleasantness), duration, and perceptual threshold—is
complex, but can be effectively accomplished with a combination of
instrumentation and the use of panels of human observers. Odor
controls increase in complexity from good housekeeping to ventilation
to masking and, finally, to aircleaning.
OTHER CHEMICAL POLLUTANTS (pp. IV-26—IV-55, IV-78—IV-93)
Nonmethane Hydrocarbon
The ratio of indoor to outdoor total nonmethane.hydrocarbon (NMHC)
concentrations is greater than 1 for about 90% of the total monitored
hours; that is, the NMHC concentrations observed in the residential
environment are almost always higher than the outdoor concentrations.
Fluctuations in the indoor concentrations may be associated with
cooking, cleaning, and other activities. Typical concentrations in
residential buildings vary between 0 and 8.0 ppm, whereas typical
outdoor concentrations are between 0 and 3.5 ppm. Measured NMHC
concentrations in new office buildings often exceed 10 ppm and reach as
high as 50 ppm; this may be attributed to the extensive use of
synthetic organic building materials and furnishings in new office
buildings, as well as cleaning Solvents and maintenance materials.
Ozone
Indoor ozone concentrations are generally lower than outdoor.
Unless there is an indoor generation source of ozone from electric
arcing or ultraviolet radiation (such as an electrostatic precipitator
or a document copier), the ratio of corresponding hourly indoor to
outdoor concentrations is almost always less than 1. Ozone is
primarily a product of outdoor photochemical reactions. Precursor
pollutants leading to the formation of ozone are primarily of
automotive origin, but other sources include the combustion of fuels
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Cor heat and electricity, the burning of refuse * the evaporation of
petroleum products, and the handling and use of organic solvents.
Ozone is highly reactive and decays rapidly by absorption on indoor
surfaces. indoor ozone has been measured at up to 120 ppbj typical
concentrations are between 0 and 20 ppb.
Sulfur Dioxide
Indoor sulfur dioxide concentrations are usually lower than
corresponding outdoor concentrations. Sulfur dioxide emission indoors
is usually small, and, because it is a relatively reactive contaminant,
it is absorbed by indoor surfaces. Indoor hourly sulfur dioxide
concentrations are typically below 20 ppb.
Particulate Chemical Composition
There is very limited information on the chemical composition of
indoor particles. Measured lead concentrations in residences are
commonly low—often below 0.S pg/m^. Lead concentrations as high
as 2 vg/m have been measured in residences with wail paints that
contain lead compounds or in residences that are near major roads.
Indoor residential concentrations of nitrates are quit6 low and are
driven mainly by the outdoor concentrations. Observed daily indoor
concentrations of nitrates do not vary widely—between 1.0 and 5
Vj/m?, with typical values at the lower end of the range.
The data base on sulfates shows that the indoor 24-h sulfate
concentration is usually lower than the corresponding outdoor
concentration. The type of fuel used for ccoking and heating is
important in determining the indoor-outdoor relationship; houses with
gas appliances have a slightly higher indoor/outdoor ratio than houses
without gas.appliances. Sulfur-containing compounds are added to
residential gas for detecting leaks of the otherwise odorless fuel.
Indoor daily sulfate concentrations range between 2.Q and 15.0
pg/m3, with typical values at the lower end of the range.
AIRBORNE MICROORGANISMS AND ALLERGENS (pp. VII-93—VI1-116)
For indoor biogenic pollutants, the sparseness of satisfactory
measurement methods arid the resulting lack of bn adequate quantitative
data base constitute serious problems. In contrast with other indoor
pollutants, biogenic pollutants bear complex and varied organic
structures that defy automatic chemical assay. Biogenic agents exhibit
limited direct toxicity, more often provoking infection or allergic
responses. Bccterial and viral agents can produce infections in
humans; however, the indoor transmission of these agents is not fully
understood. A broad array of fungi, algae, actinomycetes, arthropod
fragments, and dusts have been confirmed as airborne antigen sources
that evoke human allergic responses. Indoor biologic pollutants-—most
-------
notably bacteria and fungi—also play important roles in the
deterioration of surfaces and spoilage of stored materials.
MONITORING AND MODELING OP INDOOR POLLUTION
Indoor air quality monitoring, in addition to pollutant sampling*
must involve ventilation-rate measurements and daily activity logs of
occupants. In addition, meteorologic data and outdoor pollution
measurements may also be needed for the monitoring and assessment of
indoor pollution.
Most indoor monitorino studies have relied on instrumentation
developed for monitoring workplace or ambient air. The use of
conventional monitoring instrumentation is frequently awkward,
expensive, and suitable only for a limited number of comprehensive
indoor air quality studies. Owing to the special requirements,
instruments and sampling strategies are being developed specifically
for indoor residential and office environments. The advent of personal
monitors has permitted, in a few cases, the startup of monitoring and
exposure studies for specific pollutants—nitrogen dioxide and radon.
Personal and portable monitors are being developed for carbon monoxide,
formaldehyde, and particulate matter. Monitoring the indoor
environment, either with fixed-location sampling devices or with
personal monitors, requires special protocols addressing pollutant
sampling, instrument calibration, source operations, and occupant
activity. When indoor monitoring takes place under normal occupancy
conditions, the protocol must ensure that the act of monitoring itself
avoids influencing those occupancy conditions.
Indoor-air pollution simulation models provide a theoretical
framework for relating outdoor pollutant concentrations, meteorologic
factors, building factors, ventilation rates, and indoor source and
sink dimensions with indoor pollutant concentrations. Most
importantly, a validated simulation model must accurately predict a
desired concentration for conditions other than those tested
experimentally. Depending on ventilation conditions and the geometry
of the structure, a single room, a floor, or a whole building may be
adequately approximated as a single air-quality compartment (entity).
However, if sources and sinks are not uniformly distributed and if the
indoor environment is large, pollutant stratification occurs within a
building and a multicompartment numerical model is required to simulate
the indoor-air pollution concentrations. Almost all numerical models
are mass-balance equations that simulate the dynamic relationships
among indoor pollutant concentrations, outdoor concentrations, indoor
sources, and sinks (Including ventilation).
FACTORS THAT AFFECT EXPOSURE TO INDOOR POLLUTION
Exposure is a dynamic concept that is defined as the joint
occurrence of two perhaps independent events: the presence of a person
in a specific environment and the presence of a pollutant at a specific
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concentration in the same environment. Because both human activities
and air pollutant concentrations vary spatially and temporally,
pollutant concentrations obtained from outdoor monitoring networks are
inadequate for determining human exposure. Human activities are among
the factors that must be addressed in assessing exposure to air
pollutants. They have been studied by many researchers, mostly
sociologists, to determine population mobility patterns and time
budgets. The results indicate that, on the average, employed Americans
spend 90% of the day indoors, whereas homemakers and retired people
spend up to 95% of their time indoors. General sociologic studies may
be used in air-pollution research, but do not address specific topics
of interest for the assessment of human exposure to air pollutants.
The exact indoor location {or environmental mode) is of paramount
importance in exposure studies. Of all environmental typos, the
in-transit mode has been studied more extensively than any other
m icroenvi ronmen t.
Indoor air quality, and therefore exposure to pollutants, varies
geographically as a function of outdoor regional air quality and as a
function of the rural, urban, or suburban character of the location of
the indoor environment in question. In many residences, the indoor air
quality does not vary substantially. In larger buildings with many
ventilation zones, indoor air quality may vary in accordance with the
function (utility) of each zone. Building factors that influence
exposure include the site conditions, such as microclimate and
proximity to major outdoor pollution sources, building design (age,
size, ventilation systems), occupancy, and building operations. The
exact nature of the cause-and-effect relationships between these
factors and indoor air quality has not been established.
HEALTH EFFECTS OF INDOOR POLLUTION
Several classes of pollutants with major indoor sources were
identified as having important known or reasonably likely effects on
human health: sidestream cigarette smoke, radon and radon progeny,
mineral and vitreous fibers, formaldehyde, indoor combustion products,
agents of indoor contagion and allergens, and, to a lesser extent,
temperature and humidity extremes, noise, and odors.
Other classes of indoor pollutants may have impacts on human
health, such as consumer-product aerosols and pollutants from hobby,
interior-decorating, and maintenance activities (e.g., solvents and
pigments). Because the evidence of their effects on health is meager,
the Committee could' not determine whether specific effects were
attributable to them and concluded that effective review at an
appropriate depth was not feasible. Many airborne solvents, pigments,
mineral dusts, and other products used in hobbies and interior
decoration are present in the indoor air. The best data base on the
effects of exposure to those substances is that drawn from studies of
the industrial workplace, and the reader is therefore referred to the
occupational-health literature.
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INVOLUNTARY SMOKING (pp. VII-63—VII-81>
Tobacco smoke is a major source of both gaseous and particulate
pollution in the indoor environment, and the nonsaoker absorbs
measurable amounts of carbon monoxide and nicotine* as well as small
amounts of other smoke constituents, owing to involuntary smoking. The
carbon monoxide absorbed varies from negligible in well-ventilated
office buildings to amounts that raise the carboxyhemoglobin (COHb)
concentration by 2-3% in an exposure of 1-2 h.
The COHb produced by the most severe involuntary-smoking exposure
likely to occur in everyday living is capable of reducing the maximal
exercise capacity of normal healthy adults, but does not measurably
affect submaxioal exercise capacity. Carbon monoxide has been shown in
one study to reduce the amount of exercise that patients with hypoxic
chronic obstructive lung disease can perform before the onset of
dyspnea.
Patients with angina pectoris have a reduced exercise tolerance
after involuntary smoking that may be a combination of psychologic
stress and a carbon monoxide-induced decrease in oxygen delivery to the
myocardium. Carbon monoxide clearly reduces the amount of exercise
possible before the onset of angina in patients with angina pectoris.
Small changes in visual and auditory vigilance have been
demonstrated at COHb concentrations that can be produced by involuntary
smoking, but no change in tests of complex function has been
demonstrated. Involuntary smoking has not been shown to produce acute
changes in lung volumes or in a number of small-airway resistance
measurements in normal healthy adults. Long-term exposure to cigarette
smoke has been related to small-airway dysfunction in healthy
nonsmoking adults.
Children whose parents smoke have been shown in some studies to be
more likely to have respiratory symptoms , bronchitis, and pneumonia as
infants. This relationship has been found in some studies to be
independent of parental symptoms, socioeconomic class, and the smoking
habits of other children in the household. It shows, in those studies,
a dose-response relationship with the number of cigarettes smoked per
day by the parents. To the extent that these associations may be due
to cigarette smoke, it is reasonable to assume that the particle mass
or a specific compound contained therein, rather than nitrogen dioxide
or carbon monoxide, is responsible.
A twofold risk of cancer mortality in nonsmoking women has been
associated (in a Japanese study) with having husbands who saoke.
Apparently, the risk is proportional to the amount of passive smoking.
RADON AND RADON PROGENY (pp. VII-6—V1I-21)
The radon gas that diffuses out of radium-bearing building
materials, subsurface soil beneath buildings, and well water into the
indoor air undergoes radioactive decay. As a result, the indoor air
contains both radon gas and alpha-emitting decay nuclides in
particulate form, herein referred to as "radoa progeny."
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The health effects of radon and radon progeny are well established
from studies of workers. Exposure to radon and its progeny at high
concentrations has resulted in several hundred excess cases of lung
cancer among uranium miners in the western United States. The health
effects of ouch smaller amounts of cadon progeny froo indoor exposures
can be estimated on the basis of a linear/ no-threshold dose model,
which yields upper-limit estimates of excess cancer in populations
exposed to various indoor concentrations of radon and radon progeny.
Lifetime cumulative exposures to radon progeny that result from current
indoor exposures are lower by approximately a factor of 100-10,000 than
those xeceived by the U.S. uranium, miners who have been studied.
The reliability with which the uraniiua-miner lung-cancer experience
can be extrapolated to the effects of indoor exposures to radon progeny
among the general population is limited by several important
differences between the populations and by uncertainty about the extent
of the effect of cigarette-smoking on the incidence and latent period
for lung cancer related to radon progeny. The population differences
include: (1) an adult# male, healthy working population versus a
general population that includes the very old, the very young, and the
chronically ill; (2) coexposures to relatively high concentrations of
silica dust and diesel exhaust among the miners veisus coexposures to
relatively low concentrations of household pollutants and consumer
products among the general population; and (3) differences in the
ethnic and social backgrounds and smoking histories among the different
populations.
ASBESTOS AMD OTHER FIBERS (pp. Vll-1%—Vll-49)
The inhalation of asbestos fibers can lead, many years later, to
pulmonary fibrosis, lung cancer, and mesothelioma of the pleura and
peritoneum. All these diseases have been seen in humans who had
chronic occupational exposures to airborne asbestos fibers, and they
have all been reproduced in animals. lAing cancer and mesothelioma have
also been seen in humans who had no occupational exposures, but who
lived either in the same households as asbestos-workers or in
neighborhoods where the ambient air had increased asbestos-fiber
concentrations resulting from proximity to an asbestos-related industry
or a geologic anomaly that acted as a source of airborne fiber.
Asbestos and asbestos-containing products—such as ceiling tiles,
floor tiles, pipe insulation, and spackling compounds—were widely used
in homes and public buildings because of-their excellent thermal and
acoustic insulation and structural properties-. When these materials
and products are displaced or disturbed by abrasion of deteriorating
surfaces during housekeeping and maintenance operations, renovations,
redecorating, or, especially in public buildings, malicious mischief,
asbestos fibers can be released into the air. Concern about the
inhalation of fibers that can result has led to extensive and expensive
programs to remove asbestos, under controlled conditions, from
accessible regions of public buildings, such as schools and libraries.
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Fibrous materials used as substitutes Cor asbestos include glass
fiber, rock wool, and slag wool. They have been shown/ in animal
injection and implantation studies, to be capable of producing lung
fibrosis and mesothelioma. However# they are such less important in
this regard than asbestos, and there is no corresponding buaan-bealth
evidence associated with the forms in which they are used in industrial
and consumer products. Thus, their substitution for asbestos appears
to be beneficial, inasmuch as such substitution reduces the risk
associated with asbestos exposure.
FORMALDEHYDE (pp. VII-21—VII-37)
Formaldehyde has been the subject of numerous complaints regarding
irritation of the eyes and respiratory tract, nausea, headache, rash,
tiredness, and thirst. These symptoms have been reported mainly by
residents of mobile and conventional homes in which
formaldehyde-yielding products have been identified. Documented cases
of bronchial asthma due specifically to formaldehyde are few; more
commonly, asthma is aggravated by the irritating properties of
formaldehyde.
Aqueous solutions of formaldehyde damage the eye and irritate the
skin on direct contact. Repeated exposure to dilute solutions may lead
to allergic contact dermatitis. Poisoning from ingestion is uncommon,
because the irritancy of formaldehyde makes ingestion unlikely.
A preliminary report from the Chemical Industry Institute of
Toxicology has shown that formaldehyde induces nasal cancer in
laboratory rats and in some of the laboratory mice similarly exposed at
the high dose. Nasal cancer has developed in the group of rats exposed
at 15 ppm and 6 ppm, and dose-related histologic changes of the nasal
mucosa in rats exposed at 2 and 6 ppm. Although the human mutagenic
and teratogenic potential of formaldehyde is not known, it has
exhibited mutagenic activity in a wide variety of organisms.
Data on the health effects of other environmental factors and their
interactions—such as cigarette-smoking history, variability of health
status, age, and genetic predisposition (which may modify responses to
formaldehyde)—have not been adequately evaluated. That makes it
difficult to assess accurately the health risks attributable tc
exposure to formaldehyde. However, the complaints of residents of
homes with formaldehyde-containing products are similar to complaints
made by persons studied in the laboratory at similar formaldehyde
concentrations; hence, these health complaints may be related to
formaldehyde exposure in the hone. Accordingly, a substantial
proportion of the U.S. population may be likely to develop symptoms as
a result of exposure to formaldehyde at low concentrations. It has
been estimated, on the basis of laboratory tests and various kinds of
population surveys, that perhaps 10-20% of the general population may
be susceptible to the irritant properties of formaldehyde at extremely
low concentrations. For example, some persons report mild eye, nose,
and throat irritation and other symptoms at concentrations less than
0.5 ppm, and some note symptoms at concentrations as low as 0.25 ppm.
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These concentrations could also cause bronchoconstriction and asthmatic
symptoms in some susceptible persons, and chronic exposure to low
concentrations can result in sensitization. There appears to be a wide
range of individual susceptibility to formaldehyde exposure. We cannot
determine the exact numbers of susceptible people residing in indoor
environments where exposure to formaldehyde could produce adverse
responses. On the basis of estimates of the number of susceptible
persons among the general population and the estimate that about 11
million persons in the United States now reside in mobile homes of
varied age, construction, and quality, it may be concluded that a
substantial number pf persons are at risk of developing adverse health
effects associated with formaldehyde.
INDOOR COMBUSTION (pp. VII-49—VII-63)
The combustion of fossil fuels in air results in the generation of
effluept streams containing carbon monoxide, nitric oxide, nitiogen
dioxide, formaldehyde, carbonaceous particles, and other products of
incomplete combustion, as well as the products of complete
combustion—carbon dioxide, water, and sulfur dioxide. When the
effluents are not vented to the outside, as in the case of most gas
ranges and some space-heaters, the effluents are mixed into the indoor
air.
The percentage increase in the indoor concentration of the
combustion effluents resulting from such indoor sources is generally
greatest for nitric oxide and nitrogen dioxide. For homes with gas
ranges, indoor nitrogen dioxide concentrations are frequently twice as
high as outdoor concentrations. The long-term integrated
Concentrations can exceed the national annual ambient-air quality
standard (NAAQS) of IOC gg/m^ (0.05 ppm) in some houses. Although
chronic animal inhalation studies and community air-pollution
epidemiology studies using central raonitoring-station data have not
established that exposures at or near the NAAQS for nitrogen dioxide
produce measurable health effects, several recent studies of the health
status of children living in homes with ga? ranges have shown that they
had more respiratory illness and poorer respiratory function than
children living in comparable homes with electric ranges.
Increases in carbon monoxide sufficient to cause measurable health
effects are usually associated with improperly, operated flames or
especially prolonged use of unvented space-heaters. Both carbon
monoxide and nitric oxide bind with hemoglobin and reduce tissue
oxygenation. Carbon monoxide from indoor combustion sources and
sidestream cigarette smoke can be shown to cause measurable increases
in COHb of exposed persons, but the health implications of such
increases remain speculative. The importance of increased carbon
monoxide and formaldehyde concentrations in indoor air was discussed
above.
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INDOOR AGENTS OP CONTAGION ASP ALLERGY (pp. VH-81—VII-U6)
There is considerable evidence that a number o£ contagious-disease
organisms—including those associated with influenza, Legionnaires'
disease, tuberculosis, measles, mumps, and chicken pox—-are capable of
airborne transmission in the indoor environment. Other respirator
diseases, such as the common cold and pulmonary Infections, involve
airborne transmission. Because of the important role of respiratory
diseases in overall acute morbidity, airborne transmission of
contagious agents is important in the indoor environment.
The droplet-nucleus theory—whereby liquid particles emitted from
the human respiratory tract evaporate to a particle size that can
remain airborne for a period sufficient to be carried by natural air
currents or convective ventilation flows and later deposited in the
human airways—is generally accepted and used.as a baais for
transmission models. The effect of reduced ventilation in residences
and offices on the incidence of infections is unknown.
Only a few airborne allergens ace found in enclosed spaces. Their
health effects are difficult to estimate, although their impact is
sometimes appreciable.
EFFECTS Of INDOOR POLLUTION ON HUMAN WELFARE
Effects on human welfare are taken to include loss of productivity,
human discomfort, and effects on materials, primarily soiling and
corrosion of exposed surfaces.
SOCIOECONOMIC STATUS (pp. VIII-1—VIII-3)
Members of low income classes are more likel/ to live in poorly
insulated housing with higher air-exchange rates. Several reports have
indicated that gas stoves or unvented gas or kerosene heaters are used
for supplemental space-heating in northern cities. The percentage of
homes with smokers appears to be inversely related to parental
educational level. Lead intoxication in children occurs
disproportionately in lower-income urban populations; higher ambient
airborne-lead concentrations may contribute. However, some potential
sources of indoor pollution may occur more frequently in the middle and
upper incase brackets. Many consumer products, as well as coal and
wood stoves, exemplify such sources. Although the distributions of
these and other factors may be functions of socioeconomic status that
cause some segments of society to be more or less disadvantaged with
respect to a hazardous indoor environment, the available data allow
little more than speculation.
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PRODUCTIVITY {pp. VIII-13--VIII-19)
There Is a <3towing recognition of the difficulties in clearly
demonstrating the linkage between environmental quality and
productivity. Perhaps as a result of these difficulties, there appears
to be a slackening of research in this subject. Anecdotal or
observational evidence dan be found to support the conclusion that
improving air quality should improve productivity, but objective
documentation does not appear to exist oc to be readily available. The
most promising avenues for research appear to be those which
demonstrate direct health effects of the various pollutants.
Nevertheless, under the modern, broad definition of "productivity," a
reduction in productivity is an almost certain qonsequence of pollution
itself.
SOILING AND CORRQSIOH (pp. VIII-19--VIII-27)
Reduced indoor environmental quality can result in degradation and
deterioration of indoor materials, furnishings, and artifacts. As
efforts required for maintenance arid housekeeping increase, the
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CODES AND STANDARDS (pp. IX-2--IX-16; Appendix A)
Minimal requirements of acceptability are o£ten stated in building
codes and standards in terms of air-exchange rules, temperature limits,
and so forth. These documents tend to cause minimal requirements to be
established for such direct effects as temperature, humidity, and
odors, but may not be sufficient to provide for other effects, such, as
air pollution or noise. Nor do these codes consider the interactions
that can occur among these factors and other system features such as
lighting, thermal load, and spatial requirements.
AIR DIFFUSION CONTROL (pp. IX-16—IX-22)
Indoor air quality is most commonly controlled by forced-air
systems. However, if diffusion control is designed without considering
possible stratification of air within a room or a building, there may
be local violations of thermal) humidity, or air-quality criteria for
acceptability, end occupants may be exposed to conditions other than
expected from the design.
INDOOR ENVIRONMENTAL CONTROL SYSTEMS (pp. IX-16—2X-22)
Control methods for indoor environments require specification of
environmental criteria and definition of the control variables. The
environmental criteria that are identified in this document are health,
comfort, welfare, energy consumption, and costs. The control variables
identified are spatial requirements, lighting factors, thermal factors,
air quality, and acoustic factors. Although environmental criteria and
control variables can be identified and described, the capability of
sensing the appropriate variables and controlling the system to meet
the specified criteria is severely limited. Moreover, most indoor
environmental control systems must attempt to respond activity or
passively to all five of the control variables simultaneously.
Residential air-conditioning systems are conventionally designed to
respond to spatial, thermal, and air-quality variables and, to a
limited extent, acoustic variables. For larger facilities, such as
offices and schools, air-conditioning systems must also respond to
variations in occupancy and lighting loads, in addition to spatial,
thermal, air-quality, and acoustic factors. For other functional
spaces (e.g., concert auditoriums, art galleries, museums, and
hospitals), some or all of the variables must be controlled with
additional precision.
For many years, air-conditioning systems were designed to meet the
required environmental criteria (primarily thermal) at minimal,first
cost. Operating costs were not considered important as first costs
because energy was relatively inexpensive, compared with labor and
material. However, as the costs of energy Increased rapidly during the
last decade, operating costs became a major factor in environmental
control. Energy-conservation measures were implemented in many
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buildings to reduce operating costs. Soma of these measures (e.g.,
improved system efficiency through better maintenance) had no impact on
environmental control, but others (e.g., reduced ventilation, heat, and
lighting) had potentially adverse effects. One reason for the
occurrence of adverse effects was lack of understanding, by building
operators and owners, of the interrelationships among ventilation
rates, lighting, and health responses. As an example, changes in
lighting can affect thermal loads, which affect ventilation rates.
Conversely, results of some energy-conservation measures have indicated
that indoor environmental quality need not be degraded and, in fact,
may be enhanced by these changes (e.g., reduced stratification within
occupied spaces). Thus, two general conclusions can be drawn: control
methods may not be capable of adequately responding to environmental
changes as energy-conservation measures and cost contraints are
applied; and the quality of the indoor environment need not be
degraded, but can be enhanced if care is exercised in the selection and
implementation of the energy and cost constraints.
AIR-CLEANING BQUIPMEMT (pp. IX-22—IX-39)
Air-cleaning equipment for residential and commercial applications
is generally limited to particle filtration. Some gas and vapor
removal equipment is available, primarily for commercial applications.
Methods of rating or evaluating the performance of1 the gas and vapor
removal systems are not yet available. Methods are available for
rating and evaluating particle removal equipment, but they are
simplistic and outdated. Moreover, in-place methods of system
evaluation are available only for special cases, such as hospitals and
laborator ies.
COST EFFECTIVENESS (Appendix B)
Several economic models are available that can be used to evaluate
the costs associated with various control strategies.
Cost-effectiveness models that incorporate life-cycle costing are
needed for dec is ion-male ing.
An approach to estimating the impact of residential
energy-conservation measures on air quality is discussed in Appendix B.
The approach has not been validated or put into practical use, but is
presented for illustration and discussion.
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in
RECOMMENDATIONS
The Committee on Indoor Pollutants recognizes that decisions
affecting the quality of the indoor environment are being made by
manufacturers, government agencies, builders, building operators,
professional organizations, and private individuals. The decisions
encompass a broad range of activities in our society, with important
and long-term consequences. Federal agencies are planning
energy-conservation programs in buildings, contemplating the banning
of some products, and estimating the health risk associated with
indoor pollutant exposures, state and local government units are
considering revisions of building codes, ordinances to prohibit
smoking in public buildings, and requirements that asbestos insulation
be removed from schools.. It can be presumed that there are similar
examples of decision-making at various levels in the private sector
that affect indoor environmental quality. In view of the possible
impact of these decisions, the committee is concerned that policy,
research, and economic decisions be formulated with proper
understanding of their implications for the quality of the indoor
environment. For specific indoor contaminants, two basic inadequacies
in the available data must be resolved rapidly: poor definition of
population exposures and lack of understanding of the health and
welfare consequences of exposure to contaminants in the indoor
environment. This chapter presents the Committee's general and
specific recommendations for remedying these inadequacies.
Vie have observed that ^he existing data base is, for the most
part, derived from pilot studies or anecdotal reports. The results of
the pilot studies reveal the complexity and diversity of the
information that must be looked at in evaluating the quality of indoor
environments. In some cases, the potential health significance of
exposure to indoor contaminants has been alluded toj but the full
extent of a potential problem with respect to types of contaminants,
concentrations, and numbers of people exposed has not been determined.
He believe that the research problem is large and requires
national coordination. A national coordinated research program would
have the following advantagest
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* Xt would pcovide reasonable allocation of research efforts
among various federal agencies* national laboratories, and academic
institutions.
* It would provide standards for study design and quality
assurance that are sufficient for various decision-making purposes.
* It would provide integration of research activities and
dissemination of the information derived.
* It would provide maximal effectivenss of available funding.
The objectives of such a research program should be theses
* To determine the various sources and distribution of selected
pollutants, to measure their ranges of concentrations, and to identify
populations at risk.
* To understand how the contaminants move inside buildings, how
they mix and react, and the rate at which they are removed or
dissipated under various conditions.
* To characterize indoor pollutant emission source strengths
under actual conditions.
* To develop and test the effectiveness of control technologies.
' To determine the effects of energy-conservation measures on
indoor air quality.
To meet some of these objectives, there must be research aimed at
developing improved instruments and at strategies for using them in
the study of indoor pollutants, instruments used to characterize
indoor air quality reflect the early stages of this scientific
endeavor. The sampling devices used in indoor studies were originally
designed for sampling outdoor or industrial air. Many commercially
available ambient-ait monitors are bulky, noisy, and expensive and
have not been tested for interferences that may be encountered
indoors. These devices have raostly been judged to be inadequate for
investigating inrioor air quality, because their sensitivity, accuracy,
and preciaion are not.sufficient for the measurement of pollutants in
the small volumes of air in indoor spaces. The Committee recognizes
the importance of recent developments in the field of personal
monitors; but it also recongizes the need for a simultaneous effort
devoted to the development of air sampling devices designed
specifically for indoor environments. The new instruments must be
designed to record short-term peaks in concentrations.
Instrumentation alone is not sufficient for characterizing the
indoor environment. Numerous variables indoors (perhaps more than
outdoors) must be considereds some sources of pollutants are peculiar
to some indoor environments; there are differences in structure type,
ventilation, and other characteristics that affect pollutant
concentrations; and activity patterns and time budgets of occupants
vary. Human activity patterns and time budgets, which are essential
in determining total exposures to air pollutants, are now derived from
population"surveys. These surveys do not require (and therefore do
not obtain) information relevant specifically to indoor air quality.
The Committee sees the need for analysis of these variables and their
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effects and recommends the development of model strategies (for
sampling, etc.) or protocols as guidance for future research. (The
formulation of model sampling strategies, for example# is not meant to
stifle innovation in sampling designs, but rather to establish the
model to be used for comparing data obtained by researchers whose
objectives differ.) The Committee recommends the formulation of
strategies and protocols for measuring the strength of various indoor
pollutant-emitting sources and for assessing the effectiveness of
control devices and procedures in abating pollution.
The Conmittee recommends the formulation of a standard format for
reporting data and the development of protocols for standardized
statistical approaches that will require only minimal analysis to be
used in validating numerical models. These would help to reduce
difficulties in comparing existing data and facilitate the development
of valid conclusions; conclusions now are often based on exceedingly
small samples.
Even comprehensive information abcut the quality of the indoor
environment would not permit determination of total pollutant
exposure. It must be recognized that people are exposed to many of
the same pollutants outdoors, in transit, in the occupational-
industrial environment, and elsewhere. The relative importance of
each kind of environment can be established and priorities can be set
if and only if pollution exposures in all distinct environments are
characterized. Lack of a complete assessment may lead to inefficient
allocation of scientific effort and control funds in each kind of
environment. The Committee believes that the research efforts to
characterize indoor air pollution and human exposures indoors must
continue and intensify, if we are to determine total human exposure to
pollutants and understand environmental contamination and its effects
on health and the quality of life.
The remainder of this chapter presents specific recommendations
for research, grouped by class of indoor contaminant discussed in the
body of the report, and discusses the need for increased understanding
of indoor pollutants in general and the need for consumer protection.
RATON
Nationally coordinated investigations on radon and its progeny
should take place on two levels. A well-funded and coordinated
national survey of radon concentrations in a representative sample of
residential buildings is necessary to estimate tha exposure of the
total population to radon and radon progeny. Monitors that use the
track-etch plastic chip may be adequate for integrated measurements
for such national surveys, because they are inexpensive and are
specific to radon. However, the performance of these and other
passive devices needs to be carefully evaluated. Inexpensive
instruments for measuring radon concentrations on a short-term basis
need to be developed. These instruments should be available to local
health agencies and others for spot surveys. On another level,
research on the transport and transformation of radon inside buildings
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deserves special attention. Rates of emanation of radon from various
sources, building materials, soil, and groundwater should be evaluated
in a variety of on-site and controlled conditions. The etfectiveness
of strategies for abating or eliminating indoor radon (including the
use of material sealants and fine-aerosol collection devices) must be
evaluated.
There is an urgent need to study the health effects of radon and
radon progeny. On the baBis of known effects in miners exposed to
radon and radon progeny at relatively high concentrations, a plausible
case can be made that a substantial fraction of the lung-cancer
incidence in nonsmokers is due to the alpha-radiation dose to the
respiratory tract epithelium from inhaled and deposited radon progeny
particles. It is urgent that this observation be examined
quantitatively by studies of appropriate human populations already
known to be exposed at below 100 WLM and preferably in the range of
20-50 WLM. It is known that in some gedgraphic areas large
populations are being exposed to radon gas and radon progeny particles
in their residences at concentrations that, although much lower than
those in uranium mines, are substantially higher than those in most
residences. Epidemiologic studies of populations exposed to radon and
radon progeny are reasonable and can provide the information necessary
for the establishment of realistic and needed exposure-response
relationships. These research studies should include examinations to
determine early pathologic changes other than tumors (e.g., changes in
sputum cytology and chromosomal aberrations), with special attention
to the possibility of a relationship of those changes to the eventual
development of lung cancer. Such studies should be performed as soon
as possible*
FORMALDEHYDE
Simple and reliable passive monitors that would easily satisfy the
requirements of large surveys of buildings for formaldehyde emission
do not exist. Monitoring formaldehyde is extremely difficult, because
of the influences of temperature, humidity, and some analytic problems
that affect its detection. Both continuous and passive monitors are
needed with sensitivities in the range of 10-30 parts per billion. A
national survey for indoor formaldehyde exposures is not needed, but a
systematic study of formaldehyde concentrations in a variety of indoor
locations is needed to estimate potential exposure of humans. This
study would also identify sources of indoor formaldehyde by type of
building and decorative materials and would evaluate the effects of
ventilation rates and other variables on the concentration. Regular
measurements over specified periods would help to identify
formaldehyde emission rates of insulating building materials and
furnishings as functions of temperature, humidity, ventilation rate,
and material age.
Formaldehyde emitted from buildings and consumer products has
resulted in complaints of adverse health effects by people in some
mobile homes and in some conventional residences and other buildings.
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Some of'thia emission occurs over Ions periods. Thus, long-term
effects in humans continuously exposed to formaldehyde at low
concentrations need to be studied. There is a particular need to
assess the carcinogenic potential in the concentration ranges of human
exposures, inasmuch as one study in one strain each of ratB and mice
has shown that long-term exposure (lasting 24 mo) caused nasal
cancer. Humans have been and are now being exposed to formaldehyde in
several types of occupations and in a variety of structures.
Epidemiologic investigations are needed to assess the human health
effects of formaldehyde/ the magnitude and duration of exposure, and
the influence of cigarette-smoking habits and the presence of other
contaminants. The mutagenic, embryotoxlc, and teratogenic effects
must be included in the epidemiologic and animal studies. In humans
exposed to formaldehyde, the mechanisms of airway and target cell
responses must be evaluated and characterized as to sensitization and
adverse effects in susceptible population groups, such as asthmatics
and persons with chronic obstructive lung disease. Exposure-effect
relations and the mechanisms involved in the biologic effects require
further animal toxicologic research. Formaldehyde should be
restricted to the extent that household consumer products and building
products in normal use will not release potentially hazardous or
irritating amounts of formaldehyde into indoor air.
TOBACCO SMOKE
Tobacco smoke has shown some evidence of being a major contaminant
in many indoor envifonments. Involuntary exposure to tobacco smoke
should be assessed to identify locations and populations with high
exposure and to determine the factors that contribute to high
exposures indoors. Physical and biologic evaluation of tobacco-smoke
constituents should be continued. Tobacco-smoke constituents should
be tested for their toxic effects, their ability to act as mutagens or
promoters of carcinogenesis, and their effects in cpmbination with
other indoor pollutants. In addition, such properties of tobacco
smoke as mass and age, chemical composition, irritation factors, and
odor components should be examined to learn how they are affected by
ventilation rate, occupancy, extent of smoking, air-cleaning, and
other control strategies.
The extent to which passive exposure to sidarttream tobacco smoke
produces respiratory tract symptoms and functional decrements in
nonsmokers, especially children, needs further documentation and
measurement. Prospective studies of children in homes with ssokers
would be especially desirable to determine rates of lung maturation
and illness frequency during childhood and adolescence.
Information on the potential health effects of exposure of
nonsmokers to tobacco smoke should be widely disseminated. The
"energy-cost penalty" of providing adequate ventilation in indoor
environments that permit smoking should be analyzed in a variety of
public buildings. Increased cigarette taxation as a mect^anism of
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reimbursement for the cost of the additional air-conditioning needed
to remove tobacco smoke should be explored by governments at all
levels.
ASBESTOS AND ASBESTIFOBM FIBERS
A systematic survey is needed for the evaluation of the
distribution, integrity, and concentrations of asbestos in buildings
that contain or are thought to contain asbestos material. However,
before this survey can be conducted, there is a need to develop new
instruments to record fiber counts continuously, with size
determination and possibly asbestiform-fiber identification, because
current sampling and analytir techniques are inadequate.
Synergistic and interactive toxic effects of asbestos fibers in
combination with other air pollutants, particularly organic vapors,
should be examined in animal toxicologic ana mutagenicity studies.
Although some asbes'tiform fibers themselves do not appear to
constitute an immediate health concern, their role as initiators or
promoters in various disease processes should be studied. The
incidence of mesothelioma in humans should be monitored via a registry
and appropriate surveillance methods, to detect cases associated with
substantial nonindustrial exposure to.asbeptiform fibers.
Guidelines should be developed for the control of exposure to
airborne asbestos fibers during maintenance, renovation, and
reconstruction in buildings that contain asbestos and asbestos-bearing
shingles, tiles, plaster, etc.
COMBUSTION
Indoor combustion produces a number of contaminants. Among the
contaminants that deserve special attention are nitrogen dioxide,
carbon monoxide, respirable particles, nitrosamines, and polynuclear
aromatic hydrocarbons. The rates of their emission from sources of
indoor combustion have not been adequately evaluated. The Committee
recommends that controlled chamber experiments be conducted to
determine the products and their rates of emission from various types
of combustion under various conditions. These experiments should
focus principally on gas and electric cooking appliances and
supplemental heating systems, such as natural-gas, propane, and
kerosene heaters and coal- and wood-burning stoves. Air-venting and
air-cleaning systems should be studied as means of reducing indoor
concentrations of contaminants.
Indoor concentrations of combustion products have only recently
been surveyed. Combustion products are present in many indoor
locations, such as restaurants, cafeterias, homes, hotels, buildings
with attached garages, and recreational facilities that use gasoline-
powered equipment. Wore comprehensive and systematic surveys ara
ne«tJed to identify the range of combustion-product concentrations
encountered indoors and the numbers of people exposed to them. These
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studies should determine the population exposure to nitrogen dioxide
over both the short and the long tern, in addition, the applicability
of aablent-alr fixed-location monitors for recording nitrogen dioxide
and carbon monoxide concentrations indoors and for assessing
individual exposures should be studied.
Chemical reactions and rates of removal of emitted gases should be
determined. Nitrogen dioxide formation and removal should be examined
in detail. This will involve the simultaneous measurement of other
gaseous compounds. Hie effects of reduced air-exchange rates* zone
ventilation, and source modification on pollutant reactions should be
assessed. As with other indoor contaminants, there is a general need
to improve instrumentation. Both nitrogen dioxide and carbon monoxide
monitors are available for passive integrating sampling and for
continuous monitoring. However, for indoor use, they need to be
evaluated with respect to interferences. To evaluate short-term
personal exposures, lightweight continuous monitors for oxides of
nitrogen need to be developed. Evaluation of personal exposures to
respirable particles is currently limited to integrated samples.
Lightweight portable samplers or direct-dreading monitors that can
measure mass concentration over shorter periods are needed.
Nitrosamines can be formed during cooking and smoking. However,
very few detailed investigations of the concentrations, mechanisms of
formation, and potential control methods have been done.
The polynuclear aromatic hydrocarbons can be formed during
high-temperature combustion of organic matter. Some of them have been
found indoors as a result of emission from self-cleaning ovens and
fireplaces. Pilot studies should be initiated to evaluate the extent
of emission of polynuclear aromatic hydrocarbons and their indoor
concentrations.
The magnitude and prevalence of decreases in pulmonary function
and increases in respiratory tract infection rates among children
living in homes with gas ranges and homes with electric ranges need to
be determined more accurately, and there are several related issues
that require clarification:
* Whether the effects are due entirely to the increased
nitrogen dioxide concentration in the gas-stove homes or are
influenced by the presence of other combustion effluents from the
stoves, such as carbon monoxide, formaldehyde, and particles.
* Whether the effects can be related more closely to peak
concentrations or to long-term average exposures.
* Whether the effects of exposures to sidestream cigarette
smoke and to nitrogen dioxide are additive or synergistic.
* Whether exposure-response relationships can be developed and,
if so, whether they indicate an effective threshold concentration for
peak or average exposures.
The influence of reductions in air infiltration rates in existing
buildings on indoor concentrations of combustion products needs to be
determined. Among the potentially serious health consequences of
reductions in infiltration are:
1X1-7
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Creation of greater pressure differentials between the
indoors and the outdoors* which could reduce the effectiveness of the
venting of combustion sources, e.g., furnaces and water-heaters.
Problems in proper venting could cause substantial exposures to carbon
monoxide (which could lead to severe intoxication and fatalities), as
well as greater exposures to carbon dioxide, nitrogen dioxide,
formaldehyde, and particles.
Increase in chronic exposures to carbon monoxide, nitrogen
dioxide, formaldehyde, and particles nt low concentrations from
unvented combustion sources; this could lead to increases in
respiratory infections in children and decreases in their lung
function.
CONSUMER PRODQCTS
The use of some consumer products can lead to the release of
aerosols and gases indoors. The gaseous compounds of concern are
mostly organic vapors. Among the compounds of principal concern are
aldehydes and polynuclear aromatic hydrocarbons that evolve from
plasticizers; nitrosamines and hydrocines from rubber products,
combustion products, and cleaning agents; polychlorinated biphenyls
(PCBs) from burnt-out ballasts in fluorescent lights; and a variety of
other middle- and higher-molecular-weight organic substances from
pesticides. A few studies have noted the presence of many of these
compounds indoors. However, no systematic survey has been done. With
regard to the evolution of organic molecules from pesticides,
organochlorinated pesticides should be examined first, including
aldrin, dieldrin, endrin, benzene hexachloride, pentachlorophenol,
kepone, chlordane, and DDT. The emphasis should be on the
determination of body burdens of these compounds and specifically the
relative contributions of inhalation, ingestion, and absorption to
body burdens.
The contents of consumer products should be investigated, and the
chemical constituents should be tested for their toxic, mutagenic,
carcinogenic, and teratogenic properties. In particular, there should
be toxicologic studies of solvents, vapors, aerosols, and particulate
compounds present in these products. Their synergistic and
interactive effects with other indoor pollutants should be tested.
Consumer products whose use involves the release of gaseous and
particulate materials to the indoor atmosphere should be so labeled,
with their components. Warning labels for consumer products that can
seriously pollute the indoors should state that they are to be used.
only in areas with adequate ventilation and should stipulate the
possible consequences of their use when there is inadequate
ventilation.
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ABBOPATHOGBNS AMD ALLBflGEHS
Little is known about the sources, cancentrations, and survival
rates of many aeropathogena in homes and other buildings.
Relationships among the incidence of respiratory infections,
concentrations of aeropathogens, and air-exchuige rates in buildings
must be examined. The urgency arises from the recent modifications in
building ventilation codes that recommend reduced ventilation rates In
residential and commercial structures. A sample of commercial,
institutional, and residential buildings should be evaluated for the
types and concentrations of aeropathogens under a variety of
conditions of occupancy, human activity, ventilation, humidity,
temperature, and contaminant control. Special attention should be
given to the newer energy-efficient buildings and buildings with
drastically reduced ventilation. flie potential for infectious
contamination from air-cleaning filters, air heat-exchangers, air
humidifying systems, and air-conditioning systems deserves special
attention.
Other agents in the indoor environment known to produce allergic
responses include pollens, household mites, molds, animal dander and
excreta, and bacterial spores. Further work is needed to characterize
the size distribution of allergen aerosols, their sources, and the
conditions that are conducive to their generation. The airborne
concentration of allergens in the indoor environment has been
determined in only a few instances, and the relationship between
indoor concentration and response is poorly understood. Case-control
epidemiologic and immunologic studies are needed to clarify
exposure-effect relationships. Such studies will require improved
instrumental and analytic techniques to facilitate characterization of
concentrations of allergens and of the variety of microorganisms in
the indoor environment. Synergism of biologic and nonbiologic agents
should be explored in animal toxicology studies.
Some acute allergic responses, such as "humidifier fever," are of
unknown etiology. The pathologic agents in immunologic and case-
control epidemiologic studies need to be identified. The pathogenic
process by which repeated small exposures to some allergens often lead
to irreversible fibrotic lesions, as in bird-fancier's disease, should
be elucidated, and the potential of other, nore common indoor
pollutants to produce such disease states should be evaluated.
VEMTXIATIOM STAHDARDS AND CONTROL STRATEGIES
Knowledge a£ ventilation rates is of primary importance in studies
of indoor contaminant concentrations. Given the variety of
residential living units and other public and private facilities, it
is not surprising that very little information exists to characterize
air-exshange rates. Studies should begin to characterize air-exchange
rates in existing buildings by building type, geographic location,
occupant life styles, building operation, and observed average
pollutant concentrations during the different seasons. Smaller-scale
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studies over a considerable period are recommended to characterise air
exchange and its effects on occupant behavior in a representative
number of buildings. This information would, help to show the
relationships among air-exchange rates# pollutant concentrations#
pollutant generation# occupant behavior# and physiologic effects# as
well as the effects of energy-conservation programs aimed at reducing
air infiltration rates.
With the objective of maintaining indoor air quality, while not
adversely affecting heating and cooling costs# there is a need for
engineering studies, to determine alternative strategies for air
dilution of pollutants. Case studies of specific buildings may be
useful in determining the efficiency of selected filtration-
ventilation schemes. For example# it may be economically preferable
to filter (or scrub) recirculated air or a mixture of recirculated and
makeup air to maintain indoor air quality. Studies should be done on
the effectiveness and energy-conservation implications of pollutant
sensors used to activate air-dilution or air-cleaning systems.
Engineering studies on both air handling and air treatment systems are
encouraged. Although specific buildings may be studied in detail# the
application of the findings should be generic; i.e., the lessons
learned should be applicable to other buildings.
Standard methods should be developed and applied to evaluate the
performance of in-place environmental control systems and components.
Improved methods of providing acceptable and efficient air diffusion
for thermal and contaminant control should be developed. Life-cycle
cost evaluations should be made on the basis of current and projected
energy costs to characterize, these costs for future use in alternative
designs o£ residences and large buildings. Air-conditioning, heating,
and ventilation systems especially should be evaluated, in connection
with other building characteristics.
EXPOSURE STUDIES
Proper assessment of indoor contamination needs a perspective that
only total-exposure studies can provide. The relative contributions
to individual and population exposures of the contaminants encountered
indoors, with both indoor and outdoor sources, must be evaluated. For
contaminants with multiple entry routes, the contribution of
inhalation of indoor pollutants must be compared with all other
contributions to body burderts. Only with this evidence can research
and control efforts be prudently allocated. Under current conditions,
studies of total exposure to many contaminants are- limited by the
available instrumentation and, to a lesser extent, by analytic
methods. Such efforts are expensive. The extrapolation of their
results is constrained by the smallness and often the
unrepresentativeness of the samples of participants, by the inadequacy
of the information on activity patterns in the population at large,
and by lack of understanding of the distribution of indoor and outdoor
pollutant sources and the pathways that contribute to body burdens.
However, studies of total exposure and an understanding of
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activity-related concentration data will eventually advance our
knowledge of pollutant exposure. This knowledge is a prerequisite to
rational allocation of resources for warranted reductions in
population exposures.
The Committee urges investigation in the behavioral aspects of
indoor environments, specifically the relationships among performance,
sense of well-being, contaminant concentrations, and stress.
Temperatures, odors, and noise outside preferred ranges can reduce
productivity, especially in self-pacing tasks. The relationship
between productivity and the quality of the indoor.environment needs
to be determined. It is recognized that relationships between the
behavioral variables and pollutant concentrations may be difficult to
establish. Simultaneous measurements of trace organic vapors,
water-vapor content, conductivity, noise, light, temperature, and air
exchange rates should be pursued.
EDUCATION
Public education offers an effective way of reducing exposure of
the population to many contaminants encountered indoors. People
informed about the potential for exposure to pollutants from consumer
products, tobacco smoke, combustion products, etc., will exercise some
control to reduce the pollutant concentrations in their environments.
For the most, part, their options for controlling these pollutants are
limited to source maintenance, ventilation control, and, to some
extent, air-cleaning. Information about maintaining a clew indoor
environment and assessing indoor spaces for potential contamination
before purchasing or renting a structure and a variety.of suggestions
could be disseminated through health-maintenance organizations,
regional health-planning agencies, public-affairs offices, the
Environmental Protection Agency, the Department of Housing and Urban
Development, the Department of Energy, the consumer Product Safety
Commission, and a variety of other federal and state agencies. The
General Services Administration, the armed forces, and the. Department
of Housing and Urban Development are responsible for many residences
and other buildings. Through certification of minimal acceptable
occupancy standards, these1 federal organizations could develop
strategies to ensure that indoor spaces under their jurisdiction are
free from hazardous concentrations of contaminants.
Professional and trade associations could be instrumental in
developing'and disseminating information. These associations are
encouraged to establish standards for acceptable practice, with
respect to manufacturing, designing, building, and using products,
equipment, and structures that influence the quality of the Indoor air.
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IV
SOURCES AND CHARACTERIZATION OF INDOOR POLLUTION
This chapter addresses several chemical pollutants with respect to
their sources, concentrations, and indoor-outdoor relationships. In
addition, with the aim of characterizing the general quality of the
indoor environment, it considers temperature, humidity, unwanted sound,
and electromagnetic radiation, such as the radiofrequency, infrared,
visible, ultraviolet, and x-ray portions of the spectrum.
In the case of some pollutants, information on health effects is
scanty, at best. To the extent possible, the health effects of such
pollutants are discussed here. Detailed discussion of the health
effects of other pollutants, on which more information is available, is
to be found in Chapter VII.
Radioactivity and formaldehyde emitted indoors from building'
products are discussed in the first two sections of this chapter.
Consumer products, a generic source of indoor pollutants of many types,
are discussed next. The chapter proceeds with sections on asbestos and
fibrous glass (which occur in different forms in many indoor
environments), combustion processes (especially of unvented cooking and
heating appliances), and tobacco smoke (a highly complex and ubiquitous
mixture of pollutants). Several indoor air pollutants can be
recognized by their odors. Such odors are often the first indications
of deterioration in air quality and may themselves affect people's
well-being adversely; hence, they are treated as a distinct category of
pollutant in this chapter. Air temperature, radiant temperature, and
air velocity and humidity affect the quality of the indoor environment
through physiologic and sensory responses, so the thermal environment
is also discussed in a separate section. Other physical factors of the
indoor environment, such as noise and electromagnetic radiation, are
discussed briefly in a final section.
The diversity of subjects discussed in this chapter is evident.
Some of the (ksllutants considered here may be associated with voluntary
behavioral patterns, such as tobacco-smoking, whereas other? may be
related to involuntary and unavoidable exposure, such as exposure to
substances emitted from building materials. The reader should not infer
any order of priority among the pollutants discussed here. An effort
to attach priorities would require judgments on exposures an>j effects.
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and the order of discussion is not intended to indicate the application
of such judgment.
INTRODUCTION
Radioactivity and ionizing radiation occur naturally throughout the
biosphere, both because of the presence of primordial radioactive
elements and their decay products in the earth and because of natural
processes (primarily cosmic radiation) that produce radionuclides or
direct radiation fields. These natural, sources expose humans to
radiation both outdoors and in buildings. The magnitudes of various
contributions to total radiation dose vary from place to place and
between outdoors and indoors, and the type of radiation dose depends on
the radiation source. At one extreme, the cosmic-radiation field
delivers a dose to the entire body; this dose is not affected greatly
by the presence of a building and may be characterized primarily on the
basis, of altitude. At the other extreme, airborne alpha-emitting
radionuclides may deliver doses specifically to the lungs, and their
concentrations indoors may be strongly affected by the nature of
building materials and other sources, such as soil and water,, and by
building operations, such as ventilation. As an intermediate case, the
gamma-radiation field arising from radionuclides that are fixed in
place typically exposes the whole body and is affected by radionuclide
concentration, proximity, and shielding.
In the discussion that follows, we refer to radioactivity
concentrations and radiation fields and, by inference, to radiation
doses from sources that are inside and outside the body. Radioactivity
is given in curies; 1 Ci = 3.7 x 10*° becquerels, so 1 pCl » 0.037
Bq. Radiation fields can be specified in terms of energy flux; but it
is more conventional in the present context to use units of dose rate,
in which case the type of radiation has to be indicated. He use the
n
doses, the dose in rads is numerically equal to the dose equivalent
(DE) in rems. A distinction must be drawn between the "tissue dose,"
that actually received by tissue and therefore including self-shielding
by the body, and the "air dose," that deposited in air in the space
under consideration.
It is useful to summarize the dose-rate contribution in the United
States from radiation arising outside buildings. Three recent
summaries are those of the National Council on Radiation Protection and
Measurements"1 and the U.N. Scientific Committee on the Effects of
Atomic Radiation,*' which depended heavily on Oakley1' for U.S.
data, and the 1980 BEIR report of the National Research Council."
External radiation, that arising from sources outside the body, may be
divided into two categories, cosmic and terrestrial. The average
tissue dose rate outdoors from cosmic radiation is approximately 28
mrads/yr; the dose rate indoors is slightly reduced by overhead
RADIOACTIVITY
IV-2
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shielding {the NCRP report assumed a 10% reduction In average
exposures). This contribution has a substantial altitude dependence*
increasing from about 26 nrads/yr at sea level to about 50 mrads/yr at
1,600 m, the altitude of Denver. The average outdoor population-
weighted tissue dos$ rate from terrestrial radionuclides—due
principally to gamma rays from potassium-40, the thorium-232 series,
and the uranium-238 series—is approximately 35 mrads/yr. .This dose
rate varies substantially because of geographic variations in the
distribution of these radionuclides. For estimating average
terrestrial dose rates, the NCRP assumed that indoor dose rates were
20% lower than outdoor rates. (It also assumed that the tissue dose
was 20% less than the air dose.) Internal radionuclides contribute
important beta and gamma doses (about 2.5 mrads/yr to most of the body,
primarily from potassium-40) and an important alpha dose (even if that
to the lungs from radon and its progeny is excluded). The alpha dose
arises primarily from internally deposited uranium-238 and -234,
radium-226 and -228, and polonium-210 and varies greatly with body
organ. One of the larger contributions, about 3 mrads/yr, is the
polonium-210 alpha dose to the cells lining the bone surfaces.
However, alpha particles have a greater biologic effectiveness than
gamma rays, so the absorbed alpha dose contributes a DE some 10 times
greater than that of the same (absorbed) dose of gamma radiation.
Table IV-1 shows estimates of various contributions to DE rates, in
raillirems per year, which are numerically equal to tissue dose rates
(in millirads per year) for gamma and beta radiation. For alpha
radiation, a quality factor of 10 was assumed (based on relative
biologic effectiveness), although 20 is now recommended. 1' The value
given for lung dose from inhaled radionuclides assumed a radon-222
concentration in air of 0.15 nCi/ra3 (and slightly less than
equilibrium amounts of its radioactive decay products, or progeny).
The resulting DE has the largest value in the table. Nonetheless, this
value appears more appropriate for outdoor than for indoor air, in
which higher radon concentrations are found.
All indoor dose rates from natural radiation sources are affected
by buildings, and those from inhaled radionuclides are affected most
strongly. The only natural airborne radionuclides of importance are
radon and its progeny, principally the series beginning with radon-222,
the alpha-decay product of radium-226 (a member of the uranium-238
series). Radon is a noble gas that can move from the site of its
formation, giving it a substantial opportunity to reach air that is
inhaled by humans. The short-lived decay products of radon—polonium,
lead, and bismuth—are chemically active and thus can be collected in
the lungs, either directly or through particles to which they attach.
The most important dose arises from alpha decay of the polonium
isotopes. The decay sequence beginning with radium-226 is shown in
Figure IV-1, and, from the biomedical point of view, effectively ends
with lead-210, because of it3 half-life of about 20 yr. Because the
alpha energy associated with decays of the short-lived products to
lead-210 poses the main risk, progeny concentrations are often
expressed as the associated "potential alpha-energy concentration"
(PAEC) in air. The unit conventionally used foe PAEC is the working
IV-3
-------
TABLE IV-1
Summary of Average Dose Equivalent Rates from Various Sources
of Natural Background Radiation In the United States3
Bone
Radiation Source Gonads Lung Surfaces Marrow GI Tract
Cosmicb 28 28 28 28 28
Cosmogenic radionuclide^ 0.7 0.7 0.8 0.7 0.7
External terrestrial0 26 26 26 26 26
Inhaled radionuclides'1 — 100® —- — —
Radionuclides in the body^ 27 24 60 24 24®
Totals (rounded) 80 180 120 80 80
^Reprinted with permission from NCRP.^
kwtth 10% reduction foe structural shielding.
cUlth 20% reduction for shielding by housing and 20% reduction for shielding
by the body.
^Lung only; doses to other organs included in "Radionuclides in the body."
eLocal DE rate to segmental bronchioles ** 450 mrems/yr.
^Excluding cosmogenic contributions.
^Excluding contribution from radionuclides in gut contents.
IV-4
-------
•^U ftjli
4ft • !•» |
"tw«»
!ft • Wt
Mtv
1
1
»• tui
> ?*»¦»
] J
\
"•»» «0M S
14 d
01 01 M»V
"1*
OUf J
1*4
llaV
'"¦•dUCI -*
lirm
,oi - a) m»v
\
dun'
#1 7 M*V
1
J«« NMt
0? iCHfV
*++% ttaQP'
>1 *
<01 l»«V
FIGURE IV-1 Principal decay scheme of uranlum-238 to radon-222
to lead-206, showing alpha and beta decay; decay energies In
millions of electron voles. Reprinted with permission from National
Council on Radiation Protection and Measurements. ^p* '
IV-5
-------
level (WX.), defined as 1.3 * 105 MeV/L, the ?ABC If radon-222 at 100
nCi/n? is present with equilibrium amounts of its progeny. Dose (and
DE) rates may be inferred ftcm the PftEC on the basis of relatively
complicated modeling, provided that the progeny particle size
distribution and other factors are prescribed.
The character of a building may affect occupant radiation exposure
in three principal ways: the building serves as a container for
indoor-generated radon and its associated progeny, whether ftore
building materials, underlying soil, or water and gas; the building
materials contain natural gamma-emitters (potassium-40, the thorium-232
series, and the uranium-238 aeries)j and the building shields occupants
from cosmic or external terrestrial radiation. The last two.effects
tend to cancel one another. The building structure may, in unusual
circumstances, also protect occupants from outdoor radon-progeny
concentrations. However, the indoor concentration is ordinarily larger
than the outdoor, and outdoor-generated radon usually contributes a
small additive term to indoor concentrations« If this term is ignored,
the steady-state indoor radon concentration for a fixed indoor radon
source strength is inversely proportional to the air-exchange rate, the
rate at which the indoor air is exchanged for outdoor air. The
air-exchange rate for most U.S. buildings is around 1/h, with 0.5/h to
1.5/h typical for residences (windows closed). The air-exchange rate
and other removal mechanisms also affect the ratios of radon-progeny
concentration to radon concentration. Lack of removal implies activity
ratios o£ 1, but substantially lower values have been observed. An
equilibrium factor (F) is often defined as the ratio of the actual PABC
to the PAEC that would be associated with a specific radon
concentration if the progeny were in equilibrium with this
concentration.
This section characterizes indoor airborne radionuclides and
radiation, summarizes measurements of actual concentrations or
radiation fields, briefly indicates control measures, and suggests
subjects for further research. The major emphasis is on radon and its
progeny. The radionuclides in this decay chain, even.at typical
outdoor concentrations, cause larger radiation doses to internal organs
than all other airborne radionuclides. Furthermore, the radon and
progeny concentrations may be substantially higher indoors,
particularly in buildings with low air-exchange rates. In addition,
building occupants receive external whole-body radiation from
radionuclides fixed in building materials and soil, and these doses are
also given substantial treatment. This radiation arises principally
from several primordial radionuclides—pota9sium-40 and members of the
thorium-232 and uranium-238 decay series—with concentrations of around
0.1 pCi/g or greater in rocks, soil, and derivative building
materials. These are also the decay chains in which radon-220,
radon-222, and their progeny occur.
IV-6
-------
SOURCES OF RADIONUCLIDES AND RADIATION
Building Materials
Radionuclide Content. Pew measurements and no wide-scale surveys
of the radionuclide content of U.S. building materials have been made*
Surveys of materials in Europe are summarized in UNSCEAR 1977, • •tP* 50)
which gives activity concentrations of potassium-40, radium-226, and
thorium-232. As examples, average values for the concrete sample
groups examined range from 0.9 to 2.0 pCi/g for radium-226, 0.8 to 2.3
pCi/g for thorium-232, and 9 to 19 pCi/g for potassium-40. By
comparison, the ranges for brick are about 50% higher) those for cement
are similar, except for potassium-40 (which is 50% less); aijfl those for
natural plaster are lower by about a factor of 5.
Available U.S. data (Table IV-2) show concentrations in the same
range, assuming that the series radionuclides are sufficiently close to
equilibrium to permit comparison. In a number of cases, U.S. workers
have examined the radionuclide contents of concrete in the course of
selecting materials for low-background facilities for u3e in radiation-
counting; 2 the values obtained are consistent with the European
data, although somewhat lower, the observed concentrations are also
Within the range of values typical for major rock types and soils.
Concentrations for building materials not derived from crustal
components, such as wood, are much lower.
Measurement programs have recently been initiated to characterize
the radionuclide contents of building materials as a basis for
understanding the resulting effect on the indoor radiation
environment. Kahn et^ al_.15 have reported measurements of
concentrations in various building materials in the Atlanta area;
potassium-40, radium-226 progeny, and thorium-232 progeny
concentrations for samples of concrete, brick, and tile are given in
Table IV-2. Lawrence Berkeley Laboratory has begun to survey concretes
and other materials as part of a program on indoor air quality;
radionuclide contents for concrete and rock-bed samples from a number
of areas are given in the table.1*
Consideraoly greater radionuclide concentrations may be found in
building materials that contain residues from industrial processes.
The principal example,of such materials in the United States is.
concrete blocks incorporating phosphate slag (essentially calcium
silicate), a byproduct of phosphate production. As diseased by
Roessler et al.,*2 this slag contains most of the radium-226 and
uranium-238 found in the phosphate ore. For the electric furnace
process used in Florida, concentrations in the ore are about 60 pCl'/g»
and the slag has similar concentrations. A plant in Alabama (using
Florida and Tennessee phosphate ores) sold slag to companies in
Alabama, Mississippi, Tennessee, Georgia, and Kentucky. The concrete
produced by these companies has radium-226 concentrations estimated,
and in some cases measured, to be about 20 pCi/g.1* Phosphogypsum
(essentially calcium sulfate produced by treatment of phosphate ores
with sulfuric acid) may also be' used for building materials,
particularly wallboard. In this treatment, radium-226 follows the
IV-7
-------
TABLE IV-2
Average Radionuclide Content of U.S. Building Materials
Concentration,a pCl/g
Material
Concrete
Concrete
Brick25
Tile25
Concrete
29
25
18
Solar rock bed
18
Concrete
49
Uranium-238
Series
0.29-1.32
1.4
1.8
1.9
0.2-1.0
1.5
0.9-2.0
Thorlum-232
Series
0.28-1.58
1.5
1.8
1.1
0,2-1.0
1.4
0.8-2.3
Potas-1
8iunr-40
Comments
6.6-9.8 Summarized measurements
to select counting-room
materials
21 Atlanta area
17 Atlanta area
8 Atlanta area
5-12 Nine metropolitan areas
(preliminary values)
25 New Mexico (preliminary
values)
9-19 European concretes0
aExcept where noted, each entry is average for sample group; range is given if
several sample groups were examined.
^Because various members of decay series were detected, results in each column are
directly comparable only if series equilibrium may be assumed.
cFor comparison.
IV-8
-------
calcium, leading to tens of pCi/g in the gypsum; but such gypsum has
not been used on a large scale in U.S. wallbcard. In contrast,
concrete that incorporates phosphate slag may have been used in
approximately 100,000 homes.15 Finally/ some fly ash from coal-fired
power plants has been used in cement production, and this usa may
continue. Heretofore, it has not been thought to contribute
substantially to the radionuclide content of the resulting building
material.1' Emanation measurements on fly-ash concretes are now
being performed at Lawrence Berkeley Laboratory.
Radon Bnanation. The effective radon-222 generation rate in
building materials depends on the cadium-226 content, which varies
widely, and cn the percentage of radon formed that does not remain
lodg3d in the matrix of the material. Radon that is not fixed in place
may move through the matrix by diffusion or, if the material contains
large air spaces, by convection. Diffusive movement depends on the
diffusion length of the material in question and on its thickness. The
extent to which these processes occur depends not only on the
material's characteristics, but also on environmental conditions—
pressure, temperature, and moisture content. A rule of thumb sometimes
cited (e.g., UNSCEAR* *) is that 1% of the radon-222 generated from
materials in walls and ceilings escapes into the adjacent air space.
However, recent measurements at Lawrence Berkeley Laboratory, and
elsewhere have indicated that a considerably higher fraction can
escape, e.g., from concrete. Ingersoll et al. " cited escape-to-
production ratios of 0.08-0.25 for radon-222 fron. concrete.
(Radionuclide contents for the sample groups examined are indicated in
Table IV-2.)
Of most direct interest for indoor air quality is the actual
emanation rate, often given as picocuries per square meter per second
and sometimes as picocuries per gram per second. Measurements for
various materials give emanation rates over a wide range. For example,
European gypsum board and bricks yield radon-222 at about 0.3 x 10
pCi/m -s, whereas races for European concretes range from 0.001 to
0.2 pCi/m2-s.2<> 12 Preliminary measurements of radon-222 emanation
rate per unit mass for sample groups of concrete from U.S. metropolitan
areas (Table IV-2) give averages that range from 0.4 to 1.2 pCi/k9~h
(0.8 pCiAg-h yields approximately 0.03 pCi/m2-s tor 0.1-m-thick
concrete). Several rock samples from solar-beat storage beds averaged
0.5 pCiAg-h, although radium-226 contents were considerably higher
than those for the concrete samples." The resulting indoor
radon-222 concentrations depend on the amount of such material in the
structure, the interior volume, and the air-exchange rate. For an
air-exchange rate of 1/h and a ratio of inaoor emanating surface to
indoor volume of 0.5 m^/m^, an emanation rate of 0.03 pCi/m^-s
corresponds to a radon-222 concentration of about 0.04 nCi/m^. If
the equilibrium factor is 0.5, this would yield a PAEC of about 0.0002
WL. Direct measurement of emanation rates of materials made with
industrial byproducts (such as phosphate-slag concrete) is underway,
but results are not available. Because these materials may contain 20
times as much radium-226 as a typical concrete, radon-222 contributions
IV-9
-------
of up to several nanocuries per cubic meter of radon-222 and a
corresponding increase in the PAEC could be expected if the same
emanation ratio pertains.
Measurements of emanation rate vary by aore than an order of
magnitude,** so it is difficult to use radium content to predict the
contribution of a particular material to indoor radon content. For
this rea8on« more comprehensive information on diffusible fraction*
diffusion length, etc., and their dependence on material or
environmental factors is required before we can characterize building
materials on the basis of radionuclide content. If this information
becomes available, radionuclide contents may then be helpful in
characterizing indoor concentrations on a broad scale, e.g., by
geographic area. However, the dependence of diffusion and emanation
rates on environmental factors, such as pressure and temperature, and
on the moisture content of the material may limit the possibility for
such characterization.
In some cases, radon-220 ("thoron") and its progeny, ordinarily
present at much lower concentrations than radon-222 and its progeny,
may assume importance, particularly when mechanisms exist for
transporting emanating radon-220 rapidly into the air space of
interest. In comparison with the half-life of radon-222, the much
shorter half-life of thoron, 55 s, causes the measured radioactivity in
curies to be a characteristic of secondary interest. Bowever, the P&BC
still gives a relatively direct indication of possible dose to the
lung. One WL of radon-222 progeny has the same PAEC as that associated
with progeny in equilibrium with thoron at 7 nCi/m3. To the extent
that uranium-238 and thorium-232, which have similar half-lives, have
similar activities in source materials, the PAEC from their progeny,
radon-220 and -222, can reach similar values if rapid transport
mechanisms exist. This may occur, for example, in solar buildings that
sweep air through rock or concrete thermal-storage beds. A few efforts
have begun to measure thoron emanation rates, but results are not yet
available.
Gamma Radiation. The energies and intensities of photons from
decay of natural radionuclides have been well characterized. The
external dose from radionuclides in building materials is due to the
gamma rays emitted and depends on the geometry of the structure and
attenuation by the materials, as well as the gamma-ray energies. A
3imple expression may be derived for the gamma-ray air dose in a hole
in an infinite uniform medium:1'
" (2.43 urad/h) (%C(j + Eph'-Th + ,
where Cq, and CK are the concentrations (in picocuries per
gram) o£ uranium-238 and its progeny, thorium-232 and its progeny, and
potassium-40, respectively, and Eg, ETn,„and EK are the average
gamma-ray energies per disintegration of the same radionuclides
(including disintegration of the progeny for the uranium and thorium
series). Using Eg " 1.72 MeV, = 2.36 MeV, and Eg ¦> 0.156
KeV, " 4. « 4.2Cg + 5.70^ + o.38CK, in microrads per
rv-io
-------
hour. The stated dose contributions from the uranium and thorium
series are slightly less then those cited elsewhere* e.g.# by Krisiuk
et^al_. ,17 who may have used older information on decay schemes. For
the radionuclide contents cited in Table IV-2, the three terms in the
expression for contribute comparable amounts. (An analogous
expression for the dose from a flat plane is cited in tne section on
soil.)
For an actual structure, the geometry is complex and varied; in
addition, the building materials may attenuate the external radiation
dose from other sources. Moreover, radon-222 and its progeny may be
present in the material at less than equilibrium values, thereby
decreasing the corresponding gamma-ray dose. Tlie radon-222
escape-to-production ratio is most often in the range of low to 0.2S,
causing a small reduction in the value of X. The effects of geometry
and attenuation cannot be so simply characterized. Dose-rate
expressions from various workers, pertaining to a variety of
structures, have been summarized.17 Some of these expressions
account for reduction o^ the dose rate from outdoor sources. Moeller
et al. ' * described a computer program suitable for analysis of varied
geometries.
The infinite-geometry case yields air dose rates of about 8
urads/h for a potassium-40 concentration of 8 pCi/g and uranium-238
and thorium-232 series concentrations of 0.5 pCi/g. An infinitely
thick slab of such material would contribute about half this dose rate
at its surface. As discussed earlier, a typical outdoor ti3sue dose
rate from terrestrial radionuclides is 35 mrads/yr or 4 urads/h.
(Owing to shielding by the body, the tissue dose rate is about 20% less
than the air dose rate.)
Soil and Groundwater
Radionuclide Content. Radionuclide concentrations of major rock
types and soil have been summarized. U.S. soil values of 0.6, 1.0,
and 12 pCi/g have been stated for uranium-233, thorium-232, and
potassium-40, respectively, on the basis of 200 measurements of
gamma-ray dose rate cited by Lowder et al.10 These values vary by a
factor of around 3 from place to place. Values for crustal rocks'*
typically lie within this same range, but are considerably higher for
some formations. For example, the phosphate ro<;ks of Florida contain
the uranium-238 series at tens of picocuries per gram, but normal
amounts of thorium-232? commercial uranium ore bodies in the United
States have uranium-238 concentrations of hundreds of picocuries per
gram and higher.
Radon Emanation and Transport. The jranium-238 series, typically
present in soil3 and rocks at concentrations of about 1 pCi/g, includes
radium-226, the source of radon-222. The actual radon-222 emanation
rate from the ground depends, as for building materials, on the
percentage of diffusible radon, diffusion length, and other transport
mechanisms (including groundwater) in the soil. A review of available
IV-11
-------
measurements of radon-222 indicates a mean emanation rate from the soil
of 0.42 pCi/a^-s.*1 Given this value for the ground under a
one-story house, and assuming that the emanated cadon finds its way
into the indoor air, the soil could account for indoor radon-222 at
about 1 nCi/sr at a typical air-exchange rate of 1/h. Because
emanation rates vary by at least a factor of 10 from place to place,
this potential contribution car also be expected to vary substantially
among U.S. buildings.
The soil as a source of radon-222 can be characterized directly by
emanation measurements or, if disequilibrium and transport mechanisms
(including groundwater) are known, indirectly by measurements of
members of the uranium-238 series. Because of the relative ease of
measuring gamma rays, the indirect methods may be more appropriate for
large-scale surveys intended to characterize the contribution of soil
radon by geographic area. Gamma-ray source measurements may also be
less sensitive to changes in pressure, temperature, and moisture
content than emanation-rate measurements (see UNSCEAR*' and
NCHP1 *)• Moreover, variations in emanation rate may correlate with
factors that affect air-exchange rates and may thus complicate
assessment of the importance of soil as a source of indoor radon.
The mechanisms by which radon may be transported into buildings
have been' studied little. Soil-gas measurements, which have yielded
results of 100-2,000 pCi/L (Kranerj1' Scott;** and unpublished
measurements by Lawrence Berkeley Laboratory), may be relevant to this
question> because they may help in characterizing the radon content of
air trapped beneath buildinqs. Emanation rates themselves are useful
only for placing an upper limit on the potential of soil as an indoor
source. However, a more detailed understanding of radOn transport in
soil could provide a basis for using emanation data to estimate the
amount of radon that may accumulate beneath houses and be transported
indoors. Such collection and transport mechanisms may be greatly
affected by changes in barometric pressure, soil moisture content,
temperature gradients, and wind.
The actual pathway by which radon enters a building from the soil
appears to vary substantially with building design and construction
practice. In houses with concrete basements that are closed to the
outdoors, radon may enter by diffusion through the basement floor, by
convection within basement walls, and by movement through cracks,
designed openings, or penetrations in either of these components. Even
in communities where numerous measurements have been performed, it has
not been possible to determine the relative importance of these
mechanisms.1 1 In some mining communities, sealing of cracks has
proved relatively successful in reducing indoor radon content, but the
effectiveness of this method in general has not been evaluated. The
movement of radon from the point of entry to otner parts of the
building depends on internal construction and building use. Even in
buildings with ventilated crawlspaces, the radon concentration in the
crawlspace air may be considerably higher than outdoors, and a
substantial amount of the radon emanating from the soil may reach the
Interior space by transport from the crawlspace.
1V-12
-------
More comprehensive information on how radon is transported is
needed fot the development of techniques to prevent radon from entering
buildings and for establishment of a correlation between theradium-226
content in soil and the indoor radon content attributable to this
source.
Gamma Radiation. The gamma dose from radionuclides in soil may be
expressed in a fashion analagous to that for building materials; the
air dose rate (urad/h) at 1 m above the ground due to natural
emitters uniformly distributed in the soil has been given as Xpiane °
1.82CJJ + 2.82CTh + 0.179Cr for Cy, CTh, CR in picocuries
per gram. More current data on decay schemes may alter this
slightly. As noted above, concentrations of natural radionuclides in
soil and rock vary from place to place, causing comparable variations
in dose rates. The air dose rate is estimated at 2.6 wrads/h on the
coastal plain (the Atlantic and Gulf coastal areas), 10.2 yrads/h on
the Colorado Plateau, and 5.2 urads/h on the rest of the contiguous
United States (NCRP,3' based on nuclear-plant site surveys). The
materials in a building can provide significant shielding of occupants
frcm gamma rays from local radionuclide concentrations, but the
radionuclide content of the materials may more than compensate for this
shielding.
Radon from utilities
Water. Measured concentrations of radon-222 in well water in Maine
and New Hampshire average 53,000 and 101,000 pCi/L, respectively.11
More recent measurements have been performed in Maine.11 " Lawrence
Berkeley Laboratory has found concentrations of 100-7,500 pCi/L in
tapwater from wells or underground reservoirs associated with houses
and has correlated use of such water with increases in indoor radon
content. Radon-222 in water can quickly transfer to air, with
efficiencies of 30-909, depending on water use; 11 a concentration of
10,000 pCi/L can raise average indoor radon-222 content by about 1
nCi/m3. It is not known how widespread such water concentrations
are, nor how closely they correlate with high radium content in surface
soils and rocks.
Natural Gas. Concentrations of radon-222 in natural gas in the
Houston area have been found to average approximately 50 pCi/L at,
STP.10 Concentrations in distribution lines at various points in the
United States were found to average about 20 pCi/L.1* The resulting
concentrations in U.S. residences due to natural-gas combustion have
been estimated to be less than 0.1 nCi/m-^, even with unvented burners.
1V-13
-------
INDOOR CONCENTRATIONS AND RADIATION FLUXES
Airborne Radionuclides
Radon Concentrations. Data from several sources tabulated by
UNSCEAR** indicated that indoor radon-222 concentrations vary by two
orders o£ magnitude, with average values of about 1 nCi/m^. Such a
large range is not surprising, considering tuat the studies included
various types of buildings, building materials, underlying materials,
and ventilation conditions and used many measurement techniques. More
recent measurements have confirmed this wide variation.
A wide variation is expected even for conventional housing, because
the air-exchange rate typically ranges from about 0.5/h to l.S/h in
such buildings, and further variation in air-exchange rates occurs
because of window or door openings and mechanical ventilation systems.
The soil under a house can be expected to be the principal contributor
to the indoor radon concentration in most cases. As noted earlier, a
typical soil emanation rate, if t .• radon goes into the interior of a
house with an air exchange rate c.r 1/h,. would contribute radon-222 at
about 1 nCi/m3. Inasmuch as soil emanation rates and effective
capture by the house vary by an order of magnitude and air-exchange
rates vary widely, a large range of indoor concentrations would result.
As indicated in Table IV-3, homes monitored in New York and New
Jersey were found to have an annual average radon-222 concentration of
0.3-3.1 nCi/m3 in the living space, with a geometric mean of about
0.8 nCi/m3.' Similar measurements in Austria yielded a geometric
mean of 0.42 nCi/m3.*' In these studies the mean indoor
concentrations were 3-4 times as great as local outdoor
concentrations. Spot measurements of homes in the San Francisco area,
made during the summer with windows closed and with an average
air-exchange rate of 0.4/h, showed concentrations averaging 0.3
nCi/m3.15 Spot measurements in Illinois showed a substantial
incidence of concentrations greater than S nCi/m3; six of 22 houses
had concentrations of 10 nCi/m3 o; more.*5
High radon-222 concentrations have been found in uranium-mining
areas and in buildings that use materials high in radium. In houses
monitored in Bancroft, Ontario, 50% of the sample had concentrations
greater than 3 nCi/nr3, over 25% had concentrations greater than 7
nCi/m3, and about 6% had concentrations greater than 15 nCi/m3.11
High concentrations have also been found in homes in mining areas in
the United States; at Grand Junction, Colorado, PAECs corresponding to
radon-222 at up to hundreds of nanocuries per cubic meter have been,
measured. In a survey of several Swedish houses built with alum-shale
concrete, the average radon-222 concentration was 7 nCi/m3;** more
recent data showed average concentrations of IS nCi/m3 or more for
residences built entirely of alum shale.*7
Radon-222 concentrations of 0.6-22 nCi/m3 have been found during
spot measurements of energy-efficient homes, many of which had low
air-exchange rates; these measurements were taken with windows closed,
and the air-exchange rates were measured simultaneously."
Concentrations and air-exchange rates have also been measured in
IV-14
-------
TABLE IV-3
Selected Radon and Radon-Progeny Measurements in U.S. Resldencesa
Location
Boaton
New York-
New Jersey
Illinois
San Francisco
area
U.S.-Canada
Special Areas:
Grand Junction,
Colorado
Radoti-222 Progeny PAEC
Concentration, Concentration,b
nCi/m WL
Ho. Type of
Residences Measurement
Comments
Ordinary Areas;
Tennessee
0.008(0.0008-0.03) 15
0.07(0.005-0.2) (up to 0.002)
(0.3-33)
(0.4-0. 8)
(0.6-22)
22
26
17
0.006c
29
Grab
Crab and venti-
lation
Shale area; mostly concrete
construction
Single family; air change
rate, 1-6/h
0.8C(0.3-3.1) 0.004c(0.002-0.013) 21 Several integrated 17 single family, 3 multi-
mAoaiiVAmanf a nl a r nfn^ t W 1 anaV^maM^
measurements
over year
Grab
Grab and venti-
lation
Grab and venti-
lation
Integrated year
round
pie family, 1 apartment
building
Wood-frame construction,
unpaved crawl spaces
(windows closed)
Air .change rate, 0.02-1.0/h
(windows closed)
Energy-efficient houses;
air change rite, 0.04-
1.0/h (windows closed)
Controls for remedial-
action program (which
has included houses In
range 0.02-1 WL)
-------
Table IV-3 (contd)
Location
Florida
Butte,
Montana
Anaconda,
Montana
Radon-222 Progeny PAEC
Concentration, Concentration,'1
nCi/m WL
Mo. Type of
Residences Measurement
0.004 28
0.004(0.0007-0.01/;} 26
0-014 133
0.02 56
0.013 16
Integrated year
round
Integrated year
round
Integrated year
round
Integrated year
round
Integrated year
round
Comments
Controls on unmlneralized
soils
Controls on unmlnerallced
soils
Houses on reclaimed phos-
phate lands
Intensive mining area
Intensive mining area
aData ft on W. J. Barnes, personal communication, cited In Cenrge and Breslln.^ Single-family residences except
where noted.
^Averages; values In parentheses are ranges. All measurements are In living space; values In basements are
typically higher.
^Geometric mean.
-------
conventional houses in England* and in houses at Elliot Lake,
Ontario;*® the measured radon concentrations were consistent with
those observed for conventional houses elsewhere.
Radon-Progeny Concentrations. Radon-progeny concentrations are
often measured as potential alpha«energy' concentrations (PAEC), given
in working levels. Indoor concentrations of radon-222 progeny were
measured at the Environmental Measurements Laboratory (EML) in Hew York
City.* The concentrations were 0.02 WL in the EML basement and about
0.01 WL in the building's fifth floor, both with progeny activity
ratios of polonium-218, lead-214, and bismuth-214 of about 1:0.5:0.3.
For 21 New York and New Jersey houses, the mean annual-average PAEC foe
progeny'of radon-222 was about 0.004 WL in the living space* with a
range of values from one house to another of 0.002-0.013 WL;
equilibrium factors averaged slightly above 0.6 in the living space.
Measurements in Florida houses built on reclaimed phosphate land
yielded average radon-progeny concentrations of about 0.01 WL, but the
range extended to above 0.05 WL.11 Houses in Grand Junction,
Colorado, in which remedial action has been recommended, had pAECs
ranging from 0.02 to 1 WL. Sets of control houses monitored in Florida
and Colorado had an average PAEC similar to that in New York and New
Jersey' (see Table IV-3). Measurements have also been performed in
homes in the vicinity of uranium-mining operations. 1 1
A few measurements of individual radon-progeny concentrations have
been made, often to correlate such concentrations with possible removal
processes.11 ** These processes constitute potential control
techniques.
Some work has been done on characterizing the particle size
distribution of indoor radon progeny, as well as the dependence of
concentrations and distributions on various characteristics, including
location, particulate mass concentration, air-exchange rate, and
air-mixing rate. The fraction of radon progeny that is unattached to
particles, as well as the size distribution of attached progeny, was
measured at the EML building and in homes.* * Such measurements have
also been performed in uranium mines. The diffusion coefficients of
radon progeny have been measured,*1 and their interactions with
particles have been examined theoretically.*'
Lawrence Berkeley Laboratory has performed a few measurements of
radon progeny in solar homes in New Mexico and found PAECs of about
0.005 WL (J.G. Xngersoll, personal communication).
The simplest models of indoor radon and radon-progeny
concentrations use a set of simple equations connecting the indoor
iauon source strength, outdoor concentrations, and rate of air
exchange, assumed to be the only removal mechanism (other than
radioactive decay). An example is a computer program of Kusuda,l*
whi'rh permits step variations in air-exchange rate. Models may also
simulate diffusion of radon into a house," but transport has not
been modeled in any comprehensive way. Models have been made of
radon-progeny diffusion and attachment processes*0 " and of the
effect of such processes on progeny concentrations and unattached
fractions. 17 1 * 1 * However, no realistic models of radon and progeny
IV-17
-------
behavior in buildings. by which actual concentrations (or the effect of
control measures) might be simulated) has been attempted. More
experimental information will evidently be required to develop and
validate such models.
Gamma-Radiation Fluxes and Shielding Effects from Building Materials
As discussed above, gamma radiation from terrestrial radionuclides
may arise from both building materials and nearby soil and rock,
although the radionuclide content of these two source? may vary,
significantly. Moreover, the structural materials shield occupants
both from gamma rays from soil and rock and, to a lesser degree, from
cosmic rays. As a result, the building may affect external dose rates
of occupants.in various ways and degrees. Given information on a
particular building, the net effect may be calculated in a way similar
to that used by Moeller et al.,'' baaed on the gararaa-ray dose-rate
expressions given above and on estimation of shielding effects.
In some cases, the structure may have little effect on terrestrial
or cosmic dose rates. Exclusive use of materials that do not contain
substantial radioactivity, such as wood, has the effect of shielding
the terrestrial garata flux (tissue dose, about 35 miems/yi) by about 20
or 30% and has little effect on the cosmic-ray dose (about 28
mreraa/yr}. A concrete foundation (slab floor or basement) would have
no effect on the cosmic-ray dose and, if its radionuclide content were
similar to that of surrounding soil or rock, little effect on the
terrestrial dose. That is, although concrete substantially attenuates
gamma radiation from the soil or root, it contributes a gamma-ray flux
tl.st compensates for this reduction.
However, if a building also uses concrete in the walls and ceilings
and has a radionuclide content similar to that of local soil and rock,
an approximate doubling of the terrestrial dose rate would occur. As
some compensation, concrete walls and ceilings would tend to shield
occupants from cosmic rays in many cases by only about 20%, out by
larger fractions for large buildings.
Ordinarily, then, building materials with crustal components whose
radionuclide contents are similar to those of local soil and rock may
Increase external dose rates for occupants by up to tens of millirems
per. year or may decrease cosmic-ray rates by a somewhat smaller
amount. For building materials and surrounding soil or rock that
contain higher radionuclide contents, the dose-rate differences between
outdoors and indoors would be correspondingly larger.
COHTRPL TECHNIQUES
From the few available indoor measurements of radon-222 progeny, it
appears that variations of 0.01 WL from one building to another,
depending on air-exchange rates and on building or ground materiala,
are not unusual. The full range of values for conventional houses is
considerably larger than this, and measures that reduce the
IV-1&
-------
aLi—exchange rate can be expected to change it further. A progeny
concentration at Q.G1 >IL) it experienced two-thirds oi the time,
corresponds to an exposure of about 0.3 WLM/yr—less by about a factor
of 10 than the occupational limit of 4 WLM/yr. (Exposure of a person
to 1 HL for 170 hi a working month* yields one working-level month* or
1 WLM.J But variations in external dose rate due to ordinary building
materials are around 10 mrems/yr, less than one-hundredth of the
whole-body occupational,dose limit of 5 rems/yr. If these occupational
limits correspond to similarly valued risks, it appears that the effect
of the structure on radon-progeny exposures (given in working-level
months per year) is far more important than the effect on external
whole-body dose rates (given in rems per year). Health effects are
discussed elsewhere, but this simple comparison indicates one basis for
emphasising methods lot controlling radon-progeny exposures. Of these
inettiods, only material substitution may be. used for control.of
gamma-ray dose rates, particularly where materials have unusually high
radionuclide contents.
Techniques foe controlling indoor concentrations of radon-2.22 or
its progeny include measures tha.t decrease radbn sources, reduce
transport from sources, remove radon or its progeny from indoor air, or
exchange indoor air.for outdoor air. The easiest technique to
implement in many cases is to increase the air-exchange rate—for
example, by opening windows or installing fans. For reasons of comfort
or energy efficiency, other methods, sometimes equally straightforward,
may often be preferable. In general, not enough is known about the
cost, effectiveness, and applicability of various measures for a
judgment of their importance in the general building stock*
Material Selection or Site Preparation
In construction of a building, the use of materials whose radon-222
emanation rates are low affects the source strength directly. However,
in situations where the surrounding soil and rock contribute most of
the radon, opportunities for controlling the source strength are
limited, especially because the diffusion length of radon-222 is
relatively large and radon source strength is not often a criterion for
site selection. Attention to building materials or site materials
(underlying and surrounding soil) in new construction has a substantial
effect in cases where the emanation rate from either of these may be
unusually highr Replacing such materials (on a remedial basis) is
often difficult or expensive, so other measures may be favored.
Reducing Transport
The principal means of reducing the transport of radon to building
interiors are the sealing of materials that have high emanation rates
and, for the case of transport from surrounding soil, the plugging of
cracks and holes through which air with a high radon-222 content (e.g.,
soil gas) moves. Materials may be sealed by epoxy resins or other
T3-19
-------
coatings with up to 90% effectiveness.' * Sealing surfaces* filling
holes with impervious materials, and stopping transport by installing
plastic or other barriers have proved effective in some cases that
requited remedial action (see, for example, Atomic Energy Control
Board'), but they all require integrity of the barrier for long-term
reduction of transport. Th« general applicability or effectiveness of
these measures as long-term passive controls is not known. It should
be noted that confinement of radon by diffusion or convection barriers
also permits buildup of radon and its progeny behind the barrier,
causing an increase in gamma radiation from buildinq materials.
Nevertheless, this increase appears less important than the associated
decrease in airborne radon-222 and its progeny.1 Transport may also
be reduced by ventilating crawlspaces or basements or (in new
construction) by designing transport routes that bypass slab floors or
basements.
Removal of Progeny front Indoor Air
Methods for removing radon-222 progeny from indoor air include
filtration with fiber> electrostatic, or charcoal filters; mixing of
indoor air to cause deposition within the structure or ventilation
system; and space-charging to remove progeny ions. Filtration systems
are effective in reducing airborne particulate mass concentrations.
However, depending on the system, they may thereby raise the
concentration of unattached progeny ions, especially pclonium-218j 1'
for some particle size distributions, this would raise the ratio of
lung dose to PAEC. Nazaroff11 observed a substantial decrease in
PAEC from operation of the furnace fan (which thereby activated the
system's filter), but the unattached fraction was not measured. Holub
et al. 17 and Jonassen1' have performed related experiments on
air-mixing, ventilation, and filtration1. Finally, in many measurement
techniques, charged radon-222 progeny are collected by voltage
differentials, but it does not appear that this principle can easily be
applied as a control measure.
Exchange of Indoor and Outdoor Air
Use of air-to-air heat exchangers to remove indoor air while
conserving potentially lost energy is being investigated by Lawrence
Berkeley Laboratory. Preliminary results'* indicate that this method
is effective, in at least one configuration, in reducing radon-222 and
progeny concentrations. This method is particularly attractive because
it can be applied in both new and existing buildings and because it is
effective in reducing concentrations of other indoor contaminants.
RESEARCH NEEDS
Substantial research efforts are needed in three subjects: the
characterixation of radon sources and of the indoor concentrations and
IV-20
-------
behavior of radon and its progeny, the development and testing of
control techniques, and the modeling of radon and ita progeny in
structures. These efforts need to be supported by development of
measurement instrumentation, followed by an evaluation of indoor
concentrations, control measures, and building energy-conservation
measures, among other factors. In addition, evaluative efforts will
require further work on the health effects of radon, which have not
been discussed here.
Programs to characterize building materials by radcn emanation rate
or radionuclide content Bhojld be more widespread and complete. It is
even more important to survey soil and groundwater with respect to
radionuclide cqntent, radon emanation, and radon transport. A rapid
effort should be undertaken to determine the feasibility of geologic or
geographic characterization of soil. As part of efforts to
characterize materials, attention should be given to the effects of
moisture, pressure, and, temperature. Community water supplies 3hould
aldo be surveyed.
Studies of indoor radon and progeny concentrations should be
undertaken with two major purposes: to learn the range and
distribution,of radon and its progeny in the building stock, and to
understand the behavior of radon and its progeny in buildings. The
first purpose requires surveys of many buildings of a variety of types
and in various geographic areas. These surveys may be implemented by
associating them with other large-scale efforts, such as those for
energy-conservation retrofits or for insurance purposes. They may
measure either radon concentrations or potential alpha-energy
concentrations (PAECs), but the former may.be measured more easily and
may in fact be preferable, in that an adequate understanding of progeny
behavior could be used to infer PAECs in a way that lends itself to
generalization.
This interpretative basis must be developed through intensive
measurements to characterize .indoor radcn and progeny behavior. Such
intensive work at only a few sites would serve as a basis not only for
improving measurement techniques but also for developing control
techniques. Particular attention must be given to progeny-particlr.
Interactions and removal processes. Hesults of,intensive
investigations would be validated by less-detailed field measurements
at a larger number of sites. Ultimately, the results would serve a3 a
basis for estimates of health effects.
Many measurement programs will have to be supported by
instrumentation development. More convenient portable instruments for
field source measurements' based on alpha-scintillation techniques or. on
sodium iodide gamma-ray detectors could be developed. Further work on
integrating devices for large-scale surveys of indoor concentrations is
warranted, as is development of simple and quick progeny monitors,
presumably based on semiconductor detectors. For intensive
investigation of progeny behavior at a few sites, more versatile
special-purpose systems must be designed to measure infiltration rate,
ration, individual radon progeny, particle concentrations, and
environmental conditions automatically.
1V-21
-------
Substantial efforts to develop and study control techniques ace
required. The effects of techniques to clean the air (rather than
control the source) would have to be studied in the manner indicated
above for detailed investigations of progeny behavior.
These measurement programs must be accompanied by corresponding
modeling efforts. Models that characterize sources (on a geologic and
geographic basis) and transport (by site and building type) are
needed. Although models for physical processes involving radon progeny
have begun to be developed, much more work is needed, especially for
understanding progeny-particle interactions and control techniques.
Models of indoor-air quality that use the source and progeny models
appropriately could then be developed. Finally, the models of
indoor-air quality could be contained with models of the building stock
to represent current radon and progeny concentrations and the effects
of changes in building design and of potential control measures.
Models of indoor-air quality and the building stock will be necessary
for any indoor air pollutant and for evaluation of potential strategies
for controlling indoor-air guality.
REFERENCES
1. Atomic Energy Control Board [Canada]. Workshop on Radon and Radon
Daughters in Urban Communities Associated with Uranium Mining and
Processing, Elliot Lake, Ontario, March 7, 1978. Ottawa, Ont.,
Canada: Atomic Energy Control Board, 1979.
2. Atomic Energy Control Board [Canada]. Second Workshop on Badon and
kadon Daughters in Urban Communities Associated with Uranium Mining
ana Processing, Bancroft, Ontario, March 12-14, 1979. Ottawa, Ont.,
Canada: Atomic Energy Control Board, 1980.
3. Auxier, J. A., W. H. Shinpaugh, G. 0. Kerr, and D. J. Christian.
Preliminary studies of the effects of sealants on radon emanation
from concrete. Health Phys. 27:390-392, 1974.
4. Beck, U. L., J. A. DeCampo, and C. V. Gogolak. In Situ Ge(Li) and
Nal(Tl) Gamma-Ray Spectrometry. U.S. Department of Energy, Health
and Safety Laboratory Report HASL-258. Washington, D.C.: U.S.
Department of Energy, 1972. Available from National Technical
Information Service, Springfield, Va., as HASL-258.
5. Cliff, K. D. Assessment of airborne radon daughter concentrations
in dwellings in Great Britain. Phys. Med. Biol. 23:696-711, 1978.
6. Culot, M. V.. J. , K. J. Schiager., and H. G. Olson. Radon Progeny
Control in Buildings. Final Report. U.S. Atomic Energy Commission
Report COO-22731. Fort Collins, Col.: Colorado State University,
1973. 277 pp.
7. Culot, M. V. J., K. J. Schiager, and H. G. Olson. Prediction of
increased gamma fields after application of a racon barrier on
concrete surfaces. Health Phys. 30:471-478, 1976.
8. George, A. C. Indoor and outdoor measurements of natural radon and
radon daughter decay products in New York City air, pp. 741-750. In
J. A. S. Adams, w. M. Lowder, and T. F. Gesell, Eds. The Natural
IV-22
-------
Radiation Environment II. Proceedings of the Second International
symposium on the Natural Radiation Environment, August 7-11, 1972,
Houston, Texas, U.S.A. Available from National Technical
Information service, Springfield, Va., as CONF-720805-P-2.
9. George, A. c., and A. J. Bresiin. The distribution of ambient radon
and radon daughters in residential buildings in the New Jersey-New
York area, pp. 127X-1292 (includes discussion). In T. F. GeselJL and
W. M. Louder, Eds. Natural Radiation Environment 111. Vol. 2.
Proceedings ot a Symposium Held at Houston, Texas, April 23-28,
1978. Oak Ridge, Term.: U.S. Department ot Energy, Technical
Information Center, 1980.
1U. Gesell, T. F. Some radiological health aspects of radon-222 in
liquified petroleum gas, pp. 612-629. In R. E. Stanley and A. A.
Moghissi, Eds. Noble Gases. U.S. Energy Research and Development
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Government Printing Office, 1975.
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water to indoor radon concentrations, pp. 1347-1363. in Natural
Radiation Environment III. Vol. 2. Proceedings ot a Symposium Held
at Houston, Texas, April 23-28, 1978. Oak Ridge, Tenn.r U.S.
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12. Gesell, T. F., H. M. Prichard, and C. T. Hess. Epidemiologic
Implications ot Radon in Public Water Supplies. Paper presented at
Specialist Meeting on the Assessment of Radon and Daughter Exposure
and Related Biological Effects, Rome, Italy, March 3-7, 1980.
13. Guimond, R. J., Jr., W. H. Ellett, j. E. Fitzgerald, Jr., S. T.
Windham, and P. A. Cuny. Indoor Radiation Exposure due to
Radium-226 in Florida Phosphate Lands. Washington, D.C.: U.S.
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Revised printing. Washington, D.C.; U.S. Government Printing
Office, 1»7». U11J pp.
14. Kess, C. T., R» E. Casparius, S. A. Norton, and W. F. Brutsaert.
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Symposium Held at Houston, Texas, April 23-28, 1978. Oak Ridge,
Tenn.: U.S. Department of Energy, Technical Information Center,
1980.
15. Holiowell, C. D., et al. Building Ventilation and Indoor Air
Quality. Annual Report. Lawrence Berkeley Laboratory Report No. LBL
103?0. Berkeley, Cal.: Lawrence Berkeley Laboratory, 1979.
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Ingersoll, D. L. Krinkel, and w. W. Nazaroff. Radon in Energy
Efficient Residences. Lawrence Berkeley Laboratory Report LBL-9560.
Berkeley, Cal.: Lawrence Berkeley Laboratory, 1980.
17. Holub, R. F., R. F. Droullard, W.-L. Ho, P. K. Hopke, R. Parsley,
and J. J. stukel. The reduction ot airborne radon daughter
concentration by plateout on an air-mixing tan. Health Phys.
36:497-504, 1979.
IV-2 3
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18. Ingersoll, J. 6., B. D. Stitt, and G. H. Zapalac. A Survey of
Radionuclide Contents and Radon Emanation Rates in U.S. Building
Materials. Lawrence Berkeley Laboratory Report LBL-11771. Berkeley>
Lawrence Berkeley Laboratory, University of California, 1981.
19. International Commission on Radiological Protection.
Recommendations of the International Commission on Radiological
Protection. New York: Pergamon Press, 1977.
20. Jacobi, W. Activity and potential e-energy of 222ra
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Adans, and W. M. Lovder, Eds. The Natural Radiation Environment.
Chicagoi University of Chicago Press, 1964.
31. Lucast H. F. A fast and1 accurate survey technique foe both
radon-222 and radiua-226. In J. A. S. Adams, awl K. M. Umder, Eds.
The Natural Radiation Environment. Chicagos University of Chicago
Press, 1964.
32. McLaughin, J. P., and N. Jonassen. The effect of pressure drops on
radon exhalation from walla, pp. 1225-1236. In T. F. Gesell and
W. to. Lovder, Eds. Natural Radiation Environment III. Proceedings
of a Symposium Held at Houston, Texas, April 23-28, 1976. Oak
Ridge, Tenn.: U.S. Department of Energy, Technical Information
Center# I960.
33. Moeller, D. W., D. N, Underhill, and G. V. Gulezian. population
cose equivalent from naturally occurring radionuclides in building
materials/ pp. 1424-1443. In T. F. Gesell and W. M. Lovder, Eds.
Natural Radiation Environment III. Vol. 2. Proceedings of a
Symposium Held at Houston, Texas, April 23-26, 1976. Oak Ridge,
Tenn.) U.S. Department of Energy, Technical Information Center,
1960.
34. National Council on Radiation Protection and Measurements. Natural
background Radiation in the United States. NCRPM Report No. 45.
Washington, O.C.: National Council on Radiation Protection and
Keasureaents, 1975. 163 pp.
35. National Research Council, Committee on the Biological Effects of
Ionizing Radiations. The Effects on Populations of Exposure to Lou
Levels of Ionizing Radiation: 1980. Washington, D.C.s National
Academy PreB8,,1960. 524 pp.
36. Nazaroff, w. w., M. L. Boegel, c. D. Hollowell, and A. D. Roseme.
The Use of Medianical Ventilation with Heat Recovery for
Controlling Radon and Radon-Daughter Concentrations. Lawrence
Berkeley Laboratory Report LBL-10222. Paper presented at Third
Workshop'on Radon and Radon Daughters in Urban Communities
Associated with Uranium Mining and Processing, Fort Hope, Ontario,
Canada, March 12-14, 1980.
37. Nuclear Energy Agency. Exposure to Radiation from the Natural
Radioactivity in Building Materials. Paris: Organization for
Economic Cooperation and Development, Nuclear Energy Agency, 1979.
36. Oakley, D. T. Natural Radiation Exposure in the United States. U.S.
environmental Protection Agency Report ORP/SiD 72-1. Washington,
D.C.: U.S. Environmental Protection Agency, Office of Radiation
Programs, Surveillance and Inspection Division, 1972. 77 pp.
Available from National Technical Information service, Springfield,
Va., as PB-235 795.
39. PorstendBrfer, J., A. Wicke, and A. Schraub. The influence of
exhalation, ventilation, and deposition processes upon the
concentrations of radon (Rn-222), thoron (Th-222), and their decay
products in room air. Health Phys. 34:465-473, 1976.
40. Raabe, O. G. Concerning the interactions that occur between radon
decay products and aerosols. Health Phys. 17:177-185, 1969.
41. Ragtiunath, 8., and P. Kotrapya. Diffusion coefficients of decay
products of radon and thoron. J. Aerosol Sci. 1G:133-138, 1979.
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42. Rocssler, C. E., X. A. Smith, W. E. Bolch, and R. J. Prince.
Uranium and radium-226 in Florida phosphate materials. Health phys.
371269-277, 1979.
43. Rundo, 0., F. Markun, and M. J. Plondke. Observation of high
concentrations of radon in certain houses. Health Phys. 36»729-739,
1979.
44. Scott, A. C. The source of radon in Elliot Lake. In Workshop on
Radon and Radon Daughters in Urban Communities Associated with
Uranium Mining and Processing, Elliot Lake, Ontario, March 7, 197S.
Ottawa, Ont., Canada: Atomic Energy Control Board, 1979.
45. Smith, D. Ventilation rates and their influence on equilibrium
fraction. In Second Workshop on Radon and Radon Daughters in Urban
Communities Associated with Uranium Mining and Processing,
Bancroft, Ontario, March 12-14, 1979. Ottawa, Ont., Canada: Atomic
Energy Control Board, 1979.
46. Steinh&uslef, F., w. Hofmann, t. Pohl, and J. Pohl-Rttling. Local
and temporal distribution pattern of radon and dauahters in an
urban environment and determination of organ dose frequency
distributions with demoscopical methods, pp. 1145-1162 (includes
discussion). In T. F. Gesell and W. K. Lowder, Eds. Natural
Radiation Environment III. Vol. 2. Proceedings of a Symposium Held
at Houston, Texas, April 23-28, 19,78. Oak Ridge, Tenn.: U.S.
Department of Energy, Technical Information Center, 1980.
47. Swedjemark, G. A. Radioactivity in Rouses Built of Aerated Concrete
Based on Alum Shale. Paper presented at Specialist Meeting on the
Assessment of Radon and Radon Daughter Exposure and Related
Biological Effects, Rome, Italy, March 3-7, 1980.
47. Swedjemark, G. A. Radon in dwellings in Sweden, pp. 1237-1259
(includes discussion). In T. F. Gesell and W. M. Lowder, Eds.
Natural Radiation Environment III. vol. 2. Proceedings of a
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50. Wilkening, M. H.* W. E. Clements, and D. Stanley. Radon 222 flux
measurements in widely separated regions, pp. 717-730. In J. A. S.
Adams, w. M. Lowder, and T. F. Gesell, Eds. The Natural Radiation
Environment II. Proceedings of the Second International Symposium
on the Natural Radiation Environment, August 7-11, 1972, Houston,
Texas, U.S.A.
51. tirenn, M. E., M. Eisenbua, C. Costa-Ribeiro, A. J. Bazle, and R. D.
Siek. Reduction of radon daughter concentrations in mines by rapid
mixing without makeup air. Health Phys. 17:405-414, 1969.
FORMALDEHYDE AND OTHER ORGANIC SUBSTANCES
The infiltration of outdoor air is one source of formaldehyde and
other organic substances in the indoor environment, but the primary
IV- 26
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sources are in the indoor environment itself—building materials,
combustion appliances, tobacco smoke, and a large variety of consumer
products. A buildup of formaldehyde may be exacerbated in buildings
that have been subjected to energy-^eCficiency measures intended to
reduce infiltration and, thus, energy consumption. Emission rates for
formaldehyde and other organic pollutants emitted in the indoor
environment are generally unknown. Analytical techniques have been
applied mostly in measuring concentrations in indoor air. Very little
work has been done in measuring specific source strengths or ranking
emission sources, except on a broad relative basis.
FORMALDEHYDE
In general, indoor foriraldehyde concentrations exceed those
outdoors. The contribution of formaldehyde in outdoor air to indoor
air appears to be minor.
A recent National Research Council report deals in great detail
with the sources and effects of formaldehyde and other aldehydes.1*
The reader is referred to that report for a more comprehensive
treatment than is feasible here.
Sources and Emission Rates
Insulation. Urea-formaldehyde (UF) fonm is used as thermal
insulation in the side walls of existing buildings, especially
single-family residential buildings. OF foan> is a convenient substance
for retrofitting existing buildings, because it is injected directly
into wall cavities through small hcles that are then sealed up.
UF foams were developed in 1933 and first used as an insulating
material in the 1960s, u? foam has been used for thermal insulation in
Europe for many years, but is relatively new in the United States. In
the early 1970s, interest in and use of this material increased as the
cost of energy mounted and resulted in increased demand for residential
insulation. A production peak occurred in 1977, when the demand for
insulating products cheated shortages of other insulating materials,
such as cellulose and fiberglass.1' Approximately 170,000 houses
were insulated in 1977. The need for efficient thermal insulation in
housing has increased dramatically in the last few years. About
150,COO houses a year are now being insulated with UF foam, industry
representatives reportedly believe that more than 200,000 hones will be
insulated with UF foam during 1980."
Installation involves mixing partially polymerized UF resin with a
surfactant (foaming agent) and an acid catalyst under pressure that
forces air into the mixture to create a foam. The foam hardens within
minutes and cures and dries completely within a few days. Building
codes in the United States, concerned with the fire-safety aspects of
UF-foam insulation, rate it as a combustible material. The codes
require that UF foam, when used on the Inside of buildings, must be
protected by a thermal barrier of fire-resistant material. In England
Iv-27
-------
and Holland, OF Insulation materials ace certified for use only In
masonry cavities of buildings.
If the ingredients of UP-foan insulation are improperly formulated
or mixed* formaldehyde nay be released into the building. Long et
al.11 enumerated some of the factors that affect the release pf
formaldehyde from UF foamt
* Excessive formaldehyde in the resin-concentrate solution.
* Excessive acid catalyst in the foaming agent.
* Excess foaming agent (surfactant).
* Foaming during periods of high humidity and high temperature.
* Foaming with cold chemicals 'optimal temperature, 50-80°F).
* Improper use of vapor barriers.
* Improper use of foams (in ceilings* etc.).
Owing to ,the diversity of time factors and the complexity of their
interrelationships* the quantity and rate of formaldehyde relesase from
a house insulated with UF foam is difficult to predict.
Partlcleboard and Plywood. The superior bonding properties and low
cost cf formaldehyde polymers make them the resins of choice for the
production of building materials, especially plywood and
particleboard. Among the various formaldehyde resins used in building
materials—urea-formaldehyde, phenol-formaldehyde, and melamine-
formaldehyde—urea-formaldehyde resin is the most common adhesive used
in indoor plywood and particleboard. Plywood is composed of several
thin sheets of wood glued together with UF resin. Particleboard is
made by saturating .small wood shavings with UF resin and pressing the
resulting mixture, usually at high temperature, into the final form.
Particleboard can emit formaldehyde continuously for a long time
(several months, or even years). In buildings in which these wood
products are used for partition walls or furniture, formaldehyde may
reach concentrations sufficient to cause eye and upper respiratory
Irritation. In cases of extensive use of these products where
air-exchange rates are low, the concentration can reach 1 ppm or more.
This is due in part to the high surface-to-volume ratio of
particleboard and plywood used as building materials* The emission
rate depends on a number of factors—the original manufacturing
process, quality control of fabrication, porosity, ambient temperature,
humidity, cutting of the board for final use, etc.
UF resins contain some free formaldehyde; in addition, the resin
may hydrolyze and release free formaldehyde at high temperature and
humidity. The phenol-formaldehyde resins used for wood products that
require greater moisture resistance (i.e., exterior plywood) do not
release formaldehyde as readily as products bound with UF resin.
Phenol-formaldehyde resins are not generally used for indoor wood
products, because of their higher cost.
Combustion Appliances. Recent studies have reported on
combustion-generated indoor air pollutants, specifically contaminants
from gas stoves and heating systems in residential buildings.
IV-2 8
-------
Laboratory studies have shown that gas stoves emit substantial
quantities of aldehydes and that formaldehyde is the major component of
the aldehydes measured (Schmidt and GfltzjM G. W. Traynor, Lawrence
Berkeley Laboratory# personal communication)• Reported formaldehyde
emission from a single gas stove under test conditions has been
measured as approximately 15,000 and 25*000 wg/h for each top burner
and the oven, respectively (Traynor, personal communication).
Tobacco Smoke. Tobacco smoke is a source of several chemicals#
including several aldehydes other than formaldehyde. It may contribute
formaldehyde to the indoor environment. The smoker's exposure to these
chemicals results principally from smoke Inhaled directly into the
lungs (mainstream smoke). The smoke that is not directly inhaled into
the lungs enters the space surrounding the smoke (sidestream smoke).
It is the sidestream smoke that is the major contributor to indoor
pollution.
Analysis by Osborne et al.1 * Indicated that acrolein was an
important component of.tobacco smoke; this finding was confirmed by
Jermini et al.whose studies were conducted on a smoking machine in
an environmental chamber. Formaldehyde and acetaldehyde have also been
identified in.cigarette smoke.
Harke et al.7 ' measured concentrations of nicotine# carbon
monoxide, acrolein, and other aldehydes (expressed as acetaldehyde) in
the air of an unventilated room in which a series of experiments with a
smoking machine had been performed. Substantial concentrations, of all
four compounds were observed with this extremely low ventilation.
Other Sources. Several products that are potential sources of
formaldehyde emission are mentioned below. Because there is no
information on the rates or quantities of such emission, it is not
known which are important sources.
UF resins are used in the paper industry to increase the wet
strength of various grades of paper. Paper products typically treated
with UF resins are grocery bags, wax paper, facial tissues, napkins,
paper towels, and disposable sanitary products.
Formaldehyde polymers are used extensively in the manufacture of
floor coverings and as carpet backing. UF resins are used in. the
textile industry as binders for pigments, fire retardants, or other
materials to cloth and to impart stiffness, wrinkle resistance, and
water repellency to fabrics.
Fertilizers and pesticides used for commercially grown planes also
may use aldehydes and', theoretically, could contribute to the aldehyde
content of ambient air locally.
Urea-formaldehyde fertilizers are used not only to obtain a more
uniform release rate than is possible with soluble sources of nitrogen
but also to minimize the hazards of water pollution by nitrates leached
out of the soil. These compounds have been used with field crops,
turfgrass, pine seedlings, and geranium. The extent of their indoor
use and the amounts and rates of formaldehyde release are unknown.
Formaldehyde is used in numerous places, such as biologic
laboratories, hospitals, and hobby and craft areas.
IV-2 9
-------
Concentratlona
Indoor monitoring data for 0.8. homes are few; there are limited
nonitoring data for European hones/ particularly in the northern
European countries and they show higher indoor formaldehyde
concentrations than In the United States. Table IV-4 suaaarises recent
nonitoring data. Most of the measurements of organic substances in the
indoor environment have been made on aldehydes—specifically on
formaldehyde. Studies of the Indoor-outdoor relationships of
formaldehyde show that indoor concentrations generally exceed outdoor.
There have recently been several studies measuring indoor
formaldehyde concentrations in which emission was from particleboard
and plywood furnishings and UF-foam insulation in houses. Measurements
in Denmark,* Sweden (J. Sundell, personal communication; T. Mndvall,
personal communication), West Germany (B. Seifert, personal
communication; M. Deimel, personal communication), and the United
States (P.A. Breysse, personal communication) have shown that indoor
concentrations often exceed 0.1 ppm and may even exceed the
then-established 8-h time-weighted average safe exposure li^it (3 ppm)
for workroom air.11 In the 23 Danish houses, the average
formaldehyde concentration (the predominant source was particleboard)
was 0.62 mg/ra3 (about 0.5 ppm), and the range was 0.08-2.24 mg/m3
(about 0.07-1.9 ppm).2
As a result of occupants' complaints, formaldehyde was measured in
more than 200 mobile homes in the United States; the concentrations
reported rarged from 0.03 to 2.4 ppm (about 0.C4-;.9 mg/m3) (Breysse,
University of Washington, personal communication). A study of
formaldehyde concentrations in new office trailers with air-exchange
rates as low as 0.16/h found formaldehyde concentrations of 0.15-0.20
ppm,4 in contrast with outdoor concentrations of less than 0.01 ppm.
Formaldehyde concentrations build up in mobile home?, not only
because of emission from some building materials used in their
construction, but also because mobile homes are often more tightly
constructed than conventional homes, thus decreasing ventilation.
Aldehydes (measured by the MBTH method) were monitored in a study
of 19 homes across the United States.1* Indoor concentrations of
aldehydes were always higher than outdoor concentrations, typically by
a factor of 6 and quite often by a factor of about 10. Figure IV-2
shows the data collected in this study from a c,*s-cooking home with one
smoker. Although the source strengths were not determined in this
study/ the highest concentrations were observed in the two mobile
homer.; in general, the plywood and particleboard appeared to be the
primary sources.
In a more recent study, formaldehyde and total aliphatic -aldehyde?
(formaldehyde plus other aliphatic aldehydes) were measured at several
energy-efficient research houses at various geographic locations in the
United States.11 Results showuJ chat, at low infiltration rates
(<0.3 air change per hour, or ach), indoor formaldehyde
concentrations often exceeded 0.1 ppm, whereas outdoor concentrations
typically remained at 0.016 ppm (20 yg/m3) or less. Typical
air-exchange rates for single-family residential buildings are between
IV-30
-------
TABLE TV-4
Summary of Aldehyde Measurements In Nonoccupational Indoor Environments®
Sampling Site
Danish residences
Netherlands residences
built without formaldehyde
releasing materials
Residences in Denmark,
Netherlands, and
Federal Republic of
Germany
Two mobile home3 in
Pittsburgh, Pa.
Sample residence in
Pittsburgh, Pa.
Mobilfe homes registering
complaints in state
of Washington
Mobile homes registering
complaints in Minnesota
Mobile homes registering
complaints in Wisconsin
Public buildings and
energy-efIicisrit homes
(occupied and unoccupied)
Concentration, ppm
Range Mean
1.8 (peak) —
0.08 (peak) 0.03
2.3 (peak) 0.4
0.1-0.8b 0.36
0.5 (peak)*1 0.15
0-1.77
0-3.0
0.1-0.44
0.4
0.02-4.2 0.88
0-0.21
0-0.23b
Method of Analysis
Unspecified
Unspecified
Unspecified
BTH bubblers
MBTH bubblers
Chronotropic
acid (single
lmpinger)
Chromotropic
acid (30-min
sample)
Chromotropic
acid
Pararosanlllne
and chrono-,
tropic acid
MBTH bubblers
aReprinted from National Research Council.*^(p» 5-13)
^Formaldehyde, unless otherwise indicated.
IV-31
-------
its
jOO
rs
so
as
OUTDOORS
O O KTTCHIM
t>—-O bedroom
A A LJVINC ROOM
12/S 12/6 13/7 IS/8
12/9 12/10 12/11 12/12 12/13 12/14 12/IS 11/lfl 12/17 12/18 12/19 12/20
TIME, month and dty
FIGURE IV-2 Diurnal variation In Indoor and outdoor aldehyde concentrations at single-family house In
Chicago. Reprinted from National Research Council.5-14)
-------
0.6 and 1 ach. Figure IV-3 is a histogram showing the frequency of
occurrence of formaldehyde and total aliphatic aldehyde concentrations
measured at an energy-efficient house with an average air-exchange rate
of 0.2 ach. Data taken at an energy-efficient house in Mission Viejo,
California, are shown in Table IV-5. As shown, when the house did not
contain furniture, formaldehyde content was 80 when
furniture was added, formaldehyde rose almost threefold, A further
increase was noted when the house was occupied, very likely because of
such activities as gas cooking. When occupants opened windows to
increase ventilation, the formaldehyde content dropped substantially.
Although high, aldehyde contents observed in the majority of the
energy-efficient dwellings monitored were generally below 200 ug/ra^.
Indoor and outdoor formaldehyde and aldehyde concentrations were
found to be about the same at a public school in Columbus, Ohio, and a
large medical center in Long Beach, California, and were well below 0.1
ppm (120 pg/m^). Both buildings have high ventilation ratesj this
probably explains the low indoor concentrations, essentially equivalent
to outdoor concentrations.
Because many of the data reported from these field-monitoring
studies involved houses whose occupants had complained of indoor air
quality, these findings may not be representative of all hemes.
However, when data from a random sample in Wisconsin are compared with
those fcom the Washington mobile-home sample, most of the differences
in aldehyde concentrations can be explained by differences in the age
of the homes. The mobile homes in the complaint sample are much newer
than those in the random sample. Tabershaw Associates21 analyzed the
complaint data for mobile homes in Washington, and found that there was
no statistically valid relationship between the severity of symptoms
reported by occupants and the concentration of formaldehyde and that,
regardless of the actual exposure concentration, all persons in the
mobile homes reacted in substantially the same manner.
Foreign (particularly Danish and Swedish) houses monitored for
formaldehyde appear to have much higher concentrations than U.S.
houses. These findings probably represent differences in construction
and, hence, cannot be considered as representative of U.S. houses.
Andersen et al_. 1 formulated a mathematical model that estimates
the indoor air concentration of formaldehyde. Although use of Danish
studies may not be appropriate for U.S. houses, the treatment of
Andersen et al. illustrates the many variables that must be
considered. By conducting climate-chamber experiments, Andersen et al.
found the equilibrium concentration of formaldehyde from particleboard
to be related to temperature, water-vapor concentration in the air,
ventilation, and the amount of particleboard present. From this work,
a mathematical model was established for room-air concentration of
formaldehyde.
When this mathematical formulation was applied to the room-sampling
results, a correlation coefficient of 0.33 was found between the
observed and predicted concentrations—not a particularly good
predictive ability. The authors then modified the adjustable constants
by calculating them for each room on the basis of monitoring results.
The modified values led to a correlation coefficient of 0.88—a
considerable improvement in predictive ability.
IV-3 3
-------
Concentration (/xq/m')
FIGURE IV-3 Indoor and outdoor formaldehyde and other aldehyde con-
centrations at single-family house in Maryland. Histogram showing
the frequency of occurrence of formaldehyde and total aliphatic
aldehydes at an energy-efficient house with 0.2 ach. Reprinted from
National Research Council.
IV-34
-------
TABLE IV-5
Indoor and Outdoor Formaldehyde and Aliphatic Aldehyde Concentrations
Measured at a Single-Family House (California)3
Condition
Unoccupied, without
furniture
Number of
Measurements
Sampling Formaldehyde
Time Qi g/m
12
80 + 9%
Aliphatic
Aldehydes
(ug/m )c
90 + 162
Unoccupied, with
furniture
Occupied, dayd
Occupied, nighte
24
12
12
223 + 7%
261 + 102
140 + 31%
294 + 4%
277 + 15%
178 + 291
aReprinted from National Research Council.^(P* 5-18)
^Determined using pararosaniline method (120 ug/m^ « 100 ppb). All outside con-
centrations <10yg/m .
"¦Determined using MBTH method, expressed as equivalents of formaldehyde. All
outside concentrations <20 ug/m .
dAir exchange rate => 0.4 ach.
eWindows open part of time; air exchange rate significantly greater than 0.4 ach
and variable.
IV-35
-------
Formaldehyde release from interior particleboard occurs at a
decreasing rate with an increase in product age. Eventually the rate
of formaldehyde evolution decreases to an imperceptible point. The
time necessary for this phenomenon to occur (perhaps several years)
depends on the atmospheric conditions to which the board has been
subjected, as well as the degree of cure of the resin. The more
unstable groups degrade first, followed by the more stable free
methylol groups.
A 1977 field study in which field tests and a mathematical model
were used to determine the half-life of formaldehyde in particleboard
typically used in Scandinavian home construction reported it to be
about 2 yr when the ventilation rate in the home is 0.3 ach (C.O.
HoHowell, personal communication). Suta has analyzed the effect of
home age on formaldehyde concentrations in Danish houses. These data
give the following relationship of formaldehyde concentrations as a
function of house age when no corrections are made for other pertinent
factors, such as the amount of particleboard in the home, temperature,
humidity, and ventilation: C = 0.50e~°*012A, where C ° formaldehyde
concentration (pp
-------
particleboard would fall on the high side of this concentration range*
and houses with no particleboard would fall on the low side.
Outdoor atmospheric formaldehyde concentrations are generally much
lower than 0.1 ppo in U.S. cities. Examples of annual average
concentrations are 0.05 ppm for Los Angeles,1 " 11 0.004-0.007 ppa
for four New Jersey cities,* 0.04 ppm for Wisconsin cities (Hanrahan,
personal communication), and less than 0.03 ppm in Raleigh, North
Carolina, and Pasadena, California. Formaldehyde concentrations at
four Swiss locations ranged from 0.007 to 0.014 ppm; these
concentrations are about one-fifth the corresponding indoor Swiss
concentrations.11 A mean value of 0.004 ppm has been reported for
mainland Europe.'
Thus, formaldehyde concentrations in mobile homes and for homes
insulated with UF-foam resin are considerably higher than those of the
corresponding outdoor atmosphere.
Control Techniques
Several measures have been used in attempts to correct problems
associated with formaldehyde release from building materials, including:
* Ventilation (opening doors and windows).
* Mechanical ventilation coupled with the use of heat exchangers.
* The use of impregnated charcoal in furnace or air-conditioning
filters.
¦ The evaporation of household ammonia in closed and overheated
rooms to neutralize formaldehyde, followed by ventilation.
* Injection of ammonia into insulation through holes in walls to
neutralize formaldehyde.
* Spraying of air filters or floors with a specified odor
absorbent provided by the manufacturer.
* 08e of a "masking agent" available from the manufacturer.
* Application of vinyl wallpaper or a low-permeability paint to
interior walls.
* Removal of all or some of the insulation from the home.
Although many manufacturers claimed that they had successfully used
these remedial measures, no studies have shown that the measures will
reliably control the release of formaldehyde gas.
OTHER ORGANIC SUBSTANCES
In addition to formaldehyde, many other organic contaminants can be
present in indoor environments. Very little work has been done to
identify or measure organic contaminants that may be harmful.
Nevertheless, these compounds may provide a partial explanation for
complaints registered by people in indoor environments where It is
determined that formaldehyde and other indoor-pollutant concentrations
are low or undetectable."
IV-37
-------
The experimental tasks associated with characterizing organic
contaminants in indoor environments are formidable. The contaminants
are usually present as complex mixtures o£ many compounds at low
concentrations. Enough work has been done to outline broadly the
nature of the problem and the available information.
Sources and Emission Kates
Four major sources of organic contaminants can be identified.
People emi*. one category of organic contaminants termed "bioeffluents."
Building materials can also emit organic contaminants. The other two
categories, personal consumer {products (including insecticides,
pesticides, and herbicides) and tobacco-smoking, are discussed later in
this chapter.
Bioeffluents. Humans, throuqh normal biologic processes, emit a
category of organic substances known as "oioeffluents." Wang2"
studied bioeffluents in a school auditorium seating over 400 people.
Many organic contaminants were observed, but the major ones associated
with people were methanol, sthanol, acetone, and butyric acid. As an
example, the absolute concentrations and the emission rate per person
during a class lecture are shown in Table IV-6. Emission rates of
bioeffluents increased sharply during a class examination, considered
by Wang to be a period of stress. The findings of Wang were
corroborated in part by Johansson,10 who studied two schoolrooms in
Sweden. He observed1 that acetone and ethanol were associated with the
presence of schoolchildren. No emission rates were reported.
Building'Materials. Such products as adhesives, paints, and
sealants contain solvents and other agents that can be released during
and immediately after application. The health hazards associated with
these short-term releases of organic contaminants are acknowledged in
the warning labels regarding the use of adequate ventilation, which are
commonly applied to these products.
Less well understood is the potential for long-term emission of
organic contaminants from building materials. Slow release of. residual
solvents and other agents (e.g., catalysts, surfactants, and plastic
monomers) is one possibility, as is the gradual production of
contaminants by degradation (e.g., air oxidation, photoinitiated
reactions, and retropolymerization reactions).
Preliminary data indicate that concentrations of organic compounds
in new buildings are generally higher than outdoor concentrations. 11 "
Figure IV-4 shows comparative gas chromatograms of an indoor air sample
and an outdoor air sample taken simultaneously at the same building.
Classes of compounds consistently observed in indoor air include
hydrocarbons, alkylated aromatic compounds, and chlorinated hydrocarbon
solvents. Table IV-7 lists organic compounds identified in several
office buildings at concentrations at least 5 times greater than
outdoor concentrations."
IV-38
-------
TABLE IV-6
Average Concentracions and Emission.Races of Organic Bioeffluents
In a Lecture Class (389 People at 9:30 a.m.)
Emission Rate,
Bloeffluent Concentration, ppb mg/day per person
Acetone
20.6
+
2.8
50.7
+ 27.3
Acetaldehyde
4.2
+
2.1
6.2
+ 4.5
Acetic add
9.9
+
1.1
3.6
+ 3.6
Allyl alcohol
1.7
+
1.7
19.9
± 2'3
Amyl alcohol
7.6
+
7.2
21.9
+ 20.8
Butyric acid
15.1
+
7.3
44.6
+ 21.5
Diet rty Ike tone
5.7
+
5.0
20.8
+ 11.4
Ethyl acetate
8.6
+
2.6
25.4
+ 4.8
Ethyl alcohol
22.8
+
10.0
44.7
+ 21.5
Methyl alcohol
54.8
+
29.3
74.4
r 5.0
Phenol
4.6
+
1.9
9.5
± 1,5
Toluene
1.8
+
1.7
7.4
+ 4.9
aData from Wang.2^
IV-39
-------
Indoor
w
uu
i
Vj
Outdoor
10
I • • ¦ I ¦ ¦ 1 1 ' 1 ' 1 1 1
20 30 40
. « . i t « ' i * * » « * p ' 1 ' * * 1 1 1 1 I* I I I 1 I
Time (minutes)
o 50
100
_j
150
_l I
Temperolure
FIGURE IV-4 Comparison of chromatograos of samples taken Inside and
outside an office for trace organic substances. From C. D. Hollowell,
personal communication*
IV-40
-------
TABLE IV-7
Organic Substances Detected In Offlcesa
n-Nonane —
n-Undecane —
2-Methylpentane —
3-Methylpentane —
2,5-Dlmethylheptane
Methylcyclopentane —
Ethylcyclohexane —
Methylcyclohexane 500
Pentamethylheptane —
Aromatics:
Benzene 1
Xylenes 100
Toluene 200
Halogenalec! hydrocarbons:
Trichloroethane 350
Trichloroethylene 100
Tetrachloroethylene 100
Miscellaneous:
Hexansl —
Methylethylketone 200
aData from Schmidt et al.*®
Substance
0SHA Permissible Exposure
Limit, pom
Hydrocarbons:
n-Hexane
n-Heptane
n-Octane
500
500
500
IV-M
-------
In general) concentratone of specific organic compounds in
nonindust?ial indoor environments are will below occupational exposure
limits established by OSHA. The health hazard from the effects of
organic compounds at concentrations observed in.indoor environments
cannot now be assessed. It is important to note that OSHA criteria
were established for the industtial environment, where high exposures
to single compounds are encountered. The possibility cannot be
overlooked that cumulative exposure to several compounds at low
concentrations/ or synergistic effeces, may explain the complaints of
building occupants.
REFERENCES
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Pollution Control Association Annual Meeting, May 2, 1962, Chicago,
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Welfare, Division of Air Pollution, Public Health Service, 1962.
2. Andersen, I., G. R. Lundqvist, and L. Molhave. Indoor air pollution
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IV-42
-------
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1279. 89 pp.
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Commercial, and Light-Industry Buildings. Proceedings of tha First
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Morse. Indoor Air Pollution in the Residential Environment. Vol. 1.
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19. Sheldrick, J. E., and T. R. Steadman. Product/Industry Profile and
Related Analysis on Formaldehyde and Formaldehyde-Containing
Consumer Products. Part II. Products/Industry Profile on Urea
Formaldehyde. Report to U.S. Consumer Product Safety Commission.
Columbus, Ohio: Battelle Columbus Division, 1979. [24] pp.
20. Stahl, Q. R. Preliminary Air Pollution Survey of Aldehydes. A
Literature Review. National Air Pollution Control Administration
Publication No. APTD 69-24. Raleigh, N.C.: U.S. Department of
Health, Education, and Welfare, National Air Pollution Control
Administration, 1969.
XV-43
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21. Tabershaw, I. R., H. N. Doyle, L. Gaudette, S. H. Lamm, and 0.
Wong. A Review of the Formaldehyde Problems in Mobile Homes. Report
to National Particleboara Association. Rockvilie, Md.: Tabershaw
Occupational Medicine Associates, P.A., 1979. 19 pp.
22. U.S. Department of Health, Education, and Welfare, National Air
Pollution Control Administration. Air Quality Criteria for
Hydrocarbons. DREW Publications No. (HSM) 72-7516. Washington,
D.C.i U.S. Government Printing Office, 1970. 118 pp.
23. U.S. Department of Labor, Occupational Health and Safety
Administration. Occupational Safety and Health Standards. Subpart
Z—Toxic and hazardous substances. Code of Federal Regulations,
Title 29, Part 1901.1, July 1, 1980.
24. Wang, T. C. A study of bioeffluents in a college classroom. ASHAE
Trans. 81 (Pt. 1)-.32-44, 1975.
25. Wanner, H. U., A. Deuber, J. Satish, M. Meier, and H. Sommer. Air
pollution in the vicinity of streets, pp. 99-107. In M. W. Benarie,
Ed. Proceedings of the 12th International Colloquium on Atmospheric
Pollution, 1976. Amsterdam: Elsevier, 1976.
CONSUMER PRODUCTS
A wide array of activities and products that affect air quality can
be found in contemporary residential spaces. The full range is often
wider than is found in most occupational or public spaces. We are
concerned here with the air-pollution aspects of such activities and
consumer products.
Pollutants emitted into the indoor environment by consumer products
are usually dissipated by dilution and surface deposition. For a given
amount of such a pollutant, the rate of discharge, the volume of the
space, the ventilation rate or infiltration rate, and the presence of
occupants determine the severity and duration of human exposure. The
specifics of control strategies are discussed in Chapter IX, but it
will be clear that even an identical activity could produce radically
different exposures in different spaces, depending on the application
and efficacy of control strategies.
Consumer products introduce pollutants into the indoor air in a
number of forms and ways. For example, spray paint and sprayed-on oven
cleaners introduce an aerosol of the chemical products whenever they
are used. There are many spray products; it has been estimated that
the average U.S. residence at any given time contains 45 aerosol
sprays.11 Aerosols can also be produced indirectly, as in grinding,
sanding, cleaning, and some hobby activities. Other consumer products
and the activities associated with them introduce pollutants by
evaporation or sublimation of solvents or active ingredients, such as
paint solvents, cleaners, bleaches, and disinfectants. Still other
products—e.g., plastics, paints, and textiles with artificial fibers
and conditioners—release, or "outgas," small amounts of volatile
chemicals over long periods. The association of emission with these
types of products or activities is shown in Table IV-8. The table
represents a compilation of kinds of emission encountered in a se&rch
IV-41
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TABLE IV-8
Types of Emission of Indoor Air Pollutants Associated with
Various Activities and Consumer Products
Activity or
Product
Cleaning
Painting
Polishing
Stripping
Reflnishing
Hobbies and crafts
Intentional
Aerosol
Production
X
X
X
X
X
Unintentional
Aerosol
Production
X
X
Evaporation
or
Sublimation
X
X
X
X
X
X
Unintentional
Outgassing
X
X
X
X
X
Deodorizer X
Insecticide X
Disinfectant X
Personal groorr- X
ing product
Plastic
X
X
X
X
X
X
IV-45
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of the literature and in lists in consumer catalogs! it is clearly
incomplete.
AEBOSOL-PBODQCIHG PRODUCTS
Pressurized aerosol cans have found widespread use In a great
variety of applications. Aerosol cans typically contain a propellant
gas under a relatively low pressure—about 40 psi (3 kg/cm2)—with a
vapor pressure at naraal room temperature that allows some of the
propellant to be in equilibrium-in the liquid phase. Ontil recently,
dichlorodi fluorosis thane and trichlorofluoromethane < Eluorocarbon-12 and
fluorocarbon-U} were used widely as propeilants, but their effect on
the atmospheric ozone'layer has led to a prohibition of this
application in the United States. Propane, butane, nitrous oxide,
methylene chloride, and others are currently used as propeilants. Most
propellant gases are biologically inactive or active only at high
concentrations. Some are extremely flammable and could reach explosive
concentrations in enclosed spaces.
Active ingredients vary from product to product, and a complete
list of propeilants and active ingredients rarely appears on a can.
Cleaning agents include sodium*or potassium hydroxide in oven-cleaners>
ammonium hydroxide in window-cleaners* and teurachloroethylene and
petroleum-derived solvents in spot-cleaners. Spray paints often
contain toluene, xylene, methylchloride, and other volatile organic
substances, as well as pigttte a and a vehicle. Dravnieks2* measured
the organic chemicals present in indoor air of a high-rise apartment in
which aerosol products had been used. The use of a scented
oven-cleaner released at least 13 organic chemicals into the
residential space. An unscented aerosol deodorant and a scented
aerosol furniture polish released similarly large numbers of cheiaical
species throughout the residence.
Cote et al.' surveyed the composition of a range of aerosol
products for propeilants and active ingredients. Mokler et al.1 *
reported that under "worst reasonable conditions* some aerosol products
introduce respirable particles smaller than 6 tea in aerodynaiaic
diameter at .a concentration of over 50 mg/m3—10 times the threshold
limit value for daily average exposure in an industrial environment for
biologically inactive nuisance dust.* The same investigators found
that the conditions of discharge did net have a great effect on the
size characteristics. ,v There was no evidence of animal toxicologic
effects after a series of studies of cosmetic aerosols,1*
Marier and co-workers 11 exposed 20 human subjects to a number of
aerosol products daily for four consecutive weeks. These products
included deodorants, hair spray, frying-pan spray, room-freshaner,
insect repellent, window-cleaner, insecticide, furniture polish,
bathroom-cleaner, and a depilatory. All products were used according
to the manufacturer's instructions; after 3 wk of exposure, all
subjects were evaluated for cardiac function, respiratory function, and
hematologic and clinical biochemical characteristics. Rone of the
tests showed evidence of. toxic effects, and no fluor oca ebon was found
IV-46
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at any time in any blood sample. All the spray products used
fluorocarbon aa propellant.
In an epidemiologic study of 3,300 people in Tucson# Arizona/
Lebowitz reported in 1976 that he found respiratory effects associated
with frequent use of aerosols.17 In a followup study 5 yr after the
first one, he found that use of aerosol products was lower by a factor
of 10, and the association between aerosol use and respiratory effects
was no longer seen."
Stewart et_ al. '2 evaluated physiologic responses to different
propellant gasus (isobutane, propane, fluorocarbon-12, and
fluorocarbon-11). Theywene inhaled at concentrations of 250, 500, and
1,000 ppm for periods of 1 min to 8 h. None of the subjects showed a
decrease in pulmonary function or a change in cardiac rhythm as a
result of these exposures.
Deliberate inhalation of some aerosol sprays often leads to.serious
consequences, or even death. Lipid sprays 1 • have been shown under
such circumstances to lead to acute functional and anatomic
disintegration cf alveolar surfactant. The resulting alveolar collapse
can cause fatal hypoxemia. In one preliminary study,2* the
statistical association found between the indoor use of spray adhesives
and congenital malformations was1 sufficient to warrant further study.
PARTICLES PRODUCED AS A BYPRODUCT
The major production of particles in the indoor environment is
undoubtedly due to tobacco-smoking and food-:preparaticn (which are
considered elsewhere, as is malfunctioning heating equipment). In the
course of cleaning of floors and furniture, there is likely to be a
resuspension of dust particles that had previously settled.
Maintenance and cleaning activities have been identified as a source of
asbestos fibers in spaces that cpntain accessible asbestos.
Resuspension of settled dust in the absence of ventilation or
air-cleaning effectively increases the exposure .of occupants.1*
Even minimal exposures to asbestos fibers in hobby materials'
have been found to result in identifiable asbestos bodies in the lung,
and the asbestos fibers found in mesothelioma have been ascribed to
minimal exposures in the pursuit of hobbies. '
Hobby and home craft activities can cause substantial production o£
particles.2' The use of lead glazes by potters1" can lead to high
lead intakes, and an unknown fraction of this intake will be from
inhalation. The use of solder and flux in stained-glass fabrication
and jewelry-making results in the aerosolization of lead, cadmium, and
flux. 11 The effects of inhalation of lead and cadmium are known
better from occupational exposures, but some residential exposure must
be expected.
Some phases of woodworking result in the production of airborne
wood dust from sawing, grinding, and sanding. Acheson and co-workers
studied the risk of nasal cancer in woodworkers in the furniture
industry1 and concluded that exposure to wood dust, rather than
varnish or polish, caused an increased risk of n
-------
occupational exposures, the risk oC nasal cancer was as much as 500
times the normal, incidence.
PRODUCTS AND ACTIVITIES ASSOCIATED WITH EVAPORATION OR SUBLIMATION
Solvents are used in the indoor environment for a variety of
purposes—in clothing- and furniture-cleaners; as carriers for
polishes, paints, and varnishes; and as chemical strippers in the
refinishing of furniture—and they are inherent in many adhesives,
personal grooming products, disinfectants, and depdorizers. Most of
the chemical species involved are used in the occupational environment,
and threshold limit values have been adopted for that environment.* *
Table IV-9 contains a nonexhaustive list of substances that evaporate
or sublimate from solvents and household products and their
occupational exposure limits.1
The containers of many of the products containing substances listed
in Table IV-9 do not list their constituents or concentrations,
although hazard warnings are generally provided. The indoor air
concentrations are rarely measured; even when they are, there is
disagreement concerning the typical conditions. An example of this is
provided by two reports on methylene chloride. The first deals with
exposures to methylene chloride in paint-removers in home
workshops." One.person developed acute myocardial infarction in
three separate episodes after one use of methylene chloride for
furniture-stripping in a basement workshop. The last exposure was
fatal. In the case of a healthy younger man, it was aeci(i»".<-.?.!!y
discovered that he had a high carboxyhemoglobin (COHb) concentration
(6-8%) on each of several mornings after 2-h exposures to
paint-removers at home on the previous evening. Controlled exposures
of volunteers to methylene chloride at 50, 250, and 986 ppm for 3 h
produced COHb at concentrations of 2%, 4.5%, and 15%, respectively,
measured 1 h after the end of exposure. In the second study,'•
volunteers were exposed to methylene chlotide at 450 ppm for 26 min;
the authors considered that a typical exposure for the use of spray
paint with methylene chloride as propellant. They found "a clinically
insignificant increase" in COHb 7 h after exposure. These two reports
represent a range of reactions to methylene chloride—from nearly
undetectable to accidentally detected to fatal—that depends on
individual vulnerability, conditions of use, and criteria used for
detection. Measurements of actual concentrations of chemicals
associated with household products are scarce; where they are reported,
they can be very high, a3 in a report of benzene at 130 ppm found in a
double garage during furniture-stripping."
The use of mercury compounds as fungicides in latex paints gives
rise to long-term emission of mercury into the indoor spaces in which
such paints have been applied. Taylor'* used a radioactive tracer
and found that 20-25% of the mercury was lost in the first 90 d after
application. Foote 11 measured background ambient atmospheric mercury
concentrations in a number of homes at slightly over 2 ng/m- and in
rooms recently painted with latex paint at up to 3,000 ng/m^. In
IV-48
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TABLE IV-9
Threshold Limit Values of Various Substances3
Chemical
Acetone
Ammonia
Benzene
Carbon tetrachloride
Chlorine
Methanol
Trichloroethane
Methylene chloride
Ozone
Trichloroethylene
Turpentine
Xylene
Toluene
TLV-TWA,
mg/m
2,400
18
30
65
3
260
1,900
700
0.2
535
560
435
375
TLV-STEL,C
m&/m
3,000
27
130
9
310
2,380
870
0.6
800
840
655
560
Source
Lacquer solvent
Cleaner
Adhesive, spot cleaner,
paint remover
Spot cleaner, dry cleaner
Cleaner
Pain", spot cleaner
Cleaning fluid
Paint remover
Copying machine, electro-
static air cieaner
Dry-cleaning agent
Paint, finish
Solvent, paint carrier,
shoe dye
Solvent, paint carrier,
dry cleaning
aData from American Conference of Governmental Industrial Hygienists.^
^Threshold limit value—time-weighted average.
""Threshold limit value—short-term exposure limit.
IV-49
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rooms painted 3 yr before* he found concentrations of 68 ng/m*. The
threshold Unit value adopted by the American Conference of
Governmental Industrial Hygienists' for 8-h workdays is 50,000
hg/m . Slfiett al.11 found room-air concentrations of around
1*000-2,000 ng/ar in rooms with fresh latex paint—also well below
the TLV.and not likely to produce clinical symptoms. In comparison,
spilt mercury from broken clinical thermometers" produced
mercury-vapor concentrations in room air of about 5 ng/m*,
continuous exposure to which right produce clinical symptoms.
Residential or commercial use of insecticides, pesticides, and
herbicides both inoide and outside has the potential for contaminating
the indoor environment. Some organochlorinated or organophosphated
pesticides have specific agricultural applications, bu«. oth'irs are used
widely in urban areas by both private property-owners and
municipalities. The organlcrbaaed compounds can find their ./ay Indoors
by various routen. Some are applied directly indoors for rodent and
Insect, control. The long-term effectiveness of nun" of these compounds
la achieved by prolonged sublimation. Varltus studies have found many
Of these compounds indoors.1 ' ¦* >* in spite of the widespread use
of residential and commercial insecticides, pesticides, and herbicHes,
no systematic survey has been done to identify indoor concentrations
for the numerous compounds likely to be present.
SOME MECHANISMS OF BIOMEDICAL EPFECTS
The wide variety of the chemicals in consumer products makes it
difficult to anticipate all the possible adverse ncalth effects. Some
classes ot chemicals have common characteristics that cause them to
attack particular organ systems.
Various environmental chemicals have structural similarities that
suggest that they may have similar effects on the myocardium; these
chemicals have a lung-tissue half-life that could represent a long-term
hazard. Some examples are polyhalogenated hydrocarbons used as
insecticides and industrial chemicals, such as polychlorinated and
polybrominated biphenyls (PCB and PBB). These may produce sudden
death. The polyhalogenated hydrocarbons bind to estrogen receptors and
are estrogenic in animal systems. This may increase cholesterol and
triglyceride concentrations and so increase the risk of coronary heart
disease (CHD), of mortality from CHD, or of CHD-related death.'1
Myocardial fibers may also be damaged by toxic agents, such as
ozone. ,T Coronary-arterial-disease mortality has also been shown to
be related to concentrations of. suspended particulate matter in the
external environment." Thus, there may be many sources of
cardiotoxic agents in the indoor environment.
Organophosphorus pesticides, such as parathion, lead to clinical
symptoms resembling strong cholinergic stimulation due to a
nonreversible blockade of cholinesterase and leading to an accumulation
of endogenous acetylcholine." This accumulation disrupts the
transmission of impulses from nerve fibers to muscles.'* (In the
case of parathion, skin may be the route of entry.) Chronic effects or.
IV-50
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cerebrospinal fluid may also occur. Other disturbances of the nervous
systea may occur through exposure to such chemicals as PCB, which nay
be ingested and may be stored in fatty tissue. PCB inhibits growth in
cultured cells and interferes with the activity of a variety of
ensyaes." Pesticides occur in indoor environments through the
spraying of pesticides or herbicides and through the contamination of
items brought into the'home, including foods and flowers.1*
Solvents, especially chlorinated hydrocarbons, may damage the
kidneys and liver." Although the skin acts as an effective barrier*
serious toxicologic effects may result from exposure of the skin to
such substances as some organic phosphates, lead compounds, and acid.
Dermatitis—especially in the form of dry, scaly or fissured
reactions—-can be caused by recurrent contact with solvents,
emulsifying substances, dehydrators, or detergents. Acidic or alkaline
gases and aerosols are readily dissolved in the aqueous protective film
of the eye, on the mucous membranes of the nose and mouth, and on skin
that is moist with sweat. Such exposure may also erode teeth and
change hair structure."
These mechanisms have been demonstrated) beetuse the exposures
described can occur in nonoccupational indoor spaces, their potential
Impact should be considered. However, the importance of such exposures
is still difficult to evaluate.
SUMMARY AMD CONCLUSIONS
Among the sources of pollutants in the indoor air that are due to
consumer products or hobby or craft activities, many can harm exposed
occupants. Such products usually bear labels with hazard warnings and
instructions for use that, if followed carefully, will reduce pollutant
exposures to a point that is presumably acceptable for healthy users.
Willful abuse, as in the case of direct inhalation of aerosol products
or careless use of solvents in enclosed spaces, can result in acute or
delayed disorders or even death. The prohibition of fluorocarbons as
propellents in aerosol spray products has resulted in substitution of
other propellents that may be found to be tcxicologically less
desirable. The recognition of the carcinogenicity of vinyl chloride
and benzene has resulted in the banning of these chemicals from
consumer products, but a number of chemicals with serious toxic
potential continue to be used.
Many consumer products are used only intermittently by a given
person, and those in different households are likely to use different
products for a given purpose. For safety, most products are formulated
to avoid acute discomfort or irritation and because such acute effects
will reduce marketability. Risks of long-term or delayed adverse
health effects are not as likely to become apparent to the consumer and
are not as likely to be incorporated in hazard warnings on products.
If the constituents of the consumer products are known, it may be
possible to use a combination of occupational threshold limit values
and likely exposure concentrations and exposure durations in making
assessments of the impact of consumer products on indoor air quality.
IV-51
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Disclosure of product composition, assessment of acute, and chronic
consequences, and labeling with composition, directions for use, and
hazard turnings specific for a particular formulation amount to one of
several strategies that should be evaluated.
Monitoring or surveillance techniques now in use by such
responsible agencies as the Consumer Product Safety Commission, the
Environmental Protection Agency, and the Centers for Disease Control
are more likely to discover acute consequences than delayed adverse
health effects. The assessment of the human exposure and adverse
health consequences due to the storage and use of consumer products is
made difficult by the irregular, sporadic, and highly variable
exposures,, scarcity of measurements, and limited knowledge' about
composition of many of the products. Except for studies of accidental
poisoning, epidemiologic assessments are almost completely impossible,
owing to the episodic and irregular nature of exposures. It will be
necessary to raly on knowledge of and experience with the use of the
constituents of consumer products in the workplace. Assessment of the
impact of consumer products on nonoccupational indoor air quality must,
then, be based on constructed risks and potential exposures.
Labeling of consumer products with lists of constituents,
instructions for safe use, and hazard warnings is often inadequate, and
in any case it may be disregarded by the user and is ineffective when
the products are handled by children.
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Benzene in consumer products. Science 199>248, 1978.
ASBESTOS
"Asbestos" is a collective term fdr the fibrous or asbestiform
types of various minerals. Characteristics of flexibility, strength,
and durability have brought these mineral fibers into numerous and
varied applications involving potential exposure of large populations.
Both widespread use' and increasing investigations of the health effects
of asbestos exposure have created intense interest in asbestos as an
environmental contaminant. The health effects and toxicologic impact
of mineral fibers are covered in detail in Chapter VII.
Because the asbestiform minerals have been used in numerous
construction materials, consumer products, and appliances, the
nonoccupational environment has become an area for investigation of
asbestos contamination and human exposure. A potential foe
contamination from some types of these materials in structures during
construction, renovation, demolition, and even normal use has been
demonstrated. Repair and maintenance of household appliances,
furnaces, stoves, and asbestos-cement pipes can also result in release'
of fibers into the air.
DEFINITION OF ASBESTOS
"Asbestos" is applied to chemically varied, naturally occurring
mineral silicates of the serpentine and amphibole classification that
are separable Into fibers that are flexible and incombustible and
usually have large length-to-diameter ratios. These asbestos, or
asbestiform, mineral fibers have high tensile'strength and desirable
thermal and electric insulating properties and resist chemical
degradation. AsDestos minerals with commercial and exposure importance
are serpentine chrysotile and the amphibole group of asbestos minerals:
amosite, crocidolite, anthophyllite, and actinolite-tremolite.' 11
IMPORTANT CHARACTERISTICS OF ASBESTIFORM MINERAL FIBERS
The characteristics of durability, airborne lifetime, and fiber
dimension are especially important in determining the potential of
exposure and biologic effect.
Durability
Asbestiform fibers retain physical integrity in nearly all uses and
applications and within human tissue.'* 92
IV-55
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Potential to Remain Airborne
This potential strongly affects exposure probability. Settling
velocity depends heavily on fiber diameter and to a lesoer extent on
fiber length.* " Settling in still air in a 3-m-high room, a fiber
5 urn long and 1 tun in diameter will remain airborne for
approximately 4 h. A fiber of the same length with a 0.1-pm diameter
will remain airborne for up to 20 h." Such settling times could be
prolonged in turbulent air, and, like other suspended particles, fibers
can 'ie transported by air currents. Disruptive mechanical forces cause,
predominantly longitudinal cleavage of fibers or fiber bundle? into a
larger population of particles with smaller diameters and increased
persistence in the air.1 However, the extent of fiber cleavage by
natural forces in the environment is unknown.
Fiber Dimensions
The deposition and retention of fibers in the respiratory tract
depend on fiber dimensions, breathing conditions, and airborne fiber
concentration. Most fibers retained in human lungs are shorter than 5
ym, and have diameters less than approximately 2.5 pm,11 *•
but some thin fibers up to 200 ion have been.found in lung samples.*'
ASBESTOS PRODUCTION AND APPLICATION
Uses
The characteristics of durability, flexibility, strength, and
resistance to wear bring the asbestiform minerals into thousands of
applications. They are used in roofing and flooring products,
textiles, papers and felts, friction materials, filters and gaskets,
cement, panels, pipes, sheets, coating materials, and thermal and
acoustic insulation.1' Asbestos production began late in the
nineteenth century, when it was used as thermal insulation tor steaa
engines. Worldwide production is now nearing 5 million tons/yr, with
chrysotile the principal fiber type.*1
Production
Approximate consumption of asbestos in the United States was
600,000 tons in 1979** and is expected to be 400,000-900,000 tons in
2000. Over 90% of the asbestos used in the United States is imported,
and over 90% of the imported asbestos is Canadian chrysotile. Over 70%
of the asbestos is used in the construction industry.1
IV-56
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Spray Application
Of all the uses in the construction industry, the spray application
of asbeBtos onto structural surfaces is the most important in the
development of potential contamination situations. Such sprayed
material is usually friable or susceptible to damage and disintegration
by hand pressure. Sprayed material has been applied extensively to
steel work to retard deformation during fire and to other structural
surfaces for thermal and acoustic insulation, decoration, or
condensation control.
Spray application of asbestos fibers began in the 1930s and allowed
the rapid covering of irregular surfaces without the use of mechanical
support or extensive preparation. Early spray applications' in the
United States were mainly for decoration and acoustic insulation. In
1950, the Underwriters Laboratories approved the use of sprayed
asbestos where concrete had been required for prevention of deformation
of steel from fire in multistory buildings. This approval brought
about an intense use of sprayed asbestos material in new
construction." 19
However, evidence of the health hazards of asbestos exposure was
accumulating.21 In 1972, the New York City Council banned asbestos
spray application because of the health hazard to spray operators,
other construction workers, and the general public.11 After failure,
of attempts at on-site asbestos-contamination control,50 the EPA, in
1973, banned sprayed asbestos application for structural insulating or
fireproofing.*' Decorative materials and some heavy mix materials
were not included in the ban. In July 1978, the EPA banned spray-on
application of materials, except those in which the asbestos fibers are
encapsulated with a bituminous or resinous binder during spraying and
that are not friable after drying.A rough estimate of the total
amount of asbestos-containing materials sprayed over the 28-yr period
is 500,000 tons." Although the spraying of asbestos-containing
materials in construction ceased, such friable material in existing
structures remains a widespread asbestos-fiber source with potential
for indoor contamination (see Lumley;17 Sawyer?" and B. V. Brown,
UCLA, personal communication).
ASBESTOS CONTAMINATION OF THE ENVIRONMENT
Fiber release depends on both material coheBiveness and the
disruptive energy applied. The majority (85% or more) of asbestos in
current use is immobilized in strong binding materials, such as cement
or tiles; however, any asbestos-containing materials will release
fibers ^hen sufficiently disrupted, and the hard materials will
liberate fibers if ground, sanded, or cut. The remaining
asbestos—including that in insulation, troweled asbestos plaster, and
pi:.:e lagging—releases fibers upon minor disturbance." These
friable materials are the most important source of asbestos
contamination in structures. Friable materials can be found on open
and visible ceilings, walls, and structural members and on hidden
surfaces accessible to maintenance, renovation, or ventilatory air flow.
IV-57
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The proportion of asbestos in such material is generally 10-30% by
weight, but may vary from trace amounts to nearly 100%." Other
fibrous components include fibrous glass, mineral wools* and
cellulose. Friable materials can also contain vermiculite, talc,
perlite, diatomaceous earth, organic fibers, clays, quartz, gypsum, and
various adhesives.
Environmental contamination from asbestos-containing materials can
occur in three general ways: fallout, contact disruption, and
reentrainment of previously released but settled fibers." Fallout
is, except for very friable material, negligible. Contact disruption
and reentrainment are activity-dependent and can result in substantial
contamination and exposure.
Fibers enter occupied spaces at a relatively low rate, depending on
material friability and exposed surface area. Variations in the
fallout rate are due to structural vibration, air movement, and changes
in cohesiveness. Fallout can result in the accumulation of surface
deposits of fibers over long periods; such accumulations are then
available for later disturbance and reentrainment.
Any asbestos-containing material will release fibers if the energy
applied to it is adequate. Contact may be intentional during
demolition, renovation, or vandalism, unavoidable during maintenance,
or accidental during routine activity. Fiber release depends on
probability and energy of contact. Contamination is episodic and local
and can be intense."
The disturbance of released and accumulated fibers can cause
repeated cycles of settling and resuspension. Such reentrainment
contamination may occur after any disturbance, but can be important in
custodial activities."
ENVIRONMENTAL SAMPLING FOR ASBESTOS
Analysis of Bulk Materials
Identification of asbestos is relatively simple with mineralogic
specimens that are generally uniform in type and compositior. with
samples of construction materials, identification is more difficult.
The ainount of asbestos may be small, and construction materials may
contain other fibrous components with a variable collection of
nonfibrous components.
The primary method for asbestos identification in bulk materials is
polarized-light microscopy (PLM). X-ray diffraction (XRD) is used for
quantitative analysis of fiber type." " Transmission electron
microscopy has only limited application.1'
The petcographic microscope is a t.ransmitted-polarized-light
instrument widely used for identification and characterization of
substances based on their optical and crystallographic properties. The
techniques are established, and the equipment is inexpensive. However,
a high degree of skill and experience is required of the
microscopist.1* *1 "
IV-58
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X rays diffracted by crystalline material produce a characteristic
pattern. The technique usually yields information with a high degree
of diagnostic reliability and a printed record. It is usually used to
confirm results of petrographic microscopy; X-ray diffraction requires
a large investment in equipment, references! mineral standards, and
technical expertise. X-ray diffraction of bulk construction material
cannot define particle shape and may fail to detect concentrations o£
asbestos much below 5%. Moreover,'other silicates or crystalline
phases can interfere with asbestos identification.11 11
Specific and accurate fiber identification can be achieved by
examination of the structure of individual particles, especially in
conjunction with electron diffraction or energy-dispersive x-ray
analysis. The extrapolation of precise electron-microscope data,
however, to bulk sample information is inefficient and costly. Its use
in identification is usually confined to resolving ambiguities raised
by petrographic microscopy and x-ray diffraction. The most important
use of such analytic techniques is the identification and analysis of
inorganic particles in tissue.1 * 14
Errors in asbestiform-mineral analysis have potentially serious
consequences and are not uncommon. Fa1se-negative results will lead to
a continuation of unnecessary environmental contamination, and
false-positive results can precipitate unnecessary action. Errors
arise from analyst inexperience and from the use of phase-contrast
microscopy, rather than the appropriate polarized-light instrument.17
Measurement of Airborne Asbestos
A pump is used to draw a measured volume of air through a membrane
filter. The pump and filter are either stationary or carried on a
person, with the sampling orifice in the respiratory zone. Common
sampling rates are 2.0 L/min for personnel monitoring and 10 L/min for
general environmental sampling. Sampling times vary from minutes to
many hours, depending on anticipated fiber concentrations. Filter
segments can be examined by various methods and observers for
comparison or verification and can be stored indefinitely.19
Estimation of the amount of asbestos collected on the sampling
filters is performed by one of two methods: counting fibers by optical
microscopy with a phase-contrast light microscope and counting fibers
by electron microscopy.
The standard technique for fiber enumeration is specified by the
National Institute for Occupational Safety and Health (NIOSH) for
determination of airborne asbestos in occupational settings.11 11
Air is pumped through a membrane filter (effective pore size, 0.8
urn). A filter segment is examined with a microscope that has
phase-contrast illumination at a magnification of 400-450. particles
longer than 5 iun and with a length-to-width ratio (aspect ratio)
greater than 3 are counted. Results are presented as the numbers of
fibers per milliliter of air 15 This method enumerates only
particles of defined aspect ratio and length. It is not capable of
accurate identification of asbe:tos. Both the resolution limits of the
IV- 59
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optical microscope and the 5-ym length limit preclude enumeration of
some smaller fibers, which may be present and in numbers, greater by an
order of magnitude or more.* " However, the short fibers that.are
not counted may be less hazardous than the longer ones that are.** a>
Electron microscopy is the definitive method for both identifying
and counting small asbestos particles, when it is combined with
selected-area electron,diffraction (SAED) and energy absorption,
accurate identification of a particle is possible.11 *' laboratories
vary in techniques of sample preparation, magnification, and mass
estimation, and comparison of results has been discouraging.1' '*
Furthermore, there are no< standards for interpretation of exposure data
derived this way. Investigation of asbestos contamination by electron
microscopy is both expensive *nd extremely time-consuming. Results are
usually given in nanograms per cubic meter for mass estimations, but
can also appear as fibers per milliliter where only enumeration is
performed.1* 17 *'
Other Contamination Assessment Methods
The most relevant estimate o£ asbestos hazard is based on the
concentration of airborne, respirable asbestos fibers in the immediate
environment of building occupants. Under the usual conditions and with
the standard UIOSH optical-microscopy technique, this task is
difficult. The technique was originally intended for use,in areas, of
recognized contamination, such as asbestos production facilities. The
airborne contaminant was known, and relatively high concentrations were
readily measured. In this setting, the optical technique is effective
and appropriate. However, in the assessment of exposure situations in
other, nonoccupational structures, it has become apparent that it is
not entirely satisfactory.17 The op'-.ical-microscopy method is
truncated in its limit*. °f resolution both physically and by
regulation. The 5-pm lower limit of counted particles will preclude
the enumeration of many small fibers in the sample environment.1*
Fiber emission is nearly always local, sporadic, and activity-related.
Routine air-sampling commonly fails to describe this contamination
situation.'* *7
An alternative approach to assessment by air sampling involves a
subjective observational ranking system to provide guidance in
potential.contamination situations.11 *• This process evaluates,
relevant contamination factors that can contribute to total
contamination potential. Rating systems are an approach to a complex
process involving fiber aerodynamics, material characteristics,
structure effects, and human activity. However, the^ are not exact,
are subject to variations in factor estimation, and cannot be easily
evaluated with existing methods. They do not provide a precise
benchmark for selecting appropriate corrective actions, but can provide
consistent guidance in assessment and evaluation.
An adequate system should reflect factors that influence material
fallout, direct material disturbance, and reentrainment of f'bers.
These modes of contamination are functions of material characteristics.
IV-60
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structure configuration, and user activities. One example is a system
that considers eight factors that influence exposure." It is
predictive to the extent of estimating the probability of contamination
and exposure potential. The factors are.i
* Total asbestos content of material.
' Friability of material.
' Condition of m*terial.
• Extent o£ damage of material by water.
' Accessibility of material to activity and contact.
* Surface area of material exposed.
• Activity or movement in environment.
' Plenum or other airstream effects.
The factors are individually weighted and used in a formula to
generate a single score. Contamination evaluation by this method will
provide guidance in two wayst (1) It indicates corrective action;
scores exceeding a given value indicate that hazard potential is
substantial. (2) It establishes relative priority, the most useful
feature of the scaling system) the higher the score, the greater the
need for corrective action, and scores can be used to establish a
logical sequence of corrective actions within indoor spaces or
buildings.
ASBESTOS AIR DATA
Studies have been performed in structures containing various types
of asbestos material (classified as either friable or bonded) and under
a series of activity conditions. Tables IV-10 and IV-11 list airborne-
fiber concentration data obtained by optical microscopy (with the NIOSH
standardized technique") and electron microscopy. Nearly all the
data were collected in nonoccupational settings in apartment buildings
and private homes and in offices and schools. Both surveillance and
reenactment studies are included.
The airborn«<-fiber concentrations determined by optical microscopy
range from zero in background, quiet, and some routine activity to over
100 fibers/tal in stripping dry-spray-applied ceiling material. Fiber
contamination has an expected relationship, to activity and proximity.
The data in Table IV-11 obtained by transmission electron
microscopy are expressed as nanograms per cubic meter. Thus, they do
not distinguish between fibrous and nonfibrous asbestos, nor between
long and short fibers. Estimation of the health significance o£
mass-concentration data from Table IV-11 is impossible. There is a
lack of methodologic standardization, exposure standards, and
applicable epidemiologic information that relates fiber number
concentration to mass concentration. The electron-microscopy results
vary from zero to nearly 2,000 ng/m3. There is a progression in
contamination from background through routine and custodial activity.
Exposure probabilities can be estimated to some degree by
consideration of modes of contamination and activity in a building.
IV-61
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TABLE IV-10
Airborne Asbestos la Structures: Optical Data
Main Mode of
Contamination
Activity
Friable asbestos-containing material:
Mixed fallout
Reentrainment
Contact with
material
Mixed: con-
tact reen-
trainment
Contact
Background, city
Quiet conditions
Routine activity:
Dormitory
Schools, general
Offices
Dry sweeping, floor
Dry dusting near face
Bystander to cleaning
Heavy dusting
Laundry (contaminated
clothing)
Maintenance:
Relamping
Plumbing
Cable movement
Renovation:
Ceiling repair
Track light
Hanging light
Partition con-
struction
Pipe lagging
Ceiling damage by
vandalism
Stripping dry ceil-
ing material
Stripping wet
(amended water)
celling material
Drilling, machining
Abatement by encap-
sulation
Mean Count,
fibers/ml
0.0
o.o'
0.1
0.0
0.0
1.6
4.0
0.3
2.8
0.4
1.4
1.2
0.4
17.7
7.7
0.3
3.1
4.1
12.8
82.2
1.2
3.4
0.0
n
Range
or SD
References
42
0.0
32,33
65
0.0
32,33
10
0.0-0.8
a
79
0.1
32,33
60
0.0-0.6
32,33
5
0.7
33
6
1.3
33
3
0.3
33
8
1.6
36
12
0.0-1.2
33
2
0.1
33
6
0.1-2.4
32
24
0.2-6.4
32
3
8.2
32
6
2.9
33
12
0.8
33
4
1.1
33
8
1.8-5.8
36
5
8.0
32
11
22.4-117.0
33
96
5.2
32,33a
7
1.0-5.8
32
28
0.7
32
IV-62
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Table IV-10 (contd)
Main Mode of Mean Count, Range
Contamination Activity fibers/ml n or SD References
Bonded asbestos-containing material:
Contact Stripping cementitious 0.1 26 1.0 32
by wet ntthod
(amended water)
Machining:
Sanding tiles 1.2
Sanding concrete 7.2
Cutting concrete 6.3
Grinding concrete 0.3
Sanding taping 5.3
2
1.2-1.3
20
6
2.1
32
14
2.3
32
6
0.2
32
11
1.3-16.9
30
aH. V. Brown, personal communication.
IV-63
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TABLE IV-11
Airborne Asbeacost Electron-Microscopy Data
Location and Activity
Mean, ng/a n
Range, ng/m Reference
Urban outdoors:
48 U.S. cities
N.Y. City
N.J. schools
<10
17
14
187
22
3
2-65
3-30
23
25
25
Indoors:
Friable-asbestos,
structural surface:
Office building
N.Y. City schools
Mass. schools
N.J. schools
Office buildings
79
99
151
217
2.5-200
3
5
5
27
116
40-110
9-135
38-260
9-1,950
0-800
36
24
24
25
24
Custodial activity:
N.J. apartment
Conn, school
N.J. school
296
643
1,950
186-1,100
36
36
25
IV-64
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Quiet or background conditions say represent the usual extent of
activity in areaa with low probability of either contact or
reentrainment of asbestos. Under these conditions, contamination is
low. Routine activities in a structure containing sprayed-asbestos
surfaces will not usually result in detectable fiber concentrations.
Routine activity can result in intense contamination in sone
situations. A school population's routine activity in a building with
accessible asbestos surfaces may cause environmental contamination.
Increased fallout, occasional contact, and reentrainment may all
contribute to the highly variable fiber concentrations found under
these conditions.
Custodial work can cause disturbance and reentrainment of
accumulations of asbestos fibers. Reentrainment can be high during
custodial activity, depending on cleaning methods. Maintenance work
may involve direct contact with asbestos surfaces. Such activities may
result in marked fiber dissemination." '*
Uncontrolled removal of sprayed-asbestos surfaces during renovation
not only causes high fiber concentrations for the duration of the work,
but also increases the released-fiber burden in the structure. In such
cases, exposures involve the renovation worker and the routine
building-user as well." Before a decision on building renovation to
remove asbestos, the potential contamination during and after
renovation must be evaluated. Both contact and reentrainment release
mechanisms are involved, and very high concentrations occur during
actual contact.
STANDARDS
Estimation of the hazard associated with the airborne fiber
concentrations of Table IV-10 can be only approximate. No exposure
standards to evaluate hazard have been develc^ed for the general indoor
environment. The only existing standard is that of the Occupational
Safety and Health Administration (OSHA). Other recommendations for
occupational exposure limits are those of NIOSH and the American
Conference of Governmental industrial Bygienists (ACGIH). Although
these apply to and were intended for only occupational exposures, their
consideration in the general indoor environment may have some merit*
* The standard optical-microscopy method is used, and the air
data of Table IV-10 are comparable with the standard limits.
* The occupational exposure limits represent a distillate or
summary of both exposure and epidemiologic information. Recently
proposed changes reflect additional relevant epidemiologic evidence.
The use of the occupational exposure limits is considered by some
investigators to be acceptable for approximating the exposure
hazard.'*
Table IV-12 outlines the occupational exposure limits from 1972 to
the present. Comparison of the data in Table IV-10 with the exposure
limits of Table IV-12 demonstrates that some activities can exceed
IV-6 5
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TABLE 1V-12
Occupational Asbestos Exposure Limits
Time-Weighted Ceiling,
Limit Average (8 h/d), fibers/ml fibers/ml
OSHA original, 197246 5.0 10.0
OSHA present, 1976A5'46 2.0 10.0
OSHA proposed, 19754^ 0.5 5.0
NIOSH revised, 197741 0.1 0.5
ACGIH adopted, 1980:1
IV-66
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present time-weighted average (NA) OSHA limits. Occasional
events—such as removal, renovation* and vandalism (contact-mode
categories)—exceed the 15-min excursion limit of 10 fibers/ml.
The present 1VIA and ceiling limits were p.«t by the 1972 regulations
to become effective in 1976.** The more recent limits, the 1975
proposed ard the 1977 revised recommendedf reflect the increasing
awareness in asbestos-rdisease epidemiology and are more stringent.
With each successive regulation, the range of activities that could be
considered hazardous becomes more inclusive. The activities remaining
outside the 1977 limits are only in categories of quiet and nonspecific
routine. Occupational standards can potentially be exceeded during
renovation* maintenance, and custodial activities that disturb applied
material or accumulated fibers.
The optical-microscopy data indicate that contamination can
sometimes exceed concentrations considered hazardous. Exposures occur
in existing structuresj and the population involved is large and varied
in age, occupation, and behavior.
Children attending schools that contain friable asbestos material
constitute a population of special concern. The schoolchildren
population differs from other nonoccupational populations in age,
population density, and behavior. Any exposure would occur early in
their life, leaving a long period for development of asbestos-related
diseases. A large number of students can be exposed at one time to
asbestos that is released from asbestos-containing materials in the
school building. The school population is also very active1 Friable
asbestos-containing materials can be damaged during routine activities
and as a result of capricious behavior. Many cases of badly damaged
asbestos-containing materials have been found in schools.17
REGULATIONS
Most asbestos handling, control, and disposal in the structural
environment are subject to regulation by the EPA and the OSHA. Other
federal agencies that regulate asbestos in various settings are the
Mine Safety and Health Administration (KSHA), consumer Product Safety
Commission (CPSC),-Food and Drug Administration (FDA), and Department
of Transportation (DOT).
In accordance with section 112 of the Cledn Air Act {"National
Emission Standards for Hazardous and Air Pollutants'), the EPA
promulgated regulations on asbestos in 1973 (40 CFR 61, Subpart B,
"National Emission Standard for Asbestos").
These regulations apply to the renovation or demolition of friable
asbestos materials and to the spraying of asbestos. They specify
procedures for removal and stripping of friable sprayed-asbestos
fireproofing and insulation materials. The required work practices
include EPA notification, material-wetting, containment, container
labeling, and disposal of the removed material in an.approved
landfill. Fiber concentrations are not specified, but the regulations
require that there be no visible emission outside the structure.
IV-67
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Actions taken by the CPSC have banned the use of asbestos textiles
in general-use garments, asbestos in artificial-fireplace materials,
and asbestos-containing spackling and taping compounds.f ' Voluntary
actions by manufacturers controlled the use of asbestos in hand-held
hair-dryers.
CONTROL OF CONTAMINATION POTENTIAL
hhere a potentially hazardous situation has been identified in a
structure, asbestos-contamination control or elimination methods are
indicated.*' *• There aire four approaches to corrective action:
preventive management (a- specific management system initiated to
prevent disturbance of asbestos-containing material, with no direct
action taken on the material itself), removal and disposal by burial,
encapsulation (asbestod-containihg material is coateid with a sealant).
and enclosure , (asbestos-containing material is separated from the
building environment by. barriers, such as sealed suspended ceilings).
The corrective methods can bfe used separately or in combination,
and ech has its own advantages. Removal eliminates the. source of
expose re to- asbestosJ Both enclosure and encapsulation are containment
methods; because the asbestos material remains in the building,
enclosure and encapsulation should be considered as temporary control
methods, for use until the building is renovated or demolished.
The surface of asbestos-containing material can be damaged—causing
the friable fragments to be released—by inadvertent or uninformed
maintenance, repair, or renovation. A management system should be
implemented to control any activity by either structure personnel or
contractors. Any necessary work would be performed under controlled
conditions to protect involved personnel and other building users and
to prevent contamination of the building environment. Renovation or
demolition should include elimination of friable asbestos-containing
materials under safe conditions and protection for the worker, the
building users, and the community.
Corrective action for surfaces considered very hazardous should be
planned with priority appropriate to their contamination potential.
Removal is the ultimate solution and will end contamination potential.
Encapsulation with either penetrating or bridging sealants will enhance
the cohesiveness of the material, eliminate fallout, and protect front
minor damage. The technology of encapsulating asbestos has recently
been the subject of intense interest, and effective sealants are now
available. Management and control should be initiated for all areas
that contain friable asbestos material, no matter what other action is
planned. An asbestos management system can be implemented immediately,
has low cost, and is highly effective in exposure control." *•
SUMMARY
Asbestos is a widespread component of the structural environment.
Release of asbestiform mineral fibers from structural components
IV-6 8
-------
depends on the coheaiveneeB of the asbestos-containing material and the
intensity of the disturbing force* Asbestos-containing material that
is friable is most readily released in structures. High-energy or
machine disruption iB necessary for the release of fiberB from hard or
bound asbestos-containing materials. Durability and aerodynamic
capability have combined to produce a persistent and important
contaminant for human exposure. Contamination can be due to slight
fiber release in fallout, relatively great release by contact or direct
material disruption, or reentrainnent of fallen and accumulated
fibers. Most contamination is episodic, activity-related, and local.
Documented concentrations have been compared with existing and proposed
occupational standards. Extensive disruption of asbestos-containing
material results in substantial hazard potential. Removal# renovation,
and oemolition of friable material and machining of hard
asbestos-containing material result in a high degree of environmental
contamination in the vicinity of the disturbance. Maintenance work or
custodial care involving either friable material or accumulated fibers
can cause airborne contamination that should be considered hazardous.
REFERENCES
1. American Conference of Governmental Industrial HygieniSts. TLVs.
Threshold Limit Values for Chemical Substances in Workroom Air
Adopted by ftCGIE tor 196(1. Cincinnatii America?) Conference of
Governmental Industrial Hygienists, I960., 93 pp.
2. Asbestos Information Association of North America. Asbestos—
General Information. Washington, D.C., 1975.
3. Assuncao, J., and M.,Corn. The effects of milling on diameters and
lengths of fibrous glass and chrysotile asbestos fibers. Am. Ind.
Hyg. Assoc. J. 36:811-819, 1975.
4. Bragg, G. M., L. van Zuiden, and C. E. Hermance. The free fall of
cylinders at intermediate Reynold's numbers. Atmos. Environ.
8:755-764, 1974.
5. British Occupational Hygiene Society, Committee on Hygiene
St. idards. Hygiene standard for chrysotile asbestos dust. Ann.
Occup. Hyg. ll;47-i49, 1958.
6. Campbell, W. J., R. L, Blake, L. L. Brown, E. E. Cather, and J. J.
Sjoberg. Selected Silicate Minerals and Their Asbestiform
Varieties. Miiieralogical Definitions and Identification-
Characterization. Bureau of Mines Information Circular 8751.
College Park, Md.: U.S. Department of Interior, Bureau of Mines,
College Park Metallurgy Research Center, 1977. 64 pp.
7. Consumer Product Safety Commission. Consumer patching compounds and
artificial emberizing materials (embers and ash) containing
respirable free-form asbestos. Fed. Reg. 42:63354-63365, December
15, 1977.
8. Consumer Product Safety Commission. General use garments containing
asbestos are banned hazardous substances. Code of Federal
Regulations, Title 16, Part 1500.17 (a7), 1970.
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9. Dement,. J. M., R. D. 2umwalde, and K. M. Wallingford. Discussion
paper: Asbestos fiber exposures in a hard gold mine. Ann. K.Y.
Acad. Sci. 271:345-352, 1976.
10. Dreessen, W. C., J. M. Dallavalle, T. I. Edwards, J. W. Miller, and
R. R. Sayers. A study of Asbestosis in the Asbestos Textile
Industry. Public Health Bulletin No. 241. Washington, D.C.t U.S.
Treasury Department, Public Health Service, 1938. 126 pp.
11. Ferris, G., Jr. Asbestos Numerical Rating System. Boston!
Commonwealth of Massachusetts Special Legislature Commission on
Asbestos, September 18, 1978.
12. Fondimare, A., et al. Quantitative study of the deposition of
asbestos in the lung and pleura of subjects with diverse exposures.
In Proceedings of the Symposium on the Pathology of AsbeBtos,
Kouen, France, October 28, 1975.
13. Langer, A. M. Approaches and constraints to identification and
quantitation of asbestos fibers. Environ. Health Perspect.
9:133-136, 1974.
14. Langer, A. h., R. Ashley, V. Baden, C. Berkley, E. C. Hammond, A.
D. Mack let, C. J. Maggiore. W. J,. Nicholson, A. N. Rohl, I. B.
Rubin, A. Sastre, and I. J. Selikoff. Identification of asbestos in
human tissues. J. Occup. Mei. 15:287-295,'1973.
15. Leidel, N. A., s. G. Bayer, R. D. Zumwalde, and K. A. Busch.
USPHS/NIOSH Membrane Filter Method for Evaluating Airborne Asbestos
Fibers. DHEW(NIOSH) Publication No. 79-127. Cincinnati: U.S.
Department of Health, Education, and Welfare, National Institute
for Occupational Safety and Health, 1979. 89 pp.
16. Levine, R. J., Ed. Asbestos: An Information Resource, p. C-9. DHEW
Publication No. (NIH)79-1681. W;.3hington, D.C.: U.S. Government
Printing Office, 1978. [190] pp.
17. Lumley, K. P. S.r p. G. Harries, and F. J. 0'Kelly. Buildings
insulated with sprayed asbestos: A potential hazard. Ann. Occup.
Hyg. 14:255-257, 1971.
18. McCrone, W. C. Evaluation of asbestos in insulation. Am. Lab.
11<12)?19-31, 1979.
19. Millipore Corp. Monitoring Airborne Membrane Filter. Application
Procedure. Bedford, Mass.: Millipore Corp., 1972.
20. Murphy, R. L., B. W. Levine, F. J. Al Bazzaz, J. J. Lynch, and W..
A. Burgess. Floor tile installation as a source of asbestos
exposure. Am. Rev. Respir. Dis. 104:576-580, 1971.
21. New York City Council. Air Pollution Control Code. Local Law,
Section 1403.2-9.11(B). New York: New York City Council, 1971.
22. Nicholson, w. J., A. N. Rohl, and E. F. Ferrand. Asbestos air
pollution in New York City, pp. 136-139. In H. M. Englund and W. T.
beery, Eds. Proceeedings of the Second International Clean Air
Congress; New York: Academic press. Inc., 1971.
23. Nicholson, W. J., A. N. Rohl, R. N. Sawyer, E. Swoszowski, and J.
D. Rodaro. Measurement of Asbestos in Ambient Air. Final Report.
Contract CPA 70-92. National Air Pollution Control Administration,
1971.
24. Nicholson, W. J., A. N. Rohl, and I. Weisman. Asbestos
contamination of building air supply systems. Paper No. 29-6 in
Proceedings. International Conference on Environmental Sensing and
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Assessment. Vol. II. Institute of Electrical and Electronics
Engineers Ann. No. 75CH1044-I-29-6. Piscataway, N. J.t Institute of
Electrical and Electronics Engineers, Inc., 1976.
25. Nicholson, W. J., E. J. Swoezowski, Jr., A. N. Rohl, J. D. Todaro,
and A. Adams. Asbestos contamination in United States schools from
use of asbestos surfacing materials. Ann. N.Y. Acad. Sci.
330:587-596, 1979.
26. Pooley, F. D. Electron microscope characteristics of inhaled
chrysotile asbestos fibre. Br. J. Ind. Med. 29:146-153, 1972.
27. Pooley, F. 0. The identification of asbestos dust with an electron
microscope microprobe analyser. Ann. Occup. Byg. 18:181-186, 1975.
28. Prust, R. S. Future problems to be anticipated: Demolition, repair
and disposal. Ann. N.Y. Acad. Sci. 330:545-547, 1979.
29. Reitze, W. B., W. J. Nicholson, 0. A. Holaday, and I. J. Selikoff.
Application of sprayed inorganic fiber containing asbestos:
Occupational health hazards. Am. Ind. Hyg. Assoc. J. 33:178-191,
March 1972.
30. Rohl, A. N., A. M. Langer, I. J. Selikoff, and W. J. Nicholson.
Exposure to asbestos in the use of consumer spackling, patching-and
taping compounds. Science 189:551-553, 1975.
31. Rohl, A. N., A. M. Langer, and A. G. Wylie. Mineral
characterization of asbestos-containing spray finishes, pp. 59-64.
In U.S. Environmental Protection Agency. Asbestos Containing
Material in School Buildings: A Guidance Document. Part 1. U.S.
Environmental Protection Agency, Office of Toxic Substances
Publication No. C00090. Washington, D.C.: U.S. Environmental
Protection Agency, 1979.
32. Rohl, A. N., an^ R. N. Sawyer. Airborne Fiber Levels in Asbestos
Abatement Projects. To be presented at International Symposium on
Indoor Air Pollution, Health and Energy Conservation, Amherst,
Mass., October 14, 1981, sponsored by Harvard University School of
Public Health, Energy and Environmental Policy Center.
33. Sawyer, R. M. Asbestos exposure in a Yale building. Analysis and
resolution. Environ. Res. 13:146-169, 1977.
34. Sawyer, R. N. Indoor asbestos pollution: Application of hazard
criteria. Ann. N.Y. Acad. Sci. 330:579-586, 1979.
35. Sawyer, R. N. Yale art and architecture building: Asbestos
Contamination: Past, Present, and Future. Institute of Electrical
and Electronics Engineers, Inc., Ann. No. 75CH1044-1-20-5.
Piscataway, N.J1.: Institute of Electrical and Electronics
Engineers, Inc., 1976.
36. bawyer, R. N., and C. M. Spooner. Sprayed Asbestos-Containing
Material in Buildings. A Guidance Document. Part 2. U.S.
Environmental Protection Agency Report No. EPA-450/2-78-014.
Research Triangle Park, N.C.: U.S. Environmental Protection Agency,
1978.
37. Sawyer, R. N., and E. J. Swoszowski, Jr. Asbestos abatement in
schools: Observations and experiences. Ann. N.Y. Acad. Sci.
330:765-776, 1979.
38. Speil, S., and J. p. Leineweber. Asbestos minerals in modern
technology. Environ. Res. 2:166-208, 1969.
39. Stanton, M. F., and C. Wrench. Mechanisms of mesothelioma induction
with asbestos and fibrous glass. J. Nat. Cancer Inst. 48:797-821,
1972.
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40. Timbre11, V. Inhalation and biological effects of asbestos* pp.
429-445. In T. T. Mercer, P. E. Morrow, and W. Stober, Eds.
Assessment of Airborne Particles. Fundamentals, Applications, and
Implications to inhalation Toxicity. Proceedings of the Third
Rochester International Conference on Environmental Toxicity.
Springfield, ill.: Charles C Thomas, Publisher, 1972.
41. U.S.,Department of Health, Education, and Welfare, National
Institute for Occupational Safety and Health. Revised Recommended
Asbestos Standard. DKEW(NIOSH) Publication No. 77-169, 1977.
Washington, D.C.: U.S. Government Printing1 Office, 1977. 96 pp.
42. U.S. Department of Interior, Bureau of Mines. Mineral Industry
Surveys. Asbestos. Washington, D.C.: U.S. Department'of Interior,
Bureau of Mines, 1979.
43. U.S. Department ot Labor, Occupational Safety and Health
Administration, occupational exposure to asbestos. Notice ot
proposed rulemaking. Fed. Reg. 40:47651-47665, October 9, 1975.
44. U.S. Department of Labor, Occupational Safety and Health
Administration. Occupational safety and health standards. Emergency
standard for exposure to asbestos dust. Fed. Reg. 36:23207-23208,
December 7, 1971.
45. U.S. Department ot Labor, Occupational Safety and Health
Administration. Occupational safety and health standards.
Recodification of air contaminant standards. Fed. Reg.
40:23072-23073, May 28, 1975 129 CFR 1910.1001).
46. U.S. Department ot Labor, Occupational Safety and Health
Administration. Occupational safety and health standards, standard
for exposure to asbestos dust. Fed. Reg. 37:11318-11322, June 7,
1972.
47. U.S. Environmental Protection Agency. National emission standards
for hazardous air pollutants. Amendments to asbestos standard. Fed.
Reg. 43:26372-26374, June 19, 1978.
48. U.S. Environmental Protection Agency. National emission standards
for hazardous air pollutants. Asbestos. Fed. Reg. 3ift6820-8823,
8829-8830., April 6, 1973.
49. U.S. Environmental Protection Agency, Office ot Toxic Substances.
Asbestos Containing Material in School Buildings: A Guidance
Document, Part 1. U.S. Environmental Protection Agency, Office of
Toxic Substances Publication No. C0009U. Washington,' D.C.: U.S.
Environmental Protection Agency, 1979.
50. Villecco, M. Spray fireprooflng faces controls or ban as research
links asbestos to cancer. Archit. Forum 133(5):50-52, 1970.
51. Hagner, J. c., G. Berry, J. W. Skidmore, and V. Timbrell. The
effects ot the inhalation of asbestos in rats. Br. J. cancer
29:252-269, 1974.
52. Zoltai, T. Asbestitorm and acicular mineral fragments. Ann. N.Y.
Acad. Sci. 330:621-643, 1979.
FIBROUS GLASS
Fibrous glass is a man-made Inorganic fiber with widespread
application and distribution in the fabrication, textile, and
construction industries. It is used in thermal insulation (for
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structures, appliances, and pipe), acoustic insulation, textiles,
plastic-material reinforcement, tire cord, yarns, matting, and
filters. It is a common component of the structural environment.
Although the production of fibrous glass is a half-century old,
interest in potentially serious adverse health effects has occurred
fairly recently.
DEFINITION
The term "fibrous glass" generally includes particles composed of
glassy material with a length-to-width (or length-to-diameter) ratio
that exceeds 3. The composite elements of the glassy material form an
amorphous structure and are not well ordered or crystalline, as in the
asbestiform minerals. Contemporary conventional fibrous-glass
production blends silica sand, limestone, and soda ash as raw materials
in a continuous process. Before 1950, glassy fibrous materials,
commonly known as "mineral wools,' were commonly produced by melting
the slag of ore-smelting processes (slag wool) or naturally occurring
rocks (rock wool). Mineral-wool production began serious development
in this country after 1320 and reached a peak in the 1950s, before
modern continuous glass processes reduced the use of slag and rock as
primary materials.19 14
There are two itiajor categories of fibrous—glass products:
continuous-filament glass and glass wool.
Continuous-filament glass i's used in textiles and fabrics; as
reinforcement in plastics, rubber, and paper; and in numerous other
applications. It is produced by extruding molten glass through
dimensioned orifices to yield fiberB with fairly well-defined
diameters. Continuous glass fibers can be selectively sized to provide
the strength, hardness, or thermal properties desired for the intended
application. Most continuous-filament operations produce fibers
roughly 6 jim in diameter, with some glass reinforcing fibers having
aiameters of over 10 |im (see Pundsack;1' Smith;16 and W. Rietze,
Johns Manville Corporation, personal communication).
The most important example of glass wool is the fibrous-glass
thermal-insulation material used extensively in construction end
equipment fabrication. Contemporary glass-wool production is a
continuous processing of raw materials through melting, fiberization,
and packaging. Fiberization devices use rotors or high-velocity gas
jets either alone or in combination to produce particles of a desired
din-insion range. The diameter is important in thermal-insulation
production, because the effectiveness of the material varies inversely
with the fiber diameter. The fiber population produced in this way
does not have the well-defined diameter of the continuous-filament
process. A glass-wool fiberization system produces a range of sizes
following a frequency distribution characteristic of the process.1'
Most commercial fibrous-glass insulation has mean fiber diameters in
the range of 4.0-9.0 inn. For special applications, a small
percentage of glass wool is produced at mean diameters of 1.0 ym or
less.1' 1•
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CONCERN OVER fOTEKTIAL ADVERSE HEALTH EFFECTS
The increasing concern over the potentially serious health effects
of fibrous-glass exposure is a consequence of a number of factors:
* Interest in the carcinogenicity of asbestiform mineral fibers
ha3 raised questions concerning a possible similar effect of other
fibrous materials, including fibrous glass. 17
* The fibrogenicity and carcinogenicity of fibrous glass had
been demonstrated in animal inoculation studies in which mesotheliomas
were produced by intrapleural and intraperitoneal implantation of
fibrous glass. " 41
* Some studies of the mechanism of carcinogenicity associated
with fibers have indicated that fiber dimensions are. more important
than physical or chemical properties." The demonstration of the
apparent influence of particle size and shape indicated the possibility
of common mechanisms and effects among fibrous materials/ specifically
asbestos and fibrous glass.
* Glass fibers 1.0 toa or less in diameter are termed "nicrofibers."
In animal studies, fibers of pathologic importance are in the
microfiber range, with diameters less than approximately 0.5 n."
Fibers considered' respirable have diameters of approximately 3.5 us
or less." 29 Furthermore, the aerodynamic capability and potential
for respiration increase mainly as a function of decreasing fiber
diameter.19 21 This implicates microfibers as the most suspect in
pathologic importance, with respect to cellular effect, respirability,
and aerodynamic capability.* Microfibers are being intentionally
produced for special applications, and there is incidental microfiber
production in some glass-wool processes.
* The use of fibrous glass is widespread and increasing. There
is heavy consumption of fibrous glass by the construction industry,
including friable materials that readily release fibers in the
structural environment. The substitution of fibrous glass for asbestos
and the demand for fibrous-glass insulation products for energy
conservation will increase the use of these friable materials. The
forms, uses, and'distribution of fibrous-glass materials implies a
substantial impact if the material has marked adverse health effects.
There is concern that human exposure to fibrous glass may cause
disease. However, studies of mortality and morbidity and radiographic
examinations have failed to demonstrate discernible hazard in occupa-
tional populations with exposure to fibrous-glass particles.' ' " 11
Glass microfibers could be expected to have more airborne
persistence, respirability, and cellular.effect. However, no human
epidemiologic data support the concept.of microfiber pathogenicity.
The industrial use of microfibers is relatively small, and there have
been few accumulated years of human exposure.* However, in the older
mineral-wool production, with a wide distribution of fiber dimensions,
there has been a substantial population of particles that meet the
microfiber definition. In the mineral-wool industry, the accumulated
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exposure experience la large In numbers and years." The health
significance of microfiber exposure in human populations is not known.
IMPORTANCE OF CHARACTERISTICS OF FIBROUS GLASS
The potential for environmental contamination and exposure is
influenced by (-.he dimensions of fibrous-glass particles. Both airborne
persistence and respirability of the environmental contaminant are less
than those of asoestos, because of the relatively large diameters of
the glass particles.
Emission rates of fibrous glass depend on the proximity of the
source material, general characteristics of cohesiveness and
friability, and the intensity of the force causing the disruption.
Studies of the general environment, including space ventilation
systems, have demonstrated extremely low concentrations, less than 3
fibers/L.1 Glass-fiber concentrations in occupational and production
environments vary widely with the nature of the production process.
Most studies have shown normal production-facility concentrations well
below 1 fiber/ml as measured by the OSHA-NIOSH standard method for
airborne asbestos.9'7 18 As would be anticipated from aerodynamic
considerations, studies in microfiber production facilities have
documented airborne concentrations orders of magnitude higher than
those in conventional fibrous-glass processes.* 10
The more friable forms, such as thermal insulation, are potential
sources for environmental contamination. Studies of concentrations of
airborne fibrous particles during removal of friable insulation
material have shown high concentrations of airborne fibrous glass in
the vicinity of worker activity. During the removal of friable
spray-applied material (20% chrysotile asbestos and 70% fibrous glass) ,
fiber counts in excess of 100 fibers/ml were encountered.1*
ANALYSIS
The polarized-light microscope can be an effective instrument for
identification of fibrous glass in construction materials.
Characteristic shape, transparency, and lack cf birefringence
distinguish fibrous glass from asbestos mineral fibers. Modern fibrous
glass usually appears as isotropic particles of fairly -niloro
diameter, rod-like appearance, and high length-to-diameter ratio. Some
mineral-wool products may have highly variable dimensions, teardrop
shapes, and spherical glass "shot" of relatively large diameters. 11
STANDARDS
A TLV/TWA of 10 mg/m3 for fibrous glass or dust has been listed
by the ACGIH.This had been listed as a nuisance particle, with
the occupational exposure limit for fibrous glass given as 30 x 106
particles/ft^, or 10 mg/m^ of air.1 In a recent industry-wide
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survey, concentrations of airborne particulate matter were generally
less than 2.5 rag/m3.*
CONTROL
In consideration of the uncertainties of carcinogenicity, relevance
of the experimental tumor-production studies in animals, and the
characteristics of glass-fiber exposures of people, it appears prudent
to reduce microfiber exposure to the lowest possible point permitted by
available technology.
REFERENCES
1. American Conference cf Governmental Industrial Hygienists.
Industrial Ventilation. A Manual of Pecomnwnded Practice, p. 13-13.
14th ed. Lansing, Mich.: American Conference of Governmental
Industrial Hygienists, 1977.
2. American Conference of Governmental Industrial Hygienists. TLVs.
Tnreshold Limit Values for Chemical Substances in Workroom Air
Adopted by ACGIH for 1980, p. 19. Cincinnati; American Conference
of Governmental Industrial Hygienists, 1980.
3. Balzer, J. L. Environmental data; airborne concentrations found in
various operations, pp. 83-89. In U.S. Department of Health,
Education, and Welfare, National Institute for Occupational Safety
and Health. Occupational Exposure to Fibrous Glass. Proceedings of
a Symposium. HEW Publication No. (NIOSH) 76-151. Washington, D.C.:
U.S. Government Printing Office, 1976.
4. Dement, J. M. Environmental aspects of fibrous glass production and
utilization, pp. 97-109. In U.S. Department of Health, Education,
and Welfare, National Institute for Occupational Safety and Health.
Occupational Exposure to Fibrous Glass. Proceedings of a Symposium.
HEW Publication No. (NIOSH) 76-1S1. Washington, D.C.: U.S.
Government Printing Office, 1976.
5. Esmen, N., M. Corn, Y. Hammad, D. Wiittier, and N. Kotsko. Summary
of measurements of employee exposure to airborne dust and fiber in
sixteen facilities producing man-made mineral fibers. Am. Ind. Hyg.
Assoc. J. '.1:108-117, 1979.
6. Esmen, N. A., Y. Y. Hammad, M. Corn, D. Whittier, N. Kotsko, M.
Haller, and R. A. Kahn. Exposure of employees to man-made mineral
fibers: Mineral wool production. Environ. Res. 15:262-277, 1978.
7. Fowler, D. P., J. L. Balzer, and W. C. Cooper. Exposure of
insulation workers to airborne fibrous glass. Am. ind. Hyg. Assoc.
J. 32:86-91, 1971.
8. Gross, P., J. Tuma, and R. T. P. deTreville. Lungs of workers
e^v-osed to fiber glass. A study of their pathologic changes and
their dust content. Arch. Environ. Health 23:67-76, 1971.
9. Hill, J. W., W. S. Whitehead, J. D. Cameron, and G. A. Hedgecock.
Glass fibres: Absence' of pulmonary tuizard in production workers.
Br. J. Ind. Med. 30:174-179, 1973.
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10. Konzen, J. L. Results of environmental air-sampling studies
conductod in Owens-Corning fiberglas manufacturing plants, pp.
115-120. In U.S. Department of Health, Education, and Welfare,
National Institute for Occupational Safety and Health. Occupational
Exposure to Fibror.s Glass. Proceedings of a Symposium. HEW
Publication No. (NIOSH) 76-151. Washington, D.C.t. U.S. Government
Printing Office, 1976.
11. McCrone, W. C. Evaluation of asbestos in insulation. Am. Lab.
11(12):19-31, 1979.
12. Nasr, A. N. M., T. Ditchek, and p. A. Scholtens. The prevalence of
radiographic abnormalities in the chests of fiber glass workers. J.
Occup. Med. 13:371-376, 1971.
13. Pundsack, F. L. Fibrous glass—manufacture, use, and physical
properties, pp. 11-\n. In U.S. Department of Health, Education, and
Welfare, National Institute for Occupational Safety ani Health.
Occupational Exposure to Fibrous Glass. Proceedings of a Symposium.
HEW Publication No. ; 1IOSH) 76-151. Washington, D.C.s U.S.
Government Printing Cffice, 1976.
14. Kohl, A. N., A. M. L-r.ger, and A. G. Wylie. Mineral
characterization of i sbestos-containing spray finishes, pp. 59-64.
In U.S. EnvironmentsV. Protection Agency, Office of Toxic
Substances. Asbesto. Containing Material in School Buildings: A
Guidance Documei i. P^'t 1. Washington, D.C.: U.S. Government'
Printing Office, 1979.
15. Sawyer, R. N. Asbestos exposure in a Yale building. Analysis and
resolution. Environ. Res. 13:146-169, 1977.
IS. Smith, H. V. History, processes, and operations in the
manufacturing < :-.d u^es of fibrous glass—one company'3 experience,
pp. 19-26. Ip'j.S. Department of Health, Education, and welfare,
National Institute for Occupational Safety and Health. Occupational
Exposure to Fibrous Glass. Proceedings of a Symposium. HEW
Publication No. (NIOSH) 76-151. Washington, D.C.: U.S. Government
Printing Office, 1976.
17. Stanton, M. F. Fiber carcinogenesis: Is asbestos the only hazard?
J. Nat. Cancer Inst. 52:633-634, 1974.
18. Stanton, M. F. Some etiological considerations of fibre
carcinogenesis, pp. 289-294. In P. Bogovski, G. Gilson, V.
Timbrell, and J. C. Wagner, Eds. Biological Effects of Asbestos.
Scientific Publications No. 8. Lyon, France: International Agency
for Research on Cancer, 1973.
19.. Stanton, M. F., and C. Wrench. Mechanisms of mesothelioma induction
with asbestos and fibrous glass. J. Nat. Cancer Inst. 48:797-821,
1972.
20. Timbrell, V. Aerodynamic considerations and other aspects of glass
fiber, pp. 33-50. In U.S. Department of Health, Education, and
Welfare, National Institute for Occupational Safety and Health.
Occupational Exposure to Fibrous Glass. Proceedings of a Symposium.
HEW Publication No. (NIOSH) 76-151. Washington, D.C.: U.S.
Government Printing Office, 1976.
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21. Sawyer, R. N.f and C. M. Spooner. Sprayed Asbestos-Containing
Material in Buildings. A Guidance Document. Fart 2. O.S.
Environmental Protection Agency Report Mo. BPA-450/2-78-014.
Research Triangle Pork, N.C.i U.S. Environmental Protection Agency,
1978.
22. Nagner, J. C., C. Berry, and V. Timbrell. Mosotheliomata in rats
after inoculation with asberto9 and other materials. Br. J. Cancer
28il73-185, 1973.
23. tfrlqht, b. »i. Airborne fibrous glass particles. Chest
roentgenograms of persons with prolonged exposure. Arch. Environ.
Health 1«<17S-181, 19(8.
COMBUSTION SOURCES
Whenever unvented combustion takes place indoors or venting systems
attached to stoves, boilers, or heaters are malfunctioning, e wide
range of combustion products can be discharged directly into the indoor
atmosphere. This section susnarlxes essential information pertaining
to indoor sources of combustion products and their effects on indoor
air quality. The emphasis is on residential buildings, where research
efforts an indoor air quality have, been concentrated, but results of
United atudies of combusticn-generated pollution in other types of
buildings are also presented.
In general, the data presented here represent isolated situations
whose characteristics are highly specific to the site and the
combinations of activities that produced the effects! therefore,
transfer of these findings to other situations must be done only with
extreme care.
Smoking (which is discussed elsewhere), is the aost widely
encountered source of combustion products indoors. Besides smoking,
the primary sources of combustion byproducts in residential buildings
are usually space heaters, gas etoves, and gas water heaters. Exhaust
fico automobiles in attachec garages can al^o be a source of combustion
byproducts in buildings, as can wood fires, oil and kerosene lamps, and
candles.
The major pollutants associated with Indoor combustion are carbon
aonoxide, nitric oxide, nitrogen dioxide, aldehydes and other organic
compounds, and fine particles. These combustion products usually occur
in low concentrations, compared with the major combustion products-
carbon dioxide and water vapor. Inefficient combustion from unvented
or poorly vented space heaters, fireplaces, and lamps can also emit
carcinogenic hydrocarbon particles. Carbon dioxide and water vapor are
also produced as a result of normal metabolic processes of building
occupants and add to the buraen associated with gas appliances. Humans
produce 30-60 g of carbon dioxide and a similar amount of water vapor
per hour. An unvented space heater rated at 10,000 Btu/h, or about
2,500 kcal/h, produces around 750 g of carbon dioxide per hour.
Accordingly, depending on occupant density, space limitations, and the
extent of ventilation and infiltration, carbon dioxide concentration in
the inooor atmosphere can rise substantially above the normal range of
0.03-0.0(1. Respiration is affected when the concentration of carbon
IV-7 8
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dioxide in the air rises above 1.5%* and concentrations above 31 can
cause headachei disslness, and nausea. Above about 6-8%, carbon
dioxide causes stupor to the degree that exposed persons are unable to
take steps for self-preservation.* The Threshold Limit Value in the
occupational environment is 0.5%l—a value which has also been
applied to submarine crews, whose incidence of illness increased after
long-term, exposure to concentrations of 0.5-1%." «» ** in the
residential environment under occupied conditional carbon dioxide
concentrations are typically 0.07-0.20%.
RESIDENTIAL BUILDINGS
Space Heating
There are aany documented cases of health problems and even deaths
resulting from excessive carbon monoxide released by unvented or
improperly vented heating systems;1 11 " 11 however, few systematic
studies have provided detailed measurements of indoor air-quality
problems in such bouses. Host space heating in U.S. bouses is by
externally vented heating syatems (central furnaces or space heaters).
When the heating system is properly designed, maintained, and
functioning, combustion products that could directly affect indoor air
quality do not enter the indoor environment. However, if a negative
pressure develops in tha interior space or if there ia a faulty exhaust
system (e.g., a cracked beat exchanger or blocked flue), there can be
direct and serious degradation of indoor air quality.
Some space heating of homes is generally provided by unvented gas
and kerosene heaters. This type of heating is more commonly used in
rural areas and warm climates, such as the southern United States, and
is especially dangerous, because it emits its combustion products
directly into the living space.
In their study of indoor air quality in several homes in Rotterdam,
Blersteker and associates determined that sulfur dioxide concentrations
indoors are not normally affected by heating systems that are kept in
good condition.* However, in one older home with a faulty beater,
the indoor concentration was 3.8 times the outdoor concentration.
In a 1969-1970 study of indoor-outdoor air quality in the United
States, Yocom and co<-workers selected four homes, two public buildings,
and two office buildings for analysis.1* " One of the t-io homes
with coal beating had an antiquated central beating system with a leaky
flue. Sulfur dioxide in this borne approached 1 ppm and carbon monoxide
exceeded 50 ppm over periods of 1 b and longer, coinciding *ith periods
when coal was added to the fire and the fire was stoked.
As part of a pilot study to assess Indoor air quality in buildings,
Bollowell and co-workers showed that a gas-fired beating system in one
home, altboegh vented to the outside, produced higher nitric oxide and
nitrogen dioxide concentrations Indoors than outdoors.' In this work
and in the earlier work of Yocom et al.11 11 and Biezsteker et
al.,1 no attempt was made to measure the emission rates of the
IV-7 9
-------
combustion source or the rates at which pollutant gases enteral the
indoor environment.
In a 1973-1974 study of indoor sources ot air pollutants, Cote and
co-workers determined the emission rates o£ carbon monoxide#, nitric
oxide, and nitrogen dioxide from an unvented gas-fired space
heater.* Table IV-13 shows the emission data obtained.
Yamanaka and co-workers measured nitrogen oxides from various
unvented and vented space heaters commonly used in Japan.*' Results
on both radiant and convection types of unvented kerosene heaters, a?
well as on various water heaters and gas stoves, were reported.
Nitrogen dioxide emission from the radiant kerosene-fired space heater
averaged 46 ug/kcal (0.011 g/MJ); that from the convection type
averaged 251 pg/kcal (0.060 g/MJ).
In all the studies noted, the purpose was to measure emission of
"typical" units. The units tested were not necessarily representative
of the entire class of devices from which they were selected, nor was
there any attempt to conduct an exhaustive study of their combustion
characteristics.
Homeowners in many parts of the country ara returning to the use of
wood as a heating fuel, because of the increasing cost of oil and
natural gas. This trend is especially strong In the northeastern
states, which have depended largely on oil as a heating fuel. (The
price of No. 2 fuel oil increased by a factor of 6 or more between 1965
and 1980.)
Hood stoves and fireplaces are vented to the outdoor atmosphere,
but a number of circumstances can cause combustion products to be
emitted to the indoor atmosphere: improper installation (e.g.,
insufficient stack height), cracks or leaks in or poor fitting of
stovepipe, negative air pressure indoors, downdrafts, and accidents, as
when a log roll3 out cf the fireplace. Although much is known about
the combustion products of fuels used for space heating, little is
known about the impact of the emission from wood stoves and fireplaces
on indoor air quality—a subject urgently in need of investigation.
Combustion products of wood are highly irritating to the eyes, nose,
and respiratory system and thus provide a warning to occupants that
combustion products are present. Table ZV-14, from the work of Duncan
and co-workers, shows the types of pollutants associated with wood
burning. 7
A field monitoring program designed to compare indoor and outdoor
pollution in 10 residences and two office buildings was undertaken in
the Boston metropolitan area.1' Three of the monitored residences
used either a wood stove or a fireplace in the course of the sailing
period. Increased indoor concentrations of total suspended particles
(TSP), respirable particles, and benzo(a]pyrene were observed during
periods of wood-burning. The average indoor TSP concentrations during
days with wood-burning were about 3 times the corresponding
concentrations during days without wood-burning. Indoor 24-h
benzo[a]pyrene concentrations during days with wood-stove use were an
average of 5 times higher than those during non-wood-burning periods.
The authors concluded that the increased indoor concentrations of TSP,
IV-80
-------
TABLE IV-13
Pollutant-Gas Emission from Unvented Gas-Fired Space Heaters*
Heat Input,
Operation kcal/h
Low flame,
steady state 2,800
Kigh flame 6,200
a 6
Based on Cote et al.
IV- 81
Pollutant Emission Pollutant Emission
Factors, vig/kcal Rates, mg/h
NO NO? CO NO N0? CO
76.4 46.4 632 214 130 1,770
135 43.8 319 837 272 1,982
-------
TABLE IV-14
Emission from Residential Wood-Fired Stoves3
Emission, lb/cord^
Substance Emitted Range Average
Criteria pollutants
Particles 3-93 30.3
SO 0.5-1.5 0.7
NO 0.7-2.6 1.6
Hydrocarbons 1-146 41.6
Carbon monoxide 300-1,220 598.3
Noncrlterla pa.Tlutants
Polycycllc organic 0.6-1.22 0.9
materials
Formaldehyde 0.3-1 0.8
Acetaldehyde 0.1-0.3 0.4
Phenols 0.3-8 3.3
Acetic acid 5-48 21.1
Aluminum -- 1.3
Calcium -- 10.2
Chlorine -- 0.1
Iron -- 0.7
Magnesium -- 2.0
Manganese -- 1.6
Phosphorus -- 1.0
Potassium -- 3.6
Silicon -- 1.6
Sodium — 0.7
Titanium -- 0.02
aBased on Duncan et al.^
^The relationship used to convert from lb/ton to lb/cord was: 1 lb/ton
» 1.65 lb/cord.
IV-82
-------
respirable particles, and benzola]pyrene attributed to wood-burning may
have long-term health implications.1*
Gas Stoves; Pollutant Emission Rates and Concentrations
The early pilot studies of Yocom and co-workers, reported in 1974,
showed that, on the basis of relative indoor-outdoor concentrations of
carbon monoxide, unvented gas stoves definitely contribute to the
deterioration of indoor air quality.11
A brief study by the EPA showed that peak nitrogen dioxide
concentrations up to 1 ppm (about 1,880 iig/m^) and 1-h averages of
0.25-0.50 ppm (about 470-940 yg/m3) are reached in a closed kitchen
with no external ventilation.®
Hade and co-workers in 1973-1974 studied four homes equipped with
gas stoveb to determine the concentrations of nitric oxide, nitrogen
dioxide and carbon monoxide and their impact on indoor air quality.'*
Sampling was carried out for 2-wk periods in each home, simultaneously
at four sampling locations—three indoors and one outdoors. Table
TV-IS presents the principal data from one home included in this
study. The following were the main conclusions of the studyi
* Emission from gas stoves contributes nitrogen dioxide, nitric
oxide, and carbon monoxide to the indoor atmosphere of houses where
such stoves az» used. Kitchen concentrations of these gases responded
rapidly to stove use and, for a given house during a given season,
there was a rough correlation between average nitrogen dioxide
concentrations and average stove use.
' Nitrogen dioxide and nitric oxide were produced in roughly
equal amounts in the homes where testing was conducted. Indoor
concentrations of these pollutants were invariably higher than those
outside.
• Normal stove operations frequently resulted in nitrogen
dioxide concentrations in the kitchens averaging over 100 jg/m for
the 2-wk sampling periods.
• Comparison of samplings carried out in the spring-summer of
1973 and the fall-winter of 1973-1974 showed that in the colder
weather, when the house was closed up more often, pollutant
concentrations were more uniformly distributed in the various rooms of
the house than in the warmer months -
* A diffusion experiment conducted in one of the houses showed
that the half-life of nitrogen dioxide was only one-third that of
carbon monoxide and nitric oxide, indicating that nitrogen dioxide
decays through reaction or adsorption, in addition to normal dilution
from air exchange. This effect was observed in some of the other
houses by comparing the relative concentrations of nitrogen dioxide and
the other pollutants in various parts of the house.
Moschandreas and his associates carried out a 2-yr air sampling
program to characterize the indoor residential air environment. 11
Indoor air quality was monitored for continuous periods of
IV-83
-------
TABLE IV-15
Summary of Indoor and Outdoor Concentrations of Pollutant Gases
at a Suburban Home near Hartford, Connecticut8
Average Concentration, pg/m^
Kitchen Kitchen
over
1 m from
Living
Indoor:
Sampling
Pollutant
Stove
Stove
Room
Bedroom
Outside
Outdoor
Ratio
Period
Gas
(1)
(1A)
(2)
(3)
(4)
1:4
2:4
Spring-summer,
no2
100
61
52
44
1.39
1973
NO
--
102
64
65
26
—
2.46
CO
--
4,490
4,070
4,170
3,480
—
1.17
Fall-winter,
N09
67
60
55
—
50
1.34
1.10
1973-1974,
NO
136
134
94
—
63
2.16
1.49
first half
CO
4,190
3,520
3,230
—
1,670
2.51
1.93
Fall-winter,
no2
110
67
—
49
46
2.39
—
1973-1974,
NO
134
131
—
102
65
2.06
—
second half
CO
4,790
4,210
—
3,820
2,310
2.07
—
A 6
Based on Cote et al. House specifications: split level, two bedrooms, centrally located, well-ventllated
kitchen, 2,000-ftliving area, gas-fired stove and central heating system; occupied by two (smoking) adults
and two teen-aged children; home 6 yr old at time of tests.
-------
approximately 14 d in each of five detached dwellings, two semidetached
dwellings {townhouses), six apartment units, two mobile homes, and one
school. Three of the dwellings were referred to as "experimental,"
because they were designed to conserve energy. The remaining dwellings
were referred to either as "conventional" or by structural type. In
addition, the residences were divided according to their cooking and
heating fuel. These structures are in five metropolitan areas:
Baltimore, Washington, D.C., Chicago, Denver, and Pittsburgh. The
dwellings in Baltimore, Washington, D.C., and Chicago were monitored
twice to obtain seasonal variations. Conclusions from the study
pertaining to pollutants associated with combustion products (carbon
monoxide, nitric oxide, and nitrogen dioxide) follow:
Indoor CO concentrations are generally higher than
corresponding outdoor levels in all residences monitored.
High indoor concentrations may be attributed to . . . indoor
CO emission sources, such as gas-fired cooking appliances,
attached garages, faulty furnaces, and cigarette
smoking. . . .
The complexity of the dynunics involved in the establishment
of an indoor-outdoor relationship is clearly illustrated in
the interpretation of the data base generated for NO. From
the perspective of NO indoor variation and under real-life
conditions, three types of indoor environments have emerged:
1.) houses with electric cooking and heating appliances;
2.) houses that are heated by gas furnaces, yet serviced by
electric cooking appliances; and 3) houses that are furnished
with gas cooking and heating equipment. In houses equipped
with gas cooking appliances, observed indoor NO levels are
consistently higher than observed outdoor levels. Houses
with gas furnaces but electric cooking appliances display
higher NO indoor levels than outdoor levels, most of the
time. However, there are time intervals interspersed
throughout the monitoring period during which the observed NO
outdoor levels surpass corresponding indoor levels. Indoor
NO concentrations in totally electric homes are almost always
lower than corresponding outdoor concentrations. ...
The residential environment often provides a shelter from
high outdoor NOj levels. The three classes of residences
identified in the interpretation of the NO data also manifest
themselves in the study of NO2. The data base collected
for this project indicates that the hourly average indoor
concentrations of NO2 are almost always lower than the
corresponding ambient levels in totally electric houses.
Houses equipped with gas furnaces and electric cooking
appliances also shelter their occupants, but to a lesser
extent during peak ambient NO2 levels. Totally gas
residences do not appear to provide such protection. . . .
IV-85
-------
With the large data base generated by the study, Moschandreas and
Stark11 formulated, documented, and validated a numerical prediction
model (see Chapter VI). A secies of numerical simulations with the
model showed that, under some conditions involving gas appliances,
indoor carbon monoxide, nitric oxide, and nitrogen dioxide
concentrations increase substantially. Under these same conditions
(with the oven in use for 2 consecutive hours), carbon monoxide may
reach concentrations over 35 ppm.
The influence of gas stoves on indoor nitrogen dioxide content was
confirmed by Palmes and associates, who used integrating "personal"
monitors.15 Melia and associates used this same type of sampler in
an epidemiologic study to show that nitrogen dioxide concentrations
were significantly higher in homes with gas stoves than in those with
electric stoves.10
Puxbaum measured nitric oxide and nitrogen dioxide in a kitchen and
an adjoining room in a home with a gas stove and gas hot-water
appliance and compared indoor and outdoor concentrations. He also
compared the burning of natural and "town" gas and found that the
concentrations of both nitrogen dioxide and nitric oxide were
significantly higher during the natural-gas runs than during the
town-gas burning.17
In their 1973-1974 study, Cote and co-workers measured rates of
pollutant emission from gas appliances.' Table IV-16 presents their
data from various burner configurations and operating modes for a new
and an old stove. (These stoves produce low but continuous emission
from the pilot light, whereas current trends are toward low-heat-input
gas pilot lights and non-gas ignition systems, which will reduce this
source of indoor air pollution.)
More recently, Traynor and co-workers studied, in detail, emission
from a gas-fired stove.*' Table IV-17 summarizes some of the data
from this work, m the case of nitrogen dioxide, there was generally
good agreement between the Cote and Traynor studies. No laboratory
tests on electric stoves were carried out for comparison in these
studies, although, in an earlier field study, hollowell et^ al. did
observe small increases in kitchen ozone concentrations with
electric-stove use.*
Both Cote et al. and Hollowell et_jQ. measured gaseous pollutant
emission from top burners while water-filled pans of different
materials were being heated. Cote jet al. noted some :ninor effects on
gas-flame emission, especially with a low flame.' For example,
carbon monoxide concentrations were higher when an aluminum pan was in
place, and nitrogen dioxide concentrations were marginally lower with
all types of pans under low-flame conditions. Hollowell and
co-workers, however, could find no appreciable differences in gaseous
emission, regardless of the types of pans used.
In the Bcudy by Cote and co-workers, the efficiency of an exhaust
hood in removing stove-generated pollutants was determined.* Removal
efficiencies varied from 4% with the hood fan off to 49% with the fan
at its highest speed setting. (The low removal efficiency with the fan
off was the result of natural ventilation through the hood.) A
recirculating hood with activated charcoal, as might be expected, had
IV-86
-------
TABLE IV-16
Summary of Pollutant Emission of Gas Appliances for Typical Operating Conditions
(No Pans in Place)3
Pollutant Emission
Pollutant Emission
Heat Input
Factors
, tig/kcal
Rates, mg/h
Appliance
Operation
Rate, kcal/h
HO
co2
CO
NO NOj
CO
Older gas stove
Pilot lights
150
45.3
54.6
419
6.8 8.2
62.9
with cast iron
1 burner, high flame
2,700
92.6
51.8
382
250 140
1,031
burners
3 burners, high flame
6,780
117.0
72.8
475
793 494
3,220
Oven, steady state
2,200
91.A
73.1
530
201 161
1,166
Newer gas stove
Pilot lights
100
4.7
18.6
842
0.5 1.9
84.2
with pressed-
1 burner, high flame
3,500
130.0
79.0
510
455 277
1,795
steel burners
3 burners, high flame
10,200
138.0
65.6
315
1,408 669
3,213
Oven, steady state
2,200
77.9
50.4
1,
620
171 111
3,564
2Based on Cote et al.6
-------
TABLE IV-17
Summary of Gas-Stove Emisslona
Oven** Top Burnerc
No. No.
Experimental Experimental
Pollutant Emission, yjg/kcal Runs Emission, ug/kcal Runs
Gases:
f
00
oo
CO
CO,
MO
NO,
SO,
HCN
HCHO
Particles (<2.5 utb):
Carbon
Sulfur (as SO^)
Total respirable
mass
950
(650-1,600)
6
890 (720-1,090)
4
200,000
(195,000-205,000)
6
205,000 (196,000-217,000)
3
29
(14-50)
11
31 (21-47)
4
62
(44-74)
11
85 (69-100)
4
0.8
(0.5-1.0)
11
0.8 (0.6-0.9)
4
1.8
(1.6-2.3)
3
0.07
1
11.4
(9.9-14.2)
5
5.2 (2.0-12.0)
5
0.13
(0.05-0.24)
9
0.90 (0.86-0.96)
4
0.01
9
0.05 (0.01-0.08)
4
—
—
1.7 (1.0-2.6)
3
aBased oh Traynor e£ al. ^
''Oven operated for 1 h at 180°C (350°F).
c0perated with water-filled cooking pots.
^Ranges in parentheses.
-------
little effect on gaseous pollutants; however, such a device may
partially control organic gases and vapors responsible for odora and
aerosols released during cooking. The effect of kitchen ventilation on
carbon monoxide, nitric oxide, and nitrogen dioxide was also included
in the study by Traynor et. al.and their data on nitrogen dioxide
are presented in Figure IV-5.
Other Indoor Combustion Sources
Several other combustion sources can affect indoor air quality.
Although they tend to be site-specific and not as common as domestic
heating and gas-stove operation, several are vorthy of mention.
Water Heaters and Clothes Dryers, in two homes with gas water
heaters, Traynor observed that indoor nitrogen dioxide concentrations
were greater than outdoor (G. w. Traynor, Lawrence Berkeley Laboratory,
personal communication)- Initially, passive monitors were used to
measure average indoor concentrations aver 1 mK. Both homes were found
to have increased indoor concentrations and vera investigated in pare
detail with a continuous analyzer. In both cases, nitrogen dioxide
entered the living space from the flue collar on top of the water
heater, despite the fact that the appliances were designed to vent the
combustion products outside. Similar considerations apply to gas
clothes dryers,
Automobiles. Driving a car into or out of a basement or attached
garage can strongly affect indoor air quality, depending on the
configuration of the house and the routes for entering and leaving the
garage. In a number of documented caseg, occupants have inadvertently
left a car running in a basement garage frcwi which the resulting carbon
monoxide drifted into the associated house or apartment and caused
sickness or death of occupants, The most critical situation would
occur in a basement garage during cold weather, when the "stack effect"
of a heated house tends to draw air in fiom the garage and distribute
the pollutants captured in the garage throughout the house. A variant
of,this situation is an apartment house or office building with a
basement garage that has stairwells or elevator shafts that can
distribute pollutants throughout the building.
Little information is available on the impact on indoor air quality
of automotive exhaust emitted in garages. Yocom and associates1'
sampled one house with an attached garage and concluded that the design
of the housa (split-level) caused automotive emission from the garage
to have a greater Impact on carbon monoxide concentration than the gas
stove.
Charcoal Broiling. Charcoal cooking is usually an outdoor
activityj however, it is sometimes done in a fireplace, and some
fireplaces even include a charcoal cooker. Depending on how auch
cooking is carried out and how well the fireplace draws, the resulting
emission can enter the indoor environment. there appear to be no data
iv-a 9
-------
HOURS
FIGURE IV-5 Nitrogen dioxide concentrations in test kitchens
reported by Traynor et_ al_. as functions of use of gas oven
with different kitchen exhaust rates.
IV-90
-------
on the direct impact of charcoal broilers on indoor air quality, but a
recent study by Brookman and Birenzvige on exposure to air pollutants
from 'domestic combustion" sources provides some idea of how great
these exposures might be.* They used personal samplers to measure
hourly carbon monoxide and particulate matter in the outdoor
environment while people were operating gas lawn mowers and chain saws
and cooking with charcoal. A sampler adjacent to a charcoal cooker
recorded that hourly carbon monoxide exposures ranged from 3 to 33
ppm. Analysis of the particulate filters for polynuclear aromatic
organic matter showed that it was below the detection concentration of
the screening method used.
Hobbies. A variety of hobbies involve combustion processes, for
example, heating and soldering with an LPG torch and brazing or welding
with an oxyacetylene torch. Depending on the location, extent, and
duration of such activities, they could have an impact on indoor air
quality. Under some circumstances, the exposure of those pursuing such
hobbies to harmful contaminants could be substantial.
COMMERCIAL BUILDINGS
Only limited information is available on the effects of combustion
sources on indoor air quality in commercial buildings. Nevertheless,
any of the sources mentioned above can affect the quality of intloor air
in commercial buildings as they do in residential buildings.
Spengler and co-workers determined carbon monoxide concetrations in
several enclosed ice-skating rinks in Massachusetts10 where gasoline-
powered ice resurfacing machines are used; the concentrations were
found to exceed 50 ppm regularly.
Large public garages where traffic congestion commonly occurs in
confined spaces constitute another example of indoor air-quality
problems in commercial buildings. There are many, documented cases of
drivers and passengers who experienced acute health effects (presumably
from carbon monoxide) at times of heavy garage traffic. The most
critical situation occurs at the end of the workday or at the
completion of a major sporting event, when hundreds of cars line up
with their engines running. Stankunas and associates carried out a
study for the American Society of Heating, Refrigerating and
Air-Conditioning Engineers (ASHRAE) to measure carbon nonox.^e in
several parking garages.11 They developed a model for calculating
in-garage carbon monoxide concentrations on the basis -ȣ such variables
as ventilation volume, outdoor ambient carbon monoxide concentration,
initial carbon monoxide concentration in the quage, and garage volume.
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IV-91
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25. Waligora, J. N., Ed. Tbe Physiological Basis for Spacecraft
Environmental Limits. National Aeronautics and Space Administration
Reference ftiblication 1045. Washington, D.C.1 National Aeronautics
and Space Administration, 1979.
26. Yamanaka, S., H. Hirose, and S. Takada. Nitrogen oxides emissions
for domestic kerosene-fired and gas-fired appliances. Atmos.
Bnviroo. 131407-412, 1979.
27. YaL^s, M. W. A preliminary study of carbon monoxide gas in the
borne. J. Environ. Health 29:413-420, 1967.
28. Yoooo, j., if. Cote, and W. Clink. A Study of Indoor-Outdoor Air
Pollutant Relationships. Val. 1. Summary Report. Washingon, D.C.t
National Air Pollution Control Administration, 1974.
29. Yocoa, J., W. Cote, and W. Clink. A Study of Indoor-Oitdoor Air
Pollutant Relationships. VjI. 2. Supplementary Study. Washington,
D.C.i National Air Pollution Control Administration, 1974.
TOBACCO SMOKE
Nearly everyone is exposed to tobacco smoke at soce time or other.
Indirect exposure (i.e., exposure of nonsmokers) is referred to as
"passive exposure," "passive smoking," or 'involuntary smoking." The
extent of tbe exposure in determined by tbe number of smokers one
IV-93
-------
associates with, their Booking habits, and the characteristics of the
environment in which exposure occurs. Actual population exposures to
tobacco smoke are therefore quite variable. For some, passive exposure
to cigarette, pipe, or cigar smoke may occur routinely at work, in
transit, or at hone. For others, passive exposure may result only from
infrequent encounters with smokers in public facilities.
Over 2,000 compounds have been Identified in cigarette smoke; oany
are established carcinogens thst appear primarily in the particulate
phase. It 1b reasonable to assume that passive tobacco-snoke exposure
is many people's principal source of exposure to many of these
coat pounds.
Despite the overwhelming evidence on health effects on smokers, the
Impact of tobacco-smoke exposure on nonsmokers is not well documented.
(The health effects of gases and particles emanating from tobacco
combustion are summarized in Chapter VII.) Tobacco smoke irritates the
eyes, nose, and throat and is annoying to noncmokers, even in the
presence of "adequate" ventilation. Annoyance increases with
increasing smoke contamination and increasing dryness of air. Aside
from the irritation and annoyance that it causes, smoking in confined
spaces increased annoyance from odors and particle accumulation.
Aldehydes and ketones produced by burning tobacco give rise to odors.
Particle* that adsorb and release organic vapors can be odor sources
long after the tobacco is extinguished, and the lingering odors can be
smelled by those not desensitized.
This section discusses indoor exposure to pollution resulting from
cigarette-smoking. The factors of concern here are the number of
pepple exposed to cigarette smoke, the composition of the gases and
particles emitted, and the concentrations of pollutants encountered.
BACKGROUND
The number of people exposed to passive smoking, who might also be
termed "involuntary smokers," is not known. Howeveri given the number
of people who smoke in the United States, some involuntary inhalation
of tobacco combustion products from smoke-contaminated atmospheres by
nonsmokers is unavoidable. Passive exposure to tobacco smoke will
inevitably occur in any number of public or private activities.
In 1978, an estimated 54 million persons smoked 615 billion
cigarettes. The prevalence of regular cigarette-smoking in the adult
population declined from 42% in 1964 to 33% in 1978. Pigure IV-6 plots
the annual consumption, fioo 1950 to 1978, of cigarettes and filter-tip
cigarettes per person aged 18 and over. The adult per capita
consumption for 1978 is estimated at 3,965, which is the lowest
recorded consumption since 1958. Surveys show that fewer men are
smoking each year, but more women are smoking, particularly
teen-agers. Figure IV-7 presents the proportion of U.S. men, women,
and teen-agers that reported being regular smokers in 1974 and 1975.
This figure implies that one of every three persons between the ages of
17 and 64 regularly smokes cigarettes. Association with adult males
35-44 yr old increases the likelihood that a person will be passively
1V-94
-------
i960 55 BJ 65 70
Total
4000
• • • • • *o "4000
4 ••••
• ••**
3000- « Filternp *3000
• •
2000H •* ^
O00J • rK*X>
• • »* — — —
©50 55 60 65 70 o
Year
FIGURE IV-6 Annual consumption of cigarettes and filter-tip
cigarettes per person aged 18 yr and over, 1950-1978. 1978 per
capita consumption of cigarettes was 3,965, the lowest since
1958. Open circle, preliminary estimate. Reprinted from U.S.
Department of Health, Education, and Welfare.
IV-95
-------
w
« 30
E
Ul
x
O
z
M
K
2
Ul
cc
s
3
u
* 10
20
FmmIh
I
1
1
f
I
I
I
I
I
I
1
l
1
50
40
w
DC
Ul
3 30
%
oc
E
3
U
as
20
10
12-14 15-16 17-18
Male*
i
i
t
8
I
1
1
M
12-14 15-16 17-18
21-24 25-34 35-44 45-54 55-04 >65
AGE. YEARS
I
I
1
1
1
1
f
I
I
I
I
1
I
I
21-24 25-34 3544 45-54 55-64 >65
AGE, YEARS
FIGURE IV-7 Percentage of regular smokers in population. Teenagers,
1974. Adults.,1975, Data from U.S. Department of Health, Education,
and Welfare. A"lC» X"Ur
IV-96
-------
exposed to cigarette smoke, in 1974, the percentages of girls and boys
15-16 yr old who smoked were essentially the same. The percentage of
teen-aged boys smokingi however, has been dropping since 1970, whereas
the percentage of teen-aged girls smoking has increased dramatically.
Because cigarette smoke is ubiquitous, passive exposure to it will
be encountered in offices, industrial facilities, homes, public
sporting events, restaurants, transportation facilities, and
innumerable other locations. Professional and technical workers have
the lowest percentage of cigarette-smokersj laborers, craftsmen, and
other "blue-collar" workers have the highest. Of the maleB in
"blue-collar" occupations, 47% were smokers in 1975, whereas 36% of the
males in "white-collar" employment were smokers. Females showed the
opposite relationship; 34% of the "white-collar" females and 32% of
"blue-collar" female workers smoked. In the 1975 survey, 40% of the
women in the sanple worked outside the home; of these, 33% were
cigarette-smokers, compared with 27% of the housewives.
Information on passive exposure of nonsmokers to tobacco smoke has
never been systematically obtained, except in a limited number of
epidemiologic investigations (see Chapter VII). Data on populations
exposed at home, at work, or in other locations must be estimated from
surveys on smoking prevalence and epidemiologic studies. The National
Center on Smoking and Health (NCSK) has conducted the most extensive
surveys on American smoking habits. Marital status, educational
achievement, and income are demographic variables associated with
differences in smoking prevalence. NCSH information indicates that
divorced or separated persons smoke more than those in any other
marital-status group. For men, the highest prevalence occurs in
middle-income and high-scnool-educated groups. For women, there is a
more direct relationship between income and smoking, with more smoking
in the higher-income groups.
The demographics of smoking prevalence do not indicate exactly what
groups are passively exposed to tobacco smoke or where or when they are
likely to be exposed. We do not have information on the percentage of
the 80 million workers in the Onited States who are employed in an
environment free of tobacco smoke. He do not know what percentage of
America's 80 million residential units have smokers, but the results of
some surveys are summarized below.
Sora. 54 million adult Americans smoke (33%), so we can infer that
the number of homes and other residential units with smokers is
substantial. Summaries of prevalence of homes with smokers taken from
a study on air-pollution health effects support this contention. Table
IV-18 summarizes the response to a questionnaire in the children's
study. On the basis of 8,493 questionnaire responses obtained across
six cities (75% response rate), 70% of the homes reported having at
least one smoker. The percentages reporting at least one smoker ranged
from 63% in rural Portage, Wisconsin, to 76% in a middle-income
community in St. Louis. Lebowitz and Burrows11 reported that 53.8%
of the children in their Tucson study had smokers in their homes.
Schilling et al.11 repotted that an average of 63% of the sampled
hones in two Connecticut towns had smokers. Substantial regional
variations in the percentage of homes with snokers may be expected,
IV-97
-------
TABLE IV-18
Percentage of Hones Reporting One or More Snokersa
Proportion of Homes
Location
No. Responses
with
St. Louis, Ho.
1,922
76.1
Steubenvllle, Oh.
1,808
74.2
Kingston-Harrlman, Tenn.
810
71.8
Watertown, Mass.
838
69.8
Topeka, Kans.
1,663
63.3
Portage, Wis.
1,452
62.5
Tucson, Ariz.
676
53.8
Two towns, Conn.
376
63.3
aData from Ferris et al.,® Lebowitz and Burrows,and Schilling et al.^
IV-98
-------
owing to geographic variations in social, demographic# and religious
variables that are associated with differences in smoking prevalence.
Further stratification of the responses to the question of parental
smoking by level of parental education confirms earlier NCSH surveys.
In the Harvard aix-city study,* of the homes in which neither parent
had a high-school education, over 80% had at least one smoker. In
homc> in which one pcrent had graduated from college, only 50% had
smokers.
CONTAMINANTS IN SMOKE
A distinction can be made between mainstream smoke and sidestream
smoke in the contaminants evolved from tobacco combustion. Bath
smokers and nonsmokers are, of course, exposed to sidestream smoke.
Mainstream smoke is undiluted and is pulled through the tobacco into a
smoker's lungs. Sidestream smoke is directly from the burning
tobacco. Depending on smoking behavior, burning temperature, and type
of filter, the composition of mainstream smoke exhaled by a smoker
varies substantially. From 50% to more than 90% of water-soluble
compounds are removed from the mainstream smoke by the smoker,
depending on the depth of inhalation and the time of breath-holding.
The insoluble compounds show equal variability over a range of 20-70%.
A typical cigarette-smoker inhales mainstream smoke 8-10 times, for
a total of 24-30 s of a total 12-min burn time for a cigarette.1'
There is no dispute that the concentrations of almost all constituents
are far greater in mainstream than in sidestream smoke. However, given
approximately 24 to 1 disparity in burning tiae (i.e., the sidestream
smoke is produced during 96% of the total smoking time) and the
difference in combustion conditions, it is not surprising that
sidestream smoke is more important to the involuntary, passive smoker.
The sidestream smoke can also be enriched in many compounds.
Sidestream smoke and mainstream smoke have been characterized by many
investigators.2"* * l* " The mean particle size of fresh mainstream
smoke is slightly greater than that of sidestream smoke. Exhaled-smoke
particles are larger, on the average, than those in fresh mainstream, or
sidestream smoke, because of water absorption and coagulation. The
same processes modify the size distribution of smoke particles as they
age. If particles begin with a mass mean diameter less than> 0.2 im,
they grow by agglomeration and water absorption to a mass mean diameter
approaching 1 un within minutes.
The passive smoker by no means receives a lung dose of smoke
equivalent to that of the smoker. Several investigators have estimated
the exposure of the nonsmoker in a smoke-filled environment as
one-hundredth to one-tenth of the smoker's exposure.11 l> 11
These estimates were based primarily on measurements of carbon
monoxide, suspended particulate matter, or nicotine concentration
extrapolated from reported values for mainstream smoke. Substantial,
evidence indicates that many substances are increased in sidestream
smoke. Therefore, direct comparison on the basis of particle mass or
concentration of a specific gas may not adequately describe a passive
smoker's exposure to cigarette smoke.
IV-99
-------
The sidestream-to-mainstream ratios (s:m) of specific compounds
range from 0.7 to 46. The ratios of vapor-phase compounds vary more
than those of particulate-phase compounds. Although the composition of
mainstream smoke from nonfiltered cigarettes is quite different from
that from filtered cigarettes, the compositions of their sidestream
smoke are essentially the same. Table IV-19 presents a compilation of
the concentrations of some substances found in cigarette smoke, with
S:m ratios. Values are givet; in mass per cigarette. Unless otherwise
noted, the values refer to ronfiltered cigarettes. Sidestream
cigarette smok», because ot the length of the burn and the burn
temperature, is a more important source of local air contamination with
many substances—such as carbon monoxide, nicotine, ammonia, and
aldehydes—than mainstream smoke.
INDOOR COMCENTRATIQMS OP PARTICLES AMD VAPORS FROM CIGARETTE SMOKE
Cigarette-smoking in enclosed areas increases concentrations of
particles and gases. Increased concentrations of carbon monoxide,
nicotine, nitrosamines, and benzopyrene are among the most frequent.
Pollution measurements of air contaminated with tobacco smoke can be
conveniently divided among controlled chamber experiments and actual
exposure conditions. In many of the controlled-setting experiments,
carbon monoxide concentrations exceeding the 1-h NAAQS of 35 ppm have
been reported (see summary table on chamber studies of cigarette-smoke
exposure in U.S. Surgeon General's Report, smoking and Health)J).
Without ventilation, indoor carbon monoxide concentrations are
proportional to the amount of tobacco burned and inversely proportional
to room volume. These studies indicate that carbon monoxide
concentrations of 50-100 ppm can be obtained and that increased
ventilation substantially reduces concentrations (see Figure IV-8).
Chapter 11 of the 1979 Surgeon General's report tabulates the results
of many of the chamber experiments (Table IV-19}.
The experiments performed in controlled environments generally
involved heavier smoking than is normally encountered. Of more
interest are the observations of carbon monoxide and other pollutants
in normal indoor locations. Several studies are summarized in Table
IV-20. In general, the carbon monoxide concentrations were less than
those in the controlled experiments, probably becauoe of the heavier
smoking. Taverns, bars, nightclubs, and restaurants hava been the more
frequently reported locations in assessments of the air-quality impact
of cigarette-smoking. Concentrations less than 35 ppm for an hourly
average have been reported, primarily because of mechanical or natural
ventilation. However, studies have indicated that the 8-h NAAQS of 9
ppm could be exceeded in public facilities that permit cigarette-
smoking. Elliot and Rowe7 reported that carbon monoxide
concentrations in public assemblies of 2,000-14,000 people were between
9 and 25 ppm—up to 4 times higher than background.
As a more direct measure of exposure, several investigators have
measured COHb in nonsrookera' hlood after their exposure to cigarette
smoke. The results were as expected: modest increases in COHb.
IV-100
-------
IftDUC. -IV-17
Composition of Mainstream and Sideatreaa Smoke
Characteristic or Compound
Concentration, mg/cigarettea
Mainstream
Smoke
CD
Sldestream
Stroke
(2)
Ratio,
2:1
General characteristics:
Duration of smoke 20 550 27.5
production, s
Tobacco burned 347 411 1.2
Particles, no. per 1.05 * lO12 3.5 x 10^ 3.3
cigarette
Particles:
Tar (Chloroform extract)
20.8
44.1
2.1
10. 2b
34.5b
3.4
Nicotine
0.92
1.69
1.8
0.4&b
1<27 r
2.3
Benzo[a]pyrene
3.5 x 10"^
1.35 x,10"7
3.9
4.4 x 10 J
1.99 x 10~4
4.5
Fyrene
1.3 * 10,
3.9 x 10~4
3.0
2.70- x 10"7
1.011 x 10" J
3.7
Fluoranthene
2.72 x 10~*
1.255 x 10 3
4.6
Benzo t a]fluorene
1.84 x 10"*
7.51 x 10,
4.1
Ben2o[b/c Jfluorene
6.9 x 10"5
2.51 x 10"4
3.6
Chrysene, benz[a|anthracene
1.91 x 10
1..224 x 10'*
6.4
Benzo[b/k/j!fluoranthrene
4.9 x 10"*
1.60 x 10"
5.3
Benzo[e]pyrene
2.5 x 10"?
1.35 x 10"4
5.4
Perylene
9.0 x 10" £
3,9 x 10_:?
4.3
Diben?(a,j]a nthracene
1.1 x 10";
4.1 x 10"5
1.04 x 10"4
3.7
Diben*[a,h]anthracene,
3.1 x 10~5
3.4
ldeno-[2,3-ed]pyrene
— C
Benzo tghi] perylene
3.9 x 10 I
9.8 x 10 ^
2.5
Anthanthrene
2.2 x 10~5
3.9 x 10*5
1.8
Phenols (total)
0. 228
0.603
2.6
Cadmium
1.25 x 1C"4
4.5 x ID-4
3.6
ases and vapors:
a
Water
7.5c
293d
39.7
Carbon monoxide
18.3
86.3
4.7
—
72.6
—
Ammonia
0.16
7.4
46.3
Carbon iloxide
63.5
79.5
1.3
NO
0.O14
O. 051
3.6
HyJrogen cyanide
0.24
0.16
0.67
Acrolein
0.084
—
—
—
0.825
—
Formaldehyde
—
1.44
—
Toluene
0.108
0.60
5.6
Ace tone
0.578
1.45
2.5
Foloniunr2i0, pCi
0.04-0.10
0.10-0.16
1-4
Unless otherwise noted. Filtered cigarettes.
c3.5 tog in particulate phase; rest in vapor phase.
^5.5 mg in particulate phase; rest in vapor phase-
Reference
19
15
24
16
16
16
16
10
ia
10
18
18
18
18
18
18
18
18
18
18
18
18
13
27
13
32
26
20
20
20
11
31
26
26
32
32
7
IT-101
-------
ti SMOKERS ftNONSMOKEIIS
I.IMt (imt) llMt |nwi)
FIGURE IV-8 Calculated buildup of carbon monoxide under various conditions
of ventilation and smoking. Calculated for a room of 3,000 ft with 25
smokers on the left and for 25 nonsmokers on the right. TLV Is the threshold
limit value for carbon monoxide (50 ppm). CFM is ventilation in cubic feet
per minute. Reprinted with permission from Galuskinova.
IV-1D2
-------
TABLE IV-20
Measurement of Constituents of Tobacco Smoke Under Natural Conditions3
Level of Constituent
Reference, Location,
and Dimensions
Brunnemann and Hoffmann
Train 1 (Bar Car)
Train 2 (Bar Car)
Bar
Nightclub
Cano, et al.
Submarines 66 m3
Chappel and Parker
General public places
Government offices
Restaurants
Night clubs and taverns
Cuddeback, ejt al.
Tavern 1
Tavern 2
Elliott and Rowe
Arenas
Ventilation
Amount of
Tobacco Burned
Yes
157 cig per day
94-103 c.lg per day
6 air changes
per hour
[natural
(M.-2/hr )]
Smoking Section
dimethylnltrosamine
•13 ng/1
.11 ng/1
.24 ng/1
[.09 ng/1]
<40 ppm CO,
32 jjg/m nicotine
<40 ppm CO.
li-J5vig/m nicotine
3.5 ppm CO
2.5 ppm CO
4.0 ppm CO
13.0 ppm CO
12.5 ppm CO
.33 mg/m T
17 ppm C
.98 mg/m
CO
TPM
TPH
14.3 ppm CO
.367 mg/m3 TPM
Other
Control Section
2.0 ppm CO
2.5 ppm CO
2.5 ppm CO
3.0 ppm CO
3 ppm CO
.068 mg/m3 TPM
-------
TABLE IV-20 (continued)
Reference, Location,
and Distensions Ventilation
Galuskinova
Restaurant
Godin, et_ al.
Ferry boat compartments —
Thea r.e r —
Harke
Office building air conditioned
Office building not air condi-
tioned
Roam 78.3 ~ —
Harke and Peters
Automobile 35 km/hr speed,
no ventilation.
BO km/hr speed,
no ventilation.
30 km/hr speed,
no ventilation.
30 km/hr speed,
air jets open.
3 km/hr speed,
air jets open
& blower on.
Amount of
Tobacco Burned
Level of Constituent
Smoking Section
Other
Control Section
— .0002-.0046 mg/m^ —
benz opy rene
— 18.4 .+ 8.7 ppm CO 3.0+2.4 ppm C
— 3. 4 + 0.8 ppm CO 1.4 + 0.8 ppm C
— <5 ppm CO —
— <5 ppm CO —
3 smokers 15.6 ppm CO —
4
cig
24.3
ppm
CO
—
4
cig
12.1
ppm
CO
—
4
Cig
21.4
ppm
CO
—
4
cig
15.7
ppm
CO
—
4
cig
12.0
ppa
CO
—
-------
TABLE IV-20 (continued)
Reference, Location, Amount of
and Dimensions Ventilation Tobacco Burned
Hinds and First
Commuter train —
Commuter bus — —
Bus waiting room — —
AiiLine waiting room — —
Restaurant — —
Cocktail lounge — —
Student lounge — —
Lefcoe and Inculet
House — 1 cig
Pzadkowski, et al.
Offices —
Sebben, et al.
Night clubs
Restaurants
Bus
Slavin and Hertz
Conference room 8 air changes
pet hour
6 air changes
per hour
Level of Constituent
Other
Smoking Section Control Section
nicotine:
.0049 mg/m"* —
.0063 mg/m —
.001 mg/m^ —
.0031 mg/m —
.0052 mg/m —
.0103 mg/m;: —
.0028 mg/m —
4£ x 10 particles .9 x 10 par-
per cubic foot ~ tides per
cubic foot
2.7 ppm CO
13.4 ppm CO [6.5-41.9} 9.2 ppm CO
8-28 ppm CO —
7.3 ppm CO [6-14] 6.2 ppm CO
8 ppm CO
10 ppm CO
1-2 ppm CO
1-2 ppm CO
-------
TABLE TV-20 (continued)
Reference, Location,
and Dimensions
Self f
Intercity bus
Ventllatlon
IS air changes
per hour
U.S. Dept. transportation,
et al.
Airplane flights*
Overseas—10QZ filled 15-20 air
changes per
hour
Doioestlc—66X filled
Amount of
Tobacco Burned
23 clg burning con-
tinuous ly-
3 clg burning
contlnuously~
sReprlnted (ran U.S. Departaent of Health, Education, and Welfare.'*^
clg ¦ cigarettes; — ¦ unknown; TPH ~ total particulate matter.
Level of Constituent
Other
Smoking Section Control Section
33 ppa CO
18 ppa CO
2-5 ppa CO,
<.120 mg/a TFM
2 pptn CO,
<.120 mg/rn TFM
11-16—11-20)
-------
Hatke" shoved a COHb increase froa 0.91 to 2.1« after a 2-h exposure
to carbon monoxide at 30 ppta. Aronow1 reported siailar results In
exposed to saoice froa 15 cigarettes sacked over 2 h in a
30.8-a room without ventilation. It is possible that passive
saoking was the reason that a -portion of the nonsaoking population was
reported by Stewart et al. '• (in a national COHb survey) to :,a?e COHb
of over 1.51. But# given the range of carbon nonoxlde concentrations
reported in smoke-filled indoor locations, it ia unlikely that
cigarettes alone contribute significantly to inciaased CCHb in the
nonsmking population. Because carbon monoxide is slow to be removed
froa the envlronnr.nt, reducing fresh-air supplies to office buildings
or public facilH.i-is that permit smokir.q would necessarily increase
carbon monoxide concentrations.
Several other constituents of tobacco smoke have been measured
indoors, including nicotine, acrolein, benxo[a]pyrene, nitrosa*ines,
and aldehydes.
Under heavy-saoking conditions, acrolein is the anly gaseous
substance that has been shown V3 exceed threshold l.ait values
established for industrial environments. Acrolein is found at 1-20 ppb
in bars and restaurants} even to nonsensitive persons, these
concentrations car. cause annoying odors and eye and nose irritation.
The Indoor concentrations of benzo(a]pyrene where smoking occurs
are more ambiguous. GaluskinovS* reported concentrations of 0.2-4.6
1*3/m3 in'restaurants described as "smoky." These high
concentrations may have been due to cooking; Elliot and Rowe'
reported concentrations of 7-22 ng/n3 in the presence of total
suspended particles at 224-480 ug/m^ In public arenas with smokers.
The nicotine concentration in air is an excellent Indicator of
cigarette suite. A typical cigarette contains 2 ag of nicotine. Hinds
and First11 measured nicotine at 1-10.3 »ig/m3 in a number of
public facilities, including cocktail lounges, transportation waiting
roons, trains, and buses. The submarine contains a unique envlronaent
for observing human exposure to cigarette saoke. Cano et al.* found
nicotine in the urine of nonsaokors when the submarine environment had
nicotine at 15-35 tig/a3, and the nonsmokers' urinary nicotine
concentration was only 14 of that of the smokers. It appears unlikely
that the threshold limit value (500 ug/m3) for exposure to niootine
in industrial environments would be exceeded in indoor locations with
ventilation, although only a few studies have been reported.
Total suspended particles (TSP) and the fractions of respirable
suspended particles (RSP) have been measured in the indoor environment
in the presence of tobacco smoke. TSP concentrations of 50-400
yg/m3 nave been reported for integrated samples taken in public
arenas, lounges, bus stations, and airplanes see Table IV-2G).
There are few reported measurements of RS? in the vicinity of
tobacco-smoking. Repace and Lowrey11 reported .on 2-oin RSP samples
taken in 20 indoor environments where smoking is permitted (outdoor
measurements were also reported). The indoor RS* concentrations ranged
from 86 to 697 vg/a • These results are consists*t with
residential measurements of 24-h RSP concentrations reported by
Spengler et, aK 1' Daily indoor concentrations of RSP frequently
IV-107
-------
exceeded 200 vg/a- in hones with cigaratte-smokers. Aggregating
the date obtained from a study of €9 hoses in six cities reveals that
the indoor and outdoor concentrations in the 38 nonsmoking hoaes ace
essentially equivalent (24 iq/n3 Indoors versus 22 ig/m3
outdoors), in the 22 homes with only one cigarette-snoker, the man
concentration indoors was 43 pg/a3; the nine hoaes with two or more
smokers had a mean concentration of 75 ig/m*. These data,
collected over a 3-yr period, are presented in Figure IV-9, which shows
monthly mean RSP concentrations outside and Inside hoaes without
smokers, with one smoker, and with two or note smokers. The data
clearly illustrate the contribution c* cigarette-a»oking to indoor
particle concentrations. (The effects of pollution control on indoor
concentrations of particles generated froa tobacco-burning are
discussed in Chapter IX.)
In recent investigations of personal exposures to respirable
particles by Spengler et al_.,1 • passive smoking was shown to be an
important source. Volunteers in Topeka> Kansas, carried portable
monitors for 12-h periods on 15 sampling days. The mean RSP
concentration of samples where participants reported passive cigarette-
smoke exposure for soae time during the day was 40 ug/m^. The
nonsmoking, nonexposed participants had an overall mean concentration
of approximately 22 yg/tP, and the outdoor concentratipns averaged
less than 15 pg/a3.
CONCLUSIONS
Tobacco-smokir.g indoors can contribute to or cause increased
concentrations of respirable particles, nicotine, carbon monoxide,
acrolein, and many other fuDstances in the smoke. Hany experimental
and "real-life" aeascrements have demonstrated that where ventilation
is low or nonexistent, indoor pollutant concentrations can exceed
ambient-air quality standards and industrial standards. The indoor
concentrations have been shown to depend on the number of smokers, how
the tobacco is smoked (cigarette, pipe, or cigar), the room volume* the
volume of fresh-air makeup, the efficiency of the air-cleaning
apparatus, and the effectivenecs of air mixing in the roan. The
absorbing characteristics of building and furnlriiing materials can
affect the concentration. It has been demonstrated that the use of
makeup air (for ventilation) that has lower concentrations of the
contaminants effectively lowers the concentrations of carbon monoxide
and o'.her pollutants in tooacco smoke. Nevertheless, high respirable
and total suspended particle concentrations have been noted even in the
presence if "adequate" ventilation. Daily concentrations of respirable
particles can exceed proposed aabient-air quality standards for TSP in
homes with dmokers.
Although it needs to be documented, tobacco smoke may be the aost
important source of exposure of nonsmoking populations to
benzri[a]pyrene, nicotine, and other compounds in nonindustrialized
areas. It must, be noted, however, that there are other important
sources, both indoors and outdoors, of many of the pollutants produced
rv-ioa
-------
' 2 or mora vnokan par Kama
¦ 1 vnokar par horn*
noamofcan
outdoors
X
X
X
X
X
X
X
XJ
Nov Jan Mar May Jul
1976 1977
Sep Nov Jan Mar
1978
FIGURE IV-9 Monthly mean respirable particle concentrations.
0, outside. X, Inside nonsmoker hoaes. 1, Inside homes with
one smoker. Solid circles, Inside hones with two or oore smokers.
Sample represents 80 homes across six cities (approximately 10-15
homes per city). Reprinted with permission from Spengler et al.
IV-109
-------
by the burning of tobacco. And it is important to point out that
direct exposure of a smoker is an order of magnitude greater than the
passive exposure of a nonsmoker.
REFERENCES
1. Axonow, W. s. Effect of passive smoking on angina pectoris. N.
Engl. J. Med. 299:21-24, 1978.
2. Brunnemann, K. D., J. D. Adams, D. P. S. Ho, and o. Hoffmann. The
influence of tobacco smoke on indoor atmospheres. II. Volatile and
tobacco specific nitrosamines in main- and sidestrearn smoke and
their contribution to.indoor pollution, pp. 876-860. In 4th Joint
Conference on Sensing of Environmental Pollutants, New Orleans,
Louisiana, November 6-11, 1977. Washington, D.C.: American Chemical
Society, 1978.
3. Brunneman, ft. D., and 0. Hoffmann. Chemical studies on tobacco
smoke. XXIV. A quantitative method for carbon ponoxide and carbon
dioxide in cigarette and cigar smoke. J. Chrc.it. Sci. 12:70-75,
1974.
4. Brunnemann, K; D., and D. fciffmann. Chemical studies on tobacco
smoke. LIX. Analysis of volatile nitrosamines in tobacco smoke and
polluted indoor environments, pp. 343-356. In F. A. Walker, M.
Castegnaro, L. Griciute, and R. E. Lyle, Eds. Environmental Aspects
of N-Nitroso Compounds. 1ARC Scientific Publications No. 19. Lyon,
France: International Agency for Research on Cancer, 1978.
5. Cano, .J. P., J. Catalin, R. Badre, C. Dumas, A. Viaia, and R.
Guillerme. Determination de la nicotine par chromatagrophie en
phase gazeuse. II. Applications. Ann. Phara. Pr. 28(11):633-640,
1970.
6. Corn, M. Characteristics of tobacco sidestream smoke and factors
influencing its concentration and distribution in occupied spaces.
Scand. J. Respir. Dis. Suppl. 91:21-36, 1974.
7. Elliot, L. P., and D. R. Rove. Air quality during public
gatherings. J. Air Pollut. Control Assoc. 25:635-636, 1975.
8. Ferris, B. J., Jr., F. E. bpiezer, J. D. Spengler, D. Dockery, Y.
M. M. Bishop, M. WoLfson, and c. Bumble. Effects of sulfur oxides
and respirable particles on human health. Methodology and
demography of populations in study. Am. Rev. Respir. Ois.
120:767-7 79, 1979.
9. CaluskinovS", V. 3,4-Benzpyrene determination in the smoky
atmosphere of social meeting rooms and restaurants. A contribution
to the problem of the noxiousness of go-called passive smoking.
Neoplasma 11:465-468, 1964. (in Czech)
10. Grimmer, G., H. BShnke, B. and H.-P. Harke. Passive smoking:
Measuring of concentrations of polycyclic aromatic hydrocarbons in
rooms after machine smoking of cigarettes. Int. Arch. Occup.
Environ. Health 40:83-92, 1977. (in German; English summary)
11. Har*e, H.-P. The problem of "passive smoking." Munch. Med.
Wochenschr. 112:2328-2334, 1970. (in German; English summary|
IV-110
-------
12. Hinds, W. C., and H. W. First. Concentrations ot nicotine and
tobacco smoke in public places. N. Engl. J. Med. 292:844-845, 1975.
13. Hoegg, U. R. cigarette smoke In closed spaces. Environ. Health
Perspect. 2:117-128, 1972.
14. Johnson, W. R., R. w. Hale, J. W. Nedlock, N. J. Grubbs, and D. H.
Powell. The distribution ot products between mainstream and
sidestream stroke. Tob. Scl. 175(21):43-46, October 12, 1973.
15. Keith, C. H., and J. C. Derrick. Measurement ot t-he particle size
distribution and concentration o£ cigarette smoke by the
"coniluge." J. Colloid. Scl. lS:340-356, 1960.
16. Kotln, P., and H. L. Falk. The role and action ot environmental
agentB in the pathogenesis ot lung cancer. II. Cigarette snoke.
Cancer 13:250-262, 1960.
17. Lebowitz, M. 0., and B. Burrows. Respiratory symptoms related to
smoking habits ot tamlly adults. Chest 69:48-50, 1976.
18. Neurath, G., and H. Ehmke. Apparatur zur Untersuchung des
Nebenstromrauches. Beitr. Tabaktorsch. 2:117-121, 1964. (In German;
Erglish summary)
19. Neurath, G., and h. Horstaann. Emtluss des Feuchtlgkeitsgehaltes
von Cigaretten au£ die Zusajamensetzung des Raucftes und die
Glutzonentemperatur. Bsitr. Tabaktor&ch. 2:93-100, 1973. tin
German; English summary)
20. Partenov, y. D. Poionium-210 in the environment, and In the human
organism. At. Energy Rev. 12/1:75-143, 1974.
21. Repoce, J. L., and A. H. Lowrey. Indoor air pollution, tobacco
smokt, and public health. Science 208:464-472, 19BU.
22f Russell, M. A. H., P. V. Cole, and E. Brown. Absorption by
non-sraoners ot carbon monoxide trom room air polluted by tobacco
smoke. Lancet 1:576-579, 1973.
23. Russell, M. A. 11., and C. Feyerabend. Blood and urinary nicotine in
non-smokers. Lancet 1:179-181, 1975.
24. Scassellati Storzolim, G., and A. Savino. Evaluation ot a rapid
index ot ambient contamination by cigarette smoke, in relation to
the composition ot the gas phases ot the smoke. Riv. ltal. ig.
28:43-55, 1968.
25. Schilling, R. S. F., A. D. Letai, S. L. Hui, G. J. Beck, J. B.
Schoenberg, and A. Bouhuys. Lung function, respiratory disease, and
smoking in lamiHe**. Am. j. Epidemiol. 106:274-283, 1977.
26. Schmeltz, I., and D. Uoftmann. Chemical studies on tobacco smoke,
XXXVIII. The physiocheaical nature ot cigarette smoke, pp. 13-34.
In E. L. Hynder, D. Holtmann, and G. B. Gorl, Eds. Smoking and
Health. 1. Modifying the Risk tor the Smoker. Proceedings ot the
3rd World Conference on Smoking and Health. Washington, D.C.: U.S.
Government Printing ottice, 1976.
27. Seeholer, F., D. Hanssen, H. kabitz, and R. Schroder. Uber den
Verbleib des Wassers beim Abrauchen. 2. MitteiJLung. Beitr.
Tabaktorsch. 3:491-503, 1966. (in German; English summary)
28. Spengler, J. D., D. w. Dockery, M. P. Reed, T. Tosteson, and p.
Qulnlan. Personal Exposure to Respirable Particles. Paper 80-61.5b,
presented at 73rd Annual Meeting ot the Ait Pollution Control
Association, June 22-27, Montreal, Quebec, 1980.
IV-lll
-------
29. Spengler, J. D., D. W. Dockery, W. A. Turner, J. M. Wolfson, and B.
G. Ferris, Jr. Long-term measurements of respirable sulfates and
particles inside and outside hones. Atmos. Environ. 15(23-30/ 1981.
30. Stewart# R. D., B. D. Biretta, L. R. Platte, B. B. Stewart, J. H.
KalbfleiBch, B. Van Yserloo, and A. A. Rimm. Carboxyhemoglobin
levels in American blood donors. J. Aa. Med. Assoc. 229(1187-1195,
1974.
31. U.S. Department of Health, Education, and welfare, Public Health
Service. Smoking and Health. A Report of the Surgeon General. DHEW
Publication No. (PHS) 79-50066. Washington, D.C.t U.S. Government
Printing Office, 1979. (12&0] pp.
3 2. Weber-Tschopp, A., T. Fischer, and E. Grandjean. Physiological and
psychological effects of passive smoking. Int. Arch. Occup.
Environ. Health 37:277-288, 1976. (in Gorman; English summary)
ODORS
Some substances in the indoor environment make their presence known
primarily by their ability to evoke odor sensations. These substances
generally arise from humans or their activities. A room full of
people, for example, will invariably have "occupancy odor." A
characteristic odor like this generally emerges from a mixture of many
organic substances, each present at a low concentration. Some of the
individual constituents might cause greater concern if present alone at
much higher concentrations; as building blocks of a composite,
relatively benign odor, they receive attention only as odorants. Thus,
the smell of the indoor environment is a measure of environmental
quality. The remarkable sensitivity of olfaction encourages this
approach. That is, treating low-concentration organic contaminants on
the basis of their olfactory impact usually places stringent
requirements on the quality of the indoor air. With some notable
exceptions (e.g., the presence of carbon monoxide or mercury vapor), an
indoor environment that is odorless contains air of healthful quality.
Completely odorless conditions occur indoors only rarely. Weak
odors may go unnoticed or may be tolerated, particularly after persons
have had the opportunity to remain in a space for a while. The
lability of olfaction, evident in this phenomenon of adaptation, may
impair the credibility of the nose as an air-quality indicator. Its
sensitivity, often as good is or better than that of the most sensitive
instruments, offers some compensation for its functional instability.
This section deals with how odors arise, how human beings perceive
them, and how their status as "perceived" contaminants determines the
means to cope with them. The stringent air-quality standard
effectively imposed by high olfactory sensitivity makes odorants a
target of particular interest in any effort to keep indoor air quality
high in an energy-conscious society.
IV-112
-------
SOURCES
Occupancy Odor
Host bui.ldl.nga exist, to hold people, in some cases many people.
With the exception of churches# structures built specifically to hold
many people were relatively rare until the nineteenth century. Before
then* people avoided crowded places because oE possible
contamination—it was believed that crowded places, with their odors,
served as breeding grounds of disease. The odors were often blamed for
the apcead of infection.17 This attitude makes some sense, in view
of the imperceptibility of the actual agents of contagion. Even at the
end of the nineteenth century, many people still iound it difficult to
accept the notion that contagion is primarily fingerborne, rather than
airborr-s. Belief in the airborne route.carried no evident penalty for
the layman, merely some inconvenience. Hence, the notion that bad-
smelling air indoors signaled unhealthful conditions ecuId carry on
undisturbed. Through the burning of incense, churches had long seemed
to give credence to the idea that a good (i.e., pleasant) odor would
purify the air and thereby protect against illness. Such a practice
actually, reflected a predominant view of pre-nineteenth-century
medicine.
Only in the second' half of the nineteenth century did the toxicity
of the body effluvia responsible for occupancy odor receive scientific
attention. In a "oramon type of laboratory experiment on the matter,
animals breathed air previously breathed by other animals, or received
liquid injections of condensed organic materials from previously
breathed air. In the experiments on "rebreathing," the animals
sometimes developed infections or other difficulties; but, despite such
occurrences, experimenters could not point indisputably to any harmful
effects of the organic materials in previously breathed air.11
Experiments on injections of condensed materials yielded essentially
the same result: no consistent hazard. At the close of the nineteenth
century, the issue seemed more or less settled. On the basis of both a
review of available literature and their own experiments, Billings et,
al. 11 concluded that
[it is] very improbable that the minute quantity of organic
matter contained in the air expired from human lungs has any
deleterious influence upon men who inhale it in ordinary
foams, and, hence, it is probably unnecessary to take this
factor into account in providing for the ventilation of such
rooms. . . . The discomfort produced by crowded,
ill-ventilated rooms in persons not accustomed to them is not
due to the excess of carbonic zcid, nor to bactefia, nor, in
most cases, to dusts of any kind. The two great causes of
such discomfort, though not the only ones, are excessive
temperature and unpleesant odors. . . . The cause of the
unpleasant, musty odor which is perceptible to most persons
on passing frem the outer air into a crowded, unventilated
room is unknown; it may, in pact, be due to volatile products
IV-113
-------
of decomposition contained in the expired air of persons
having decayed teeth, foul mouths, or certain disorders o£
the digestive apparatus* and'it is due* in part, to volatile
fatty acids given off with, or produced from, the excretions
of the skin, and from clothing soiled with such excretions.
It may produce nausea and other disagreeable sensations in
specially susceptible persons, but moBt men coon become
accustomed to it, and cease to notice it, as they will do
with regard to the odor of a i»moking-cai, or of a soap
factory, after they have been for some time in the place.
The direct *nd indirect effects of odors of various kinds
upon the comfort, and perhaps also upon rhe health, of men
are more considerable than would be indicated by any tests
now known for determining the nature and quantity of the
matters which give rise to them. (pp. 24, 26-27)
This statement would prompt little dispute today.
A quarter-century after the experiments of Billings and colleagues,
a New York State commission focused on ventilation requirements for
occupied classrooms.*' Tests of such varied functions and indexes as
comfort, body temperature, intellectual performance, motivation,
respiration, metabolism, condition of the nasal mucosa, frequency of
colds, blood pressure, hematocrit, appetite, and rate of physical work
uncovered no cause for medical concern under normal conditions of
occupancy. This 8-yr effort reinforced notions that control of
occupancy odor should figure prominently in indoor-air quality control,
but the justification had to rest on grounds of comfort, rather than on
grounds of health. The first truly quantitative studies of ventilation
requirements started with the premise that ventilation primarily must
control occupancy odor.
Tobacco Smoking. Througnout the twentieth century, the air in
occupied rooms has commonly been smoky. Mainstream cigarette smoke
contains approximately 3,000 gaseous constituents,7* and these and
associated particulate matter may both constitute health hazards for
occupants. To add insult to injury, tobacco smoke forms the most
annoying and persistent indoor odor nuisance.** A survey of
professional ventilating engineers placed it well ahead of the next two
most disturbing indoor odorous contaminants, occupancy and cooking
odors. Its severity as a nuisance derives from its properties: it is
an apparent allergen for some persons; it is an eye, nose, and throat
irritant for most persons; it is an odorant; it is a soiling agent; and
it is a stimulus for chest discomfort in persons with angina pectoris.1' Tl
Its "tar" content causes it to adsorb strongly to surfaces. After
adsorption, it desorbs slowly and thereby promotes so-called secondary
sources of odor. In general, such sources concentrate previously
airborne odorants on their surfaces (e.g., air-conditioning coils) or
in their interstices (e.g., fabric). When the adsorbed odorants
desorb, they often have an odor character somewhat different from that
of the parent contaminant, and this generally seems true of tobacco
smoke.1 *
IV—114
-------
Tobacco-smoke odor increases in intensity and unpleasantness
immediately after active smoking has ceased and after the particulate-
vapor complex has adsorbed to surfaces." Figure IV-10 demonstrates
how odor increased in intensity during a period after cigarettes were
extinguished in an unventilated room. During this time* the odor
character changed from pungent and burnt to stale and sour. This
presumably reflected some chemical instability of the airborne matter.
The contaminants of mere occupancy also seem somewhat unstable; but,
unlike tobacco odor, occupancy odor diminishes rapidly and dramatically
with time (see Figure IV-10).
Cooking. One brand of cigarettes differs from another in type and
blend of tobacco, type of additives sprayed on the tobacco or paper,
and various other characteristics, such as porosity of paper and
temperature of the ember. *1 In spite of these variations, all
cigarettes give rise to an odor readily identifiable perceptually as
tobacco odor." In similar fashion, cooking gives rise to
perceptually characteristic odors. These do not possess quite the
simple integrity as a perceptual class as does tobacco-smoke odor.
Some cooking odors constitute more serious nuisances th*n others. Some
(e.g., cabbage odor) are generally considered disagreeable, whereas
others (e.g., baking odors) are generally considered inoffensive. Some
vapors (e.g., those from deep frying) adsorb tenaciously to surfaces
and therc.oy become long-term contaminants. During initial generation,
such vap?rs may evoke pungency, as well as odor; whether the pungency
derives ):rom organic gases generated by the reaction of tt> People will tolerate
inadequate control of cooking odors (e.g., operation of a ductless
range hood with a spent carbon filter) much more readily than
inadequate control of bathroom odors.
Odor Control. Elimination of the odor source, local axhaust,
general ventilation, and filtration (usually adsorption) are the
principal ways of controlling indoor malodors physically. Iri some
places, such as bathrooms and smoking areas, generation of malodoc may
exceed the limits of physical control and persons in ct.arge of
IV-115
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TIME AFTER SOURCE OF ODOR REMOVED (min.)
FIGURE IV-10 Decay of odor in still air in an unventilated
chamber after an open flask of valeric acid had been removed,
five cigarettes had been smoked, and a number of nonsmoking
occupants had left the chamber ("body odor"). Odor Judgments
were made by observers who entered momentarily from time to
time. Reprinted with permission from Yaglou and Witheridge.
IV-116
-------
maintenance resort to commercially marketed odor counteractants.*'
Such products generally comprise a fragrance base made up of many aroma
chemicals and possibly a single proprietary "active" ingredient.
Typically, a manufacturer claims that the product has eliminated the
objectionability or diminished the intensity of some standard malodor
in laboratory tests. The claim Invariably has some validity, because
all odorants, including malodorants, can influence the perception of
other odors. This rule forms the foundation of practical perfumery."
Basic research in olfaction supports the notion that a gas-phase
mixture of components generally has an oior less intense than the total
of the separate odors of the unmixed components,10 perhaps less
intense than some of its constituents alone—an extreme case of
perceptual hypoadditivity. 11 " The matter of alterations in odor
quality (character) has received little attention in the scientific
laboratory. The perfumer knows through experience how to manipulate or
blend malodorants to produce acceptability. Hence, some fruity-
smelling natural essences (always mixtures of constituents) may contain
some "subsurface" putrid-smelling constituents. The perfumer may
therefore blend a "deodorizing" fragranca that will assimilate a
putrid-smelling contaminant into a-fruity complex. When unable to
anticipate the particular malodorous quality of interest, the perfumer
generally blends a fragrance with a nondescript, unnameable odor
character. Such a broad-band masker may assimilate some malodors
readily, but at the very least adds perceptual "noise" to the
maldodorous environment. Eventually, the usual or frequent occupants
of a space may come to smell the malodorant through the olfactory
noise. Persons who ride airplanes often, for instance, eventually find
that the smoking area smells strongly of both tobacco smoke and masking
agent.
It might seem that deodorizing products are used commercially only
in special locations (e.g., bathrocis) or only on the occasions of
uncontrollable lualodorous emission (e.g., in the case of water damage
to upholstery). In fact, such products, under the generic name of
"reodorants," appear in virtually every cleaning product (e.g.,
degreasers, detergents, soaps, and fabric shampoos) and in many other
materials (e.g., fabrics, plastics, floor finishes, and carpets).
Reodorants are sometimes used to cov®r up undesirable ambient odors
(e.g., mildew in damp spaces) and often tc cover up the intrinsic odors
of manufactured products themselves (e.g., formaldehyde in
permanent-press fabrics). No matter what their purpose, reodorants and
odor counteractants have become permarjnt parts of the indoor
environment.*9
Building Materials and Furnishings
Almost any object indoors may serve as a primary or secondary
source of odor. Accordingly, the list of indoor odorous contaminants
could go on indefinitely. In fact, Jarke1" identified over 200
organic constituents in residences under conditions designed to
minimize active generation of contaminants. M^lhave and Miller*0
IV-117
-------
identified a similar number and noted that only six of 46 dwellings
seemed odorless.
The identities of the more common indoor contaminants led jarKe to
conclude that notable, more or less permanent sources include food*
plants, bodies, dry-cleaned clothes, cosmetics, household products,
attached garages, heating systems, new furniture, carpeting, and
redecorated surfaces. Chemical contamination is apprently much higher
in new than in old homes.'9 New materials require a considerable
amount of time to "cure" before the off-gassing of volatile odorous
substances diminishes to an imperceptible point. One pf the most
notorious of the odorous contaminants in new buildings is
formaldehyde.* It emanates from chipboard, panel adhesive, carpet
backing, vinyl wall-covering, resin-treated fabrics, and urea-
formaldehyde foam insulation. In some Danish homes, the concentration
of gas-phase formaldehyde has exceeded threshold limit values for
occupational exposure.9
Although formaldehyde has an odor, it has developed a reputation as
an olfactory anesthetic.51 The reason for its putative anesthetic
properties has not been fully studied. Conceivably, its irritant
properties play a role in the anesthetic phenomenon. Cain and
Murphy3* have reported that an irritant can immediately diminish and
actually block olfaction. This effect seems to occur through interplay
between sensory activity in the trigeminal nerve system and sensory
activity in the olfactory nerve system. The trigeminal nerve mediates
all cutaneous sensations of the face, as well as the pungency,
irritation, warmth, cooling, and pain that can arise from chemical
stimulation of mucosal tissue in the nose, mouth, and eyes. The
evidence suggests that the interaction between odor and irritation
takes place in the central nervous system and, hence, that it'would
hold true for virtually all combinations of odorous and irritating
stimuli. It seems relevant that various successful deodorizers have
contained irritants or pungent materials. For example, one commonly
used deodorizer of the wick type contained formaldehyde, and other
types of deodorizers contained other aldehydes. Ozone, a pungent gas,
has long had a reputation as a deodorizer, even at concentrations too
low to eliminate rnalodors through oxidation.75 The "fresh-air" smell
that deodorizers sometimes are claimed to produce can stem from the
pungency produced by these substances at low concentrations in the
product. Fresh Arctic air generally contains noticeable amounts of
ozone. Hence, the association of pungency with "fresh air" has some
basis in common experience. Nevertheless, the deliberate addition,
even at low concentrations, of products that aro irritating has
questionable justification.
Odors That Enter from Outdoors
in theory, ventilation dilutes and displaces contaminants that are
generated indoors. Bringing in odor-contaminated air for use in
ventilation to reduce odors obviously can defeat the purpose. Odorous
outside air is encountered in areas of great industrial pollution or
IV-118
-------
where micrqmeteorologic conditions allow entrainmerit of emitted
substances from local sources into intake vents. In recognition of the
possibility that the air used for ventilation sometimes fails to meet
normal standards of quality, the American Society of Heating,
Refrigerating and Air-Conditioning Engineers (ASHRAE) specified, in
Standards for Natural and Mechanical Ventilation,' that intake air
should meet both objective and subjective criteria for cleanliness. A
draft revision of this standard contains a list of notable outdoor
contaminants, some odorous and some nonodorous, and concentrations not
to be exceeded (see Table IV-21). Adherence to these criteria will not
guarantee the odorlessness of air, but will probably minimize
difficulties in polluted regions.
Odors may also be generated in the air delivery system itself.
Berglund and Lindvall11 discovered cases where the air supplied to a
room had a higher degree of odorant contamination than the air already
in the room. That can occur when air-to-air heat exchangers, installed
to conserve energy, allow exchange of organic materials between exhaust
and makeup air. Another source may be the accumulation of odorous
materials on roughing filters and cooling coils and in humidifiers in
the intake system.
MEASUREMENT OF ODOR
Odors have various attributes: intensity, quality (character),
affective charge (acceptability-objectionability), and duration. Most
environmental odorants are mixtures of substances. Hence, intensity
and character generally represent the net action and nonlinear
perceptual combination of various constituents. Figure IV-11 depicts a
gas chromatogram of a sample of odorous air (perspiration odor). In
this case, the odorous sample is split into two streams after it passes
through the column of the chromatograph.51 One stream goes to a
flame ionization detector and the other to a sniffing ^rrt, where the
experimenter can note the odor character associated with the various
chromatogram peaks. Such an odor-annotated chromatogram, called an
"odorogram," can help in deciding how many peaks (constituents) seem
odor-relevant, whether a few constituents seem particularly redolent of
the unfractionated sample, and whether there is a relationship between
the height of a peak and the magnitude of its odor. Often, a barely
detectable peak is related to a strong odor and an enormous peak to a
barely detectable odor. This situation reflects the nonuniform
sensitivity of the nose; some substances stimulate at much lower
concentrations than others. Table IV-22 shows, for instance, that
ethyl acr'/late stimulates at a concentration six orders of magnitude
below that of ethylene and five orders of magnitude below that of
acetone.Odor science has long sought, with limited success, to
account for such large disparities in stimulating efficiency.1' 26
IV-119
-------
TABLE IV-21
Ambient-Air Quality Standards for Notable Contaminants Unregulated
by Federal Clean Air Act®
Contaminant*"
Acetone
Acroleijj
Ammonia
Beryllium
Cadnium
Calcium oxide (l^me)
Carbon disulfide
Chlorine
Chromium
Cresol
Dichloroethan|
Ethyl acetatg
Formaldehyde
Hydrochloric aci^
Hydrogen sulfide
Mercaptans
Mercury
Methyl alcohol
Methylene chloride
Nickel
Nitrogen nonoxide
Phenol*
Sulfates
Sulfuric acid*
Trichloroethylene*
Vanadium
Zinc
LonR-Term Standard
Concentration
7 rog/m
0.5 mg/m3
0.01 lig/m
2.0 yg/nr
0.15 mg/m^
0.1 mg/m;j
1.5 yg/m
0.1 mg/m
2.0 mg/m-3
14 mg/m
0.4 mg/m"'
40-50 p g/m
2 ug/m^
1.5 ng/m
20 mg/ra
50 mg/m
2 yg/m ,
0.5 mg/m
0.1 mg/m
4 yg/m3..
12 vg/m
50 yg/ra
100 yg/n
2 mg/ra
5 mg/m
2 u g/n
50 ug/m
100 jjg/m
Period
24 h
1 yr
30 d
24 h
24 h
24 h
Short-Term Standard
Concentration Period1"
24
24
24
24
24 h
24 h
24 h
1 yr
24 h
24 h
24 h
24 h
1 yr
24 h
1 yr
24 h
1 yr
24 h
24 h
1 yr
24 h
24 mg/m
25 us/ar
7 mg/m
20-30 y
0.45 mg/m
0.3 mg/m
1
6.0 mg/m
42 mg/m3
150 yg/m
3 mg/m
*~2 yg/m
20 yg/m
O
4.5 mg/nr
150 mg/m
1 mg/m
200 yg/m"
16 mg/m
30 min
C
C
C
30 min
30 min
30 min
30 min
C
30 min
1 h
1 h
30 min
30 min
30 min
30 min
30 min
aReprinted with permission from ANSI/ASHRAE.^ Concentrations listed should be
corrected to standard conditions—25°C and 760 mm Hg.
^Contaminants marked with an asterisk have odor3 at concentrations sometimes
found in outdoor air; concentrations listed do not necessarily result in
absence of odor.
cC, ceiling (maximal allowable concentration).
IV-120
-------
KOVATS INDEX
600 1200 1400 1600 1800 2000
RETENTION TIME (min.)
FIGURE TV-11' Odor-annotated gae chrooatogram, called an
"odorogram." Test vapor was human perspiration. Annota-
tions refer to odor qualities noted by an observer when
various constituents (represented by peaks) eluted from
the chromatographic column. Reprinted with permission
from Dravnieks.
IV-121
-------
TABLE IV-22
Odor
Threshold and Quality of
Various Petrochemicals3
Threshold
Concentration
, ppm
50X
100X
Recog-
Recog-
Compound
Absolute
nition
nition
Quality
Acetone
20.0
32.5
140
Sweet-fruity
2,6-Butanol
0.30
1.0
2.0
Rancid-sweet
Di-N-butylamine
0.08
0.27
0.48
Fishy-amine
Dlethylamine
0.02
0.06
.0.06
Musty-fishy-amine
Ethyl acetate
6.3
13.2
13.2
Sweet-ester
Ethyl acrylate
0.0002
0.00030
0.00036
Sour-pungent
Ethylene
260
400
700
Olefinic
N-Ethyl morpholine
0.08
0.25
0.25
Ammonlacal
Isobutyl acetate
0.35
0.50
0.50
Sweet-ester
Isobutyl acrylate
0.002
0.009
0.012
Swee t-mus ty
Methanol
A.26
53.3
53.3
Sour-sharp
We thy letfty lketone
2.0
5.5
6.0
Sweet-sharp
2-Methyl-5-ethyl
0.006
0.008
0.010
Sour-pungent
pyridine
2,4-Pentanedione
0.01
0.020
0.024
Sour-rancid
Propanal
0.009
0.040
0. 080
Sweet-ester
Propionic acid
0.028
0.034
0.034
Sour
Propylene
22.5
67.6
67.6
Sharp-amine
a A
Data from Hellraan and Small.
IV-122
-------
Sample Collection
Procedures used to collect environmental samples for odor analysis
have begun to approach standardization. Figure IV-12 displays a
collector that contains the porous polymer material Tenax GC." Use
this adsorbent material avoids the need Cor solvents in collection
and analysis of air samples. A 2-L sample drawn through the collector
typically retains organic materials in a quantitatively faithful
fashion if their molecules have more than about six carton atoms. For
analysis of its contents/ the collector is connected to a gas
chromatography where flash-heating desorbs the contents into a stream
of inert carrier gas. New techniques, such as high-pressure
capillary-column chromatography, allow greater resolution and
sensitivity than could be achieved with packed columns of the sort used
to analyze the sample in Figure IV-11. Unfortunately, there is some
incompatibility between capillary injection and the odorogram procedure.
Psychophysical Analysis
The standardization that has evolved in the collection of samples
has extended also to psychophysical procedures foe evaluation of
environmental odors. The choice of procedures obviously depends on the
question of interest. A variety of techniques are used in the
laboratory, and a considerable number of techniques compete for
attention in the field. Nevertheless, techniques that have recently
emerged from activities of the ASTM Committee on Sensory Evaluation
seem reasonably stable and precise and therefore legitimate for use as
standard techniques. This section highlights these methods for the
assessment of important attributes of odor3.
Odor Character. The odor of any substance can be described
precisely by only one terra—the name of the substance itself. Stated
otherwise, the only precise name for the odor of a lemon is "lemon
odor," for the odor of a rose, "rose odor." and for the odor of a goat,
"goat odor." Unlike colors, tastes, and sounds, odors have never
given rise to their own glossary.17 Moreover, people often find it
difficult to retrieve the names of even familiar odors, not to mention
describing unfamiliar ones. ' * This situation motivated the
derivation of a list, of 146 descriptors to aid in the characterization
of odors (Figure IV-13).11 It seems necessary, if unwieldy, and has
led to surprising reliability in a multilaboratory comparison.'*
Earlier systems of odor classification, generally hierarchic, with a
small number of. major categories and associated subdivisions never
proved practical.ts
Data derived from the list of 146 odor descriptors can have
particular use in an effort to track down the source of a tnalodor,
particularly an episodic tnalodor. The list enables persons influenced
¦"by the sama malodor to express possible consensus regarding its
character. Without such uniform terminology, even articulate persons
often give such impoverished qualitative descriptions of malodors as
"stinky," "rotten," "yucky," and "foul."
IV-123
-------
Tenax GC
Glass
Wool
G C Port
l
I . iii.l
A
Collector
FIGURE IV-12 Tenax-filled collector for organic contaminants.
Insert shows details of connecting tha end of the collector to
the injection port of a gas chromatograph. Length of collector,
200 mm; outside diameter, 3.1 mm. Reprinted with permission
from Jarke.
IV-124
-------
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National Research Council. ¦*
-------
Odor Intensity. Prom the standpoint of environmental engineering»
intensity is the most important attribute of an odor. It also permits
relatively precise measurement by matching. A recently adopted ASTM
butanol reference scale has already served well in this capacity.*
The reference scale entails the use of an olfactometer that sets up
eight concentrations of butanol spanning a range of subjective
intensity from very wealt to very strong. As Figure IV-14 shows, an
observer seeks to find a nozzle on a lazy Susan that matches the
intensity of a test odor.11 Figure IV-15 gives an example of some
results obtained in this fashion."
Intranodality matching,, such as that used with the butanol
reference
-------
FICURE IV-14 A subject using the butanol olfactometer (lazy Susan
configuration.) to find an odor that matches an unknown stimulus.
As customarily arranged, t.ie device delivers concentrations that
range from 16 to 2,000 ppm. Concentration changes by a factor of
2 from port to port. Reprinted with permission from flavot Quality:
Objective Measurement. ^p* '
IV-127
-------
B
$
5
K
1
$
101 10^ lO1 10*
RELATIVE CONCENTRATION
FIGURE IV-15 Psychophysical functions for five odorants. Functions
were obtained by matching butanol (note left ordinate) to various
concentrations of each odorant. Right ordinate shows odor intensity
derived via the psychophysical function for butanol. Data from
Dravnieks and Laffort.
IV-128
-------
the same techniques as its Intensity. For Instance, Lindvall and
Svrisaon** used matching to hydrogen sulfide (rotten-egg odor) to
assess the unpleasantness of combustion-toilet emission. Many
investigators have used numerical scaling, sometimes ratio scaling,"
and sometimes category scaling.'* The category scales have typically
been bipolar, ranging, for instance, from -i (very unpleasant) to +3
(very pleasant),* Unfortunately, such a scale seems often to
misrepresent the variability of acceptability and objectionability in
the extremes of tne hedonic continuum. Accordingly, some persons have
used a line-marking or line-producing technique.41 This generally
involves a bipolar scale, but without fixed categories, and seems to
yield a mote realistic picture of response variability than does
category scaling.1* Other techniques of continuous, rather than
categoric, judgment may befiave just as well as line-marking, with
respect to response variability.
Odor Threshold. The measurement of odors has.often comprised
merely the measurement of the concentration (or dilution} necessary to
achieve some criterion of detectability. The literature on olfaction
contains well over 1,000 threshold values for odorants. All too
commonly, these were obtained by techniques devised specifically for
particular investigationsj*1 11 for this reason, the threshold value
for a particular odorant may vary widely, even by orders of magnitude,
from one investigation to another. Specific factors contributing to
this variability include the means of stimulus presentation to the
odor-panel member, judgmental factors, and the implicit or explicit
definition of threshold. Few experimenters have sought to verify the
reliability of the vessels or olfactometers used to present odorous
stimuli. Furthermore, each device customarily uses arbitrarily chosen
conditions [e.g., flowcate, temperature, humidity, and solvent), and
this often precludes comparison with results obtained with other
devices or, more Important, may preclude a comparison with typical
environmental conditions.
The psychophysical means of eliciting information on detectability
can alter apparent sensitivity by a factor of 100 or more.15
Presenting a pair of stimulus samples—one containing an odorant at a
fixed, weak concentration and the other containing only air—and
forcing the subject to choose one of the two in each of scores or
hundreds of trials will maximize detection. (This forced-choice
procedure could also offer one odorous sample and two blanks, etc.)
But presenting various concentrations randomly with no direct
comoarison stimulus ("blank") invites variability. One subject may set
a low criterion and say "yes* to almost anything. Another subject may
behave much more conservatively. Such differences between subjects
have given incentive to erect a new psychophysics of signal detection.*%
Because of its time-consuming demands in data collection, the theory of
signal detection i3 not popular with researchers. That theory
challenges the concept of threshold and Instead specifies, in
probabilistic ar.d relatively bias-free terms, the detectability of any
given signal. In this respect, it highlights the probabilistic nature
of all thresholds. Despite the layman's view, "threshold" hardly
IV-120
-------
refers to a concentration below which a normal person can never detect
odor. Even concentrations well below "threshold" may be detectable
with sufficient frequency to cause concern about the validity of the
threshold concentration.
Complications involved in the interpretation of existing threshold
data and pitfalls in the collection of new data raise the question of
whether "thresholds," or comparable indexes of detection, offer greater
benefits than suprathreshold matching. Nevertheless/ some persons will
undoubtedly choose threjhold measurement over matching. A relatively
new ASTM procedure at least offers some standardization. ' It
recommends three-alternative forced-choice presentations wherein one
nozzle of an air-dilution olfactometer presents an odorous stimulus at
a given dilution and two companion nozzles present odorless air.
Testing begins at a very low concentration and progresses to higher
concentrations until the subject detects the stimulus reliably.
Although the method contains arbitrary ingredients, it combines various
important features designed to minimize response bias; and it allows a
relatively speedy, if gross, estimate of the degree of dilution that a
sample of odorous air can withstand before it ceases to be detected
readily.
ODOR CONTROL
The control of odor should follow the same strategy as the control
of virtually any other type of indoor contaminant. The first 3tep
should involve gpod housekeeping and prevention of the source. This
will obviously fail in the many cases where tiie. mere presence and
normal activities of occupants inevitably give rise to odorous organic
materials. A second step would eliminate airborne contaminants, such
as kitchen odors, by lo^al exhaust.
In principle, the removal of odorous contaminants can follow one or
more of the classical strategies: oxidation (e.g., incineration),
scrubbing (e.g., spray-washing), chemical conversion (e.g.,
chlorination), filtration, and dilution.70 The first three of these
are used almost exclusively in the control of industrial odorous
emission. For odors in residential, commercial, and institutional
spaces, filtration and dilution are the methods of choice. The use of
deodorizers is justified only under unusual and temporary conditions.
Ventilation
Before the. development of mechanical ventilation, the entrance of
outsitfe air through windows was the means of both thermal and
contaminant control. The need for thermal control often dictated the
demand for outside air.11 Mechanical ventilation ^ysiems, however,
allowed separate control of the temperature and contaminants. The
amount of ventilation air necessary for control of contaminants
historically has been a matter of contention. Some persons argued for
ventilation rates that would render the air odorless. This strategy
IV-130
-------
rested on the premise that odor-laden air necessarily contained harmful
organic contaminants. Similarly, some argued for rates that would
maintain carbon dioxide at a concentration only twice that of the
ambient air.11 Here again, the strategy rested on the notion that
conservative control of a measurable (or, in the case of odors,
perceptible) contaminant, even a rather innocuous one, would take care
of unknown, but possibly harmful, airborne substances. This strategy
led to unreasonably high ventilation rates. To achieve a criterion of
approximate odorlessness, the ventilation rate must generally exceed 30
ft3/min (abput 14 L/sJ per occupant, even during nonsmoking occupancy.
The Hew York State Commission on Ventilation found that the
concentration of carbon dioxide in a normally ventilated schoolroom
correlated only weakly with odor.*' Hence, the use of one
contaminant seemed unable to predict the concentrations of all
contaminants. The correlation rule may actually work reasonably well
under conditions of active control of the delivery of ventilation
air.*1 Nevertheless, the New York State commission found that a rate
of 10-15 ft /min (about 4.7-7.1 L/s) per student in.a classroom with
about 250, ft (9 m3) per student sufficed to control odor and
carbon dioxide concentration reasonably well; furthermore, it seemed
acceptable on the basis of criteria of comfort, health, and
performance. In Winslow's7* words:
The chemical vitiation of the air of an occupied room (unless
poisons or dusts from industrial processes or defective heating
appliances are involved) is of relatively slight importance. The
organic substances present, manifest as body odors, may exert a
depressing effect upon inclination to work and upon appetite;
therefore occupied rooms should be free from odors which are
obvious to anyone entering from without. (Such odors are never
perceived by those who have been in the room while they have been
accumulating.) Objectionable effects of this sort have only been
demonstrated, however, with a carbon dioxide content of over .2
per cent, which would correspond to an air chanqa of less than 6
cubic feet per person per minute, (pp. 77-78)
As mechanical ventilation systems became more common, there was
more interest in discovering how the odor of a room would vary with
changes in the proportion of total supply air that consisted of
ventilation (.outdoor) air. Figure IV-16 depicts a functional relation
that Houghten and colleagues"7 erected from judgments in a juniop-
high-school classroom. The function, derived from judgments of
visitors who entered the occupied classroom briefly, intersects the
line equal to a judgment of 2 ("noticeable [odor] Dut not
objectionable") at a ventilation rate of about 11 ft3/min (about 5.2
L/s) per student. This outcome seemed to confirm the findings of the
New York State commission.
Experiments performed at the Harvard School of Public Health
shortly after the study of Houghten and colleagues implied that
ventilation requirements per occupant would vary with the amount of
space (volume) available to each occupant. Yaglou and colleagues71
IV-131
-------
L/SEC-PERSON
OUTDOOR AIR SUPPLY (CFM/PERSON)
FIGURE IV-16 Relation between odor intensity and ventilation ail
in junior-high-school classrooms. Observers entered the occupied
classroom from a relatively odor-free corridor. Adapted from
Houghten et al.
IV-132
-------
of Harvard, like Houghten et al., derived functions that related odor
to ventilation rate and added aucb variables as relative crowding,
hygiene* and age, Each variable had some influence* but crowding
(i.e.* occupant density in an experimental room) had the most
noteworthy influence. Figure IV-17 depicts ventilation requirements
decided by various criteria versus air space per occupant. Function C
represents requirements according to an odor criterion of "moderate" (a
rating of 2 on a scale of 0-5). It reflects the Intersection of this
perceived extent of odor with the various combinations of ventilation
rate and air space per person in the functions for occupancy odor
depicted in figure IV-18.
Although admittedly incomplete, the work of faglou et al. stands aa
the most definitive investigation of ventilation requirements ever
performed. It seemed to figure at least implicitly in the
recommendations of ASHHAE Standard 62-73* a standard based on
professional consensus.' As Figure IV-19 shows* the recommended
ventilation rates for a diverse group of residential and commercial
spaces follows much the sane curvature as the function of Yaglou et^
al.Almost all the recaimended rates fall above the function—an
unsurprising feature, inasmuch as most epaces have a higher odor load
than that imposed merely by sedentary occupancy. Cigarette-smoking,
for instance, leads to much higher ventilation requirements.
Unfortunately, the study shown in Figure IV-20 proffered the only
thorough look at the ventilation requirements necessary to control the
odor of fresh tobacco smoke.77 In many of the spaces represented in
Figure IV-17, smoking or some physical activity might occur. Curve D
in Figure IV-17 formed one attempt to account for the requirements In
spaces with such activities. The function, a 504 upward transposition
of curve C, apparently has no experimental justification, but may
nevertheless serve well as a rough guide for ventilation
requirements.71
See Chapter IX for more complete discussion of ventilation
standards.
Air-Cleaning
The principles of contaminant dilution and displacement, achieved
through ventilation, offer the simplest means of indoor contaminant
control. In some instances, however, ventilation alone proves
inefficient or ineffective. Other means of control can thvn assist.
Outdoor air sometimes contains unwanted concentrations of ccr-taminantB,
and recirculation of indoor air becomes desirable. For instance, the
outdoor air may contain enough sulfur dioxide to damage sensitive
electronic equipment. Filtration of one sort or another can reduce the
concentrations of the contaminant in the incoming air or, sometimes
more productively) can reduce the concentrations of the various
contaminants generated indoors and thereby, reduce reliance on the use
of contaminated outdoor air.** In principle, filtration of
recirculated air can achieve indoor air quality that exceeds that of
outdoor air. But in practice, filtration leaves some contaminants
(e.g., carbon monoxide and carbon dioxide) unattenuated. Only very
expensive procedures will eliminate these contaminants. Thus, an
IV-133
-------
FIGURE IV-17 Relation between ventilation rate and air space per
occupant according to four criteria: A, maintenance of oxygen;
B, control of carbon dioxide (<0.6%); C, control of body odor under
sedentary conditions (no smoking); and D, control of odor when
occupants were slightly active and when smoking was permitted.
Lower curve derived from data of Yaglou ££ al. Adapted from
Viessman.
IV-134
-------
AIR SPACE PER PERSON {m3J
9 10 <9
AIR SPACE PER PERSON (CO. FT.)
FIGURE IV-18 Odor intensity versus net air space per person for
ventilation rates of 5-30 cfm (2.5-15 L/s). Adapted from
Yaglou et_ al.
IV-IJ5
-------
AIR SPACE PER PERSON
-------
L/SEC • SMOKER
OUTSIDE AIR SUPPLY (cfm per smoker)
FIGURE IV-20 Variation in odor intensity with fresh air supply
when nine persons, including six smokers, occupied Yaglou's
chamber and smoked cigarettes at a iate of 24 per hour. Functions
labeled "smokers" amd "nonsmokers" depict judgments of occupants*
Function labeled "observers" depicts Judgments of persons who
entered briefly from an odor-free room. Adapted from Yaglou.
IV-137
-------
engineer or designer cannot rely entirely on recirculation, but must
deliver some minimal quantity of outdoor air. According to ASHRAE
guidelines,* the minimum should equal 5 ft^/iuin (about 2.4 L/s) P®r
person when the filtration system has high efficiency. This quantity
of air guarantees adequate control of carbon dioxide with a substantial
margin of safety. In a space that might normally demand outdoor air
at, say, 20 ft^/min (about 9.4 L/s) per occupant to control the
concentrations of organic materials generated during occupancy, use of
a high-efficiency filtration system could save considerable amounts of
the eneroy generally used to heat or cool ventilation air.
The characteristic way to clean indoor air involves the use of
granular filter media and', if necessary, particle filters.4 Particle
filtration will prove necessary in the presence of cigarette-smoking.
Some portion of tobacco-smoke odor is presumably eliminated by such
filtration. Particle filters protect the granular filter.
Activated carbon is the most common type of granular medium for
control of airborne organic matter." It removes most odorous
material and generally renders the air "fresh-smelling." Its adsorbent
property leads to actual retention of the contaminant up to a'
saturation point, when the filter b-ad must be replaced. Activated
carbon is available in many varieties, depending on starting materials
and production conditions,. Efficiency varies considerably, and life
span may be unpredictable. Such technical vagaries detract from the
use of activated carbon by nonspecialists, and it currently is little
used in ordinary ventilation systems. Other adsorbent materials, such
as porous polymers, have been.developed for gas chromatography,*• and
perhaps these now-costly materials will become cheap enough for 'use in
ventilation.
Finally, activated carbon or activated alumina can be impregnated
with other materials to increase efficacy against particular
contaminants. Activated alumina impregnated with postassium
permanganate, developed specifically for odor control, offers the most
readily available commercial alternative to activated charcoal.** It
operates by adsorption and oxidation and thereby capitalizes on an
empirically observed rule that a malodorant may lose its malodorous
properties when oxidized.
RESEARCH HEEDS
Ventilation Codes
A survey of building codes in the 1960s uncovered a tenfold
variation in the lists*? ventilation rates.1" Such variation reflects
in part the change in modes of thought regarding ventilation
requirements through the years. Some codes apparently arose from local
notions of "good engineering practice" and had seen little or no
revision in decades. In the late nineteenth century, the American
Society of Heating and Ventilating Engineers recommended 30 ft^/min
per occupant. As mentioned above, this value arose froT the notion
that ventilation should Keep the indoor concentration of carbon dioxide
IV-138
-------
at leas than twice its outdoor concentration. Forty years later, the
Society recommended a rate of 10 ftVmin per occupant. Although the
studies of the New York State commission and other researchers had made
it clear that a rate as low as 10 ft^/min per occupant would not lead
to harm, the members of the Society's committee apparently felt the
need for considerably more data. W. H. Driscoll, a member of the
committee, noted:7*
When we finally decided that we would take 10 cfm per person as
the minimum it was a sheer compromise* merely an attempt to finish
the work of the Committee and get the report before the Society.
There was a difference of opinion as to whether the 30 cu ft that
have been set up as a standard since time immemorial should be
adopted, or whether no cubic feet, tor which there wa3 very
aggressive support, not necessarily within the committee but from
outside of the Committee, on the theory that no scientific studies
had ever been made to support the necessity for the introduction
of any outdoor air as a ventilation requirement.
-------
Conservation in New Building Design.' The various model-code groups
(Building Officials and Codes Administrators International,
International Conference of Building Officials, and Southern Building
Code Congress International) have since cooperated with the National
Conference of States on Building Codes and Standards (NCSBCS) in
drawing up an energy-conservation code, Code for Energy Conservation in
New Building Construction. •' It too incorporated the minimal rates
of the ASHRAE ventilation standard.
An NCSBCS survey of building codes** conducted in May 1979
revealed widespread adoption of energy conservation in ventilation
(Table IV-23). Virtually all large jurisdictions have conformed or
will soon conform to conservation standards through adherence to one or
another model code, a. separate state code rooted in a model code, or
ASHRAS Standard 90-75. At the time of the survey, only five
jurisdictions had failed to take overt action toward the adoption of an
energy-efficient code.
Energy Efficiency, Comfort,.and Health
Both the recommended and minimal ventilation rates in ASHRAE
Standard 62-73 comprise consensus values. Except, perhaps, for spaces
with unexpectedly high rates of cigarette-smoking, the recommended
values probably serve well. In some spaces with' heavy smoking or
cooking, the minimal values will probably serve very poorly. Without s
foundation of mclern research on a variety of contaminants, the
justification of the minimal values will rest heavily on considerations
of energy, rather than health. The research must seek to specify rates
and strategies that will achieve both energy efficiency and healthful
conditions. This will eventually require strict control over the
internal atmosphere. Without guidance, some engineers will shut down
intake-air dampers to save fuel and will thereafter rely on
infiltration alone for fresh air. This strategy actually reduces,
rather than increases, the engineer's active control over the building.
The dimensions of ventilation research are roughly the same now as
in the time of the work of Yaglou e£ al. Ventilation dilutes
contaminants. Its efficacy depends on the nature of indoor
contaminants, the size of a space, environmental variables,
furnishings, duration of occupancy, aesthetic standards of occupants of
or visitors to the space, and sensitivity of occupants. Modern methods
available for experimentation include the newly standarized
psychophysical methods discussed here and mor.itoring equipment not
available during earlier research on ventilation (e.g., continuous
carbon monoxide analyzer, continuous carbon dioxide analyzer, gas
chromatograph, mass spectrometer, particle-mass monitor, condensation
nucleus counter, and electric aerosol analyzer), with these various
tools, it is now possible to characterize the indoor environment in
both a psychophysical and a physicochemical manner. Such
characterization has now begun in North America and Europe."
IV-140
-------
TABLE IV-23
NCSBCS Survey of Energy-Conservation Codes3
Energy-
Conservation
Jurisdiction
Code
Alabama
SBCCI
Alaska
(ASHRAE 90-7|)
Arizona
(Slate coJe)^
Arkansas
(State code)
California
State code
Colorado
MCEC
Connecticut
State code
Delaware
(MCEC)
District of
(City code)
Columbia
Florida
State code
Georgia
MCEC
Hawaii
ICBO
Idaho
tCBO
Illinois
(State code)
Indiana
MCEC
Iowa
MCEC
Kansas
State code
Kentucky
MCEC
Louisiana
(MCEC)
Maine
(State code)
Maryland
(ASHRAE 90-75)
Massachusetts
MCEC
Michigan
ASHRAE 90-75
Minnesota
ASHRAE 90-75
Mississippi
(MCEC)
Missouri
(MCEC)
Montana
MCEC
Energy-
Conservation
Jurisdiction
Code
Nebraska
(ICBO)
Nevada
MCEC
New Hampshire
MCEC
New Jersey
BOCA
New Mexico
ICBO t
New York
State code
North Carolina
State code
North Dakota
ICBO
Ohio
MCEC
Oklahoma
None
Oregon
ICBO
Pennsylvania
(ASHRAE 90-75)
Rhode Island
ASHRAE 90-75
South Carolina
SBCCI
South Dakota
(MCEC)
Tennessee
MCEC
Texas
(MCEC)
Utah
MCEC
Vermont
(ASHRAE 90-75)
Virginia
BOCA, ASHRAE 90'
Washington
State code
West Virginia
None
Wisconsin
State code
Wyoming
ICBO
American Samoa
MCEC
Guam
ICBO
Puerto Rico
MCEC
a( ) denotes that legislation Is pending.
ASHRAE 90-75' = ASHRAE STANDARD 90-75.
BOCA 3 Model Code, Building Officials & Code Administrators International,, Inc.
ICBO = Model Code, International Conference of Building Officials.
MCEC *» Modal Code for Energy Conservation In New Building Construction.
SBCCi = Model Code, Southern Building Code Congress International Inc.
Asterisk denotes obvious incorporation of energy-conserving aspects of a model
code or ASHRAE 90-75; codes or pending codes for California, Maine, and
North Carolina also include some such aspects.
IV-1A1
-------
REFERENCES
1. American National Standards Institute* and Society of Heating*
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Air-Conditioning Engineers, Inc., 1981. 48 pp.
2. American Society for Testing and Materials. ASTM E 544-75. Standard
Recommended Practices for Referencing Suprathreshold Odor
Intensity. Philadelphia: American Society for Testing and
Materials, 1975.
3. American Society for Testing and Materials. ASTM D 1391. Standard
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1978.
4. American Society of Keating, Refrigerating and Air-Conditioning
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5. American Society of Heating, Refrigerating and Air-Conditioning
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Refrigerating and Air-Conditioning Engineers, Inc., 1975. 53 pp.
6. American Society of Heating, Refrigerating anr. Air-Conditioning
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9. Andersen, I., G. R. Lundqvist, and L. Molhave. Indoor air pollution
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10. Berglund, B. Quantitative and qualitative analysis of industrial
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IV-142
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12. an^insa, J. S., s. w. Mitchell, and D. H. Bergey. The composition
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15. Cain* W. S. History of research on smell, pp. 197-229. In E. C.
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16. Gain, w. s. Interactions among odors, environmental factors and
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17. Cain, W. S. Physical and cognitive limitations on olfactory
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13. Cain, W. S. To know with the nose: Keys to odor identification.
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19. Cain, W. S. Sensory attributes of cigarette smoking. In G. B. Gori
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20. Cain, W. S. The odoriferous environment and the application of
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21. Cain, W. S. Ventilation and odor control: Prospects for energy
savings. ASHRAE Trans. 8S(Pt. 1):784«793, 1979.
22. Cain, W. S., L. G. Berglund, R. A. Duffee, and A. Turk. Ventilation
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23. Cain, W. S., and M. Drexler. Scope and evaluation of odor
counteraction and masking. Ann. N.Y. Acad. Sci. 237:427-439, 1974.
24. Cain, W. S., and T. Engen. Olfactory adaptation and the scaling of
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The Rockefeller University Press, 1969.
25. Cain, w. S., and F. Johnson, Jr. Lability of odor pleasantness:
Influence of mere exposure. Perception 7:459-465, 1978.
26. Cain, W. S., and C. L. Murphy. Interaction between chemoreceptive
modalities of odor and irritation. Nature 284-255-257, 1980.
2 7. Chapln, C. V. The Sources and Modes of Infection. New York: John
Wiley l Sons, 1910. 399 pp.
IV-143
-------
28. Davies, J. T. Olfactory theories, pp. 322-350. In L. M. Beidler,
Ed. Handbook of Sensory Physiology. Vol. IV. Chemical Senses. Part
1. Olfaction. Berlin: Springer-Verlag, 1971.
29. Degobert, P. Hedonic and intensity ranking of different malodours
by category estimation and paired comparison, pp. 107-121. In J. H.
A. Kroeze, Ed. Preference Behaviour and Chemoreception. London:
Information Retrieval Ltd., 1979.
30. Doty, R. L. An examination of relationships between the
pleasantness, intensity, and concentration of 10 odorous, stimuli.
Percept. Psychophys. 17:492-496, 1975.
31. Dravnieks, A. Correlation of odor intensities and vapor pressures
with structural properties of odorants, pp. 11-28. In R. A.
Scanlan, Ed. Flavor Quality: Objective Measurement. American
Chemical Society Symposium Series, No. 51. Washington, D.C.:
American Chemical Society, 1977.
32. Dravnieks, A. Evaluation of human, body odors: Methods and
interpretations. J. Soc. Cosinet. Chem. 26:551-571, 1975.
33. Dravnieks, A. Fundamental considerations'and. methods for measuring
air pollution odors, pp. 429-436. In J. LeMagren and P. MacLeod,
Eds. Olfaction and Taste. VI. London: Information Retrieval Ltd.,
1978.
34. Dravnieks, A. Measurement of odors in an indoor environment, pp.
127-139. In P.O. Fanger, and 0 Valbj^rn, Eds. Indoor Climate.
Effects on Human Comfort, Performance, and Health in Residential,
Commercial, and Light-Industry Buildings. Proceedings of the First
International Indoor Climate Symposium1, Coperlhagen, August 30-
September 1, 1978. Copenhagen: Danish Building Research Institute,
1979.
35. Dravnieks, A. Organic Contaminants in Indoor Air and Their
Relationship to Outdoor Contaminants. Phase I, ASHRAE Research
Project 183. IIT Research Institute. New York: American Society of
Heating, Refrigerating and Air-Conditioning Engineers, Inc.,
February 1977. (unpublished)
36. Dravnieks, A., F. C. Bock, J. J. Powers, M. Tibbetts, and M. Ford.
Comparison of odors directly and through profiling. Chem. Senses
Flavor 3:191-225, 1978.
37. Dravnieks, A., and P. Laffort. Physico-chemical basis of
quantitative and qualitative odor discrimination in humans, pp.
142-148. In D. Schneider, Ed. Olfaction and Taste. IV. Stuttgart:
Wissenschaftliche Verlagsgesellschaft MBH, 1972.
38. Engen, T. Psychophysics. 1. Discrimination and detection, pp.11-46.
In J. W. Kling and L. A; Riggs, Eds. Woodworth and Schlosberg's
Experimental Psychology. 3rd ed. New York: Holt, Rinehart and
Winston, .Inc., 1972.
39. Engen, T., and D. H. McBurney. Magnitude and category scales of the
pleasantness of odors. J. Exp. Psychol. 68:435-440, 1964.
40. Evans, ,C. D., K. Warner, G. R. List, and J. C. Cowan. Room odor
evaluation of oils and cooking fats. J. Am. Oil Chem. Soc.
49:578-582, 1972.
41. Fazzalari, F. A., Ed. Compilation of Odor and Taste Threshold
Values Data. Philadelphia: American Society for Testing and
Materials, 1978. 497 pp.
IV-144
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42. Gori, G. B. Low-risk cigarettes: A prescription. Science
194:1243-1246, 1976.
43. Haggard, H. W. Devils, Drugs, and Doctors. The Story of the Science
of Healing from hedicine-Man to Doctor. New York: Harper &
brothers, 1929. 405 pp.
44. Banna, G. P., and R. L. Kuehner. Critical Factors in Odorant
Measurement and Control. ASHRAE Symposium Bulletin CH-69-2:66-72,
January 27-30, 1969.
45. Hanna, G. F., R. L. Kuehner, J. D. Karnes, and R. Garbowicz. A
chemical method for odor control. Ann. N.Y. Acad. Sci. 116:6.63-675,
1964.
46. Hellman, T. M., and F. H. Small. Characterization of the odor
properties ot 101 petrochemicals using sensory methods. J. Air
Follut. Control Assoc. 24:979-982, 1974.
47. Houghten, F. C., H. H. Trimble, C. Gutberlet, and M. F.
Lichtenfels. Classroom odors with reduced outside air supply. ASHVE
Trans. 41:253-267, 1935.
48. Jarke, F. H. Organic Contaminants in Indoor Air and Their Relation
to Outdoor Contaminants. Final Report of ASHRAE Research Project
183, December 1979.
49. Jellinek, J. S. The Use of Fragrance in Consumer Products. New
York: John Wiley & Sons, Inc., 1975. 219 pp.
50. Kalika, P. W., J. K. Holcombe, and W. A. Cote. The re-use of
interior air. ASHRAE J. 12(11):44-48, 1970.
51. Klauss, A. K., K. H. Tull, L. H. Roots, and J. R. Pfafflin. History
of the changing concepts in ventilation requirements. ASHRAE J.
12(6}:51-55, 1970.
52. Kulka, K. Odor control by modification. Ann. N.Y. Acad. Stfi.
116:676-681, 1964.
53. Kusiida, T. Control of ventilation to conserve energy while
maintaining acceptable indoor air quality. ASHRAE Trans.
82(Pt.l):1169-1181, 1976.
54. Leonardos, G., and D, A. Kendall. Questionnaire study on odor
problems of enclosed space. ASHRAE Trans. 77(Pt. 1) :101-112, 1971.
55. Lindvall, T. On sensory evaluation of odorous air pollutant
intensities. Measurements of odoi intensity in the laboratory and
in the field with special reference to effluents of sulfate pulp
factories. Nord. Hyg. Tidskr. Suppl. 2:1-181, 1970.
56. Lindvall, T., and L. T. Svens'son. Equal unpleasantness matching of
maloaorous substances in the community. J. Appl. Psychol.
59:264-269, 1974.
57. Lundqvist, G. R. The effect of smoking on ventilation requirements,
pp. 275-292 (includes discussion). In P.O. Fanger, ana 0. Valbj^rn,
Eds. Indoor Climate. Effects on Human Comfort, Performance, and
Health in Residential, Commercial, and Light-Industry Buildings.
Proceedings of the First International Indoor Climate Symposium,
Copenhagen, August 30-September 1, 1978. Copenhagen: Danish
Building Research Institute, 1979.
58. Marks, L. E. Sensory Processes. The New Psychophysics. New York:
Academic Press, Inc., 1974.
IV-145
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59. McCord, C. P., and W. N. Witheridge. Odors. Physiology and control.
New York: McGraw-Hill Book Company, Inc., 1949. 405 pp.
60. Mjilhave, L., and J. Miller. The atmospheric environment in modern
Danish dwellings—Measurements in 39 Ilats, pp. 171-166. In P. 0.
Fanger and 0. Valbj^rn, Eds. Indoor Climate. Effects on Human
Comfort, Performance, and Health in Residential, Commercial, and
Light-Industry Buildings. Proceedings of the First International
Indoor Climate Symposium, Copenhagen, August 30-September 1, 1978.
Copenhagen: Danist. Building Research Institute, 1979
61. Moskowitz, H. R., A. Dravriieks, W. S. Cain, and A. Turk,
standardized procedure for expressing odor intensity. Chem. Senses
Flavor 1:235-237, 1974.
62. Moskowitz, H. R., A. Dravnieks, and L. A. Klarman. Odor intensity
and pleasantness for a diverse set of odorsnts. Percept.
Psychophys. 19:122-128, 1976.
63. National Conference of States on .Building Codes and Standards. Code
for Energy Conservation in,New Building Construction. McLean, Va.:
National Conference of States on Building Codes and Standards, 1977.
64. National Conference of States on Building Codes and Standards.
Survey of Energy Efficient Building Codes. McLean, Va.: National
Conference of States on Building Codes ana Standards, 1979.
65. National Research Council, Committee on Odors from Stationary and
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Washington, D.C.: National Academy of Sciences, 1979. 491 pp.
66. New York State Commission on Ventilation. Ventilation. New York:
E. P. Dutton & Company, 1923.
67. Stevens, S. S. Psychophysics: Introduction to Its Perceptual,
Neural, and Social Prospects. New York: John Wiley 6 Sons, Inc.#
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68. Turk, A. Absorption, Chapter 8. In A. C. Stern, Ed. Air Pollution.
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70. Turk, A., R. C. Haring, and R. W. Okey. Odor control technology.
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IV-146
-------
77. Yaglou, C. P. Ventilation requirements for cigarette smoke. ASHAE
Trans. 61:25-32, 1955.
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(Part 2). ASHVE Trans. 43:423-436, 1937. (includes discussion)
TEMPERATURE AND HUMIDITY
The atmosphere not only has an important role in respiratory gas
exchange (supplying oxygen and accepting carbon dioxide), but also
serves as the heat-exchange medium surrounding the human body.
Atmospheric pressure, including its constituents and especially
water-vapor pressure, environmental temperature, and the rate of air
movement all affect rates of heat loss and heat gain. A change in the
rate of heat loss or heat gain ultimately has an effect on body heat
content and body temperature.
Human body temperatures are maintained w'thin very narrow ranges
either by involuntary physiologic responses controlled by the
thermoregulatory system or by behavioral adjustments that modify the
thermal environment toward thermal equilibrium. The physiologic
responses are proportional to deviations from preferred body
temperature, especially chose associated with the hypothalamic region
of the brain. Behavioral adjustments are proportional to deviations in
thermal sensation and thermal comfort from thermoneutral and
acceptable, respectively. In general, people prefer to use the
behavioral adjustments, rather than having to rely on the physiologic
responses.
The thermal state of the human body can be described by the heac
balance equation:
S=»M-E-W-R-C, (1)
in which S = rate of storage of body heat,
M » rate of metabolic heat production,
E » rate of evaporative heat loss,
W a rate of external work done,
R a rate of radiant heat loss, and
C » rate of convective heat loss.
All the above terms are usually expressed in watts pec square meter of
skin surface aroa. Body surface areas in adults range from 1.6 to 2.2
m2 and can be estimated by Equation 2 from height and weight:
Aq » 0.202 m°-425H°-725, (2)
in which AD = body surface area, m2,
m = body weight, kg, and
H = body height, m.
IV-147
-------
Except for short periods, Equation 1 should result in values o£ S
very near zero. Any deviation from zero results in lowering or
raising of body temperature (hypothermia or hyperthermia,
respectively), with adverse consequences for health and well-being.
The metabolic heat generated in the body varies from a minimum of 45
W/ra2 to a maximum that varies between 600 and 900 W/ra2 for short
periods.
2
Heat losses in- excess of 45 W/m in the resting state tend to
produce hypothermia in some people. Depending on the individual,
evaporative heat loss roust be at least 100-300 W/m to prevent
hyperthermia under conditions of sustained hard work. The range of
deep-body temperatures that can be encountered is shown in
diagrammatic form in Figure IV-21. A range of ambient temperatures
with the appropriate responses is shown in Figure IV-22, and a range
of metabolic rates associated with some typical activities is
presented in Figure IV-23.
As is evident from the heat-balance equation, many factors
determine the heat balance, and they must always be evaluated
simultaneously. Energy-conservation strategies may involve lower or
higher air temperatures, higher or lower vapor pressures, and higher
or lower air velocities. Interruptions in energy supplies can result
in sharply higher or lower air temperatures, t-rhich can have additional
adverse health effects.
HEAT EXCHANGE WITH THE INDOOR ATMOSPHERE
A complete assessment of heat exchange between man and his thermal
environment can be found in a recent review by Gagge and Nishi.'
The following is a limited overview.
Whenever the value of S differs from zero in the heat-balance
equation, body temperature will change. At an average body weight of
40 kg/m2 and a weighted average specific heat of 36.5
Wh,0C*:n-2, it follows that, for example, with S at 36.5 W/m2
for 1 h, the average body temperature will rise by 1°C.
The rate of metabolic heat production, M, cannot be reduced to
below about 40 W/m , but can rise to as high as 800 W/m2 during
maximal exercise. Heat exchange by convection (C), by radiation (R),
and by evaporation (E) is affected by ambient temperature Ta, by air
velocity, and by clothing insulation. For a nude person, convective
heat exchange in still air (velocity, V, less than 1 m/s) is
approximated by:
C. = hp (Tg — Tj) , (3)
in which C = convective heat exchange, W/m2,
hc = convective-heat-transfer coefficient, W*m-2*aC-^,
Ts mean weighted skin temperature, °C, and
Tfl = ambient air temperature, °C.
IV-148
-------
°F
108
106 —
104
102 —
100 —
98 —
°C
42
41
40
¦ 39
-38
- 3?
— 36
96-
94 —
92 —
- 35
-34
Hyperthermia
Very Hard Exercin
Hard
* Exercise
Moderate
• Normal
Range
at Rett
Early Morning
Cold Weather
Exposure
Hypothermia
— 33
RECTAL TEMPERATURE
FIGURE IV-21 Range of rectal temperatures encountered in different
conditions. Temperatures designated as "hyperthermia* and "hypo-
thermia" are associated with Increased risk to health and should be
avoided.
IV-149
-------
- 40
-30n
30-
20-
c
50
F
i20-
110 —
100-
90-
80-
70-
60-
50-- 10
40-
BEHAVIORAL
REGULATION
- 20
THERMAL
COMFORT
- 0
I--10
BEHAVIORAL
REGULATION
PHYSIOLOGIC
THERMOREGULATION
FIGURE IV-22 The range for thermal comfort assumes minimal clothing
at the high end and substantial clothing at the low end and thus
includes somj behavioral regulation. The zones designated "behavioral
regulation" require modification by neanG other than clothings "Phys-
iologic thermoregulation" indicates the limits of short-term physio-
logic regulation in a healthy person at rest with minimal clothing.
IV- ISO
-------
w/m2
300
280
260
240
220
200
180
160 f—
140
120
100
80
60 -
40
Sawing Wood by Hartd
Ttbte Ttfinit
— Slow Walking
Typing
Sloping
METABOLIC RATES
FIGURE IV-23 Metabolic heat production rates associated with various
activities. Adapted from Aerenson and Robertson.
IV- 151
-------
The convective-heat-transfer coefficient depends on position and
posture and on air velocity. Seasonable estimates of hc are about 4
W*m~2«°c~^ in still air and 11.6 V0'® air with a velocity of
over 0.2 m/s.11 The human body also exchanges heat by radiation.
The radiant environment is usually characterized by a mean radiant
temperature (Tr) or by an effective radiant field (Hr) in watts per
square meter. Equation 4 shows the conversion between these terms:
Hr = hr{Tr-Ta), (4)
in which hr = radiant-heat-transfer coefficient.
A reasonable approximation of hc is 4.5 W»m""2«0C-1 at a
skin temperature of 34°C and an ambient temperature of 29°C. It is
often convenient, especially when Tr and Ta are relatively close
together, to combine radiation and convection into an overall
neat-transfer coefficient, h, and to use the operative temperature,
Tq, for the thermal environment. Operative temperature is the
temperature of an environment with uniform air and wall temperature
thci; exchanges heat with the body at the same rate as with the complex
environment that it describes. The combined heat-tiansfer coefficient
(h) in still air is about 8-10 W»m~2,0C-1.
The use of clothing reduces the heat exchange with the
environment. This insulation, IciQ, is usually expressed in clo
units; 1 clo unit corresponds to insulation at 0.155
¦ra2,"C'Vk-1. The reciprocal of Ici0 is hc^, the conductance
of clothing. If clothing efficiency is F^, then
*cl n Ucl/thcl + h) = 1/(1 + 0.155hIclo), (5)
and the total radiant and convective heat transfer with clothing
becomes:
R+C = Fclh{Ts - Tq). (6)
Fc^ varies from 1 for a nude man down to 0.25 for heavy,winter
clothing, including an overcoat. The temperature at which man feels
thermoneutral at rest varies with clothing. At Fc^ = 1,
thermoneutrality occurs at 28°C; at Fc^ " 0.25, it occurs at 15°C.
Figure IV-24 further illustrates the relationship between clothing and
temperature for thermoneutrality.
At temperatures above thermoneutrality, or when increased metabolic
heat production' exceeds loss of "dry" heat to the environment, sweat is
secreted and the resulting evaporative heat loss (E) restores overall
thermal equilibrium., For every gram of sweat that evaporates from the
skin, 0.68 Wh of heat is lost from the skin. The maximal evaporative
heat loss is limited by the maximal amount- of sweat that can be
secreted (about 1,500 g/h) and by the evaporative power of the
environment. The maximal rate of evaporation, E^x, from *>.
completely wetted skin is given in Equation 7:
IV-152
-------
o
-I
o
2
O
D
(/)
Z
o
X
I-
o
-I
o
OPERATIVE TEMPERATURE < C)
18 20 22 24 26
68 72 76 80
OPERATIVE TEMPERATURE (°F)
FIGURE IV-24 Effect of interaction of operative temperature and clothing
insulation on thenaoneutrality, and aabient temperatures accepted by 802
of people when sedentary at minimal air velocity.
IV- 153
-------
®ma x
2.2hc(Psj( - pdp^ypcl' C'
in which Emax " naximal evaporative rate# W/ta2,
2.2 - Lewis relation, *C/Torr,
hc a convective beat transfer coefficient,
W«a~2*°C~l,
psk a saturated water-vapor pressure at skin,
Pjp » water-vapor pressure in the atmosphere, Torr, and
Fpcl 11 Nishi permeation factor. "
For most types of porous clothing, Niahi and Gagge11 have shown
experimentally that
Fpcl = I/*1 + 0.143hcXclo). (8)
If the evaporative heat loss required for thermal equilibrium (Ereg'
is less than Bmax, the skin vij.1 be less than 100% wet. If W is the
percent of 9kin surface area wetted by sweat, then
E
re^^max*
Increasing values of w produce increasing discomfort. The value of
Eroaj, is decreased by adding clothing, by increasing water-vapor
pressure, and by lowering air velocity. Lowering the humidity,
reducing clothing, and increasing air velocity reduce W and physiologic
3train and increase thermal comfort.
PHYSIOLOGIC RESPONSES TO THE THERMAL ENVIRONMENT
In environments in which the body tends to lose or gain heat, body
temperature changes. Such changes produce physiologic responses aimed
at keeping body temperature constant. When body temperature falls,
skin temperature tends to fall first, and then (more gradually)
deep-body temperature. The first physiologic response is a reduction
in blood flow to the extremities and to the skin in general.
Peripheral vasoconstriction reduces the convective heat transfer
between the skin and the trunk core and causes rapid lowering of the
temperature of hands and feet while reducing the loss of heat from the
core, normal skin blood flow is at about 250 ml/oin and can easily be
reduced to 50 ml/min or less. If further reduction occurs in body
temperature, the thermoregulatory system causes an increase in
metabolic heat production through involuntary shivering, which can add
100-150 W/m^ to the basal 40 W/m^.
If, however, the thermal environment causes body temperature to
rise, the initial physiologic response is an increase in blood flow to
the extremities and the skin, vasodilatation increases the convective
heat transfer between the skin and the trunk core. The normal skin
blood flow of 250 ml/min cau be increased to as much as 3,000 ml/min-
affective overall thermal conductance between skin and core is about 16
with a low of S W*te~2*°C"3' in the cold and a high
IV-154
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of 100 in the heat. Increased body temperature also
causes the secretion of sweat over most of the skin suiface area at
rates proportional to the body-temperatuce increase. Above the
sweating threshold, a further laC rise in nean body temperature
produces sweat secretion st 200-600 q "ni~2 corresponding to
evaporative heat loss at 150-400 W/m . Foe a more complete and
quantitative review of human tnermoregulation, the reader is referred
to Stolwijk and Hardy. 14
The involuntary physiologic responses just described are usually
associated with feelings of thermal discomfort. Relationships among
ambient temperature, therijial pleasantness, comfort, and temperature
sensation are illustrated in Figure XV-25. Prediction of thermal
sensation, thermal comfort, and thermal acceptability must take into
account all factors involved in heat production, heat los3, and
heat transfer; and it must do it simultaneously. In a nearly steady
state, this is fairly feasible, but it becomes more complex when body
temperature or ambient temperature is changing.
Berglund and Gonzalez' evaluated the effect of slowly changing
ambient temperature and water-vapor pressure and found that
environmental temperature changes of 0.6®C/h from a 25°C starting point
were quite acceptable, as were changes in the water-vapor pressure, as
long as the instantaneous water-vapor pressure was kept below 16 Torr.
Internal body temperature has a considerable effect on comfort
sensation. When the body interior is hyperthermic, as after vigorous
exercise, a low air temperature even at high velocity (cold draft) is
felt as comfortable and pleasant, although the same cold draft would be
extremely uncomfortable to a person who is already slightly hypothermic
from a previous exposure to colcl. A hypothermic pecsan would prefer
very warm air, which in turn would be felt as very uncomfortable by
someone in a hyperthermic state.
There is general agreement that age, gender, and physical fitness
do not affect preferred ambient temperature, if metabolic heat
production and clothing insulation are constant.
When people are exposed to thermal conditions outside the comfort
range, the extent of their discomfort is affected by age, gender, and
physical fitness, even if activity and. clothing are controlled. The
extent' of discomfort is closely correlated with physiologic
thermoregulatory responses. Those who have a vigorous involuntary
response', such as sweat secretion on body warming, experience more
intensive and earlier discomfort than those whose sweat secretion
begins at higher body temperature.
When a space has thermal nor.uniformities (such as vertical
temperature gradients} or radiant nonuniformities (such as radiant
temperature in one direction 10°C higher than in another direction),
such nonuniformitiea can be perceived as uncomfortable, even if the
average temperature is in the comfortable zone.
In a cool or thermoneutral environment, increased air movement is
felt as uncomfortable; but at temperatures above thermoneutrality,
increased air movement is desirable and extends the comfort zone to
higher ambient temperatures.
IV-155
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Pleatantneif
Comfort
unpleasant
*er' uncomfortable
Slightly unpleasant
Uncomfortable
Indifferent
Slightly uncomfortable
Pleasant
Comfortable
~ Pleatantnet*
O Comfort
• Temperature Seniallon
Thermal
Seniotion
Cold Hot
Cool Warm
"am
Neutral
15 20 23 30 35 40 45
AMBIENT AIR TEMPERATURE
50 *C
FIGURE IV-25 Reports "of pleasantness, comfort sensation, and thermal sensation from sedentary
subjects In minimal clothing In environments with low air velocities and uniform air an
-------
HEALTH CONSEQUENCES OF EXTREMES OF TEMPERATURE AMD HUMIDITY
Adverse health effects of extremes of temperature and humidity are
in several categories. As extremes of temperature and humidity, we
designate operative temperatures below 18®C and above 30°C and
humidities below 4 Torr and above 16 Torr water-vapor pressure, for
people in conventional clothing, and at rest. Any temperature or water-
vapor pressure that requires physiologic responses makes demands on the
reserves of the systems that regulate cardiovascular function or fluid
balance. In healthy people, these responses reduce such reserves, thus
perhaps interfering temporarily with work capacity or limiting athletic
achievement. In diseased persons, such as those with cardiovascular
disease, such reserves are very small or nonexistent; such persons can
be seriously threatened by even small excursions of temperature or
water-vapor pressure.
Assessments of health consequences o£ extremes of temperature and
humidity tend to be based on two kinds of observations: observations
of acutely ill j-opie whose status call be correlated with temperature
measurements in their hospital rooms, and observations in epidemiologic
studies of whole populations, with daily outdoor temperatures
correlated with daily mortality or with the number of emergency-room
visits. In the firBt case, the number of patients observed is
relatively small, and each patient has a different disease stater it is
difficult to draw very detailed conclusions from such observations. In
the second case, very large populations can be observed, but it is
difficult to evaluate actual exposure and to assess the pre-existing
disease of those who have died.
Clinical reports of particular sensitivity of patients with
congestive heart failurs to hot and humid environments have been
presented by Burch and co-workers.'"* Ellis,' Schuman,1* and
Oechsli and Buechley1' have reported on excess mortality in
populations exposed to unusually hot weather. Thi9 excess mortality
occurred particularly among the aged, tne hypertensives, diabetics, and
patients with arteriosclerotic and other cardiovascular disease and
chronic respiratory disease.
Exposure to low temperatures can produce accidental hypothermia,
especially in the aged .[Watts;1' McNicol and Smith10). Low winter
temperatures are associated with increased mortality,7 although few
studies have specifically addressed thi3. asf»r*siatior.
REFERENCES
1. Berenson, P. J., and w. G. Robertson. Temperature, pp. 65-148. In
J. F. Parker, Jr. and V. R. West, Eds. Bioastronautics Data Book.
2nd ed. National Aeronautics and Space Administration Publication
No. NASA SP-3006. Washington, D.C.s U.S. Government Printing
Office, 1973.
2. Berglund, L. G., and R. H. Gonzalez. Application of acceptable
temperature drifts to built environments as a mode of energy
conservation. ASHRAE Trans. 84(1):110-121, 1978.
IV-157
-------
3. Batch, G. S. The influence of environmental temperature and
relative humidity on the rate of water loss through the skin in
congestive heart failure in a subtropical climate. Am. J. Med. Sci.
211^181-183, 1946.
4. Burch, G. E., and A. Ansari. Artificial acclimatization to heat in
control subjects and patients with chronic congestive heart failure
at bed rest. Am. J. Med. Sci. 256:180-194, 1968.
5. Burch, G. E., and N. DePasquale. Influence of air conditioning on
hospitalized patients. J. Am. Med. Assoc. 170:160-163, 1959.
6. Burch, G. E., and G. C. Miller. The effects of warm, humid
environment on patients with congestive heart failure. South. Med.,
J. 62:816-822, 1969.
7. Ellis, F. P. Mortality from heat illness and heat-aggravated
illness in the United States. Environ. Res. 5:1-58, 1972.
3. Gagge, A. P., and Y. Nishi. Heat exchange between human skin
surface and thermal environment, pp. 69-92. In 0. H. K. Lee, H. L.
Falk, S. D. Murphy, and S. R; Geiger, Eds. Handbook of Physiology.
Section 9. Reactions to Environmental Agents. Bethesda, Md.:
American Physiological Society, 1977.
9. Hardy, J. 0., J. A. J. Stolwijk, and A. P. Gagge. Man, p. 342. In
G. C. Whittow, Ed. Comparative Physiology of Thermoregulation. Vol.
II. Mammals. New York: Academic Press, Inc., 1971.
10. McNicol, M. V)., and R. Smith. Accidental hypothermia. Br. Med. J.
1:19-21, 1964.
11. Nishi, Y., and A. P. Gagge. Direct evaluation of convective heat
transfer coefficient by naphthalene sublimation. J. Appl. Physiol.
29:830-838, 1970.
12. Nishi, Y., and A. P. Gagge. Moisture permeation of clothing—A
factor governing thermal equilibrium.and comfort. ASHRAE Trans.
76(Pt. 1):137-145,. 1970.
13. Oechsli, p. w., and R. W. Buechley. Excess mortality associated
with three Los Angeles September hot spells. Environ. Res.
3:277-284, 1970.
14. Schuman, S. H. Patterns of urban heat-wave deaths and implications
for prevention: Data from Hew York and St. Louis during July, 1966.
Environ. Res. 5:59-75, 1972.
15. Stolwijk, J. A. J., and J. D. Hardy. Control of body temperature,
pp. 45-68. In D. H. K. Lee, H. L. Falk, S. D. Murphy, and S. R.
Geiger, Eds. Handbook of Physiology. Section 9. Reactions to
Environmental Agents. Bethesda, Md.: American Physiological
Society, 1977.
16. Watts, A. J. Hypothermia in the aged: A study of the role of
cold-sensitivity. Environ. Res. 5:119-126, 1972.
CHARACTERIZATION OF ADDITIONAL PHYSICAL INDOOR POLLUTANTS
The indoor pollutants thus far described have been defined
primarily as airborne contaminants. Other forms of pollution do not
depend on mass concentration, such as sound and electromagnetic
radiation. Electromagnetic radiation occurs in the radiofrequency,
IV-158
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infrared, visible light, ultraviolet, and x-ray portions of the
electromagnetic spectrum. The frequencies of the electromagnetic
radiation discussed here range from 10^ Hz (radiofrequency) to 10^5
Hz (ultraviolet). Table IV-24 summarizes the. frequency distribution
for each of these portions of the spectrum and of audible sound# which
is transmitted via the vibration of air molecules.
SOUND AtlD NOISE
Physical Characteristics
The audibility of sound depends on1 intensity and frequency, with a
maximal human response in the region near 3 x 103 Hz. A sound with
predominant frequencies below 100 Hz or above 10^ Hz may require a
million times more energy to have the same audibility a& a sound with a
predominant frequency of 3 x 10^ Hz. A method of weighting the
pressure exerted by the sound waves at different frequencies has been
developed to compensate for these variations. The decibel values
(which constitute a logarithmic intensity scale) cited herein are
measurements with level A weighting, the scale that most closely
matches the response of the human ear. The differences in the
treatment of the intensity content of a sound are slight and do not
change substantially from' one source to another.
Sounds in the indoor environment are generated both outside and
inside the occupied space. Table IV-25 gives examples of sound
intensities in the outdoor environment. Table IV-26 lists sound
intensities produced by typical household appliances in the indoor
environment.
Sound intensities are usually measured by a meter satisfying the
requirements of American National Standards Institute Specification
SI.4-1971 (for sound meters).
Psychophysiologic Effects
The possible effects of sound include permanent and temporary loss
of hearing, cardiovascular disease, sleep disruption, and psychologic
effects.1* The physiologic and psychologic responses to sound may be
transitory; 1 * however, there is insufficient information on the
effects of sound by itself or in combination with other stressors.
Sound at intensities that are found to be objectionable will affect
productivity and decrease enjoyment of the environment.1*
The EPA has identified sound intensities that, if not exceeded,
should protect against some of the adverse effects of sound. l* These
values are expressed in terms of maximal 8-h (75 dB) and 24-h (70 dB)
averages required to protect against hearing loss. There are also
yearly average long-range environmental goals of 55 dB outdoors and 45
dB indoors, which are recommended to avoid activity interference or
annoyance. 11 There is still debate in professional circles about the
maximal intensities of short-duration environmental sound that can be
IV-159
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Type of Radiation
Ultraviolet
Ultraviolet C
Ultraviolet B
Ultraviolet A
Visible light
Infrared
Near Infrared
Infrared
Far infrared
Radlofrequency
Microwave
Very high frequency
High frequency
Medium frequency
Low frequency
Very low frequency
Sound, audible
TABLE IV-24
Radiation Wavelengths and Frequencies
Wavelength Frequency, Hz
0.19-0.28 vn 1.07 x 10l^-1.58 x 101*
0.28-0.315 pm 9.5 x lO^-l.O? x 10*5
0.315-0.4 vi o 7.5 x 10 -9.5 x 101-+
0.4-0.7 vm 4.29 x 1014-7.5 x 101*
0.7-1.4 ym
1.4-3 pm
3-1,000 vm
2.14 x 10^-4.29 x
10-2.14 x
1.00
3
10U-1.00 x
14
14
1014
1-1,000 can
3
X
10®-3
X
10:
1-10 m
3
X
10-3
X
10:
10-100 a
3
X
10^-3
X
10
100-1,000 m
3
X
10f-3
X
10'
1,000-10,000 n
3
X
10^-3
X
10
10,000-30,000 n
1
X
10-3
X
10
0.016-20.0 m
15-2
X
10'
IV- 160
-------
TABLE IV-25
Examples of Outdoor Day-Night ,'verage Sound Intensities
at Various Locations9
Location
Apartment next to freeway
Downtown with some construction
Urban high-density apartment
Urban row housing on major avenue
Old urban residential area
Wooded residential area
Agricultural cropland
Rural residential area
Wilderness ambien
Average Sound
Intensity, dB(A)
88
79
78
68
59
51
44
39
35
1Data from Council on Environmental Quality.
TABLE IV-26
Examples of Sound Intensities Generated Indoors
by Household Appliances3
Average Sound
Appliance Intensity, dB(A)
Blender 80-90
Garbage disposer 80
Window air conditioner 60
Refrigerator 45
Vacuum cleaner 70-75
Hair dryer 78
Mixer 82
a 8
Data fran Jones.
IV-161
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considered safe. However, above 110 dB, sound ia so intense that most
people experience pain or a tickle in their ears. '*
Although it is difficult to determine the exact day and night
indoor sound intensities, studies have indicated that an intensity of
60.4 dB with a standard deviation of 5.9 dB can be expected in a
typical urban residential area, with instantaneous intensities
exceeding 80 dB. 11 An expected intensity of €0.4 dB is below the 70
dB recommended by the EPA to prevent hearing loss, but it is veil above
the intensity recommended to avoid interference' and annoyance,
therefore, day and night sound intensities in the 100-site EPA survey
may contribute to speech interference, reduced worker productivity, and
annoyance. 1066-69)
A high intensity of background noise in urban areas* stemming
primarily from transportation appears to affect the developing fetus.
Women exposed to aircraft noise have a higher proportion of
low-birthweight children, who are at higher risk of mortality and both
physical and, mental effects. 10(PP* 110-111) This association
cannot be separated from the social status of the women (a
codetermining variable), inasmuch as many members of the lower social
classes live in "noisy" areas.
Exposure to high intensities of sound affects communication and
learning, including the acquisition of language. 1 °^P*
Adaptation or resignation to anncyance may occur, and there do not
appear to be groups of people that are particularly sensitive.
After-effects of noise have been noted at home and at work, and noise
appears to influence aggressiveness and minimize voluntary helping
behavior. "(PP.- ^0-121]
RADIOFREQUENCY AND MICROWAVE RADIATION (104 to 3 x 101-1 Hz)
Physical Characteristics
Although the physical characteristics of all electromagnetic
radiation are similar, the frequency is inversely proportional to
wavelength, and the effects of the' longer wavelengths, such as
radiofrequency radiation, are radically different from those of the
shorter-wavelength ionizing radiation, such as x rays and gamma r^ys.
The photon energy in radio waves is so small that there is no
ionization when it is absorbed in an organism.19
Table IV-27 summarizes the radiation properties of some common
nonionizing-radiation systems and their expected far-field power
densities. Energy radiated by these systems can be additive, provided
that the frequencies are within the same octave band.
For the purposes of this report, the densities of all radio-
frequency energies generated outdoors are defined as "background power
densities," and those of radiofrequencies generated indoors as
"generated power densities."
Some radiofrequency energy is generated in the indoor environment.
In general, all electric equipment produces some radiofrequency
radiation. However, all but a few electric devices radiate energy at
IV-162
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TABLE IV-27
Comparison of Radiation Properties of Some Common Radiofrequency-Generating Systems
Radiating System
AM radio transmitter
FM radio transmitter
VHF TV
UHF TV
Acquisition radar3
(ARSR)
Tracking radar:8
Type A
Type B
Frequency
500 kHz
88-108 MHz
174-216 MHz
470-890 MHz
1 GHj:
10 CHz
1.3 GHz
Average Transmitter Power
50 kW (maximum allowed)
100 kW
300 kW (maximum allowed)
5,000 kW (maximum allowed)
20 kW
5 kW
150 kW
Far-Field Power Density
ct Selected Distance
0.016 mW/cm^ at 400 m
0.03 mU/cmg at 500 m
0.04 mW/cm at 500 m
0.5 mW/cm at 500 m
0.05 mW/cu at 3,000 m
(near field, 100 mW/cm
at 30 m)
0.01 mW/cm^ at 3,000 m
(near field, 800 nW/cm
at 9 m)
1 mW/cm at 5,000 m (near
field, 56 mW/cm at 523 m)
aRadar power densities given along line of sight of transmitted power; off axis, power densities are
generally 0.01 less than those along line of sight.
-------
well below the American National Standards Institute recommended
exposure limits, even in combination with one another. One major
exception is the microwave oven. Under normal operating conditions! a
residential microwave oven radiates approximately 1 raW/cm2 at the
seal on the door. However, if the door is defective, values in excess
of 1 W/cn? can be achieved.
Psychophysiologic Effects
Effects of radiofrequency radiation can be divided into two major
categories': 19 thermal effects (when the radio-wave energy is
converted into heat) and nonthermal effects (which cannot be directly
explained by thermal equivalents).
Biologic effects depend on the frequency and the intensity of the
radiation; the duration of exposure; the dielectric constant,
temperature, and thermal conductivity of the irradiated tissue; the
ability of the tissue to dissipate heat; and the dimensions of the
body. Absorption of microwave radiation by body tissues results in an
increase in temperature, often producing internal burns due to local
hot spots caused by nonuniformity in the field. The eyes and cestes
were found to be the most sensitive. 17
Specific effects at the cellular or molecular level were postulated
more than a decade ago without resolution of the importance of these
effects with respect to biologic damage.1 The possibilities of
nonthermal effects, such as rearrangements within macromolecules and
subcellular structures, have been under investigation for many years,
but further studies will be necessary to clarify the issues. It is
relatively clear that metabolic and functional disturbances at the
cellular level can be caused by microwave radiation, but the mechanisms
of these effects are not yet well understood.
Table IV-28 characterizes the relative rates of absorption by the
human body; however, it is difficult to determine the exact effect of
each frequency. Because the radiofrequency energy generated indoors is
low, the major emphasis should be on outdoor sources. Indoor
radiofrequency fields are generally lower than outdoor. Osepchuck has
discussed sources of microwave and other forms of radiofrequency
energy. 11
FAR-INFRARED AND INFRARED RADIATION (3 x 1011 Hz to 4.3 x 1014 Hz)
Physical Characteristics
The infrared energy spectrum ranges from far-infrared (3 x 10^1
Hz to 1014 Hz), through infrared (1.0-2.14 x 1014 Hz), to near-
infrared (2.14-4.29 x 101 Hz). Infrared radiation is produced
naturally by the sun and by all common heating and artificial-light
sources. The incandescent lamp is one of the major sources of infrared
radiation and the most common artificial-light source in the indoor
environment. Of the total input wattage of an incandescent lamp,
IV-164
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TABLE IV-28
Relative Absorption of Radiofrequencles by Human Body9
Maximal Absorption
Frequency, 10 Hz by Human Body, %
<400 <50
400-1,000 50-100
1,000-3,000 20-100
3,000-10,000 >50
Data from U.S. Department of Health, Education, and Welfare.
IV- 165
-------
75-80% is converted to near-infrared and infrared radiation.' The
ACGIH has adopted a TLV of 10 raW/cm2 for infrared radiation in the
workplace. 1 Ihe power density 2 m from a 100-W lamp is approximately
0.6 mW/cm2 for the total infrared spectrum. Sunlight on the earth's
surface produces a flux of about 70 raW/cm2, of which about half is
infrared.
Psychophysiologic Effects
Depending on its wavelength, infrared is absorbed in the surface of
the skin (wavelengths larger than 2 un) or can penetrate several
millimeters (wavelengths between 0.7 and 1.5 urn). Safety standards
in industrial environments are based on the risk that, infrared
radiation may induce cataracts in the eyes of persons exposed to
excessive infrared radiation, such as glassblowers or open-hearth
steelworkers. 16
Excessive infrared radiation is r.ost easily controlled by shielding
the source with reflecting metallic foils.
VISIBLE RADIATION
Physical Characteristics
Radiation in the near-infrared and visible spectrum is produced by
many sources, both natural and artificial. Our sense of. sight, feeling
of well-being, and comfort are all, to a great extent, influenced by
visible and near-infrared radiation.
Psychophysiologic Effects
Retinal burns from observation of the sun have been described
throughout history. Chorioretinal burns rarely occur from exposure to
artificial light, because the normal aversion to high-brightness light
sources (the blink reflex) provides adequate projection, unless the
exposure is hazardous within the duration of the blink reflex.
Many factors affect the usefulness of visible light. Among the
most important are discomfort glare and disability glare. 1 Light
sources can cause a reduction in contrast of an. image, owing to
scattered visible radiation, by adding a uniform veil of luminance to
the object. This effect, commonly called "veiling luminance," may
cause a reduction in visual performance without physical damage.
Discomfort glare is a sensation of annoyance or pain caused by
brightness in the field of view that is greater than that to which the
eyes are adapted. It has been shown that the threshold of dis.comfort
glare changes as a function of age.3 Although discomfort glare does
not necessarily interfere with visual performance, it can cause eye
strain and contribute to fatigue. Disability glare and ocular stray
light influence one's ability to perform a task by artificially veiling
IV-16S
-------
the contrast o£ the visual target. It is therefore a great contributor
to eye. fatigue.
ULTRAVIOLET RADIATION (0.75-1.58 X 1015 Hz;
wavelength, 0.19-0.400 urn)
Physical Characterstica
Ultraviolet radiation is divided into three wavelength categories:
ultraviolet-A {UV-A), 0.315-0.400 nn; ultraviolet-B (UV-B),
0.28-0.315 urn; and ultraviolet-C (UV-C), 0.19-0.28 van. All
fluorescent lamps emit UV-A, but not UV-B or UV-C. High-intensity
discharge lamps produce UV-A, UV-B, and some UV-C. Incandescent lamps
produce small amounts of UV-A, and essentially no UV-6 and UV-C.
Ultraviolet radiation is measured with specialised radiometric
photometers.
Psychophysiologic Effects
UV-B and UV-C are known photocarcinogens.5 Doses of UV-B and
UV-C 10 times the human minimal erythema dose (MED) have initiated
squamous cell carcinomas, and chronic continuous exposure to UV-A can
also have a carcinogenic effect.5
The ACGIH recommends limits on workplace ultraviolet exposure that
depend on wavelength an<^ on the duration of exposure. 1 For UV-A, the
intensity should not exceed 1 mW/cm^ for more than 1,000 s, nor
should the dose exceed 1 J/zn? if given in less than 1,000 s. For
UV-B and UV-C, the dose should not exceed about 3-10 mJ/cm2 in any
8-h period. The degree of hazard seems to be associated with the
erythemal efficiency of each frequency. 1 5
SUMMARY
Ionizing and nonionizing electromagnetic radiation occurs in the
indoor environment. This radiation can be harmful, and one cannot
always sense its presence.
Sound can generally be heard and in some cases felt. Excessive
sound can cause deterioration of hearing acuity and, if extremely
intense or prolonged, cause deafness. Background sound in the urban
residential environment can exceed the recommended intensities and
result in interference and annoyance. Sound of 70-80 dB, commonly
found in indoor environments, can inhibit task performance and possibly
contribute to aggressive human behavior.*
Infrared, far-infrared, and radiofrequency radiation produce no
visible o; audible evidence of their presence. However, infrared
radiation does provide sensory indication of its presence by heating of
human tissue. Far-infrared and radiofrequency radiation,, however,
provide no indication of their presence, unless their power levels are
IV-167
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so high a9 tc increase skin temperature. Heating of human tissue
occurs because of the infrared output of incandescent lamps. However,
the detrimental effects of this heating have not been fully
investigated. Surveys have shown that in several cities 98% of the
people are exposed to less than 1 itf/cm2 from broadcasting
transmitters.7 However, ultrahigh-frequency television transmitters
can radiate radiofrequency pollution to adjacent buildings at 5-200
iM/cra2.
Ultraviolet-A, vis-ible light, and near-infrared radiation can
produce surface heating of human and animal tissue. These frequencies
are of concern because of thexr ability to affect human performance.
The veiling reflections caused by most artificial lighting systems can
have substantial influence on human visual performance. Reduction of
veiling reflections can increase' visual performance and decrease the
energy consumed by lighting systems. Transient adaptation (dilation
during or immediately after eye movements) is caused by sudden changes
in the visual spectrum power. Transient adaptation contributes to eye
fatigue and decreased visual performance.
REFERENCES
1. American Conference of Governmental Industrial Hygienists. TLVs.
Threshold Limit Values for Chemical Substances in Workroom Air
Adopted by ACGIH for 1980. Cincinnati: American Conference of
Governmental Industrial Hygienists, 1980. 93 pp.
2. Bennet, H. J. Discomfort Glare:' Demographic variables, p. 6. IERI
Special Report No. 118, 1976.
3. Cleary, E. Biological Effects and Health Implications of Microwave
Radiation. Symposium Proceedings. Richmond, Virginia, September
17-19, 1969. 'J.S. Department of Health, Education, and welfare.
Bureau of Radiological Health Publication No. BRH/DBE 70-2.
Washington, D.C.: U.S. Government Printing Office, 1971. 265 pp.
4. Council on Environmental Quality. Noise, pp. 533-576. In
Environmental Quality—1979. The Tenth Annual Report of the Council
on Environmental Quality. Washington, D.C.: U.S. Government
Printing Office, 1980.
5. Cunningham-Dunlop, S., and B. H. Kleinstein. wavelength dependence,
pp. 51-61. In Carcinogenic Properties of Ionizing and Nonionizing
Radiation. Vol. I. Optical Radiation. DHEW (NIOSH) Publication No.
78-122. Washington, D.C.: U.S. Government Printing Office, 1977.
6. Geen, R. G., and E. C. O'Neal. Activation of the cue-elicited
aggression by craneral arousal. J. Pers. Soc. Psychol. 11:289-292,
1969.
7. Janes, D. E., Jr. Radiation surveys—Measurement of leakage
emissions and potential exposure fields. Bull. H.I. Acad. Med.
55:1021-1041, 1979.
8. Jones, H. W. Noise °in the Human Environment. Edmonton, Alberta:
Environmental Council of Alberta, 1979.
9. Kaufman, J. E., and J. F. Christensen, Eds. IES Lighting Handbook.
The Standard Lighting Guide. 5th ed. New York: Illuminating
Engineering' Society, 1972.
IV-168
-------
10. National Research Council, Committee on Appraisal oC Societal
Consequences of Transportation Noise Abatement. Noise Abatements
Policy Alternatives for Transportation. Washington, D.C.: National
Academy ot Sciences, 1977. 206 pp.
11. Osepchuck, J. M. Sources and basic characteristics ot microwave/RF
radiation. Bull. N.Y.,Acad. Med. 55:976-998, 1979.
12. Schultz, T. J. Noise Assessment Guidelines. (Technical. Background
tor Noise Abatement in HUD's Operating Programs.) U.S. Department
ot Housing and Urban Development Report No. TE/NA 172. Washington,
D.C.: U.S. Government Printing Office, 1971. 210 pp.
13* Smith, S. w., and 0. G. Brown. Radio Frequency and Radio Microwave
Radiation Levels Resulting from Man-Made Sources in the Washington,
D.C. Area, pp. 1-13. U.S. Department ot Health, Education, and
Welfare Pub. No. (FDA)72-8015. Washington, D.C.: U.S. Government
Printing Office, 1972.
14. U.S. Envirc'.uiiental Protection Agency, Office ot Noise Abatement and
Control. Information on Levels ot Environmental Noise Requisite to
Protect Public Health and Welfare with an Adequate Margin ot
Safety. U.S. Environmental Protection Agency Report No.
550/9-74-004. Washington, D.C.: U.S. Government Printing Office,
1974. [214J pp.
15. Vogelman, J. H. Physical characteristics ot microwave and other
radiofrequency radiation, pp. 7-10. In s. F. Cleary, Ed. Biological
Effects and Health Implications of Microwave Radiation. Symposium
Proceedings. Richmond, Virginia, September 17-19, 1969. U.S.
Department ot Health, Education, and Welfare, Bureau ot
Radiological Health Publication No. BRH/DBE 70-2. Washington, D.C. :
U.S. Government Printing Office, 1971.
16. Wallace, J., P. M. Sweetnam, c. G. Warner, P. A. Graham, and A. L.
Cochrane. An epidemiological study ot lens opacities among steel
workers. Br. J. Ind. Med. 28:265-271, 1971.
17. World Health Organization. Health Hazards in the Human Environment.
Geneva: World Health Organization, 1972. 367 pp.
IV-169
-------
V
FACTORS THAT INFLUENCE EXPOSURE TO INDOOR AIR POLLUTANTS
The types and quantities of pollutants found indoors vary
temporally and spatially. Depending on the type of pollutant and its
sources, sinks, and mixing conditions, its concentration can vary by a
factor of 10 or more, even within a small area.
Human mobility constitutes an important kind of complexity in the
determination of exposure to air pollutants. Human activity patterns
differ between midweek and weekend, between one season and another, and
between one part of one's lifetime and another. Activity patterns
determine when and how long one is exposed to both indoor and outdoor
pollutants. Therefore, in reviewing the'factors that influence
air-pollution exposures, we have specifically separated them into two
major components: time (activity) and concentration (location).
Information on the time spent in various activities is summarized
first, and then the variations iii concentration encountered in
different locations. Unfortunately, most of the studies discussed were
not longitudinal and thus do' not offer information on seasonal
differences in time spent indoors and outdoors or on regional
differences in activity patterns.
Outdoor concentrations of pollutants and rates of infiltration
affect the concentrations to which people are exposed indoors. The
emphasis of the second section of this chapter is on geographic
variations in outdoor pollution and their impact on indoor pollution.
Building construction techniques, as they vary geographically, and
their effect on pollution infiltration ratc3 are particularly
important. But the measurement techniques available are limited; the
need for additional studies is discussed. The rates of infiltration on
a neighborhood scale have been studied by only a few researchers.
Although their work has focused on energy conservation, their findings
can easily be applied to the study of the impact on indoor pollution.
As shown in Chapter IV, there can be large indoor-outdoor
differences in pollutant concentrations. Concentrations also vary
among indoor locations and from one time to another. In determining
total exposure to pollutants, therefore, both indoor and outdoor
concentrations must be well characterized. The ways in which building
characteristics affect indoor pollution vary with type of pollutant.
7-1
-------
type of building, building location and orientation, and even room use
within a given building. Building characteristics are the subject of
the final section of this chapter.
HUMAN ACTIVITIES
Patterns of human behavior and activity determine the time spent in
any specific location, and thus knowlege of them is essential in
estimating exposures of populations to pollutants. As indicated by
Ott,SI a large number and variety of studies in which data on human
activities were collected from population samples have been completed
over the last 50 yr.
When one examines the literature on human activities, the term
"time budget" fzeitbudget," "budget de temps") is encountered often.
A time budget produces a systematic record of how time i3 spent by a
person in some specified period, usually 24 h. It contains
considerable detail on a person's activities, including the locations
in which the activities take place.**
One way of obtaining time budget information from the populations
surveyed is to ask each respondent to maintain a diary of his or her
activities over a 24-h period or longer. In another approach, the
so-called "yesterday" survey approach, the interviewer asks each
respondent about his or her activities on the preceding day.
Several summaries of the historical development of time-budget
research have been published.11 " 51 7° Ott51 discussed the
literature on activity patterns in the context of estimation of
exposure to air pollution.
The Multinational Comparative Time Budget Research Project,
launched in September 1964 by a small group of social scientists from
eastern and western countries, used common principles for sampling,
interviewing, and data coding and tabulation on an international
basis. The population sample consisted of nearly 30,000 persons in 12
countries (Belgium, Bulgaria, Czechoslovakia, France, East Germany,
West Germany, Hungary, Peru, Poland, United States,.Soviet Union, and
Yugoslavia) . A standardized coding sytem, was developed foe coitparinq
activities in different countries. The multinational study developed a
coding system with 100 categories of activities represented oy a
two-digit code (from 00 to 99). The activities represented by these
codes can be grouped into 10 classes: working time and activities
related to work, domestic house work, care of children, purchasing of
goods and services, private needs (such as1meals and sleep), adult
education and professional training, civic and collective
participation, sports and active leisure, passive leisure, and
spectacles, entertainment, and social life.'**
The Project yielded a rich data base that has been summarized in a
number of tables, figures, and articles.*' For example, the average
time spent by employed men, employed women, and married housewives in
various locations in 12 countries is shown in Table V-l. The data show-
that employed men in the 12 countries spend between 12 h (in Hungary)
and 15.2 h (in Belgium) in their homes, whereas housewives spend
V-2
-------
table V-l
Tine Spent in Various Locations In 12 Countries
(Average Hours per Day)a
Reproduced from
feeil available copy.
7 11 Employed am. U4>rl
taudr om"thoir*
IS 1
IJ S
\» i
1 S fc
134
M 1
US
(Iff
1/9
14 0
IU
116
?J4
11*
IJ A
pan Duiuftr onr'k luxm
OS
0 ?
0 I
0 1
i 0
05
04
1 0
4 1
n 2
0 1
0 1
0 )
01
1 4
•t pot'i workplace
10
? 1
1 9
11
34
1 i
A B
1 3
ft 4
y o
6 1
6 S
6.0
3 1
6 I
fS UMBI
t s
J1
1 6
1 \
1 1
2 1
1 1
1 0
IS
11
I i
1 J
30
>1
3 )
t» other prop^'t ton*
05
0 3
0)
0)
OS
Oft
0 )
0 J
03
0.3
Of
06
01
01
0 i
u plac*» oTbuioicu
07
04
06
OS
0«
04
0 6
04
Q 1
0«
0 1
Ot
0 4
Ot
0 f
B MtMWli ind tet
0.2
00
0 1
01
OS
04
0 1
0/
0 J
00
04
04
0 i
01
0"
fe iff other tociboen
C4
ot
0t
01
ot
04
6 3
04
04
Qt
Of
04
0 1
0 3
0 ?
lotat
W«
un
14 0
340
34 t>
24 0
14 «
14 0
14 0
14 0
M.O
*40
U 0
34 a
24 0
J-J / *oewe.afl 4syt
inwU onc'i Hon*
IT I
14 t>
110
IS.)
170
16 1
St 1
14 J
16 1
r o
IS 4
IS 1
140
i»0
no
}luI ouliid* ooe'i h9«*
01
0 ]
0 1
00
0 1
0.1
0 1
0 1
04
0 1
00
01
0 (
0.*
04
if otn'i workpUrc
).i
* s
i t
c r
St
J6
4 9
6 J
44
SB
} J
SO
11
6.1
64
« otntil
f 3
fa
ti
i.i
J 1
1 3
> I
J 4
1 1
1 i
1 3
n
1 1
1 4
1 s
¦a otter propfc'1 how
04
0 2
0 2
03
04
09
0 ]
01
Ob
06
0.1
06
01
n pt*cri bkWMu
i fi
04
01
06
06
0 1
0 1
OS
0.1
0.1
01
11
06
04
0 4
h M-fiauia^H igtd bar»
03
00
Ot)
0 1
01
0)
0 1
00
0 1
00
03
02
0 J
00
00
b ill uthct tocitioat
04
0.]
04
0 1
04
0 1
0 i
01
0.1
0 1
01
04
OS
02
0 I
tOffl
34.0
14 0
1-4 0
24 J
i* a
14 0
14 0
14.0
1*0
34 0
340
34 ft
14.0
HO
14,0
T-t JttQ*my*tva, tU dtft {mtnmJ o*jv)
nddt ow '• fcoew
21 t
20 4
10*
31 7
10 4
10 5
11 1
Itt
ll.O
10 9
10 5
109
If 4
70S
49 1
JUil QW<«I« OAf'llKMM
01
1 4
0 )
Ot
CI
0.4
0.)
2 1
03
0 1
0 t
0 1
0 4
06
1 1
M u»nHI
1 0
0.4
11
9 9
14
10
1 0
0*
1 3
1.3
kO
09
1 t
1 .*
1 t
» cjflll ffOpk'lllCIIK
0#
04
01
OS
Oft
06
0 >
ot
04
OS
• 1
01
l)»
D >
n l
fc fltoff of buAWIf
05
0 J
11
06
01
11
09
09
0*
1 2
1 )
i 1
1.1
04
OS
m ntuttim t) »nd bni
01
Q.I
0.0
0.0
0 1
0.1
00
00
00
0.0
0 1
0 1
00
00
0 0
to ril otfcei locaueat
0}
a i
0 I
0 1
04
O]
03
02
0 I
0 t
01
01
0 I
0 1
Ot
ictMi
34 0
34 a
*4 0
14 o
14 0
14 0
14 0
14 0
>4 0
14 0
14 0
34 0
14 0
34 0
24 0
'Reorlnted vlth permission from Snalat." Data are weighted to ensure equality of daye of the week and
i;un.ber of eligible respondents per household.
-------
between 19.7 h (in Hungary) and 21.6 h (in Belgium) in their homes. In
the 12 countries, therefore, employed men spend, on the average, 50-63%
of the day in their homes, and housewives spend 82-90% of the day in
their homes. It is difficult to determine the overall amount of time
spent indoors from these data, because categories like "at one's
workplace" do not distinguish between indoor and outdoor workplaces.
Similarly, the categories "in places of business" and "in all other
locations" do not specify whether they are indoors or outdoors.
However, if one assumes that all ""workplaces," "places of business,"
and "restaurants and bars" are indoors, along with the category "in
other person's homes," and that the category "in all other locations"
is assumed to be entirely outdoors, then it is possible to estimate the
amount of time spent by respondents in three general categories:
indoors, outdoors, and in transit (sea Table V-2).J1
With these assumptions and the restructured data shown in Table
V-2, it is estimated that employed men .in the 12 countries spend
between 84% (in Maribor, Yugoslavia) ana 92% (in France) indoors. It
should be emphasized, however, that many'of the entries in Table V-2
cannot be compared with each other on a statistical basis, because the
numbers of respondents in the samples vary. Also, the
representativeness varies, because some countries, such as the Soviet
Union, are represented by a single city and its suburbs (Pskov,
population 115,000), whereas others, such as the United States (44
cities), are represented by a national sample of metropolitan areas.
Finally, some assumptions as to whether a location was indoors or
outdoors need to be examined, because they may introduce error.
However, the estimates in Table V-2 appear uset.il as rough
approximations of the times spent by residents of 12 countries indoors,
outdoors, and in transit.51
If only the data for the United States (44 cities) are considered,
it appears that, on the average, employed men spend 90% of the day
(21.7 h) indoors, whereas married housewives spend 95% of the day (22.8
h) indoors. Employed men in the United States are estimated to spend
2.9% of the day (0.7 h) outdoors, and housewives 1.7% (0.4 h).
Although the estimates in Tables v-1 and v-2 are useful for
determining the total amount of time spent in various locations, they
give little information about the time of day when persons are present
in each location. Data from the multinational study can be displayed
in a composite profile that shows the proportion of the population that
are engaged during the day in selected activities, such as sleeping,
eating, working, travel, and watching television (Figure V-1).
In addition to the studies of activities in the United States by
Robinson,®'"" activity-pattern studies have been carried out in
Durham, N.C., by Chapin and Hightower," on a sample of 43 Standard
Metropolitan Statistical Areas (SMSAs) by Chapin and Brail,11 on a
followup U.S. national sample by Brail and Chapin,' and on the
Washington, D.C., metropolitan area by Hammer and Chapin.11
Information supplied in this section is limited to urban areas; this
reflects the available published information. No comments are made on
variations in numbers, because.it is beyond the scope of this document
to assess their reliability.
V-4
-------
TABLE V-2
Estimated Time Spent in Three Environmental Categories*
Country
Average
Time Spent,
h/d
Employed
Men
Housewives"
Indoors
Outdoors
In transit
Indoors
Outdoors
In transit
Belgium
21.6
0.9
1.5
23.2
0.4
0.4
Bulgaria (Kazanlik)
21.0
0.9
2.1
22.1
1.5
0.4
Czechoslovakia (Olomouc)
21.3
1.1
1.6
23.2
0.5
0.4
France (six cities)
22.0
0.5
1.5
23.3
0.2
0.5
West Germany (100 districts)
20.4
1.9
1.7
22.2
1.2
0.6
West Germany (Osnabruck)
20.7
1.1
2.2
22.7
0.7
0.6
East Germany (Hoyerswerda)
21.6
0.7
1.7
23.2
0.5
0.3
Hungary (Gyor)
20.4
1.6
2.0
21.5
2.3
0.2
Peru (Llma-Callao)
20.8
0.7
2.5
22.9
0.7
0.4
Poland (Torun)
21.9
0.4
1.7
2J.3
0.2
0.5
United States (44 cities)
21.7
0.7
1.6
22.8
0.4
0.8
United States (Jackson, Mich.)
21.8
0.7
1.5
23.0
0.3
0.7
U.S.S.R. (Pskov)
21.0
1.0
2.0
22.6
0.7
0.7
Yugoslavia (KraguJevac)
21.4
0.8
1.8
22.4
0.9
0.7
Yugoslavia (Maribor)
20.1
1.7
2.2
21.3
2.4
0.3
"Reprinted from Ott.^* Derived from data originally published in Szalai;^^p" data are
weighted to ensure equality of days of the week and number of eligible respondents per households
^Married persons only.
-------
MIDNIGHT 6 AM NOON 6 PM MIDNIGHT
TIME
FIGURE V-l Diurnal profiles showing percentage of employed men in
United States (44 cities) engaged In nine types of activities as a
function of tine of day (weekdays only). Data weighted to ensure
equality of days of the week and number of eligible respondents.
Reprinted with permission from Szalal.
V-6
-------
In the United States, legislation passed in 1952 required urban
areas to conduct metropolitan-area transportation studies as a
prerequisite for receiving federal funds for highway construction.*'
As a result, transportation studies have been undertaken in 200 areas
of the United States," and these studies have usually involved
collection of considerable detail about the transportation activities
of the urban population, particularly in cities with populations in
excess of 50,000. As reported by Robinson,, Converse, and Szalai,*®
the multinational research project also collected information' on the
average time spent in commuting to and from work in various countries
(see Table V-3). Most of the summaries of findings from time-budget
studies have presented only average values and seldom given histograms
or information on the variance of the time spent in various locations
or activities.
In 1969-1970, the U.S. Department of Transportation made
arrangements with the Bureau of the, Census to carry out a nationwide
study of the transportation-related activities of the U.S population.
This study, called the Nationwide Personal Transportation Study, was
based on home interviews and covered individual activities in
considerable detail.1 * * " i7 'J s* Figure V-2 shows a
frequency distribution of the amount of time spent in commuting based
on these data. Assuming two trips per day, the overall average o£ 22
min/trip compares reasonably well with the average of 46 min/d reported
by Robinson, Converse, and Szalai.'0
There is a need for a special-purpose activity-pattern study
specifically tailored to the problem of estimating air-pollution
exposures. Previous activity-pattern studies have not considered
questions that apply to exposures to air pollutants. Such a survey
should begin with a pilot study on a single city, to perfect the
experimental design and data-collection methods, and should use.
personal monitoring instruments to measure exposures. Once the pilot
study is completed and the results are evaluated, a large-scale'
research investigation could be carried out on a number of cities or on
a national probability sample. The large-scale survey would use
diaries and personal monitoring instruments to characterize the
frequency distribution of air-pollution exposures of the population as
a whole and in selected cities. Information from the diaries could be
compared with the measurements of exposure to determine how different
activities affect papulation exposure rates.
GEOGRAPHIC AND LOCAL VARIATIONS
The air quality of an indoor environment is often described on the
basis of one 24-h average obtained from one indoor sampling' location.
The spatial distribution of indoor air pollutants within a structure is
a little-studied subject. Therefore, recent or current unpublished
works and Lcc^iiical papers related to environmental concerns, but not
necessarily t: indoor air quality, are incorporated in this review.
Son>e of the associations made and conclusions reached are clearly based
on explicitly stated assumptions, rather than on scientific
documentation.
V-7
-------
TABLE V-3
Average Time Spent Traveling To and From Work, by Mode of Transportation3
Average Time Spent, min/d
Public
Country
Transport
Automobile
Walking
All Travel
Belgium
98
55
52
66
Bulgaria (Kazanlik)
93
73
47
57
Czechoslovak;}a (Olomouc)
73
62
46
59
France (six cities)
82
46
44
50
West Germany (100 districts)
—
—
—
40
Meat Germany (Oanabruck)
71
41
46
47
East Germany (Hoyerswerda
82
66
30
62
Hungary (Gyor)
104
48
40
64
Peru (Lima-Callao)
103
93
4b
89
Poland (Torun)
71
50
41
60
United States (44 cities)
81
46
30
50
United States (Jackson, Mich.)
—
39
34
38
U.S.S.R. (Pskov)
67
—
32
—
Yugoslavia. (Kragujevac)
70
53
47
51
Yugoslavia (Maribor)
71
44
40
51
Average
82.0
55.1
41.2
56.0
Standard deviation
13.3
15.1
7.2
12.7
aReprinted with permission from Robinson et al.^
-------
40
35
36.6%
2
o
e
O-
30
25
Aver aye
22 minutes
<
i
to
20
15
10
19.0%
15.8%
14.1%
-L
7 G%
3.8%
0.8%
i
greater than
65 - 2.2%
10
15
20
25
30 30
Time, Minutes
40
45
50
55
GO
65
FIGURE V-2 Frequency distribution of home-to-work commuting times for employed persona In the
United States (excludes persons who work at home or at no fixed address). Reprinted from
Svercl and Aaln.
-------
The types of pollutants and the concentrations of each type vary
between locations within a structure, between structures within a
geographic area, and between geographic areas. This section discusses
some of these interrelationships.
GEOGRAPHIC VARIATIONS IN INDOOR AIR QUALITY
Owing to the small number of field monitoring studies, the
geographic distribution of indpor air pollutants has not been
determined. However, it is instructive to review the geographic
distribution of the major factors that affect variations in the
concentrations of pollutants and their impact on the quality of the
indoor environment. Outdoor air quality, air-infiltration rates, and
sources of emission of indoor pollutants are the major factors.
Outdoor air quality has been studied .'with respect to some pollutants,
and the geographic distribution of these few pollutants is well
understood. Descriptive statistics published annually by EPA and state
and local air-quality agencies furnish much scientific information
useful in discerning regional and local differences in concentrations
of carbon monoxide, total suspended particles, ozone, NQ^, sulfur
dioxide,, sulfates, and otners. Clearly, it is beyond the scope of this
document to summarize the existing information on geographic variations
in the types and concentrations of all ambient pollutants. It should
be noted that the geographic distribution of some criteria pollutants
has been studied and is easily accessible from the literature;
information on noncriteria pollutants is sparse and often collected and
analyzed by questionable methods.
Concentrations of chemically nonreactive pollutants in residences
generally correlate with those outdoors. Results from the six-city
study,*3 which monitored indoor and outdoor environments for an
extended period, clearly showed the influence of outdoor concentrations
on the indoor environments (see Figure V-3). Another study,*7
sponsored by EPA, supported the conjecture that indoor concentrations
of inert gaseous contaminants correlate with outdoor concentrations.
The available data base is not large enough to support statistical
conclusions, but there is little doubt that the variations in indoor
pollutant concentrations correlate with variations in outddor
concentrations. Thus, it is expected that a city with high outdoor
pollutant concentrations will have high indoor concentrations, unless
control strategies are, used. Although this is a broad, general
conclusion, it must be emphasized that the indoor concentration of a
given pollutant is expected to vary widely among residences within one
city. This variation may be sufficient to mask the impact of varying
outdoor concentration.
Distribution of indoor air quality is extremely difficult to
describe on a geographic scale, because indoor air quality is
determined by complex dynamic relationships that depend heavily on
occupant activity and highly variable structural characteristics.
Weather, which has a regional character, influences indoor air
concentrations of some chemicals, such as formaldehyde, and biologic
V-10
-------
70
POP! TOPL KING WAT. ST.L. STEU.
S Out doc*
n ^Xloof r&ctrtc tvokmq
S fat ceoiatf
¦£* runb*f ed ^Ot/rteCtrC c«*r*3 home*
FIGURE V-3 Annual nitrogen dioxide concentration outside and
inside electric- and gas-cooking homes, averaged across efich
community's indoor and outdoor network (May 1977-April 1978).
Reprinted with permission from Spengler et al.
V-U
-------
contaminants, such as bacteria and molds. Therefore, the influence of
relative humidity and other weether-related conditions affecting indoor
environmental quality needs to be studied geographically. Research
specifically addressed to geographic distribution of indoor air quality
is needed.
Other sections of this document address ventilation rates of large
buildings^ and the discussion of the geographic distribution of
air-infiltration rates in this section focuses on residences.
Typically/ the air-infiltration rate for American residences is assumed
to be 0.5-1.5 ach. This assumption is supported by the results of
several energy and air-quality studies that expetimentally determined
the range of ventilation rates for typical residences to be between 0.7
and 1.1 ach [Moschandreas and Morse;4* C. 0. Hollowell, personal
communication). Recently built or retrofitted residences had lowex
infilcration rates, between 0.5 and 0.B ach (J. Hoods, personal
communication). However, the sample that yielded the.data is small,
and statistical documentation for such statements is not strong.
Only one experimental study appears to have been broad enough to
allow generalizations on the spatial distribution of air-infiltration
rates. A 1979 reportpresented air-lealtage characteristics of
low-income residences 10-90 yr old in 14 cities in ail climatic zones
of the United States. Two measurement techniques were used: a
tracer-gas decay technique with air bags to measure natural air
infiltration,14 and a fan-depressuiization test that measures induced
air-exchange rates.** Of the 266 low-income residences tested with
these two techniques, 68% were frame buildings, 16% masonry, and 11%
masonry-veneer. These proportions do not necessarily reflect those of
the universe of low-income dwellings. Figure V-4 illustrates the
findings of the 'study on air-infiltration rates from three cities.
With the tracer-gas technique( it was found that 19% of the rates were
below 0.5 ach; 40% were moderate, between 0.5 and 1.0 ach; 20% were
high, between 1.0 and 1.5 achj and 20% were very high, greater than 1.5
ach. This characterization of the rates as moderate, high, and very
high was given by Grot and Clark, and does not reflect a universally
accepted nomenclature. Although their paper did not discuss the
general geographic distribution of air-infiltration rates,
investigations of the data base are continuing. They observed that,
the higher the number of degree days, the lower the infiltration rate
of the residences. This observation is preliminary {R. A. Grot,
personal communication), and further work is needed to verify it.
Furthermore, this was a study of low-income residences, not typical
residences.
There have been studies that indicate the geographic distribution
of residential indoor sources. The residential energy consumption in
various geographic regions (Table v-4) shows the use of fuel types that
are potential sources of high concentrations of nitric oxide, nitrogen
dioxide, and carbon monoxide in residences with gas cooking and
heating. A second example shows the number of mobile homes in each
state (Table V-5)—an indoor environment with a reported potential for
high formaldehyde concentrations. Finally, residences in Polk County,
Florida, Grand Junction, Colorado, and Butte, Montana, are built with
V-1Z
-------
40
£ 30
20
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30
20
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A. Charleston, S.C.
Ho. of Houses B 23
No. of Readings B 134
Average N = 1.20 Hr-1
a = 0.86 Hr"'
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No. of Houses - 17
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FIGURE V-4 Histograms of measured natural air-infiltration rates for
three cities. Reprinted with permission from Grot and Clark.
V-13
-------
TABLE V-4
Distribution of Residential Energy Consumption by Fuel Type
and Re^'on, 1970 (Single-Family Detached Homes)3
Distribution of Fuel Use, %
Region Gas Oil Electricity Coal and Wood
Northeast
New England 20 76 3 1
Middle Atlantic 46 45 3 6
North central
East north central 71 23 2 4
West north central 76 20 2 2
South
South Atlantic 41 39 13 7
East south central 60 4 20 16
West south central 93 — 4 3
West
Rocky Mountain 81 8 5 6
Pacific 76 12 10 2
a 37
Reprinted from Keyes.
V-14
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TAB\E V-5
Estimated Sa>ck of Year-Round Occupied Mobile Homes at End of 1977
No. Mobile
% of
No. Mobile
Z of
State
Homes
Total
Scate
Homes
Total
Alabama
104,272
2.80
Montana
30,363
0.82
Alaska
14,215
0.38
Nebraska
25,957
0.70
Arizona
104,711
2.8J
Nevada
28,937
0.78
Arkansas
57,616
1.55
New Hampshire
17,853
0.48
California
286,888
7.71
New Jersey
20,387
0.55
Colorado
54,245
J.„46
New Hexico
44,930
1.21
Connecticut
10,017
0.27
New York
104,216
2.80
Delaware
17,661
0.47
North Carolina
192,893
5.18
Florida
117,708
8.54
North Dakota
13,561
0.50
Georgia
153,349
4.12
Ohio
135,374
3.64
Hawa i i
231
0.01
Oklahoma
53,121
1.43
Idaho
34,599
0.93
Oregon
85,431
2.30
Illinois
106,125
2.85
Pennsylvania
150,838
4.05
Indiana
104,601
2.81
Rhode Island
2,842
0,08
Iowa
38,280
1.03
South Carolina
103,071
2.77
Kansas
48,396
1.30
South Dakota
19,641
0.53
Kentucky
83,360
2.24
Tennessee
92,750
?.49
Louisiana
83,682
2.25
Texas
232,550
6.25
Maine
26,675
0.72
Utah
20,520
0.55
Maryland
26,724
0.72
Vermont
11,049
0.30
Massachusetts
13,558
0.36
Virginia
83,576
2.25
Michigan
134,353
3.61
Washington
88,330
2.37
Minnesota
58,103
1.56
"•Jest Virginia
53,758
1.44
Mississippi
69,961
1.88
Wisconsin
53,737
1.44
Missouri
84,993
2.28
Wyoming
16,988
0.46
Total
3,721,996
100
V-15
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or on radon-emitting materials and have high indoor radon
concentrations* The geographic distribution of.radon-emitting
materials ia being generated jay DOB and should be available soon.
Spatial distributions of this kind have not been generalized to
document variations in indoor air quality*
URBAN, SUBURBAN, AND NEIGHBORHOOD VARIATIONS IN INDOOR AIR QUALITY
Th^ quality of indoor air is a function of outdoor air quality,
emission from indoor sources, air-infiltration ratejj, and occupant
Activity and is likely to wary within each metropolitan and suburban
area, and indeed within each neighborhood, within & metropolitan area,
it has been shown that an urban complex leads to the so-called urban
heat reservoir.1 Urban characteristics—such as city size, density
of buildings, and population—correlate with such meteorologic, factors
as temperature? pressure, and wind velocity.15 The urban heat island
affects both urban pollution patterns and meteorologic characteristics
that affect the infiltration rates of buildings. Thus, although the
exact nature of the impact on indoor air quality is not known, it is
fair to expect the heat island to have an impact on the indoor
environment that is likely to be adverse. Also, the variations due to
mechanical ventilation, structural differences, and air infiltration
may vary within a neighborhood as a Lunction of such factors as house
orientation, tree barriers, and terrain roughness.
Occupant activity, air-infiltration rates, the indoor sources of
pollutants, and their chemical natures are some of the factors that
cause variations within a city. A recent study11 in the Boston
metropolitan area obtained indoor air samples from 14 residence.", under
occupied "real-life" conditions for 2 wk each. As illustrated in
Figure v-5, the indoor-air character not only was driven by outdoor
concentrations* but was greatl> affected by other factors, such as
indoor activities.
Air-infiltration rates may be estimated by many dynamic
models. 5 ls ** ** 1,0 ** Tl 11 Network computer models1 are also
available. For tall buildings, there are methods for calculating
infiltration rates on an overa]l and floor-by-floor basis.7*"'* The
models vary in complexity and applicability. Their operational use
also varies considerably, and only a few have been experimentally
verified. Each of these models requires a number of input parameters
for estimating the air infiltration: number of exterior walls and
windows; use of each ruom; wind speed, direction, and pressure
differentials', indoor-outdoor temperature difference; heating,
ventilating, and air-conditioning (HVAC) systems; structural
characteristics; and terrain characteristics.
Hind 9peed, temperature difference, pressure differential, terrain
characteristics (roughness aud barriers* 3uch as trees and fences),
building orientation, and structure characteristics may be aEfected by
the location of one residence relative to another within a
neighborhood. Energy-consumption patterns in residences were the
subject of a 3-yr pcograa at Princeton University's Center for
V—16
-------
J3
o.
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200-
180-
160
140
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100
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Site
09
FT.GURE V-5 Mean of hourly indoor and outdoor nitric oxide concentrations (ppb) in Boston metropolitan
area with confidence Units. Reprinted with perroiriion from Moschandreas et al.
-------
Environmental Studies. An important segment of this work was to
determine the effects of barriers to prevailing winds on air
infiltration in residences. A series of wind-tunnel tests were used to
validate the air-infiltration model reported by Princeton
researchers.4* Figure V-6 describes quantitative results for end
units and interior units with and without tree sheltering. The "X"
shows the unit tested in the configuration of "townhouses" oriented to
the wind. The three wind speeds tested were 92 ft/s (28 m/s), 120 ft/s
(37 m/s), and 140 ft/s (43 m/s). The figures shown for air
infiltration were averaged for the three wind speeds. The authors
reached the following conclusions relevant to this section:
• Significant differences occur for the variety of
house/wind configuta.ti.ons tested. Depending upon the
particular house/wind configurations, end units experienced'
about 20 to 30% more infiltration than interior units clue to
the large expanse of side wall exposed to the wind.
• Sheltering effects, such as small, solid fences and
tall evergreen trees were found to significantly reduce
wind-produced air infiltration losses.
• The most effective windbreak tested in the present
quantitative study is that of a straight row of tall
evergreen trees. This type of windbreak produced a reduction
in air infiltration of 40% compared to the unsheltered
interior house. The combination of trees and fences results
in a reduction of 60%, compared to the case without tcees.
A foilowup study collected data on the air infiltration ip an
occupied residence before, during, and after a temporary tree windbreak
was installed. The benefits of tree-row sheltering were amply
illustrated with a wind speed of 5.6 m/s (12.6 mph) and air temperature
of 18°C (32.5®F). The air infiltration was reduced from 1.13 to 0.66
ach, a 42% reduction. Analysis of the weather conditions prevailing
during the heating season led to the conclusion that the tree barrier
would cause an overall reduction in air infiltration. A final
report' documented that the wind-velocity profile varies with the
roughness of terrain; the wind pressure distribution is changed and the
absolute pressure on a building is decreased by the presence of
obstacles within a few building lengths.
In conclusion, the studies done at Princeton showed that the
location and orientation of a residence within a neighborhood and the
tecrain and barriers surrounding it do affect the rate of air
infiltration. The difference between urban and suburban surroundings
also contributes to the complexity of determining the effect3 of
location on rates of air infiltration in residences. The functional
relationship between air infiltration and indoor air quality has not
been fully established, nor have the distribution patterns of indoor
air quality in the urban, suburban, and neighborhood areas. Further
research is warranted to study the cause-and-effeet relationship
between air infiltration and air quality and to formulate the best
V-18
-------
Houte-Wtnd Orientation
End Units
Air Infiltration
Average
Interior Units and
Tret Sheltering
Air Infiltration
Average
m
1.4 S«
2.35B
2.3M
1.098
0.7B6
0.0M
. . t .
• afi
~
E
1.240
1.2S9
o.m
0.853
0.738
0.650
0.498
FIGURE V-6 Effects of orientation and wind barriers on air
infiltration in tounhouse units. Arrow indicates wind directior.,
X.Indicates unit tested* Dashed lines indicate wind breaks.
Infiltration average in ach. Reprinted with permission from
Mattingly and Peters.
V-19
-------
balance between energy conservation and Indoor air quality in
commercial! as well as residential buildings.
A recent HUD publication, T'"" entitled Air Quality
Considerations in Residential Planning, is designed for routine use by
HUD staff to determine air quality at potential housing sites. A
special HUD environmental clearance rating is used to assess the
relationship between estimated air quality and ambient-air standards
and to determine whether the potential project should be rejected,
proceed with standard construction practices, or proceed after
mitigating steps are imposed. The mitigating steps include setting
residences away from major roads and specifying air-infiltration rates
and the use of pollutant control devices.
In a business district, ambient air quality and, correspondingly,
indoor air pollution are affected by the amount of local automobile
traffic. The General Electric Co.'* investigated the indoor-
pollution variations caused by traffic in the area of two complex
high-rise buildings. One of the buildings was an air-rights apartment
building that straddles the Trans Manhattan Expressway; the second was
a more conventional high-rise structure on a canyon-like street in
midtawn Manhattan. Several observations in this study are pertinent
when one is considering the distribution patterns of outdoor and indoor
pollutant concentrations as they are affected by site configuration.
• The vertical wind profile was different at the two
sites. At the air-rights building, a wind vortex was present at
times; at the canyon structure, road winds were limited to
particular directions only.
• The traffic flow rate and wind direction between the
street level and the third-floor level of the air-rights building
resulted in a random relationship, but "significantly lower"
carbon monoxide concentrations at the third-floor level.
However, at the other site, a linear relationship was observed
between street- and third-floor-level concentrations, regardless
of wind direction. This resulted in third-floor carbon monoxide
concentrations that ware only slightly lower than those observed
at street level.
• It was found that "pollutants generated at road level
diffuse as a function of vertical distance." Specifically,
typical exponential reductions in CO concentrations from the
bottom to top floors" were observed outdoors at both sites. This
elevation-related reduction in pollutant concentration was also
observed indoors, but it is less pronounced.
In addition, the General Electric study made a number of
recommendations that are relevant to air quality, its relationship to
neighborhood building planning, and specific efforts to reduce indoor
pollutant concentrations; lower floors of high-rise buildings must be
specially sealed from traffic-generated pollutants; building entrances
should be placed so that prevailing road winds are parallel to them;
convection paths inside buildings should be minimized; elevator control
rooms at roof level should be force-ventilated to reduce pollutant
V-20
-------
entrapment) and a parking garage in a large complex building should be
force-ventilated outside the building at a point that will minimize
reintroduction of the exhaust into the structure.
VARIATIONS IN INDOOR MR QUALITY IN BUILDINGS
The indoor air quality of an individual building is often
characterized by the 24-h average for the concentration of one
pollutant measured at one sampling location. Because the activity
patterns of persons are such that more time is spent in some indoor
areas than in others, the question arises:"* "Do indoor zones
(independent areas) with distinct pollutant patterns exist?" At issue
here is whether sampling from one monitoring zone is sufficient to
characterize the air quality of an entire building. Hoschandreas and
co-workers tried to answer this question with data obtained from 24
residences monitored under "real-life" conditions. Four-minute average
pollutant concentrations were obtained sequentially from four sampling
sites (kitchen, bedroom, living room, and one outdoor site). Hourly
averages of concentration were calculated from the 4-min information.
Corresponding hourly average concentrations of pollutants at the three
indoor sampling sites were not always equal. Indoor nitrogen dioxide
concentrations (Figure V-7) from two residences, one with gas cooking
facilities and the other with electric cooking facilities, illustrate a
more pronounced increase in the room with an indoor pollutant-
generating source.9' Statistical analysis did show significant
differences in the concentrations of pollutants between different
locations within a residence. Air-quality measurements are made to
determine the concentrations to which people are exposed. If there are
indoor zones where concentrations of pollutants are high and where
people spend substantial amounts of their indoor residence time, their
calculated exposure could be very different from that calculated on the
basis of a single measurement for an entire building.
The null hypothesis, tested by a two-tailed, paired t-test, was
that the mean of the differences between corresponding hourly average
pollutant concentrations at two indoor sites is equal to zero. This
null hypothesis was rejected in more cases than it was accepted in.
Comparison of the observed range and calculated differences led to the
conclusion that, although corresponding hourly indoor pollutant
concentrations are not uniform throughout a residence,• the differences
between sampled sites are small and probably of minimal health
importance.
In an extensive analytic study of indoor air quality, Shair and
Heitner'1 assumed that tt.ere are no pollutant gradients in the indoor
environment. The experimental data base of Hoschandreas and
co-workers10 verified that the gradients in concentrations of several
gaseous pollutants in the residential environment are negligible. J.D.
Spengler, R.E. Letz, J.B. Ferris, Jr., T.Tibbets, and C. Duffy reported
(at the annual meeting of the Air Pollution Control Association, in
June 1981) on weekly nitrogen dioxide measurements in 13S homes in
Portage Wisconsin. On the average, kitchen concentrations were twice
V-21
-------
TIME OF DAY TIME OF DAY
FIGURE V-7 Hourly concent rations of nitrogen dioxide at thre« Indoor locations In veaidencea with
gas (R14G) and electric (R!>E) cooking facilities. Reprinted with permission from Monchandieaa et al.^®
-------
those in bedrooms in homes that had gas stoves* A study of the air
quality in a scientific laboratory by West'* showed an almost uniform
distribution of an inert tracer continuously released in the room.
Similar experiments performed by Hoscbandreas et al. in residential
environments showed that equilibrium is reached throughout a house
within an hour. Episodic release of sulfur hexafluoride tracer gas
also illustrates this point. Figure V-8 shows the measured sulfur
hexafluoride concentrations plotted against time. The source location
was the living room; adjacent locations were the kitchen and the hall.
Episodic release of this inert gas in 24 residences vas followed by
uniform indoor distributions within 30 min.*T ** The one-zone
concept does not require instantaneous mixing, because it is based on
the behavior of hourly average pollutant concentrations.
Moschandreas and associates*° used a different data base derived
from the monitoring of 14 indoor environments in the Boston
metropolitan area. Analysis of variance was used to reach the
following conclusions:
* Pollutants (ozone and sulfur dioxide} generated principally
outdoors have little or no interzonal statistical difference indoors.
* Pollutants with strong indoor generation have interzonal
statistical differences in residences with gas facilities and offices,
but not in electric-cooking residences. In general* the observed
differences are not large, and the health differences are not expected
to be serious.
* Depending on indoor activity and outdoor episodic pollutant
activity, the indoor arithmetic 24-h average may or uay not adequately
represent the variation of hourly indoor concentrations.
* Although more th*n one zone would be preferable, hourly
pollutant concentrations- obtained from one indoor zone adequately
characterize the indoor environment.
These conclusions were arrived at in a particular investigation. A
properly designed, much larger experimental study is required to
determine the general significance and applicability of these findings.
The above conclusions are not applicable to short-lived
pollutants. Contaminants associated with tobacco smoke, bathroom
odors, allergens, and other pollutants related to dust are expected to
vary considerably in a given residence. Additional documentation is
needed to determine the extent of this variation.
BUILDING FACTORS
Site characteristics, desian, opevation, and occupancy all may
affect indoor air quality. Each affects the adequacy of a building's
systems for controlling environmental quality. They are components of
an environmental control system with the following functions: to
mitigate adverse ambient conditions, to provide for variations in the
intended occupant activity, to sustain the integrity of the structure
of the building, and to support continuous operation over the
V-23
-------
PITTSBURGH HIGH-RISE II
17 JUNE 77
TIME 1645
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TIME, minute]
FIGURE V-8 Episodic release of sulfur hexafluoride gas. Reprinted
with permission from Moschandreas et al.
V-24
-------
building's service life. The relationship between building factors and
indoor air quaLLty has not been quantified? or for that matter
extensively studied, but it Is important. Designing and controlling
building factors may prove to be an effective mechanism for achieving
desirable indoor air quality.
SITE CHARACTERISTICS
The characteristics of a building site that influence indoor air
quality are addressed as three related subjectsi air flow around
buildings# proximity to major sources of outdoor pollution and type of
utility service available.
The air flow around a building has been shown to be determined by
the local characteristics of the geometry of surrounding buildings/
the location and type of surrounding vegetation,71 the terrain,aj
and the size and shape of the building itself." Pollutants can be
transported by the air flow from street level, over the facade of the
building, and onto the roof.10 14 55 Field tests of isolated
tfuildings have been used to develop scaling coefficients for both
isothermal and stratified cases of surface wind pressures, turbulence,
and dispersion.17 11 Air flow around a building creates low pressure
on the leeward side and/or the sides adjacent to the windward face, as
well as the roof.90 Air pollutants released from stacks, flues,
vents, and cooling towers in the region can reenter the building
through makeup-air intakes for ventilation. 19
Trees and forests have been generally studied as shelter belts in
an agricultural context. Shelter belts affect air flow around
buildings. When an air current reaches a shelter belt, part of it is
deflected upward with only a slight change in velocity, part passes
through the crowns of the trees with very low velocity, and part is
deflected beneath the canopy with rapidly decreasing velocity.11 1'
The changes in velocity of air flow outside may change the infiltration
rate and thus affect indoor air quality.
The location of a building relative to a major outdoor pollution
source can affect irdoor air quality. For example, buildings near
major streets or highways often have high carbon monoxide and lead
concentrations, owing to the infiltration of these pollutants.1* 11 **
The type of utility service available is also related to the siting
of a building and may affect the character of its indoor environment.
The availability of particular fuels (e.g., natural gas and oil)
influences the types and concentrations of pollutants (e.g., combustion
products) emitted by space- and water-heating. Service moratoria,
development timing, and development scale are institutional elements
that contribute to the variability of utility services and thus can
affect indoor air quality.
OCCUPANCY
Occupancy factors that affect indoor air quality include the type
and intensity of fiuwan activity, spatial characteristics of a given
activity, and the operation schedule of a building.
V-25
-------
Several human activities-such as smoking, cleaning, and
cooking—generate gaseous and particulate contaminants indoors. The
number of occupants of a space and the degree of their physical
activity (i.e.i metabolic rate at rest or under intense activity) are
related to the production of various pollutants/ such as carbon
dioxide, *atei vapor, and biologic agents. If the only source of
indoor carbon dioxide production is that caused by occupants,
ventilation rates may be proportional to the number of people and their
metabolic rates.,s Although studies have shown no constant
relationship between carbon dioxide concentrations and the
concentrations of other pollutants, carbon dioxide concentration is
often used as a general indicator of the adequacy of ventilation in an
occupied space.
Building occupancy is often expressed as occupant density and the
ratio of building volume to floor area. The importance of occupancy in
indoor air quality is illustrated by the fact that the choice of
natural or mechanical ventilation is based on occupant density and the
spatial characteristics of the buiding under consideration. The use of
Yaglou's early work on the relationship between occupant density and
detectable body odor in determining necessary ventilation rates is
discussed elsewhere.
Occupancy schedules and associated building use may affect the
type, concentration, and time and space distribution of indoor
pollutants. Because most buildings are unoccupied for substantial
portions of each day, the manipulation of "operating schedule" is a
means of controlling energy use.1 Efforts to conserve energy through
the design of ventilation systems can result in the degradation of
indoor air quality.s> However, detailed studies relating ventilation
capacity, occupancy schedules, energy requirements, and indoor air
quality have only recently been implemented.
DESIGN
Elements of building design that affect the indoor environment
include interior-space design (space planning), envelope design, and
selection of materials.
The evolution of space planning in many building types has resulted
in flexibility in assigning functions to specific locations. However,
this flexibility is accompanied by a decrease in the ability to predict
exposure to air pollutants. In particular, "open-plan" offices and
schools have serious technical problems of redundant service
distribution, limited acoustic control, incomplete air diffusion, and
incomplete pollutant dispersion indoors, compared with "fixed-plan"
floor layouts.
Evaluation of the success of a floor plan in achieving space
efficiency, structural economy, and energy efficiency is usually in
terms of net area per occupant and ratio of net usable area to total
area. Explicit planning for environmental quality must be included to
ensure that spatial arrangements are acceptable to the occupants.
A building's structural envelope consists of both primary
elements—foundations, floors, walls, and roofs—and secondary "skin"
7-26
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elements—facings, claddings, and sheathing. To various degrees, the
function of these is to maintain the integrity of the structure under
the stresses caused by structural load, wind pressure, thermal
expansion, precipitation, earth movement, and fire. The integrity of
the building envelope is a major consideration in uncontrolled air
movement into and out of a building—usually referred to as
"infiltration." This is a major factor in indoor air quality. There
has been no systematic survey of infiltration rates of buildings in the
United States. The dominant factor in determining a building's
infiltration rate is the total area of effective leakage, as measured
with fan pressurization. Following the leakage area in importance are
the terrain and shielding near the building, the mean climatic
conditions during heating (or cooling) periods, and the building
height.'2 There is much evidence,1' both in the United States and
in Europe, that houses in mild climates are "very leaky," whereas
houses in severe climates are "tight."
Greater height of a building increases the "stack effect," or
updrafting, and exposes the building to higher wind speeds. Thus,
higher wind pressures drive air through existing openings, referred to
as "leakage," increasing the infiltration rate."' "
The dominant building factors that determine infiltration have not
been identified, but a catalog of leakage openings found in typical
structures is as follows:
• Walls: Leakage around sill plates (the openings at the bottom
of wallboard), electric outlets, plumbing penetrations, and headers in
attics for both interior and exterior walls.
• Windows and doors: Window type is more important than
manufacturer in determining window leakage.77 This source of leakage
tends to be overrated; it contributes only about 20% of the total
leakage o£ a house.9 71
Fireplaces: This includes dampers, glass screens, and
fireplace caps.
• Heating and cooling systems: The variables include combustion
air for furnaces, dampers for stack air draft, air-conditioning units,
and location of ductwork.
• Vapor barrier and insulation penetrations.
• Utility accesses: This includes recessed lighting and
plumbing and electric penetrations leading to attic or outside.
• Terminal devices in conditioned space: This includes leakage
of dampers, especially those for large air-handling systems.
• Structural types: Examples are drop ceilings above cupboards
or bathtubs, prism-shaped enclosures over staircases in two-story
houses, and elevator and utility shafts that lead from basement to
attic.
Wall and ceiling materials and floor finishes are the constituents
of the building interior. Modular components, weight, strength,
thermal insulation, thermal stability, sound insulation, fire
resistance, ease and speed of installation, and ease of maintenance are
among the criteria considered in the selection of materials for walls,
ceilings, and floors. But emphasis on first cost, ease of
installation, maintenance, and long service life has also led to the
V-27
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use of materials that may be sources of indoor contaminants, as
mentioned in Chapter IV.
OPERATIONS
Depending on the type of ownership (owner-occupied or
developer -owned), building operation may vary considerably* and this
variation may have an impact on indoor air quality. "Building
operation" pertains to the following elements of .a buildings'1 the
building envelope, service and plant, building facilities, equipment,
and landscaping. Cleaning, preventive maintenance, and replacement and
repair of defects are also included in building operation. The staff
responsible for building operation include management, engineering, and
custodial personnel. The care responsibilities are operation of the
heating, ventilation, and air-conditioning systems and building
services, such as hot water, lighting, and power distribution.
Building operation has an impact on indoor air quality in numerous
ways, but the magnitude of this impact is not known.
SUMMARY AND RECOMMENDATIONS
The nearness of a building to pollution sources and its orientation
with respect to wind affect the impact of airborne pollutants within
its envelope and the performance of its HVAC system. Air flow around
buildings, protective building placement, and landscaping at the site
and on an urban scale are useful in mitigating indoor contamination.
The magnitude and duration of activity in a building affect the
generation and dispersion of pollutants. Building classifications that
specify occupancy limits for safety and fire protection can also be
used to determine its environmental control requirements. The control
of indoor pollutants depends on floor layout, pollutant concentrations,
emission rates of sources, and type of ventilation system. These
factors vary with the age, region, and type of construction of the
buildings.
A systematic formulation of interactions of air turbulence,
stratification, and pressure distribution between buildings needs to be
developed to predict the effect of site conditions and design measures
for buildings. Also, objective measurements of concentrations of
contaminants for major classes of buildings need to be made for use in
predicting the effects of building factors on the requirements for
pollution mitigation within buildings. The measurement of dispersion
characteristics for basic floor layouts and systems should be
undertaken to identify methods of dilution or masking of pollutants.
The amount of energy required for mitigation with various control
strategies should be studied to optimize energy efficiency and indoor
air quality. The lifetime costs of various mitigation strategies
should be measured to identify promising firsts-cost and annual-cost
alternatives both for the design of new buildings and for the redesign
of existing buildings.
V-28
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25. Gibson, U. E., and R. E. Cawley. The heat pump solar collector
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29. Grot, R. A., and R. E. Clark. Air Leakage Characteristics and
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30. Iialitsky, J. Air flow and pressures near exterior building
surfaces. ASHRAE J. 7(7):37-38, 1965.
31. Halitsky, J. Gas diffusion near buildings. ASHRAE Trans.
69:464-484, 1963.
32. Hammer, P. G., Jr., and F. S. Chapin, Jr. Human Time Allocation: A
Case Study of Washington, D.C. Technical Monograph. Chapel Hill:
University of North Carolina, Center for Urban and Regional
Studies, 1972. 242 pp.
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33. hatley, R. K. Nationwide Personal Transportation Study.
Availability of Public Transportation and Shopping Characteristics
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34. Hittman Associates, Inc. Residential Energy Consumption in
Single-Family Housing. March 1973. U.S. Department of Housing and
Urban Development Publication No. HUD-PDR-29-2. Washington, D.C.s
U.S. Government pointing Office, 1974. 174 pp.
35. Jensen, M. The model-law for phenomena in natural wind. Ingenijfren
2:121-128, 1956.
36. Jordan, R. C., G. A Erickson, and R. R. Leonard. Infiltration
measurements in two research houses. ASHRAE Trans. 69:344-350, 1963.
37. Keyes, D. L. Population redistribution*. Implications for
environmental quality and natural resource consumption, p. 213. In
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and Public Policy. Washington, D.C.: National Academy of Sciences,
1980.
38. Kittredge, J. Forest Influences. The Effects of Woody Vegetation on
Climate, Water, and Soil, with Applications to the Conservation of
Water and the Control of Floods and Erosion. 1st ed. New York:
McGraw-Hill Book Company, Inc., 1948. 394 pp.
38. Kronvall, J. Testing of houses for air leakage using a pressure
method. ASHRAE Trans. 84(Pt. l):72-79, 1978.
40. Laschober, R. R., and J. H. Healy. Statistical analyses of air
leakage in split-level residences. ASHRAE Trans. 70:364-374, 1964.
41. Malik, N. Field studies of dependence of air infiltration on
outside temperature and wind. Energy Build. 1:281-292, l'J78.
42. Manasseh, L., and R. Cunliffe. Office Buildings. New York: Reinhold
Publishing Corporation, 1962. 208 pp.
43. Marin, A. Influence of stack effect on the heat loss in tall
buildings. ASHVE Trans. 40:377-386, 1934.
44. hattingly, G. E., and E. F. Peters. Wino and trees: Air
infiltration effects on energy in housing. J. Ind. Aerodyn. 2:1-19,
1977.
45. Mclntyre, D. A. Indoor Climate. London: Applied Science Publishers
Ltd., 1980. 443 pp.
46. Michelson, W. Time-budgets in environmental research: Some
introductory considerations, pp. 262-268. In W. F. E. Preiser, Ed.
Environmental Design Research. Vol. 2. Symposia and Workshops.
Fourth international EDRA Conference. Stroudsburg, Pa.: Dowden,
Hutchinson, and Ross, Inc., 1973.
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Pollutant Release Experiments and Numerical Analyses. U.S.
Environmental Protection Agency Report No. EPA-600/7-78-229b.
Research Triangle Park, N.C.: U.S. Environmental Protection Agency,
Environmental Monitoring and Support Laboratory, 1978. 240 pp.
48. Moschandreas, D. J. and S. S. Morse. The Relationship between
Energy Conservation Measures and Exposure to Indoor Toxic
Pollutants. Paper No. 27b, presented at the American Institute of
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Chemical Engineers «7th National Meeting, Boston, Massachusetts,
August 19-22, 1979.
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Morse, Indoor Air Pollution in the Residential Environment. Vol. 1.
Data Collection, Analysis and Interpretation. U.S. Environmental
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Monitoring and Support Laboratory, 197U. 201 pp.
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Indoor-Outdoor Concentrations ot Atmospheric Pollutants. GEOMET
Report No. ES-H23. Palo Alto, Cal.s Electric Power Research
Institutei 198Q.
51. ott, W. R, Human Activity Patterns* A Review ot the Literature tor
Air Pollution Exposure Estimation. SIMS Technical Report. Stanford,
Cal.: Stanford University, Department ot Statistics, (to be
published)
52. Ottensmann, J. R. Systems ot Urban Activities and Time: An
Interpretive' Review ot the Literature. An Urban Studies Research
Paper. Chapel Hill, N.C.: University ot North Carolina, Center tor
Urban ana Regional Studies, 1972. 45 pp.
53. Panotsky, H. A. The atmospheric boundary layer below 150 meters.
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447-463. In K. J. Eaton, Ed. Proceedings'ot the Fourth
International Conterence on Wind Eitects on Buildings and
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1977.
55. Rand, G. H. Caution: The ottice environment may be hazardous to
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49 pp.
57. Robinson, J. P. Changes in Americans* Use ot Time: 1965-1975: A
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Communications Research Center, 1977.
58. Robinson, J. P. How Americans UseJ Time in 1965. Ann Arbor:
University ot Michigan, University Microtilms International, i.977.
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60. Robinson, J. P., P. E. Converse, and A. szaiai. Everyday lite in
twelve countries, pp. 113-144. In A. Szalai, Ed. The Use ot Time:
Daily Activities ot Urban and Suburban Populations in Twelve
Countries. The Hague: Mouton & Co., 1972.
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indoor pollution concentrations to those outside. Environ. Sci.
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62. Sherman, M. H. Air Infiltration in Buildings. Berkeley, Cal.:
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63. Spengler, J. 0., B. G. Ferris, Jr., and 0. W. Dockery. Sulfur
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Occupancy. Report No. 1. Washington, D.C.: U.S. Department of
Transportation, Federal Highway Administration, Office of Highway
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Department of Transportation, Federal Highway Administration.
Washington, D.C.: U.S. Government Printing Office, 1972. 28 pp.
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VI
MONITORING AND MODELING OF INDOOR MR POLLUTION
This chapter discusses tt»e research tools required foe nea.suci.ng or
estimating indoor pollution &r.d exposure to i-t.
Techniques and instruments used for the measurement of outdoor
pollution, may be acidified far t)-.e sampling of indoor ernronneiit3.
Several problems eaerge with such modifications. and those problems are
discussed here, as well a3 instruments designed specifically for the
sampling of indoor air.
Personal monitors are increasingly recognized as powerful
scientific tools for determining individual, ari6 population exposure to
air pollutants. Although tiiey are still in the early stages of
application, it is clear the personal monitors can yield data that are
L'seful in associating human activities with exposure to air pollution.
The benefits and deficiencies of personal noniters are discussed in a
separate section of thjs chapter.
The extent of indoor air pollution can be estimated with numerical
models; mass-balance equations are used to estimate concentrations of
indoor pollutants as fractions of outdoor concentrations and to
estimate infiltration rates, indoor source strengths, pollutant decay
rates, and mixing factors. Several models have been developed, but few
have been validated against data obtained from measurements•
In estimating the total exposure of hu*atis to pollutants (exposure
to pollutants encountered indoor and outdoors, in industrial sites and
other woi^-iplaces, etc.), it is essential to know not only the pollutant
concentrations, but also individual patterns of nobility and use of
tine. The available information pertinent to the last two
characteristics has been gathered mostly by social scientists and,
although interesting, does not raeet the information needs for assessing
exposure to air pollution. The final section of this chapter discusses
the Idea of total exposure and what knowledge is needed to measure it.
FIXED-STATION SAMPLING AMD MONITORING
There is an extensive data base on outdoor air quality * and much of
the knowledge gained from studies of outdoor air quality is applicable
VX-1
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to the characteriiation of nanindustrial Indoor environments. However,
the characteristics of indoor air quality in residential and commercial
buildings and at other indoor sites can be quite different from those
of outdoor and heavy-industrial environments. Thus, a number of
special problems arise: the quality of indoor air is affected by a
broad spectrum of pollutants from both outdoor and indoor sources;
measurements of indoor air concentrations may require sampling
instruments considerably different from those used in the outdoor or
industrial environment; and the air volume inside a building is finite*
and the rate of air exchange (especially in residential units) may be
very low, and therefore, when air samples are drawn from an occupied
space by external samplers, the sampling flow rate must be so low as to
have only a negligible effect on indoor air movement and on the air-
exchange rate.
Because of the effects of equipment heat and noise, as well as
occupant inconvenience, sampling and monitoring equipment should (and
usually can] be placed in remote locations outside the building being
evaluated. Thus, it is common practice is to locate the instruments
outside the building space and draw air-sample streams to them.
Sampling techniques fall into the following broad categories:
• Continuous samplings Provides "real-time" sampling; required
to observe temporal fluctuations in concentration over short periods.
• Integrated or continuous sampling; Provides an average
sampling over a specified period; used when the mean concentration is
either desirable or adequate for the purpose.
• Grab or spot sampling; Provides single samples taken at
specified intervals; typically consists cf admitting an air sample into
a previously evacuated vessel', drawing a sample into a deflated bag for
later analysis, or drawing (by mechanical pump) a sample through a
sample collector to extract a contaminant from, the air; suitable when
"spot" samples are adequate for the measurement of a pollutant and
knowledge of temporal concentration variation over short periods is not
iraportant.
Some instruments sample and measure pollutants directly, and others
sample for later laboratory analysis. The direct-reading instruments
required for continuous monitoring use various types of physicocheaical
detectors that can measure the concentrations of pollutants ill situ.
Integrated or grab-sampling methods are used when there is no suitable
concentration sensor available, when the pollutants of interest are
present at concentrations too low to permit use of direct-reading
instruments, or when sampling sites are inaccessible to bulky
instruments. Further information on sampling and measurement methods
for air pollutants is available elsewhere.1 11
CONTINUOUS MONITORING
Continuous monitoring is a technique for sampling and measuring the
real-time concentration of pollutants. Indoor air quality is subject
VI-2
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to both temporal and spatial variations, and data on these variations
would be needed to determine the concentrations to which occupants are
exposed or to model indoor air pollution. The choice of monitoring
techniques must be consistent with the types of information desired and
the resources and manpower available. Mthcugh continuous monitoring
has numerous benefits, it also has a number of disadvantages.
Two positive features of continuous monitoring are that peak
short-term concentrations can be determined, in addition to average
concentrations calculated over any period, and that concentration
variation as a function of time can be correlated With source
generation, infiltration-ventilation, and other characteristics.
The availability of continuous-monitoring instrumentation depends
on many factors, including the chemical properties of the pollutant and
the range of concentrations to be measured. Continuous monitors are
commercially available for all the gaseous pollutants that are
designated "criteria" pollutants by the EPA—carbon monoxide, sulfur
dioxide, nitrogen dioxide, ozone, and total nonmethane hydrocarbons.
The EPA! has specified performance criteria for the instruments used to
measure each of these pollutants, and all analyzers that meet these
specifications in performance tests are designated "EPA-approved."
Continuous-monitoring systems, even with high-quality
instrumentation, are not trouble-free. For example, continuous
monitors are expensive and require frequent calibration and routine
maintenance. In addition, they have their own power and ambient-
temperature requirements and can create safety, heat, and noise
problems if they are placed at the sampling points. For these reasons,
monitoring systems are generally designed to have all equipment for
continuous analysis and recording at a single remote site, often a
mobile laboratory. Such a laboratory usually contains facilities for
calibration and maintenance, and it may also provide electric power and
suitable environmental conditions for the equipment. If sampling lines
made of flexible fluorocarbon tubing or other nonreactive materials are
used, air from several sampling points can be drawn into the laboratory
for analysis. One set of continuous monitoring equipment can be shared
by several sampling sites if the individual lines are sequentially
sampled.71 In this scheme, all instruments obtain air samples from a
common manifold, which, in turn, is supplied with air from one of four
sampling sites (one of which is usually outdoors) or from a calibration
system.71 The length of the sampling interval for each site can be
determined by the response times of the individual instruments, the
actual transit time in the sampling line, and the details of temporal
information required at each sampling site.
Continuous monitoring requires highly trained field personnel,
rigorous quality-control (calibration) procedures, and provisions for
quality assurance (independent performance audits of routine monitoring
and data-handling operations). Securing electric power and a suitable
location for a mobile laboratory equipped with sampling lines ar.d
cables can require long-term planning and entail considerable expense.
This type of fixed-station monitoring is not suitable for large-scale
surveys, because of these time and cost considerations. For
large-scale survey work, integrated sampling snd grab-sampling
techniques are generally more appropriate.
VI-3
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INTEGRATED SAMPMHS
Integrated sampling, in which a known sampling rate is maintained
over some period, ia commonly used for pollutants that must be
accumulated to permit analysis. The period of collection may be
several minutes or several weeks or months. Analysis nay be performed
at the collection site or in a laboratory. The data resulting from
analysis of integrated samples are expressed as an average
concentration over the sampling period. A variety of particles, gases,
and vapors are sampled by this technique.
Particles can be collected on filter media for later eraviaetric
and chemical analyses. Size-selective particle samplers, such as
various dichotomous air samplers1* and portable cyclone samplers,* * 141
are used in indoor aerosol sampling when it is desirable to determine
the concentration of fine particles (less than 2.5 ym in aerodynamic
diameter) or respirable particles [less than 3.5 ian in aerodynamic
diameter). The samples can be analyzed by beta gauge or gravimetric
techniques capable of determining mass concentrationf by x-ray
fluorescence, neutron-activation analysis, etc., to determine their
elemental composition; and by a variety of separation and analytic
techniques to determine chemical composition. Aerosol samplers must be
placed directly at the sampling sites, to avoid the particle losses
that occur when air is drawn through sampling lines. The
sophistication of particle samplers ranges from hand-held units that
require manual operation to fully automated units that can be programed
to operate unattended for several weeks.
Gaseous substances can be collected by both passive
(diffusion-controlled) and active [powered bulk air-flow) samplers.
Soluble vapors, such as formaldehyde and amaonia, can be collected by
liquid gas washers and bubblers. Air sampling with bubblers, as well
as with other accumulating sample collectors (such as adsorbers and
condensation traps), requires that the total volume of the air sample
be accurately known. This can be accomplished with dry- or wet-test
meters, which measure sampled volume directly, or by measuring or
controlling the sampling rate and time.
Many techniques have been used to measure the concentrations of
radon and radon daughters. Because of the low level,of radioactivity
usually found in buildings, integrated measurements are often
necessary. Passive devices that use sensitive thermoluminescent
dosimeter (TLD) chips,1' passive film, or track-etch techniques15
can record alpha decay over periods of weeks or months to determine
average radon concentrations. Radon-daughter concentrations can be
determined by passing a known volume of air through a filter paper
(typically for ID min) and then measuring total alpha activity on the
filter with an alpha-decay ratemeter.
Integrated sampling techniques have several advantages: they are
less expensive and requite less manpower than continuous monitors, they
can be used to measure concentrations that are too low to be measured
directly, samples can often be analyzed later at a more convenient time
or place, and average concentrations over long periods are easily
obtained. But they also have some disadvantages: short-term temporal
VI-4
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information is lost; samples must be taken frequently if tenporal
variability in concentration is to be assessed; transporting the sample
to its point of analysis may require special handling, special
environmental conditions, or rapid delivery to avoid deterioration; and
quality control may be more difficult to implement.
GRAB SAMPLING
In grab sampling, one sample is collected over a very short
period. Grab samples have to be taken frequently, if temporal
variability in pollutant concentrations is to be assessed. It is
usually the least expensive technique for field sampling, unless very
frequent samples are required. It may simply involve filling a
container with an air sample and transporting it to a laboratory for
analysis, or it may involve extractive sampling, as in colorimetric
detector tubes. It is most useful when the laboratory equipment
required for analysis is at a remote location, when a very large number
of samples are required, or when manpower and equipment are limited.
Sampling vessels commonly used include plastic bottles, glass tubes
filled with adsorbent, stainless-steel containers, and bags of aluminum
polyester (Mylar), PVC film, and fluoropiastic film.*1 Grab sampling
has been used to estimate concentrations of radon, tracer gases, and
organic compounds.
Grab sampling can be used to measure radon concentrations by
pumping a known volume of air through a filter into a Tedlar1* bag,
which is impervious to r^don. The time at which the sample is taken
must be recorded, and, .ause of the decay properties of radon gas,
analysis must be performed within a few days. If necessary, the sample
can be concentrated with a cryogenic trap or transferred directly into
a zinc sulfide scintillation chamber59 for alpha-counting. The bags
are inexpensive and can be mailed, with manual pumps, to field sites.
Similarly, air samples can be qualitatively and quantitatively analyzed
for organic compounds with gas-chromatographic techniques.
Grab sampling, with its low cost and minimal manpower requirement,
is suitable for large-scale survey work. However, a number of problems
are associated with this technique. No information other than an
"instantaneous" concentration can be obtained, and this value could be
greatly affected by something as simple as the opening of a door or
window. Sampled volumes are relatively small, and the laboratory
measurement technique must be sensitive enough to determine ambient
concentrations directly. Inward and outward diffusion of various gases
has been observed for many materials used in collection bags, and leaks
in the containers and connectors are common. Particular attention must
be given to degradation, adsorption, contamination, transformation, and
the possible formation of artifact pollutants.*' The expeditious
transport of grab samples with reference to time, temperature, sealing,
and handling is important. Quality control is difficult to maintain,
but must be established before this technique can be U3ed with
confidence.
VI-5
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MONITORING OF VENTILATION RATE
Indoor air quality is directly affected by the rate at which
outdoor air enters a building. Ventilation can be t'sed to maintain low
concentrations of indoor-generated pollutants. In turn, human comfort
conditions, such as temperature and relative humidity, can be the
determining factors in setting ventilation rates. Measurement of the
infiltration-ventilation rate* the meteorologic factors that affect it
(outdoor temperature, wind speed, and wind direction), and comfort
factors (temperature and relative humidity} can be an integral part of
fixed-location field monitoring.
Ventilation systems vary considerably. Detached single residential
units are ventilated primarily by infiltration—the uncontrolled
leakage of air through cracks in the building envelope (around doora
and windows, through walls and, floor joints, etc.)—and by the
controlled opening of windows and doors. Large buildings are usually
ventilated by mechanical systems of varied complexity.
So-called fresh air enters detached residential structures by
infiltration; the term "air changes per hbur" (ach) is routinely used
far this gourde of ventilation—"1 ach" means that a volume of outdoor
air equal to the volume of the interior building space "leaks" inside
each hour. That does not imply that the incoming air drives out or
displaces the old air as it enters; rather, it i3 assumed that perfect
mixing takes place. In practice, however, perfect mixing is impossible
to achieve. Therefore, an estimate of outdoor-air flow rate is based
on the assumption of perfect mixing and homogeneity of Lndoor air to
facilitate calculating infiltration rates.
By far the most commonly used method of estimating air-exchange
rates is the tracer-gas decay technique."' In this method, a tracer
gas is released into the building space at one or more points, possibly
with the use of fans. In this way, an attempt is made to produce a
uniform concentration throughout the building space. If homogeneity is
maintained, the decay of the tracer gas is exponential, and the
infiltration rates can be determined by sampling the air at several
times. The air-exchange rate can be obtained from the slope of a
semilogarithmic plot of the natural logarithms of the pollutant
concentration versus time.
In a similar method, the equilibrium-concentration method, a tracer
gas is released at a constant rate into the building space.** In the
steady-3tate condition with perfect mixing, the indoor concentration
will reach a steady-state value. From this and the injection rate, the
infiltration rate can be calculated. With this technique, although it
is simple to perform, it often takes many hours to reach a steady-state
equilibrium.
More complex tracer-gas systems can measure infiltration rates on a
semicontinuous or continuous basis.1*7 Many gases have been used for
tracer-gas measurements. Some of the properties that such a gas should
have are easy measurement at low concentrations, minimal interference
from other air constituents, chemical stability, nonreactivity, lack of
absorption by building contents, a density comparable with that of air,
safety for humans, lack of explosiveness and flammability, absence of
Vl-6
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other interior or exterior sources/ low cost, and ready availability.
Some gases commonly used are sulfur hexafluoride, nitrous oxide, and
ethane.*•
Mechanical ventilation systems vary considerably in design and
complexity, and methods chosen to estimate ventilation rates must be
suitable for the systems under consideratSon. The methods commonly
U3ed to estimate the ventilation rate for systems that use
recirculation include pressure-measuring devices (such as inclined
manometers and U-tubes), velocity meters {such as pitot tubes, hot-wire
flowmeters, heated-thermistor flowmeters, and heated-thermocouple
flowmeters), mechanical gas-flow indicators {such as rotating and
deflecting-vane anemometers), tracer-gas techniques, and heat-balance
techniques. '* Care must be taken to distinguish between the total
rate at which air enters a particular zone and the rate at which
outside air enters the zone.
Temperature-measuring devices suitable for continuous monitoring
include thermocouples, semiconductors, and thermistors. Typical indoor
temperatures range from 15 to 40°C. Thermocouples present problems
with low voltage outputs near 0°C and have nonlinear characteristics,
but only when the cold junction is at 0°C. Semiconductor temperature
sensors that use integrated circuits and have a voltage output linear
with temperature are suitable for continuous recording. The most
common temperature probe for measuring temperatures in this range is
probably the thermistor, because of its high resistance ratio (which
yields large voltage changes for small changes in temperature), its
linearized output, and its wide operating range. Temperature gradients
can be large in a building and even in an individual room. Probes
should be placed where they will sense the temperature experienced by
the occupants. Temperature probes should be calibrated against mercury
thermometers that meet the specifications of the American Society for
Testing and Materials (A.STM) .
Relative humidity can be measured with sensors of the "human hair"
type, which expand and contract with changes in humidity) or with
dewpoint-measuring devices. Commercially available dewpoint
hygrometers, based on the principle that the vapor pressure of water is
decreased by the pressure of an inorganic salt, are well suited to
continuous monitoring. Relative humidity can be readily calculated
from dry-bulb and dewpoint temperatures. Relative-humidity measuring
devices can be calibrated with the aid of sling psychrometers.
PERSONAL MONITORS
Over the last 2 decades, a wide variety of miniaturized air
samplers have become available that collect gaseous and particulate
samples from the immediate vicinity of people, even as they conduct
their normal activities. The initial devices used battery-powered
samplers, defined as "nonpassive." Although widely used, these devices
are often larger and heavier than desirable. More recently, a variety
of diffusion- and permeation-controlled samplers have become
available. These "passive* devices are applicable solely to gas- and
Vl-7
-------
vapor-sampling and are very snail and light. They all use sensitive
chemical or physical analytic methods.
Three recent workshops reviewed candidate technologies for personal
sampling and monitoring of air-pollution exposure. A Brookhaven
group*7 identified potential methods tor gas- and paftide-
monitor ing. An EPA feasibility study" identified useful methods for
monitoring sulfur dioxide, nitrogen dioxide* and ozone. Another EPA
symposium*4 explored the use of available technology for
health-effects studies and other uses.
Blood carboxyhemoglobin (COHb) can be used as a measure of the
actual dose of carbon monoxide received by a person.
Respirable-particle concentrations are also of prime concern in
health-effects studies; some of the factors involved in obtaining
reliable data have been evaluated.*1 101
PERSONAL SAMPLING DEVICES
Gas-Sampling
The major techniques developed for sampling gaseous pollutants are
passive (based on membrane permeation or diffusion through a
geometrically defined air apace) and nonpassive (in which air-pumping
devices draw defined air volumes through devices of known collection
efficiency).
Passive Samplers. Passive samplers use the kinetic energy of gas
molecules and the efficiency of the adsorbent collector to extract
pollutant molecules from the air at a known rate. The sampler must be
placed at the collection site, but has no requirement for a pump, flow
regulator, or batteries. Such samplers therefore have major advantages
with respect to weight, cost, .and maintenance. There are two basic
types: diffusion and permeation. Their use is limited by the rate and
amount of gaseous diffusion through a geometrically controlled air
space or by transport through a permeable membrane that is specific for
the pollutants being sampled.
The choice and use of the diffusion-collector technique require
knowledge of the coefficient of diffusion of the pollutant to be
sampled in air under conditions similar to those normally encountered.
Humidity effects have been encountered; these are most probably caused
by changing absorbent efficiency.
One diffusion sampler has been developed'1*" for the measurement
of ambient nitrogen dioxide. It uses the principle of diffusion
through the bore of an open tube that defines the rate of transport to
the collector., The quantity of nitrogen dioxide diffused from the open
end of the tube to the collector surface (triethanolamine) is .
calculable by Tick's first law of diffusion, which may be expressed as:
Qn0^ = D(A/L)Ct,where 0^02 " number moles of nitrogen dioxide
VI-8
-------
transferred during time t, A » cross-sectional area of tube {cm2},
L « distance from open end to collector surface {cm), C = concentration
difference between tube entrance and closed end (mol/cm^), and D *»
coefficient of diffusion of nitrogen dioxide in air (c»2/s). The
required nitrogen dioxide absorbed** ia given as a time-weighted
average concentration for the sampling period.
Substituting typical values of the parameters—D ¦ 0.154 cm2/s,
A • 0.71 on2, and L » 7.1 cm—simplifies the expression tos
QnO; " (ppm-h) X 10"9.
In principle, this method is applicable to determination of any
gaseous air pollutant foe which an efficient, selective absorbent is
available and for which an appropriate analytic chemical procedure may
be devised. The size of the sampler can be varied, but attention must
be given to scaling factors.*' 14 Diffusion samplers have reportedly
been used for water vapor and sulfur dioxide, *' nitric oxide," ' 5
aniline, 11 benzene,' >s ammonia,*1 carbon monoxide," and
NCtjj.*5 An activated-carbon element has been used as the collector
in a badge that has an open grid to define the geometry of the gaseous
diffusion port. ,l This method of sampling requires use of
gas-chroraatographiq (GC! analysis, for measurement of the specific
gaseous pollutant absorbed. A variety of organic compounds can be
sampled and measured by this technique*
A large latiety o£ permeation sassplecs vised Eos rsonitot ¦systems ate
available commercially. All use membranes fabricated and calibrated to
control the rate of permeation of the pollutant tb the collector, which
may be a solid medium, such as charcoal or Tenax GC for specific
chemicals. Processing of the collected sample varies widely;
chromatographic or colorimetric procedures are commonly applied for
measurement.
Transport of a gaseous pollutant across a membrane resembles the
diffusion process.10'' However, permeation involves solution of the
gaseous species in the membrane. Specific interaction between the gas
and the polymer matrix introduces variables. As in a diffusion
collector, the concentration of the gas approaches zero on the aide of
the membrane next to the collector, causing a gradient that results in
flow froa the ambient-air side.
The permeability constant, P, of a membrane is defined by the
equation K = PA(C^ - Cjl/S, where U » fate of transport across the
membrane (raol/s), P = permeability constant {cm2/s), A - cross-
sectional area
-------
Merabranes used in permeation collectors are made from polymeric
materials, such as dimethylsilicones, silicone polycarbonate,
silicones, cellulose acetate, TFE Teflon, FEP Teflon, Mylar, polyvinyl
fluoride, Iolon, and Silastic. Thicknesses of 2.5-2S x 10~3 cm have
been tested."
The permeation collector with activated absorbents is particularly
useful for organic pollutants when GC analysis is applied. Commercial
monitors are available from the 3M Corporation1® and Du Pont that
allow determination of more than 80 compounds by this method. Sulfur
dioxide,11 ## 1Q1 chlorine, 17 ltt vinyl chloride,75 ,t5 147
nitrogen dioxide, lB* alkyl lead, 187 and benzene 107 have been
determined. The utility of a spectrum of absorbents ir. these passive
collectors has been tested.'
Nonpassive Systems. A considerable variety of sampling systems
using pumps to move the air have come into use over the last 2 decades,
including impinger systems and solid adsorbers for gases and impingers,
filters, and inpactors for solid particles. Directly indicating
devices using impregnated papers, chalks, and crayons and
stain-detector tubes have also been used. These techniques have been
reviewed in detail by Linch55 and Saltzman.®1
A recent development in personal monitors involves a pump that is
positioned next to the wearer's diaphragm by a light harness. The
volume of air pumped by the motion of the thoracic cavity,is recorded
by an electronic package, which may be checked by a detached readout
system. This system samples air for gases through coaled
diffusion-tube collectors or for particles through small filters at
flow rates of 75-500 ml/min, depending on the wearer's breathing rate.
The complete apparatus weighs 590 g.. In conjunction with spirometer
calibration, actual exposures to measured pollutants may be calculated.
Particle-Sampling
Particulate samples are collected by using the same principles used
for large-scale samplers: filtration, impaction, and liquid
impingement. The separation of the respirable fraction of particles is
of considerable importance for personal monitors, and collection of
adequate numbers of samples for analysis is critical. All'particle-
samplers use some'device for moving the air sample and for separating
the respirable-particle fraction. Collection is preceded by 3uch a
device as a cyclone presampler. The relatively low power available to
drive the air-sampling pump usually limits particle collection by
personal monitors to filtration, either in a single stage or in a
second stage that follows a cyclone that collects the large,
nonrespirable particles. For respirable-paiticle-sampling, the
air-flow rate must be precisely controlled.
The theory of aerosol collection bv filtration has been extensively
reviewed by Dorman,11 Pich,'7 Fuchs,1* Green and Lane,1* Liu
and Lee,*7 and Lippmann.1* Small-scale impaciors suitable for
respirable-dust-sampling with a personal monitor have been described by
Marple'1 and Willeke. I0*
VI-10
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Biologic Monitoring
Measurements made on the human body and its excretions constitute
an alternative way of measuring exposure to environmental pollutants.
They include measurements of blood, urine, feces, and hair. The
methods that can be used to relate environmental pollutant exposure to
human composition have been reviewed at length in other NRC reports (on
carbon monoxide, nitrogen oxides, and various trace metals).
USE OF PERSONAL MONITORS IN EXPOSURE STUDIES
Exposures to air pollution usually vary with a person's mobility
patterns and activities. Therefore, estimating the total exposure of a
person from one or a few air-pollution measurements at stationary
locations cannot properly characterize the variation in a population's
or a person's actual exposures. To evaluate health effects, it is
necessary' to know actual personal exposures and the distribution of
thos£ exposures in' a population. The need for direct measurement of
personal exposure to pollution has been noted by several authors.*' *'
Personal monitors for various pollutants are commercially
available. The Brookhaven workshop identified four basic experimental
designs:,e
1. Use of Individual Air Pollution Monitors for Direct
Determination of Exposure. Each person in the study
population would wear or carry an individual air pollution
monitor during the course of the study. The same individuals
would also be subjected to continuous or periodic evaluation
of health responses. Individual exposure and response would
thus be measured. . . . Because of economic constraints, only
relatively small populations could be studied by this direct
approach.
2. Use of Individual Air Pollution Monitors to Adjust
Results from Fixed Stations. As previously indicated, there
can be substantial variations between area level measurements
and personal exposure measurements. By monitoring exposure
of individuals with individual air pollution monitors in
areas also monitored with fixed stations, one would obtain
the distribution of individual exposures in relation to
measurements obtained at the fixed stations. If one or
several relatively constant relations were found in various
areas, fixed-station data would then be corrected for use in
estimating population exposures.
3. Use of Representative Sampling to Determine Subgroup
Exposure. A carefully selected sample of the study
population would be asked to wear or carry individual air
pollution monitors. The sample would be stratified, grouping
those expected to have similar exposures (e.g., office
VI-11
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workers or street Workers) . The measured exposure of each
subgroup in the sample could be used as rapresentative of the
entire group.
4• Use of Individual Air Pollution Monitors to Calibrate
Personal Activity Models. Activity models have been
developed that describe how and where people spend their
time. . . . These models could prove to be useful in
estimating population exposure. They have not been applied
in air pollution epidemiology except in a very limited way,
and they could be best calibrated or verified through
experiments using individual air pollution monitors.. In such
an experiment, a carefully selected sample of the study
population would be asked to wear individual air pollution
monitors, and their measured exposure would be compared with
the estimated exposure of the activity model.
Gaseous Pollutants
Carbon Monoxide. Ott and Mage7® collected 425 integrated carbon
monoxide samples over 21 d in November 1970 and January 1971 in
downtown San Jose, California. Breathing-zone samples collected while
the subjects walked typical pedestrian routes were compared with tnose
measured at the fixed monitoring stations. The mean pedestrian
exposure was 1.6 times the mean concentration measured by the fixed
monitors, but individual measurements of exposure varied from those
measured at the fixed stations by a factor of up to 10. Ott and Mage
concluded that the fixed-station monitoring data "provide a relatively
poor measure of the true' exposure of members of the general public to
air pollutants."
Wright et al. 111 sampled exposures in Toronto with portable
carbon monoxide monitors. They demonstrated a "substantial discrepancy
between the carbon monoxide concentrations detected by Hie provincial
network of fixed-site sampling stations and the much higher
concentrations commonly met by people living and working in a large
metropolitan area such as Toronto."
Cortese and Spengler" measured exposure of Boston commuters
equipped with portable carbon monoxide instruments (Ecolyzers). They
reported that 1-h exposures exceeded fixed-monitor measurements by a
factor of 1.3-2.1? 8-h mean exposures were considerably below the 8-h
mean from the fixed monitor.
Wallace 1#* carried a carbon monoxide dosimeter during 30
commuting trips by bus to his office in Washington, D.C.
Concentrations inside the vehicles were typically 2-4 times those
continuously measured in the central city at the fixed monitoring
station (Figure VI-1). There was no correlation between the ambient
and personal in-vehicle measurements.
Nitrogen Dioxide. In a personal-monitoring study of children in
Ansonia, Connecticut,# nitrogen dioxide and sulfur dioxide were
VI-12
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35 i—
30
25
iM
3
8 15
10
Carbon Menoxld*
Concentration: in Vchicla
' ' ' ' ' ' '
Ambient CO Concentration* in City
During Commuting Hour*
8 101214 161820 22
JULY
-h
_L
J L_i__L
4 6 8 101214 16
AUGUST
FIGURE VI-1 Carbon monoxide concentrations in vehicle,
compared with ambient concentrations in city. Reprinted
from Wallace.
VI-13
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measured with bubblers." Twenty boys were equipped with suitcase
samplers that they carried for one 24-h day. Exposure to nitrogen
dioxide tended to be greater in children exposed to smoking at home,
but the differences were not statistically significant. As with sulfur
dioxide, mean personal exposure values (61.3 ± 7.2 yg/m3) were
significantly lower than mean outdoor nitrogen dioxide concentrations
(100.1 19.0 iq/a?).
Palmes et_aK ' * has described a passive personal sampler for
nitrogen dioxide suitable for occupational exposures. The same device
has been used to estimate 1-wk average indoor nitrogen dioxide
concentrations in 109 dwellings with gas stoves and nine with electric
stoves in metropolitan New York." It wad found that the homes with
gas stoves had significantly higher nitrogen dioxide concentrations
than those with electric stoves. Average values in the kitchens with
gas scoves approached the U.S. primary ambient-air quality standard of
50 ppb (annual average).
These dosimeters were used in a personal-monitoring study of five
families with gas stoves and four families with electric stoves in
Topeka, Kansas.1' In each family, the husband, wife, and one child
wore the dosimeters for four 1-vk samples. Dosimeters were also placed
outside, in the kitchen, and in the bedroom. No significant
differences were found between the personal-monitor and outdoor
measurements for the families with electric stoves (Figure VI-2). For
the, families with gas stoves, personal exposures were significantly
higher than outdoor values and correlated best with the fixed
dosimeters in the bedroom. No significant differences in exposures
were found between family members.
Sulfur Dioxide. Exposure to sulfur dioxide has been estimated in
several studies by the calculation of a time-weighted average exposure
from the time spent and average concentrations in various places.1* *T
Sulfur dioxide personal monitors have not been extensively used in
field studies.
In the personal-monitoring study of children in Ansonia,
Connecticut, no significant difference was found among the sulfur
dioxide personal exposure measurements of the boys.* The personal
samplers had a mean of 5.5 ± 0;07 ig/m*, which was significantly
lower than the outdoor mean of 12.0 ± 2.2 ug/n>^. The reports of
daily activities showed that the children were indoors between 60% and
80% of the day.
Passive personal monitors using the collection principle of gas
permeation through polymer membranes have been shown to be sensitive to
24-h average concentrations of sulfur dioxide down to 0.01 ppm.1 1,7
Sampling at ambient concentrations with treated filters also appears
feasible.®7 However, no personal-monitoring results with these
techniques have been reported.
Organic Substances. Several passive monitors have been developed
that may have the sensitivity to measure mean personal exposure to
organic substances for sampling periods of 1 d to 1 wk.* '1 " "
Their use has yet to be demonstrated in personal-monitoring programs in
nonindustrial environments.
VI-14
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Z 50
O
Electric Stove
FIXE 0 r PERSONAL
<
ce
K
Z
ILI
O
z
o
o
N
o
z
30
10
_L
-L.
JL
Wife
_L
2 3
WEEK
Gat Stove
70
— K
z
o
<
IE
t-
Z
UJ
U
z
o
o
o
O
z
50
30
10
_1_
J_
1 2 3
WEEK
PERSONAL
.Wife
Hutbartd
Child
1 2 3
WEEK
2 3
WEEK
FIGURE VI-2 Week-long nitrogen dioxide concentrations, vigJ
for an electric-cooking and a gas-cooking family in Topeka,
Kansas, May-June 1979. B, bedroom; K, kitchen: 0, outdoor.
Reprinted with permission from Dockery et al.
VI-15
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Particles
Resplrable Particles, in the Ansonla study,• personal exposures
to resplrable particles were significantly higher among children who
lived with one or more amokers. The mean personal exposure, 114.5 ±
9.0 yg/ra , was significantly higher than the mean outdoor
concentration, 58.4 ±5.9 jig/ra3. The outdoor high-volume
samplers, however, collected both resplrable and nonrespirable
particles. The principal conclusion of this study was that a child's
exposure "load" of air pollutants, especially resplrable particles, is
determined primarily by indoor exposures.
Personal exposure to resplrable particles and sulfates has been
measured in two cities as part of the Harvard six-city study, 11 in
which 37 people carried personal respirable-particle monitors with them
during the day. Fixed-station monitors were run simultaneously in the
main activity room of each home and at several locations outside.
There were at least three complete sample days for each person.
Mean personal exposures to resplrable particles and sulfates for
each city were determined on the basis of mean outdoor concentrations.
In each city., there wore significant differences in results between
individuals, as determined by their activities. A linear; increase in
personal exposure to resplrable particles with the number of smokers in
the home and workplace was found.
Lead. Berlandi et al.' have reported personal lead-exposure
measurements from 2 d of sampling in metropolitan Boston. Samples
collected while subjects were driving into Boston had a time-weighted
average of 4.5 yg/m the first day and 3.7 pg/m3 the second;
indoor personal samples were all less than 1 pg/m3. FugaS et
al.2 * estimated average air lead exposure of an office worker in
Zagreb. Air lead was measured with a personal monitor inside and
outside her home and her office and at other sites. Table vl-1 shows
that the average concentrations were highest in association with
outdoor activities—6.3 pg/m3—with only 1.7 pg/m3 or less from
indoor sampling. A time-weighted average exposure was then calculated
on the.basis of her activities each week (Table VI-1). The average
weekly exposure was estimated to be 1.1 pg/m3, compared with the
average measured value of 0.72 pg/m3 outside the subject's home.
Fugas17 extended this method of estimating exposure to lead in
air to a middle-sized industrial town in Yugoslavia. Air lead was
measured ac various locations indoors and outdoors during the winter of
1972-1973. Estimated exposures were considerably higher than the
average urban monitoring-station value of 0.9 pg/m3.
Lead concentrations up to 10 times that found in buildings may be
found in vehicles or outdoors. The contribution of outdoor and
vehicular exposure to mean personal exposures may be small, because of
the comparatively short exposure times.
Vl-16
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TABLE VI-1
Calculation of Time-Weighted Weekly Average Exposure of
Office Worker In Zagreb to Airborne Leada
Average Lead Integrated
Concentration, Duration of Exposure,
Location or Activity ug/rc Exposure, h/wk yg-h/m
Workplace 1.2 42 50.4
Outdoor activities 6.3 14 88.2
Recreation 0.2 6 1.2
At hone:
Rest of day 0.7 22 15.4
Night 0.3 48 14.4
Weekends 0.5 36 18.0
Total — 168 187.6
Weighted-average weekly exposure: 1.1 ug/m^
aData from Fugas et al.
VI-17
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Biologic Indicators
Direct measurement of individual dose by biologic means is possible
for several pollutants. This method intrinsically compensates for
different rates of uptake by different persons, as well as for
differences in exposJre.
Carbon Monoxide. Actual carbon monoxide dose received can be
measured directly by measuring blood carboxyheraoglobin.
Stewart ejt al.'measured COHb of blood donors in 25 American
cities. They reported COHb concentrations higher than those expected
from fixed-station monitoring data. Goldmuntz1* ccapared COHb
measurements for nonsmokers from 1969 through 1972 with carbon monoxide
measurements from 37 EPA fixed-station monitors in 1973. Goldmantz
argued that the measurements from so'ie of these fixed stations may be
inappropriately high, because of their siting.
Morgan and1 Morris" calculated COHb concentrations that would be
expected if the population were in equilibrium with the measured
fixed-station carbon monoxide concentrations by the relation, % COHb ¦
0.16JCO] + 0.3, where [CO] is the carbon monoxide concert.ation (ppnt),
Comparing these calculations with nonsmoker COHb measurements, they
concluded that "the average dose indicated &y COHb levels exceeded that
predicted from the fixed-station data by a factor of 2."
Stewart et al., in a similar analysis of data obtained in
Chicago in 1970 and 1974, reported COHb concentrations close to, but
consistently higher than, those predicted from fixed-station
measurements. They noted that the use of fixed-station measurements to
define population exposure may not reflect worst-exposure situations,
indoor exposures to caroon monoxide from cigariette smoke, or exposures
from faulty heatir.g systems. Kahn e^t al_. s® demonstrated that COHb
concentrations among nonsmokers in the St. Louis population are
strongly affected by occupational exposure and by exposure to smokers.
Lead. There is little doubt of a correlation between the high
exposures to lead in the air of industrial areas and indexes of lead
absorption, such as blood lead, urinary lead, delta-aminolevulinic acid
dehydrase (ALAO), and delta-aminolevulinic acid (DALA). The
relationship between these measures of lead dose and the lower
concentrations of air lead characteristic of the community—i.e., less
than 10 yg/m^—is not well established. A National Research
Council ccramittee has stated that "more precise studies are needed of
the relation between atmospheric lead exposure in the urban environment
and the concentration of lead in the blood, perhaps by the use of
personal monitors.""*
In an attempt to characterize this relationship, Azar et al.*
compared average, exposures to lead in air measured by personal
monitoring with the biologic indexes of lead absorption. Tvto groups of
30 U.xl drivers Ln two cities cx.c three groups of 30 Uu Pent employees
in three cities carried personal particle monitors with them for 2-4
wk. Their exposure to air lead was calculated as a time-weighted mean
for their exposures at home and at work. Blood lead was determined
VI-18
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weekly, and urinary lead daily. Different relationships were found
between average exposure to airborne lead and the logarithm of the
blood lead concentration in each city. The plots of the data for all
five groups, however, had a cimilar slope, with different Intercepts.
The authors suggested that the different intercepts indicate that
variables other than airborne lead, presumably ingested lead, are
affecting blood lead content. No comparisons with fixed monitoring
were made.
MODELING OF INDOOR AIR QUALITY
The value of an indoor air pollution model is twofold. First, it
provides a framework for interpreting experimental results and for
planning new experiments. Specifically, a model is useful in relating
indoor pollutant concentrations to various geometric, ventilation,
source, and sink parameters. Modeling cart be used to determine the
accuracy and precision to which various quantities must be measured if
the desired accuracy of prediction is to be achieved. It car also oe
used in sorting out trends in tha experimental data.
Second, and more important, a model provides a means to predict
accurately some desired function of concentration (such as peak
concentration or dosage) for places and conditions other than those
tested experimentally.
In epidemiologic studies, it is important to consider the quality
of the air to which subjects are actually exposed; in many case3, the
air quality associated with the home, the mode of transportation, and
the workplace should not be taken to be the same as that associated
with the outside.
Indoor-air-quality models are developed to aid in understanding and
predicting indoor air-pollutant concentrations and dosages as functions
of outdoor air-pollutant concentrations, indoor-outdoor air-exchange
rates, and indoor aii-pollutant sources and sinks.
Air pollution indoors may be of outdoor or indoor origin. Outdoor
pollutants may enter a structure through infiltration or ventilation.
Pollutants of indoor origin may arise from point or diffuse sources.
Regardless of their source, air pollutants may be transported and
dispersed throughout various regions of the enclosure. Some pollutants
may be removed by filters through which the makeup air or the
recirculated air flows, by exfiltration or ventilation to the outdoors,
and by chemical change. In the case of particles, surface removal and
generation are often important.
Given familiarity with the system to be described and with the
purpose of developing and using an indoor air pollution model, the
starting point in developing a model is usually a statement of. the mass
balance concerning the pollutant of interest. For example, consider a
structure of volume V, in which makeup air enters from the outside and
passes trough a filter at a rate qg. Part of the building air is
recirculated through another filter at a rate q^, and air infiltrates
the structure at a rate qj* Each filter is characterized by a factor
F 3
-------
concentration is assumed to be uniform throughout the structure. The
indoor and outdoor pollutant concentrations at time t are C and Cg,
respectively. The rate at which the pollutant is added to the indoor
air owing to internal sources is S. The rate at which the pollutant is
removed from the air owing to Internal sinks is R. In this case, the
appropriate starting equation is:
Vi!f =
-------
adequate description. For example, stratification in a room cannot be
neglected when one is describing the movement of smoke and toxic gases
associated with building firesj111 however, even in such a case
(where intense stratification is to be expected), only two compartments
(coupled) were needed to obtain a satisfactory description.
Sulfur hexafluoride tracer experiments, conducted with average-
sized rooms (20 x 20 x 8 ft) in which one or more persons were moving
and in which the air was being exchanged about 3 times per hour, have
suggested that associated eddy diffusivities are around 10^ cm2/s
(D. D. Reible and F. H. Shair, personal communication); thus, about 5
min after an instantaneous point-source release, tracer concentrations
(although decreasing) were about equal throughout most of a room.
The solution to the two-compartment model with constant
coefficients is presented below, after a brief general discussion of
multicompartment models. Examples of two-compartment and single-
compartment models of indoor air quality are also discussed.
MULTICOMPARTMENT MODELS
Most n-compartment models have been (or probably will be) described
by n coupled first-order linear ordinary differential equations of the
form:
dx^
— + » a2X2 + a3X3 + anXn + an + ±
dx2 (2)
+ bxX2 = b2X! + b3X3 + bnXn + bn + i
dxn
dt~ +
In general, the terms aj_, b^, etc., represent the sum of
first-order losses from the compartment due to exhaust streams,
filtration of any recirculating streams, and sources and sinks due to
first-order chemical reactions. In most cases, the sources and sinks
due to chemical reactions may be simulated as pseudo first-order,
because of the low concentrations (parts per million, or less) of the
pollutant. In cases where higher-order chemical reactions are
important, the model equations will be nonlinear and generally will
have to be solved numerically. In the case of particulate pollutants,
the parameters a^, bj, etc., will probably contain loss terms,
owing to surface deposition. The coefficients a2 ... an, b2
... bn, etc., represent the gain of pollutants in various
compartments that may result from the intrusion of air from other
compartments. The terms an + i» bn + etc., represent the sums
of the zeroth-order source and sink terms associated with each of the
compartments.
As indicated by Equations 2, an n-compartraent model will contain
n(n + 1) parameters, whose values should be determined independently.
Any temptation merely to fit the data through blind adjustment of the
VI-21
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values of the parameters should be resisted, If the model is to be of
broad value. The aim of any model should be to explain (and predict)
as many data as possible with the smallest possible number of
"adjustable parameters."
Because it is always possible to define X,, as the concentration
of the pollutant in the nth compartment at any time minus the initial
concentration, the initial conditions for Equations 2 may be taken as
XjJO) - X2(0) - ... Xn(0) - 0.
TWO-COMPARTMENT MODELS
In general, the equations that describe two-compartmen«. models are
of the form:
dXt
dt
and
ajX^ 3 a2X2 ^ a^«
(3)
dX2
+ = b2xl + ^3• ^4)
dt
The initial conditions are:
X,
at t
(5)
When the coefficients of Equations 3 and 4 are constant.
_ aibi_+aIbi /a3b, \ _a / \
ajb, —a3b2 \a,bi + ajb3/ \[(a] — bj3 + 4a5b2]14 / \ ((ai —b|)5+4aibj]w/
(6)
VI-2 2
-------
and
aib3 + a3ba /aibj_*ajbj\ / 0e~a1 — ae*^ \
1 iibi-ajbj \aibi — ajbj/ \[(3| — b|)1+4ajbj]wj
where
o=(a, + bt)/2 + [(a i — b|)J +4aJbj]V4/2
and
P=(as + b|)/2 - [(ai - ba)a +4a3b]]w/2.
In Equations 6 and 7, the first term on the right side represents the
steady-state solutions that are reached after the transient terras decay.
Woods et_ al. 118 used a two-compartment model in their analysis of
thermal and ventilation requirements for laboratory-animal cage
environments {see also Woods1"). The two compartments were the room
and the animal cage. Mass or energy balances for each compartment were
coupled by both free convection and forced circulation of room air
through the cage. Their models permit estimation of dry-bulb and
dew-point temperatures and concentrations of gaseous particulate
contaminants in cages, as well as in a laboratory room. Such models
can be used to determine an acceptable means of safely reducing room
ventilation rates with implications of reduced energy consumption and
operational costs.
Miller" has used a two-compartment model in his description of
the reentry of the ex.-^usts from laboratory fume hoods. The two
coraf\rtments were the building and the building wake (from which the
makeup air is drawn). Miller** and Sasaki et al.1,1 tw,*e shown that
the reentry of fume-hood exhaust is a much more pervasive problem than
is commonly recognized. Sulfur hexafluoride tracer experiments have
shown that reentry of a portion of the fume-hood exhaust is usually the
dominant factor in determining the concentrations of the pollutants to
which all persons are exposed in the laboratory building. Indoor
concentrations of fume-hood exhausts, normalized to the source
-b,
/ e^'-e-*' \
VI-23
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strengths, range from about 1 to about 350 ppb per mole released per
hoar. Although the chemical nature of the fume-hood emission is of
prime importance, persons typically complain often when they are in
buildings whose normalized indoor concentrations are above 100 ppb per
mole released per hour from fume hoods.
SINGLE-COMPARTMENT MODELS
Lidwell and Lovelock1* were apparently among the first to compare
concentrations of a pollutant with a mass-balance model. Their model
involved the instantaneous introduction of a nonreactive pollutant into
a- room and' considered the dilution resulting from a constant
ventilation rate in which the input air was pollutant-free. They noted
that, when the air in the room was not well mixed, the dilution by
ventilation air was not necessarily exponential; nor were the rates of
dilution the same in all parts of the room. A portion of the inlet air
stream often tends to bypass part of the room. For instance, when both
the inlet and exhaust ducts are on the ceiling, the lower half of the
room (and especially the corners) is apparently bypassed and the air in
it is diluted more slowly than expected.
Brief6 suggested the use of a mixing factor (a constant, usually
ranging in value between 1/3 and 1/10, that multiplies the ventilation
rate) to account for dilution rates that are lower than would exist if
the room air were continually well mixed. Constance11 also
recommended the use of mixing factors. Drivas et al.11 derived
mixing factors ranging in value between 0.3 and 0.7, except when fans
were used; with fans, the characteristic time for mixing the air
throughout the room was short, compared with the characteristic
residence time, and the mixing factors were close to unity.
Milly'3 used a single-compartment model involving the
instantaneous introduction of a nonreactive contaminant with a
pollutant-free input air stream in his discussion of chemical attack of
tanks and fortifications. Calder 11 used a single-compartment model
in his analysis of the protection afforded by buildings against
biologic-warfare aerosol attack; he permitted the outside concentration
to vary with time and took into account the surface removal of aerosol
by means of a first-order sink term; his results can also be used to
describe doses associated with radioactive or chemical contaminants.
Calder11 also used a single-compartment model to calculate dosages
associated with the penetration of a forest canopy by aerosols. Milly
and Thayer®* developed a technique for predicting indoor dosages of
pollutants generated outdoors, 'on the basis of a single-compartment
model.
Turk141 presented a detailed analysis of the transient behavior
of a single-compartment model involving a constant generation term, and
a constant outside concentration; he then considered several special
cases during his analysis of the measurement of odorous vapors in test
chambers.
Hunt** used z single-compartment model with a constant internal
source and a first-order sink term to interpret data regarding airborne
V.-24
-------
dust in post-office facilities. Hunt et al. *• and Cote and Holcombe"
used a single-compartment model in their investigations of nonreactive
gaseous pollutants indoors. Bridge and Corn' used a single-
compartment model to predict concentrations of carbon monoxide and
particles associated with smoking of cigarettes and cigars; their
resulta were in good agreement with measured values. Saberaky et
al.* * reported that a single-compartment model involving an outdoor
concentration that varied sinusoidally in time and a first-order
heterogeneous (surface) decomposition term gave qualitative agreement
with data for indoor concentrations of ozone. Shair and Heitner"
started with a single-compartment model to develop a "linear-dynamic"
model by which the indoor concentrations of ozone can be related to
those outside by means of a simple expression. Tests conducted with 24
forced-ventilation systems in 13 laboratory-office buildings yielded
Values of k (the heterogeneous-loss constant) of 0.02-0.08 cmvcm^-s,
with an average of 0.04 cm3/cm2-s.'*
To save energy, the makeup-air flow rate in buildings has been
reduced. In one case, the reduction in *che makeup-air flow rate was
sufficient to permit economical selective filtering of the makeup
airstream (with activated charcoal) during the times when the outdoor
*iir quality was relatively poor (see Figure VI-3); use of the
activated-charcoal filters only when needed and replacement of
inexpensive pifefilters every couple of mcnths extended the life of the
activated-charcoal filters to about 3 yr. This system was designed
with the aid of the "linear-dynamic" model.'* Kusuda51 used a
single-compartment model to examine the feasibility of intermittent
operation of mechanical ventilation systems with an eye to conserving
energy while maintaining acceptable indoor air quality.
Moschandreas (personal communication) used a single-compartment
model of air pollution in nonwor.kplace indoor environments ¦ in
Baltimore, Washington, D.C., Pittsburgh, Chicago, and Denver. He
monitored carbon monoxide, nitric oxide, nitrogen dioxide, sulfur
dioxide, ozone, methane, total hydrocarbons, and carbon dioxide
continuously for periods of approximately 14 d in each of five detached
dwellings (townhouses), six apartrent units, two mobile homes, and one
school. In addition, there was a S-d period of monitoring in one
hospital. The model discussed by Moschandreas et. al..71 71 explicitly
included a chemical-decay term that was validated with the data base
just mentioned. Numerical predictions of hourly carbon monoxide,
nitric oxide, nitrogen dioxide, carbon dioxide, and nonmethane-
hydrocarbon concentrations were found to be within 209 of the observed
values 80% of the time. The model did less well in predicting the
indoor sulfur dioxide and O2one concentrations; this was attributed to
the chemical reactivity of the pollutants. A study was implemented to
rank the sensitivity in magnitude changes in output of the model caused
by perturbation of an input parameter. The ranking of input
parameters, in ascending order of sensitivity, is as follows: initial
condition and volume of the structure, indoor source, and pollutant
decay and air-infiltration rate of the structure.71
Shair et_al.®* used a slngle-compairtment model to describe the
moisture content of bathroom air during and aft»r the use of a showerj
VI-25
-------
0.45
0.40
0.35
0.30
N
0.25
PPM
0.20
0.15
0.10
0.05
0
i—r
RUN NO. 12
JULY 22,1975
OUTDOOR CONCENTRATION
OF OZONE
INDOOR CONCENTRATION
OF OZONE WITHIN 1st. 2nd
ond 3rd FLOORS OF
SPALDING LABORATORY
h y
/\x
VS
i
\
2:00
2:30
TIME (PD.T.)
3:00
3:30
Figure VI-3 Relative indoor and outdoor ozone concentrations. From
F. H. Shair (personal communication).
VI-26
-------
they found good agreement with experimental results by considering the
solid surfaces in the bathroom to be a sink while the shower is on and
a source shortly after the shower is turned off.
Repace and Lowrey** have developed a one-compartment.model that
describes growth equilibrium and decay of tobacco-smoke aerosol under
different room mixing conditions.
Hollowell et al.** have discussed the impact of radon on indoor
air quality. Kusuda et_ al_.'' used the available indoor-radon data to
develop a single-compartment model with a t'irst-order radioactive-decay
term and a constant generation rate:
ydC
— = qC0 - XVC + VS, (10)
dt
in which V is' volume, Cg is outdoor concentration, and C is indoor
concentration. In addition to terms previously defined, there is the
radon-decay constant X = 1.258 x 10~4/min and the average source
strength per unit volume of air* S. Setting the left-hand side of the
above equation to zero and solving for the air-exchange rate yields:
q/v a is ¦ xc)/{c - c0). (ii)
To facilitate determination of effective radon source strengths, future,
measurements of indoor-radon concentrations 3hould be accompanied by
corresponding outdoor measurements and air-exchange rates, as
determined, for example, by a tracer-dilution technique.
SUMMARY AND CONCLUSIONS
The main purpose of an indoor air quality model is to show the
relationships of indoor pollutant concentrations to those outside, to
geometric and ventilation characteristics of a structure,
-------
ventilation rates, and, if possible, sink and source strengths. Such
information is required for any model based on a pollutant mass balance.
ESTIMATION OF TOTAL EXPOSURE TO AIR POLLUTION
Today's data on urban air quality cone mostly from measurements at
fixed monitoring stations. Such data probably show accurately the
exposure of a hypothetical person who spends all his time at the
station's intake probe. However, people are in constant motion in
urban areas, moving from residential areas to places of work to
commercial areas, etc. To determine individual human exposure to air
pollution accurately, it is necessary to find some means to measure and
correlate the movement of individuals in a population and the spatial
variation in concentrations of pollutants, whether indoors or outdoors.
One way to estimate better the total individual exposure to
environmental pollutants is to equip a large number of persons with
monitoring instruments and allow them to go about their daily
activities in a normal manner. However, no large-scale personal
monitoring studies have been done or are in progress, at least partly
because the development of total-exposure monitoring is still in an
early stage. Although no large-scale national program to develop
personal monitors has evolved, limited funds from federal agencies have
resulted in the development of specific monitors, and private companies
have developed some instruments that are' portable, small, and
reasonably priced.1* " 71
Other approaches have used theoretical analyses and models for
estimating total exposure. Fugas17 made one of the first attempts to
compute total exposure from experimental data; her approach was
intended only as an illustrative example. She obtained measurements of
average concentrations of lead, manganese, and sulfur dioxide during
the winter of 1972-1973 from official air-monitoring stations in the
city. The measurements were taken at the breathing zone in several
streets during business hours, indoors close to the streets during
business hours, and in the countryside. By estimating the time spent
by inhabitants of.the city in five locations—home, work, street 1,
street 2, and the countryside—Fugas calculated the "weighted weekly
exposure" (WWE) for each of these air pollutants (see Table VI-2). An
intermediate computation is the "integrated exposure," which is the
product of the average concentration and the time during which
pollution occurs. To calculate the WWE for sulfur dioxide, for
example, we note that a person spent an average of 110 h/wk at home,
where the average concentration was 89 pg/m3, for an integrated
exposure of 9,790 yg-h/ra3 for the time spent at home. By adding
all the integrated exposure components, Fugas obtained the total of
16,696 vig-h/m3 for the week. The WWE to sulfur dioxide was then
obtained by dividing by the number of hours in a week: 16,896/168 * 101
vg/m3 •2 7 ^
Duan1* has modified Fugas's approach by substituting the term
"microenvironment types" for the "locations" used to compute WWE. In
Duan's model, a person's integrated exposure over some period (for
VI-28
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TABLE VI-2
v a
Example by Fugas Illustrating Computation of Weighted Weekly Exposure
Sulfur
Type of
Duration of
Dioxide
Lead
Mangane
se
Exposure
Exposure, h/wk
C
Ct
C
Ct
C
Ct
Home
110
89
9,790
2.5
275
0.04
4.4
Work
42
8
336
0.3
12.6
0.02
0.84
Street 1
10
600
6,000
6.0
60
0.80
8.0
Street 2
4
180
720
3.5
14
0.12
0.48
Countryside
2
25
50
0.1
0.2
0.01
0.02
Total
168
—
16,896
—
361.8
—
13.74
Weighted
—
—
101
—
2.2
—
0.08
weekly
exposure
aData from Fugas.^ Values for C (concentration) are expressed in Pg/m^, and
values for Ct (integrated exposure) are expressed in yg—h/m .
VI-29
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example, a week) is computed as a weighted average of the exposures
from various microenvironment types, weighted by the proportion of time
spent in each microenvironment type:
K
V z *
1
where E^j is the integrated exposure of the ith individual during
the jth period, c^jk is the average concentration in the kth
microenvironment type during the jth period, and t^^ is the
activity-pattern coefficient denoting the time the ith individual spent
in the kth microenvironment type during the jth period. Duan"
suggested that a microenvironment type should be defined "finely"
enough to be homogeneous; that is, the concentration coefficients
should not vary appreciably over the individuals. However, the
microenvironment types have to.be somewhat "coarse," so that the
analyst will not have too many types to deal with. Some types might be
"rush-hour highway commuting," "daytime urban office with air-
conditioning," and "weekend daytime outdoors in the park."1'
Moschandreas and Morse79 have suggested an analogous approach for
computing air-pollution exposure and have applied it to real data.
They introduced the application of "mobility patterns," which are
designed to capture "the daily movements of individuals as they move to
and from work, from home to points of amusements, adventure, business,
and so on."70 By examining the literature on activity patterns and
"time budgets," they arrived at the estimated time that all persons—
all races, ages, socioeconomic groups, workers, students, etc.—spend
in various "environmental modes" (which are analogous to the
•microenvironment types" of Duan11 and the "locations" of
Fugas17). The population spends 72.8% of its time inside homes, but
the figure is different for different population subgroups (workers,
children, the elderly, etc.).
Because of the importance of considering the mobility patterns of
population subgroups, Moschandreas and Morse" examined U.S. census
data to define the percentage of each of six subgroups in the total
population: housewives, office personnel, industrial workers, outdoor
workers, elderly and infirm people, and students. However, students
are not considered in the overall model, because few studies have been
made of their mobility patterns. The model can be viewed as a
three-dimensional drawing in which persons move through time occupying
different environmental modes, thereby exposing themselves to the
particular concentration that is associated with each environmental
mode and period. On the basis of data on typical diurnal ozone
concentrations for three environmental modes (residential, office, and
indoors) in the Boston area and estimates of the percentage of the
population in each environmental mode as a function of time,
Moschandreas and Morse7" estimated that 21% of the population is
exposed to ozone at 80 ppb or more. At the time, the federal NAAQS for
ozone (1-h average) was 80 ppb, but it has since been raised. Among
individual population subgroups, Moschandreas and Morse estimated that
VI-30
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outdoor workers ate exposed to high ozone concentrations (oyer 80 ppb)
for about 6 h and industrial workers for the 1-h period between 4:00
and 5:00 p.m. if we take a "snapshot" of the estimated population
exposures at some particular point in time, such as 3:00 p.m. (that is,
1500j see Figure VI-4), some 25% of the population (3.9% in outdoor
activities and 21.3% in transit) is exposed to ozone at 80 ppb or more.
Although these are excellent recent examples of ways to estimate
population exposure to air pollution, they have several limitations.
Health-related air quality standards usually do not have weekly^,
averaging times. Thus, the value of the WWE calculated by Fugas17
cannot be compared directly with existing air quality standards. Duan's
formulation21 was intended to be more flexible, allowing any
averaging period (for example, a week or a month) to be used. The
computation of exposure by Moschandreas and Morse'0 did not cause
difficulties with averaging periods, because ozone has a 1-h NAAQS, and
the population is assumed to spend 1-h increments (or multiples of 1
h), in each environmental mode.
Each of the above approaches for calculating exposure gives the
population's average exposure over some specified period, and a problem
arises from the emphasis on the arithmetic mean. In any given period,
¦somis people will be involved in combinations of activities that can
result in exposures much higher and much lower than the mean. In
addition, the time spent in each activity varies from day to day and
from person to person. Thus, the mean value for exposure concentration
is not adequate to characterize the' highest concentrations to which
members of.the population are exposed, and the variance of exposures
also must be considered. Ideally, there would be an effective
technique for determining the entire frequency distribution of
exposures of the population to air pollution.
As discussed above, two.approaches are used for estimating the
frequency distribution of human air-pollution exposures: modeling,
which relate? the activities of persons as a function of time and the
concentrations to which they are exposed; and field studies, which use
personal monitors to cover a large enough population sample (or a
stratified sample) to represent statistically the distribution of
exposures. Although a large-scale field study of exposure has not been
completed, efforts are under way to use computer simulation to codel
human exposures to air pollution.
Ott77 7# has developed a computer-simulation model of human
exposure to air pollution that includes the movements of individual
people in a metropolitan area as a series of transitions from one
"microenvironment" to another. Ott's computer program, "Simulation of
Human Air Pollution Exposures" (SHAPE), uses probability distributions
of the time that people spend in each microenvironment—distributions
derived from studies of human activity patterns. In each
microenvironment, the concentration to which an individual is exposed
is treated stochastically, with distributional models that are brsed on
field studies of air-pollutan'c concentrations reported in the research
literature. In the simulation, the computer keeps track of the
exposure received by each person as ha or she moves forward in time and
occupies successive microenvironments.
tTT — ^ 1
-------
c/
.9
72
B
«4 J
I
c/
66 L
•/
W
*9b
c
o
40 r
u
32 L
' oinfr'-i
' o*!Z„lr"du""°i
' oV:?"'
FIGURE Vl-4 Example showing proportion of population exposed to hourly, ozone concentrations during
the 1500 hour (3:00 p.m.) in each environmental mode (numbered above). Reprinted with permission
from Moschandreae and Morse.'0
-------
Qtt'T defines an "exposure" of parson i to concentration c
statistically as the joint occurrence of two independent events:
person I 1b present in nicioenvLronment j, and the concentration C[j) ¦
c occurs In microenviionraent j. C{j) denotes the probability
distribution oC the concentrations associated with the microenvlronment
and is based on field monitoring data. Then, the integrated exposure
of person i is computed as the sum of the products of the
concentrations encountered in each raicroenvironment and the tine spent
there:
£ = Y) ct ,
i = i
where Cj is the concentration associated with microenvironment j,
tj. is the time spent by person i in microenvironment j, and j is the
total number of raicroenvironraents occupied by person i in some period
of interest. Conceptually, this model can be represented by a
three-dimensional array (see Figure VI-5) that is similar to a
three-dimensional space developed by Moschandrea3 and Morse."
However, the computer simulation follows one person at a tine through
his or her daily activities, and the resulting distribution of
exposures is obtained by considering those of all persons in the
simulation. The times t^j spent in the microenvironments are
variable and do not need to be integer multiples of 1 h.
REFERENCES
1- Amass, C. E. Passive membrane-limited dosimeters using specific
ion electrode analysis, pp. 437-460. In D. T. Mage, and L.
Wallace, Eds. Proceedings of the Symposium on the Development and
Usage of Personal Monitors for Exposure and Health Effect
Studies. U.S. Environmental Protection Agency (Environmental
Monitoring and Support Laboratory, and Health Effects Research
Laboratory) Report Mo. EPA-6G0/9-79-032. Washington, D.C.: U.S.
Government Printing Office, 1979.
2. American Conference of Governmental Industrial Hygienists. Air
Sampling Instruments for Evaluation of Atmospheric Contaminants.
5th ed. Cincinnati: American Conference of Governmental
Industrial Hygienists, 1978.
3. Azar, A., R. 0. Snee, and K. Habibi. Relationship of community
levels of air lead and indices of lead absorption, pp. 591-594.
In D. Barth, A. Berlin, R. Engel, P. Recht, and J. SmeetS/ Eds.
Proceedings. International Symposium, Environmental Health
Aspects of Lead, Amsterdam, October 2-6, 1972.
4. Bamberger, R. L., G. G. Esposito, B. W. Jacobs, G. E. Podolak,
and J. F. Mazur. A new personal sampler for organic vapors. Am.
Ind. Hyg. Assoc. J. 39:701-708, 1978.
5. Berlandi, F. J., G. R. Dulude, R. M. Griffin, and.E, R. Zink.
Electrochemical air lead analysis for personal environmental
VI-33
-------
II "¦
VJ
UJ
ft.
>
A.
o
UJ
FIGURE VI-5 Graphic representation, of person-environment-time array in computer
simulation model of exposure to air pollution suggested by Ott«
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movement in building fires. Fire' Mater. 4:17-27, 1980.
VI-43
-------
VII
HEALTH EFFECTS OF INDOOR POLLUTION
INTRODUCTION
The Committee, charged with characterizing the quality of the
indooi environment and determining the potential adverse health effect's
of pollutants in that environment, selected the following pollutants
for detailed discussion: radon and radon progeny, formaldehyde and
other organic substances, fibrous building materials, combustion
products (resulting from combustion of fuels in space-heating.,
water-heating, cooking, hobbies and crafts, etc.), involuntary smoking,
airborne agents of contagion, and airborne allergens. These are
obviously only examples of hazardous pollutants. They were chosen
because there was a large volume of published material available on the
sources of their presence indoors that could be used to document the
adverse effects of human exposure to them. The sources of these and
other pollutants are described in Chapter IV; the biologic responses to
the selected pollutants are discussed here.
It is beyond the scope of this report to list all the pollutants
found indoors that are hazardous to human health. Some pollutant
sources have been known for a long time but only recently recognized as
important. Cigarette-smoking is an example; although the smoke
components that cause adverse health effects need more study,
considerable progress has been made, as reported in this chapter. The
examples given in this chapter make it plain that humans are exposed to
a variety of potentially hazardous indoor pollutants from diverse
sources. It is hayed that this report will encourage researchers to
broaden the list of hazardous indoor pollutants and to characterize the
hazards, so that the general public and those responsible for pollution
control and abatement can be informed.
Throughout this report, pollutants are mentioned without discussion
of their health effects. This aoes not constitute an oversight on the
part of the Committee, but rather reflects a decision that the
discussion here be adequate to show that there are indoor pollutants
that cause adverse health effects in humans. The reader's attention is
directed to Chapter III, which offers some recommendations for further
health research with respect to these pollutants, for further exposure
VII-1
-------
studies, and for public education about effective ways of reducing
exposure to many contaminants encountered indoors.
Pollutants are inhaled, ingested, and absorbed. They may have
effects at their first point of contact with the body, or they may
affect internal organs. They may be changed physically or chemically
(metabolically) in the process of exerting their effects, or they may
undergo intermediate physical or metabolic changes before exerting an
effect. They may be stored in tissue for a time and be released later;
many of them are eventually excreted. Their own behavior helps to
shape the mechanisms of their effects. Pollutants may act
independently, antagonistically, or synergistically.
InhaLation is generally the most important route by which toxic
substances enter the body. Inhaled substances may exert their effects
in the lungs, or they may pass from the lungs to other organ systems in
blood, lymph, etc. Ingestion is far less common than inhalation as a
route of exposure, but is important for some toxic substances, such as
lead, arsenic, and mercury. In additiori to the direct physical or
chemical effect of ingested substances in the gastrointestinal tract,
they may pass through the tract into the blood and be distributed to
other organs. Liquid and vapor-phase pollutants may be absorbed
through the skin and affect the skin, pass through the skin and then
conjugate with tissue protein, or enter the bloodstream and be
distributed further.1' 21 ** 15
Environmental agents may exert their effects either by physical or
by chemical-physiologic (enzymatic) means. The fulJ toxic potential of
most substances is usually not expressed in normal healthy people,
because of the body's defense mechanisms and mechanisms of elimination
or because the substances are sequestered in inactive forms at various
tissue sites (bone, skin, hair, and nails). However, impairment of the
body's defensive processes may lead to increased toxicity, owing to the
higher concentrations of the substances that build up when the usual
means of elimination or reduction are blocked. Effects can occur
metabolically at the cell or organ level. Various trace substances
(e.g., halogenated hydrocarbons and trace metals) can have their
effects at both levels. 13 11 25
Some physical signs give evidence of primary toxicity, such as
contact with substances that produce irritation, inflammation, or
contraction. Some gases, such as carbon monoxide and nitiogeri dioxide,
when inhaled can affect the body's capacity to absorb oxygen.
Secondary mechanisms of toxicity include metabolic alteration of
the substance and accumulation of the byproducts fr^a the initial
action of the pollutant. Some substances are detoxified by metabolic
processes (oxidation, reduction, and synthesis), and the detoxification
mechanisms may themselves cause damage, as in the oxidation of alcohol
to formaldehyde and the reduction of arsenic or manganese, which may
produce more toxic forms.
Respiratory effects can be directly attributed to only a few
pollutants encountered at high concentrations indoors: nitrogen
dioxide, carbon monoxide, formaldehyde, and probably particles are
important \n this regard.
VII-2
-------
Physical factors (such as temperature, humidity, noise, nonionizing
radiation, and light} and their effects are discussed in Chapters IV
and VIIIj knowledge of their effects in the indoor environment is
sketchy and difficult to assess. Information on the health effects of
pollution due to consumer products in general has the same limitations
and is treated in the same way.
A variety of trace metals may be present indoors as a result of
filtration of outdoor air and as a result of indoor sources of
pollutants. These trace metals are also found in the domestic water
and in the diet. Some of them, especially lead and mercury, have
adverse health effects.® 9 15 Exposure to mercury indoors may result
from spills of liquid mercury and deterioration of paint. Mercury
vapor is quickly and efficiently .absorbed by the lung and may be
absorbed through the skin.12 Although much of the body burden of.
lead may come from the diet, the combined effects of air, soil1, house
dust, and water as sources of indoor lead are appreciable. 1 1728
The effects of lead and mercury on the brain are well
known. 1 3 ' 1,1 17 "20 11 13 **-*' Behavioral dysfunctions caused oy
lead may occur through modification of the enzymatic response to a wide
variety of toxic agents and through interference with neuromuscular and
ganglionic transmission.3 10
Gastrointestinal symptoms may be produced by inhalation of. toxic
substances, such as lead and mercury, that reach the gastrointestinal
tract through the bile duct.* 22 Organic mercury is also hepatotoxic
and may cause kidney damage by destroying cells in the tubular
system. 17 Lead and arsenic deposited in the kidney at low
concentrations may produce sensitization^ to damage by endotoxins or
exotoxins, such as analgesics and bacteria, although this is still
debatable.1' Mercuric chloride may produce acute renal failure.12
Mercury has toxic effects on the thyroid and therefore may have further
systemic effects. 11 Cadmium interacts with other nutrients and may
be stored in the kidney and damage capillaries there.7 ls 27 2> It
also accumulates in the liver at concentrations that depend on age and
smoking habits.7 Lead can inhibit heme synthesis,13 especially in
school-age children. Lead, zinc, and delta-aminolevulinic acid (ALA-D)
interact, and porphyrins (free erythrocyte porphyrins and zinc
protoporphyrins) are active in the blood; that activity determines the
influence of lead on heme synthesis. 27217-2 2) Lga
-------
ana it produces irritation in the mouth.11 11 Mercury poisoning may
affect the sense of touch, owing to the swelling of all extremities,
including ears and nose.M Except for spills of inorganic mercury
and excessive use of mercury-based paint, it is debatable whether
indoor concentrations of mercury are ever high enough to produce those
effects.15
This chapter deals with the biologic responses to specific
pollutants and biologic agents. The pollutants discussed are
sidestream cigarette smoke, radon progeny, mineral and vitreous fibers,
formaldehyde, and products of indoor combustion (predominantly carbon
monoxide and nitrogen oxises). Gases not usually found indoors in
moderate or high concentrations—such as sulfur oxides and ozone—are
not discussed at length. Nor are sources like cooking, which may
produce some particles or hydrocarbons, but about which little is
known. For information on substances that are known to have adverse
effects in the occupational environment or on solvents, dusts, etc.,
which have been reviewed thoroughly, the reader is referred to the
published literature (e.g., reports issued by FDA and CPSC).
Environmental factors that are not known to have adverse biologic
impact are not discussed here; rather, there are appropriate references
to other chapters.
REFERENCES
1. Angle, C. R., and M. S. Mclntire. Environmental lead and children:
The Omaha study. J. Toxicol. Environ. Health 5:855-870, 1979.
2. Berkout, p. G., N. J. Paterson, A. C. Ladd, and L. J. Goldwater.
Treatment of skin burns due to alkyl mercury compounds. Arch.
Environ. Health 3:592-593, 1961.
3. Bull, R. J. Effects of trace metals and their derivatives on the'
control of brain energy metabolism, pp. 425-440. In S. D. Lee, Ed.
Biochemical Effects of Environmental Pollutants. Ann Arbor, Mich:
Ann Arbor Science Publishers, Inc., 1977.
4. Dahlgren, J. Abdominal pain in lead workers. Arch. Environ. Health
33:156-159, 1978.
5. Oaines, R. H., D. W. Smith, A. Feliciano, and J. R. Trout. Air
levels of lead inside and outside of homes. Ind. Med. Surg.
41(10):26-28, 1972.
6. DuBois, K. P. Interactions of chemicals as a result of enzyme
inhibition, pp. 95-107. In D. H. K. Lee. and P. Kotin, Eds.
Multiple Factors in the Causation of Environmentally Induced
Disease. New York: Academic Press, Inc., 1972.
7. Elinder, C.-G., T. Kjellstrom, L. Friberg, B. Lind, and L. Linnman.
Cadmium in kidney cortex, liver, and pancreas from Swedish
autopsies. Arch. Environ. Health 31:292-302, 1976.
8. Finelli, V. N . Lead, zinc, and 5-aminolevulinate dehydratase,
pp. 351-363. In S. D. Lee, Ed. Biochemical Effects of Environmental
Pollutants. Ann Arbor, Mich.: Ann Arbor Science Publishers, Inc.,
1977.
9. Foote, R. S. Mercury vapor concentrations inside buildings. Science
177:513-514, 1972.
VII-4
-------
10. Goldberg, A. M. Neurotransmitter Mechanisms in inorganic lead
poisoning, pp. 413-423. In S. D. Lee, Ed. Biochemical Effects of
Environmental Pollutants. Ann Arbor, Mich.: Ann Arbor Science
Publishers/ Inc., 1977.
11. Goldsmith, J, R., and L. T. Friberg. Effects of air pollution on
human health, pp. 457-610. In A. C. Stern, Ed, Air Pollution. 3rd
ed. Vol. II. The Effects of Air Pollution. New York: Academic
Press, Inc., 1977.
12. Hayes, h. J., Jr., R. A. Neal, and H. H. Sandstead. Role of tody
stores in environmentally induced disease - DDT and lead,
pp. 136-164. In D. H. K. Lee and P. Kotin, Eds. Multiple Factors in
the Causation of Environmentally Induced Disease. New York:
Academic Press, Inc., 1972.
13. Hernberg, S. Lead, pp. 715-769. In C. Zenz, Ed., In Occupational
Medicine. Principles and Practical Applications. Chicago: Year Book
Medical Publishers, Inc., 1977.
14. Hirschman, S. Z., M. Feingold, and G. Boylen. Mercury in house
paint as a cause of acrodynia. Effect of therapy with N-acetyl-D,L-
penicillamine. N. Engl. J. Med. 269:889-b93, 1963.
15. Joselow, M. M. Indoor air pollution by mercury. Ann. Intern. Med.
78:449-450, 1973.
16. Kass, E. H. Multiple factors in the causation of renal disease, pp.,
83-91. In D. H. K. Lee and P. Kotin, Eds. Multiple Factors in the
Causation of Environmentally Induced Disease. New York: Academic-
Press Inc., 1972,
17. Morse, D. L., W. N. Watson, J. Housworth, L. E. Witherell, and
P. J. Landrigan. Exposure of children to lead in drinking water.
Am. J. Public Health 69:711-712, 1979.
18. Needleman, H. L., C. Gunnoe, A. Leviton, R. Reed, H. Peresie, C.
haher, and P. Barrett. Deficits in psychologic and classroom
performance of children with elevated dentine lead levels. N. Engl.
J. Med. 300:689-695, 1979.
19. Petering, B. G., L. Murthy, and F. L. Cerklewski. Role of nutrition
in heavy metal toxicity, pp. 365-376. In S. D. Lee, Ed,. Biochemical
Effects of Environmental Pollutants. Ann Arbor, Mich.: Ann Arbor
Science Publishers, Inc., 1977.
20. Roels, H., J.-P. Buchet, R. Lauwerys, G. Hubermont, P. Bruaux,
F. Claeys-Thoreau, A. Lafontaine, and J. Van Overschelde. Impact of
air pollution by lead on the heme biosynthetic pathway in
school-age children. Arch. Environ. Health 31:310-316, 1976.
21. Schanker, L. S. Flow of environmental agents in reaching their site
of action, pp. 6-14. In D. H. K. Lee, and D. Minard, Eds.
Physiology, Environment, and Man. New York: Academic Press Inc.,
1970.
22. Sexton, D. J., K. E. Powell, J. Liddle, A. Smrek, J. C. Smith, and
T. W. Clarkson. A nonoccupational outbreak of inorganic mercury
vapor poisoning. Arch. Environ. Health 33:186-191, 1978.
23. Shy, C., J. Goldsmith, J. Hackney, M. D. Lebowitz, and D. Menzel.
Statement on the Health Effects of Air Pollution: ATS News 4:22-62,
Spring, 1978.
VII-5
-------
24. Stokinger- H. E. Means of contact and entry of toxic agents, pp.
7-11. In W. M. Gafafer, Ed. Occupational Diseases: A Guide to Their
Recognition. U.S. Department of Health, Education, and Welfare,
Public Health Service Publication No. 1097. Washington, D.C.t U.S.
Government Printing Office, 1964.
25. Stokinger, H. E. Mode of action of toxic substances, pp. 13-26. In
W. M. Gafafer, Ed. Occupational Diseases: A Guide to Their
Recognition. U.S. Department of Health, Education, and Welfare,
Public Health Service Publication No. 1097. Washington, D.C.: U.S.
Government Printing Office, 1964.
26. Ter Haar, G. An investigation of elevated blood lead levels in
Detroit children. Arch. Environ. Health 34:145-150, 1979.
27. Waldbott, G. L. Health Effects of Environmental Pollutants. Saint
Louis: The C. V. Mosby Company, 1973. 316 pp.
28. World Health Organization. Health Hazards of the Human Environment.
Geneva: World Health Organization, 1972. 387 pp.
RADON AND RADON PROGENY
The physical, chemical, and radiologic properties of radon-222
(referred to as radon), radon-220 (thoron), and their progeny and the
principles of dosimetry are summarized in Chapter IV.
The unit of exposure of man is the working level (WL), defined as
the quantity of short-lived proqeny that will result in 1.3 x 10^ MeV
of potential alpha energy per liter of air. This is equivalent to a
concentration of short-lived radon progeny in complete equilibrium with
radon-222 at 100 pCi/L in air. The working-level monf.n (WLM) is a term
defined originally for occupational exposure, and 1 WLM is exposure at
1 WL for 170 h. Thus, the working-level month is a measure of
cumulative exposure.
The working level is a measure of exposure rate; it has been widely
assumed that, over a 70-yr lifetime, typical total-lifetime background
exposures are in the range of 5-20 \JLM. Howevet, the average and
distribution in the United States are not well studied. Some
restrictions on the use of the working level must be noted. First, it
is not useful for thoron progeny, because the dose delivered to the
bronchial epithelium for the same amount of potential alpha energy
(1.3 x 105 MeV) per liter of air can be much higher than that of
radon progeny. Second, characterization of the dose to lung airways
based solely on the working level involves a degree of uncertainty:
the distribution of the lung dose depends on the unattached fraction,
the particle size distribution of the aerosol to which the radon
progeny are attached, lung morphometry, breathing rate, etc. Even with
a general knowledge of the physical factors, other uncertainties in
calculating dose are sufficiently great that characterization of the
exposure atmosphere in terras of any measure more precise than working
level is inappropriate for r^se approximations. The difficulties in
characterizing dose and relating it to effects have been reviewed
recently by Cross et a^.. It should be noted that deviations in the
exposure environment from reference conditions may result in actual
VII-6
-------
lung doses that differ from those expected on the basis of the
reference conditions assumed.
REVIEW OP DOSE AND EXPOSURE CALCULATIONS
The inhalation of radon progeny leads to a very inhomogeneous alpha
dose to the human lung. For a variety of reasons—including
preferential deposition, mucociliary clearance of aerosols deposited on
conductive airways, and the observed tumor sites and types—it is
believed (but by no means certain) that the radiation from the
alpha-particle irradiation of the tasal cells of the upper bronchial
epithelium is the exposure characteristic most closely relatable to
carcinogenic risk. However, it is difficult to determine the
alpha-particle dose, because of the intractable difficulty of measuring
it in. vivo. Hence, dose calculations have been based on physical and
biologic models. Dosimetric models have been developed for adults and
have been summarized in several recent reports.11 *' Recently, an
age-dependent model was developed by Bofmann et al.11 Moreover, the
reference atmosphere is important for dose calculations, which are
influenced by the fraction of unattached progeny and the particle size
distribution of the progeny. Breathing rate, mucociliary clearance,
lung morphometry, age, and sex must also be considered.
Depending on assumptions about the equilibrium, unattached fraction
of progeny, carrier aerosol distribution, and the locus of target cells
chosen for th? estimates, calculated dose estimates per working-level
month can vary by up to a factor of. 100. A comprehensive evaluation of
the dose through the various regions of the lung, talcing into account
attached and unattached fractions and particle size distributions, has
recently been published.11
The table of background dose rates cited in Chapter IV is taken
from National Commission on Radiation Protection and Measurements
(NCRP) Report 45, which assumes that the reference exposure atmosphere
for the United States is at about the concentration found in outdoor
air, assumed to be radon-222 at 150 pCi/m3 in equilibrium with the
progeny. George and Breslin" measured radon working levels in
cellars, first-floor spaces, and outdoors for 21 houses in New York and
New Jersey and found the ratio of first-floor to outdoor average annual
radon content to be 4.6, with median outdoor content of 180 pCi/m^.
The first-floor-to-outdoor working-level ratio was lower, 2.6j that
suggests a reduced equilibrium indoors, as might be expected. The
annual mean on the first floor was 0.004 WL. Bow representative these
are of the metropolitan New York area or other areas is not known.
On the assumption that there was an 80% occupancy factor in the
houses, with the 20% balance spent outdoors, the annual weighted
estimate for the New York-New Jersey study was 0.11 WUt/yr. Over a
70-yr life, that would produce roughly 8 wm.
VI1-7
-------
BIOLOGIC EFFECTS
This section deals with the estimation of potential risk to man
£rom inhalation exposure to radon progeny, the basis Cor the estimates
of risk* and the ?hortcomings in our knowledge related to the exposures
normally encountered.
Underground Miners
Much of our knowledge aboiit the human health effects of radon and
its progeny is based on the experience of underground miners whose
exposures must be characterized, in relation to environmental
characteristics, as having high dcse rates (working levels) and high
cumulative doses (working-level months). Table VII-1 shows
representative values for underground mines and typical indoor
measurements in houses, to provide perspective on the use of the term
"high."
In the general population, exposure to radon progeny occurs under
conditions rather different from those in underground mines, and i* is
therefore necessary to consider the extent to which epidemiologic
studies in miners ace germane to the general population. The
feasibility of conducting epidemiologic studies of nonmining
populations has recently been examined, and populations of health-spa
workers were identified as promising.*7 There have been five majoi
reviews of results of studies on underground miners. The analysis here
draws partly on those and on the reports cited in them. All five
reviews dealt with underground-nr.ning experience and with miners who
were, for the most part, adult males.
Conclusions patterned after those of Seltser derived from those
studies are as fellows:
• There is no reason to doubt an excessive lung-cancer risk
among the early Bohemian uranium-miners in Schneeberg and
Joachimstal, " the U.S. uraniiun-miners at the Colorado Plateau,2'
and Czechoslovakian uranium-mirars.1 * *1 In addition, there were
increased occupational lung-cancer rates, relative to.thos>e of
equivalent smoking groups in tha general population, among underground
miners with large exposures to radon and progeny iri hematite,
fluorspar, and zinc mines in several countries.10
• It is cliar that the respiratory tracts or" the uranium-miners
received massive exposure from the alp!ia-emitt^ ng progeny, wliich are
responsible for iguch more of the r-jdiation exposure than the parent
radon itself.
• There appears to be no convincing evidence that there are any
other components of thu mine environment the.: are responsible for the
excess lung-cancer risk- Conversely, there is no evidence to rule out
a contributory role of. other components of this unusual environment,
i.e., respirable silica dust and variable background dust
concentrations and size distributions.
VII-8
-------
TABLE VII-1
Representative Exposures to Radon-222 Progeny
Subjects or
Location WLa WLMa,b
Uranium miners0 1-20 LOCM0,000
Outdoors <0.001
Indoors
-------
* There has been no definitive study in which a valid comparison
group foe the highly selected occupational populations was used. The
observed-to-expected ratios have generally been expressed in relation
to the general population or to a selected portion of the general
population, and not to other underground miners. Such a comparison nay
be difficult to obtain, because most underground mining invol'et
exposure to radon progeny at a higher-than-background concentration.
• Cigarette-smoking is clearly important, but not essential, in
the Induction of lung cancer. Lung cancer Is greatly increased in
these studies among uranium-miners who smoke, but is also higher among
non-clgarette-amoklng miners. Inferences from both the human
epidemiologic Work and the animal toxicologic studies are
contradictory: in each case, one can cite opposite conclusions on the
importance of smoking.
Fundamentally, the existing information is Insufficient for a
decision of whether radiation exposure multiplies the' risk of lung
cancer associated with other factors, such as smoking, or whether it
produces a cancer risk that is proportional to the radiation exposure
and merely additive to these other risks. In this review, a model
based on the latter idea; the "absolute-risk model," has been adopted,
although it must be kept in mind that it may not represent the true
situation. 1'
Epidemiologic studies of carcinogenesis may be considered complete
if all the population at risk has died and the follovup is complete.
Thus what is usually measured is some cumulative tumor incidence in the
population up to the time of the analysis, which is lower than the
lifetime excess risk.
For such data, risks may be defined as cumulative incidence to time
t from exposures X. Or one may try to express the risk in trrms of
appearance per unit time (usually years), being careful to define the
period over which tumors appear. One must distinguish between latent
period and followup time of the study group. Sometimes, average risk
per year is found by dividing cumulative incidence to time t by the
followup time (i.e., as is done by UNSCEAR'sj; but recently the
National Research Council Committee on the Biological Effects of
Ionizing Radiations (the BEIR Committee) excluded the latent period to
define the risk per year. Thus, risk estimates (in cancers/106
person-years per WLH) should not be directly compared with other
dimensionally equivalent risk estimates found for a different period.
The method chosen here uses the cumulative incidence divided by the
followup time. In any event, the time over whicn a time-dependent risk
estimate is derived is always specified.
The results of studies of lung cancer in underground uranium-miners
In the United States and Czechoslovakia and non-uranium-miners in
Sweden, Canada, and the United Kingdom, analyzed as a linear,
no-threshold phenomenon, are summarized in Table VII-2. The first
column shows the excess risk in terr.s of the number of expected
lung-cancer cases per working-level ponth per yearj these range between
2.2 x 10~® and 8 x 10~®. Column 1 is obtained bv dividing the
observed number of lung cancers in the study group by the followup time
VII-10
-------
a
w
I
Humana
Lung-Cancer
Risk,
no./WLM/yr
2.1 x 10
-6
-6
to 2.9 x 10
8 x 10"6
6 x 10~6
to 16 x 10"6
3.4 x 10~6
2.2 x 10~6
7 x 10~6
Experimental Anlmala
Lung-Tumor Risk.,
no./WLM
Followup
Time,
11
19-23
21-26
-6
280 x 10
9 x 10"6
33 x 10"6
Animal
Rat
Reagle
Beagle
TABLE VI1-2
Summary of Lung-Cancer Risk Estimates
Cumulative
Excess Risk,
no./WLM
170 x 10
-6
230 x 10
-6
Type
of Mine
Uranium
Uranium
Nonuraniutu
Fluorspar
Iroa
Exposure, WLM
Average
740
Range
0-10,000
Location
Reference
Exposure, WLM
170
11,000
12,000
Other Exposures
None
Ore dust, smoking
Ore dust
Colorado plateau 45
Czechoslovakia 41
— 24
Sweden
Canada
U.K.
Reference
11
15
15
45
45
45
-------
in years and the average exposure o£ the population. The second column
shows the followup tine of the study in years. These atudies in
general have not followed the exposed populations until the end of
life. Therefore, a valid estimate of the cumulative risk to the end of
life cannot be derived .from these studies. Column 3 is an under-
estimate of lung-cancer risk to the end of life. Indeed, UNSCEAR**
has suggested that, beyond 15 yr of exposure/ the risk per working-
level month per year decreases from 4 x 10~® to 2.2 x 10~6 up to 25
yr of exposure. UNSCEAR has suggested that the cumulative lifetime
lung-cancer risk among these miners might be as high as 200 x 10"^ or
450 x 10~® per working-level month.
In the study of Czechoslovakian miners, Kunz et al.** found, that
the proportion of cigarette-smokers in the underground miners was about
70%, roughly equa.'-. to the proportion in their general male population,
and concluded that the risk increases with age at onset of exposure. A
more recent reanalysis of the data from the uranium-miners in the
Colorado Plateau done by Lundin et al.J* concluded that the risk
increased progressively from nonsmokers through light to heavy
cigarette-smokers, but the excess risk over that to, nonminsrs with
equivalent smoking was much less f6r nonsmokers and was about the same
for light and heavy smokers. ' Lundin et al,. further suggested that
smoking promotes the appearance of lur.g tumors and thus that lung
cancers appear earlier in smokers than in noncrxskers. If true, this
would effectively result in a lower cumulative incidence in nonsmokers.
Saccomanno et^al. (personal communication), in analyzing ages of
smokers and nonsmokers among 302 Colorado Plateau miners with lung
cancer, found the average age at death to be earlier in the nonsmokers
(48.5 yr) than in the smokers (55.5 yr).
Thus, the risk estimates shown in Table VII-2 seem to cluster in
two groups, 2.2 x 10-^ to 3.4 x 10~® WLM/yr in the U.S. uranium-
miners and the Swedes and fluorspar-miners and 3-4 times higher in the
Czechoslovakians and iron-miners.
The physical measurements of mine atmospheres in the U.S. and
Czechoslovakian studies have not been compared, although systematic
errors exceeding 50% seem unlikely (Domanski, personal communication).
The reason for the higher risk among the Czechoslovakian miners is
not clear. Lundin jit al.J* suggested that they may be higher because
Czechoslovakian miners started mining at younger ages. This hypothesis
is not consistent with the observed dependence on age for equal doses
in animals.
Thus, the risk estimates differ between the various studies by a
factor of 3 or more for linear, absolute-risk estimates. However,
greater uncertainties are involved in extrapolating to lower exposures
in the range below 100 WLM, and further uncertainties are involved in
extrapolating to populations with a wide distribution in ages. The
question of the influence of age and gender on effect is not yet
settled in either experimental animals or man.
Archer 1 has recently plotted his evaluation of the excess annual
risk per working-level month (i.e., that above the risk established for
the control population) for lung cancer versus the estimate of
cumulative working-level months. This is reproduced in slightly
VII-12
-------
modified form in Figure VII-1. The risk per working-level month
increases monotonically down to several hundred working-level months.
Although the reliability of the individual points is poor, the fact
that all are well below the maximum is highly suggestive.
Histologic and Cytogenetic Studies in Mar—Lung Cancer
Exposure to radon and thoron progeny has been shpwn to be
correlated with chromosomal aberrations measured in peripheral blood
lymphocytes. 11 " In uranium-miners, there appears to be a good
correspondence between increased prevalence of chromosomal aberrations
and cytologic sputum changes characteristic of markedly atypical cells
and carcinomas ^n situ.'
On the basis of pathologic examination of 52 lung cancers in
uranium-miners in the Colorado Plateau, Saccomanno et al. in 1964
reported that there was a predominance of small-cell undifferentiated
carcinoma,18 and in 1971 150 cases were evaluated by a panel of
pathologists, who came to the same conclusion. 15 An interesting
conclusion of this group was that the mean latent period for the
small-cell types in miners with fewer than 700 WLM was 9.4 yr, compared
with mean latent periods of 17.8 yr for.all cancer types for exposure
greater than 700 WLM.
The prevalence of the small-cell type seems to be decreasing with
time, from 76% (13 of 17) in the period 1954-1959 to 22% (13 of 58) in
the period 1975-1979 (Saccomanno, personal communication). The meaning
of this is unclear, although the small-cell type of cancer may be
associated with the higher dose rates (in working levels) of the 1950s
and early 1960s in uranium mines in the Colorado Plateau.. Archer et^
al.J analyzed lung cancer by type in a study group of 3,366 uranium-
miners between 1950 and 1970 and found 66 small-cell cancers, compared
with two expected. Saccomanno et^al_. '7 have shown that an early
indicator of both precancerous lesions and carcinoma of the lung can be
obtained by cytologic examination of cells from the sputum; this offers
the opportunity to identify persons at risk early and to provide early
treatment.
Auerbach et al.7 have made detailed histologic examinations of
iungs of uranium-miners and nonmining controls matched for age and
smoking history obtained at autopsy. They concluded "that the
synergistic effect of the exposure to uranium dust along with cigarette
smoking increases the risk of lung cancer and that in addition to a
main tumor mass, other sites of tissue alterations, leading to tumor
development are frequently already present in the lung."
In epidemiologic studies in nonrainers, Hess et al.10 have
demonstrated a correlation between high radon concentrations in well
water in Maine and mortality from lung cancer and all cancers, on the
basis of available vital statistics. There were no controls for
smoking. The lung-cancer incidence in Maine is lower than the national
incidence,, and a definitive analysis of the relationship of radon in
water and long-term radon concentration in indoor air was not
presented. These studies should be followed up with detailed
VII-13
-------
to
c
u;
CJ
Z
<
o
o
- s
- -I
CD _
< >.
t- .
CO %
£ ~
t ci
< z
35 -
30
25
20
15
10
a
o
tf
~ Swwdan (protactinium, line, iron)
O Czachostovtkla (uranium)
A United Statm (uranium)
• Canada (uranium)
A Unitad Stata Miita rural nommokart)
¦ Schnaaburg-Joachirrathal
• Canada (fluonpar)
6
100 200 300 400 500 600 700 f 1200 or more
(0.35) (0.71) (1.1) (1.4) (1.8) (2.1) (2.5) <4ormore)
CUMULATIVE WLM (Mean Exposure Rate, WL)
FIGURE VI1-1 Attributable lung cancer per unit of radiation fro-n radon
progeny as function of cumulative exposure and exposure rate. Adapted
from Archer.
VII-14
-------
case-control studies In which the long-tern radon concentrations in air
are carefully evaluated.
Axelson et al.* conducted a case-control study based on death
certificate* and housing types in Sweden and concluded that there may
be a relationship between housing type and lung cancer. Residence in
stone houses was more common among those with lung cancer than
residence in wooden houses. Mo exposure data on radon or radon progeny
were correlated, nor was Information available on heating and cooking
practices.
Although both studies suggest a link between radon exposure and
long cancer, neither is s-^ficient to suggest causality.
Inhalation-Toxicology Studies in Animals
Experimental studies In animals offer the opportunity to test
hypotheses related to the effects of smoking on animals and whether
smoking is additive or synergistic in inducing or accelerating the
appearance of lung cancer. Until recently, lung cancers had net been
produced with radon progeny in animals. Early experiments with very
large exposures showed no short-term effects on the lung» and, although
dogs were exposed, the negative short-term pathologic results
discouraged the pursuit of such studies in the United states until
recently.
Studies of carcinogenesis of radon progeny are being conducted in
France by researchers at CEA11 and in the United States at the
Battelle Pacific Northwest Laboratory.1* Short-term exposures
conducted at the University of Rochester showed little pathologic
change in lungs of dogs for short followup times (D. Morken, personal
communication} . There has also been work on lung carcinogenesis after
intratracheal instillation or inhalation of long-lived alpha-emitters.
Those studies in which exposures are primarily of the pulmonary regions
of the lung, rather than of the bronchial airways, are not considered
relevant.
The combined effects of smoking and inhalation of uranium-ore dust,
radon progeny, and diesel-engine exhaust have been studied in Syrian
hamsters and dogs.11 One conclusion was that the Syrian hamster was
not an appropriate animal model for the study of pulmonary
carcinogenesis, inasmuch as it appeared to be resistant to carcinoma
induction by realistic exposures in lifespan exposure studies.
Information obtained with beagles was useful, although limited. Four
groups of 20 dogs were studied. All animals with lung tumors had
cumulative exposures greater than 13,000 WLM. It was observed that
3raoking decreased the number of observed tumors. The tumors in
uranium-miners are in the smaller bronchi, whereas in animals,they are
bronchioalveolar and in the nasal epithelium. It was suggested from
this study that the human and animal data are not directly comparable-
However, it is to be expected that the morphometric differences between
animals and man and differences in exposure conditions will change the
relative sites of particle deposition, the cell types being irradiated
most heavily, and the loci and cellular origin of tumors.
VI1-15
-------
Complementary studies were done in Prance with rodents exposed to
radon progeny with and without concurrent exposure to other
substances." This very extensive program of studies on lung
tumorigenesis in the rat demonstrates that it is a suitable model Cor
sane aspects of radon-progeny tumorigenesis in the lung. Die tumors
that are examined in histopathologic studies at death appear very late
in life, grow slowly (relative to the rat's life span), and are rarely
fatal.*•
The data on rodents indicate a cumulative incidence per working-
level month that is rather similar to that estimated for man, even
though the tumor types and sites in rodents differ considerably from
those found in humans. The pathologic basis for this and the
comparability have been discussed elsewhere.11 Similar studies of
rats are underway at Battelle-Pacific Northwest. These are not yet
complete; exposure began later than in the French studies. Because
lung tumors in rodents show up after the median life span and are
therefore restricted to less than half the population at risk. it is
premature to speculate on the eventual results of the studies'* and
their relationship to the French studie3.
SUMMARY AND CONCLUSIONS
There is no doubt that radon and its progeny in sufficient doses
can produce lung cancer in man.
It is also generally believed, on the basis of dosimetric
considerations, that the short-lived progeny are responsible for most
of the lung-cancer risk.
Some epidemiologic studies of underground miners have suggested
that smokers seem to be at higher risk of lung cancer than nonsmokers,
but the risk to nonsmokers is also increased, whether the risks are
additive or synergistic is not yet clear.
The cumulative exposures (in working-level months) at which human
and animal carcinogenesis has teen observed are generally higher by an
order of r^gnitude or more than those characteristic of the normal
indoor environment. Excess cancers have been seen in association with
exposures that were 2-3 orders of magnitude greater than those fopnd in
normal indoor environments.
Thus, to predict the results of the effects of decreased indoor
ventilation on exposure to radon progeny, it is necessary to
extrapolate beyond the range of exposures for which effects have
clearly been documented.
Although the generally accepted linear dose-response function does
not fit the available data very well, there is no established
alternative dose-response function. He can conclude that dose rate or
fractionation has an eftect that cannot yet be adequately described.
Only by a combination of human, animal, and cellular studies will
it be possible to estimate with any confidence the risk coefficients
for natural indoor exposures in the range of interest, as enhanced by
low air turnover associated with energy-conservation efforts.
VII-16
-------
Although there are legitimate reasons to criticize it, the
working-level month is probably the best available measure of potential
dose as related to likely biologic effect. Its use should be judicious.
REFERENCES
1. Archer, V. E. Effects of Low Levels of Radon on Kan. Paper
presented at the Specialist Meeting on Assessment of Radon and
Daughter Exposure to Man and Related Biological Effects, Rome,
1980.
2. Archer, V. E. Factors in exposure-response relationships of radon
daughter injury, pp. 324-367. In Conference/Workshop on Lung
Cancer Epidemiology and,Industrial Applications of.Sputum
Cytology. Golden, Colo: Colorado School of Mines Press, 1979.
3. Archer, V. E., G. Sacconianno, and J. H. Jones. Frequency of
different histologic types of bronchogenic carcinoma as related
to radiation exposure. Cancer 34:2056-2060, 1974.
4. Archer, V. E., J, K. Wagoner, and p. E. Lundin, Jr. Cancer
mortality among uranium mill workers. J. Occup. Med. 15:11-14,
1973.
5. Archer, V. E., J. K. Wagoner, and F. E. Lundin. Lung cancer among
uranium miners in the United States. Health Phys. 25: 351-371,
1973.
6. Archer, V. E., J. K> Wagoner, and F. E. Lundin, Jr. uranium
mining and cigarette smoking effects on man. J. Occup. Med.
15:204-211, 1973.
7. Auerbach, 0., G. Saccomanno, M. Ruschner, R. D. Brown, and L.
Garfinkel, Histologic findings in the tracheobronchial tree of
uranium miners and non-miners with lung cancer. Cancer
42:483-489, 1978.
B. Axelson, O., C. Edling, and H. Kling. Lung cancer and residency—
A care referent study on the passible impact of exposure to radon
and its daughters in dwellings. Scand. J. Work Environ. Health
5:10-15, 1979.
9. Brandom, W. F., G. Saccomanno, V. E. Archer, P. G. Archer, and
A. D. Bloom. Chromosome aberrations as a biological dose-response
indicator of radiation exposure in uranium miners. Radiat. Res.
76:159-171, 1978.
10. Budnitz, R. J., J. V. Berk, C. D. Hollowell, W. W. Nazaroff,
A. V. Nero, and A. H. ,Rosenfeld. Human Disease From Radon
Exposures: The Impact of Znecgy -Conservation in Residential
Buildings. Lawrence Berkeley Laboratory Report LBL-7309, Revised
EEB-Vent-78-5. Berkeley, Cal.: Lawrence Berkeley Laboratory, 1979.
11. Chameaud, J.^ R. Perraud, R. Masse, and J. Lafuraa. Cancers
induced by ^'^Radon in the rat. Paper presented at the
Specialist Meeting on Assessment of Radon and Daughter Exposure
and Related Biological Effects, Rome, 1980.
12. Costa-Ribeiro, C., M. A. Barcinski, N. Figueiredo, E. Penna, F.
Loblfo, N. Lobao, and H. Krieger. Radiobiological aspects and
radiation levels associated with the milling of monazite sand.
Health Phys. 28:225-231, 1975.
VII-17
-------
13. Cross, F. T. Exposure standards for uranium mining. Health Phya.
37:765-772, 1979.
14. Cross, P. T., R. F. Palmer, R. H. Busch, and R. L. Buschbom.
Influence of Radon Daughter Exposure Rate and Uranium Ore Oust
Concentration on Occurrence of Lung Tumors. Paper presented for
Battelle Pacific Northwest Laboratories at the Specialist Meeting
on Assessment of Radon and Daughter Exposure and Related
Biological Effects, Rome, 1980.
15. Cross, F. T., R. F. Palmer, R. E. Filipy, R. H. Busch, and B. 0.
Stuart. Study of the Combined Effects of Smoking and Inhalation
of Uranium Ore Dust, Radon Daughters and Diesel Oil Exhuast Fumes
in Hamsters and Dogs. Final Report. Battelle Pacific Northwest
Laboratories Report No. PNL-2744-UC-48. Washington, D.C.: U.S.
Department of Energy, 1978. 143 pp.
15a. Eadie, G. G., R. F. Kaufmann, D. J. Markley, and R. Williams.
Report of Ambient Outdoor Radon and Indoor Radon Progeny
Concentrations during November 1975 at Selected Locations in the
Grants Mineral Belt, New Mexico. U.S. Environmental Protection
Agency, Office of Radiation Programs Report No. ORP/LV-76-4. Las
Vegas: U.S. Environmental Protection Agency, Las Vegas Facility,
1976. 53 pp.
16. Federal Radiation Council. Guidance for the Control of Radiation
Hazards in Uranium I.ining. Staff Report No. 8. Revised September
1967.
17. Fisher, D. R. Estimating Population Health Risk from Low-Level
Environmental Radon. Paper presented foe Battelle Pacific
Northwest Laboratories at the Specialist Meeting on Assessment of
Radon and Daughter Exposure and Related Biological Effects, Rome,
1980.
17a. Fitzgerald, J. E-, Jr., R.-J. Guimond, and R. A. Shaw. A
Preliminary Evaluation of the Control of Indoor Radon Daughter
Levels in New Structures. U.S. Environmental Protection Agency
Report No. EPA-520/4-76-018. Washington, D.C.: U.S. Environmental
Protection Agency, Office of Radiation Programs, 1976. 88 pp.
18. George, A. C., and A. J. Breslin. The distribution of ambient
radon and radon daughers in residential buildings in the New
Jersey-New York area, pp. 1272rl292 (includes discussion). In T.
F. Gesell and w. M. Lowder, Eds. Natural Radiation Environment
III. Vol. 2. Proceedings of a Symposium Held at Houston, Texas,
April 23-28, 1978. Oak Ridge, Tenn.: U.S. Department of Energy,
Technical Information Center, 1980.
19. Guimond, R. J., Jr., W. H. Ellett, J. E. Fitzgerald, Jr., S. T.
Windham, and P. A. Cuny. Indoor Radiation Exposure Due to
Radium-226 in Florida Phosphate Lands. U.S. Environmental
Protection Agency (Office of Radiation Programs) Report No. EPA
520/4-78-013. Washington, D.C.: U.S. Government Printing Office,
[206] pp.
20. Hess, C. T., S. A. Norton, W. F. Brutsaert, R. E. Casparius, E.
G. Coombs, and A. L. Hess. Radon-222 in potable water supplies in
New England. J. N. Engl. Waterworks Assoc. 94:113-129, 1980.
VII-18
-------
21. Hofmann, W., S. SteinhMusler, and E. Pohl. Age-/ sex-, and
weight-dependent dose patterns due to inhaled natural
radionuclides, pp. 1116-1144. In T. F. Gesell and W. M. Lewder,
Eds. Natural Radiation Environment III. Vol. 2. Proceedings of a
Symposium Held at Houston, Texas, April 23-26, 1976. Oak Ridge,
Tern.s U.S. Department of Energy, Technical Information Center,
19B0.
22. Jacobi, W., and K. Eisfeld. Dose to tissueB and effective dose
equivalent of radon-222, radon-220 and their short-lived
daughters. Institut filr Strahlenschutz dec Gesellschaft fllr
Strahlen und Unweltforschung nbH, 1980.
23. Johnson, R. H., Jr., D. E. Bernhardt, N. S. Nelson, and H. W.
Calley, Jr. Assessment of Potential Radiological Health Effects
from Radon in Natural Gas. U.S. Environmental Protection Agency
Report No. EPA-520/1-73-004. Washington, D.C.: U.S. Environmental
Protection Agency, Office of Radiation programs, 1973. 68 pp.
24. Kunz, E., J. £evc, V. Placek, and J. Horacek. Lung cancer in man
in relation to different time distribution of radiation exposure.
Health Phys. 36:699-706, 1979.
25. Letourneau, E. G., and D. T. Wigle. Mortality and Indoor Radon
Daughter Concentrations in 13 Canadian Cities. Paper presented at
the Specialist Meeting on Assessment of R-don and Daughter
Exposure and Related Biological Effects, Rome, 1980.
26. Lundin, F. E., Jr., V. E. Archer, and J. K. Wagoner. An
exposure-time-response model for lung cancer mortality in uranium
miners: Effects of radiation exposure, age, and cigarette
smoking, pp. 243-264. In,Proceedings of Sims Conference on Energy
and Health, 1978.
27. Lundin, F. E., Jr., J. K. Wagoner, and V. E. Archer. Radon
Daughter Exposure and Respiratory Cancer: Quantitative and
Temporal Aspects. National Institute for Occupational Safety and
Health, and National Institute of Environmental Health Sciences
Joint Monograph No. 1, 1971. 175 pp.
28. Masse, R. Histogenesis of lung tumors induced in rats by
inhalation of alpha emitters, pp. 498-521. DOE Symposium Series
53, CONF 79 10002. Washington, D.C.: U.S. Department of Energy,
1979.
29. Momeni, M., J. B. Lindstrom,. C. E. Dungey, and W. E. Kisieleski.
Radon and Radon-Daughter Concentrations in Air in the Vicinity of
the Anaconda Uranium Mill. U.S. Nuclear Regulatory Commission
Report No. NUREG/CR-1133. Washington, D.C.: U.S. Nuclear
Regulatory Commission, Office of Nuclear Regulatory Research,
1979. 97 pp.
30. National Research Council, Committee on the Biological Effects of
Ionizing Radiations. The Effects on Populations of Exposure to
Low Levels of Ionizing Radiation: 1980, pp. 308-331. Washington,
D.C.: National Academy Press, 1980.
31. National Research Council, Advisory Committee on Biological
Effects of Ionizing Radiations. The Effects on Populations of
Exposure to Low Levels o£ Ionizing Radiation, pp. 145-157.
Washington, D.C.: National Academy of Sciences, 1972.
VII-19
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32. Pohl-Ruling, J.» and P. Fischer. An Epidemiological Study on
Chromosome Aberrations in a Radon Spa. Paper presented at the
Specialist Meeting on the Assessment of Radon and Daughter
Exposure and Related Biological Effects, Home, Italy, March 3-7,
1980.
33. Pohl-Riiling, J., and P. Fischer. The dose-effect, relationship of
chromosome aberrations to a and y irradiation in a population
subjected to an increased burden of natural radioactivityI
Radiat. Res. 80:61-81, 1979.
34. Royal Commission on Health and Safety of Miners (Ontario). Report
of the Royal Commission ,on Health and Safety of workers in Mines.
Toronto, Canada:. Province of Ontario, Ministry of Attorney
General, 1976. [3491 pp.
35. Saccomanno, G., V. E. Archer, 0. AUerbach, M. Kuschner, R. P.
Saunders, and M, G. Klein. Histologic types of lung cancer among
uranium miners. Cancer 27:515-:523, 1971.
36. Saccomanno, G., V. E. Archer, 0. Auerbach, R. P. Saunders, and
L. M. Brennan. Development of carcinoma of the lung as reflected
in exfoliated cells. Cancer '33:256-270, 1974.
37. Saccomanno, G., V. E. Archer, R. P. Saunders, 0. Auerbach, and
M. G. Klein. Early indices 'of cancer risk among uranium miners
with reference to modifying factors. Ann. N.Y. Acad. Sci.
271:377-383, 1976.
38. Saccomanno, G., V. E. Archer, R. P. Saunders, L. A. James, and
P. A. Beckler. Lung cancer of uranium miners on the Colorado
Plateau. Health Phys. 10:1195-1201, 1964.
39. Saccomanno, G., R. P. Saunders, M. G. Klein, V. E. Archer, and L.
Brennan. Cytology of the lung in reference to irritant,
individual sensitivity and healing. Acta Cytol. 14:377-381, 1970.
40. Seltser, R. Lung cancer and uranium mining. Arch. Environ. Health
10:923-936, 1965.
41. Sevc, J., E. Kunz, and V. Pla"cek. Lung cancer in uranium miners
and long-term exposure to radon daughter products. Health Phys.
30:430-437, 1976.
42. Snihs, J. O. The approach to radon problems in non-uranium, mines
in Sweden,1pp. 900-911. In Proceedings of the Third International
Congress of the International Radiation Protection Association,
Washington, D.C., September 3-14, 1973. U.S. Atomic Energy
Commission Report CONF-730907-P2. Washington, D.C.: U.S. Atomic
Energy Commission, 1974.
43. Steinhausler; F., E. Pohl, and W. Hofmann. On the Suitability of
Epidemiological Studies of Population Groups Exposed to Elevated
Levels of Radon- and Daughters. Paper presented at the Specialist
Meeting on the Assessment of Radon and Daughter Exposure and
Related Biological Effects, Rome, Italy, March 3-7, 1980.
44. Turner, J. E., C. F. Holoway, arid A. S. Loebl, Eds. Workshop on
Dosimetry for Radon and Radon Daughters, Oak Ridge National
Laboratory, April 12-13, 1977. Oak Ridge National Laboratory
Report No. ORNL-4343. Oak Ridge, Tenn.: U.S. Department of
Energy, Oak Ridge National Laboratory, 1978. 54 pp.
VII-20
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45. United Nations Scientific Committee on the Effects of Atonic
Radiation. Sources and Effects of Ionizing Radiation, Report to
the General Assembly, with Annexes, pp. 200-226, 394-399. New
York: United Nations, 1977.
46. U.S. Environmental Protection Agency. Preliminary Findingsi Radon
Daughter Levels in Structures Constructed on Reclaimed Florida
Phosphate Land. U.S. Environmental Protection Agency, Office of
Radiation Programs Report No. ORP/CSD-75-4. Washington, D.C.:
U.S. Environmental Protection Agency, 1975. 40 pp. Available from
National Technical Information Service, Springfield, Va., as
PB-257 679.
47. Wrenn, M. E., F. Steinhausler, and G. Clemente, Eds. Proceedings
of the Specialist Meeting on the Assessment of Radon Daughter
Exposure and Related Biological Effects, Rome, Italy, March 3-7,
1980. (in press)
FORMALDEHYDE AND OTHER ORGANIC SUBSTANCES
This section reviews the potential effects of formaldehyde and some
other indoor organic pollutants. The sources of such pollutants are
discussed in Chapter IV. The concentrations of most of the organic
substances in question are usually unknown, because they are identified
mainly as peaks on chromatograms. Their health effects must be
discussed as potential, rather than known, Jnasmuch as the
characteristics of their presence indoors have not beer, studied.
Committees of the National Research Council have reviewed the effects
of particulate polycyclic organic matter®7 and vapor-phase organic
pollutants.11
Adverse health effects due to formaldehyde nay occur after exposure
by inhalation, ingestion, or contact. Ascribing specific health effects
to specific concentrations of. formaldehyde is difficult, because people
vary in their subjective responses and complaints. Moreover,
hypersensitive persons, those with disease, and hyposensitive persons
may not have been evaluated in epidemiologic studies. Thus, the
threshold for response will not be constant among all segments of the
population. Interpretation of the health effects of formaldehyde must
also consider the duration of exposure of subjects. A short-term
inhalation study cannot accurately predict the effects of formaldehyde
exposures of residents oif conventional or mobile homes who may oe
exposed continuously to low concentrations. Odor irritation and
tolerance may develop after several hours of exposure and modify the
response to formaldehyde.
EFFECTS OF FORMALDEHYDE IN ANIMALS
The reader is referred to the NRC report, Formaldehyde and Other
Aldehydes. '* for detailed discussion^ of the effects of formaldahyde
exposure reported in experimental animal studies.
VII-21
-------
The carcinogenic effects o£ formaldehyde exposure in humans have
not been assessed. However, studies in cats and mice done by the
Chemical Industry Institute of Toxicology have found that formaldehyde
induces nasopharyngeal carcinoma after several months of exposure at 15
and. 6 ppm for 6 h/d, 5 d/wk. Dose-related histologic changes were
observed in the' nasal mucosa of rats exposed at 2 and 6 ppm for the
same times. formaldehyde has mutagenic activity in a variety of
microorganisms and in some insects. More work is necessary to
ascertain its mutagenic potential in germinal or somatic mammalian
cells. Such information would be used to assess the potential hazard
to persons exposed to formaldehyde. Formaldehyde has not been shown to
be teratogenic in animals.
EFFECTS OF FORMALDEHYDE IN HUMANS*
The principal effect of low concentrations of formaldehyde observed
in humans is irritation of the eyes and mucous membranes. A wide range
of concentrations of airborn formaldehyde have been reported to cause
specific human health effects. Table VII-3 shows the variability and
overlap of responses among subjects. Some persons develop tolerance to
olfactory, ocular, or upper respiratory tract irritation. Such factors
as smoking habits, socioeconomic status, preexisting disease, various
host factors, and interactions'with other pollutants and aerosols are
expected to modify these responses.
Eye
Human eyes are very sensitive to formaldehyde, responding to.
atmospheric concentrations of 0.01 ppm in some cases (when mixed with
other pollutants) and producing a sensation of irritation at 0.05-0.5
ppm. Lacr^mation is produced at 20 ppm, but damage is prevented by
closing of the eyes in response to discomfort. See Table VII-4 for
summaries of effects at various concentrations.
Olfactory System
The odor threshold of formaldehyde is usually around 1 ppm, but may
be'as low as 0.05 ppm in some people.® 9 1 * 11 *' 7 5 7 7 91 **
Olfactory fatigue—as determined on the basis of increased olfactory
thresholds for rosemary, thymol, camphor, and tar—was reported among
plywood and particleboard workers and is presumed to be associated with
formaldehyde.91 98 Olfactory fatigue can be important in the home
owing to reduced sensitivity to odors; a person exposed to formaldehyde
might not smell other substances, such as leairing gas or burning
materials.
•Much of this discussion is derived from the National Research Council
report, Formaldehyde and Other Aldehydes,J> to which the reader is
referred for additional details.
VI1-22
-------
TABLE VI1-3
Reported Health effects' of Formaldehyde at Various Concentrations3
Approximate
Formaldehyde
Concentration,
PPm
Effects
None report, i
Neurophysiology effects
Odor threshold
Eye Irritation
Upper airvsy irritation
Lower air*'. ? and pulmonary
effect?
Pulmonary edema, inflam-
mation, paeumonia
Death
0-0.05
0.05-1.5
0.05-1.0
0.01-2.0°
0.10-25
5-30
50-100
100+
aDerived from Rational Research Council.^
''The low concentration (0.01 ppm) was observed in the
presence of other pollutants that may have been acting
synergistically.
VI1-23
-------
TABLE VtI-4
Eye Irritation Effects of Formaldehyde*
Formaldehyde
Concentration, ppm
0.03-3.2
13.8
20
0.25
0.42
0.83-1.6
Duration of
Exposure
4-5
0.9-2.7
0.3-2.7
0.9-1.6
0.13-0.45
0.067-4.82
0.02-4.15
0.03-2.5
Chamber—single;
20-35 min; gradually
Increasing concen-
tration
30 nln
Less than 1 nln
Chamber—repeated:
5 h/d for 4 d
5 h/d for 4 d
5 h/d for 4 d
Occupational:
Indoor residential:
Effects on Eyes
Increase In blink
rate; Irritation
Irritation (»»>d
nose Irritation)
Discomfort and
lacrlisatlon
19Z "slight dis-
comfort"
31Z. "slight discom-
fort" and conjunc-
tival irritation
942 "slight discom-
fort" and conjunc-
tival irritation
Irritation, lacrima-
tlon, and discomfort
in 30 min
Tearing
Prickling and tearing
Intense irritation
and itching
Stinging and burning
Tearing
Irritation
Irritation
aReprinted from National Research Council.
VII-24
-------
Respiratory Tract
The nose adjusts the temperature and water-vapor content of air and
removes a large proportion of foreign gases and dusts," and the
nasal mucociliary system clears foreign material deposited on it.
Nasal congestion from injury may lead to partial mouth-breathing; when
nasal functions are irepaired or the nose is otherwise bypassed for
mouth-breathing, the burden of conditioning and cleaning the air falls
on the oral airways and the lungs. If the naeal defense system is
disturbed or if mouth-breathing occurs, greater concentrations of
formaldehyde will reach the lungs, and other noxious materials
ordinarily cleared from the airways may be retained.
Upper Airway Irritation. Symptoms of upper airway irritation
include the feeling of a dry throat, tingling sensation of the nose,
and sore throat, usually co-existent with tearing and pain in the
eyes. Irritation occurs over a wide range of concentrations! usually
beginning at approximately 0.1 ppa, but reported more frequently at
1-11 ppm1 • " ** 11 »• •• (see Table VII-3]. Tolerance to eye
and upper airway irritation may occur after 1-2 h of exposure. 1 ** 71
However, even if tolerance develops, the irritation symptoms can return
after a 1- to 2-h interruption of exposure.1 s '* ** 11 " As in the
case of eye irritation, some persons seen to tolerate higher
concentrations, 16-30 ppm; it is not known whether subjects develop
tolerance.
Lower Airway and pulmonary Effects. Lower airway izritation that
is characterized clinically by cough, chest tightness, and wheezing is
reported often in people exposed to formaldehyde at 5-30
ppa." l> ** ** " ** 100 Chest x rays of persons apparently exposed
to formaldehyde at high concentrations are usually normal, except foe
occasional reports of accentuated bronchovascular markings, but
pulmonary-function test results may be abnormal.1*®
Pulmonary edema, pneumonitis, and death result from very high
formaldehyde concentrations, 50-100 ppm.* *• l,c It is not known
what concentrations are lethal to humans, but concentrations exceeding
100 ppm would probably be extremely hazardous to most and might be
fatal in sensitive persons.
Asthma. Formaldehyde has been shown to cause bronchial asthma in
humans.1* «»•»»! »»»»«» in some cases, asthmatic
attacks are due specifically to formaldehyde sensitization or allergy;
controlled inhalation studies with formaldehyde are positive in these
instances." More commonly, formaldehyde seems to act as a direct
airway irritant in persons who have bronchial asthmatic attacks from
other causes. Concentrations at which attacks occur are highly
variable. Bronchial asthma is characterized by hyperreactivity of
airways, and the airways respond to many nonspecific inhaled irritants,
including formaldehyde.
The exact mechanism of the asthma syndrome related to formaldehyde
exposure is not known. It has been suggested that an immunologic basis
VI1-25
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is sometimes operative. However, no studies have demonstrated the
presence of specific circulating immunoglobulins (IgE or IgG) in
affected persons. Although formaldehyde at low concentrations may
cause asthmatic symptoms in some sensitized subjects, in irritant
concentrations it produces bronchoconstriction in even normal persons.
Inhalation of formaldehyde fumes may cause airway hyperreactivity, an
important component of bronchial asthma.1' ** ,s 1% Methacholine and
histamine challenge tests have demonstrated this hyperreactivity with
other environmental pollutants.1' 11 11 17 1'
Skin
Skin contact with formaldehyde ha3 been reported to cause a variety
of cutaneous problems in humans, including irritation, allergic contact
dermatitis, and urticaria.*1 71 '* Allergic contact dermatitis from
formaldehyde is relatively common, and formaldehyde is one of the more
frequent causes of this condition both in the United States'* and in
other areas.27 , The North American Contact Dermatitis Group reported
that formaldehyde is the tenth leading cause of skin reactions among
dermatitis patients patch-tested for allergic contact dermatitis.
Approximately 4% of 1,200 patients had positive skin reactions when
tested with 2% formalin (0.8% formaldehyde) under an occlusive
patch.'8 Minor epidemics of allergic contact dermatitis have been
described in diverse situations, for example, among nurses who handled
thermometers that had been immersed in a 10% solution of formaldehyde71
and among those who were exposed to formaldehyde in hemodialysis
units.7'
In many cases, either the initiation or t'he elicitation of the
allergy has been caused by contact with formaldehyde or formalin, but
it may also result from formaldehyde-releasing agents used in
cosmetics, medications, and germicides, from incompletely cured resins,
and from the decomposition of formaldehyde-containing resins used in
textiles.*' People with cutaneous allergy to formaldehyde have
particular problems because there are so many sources of formaldehyde
exposure in ordinary daily life (for example, the FDA listed 846
cosmetic formulations containing formaldehyde12). The skin reaction
rate from cosmetic formulations containing formaldehyde has not been
excessive, because it is used mainly as a preservative in shampoos,
whose contact time with skin is short. Formaldehyde-releasing cosmetic
preservatives, such as Quaternium-15, have shown a greater reaction
frequency than formaldehyde itself (unpublished data from Cosmetics
Technology Division, Bureau of Foods, FDA).
Low concentrations of formaldehyde are associated with many
sources, and repeated contact with them may be sufficient to provoke
responses in people with allergic coi:c3Ct sensitization. These sources
include components of plastics, glue:;antifungal disinfectants,
preservatives, paper, fabrics, leather, coal and wood smoke, fixatives
for histology, and photographic materials.1' Available data do not
permit the determination of a degree of exposure to formaldehyde-
containing products that would be safe once sensitization has occurred.
VII-26
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Most sensitized persons can tolerate topical axillary products
containing formaldehyde at up to about 30 ppm.*1, With increasing
concentration« one sees a higher frequency of resporvders,11 probably
because skin penetration by formaldehyde varies from one person to
another and even from one site to another on the sane person. Thus,
different amounts of formaldehyde may reach different target sites.
The dose needed to elicit a response depends on these factors and
others, such as occlusion, temperature, contact time, and vehicle.
Allergic contact dermatitis is a manifestation of cell-mediated
immunity. The standard diagnostic test for thiB condition is the
epidermal patch test.. Patch testing for skin sensitization to
fortaldehyde resin is performed with a 5-10% concentration of the resin
in petrolatum.1
Although formaldehyde has been reported to cause contact urticaria,
it is not yet clear whether this is irnmiinologically mediated.*1
Formaldehyde is a potent sensitizer and irritant; repeated exposure to
it may also result in dermatitis.
Central Nervous System
Central nervous system responses to formaldehyde have been tested
in a variety of ways, including by determination of optical
chronaxy,* electroencephalographically,** and by the sensitivity of
the dark-adapted eyes to light.'1 Responses are reported in some
persons at 0.05 ppm and are maximal at about 1.5 ppm., Formaldehyde at
below 0.05 ppm probably has little or no objective adverse effect.**
Fel'dman and Bonashevskaya reported that formaldehyde at 0.032 ppa
produced no electroencephalograph^ changes and did not reach the odor
threshold in five extremely sensitive subjects.** Melekhina
demonstrated changes in the sensitivity of the dark-adapted eye to
light at about 0.08 ppra'. 51
Alimentary Tract
Ingestion of formaldehyde has been reported to cause headache-,
upper gastrointestinal pain," 2 0 2 1 *' lc •• allergic reactions,
corrosive effects on gastrointestinal and respiratory tracts,21 **
and systemic damage.11 *• Accidental or suicidal poisoning with
formaldehyde usually involves the ingestion of aqueous solutions; death
occurs after the swallowing of as little as 30 ml of formalin.' **
Gastrointestinal tract damage is most marked in the stomach and lower
esophagus, with the tongue, oral cavity, and pharynx generally not
severely affected." The small intestine may occasionally be
involved; perforated appendix is a rare complication. When the
chemical infiltrates around the epiglottis, injury to the larynx and
trachea may occur.* *4 *6 After ingestion, there may be loss of
consciousness, vascular collapse, pneumonia, hemorrhagic nephritis, and
spontaneous abortion.* 1,3 One autopsy report of a fatal ingestion
described hardening of organs adjacent to the stomach (lung, liver.
VII-27
-------
spleen, and pancreas)# hyperemia and edema of the lungs, bilateral
diffuse bronchopneumonia, fatty degeneration of the liver with
subcapsular he- rrhage, renal tubular necrosis, and involvement of the
brain.* ** '*
Consumer Complaints in Residential Environments
A number of studies have been undertaken to determine the magnitude
and extent of formaldehyde exposure of persons in the residential
environment.1 " 11 ,T '* *° " * * Breysse reported a study of 325
persons living in 272 mobile homes, all of whom had eye and upper
respiratory tract irritation.1' #0 Formaldehyde concentrations
(measured in 138 instances) ranged from 0 to 2.S ppm; approximately 90%
were less than 1 ppm, and 9.4% were above 1.0 ppra. " Of 121 persons
studied, 15% had no symptoms, and approximately 34% had three or more
symptoms. Symptoms reported moat often included eye irritation (about
30%), nose irritation (5%), respiratory tract involvement (24%),
headache (21%), nausea (5%), and drowsiness.
In November 1977, the Connecticut Department of Health and Consumer
Protection began receiving complaints from state residents who had
urea-formaldehyde foam insulation installed in their homes.'1 By
September 1978, 84 complaints had been received. The Department tested
the 84 homes and found formaldehyde in the air in 75. The sensitivity
of the testing system was reported to be less than 0.05 ppm. Health
symptoms were reported by 224 residents of 74 homes, in which
detectable concentrations of formaldehyde ranged between 0.5 and 10
ppm, with a mean of 1.8 ppm. The symptoms of the residents included
eye, nose, and throat irritation; GI tract symptoms; headache; skin
problems; and some miscellaneous complaints, such as fatigue, aches,
and swollen glands. In. 37%, however, symptoms occurred when
formaldehyde was not detectable by the methods used. When formaldehyde
was detectable (0.5-10 ppm), 49% of the occupants had eye irritation,
37% nose and throat irritation. 46% headache, and 22% GI tract
symptoms; in homes with no detectable formaldehyde, 26% had eye
symptoms, 41% nose and throat irritation, 26% headache, and 42% GI
tract symptoms.
Occupational Standards for Formaldehyde
It is important to consider total exposure to formaldehyde.
Therefore, it should be noted that some people are exposed to it at
work. The present Occupational Safety and Health Administration (OSHA)
standard for formaldehyde is 3 ppm, as a time-weighted average
concentration over an 8-h workshift. In 1974, the American Conference
of Governmental Industrial Hygienists (ACGIH) recommended a limit o£ 2
ppm, mainly because irritation might occur above this concentration.
The National Institute for Occupational Safety and Health (NIOSH) has
recourcended a workplace ceiling limit of 1 ppm.1*
VII-28
-------
Significance of Adverse Health Effects In Regard to Population at Risk
The total number of people who are exposed to formaldehyde and who
manifest adverse health effects is difficult to determine. There is
evidence that such responses may occur in a substantial proportion of
the exposed population in the United States. The variability in
response among exposed persons makes it particularly difficult to
assess the problem.
Millions ol persons live in mobile or conventional homes that
contain either urea-formaldehyde (UF) loam insulation or particleboard
made with UF resins. When measurements have been performed, a wide
range of formaldehyde concentrations, from 0.01 ppm to 10.6 ppm, have
been reported. In most indoor environments, 24-h average formaldehyde
concentrations of 0.05-0.3 ppm are not uncommon today. Because people
may spend over 70% of their time indoors, exposure to formaldehyde from
gas cooking and smoking combined with that from UF foam, particleboard,
and plywood could be substantial. In addition, people are exposed to
formaldehyde from occupational sources, consumer products, and outdoor
ambient air.
Formaldehyde concentrations measured in ambient air are lower than
in residences. Concentrations vary, but atmospheric concentrations are
usually less than 0.1 ppm and very often less than 0;05 ppm. The dose
received by the 220 million people in the United States from outdoor
exposure appears to be minimal, except for unusual circumstances of
traffic, fuel use, or automobile density. Consumer exposures are
mainly by direct contact, and contact dermatitis is an important
consideration, as has been discussed.
Little is known about the magnitude of the population that is more
susceptible to the effects of inhaling formaldehyde vapor. Asthmatics
may constitute a segment of the general population that is more
susceptible; inhalation even at low concentrations may precipitate
acute symptoms. Airway hyperactivity may explain the susceptibility of
iasthmatics to formaldehyde at low concentrations. Using data gathered
from over 1,500 methacholine challenge tests, one can estimate the
prevalence of airway hyperreactivity in the population at large.sl
About 9 million people in the United States have bronchial »a+hma.
Essentially all will react positively to methacholine challenge tests
and thus be considered to have hyperreactive airways. The degree
of airway reactivity is variable and depends on a number of factors. 11
It has been estimated that 30% of atopic nonasthmatic people—perhaps
10 million—have positive methacholine tests." Townley et al.
reported that 5% of nonatopic persons—another 8.5 million—have
positive methacholine tests.'1 Therefore, on the basis of
calculations reported for positive methacholine challenge tests, it can
be estimated that about 25 million persons in the United States, or
10-12% of the population, may be considered to have some degree of
airway hyperreactivity. This population could potentially be more
susceptible to formaldehyde.
Information on other assumed susceptible populations is limited.
The U.S. Department of Bealth, Education, and Welfare, in a 1977 report
on prevention, control, and elimination of respiratory disease,'
VII-29
-------
estimated that 10 million persons in the United States had chronic
obstructive lung disease (excluding asthma).'7 An unknown percentage
oE then will have positive methacholine challenge tests. Britt et
al. l* suggested that the presence of methacholine sensitivity and
evidence of airway hyperreactivity are risk factors .for the development
of chronic obstructive pulmonary disease (COPD). Perhaps patients with
COPD who manifest airway hyperreactivity constitute a susceptible
population, inasmuch as they react more acutely to airborne irritants,
including formaldehyde.
On the basis of sensitivity to methacholine, some atopic persons,
some nonatopic subjects, and some COPD patients may constitute a
potential formaldehyde-susceptible population. This population could
also have greater eye and upper respiratory tract sensitivity.
However many apparently normal people also reacc to the' irritant
properties of formaldehyde; this makes it more difficult to determine
the susceptible population.
In another attempt to estimate the susceptible population
(particularly in relation to eye, nose, and throat sensitivity} ,
information on a small number of healthy young adults .exposed to-
formaldehyde at various concentrations for short periods was
considered. " At 1.5-3.0 ppm, more than 30% of the subjects tested
reported mild to' moderate eye, nose, and throat irritation symptoms,
and 10-20% had strong reactions. When test subjects were exposed at
0.5-1.5 ppm, slight or mild eye, nose, and throat irritation was noted
in more than 30%, but 10-20% still had more marked reactions.
Approximately 20% of the subjects had slight ear, nose, and throat
irritation in response to fotmaldehyde at 0.25-0.5 ppm. Finally, at
the lowest concentration tested, less than 0.25 ppm, some exposed
subjects ("less than 20 percent") still reported minimal to slight eye,
nose,, and throat discomfort. These data might be interpreted as
suggesting that there are subjects, perhaps 10-20% of those tested, who
react to formaldehyde at any given concentration.
We may get further information from mobile-home surveys from which
environmental and clinical data are available. Irritation symptoms'
were reported by 30-50% of subjects when formaldehyde concentration was
greater than 0.5 ppm. When the concentration was less than 0.5 ppm,
irritation symptoms were reported in fewer than 30% of subjects.
Finally, in a more controlled study in which irritation symptoms were
investigated, mild irritation responses (doubling of blinking rate)
occurre'd in 11% of subjects tested at 0.5 ppm.
In summary, fewer tlian 20% but perhaps more than 10% of the general
population may be susceptible to formaldehyde and may react acutely at
any concentration, particularly if it is greater than 1.5 ppm. People
report mild ENT discomfort and other symptoms at less' than 0.5 ppm,
with some noting symptoms at concentrations below 0.25 ppm. Low-
concentration formaldehyde exposures may produce eye, nose, and throat
symptoms and possibly lower-airway complaints. In some susceptible'
persons, an "allergic" reaction to formaldehyde may occur at very low
concentrations, causing bronchoconstriction and asthmatic symptoms.
This particular type of reaction to formaldehyde appears to be
uncommon; its prevalence cannot now be estimated.
VII-30
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EFFECTS 0? OTHER ORGANIC SUBSTANCES
Cardiac arrhythmia may occur through proteination of endogenous
catecholamines produced by a number of chemicals present in the
environment. Various environmental chemicals have structural
similarities to other chemicals that may have similar effects on the
myocardium) thes' chemicals have a lung tissue half-life that could
represent a long-term hazard. Examples include the polyhalogenated
hydrocarbons, which may cause sudden death. The polyhalogenated
hydrocarbons also bind to estrogen receptors and have been shown to
have estrogenic effects in animal systems. These effects may increase
HDL cholesterol and triglyceride concentrations and thus increase
coronary-heart-disease incidence or mortality risk.'*
Disturbances of the nervous system may occur through exposure to
such chemicals as polychlorinated biphenyls (PCBs), which may be stored
in fatty tissue and result in a long-term body burden. PCBs inhibit
growth in cell cultures and interfere with' the activity of a- variety of
enzymes.'*
Vapor-phase organic pollutants undergo biologic transformation
sequences and metabolic reactions in the intestine, and the metabolites
may be conjugated or excreted directly. Both forms may have a primary
effect on the gastrointestinal tract.5* The enzymatic activity of
the microflora of the gastrointestinal tract may also lead to the
conversion of ingested substances, such as nitrites to nitrates.
Formation of nitrosamines by the reaction of secondary amines with
nitrates may lead to cancer.
Vapor-phase organic pollutants are enzymatically converted in the
kidney and in the liver to more polar compounds, which are then
excreted.1' These hydrocarbons may have nephrotoxic action.
Solvents and chlorinated hydrocarbons may produce kidney land liver
damage.'7
Primary skin irritants include polycyclic organic matter and other
vapor-phase organic pollutants. Various pathologic responses in man
have been related to the use of polycyclic organic matter. Polycyclic
aromatic hydrocarbons are reportedly associated with the same kinds of
work exposures that have produced skin cancer. These materials include
derivatives of1 fossil fuel, paraffin distillates, asphalt, and
lubricating oils.57 Polycyclic organic matter may produce changes in
hair follicles and sebaceous glands.57 Vapor-phase organic
pollutants (like formaldehyde) may produce a variety of skin effects.
They may produce eczematous contact dermatitis and dermal contact
sensitivity.*1 They may be absorbed percutaneously because o£
solubility in the water-lipid system, they may produce skin
paresthesis, '* and they may produce eczematous reactions of an acute
or chronic nature, including eruptions and exacerbations." 11
Highly water-soluble pollutants are most likely absorbed by the
conjunctiva locally and systemically. The vapor-phase organic
pollutants, for instance, will affect the conjunctival membranes, the
cornea, and the nasal mucous membranes and cause mild to acute
inflammation.58
VII-31
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Washington, D.C.: National Academy of Sciences, 1976. 411 pp.
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—An Assessment of Its Health Effects. Washington, D.C.: National
Academy of Sciences, 1980. 38 pp.
60. North American Contact Dermatitis Group. Epidemiology of contact
dermatitis in North America: 1972. Arch. Dermatol. 108:537-540,
1973.
61. Nova, H., and R. G. Touraine. Asthme au formol. Arch. Mai. Prof.
18:293-294, 1957. (in French)
62. Odom, R. B., and H. I. Maibach. Contact urticaria: A different
contact dermatitis, pp. 441-453. Chapter,15 in F. N. Marzulli,
and H. I. Maibach, Eds. Advances in Modern Toxicology. Vol. 4.
Dermatotoxicology and Pharmacology. Washington, D.C.: Hemisphere
Publishing Corporation, 1977.
63. Orringer, E. P., and W. D. Mattern. Formaldehyde-induced
hemolysis during chronic hemodialysis. N. Engl. J. Med.
294:1416-1420, 1976.
64. Paliard, F., L. Roche, C. Exbrayat, and e. Sprunck. Chronic
asthma due to formaldehyde.. Arch. Mai. Prof. 10:528-530, 1949.
(in French)
65. Parker, C. D., R. E. Bilbo, and C. E. Reed. Methacholine aerosol
as test for bronchial asthma. Arch. Intern. M?d. 115:452-458,
1965.
66. Pepys, J., C. A. C. Pickering, A. B. X. Breslin, and D. J. Terry.
Asthma due to inhaled chemical agents—tolylene di-isocyanate.
Clin. Allergy 2:225-236, 1972.
67. Popa, V., D. Teculescu, D. Stanescu, and N. Gavrilescu. Bronchial
asthma and asthmatic bronchitis determined by simple chemicals.
Dis. Chest 56:395-404, 1969.
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68. Porter, J. A. H, Acute respiratory distress following formalin
inhalation. Lancet 2:603-604, 1975.
69. Proctor, D. F. The upper airways. I. Nasal physiology and defense
of the lungs. Am. Rev. Respir. Dis. 115:97-129, 1977.
70. Rathery, F., R. Piedelidvre, and J. Delarue. Death by absorption
of formalin. Ann. Med. Leg. Criminol. 20:201-206, 1940. (in
French)
71. Rostenberg, A., Jr., B. Bairstovr, and T. W. Luther A study of
eczeraatous sensitivity to formaldehyde. J. Invest. Dermatol.
19:459-462, 1952.
72. Roth, w. G. Tylosic palmar and plantar eczema caused by steaming
clothes containing formalin. Berufsdermatosen ' 17:263-268, 1969.
73. Sakula, A. Formalin asthma in hospital laboratory staffLancet
2:816, 1°75.
74. Schoenberg, J. B., and C. A. Mitchell. Airway disease caused by
phenolic (phenol-formaldehyde) resin exposure. Arch. Environ.
Health 30:574-577, 1975.
75. Shipkovitz, H. D. Formaldehyde Vapor Emissions in the
Permanent-Press Fabrics Industry. Report No. TR-52. Cincinnati:
U.S. Department of Health, Education, and Welfare, Public Health
Service, Consumer Protection and Environmental Health Service,
Environmental Control Administration, 1968. 18 pp.
76. Shy, C. M., J. R. Goldsmith, J. D. Hackney,- M. D. Lebowitz, and
D. B. Menzel. Health effects of air pollution. Paper presented at
meeting of American Thoracic Society, Medical Sectior of American
Lung Association, 1978;
77. Sim, V. M., and R. E. Pattle. Effect of possible smog irritants
on human subjects. J. Am. Med. Assoc. 165:1908-1913, 1957.
78. Sneddon, I. B. Dermatitis in an intermittent haemodialysis unit.
Br. Med. J. 1:183-184, 1968.
79. Spector, S. L., and R. S. Farr. A comparison of raethacholine and
histamine inhalations in asthmatics. J. Allergy Clin. Immunol.
56:308-316, 1975.
80. Tabershaw, I. R., H. N. Doyle, L. Gaudette, S. H. Lamm, and 0.
Hong. A Review of the Formaldehyde Problems in Mobile Homes.
Report to National Particleboard Association. Rockville, Md.:
Tabershaw Occupational Medicine Associates, P.A., 1979. 19 ppj
81. Townley, R. G., A. K. Bewtra, N. M- Nair, ?. D. Brodkey, G. D.
Matt, and K. M. Burke. Methacholine inhalation challenge studies.
J. Allergy Clin. Immunol. 64:569-574, 1979.
82. Turiar, C. Asthma through sensitivity to formaldehyde. Soc.
Franc. d'Allergie, Seance d" 18 Nov. 1952.
83. Uehara, M. Follicular contact dermatitis due to formaldehyde.
Dermatologica 156:48-54, 1978.
84. U.S. Consumer Product Safety Commission. News from CPSC.
Wednesday, August 1,' 1979.
85. U.S. Consumer Product Safety Commission, Directorate for Hazard
Identification and Analysis—Epidemiology. Summaries of in-depth
investigations, newspaper clippings, consumer complaints and
state reports on urea-formaldehyde foam home insulation.
Washington, D.C.: U.S. Consumer Product Safety Commission, July
1978.
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86. U.S. Department of Health, Education, and Welfare, National
Heart, Lung, and Blood Institute. Working Group on Heart Disease
Epidemiology. DHEW (NIH) Publication No. 79-1667. Washington,
D.C.: U.S. Department of Health, Education, and Welfare, 1979.
69 pp.
87. U.S. Department of Health, Education, and Welfare, National
Heart, Lung and Blood Institute, Division of Lung Disease.
Respiratory Diseases. Task Force Report on Prevention, Control,
Education, pp. 84-91. DHEW Publication No. (NIH) 77-1248.
Washington, D.C.: U.S. Government Printing Office, 1977.
88. U.S. Department of Health, Education, and Welfare, National
Institute for Occupational Safety and Health. Criteria for a
Recommended Standard... Occupational Exposure to Formaldehyde.
DHEW (NIOSH) Publication No. 77-126. Washington, D.C.s U.S.
Government Printing Office, 1976. 165 pp.
89. Vaughan, W. T. The Practice of Allergy, p. 677. St. Louis: The C.
V. Mosby Company, 1939.
90. Waldbott, G. L. Health Effects of Environmental Pollutants. SAint
. Louis: The C. V. Mosby Company, 1973. 316 pp.
91. Walker, J. F. Formaldehyde, pp. 77-99. In A. Standen, Ed.
K,irk-Othmer Encyclopedia of Chemical'Technology. 2nd rev. ed.
Vol. 10. New York: Interscience Publishers, 1966.
92. Wayne, L. G., R. J. Bryan, and K. Ziedman. Irritant Effects of
Industrial Chemicals: Formaldehyde. DHEW (NIOSH) Publication No.
77-117. Washington, D.C.: U.S. Government Printing Office, 1976.
[138] pp.
93. Weger, A. Thalamischer Symptomenkomplex bei Fortaalinintoxikation.
Z. Ges. Neurol. Psych. 111:370-382, 1927. (in German)
94. Wisconsin Division of Health, Bureau of Prevention. Formaldehyde
Case Filfe Summary, October 23, 1978. Madison: Wisconsin Division
of' Health, 1978. 3 pp.
95. Wisconsin Division cf Health, Bureau of Prevention. Statistics of
particle board related formaldehyae cases through December 15,
1978. Madison: Wisconsin Division of Health, 1978. (41 pp.
96. Woodbury, J. w. Asthmatic syndrome following exposure to tclylene
dissocyanate. Ind. Med. Surg. 25:540r543, 1956.
97. World Health Organization. Health Hazards of the Human
Environment. Geneva: World Health Organization, 1972. 387 pp.
98. Yefremov, G. G. State of the uppT respiratory tract in
formaldehyde production workers. Zh. Ushn. Nos. Gorl. Bolezn.
30(5):11-15, 1970. (in Russian; English summary)
99. Zaeva, G. N., I. p. Ulanova, and L. A. Dueva. Materials for
revision of the maximal permissible concentrations of
formaldehyde in the inside atmosphere of industrial premises.
Gig. Tr. Prof. Zabol. 12:16-20; 1968. (in Russian)
100. Zannini, D., and L. Russo. Long-standing lesions in the
respiratory tract following acute poisoning with irritating
gases. Lav. Um. 9:241-254, 1957. (in Italian; English summary)
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FIBROUS BUILDING MATERIALS
Current knowledge of the adverse health effects of flt.'oos building
materials is reasonably coaplete for only one such material; asbestos.
Other materialsi such as fibrous glass and rock wool, are becoming wore
widely used, but little is known about their heclth effects in humans.
The continuing widespread use of fibrous building materials in the
absence of an adequate understanding of their potential health impacts
has led to public-health concern. The details of their production,
use, emission, and control are reviewed in Chapter IV.
The nr.ture of health problems varies with the organ system that may
be affected. Fibrous materials can have a direct effect due to contact
with the skin, can affect the lungs because of inhalation, and can
affect the gastrointestinal tract because of inadvertent ingestion.
Furthermore, every organ in the body may be affected through transport
of fibers by the hematogenous or lymphatic systems. There does not
appear to be any uptake of fibrous material through the skin.
Inhalation is the major route of, entry of fibrous particulate
matter. Deposition and retention depend on the usual factors of
respiratory physiology and on fiber dimension. Host inhaled fibrous
material is cleared by the mucociliary escalatory clearance mechanism,
which results in inadvertent ingestion. Other inhaled particles are
retained in the lung, where they accumulate. Some fitxrs, through
uncertain routes, migrate to the pleura and stay there. Fiber
translocation from the lung also occurs via the hematogenous and
lymphatic systems, with eventual accumulation of fiber> in virtually
every organ of the body. The fractions that are dissenrnated by this
mechanism and through the gastrointestinal system are n-->t known.
That dispersion takes place through the gastrointestinal tract has
been clearly shorn in animals.' Gavag: of asbestos or the presence
of asbestos in drinking water or food results in transport across the
intestinal wall into the peritoneal cavity and into the bloodstream,
which leads to deposition throughout the body. After gavage, asbestos
has been found in all organs examined, including kidney, liver,
pancreas, and brain. It can also cross the placenta.1
Asbestos and other fibrous materials are not metabolized after
entering the body, but there is leaching of chemical constituents,
which varies with fiber type and sixe. Fibers can take up biologic
residence in many organs, and most fibers remain uncoated. Some fibers
become coated with an iron-prctein matrix and form an "asbestos body9
when asbestos is the core material. Nhen the core is not identified,
it is known as a "ferruginous body." The intracellular process that
produces this coating has been well documented by Susuki and Churg.**
Some structural and compositional changes occur after fibers are taken
up in tissue, particularly in the lung. In the case of chrysotile,
magnesium leaches out of the fiber; this ultimately changes the
structure of chrysotile and makes quantitative recovery from lung
tissue less secure over time. The mechanism r
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interaction of asbestos and macrophages l_n_ vivo is less well
understood, but some intact macrophages contain snail fibers, and
others surround parts of large fibers.
SPECIFIC HEALTH EFFECTS
Health effects resulting from exposure to fibrous materials can be
divided into nonmalignant and malignant effects. A division into acute
and chronic effects is of little value. Except for the acute cutaneous
irritation produced by fibrous glass products, including those treated
with resins and lubricants, the important effects of exposure to
fibrous materials are chronic, and they often have very long latent
periods. No initial short-term health effects of any major consequence
are seen in either healthy adults or persons with pre-existing
conditions, because of the long latent period of the effects.
All mineral fiber types have been shown in laboratory animals to be
capable of producing a wide spectrum of disease when administered as
long, thin fiber3.
Nonmalignant Effects
Cutaneous Effects. Asbestos has been shown to produce
granulomatous warts on the hands, and asbestos fibers have been found
in these growths. Whether asbestos alone is the causative agent or
viruses play a role has not been studied. It has been known for
»«veral decades that fibrous glass materials can produce severe
irritation in those working with them. This may be a function of
direct physical contact or of a chemical process related to resins and
lubr-.cants. It can be prevented by the wearing of long-sleeved
clothing and gloves.
Findings in Sputum. Asbestos bodies were first described (although
noc so named until 1929) on the basis of autopsy findings in two-deaths
in 1906." These fibers coated with iron-protein have been used as a
marker for previous asbestos exposure, not as an indicator of disease
or severity cf disease. As a marker of exposure, their appearance
works well. The coating of fibers jLn vivo varies with species.
Both uncoated fibers and asbestos bodies have been found in sputua
and give some guidance as to extent of exposure, particularly if the
exposure has been Intense. Digestion and examination of lung tissue
often reveal the presence of asbestos bodies and fibers; in
approximately half of 3,000 consecutive autopsies in New York City,
optical microscopy uncovered asbestos bodies in lung tissue.1*
Electron microscopic examination is preferred for more complete
evaluation.
Pulmonary Disease. The most important nonmalignant health effect
of asbestos exposure is the change in the pulmonary system.
Asbestosis, lung scarring, can lesult from asbestos exposure and is a
VII-39
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leading cause of death tunong some occupationally exposed groups.
"Asbestosis" refers to the fibrotic process of either the lung
parenchyma or the visceral pleura, if one is referring only to lung
tissue# the term "parenchymal asbestosis" is preferable. "Asbestosis"
is a clinical diagnosis that can be made in the absence of active
symptoms or any appareiit ill health* "Impairment" is a clinical
judgment based on findings in the history and in physical and
laboratory examinations. Not everyone with disease is impaired. The
presence of disease, without impairment should always suggest the
possibility of future impairment or future additional disease.
"Disability" is a legal concept related to the absence or presence of
disease and impairment, often with regard to specific functions.
Fibrosis of the lung parenchyma after asbestos exposure is related
to the degree of exposure and the period since the beginning of
exposure. It has been documented*' that increasing exposure leads to
an increase in the incidence of asbestosis and an increase in its
severity. The degree of asbestosis is usually measured in terms of the
ILO-u/C classification for x-ray films (issued by the international
Labour Office, 1971, Geneva), which evaluates changes on a 12-point
scale and includes types of changes and associated findings.
Radioloijically evident asbestosis generally develops only after
considerable time has passed since first exposure, unless exposure has
been intense. The appearance of extensive asbestosis in less than 20
yr is unusual. If asbestosis does occur within that period, it will
probably not be fac advanced. The exposure1 need not be continuous over
this period; and relativiely brief exposure may be sufficient to cause
disease many years later.
In addition to parenchymal asbestosis, changes may develop in the
pleura. Pleural fibrosis, with or without calcification, is a common
finding after asbestos exposure. There is increasing evidence that the
extent of exposure required to produce pleural .changes may be less than
that associated with parenchymal changes." There is no reliable
correlation between a finding of nonmalignant pulmonary changes and the
predictability of development of neoplasia, which can develop without
radiologic evidence of asbestosis.
Malignant Effects
A variety of malignant neoplasms are associated with exposure to
asbestos.
Lung Cancer. Lung cancer is found in great excess among workers
occupationally exposed to asbestos. This has been noted with all
commercially important types of asbestos. Asbestos-related tumors tend
to be in the lower lobes and peripheral, following the pattern of the
parenchymal changes of asbestosis, although neoplasms are also
increased in the upper lobes. The cell type distribution does not
appear to be altered with asbestos-related cancers.12 Cigarette-
smoking acts synergistically to increase the risk of developing lung
cancer.*1
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Mesothelioma. Both pleural and peritoneal mesotheliomas are Been
after exposure to asbestos. Pleural mesotheliomas are generally aoce
common) peritoneal meeathelLaaaa tend to take longer to develop and
tend to occur in large numbers only among note heavily exposed
populations. Their incidence is not related to cigarette-smoking•
Ott>«-T Cancers, other malignancies are found in excess after
aabestcs exposure. Of particular importance is the increase in
gastrointestinal tract cancers, particularly of the colon and rectum,
stomach, and esophagus.*2 Pancreatic cancer does not appear to be
increased. Oropharyngeal cancers and laryngeal cancers are also
increased.*1
Among women, ovarian cancer has been reported after asbestos
exposure, 19 but more data on this question are needed.
LABORATORY EVIDENCE Q1- aZ? IT3 EFFECTS
An increasing number of reports have demonstrated adverse effects
in vivo or _in vitro, many in parallel with demonstrated huaan health
effects.
In Vivo Effects
In vivo experimentation has documented all the major health effects
caused by asbestos; and in some cases other materials have caused
similar changes.
Inhalation. Inhalation studies with asbestos of several fiber
types have documented the risk in animals of developing asbestosis and
malignancy, including lung cancer and mesothelioma. Wagner et al.'*
and Davis et al." have sho**n that all major fiber types produce both
malignancies noted, and that the usual dose-response relationship
holds. Wagner et al. and Bernstein et al.' are conducting studies to
evaluate the hazards associated with inhalation of fibrous glass
products and talc.
Injection. Intratracheal, intrapleural, and intraperitoneal
injections into laboratory animals of asbestos, fibrous glass, and
other¦fibrous material have been associated with disease production.
Lung cancer has been produced in hamsters with intratracheal
instillation."* Peritoneal mesothelioma has been produced by
injections or other placement of asbestos into the pleural cavity.
Stanton et al.*7 *• produced neoplasms with long, thin fibers of
various kinds, including asbestos, fibrous glass products, and aucb
other fibrous materials as fibrous dawsonite, an aluminum carbonate.
Peritoneal mesotheliomas have developed after intraperitoneal
injections of asbestos.** Wright and Kuschner" instilled
asbestos, glass, and other fibers into guinea pigs intratracheally;
when the fibers were long and thin, all the materials produced lung
fibrosis.
VI1-41
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In Vitro Effects
In vitro techniques are increasingly being used to study the
effects of asbestos and other fibrous materials. A comprehensive
review on this subject was published, by Harington et al. 17
Macrophages. Asbestos and other fibrous materials may be tonic to
macrophages. This was first shown by Harington et al.. 17 in
preparations of freshly prepared macrophages and more recently by Wade
et. al_. 11 in continuously cultured malignant macrephage-like cells..
Thus, the cytotoxic potential of a variety of fibers is clear. There
is new evidence that the cytotoxic potential of fibrous materials may
.parallel their carcinogenic potential.' 11 Miller has reviewed the
effects of asbestos on macrophages as shown with electron
microscopy.**
Fibroblasts. Addition of asbestos to cultjres of fibroblasts has
demonstrated alterations in both ceilular bio nemistry and morphologic
appearance." " These chemical alterations have not yet been
related to changes in human lung tissue.
Other Cell Systems. .Other cell systems have been used to study the
effects of asbestos. Schnitzer et al. " used erythrocytes as a test
system for the evaluation of biologic effects of a variety of dusts,
and work with mesothelial cell culture11 has begun to increase the
understanding of changes in this cell type brought about by exposure to
such dusts as asbestos..
Organ Culture
Another approach to the understanding of the effects of asbestos
and other dusts has been the use of organ culture systems. Mossman et
al. 11 investigated the effects of crocidolite on hamster tracheal
cultures, and Frank12 studied the effects of amosite and chrysotile.
Hyperplasia of basal cells was the most prominent morphologic change
noted. Rajan et al. " studied the effects of asbestos on human
pleura in organ culture and jalso noted hyperplasia after the addition
of asbestos. Fibrous glass products are currently under study with
organ culture techniques.
EPIDEMIOLOGY AND OCCUPATIONAL EXPOSURE
The first case of asbestosis reviewed for compensation purposes was
observed in 1906 in England by Murray.11 Additional cases were
reported later, and the disease wa3 better understood by 1930. In
1935, Lynch and Smith17 reported the first case of lung cancer in a
man who worked in an asbestos factory and suggested a causal
relationship. The historical development of the understanding of
asbestos-related disease was reviewed by Selikaff and Lee.*1
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Asbestos13
Cases of asbeatosis were known earlier, but it was daring 1930 that
Merewether and Price*' extensively reviewed the association of
asbestos exposure and the development of fibrosis. More than 25% of
363 asbestos manufacturing workers had evidence of pulmonary fibrosis
related to their exposure to asbestos. Similar findings were reported
in the United States by Lanza el al.11 For the development of
asbestosis in relation to exposure and to the period from onset of
exposure, the information reported by Selikoff and Lee*' clearly
demonstrated a dose-response relationship and showed that development
and severity of asbestosis increase with time.
Other Chronic Lung Diseases
There have been few epidemiologic reports of other chronic lung
disease after exposure tc nonasbestos fibrous materials. Bayliss eit
al.1 reported no increased lung-cancer mortality, but an increase in
nonraalignant respiratory-disease deaths among fibrous-glass production
workers. Boehlecke eit al_. 9 have reported on a group of workers
exposed to wollastonite, a fibrous monocalciura silicate used as an
asbestos substitute. They observed none of the clinical stigmata
usually seen with asbestos exposure. Only 36% of workers had been
exposed more than 15 yr before the study.
Cancer Epidemiology
The 1955 report by Doll11 was a landmark in the establishment of
a relationship between lung cancer and asbestos exposure. Other
reports soon followed; several were represented at the Hew, York Academy
of Sciences in 1965. 17
Before 1960, mesothelioma had been a rarely reported disease,
although some cases had been seen in asbestos workers. In that year,
Wagner et al.Si reported 47 cases that had occurred during a 4-yr
period in the asbestos-mining area of South Africa. Further reports
appeared soon after, and the strong causal relationship with asbestos
exposure has now been firmly established. Cochrane ¦ and Webster*
found that 69 of 70 cases of mesothelioma at one South African hospital
were associated with substantial asbestos exposure.
Principles
Through the epidemiologic investigations of occupationally exposed
groups, several principles of exposure-disease relationship have become
clear. The question of latency is now well understood: in general,
15-20 yr must pass before the signs of marked asbestos-related disease
are detected, by either x-ray study, pulmonary-function results, or
physical findings. The exposure may have been brief; if it was intense
VI1-43
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enough, disease may result, although in almost all cases there is a
long latency period.
It has become clear that both the severity of asbestosis and the
risk of developing lung cancer or mesothelioma depends on the total
exposure to fibers. Because of the paucity of data on workplace or
environmental concentrations, exposures are almost never known exactly,
and only rough estimates of exposure can be agreed on by most
authorities.
Exposure in the workplace can be either direct or indirect. In
many cases, indirect, or "bystander," exposure has proved hazardous.
This has been established,in shipyard workers16 19 and maintenance
workers.1' Thus, indirect exposure can be hazardous to people who
work near those specificially assigned to handle asbestos.
Other Fibrous Mineral Materials and Dusts
No epidemiologic investigation has demonstrated substantial health
hazards related to other fibrous materials and dusts that might
contaminate the indoor, environment. The asbestos substitutes used in
construction are relatively new, at least with respect to their
possibly producing hunan health effects, and little is known of their
hazards. Those materials include the slag wools, rock wools, glass
wools, and filaments. The subject of man-made mineral fibers has been
reviewed by Hill20 and Wagner et al.**
NONOCCUPATIONAL EXPOSURE
Much less is known about exposure to fibrous materials away from
the workplace than about occupational exposure.
Neighborhood Exposure
There have been several studies of exposures of persons living near
asbestos production facilities. Wagner's original report on cases of
mesothelioma in South Africa included mainly persons who lived near
asbestos mines or along the routes of transport. Newhouse and
Thompson'1 showed that a substantial number of cases of mesothelioma
at the London Hospit.al between 1910 and 196S were in persons who lived
within 0.5 mile of
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Family Exposure
Among the best recorded relationships between household
contamination and disease development are those among families of
asbestos workers. Particularly striking is the development of
mesotheliomas among wives, children, and other family contacts of
asbestos workers who have brought asbestos home on their persona and
clothing. Contamination of the living environment resulted; 20 yr or
more later, mesotheliomas appeared. In addition, roughly one-third of
such persons had x-ray changes consistent with asbestosis.> Studies on
this subject were recently reported by Anderson et al.1 and Tagnon et
al.s«
Exposure in Buildings
Only within the last several years has the scientific community
become aware of the widespread use of asbestos in public buildings in
ways that might be related to substantial risk. Asbestos is used in
insulation and fireproofing materials, in ornamental decoration and
soundproofing, and in large quantities on surfaces in public areas.
Its use in school buildings has been the subject of recent reviews'* *• *5
that included discussion of potential health problems and suggestions
of control measures. Public areas in other buildings can also become
contaminated, especially during routine or other maintenance
procedures, which may aerosolize friable asbestos coatings.
There have been few measurements of air concentration. Especially
lacking are studies that put members of the general population or
schoolchildren under prospective surveillance to see what (if any)
adverse health effects occur. Refinement of risk estimates of effects
in the general population awaits additional understanding and
measurement of the potential effects of long-term low-concentration
exposure. The relationship of total exposure to the age when first
exposure occurs is not known.
Other Exposures
The general environment may become contaminated from ambient air or
water pollution with asbestos or other fibrous material. This is of
special concern for houses in communities with mining and processing
facilities. Household exposures can also occur elsewhere, although few
measurements have been made to demonstrate the extent of such exposures.
In Montgomery County, Maryland, widespread ambient-air
contamination has resulted from the long use of. crashed rock containing
asbestos for the paving of roads, parking lots, and playgrounds. Air
concentrations in the community were reported to be similar to those in
some working environments,17 and the particular asbestos that was
contaminating the air was shown to have substantial biologic
activity.1 ¦
vti-45
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Water contamination can also occur from the dumping of industrial
wastes into lakes* as evidenced by tbe asbestos found in the water of
some communities that take theic municipal supplies from Lake
Superior.1'
Consigner products brought into the home may contain asbestos. The
Consumer Product Safety Commission has banned artificial, fireplace logs
and hair-dryers containing asbestos. The subject of consumer-product
asbestos hazards has been discussed by Franklin.l
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13. Frank, A. L., A. N. Rohl, M. J. Wade, and L. E. Lipkin. Biological
activity in vitro of chrysotile compared to its quarried parent
rock (platy serpentine). J. Environ. Pathol. Toxicol. 2:1041-1046,
1979.
14. Franklin, B. H. Public health control of environmental asbestos
disease: Consumer products. Ann. N.Y. Acad. Sci. 330:497-501, 1979.
15. Graham, J., and R. Graham. Ovarian cancer and asbestos. Environ.
Res. 1:115-128, 1567.
16. Hammond, E. C., L. Garfinkel, I. J. Selikoff, and w. J. Nicholson.
Mortality experience of residents in the neighborhood of an
asbestos factory. Ann. N.Y. Acad. Sci. 330:417-422, 1979.
17. Harington, J. S., A. C. Allison, and D* V. Badami. Mineral fibers:
Chemical, ptiysiochemical, and biological properties. Adv.
Pharmacol. Chemother. 12:291-402, 1975.
18. Harries, P. G. Asbestos hazards.in Naval Dockyards. Ann. Occup.
Hyg. 11:135-145, 1968.
19. Harries, P. G. Experience.with asbestos disease and its control in
Great Britain's Naval Dockyards. Environ. Res. 11:261-267,. 1976.
20. Hill, J. w. Health aspects of man-made mineral fibres. A review.
Ann. Occup. Hyg. 20:161-173, 1977.
21. Jaurand, M.-C., H., Kaplan, J. Thiollet, M.-C. Pinchon, J.-F.
Bernaudin, and J..Bignon. Phagocytosis of chrysotile fibers by
pleural mesothelial cells in culture. Am. J. Pathol. 94:529-538,
1979.
22. Kannerstein, M., and J. Churg. Pathology of carcinoma of the lung
associated with asbestos exposure. Cancer 30:14-21, 1972.
23. Langer, A. M., C. M. Maggiore, W. J. Nicholson, A. N. Rohl, I. B.
Rubin, and I. J. Selikoff. The contamination of Lake Superior with
amphibole gangue minerals. Ann. N.Y. Acad. Sci. 330:549-572, 1979.
24. Langer, A. M., I. J. Selikoff, and A. Sastre. Chrysotile asbestos
in the lungs of persons in New York City. Arch. Environ. Health
22:348-361, 1971.
25. Lanza, A. J., W. J. McConnell, and J. H. Fehnel. Effects of the
inhalation of asbestos dust on the lungs of asbestos workers.
Public Health Rep. 50;1-12, 1935.
26. Lilis, R., S. Daum, H. Anderson, M. Sirota, G. Andrews, and I. J.
Selikoff. Asbestos disease in maintenance workers of the chemical
industry. Ann. N.Y. Acad. Sci. 330:127-135, 1979.
27. Lynch, K. M., and w. A. Smith. Pulmonary asbestosis. 111. Carcinoma
of lung in asbesto-silicosis. Am. J. Cancer 24:56-64, 1935.
28. Marchand, F. Ober Eigentumliche Pigraentkristalle in den Lungen.
Dtsch. Path. Ges. Verh. 17:223, 1906.
29. Merewether, E. R. A., and C.W. Price. Report on Effects on
Asbestos Dust on the Lungs and Dust Suppression in the Asbestos
Industry. London: His Majesty's Stationery Offige, 1930. 34 pp.
30. Miller, K. The effects of asbestos on macrophages. CRC Crit. Rev.
Toxicol. 5:319-354, 1978.
31. Mossman, B. T., J. B. Kessler, B. W. Ley, and J. E. Craighead.
Interaction of crocidolite asbestos with hamster respiratory mucosa
in organ culture. Lab. Invest. 36:131-139, 1977.
VII-47
-------
32. Murray, H. M. Report of the Departmental Committee on Compensation
for Industrial Disease. London: His Majesty's Stationery Office#
1907.
33. Newhouse, M. L., and H. Thompson. Mesothelioma of pleura and
peritoneum following exposure to asbestos In the London area. Br.
J. Ind. Med. 22:261-269, 1965.
34. Nicholson, W. J., A. N. Rohl, R. N. Sawyer, E. J. Swoszowski, ijr.,
and J. D. Todaro. Control of sprayed asbestos surfaces in school
buildings: A feasibility study. Report, to the National Institute of
Environmental Health Sciences. New York: City University of New
York, Mount Sinai School of Medicine, Environmental Sciences
Laboratory, 1978. [121] pp.
35. Rajan, K. T.« J. C. Wagner, and P. H. Evans. The response of human
pleura in organ culture to asbestos. Nature 238:346-347, 1972.
36. Richards, R. J., and F. Jacoby. Light microscope studies on the
effects of chrysotile asbestos and fiber glass on the morphology
and reticulin formation of cultured lung fibroblasts. Environ. Res.
11:112-121, 1976.
37. Rohl, A.N., A. M. Langer, and I. J. Selikoff. Environmental
asbestos pollution related to use of quarried serpentine rock.
Science. 196:1319-1322, 1977.
38. Sawyer, R. N., and E. J. Swoszowski, Jr. Asbestos abatement in
schools: Observations and experiences. Ann. N.Y. Acad. Sci.
330:765-775, 1379.
39. Schnitzer, R. J., G. Bunetcu, and v. Baden. Interactions of mineral
fiber surfaces with cells in vitro. Ann. N.Y. Acad. Sci.
172:759-772, 1971.
40. Seidraan, H., I. J. Selikoff, and E. C. Hammond. Short-terra asbestos
work exposure and long-term observation. Ann. N.Y. Acad. Sci.
330:61-89, 1979.
41. Selikoff, I. J., E. C. Hammond, and J. Churg. Asbestos exposure,
smoking, and neoplasia. J. Am. Med. Assoc. 204:106-112, 1968.
42. Selikoff, I. J., E. C. Hammond, and H. Seidman. Mortality
experience of insulation worker is in the United States and Canada,
1943-1976. Ann. N.Y. Acad. Sci. 330:91-116, 1979.
43. Selikoff, I. J., and 0. H. K. Lee. Asbestos and Disease. New York:
Academic Press Inc., 1978. 549 pp.
44. Shin, M. L., and H. I. Firminger. Acute and chronic effects of
intraperitoneal injection of two types of asbestos in rats with a
study of the histopathogenesis and ultrastructure of resulting
mesotheliomas. Am. J. Pathol.' 70:291-313, 1973.
45. Silver,- R. Z. Asbestos in school buildings: Results of a
nation-wide survey. Ann. N.Y. Acad. Sci. 330:777-786, 1979.
46. Smith, W. E., L. Miller, R. E. Elsasser, and D. D. Hubert. Tests
for carcinogenicity of asbestos. Ann. N.Y. Acad. Sci. 132:456-488,
1965.
47. Stanton, M. P., M. Layard, A. Tegeris, E. Miller, M. May, and E.
Kent. Carcinogenicity of fibrous glass: Pleural response in the rat
in relation to fiber dimension. J. Nat. Cancer Inst. 58:587-603,
1977.
VII-48
-------
46. Stanton, M., and C. Wrench. Mechanisms of mesothelioma induction
with asbestos and fibrous glass. J. Nat. Cancer Inst. 48:797-821,
1972.
49. Suzuki, Y., and J. Churg. Structure and development of the asbestos
body. Am. J. Pathol. 55:79-107, 1969.
50. Tagnon, I.,, W. J. Blot, R. B. Stroube, N. E. Day, L. E. Morris,
D. B. Peace, and J. F. Fraumeni, Jr. Mesothelioma associated with
the shipbuilding industry in coastal Virginia. J. Cancer Res.
40:3875-3879. 1980.
51. Wade, M. J., L. E. Lipkin, and A. L. Frank. Studies of in vitro
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cytotoxicity in a long term macrophage-like cell culture. Nature
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in vitro cytotoxicity assay as applied to asbestos and other
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1980.
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effects of the inhalation of asbestos in rats. Br. J. Cancer
29:252-269, 1974.
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mesothelioma and asbestos exposure in the North Western Cape
Province. Br. J. Ind. Med. 17:260-271, 1960.
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455-472. In W. H. Walton Inhaled Particles IV. Proceedings of an
International Symposium Organized by the British Occupational
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Pergamon Press, 1977.
COMBUSTIOS PRODUCTS
This section concerns the effects of the exposute of people in
buildings to the products of fossil-fuel combustion that takes place in
those buildings. Such fuels are consumed in space- and water-heating,
clothes-drying, cooking, and operating gas-powered refrigerators and
propane torches. When unvented flames are used in maintenance,
modification, and repairs or in hobby activities, some of the effluents
are similar to those of flames used for cooking and space-heating—
carbon monoxide and nitrogen dioxide. As discussed in Chapter IV,
additional toxicants may also be released, depending on the composition
of the objects heated and the temperatures attained.
VII-49
-------
The present discussion is limited to the effects of the products of
fossil-fuel corabusion. It excludes, for example, the materials
vaporized by the application of a flame to a cooking pot, frying pan,
or metal object involved in maintenance or hobby activities. With
respect to cooking, this exclusion can be justified on the basis that a
gas range and an electric range do not differ substantially in the
composition and magnitude of pollutants released during cooking. The
contribution of the cooking processes ihemselves to overall indoor
pollution may be important, especially with respect to odor
characteristics and the concentrations of suspended particles. But the
effluents of cooking processes are highly variable, and their effects,
if any, on the health of residents are generally not known. Cigarette
combustion is also excluded, in that it is discussed in the next
section of this chapter.
For the products of indoor combustion to constitute a health
stressor, they must be able to cause toxic effects and they must be
present in occupied spaces at sufficient concentrations and for
sufficient durations to manifest their toxicity in a substantial part
of the exposed population. The extent to which products of combustion
contaminate indoor air depends on the composition of the fuel, the
temperature of combustion, the efficiency of combustion, the efficiency
of the venting of the combustion products tc the outdoor air, and the
isolation of discharged air from makeup air 'hat enters the occupied
space. The most important factor is usually the presence or absence of
effective venting of the combustion products to the outdoor air. If
the venting is effective, there should be relatively little buildup of
combustion effluents indoors, even when liquid fuels (such as kerosene)
or solid fuels (such as wood, charcoal, coke, and anthracite) are
burned. However, the use of liquid and solid fuels makes it more
difficult to achieve effective venting.
When venting of combustion effluents is incomplete, even the
burning of the cleanest of. fuels (natural gas) may liberate excessive
amounts of toxic gaseous effluents, specifically carbon monoxide and
nitrogen dioxide. There may also be measurable amounts of nitric
oxide, unburned fuel (methane, ethane, propana, etc.), products of
pyrosynthesis (e.g., aldehydes), and carbonaceous particles.
The products of indoor combustion that are most often of health
concern are carbon monoxide and nitrogen dioxide. Airborne
concentrations of these pollutants have h"en measured in a number of
epidemiologic studies; but other air pollutants were also present, and
their concentrations were usally not measured. At best, epidemiology
can demonstrate an association, but it cannot establish causality.
CARBON MONOXIDE
Exposure to carbon monoxide (a product of incomplete combustion of
any fossil fuel) constitutes a long-established and well known acute
hazard. Exposure at over 500 ppm for more than 1 h can lead to
approximately 20% of carboxyhemoglobin saturation. Exposure at 1,500
ppm for 1 h is dangerous to life. 1 Such high concentrations can
VII-50
-------
result from improper combustion—e.g., without an adequate supply of
combustion air. The issue of a threshold for adverse carbon monoxide
effects was addressed in a 1977 National Research Council report: 11
Whether there is a threshold carboxyhemoglobin
concentration for an adverse effect is still unknown. . . .
The mechanism for adverse carbon monoxide effects is a fall in
capillary oxygen partial pressure (p02) due to carbon
monoxide binding to henoglobin, and therefore a pertinent
question is whether any fall in capillary p02, no matter how
small, results in an adverse effect on tissues. It is known
that many tissues, in order to keep intracellular pOj nearly
constant, can adapt to acute falls in arterial p02 with
resulting falls in capillary p02< The major adaptation
mechanism in many tissues is probably recruitment of
capillaries to give a decrease in oxygen diffusion distance
between capillary olood and mitochondria. If such a mechanism
occurs as carboxyhemoglobin increases, it is unlikely that
adverse carbon monoxide effects occur at carboxyhemoglobin
concentrations near zero and more probable that a threshold
exists at a carboxyhemoglobin concentration where adaptation
cannot compensate.
. . . The tissues most sensitive to the adverse effect of
carbon monoxide appear to be heart, brain, and exercising
skeletal muscle. Evidence has been obtained that
carboxyhemoglobin concentrations in the 3-5% saturation range
may adversely affect the ability to detect small unpredictable
environmental changes (vigilance). There is evidence that
acute increases of carboxyhemoglobin to above 4-5% in patients
with cardiovascular disease can exacerbate their symptoms when
the carboxyhemoglobin is as low as 5%. . . .In the studies of
the effect of carbon monoxide on vigilance and cardiovascular
symptoms, there was no attempt either to determine the effect
of lower carboxyhemoglobin concentrations or to look for a
threshold. When aerobic metabolism of exercising skeletal
muscle was studied, an apparent threshold was found. At a
carboxyhemoglobin concentration below 5%, a measurable effect
on oxygen uptake could not be demonstrated.
* * *
The current EPA standard for carbon monoxide is 9-ppm
maximum for 8-hr average exposure, or 35-ppm maximum for 1-hr
average exposure. Approximate calculated carbon monoxide
uptakes for varying levels of activity after exposure to these
concentrations are given below.
Exposure
Resting
Moderate Activity
Heavy Activity
9 ppm, 8 hr
1.3% sat
1.4% sat
1.4% sat
35 ppm, 1 hr
1.3%
2.2%
2.9%
VII-51
-------
... The current EPA standard is mainly justified on the
basis of adverse carbon monoxide effects in patients with
cardiac and peripheral vascular disease and effects of carbon
monoxide on oxygenation of skeletal muscles in exercising
normal human subjects. There appears to be an adequate safety
factor between the lowest carboxyhemoglobin concentration that
has been demonstrated to cause adverse effects and the maximal
carboxyhemoglobin concentration that can occur at 9-ppm carbon
monoxide for 8 hr or 35 ppm for 1 hr. (pp. 164-167)
The experimental studies on carbon monoxide health effects
performed in recent years are summariied in Table VII-5. They have
tended to confirm the judgments expressed in the 1977 NRC report.
Moderately severe exposures to carbon monoxide—e.g., at 50 ppm for
up to about an hour—can occur in kitchens as a result of ordinary u*e
of a gas range, especially when the cooking uter.sils divert or quench
the flame. Higher exposures can be found indoors in public buildings,
such as ice-skating rinks, where mean concentrations of carbon monoxide
as high as 100 ppm have been measured (Spengler, personal
communication). The health effects of indoor exposures to carbon
aot.oxide are addressed in the next section of this chapter, which deals
with involuntary smoking; carbon monoxide is, of course, a pollutant
that it' common to cigarette-smoke and fossil-fuel combjstion
effluents, The effects of carbon monoxide from indoor combustion
cahnot be adequately assessed without considering the influence of
exposure to cigarette smoke. For smokers, mainstream smoke is the
dominant source of carboxyhemoglobin (COHb) in the blood. For
nonsmokers, the lower COHb values c*n be attributed to metabolism, to
carbon monoxide in the outdoor air, to carbon monoxide in sidestream
smoke, and to carbon monoxide from indoor combustion sources. The
extent of COHb saturation associated with metabolism is 0.7%.
Community air pollution or exposure to sidestream smoke ctn raise COHb
in nonsmokers to 2-3%." The influence of indoor combustion on COHb
saturation depends on many factors. Carbon monoxide from indoor
combustion may be dominant when there are no smokers in the occupied
space and when outdoor carbon monoxide concentration is low. It can
also be dominant even when cigarette use and outdoor concentration are
high when the indoor combustion source is large (as in the case of
unvented space-heaters) or when combustion efficiency is poor because
of poor burner maintenance or blockage of the air supply. A summary of
measurements of indoor carbon monoxide concentrations is provided in
Chapter IV.
NITROGEN OXIDES
Inaoor combustion can have an important effect on the indoor
concentrations of nitric oxide and nitrogen dioxide. Nitric oxide
binds to hemoglooin to produce methemoglobin-. Many of the adverse
effects reported in the past for carbon nonoxide alor.e may be related
to the combined action of CCHb and methemoglobin, especially inasmuch
VI1-52
-------
TABLE VII-5
Controlled Exposure to Carbon Monoxide
Species
Hunan (normal)^
Human (n ¦ 18)^8
Human
29
Hums:; (n
Hunan (n
19)
37
20)
43
Huaan
44
Pigeon (norraocholes-
terolenic and hyper-
cholesterolemia)
Rabbit (hypercholes-
ternlemic)
Dog (myocardial
Injury)
Dog (anesthetized,
norm^}., open-chested)
Monkey*"'
Rabbit40
Rat (n - fl-16)
Rat (n ¦ 4)'
Rat (exposed pre-
natally)
Exposure
Health Effects Observed
100 ppn, 1 h
200 ppm, 3 h
15-20
13-18 ppm, 30 d
10 mg/rn^, 9 ppm,
90 d
50 ppm, 4 h
150 ppm, 3.5 h
3.2-4.7X COHb
82 COHb
4.92Z COHb
150 ppm, 52 and
84 wk
250 ppm, 10 wk
100 ppm, 2 h
100 ppm, 2 h
100 ppm, 6 h,
9.32 (ave.)
COHb
180 ppm, 4 h
Mean exercise time until exhaustion
significantly decreased
No significant effect on scotoplc
sensitivity, reaction tine, eye
movements, visually evoked
cortical potentials
Increased albumin, 3-glotaiins,
total lipids, cholesterol,
6-lipoproteins; decreased blood
sugar
None
No significant changes in lung
function
No effect on critical flicker-
fusion frequency; in monotonous
situation, relative ."activation"
of subjective feelings
Increased errors in auditory dis-
crimination Jn open oifieea
Less difficult task: no signifi-
cant effects in isolation booth®
Less difficult task: no signifi-
cant effects3
In hypercholesterolemic birds,
atherosclerosis more severe
Coronary arterial atherosclerosis
significantly higher
Decreased ventlcular fibrillation
threshold
Decreased ventlcular fibrillation
threshold
Ventricular fibrillation nore
easily induced
Focal lntlmal edema in aorta
100 ppm, 200 ppm. Changes in blood glucose and lactic
500 ppm; 4 h
100-1,000 ppm,
1.5 h
150 ppm, contig-
uous , 153 COHb
acid; no significant plasma
cortlcosterone increase
Lever-pressing response rate
decreased at increasing concentra-
tion.
Reduced .irthwelght, decreased weight
gain, 1 -wer behavlorai activity,
altered central catecholamine
activity, less tocal brain protein
at birth
"Environment and task difficulty aay alteT effects.
^Response decrease inconsistent at lower concentrations.
VII-53
-------
aa sources that emit carbon monoxide o£ten produce nitric oxide as
well. I£ present data are indicative* nitric oxide at 3 ppo (3.75
mg/a?) is physiologically comparable with carbon monoxide at 10-15
ppm (11-17 ng/m3).* Thus, NOjj may increase cardiovascular stress
due to hypoxia, although the NC^ does not shift the oxygen binding
equilibrium Cor hemoglobin, and the effects of N0X are not
quantitatively identical. The work of Case et al_. * has suggested,
that N0^ generated by household combustion appliances accounts for a
substantial fraction of the total methemoglobin present in the blood of
most humans. N0X concentrations i fficient to generate 2% cr more
methemoglobin may be encountered often in the home (and in roadway
tunnels). l*
Nitrogen oxides may change heme by producing polycythemia with
increased hematocrit and with decreased mean corpuscular volume. They
may also produce leukocytosis and other hematologic abnormalities, as
well as vascular membrane injury and leakage that lead to edema.**
Nitrogen dioxide exposure affects the activity of several enzymes: it
decreases erythrocyte memorane acetylcholinesterase, increases
peroxidized erythrocyte lipids, &nd increases glucose-6-phosphate
dehydrogenase. It also produces substantial decreases in hemoglobin
and hematocrit values."
Both nitric oxide and nitrogen dioxide are formed from atmospheric
nitrogen and oxygen in the high-temperature part of a flame by the
temperature-dependent process of nitrogen fixation. Acute toxicity is
not to be expected from the nitrogen dioxide formed in unvented indoor
combustion, because not enough nitrogen dioxide is generated. But
nitrogen dioxide concentrations equal to or greater than the current
ambient-air quality standard of 0.05 ppa are not unusual in kitchens
where gas is used for cooking (see Chapter IV). At those
concentrations, nitrogen dioxide may affect senuory perception,
especially dark adaptation,'* and produce eye irritation, especially
with hydrocarbons.1'
Nitrooen dioxide can produce transient and long-term damage to both
small bronchial airways and alveolar tissue. In the bronchial airways,
exposure of rats to nitrogen dioxide at as low as 2 ppm for 4 h
stimulated the differehtation of nonciliated cells into mature Clara
cells and ciliated cells;1* that effect raises the possibility that
chronic exposure' could lead to chronic bronchitis. The nitrogen
dioxide also destroyed Type I epithelial cells and stimulated the
proliferation of Type II cells. Thus, chronic exposure might
contribute to the development of emphysema. In addition, in animals
challenged with bacterial aerosols after exposure to nitrogen dixoide
at 1.5 ppm for 2 h or at 0.5 ppm for ,2 wk, there was significantly
increased mortality, compared with that in animals challenged with the
same bacterial aerosols without nitrogen dioxide.1*
Further information on the acute and chronic toxicity of nitric
oxide and nitrogen dioxide can be found in the 1977 NRC report on the
nitrsgen oxides'* and in the 1981 EPA criteria document on NOjj.**
Tables VII-6 and VII-7, from the NRC report, summarized observed
effects of short-term exposures of humans to nitrogen dioxide at high
and low concentrations. Table. VXI-8 summarizes some of the more recent
experimental exposure studies.
VII-54
-------
TABLE VI1-6
Human Effects of Acute Exposure to High Nitrogen Dioxide Concentrations3
Nitrogen
Dioxide
Concentration
tag/mJ
PP°i
Clinical Effect
940
500
Acute pulmonary edema—fatal
564
300
Bronchopneuaonia—fatal
282
150
Bronchiolitis fibrosa obliterans—
fatal
94
50
Bronchiolitis, focal pnr.uoonltls—
recovery
47
25
Bronchitis, bronchopneumonia—
recovery
aReprlnted frc® National Research Council.269)
Tine between Exposure
and Termination of Effect
Within 48 h
2-10 d
3-5 vk
6-8 vk
6-8 vk
VI1-55
-------
TABLE VI1-7
Summary of Human Responses to Short-Term Nitrogen Dioxide
Exposures Alone*
Nitrogen Dioxide
Concentration
Effect
mg/m
ppm
Time to Effect
Odor threshold
0.23
0.12
Immediate
Thfeshold for dark adapta-
0.14
0.075
Not reported
tion
0.50
0.26
Not reported
Increased airway
1.3-3.8
0.7-2.0
20 min^
resistance
3.0-3.8
1.6-2.0
15 min
2.8
1.5
45 nin^
3.8
2.0
45 min
5.6
3.0
45 rain®
7.5-9.4
4.0-5.0
40 min
9.A
5.0 '
15 min
11.3-75.2
6.0-40.0
5 min
13.2-Jl.8
7.0-17.0
10 .tnin®
Decreased puloonary
7.5-9.4
4.0-5.0
15 min
diffusing capacity
Increased alveolar-
9.4
5.0
25 minh
arterial p02
difference
No change In sputum
0.9-61.6
0.5-3.0
45 min
histanine concentration
Reprinted from National Research Council. ^
^Exposure lasted 10 min. Effect on flow resistance was observed 10 min after
termination of exposure.
cEffect was produced at this concentration when normal subjects and those
with chronic respiratory disease exercised during exposure.
"^Effect occurred at rest in subjects with chronic respiratory disease.
eEffect occurred at rest in normal subjects.
^Exposure lasted 10 min- Maximal effect on flow resistance was observed
30 min later.
®Also failed to find Increased flow, resistance over the range of nitrogen
dioxide exposures from 5.1 to 30.1 mg/ra (2.7-16.0 ppo).
^Effect occurred 10 min after termination of 15-min exposure.
VII-5 6
-------
TABLE VI1-8
Controlled Exposure to Nitrogen Oxides
Species
Exposure
Health Effects Observed
Mouse (6-8 wit JJC
Mouse
27
Guinea pig
25
1C Ppffly
2 h/d, 5 d/wk,
up to 30 wk
NO', 10 ppm
NOj, 0.5-28 ppm,
6 mo to 1 yr
NOx, 1 ppm, 6 mo
Human (asthma, n » 13: N0o, 0.5 ppm, 2 h
bronchitis, n - 7>" *
Lung damage, suppressed immune function
with chronic exposure, enhanced imau'ne
reactivity with shorter exposures
Paraseptal emphysema, suppressed immune
function with chronic exposure,
enhanced immune reactivity with shorter
exposures
Mortality atter Streptococcus pyogenes,
mortality increased with increasing
dose and exposure time
Disturbed glycolysis, enhanced catabolic
processes in brain, Inhibited respira-
tion, decreased brain aminotransferase
activity, morphologic alterations in
blood vessels
Lightness in chest, burning of eyes,
headache, or dyspnea; pulmonary-
function changes; nasal discharge
Human (asthus
n - 20)
Cat
26
Guinea pig
41
Mouse
Mouse
12
38
Hamster
24
NO2, 0.1-0.2 ppm Increased bronchoconstriction8
NO2, 80 ppm, 3 h Diffuse alveolar damage
NO2, 0.506 ppm;
NO, 0.05 ppm;
122 d
N07, 1.5-5.0 ppo,
3 h
NO-}, 0.5 ppm; .10,
12, 14 d
NO2, 30 ppm, 3 wk
In lungs: decreased phosphatidyl-
ethanolamine, sphlx -omyelin, phosphati-
dylserine, phosphatidic acid,
phosphatidylglycerol S-phosphate;
Increased lysophosphatidylethanolamine
Mortality in nice challenged with
Streptococcus aerosol significantly
increased at 2.0 ppm and above
Average protein content of lungs
significantly higher
Loss of body weight, increased dry lung
weight, decrease in lung elastln and
collagen
lCarbachol provocation.
Elastln and collagen later returned to normal.
VII-57
-------
The evidence of health effects after prolonged exposure at low
concentrations is inconsistent. This should not be surprising, in that
much of the evidence was obtained from epidemiologic studies in which
the observed effects coul
-------
longitudinal study of schoolchildren in England and Scotland, 4,827
boys and g.'rls aged 5-10 yr in 27 randomly selected areas were examined
in 1977, the last year of the study. The authors .eported that
prevalence of one or more respiratory symptoms or diseases was higher
in children from gas-cooking homes than in those from electric-cooking
homes and that the association appeared to be independent of age, sex,
social class, number of cigarette-smokers in the home, and latitude.
However, it was found only in urban areas (for boys, £ < 0.005; for
girls, £ » 0.08}. In children aged 6-7.5 yr in 1973 who were
followed until the last year of the study, there was some indication
that the association between respiratory illness and gas cooking
disappeared as the children grew older; this trend was not obvious in
the children in the other age groups, who were follwed for 2-4 yr. The
evidence from the 1977 study did show a relationship between gas
cooking and respiratory illness that supported results of the ,1973.
stuay in the same group, although the results on cohorts showed some
indication that the relationship may disappear as children grow older.
Florey et al. 11 examined the relation between lung function and
respiratory illness in a population of 808 primary-school children aged
6-7 yr and the concentrations of nitrogen dioxide in the kitchens and
bedrooms of their home?. Complete data were collected on about 66% of
the population. The children lived in a defined 4-km2 area in
Middlesborough (United Kingdom). One-week average outdoor nitrogen
dioxide concentrations varied little over the area: 25-43 pg/m3
(14-24 ppb). The prevalence of respiratory illness was higher in
children from gas-cooking than from electric-cooking homes (£ a 0.1).
Although prevalence was not related to kitchen nitrogen dioxide
concentration (9-570 yg/m^), it increased with increasing nitrogen
dioxide in the children's bedrooms in gas-cooking homes (4-169 ppb;
p > 0.1). Lung function was not related to nitrogen dioxide content
in the kitchen or bedroom. Because of the very low nitrogen dioxide
concentrations at which an association with illness was observed and
the inconsistency between these results in the united Kingdom and those
from several studies in the United States, the authors speculated that
the nitrogen dioxide concentrations were a proxy for some other factor
more directly related to respiratory disease, such as temperature or
humidity.
A similar study by Keller et al.,L in Columbus, Ohio, failed to
establish any increase in respiratory disease or decrease in pulmonary
function (SVC and FEVg^s) associated with the use of gas for
cooking. Their sample included 441 families, divided into two groups:
those using gas and those using electricity in cooking. Family health
and demographic data were obtained from the participants. Reports of
acute respiratory illness were obtained through biweekly telephone
calls to each household. Respondents were asked to report respiratory
illness in any member of the household and to indicate the presence or
absence of a set of signs and symptoms. Ambient air was analyzed
indoors and outdoors in a sample of the households, and pulmonary-
function tests were conducted on a subsample of the participants
representing both types of households. The mean nitrogen dioxide
concentrations were 0.05 ppm (90 ug/m3) in the gas-cooking homes
VII-59
-------
and 0.03 ppm (50 pg/m^) in the electric-cooking hones. Xn an
extension of this stud/, Keller et_ al_.11 selected 120 households with
school-age children from the gas-cooking and electric-cooking cohorts.
Reports of respiratory illness and symptoms were obtained by telephone
interview every 2 wk for 13 mo by a nurse-epidemiologist. If the onset
of respiratory illness occurred within 3 d of the call, a household
visit was arranged to examine the person reported ill and to obtain a
throat culture. In addition, two sets of "well" controls were
examined. The results va?.idated the reporting method and replicated
earlier findings of no significant difference in incidence of acute
respiratory illness betwesn gas- and electric-cooking households.
The largest and most recently reported study of the effects of gas
cooking on the health of children is that of Speizer et al." As
part of a long-range prospective study of the health effects of air
pollution, they studied approximately 8,000 children aged C-10 yr in
six communities. Questionnaires were completed by their parents, and
simple spirometry was performed in school. Comparisons were made
between children living in homes with gas stoves and those living in
homes with electric stoves. Children from households with gas stoves
had a greater history of respiratory illness before age 2 (average
difference, 32.5/1,000 children) and small but significantly lower FEV
and FVC values corrected for height (average difference, 16 ml and 18
ml, respectively). These findings were not explained by differences in
social class or in parental smoking, habits. Measurements taken in the
homes for 24-h periods showed that nitrogen dioxide concentrations were
4-7 times higher in homes with gas stoves than in homes with electric
stoves. However, these 24-h measurements were generally well below the
current federal 24-h outdoor standard of 100 ug/m3. Short-term
peak exposures, which were in excess of 1,100 ng/m3, occurred
regularly in kitchens. Further work will be required to determine the
role of these short-term peaks in the effects noted.
REFERENCES
1. American Industrial Hygiene Association. Hygienic guide series.
Carbon monoxide. Am. Ind. Hyg. Assoc. J. 26:431-434, 1965.
2. Armitage, A. K., R. F. Davies, and D. M. Turner. The effects of
carbon monoxide on the development of atherosclerosis in the White
Carneau pigeon. Atherosclerosis 23:333-344, 1976.
3. Aronow, H. S., and J. Cassidy. Effect of carbon monoxide on maximal
treadmill exercise: A study in normal persons. Ann. Intern. Med.
83:496-499, 1975.
4. Aronow, H. S.r E. A. Stemmer, B. Wood, S. Zweig, K. Tsao, and L.
Raggio. Carbon monoxide and ventricular fibrillation threshold in
dogs with acute myocardial injury. Am. Heart J. 95:754-756. 1978.
5. Aronow, W. S., E. A. Stemmer, and S. Zweig. Carbon monoxide and
ventricular fibrillation threshold in normal dogs. Arch. Environ.
Health 34:184-186, 1979.
VII-60
-------
6. Atland, P. D., and B. A. Rat trier. Effects of nicotine and carbon
monoxide on tissue and systemic changes in rats. Environ. Res.
19:202-212, 1979.
7. Ator, N. A., W. H. Merigan, Jr., and R. W. Mclntire. The effects of
brief exposures to carbon monoxide on temporally differentiated
responding. Environ. Res. 12:81-91, 1976.
8. Case, G. D., J. s. Dixon, and J. C. Schooley. Interactions of blood
metalloproteins with nitrogen oxides and oxidant air pollutions.
Environ. Res. 20:43-65, 1979.
9. Case, G. D., J. C. Schooley, and 5. D. Jonathan. Uptake and
Metabolism of Nitrogen Oxides in Blood. Papsr presented at the 20th
Annual Meeting of the Biophysical Society, Seattle( Washington,
February 24-27, 1976.
10. Davies, R, P., D. L. Topping, and D. M. Turner. The effect of
intermittent carbon monoxide exposure on experimental
atherosclerosis in the rabbit. Atherosclerosis 24:527-536, 1976.
11. DeBias, D. A., C. M. Banerjee, N. C. Birkhead, C. H. Greene, S. D.
Scott, and w. V. Harrer. Effects of carbon monoxide inhalation on
ventricular fibrillation. Arch. Environ. Health 31:42-46, 1976.
12. Ehrlich, R., J. C. Findlay, J. D. Fenters, and 0. E. Gardner.
Health effects of short-term inhalation of nitrogen dioxide and
ozone mixtures. Environ. Res. 14:223-231, 1977.
13. Evans, M. J., and G. Freeman. Morphological and pathological
effects of NO2 on the rat lung, pp. 243-265. Iii S.D. Lee, Ed.,
Nitrogen Oxides and Their Effects on Health. Ann Arbor, Mich.: Ann
Arbor Science Publishers, Inc., 1980.
14. Fechter, L. 0., and Z. Annau. Toxicity of mild prenatal carbon
monoxide exposure. Science 197:680-682, 1977.
15. Florey, C. du V., R. J. W. Melia, S. Chinn, B. D. Goldstein, A. G.
F. Brook?, H. H. John, I. B. Craighead, and X. Webster. The
relation between respiratory illness in primary schoolchildren ana
the use of gas for cooking. III. Nitrogen dioxide, respiratory
illness and lung infection. Int. J. Epidemiol. 8:347-353, 1979.
16. Gardner, D. E., F. J. Miller, E. J. Blommer, and D. L. Coffin.
Influence of exposure mode orr the toxicity of NOj. Environ.
Bealth Perspect. 30:23-29, 1979.
17. Goldsmith, J. R. and L. T. Friberg. Effects of air pollution on
human health, pp. 458-611. In A. C. Stern, Ed. Air Pollution. 3rd.
ed. Vol. II. The Effects of Air Pollution. New York: Academic
Press, Inc.. 1977.
18. Hollowell, C. D., R. J. Budnitz, C. D. Case, and G. Traynor.
Combustion Generated Indoor Air Pollution: Field Studies
8/7i-10/75. Lawrence Berkeley Laboratory Publ. LBL-4416. Berkeley,
Cai.: Lawrence Berkeley Laboratory, 1976.
19. Holt, P. G., L. M. Finlay-Jones, D. Keast, and J. Papadimitrou.
Immunological function in mice chronically exposed to nitrogen
oxides (NOjj). Environ. Res. 19:154-162, 1979.
20. Hugod, c., L. H. Hawkins, and P. Astrup. Exposure of passive
smokers to tobacco smoke constituents. Int. Arch. Occup. Environ.
Health 42:21-29, 1978.
VII-61
-------
21. Keller, M. D., R. R. Lanese, R. I. Mitchell, and R. W. Cote.
Respiratory illness in households using gas and electricity £or
cooking. I. Survey of incidence. Environ. Res. 19:495-503, 1979.
22. Keller, M. D., R. R. Lanese, R. I. Mitchell, and R. W. Cote.
Respiratory illness in households using gas and electricity for
cooking. II. Symptoms and objective findings. Environ. Res.
19:504-515, 1979.
23. Kerr, H. D., T. J. Kulle, M. L. Mcllhany, and P. Swidersky. Effects
of nitrogen dioxide on pulmonary function in human subjects: An
environmental chamber study. Environ. Res. 19:392-404, 1979.
24. Kleinerman, J., and M. P. C. Ip. Effects of nitrogen dioxide on
elastin and collagen contents of lung. Arch. Environ. Health
34:228-232, 1979.
25. Ko^mid
-------
36. Posin, C., K. Clark, M. P. Jones, J. V. Patterson, R. D. Buckley,
and J. D. Hackney. Nitrogen dioxide inhalation and human blood
biochemistry. Arch. Environ. Health 12:318-324, 1978.
37. Raven, P. B., J. A. Gliner, and J. C. Sutton. Dynamic lung function
changes following long-term work in polluted environments. Environ.
Res. 12:18-25, 1976.
38. Sherwin, R. P., and L. J. Layfield. Protein leakage in the lungs of
mice exposed to 0.5 ppm nitrogen dioxide. A fluorescence assay for
protein. Arch. Environ. Health 31:116-118, 1976.
39. Speizer, F. E., B. Ferris, Jr., Y» M. M. Bishop, and J. Spengler.
Respiratory disease rates and puljnonary function in children
associated with NO2 exposure. Am. Rev. Respir. Dis. 121:3-10,
1980.
40. Thomsen, H. K., and K. Kjeldsen. Aortic intimal injury in rabbits:
An evaluation of a threshold limit. Arch. Environ. Health
30:604-607, 1975.
41. Trzeciak, H. I., S. Kosmider, K. Kryk, and A. Kryk. The effects of
nitrogen oxides and' their neutralization products with ammonia on
the lung phospholipids of guinea pigs. Environ. Res. 14:87-91, 1977.
42. U.S. Environmental Protection Agency. Air Quality Criteria for
Oxides of Nitrogen. Research Triangle Park, N.C.: U.S.
Environmental Protection Agency, Environmental Criteria and
Assessment Office, 1981. (in press)
43. Weber, A., C. Jermini, and E. Grandjean. Effects of low carbon
monoxide concentrations on flicker fusion frequency and on
subjective feelings. Int. Arch. Occup. Environ. Health 36:87-103,
1975. (in German; English summary)
44. Wright, G-. R., and R. J. Shephard. Carbon monoxide exposure and
auditory duration discrimination. Arch. Environ. Health 33:226-235,
1978.
INVOLUNTARY SMOKING
The combustion of tobacco products is responsible for only a small
fraction of the total atmospheric pollution,1" and it is only in the
enclosed indoor environment that smoking produces a major fraction of
the airborne environmental contamination. The potential health effects
of this contamination have recently becc.ne a subject of considerable
concern and controversy.*" tJ(PP-H~l 11-41) health
effects of smoking on smokers have been extensively studied." But
the health effects on nonsmokers have received far less study, and this
section documents what is known about these effects.
The exposure of nonsmokers to environmental contamination by the
combustion products of tobacco has been referred to as "passive
smoking," "second-hand smoking," and "involuntary smoking." We use the
term "involuntary smoking" for this kind of exposure; it provides
exposure to many of the same constituents of tobacco smoke that
voluntary smokers experience, and it is involuntary, in that the
exposure occurs as an unavoidable consequence of breathing in a
smoke-filled room.
VII-63
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The chemical constituents found in the atmosphere due to tobacco
smoke are derived from two sources—mainstream and sidestream siooke.
Mainstream smoke emerges from the tobacco product after being drawn
through the tobacco during puffing. Sidestreara smoke rises from the
burning cone of tob^co. For several reasons, mainstream smoke and
sidestream smoke conv.ti.bJte different concentrations of many substances
to the atmosphere: different amounts of tobacco are consumed in thi
production of mainstream and sidestream smoke; the temperature of
combustion for tobacco is different during puffing and during
smoldering; and some substances are partially absorbed from the
mainstream smoke by passage through the cigarette and the lungs of the
smoker. The amount of a substance absorbed by the smoker depends on
the characteristics of the substance and the depth of inhalation by the
smoker. When the smoker does not inhale the smoke into his or her
lungsi the smoke exhaled contains less than half its original amount of
water-soluble volatile compounds, four-fifths of the original
non-water-soluble compounds and particulate matter, and almost all the
carbon monoxide.11 When the smoker does inhale the mainstream smoke,
that exhaled into the atmosphere contains leas than one-seventh of the
original amount of volatile and particulate substances and less than
half the original concentration of exhaled carbon monoxide.11 The
differential impact of these factors on the extent of contamination is
discuissed elsewhere in this report.
The differences in chemical composition between sidestreara and
mainstream smoke and the differences between the low-dose, continuous
exposure of the involuntary smoker and the high-dose, intermittent
exposure of the voluntary smoker make the comparison of dosage in terras
of "cigarette equivalents" highly speculative. The qualitative and
quantitative differences between the two kinds of exposures prevent the
extrapolation of the well-established health effects of
cigarette-smoking to the involuntary smoker. We therefore try to
identify health effects on the basis of actual exposures, rather than
on the basis of effects on smokers«,
ABSORPTION OF SMOKE CONSTITUENTS
There are no direct measurements of absorption of most of the
constituents of tobacco smoke. However, Hugod et al_. ' * found that
the concentrations of carbon monoxide, nitric oxide, acrolein, hydrogen
cyanide, and nitrogen dioxide in a sealed chamber decreased when
nonsmokers were present, but rot when the chamber was empty; hence,
either absorption by the nonsmokers or adsorption onto their clothing
occurs. A number of studies that have examined carbon monoxide
absorption are summarized in Table VII-9. Carbon monoxide is often
used as a measure of tobacco-smoke pollution and absorption, because it
is readily measured and has been implicated in the pathogenesis of
atherosclerosis. But there are several problems in the use of carbon
monoxide as a measure of total smoke exposure. Sraoking is oftly one
source of carbon monoxide in the environment and great care must be
taken to establish that the carbon monoxide measured is indeed from
vir-64
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TABLE VII-9
Absorption of Smoke Constituents from Environmental Exposure
Location and
Dimensions
t ?
Room (80 ra~)
Isolated
community
18
I'ospital out-
patient
18
department
Office build-
ing"
Room (170 ra3)2A
Room (68.1 m3)28
Chamber „
(14.6 m3)38
Amount of
Ventilation® Tobacco Burned
6.4 ach
Room (30.8 m3)3 11.4 ach
None
None
1.2 ach
2.3 ach
one
None
3 pipefuls
15 cigarettes in
2 h
15 cigarettes in
2 h
Smoking
permitted
Smoking
permitted
105 cigarettes
107 cigarettes
101 cigarettes
20 cigarettes by
machine; addi-
tional smoke
added to keep
smoke constant
for 3 h
4 cigarettes ini-
tially + 1 cig-
arette per 30
min by machine
Concentrations
of
Constituents
46 cigarettes and CO, 4.5 ppra;
nicotine, 377
ng/ m
CO, 1 ppm
CO, 2-4 ppm
CO, 3-8 ppm
CO, 30 ppm
CO, 5 pptn
CO, 75 ppm
CO, 18-26 ppm
CO, 24 ppm
Measure of
Absorption
No change in
COHb, 0.6%
Nonsmokers:
COHb, 1.25-
1.77%
Nonsmokers:
COHb, 1.30-
2.28%
Nonsmokers:
COHb, 0.68%
Nonsmokers:
COHb, 0.97%
Nonsmokers:
COHb, 1.12%
Smokers:
COHb, 7.5%
Nonsmokers:
COHb, 2.1%
Smokers:
COHb, 5.8%
Nonsmokers:
COHb, 1.3%
Smokers:
COHb, 5.0%
Nonsmokers:
COHb, 1.6%
Nonsmokers:
COHb, 0.73-
1.63%
Nonsmokers:
COHb, 0.75-
1%
V2I-65
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TABLE VH-9 (continued)
Concentrations
Location and Amount of of
Dimensions Ventilation* Tobacco Burned Constituents
Room (43 m3)"'*5 None 80 cigarettes and CO, 38 ppm
2 cigars per hour
Restaurants
and offices
51
Room (37.5 m3)^® None
8-h workshlft
126 cigarettes
by smokers in
0.2 h
CO, 2.5-15 ppm
CO, 30 ppm
Car, engine None
off (2.09 m )
10 cigarettes
in 1 h
CO, 90 ppm
Office build-
ing56
CO, 2.7 ppm
ach = air changes per hour.
Measure of
Absorption
Smokers:
COHb, 9.62;
urinary
nicotine,
1,236 ng/ml
Nonsmokers:
COHb, 2.62;
•jrlnary
nicotine,
£.0 ng/ml
No change in
COHb, 2.12
Smokers:
COHb, 9.12
Nonsmokers:
COHb, 2.22
Smokers:
COHb, 10%
Nonsmokers:
COHb, 52
Nonsmokers:
COHb. 0.63-
0. 'j22
VII-66
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cigarette smoke. Carbon monoxide ia part of the gas phase o£ smoke and
so does not settle out of the atmosphere passively/ but is quite avidly
absorbed from the atmosphere by breathing. As a result, the time
course of carbon monoxide concentration differs from that of the
particulate phase of the smoke, and the impact on carbon monoxide of
filtration, ventilation# and number of persons in the room is also
different from the impact on particulate constituents.
Because carbon monoxide is bound to hemoglobin with 210 times the
affinity of oxygen, very low concentrations of carbon monoxide in the
air can result in substantial carboxyhemoglobin (COHb) concentrations
in the blood. A small amount of carbon monoxide 1b produced by the
body, resulting in COHb content of approximately 0.7%. COHb values are
about the same in rural communities'* and increase to about 2.5-3*
when there is marked smoke pollution. Two studies examined carbon
monoxide absorption by nonsmoking workers under conditions where
smoking was allowed as part of the normal work environment. Szadkowski
et al.s* found very low concentrations of carbon monoxide in an
office setting and no change in COHb. Sepp&nen and uusitalo*1 found
higher carbon monoxide content in restaurants and offices (2.5-15 ppm)
and still no change in COHb, but the workers began the day with COHb
concentrations (2.1%) comparable with those that would be expected from
such atmospheric carbon monoxide content and therefore would not be
expected to change. A number of studies have documented increases in
COHb secondary to smoke exposure under experimental conditions (see
Table VII-9), and the greatest extent of smoke pollution that would
normally be tolerated produces COHb of approximately 2.5-3% after
1-2 h. Srch5* found COHb of 5% in nonsmokers, but there was more
smoke than would be tolerated under normal conditions.
Russell et al.* * " also measured nicotine excreted by nonsmokers
and found that they absorb measurable amounts of nicotine from the
environment, but only 6.5% of that absorbed by r-iol.ers.
Repace and Lowrey"2 estimated the exposure o£ nonsmokers to
respirable suspended particles from cigarette ...^e. They predicted
that a nonsmoker working in an office wh*»re s ;*ing was allowed would
inhale particles at a rate 3 times greater tnan without t.iis exposure.
In summary, the literature sugge3ts that nonsmokers would be
expected to have slight increases in their COHb content (1-2%) from
cigarette smoke in the normal' working environment ar.d more (2-3%) under
conditions of heavy smoke pollution. Nonsmokers also absorb nicotine
and an unknown quantity of other smoke constituents.
EFFECTS ON HEALTHY PERSONS
The effect of involuntary smoking on a person is determined not
only by the qualitative and quantitative aspects of the smoke-filled
environment, but also by the characteristics of the person. Reactions
may vary with age and with the sensitivity of a person to the
components of tobacco smoke.
VII-67
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Annoyance
In 1975, a national probability sample of U.S. telephone
households" was asked to agree or disagree with the statement, "It
is annoying to be near a person who is smoking cigarettes." Among
"never smokers," 77% of the males and 80.5% of the females agreed with
the statement; among current smokers, 35% of the males and 34.5% of the
females also agreed with the statement.
Several federal agencies'1 cooperated to survey the symptoms
experienced by travelers on military and commercial aircraft. They
distributed a questionnaire to passengers on 20 military and eight
commercial flights; 57% of the passengers on the military flights and
45% of the passengers on the commercial flights were smokers. The
planes were well ventilated, and carbon monoxide content was always
below 5 ppm, with low concentrations of. other pollutants as well. In
spite of the low measurable pollution, over 60% of the nonsmoking
passengers and 15-22% of the smokers reported being annoyed by the
other passengers' smoking. These feelings were even more prevalent
among nonsmokers who had a history of respiratory disease.
Seventy-three percent of the nonsmoking passengers on the commercial
flights and 62% of the nonsmoking passengers on the military flights
suggested that some remedial action be taken; 84% of those who
suggested remedial action felt that segregating the smokers from
nonsmokers would be a satisfactory solution. Such segregation is now
required on commercial aircraft.
The annoyance reaction may be due to the odor, probably
attributable to both the particulate and vapor phases; the odor
threshold appears to be low." *7
Irritation
Many of the substances in cigarette smoke are irritating; the major
sites of irritation are the eyes and nasopharynx. Speer51 assessed
the nature of this irritation by interviewing 250 nonallergic patients
about their reaction to cigarette smoke; 69.2% reported eye irritation,
31.6% headache, 29.2% nasal symptoms, and 25.2% cough. Barad"
surveyed 21,366 employees of the Social Security Administration and
found that nonsmoking workers reported high prevalences of conjunctival
irritation (47.7%), nasal discomfort (34.7%), and cough, sore throat,
or sneezing (30.3%) when exposed to cigarette smoke.
Weber et al." ,e exposed subjects to various concentrations of
cigarette smoke in a sealed chamber and noted that the eyes were most
sensitive to the irritants in the smoke, followed by the nose.
Self-reported eye irritation was closely related to such objective
signs as tear flow and eye closing or rubbing. Annoyance was the same
for pollution caused by whole smoke and by only the gas phase; that
indicates that it is the gas phase that is annoying. But whole smoke
produced considerably more irritation as expressed by eye and nose
symptoms, and that indicates that the particulate phase is responsible
for irritation. Hugod e_t al. " confirmed that the eyes are the most
VII-68
-------
sensitive site and found that acrolein at the concentrations found in
smoke-filled environments did not cause significant irritation, fcrtho
and Koch* have reported 11 unpleasant-smelling constituents in the
volatile phase and 50 in the semivolatile phase of cigarette smoke.
The eye and nose irritation experienced by nonsmokers in a
smoke-filled environment is influenced by the humidity of the air, as
well as by the concentration of irritating substances. Johansson"
and Johansson and Ronge" have shown that eye and nose irritation due
to cigarette smoke is maximal in warm, dry air and decreases with a
small rise in relative humidity.
Physiologic Responses to Smoke
At Rest, Harke and Bleichert15 studied 18 adults (11 smokers and
seven nonsmokers) in a 170-m^ room in which ISO cigarettes were
smoked or allowed to burn in ashtrays for 30 min. They noted that the
subjects who smoked during the experiment had a significant lowering of
skin temperature and a rise in blood pressure. Nonsmokers who were
exposed to the same smoke-contaminated environment showed no change in
either of these measures. Luquette et al.J* performed a similar
experiment with 40 children exposed alternately to smoke-contaminated
and clean atmospheres, but otherwise under identical experimental
conditions. Exposure to the smoke was associated with increases in
heart rate (5 beats/min) and in systolic and diastolic blood pressure
(4 and 5 mm Hg, respectively). The differences in results between
these studies may be due, in part, to the age of the subjects:
children may be more sensitive to the cardiovascular effects of
involuntary smoking than adults. Or the increases in heart rate and
blood pressure may be due to a difference between children and adults
in the psychologic response to being in a smoke-filled atmosphere.
Pimm et al. " found a slight decline in heart rate in control
subjects of both sexes (thought to be secondary to prolonged
inactivity) and a similar decline in heart rate in males exposed to
cigarette smoke. However, women exposed to smoke had a small but
significant increase in resting heart rate. The authors suggested t-.hat
this may be due to a difference in psychologic, rather than
physiologic, response in the women.
Rummel et al."' examined this question with a group of 56
students exposed tc cigarette smoke. There was a slight increase in
the entire group in systolic blood pressure on exposure to smoke. When
the group was divided into those who were indifferent to cigarette
smoke and those who expressed a dislike for it, both groups again had a
rise in systolic blood pressure on exposure to smoke, but the "dislike"
group also had a significantly higher heart rate at the start and
during the entire course of the study; that suggests that psychologic
factors may play a role in the physiologic response to involuntary
sraoking.
Pimm et al. " examined the effect of exposure to machine-produced
smoke on ventilatory function in healthy young adults. There were no
significant changes in the subdivisions of lung volume, maximal
VII-69
-------
expiratory flow volume, or single-breath nitrogen washout after
exposure.
With Exercise. Several authors have found small decrements in
maximal aerobic capacity at COHb contents corresponding to those
associated with involuntary smoking;* '• w for a given degree of
exercise, there are reductions in exercise time to exhaustion and
maximal oxygen consumption, and there is a higher heart rate. These
effects were more pronounced in older than in younger subjects.
Gliner et al.1 * evaluated submaximal exercise and found no change
with COHb at 3-6%. Pimm et_ al,.1 * evaluated young adulcs after
exposure to cigarette smoke for 2 h {COHb, 1?; and found no change with
submaximal exercise. Shephard et al.il studied 23 healthy young
adults after 2 h of passive smoke exposure with intermittent bicycle
ergometer work sufficient to increase respiratory minute volumes by a
factor of 2.5. Carbon monoxide equivalents of 20 ppm and 31 ppra did
not change static lung volumes and produced 3mall changes (3-4%) in
FVC, FEV, Vmax 50%, and vmax 75%, equivalent to cigarette
consumption of less than 0.5 cigarette in 2 h.
Psychomotor Function
There has been some concern over the effects of relatively low
concentrations of carbon monoxide dn psychomotor functions (which
involve perception of and reaction to stimuli), especially those
related to driving an automobile. There is an extensive and'sometimes
contradictory literature on this subject; but it is beyond the scope of
this report, and the reader is referred to several recent
reviews.11 '• 19 Most of the documented effects occur at COHb
concentrations well above those produced by involuntary smoking;
however, slight changes in acoustic and visual vigilance have been
reported at COHb as low as 2%. The impact of these changes on complex
functions such as driving, and their interactions with fatigue and
alcohol have not been evaluated for COHb in the range of 2-3%.
Long-Term Effects
The question of long-term effects on the nonsmoker of exposure to
cigarette smoke has only recently been raised. The difficulty of
measuring the exposure, the complex interaction of cigarette-smoking
with behavioral and socioeconomic factors, and the problem of
con.rolling for past smoking history, air pollution, and industrial
exposure make it very difficult to isolate the effect of cigarette
smoke on the nonsmoker. Recent population studies that accounted for
i'hese confounding factors indicated that passive smoke exposures are
associated with increased incidences of respiratory mechanical function
abnormalities.1' "
White and Froebt# examined the relationship of exposure to
cigarette smoke in the workplace and tests of lung function. They
VII-70
-------
found that nonsmokers who had worked where smoking was allowed had
unadjusted midexpiratory (PEP 25-75%) and end-expiratory (FEF 75-85%)
flow rates lower than those of workers in workplaces where smoking was
restricted, but not significantly when adjusted for sex, age, and
height. They suggested that the differences represent small-airway
dysfunction produced by smoke exposure, and small-airway dysfunction is
thought to be an early precursor of clinically significant chronic
obstructive lung disease. They controlled for occupational and
air-pollution exposure and for smoking in the home. It is difficult to
prove an association from a single study, especially in a subject as
complex as involuntary smoking} however, their data do suggest that
exposure to cigarette smoke may have a deleterious effect on the health
and function of the healthy nonsmoker in the wo: ; environment.
Hirayama,1' in a study of mortality records in 29 health-center
districts in Janan, followed 91,540 nonsmoking wives, aged 40 and
above, for 14 yr (1966-1979) and assessed the standardized mortality
rates for lung cancer according to the smoking habits of their
husbands. Wives of heavy smokers (greater than 20 cigarettes/d) were
found to have a relative risk of developing lung cancer of 2.1, whereas
wives of ex-smokers and of smokers of fewer than 20 cigarettes/d had a
relative risk of 1.6. The relation'between a husband's smoking and a
wife's risk of developing lung cancer showed a similar pattern when
analyzed by age and occupation of the husband. The husband's smoking
habits die! not affect his wife's risk of dying from other diseases,
such as stomach cancer, cervical cancer, and ischemic heart disease.
The risk of developing emphysema and asthma seemed to be higher in
nonsmoking wives of heavy smokers, but the effect was not statistically
significant. The husbands' drinking habits seemed to have no effect on
any cause of death in their wives, including lung cancer.
Trichopoulos et al.*a interviewed 51 women with lung cancer and
163 other hospital patients in Greece regarding their smoking habits
and their husbands' smoking habits. Forty of the lung-cancer patients
and 149 of the other patients were nonsmokers. Among the nonsmoking
women, there was a statistically significant difference between the
cancer patients and the other patients with respect to their husbands'
smoking habits. Estimates of relative risk of lung cancer associated
with having a husband who smokes were 2.4 for smokers of less than one
peck per day and 3.4 for smokers of more than one pack per day.
In two studies indicating a similar effect, it appears that chronic
passive smoking significantly increases the incidence of lung cancer.
EFFECTS ON SPECIAL POPULATIONS
The studies mentioned examined the effects of involuntary smoking
on relatively healthy populations. An exposure that is harmless for
someone who is healthy may have a very different effect on someone with
heart or lung disease or hypersensitivity to substances found in
smoke. Effects may differ in children, owing to their greater
ventilation per unit of body weight. This section reviews the evidence
on the effects of involuntary smoking on each of these special
populations.
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Cardiovascular Disease
Carbon monoxide Impairs oxygen transport in two ways. First, it
competes with oxygen for hemoglobin binding sites. Second, It
increases the affinity of oxygen for the remaining hemoglobin, thereby
requiring a larger gradient in pO^ between the blood and tissue to
deliver a gJven amount of oxygen. Carbon monoxide also binds to other
heme-containing pigments, most notably myoglobin, for which it has an
even greater affinity than for hemoglobin at low p02- The
significance of this binding is unclear, but it may be important in
some tissues (such as heart muscle) that have both high oxygen
requirements and large aiaounts of myoglobin.
In healthy people, the COHb content due to involuntary smoking is
probably functionally insignifleant, with small changes demonstrable
only under extreme exertion. In those with a limited cardiovascular
reserve, however, any reduction in the oxygen-carrying capacity of the
blood may be of greater importance.
Ayres et^al. 11 '» exposed a group of patients to various
concentrations of carbon monoxide (COHb, 9%) and found that they had
lower arterial, mixed venous, and coronary sinus pc>2 and decreased
lactate extraction.
Aronow and isbell® and Anderson et al.1 have shown a decrease
in the mean duration of exercise before onset of pain in patients with
angina pectoris exposed to carbon monoxide at low concentrations (50
and 100 ppm). Carboxyherooglobin was significantly increased (2.9%
after 50 ppm; 4.5% after 1QQ ppm), and the systolic blood pressure,
heart rate, and product of systolic blood pressure and heart rate (a
measLire of cardiac wore) were all significantly lower at the onset of
angina pectoris.
In a continuation of this work, Aronow et al.! 7 studied eight
patients with angiographically demonstrated coronary arterial disease
(>"75* obstruction of at least one coronary artery) during two cardiac
catheterizations. During the first, each patient smoked three
cigarettes; during the second, each patient inhaled carbon monoxide
until the maximal coronary sinus COHb content equaled that produced by
smoking during the first catheterization. Smoking increased the
systolic and diastolic blood pressure, heart rate, left ventricular
end-diastolic pressure {LVEDP}, and coronary sinus, arterial, and
venous COHb; no changes were noted in left ventricular contractility
and venous
p02. When carbon monoxide was inhaled, increased LVEDP and coronary
sinus, arterial, and venous COHb were noted; there were no changes in
systolic and diastolic blood pressure, heart rate, or systolic ejection
period; and there wert; decreases in left ventricular dp/dt, stroke
index, cardiac index, and coronary sinus, arterial, and venous pOj.
These data suggest thet carbon monoxide has a negative ionotropic
effect on myocardial tissue, which results in the decreased dp/dt and
stroke index. When the positive effect of nicotine on contractility
and heart rate is added by smoking, the net effect is increased cardiac
work for the same cardiac output.
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Aronow' also examined the effect of involuntary smoking on
patients with angina pectoris. Ten patients (two smokers and eight
nonsmokers) exercised after a control exposure to uncontaminated air,
after exposure to 15 cigarettes smoked over 2 h in a well-ventilated
30.8-m3 room, and after exposure to 15 cigarettes smoked over 2 h in
an unventilated 30.8-nP room. Carboxyhemoglobin rose ftora 1.25% in
the control situation to 1.77% after exposure in the ventilated room,
and to 2.28% after exposure in the unventilated room. The mean time of
exercise until onset of angina decreased by 22% after exposure in the
ventilated room and by 38% after exposure in the unventilated room.
The patients also had onset of angina at a lower heart rate and
systolic blood pressure, and they had increases in heart rate and
systolic and diastolic blood pressures. Aronow attributed this to the
possible absorption of nicotine (nicotine was not measured). The
relatively low nicotine absorption documented under these conditions
(see the previous section) makes it unlikely that nicotine would be
responsible for these physiologic changes. Another possible
explanation is that anxiety or aggravation associated with being in the
smoke-filled room resulted in a stress response." The combination
of increased blood pressure and pulse at the start of exercise and' the
increase in carboxyhemoglobin resulted in a greater decline in exercise
time until angina for the measured carboxyhemoglobin than had been
shown for carbon monoxide exposure alone.
In summary, there is evidence that increases in carboxyhemoglobin
capable of being produced by involuntary smoking can reduce the
exercise duration required to induce angina in some patients with
coronary arterial disease.
Chronic Obstructive Lung Disease
Patients with chronic lung disease constitute a second group who
are limited in their ability to exercise and who might be particularly
susceptible to involuntary smoking. Aronow et al. had 10 patients
with hypoxic chronic lung disease (pO^ < 70 torr) exercise before
and after a 1-h exposure to carbon monoxide at 100 p?m (COHb increased
from 1.43% to 4.08%). There was a significant reduction in mean
exercise time until marked dyspnea, from 218.5 s to 146.6 s. There was
no difference in exercise mean systolic or diastolic blood pressure,
heart rate, product of systolic blood pressure and heart rate, or
arterial pOj, pCC^, or pH before or after carbon monoxide
exposure. The mechanism for this earlier induction of dyspnea remains
unclear, because decreased oxygen transport to the exercising tissues
should have been reflected in a shift to anaerobic metabolism and the
development of acidosis.
Persons with Allergies
The existence of a true tobacco allergy remains unclear. There is
no proof that specific sensitization to cigarette smoke occurs.59
VII-73
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However, it is cleac that allergic patients are more sensitive to a
variety of environmental irritants, including tobacco smoke.** The
manifestations of this irritation may often mimic the allergic symptoms
experienced by these patients when they come into contact with
well-established allergens. It has also been demonstrated that
cigarette-smoking by parents is a significant exacerbating factor in
childhood asthma."
Infants and Children
Children have a higher incidence of acute respiratory illness than
adults and may be more susceptible to air pollutants than adults, owing
to their greater minute ventilation per unit of body weight. Several
researchers have investigated the effects of parental smoking on the
health of children.
Colley" found a relationship between parental smoking habits and
the prevalence of respiratory illness in children. However, an even
stronger relationship was found between cough and phlegm production in
parents and respiratory infections in children. They postulated that
the latter relationship resulted from the greater infectivity of these
parents due to their cough and phlegm production. The relationship
between parental cigarette-smoking and respiratory infection in their
children would then occur because cigarette-smoking caused the parents
to cough and produce phlegm and would not be indicative of a direct
effect of smoke-filled air on the children. Bland et al. reported
similar relationships.
There have been several other research reports of associations
between passive smoking in the home and symptoms or illnesses in
children.1* ** A telephone survey14 confirmed an earlier
survey,1® in that children and adult nonsmokers subjected to
household tobacco smoke had had a higher prevalence of acute
respiratory illness in the preceding week than children and adult
nonsmokers not so exposed. Reporting biases of the telephone
respondents were not examined or controlled. Said and zalokar**
questioned Parisian high-school students (aged 9-19) about parental
smoking and about their history of adenoidectomies and
tonsillectomies. They found increases in the latter related to amount
of tobacco smoked by either or both parents. This relationship was not
always consistent (e.g., the% of such operations did not increase with
increases in maternal smoking if paternal smoking was high). The
prevalence of appendectomies was related to maternal smoking as well
{and appendectomies were significantly correlated with the other
operations). Social status was not controlled; and the effect of
actual (voluntary) smoking, a critical factor in this age group,11
was not evaluated in this study, thereby limiting its usefulness.
Harlap and Davies34 studied infant admissions to Hadassah
Hospital in West Jerusalem and found a relationship between admissions
for bronchitis and pneumonia in the first year of life and maternal
smoking habits during pregnancy. Data on postnatal maternal smoking
habits were not obtained, but it can be assumed that moat of the
VII-74
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mothers who smoked during pregnancy continued to smoke during the
following year. A relationship between infant admission and maternal
smoking habits was demonstrable only between the sixth and ninth months
of infant life and was more pronounced during the winter months.
Mothers who smoke during pregnancy are known to have Infants with a
lower average birthweight than nonsmoking mothers. The relationship
between maternal smoking and infant admission to the hospital found in
this study was greater for low-birthweight infants, but the same
relationship was found for normal-birthweight infants, Harlap and
Davies'* demonstrated a dose-response relationship between maternal
smoking and infant admission for bronchitis and pneumonia; however,
they also found a relationship between maternal smoking and infant
admission for poisoning and injuries. This may indicate a bi?a in the
study due to relationships that may,exist between smoking and such
factors as parental neglect and socioeconomic class. In addition,
hospital admission rates may not be an accurate index of infant
morbidity.
Colley et al.10 and Leeder et al.V studied the incidence of
pneumonia and bronchitis in 2,205 children over the first 5. yr of life
in relation to the smoking habits of both parents. They found that a
relationship between parental smoking habits and respiratory infection
in children occurred only during the first year of life. They also
showed a relationship between infant infection and parental cough and
phlegm production that was independent of the effect of parental
smoking habits. The relationship between parental smoking and infant
infection was greater when both parents smoked and increased with the
number of cigarettes smoked per day. The relationship persisted when
social class and birthweight were controlled' for.
Rantakallio14 has also found an increased incidence of
pneumonia in children under the age of 5. She studied 12,000 children
born in northern Finland in 1966 and matched smoking mothers with
nonsmoking mothers for various factors, including marital statue,
maternal age, and socioeconomic status. Children of smoking mothers
had significantly higher morbidity {g < 0.001) and were more likely
to be hospitalized (£ < 0.001), and their hospitalizations were
longer. Most of this excess morbidity was due to respiratory illness
and was present in the first 5 yr of life, with the most pronounced
effect occurring in the first year of life.
Cederl&f and Colley" stated that, "when parents' respiratory
sympton3 were taken into account, exposure of the child to cigarette
smoke generated by the parents' smoking had little if any effect upon
the child's respiratory symptoms." Lebowitz and Burrows51 and
Schilling et_aL.*s reported nonsignificant relationships between
parental smoking and children's symptoms when parental symptoms were
taken into account. They concluded that parents had a "bias" toward
reporting symptoms in their children when they themselves had such
symptoms.
Tager et al.57 '* examined the relationship, of parental smoking
habits and expiratory flov rates in children. They found a dose-
dependent decline in the K3F (25-75%) in the children, with a greater
decline occurring if both parents smoked than if one parent smoked, and
VI1-75
-------
with the decline increasing with number of cigarettes smoked. This
effect was Independent of the smoking habits of the children.
Pulmonary infection early in life has been shown to affect pulmonary
function in children and adults adversely, and the decline in flow
rates reported by Tager et al^ may be secondary to the excess risk of
pneumonia in infants whose parents smoke. They attempted to examine
this by retrospectively asking the parents about childhood illness* but
did not show an association between parental smoking and childhood
infection, in contrast with the results of Rantakallio and Harlap. It
is not clear whether this represents a true difference in the
populations.
In a further study of 5- to 9-yr-old children in the same
population, Weiss e£ al_. *7 reported that parental cigarette-smoking
was linearly related to the occurrence of persistent wheeze (£^= 0.012)
and lower degrees of mean forced midexpiratory flow. Current
persistent wheeze occurred in one.of 57 children (1.8%) from households
where both parents had never smoked; in 10 of 146 children (6.8%) with
one parent currently smoking; and in 20 of 169' children (12%) with both
parents currently smoking. When the analysis was repeated with the
exclusion of mothers with wheeze, the results were similar—0, 1.8, and
7.7% wheeze in children with no smoking parents, one smoking parent,
and two smoking parents, respectively. Exclusion of fathers with
wheeze gave 0, 6.7, and 14% wheeze,- respectively;
In summary, children of smoking parents have an increased incidence
of persistent wheeze and may be at excess risk of repiratory infection
at least for the first year of life. They may also have reduced
pulmonary function as adults. The exact interplay among the effects of
maternal smoking during pregnancy, involuntary smoking by children, and
actual occurrence of infection has not been established.
CONCLUSIONS
* Tobacco smoke is a major source of pollution in the indoor
environment.
* The nonsmoker absorbs measurable amounts of carbon monoxide
and nicotine and may absorb small amounts of other constituents, owing
to involuntary smoking.
* The amount of carbon monoxide absorbed owing to exposure to
tobacco smoke in the environment varies from negligible anounts in
well-ventilated office buildings to enough to raise carboxyhemoglobin
contents by 2-3% in a 1- to 2-h exposure.
* The carboxyhemoglobin produced by the most severe involuntary
smoking exposures likely to occur in everyday living can reduce the
maximal exercise capacity in normal, healthy adults, but does not
effect submaximal exercise to any measurable degree.
* Involuntary smoking has not been shown to produce acute change
in lung volumes, expiratory flow rates, closing volumes, or the slope
of phase III of the single-breath nitrogen washout in normal, healthy
adults; but long-term 'exposure to cigarette smoke is celated to
small-airway dysfunction and an increased incidence of lung cancer in
healthy nonsmoking adults.
VII-76
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* Small changes in visual and auditory vigilance have been
demonstrated at cacboxyhemoglobin contents capable o£ being produced by
involuntary smoking, but no change in tests of complex function has
been demonstrated. The interaction of fatigue, alcohol, and carbon
monoxide exposure on complex functions, such as automobile driving, has
not been investigated for COHb contents capable of being produced under
normal conditions of involuntary smoking.
* Patients with angina pectoris have reduced exercise tolerance
after involuntary smoking that may be a combination of psychologic
stress and a reduction in oxygen delivery to the myocardium induced by
carbon monoxide. Carbon monoxide clearly reduces the amount of
exercise possible until the onset of angina in patients with angina
pectoris at COHb contents that may be reached as a result of
involuntary smoking.
* Carbon monoxide has been shown in one study to reduce the
amount of exercise that patients with hypoxic chronic obstructive lung
disease can perform until the onset of dyspnea.
* Most nonsmokers find it annoying to be exposed to cigarette
smoke. This annoyance is probably due to substances in the gas phase
of the smoke.
* Cigarette-smoke exposure results in eye, nose, throat, and
respiratory irritation. The eyes are most sensitive, followed by the
nose and throat. The particulate phase of cigarette smoke seems to be
predominantly responsible for this irritation.
* Persons with allergies are more sensitive to the irritant
effects of cigarette smoke. However, there is no proof of tobacco
allergy.
* Children whose parents smoke may be more likely to have
respiratory symptoms, bronchitis, and pneumonia as infants and may have
poorer pulmonary function as adults, compared with children of
nonsmoking parents. This relationship is not independent of parental
symptoms, socioeconomic class, and the smoking habits of the children;
and it is associated with the number of cigarettes smoked per day by
the parents.
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68. White, J. R., and H. F. Froeb. Small-airways dysfunction in
nonsmokers chronically exposed to tobacco smoke. N. Engl. J. Med.
302:720-723, 1980.
69. Yabroff, I., E. Meyers, V. Fend, N. David, M. Robertson, R. Wright,
and R. Braun. The role of atmospheric carbon monoxide in vehicle
accidents. Menlo Park; Cal.: Stanford Research Institute, February
1974.
INDOOR AIRBORNE CONTAGION
Among the pollutants of indoor air are biologic aerosols produced
by people when they cough, sneeze, sing, spit, blow their noses, or
even talk. Discussion of airborne infection is as old as recorded
history, but refined concepts of contagion, expressible in quantitative
terms, are surprisingly recent. Less then 50 yr ago, William F. Wells
synthesized a coherent theory that has now been tested and
amplified.*1 Even though the ideas are not yet imbedded in medical
thinking and teaching, they pertain to a very important medical and
public-health problem. Airborne contagion is the mechanism of
transmission of most acute respiratory Infections, and these are the
greatest of all causes of morbidity. Primary pulmonary tuberculosis if>
also transmitted in this way. Airborne contagion from person to person
is mostly an indoor phenomenon.
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ASSESSING INDOOR BIOGENIC POLLUTANTS
In approaching biogenic pollutants, the dearth of data on indoor
prevalence and the lack of satisfactory study methods constitute a
single complex problem. Although most indoor biologic agents are
distinctive microscopically, many categories of biogenic particles are
not. For those which also fail to grow recognizably in culture, no
practical enumeration is yet possible.
The penetration of biologic particles into buildings has been
little studied, but seems to depend most on the extent of mass flow
through windows and doors. Additional factors in ventilation' * '*
include incident-wind speed and direction, negative pressurization by
exhaust fans, and stack effects (which may be minor in warm periods).
Air leaks between structural members ("crackage") foster ventilation;
window and door frames contribute less.*" Tracer gases often have
suggested brisk infiltration of air into structures; however, the
capacity of windborne particles to negotiate minute cracks, certainly
less, remains to be estimated. Sampling for biologic agents both
indoors and outdoors is fundamental to studies of their sources.
Furthermore, because particles may remain indoors for a long time after
infiltration from free air, analyses of indoor-outdoor relationships
must be sensitive to the resulting lag effects.'''
Biogenic pollutants bear complex and varied organic structures,
which defy automated chemical assay. Culture or direct microscopic
enumeration offers a workable, although tedious, alternative for some
particles;, for others, immunofluorescence and multiphasic
microscopy" have demonstrated potential. Concentrations of airborne
biogenic dusts that lack morphologically defined units might be
estimated by subjecting extracts of bulk aerometric samples to
immunoassay; methods suitable for amorphous components of house dust
have been discussed elsewhere.67
Because many biologic pollutants are relatively large
aerodynamically, whereas others are quite small or undefined,
precautions to minimize size-related collection bias are essential.
Rates of circulation indoors are generally lower and often more nearly
constant than those outdoors. However, the velocities generated by
fans, human activity, and pronounced convection are important; they
readily bias recoveries based on fallout and may affect collection with
suction traps.*' As a result, differences in particle recovery
between indoor and outdoor sites may reflect prevailing flow conditions
more than real transmural differences in aerosol prevalence.
Despite their longstanding popularity, "gravitational" methods
involve particularly marked, size-related bias in collections.82 And
the small samples obtained and the lack of volumentric capability
further limit the usefulness of data obtained in this way. Suction
devices have been used sucessfully for indoor studies, and miniature
impactors are adaptable for this purpose. In all applications, the
siting of samplers vis-a-vis probable pollutant sources should be
considered and points of low flow avoided.
In contrast with chemically simpler pollutants, biogenic agents
exhibit limited direct toxicity, more often provoking infection.
VII-82
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Airborne transmission of infectious agents is facilitated indoors by
the prompt dispersion of particles.12 In general* indoor bacteria
appear to have indoor sources; data on outdoor airborne bacteria are
severely limited. One study has reported bacteria in outdoor air at up
to 4,000/m .* Another study presented indoor-to-outdoor ratios of
0.76-14.25,7# with much site-to-site variation. Outdoor
concentrations may depend oh high wind velocity and temperature' and
are apparently highest in summer.7 '*
Bacteria from outdoors do contaminate interiors, but to an unknown
degree. Clostridium perfringens, primarily a soil bacterium, has been
found in room air and house dust.7*
The primary source of bacteria in most indoor places is the human
body.®1 Although the major source is the respiratory tract,11 *'
there are other sources. According to Clark and Cox, '* 7 million
skin scales are shed per minute per person, with an average of four
viable bacteria per scale. Abrasion is the primary factor in the rate
of loss1" 51 and showering increases the rate of loss of
bacteria."' " * *
EVIDENCE OF INDOOR AIRBORNE INFECTION
Droplet nuclei are the dried residues of the smallest respiratory
droplets. They range in size from 1 to 3 un, disperse rapidly
throughout the air of a room, and are carried wherever the air goes.
Settling velocity is negligible in comparison with tha velocity of air
movement in occupied rooms. The concentration of viable organisms
attached to droplet nuclei may be reduced by natural die-away, air
filtration, or exchange with outdoor air. Standard filters used in
ventilating systems remove a small fraction. There is no reservoir of
infectious droplet nuclei other than the respiratory tracts of people
carrying the organisms. Hells10 believed that aerial transmission
from person to person occurs indoors where droplet nuclei are in
sufficient concentration to be a hazard. Infectious contact
(contagion) requires proximity in time and [.pace between host and
victim, but can be extended to the confines of the enclosed atmosphere
and to a shared ventilating system if. the air within the system is
recirculated; '* the recirculating system then becomes a common
enclosed atmosphere.
Tuberculosis
In the 1950s, a study was carried out at the Veterans'
Administration Hospital in Baltimore in which guinea pigs breathed air
vented from a tuberculosis ward.70 Tubercle bacilli from the
patients, which had gone through the ventilating ducts and through the
upper respiratory tracts of the guinea pigs, were positively identified
in the lungs of infected animals.** On the ba3is of this and oth^r
evidence, it is generally agreed that the initial infection of the
lungs with tuberculosis is airborne.
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Measles
An early demonstration of airborne infection involved the indirect
approach—the control of epidemic spread by disinfecting the air. The
study was carried out in the 1940s in schools in Germantown and
Swarthntore, Pennsylvania, by Wells et^al,.'1 Shortly after
ultraviolet {UV) air-disinfection fixtures had been installed in the
test schools, a major measles epidemic struck. In both communities,
the nonirradiated schools had sharp outbreaks of measles, and the
UV-irradiated schools did not. The reduced spread of infection in the
irradiated schools could be attributed to the single factor that was
different, namely, the concentration of viable airborne measles virus.
During the spring of 1974, a sharp outbreak of measles occurred in
an elementary school near Rochester, New fork."1 Measles was
introduced into the school by a girl in the second grade. Twenty-eight
secondary cases followed after an incubation period of about 10 d;
these were distributed among 14 classrooms served by the same
ventilating system. The wide distribution of the 28 secondary cases
among children who had never even occupied the same room as the child
with the index case and the fact that about 70% of the air was
recirculated, and hence shared by all children served by the
ventilating system, led to the conclusion that measles reached the
various classrooms via the ventilating system.
Asian Influenza
During the 1957-1953 pandemic of Asian influenza, the main building
of the Veterans' Hospital in Liverraore, California, had UV air
disinfection installed throughout, and the patients la the. building
constituted a test group.97 Patients in neighboring nonirradiated
buildings served as controls. No mixing of test and control groups was
allowed. Hospital personnel and visitors who mingled in the outside
community were relied on to introduce infection into the two patient
populations. The incidence of serologically diagnosed influenza among
the 209 patients living in the UV-irradiated building was 2%; among the
396 patients living in nonirradiated buildings, it was 19%. Like the
measles study, this demonstration provided evidence consistent with
transmission of the infectious virus by air.
Schulman demonstrated that natural transmission of influenza from
mouse toimouse is airborne,7* and the studies of various viral
infections by Knight and collaborators are compatible with aerial
transmission in humans."'
Smallpox
In 1970, in a West German hospital, a patient with smallpox
infected 19 other persons, despite rigid isolation procedures.
Investigators from the World Health Organization and west Germany
demonstrated that smallpox, like influenza, could be transmitted by air
VII-84
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currents, but smallpox has been eradicated and need not be considered
further.M
These selected epidemiologic studies show the Kind of evidence
supporting the droplet-nucleus concept o£ indoor airborne contagion.
There have, of course, been many other studies, including unsuccessful
attempts at confirmation of some of those mentioned. In retrospect,
the failures appear to be attributable to inadequacies of experimental
design. The droplet-nucleus mechanism of Wells is emerging as the
successor, for most respiratory infections, to the direct-contact
mechanism of Chapin.
Other Types of Airborne Infection
Infections in hospitals have not been shown to be primarily
airborne, and such organisms as staphylococci, streptoccci, and
gram-negative bacilli are not characteristically transmitted by air.
Nevertheless, hospital-acquired infections of the lower respiratory
tract are presumptively airborne, inasmuch as inspired air is the most
likely vehicle for carrying organisms to the lungs. Hospital patients
are often hypers'usceptible to infection, and transmission nay occur in
ways not often seen in the general population.
A major epidemic of Legionnaire's disease occurred in a hospital
into which outside air contaminated with Legionella pneumophila leaked
during adjacent construction.* * This organism is unusual among
bacterial pathogens, in that it apparently exists in outdoor natural
reservoirs (soils) and infection is possible through inhalation of
contaminated outdoor air." 91 The most common mode of spread of
Legionnaire's disease involves air-cooling equipment that becomes
contaminated and produces concentrated bacterial aerosols." 17 "
Air-conditioning and -humidifying equipment can be a source of
intcaraural bacterial aerosols. Cool-mist vaporizers and nebulizers
that can produce heavily contaminated aerosols are of special
concern.1 11 " " 11 *0 ** *¦ si " 7 7 8 '• Apparently, bacterial
contamination of such units approaches 11)0%.19 71 pseudomonas
appears to be the most comroouly isolated bacterial genus. 1 c *5 *• *'
Smith" reported several cases of Acinetobacter Infection resulting
from contaminated coOl-mist vaporizers. Evaporative humidifiers,
although often contaminated with bacteria, are less likely to produce
bacteria-laden aerosols.* ' " Disinfection of any humidifying unit
i3 effective only temporarily,* " ** and Rosenstweig7 1 has
recommended banning cool-mist humidifiers for home or hospital use.
Other appliances reported to be potential sources of indoor
bacterial aerosols are flish toilets.'1 Ice machines are also
potential foci for bacterial contamination.5 Rylander et al.11
discussed carpeting as a foc^s for bacterial contamination, but
concluded that carpeting can, in fact, reduce airborne bacterial
concentrations by trapping bacteria-laden particles in the pile.
There are specific sites at which bacteria may become airborne at
high concentrations. Factories that process organic materials may
contain dense bacteiial aerosols." *1 " **
VII-85
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In some Interior situations/ even low bacterial concentrations are
of concern, A submarine constitutes a closed system in which
human-source bacteria, could accumulate to an undesirable extent.
Morris and Pallor5' " and Wright et al." discussed this subject
and concluded that modern air-cleaning in submarines creates an
environment unusually low in bacteria.
Also of concern are bacterial concentrations and patterns of
bacterial distribution in aircrfift, especially those used to transport
infectious patients. Clayton et al." reported that, whereas in the
Boeing 707 artificially aerosolized indicator bacteria are confined to
the rear portions of the aircraft, in the C130E Hercules such bacteria
become rapidly disseminated throughout !;he vehicle.
Bacteria (both surface and airborne] in the hospital environment
warrant- attention. Bacterial content in a hospital environment depends
primarily on the preser.ee of humans and on the degree and types of
their activity.* •* "* JI 81 "•
Bacterial products may contaminate indoor air in the absence of
bacterial cells. Pine dust in 3 detergent factory was found to contain
Bacillus subtilis enzymes." workers became ill when exposed to
sewage-sludge dust; the active factor, was presumed to be airborne
endotoxin.1® Finally, laboratory illness has occurred as the result
of inhalation of tuberculin aerosols during operation of a high-dpeed
centrifuge, 1 *
Several fungi—Blastomyces, Cryptococcus, Coccidloldes, and
Hlstoplasma, all V.nown primarily as human pathogens—exist in natural
reservoirs, usually associated with bird or animal
emanations.1 ' 11 •* The extent of contamination of interior
situations by these fungi is unXnown. Howover, all are known to enter
the body by the respiratory route,1 11 " '1 " " and
Coccidloides and Histoplasma are known to be highly infective.ts
Thus, natural reservoirs near human habitation will surely result in
some interior contamination leading to a possible risk of
infection.J 3 1 *• 11 »i »s pot example, S * 10^ viable
Cryptococcus spores liave been found per gran of dry pigeon feral
material,2 and the spores were present in more than half the pigeon
droppings examined"—droppings that are often abundant in areas of
dense human population.
Candida albicans and dermatophytes have been recovered from air and
dtiat samples in clinic rooms especially during and after examination of
infected patients.1* " ** However, Pri€drich,> reported only
3% of air samples .and 14% of dust samples positive in examining rooms
during pei'lixls with no patients.
IMPORTANCE OF AIRBORNE CONTAGION
In a 9.5-yr study of 85 families in Cleveland, Ohio, Dingle found
that 63% of all illnesses were respiratory.®* According to the
National Health Survey, respiratory conditions (predominantly upper
respiratory disease and "influenza") account for more than half of all
acute conditions, including illnesses and injuries." The incidence
VII-86
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of respiratory conditions is just under one per person per year* and,
on an average, each person's activity is restricted for 4.5 d. If one
grants that the respiratory conditions referred to are mostly in the
category of indoor airborne contagion, the problem is seen to be
enormous. Loss of time from work or from school exceeds that from any
other cause.
PREVENTION OP IKDOOR AIRBORNE CONTAGION
Less-crowded living conditions, isolation, and vaccination have
helped to reduce airborne contagion. We consider here a measure that,
although neglected in the past, is assuming increasing importance: air
disinfection in buildings.
Control of epidemic spread of airborne contagion requires that each
infectious case beget, on the average, no more than one new case. The
concentration of infectious droplet nuclei must be reduced to the point
where susceptible people stand but a small chance of inhaling an
infectious particle. Ir. relatively airtight buildings where the
capacity of the ventilating system, the fraction.of fresh-air makeup,
and the efficiency of the filters are known, where the number of
infections in each generation of an epidemic is available from records,
and where the pulmonary ventilation and duration of exposure of the
occupants can be estimated, the essential characteristics of airborne
contagion can be dealt with quantitatively. In the 1974 measles
epidemic in a school near Rochester, New York, this was done. '*
During the first generation, the number of infectious particles (quanta
of infection) produced pec minute in the index case was 93—an amount
that produced a concentration in recirculated air of 1 per 5.17 m^.
Twenty-six susceptible children breathing this sparsely infected air
acquired measles and appeared as cases in the second generation. Such
calculations provide architects and engineers with an appreciation of
the particulate nature and the quantitive aspects of a characteristic
airborne infection.
Thus, the routes of transmission are airborne through infiltration
and ventilation, from person to person, and via fomites. The effects
of ventilation rates are unknown.11 " There are interactions
between microorganisms and pollutants, as between indoor combustion and
smoking, in producing respiratory illness, especially in children and
the infirm.11 '* 7t
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the atmosphere of plants processing vegetables for freezing. Health
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62. Nelson, C. L. Environmental bacteriology in the unidirectional
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63. Pennington, J,. H., J. Lumley, and F. O'Grady. The growth of
Pseudomonas pyocyanea in Garthur condenser humidifiers. An
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64. Peterson, J. E. Estimating air filtration into houses: An
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65. Pike, R. M. Laboratory-associated infections: Incidence,
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66. Radonic, M. Systemic allergic reactions due to occupational
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67. Reznikov, M., J. H. Leggo, and D. J. Dawson. Investigation by
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M. scrofulaceum group from house dusts and sputum in southeastern
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68. Riley, E. C., G. Murphy, and R. L. Riley. Airborne spread of
measles in a suburban elementary school. Am. J. Epidemiol.
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69. Riley, R. L., C. C. Mills, F. O'Grady, L. U. Sultan, F. Wittstadt,
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Ultraviolet irradiation of infected air: Comparative infectiousness
of different patients. Am. Rev. Respir. Dis. 85:511-525, 1962.
VII-91
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70. Riley, R. L., W. P. Wells, C. C. Mills, W. Nyka, and R. L. McLean.
Air hygiene in tuberculosis! Quantitative studies of infectivity
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71. Ro*enzweig, A. L. Contaminated humidifiers. N. Engl. J. Med.
2e3tl056, 1970.
72. Rutter, D. A., and C. G. T. Evans. Aerosol hazards from scae
clinical laboratory apparatus. Br. Med. J. 1:594—5t»7» 1972.
73. Rylander, R., K.-E. Myrb&ck, B. Verner-Carlson, ar\d M. Ohrstrilm.
Bacteriological investigation of wall-to-wall carpeting. Am. J.
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74. Sayer, W. J., N. M. MacKnight, and H. W. Wilson. Hospital airborne
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ALLERGIC REACTIONS IN THE INDOOR ENVIRONMENT
Only a few airborne allergens are found in enclosed spaces.
Although human exposure to them is recurrent and of variable duration,
the health effects of exposure to them alone are difficult to
estimate. Despite this uncertainty, the impact of some agents is
clearly appreciable. House dust and pollen, for example, are
acknowledged as two of the most important factors in provoking symptoms
of allergic rhinitis and asthma in many locales. Clinically evident
allergy to animal danders is
-------
Allergic reactions can occur on the skin and in the noser airways,
and alveoli. Although increasingly recognized as important causes of
allergic lung diseases, occupational agents are considerably less
prevalent as causes of these diseases than such allergens as pollen,
moulds, mites, and animal dander and excreta, to which exposure occurs
in the home environment.
ALLERGIC REACTIONS OH THE SKIN
Both primary irritants and allergic sensitizers may produce
inflammation of the skin or an eczematous process. Primary irritation
causes contact dermatitis. The effect is through direct action on the
skin. Irritants act by removing lipid films, producing denaturation of
keratin, or interfering with the barrier layer. Through the production
of dehydration, the effects may occur by protein precipitation or
oxidation. Sensitizers produce cutaneous changes after previous
contacts, either immediately on recontact or shortly thereafter.
Almost any chemical may be a sensitizer. A sensitizer stimulates the
immune mechanisms by producing an antigen, usually by combining with a
protein. Immediate hyperreactivity is produced by a binding with igE
on basal cells. Delayed hyperreactivity may be produced by IgG
mediation.1 1
Photoallergic reactions may be produced by ultraviolet (UV) light,
which leads to an inflammatory response. The antigenic agent may be a
UV-raediated degradation product or a visible-light photosensitizer that
produces an immediate hypersensitivity response.
Secondary effects may occur after the cutaneous defenses have been
removed. Some fatty acids on the surface lipid film may act as
antimicrobials.'"' Bacteria may grow on an oozing or fissured
surface. Other toxins may also enter the system at that point.
Lesions may be highly variable, with a range from slight inflammation
to tumor. Acute contact eczematous dermatitis can be due to a primary
irritant or a sensitizer and is characterized by inflammation changes,
crusts, and sloughing.
ALLERGIC REACTIONS IN THE RESPIRATORY TRACT
Allergic reactions in the respiratory tract can be distinguished by
the site and the nature of the reaction and by the underlying
immunologic mechanisms.
Site and Nature of Reactions
Allergic responp.es to inhaled materials cause a local inflammatory
reaction that affects predominantly the nose (allergic rhinitis), the
airways (allergic asthma), the airways and adjacent alveolar spaces
(allergic asthma with pulmonary eosinophilia—allergic bronchopulmonary
aspergillosis), or alveoli and peripheral bronchioles (hypersensitivity
VI1-94
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pneumonitis oc extrinsic allergic bronchioloalveolitis). Similar
reactions can occur in each of these separate sites, often producing
similar pathologic changes, in the absence of any recognized extrinsic
cause.
Allergic rhinitis is characterized by vasodilatation and edema of
the nasal mucosa with mucus hypersecretion, which causes nasal
discharge and obstruction.
Asthma is most usefully defined in functional terms as partial
narrowing of the airways that is reversible over short periods, either
spontaneously or as a result of treatment. The defining criterion of
asthma is therefore variable airway narrowing. This airway narrowing
may be due to contractions of airway smooth muscle, edema of the
bronchial mucosa, accumulation of bronchial mucosal secretions, or any
combination of those. If the cause of the airway narrowing can be
identified as an allergic reaction to an extrinsic agent, the term
"allergic asthma" can be used.
Pulmonary eosinophilia (pulmonary infiltration with eosinophilia,
or PIE) is defined as transient shadowing on a chest roentgenogram
accompanied by an increased blood eosinophil count. Histologically,
the alveolar spaces in the affected parts of the lung are consolidated
with eosinophils. Pulmonary eosinophilia may be caused by a reaction
to drugs or to helminths migrating through the lung. Aspergillus
fumigatus is the only important inhaled allergen identified as a cause
of the syndrome; when it is the cause, the syndrome is called "allergic
bronchopulmonary aspergillosis," or ABPA. AfiPA episodes are often
accompanied by asthmatic attacks.
Hypersensitivity pneumonitis is characterized, at least during its
early stages, by the infiltration of alveolar walls and peripheral
bronchioles with mononuclear cel.13. The condition is often associated
with the formation of epithelioid ^nd giant-cell granulomata. The
disease may be accompanied by progressive fibrosis, which makes it
difficult to distinguish the changes in the lung from other causes of
alveolar wall fibrosis.
Mechanisms of Reactions
Allergic reactions are conventionally distinguished from reactions
of protective immunity by the extent of tissue damage. The immunologic
mechanisms underlying allergic reactions differ little from those
involved in immune reactions. They are distinguished by outcome:
whereas little or no tissue damage occurs in immune reactions, allergic
reactions are characterized by the disproportionate damage caused in
most tissues. The different types of immunologic reaction that may
cause tissue damage have been classified by Gell et al_. 51 Of their
four types of allergic reactions, three are of particular importance in
relation to allergic lung disease: immediate (Type I) reactions,
Arthus or local immune complex (Type III) reactions, and cell-mediated
delayed-hypersensitivity {Type IV) reactions. It is important to
appreciate that, although these types are considered separately, more
than one type is involved in most, if not all, cases of allergic lung
disease.
VII-95
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Immediate (Type I) Reactions. In this type, antigen reacts with
antibody, primarily IgE antibody on the surface of circulating
basophils and mast cells, which are present in the submucosa in the
nose and airways {as well as in the skin and gastrointestinal tract).
IgE antibody is attached to surface receptors on the cell through its
Fc portion. Bridging of two adjacent IgE molecules by reaction of
antigen with the Fab portion of the molecules stimulates intracellular
metabolic changes that lead to the release of pharmacologically active '
mediators from the cytoplasmic granules of the cells. The mediators
released' include histamine and slow-reacting substance of anaphylaxis
(SRS-A), both of which increase the permeability of small blood vessels
to intravascular protein molecules, as well as stimulating
smooth-muscle contraction. In addition, eosinophil chemotactic factor
of anaphylaxis (ECF-A) is released. The mediators released from these
cells during the reaction have pharmacologic properties that could
mediate many of the changes observed in the nose and airways in
allergic.rhinitis and asthma.
Arthus Local Immune Complex (Type III) Reactions. Immune complexes
formed in tissue spaces of antigen and IgG antibody in relative antigen
excess can cause local tissue damage. Such complexes fix complement,
and several of the complement cleavage products released have
pharmacologic activity. C3a and Csa are anaphylotoxins that
stimulate histamine release from mast cells. Cis chemotactic
both for neutrophils and eosinophils. Neutrophils that have surface
receptors for 03^ and the Fc portion of IgG phagocytose immune
complexes formed in antigen excess when ingested and provoke the
release of proteolytic lysosomal enzymes from neutrophils. This is
referred to as "regurgitation during feeding" and causes local tissue
damage. This mechanism is probably important in th« tissue damage that
occurs in the aixways in ABPA and in the inflammatory reaction in
alveolar walls in hypersensitivity pneumonitis.
Cell-Mediated Delayed-Hypersensitivity ' (Type IV) Reactions. •In
these reactions, antigen reacts not with antibody, but with
specifically sensitized T-lymphocytes. The reaction stimulates the
release from the lymphocyte of a number of biologically active soluble
substances known as "lymphoklnes," which are capable of mediating &
local inflammatory reaction. Among these biologic activities,
iymphokines have been shown to be chemotactic for macrophages, to
induce activation of macrophages) and to inhibit their migration. The
interaction of antigen with specifically sensitized T-lyraphocyces can
therefore stimulate local recruitment and activation of macrophages, in
addition to maintaining them at the site of reaction. This type of
reaction is well recognized in the delayed hypersensitivity to
tuberculin and has also been shown to participate in the inflammatory
reaction in alveolar walls in hypersensitivity pneumonitis. (Type IV
reactions occur with some bacteria, such as M. tuberculosis, and with
fungi, as discussed in the previous section.}
These immunologic reactions participate in the different allergic
reactions to inhaled materials in the respiratory tree, as shown in
Table VII-10. Other immunologic mechanisms, not yet clearly
identified, may also be involved in these diseases.
VII-96
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TABLE VII-10
Immunologic Mechanisms in Allergic Lung Diseases
Reaction
Site
Disease
Nose
Airways
Airways ^nd alveolar
spaces
Alveolar walls and
peripheral
bronchioles
Allergic rhinitis
Allergic rhinitis
Asthma with pulmonary eoslnophilia,
allergic bronchopulmonary asper-
gillosis
Hypersensitivity, pneumonitis
(extrinsic allergic bronchiolo-
alveolltis
Immunologic Mechanism
IgE
IgE
IgE, IgG, immune com-
plexes
IgC, immune complexes,
sensitized T-lympho-
cytea
VII-97
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FACTORS THAT DETERMINE ALLERGIC REACTIONS IN THE RESPIRATORY TRACT
Allergic reactions to inhaled materials in the respiratory tract
are determined by a number of identifiable factors, which include the
physical and chemical properties of the inhaled particles, the
immunologic reactivity of the host, and the pattern of exposure.
Nature of the Inhaled Material
Most inhaled materials that stimulate an allergic response in the
respiratory tract are particulate and approximately spherical. To
cause this kind of response, particles must remain suspended in
atmospheric air long enough to be inhaled; for an immunologic reaction
to occur, they must penetrate to a reaction site in the lungs. Inhaled
particles are deposited on the surfaces of the nose, airways, and
alveoli. Three separate mechanisms contribute to this deposition:
gravitational sedimentation, inertial impaction, and diffusion. Any
particles suspended in air will fall under the force of gravity and
reach a terminal velocity tha- is determined by diameter and density.
In addition, a particle suspended in an airstream that is changing in
direction, as occurs in the nasopharyngeal or branching bronchial
airways, will continue for some distance in the original direction of
airflow, owing to inertia. The distance traveled by a particle in the
original direction of airflow is determined by its density and
diameter, the velocity of airflow, and the angle of change of
direction. Impaction of particles due to this mechanism is of most,
importance with large particles (aerodynamic diameter, greater than
3 vm) in the nose and proximal airways, the portions of the
respiratory tract in which the velocity of airflow and angles of change
of direction are greatest. Gravitational sedimentation is of greater
importance in determining deposition of smaller particles {aerodynamic
diameter, 0.5-3 un) in the smaller, more peripheral airways and in
the alveoli. Very small particles (aerodynamic diameter, less than 1
un) may be deposited by diffusion, owing to their Brownian movement
resulting from the impact of surrounding gaseous molecules.
Most particles whose aerodynamic diameter is 20 un or more and
50% of paiticles down to 5 urn are deposited in the nose. Almost
complete deposition of particles of 5 un or more occurs in the
tracheobronchial tree. Alveolar deposition (the so-called respirable
fraction) is maximal for particles whose aerodynamic diameter is
between 2 and 4 ym. Once deposited, a particle is not resuspended in
respired air. Particles not deposited are expelled in the exhaled air.
Particles deposited in the airways are trapped in the mucus blanket
on the mucosal surface and are moved centrally by the coordinated
beating of the cilia, which extend distally as far as the terminal
bronchioles (the "mucociliary escalator"). Some particles deposited in
the airways are usually cleared within 24 h. Particles deposited in
the alveoli are phagocytosed and cleared by alveolar macrophages; they
migrate from the alveoli with their engulfed particles either
proximally into the airways on to the mucociliary escalator or out into
VII-9H
-------
the draining lymphatics. Clearance of particles deposited in the
alveoli takes place in several phases, with characteristic tines
measured in hours, days, weeks, and years.
Of the potentially allergenic particles, the moulds and organic
dusts (including animal excreta) have aerodynamic diameters that allow
their penetration into the airways and alveoli. The majority of
pollens, however, have diameters greater than 12 tin, with aerodynamic
diameters somewhat different because of'their density. However, pollen
grains have been recovered from the airways by endoscopy and from
resected lungs.1*0
The chemical properties of a molecule that determine its
antigenicity are poorly understood. In general, "complete" antigens
that are able to stimulate antibody production are proteins or
polysaccharides of high molecular weight. Both organic and inorganic
molecules of low molecular weight (less than 1,000) can act as
haptenes, stimulating antibody production when coupled to
high-molecular-weight carrier molecules.
Immunologic Reactivity of the Host—Atopy
Coca and Cooke11 introduced the term "atopy" to describe persons
who were readily sensitized to proteins in their environment. These
reactions have since been shown to be mediated by I^jE antibody.'7
Pepys111 has redefined "atopy".as "that, form of immunological
reactivity of the subject in which reaginic antibody, now identifiable
as IgE antibody, is readily produced in response to the common
allergens of the subject's environment." The presence of IgE antibody
specific to a particular allergen can be demonstrated, by its ability to
elicit an immediate "weal and flare" skin prick test reaction. The
atopic status of a person—but not clinical reactivity—can therefore
be defined by reactions to skin tests with allergens appropriate to the
particular environment.
Several studies'9 121 have shown atopy to be familial. Its
genetic basis, however, remains unclear. Atopy (defined as one or more
positive skin test reactions to common inhalant allergens) in
asthmatics is strongly related to the frequency in first-degree
relatives of eczema and hay fever and less to the frequency of asthma.
Circumstances of Exposure to Inhaled Allergens
Evidence from the investigations of allergic reactions to inhaled
particles in industry has suggested a relationship between exposure and
disease. Juniper et al." showed, in a study of IgE-mediated
allergic reactions to B_. subtilis enzymes, particularly alcalase, in
the enzyme-detergent industry, that the incidence of skin test reactions
to alcalase was increased in groups with heavier exposures, but that
the incidence in atopics exceeded that in nonatopics at each exposure.
The effects of differences in intensity and duration of exposure in
determining sensitization have not been studied.
VII-99
-------
Exposure to allergens during the earl/ months of life may be
important in determining the tendency to produce IgE antibody to
inhalant allergens. Taylor et al_. 111 demonstrated an association
between transient IgA deficiency in infancy and later development of
atopy. They suggested that inhalant and ingested (particularly milk)
allergens traverse mucosal barriers in IgA-deficient persons during
this "vulnerable" period and stimulate the production of IgE antibody.
If this hypothesis is correct, it presents an opportunity for the
prevention of atopy: exclusion of potential allergens from the
environment during this period may prevent the stimulus to IgE
production.
ALLERGIC LUNG DISEASES AND THEIR CAUSAL ALLERGENS
Allergic Rhinitis and Asthma
IgE-raediated rhinitis and asthma may be caused by a wide variety of
allergens common in the environment,,which include the house dust mite,,
pollens, moulds, and anin.c.1 dander and excreta. The particular
allergens that cause these diseases have great geographic variation:
exposure to different moulds and pollens and to the house dust-mite
varies greatly according to climatic conditions; which determine their
prevalence in a particular environment.
Pollen. Among biogenic particles, pollen grains can perhaps be
most confidently ascribed to sources in nature, and their presence in
enclosed spaces generally reflects incursions from outdoor air.
Wind-pollinated plants typically have drab, scentless, individually
minute flowers, unlike the large showy blooms of many popular house
plants. However, with sizable indoor planting, pollens of cyclamen and
impatiens have been found to reach concentrations of hundreds of grains
per cubic meter; their possible effects have not been studied (H. Burge
and W, Solomon, unpublished iata) .
The few studies of the flux of pollens into homes have emphasized
the importance of free ventilation and indicated that even partial
closure of windows can substantially exclude these particles.1
Undisturbed, closed rooms were recognized as pollen "refuges" many
years ago. However, pollen grains are known to enter fully closed
structures through faults between structural members ("crackage")—an
effect positively related to outdoor wind speed " and probably
heavily dependent on gust-induced effects. The opening of doors as
occupants enter and leave further enhances the entrance of pollen and
limits the barrier function of any building. After penetrating
indoors, pollen may remain airborne or be deposited, with secondary
reflotation possibly due to scouring air currents and disturbance of
substrates.
Many different pollens from grass, trees, and flowers have been
shown to cause allergic rhinitis and asthma. Pollen counts vary
greaHy during the year and from year to year, and symptoms in
sensitized people are closely related to the prevalence of the
VII-100
-------
particular pollen causing disease. Grass and ragweed pollen, which ace
particularly cannon causes of allergic rhinitis and asthma, are most
abundant in the summer months. In some areas, the pollens of mulberry
and other trees are alao important.
Although soluble extracts of pollen have been shown to provoke
asthmatic reactions in symptomatic persons/ pollen grains are generally
too large to penetrate into the respiratory tract beyond the trachea.
Various suggestions have been made to explain how in these
circumstances pollen can penetrate into the airways and react with IgE
on the surface o£ submucosal mast cells to provoke an asthmatic
reaction. Pollen grains and fragments bE pollen grains {or plant
bract) may be scnall enough to penetrate into the airways and have been
so found in an autopsy study. Kimura et al. " have identified
basophils and mast cells in the lumen of the airways. Inhaled pollen
grains may therefore stimulate an IgE-dependent mast cell and basophil
degranulation that occurs initially in the bronchial lumen.
House Dust Mite. Interest in acarlds has been stimulated largely
by some pyroglyphid mites that contribute sensitizing materials to
domestic dusts. Bouse dust is a poorly characterized and variable
substance that Is universally recognized to produce allergic rhinitis
and asthma." " 1,1 In many areas, two mite species,
Dermatophagoides pteronyssinus and farinae f are abundant indoors and
may be recovered, from air in domestic interiors.1* 78 l" 1J'
Parallel allergic reactivity to these agents and to crude house dust
has been described widely, 1 •*. 1J15 although exceptions are well
documented¦31 A possible role for nits allergy has been proposed in
urticaria (hives) " and in other skin disorders.*1
House dust mites are most abundantly associated with mattresses,
bedclothes, and heavily used upholstered furniture.75 '' A
temperature of around 25°C appears most favorable, and a relative
humidity of at least 45% is essential to prevent death from
desiccation. Populations vary with atmospheric moisture, often being
highest in autumn, but also in summer or winter, especially in damp
houses." 107 ll* 14* Pyroglyphid mites have varied diets, but
lelish especially human epidermal scales} specific fungi may also be
favored, 1,1 but nutritive factors may not1 be important for
concentration.77 Indoor temperature doas not appear to be
important.77 1,7 Mite numbers may be reduced by decreasing indoor
humidity, avoiding fibrous floor and furniture coverings, and encasing
pillows and mattresses in plastic. Safe and effective chemical
miticides for the home are still needed.1**
Extensive surveys of indoor acarids have disclosed additional
commonly recovered genera (Glycyphagus, Hirst.ia, Tvrophagus, and
EurogLyphual that inhabit dust. In. addition,¦interiors used to process
or store agricultural products often yield large and specialized mite
populations.7* ll* 144 Although the whole house dust mite is about
300 im long, the allergens are probably present In its debris,
particularly the excreta, whose particles are of an inhalable size.
VII-101
-------
Moulds. The moulds that may cause allergic rhinitis and asthma are
predominantly of the genera Alternaria, Cladosporlum, and Aspergillus,
as well as Merullus lachrymana, the cause of dry rot. Atmospheric
spore counts of these moulds ara usually highest in the late summer and
autumn, although spore counts of Aspergillus fumigatus are maximal in
the autumn and winter.
Cladosporiura was by fat the most frequent taxon recovered both
outdoors and in domestic and other "clean" interiors during summer in
the United States,14 4" *» 74 •» 41 111 124 1,4 147 in Europe,1 4* 1,4 lit
and in Asia,'1 but was always more abundant outdoors than indoors.' 14 14
Penicillium usually dominated wintertime U.S. collections1* 44 1,1 1,4
and some European sites'7 44 1,4 144 and is often considered an
"indoor* fungus, being frequently more abundant indoors than
outdoors.1 10 *7 44 121 Penicillium concentrations also increase
substantially with housecleaning and repair.43 112 Alternaria was
the n;st frequent indoor fungus in the summertime in two southwestern
U.S. studies,1" 85 although the contribution of outdoor air was
uncertainl Aspergillus was dominant in only two studies, one in
China 25 and one in Great Britain,44 but is considered one of tne
most common groups of indoor fungi. 1 14 Aspergillus species were
usually other glaucus groups (e.g., A. amestelodami and A. repens) or
A. versicolor, with relatively few A. fumigatus or A. flavus
recoveries. Mucor was consistently more frequent indoors10 than
outdoors.
Cases of contamination of domestic interiors usually involved
outdoor fungi that increased indoors on specific substrates.
Floodwater disasters often produce abundant mold growth with attendant
increase in airborne spore counts.14 79 Any organic material may
support mold growth when wet. Damp walls may acquire abundant
Cladosporium cladosporioides Aureobasidum, 07 41 and damp leather,
cotton, and paper often are covered with Penicillium or Aspergillus
spores. Fireproofing materials,* furniture stuffing (e.g., kapok,
feathers, and hair14 145 lt0), carpets,4* and stored organic
material'7 " all have been implicated as foci of mold
contamination. House dust contained 10,000-3,000,000 spores/g in one
study, 1 *' and dust-raising activities clearly increased spore counts
in libraries 14 and domestic interiors.47 1,1 Repair work increased
counts up to'20-fold, presumably because of dust dispersion) and
contamination was not restricted to the actual repair site, but spreaa
throughout the home.** Fungal taxa in dust may occur in proportions
different from those in air;51 in fact, some fungi may grow in dust. "* 1,4
Several additional reports have implicated house dust4' 114 141 as a
source of airborne fungi. House plants have been implicated as sources
of increased A. fumigatus concentrations in homes and hospital
rooms;1'4 147 however, Burge and Solomon (unpublished data) did not
find evidence of this ubiquitous soil fungus in domestic air associated
with hpuse plants. Pets have also been blamed for increased A.
fumigatus counts,4" but Burge e£ al.11 did not find evidence of
direct animal contributions to the A. fumigatus in a series of
animal-care rooms. Poor landscaping practices, including accumulation
of organic debris and high shade,74 and such appliances as
VII-102
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evaporative humidifiers1* 1,4 181 and air-conditioners1" '** have
been named as potential sources of airborne fungal cbntamination. The
wood-rotting fungus Merulius lacrymans. contaminating damp timbers in
old and damaged English homes, may produce potentially sensitizing
spores indoors at up to 360,000/n^ of air." ' * Spores released in
(or allowed to enter) one area of a home spread rapidly to all areas
with open doors.1*
The situation differs markedly in interiors used specifically for
processing or handling of biologic materials * * 17 1% 17 11 ** " 11
*7 •« (» t< e* 110 11? lit 11« 111 11« lt« IS*
Aspergillus fumigatus is a ubiquitous soil fungus and can be
present wherever organic material provides a suitable substrate.** 11 *
In outdoor urban air, A. fumigatus rarely exceeds 150 spores/m3 and
is not necessarily frequent." l*° ,*1 In the presence of compost,
counts can rise into the millions per cubic meter,t#1 1,7 with the
possibility of attendant indoor pollution. In relatively clean
interiors, A. fumigatus counts generally are low:
0-200/m3.5 11 *' ** 111 1" However, in interiors in which organic
material is stored or handled, they can exceed 2 x 1010 spores/m3.* '7 '*
The incidence of invasive aspergillosis in the normal population
appears quite low, even in persons exposed to spores at high counts," **
but the risk of hypersensitivity disease in overexposed people is
substantial."-* 50 #1 •* ** 1,1 11 * »" 14'
A wide variety of fungi that are normally saprophytic (as is A.
fumigatus) may opportunistically become invasive human pathogens.1*
Some data on indoor contamination by these organisms are available from
general surveys of indoor mould concentrations,1 * 9 " 11 ss 57 7' *' ,1'
but none has been studied with respect to possible risk factors that
foster human infection.
Algal Particles. Algal cells, including viable units, are regular
components of outdoor aerosol and have been regarded as potential human
allergens for decades.* • " Algae reside in soil and on natural
surfaces, as well as in aquatic habitats, from which they may become
airborne in the bursting of bubbles11* or the fragmentation of
foams.117 These processes, as well as dry dispersion from soil, all
increase with rising wind speed and with physical (e.g., agricultural)
disturbance of substrates.1*
Although concentrations of algae in indoor air have not been
systematically studied, they are often present in water reservoirs and
in house dust and are undoubtedly dispersed periodically. Soil
particles and aerosols from water reservoirs are the most probable
sources of algae recovered indoors. Sensitization to dusiborne green
algae (Chlorella 3pp.) has been amply documented; however the impact
of indoor exposure to these or related organisms remains uncertain.11
Animal Dander and Excreta. Domestic animals, particularly cats,
are important causes of allergic rhinitis and asthma. Other animals
that can cause these diseases include dogs, rabbits, guinea pigs, and
horses. It has been generally accepted that the source of allergens is
the animal dander. Recent studies of laboratory-animal workers with
rhinitis and asthma due to XgE-mediated reactions to rats snd mice have
VIl-103
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identified the animals' urine as an important source of allergenic
protein. The urine of the other animals has not yet been investigated
as a possible source of allergens.
Sensitivities to pets are discrete/ shoving species specificity and
often breed specificity.181 Washed hair is generally antigen-poor,*1
but epidermal scales and body fluids109 appear to carry potent
activity.
Highly sensitive persons may develop urticaria or flares of
allergic eczema from direct physical contact with the implicated
species. Whether airborne antigen alone can cause these skin, problems
is not clear. However, respiratory symptoms often continue for many
weeks after an implicated pet has left the home, and that suggests that
minute inhaled doses of dander can sustain a clinical response.
Because the airborne antigen has not been measured, more explicit
dose-response relationships also remain unknown.
Although more commonly associated with hypersensitivity
pneumonitis, 163 serum proteins in the feces of birds, particularly of
parakeets (budgerigars) and pigeons, can stimulate igE antibody
production, especially in atopic persons,"0 and cause asthma.
Feathers, present largely in bedding and clothing, are familiar
sensitizers that seem to acquire increasing antigenic potency with
agei,s although this change could reflect progressive invasion by
mites (or microbial contamination); differences between purified
antigens of feathers and house dust have been claimed." The
offending materials seem to bs derived primarily from serum and
intestinal secretory componentsr®* although feather and egg proteins
also may contribute antigens.
The cause of rhinitis and asthma associated with an IgE-taediated
reaction can usually be readily identified from the history and from
skin prick test reactions. A history of symptoms that are temporarily
related to a particular exposure (i^e., seasonal variation in symptoms
or symptoms occurring after exposure to domestic animals or bedmakings)
strongly suggests the relationship. The presence of IgE antibody
specific to the particular allergen will be revealed through skin prick
testing with the putative allergens.
Fragments of epidermis and skin appendages, (danders) are shed by
all vertebrates and undoubtedly are dispersed indoors. With components
of sweat, saliva, and waste discharges, these particles may contribute
substantial quantities of species-specific materials to the indoor
environment. Although nontoxic, the dispersed materials are 3trong
sensitizers and commonly elicit allergic rhinitis and asthma. In
addition, emanations of birds and of at least one small mammal, the
gerbili 1,1 have been implicated as agents of allergic alveolitis.
Insects. Insect emanations are ptrong sensitizers, can elicit
respiratory allergic reactions, and a-:e often evident in outdoor
air.9* Symptoms have occurred as a result of local swarming of
caddis flies,111 mushroom flies, may flies, *1 and box elder
beetles? 11 * and antibody responses to other types are easily
demonstrable. In addition, species that establish themselves .
indoors—including roaches, houseflies, bedbugs, and carpet
VII-104
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beetles—have been implicated as human sensitizers.11* Beaches have
received special attention because o£ their widespread abundance and
the capacity of aqueous extracts of common species to elicit
respiratory responses in challenged sensitive subjects.'1 Roach
fecal pellets appear to share antigens with the bodies of the insects
that produce them and, on dissolution, may contribute importantly to
air contamination." Sensitization to roach antigens is particularly
frequent in persons of low income; this apparently reflects an
association with poor sanitary conditions. 11 In addition to pests, a
variety of insects exploited commercially for research purposes can
produce indoor contamination and respiratory allergy in exposed
persons."4 '• l**
Human dander. Epidermal scales of human origin are often the most
abundant and microscopically distinctive component of indoor dusts. 15 '5
These structures readily serve as "rafts" for aerial transport of
bacteria and other microorganisms. However# the role of human dander
as an antigen for allergic subjects is highly controversial. Antibody
responses to this material have been reported, 15 IM but confirmatory
data and evidence of clinical impact are still awaited.
Asthma and Pulmonary Eosinophilia Due to Allergic Bronchopulmonary
Aspergillosis
ABPA is caused by an allergic reaction in'the airways to inhaled
Aspergillus fumigatus. The disease is characterized by recurrent
episodes of pulmonary eosinophilia, usually associated with attacks of
asthma. In addition to asthma and pulmonary eosinophilia, ac the
disease progresses, bronchiectasis (typically proximal, but sometimes
widespread), airway narrowing that becomes increasingly less
reversible, and pulmonary fibrosis that particularly involves the upper
lobes may also develop.
Aspergillus fumigatus is widely distributed. Its spores are about
3 w in diameter, but tend (unlike such other members of the genus as
A.. clavatua, the cause of malt-worker's lung) to form spore chains up
to 10 i*n in length, which when inhaled deposit in proximal airways.
Unlike the other moulds that may cause asthma, such as the genera
Alternaria and Gladosporium, A. fumigatus grows at body temperature,
and its septate hyphae may be found in.sputum. Spore counts are
usually highest during the winter, when exacerbations of the disease
most frequently occur.
In common with such allergens as Dermatophlagoides pteronyssinus
and grass pollen, A. fumigatus inhaled into the respiratory tree can
stimulate production of specific IgE antibody. Its ability to persist
and to grow in the airways can also stimulate IgG antibody production.
A. fumigatus inhaled into the airways of a person with IgE and IgG
antibody not only provokes release of mediators from mast cells, but
can form immune complexes, which in antigen excess cause a local
tissue-damaging inflammatory reaction. This is thought to be the cnuse
of the proximal bronchiectasis that is characteristic of the disease.
VII-105
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Eosinophil cheraotactic factors released froa mast cells and from
complement activation may be responsible for the associated
eosinophilic consolidation.
Allergic bronchopulmonary aspergillosis is an uncommon disease,
although in the United Kingdom it is the commonest cause of pulmonary
eosinophilia. in one series, it was responsible for 116 of 143 cases
of pulmonary eosinophilia. It appears to be less prevalent in the
United States than in the United Kingdom. That is probably due to
climatic differences: conditions in the United States are generally
less favorable to the growth of A. fumigatus, although the difference
may be due in part to differences in diagnostic convention.
The disease should be suspected in those with episodes of pulmonary
eosinophilia, usually with asthma, which occur particularly during
periods of the year when A. fumigatus spores are most prevalent. Those
with asthma whose chest roentgenograms show changes of bronchiectasis
or upper lobe fibrosis are also likely to have ABPA.
Hypersensitivity Pneumonitis (Extrinsic Allergic Alveolitis)
Hypersensitivity pneumonitis is an inflammatory reaction in
alveolar walls and peripheral bronchioles due to an allergic reaction
between inhaled organic particles and circulating antibodies and
sensitized lymphocytes. In the acute stages of the disease, alveolar
walls and peripheral bronchioles are infiltrated with mononuclear
cells, vhich form noncascading giant and epithelioid cell, granulomata.
With progression of the disease (due to repeated or continuous allergen
exposure), pulmonary fibrosis, particularly involving the uE-oer lobes,
may develop. The disease is thought to be the result both of the
formation of immune complexes in antigen excess in alveolar walls and
bronchioles and of a reaction between inhaled allergen and sensitized
lymphocytes.
An increasing number of organic materials have been identified as
capable of causing hypersensitivity pneumonitis. Exposure to most of
these, such as Hicropolyspora faeni (the cause of farmer's lung), is
occupational. Two important causes of the disease are nonoccupational:
bird fancier's lung and ventilation pneumonitis. Bird fancier's lung
is caused by the inhalation of serum proteins in the feces of pigeons
and parakeets. The disease may develop in pigeon fanciers or in those
who keep parakeets in their homes. Ventilation pneumonitis is due to a
reaction to thermophilic actinomycetes growing in ventilation systems;
they have been shown to cause hypersensitivity pneumonitis both in
offices and in homes with ventilation systems contaminated by these
organisms. Thermophilic actinomycetes are not common in outdoor air,
but may be extremely abundant in interiors where organic material is
handled1* 1' S1 '* 1" 1,1 and are apparently common in domestic
interiors.7 14 Concentrations in barns and cotton mills can exceed
30,000/m^ of air," 11 11 " *' ** " l" whereas recoveries in
domestic interiors rarely exceed 3,000/m3.t#
Domestic sources of actinomycetes are less clearly identified.
Thermophilic actinoaycetes have been recovered from humidifier
VII-106
-------
fluid,1* ** *»-*• •• 11 * 1,1 *»• »*' air-conditioners,6 ** •• 14'
and an evaporative cooler." However, their presence in a humidifier
does not imply dispersion in the air,T ** and airborne taxa may
differ from those commonly recovered from humidifier fluid.1*
The pattern of symptoms in those affected is related primarily to
the circumstances of exposure to the causal allergen. Those with
intermittent exposure to high concentrations of allergens, as occurs in
pigeon fanciers, develop recurrent episodes of breathlessness
accompanied by flulike symptoms of malaise, headache, myalgia, and
fever. Measurements of lung function during such an acute episode show
a restrictive ventilatory defect with a decrease In gas transfer. In
the absence of further exposure to the causal allergen, symptoms
resolve over a period of 7-10 d, with improvement in lung-function
measurements and chest-roentgenogtam abnormalities over a month. With
further exposures, lung-function tests and radiographic abnormalities
can persist, and pulmonary fibrosis develop.
Those who have more continuous exposure to low concentrations of
allergen, such as those exposed to parakeet excreta in their homes,
often do not develop constitutional symptoms, but later, less
reversible stages of the disease with increasing exertional dyspnea.
The abnormalities of lung function are similar to those found in acute
disease: a restrictive ventilatory defect with impairment of gas
transfer. There may also be loss of volume of the upper lobes with
linear shadows and cystic change due to fibrosis.
A disease that is probably due to an allergic reaction in the
alveolar wall to contaminants of humidification systems, but which has
several important features that distinguish it from typical
hypersensitivity pneumonitis, has recently been described and called
"humidifier fever."iS 17 The particular contaminants responsible are
unknown, but may be amebae growing,in the water. Those affected have
recurrent episodes of flulike symptoms and fever that are often severe
enough to overshadow the associated breathlessness. Symptoms develop
4-6 h after the onset of exposure and resolve spontaneously, whether or
not exposure continuesj and they recur only on reexposure after an
absence of several days from exposure. Lung-function measurements
during an attack show a restrictive ventilatory defect with impairment
of gas transfer that improves over a period of days with the resolution
of symptoms, despite continuing exposure. Unlike hypersensitivity
pneumonitis, it is not accompanied by abnormalities on the chest
roentgenogram during the acute attack, and pulmonary fibrosis does not
occur, even in those who have had recurrent episodes of the disease for
several years. Precipitins to an extract of the humidifier water or of
the "jelly" growing in the humidifier are found in the serum of those
affected, but may also be found in the serum of ot*er exposed persons
who do not get the disease. Immunofluorescent antibodies to various
species of amebae, particularly Negleria grubeti and ftcanthamoebae,
have been found in the serum of those with precipitins to tue
humidifier water, but the relationship of these antibodies to disease
remains unclear.
Concentrations of protozoa in interior air have not been
sytematically reported; however, their occurrence indoors from both
VII-107
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external and intramural sources may be anticipated. Protozoa have been
recovered, In culture, from free air by several investigators, as
summarized by Schlichting, 117 although the indicated concentrations
have been well below those of pollens, algae, and fungal spores. Hind
scourins dry soil has been favored as a source of aizborne isolates,
although foams and such factors as sewage-processing may contribute
locally. 117
Indoor fluid collections—such as aquariums, humidifier coservoizs,
and physiotherapy pools—are among the sites of potential colonization
by protozoa. Recoveries of an ameba (Hartmannella castellanli) from
air in a pediatric respiratory-care facility may implicate similar
sources; however, many strains of the same species, as well as
Naegleria and Schizopyrenus, also were taken from outside air.7*
Suspicion has also been cast on protozoa as agents responsible foe
"humidifier fever" in office and factory workers.15 17 Some species
(i.e., Naegleria fowler and Acanthamoeba spp.) are known to cause
dangerous neurologic infections, although aerial transmission has not
been demonstrated.15
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71. Xang, B. study on cockroach antigen as a probable causative agent
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74. Kern, R. A. Asthma due to sensitization to a mushroom fly
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105. Moore, B. S., and J. S. Hyde. Characterization of breed-specific
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115. Peterson, J. E, Estimating air filtration into houses: An
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117. Popescu, I. G., E. Capetti, C. Galalaie, and I. Spiegler. Study
of atmospheric fungi in a big cereal silo over a period of one
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1975.
118. Prince, H. E., M. B. Morrow, and G. H. Meyer. Molds in
occupational environments as causative factors in inhalant
allergic diseases. A report of two cases. Ann. Allergy
22:688-692, 1964.
119. Raper, K. B., and D. I. Fennell. The genus Aspergillus.
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120. Refai, M., and A. Loot. Studies of mould contaminations of meat
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12:621-624, 1969.
121. Richards, M. Atmospheric mold spores in and out of doors. J.
Allergy 25:429-439, 1954.
122. Ripe, E. Mould allergy. I. An investigation of the airborne,
fungal spores in Stockholm, Sweden. Acta Allergol. 17:130-159,
1962.
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123. Samsffe-Jensen, T. Mould allergy. Sensitization by special
exposure illustrated by two cases of allergy to Cladosporiun
fulvum. Acta Allergol. 9:38-44, 1955.
124. Samson# R. A., and B. van der Lustgraaf. Aspergillus
penicilloides and Eurotium halophilicum in association with
house-dust mites. Mycopathologia 6-J: 13-16, 1978.
125. Schaffec, N., E. E. Seidmon, and S. Bruskin. The clinical
evaluation of air-borne and house dust fungi in New Jersey. J.
Allergy 24:348-354, 1953.
126. Schlichting, H. E., Jr. Ejection of microalgae into the air via
bursting bubbles. J. Allergy Clin. Immunol. 53:185-188, 1974.
127. Schlichting, H. E., Jr. The importance of airborne algae and
protozoa. J. Air Pollut. Control Assoc. 19:946-951, 1969.
128. Schlueter, D. P., J. N. Fink, and G. T. Hensley. wood-pulp
workers' disease: A hypersensitivity pneumonitis caused by
Alternaria. Ann. Intern. Med. 77:907-914, 1972.
129. Schwartz, M. Heredity in bronchial asthma. Acta Allergol. 5
(Suppl. II), 1952.
130. Seabury, J., B. Becker, and J. Salvaggio. Home humidifier
thermophilic actinomycete isolates. J. Allergy Clin. Immunol.
57:174-176, 1976.
131. Seabury, J., J. Salvaggio, H. Buechner, and V. G. Kundur.
Bagassosis. III. Isolation of thermophilic and mesophilic
actinoroycetes and fungi from moldy bagasse. Proc. Soc. Exp. Biol.
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132. Seabury, J., J. Salvaggio, J. Domer, J. Fink, and T. Kawai.
Characterization of thermophilic actinomycetes isolated from
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Immunol. 51-.161-173, 1973.
133. Segretain, G. Infection by fungi that ordinarily are saprophytes.
Pulmonary aspergillosis. Lab. Invest. Il:lu46-1052, 1962.
134. Sherman, H.,'and ~. Merksamer. Skin test reactions in
mold-sensitive patients in relation to presence of molds in their
homes. N.Y. State J. Med. 64:2533-2535, 1964.
135. Sidransky, H. Experimental studies with aspergillosis, pp.
165-176. In E. W. Chick, A. Balows, and M. Furcolow, Eds.
Opportunistic Fungal Infections. Proceedings of the Second
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Publishers, 1975.
136. Slnha, R. N., J. E. M. H. van Bronswijk, and H. A. H. Wallace.
House dust allergy* mites and their fungal associations. Can.
Med. Assoc. J. 103:300-301, 1970.
137. Slavin, X. G., and P. Winuenburger. Epidemiologic aspects o£
allergic aspergillosis. Ann. Allergy 38:215-218, 1977.
138. Solomon, W. R. Assessing fungus prevalence in domestic interiors.
J. Allergy Clin. Immunol. 56:235-242, 1975.
139. Solomon, W. R. Fungus aerosols arising from cold-mist vaporizers.
J. Allergy Clin. Immunol. 54:222-228, 1974.
140. Solomon, W. R., and H. P. Burg®. Aspergillus fumigatus levels in-
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141. Solomon, W. R., H. P. Burge, and J. R. Boise. Airborne
Aspergillus fumigatus levels outside and within a large clinical
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143. Spendlove, J. C. Penetration of structures by microbial aerosols.
Dev. Ind. Microbiol. 16:427-436, 1975.
144. Sreeramulu, T. Concentrations of fungus spores in the air inside
a cattle shed. Acta Allergol. 16:337-346, 1961.
145. Staib, F., T. Abel, S. K. Mishra, G, Grosser M. Fock'ing, and A.
blisse. Occurrence of Aspergillus fumigatus in West Berlin—
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comparative study of antigens of Aspergillus fumigatus isolates
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1978.
148. Stevenson, D. D., and K. P. Mathews. Occupational asthma
following inhalation of moth particles. J. Allergy 39:274-203,
1967.
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Turner-Warwick. Respiratory allergy to a factory humidifier
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VIII
EFFECTS OF INDOOR POLLUTION ON HUMAN WELFARE
"Indoors" is the place of escape from extremes of temperature,
humidity, and environmental conditions and from exposure to some
pollutants found in, the "outdoors." It is the place where rest,
relaxation, and the general welfare afforded by bodily comforts are
sought. It is known that attempts to reduce energy consumption in
buildings can affect the quality of indoor environments. This chapter
discusses some of the effects on human welfare—e.g., discomfort,
decreased productivity, soiling, corrosion, and maintenance and
housekeeping needs—caused by alterations in environmental control
systems.
Discomfort is the result of undesirable sensory stimuli, such as
noise, malodors, glare, and extremes of humidity and temperature.
These often invoke a human response, identified as "discomfort," that
is straightforward and physical and that may sometimes be relieved by
attenuation of the stimulus. However, mere attenuation of the sensory
stimulus sometimes does not suffice. Discomfort is a sensitive
indicator of the need for adjustments in environmental quality control.
The relationships between indoor pollution and productivity can be
evaluated only after one carefully defines productivity and determines
how it is to be assessed. Originaly, productivity was conceived simply
as quantity of output; but it has come to be addressed in terms of
economy—the cost per unit of production. This chapter discusses some
attempts to measure the effects of environmental quality, with
productivity as a tool.
Indoor air pollution is a source of soiling and contributes to the
deterioration and corrosion of equipment, furnishings, and appliances.
Soiling increases needs for maintenance and housekeeping and for some
equipment in the ventilation system.
RELATIONSHIPS BETWEEN SOCIOECONOMIC STATUS AND INDOOR POLLUTION
The relationships between housing characteristics, and the health of
the occupants among the various socioeconomic groups are not well
known. The available information, although limited, is important if we
VIII-1
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are to understand and identify the problems involved and if we are to
learn the relationships between housing types, housing quality, indoor
environmental quality, and pollutant types, on the one hand, and the
health and welfare of the people in the several socioeconomic groups,
especially those in the lover groups, on the other hand.
h comprehensive treatment of socioeconomic status (SES) and indoor
air pollution may be important to the formulation of control strategies
(local, state, or federal) in matters that influence indoor pollution,
such as energy-conservation assistance programs and low-income and
rent-subsidy programs.
Housing characteristics are related to social status or income
level.'® 51 47 Status and income often have been shewn to be related
to health and probably constitute an intervening variable in the
relationship between selected housing characteristics and health. 14 51
The role of housing itself in determining health is still
unclear.'1 " " 47 49 Crowding indoors is thought to be an
important contributor to the spread of infectious diseases and a
potential source of physiologic stress." 51 47 49 A,substantially
higher proportion of persons in low-income groups have chronic health
conditions that limit their activities * * ana keep them indoors.
Some characteristics of housing constitute definite risks to
health—e.g., carbon monoxide poisoning from faulty venting of
space-heating systems72 and lead poisoning from paints.*0 The two
mentioned are also related to low-income houses, which often have
greater rates of air infiltration and, because they are close to
sources of pollution, transport pollution more freely from outdoors to
indoors.'i 5* Spivey and Radford" found that a high proportion of
gas stove? ano gas space-heaters (60% in lower-SES homes in east
Baltimore) had higher indoor than outdoor concentrations of carbon
monoxide (8-8.9 ppm versus 5.5-6.1 ppm). In two sets of homes studied,
the amount of passive smoking did not appear to be related to any
differences observed in indoor carbon monoxide concentrations. In over
70% of these homes, the lead content in dust and paint samples exceeded
currently recommended standards. Blood lead contents are lower in
persons who live in SES-equivalent houses with air-conditionirig than
without.20 Binder et al.12 found that indoor respirable-particle
concentrations were higher in homes with higher ratios of persons to
room volume.
The following tentative conclusions can be drawn: Homes with
controlled ventilation systems, air filtration, good maintenance, and
properly working appliances have lower concentrations of indoor
pollutants. That implies that the middle and upper socioeconomic
groups are at lower risk. However, there are sources of pollution
other than those mentioned in upper-income houses, specifically, newer
and more carpets, curtains, and furniture. Low-income housing is more
likely to have improper ventilation, poor maintenance, defective
appliances (such as improperly operating stoves and space-heaters), and
lead^based paint—all of which contribute to higher indoor
concentrations of pollutants.10 51 54 40 Furthermore, persons in the
low-income groups are more likely to live in mobile homes or
apartments,'7 which frequently are crowded (high ratio of persons to
VIII-2
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volume)." Mobile homes generally are very airtight, and crowding
can result in high concentrations of indoor pollutants.1 * ••
Recreational vans and trailers have many of the physical
characteristics of mobile homes and can have similar pollution
problems. Those who can afford to "tighten" their conventional homes
for energy conservation may also have higher indoor concentrations of
some pollutants, although one would expect an eventual balance between
"tightening" and proper ventilation in those homes.
HUMAN DISCOMFORT '
The incentive to control the indoor environment is derived as much
from consideration of human comfort as from consideration of health.
Discomfort provides an immediate incentive to control the quality of
the indoor environment. Undesirable sensory signals (e.g., noise,
glare, and cold) register as discomfort. These signals have
straightforward physical correlates (e.g., sound pressure; contrast
ratio, and temperature) with the need for controls, such as the
installation of sound-absorbing tiles. A person annoyed initially by
the loud conversation of co-workers may eventually become annoyed even
by whispered exhanges; thus, mere attentuation of noise may not
suffice. A person annoyed frequently by sidestream cigarette smoke
from the person at the next desk may eventually become angered by the
slightest trace of tobacco-smoke odor. Such time-dependent changes in
sensitivity show a cognitive contribution to discomfort. Some persons
can become annoyed merely by the information carried by a stimulus, and
this reaction can be as important as a reaction to the stimulus itself.
Whether discomfort is caused by the intensity of stimulation or by
the conditioned response resulting from sensitization, the questions
arise: Will avoidance or elimination of discomfort ensure a reasonably
healthful indoor climate? Does endurance of discomfort take a
psychologic or physiologic toll?
Our senses are remarkably adaptive. Therefore, they do not provide
infallible sensory signals about the safety of the environment, owing
to their inability to register some types of energy or potential
stimuli. For instance, a person may view a solar eclipse without
knowledge that the ultraviolet rays, unregistered by the photo-
receptors, may damage the eye. A person may bask in the warmth of the
summer sun without awareness that ultraviolet rays, poorly registered
in this case by cutaneous receptors, may cause serious, even lethal
burns. Similarly, a person may eat a bacteria-laden, although
delicious, meal without any sensory warning of the ptomaine toxins
present. The sense of smell also fails to register some harmful
stimuli, such as carbon monoxide. With only a limited number of
notable exceptions, however, the absence of annoying stimuli indoors
may be misleading, but generally does signify safe conditions of
occupancy.
Regarding the endurance of discomfort, possible long-term effects
include irritability, depression, ¦inability to concentrate, anxiety,
indigestion, headaches, back pain, and insomnia.17 Short-term
VIII-3
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effects of discomfort are often rather specific to a particular
modality. Hence, malodors may cause symptoms of digestive upset, poor
lighting may cause headaches, and cold drafts may cause muscle
stiffness. Objective verification of direct causes of these various
symptoms is difficult. For this reauon, the symptoms, even when
severe, fail to qualify as adverse health effects.
This section briefly discusses some of the indoor-polution aspects
of discomfort.
MALODORS
The olfactory senses signal the presence of some harmful airborne
stimuli, but sometimes they fail to do so, and there are frequent
"false aiarms:" As mentioned in Chapter IV, people have historically
avoided bad-smelling, air for fear that it signaled illness-causing
conditions, in the nineteenth century, the criteria for ventilation
commonly arose from the notion that odorous air contained harmful
ingredients Known variously as crowd poison, morbific matter, and
anthropotoxin. 18 For instance, Russell stated in The Atmosphere in
Relation to Human Life and Health:sJ
Organic matter is given off from the lungs and skin, of
which neither the exact amount nor the composition has been
hitherto ascertained. Their quantity is very small, but of
its importance there can be no doubt. . . . Since this organic
matter has been proved to be highly poisonous, even apart from
carbon dioxide and vapor, we may safely infer that much of the
mischief resulting from the inspiration of rebreathed air is
due to.the special poisons exhaled by the body.
In the absence of instrumentation to detect the presence of small
amounts of odorous organic vapors, the nose remains a sensitive
indicator. Surprisingly, even today there are no good rules for laymen
or scientists to relate perceived odor quality to toxicity. Some
odorous signals are used to warn about toxic hazards (e.g., mercaptans
are used in natural gas to signal leaks). We may know from experience
that some foul-smelling living spaces pose no overt danger, but people'
will still avoid such places. We may argue that this avoidance is
derived from mere discomfort, but occupants may fail to see the
situation in such benign terms.
In the early twentieth century, the New York State Commission on
Ventilation performed a set of experiments regarding the effects of
occupancy odor on human comfort and performance.** In a popular
synopsis of this 8-yr effort, Winslow70 stated:
We may summarize our discussion of the physiology of
ventilation as follows: The chemical vitiation of the air of
an occupied room (unless poisons or dusts from industrial
processes or defective heating appliances are involved) is of
relatively slight importance. The organic substances present.
VIII-4
-------
' manifest as body odors, may exert a depressing effect upon
inclination to work and upon appetits; therefore, occupied
rooms should be free from body odors which are obvious to
anyone entering from without. (Such odors are never perceived
by those who have been continuously in the room while they
have been accumulating.) Objectionable effects of this sort
have only been demonstrated, however, with a carbon dioxide
content of over .2 per cent, which would correspond to an air
change of less than 6 cubic feet per person per minute.
During the 1930s, Winslow and Herrington71 demonstrated that "dust
odor" similar to that from a heating system could also depress appetite.
Winslow implied that the olfactory sense generally adapts to
prevailing odorous stimulation in such a way as to reduce discomfort.
Similarly, Cain reported that a temporary reduction in olfactory
sensitivity, perhaps in conjunction with affective habituation,
presumably explains why workers in some malodorous industries
eventually find the odorous atmosphere unobjectionable. 17 In
contrast, people who live near malodorous sources of pollution seem to
experience adverse olfactory reactions of constant or even increasing
severity. For example, residents exposed frequently to malodorous
emission of factories complained of chronic headaches, nausea,
coughing, .disturbance of sleep, and loss of appetite.*4 Those
' adverse reactions, se
-------
offices, schools, and hospitals. The context can have a strong bearing
on the degree of annoyance. Nemecek and Grandjoan*1 surveyed a large
office and found that most of the employees were disturbed by noise
that w»3 considered well within professional design standards. The
"noise" came from conversations, and it was content, rather than,
intensity, that was the disturbing attribute.
Experiments in both human beings and animals have shown that
stressful effects from nondeafening noise arise without respect to the
"meaning" of the auditory stimulation.41 Physical attributes that
seem particularly relevant to annoyance 1 include intensity,
concentration of energy within high frequencies, temporal and spectral
complexity, duration, and the suddenness of sounds.'* Table VIII-1
shows results of a survey made to determine the importance of various
physical and perceived attributes of annoying sounds." The
respondents judged loudness the most important attribute, witn
suddenness next in line. The next three most important attributes
comprised cognitive features (sound is man-made, sound cannot be turned
off, sound is unnecessary). The preeminence of loudness in the
determination of annoyance has led to recommendations, such,as those in
Table VII1-2, for tolerable maximal loudness in various types of
rooms." The loudness values listed here refer to continuous noise
in the period between 7 a.m. and 10 p.m.
Both human and animal laboratory experiments have shown hormonal
effects of noxious, although nondeafening, noise exposure. Even
exposures of about 70 dB can increase the output of adrenal
corticosteroids.* l' Sound intensity this low can also cause
constriction, of peripheral blood vessels. '• Such changes, and other
physiologic manifestations, usually fail to outlast the stimulus, but
do cause concern that noise might eventually lead to more chronic
symptoms of stress or affect sleep. Frequent interruption of sleep or
alteration in the normal progression of sleep patterns may be thought
to jeopardize physical or mental health eventually. Fortunately,
adaptive alterations in the pattern of sleep seem to minimize most
short-term consequences of disruption by noise.'*'
In addition to physiologic manifestations, noise exposure produces
adverse behavioral manifestations. Experimental exposure to noise
diminished the quality of interpersonal contact,11 increased
aggressiveness,17 and impaired willingness to help persons in
need."1 Loud noise, particularly intermittent noise, may alter
productivity. The effect may be facilitative, rather than inhibitory;
that has led to the speculation that noise may interact' with other
environmental factors and ~.ith personal factors to achieve a aegree of
arousal desirable for work.1*
TEMPERATURE
There is little scientific information on the connection between
thermal conditions and productivity."1 In laboratory experiments at
65-85°F (18-298C), productivity often reached a peak at nonpreferred
temperatures.71 In an apparel factory, productivity (i.e.,
VIII-6
-------
TABLE.VIIT-l
Contributions of Various Characteristics of
Sound Characteristic
Steady high-pitched sounds
Steady low-pitched sounds
Intermittent high-pitched sounds
Intermittent' low-pitched sounds
Loudness ol sounds
Suddenness of sounds
Feeling that a sound cannot be turned off
Feeling that a sound is unnecessary
Feeling that a sound con.es from a source
of little benefit
Sounds that clash (unharraonious)
Sounds that catch one's attention at a
distance and then get louder and louder
Sound is man-made
Sound to Annoyance3
Relative Annoyance
(Scale Value)
3.94
3.66
4.54
3.81
6.46
5.80
5.55
5.38
4.81
4.43
5.23
5.65
aData from Dunn.^
VIII-7
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TABLE VIII-2
Suggested Maximal Tolerable intensities In Various Indoor Locations
for More or Less Continuous Noise between 7 a.m. and 10 p.m.3
Intensity,
Type of Space . ¦ dB(A)
Broadcast studio 28
.Concert hall 28
Legitimate theater (500 seats, no amplification) 33
Music room 35
Schoolroom (no amplification} 35
Apartments, hotel 38 '
Assembly hall 38
Home 40
Motion-pict'.ire theater 40
Hospital 40
Church 40
Courtroom 40
Library 40
Office
Executive 35
Secretarial (mostly typing) 50
Drafting 45
Meeting room (sound amplification) '45
Retail store ,47
Restaurant 55
aData from Kryte*."^
VTII-8
-------
piecework) varied little, if at 3ll, with thermal conditions (note#
however, that workers were paid by the piece).** When giveni the
opportunity to express an opinicn, people will be consistent in their
preference regarding environmental conditions. The "comfort vote" has
literal meaning in research on thermal acceptability. It refers ,to a
subjective rating on a seven-po:.nt scale of comfort, on which the
midpoint signifies thermal neutrality. A large body of research has
made it possible to determine, 'ry means of "comfort equations," the
combinations of several factors.—notably air temperature, humidity,'
radiant temperature, air velocity, degree of activity, and type of
clothing—that will minimize discomfort. The range of acceptable
combinations of environment'1 conditions is known as the "comfort zone."
Figure VIII-1 depicts summer and winter comfort zones adopted in
1981 by The American Society ol Heating, Refrigerating, and
Air-Conditioning Engineers (ASl;RAE).1 10 The comfort zones show the
relationship of comfort to temperature and humidity during "light"
activity. At least 80% of occupants should feel comfortable—no'more
than slightly warm or slightly cool—in these zones. The comfort zone
is different between summer and winter, because people wear more
clothing during the winter. The thermal resistance of a clothing
ensemble can be measured precisely in "clo" units. Table'VIII-3 offers
an example of how a change in clothing will be reflected quantitatively
in clo-values and optimal operative temperatures. Operative
temperature is determined on the basis of air temperature and average
radiant temperature. In an interior zone with only a slight radiant
component, the operative temperature approximately equals dry-bulb
temperature.
Insulation from clothing and degree of activity interact in
determining acceptable temperature. The ASHRAE standard therefore
offers an equation to convert acceptable operative temperature (°C) for
sedentary occupancy (1.2 mets) to that for more active occupancy (e.g.,
housework at 2 mets, garage work at 3 mets); *o(active) =
tQ(sedentary) ~ 3(1 + cl°)(met " 1*1)' wh®re fc0 represents
operative temperature. In addition to steady-state features of the
thermal environment, the standard considers temporal nonuniformities
(e.g., temperature cycling) and spatial nonuniformities (e.g., verticail
temperature differences). Some limited nonuniformities, such as
monotonic temperature drifts, may prove both economical and
acceptable.11
Conditions for thermal comfort seem to vary little, if at all, with
such factors as geographic location, sex, body build, ethnic
background, and even age.2" The effects of aging seem to merit some
special consideration. Basal metabolic rate decreases progressively
with age, but, according to Fanger,1'' evaporative heat loss does, ,
also. The two changes seem to offset each other, although the elderly
spend much more time than the young in sedentary activities.
Furthermore, with the lower temperatures now common indoors during
winter, the elderly seem to have a narrower temperature range over
which they can increase their thermal resistance.5' Because of
sensory adaptation, a sedentary old person may fail to notice the
symptoms of impending hypothermia until it becomes severe. Adequate
VIII-9
-------
Ill
e
3
i-
<
«C
Id
0.
2
in
O
CL
*
U1
Q
_ 0.010
0.015
H
<
e
>
t-
.005
3
I
0.0
70 80
OPERATIVE TEMPERATURE
FIGURE VIII-1 Acceptable ranges of operative temperature and humidity
for persons wearing typical summer clothing and typical winter clothing.
These "comfort zones" assume that occupants are engaged in only light
activity. Reprinted with permission from American Society of Heating,
Refrigerating, and Air-Conditioning Engineers.
VIII-10
-------
TABLE VIII-3
Temperatures for Thermal Acceptability (Comfort) of Sedentary or Slightly
Active Persons (<1>2 nets) at 502 Relative Humidity3
Season Typical Clothing
Winter Heavy slacks, long-sleeved
shirt, sweater
Summer Light slacks, short-
sleeved shirt
clo
Optimal
Operative
Temperature
°C 2E
71
0.9 21.7
0.5 24.4
Operative Temperature
for 80% Thermal
Acceptability0
.""C *F
20-23.6
68-74.5
76 22.8-26.1 73-79
Minimal
0.05 27.2
81 26-29
79-84
aData from American Society of Heating, Refrigerating, and Air-Conditioning
Engineers. Other than clothing, there are no seasonal or sex variations for the
temperatures listed. For infants, some elderly persons, and physically disabled
persons, the lower temperature limits should be avoided, met = measure of energy
production per unit of surface area of a seated person at rest. 1 met «¦ 58.2 W/m^
or 18.4 Btu/h.ft . Surface area of average man = 1.8 m (19 ft ).
^Indoor operative temperature is a weighted mean of average air and average
radiant temperatures.
cSlow air movement (^0.15 m/s =¦ 30 ft/min).
J o
clo = measure of thermal resistance of a clothing ensemble: 1 clo = 0.155 m »K/W
or 0.88 ft •h«°F/Btn-
VIII-11
-------
clothing is the best precaution against cold distress. In the United
States, people were not energy-conscous until rather recently, and both
young and elderly seem to need more education regarding the way to
match clothing to the thermal load of the environment. .
INTERRELATIONSHIPS OF ENVIRONMENTAL FACTORS
Other prominent factors in the indoor environment include lighting,
furnishings, and che size and configuration of the space. Control of
type and quality of illumination is often an aspect of design.
Professional and aesthetic preferences can govern the choice of
intensity, placement of sources, hue, and degree of contrast of
lighting. These matters often receive much attention in the
workplace. The question of whether light, temperature, and sound are
optimal should be viewed in terms of such needs as productivity and
accident prevention. In the home, the considerations are different
from those of the workplace—questions of efficiency and productivity
place few constraints on the physical environment at home, and few
persons obtain professional advice regarding ways to maximize comfort
and minimize hazards in the home.
Proshansky and colleagues10 stated that "behavior in relation to
a physical setting is dynamically organized: a change in any component
of the setting has varying degress of effects,on all other components
in that setting, thereby changing the characteristic behavior pattern
of the setting as a whole." That conclusion may seem obvious; however,
the need to consider it arises in experiments where a source of
discomfort is expected to decrease productivity, but increases it
instead. Such studies may often fail to give precise answers regarding
the importance of one or another environmental factor, but they can
help to heighten our awareness. Awareness is a powerful tool in
recognizing and dealing with the complex interplay of safety, health,
comfort, and productivity indoors.
SUMMARY
A person's perception of discomfort can provide a useful indicator
of possible adverse effects of environmental agents. Discomfort gives
immediate incentive to avoid or to correct environmental deficiencies.
There is little information regarding whether long-term exposure to
sources of discomfort will eventually cause adverse health effects.
This question has no global answer. The discomfort caused by a
thermally variable environment may lead to physiologically useful
acclimatization and to behavioral strategies that diminish the impact
of environmental challenges, in contrast, exposure to moderately
intense noise—«.g., 80 dB(A)—leads to no such physiologic
accommodation in the auditory system and may eventually cause hearing
loss in susceptible persons. As an added complication, low-intensity
sound may cause considerable discomfort and even intense autonomic
reactions in persons sensitized to the "meaning" of the sound. The
VIII-12
-------
long-term deleterious effects of continuous activation of the autonomic
nervous system are not known, and efforts to measure such symptoms as
nausea, headaches, and dizziness and learn their clinical significance
should be encouraged.
Some airborne chemical contaminants cause discomfort via
stimulation of the olfactory sense or the common chemical sense. This
probably serves a useful purpose, inasmuch as people will often avoid
'bad;-8melling atmospheres, regardless of any known toxic properties.
The discomfort can also lead to closer investigation of the source of
malodors.
A generic relationship between discomfort and productivity has
eluded specification. It seems possible at best to state only that the
point of maximal productivity may not coincide with the point of '
minimal discomfort, but will hardiy fall at the point of maximal
discomfort. Comfort is derived from the harmonious interactions of
many things, including physical factors, context, motivation, social
factors, attitudes, and skill at the task at hand. Therefore, it is
related to all aspects of a person's behavior and may prove just as
difficult to predict. Nevertheless, appropriate attention to the
maintenance of proper lighting, air, and thermal conditions increases
the diversity of activities and the numbers of 'people that can be
accommodated in comfort.
RECOMMENDATIONS'
• Subtle forms of discomfort often arise from the use of
manufactured products, building materials, and consumer products.
Therefore, identification of the products leading to'irritation and of
its duration1can be used by manufacturers in the design of safer
products.
• The relationships of subjective complaints of discomfort to
associated symptoms—such as.headaches, nausea, and other health
effects—should be studied in persons of different ages and in
different categories of other kinds, such as socioeconomic status.
Objective data from these studies could be useful in targeting the
design characteristics of buildings. .
• For each type of discomfort ie.g., noise-induced discomfort
and odor-induced discomfort), there is a need for research on how to
relate stimulation to discomfort.
DECREASED PRODUCTIVITY
Direct relationships between indoor pollution and decreased
productivity can be evaluated only if one carefully defines
"productivity" and how it is to be assessed. Productivity was
originally conceived of as simply the quantity of output; Sumerian
documents dating to 5000 B.C. have been identified as organizational
records of productivity. Although employee counseling appears in
Egyptian records of around 4000 B.C., productivity at the beginning of
VIII-13
-------
the twentieth century was still viewed as essentially the output of
robot-like workmen; the production line of the 1920s was simply a way
of organizing the.work to increase output. As the numbers of workers
rose and.hourly wages and investment in equipment increased,
productivity began to be measured in economic terms, such as cost per
unit of production. More attention was later given to devising work
methods for decreasing cost3 per unit of production. ThiB focus on
increasing productivity while reducing costs led, almost inevitably, to
a degradation of pioduct quality. Therefore, quality became a
consideration in measuring productivity, and again the definition of
"productivity" had to be revised.
DEFINITION OF "PRODUCTIVITY"
There is national recognition that our resources are not infinite,
and this recognition has led to reexamination of the earlier
definitions of "productivity." The demands for increasing productivity
have, had a serious impact on the physical and mental well-being of both
the workforce and the consumers of its production, to say nothing of
the impact on "quality of life" in our society. Thus, the measure of
productivity was expanded to consider the "efficiency of the output."
Productivity is currently addressed in terms of cost effectiveness—
"Does it work?"—with considerations of timeliness, effects obtained or
results achieved, and such humanistic elements as manner of performance
and methods of achieving the results. The periods of redefinition of
"productivity," at the national level, can be dated by Presidencies.
The simple concept that productivity equaled output w?.s displaced,
during the Franklin D. Roosevelt era, by consideration of cost per unit
of production. This idea was displaced, during and after the Kennedy
administration, by consideration of the effectiveness of policies to
improve productivity. Over roughly the last 50 yr, the definition of
"productivity" has used a complex of interacting entities and
characteristics, including quantity and quality of product, monetary
cost, timeliness, and human costs. Human costs include those
engendered by the manner of performance, the method of achieving the
results, and the actual benefits, as compared with the social costs.
As long as ;>eople are involved in the definition, productivity can be
adversely affected by pollution (defined as the presence of any
unwanted or unnecessary element in the environment).
PRODUCTIVITY IN INDUSTRIAL ENVIRONMENTS
Pollution will affect productivity at two distinct levels: its
physical effects on the means of production, or on the product itself,
which are directly related to the quality of the product; and the
effects on the health of the worker. Air contaminants can be
categorized into particulate and gaseous, organic and inorganic,
visible and invisible, subraicroscopic and microscopic, or toxic and
harmless.
VIII-14
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With even "clean," country air containing particles bigger than 0.3
wo at over 106/ft and atmospheric dust loads of 20-200
tons/mi^ per month in cities, the physical effects of pollution can
be substantial. Solid particulate contaminants accumulate on surfaces,
contaminate food products, and discolor walls, ceilings, floors, and
furnishings; nonparticulate contaminants (vapors and gases) also affect
food products, discolor surfaces and furnishings, and cause
deterioration of fabrics and finishes. When one considers that
unnecessary cleaning, repairs, and painting and untimely replacement
are nonproductive, one can see that the physical effects of pollution
are a drain on productivity. The' loss of light to dirt on windows, the
role of dirty car windows in.causing accidents, the inefficiencies of
dir.ty'cooling coils or heating elements, the erosion of building
structures, and. the diversion of resources (both money and time)
because of these problems all contribute to a lowering of
productivity. Indeed, tobacco smoke and cooking and body odors form
the primary requirement for ventilation in nonindustrial occupied
spaces. About 17% of the national energy use is,devoted to moving,'
heating, or cooling air for ventilation; such pollutants can be
considered a major factor in limiting the energy availaDle for
productivity.
Even though many contaminant effects are related to specific
products.or processes, their effects on the health of workers are not,
and they can be dealt with generically. As opposed to the physical,
classification of contaminants mentioned above, a spectrum of health
effects of pollutants can be suggested; lethal-disabling-sickenina-
irritating-annoying-distracting-discomforting.
Although the lethal end of this spectrum has captured more
attention (e.g., consider lead poisoning and asbestos exposure), in the
present social climate, where productivity depends more on what people
will produce than on what they can produce, the greatest effects or.
productivity will probably be incurred toward the discomfort end of the
spectrum. Obviously, premature death or chronic disability removes the
individual producer. But even a slight increase in illness' or malaise
can reduce productivity, by absenteeism or by "taking it easy" for a few
days. Indeed, even momentary distraction, discomfort, annoyance, or
physical irritation will reduce the quantity or quality of production.
In a 1979 NIOSH pilot study in industrial plants in Oregon and
Washington, workers were examined for. occupational diseases and other
conditions. Hearing loss (noise pollution?) was thr> f.oat frequent
(28%) , and skin conditions were next (18%), followed by lower
respiratory conditions (14%), toxic jr.d low-grade toxic effects (14%),
upper respiratory conditions (11%), and eye conditions (9%).41 No
such data exist for nonindustrial environments, but, if one considers
today's nonindustrial and social environments (discos, lounges, rock
concerts, radios, and record-players and their sound intensities), it
seems probable that decrements in hearing due to "noise pollution"
represent one of the leading correlates of productivity losses.
Although the incidences .of the other health effects mentioned above may
differ in a nonindustrial setting, they are all likely to occur.
VIII-15
-------
The Impact on productivity from pollutants that are simply
annoying, distracting, or discomforting (temperature, odor, and
soiling) has been largely Ignored until recently. However, insight
into their anticipated effects can be gained by examination of the
tables of "relaxation allowances" established to develop production
standards for jobs or of "environmental, differential-pay pLans"
developed to provide extra compensation for putting up with a variety
of undesirable conditions. Allowances of formal rest breaks and pay
differentials, based prifnarily on physical strain, began to be common
around 1950. These allowances have expanded) they were based
increasingly on psychologic factors in tlie 1960s and on environmental
factors in the 1970s. Some rest allowance seems appropriate to lessen
the abuse of the worker, but growing public concern over environmental
factors may have led to increases in rest' allowances and pay
differentials. These provide documentation of the costs of the adverse
effects of environmental pollution better than anything else available.
The relaxation allowances consider four elements. A standard 10%
time break, 18 min every 3 h, is considered adequate for personal
needs, such as a trip to the r?st room or a coffee break, although in
practice it tends to be more generous in most industrial settings. A
second set of relaxation allowances are oased on such physiologic
factors as energy demands', postures, body motions, and restrictive
protective clothing; a third is based o-.i psychologic factors associated
with timing, monotony, and the required concentration (diligence). A
fourth deals with environmental factors, such as thermal quality,
humidity, other air pollution, noise, dirt, and vibration.
Williams45 suggested that relaxation allowances ti.e., percent of
productive time lost) be determined as a function of environmental
conditions, as follows:
1. Thermal and atmospheric conditions:
Consider whether, despite or in the absence of protective clothing
or equipment, and extractors or ^ir-conditioning equipment, the air
conditions in terms of temperature and purity are such that
additional demands are made when performing the work; air
conditions are defined as:
A. Adequate ventilation and circulation with formal climatic
humidity.
B. Inadequate ventilation and circulation with non-standard
climatic conditions causing some discomfort.
C. Very poor ventilation and circulation. Fumes, dust,
steam, causing irritation to eyes, skin, nose, throat.
VIII-16
-------
Temperature
Air Condition
•P °C ABC
'relaxation allowance"
55" to 75°
13° to
24°
0«
0 to
5%
5 to
10%
76° to 100°
24° to
38°
1 to
10%
5 to
15%
10 to
20%
55° to 30°
13° to
-1°
1 to
10%
5 to
15% '
10 to
20%
Below 30°
-1°C
•
10 to 20%
20
to 25%
20
to 30%
2. Physical conditions, including noise.
Consider the general physical conditions of the environment in
relation to the work being performed and the degree of discomfort
caused by dirt, oil, grease or water and other liquids, ice,
chemicals, etc. Consider also whether noise is irritating by '
irregularity, or uncomfortable pitch or volume.
A. Clean, bright, dry surroundings.
Normal "machine" and human noise.
B. Dirty, wet, greasy and contaminated surroundings
C. Uncomfortable noise
D. Combination of several factors
In an effort to check the allowances, some 16 establisiMnents and
145 different jobs, including about 6% female workers, were examined.
In general, the findings supported the relaxation-allowance approach.
The allowances tor these environmental factors are obviously only
suggestions. Therefore, it is doubtful whether additional research
would provide any reliable refinement of the productivity losses due to
environmental factors, because such psychologic factors as motivation,
leadership, expectation, and need (and their interactions) are as
important as the environmental factors in determining productivity.
In the environmental pay-differential approach. Federal Personnel
Manual letter 532-17 established specific pay differentials for
exposure after November, 1970, to "various degrees of hazards, physical
hardships and working conditions of an unusual nature," as follows:
Dirty Work: Performing work which subjects the employee **
to soil of body or clothing: a) beyond that normally expected in
performing the duties of the classification; and b) where not
adequately alleviated by mechanical equipment or protective devices
. . .; or c) when their use results in an unusual degree of
discomfort.
Cold or Hot Work: At or below 32°F or above 110°F 4%
" rking with or near:
0%
0 to 3%
0 to 4%
0 to 8%
VIII-17
-------
A. Poisons (Toxic Chemicals)
High hazard
Low hazard
B. Micro-Organisms - High hazard
High hazard
Low hazard
Although these pay differentials are not directly relatable to
productivity decrements, the increases in direct costs of protection
are explicit, and productivity decrements are therefore also explicit;
hence productivity losses can be inferred. However, the basis for such
pay differentials is at least as much political as factual; additional
research along these lines is not likely to be very informative.
Determining productivity losses caused by pollution is extremely
complex. Even with careful definitions and measurement, it appears
unlikely that any simple cause-effect correlations can be established
that would not be destroyed by alterations in motivation, leadership,
expectation, and need.
PRODUCTIVITY IN NONINDUSTRIAL ENVIRONMENTS
These very limited considerations of interaction between air
quality and productivity can be defined in terms of units of
production, percentage of rejects, or costs per unit of salable
product. Models have been developed to show the influence of heat
exposure on productivity,• but, as with the comfort models, there has
not been much work on validating them. Thus, the models provide only a
theoretical prediction of reductions in work capacity. Few studies
have been carried out on the causes of productivity decreases in
industry, and even fewer in institutional settings. The American
Society of Heating, Refrigerating and Air-conditioning Engineers
(ASHRAE) has supported studies of the potential benefits of
air-conditioning in schools.** Air-conditioned classrooms and
libraries were heavily preferred (by about 95%), but it could be
inferred that air-conditioned schools attract better teachers and that
better teachers get better results. Similarly ambiguous results have
attended most of the numerous ASHRAE studies on air-conditioning
criteria.1 The difficulties rest in part with the variability of
actual environmental conditions, as distinct from those supposedly
maintained by the control systems, and 'in part with the difficulty
(suggested by Wyon7*) of defining the criteria for such environmental
qualities as "comfort" and air quality, as distinct from the criteria
for performance.
There has been growing recognition of the difficulties in
demonstrating linkages between environmental quality and productivity,
and the pace of research in this subject appears to have slackened in
the last few years. Concerns about productivity have been focused more
and more on workplace layout and worker motivation; that is probably
appropriate, because they have direct and tangible impacts on
productivity. The most tangible effects of air quality on productivity
VII3-18
8%
4%
8«
4*
-------
and quality of life are the. adverse effects on health and longevity;
even so, experimental confounding easily blurs any direct linkages.
E.g., when the U.S. Amy introduced its "MUST" field hospital, which,
used air-conditioning, in Vietnam, patient survival ant? hospitalization
time were ciearly improved, but argument arose as to whether the
improvements were caused by air-conditioning or by staffing.
SOILING, CORBOSIOH, MAIOTSNAMCE. AMD HOUSEKEEPING
Indoor air pollution is a source of soiling and contributes to the
deterioration and corrosion of equipment', furnishings, and appliances ,
Changes in ventilation, such as a decrease in the amount of outside air
used in ventilation to save energy or an increase to accomplish the
same end by making greater use of natural ventilation during mild
'weather, can affect the rates of soiling and deterioration. Even.,if
indoor pollutants do not adversely affect occupants or the rate of
soiling, deterioration, or corrosion, they increase requirements for
housekeeping and associated environmental control systems to maintain
the value of materials and property.
PAjyriCLg DEPOSITION
Deposition of dust particles on .walls and other surfaces is the
most common cause of soiling. The number and surface and mass
relationships of particles are important in soiling. A 5-wa-diaraeter
spherical particle has 1,000 times the mass of a 0.5-yro particle of
the same material, but only 100 times the surface area. Thus, it is
the submicrometer particles that have greater soiling potential,
although, the relationship between particle size, optical
characteristics, and soiling is complex. However, larger particles
contribute more to abrasion, and'lint can foul equipment. Mechanical
heating, cooling, and ventilating systems commonly include air filters
to remove lint and larger particles. In some manufacturing operations,
such as production of microelectronic circuits,7 it is essential to
have' very-high-efficiency filtration for removal of submicrometer
particles.' The average home or place of business does not approach
these high standards of air cleanliness, although an increasing number
of residences are using electronic air-cleaners capable of removing
submicrometer particles.
Larger particles settle faster than smaller ones. Gravity
sedimentation is an important mode of deposition, but it may be
comparatively unimportant in deposition of very small airborne
particles. Figure VIII-2 is a plot of Stokes diameter of a particle as
a function of time required to settle 1 i in air. Settling times ate
plotted for particles with densities of 1 and 2 g/cm^. Water and oil"
droplets have densities of about 1 g/cm^. Figure VIII-2 is a
somewhat idealized representation, but it permits a visual estimate of
the relative sedimentation rates of large and small particles.
Particles larger than .5 m in Stokes diameter settle in a
VIII-19
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TIME, h
FIGURE VIII-2 Particle diameter (d) and density (pp) 33 a function,
of time required to settle 1 m in air, according to Stokes's law.
VIII—20
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comparatively short time; particles smaller than 1 10 may remain
suspended for hours, unless they become attached to other particles,
walls, or surfaces. Davies has reviewed deposition from moving
aerosols.11
Electrostatic and thermal precipitation are two important
mechanisms by which particles are deposited. Penney and Ziesse*7
have measured the mobilities of airborne dust particles under the
influence of thermal and electrostatic gradients and have estimated an
average effective thermal mobility of 2.4 x 10~® m^/'C*s and an
effeccive electric mobility of about 11 x 10~® m^/V*s. These
values can vary widely for different dust particles, but they are
useful approximations for the design of dust-collecting equipment.
Penney andziesse also noted that an electrostatic precipitator that
does not capture all particles causes more soiling than an air-cleaner
o,f the same efficiency that does not charge particles. Apparently, the
particles become electrically charged, and that causes, them to attach
to surfaces more' readily. Thus, it is important that the precipitator
be designed for maximal capture.
The force of attraction between two molecules (London-Van der waals
force), varies as the inverse of the 7th power of the distance between
them" and plays a role in interparticle adhesion or adhesion to
surfaces. The electrostatic attraction of particles to surfaces is
very strong at distances of a few angstroms, but diminishes rapidly
with increasing distance. From the standpoint of soiling, London-Van
der Waals forces are probably important in particle letention after a
particle contacts a surface. Corn11 calculated the electrostatic
attraction between a charged particle 1 m in diameter and an
adhering particle or surface in which it induces an equal and opposite
charge. Assuming a particle charge of 15 electrostatic units
(e.s'.u.)—i;e., 15 x 10~® coulombs—and a separation of 1 nm (10
A), he estimated a force of 5.2 x 10"^ dynes, which is about 107
times the gravitational force, assuming a density of 1 g/cra^.
However, this is only one one-thousandth of the estimated Van der Waals
force.
Capillary attraction is a mechanism of particle retention due to
adsorbed liquid films. Capillary attraction is probably more important
in fouling (where air comes into contact with damp coils or pipes) or
in particle filtration (where adhesive liquids are applied to the
filter) than in most everyday soiling of walls and surfaces. When the
radius of the liquid film at the point of contact is small, compared
with the radius of the particle, the force of attraction between a
sphere and a plane surface, with a film of liquid interposed, may be
expressed by the relationship F = 411-rr, where F is the capillary
force, f is the surface tension of the liquid, and r is the particle
radius.* * Corn1' has suggested v.hat that equation is approached
only at relative humidities near i00%, where water is in the liquid
phase. At lower vapor pressures, the force is less.
The surface-to-volume relationship of particles increases
dramatically as particles become very small, and this relationship is
important in soiling. Surface forces have a much greater ::>le in
r" ^termining soiling properties of small particles than of larger
VIII-21
-------
particles. Very fine particles cling to a glass slide when the slid6
is inverted. Walker and Fish** demonstrated that removing small
particles by Either liquids, airstreams, brushing, or gravity was more
dif£icult than removing large particles.
Human activities can cause agitation that resuspends deposited
particles. Primarily, it is the larger particles that are more readily
redispersed by this means. Hunt," in experiments using a light-
scattering-particle counter, showed that vacuum-cleaning a rug or
operating an electric fan caused a severalfold increase in the number
of particles larger than 3 wn, but only a slight perturbation in the
number of smaller particles. But other activities—such as smoking,
heating, or cooking—produced primarily submicrometer particles. Also,
aerosols in this size range are probably produced by condensation from
the vapor phase, rather than by dispersing preexisting particles from
surfaces or from a powder.
MOISTURE AND FUNGAL GROWTH
Fungal growth is another cause of soiling and deterioration that
generally occurs in areas with high humidity and low ventilation.
Microbial slimes in air-cooling and -humidifying units, plumbing
fixtures, condensation trays, and drains cause serious and often costly
mechanical problems. These and other airborne organisms can discolor
paint, weaken fabrics, and degrade foodstuffs. Microorganisms can also
lead to odors, such as the musty smell of a damp basement.
Schafferss has reviewed many of the effects of moisture in buildings,
including the promotion of fungal growth. Moisture can be generated
internally from combustion during heating and cooking, drying clothes,
bathing, and even1 breathing, and it can come from the outside during
periods of high humidity. Moisture generated indoors can result in
high humidities when there is no dehumidification, when ventilation
rates are low, or when a structure has tight vapor barriers in walls
and partitions. Fungal growth in ducts or on walls and surfaces has
been observed after the use of large amounts of outside air for
ventilation during damp periods.
Water vapor is not ordinarily regarded as a pollutant. Not only is
it essential to suppcrt the growth of microorganisms, but, if it is
present in excessive amounts, it can cause more visible effects, such
as peeling of paint and wallpaper. ,It also has an effect on comfort
. (as discussed earlier), and it can'enhance the effect of other
pollutants. Hermance et^al.-'14 ^or example, have noted this in
studying damage to telephone contacts by airborne nitrates.
iGASEOUS POLLUTANTS
The important gaseous pollutants—such as ozone, sulfur dioxide,
oxides of nitrogen, and carbon monoxide—affect the corrosion and
deterioration of materials. Ozone can cause cracking of rubber and
some other elastomers. The amount or rate of cracking of stretched
VIII-22
-------
rubber bands has been used as a method for determining low
concentrations of ozone.1" " Not only does ozone occur in the
outdoor air, but trace amounts can be produced indoors by arcing of
electric motors in tools and appliances and by corona discharges of
electrostatic air-cleaners. Sulfur1 dioxide and oxides of nitrogen may
also contribute to corrosion and deterioration, but they are more often
considered as potential health hazards. Carbon monoxide is
comparatively inert and does not react on surfaces; although it is a
hazard to health and safety, it does hot normally cause soiling or
deterioration.
EFFECTS OF TIGHT CONSTRUCTION
Reduction of i\filtration resulting from tighter construction
decreases the amounts of pollutants coming from outside, but can cause
increases in the concentrations of those.generated indoors, unless
there is a change in ventilation rate. To achieve the full benefit of
tight construction without increasing soiling, corrosion, and
deterioration, provision must be made to abate or eliminate indoor-
generated moisture and the indoor pollutants at their source.
Particles and moisture are probably the most important agents that
affect the rates of soiling, corrosion, and deterioration. Particle
counts are usually lower indoors,' but not always. Cooking,
cleaning, and other indoor activities intermittently distribute
particles, as well as moisture. Sources of many other pollutants are
discussed in Chapter IV.
As mentioned earlier, increased tightness of buildings can result
in increased moisture indoors. Previously, moisture generated indoors
has leaked out through the building structure, but, as these paths of
elimination are reduced, it may be necessary to use dehuraidifiers.
EFFECTS ON MAINTENANCE FOR CORROSION AND DETERIORATION
Andrews5 estimated that the cost of corrosion in the United
States exceeds $25 billion per year. This expense is reported to be
due to additional fuel, maintenance, or replacement costs. Although
the fraction of these costs caused by indoor pollution was not
reported, it can be assumed that even a small percentage could
represent a great financial impact over the lifetime of a building.
Four types of corrosion, which must be controlled in building
environmental control systems, are shown in Table VIII-4, with some
methods of prevention.
If the quality of the indoor air is degraded, the increased
concentration of contaminants can aggravate scaling of heat-exchanger
surfaces.9 For example> the air in a space with relatively high
moisture content often is recirculated across a cooling coil for
dehumidification. Increased carbon dioxide and sulfur dioxide of the
indoor air may react with the condensed water and accelerate corrosion
on the cooling coil.
VIII-23
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TABLE V1II-4
Types of Corrosion and Methods of Environmental Control in Buildings3
Type of Corrosion
Uniform
Pitting
Galvanic
Result
Maintenance Action
Stress
Direct chemical attack
Local deposits of parti-
cles on metal surfaces
Electrochemical reaction
between dissimilar
metals (less noble metal
is corroded)
Corrosion attacks stress-
weakened metal
Apply protective coatings
Inspect and remove solid
deposi ts
Remove solids in suspension
Apply such coatings as
plastics, paints, and
asphaltum (protect both
metals with same material)
Apply appropriate chemical 1
inhibitors
Replace
Data from Andrews.'
VIII-24
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Reports of increased maintenance of heat-exchangers or rotating
equipment necessitated by degradation of indoor air quality were not
found in the literature, but the appropriate conditions for increased
corrosion have been reported.' " ** 11 " For example, Hermance
et_aJL.'' reported that telephone switching equipment required
increased maintenance because of nitrates.
Inasmuch as nitrogen oxides and sulfur oxides can be present in
indoor environments, either from indoor sources or from outdoors, the
potential exists for corrosion of electric components in most indoor
environments.
EFFECTS ON HOUSEKEEPING
Cleaning and care of materials and properties in institutional
spaces represent approximately 15-20% of the total annual operating
costs of these facilities (W. w. Whitman, personal communication). In
turn, annual operating costs can be approximately 50-75% of the
annualized initial investment of buildings.* Thus, any degradation of
the indoor air quality that causes an increase in housekeeping can
seriously affect the life-cycle cost of a building.
As buildings' have become more energy-efficient, the moisture
content has been generally leported to have increased, owing' to
decreased infiltration.55 Additionally, the concentration? of smoke
particles and other contaminants from smoking and other indoor
activities have increased (see.Chapter IV). Thus, the rates of soiling
and deterioration of exposed surfaces may be accelerated, as a result
of degradation of indpor air quality.
Windows are a primary site for accelerated soiling, especially
during the heating season. Because resistance to heat transfer through
windows is usually one-tenth to one-third that of adjacent walls, the
inside surface temperatures of the windows will be much lower than
those of the walls. If the inside surface temperatures of the windows
are lower than the dewu).. _.;t temperature of the occupied space,
condensation will occur at these surfaces. Particles and gaseous
contaminants in equilibrium with the water vapor will be deposited on
the window surfaces with the condensate. As the condensate leaves the
windows by evaporation or draining, the other contaminants will be left
on the surfaces as residue, thus increasing the required frequency of
cleaning. Boyce 11 reported that, when windows are not thoroughly
cleaned periodically, a cloudy film builds up that can be removed only
with muriatic acid. To combat pollution in Los Angeles, Boyce stated,
aluminum mullions and transoms on the CNA Park plaza Building oust be
cleaned annually with mild steel wool and oil must then be applied to
protect the metal. If outdoor pollutants are transported indoors, or
if similar pollutants are generated indoors, the interior surfaces of
windows might require similar treatment.
*The annualized initial investment is based or a present cost of
$70/ft^ amortized over 50 yr at an inflation rate of 9%. Current
annual operating costs are approximately 33/ft2.
VIII-25
-------
Indoor lighting efficiency is also affected by indoor air quality.
Williams'* reported that dirt accumulations on lamps and fixtures can
reduce light output by 10-50% over the rated "end-of-life" of the
lamps. Thus, as dirt and film accumulate on fixtures and lamps,
cleaning and relamping frequencies must be increased to maintain proper
illumination.
Another major category of housekeeping expense is related to the
care of floors and carpeting. Darling21 reported that# on a national
average, 40-60% of the working hours of cleaning crews is required for
floors and carpeting and that carpeting soils more, quickly in
industrial centers than in suburban areas, where air pollution is less
severe.
Furniture, paintings, sculptures, and musical instruments are also
affected by indoor air quality. The special requirements for
environmental control in museums, art galleries, and auditoriums are
indicative of the care that is required to protect these properties. 1
METHOD OF TREATMENT
There are ways to' reduce the indoor pollution that causes soiling
and deterioration. For example,'air filtration reduces the amount of
airborne dust. Most central heating and air-conditioning systems
contain air filters., Although these are usually not of high '
efficiency, they do reduce dust. An electronic air-cleaner designed
for a specific system can remove still more particles.
' The visible .effects of undesirable thermal precipitation of dust on
walls near grilles and radiators may be reduced by shields that direct
air away from walls.
Dehumidifiers remove excessive moisture. However, during the
heating season, humidity is often low indoors, and it may be necessary
to add moisture t Activated carbon and other adsorbent air-cleaners are sometimes
used in buildings in high-pollution areas to remove gaseous
pollutants. However, these are not in general use, and they present
some special problems. For example, it is harder to determine when an
adsorbent filter needs to be changed than a particulate filter (see
also Chapter IX).
RECOMMENDATIONS
Some of the commonly recognized agents that produce soiling and
deterioration have been discussed in the foregoing paragraphs, but
VIII-26
-------
additional questions need investigation. With regard to removal of
indoor particles, where is the point of diminishing returns in
improving the efficiency of particulate filters? Likewise, where is
the point of diminishing returns reached in increasing the rate at
which air is removed from an occupied space and filtered? Dust
composition may jIpo be important. There have been a few analyses of
indoor dust,11 %,,but much less work that has tried to relate '
soiling, corrosion, or other deleterious effects to dust composition
ana particle size. Thus, the effectiveness of dust removal technology
and the specific nature of the dust, as tphey relate to soiling and
deterioration, need further investigation.
Information on the role of gaseous pollutants in soiling or
corrosion is lacking.
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Geneva: World Health Organization> 1972. 387 pp.
73.,Wyon, D. P. Human productivity in thermal environments between 65F
and 85F (18-30C), pp. 192-216. In J. A. J. Stolwijk, Ed. Energy
Conservation Strategies in Buildings. New Haven: John B. Pierce
Foundation of Connecticut, Inc., 1978.
74. Wyon, D. P. The role of the environment in buildings today: Thermal
aspects. Factors affecting the choice of a suitable room
temperature. Build Int. 6:39-54, 1973.
VIIT-31
-------
IX
CONTROL OF INDOOR POLLUTION
The quality of the environment in a building is inherently
dependent on the design and operation of the building's environmental
control system. Several factors that affect the design and operation
of control systems are identified in Chapter V, including human
activities' and geographic and building characteristics. Optinally,
control systems are designed to maximize human comfort, and it is
essential to know the acceptable ranges for environmental
characteristics (comfort and air-quality factors). Some constraints
that must be 'Imposed on control systems are related to cost and energy
consumption. As a result of the application of these constraints,' the
goal of maximal comfort is usually compromised. The ranges of
conditions within which control systems operate are usually based on
codes and standards that have been developed and promulgated to protect
the health and welfare of occupants. This chapter begins with a review
of codes and standards that pertain to indoor pollution.
Codes end standards have beer developed as prescriptive guidelines
based on consensus, but, as energy conservation and operating cost
become more important, the need for evaluation of control-system
performance increases. Criteria of system acceptability are also
changing—codes and standards are becoming oriented more toward
performance, and life-cycle costs are receiving more attention.
Changes in the attitude toward environmental control present
several difficulties. Feedback control for. acceptable indoor air
quality is recognized and needed, but the availability of reliable and
inexpensive controllers is seriously limited. Performance-oriented
standards have not been widely accepted by contractors and enforcement
officials, because cf barriers in technology transfer and increased
costs of implementation and liability. And economic decisions based on
life-cycle costing have not been accepted by contractors and building
developers, who have resisted because of a lack of incentives, such as
amortization periods and allowance of pass-through of operating costs,
and because of the high cost of capital. Appendix B considers energy
environmental, and economic factors and presents a method for providing
acceptable control of indoor air quality at acceptable costs of money
and energy.
IX-1
-------
VENTILATION CODES AND STANDARDS
Control of indoor environments in residential and commercial
buildings to achieve.what is termed "comfortable" or an "acceptable"
thermal quality requires approximately one-third of the total annual
energy consumption in the United States.'* An additional 10% may be
required to maintain conditions that are acceptable for occupants in
industrial facilities. Ventilation systems have been reported to
require as much as 50% or 60% of the total energy consumed in
buildings." *'
For energy conservation, rather arbitrary changes in building codes
and standards are being proposed.'* " Reduction of ventilation in
residential, commercial, and industrial buildings could jeopardize the
health, safety, or welfare of those who occupy them. Reduction of
energy consumption is a necessary but .'insufficient step in the
development of acceptable building energy management programs. Also
required is the maintenance of environmental conditions that are not
deleterious to the occupants or harmful to property. These conditions
include spatial, thermal, illumination, and acoustic qualities of the
environment, as well as the gaseous and particulate qualities of the
air. ventilation is the historically and currently practical means of
providing acceptable indoor air quality.
To protect the health, safety', and welfare of the general public,
building codes have been adopted and'enforced by local, state, and
federal government agencies. These codes generally specify minimal'
acceptable ventilation criteria to be maintained in the buildings.
Note that "ventilation air," as used here and elsewhete in this ¦
document, refers to outdoor air or recirculated, treated air.
Compliance with building codes is usually the responsibility of
licensed professional engineers and architects during design.
.Responsibility for compliance during operation often is'vague, if
specified at all. After a building has been designed and constructed,
the owner or manager usually assumes responsibility for maintaining the
quality of the indoor environment, and there is normally no official
enforcement.
State and local building codes are normally based, directly or with
modification, on one of. three model building codes published in the
United States: The BOCA Basic Building Code" " of the Building
Officials and Code Administrators International (BOCA); the' Uniform
Building Code 2' of the International Conference of Building Officials
(ICBO); and the Southern Building Code3* of the Southern Building
Code Congress International, Inc. (SBCCI).
Building codes are usually derived from standards that have been
promulgated by authoritative bodies, such as the American National
Standards Institute (ANSI), the National Fire Protection Association
(NFPA), and the American Society for Testing and Materials (ASTM).
Other organizations that publish standards for the building industry
are the American Society of Heating, Refrigerating, and Air-
Conditioning Engineers (ASHRAE), the American Society of Mechanical
Engineers (ASME), the Illuminating Engineering Society (IES), the
IX-2
-------
American Concrete Institute (ACI), the Air Conditioning and
Refrigeration Institute (ARI), and the Sheet Metal Contractors
Association (SMACNA). {In preparing proposed procedures for listing
voluntary standards bodies for federal agency support and
participation, the Department of Commerce held discussions with some 37
voluntary standard^ bodies.'2)
Standards published by these organizations are usually developed by
a consensus method and are known as "voluntary standards" or "consensus
standards." 1 '* ri Voluntary standards are usually adopted, after
periods of open review, as guidelines of recommended practice or
minimal performance criteria by which an organization may govern
itself. However, a voluntary standard may become mandatory if it is
adopted within legal documents, such as government standards or
building codes.
Standards also are developed in response to state or federal laws.
These are known as "mandatory standards"'1 11 and are promulgated in
the form of state or federal regulations after they have been subjected
to public hearings. Agencies responsible for the promulgation and
enforcement of mandatory standards relevant to the building industry
include the Department of Housing and Urban Development (HUD), the
Department of Health and Human Services (DHHS, formerly the Department
of'Health, Education, and Welfare, or DHEW), and the Department of
Energy (DOE).
BACKGROUND
By selecting the site, size, ,shape, and orientation of housing, man'
has nearly always taken advantage of natural ventilation for thermal ,
and, air-quality control. Ventilation requirements in buildings have
been specified since the eighteenth century. The early history of the
development of ventilation codes and standards has been reviewed by
Nevins,*1 Klauss et al., '2 and Arnold and O'Sheridan, Inc. 11
As shown in Figure IX-1, ventilation rates increased from 4
cfm/person in 1824 to 30 cfm/person in 1895. A minimal requirement of
30 cfm/person dominated design of ventilation systems during the first
quarter of the twentieth century, as evidenced by the fact that in 1925
the codes of 22 states required a minimal ventilation rate of 30 cfm of
outdoor air per person.'1
•A major change in ventilation standards resulted from experimental
work reported by Yaglou et al." in the 1930s. .These studies
recognized the importance of controlling indoor air quality, as well as
ventil?.tion-air quantity, and reported ventilation rates in cubic feet
per minute per. person required to provide "odorfree" environments as
functions of available air space per person. It should be noted that
these ventilation rates were based on the assumption that outdoor air
("fresh air") was odcrtrte.
The Yaglou studies, conducted under controlled experimental
conditions, have served as the primary reference in codes and standards
for the last 40 yr. However, because of the difficulty in accurately
estimating occupancy and the lack of feedback control methods fpr
IX-3
-------
z
o
CO
c
UI
a.
S
LL
U
Ui
H
<
IE
Z
o
H
<
Z
UJ
>
30
25
20
15
10
Billing! (18951
ASHVE Rcquiramsna
Plug* (1905)
Tradgold (1834)
_L
Accaptad Requirement!
Subject to R«vsl union
Basiafor
ASA Standard
Yaglou (1936)
ASHVE R«quirtmcnts
ASHRAE Standard
62-73 (1973)
Currant
Revaluation
I
!
1325 1830
1875
1900
YEARS
1925
1950 1975
1980
FIGURE IX-1 Historical development of ASHRAE Standard 62-73.
After Klauss et al.
IX-A
-------
ventilation, many codes and standards, including several now in
effect,have specified ventilation requirements as
room-air changes per hour, rather than exchange rate per person.
Theoretically, these criteria should be synonymous, but they are not.
When ventilation rates are specified as room-air changes per hour,
sensitivities to spatial dimensions and occupancy are lost. For
example, 5 air changes per hour (ach) in a theater with a 20-ft (6.1-m)
ceiling height.and a sparse occupancy of 100 ft^ (9.3 m^) of floor
area per person would result in 167 cfm (79 L/s) per person, whereas
the same room-air exchange rate and occupancy in a classroom with an
8-ft (2.4-m) deiling would mean 67 cfm (32 L/s) per person. However,
at full-load occupancies of 10 ft^,(0.9 m?) per person in the
theater and 20 ft^' (1.9 m^) per person in the classroom, 5 ach
would result in 17 cfm (8 L/s) per person in the theater and 13 cfm (6
L/s) per person in the classroom.. Thus, at less than full-load
occupancies, the ventilation rates per person would exceed the values
shown in Figure IX-2, whereas at full loads, the ventilation would be
insufficient to provide "odorfree" air.
The inherent problems associated with specifying air changes per
hour have been recognized in some standards for several years.' In
1946, the American Standard Building Requirements for Light and
Ventilation, A53.1, was publisned by the American Standards Association
(ASA) with primary criteria in. cubic feet per minute per square foot of
floor area.1® A revision and update of A53.1 was published in 1973
by ASHRAE with primary criteria in cubic feet per minute per person. *
The latter standard was adopted by the ANSI (formerly ASA) in 1977 and
has been designated ANSI Standard B194.1. For the first time in a
ventilation standard, Standard 62-73 provided a quantitative definition
of "acceptable outdoor air" and specified conditions under which
recirculated air could be used. Both minimal and recommended '
ventilation rates were specified in the ASHRAE standard to accommodate
fuel economy (minimal values) or comfort in odorfree environments
(recommended values). Energy savings at design summer and winter
conditions resulting from minimal ventilation rates specified in
Standard 62-73 have been estimated to range from 27 to 81% for various
occupied spaces, compared with rates in Standard A53.1."°
In response to demands for energy-efficient buildings, ASHRAE
developed a new standard, which was published in 1975: Standard 90-75,
Energy Conservation in New Building Design.7 Through a contract with
DOE, the National Conference of States on Building Codes and Standards;
Inc. (NCSBCS), undertook, with the three model-code groups recognized
in the United States, to write a model Code for Energy Conservation in
New Building Construction. 17 This model code was based on ASHRAE
Standard 90-75 and is generally considered to be its codified
counterpart. By 1980, legislation either had been passed or was being
considered by 45 states for energy-conservation regulations 'based on
these two documents. 67
ASHRAE Standard 90-75 was expected to reduce energy requirements in
new buildings by 15-60%, 12 but efforts to promulgate the standard
resulted in a conflict with Standard 62-73. Standard 90-75 stated that
the "minimum" column in Standard 62-73 for each type of occupancy
IX-5
-------
AIR SPACE PER PERSON (ft3)
FIGURE IX-2 Ventilation rates resulting from the Yaglou studies.
IX-6
-------
"shall" be used foe design purposes. This statement in Standard 90-75
effectively deleted the "recommended" column in Standard 62-73 and
caused serious concern regarding the possibility of insufficient
ventilation in new buildings. For example, when smoking was allowed in
a room ventilated at the minimal rate of 5 cfm (2.4 L/s) per person,
the carbon monoxide concentrations approached.the limits specified by
the EPA primary ambient-air quality standards, and particle
concentrations exceeded the proposed limits by a factor of 30-60. 11
There is still controversy about what are acceptable concentrations of
pollutants and ventilation rates.
In January 1981, ASHRAE adopted Standard 62-1981' in an effort to
resolve some of the problems with Standard 90-75 and to reflect newer
design requirements, equipment, systems, and instruments. & comparison
of the newly revised Standard 62-1981, Standard 62-73, and the obsolete
Standard A53.1 is shown in Table IX-1. Several major revisions have
been made in an effort to resolve the apparent conflict between
operating ventilation control systems for energy savings and operating
them foe protection of the health and comfort of the occupants.
• The quality of outdoor air to be used for dilution and control
of indoor air pollution has been defined, not only in terms of the EPA
primary standards, but also in terms of other recognized guidelines and
professional judgment.
• ¦ Values for minimal and recommended ventilation rates have been
replaced with required values for smoking and nonsmoking areas.
Nonsmoking areas have proposed values similar to the existing minimal
values, and those for smoking areas are similar to or greater than the
values currently recommended.
• A method has been specified that will determine the amount of
recirculation air required to compensate for allowable reductions in
outdoor air. The amount is determined as a function of air-cleaner
efficiency.
• The operation of mechanical ventilation systems during periods
of occupancy is specified as a function of the source of indoor
pollutants.
• An alternative method specifies both objective and subjective
criteria for indoor air-quality, but the method of achieving control is
left to the discretion of the operator.
With the advent of performance criteria for indoor pollutant •
control, conflicts between various codes and standards could become
more intensive.
IMPLEMENTATION OF CODES AND STANDARDS
Ventilation codes and standards have been published by several
agencies and organizations. As a result, the designer or operator of a
system has the responsibility of reviewing the relevant documents and
then deciding which of them apply. In many cases, the values in thoae
codes and standards will not be consistent. Thus, it can present a
IX-7
-------
TABLE IX-1
Comparison of Ventilation Requirements in ASHRAE Standard 62-73 (1973),
ASA Standard A 53.1.(1946), and ANSI/ASHRAE Standard 62-1981 (1981)
Subject
Outdoor-air
quality
ASA 53.1
10
Accepted ambient
conditions
ASHRAE 62-736
Acceptable
criteria
specified
ANSI/ASHRAE 62-1981*
Acceptable criteria
more precisely
specified''
Ventilation air
Same as for out-
door air
Treated recir-
culated air
allowable
Treatment more pre-
cisely specified
Mechanical
ventilation
Requirements same
as for natural
ventilation
Reduced rates
allowable
Methods for variable
ventilation describe
Primary venti-
lation
criteria
cfm/ft , minimal
values
cfm/person, min-
imal and recom-
mended values
Required values of
cfm/person specified
for smoking and non-
smoking areas
Indoor-air
quality
Not specified
Not specified '
Alternative performanc
method specified
IX-8
-------
challenge to the building designer and operator to select a ventilation
rate that will meet the requirements of all relevant codes and
standards. Under these circumstances, the usual procedure has been to
select the largest value tha.t would satisfy the requirements of all the •
codes and standards.
Because of recent concerns regarding energy consumption and costs,
some regulations have been promulgated or proposed that are in direct
conflict with those promulgated to protect the health or comfort of
occupants; an example is the 1977 Assembly Bill 983 of Wisconsin,
Ventilation Requirements cor Public Buildings and place's of
Employment. Bill 983 would have eliminated mandatory minimal
ventilation requirements specified in the state building code (i.e., 5
cfm per person) during the period October 1 to April 1 of each year.
Building owners would have been allowed to close or otherwise regulate
outside-air intakes to conserve energy during these periods. Bill 983
was passed by the 1977 General Assembly and vetoed by the governor? the
veto was overridden by the Senate and sustained by the House. This
legislation was reintroduced as a rider to an appropriations bill in
the 1979 General Assembly. It was later amended to allow reduced
ventilation only through adminstrative action; in that form, it
passed. The state Department of Industry, Labor and Human Relations,
previously responsible for ventilation requirements, will administer
the law.
A summary of the most commonly cited ventilation codes and 1
standards is shown in'Table IX-2'. Several model codes and ASHRAE
Standard 62-73 may be applied to each of the nine functional catagories
of buildings listed in Table IX-2.5® Other voluntary and mandatory
standards are shown as they apply to particular functions. It should
also be noted that the NCSBCS model Code for Energy Conservation in New
Building Construction was developed with the three model-code groups
and applies to all. functional catagories.17 This model code
specifies ventilation rates for energy calculations as the minimal
values in Standard 62-73. The ASHRAE standard, in turn, defers to
other standards or codes when they have precedence and require higher
ventilation rates.
Domiciles
As indicated in Table IX-2, the two primary sources for ventilation ,
requirements are ASHRAE standards * ® and the HUD Minimum Property
Standards (MPS)."'71 Both sets of standards are considered
voluntary, but may become mandatory under specific conditions—Standard
62-73 when adopted as part,of a state energy code, and the MPS if
housing is financed through the, Federal Housing Administration (FHA).
Ventilation rates for various spaces throughout private dwelling
places are specified in Standard 62-73 as 5-20 cfm/person (minimum) and
7-50 cfm/person (recommended). The higher rates are for bathrooms and
kitchens and are for intermittent operation. The MPS also set
intermittent exhaust rates in kitchens and baths at 15 and 8 ach,
respectively. The 1979 revisions of the MPS allow ventilation by
IX-9
-------
TABLE IX-2
Sources of VenCilatlon Codes and Standards for Occupied Spaces
Building-Function
Category
Domicile: place of
residence, such as a
single-family dwell-
ing, multifamily
dwelling, public
housing, rowhouse^
apartment, or con-
dominium
Educational: build-
ing used for class-
rooms or instruction
Laboratory: building
used predominantly
for research and
diagnostic work, and
not necessarily for
instruction
Medical: building used
for health-care
facilities, such as
hospital, clinic,
medical center, sani-
tarium, day nursery,
infirmary, orphanage,
wrsing home, or
mental-health Institu-
tion
Office: such buildings
as used for offices,
civil administration,
or radio or tele-
vision station
Public assembly: build-
1 ing where groups can
meet for such func-
tions as theater,
restaurant, cafeteria,
retail store, art
gallery, museum, bank,
post office, court-
house ,•assembly hall,
church, dance hall,
coliseum, passenger
terminal, or library
Voluntary Standards Mandatory Standards
ASHRAE6'9
MPS 4900
MPS 491070
Model Building
Codes
BOCA15'16
UBC '
SBCCI55
NCSBCS
ASHRAE
6,9
ILAR guide and
standards /"
NIH guidelines66
ASHRAE6'9
>74
9 CFR 1.1, 1979'
29 CFR 1910, 1979
BOCA*5'16
49
55
UBC
SBCCI
NCSBCS
17
BOCA1^16
UBC29
SBCCI55
NCSBCS17
ASHRAE6'9 HRA 79-1450068 ' 30CA15'16
MPS 4920 1 UBC29
SBCCI55
NCSBCS17
ASHRAE6,9
BOCA15'16
UBC29 .
SBCCI55
NCSBCS1
ASHRAE6'9
BOCA15'16
UBC29
SBCCI55
NCSBCS17
IX-10
-------
Table IX-2 (contd)
Building-Function
Category
Rehabilitation: non-
health-care building
used for instruction,
but not of the,regi-
mented 'classroom type;
pertains more to ¦
readjustment, such as
iail, prison, reform-1
ato-;', or half-way
houses
Warehouse: building
used for storage of
materials and sup-
plies, such as. stor-
age facility, main-
tenance facility, 1
garage, airplane
hangar, or bus barn
Industrial: such
buildings as
factories, assembly
plants, foundries,
mills, power plants,
telephone-exchange ¦
facilities, water and
waste-water treatment
plants, solid-refuse
plants, zoos, green-
' houses, aviaries,
arboretuns, or others
requiring environ-
mental control for
process control
Model Building
Voluntary Standards Mandatory Standards Codes
ASHRAE6'9 — . BOCA*5'16
UBC29 ,
SBCC1
NCSBCS
ASHRAE6'9 OSHA72 BOCA15'16
UBC
. SBCCI55_
NCSBCS17
ASHRAE6'9 OSHA72 BOCA15'16
UBC29
SBCCI
NCSBCS17
1X-11
-------
infiltration cates of 0.5 ach and natural ventilation through operable
windows, which must have a total area of at least one-twentieth of the
floor area of the room. ANSI/ASHRAE Standard 62-1981 specifies 10 cfm
(5 L/s) per room for spaces other than bathrooms and kitchens, for
which values are set at 50 and 100 cfm (24 and 47 L/s) per room,
respectively. Although the ventilation rates are specified differently
in these voluntary standards, the results are intended to be
equivalent. Moreover, the 1979 revisions to the MPS and the values in
Standard 62-1981 are in close agreement with values recommended
internationally.*1 ,s
Educational Facilities
The mechanical-ventilation rate for classrooms is specified in
Standard 62-73 and in the model codes as a minimum of 5 cfm/person for
a full-load occupancy of 20 ftfyperson. However, the minimal
supply-air rate (i.e., ventilation plus recirculation) is specified as
10 cfm/person in Standard 62-73 and 15 cfm/person in the model codes.
Natural ventilation is specified in the model codes as that obtainable'
through operable windows with areas one-twentieth of the floor areas;
Standard 62-73 specifies minimal and recommended natural-ventilation
rates of. 10 and 10-15 cfm/person, respectively. Standard 62-1981
specifies required ventilation rates of 5 cfm (2.5 L/s) and 25 cfm
(12.5 L/s) per person for nonsmoking and smoking areas, respectively,
in classrooms.
Laboratories
Specific controls for ventilation in laboratory spaces are required
for protection of the health ana comfort of laboratory personnel and
for the preservation of specimens and critical experimentation
conducted in the facilities. A differential in air pressure may be
required between laboratory areas and public spaces, such as meeting
rooms and reception areas, to protect the general public. Thus, the
nature of ventilation control is moru complex in these facilities than
in most other indoor environments.
Toxic and hazardous materials used in the laboratory must be
controlled to within the limits prescribed.by OSHA.7i Control may be
by isolation or enclosure of the pollutants, dilution, or air-cleaning,
but OSHA does not mandate a particular control method. This type of
standard has become known ar- a "performance standard."
Indoor areas in which substances suspected of being carcinoqenic
are used or where recombinant-DNA research is conducted must be kept
under negative static pressure relative to the surrounding
areas.6' 'J Local exhaust and clean makeup air may be u3ed for
pressure control, but the exhaust must be decontaminated before
discharge. Also, "experiments," procedures, and equipment that could
produce aerosols must be confined to laboratory hoods or glove
boxes. 71
IX-12
-------
When laboratory animals are used in experiments) their care and
wall-being must also be maintained. The Animal Welfare Act7*
specifies many procedures for the care and handling of the animals, but
is vague and nonspecific about environmental control in the laboratory
or the cage.** The standards published by the Institute of
Laboratory Animal Resources (ILAR) of the National Research council are
somewhat mor« specific in "recommending" ventilation rates.'*
However, these standards often require 10-20 ach with 100% outside air,
which is energy-intensive, and the use of 100% outside air may have
little or no impact in the cage mlcroenvironment. **
ASHRAE Standard 62-73 specifies 15 cfm/person as minimal and 20-25
cfm/person as recommended ventilation rates for spaces without
animals. With animals, the minimal rate is 40 cfm/person and the
recommended rate is '.5-50 cfm/person. These outdoor-air requirements
may be reduced by two-thirds for mechanical ventilation systems with
adequate particle filtration.
Standard 62-1981 specifies a required ventilation rate of 10 cfm
(5 L/s) per person for nonsmoking areas and recognizes that other
standards may override this rate.®
Medical Facilities
Ventilation and control of biologic contamination in medical
facilities, especially in some hospital treatment areas, have been the
subject of much research since the middle of the nineteenth century. 11 "
The Health Resource Administration (HRA) publishes requirements"
that must be maintained if federal funds (i.e., Hill-Burtqn funds) are
used for new construction or major modifications.
Since 1969, these regulations have allowed recirculation in
sensitive areas, such as operating rooms. However, changes have
occurred in the specified number of air changes per hour of supply air
and the percentage of outside air." Currently, HRA allows
recirculation of air in all areas of hospitals, with the following
restrictions: *'
* In sensitive area's, such as operating rooms, two ait filters
are required—a preiilter and a final filter, rated at 25% and 90% ¦
efficiency, respectively, according to ASHRAE Standard 52-76.*
* Each space in which inhalation anesthetic agents are
administered must be supplied wi.th a separate scavenging system for
exhausting waste anesthetic gases.
* Appropriate air-pressure relationships must be maintained with
respect to adjacent areas.
Changes specified in the minimal requirements of construction and
equipment for hospital and medical facilities*' allow reductions of
up to 25% when specific rooms are unoccupied, provided that the
specified pressure relationships are maintained when they are
occupied. When this feature is used, positive provisions, such as an
electric interconnect between the ventilation system and room lights.
IX-13
-------
nust be included, to ensure that the specified ventilation rates are
automatically resumed when the rooms are reoccupied.
Standard 62-73 specifies ventilation rates for hospitals and
nursing and convalescent homes in terms of minimal and recommended
cubic feet per minute per person and allows reductions in the use of,
outdoor air to one-third of the specified values when mechanical
ventilation is used.
Standard 62-1981 specifies required ventilation rates for patient
rooms as 35 cfm (17.5 L/s) and 7 cfm (3.5 L/s) per beu for smoking and
nonsmoking spaces, respectively. In other hospital areas, Standard
62-1981 values are per person for nonsmoking spaces and are similar to
the minimal values previously' specified.
As shown in Table IX-3, the ventilation and total air-supply rates
specified'in HRA 79-14500 are generally greater than those specified in
ASHRAE Standard 52-73 or 62-1981."
The ventilation rates specified in MPS 4920" are primarily in
terms of allowable infiltration rates and exhaust rates for kitchens
and patient-room lavatories.
Other Nonindustrial Spaces
The ASHRAE standards' ' are primary sources for ventilation rates
for offices, public-assembly buildings, and rehabilitation facilities.
Currently, no other standards are generally used in the United States.
In Standard 62-73, ventilation rates are specified as minimal and
recommended rates per person with reductions in outdoor air of
one-third of the' specified values allowed for mechanical ventilation,
if adequate' filtration is provided. Standard 62-1981 specifies
ventilation rates as required for smoking and nonsmoking areas with
reductions in outdoor air allowed for mechanical ventilation as a
function of filter efficiency.
SUMMARY
State and local building codes usually are based on one of the
three model-code documents. These become legal documents when adopted
by appropriate government' agencies. The ventilation rates specified in
the building code's are usually derived from standards, such as those
published by ASHRAE.
Traditionally, other.mandatory standards have taken precedence over
a building code when the values in standards exceeded those in the
building code. However, model energy-conservation codes have been
promulgated by the model-code groups, and there can now be conflicts in
required ventilation rates between codes and mandatory standards. With
the advent of indoor-pollutant criteria, the conflicts could become
more extensive, because methods of pollution control that do not
require the traditional ventilation rates may be used.
IX-14
-------
TABLE tX-3
Comparison of Hospital Ventilation Standards3
ASHRAE Standards: Hlll~Burton Standards
Equivalent Air Changes per Hour''
Outdoor-Air Changes
per
Total-Air Changes
per
ASHRAE
62-73 ANSI/ASHRAE 62-1981
Hour,
Minimum
Hour,
Minimum
Mini-
Non-
Pre-
Pre— -
Area
mum
Recommended Smoking
smoking
1969
1969.
1974
1979
1969
1969
1974
1979
Operating
5
— —
1.2
12
5
5
5
12
12
25
25
roam
Recovery
4C
—
3d
6
2
2
2
6
6
6
6
room
Patient
1
1.5-2 2.5
0.5
.2
2
2
2
2
2
2
2
- room
Ward
1.5
2-2.5 2.5
0.5
2
2
2
2
2
2
2
2
Medical
—
2.5
0.5
6
2
2
2
6
6
6
6
procedure
(treatment)
Physical
2
2.5-3 —
2.5
6
2
2
2
6
6
6
6
therapy
Autopsy
2
2.5-3 —
7
6
2
2
2
15
12
12
12
aFrom Woods.^
''Celling height assumed to be 10 ft (3 m).
cSpecial requirements or codes may determine ventilation rates*
^Activities generating contaminants may require higher rates.
eAir shall not be recirculated.
-------
RECOMMENDATIONS
The general public Is not aware of the distinction between
ventilation control and indoor air-quality control. The techniques and
terminology used in air-quality control and ventilation design,
operation, and codes should be described in clear and consistent
language.
We recommend that professional and government organizations
coordinate tc. establish a model code for indoor air quality that would
meet health, energy, and economic criteria.
Responsibility for enforcement of acceptable control of indoor air
quality should be defined for various building categories. Enforcement
procedures should be considered wi,th respect to building construction
and building operation.
AIR DIFFUSION CONTROL
Air is supplied to ventilate an enclosed space (i.e., a room or
group of rooms in a building) for two main reasons: .
* To maintain acceptable oxygen concentration and to dilute (and
remove) carbon dioxide and other contaminants for safety of the
occupants. ,(and some times to provide a differential in air pressure as
required by building codes or standards). , Ventilation air flow rates
are specified in codes and standards.4 Ic should be noted that
supplying the specified or mandated rates for ventilation does not ,
guarantee adequate dilution or removal of contaminants if the air is
not uniformly diffused throughout the,occupied space.
* To provide a thermally controlled environment that is
acceptable to the occupants. An acceptable thermal environment has
been defined as one in which at least 80% of the occupants clothed
normally and engaged in sedentary or near-sedentary activities would
express thermal comfort, which is defined as "that condition of mind
which expresses satisfaction with the thermal environment."
Depending on the activity and typical clothing of the occupants, the
combination of air temperature, mean radiant temperature, relative
humidity, and air velocity must be appropriate for the occupants to
feel comfortable (see Chapters IV and VII).1* 15 51
Conventionally, air diffusion control has been designed and
installed to ceet the criteria for thermal comfort, with the assumption
that the air-qiality criteria will be met simultaneously.
AIR DIFFUSION EQUIPMENT
The supply air for ventilation is usually treated at a central
location (i.e., filtered and conditioned for an appropriate dry-bulb
and dew-point temperature) and then distributed by a duct system to the
intended space. The amount of air supplied to each space is controlled
by the terminal units of the duct system.
IX-16
-------
Four types of terminal units are commonly available:1 grilles,
slot diffusers, celling diffusers, and perforated ceilings.
' Grilles, which can have different configurations (e.g., adjustable
bar grilles, fixed bar grilles, stamped grilles, and vaiiable-area
grilles), are.usually in a high sidewall position, in a perimeter
installation, or in the ceiling. . The air from a high sidewall position
is thrown across the ceiling and.drops toward the floor as it traverses
the room. Prom a floor or sill grille, the air is directed vertically
upward along the perimeter walls to which the airstreara adheres, owing
to the Coanda effect. (The Coanda effect can be defined as the ability
of a jet to cling to a curved or deflected surface while increasing its
mass flow rate along the flow path.10) When grilles are installed in
the ceiling, curved vanes deflect the air along the ceiling so that the
Coanda effect causes the airstream to follow a horizontal distribution.
A slot diffuser is usually installed in long continuous lengths in
several different locations similar to those described for grilles.
Ceiling diffusers usually are series of rings or louvers (not
necessarily circular) that direct the airstream across the ceiling.
In perforated ceilings, the air is contained in a supply plenum
above the ceiling and delivered through holes or slots in the ceiling
material.
AIR-DIFFUSION CRITERIA
The velocity of the air i!s important—if the appropriate velocity
is exceeded, conditions can become drafty and thus uncomfortable." 51
The force of the air supplied must be such that it stirs the air
already in the space so that mixing is accomplished, to reduce the
variance of air properties, both thermal and chemical, throughout the
space. However, complete mixing of the air in the space is seldom
achieved.
In some cases, especially when there are high ceilings (i.e.,
commercial or institutional spaces), various zones can be identified as
occupied and unoccupied spaces. There is little thermal and
respiratory .exchange between people and the air above head level, and
the space between head level and the ceiling is called "unoccupied
space." Uniform mixing of the air is necessary for the comfort of .
those in the occupied space, but is not needed in unoccupied space.'
Because there may be incomplete mixing of the air in the unoccupied
space, the chemical and thermal composition may be noticeably different
from that of the occupied space.
Nonuniform mixing may be caused by the type and location of the
terminal units selected for the space or by such deficiencies as:
* Direct air flow from the terminal supply unit to the exhaust
or return air grilles that bypasses a part (or most) of the occupied
space.
* An air circulation pattern that causes secondary air currents
where the supplied air does not have sufficient force to cause complete
mixing, thus leading to air stratification within the enclosure.*1
IX-17
-------
Mathematical models to determine the effective mixing rate that
occurs in a space have been proponed, but extensive research is still
needed to obtain reliable methods to quantify mixing.11 *• 11 "
When mixing in an occupied space is nonuniform, comfortable
conditions cannot be ensured for the occupants in the stagnant
(secondary flow) zones. To minimize nonuniform mixing, the location,
type, and size of the terminal units must be selected correctly. There
are very few definite criteria to make this selection for a particular
application, but the concept of air-diffusion performance index
(ADPI)*' is commonly used to characterize a terminal unit.
The ADPI is based on subjective responses to drafts. The effective
draft temperature (6) is determined from the local velocity (Vx),
in feet per minute, and the difference in dry-bulb temperature, in
degrees Fahrenheit, between the local point and the control
temperature (tc): 0 ® (tx - tc) - 0.07(Vx - 30). The ADPI is
the percentage of the total number of measured points that have
effective draft temperatures of -3.0 to +2.0°F and local velocities of
70 ft/min or less (see Figure IX-3). ADPI values have been
experimentally calculated for typical applications of terminal units as
a function of the airflow characteristics from the units and the
thermal loads of the spaces (see Tables IX-4, IX-5, and IX-6 and Figure
IX-4). From the values lidted in Table IX-4, types and sizes of
terminal unit! can be selected to provide acceptable mixing in the
occupied spacy.
The ADPI, although practical, may not yield the best selection in
all cases. Several points should be considered:
* The location of the exhaust outlet influences air movement
only in a small zone near the outlet itself. Thus, the ADPI does not
depend on the location of the exhaust outlet.1" However, there are
studiesss 11 * that have shown that different locations of the supply
and exhaust units cause different patterns of airflow, some of which
may be unstable and some unacceptable for thormal comfort.
* Airflow patterns are different during heating and cooling
cycles. Commonly, the same terminal units are used for both
situations. Thus, the cool air from a ceiling diffuser would drop into
the occupied space, but hot air supplied by the same terminal mixes to
provide thermal comfort of the occupants. However, the ceiling
location may not be appropriate for a heating situation, inasmuch as
the hot air supplied by the ceiling diffuser would tend to stay near
the ceiling, owing to buoyancy; this results in ait stratification near
the floor. A similar situation may occur' when the terminal units are
placed low in the occupied space; the hot-air supply tends to rise and
affect the whole room, whereas the cold-air supply tends to stay low,
thus possibly causing development of a stagnant layer near the
ceiling. Therefore, for spaces where both heating and cooling are
needed, care should be taken to ensure that the terminal unit will have
an appropriate ADPI in both situations.
* Calculation of an ADPI assumes that steady conditions exist
and that the room has no airflow obstructions. Some attempts have jeen
made to study the effects of obstructions in the occupied space,"
IX-18
-------
-C -4 -2 o 2 4
DRAFT TEMPERATURE DIFFERENCE (tx - tcl.°F
FIGURE IX-3 Comfort criteria used to evaluate the air
diffusion performance index (ADPI).
VERTICAL CROSS SECTION
PLAN VIEW
FIGURE IX-4 Airstream characteristics. Reprinted with
permission from Nevins.
IX-19
-------
TABLE IX-4
Air Diffusion Performance Index for Common Diffuser Applications3
Terminal Device
Room Load,
Btuh/ft
Tijq/L for
Max. ADPI
Maximal
ADPI
For ADPI
Greater Than
Range of
T<;n/L
High-sidewall grilles
80
1.8
68
60
1.8
72
70
1.5-2.2
40
1.6
78
70
1.2-2.3
20
1.5
85
80
1.0-1.9
Circular ceiling
80
0.8
76
70
0.7-1.3
diffusers
60
0.8
83
80
0.7-1.2
40
0.8
88
80
0.5-1.5
20
0.8
93
-90
0.7-1.3
Sill grille straight
80
1.7
61
60
1.5-1.7
vanes
. " 60 -
1.7
72 -
70
1.4-1.7
40
1.3
86
80
1.2-1.8
20
0.9
95
90
0.8-1.3
Sill grille spread
80
0.7 -
94
90
0.8-1.5
vanes
60
0.7
94
80
0.6-1.7
40
C. 7
94
—
—
20
0.7
94
— -
—
Ceiling slot diffusers
80
0.3^
85
80
0.3-0.7
60
0.3
88
80
0.3-0.8
40
0.3°"
91
80
0.3-i.l
20
0.3
92
80
0.3-1.5
Light troffer diffusers
60
2.5
86 -
80
<3.8
40
1.0
92
90
<3.0
-
20
1.0
95
90
<4.5
Perforated and louvered
11-51
2.0
96
90
1.4-2.7
ceiling diffusers
80
1.0-3.4
——
av
Reprinted with permission from Mevins. T^q = throw of isothermal airstream to a terminal velocity of
50 ft/min (see Figure IX-4 and Table IX-5). L - characteristic dimension of the space (see Table IX-6)..
^loo/1-
-------
TABLE IX-5
Definitions of Airstream Characteristics
Throw: Horizontal distance measured from plane of supply dlffuser' to
farthest point of airstream center line at which airstream
velocity equals selected velocity, i.e., terminal velocity
(Tcq if terminal velocity is 50 ppo or T,0« if terminal velocity
is 100 fpm).
Spread: Divergence of airstream in horizntal or vertical plane»
Drop: Vertical distance between center line of terminal unit and point,
to vhich throw is measured.
TABLE IX-6
Characteristic Dimensions for Different Air Diffusers3
t
Diffuser Type Characteristic Length
High-sidewall grille
Circular ceiling diffuser
Sill grille
Ceiling slot diffuser
Light troffer diffusers
Perforated, louvered
ceiling diffusers
aReprinted with permission from Nevlns.^
IX-21
Distance to wall perpendicular to jet
Distance to closest wall or intersecting
air jet
Length of room in direction of jet flow
Distance to wall or midplane between out-
lets
Distance to midplane between outlets plus
distance from ceiling to top of
occupied zone
Distance to wall or midplane between out-
lets '
-------
but more research is needed to analyze the effects better. Moreover,
actual conditions in the occupied space (i.e., normal working
conditions) may be very different from those predicted by the ADPI
method., because the obstructions, people, and appliances in the space
may cause a different air pattern.
*, ADPI relates comfort to local air temperature and local air
velocity a3 they deviate from a setpoint suitable for providing
thermally comfortable conditions. This setpoint must be established by
other methods, such as percentage of people dissjatisf ied (PPD),1* KSU
thermal sensation index,51 and standard effective temperature
(SET).25 All these methods determine the proper combination of
ambient air temperature, relative humidity, mean radiant temperature,
and air velocity that must exist in the room as a function of the
occupants' activity and clothing.
CONCLUSIONS
Currently, air-diffusion systems are designed for1 two main
purposes: to supply ventilation air according to type of room and
intended use,, as required by codes; and to locate supply-air terminal
units and define setpoints' on the basis of occupant comfort, which
depends on thermal factors.
RECOMMENDATIONS
Interactions between thermal factor^ and mass factors (i.e.,
concentrations of water vapor, odors, and other gaseous contaminants
and suspended particles) that influence the comfort or health of
occupants must be studied, and the results must be incorporated into
the design procedure. The measurement of air quality in a space is
still quite difficult. It is recommended that research be
conducted to provide design guidelines for the selection and placement
of air-supply and -return units that will ensure both the mass air
quality and the thermal air quality required in a space under
conditions of use.
AIR-CLEANING EQUIPMENT
The principles that govern the process of cleaning air to improve
its quality for use indoors are similar to those for industrial
processes to remove effluent gases before discharging exhaust air to
the atmosphere. However, these processes and the equipment involved to
process air for ventilation are radically different from their
industrial counterparts.
IX-22
-------
LOCATION OF INDOOR-AIR Ci.EANERS
As shown schematically in Figure IX-5, the location of air-cleaning
equipment in a ventilation system will vary with the type of system and
its application. (Strategies for control of indoor pollutants are
discussed in tne final section of this chapter.) First* if the
concentrations of contaminants in outdoor air are unacceptable,* '
the outdoor air must be cleaned. Second^ recirculated air from
occupied spaces must be cleaned to achieve the sane quality as
specified for the outdoor air used for ventilation. Third, special
ventilation systems, such as fume hoods, may use air-cleaners in the
supply and exhaust airstreains.
TYPES OF AIR-CLEANERS
An air-cleaner capable of controlling particulate, vaporous, and
gaseous contaminants does not exist. Filters and electronic cleaners
are used to remove airborne particles from ventilation air; and
commercial and institutional facilities may use wet collectors. Viable
biologic particles are usually removed by special filters, electronic
air-cleaners, or wet collectors; in some cases, ultraviolet (UV) lamps
may be used to inactivate the viable contaminants. It should be noted
that UV radiatiqn is used to kill bacteria, but not to remove them from
the airstream.
Filters and electronic air-cleaners are not effective for removing
gases or vapors. Sorption devices are usually selected to remove these
contaminants from the airstream. If both particles and gases or vapors
must be removed, air-cleaners first reiftove the particles,' then the
gases or vapors. In some critical applications, such as hospital
operating rooms, a "final" filter may be required to remove residues or
particles' sloughed from the gas-removal devices.'7
Devices for Particle Removal
. Airborne particles are commonly removed by mechanical filter units
that use one or a combination of the following mechanism:22
Inertial impingement (impaction): An abrupt change in
direction of the airstream causes airborne particles to collide with
the filter fiber. This method of collection is most effective with
larger particles.
• Interception: This method of collection is a special case of
impingement in which a particle collides with a fiber, independently of
inertia., This method may be more effective than impingement at low
velocities.
* Straining: Airborne particles are captured as they attempt to
pass between two adjacent fibers.
Diffusion: Very small airborne particles are driven to the
filter fiber by random molecular bombardment by air molecules. This
method is most effective for the smallest particles.
IX-23
-------
Exhaust
Infiltration Air
Outdoor
Makeup
Air (or
Ventilation
Other
Air-Cleaner
Location
i
N
Alternate
Paths for
Recirculated
Air
Ventilating /
Air /
Other
Air-Cleaner
^ Locations
General
Exhaust
Occupied
Space
Other
Air-Cleaner
Location -
Local
.9 r-^3~ Makeup
-ir
3 c'
a>
>
Return Air
Air for
Ventilation
Local
Exhaust
- Exfiltration
FIGURE IX-5
Schematic of a ventilation system. Adapted from ANSI/ASHRAE 62-1981.2
-------
The relationship between filter efficiency and particle size is
shown in Figure IX-6. The effectiveness of diffusion is greater for
.smaller' particles,, whereas the effectiveness of' impingement,
interception, and straining is greater for larger particles. Thus, a
characteristic performance curve, similar to the upper curve in Figure
IX-6, shows a minimal effectiveness of a filter to remove a given
particle size.*1
The performance of a mechanical filter is usually expressed in
terms of its particle removal efficiency, its loading capacity, and its
resistance to air flow.1' Removal efficiency may be expressed as a
function of the mass, physical or aerodynamic size (e.g., Stokes
diameter), or number of,particles removed.1' " \ relationship among
these efficiencies can be expressed mathematically," but the filters
must be tested to express the appropriate efficiencies numerically.
Although many test methods for evaluating filter efficiencies have been
published, IS * * those generally accepted for indoor environments
in the United States are ASHRAE Standard 52-76 for mass and size
efficiencies* and MIL Standard 282 for number efficiency.*1 A
method for rating the loading (i.e., dust-holding) capacity is also
specified in ASHRAE Standard 52-76. Both standards result in single
value ratings. MIL Standard 282 specifies a means foe rating the
efficiency of DOP (dioctylphthalate) produced by a special generator in
removing 0.3-ym particles. ASHRAE Standard 52-76 specifies a means
for rating the size removal efficiency of a filter challenged with a
standardized "atmospheric dust." A "weight arrestance" (i.e., mass
removal efficiency) procedure specified in ASHRAE Standard 52-76
results in a single value rating for a filter challenged with a
"synthetic dust." This dust is used to rate the dust-holding -capacity
of a filter (i.e., the amount of dust a filter can retain before a
specified pressue drop is reached). 1 A major shortcoming of these
standards is the lack ' defined procedures to rate mass, size, and
particle removal efficiencies as functions of particle size.
The other characteristics necessary to rate the performance of
mechanical filters are the air flow rate at which the efficiencies are
determined and the air pressure drops imposed by the filter when it is
clean and when it is fully loaded. Both standards specify procedures
for determining these characteristics. Characteristics for several .
~-.ypes of mechanical filters are summarized in Table IX-7.
Mechanical filters are used for three kinds of applications in
which the three types of removal efficiencies are required:
• Filters used' to remove the largest and heaviest particles from
an airstream are usually rated by weight efficiency (see Table IX-7).
They are often described as low-efficiency filters and are used as
upstream prefilters to remove some of the load before the final
filters3 or to protect such mechanical devices as fans and
heat-exchangers. Probably the most common use for this type of filter
is in residential furnaces and central air-conditioning systems.
« Medium-efficiency filters, usually rated by size or dust-spot
efficiency," are used when smaller particles must be removed from the
air. They are more expensive than low-efficiency filters. They are
IX-25
-------
100 (-
>
u
z
<
>
o
s
10 -
yj 0.1 —
H
C
2 0.01
0.001 -
0.0001
0.001
y X,
/
>
z
0.01 0.1 1
PARTICLE SIZE./im
10
FIGURE TX-6 Filter efficiency as a function of particle size for a typical
impingement filter. Adapted from Crawford.
IX-26
-------
TABLE IX-7
Typical Characteristics of Mechanical Filters'
Type of Air Cleaner
Viscous-impingement filter
>ry-type extended surface:
Control
Mechanism
Impingement
Impingement
Pressure Efficiency, 3!
Drop, Pa Weight1" SlzeJ
Number
<125
20-50
50-75
60-80
70-85
5-10
5-15
5-20
10-25
x
i -
K>
filters)
aAdapted from ASHRAE.
''Pressure drop at air velocity of 1-4 m/s through media; tllter-face velocity usually higher.
cAlso described as dust arrestance in ASHRAE Standard 52-76.4
dAlso described as atmospheric dust spot efficiency in ASHRAE Standard 52-76.4
ePartide-removal efficiency of 0.3 pm (i.e., UOP method), as described in Mil Standard 282.63
fAs described in ASHRAE Standard 52-76.4
Dust-Holding
Capacity,
g/(l,700 mJ/h)
70-140
120-560
180-540
240-760
Open-cell foams
and
12-250
7C-80
15-30
—
180-425
Cellulose glass-fiber mats
intercep-
80-90
20-? 35
—
90-180
Multi-ply glass-fiber mats
tion
85-90
25-40
5-10
90-180
5- to 10-ti m fibers, 6-12 mm
90-95
40-60
15-20
270-540
thick
3- to 5-Vim fibers, 6-20 mm.
>95
60-80
35-40
180-450
thick
1- to 4-gm fibers and asbestos
>95
80-90
50-55
180-360
0.5- to 2->pm glass fibers
—
90-98
75-90
90-270
0.1- to 1-ym fibers (HE?A
—
—
99.97-99.999
500-1,000
-------
often used with prefilters to extend their useful lives. They are also
specified for sensitive areas in hospitals'7 and are used for removal
of tobacco smoke or for protection of materials fr6m soiling.
* High-efficiency particulate air (HEPA) filters are rated by
number efficiency*' and are used when "absolute" filtration is
required. These filters were originally developed for industrial
applications and are generally used in nuclear reactor.facilities and
for cleanroom applications. HEPA filters are expensive and are
therefore normally protected by prefilters. Medical facilities use
them in isolation wards, pharmacies, and surgical
suites.'•IPP* 51-73) In these areas, it is often necessary to tust
the filters after installation. Test procedures developed for some of
these applications are available in the literature.1'^PP* .193-213)
Small HEPA filters have recently been used to create "clean-air zones,"
especially about the heads of allergic persons during sleep. Air is
drawn through the filters and distributed from headboard emission poets
as a discrete laminar-flow field." Claims of removal of various
inhalant allergic substances and reduction in associated problems have
been made; however, the effect on removal of biogenic particles
requires more study.
It should be noted that mechanical filters are effective only when
the particles remain airborne in the ventilation system,, and particles
from an occupied space must be transported to a filter in the system
(Figure IX-5). Particles that have settled are a residual source of
contamination if re-entrained. In removal or cleaning of filters, care
must be exercised to minimize re-entrainment and exposure of
maintenance personnel.
Electrortatic precipitators are also commonly used to remove
airborne particles. The precipitation proems consists of providing an
electric charge or. the particle, establishing an electric field, and
removing the particle from the precipitator.*?^P*
Electrostatic precipitators, used for outdoor pollution control,
typically are of single-stage design and use a high direct-current
(d-c) voltage (20-100 kV) to produce a negative corona (see Figure
IX-7). The corona generated provides the necessary charge to particles
for the electric field to cause them to drift to the .collecting
electrodes.
Electrostatic precipitators, which are used only for cleaning
ventilation air, are designated as "electronic air-cleaners."' Three
types of electronic air-cleaners are commonly used for control of
particulate matter in residential and commercial environments:
• Ionizing-plate type; These devices are typically of the
two-stage d'e3ign, as shown in Figure IX-8. A high d-c voltage (e.g.,
12 kV) produces a positive charge on the rirborne dust, which is then
precipitated on the collection,plates. Tie positively charged corona
is less effective as a particle-collector than the negatively charged,
but produces much less ozone.
IX-28
-------
I
Collected Dust
FIGURE IX-7 Schematic of a single-stage ^yire and pipe) ulectrostatic
precipitator. After Oglesby and Nichols.
IX-29
-------
Icn Path
Air
Flow
Discharge
Electrode
(wire)
Stage
Collection Electrodes
(plates alternately
charged)
Air Flow
->
Path of Charged
Dust.Particles
Air Flow
Downstream
mecnanical
filter
(optional)
FIGURE IX-8 Schematic of a two-stage ionizing-plate electronic air-
cleaner. After .ASHRAE.
IX-30
-------
* Charqed-media, nonionizing type: A dielectric filtering
medium (e.g., glass-fiber mat or cellulose mat) is supported on or in
contact with an alternately charged and grounded gridwork (e.g., +12 kV
d-c). Airborne particles are polarized in the resulting field and
electromagnetically attracted to the filaments of the filter.
* Charged-media, ionizing type: Airborne particles are charged
by positive ions from a discharge electrode. The chargsd particles are
then collected on a charged filter mat downstream from the ionizer.
The performance of electrostatic precipitators is; often evaluated
in terms of the Deutsch equation: *7 n ¦ 1 - exp[-Av//Qj, where '
,n = particle removal efficiency, A = area of collecting surface
(m2), Q = gas volume flow rate (nP/s), and w =¦ migration velocity
of particle (m/s). This equation can only approximate the actual
removal efficiency. Manufacturers often publish performance data on
removal efficiency, particle size, and an empirically derived migration
velocity (callad "precipitation rate parameter," wp) . *7'P*
Unlike the migration velocity (w), the parameter wp includes effects
due to rapping losses (i.e., for industrial precipitators), gas flow
distribution within the precipitator, .particle size distribution, and
dust resistivity.*7^P* 2*4) A performance curve for a typical
electrostatic precipitator is shown in Figure IX-9.
Conversely, the performance of electronic air-cleaners is not
usually rated in terms of the Deutsch equation, but rather in terms of
dust-spot efficiency" or the DOP method." Their performance '
compares favorably with that of medium- to high-efficiency mechanical
air filters, and their major advantage is the low resistance to air
flow, Compared with that of mechanical filters. However, this low
resistance can be a disadvantage, if they are not installed so that
there is uniform air velocity at the entrance of the cleaner. As shown
in Table IX-8, compromises are often required with respect to removal
efficiency, pressure drop, and space limitation when selecting
electronic air-cleaners.
Electronic air-cleaners are often used for the same applications as
described for medium-efficiency and HEPA filters and normally require
the same type of prefiltering as medium- to high-efficit.-sy mechanical
filters to remove larger particles. Special care is needed in
. servicing, and any of three methods is acceptable:
Removal of collection plates or charged media, washing with a
detergent, and drying before reinstallation.' This method is most
common for residential units and small commercial applications.
' *, Washing of collecting plates in place with an integral
washer. This method is commpnly used in larger commercial
installations.
* Collection of dry agglomerates dislodged from the collection
plates. An automatic replaceable-medium filter is usually used for
this purpose in large and small commercial installations (sec Figure
IX-8).
IX-31
-------
PARTICLE DIAMETER, urn
FIGURE IX-9 Typical removal efficiency of electronic air-cleaner. After
ASHRAE.3
IX-32
-------
TABLE tX-,6 ,
Relative Performance of Electronic Air-Cleaners by Type3
Type of Cleaner
TonLzing plate
Charged inedia,
nonionizing
Charged media,
ionizing
Removal Efficiency, % Pressure
Dust Spot Method POP Method Drop, Paa
85-90
25-35
mO— 60
65-80
10-20
25-35
25-40
40-75
40-75
Relative Space
Requirement
Maximal
Minimal
Moderate
Values reported are approximate and were obtained by personal communica-
tion with C. W. Soltis, Filterlab, Inc., Houston, TX.
v *y
At face velocities of 1.5-2.5 m/s. 1 pascal (Pa) = 1 newton/m .
IX-33
-------
There are some problems to be considered with electronic
air-cleaners. There is a potential hazard associated with the high
voltage at the ionizing electrode, collection plates and charged
media; ' ozone can be produced by the high voltage, even with the
positive corona;*7^* 19®)*• and soiling can be,caused by charged
dust particles that penetrate the air-cleaner.H' '7
Disinfection with Germicidal Ultraviolet Radiation
Airborne contagion may be controlled with germicidal UV radiation
produced by mercury-vapor discharge lamps. Modern germicidal lamps can
be made of.glass that blocks radiation in the ozone-producing range,
but transmits the germicidal rays of 254-nm wavelength. This radiation
is effective in disinfecting most pathogenic airborne bacteria and
viruses, provided that the relative humidity does not exceed 70%; but 1
it is less effective against fungi.
Direct exposure to germicidal UV radiation causes superficial skin
and eye irritation, fading of fabric colors, and browning of plant
leaves. The UV source must therefore be placed so as to prevent direct
exposure. Usually, this is accomplished by irradiating the air above
the heads of occupants. The UV lamp fixtures are' relatively
inexpensive to install and operate. Frequency of maintenance depends
on dustiness of the environment. For example, in room installations
with cold cathode tubes, yearly cleaning and biennial replacement are
ordinarily adequate.
Upper-air irradiation is provided by lamp fixtures mounted on the
wall or. suspended from the ceiling at a height of about 7 ft. ,l
Occupants of the room are protected from direct exposure to UV
radiation by baffles. The effectiveness of disinfection depends on
good mixing of the air in the upper and lower portions of the room;
thus, stratification for energy conservation may be counterproductive
for contamination control with UV irradiation. However, the
concentration of airborne organisms in the breathing zone in a
uniformly mixed space can be reduced to one-tenth to one-fifth that in
the absence of UV radiation.
Upper-air irradiation is well suited to rooms with high ceilings if
stratification is prevented, such as classrooms. Success in blocking
the spread of measles has indicated' that inactivation of measles virus
with UV radiation is feasible. Improved UV lamps are being developed,
but the modern trend toward low ceilings in homes will seriously limit
the applicability of upper-air UV irradiation.
"JV irradiation of air in supply-air ducts is technically easy,
because intense radiation can be used there without hazard to people.
The amount of radiation required depends on the size of the ducts and
the supply-aii: flow rate." 71 When air is recirculated within the
ventilation system, UV irradiation is very useful to reduce the
concentrations of infectious organisms or droplet nuclei throughout the
areas supplied by the forced-air system. UV irradiation in the ducts
cannot stop the spread of infection in the room of a person with an
infectious disease. When the source of infection is in the room, the
IX-34
-------
concentration of infectious droplet nuclei is relatively high.
Therefore, UV irradiation is required in the room itself, or other
methods of contamination removal may be required.
Devices for Gas and Vapor Removal
Gas and vapor molecules cannot be effectively removed from
airstreams by the mechanical and electrostatic principles so far
described. Sorption is generally used for gas or vapor removal; there
are three basic mechanisms, as described by Heser: 15
•, . Absorption: Penetration of molecules of the pollutant into
the sorbent material (i.e., absorbing phase;, which may be either solid
or liquid. An example is absorption of nitrogen dioxide in a wet
air-scrubber.
* Adsorption on external surfaces: Physical or chemical
fixation on free surfaces. .Examples,of physical adsorption include
fixation of noble gases or nitrogen on nonporous solids, such as
aluminum oxide, graphite, ionic crystals, and metal foils. An example '
of chemical adsorption (chemisorption) is the jptake of carbon monoxide
on transition metals, such as iron and nickel.
• , Sorption on internal surfaces and in porest Physical
adsorption or chemisorption fixation on internal surfaces or within
pores of porous solids. Capillary condensation within pores and
occlusion of'molecules or ions also occur. Examples o£ these sorbents
are silica gel, aluminum hydroxide, activated carbon, clay minerals,
and molecular sieves. An application of this mechanism would be radon
sorption on activated carbon.
Although absorption is an important gas- or vapor-removal mechanism
for industrial, and military applications,ss it is seldom used for
environmental control in residential or commercial buildings, but is
used to control odorous gases or vapors.
Adsorption is a dynamic process in which the net rate of adsorption
is expressed as:*1 net rate of adsorption « (ks - d)-, wher« s =
rate of transfer of gas molecules to the adsorbent surface, k ¦»
fraction of molecules retained on the surface, and d 3 desorption
rate. Because d increases with amount adsorbed, the performance of
adsorption devices is not usually rated in terms of efficiency, but
rather in terms of adsorption capacity and penetration time.'* '7, 41
Adsorption capacity is usually measured in terms of the amount
(grams, moles, or cubic centimeters) adsorbed per gram of solid
adsorbent as functions of the partial pressures of the adsorbates at
constant temperatures (isotherms). Adsorption can be classified as
physical, chemical, surface, or internal. Lieser" has reported on
variations in adsorption efficiency as functions of relative partial
pressure.
Because the adsorption process is dynamic, specification of the
adsorption capacity is not sufficient to describe the effectiveness of
the process. A measure of its desorption rate or its correlate, the
IX-35
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penetration time, is also necessary. Penetration time has also been
described as the "duration of adsorbent service before saturation"'1
and the "breakthrough time," or "time in which the maximum permissible
concentration will not be exceeded."74 Methods described by Turk41
can provide a means to evaluate the dynamic performance of sorption
devices that is consistent with those used to evaluate the performance
of' particle removal devices.
Standard test methods for evaluating the effectiveness of gas and
vapor removal devices are not yet available in the heating,
ventilating, and air-conditioning (HVAC) industry in the United
States. However, some standard test procedures have been developed in .
western Europe.74 The development of such a standard in¦the United
States has recently been initiated' by ASHRAE. The conventional method
of selecting gas and vapor removal equipment has been to define the
potential sources of contamination, describe the problem to equipment
manufacturers, ask for equipment specifications,'sometimes ask for a
performance guarantee, and, less frequently, ask that the equipment be
tested for compliance after it is installed (H. E. Burroughs, personal
communication).
Performance of gas and vapor removal equipment depends on several
factors:41 concentration of the sorbate in>the airsttaam, total
surface area of the adsorbent, total volume of pores small enough to
facilitate condensation of the adsorbed gases, presence of other qases
or vapors (e.g., water vapor) that will compete with the adsorbate for
a place on the adsorbent, physical and chemical characteristics of the
adsorbate (weight, electric polarity,, size, and shape), and electric
polarity of the adsorbent surfaces.
Activated carbon consists mostly of neutral atoms of a single
element and presents a surface with a relatively homogeneous electric
charge. But oxygenated adsorbents (e.g., activated alumina,' silica
gel, and molecular sieves) contain nonhomogeneous distributions of
electric charges and are polar. Oxygenated adsorbents have
considerably greater selectivity than activated carbon and have much
greater preferences for polar than for nonpolar molecules. Thus,
oxygenated adsorbents are more useful for separation of pollutants, and
activated carbon is generally more useful for overall decontamination.
Because oxygenated adsorbents have a strong affinity for water vapor,
which is highly polar, they are essentially ineffective for direct
decontamination of moist air.41
To enhance adsorption, the adsorbent may be impregnated by other
substances. Enhancement1 is achieved by chemical conversion of the
pollutant by the impregnant to harmless or adsorbable products, the
impregnant's functioning as a continuous catalyst for oxidation or
decomposition, and the impregnant's functioning as an'intermediate
catalyst."
Table IX-9 shows some examples of adsorbents and pollutants arid the
mechanisms of action. Except for formaldehyde, ammonia, and perhaps
mercury, the pollutants listed may be found more commonly in the
industrial environment. But this table illustrates the broad range of
vapors and gases that might pollute the impregnated adsorbents. Note
that activated carbon impregnated with sodium sulfite and activated
IX-36
-------
TABLE IX-9
Adsorbent
Activated
carbon
Activated
alumina
Impregnant
Adsorbent Impregnations3
Pollutant
Bromine
Lead acetate
Phosphoric acid
Sodium silicate
Iodine
Sulfur
Sodium sulfite
Sodium carbonate
or bicarbonate
Oxides of copper,
chromium,
vanadium, etc.;
noble metals
(palladium,
platinum)
Potassium perman-
ganate
Sodium carbonate
or bicarbonate
Ethylene; other
alkenes
Hydrogen sulfide
Ammonia; amines
Hydrogen fluoride
Mercury
Mercury
Formaldehyde
Acidic vapors
Oxidizable gases,
including re-
duced sulfur com- .
pounds, such as
hydrogen sulfide,
COS, and mercaptans
Easily oxidizable
gases, especially
formaldehyde
Acidic gases
Action
Conversion to dibro-
mide, which remains
on carbon
Conversion to lead
sulfide
Neutralization
Conversion to
fluorosilicates
Conversion to
mercuric iodide
Conversion to
mercuric sulfide
Conversion to addition
product
Neutralization
Catalysis of air
oxidation
Oxidation
Neutralization
aReprinted with permission from Turk.^*
IX-3 7
-------
alumina impregnated with potassium permanganate are both effective in
adsorbing formaldehyde. This point is important, because formaldehyde
has been found indoors in concentrations above those considered
acceptable by some European standards and ANSI/ASHRAE Standard
62-1981. Gas-cleaning devices with the required impregnated adsorbents
are commercially available in the United States for use in residential
and commercial buildings. For example, activated carbon doas not
adsorb carbon monoxide, but a combination of a desiccant (silica gel)
and an oxidation catalyst, Hopcalite (a mixture of cupric oxide and
manganese dioxide), has been reported to be effective,'5 although the
Hopcalite must be kept scrupulously dry.
Preconditioning of the adsorbate can be used to enhance gas- or
vapor-cleaning.61 Some of the techniques are as follows:
* Use of a particulate prefilter to reduce loading of the
adsorbent.
* Concentration of the adsorbate (e.g., by pressurizing the
system).
Removal of moisture from the airstream by dehumidification to
a relative humidity below 50%.
* Cooling of the airstream to below 38°C (100°F).
Some of these techniques may be more energy-intensive than reducing
pollutant concentration by dilution ventilation. Thus, limitations to
the enhancement potential must be considered, including:
* Penetration time through the adsorbent is inversely
proportional to the air flow rate and the concentration or vapor
pressu'i of the adsorbate.JS 41
* Resistance to air flow (i.e., pressure drop) increases with
the air flow rate or velocity, the mesh size of the adsorbent, and the
thickness of bed.*1
* Adsorption capacity decreases as the temperature or relative
humidity of the airstream increases.41 75
Servicing tehniques for gas and vapor removal equipment include
replacement or regeneration of the sorbent and are similar to those for
replacing mechanical filters. The sorbent may be contained in panel-
like trays, canisters, or pleated retainers.91 Discarding old
sorbent and replacing with new is normally cost-effective, if the
penetration time exceeds a month and the sorbate concentration is low
(as in residential air-conditioning systems) or if the sorbent requires
impregnation." However, in some large HVAC systems, such as in ,
airline terminals, where the adsorbate concentrations are relatively
high (penetration times relatively short) and impregnated sorbents are
not required, regeneration may be cost-effective. Regeneration is
accomplished primarily by thermal methods, but techniques wijth ionizing
radiation and chemical activation are also available.1* Z1 ,l 11
Regeneration may be accomplished on site, or the sorbent may be
returned to the manufacturer for processing, as is usually done for
air-conditioning applications.
IX-38
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SUMMARY
Air-cleaning devices for residential and commercial applications
are commercially available. However, no single type of air-cleaning
process is available that can control particles, gases, and vapors.
Therefore, it is necessary to rely on multistage systems to obtain the
desired control, if all three types of contaminants are to be removed.
These systems consist of combinations of mechanical filters, electronic
air-cleaners, and gas and vapor removal devices. The systems can be
used as components within central air-conditioning systems or as
unitary appliances {fan-filter modules).
Voluntary standards exist in the United States for methods of
rating performance of particle-removal devices, and corresponding
standards for gas- and vapor-removal devices are now being developed.
However, no standards provide procedures for rating performance of
fabricated or assembled air-cleaning subsystems, whether they are
installed as components or used as unitary appliances.
Some effort toward predicting dynamic performance of gas-cleaning
from liquids has been reported,77 but dynamic modeling of indoor
air-quality control systems has received little attention.
Many of the air-cleaning control devices impose substantial
resistance to'air flow (i.e., system pressure drop). This resistance
requires additional energy consumption. Costs of installing and
servicing these devices must also be considered. Thus, optimization
techniques should be considered to decide between alternatives that
will provide acceptable indoor air quality, energy consumption, and
life-cycle costs.
STRATEGIES FOR CONTROL OF INDOOR POLLUTION
The demarcation between healthful and unhealthful air is not well
defined. Although air-quality standards exist for outdoor air and for
the industrial environment, few standards directly address the indcor,
nonindustrial environment (see Appendix A). Occupants of indoor
environments are expected to be exposed to long-term low concentrations
and intermittent high concentrations of pollutants. Control strategies
designed to limit indoor concentrations must consider the possible time
dependence between exposure and' effects, as well as the specifics of
source configuration and contaminant characteristics (i.e., gas versus
particles, reactivity versus nonreactivity, molecular weight, particle
size).
Five general control strategies (see Table IX-10) have been
identified and may be applied in indoor environments: ventilation,
source removal, source modification, pollutant removal, and education.
These strategies may not be mutually exclusive; combinations, such as
source modification plus ventilation, may be preferred in some
situations. This section briefly discusses these strategies and
tabulates the relative effectiveness of some of them for various
contaminants. More details on controls are provided in Chapter IV,
with respect to individual contaminants or sources.
IX-39
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TABLE 1X-10
Indoor-Pollution Control Strategies
Control by Ventilation
A. General ventilation
B. Spot (zone or localized) ventilation
C. , Infiltration
Control by Source Reooval
A. Material or product substitution
B. Restrictions on source use, sales, and activities by type
of Indoor facilities
Control by Source Modification
A. Change in combustion design
B. Material substitution
C. Reduction in emission rates by intervention of barriers
Control by Air-Cleaning (Pollutant P tnoval)
A. Particle filtering
B. Gas and vapor removal
C. Passive scavenging or absorption
Education
A. Consumer information on products and oaterials
B. Public Information on health, soiling, productivity, and
nuisance effects
C. Resolution of legal rights and liabilities of consumer,
tenant, oanufacturer,' etc., related to Indoor quality
IX-AO
-------
Ventilation is the principal means of controlling residential
indoor pollution by dilution with outdoor fresh air. (See Figure IX-10
for schematic of HVAC system for nonresidential building.) Outdoor air
is brought in and dilutes the indoor-generated pollution. This
strategy is in conflict with energy conservation* in that the heat and
humidity of the displaced indoor air are not conserved. Control by
dilution requires a well-ventilated indoor space; energy conservation
requires reduction in the amount of unconditioned air brought in from
outdoors. Optimal air ventilation must be estimated* or energy must be
conserved and indoor quality preserved without reducing ventilation
rate. . Heat-exchangers provide the technologic capabilities to conserve
energy while not substantially reducing the.ventilation rate.
Control of indoor air quality in many buildings depends, on the HVAC
system. Maintaining acceptable indoor air quality has not yet been a
design feature of HVAC systems (see earlier sections of' this chapter)..
The American Society of Heating, Refrigerating, and Air-Conditioning
Engineers has recently included indoor air quality as additional design
and operating criteria for HVAC in its new ventilation standard.1
The use of HVAC systems as a means of controlling the quality of indoor
air is promising.
HVAC systems can be divided into several categories, as listed in
Table IX-11. Each category has advantages and disadvantages that
broadly define the characteristics of the individual system.'
Potentially, the mass concentration and thermodynamic requirements can
be met by any of several HVAC systems. However, proper design will
optimize equipment selection and component configuration and the
functional and economic requirements of a building's HVAC system.
Table IX-12 indicates' typical applications for various HVAC systems.
Local exhaust—e.g., forced ventilation near a known or well-defined
source of indoor pollution—is widely used in industrial environments
and to a lesser extent in resiiences. Control is achieved by
exhausting the pollutant at the source to the outdoor environment.
Examples of such residential use are bathroom vents and vents over
cooking and heating facilities. It is important that exhaust air not
be re-entrained into the building.
Some are^s in a structure may have unique requirements .for spot
ventilation—for example, positive- and negative-air-pressure zones.
Exhaust fans may be required to control moisture and odors in bathrooms
without windows. Kitchens and kitchen,stoves usually have'some form of
filtered, unvented forced draft for contaminant control, and unvented
range hoods with charcoal filters have recently become popular. These
may be effective for grease, odors, and other large molecules, but not
for removing carbon monoxide and other small molecules. Furthermore,
the filters are somewhat expensive and in normal practice are not
changed often enough to be reliable. For these reasons, the unvented
range hood cannot be considered a reliable pollution control device.
A further problem with the use of spot-ventilation exhaust fans in
airtight houses is that too much powered exhaust reduces the natural
draft in the furnace vent and can cause combustion products from the
furnace to be drawn into the living space. Spot ventilation or exhaust
is not provided for gas stoves, gas ovens, small gas water-heaters, and
IX-41
-------
Exhaust
Air
Outside
Air
Exhaust
Damper
Return
Fan
T
U
?
i i
Control Damper
for Air Recirculation
^ V
—t Mixed ^
1—Air
1
1
(J-
Inlet
Damper
/ Supply Fan
Filters, ,
Heating, Cooling Coils
Air from
Occupied
Space
Air to
Occupied
FIGURE IX-10 Schematic of conventional heating, ventilating,
and air-conditioning (HVAC) air-supply system for nonresiden-
tial buildings.
IX-42
-------
TABLE IX-11
Air-Handling i!ystems
Category
All air
Description
Provides all required
sensible and latent
heat-exchange capac-
ity in air supplied
by thfe system
Advantages
1. Centralized location
of all major equipment
2. Removes major compo-
nents from conditioned
area '
3. Greatest potential for
use of free cooling
4. Flexibility under
varied operating con-
ditions
5. Easily adapted to heat
recovery
6. Optimal distribution -
for'air motion control
7. Suitable for large
makeup-air require-:
ments
8. Adaptable to automatic
seasonal changeover
9. Adaptable to winter
humidification
Disadvantages
1. Additional duct
clearance require-
ments
2. Additional fan
energy required
for perimeter load
during unoccupied
hours ¦
3. Air balancing
difficult
4. Accessibility .to
terminal devices
required
Air-water Both air and water
distributed to space
to provide required
heating and cooling
1. Individual room tem-
perature control
2. Flexibility under
varied operating con-
ditions
3> Low distribution space
requirement
4. Reduced central equip-
. ment space requirement
5. Horsepower savings by •
using water instead of
air
6. Reduction in fan power
requirements during'
occupied period
7. Can eliminate cross-
contamination. .
8. Long life of compo-
nents
1. Low primary air
quantities make
design o^ two-pipe
system critical
for proper inter-
mediate-season
control
2. System changeover
can be complicated
3. Usually limited to
perimeter spaces
A. Controls tend to be
more complex
5. Secondary air flows
create high main-
tenance requirements
6. Primary air supply
usually constant
7. Primary air provides
all dehumidifica-
tlon, so low-dew-
point air Is pro-
vided
8. Not able to handle
high-exhaust
• applications
IX-43
-------
Table IX-11 (contd)
Category Description
All water
Provides space required
for heating and cool-
ing by distributing
hot and chilled water
to terminal unite
Unitary
Packaged system that can
provide heating and
cooling
Advantages
1. Flexibility for adapta-
tion to many building
configurations
2. One of lowest-first-
cost central-perimeter
systems
3. Easy to retrofit to
existing structures
A. Low system distribution
requirements
5. Low cross-contamination
potential
6. Individual room control
with quick response to
¦ varying loads
7. No seasonal changeover
need be required
Disadvantages
1. Individual room control
2. Individual air distri-
bution control
3. Heating and cooling in-
dependently controlled
by zone
4. Individual ventilation
air control
5. Usually space-saving
6. Usually low installation
costs
7. Usually lower initial
costs
8. Allows zone shutdown
1. Inadequate rela-
tive-humidity
control
2. No' positive venti-
lation for many
types of designs
3. Through-therwall'
units may be
unsatisfactory in
appearance on out-
side of building
A. Two-pipe systems
require seasonal
changeover
5. Maintenance and
service work re-
quired in occupied
space
6. Filters, coils, and
condensate drain
lines must be kept
clean to limit
bacterial growth .
1. Limited options
available' for size
and control
2. Limited capability
for exceptionally
high or exception-
ally low relative
humidity
3. Acoustics must be
carefully con-
sidered
A. Maintenance in
occupied space
required
5. Exterior building
aesthetics may be
affected
6. Higher operating
costs
IX-44
-------
Category
All air
Air-water
All water
Unitary
Systen
TABLE IX-12
HVAC System Typical Applications
. Typical Applications
Single zone
Variable air volume
Reheat
Dual duct
Multizone
Induction
Dual-duct induction
Fan coil
Valance units
Window air condi-
tioners
Through-t he-wal1
' conditioners
Rooftop
Water loop heat
pumps
Small department stores, individual shops,
computer rooms, single-family residences,
warehouses
Offices, institutional and public-assembly
buildings
Offices, laboratories, hospitals
Offices, institutional and publie-assembly
buildings
Small buildings, small offices
Offices, hospitals
Offices
Motels, hospitals, offices, apartments
Warehouses
Residences, small office buildings
Residences, small office buildings
Department stores, malls, offices
Large offices
IX-45
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space-heaters fueled with gas or oilj therefore, large amounts of ¦
carbon dioxide and water vapor are introduced indoors.
The indoor-pollution problems caused by the lack of spot
ventilation or exhaust in single-family residences are only now being
studied. The information is inadequate to assess the magnitude of the
problems or to define the amount of ventilation air needed to abate the
pollutants produced by these sources.
Source removal is the mast effective means of controlling indoor
pollution. Examples of source removal are no-smoking areas a.-.d
prohibition of u:ea-formaldehyde foam insulation and kerosene heating
units for indoor spaces occupied by people. These strategies ars more .
effective when substitute products are available and less effective
when they rely on enforcement to ensure compliance. Where source-
removal strateqies modify human'behavior, conflict with consumer
preference, or involve an economic penalty, they are less l\kely to be
adopted by regulatory bodies. The adverse effects of indoor
contaminant exposure must be well established in, the public
perception. Public debate centered on tne restriction of smoking in
public places illustrates the controversy that surrounds source-remo»al
strategies for maintaining indoor air quality. However, when material
or product substitution is net disruptive or expensive, source removal
is clearly the strategy of choice. It is obvious that these decisions
should be made early in the design stages of new facilities. If a
macerial or product already in use :s determined to be hazardous,
removal may still' be the strategy'of choice. Source removal has been'
applied in the removal of lead from house paint both in the product and
by paint removal. A current widespread effort to remove all asbestos
from school buildings is another example of the source-removal control
strategy. Cost consideration must be carefully compared with the
likely benefits in reduced health risks and property damage and with
other imputed benefits. Source removal may cause a displaced problem,
such as occupational exposure during removal or a hazaidous-waste
disposal problem. These and other factors must be carefully considered
before the institution of a program to remove an existing source.
Air-cleaning devices have been used in large indoor commercial,
industrial, and institutional environments to eliminate or reduce
indoor pollutants., This strategy has not been widely used in
residences, because the devices are expensive to buy and operate and
can be bulky and noisy. Small commercial electrostatic precipitators,
ion generators, air filters, and gas absorbers (charcoal filters) are
used to remove contaminants in some indoor environments. Many of these
devices are advertised to provide particlef.ree and odorfree clean
indoor environments. The efficiencies of these devices need to be
evaluated by independent organizations.
Source modification is an alternative to source removal. The
objective of source modification is to reduce the rate of pollutant
emission into the indoor environment. Source modification includes
maximizing the efficiency of gas cooking and heating facilities that
reduce emission of some pollutants. Coating of lead-based paints and
asbestos-containing building materials to seal the surface and prevent
emission is effective and practical. Coating radon- and formaldehyde-
IX-46
-------
emitting surfaces is promising and warrants further study. A source
should not be modified rfhen it can be assumed that the modification
will cause emission ol a different contaminant. The spraying of
surfaces that are formaldehyde-emitters may itself constitute a source
of indoor contamination.
Table IX-13 summarizes control strategies available for several
types of pollutants. The table identifies strategies proved effective
in controlling a pollutant, but interactive effects must be considered
if several pollutants are to be controlled simultaneously. This
requirement and the complexity of control strategies lead to the
necessity of an overall systems designer.
Control of indoor contaminant concentrations by dilution with
outdoor air will continue to be a major control.strategy. Direct
control of the ventilation system based on indoor contaminant
concentration is the best means of achieving the optimal compromise
between energy conservation and pollution control.
Some provision is needed to add or conserve moisture. Homes in
cold climates need to conserve humidity in the indoor air in winter and
reject as much water as possible to the outside1in summer. Simple
energy-conserving means for this kind of moisture control are not yet
available, but the latent heat associated with moisture movement can
represent substantial energy that is not conserved.
N»w ventilation control strategies are needed. Positive
ventilation with heat recovery should be introduced in the building
industry. Past practice fixed the temperature of the mixed air
(outside air plus recirculated air) . This simplified comfort control,
but. usually resulted in excessive energy loss. A floating mixed-air
temperature based on outside-air temperature can proyide closer control
of. the ventilation air and energy savings.
New sensors for optimal control of ventilation should be
developed. Although laboratory instruments can measure the
concentration of some indoor pollutants, often these instruments, are
too bulky, too expensive, too complex, and generally not suitable for
extended, unattended use that might be required in measuring indoor
environments.
Greater emphasis should be placed on controlling specific
pollutants at their sources. Combustion-generated pollutants—
including carbon dioxide, water vapor, carbon monoxide, and nitrogen
oxides—can be removed at the source. New inexpensive, small, and
uncomplicated pollutant control devices are also needed. New
construction materials must be examined ca.efully for undesirable
environmental effects.
The efficiency of each control strategy must be studied both in the
laboratory and under "real-life" conditions. As indicated earlier, a
systems approach may be required in large structures; however, less
elaborate and inexpensive means of controlling contamination in indoor
residential environments are conceptually possible,' are needed, and can
become practicable.
Some indoor pollution problems can be controlled through the
marketplace choices of an educated consuming public. The general
public must be informed of the sources of Indoor contaminants'and the
IX-47
-------
TABLE IX-13
Summary of
Control Strategies for Sources of Indoor Air
Pollutantsf-
Source Modification " Ventilation
Pollutant
Removal -
Material
General
Spot
Gas and
Substi-
Contain- Local
Ventil-
Ventil
Particle
Vapor
Pollutants
tution
ment ~ Exhaust
ation
ation
Removal
Removal
•Other
Radon and
R
R NR
R
NR
R
NR
proge ny
-
Formaldehyde
R
R NR
R
NR
NR
- R
—
and other
organic
substances
Asbestiform
R
R NR
NR
NR
R
. NR
—
minerals
and fibrous
glass
00
Combustion
Rb
NR Rc
R
Rc
Rd
Rd
. —
products
Cons ume r
R
R NR
R
NR
Rd
Rd
—
products
Tobacco smoke
R
NR NR
R
NR
Rd
Rd
—
"Odors
NR
R Rc
R
Rc .
Rd
Rd
Mask-
-
ing
(R)
Biologic
R
R R
R
R
R
NR
UV dis-
agents
infect'
(particles)
ion (R
Carbon dioxide
NR
NR R
R
R
NR
NR
—
Moisture
NR
NR R
R
R
NR
. R
Thermal
R
R R
R
R
NR
R
—
extremes
"
"R » recommended;
NR » not recommended.
^Source of heating can be substituted (e.g., heat pump,
electric
range).
£
Usually combined
atrategles
for a given pollutant.
Both cleaning methods usually required.
-------
adverse consequences of acute and chronic exposures. It,must be
informed about the cost and effectiveness of various control options
and the efficiencies of commercially available air-cleaning equipment.
The public should be informed of its legal rights with respect to
product liability. The obligation and rights under purchase and lease
agreements pertaining to healthful indoor environments for residential,
commercial/ and public places must be defined. Education provides easy
and inexpensive steps that help to improve indoor air quality. Such
steps include reduction in indoor smoking, ban of potentially harmful
indoor sprays, use of proper paint, changes in daily routines to avoid
exposing all family members to pollutants, and the'like. The
efficiency of this control strategy cannot be estimated, but most would
agree that only' a properly educated public can require steps toward
implementing one or more combinations of the other control strategies.
Public-interest organizations, public utilities* professional
societies, trade and manufacturing associations, and government
agencies all have a responsibility to ensure that the public.receives
factual information related to. indoor contaminants.
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IX-49
-------
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IX-52
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IX-55
-------
APPENDIX A
AIR-QUALITY STANDARDS
The possibility of establishing standards for indoor air quality is
under consideration, because its importance for protecting human health
is recognized as a major national environmental issue. The eve
increasing cost of energy has heightened the need for considering such
standards, inasmuch as a cost-effective method of reducing energy use
in buildings is to reduce ventilation, an action that can increase
indoor air pollution.
There is a regulatory indoor air standard for nonoccupational air
in the United States only for ozone. There are voluncary standards for
indoor air quality that may serve as guidelines to federal, state, or
local government agencies on formaldehyde, carbon monoxide, chlorine,
radon, carcinogenic aerosols, and other chemical substances. The ozone
standard applies only to devices that produce ozone as a waste
product. The radon standards and guidelines apply only to buildings
that are contaminated as a result of uranium-processing (e.j., by the
use of mill tailings as landfill) and buildings that are on phosphate
land in Florida.
Tables A-l through A-8 list a number of U.S. outdoor air-quality
and occupational standards and some relevant foreign standards. They
are presented not as an exhaustive list of aic-quality standards,.but
rather to impart perspective to the many allusions to standards
throughout this report.
A-l
-------
TABLE A.-1
National Primary Ambient-Air Quality Standards ad Set by
the U.S. Environmental Protection Agency
Contaminant
Sulfur oxides,
measured as
sulfur dioxide
Particulate
matter
Carbon monoxide
Ozone
Hydrocarbons
Nitrogen dioxide
Lead
Long Term
Concentration,
yi g/m
80
75
100
1.5
Averaging
Time 1
1 yr
1 yr
1 yr
3 moe
May be exceeded only once per year.
Geometric mean.
Short Term
Concentration,
U g/m ¦
365a
260
10,000*
40,000*
235°
160
Averaging
Time
24 h
24 h
8 h
1 h
1 h
3 hd
Reference
15
14
16 '
16
20
17
19
18
%
'Standard is attained when expected number of days per calendar year with maximal
hourly average concentrations above 0.12 ppn (235 yg/m ) is equal to or less than
1, as determined by Appendix H to subchapter C, 40 CFR 50.
J
3-h period is 6 a.m. to 9 o.m.
"3-mo period is a calendar quarter.
A-2
-------
Table A-2
Additional Ambient Air Quality Guidelines3
Long Term Short Term
Contaminant
Concentration1"
Time
Concentration1*
Time
Acetone - 0
7 mg/m
24 h
24 mg/m;?
30 mLn
Acrolein - 0
<5
—
25 yg/m3
7 mg/m
C
Ammonia - 0
0.5 mg/m
0.01 y g/m
,2.0 y g/m
Yr
C
Beryllium
30 d
—
—
Cadmium
24 h
—
--
Calcium oxide (line)
<1
—
20-30 yg/m3
0.45 mg/m3
0.3 mg/m
C
Carbon disulfide - 0
0.15 mg/mJ
24 h
30 min
Chlorine - 0
0.1 mg/m
24 h
30 min
Chromium
1.5 yg/m
24 h
—
—
Cresol - 0 .
0.1 mg/m;:
24 h
—
—
Dichloroethane - 0
2.0 mg/m3
24 h
6.0 mg/m3
30 min
Ethyl acetaf a - 0
14 mg/m
24 h
42 mg/m
30 min
Formaldehyde - 0
—
120 yg/m3
C
Hydrochloric acid - 0
0.4 mg/m
24 h
3 mg/m3
30 min
Hydrogen sulfide - 0
40-50 ug/m
24 h
42 ug/m
1 h
Mercaptans - 0
•5
— •
20 yg/ra3
1 h
Mercury
2 yg/m
' 24 h
— '
Methyl alcohol - 0
1.5 mg/m
24 h
5 mg/m
30 min
Methylene
20 mg/m3
• Yr
150 mg/m
30 min
chloride - 0 ,
50 mg/m
2 Ug/m ,
24 h
Nickel
24 h
—
—
Nitrogen monoxide
0.5 mg/m3
24 h
1 mg/m3
30 min
Phenol - 0
0.1 mg/m
24 h
—
—
Sulfates
4 ug/m
Yr
—
—
12 yg/m3
24 h
Sulfuric acid - 0
50 pg/m
100 v g/m
Yr
24 h
200 yg/m3
30 min
Trichloroethylene - 0
2 mg/m3
5 mg/m
Yr
24 h
16 tng/ra3
30 min
Vanadium
2 yg/m
24 h
—
—
Zinc
50 yg/m
'100 y g/m
Yr
24 h
aReprinted with permission from ANSI/ASHRAE, which states: "Outdoor'air shall be
considered unacceptable if it is known to contain any contaminant at a concentra-
tion above that listed in Table [A-2]. This table covers other common contaminants
¦for wl.ich no EPA ambient air quality standards exist. These [concentrations] were
selected from current practices in various states, provinces and other countries."
o
,^Contaminants narked "0" have odors at concentrations sometimes found in outdoor
air. The tabulated1 concentrations do not necessarily result in odorless conditions.
cUnless otherwise specified, all air quality measurements should be corrected to
standard conditions of 25°C (77°F) temperature and 760 nm (29.92 in.) of mercury
pressure (101.3 kPa).
^C, ceiling, or maximal allowable concentration..
A-3
-------
TABLE A-3
Selected Occupational-Safety and -Health Standards as Sec iy
U.S. Occupational' Safety and Health Adtslnlstratlana
Concentration^
Contaminant ppm mg/m"1
Carbon dioxide 5,000 9,000
Carbon monoxide 50 55
Formaldehyde .2 3
Nitric oxide 25 30
Nitrogen dioxide 5 9
Ozone 0.1 0.2
Sulfur dioxide 5 13
Inert or nuisance — 5 '
dust, respirable
fraction
Asbestos c c
aData from 29 CFR 1910.1000.U
b8-h time-weighted averages, except values for nitrogen dioxide,
which are celling values.
c
Fewer than two fibers longer than 5 ym per cubic centimenter.
A-4
-------
TABLE A-4
Radon Standards
Country
Indoor:
United States:
Sites contaminated
by uranium-process-
ing
Phosphate land,
Florida:
Existing housing
New housing
Canada:
Sweden:
Max., existing
buildings
Max., new buildings
Occupational:
U.S. miners:
Instantaneous maximum
Maximal cumulative dose
Average Annual
Working Level
0.015
Action
Status
<0.02
>0.02
Normal indoor
background
>0.01
>0.02
>0.15
200 Bq/m3a
70 Bq/m3a
1 WL
4 WLM/yrb
Cost-benefit analysis
-required when level Is
only slightly above
maximum
Reduce to as low as rea-
sonably achievable
Action Indicated
Investigate 1
Primary action criterion
Prompt action
Interim and proposed clean-
up standard for buildings .
contaminated by uranium-
processing sites
Recommendation to governor
of Florida
Policy statement by AECB
i
Proposed standard
MSHA standard
Reference
13,21
12
22
Assuming an equilibrium factor of 0.5, these values are 0.027 WL and 0.009 WL, respectively.
^Period is a calendar year. Dose for any month is defined as cumulative dose in WL-h' divided by 173. Assuming
173 h worked per month (i.e., 2,076 h/yr), average annual working level is 1/3 UL.
-------
TABLE A-5
Formaldehyde Standards
Country
Indoor air;
United States
Denmark
Netherlands
Sweden
Federal Republic of
Germany
Occupational air;
United States
Concentration,
£ee!
0.12 ppm maximum
0.1 ppm maximum
0.1 ppm maximum, new buildings
0.4 ppm minimum, old buildings0
0.7 ppm maximum, old buildingsc
0,1 ppm maximum
3 ppm; 8-h time-weighted average
5 ppm, celling
1 ppm, 30-min maximum
Status
Recommended
Recommended by ministers of
housing and health
Proposed by National Board
of Health and Welfare
Recommended by Ministry of
Health
Promulgated by 0SHA
Promulgated by 0SHA
Recommended by NIOSH
Reference
3
5
23
11
11
10
r
t
a0.1 ppm J.120ng/m .
b,
Several states have proposed indoor standards in the. range of 0.2-0.5 ppm.
c0.4-0.7 ppra is.a border range. Concentrations higher than 0.7 ppm do not meet the standard. Those
lower than 0.4 ppm do meet the standard.. Those within the range do not meet the standard if dwellers
complain. In recently built houses, 0.7 ppm should'be acceptable during first 6 mo.
J. E. Woods (personal coumunication).
-------
Table A-6
Selected Guidelines for Air Contaminants of Indoor Origin
Contaminant
Concentration • Exposure Time
Comments
Acetone - 0
Ammonia - 0
Asbestos
Benzene - 0
Carbon dioxide
Chlordane - 0
Chlorine
Cresol - 0
Dichloromethane - 0
Formaldehyde - 0
Hydrocarbons, aliphatic - 0
Hydrocarbons, aromatic - 0
Mercury
Ozone - 0
Phenol - 0
Radon
Tetrachloroethylene - 0
Trlchloroethane - 0
Turpentine - 0
Vinyl chloride - 0
4.5
5 ug/m
1?0 yg/m"
100 pg/m
0.01 working
level (WL)
Known human carcinogen;
best available con-
trol technology
Known human carcinogen;
best available con-
trol technology
.Continuous
Continuous
Continuous
Continuous
Annual average
W. German and Dutch
guidelines
Background 0.002-
0.004 WL
Known human carcinogen;
best available con-
trol technology
aReprinted with permission from ANSI/ASHRAE,1 which states: "If the /iir is thought to
contain any contaminant not listed [in various tables], guidance on acceptable
exposure . . . should be obtained by reference to the standards of the Occupational
Safety and Health Administration. For application to the general population the
concentration of these contaminants should not exceed 1/10 of the limits which are
used in industry. ... In some cases, this procedure may result in unreasonable
limits. Expert consultation may then be required." "These substances are ones for
which indoor exposure standards are not yet available."
^Contaminants marked "0" have odors at concentrations sometimes found in Indoor air.
The tabulated concentrations do not necessarily result in odorless conditions.
-------
Other
Contaminant
United States:
Ozone
Japan:
Carbon dioxide
Carbon monoxide
Particles
TABLE A-7
Indoor Air-Quality Standards
Concentration
0.05 ppm (100 yg/m^)
1,000 ppm (1,800 mg/ra^)
10 ppm (11 mg/m ),
150 yg/m
A-8
-------
TABLE A-8
U.S. STANDARDS
Ventilation Standards for Dwellings
ASHRAE Standard 62-73:,
Single-Unit Dwellings,'
ANSI/ASHRAE Standard 62-1981:
Single or Multiple Units,
cfm/room
Area
Minimum
Recommended
Minimum
General living areas
5
7-10
10
Bedroaas
5
7-10
10
Kitchens
20
30-50
100 (Intermittent operation)
Toilets, bathrooms
20
30-50
50 (intermittent operation)
All other rooms
NA
NA
10
Basements, utility
5
5
NA
rooms
PROPOSED NORTHERN EUROPEAN STANDARDS7
Area Standard
General living areas 0.5 ach measured in spring and autumn, bat not less than
4 L/s per beda
Kitchens 10 L/s continuously,3 plus:
For an electric stove with more than two rings, an
adjustable fan capable of removing at least 80% of the
gaseous cooking products
For other electric stoves, an exhaust fan of at least
30-L/s capacity
For gas stoves, an exhaust fan of the size necessary to
remove the combustion products
Toilets 10 L/s continuously,3 plus an openable window or vent or
an exhaust fan capable of 30 L/s
al L/s equals approximately 2 cfm.
A-9
-------
REFERENCES
1. American National Standards Institute, and American Society of
Heating, Refrigerating and Air-Conditioning Engineers. ANSI/ASHRAE
Standard 62-1981. Ventilation for Acceptable Indoor Air Quality.
New York: American Society of Heating, Refrigerating and
Air-Conditioning.Engineers, Inc., 1981. 48 pp.
2. American Society of Heating, Refrigerating and Air-Conditioning
Engineers. ASHRAE Standard 62-73. Standards for Natural and
Mechanical Ventilation, p. 6. New York: American Society of
Heatingv Refrigerating and Air-Conditioning Engineers, Inc., 1973.
3. Andersen, I. Formaldehyde in the indoor environment—Health
implications $nd the setting of standards, pp. 65-77. In P.O.
Fanger, and 0. Valbj^rn, Eds. Indoor Climate. Effects on Human
Comfort, Performance, and Health in Residential, Commercial, and
Light-Industry Buildings. Proceedings of the First International
Indoor Climate Symposium, Copenhagen, August 30-September 1, 1978.
Copenhagen: Danish Building Research Institute, 1979.
4. Atomic Energy Control Board [Canada] (AECB). Criteria for
Radioactive Clean-up in Canada. AECB Information Bulletin 77-2.
Ottawa, Ont., Canada: Atomic Energy Control Board, 1977.
5. Baars, R. The formal aspects of the formaldehyde problem in the
Netherlands, pp. 77-82. In P.O. Fanger, and 0. ValbjfSrn, Eds.
Indoor Climate. Effects on Human Comfort, Performance, and Health
in Residential, Commercial, and Light-Industry Buildings.
Proceedings of the First International Indoor Climate Symposium,
Copenhagen,. August 30-September 1, 1978. Copenhagen: Danish
Building Research Institute, 1979.
6. National Technical Information Service..Building Control Law and '
Dust Collectors, (in Japanese; English abstract) 1974. APTIC No.
63252.
7. NKB. Forslag till Nordiska riktlinjer for byggnadsbestammelser
rorande: Luftkvalitet. [Proposed Nordic Guidelines for Building
Codes: Air Quality] Stockholm, Sweden: NKB, 1979.
8. Swedish Ministry of Agriculture. Preliminary Proposal for Measures
to Minimize Radiation Risk in Buildings, Sections 3.2.2 and 3.2.4.
Stockholm: Swedish Ministry of Agriculture, 1979.
9. U.S. Department of Health, Education, and Welfare, Food and Drug
Administration. Standard for equipment producing ozone as a
byproduct. Maximum acceptable level of ozone. Code of federal
Regulations, Title 21, Part 801.415, July 1, 1979.
10. U.S. Department of Health, Education, and Welfare, National
-Institute for Occupational Safety and Health. Criteria for a
Recommended Standard....Occupational Exposure to Formaldehyde. DHEW
(NIOSH) Publication No. 77-126. Washington, D.C.: U.S. Government
Printing Office, 1977.
11. U.S. Department of Labor, Occupational Safety and Health
Administration. Occupational safety and health standards. Air
contaminants. Code of Federal Regulations, Title 29, Part
1910:1000, July 1, 1979.
A-10
-------
12. U.S. Environmental Protection Agency. Indoor radiation exposure due
to radium-:226 in Florida phosphate lands: Radiation protection
recommendations and request for comment. Fed. Reg. 44:38664-38670,
July 2, 1979.
13. U.S. Environmental Protection Agency. Interim cleanup standards for
inactive uranium processing sites. Fed, Reg. 45:27366-27368, April
22, 1980.
14. U.S. Environmental Protection Agency. National primary ambient air
quality standards for particulate matter. Code of Federal
Regulations, Title 40, Part 50.6, July 1, 1980.
15. U.S. Environmental Protection Agency. National primary ambient air
quality star&ards for sulfur oxides (sulfur dioxide). Code of
Federal Regulations, Title 40, Part 50.4, July 1, 1980.
16. U.S. Environmental Protection Agency. National primary and
secondary ambient air quality standards for carbon monoxide. Code
of Federal Regulations, Title 40, Part 5C.8,.July 1, 1980.
17. U.S. Environmental Protection Agency. Notional primary and
secondary ambient air quality standard for hydrocarbons. Code of
Federal Regulations, Title 40, Part 50.10, July 1, 1980.
18. U.S. Environmental Protection Agency. National primary and
secondary ambient air quality standards for lead. Code of Federal
Regulations, Title 40, Part 50.12, July 1, 1980.
19. U.S. Environmental Protection Agency. National primary and
secondary ambient air quality standard for nitrogen dioxide. Code
of Federal Regulations', Title 40, Part 50.11, July 1, 1980.
20. U.S. Environmental Protection Agency. National primary and
secondary ambient air quality standards for ozone. Code of Federal
Regulations, Titie 40, Part 50.9, July 1, 1980.
21. U.S. Environmental Protection Agency. Proposed cleanup standards
for inactive uranium processing sites. Fed. Reg. 45:27270-27375,
April 22, 1980.
22. U.S. Mine Safety and Health Administration. Regulations and
standards applicable to metal and nonmetal mining and milling
operations. Code of Federal Regulations, Title 30, Part 57.5-38 and
¦ 57.5-39, July 1, 1979.
2 3: Wahren, H. Formaldehyde Indoor Air Standards in Sweden. Paper
presented at the Consumer Product Safety Commission Technical,
Workshop or rormaldehyde, Washington, D.C., April 9-11, 1980.
A-ll
-------
APPENDIX B
ESTIMATING THE IMPACT OP RESIDENTIAL
ENERGY-CONSERVATION MEASURES ON
AIR QUALITY: A HYPOTHETICAL CASE
HYPOTHETICAL CASE STUDY
Two of the simple-*- and most cost-effective methods of reducing the
energy consumption of & residence are to increase the insulation and to
decrease air infiltrati'>n. However, infiltration , is the primary source
of ventilation for residences, and reducing it may adversely affect air
quality. Therefore, a1though caulking and weatherstripping a home may
reduce energy consumption, they may also adversely affect the health
and reduce the comfort of the occupants, unless alternative methods of
controlling air guali:t' are applied.'
Attempts to etitimav- the impact of residential energy-conservation
measures on air quality in,the home and, consequently, on the health
and comfort of the residents are frauglit with difficulty. Most
troublesome is the issue of incommensurability: one cannot confidently
compare the dollar costs of insulating a house and the associated
reductions in fue*.. bills with the essentially nonquantifiable potential
adverse effects 'jr. air quality, health, and comfort. Furthermore,
numerous assumptions must be made. Some of the assumptions are.
relatively reliabJa; for example, demographic studies can provide
evidence on average family size, lifestyle characteristics (such as
smoking habits), and proportion of homes with a particular appliance
(such as a gas oven). 1 Other assumptions may be based on evidence and
experience from the building trades—for example, the effectiveness of
caulking the windows of a home. (Engineering analyses of related
interactions have been performed.) Assumptions'concerning the air
quality in homes before and after.the institution of energy-
conservation measures can be based on evidence now being accumulated or
on data already in hand.
The following case study is an unvalidated example of the type of
analysis that might be considered to assist in making decisions
concerning energy conservation versus'indoor air quality. It is
proposed not as a solution to the analytic problem, but as an approach
subject to further study and refinement. As a discussion piece,, it may
assist in identifying the types of data needed for analysis, the most
appropriate mathematical models, and, most important, the assumptions -
B-l
-------
that auy be validly applied. The reader must be aware that the models
presented here have not been validated or tesced in practical caeea to
determine their effectiveness in predicting results. This presentation
is for the purpose of illustration and discussion of a possible
approach.
EXISTING CONDITIONS
To evaluate the possible impact of energy-conservation measures on
single-family residences, conditions in a hypothetical hone in central
Iowa are simulated. It is a 15-yr-old, split-level house with a
basement and an attached two-car garage. The total heated floor space
is 2,100 ft2, of which 700 ft2 is below grade. The house is of ,
wood frame construction on a concrete-block foundation. It has
insulation values of R7 in the walls and Rll in the ceilings,
double-pane windows, and an Infiltration rate of 0.8 air change per
hour (ach). with windows and ,doors closed. The house is heated .with a
natural-gps, foroed-air furnace and cooled with an-electric central
air-conditioning system. The house is occupied by a family of Civet a
father, who smokes cigarettes: his wife} her mother; and two children,
2 and 10 yr old. Appliances, include a natural-gas stove, a gas
clothes-dryer, an electric washing machine, an electric dishwasher, and
a gas water-heater.
All this is assumed to be fairly typical of a middle-class family
in central Iowa. 1 These conditions were used as the basis of an energy
and air-quality analysis of the hone. The hone was then reanalyzed for
two mutually exclusive conservation measures, to determine the changes
in energy consumption and air quality. The first measure was to
relnsulate the walls to a value of Rll (1 additional inch of cellulose
insulation}' and the celling to'R19 (2 additional inches of cellulose
Insulation); this measure was assumed to be accompanied by a reduction,
in the infiltration rate to 0.S ach. The second measure was a higher
Insulation alternative in which the walls were increased to Rll and the
ceiling to R30» the infiltration rate was assumed to decrease to 0.3
ach. Two other independent measures were analyzed for air-quality
impacti the installation of an electronic air-cleaner and the
cessation of cigarette-smoking. A summary of these alternatives is
shown in Table B-l. The results of the energy-consumption'and
air-quality analyses for these alternatives were either directly or
indirectly, used in an economic model to determine' the rate of return
available to the homeowners for the various alteratives.
CASE ANALYSIS
Energy Consumption
The annual heat loss and heat gain for the building were calculated
from a simple steady-state model, with an overall heat-transfer
coefficient and annual degree-days for heating and cooling. The model
was exe'cised for each of the three cases listed in Table B-2. Values
B-2
-------
TABLE B-l
Summary of Scenario Analyzed in Hypothetical Example
Insulation
Infiltration
Air
Condition
Case
Wall ,
Celling
(ach)
Cleaner
Smoker
Existing
P
R-7
R-ll
0.8
No
Yes
Alterna-
A-l
R-ll
R-i9
0.5 ,
i
No
Yes
tive
A-2
R-ll
R-19
0.5
Yes
Yes
B-l
R-ll
R-30
0.3 '
No '
Yes
B-2
R-ll
R-30 '
0.3
Yes
Yes
B-3
R-ll
R-30
0.3
, No
No
TABLE B-2
Insulation Alternatives
R Value (h « ft2 . °F/Btu)
Case
Description
Wall
Ceiling
Infiltration
P
Existing condition
7
11
0.8
A
Low insulation
11
19
0.5
B
High insulation
11
30
0.3
B-3
-------
for the overall heat-transfer coefficient (UA) were calculated in
accordance with the method used b/ ASHRAE;1 the results are listed in
Table B-3.
The amual degree-days11 are based on 30-yr averages for Des
Moines, Iowa, and are based on 65°F. The values used for heating and
cooling were 6,710 and 928 degree-days/yr, respectively. These values
for the overall heat-transfer coefficient and degree-days were used in
the following equation to calculate the annual heat loss and heat
gain: Q = 24(UA)(DD), where Q » annual heat loss or heat gain (Btu),
UA <* overall heat-transfer coefficient (Btu/h *°F), and DD - annual ,
heating (coding) degree-days. The results of these calculations are
also listed in Table B-3.
To estimate more accurately the energy consumed for heating, a
seasonal furnace efficiency had to be determined. This efficiency
depends on the steady-state efficiency of the furnace and' the amount by
which it is oversized. As the heating load is reduced, owing to the
conservation measures, the seasonal furnace efficiency is also
reduced—by approximately 2% for each 10% oversize increment (John E.
Janssen; personal communication). The seasonal furnace efficiencies
used for each of the cases are shown in Table B-4. By dividing these
efficiencies into the heating loads, the energy input to the house can
be calculated; by applying the energy conversion factor for natural gas
(100,000 Btu/ccC), the annual fuel consumption can be determined.
These results are shown in Table B-4.
The annual electric consumption for cooling is calculated from the
following equation: Qelec = l«3Q/(COP)(3,412), where Qej.ec B
electric-energy consumption (kWh), Q =» sensible heat gain (Btu), 1.3 =
adjustment for latent load (assumed to be 30% of sensible load), COP =>
seasonal coefficient of performance (assumed to be 2.5), and 3,412 B
conversion factor (Btu/kWh). The results of these calculations are
listed in Table B-5.
Air Quality
The air quality in the conditioned space was evaluated for the
three cases and for the two independent measures (installation of an
air-cleane: and cessation of cigarette-smoking). The contaminants
evaluated were carbon monoxide, nitrogen dioxide, formaldehyde, radon,
and respirable suspended particles (RSP), which include dust and
cigarette smoke. The models used in these evaluations are simple ones
that have not been experimentally validated. There is a need to
validate these findings not only experimentally, but also in practical
test cases. The objective of these analyses was to determine the
sensitivity of various parameters to the contaminant concentrations,
and absolute values may only be assumed as approximate.
General Models. The general model used to calculate the
contaminant concentration profiles (except that for radon) is shown
B-4
-------
TABLE B-3
Overall Heat-Transfer Coefficients
Heat Loss, Heat Gain,
Case Description 13A (Btu/h > °F) 10 Btu/yr 10 Btu/yr
P Existing condition 737 119 16
A Low insulation 582 94 13
B High Insulation 502 81 11
TABLE B-4
Annual Natural-Gas Consumption for Heating
Seasonal
Heat Loss, Furnace Natural-Gas Corsumption
Case
10 Btu/yr
Efficiency
10" Btu/yr
a-F/yr
P
119
0.60
198
1,980
A
94
0.56
168
1,680
B
81
0.53
153
1,530
TABLE B-5
Annual Electricity Consumption for Cooling
Heat Gain, Electric Consump-
Case 10 Btu/yr tion, kWh
P 16 2,400
A 13 2,000
B 11 1,700
B-5
-------
schematically in Figure B-l. The assumptions and nomenclature used are
as follows:
* Equal infiltration and exfiltration rates (V^).
* Uniform contaminant concentration (C) in the occupied volume .
(V).
* Constant outdoor contaminant concentration (CQ).
* An electronic air-cleaner with an RSP-removal efficiency#of
c, operating continuously with a constant-supply airflow rate (Vs).
* A net contaminant generation rate (N)—decay rates are;
neglected. A mass balance equation that describes the air quality of
the house is given as follows:
. VjfCo - C) + V8(Cg - C) ~ N » VdC (1)
dt
and
Cs o (1 - c)C.
This set of equations can be combined and rearranged to give the
following differential equation for the indoor concentration (C)
+' (vi + cVs)C p N + (2)
dt
' rate of dilution generation
change and and
in air ', removal infiltration
quality effects effects
The solution of this equation is:
where Cj is the initial condition for the concentration. This
1 t « *
equation is valid only for constant values of N, V^, Vgf e, and
CQ. For this analysis, the generation rate is assumed to vary by
steps. Therefore, Equation 3 can be applied to each step separately,
with the initial condition for a given step being the final
concentration of the previous step.
A slightly different model is used for radon, because of the
assumption of different concentrations above and below grade. The
model is shown schematically in Figure R-2 and includes an air exchange
(Vab) between the above- and below-grade spaces and no generation in
B-6
-------
FIGURE B-l General air-quality model for hypothetical single-family
residence.
B-7
-------
above grade
C , V
a a
Vib» Co
v, » C
la o
Vab» Cb
Cb» \
below grade
.
FIGURE 8-2 Radon oodel.
B-8
-------
the above-grade space. All concentrations, air-exchange rates, and the
generation rate are assumed to be constant? to give the following mass
balances:
below: Vib(Cb - CQ) + Vab(Cb - Ca) « N, and (4)
above: Via(Ca - CQ) + Vab(Ca - Cfa) - 0.
These equations can be solved simultaneously for the above- and
below-grade radon concentrations (Ca, Cb):
C = (——: ¦ . ^,'b : — ^N + C , (5a
1 \ViaVib+ViaVab+VjbVib/ - <5a
Cb = /-—:—V|a4.Vab . . Wc . (5b
" \Vi»Vib + Vi4Vab + VibVlb/ «,
Generation Rates. The contaminants are generated from several
sources, including cooking (caroon monoxide, nitrogen dioxide,, and
formaldehyde), smoking (carbon monoxide; nitrogen dioxide,
formaldehyde, and RSP), material outgassing (formaldehyde and radon),
and indoor dust generation (RSP). The assumed daily generation
profiles of these sources are shown in Figure B-3. The generation
rate for cooking is assumed to be constant and occurs at 7 a.m., 12
noon, and 5 p.m. for IS, 30, and 60 min, respectively. Smoking occurs
at 7 a.m. and 7:30 a.m. and every half-hour from 5:30 p.m. to 11:30
p.m., inclusive, "he duration of each occurrence of smoking is 10
min. * Material outgassing is assumed to be constant throughout the
day< Indoor dust is generated from 7 a.m. to 11 p.m., primarily owing
to resuspension of particles from carpeting. The generation rates for
all these sources are listed in Table B-6, with the outdoor
concentrations.
Concentration Profiles. To determine the daily indoor-contaminant
concentration profiles, a daily generation profile for each
contaminant (carbon monoxide, nitrogen dioxide, formaldehyde, and RSP)
was determined by summing the generation rates of the appropriate
sources. This provides an overall generation profile consisting of
step changes to which Equation 3 can be applied, as discussed
previously. The solution is started by choosing an initial condition '
(usually D CQ) at the beginning of a period (usually 7 a.m.)
and applying Equation 3 to each,interval of constant generation rate.
The solution proceeds throughout the day and is repeated until no
changes occur in t{ie initial conditions from one day to the next.
The concentration profiles for carbon monoxide, nitrogen dioxide,
and formaldehyde are shown in Figures B-4 through B-6 for cases P, A,
and B (0.8, 0.5, and 0.3 ach) . Figure B-7 shows the estimated
concentration profiles for RSP for each of the infiltration rates and
B-9
-------
Generation
Rateu
N
FIGURE B-3 Generation profiles of indoor pollutants for hypothetical
single-family residence.
B-10
-------
Outdoor
Concentration
TABLE B-6
Assumed Contaminant Source Summary
Indoor
aSee Hollowell et> al.^
Total
Contaminant
-------
Time, hrs
FIGURE B-4 Carbon monoxide'concentrations.
-------
Time, hrs
FIGURE B-5 Nitrogen dioxide concentrations.
-------
Time, hrs
FIGURE B-6 Formaldehyde concentrations.
-------
. Time, hrs
FIGURE B-7 Concentrations of respirable suspended particles.
-------
a fourth profile for the effect of the electronic air cleaner (c •
0.93, Va • 1,000 cf&j.* The Infiltration rate has a negligible
effect on the concentration profile after inclusion of the
air-cleaner} therefore, only one ptofile for a).l infiltration rates Is
shown.
The cessation of cigarette-smoking has no significant effect on
the carbon monoxide* nitrogen dioxide# or formaldehyde concentration
profiles. However, It does have a significant effect on RSP
concentrations, as shown in Figure B-8 for an infiltration rate of 0.3
ach.
Radon, an inert gas, is generated from the ftcay of radium ir. the
below—grade building materials (i.e., concrete).,7 The hazardous
radiation effects of radon *re due primarily to its progeny (RaA,
and RaC). The combined radiation effect of these progeny is taken
into account with the working level (WL) defined as:7 WL • 0.00103
RaA ~ 0.00507 Rafl ~ 0.00373 RaC, where RaA, RaB, and RaC are
concentration in picocuries per liter. The decay rate of rador. is
0.0075/h, which is negligible, compared with the assumed lnf il'a-ation
rates of 0.8, 0.5, and 0.3 ach. Therefore, infiltration was assumed
to be the only method of rado.i removal in the model.
To calculate the radon concentration profiles, radiation of 0.5
and 1.0 pCi/L was assumed for the above- and below-grade spaces at the
present condition (P). When these values are substituted for Ca and
Cb in Equations 5 and it is assumed that the outdoor rado>i
concentration is negligible, compared with, the indoor concentration
(CQ ¦ 0), values of Vab ¦ 8,960 ft^/h and H ¦ 256,000 pCi.h are
obtained. The values for the cir-exchange rate.between tie above- and
below-grade spaces a
-------
Time, hrs
FIGURE B-8 Effects of cigarette smoke and air cleaner en concentrations of resplrable suspended
particles.
-------
TABLE B-7
Radon Concentrations and Working Levels
Above Grade
Below Grode
Radon
Radon
Equilibrium
Concentra-
Concentra-
Case Factor
(F)
tion, pCi/L
WL
tion,
, pCi/L WL
P 0.84
0.50
0.004
1.00
0.008
A 0.84
0.88
0.007
1.43
0.012
B . 0.84
1.58
0.013
2.17
0.018
A filtered 0.32
0.88
0.003
1.43
0.005
B filtered 0.32
1.58
0.005
2.17
. 0.007
table B-8
Air-Quality Standards3
Contaminant
Concentration
Tine
Standard
Carbon monoxide
40 pg/m3
1 h
NAAQS
10 pg/nr
8 h
NAAQS
Nitrogen, dioxide
100 pg/m3
1 yr
NAAQS
Total suspended particles
75. pg/m3
1 yr
NAAQS
•
260 pg/m
24 h
NAAQS
Formaldehyde
120 pg/m3
Continuous
West German
Radon
0.01 WL
Continuous
37 FR 25918
aDerived from ANSI* and
ASHRAE.
1
B-18
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acceptable values are also plotted in Figures B-5, B-6, and B-7 for
nitrogen dioxide, formaldehyde# and RSP, respectively, for comparison .
with the predicted indoor contaminant concentrations. The carbon
monoxide health standard greatly exceeds the predicted values in
Figure B-4 and thus are not shown there. Figure D-5 shows that the
long-term standard (1 yr) for nitrogen dioxide concentration would be
exceer^i for approximately 1 h/d for the present condition (P),
whereas cases.A and B would exceed the standard for 2 and 4 h/d,
respectively. The formaldehyde concentration in Figure B-6 would
reach 41% of the short-term standard (continuous) for the present
condition (P), 58% for case A, and 86% for case B. Figure Br-7 shows
that the RSP concentrations would exceed the short-term standard (24
h) for case A during 3.5 h/d and case B'during 6 h/d, whereas the
present condition never exceeds this standard. The long-term standard
(1 yr) would be exceeded by cases P and A for 11 and 17 h/d,
respectively, and case B would constantly exceed the short-term
standard. The inclusion of the electronic air-cleaner would reduce
the RSP concentration to a point below the long-term standard for all
cases. The cessation of cigarette-smoking without the air-cleaner
would also reduce RSP concentrations below this standard for cases P
and A. However, case B would exceed the standard slightly for 13 h,
owing to indoor dust generation, as shown in Figure B-8. Table B-7
shows that the short-term standard (continuous) of 0.01 WL for radon
would be exceeded below grade for case A and above and below grade for
case B, unless the electronic air-cleaner were used.
Economics
To perform the economic analysis, estimates for the installation
costs and energy-cost, savings were needed for each of the conservation
measures considered.' • 10 Present annual energy costs for natural
gas and electricity were calculated by multiplying the annual energy
requirements (Tables B-3 and B-4) by the present fuel costs in Ames,
Iowa (0.28 $/ccf for natural gas and 0.057 $/kWh for electricity) for
each of the three cases (P, A, and B). Energy-cost savings for each
of the insulation alternatives (A and B) over the present condition
(P) were then calculated. The results are listed in Table B-9.
The assumed method of insulating for each of the alternatives was
to add sufficiient cellulose insulation to the walls and ceiling to
obtain the desired R value. Installation and material cost estimates
from a local insulation contractor in Ames, Iowa, wpre 0.20 3/ft of
ceiling area to upgrade from Rll to R19 (case A), 0.31 3/ft2 of
ceiling area to upgrade from Rll to R30 (case B), and 0.50 3/ft of
gross exterior wall area to upgrade from R7 to Rll (cases A and B).
With an insulated ceiling area of 1,400 ft2 and a gross exterior
wall area, of 1,576 ft , total' installed insulation costs of $1,218
and 31,378 were obtained for cases A and B, respectively. These costs
include $150 for caulking and weatherstripping. The only other first
cost needed in the economic analysis war 3726 for the installed cost
of the electronic air-cleaner.
B-19
-------
Salvage values at the end of the economic life for the various
alternatives were also needed. The economic life used was the length
of time that the present owner would continue to own the house. At
the end of this life (assumed to be 7 yr), it was assumied that the
salvage value of the insulation in terms of today's dollars would be
the same as its first cost, owing to the increase in resale value of .
the house. The salvage value of the electronic air-cleaner was
assumed to be $250.
Rates for electricity and natural gas were assumed to increase by
18 and 22%/yr, respectively, and the rate of general inflation was
assumed to be 10%/yr.
The economic analysis was' performed for three distinct situations,
each containing two mutually exclusive alternatives, as shown in Table
B-10.
The inflation-adjusted rates of return, shown in Table B-10, were
calculated for each alternative over present condition, as well as the
inflation-adjusted rate of return on the incremental costs for each
pair of alternatives.
If the homeowner's marginally acceptable rate of return (MARR)
were 10%, he should choose alternative B for situation I, alternative
A for situation II, and alternative B for situatior III.
SUMMARY
Care must be exercised when considering estimates based on models
that have not been validated against measurements. In such cases, the
magnitude of the estimated values may not be equivalent to that of the
observed values. Model estimates can be used, however, for
comparative studies to illustrate cause-effect relationships among
various parameters. From this perspective, the scenarios described in
this appendix show that energy-conservation measures may adversely
affect the indoor air quality of single-family residences. The
inclusion of the cost of air-quality control may reduce the economic
attractiveness of some energy-conservation measures. Although these
simulations have been based on several assumptions, they demonstrate
the inter- relationships between energy conservation and indoor air
quality. In addition, the'simulations of this hypothetical residence
focus attention on the factors that must be considered in the
regulation of indoor environments.
RECOMMENDATIONS
Some parts of the models presented, here have not been validated in
practical cases that show their utility. Further research is needed
to develop models and to test and validate their usefulness in
assessing the relationships between air quality and energy
conservation in residential and commercial buildings. A large program
should be established to develop this research tool further and to
demonstrate the usefulness of models in evaluating indoor
B-20
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TABLE B-9
Present Annual Energy Costs
Cost, $
Case Natural Gas Electricity Total
P , 550 140 690
A 470, 110 580
B 430 100 530
,P - A 80 30 110
P - B 120 40 160
TABLE B-10
Inflation-Adjusted Rates of Return for Hypothetical Examples
R0R over ROR on Incremental
Situation Alternative P cond, Z Investment ov<»r A, Z
I A-l 18.3 —'
B-l 23.0 55.1
II A-l ' ' 18.3 —
B-2 13.8 6.2
III A-2 9.5 —
B-2 13.8 55.1
B-21
s'
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environmental conditions. Models may be used in the design of future
structures to ensure the health and comfort of the public and
conservation of natural resources.
REFERENCES
I. American National Standards Institute, and American Society of
Heating, Refrigerating and Air-Conditioning Engineers. ANSI/ASHRAE
, Standard 62-1981. Ventilation for Acceptable Indoor Air Quality.
New York: American Society of Heating, Refrigerating and Air
Conditioning Engineers, Inc., 1980. 48 pp.
2 American Society of Heating, Refrigerating, and Air Conditioning
Engineers. ASHf.XE Handbook and Product Directory. 1977
Fundamentals, Chapter 22. New York: American Society of Heating,
Refrigerating, and Air Conditioning Engineers, Inc., 1977.
3. Engineering Research Institute. Manual of Procedures for
Authorized Class A Energy Auditors in Iowa. Ames, Iowa:. Iowa State
University Press; 1979.
4. Hollowell, C. D., J. V. Berk, M. L. Boegel, R. R. Miksch, W. w.
Nazaroff, and G. w. Traynor. Indoor air quality in residential
buildings. In F. E. de Oliveira, J. E. Woods, and A. Faist* Eds.
Building Energy Management—Conventional and Solar Approaches.
Proceedings of the International Congress, May 12-16, 1980, povoa
de Varzim,¦Portugal. New York: Pergamon Press, 1980.
5. Hollowell, C. D., J. V. Berk, C. Lin,, and I. Turiel. Indoor Air
Quality in Energy Efficient Buildings. Lawrence Berkeley
Laboratory Report LBL-8892. Berkeley, Cal.: Lawrence Berkeley
Laboratory, 1979. .
6. Hollowell, C. D., J. V. Berk, and G. W. Traynor. Impact of reduced
infiltration and ventilation on indoor air quality. ASHRAE J.
21(7):49-53, 1979.
7. Jonassen, N. Indoor radon concentrations and building materials
control of airborne radioactivity. In F. E. de Oliveira, J. E.
Hoods, and A. Faist, Eds. Building Energy Management—Conventional
and Solar Approaches. Proceedings of the International Congress,
May'12-16, 1980, Povoa de Varzim, Portugal. New York: Pergamon
Press, 1980.
8. Montag, G. M. A commercial building ownership energy cost anaysis
model. In F. E. de Oliveira, J. E. Woods, and A. Faist, Eds•
Building Energy Management—Conventional and Solar Approaches.
Proceedings of the International Congress, May 12-16, 1980, Povoa
de Varzim, Portugal. New York: Pergamon Press, 1930.
9. Repace, J. L., and A. H. Lowtey. Indoor air pollution, tobacco
smoke, and public health. Science 208:464-471, 1980
10. Smith. G. w. Engineering Economy. 3rd ed. Ames. Iowa:. The Iowa
State University Press, 1979.
II. U.S. Department of Commerce, National Climatic Center. Local
Climatological Data. Asheville, North Carolina.
12. woods, J. E., Ventilation, health and energy Consumption: A status
report. ASHRAE J. 21 (7.) :23-27, 1979.
B-22
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£
£
[NASI
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