September 13 and 14, 1983
      Sheraton Palace Hotel
        San Francisco, CA

                      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

                    EPA Region 9 presents an

                     AIR TOXICS CONFERENCE

                   Septenber 13 and 14, 1983

                     Sheraton Palace Hotel

                   San Francisco, California


         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


 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


                      AIR TOXICS CONFERENCE

                        September 13, 1983


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
            California Department of Health Services

                        September  14,  1983


 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
          Mike Johnston - Chief,  Air Operations Section
          Dana Davoli - Environmental  Scientist
          EPA, Region  10

 10:00   Break

                      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


 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

             David Patrick
   Chief, Pollutant Assessment Branch
  U.S. Environmental Protection Agency
       Research Triangle Park, NC


     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
      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.

     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

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


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.

     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,

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.


     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

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

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

 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.


                   FRAMEWORK FOR AIR TOXICS
                       Michael Scheible
Chief, Office of Program Planning,  Evaluation, and Coordination
                California Air Resources Board
                        Sacramento, CA



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
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
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
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

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 (
      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*'
        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'
                                    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
                                                          scientists to idrntify some of them
                                                          four years ago after deciding the
                                                          Environmental Protection Agency
                                                          was moving too slowly on the prob-

                                                            The toxics in question include
                                                                nrsenir from wood pre-
                                                                          , cadmi-
 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?






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)
* As regulated under Clean Air Act, except Lead






  Plus 2OOO-5OOO per year

AB 1OO5  -  1981/82
AB 18O7 -  1983





    — ARB	









               — 1O MONTHS —
            Substance • by • Substance

         8 MONTHS
                       6 MONTHS










               RISK REDUCTION



             MARGIN OF SAFETY


  — ARB






Health Effects
Long Teim

     - ARB
     - DOHS
     - 1O MONTHS

     -- ARB/APCD's
     - 14 MONTHS

                      Dr. Kim Hooper
                    Research Scientist
         California Department of  Health  Services
                        Berkeley, CA

                                                                Kim Hooper, Ph.D.
  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


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

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).

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

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


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

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.


"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

 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)

              Dr. Hanwant Singh
   Director, Atmospheric Chemistry  Program
              SRI International
                Menlo Park, CA

                          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

  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
                          1* Un 12

Table I.  Sources, Sinks, Background Levels, and Toxic Effect* of Chemicals of Interest

     methyl chloride
     methyl bromide
     methyl iodide
     carbon tetrachloride
     1,2-dibromoe thane
     1,1,1-trichloroe thane
     1,1,2-tric.Moroe thane
     3-chloro-1 -propene
     hexachloro-1,3 butadiene
major source0

 N(O), MM
 N(O), MM
 N, MM

loss,c '.
HO, hv(T)

                                                                     surface level
                                                                    bckgrnd concnd


  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, 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




Table H. Concentrations of Chemicals
lta««tM~lV24 Hey M
(ut. «nr UM> *)*i)')
ChMltll €••«•
ri^ i •! i »Fc
Mthrl c»l»ct*« 9)) (4011*
HHkjri to*!* 100 ()•)
Mlhyl l«4l«* 4 (1)
•IUilaiia»iHana *74 ())))
Oa»r.*l*n 42) (749)
Carte* titrttckjlwUt 404 (449)
29 M
1.1-DlchUrMttaM 1)12 ( 1«J)
7 WO
1.1-Olkrw.thA** )9 (72)
1.1.1-TTtchlorMttaM ))) (14))
1.1.2-Trlchlorwth.MM )} (24)
1.1,1.1-tttrKhUrMtlwaM U (|)
l,l-»lcM*r«fT«9>*M (I ()r)
l,l-Mclil»rMCkrl«M 2) (H)
1tlcia*r*«thrUM 144 (19))
T*tr«chlw.MthyUM 401 (59|)
3, Oiler o-l-pr***** <) (-)

•»••»»• )T*0 (SMO)
Fotwltteiiy** - (->
IHI (111)

III (12))

21 (11)

1991 (1911)

20)) (HM)

2>M (2122)

4110 (1)21)

4)0 ())0)

112) (14)1)

174 (111)

7) (42)

174 (1)1)

99 (141)

771 (1047)

2717 (40)2)

7)1 (IM) 1)09 (214)
•i (») m (to
) (2) I) <9)
411 (ID) 1441 (2011)
7) (») ))) (144)
129 (4) 111 ()•>
124 (101) )Q1 (41)1)
14 (4) 122 ()l)
21) (114) 1211 (7*1)
1) (4) 12 ()))
4 (2) 41 (14)
51 (12) 244 ()))
* ()) )4 (20)
112 (1)4) 60! (127)
124 (9))) 2209 (6471)
<3 (-) 
1410 ( 1190) 4489 (1719)
11)00 (4)00) 1M34 11)10)
• 100
0*»*«r»l4-24 JWM CO
Co ac*«t ratio*
Ffl •»/•'

124 ()l) 411 (IM)
2 (1) 10 (4)
94-1 (924) )))) (Mil)
11) (204) 199 (1001)
174 ( 19) 1094 ( 1)9)
1 16
2*1 (297) 974 (1100)
11 (1)) IV (1)4)
711 ()))) )H) (HMJ)
27 (10) 1*7 ()4)
10 ()) 69 (11)
4« (14) 121 (6))
11 (49) 12) (194)
198 (111) 104) (16*0)
)94 (111) 2670 (1071)
<) (-)  (-)
2 (1) 11 (II)
<) (-) 16 (-)
4)90 (1940) 11976 (12)**)
I2NO O900) 1)041 (7224)
* Arithmetic average (standard deviation). * Maximum concentration. * Minimum
•lMralaV—2-11 July 10
C*nc« ait ration
•pt nc/a1
70) (179) 1449 ()69)
2)9 (147) 1004 (441)
) U) 16 (7)
194* (1404) 4762 (4*78)
70) (798) Ml) (1874)
17) (2)) 1100 (14))
137 (12)) 1442 (1)11)
22 (7) 168 ()))
7*7 (2)7) 4070 (1*00)
41 (21) 21) (II*)
11 (') 12 (62)
)7 (1)) 26) (49)
9 (4) )6 (14)
lit ())) 6)1 (29))
4*4 (IM) )279 ( 1)99)
<) (-) <16 (-)
4 ()) 4) ()2)
<) (-) 26 (-)
)9)0 (1910) 12)76 (40*1)
19000 (7400) 2)24) (9)06)
Stat«« Ulawd — 27 Hatth-J April 81
(Ut. 40*))' L0o*. 74°12')
COBC«*U rat Ion
•pl ««/»J
701 (114) 144) ()D)

•4 (I0f) 124 (419)
1 (1) 12 (4)
140) (2947) )I44 (10214)
144 (117) 709 ()•*)
• 72

309 (101) 194] (1270)
2)4 ()20) 10)* (1101)
20 (6) ID (*6)
468 (2*8) 2110 (1)11)
7 (i) )8 (II)
- (-) - (-)
16 (1)) 120 (69)
- (-) - (-)

167 (199) 896 (10*8)
292 (200) 1971. (1))))
- (-) - (-)
- (-)
- (-)
- (-> - (-)

- (-) - (-)
420* (4217) 1)18* (1)641)
14)00 (9100) IMIO (1114))

rittaa«rfhr--*-14 April 11
(Ut. '•*• 24' Ua«. 79* )*')
ri»« My.3
66) (10)1 1)71 (216)
41 ( ) 1)9 (21)
1 ( ) 6 (4)

)90 (144) )))) (847)
97 (41) 471 (199)
))l (107) 20fl (47))
111 ())> *M 1141)
16 (ID) 122 (74)
486 (272) 16*8 ( 1*81)
6 (2) 1) (II)
* ( 1) 27 (M
1) (!) 104 (17)
- (-) - ( -)

94 (91) 111 (499)
409 (1)7) 2771 (2*19)

4 (7) 44 (7))
- (-) - (-)
• (-)
- (.)
- (-) - ( -»
)00) (»•!«> 1)918 (111)7)

20*00 O200) 2)11* (6)67)

O» t «•«.•—
(Ut. *1°
• M (168)

47 (|7)
2 (2)

1446 (44)))
•1 (26)
140 ()1)
II) (140)
If- (17)
476 (IM>
7 ()>
) (1)
29 (7)
22 (19)
11) (1«1)
)90 (4)1)
- (-)
- <->
- (-)
- (-)

- (-)
2)61 (1779)
12800 (1300)
I 7200

21-30 4»rll tl
4)' LM«. |7»4D
1764 (M6)

III (44)

12 (11)

H80 (130*2)

>9) (124)

14)4 (12:)

7U (1)74)

198 (2*1)

2)94 t*4l)

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21 (7)

IM on

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120* (1)14)

)998 (304))

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81)1 O444)

1)47) (4041)


| woo
\ 2000
I 1500
o 1000
1 ' ' • ' ' '
. •
••• • .
. • "V '.*
• •' i •
. • * '• • • •
i i i i i i ) . ; . i
                        TIME — 0*11
                    (•I  HOUSTON. TX

       $ 2800

       i 1500
       o 1000
f* •-
                         TIME —
                    Ital ST. LOUIS. MO
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
                                                      10     IS

                                                      TIME — hour

                                                   III HOUSTON. TX
C 8
n 4
I ^


j n * i h u J H"

0 5 10 15 20 25
TIME — hour
                                                  Ibl RIVERSIDE. CA
                              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

I 3000
fc 2500
1 2000
1 1500
	 . 	 , 	 . 	 , 	 . 	 r 	 _- , 	

T '.
•J .
I i * , , i I
1 ' 1 I .MIi!,'!,
_ _ 	 	 . 	 _
0 5 10 15 20 2
TIME — hout
& 3000
f 2500
* 1500
I 500
• T - -
' , T j

" t

T 1 ' _

. , .1,1 . ! 1, .1
3 5 10 16 20-1- 2
TIME — hour
9 3500
* 3000
f 2SOO
i 2000

i • t

:HH !




: i;
0 5 tO 15 20 2
TIME — hour
                   Id  RIVERSIDE. CA

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
                                  O _    DO,
                                   0   a  » o
                                  °o    „  °
                                  o o   °   on
                                                         Figure 4. Atmospheric concentrations of chloroform at Staten Island,
                         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

J 3500
f 2800
0 1500
g 100°
5 HO





0 J


L S 10


' * J, — ' 	
TIME — hour




20 2

              III HOUSTON. TX •
                             15-24 MAY I960
| 3500
- 3000
. 2SOO
O 1500
u 1000
Z 800



                         10     15 J-   20
                        TIME — hour

            (b) RIVERSIDE. CA	 7-12 JULY 1980
Flgur* 6. Mean dumal variation of 1,2-dteNoroethane.


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
1 isor
8° 500


-ill! , -
I1! 1 ii i • j . i
i - i i i
                                                                                   TIME — hour

                                                                               U) HOUSTON. TX
| 1500
8 1000





: I

T 1
.1 J
                                                                                   10     IS
                                                                                   TIME — hour
                     (bl  DCNVER. CO
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

| 400
i r i




1. 1

1,. .1 i j ' ,1 *
0 6 10 15 20 3
TIME — hour
| 800
& 600
| 400
J1 **>



0 t

10 15 J

, I
20 2
                    TIME — hour
                   Ib)  DENVER. CO
    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
 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
 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

                        to   1  is
                        TIME — hour

                    (•I  HOUSTON. TX


| 15
o" 10
5 10 15 20 2
TIME — hour


                  5     10     15

                       TIME 	 hour

                  Ic) STATEN ISLAND. NY
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.


   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
  (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,
   (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,
  (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,
  (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

(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,
 (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.

                     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

                   Suranary of Comments on Ambient
              A1r Monitoring for Toxic Compounds by  the
                         Air Resources Board
                          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

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-
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).

                               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


                      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:
         Carbon Tetrachloride
         Ethylene Oxide
         Ethylene Dibromide
Methyl Bromide
Mehtyl Chloroform
Methylene Chloride
Vinyl Chloride

 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.


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.
    •    "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

    •    "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.



    BENZENE                XYLENE




    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.

                      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


                 Suaaary of Presentation of David Grinsrud
                      Region 9 Air Toxics Conference
                            September 13, 1983
     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.

     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


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.


     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

     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.

     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.


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.


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

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


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


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.


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

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.


                      Dr. Donald  Austin
Chief, Resource for Cancer  Epidemiology  and  California  Tumor  Registry
           California Department  of  Health Services
                         Emeryville,  CA

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 to the Son-industrial  portion.  The incidence of lung cancer
for the county as a whole was unremarkable as cocpared to four other local

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.

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.

                                 PROJECT SOWARY



                         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


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.

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.


     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:


 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.


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


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.


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

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,


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.


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



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


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

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


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.


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


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.


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

measure of total lifetime dose of  SO. from Contra Costa County was used,

no elevated risk was apparent.


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.

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.

             Kathleen  Shimmin
      Chief, Field Operations  Branch
   U.S. Environmental  Protection  Agency
            San  Francisco,  CA

            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

Nov. 1980
Dec. 1980

Jan. -Feb. 1982
Feb. 1982
Mar. 1982
Apr. -Aug. 1982

Sept. 1982
Apr. 1983

Summer 1983

Fall 1983
Refinery Acid Sludge Disposal
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

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

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

                       Michael Johnston
                Chief, Air Operations Section
             U.S. Environmental Protection Agency
                         Seattle, WA
                         Dana Davoli
                   Environmental Scientist
             U.S. Environmental Protection Agency
                         Seattle, WA

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

                 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

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%

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.


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.


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.

 Hynre I
                                                Conci-ptual  Framework  for Arsenic
                                                          Ambient  Environment
       Human Exposures
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)
hair , ,,. Slgnl f leaner /Heal th Riskc 	
	 * blood
Air ./Couiplex ^v
'Jo 11 r Environuw>nt4l )
Vegi'tation Recycling^/
Siirliico W.itor L"xpo«;nre
*" Ground Water Pathways
Health Effects
Mortal ity
> Morbidity
IJisk Assessments
Lpideintological Studies
drinking water
Ueruidl Ahsorpt tin- 	


tP/yiiif/rVotein Levels


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.

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.

             Michael Naylor
         Director, Air  Quality
      Clark County Health  District
             Las Vegas,  NV


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

The toxic air pollutants in the Southeast Valley consist of:

            hydrogen chloride
            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.
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.

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.

             Milton Feldstein
      Air Pollution Control Officer
 Bay Area Air Quality Management District
            San Francisco, CA


           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

     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.


     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

     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

     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

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

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.

     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

     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

     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
BAAQMD 9/1U/83


                                      FIGURE  1

                             SEMICONDUCTOR MANUFACTURING
Molten  v
-> Ingots

            SOLVENTS             SOLVENTS

 ,  Silicon
•>  Wafers

t .

— >

, these steps are.'


— ^-

many times

                               Soft  bake
       Laser Scribe
BAAQMD 9/14/83

                Ed Camarena
       Director, Enforcement  Division
South Coast Air Qaulity  Management  District
                El Monte,  CA

South Coast


          PRESENTED SEPTEMBER 14,  1983

                    AT THE


                  SPONSORED BY

                 EPA, REGION IX




                EDWARD CAMARENA




                         PRESENTED SEPTEMBER 14, 1983
                                    AT THE
                            AIR TOXICS CONFERENCE
                         SPONSORED BY EPA. REGION IX. IN
                          SAN FRANCISCO, CALIFORNIA


     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

     C.  Enforcement of the state and District air pollution emergency plan,
     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

                                 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

     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

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


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


     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."

     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:

    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
petition for an Order for Abatement  which would:


     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
     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.

     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


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
     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

     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
     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.

     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

                               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


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.

              David Chelgren
       Manager, Compliance Section
  Arizona Bureau of Air Quality Control
               Phoenix, AZ

                       A  case  study  in  air toxics response

                    David 0. Chelgren,  Manager for  Compliance
                  in the  Arizona Bureau of Air Quality  Control

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.


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


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.


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.


 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

 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.


 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.


 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.


 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

 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


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.


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

                      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

                        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?



                   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.

     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.

                             ~129'                 ft£GION 8
                                                  COMH CNTR

SEPTEMBER 14, 1983
                                              fcp 23   I  33 PN '83

                   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.


     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


     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.


     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

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

Air Quality Director
4275 Grand Av.
Ojai, Ca.  93023

           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.

         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

         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.


                           LIST OF PARTICIPANTS


                        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

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
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
401 M  Street, SW
Washington, D.C.   20460

Mr. Don  Crowe
California Air Resources Board
1102 Q Street
Sacramento, CA  95814

Hr. David Calkins
E.P.A., Region 9
215 Fremont Street
San Francisco, CA  94105

Vinh Cam
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
600 Bancroft Way
Berkeley, CA  94710
Dr. Larry T. Cupitt
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

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
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
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

Mr. Dan Goalwin
Bay Area AQMD
939 Ellis Street
San Francisco, CA
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
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

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
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

Mr. Herman Myer
Sacramento County APCD
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
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
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

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
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
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
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

Mr. Ray Seid
E.P.A., Region 9
215 Fremont Street
San Franciso, CA  94105

Mr. Richard Seraydarian
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
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

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

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