PROCEEDINGS
EPA REGION 9 AIR TOXICS CONFERENCE
September 13 and 14, 1983
Sheraton Palace Hotel
San Francisco, CA
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TABLE OF CONTENTS
Final Conference Agenda 1
Air Toxics Programs and Policies
EPA'S Regulatory Process for Air Toxics 4
California Air Resources Board's Framework 15
for Air Toxics
California Department of Health Services
Carcinogen Policy 41
Background Information on Air Toxics
Ambient Monitoring for Air Toxics in Region 9 48
Sources of Air Toxics in California 58
Air Toxics in the Indoor Environment 66
A Study of the Relationship Between Cancer 73
Incidence and Air Pollution in Contra Costa
County, California
Air Toxics Case Studies
Air Emissions From a Former Disposal Site 88
Emissions from the ASARCO Copper Smelter 93
in Tacoraa, Washington
Toxic Air Pollution in Henderson, Nevada 100
Emissions from the Semiconductor Industry 103
Volatile Organic Emissions From Landfills 108
Asbestos Decontamination in Globe, Arizona 121
Panel Discussion 126
List of Participants 135
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EPA Region 9 presents an
AIR TOXICS CONFERENCE
Septenber 13 and 14, 1983
Sheraton Palace Hotel
San Francisco, California
Co-Sponsors
United States Environmental Protection Agency
California Air Pollution Control Officers Association
California Air Resources Board
League of Women Voters of California
FINAL AGENDA
Conference moderator: David Howekamp
Director, Air Management Division
EPA, Region 9
September 13, 1983
8:30 Welcome and introduction
John Wise - Acting Regional Administrator
EPA, Region 9
AIR TOXICS PROGRAMS AND POLICIES
8:45 EPA1 s regulatory process 'for air toxics
David Patrick - Chief, Pollutant Assessment Branch
EPA, Research Triangle Park, NC
9:30 California Air Resources Board's
framework for air toxics
Michael Scheible - Chief, Office of Program Planning,
Evaluation, & Coordination
California Air Resources Board
10:15 Break
10:30 California Department of Health Services
carcinogen policy
Dr. Rim Hooper - Research Scientist
California Department of Health Services
11:15 Lunch
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-2-
AIR TOXICS CONFERENCE
September 13, 1983
BACKGROUND INFORMATION ON AIR TOXICS
12:30 Ambient monitoring for air toxics in Region 9
Dr. Hanwant Singh - Director, Atmospheric
Chemistry Program
SRI International
1:15 Sources of air toxics in California
6. C. Hass - Chief, Haagen-Smit Laboratory Division
California Air Resources Board
Terry HcGuire - Assistant Division Chief,
Stationary Source Control Division
California Air Resources Board
2:00 Break
2:15 Air toxics in the indoor environment
Dr. David Grimsrud - Co-Leader, Building Ventilation
and Indoor Air Quality Program
Lawrence Berkeley Laboratory
Dr. Ren Sexton - Director, Indoor Air Quality Program
California Department of Health Services
3:30 A study of the relationship between cancer incidence
and air pollution in Contra Costa County, California
Dr. Donald Austin - Chief, Resource for
Cancer Epidemiology and California Tumor
Registry
California Department of Health Services
*
September 14, 1983
AIR TOXICS CASE STUDIES
8:30 Air emissions from a former disposal site
Kathleen Shimmin - Chief, Field Operations Branch
EPA, Region 9
9:15 Emissions from the ASARCO copper smelter in
Tacoma, Washington
Alexandra Smith - Director, Air & Waste Management
Division
Mike Johnston - Chief, Air Operations Section
Dana Davoli - Environmental Scientist
EPA, Region 10
10:00 Break
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-3-
AIR TOXICS CONFERENCE
September 14, 1983
10:15 Toxic air pollution in Henderson, Nevada
Michael Naylor - Director, Air Quality
Clark County Health District
11:00 Emissions from the semiconductor industry
Milton Peldstein - Air Pollution Control Officer
Bay Area Air Quality Management District
11:45 Lunch
1:00 Volatile organic emissions from landfills
Ed Camarena - Director, Enforcement Division
South Coast Air Quality Management District
1:45 Asbestos decontamination in Globe, Arizona
David Chelgren - Manager, Compliance Section
Arizona Bureau of Air Quality Control
2:30 Break
PANEL DISCUSSION
2:45 Panel moderator: Dr. Herschel Griffin - San Diego
State University
Panel members:
Milton Feldstein - California Air Pollution Control
Officers Association
Jeanne Harvey - League of Women Voters of California
Maureen Lennon - Atlantic Richfield Company
David Patrick - Environmental Protection Agency
Michael Scheible - California Air Resources Board
4:30 Closing remarks-EPA, Region 9
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-4-
EPA'S REGULATORY PROCESS FOR AIR TOXICS
David Patrick
Chief, Pollutant Assessment Branch
U.S. Environmental Protection Agency
Research Triangle Park, NC
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EPA'S TOXIC AIR POLLUTANT REGULATORY PROCESS
The principal authority under the CAA for control of toxic air pollutants
1s section 112, entitled National Emission Standards for Hazardous A1r
Pollutants. Section 112 defines "hazardous pollutant" as an "air pollutant
to which no ambient air quality standard 1s applicable and which 1n the
judgment of the Administrator causes, or contributes to, air pollution
which may reasonably be anticipated to result 1n an Increase 1n mortality or
an Increase 1n serious Irreversible, or Incapacitating reversible, Illness."
Regulations under section 112 must be established at a level to protect the
public health with an "ample margin of safety." Section 111 (New Source
Performance Standards) also provides for control of pollutants which adversely
affect human health or welfare but are not "hazardous" as defined under
section 112. Seven pollutants have been listed as hazardous under section
112 and to date emission regulations have been promulgated to control four.
Regulations for the remaining three hazardous air pollutants have been proposed.
One additional pollutant has been regulated under section 111 for health
reasons.
EPA's activities 1n dealing with these pollutants have been, as I am
sure you know, a matter of considerable debate both within the Agency
and outside. We attempted to articulate a decision-making policy In 1979
by proposing the Airborne Carcinogen Policy. Recently, we have been
attempting to develop a more general A1r Toxics Policy. While there 1s
clear agreement that resolution 1n the near future 1s Important, the Issues
and options remain broad and complex. Let me describe some of them first.
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In evaluating the extent of the toxic air pollutant problem, we must
first determine whether pollutants emitted to the ambient air pose significant
risks to public health. Available ambient exposure and health effects
Information and the scientific interpretation of that information do not
allow a clear-cut, absolute determination of the extent of the health risks
associated with toxic air pollutants for the nation as a whole. The magnitude
of the toxic air pollutant problem in terms of number of pollutants and
sources of emissions also is difficult to determine with precision. A 1976
EPA survey of the organic chemical industry Identified over six hundred
commercially important chemicals, of which about 50 were identified from
preliminary health information or production volume as possible toxic air
pollutants requiring more detailed assessment. Many source categories
other than those 1n the organic chemical Industry also may be significant
emitters of toxic air pollutants. These sources include mining, smelting,
refining, manufacture and end-use of minerals and other Inorganic chemicals;
combustion; petroleum refining, distribution, and storage; solvent usage
and disposal; mining, processing, use and disposal of radioactive substances
and radioactive by-products; waste treatment, storage and disposal facilities;
and various sources of non-toxic emissions which are chemically transformed
Into toxic air pollutants In the atmosphere. Notwithstanding, while the
existence of significant widespread risks resulting from exposure to ambient
concentrations of toxic air pollutants 1s the subject of considerable
scientific debate, clearly there are individuals that are at increased risk
from exposure to relatively high concentrations of air pollutants that may
be toxic and are emitted from uncontrolled or partially controlled sources.
In addition, there 1s the concern that exposures to these pollutants at low
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-7-
levels may result 1n chronic adverse effects which may not become evident
for many years.
EPA is concerned with all human health effects that could result from
exposure to toxic air pollutants, although cancer is of special concern because
of the high Incidence of mortality associated with it. While the total number
of cancer deaths each year is well known, the contribution of air pollution to
this total 1s uncertain. Ambient air pollutants generally are believed to
rank well below smoking, occupational exposure, and diet as an incremental
cause of cancer, although the risk associated with voluntary personal
habits, such as diet and smoking, tends to be of lesser concern than that
resulting from involuntary exposures to air and water pollution.
As I mentioned earlier, there are two principal alternatives provided
under the Clean Air Act for dealing with emissions of toxic air pollutants
from stationary sources: section 112 and section 111.
Section 112 has been considered 1n the past to be the primary statutory
mechanism for controlling toxic air pollutants. However, a major issue
complicating its implementation is the establishment of toxicity to humans
based on uncertain mathematical extrapolation from high-dose animal tests
or occupational exposure to low-dose public exposure at ambient air
concentrations. Another 1s identification of the appropriate level of
emission controls for pollutants for which health effects thresholds have
not been demonstrated. In other words, what Is an ample margin of safety
for a carcinogen?
There also 1s considerable uncertainty with exposure estimation because
of the difficulty In obtaining precise data on long-term emission rates,
atmospheric dispersion patterns and population concentrations around
individual sources, and because of the lack of information on short-term
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and long-term movement (migration) of people and indoor versus outdoor
toxic air pollutant concentration patterns. Further, ambient monitoring
data are limited and would be both very costly and time consuming to obtain
for use in exposure assessment. Finally, there are uncertainties concerning
exposure to multiple pollutants and to a single pollutant from multiple
sources, and the possibility of synergistic actions and heightened
susceptabiTitles to some cancers by some population groups. These factors
make it difficult if not Impossible to determine, or even estimate with any
confidence, the real magnitude of the risk to human health based on the
available data or to establish any epidemlological association between
cancer and public exposure to ambient concentrations of a specific substance.
Finally, section 112 does not mention economics. Thus, a literal
Interpretation of section 112 would require zero emissions to achieve zero
exposure to non-threshold pollutants. As I am sure you know, zero emissions
requirements would likely result in widespread industry shutdown. We do
not believe Congress Intended that.
Principally because neither the language nor the legislative history of
the Clean Air Act provide any specific Congressional Intent on these Issues,
It has been difficult to establish definitive criteria for the evaluation
and control of toxic air pollutants under section 112. Administrative,
legal, and legislative requirements, coupled with a lack of acceptable
criteria for decision-making, have resulted In an evaluation process that
can take from 5 to 7 years from Initial identification to promulgation of
regulations. As a result of this lengthy process, while many substances
are under evaluation as possible toxic air pollutants, few have reached the
final decision stage.
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The air toxics policy, that I mentioned earlier 1s under development,
attempts to respond to these Issues and concerns 1n the following way. In
general, 1t would continue use of section 112 to control air toxics which
are clearly "hazardous" 1n the sense that exposure at ambient levels may
reasonably be anticipated to result 1n an Increase in mortality or serious
Illness. However, where population exposure, the number and location of
sources, or the estimated health risks warrant consideration of other
sections of the Clean Air Act, or where the use of other legislative authorities
or nonregulatory control options are clearly Indicated, the process provides
the flexibility to use these alternatives. In order to ensure that public
health concerns are dealt with 1n the most timely and efficient manner, and
1n order to optimize resource use, the process provides for several levels
of Increasingly detailed analysis. At each level, decisions are made to
ensure that the pollutants which receive the most detailed and resource
Intensive analysis are the most Important to public health.
More specifically, candidate pollutants would be Identified periodically
and then ranked using available health and source Information. The highest
ranked candidates would be screened to assess their potential for health
risks at ambient exposures. One of the following actions then would be
taken: (1) Where Information 1s not adequate to determine the appropriate
next step, that Information would be gathered. (2) Where there clearly 1s
no significant risk to public health, the candidate would be dropped from
further active consideration. (3) Where source categories of a toxic
pollutant clearly pose a health concern but can be dealt with more efficiently
with using a statute (e.g., Federal or State) other than the Clean A1r Act,
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Jur1sd1ct1on would be transferred to the appropriate program. (4) Where
Information warrants, the candidate would undergo comprehensive health and
exposure assessment.
Development of the comprehensive health assessment document 1s a
detailed and resource Intensive process that normally leads to formal Science
Advisory Board review 1n public meetings and closure by the Board when it
1s satisfied that the document 1s scientifically sound and adequately
represents the latest scientific knowledge. Following closure, this document
along with other relevant Information 1s provided to the Administrator and
all feasible control options are Identified.
Several responses are possible at this point: (1) Where Federal regul-
atory action 1s appropriate, the necessary legislative authority would be
Implemented. (2) Where State/local, voluntary or other non-Federal actions
are appropriate, EPA would provide necessary technical or support Information.
(3) Where public health needs Indicate that further action at this time 1s
not required, activities would be halted and the candidate placed in a
category for periodic reassessment.
Under the Clean A1r Act, the process for developing standards under
§112 begins with the listing of a hazardous air pollutant. Source
categories that result 1n significant risks would be evaluated to determine
those for which proposal of regulation 1s appropriate and those for which
proposal 1s not. The basis for control using this approach would be best
available technology, or BAT, with additional control applied 1f the
risk remaining after application of best available technology Is determined
to be unreasonable.
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By BAT, EPA means the best control available, considering economic,
energy, and environmental Impacts. BAT may be different for new and existing
sources within a source category and may be equal to or more stringent than
the best technology defined for New Source Performance Standards under §111.
Whether a source category Is estimated to cause a significant risk would be
decided 1n light of the estimated risks to Individuals, and the estimated
cumulative risks to populations affected by that source category. Whether
the estimated risks remaining after application of BAT are unreasonable
would be decided 1n light of a judgmental evaluation of the estimated
maximum lifetime risk and cancer Incidences per year remaining after application
of BAT, the Impacts, Including economic Impacts, of further reducing those
risks, the readily available benefits of the substance or activity producing
the risk and the availability of substitutes and possible health effects
resulting from their use. In all cases where estimated risks are used, the
significant uncertainties associated with those numbers would be weighed
carefully 1n reaching the final decision.
In this approach, the use of risk numbers generally 1s confined to
areas of broad comparisons, e.g., In selecting source categories to evaluate
and 1n assessing the Incremental change 1n risk that results from application
of various control options. The use of risk numbers 1n an absolute sense
1s avoided because of the many uncertainties.
Obviously, there are legitimate concerns with this approach, particularly
1n Its United use of risk assessment and predominant use of technology and
cost. However, this approach has been generally followed for several
reasons: 0) *« did not have to rely on very uncertain risk estimates, (2)
we are able generally to precisely quantify technology and cost, and (3) 1t
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provldes consistency with section 111. Then, 1n June the Administrator
spoke before the National Academy of Sciences and Issued a call for a more
rational system for assessing and managing risks to the American public.
Mr. Ruckelhaus stated, among other things, that risk assessment should be
Improved, that risks should be weighed against the benefits of continued
use and the risk of substitutes and environmental transfer, and that the
public should be Involved In risk management to a greater extent.
In response to this, we have begun to explore other decision-making
criteria and procedures. Our goal Is to expand the use of risk assessment
1n order to relate regulation more directly to public health concerns, add
across pollutants and sources more consistency to regulations and their
effects, and provide more balance 1n benefits and costs. Clearly these
concerns must be addressed quickly since regulations for benzene, radlonucl1des
and arsenic now have been proposed.
Some options being considered are the following:
1. Specify risk number cutoffs to eliminate source categories
from consideration for regulation.
2. Adopt target after control risk number levels.
3. Use population density around sources to assist 1n determining
the extent and level of control.
4. Orient regulation more specifically to Individual sources.
Several other aspects of our toxic air pollutant program should also
be of Interest to you. First, EPA is beginning to take a more active role
in working with EPA Regional Offices and State/local air pollution control
agencies on toxic air pollutants. This 1s appropriate because of the
widespread and growing interest 1n toxic pollutants at the State/local
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level. For example, regional workshops like this one for State and local
officials were held last year 1n Boston, Atlanta, and Philadelphia to
consider a wide range of toxics Issues and problems. Others are being
planned. We have also begun to develop an Air Toxics Clearinghouse to
provide pertinent Information to State and local agencies on sources,
/
emissions and control Information, health summaries, exposure assessment
methodologies, monitoring Information and regulatory progress 1n other
State and local areas. He are working closely with STAPPA and ALAPCO In
developing this Clearinghouse. Next, EPA recently completed a detailed
assessment of the eight most active State and local air pollutant control
programs, and this report was circulated to State and local program offices.
A follow-up questionnaire was sent out by STAPPA and a final report 1s
expected from them soon summarizing Its results. I think a major new step
1s the recent start-up of the first of 10-12 planned air toxics monitoring
centers. It 1s located 1n Philadelphia and will provide our first opportunity
to begin obtaining long-term toxics trend data and to develop and test
sampling and analytical mehtods for potentially toxic air pollutants.
Research also 1s on-going by EPA 1n several other areas. These Include
basic health effects research, such as the evaluation of the mechanisms and
effects of potential air toxics on humans, atmospheric fate and transport
studies, development of control technologies, sampling and analytical
techniques and ambient monitoring.
In a related area, study and control of air toxics must mesh properly
with other environmental control programs. Of principal Interest are the
Interfaces with the toxic water pollutant program under the Clean Mater
Act, the hazardous waste program under the Resource Conservation and Recovery
Act, and the hazardous substance control efforts under the Superfund
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legislation. In each of these programs, there 1s an air pollution component,
particularly with volatile organic compounds, and we are beginning to
Interface more closely with these programs.
In conclusion, we have a growing toxic air pollutant evaluation and
EPrt ,'i
control program. Ue-are proceeding to streamline the process for evaluation
and control of air toxics and to articulate this process to the public,
Congress, Industry, and environmental groups so that everyone will understand
^4\w ^uxv
how we'Intend to fulfill our mandate to protect the public health from
"TtuS (.'.£» ' {'>' f'i\c£ f>rpCM£V7d ,
toxlc a1 r pol 1 utants. We take th1 s mandate very seriously, and I appredate
>,
the opportunity to discuss this Important program^rf-th-you-today.
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CALIFORNIA AIR RESOURCES BOARD'S
FRAMEWORK FOR AIR TOXICS
Michael Scheible
Chief, Office of Program Planning, Evaluation, and Coordination
California Air Resources Board
Sacramento, CA
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«H\L
1}
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Summary of Health and Safety Code Section 39650 et seq (AB 1807 of 1983)
Relating to Toxic Air Contaminants
Section 39650. INTENT. Establish a program to identify and control toxic
air contaminants so that the public health is protected.
Section 39655. DEFINITIONS.
T)Toxic air contaminant = air pollutant which may cause or contribute to
Increased mortality or serious illness or pose present or potential health
threat. Includes NESHAP substances.
2) Airborne toxic control measure = recommended methods to be used by
districts to reduce emissions of toxic air contaminants.
Section 39660-62. SUBSTANCE IDENTIFICATION PHASE (risk assessment).
TJARB requests DOHS evaluation of substance's health effects.
2) DOHS submits written evaluation and recommendations within 90 days (30 day
extension).
3) ARB prepares report with DOHS participation.
4) Scientific Review Panel considers report and submits written findings to
ARB within 45 days (15 day extension).
If panel finds deficiencies, ARB has 30 days to revise and resubirn' .
ARB prepares hearing notice and proposed regulation within 10 days
after panel reports.
5) Public hearing.
6) ARB determines that substance is a TAC and specifies threshold if
applicable.
7) DFA in charge of pesticide health effects evaluation and designation.
Section 39665-67. CONTROL DECISION PHASE (risk management).
TJARB reports on need and degree of emission control; districts participate,
affected parties and public consulted.
a) If threshold, control to threshold; if no threshold, reduce risks.
b) ARB must consider technology, cost, risk and adverse environmental
impacts.
2) Public hearing (45 day notice).
3) ARB to use existing rulemaking authority for controlling mobile sources or
motor vehicle fuels.
4) ARB adopts airborne toxic control measure to guide district action on
stationary sources.
5) Districts propose regulations within 120 days of ARB adoption of measures.
6) Districts adopt rules within 6 months of step 4).
7) Seasonal food/fiber processors exempt from district NSR rules until 1987.
8) DFA in charge of pesticide controls.
Section 39670. SCIENTIFIC REVIEW PANEL.
TJConsists of 9 members: 5 appointed by the Secretary of Environmental
Affairs, 2 by Senate Rules, 2 by Assembly Speaker, from list supplied by
the President of U.C.
2) Areas of expertise, qualifications, terms (3 years) and disclosure
requirements specified.
3) ARB, DOHS, DFA provide staff support.
Section 39674. PENALTIES. $10,000/day if violation of emission or other
condition.
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A14 TIM
October Hi 1Mft
Sharp Debate on ARB's Toxic-Air Proposal
Board Says Hearing 'Only A First Step," Calls For Further Discussion
By MM Miller
M>Jttff WrtMf
Conflicting oplf
measure actual rif
public hearing W
state Air Resottrc.
sresently-unreg •;
pounds Into the
atace even
Clement In ti
health risk. O
alto subject (
of.
and carcinogens to the federal Environmental
Protection Agency, told the hearing there to a
sound scientific reason for public concern about
• -•Hnogens in the air."
t Urged the ARB "to set priorities for identify-
earciaogeoi so the worst will be dealt with
i.* Bat, he added, "fee proposed regulations do
conform to scientific methods of identify*'
rcinogens."
Dr. Roy Albert, professor of
«dldne at New York Unlver-"
4 the EPA'i Carcinog*-
irged the. board to _^ % m ^
He urged that the ARB r%
include criteria consists'
concepts.
Panel OKs Bill That Targets
*&$£%*£ Airborne Toxic Chemicals
#i«l^^?d*!5 By Tberae Gray
*&#
A bill that would launch a long-
Hack on airborne toxic
chemicals won approval Tuesday in
Senate
scientists to idrntify some of them
four years ago after deciding the
Environmental Protection Agency
was moving too slowly on the prob-
lem.
The toxics in question include
nrsenir from wood pre-
, cadmi-
""•Iters,
l^cancer agents in air
•••rifv the
aS2u**»ftiStlei»**Sft ^ «* fJ°*»*«fl*i«*Zr"»'wc ^ ^^
-------
Why are toxic air contaminants important?
* What is the ARB approach?
* What is happening now?
00
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TOXIC AIR CONTAMINANTS
AND
TRADITIONAL POLLUTANTS
-------
TOXIC AIR CONTAMINANT
CAUSES OR
CONTRIBUTES
TO INCREASED
MORTALITY
OR SERIOUS
ILLNESS
OR
MAY POSE
PRESENT OR
POTENTIAL
HUMAN HEALTH
HAZARD
INCLUDES NESHAP's POLLUTANTS
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Traditional Pollutants*
Toxic Air Contaminants
Few (6)
Not Bioaccumulated
Lung Primary Target
Organ (Except CO)
Readily Available Human
Health Effects Data
Effects Generally Occur
From Minutes to Months
Potentially Numerous
Some may Bioaccumulate
Many Target Organs
Dose-Response Data For
Humans Rarely Available
Effects Generally Occur
After Long Latent
Period (Years)
ISJ
r
* As regulated under Clean Air Act, except Lead
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LOW
CHRONIC
FROM
RELATIV
VELS
ACUTE
NJ
H EFFECTS
TERM
-------
SUSPECTED AND. KNOWN TOXIC SUBSTANCES
CATEGORY
NIOSH REGISTRY OF TOXIC EFFECTS OF
CHEMICAL SUBSTANCES (1979)
IARC LIST OF ANIMAL CARCINOGENS WITH
SUFFICIENT EVIDENCE OF CARCINOGENICITY
(1982)
IARC LIST OF KNOWN AND PROBABLE HUMAN
CARCINOGENS (1982)
NESHAP SUBSTANCES
SUBSTANCES PROPOSED FOR NESHAP REVIEW
APPROX. NO.
OF SUBSTANCES
4O,OOO*
180
8O
6
BO
to
Ul
POTENTIAL TOXIC AIR CONTAMINANTS
40-50
Plus 2OOO-5OOO per year
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HISTORY
AB 1OO5 - 1981/82
ARB REGULATIONS - 1982/83
AB 18O7 - 1983
-------
RATIONALE FOR CONTROL OF
TOXIC AIR CONTAMINANTS
AMBIENT AIR DATA
PUBLIC EXPOSURE DATA
cn
EXISTENCE OF FEASIBLE CONTROL
TECHNOLOGIES
NEEDS OF LOCAL AIR POLLUTION
CONTROL DISTRICTS
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PROCESS
-------
SCIENTIFIC
KNOWLEDGE
RISK CONSIDERATION
BEST
AVAILABLE
EMISSION
CONTROLS
GOAL:
PROTECTION
OF
PUBLIC
HEALTH
NJ
-------
SUBSTANCE
IDENTIFICATION
CO
CONTROL
DECISION
-------
SUBSTANCE
IDENTIFICATION
ARB
—-DOHS
CONTROL
DECISION
APCD's
— ARB
-------
SCIENTIFIC
REVIEW
PANEL
o
-------
SUBSTANCE IDENTIFICATION
RISK
ASSESSMENT
U)
CONTROL DECISION
RISK
MANAGEMENT
-------
SUBSTANCE
IDENTIFICATION
PROCESS
ARB
Request
to
DOHS
DOHS
Health
Effects
Evalu-
ati
ion
ARB
Report
Scientific
Review
Panel
Public
Hearing
ARB
Decision
Adminis
trative
Review
Proce-
dures
OJ
r\j
I
APPROXIMATELY
— 1O MONTHS —
Substance • by • Substance
-------
Regulatory
Needs
Report
Public
Hearing
ARB
Adopts
Airborne
Toxic
Control
Measure
APCD
Proposes
Non-Vehicular
Source
Regulation
APCD
Adopts
Regulations
APPROXIMATELY^
8 MONTHS
MAXIMUM
6 MONTHS
U)
U)
CONTROL
DECISION
PROCESS
-------
FACTORS TO BE ADDRESSED IN DEVELOPING
AIRBORNE TOXIC CONTROL MEASURES;
* SOURCES, SOURCE CATEGORIES, EMISSION
LEVELS
* PHYSICAL/CHEMICAL CHARACTERISTICS OF
SUBSTANCE IN AIR
* PUBLIC HEALTH EFFECTS OF EXPOSURE
* AVAILABILITY AND COSTS OF CONTROLS
AS RELATED TO RISK LEVELS
* SUITABILITY OF LESS HAZARDOUS SUBSTANCES
u>
*»
-------
RISK REDUCTION
NO KNOWN THRESHOLD
-------
THRESHOLD PLUS
MARGIN OF SAFETY
U)
c
KNOWN THRESHOLD
-------
MOTOR VEHICLES
— ARB
NON-VEHICULAR SOURCES
— LOCAL AIR POLLUTION
CONTROL DISTRICTS (APCD's)
— ARB COORDINATION
to
•x]
-------
SUMMARY
OJ
03
-------
Health Effects
Long Teim
'
.
-------
SUBSTANCE
IDENTIFICATION
- ARB
- DOHS
•• RISK ASSESSMENT
- SCIENTIFIC REVIEW
PANEL
- 1O MONTHS
CONTROL
DECISION
-- ARB/APCD's
- RISK MANAGEMENT
-- AIRBORNE TOXIC
CONTROL MEASURES
- 14 MONTHS
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-41-
CALIFORNIA DEPARTMENT OF HEALTH SERVICES CARCINOGEN POLICY
Dr. Kim Hooper
Research Scientist
California Department of Health Services
Berkeley, CA
-------
Kim Hooper, Ph.D.
HESIS
12/16/83
-42-
Epigenetic Carcinogens: Problem with Identification and Risk Estimation
There is recent interest in the broad classification of carcinogens into two
categories based on their mechanism of action: those that act through genetic
mechanisms by interacting with DMA, causing gene mutation or duplication, or
change in chromosome structure or number; and those that do not interact with
DNA, but may cause changes in methylation patterns or tertiary structure of
DNA, and are termed epigenetic carcinogens (IARC, 1983). Carcinogens which
produce a consistent response in short-term tests for mutagenicity are desig-
nated as acting by a genetic mechanism, and are frequently called initiators
or early stage carcinogens, indicating that they affect one of the early
stages of the multi-step process of carcinogenesis. Carcinogens that do not
produce responses in assays for mutation, cell transformation, chromosome
aberration, or DNA binding or damage, are described as producing their car-
cinogenic effect by epigenetic mechanisms. Evidence for mechanism may be
supplemented by initiation/promotion studies in specific organ systems, in-
cluding mouse skin, rat liver, and urinary bladder to identify initiators or
promoters.
The mechanisms of carcinogenesis are just beginning to be understood, and
recent advances in the techniques of molecular biology have enabled us to
describe and speculate on the actions and regulation of "oncogenes" (role of
enhancers, promoter insertion models, role of various growth factors, etc.)
and hold the promise to unravel the manner by which normal cells are trans-
formed into the neoplastic state. It is likely that carcinogenesis is
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complex, and that there are be many ways In which the cell's normal function-*
ing can be disrupted and lead to neoplasia. Thus, in large part the proposed
simple dichotomy of genetic and epigenetic carcinogens arises from and
reflects our present limited knowledge of carcinogenesis. As we develop our
ability to determine the mechanisms of action of individual carcinogens, such
general terms as genetic and epigenetic will likely be replaced by more
specific and meaningful terms. This view has been expressed by the
International Agency for Research on Cancer (1ARC), which concluded that "at
* *
present, no classification of carcinogens according to mechanism could be
exhaustive or definitive. On the other hand, classification of mechanisms
has considerable value for particular scientific purposes." (IARC, 1983)
A further significant proposal is that epigenetic carcinogens have
"thresholds," dose levels at or below which no carcinogenic effects are
produced. Consequently, risks of cancer from exposures to epigenetic car-
cinogens at low doses are presumed to be much lower than those for
carcinogens which act by genetic mechanisms. A risk assessment method has
been proposed which produces low estimates of cancer risks from exposures to
epigenetic carcinogens. When applied to data from several cancer tests, this
method would, in effect, permit public exposure to epigenetic carcinogens at
levels 100-300 fold higher than would be permitted for genetic carcinogens
using a standard method for estimating cancer risks. Such a proposal has
enormous public and occupational health significance because several large
volume industrial chlorinated carcinogens (e.g. DDT, dicldrln, PCBs,
perchloroethylene, and trichloroethylene) have been described as acting by
epigenetic mechanisms (Weissburger, 1983).
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There are several problems with this proposal. First, there is at present no
direct and validated means of identifying epigenetic carcinogens, except
those that are active in an ase; "or promoters. Whereas genetic carcinogens
may be directly identified by ™s:f.ive responses in DNA-binding studies or in
a battery of short-term tests, epigenetic carcinogens are identified only
indirectly by their failure to produce a response in one of the above short-
term assays. For us to feel confident of an Identification based on negative
results, the frequency of false negatives in these tests must be known and be
quite low. Unfortunately, the sensitivity of several of these assays is
suspect and may lead to false negative results. In DNA-binding assays, for
example, several thousand molecules of a carcinogen may be adducted to DNA
per cell and not produce a significant positive response, even when radioac-
tive carcinogens of the highest available specific activity are used. In
fact, short-term test systems failed to detect most (all but direct-acting)
carcinogens before metabolic activation was introduced. Under the proposed
system, these would have been mistakenly classified as epigenetic car-
cinogens, even though they would be shown subsequently to directly interact
with DNA after metabolic activation and be correctly classed as genetic
carcinogens. Similarly, classic carcinogens which have been detected only
after test systems were improved (e,g. large insoluble polycyclic aromatic
hydrocarbons, aromatic amines, conjugated compounds and agents which
presumably act through free-radical or oxidative mechanisms) would have been
incorrectly designated as "epigenetic" agents because of the lack of response
of the earlier test systems.
In summary, designating a substance an epigenetic carcinogen by the absence
of response in a short-term test for mutageniclty or DNA-damage has obvious
-------
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shortcomings. At present, we can only tentatively identify agents as
epigenetic carcinogens. Given this uncertainty, it appears unwise to permit
exposure to 1>. ?00 fold higher levels than would be permitted for genetic
carcinogens.
Second, even if epigenetic carcinogens could be conclusively identified,
there is not clear evidence that "threshold" dose levels exist for either
genetic or epigenetic carcinogens. For genetic carcinogens, the Food Safety
Council plotted dose-response curves for the available multi-dose* (greater
than 3 dose levels) cancer bioassays (Report of the Food Safety Council,
1978). In tests of four genetic carcinogens (aflatoxin, vinyl chloride,
dimethyInltrosamine, and bis-dichloromethylether) there was no evidence of a
threshold. Instead, there are dose levels at vMcl? less than one tumor is
expected to appear based on the dose response curve, and no tumors appear.
Hulti-dose studies using large numbers of animals with 2-acetylamtnofluorene
(6 doses; 20,000 mice) (Littlefield, 1979) and dimethylnitrosamine (A doses;
5,000 rats) (Peto, personal communication, 1983) give no indication of
•
thresholds. The dose response curve for bladder cancer in the 2-AAF experi-
ment gives the impression of a threshold, but a re-plot of this data on an
enlarged scale at improved resolution indicated that the tum°r rates ln"
crease with dose even at the lower doses (Gaylor, 1980). The large study
with DMN in rats produced a dose-response relationship that is linear in the
low dose range (Peto, personal communication, 1983).
The Food Safety Council Report also contains dose-response plots for three
chemicals which have been designated as promoters or epigenetic carcinogens
(DDT, dieldrin, and saccharin) and there is no evidence for threshold dose
-------
-46-
levels. Instead, there are dose levels where no tumors are expected, and no
tumors appear. Promotion studies using saccharin (Nakanishi, et al., 1980)
or phenobarbltal (Peralno, et al. 1977; Kunz, et al., 1983), are cited as
demonstrating thresholds, but provide no such evidence.
A cancer bioassay of nitrilo-triacetlc acid (NTA) (Food Safety Council, 1978)
at 5 dose levels has been cited as the best documentation of a threshold or
"no effect" level. In fact, no threshold Is evident even though there are no
tumors at the two lowest dose levels. The number of kidney tumors "expected"
in these two low-dose groups is much less than 1. Thus, the fact that no
tumors (or less than 1 tumor) appear in these dose groups is a reasonable
finding. The NTA case is representative of other examples where the "no
effect" or threshold level" appears to be confused with the "no sensitivity"
level. The apparent "no effect" level is, in fact, the dose level at which
the study lacks the sensitivity to detect the expected response.
Thtse above findings support the positions taken by the proposed DOHS
Carcinogen Policy: that present knowledge is inadequate to justify separate
risk assessment methods for genetic and epigenetic carcinogens; and that un-
less convincing evidence is presented to the contrary, quantitative estimates
of carcinogenic risk will be made using non-threshold models.
-------
-47-
"Approaches to Classifying Chemical Carcinogens According to Mechanism o'f
Activity," IARC Working Group Report, May, 1983
Gaylor, D.W. as reported in Assessment of Technologies for Determinin
Cancer Risks from the Environment. Office of Tech. Assess. Jour 1981 24
PP-
Ito, N. et al. "Effects of Promoters on N-butyi-N-(4-hydroxylbutyl)
nitrosamine-Induced Urinary Bladder Carcinogenesis in the Rat" Env. Health
Persp. 50 61-69 (1983)
Kiinz, H.W. et al., "Quantitative Aspects of Chemical Ca .-inogenesis and
Tumor Promotion in Liver," Env. Health Persp. JO 113-2? f 983-X. -
Little fie Id, N.A. et al. "Effects of Dose and Time in a Long-term Low-dose
Carcinogenic Stud" J. Envir. Pathol. Toxicol. ^ 17-37 (1979)
Nakanishi, ft. et al. "Dose-Response of Saccharin in Urinary Bladder
Hyperplasias in Fisher 344 Rats pretreated with N-butyl-N-(4-hydroxybutyl)
nitrosamine," JNCI ^5 1005-1009 (1980)
•
Peraino, C., Fry, T.J.M., and Statteldt, E. "Effects of Varying the Onset
and Duration of Exposure to Phenobarbltal on its Enhancement of 2-
acetylaminofluorene-induced hepatic tumorigenesis" Cancer Res 37 3623-3627
(1977) ~~
Peto, T. personal communestion, December 1983
Report of Food Safety Council Food and Cosmetic Toxicology
Weissburger, J.H. & Williams, G.M. "The Distinct Health Risk Analyses
Required for Geootoxic Carcinogens and Promoting Agents," Env. Health Persp.
50 233-245 (1983)
-------
-48-
AMBIENT MONITORING FOR AIR TOXICS IN REGION 9
Dr. Hanwant Singh
Director, Atmospheric Chemistry Program
SRI International
Menlo Park, CA
-------
-49-
Reprinted from Environmental Science and Technology, 1982,16, 872.
Copyright © 1982 by the American Chemical Society and reprinted by permission of the copyright owner.
Distribution off Selected Gaseous Organic Mutagens and Suspect
Carcinogens In Ambient Air
Hanwant B. Singh/ Loub J. Sala*, and Robin E. StflM
SRI International. Mento Park, Calfomte 94025
• An on-site field data collection program, based on
short-term studies, was conducted in seven U.S. cities.
Atmospheric concentrations, variabilities, and diurnal
behaviors of 20 gaseous organic bacterial mutagens or
suspect carcinogens are described. Except for benzene and
formaldehyde, average concentration levels for all chem-
icals measured were in the 0-1-ppb range. Benzene and
formaldehyde average levels were in the 1-6 and 10-20-ppb
range, respectively. Typical diurnal profiles show highest
concentrations during nighttime or early morning hours,
with minimum concentrations in the afternoon hours;
chemistry plays only a nominal role in defining this diurnal
behavior in most cases. It is concluded that organic mu-
tagens have always existed in the atmosphere (and the
ocean), although at relatively low background concentra-
tions. Our measurements for this group of 20 chemicals
show that in the cleanest environments the present ex-
poeure is more than twice the natural background, whereas
in the U.S. cities we studied exposure may be 15-30 times
greater.
Introduction
In a recent report the surgeon general stated that Tone
chemicals are adding to the disease burden of the United
States in a significant, although as yet not precisely defined
way" (1). Estimates suggesting that 50-90% of human
cancer may be of chemical origin persists (1,2). The degree
to which synoptic and macro- and microenvironmenta in-
dividually contribute to human cancer is a matter of on-
going research and debate (3,4). Although the risks may
be highly uncertain, there is little doubt that significant
quantities of a growing number of synthetic organic
chemicals have been released into the ambient enviorn-
ment during recent decades. In many cases, virtually the
entire quantity of the chemical manufactured is released
into the environment as a necessary outcome of use (5,6).
A key parameter in assessing risk from ambient exposure
entails the characterization of ambient atmospheres in
which the affected population resides. Because of the
relatively recent interest in ambient hazardous chemicals,
the atmospheric abundance, sources, and sinks of this
group of pollutants are poorly understood. Although en-
vironmental episodes (e.g., the "Love Canal" incident) have
received considerable attention (1), the extent of human
exposure to chemicals in normal ambient atmospheres
remains relatively poorly determined.
The present study was initiated to measure selected
organic chemicals in several U.S. cities. Although we
measured 44 organic chemicals, results presented here are
limited to 20 bacterial mutagens and suspect carcinogens.
Table I lists chemicals that have been defined as bacterial
mutagens or suspect carcinogens. References 8-14, shown
in the last column of Table I, often refer to additional
studies that support their findings. Other chemicals for
which concurrent ambient data were collected but not
included here are fluorocarbons F 12, F 11, F 113, and F
114, ethyl chloride, 1,1-dichloroethane, 1,1,1,2-tetra-
chloroethane, 1,2-dichloroethylene, monochlorobenzene,
o-dichlorobenzene, m-dichlorobenzene, 1,2,4-trichloro
benzene, toluene, ethylbenzene, m- and p-xylenes, o-xylene;
4-ethyltoluene, 1,2,4- trimethylbenzene, 1,3,5-trimethyl-
benzene, acetaldehyde, phosgene, peroxyacetyl nitrate, and
peroxypropionyl nitrate. These excluded chemicals are not
considered to be mutagenic or carcinogenic at the present
time. The data can be found in ref 15. Empirical tests
have shown that nearly 90% of tested animal carcinogens
are also bacterial mutagens, while an equal percentage of
noncarcinogens are nonmutagens (7). Bacterial muta-
genicity tests are simple and direct and provide a useful
screening test for carcinogenicity. The carcinogenicity
information is based on tests involving epidemiology and
a critical and comprehensive evaluation of carcinogenicity,
mutagenicity, and other lexicological data (8-10). The
terms "bacterial mutagens" (BM) and "suspect
carcinogens" (SC) as used here do not imply that a proven
human health hazard exists; however, these chemicals are
fiaf
1* Un 12
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Table I. Sources, Sinks, Background Levels, and Toxic Effect* of Chemicals of Interest
chemical
methyl chloride
methyl bromide
methyl iodide
dichloromethane
chloroform
carbon tetrachloride
1,2-dichloroethane
1,2-dibromoe thane
1,1,1-trichloroe thane
1,1,2-tric.Moroe thane
1,1,2,2-tetrachloroethane
1,2-dichloropropane
1,1-dichloroethylene
trichloroethylene
tetrachloroethylene
3-chloro-1 -propene
hexachloro-1,3 butadiene
o-chlorotoluene
benzene
formaldehyde
major source0
N(O), MM
N(O), MM
N(0)
MM
MM
MM
MM
MM
MM
MM
MM
MM
MM
MM
MM
MM
MM
MM
MM
N, MM
dominant
removal
mechanism''
HO
HO
hi>(T)
HO
HO
hi>(S)
HO
HO
daily
loss,c '.
0.4
0.4
12.2
1.3
0.9
-0.0
1.9
2.2
HO
HO
HO
HO
HO
HO
HO
HO
HO
HO
HO
HO, hv(T)
2.8
<0.1
10.2
29.2
17.2
1.5
91.1
22.8
11.4
88.2
surface level
bckgrnd concnd
PPt
650
20
2
50
20
135
40
2
160
15
50
400
ng/mj
1340
78
12
173
97
848
168
15
981
80
337
490
toxicity (ref)*
BM (8, 9)
BM (8, 9)
BM,SC(8, 9, 12)
BM (8, 9)
BM, SC(8, 10, 11)
NBM, SC(8, 9, 10)
BM, SC (8, 9, 10)
BM, SC (8, 10)
weak BM (8, 9)
NBM, SC(8, 9, 13)
BM, SC (8)
BM(8)
BM, SC (8, 9, 10)
BM, SC (8, 9, 10)
SC (8, 10, 14)
SC (8, 10)
BM, SC(8)
SC (8, 10)
BM, SC (8, 10)
0 N, natural; O, oceanic; MM, man-made. b HO, hydroxyl radical; hv, photolysis; T, troposphere; S, stratosphere. c With-
in the boundary layer (12 sunlit h); calculated based on estimated daytime (12 h) average HO abundance of 2 X 10* mole-
cules/cm3 and mean temperature of 300 K. d At 40° N. * BM, bacterial mutagen (positive Ames test); NBM, not bacteria]
mutagen (negative Ames test); SC, suspect carcinogen.
considered to be of present and future atmospheric interest
for both the environment and human well-being.
Experimental Program
Chemicals were measured on site and in real time by
using an instrumented mobile environmental laboratory.
All compounds listed in Table I (excluding benzene and
formaldehyde) were measured with electron capture (EC)
gas chromatography (GC). Benzene was measured with
a flame ionization GC system. Formaldehyde was mea-
sured by the chromotropic acid method as well as by the
analysis of its 2,4-dinitrophenylhydrazone (DNPH) de-
rivate with high-performance liquid chromatography (15).
For the analysis of all chemicals (except formaldehyde)
listed in Table I, a 400-mL air sample was preconcentrated
on a Vie m- o.d. loop filled with glass wool (4-in. length)
and held at liquid oxygen temperature. Sampling volume
for formaldehyde analyses was approximately 120 and 60
L (2-h sampling time) for the chromotropic acid and the
DNPH methods, respectively. A 24-h around-the-clock
measurement schedule was followed for a period of 1-2
weeks at selected sites (Table II), allowing us to collect a
body of data to study mean diurnal variations. Primary
standards were generated by using a complex array of 40
permeation tubes. For approximately 15 of the 20 chem-
icals listed in Table I, high concentration standards (5-10
ppm) were also stored. (The high concentration was
chosen to ensure long-term stability). These were obtained
commercially from Scott-Marrin Inc. (Riverside, CA).
Field calibrations were performed by pressurizing a large
volume of urban air to 40 psi in a 35-L electropolished
cylinder. After allowing the air to stabilize for a few days,
it was calibrated against the primary standard, which then
became a secondary field standard, routinely analyzed two
to three times a day. In addition, 10-15-ppb secondary
standards, prepared from the ppm standards, were carried
aboard and also routinely analyzed. On the basts of limited
intra- and interlaboratory comparisons, we estimate the
overall accuracy of these measurements to be within
±15%. The measurements for formaldehyde might be
accurate to within ±30%. Additional measurement details
can be found in ref 15.
Results and Discussion
Table I summarizes the estimated daily loss rate of
chemicals, their major source, toxicity, and background
concentrations. The loss rates are estimated on the basis
of hydroxyl (HO) radical reactivity and photolysis. Methyl
iodide and formaldehyde are the only two chemicals for
which photolytic loss is important. The background con-
centrations are based on surface level measurements con-
ducted around the globe, but especially at a Pacific marine
site at Point Arena, CA (39.9° N) (5, 16-18). Reliable
formaldehyde measurements are not available from remote
sites, but a 400-ppt mixing ratio is not inconsistent with
either limited measurements or estimates from photo-
chemical models. Concentration data are provided both
as mixing ratios and in nanograms per cubic meter (ng/
m8). This redundancy is provided for convenience because
exposures are invariably expressed in mass concentration
units. Table n summarizes field data on the 20 bacterial
mutagens and suspect carcinogens. Measured average
(arithmetic averages) concentrations and the corresponding
standard deviations are presented in units of ppt and
ng/m8. Maximum and minimum concentrations are pro-
vided in ppt units.
Methyl halides constitute a unique group of bacterial
mutagens that are ubiquitously distributed in atmospheric
as well as oceanic environments (16, 18, 19). There is
currently no doubt that these three methyl halides are
bacterial mutagens with a relative mutagenic potential
(revertanto per unit weight) of CH3C1 = 1, CH,Br = 30,
and CHjI - 3 (9). Evidence suggests that methyl chloride,
methyl bromide, and methyl iodide are dominant natural
chlorine, bromine, and iodine carriers in the atmosphere
(16). Their biogeochemical roles, however, are not yet fully
understood; the possibility exists that these chemicals
regulate the burden of stratospheric ozone. We also
speculate that such chemical mutagens of natural origin
may have played a hitherto undefined role in the processes
Environ. Sd. Tachnol., Vol. 16. No. 12. 1982 173
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Figure 1. Methyl chloride in the ambient air of selected cities.
of biological evolution; chemical bacterial mutagens have
been a part of our environment since prehistoric time.
Table II summarizes the urban methyl halide levels at
seven sites in selected U.S. cities. Methyl chloride average
levels of 0.66-0.96 ppb are close to or marginally above the
background of 0.6-0.7 ppb. Clearly, local sources of methyl
chloride in urban areas exist. Figure 1 shows elevated
methyl chloride levels in Houston, while St. Louis levels
are near background. It appears unlikely that primary
methyl chloride emissions could account for this difference.
We suspect secondary sources of methyl chloride (e.g.,
combustion) exist but have not yet been fully character-
ized. Methyl bromide levels (average of 0.04-0.26 ppb)
were found to be well above background in all cities.
Average methyl iodide levels of 1-4 ppt at all urban sites
are slightly lower or indistinguishable from their back-
grounds. Thus, methyl iodide remains a chemical of vir-
tually exclusive natural origin. Its low abundance is, in
part, attributable to its high reactivity (12% daily loss
rate). Figure 2 shows a mean diurnal methyl iodide profile
at two selected sites; the afternoon minimum is attribut-
able to its high reactivity. Overall maximum methyl
chloride, methyl bromide, and methyl iodide concentra-
tions of 2.3 ppb (Houston), 1.0 ppb (Riverside), and 0.01
ppb (Houston) were measured, with minimum concen-
trations being indistinguishable from background levels.
Urban methyl halide data from the literature are scarce,
partly because solid sorbents such as Tenax, which have
been used extensively for routine data collection, do not
appear to collect methyl halides (20, 21) although the
presence of methyl bromide was noted (20). Chameides
and Davis' recently summarized methyl iodide data from
clean as well as from polluted environments point to a
great deal of variability (22). A substantial part of this
variability, especially in urban areas, we believe to be as-
sociated with earlier measurement problems.
Dichloromethane (methylene chloride) is also a bacterial
mutagen (9), but is only about a quarter as potent as
methyl iodide. Average concentrations (Table II) were in
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Flgur* 2. Mean diurnal variation of methyl Iodide.
the 0.4-2-ppb range, which are at least an order of mag-
nitude higher than the background concentration of 0.05
ppb. Maximum concentrations of 18 and 9 ppb were
measured at Staten Island and Riverside, respectively.
Even though methylene chloride is a typical solvent likely
to find most use during daytime, in virtually all cases
(except Riverside) the highest values were encountered
during nighttime, with afternoon lows. Figure 3 provides
an example of this typical diurnal behavior at the Houston
and Denver sites and the reverse behavior at Riverside.
Although conclusive data interpretation is not possible in
the absence of accurate daily emission inventories, the very
high methylene chloride levels reported earlier from Los
Angeles (average = 3.7 ppb) (23) and the downwind nature
of the Riverside site can provide part of the explanation.
The afternoon minimums cannot be attributed to chemical
loss because of the relatively unreactive nature of this
chemical (Table I). As we shall see, the afternoon mini-
mum is a fairly general feature and can only be attributed
to dilution caused by deep vertical mixing typical of af-
ternoon hours.
Pellizzari and Bunch (20), using the Tenax collection
procedures, have also reported methylene chloride con-
centrations from several industrial sites and show signif-
icantly greater variability as compared with our data.
Although our data are not necessarily inconsistent with
these measurements, certain discrepancies are evident For
example, concentrations significantly iower than geo-
chemical background have been frequently reported, a
phenomenon also found to be true in cases of carbon
tetrachloride, 1,1,1-trichloroethane, 1,2-dichloroethane,
trichloromethylene, and tetrachloroethylene (20). The
causes of this problem are unclear. By and large, urban
methylene chloride data are scarce.
Chloroform, a mutagen and a suspect carcinogen (9-11),
has received considerable attention because of its high
levels in drinking water (24). Average concentrations of
about 0.7 ppb at Riverside, 0.4 ppb at Houston, and about
0.1 ppb at the other sites are clearly 1-2 orders of mag-
Environ. Set Techno!., Vol. 16, No. 12. 1982 87S
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Figures. Mean dkmal variation of methylene chloride at selected sites.
nitude higher than background concentrations. Maximum
concentrations of about 5 ppb were measured at more than
one site. Figure 4 clearly points to the existence of urban
sources. As shown earlier (15, 23), the highest levels of
chloroform are measured during the night. The direct
sources of chloroform (U.S. emissions are <0.02 million
tons/year) appear to be too small to account for its per-
vasiveness in urban environments. In a recent review (25),
chlorination of water and possibly automobile exhaust were
suggested as two important sources of chloroform. Pel-
lizzari and Bunch (20) report concentrations that vary from
unquantifiable levels to 7 ppb, a range comparable to that
found in our study.
Carbon tetrachloride, a man-made chemical, is nearly
uniformly distributed around the globe (78, 26). Urban
carbon tetrachloride levels are higher than background
levels by a factor 1.5-3. At all sites (except Houston)
average concentrations were between 0.2 and 0.3 ppb. At
Houston the maximum and average concentrations were
2.9 and 0.4 ppb, respectively. The diurnal behavior of
carbon tetrachloride was typical of other pollutants. The
Staten Island mean diurnal behavior is shown in Figure
QUO
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Figure 4. Atmospheric concentrations of chloroform at Staten Island,
NY.
TIME — dwt
Figure 5. Mean dturnal variations of carbon tetrachtorkJe at Staten
Island, NY.
5. Concentrations during the afternoon minimum are
comparable to background levels (0.14 ppb) of carbon
tetrachloride, a condition caused by deep vertical mixing
during afternoon hours. Very little urban data from other
sources have been available, although its background ap-
pears well characterized (17, 18, 26). Limited urban
measurements from Lillian et al. (27) and Simmonds et
al. (28) are consistent with our measurements. Ohta et al.
(29) reported significantly higher values (average =1.4
ppb) from Tokyo.
1,2-Dichloroethane, a large-volume chemical (U.S.
emissions approximately 0.2 million tons/year), is a bac-
terial mutagen and a suspect carcinogen (Table I). Average
concentrations of 0.1-1.5 ppb point to a considerable
difference in abundance at various sites. Maximum con-
centration of 7.3 ppb was measured at Houston; Figure 6
shows the mean diurnal profile of 1,2-dichloroethane at
Houston and Riverside. Once again, the highest values are
encountered during the night and early morning hours.
Previous atmospheric data on 1,2-dichloroethane are ex-
tremely sparse. Bozzelli (27) could quantify only 2 samples
from a total of 250 collected. Pellizzari and Bunch (20)
provide abundant data that are well below the measured
as well as the estimated background of about 30-50 ppt
(6, 17), although their higher concentrations are compa-
rable to data presented here.
1,2-Dibromoethane is expected to be a potent carcinogen
with a unit risk 50 times greater than 1,2-dichloroethane
(10). This chemical is used primarily as a gasoline additive
and a fumigant (U.S. production is 0.1 million tons/year).
Average 1,2-dibromoethane concentration at no study site
876 Environ. Set. Techno).. Vol. 16, No. 12, 1982
-------
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Flgur* 6. Mean dumal variation of 1,2-dteNoroethane.
10
TIME
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hour
Flgwe 7. Mean dumal variation of 1,2-dfcromoelnane at Denver, CO.
exceeded 0.06 ppb (average range 0.02-0.06 ppb), although
concentrations as high as 0.37 ppb were measured. A
typical mean diurnal profile for the Denver site is shown
in Figure 7. The highest average levels were again en-
countered during night and early morning hours. Typical
ambient concentration data available from the literature
suggest a concentration range of 0-0.3 ppb (20, 30, 31).
BozzeUi et al. (21) report some exceptionally high values
from New Jersey.
1,1,1-Trichloroethane, a popular solvent in recent years,
has undergone a rapid growth (17,18). It is weakly mu-
tagenic, although considerable disagreement as to its health
effects exists (8, 9, 32). Virtually all the manufactured
amount is released into the environment. This chemical
is quite stable in the atmosphere and a global residence
time of about 8 years has been estimated (18). About 15%
of this chemical could enter the stratosphere where it could
interreact with the ozone layer in a manner similar to
fluorocarbons. Typical average concentrations (Table n)
were measured to be hi the 0.25-0.75-ppb range. The
highest concentration of 2.7 ppb was measured in Denver.
Figure 8 shows a typical diurnal behavior in Houston and
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Figure 8. Mean rJumal variation of 1.1.1-trlchloroethane.
Denver. Very little recent urban data have been published.
Simmonds et al. (28) found an average concentration of
0.37 ppb in Los Angeles in 1973, which is in reasonable
agreement with our Riverside data (average = 0.7 ppb),
if we recognize that the emissions of 1,1,1-trichloroethane
have more than doubled during the last 8 years. A great
deal of 1,1,1-trichloroethane data from remote environ-
ments have been collected (17, 18), even though urban
measurements are sparse.
1,1,2-TrichJoroethane was found at extremely low con-
centrations (average 0.01-0.04 ppb) at all sites. At no time
did its concentration exceed 0.15 ppb. These data are not
inconsistent with those reported by Pellizzari (20), who
found levels of <0.01-2 ppb at sites in New Jersey, Texas,
and Louisiana. This 1,1,2 isomer is nearly 30 times more
reactive than the 1,1,1 isomer of trichloroethane (Table
I). 1,1,2,2-Tetrachloroetnane was measured at an average
concentration of 0.01 ppb or less (Table II). Its highest
concentration never exceeded 0.1 ppb. 1,2-Dichloroprane
was also present at an average concentration of 0.02-0.07
ppb, and its highest measured concentration never ex-
ceeded 0.25 ppb. Compared with chloroethanes, this
chloropropane is considerably more reactive, and a 10%
daily loss rate is esimated (Table I). In the only data
available (20), 1,1,2,2-tetrachloroethane and 1,2-dichloro-
propane levels of about 0.01 and 0.02 ppb, respectively,
have been reported.
Five chloroalkenes were measured, and of these, allyl
chloride (3-chloro-l-propene), a suspect carcinogen, could
not be detected at concentrations exceeding 5 ppt. 1,1-
Dichloroethylene (vinylidene chloride) was present at an
average concentration of 0.01-0.03 ppb. However, it was
below our detection limit of 5 ppt during 30-50% of the
time of all sites. These values are quite consistent with
the very low emissions (1-4 tons/year for 1,1-dichloro-
ethylene and 500 tons/year for allyl chloride) and high
reactivity (Table I). Although vinylidene chloride has been
identified in Tenax air samples (20), quantification has not
been possible for lack of sensitivity (detection limit of
Environ. Sd. Tecrmol., Vol. 1«. No. 12. 1982 877
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9. Mean diurnal variation of trichloroethylene
0.05-0.1 ppb). Occasionally, however, scattered data in
the concentration range of 0.01-0.6 ppb have been reported
m.
Of the chloroalkenes measured in this study, trichloro-
ethylene (TCE) and tetrachloroethylene (called per-
chloroethylene, PCE) are two large-volume chemicals.
Considerable debate on the potential carcinogenicity of
these alkenes currently exists (8,10,33). Their annual U.S.
emissions are estimated to be 0.15 and 0.3 million tons,
respectively. As is clear from Table I, TCE is substantially
Bore reactive in the atmosphere. TCE and PCE average
concentrations range from 0.1 to 0.2 and 0.3 to 0.6 ppb,
respectively. The concentration ratio (PCE/TCE) lies
between 2 and 4. The highest PCE concentration, 7.6 ppb,
• also about 3 times the highest TCE concentration of 2.5
ppb. In both instances a significant elevation above
background levels is evident. Their diurnal behavior was
very nearly identical; Figure 9 demonstrates a typical
diurnal profile of TCE. PCE diurnal behavior is similar,
but the nighttime-daytime gradients are somewhat less
pronounced.
Although TCE and PCE have been measured by several
investigators, data are sporadic. Lillian et al. (27) reported
nerage concentrations of 0.1-0.9 ppb (maximum 18 ppb)
(at TCE and 0.1-4.5 ppb (maximum 8 ppb) for PCE from
ttveral Eastern coastal cities. Bozzelli et al. (21) could
quantify only a small fraction of the collected samples and
reported an average concentration range of 1-2 ppb of
TCE and 0.3-4 ppb of PCE from six sites in New Jersey.
Contrary to our findings, their average PCE/TCE con-
centration ratio was greater than 1 at only three of the six
«ites. Ohta et al. (29) reported from Tokyo average con-
centrations of 1.2 ppb for both. Other measurements by
Singh et al. (5) have been reviewed (14). Unlike other
chloroalkenes, hexachJoro-l,3-butadiene (HCBD), a bac-
terial mulagen, is no longer manufactured in the U.S.
HCBD, however, has been identified in the effluents of
sewage treatment plants and as a byproduct of the com-
bustion of plastics; secondary sources do exist HCBD was
measured at an average concentration of less than 0.01 ppb
at all sites; its highest measured concentration was 0.15
ppb. No information is available op the reactivity of this
chemical, but its structure would suggest that it is highly
reactive. Limited measurements from Niagara Falls,
Louisiana, and Texas (20) show a concentration range of
0-0.1 ppb.
Although several chloroaromatics were measured during
this study (75), a-chlorotoluene (benzyl chloride) is the
only member that shows clear evidence of bacterial mu-
tagenicity (Table I). Ambient concentrations as high as
0.11 ppb were measured, but by and large this chemical
was not detectable at 5-ppt levels. A daily loss rate of 23%
(Table I) and an estimated U.S. emission strength of 45
tons/year are entirely consistent with its nondetectability
in urban atmospheres (75). No abmient data could be
found in the literature, although concentrations in the
1-2-ppb range have been reported near a Stauffer chemical
plant in Edison, NJ (20).
Eight important aromatic hydrocarbons were measured;
of these, benzene is a suspected carcinogen (8,10). Because
the mutagenicity of toluene is strongly disputed (1, 10),
it is not included here. The average benzene concentra-
tions at all sites were between 1.5 and 6 ppb, although
concentrations as high as 65 ppb were measured. Toluene
was typically 1-2 times more abundant than benzene. The
diurnal behavior of benzene, shown in Figure 10, was
representative of all aromatic hydrocarbons. The mean
diurnal behavior of benzene is not atypical of other pol-
lutants discussed here. Much of the literature data on
benzene were obtained during the daytime (34), and these
average concentrations are comparable to daytime con-
centrations reported here. No diurnal profiles of benzene
could be found in the published literature.
Formaldehyde, a mutagen and a suspect carcinogen, is
also a natural component of the global atmosphere (Table
I). Its average urban concentrations of 10-20 ppb are
significantly higher than an estimated background of 0.4
ppb (Table I). Despite its extremely high reactivity,
formaldehyde was the most dominant bacterial mutagen
found in the urban atmosphere, some 4 times (range of 3-8
times) more abundant than benzene. Formaldehyde was
measured by two different methods, both with comparable
results (±30%). Acetaldehyde, a nonmutagen, was also
measured at an average concentration of 1 and 2 ppb
(range of 0.2-3.4 ppb) at the Pittsburgh and Chicago sites,
respectively. These data and those of others have been
presented in greater detail in ref 15.
Although the chemicals listed in Table I can differ sig-
nificantly as to their mutagenic and carcinogenic capacities
(9, 10), a simple summation of their mass concentration
is of interest for comparison with background levels.
Collectively, the aggregate daily mean exposure to all
chemicals in Table II is found to lie between 27 and 59
Mg/m3 at all sites. (Formaldehyde data in Houston could
not be collected because of technical difficulties, so the
Houston data of Joshi (35) are used). The daily average
exposure in an unpolluted environment from the four
naturally occurring mutagens (methyl halides and form-
aldehyde) is determined to be about 1.9 Mg/m3 from data
in Table I. Total exposure to all mutagens and suspect
carcinogens (both natural and man-made) in the present
remote environments is 4.4 ng/m3 (Table I). Thus, even
in a locally unpolluted environment, the present exposure
Environ. SO. Tschnol., Vol. 16, No. 12, 1982
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-56-
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Hiur* 10. Mean dumal variation of benzene.
to this group of chemicals has more than doubled. In
urban environments this exposure is at least 15-30 times
the natural background (1.9 vs. 27-59 Mg/ms).
The total exposure to mutagens and carcinogens from
urban ambient air is, of course, much higher because of
nongaseouB species (e.g., polyaromatic hydrocarbons) (36)
at well as other gaseous species for which either toxicity
studies are inconclusive or measurement methods inade-
quate (e.g., oxygenated chemicals). More extensive mea-
surements are clearly needed to refine further the quan-
titative relationships developed here.
Concluding Thoughts
A number of synthetic organic chemicals that are known
to be toxic at concentrations much higher than those found
in ambient air are present in the urban as well as remote
atmospheres. The data base to define the abundance of
guch chemicals is currently very limited. Most synthetic
rfi»tni/<«la listed in Table I came into major use after 1950,
•ad since then their production and release have continued
to grow exponentially, with a doubling time of about 6
years (5). Because of the long lag times (10-50 years)
associated with the onset of cancer (1,2), a significant risk
nay not be identified until a future date. Continuous
exposure to low levels of such chemicals could erode any
human threshold that may exist or enhance the frequency
of cancer's occurring from other primary causes such as
cigarette smoking (37). The ubiquitousne&s of organic
mutagens of natural origin in the air and oceans leads us
to speculate that they may have played a role similar to
that attributed to radiation in the processes of biological
evolution. A comparison of the mutagenic activity of these
natural organic* with natural low-level radiation would
help to understand better the part natural chemicals might
have played in those processes.
Acknowledgments
Helpful discussions with L. Cupitt of the U.S. Envi-
ronmental Protection Agency are appreciated.
Literature Cited
(1) Report prepared for U.S. Senate, Serial No. 96-15, "Health
Effects of Toxic Pollutants: A report from the Surgeon
General, Department of Health and Human Services", Aug
1980.
(2) LaFond, R E., Ed. "Cancer The Outlaw Cell"; American
Chemical Society: Washington, D.C., 1978.
(3) Epstein, S. "Politics of Cancer"; Sierra Club Books: 1978;
revised in Anchor Press, 1979.
(4) Peto, R. Nature (London) 1980, 284, 297.
(5) Singh, H. B.; et aL "Atmospheric Distribution, Sources, and
Sinks of Selected Halocarbons, Hydrocarbons, SF6 and
N,O"; EPA-600/3-79-107,1979.
(6) Altshuller, A. P. Adv. Environ. Sci. Techno/. 1980, 10,
181-215.
(7) McCann, J.; Ames, B. N. Cold Spring Harbor Con/. Cell
Proliferation 1977, 4, 1431-1450.
(8) Helmes, C. T.; et al. "Evaluation and Classification of the
Potential Carcinogenicity of Air Pollutants"; SRI Inter-
national NCI Contracts N01-CP-33285 and 95607, Menlo
Park, CA, 1980.
(9) Simmon, V. F.; Kauhaven, K.; Tardiff, R G. Dev. Toxicol.
Environ. Sci. 1977, 2, 249.
(10) Albert, R. E., The Carcinogen Assessment Reports, sub-
mitted for publication to the U.S. EPA, 1980.
(11) NCI report on carcinogenesis, Bioaasay of Chloroform, NIH,
MD, 1976.
(12) Poirier, L. A.; Stoner, D. K.; Shimkin, M. B. Cancer Res.
1975, 35, 1411-1415.
(13) NCI carcinogenesis technical report series, No. 74, 1978.
(14) Greenberg, M. M.; Parker, J. C. "Health Assessment
Document for Tetrachloroethylene"; U.S. Environmental
Protection Agency, External Review Draft No. 1, Research
Triangle park, NC, 1976.
(15) Singh, H. B.; Salas, L.; Stiles, R.; Shigeishi, H.
"Measurements of Hazardous Organic Chemicals in the
Ambient Air"; Project 7774 final report, EPA, 1982.
(16) Singh, H. B.; Salas, L.; Stiles, R, submitted for publication
in J. Geophyi. Ret.
(17) Singh, H. B.; Salas, L. J.; Stiles, R, submitted for publi-
cation in J. Geophyt. Res.
(18) Singh, H. B.; Salas, J.; Shigeuhi, H.; Scribner, E. Science
(Wathington, D.C.) 1979, 203, 899-903.
(19) Lovelock, J. E. Nature (London) 1975, 256, 193-194.
(20) Pellizzari, E. D.; Bunch, J. E. "Ambient Air Carcinogenic
Vapors—Improved Sampling and Analytical Techniques
and Field Studies"; EPA-600/2-79-081, 1979.
(21) Bozzeffl, J. W.; Kebbekut, B. B.; Greenberg, A., final report
submitted to New Jersey Department of Environmental
Protection by New Jersey Institute of Technology, 1980.
(22) Chameides, W. L.; Davis, D. D. J. Geophyt. Ret. 1980,85,
7383-7398.
(23) Singh, H. B.; Salas, L.; Smith A.; Shigeishi, H. Atmos.
Environ. 1981, 15, 601-612.
(24) Symons, J. M.; et al. J.—Am Water Works Attoc. 1975,
634-637.
(25) Batjer, K.; et aL Chemotphere 1980, 9, 311-316.
(26) Singh, H. B.; Fowler, D. P.; Peyton, T. 0. Science (Wash-
ington, D.C.) 1976,192,1231-1234.
Sri Tuchnri VrJ. 16 to 12 1082 170
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(27) Lillian, D.; et aL Environ. Sci. Technol. 1975,9,1042-1048.
(28) Simmonda, P. G.; Kerrin, S. L.; Lovelock, L. G.; Shair, P.
H. Atmos. Environ. 1974, 8, 209-216.
(29) Ohta, T.; Morita, M.; Mizoguchi, L At mot. Environ. 1976,
10, 557-560.
(30) Going, J. E.; Spigarelli, J. L. "Sampling and Analysis of
Selected Toxic Substances Task IV—Ethyiene Dibromide";
EPA 560/6-76-021,1976.
(31) Leinrter, P.; Perry, R.; Young, P. J. Atmos. Environ. 1978,
12, 2383-2387.
(32) Farber, H. P. "1,1,1-Trichloroethane as an Industrial Sol-
vent: A Review of Current Health and Environmental
Knowledge"; Dow Chemicals: Midland, MI, 1979.
(33) Demopoulas, H. B.; Wagner, B.; Cimino, J. "An Academic
Review of the Hazards Posed by Trichloroethylene", New
York University Medical Center, unpublished.
(34) Mayrsohn, H.; Kuramoto, M.; Crabtree, J. H.; Sothern, R.
B.; Mano, S. H. "Atmospheric Hydrocarbon Concentration
June-September 1975"; DTS-76-15, California Air Re-
sources Board.
(35) Joshi,S.B. "Houston Field Study—1978 Formaldehyde and
Total Aldehydes Monitoring Program"; EPA Contract
68-02-2566, Northrop Services Inc. Report ESC-TR-79-22,
1979.
(36) National Academy of Sciences, "Paniculate Polycyclic
Organic Matter"; Washington, D.C., 1972.
(37) Albert, R. E.; Burns, F. J. Cold Spring Harbor Conf. Cell
Proliferation 1977,1, 289-292.
Received for review March 12, 1982. Accepted July 23, 1982.
Research funded in part by U.S. Enviromental Protection Agency
under Grant 806990.
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SOURCES OF AIR TOXICS IN CALIFORNIA
G. C. Hass
Chief, Haagen-Smit Laboratory Division
California Air Resources Board
El Monte, CA
Terry McGuire
Assistant Division Chief, Stationary Source Division
California Air Resources Board
Sacramento, CA
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Suranary of Comments on Ambient
A1r Monitoring for Toxic Compounds by the
Air Resources Board
by
G. C. Mass, Chief
Haagen-Smit Laboratory Division
El Monte
The Air Resources Board began monitoring for toxic compounds in the
vicinity of suspected sources of particular compounds; e.g., vinyl
chloride, halogenated hydrocarbons, benzene, etc. It was standard
practice to locate a control sampling point some distance removed from
the source. NQt infrequently, measurements at the control point
exceeded those near the source. This led to the beginning of our
current program to monitor the general urban air on a regular basis.
Currently, we collect four 24-hour samples weekly at our El Monte lab
headquarters. Three other locations, Riverside, downtown Los Angeles,
and Dominguez are sampled on a three-day rotating schedule.
The samples are collected in Tedlar bags and taken to the El Monte
facility for analysis within a few hours of the end of the collection
period. An aliquot of the bag contents is transferred by syringe to the
freeze out loop of a gas chromatograph equipped with an electron capture
detector. Our standard procedure yields results for nineteen halogenated
hydrocarbons (not all of interest as toxics). It 1s our intention to
add a separate GC analysis for benzene.
The El Monte station has been in operation since November, 1982, and the
satellites from one to three months later. Mean results from the stations
are shown for six compounds in Table I. These six compounds are believed
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to be of significant toxic interest. Some were found above the limit
of detection in all samples, while the others were found often enough
to yield an estimate of their mean concentration. Carbon tetrachloride
behaves much like a "clean air" background compound in terms of spatial
and temporal distribution. Our mean value, however, is only about one
third the background value reported by Dr. Singh in the previous presen-
tation.
This raises the question of the reliability of those measurements. The
concentrations reported are about three orders of magnitude lower than
those encountered in conventional air pollution work. Opportunities for
error in sampling, sample transfer, standardizing procedures, and
analysis are correspondingly amplified. Nevertheless, the numbers cannot
be ignored pending attainment of the confidence limits to which we are
accustomed. In the case of carbon tetrachloride cited above, which shows
an apparent discrepancy of a factor of three, either number is of social
concern when considered in the context of published cancer risk factors
and the population at risk.
The ARB Haagen-Smit Laboratory has benefitted by being close neighbors to
the South Coast Air Quality Management District facilities. Professional
cooperation has been beneficial to both laboratories. The ARB now proposes
to extend this cooperation to other governmental organizations in Califor-
nia by establishing in the near future a Toxic Substances Technical
Advisory Committee (TOXTAC).
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TABLE I
TOXIC ORGANIC SURVEY
MEAN VALUES OF COMPOUNDS
AT FOUR SAMPLING SITES
INCLUSIVE DATES: 11/14/82 TO 6/26/83
EL MONTE DOLA DOMINGUEZ RIVERSIDE
SAMPLING SITE CONC. CONC. CONC. CONG.
COMPOUNDS PPb PPb PPb PPb
1. DICHLOROMETHANE 1.47 0.89 1.62 1.09
2. TRICHLOROMETHANE 0.05 0.17 0.05 0.05
3. TETRACHLOROMETHANE 0.04 0.06 0.04 0.04
4. TRICHLOROETHYLENE 0.32 0.63 0.34 0.25
5. 1,2-DIBROMOETHANE 0.01 0.01 0.01 0.01
6. TETRACHLOROETHYLENE 1.20 1.38 1.36 0.44
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Sources of Air Toxics in California
Terry McGuire - Assistant Division Chief
Stationary Source Division
California Air Resources Board
The California Air Resources Board is working in a number of areas to
identify and inventory sources of potentially toxic substances in
California. Current activities in this field include:
Identification of substances to be inventoried
Literature studies and preparation of preliminary Inventories
Extramural research
Field evaluation and testing
Coordination with air pollution control districts
Utilization of existing organic gas emission data
Identification of Substances
Lists have been established by the EPA and the ARB of more than forty
substances of concern because of their potential toxicity. To date, the EPA
has identified seven substances as hazardous pollutants under Section 122 of
the Clean Air Act (National Emission Standards for Hazardous Air
Pollutants). A.recently enacted law (AB 1807, Tanner) has added to the State
Health and Safety Code, procedures for identifying substances as toxic. No
substances have been identified to date.
Present inventory efforts are concerned with a number of substances of high
current interest. The Emission Inventory Technical Advisory Committee
(EITAC), composed of representatives from the EPA, the ARB, and six of the
air pollution control districts -in the state, is considering a statewide
survey of the following 13 substances:
Arsenic
Benzene
Carbon Tetrachloride
Chloroform
Ethylene Oxide
Ethylene Dibromide
Methyl Bromide
Mehtyl Chloroform
Methylene Chloride
Perchloroethylene
Trichloroethylene
Vinyl Chloride
Formaldehyde
Literature Studies and Preparation of Preliminary Inventories
A study has been 1n progress for more than a year to Identify sources and
compile a preliminary inventory of emissions of selected substances. The
Inventory is primarily based on Information in the literature, but includes
applicable information from current research studies and field evaluation and
testing. The preliminary Inventory is being revised and will include
Information on the properties, present uses, emission potential, and
statewide emissions for twenty-five substances.
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Information available in the literature has a number or nmltations:
• Information is incomplete.
• Information available is not always for the same'year. (Use of some
substances has changed significantly in recent years.)
t There are sometimes conflicting information in different references.
t There is a lack of quantitative and source-specific data.
Typical sources of potentially toxic substances that have been identified
from the literature and examples of the substances emitted are shown in
Figure I.
Extramural Research
Several ARB sponsored research projects, either completed or are in progress,
are providing data to support this inventory effort.
• "An Inventory of Carcinogenic Substances Released into the Ambient
Air in California," Science Applications and KVB. The study
Investigated: Arsenic, Asbestos, Benzene, Cadmium, Carbon-
tetrachloride, Chloroform, Ethylene Dibromide, Ethylene Dichloride,
Nitrosamines, Perchloroethylene, Polycyclic Organic Matter. Tests
were concluded on: lead smelters, a steel mil.l, an asbestos cement
plant, and four organic chemical manufacturing plants.
• "Formaldehyde - A Survey of Airborne Concentrations and Sources,"
Science Applications, Inc.
t
• "Improvement of Emission Inventories for Reactive Organic Gases and
Oxides of Nitrogen in the Sourth Coast Air Basin," Systems
Applications. The study will provide improved organic speciation
data.
• "Development and Improvement of Organic Compound Emissions," Science
Applications, Inc.
Field Evaluation and Testing
The ARB staff has been active in the evaluation and testing of facilities
known to emit potentially toxic substances. This activity includes designing
test procedures and conducting material balances; conducting tests-such as
stack and ambient monitoring for Ethylene Oxide, tests on the incineration of
waste solvents in the General Portland cement kiln, and monitoring at the BKK
and Kettleman dump sites; and evaluating a wet air oxidation unit jointly
with the Santa Barbara County Air Pollution Control District.
Coordination with Air Pollution Control Districts
A number of the air pollution control districts in the state have initiated
programs to identify and Inventory potentially toxic substances. This
activity has been coordinated with the EPA and the ARB through the Emission
Inventory Technical Advisory Committee.
• The South Coast Air Quality Management District is conducting a
survey of approximately 1600 facilities for 20 substances.
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FIGURE I.
TYPICAL SOURCES OF POTENTIALLY TOXIC AIR CONTAMINANTS
INDUSTRIAL
• CHEMICAL INDUSTRY
BENZENE
CARBON TETRACHLORIDE
CHLOROFORM
O PETROLEUM INDUSTRY
BENZENE
O CLEANING AND DECREASING
METHYLENE CHLORIDE
METHYL CHLOROFORM
• FUEL COMBUSTION
ARSENIC
BERYLLIUM
CADMIUM
CHROMIUM
• METAL SMELTING
ARSENIC
CADMIUM
AGRICULTURE
O PESTICIDES AND FUMIGANTS
ARSENIC
CARBON TETRACHLORIDE
ETHYLENE DIBROMIDE
MOTOR VEHICLES
• EXHAUST AND EVAPORATION
BENZENE
ETHYLENE DIBROMIDE
ETHYLENE DICHLORIDE
WASTE DISPOSAL
• HAZARDOUS WASTE LANDFILLS
BENZENE TETRACHLOHOETHYLENE
CHLOROFORM VINYL CHLORIDE
METHYL CHLOROFORM
• SANITARY LANDFJLLS
BENZENE XYLENE
DICHLOROBENZENE
• INCINERATION FACILITIES
• CHEMICAL DESTRUCTION FACILITIES
DIOXANE
TRICHLORCETHYLENE
FORMALDEHYDE
TRICHLOROETHYLENE
FORMALDEHYDE
LEAD
MERCURY
LEAD
ETHYLENE DICHLORIDE
METHYL BROMIDE
FORMALDEHYDE
LEAD
POLYCYCLIC AROMATIC
HYDROCARBONS
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t The Ventura County APCD is conducting a survey of dry cleaners,
hospitals, plastic and electronic industries;
t The Santa Barbara County APCD is conducting a survey of 550
companies and is.planning to- test a dump site in Santa Maria.
-;
t The Sacramento County APtD contracted with KVB to inventory
emissions of potentially toxic substances within the county.
• The Bay Area Air Quality Management District has been obtaining
Inventory data for some potentially toxic substances as part of its
normal Inventory procedures.
Members of the EITAC are developing a uniform survey format that can be used
by the districts to report emission data for potentially toxic substances to
the state emission data system.
Utilization of Existing Organic Gas Emissions Data
A potential exists for locating and quantifying some potentially toxic
emissions by using the present organic gas data base and speciation
profiles. A speciation profile for a process shows what fractions of the
total organic gas emissions are various organic compounds. Using the
speciation profile and the total organic gas emitted by a process provides an
estimate of the emissions for a specific organic substance. Existing
speciation profiles include fourteen substances that have been identified as
potentially toxic. A preliminary evaluation of benzene emissions using
speciation profiles and the 1979 organic gas emission inventory indicates
that more accurate speciation profiles are needed.
Work is in progress at the Air Resources Board to establish a data system to
store in a consistent manner, the information on emissions of potentially
toxic substances that is being compiled by the local air pollution agencies.
The system will link to the existing data base of criteria pollutants to
utilize existing organic emissions information.
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AIR TOXICS IN THE INDOOR ENVIRONMENT
Dr. David Grimsrud
Co-Leader, Building Ventilation and Indoor Air Quality Program
Lawrence Berkeley Laboratory
Berkeley, CA
Dr. Ken Sexton
Director, Indoor Air Quality Program
California Department of Health Services
Berkeley, CA
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Suaaary of Presentation of David Grinsrud
Region 9 Air Toxics Conference
September 13, 1983
Introduction
Prior to any discussion of indoor air quality I must point out that
there are no indoor air quality standards that govern general public access
buildings. Thus, the definition of toxics used in this conference applies
to all pollutants monitored within buildings. This lack of standards
forces us to apply occupational or ambient air quality standards to
measurement results as reference guidelines. However, this is, at best, a
questionable practice and in some cases is clearly inappropriate.
Background
Indoor air quality began to be an issue in the mid-seventies when
research scientists began to Investigate movement of outdoor pollutants
Indoors using equipment that had been developed for outdoor monitoring. It
quickly became apparent that some pollutants found indoors could not be
associated with outdoor sources; since those observations many important
indoor pollutant sources have been found.
At approximately the same time energy conservation in buildings began
to receive national attention. Since an inexpensive weatherization measure
that had large potential energy savings was the reduction of outdoor
ventilation air, concern began to be expressed about this measure's impact
on indoor air quality. If the pollutant source strength remains constant,
a decrease in ventilation rate (the most important pollutant removal
process) should increase pollutant concentrations. As a result of these
concerns the research program of our group, and others studying indoor air
quality, was directed toward two major questions:
(1) What effects do weatherization and/or new building practices have on
indoor air quality?
(2) What minimum ventilation rates are required to assure adequate indoor
air quality in buildings?
Our work and the work of other research groups have shown that neither
question has a unique answer. As a result, the emphasis of our group has
shifted to the characterization of the physics and chemistry of pollutants
found within buildings. This includes monitoring the concentrations found
within buildings—often using instrumentation developed for studies in our
laboratory experiments and using procedures developed for our laboratory
studies* It does not Include health studies, although our laboratory and
field monitoring work informs those who study health effects about the
concentrations that will be present within buildings. It does support the
development of techniques that are specific to a single pollutant.
A major emphasis of our work continues to be the building. The
building shell defines the volume and the environmental conditions in which
pollutants are released. Changes in building operation, materials used in
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building construction, and appliance use all affect pollutant concentra-
tions and transformations.
LBL Research Project Areas
Combustion Products.
in this project we have studied the emission rates of gas stoves,
unvented gas and kerosene space heaters, and wood stoves. Using these
measured emission rates we have compared concentrations that would be
predicted by modeling with concentrations obtained in field measurements
made in research houses. These results show that concentrations of oxides
of nitrogen or carbon can reach high levels indoors (levels in excess of
NAAQS or OSHA standards).
Major questions remain in this area concerning the transport and
transformation of pollutants—and ultimately the control of combustion
pollutant concentrations.
Radon and Radon Progeny.
in the United States the emission rates of radon from common building
materials are too small to explain the radon concentrations seen within
buildings. This observation and other direct evidence of radon entry point
to the soil as the major source of radon in buildings. Comparisons of
radon concentrations and ventilation rates show that the large variability
in concentrations seen in buildings is primarily due to source variations
rather than to variations in ventilation rates in buildings. These obser-
vations define a series of important questions that must be investigated
before the problem of radon and radon progeny can be resolved. These
include the mechanisms of radon entry into buildings, the behavior of radon
and radon progeny in the air after entry, and ultimately the control of
these pollutant species.
Formaldehyde and Other Organics.
Work in this area has demonstrated a clear dependence of indoor
concentrations on building materials and furnishings found within the
space. Many questions remain to be addressed and answered in the study of
airborne organics. Included are the detailed identification of source
emission rates, the dependence of emission rates on environmental factors,
the development of reliable and low-cost methods of sampling the concentra-
tions of organics in the indoor air, and development of an improved under-
standing of the health effects associated with any single contaminant or
combination of these contaminants.
instrumentation Development.
This Is an ongoing part of any research effort and has been an Impor-
tant part of our program. Instruments developed range from the sophistica-
tion of an automated device that samples radon progeny remotely under
microprocessor control to the simplicity of passive samplers that combine
low cost and ease of operation with measurement precision.
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Efforts to develop and test passive samplers have been a particular
Interest for our project. Passive samplers will allow a large-scale survey
of Indoor air quality In buildings to be conducted. The samplers that are
presently available include those that measure radon, nitrogen dioxide,
formaldehyde, carbon monoxide, and water vapor. We are currently beginning
studies to develop a carbon dioxide sampler.
Major issues yet to be resolved include developing a better under-
standing of the limitations of passive samplers through field experience
and testing. Even more important is the issue of the utility of passive
sampler results, i.e., long-term average concentrations. If health risks
depend more on short-term peak concentrations than on long-term exposure to
some average pollutant concentration, then passive samplers are
Inappropriate for monitoring purposes. However, their low cost and simpli-
city make them very attractive for possible future use, particularly for
screening large numbers of buildings for potential air quality problems.
Indoor Air Quality Control Techniques.
Our major effort in this area in the past has been the study of
ventilation using mechanical systems employing air-to-air heat exchangers
that minimize energy use. Construction trends (in colder climates) are
moving to tight buildings where ventilation is supplied mechanically.
Energy use in these buildings is minimized if the mechanical systems employ
heat recovery from the exhaust air. Our group has measured the thermal
effectiveness of these systems, their ability to remove pollutants from the
air, and ventilation effectiveness (the ratio of air delivered to a space
to the amount predicted by the manufacturer). Cost effectiveness studies
show that heat exchangers are not always the best solution; their utility
depends on the cost of energy, building tightness, and the climate of an
area.
The controls project is moving away from studies of ventilation
systems to studies that Investigate pollutant-specific control techniques.
Studies in progress or planning include air washing to remove formaldehyde,
ultraviolet photodecomposition to remove formaldehyde, and reactivity
studies to control nitrogen dioxide.
Summary
Our group, and others, have shown the importance of indoor pollutant
sources in determining indoor pollutant concentrations. While ventilation
continues to be an important indoor air quality control technique, one must
consider both sources and removal mechanisms to adequately describe air
quality within buildings.
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•
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furniture), combustion (e.g., unvented apace heaters, gas-fired appliances,
fireplaces), sidestream tobacco smoke, pesticides, consumer products (e.g.,
personal care and cleaning products), and human activities (e.g., cooking,
hobbies). Among the organic air pollutants which have been measured indoors
are aliphatic, halogenated, and aromatic hydrocarbons, alcohols, ketones,
esters, monomers, plasticizers, acetaldehyde, acrolein, chlordane, malathion,
and dichlorvos.
Because society has been slow to recognize the importance of indoor air
quality, there are insufficient data to evaluate health consequences. In many
cases it is not feasible to delineate the relative contribution of indoor and
outdoor sources to toxic air pollutant exposures. However, information on
hand indicates that evaluation of indoor as well as outdoor exposures is
essential for realistic health effects assessment. The importance of
Bafeguarding indoor air quality is underscored by the high toxicity of many
identified indoor pollutants, evidence of elevated concentrations indoors, and
the large number of people potentially at risk.
PUBLIC POLICY ISSUES
Tor a given dose of a specific chemical, the toxic effects are the same
whether exposure occurs indoors or outdoors, all other factors being equal.
However, there are critical differences between indoor and outdoor air
pollution which have ramifications for policy choices about appropriate public
responses.
The rationale for government regulation to control outdoor sources focuses on
the issue that those who suffer the effects are not compensated, nor is their
interest in cleaner air readily effective in influencing polluters. In
economic terms, outdoor air is a "public good" since members of a community
breathe basically the same ambient air. Public intervention has been deemed
appropriate in the case of ambient air pollution, because 1) no rational
individual will attempt to cleanup dirty air over cities since his or her
share of the benefits are much smaller than the costs, 2) efforts at
voluntary cooperation to reduce pollution are doomed, since those who refuse
to contribute can not be excluded from the benefits, and 3) no pollution
source will spend enough on abatement in the absence of regulations or legal
liability due to the difficulties of collecting from beneficiaries.
Although indoor air quality is often spoken of in a generic sense, there are
in fact a wide range of indoor environments. Among important distinctions are
1) occupational, both industrial and nonindustrial, 2) nonoccupational,
including residential, commercial, institutional, and public, and 3)
transportation microenvironments, including automobiles, airplanes, and
subways. It is therefore clear that there are both private and public indoor
settings; a fact which may influence decisions about public intervention.
Indoor air in private residences does not have the characteristics of a public
good, since the costs and benefits of abatement are internalized within the
household. If occupants foul the air in their own home, they are forced to
breathe it. If they attempt to improve its quality by increasing ventilation
or installing air-cleaning devices, they bear the costs and enjoy the
benefits. Prescription of indoor air quality standards and regulations must
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confront the fact that households are already making decisions about their own
air quality.
However, not all buildings are residences and not all residences are owner-
occupied. Air quality in large public buildings shares some characteristics
with outdoor air. The case for indoor air quality regulations is much
stronger in hospitals and convention halls than in private dwellings. It is
common practice to regulate construction and operation of public buildings to
ensure that adequate provisions are made for health and safety. In addressing
the issue of indoor air quality, decision-makers must remember that the role
of government may depend on the degree of "publicness" of a particular
building.
CALIFORNIA'S INDOOR AIR QUALITY PROGRAM
Assembly Bill No. 3200 directs the Department of Health Services to coordinate
efforts to assess, protect, and enhance indoor environmental quality.
Specifically, the State Legislature declared "...that the public interest
shall be safeguarded by a coordinated, coherent State effort to protect and
enhance the indoor environmental quality in residences, public buildings, and
offices in the state." In accordance with the directives outlined in Assembly
Bill Ifo. 3200, the Indoor Air Quality Program was established within the
Department of Health Services, Air and Industrial Hygiene Laboratory.
The California Indoor Air Quality Program is a multidisciplinary unit
responsible for promoting and conducting research aimed at understanding the
determinants of healthful indoor environments. The ultimate goal is to assess
the nature and magnitude of potential hazards within the State so that health
risks can be evaluated rationally. This information is an essential component
of policy decisions about the need for public intervention.
SjMMARY
Most of the current discussion concerning control strategies for toxic air
pollutants has focused on outdoor sources. It is becoming increasingly
apparent, however, that development of an effective program to reduce
population exposure must take indoor environments into account. In order to
assess health risks, establish suitable standards, and implement appropriate
control strategies, information is required about the number of people
exposed, severity and pattern of exposures, and dose-response relationships.
Evaluation of indoor exposures to toxic chemicals is an integral part of this
process.
A sore indepth discussion of the issues raised here may be obtained from the
following references.
Ken Sexton and Robert Repetto, Indoor Air Pollution and Public Policy,
Environment International 8;5-10, 1932.
John Spongier and Ken Sexton, Indoor Air Pollution: A Public Health
Perspective, Science 221:9-17, 1983.
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A STUDY OF THE RELATIONSHIP BETWEEN CANCER INCIDENCE
AND AIR POLLUTION IN CONTRA COSTA COUNTY, CALIFORNIA
Dr. Donald Austin
Chief, Resource for Cancer Epidemiology and California Tumor Registry
California Department of Health Services
Emeryville, CA
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A3T7PACT
A study cf tho relationship of lung cancer incidence in Contra Costa County to
acbient levels of air pollution has been concluded. The study was generated as
the result of public officals and private citizens groups concerned about
reports of elevated lung cancer incidence in the county. It had been suspected
by soP!e that the presence of industrial plants in the county, mainly petro-
cherical refineries, could be a contributing factor. The study, initiated
with a grant from the EPA, consisted of five parts.
First, an incidence analysis established that when the county was divided into
tvo parts, the Industrial portion of the county had ac excess of lung cancer as
conpp.red to the rerair.ing Son-industrial portion. The incidence of lung cancer
for the county as a whole was unremarkable as cocpared to four other local
counties.
Kore detailed information on the patterns of air pollution in the county were
obtained in the second phase of the study. Five percanent air monitoring
stations and ten temporary stations monitored the levels of 12 air pollutants
for e reriof of one year. These data were incorporated into later phases of
the study.
Ir the third portion of the study, through a correlation analysis of 1970-"°
lung cancer rctes ar.d various air pollution constituents, a relationship
between ertiert air CC1 and lung cancer in males, but not in females, was
found to be statistically significant. However, the percent of the working
population categorized as blue collar was also associated with lung caacer ir
Bales ar.d the previous association between lung cancer ir Bales and ambiect air
SC levels was eliminated when this third factor was taken into consideration.
Fart fcur of the study was to have consisted of s linkage of occupational group
cohorts to registry cancer incidence files but was not conducted for lack cf
easy availability of occupational group records.
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Part five of the study was an analysis of case-control interview data on a
final annple of €?2 individuals. Demographic, work history, residential
history, dietary, an* sacking history questions corprised the bulk of the date
collected. Analysis of the data indicated that the najor contribution to
lung cancer in Contra Costa County was due to cigarette snoking.
Further, there was no identified effect on lung caccer risk contributed fron
any oeasured constituent of air pollution. Of five broad occupational
categories (indicating possible hasardous exposures) none had any significant
relationship to lung cancer, retailed evaluation of the effect of specific
occupational groups awaits final analysis.
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PROJECT SOWARY
EPIDEKIOLOGICAL STUDT 0? THE HCIDWCE Of CAHCER
AS RELATED TO INDUSTRIAL WISSIOIS IF
CONTRA COSTA COUNTY, CALIFORNIA
Donald F. Austin, M.I>., Terne Nelson, Biz Swain,
Linda Johnson, Susan Lam, Peter Plesael
The purpose of this study was to exanine the relationship of lung cancer
incidence in Contra Costa County to ambient levels of air pollution. It was
suspected that the presence of heavy industry in the county, mainly petro-
cheBical plants and oil refineries, could be a contributing factor.
Initially, an incidence analysis established that tfce Industrial portion of the
county had an excess of lung cancer as compared to the remaining Non-industrial
portion.
Air pollution patterns were subsequently determined by five permanent air
monitoring stations and ten temporary stations which monitored the levels of 12
air pollutants for a period of one year.
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By correlating the 1970-79 lung cancer rates for each census tract and tract
levels of air pollution constituents, a statistically significant relationship
between ambient air SO. and lung cancer in Bales, but not in females, was
found. However, when adjusted for the percent of the working population
categorized as blue collar, the association was eliminated.
An interview study of 249 cases and 373 controls was then conducted. Demo-
graphic, work history, residential history, dietary, and smoking history
questions comprised the bulk of the data collected. Analysis indicated that
the major contribution to lung cancer in the county was due to cigarette
smoking. Ho significant association between lung cancer risk and measured
constituents of air pollution was found. Of five broad occupational categories
(indicating possible hazardous exposures) none had any significant relationship
to lung cancer.
IHTRODUCTION
Contra Costa County, located in the northeastern part of the San Francisco
Bay Area, is one of 39 OS counties found to have a high mortality rate for
specific cancer sites. The fact that the county also has five major
petroleum refineries and numerous petrochemical plants, and that 68? of
the total stationary air pollution in the Bay Area originates from the
county, prompted an epidemiological study of the incidence of cancer in
Contra Costa County. The major objective was to determine whether
industrial emissions have a measurable effect on cancer occurrence. The
study consisted of four parts:
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1. A comparison of cancer incidence in heavily industrialized sections
of the county to nonindustrialised sections.
2. Ambient air monitoring, consisting of sampling and chemical analysis
of components of particulate pollution.
3« Correlation analysis of lung cancer incidence rates with air
pollution constituents and census tract characteristics.
4. A case-control study to identify specific environmental factors
associated with lung cancer incidence in the county.
HETHOPS
Cancer Incidence
Cases included for analysis were malignant, invasive, resident incidence
cases with primary sites of lung, bronchus or trachea for the period of
1969-19rr8. Age adjusted incidence rates were generated for the Industrial
and Hoc-Industrial areas.
Air Pollution Monitoring
A total of 15 hi-volune particulate saaplers were strategically sited at
13 locations in Contra Costa County and two locations in adjacent
counties.
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Air particulate material was collected every sixth day at each of the 15
sampling sites from November, 1978 to October, 1979« Particulate matter
was analysed for total suspended particulates (TSP), beneene soluble
organics (BSD), sulfate (SO.), nitrate (HO,), lead (Pb), selected
polycyclic aromatic hydrocarbons (PAH), and «utagenie activity. Standard
chemical techniques vere used to analyze TSP, BSD, SO., HO,, and Pb.
Specific PAH vere separated by high preformance liquid chromatography and
analyzed using ultraviolet absorption and fluorescence. Hutagenicity vas
measured using the Ames test.
Correlation of cancer incidence data to air pollution measurements
required interpolation of the station data to 115 census tract population
centroids using a contour mapping program called STHAP.
Correlation analysis
Pearson correlation coefficients for census tract data between each air
pollutant constituent and the 5- and 10-year average annual age-adjusted
lung cancer incidence rates were computed for white males and females (two
atypical tracts were removed from the analysis). Partial correlation
coefficients for the same data were compared using socio-economic
variables as controls.
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Case-control Study
A case-control questionnaire study was conducted. All cases of cancer of
the trachea, bronchus or lung among black or white residents of Contra
Costa County, diagnosed between May 8, 1980 and July 31, 1981, and who
were at least 35 years of age and less than 75 years of age at diagnosis,
comprised a group of 332 eligible cases. Proxies were interviewed where
cases were too ill or were deceased.
Controls were Batched to cases of the same race and sex, and 5-year age
group in each of 32 age, race, and sex strata. Controls were selected
from the general population of Contra Costa County by random digit dialing.
At the end of the matching and data editing processes 19 cases and 37
controls were deleted leaving 249 cases and 3"73 controls for analysis.
The measure of the respondent's exposure to air pollution was expressed as
an estimated cumulative dose for each pollutant, based on the residential
history in the county.
The respondents' smoking experience was characterized by several
parameters; total smoking duration, total pack years and average packs
smoked per day.
The occupational exposure analysis was based on the coding of each work
experience using occupation and industry titles in the Census' 1980
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Alphabetical Index of Industries and Occupations. Each blue collar job
experience was assigned to one of four broad industry categories:
construction, petrochemical, metal, and other industries.
The duration of time worked in an industrial category was calculated and
accumulated for each respondent.
An asbestos exposure variable was created from various occupational
categories. All shipyard occupations plus all other jobs for which
asbestos exposures were reported were combined to form a total duration of
asbestos exposure per respondent.
Each respondent was assigned a water source based on the water source for
each census tract of residency at the tine of interview or, for cases,
diagnosis.
Certain census tracts in Contra Costa County contain known dumps of toxic
or chemical waste. Each respondent was coded to indicate whether or not
their census tract of residence contained a dump site.
To evaluate possible response variation among controls, the number of
controls expected from each census tract was computed and compared to the
number actually obtained. One area of the county was overrepresented and
a separate small area of the county was underrepresented so that these
responses were appropriately weighted in the analysis.
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The amount of alcohol consumed per week was determined by history and
formed an estimate of alcohol consumption. A dietary questionnaire
provided estimates of weekly consumption of certain dietary items.
Vithin a particular race, sex and 5-year age group, controls were matched
to cases by age using a variable matching ratio. Thus a case may have one
or more matched controls.
Analysis of the data was carried out using multiple logistics regression
procedures.
CONCLUSIONS
Incidence Analysis
The incidence analysis established that when the county was divided into
two parts, the Industrial portion of the county had a 40£ excess of lung
cancer as compared to the Bon-industrial portion in the 1975-79 time
period.
Air Pollution Monitoring
The Pb map was consistent with the fact that the largest source of Pb in
the area is the automobile and the map conformed approximately to the
paths of freeways. Comparison of the BSD and Pb maps suggests the
contribution of the automobile to the BSD levels may be significant. The
SO distribution differs from the Pb by conforming to the industrial
4
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belt. This is consistent irith the fact that SO-, the precursor of SO.,
is emitted by stationary sources, primarily chemical industries,
refineries and power plants, all located along the industrial- belt. The
patterns of the five PAH are similiar to one another and to lead.
The correlation coefficients between pollutants for the 15 monitoring
stations show very similar relationships to those based on the 113 census
tracts which provided validation for their use in subsequent correlation
analyses.
Correlation Analysis
A correlation analysis of 1970-79 lung cancer rates by census tract and
various air pollution constituents showed only one statistically
significant relationship. That relationship was between ambient air SO^
and lung cancer in males, but not in females. However, when controlled
for the percent of the population categorized as blue collar workers the
relationship was eliminated.
Case-control Study
Using multiple logistics regression analysis, all air pollution
constituents were individually reviewed for their relationship with lung
cancer. Hone of the measured air pollutants showed a statistically
significant relationship. However, because SO^ had shown a relationship
in correlation analysis, it was included in the study as discussed below.
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Because of the relevance of smoking to lung cancer, two statistically
significant sacking variables for Bales (p<.0l), average packs smoked per
day and total sacking duration, were analysed in conjunction with any
other single variable. In this series of analyses only one additional
variable emerged as a statistically significant factor in reducing the
risk of lung cancer, but only for vales. This was an Indirect measure of
dietary intake of vitamin A: the consumption of green vegetables
(p<0.0l). A similar but not statistically significant effect was found
for females (P<0.16).
Although no other variables suggested a significant effect on the risk of
lung cancer, further analyses were done adding more variables in different
combinations, to identify possibly significant relationships obscured in
simpler models. In more complex analytical models the effect of SO.
dose, TSP dose, and other pollutant doses were analyzed separately
controlling for the effects of smoking, drinking, diet, occupation and
asbestos exposure. Again, no variables for males, other than green
vegetables and the smoking variables emerged as statistically
significant. For females, one smoking variable, average packs smoked per
day, was significant.
The most complex analysis contained all variables which, in simpler
models, had shown a statistically significant relationship to lung cancer,
or was a known causal factor, or was of particular interest because of
previous analyses. This analysis contained a total of 13 variables and
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represents a "saturated" model. The model included variables related to
smoking, diet, alcohol, asbestos, SO. dose, occupation, and water source.
No additional statistically significant relationships with lung cancer
risk appeared. Other than smoking, and the one dietary factor for Bales,
no other relationships approached statistical significance.
DISCUSSION
This analysis of case-control data suggests that the major contributor to
lung cancer in Contra Costa County is smoking. Further, smoking accounts
for most of the previously identified difference in lung cancer incidence
between the Industrial and Non-Industrial areas.
There was no identified effect on lung cancer risk contributed fror any
measured constituent of air pollution. The one air pollutant (SO^)
significantly correlated with male lung cancer incidence in the indirect
correlational analysis, had a positive but not statistically significant
relationship with lung cancer risk in the case-control analysis only when
SO. level at the current address was used as the measurement. Yhen a
4
measure of total lifetime dose of SO. from Contra Costa County was used,
no elevated risk was apparent.
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One dietary factor had a significant (p<0.0l) protective effect for males
and a similar but not statistically significant (p<0.l6) effect for
females. This factor, weekly servings of green vegetables, is a crude
measure for several dietary constltituents believed to reduce the risk of
cancer of several types. Both vitamin A and cruciferous vegetables would
be included in this dietary measure. The dietary measure, weekly servings
of yellow vegetables, did not discriminate between cases and controls.
•one of the occupational categories had any significant relationship to
lung cancer risk in males. The occupational categories are very broad and
undoubtedly contain specific occupations that are of higher and lower
risk. The occupational analysis therefore likely explains less lung
cancer than potentially it could. This supposition is supported by the
fact that a higher proportion of lung cancer among females is explained in
the analytical models than among males. Hales would be expected to
have a higher proportion of their numbers in occupations with carcinogenic
hasards. A more detailed analysis of the effect of various occupations on
lung cancer risk is planned.
The effect of asbestos exposure, as measured, did not bear a statistically
significant relationship to lung cancer in this analysis. In any
subsequent analysis a more quantitative measure of asbestos exposure would
be desirable.
There was no apparent effect of source of drinking water or proximity to
known toxic waste dumps on the risk of lung cancer.
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Theae data confirm the known causal relationship between smoking and lung
cancer. They provide some reassurence that constituents of particulate
air pollution do not contribute Beasurably to the risk of lung cancer.
This is consistent with the findings of several other studies. These data
provide supportive evidence for the protective effect of dietary factors
on cancer risk, a finding consistent with other epidemiologic and
laboratory studies. The need for a »ore detailed analysis of occupation
and lung cancer risk is apparent.
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AIR EMISSIONS FROM A FORMER DISPOSAL SITE
Kathleen Shimmin
Chief, Field Operations Branch
U.S. Environmental Protection Agency
San Francisco, CA
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Air Emissions From a Former Disposal Site
and the Process of Solving a Hazardous Waste Problem
The McColl site is located in Fullerton, Orange County,
California, adjacent to a residential area which grew up around
what was originally vacant land. In the 1940's, acid refinery
sludge, from the wartime production of high octane aviation fuel,
was deposited in sumps in the ground. Later, from 1951 to 1964,
drilling mud was placed over the sludge to cover the sumps. The
public perception of problems at the site intensified as housing
development increased in the vicinity. Table One, Chronology of
McColl Site, chronicles the history of the site development and
subsequent measures to remedy problems.
Because of the complex and inter-related nature of the issues
which led to identification of McColl as a significant hazardous
waste site in California, a group was formed representing all
pertinent governmental agencies, land owners, and potentially
responsible industries. This group formalized its existence
through memoranda of understanding and identified the McColl
solution in three phases: Phase I, Characterization of the Site;
Phase II, Selection of Remedial Alternatives; Phase III, Site
Cleanup. Voluntary funding for Phase I, in excess of $1 million
was provided by industry and the State of California. Phase II
was funded by the State. Funding for Phase III is being negotiated.
At each step, the coalition of entities tried to anticipate
problems and make orderly plans for timely solutions. Public
review of progress was a key element to the process.
As a result of the site characterization studies, which
focused on air quality, odors, water quality, soil and waste
description, and identification of health symptoms, it was
determined that odor, sulfur dioxide, and benzene were the
emissions of concern (Table Two: Air/Odor Results, Undisturbed
Site). These three factors had to be controlled in any site
remedy. The remedial alternative selected by the-California
Department of Health Services - excavation of the waste - was
first pilot tested to determine that these factors could be
controlled to a level satisfactory for the protection of public
health (Table Three: Findings during Pilot Excavation).
As the final remedy is approached at this site, there are
inescapable conclusions which may be drawn from the process:
1) technical problems in a vacuum usually may be solved without
incident: it is rare, however, that such a situation exists with
a significant hazardous waste site - the public has expectations
of success, wants to scrutinize the process and may have an
inherent distrust of motivations for government and industry;
2) the key is to lay out an orderly process of problem assessment
and to make practical estimates of schedules and costs. All of
this must be done with public involvement at each stage and
education of everyone so that options are understood and reasonable
choices undertaken.
Prepared by: Kathleen G. Shimmin, Chief, Field Operations Branch
Toxics & Waste Management Division, EPA Region 9
October, 1983
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1942-46
1951-64
1960
1968
1970's
1980
1980
Nov. 1980
Dec. 1980
1981
Jan. -Feb. 1982
Feb. 1982
Mar. 1982
Apr. -Aug. 1982
Sept. 1982
Apr. 1983
Summer 1983
Fall 1983
Refinery Acid Sludge Disposal
4
Drilling mud cover placed
Golf course built
Residential development to east of site
Ownership changes
Residential development east, south, north
Government conducts abbreviated study of site
Public hearing
EPA sends information request to potentially
responsible parties
Negotiations — > MOA (Phase I)
Site characterization
Technical Study plans developed
Process defined and initiated
$1 million committed and contractor selected
Public review of plans
CA Hazardous Site List published. McColl is #1
Technical Studies conducted
(Site characterization)
Phase II MOA. Evaluation of remedial alternatives
Alternative selected
Pilot excavation conducted
Early preparations commence
Environmental assessment report completed
Cleanup to commence (Phase III)
Table One:
Chronology of McColl Site
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Findings; Odor
Components include: aroraatics, tetrachloroethane, phenols,
ethylbenzenef alkenes, cyclic compounds,
tetrahydrathiophene, carbon disulfide
Identifiable pattern for "McColl Odor"
Findings; Air
Sulfur Dioxide (100 Samples)
Background, ambient: 0.012 + 0.022 ppm (v)
Site concentrations: 96% of samples less than two
times background. Average
concentration is 0.011 ppra (v)
Total Hydrocarbon (100 Samples)
Background: 2.0 _+ 0.7 ppm (v)
Site: 100% of samples less than twice background
Table Two: Air/Odor Results. Undisturbed Site. McColl
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Findings, Pilot Excavation
- Odor can be controlled
Baffles, shields, foams, covering used
- Backup system for contingency
Tent enclosure
- Estimated Magnitude
Maximum; 200,000 cubic yards material
(approximately 8000 truckloads)
Table Three: Findings, during Pilot Excavation
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EMISSIONS FROM THE ASARCO COPPER SMELTER IN TACOMA, WASHINGTON
Michael Johnston
Chief, Air Operations Section
U.S. Environmental Protection Agency
Seattle, WA
Dana Davoli
Environmental Scientist
U.S. Environmental Protection Agency
Seattle, WA
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Arsenlc Emissions from the ASARCO Swelter
Tacoma, Washington
Presented by
Michael M. Johnston
Dana Davoli
US Environmental Protection Agency
Region 9
A1r Toxics Conference
September 13-14, 1983
San Francisco, California
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Arsenic Emissions from the ASARCO Smelter in
lacoma, Washington1
On July 11, 1983, the US Environmental Protection Agency (US EPA) proposed an
arsenic NESHAP (National Emission Standard for Hazardous Air Pollutants) under
Section 112 of the Clean Air Act. This NESHAP was proposed for three
industrial categories, copper smelters processing high-arsenic feed ore,
copper smelters processing low-arsenic feed ore, and glass manufacturing
plants. EPA's approach in developing this NESHAP was to require at a minimum
best available technology (BAT) for control of arsenic emissions at source
categories estimated to cause a significant public health risk. More
stringent controls could he reouired if necessary to prevent unreasonable
health risks remaining after BAT (taking costs and technical feasibility into
account).
The only facility in the first industrial category (high-arsenic copper
smelters) is the ASARCO smelter in Tacoma, Washington. It was built in 1890
and operated as a lead smelter until ASARCO nought it in 1905 and converted it
to a copper smelter. This copper smelter processes copper ores (many of which
are from foreign sources) with an average arsenic content of 4% compared to
the other copper smelters in the US which use feed ores with less than Q.6%
arsenic.
EPA has estimated that current emissions of arsenic from this facility are
about 311 tons per year - 165 tons per year from stack emissions and the rest
from fugitive sources.* Proposed BAT, which is hooding over one of the
processes at the plant to capture fugitive emissions, is projected to reduce
arsenic emissions from 311 to 189 tons per year.
Several epidemiological studies done on workers, including those at the ASARCO
facility, indicate that exposure to airborne arsenic causes respiratory
cancer. Because it is a carcinogen, EPA has presumed that arsenic is a
no-threshold pollutant and that effects may occur at any level of exposure.
The risk assessment for residents living near the smelter was extrapolated
from the cancer risks seen in the workplace at higher levels of arsenic
exposure, using a linear model. Estimates of exposure in the population
around the smelter were developed from population data and the projected
ambient air concentrations calculated from dispersion modeling. It was
estimated that in a population of 368,000 people living near the smelter the
excess lung cancer cases expected to result from ASARCO emissions ranged from
1.1. to 17.4 per year before BAT is installed to 0.21 to 3.4 following BAT.
Lifetime risks for the highest calculated level of exposure (30 ug/m3) was
9/100 before controls and 2/100 after BAT. Because of the assumptions made
(e.g., linear extrapolation model), these estimates are thought to be
conservative and indicative of upper bound life-time cancer risks. There is
also much uncertainty in these numbers because of the difficulty in obtaining
fugitive source emission data and because many assumptions must be made in
developing the risk assessments.
*These estimates will likely be lowered based upon additional testing done
at the facility during September and October.
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Much attention has been focused upon the arsenic NESHAP for the Tacoma
facility because the estimated residual health risks remaining after BAT are
high relative to those estimated for other sources regulated by NESHAPs.
Additionally, William Ruckelshaus, the Administrator of EPA, has decided to
involve the public more in the risk management decisions made by EPA. The
arsenic NESHAP is the first such regulation targeted for enhanced public
involvement, with EPA's efforts directed thus far on the ASARCO facility. To
Involve the public, EPA has put much effort into press releases and other
published material, attempting to explain technical information and the
decision-making process in terms the public can understand. Three public
workshops were conducted to present the data and answer the public's questions
and numerous presentations were made before interested groups. Although it
has been reported in the press that EPA has asked the citizens living around
the smelter to "vote on the issue of health versus jobs", this 1s not the
case. This decision will be made by the Administrator of EPA alone. The
purpose of the workshops and other public programs 1s to provide as much
information to the public as possible so that their comments will be made with
the full knowledge of the technical and other Issues upon which the regulatory
decision will be made.
The proposed arsenic NESHAP deals with controls of current emissions of
arsenic from the ASARCO smelter. However, potential problems also exist in
the community surrounding the smelter as a result of historic emissions of
arsenic. Deposition of arsenic has resulted in contamination of soils,
household dusts, and vegetables, with the highest levels occurring closest to
the smelter. For example, recent sampling of surface soil close to the
facility has shown soil arsenic levels of several thousand parts per million
(ppm) while garden soil (which 1s tilled and often mixed with non-soil
nutrients) is at levels of several hundred ppm. The most recent analyses have
shown that the average arsenic content of vegetables from these gardens is
about 24 ppm, while maximum values of over 400 ppm have been found. Household
dust has been shown to contain levels of arsenic as high as 4641 ppm.
Analyses of urine samples from children living near the smelter also show that
arsenic levels are significantly above normal. Average urinary arsenic levels
have ranged from 20-300 ug/1 (micrograms per liter) with maximum levels up to
890 ug/1. (Background levels for unexposed populations are usually less than
25 ug/1).
The flow diagram shown In Figure 1 Illustrates the pathways and routes of
exposure that may be responsible for the Increased arsenic body burden 1n
these children. In addition to Inhalation of recently emitted arsenic,
Inhalation of resuspended soils and dusts are also possible. Contaminated
soils and dusts are of particular concern for young children because they
Ingest small amounts 1n normal hand-to-mouth activity. It has been estimated
that children with pica, an abnormal craving for dirt, can ingest several
grams of soil a day. Studies around lead smelters have confirmed that this
can be a significant exposure route for children. Finally, Ingestlon of
contaminated vegetables and water are potential sources of arsenic, although
studies thus far do not show problems with drinking water supplies 1n the
smelter area.
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Hhlle current arsenic emissions are to be controlled through the arsenic
NESHAPs, the potential problems resulting from past emissions are being dealt
with through EPA's Superfund program. The Washington Department of Ecology
(HDOE) under a cooperative agreement with EPA, is the lead agency in these
Superfund efforts and is working with EPA and the state and local health
agencies to design the investigations discussed below.
The high urinary arsenic levels of children living near the smelter show that
they are exposed to arsenic, but the pathways leading to this exposure are not
clear. These pathways must be determined before decisions can be made about
implementing remedial actions which will result in lowered urinary arsenic
levels. For example if current emissions are a significant source, then
controls on these emissions at the plant are appropriate. If resuspended soil
is an important exposure source, it may be necessary to remove soil or cover
it with sod or paving. The Superfund Investigations are being designed to
provide data on sources of exposure which will in turn be used to plan
remedial measures.
Although several samplings of soils, vegetables and urine have been made in
the past, much of this data may not reflect the current situation and was not
collected in a way that answers the questions on exposure pathways. Therefore
several types of additional studies have been proposed and are in the design
stage, Including an Exposure Assessment Study. (See Table 1 for examples).
The Exposure Assessment Study will be patterned after those already conducted
around several lead sources in the US. It involves taking measurements of
contaminants In various media (e.g., soil, dust) concurrently with
measurements of body burden (urinary arsenic in this case). Multivarient
statistical techniques will then be used to attempt to correlate excess
urinary arsenic levels with contamination levels in the different media.
Studies such as these can include measurements of contaminants in soils, house
dusts, and vegetation. To obtain an estimate of the amount of contamination
on children's hands, hand loading studies are done. This involves dipping
children's hands Into a dilute acidic solution (about the pH of vinegar) and
analyzing the solution. The Center for Disease Control is now working with
WDOE, EPA and the local health agencies to design and implement this Exposure
Assessment for the ASARCO area.
The State health department 1s also assessing the need for further
epidemiological studies. Two lung cancer mortality studies done In the Tacoroa
area did not demonstrate an increased risk for persons living near the
smelter, however this effect Is probably too small to study
epldemiologically. Blood analyses and hearing tests on children attending the
school near the smelter also appear normal.
As can be seen from this discussion, emissions of arsenic from the ASARCO
smelter have resulted 1n potential problems due to air pollution as well as to
contamination of other environmental media. This situation stresses the need
for pollution control agencies to take a more Integrated approach In dealing
with toxicants.
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Hynre I
Conci-ptual Framework for Arsenic
Exposure
Sources
Ambient Environment
Human Exposures
1
00
o>
lAComa i>mel tcr
Current Air Emissions
short term peaks (upsets)
average (annual)
Historic Atr Lmisslons Source
Other Anthio|iOijcnlc Sources Contrihutlnns
Natural UrtLkijroui'd (direct t indirect)
Indices
As
urine
hair , ,,. Slgnl f leaner /Heal th Riskc
* blood
bone
Air ./Couiplex ^v
'Jo 11 r Environuw>nt4l )
Vegi'tation Recycling^/
Siirliico W.itor L"xpo«;nre
*" Ground Water Pathways
etc.
Health Effects
Outcomes
Mortal ity
> Morbidity
IJisk Assessments
Lpideintological Studies
Inhalation
Ingestton
foods
drinking water
pica
Ueruidl Ahsorpt tin-
Undy
llurden
Measures
organs
tP/yiiif/rVotein Levels
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Table 1
Examples of Planned Studies
Exposure Assessment Study - May Include measurements of contaminants in
sous, vegetaDies, Household dusts and air concurrent with measurements of
body burden levels (such as urinary and hand loadings). This 1s done for a
sampling of residents 1n the affected areas. Mult1var1ate statistical
analysis 1s performed on the resulting data to delineate and quantify sources
of exposure and to predict the effectiveness of different remedial actions
(Already completed or 1n progress at smelters 1n Texas, Idaho and Montana).
Deposition Monitoring - Use of acid precipitation equipment to determine the
level of current deposition of arsenic occurring near the smelter. Related to
past vs. present smelter operation Issues as well as potential remedial
actions Involving soil clean up.
Soils - Isopleth Study - Soil sampling of areas near the smelter to determine
the geographic extent of the most contaminated areas and the areas that may
require remedial action.
Drink1ng Water Survey - Sampling and analyses of well water cisterns and
other drinking water supplies 1n areas of high arsenic in soil or air.
Soil Leaching Tests - Leaching tests on soils with high contamination levels
to determine potential for environmental movement, especially to groundwater.
1
Source Apportionment Model - Uses chemical mass balance approaches to
determine the contribution of specific emission points within a facility to
artnent pollutant levels as well as the contribution of resuspended
contaminated soils and dusts. Distinguishes between air contamination due to
current vs. historical deposition.
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TOXIC AIR POLLUTION IN HENDERSON, NEVADA
Michael Naylor
Director, Air Quality
Clark County Health District
Las Vegas, NV
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TOXIC AIR POLLUTION IN HENDERSON, NEVADA
The first part of the presentation consisted of aerial photo-
graphs of the Southeast Valley cloud, as observed by a helicop-
ter traversing from downtown Las Vegas to Henderson. The slides
displayed the low vertical depth of the cloud and its proximity
to the Industrial Complex.
I discussed some of the examples of complaints we have received
from citizens, which include: odor, eye burning, visibility
and breathing difficulty, and frustration with continuing air
pollution.
The toxic air pollutants in the Southeast Valley consist of:
chlorine
hydrogen chloride
ammonia
Southeast Valley cloud
peroxyacetylnitrate (PAN)
peroxybenzoylnitrate (PB N)
formaldehyde z
The criteria air pollutants of concern are:
ozone, and
total suspended particulate
Chlorine is important because: it is a precursor for ozone,
eye irritants hydrochloric acid and nitric acid, and it contri-
butes to odor occurrences.
Ozone levels have exceeded the standard, and we have determined
that chlorine emissions cause the unusual winter-time morning
ozone excursions. The key component in the ozone generation
is the photolysis of chlorine molecules (emitted from the In-
dustrial Complex) into radical chlorine atoms. The radical
chlorine atoms attack hydrocarbon molecules and remove hydrogen
atoms, yielding a reactive hydrocarbon radical and hydrogen
chloride. These reactive hydrocarbons then initiate the con-
ventional ozone generation cycle which involves the oxidation
of NO to NO_. Similar reactions lead to the formation of eye
irritants PATJ and PB N.
Z
Some of the principal aerosol components in the Southeast
Valley cloud include: ammonium, nitrate, chloride, organic
carbon, and elemental carbon. We have observed that ammonium
and Bscat (light scattering measured by a nephelometer) are
correlated with an r of approximately 0.9.
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Visual ranges asociated with the cloud occurrence vary from
two to twenty-four miles. We believe the primary components
responsible for visibility impairment, in order of importance,
are: ammonium nitrate, ammonium chloride, elemental carbon,
and ammonium sulfate. The ammonium nitrate results from the
combination of ammonia and nitric acid. The nitric acid re-
sults from oxidation of nitrous oxide initiated by chlorine
photolysis. One of the major research problems remaining for
the cloud is to develop a model which relates precursor emis-
sions to cloud intensity.
Chlorine emissions from the Industrial Complex have been drop-
ping over the last eight years, from roughly 400 Ibs/hr to
approximately 25 Ibs/hr. Ammonia emissions from documented
sources have declined from about 15 Ibs/hr to about 4 Ibs/hr.
However, there appears to be an unknown source of ammonia emis-
sions (near the Industrial Complex) which seems to emit approx-
imately 30 Ibs/hr. As a result of these emission reductions,
we have seen air quality improvements since 1980 for ozone,
eye irritation, and odor complaints. However, there has been
no improvement for the cloud occurrence and intensity.
Our work plan for 1983 and 1984 is to concentrate on several
actions which could result in eventual further abatement of
the air pollution problems, with particular emphasis on im-
provements in the cloud. These will include: smog chamber
experiments; short-term low production runs at the remaining
source of chlorine emissions; continuous in-plant monitoring
for fugitive ammonia emissions; adopting a regulation requiring
LAER for chlorine-emitting sources; and continuing ambient
monitoring for aerosol compounds and gaseous pollutants.
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EMISSIONS FROM THE SEMICONDUCTOR INDUSTRY
Milton Feldstein
Air Pollution Control Officer
Bay Area Air Quality Management District
San Francisco, CA
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BAY AREA AIR QUALITY MANAGEMENT DISTRICT
Emissions From The Semiconductor Industry
Milton Feldstein
Air Pollution Control Officer
The semiconductor industry emits precursor organic
emissions which contribute to ozone standard exceedances. Be-
cause of chemicals used by this industry, exotic gases and chlor-
inated solvents which are potentially of concern as air toxics
are also emitted. Chlorinated solvents are used extensively in
cleaning processes during semiconductor manufacture. The exotic
gases such as phosphine, arsine, silane and diborane are used
as "dopants" in the semiconductor manufacturing process. The
District adopted Regulation 8, Rule 30 to control the precursor
organic emissions from the semiconductor industry. This rule
affects approximately 200 companies in the Bay Area and will accom-
plish a 3.5 ton/day reduction in precursor organic emissions by
requiring 90% control from photoresist processes and controls for
solvent sinks. The rule includes a provision to allow for an
alternative compliance plan (bubble). This reduction of 3.5 tons/day
is part of the 1982 Plan's overall reduction of 85 tons/day. All
large sources of precurors have already been controlled. We are
now controlling the smaller sources and these controls are gen-
erally more expensive in terms of cost per ton of emission reduced.
With respect to toxic emissions, a determination needs to be
made as to what substances need to be controlled. This identifica-
tion needs to define threshold levels where possible. Federal and
state agencies have the resources to do this. Once a list of air
toxic contaminants is defined, then local air pollution control
districts can proceed with the development of rules to control
emissions of these substances. The technology to control emissions,
especially the organic emissions, is available in the form of in-
cineration or carbon absorption. This is a new area for air pol-
lution regulatory agencies. The quantities of toxic air contam-
inants emitted is very small when compared with emission of criteria
pollutants.
The Bay Area Air Quality Management District is currently con-
ducting source tests to speciate the organic emissions from semi-
conductor sources and to quantify the emissions of arsine, phosgene,
and HC1. The second phase of this program is to extend this source
testing to other source categories as well as other compounds. This
data will serve as the beginning of an emission inventory data base
for air toxic contaminants.
Control of sources of these emissions will occur after the
regulation development process is completed. This process for air
toxic contaminants begins with the identification of the toxic
contaminant at the state/federal level (ARE, DOHS, EPA). Once
this occurs, then local districts can begin the development of rules
to control the emission of the contaminant. This involves a
participatory process which includes the affected sources as well
as the public.
This is a logical way to proceed. We need to begin on a
compound by compound basis to control these contaminants.
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SEMICONDUCTOR MANUFACTURING
Chlorinated solvents are primarily used in semiconductor
manufacture as surface cleaners and strippers; they are also
used as diluents for surface coatings.
Hydrocarbon solvents (both chlorinated and un-) are used
to clean and prepare wafer surfaces before virtually every step
in the fabrication process. Strict quality control requirements
restrict the reuse of cleaning solvents, resulting in high volumes
of solvent usage. Used solvents are reclaimed and sold to other
industries; most semiconductor firms will use nothing but virgin
solvents.
Cellosolves are non-chlorinated hazardous solvents used as
diluents for positive photoresist. Low volatility and low pre-
cursor organic emission rates make positive photoresist preferred
over negative photoresist, at least from an ozone production
standpoint.
Various chlorinated solvents are used as diluents for nega-
tive photoresist.
An average company uses about 30,000 gallons/yr of chlorinated
(non-precursor) solvents; it emits about 3 tons/yr of atmospheric
emissions.
Process Description
The manufacture of electronic devices from raw materials in-
volves many steps (Figure 1). Toxic hydrocarbon solvents are used
during some of these operations to act as a carrier or diluent for
coatings and to strip material from the surface of the circuits.
Most of the solvents used are collected and reclaimed or disposed of,
A fraction evaporates and is exhausted to the atmosphei-e.
Wafer Production
CRYSTAL GROWTH: Molten silicon is grown into cylindrical
ingots; a tiny crystal" is used as a "seed" to allign the crystal
lattice, making the entire ingot one single crystal.
WAFER MANUFACTURE: The ingot is sliced with a diamond saw
into round, ultr-thin wafers and polished to a perfect mirror
finish.
Integrated Circuit Fabrication
OXIDATION: The wafer is exposed to pure oxygen at an
elevated (1200 C) temperature. A layer of silicon dioxide
grows on all sides of the wafer.
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PHOTORESIST APPLICATION (Negative Photoresist): The wafer
is coated_with photoresist, an emulsion that hardens when exposed
to ultraviolet light. This process frequently employes one or more
cleaning steps, using a hydrocarbon solvent to remove contaminants
and prepare the surface. The photoresist emulsion may contain
solvents as well.
PHOTORESIST EXPOSURE: A glass mask is alligned with the
wafer and ultraviolet light is projected through the mask. The
shaded areas on the mask prevent light from reaching portions of
the wafer; photoresist in these areas stay soft. Exposed photoresist
hardens.
PHOTORESIST DEVELOPING: The wafer is washed in a solvent
that removes the soft photoresist but leaves the hardened resist on
the wafer. The oxide layer on the wafer surface is exposed wher-
ever soft resist is removed.
ETCHING: Exposed oxide surface is removed using either an
acid bath or a plasma etcher, revealing the original silicon
surface; the oxide now forms a stencil of the mask pattern. The
remaining photoresist is removed.
DIFFUSION: The wafer is placed in a diffusion furnace and
exposed to dopant gases (phosphorous, arsenic, antimony, etc.) at
high temperatures. The dopant atoms enter the exposed silicon,
but are blocked by the oxide stencil.
EPITAXIAL GROWTH: The wafer is exposed to silane gas at high
temperatures; a layer of silicon is grown over the entire wafer
surface.
The steps will be repeated many times during integrated cir-
cuit fabrications; toxic organic solvents are used as surface clean-
ers, photoresist strippers and photoresist carriers throughout the
operation.
BAAQMD 9/1U/83
MF:gp
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FIGURE 1
SEMICONDUCTOR MANUFACTURING
WAFER PRODUCTION
Molten v
Silicon-*
Crystal
Growth
Silicon
-> Ingots
INTEGRATED CIRCUIT FABRICATION
SOLVENTS SOLVENTS
SOLVENTS
t
Wafer
Manufacture
, Silicon
•> Wafers
POPAWTS
Wafer__
*
*
t .
*
Oxidation
— >
, these steps are.'
Photoresist
->
Etching
-*
— ^-
'repeated
Diffusion
\
many times
Circuit
Separated
M
O
71
.Integrated
^Circuit
Oxidation
Furnace
Photoresist
Spinner
Soft bake
Exposure
Hardbake
Developer
Etching
Bath
Plasma
Etcher
Diffusion
Furnace
Epitaxial
Reactors
Diamond
Scribe
Laser Scribe
BAAQMD 9/14/83
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VOLATILE ORGANIC EMISSIONS FROM LANDFILLS
Ed Camarena
Director, Enforcement Division
South Coast Air Qaulity Management District
El Monte, CA
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South Coast
AIR QUALITY MANAGEMENT DISTRICT
9150 E. FLAIR DRIVE. EL MONTE. CA 91731
CONTROL OF VOLATILE ORGANIC
EMISSIONS FROM LANDFILLS
PRESENTED SEPTEMBER 14, 1983
AT THE
AIR TOXICS CONFERENCE
SPONSORED BY
EPA, REGION IX
IN
SAN FRANCISCO, CALIFORNIA
BY
EDWARD CAMARENA
DIRECTOR OF ENFORCEMENT
SOUTH COAST AIR QUALITY MANAGEMENT DISTRICT
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CONTROL OF VOLATILE ORGANIC EMISSIONS FROM LANDFILLS
PRESENTED SEPTEMBER 14, 1983
AT THE
AIR TOXICS CONFERENCE
SPONSORED BY EPA. REGION IX. IN
SAN FRANCISCO, CALIFORNIA
BY
EDWARD CAMARENA, DIRECTOR OF ENFORCEMENT
SOUTH COAST AIR QUALITY MANAGEMENT DISTRICT
INTRODUCTION
Traditionally air emissions have been regulated from the perspective of
their contribution to the overall air pollution problem. The control efforts
have been primarily focused on at those air contaminants for which either
state or federal ambient air quality standards have been adopted. In recent
years however, attention has been increasingly focused on toxic or hazardous
air contaminants which may not be a region wide problem but which have a
potential for creating a localized problem.
Included In the mission of the South Coast Air Quality Management
District Is the abatement of emissions of toxic and hazardous air contaminants
in order to protect public health and welfare. This is done through:
A. Enforcement of applicable sections of the California Health and
Safety Code and District rules and regulations;
B. Enforcement of National Emission Standards for-Hazardous Air
Pollutants (NESHAPS). These have been incorporated into District
rules,
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C. Enforcement of the state and District air pollution emergency plan,
and
D. Assistance rendered to other agencies in the event of a spill of
toxic or hazardous materials which may become airborne.
This paper Mill review some of the South Coast Air Quality Management
District's efforts to control toxic and hazardous air contaminates from
landfills.
TOXIC DUMPS
The toxic/hazardous nature of certain industrial wastes and their impact
on the environment is only in recent years being recognized. Wastes from
refineries, chemical plants, etc., have been deposited in convenient "rural"
sites in the past without significant controls or consideration for their
ultimate fate. As a result of our growing population, these formerly rural
sites are now, in many instances, immediately adjacent to residential areas
and have caused a myriad of problems.
•»
Wastes at these sites may pose water and air pollution problems depending
on the circumstances. Although there are a number of potential mitigation
measures the most practical and effective seem to be;
A. Encapsulation, or
B. Excavation followed by proper disposal at an approved site.
Recent South Coast Air Quality Management District experience indicates
that excavation Is the method preferred by most regulatory agencies and the
affected public. This method however, has been shown to cause some very
significant though temporary air pollution problems including;
A. Temporary Illness (nausea, headache) of hundreds of people and
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B. Odor complaints as far as five miles downwind.
Refinery wastes have been most often Identified as the problem for sites
in the South Coast Air Quality Management District and the contaminants posing
the greatest short term hazard from these sites have been identified as sulfur
dioxide and tetrahydrothiophenes.
The South Coast Air Quality Management District has recently adopted Rule
1150, Excavation of Landfills which requires that prior to any landfill
excavation, that an air pollution control plan be submitted and approved by
the District. This provides the mechanism to require proper site content
characterization and development and Implementation of air emission mitigation
uieasures prior to the start of a project. Depending on the type of materials
to be excavated the plan may provide:
A. Emission mitigation measures such as work face size restrictions,
truck covering requirements, use of foams to blanket workface, etc.,
B. Offslte monitoring,
C. Work stoppage criteria based on monitoring data and odor level,
D. Public notification and complaint hotlines,
E. Evacuation contingency plans.
The planning process for excavation of a site Is a multi-entity activity
usually involving the South Coast Air Quality Management District, state and
county departments of health services, the Regional Water Quality Control
Board, the State Solid Waste Management Board, other city/county agencies as
well as the property owners, other responsible parties and the affected
public. In an extreme case as the McColl site 1n Fullerton, the site
characterization and mitigation planning process may take two or more years
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and Involve over a million dollars in expenditures before excavation,
encapsulation or other mitigation work actually begins.
During an excavation, South Coast A1r Quality Management District
enforcement personnel are present on-site at all times and are responsible for
assuring all excavation plan requirements are carried out and may require work
stoppage when predetermined odor levels or air contaminant concentrations are
reached. In addition, SCAQMD technicians, chemists and meteorologists provide
a variety of services such as quality assurance checks on monitoring (usually
done by contractor), odor dispersion estimates and stability and wind pattern
predictions (to assist 1n daily activity planning). Depending on the nature
and size of the site, a properly controlled excavation may take from a few
days to several months of actual work.
ACTIVE LANDFILLS
Active landfills, whether they be Class I (can accept toxic/hazardous
wastes) or Class II (cannot accept toxic/hazardous wastes), can be significant
air pollution problems if not carefully managed. Below are two case histories
describing the problems encountered at active landfills and the actions taken
by the SCAQMD.
BKK LANDFILL (odors and vinyl chloride)
In October I960, odor complaints from residents in the vicinity of the
BKK Landfill (Class I) In West Covina prompted the District to issue violation
notices alleging violations of Rule 402 (nuisance) and Section 41700
(nuisance) of the California Health and Safety Code. Odors emanating from the
landfill were determined to originate almost entirely from the anaerobic
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decomposition of wastes within the fill rather than directly from the daily
disposal activities. The District required expansion of an existing gas
collection and incineration system composed of a series of gas wells venting
to a flare. Testing of the composition of the collected landfill gases
revealed concentrations of vinyl chloride ranging up to 2,000 ppm. Although
the collected gases containing high concentrations of vinyl chloride were
efficiently destroyed by the flare, it was known that not all of the landfill
gas was being collected and that emissions from the landfill surfaces was
still a problem.
The South Coast Air Quality Management District immediately began
Monitoring ambient air in the residential areas to determine whether the
remaining uncontrolled emissions could result in an exceedance of the ambient
air quality standard for vinyl chloride. It was found that the vinyl chloride
standard was being exceeded off-site about fourteen days a month and the
maximum 24-hour average concentration was 0.05 ppm (five times the air quality
4
standard).
The District immediately notified the state and local departments of
health services and requested an evaluation of the data. A senior official of
the Epidemiological Studies Section of the California Department of Health
Services stated in a July 1981 letter to the District commenting on the vinyl
chloride measurements taken 1n May and June 1981 near the BKK landfill: "We
believe that these levels of vinyl chloride pose no Imminent health hazard to
the surrounding population, but they are of sufficient concern to require that
effective mitigation measures be taken at the earliest possible time."
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An interagency task force Mas created to develop a program to update
emission control efforts in the West Covina landfill area. The task force,
which included the District, the city of West Covina, Los Angeles County
Health Department, State Solid Waste Management Board, State Department of
Health Services and the Regional Water Quality Control Board began meeting
regularly in May 1981 to develop ways to further reduce odors and emissions of
volatile organic compounds, including vinyl chloride, at the landfill site.
BKK Corporation also was prohibited by the State Department of Health Services
from accepting industrial wastes containing vinyl chloride.
The task force implemented a program of additional gas well installation
and waste gas incineration designed to reduce the concentration of odorous gas
emitted to the atmosphere. Such incineration also controls vinyl chloride
emissions. Since the implementation of this program in 1981, there have been
fewer odor complaints and vinyl chloride concentrations have been reduced
significantly. Whereas the standard was exceeded about fourteen days per
month in 1981, it is now exceeded about two days per month and the maximum
concentration detected in recent months is one fifth that found in 1981.
During July-October 1982, the District, in cooperation with the State
Department of Health Services and the California Air Resources Board,
conducted an extensive monitoring project to determine the concentration and
health impact of other potentially toxic emissions from the BKK landfill. It
was concluded that certain compounds were present at levels higher than at the
selected control site (Pico Rivera). The State Department of Health Services
concluded that:
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A. Even at the highest observed concentrations, that the substances
measured were present at concentrations well below their threshhold
for toxic, non-carcinogenic action,
B. At the low level of exposure that it 1s not possible to calculate
excess cancer risks. However, worst case estimates of the individual
cancer risks suggests that those living immediately adjacent to the
landfill may have accumulated excess risks to date of 5/100,000,
C. Based on the estimated exposed population within a one-mile radius,
no additional cases of cancer are expected from exposure to date and
exposure levels are declining, and
D. The individual cancer risks are at a relatively low level and do not
constitute a public health emergency.
E. Since the stations around the site are not known to be near other
sources of emissions of these compounds (dry cleaning establishments,
plastics products manufacturers, metal finishing industries, etc.),
the data suggest that the BKK site is a source of these compounds.
The elevated levels of the chlorinated compounds in particular
Indicate a need for mitigation measures such as expansion of the
landfill gas gathering system, upgraded maintenance programs, and
changes in handling of wastes containing these compounds.
F. Further action 1s also mandated by the continued, periodic
exceedences of the State's Ambient A1r Quality Standard for vinyl
chloride of 0.01 ppm (10 ppb).
The South Coast A1r Quality Management District has recently filed
m
petition for an Order for Abatement which would:
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A. Require a plan to expand existing gas coll lection and incineration
system to assure no further exceedances of vinyl chloride ambient air
quality standard,
B. Require Implementation of the plan as soon as possible after approval
by Executive Officer and according to a schedule specified by Hearing
Board,
C. Require BKK to contract for monitoring for vinyl chloride, and
D. Require BKK to install monitors within fill to check effectiveness of
gas collection system.
OPERATING INDUSTRIES, INC., LANDFILL
On April 5, 1983, the District Hearing Board issued an Order for
Abatement against Operating Industries, Inc. (Oil), the operator of a class II
landfill located 1n the City of Monterey Park. This abatement order was
stipulated to by Oil and was in response to many problems at the landfill
site, and its vicinity, including odors, migrating gases, and exposed
leachate. The stipulation for the Order for Abatement was developed with the
tooperation and assistance of other agencies to ensure that there would be no
conflict with their requirements.
The abatement order provides a comprehensive program and strict
compliance schedule for odor control, Including an extensive gas collection
and Incineration system, leachate controls, gas monitoring, cover
requirements, and final closure by December 31, 1984.
Subsequent to the Issuance of the abatement order, District tests
detected an Increase in the concentration of vinyl chloride in the landfill
gases above those trace amounts normally found at such sites. The cause of
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the recent Increase is not known at this time. While monitoring had not yet
shown an exceedance of the state ambient air quality standard for vinyl
chloride, calculations by District staff indicated that the emission rates
were expected to result in exceedances under more stable weather conditions,
unless prompt action was taken to minimize concentrations of this toxic
contaminant.
In addition, District inspectors uncovered deficiencies in Oil's system
for screening and prohibiting the illegal disposal of toxic/hazardous wastes
at the site. Such disposal may result in air emissions of toxic/ hazardous
materials.
In order to prevent exceedances of the ambient air quality standard for
vinyl chloride and to assure that no further illegal disposal of
toxic/hazardous occurs, the District filed a petition for modification of the
abatement order which, if approved by the Hearing Board, would:
A. Immediately stop disposal at Oil of all liquid and solid wastes
until ;
1. Oil can screen out and prohibit the disposal of illegal hazardous
loads; and
2. Oil completes and places the gas collection system into full
operation to minimize odors and emissions, including vinyl
chloride;
B. Require Oil to pay the costs of continuously monitoring vinyl
chloride in the residential area; and
C. Require Oil to post a bond to assure completion and continuous future
operation of the gas collection system after final closure.
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Exceedances of the vinyl chloride standard were subsequently detected In
the residential community adjacent to the landfill. The abatement order
hearing is pending at this writing.
Immediately adjacent to the Oil landfill is the Getty" Synthetic Fuels,
Inc. gas recovery facility. This facility draws landfill gas through a series
of wells at Oil, removes carbon dioxide (which is vented to the atmosphere)
and sells the cleaned methane to the Southern California Gas Company. Vinyl
chloride is vented along with the carbon dioxide. To prevent exceedances of
the vinyl chloride air quality standard in the vicinity of the Getty facility,
the District required the immediate relocation of the vent as far away from
any residences as possible as a stop-gap measure. Destruction of the vinyl
chloride through flaring (burning) is being required as the ultimate control.
In addition, Getty's pending permit to operate application was denied due to
the present inability to control vinyl chloride emissions.
The District will continue to inspect the Oil and Getty sites at least
three times per week to assure compliance with the abatement order and will
continue ambient monitoring for vinyl chloride and landfill gas emissions
testing and take appropriate enforcement actions until the problem is
resolved.
CLOSING COMMENTS
Toxic Enforcement 1s a Resource Intensive Activity
In the absence of NESHAPs rules or ambient air quality standards for all
but a few toxic/hazardous materials, the South Coast Air Quality Management
District's approach has been to monitor air quality in the vicinity of
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-],2Ch
suspected sources and to present the data to the county or state departments
of health services for a risk assessment analysis. This procedure is
extremely resource intensive and time consuming and must be done on a case by
case basis.
This enforcement process could be shortened considerably by the adoption
of ambient air quality standards followed by rule adoption where emission
reductions are needed, buch a process would permit the priortizaFfoh of
efforts based on which standards have been adopted. At present, in the
absence of standards local districts are at a loss as to which contaminants
and sources should receive attention first.
Cooperation with Other Agencies
More than with any other area of air pollution enforcement, local
districts must work closely with other state and local agencies where toxic
and hazardous air emissions are concerned. There are some areas of regulatory
overlap. Solutions to one environmental problem, if not carefully
coordinated, may result in creation of another. Through this close work,
local districts and other agencies can find areas of mutual benefit, such as
the sharing of data. Also, when there are air emissions problems involving
toxic/hazardous materials, there are usually violations of other environmental
regulations involved. When these are found, coordinated multi-agency
enforcement action against a source can be very effective in bringing about
prompt compliance and can avoid problems brought about by the source
attempting to play one agency's requirements against another.
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ASBESTOS DECONTAMINATION IN GLOBE, ARIZONA
David Chelgren
Manager, Compliance Section
Arizona Bureau of Air Quality Control
Phoenix, AZ
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ASBESTOS DECONTAMINATION IN GLOBE, ARIZONA
A case study in air toxics response
David 0. Chelgren, Manager for Compliance
in the Arizona Bureau of Air Quality Control
BACKGROUND
Chrysotile asbestos has been an important natural resource of Arizona since the early
1900's. During the first few decades of asbestos mining, the raw fiber was transported
as far as 50 miles to the mills by pack animal. Impurities such as serpentine and
limestone were first removed by hand cobbing in the mine before transport to the mills,
which were located near Globe. There are over eighty registered asbestos claims in
Arizona including two in the Grand Canyon. However, about seventy five of the minesites
are located in Gila County. As many as fourteen asbestos m'lls were operating in and
around Globe, Arizona at one time. The General Service's Administration established a
depot in Globe in 1952 for the purchase and storage of strategic grades of asbestos
fibers. In addition to the locally mined material some additional ore was brought into
Arizona from sources outside of the state including overseas, for milling.
In a number of cases the milling of hand cobbed ore was accomplished at the minesite
but starting in about 1939 several mills were built and operated in Globe. These
included the Arizona Asbestos Company (Town) Mill, the Jaquays Asbestos Company Mill,
and the Metate Asbestos Corporation Mill located at the junction of U.S. 70 and Arizona
77 east of Globe. These mills were operating when the National Emission Standard for
Hazardous Air Pollutants (NESHAPs) relating to asbestos was promulgated in 1973, and
were subject to regulation by the Pinal-Gila Counties Air Pollution Control District (PGCAPCD)
The Town Mill was shut down in 1973 because of violations of the applicable standards.
The Metate Mill was denied an air pollution control operating permit in 1972 but did
obtain a conditional permit for limited operations from the Gila County Air Pollution
Control Hearing Board. An order to cease operation in violation of its Conditional
Permit was issued to Metate by the local air agency in December, 1973. At this point
Metate had already started subdividing the property around the mill as a mobile home
park. The Globe City Council approved the subdivision plan in spite of a written re-
cownendation by the Director of the PGCAPCD to the Mayor that residences should not be
permitted in such close proximity to asbestos mills. A temporary injunction against
Metate was obtained in early 1974 when it was determined that it was operating at night
after a number of residents had moved into the park. A permanent injunction was issued
on April 30, 1974. The Arizona Real Estate Department (ARED) which had also approved
the subdivision negotiated an agreement with Metate in 1976 to resolve numerous con-
plaints by the residents including a provision that the mill would be removed after
forty two lots were sold.
ARIZONA STATE INVOLVEMENT
The Arizona Department of Health Services (ADHS) became aware of the asbestos contamina-
tion during an inspection of the park's waste water treatment plant by a representative
of the Bureau of Water Quality Control in early October, 1979. Exposed tailings and
contaminated equipment were observed at numerous locations in the subdivision and on the
adjacent railroad' right-of-way (ROW). Other former asbestos facilities exhibiting
exposed asbestos containing materials were located and inspected by representatives of
the Bureau of Waste Control including the Town, inactive Jaquays, and Kyle mill sites.
Bulk soil samples exhibited asbestos contamination ranging from five to sixty percent
in most lots of the subdivision, on the ROW, and at the other millsites. Water samples
from Globe, the Salt River and in the Phoenix Water System were determined to contain
from 200,000 to 2,000,000 chrysotile fibers per liter along with much lower levels of
amphiboles. Once the results of the soil sample analyses started corning in it was
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apparent that a potential for high level exposure to airborne asbestos was present and
a meeting was held with representatives of the City of Globe, the Gila County Health
Department, the PGCAPCD and the State Real Estate Commissioner to advise them of the
problem. Additional lot sales were prevented by the withdrawal of the subdivision
approval by ARED. A letter was also sent to each of the residents in the subdivi-
sion advising them of the soil sample results and recomnending precautions to minimize
the potential for exposure to and inhalation of asbestos fibers. Personal monitor air
samples taken during soil sampling, vacuuming inside a mobile home and outside the
trailers were analyzed by the Arizona Industrial Commission usinq the Occupational
Safety and Health Administration (OSHA) approved optical microscopy method and were later
reported to contain between 0.003 and 0.350 fibers per cubic centimeter.
REMEDIAL RESPONSE
By mid-December, 1979 the Director of ADHS asserted jurisdiction of the inactive
millsites which was later modified to include all asbestos facilities subject to
NESHAPs in Gila County. Letters were sent to each of the mill operators orderinq them
to submit plans for decontamination to achieve compliance with NESHAPs within thirty days.
The responsibility for the planning and verification of the decontamination activities
was then assigned to the Bureau of Air Quality Control (BAQC) because NESHAPs were the
only regulations that could be enforced to achieve the resolution of the problem.
The site was also inspected by representatives of the Centers for Disease Control and
the National Institute for Occupational Safety and Health who then recommended immediate
evacuation of the residents as well as restricting public access to the site. This
recommendation was supported in a letter from an Assistant U.S. Surgeon General as well
as by knowledgeable members of the Department staff. These recommendations were passed
on to Governor Babbitt who declared the State of Emergency on January 16, 1980 in order
to free up funds for temporary relocation of residents and contracts for cleanup of
the ROW and the lots and mobile homes in the park by the Governor's Division of Emer-
gency Services. An agreement was reached with Metate relative to its demolition and
decontamination of the mi 11 site. Written instructions were provided to the residents
for the evacuation and they were advised of the plans for evacuation in a meeting on
February 1, 1980. Air monitoring stations were placed in and around the park which were
activated at that time. Residents desiring temporary relocation were evacuated and the
initial decontamination of the affected areas then oroceeded under the continuing sur-
veillance of BAQC in the following steps, starting on February 6, 1980:
1. Metate Mill demolished and buried on site with a minimum cover of two feet of clean
compacted cover.
2. Exposed tailings and stored fibers and ore buried under two feet of clean compacted
cover at Town Mill.
3. Rip rap installed on wash bank and exposed asbestos covered with clean fill at
inactive Jaquays millsite.
4. No action taken at Kyle millsite because the property was in estate probate and the
estate had no funds for cleanup, and low potential for release of airborne fibers
at its location.
5. Contaminated equipment on ROW cleaned and removed, tailings buried and minimum of
two feet of clean compacted fill placed.
6. Lots analysed as positive for soil asbestos were provided with six inches of top-
soil and grass seed where requested by residents. Bulk soil samples after the cover
was placed contained less than one percent asbestos.
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7. Interiors of mobile homes cleaned up by commercial cleaninq company and residents
allowed to return.
8. Metate slab scrubbed, pump well debris removed, and cracks sealed with asphalt
sealant.
9. Wash qunited.
10. Residents were offered delivery of additional topsoil and grass seed.
11. State of Emergency was ended on June 30, 1980. Cost of cleanup to State was
approximately $260,000.
12. Analysis of random soil samples at Metate millsite reported as less than one
percent by U.S. Bureau of Mines.
13. Restriction on lot sales lifted on condition that Metate maintain millsite to
prevent exposure or releases of asbestos fibers from millsite.
FINAL GLOBE HILLSITE DECONTAMINATION
The initial decontamination of this inactive Jaquays millsite was ineffective because
of persistent erosion of the cover over the asbestos tailings. However, we negotiated
a voluntary cleanup of this property by Junction Partners, Inc. which bought the property
for commercial and residential development. Over 9,000 yards of contaminated material
was excavated and buried on site under a plastic barrier with about nine feet of clean
compacted cover. This work was completed under Bureau supervision and in full compliance
with all applicable air and OSHA regulations.
KYLE MILLSITE STATUS
Negotiations for decontamination and disposal of the limited asbestos containing
material were initiated in September, 1982. However, the Administrator of the Estate
has refused to perform a voluntary cleanup. An Order of Abatement requiring decontaninatitn.
was issued in June, 1983. The Order specifying compliance with NESHAPs Regulations has
thus far been ignored. We are now preparing to file for injunctive relief to require
compliance with the Order.
AIR QUALITY MONITORING
Ambient air monitoring for asbestos has continued to determine the effectiveness of the
initial decontamination of the subdivision as well as to monitor the potential exposure
to emissions from the adjacent Jaquays Mill. The mill has not operated since the end
of 1981 but still represents a-potential source of asbestos emissions from its exposed
tailings piles. The data was analyzed as it became available. Once the data base from
our original sampling station was available, statistical analyses showed a clear trend
toward increasing levels of exposure over time. This potential was also supported by
continuing on site inspections which indicated that the vegetative cover had not been
established or maintained in the topsoil cover provided and that the resulting erosion
had exposed asbestos contaminated materials.
When the probability of increasing levels of exposure to airborne asbestos fibers became
apparent the site was nominated and qualified for Superfund cleanup, which is now in
progress.
Statistical analyses of the air samples were undertaken in an attempt to identify the
source of ambient exposure. No conclusive correlations were established within an
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acceptable confidence level. In fact measured asbestos concentrations were generally
higher at low wind speeds than at high average wind soeeds. Thus, it might be concluded
that the higher levels of exposure were associated with activities in the near vicinity
of the monitoring site. A slight positive correlation with wind speed did occur in the
sector containing the Jaquays millsite but the limited number of valid data points pre-
vents any conclusions within an acceptable level of confidence.
The usable data base for the wind analyses was very limited due to poor data recovery
by the wind instruments. The monitoring station is now equipped with more reliable
data recorders and data averaging to expedite data reduction.
Simultaneous high volume and cassette samples were collected for a large number of the
early measurements using millipore filters of 5.0 and 0.8 pore size respectively.
Significantly higher fiber counts were detected on the cassette filters. Although this
might be attributed to the difference in filter pore size, it may also have resulted from
differences in the method of preparing Transmission Electron Microscopy sample grids
by different laboratories.
Laboratory quality assurance checks at the two commercial laboratories was limited to
the counting of blanks and prototype NBS specimen counting grids which were satisfactorily
reported. Prepared TEM grids were also interchanged between laboratories. Interlab
correlation was virtually non-existent. However, this lack of correlation may have
resulted from non-uniform distribution of fibers on the orids. We intend to specify
the use of "Finder Grids" in future TEM work so that specific grid openings can be
identified for interlab verifications.
SITE MAINTENANCE
Independent of the specific method of decontamination and on-site disposal there is
a need to provide for long term maintenance to assure that asbestos contaminated material
is not disturbed or exposed. Simple compliance with the current NESHAPs provisions
which formed the basis for the initial decontamination was obviously inadequate in this
respect. However, we believe that on-site disposal, similar to that utilized at the
Globe millsite and contemplated at the Kyle millsite, will minimize long term maintenance
requirements.
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PANEL DISCUSSION
Dr. Herschel Griffin (Panel Moderator)
Associate Dean, College of Human Services
San Diego State University
San Diego, CA
Milton Feldstein
Air Pollution Control Officer
Bay Area Air Quality Management District
San Francisco, CA
Jeanne Harvey
State Water and Air Quality Director
League of Women Voters of California
Ojai, CA
Maureen Lennon
Advisor, Regulatory Affairs Group
Atlantic Richfield Company
Los Angeles, CA
David Patrick
Chief, Pollutant Assessment Branch
U.S. Environmental Protection Agency
Research Triangle Park, NC
Michael Scheible
Chief, Office of Program Planning, Evaluation, and Coordination
California Air Resources Board
Sacramento, CA
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PANEL QUESTION
In a speech entitled "Science, Risk, and Public Policy"
delivered to the National Academy of Sciences on June 22,
Mr. Ruckelshaus stated that:
...we must now deal with a class of pollutants for which
a safe level is difficult, if not impossible, to establish..
we must assume that life now takes place in a minefield of
risks from hundreds, perhaps thousands, of substances.
At the same time, Section 112 of the Clean Air Act charges EPA
with establishing standards for air toxics such that "an ample
margin of safety is provided to protect the public health."
Given the difficulty of establishing safe levels for air
toxics, what directions should EPA take regarding policy and/or
research in an effort to apply the Clean Air Act's mandate to
the regulation of air toxics?
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BAY AREA AIR QUALITY MANAGEMENT DISTRICT
Response To Panel Question
Milton Feldstein
Air Pollution Control Officer
Standards can be set for toxic air contaminants based
on thresholds or acceptable risk. EPA does have or should
have the reources necessary to develop these tandards. Methods
to analyze for these contaminants need to be developed. EPA
needs to increase their resources devoted to research and meth-
odologies for data base (emission inventory and ambient monitoring)
compilation for these contaminants. There will always be disa-
greement as to what is an appropriate threshold level or risk
level. More resources need to be devoted to the study of the
effects these contaminants are currently having on people. This
should be done through increased epidemiological studies, with
adequate resources devoted to the studies.
Control of organic toxic emissions is not a mystery. Control
can be accomplished through incineration or carbon absorption.
There are trade-offs in emissions since incineration will result in
increased NO emissions. The benefit of reduced toxic emissions
and the effects of increased NO emissions need to be balanced.
A
The public needs to be actively involved in policy develop-
ment and in the development of the criteria used to assess risk.
The "public" which especially needs to be actively involved are
those people who are exposed. In order for this "public" to
effectively participate, they have to be informed of the risks
involved. Better public information on the risks involved needs
to be prepared and made available. This information needs to be
understandable and readily available (e.g. made available through
the media rather than through the Federal Register).
Local air pollution control districts have the expertise to
control the emissions through the development, adoption, and en-
forcement of regulations. EPA needs to define the contaminants
of concern , appropriate thresholds and risk analysis.
EPA should also accelerate reserach for analytical methods
and new methods of control.
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19Q
~129' ft£GION 8
COMH CNTR
SEPTEMBER 14, 1983
fcp 23 I 33 PN '83
STATEMENT BY THE LEAGUE OF WOMEN VOTERS TO BE PRESENTED
AT THE E.P.A. CONFERENCE ON TOXIC AIR
I represent the League of Women Voters of California, a grass
roots citizens organization with well over 12,000 members. All with
a long standing interest in human and environmental affairs.
The League is committed to the principle that democratic govern-
ment depends upon the informed and active participation of its citi-
zens in all areas of public policy. We are pleased to think that this
conference represents a renewed trend toward a broad based citizen
involvement in EPA policy decision making.
Our historical position with respect to the CLEAN AIR ACT has
bee*one of strong support. Without belaboring the past, I should say
that in early 1980, when the Act came up for review and reauthorization
and was the target of attack from industrial interests as well as a
showcase for regulatory relief^ the League made it a priority to oppose
any retreat from the public health and environmental safeguards con-
tained in the law. And one of the key provisions that we have sought
to strengthen has been the acceleration in control of toxic air pol-
lutants .
As for the mandate "to establish standards to provide for the
protection of public health" the wording seems clear. It reflects
the will of the people as perceived by Congress.
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I shall speak of the ambiguities in the CLEAN AIR ACT and the
problems of its implementation as they seem to be viewed by the
decision makers. I shall also take this opportunity to present
some of the needed changes as perceived by the League.
That the setting of standards should be predicated upon what
scientific and medical information exists seems evident. The paralysis
occurs when a decision is required to take that scientific information,
imperfect and incomplete as it may be, and act upon it. Yet this is
the administrative burden of the EPA. If indeed, Section 112 is not
enforceable, then legislation may be the only answer. It is our con-
tention that such is the case and that an amendment of the Act must be
sought. EPA would be strengthened by an amendment to the CAA that
would set standards by imposing a known scientific criterion.
Standards that would be at least as strict as a more clearly defined
Best Available Technology. The EPA continues to rely heavily on the
economic aspects of BAT, much more so than the League thinks is
justified.
Which brings us to some economic considerations. We do not rec-
ognize cost as a valid criterion for setting acceptable levels of risk.
While costs are not to be denied, they can be taken into account when
strategies and technologies to achieve reduction goals are chosen. At
that time alternate processing methods and compounds can be studied.
For example, we suggest a combination of population density and cancer
incidence as being appropriate considerations in risk managment plans.
As an adjunct to this thinking, industry must recognize that developing
effective controls are a cost of doing business.
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Realistically, political considerations have been high on the list
of uncertainties in the administration of all public agencies. Re-
peated and recent polls point to an enormous political force favoring
implementation of the CAA, even at the risk of some loss of jobs. The
public does not demand absolute scientific proof of how toxins endanger
their health, but the past few months have given us ample evidence
that they are quick, to place blame when protection has not been afforded
them. The disovery of dioxin that necessitated the abandonment and
reparations for a whole town in Missouri as well as the identification
in California of toxins in the Stringfellow Pits and the ground water
contamination in San Jose are good examples. It seems better to err on
the side of strict regulation than to run these risks. On-going scien-
tific findings can be easily folded into an existing program, particu-
larly if it involves reduction of control and cost.
Another EPA concern exists for the rights of states, localities
and industry. However, the suggestion that they undertake to volun-
tarily set their own control standards is, unfortunately, highly im-
practical. The proposal for the Agency to carry on a continuous mon-
itoring program of multiple entities is inefficient and fraught with
opportunity for inaction. The costs of scientific expertise, in itself,.
would be prohibitive. In addition, states need the authority of the
Federal government in drder to expedite reforms. Without such support,
competition for development is bound to impair individual states ability
to set and enforce standards in the public interest.
As I mentioned at the beginning, any evidence of opportunity for
public review is welcomed by the League. By this I do not mean that
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the public should be burdened with making repeated decisions about what
they want. That decision has been made. And a further cautionary note,
all public information and opportunities for participation are useless
if a course of action has been predetermined. Clearly defined channels
for participation and provision for dessiminating objective information
must be provided in order that citizens can fill the important role of
helping to develop policy decisions, such as how to make the best use
of the limited dollars.
To summarize - the League would like to see some changes in the
law that would give EPA the necessary authority and incentive to set
a timetable to identify air toxins and implement control measures -
and that proper channels for public input continue to be given a high
priority.
PRESENTED BY JEANNE G. HARVEY
Air Quality Director
LEAGUE OF WOMEN VOTERS OF CALIFORNIA
4275 Grand Av.
Ojai, Ca. 93023
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Summary of Remarks Made by Michael Scheible
at Panel Discussion at Region IX Toxics Conference
September 14, 1983
The question that we were asked to address raises the
issue of whether the Clean Air Act has placed EPA in an
impossible situation of eliminating all exposures to substances
for which no safe level can be established. First/ it is my
personal view that the goal established by Congress to protect
public health with an ample margin of safety and the statement
by Administrator Ruckelshaus are both correct, and from a
policy perspective these two positions do not present
irreconcilable conflicts. Although legal interpretations may
be applied to the Clean Air Act that would make it difficult to
totally resolve this issue, I believe that progress can be
made. There are clearly other technical-legal inconsistencies
in the Act of comparable magnitude. Perhaps the best example
is the requirement that the ozone standard be attained in the
South Coast Air Basin by 1987. While these inconsistencies
have caused problems, they have not prevented state and local
actions that will result in very significant progress in
cleaning the air.
Second, I believe that the current process used by EPA
relies too heavily on federal actions and that the Act requires
EPA to devise controls in an unrealistically short timeframe
once a substance has been identified as a hazardous air
pollutant. In many cases, airborne exposures to hazardous
substances result from the emissions from thousands, or in the
case of pollutants emitted from automobiles, millions of
sources. It will take time to design effective strategies in
such cases. To deal with the complexity of the problem, EPA
needs to rely more on the capabilities of local agencies,
perhaps in a process similar to that used to develop attainment
plans for criteria pollutants, to identify and implement
actions to reduce emissions of hazardous pollutants to
acceptable levels.
Third, EPA needs to develop an overall policy and
context for making decisions on how sources of hazardous
pollutants will be controlled. I think it is unfortunate that
much of this overall policy may be made based on experiences
with the Tacoma Copper Smelter, a situation largely seen by the
public as a conflict between health and jobs. I believe that
such situations will be the exception and that trying to
produce reasonable policies out of such an emotional setting
will be very difficult.
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Fourth, EPA needs to expedite its process to make
decisions on the identification of additional hazardous
pollutants. The review pipeline has been full for some time,
and it is doubtful that significant additional information that
would aid the resolution of existing scientific controversies
will become available in the near future. Because state and
local agencies must rely very heavily on the federal government
for health assessments it is imperative that EPA break the
current logjam and make decisions on the substances now under
review.
Finally, I would like to echo support for more public
involvement. Ultimately, it is the public who both pays for
and benefits from the control of hazardous air pollutants.
However, as is true in most cases, the cost and benefits are
not equally distributed. Rarely is the public that must bear
the increased health risk the same as the public that derives
benefits from the economic activities that result in emissions
of hazardous materials. EPA, states and local agencies must
improve our past efforts to inform and involve the public in
decisions that ultimately involve the public acceptance of some
level of risk. We must make explicit the scientific and
economic issues involved and better educate the public.
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LIST OF PARTICIPANTS
EPA REGION 9 AIR TOXICS CONFERENCE
September 13 and 14, 1983
Sheraton Palace Hotel
San Francisco, CA
Mr. Ben Almario
U.S. Department of the Navy
P.O. Box 727
San Bruno, CA 94066
Mr. Gerald Anderson
Systems Applications, Inc.
101 Lucas Valley Road
San Rafael, CA 94903
Mr. Donald Ames
California Air Resources Board
1102 Q Street
Sacramento, CA 95812
Mr. Donald F. Austin, M.D.
Department of Health Services
5850 Shellmound, #200
Emeryville, CA 94608
Mr. Lynn Baker
1615 Phantom Avenue
San Jose, CA 95125
Mr. Richard Baldwin
County of Ventura APCD
800 South Victoria Avenue
Ventura, CA 93009
Mr. Bob Barham
California Air Resources Board
1102 Q Street
Sacramento, CA 95812
Mr. William Barker
University of California
Los Angeles Graduate School
1427 - 25th Street, #4
Santa Monica, CA 90404
Mr. Cliff Bast
Hewlett Packard
300 Hanover Street, 20DJ
Palo Alto, CA 94304
Mr. Michael Belliveau
Citizens for a Better Environment
88 First Street
San Francisco, CA
Mr. Ravi Bhatia
Envirosphere Company
444 Castro Street
Mountain View, CA 94041
Mr. Robert Bishop
E.P.A., Region 9
215 Fremont Street
San Francisco, CA 94105
Mr. Phil Bobel
E.P.A., Region 9
215 Fremont Street
San Francisco, CA 94105
J.M. Bodie, M.D.
San Mateo County Department of
Health Services
225 - 37th Avenue
San Mateo, CA 94403
Mr. Steve Body
E.P.A., Region 9
215 Fremont Street
San Francisco, CA 94105
Meredith Boli Associates
8857 West Olympic Blvd.
Suite 200
Beverly Hills, CA 90211
Mr. Frank Bonamassa
California Air Resources Board
9528 Telestar Avenue
El Monte, CA 91731
Mr. Michael L. Borden
Safety Specialists, Inc.
P.O. Box 4420
Santa Clara, CA 95054
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Hr. David Bauer
IT Corporation
336 West Anaheim Street
Wilmington, CA 90744
Ms. Rebecca L. Beemer
Thermal Power Company
601 California Street
San Francisco, CA 94108
Ms. Kandice Bellamy
E.P.A., Region 9
215 Fremont Street
San Francisco, CA 94105
Mr. Richard Bradley
California Air Resources Board
P.O. Box 2815
Sacramento, CA 95812
Mr. Tom Brady
Los Angeles Mayor's Office
City Hall, Room M-l
Los Angeles, CA 90012
Mr. Joseph J. Brecher
506 - 15th Street
Oakland, CA 94612
Mr. James Breitlow
E.P.A., Region 9
215 Fremont Street
San Francisco, CA 94105
Mr. T. Brennan
Bay Area AQMD
939 Ellis Street
San Francisco, CA 94109
Ms. Debbie Bright
Bright and Associates
1200 North Jefferson, Suite B
Anaheim, CA 92807
Ms. Kim Brobeck
University of San Francisco
400 Willamette Drive
Vacaville, CA 95688
Mr. Dave Brooks
Hewlett Packard
300 Hanover Street, 20 DJ
Palo Alto, CA 94304
Mr. Timothy Bruce
City of West Covina
1444 West Garvey
West Covina, CA 91790
Mr. Larry Bowen
South Coast AQMD
9150 Flair Drive
El Monte, CA 91731
Mr. Larry Bowerman
E.P.A., Region 9
215 Fremont Street
San Francisco, CA 94105
Ms. Jan Bush
CAPCOA
254 Day Road
Ventura, CA 93003
Mr. Michael Cardin
Union Oil Company of California
461 South Boylston Street
Los Angeles, CA 90017
Mr. Robert W. Carr
San Luis Obispo County APCD
2146 Sierra Way, Suite B
Arroyo Grande, CA 93420
Mr. Willard Chin
E.P.A., Region 9
215 Fremont Street
San Francisco, CA 94105
Mr. Robert C. Cofer, P.E.
Sacramento County APCD
3701 Branch Center Road
Sacramento, CA 95827
Mr. Joel Cohen
J. M. Cohen, Inc.
Ill Winding Way
San Carlos, CA 94070
Ms. Carol B. Coleman
Atlantic Richfield Company
515 South Flower Street, Room 4084
Los Angeles, CA 90017
Mr. Garry D. Criscione
Tulare County APCD
Health Department
County Civic Center
Visalia, CA 93291
Mr. Randy Crissmon
E.P.A.
401 M Street, SW
Washington, D.C. 20460
Mr. Don Crowe
California Air Resources Board
1102 Q Street
Sacramento, CA 95814
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Hr. David Calkins
E.P.A., Region 9
215 Fremont Street
San Francisco, CA 94105
Vinh Cam
U.S. EPA
Air Programs Branch
Room 1005
26 Federal Plaza
New York, NY 10278
Mr. Ed Camarena
South Coast AQMD
9150 Flair Drive
El Monte, CA 91731
Mr. Ken Davis
Monsanto Company
1121 L Street, Suite 1906
Sacramento, CA 95814
Ms. Dana Davoli
E.P.A., Region 10
1200 - 6th Avenue, M/S 532
Seattle, WA 98101
Mr. Bill DeBoisblanc
Bay Area AQMD
939 Ellis Street
San Francisco, CA 94109
Ms. E. DeFalco
League of Women Voters, Bay Area
117 Natalie Drive
Moraga, CA 94556
Mr. Jeffrey H. Desautels
Anaconda Minerals Company
555 - 17th Street
Denver, CO 80202
Mr. David DiJulio
Southern California Association
of Governments
600 South Commonwealth Ave., Suite 1000
Los Angeles, CA 90005
Ms. Paulette Durand
University of San Diego
Alcala Park
San Diego, CA 92110
Mr. Dennis Dykstra
Chevron Research
576 Standard Avenue
Richmond, CA 94802
Ms. Janise Ehman
Engineering-Science
600 Bancroft Way
Berkeley, CA 94710
Dr. Larry T. Cupitt
GKPB, MD-84
U.S. Environmental Protection Agency
Research Triangle Park, NC 27711
Ilene R. Danse, M.D.
Chevron Environ. Health Center, Inc.
P.O. Box 4054
Richmond, CA 94804
Mr. Allen Danzig
San Diego, APCD
9150 Chesapeake Drive
San Diego, CA 92123
Ms. Anna Fan
Department of Health Services
2151 Berkeley Way
Berkeley, CA 94704
Mr. Don Fast
IBM Corporation
5600 Cottle Road
San Jose, CA 95193
Mr. Milton Feldstein
Bay Area AQMD
939 Ellis Street
San Francisco, CA 94109
Mr. Bryant Fischback
The Dow Chemical Company
P.O. Box 1398
Pittsburg, CA 94565
B. N. Fleischer
Allied Chemical
Nichols Road
Pittsburg, CA 94565
Mr. Chuck Flippo
E.P.A., Region 9
215 Fremont Street
San Francisco, CA 94105
Mr. James Forrest
E.P.A., Region 9
215 Fremont Street
San Francisco, CA 94105
Mr. Michael S. Foster
Cheveron U.S.A.
575 Market Street Street, Room 1566
San Francisco, CA 94105
Mr. C. Lee Fox
Pima County Health Department
151 West Congress Street
Tucson, AZ 87501
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Ms. Victoria A. Evans
Gaia Associates
Golden Gate Energy Center
Fort Cronkhite, Building 1055
Sausalito, CA 94965
Mr. Robert W. Evans
Maricopa County APCD
P.O. Box 2111
Phoenix, AZ 85001
Mr. Gerry Fait
Pillsbury, Madison & Sutro
225 Bush Street
San Francisco, CA 94104
Mr. Patrick Frost
SMUD
3580 Buoy Way
Sacramento, CA 95871
Mr. George Fujimoto
Hawaii Department of Health
645 Halekauwila, 3rd Floor
Honolulu, HI 96813
Mr. Barry Garelick
Woodward-Clyde Consultants
1 Walnut Creek Center
100 Pringle Avenue
Walnut Creek, CA 94596
Mr. Morris G. Gary
IBM Corporation
Dept. 843/124
5600 Cottle Road
San Jose, CA 95193
Mr. Bob Gaynor
Bay Area AQMD
939 Ellis Street
San Francisco, CA 94109
Mr. Ralph George
BKK Corporation
2550 - 237th Street
Torrance, CA 90505
Mr. D.J. Gladen
SoCalGas
810 South Flower
Los Angeles, CA 90017
Ms. Caren Glassel
E.P.A., Region 9
215 Fremont Street
San Francisco, CA 94105
Mr. Robert S. Frederick
State Board of Fabric Care
1900 San ysidro
Beverly Hills, CA 90210
Ms. Terry Freeman
SRI International
333 Ravenswood Avenue
Menlo Park, CA 94025
Mr. Jim Frolich
Ch2m Hill
2200 Powell Street, 8th Floor
Emeryville, CA 94608
Mr. Roger D. Griffin
KVB, Inc.
18006 Skypark
Irvine, CA 92714
Mr. Herschel Griffin
San Diego State University
College of Human Services
San Diego, CA 92182
Mr. David Grimsrud
Lawrence Berkeley Laboratory
Building 90 - 3058
Berkeley, CA 94720
Mr. Jack Grisanti, President
Cal-Alga Resources
15509 Mountain View
Kingsburg, CA 93631
Mr. Colin K. Guptill
Pinal-Gila APCD
Box 426
Kearny, AZ 85237
Mr. Don Harvey
E.P.A., Region 9
215 Fremont Street
San Francisco, CA 94105
Ms. Jeanne Harvey
League of Women Voters
4275 Grand Avenue
Ojai, CA 93023
Mr. G. C. Hass
California Air Resources Board
1102 Q Street
Sacramento, CA 95814
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Mr. Dan Goalwin
Bay Area AQMD
939 Ellis Street
San Francisco, CA
94105
Mr. Kevin Golden
E.P.A., Region 9
215 Fremont Street
San Francisco, CA 94105
Mr. Mary Gothberg
Ford Aerospace
3939 Fabian Way
Palo Alto, CA 94303
Ms. Lois Green
E.P.A., Region 9
215 Fremont Street, MS: A-3-3
San Francisco, CA 94105
Mr. J. T. Hoicombe
Pacific Gas and Electric Company
77 Beale Street, Room 1373
San Francisco, CA 1373
San Francisco, CA 94106
Dr. Kim Hooper
Department of Health Services
2151 Berkeley Way
Berkeley, CA 94704
Barry R. Horn, M.D.
Bay Area AQMD
2063 Oakland Avenue
Piedmond, CA 94611
Mr. David Howekamp
E.P.A., Region 9
215 Fremont Street
San Francisco, CA 94105
Ms. Mary Humboldt
Campaign for Economic Democracy
1337 Santa Monica Mall, 1310
Santa Monica, CA 90401
Ms. Sharon Huse
WESTNAVFACECOM
P.O. Box 727
San Bruno, CA 94066
Ms. Betty Ichikawa
California Air Resources Board
P.O. Box 2815
Sacramento, CA 95812
Mr. Miles R. Imada
Department of Health Services
2151 Berkeley Way
Berkeley, CA 94704
Ms. Stana Hearne
League of Women Voters, Bay Area
5931 Rincon Drive
Oakland, CA 94611
Ms. Evelyn F. Heidelberg
California Council for Environmental
and Economic Balance
215 Market Street, Suite 1311
San Francisco, CA 94105
Mr. Steven Hill
Bay Area AQMD
939 Ellis Street
San Francisco, CA 94109
Ms. Kay Jensen
California Air Resources Board
1102 Q Street
Sacramento, CA 95814
Ms. Jeri Johnson
E.P.A., Region 9
215 Fremont Street
San Francisco, CA 94105
Mr. Joseph R. Johnson
BKK Corp.
2550 - 237th Street
Torrance, CA 90505
Mr. Neal Johnson
Waste Management Board
1020 - 9th Street, Suite 200
Sacramento, CA 95814
Ms. Kathleen M. Kahler
American Lung Association
833 Market Street
San Francisco, CA 94103
Mr. Charles B. Kay
Texaco Inc.
3350 Wilshire Boulevard
Los Angeles, CA 90010
Mr. Larry Kerrigan
Los Angeles Dept. of Water & Power
111 North Hope Street, Room 632
Los Angeles, CA 90051
Mr. Peter King
E.P.A., Region 9
215 Fremont Street
San Francisco, CA 94105
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Ms. Laura King
Natural Resources Defense
Council, Inc.
25 Kearny Street
San Francisco, CA 94108
Ms. Jean Kitchens
League of Women Voters
318 Randloph Street
Napaf CA 94558
Mr. Kent Kitchingman
E.P.A., Region 9
215 Fremont Street
San Francisco, CA 94105
Ms. Meredith Jane Klein
Pillsbury, Madison & Sutro
P.O. Box 7880
San Francisco, CA 94120
Mr. Irwin Koehler
Roy F. Weston, Inc.
153 Kearny Street, Suite 506
San Francisco, CA 94108
Ms. Ruth H. Koehler
League of Women Voters
64 Stuart Court
Los Altos, CA 94022
Mr. Carl Kohnert
E.P.A., Region 9
215 Fremont Street
San Francisco, CA 94105
Mr. Imants Krese
E.P.A., Region 9
215 Fremont Street
San Francisco, CA 94105
Mr. Bob Kuhlman
California Air Resources Board
1102 Q Street
Sacramento, CA 95814
Mr. Linda Larson
E.P.A., Region 9
215 Fremont Street
San Francisco, CA 94105
Mr. Sven A. Larsson
Formica Corp.
P.O. Box 519
Rocklin, CA 95677
Mr. Ron Leach
E.P.A., Region 9
215 Fremont Street
San Francisco, CA 94105
Mr. Olaf Leifson
Department of Food and Agriculture
1220 N Street
Sacramento, CA 95826
Ms. Maureen Lennon
Atlantic Richfield Co.
515 South Flower St., AP 410
Los Angeles, CA 90071
Mr. Richard Lewis
c/o Mike Miller
City of West Covina
P.O. Box 1440
West Covina, CA 91768
Mr. Alan C. Lloyd
Environmental Research
& Technology, Inc.
2625 Townsgate Road
Westlake Village, CA 91361
Mr. William Loscutoff
California Air Resources Board
1102 Q Street
Sacramento, CA 95814
Mr. Dick Lundquist
California Air Resources Board
1102 Q Street
San Francisco, CA 94105
Ms. Barbara Maco
E.P.A.
236 - 4th Avenue
San Francisco, CA 94118
Mr. Tirlochan S. Mangat
Bay Area AQMD
939 Ellis Street
San Francisco, CA 94109
Mr. Terry McGuire
California Air Resouces Board
1102 Q Street
San Francisco, CA 95814
Mr. J. Craig Mckenzie
Chemical Waste Management
P.O. Box 471
Kettlemen City, CA 93239
Mr. Ralph Mead
255 Sycamore Avenue
Mill Valley, CA 94941
Mr. Raymond Menebroker
California Air Resources Board
1102 Q Street
Sacramento, CA 95814
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Mr. Herman Myer
Sacramento County APCD
37018BranchaCentertRoad
Sacramento, CA 95827
Mr. Edward Miller
Bay Area AQMD
939 Ellis Street
San Francisco, CA 94109
Mr. Michael L. Miller
City of West Covina
P.O. Box 1440
West Covina, CA 91793
Mr. Jerry Miller
Teknekron, Inc.
2118 Milva Street
Berkeley, CA 94704
Mr. David A. Monroe
Union Oil of California
461 South Boylston Street
Los Angeles, CA 90017
Mr. Walter R. Mook
San Bernardino County APCD
15579 - 8th Street
Victorville, CA 92392
Mr. David Morel1
E.P.A.
215 Fremont Street
San Francisco, CA 94105
Mr. Wayne Morgan
Stanislaus County APCD
1716 Morgan Road
Modesto, CA 95351
Mr. Joel D. Mulder
E.P.A. Center for Disease Control
215 Fremont Street
San Francisco, CA 94105
Carol or Arthur Murray
13 Miramonte Drive
Morage, CA 94556
Mr. Michael Naylor
Clark County Health District
P.O. Box 4426
Las Vegas, NV 89127
Mr. Michael Neale
Dow Chemical U.S.A.
2800 Mitchell Drive
Walnut Creek, CA 94598
Mr. Fernando I. Nell
Safety Specialists, Inc.
P.O. Box 4420
Santa Clara, CA 95054
Ms. Emily Pearson Nelson
Graduate Research Assistant
715-1/2 North Marguerita
Alhambra, CA 91801
Mr. Lyler R. Nelson
Southern California Edison Co,
2244 Walnut Grove Avenue
Rosemead, CA 91770
Mr. James F. Norton
1885 Ridgeview Drive
Roseville, CA 95678
Mr. Leslie Norton
Engineering-Science
125 West Huntington Drive
Arcadia, CA 91006
Ms. Mitsi Okamoto
E.P.A., Region 9
215 Fremont Street
San Francisco, CA 94105
Mr. William Rogers Oliver
Systems Applications, Inc.
101 Lucas Valley Road
San Rafael, CA 94903
Mr. John Ong
E.P.A., Region 9
215 Fremont Street
San Francisco, CA 94105
Ms. Jean J. Ospital
Southern California Edison
P.O. Box 800
Rosemead, CA 91770
Ms. Patricia M. O'Toole
Union Oil Company of California
461 South Boylston Street
Los Angeles, CA 90017
Mr. Charles E. Owens
United Airlines M.O.C.
San Francisco Internaitonal Airport
San Francisco, CA 94128
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Mr. Coe Owen
E.P.A., Region 9
215 Fremont Street
San Francisco, CA 94105
Mr. Gordon Palmer
Southern California Association
of Governments
600 Commonwealth Avenue
Suite 1000
Los Angeles, CA 90005
Mr. David Patrick
E.P.A., Air Quality Planning
& Standards
Research Traingle Park, NC 27711
Ms. Joan Patton
League of Women Voters, Bay Area
5845 Ocean View Drive
Oakland, CA 94618
Mr. Thomas A. Peters
Engineering-Science
125 West Huntington Drive
Arcadia, CA 91016
Mr. Daniel V. Phelan
155 Jackston, Suite 305
San Francisco, CA 94111
Mr. Ralph Propper
Coalition for Clean Air
309 Santa Monica Blvd., |312
Santa Monica, CA 90401
Mr. Doug Quetin
Monterely Bay Unified APCD
1064 Monroe Street, Suite No. 10
Salinas, CA 93901
Mrs. Doroty M. Rankin
Pinal-Gila Counties AQCD
P.O. Box 1076
Florence, AZ 85232
Mr. Tom Rarick
E.P.A., Region 9
215- Fremont Street
San Francisco, CA 94105
Mr. Michael Redemer
Beacon Oil Company
525 West 3rd Street
Hanford, CA 93230
Mr. Ralph M. Riggin
Battelle
505 King Avenue
Columbus, OH 43085
Ms. Joan E. Riley
Chemical Manufacturers Association
2501 M Street, N.W.
Washington, D.C. 20037
Mr. Donald Robbins
Asarco Inc.
3422 South 700 West
Salt Lake City, UT 84119
Mr. Richard Rollins
National Semiconductor
2900 Semiconductor Drive, M/S B540
Santa Clara, CA 95051
Mr. Scott Ross
UCLA-SPH
1427 - 25th Street
Santa Monica, CA 94025
Mr. Marc Rothschild
E.P.A., Region 9
215 Fremont Street
San Francisco, CA 94105
Ms. Sharon F. Rubalcava
McCutchen, Black, Verleger & Shea
600 Wilshire Boulevard
Los Angeles, CA 90017
Mr. Kelly Runyuon
S.F. Sold Waste Managment Program
City Hall, Room 271
San Francisco, CA (4102
Mr. Hanafi Russell
Department of Health Services
2151 Berkeley Way
Berkeley, CA 94704
Ms. Adelia Sabiston
League of Women Voters, Bay Area
3953 Campolinda Drive
Morago, CA 94556
Ms. Sue Sakaki
E.P.A., Region 9
215 Fremont Street
San Francisco, CA 94105
Mr. Mark Saperstein
Electric Power Research Insititue
3412 Hill iew Avenue
Palo Alto, CA 94303
Mr. Michael Seaman
California Air Resources Board
1102 Q Street
Sacramento, CA 95814
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Mr. Ray Seid
E.P.A., Region 9
215 Fremont Street
San Franciso, CA 94105
Mr. Richard Seraydarian
WESTNAVFACENGCOM, CODE 1144
P.O. Box 727
San Bruno, CA 94066
Dr. Ken Sexton
Deparmtent of Health Services
2151 Berkeley Way
Berkeley, CA 94704
Mr. Michael Scheible
California Air Resources Board
1102 Q Street
Sacramento, CA 95814
Mr. Rolf D. Schmued
Rockwell International
Rocketdyne Division
6633 Canoga Avenue - d/543-FB66
Canoga Park, CA 91304
Mr. Herb Schuyten
Chevron U.S.A.
575 Market Street, Room 1564
San Francisco, CA 94105
Dr. J.C. Schwegmann
Kaiser Aluminum & Chemical Corp.
300 Lakeside Drive
Oakland, CA 94643
Ms. Celia Shen
California Air Resources Board
1309 T Street
Sacramento, CA 95814
Mr. J. Gareth Shepherd
Kaiser Refractories
Moss Landing, CA 95039
Mr. James M. Shikiya
California Air Resources Board
9528 Telestar Avenue
El Monte, CA 91731
Ms. Merceditas Shikiya
South Coast AQMD
9150 Flair Drive
El Monte, CA 91731
Ms. Kathleen Shimmin
E.P.A., Region 9
215 Fremont Street
San Francisco, CA 94105
Mr. Bart Simmons
Department of Health Services
2151 Berkeley Way
Berkelehy, CA 94704
Dr. Hanwant B. Singh
SRI International
333 Ravenswood
Menlo Park, CA 94025
Mr. Eric P. Skelton
Sacramento County APCD
3701 Branch Center Road
Sacramento, CA 95827
Kathryn Smick, M.D.
1115 Oakhill Road
Lafayette, CA 94549
Mr. Robert N. Smiley
Vulcan Chemicals
333 Hegenberger Road, #208
Oakland, CA 94621
Ms. Alexandra B. Smith
E.P.A., Region 10
1200 - 6th Avenue, M/S 529
Seattle, EA 98101
Mr. Ted Smith
Silicon Valley Toxics Coalition
1025 North 4th Street
San Jose, CA 95112
Mr. David Solomon
E.P.A., Region 9
215 Fremont Street
San Franciso, CA 94105
Mr. Todd I. Sostek
SoCalGas
Box 3249, Terminal Annex
Los Angeles, CA 90051
Mr. David R. Souten
System Application, Inc.
101 Lucas Valley Road
San Rafael, CA 94903
Ms. Pat Springer
E.P.A., Region 9
215 Fremont Street
San Francisco, CA (4105
Mr. Arnold Stein
Engineering Science
125 West Huntington Drive
Arcadia, CA 91006
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Mr. Mike Stenburg
E.P.A., Region 9
215 Fremont Street
San Francisco, CA (4105
Mr. R. Stephens
Department of Health Services
215 Berkeley Way
Berkeley, CA 94704
Ms. Leslie Stewart
League of Women Voters
3557 Mt. Diablo Boulevard
Lafayette, CA 94549
Ms. Alexis Strauss
E.P.A., Region 9
215 Fremont Street
San Francisco, CA 94105
Mr. J.A. Stuart
South Coast AQMD
9150 Flair Drive
El Monte, CA 91731
Mr. Rick Sugarek
E.P.A., Region 9
215 Fremont Street
San Francisco, CA 94105
Ms. Andree Tamony
Dow Chemical
P.O. Box 1398
Pittsburg, CA 94509
Ms. Melinda Taplin
E.P.A., Region 9
215 Fremont Street
San Francisco, CA 94105
Ms. Ruby Tarleton
League of Women Voters
2243 Redwood Road
Napa, CA 94558
Mr. Russ Tate
California Air Resources Board
P.O. Box 2815
Sacramento, CA 95812
Ms. Vivian Thomson
E.P.A., Region 9
215 Fremont Street
San Francisco, CA 94105
Ms. Phyllis Tichinin
Toxic Assessment Group
2530 J Street
Sacramento, CA 95816
Mr. G. Tsou
California Air Resources Board
1102 Q Street
Sacramento, CA 95814
Ms. Lucille van Ommering
E.P.A., Region 9
215 Fremont Street
San Francisco, CA 94105
Mr. Peter Venturini
Callifornia Air Resources Board
1102 Q Street
Sacramento, CA 94105
Mr. Mark Volmert
Los Angeles County
856 Hall of Administration
500 West Temple
Los Angeles, CA 90012
Mr. Alan Waltner
E.P.A., Region 9
215 Fremont Street
San Francisco, CA 94105
Mr. Jerry Wesolowski
Department of Health Services
2151 Berkeley Way
Berkeley, CA 94704
Ms. Alice Westerinen
California Air Resources Board
1131 S Street
Sacramento, CA 95815
Ms. Deanna Wieman
E.P.A., Region 9
215 Fremont Street
San Francisco, CA (4105
Mr. Daniel Wilkowsky
National Semiconductor
2900 Semiconductor Drive, M/S d3940
Santa Clara, CA 95051
Ms. Stell Wilcox
San Diego APCD
9150 Chesapeake Drive
San Diego, CA 92123
Ms. Julie Williams
Signetics Corporation
811 East Arques Avenue, M/S 0458
Sunnyvale, CA 94088
Mr. John Wise
E.P.A., Region 9
215 Fremont Street
San Francisco, CA 94105
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Mr. Harmon Wong-Woo
California Air Resources Board
1102 Q Street
San Francisco, CA 95814
Mr. Michael Work
E.P.A., Region 9
215 Fremont Street
San Francisco, CA 94105
Robert A. Wyman, Esq.
Lathraan & Watkins
555 South Flower Street
LOs Angeles, CA 90071-2466
Dr. Terry Young
Environmental Defense Fund
2606 Dwight Way
Berkeley, CA 94704
Mr. Thomas Zosel
3M Company 33331
St. Paul, MN 55133
Mr. Mark Zuckerraan
Signetics Corporation
811 Esta Arquest Avenue, MS-2539
Sunnyvale, CA 94088
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