Meeting Overview

MINUTES

ZONING  BOARD  OF APPEALS

JUNE  17, 2015

 

 

 

MEMBERS  PRESENT:

 

DANSULLNAN JOAN SALOMON

LEONARD FEROLDI, ALTERNATE

PATRICIA CASTELLI MICHAEL BOSCO THOMAS QUINN

ABSENT:

 

 

NONE

 

 

 

 

ALSO PRESENT:

Dennis Michaels, Esq. Ann Marie Ambrose, Deborah Arbolino,

Deputy Town Attorney Official Stenographer Administrative Aide

 

 

 

 

This meeting was called to order at 7: 00 P .M. by Mr. Sullivan, Chairman.

Hearings on this meeting’s agenda, which are made a part of this meeting, were held as

noted below:

 

 

 

PUBLISHED ITEMS

 

APPLICANTS

 

 

 

NEW ITEMS:

DECISIONS

 

KIM DeTEMPLE

45 Grand Avenue, Tappan,NY

77.10 I 2 I 21; R-15 zone

• 5.153 DISTANCE BETWEEN ACCESSORY STRUCTURE VARIANCE

APPROVED

ZBA#15-49

 

Di DOMENICO

8 Sargent Hartz Drive,

Tappan,NY

77.09 I I I 30.2; R-15 zone

R-80, COLUMN 2, PARAGRAGH              ZBA#lS-50·

#7 SIZE OF SUBORDINATE DWELLING VARIANCE APPROVED

 

VARGA

56 Conklin Avenue,

Tappan,NY

77.11III61;  R-15 zone

 

BARSANTI

66 Andre Avenue, Tappan,NY

77.10 I 3 I 65; R-15 zone

FLOOR AREA RATIO, SIDE YARD, AND REAR YARD VARIANCES

APPROVED

 

 

 

• 5.12 DISTRICT BOUNDARY, FLOOR AREA RATIO, FRONT YARD AND BUILDING HEIGHT VARIANCES APPROVED

ZBA#lS-51

 

 

 

ZBA#15-52

 

 

MERRIT SUBDIVISION     NYS TOWN LAW §280A FOR                    ZBA#lS-53

390 Ehrhardt Road                 LOTS 3A, 3B AND SB; STREET FRONTAGE Pearl River, NY                      FOR LOTS 3A, 3B AND SB; FRONT YARD FOR

64.18 I 1I78.l   &                   LOT 3B; REAR YARD FOR LOT 3B; AND BUILDING

78.3; R-15 zone                     HEIGHT FOR LOTS 3A, 3B, AND SB APPROVED

 

 

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Minutes

Page2

 

 

OTHER   BUSINESS:

 

In response  to requests  from the Orangetown   Planning  Board,  the Zoning  Board of Appeals:  RESOLVED,  to approve  the action of the Acting  Chairperson  executing  on behalf  of the Board   its consent  to the Planning  Board  acting   as Lead Agency   for the State Environmental  Quality  Review  Act (SEQ RA) coordinated  environmental  review of actions pursuant  to SEQRA  Regulations§    617.6   (b)(3) the following  applications:

60- 70 West Dexter Plaza Condominium   Interior  Commercial  Subdivision  plan, 60- 70

Dexter Plaza,  Pearl River, NY;  68.20 I 1  I  1.130;   LI zone;  4-6 East Dexter Plaza Interior Commercial  Subdivision   Plan,  4-6 East Dexter  Plaza,  Pearl River,, NY 68.20   I 1   I 1.140; LI zone; The Club at Pearl River site plan amendment,  Blue Hill South and Veterans Memorial  Drive,  Pearl River, NY,  73.10  I 114;  PAC & OP zone;  Henry Kaufman Campgrounds/  JCC Manhattan  Amendment  to Preliminary approval  of master plan,  667

Blauvelt  Road,  Pearl River, NY 69.14 I 1I28    & 69.10   I 2 I 21;   R-80 zone;Bracken Site

Plan,  retaining  wall and patio,  31 Tweed Blvd,  Nyack,  NY 71.09  I 11    43;  R-22 zone; Brightview  Senior  Living  Lake Tappan  Site Plan,  31   Hunt Road,  Pearl River, NY 73 .15  I

1I10;     R-80 zone;  American  Legion Parking  Site Plan ,61  Hunt Road, Pearl River,  NY

73.15   I 1I2;    R-80  zone;  Pearl River Properties  Interior  Commercial  Subdivision  Plan,  73

Route 304,  Pearl River, NY 68.19  /4 I 16;   CO zone;  and FURTHER  RESOLVED,  to request   to be notified  by the Planning  Board  of SEQ RA proceedings,  hearings,  and determinations   with respect to these matters.

 

 

 

 

 

 

ADDITIONAL    BUSINESS:

Proposed Local Law relating  to Prohibited  Uses Town wide§  10.5 Review

See attached

 

 

THE DECISIONS  RELATED  TO THE ABOVE  HEARINGS   are inserted herein and made part of these minutes.

 

 

The verbatim  minutes,  as recorded  by the Board’s  official  stenographer  for the above hearings,  are not transcribed.

 

 

There being no further business  to come before the Board,  on motion  duly made, seconded  and carried,  the meeting  was adjourned  at 9: 1 OP  .M.

 

Dated: June  17,  2015

 

 

 

 

DISTRIBUTION: APPLICANT

TOWN ATTORNEY

DEPUTY TOWN ATTORNEY TOWN BOARDMEMBERS

BUILDING INSPECTOR (Individual  Decisions) Rockland County Planning

 

::c:z=o~

ZONING  BOARD  OF APPEALS

 

 

 

Deborah  Arbolino,  Administrative  Aide

 

 

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Debbie Arbolino

 

From: Sent: To:

Subject: Attachments:

Dan Sullivan <dansully113@gmail.com> Thursday, June  18,  2015 12:08 PM Debbie Arbolino

FW:  Town Board Response

CaliforniaBenzeneReference.pdf;    WisconsinCastMetalsAssociation.pdf

 

 

 

See attached. Thanks.

 

 

From: Dan Sullivan  [mailto:dansullyll3@gmail.com]

Sent: Wednesday, June 17, 2015 11:20 AM

To: Debbie Arbolino

Cc: michaelb@sabey.com;   patriziac@verizon.net;  Tjg217@aol.com;  Feroldi@optonline.net;    DrJoanSalomon@gmail.com; Dennis  Michaels

Subject: Town Board Response

 

Hi  Debbie,

Please  forward the following  to the Town Board. Thanks,

Dan.

 

 

 

Honorable    Board  Members,

 

 

With regards to the memo from John Edwards,  Town  Attorney,  dated May 27, 2015,  with regards to Proposed   Local  Law which would  add “solvents   and similar  such materials,    including   benzene,   toluene,   xylene” to the Town Code 4.41 listing of prohibited  manufacturing   uses, while we, the  Town of Orangetown  – Zoning  Board of Appeals, understand  the  desire of the Town board to expediently  address the concerns  of some town residents,  we request that the Town Board abstain from voting on this proposed law change until  further   reviews  are  performed and completed.

 

From the expert  reports  with  which   we were provided,   as well  as from the  attached documentation,    it is known that the three  gasses  mentioned surround  us, as they are found  in  nail   polish,   nail  polish   remover, gasoline,  paint  and paint thinners,   adhesives,  car exhausts,   etc. and are  the byproduct of heat  sources   such  as fireplaces,  furnaces, cars,

campfires,   grills,  charcoal,   lawnmowers,   etc. Though  undesirable,  there  are  many  areas  in the  country where foundries and refineries   operate  in close proximity  to towns  and villages.

 

We therefore  suggest that the Town  Board take the  time to hire the proper resources  to do a thorough  review  of all gases, emissions   and other  manufacturing   by-products  with the  end goal  of establishing   a local  Clean  Air Act that would address any   gasses  and  emissions   that  are found  to be dangerous. To limit  the law to the three gasses mentioned, without  a thorough,  expert review,   may  be doing  the Town  of Orangetown   and our neighbors   an  injustice.   This act would   establish a process  for independent    reviews by professional  engineers   of future  manufacturing   and R & D projects to determine  the  impact  of each  project on the  environment.    Clearly,   all new applications  would  be subject to the guidelines established   in the  Clean  Air Act, which we are sure would  also  require  that all new applications   would   be required to install   the  newest, most effective  control  measure available   at the time of review, and   be subject  to continued   regulation   by way periodic  inspections, of at least once   a year, to insure compliance with all  provi~ons of the

Clean  Air Act.                                                                                                                 381:1.:!0    ~)1~318    NMOJ.

 

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1

 

We would  also suggest that  the Town  Board create  a committee,   headed  by a Town  Board member,  which  would include  representation    from  the  Land Use Boards,  town  engineers  and  legal counsel  to work  with  the  expert consultants   to establish  the Town  Clean Air Act.

 

Kind regards, ZBA

 

 

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OFFICE     OF  THE   TOWN   ATTORNEY TOWN     OF  ORANGETOWN TOWN    HALL

26  ORANGEBURG ROAD

ORANGEBURG,   NY  10962

 

JOHN S.  EDWARDS

TOWN ATTORNEY                                                                                                                                                                                                                               TELEPHONE

(845)  359-5100

 

TERESA  M.  KENNY

FIRST  DEPUTY TOWN ATTORNEY

FAX

(845)  359-2715

 

 

 

Zoning  Board  of Appeals

20 Greenbush  Road

Orangeburg,  New York  10962

 

Attn.:   Debbie  Arbolino,  Clerk  to the Board

May 27,  2015

 

[R1~(Cf~u~~[Q)

 

MAY  2·9  2015

 

 

TOWN OF ORANGETOWN LAND USE BOARDS

 

 

Re:       Proposed   Local   Law  relating   to Prohibited  Uses Town-wide   § 10.5  Review

 

Dear Debbie:

 

 

I enclose  herewith   a copy  of  a proposed   Local  Law  under  consideration   by  the  Town Board,  which,  if  adopted,  would  add  “solvents   and  similar  such  materials,    including  benzene, toluene,    xylene”,    to  the  Town  Code   §  4.41  listing  of  prohibited    manufacturing   uses,   which

involve   the primary  production  of such items  from raw materials.

 

 

 

 

wide.

The  proposed  amendment   would  further  prohibit   waste  gasification   as a process  Town-

 

 

 

Pursuant  to Chapter  43,  § 10.5  of the Town  Code,  the Town  Board  seeks  the review  and recommendation   of the Planning  Board  with  respect  to the proposed  amendments.    Although  not required  under  the Code,  the Town  Board  would  be interested   in  the comments  of the Zoning Board  as well.  (Town Code§§   10.521     and I 0.522 identifies  the various   matters  to be considered by the Planning  Board  when making  its  comments  and recommendations,  if any.  Those  sections might  also  help  guide the ZBA.)

 

Consistent    with   the  referenced    Code  section,   the  Town   Board   would   appreciate   the Planning   Board’s    recommendation    within   30  days,  but  preferably   on  or  before  June   16,   if possible.

 

 

Thank  you,  in advance,  for your  assistance.    Please  call if you have any questions.

 

 

 

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Zoning Board of Appeals

Attention:  Debbie Arbolino, Board Clerk

May 27, 2015

Page2

 

 

 

Encl.

CC:     Supervisor and Town Board (w/o encl.) John Giardiello, Director, OBZPAE

Dennis D. Michaels, Deputy Town Attorney

Robert Magrino, Deputy Town Attorney

 

 

 

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JOHN  S.  EDWARDS

OFFICE     OF  THE     TOWN  ATTORNEY TOWN     OF   ORANGETOWN TOWN    HALL

26  ORANGEBURG  ROAD

ORANGEBURG,   NY  10962

 

TOWN ATTORNEY                                                                                                                                                                                                                                TELEPHONE

(845)  359-5100

 

TERESA  M.  KENNY

FIRST DEPUTY TOWN ATTORNEY

FAX

(845) 359-2715

 

 

 

May 26, 2015

 

Ms.  Arlene Miller

Deputy  Commissioner

Rockland  County  Department   of Planning

Dr. Robert  L. Yeager  Health  Center, Building  T

50 Sanatorium  Rd.

Pomona,  New York    10970

 

Re:       GML 239 (1) & (m) Referral

 

Proposed  Text Amendment,  Amending Town Zoning Law with Respect to

Prohibited Uses Throughout  the Town.

 

Dear Ms.  Miller:

 

 

Pursuant  to  General  Municipal   Law  §§ 239-1   & m,  enclosed  please  find Referral  Fann and supporting   documents relating  to a proposed  Local  Law,  that would  amend  the Town  Code of  the  Town  of  Orangetown,   Chapter   43,  entitled   “Zoning”,   with  respect  to  uses  prohibited throughout  the Town.

 

Also  enclosed  is a Lead  Agency  Circulation   Letter  from  the Town Board,   indicating  its intention  to act as Lead Agency  with respect  to the action.    To the extent you are able to provide you review  comments  and a response  on the issue  of Lead Agency  status prior  to June  16,   2015, your cooperation  would  be appreciated.

 

Thank  you for your attention  to the referenced  matters.

 

 

Encl.

CC:        Supervisor   Stewart  & Town  Board  (w/o encl.)

 

 

 

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ROCKLAND   COUNTY  DEPARTMENT   OF PLANNING

REFERRAL  FORM FOR GENERAL  MUNICIPAL  LAW REVIEWS

 

 

Municipality:  TOWN  OF ORANGETOWN

 

Date Sent:      April  15, 2015

 

Board         · _ Planning      

 

 

ZBA   _X_ Town!Village        Meeting Date:  May  19. 2015

 

 

File Name:                  Town  of Orangetown-  Proposed  Text Amendment  I Local Law, amending Chapter 43

• § 4.41, 4.42 and 4.45 of the Town Code, relating to Prohibited  Uses throughout the

Town  of Orangetown,  to include  additional  uses and processes

 

Contact  Person: Address

Andrew  Y. Stewart,  Town  Supervisor

26 Orangeburg  Road,  Orangeburg,  New York   10962

 

 

 

Referral  Agencies

(Please indicate the agencies that have also received copies of this application)

RC Highway  Department

RC Division  of Enviromnental   Resources

RC Drainage  Agency

RC Department   of Environmental   Health  (Sewers,  Water,  Mosquito  Code, Underground  Tanks) RC Sewer District  #1

NYS Department   of Environmental   Conservation

NYS  Department   of Transportation

NYS Thruway  Authority

NY-NJ  Trail  Conference  (Long Path) Palisades  Interstate  Park  Commission

• US Anny Corps of Engineers

Cornell  Cooperative   Extension  of Rockland  County

Adjacent  Municipality                                                                                                                                  _

.x.,    Other:   TOWN  OF ORANGETOWN   PLANNING   BOARD

 

Pursuant  to the General  Municipal  Law Article  12-B, Section

239 (n)                                    Subdivision

239 (1) & (m):              _       Site Plan    _Variance        _Special     Permit     _A_  Zone Change/Amendment

Other – Please list ———–~

Location  of Parcel( s)_  _..::;:;T…;:;o…:..;wn~-wi.;..;..;;;..;:·  d;;..;;:;e_;;;Z_.o     n=in-.;g……T-=—ex t“””‘AI-=n.._en~d=m==en:.=..:t’—————-

 

Acreage  of Parcel  (s)  N/A.                                                                                                .,.     -c::~~-

Existing  Sq. Footage                                                Proposed  Sq. Footage                      …o…. E—~-~-   0

 

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_x_

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• Brief Project Description:  Chapter 43,  §  4.4 of the Town  Code, entitled “Prohibited Uses” identifies various manufacturing  uses and processes that have been determined by the Town to be inconsistent or otherwise  not  compatible  with  the  general health,  safety  and  welfare  of  the  residents of  the  Town, particularly given the relatively dense population, and largely residential nature, of the Town. The proposed text amendment would add “solvents and similar such materials, including benzene, toluene, xylene”, to the
• 4.41 listing of prohibited manufacturing uses which involves the primary production of such items from raw materials.

 

 

The proposed amendment would further prohibit waste gasification as a process Town-wide. Variances  Needed (if applicable)                             Required                                 Provided NIA

 

Rockland County Department of Planning 9113                  {G:\All\GML\GML Referral Form]

 

 

 

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LOCAL  LAW  NO. _   OF 2015, AMENDING  CHAPTER  43, § 4.4, OF THE ZONING LAW OF THE TOWN OF ORANGETOWN  RELATING TO PROHIBITED   USES

 

Be it enacted by the Town Board of the Town of Orangetown as follows:

 

Section 1:       Chapter  43  §§  4.41,  4.42  and  4.45  of  the  Town  Code, relating  to Prohibited Uses throughout the Town of Orangetown, is hereby amended to include additional uses  and processes,  and otherwise to  clarify the nature and extent of the prohibition in the context of all such uses and processes determined to be inconsistent with the general health, safety and welfare of residents of the Town.  As amended, the said sections of the Code shall read as follows:

 

• 4.4 Prohibited uses.

 

The uses which are listed in this section are prohibited in the Town.

 

4.41    Manufacturing   uses   involving   primary  production   of   the   following products from raw materials: asphalt, cement, charcoal and fuel briquettes; chemicals, solvents and similar such materials. including benzene. toluene. xylene. aniline dyes, ammonia, carbide, caustic soda, cellulose, chlorine, carbon black and bone black, creosote, hydrogen  and oxygen, industrial alcohol, nitrates (manufactured and natural) of an explosive nature, potash, plastic    materials   and   synthetic   resins,   pyroxylin,   rayon   yarn   and hydrochloric, nitric, phosphoric, picric and sulphuric acids; coal, coke and tar products, including gas manufacturing; explosives; fertilizers; gelatin, glue and size (animal); linoleum and oilcloth; matches; paint, varnishes and turpentine; rubber (natural or synthetic); soaps, including fat rendering; and

starch.

 

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The following processes: nitrating of cotton or other materials; milling or

 

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processing of flour, feed or grain; magnesium foundry; reduction, refining,

smelting and alloying of metal or metal ores; refining secondary aluminum;

 

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refining  petroleum  products,  such  as  gasoline,  kerosene,  naphtha  and lubricating oil; distillation of wood or bones; and reduction and processing

 

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4.45

Dumps; junkyards; sewage treatment plants; waste gasification and similar

such facilities; incinerators not accessory to a principal use; and sanitary

 

landfill  operations  not accessory  to a principal  use;  except any of the above when municipally   owned  and operated.

 

 

 

State.

Section 2:       This law shall take effect immediately upon filing with the Secretary of

 

 

 

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JOHN  S. EDWARDS

OFFICE      OF   THE     TOWN      ATTORNEY

TOWN     OF   ORANGETOWN

TOWN     HALL

26  ORANGEBURG    ROAD ORANGEBURG,            NY  10962

 

TOWN ATTORNEY                                                                                                                                                                                                                                TELEPHONE (845) 359-5100

 

TERESA  M. KENNY

FIRST DEPUTY TOWN ATTORNEY

FAX

(845) 359-2715

 

 

 

May 26, 2015

 

 

 

 

Lead Agency Coordination  Letter  From The Town of Orangetown, With Request for Expedited  Response

 

 

 

Re:      Proposed Text Amendment,  Amending Town Zoning Law with Respect to

Prohibited  Uses Throughout   the Town.

 

 

 

Dear Sir or Madam:

 

The Town Board of the Town of Orangetown, Rockland County, New York is hereby notifying you that, at its meeting held on the lih  day of May 2015, the Town Board adopted a resolution in connection with a proposed action, to wit, a proposed Local Law, that would amend the Town Code of the Town of Orangetown, Chapter 43, entitled “Zoning”, with respect to uses prohibited throughout the Town  (i) declaring its intention to act as Lead Agency under SEQRA; (ii) making the preliminary determination that the action is an ”unlisted” action under SEQRA; (iii)  directing  that  a  SEQRA  Coordination  letter be  circulated to  all potential  Involved or Interested Agencies;  and  (iv) directing that the matter be circulated to the  County Planning Department   for   GML   review   and  to   the   Town   Planning   Board   for  its  review  and recommendation under the Town Code.

 

As stated, the Town Board has made a preliminary determination that the action proposed is subject to review under the State Environmental Quality Review Act (“SEQRA”), and that such action constitutes an “Unlisted” action. The Town Board, by Board resolution, has expressed its intention to serve as Lead Agency for the action and, pursuant to Sections 617.6(b) and (c) of the N.Y.C.R.R., and requests your agreement that it be so designated.

 

The Town Board further wishes to expedite the designation of the Lead Agency and has enclosed a self-addressed, stamped envelope for your prompt reply.  If you agree to the Town Board being

designated Lead Agency, please sign the enclosed copy of this letter and return ~t to the ~fihcf of

the Supervisor of the Town of Orangetown as soon as possible.  If yOb~ ~He~ d~~hit   s{illm1t a

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NM013DN\1’d0  .:10   Nfl\01

 

SEQRA Coordination  Letter

May26,2015

Page2

 

 

 

 

written objection within 30 days of the mailing of this notification, the Town Board will assume the role of lead agency for this action.

 

Enclosed please find a Short Environmental Assessment Form, and other relevant documents and information, including vicinity maps and the referenced earlier reviews.

 

 

Very truly yours,

 

 

 

The                                                                        agrees to the designation of the Town Board of the Town of Orangetown as lead agency for the above-referenced project.

 

(Print Name and Title) Encl.

CC:     Andrew Y. Stewart, Supervisor

Charlotte Madigan, Town Clerk

TO:       INVOLVED AND INTERESTED  AGENCIES: Rockland County Department of Planning

BuildingT

50 Sanatorium Rd.

Pomona, New York  10970

 

Orangetown Planning Board

20 Greenbush Road

Orangeburg, New York  10962                                 30\.:1.:10 S~l!31Q    NMOl

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617.20

Appendix B

Short Environmental  Assessment  Form

• ··——–·—··-·——·———·—–··——–·—-·—-·-.. ————————–·–·-·-·—-··-···———-~—-·-··—·–······-·-·—·-··

 

Instructions for Completing

 

Part  1  – Project  Information.  The applicant or project sponsor is responsible  for the completion  of Part  1.  Responses become part of the application for approval or funding, are subject to public review, and may be subject to further verification. Complete Part 1  based on information currently available. If additional research or investigation would be needed to fully respond to any item, please answer as thoroughly as possible based on current information.

 

Complete all items in Part 1.  You may also provide any additional information which you believe will be needed by or useful to the lead agency; attach additional pages as necessary to supplement any item.

 

Part  1 – Project  and Sponsor Information

 

 

Name of Action or Project:

Local Law Amendment of Chapter 43, •zoning Code”, Section 4.4, “Prohibited Uses”

 

Project Location (describe, and attach a location map):

 

Town Of Orangetown

 

Brief Description of Proposed Action:

Amend section 4.4 of the Town’s Zoning Code to add other prohibited uses and processes. See attached amendments.

 

 

Name of Applicant or Sponsor:                                                                           Telephone:  845.3ss-8410

Town Of Orangetown Town Board                                                                             E-Mail: Address:

26 Orangeburg Road

 

City/PO:                                                                                                                            State:                          Zip Code:

Orangeburg                                                                                                                        NY                              10962

 

1. Does the proposed action only involve the legislative adoption of a plan, local law, ordinance, NO  YES

administrative rule, or regulation?

If Yes, attach a narrative description of the intent of the proposed action and the environmental resources that

may be affected in the municipality and proceed to Part 2.  If no, continue to question 2.                                                  ~

2. Does the proposed action require a permit, approval or funding from any other governmental Agency?  NO  YES

IfY es> list agency(s) name and permit or approval:

D  D

 

3.a. Total acreage of the site of the proposed action?                                                       acres b.Total  acreage to be physically disturbed?                                                                   acres

1. Total acreage (project site and any contiguous properties) owned

or controlled by the applicant or project sponsor?                                                    acres

 

OUrban    D Rural (non-agriculture) D Industrial D Commercial   0Residential (suburban) OForest      OAgriculture 0Parldand 0Aquatic OOther (specify): 301.:L:!O   S~n1310   N

4. Check all land uses that occur on, adjoining and near the proposed action.

 

 

 

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—

D

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5. Is the proposed action,  NO YES    N/A
6. A permitted use under the zoning regulations? D  D  D

.   —-b.-Consistent wlth.the.adopted.comprehensive, plan?              ——————————-            –D- -D—D-

6. Is the proposed action consistent with the predominant character of the existing built or natural NO  YES

landscape?                                                                                                                                               D D

7. Is the site of the proposed action located in, or does it adjoin, a state listed Critical Environmental.Area? NO  YES

TfYes, identify:                                                                                                                                            D D

8. a. Will the proposed action result in a substantial increase intraffic above present levels?  NO  YES

9. Does the proposed action meet or exceed the state energy code requirements? If the proposed action will  exceed requirements, describe design features and technologies:     10. Will the proposed action connect to an existing public/private water supply?   If  No, describe method for providing potable water:     11. Will the proposed action connect to existing wastewater utilities?   If  No, describe method for providing wastewater treatment: NO D YES D NO YES D D NO D YES D 12. a. Does the site contain a structure that is listed on either the State or National Register of Historic NO YES

D  D b. Are public transportation service(s) available at or near the site of the proposed action?                          D  D c. Are any pedestrian accommodations or bicycle routes available on or near site of the proposed action?    D  D

 

 

 

Places?

1. Is the proposed action located in an archeological sensitive area?

D  D

D  LJ

13. a. Does any portion of the site of the proposed action, or lands adjoining the proposed action, contain NO  YES

D  D

wetlands or other waterbodies regulated by a federal, state or local agency?                                           D  D

1. Would the proposed action physically alter, or encroach into, any existing wetland or waterbody?

If Yes, identify the wetland or waterbody and extent of alterations in square feet or acres:                                     ·.                                                  …            ·

 

 

.                       ·.’.          .

D Shoreline DForest   · D Agricultural/grasslands D Early mid-successional D Wetland OUrban 0Suburban

14. Identify the typical habitat types that occur on, or are likely to be found on the project site. Check all that apply:

 

 

 

15. Does the site of the proposed action contain any species of animal, or associated habitats, listed NO  YES

by the State or Federal government as threatened or endangered?                                                             D  D

16. Ts the project site located in the I 00 year flood plain? NO  YES

I        I   .             ri

17. Will the proposed action create storm water discharge, either from point or non-point sources? NO  YES

D  D

If Yes,

1. Will storm water discharges flow to adjacent properties? ONO       DYES

..

1. Will storm water discharges be directed to established conveyance systems Doffandstorm drains)?  :

1.

If Yes, briefly describe:                                                                                         NO    []YES              M ~

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18. Does the proposed  action  include  construction   or other  activities  that result  in the impound.ment  of                  NO  YES

water or other liquids (e.g. retention pond, waste lagoon, dam)?

If Yes, explain purpose and size:

-Gl–·

——-·-··–·——–·——-·—-·—————–·—-··—-·-.-·—–·——-·-·- -r;J-

 

19. Has the site of the proposed action or an adjoining property been the location of an active or closed NO  YES

solid waste :management facility?

IfYes,  describe:                                                                                                                                                            D D

 

20. 20. Has the site of the proposed action or an adjoining property been the subject of remediation (ongoing or NO  YES

completed) for hazardous waste?

Tf Yes, describe:                                                                                                                                                           D D

 

I AFFIRM  THAT  THE  INFORMATION   PROVIDED  ABOVE IS TRUE AND ACCURATE  TO THE BEST OF MY KNOWLEDGE

Applicant/sponsor name:  Town of Orangetown                                                               Date: 5/22115

Signature:

 

 

 

Part  2-  Impact  Assessment. The Lead Agen~y Is responsible for the completion of Part  2.  Answer a11 of the fo11owing questions in Part 2 using the information contained in Part l and other materials submitted by the project sponsor or otherwise available to the reviewer.  When answering the questions the reviewer should be guided by the concept “Have my responses been reasonable considering the scale and context of the proposed action?”

 

• .·. .                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                     No, or       Moderate

.   –                                                                                                                                                …

.       .                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                   small          to large

0     D

D

impact         impact

–   .                                                                                                                                                                                                                                                                                                         ..                             [  may               may

..                                                            .    .                                                                                                                                                                                                                                                                                                                                                    occur            occur

1. Will the proposed action create a material conflict with an adopted land use plan or zoning regulations?
2. Will the proposed action result in a change in the use or intensity of use ofland?  0     D
3. Will the proposed action impair the character or quality of the existing community?  0     D

0     D

4. Will the proposed action have an impact on the environmental characteristics that caused the establishment of a Critical Environmental Area (CEA)?

 

0     D

5. Will the proposed action result in an adverse change in the existing level of traffic or affect existing infrastructure for mass transit, biking or walkway?

 

6. Will the proposed action cause an increase inthe use of energy and it fails to incorporate

D

reasonably available energy conservation or renewable energy opportunities?                                      ~

7. Will the proposed action impact ‘existing:
8. public I private water supplies? ~

0     D

1. public I private wastewater treatment utilities? ~               D
2. Will the proposed action impair the character or quality of important historic, archaeological, architectural or aesthetic resources?

 

131 ~~l             D

9. Will the proposed action result in an adverse change to natural resources (e.g., wetlands, waterbodies, groundwater, air quality, flora and fauna)?                                   301.:! .:! e  s }~}

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-·———–·-·–·–·–·-·

..

No,or        Moderate

small           to large impact         impact

  may_           may      .

occur      occur

 

 

D

10. Will the proposed action result in an increase in the potential for erosion, flooding or drainage problems?    ~
11. Wi11 the proposed action create a hazard to environmental resources or human health? ~              D

Part  3 – Determination of significance.  The Lead Agency is responsible  for the completion of Part  3. For every question inPart 2 that was answered “moderate to large impact may occur”, or if there is a need to explain why a particular element of the proposed action may or will not result ina sigrrificant  adverse environmental impact, please complete Part 3. Part 3 should, insufficient  detail, identify the impact, including any measures or design elements that have been included by the project sponsor to avoid or reduce impacts. Part 3 should also explain how the lead agency determined that the impact may or wiJ I  not be significant. Each potential impact should be assessed considering its setting, probability of occurring, duration, irreversibility, geographic scope and magnitude.  Also consider the potential for short-term, long-term and cumulative impacts.

 

The proposed amendment to Chapter 43, section 4.4 will not have moderate to large environmental impacts since it will prohibit certainuses

involving primary production and processes in the Town. See attached amendment.

 

 

 

D

Check this box if you have determined, based on the information and analysis above, and any supporting documentation, that the  proposed  action may  result in one or more potentially large or significant adverse impacts and an environmental impact statement is required.

Check this box if you have determined, based on the Information and analysis above, and any supporting documentation, that the proposed action will not result in any significant adverse environmental impacts.

 

Town Board of the Town of Orangetown                                              5/22115

Name of Lead Agency                                                                               Date

Andy Stewart

Print or Type Name of Responsible Officer in Lead Agency

 

 

Signature of Responsible Officer in Lead Agency

 

 

 

 

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Benzene  Reference   Exposure   Levels Technical Support Document for the Derivation of Noncancer Reference Exposure Levels Appendix D1

 

Public  Review Draft

June 2013

 

Air,  Community, and Environmental Research Branch Office  of Environmental Health Hazard Assessment California En9H-ldi:imitilltiall~~’l~qtion  Agency

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Benzene Reference  Exposure  Levels

Technical Support Document for the Derivation of

Noncancer Reference Exposure Levels

Appendix D1

 

 

 

 

Prepared by the

Office of Environmental Health Hazard Assessment

George V. Alexeeff, Ph.D., Director

 

 

 

 

Author

James F. Collins, Ph.D

 

 

 

 

Technical Reviewers Andrew  C. Salmon, M.A., D.Phil. Melanie A. Marty, Ph.D.

 

 

 

June 2013

 

 

 

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.     ‘   -·     .. ·-

 

Benzene RELS                                                                        PUBLIC REVIEW DRAFT  June 2013

 

 

 

 

Benzene Reference  Exposure  Levels

 

(benzol; benzo/e; cyc/ohexatriene)

 

CAS: 71-43-2

 

 

 

0

 

 

 

1      Summary

 

The Office of Environmental  Health Hazard Assessment  (OEHHA) is required to develop  guidelines for conducting health risk assessments  under the Air Toxics Hot Spots  Program (Health and Safety Code Section 44360(b)(2)).   In response to this statutory  requirement OEHHA developed a Technical Support Document (TSD) that describes  acute, 8-hour, and chronic RELs.  The TSD was adopted in December 2008 (OEHHA,  2008) and presents methodology  reflecting the latest scientific knowledge and techniques, and in particular explicitly includes consideration of possible differential effects on the health of infants, children, and other sensitive subpopulations,  in accordance with the mandate of the Children’s Environmental  Health Protection Act (Senate Bill 25, Escutia, Chapter 731, Statutes of 1999, Health and Safety Code Sections  39669.5 et seq.).  These guidelines have been used to develop the RELs for benzene presented in this document; this document will be added to Appendix  D of the TSD.

 

Benzene is a solvent, and acute high inhalation exposure may lead to eye, nose, and throat irritation and central nervous system depression  in humans.  Prolonged or repeated exposures have been associated with both blood cell proliferation and reduction in blood cell numbers, including peripheral lymphocytopenia,  pancytopenia, and aplastic anemia.  The non-cancer adverse health effects of benzene result from the ability of its metabolites to adversely affect rapidly dividing cells, especially in the bone marrow where detoxifying enzymes for its toxic metabolites are present at low levels compared to the liver.  Children may be more sensitive to benzene because so many of their tissues are undergoing rapid cell division and differentiation for growth and development to stimulate and maintain growth.  This review includes relevant material published through January 2013 and is a technical review of those studies specifically

applicable to developing non-cancer ~~..’1      §-~~ !l~’3dwMWf ic inhalation RELs for

benzene.                                                ..

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Appendix 01                                        1                                                                                             Benzene

 

Benzene RELS                                                                        PUBLIC REVIEW DRAFT   June 2013

 

 

Although benzene is  a known human carcinogen  (IARC  Group 1 ),  this document does not discuss issues  related  to the cancer potency factor.  That was derived  previously and is available   at www.oehha.ca.gov/air/hot      spots/index.html.

 

 

1.1           Benzene Acute  REL

Reference Exposure Level

 

Critical effect(s) Hazard Index target(s)

 

1.2    Benzene 8-Hour REL Reference  Exposure Level Critical effect(s)

 

Hazard Index target(s)

 

1.3   Benzene ChronicREL Reference Exposure Level Critical effect(s)

 

Hazard Index target(s)

 

27 µglm3   (0.008 ppm; 8 ppb) (for a 6 hour exposure)

Developmental   hematotoxicity   in fetal  and

neonatal   rats

Developmental;   Immune System; Hematologic  System

 

 

 

7 µg/m3   (0.002  ppm; 2 ppb)

Decreased peripheral   blood cells  in

Chinese workers

Hematologic System

 

 

 

7 µg/m3   (0.002 ppm; 2 ppb)

Decreased peripheral    blood cells  in

Chinese workers

Hematologic System

 

 

 

 

2   Physical and Chemical Properties (HSDB,   2007)

 

Description Molecular formula Molecular weight Density/Specific gravity Boiling point

Melting point

Vapor pressure Flashpoint Explosive limits

 

Solubility

 

 

 

Octano//water partition coefficient Odor threshold

 

 

 

Appendix  01

clear,   colorless   liquid

CsHs

78.1   g/mol

0.8787@  15°C/4°C

80.1  °C

5.5°C

94.8 mm Hg@  25°C  (0.125    atm)

-11 °C

upper=  8.0%   by volume   in  air lower=    1.4%  by volume   in air

miscible   with ethanol,   chloroform,    ether,   carbon

disulfide,   acetone,   oils,   and glacial   acetic acid;

slightly   soluble   in water (1,790   mg/L@  25°C)

log  Kow = 2.13

301.:l.:lO   ~)0:!318   NMOI

·~’!~

0.875 ppm (2.8 mglm3)      (Haley,   1977)

4              19??033· 21lW)srnz

 

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2                                                   Benzene

 

Benzene RELS                                                                        PUBLIC REVIEW DRAFT  June 2013

 

 

Odor description Metabolites Conversion factor

aromatic odor (sweet); gasoline-like  odor hydroquinone, .benzoquinone,  catechol, phenol

1   ppm = 3.26 mg/m3  = 42 µmol/m3

 

 

3   Occurrences and Major Uses

 

Benzene was widely used in the past as a multipurpose organic solvent.  This use was discouraged due to its high toxicity and, at least in the United States, its use as a solvent has decreased.   Present uses include benzene as a raw material in the synthesis of styrene, phenol, cyclohexane,  aniline, and alkyl benzenes and in the manufacture of various plastics, resins, and detergents.  Synthesis of many pesticides and pharmaceuticals  also involves benzene as a chemical intermediate    Benzene is emitted in large quantities from oil refineries and petroleum storage facilities.  The tire industry and shoe factories use benzene extensively.  Annual production in the U.S. was estimated to be 12.32 billion pounds (6.16 million tons) in 1993 (HSDB, 2007).  In

2010 estimated U.S. production was 1.8 billion gallons (13.3 billion pounds) (Balboa,

2011 ).

 

Benzene exposure also arises from cigarette smoking (including passive smoking), home use of solvents or gasoline, and leaking underground storage tanks (Goldstein and Witz, 2009).

 

Estimates for benzene emissions from the Statewide 2008 California Toxics Inventory

(CTI) were 1,284 tons from stationary sources,  117 tons from area-wide sources,

5,024 tons from on-road mobile sources, 4,393 tons from other mobile sources, and 46 tons from natural sources (CARB, 2008).  The top 25 benzene emitters in the Air Toxics Hot Spots program in 2008 emitted between 4.000 and 49,000 pounds per year.

 

A survey of indoor levels of volatile organic chemicals reported a geometric mean of

0.69 µg/m3  (0.22 ppb) for benzene (range=  0.29-   2.11 µg/m3)  in 29 small- and medium-sized commercial buildings in California (Wu et al., 2011 ).

 

Indoor benzene levels were measured prior to and after the Ireland Public Health Tobacco Act of 2002 ban on smoking in pubs (McNabola et al., 2006).  The average ambient concentration  of benzene measured inside two Dublin pubs in March 2004 prior to the ban was 4.83 µg/m3  (1.5 ppb ).  The average ambient level outside the pubs was

0.84 µg/m3  (0.26 ppb).  In August 2004 after the ban the average indoor level was

0.54 µg/m3  (0.2 ppb). The average ambient outside level was 0.13 µg/m3  (0.04 ppb).

 

The TEACH (Toxic Exposure Assessment,  Columbia/Harvard)  study characterized personal exposures to urban air toxics among 41 high school students living in Los Angeles in 2000 (Sax et al., 2006).  Exposure was analyzed using 48-hr personal monitoring, outdoor ambient monito~1  and in-hp..f!I~ Cl~~t     monitoring. The students

were mainly Hispanic (93%)., and w     ;   te~t9ir~~\b1titt ntffl!     okers from non-smoking

families. The mean outdoor concent~i°lfff!nfn9iYfr55fut2          µg/m3  (1  ppb), while the

 

 

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Appendix 01                                            3                                                   Benzene

 

Benzene RELS                                                                        PUBLIC REVIEW DRAFT  June 2013

 

 

mean in-home concentration was 3.87 µg/m3 (1.2 ppb). The mean personal concentration was 4.64 µg/m3  (1.4 ppb).        .

 

Nazaroff and Singer studied hazardous air pollutants including benzene within US residences. Data analyses indicated that some 16 million US juveniles (2 months to 16 years old) were exposed to benzene from Environmental  Tobacco Smoke (ETS) in the home (Nazaroff and Singer, 2004 ).  Assuming  that from 14 to 20 cigarettes are smoked per day in each residence, with an average of 430 µg benzene per cigarette, the resulting indoor air level was calculated to be 1.1-2.5 µg/m3 (0.3-0.8 ppb) and the daily intake of benzene for juveniles was 14-  31  µg.

 

In 2002 the estimated statewide ambient concentration of benzene was approximately

0.6 ppb (-2 µg/m3) (CARB, 2004). Statewide the annual average benzene concentration has decreased from -2.5 ppb in 1990 to -0.5 ppb in 2007 (CARB, 2009).

Table 3.1 shows benzene  levels in ambient air at various sampling stations in the Bay

Area Air Quality Management District in 2008. Benzene levels were determined by a modification of USEPA method T0-15, which uses gas chromatography/mass spectrometry. The minimal detectable level for benzene  is 0.014 ppb (0.046 µg/m3).

 

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Appendix 01                                        4                                              Benzene

 

Benzene RELS                                                                        PUBLIC REVIEW DRAFT  June 2013

 

 

Table 3.1. Benzene Levels llr>pb) at Monitoring Stations in the Bay Area in 2008

Station                          Average         Maximum        Minimum     Samples

Benicia –  VIP                               0.106             0.350               0.030                60

Berkeley                                       0.269             1.00                0.050               122

Bethel Island                                0.135             0.510               0.040                62

Concord – Treat Blvd.                  0.167             0.450               0.050                62

Crockett – Kendall Ave                0.116             0.250               0.040                 62

Fremont-Chapel Way 1                            0.195             0.630               0.070                40

Fremont-Chapel Way 2              0.230             0.590               0.100                31

Fort Cronkhite                              0.0681           0.200               0                       62

Livermore – Rincon Ave.             0.197             0.540               0.060                62

Martinez – Jones St                     0.172             0.610               0.030                60

Napa – Jefferson St                     0.321             1.05                0.080                62

Oakland                                        0.234             0.520               0.060                62

Oakland – Filbert St.                    0.191             0.610               0.040                60

Redwood City                              0.244             0.710               0.090                62

Richmond – 7th St                       0.165             0.320               0.020                62

San Francisco – Arkansas  1              0.176             0.410               0                       62

San Francisco -Arkansas  2       0.182             0.470               0.060                31

San Jose – Jackson St. 1                       0.316             1.11                0.050               120

San Jose – Jackson St. 2            0.296             1.00                0.110                31

San Pablo – Rumrill                     0.232             0.440               0.100                62

San Rafael                                   0.190             0.370               0.050                62

Santa Rosa – 5th St                     0.210             0.800               0.030                62

Sunnyvale – Ticonderoga            0.153             0.430               0.050                56

Vallejo – Tuolumne St                 0.196             0.660               0.060                62

Source: BAAQMD. Toxic Air Contaminant Air Monitoring Data for 2008

 

Table 3.2 shows benzene levels in ambient air at ten fixed sampling locations in the South Coast Air Quality Management  District between 2004 and 2006 taken as part of the Multiple Air Toxics Exposure Study (MATES) Ill study.  Year 1  was April 2004 through March 2005.  Year 2 was April 2005 through March 2006.  The analytical method used generally followed the EPA Method T0-15;  determination of volatile organic compounds collected in specially prepared canisters and analyzed by gas chromatography/mass  spectrometry.

 

 

 

 

 

301.:1.:10   S)IH310  NM01

Sh 2r w d    s  1nr   s102

 

– NM013~Nv}J0 .:10  NMO!

 

Appendix 01

5                                                    Benzene

 

Benzene    RELS                                                                                 PUBLIC   REVIEW   DRAFT    June  2013

 

 

Tabl e 3 2   Benzene

Leves  at 10 F’rxe d Sites  m.    SOUth Coas t m.    2004 through  2006

Year  1   (4/2004  –  3/2005)              Year  2 (4/2005  –  3/2006)

 

Location Anaheim	Mean 0.44	ppb	SD 0.28	Samples 118	Mean 0.42	ppb	SD 0.33	Samples 115
Burbank	0.73		0.42	118	0.69		0.44	122
Central   LA	0.59		0.30	117	0.57		0.31	121
Compton	0.82		0.70	118	0.78		0.67	118
Inland  Valley	0.49		0.24	115	0.49		0.24	116
Huntincton   Park	0.76		0.46	98	–		–	–
North  Lone  Beach	0.56		0.35	119	0.48		0.34	118
Pico  Rivera	0.57		0.32	121	–		–	–
Rubidoux	0.45		0.25	114	0.43		0.26	120
West  Lonq  Beach	0.57		0.44	114	0.50		0.38	120

Source:   http://www.aqmd.gov/prdas/mateslll/Final/Appendices/f•

MA TESI  I IAppendixVI    Final92008.pdf

 

Note that  all the  levels   in Table   3.2   are higher  than  the  highest   mean  value   (0.321   ppb) in the  Bay Area  {Table   3.1  ).   Table   3.3   shows  benzene   levels   from  ten  sites   in  a subproject   of MATES  Ill  in which  mobile   monitoring    stations   (microscale)    were intentionally     put near  a known  emission    source  and  the  results   compared   to a fixed  site nearby  over  a period  of three  to ten  months.

 

Site Monitor Mean (ppb) SD Samples Time  interval Commerce Microscale* 0.69 0.33 62 11   /2004  –  5/2005 Huntinoton   Park Fixed 0.93 0.52 46 “ Indio Microscale 0.21 0.1 26 3/2005  –  5/2005 Rubidoux Fixed 0.39 0.23 26 “ San  Bernardino Microscale 0.73 0.38 45 10/2004  –  2/2005 Inland   Valley(SB) Fixed 0.51 0.28 46 “ Sun Valley Microscale 0.52 0.23 91 6/2005  –  3/2006 Burbank Fixed 0.75 0.46 101 “ Santa  Ana Microscale 1.04 0.6 47 9/2005  –  1 /2006 Anaheim Fixed 0.61 0.4 46 “

Table 3.3.   Benzene Levels (ppb) at Monitoring Stations in South Coast 2004–2 006

 

 

 

*A mobile   monitoring   device   was  intentionally   located   near  a known  emission    source. Source:   http://www.aqmd.gov/prdas/mateslll/Final/Document/e•

MATESlllChapter5Final92008.pdf

 

Benzene    exists   mostly  in  the vapor  phase.     It reacts  with  photochemically    produced hydroxyl   radicals    with  a calculated     half-life    of 13.4   days.    In atmospheres    polluted  with NOx or S02  the  half-life    can be as short  as 4-6  hours

(http://www.   epa. gov Iogwdw/pdfs/f  actsheets/voc/tech/benze    n e. pdf).

 

 

Appendix   01

–3_?1.:LJO  S>ltl310     N!r\Ol

OS ~I Lid    8    1nr  SIOZ

 

N~OL3vN\;tliQ    .:10  Nlt\Ol               Benzene

 

Benzene RELS                                                                         PUBLIC REVIEW DRAFT  June 2013

 

 

4   Metabolism

 

Inhalation of benzene is the principal route of concern for the general public; approximately  half the benzene inhaled by humans is absorbed (Nomiyama and Nomiyama,  1974; Pekari et al., 1992).  In men and women exposed to 52-62 ppm benzene for 4 hours, 46.9 percent of the inhaled dose was absorbed.  Of this absorbed fraction, 30.1 percent was retained and 16.8 percent was excreted unchanged in the expired air (Nomiyama and Nomiyama, 1974 ).

 

After absorption, benzene targets the liver, the kidney, the lung, the brain, and the blood-forming  bone marrow.  The parent compound likely causes the acute neurotoxic effects.  Benzene metabolism is depicted in Figure 4.1.

 

(1) Benzene is metabolized in the liver to benzene epoxide by the cytochrome  P450 system, primarily CYP2E1 (but also to varying extents by CYP1A1, CYP2B1, CYP2F1, and CYP2F2).  Benzene epoxide has a half-life of approximately  8 minutes in rat blood (Lindstrom et al., 1997) and thus could travel from the liver to other organs including bone marrow.

 

(2) Benzene epoxide rearranges nonenzymatically  to phenol, initially the major metabolite of benzene.  Phenol is oxidized, also by CYP2E1, to hydroquinone. Hydroquinone can be oxidized to the toxic metabolite benzoquinone  non-enzymatically by 02 or enzymatically  by myeloperoxidase  (MPO) in bone marrow.  Benzoquinone can be converted back to hydroquinone by NAD(P)H:quinone  oxidoreductase  (NQ01 ), a detoxifying reaction.

 

(3) Benzene epoxide is enzymatically transformed  by microsomal epoxide hydrolase to benzene dihydrodiol, which is then dehydrogenated  to catechol by dihydrodiol dehydrogenase.

 

Most of the catechol and phenol metabolites are excreted within 24 hours in the urine, while hydroquinone  requires 48 hours {Teisinger et al., 1952).

 

(4) Benzene epoxide is also metabolized to a ring-opened product, trans, trans• muconaldehyde.   t,t-Muconaldehyde  can be metabolized to t,t-muconic acid (oxidation) and to 6-hydroxy-t,t-2,4-hexadienal   (reduction)(not  shown in Figure 4.1 ).

 

(5) Benzene epoxide can be conjugated with glutathione by glutathione-S-transferases to ultimately form S-phenylmercapturic  acid (SPMA).

 

(6) Benzene epoxide also equilibrates with its oxepin, a seven-atom  monocyclic structure, which may be an intermediate in one or more of the previous pathways (Figure 4.1 ).

 

(7) The benzene metabolites ~~~.:\iV6~~~~1Bu~h’8>henol,  catechol, hydroquinone, and

1,2,4-benzenetriol)  can form 8!f~~5Lf8d  ~~c~Hrim~s   (Nebert et al., 2002), and

 

 

NMOl3~NVhlO   .:10   NM01

Appendix01                                      7                                               Benzene

 

Benzene  RELS                                                                        PUBLIC REVIEW DRAFT   June 2013

 

 

quinol  thioethers   after  reaction with  glutathione   (Bratton  et al.,   1997)  as part of phase II

metabolism (not  shown in  Figure 4.1 ).

 

(8) Benzene  metabolites  can form adducts  with  DNA and proteins,   especially  albumin.

 

Figure 4.1.  Intermediary   metabolism  of benzene

 

 

 

~

HOY

SG

H   H

I                         I

OHC -C=C-C=C-CHO

I                    I

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H

TR.o:..r~s. TRi’.NS•

 

PREMERCAPTURIC

ACID     \G\s H

o~   ~o

yr·..iu,coXr1J,O:..LD:EH]YDE

 

~ I                            cy_to_P__-4_5o..

• HZJ ~l OH           [OJ

~SH

0

 

O-c-,                      [OJ

srnzrnE       1     srnzrnE

EPOXIDE          ~~H          ?

t0oH

DIOL

 

OXIDE                         OXEPlrv

f•JOf•JEf•JZYMATIC          RE.’,RR~.f·JGEMEfoIT

 

6

OH                                                   OH

0   [OJ

HYDROLi’.SE

 

 

 

[OJ

DIHYDRODIOL

DEHYDROGrn.O:..SE

 

 

OH

-yoH

EPOXIDE

 

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OH

HYDROQUlr~ONE

..,

PHErvOL

i

,.     CMECHOL

 

0o                           “-. ”,,.._ i:O$H r

 

,, … “‘

 

“-…,)OJ                                                         [OJJ,..,..,.

 

OH_../

 

 

0                                                             OH

(0Jo

 

 

p . BErvZOQU1rvor1JE

1,    2, 4 . TRIHYDROXY  srnzrnE

o-  BErvzoqu1rvorvE

 

 

Source: Benzene.  Environmental    Health   Criteria.    150 (World  Health  Organization,    1993)

 

The metabolites  found  in  individual   experiments   depend  on the  species  and  the exposure conditions.     As an  example,  Table  4 compares the percentage   of water soluble metabolites in 24 hour urine samples  from mice  and  rats exposed to either

5 ppm  or 600 ppm benzene  for the first  6 of the 24 hours (Sabourin   et al.,   1989).

 

 

Appendix   01

30l.:1.:JO   9:18310     NMOl

es 2I   Lld    s   1nr srnz

 

NMOl3DN\;fUO     .:JO    Ni\°Wl

 

 

Benzene

 

Benzene RELS                                                                        PUBLIC REVIEW DRAFT  June 2013

 

 

5ppm (3 mice) 600 ppm (3 mice) 5ppm (2 rats} 600 ppm (3 rats) Phenyl glucuronide 1 15 1.4 1 Catechol glucuronide Non-detect Non-detect Non-detect Non-detect Phenyl sulfate 36 52 56 73 Hydroquinone monoglucuronide 26 9 8.5 0.5 Hydroquinone 6.6 2.3 2.9 1.5 sulfate         Pre- phenylmercapturic 6 15 9.5 17 acid         Phenylmercapturic 1 Non-detect 1.3 1 acid         Muconic acid 23 5 18.5 4 Unknown Non-detect Non-detect 1.4 Non-detect Total 99.6 98.3 99.5 98

Table 4.1. Percentageof water soluble metabolites in 24 hour urines (Sabourin et al., 1989)

 

 

 

Benzene causes hematotoxicity through its phenolic metabolites, which lead to DNA strand breaks, chromosomal damage, sister chromatid exchange (SCE), inhibition of topoisomerase  II, and damage to the mitotic spindle.  The myelotoxic (and carcinogenic) effects of benzene are associated with free radical formation either as benzene metabolites, particularly benzoquinone, or as lipid peroxidation  products (Smith et al.,

1989; USEPA, 2002; Rana and Verma, 2005).  The effects of intraperitoneal  injection of benzene and various of its metabolites on erythropoiesis were studied in mice in vivo (Snyder et al., 1989).  The most potent inhibitor of red blood cell (RBC) production was

a mixture of hydroquinone (50 mg/kg) and t,t-muconaldehyde  (1  mg/kg).  Several other

metabolites also inhibited red cell formation.

 

Transgenic  mice, in which the gene for CYP2E1 has been knocked out (cyp2e1-1-),  do not show toxicity when exposed to 200 ppm benzene for 6 hr (Valentine et al., 1996). CYP2E 1   protein and its associated enzymatic activity were not detected in early fetal human liver samples (Vieira et al., 1996).

 

Transgenic  male mice, in which the gene for microsomal epoxide hydrolase was knocked out, did not show benzene toxicity (e.g., decreased white blood cell (WBC) counts) when exposed to 50 ppm benzene for two weeks, while control male mice did

 

(Bauer et al., 2003).  In humans, susceptibility to chronic benzene poisoning has been related to the epoxide hydrolase QJO~      ~~~b8n,..?,pP8).  Specifically the risk of

benzene poisoning increased in the subjects wffh m1cPO~oma1 epoxide hydrolase

(EPHX1)GGAC/GAGTdiplotypeQt~J~:W-5~ orilfr’\’frlrAGT  diplotype(P =

 

NMOl3DN’t/~O  .:IO NMOl

Appendix 01                                        9                                               Benzene

 

Benzene RELS                                                                 PUBLIC REVIEW DRAFT June 2013

 

 

0.00086).  Surprisingly, neither diplotype altered the level of microsomal epoxide hydrolase enzyme activity.

 

Yoon and co-workers investigated the involvement of the aryl hydrocarbon receptor (AhR) in benzene hematotoxicity using wild-type (AhR+/+),heterozygous (AhR+1-),   and homozygous null (AhR_,_) male mice (Yoon et al., 2002).  No hematotoxicity and no changes in peripheral blood and bone marrow cells were induced in AhR_,_ mice by a 2- week inhalation exposure to 300 ppm (978 mg/m3)  benzene.  The lack of hematotoxicity

was associated with the lack of p21 over-expression,  regularly seen in wild-type mice

following benzene inhalation.  (p21, also known as Cdkn1a in mice and CDKN1A in humans, is a cyclin-dependent  kinase inhibitor important in the braking of the cell division cycle.)  Combined treatment of AhR_,_ mice with two benzene metabolites (phenol and hydroquinone) induced hematopoietic toxicity.  The aryl hydrocarbon receptor may have a role in the regulation of hematopoiesis and in benzene-induced hematotoxicity (Gasiewicz et al., 2010).

 

In Wistar rats of both sexes with a large body fat content, benzene was eliminated more slowly and remained in the body for a longer time than in rats with a small body fat content.  Accordingly, the decrease in WBC during chronic benzene exposure was seen only in rats with large volumes of fat tissue. In humans, the elimination of benzene was slower in women than in men. The slower elimination in women is due primarily to the bulky distribution of body fat tissue. The authors concluded that women may be inherently more susceptible to benzene, which has a high affinity for fat tissue (Sato et al., 1975).

 

The pharmacokinetics  of benzene follows a two-compartment  model in the rat.  The rapid phase has an elimination half-life (t112)   of 0. 7 hours, and the t112  for the longer phase is 13.1 hours  (Rickert et al., 1979).  The long elimination half-life for benzene is due to the formation of catechol, quinone, and hydroquinone in the bone marrow.

These reactive metabolites are not readily excreted, and are cytotoxic to the stem cells

in the bone marrow (Greenlee et al., 1981).

 

A three-compartment  model was fit to human data on benzene disposition and bone• marrow metabolism (Watanabe et al., 1994).  The general relationship between cumulative quantity of metabolites produced and inhalation concentration, was S• shaped, inflecting upward at low concentrations, and saturating at high concentrations.

 

Kim, Rappaport and associates studied the relationships between levels of five benzene  metabolites and benzene exposure among 250 exposed and 136 control Chinese workers (Kim et al., 2006a; Kim et al., 2006b}.  Benzene metabolism was nonlinear with  increasing benzene levels above 0.03 ppm.  They then statistically tested whether  human  metabolism of benzene is better fit by a kinetic model having two pathways  rather than only one (i.e., CYP2E1) (Rappaport et al., 2009).  Michaelis• Menten-like  models were fit to urinary benzene metabolites and the corresponding air concentrations  of benzene (range:<  0.0013feR913″{)299.):bpiffi(~*  mg/m3))   for 263 nonsmoking  Chinese females.  The different values of Akaike~  i.nf.c,)fmation criterion

es zi~tJd   9   1nr ~tut

 

 

Appendix 01

tU\013~NV”d0 .:!O  NMOl

Benzene

 

Benzene RELS                                                                         PUBLIC REVIEW DRAFT  June 2013

 

 

(AIC) obtained with the two models gave strong statistical evidence favoring two metabolic pathways.  The low-affinity pathway (likely due to CYP2E1.) had an affinity (“Km11)        of 301 ppm (981 mg/m3)  for benzene in air; the value for the high-affinity pathway (unknown but possibly due to CYP2F1 or CYP2A13) was 0.594 ppm, a 500- fold difference. The exposure-specific  metabolite level predicted by the two-pathway

model at non-saturating  benzene concentrations was 184 µM/ppm of benzene, which is

close to an independent estimate of 194 µM/ppm for a nonsmoking Chinese female (Weisel et al., 2003).  Rappaport estimated that a nonsmoking woman would metabolize about three times more benzene from the ambient environment  under the two-pathway model (184 µM/ppm) than under the one-pathway  model (68.6 µM/ppm). A follow-up study examined the individual urinary metabolites of benzene in each woman

(Rappaport et al., 2010).  The data indicated that the predicted high-affinity enzyme is

predominant at less than 1   ppm and favors the ring-opening pathway to t, t•

muconaldehyde  (see Figure 4.1 ).  The concept of increased efficiency

in benzene metabolism at levels below 3 ppm has important implications for low level environmental  exposures.  The concept has been challenged (Price et al., 2012; 2013) and defended by the original authors (Rappaport et al., 2013).

 

4.1  Physiologically-based  Pharmacokinetic Modeling

 

Based partly on an early PBPK model for styrene (Ramsey and Andersen,  1984), Medinsky and coworkers developed a model to describe the uptake and metabolism of benzene in F344/N rats and 86C3F1  mice and to determine if the observed differences in toxic effects between mice and rats could be explained by differences in metabolic pathways or by differences in uptake (Medinsky et al., 1989a).  For inhalation concentrations  up to 1,000 ppm (3,260 mg/m3)  for six hours, mice metabolized at least two to three times as much total benzene (per kg body weight) as rats.  In regard to metabolites, rats primarily formed phenyl sulfate, a detoxification  product (see Table 4). In addition to phenyl sulfate, mice formed hydroquinone glucuronide and muconic acid

which are part of toxicity pathways.  The formation of hydroquinone showed the greatest difference between mice and rats.  Metabolic rate parameters (Vmax and Km) were

affinity, high capacity.  Model simulations suggested that hydroquinone and muco~c ~ –f acid comprised a larger fraction of the total benzene metabolized at lower benze~ levels for both rats and mice than at higher levels (where detoxification  metabolites: tM 2 ~ z predominated).  (See also Table 4.1)                                                                           ~ .- ~ rn 0) o

very different for hydroquinone conjugation and muconic acid formation compared to formation of phenyl conjugates and phenyl mercapturic acids.  Assumed toxication pathways had high affinity, low capacity kinetics; detoxification  pathways were low

 

 

 

 

 

 

The animal model was extended to predict benzene metabolism in people expos~   near     ~

occupational exposure limits in effect at the time of the paper’s publication (Medin~y @    ~

al., 1989b). For 8 hr inhalation exposures less than 10 ppm (32.6 mg/m3),  metabo1iles,of 1                    ~

hydroquinone, the precursor of the toxic benzoquinone,  were predicted to predomlaat&’l  1                     o

in people.  Lower levels of muconic acid, a metabolite of muconaldehyde,   were   ~    ·    ~      ~

predicted below 10 ppm.  Above 10 ppm, detoxification  metabolites, including phenyl conjugates, predominated  (Medin-sky-et al., 1989a).

…..                         .     ……

 

 

 

Appendix 01                                       11                                                                Benzene

 

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A PBPK model, based on that of Medinsky above,   was developed to describe  the disposition    of benzene in 3 and 18  month-old C57BL/6N  mice and to examine  the key parameters   affecting changes in  benzene  disposition    with  age (McMahon et al.,  1994). The model  included a rate constant  for urinary elimination    of metabolites   as an age• related   increase in  Km for production  of hydroquinone   conjugates from benzene.   The study indicated that age-related   changes in physiology,    including   decreased elimination of hydroquinone  conjugates at 18 months,   were  responsible for altered disposition    of benzene  in aged  mice.

 

Travis  and colleagues   developed  three PBPK models  to describe  the pharmacokinetics of benzene  in mice,  rats,  and humans,   respectively,    using  five  anatomical compartments:   liver,  fat,  bone  marrow,   muscle (poorly  perfused),   and other  richly perfused  organs (e.g.,    brain,   heart,   kidney, and viscera),    all  interconnected   by the

arterial  and venous blood flow (Travis  et al.,  1990).     Benzene metabolism  showed Michaelis-Menten  kinetics and occurred  primarily in the liver  (human   Vmax = 29.04 mg/h) and  secondarily   in the bone  marrow (human  Vmax = 1.16  mg/h).  Graphical

comparison of model results  with empirical   data in  the three species  from previously published reports was quite   favorable for exposure by inhalation   and gavage,  and from intraperitoneal    and subcutaneous    injection.

 

Bois  and colleagues   modeled   the distribution   and metabolism   of benzene in  humans using population   pharmacokinetics,   Bayesian   statistical   inference,  and  PBPK modeling (Bois et al.,  1996).    Using  existing data, they derived  distributions    for  model parameters. The model  adequately  fit both  prior physiological    information   and recent experimental data (Pekari  et al.,   1992).    An estimate  of the  relationship   between  benzene  exposure

up to 10 ppm (32.6 mg/m3)  and the median population    fraction metabolized  in  the bone marrow is 52 percent  (90% Cl =  47-67%),   and was linear in  the  three subjects   studied

by Pekari   et al.  (1992).     At 1   ppm continuous   exposure, the occupational   inhalation exposure threshold   in the U.S.,  the estimated  quantity metabolized in the bone marrow ranged from 2 to 40 mg/day, a 20-fold  variation.

 

Cole and coworkers developed  a PBPK model in mice  to relate  inhaled   benzene  levels to tissue  doses of benzene,   benzene   oxide,  phenol,   and  hydroquinone   (Cole  et al.,

2001 ).   Parameter values  in  the  literature   were used.  Additional parameters, estimated by fitting the model   to published   data, were first-order rate constants (ki)  for pathways lacking in vitro data  and the concentrations   of microsomal   and cytosolic  protein.   The model was constrained by using   the in  vitro metabolic   parameters  (Vmax, first-order

rate constants  (ki),  and saturation   parameters),   rather than in vivo values.   Even  though data from  multiple laboratories   and experiments   were  used,  model simulations    matched the data reasonably   well in  most cases.  No extrapolation  to humans  was attempted.

 

Yokley and associates  developed a human  PBPK model  that quantified    tissue  levels  of benzene, benzene  oxide,   phenol,    and hydroquinone   after inhalation   and oral benzene exposures   (Yokley  et al.,   2006).    The model  was i~~~~)’fc»l~W1 framework that acknowledges   sources of variation  due to inh1{§n~W1)   a~   inl’~dual

 

 

 

Appendix 01                                           12

 

Benzene RELS                                                                         PUBLIC REVIEW DRAFT  June 2013

 

 

variation, measurement  error, and other data collection issues. They estimated the population distributions of key PBPK model parameters. They hypothesized that observed interindividual variability in the dosimetry of benzene and its metabolites resulted primarily from known or estimated variability in key metabolic parameters and that a statistical PBPK model that explicitly included variability in only those metabolic parameters would sufficiently describe the observed variability. They identified parameter distributions for the PBPK model to characterize observed variability through the use of Markov chain Monte Carlo analysis applied to two data sets. The identified parameter distributions described most of the observed variability, but variability in physiological parameters such as organ weights may also be helpful to predict the observed human-population  variability in benzene dosimetry.

 

Various benzene exposure scenarios were simulated for adult men and women using

PBPK modeling (Brown et al., 1998). Women had a higher blood/air partition coefficient

and maximum velocity of metabolism for benzene than men.  Women generally h~   a S   ~

higher body fat percentage than men.  Physicochemical  gender differences  resulbid in~      :E

women metabolizing 23-26 percent more benzene than men in the same scenari~    ;:=    ~

although benzene blood levels are generally higher in men.  The authors stated tnat            .,,

women may be at higher risk for certain effects of benzene exposure.

 

 

5  Acute  Toxicity  of Benzene

 

5.1 Acute Toxicity to Adult Humans

11   f-..& I       “1

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Deaths from acute exposure to benzene are often related to physical exertion and release of epinephrine with subsequent cardiac failure.  Frequently, the person trying to rescue a collapsed victim will die during the effort of lifting the unconscious person (HSDB, 2007).  Anesthesia  may develop at concentrations  above 3,000 ppm (9,600 mg/m3).       At exposures greater than 1,000 ppm (3,200 mg/m3)    (duration unspecified), CNS symptoms include giddiness, euphoria, nausea, and headaches; heightened cardiac sensitivity to epinephrine-induced  arrhythmias may develop (Snyder, 1987). These effects may be accompanied  by symptoms of mild irritation to the eyes and mucous membranes.  Acute hemorrhagic pneumonitis is highly likely if benzene is aspirated into the lung (HSDB, 2007).  Respiratory tract inflammation,  pulmonary hemorrhages,  renal congestion, and cerebral edema have been observed at autopsy in persons with acute benzene poisoning.  In these cases, blood levels of 2 mg percent (2 mg/100 ml) benzene were not associated with hematological changes (Winek and Collom, 1971).

 

A case report described three deaths due to acute benzene poisoning from a shipboard accident (Avis and Hutton, 1993).  Exposure levels were not estimated.  Autopsies showed skin, respiratory, and cerebral injury.  Benzene levels in body fluids and tissues were consistent with the lipophilicity of benzene.  In a single fatal acute case of benzene intoxication aboard a chemical cargo ship (Barbera et al., 1998), the authors found

blood clots inside the heart and main vessels, multi-organ congestion, and pulmonary

 

 

 

Appendix 01                                           13                                                  Benzene

 

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edema.  They also  measured benzene (rounded to whole numbers) in several organs: liver (379 µg/g tissue),   heart (183 µg/g  tissue), brain (179 µg/g tissue),   kidneys (75 µg/g tissue),  lungs (22 µg/g tissue),  blood  (32 µg/ml),   and urine (2 µg/ml).

 

Systemic poisoning by benzene can occasionally result in neuroretinal  edema and in retinal  and conjunctiva!  hemorrhage (Grant, 1986).  Additionally,    petechial  hemorrhages of the brain,  pleura,   pericardium,  urinary tract,  mucous membranes,   and skin  may occur in cases of fatal,  acute benzene poisoning (Haley,   1977).

 

Major concerns of systemic benzene toxicity   include pancytopenia and acute myelogenous leukemia (IARC,   1982).    Both are typically   seen in chronic and subchronic exposures,   but may be of concern following   acute exposures as well.    Cells  of the

myeloid   pathway,  erythroid  in particular,  are specific targets of benzene toxicity.

 

Fifteen degassers were acutely  exposed over several   days to > 60 ppm benzene during removal  of residual  fuel  from fuel  tanks on ships (Midzenski et al.,  1992).   The maximal level  was approximately   653 ppm (2, 129 mq/rn”).    Volatilization   of benzene  from the residual fuel was the suspected source of benzene.  Twelve workers reported mucous membrane irritation.    Eleven   reported  neurotoxic   symptoms.    Workers  with  more than 2 days (8  hours/day)  of acute exposure were significantly  more likely  to report dizziness and nausea  than those with  2 or fewer  days.    Blood cell  analyses over a 4-month   period

after exposure found at least one hematologic  abnormality   consistent   with  benzene exposure in 9 degassers.   For example,   white blood  cell counts were below normal  in  4 workers.   At one year,  6 workers had  persistent abnormalities;   an additional worker,   with normal hematologic    parameters initially,    later developed an  abnormality  consistent  with benzene exposure.    Many large  granular lymphocytes  were found  in the peripheral

blood smears of six of the workers.   There were no significant associations between the presence  of hematologic abnormalities and  either the number of hours of acute

benzene exposure or the duration   of employment as a degasser    in  this study.

 

Two studies  may indicate   an acute  NOAEL   for adult humans.   Japanese students between the age of 18 and 25 breathed one of seven  organic solvents for 2. 7 to 4 hours in  a 60 m3 chamber.  No adverse effects were reported in three  males  and three females exposed  to 52-62 ppm benzene  for the full 4 hours  (Nomiyama and Nomiyama,

1974).   In  a study of the absorption  and elimination   of inhaled  benzene (Srbova et al.,

1950), the authors mentioned  that no adverse effects were seen in  23 adult volunteers exposed to 47 to 110 ppm benzene for 2 to 3 hours.   Thus 110  ppm (359 rnq/rrr’)  is a possible 3-hour NOAEL for acute effects  of benzene in humans (National   Academy of Sciences,  2009) .

 

5.2  Acute Toxicityto Infantsand  Children

 

No studies  of the effects of acute or short-term inhalation  exposure to benzene in infants and children were found in  the published  literature.381.:.L:JO      S)l>3318    NMOl

 

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5.3  Acute Toxicity to Experimental Animals

 

The oral LD50 in rats was calculated to be 3.4 g/kg in young rats and 4.9 g/kg in older rats  (Kimura et al., 1971).  Death was observed in 2 out of 10 rats exposed to

33,000 mg/m3  (10,300 ppm) for 12.5-30 minutes daily for either 1   or 12 days ((IARC,

1982)).  A 4-hour LC50 of 13,700 ppm (43,800 mg/m3)   was reported in female rats (Drew and Fouts, 1974; IARC, 1982).  An LCLo of 45,000 ppm (144,000 mg/m3)   is reported in rabbits (NIOSH, 1994 ).   In mice, an LC50 of 9,800 ppm (31,400 mg/m3)   is reported (NIOSH, 1994 ).   Leukopenia has been demonstrated to occur in rabbits exposed to 240 ppm (767 mg/m3)   for 10 hours/day for 2 weeks (IARC, 1982).

 

Brief inhalation of air saturated with benzene vapor (concentration  unknown) resulted in ventricular extrasystole in cats and primates, with periods of ventricular tachycardia that occasionally terminated in ventricular fibrillation (Sandmeyer,  1981a).

 

The RD50 is a chemical concentration that depresses the respiratory rate in mice by 50 percent due to sensory irritation of the upper respiratory tract.  An attempt to determine the inhalation RD50 for benzene was not successful (Nielsen and Alarie, 1982).  The investigators showed that inhalation of 5,800 ppm (18,800 mg/m3}  benzene in mice caused an increase in respiratory rate beginning at 5 minutes following onset of exposure.  They speculated that the stimulation of respiratory rate resulted from the action of benzene on the central nervous system.  In this study, the authors reported that benzene was not irritating to the upper airways of the animals up to 8,500 ppm (27,710 mg/m3).

~

Repeated subcutaneous  dosing of mice with benzene for 6 to 20 days resulted in E¢    ~    ~

dose-related  decrease in red blood cell production as measured by the incorporatide of~      ~

59Fe into developing erythrocytes.   The DBA mouse strain was more sensitive tharrihe  r-      o

CD-1 and C5786 strains.  Research using multiple species indicated that mice ar~ora,,      ~ sensitive to adverse effects on erythropoiesis from benzene than are rabbits whic~re         ;:u more sensitive than rats (Longacre et al., 1980; Longacre et al., 1981a; IARC, 19~).    ~      ~

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Acute exposure to benzene may disrupt erythropoiesis  and result in genotoxicity.~               6

Subcutaneous  injection of 51      13, 33, and 80 mmol/kg (390, 915, 2,577, and 6,24~     ·   :;!]     :e

mg/kg) benzene in 8- to 10-week-old, male, Swiss-Webster  mice inhibited                            :z:

erythropoiesis  in a dose-dependent  manner, as measured by uptake of radiolabeled iron in the bone-marrow 48 hours after benzene injection (Bolcsak and Nerland, 1983). Three metabolites of benzene (phenol, hydroquinone,  and catechol) also inhibited iron uptake.

 

Results from subacute exposures further illustrate the hematotoxic effects of benzene and the potential for immunotoxicity.   Inhalation of 103 ppm (334 mg/m3)   benzene for 6 hours/day for 7 days by mice caused decreased spleen and marrow cellularity and decreased spleen weights  (Green et al., 1981).  Benzene inhalation at 01      10, 30, 100, and 300 ppm (0, 32.6, 97.3, 326, and 973 mg/m3}  for 6 hours/day for 5 days resulted in a decreased host-resistance to bacterial infection by Listeria monocytoqenes

 

 

 

Appendix 01                                       15                                                  Benzene

 

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(Rosenthal and Snyder, 1985).  The numbers of L. monocytogenes  isolated from the spleen were increased in a dose-dependent  manner on day 4 of infection.  The total numbers of T- and B-lymphocytes in the spleen and the proliferative ability of the splenic lymphocytes were decreased in a dose-dependent  manner by benzene exposures of 30 ppm (97 .3 mg/m3)   or greater.  No decrement in host resistance or immune response was observed at 10 ppm (32.6 mg/m3)    benzene.  Later studies in mice have also shown that exposure to 10 ppm for a subacute duration does not significantly alter hematological parameters in blood, spleen, thymus, or bone marrow.

 

Inhalation of 0, 10, 31, 100, or 301 ppm (0, 32.6, 100.4, 326, or 978 mg/m3)  benzene for

6 hours/day for 6 days resulted in a dose-dependent  reduction in peripheral lymphocytes, and a reduced proliferative response of B- and T-lymphocytes  to mitogenic agents in mice (Rozen et al., 1984).  Total peripheral lymphocyte numbers and B-lymphocyte proliferation in response to lipopolysaccharide  (LPS) were significantly reduced at 10 ppm (32.6 mg/m3).   The proliferation of T-lymphocytes was significantly reduced at 31 ppm (100.4 mg/m3).

 

Farris et al. (1997) reported the hematological consequences of benzene inhalation in

12-week-old male B6C3F1/CrlBR mice exposed to 1, 5, 10, 100, and 200 ppm (3.26,

16.3, 32.6, 326, and 652 mg/m3)  benzene for 6 hr/day, 5 days/week for 1, 2, 4, or 8 weeks.  The study also evaluated hematology in small recovery subset groups at each

concentration  (4 weeks exposure to benzene, then up to 25 days in air).  There were no significant effects on hematopoietic parameters from exposure to 10 ppm benzene or less.  Thus 10 ppm (32.6 mg/m3)  was a NOAEL for up to 8 weeks of exposure in this study.  Exposure to 100 and 200 ppm benzene reduced the number of total bone

marrow cells, progenitor cells, differentiating  hematopoietic cells, and most blood

parameters.  Replication of primitive progenitor cells in the bone marrow was increased during the exposure period as a compensation for the cytotoxicity.  At 200 ppm, the primitive progenitor cells maintained an increased percentage of cells in S-phase through 25 days of recovery compared with controls.

 

Evans and coworkers used CD1 and C57BU6J  mice in a time-sampling  protocol to

• quantify seven categories of behavior (stereotypic, sleeping, resting, eating, grooming, locomotion, and fighting). Animal were exposed 6 hours per day for 5 days to 0, 300, or
• goo ppm (0, 960 or 2,930 mg/m3) benzene followed by two weeks of no benzene

exposure.  The authors designed the inhalation exposures to “reflect” occupational

exposure at that time.  An increase in active behavior in the form of eating and grooming was observed in both strains of mice following exposure to 300 ppm and 900 ppm benzene for 6 hours/day for 5 days (Evans et al., 1981).

 

Exposure of BALB/c male mice to 50 ppm ( 162 mg/m3)  benzene on 14 consecutive days resulted in a significantly reduced blood leukocyte count (Aoyama, 1986).

 

 

 

 

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6  Chronic Toxicity of Benzene

 

6.1  Chronic Toxicity to Adult Humans

 

The primary toxicological  effects of chronic benzene exposure are on the hematopoietic system.  Neurological and reproductive/developmental  toxic effects are also of concern

at slightly higher concentrations.   Impairment of immune function and/or various types of

anemia may result from the hematotoxicity.  The hematologic lesions in the bone marrow can lead to peripheral lymphocytopenia  and/or pancytopenia following chronic exposure.  Severe benzene exposures can also lead to life-threatening  aplastic anemia. These lesions may lead to the development of leukemia years later, after apparent recovery from the hematologic damage (Degowin, 1963).

 

Investigators observed 28 cases of pancytopenia among 32 patients in Turkey, who were chronically exposed to benzene vapors from adhesives ranging from 150 to 650 ppm (489 to 2, 119 mg/m3)  for 4 months to 15 years(Aksoy et al., 1972).  Bone marrow punctures revealed variable hematopoietic  lesions, ranging from acellularity to hypercellularity.   Central nervous system (CNS) abnormalities were reported in four of six individuals with pancytopenia following chronic occupational exposure to unknown concentrations  of benzene for an average of 6 years (Baslo and Aksoy, 1982).  The abnormalities  included reduced sensory and motor nerve conduction velocities.

 

A retrospective longitudinal study correlated average benzene exposure with total white blood cell counts in a cohort of 459 Pliofilm rubber workers in Ohio (Kipen et al., 1988). The authors found a significant (p < 0.016) negative correlation between average workplace benzene concentrations  and white blood cell counts for the years 1940-1948. A reanalysis of these data (Cody et al., 1993) showed significant decreases in red

(RBC) and white (WBC) blood cell counts among a group of 161 workers during the

During the course of employment, workers with low monthly blood cell counts were   ti ~ Cj transferred to other areas with lower benzene exposures; this potentially created a b~ c; <

1946-1949 period compared with their pre-exposure  blood cell counts.  The decline in blood counts was measured over the course of 12 months following start of exposure.

 

 

towards non-significance  by removing sensitive subjects from the study population.  0          ::==      ~ Since there was a reported 75 percent rate of job change within the first year of       f:;               .,, employment, this bias could be highly significant.   In addition, there was some indic~on en   g

that blood transfusions were used to treat some “anemic” workers, which would cause   ,,      l;:i.. serious problems in interpreting the RBC data, since RBCs have a long lifespan (1~       :3     ~ days) in the bloodstream.  Two of Cody’s co-authors performed the exposure analyms  ~   J        ~ and determined a range of monthly median exposures of 30-54 ppm throughout thg12-cr,      ~

month segment examined (Crump and Allen,  1984).  Despite the above-mentioned       ~       z

potential biases, workers exposed above the median concentrations  displayed

significantly decreased WBC and RBC counts compared with workers exposed to the lower concentrations  using a repeated measures analysis of variance (ANOVA).

 

The mortality from all cancers and leukemia, in addition to hematologic parameters, was investlqated !n-male workers exposed to benzene for 1-21 years between 1952 and

 

 

 

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1978   at a Gulf Oil refinery in Texas (Tsai  et al.,   1983).    The cohort  of 454 included maintenance workers and  utility men  and  laborers  assigned to benzene  units  on a “regular  basis”.  Exposures to benzene  were determined using personal   monitors.    The median  air concentration  was 0.53  ppm (1.7   rnq/rrr’) in  the work areas of greatest exposure to benzene  and the average length  of employment was 7.4 years.   The analysis of overall  mortality revealed   no significant   excesses.   Mortality from all  causes (SMR = 0.58,  p :5  0.01) and from diseases of the circulatory system (SMR  = 0.54, p :5

0.05)  was significantly   below expected  values based  on comparable groups of U.S. males.    The authors concluded that a healthy  worker effect was present.   An internal comparison  group  of 823 people, including 10 percent of the workers  who were employed  in  the same plant in operations not related   to benzene,   showed  relative  risks (RR) of 0.90  and 1.31    for all causes and cancer at all  sites,  respectively  (p < 0.28 and

0.23).  A subset of 303 workers was followed  for medical   surveillance.    Up to four hematological    tests per year were  conducted.    Total  and differential   WBC counts, hemoglobin,    hematocrit,   RBC,  platelets, and clotting times were found to be within normal   (between  5% and 95% percentile)   limits  in  this group.   (This study was the basis of OEHHA’s  previous  chronic REL of 60 µg/m3.)

 

Complete blood count (CBC)  data from employees  who had  ever participated    in the Shell  Benzene   Medical  Surveillance    Program were compared to employees  who had not participated (Tsai et al.,  2004 ).   The study  included   1,200 employees   in the surveillance   program (mean  eight  hour TWA benzene   exposure of 0.60 ± 5.60 ppm (median   = 0.1   ppm)  (2 ± 18  mg/m3)  from 1977  to 1988  and of 0.14  ± 0.82  ppm (median=   0.1 ppm) (0.5  ± 2.7  mg/m3)  since  1988) and  3,227 comparison  employees. The study  evaluated  abnormality   of six blood  count parameters    (WBC,   lymphocytes, RBC,   hemoglobin,    mean  corpuscular   volume (MCV),   and platelets)   and  the  adjusted mean  values of these parameters in  the  exposed   group.  No  increased abnormality  of the six  parameters was found among  exposed employees,    however   a significant

decrease (p = 0.02)  in the MCV was seen in the exposed  workers.  The mean values of the exposed employees,  adjusted for age, gender,   race, amount of time between  first and last  exam, and current  smoking,   were similar to those in the comparison group.  No adverse hematological    effects were found.   However,  the “exposed”  group  had  a very wide range  of benzene  exposure levels  as evidenced  by the reported  mean,  standard deviation,  and median values.   The coefficient of variation (SD/mean) was greater than

100  percent.   The median exposure value of 0.1 ppm (0.326  mg/m3)  means that half  the workers were exposed  below  that  level.

 

Routine  data collected from 1980 to 1993  for Monsanto’s   medical/industrial     hygiene system were used  to study  387 workers with  daily  8-hour  time-weighted  average exposures (TWA)  of 0.55 ppm benzene  (1.8   mq/rn”)  (range=   0.01   –  87.69  ppm;  based on 4213 personal  monitoring  samples;    less than 5 percent exceeded 2 ppm)  (Collins et al.,  1997).    Controls were 553 unexposed workers.   There was no  increase in the prevalence of lymphopenia,   an early,  sensitive  indicator of benzene  toxicity,   among

exposed  workers (odds  ratio=   0.6;   95% confidence   interval  (Cl)=   0.2 to 1.8),   taking into

account smoking,   age, and sex.  There also  was no increase  in  risk am~~!!J.:@j) W<iir.fil!ltS)  NMG 1

exposed for 5 or more years (odds   ratio=   0.6;  95% Cl = 0.2 to 1.9).   There were no        lnp  SlUZ

19  Zl   Lld   9       II       .

 

 

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Nh\OJ  3~N’ftl0   ::10   Nri\Ol

Benzene

 

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differences between exposed and unexposed workers for other measures of hematotoxicity,  including mean.corpuscular  volume and counts of total white blood cells, red blood cells, hemoglobin, and platelets.

 

Between 1967 and 1994 a cohort of 105 workers exposed to low levels of benzene (as measured by personal monitors) was studied at a small petroleum company in Texas (Khuder et al., 1999).  The exposure ranged from 0.14 ppm to 2.08 ppm (0.46. to 6.78 mg/m3)  (8-hour TWA) (mean±  1   SD=  0.81±0.72  ppm).  The mean complete blood counts (CBC) were within the normal range, as were the WBC.  Other CBC values (RBC, hemoglobin level, MCV, and platelet count) were significantly reduced during the follow-up period.  Duration of employment was significantly related to the changes in MCV and platelet counts.  The reductions in MCV were statistically significant only

among workers employed for more than 10 years. The study suggests that low levels of benzene may affect some CBC values.

 

A collaboration  among the National Cancer Institute, the Shanghai Hygiene and Anti• Epidemic Center, the University of California Berkeley, and other institutions has produced an impressive amount of data on levels of benzene exposure and their effects on nearly 75,000 Chinese workers in 672 factories in 12 cities (Dosemeci et al., 1994; Yin et al., 1994; Hayes et al., 1996; Rothman et al., 1996b; Qu et al., 2002; Lan et al.,

2004).  The initial studies were on exposure between 1949 and 1987 (Dosemeci et al.,

1994), but subsequent reports include later years.  Chronic benzene poisoning, defined by a WBC level less than 4000 cells per microliter over several months duration, is a compensable  adverse health effect for workers in China and a precursor of chronic disease.

 

In a cross-sectional  study, hematologic outcomes were assessed in 44 (23 male and 21 female) workers heavily exposed to benzene (median=  31 ppm (101 mg/m3)  as an 8-hr TWA) for six months to 16 years (mean=  6.3 years) at three workplaces  in Shanghai (Rothman et al., 1996a).  Controls were 44 age and gender-matched  unexposed

workers at two other workplaces.   Hematologic parameters (total WBC, absolute lymphocyte count, platelets, RBC, and hematocrit) were decreased among exposed workers compared to controls (Table 6.1 ); an exception was the red blood cell mean corpuscular volume (MCV), which was higher among exposed subjects.  In a subgroup of 11  workers with a median 8 hr TWA of 7.6 r,pm (24.8 mg/m3)  (range=  1-20 ppm) and not exposed to more than 31  ppm (101 mg/m ) on any of 5 sampling days, only the absolute lymphocyte count was significantly different between exposed workers and

controls (p = 0.03).  Among exposed subjects, a dose response relationship with various

measures of current benzene exposure (i.e., personal air monitoring, benzene metabolites in urine) was present only for the total WBC count, the absolute lymphocyte count, and the MCV.  The results support the use of the absolute lymphocyte count as the most sensitive indicator of benzene-induced  hematotoxicity.

 

Appendix 01

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19                                                  Benzene

 

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Table  6.1.  Selected

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heral blood cell count  data from  Rothman  et al.  1996

 

	Controls	:5 31  ppm benzene Median   (8  h TWA)=	> 31  ppm benzene Median  (8 h TWA)
	N=44	13.6       m  N=22	= 91.9     m   N=22
WBC (mean (SD)/µL)	6800 (1700)	6400(1800)	5600(1900f
Absolute  lymphocyte
count   mean  SD I  L	1900  400	1600  300 a	1300    300 c
RBC(mean	4700 (600)	4600 (460)	4200 (600t
x103  SD I  L
Platelets   (mean SD I  L	166   (59)	132 (45)	121   {43)a
MCV (µm )(mean(SD))	88.9  (4.9)	89.8  (3.9)	92.9 {3.4)c
a  p < 0.01;      p < 0.05; c  p	< 0.001

 

Subsequently  the research  group reported  that in a case-control   (50  cases,  50 controls) study within  the Shanghai worker cohort,   benzene   poisoning  was two to three times more likely  if a person had either  high CYP450 2E1 activity or no NAD(P)H:quinone reductase  (NQO 1)  activity  (NQO 1 *2/*2 genotype),   and seven to eight  times more likely with both high   CYP450 2E1   activity  and  no NQ01  activity  {Table  6.2) (Rothman  et al.,

1997).    The percentage of Chinese  with the null activity NQ01 *2/*2 genotype   is five

times  that of non-Hispanic   whites (22.4  % vs 4.4 %) (Ross,   2005).    The data support the role of benzoquinone  as a key metabolite in benzene-induced  toxicity.

 

CYP2E1 activity NQ01 qenotvpe   Odds ratio 95%CI No. cases Slow +/+and +/- 1   – 8 Slow -/-   2.4   0.6-9.7 6 Rapid +/+and +/- 2.9   1.0-8.2 21 Rapid -/-   7.6   1.8-31.2 13

Table  6.2.   Joint effects of CYP2E1 activiyt and NQOI genotypeon benzene poisoning  from  Rothman et al. (1997)

 

 

In a study  that partially confirmed and  extended the study of Rothman  and colleagues, Chen  and coworkers studied   single   nucleotide polymorphisms    (SNPs) in  CYP2E1, NQ01,   MPO,  GSTM1   and  GSTT1 in 100 benzene-exposed   workers diagnosed   with chronic benzene poisoning   and  90 benzene-exposed   matched controls (Chen  et al.,

2007). There was a 2.82-fold  (95%  Cl  = 1.42-5.58)   increased risk of benzene   poisoning in  the workers with the NQ01   609C > T mutation  genotype  (T/T) compared with  the heterozygote   and the wild-type   (C/C).   Workers with  the  GSTT1   null genotype   had a

1.91-fold     (95% Cl=    1.05-3.45) increased    risk  of poisoning   compared with those with

GSTT1   non-null  genotype.  A three  genes’  interaction   revealed   a 20.41-fold    (95% Cl  =

3. 3. 79-111.11) increased  risk of! p©.il>b9ii~gl  fh3s°1J:>j~~~+vith the NQ01  609C > T TIT genotype   and  with  the  GSTT1 nuJ,l,g~p9tyPie  aq,QnthMrffSTM1  null  genotype compared with  those carrying the NQOiS~~    Wet cm- arlH1cl~enotype,    GSTT1   non-null genotype,  and GSTM1 non-null genotype.  These auihors  found  no association  of

NM013DN\1’UO      ju NN\Ul

 

 

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CYP2E1 and MPO genotype with chronic benzene poisoning in this benzene-exposed population.

 

Personal benzene exposure and blood cell counts were measured in 130 exposed workers (62 men and 68 women) in three factories in Tianjin, China and in 51 age- and gender-matched  unexposed subjects (Qu et al., 2002).  Benzene air levels on the day of blood sampling ranged from 0.06 to 122 ppm (0.2 to 398 mg/m3).    The 4-week average exposure levels were 0.08 to 54.5 ppm (0.26 to 178 mg/m3).     Significant decreases of RBC, WBC, and neutrophils were observed (Table 6.3). The decreases correlated with both personal benzene exposures and levels of biomarkers: the urinary metabolites S• phenylmercapturic  acid and trans,trans-muconic  acid, and the albumin adducts of benzene oxide and 1,4-benzoquinone.  The depressions  in RBC, WBC, and neutrophils were exposure dependent and were also significantly different in the lowest exposed group (S 0.25 ppm) compared with unexposed subjects. The results suggested to the authors that lymphocytes  may not be more sensitive than neutrophils to chronic

benzene exposure.  Unfortunately the results may be confounded since the workers were also exposed to toluene, which protects against the adverse effects of benzene (Snyder et al., 1989).  The statement that some cell counts were significantly depressed at s 0.25 ppm benzene is potentially important, but it was difficult to ascertain from the presentation of the data how many workers were exposed at that level.

 

Table 6.3.  Selected

heral blood cell count data from Qu et al.  2002

 

Workers   N                                        54                    36                29                  11

 

Mean (SD)

cumulative

32(21)             74(51)         123(65)         237(188)

 

 

0.004                 3.07 (2.9)        5.89 (4.8)    17.4 (15.5)    50.6 (0.003)               (55.4)

 

463  52            403  62           396  57       404  51         391  39

6671 (1502)     6383 (1330)    6089            6103              4727

1455            1560             548

Neutrophils (per µL)*   4006 (1108)     3377 (868)      3491            3501              2480

1121            1314             451

*p < 0.001, test for exposure-response  trend

#p < 0.01 vs. control by t test for difference between the means (only lowest benzene tested)

 

A cross-sectional  survey studied 250 (86 male and 164 female) Chinese workers exposed in two shoe manufacturing facilities to glues containing 0.6 to 34 percent benzene for 6.1 ± 2.1 years (Lan et al., 2004 ).   For each worker, individual benzene (and toluene) exposure was monitored repeatedly (up to 16 months) before blood samples were drawn.  WBC and platelet counts were significantly lower than in the 140

control garment workers, even for exposure below 1   ppm benzene in air (mean=  0.57 ±

0.24 ppm) (1.86 ± 0.78 mg/m3)  (Table 6.4).  Progenitor cell colony formation declined significantly with increasing benzene exposure and was more sensitive to the effects of

 

 

 

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benzene  than  was  the  number  of mature  blood  cells.  Genetic  variants   in myeloperoxidase     (MPO)  and  NQ01   influenced   susceptibility    to benzene   hematotoxicity. Increased   myeloperoxidase    activity  and  decreased   NQ01   activity  were  associated   with increased   hematotoxicity.     The  authors  concluded   that  hematotoxicity    from  benzene exposure   may  be evident  among  genetically   susceptible   subpopulations.     A confounder is the  co-exposure   of the workers   to toluene,   a competitive   inhibitor  of benzene metabolism.

 

In response   to criticism   (Lamm  and  Grunwald,   2006)  of the adequacy   of their  dose• response   data,  the authors  (Lan  et al., 2006)  confirmed   the monotonicity   of their  data  by spline  regression   analysis   of benzene   exposure   and WBC  counts.   They  found  no apparent   threshold   in their  exposure   range  of 0.2 to 75 ppm  (0.65  to 245  mg/m3) benzene.

 

Table 6.4. Selected peripheral blood cell count data from Table 1  of Lan et al.

2004

 

Controls

Low

Medium

High

pfor

 

 

 

 

 

WBC

(< 0.04 ppm)    exposure

(n = 140)          0.57 ppm

n = 109

2.85 ppm

(n = 110)

28.73 ppm

(n = 31)

0.57 ppm vs. controls

 

< 0.0001

< 0.0001

0.018

0.003

0.003

0.018

 

Platelets           230 (60) x 10    214 (49) x 10    200 (53) x 10    172 (45) x 10

* Unadjusted mean cell number (± 1   SD) per microliter of blood

0.023

 

 

In order to identify specific genes involved in the cell count changes above, the authors used a commercial assay (Golden Gate assay by lllumina) to analyze 1,395 single nucleotide polymorphisms  (SNPs) in 411 genes in the 250 benzene-exposed workers and the 140 unexposed controls (Lan et al., 2009).  Highly significant findings clustered in five genes (BLM, TP53, RAD51, WDR79, and WRN) that have important roles in DNA repair and genomic maintenance.  TP53 (tumor protein p53), the “guardian of the genome,” is a tumor suppressor gene and is mutated in up to 50 percent of human cancers.  WDR79 is located next to TP53 on chromosome  17 and is also known as TCAB 1   and WRAP43 (for WD40-encoding  RNA antisense to p53).  BLM (for Bloom syndrome) codes for a member of the RecQ helicase family which is involved in DNA replication fork repair processes.  WRN (Werner’s syndrome) codes for an enzyme(s) with helicase, exonuclease, and ATPase properties.  RAD is a homologue of RecA involved in homologous recombination and repair.  One or more SNPs in each gene

were associated with statistically significant reductions of 10-20 percent in the WBC

count among benzene-exposed workers (p = 0.0011to0.0002)    but not among controls.

 

 

 

 

 

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A further study of this cohort involved 1,023 tag SNPs in 121 gene regions important for benzene effects (Hosgood et al., 2009).  Linear regression was used to relate genetic polymorphisms  and total white blood cell (WBC) count and its subtypes. The minp (minimal p value) test assessed the association on the gene region level. The false

discovery rate (FDR) method was used to control for multiple comparisons. 1      Vascular endothelial growth factor (VEGF) (minp = 0.0030) and ERCC3 (a gene involved in

nucleotide excision repair of DNA) (minp = 0.0042) were the gene regions most

significantly associated with altered WBC counts among benzene-exposed  workers,

after accounting for multiple comparisons.   Statistically significant changes were also found for WBC subtype counts, including granulocytes,  CD4+ T cells, and lymphocytes for VEGF, and granulocytes and NK cells for ERCC3.  Further, in workers exposed to

<1 ppm benzene, a SNP in VEGF was associated with changes in WBC and granulocyte counts, and SNPs in ERCC3 were associated with changes in WBC, NK cell, and granulocyte  counts.

 

A cross-sectional  study of the same workers evaluated the association between SNPs in genes involved in innate immunity and benzene hematotoxicity. A total of 1,236 tag SNPs in 149 gene regions of six pathways were analyzed (Shen et al., 2011 ). Six regions were significant for their association with WBC counts based on gene-region  (p

< 0.05) and SNP analyses (False Discovery Rate<  0.05): MBP (myelin basic protein),

VCAM1 (vascular cell adhesion molecule 1), ALOX5 (arachidonate 5-lipoxygenase), MPO (myeloperoxidase),  RAC2 (a member of a group of small GTPases), and CRP (C reactive protein). Specific SNPs for VCAM1, ALOX5, and MPO were the three most significant SNPs and showed similar effects on WBC subtypes: granulocytes, lymphocytes, and monocytes. A 3-SNP block in ALOXE3 showed a global association (omnibus P = 0.0008) with WBCs, but the SNPs were not individually significant.

 

Other recent studies have not found effects of benzene on blood cells at such low levels.  Swaen and colleagues studied hematological  effects at low benzene air levels among Dow Chemical Company employees in the Netherlands (Swaen et al., 2010). They compared 8,532 blood samples from 701 male workers with low benzene exposure to 12,173 samples from 1,059 male workers with no occupational  benzene exposure for the years 1981-2007.  A Job Exposure Matrix was constructed using

21,584 benzene air measurements for the exposed employees. The Matrix was used to estimate benzene exposure in the year in which each blood sample was collected. The average lymphocyte counts for the unexposed and exposed group were similar:

2,090.29 and 2,097.02 cells per microliter, respectively.  Adjustments for smoking, age, and month of blood sample did not change the results.  No adverse effect on any blood parameters was seen.  Stratification into three exposure subgroups (<0.5 ppm (1.63 mg/m3),  0.5-1 ppm, and >1 ppm (3.26 mg/m3))  showed no significant differences for any of the blood parameters among the exposure categories including the non-exposed.

 

1    The False Discovery  Rate (FDR) of a set of predictions is the expected percent of false predictions in the set. If the algorithm returns 100 genes with an FDR of 0.3, expect 30 of them to be false and 70 to be correct.

 

 

 

 

 

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In 1981, South Korea banned use of glues or solvents containing more than 1   percent benzene from the workplace, except where benzene is used in a completely sealed process.  After the ban (in 2000), the number of workers possibly exposed to benzene was estimated to be 196, 182 workers in 6,219 factories.  Benzene exposure in different industries was assessed by reviewing the claimed cases for workmen’s compensation due to hematopoietic diseases related to benzene which were investigated by Korea OSHA between 1992 and 2000 (Kang et al., 2005).  Six factories were evaluated for benzene exposure.  Personal air monitoring was performed in 61 workers; urine samples were collected from 57 to measure trans,trans-muconic  acid (t,t-MA); and hematologic examination was performed.  The geometric mean of benzene in air was

0.094 ppm (range=  0.005-5.311 ppm) (0.3 mg/m3;   range=  0.02-17 mg/m3).   Seven

samples were higher than 1   ppm but less than 10 ppm, the occupational exposure limit in Korea. The geometric mean of t,t-MA in urine was 0.966 mg/g creatinine (range =

0.24-2.74). The benzene exposure level was low except in a factory where benzene

was used to polymerize other chemicals. Ambient benzene from 0.1 to 1   ppm (0.326 to

3.26 mg/m3)  was significantly correlated with urinary t,t-MA concentration  (r=O. 733, p<0.01).  Hematologic parameters did not show any significant differences among groups divided by the level of exposure. Korean workers were not highly exposed to

benzene and the level of exposure was mostly less than 1   ppm.

 

6.2  Chronic Toxicityto Infants and Children

 

Several epidemiological  and ecological studies have been published, which examine the association between benzene exposure and health outcomes in children, notably leukemia (Brosselin et al., 2009).  However, these studies use proximity to gasoline stations or roads with high traffic volumes as proxies for benzene exposure.  Since the resulting exposures are to complex mixtures of VOCs and/or vehicular exhaust of which benzene is one component among many, the role of benzene in the reported health effects is not clear.  Nonetheless, we briefly describe some below.

 

In France, Brosselin and colleagues studied the association between acute childhood leukemia and residing next to gas stations and automotive repair shops for 2003-2004 (the ESCALE study (SFCE))(Brosselin  et al., 2009).  A total of 765 cases of acute leukemia and 1,681 controls under 15 years of age was studied. Acute leukemia was significantly associated with residence next to either gas stations or automotive-repair garages (odds ratio (OR)=  1.6 [95% Cl = 1.2-2.2]) and next to a gas station only (OR=

1.9 [95% Cl = 1.2-3.0]). The OR did not show a tendency to increase with exposure duration. The results were not modified by adjustment for potential confounders including urban/rural status and type of housing (Brosselin et al., 2009).  In a further study of this population, acute leukemia was significantly associated with higher estimates of traffic N02 levels at the home (> 27.7 µg/m3)  compared with lower N02 levels(<  21.9 µg/m3)  [OR=  1.2; 95% Cl=  1.0-1.5] and with the presence of a heavily•

trafficked road within 500 meters (m) of the home compared with the absence of such a

road in the same area (OR=2.0; 95% Cl, 1.0-3.6). There was a significant association between acute leukemia and a high density of heavy-traffic roads within 500 m

 

 

 

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compared with the reference category with no heavy-traffic road within 500 m (OR=

2.2; 95% Cl, 1.1-4.2), and a significant positive linear trend of the association of acute leukemia with the total length of heavy-traffic road within 500 m (Amigou et al., 2011 ).

 

An earlier case-control study in France for the years 1995-1999 involved 280 leukemia cases and 285 controls.  There was no association between the mothers’ work

exposure to hydrocarbons during pregnancy and leukemia, or between residential traffic density and leukemia. There was a statistically significant association between residences near a gas station or an automotive repair shop during childhood and the

risk of childhood leukemia (OR=  4.0, 95% Cl=  1.5-10.3), with a positive duration trend.

The association was strong for acute non-lymphocytic  leukemia (OR=   7.7, 95% Cl 1.7-

34.3) and was not altered by adjustment for potential confounders  (Steffen et al., 2004).

 

An ecologic analysis studied 977 cases of childhood lymphohematopoietic  cancer diagnosed from 1995-2004 in Texas (Whitworth et al., 2008).  Exposure values were the U.S. Environmental Protection Agency’s 1999 modeled estimates of benzene and 1,3- butadiene for 886 census tracts surrounding  Houston.  Census tracts with the highest benzene levels had elevated rates of all leukemia [rate ratio (RR) = 1.37; 95% Cl =

1.05-1.78]. The association was higher for acute myeloid leukemia (RR=  2.02; 95% Cl,

1.03-3.96) than for acute lymphocytic leukemia (RR = 1.24; 95% Cl, 0.92-1.66). Among census tracts with the highest 1,3-butadiene levels, the authors observed RRs of 1.40 (95% Cl, 1.07-1.81 ),  1.68 (95% Cl, 0.84-3.35), and 1.32 (95% Cl, 0.98-1.77) for all leukemia, acute myeloid leukemia, and acute lymphocytic leukemia, respectively.

 

6.3  Chronic Toxicity to Experimental Animals

 

A number of animal studies have demonstrated that benzene exposure can induce bone marrow damage, changes in circulating blood cells, developmental  and reproductive effects, alterations of the immune response, and cancer.  With respect to chronic toxicity, hematological changes appear to be the most sensitive indicator (Table

6.5).

 

Wolf and coworkers conducted repeat benzene exposures (7-8 h/day, 5 days/week) in several species.  Rabbits were exposed to 80 ppm (261 mg/m3)  for 175 total exposures; rats were exposed to 88 ppm (287 mg/m3)  for 136 total exposures; and guinea pigs

were exposed to 88 ppm (287 mg/m3)  for 193 total exposures (Wolf et al., 1956).  The

observed effects included leukopenia, increased spleen weight, and histological changes to the bone marrow.

 

Hematologic effects, including leukopenia, were observed in rats exposed to mean concentrations  of 44 ppm (143 mg/m3)  or greater for 5 to 8 weeks.  Exposure to 31 ppm (100 mg/m3)   benzene or less did not result in leukopenia after 3 to 4 months of

exposure (Deichmann et al., 1963).

 

 

 

 

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Among Sprague-Dawley  rats and AKR/J mice exposed to 300 ppm (972 mg/m3) benzene, 6 hours/day, 5 days/week for life, Snyder and coworkers found lymphocytopenia,  anemia, and decreased survival time (Snyder et al., 1978).

 

Male mice exposed to 400 ppm (1,304 mg/m3)  benzene, 6 hours/day, 5 days/week for

9.5 weeks showed depressed bone marrow cellularity, decreased stem cell count, and altered morphology in spleen colony-forming  cells (Cronkite et al., 1982)

 

Mice are more sensitive than rats or rabbits to the hematologic and leukemic effects of benzene (IARC, 1982; Sabourin et al., 1989).  Metabolism of benzene to hydroquinone, muconic acid, and hydroquinone glucuronide is much greater in mice than rats, whereas the detoxification pathways are approximately equivalent between the two species (Sabourin et al., 1988).

 

A study on the chronic hematological effects of benzene exposure in C57 81/6 male

mice (5 or 6 per group) showed that peripheral lymphocytes, red blood cells and colony• forming units (CFUs) in the bone marrow and spleen were significantly decreased in number after treatment with 10 ppm (32.4 mg/m3)  benzene for 6 hours/day, 5

days/week for 178 days compared to unexposed controls (Baarson et al., 1984).  Ten ppm, the only concentration studied, was the workplace exposure standard at the time.

 

Male and female mice (9or10   per group) were exposed to 10, 25, 100, 300 and 400 ppm benzene for 6 hours/day, 5 days/week for 2 to 16 weeks (Cronkite et al., 1985). After 2 weeks at 100 ppm (326 mg/m3)  benzene and higher, mice showed both decreased bone marrow cellularity and a reduction of pluripotent stem cells in the bone marrow.  The decrease in marrow cellularity continued for up to 25 weeks following a

16-week exposure to 300 ppm (972 mg/m3)  benzene.  Peripheral blood lymphocytes (PBLs) were dose-dependently  decreased with benzene exposures of greater than 25 ppm (81 mg/m3)  for 16 weeks, but recovered to normal levels following a 16-week recovery period.         ·

 

Fifty Sprague-Dawley  rats and 150 CD-1 mice of both sexes were exposed to 0, 1, 10,

30, or 300 ppm (0, 3.26, 32.6, 97.2, or 972 mg/m3)  benzene, 6 hours/day, 5 days/week for 13 weeks (Ward et al., 1985).  Serial necropsies were conducted at 7, 14, 28, 56,

and 91 days (20 percent of each group of rodents at each time point).  No hematological

changes were found for mice and rats at 1, 10, or 30 ppm.  In male and female mice significant increases in mean cell volume and mean cell hemoglobin values and decreases in hematocrit, hemoglobin, lymphocyte percentages, and decreases in red cell, leukocyte and platelet counts were observed at 300 ppm.  The changes were first observed after 14 days of exposure.  Histological changes in mice included myeloid hypoplasia of the bone marrow, lymphoid depletion in the mesenteric lymph node, increased extramedullary  hematopoiesis in the spleen, and periarteriolar lymphoid sheath depletion.  Effects were less severe in the rats.  In this subchronic study 30 ppm (97 .2 mg/m3)  was a NOAEL.

 

 

 

 

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The National Toxicology Program (NTP, 1986) conducted a chronic (2 year) toxicity “bioassay” in F344 rats and B6C3F1 mice of benzene by gavage in corn oil.  Doses were 0, 25, 50, and 100 mg/kg-day for females and 0, 50, 100, and 200 mg/kg-day for males.  Dose-related  lymphocytopenia  and leukocytopenia were observed in both species in all dosed groups.  Mice exhibited lymphoid depletion of the thymus and spleen and hyperplasia of the bone marrow.

 

Investigators at Brookhaven National Laboratory exposed CBA/Ca mice to 10, 25, 100,

300, 400 and 3,000 ppm (32.6, 82, 326, 972, 1,304 and 9, 720 mg/m3)  benzene 6 hours/day, 5 days/week for up to 16 weeks (Cronkite et al., 1989).  No effects were observed at 10 ppm.  Lymphopenia was observed in the 25 ppm exposure group. Higher concentrations  of benzene produced dose-dependent  decreases in blood lymphocytes,  bone marrow cellularity, spleen colony-forming  units, and an increased percentage of CFU-S in S-phase synthesis.

 

Farris et al. exposed B6C3F1   mice to 1, 5, 10, 100, and 200 ppm (3.26, 16.3, 32.6, 326, and 652 mg/m3)  benzene for 6 hr/day, 5 days/week, for 1, 2, 4, or 8 weeks (Farris et al.,

1997).  In addition some animals were allowed to recover from the exposure for up to 25 days.  There were no significant effects on hematopoietic  parameters from exposure to

1 O  ppm benzene or less.  Exposure to higher levels reduced the number of total bone

marrow cells, progenitor cells, differentiating  hematopoietic cells, and most blood parameters.  The replication of primitive progenitor cells was increased.  The authors suggested that this last effect, in concert with the genotoxicity of benzene, could play a role in the carcinogenicity  of benzene.

 

Study (Farris et al., Animal Mice Exposure 6 h/d, 5 Duration 1, 2, 4, or Effect hemato- NOAEL    LOAEL 10 ppm     100 ppm 1997)   d/wk 8wk poiesis   (Cronkite et Mice 6 h/d, 5 Up to 16 hemato- 10 ppm    25ppm al., 1989)   d/wk wk poies is   (Aoyama, Mice 6 h/d 14 days hemato- not            50 ppm 1986) (Ward et al.,   mice & rats   6 h/d, 5   13 weeks poiesis hemato- found 30 ppm    300 ppm 1985)   d/wk   poies is   (Cronkite et Mice 6 h/d, 5 2-16 wk hemato- 25ppm      100 pm al., 1985)   d/wk   poies is   (Baarson et Mice 6 h/d, 5 178 d hemato- not            10 ppm al., 1984)   d/wk   poiesis found (Deichmann Rats 5 h/d, 4 5wk-4  mo hemato- 31  ppm    44 ppm et al., 1963)   d/wk   poies is   (Wolf et al., rabbits, 7 h/d 136-193 hemato- not            80-88 1956) rats, guinea   exposures poiesis found        ppm   pigs

Table 6.5.

I rnportant  non-acute ammaI.mh a I atilon s u  ies ofb enzene

 

 

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7   Developmental and Reproductive   Toxicity

 

7.1  Human Studies

 

Based on blood samples taken at birth from mother and infant, benzene can cross the human placenta and be in the umbilical cord at a level equal to or greater than in maternal blood {Dowty et al., 1976).  The database of benzene effects on human reproductive and developmental toxicity is limited to a few reports which usually have small samples, unmeasured exposure to benzene, and exposure to other chemicals. CYP2E1, which is a key enzyme in the pathway from benzene to its toxic metabolites, was not detected in human livers in the early fetal period (Vieira et al., 1996) but was detectable at low levels in some fetuses beginning in the second trimester {Johnsrud et al., 2003).  In the third trimester CYP2E1 is present in most fetuses at 10-20 percent of adult levels {Table 7 .1 ).   However, many phase II enzymes which detoxify benzene metabolites are also low in the fetal period (Mccarver  and Hines, 2002).  For example, for seven of eight substrates of UDP-glucuronyltransferase  in human liver, the level during the fetal period ranged from less than 1   to 30 percent of adult levels and the level at the end of the fetal period ranged from 6 to 31 percent of adult levels.  For only one substrate (5-hydroxytryptamine)  were adult levels of UDP-glucuronyltransferase  present in the fetal period (Leakey et al., 1987).

 

Table 7 .1.  Changes  of CYP2E1 with  age in human  liver  (Hines,  2007)

Age 151   trimester fetus: 8-13.4 weeks	N 14	omol CYP2E1/mg protein – (not detectable)
~na trimester fetus: 13.6-25 weeks	45	0.3 ± 0.6 (mean ± SD)
3ra trimester fetus: 27-40 weeks	14	5.8 ±4.6
Neonate: 0-29 days	42	13.4 ± 16.0
Infant: 1.1-11.3 months	64	36.2 ± 20.3
Prepubertal: 1.1-10.0 years	41	43.1±20.6
Adolescent:  11.0-17.7 years	20	-68  (median)
Adult	–	-50  (median)

 

The EDEN Mother-Child Cohort Study Group assessed the relation between personal exposure to airborne benzene in non-smoking pregnant French women and fetal growth

{Slama et al., 2009).  A group of 271 mothers recruited from the University Hospitals of Nancy and Poitiers from September 2003 through June 2006 carried a diffusive air sampler during week 27 of gestation to assess benzene exposure.  The authors estimated head circumference of the offspring by ultrasound measurements during the second and third trimesters of pregnancy and at birth.  Median benzene exposure was

1.8 µg/m3  {0.5 ppb) {5 and 95th percentiles, 0.5 and 7.5 µg/m3).    An increase of 1   in log•

 

transformed benzene exposure was associated with a gestational age-adjusted decrease of 68 g in mean birth weight {95% Cl, -135 to -1  g; p = 0.05) and of 1.9 mm in

mean head circumference  at birth {95% Cl, -3.8 to 0.0 mm; p = 0.06).  Similarly, this differential in exposure was also associated with an adjusted decrease of 1.9 mm in

head circumference during the third trimester {95% Cl, -4.0 to 0.3 mm; p = 0.09) and of

1.5 mm in head circumference at the end of the second trimester {95% Cl, -3.1 to 0 mm;

 

 

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p = 0.05).  The association cannot necessarily be attributed solely to benzene, particularly since the benzene exposure may reflect exposure to a mixture of associated traffic-related  air pollutants.  Traffic-related  air pollutants have been associated in a number of studies with adverse birth outcomes including low birth weight.

 

Lindbohm and colleagues reported a statistically significant increase in spontaneous abortions in women whose husbands worked at petroleum refineries or with petroleum

derived solvents including benzene (16 spontaneous  abortions among 93 preqnancles:

odds ratio = 2.2; 95% Cl = 1.3-3.8) (Lindbohm et al., 1991 ).

 

The Texas Birth Defects Registry contained data on neural tube defects (533 cases of spina bifida and 303 cases of anencephaly)  in babies delivered between 1999 and 2004 (Lupo et al., 2011 ).  Census tract-level estimates of annual benzene, toluene, ethylbenzene,  and xylene (BTEX) levels were obtained from the U.S. EPA’s 1999

Assessment  System for Population Exposure Nationwide.  Mothers living in census tracts with the highest benzene levels were more than twice as likely to have offspring

 

with spina bifida than were women living in census tracts with the lowest levels (odds ratio = 2.30; 95% Cl = 1.22-4.33).   No other significant associations were observed for

benzene and no associations were found for toluene, ethlybenzene,  and xylene.  A variety of confounders such as race/ethnicity, maternal age, and socioeconomic  status were taken into account.

 

Ghosh and colleagues investigated the effect of ambient air pollution in Los Angeles

County on birth weight among 8, 181 term tz 37 wk gestation), low birth weight (LBW;

<2,500 g) children and 370,922 term normal birth weight children born from 1995

through 2006; all mothers lived within 5 miles of at least one of four stationary toxic air contaminant  monitors (Ghosh et al., 2012).  The influence of local variation in traffic pollution was assessed by land-use-based,  regression-modeled  estimates of oxides of nitrogen. Adjustments were made for maternal age, race/ethnicity, education, and

parity, and for infant gestational age (and gestational age squared).  Logistic regression indicated that the odds of term LBW increased 2-5  percent (range of 95% Cl=  0%-9%) per interquartile-range  increase in modeled traffic pollution estimates and in monitoring• based air toxics exposure estimates for (1) the entire pregnancy, (2) the third trimester, and (3) the last month of pregnancy.  Models stratified by monitoring station (to investigate air toxics associations  based solely on temporal variations) resulted in

2-5 percent increased odds per interquartile-range  increase in third-trimester  exposures to benzene, toluene, ethyl benzene, and xylene (BTEX); some confidence intervals indicated statistically significant effects.  However, benzene was not a better predictor of LBW than toluene, ethyl benzene, xylene, or PAHs (Polycyclic Aromatic Hydrocarbons excluding naphthalene).

 

In the latter 1990s, the level of benzene in gasoline sold in the United States decreased as the result of regulation.  Zahran and coworkers investigated the relationship between maternal exposure to benzene and birth weight outcomes among US residents in 1996 and 1999. A total of 3.1 million singleton births registered with the U.S. National Center for Health Statistics were included (Zahran et al., 2012).  Maternal benzene

 

 

 

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concentrations were estimated at the county level using data from the US EPA’s National Air Toxics Assessment.   Regression analysis estimated that a 1   µg/m3  (0.3 ppb) increase in maternal exposure to benzene (1) reduced birth weight by 16.5 g (95% Cl, 17.6-15.4), (2) increased the odds of a low birth weight (LBW) child by 7 percent,

and (3) increased the odds of a very LBW child by a multiplicative factor of 1.23 (95% Cl, 1.19-1.28). In counties where benzene levels decreased 25 percent from 1996 to

1999, birth weight increased by 13.7 g (95% Cl, 10.7-16.8) and the risk of low birth weight (LBW) decreased by a factor of 0.95 (95% Cl, 0.93-0.98).  The authors admit that concentrating on benzene is a limitation since PM also affects birth weight.

 

Xing and coworkers used multicolor fluorescence in situ hybridization (FISH) to measure the incidence of sperm with numerical abnormalities of chromosomes X, Y, and 21among33 benzene-exposed  men and 33 unexposed men from Chinese factories (Xing et al., 2010).  Passive air monitors were used to measure benzene as

well as toluene and xylene.  Benzene levels for the exposed ranged from zero (i.e., limit of detection) to 24 ppm (78 mg/m3);   nine had levels s 1   ppm (S 3.26 mg/m3).   Exposed

men were grouped into low and high exposure based on levels of urinary t,t-muconic acid.  Compared to controls, sperm aneuploidy increased across low- and high-exposed groups for disomy X [incidence rate ratio (IRR) for low=  2.0: 95% Cl=  1.1-3.4; and IRR for high = 2.8: 95% Cl = 1.5-4.9], and for overall hyperhaploidy for X, Y and 21 chromosomes  (IRR for low=  1.6; 95% Cl, 1.0-2.4; and IRR for high = 2.3; 95% Cl, 1.5-

3.6, respectively). Even for the nine exposed to s 1   ppm, the authors found statistically

significantly elevated disomy X (IRR = 1.8; 95% Cl = 1.1-3.00) and hyperhaploidy ( IRR

= 2.0; 95% Cl= 1.1-3.9) compared with the 33 unexposed men.  In this study benzene increased the frequencies of aneuploid sperm for chromosomes associated with chromosomal abnormality syndromes in human offspring at surprisingly low levels. Further studies with this cohort using chromosome  1   and low, moderate and high exposure groups yielded IRRs and 95% Cls for all structural aberrations combined of

1.42 (95% Cl= 1.10-1.83), 1.44(Cl=1.12-1.85), and 1.75 (Cl=  1.36-2.24) and for deletion of 1p36.3 alone of 4.31(Cl=1.18-15.78),  6.02(Cl=1.69-21.39),  and 7.88 (Cl

= 2.21-28.05) for men with low, moderate, and high exposure, respectively, compared with unexposed men (Marchetti et al., 2012).

 

 

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7.2  Animal Studies

 

Inhalation of 14C-benzene by pregnant mice resulted in labeled material in the fetuses

(Ghantous and Danielsson, 1986).

 

Groups of 40 female Sprague-Dawley  rats were exposed to 0, 1,  10, 40, and 100 ppm

(0, 3.26, 32.6, 129.6, or 326 mg/m3}  benzene for 6 hours/day during days 6-15 of gestation (Coate et al., 1984).  At least 80 percent of the 40 females in each group .

littered (mean litter size = 13 fetuses).  The viscera and skeletons of the fetuses were

evaluated for variants and the fetal body weight and length were measured.  No

increase in variants was noted.  A significant decrease was noted in the body weights of fetuses from dams exposed to 100 ppm (326 mg/m3)   benzene (Table 7.2).  No effects were observed at 40 ppm ( 130 mg/m3},   the NOAEL for this experiment.

 

Table 7.2. Fetal body weights from Table 5 of Coate et al. (1984)

Group	Litters      ppm          Fetal male bw      Fetal female bw    Livet  fetuses per
		benzene	(mean±  SD)		litter  (mean±SD)
1	32/40	0	4.02 ± 0.349 g	3. 78 ± 0.303 g	13.0 ± 3.10
2	33/40	0	4.06 ± 0.430	3.85 ± 0.477	12.5 ± 2.98
3	37/40	1	3.86 ± 0.381	3.69 ± 0.350	13.8 ± 2.47
4	37/40	10	3.88 ± 0.303	3.70 ± 0.385	13.3 ± 2.56
5	37/40	40	3.91±0.492	3.64 ± 0.382	12.9 ± 2.90
6	35/40	100	3.77 ± 0.226*	3.56 ± 0.274*	13.8 ± 2.43

* significantly lower than 0 ppm groups; p < 0.05

t  There were no dead fetuses.

 

Exposure of pregnant Swiss Webster mice to concentrations  as low as 5 ppm

(16 mg/m3}  benzene on days 6-15 of gestation (6 hr/day) resulted in bone-marrow hematopoietic changes in the offspring that persisted into adulthood (Keller and Snyder,

1986).  However, the hematopoietic effects (e.g., bimodal changes in erythroid colony•

forming cells) were of uncertain clinical significance.

 

In a subsequent,  similar study, the authors (Keller and Snyder, 1988) found that exposure of mice in utero for 6 h/day to 5, 10 and 20 ppm (16.3, 32.6, and 65.2 mg/m3) benzene on days 6-15 of gestation resulted in suppression of erythropoietic  precursor cells and persistent, enhanced granulopoiesis  in peripheral blood cells of 2-day

neonates (Table 7.3) and increased granulocytes  in the livers of 2-day neonates and the

spleens of adults at 6 weeks (data not shown).  There was a dose-dependent  decrease in early nucleated red cells (basophilic normoblasts)  (Table 7.3).  The authors

considered these effects to be significant bone-marrow toxicity.  OEHHA staff previously used this study to develop a Maximum Allowable Daily Level (MADL) for Proposition 65 (OEHHA, 2001 ).  The benzene MADL is 49 µg/day for an inhalation exposure and 24

µg/day for an oral exposure.

 

 

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Table 7.3. Differential peripheral blood cell counts in fetuses of benzene-exposed eresnant  m.ice.#

 

		Dividing Granulo-	Nondividing	Early nucleated	Late nucleated	Primitive nucleated    Lympho-
Exposure	Blasts	cytes	granulocytes	red cells	red cells	red cells      cvtes
16-day fetuses
Air	0.00±0.00	0.50±0.16	1.60±0.50	5.10±1.34	0.40±0.22	92.4±1.95
5ppm	0.00±0.00	2.10±0.67	3.60±1.57	5.80±1.88	0.80±0.25	87.4±4.11
10 ppm	0.10±0.00	0.90±0.28	1.30±0.33	4.00±0.60	1.20±0.39	92.4±1.20
20 ppm	0.10±0.00	1.50±0.50	2.20±0.63	3.90±0.79	1.50±0.34	90.7±1.48
2-day neonates
Air	0.00±0.00	3.80±0.66	67.60±2.44	7.30±1.36	6.20±1.79	14.0±3.1
5 ppm	0.20±0.14	3.10±0.57	72.30±3.09	1.70±0.62*	3.60±0.88	17.9±2.4
10 ppm	0.10±0.10	5.90±1.04	67.90±2.88	0.50±0.22*	7.30±0.83	16.9±2.0
20 ppm	0.10±0.10	2.10±0.62	80.40±2.67*	0.00±0.00*	1.60±0.45*	14.2±2.5
6-week adults
Air	0.00±0.00	2.20±0.47	19.3±2.28	0.00±0.00	0.20±0.14	75.0±3.0
5ppm	0.00±0.00	1.20±0.47	22.0±2.47	0.10±0.10	0.20±0.13	72.3±3.1
10 ppm	0.00±0.00	0.60±0.22	24.2±2.59	0.00±0.00	0.10±0.10	75.1±2.9
20ppm	0.10±0.10	2.20±0.63	16.7±2.27	010±0.10	0.20±0.13	77.6±2.4

# 100 cells were counted from 1   male and 1   female from each of 5 litters per treatment

(n=10)

*p < 0.05 vs corresponding control by Dunnett’s test. Values are mean±SE.

 

An exposure of 500 ppm (1,600 mg/m3)    benzene for 7 hours per day through days 6-15 of gestation was teratogenic in the fetal brain of Sprague-Dawley  rats, while 50 ppm (160 mg/m3)    and 500 ppm resulted in reduced fetal weights on day 20 of gestation (Table 7.4) (Kuna and Kapp, 1981).  The higher exposure levels also had significantly more fetuses with skeletal variants.  No fetal effects were noted at an exposure of

10 ppm (32.6 mg/m3),   which is the NOAEL for this study.

 

 

 

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Table 7.4. Fetal bod          ht and len  th  Kuna and Ka

Benzene                                              0  m           10                                   500     m

17               18                                   19

107/119      188/197                          151/165

 

Mean body weight of live fetuses      4.4 ± 0.6

4.4±  0.5

3.8 ± 0.7*   3.6 ± 0.8*

 

 

Mean crown-rump length (cm) in      4.1 ± 0.2     4.1 ± 0.2     3.9 ± 0.3     3.8 ± 0.4*

live fetuses

Fetuses (litters) with skeletal or         3 (3)            2 (1)            23** (6)       30** (6)

visceral variants   n

Fetuses with brain anomalies or        0/35            0/56            5/35            7/44***

variants

* statistically significant difference from control (p < 0.05); values are mean ± 1   SD.

** significantly different by chi-square test

***statistically   different from control (p<0.05) by Fisher Exact Test (2-tailed)

 

Inhalation of 500 ppm benzene (the only concentration tested) for 7 hours/day on gestational days 6 to 15 in CF-1 mice and days 6 to 18 in white New Zealand rabbits induced minor skeletal variations that the authors did not consider to be teratogenic (Murray et al., 1979).

 

Exposure of CFY rats to continuous benzene inhalation (24 h/day) at 150, 450, 1500, or

3000 mg/m3  (50, 150, 500, or 1000 ppm) from days 7-14 of gestation led to decreased fetal body weights, elevated liver weights, and signs of skeletal retardation at 150 mg/m3 (50 ppm) benzene, the lowest concentration tested (Tatrai et al., 1980).

 

Female CFLP mice and NZ rabbits were exposed by inhalation to 0, 500, or 1,000 mg/m3  (0, 153, or 307 ppm) benzene for 24 h/day from day 6 to day 15 of pregnancy (Ungvary and Tatrai, 1985).  Maternal toxic effects were moderate and dose dependent. Benzene induced skeletal variations and weight retardation in fetuses of rabbits at 1,000 mg/m3 and in fetuses of mice at 500 and 1,000 mg/m3.    Benzene increased the post• implantation loss (percent fetuses dead or resorbed) in rabbits at 1,000 mg/m3•

Benzene induced spontaneous  abortion in rabbits at 1,000 mg/m3.

 

In order to determine if prenatal exposure to benzene induces neurobehavioral  changes in offspring, 0.1 mg/kg benzene was injected subcutaneously  on gestation day 15 into four pregnant female Sprague-Dawley  rats (Lo Pumo et al., 2006).  There were no changes in total number of neonates, body weight, and eye opening time between progeny of benzene-exposed  dams and controls, and no malformations.  At birth, neonatal reflexes (cliff aversion, forelimb, placing, bar holding, forelimb grasping, startle) were scored in benzene-exposed  pups.  More benzene-exposed  pups exhibited

reflexes each day compared to controls. Also, the completion (maximum appearance, i.e. 100 percent of the litter exhibited each reflex) of neonatal reflexes in benzene• exposed animals preceded that of controls. Beginning at 2 months after birth, cognitive and motor performance was assessed in males of the prenatally benzene-exposed progeny. Motor activity in the open-field test showed reduced ambulation in benzene-

 

 

 

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exposed rats compared to controls. Acquisition of active avoidance responses in the shuttle-box test was impaired in benzene-exposed  rats vs. controls. Prenatal benzene exposure was associated with reduced retention latency in a step-through passive avoidance task.  The authors concluded that acute exposure to benzene during gestational organogenesis  may cause long-lasting changes in motor behavior and cognitive processes.  It is problematic to extrapolate this acute subcutaneously administered dose to an equivalent inhalation exposure.

 

Exposure of rabbits to 80 ppm (261 mg/m3)  and of guinea pigs to 88 ppm (277 mg/m3) benzene 7 hours/day, 5 days a week for 8 months caused testicular degeneration (Wolf et al., 1956).

 

In a one-generation  reproduction study, groups of 26 female Sprague-Dawley  rats were exposed for 6 hours per day by inhalation to 1,  10, 30, and 300 ppm benzene during a

10-week premating period and during mating (to proven fertile males), gestation, and

lactation (Kuna et al., 1992).  There was no effect on female reproductive performance at any benzene level.  Performance measures included number of litters (range=  19-

24), mean gestation length (21.6-21.9 days), mean pup number per litter (11.7-12.6),

and viability index (96.9-99.5%).  At 30 and 300 ppm there was a trend for 21-day-old pups toward reduced body and organ weight but differences were statistically significant (p < 0.05) only for female pups at 300 ppm (32.59 ± 5.05 g vs. 36.3 ± 5.20 g in controls).

 

7.3  Genotoxicity

 

A review of the data from more than 1400 genotoxicity tests for benzene and its metabolites (Whysner et al., 2004) led to the conclusion that benzene and its metabolites do not produce reverse mutations in Salmonella typhimurium but are clastogenic and aneugenic, producing micronuclei (MN), chromosomal aberrations (CA), sister chromatid exchanges (SCE), and DNA strand breaks.

 

The International Agency for Research on Cancer (IARC) recently summarized the genotoxicity of benzene (IARC, 2012): “There is strong evidence that benzene metabolites, acting alone or in concert, produce multiple genotoxic effects at the level of the pluripotent haematopoietic stem cell resulting in chromosomal changes in humans consistent with those seen in haematopoietic cancer. In multiple studies in different occupational populations in many countries over more than three decades a variety of genotoxic changes, including chromosomal abnormalities, have been found in the lymphocytes of workers exposed to benzene.”

 

 

 

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In the most sensitive inhalation study of genotoxicity  in animals, inhalation of 3, 10, and

30 ppm (9.7, 32.6, and 970 mg/m3)  benzene for 6 hours by adult .male Sprague-Dawley rats resulted in a significant increase over controls in the frequency of sister chromatid exchanges ~SCE) in peripheral blood lymphocytes  (Erexson et al., 1986).  One ppm (3.26 mg/m ) was a tentative NOAEL for the effect.  Male DBA/2 mouse peripheral blood lymphocytes showed a significant concentration-related  increase in SCE frequency over controls at 10, 100, and 1,000 ppm (32.6, 326, and 3,260 mg/m3) benzene, the three concentrations  tested.  Mouse femoral bone marrow also showed a significant concentration-dependent  increase in micronuclei at 10, 100, and 1,000 ppm over controls (Erexson et al., 1986).

 

7.4  Toxicogenomics

 

In order to study hematotoxicity at the level of altered multigene expression, cDNA microarray analyses were performed on mouse bone marrow tissue extracts during and after a 2-week exposure to 300 ppm benzene (Yoon et al., 2003).  Expression of fifteen genes was at least doubled by benzene exposure compared to controls.  Two of these were increased nearly five-fold (a polycomb binding protein and Metallothionein  1 ). CYP2E1 expression was increased 2.13 fold.  Conversely this high-level benzene exposure decreased expression of a G-protein coupled receptor to 1   percent of its normal output.

 

One of the cohorts of Chinese workers described above (Lan et al., 2004) was analyzed by microarray analysis for global gene expression  in the peripheral blood mononuclear cells (WBC) of 83 workers exposed to benzene levels ranging from<  1   ppm to>  10 ppm.  The workers were divided into 4 exposure groups and compared to a group of 42 controls (Table 7.5) (McHale et al., 2011).  Changes in many metabolic pathways and extensive increases (and probably decreases, which are not discussed) of the expression of specific genes were found at all benzene exposure levels (McHale et al.,

2011 ). The AML (acute myeloid leukemia) pathway was among the pathways most significantly associated with benzene exposure. Alterations in immune response pathways (e.g., toll-like receptor signaling pathway, T-cell receptor signaling pathway) were associated with most exposure levels.  A 16-gene increased expression signature (relative to no exposure) was associated with all levels of benzene exposure.  The three genes with the highest increased expression were a serpin peptidase inhibitor, a tumor necrosis factor, and interleukin 1  alpha.

 

The above summaries of acute and chronic toxicity of benzene are intended to give an overview of the data and to analyze reports most relevant to developing  Reference Exposure Levels (RELs) for benzene, i.e., inhalation studies.  More comprehensive reviews of benzene toxicity are available (Sandmeyer,  1981b; World Health Organization,  1993; USEPA, 2002; ATSDR, 2007; Wilbur et al., 2008; Goldstein and Witz, 2009; IARC, 2012; Wang et al., 2012).

 

 

 

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8   Derivation  of Reference  Exposure  Levels

 

8.1 Acute Reference Exposure Level for Benzene

 

Key study

Study population Exposure method Exposure continuity Exposure duration Critical effects

 

LOAEL NOAEL BMCLo.sso

Human equivalent concentration

Time adjustment factor

LOAEL uncertainty factor (UFL)

Interspecies uncertainty factor Toxicokinetic (UFA-k) Toxicodynamic (UFA-d)

lntraspecies uncertainty factor Toxicokinetic (UFH-W Toxicodynamic (UFH-d)

Database uncertainty factor Cumulative uncertainty factor Acute Reference Exposure Level

Keller and Snyder, 1988 pregnant female rats

inhalation of 0, 5, 10, or 20 ppm benzene

6 hours per day

10 days (days 6-15 of gestation)

decreased early nucleated red cell counts

(Table 7.3)

5 ppm ( 16 mg/m3)

not found

not used due to poor fit (Table 8.1)

5 ppm (RGDR* =  1 )(systemic effect) Not done (see below)

‘110 (see below)

 

2 (default) (OEHHA, 2008)

‘110 (default)

 

10 (default)

’11 O (default)

1   (developmental studies are available)

600

8 ppb (27 µg/m3)

 

 

*The Regional Gas Dose Ratio (RGDR) is the ratio of the regional gas dose calculated for the respiratory region affected by the inhaled toxicant in the animal species to the regional gas dose in the corresponding region in humans.  For a toxicant with a systemic effect, the default value is 1.

 

Reference Exposure Levels are based on the most sensitive, relevant health effect reported in the medical and toxicological literature.  Acute Reference Exposure Levels are levels at which infrequent one-hour exposures are not expected to result in adverse health effects (see Section 5 of the Technical Support Document (OEHHA, 2008)). Studies of developmental toxicity usually use repeat exposures in utero, either throughout gestation or during organogenesis.  The acute REL for benzene is based on a developmental study (Keller and Snyder, 1988) in which pregnant rats were exposed

6 hours per day during days 6 through 15 of gestation.  However, developmental toxicity

may occur in response to just one exposure during a specific window of

susceptibility.  A literature search found 133 single-day exposure developmental toxicity studies involving 58 chemicals (Davis et al., 2009). The same endpoints observed in repeat dose studies are often observed with single exposures, an acute effect. The acute REL derived above is a level not to be exceeded in any one hour period, which is the default application for acute RELs based on developmental studies (OEHHA, 2008)

 

 

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In the key study, which OEHHA earlier used to develop a Proposition 65 MADL for benzene (OEHHA, 2001), a monotonic dose response was seen for early nucleated red cells in 2 day neonates.  The LOAEL was 5 ppm.  A NOAEL was not detected.  The several continuous  models in BMDS version 2.2 were fit to the data.  The Hill Model calculated a BMCLo.ssoof 0.0112 ppm, which was much smaller than the model’s BMCo.sso of 0.92 ppm, while other models had poor fits (p < 0.1) (data not shown).  The poor results were in part due to the high adverse response (> 75 percent decrease in differential cell count) at 5 ppm, the lowest dose, and hitting a bound of O at 20 ppm, the highest dose.  The data from the highest dose were omitted and the BMDS linear model was fit to the data.  The value for fit was also below 0.1 (Table 8.1 ).  The BMDS results were not used as the point of departure for the REL. However, despite the relatively

poor fit to the data, the proximity of the BMCLo.ssoof 1.51 ppm to the LOAEL of 5 ppm provides some support for the use of “110 for the LOAEL to NOAEL UF.

 

Variance Constant Deviation 1   SD BMC(ppm) 4.14 BMCL(ppm) 3.01 p for fit     AIC* (fitted) 0.0364        98.0831 Constant 0.5SD 2.07 1.51 0.0364      98.0831 Constant 0.05 Relative 0.48 0.40 0.0364        98.0831 Not 1   SD 8.11 5.18 0.015         76.4167 Not 0.5SD 4.06 2.59 0.015          76.4167 Not 0.05 Relative 0.548 0.512 0.015          76.4167

Table 8.1. Benzene 2d neonate data ~’drop 20 ppm~ in BMDS 2.2 Linear Model

 

 

*Akaike Information Criterion

 

The default interspecies UFA-k of 2 for residual pharmacokinetic  differences was used. As indicated above PBPK models for benzene are available in mice, rats, and humans. The hematological effects in the key study have a plausible mechanism involving the toxic metabolites of benzene.

 

The default intraspecies UFH-k of 10 was used.  Screening PBPK modeling by OEHHA staff for toluene, xylene, and naphthalene (OEHHA, 2008) indicated that a factor of …/1 O may be adequate for benzene,  However, the modeling did not include metabolism. Several benzene-specific  reports supported the default value of 10 and possibly a greater value.  In one study of Chinese workers, those with high CYP2E1 and no NQ01 had an odds ratio (OR) of 7.6 for benzene poisoning compared to those with low CYP2E1 and normal NQ01  activity (Table 6.1.2) (Rothman et al., 1996b).  The prevalence of no NQ01  activity is five times greater (22.4% vs. 4.4%) in the Chinese population compared to non-Hispanic whites (Ross, 2005).  A three genes’ interaction revealed a 20.41-fold increased risk of poisoning in Chinese subjects with the NQ01

TIT genotype and with the GSTT1 null genotype and the GSTM1 null genotype compared with those carrying the NQ01  CIT and CIC genotype, GSTT1 non-null genotype, and GSTM1 non-null genotype (Chen et al., 2007).  In a study not involving Chinese adults, at 1   ppm benzene continuous exposure, the PBPK model-estimated quantity of benzene metabolized in human bone marrow ranged from 2 to 40 mg/day, a

20-fold variation (Bois et al., 1996).

 

 

 

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CYP2E1, a principal enzyme in the pathway of benzene metabolism which produces toxic metabolites, has not been detected early in human fetal liver (Vieira et al., 1996) and rises to only 10-20 percent of the adult level by the third trimester (Johnsrud et al.,

2003)(Table 7 .1 ).   However, since many detoxifying enzymes are also low during this period (Mccarver  and Hines, 2002), bone marrow toxicity from benzene metabolites can occur in the fetus.  The 8-fold variation in CYP2E1 levels between the third trimester fetus and the adult (Table 7.1) is also compatible with the default value of 10 for toxicokinetic variability among humans.

 

The default intraspecies UFH-d (toxicodynamics) of ~10 was used to account for pharmacodynamic  variability among pregnant women and their fetuses and among infants, children, and adults (OEHHA, 2008).  During embryonic and fetal development, hematopoiesis occurs first (mesoblastic period) in the extraembryonic yolk sac beginning in the 2nd week and ceasing by the eighth week of gestation, then in the liver (hepatic period) and to a lesser extent in thymus and spleen beginning at the

5th_5th week of gestation, and finally in the bone marrow (myeloid period) beginning at

the 16th_18th week of gestation or even earlier (Charbord et al., 1996; Peault, 1996; Brugnara and Platt, 2003).  The bone marrow volume increases linearly with body weight between 29-33 weeks of gestation and term (Hudson, 1965).

 

Blood cell type and rates of formation change with age (e.g., Table 7.3) and hematopoiesis would be expected to be more dynamic during developmental  (growth) stages than in the adult.  The erythroblast count, a marker of the contribution of the liver to erythropoiesis, decreases exponentially from 83/100 leukocytes at 17 weeks

gestation to 4/100 at term (Nicolaides et al., 1989).  The third trimester fetus is said to

produce red cells at three to five times the rate in adults at steady-state (Palis and Segel, 1998).  The estimate is based on the linear decline in reticulocytes per 100 red blood cells from -10  percent at 17-24 weeks of gestation to -4  percent at term (Matoth et al., 1971; Zaizov and Matoth, 1976; Nicolaides et al., 1989), a comparison of reticulocytes/1000  red cells in newborns (mean=  51.9) versus adults (mean=  15.7) (Seip, 1955), and a computerized simulation analysis of total red cell volume and life span at different life stages (Bratteby et al., 1968).

 

In a study of infants born prematurely, the body weight steadily increased (tripled) with gestational age, the percent reticulocytes declined overall, and the red blood cells (RBC) per volume was fairly constant (Table 8.2) (Zaizov and Matoth, 1976).  Since both the bone marrow volume (Hudson, 1965) and the red blood cell volume (Bratteby,

1968) increase with gestational age and body weight, the net formation of RBCs must be substantial.

 

At birth a large drop in red cell production results in a transient physiological anemia of clinical concern (Palis and Segel, 1998). which reaches a low point in total red cells and hematocrit at 6-9 weeks of life after which red cell counts increase again (Matoth et al.,

1971).

 

 

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Table 8.2. Red cell values on first postnatal day in infants born prematurely

(Zaizov and Matoth, 1976)

Gestation (wk)      N (infants)             Body wt (g)8                     % reties.               RBC x 104

24-25                    7                            725 ± 185             6.0 ± 0.5               4.65 ± 0.43

26-27                     11                                  993 ± 194             9.6 ± 3.2               4.73 ± 0.45

28-29                    7                            1174±128           7.5 ± 2.5               4.62 ± 0.75

30-31                    25                          1450 ± 232           5.8 ± 2.0               4.79 ± 0.74

32-33                    23                          1816 ± 192           5.0 ± 1.9               5.0 ± 0.76

34-35                    23                          1957 ± 291           3.9 ± 1.6               5.09 ± 0.5

36-37                    20                          2245 ± 213           4.2 ± 1.8               5.27 ± 0.68 term0             19                                                       3.2 ± 1.4               5.14±0.7

a  mean ± standard deviation

b  term data based on {Matoth et al., 1971)

 

Although hematopoiesis  is dynamic during development, we were unable to find pertinent quantitative data justifying  a UFH-ct factor greater than the default factor of v10.

 

In the study {Coate et al., 1984)that was the basis of OEHHA’s previous acute REL for benzene {OEHHA, 1999), statistically significant decreased fetal body weight was seen only at 100 ppm, the highest dose tested {Table 7.2).  A mechanism for the fetal effect of decreased body weight in the study is not obvious.  The effects on fetal body weight may be due to the parent compound, which can cross the placental wall, and/or to one of more benzene metabolites.  The Keller and Snyder {1988) study is a much more sensitive study than the Coate et al. study showing effects on the hematopoietic system in neonates at much lower gestational exposure levels than Coate et al. found affecting

fetal body weight.

 

 

 

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8.2  8 hour Reference Exposure Level for Benzene

 

The 8-hour Reference Exposure Level is a concentration at or below which adverse noncancer health effects would not be anticipated for repeated 8-hour exposures (see Section 6 of the Technical Support Document (OEHHA, 2008)).

 

For a health protective approach, OEHHA determined that the 8 hour REL should be the same as the chronic REL: 0.002 ppm (7 µg/m3).     It is unclear whether the

adverse effects of repeated benzene exposure are reversed by overnight or over•

the-weekend  periods of non-exposure and they are likely to continue to worsen with additional exposure.

 

8.3  Chronic Reference Exposure Level for Benzene

 

Study

Study population

 

 

 

Exposure method

Exposure continuity

 

Exposure duration

Critical effects

 

LOAEL NOAEL BMCLo.5SD

 

Average occupational exposure

Human equivalent concentration

 

LOAEL uncertainty factor (UFL) Subchronic uncertainty factor (UFs) Interspecies uncertainty factor

Toxicokinetic (UFA-k) Toxicodynamic (UFA-d)

lntraspecies  uncertainty factor

Toxicokinetic (UFH-k} Toxicodynamic(UFH-d)

Database uncertainty factor

Cumulative uncertainty factor

Chronic Reference Exposure Level

Lan et al. (2004)

250 male and female Chinese shoe workers aged 29.9 ± 8.4 years (vs. 140 controls)

Discontinuous occupational exposure

8 hr/day (10 m3 per 20 m3 day), 6 days/week

6.1 ± 2.1 years

Decreased peripheral blood cell counts

(7 categories; see Table 6.4)

0.57 ± 0.24 ppm (1.86 ± 0.78 mg/m3)

Not found

0.476 ppm (Hill Model version 2.15){Table

8.3)

0.204 ppm (0.476 ppm x 10/20 x 6/7)

0.204 ppm (0.665 mg/m3)

 

Not applicable with BMC

“10  (8-S12% expected lifetime)

 

1   (default, human study)

1   (default, human study)

30 (see explanation below)

 

 

 

1   {developmental studies are available)

100

2 ppb (7 1-1g/m3)

 

 

The chronic Reference Exposure Level is a concentration at which adverse noncancer health effects would not be expected from continuous chronic exposures {see Section 7 in the Technical Support Document {OEHHA, 2008)).

 

 

 

 

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The point of departure for the REL was derived using the changes in B cell levels (Lan et al., 2004 ), which were considered the most sensitive endpoint, as a function of benzene concentration  (Table 6.1.4) and the continuous models in the BMDS software. The Hill model (version 2.15) in the BMDS software gave acceptable values for fit and the lowest AIC.  We specified a risk of 0.5 estimated standard deviation from the control mean as the benchmark and obtained a BMC of 1.62 ppm and a BMCL of 0.476 ppm (p value for fit=  0.303) (Table 8.4).  The U.S. En.vironmental  Protection Agency (USEPA) has suggested use of 1   standard deviation from the control mean as a benchmark but a BMCL1so could not be obtained with the B cell data using the Hill model (Table 8.4).

 

Table 8.4. Benzene  B cell data in BMDS 2.2 (Hill Model Version:  2.12; 02/20/2007) Model           BMC         BMCL         BMC/BM CL     p (test 4)          AIC (fitted)

(ppm)       (ppm)

Constant variance (rho = 0)

Polynomial 0.5 SD          3.04          2.05            1.5                   0.04099           3907.44

Exponential 0.5 SD         1.22         0.44           2.8                   0.1105             3905.811 (Models 4 and 5)

Power0.5  SD                 20.35        14.03          1.7                     0.0006241       3916.02

Linear 0.5 SD                  20.35        14.03         1.7                   0.0006241       3916.02

Hill  0.1 SD                      0.131        0.0299       4.4                    0.303                3904.325

Hill  0.25 SD                    0.422        0.1039       4.1                    0.303                3904.325

Hill  0.5 SD                     1.624       0.4764       3.4                   0.303               3904.325

Hill  0.05 Relative Dev    0.164        0.038         4.3                    0.303                3904.325

Hill 0.1 SD 0.129 Failed         – 0.663                3904.575 0.663                3904.575 Hill 0.25 SD 0.427   Hill 0.5 SD 1.813 Failed         – 0.663 3904.575 Hill 1.0 SD Failed ( MR not in range o f mean function)

Hill  1.0 SD                      Failed (BMR not in range of mean function) Variance not constant (rho¢. 0)

 

Failed         –

 

 

 

 

The Lan et al. (2004) study is more sensitive than both the Tsai et al. (1983) study, used previously by OEHHA for its chronic REL (OEHHA, 2000), and the Rothman et al.

(1996) study used by USEPA for its Reference Concentration (RfC).  Effects on the hematologic system are seen at a level where Tsai et al. did not find significant

changes.  However, as indicated above, at least half(;;:: 50%) of the exposures in Tsai et al. were less than 0.1 ppm, the median concentration.   In Lan et al., 0.09 ppm is two standard deviations below the mean of 0.57 ppm indicating that in Lan et al. only 2.5 percent of the exposures were below 0.09 ppm.  The findings of significant depression

in some blood cell counts at s 0.25 ppm by Qu et al. (2002) and at 0.79 ppm by Khudar

et al. (1999) are compatible with the results of Lan et al. (2004).

 

A combined intraspecies uncertainty factor(UFH) of 30 was used as a compromise instead of separate toxicokinetic  and toxicodynamic  factors since there were reasons for and against higher and lower values for each subfactor.

 

 

 

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Figure 8.3. The continuous  Hill model fit to the B cell data of Lan et al. (2004).

 

 

Hill Mxfel wth o.95 Confidence Level

 

I

240   f

 

 

220

 

200

Hill

 

 

1. Q) crt.:I a.

Q)

rt.I

c::

 

180

 

c:     160

(0

Q)

~

——·–·—–        —    —     –   —       —    ——-·—

 

140

 

1~    t

 

100  ~

BMDL •                              :Bl’vD

0

 

 

11:5710/042011

 

 

5                       10                      15                      20                      25                         30 dose

 

 

As discussed for the acute REL, several benzene-specific  reports supported the default value of 10 for UFh-k (and possibly a greater value).  Chinese workers with high CYP2E1 and no NQ01  had an odds ratio (OR) of 7.6 for benzene poisoning compared to those with low CYP2E1 and normal NQ01  activity (Table 6.1.2) (Rothman et al., 1996b). The prevalence of no NQ01  activity is five times greater (22.4% vs. 4.4%) in the Chinese population compared to non-Hispanic whites (Ross, 2005).  A three genes’ interaction revealed a 20.41-fold increased risk of poisoning in subjects with the NQ01  TIT

genotype and with the GSTT1 null genotype and the GSTM1 null genotype compared with those carrying the NQ01  CIT and CIC genotype, GSTT1 non-null genotype, and

GSTM 1   non-null genotype (Chen et al., 2007).  Some of these variations may already be incorporated in the population of Chinese workers studied in Lan et al. (2004 ), which

was used as the basis of the 8-hour and chronic RELs, so that a U Fh-k less than 1 O might be applied.  However, in a study not limited to Chinese adults, at 1   ppm benzene continuous exposure the PBPK model-estimated  quantity of benzene metabolized in

human bone marrow ranged from 2 to 40 mg/day, a 20-fold variation (Bois et al., 1996; Lan et al., 2004 ). The observation that CYP2E 1   levels vary 8-fold between third trimester fetus and adult (Table 7.1) also supports use of the value of 10.

 

The intraspecies UFH-d  (toxicodynamics) was used to account for pharmacodynamic variability among pregnant women and their fetuses and among infants, children, and adults (OEHHA, 2008).  During embryonic and fetal development hematopoiesis first

 

 

 

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occurs in the extraembryonic  yolk sac, then in the liver and thymus, and finally in the bone marrow during the second and third trimesters (Peault, 1996).  Blood cell type and rates of formation change with age (e.g., Table 7.3) and would be expected to be more dynamic during pre- and post-natal developmental  stages than in adults.  Further discussion of this subfactor can be found in the acute REL derivation above.  However, unlike the acute REL where a sensitive developmental  stage was the critical effect, the key study for the chronic REL involved only exposures and effects in adult workers.

 

The federal Agency for Toxic Substances and Disease Registry (ATSDR) developed a draft Minimal Risk Level (MRL) for chronic (365 days or more) exposure to benzene of

0.003 ppm (10 µg/m3)   based on the Lan et al. (2004) study (ATSDR, 2005; Wohlers et al., 2006; Wilbur et al., 2008).  ATSDR also used the data on B cells (see Table 3 above) in the continuous  Hill model.  However, they defined the BMR as 0.25 standard deviation from the mean, and got a BMC of 0.42 ppm and a BMCL of 0.1  O ppm.

 

In 2003, USEPA derived a Reference Concentration  (RfC) for benzene of 10 ppb (30

µg/m3)  using the Rothman et al. (1996) study, a benchmark dose approach, and their judgment  of appropriate uncertainty factors (IRIS, 2007).  This RfC was derived prior to the publication of Lan et al. (2004 ).

 

8.4  Data Strengths and Limitations for Development of the RELs

 

Both the animal and human databases for benzene are extensive compared to many other chemicals in commerce.  However, a major data gap is the absence of health effects data in infants and children and in young animals.  The hematopoietic system of a growing child must not only keep up with blood cell turnover but must also supply

extra cells for a growing body.  Rapidly dividing cells are more prone to mutation and other cellular changes resulting from chemical exposure.  Thus infants and children may be more sensitive to benzene and its metabolites.

 

A data gap of a specific test is that of a two-generation  reproductive  study (Chapin and Sloane, 1997).  USEPA considered that this gap warranted an additional “database” uncertainty factor in its benzene RfC derivation.  Due to the otherwise extensive animal and human data available for benzene, including developmental  studies in animals, we did not apply such a factor.  OEHHA’s acute REL is based on a developmental  study in rats.

 

8.5  Benzene as a Toxic Air Contaminant Especially Affecting  Infants and Children

 

In view of the wide-spread  exposure to benzene, the documented toxicokinetic variability  in benzene metabolism, and dynamic hematopoiesis during development, there is valid concern that benzene exposure may disproportionately  impact infants and children.   Benzene causes leukemia in exposed workers, including acute myeloid leukemia, and acute non-lymphocytic  leukemia. A positive association has also been found between  benzene exposure in workers and acute lymphocytic leukemia, chronic

 

 

 

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lymphocytic leukemia, multiple myeloma and non-Hodgkin lymphoma. Acute lymphoblastic leukemia is the most common. childhood cancer; other types of leukemia also occur in children.  (IARC, 2012).   OEHHA recommends that benzene be identified as a toxic air contaminant which may disproportionately  impact children pursuant to Health and Safety Code, Section 39669.5(c).

 

 

 

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WISCONSIN CAIT ITALI ASSOCIATION

 

 

Understanding Benzene Emissions from  Iron & Steel Foundries

 

 

 

 

INTRODUCTION

 

The Wisconsin   Cast Metals  Association    (WCMA)  represents the majority of the foundries  in Wisconsin.    This document was developed  by WCMA  to provide  background  information  on benzene  released  during the manufacturing  of metal castings. Any discharges  from foundries,  including  benzene,  are strictly regulated   by   the   U.S.    Environmental    Protection    Agency (USEPA)  and the   Department  of Natural   Resources  (DNR). However,    it  is   important    to  recognize   that  foundries    are relatively     small   contributors    of   benzene   releases    to   the atmosphere.

 

 

BACKGROUND

 

Few  industrial  processes  actually  manufacture  benzene.     It is typically created as an incidental  by-product  of a manufacturing or combustion   process.     For  example,  foundries  do  not use benzene  as a raw material.  However,   it  is  a trace by-product from the combustion  which  occurs during  the casting  process when  the   molten    iron  contacts   the  sand  mold   .       In  fact, combustion  of any kind  including  the burning  of natural  gas, fuel  oil,  gasoline or wood,  creates benzene   as a by-product.

 

 

SOURCES OF BENZENE

 

USEPA  reports  that mobile  sources  such  as cars,  buses  and trucks   account   for   the   majority   of   nationwide    emissions. Benzene  is  a component   of gasoline.    Cars and gasoline-fueled engines   emit   small  quantities   of  benzene  in  unburned   fuel. Benzene is also released  when it evaporates  due to the handling of gasoline  such as filling  the gas tank of a car.

 

• Evaporative Emissions

 

 

Table   l presents   estimates   of benzene   emissions    to the outdoors in    Wisconsin      during     1996     as   reported     by   the   Wisconsin Department     of Natural   Resources    and  the  U.S.    Environmental Protection    Agency.

 

 

Table  1

Wisconsin  Benzene  Emissions

 

Category                   Emissions                 Contribution

(tons  per year)                    (%)

 

Point Sources                      88                                      I

 

Area Sources                   2,003                              18

 

Onroad                         3,650                              33

Mobile  Sources

 

Nonroad                        5,370                             48

Mobile Sources

 

All Sources                    J  l, 111                             100

Source:  References  1   and 2.

 

 

Industrial  operations,   or point  sources,   are the most  tangible category of benzene sources, but they are by far not the largest. Industrial operations are typically the most regulated and utilize sophisticated  methods to reduce emissions.    As shown in Table I,  industrial  operations  contribute  less than 1 % of the benzene emissions   released  in Wisconsin.

 

Over  99%  of  benzene  emissions are   generated   by   non-industrial sources.    These are referred  to as area  and  mobile   sources.     Area sources  include  a wide  variety of common   activities    including   the heating      of     residential        and commercial  buildings   with  natural

gas  and  fuel  oil,  fireplaces   and  woodstoves,   and  wildfires. Onroad  mobile sources  include  automobiles,  trucks and buses. Nonroad mobile sources include airplanes,  trains, lawnmowers, snowmobiles,   construction   vehicles,  and farm machinery.

 

 

 

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Table   2 presents   a comparison    of emissions    from  more  common sources   of benzene   such  as  lawnmowers    and current   automobile traffic   with  those  from  Wisconsin      foundries.

 

 

 

Table 2

Common Sources of Benzene Emissions to the Air

cleveloJ?ed with  t~1e state fou~1dry  industry.  Under this program, each   foun~t)’    is   responsible    for   researching    alternative manufactunng    methods   and  must  demonstrate   reductions    in emissions.     Some  methods   include  use  of  less  combustible organic   materials    in  the  sand  molds    or  water   containing reactants   to  destroy   the  benzene   or  prevent   its .  formation. Foundries  must subrl?-it periodi~   reports to the DNR to verify the success  of the pollution  reduction  programs.

 

Foundries  in Wisconsin  must obtain an air quality permit from

 

 

 

Activity Benzene Released (lbs per the DNR.   These permits  will contain  limitations  on benzene emissions .and  addition.al  ‘.equirements  for monitoring,  testing,   year) and reducing  ~hese  em1ss10~1~.    Prior to issuance  of the permit, the DNR pro~1des  opportumttes for the general public to review Average  car traveling  15,000   miles 4 a draft  permit  and its supporting  analysis.     Comments  on the draft permit and benzene control requirements  can be submitted Lawn  mower 5 to  tl~e  DNR  during    a 30-day  comment   period  and  a public hearing. Residential    wood stove 16     Snowmobile   37 WCMA PARTICIPATION IN POLLUTION REDUCTION   Traffic  on a Mile   of Main   Street in Reedsburg   1,854 The   Wisconsin     Cast  Metals    Association    and   its   member found~·ies  ha.ve  been active  participants  in  the development   of Traffic on a Mile   of Interstate  43 in  Green  Bay 3,015 the Wisconsin  benzene reduction program for foundries.   They Traffic  on a Mile of Highway  51  in  Stevens  Point 3,406   Traffic  on a Mile  of Interstates  90/94  in  Madison 4,260   Typical  Iron Foundry  Emissions 6,140   Traffic  on a Mile of Interstate   94 in  Milwaukee 16,208

Source:  References  3, 4 and 5.

 

 

WISCONSIN REQUIREMENTS FOR FOUNDRIES

 

There  are  no national   standards  for  benzene  emissions    from foundries,     However,   in   Wisconsin,    the  DNR  has  set a low threshold   of 300  pounds  per year at which   industrial   sources must  evaluate  control   of  their  benzene  emissions.      Benzene emissions  from  non-industrial      sources   such  as  zas  stations vehicles    and  small  engines    are  not  regulated   by  the  DNR’. Benzene emissions   from each foundry  are estimated,   and then carefully  reviewed  and  approved  by  the  DNR.     The  agency must  insure  the emissions  cause no adverse  impacts   on h~man health and the environment.

 

Based on its  review of available   emission  control methods, the

D~.  has  c?ncl~ded    that  the  control    of  foundry   benzene

~llliss1ons  usm~ a.u pollution control equipment  is economically infeasible,     This is due to very low concentrations    of benzene in  the ~xhaust   gases,   high  energy  and  equipment    costs,  and

uncertamty  about the effectiveness  of available  technology.

 

Benzene  .can be present  in foundry  exhaust  gases at concentrations  of 0.1  to 3 parts  per million.     These concentrations     are  up  to  l 0  times   lower   than   the  OSHA standards    for  the  workplace.  Controlling  the  benzene  would require  the use of additional   equipment.    It would require  large amounts   of  natural  gas  to  heat  the  air  and  incinerate   the benzene.    The  burning  of natural  gas,  in and of itself,  would generate  benzene and other emissions.

 

~s   a  more . cost-effective   alternative,     DNR   requires   each foundry  to follow  a pollution  reduction   program  to research methods  for  reducing  benzene  emissions.    This  program  was

 

 

 

have sponsored  numerous  tests to measure benzene  emissions, and   many   WCMA   foundries    have   already   implemented benzene reduction   methods.

 

 

EFFECTS OF BENZENE EXPOSURE

 

The  health  effects  of  pollutants   in  the  air  depend  on  their concentration   and an individual’s   length  of exposure.    High concentrations      or   acute   exposure    may   be   immediately noticeabl~.   Low concentrations  over extended periods of time, or  chrome   exposure,   may  require   years  for  the  effects   to become apparent.  The concentrations  of benzene in the outdoor air are far below   the level  where  effects  are  noticeable.   The level  at which  severe  toxic  effects  due  to benzene  exposure occur  is approximately   3 million   times  greater  than a typical rural  background  concentration,   and  9  million  times  greater than  the  maximum    concentration    generated   at  the  property boundary  by operations  at a typical  iron foundry.

 

Some  air  pollutants,  such  as  benzene,   have  been  proven  to cause  cancer  in  humans.    This  conclusion   is either  based on exposure  to high concentrations  that have occurred to people in their workplace,  or based on laboratory  experiments  in  which animals receive very high closes.   People are rarely exposed  to the high  concentrations   which  occurred  in the  workplace  or

 

 

Page 2

 

were  used  in  the  laboratory    experiments.       Low  level   exposures may   still   pose   health     risks,    so   efforts    are   taken    to  reduce emissions     of these  pollutants.

 

It is  important    to note  that  emissions      and  exposure    are  not  the same.    The  concentration     of benzene   released    while  filling  a gas tank  or operating   a lawn   mower   may  result  in a higher   exposure than  the emissions     released   by the tall  stacks  used  by industries.

 

For  a  typical    foundry,    the  downwind     benzene    concentrations are  well   below    the  concentrations       due   to  common    activities such  as filling   a gasoline   tank  or traveling    in  a car.

 

USE OF RISK ASSESSMENT

 

To evaluate  foundry benzene emissions,  the DNR must rely  on the     use     of     computer modeling  to simulate  worst• case  weather  conditions  and estimate    concentrations      at various   locations.     This  is  a more        practical           and conservative     approach   than placing   monitors  all around the    foundry     to    measure actual concentrations.

 

During its review of foundry benzene emissions,  the DNR must verify that foundry benzene emissions   will not harm the environment  or people living near the foundry.    For this purpose,  the DNR conducts  a risk assessment,  a common tool for evaluating the hazards posed by low level exposure to environmental  pollutants.     The risk assessment  will  estimate  the possibility  that the emission  will cause any harm.

 

The DNR risk assessment  conservatively  assumes that an individual  is present at the location of maximum  concentration near the plant  and will be exposed  to this concentration  for a

70-year lifetime. To assess the risk posed to this individual,  the predicted  concentration  is converted  to risk  using   a unit risk value. Toxicologists  and epidemiologists  use information on the

effects   of  a  pollutant   to  establish    a  relationship    between exposure  and risk and

errussions.      A predicted   risk   of Jess  than  10 in  a million  or

0.00001 represents  nearly zero risk and is  typically  considered insignificant   by regulatory  agencies.

 

Table  3 presents  the predicted  risk due to benzene  emissions from  a typical  foundry  at  various  distances  from  the  plant. These  theoretical  risks of developing  cancer  are compared  to other risks  of death  in  the Wisconsin  due  to such  causes  as smoking,  driving   or being  struck  by  lightning.     The  risk  or probability of harm due to the emissions  from a foundry is well below  that for more common activities,  and even  the risk  due to urban and rural background  concentrations  of benzene.

 

Table 3

Risk Comparison

 

Certainty

Cause of Death or Illness                        of Harm

(Frequency  in

Million)

 

Smoking                                                                 210,000

 

Motor vehicles accidents                                         9,430

 

All home accidents                                                  7,700

 

Passive  smoking                                                      7,000

 

Fi.rearms                                                                   1,520

 

Average diagnostic  medical   xrays                         1,400

 

Drowning                                                                   890

 

Aircraft accidents                                                      290

 

Electrocution                                                                150

 

Excessive  cold                                                           130

 

Accidental   foils                                                          40

 

develop   the  unit  risk value.                This information           is typically       obtained from  epidemiological studies      of    human exposure            and laboratory       animal tests,   both  based   on high      levels         of e  x  p  o  s  u  r  e  . Mathematical    models

are         used           to       0 conservatively

estimate    the   hazards

Cancer

R!?sponse

 

 

 

Oose

Lightning                                                                     35

 

Urban benzene concentration                                    16

 

Rural benzene concentration                                      12

 

Iron foundry  benzene concentration                           4 at the facility property  line.

 

Yi mile  from an iron  foundry                                    0.5

 

1   mile  from an iron  foundry                                     0.3

Source: References  7, 8 and 9.

 

found during  these studies   to those  that might be expected  at

low  levels  of exposure.    The  end  result  is a unit risk  value which can be used to estimate the relative  risk of harm posed by a low level of exposure.    In  the case of benzene,   the risk of contracting  cancer from the exposure  is  estimated.

 

A risk of zero indicates  that no harm will occur.  A risk of one concludes  that harm will occur.   The risk assessment  must conclude  that insignificant   risk  will result  due to the foundry

CONCLUSIONS

 

The  DNR  has  concluded   that the risk   posed  by  the  benzene from foundries  is small and insignificant,    and  these emissions are unlikely  to cause  harm  to individuals  or the environment. Continued   efforts  by Wisconsin  Cast Metals  Association   and Wisconsin  foundries  to identify  lower polluting  manufacturing methods will further reduce benzene emissions   and impacts.

 

 

Page 3

 

REFERENCES

 

1. 1. Wisconsin Department of Natural Resources,  NR 438 Annual

Emissions Inventory,   1996.

 

2. USEPA, National   Air  Toxics   Assessment   internet   site:

www.epa.gov/ttn/uatw/nata.

 

3. 3. USEPA,   Locating   and   Estimating   Air   Emissions  from

Sources of Benzene, EPA-454/R-98-011,    June 1998.

 

4. 4. Wisconsin  Department   of Transportation,    Annual  Traffic

Counts for Wisconsin  Highways,  2000.

 

5. Wisconsin Department  of Natural   Resources,  Summary  of

Iron Foundries  Subject to State Benzene Regulations,  2000

 

6. 6. Wallace, , Major Sources  of Exposure  to Benzene   and Other Volatile Organic  Chemicals,  Risk  Analysis,   Volume   10, No. 1,   1990.

 

7. 7. USEPA, National Air  Quality and Emissions  Trend Report,

1998.

 

8. 8. Bureau  of  Health  Information,   Division   of  Health    Care Financing,     Department    of   Health    and   Family     Services, Wisconsin Deaths,  1998.   January 2000.

 

9. 9. Travis, and Cook,  S.,  Hazardous  Waste Incineration.   and

Human Health,  CRC Press, Inc.,   1989.

 

10. 10. Graphics  courtesy of the USEP

 

Prepared  by  \Vi11gra  Engineering,   S.C..  Madison.   \Visconsin.  October  2000.

 

Printed  011 Recycled  Paper

 

 

 

WISCONSIN C  11        ~ ASSOCIATION

660 East Mason  StrectO    Milwaukee,    WI  53202 0  414-227-1292

 

 

 

“Understanding  Benzene Emissions from  Iron & Steel Foundries”

 

 

 

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Home  -» Air-~> Hot Spots ..»Revlsed  Air Toxics Hot Spots Program Technical Support Document for the

Derivation of Noncancer Reference Exposure Levels and RELs for Six Chemicals

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ADOPTION OF THE REVISED AIR TOXICS HOT SPOTS PROGRAM TECHNICAL  SYf  PORT  ~

DOCUMENT FOR THE DERIVATION OF NONCANCER  REFERENCE EXPOSURE LEVE(:%    ~ AND RELS FOR SIX CHEMICALS                                                                                      ~     :3     ~ [12/19/08]                                                                                                                                ::!!     l’\l   :      ~

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updated August, 2013

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The Office of Environmental Health Hazard Assessment  (OEHHA) is required to develop guidelines for conducting health risk assessments  under the Air Toxics Hot Spots Program (Health and Safety Code Section 44360(b)(2)). OEHHA initially developed Technical Support Documents (TSDs) in 1999-2000  in response to this statutory requirement, including two which described acute and chronic Reference Exposure Levels (RELs). (A REL is an airborne level of a chemical that is not anticipated to presenta significant risk of an adverse non-cancer health effect.) OEHHA has developed a revised draft TSO, “Air Toxics Hot Spots Program Technical Support Document for the Derivation of Noncancer Reference Exposure Levels, n  which is designed to replace those two original TSDs. This presents methodology revised to reflect scientific knowledge and techniques developed since the previous guidelines were prepared, and in particular to explicitly include consideration of possible differential effects on the health of infants, children and other sensitive subpopulations, in accordance with the mandate of the Children’s Environmental Health Protection Act (Senate Bill 25, Escutia, Chapter 731, Statutes of 1999, Health and Safety Code Sections

39669.5 et seq.). In addition to the previously defined acute and chronic RELs, the new method allows for the estimation of 8-hour RELs, which may be useful in dealing with some special circumstances  in Hot Spots risk assessments.

 

A draft of the TSO was released on November 2. 2007 to solicit public comment. The document was then reviewed by the State’s Scientific Review Panel on Toxic Air Contaminants (SRP). It was initially presented to the SRP on

February 28, 2008. Revised versions of the document reflecting new data and comments from the public and the SRP

were discussed at meetings held on May 16, 2008 and June 18, 2008. At the latter meeting, the SRP approved the

final versions of the methodology section and the associated methodological appendices.

 

Following this process, and by this memo, OEHHA is finalizing and adopting the TSO, along with acute, 8-hour and chronic Reference Exposure Levels (RELs) for six chemicals (acetaldehyde, acrolein, arsenic, formaldehyde, manganese [no acute REL was derived for this chemical], and mercury). The values of the RELs are listed in the table attached. OEHHA also hereby adds acetaldehyde, arsenic, formaldehyde,  manganese, and mercury to the list of

Toxic Air Contaminants that may cause infants and children to be especially susceptible to illness. Acrolein has already been listed in this way. This listing, specified by the Children’s Environmental Health Protection Act, requires that any Air Toxic Control Measures which CARB determines to be necessary for listed chemicals shall be adequate to protect the health of infants and children.

 

Adoption of the TSO does not automatically affect the other existing acute and chronic RE Ls (which are listed  in the appendices to the TSO). However, the RELs for the six chemicals that OEHHA is adopting today illustrate the use of the new guidelines. These proposed RELs were initially presented for public comment and SRP review along with the Technical Support Document, and were discussed further at the meeting of the Scientific Review Panel on October 30,

2008. At the meeting of the Scientific Review Panel on December 5, 2008, the RE Ls and their supporting documentation were approved. The toxicological summaries describing their derivation, and the values for acute,

8-hour and chronic RELs, are presented  in the appendices to the new TSO. Any further new or revised RELs approved by the SRP will be adopted and also included  in these appendices.

 

Follow the links below to donwload the Technical Support Documents

 

Air Toxics Hot Spots Program Technical Support Document for the Derivation of Noncancer Reference Exposure

Levels (OEHHA. 2008)

 

 

 

http://oehha.ca.gov/air/hot_spots/rels_dec2008.html                                                                     61212015

 

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• -» Appendix A – Acronyms

 

• ·?>> Appendix B -Appendix B. Acute. 8-Hour. and Chronic Reference Exposure Levels (RELsl Summarv Table

(updated 10/18/13}

 

-:>>     Appendix C. Substances for which Emissions Must Be Quantified

 

..)>    Appendix  D.1 Individual Acute. 8-Hour. and Chronic Reference Exposure Level Summaries (updated 07/09/14)

 

..:>>     Appendix  D.2 Acute RELs and toxicity summaries using the previous version of the Hot Spots Risk Assessment guidelines  COEHHA 1999) (updated  08/20/13}

 

-)>   Appendix D.3 Chronic RELs and toxicity summaries using the previous version of the Hot Spots Risk

Assessment guidelines (OEHHA 1999) (updated 08/20/13}

 

.. :>>      Appendix  E. Application  of Toxicokinetic  Modeling and Analysis of Toxicokinetic  Differences  by Age at Exposure

 

• ·:>> Appendix F:  Estimating Human Equivalent Concentrations Using the U.S. EPA Default Approach

 

• ·)> Appendix G. Value of the Haber’s Law Exponent (n) for various gases and vapors for acute RELs developed using OEHHA (1999) procedures

 

.. ::>>       Appendix  H. Target Organs or Systems used in Acute. 8-Hour and chronic Hazard Index Calculations

 

 

 

Acute (A), 8-hour (8) and Chronic (C) Reference Exposure Levels

(Follow the links in the chemical names below to view the documentation}

 

!Substance                                             Inhalation REL Oral REL (ug/kg Hazard Index Target Organs Huma Data     (ug/m3) BW-day)       Acetaldehvde (75-07-0)   A   470     Sensory irritation; bronchi, eyes, nose, throat x     8   300     Respiratory system       c   140     Respiratory system     Acrolein  (107-02-8)   IA   2.5     Sensory irritation; eyes x     8   0.7     Respiratory system       K:   0.35     Respiratory system     Arsenic (7440-38-2) & inoraanic   ~   0.20     Development (teratogenicity);   arsenic comoounds lincludina  arsine)       cardiovascular system; nervous           system       8   0.015     Development; cardiovascular system; nervous system; lung; skin x     ~   0.015   0.0035   Development; cardiovascular  system; x         nervous system; lung; skin     Formaldehvde (50-00-0)   ~   55     Sensory irritation; eyes x

n

 

 

 

http://oehha.ca.gov/air/hot_   spots/rels _dec2008.html                                                                              6/2/2015

 

OEHHA  Air- Revised  Air Toxics Hot Spots Program  Technical   Support Document  for th…     Page 3  of 3

 

 

 

	8	9		Respiratory  system	x
	le	9		Respiratory  system	x
Manaanese   17439-96-5)  & manaanese lcomnounds	l.l!	—
	8	0.17		Nervous system	x
	k:	0.09		Nervous system	x
Mercurv  (7439-97-6) & inoruanic mercurv  comnounds	lA	0.6		Nervous system,   development
	8	0.06		Nervous system	x
	IC	0.03	0.16	Nervous system	x

 

 

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All OEHHA Acute,  8-hour  and Chronic   Reference  Exposure   Levels  (chRELs)  as of June  2014

Follow the links below to download documentation  on the reference exposure  levels. Footnotes:

c11REL  types: A=  acute, 8 = 8-hour, C =chronic.  Exposure averaging time for acute RELs is 1   hour.  For 8-hour RELs, the exposure averaging time is 8 hours, which may be repeated.   Chronic RELs are designed to address continuous exposures for up to a lifetime: the exposure metric used is the annual average exposure.

 

C2Jspecies  used in key study for REL development:  D = dog; Gb = gerbil; GP = guinea pig: H = human; Ha = hamster; M

= mouse; Mk = monkey; R = rat; Rb = rabbit

 

l3Jrhese peer-reviewed  chronic REL values were developed  under the Toxic Air Contaminant  (TAC) Program mandated by AB1807.

 

l41REL based on benchmark dose (BMC) approach.

 

l5JREL developed  using the revised methodology  (OEHHA, 2008)].

 

 

OEHHA  Acute,  8-hour  and Chronic   Reference  Exposure   Level  (REL) Summary 1

 

 

 

Substance

 

 

REL Inhalation Oral REL Hazard  Index type       REL (ug/kg  BW-day) Target  Organs

[1]       (ug/m3)

Species

[2]

 

 

 

Acetaldehyde    (75-07 -0)                   Acrolein    (107-02-8)	A	470!5}	Eyes; respiratory system (sensory irritation)	H
	8	30014•5]	Respiratory system	R
	c	140£4•51	Respiratory  system	R
	A	2.5/5}	Eyes, respiratory system (sensory irritation)	H
	8	0.7(5}	Respiratory system	R
	c	0.35/SJ	Respiratory  system	R
Ac~lic   Acid   (79-10-7)	A	6,000	Respiratory system; eyes	R
Acrvlonitrile  (107-13-1)	c	sf41	Respiratory system	R

 

 

 

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OEHHA  Air – Table of All Acute, Chronic  and 8 hour Reference  Exposure  Levels                  Page 2 of IO

 

 

 

 

 

Ammonia   (7664-41-7)

A      320of41                                                                                             H

Q           200                                    Respiratory system                  H A          0.20£5}                                              Development;                            M

cardiovascular  system;

nervous system

 

 

 

8      0.015{5}                               Development;                            H

cardiovascular  system; Arsenic   (7440-38-2}  & inorganic arsenic                                                                      nervous system; compounds   (including  arsine)                                                                                       respiratory system; skin

 

c     0.015£5}             0.0035£51          Inhalation & oral:                   H Development;

cardiovascular  system; nervous system; respiratory system; skin

 

Benzene   (71-43-2)

A          27                                     Developmental;  Immune         M

system; Hematologic system

 

8           a                             Hematologic  system                 H

 

c       ~                                             Hematologic  system                 H

 

 

Benzyl  Chloride(100-44-7)                                          A         240                                    Respiratory system; eyes     M,R

 

c     0.007                2.0            Inhalation: Respiratory             H Bervllium&  bervllium   compounds    (7440-41-7)                                                           system; immune system

Oral: Alimentary  system

(Gastrointestinal  tract)

 

 

A       660(4•51

Development

M

 

 

Butadiene   (106-99-0)                                                 8         9(4,5)                                                 Reproductive  system               M

 

 

c      2(4,5}                                             Reproductive  system               M

 

 

Cadmium   & cadmium   compounds   (7440-

c     0.02                  0.5            Inhalation: Kidney;                   H

respiratory system

 

43-9)                                                                                                                                   Oral: kidney

 

 

Carbon  disulfide  (75-15-0)

A       6.200                                  Reproductive/                            R Development;  nervous

system

 

 

Q       aoo£41                                     Nervous system;                       H

re(:’!roductivesystem

 

 

Carbon  monoxide   (630-08-0)                                   A       23,000                                 Cardiovascular  system            H

 

 

 

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OEHHA  Air – Table of All Acute,  Chronic  and 8 hour Reference  Exposure  Levels                  Page 3of10

 

 

 

 

A          50                                     Eyes (sensory irritation)           H

 

Caprolactam   (105-60-2)	8	7		Respiratory  system	R
	c	2.2		Respiratory  system	R
	A	1.900		AlimentaQ( system (liver); Re12roductive/	R
				Develo12mental; nervous
Carbon  tetrachloride  (56-23-5)				system
	Q	40		AlimentaQ( and nervous	GP
				systems: development
Chlorinated dibenzo-p   dioxins   and	c	0.00004	1×10-5	Inhalation and Oral:	R
dibenzofurans				Alimentary  (liver)
				reproductive,  endocrine,
Unspeciated  mixtures treated as				respiratory,  hematologic
2,3,7,8-tetrachlorodibenzo-p-dioxin    (1746-01-6)				systems; development
	A	210		RespiratoQ( system; eyes	H
Chlorine (7782-50-5)
	Q	0.2£41		RespiratoN  system	R
Chlorine dioxide   (10049-04-4)	c	0.6		Respiratory  system	R
	c	1,000		Alimentary  system (liver);	R
Chlorobenzene    (108-90-7)				kidney; reproductive
				system
	A	150		Re12roductive/ Developmental;	R
				respiratoQ( system;
Chloroform  (67-66-3)				nervous system
	~	300		AlimentaQ( system; kidney: development	R
	A	29		RespiratoQ( system; eyes	M
Chloropicrin  (76-06-2)
	Q	0.4[4]		Res12iratoQ( system	M
	c	0.002	20	Inhalation: Respiratory	H
Chromic trioxide   (as chromic acid mist)				system
				Oral: Hematologic  system
Chromium {hexavalent)   (18540-29-9)  & soluble	c	o.2r41	20	Inhalation: Respiratory	R
hexavalent chromium compounds  (except				system
chromic trioxide)				Oral: Hematologic  system
Copper  and compounds	A	100		Respiratory  system	H

 

 

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OEHHA  Air – Table  of All Acute,  Chronic  and 8 hour Reference  Exposure  Levels                  Page 4of10

 

 

 

Cresol  mixtures (1319-77-3)	c	600	Nervous system	R
Dichlorobenzene    {1 A-} (106-46-7)	c	800	Nervous and respiratory; –       alimentary systems	R
			(liver}; kidney
Dichloroethylene    1.1.J.} (75-35-4)	c	70	Alimentary  system (liver)	GP
Diesel  Exhaust	c	5£3)	Respiratory system	R

 

 

Diethanolamine     (111-42-2)

c       3                                      Respiratory and                        R

hematologic  systems

 

 

Dimethvlformamide     (N.N-) (68-12-2)                      c       80                                    lAlimentary (liver) and               H

respiratory systems

 

 

A     3,000                                  Resoiratorv svstem: eves        H

 

 

 

Dioxane  (1,4-) (123-91-1) Q 3,000 Alimentarv svstem: kidnev: cardiovascular svstem R   A   1,300   Resoiratorv svstem: eves   H Epichlorohydrin  (106-89-8)               Q ~ Resoiratorv svstem: eves R     c   20   Respiratory system;   M         cardiovascular  system         c   2,000   Alimentary  system (liver);   M,R Ethylbenzene(100-41-4)       kidney; endocrine           system; development     Ethyl  chloride (75-00-3)   c   30,000   Development;  alimentary system (liver)   M   Ethylene  di bromide   (106-93-4)     c   0.8   Reproductive  system   H   Ethylene  dichloride  (107-06-2)   c   400   Alimentary  system (liver)   R     c   400   Respiratory system;   H         kidney; development     Ethylene  glycol  monobutyl ether   (111-76-2)   A   14,000   Respiratory system; eyes   H   Ethylene  glycol  monoethyl   ether   (110-80-5)   A   370   Reoroductive/ Develooment   R       ~   70   Reoroductive  svstem·   Rb         hemotoloaic  svstem

E~oxybutane   {112-}   (106-88-7)

 

 

 

EthyJene glycol  (107-21-1)

 

 

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OEHHA  Air – Table of All Acute,  Chronic  and 8 hour Reference  Exposure  Levels                  Page 5of10

 

 

 

Ethylene glycol monoethyl ether acetate	A	140	Reoroductive/                            R Develooment’  nervous svstem
(111-15-9)
	Q	300		Develooment	Rb
Ethylene glycol monomethyl ether {109-86-4)	A	93		Reoroductive/ Develocment	R
	Q	60		Reoroductive  svstem	Rb
Ethl£lenegll£col monomethl£1ether acetate (110-49-6)	c	90		Reproductive  system	Rb
Ethl£leneoxide (75-21-8)	c	30		Nervous system	R
Fluorides (except Hydrogen Fluoride – listed	c	13£4)	40	Inhalation:  Bone and	H
below separately)				teeth; respiratory system
				Oral: Bone and teeth
	A	55£5)		Eyes {Sensory  irritation)	H
Formaldehl£de (50-00-0)	8	9(5)		Respiratory  system	H
	c	9(5)		Respiratory  system	H
Glutaraldeh~de (111-30-8)	c	o.08r41		Respiratory  system	M
Hexane (n-)(110-54-3)	c	7000		Nervous system	H
Hlldrazine  {302-01-2)	c	0.2		Alimentary  system (liver);	Ha
				endocrine system
	A	2.100		Resoiratorv  svstem· eves	H
Hydrogen chloride (7647-01-0)
	Q	!l		Resoiratorv  svstem	H
	A	340		Nervous svstem	H
Hydrogen cyanide (74-90-8)	Q	!l		Nervous svstem· endocrine  svstem·	H
				cardiovascular  svstem
Hydrogen fluoride (7664-39-3)	A	240		Resoiratorv  svstem· eves	H
	Q	14£41	40	Inhalation: Bone and	H
				teeth· resoiratorv svstem
				‘See “fluorides”
				summarv)

 

 

 

http://oehha.ca.gov/air/allrels.html                                                                                                               6/2/2015

 

OEHHA Air – Table of All Acute,  Chronic  and 8 hour Reference  Exposure  Levels                  Page 6of10

 

 

 

Oral: Bone and teeth

 

 

Hxdrogen selenide (7783-07-5)                          A          5                                  Respiratory system; eyes     GP

 

 

 

 

Hydrogen sulfide (7783-06-4)

A          42                                 Nervous svstem                    H

 

Q        10                                Resoiratorv svstem               M

 

 

lso(;!horone (78-59-1)                                          c     2,000                              Development; alimentary    R,M

system (liver)

 

 

 

 

lsopropanol (67-63-0)

A       3.200                              Eves·  resoiratorv svstem       H

 

Q      7.000                              Kidnev: develooment          R,M

 

 

 

Maleic anhxdride (108-31-6)                               c     0.1£41                                       Respiratory system            R,Ha, Mk

 

 

 

Manganese {7439-96-5}   & manganese

8      0.11£4•51                                    Nervous system                    H

 

development   nervous svstem· develooment       A   68.000     Nervous svstem   H Methyl chloroform  (71-55-6)             Q 1000   Nervous svstem Gb   Methylene chloride (75-09-2)   A   141000       H

4•51

compounds                                                          c    0.09(

Nervous system                    H

 

 

A	0.6r51	Nervous system;	R
		development

 

Mercu(Y (7439-97-6} & inorganic me compounds	rcu(Y          8	0.06(51		Nervous system; development;  kidney	H
	c	o.03rSJ	0.16f5l	Inhalation & Oral:	H
				Nervous system;
				development;  kidney
	A	28.000		Nervous svstem	H
Methanol (67-56-1)
	Q	41000£4}		Develooment	M
	A	3900		Nervous svstem; respiratory system;	H
				Reproductive/
Methyl bromide (74-83-9)
	Q	§		Resoiratorv svstem:	R

 

 

 

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OEHHA  Air -Table  of All Acute,  Chronic  and 8 hour Reference  Exposure  Levels                  Page 7of10

 

 

 

Cardiovascular  svstem· H nervous svstem

Cardiovascular  svstem: Nervous svstem

 

 

~        400

 

 

Meth)llene  dianiline   (4.4′-) (101-77-9)                     c      20                                     Eyes; alimentary  system        GP

(liver)

 

Meth)llene  di12hen)ll isoc)lanate

(101-68-8)

c     0.1£41

Respiratory  system

R

 

Meth)ll

eth)ll  ketone  (78-93-3)

A

13,000

Respiratory  system; eyes

H

 

 

Meth)ll  isoc)lanate   (624-83-9)

 

 

 

c   1   c     8,000

Naohthalene   (91-20-3) c   9 Respiratory  system   H     A   0.2£5]   Immune system   M   Nickel  & nickel  comnounds   (except nickel oxide for chronic inhalation exposures)   8   0.05151 Respiratory,  immune systems   R (Inhalation concentrations  as µg Ni/m3: oral dose as µg Ni/kg-day) c   0.014£51                1   1               Inhalation:   Respiratory   R

Meth)ll  t-bu1)ll ether  (1634-04-4)

Respiratory  system;                 R

reproductive  system

 

 

Kidney; eyes; alimentary          R

system (liver)

 

 

 

[5]
				system; hematologic
				system
				Oral: Development
Nickel  oxide  (1313-99-1)  (Inhalation	c	0.02£51	11£5]	Inhalation: Respiratory	M
concentration  as µg Ni/m3: oral dose as µg Ni/kg-day)				system Oral: Development	R
Nitric  acid   (7697-37-2)	A	86		Respiratory system	H
Nitrogen  dioxide  (10102-44-0)	A	470		Respiratory  system	H
Ozone  (10028-15-6)	A	180		Respiratory  system; eyes	H
	A	20.000		Nervous svstem·	H
resoiratorv svstem· eves Perchloroethylene     (127-18-4) (syn. Tetrachloroethylene)[3J
~		35		Kidnev· alimentarv	M
				svstem (liver)
Phenol   (108-95-2)                                                     A		5.800		Resoiratorv  svstem· eves	H
Q		200		Alimentarv  svstem:	R
				cardiovascular  svstem·
				kidnev: nervous svstem

 

 

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OEHHA Air – Table  of All Acute, Chronic  and 8 hour Reference  Exposure  Levels                  Page 8of10

 

 

 

Phosaene  (75-44-5)	A	4	Respiratory system	R
Phosphine   (7803-51-2)	c	0.8	Respiratory system; alimentary  system (liver);	M
			nervous system; kidney;
			hematologic  system
Phosohoric   acid  (7664-38-2)	c	7(4)	Respiratory system	R

 

 

Polychlorinated    biphenyls (PCBs)                         c        –                     –

Inhalation & oral:

~limentary  (liver)                      R

 

Individual congeners  evaluated  using TEF                                                                     reproductive,  endocrine, methodology,  relative to as                                                                                               respiratory,  hematologic

2,3,7 ,8-tetrachlorodibenzo-p-dioxin   (see                                                                         systems; development

Appendix C in the TSO for Cancer Potency

Factors-  online at: htt12://oehha.ca.gov/air/hot  SQots/tsd052909.html
Phthalic  anh)ldride   (85-44-9)	c	20		Respiratory system	H
Prop)llene(115-07-1)	c	3,000		Respiratory system	R
Prop)llene  gl)lcol  monometh)ll   ether  (107-	c	7,000		~limentary  system (liver)	R
98-2)
Propylene   oxide  (75-56-9)	A	3.100		Resoiratorv svstem: eves· reoroductive/develooment	H
	Q	30		Resoiratorv svstem	R
	c	20	5	Inhalation & oral:	H
Selenium  and selenium comQounds (other than				~limentary  system (liver);
hydrogen selenide)				cardiovascular  system;
				nervous system
Silica  (crystalline,  respirable)	c	3(4)		Respiratory  system	H
Sodium  hvdroxide   (1310-93-2)	A	8		Respiratory system; eyes;	H
				skin
	A	21.000		Resoiratorv  svstem: eves· reoroductive/develooment	H
Styrene  (100-42-5)
	Q	900£41		Nervous svstem	H
Sulfates	A	120		Respiratory system	H
Sulfur  dioxide   (7446-09-5)	A	660		Respiratory  system	H
Sulfuric acid  (7664-93-9)  [& oleum,  acute only]	A	120		Resoiratorv svstem	H

 

Q          1                                   Resoiratorv svstem                 Mk

 

 

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OEHHA Air – Table  of All Acute,  Chronic  and 8 hour Reference  Exposure  Levels                  Page 9of10

 

 

 

Toluene  (108-88-3)	A	37,000	Resoiratorv.  nervous svstems;  eyes	H
			reproductive/development
	_g	300	Nervous svstern: resoiratorv  svstem: develooment	R
Toluene  diisocl{anates  {2,4-  & 2,6-}	c	0.07	Respiratory system	H
Trichloroethl{lene     (79-01-6)	c	600	Nervous system;  eyes	H
	A	2,800	Nervous svstem· eves	H
Triethylamine   (121-44-8)
	c	200	~	R
Vanadium   ~entoxide(1314-62-1)	A	30	Respiratory   system;  eyes	H
Vi nJl I  acetate  ( 108-05-4)	c	200	Respiratory  system	R,M

 

Vinlll  chloride   (75-01-4)	A	180,000	Nervous system; respiratory   system;  eyes	H
Xylenes:  technical  mixture  (1330-20-7)  and	A	22000	Nervous & resoiratorv svsterns:  eves	H
o-xylene  (95-47-6),  m-xylene   (108-38-3)    and
p-xylene (106-42-3)   isomers.	_g	700	Nervous & resoiratorv	H
			svstems: eves

 

 

 

 

 

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DECISION

ZONING CODE SECTION  5.153 VARIAN  CE APPROVED

 

To:   Kim DeTemple

23 Lafayette Road

Tappan, New York 10983

ZBA#IS-49

Date: June 17, 2015

 

 

FROM: ZONING BOARD OF APPEALS: Town of Orangetown

 

 

ZBA#lS-49: Application of Kim DeTemple for a variance from Zoning Code (Chapter

43) of the Town of Orangetown Code, R-15 District, Group M, Section 5.153 (Location of accessory buildings or structures: 15′ required between structures, 5.3′ existing between deck and garage) at an existing single-family residence. The premises are located at 45 Grand Avenue, Tappan, New York and are identified on the Orangetown . Tax Map as Section 77.10, Block 2, Lot 21; in the R-15 zoning district.

 

 

 

 

Heard by the Zoning Board of Appeals of the Town of Orangetown at a meeting held on Wednesday, June 17, 2015 at which time the Board made the determination  hereinafter set forth.

 

Kim DeTemple appeared and testified. The following documents were presented:

1. Plot plan showing the existing structures and the distance between them. (1 page).
2. A hand drawing of the existing deck.

 

Mr. Sullivan,  Chairman, made a motion to open the Public Hearing which motion was seconded by Ms. Castelli and carried unanimously.

 

On advice of Dennis Michaels, Deputy Town Attorney, counsel to the Zoning Board of Appeals, Mr. Sullivan  moved for a Board determination that the foregoing application is a Type II action exempt from the State Environmental Quality Review Act (SEQRA), pursuant to SEQRA Regulations §617.5 (c) (9), (10), (12) and/or (13); which does not require SEQRA environmental review. The motion was seconded by Ms. Castelli and

carried as follows: Ms. Castelli, aye; Ms. Salomon, aye; Mr. Bosco, aye; Mr. Quinn, aye;

and Mr. Sullivan, aye.

 

 

 

 

Kim DeTemple testified that the house belonged to her mom, that the existing structures have been there for years; that the estate is selling the house and found out that a variance is needed because the deck on the garage is too close to the back of the house; that she would like to legalize the existing condition in order to sell the house.

 

 

 

301.:J.:JO  SY:U31Q  NMO!

£h  21  Wd   s   1nr  5102

 

NM013t)N’Vhl0  .:10   N/~01

 

De Temple

ZBA#lS-49

Page2 of 4

 

 

 

 

Public Comment:

 

No public comment.

 

The Board members made personal inspections of the premises the week before the meeting and found them to be properly posted and as generally described on the application.

 

A satisfactory statement in accordance with the provisions of Section 809 of the General

Municipal Law ofNew York was received.

 

Mr. Sullivan made a motion to close the Public Hearing which motion was seconded by

Ms. Castelli and carried unanimously.

 

FINDINGS OF FACT AND CONCLUSIONS:

After personal observation of the property, hearing all the testimony and reviewing all the documents submitted, the Board found and concluded that the benefits to the applicant if the variance(s) are granted outweigh the detriment (if any) to the health, safety and

welfare of the neighborhood or community by such grant, for the following reasons:

 

 

 

1. The requested Section 5 .153 variance, for the distance between the rear of the house and the deck on the garage, will not produce an undesirable change in the character of the neighborhood or a detriment to nearby properties. The structure has existed in its present state for many years without complaint.

 

 

 

2. The requested Section 5, 153 variance, for the distance between the rear of the house and the deck on the garage, will not have an adverse effect or impact on the physical or environmental conditions in the neighborhood or district. The structure has existed in its present state for many years without complaint.

 

3. The benefits sought by the applicant cannot be achieved by other means feasible for the applicant to pursue other than by obtaining a variance.

 

 

 

4. The requested Section 5,153 variance, for the distance between the rear of the house and the deck on the garage, although somewhat substantial, afford benefits to the applicant that are not outweighed by the detriment, if any, to the health, safety and welfare of the surrounding neighborhood or nearby community.  The structure has existed in its present state for many years without complaint.

 

 

 

5. The applicant purchased the property subject to Orangetown’s Zoning Code (Chapter

43) and is proposing a new addition and/or improvements, so the alleged difficulty was self-created, which consideration was relevant to the decision of the Board of Appeals, but did not, by itself, preclude the granting of the area variances.

 

 

301.:1.:10  S>!H310   NMO!

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De Temple

ZBA#lS-49

Page 3   of 4

 

 

 

DECISION: In view of the foregoing and the testimony and documents presented, the Board: RESOLVED, that the application for the requested Section 5.153 variance, for the distance between the garage and house, is APPROVED; and FURTHER RESOLVED, that such decision and the vote thereon shall become effective and be deemed rendered on the date of adoption by the Board of the minutes of which they· are a part.

 

 

 

 

General Conditions:

 

(i) The approval of any variance or Special Permit is granted by the Board in accordance with and subject to those facts shown on the plans submitted and, if applicable, as amended at or prior to this hearing, as hereinabove recited or set forth.

 

(ii) Any approval of a variance or Special Permit by the Board is limited to the specific variance or Special Permit requested but only to the extent such approval is granted herein and subject to those conditions, if any, upon which such approval was conditioned which are hereinbefore set forth.

 

 

 

(iii) The Board gives no approval of any building plans, including, without limitation, the accuracy and structural integrity thereof, of the applicant, but same have been submitted to the Board solely for informational and verification purposes relative to any variances being requested.

 

 

 

(iv) A building permit as well as any other necessary permits must be obtained within a reasonable period of time following the filing of this decision and prior to undertaking any construction contemplated in this decision. To the extent any variance or Special Permit granted herein is subject to any conditions, the building department shall not be

obligated to issue any necessary permits where any such condition imposed should, in the sole judgment of the building department, be first complied with as contemplated hereunder. Occupancy will not be made until, and unless, a Certificate of Occupancy is issued by the Office of Building, Zoning and Planning Administration and Enforcement

which legally permits such occupancy.

 

 

 

(v) Any foregoing variance or Special Permit will lapse if any contemplated construction of the project or any use for which the variance or Special Permit is granted is not substantially implemented within one year of the date of filing of this decision or that of any other board of the Town of Orangetown granting any required final approval to such project, whichever is later, but in any event within two years of the filing of this decision. Merely obtaining a Building Permit with respect to construction or a Certificate of Occupancy with respect to use does not constitute “substantial implementation” for the purposes hereof.

 

 

301.:JdO S>!H310   NMOl

 

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NM013~N\iUO  dG Nh\01

 

 

DeTemple

ZBA#l5-49

Page  4 of  4

 

 

The foregoing  resolution  to approve  the application  for the requested  Section  5.153 variance,  for the distance  between  the deck on the garage  and the rear of the house, was presented   and moved by Mr. Bosco,  seconded  by Mr. Quinn  and carried as follows:   Mr. Bosco,  aye; Mr.  Feroldi,   aye; Mr.  Quinn,  aye; Ms.  Castelli,  aye; Ms.  Salomon,  aye; and Mr. Sullivan,  aye.

 

The Administrative   Aide to the Board is hereby  authorized,   directed  and empowered  to sign this decision  and file a certified  copy thereof  in the office of the Town  Clerk.

 

DATED:    June 17,  2015

 

ZONING  BOARD  OF APPEALS TOWN  OF ORANGETOWN

 

 

DISTRIBUTION:

 

APPLICANT

ZBA MEMBERS SUPERVISOR

TOWN BOARD MEMBERS TOWN ATTORNEY

DEPUTY   TOWN ATTORNEY

OBZPAE

BUILDING    INSPECTOR-M.M.

By-L-~.-..+-<—‘-‘a<>G.-=–f=~ Deborah  Arbolino Administrative   Aide

 

 

TOWN  CLERK

HIGHWAY   DEPARTMENT ASSESSOR

DEPT.  of ENVIRONMENTAL MGMT. and ENGINEERING FILE,ZBA,    PB

CHAIRMAN,    ZBA, PB, ACABOR

 

 

 

:381.:l.:lO     S)l)Bl8   NMCl

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DECISION

ZONING CODE USE TABLE R-80, COLUMN 2 PARAGRAPH  7, 600 SQ. Ff.

PERMITTED;  672 SQ. FI’. EXISTING;  VARIANCE APPROVED (LOCAL LAW

7OF1981)

 

To:   Christine DiDomenico

8 Sgt. Hartz Drive

Tappan, New York I 0983

ZBA#l5-50

Date: June 17, 2015

 

 

FROM: ZONING BOARD OF APPEALS: Town of Orangetown

 

 

ZBA#15-50: Application of Christine Di Domenico for a variance from Zoning Code

(Chapter 43) of the Town of Orangetown Code, R-15 District, Group M, refers to R-80

District, Column 2, paragraph 7 (conversion of a detached, owner occupied, single-family

dwelling so as to add 1  additional dwelling unit clearly subordinate to the main 1  family use to occupy not more than 600 sq. ft.: 672 sq. ft. existing) for a Local Law 7of1981

conversion of an existing single-family residence. The premises are located at 8 Sargent

Hartz Drive, Tappan, New York and are identified on the Orangetown Tax Map as

Section 77.09, Block 1, Lot 30.2; in the R-15 zoning district.

 

 

 

 

Heard by the Zoning Board of Appeals of the Town of Orangetown at a meeting held on Wednesday, June 17, 2015 at which time the Board made the determination hereinafter set forth.

 

Christine DiDomenico appeared and testified. The following documents were presented:

1. Copy of survey dated May 7, 1997 by William Youngblood Associates. (1 page).
2. A hand drawing of the proposed space for the subordinate dwelling unit.
3. A restrictive covenant dated 04/08/2015 Instrument Number-2015-00009565

filed with the Rockland County Clerk by Christine DiDoinenico,  8 Sgt. Hartz

Drive, Tappan, New York.

4. A letter is support of the application from an abutting property owner.

 

 

 

Mr. Sullivan, Chairman, made a motion to open the Public Hearing which motion was seconded by Ms. Castelli and carried unanimously.

 

On advice of Dennis Michaels, Deputy Town Attorney, counsel to the Zoning Board of Appeals, Mr. Sullivan moved for a Board determination that the foregoing application is a Type II action exempt from the State Environmental Quality Review Act (SEQRA), pursuant to SEQRA Regulations §617.5 (c) (9), (10), (12) and/or (13); which does not require SEQRA environmental review. The motion was seconded by Ms. Castelli and . carried as follows: Ms. Castelli, aye; Ms. Salomon, aye; Mr. Bosco, aye; and Mr. Quinn, aye; and Mr. Sullivan, aye.

 

Christine DiDomenico testified that the apartment was built for her daughter; that her daughter got pregnant and married very young; that the kids lived in the lower portion of the house and shared the kitchen for a while; that she also had two other children at home; that when the baby was born they were coming up and down to the kitchen at all hours; that she installed the second kitchen at that time; that was probably about nine years ago; that she came in to legalize the apartment couple of months ago and filed a

restrictive covenant; that when the inspector came out to the house they found out that the apartment was 72 sq. ft. too large; and that she is selling the house; and the people

interested in purchasing the house would like to continue the use of the apartment for

their parents.                                   301.:J.:JO  S)1H310  NM01

..

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DiDomenico

ZBA#lS-50

Page2  of  4

 

 

 

 

Public  Comment:

 

 

No public  comment.

 

The Board members  made personal  inspections  of the premises  the week before the meeting  and found them to be properly  posted  and as generally  described  on the application.

 

A satisfactory  statement  in accordance  with the provisions  of Section  809 of the General

Municipal  Law ofNew   York was received.

 

 

Mr. Sullivan made a motion  to close the Public  Hearing  which motion  was seconded by

Ms. Castelli   and carried unanimously.

 

 

FINDINGS  OF FACT AND CONCLUSIONS:

After personal  observation  of the property,  hearing  all the testimony  and reviewing  all the documents  submitted,  the Board  found and concluded  that the benefits  to the applicant  if the variance(s)  are granted  outweigh  the detriment  (if any) to the health,  safety and

welfare  of the neighborhood   or community  by such grant, for the following  reasons:

 

 

 

1. The requested  R-80,  Column  2, paragraph  7 variance  will not produce an undesirable change in the character of the neighborhood or a detriment to nearby properties. The additional 72 sq. ft. is minimal and the entrance to the apartment is in the rear of the house.

 

2. The covenant required by Orangetown Zoning Code Section 4.51 (a/k/a Local Law

#7) of 1981) has already been executed by the property owners and recorded in the

Rockland County Clerk’s Office on 04/08/2015 as Instrument #2015-00009565.

 

 

 

3. The requested R-80, Column 2, paragraph 7 variance will not have an adverse effect or impact on the physical or environmental conditions in the neighborhood or district. The additional 72 sq. ft. is minimal and the entrance to the apartment is in the rear of the house.

 

 

4. The benefits sought by the applicant cannot be achieved by other means feasible for the applicant to pursue other than by obtaining a variance. The additional 72 sq. ft. is minimal and the entrance to the apartment is in the rear of the house.

 

 

 

5. The requested R-80, Column 2, paragraph 7 variance for an additional 72. Sq. ft. is not substantial.

 

6. The applicant purchased the property subject to Orangetown’s Zoning Code (Chapter

43) and is proposing a new addition and/or improvements, so the alleged difficulty was self-created, which consideration was relevant to the decision of the Board of Appeals, but did not, by itself, preclude the granting of the area variances.

 

30f.:l.:W  S)fH310 NMOl

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NM013~NVUO  .:lO  NA\01

 

DiDomenico

ZBA#lS-50

Page 3   of 4

 

 

 

DECISION: In view of the foregoing and the testimony and documents presented, the

Board: RESOLVED, that the application for the requested R-80, Column 2, paragraph 7 variance for an additional 72 sq. ft. is APPROVED; and FURTHER RESOLVED, that such decision and the vote thereon shall become effective and be deemed rendered on the date of adoption by the Board of the minutes of which they are a part.

 

 

 

General Conditions:

 

(i) The approval of any variance or Special Permit is granted by the Board in accordance with and subject to those facts shown on the plans submitted and, if applicable, as amended at or prior to this hearing, as hereinabove recited or set forth.

 

(ii) Any approval of a variance or Special Permit by the Board is limited to the specific variance or Special Permit requested but only to the extent such approval is granted herein and subject to those conditions, if any, upon which such approval was conditioned which are hereinbefore set forth.

 

 

 

(iii) The Board gives no approval of any building plans, including, without limitation, the accuracy and structural integrity thereof, of the applicant, but same have been submitted to the Board solely for informational and verification purposes relative to any variances being requested.

 

 

 

(iv) A building permit as well as any other necessary permits must be obtained within a reasonable period of time following the filing of this decision and prior to undertaking any construction contemplated in this decision. To the extent any variance or Special Permit granted herein is subject to any conditions, the building department shall not be

obligated to issue any necessary permits where any such condition imposed should, in the sole judgment of the building department, be first complied with as contemplated hereunder. Occupancy will not be made until, and unless, a Certificate of Occupancy is

issued by the Office of Building, Zoning and Planning Administration and Enforcement which legally permits such occupancy.                                      ·                                                                                                                                                                                                                                 ·

 

 

 

(v) Any foregoing variance or Special Permit will lapse if any contemplated construction of the project or any use for which the variance or Special Permit is granted is not substantially implemented within one year of the date of filing of this decision or that of any other board of the Town of Orangetown granting any required final approval to such project, whichever is later, but in any event within two years of the filing of this decision. Merely obtaining a Building Permit with respect to construction or a Certificate of Occupancy with respect to use does not constitute “substantial implementation” for the purposes hereof.

 

 

 

 

301.:L:!O  S>!~310 NMO!

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Di Domenico

ZBA#l5-50

Page  4 of  4

 

 

 

The foregoing  resolution  to approve  the application  for the requested  R-80,   Column  2, paragraph  7 variance  for an additional   72 sq. ft.was presented  and moved by Mr.  Quinn, seconded  by Mr. Bosco   and carried  as follows:  Mr.  Bosco,   aye; Mr. Sullivan,  aye;   Mr. Quinn,  aye ;Ms. Castelli,   aye; and Ms.  Salomon,  aye.

 

The Administrative  Aide to the Board is hereby  authorized,  directed  and empowered  to sign this decision  and file a certified  copy thereof  in the office of the Town Clerk.

 

DATED:    June 17,  2015

 

ZONING  BOARD  OF APPEALS TOWN  OF ORANGETOWN

 

 

 

 

DISTRIBUTION:

 

APPLICANT

ZBA   MEMBERS SUPERVISOR

TOWN BOARD  MEMBERS TOWN ATTORNEY

DEPUTY  TOWN ATTORNEY OBZPAE

BUILDING    INSPECTOR-R.A.O.

ByL….i.<:~:……..=…~=o….>..~~= Deborah  Arbolino

Administrative   Aide

 

 

TOWN CLERK

HIGHWAY   DEPARTMENT ASSESSOR

DEPT.  of ENVIRONMENTAL MGMT.   and ENGINEERING FILE,ZBA,    PB

CHAIRMAN,     ZBA,  PB,  ACABOR

 

 

 

:3Ql::l.:l0    s \B318    NMOl

 

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Nh\Ol3~N\-itio    ::JO   Nfr\01

 

DECISION

FLOOR AREA RATIO, SIDE YARD AND REAR YARD VARIANCES APPROVED

 

To: Andrew and Ann Varga

56 Conklin Avenue

Tappan, New York 10983

ZBA #15-51

Date: June 17, 2015

 

 

FROM: ZONING BOARD OF APPEALS: Town of Orangetown

 

 

 

ZBA#lS-51: Application of Andrew and Ann Varga  for variances from Zoning Code (Chapter 43) of the Town of Orangetown Code, R-15 District,  Group M, Section 3.12, Columns 4 (Floor Area Ratio: .20 permitted, .23 proposed), 9 (Side Yard: 20′ required,

11.5′ proposed), and 11 (Rear Yard: 35′ required, 31.5′ proposed)  for an addition to an existing single-family residence. The premises are located at 56 Conklin Avenue, Tappan, New York and are identified on the Orangetown Tax Map as Section 77.11, Block 1, Lot 67; in the R-15 zoning district.

 

 

 

 

Heard by the Zoning Board of Appeals of the Town of Orangetown at a meeting held on Wednesday, June 17, 2015 at which time the Board made the determination hereinafter set forth.

 

Andrew Varga and Richard Bouchard, Architect, appeared and testified. The following documents were presented:

1. Architectural plans dated 04/16/2015 signed and sealed by Richard A. Bouchard, Architect, (2 pages).
2. Historic Areas Board of Review Decision #15-11 dated June 9, 2015.

 

 

 

 

Mr. Sullivan, Chairman, made a motion to open the Public Hearing which motion was seconded by Ms. Castelli and carried unanimously.

 

On advice of Dennis Michaels, Deputy Town Attorney,  counsel to the Zoning Board of Appeals, Mr. Sullivan moved for a Board determination that the foregoing application is a Type II action exempt from the State Environmental Quality Review Act (SEQRA), pursuant to SEQRA Regulations §617.5 (c) (9), (10), (12) and/or (13); which does not require SEQRA environmental review. The motion was seconded by Ms. Castelli and

carried as follows: Ms. Castelli, aye; Ms. Salomon, aye; Mr. Bosco, aye; Mr. Quinn, aye;

and Mr. Sullivan, aye.

 

Richard Bouchard, Architect, testified that the house is a Cape Cod style house; that currently there is a screened-in porch that runs the entire width of the house in the rear and a little beyond; that they would like to expand by three feet and enclose half of it to make it living space; that they would like to expand their existing kitchen and add a living area and enclose the other half as a three season room and add a small deck for the

grill; that the small deck in the rear with steps going into the backyard is causing the need for the rear yard variance; that presently there is no way into the rear of property from

that level of the house; that the proposal stays in line with the existing house along the

11.5′ property line; and the lot is only 9, 400 and change and should be 15,000 sq. ft.;

that this undersized lot triggers the floor area ratio variance; and that they would not mind qualifying for the undersized lot which would require a 15 foot side yard.

 

 

Andrew Varga testified that the hou~3’PJ9~ ~~~~      Qiiki  AA addition; that the next door neighbor has a large rear deck that required a vanance £ff’Hmt there are four in family

and the dog.                                        h~  ?_! IJd     9     1nr   5IOZ

 

NA\Ol3~N’v’ci0  .:10  NMOl

 

Varga

ZBA#lS-51

Page2 of 4

 

 

 

 

Public Comment:

 

No public comment.

 

The Board members made personal inspections of the premises the week before the meeting and found them to be properly posted and as generally described on the application.

 

A satisfactory statement in accordance with the provisions of Section 809 of the General

Municipal Law ofNew York was received.                                ·

 

Mr. Sullivan made a motion to close the Public Hearing which motion was seconded by

Ms. Castelli and carried unanimously.

 

FINDINGS  OF FACT AND CONCLUSIONS:

After personal observation of the property, hearing all the testimony and reviewing all the documents submitted, the Board found and concluded that the benefits to the applicant if the variance(s) are granted outweigh the detriment (if any) to the health, safety and welfare of the neighborhood or community by such grant, for the following reasons:

 

 

 

1. The requested floor area ratio, side yard and rear yard variances will not produce an undesirable change in the character of the neighborhood or a detriment to nearby properties. The proposed addition is only enlarging the existing structure by three additional feet to the rear.

 

 

 

2. The requested floor area ratio, side yard and rear yard variances will not have an adverse effect or impact on the physical or environmental conditions in the neighborhood or district. The proposed addition is only enlarging the existing structure by three additional feet to the rear.

 

3. The benefits sought by the applicant cannot be achieved by other means feasible for the applicant to pursue other than by obtaining variances.

 

 

 

4. The requested floor area ratio, side yard and rear yard variances, although somewhat substantial, afford benefits to the applicant that are not outweighed by the detriment, if any, to the health, safety and welfare of the surrounding neighborhood or nearby community. The proposed addition is only enlarging the existing structure by three. additional feet to the rear.  ·

 

 

 

5. The applicant purchased the property subject to Orangetown’s Zoning Code (Chapter

43) and is proposing a new addition and/or improvements, so the alleged difficulty was self-created, which consideration was relevant to the decision of the Board of Appeals, but did not, by itself, preclude the granting of the area variances.

 

 

 

 

 

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Varga

ZBA#lS-51

Page 3   of 4

 

 

DECISION: In view of the foregoing and the testimony and documents presented, the Board: RESOLVED, that the application for the requested  floor area ratio, side yard and rear yard variances are APPROVED; and FURTHER RESOLVED, that such decision and the vote thereon shall become effective and be deemed rendered on the date of adoption by the Board of the minutes of which they are a part.

 

 

 

 

General Conditions:

 

(i) The approval of any variance or Special Permit is granted by the Board in accordance with and subject to those facts shown on the plans submitted and, if applicable, as amended at or prior to this hearing, as hereinabove recited or set forth.

 

(ii) Any approval of a variance or Special Permit by the Board is limited to the specific variance or Special Permit requested but only to the extent such approval is granted herein and subject to those conditions, if any, upon which such approval was conditioned which are hereinbefore set forth.

 

 

 

(iii) The Board gives no approval of any building plans, including, without limitation, the accuracy and structural integrity thereof, of the applicant, but same have been submitted to the Board solely for informational and verification purposes relative to any variances being requested.

 

 

 

(iv) A building permit as well as any other necessary permits must be obtained within a reasonable period of time following the filing of this decision and prior to undertaking any construction contemplated in this decision. To the extent any :variance or Special  · Permit granted herein is subject to any conditions, the building department shall not be

obligated to issue any necessary permits where any such condition imposed should, in the sole judgment of the building department, be first complied with as contemplated

hereunder. Occupancy will not be made until, and unless, a Certificate of Occupancy is issued by the Office of Building, Zoning and Planning Administration and Enforcement which legally permits such occupancy.

 

 

 

(v) Any foregoing variance or Special Permit will lapse if any contemplated construction of the project or any use for which the variance or Special Permit is granted is not substantially implemented within one year of the date of filing of this decision or that of any other board of the Town of Orangetown granting any required final approval to such project, whichever is later, but in any event within two years of the filing of this decision. Merely obtaining a Building Permit with respect to construction or a Certificate of Occupancy with respect to use does not constitute “substantial implementation” for the purposes hereof.

 

 

 

30\.:HO s;n\310  NM01

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Varga

ZBA#15-51

Page  4 of  4

 

 

 

The foregoing  Resolution  to approve  the application   for the requested  floor area ratio, side yard and rear yard variances   was presented  and moved by Ms. Salomon,   seconded by Ms.  Castelli   and carried as follows:   Mr. Bosco,   aye;  Mr. Sullivan, aye;  Mr. Quinn, aye; Ms. Castelli, aye;  and Ms. Salomon, aye.

 

The Administrative Aide to the Board is hereby authorized,  directed and empowered to sign this decision and file a certified copy thereof in the office of the Town Clerk.

 

DATED: June 17, 2015

 

ZONING BOARD OF APPEALS TOWN OF ORANGETOWN

 

 

 

DISTIUBUTION:

 

APPLICANT

ZBA   MEMBERS SUPERVISOR

TOWN BOARD MEMBERS TOWN  ATIORNEY

DEPUTY   TOWN ATIORNEY OBZPAE

BUILDING    INSPECTOR-R.A.0.

By..Lf~~–=-=::~~;,Li~~l

Deborah Arbolino

Administrative Aide

 

 

TOWN   CLERK

HIGHWAY    DEPARTMENT ASSESSOR

DEPT.  of ENVIRONMENTAL

MGMT.  and ENGINEERING FILE,ZBA,    PB

CI-IAIRMAN,     ZBA,   PB,  ACABOR

 

381.:1.:10    S,.)\318    NMOl

hh  zi Wd   9    1nr srnz

 

NM 013  8 N ·1ti0   .:I 0  Vi f-,\ 01

 

DECISION

ZONING CODE SECTION 5.12 DISTRICT BOUNDARY, FLOOR AREA RATIO, FRONT  YARD AND BUILDING HEIGHT VARIANCES   APPROVED

 

To:   Peter and Elizabeth Barsanti

66 Andre Avenue

Tappan, New York 10983

ZBA #15-52

Date: June 17, 2015

 

 

FROM: ZONING BOARD OF APPEALS: Town of Orangetown

 

 

 

ZBA#l 5-52: Application of Peter and Elizabeth Barsanti for variances from Zoning Code (Chapter 43) of the Town of Orangetown Code, R-15 District, Section 5.12 (Lot divided by district boundary applies): Section 3.12, Group M, Columns 4 (Floor Area Ratio: .20 permitted, .215 existing, and .272 proposed) 8 (Front Yard:  30′ required,

16.54′ existing & proposed)  and 12 (Building Height: 16.67′ permitted, 20.16′ existing

& proposed) for an addition to an existing single-family residence. The premises are located at 66 Andre Avenue, Tappan, New York and are identified on the Orangetown Tax Map as Section 77.10, Block 3, Lot 65;  in the R-15 zoning district.

 

 

 

 

Heard by the Zoning Board of Appeals of the Town of Orangetown at a meeting held on Wednesday, June 17, 2015 at which time the Board made the determination hereinafter set forth.

 

Peter Barsanti and Robert Hoene, Architect, appeared and testified. The following documents were presented:

1. Architectural plans dated 04/21/2015 signed and sealed by Robert Hoene,

Architect.(3 pages with the site plan and bulk table)

2. Zoning Board of Appeals Decision #03-24 dated 04/02/2003.
3. A letter dated June 4, 2015 from the County of Rockland Department of Planning

signed by Douglas J. Schuetz, Acting Commissioner of Planning.

4. A letter dated June 15, 2015 from the County of Rockland Department of

Highways signed by Sonny Lin, P .E..

 

 

 

 

Mr. Sullivan, Chairman, made a motion to open the Public Hearing which motion was seconded by Ms. Castelli and carried unanimously.

 

On advice of Dennis Michaels, Deputy Town Attorney,  counsel to the Zoning Board of Appeals, Mr. Sullivan moved for a Board determination that the foregoing application is a Type II action exempt from the State Environmental Quality Review Act (SEQRA), pursuant to SEQRA Regulations §617.5 (c) (9), (10), (12) and/or (13); which does not require SEQRA environmental review. The motion was seconded by Ms. Castelli and

:z     ~             as follows: Ms. Castelli, aye; Ms. Salomon, aye; Mr. Bosco, aye; Mr. Quinn, aye;

;r;   ·    :::iarid Mr. Sullivan, aye.

0        IN            u,

tw-       Ir-(              lJ..

<-?        eft.oben Hoene, Architect, testified that the proposal before the Board is for an addition

~     ‘bver ~e  existing first floor; that they are proposing to add 3 81 sq. ft. over the existing

~     c&st flPor; that the Barsantis’ have three children; that their son has a small bedroom and

L1-           the ~    girls presently share a room; that the proposal would afford a bedroom for each

0          :aind:and a small study area; that there was a mistake on the original plan submitted; that

~     JLe t@>r area ratio was calculated including the existing first floor and should be that

~      [iey  hre proposing to add 381 sq. ft. over the existing first floor; that the original application stated that they were adding 500 sq. ft.; that they have an existing floor area ratio of .21 and are looking for .255; that the addition is modest in size; that the property in New Jersey was calculated into the total land; and that he would like to submit the revised site plan and bulk table with the correct floor area ratio request.

 

Barsanti

ZBA#15-52

Page2 of 4

 

Peter Barsanti testified that one of the existing bedrooms is so small that it doesn’t even have a closet and that they would like for all three children have their own bedrooms.

 

 

 

 

Public Comment:

 

No public comment.

 

The Board members made personal inspections of the premises the week before the meeting and found them to be properly posted and as generally described on the application.

 

A satisfactory statement in accordance with the provisions of Section 809 of the General

Municipal Law of New York was received.

 

Mr. Sullivan made a motion to close the Public Hearing which motion was seconded by

Ms. Castelli and carried unanimously.

 

FINDINGS OF FACT AND CONCLUSIONS:

After personal observation of the property, hearing all the testimony and reviewing all the

documents submitted, the Board found and concluded that the benefits to the applicant if

the variance(s) are granted outweigh the detriment (if any) to the health, safety and welfare of the neighborhood or community by such grant, for the following reasons:

 

 

 

1. The requested Section 5.12 district boundary, floor area ratio as modified to .255,

front yard and building height variances will not produce an undesirable change in the

character of the neighborhood or a detriment to nearby properties. A portion of the

property is in New Jersey; because of the property line being split by state

boundaries, any addition to the residence requires variances.

 

 

 

2. The requested Section 5.12 district boundary, floor area ratio as modified to .255, front yard and building height variances will not have an adverse effect or impact on the physical or environmental conditions in the neighborhood or district. A portion of the property is in New Jersey; because of the property line being split by state boundaries, any addition to the residence requires variances.

 

3. The benefits sought by the applicant cannot be achieved by other means feasible for the applicant to pursue other than by obtaining variances. A portion of the property is in New Jersey; because of the property line being split by state boundaries, any addition to the residence requires variances.

 

4. The requested Section 5.12 district boundary, floor area ratio as modified to .255, front yard and building height variances, although somewhat substantial, afford benefits to the applicant that are not outweighed by the detriment, if any, to the

 

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health, safety and welfare of the surrounding neighborhood or nearby community. A portion of the property is in New Jersey; because of the property line being split by state boundaries, any addition to the residence requires variances.

 

 

 

The applicant purchased the property subject to Orangetown’s Zoning Code (Chapter

43) and is proposing a new addition and/or improvements, so the alleged difficulty

was self-created, which consideration was relevant to the decision of the Board of

Appeals, but did not, by itself, preclude the granting of the area variances.

 

Barsanti

ZBA#15-52

Page 3   of 4

 

 

 

 

 

DECISION: In view of the foregoing and the testimony and documents presented, the Board: RESOLVED, that the application for the requested Section 5.12 district boundary, floor area ratio as modified to .255, front yard and building height

variances are APPROVED; and FURTHER RESOLVED, that such decision and the vote thereon shall become effective and be deemed rendered on the date of adoption by the Board of the minutes of which they are a part.

 

 

 

General Conditions:

 

(i) The approval of any variance or Special Permit is granted by the Board in accordance with and subject to those facts shown on the plans submitted and, if applicable, as amended at or prior to this hearing, as hereinabove recited or set forth.

 

(ii) Any approval of a variance or Special Permit by the Board is limited to the specific variance or Special Permit requested but only to the extent such approval is granted

herein and subject to those conditions, if any, upon which such approval was conditioned which are hereinbefore set forth.

 

 

 

(iii) The Board gives no approval of any building plans, including, without limitation, the accuracy and structural integrity thereof, of the applicant, but same have been submitted to the Board solely for informational and verification purposes relative to any variances being requested.

 

 

 

(iv) A building permit as well as any other necessary permits must be obtained within a reasonable period of time following the filing of this decision and prior to undertaking any construction contemplated in this decision. To the extent any variance or Special Permit granted herein is subject to any conditions, the building department shall not be

obligated to issue any necessary permits where any such condition imposed should, in the sole judgment of the building department, be first complied with as contemplated hereunder. Occupancy will not be made until, and unless, a Certificate of Occupancy is issued by the Office of Building, Zoning and Planning Administration and Enforcement which legally permits such occupancy.

 

 

 

(v) Any foregoing variance or Special Permit will lapse if any contemplated construction of the project or any use for which the variance or Special Permit .is granted is not substantially implemented within one year of the date of filing of this decision or that of any other board of the Town of Orangetown granting any required final approval to such project, whichever is later, but in any event within two years of the filing of this decision. Merely obtaining a Building Permit with respect to construction or a Certificate of Occupancy with respect to use does not constitute “substantial implementation” for the

purposes hereof.

 

 

 

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Barsanti

ZBA#l5-52

Page 4 of 4

 

 

The foregoing Resolution  to approve the application   for the requested Section  5.12 district  boundary,  floor area ratio  as modified to .255,  front yard and building  height variances   was presented and moved by Mr. Sullivan,  seconded by Ms.  Castelli  and carried as follows:  Mr. Bosco,  aye;  Ms.  Castelli,  aye;  Mr. Sullivan,  aye;   Mr. Quinn,  aye; and Ms.  Salomon,   aye.

 

The Administrative  Aide to the Board  is hereby authorized,   directed and empowered  to sign this decision  and file a certified  copy thereof in the office of the Town Clerk.

 

DATED:  June 17,  2015

 

ZONING BOARD OF APPEALS TOWN OF ORANGETOWN

 

 

DISTRIBUTION:

 

APPLICANT

ZBA MEMBERS

SUPERVISOR

TOWN BOARD MEMBERS TOWN ATTORNEY

DEPUTY  TOWN ATTORNEY OBZPAE

BUILDING    INSPECTOR-M.M.

By—<-.ir,,.=..a..<…..=..:::=-==:_:::…..<…<~- Deborah  Arbolino Administrative Aide

 

 

TOWN  CLERK

HIGHWAY   DEPARTMENT

ASSESSOR

DEPT.  of ENVIRONMENTAL

MGMT. and ENGINEERING FILE,ZBA,   PB

CHAIRMAN,     ZBA,  PB,  ACABOR

 

 

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DECISION

NEW  YORK  STATE  TOWN  LAW  SECTION 280A EXCEPTION  VARIANCE FOR  LOTS  3A, 3B & SB; STREET FRONTAGE  FOR  LOTS  3A, 3B & SB; FRONT YARD  FOR  LOT  3B, REAR  YARD  FOR  LOT  3B, AND BUILDING HEIGHT  FOR  LOTS  3A, 3B & SB; VARIANCES    APPROVED

 

To:   Edward  Merritt

9 Merritt  Drive

Nanuet,  New York  10954

ZBA#l5-53

Date:  June  17, 2015

 

 

FROM:  ZONING  BOARD  OF APPEALS:  Town  of Orangetown

 

 

ZBA#lS-53:   Application  of  Merritt  Subdivision   for variances  from Zoning  Code (Chapter  43) of the Town  of Orangetown  Code, R-15 District,   Group M, Section 3.12, Columns  7 (Street Frontage:   75′  required,  O’ proposed  for lots 3A, 3B & SB),  8 (Front Yard: 30′ required,  22′  proposed  for lot 3B ),  11  (Rear Yard:  35′ required,  30.9′ proposed  for lot 3B), and 12 (Building  Height:  20.3′  permitted  for lot 3A, 30′ proposed;

22′ permitted  for lot 3B, 30′ proposed,  and 20.3′  proposed  for lot SB, 30′  proposed)   and an exception  from New York  State Town Law Section  280A variances  for lots 3A, 3B

and SB for a residential  subdivision.  The premises  are located  at 17 Merritt  Drive and 390

Ehrhardt  Road, Pearl River, New York  and are identified  on the Orangetown  Tax Map as

Section  64.18,  Block  1, Lots  78.1 & 78.3; in the R-15 zoning district.

 

 

 

Heard by the Zoning Board of Appeals  of the Town  of Orangetown  at a meeting  held on Wednesday,  June 17, 2015 at which time the Board made the determination  hereinafter set forth.

 

Edward Merritt,  TJ Ryan and Donald  Brenner,  Attorney,  appeared  and testified. The following  documents  were presented:

1. Minor  Subdivision  Plat for Merritt  dated 01115/2015 with the latest revision  date

of 03/14/2015  signed and sealed by William  D. Youngblood,  PLS and Steven

Michael  Sparaco. P .E..

2. A letter dated  May  19, 2015 from the County of Rockland  Department  of

Planning  signed by Douglas  J. Schuetz,  Acting  Commissioner  of Planning.

3. A letter dated June  16, 2015 from the County  of Rockland  Department  of

Highways  signed by Sonny  Lin, P .E ..

4. A letter dated May 8, 2015 from the County of Rockland  Department  of Health signed by Scott Mc Kane,  P .E ..

 

Mr. Sullivan,   Chairman,  made  a motion  to open the Public Hearing  which motion  was seconded  by Ms. Castelli   and carried unanimously.

 

On advice of Dennis Michaels,  Deputy Town  Attorney,   counsel to the Zoning  Board of Appeals,  Mr. Sullivan moved  for a Board determination   that since the Planning  board noticed  its intent to declare itself Lead Agency  and distributed  that notice of intention  to all Involved  Agencies,  including  the ZBA who consented  or did not object to the Planning  Board acting as Lead Agency  for this application,  pursuant  to coordinated review under the State Enviromnental   Quality  Review  Act Regulations  §617.6 (b) (3); and since the Planning  Board  conducted  a SEQRA  review  and on April 22, 2015, rendered  an environmental  determination  of  no significant  adverse environmental impacts  to result from the proposed  land use action (i.e., a “Negative  Declaration”  or “Neg, Dec”),  the ZBA is bound by the Planning  Board’s  Neg Dec and the ZBA cannot

iy!~:R.R.

req~ire  further  SEQRA review  pursu~t  to SE~RA Regulation§   617,6 <12)13). Thc;..,     .                                         -.                                                                            ‘·  1

motion  was seconded  by Ms. Castelh  and earned  as follows:  Mr. Quinn,                 5 ~ H 31 a NM Q_

Salomon,  aye;  Mr. Sullivan,  aye;  Mr. Bosco,  aye; and Ms. Castelli,  ayi;b    21  lJd    9    1nr  5102

 

 

NM013~N\1tiQ     .:JG   NN\01

 

Merritt

ZBA#lS-53

Page2  of  4

 

Donald  Brenner,  Attorney,  testified  that the property  is unique,  it is the only original clay courts in Rockland  County;  that the person  that was in charge of the courts passed  away and the property  has been used less and less; and that the proposed

subdivision  has already received  a preliminary  approval  and a neg dee; and that it will be returning  to its intended  residential  use.

 

Public  Comment:

 

 

No public  comment.

 

 

The Board members  made personal  inspections  of the premises  the week before the meeting  and found them to be properly  posted  and as generally  described  on the application.

 

A satisfactory  statement  in accordance  with the provisions  of Section  809 of the General

Municipal  Law ofNew  York was received.

 

 

Mr. Sullivan made a motion  to close the Public Hearing  which motion was seconded  by

Ms. Castelli   and carried unanimously.

 

 

FINDINGS  OF FACT AND CONCLUSIONS:

After personal  observation  of the property,  hearing  all the testimony  and reviewing  all the documents  submitted,  the Board  found and concluded  that the benefits  to the applicant  if the variance(s)  are granted  outweigh  the detriment  (if any) to the health,  safety and

welfare  of the neighborhood  or community  by such grant, for the following  reasons:

 

 

 

1. The requested  New York  State Town  Law Section  280A  Exception  for lots 3A, 3B

and SB; Street Frontage  variances  for lots 3A, 3B &SB, Front Yard  variance  for lot·

3B, Rear Yard variance  for lot 3B, and Building  Height variances  for lots 3A, 3B & SA; will not produce  an undesirable  change  in the character  of the neighborhood  or a detriment  to nearby properties.  The property  is reverting  back to its original

residential  use.

 

 

 

2. The requested  New York  State Town  Law Section  280A  Exception  for lots 3A, 3B

and SB; Street Frontage  variances  for lots 3A, 3B &SB, Front Yard variance  for lot

3B, Rear Yard variance  for lot 3B, and Building  Height variances  for lots 3A, 3B & SA; will not have an adverse  effect or impact  on the physical  or environmental conditions  in the neighborhood   or district.  The property  is reverting  back to its original residential  use.

 

 

3. The benefits  sought by the applicant  cannot be achieved  by other means  feasible  for the applicant  to pursue  other than by obtaining  variances.

 

4. The requested New York  State Town  Law Section  280A  Exception  for lots 3A, 3B

and SB; Street Frontage  variances  for lots 3A, 3B &SB, Front Yard variance  for lot

0

3B, Rear Yard variance  for lot 3B, and Building  Height variances  for lots 3A, 3B &

 

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SA;  although  somewhat  substantial,  afford benefits  to the applicant  that are not

 

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outweighed  by the detriment,  if any, to the health,  safety and welfare  of the

surrounding  neighborhood   or nearby  community.    The property  is reverting  back to its original residential  use.

 

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5-? The applicant  purchased  the property  subject to Orangetown’s   Zoning  Code (Chapter

~  43) and is proposing  a new addition  and/or improvements,   so the alleged difficulty

~was   self-created,  which  consideration  was relevant  to the decision  of the Board of

Appeals,  but did not, by itself, preclude  the granting  of the area variances.

 

Merritt

ZBA#IS-53

Page 3   of 4

 

 

 

DECISION: In view of the foregoing and the testimony and documents presented, the

Board: RESOLVED, that the application for the requested New York State Town Law Section 280A  Exception for lots 3A, 3B and SB; Street Frontage variances for lots 3A, 3B &SB, Front Yard variance for lot 3B, Rear Yard variance for lot 3B, and Building Height variances for lots 3A, 3B & SA; are APPROVED; and FURTHER RESOLVED, that such decision and the vote thereon shall become effective and be deemed rendered on the date of adoption by the Board of the minutes of which they are a part.

 

 

 

 

General Conditions:

 

(i) The approval of any variance or Special Permit is granted by the Board in accordance with and subject to those facts shown on the plans submitted and, if applicable, as amended at or prior to this hearing, as hereinabove recited or set forth.

 

(ii) Any approval of a variance or Special Permit by the Board is limited to the specific variance or Special Permit requested but only to the extent such approval is granted herein and subject to those conditions, if any, upon which such approval was conditioned which are hereinbefore set forth.

 

 

 

(iii) The Board gives no approval of any building plans, including, without limitation, the accuracy and structural integrity thereof, of the applicant, but same have been submitted to the Board solely for informational and verification purposes relative to any variances being requested.

 

 

 

(iv) A building permit as well as any other necessary permits must be obtained within a reasonable period of time following the filing of this decision and prior to undertaking any construction contemplated in this decision. To the extent any variance or Special Permit granted herein is subject to any conditions, the building department shall not be

obligated to issue any necessary permits where any such condition imposed should, in the sole judgment of the building department, be first complied with as contemplated hereunder. Occupancy will not be made until, and unless, a Certificate of Occupancy is issued by the Office of Building, Zoning and Planning Administration and Enforcement which legally permits such occupancy.

 

 

 

(v) Any foregoing variance or Special Permit will lapse if any contemplated construction of the project or any use for which the variance or Special Permit is granted is not substantially implemented within one year of the date of filing of this decision or that of any other board of the Town of Orangetown granting any required final approval to such project, whichever is later, but in any event within two years of the filing of this decision. Merely obtaining a Building Permit with respect to construction or a Certificate of Occupancy with respect to use does not constitute “substantial implementation” for the

purposes hereof.

 

 

 

301.::l.:lO  S)rt1310 NA\01 h~ ~! lJd    9    1nr  SIUZ NMOl30NVtW       :10  NMOl

 

Merritt

ZBA#lS-S3

Page  4 of  4

 

 

 

The foregoing  resolution  to approve  the application  for the requested   New York  State Town Law Section  280A  Exception  for lots 3A,  3B and SB; Street Frontage  variances for lots 3A,  3B &SB,   Front Yard variance  for lot 3B,   Rear Yard variance  for lot 3B, and Building  Height variances  for lots  3A, 3B & SA; was presented  and moved by Ms.

Castelli,  seconded  by Ms.  Salomon    and carried  as follows:   Mr. Bosco, aye; Mr. Sullivan,

aye;  Mr. Quinn,  aye ;Ms.  Castelli,  aye;  and Ms. Salomon,  aye.

 

 

The Administrative  Aide to the Board is hereby  authorized,   directed  and empowered  to sign  this decision  and file a certified  copy thereof  in the office of the Town Cleric

 

DATED:   June 17,  201S

 

ZONING  BOARD  OF APPEALS TOWN  OF ORANGETOWN

 

 

 

DISTRIBUTION:

 

APPLICANT

ZBA MEMBERS SUPERVISOR

TOWN BOARD  MEMBERS TOWN ATTORNEY

DEPUTY   TOWN ATTORNEY

OBZPAE

BUILDING   INSPECTOR-N.A.

 

By…,L.L~~~~~~—.!.–‘ /l-“~~-L~

Deborah  Arbolino

Administrative  Aide

 

 

TOWN CLERK

HlGHWAY    DEPARTMENT ASSESSOR

DEPT.  of ENVIRONMENTAL MGMT. and ENGINEERING FlLE,ZBA,   PB

CHAIRMAN,     ZBA,  PB,  ACABOR