Hydrologics, Inc. System Wide Zero Discharge Flushing & Water System Video Inspection
2 If changes in the work seem merited by Consultant or the City, and informal consultations with the other party indicate that a change is warranted, it shall be processed in the following manner: a letter outlining the changes shall be forwarded to the City by Consultant with a statement of estimated changes in fee or time schedule. An amendment to this Agreement shall be prepared by the City and executed by both Parties before performance of such services, or the City will not be required to pay for the changes in the scope of work. Such amendment shall not render ineffective or invalidate unaffected portions of this Agreement.
4. Maintenance of Records.
Books, documents, papers, accounting records, and other evidence pertaining to costs incurred shall be maintained by Consultant and made available at all reasonable times during the contract period and for four (4) years from the date of final payment under the contract for inspection by City.
5. Term
The term of this Agreement shall be from October 13, 2026, to June 30, 2027, unless earlier terminated as provided herein. The Parties may, by mutual, written consent, extend the term of this Agreement if necessary to complete the Project. Consultant shall perform its services in a prompt and timely manner within the term of this Agreement and shall commence performance upon receipt of written notice from the City to proceed (“Notice to Proceed”). The Notice to Proceed shall set forth the date of commencement of work.
6. Delays in Performance.
a. Neither City nor Consultant shall be considered in default of this Agreement for delays in performance caused by circumstances beyond the reasonable control of the nonperforming party. For purposes of this Agreement, such circumstances include but are not limited to, abnormal weather conditions; floods; earthquakes; fire; epidemics; pandemics; war; riots and other civil disturbances; strikes, lockouts, work slowdowns, and other labor disturbances; sabotage or judicial restraint.
b. Should such circumstances occur, the non-performing party shall, within a reasonable time of being prevented from performing, give written notice to the other party describing the circumstances preventing continued performance and the efforts being made to resume performance of this Agreement.
7. Compliance with Law.
a. Consultant shall comply with all applicable laws, ordinances, codes and regulations of the federal, state and local government, including Cal/OSHA requirements. b. If required, Consultant shall assist the City, as requested, in obtaining and maintaining all permits required of Consultant by federal, state and local regulatory agencies. c. If applicable, Consultant is responsible for all costs of clean up and/ or removal of hazardous and toxic substances spilled as a result of his or her services or operations performed under this Agreement.
Hydrologics, Inc. System Wide Zero Discharge Flushing & Water System Video Inspection
3 8. Standard of Care; Performance of Employees
a. Consultant’s services will be performed in accordance with generally accepted professional practices and principles and in a manner consistent with the level of care and skill ordinarily exercised by members of the profession currently practicing under similar conditions. b. Consultant’s employees and subcontractors shall have sufficient skill and experience to perform the Services assigned to them. Consultant represents that it, its employees and subcontractors have all licenses, permits, qualifications and approvals of whatever nature that are legally required to perform the Services, including a City Business License, and that such licenses and approvals shall be maintained throughout the term of this Contract. As provided for in the indemnification provisions of this Contract, Consultant shall perform, at its own cost and expense and without reimbursement from the City, any services necessary to correct errors or omissions which are caused by the Consultant’s failure to comply with the standard of care provided for herein. Any employee of the Consultant or its sub-consultants who is determined by the City to be uncooperative, incompetent, a threat to the adequate or timely completion of the Project, a threat to the safety of persons or property, or any employee who fails or refuses to perform the Services in a manner acceptable to the City, shall be promptly removed from the Project by the Consultant and shall not be re-employed to perform any of the Services or to work on the Project.
9. Assignment and Subcontracting
Consultant shall not assign, sublet, or transfer this Agreement or any rights under or interest in this Agreement without the written consent of the City, which may be withheld for any reason. Any attempt to so assign or so transfer without such consent shall be void and without legal effect and shall constitute grounds for termination. Subcontracts, if any, shall contain a provision making them subject to all provisions stipulated in this Agreement. Nothing contained herein shall prevent Consultant from employing independent associates and subcontractors as Consultant may deem appropriate to assist in the performance of services hereunder.
10. Independent Contractor
Consultant is retained as an independent contractor and is not an employee of City. No employee or agent of Consultant shall become an employee of City. The work to be performed shall be in accordance with the work described in this Agreement, subject to such directions and amendments from City as herein provided.
11. Insurance. Consultant shall not commence work for the City until it has provided evidence satisfactory to the City it has secured all insurance required under this section. In addition, Consultant shall not allow any subcontractor to commence work on any subcontract until it has secured all insurance required under this section. a. Commercial General Liability
(i) The Consultant shall take out and maintain, during the performance of all work under this Agreement, in amounts not less than specified herein, Commercial General Liability Insurance, in a form and with insurance companies acceptable to the City. (ii) Coverage for Commercial General Liability insurance shall be at least as broad as the following:
Hydrologics, Inc. System Wide Zero Discharge Flushing & Water System Video Inspection
4 (1) Insurance Services Office Commercial General Liability coverage (Occurrence Form CG 00 01) or exact equivalent. (iii) Commercial General Liability Insurance must include coverage for the following:
(1) Bodily Injury and Property Damage
(2) Personal Injury/Advertising Injury
(3) Premises/Operations Liability
(4) Products/Completed Operations Liability
(5) Aggregate Limits that Apply per Project
(6) Explosion, Collapse and Underground (UCX) exclusion deleted
(7) Contractual Liability with respect to this Agreement (8) Property Damage
(9) Independent Contractors Coverage
(iv) The policy shall contain no endorsements or provisions limiting coverage for (1) contractual liability; (2) cross liability exclusion for claims or suits by one insured against another; (3) products/completed operations liability; or (4) contain any other exclusion contrary to the Agreement.
(v) The policy shall give City, its officials, officers, employees, agents and City designated volunteers additional insured status using ISO endorsement forms CG 20 10 10 01 and 20 37 10 01, or endorsements providing the exact same coverage. (vi) The general liability program may utilize either deductibles or provide coverage excess of a self-insured retention, subject to written approval by the City, and provided that such deductibles shall not apply to the City as an additional insured. b. Automobile Liability
(i) At all times during the performance of the work under this Agreement, the Consultant shall maintain Automobile Liability Insurance for bodily injury and property damage including coverage for owned, non-owned and hired vehicles, in a form and with insurance companies acceptable to the City.
(ii) Coverage for automobile liability insurance shall be at least as broad as Insurance Services Office Form Number CA 00 01 covering automobile liability (Coverage Symbol 1, any auto).
(iii) The policy shall give City, its officials, officers, employees, agents and City designated volunteers additional insured status. (iv) Subject to written approval by the City, the automobile liability program may utilize deductibles, provided that such deductibles shall not apply to the City as an additional insured, but not a self-insured retention.
c. Workers’ Compensation/Employer’s Liability
Hydrologics, Inc. System Wide Zero Discharge Flushing & Water System Video Inspection
5 (i) Consultant certifies that he/she is aware of the provisions of Section 3700 of the California Labor Code which requires every employer to be insured against liability for workers’ compensation or to undertake self-insurance in accordance with the provisions of that code, and he/she will comply with such provisions before commencing work under this Agreement.
(ii) To the extent Consultant has employees at any time during the term of this Agreement, at all times during the performance of the work under this Agreement, the Consultant shall maintain full compensation insurance for all persons employed directly by him/her to carry out the work contemplated under this Agreement, all in accordance with the “Workers’ Compensation and Insurance Act,” Division IV of the Labor Code of the State of California and any acts amendatory thereof, and Employer’s Liability Coverage in amounts indicated herein. Consultant shall require all subconsultants to obtain and maintain, for the period required by this Agreement, workers’ compensation coverage of the same type and limits as specified in this section.
d. Professional Liability (Errors and Omissions)
At all times during the performance of the work under this Agreement the Consultant shall maintain professional liability or Errors and Omissions insurance appropriate to its profession, in a form and with insurance companies acceptable to the City and in an amount indicated herein.
This insurance shall be endorsed to include contractual liability applicable to this Agreement and shall be written on a policy form specifically designed to protect against acts, errors or omissions of the Consultant. “Covered Professional Services” as designated in the policy must specifically include work performed under this Agreement. The policy must “pay on behalf of” the insured and must include a provision establishing the insurer's duty to defend. e. Minimum Policy Limits Required
(i) The following insurance limits are required for the Agreement:
Combined Single Limit
Commercial General Liability $1,000,000 per occurrence/ $2,000,000 aggregate for bodily injury, personal injury, and property
damage
Automobile Liability $1,000,000 combined single limit
Employer’s Liability $1,000,000 per accident or disease Professional Liability $1,000,000 per claim and aggregate (errors and omissions)
(ii) Defense costs shall be payable in addition to the limits. (iii) Requirements of specific coverage or limits contained in this section are not intended as a limitation on coverage, limits, or other requirement, or a waiver of any coverage normally provided by any insurance. Any available coverage shall be provided to the parties required to be named as Additional Insured pursuant to this Agreement.
Hydrologics, Inc. System Wide Zero Discharge Flushing & Water System Video Inspection
6 f. Evidence Required
Prior to execution of the Agreement, the Consultant shall file with the City evidence of insurance from an insurer or insurers certifying to the coverage of all insurance required herein. Such evidence shall include original copies of the ISO CG 00 01 (or insurer’s equivalent) signed by the insurer’s representative and Certificate of Insurance (Acord Form 25-S or equivalent), together with required endorsements. All evidence of insurance shall be signed by a properly authorized officer, agent, or qualified representative of the insurer and shall certify the names of the insured, any additional insureds, where appropriate, the type and amount of the insurance, the location and operations to which the insurance applies, and the expiration date of such insurance.
g. Policy Provisions Required
(i) Consultant shall provide the City at least thirty (30) days prior written notice of cancellation of any policy required by this Agreement, except that the Consultant shall provide at least ten (10) days prior written notice of cancellation of any such policy due to non-payment of premium. If any of the required coverage is cancelled or expires during the term of this Agreement, the Consultant shall deliver renewal certificate(s) including the General Liability Additional Insured Endorsement to the City at least ten (10) days prior to the effective date of cancellation or expiration.
(ii) The Commercial General Liability Policy and Automobile Policy shall each contain a provision stating that Consultant’s policy is primary insurance and that any insurance, self-insurance or other coverage maintained by the City or any named insureds shall not be called upon to contribute to any loss.
(iii) The retroactive date (if any) of each policy is to be no later than the effective date of this Agreement. Consultant shall maintain such coverage continuously for a period of at least three years after the completion of the work under this Agreement. Consultant shall purchase a one (1) year extended reporting period A) if the retroactive date is advanced past the effective date of this Agreement; B) if the policy is cancelled or not renewed; or C) if the policy is replaced by another claims-made policy with a retroactive date subsequent to the effective date of this Agreement.
(iv) All required insurance coverages, except for the professional liability coverage, shall contain or be endorsed to provide a waiver of subrogation in favor of the City, its officials, officers, employees, agents, and volunteers or shall specifically allow Consultant or others providing insurance evidence in compliance with these specifications to waive their right of recovery prior to a loss. Consultant hereby waives its own right of recovery against City, and shall require similar written express waivers and insurance clauses from each of its subconsultants.
(v) The limits set forth herein shall apply separately to each insured against whom claims are made or suits are brought, except with respect to the limits of liability.
Further the limits set forth herein shall not be construed to relieve the Consultant from liability in excess of such coverage, nor shall it limit the Consultant’s indemnification obligations to the City and shall not preclude the City from taking such other actions available to the City under other provisions of the Agreement or law.
h. Qualifying Insurers
Hydrologics, Inc. System Wide Zero Discharge Flushing & Water System Video Inspection
7 (i) All policies required shall be issued by acceptable insurance companies, as determined by the City, which satisfy the following minimum requirements:
(1) Each such policy shall be from a company or companies with a current A.M. Best's rating of no less than A:VII and admitted to transact in the business of insurance in the State of California, or otherwise allowed to place insurance through surplus line brokers under applicable provisions of the California Insurance Code or any federal law.
i. Additional Insurance Provisions
(i) The foregoing requirements as to the types and limits of insurance coverage to be maintained by Consultant, and any approval of said insurance by the City, is not intended to and shall not in any manner limit or qualify the liabilities and obligations otherwise assumed by the Consultant pursuant to this Agreement, including but not limited to, the provisions concerning indemnification.
(ii) If at any time during the life of the Agreement, any policy of insurance required under this Agreement does not comply with these specifications or is canceled and not replaced, City has the right but not the duty to obtain the insurance it deems necessary and any premium paid by City will be promptly reimbursed by Consultant or City will withhold amounts sufficient to pay premium from Consultant payments. In the alternative, City may cancel this Agreement.
(iii) The City may require the Consultant to provide complete copies of all insurance policies in effect for the duration of the Project. (iv) Neither the City nor any of its officials, officers, employees, agents or volunteers shall be personally responsible for any liability arising under or by virtue of this Agreement.
j. Subconsultant Insurance Requirements. Consultant shall not allow any subcontractors or subconsultants to commence work on any subcontract until they have provided evidence satisfactory to the City that they have secured all insurance required under this section.
Policies of commercial general liability insurance provided by such subcontractors or subconsultants shall be endorsed to name the City as an additional insured using ISO form CG 20 38 04 13 or an endorsement providing the exact same coverage. If requested by Consultant, City may approve different scopes or minimum limits of insurance for particular subcontractors or subconsultants.
12. Indemnification.
a. To the fullest extent permitted by law, Consultant shall defend (with counsel of City’s choosing), indemnify and hold the City, its officials, officers, employees, volunteers, and agents free and harmless from any and all claims, demands, causes of action, costs, expenses, liability, loss, damage or injury of any kind, in law or equity, to property or persons, including wrongful death, in any manner arising out of, pertaining to, or incident to any acts, errors or omissions, or willful misconduct of Consultant, its officials, officers, employees, subcontractors, consultants or agents in connection with the performance of the Consultant’s services, the Project or this Agreement, including without limitation the payment of all damages, expert witness fees and attorney’s fees and other related costs and expenses. Consultant's obligation to indemnify
Hydrologics, Inc. System Wide Zero Discharge Flushing & Water System Video Inspection
8 shall not be restricted to insurance proceeds, if any, received by Consultant, the City, its officials, officers, employees, agents, or volunteers.
b. If Consultant’s obligation to defend, indemnify, and/or hold harmless arises out of Consultant’s performance of “design professional” services (as that term is defined under Civil Code section 2782.8), then, and only to the extent required by Civil Code section 2782.8, which is fully incorporated herein, Consultant’s indemnification obligation shall be limited to claims that arise out of, pertain to, or relate to the negligence, recklessness, or willful misconduct of the Consultant, and, upon Consultant obtaining a final adjudication by a court of competent jurisdiction, Consultant’s liability for such claim, including the cost to defend, shall not exceed the Consultant’s proportionate percentage of fault.
13. California Labor Code Requirements.
a. Consultant is aware of the requirements of California Labor Code Sections 1720 et seq. and 1770 et seq., which require the payment of prevailing wage rates and the performance of other requirements on certain “public works” and “maintenance” projects (“Prevailing Wage Laws”). If the services are being performed as part of an applicable “public works” or “maintenance” project, as defined by the Prevailing Wage Laws, and if the total compensation is $1,000 or more, Consultant agrees to fully comply with such Prevailing Wage Laws. Consultant shall defend, indemnify and hold the City, its officials, officers, employees and agents free and harmless from any claims, liabilities, costs, penalties or interest arising out of any failure or alleged failure to comply with the Prevailing Wage Laws. It shall be mandatory upon the Consultant and all subconsultants to comply with all California Labor Code provisions, which include but are not limited to prevailing wages (Labor Code Sections 1771, 1774 and 1775), employment of apprentices (Labor Code Section 1777.5), certified payroll records (Labor Code Sections 1771.4 and 1776), hours of labor (Labor Code Sections 1813 and 1815) and debarment of contractors and subcontractors (Labor Code Section 1777.1). The requirement to submit certified payroll records directly to the Labor Commissioner under Labor Code section 1771.4 shall not apply to work performed on a public works project that is exempt pursuant to the small project exemption specified in Labor Code Section 1771.4. b. If the services are being performed as part of an applicable “public works” or “maintenance” project, then pursuant to Labor Code Sections 1725.5 and 1771.1, the Consultant and all subconsultants performing such services must be registered with the Department of Industrial Relations. Consultant shall maintain registration for the duration of the Project and require the same of any subconsultants, as applicable. Notwithstanding the foregoing, the contractor registration requirements mandated by Labor Code Sections 1725.5 and 1771.1 shall not apply to work performed on a public works project that is exempt pursuant to the small project exemption specified in Labor Code Sections 1725.5 and 1771.1. c. This Agreement may also be subject to compliance monitoring and enforcement by the Department of Industrial Relations. It shall be Consultant’s sole responsibility to comply with all applicable registration and labor compliance requirements. Any stop orders issued by the Department of Industrial Relations against Consultant or any subcontractor that affect Consultant’s performance of services, including any delay, shall be Consultant’s sole responsibility. Any delay arising out of or resulting from such stop orders shall be considered Consultant caused delay and shall not be compensable by the City. Consultant shall defend, indemnify and hold the City, its officials, officers, employees and agents free and harmless from any claim or liability arising out of stop orders issued by the Department of Industrial Relations against Consultant or any subcontractor.
Hydrologics, Inc. System Wide Zero Discharge Flushing & Water System Video Inspection
9 14. Safety.
Consultant shall execute and maintain its work so as to avoid injury or damage to any person or property. In carrying out its Services, the Consultant shall at all times be in compliance with all applicable local, state and federal laws, rules and regulations, and shall exercise all necessary precautions for the safety of employees appropriate to the nature of the work and the conditions under which the work is to be performed. Safety precautions as applicable shall include, but shall not be limited to: (A) adequate life protection and life-saving equipment and procedures; (B) instructions in accident prevention for all employees and subcontractors, such as safe walkways, scaffolds, fall protection ladders, bridges, gang planks, confined space procedures, trenching and shoring, equipment and other safety devices, equipment and wearing apparel as are necessary or lawfully required to prevent accidents or injuries; and (C) adequate facilities for the proper inspection and maintenance of all safety measures.
15. Verification of Employment Eligibility.
By executing this Agreement, Consultant verifies that it fully complies with all requirements and restrictions of state and federal law respecting the employment of undocumented aliens, including, but not limited to, the Immigration Reform and Control Act of 1986, as may be amended from time to time, and shall require all subconsultants and sub-subconsultants to comply with the same.
16. INTENTIONALLY DELETED
17. Laws and Venue.
This Agreement shall be interpreted in accordance with the laws of the State of California.
If any action is brought to interpret or enforce any term of this Agreement, the action shall be brought in a the Superior Court of California for the County of Napa.
18. Termination or Abandonment
a. City has the right to terminate or abandon any portion or all of the work under this Agreement by giving ten (10) calendar days written notice to Consultant. In such event, City shall be immediately given title and possession to all original field notes, drawings and specifications, written reports and other documents produced or developed for that portion of the work completed and/or being abandoned. City shall pay Consultant the reasonable value of services rendered for any portion of the work completed prior to termination. If said termination occurs prior to completion of any task for the Project for which a payment request has not been received, the charge for services performed during such task shall be the reasonable value of such services, based on an amount mutually agreed to by City and Consultant of the portion of such task completed but not paid prior to said termination. City shall not be liable for any costs other than the charges or portions thereof which are specified herein. Consultant shall not be entitled to payment for unperformed services, and shall not be entitled to damages or compensation for termination of work.
b. Consultant may terminate its obligation to provide further services under this Agreement upon thirty (30) calendar days’ written notice to City only in the event of substantial failure by City to perform in accordance with the terms of this Agreement through no fault of Consultant.
Hydrologics, Inc. System Wide Zero Discharge Flushing & Water System Video Inspection
10 19. Ownership of Documents and Confidential Information. a. All deliverables and other documents generated by Consultant in the performance of the Services, including all work papers, work-in-progress, designs, drawings, documents, data, computations, specifications, studies and reports prepared by Consultant as a part of the Services or authorized Additional Services (“Consultant Work Product”) shall belong to and be subject to the sole ownership and use of City. b. Except as otherwise provided in “Termination or Abandonment,” above, all original field notes, written reports, drawings and specifications and other documents, produced or developed for the Project shall, upon payment in full for the services described in this Agreement, be furnished to and become the property of the City. c. During the course of the performance of this Agreement, Consultant may receive written or verbal information from City, its representatives or agents, not in the public domain. Such information may include City’s know how, trade secrets, and other proprietary and confidential information and Consultant agrees to treat such information as confidential information belonging to City. Consultant agrees that neither it, nor its officers, employees, representatives, agents, successors, or assigns, will disclose such information to any third party or use the same in any manner without the prior written consent of City. Moreover, Consultant agrees to safeguard such proprietary and confidential information from unauthorized disclosure and/or use using the same degree of care it uses to protect its own proprietary and confidential information, but not less than a reasonable standard of care. In the event that disclosure of such information is sought pursuant to any law or regulation, Consultant shall promptly notify City of such fact to allow City to assert whatever exclusions or exemptions may be available to it under applicable law or regulation.
20. Organization
Consultant shall assign Gunther Mueller as Project Manager. The Project Manager shall not be removed from the Project or reassigned without the prior written consent of the City.
21. Limitation of Agreement.
This Agreement is limited to and includes only the work included in the Project described above.
22. Notice
Any notice or instrument required to be given or delivered by this Agreement may be given or delivered by depositing the same in any United States Post Office, certified mail, return receipt requested, postage prepaid, addressed to:
CITY:
City of St. Helena
1088 College Ave
St. Helena, CA 94574
Attn: Joseph Leach P.E. PW Director
CONSULTANT:
Hydrologics, Inc.
500 S Australian Ave, Ste 600-1008
West Palm Beach, FL 33401
Attn: Gunther Mueller
Hydrologics, Inc. System Wide Zero Discharge Flushing & Water System Video Inspection
11 and shall be effective upon receipt thereof.
23. Third Party Rights
Nothing in this Agreement shall be construed to give any rights or benefits to anyone other than the City and the Consultant.
24. Equal Opportunity Employment.
Consultant represents that it is an equal opportunity employer and that it shall not discriminate against any employee or applicant for employment because of race, religion, color, national origin, ancestry, sex, age or other interests protected by the State or Federal Constitutions. Such non-discrimination shall include, but not be limited to, all activities related to initial employment, upgrading, demotion, transfer, recruitment or recruitment advertising, layoff or termination.
25. Entire Agreement
This Agreement, with its exhibits, represents the entire understanding of City and Consultant as to those matters contained herein, and supersedes and cancels any prior or contemporaneous oral or written understanding, promises or representations with respect to those matters covered hereunder. Each Party acknowledges that no representations, inducements, promises or agreements have been made by any person which are not incorporated herein, and that any other agreements shall be void. This Agreement may not be modified or altered except in writing signed by both Parties hereto. This is an integrated Agreement.
26. Severability
The unenforceability, invalidity or illegality of any provision(s) of this Agreement shall not render the remaining provisions unenforceable, invalid or illegal.
27. Successors and Assigns
This Agreement shall be binding upon and shall inure to the benefit of the successors in interest, executors, administrators and assigns of each Party to this Agreement. However, Consultant shall not assign or transfer by operation of law or otherwise any or all of its rights, burdens, duties or obligations without the prior written consent of City. Any attempted assignment without such consent shall be invalid and void.
28. Non-Waiver
None of the provisions of this Agreement shall be considered waived by either Party, unless such waiver is specifically specified in writing.
29. Time of Essence
Time is of the essence for each and every provision of this Agreement.
30. City’s Right to Employ Other Consultants
Hydrologics, Inc. System Wide Zero Discharge Flushing & Water System Video Inspection
12 City reserves its right to employ other consultants, including engineers, in connection with this Project or other projects.
31. Prohibited Interests
Consultant maintains and warrants that it has not employed nor retained any company or person, other than a bona fide employee working solely for Consultant, to solicit or secure this Agreement. Further, Consultant warrants that it has not paid nor has it agreed to pay any company or person, other than a bona fide employee working solely for Consultant, any fee, commission, percentage, brokerage fee, gift or other consideration contingent upon or resulting from the award or making of this Agreement. For breach or violation of this warranty, City shall have the right to rescind this Agreement without liability. For the term of this Agreement, no director, official, officer or employee of City, during the term of his or her service with City, shall have any direct interest in this Agreement, or obtain any present or anticipated material benefit arising therefrom.
[SIGNATURES ON FOLLOWING PAGE]
Hydrologics, Inc. System Wide Zero Discharge Flushing & Water System Video Inspection
13 SIGNATURE PAGE FOR PROFESSIONAL SERVICES AGREEMENT
BETWEEN CITY OF ST. HELENA
AND HYDROLOGICS, INC.
IN WITNESS WHEREOF, the Parties have executed this Agreement as of the date first written above.
CITY OF ST. HELENA HYDROLOGICS, INC.
By: By:
James McCann Its:
Interim City Manager
Printed Name:
ATTEST:
By:
Ethan Walsh, City Attorney
Hydrologics, Inc. System Wide Zero Discharge Flushing & Water System Video Inspection
14 EXHIBIT A
Scope of Services
Hydrologics, Inc.
500 S Australian Ave Ste 600-1008
West Palm Beach, FL
33401-6223
8884933123
Quotation 240257
ADDRESS SHIP TO
City of St. Helena
1088 College Ave.
St. Helena, CA 94574
City of St. Helena
1088 College Ave.
St. Helena, CA 94574
DATE
08/25/2026
TOTAL
$429,195.00
PROJECT
Camera 47 day
QTY RATE AMOUNT
Mobilization
To move camera equipment and secondary crew to customer site. 1 4,960.00 4,960.00
Camera work
Daily rate for Camera work for a 3 man crew-2 probes per day with pre and post videos to show conditions on particular mains
47 6,000.00 282,000.00
Prevailing Wage Addition
Additional wages for a 3 man crew Davis-Bacon Act # GA20230309 47 3,000.00 141,000.00
Stand Down
Daily rate is charged for each day Hydrologics is not able to perform camera work due to no fault of Hydrologics.
0 3,800.00 0.00T
Administrative Fee
Compliance paperwork preparation
1 1,235.00 1,235.00
SUBTOTAL 429,195.00
TAX 0.00
TOTAL $429,195.00
THANK YOU.
Accepted By Accepted Date
Exhibit A
Hydrologics, Inc.
500 S Australian Ave Ste 600-1008
West Palm Beach, FL
33401-6223
8884933123
Quotation 240245
ADDRESS SHIP TO
City of St. Helena
1088 College Ave.
St. Helena, CA 94574
City of St. Helena
1088 College Ave.
St. Helena, CA 94574
DATE
08/25/2026
TOTAL
$487,877.02
PROJECT
System Wide ZDF Project
QTY RATE AMOUNT
Flushing
Standard ZDF flushing process includes (1) ZDF unit operated by (2) Hydrologics employees and all necessary equipment to perform the flushing operation in a normal potable water distribution system (per 8-hour day)
47 9,800.00 460,600.00
Flushing Discount
Flushing Discount -
47 -1,960.00 -92,120.00
Prevailing Wage Addition
Additional daily expense for the increased cost of additional wages required per prevailing wage laws in the city or local of operations. The rate is not inclusive of weekend, overtime, or holiday hours and is subject to increase if work performed falls after the date of the next determination increase posted by the Department of Labor/DIR.
49 765.00 37,485.00
Stand Down
Daily rate is charged for each day Hydrologics is not able to perform flushing days due to no fault of Hydrologics.
0 3,800.00 0.00T
Mobilization
A mobilization fee is charged to move ZDF equipment to/from the customer's site. This fee is charged at the start of a project and upon return visits.
1 3,880.00 3,880.00
Disinfection
Disinfection of ZDF equipment before use in the customer's system. This fee is charged when a project is started and before any return visits.
1 4,860.00 4,860.00
ZDF OHM Filters
OHM Polypropylene #2 Size Bag Filter, Extended 32" Finished Length, 7 Layers, "FS" Flange Top, 1 Micron Rating
Note: This estimate assumes the use of 36 filters per day. The customer will be billed for the actual number of filters used.
1,692 39.95 67,595.40T
Administrative Fee
Permitting, Licensing, Insurance Certificates, & Compliance Documentation if required 0 490.00 0.00
SUBTOTAL 482,300.40
TAX 5,576.62
TOTAL $487,877.02
Service Time Disclaimer
The ZDF service time provided in this estimate is based on industry averages and historical data. Actual service time may vary depending on the specific conditions of the customer’s water quality. As water quality can significantly impact the duration of services, final service time will be determined during performance of the work.
THANK YOU.
Exhibit A
Outlook
Agenda Item 10.3
From Joshua Parke <[email protected]>
Date Tue 10/13/2026 12:46 PM
To Andrew Bradley <[email protected]>
Cc Paul Dohring <[email protected]>; Michelle Deasy <[email protected]>; James McCann <[email protected]>; Joseph Leach <[email protected]> 7 attachments (3 MB)
1Original Outreach ReFlushing.pdf; 2Response 2JM.pdf; 3ZDF_Response to AC Pipe_rev 2_101326.pdf; 4Consultant Response Email Thread .pdf; 5Response 2JL.pdf; 6WaterborneAsbestos-2026Mar23.pdf; 7ph4asbestos92603.pdf; Hi Andrew,
I’m not able to be at the computer this afternoon and will not have time to post comment beyond this email so I am including the document set from the correspondence with the city regarding agenda item
10.3. Please also post the body of this email as the first comment.
Documents are presented in chronological order below please post accordingly.
I want to emphasize that in no way am I insinuating there is an issue in our system around this. I am simply emphasizing that i think it is important that we execute the work properly so that we are sure we are not creating potential for harm. We have an opportunity to address this with the level of responsibility it deserves. Given the current status of the issues with our water infrastructure and quality of service everyone needs to know that the level of urgency exists as well as the level of care required.
This type of pipe is everywhere all over the world, hundreds of thousands of miles of it. It is not a problem unique to our town. I am not writing this to create or enflame a situation. We simply need to make sure we know where we stand and do something about it. As mentioned before it is an opportunity to set a positive proactive example for many communities that are up against this.
My hope is that this can easily become another aspect of dealing with the issue and can simply be incorporated in the proper sequence of procedures needed.
Again please post the body of this email as comment number 1 and the proceeding documents in order after.
Thank you,
Joshua Parke
From: Joshua Parke <[email protected]>
Subject: Hydrologics Agenda Item
Date: October 12, 2026 at 11:35:50AM PDT
To: James McCann <[email protected]>
Hi Jim,
Realize I may be writing you on a day off, no need to respond today.
Reading over the Tuesday agenda item for the high velocity pipe scrubbing i’m deeply concerned that the asbestos pipe aspect is being overlooked along with the distinct possibility of simply redistributing dissolved manganese into the system. The 1 micron filter diameter does not capture the majority of asbestos fibers nor does it capture undissolved manganese or various bacteria etc.
The treatment process often uses chlorine as a last treatment stage but the chlorine could just oxidize the dissolved manganese after the fact. Jay mentioned that we have about 5% dissolved manganese still exiting the plant.
The asbestos is the biggest concern. It’s a known carcinogen and there is lots of data around the correlation between ingestion and increased cancer risks. I’m not drawing the line of direct causation but I am communicating that it is exceptionally irresponsible to be using a high velocity scrubbing technique on asbestos pipes of which we have no data regarding their material state of deterioration. There are water pipe flow studies around the increased fiber release from just high flushing flow, let alone high velocity scrubbing, and they are based on pipe that is about 10 years old. The life span of ACP is about 50 years before deteriorating (the break of the main at Stonebridge is a good example of evidence of deterioration). The only tests we have regarding fiber shedding is from source locations and one test on Allison Ave while the majority of the ACP pipe is located on the west side of town where the oldest infrastructure is.
We need to be responsible in the approach of how we deal with this. Asbestos pipe is essentially the leaded gasoline of our time and it is a problem the world over. Italy, where the pipe first originated, is an example of a country dealing with the issue and has the most recent health focused data. It’s entirely possible that we have levels in the distribution system well exceeding EPA levels and until we test in the system we simply don’t know. The additional risk aside from health implications is the potential for scarifying the pipe surface of old pipes and having them continue to shed vigorously long after the scrubbing is done.
Water can appear “clear” and have tens of millions of fibers. This is a serious issue.
We need to add testing for asbestos levels to the city’s testing plan to determine the extent of the health issue it presents in town. The data will help to determine proper pipe
cleaning procedures and how we can prioritize steps and chronology moving forward based on known exposure data..
The community needs to know the city cares about its wellbeing and this is yet another way to show we are doing things properly.
For the meeting I would suggest presenting a proper work plan detailing actions and chronology, not just a list of potentials. Start with the plant, then the tank, then the main transmission line and talk about the issues clearly and discuss the appropriate steps.
We can be focusing on non the plant/tanks/main line while we determine the best plan of action for the pipes in town.
Long term if the Hydrologics approach is determined to be the best one based on the age of pipes at a minimum run through the typical process of closed loop scrubbing and filtering of 1 micron and larger contaminants but do not keep the water in the pipe system to redistribute. Flush the pipes afterward to clear the remaining water.
I have a great deal of scientific research papers and articles etc on the subject and detailed potential proper procedures etc. and would happy to share.
Please do this properly. There is an immense amount of opportunity in setting an example for other communities as well as rebuilding good will within this one.
Looking forward to hearing your thoughts. Please let me know tomorrow morning if the item will be staying on the agenda. If so I need to think through an appropriate public comment that delivers the messaging in an appropriate way.
Hope this finds you well,
Sincerely,
Joshua
On Oct 12, 2026, at 12:46PM, Joshua Parke <[email protected]> wrote:
Hi Jim,
Thank you for the prompt response and I apologize I didn’t reach out sooner. Typical government verbiage on this historically has been to simply stay that "levels are within EPA testing range” but when the EPA established it’s standards for testing in ’92 it simply stated that if elevated levels were found at the source then municipalities were required to test within the system, this completely negates the existence of now deteriorated pipes supplying drinking water. California has somewhat more stringent regulation but the single source test at Allison last year while strategically checks the box does not reflect an actual standing of our situation.
Consultants are motivated to sign contracts and the city is motivated to show action. I get that.
Here’s some contemporary data from our neighbors to the north who supplied the world with a significant amount of the mined asbestos that exists in our built environment:
On Oct 12, 2026, at 12:10PM, James McCann <[email protected]> wrote:
Hello JoshuaThank you for the early comment regarding the agenda item and proposed action.
I’ll share your email with Joe Leach for his info and response. We certainly need to consider the range of potential effects of our actions; I appreciate your call to attention.
We’ll be in touch.
-Jim
Hydrologics | Technical Response
Response to Concerns Regarding Zero Discharge Flushing
Asbestos Cement Pipe Manganese Filtration Water Quality Monitoring Joshua,
Thank you for taking the time to provide such a detailed comment. We share your underlying objective: any work performed in St. Helena's drinking-water system should protect public health, preserve the integrity of the infrastructure, and be supported by measurable data.
Below we’ve addressed each of your concerns. While we welcome the comments, it’s important to note that several statements are overstated, technically incomplete, or presented as established facts when they are not.
Asbestos Cement Pipe
Your concern that deteriorated asbestos-cement pipe can release fibers under certain conditions should be considered. High-flow can mobilize material already present in a water main, and significantly deteriorated AC pipe warrants additional care. That does not, however, establish that the proposed ZDF work will damage the pipe or create an unsafe condition. Pipe age and a history of main breaks are reasons for condition assessment, but they do not by themselves establish the condition of every AC main.
It is also extremely important to distinguish Zero-Discharge Flushing from mechanical scraping or pigging. ZDF does not insert a scraper, brush, or abrasive device into the pipe. It creates a controlled hydraulic loop, circulates water at a prescribed velocity, removes suspended sediment and particulate material through filtration, monitors turbidity, and returns the treated water to the distribution system. And we monitor our sample ports and if we identify any particulates, we lower the velocity and flush out any of the particles that may have come loose the liner pipe. This is another safeguard.
Filtration and Asbestos Measurement
The statement regarding the 1-micron filter requires clarification. EPA regulates asbestos in drinking water based on the number and length of fibers, while a filter rating describes particle-retention performance. Those measurements are not directly interchangeable. Consequently, it would not be technically supportable either to claim that the filter captures all asbestos fibers or to claim, without testing, that it captures almost none of them. If AC-pipe segments are included in the work, representative asbestos sampling is the appropriate way to determine actual performance.
Manganese and Disinfection
The manganese issue similarly requires differentiation between dissolved and particulate manganese. ZDF is designed to remove particulate manganese, sediment, biofilm, and other accumulated material. Dissolved manganese is not removed merely by passing through a particulate filter. Chlorine can oxidize dissolved manganese into a particulate form, but the extent and location of that reaction depend on pH, dose, contact time, temperature, and other water-chemistry conditions. For that reason, dissolved, particulate, and total manganese should be evaluated separately.
The 1-micron filtration system should not be characterized as a sterilization barrier. Distribution-system microbial control depends on disinfectant management, operational controls, and bacteriological verification. Those measures should be included in the work plan.
Health and Regulatory Context
Current scientific and regulatory guidance also requires precision regarding health risk. Asbestos is a known carcinogen when inhaled. The evidence concerning ingestion through drinking water is less conclusive, although EPA maintains an enforceable drinking-water standard of 7 million fibers per liter for fibers longer than 10 micrometers. The concern should therefore be taken seriously and evaluated through properly located sampling rather than through assumptions in either direction.
Hydrologics | Technical Response
Recommended Work Plan
Like all of our projects, Hydrologics supports and adheres to a cautious, data-driven work plan that includes the following safeguards:
• Identify the AC-pipe segments affected by the project. • Review available pipe-condition, break-history, and water-chemistry information. • Collect representative baseline asbestos samples at taps served by AC pipe, including locations where release would be most likely.
• Establish operating limits, acceptance criteria, and stop-work thresholds before flushing begins. • Monitor turbidity, pressure, flow, disinfectant residual, and manganese during the work. • Conduct post-flushing asbestos and water-quality sampling where AC pipe is involved. • Compare inlet water, filtered return water, and representative downstream water-quality results. • Provide a written comparison of baseline, operating, and post-project results.
If those results indicate that a segment should not be subjected to the proposed hydraulic conditions, the operating plan should be modified or that segment excluded. If the results show that the process safely removes accumulated material without adversely affecting the pipe or water quality, the City will have objective evidence supporting its next steps.
We believe that approach addresses the concern responsibly: neither ignoring a potential risk nor assuming harm before the relevant condition and water-quality data have been collected.
Sincerely,
Gunther Mueller
HydroLogics
Technical References
• American Water Works Association. Policy Statement on Distribution System Water Quality. • U.S. Environmental Protection Agency. National Primary Drinking Water Regulations, asbestos maximum contaminant level and monitoring requirements.
• U.S. Environmental Protection Agency. Protecting Water Quality Through Distribution System Flushing. • World Health Organization. Asbestos in Drinking Water, Guidelines for Drinking-water Quality fact sheet, 2022. • The Water Research Foundation. Guidance Manual for Managing Long Term Performance of Asbestos Cement Pipe.
On Oct 13, 2026, at 10:19AM, Joshua Parke <[email protected]> wrote:
Thank you Joe.
This is a confusing AI generated response. It agrees and disagrees and seems to contradict itself.
Do you have the asbestos testing and field reports mentioned for the 9 miles of flushing work that was executed in June?
On Oct 13, 2026, at 9:59AM, Joseph Leach <[email protected]> wrote:
Good a.m. Joshua,
Please see the attached response from Hydrologics related to your inquiry...
Mr. Mueller will be present virtually this evening to field any additional questions you might have.
Cordially,
JOE LEACH, PE
ASSISTANT CITY MANAGER/DIRECTOR OF PUBLIC WORKS/CITY ENGINEER City of St. Helena | Public Works
1088 College Avenue | St. Helena, CA 94574
Direct: (707) 968-2629 | [email protected] | http://cityofsthelena.gov/publicworks Celebrating St. Helena's Sesquicentennial: 150 Years of Service Learn more about celebrations throughout 2026 at celebratesthelena.com From: Gunther Mueller <[email protected]>
Sent: Tuesday, October 13, 2026 7:00 AM
To: Joseph Leach <[email protected]>; Bruce Zaeni <[email protected]>
Cc: issam.najm <[email protected]>; James McCann
<[email protected]>; Andrew Bradley
<[email protected]>; Carlos Uribe
<[email protected]>; issam.najm
<[email protected]>
Subject: RE: StH-Hydrologics Contract Public Comment
Joe & Bruce,
Attached, Please find our response to the Public Comment.
I see you booked a morning call… see you then. I am also available for the Council meeting Tuesday Evening virtually.
In Service of Your Success,
Gunther Mueller
Hydrologics.com – Chief Revenue Officer
The Home of Zero Discharge Flushing
505-738-3851
Book A Meeting with Gunther
From: Joseph Leach <[email protected]>
Sent: Monday, October 12, 2026 2:04 PM
To: Bruce Zaeni <[email protected]>; Gunther Mueller <[email protected]>
Cc: issam.najm <[email protected]>; James McCann
<[email protected]>; Andrew Bradley
<[email protected]>; Carlos Uribe
<[email protected]>
Subject: StH-Hydrologics Contract Public Comment
Bruce & Gunther,
[EXTERNAL] CAUTION: This email is from an external source.
Verify the sender's address before clicking any links or providing
Attached is a public comment we received related to the item scheduled to be awarded by the City Council at their meeting tomorrow evening.
Please provide a response ASAP.
Let me know if we need to schedule a mtg to discuss.
Thanks,
JOE LEACH, PE
ASSISTANT CITY MANAGER/DIRECTOR OF PUBLIC WORKS/CITY ENGINEER City of St. Helena | Public Works
1088 College Avenue | St. Helena, CA 94574
Direct: (707) 968-2629 | [email protected] | http://cityofsthelena.gov/publicworks Celebrating St. Helena's Sesquicentennial: 150 Years of Service Learn more about celebrations throughout 2026 at celebratesthelena.com <ZDF_Response to AC Pipe_rev 2_101326.pdf><Parke Comment_Hydrologics Item_101226 1323.pdf>
On Oct 13, 2026, at 10:36AM, Joshua Parke <[email protected]> wrote:
Joe,
Here’s some additional data generated by the state regarding the issue as well as a current document from Canada. We have manganese levels coming in from residents that is exponentially beyond stated safe levels. We need to make sure we do this properly.
Also missing from the staff report is any statement of chronology for the execution of the work. I’m assuming the main line from Bell canyon will be cleaned prior to executing this work?
The testing is the primary concern. What is the current state of the amount of shedding we have within the pipes and is the process adequate for filtering the material? I understand the easy interpretation of saying the EPA regulates by length of fiber. The length is different from the diameter however and the diameter of the fibers are much less than 1 micron so the length of the fiber is not an adequate statement of fact that the material does not pass through the filter. What testing do they do in the field to make sure the quantity released back into the system is not beyond EPA standards?
1 Friends of the Earth Canada
Comments and recommendations regarding:
Draft Guidance on Asbestos in Drinking Water
Guidance document for public consultation
https://www.canada.ca/en/health-canada/programs/consultation-guidance-asbestos-drinkingwater/document.html Submitted to Health Canada
Email: [email protected]
March 23, 2026
Respectfully submitted by:
Meg Sears PhD
Chair, Prevent Cancer Now
Theresa McClenaghan,
Executive Director and Counsel, Canadian Environmental Law Association Bea Olivastri, CEO, Friends of the Earth Canada
2 Table of Contents
Summary ..................................................................................................................................................... 3 Recommendations for Actions.................................................................................................................... 6 Introduction ................................................................................................................................................ 8 Drinking water contamination from asbestos-reinforced cement pipes.................................................... 9 Measuring asbestos in water.................................................................................................................. 9 Carcinogenicity of ingested asbestos.......................................................................................................... 9 Comments on the consultation summaries of carcinogenicity research ............................................. 10 When exposure is primarily airborne, how does asbestos cause cancers beyond the lungs?............. 11 Scope of the problem and elements of solutions................................................................................. 11 Examples of international actions regarding asbestos cement pipes................................................... 12 Conclusions............................................................................................................................................... 13 Water contamination measurement, and standard to protect public health ...................................... 13 Reflection in conclusion ........................................................................................................................ 14 Appendix 1: Doorhanger following repair of an asbestos-cement pipe in Regina ................................... 15 Appendix 2: Sample waterworks maps with asbestos cement water pipes —Winnipeg and Regina...... 16 REFERENCES .............................................................................................................................................. 17
3 Summary
The draft guidance for waterborne asbestos marks the first invitation by the Canadian government for public discussion of asbestos in drinking water, and asbestos-cement pipes.
Prevent Cancer Now, Canadian Environmental Law Association, and Friends of the Earth Canada submit the following comments and recommendations in response to the Consultation Document: Draft Guidance on Asbestos in Drinking Water - Guidance document for public consultation released on January 23 2026.
We call for Health Canada to recognize that asbestos—a known human carcinogen—is hazardous and causes cancer when it is waterborne; and to establish a formal Guideline for drinking water quality.
With corrections to data and interpretations presented in the consultation document, plus the peerreviewed literature discussed below, the three criteria outlined by Health Canada are met to develop a maximum acceptable concentration (MAC) for asbestos in drinking water:
1. exposure to the substance could lead to adverse health effects;
2. the substance is frequently detected or could be expected to be found in a large number of drinking water supplies throughout Canada;
3. the substance is detected, or could be expected to be detected, at a level that is of possible health significance.
The Health Canada draft assessment has substantial methodological and scientific shortcomings. We offer the following analyses and commentary to support development of asbestos drinking water guidelines for all Canadians, particularly to protect those who are at higher risk of exposure and most vulnerable to the impacts of asbestos (e.g. workers, and families including young children whose water supply relies on cement asbestos pipes). We take this opportunity to direct attention to:
• correction of summarized peer-reviewed data (e.g., Donham et al. clearly demonstrates carcinogenicity of ingested asbestos, comparing the exposed animals to two control groups of equal numbers);
• interpretation of data, while recognizing that studies investigating the impacts of oral ingestion of asbestos fibres are limited and many are older;
• the facts of inhalational exposure from dried residues (e.g., laundry), as well as boiling water, showers and humidifiers—e.g., potentially releasing millions of asbestos fibres into the breathing zone of a child;
• the lack of relevant, recent analyses of asbestos in Canadian drinking water sources; and • the need for an accredited Canadian laboratory to measure concentrations and size distributions of asbestos fibres in water samples.
Over decades, Canada provided the world with approximately 40% of its chrysotile asbestos, and Canadian researchers contributed to the body of science demonstrating carcinogenicity in affected workers and communities. In 2018 the federal government took regulatory action against bulk and airborne asbestos to prevent cancer, while noting a lack of “consistent, convincing evidence” regarding swallowing asbestos. This is a high bar of proof given data scarcity, and limitations of research investigating harms of ingesting asbestos in drinking water. Similar claims have been made in the consultation document.
4 Canada’s asbestos-cement water pipes have been aging and breaking, and asbestos is increasingly contaminating drinking water in affected neighbourhoods. Responses focus on pipe replacement, but not public health implications. The present consultation should fill this important public health scientific and regulatory gap.
The consultation document reiterates a need for, “consistent, convincing evidence” that asbestos, a known human carcinogen according to the International Agency for Research on Cancer, 1 is harmful
when swallowed. As noted, such evidence is thwarted by Canada’s lack of an analytical method, laboratory capacity and data on asbestos contamination of drinking water, all of which is a consequence of the assumption that drinking asbestos is “safe.” Within this circular reasoning, there is certainly no “consistent, convincing evidence” that drinking asbestos is safe. Furthermore, with millions of Canadians ingesting increasingly contaminated water from aged, degrading asbestos cement pipes, the cumulative impacts could be considerable, and may already be reflected in Canada’s increasing incidence of cancers; particularly colorectal cancer. A 2022 Statistics Canada infrastructure survey found that approximately 14,000 km of asbestos cement pipes carrying drinking water were reported by 64% of surveyed jurisdictions.2
Asbestos is one of the most-studied toxicants, with extensive scientific literature spanning many decades. Inhaling, then swallowing fibres cleared from lungs, was described by the International Agency for Research on Cancer in their conclusion that asbestos is a known human carcinogen.1 Abdominal cancers associated with airborne asbestos are presumed to arise from swallowing contaminated phlegm cleared from the respiratory tract, but contaminated drinking water is another potential exposure route. Water-borne asbestos can contaminate air when boiled, aerosolized in humidifiers or when showering, and shed from laundered linens and clothing, resulting in airborne exposures.
Asbestos fibres have been visualized in gastrointestinal and liver cancers (cholangiocarcinoma). 3,4,5,6
Moreover, visualized fibres in these tissues are often smaller than 10 µm, consistent with the shorter fibres seen in drinking water.7,8
Importantly, academic research methods and reporting styles have evolved over time, often resulting in discounting of older studies. Health Canada leans on a systematic review (Go, et al.) published in 2025, that clearly illustrates carcinogenic potential of ingested asbestos. 9 Some of this work is included
in the consultation document.
Human epidemiological studies, published from 1974 to 2015, reported that ingestion of asbestos was significantly associated with cancer incidence and/or mortality in 11 out of 14 studies. A 2024 systematic review of asbestos ingestion and gastrointestinal cancers, with a somewhat different selection of included studies found a causal link between occupational asbestos exposure and the risk of oesophageal, stomach and colorectal cancer.10
Animal studies are not reported as having as many significant findings, but the consultation document misrepresents the Donham et al. study. This key, early study had two control groups—one fed cellulose to mimic the bulk of the asbestos loading, and one a simple control group, so there were twice as many “unexposed” animals and the incidence of cancer in the asbestos-exposed animals was substantially higher. As well, ashed tumour samples identified fibres in the “control” group tumours, so it was not a clean comparison. This initial large experimental study details experimental challenges, and did find
5 that waterborne asbestos caused cancers. Thus, two animal studies support that ingested asbestos is a carcinogen.
Regulation of asbestos in water would require water quality analytical methodology and capacity to meet regulatory obligations. Water quality data could assist with prioritization of pipes replacement, beyond responding to increasing pipe breaks. The consultation draft suggests that a science-based MAC (maximum allowable contamination level) is necessary for a standard (action level) before pipes replacement can be directed.
It is not good governance nor in the interest of public health to await unprioritized research, to identify a threshold that may not exist, before taking action to minimize asbestos in drinking water.
An asbestos standard to highlight risks and to track progress would specify: 1. the fibre size range of interest; and 2. a maximum concentration of fibres in water. These could be set pragmatically, now.
Particle size: The U.S.A. standard to count only large fibres, 10 µm (micrometres or microns) and larger, was set decades ago to ensure adequate access to current day analytical capacity.
The vast majority of particles are much smaller than 10 µm, and these are harmful, so the U.S.A. standard is insensitive and is outdated.11 With modern technologies and knowledge of hazards of smaller fibres, we recommend that the size range of interest be consistent with other waterborne particulate contaminants. The consultation notes asbestos fibre size distributions with peaks at 4 µm or smaller. Modern analyses of particle size distributions, and a smaller regulatory particulate size minimum (e.g., ESML labs report fibres both >10 µm and >0.5 µm 12). would be a more meaningful threshold of concern.
Contaminant levels: The consultation document indicates that utilities’ drinking water treatment removes asbestos from source water. Thus, if there is no source of asbestos in the water distribution network, asbestos fibre counts will be very low. A maximum fibre count should signal early concerns in the context of background levels with robust infrastructure in place. There is no “safe” level of asbestos exposure—"millions of fibres per litre” represents substantial contamination; not a precautionary approach. A guidance value should be much lower.
Internationally, several nations are expediting replacement of asbestos cement pipes because of concerns that waterborne asbestos is contributing to increasing cancer rates, as well as the disruption and costs of frequent pipe breakages.
13,14,15 Canada has not yet made such a commitment.
Enabling important Canadian cancer research
When the present and historical locations of asbestos cement pipes are available, this data would help to enable epidemiological research including cohorts of newly diagnosed relevant cancers such as colorectal—a rapidly increasing malignancy in younger and younger Canadians.16
6 Recommendations for Actions
1. Establish Guidelines for asbestos in drinking water. Acknowledge that asbestos in drinking water is a human health concern. Health Canada has a role to state this unequivocally and publicly, and to counter misinformation such as by local municipalities that citizens need not worry about cloudiness, sludge or sediment in drinking water impacted by asbestos cement pipe degradation and breakage, notably during and following pipe repairs.
2. Do not support the draft consultation proposal by Health Canada which recommends no action to develop a Maximum Allowable Contaminant (MAC) level for asbestos in water. The criteria to support the development of guidelines seem to have been met, and action to establish a MAC is a priority.
3. In affected areas, the government should test drinking water for asbestos annually and following repair of asbestos cement water pipes, and report results to the public.
4. Develop guidelines for asbestos in drinking water by Health Canada in collaboration with the Federal-Provincial-Territorial Committee on Drinking Water with an initial, interim goal of “As Low As Reasonably Achievable” (ALARA) in terms of both fibre size and concentrations.
Recommended limits must include a substantial majority of asbestos fibres, including particles as small as 0.5 µm and larger, as for some other airborne pollutants.
Report the spectrum of fibre counts over size ranges, as is currently available from some laboratories.
Establish Laboratory Accreditation and Facilities for analysis of asbestos in drinking water
5. Establish accredited laboratory test methods for asbestos in drinking water.
6. Establish Canadian analytical laboratory capacity to measure asbestos in water, with reporting of the spectrum of fibre sizes ranging from less than one micrometre to greater than 10 micrometre (0.5 µm to >10 µm) length; substantially more sensitive than the U.S.A. limit (7 million fibres per litre [MFL] for fibres ≥ 10 µm).
Testing and Reporting of asbestos in drinking water
7. Establish a periodic water testing survey for affected municipalities as suggested in Health Canada’s draft guidance (e.g., sampling from fire hydrants) in order to: establish baseline data; to guide recommendations for water treatment (private or public); and to support prioritization of asbestos-cement pipe replacement.
Advancing Asbestos Eradication in Canada
8. Support and expand research and capacity for asbestos eradication in Canada, with goals to: 1. outline and validate best practices to measure, to prevent and to minimize asbestos in drinking water; 2. establish best practices for asbestos-cement pipe removal, disposal, and replacement; and 3. support continuing medical education and research to investigate roles of asbestos in increasing related disease, including cancers.
9. Commit to work with all levels of governments to develop and execute a plan to identify and to replace existing cement water pipes with non-asbestos alternatives: 1. expedite and help to finance
7 identification and safe replacement of asbestos cement water pipes, as well as any connected lead service lines; and 2. ensure reporting of the progress in completion of this work.
10. Where drinking water flows through asbestos cement pipes to points of use:
- establish downstream local water treatment if appropriate, and/or - support in-home treatment to remove ultrafine particulate matter.
11. Assemble and make accessible historical and present-day mapping of areas serviced by asbestos cement pipes, and downstream of asbestos cement pipes, to enable epidemiological research.
12. Support research, education and capacity to include asbestos in differential clinical diagnoses of cancers potentially associated with ingestion of asbestos.
International Commitment
13. Support the listing of Chrysotile Asbestos under the Rotterdam Convention for Prior Informed Consent.
Recommendations for New Financial Commitments
Many of our recommendations could be accommodated in Health Canada’s existing operations. Several will require new financial commitments which we request as inputs to Budget 2026.
New operating funds will be required for the following recommendations:
• Significant investment for planning and action on replacement of existing cement water pipes with public reporting on progress;
• Establishing Laboratory Accreditation and Facilities for analysis of asbestos in drinking water; • Establishing a periodic water testing survey for affected municipalities and develop a public facing portal for test results and other relevant information; • Testing drinking water for asbestos annually and following repair of asbestos cement water pipes, and report results to the public;
• Funds for downstream local water treatment if appropriate and/or in home treatment technology to remove ultrafine particulate matter; and,
• Funds for research, education and capacity to include asbestos in differential clinical diagnoses of cancers potentially associated with ingestion of asbestos. • Advancing Asbestos Eradication in Canada Research on best practices and support for continuing medical education and research to investigate roles of asbestos in increasing related disease, including cancers;
• Quantifying financial amounts is beyond the scope of this consultation response, but the submitting organizations will consider the necessary levels of funds in the coming months and strongly recommend a financial commitment in Budget 2026.
In the following sections, we offer expanded comments supporting the recommendations on concerns with impacts of asbestos on health of Canadians, the contributions of asbestos from current and presence of asbestos in cement water pipes in Canada, and the uncertainties and scientific limitations in studies focused on contribution of asbestos from oral ingestion to adverse effects. We also discuss replacement of asbestos-cement water infrastructure.
8 Introduction
Over the past century, asbestos has fallen from use as a “miracle mineral” that was fire-proof and insulating, and used widely in industries, buildings and products. Asbestos is a known human carcinogen,1that was largely prohibited in 2018 under the Canadian Environmental Protection Act, and subject to regulation restricting use, (e.g., asbestos may be permitted for the military, and nuclear power), and prescribing removal and disposal of hazardous materials.17 Canadian asbestos regulations and water quality guidance, however, are silent on water pipes.
Canada was “rich” with asbestos, and over time exported approximately 40 percent of the chrysotile asbestos used globally. The dark underbelly of sharp microscopic asbestos fibres was first identified in previous generations, with ailments in miners, factory employees, and tradesmen working with asbestos-containing materials. Workers’ lives were too-often too short, ending with the breathlessness of asbestosis stiffening lungs, and cancers such as lung cancer, mesothelioma, and stomach, gastrointestinal, rectal, liver, ovarian and bladder cancers. Workers were worst affected; but fibres clinging to clothes, or even brought home in bulk for insulation (compliments of generous employers, as in Peterborough ON), continue to impact families through generations. Homes and neighbourhoods can be impacted by dust, and there is dread of upcoming remediation of asbestos-contaminated sites.
Distinct from industrial sites, contaminated buildings and exposures to dust, asbestos also contaminates drinking water. Fibres originate in natural erosion of asbestos-rich rock, industrial runoff, asbestos-impacted aquifers, or water transported via asbestos-reinforced cement (asbestos-cement or “transite” pipes; approximately 20% asbestos when new) carrying drinking water to homes and businesses. Over time minerals in cement (calcite) dissolve and wash away, the internal pipe surface erodes, and asbestos is shed into drinking water. Asbestos fibres remain as the cement dissolves, and according to a WorkSafe BC fact sheet, “Aged, failing pipes, from which the binding materials have leached, can be up to 80 percent asbestos.”18,19
Asbestos is a potent multi-site carcinogen, and incidence of colorectal cancer is increasing rapidly in ever-younger Canadians.16 Although diet and diverse other exposures are reasonably expected to be contributing to this scourge, the increasing ingestion of asbestos in some households cannot be discounted. Informed citizens, clinical awareness and analytical capacity are essential to support epidemiological research and measures to protect public health.
It is essential to have means and capacity to measure and characterize waterborne asbestos, in order to manage it. Unfortunately, Canada has no standard or policy for asbestos in drinking water, nor even an accredited methodology to measure asbestos in water. With no domestic commercial laboratory capacity, Canadian laboratories send samples to the U.S.A. for analysis according to American methodology and standards.
20 The present draft guidance for waterborne asbestos marks the first Canadian federal invitation for public discussion of asbestos in drinking water, and asbestos cement pipes. Prevent Cancer Now and Waterborne asbestos assessment and response are impacted by scientific limitations as to what is “known” and “knowable,” lack of awareness, and common misconceptions:
• limitations of knowledge of exposure to waterborne asbestos, in turn, limit linking with cancers;
9 • hazard characterization to inform a precautionary public health approach to asbestos-containing waterworks, measures to minimize asbestos in Canadian drinking water, and research needs; • late-day national and international experiences with asbestos-cement pipes contaminating drinking water; and
• asbestos-cement pipes management and replacement, with secure waste disposal.
Drinking water contamination from asbestos-reinforced cement pipes Naturally occurring asbestos should be captured with appropriate filtration of communities’ source water, but asbestos-reinforced cement pipes (asbestos-cement pipes) shed asbestos into pre-treated drinking water enroute to homes and businesses. Unfortunately, citizens may be misinformed about potential asbestos contamination (Appendix 1).
Across Canada, asbestos cement pipes were installed from the 1930s to the 1990s. Many jurisdictions still rely on extensive asbestos-cement pipe networks to supply drinking water (see sample map examples in Appendix 2).
A National Research Council centre at the University of Regina studied the city’s extensive asbestos cement pipes network and published ten reports citing “health hazard” and “cancer”. 21 This failing
infrastructure contaminates drinking water and is over-due for replacement, to ensure reliable, safe, essential water supplies.
Pipe breaks often occur in regions with clay soil, which expands and contracts with moisture, or lack thereof, promoting pipe breakage. Extreme heat and deluges are worsening with climate change, risking increasing breaks. Secondly, calcite in the cement dissolves over time (particularly with soft water), the pipes weaken, increasing quantities of asbestos are shed into drinking water, and the pipe eventually breaks (too often “catastrophically”).
Canada’s asbestos cement pipes are reaching this stage, with increasing breakages causing water outages, floods, and expensive emergency repairs, and asbestos contamination of drinking water including asbestos-laden sludge.
Asbestos cement pipes deliver water to thousands of Canadian homes, schools and businesses.
Statistics Canada reported approximately 14,000 km of asbestos cement pipe, with more asbestos cement pipe in the west than the east, based on Statistics Canada Infrastructure Survey answers from 64% of jurisdictions for 2022.
2 This question was repeated for the year 2024, with results anticipated later in 2026.
Measuring asbestos in water
Focusing attention and credence, and following progress in asbestos eradication, requires Canadian laboratory accreditation, for detailed data characterizing asbestos contamination in water. Presently all samples are sent to U.S.A. laboratories.
Carcinogenicity of ingested asbestos
Asbestos is one of the most-studied toxicants, with extensive scientific literature spanning many decades. Inhaling, then swallowing fibres cleared from lungs, was described by the International
10 Agency for Research on Cancer in their conclusion that asbestos is a known human carcinogen.1 Abdominal cancers associated with airborne asbestos are presumed to arise from swallowing contaminated phlegm cleared from the respiratory tract, but contaminated drinking water is another potential exposure route. Water-borne asbestos can contaminate air when boiled, aerosolized in humidifiers or when showering, and shed from laundered linens and clothing, resulting in airborne exposures.
Asbestos fibres have been visualized in gastrointestinal and liver cancers (cholangiocarcinoma). 3,4,5,6
Moreover, visualized fibres in these tissues are often smaller than 10 µm, consistent with the shorter fibres seen in drinking water.7,8
Importantly, academic research methods and reporting styles have evolved over time, often resulting in discounting of older studies. Health Canada leans on a systematic review (Go, et al., 2025), that clearly illustrates carcinogenic potential of ingested asbestos.9 Selections from this work is included in the consultation document.
Comments on the consultation summaries of carcinogenicity research Human epidemiology is strong, that ingestion of asbestos causes cancers. The consultation document summarizes human epidemiological studies, published from 1974 to 2015, that reported that ingestion of asbestos was significantly associated with cancer incidence and/or mortality in 11 out of 14 studies.
A 2024 systematic review of asbestos ingestion and gastrointestinal cancers, with a somewhat different selection of included studies found a causal link between occupational asbestos exposure and the risk of oesophageal, stomach and colorectal cancers. 10 Animal studies are not reported as having as many significant findings, but the consultation document misrepresents the large Donham et al. study. This key, early study had two control groups—one fed cellulose to mimic the bulk of the asbestos loading, and one a simple control group, so there were twice as many “unexposed” animals. In fact, counter to the consultation report, the incidence of cancer in the asbestos-exposed animals was substantially higher. As well, ashed tumour samples identified fibres in the “control” group tumours, so it was not a clean comparison. This initial large experimental study details experimental challenges, and did find that waterborne asbestos caused cancers. Thus, at least twice as many animal studies support that ingested asbestos is a carcinogen.
Asbestos inhalation versus ingestion is a false dichotomy Asbestos is a known human carcinogen, and was one of the first substances examined by the nascent International Agency for Research on Cancer (IARC, 1977).1 The initial focus was on occupational airborne exposures in mining and manufacturing, with workers and families dying of lung cancers and mesothelioma. The draft guidance document details studies reporting asbestos fibres have been found in numerous tissues and in urine, in animal studies and in humans. Cancers that were elevated with asbestos exposures including:
buccal cavity, pharynx, esophagus, trachea, bronchus, lung, mesothelioma, stomach, liver, gallbladder, pancreas, intestines, rectum, peritoneum, genitalia, bladder, ovary, breast, and eye.
11 Are “smaller” asbestos fibres removed by phagocytes, so they do not pose cancer risks? This is briefly aired in the draft guidance, and has been proposed in the literature. In contrast, the draft guidance reports observations of asbestos fibres traversing membranes and entering lymph and blood circulatory systems, and appearing in urine. This is consistent with observations of fibres being widely dispersed in animal tissues (as discussed by Donham et al.), and the many cancer sites listed above.
When exposure is primarily airborne, how does asbestos cause cancers beyond the lungs? There is no “bright line” between exposure to asbestos in drinking water, versus airborne asbestos and handling of solid materials. Swallowing is not distinct from inhaling asbestos:
• Inhaled asbestos is cleared from the lungs via mucociliary action, then swallowed; • Waterborne asbestos fibres become airborne many ways, such as when water is boiled, sprayed in showers, dispersed via a humidifier; or later when fibres on surfaces, clothing or bedding are re-mobilized.
Beyond swallowing asbestos as it is cleared from the respiratory tract, other cancers associated with airborne asbestos fibres include mesothelial and more distant bladder and ovarian cancers. These reflect migration of fibres to underlying tissue, and to circulatory systems for blood and lymph. Early animal studies of asbestos reported fibres widely distributed throughout the body, and in urine as well as feces. Indeed, excreted asbestos represents a containment challenge in the laboratory. 23 Scope of the problem and elements of solutions
In 2026, deteriorating asbestos cement pipes deliver water to millions of Canadians, who are at risk of increasingly frequent pipe breaks, water outages and floods, and asbestos-contaminated domestic water. Despite absence of Canadian laboratory quantification, wherever this aging infrastructure is in use, residents of all ages, in entire households, are encountering increasing levels of asbestos in drinking water, showers, laundry and humidified air.
Surveillance strategies such as monitoring asbestos levels and condition assessment of pipes to inform infrastructure replacement schedules.
Surveillance must be based on knowledge of where pipes are located in individual jurisdictions, with mapping as in the Appendix.
Progress may be followed with successive Canada-wide via Statistics Canada infrastructure surveys.2 Healthy drinking water is a national priority, and expedited safe replacement of asbestos cement pipes fits the rubric of a “nation building project.” This is an opportunity for the country that led the world in use of asbestos, now to lead in cleanup with technology for efficient “trenchless” asbestos cement pipe removal, safe disposal and replacement.
Asbestos eradication. Canada has regulated asbestos in air, and existing asbestos in buildings and equipment have been identified, contained, and targeted for elimination. (Prohibition of Asbestos and Products Containing Asbestos Regulations, SOR/2018-196)
1. Asbestos removal and disposal are guided by detailed occupational health and safety (OHS) and hazardous waste disposal rules and practices at the provincial level. Protocols are required for
12 removal and disposal of asbestos cement pipes, such as detailed in resources from WorkSafe BC.19
Public awareness for personal protective actions. When public health officials, from local to national, tell the public not to worry or take protective action against a scientifically robust risk, then the public is in fact put at risk. They do not take even the simplest steps to protect the health of themselves and their family. Appendix 1 includes images of door hangers used in Regina, that misinform residents and dissuade them from reducing their exposure to asbestos fibres when asbestos-cement pipes are broken, repaired or replaced.
Setting a standard is central to consistent regulatory actions, but the present day U.S.A. 10 µm threshold excludes the majority of fibres, which are smaller. This standard was set at a time when technologies were not developed or readily available to count smaller fibres routinely; it was based on pragmatism to accommodate as well as possible the science and analytical capacity of the day.
According to sources referenced in the consultation, the U.S.A. >10 µm threshold can exclude 90% or more of asbestos in samples from aging asbestos-cement pipes(pp 13-14 in the consultation document). Canada’s standard must include particle sizes comparable to those regulated for air.
Disposal of Asbestos Cement Pipes creates toxic sites
There is broad consensus that pipes must not be left in the ground, as asbestos pipe residues create a toxic site that must be documented and protected, and is likely to be disturbed in the future.
It is overdue for asbestos shed from deteriorating water infrastructure to be treated as a preventable hazard.
Examples of international actions regarding asbestos cement pipes Internationally, many nations are expediting replacement of asbestos cement pipes because of concerns that waterborne asbestos is contributing to increasing cancer rates, as well as the disruption and costs of frequent pipe breakages. The following are a few examples. No such commitment has been made in Canada, yet.
Scottish Water recently announced a plan to spend 143-million pounds to replace 6,000 kilometres of old asbestos cement water pipe in 15 years.13
Malaysia is even more ambitious, planning to replace almost 40,000 kilometres of asbestos cement water pipe by 2040. (Recent media reports extend the replacement timeframe to 2050).14 In Tetu, Kenya, the state is to replace ageing water pipes over health concerns including high rates of cancer according to a September 24, 2025 Government Advertising Agency news release. 15
13 Conclusions
Canada supplied the world with 40% of its asbestos, but despite growing knowledge, Canada has been slow to regulate this hazardous material. Canada is over-due to issue and to act upon drinking water quality guidance, with the goal for particle loadings of all sizes to be As Low As Reasonably Achievable (ALARA). Canada has regulated asbestos in air, and existing materials in buildings and equipment are contained, labelled, and targeted for elimination.
Asbestos removal and disposal are guided by detailed occupational health and safety (OHS) and hazardous waste disposal rules and practices. Protocols are required for removal and disposal of asbestos cement pipes.
The Health Canada draft assessment has substantial methodological and scientific shortcomings, but the evidence is clear that asbestos causes cancer when it is ingested, as well as when it is inhaled.
The most recent, albeit incomplete, data indicates that approximately 14,000 km of deteriorating asbestos cement pipes deliver water to a substantial number of Canadian households and businesses.
These aging pipes are breaking increasingly frequently, causing water outages and floods. Regardless of absence of Canadian laboratory quantification, where this aging infrastructure is in use, increasing asbestos levels in drinking water, showers, laundry, humidified air, etc. are exposing all ages to hazardous fibres. (Quantities of particles aerosolized vary with humidifier design.) Asbestos is a potent carcinogen, and incidence of cancers—particularly colorectal cancer—are increasing rapidly in ever-younger Canadians and populations globally, with calls to identify early life exposure risk factors.
16,24 Although diet and other exposures are reasonably expected to be contributing to this scourge, the increasing ingestion of asbestos in many communities cannot be discounted. Knowledgeable citizens, clinical awareness and analytical capacity are essential to support informed care and epidemiological research. Informing citizens that asbestos residues pose no health concern, as done in Regina (Appendix 1), is counter to public health principles.
Across Canada, asbestos cement pipes were installed from the 1930s to the 1990s. Many jurisdictions still rely on extensive asbestos-cement pipe networks to supply drinking water (see sample maps in Appendix 2). Healthy drinking water is indeed a national priority, and expedited safe replacement of asbestos cement pipes fits the rubric of a “nation building project.” This is an opportunity for the country that led the world in use of asbestos, now to lead in cleanup with technology for efficient “trenchless” asbestos cement pipe removal, responsible asbestos disposal and pipe replacement.
There is broad consensus that pipes must not be left in the ground, as this creates a toxic contaminated site that is highly likely to be disturbed in the future.
Water contamination measurement, and standard to protect public health It is essential to establish a Canadian analytical method and laboratory capacity to test for asbestos in water. Canadian laboratories presently ship samples to the U.S.A.
There is no Canadian recommended limit for asbestos in drinking water. Thus, there is no routine water quality data on which to base decisions, let alone scientific research including epidemiology and biological identification (e.g., in tumor samples).
14 Coincidentally, gastrointestinal cancers (particularly colorectal cancers) are increasing rapidly in everyounger Canadians. 25 Increasing ingestion of asbestos as aging pipes degrade and contaminate drinking water, bears investigation as a potential contributor, and appropriate action for safe replacement of essential infrastructure.
Small fibres may contribute to development of these cancers. International knowledge, epidemiological and experimental (animal) research, and regulation of other particulate matter (PM) include particles much smaller than 10 µm. Suggestions that phagocytosis will clear fibres shorter than 10 µm, supporting this size cutoff, are not consistent with many reports of smaller fibres in tumours, including citations in the consultation document. Public health should be protected with a standard to regulate asbestos that is consistent with other particulate matter such as smoke and industrial emissions, both of which have effects on multiple organs due to particles as well as toxic chemicals.
The starting point is to address all asbestos particles 0.5 µm length and greater, as are measured by commercial laboratories in the U.S.A.
In summary, the proposed guidance document has many shortcomings, including errors of fact and interpretation. A precautionary, more fulsome synthesis and analysis would address remaining doubts that it can be hazardous to drink asbestos. Along with particular chemicals over generations, asbestos should be reasonably anticipated to be a contributor to the accelerating increases in cancers (particularly gastro-intestinal), in ever-younger Canadians and global citizens.
Reflection, in conclusion
In 1977, IARC classified asbestos as a Group 1 carcinogen. That same year, the Science Council of Canada produced a report entitled Regulatory Processes and Jurisdictional Issues in the Regulation of Hazardous Products in Canada. It states:
“Among the six cases discussed in this report and in the Science Council’s Policies and Poisons study, the asbestos case is perhaps most indicative of the inadequacies of the Canadian regulatory process, both at the regulation-making and the compliance levels.” Today, a half century later, asbestos-cement drinking water pipes remain in use. These should be replaced urgently as a national priority, with technology to remove the pipes and to ensure robust waste management.
15 Appendix 1: Doorhanger following repair of an asbestos-cement pipe in Regina Note reassurance that, “This disturbed sediment does not pose a health concern.”
16 Appendix 2: Sample waterworks maps with asbestos cement water pipes —Winnipeg and Regina
Winnipeg MB 26
April 2023
740 km of A-C pipe
population: 850,000
Asbestos-cement pipes in green
Click image for full size
Regina, SK 27
April 2023
500 km of AC pipe
population: 227,000
Asbestos-cement pipes in purple
Click image for full size—
17 REFERENCES
1. International Agency for Research on Cancer (IARC). Asbestos - IARC Monograph on the Evaluation of Carcinogenic Risk of Chemicals to Man [Internet]. Vol. 14. 1977 [cited 2026 Mar 10]. Available from:
https://publications.iarc.who.int/Book-And-Report-Series/Iarc-Monographs-On-The-IdentificationOf-Carcinogenic-Hazards-To-Humans/Asbestos-1977
2. Prevent Cancer Now. Where are Canada’s asbestos cement drinking water pipes? Check the data for where you live [Internet]. 2025 Sep 30 [cited 2026 Mar 11]. Available from:
https://preventcancernow.ca/where-are-canadas-asbestos-cement-drinking-water-pipes-check-thedata-for-where-you-live/
3. Brandi G, Tavolari S. Asbestos and Intrahepatic Cholangiocarcinoma. Cells. 2020 Feb 12;9(2):421. doi:10.3390/cells9020421 PubMed PMID: 32059499; PubMed Central PMCID: PMC7072580.
4. Grosso F, Croce A, Libener R, Mariani N, Pastormerlo M, Maconi A, et al. Asbestos fiber identification in liver from cholangiocarcinoma patients living in an asbestos polluted area: a preliminary study.
Tumori J. 2019 Oct 1;105(5):404–10. doi:10.1177/0300891619839305
5. Kogan FM, Vanchugova NN, Frasch VN. Possibility of inducing glandular stomach cancer in rats exposed to asbestos. Occup Environ Med. 1987 Oct 1;44(10):682–6. doi:10.1136/oem.44.10.682 PubMed PMID: 3676121.
6. Szendröi M, Németh L, Vajta G. Asbestos bodies in a bile duct cancer after occupational exposure.
Environ Res. 1983 Apr 1;30(2):270–80. doi:10.1016/0013-9351(83)90213-X
7. Toft P, Wigle D, Meranger JC, Mao Y. Asbestos and drinking water in Canada. Sci Total Environ. 1981 Apr 1;18:77–89. doi:10.1016/S0048-9697(81)80051-4
8. Millette JR, Clark PJ, Stober J, Rosenthal M. Asbestos in water supplies of the United States. Environ Health Perspect. 1983 Nov;53:45–8. doi:10.1289/ehp.835345
9. Go J, Farhat N, Leingartner K, Insel EI, Momoli F, Carrier R, et al. Review of epidemiological and toxicological studies on health effects from ingestion of asbestos in drinking water. Crit Rev Toxicol. 2024 Nov 25;54(10):856–94. doi:10.1080/10408444.2024.2399840 PubMed PMID: 39436319.
10. Koehoorn M, McLeod CB, Fan J, Arrandale VH, Davies HW, Dement JM, et al. Occupational asbestos exposure and gastrointestinal cancers: systematic review and meta-analyses. Occup Environ Med. 2024 Dec 1;81(12):639–46. doi:10.1136/oemed-2024-109707 PubMed PMID: 39929711.
11. Dodson RF, Atkinson MAL, Levin JL. Asbestos fiber length as related to potential pathogenicity: A critical review. Am J Ind Med. 2003;44(3):291–7. doi:10.1002/ajim.10263
12. EMSL | Asbestos in Water [Internet]. [cited 2025 Jun 11]. Available from:
https://www.emsl.com/Services.aspx?action=list&ServiceCategoryID=52
18 13. Hakimian R. Scottish Water details £13.4bn business plan including targeted investments in assets. New Civil Engineer [Internet]. 2026 Mar 3 [cited 2026 Mar 20]. Available from:
https://www.newcivilengineer.com/latest/scottish-water-details-13-4bn-business-plan-includingtargeted-investments-in-assets-03-03-2026/
14. Media Selangor. Fed govt sets 2040 deadline to replace all critical asbestos cement water pipes [Internet]. 2025 Dec 4 [cited 2026 Mar 20]. Available from: https://newswav.com/article/fed-govtsets-2040-deadline-to-replace-all-critical-asbestos-cement-water-p-A2512_nc2cvj
15. KNA. State to replace ageing water pipes in Tetu over health concerns. The Star, Kenya [Internet]. 2025 Sep 19 [cited 2026 Mar 20]. Available from: https://www.thestar.co.ke/counties/central/2025-09-19-state-to-replace-ageing-water-pipes-in-tetu-over-healthconcerns
16. Brenner DR, Heer E, Sutherland RL, Ruan Y, Tinmouth J, Heitman SJ, et al. National Trends in Colorectal Cancer Incidence Among Older and Younger Adults in Canada. JAMA Netw Open. 2019 Jul 31;2(7):e198090. doi:10.1001/jamanetworkopen.2019.8090 PubMed PMID: 31365108; PubMed Central PMCID: PMC6669779.
17. Government of Canada, Legislative Services Branch. Prohibition of Asbestos and Products Containing Asbestos Regulations [Internet]. 2018 Dec 30. Available from: https://lawslois.justice.gc.ca/eng/regulations/SOR-2018-196/FullText.html
18. WorkSafe BC. Asbestos-containing pipes in municipal underground works projects [Internet]. 2018. Available from: https://www.worksafebc.com/en/resources/health-safety/informationsheets/asbestos-containing-pipes-in-municipal-underground-works-projects?lang=en
19. WorkSafeBC. OHS Regulation Part 6: Substance Specific Requirements [Internet]. [cited 2026 Mar 15]. Available from: https://www.worksafebc.com/en/law-policy/occupational-healthsafety/searchable-ohs-regulation/ohs-regulation/part-06-substance-specificrequirements#SectionNumber:6.25
20. Asbestos in Water Testing Overview & FAQ - Laboratory Testing [Internet]. 2025 Nov 16 [cited 2026 Feb 21]. Available from: https://laboratorytesting.com/resources/asbestos/asbestos-in-watertesting-overview-faq/
21. Prevent Cancer Now. Canada’s asbestos cement water pipe research — a brief history [Internet]. 2023 [cited 2024 Mar 13]. Available from: https://preventcancernow.ca/asbestos-cement-waterpipe-research-in-canada/
22. https://UKWIR.org [Internet]. [cited 2026 Mar 12]. Asbestos Cement water mains deterioration and failure prediction models. Available from: https://UKWIR.org/water-industry-technicalreport?object=15332497-3056-4e13-b1c2-ce683c829042
19 23. Donham KJ, Berg JW, Will LA, Leininger JR. The effects of long-term ingestion of asbestos on the colon of F344 rats. Cancer. 1980;45(S5):1073–84. doi:10.1002/1097- 0142(19800315)45:5+<1073::AID-CNCR2820451308>3.0.CO;2-W
24. Murphy CC, Zaki TA. Changing epidemiology of colorectal cancer — birth cohort effects and emerging risk factors. Nat Rev Gastroenterol Hepatol. 2024 Jan;21(1):25–34. doi:10.1038/s41575- 023-00841-9
25. O’Sullivan DE, Hilsden RJ, Ruan Y, Forbes N, Heitman SJ, Brenner DR. The incidence of youngonset colorectal cancer in Canada continues to increase. Cancer Epidemiol. 2020 Dec 1;69:101828. doi:10.1016/j.canep.2020.101828
26. Winnipeg Water Main Material Map [Internet]. City of Winnipeg; 2023 [cited 2026 Mar 30].
Available from:
https://legacy.winnipeg.ca/waterandwaste/pdfs/water/WATER%20MAIN%20BY%20MATERIAL.pdf
27. City of Regina. Regina Water Main Pipes Material Categories [Internet]. 2023. Available from:
https://openregina.ca/dataset/30c8dcec-0f5f-4b80-bede-5fe276ac8fe5/resource/80cf0503-085b4cbc-9674-ddd98d3d81b9/download/map--water-main-pipes.pdf
PUBLIC HEALTH GOALS FOR
CHEMICALS IN DRINKING WATER
ASBESTOS
September 2003
Governor of the State of California
Gray Davis
Secretary for Environmental Protection
California Environmental Protection Agency
Winston H. Hickox
Director
Office of Environmental Health Hazard Assessment
Joan E. Denton, Ph.D.
Public Health Goal for
ASBESTOS
In Drinking Water
Prepared by
Office of Environmental Health Hazard Assessment
California Environmental Protection Agency
Pesticide and Environmental Toxicology Section
Anna M. Fan, Ph.D., Chief
Deputy Director for Scientific Affairs
George V. Alexeeff, Ph.D.
September 2003
LIST OF CONTRIBUTORS
PHG PROJECT
MANAGEMENT
Project Director
Anna Fan, Ph.D.
Public Workshop
Robert Howd, Ph.D.
Juliet Rafol
Coordination of
External Review
Yi Wang, Ph.D.
Moira Sullivan, M.S.
Revisions/Responses
Robert Howd, Ph.D.
REPORT PREPARATION
Authors
Moira Sullivan, M.S.
Yi Wang, Ph.D.
Richard Ames, Ph.D.
Primary Reviewer
Michael Lipsett, M.D.
Final Reviewers
Robert Howd, Ph.D.
Anna Fan, Ph.D.
George Alexeeff, Ph.D.
SUPPORT
Administrative Support
Edna Hernandez
Coordinator
Sharon Davis
Hermelinda Jimenez
Genevieve Vivar
Michelle St. Croix
Library Support
Charleen Kubota, M.L.S.
Web site Posting
Edna Hernandez
Laurie Monserrat
We thank the U.S. Environmental Protection Agency (Office of Water; National Center for Environmental Assessment) and the faculty members of the University of California with whom the Office of Environmental Health Hazard Assessment contracted through the University of California Office of the President for their peer reviews of the public health goal documents, and gratefully acknowledge the comments received from all interested parties.
ASBESTOS in Drinking Water
California Public Health Goal (PHG) ii September 2003
PREFACE
Drinking Water Public Health Goals
Pesticide and Environmental Toxicology Section
Office of Environmental Health Hazard Assessment
California Environmental Protection Agency
This Public Health Goal (PHG) technical support document provides information on health effects from contaminants in drinking water. PHGs are developed for chemical contaminants based on the best available toxicological data in the scientific literature.
These documents and the analyses contained in them provide estimates of the levels of contaminants in drinking water that would pose no significant health risk to individuals consuming the water on a daily basis over a lifetime.
The California Safe Drinking Water Act of 1996 (amended Health and Safety Code, Section 116365), amended 1999, requires the Office of Environmental Health Hazard Assessment (OEHHA) to perform risk assessments and publish PHGs for contaminants in drinking water based exclusively on public health considerations. Section 116365 specifies that the PHG is to be based exclusively on public health considerations without regard to cost impacts. The Act requires that PHGs be set in accordance with the following criteria:
1. PHGs for acutely toxic substances shall be set at levels at which no known or anticipated adverse effects on health will occur, with an adequate margin of safety.
2. PHGs for carcinogens or other substances that can cause chronic disease shall be based upon currently available data and shall be set at levels that OEHHA has determined do not pose any significant risk to health.
3. To the extent the information is available, OEHHA shall consider possible synergistic effects resulting from exposure to two or more contaminants.
4. OEHHA shall consider the existence of groups in the population that are more susceptible to adverse effects of the contaminants than a normal healthy adult.
5. OEHHA shall consider the contaminant exposure and body burden levels that alter physiological function or structure in a manner that may significantly increase the risk of illness.
6. In cases of insufficient data to determine a level of no anticipated risk, OEHHA shall set the PHG at a level that is protective of public health with an adequate margin of safety.
7. In cases where scientific evidence demonstrates that a safe dose-response threshold for a contaminant exists, then the PHG should be set at that threshold.
8. The PHG may be set at zero if necessary to satisfy the requirements listed above.
ASBESTOS in Drinking Water
California Public Health Goal (PHG) iii September 2003
9. OEHHA shall consider exposure to contaminants in media other than drinking water, including food and air and the resulting body burden.
10. PHGs published by OEHHA shall be reviewed every five years and revised as necessary based on the availability of new scientific data.
PHGs published by OEHHA are for use by the California Department of Health Services (DHS) in establishing primary drinking water standards (State Maximum Contaminant Levels, or MCLs). Whereas PHGs are to be based solely on scientific and public health considerations without regard to economic cost considerations, drinking water standards adopted by DHS are to consider economic factors and technical feasibility. Each standard adopted shall be set at a level that is as close as feasible to the corresponding PHG, placing emphasis on the protection of public health. PHGs established by OEHHA are not regulatory in nature and represent only non-mandatory goals. By federal law, MCLs established by DHS must be at least as stringent as the federal MCL if one exists.
PHG documents are used to provide technical assistance to DHS, and they are also informative reference materials for federal, state and local public health officials and the public. While the PHGs are calculated for single chemicals only, they may, if the information is available, address hazards associated with the interactions of contaminants in mixtures. Further, PHGs are derived for drinking water only and are not intended to be utilized as target levels for the contamination of other environmental media.
Additional information on PHGs can be obtained at the OEHHA Web site at www.oehha.ca.gov.
ASBESTOS in Drinking Water
California Public Health Goal (PHG) iv September 2003
TABLE OF CONTENTS
LIST OF CONTRIBUTORS....................................................................................II PREFACE................................................................................................................ III TABLE OF CONTENTS.......................................................................................... V PUBLIC HEALTH GOAL FOR ASBESTOS IN DRINKING WATER .............1 SUMMARY.................................................................................................................1 INTRODUCTION......................................................................................................2 CHEMICAL PROFILE.............................................................................................5 Chemical Identity and Properties .....................................................................5 Fiber Characterization................................................................................6 Production, Import and Export.........................................................................7 Production ..................................................................................................7 Import and Export ......................................................................................8 Uses and Disposal ............................................................................................9 Uses ............................................................................................................9 Disposal....................................................................................................10 ENVIRONMENTAL OCCURRENCE AND HUMAN EXPOSURE.................13 Air...................................................................................................................13 Soil .................................................................................................................14 Water ..............................................................................................................14 Food and Other Sources .................................................................................17 METABOLISM AND PHARMACOKINETICS..................................................17 Absorption......................................................................................................18 Study Limitations.....................................................................................19 Distribution.....................................................................................................19 Metabolism.....................................................................................................22 Excretion ........................................................................................................22 ASBESTOS in Drinking Water
California Public Health Goal (PHG) v September 2003
TOXICOLOGY........................................................................................................23 Toxicological Effects in Animals...................................................................23 Acute, Subacute, and Chronic Noncancer Effects ...................................23 Immunological and Lymphoreticular Effects ..........................................26 Neurological Effects.................................................................................28 Reproductive Effects................................................................................28 Developmental Effects .............................................................................28 Genotoxicity.............................................................................................28 Cancer.......................................................................................................34 Toxicological Effects in Humans: Oral Exposure..........................................40 Acute, Subacute, and Chronic Noncancer Effects ...................................40 Cancer.......................................................................................................40 Toxicological Effects in Humans: Inhalation and Other Exposures..............43 Acute, Subacute, and Chronic Noncancer Effects ...................................43 Immunological and Lymphoreticular Effects ..........................................44 Genotoxicity.............................................................................................45 Cancer.......................................................................................................46 DOSE-RESPONSE ASSESSMENT .......................................................................50 Noncarcinogenic Effects ................................................................................50 Carcinogenic Effects ......................................................................................51 CALCULATION OF PHG......................................................................................54 Noncarcinogenic Effects ................................................................................54 Carcinogenic Effects ......................................................................................55 Risk Estimate Based on Human Inhalation Data .....................................55 Risk Estimate Based on Animal Data ......................................................55 RISK CHARACTERIZATION..............................................................................57 REGULATORY STANDARDS..............................................................................58 Maximum Contaminant Level (MCL) and Drinking Water Standards .........58 Other Regulatory Standards ...........................................................................59 REFERENCES.........................................................................................................61 ASBESTOS in Drinking Water
California Public Health Goal (PHG) vi September 2003
PUBLIC HEALTH GOAL FOR ASBESTOS IN DRINKING
WATER
SUMMARY
A public health goal (PHG) of 7 million fibers per liter (MFL) or 7×106 fibers/L, for asbestos fibers exceeding 10 µm in length, has been developed for asbestos in drinking water. The derivation of this PHG follows the approach of the United States Environmental Protection Agency (U.S. EPA), which was based on tumorigenic effects observed in experimental animals. An increased incidence of benign adenomatous polyps of the large intestine was observed in male Fischer 344/N rats exposed to chrysotile asbestos fibers, 65 percent of which were greater than 10 micrometer (µm) in length, in a lifetime diet study performed by the National Toxicology Program (NTP, 1985). An elevated risk for adenomatous polyps and colorectal cancer has also been observed in human subjects with a history of exposure to asbestos (Neugut et al., 1991).
This is further supported by epidemiological data on risk of gastrointestinal tumors after inhalation exposures, as evaluated by the National Academy of Sciences (NAS, 1983).
The potential for tumorigenic effects is also supported by findings of genotoxicity in bacterial and mammalian systems both in vitro and in vivo (IARC, 1996; NTP, 2000).
The voluminous body of evidence that exposure to asbestos through inhalation increases the risk of lung cancer and mesothelioma in humans and animals (ATSDR, 1995; Cantor, 1997; IARC, 1996; IPCS, 1998; Kang et al., 1997; U.S. EPA, 2000) substantiates the overall assessment of human carcinogenicity of asbestos. Asbestos exposure has also been linked with increased risks of stomach cancer, colorectal cancer and renal cell carcinoma (RCC) in humans. The Office of Environmental Health Hazard Assessment (OEHHA) concurs with the U.S. EPA and the NAS that all the data mentioned above contribute to the overall weight of evidence for asbestos carcinogenicity.
For the calculation of the PHG, oral cancer potency estimates developed by the U.S. EPA (1985b) were used. It is plausible that the true value of the human oral cancer potency for asbestos in drinking water has a lower bound of zero based on statistical and biological uncertainties. Part of this uncertainty is due to limited suggestive evidence to support a genotoxic mechanism. However, due to the absence of specific scientific information explaining why the animal tumors are irrelevant to humans at environmental exposure levels, a standard health-protective approach was taken to estimate cancer risk.
The cancer potency estimate derived from the cancer slope factor (CSF) of the male rat intestinal polyps was 1.4×10-13 (fibers/L)-1. The PHG was calculated assuming a de minimis theoretical excess individual cancer risk level of 10-6 (one in a million) from exposure to asbestos. Based on these considerations, a PHG for asbestos in drinking water of 7 MFL (for asbestos fibers exceeding 10 µm in length) is established, which is the same value as the Maximum Contaminant Level (MCL) established by the U.S. EPA (1991a). This PHG is considered to provide an adequate margin of safety for all the noncarcinogenic effects of asbestos, including potential genotoxicity and adverse effects on the gastrointestinal system, immune system, kidney, and body weight.
ASBESTOS in Drinking Water
California Public Health Goal (PHG) 1 September 2003
Based on a subchronic study in rats reported by Cemerikic (1977), a LOAEL of 107 mg/kg-day (1x1012 fibers/kg-day) for nephrotoxicity was selected for assessment of noncarcinogenic effects of asbestos in drinking water. A relative source contribution of 20 percent, a combined uncertainty factor of 3,000 (10 for estimation of a NOAEL from a LOAEL, 10 to account for the uncertainty in inter-species extrapolation, and 10 for human variability), an uncertainty factor of 3 to account for subchronic to chronic study duration extrapolation, and an adult daily water consumption rate of 2 L/day were used.
The calculated public health protective concentration for asbestos in drinking water based on noncarcinogenic effects is 2.4x109 fibers/L, or 2350 MFL.
INTRODUCTION
This document examines available data and evidence on the toxicity of asbestos for establishing a public health goal (PHG) for asbestos in drinking water. The U.S. EPA, in its drinking water criteria documents (U.S. EPA, 1985a; 1985c) and an evaluation of the available literature for the 1993 updates of the Integrated Risk Information System (IRIS) database (U.S. EPA, 2000), concluded that inhalation of asbestos increases the risk of lung cancer and mesothelioma in humans and animals. Human data on asbestos ingestion exposure was considered to be suggestive of carcinogenicity. Data from the National Toxicology Program (NTP) animal studies on ingestion exposure provided “some evidence” of carcinogenicity for intermediate-range [65 percent greater than 10 micrometers (µm) and less than 14 percent greater than 100 µm] chrysotile fibers, but not for short-range (98 percent smaller than 10 µm) chrysotile fibers (NTP, 1985; 1990a).
The National Academy of Sciences (NAS, 1983) and the Agency for Toxic Substances and Disease Registry (ATSDR, 1995) also made similar conclusions based on tumorigenic effects observed in experimental animals in the NTP studies (1985).
Asbestos is a generic term used to describe a group of six different types of naturally occurring hydrated silicate minerals that crystallize in fibrous habit: amosite, chrysotile, crocidolite, and the fibrous varieties of tremolite, actinolite, and anthophyllite. The three most common types are chrysotile, amosite, and crocidolite. Asbestos is composed of silicon, oxygen, hydrogen, and various positively charged metal ions. The basic unit of asbestos minerals is the silicate group (SiO4). The U.S. EPA (1985c) and other regulatory agencies have considered that fibers with an aspect ratio (ratio of length to width) greater than three to one should be regulated, although this definition has been criticized (Skinner et al., 1988). Asbestos fibers are resistant to heat and most chemicals.
These properties make asbestos useful for insulation, friction products, and a variety of other products. Asbestos may have been so widely used because few other available substances combine the same qualities. However, asbestos mining and use has been greatly decreased in the U.S. due to the potential health hazards of this mineral.
Contamination of municipal drinking water occurs in three ways: through industrial contamination of source water, natural contamination of source water, and the use of asbestos-cement distribution pipes. Industrial contamination occurred in Duluth, Minnesota when taconite mine tailings were dumped into the source water, exposing a ASBESTOS in Drinking Water
California Public Health Goal (PHG) 2 September 2003
city of 100,000 population for over 25 years. Natural contamination occurs in the San Francisco Bay area and in parts of Washington State where source waters flow through serpentine rock formations. Asbestos-cement distribution pipe contamination has been studied in Florida and New York.
Inhalation of asbestos fibers has been clearly associated with lung cancer and mesothelioma. This finding led to the U.S. EPA’s intention to ban new uses of asbestos in the U.S. by 1997; however, a federal court overturned the regulation (U.S. EPA, 1989) in October 1991. It is still legal to manufacture, process, and import most asbestos products. Fibers are defined as having an aspect ratio of three to one or greater (U.S. EPA, 1985c). Longer fibers are considered to have greater toxicity (Winner and Cossette, 1979). The U.S. EPA (2000) lists asbestos as a Group A human carcinogen through the inhalation exposure route on its IRIS database. The International Agency for Research on Cancer (IARC) of the World Health Organization (WHO) lists asbestos as a Group 1 human carcinogen through inhalation (IARC, 1973, 1977, 1987).
Recent comprehensive reviews have described in detail the histopathological and clinical features of asbestos related diseases (Kamp and Weitzman, 1999). Asbestos is an established genotoxic and carcinogenic agent that can induce DNA damage, gene mutation, gene transcription, and protein expression in modulating cell proliferation, apoptosis, inflammation, and cell death (IARC, 1996; McDonald, 1998). Evidence implicating various pathways of asbestos-induced diseases includes: 1) the chemical and structural properties of the fibers, 2) the lung fiber burden, 3) fiber uptake by pulmonary epithelial cells, 4) iron-catalyzed free radicals, 5) DNA damage, 6) alterations in cytokines, growth factors, and other inflammatory cell products, and 7) interactions with cigarette smoke and other carcinogens in the environment (Kamp and Weitzman, 1999).
The toxicity of ingested asbestos fibers is less certain. Many animal studies have been inconclusive or negative for ingested asbestos. The NTP (1985) animal studies showed increased benign adenomatous polyps of the large intestine after oral exposure to intermediate-range chrysotile fibers, 65 percent of which were greater than 10 µm in length. A parallel NTP (1985; 1990a) study of short-range fibers, 98 percent of which were shorter than 10 µm in length, did not produce a response in male or female rats.
The results for intermediate-range fibers were not statistically significant compared with the concurrent controls. However, the incidence of the neoplasms was highly significant when compared with the incidence of combined benign and malignant epithelial neoplasms of the large intestine of the pooled control groups of all the NTP oral asbestos lifetime studies. The NTP has interpreted the animal studies as providing "some evidence" of carcinogenicity for intermediate-range fibers.
Human studies of ingested asbestos have yielded conflicting results. Some ecological mortality follow-up studies have yielded evidence of carcinogenicity at intermediate stages in the follow-up; none, however, have shown statistically significant evidence of carcinogenicity at the conclusion of the follow-up period. Reviews evaluating the human ingestion epidemiology studies have concluded that it would be impossible for any of the ecological studies to have sufficient power or control over extraneous factors to establish convincing evidence of carcinogenic effect from asbestos consumption through water supply contamination. Therefore, the human evidence of toxicity from ingested asbestos ASBESTOS in Drinking Water
California Public Health Goal (PHG) 3 September 2003
does not appear to be useful in establishing drinking water standards or public healthprotective concentrations of asbestos fibers in drinking water.
Given a lack of usable human data on the risk of asbestos ingestion, risk evaluators have turned to two other sources of information: human occupational inhalation studies focusing on gastrointestinal tract cancer, and animal studies of ingested asbestos. Each approach requires extrapolation, either across exposure modality or across species. The use of the occupational inhalation studies assumes that a certain percentage of inhaled particles are cleared from the lungs and swallowed and that gastrointestinal tract cancer is the appropriate endpoint.
The NAS (1977, 1983) evaluated five occupational inhalation studies under the assumption that 30 percent of inhaled particles are cleared and swallowed. Further adjustments were made to transform occupational workday exposures to the exposures anticipated from consumption of contaminated drinking water. Based upon the inhalation studies and the assumptions made to allow transformation to approximate ingestion exposures, the NAS established a 10-6 risk level as 0.01 MFL or 1×104 fibers/L for excess cancer risk. However, the NAS (1984) concluded “the association of asbestos with an increased risk of malignancies other than lung cancer and mesothelioma has not been confirmed in animal studies and has not been observed consistently in human studies.” The U.S. EPA (1991a) Science Advisory Board stated that “given the positive signal seen in some epidemiologic studies, plus well-documented evidence for the association between asbestos fiber inhalation and lung cancer, it is hard for the Committee to feel comfortable in dismissing the possibility of an increased risk of gastrointestinal cancer in humans exposed to asbestos fibers from drinking water.” The U.S. EPA (1991a) has treated asbestos as a Category II contaminant and established a primary drinking water standard Maximum Contaminant Level (MCL) of 7 MFL for asbestos fibers exceeding 10 µm, as identified by X-ray diffraction and quantified by transmission electron microscopy (TEM) (U.S. EPA, 1985b). The non-enforceable MCL Goal (MCLG) based mainly on evaluation of health effects is also set at 7 MFL by the U.S. EPA (1991a). The ATSDR (1995) used animal toxicology data to establish a 10-6 risk level as 7.1 MFL for excess cancer risk.
OEHHA was unable to establish an audit trail on the figures used by NAS (1977, 1983, 1984) in their calculation of 0.01 MFL as the 10-6 excess cancer risk level, and considers the quantitative evaluation of cancer risk from the human data used by NAS to be problematic. OEHHA supports the U.S. EPA’s approach as more appropriate for deriving a PHG for ingested asbestos in municipal drinking water. The U.S. EPA (1991a) and approximately nine states have set either 7 or 7.1 MFL as a drinking water standard (ATSDR, 1995). According to statute (HSC 116365), OEHHA “may review, and adopt by reference, any information prepared by, or on behalf of, the United States Environmental Protection Agency for the purpose of adopting a national primary drinking water standard or maximum contaminant level goal when it establishes a California maximum contaminant level or publishes a public health goal.” In this document, we evaluate the available data on asbestos toxicity, with a primary focus on the oral exposure literature that is deemed most appropriate to establish a PHG for drinking water. The studies that can be used to identify public health-protective ASBESTOS in Drinking Water
California Public Health Goal (PHG) 4 September 2003
levels are reviewed and evaluated; many studies on other aspects of asbestos toxicity not directly applicable are not cited. Portions of this document are abstracted from “Toxicological Profile for Asbestos Update” (ATSDR, 1995) as well as “Drinking Water and Health, Volume 5” (NAS, 1983).
CHEMICAL PROFILE
Asbestos is the general name applied to a group of six different fibrous minerals that occur naturally in the environment, including the three most common types: chrysotile, amosite, and crocidolite; and the fibrous varieties of tremolite, actinolite, and anthophyllite. Nonasbestos, nonfibrous forms of tremolite, actinolite, and anthophyllite with similar physical and chemical properties as asbestos are also found naturally.
Asbestos can be found naturally in both soil and rocks in some areas. The most common asbestos mineral type is white chrysotile; other types include blue crocidolite, gray anthophyllite, and brown amosite. Other natural mineral fibers that may be considered potentially hazardous because of their physical and chemical properties similar to asbestos are erionite, wollastonite, attapulgite and sepiolite.
The asbestos minerals are made up of fibers that vary in length and may be straight or curled. Asbestos fibers do not have any detectable odor or taste. Asbestos fibers are resistant to heat and most chemicals. The major properties of concern for commercial uses are length, granular content, degree of openness or effective surface area, surface charge, drainage or filtration rate, color, absorption, electrical resistivity, bulk density, and tensile strength. Because of these properties, asbestos fibers have been mined for use in a wide variety of man-made products, mostly in building materials, friction products such as brake shoes, and heat-resistant fabrics. Asbestos content of products is not necessarily an indication of its relative health risk, for in many products fibers are tightly bound to the matrix or encapsulated. Potential health risks arise when asbestos fibers are set free, for example during drilling or sawing of asbestos cement sheets (HSDB, 2000), or when asbestos-reinforced concrete pipe releases fibers into the water.
Chemical Identity and Properties
Asbestos is a generic term for a class of six naturally-occurring hydrated fibrous minerals with a basic unit of the silicate SiO4 group. This group can form a variety of polymeric structures through formation of Si-O-Si bonds. Asbestos fibers are generally white, gray, green, or brown fibers. They have exceptional tensile strength, and are moldable with varying textures and degrees of flexibility (ATSDR, 1995). Table 1 lists common synonyms and other pertinent identification information for generic asbestos and the six individual asbestos minerals (ATSDR, 1995).
Asbestos is divided into two groups, namely, serpentine and amphibole. Serpentine asbestos is the mineral chrysotile, also called white asbestos. Serpentine is the most common form of asbestos. Chrysotile is a magnesium silicate with strong, flexible fibers.
It is possible to spin the longer serpentine fibers. For the serpentine class, the polymeric form is an extended sheet. This extended sheet tends to wrap around itself, forming a ASBESTOS in Drinking Water
California Public Health Goal (PHG) 5 September 2003
tubular fiber structure. These serpentine fibers are usually curved in contrast to the straight morphology of the amphiboles.
Amphibole asbestos includes various silicates of magnesium, iron, calcium, and sodium.
Subdivisions of amphibole asbestos include five species identified as actinolite, amosite, anthophyllite, crocidolite, and tremolite. Crocidolite is also called blue asbestos, while amosite is also called brown asbestos. For the amphibole class of asbestos, the polymeric structure consists of a linear double chain. These chains crystallize into long, thin, straight fibers, which are the characteristic structure of this type of asbestos.
Table 2 summarizes the physical and chemical properties of the six asbestos minerals (ATSDR, 1995). Asbestos fibers are basically inert chemically, or nearly so. They are noncombustible and conduct heat poorly. They are odorless, and do not evaporate, dissolve, burn, rot, or undergo significant reactions with most chemicals. It is these properties that have made asbestos so useful, with modern industrial use dating from about 1880 when the Quebec chrysotile fields began to be exploited (IARC, 1977).
Asbestos fibers are resistant to acids, bases, and high temperature; only chrysotile is not stable in acids and hydroxides (HSDB, 2000). In tissues, chrysotile fibers are more soluble than amphiboles, which tend to remain intact (ATSDR, 1995). However, case studies of chrysotile asbestos and related lung cancer cases show fibers 40 years after exposure. Asbestos is nonbiodegradable and environmentally cumulative (HSDB, 2000).
Asbestiform refers to a group of natural fibrous minerals comprised of fibrous clays and other fibrous silicates. Fibrous clays include attapulgite and sepiolite. Attapulgite is also named palygorskite. Other fibrous silicates include wollastonite, nemalite, talc, and zeolites. Nemalite is also named fibrous brucite. Zeolites can be divided into erionite and mordenite. These materials have characteristics and biological activities similar to asbestos (Bignon, 1989).
Fiber Characterization
Fiber characteristics make for differences in toxicity and potency. In general, fibers that are long and thin appear to be more carcinogenic than fibers that are short and thick (Stanton et al., 1977). The full characterization of asbestos fiber in a test sample is an essential step in the understanding of the mechanisms of fiber carcinogenesis. The consensus report (IARC, 1996) prepared by the group of invited experts convened at IARC in 1996 provided an in-depth review of the parameters necessary for fiber characterization and the methodology needed to obtain these data.
The only analytical method approved by the U.S. EPA (1991a) to comply with the federal drinking water monitoring requirements beginning December 31, 1995, is the use of transmission electron microscopy (TEM) for quantification, together with X-ray diffraction for identification. The accuracy of this method is sensitive to the quality of the water sample and to the presence of interfering substances. U.S. EPA (1985b, 1991a) has determined that TEM is the best available technique because of its ability to differentiate chrysotile from amphibole asbestos fibers, its effectiveness in distinguishing between asbestos and nonasbestos fibers, and its ability to determine the number of fibers per volume and quantitate both length and width of the fibers. U.S. EPA (1991a) established the MCLG for asbestos based on assessments using data from TEM analyses.
ASBESTOS in Drinking Water
California Public Health Goal (PHG) 6 September 2003
The physico-chemical and structural properties of fibers, such as surface charge, solubility, surface chemistry, surface area, dimensions, aspect ratio, size distribution, exposed surface, chemical composition, etc., are generally considered to be the primary determinants of their biological effects (Bonneau et al., 1986; Fubini, 1996).
Measurements of dimensions are best accomplished by TEM. The carcinogenic potential of a fiber is associated with the length and aspect ratio of the fiber (U.S. EPA, 1985c).
Crystallinity and the type of exposed crystal faces determine reactivity and solubility, and consequently, biopersistence. Micromorphology such as surface irregularities, indenting, steps, kinks, and edges also affect reactivity, durability, and solubility (Kane, 1996).
The chemical composition of a fiber determines its adsorption of exogenous or endogenous materials, its potential for free-radical generation at the solid-liquid interface, its potential for the mobilization of metal ions by endogenous chelators, and its propensity for selective leaching. The free radicals may cause reactive oxygen/nitrogen species formation, DNA damage and lipid peroxidation (Kane, 1996). Asbestos can stimulate cells to generate reactive oxygen species via reactions mediated by iron present on the surface of asbestos. This transition metal catalyzes the reduction of hydrogen peroxide to generate hydroxyl radical, and the hydroxyl radical can damage various cellular components, causing DNA strand breaks, protein modification, and lipid peroxidation (Fubini and Mollo, 1995). Asbestos can trigger a number of molecular and cellular events via reactions mediated by reactive oxygen species, including proinflammatory cytokine expression, enhanced toxicity, development of asbestosis, and carcinogenesis (Ding et al., 1999; Jaurand, 1997).
Production, Import and Export
Because asbestos fibers may produce adverse health effects in exposed persons, the U.S.
EPA (1989) published a final rule of commerce prohibitions in manufacture, importation, processing, and distribution in 1989 (40 CFR Part 763, Subpart I). The rule would have banned by 1997 about 94 percent of the new uses of asbestos in the U.S. based on 1985 estimates. Uses established before July 12, 1989 would still be allowable. However, in 1991, the U.S. Court of Appeals, Fifth Circuit, vacated and remanded the majority of the rule. Currently, the manufacture, importation, processing and distribution of most asbestos-containing products is still legal. Proper destruction and disposal of these asbestos-containing products are required under regulations.
Production
The asbestos mineral is mined or quarried with its parent rock. Historical records show that asbestos has been known for more than 2,000 years. Chrysotile, amosite, and crocidolite are the asbestos species of major commercial significance (HSDB, 2000).
Chrysotile is the predominant form of asbestos in international commerce and accounts for 99 percent of current world production of 2 million tonnes (Landrigan et al., 1999).
The production volume of asbestos in the U.S. has decreased substantially from peak production of over 299 million pounds (about 136,000 metric tons) estimated in the late 1960s and early 1970s (SRI, 1982), to 112 million pounds (about 51,000 metric tons) ASBESTOS in Drinking Water
California Public Health Goal (PHG) 7 September 2003
estimated in 1987, 37 million pounds (about 17,000 metric tons) estimated in 1989, to a low of 15,000 metric tons estimated in 1993 (HSDB, 2000; U.S. Bureau of Mines, 1994).
In the U.S., asbestos was commercially mined and milled in California, Arizona, North Carolina, and Vermont, but many of these companies suspended asbestos mining operations in the 1970s (HSDB, 2000). Over 30 million tons of asbestos have been mined, processed, and applied in the U.S. since the early 1900s (Kamp and Weitzman, 1999). In 1985, three U.S. companies produced asbestos fibers including Calaveras Asbestos, Ltd., Calaveras County, California; KCAC, Inc., San Benito County, California; and Vermont Asbestos Group, Orleans County, Vermont. By 1991, only two firms produced asbestos, one each in California and Vermont (U.S. Bureau of Mines, 1994).
In the U.S., asbestos was primarily mined in open pits. Ore is blasted or drilled from the pit, crushed, dried, and stored until milling. The milling process removes asbestos fibers from the ore by a series of crushing, fiberizing, screening, aspirating, and grading operations. More recently, an alternative method of mining was developed in order to reduce air emissions of fibers. This method uses bulldozers and scrapers (rather than blasting) to remove the ore from the pit. The ore is watered down to prevent air dispersion of the fibers, and is crushed, sized, and screened in a wet condition. After being dewatered, the fibers are pelletized, dried, and prepared for shipment either as pellets or further processed to yield open fibers (U.S. EPA, 1988).
Sales of chrysotile asbestos have significantly decreased in Northern America and Western Europe because of widespread recognition of its health hazards. However, asbestos sales remain strong in Japan and across Asia as well as in developing countries worldwide (Landrigan et al., 1999).
Import and Export
Most asbestos used in the U.S. is imported. Imports from 1950 to 1974 varied from about 1,287 million pounds to 1,580 million pounds (about 585,000 to 718,000 metric tons) per year. During the late 1970s, imports began decreasing, with a sharp drop after 1980. By 1984, imports were down to 462 million pounds estimated (about 210,000 metric tons), to 81 million pounds (about 35,000 metric tons) estimated by 1991, and to 33,000 metric tons estimated in 1993. Most asbestos, about 98 percent, imported to this country came from Canada, but about one percent was imported from South Africa (ATSDR, 1995).
Exports of asbestos were small until the mid-1960s, when a significant increase in exports occurred. In recent years, export volumes have generally decreased from 132 million pounds (about 60,000 metric tons) estimated in 1987 to 48 million pounds (about 22,000 metric tons) estimated in 1991 (SRI, 1982; U.S. Bureau of Mines, 1992; 1994). Exports then increased to an estimated 32,000 metric tons in 1993, mainly as asbestos-containing finished products.
ASBESTOS in Drinking Water
California Public Health Goal (PHG) 8 September 2003
Uses and Disposal
Uses
It is estimated that asbestos, almost exclusively chrysotile, has been used in over 3,000 different products in the U.S. as well as worldwide. Chrysotile accounts for over 95 percent of world asbestos consumption (Kamp and Weitzman, 1999). The largest use is in asbestos cement for products such as pipes, ducts, and flat and corrugated sheets.
Asbestos is widely used in manufactured goods in construction, mostly roofing shingles, ceiling, and floor tiles, and asbestos cement sheets are used in a wide variety of construction applications. Other main uses have been in paper products, friction products, fire-resistant textiles, packings and gaskets, coatings, and asbestos-reinforced plastics. There have also been numerous other miscellaneous uses. Pipe products are used in water supply, sewage disposal, and irrigation systems (HSDB, 2000).
The U.S. used approximately six percent of the world production of asbestos in 1982.
Reported consumption of asbestos in the U.S. was 790 million pounds (about 359,000 metric tons) in 1980, 497 million pounds (about 226,000 metric tons) in 1984, 185 million pounds (about 84,000 metric tons) in 1987, 81 million pounds (about 35,000 metric tons) in 1991, and 33,000 metric tons in 1994 (SRI, 1982; U.S. Bureau of Mines, 1992, 1994). In 1993, 30 percent of the total apparent asbestos consumption was used for friction products such as automobile clutch, brake, and transmission components, with five percent used for asbestos-cement pipe, 50 percent for roofing products, 10 percent for packing and gaskets, and five percent for other uses (U.S. Bureau of Mines, 1994). Approximately 99 percent of asbestos used in the U.S. in 1993 was chrysotile (ATSDR, 1995; U.S. Bureau of Mines, 1994). In Europe, asbestos consumption in 1994 ranged between 0.004 kg per capita in Northern Europe and 2.4 kg in the former Soviet Union (Albin et al., 1999).
The Consumer Product Safety Commission (CPSC) banned general use garments containing asbestos in 1978. However, the use of asbestos in special garments such as fire fighting suits is permitted if they are constructed so that asbestos fibers will not become airborne under normal conditions of use (HSDB, 2000). At present, only asbestos-containing products that were not being manufactured, imported, or processed on July 12, 1989 are subject to the prohibition requirements of the U.S. EPA (1992a) regulation.
The largest use of asbestos is in asbestos cement for products such as pipes, ducts, and flat and corrugated sheets. Pipe products are used in water supply, sewage disposal, and irrigation systems. Asbestos cement sheets are used in a wide variety of construction applications. Other uses of asbestos include fire resistant textiles, friction materials such as brake linings, underlayment and roofing papers, and floor tiles (HSDB, 2000).
Substitutes for asbestos are constantly being developed (U.S. EPA, 1989). Nonasbestos friction materials are currently being used in disk brake pads, and substitutes are being developed for drum brake linings. Primary substitutes include semi-metallic materials for disc brakes and nonasbestos organics (e.g., fiberglass, para-aramid, mineral fibers, steel ASBESTOS in Drinking Water
California Public Health Goal (PHG) 9 September 2003
wool and fibers, and resins) for brake drums. Since it is not possible to use asbestos safely, safer substitutes should be considered for all uses (Landrigan et al., 1999).
Disposal
Currently, asbestos-containing wastes may only be deposited in landfills that are approved and regulated by the federal government. Regulations include wetting or using dust suppression agents, covering with at least 15 centimeters (about six inches) of nonasbestos-containing material, and deterring public access with a fence or natural barrier (U.S. EPA, 1990). These regulations are intended to ensure that asbestos at these sites is not dispersed into the environment. No data were located on amounts of asbestos in such sites.
ASBESTOS in Drinking Water
California Public Health Goal (PHG) 10 September 2003
Table 1. Chemical Identity of Asbestos
Characteristic Asbestos Chrysotile Actinolite Amosite Anthophyllite Crocidolite Tremolite Synonyms No data Serpentine asbestos,
white asbestos
No data Mysorite, brown
asbestos, fibrous cummingtonite/ grunerite
Ferroanthophylliteaz bolen asbestos
Blue asbestos Silicic acid,
calcium magnesium salt (8:4)
Trade name No data Avibest; Cassiar AK,
Calidria RG 144, Calidria RG 600
No data No data No data No data No data
Chemical formula No data Mg3Si O2 5(OH)4
n
5 Fe)
]2
,
H)
g
(O
(M
22 2 a
O
[C
8 Si
[(Mg,Fe)7Si8
O22(OH)2]n
[(Mg,Fe)7Si8
O22(OH)2]n
[NaFe3 2+Fe2 3+
Si O8 22(OH)2]n
[Ca Mg 2 5Si O8 22
(OH)2]n
Chemical structure N/A Extended sheet Double chain Double chain Double chain Double chain Double chain Identification numbers: CAS registry 1332-21-4 12001-29-5 13768-00-8 12172-73-5 17068-78-9 12001-28-4 14567-73-8 NIOSH RTECS CI6475000 GC2625000 AUO550000 BT6825000 CA8400000 GP8225000 XX2095000
DOT/UN/NA/
IMCO shipping
IMCO 9.0 UN2212
IMCO 9.3 UN2590
No data No data
UN2212
No data No data
UN2212
No data
HSDB 511 2966 No data 2957 No data No data 4212
NCI CO8991 C61223a No data No data No data CO9007 CO8991 Abstracted from ATSDR (1995), Table 3-1; sources: HSDB (2000); IARC (1977); U.S. EPA (1985b). CAS = Chemical Abstract Service; DOT/UN/NA/IMCO = Department of Transportation/United Nations/North America/International Maritime Dangerous Goods Code; HSDB = Hazardous Substances Data Bank; NCI = National Cancer Institute; NIOSH = National Institute for Occupational Safety and Health; RTECS = Registry of Toxic Effects of Chemical Substances. ASBESTOS in Drinking Water California Public Health Goal (PHG) 11 September 2003
Table 2. Physical and Chemical Properties of Asbestos Materials Property Chrysotile Actinolite Amosite Anthophyllite Crocidolite TremoliteMolecular weighta Not applicable licable Not app applicable Not Not applicable licable Not app applicable Not Color
h
gray,
ellowis
White,
yn,gree
No data Brown, gray,
greenish
Gray, white, brown-gray, green
Lavender, blue,
green
White to light green
Physical state Solid Solid Solid Solid Solid Solid
Melting point/decomposition temperature 800-850οC No data Cο 90000-6 Cο 509 800οC C ο 0041, yitvgraSpecific 552. dataNo 433. 1.3-852. 373. dataNo
Solubility:
r eWat
Organic solvents
sd Aci b
b Bases
ble luoInsble luoIns
0 .056
03 1.
ble luoInsble luoIns
No data No data
ble luoInsble luoIns
0 .012
82 6.
ble luoInsble luoIns
13 2.77 1.
ble luoInsble luoIns
14 3.20 1.
ble luoInsble luoIns
No data No data
Isoelectric point 11.8 No data 5.2-6.0 No data No data No data Electrical charge at neutral pH Positive data No Negative Negative Negative dataNo Length distribution in UICC reference samples m µ1 % >
m µ5 % >
m µ 10 % >
44 -36
6 3-
1-3
No data No data No data
46 6 1
46 5 1
36 3
7 0.
No data No data No data
sty timilabilimmFla Nonflammable able Nonflamm ablelamm Nonf able Nonflamm ablenflamm No able Nonflamm Abstracted from ATSDR (1995), Table 3-2; sources: HSDB (2000); IARC (1977); NAS (1977); SRI (1982); U.S. EPA (1980, 1985b). nite polymers. s of asbestos are indefi a All form
ains intact. ure rem ter-ions; silicate struct oun c f s oso l toe duthgiew in ss lotnecrePb ASBESTOS in Drinking Water California Public Health Goal (PHG) 12 September 2003
ENVIRONMENTAL OCCURRENCE AND HUMAN EXPOSURE
Asbestos is widely distributed in the earth’s crust. Chrysotile, which accounts for more than 95 percent of the world asbestos trade, is exploited in more than 40 countries, mostly in Brazil, Canada, China, Kazakhstan, the Russian Federation, South Africa, and Zimbabwe. Asbestos deposits are located in many parts of California and are commonly associated with serpentine rock, although other types of asbestos are also found in California. Serpentine rock, which often contains chrysotile asbestos, is abundant in the Sierra foothills, the Klamath Mountains, and the Coast Ranges, and is the California state rock. Asbestos is ubiquitous in the environment because of its extensive industrial use and the dissemination of fibers from natural sources.
Asbestos minerals occur naturally as fiber bundles that may be several centimeters long.
However, when manipulated, they break down into smaller fibers that may have dimensions in the submicron range. It is these small fibers that can pose health risks.
Occupational exposure appears to be the major cause for diseases in humans related to asbestos exposure. Population surveys indicate that male workers in construction or in shipyards have had the highest potential for asbestos exposure (Albin et al., 1999).
People have also been exposed to asbestos by living with asbestos workers or living in the vicinity of asbestos mines and factories. Indoor air in buildings with asbestoscontaining materials can be a major source for nonoccupational asbestos exposure (HEI, 1991).
Asbestos fibers are not able to move through soil and are not broken down to other compounds in the environment. Therefore, they can remain in the environment for decades or longer (ATSDR, 1995). Asbestos fibers may bioaccumulate in animals and humans. The general population may be exposed to asbestos fibers in outdoor and indoor air, beverages, drinking water, food, pharmaceutical and dental preparations, and by consumer use of asbestos-containing products (IARC, 1977).
Air
Although asbestos is not volatile, small fibers and clumps of fibers may be released to air as a dust-like suspension. Chrysotile appears to be the predominant fiber found in the outdoor air. IPCS (1986; 1998) reported asbestos concentrations of fibers longer than 5 µm measured at various locations in Austria, Canada, Germany, South Africa, and the U.S. ranging from less than 1×10-4 to about 1×10-2 fibers/mL, mainly analyzed by TEM.
Analyzed by light microscopy (LM) and expressed as phase-contrast optical microscopy (PCOM) equivalent fibers longer than five µm, asbestos concentrations in outdoor air are generally less than 5×10-4 fibers/mL in remote areas in the U.S., and up to 2×10-3 fibers/mL in urban areas (IPCS, 1998). Measurements reported by the California Air Resources Board (1986) ranged from 8 to 500 fibers/m3
, with the higher concentrations
associated with proximity to production and use facilities.
U.S. EPA (1991b) requires the establishment of an administrative record of asbestos in buildings, especially in school buildings where children may be exposed to airborne asbestos through indoor air inhalation. IARC (1976) summarized indoor air measured in ASBESTOS in Drinking Water
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1972 in U.S. school buildings with sprayed-on asbestos, showing as high as
3.8 fibers/mL. Indoor air concentrations measured in various buildings in the U.S., Canada, and Germany ranged from below the detection limit of the analytical method to 1×10-2 fibers/mL (IPCS, 1986; 1998).
One source of asbestos in the environment is the erosion of natural deposits of asbestosbearing rocks. Asbestos can also be released into the environment by human activities.
It is estimated that emissions from asbestos processing, including milling, manufacturing, and fabrication are about 2,240 pounds per year (U.S. EPA, 1992b). This estimate assumes full compliance with the current National Emission Standards for Hazardous Air Pollutants (NESHAP) (U.S. EPA, 1986, 1990) applicable to asbestos. Occupational exposures to asbestos in air were reported as high as 3×109 fibers/m3 in 1949 and reduced
to 2×108
fibers/m3 (200 fibers/mL) in 1965 (IPCS, 1998). The current OSHA permissible exposure limit is 0.1 fibers/mL (1 x 105 fibers/m3).
An estimated total of 11,264 pounds (about 5.1 metric tons) of asbestos, amounting to about 4.5 percent of the total environmental release, was discharged to the air from manufacturing and processing facilities in the U.S. in 1992 (TRI92, 1994). The TRI data should be used with caution since only certain types of facilities are required to report.
This is not an exhaustive list.
Other sources of asbestos release include releases from clutches and brakes on cars and trucks, as well as releases of asbestos from insulation or other building materials.
Estimated asbestos emissions from waste disposal from all sources were about 499,000 pounds (about 227 metric tons) per year (U.S. EPA, 1990). If all sources were in full compliance with the NESHAP for asbestos, waste disposal emissions would be reduced to 1,320 pounds (about 600 kilograms) per year (U.S. EPA, 1990a).
Soil
Soil may be contaminated with asbestos by the weathering of natural asbestos deposits, or by land-based disposal of waste asbestos materials. While disposal of waste asbestos to landfills was a common practice in the past, current regulations restrict this practice.
An estimated total of 235,900 pounds (about 107 metric tons) of asbestos, amounting to about 95.3 percent of the total environmental release, was discharged to land from manufacturing and processing facilities in the U.S. in 1992 (TRI92, 1994). The Toxics Release Inventory (TRI) data collected by the U.S. EPA should be used with caution since only certain types of facilities are required to report. This is not an exhaustive list.
Water
Asbestos is released to water from a number of sources, including erosion of asbestosbearing rocks and surficial materials in the watershed, erosion of natural deposits, corrosion from asbestos-cement pipes, and disintegration of asbestos roofing materials with subsequent transport via rainwater into cisterns, and the like. Wastewater from asbestos mining activities and asbestos-related industries as well as atmospheric input also carry significant burdens of asbestos fibers in water (U.S. EPA, 1976). In the U.S., ASBESTOS in Drinking Water
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asbestos in drinking water has been shown as primarily chrysotile (Millette et al., 1981; IPCS, 1998; Speil, 1974). In areas such as San Francisco, Sherbrooke, and Seattle, chrysotile in water supplies has been attributed to erosion from natural asbestos rocks and ores (Millette, 1983). The fibers may remain in suspension in the water for long periods of time. In addition, suspended chrysotile fibers may adsorb organic materials, which eventually cover the entire fiber surface and consequently affect the biological activities of the fiber (Bales and Morgan, 1985; IARC, 1996; IPCS, 1998).
The total amount of asbestos released to water has been estimated to be 1.1×105 to
2.2×105
pounds (about 50 to 100 metric tons) per year (NAS, 1984). Chrysotile concentrations in lakes and streams have been variable, depending on proximity to source areas and river flow pattern (IPCS, 1998; Schreier, 1989). Concentrations of 1×106 to
1×108
fibers/L are typical in most rivers draining serpentinic rock formations, with seasonal fluctuations. Concentrations up to 1×1013 fibers/L have been reported in a stream draining asbestos-bearing bedrock (IPCS, 1998; Schreier, 1987; 1989). Bishop et al. (1985) identified asbestos and glass fibers ranging from about 5 µm in diameter to 50 µm in length in Los Angeles municipal sewage sludges at 106 to 108 fibers per gram sludge dry weight.
An estimated total of 250 pounds (about 0.11 metric tons) of asbestos, amounting to less than one percent of the total environmental release, was discharged to surface water from manufacturing and processing facilities in the U.S. in 1992 (TRI92, 1994; not an exhaustive list).
Cunningham and Pontefract (1971) reported asbestos in drinking water in Quebec and Ontario in Canada (ranging from 2×106
to 1.73×108 fibers/L) with the highest levels in
unfiltered tap water near a mining area. Asbestos concentrations in drinking water in Austria were higher in an area with natural deposits at the source of the water supply (1.9×105
fibers/L) compared to a median of 3.2×104 fibers/L from 10 areas with asbestos deposits, or 14 areas with use of asbestos cement pipes, or six control areas. However, a sample of surface water from a cistern showed considerable asbestos contamination and raised concern about the use of water for room air humidification (Neuberger et al., 1996). Similar concern was discussed in the U.S. (Webber et al., 1988).
Average asbestos concentrations from 0.3 to 1.5 µg/L were measured in eastern U.S. river water samples and chrysotile levels up to 12 µg/L were found in the Jumata and Connecticut rivers (IARC, 1977; Nicholson, 1974; Nicholson and Pundsack, 1973).
Cook et al. (1974, 1976) reported average asbestos concentrations of about 1.7×106 fibers/L in the Great Lakes and Saint Lawrence River bywaters with higher counts along the north shore of Lake Superior between Silver Bay and Duluth, along the Saint Clair River in the U.S., and downstream from Montreal and in the asbestos mining district in Quebec (IARC, 1977). This led to national surveys of asbestos in drinking water in the late 1970s in the U.S., Canada, the United Kingdom, Germany, and other countries that resulted in findings of 105
to 106 fibers/L in water supplies. Approximately 10 percent of water supplies in the U.S. and five percent in Canada contained 108 to 109 fibers/L due to
naturally occurring asbestos-rich bedrock or asbestos mining activities (IARC, 1977; Millette, 1983; Schreier 1989).
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In the U.S., northern California, where asbestos-bearing rocks are abundant, is known for high asbestos levels in water supplies. Because California is a water deficient state and water distribution systems for drinking water and irrigation are extensive and interconnected, this has the potential to compound the degree of asbestos contamination.
Once asbestos-rich sediment gets into the system, the fibers are distributed over large areas, thus affecting drinking water quality for a large segment of the population (Hayward, 1984; Jones and McGuire, 1987; Tarter et al., 1983). Other areas in the U.S. with high asbestos concentrations in drinking water are the Puget Sound area of Washington, part of the Appalachian Mountains in New York, New Jersey, and Maryland, the Duluth area in Minnesota, and sections of New Mexico (Schreier, 1989).
Groundwater in the Rio Grande Valley in New Mexico was also found to contain asbestos (Oliver and Murr, 1977).
In 1973, amphibole asbestos fibers were discovered in the municipal water supply of Duluth, Minnesota ranging from 107 to 109 fibers/L (Cook et al., 1974). The entire city population of 100,000 was exposed from the late 1950s through 1976 at levels of 1×106 to 6.5×107
fibers/L of water (Sigurdson, 1983; Sigurdson et al., 1981).
Drinking water concentrations of asbestos are usually less than 1×106 fibers/L for fibers
of all sizes, although significantly higher values up to 1×109 fibers/L have been found in
circumstances where water systems have been in contact with asbestiform minerals or where contamination of the water supply exists (Cotruvo, 1983). The fiber mass concentrations corresponding to these fiber concentrations are usually less than
0.01 µg/L. Thus direct water ingestion usually leads to exposure of less than 0.02 µg/day (U.S. EPA, 1980). Estimated annual doses of ingested asbestos for drinking water in the United States range from 9x105 to 4x1011 fibers, as shown in Table 3.
Reported data suggest that fibers of all lengths at 1×106 fibers/L correspond to anywhere
from 2×10-4 to 2×10-3 µg/L, with up to 2×108
fibers/L in water systems (IPCS, 1986,
1998; U.S. EPA, 1980). Data on asbestos concentrations from erosion of fibers from asbestos cement cooling tower panels indicate that the mass of 1×106 fibers is from 0.01
to 0.2 µg (U.S. EPA, 1980). From 1984 to 2000, asbestos was detected in 80 out of 1933 samples from public drinking water systems in California. The detection limit for purposes of reporting (DLR) was 0.2×106
fibers/L or 0.2 MFL as reported by DHS at
http://www.dhs.cahwnet.gov/ps/ddwem/chemicals/phgs/mclcomparison.htm (accessed January 21, 2001).
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Table 3. Estimated Ingested Dose from Drinking Water in U.S.* Reference Concentration in
water
Yearly ingested dose
(EM fibers ) §
Office of Toxic Substances estimate of
asbestos-contaminated water
(Bishopville, SC)
547 x 106 fibers/L 3.99 x 1011
Natural contamination; geological
source (San Francisco, CA)
130 x106 fibers/L 9.49 x 1010
Groundwater (ambient) 3.2 x 105 fibers/L 2.34 x 108
Office of Water Regulations and
Standards, Survey of Drinking Water
1 x105 to 100 x106
fibers/L
7.3 x 107
to 7.3x1010
American Water Works estimates
(municipal water systems):
•Memphis District System
•Providence District System
•Saginaw Source
1.7 µg/L
0.27 µg/L
0.0032 µg/L
4.69 x 108
7.45 x 107
8.83 x 105
*Adapted from Rowe (1983).
§
Yearly dose estimates: OTS, OWRS: conc. in water x 2 L/day x 365 days/yr; AWWA: conc. in water x 2 L/day x EM fibers/µg x 365 days/year.
Food and Other Sources
In the past, filters made from asbestos, and talc containing asbestos as an impurity were employed in the preparation of wines, beers, coated rice, processed sugar, vegetable oil, lard, and other items consumed by humans (IARC, 1977). Asbestos concentrations in British, Canadian and American beer ranged from 1 to 10×106 fibers/L and in various
sherries, ports, vermouths, and soft drinks ranged from 1.7 to 12.2×106 fibers/L (Biles
and Emerson, 1968; Cunningham and Pontefract, 1971, 1974; IARC, 1977). Chrysotile fibrils at 13 to 24×106
fibers/L were found in spirit filtered with asbestos filters (IARC, 1977; Wehman and Plantholt, 1974). Wines have been shown to contain as much as 64×106
fibers/L (U.S. EPA, 1985c). Analysis of 47 brands of sake purchased in Japan during 1983-1985 showed asbestos concentrations from less than the detection limit of
7.8×103
fibers/L to 196×106 fibers/L (Ogino et al., 1988).
The use of asbestos filters in food or pharmaceutical preparations has been discontinued in the U.S. since 1976, and intake of asbestos through foods or drugs is now unlikely.
However, asbestos has been found in art supplies such as crayons, probably as a contaminant of the talc used to strengthen the crayons.
METABOLISM AND PHARMACOKINETICS
Asbestos fibers may enter the body after inhalation or oral exposures. It is unlikely that any appreciable uptake of asbestos fibers will occur after dermal exposure. The ASBESTOS in Drinking Water
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deposition and fate of fibers in the lungs is largely dependent upon their size and shape.
Fibers deposited in the lungs may be removed from the lungs by mucociliary clearance or by macrophages, or they may be retained in the lung. It has been estimated that 25 to 75 percent of inhaled fibers are cleared from the respiratory tract by the mucociliary escalator, and subsequently swallowed (Lee, 1974).
Longer fibers that are retained in the lung may undergo a number of processes including translocation, dissolution, fragmentation, splitting or protein encapsulation. Long fibers that become encapsulated in protein form what is often referred to as an “asbestos body;” the term “ferruginous body” is used when the nature of the core fiber is not known.
These bodies are golden brown in appearance, owing to the presence of iron. The protein coat is rich in ferritin, an iron storage protein, possibly arising from macrophages and giant cells. The formation of asbestos bodies may represent an attempt of macrophages to digest long fibers extracellularly (Koerten et al., 1990a,b). Ferruginous coatings form on a population of asbestos fibers that are greater than eight µm. Ferruginous bodies, when seen in lung tissue sections in combination with fibrosis, are important in establishing the diagnosis of asbestosis (Dodson et al., 1999).
An intraperitoneal injection in mice of 200 µg UICC crocidolite fibers, about 91 percent of which were shorter than two µm, resulted in clearance by the lymphatic system, producing minimal inflammation and mesothelial cell proliferation. However, for fibers about 60 percent longer than two µm, the injection resulted in accumulation of inflammatory cells, mesothelial cell injury, and proliferation due to fiber persistence up to six months after the treatment, with limited lymphatic clearance (Moalli et al., 1987).
Absorption
There is considerable controversy as to whether ingested asbestos fibers can penetrate and pass through the walls of the gastrointestinal tract in sufficient numbers to cause adverse effects (Cook, 1983; Hilding et al., 1981; Meek, 1983; Volkheimer, 1973, 1974).
While the data are inconclusive, a number of toxicokinetic studies have shown that asbestos fibers do penetrate the gastrointestinal mucosa, and collect in other tissues (Amacher et al., 1974; Carter and Taylor, 1980; Cook and Olson, 1979; Craun and Millette, 1977; Epstein and Varnes, 1976; Lee, 1974; Pontefract and Cunningham, 1973; Storeygard and Brown, 1977; Wells, 1975; Westlake et al., 1965; Westlake, 1974).
Electron micrographic studies indicate that some fibers penetrate into the gastrointestinal epithelium (Storeygard and Brown, 1977; Westlake et al., 1965). In addition, some fibers pass through the gastrointestinal wall and reach the blood, lymph, urine, and other tissues (Carter and Taylor, 1980; Cunningham and Pontefract, 1973; Cunningham et al., 1977; Hallenbeck and Patel-Mandlik, 1979; Kaczenski and Hallenbeck, 1984; Ogino et al., 1987; Patel-Mandlik and Millette, 1980, 1983; Pontefract and Cunningham, 1973; Sebastien et al., 1980; Weinzweig and Richards, 1983). The mechanism by which asbestos fibers pass through the gastrointestinal wall is not known with certainty, but it has been noted that a wide variety of µm-sized particles, e.g., starch granules, cellulose particles, or pollen, can cross the gut by passing between (not through) the cells of the epithelial layer in a process termed persorption. It seems likely that this may account for ASBESTOS in Drinking Water
California Public Health Goal (PHG) 18 September 2003
uptake of asbestos fibers as well (Volkheimer, 1973, 1974). Several researchers have found that the average length of fibers in extra-gastrointestinal tissues or fluids is shorter than the average length of the fibers ingested (Cunningham et al., 1977; Patel-Mandlik and Millette, 1983; Weinzweig and Richards, 1983), suggesting that short fibers pass through the gastrointestinal epithelium more easily than long fibers.
Although several researchers have found no clear evidence of transmigration (Davis et al., 1974; Holt, 1974; Pooley, 1974), the weight of evidence supports the conclusion that some asbestos fibers do cross the gastrointestinal tract barrier. Data are insufficient to precisely estimate the fraction of ingested fibers which pass through the gastrointestinal wall, but Sebastien et al. (1980) estimated that a maximum of 10-4 to 10-7 times the number of chrysotile or crocidolite fibers introduced to the stomach appeared in the lymph fluid of rats. Cook and Olson (1979), analyzing human urine, detected from 10-3 to 10-5 of the concentration present in the subject’s drinking water. Neither the lymph fluid nor the urine can account for all fibers that may migrate across the gastrointestinal tract mucosa.
Study Limitations
Many of the studies on gastrointestinal penetration by ingested asbestos fibers provide incomplete information for defining analytical sensitivity, fiber recovery, sample contamination, latency period determination, etc. The absence of clear definitions of detection limits and/or positive tissue control samples make the reports of no fiber presence in some studies difficult to evaluate. For example, in the Gross et al. (1974) rat study, although clearly most of the ingested asbestos fibers were not absorbed across the gastrointestinal tract, the detection limit information was incomplete, there were no positive controls, and the negative control samples were contaminated. Many of the gut penetration studies entail exposures to chrysotile asbestos, the most common contaminant of water, food and beverages. However, chrysotile asbestos fiber concentrations are the most difficult to estimate because, in addition to having extremely thin diameters that make them difficult to identify, these fibers are readily reduced to individual fibrils.
Distribution
Asbestos is reported to be disseminated in the body of experimental animals following its initial primary site of absorption or deposition (Pontefract and Cunningham, 1973; Westlake et al., 1965; Volkheimer, 1973, 1974). Asbestos fibers have been detected in blood (Weinzweig and Richards, 1983), lymph (Sebastien et al., 1980), human fetuses, and fetuses (Haque et al., 2001) of rats exposed to oral doses of asbestos, suggesting that fibers penetrating the gut might be carried to tissues throughout the body. In support of this, asbestos fibers have been detected in lung, kidney, liver, brain, heart, and spleen of rats exposed to asbestos in the diet (Cunningham et al., 1977; Pontefract and Cunningham, 1973). Highest levels of fibers were found in the omentum, which is a fold of the peritoneum interconnecting the abdominal viscera, supporting the idea that the fibers were emanating from the gastrointestinal tract. Although the diet fed to the animals was prepared using corn oil to minimize asbestos fiber inhalation, the possibility that some fiber inhalation took place cannot be eliminated (Cunningham et al., 1977).
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Suzuki and Kohyama (1991) reported that inhaled asbestos can be translocated into extrapulmonary tissues. Masse et al. (1980) provided clear evidence of penetration of the gut in animals. Sebastien et al. (1980) recovered chrysotile and crocidolite fibers in the lymphatic and blood circulatory systems of rats following both a single dose ingestion and chronic ingestion. Kaczenski and Hallenbeck (1984), in a study on baboons, demonstrated clear evidence of hematogenous migration of chrysotile asbestos after gavage feeding. Webster (1973, 1974) reported finding iron-containing macrophages in the duodenal and ileal mucosa of baboons fed asbestos for up to five years.
Kobayashi et al. (1987) reported on the asbestos distribution/burdens in extrathoracic organs of human subjects exposed to chrysotile. Twenty-six male autopsy subjects were subdivided into three groups according to the degree of asbestos bodies (ABs) in the lung. Group I had from 100-1000 ABs/g of wet lung, Group II had ABs ranging from 10 to 99, and group III had no detectable ABs in the lung. The incidence and the number of ABs in extrapulmonary organs usually increased as the pulmonary exposure level rose.
The esophagus was one of the preferential sites of exposure. In Group I, ABs were found in the esophagus, spleen, pancreas, bone marrow, and thyroid gland; one or more ABs were identified in at least 54 percent of the examined organs. In group II, 24 percent of the organs had one or more ABs. No extrapulmonary ABs were found in Group III subjects. The authors reported that the Group I subjects had no direct occupational exposure to asbestos. Fiber count, identification of fiber types, and the determination of fiber size could not be undertaken because of the limitations of light microscopic analysis.
Huang et al. (1988), using transmission electron microscopy, reported finding asbestos fibers in human pulmonary and extrapulmonary tissues of three autopsy cases with known asbestos burdens (one had suffered from asbestosis). In addition to lung tissue, asbestos fibers were found in tissues from the liver, spleen, pancreas, kidney and gastrointestinal tract. Of the extrapulmonary organs examined, kidney tissue displayed a markedly higher asbestos level than any other organs. The number of asbestos fibers in extrapulmonary tissues tended to increase with the pulmonary asbestos level. Just as was found in lung tissue, a large range of fiber length was also observed in extrapulmonary tissues. Moreover, the geometric mean length of fibers in lung and other organs was not significantly different. The authors suggest that this may indicate that asbestos fiber migration within the body may be accomplished with little size restriction.
A few human studies also suggest asbestos uptake from the gastrointestinal tract and its circulation and migration to other organs. Langer (1974) reported concentrations of asbestos bodies and uncoated fibers, in the order from high to low, in lungs, kidneys, pancreas, and liver, for asbestos workmen. Carter and Taylor (1980) detected amphibole asbestos in the lung, liver, and jejunum of autopsied residents of Duluth, Minnesota, with long-term high-level oral exposure to amphibole asbestos through a contaminated water supply. Sixty percent of the 19 persons studied had levels of amphibole fibers greater than 2×105
fibers/g in the lung, liver and intestinal wall. Total counts of these amphibole fibers in the drinking water ranged from approximately 2×106 to 2×108 fibers/L with an
average of 2×107
fibers/L.
Several authors have described the presence of asbestos fibers and asbestos bodies in tumor tissue (Ehrlich et al., 1985; Henderson et al., 1975). Henderson et al. (1975) found ASBESTOS in Drinking Water
California Public Health Goal (PHG) 20 September 2003
amphibole and chrysotile asbestos fibers in stomach tumors and adjacent gastric mucosa in Japanese men with oral exposure to chrysotile. Not all of the tumor tissue examined contained asbestos fibers. The occupational history of the patients was not known. Other silicates besides asbestos were also found in some of the tissues. In at least one case, asbestos bodies were found in a carcinoma of the colon in an insulation worker with asbestosis (Ehrlich et al., 1985).
A group of investigators reported finding many asbestos fibers in electron microscopic analyses of placenta and body tissues taken from some stillborn infants, but very few in placental digests from liveborn infants (Haque et al., 1992, 1996, 1998). Haque et al. (1998) summarized the results from the study of 82 stillborn and 45 liveborn infants.
Twenty-three percent of the placentas of stillborn infants contained asbestos fibers, with mean numbers of about 53,000 fibers per gram in the positive tissues. Fifteen percent of placentas from liveborn infants contained asbestos fibers, but at much lower levels. The mean level was reported as 19 fibers/g, although this contradicts the reported sensitivity level, where one fiber is equivalent to 11,000 fibers/g. The discrepancy may be due to subtraction of reagent blank readings, which would correspond to a fraction of a fiber per gram. Asbestos fibers were also detected in other tissues of the stillborn infants. The mean fiber counts were highest in the liver (59,000/g), followed by lung (39,000/g) and skeletal muscle (32,000/g). Actual numbers of asbestos fibers counted, based on the indicated conversion factor, ranged from zero to 33 per gram of processed tissue. Fiber sizes in the stillborn infants ranged from 0.5 to 16.8 µm in length and 0.03 to 0.8 µm in width, with a mean length of 1.55 µm and a mean width of 0.098 µm. Eighty-eight percent of the fibers were chrysotile. In the liveborn infants, the fibers tended to be longer and thicker. However, differences in processing and examination between the groups make this finding uninterpretable. A highly significant association was noted between fiber presence and previous abortions (p<0.007), and a smaller but still significant association with placental disease (p<0.04). The authors postulate that disease processes resulting in a stillbirth might result in increased transfer of maternal fibers to the placenta and infant. They also suggest that rapidly dividing fetal cells may be especially susceptible to the carcinogenic and mutagenic effect of asbestos.
Several studies have demonstrated transplacental transfer of asbestos in animal models.
After asbestos fibers were injected intravenously, transplacental transfer of asbestos was shown in rats (Cunningham and Pontefract, 1974). Haque and Vrazel (1998) demonstrated transfer of asbestos fibers to the fetus and placenta within one hour following a single intravenous injection via the tail vein in pregnant mice. The asbestos suspensions contained approximately 345,000 fibers/mL. Histologic examination of sections from fetuses and placentas showed focal areas of coagulative necrosis with mild neutrophil infiltration in some placentas. Electron microscopy of the placental tissue taken from the areas of necrosis showed the presence of very small (100 to 700 nm) asbestos fibers within the cytoplasm and nuclei of placental cells. Asbestos fibers were found in fetal lungs and liver following the injection of one to three mg (one mg/mL water) of chrysotile asbestos fibers into the femoral vein of pregnant Wistar rats at twoday intervals from days 10-14 of gestation (Cunningham and Pontefract, 1974). Total dose varied from four to 12 mg (4×105
to 12×105 fibers) of asbestos. The highest number
of fibers found in fetal liver (27×106 fibers/g) and lungs (140×106 fibers/g) came from a
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California Public Health Goal (PHG) 21 September 2003
dam administered four 3-mg injections (total dose = 12 mg or 12×105 fibers). In a recent
work, Haque et al. (2001) demonstrated the transfer of asbestos fibers to the fetus following gavage feeding of pregnant mice with chrysotile asbestos. Groups of mice (6/group) were given two doses of either 50 µg chrysotile suspension in 0.2 ml sterile normal saline (treated) or 0.2 ml saline (control), and were allowed to mate two days later. After pregnancy was confirmed, the treated and control groups received two additional doses of chrysotile asbestos or saline on gestational days 7 and 12. Both groups were allowed to deliver naturally and the pups were sacrificed at 8, 11, 19 or 20 days after birth. The lungs and liver of two pups from each dam were processed for fiber counts using electron microscopy. All pups of the treated group had chrysotile fibers, while none were present in pups from controls. The mean fiber count of the lungs and liver of the treated pups was 780 and 214 fibers/g, respectively. Mean lengths of the fibers in the lung and liver were 18.5 and 18.3 µm, respectively. There was no significant difference in weight gain between the two groups. The postnatal fetal mortality, 8.2 percent for the treated and 4.5 percent for the control group, was not statistically significant.
Metabolism
No studies were located regarding any changes in asbestos fibers in the gastrointestinal tract per se. However, chrysotile fibers incubated in simulated gastric juice underwent leaching of magnesium ion from the silica framework, with a resultant change in net fiber charge from positive to negative (Sheshan, 1983), and chrysotile fibers with altered appearance and X-ray diffraction patterns were detected in the urine of animals (Hallenbeck and Patel-Mandlik, 1979; Patel-Mandlik and Millette, 1983). These observations, although limited, suggest that chrysotile fibers undergo some metal ion exchange and alterations in gross structure in biological fluids after oral exposure.
Asbestos bodies have been detected in tissues such as the colon (Ehrlich et al., 1992), suggesting that encapsulation of asbestos fibers may occur in extrapulmonary tissues as well.
Excretion
It has been demonstrated that ingested fibers are eliminated through the urine and feces.
Several authors have reported on the excretion of asbestos fibers in urine (Boatman et al., 1983; Cook and Olson, 1979; Hallenbeck and Patel-Mandlik, 1979). Cook and Olson (1979) detected amphibole fibers in the urine of persons with varying exposure to unfiltered drinking water drawn from Lake Superior. In some cases, the urine samples contained more than 10 times the number of fibers corresponding to the detection limits (10 to 40 amphibole fibers/mL urine). A single day’s ingestion of water was observed to result in a urine amphibole load of 10-3 to 10-5 of the number of fibers ingested, with fibers detectable in urine at least 10 days after ingestion. The authors felt this ratio to be remarkably large. Urinary asbestos levels of workers occupationally exposed (inhalation and ingestion) to chrysotile asbestos in a factory producing roof coatings were significantly greater than the concentrations found in a control group (both on a number and mass basis) (Finn and Hallenbeck, 1985), even though airborne asbestos ASBESTOS in Drinking Water
California Public Health Goal (PHG) 22 September 2003
concentrations were always below the OSHA eight-hour-time-weighted average (2 fibers/cc by PM). Detection of asbestos in the control group indicates that asbestos may appear in the urine of individuals in the general population. Hallenbeck and PatelMandlik (1979) reported that chrysotile fibers administered orally to baboons may be recovered in urine. Gross et al. (1974), in a study on rats, reported that nearly all ingested asbestos fibers are excreted in the feces. This is essentially complete within 48 hours following a single oral dose.
TOXICOLOGY
Asbestos was suspected to have links with some human cancers as early as 1935 (Lynch and Smith, 1935). A number of authoritative bodies have listed asbestos as a known human carcinogen via the inhalation route. NTP (2000) and IARC (1987) reported that there is sufficient evidence of carcinogenicity of asbestos as well as chrysotile, amosite, anthophyllite, and crocidolite in experimental animals. NAS (1977, 1983, 1984) and ATSDR (1995) are also in agreement with the determination of asbestos carcinogenicity.
There are numerous publications on toxicological evaluations of asbestos, mainly on occupational groups exposed to airborne asbestos. It is well recognized that the greatest risks with occupational exposure to asbestos, mainly through inhalation as well as some through accidental ingestion, are mesothelioma, bronchial carcinoma in the lung, and asbestosis (IPCS, 1998). Mesothelioma is a primary malignant tumor of the pleura and peritoneum whereas asbestosis is described as a diffuse pulmonary fibrosis. Numerous studies in various animals also support the carcinogenicity of asbestos fibers, especially through inhalation exposure (Reeves et al., 1971, 1974; Smith et al., 1965; Wagner et al., 1974).
However, this PHG technical support document focuses mainly on toxicological data needed for characterization of the risk from ingestion of asbestos in drinking water since the purpose of this document is to develop a health protective concentration of asbestos in drinking water. Special attention has been paid to carcinogenicity and genotoxicity as the supporting evidence for selecting carcinogenicity as the most sensitive toxicity endpoint for deriving a public health protective concentration in drinking water.
Toxicological Effects in Animals
Acute, Subacute, and Chronic Noncancer Effects
Most studies conducted in animals seem to indicate that ingestion of asbestos causes little or no risk of noncarcinogenic injury. No studies were located regarding respiratory, musculoskeletal, hepatic, endocrine, dermal, ocular, metabolic, or other systemic effects in animals after oral exposure to asbestos (ATSDR, 1995; HSDB, 2000).
In the literature search, no studies have been located regarding death in animals after acute, intermediate, or chronic oral exposure to asbestos. Feeding studies in rats and hamsters indicate that ingestion of high amounts in the diet (one percent), equivalent to doses of 500 to 800 mg/kg-d of chrysotile, amosite, crocidolite, or tremolite, does not ASBESTOS in Drinking Water
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cause premature lethality, even when exposure occurs for a lifetime (ATSDR, 1995; NTP, 1983, 1985, 1988, 1990a,b,c).
Kidney Effects
Cemerikic (1977) exposed male and female Wistar rats (seven per sex) to chrysotile asbestos in drinking water for 3 months. The ten male and seven female controls received tap water. A suspension of asbestos fibers in drinking water was prepared by shaking 2.5 g of chrysotile asbestos in 500 ml of water; this was allowed to settle for 30 minutes and the top 250 ml, which contained about 9.4x109 (1 mg) fibers/ml was drawn off (the technique of Pontefract and Cunningham, 1973). Blood pressure was measured by tail cuff at one or more time points (3, 6, 9, 12, 15 weeks). A moderate increase of blood pressure, evidence of hypertension, was found by the tail cuff procedure in exposed females after 6, 9 and 12 weeks, and in males at 9 and 15 weeks, compared with controls. Arterial pressures measured in the anesthetized animals via cannulation at 12 weeks in females and 15 weeks in males were also shown to be elevated. One male and three females were judged to be hypertensive (blood pressure >two standard deviations above the mean control level). Females were sacrificed after 12 weeks and males after 15 weeks. The organs were measured and the kidneys and bladders examined histopathologically. Pathologic presence of red blood cells and hyaline casts in the urine sediment of four males indicated damage to the kidneys.
Kidneys of experimental females showed only discrete perivascular infiltration. Results were interpreted by the authors as indicating that “asbestos may be nephrotoxic in male and hypertensive in female rats.”
Gastrointestinal Effects
A number of researchers have investigated nonneoplastic and biochemical effects of ingested asbestos on the gut wall since the tissue most directly exposed to ingested asbestos is the gastrointestinal epithelium (ATSDR, 1995). In addition, studies in rats by Evans et al. (1973) have shown that the gastrointestinal tract receives, via pulmonary clearance, much of the asbestos load of the lung. Several researchers have described significant biochemical or histological alterations at the subcellular level in the gastrointestinal tract after oral exposure to asbestos.
Jacobs et al. (1978a) examined the gastrointestinal tract tissues of an unspecified number of rats fed 0.5 or 50 mg of chrysotile per day for one week or 14 months. Light microscopy revealed an accumulation of cellular debris and Alcian blue-positive material in the lumen of the ileum, colon and rectum. There was also marked vacuolation in the surface epithelial cells of the mucosa, and in the loose tissue core of the lamina propria.
Analysis by electron microscopy revealed marked separation of cells along the intracellular membrane in the colon and ileum. Loss of the brush border and discharge of the cell contents into the lumen was common, with adherence to the luminal surface.
Microvilli were often less compact, organized and evenly stained than those of the control animals, and abnormal blebbing of the surface was present. In addition, mitochondria were swollen in intact cells. The esophagus, stomach, and cecum in treated animals appeared unaffected. Significant alterations, consistent with a mineral-induced ASBESTOS in Drinking Water
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cytotoxicity, were found in the lining cells of the rat small intestine in animals fed diets containing chrysotile asbestos (0.5 to 50 mg/day) for 10 months (Jacobs et al., 1977), then starved for 24 hours before sacrifice. The DNA content of washings from the small intestine lumen increased and RNA levels decreased in asbestos-treated rats. The level of DNA in the lumen washings of treated animals maintained on both concentrations of asbestos in the diet was twice as high as that found in control animals. Enzyme levels within the lumen were also significantly higher than those found in a similar number of control rats. Levels of DNA, RNA and protein in the mucosal lining cells of the gut remained unchanged, although intracellular enzyme levels were consistently elevated.
The higher levels of DNA and enzymes in the intestinal lumen of fasted rats that have previously ingested asbestos may be the result of mineral-induced cellular damage (i.e., cytotoxicity to mucosal cells).
Amacher et al. (1974, 1975) conducted several dose-response studies in rats to measure DNA synthesis by tritiated thymidine uptake in tissues. In the first study, three groups of five Charles River rats were gavaged with 5, 100, or 500 mg/kg chrysotile. There were 21 control animals. Two weeks following administration of the 5 mg/kg dose, DNA synthesis was significantly increased in the colon and small intestine and significantly reduced in the liver. At the 500 mg/kg dose, DNA synthesis was significantly reduced in the small intestine two weeks following administration. No significant changes were noted in the stomach or liver. Increases in DNA synthesis were noted in the stomach and small intestine at one and two days respectively, and in the colon from 23-68 days following administration of 100 mg/kg chrysotile to five groups of five rats. An additional study (Amacher et al., 1975) was conducted in which five groups of five rats were administered 0.5, 5.0, 25.0, 50.0 and 100 mg/kg chrysotile by gavage following fasting for 24 hours. At three days, incorporation of tritiated thymidine was significantly elevated in the whole stomach, duodenum, and jejunum in the 5-100 mg/kg dose range; incorporation in the liver was reduced.
Increased numbers of aberrant crypt foci (ACF), preneoplastic lesions of colon cancer, were induced in rats one month following bolus administration of either a single dose (70 mg/kg-day) of chrysotile, a single dose (40, 80 or 160 mg/kg-day) of crocidolite, or three doses (33 mg/kg-day) of crocidolite over a 5 day period (Corpet et al., 1993). Rats given any asbestos (any form or dose) had more ACF in the colon than water treated controls. Chrysotile (70 mg) induced as many ACF as crocidolite (80 mg). No aberrant crypt foci were seen in the controls (p < 0.05 with each one of the four treated groups).
No dose response was noted however, since increasing doses of crocidolite did not induce increasing numbers of ACF (all different from control, all p<0.05, but no difference between treated groups). The aberrant crypt foci were distributed primarily in the middle colon and rectum in all groups. Mice administered either a single dose (100 mg/kg) of chrysotile or three doses (50 mg/kg-day) of crocidolite did not show any increases.
Delahunty and Hollander (1987) exposed an unspecified number of Sprague-Dawley rats to 0.5 g/L chrysotile asbestos in their drinking water, approximately seven mg/day ingested, for 1.5 years. In vivo intestinal permeability studies showed that asbestos treatment resulted in a significant reduction in the ability of the intestine to absorb the non-metabolizable sugars lactulose and mannitol in comparison to control animals, as determined by significant decreases in the urinary elimination. However, no decrease ASBESTOS in Drinking Water
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was found in the elimination of rhamnose, another non-metabolizable sugar. Previous experiments by the authors showed that the permeability function of rat intestine could be monitored by the oral administration of non-metabolizable compounds (permeability probes) such as lactulose, rhamnose, and polyethylene glycol. The entire intestinal mucosal surface of each animal was removed and examined macroscopically for obvious lesions. Multiple representative sections of the small and large intestines of asbestostreated and control animals were processed for light microscopy and assessed for any abnormalities. No specific findings of these examinations were reported except the absence of asbestos fibers in the sections. There were no differences in the weight or appearance of the treated rats, compared to controls.
No excess non-neoplastic lesions of the gastrointestinal epithelium have been detected in a number of other animal feeding studies (Bolton et al., 1982; Donham et al., 1980; Gross et al., 1974), including an extensive series of lifetime studies in rats and Syrian hamsters in which such effects were carefully investigated (NTP, 1983, 1985, 1988, 1990a,b,c).
Body Weight Effects
An NTP toxicology/carcinogenesis study reported decreased (15-37 percent) body weight gain in rats exposed to amosite asbestos in the diet (NTP, 1990b). Amosite (target concentration of 10,000 ppm, one percent by weight of study diet) was given to two groups of male and female rats. One group (amosite group) was exposed from weaning throughout life. The second group received chrysotile asbestos (by mistake) beginning at birth by preweaning gavage and then amosite in feed from weaning throughout the lifespan (amosite + PW group). Group sizes varied from 100-250. Litter size was the same, but the offspring from mothers exposed to amosite asbestos were smaller at weaning than those from non-exposed mothers, and remained smaller throughout their life. Changes in food consumption do not explain the decreased body weight gain since treated rats had slightly higher food intakes than controls. This did not appear to negatively effect the survival of amosite-exposed rats since they show enhanced survival compared with the non-exposed rats. Effects on body weight gain have generally not been observed in other studies (Gross et al., 1974; NTP, 1983, 1985, 1988, 1990a,c; Delahunty and Hollander, 1987). The significance of this finding is therefore uncertain.
Immunological and Lymphoreticular Effects
Asbestos exposure has been associated with changes in both humoral and cellular immune functions in experimental animals in vivo as well as in vitro. For example, the chronic inflammatory response after asbestos exposure represents a complex immunological process initiated by fiber deposition which involves multiple types of immune cells (Luster and Rosenthal, 1993; Rosenthal et al., 1998, 1999).
An intraperitoneal injection of 200 µg UICC crocidolite fibers (about 60 percent of which were longer than two µm) in mice resulted in accumulation of inflammatory cells, mesothelial cell injury and proliferation (Moalli et al., 1987). Repeated weekly intraperitoneal injection of 200 µg UICC crocidolite in mice for 3 to 42 weeks resulted in ASBESTOS in Drinking Water
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inflammation and submesothelial fibrosis associated with fiber clusters after 6 to 12 weekly injections. Mesothelial cell proliferation with thymidine incorporation increased progressively over 42 weekly injections. Mesothelial cell proliferation was dissociated spatially and temporally from the development of submesothelial fibrosis (MacDonald and Kane, 1993).
Choe et al. (1999) assessed the effects of in vitro and in vivo asbestos exposure on the adhesion of rat pleural leukocytes (RPLs) to rat pleural mesothelial cells (RPMCs).
Exposure for 24 hours to either crocidolite or chrysotile at 1.25 to 10 µg/cm2 increased
the adhesion of RPLs to RPMCs in a dose-dependent fashion, an effect that was potentiated by interleukin-1beta (particulates were added to RPMC cultures at concentrations ranging from 1.25-10.0 µg/cm2). Crocidolite or chrysotile plus interleukin-1beta (IL-1beta) also upregulated vascular cell adhesion molecule-1 mRNA and protein expression in rat pleural mesothelial cells, and the binding of rat pleural leukocytes to asbestos-treated rat pleural mesothelial cells was also abrogated by antivascular cell adhesion molecule-1 antibody. In the in vivo experiments, rat pleural leukocytes exposed by intermittent inhalation to crocidolite for two weeks manifested significantly greater binding to RPMCs than did RPLs from sham-exposed animals. The time weighted exposure concentration for crocidolite in this experiment was 10.5 + 2.3 (SE) mg/m3
. These exposure levels were comparable with historic asbestos dust concentrations recorded in the workplace environment of asbestos mines and mills. The ability of asbestos fibers to upregulate RPL adhesion to RMPCs may play a role in the induction and/or potentiation of asbestos-induced pleural injury.
Asbestos may cause pathological lesions via an autocrine-like process in which the response evoked by fibers acts to enhance subsequent interactions of asbestos with tissue (Xie et al., 2000). Exposure of rat alveolar macrophages in vitro to crocidolite increases the production of tumor necrosis factor alpha (TNF-alpha) and IL-1beta (Mongan et al., 2000). The role that cytokine TNF-alpha and chemokine macrophage inflammatory protein-2 (MIP-2) play in asbestos-induced inflammation in the lung has been reviewed recently (Driscoll, 2000). Asbestos fibers stimulate TNF-alpha production by macrophages, and TNF-alpha is released from alveolar macrophages after phagocytosis of fibers. TNF-alpha initiates adhesion molecule expression and production of chemotactic cytokines that ultimately results in the infiltration of inflammatory cells to a site of infection or tissue injury in the respiratory tract. MIP-2 produced by macrophages and epithelial cells mediates the neutrophilic inflammatory response of the rodent lung to crocidolite. Expression of the MIP-2 gene in rat lung epithelial cells is dependent on the transcription factor (NF), NF-kappaB, and is regulated partially by oxidative stress induced by asbestos exposure (Driscoll, 2000). TNF-alpha increases epithelial fiber binding by an NF-kappaB-dependent mechanism, while macrophage TNF-alpha production acts to enhance subsequent tissue fiber interactions (Xie et al., 2000). The stimulus for pleural macrophage recruitment after chrysotile or crocidolite exposure is the induction of monocyte chemoattractant protein-1 (MCP-1) synthesis by pleural mesothelial cells, as shown by both in vivo and in vitro experiments (Tanaka et al., 2000).
Asbestos-induced binding to epidermal growth factor receptor initiates signaling pathways responsible for increased expression of protooncogene c-fos and the development of apoptosis. Crocidolite abolished binding of epidermal growth factor to ASBESTOS in Drinking Water
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its receptor in rat pleural mesothelial cells in vitro. Crocidolite interacts with the epidermal growth factor receptor and stimulates steady state mRNA levels and synthesis of epidermal growth factor receptor protein. Stimulation of epidermal growth factor receptor phosphorylation by asbestos is linked to the induction of c-fos, but not of c-jun.
Inhibition of signaling through this pathway with tyrphostin AG-1478, but not with the nonspecific tyrphostin A-10, decreases apoptosis in vitro (Zanella et al., 1999).
Neurological Effects
No histological or clinical evidence of neurological injury was detected in rats or hamsters chronically exposed to high doses (500 and 830 mg/kg-day, respectively) of chrysotile, amosite, crocidolite, or tremolite in the diet (NTP, 1983, 1985, 1988, 1990a,b,c).
Reproductive Effects
Limited evidence from animal studies suggests that chronic ingestion of asbestos does not injure reproductive tissues, and that exposure during gestation does not reduce fertility (NTP, 1983, 1985, 1988, 1990a,b,c). No histopathological changes in reproductive organs or effects on fertility were observed in Syrian hamsters exposed to chrysotile, amosite, crocidolite, or tremolite (500 and 830 mg/kg-day, respectfully) in the diet during breeding, gestation, and lactation (NTP, 1983, 1985, 1988, 1990a,b,c).
Developmental Effects
Although detailed studies were not performed, no teratogenic effects were noted in the offspring of rats or hamsters exposed to chrysotile, amosite, crocidolite, or tremolite (500 and 830 mg/kg-day, respectively) during gestation (NTP, 1983, 1985, 1988, 1990b,c).
However, decreased body weight at birth and later in life was noted in some of the studies (McConnell et al., 1983a; NTP, 1985, 1990a). No teratogenic effects were seen in CD-1 mice given doses up to 33 mg/kg-day of chrysotile in their drinking water, or 143 mg chrysotile asbestos per mL, during days 1-15 of gestation (Schneider and Maurer, 1977). Studies carried out with blastocyst exposure to chrysotile in drinking water found some decrease in postimplantation survival (Hall and Rumack, 2000).
Genotoxicity
Regulation of DNA synthesis, measured via the uptake of tritium labeled thymidine, was altered in the stomach, small intestine, and liver of the young adult male Charles River CD rats gavaged with chrysotile suspensions (mainly between five and 120 µm in diameter) in normal saline at 5, 100, and 500 mg/kg doses (Amacher et al., 1974, 1975).
Epstein and Varnes (1976) also demonstrated changes in DNA metabolism in tissues lining the gastrointestinal tract and other body organs in rats gavaged with 5 to 100 mg/kg chrysotile. These investigators concluded that asbestos penetrates the mucosal layer of the gut and either enhances mitosis by interaction with nuclear DNA, or causes accelerated cell death and thus stimulates a mitotic burst of replacement cells.
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Inclusion of 0.5 to 50 mg chrysotile in the diet of rats initiated changes in the small intestinal lumen content of DNA and RNA, and produced changes in both lysosomal and brush-border enzymes (Jacobs et al., 1977). The asbestos-induced cytotoxicity in the mucosal cells lining the small intestine in rats exposed for one week or for five to 15 months was confirmed using electron microscopy (Jacobs et al., 1978a). The incorporation of tritium-labeled thymidine into DNA was significantly increased in the small intestine, colon, rectum, stomach, and spleen, but was decreased in the liver (Jacobs et al., 1978b).
DNA fingerprint analysis of rat peritoneal tumors induced by intraperitoneal injections of crocidolite or benzo(a)pyrene revealed similar mutational frequencies by crocidolite (14.8 percent) and benzo(a)pyrene (18.2 percent). Only deletions of bands were observed in the DNA from asbestos-induced tumors, whereas the alterations in the benzo(a)pyreneinduced tumors were exclusively additional bands (Kociok et al., 1999).
Asbestos fed to male mice in doses of 20 mg/kg-day for 60 days did not result in genotoxic effects on sperm and germinal cells (Rita and Reddy, 1986). An intraperitoneal injection of 10 mg asbestos per CBA mouse induced micronuclei in polychromatic bone marrow erythrocytes and the combination of radiation increased the mutagenic effect (Frash et al., 1999).
Yamaguchi et al. (1999) reported an increase of 8-hydroxyguanine in DNA and its repair activity in the lung of Syrian hamsters or Wistar rats after intratracheal instillation of crocidolite asbestos, indicating a type of oxidative DNA damage. Crocidolite induced activator protein (AP-1) transactivation in the pulmonary and bronchial tissues of transgenic mice at two days after intratracheal instillation. It also caused a dose-and time-dependent induction of AP-1 activation in cultured JB6 cells persisting for at least 48 hours, indicating cell proliferation (Ding et al., 1999). The upregulation of the protooncogenes c-myc, fra-1, and egfr monitored at different stages of asbestos-induced carcinogenesis in rats showing the mRNA expression patterns was demonstrated by suppression subtractive hybridization and array assay. A possible role of fra-1 as one of the dimeric proteins generating the AP-1 transcription factor was substantiated by its dose-dependent expression in mesothelial cells treated with asbestos in vitro (Sandhu et al., 2000).
Drosophila melanogaster fed asbestos induced aneuploidy in germinal cells. Chrysotile, nonfibrous tremolite, and amosite induced aneuploidy in the fruit flies but crocidolite did not induce significant chromosomal changes (Osgood, 1994; Osgood and Sterling, 1991).
There are many reviews (Daniel, 1983; IARC, 1973, 1977, 1980, 1987, 1989, 1996; IPCS, 1986, 1998; Jaurand, 1991, 1996, 1997) that summarize the use of in vitro genotoxicity and cell transformation assays to evaluate the potential carcinogenicity of fibers. Some of these studies are described below.
Mutagenicity
Chamberlain and Tarmy (1977) found negative gene mutation results of chrysotile, crocidolite, amosite, anthophyllite, and man-made vitreous fibers in Salmonella typhimurium TA1535 and TA1538 as well as several strains of Escherichia coli.
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However, an alkali-rich analogue of tremolite induced a significant number of mutants in Escherichia coli CSH50 with exogenous liver homogenate S9 fraction (Cleveland, 1984).
Jaurand (1989) postulated that this might be due to the test fiber being ground just prior to adding to the bacterial cultures and new sites being opened on the fiber surfaces for the formation of mutagenic oxidants. Using Salmonella typhimurium TA102, which is sensitive to oxygen free-radical DNA damage, Faux et al. (1994) found that UICC crocidolite, but not UICC chrysotile, produced gene mutations. Athanasiou et al. (1992) did not observe gene mutations with tremolite in TA102. With the addition of hydrogen peroxide, asbestos-induced lipid peroxidation leading to DNA adduct formation in Salmonella typhimurium TA104 and rat lung fibroblasts was observed. Howden and Faux (1996) concluded that the DNA damage might be related to the amount of iron mobilized from the fibers.
Most in vitro mutagenesis studies have revealed negative results (Kelsey et al., 1986; Kenne et al., 1986; Oshimura et al., 1984; Reiss et al., 1980, 1982). However, Huang et al. (1978), using Chinese hamster lung cells, reported a weak mutagenicity of chrysotile, crocidolite, or amosite at the hypoxanthine guanine phosphoribosyl transferase (hprt) locus with 6-thioguanine as the selective agent (Huang, 1979). On the other hand, no mutagenic response was observed 1) at the hprt locus in adult rat liver cells treated with chrysotile, crocidolite, or amosite (Reiss et al., 1982); 2) at the hprt and Na+ /K+
ATPase locus in Syrian hamster embryo cells treated with chrysotile or crocidolite (Oshimura et al., 1984) or 3) at the hprt locus in Chinese hamster ovarian (CHO) cells treated with crocidolite (Kenne et al., 1986). Hei et al. (1991, 1992, 1995) have shown that both chrysotile and crocidolite fibers are highly mutagenic to mammalian cells in culture, and induce large chromosomal deletions in a dose-dependent manner in the AL hamster-human hybrid cell line by DNA analysis. A significant rate of mutation was detected at the S1 locus in AL hamster-human cell hybrids with chrysotile or crocidolite.
No mutagenic response was observed at the hprt locus in AL hamster-human cell hybrids with chrysotile or crocidolite (Hei et al., 1992), or tremolite or erionite (Okayasu et al., 1999b).
At a dose of 50 µg/mL, chrysotile was mutagenic in the autosomal HLA-A locus in human peripheral lymphocytes but 400 µg/mL crocidolite or erionite was not (Both et al., 1994). Crocidolite did not increase mutation frequency in the HLA-A locus in a mesothelioma cell line (Both et al., 1995). Loss of heterozygosity was detected in human lymphocytes treated with crocidolite or erionite (Both et al., 1994), as well as in mesothelioma cells treated with crocidolite (Both et al., 1995) but not with chrysotile (Both et al., 1994). As demonstrated by the protective effect of the antioxidant enzyme, manganese superoxide dismutase, in AL hamster-human cell hybrids, asbestos-induced mutagenesis may be caused by oxygen-derived molecules (Hei et al., 1995).
Clastogenicity
There is general agreement about the ability of asbestos fibers, mainly chrysotile and crocidolite, to induce chromosomal mutations including aneuploidy, polyploidy, and aberrations in a variety of mammalian cells (Athanasiou et al., 1992; Babu et al., 1980; Barrett, 1991; Chamberlain and Tarmy, 1977; Donaldson and Golyasnya, 1995; Dopp ASBESTOS in Drinking Water
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et al., 1995; Emerit et al., 1991, 1995; Hart et al., 1992; Hesterberg and Barrett, 1985; Hesterberg et al., 1993; Huang et al., 1978; Jaurand et al., 1983, 1986; Jaurand, 1989; Kelsey et al., 1986; Kenne et al., 1986; Kodama et al., 1993; Korkina et al., 1992; Lavappa et al., 1975; Lechner et al., 1985; Lu et al., 1994; Oshimura and Barratt, 1986; Oshimura et al., 1984, 1986; Palekar et al., 1987; Pelin et al., 1995a, 1995b; Price-Jones et al., 1980; Rieder et al., 1991; Sincock and Seabright, 1975; Sincock et al., 1982; Valerio et al., 1980, 1983; Verschaeve and Palmer, 1985; Yegles et al., 1993). There is also agreement that asbestos can cause chromosome breaks and other chromosomal aberrations (Jaurand et al., 1986; Kelsey et al., 1986; Kenne et al., 1986; Korkina et al., 1992; Valerio et al., 1983). Several authors have reported that asbestos fibers increase the frequency of sister chromatid exchanges (SCEs) in vitro (Babu et al., 1980; Fasy, 1991; Livingston et al., 1980). Casey (1983) reported SCEs in Chinese hamster ovary K1 cells, human fibroblasts, and lymphoblastoid cells exposed in vitro to asbestos.
Chrysotile exhibited clastogenic and aneuploidogenic effects in Chinese hamster lung fibroblast V79 cells (Lu et al., 1994).
Dopp and Schiffman (1998) investigated mitotic disturbances caused by amosite, crocidolite, and chrysotile in Syrian hamster embryo fibroblasts. All three fiber types induced a significant increase of micronuclei in Syrian hamster embryo cells. The micronuclei formation occurred in a dose-dependent manner. Amosite was the most potent fiber, with the highest micronuclei frequency at the lowest fiber concentration.
Asbestos fibers also induced disturbances during mitosis in the absence of spindle fiber damage, misaggregation of chromosomes, and changes in chromatin structure.
Chrysotile induced micronuclei in Chinese hamster lung fibroblast V79 cells (Keane et al., 1999). Exposing Syrian hamster embryo fibroblasts to one µg chrysotile per cm2 for
66 hours induced micronuclei (p < 0.05), and kerosene soot enhanced the clastogenicity (Lohani et al., 2000).
Structural chromosomal aberration was induced in human embryo lung cells exposed to 5 µg/mL chrysotile for 24 hours (Wang et al., 1999). Structural chromosomal aberrations in human lymphocytes were reported due to reactive oxygen/nitrogen species, probably generated by monocytes present in the incubation medium (Korkina et al., 1992). The occurrence of chromosomal aberrations in human lymphocytes following treatment with conditioned medium from chrysotile-treated mesothelial cells was judged to confirm the role of reactive oxygen/nitrogen species in asbestos clastogenicity. In this study, neither a cell-free nor an asbestos-free control conditioned medium produced chromosome damage. The addition of catalase and manganese superoxide dismutase to the culture medium of asbestos-treated mesothelial cells reduced the clastogenic potency of the resultant conditioned medium (Emerit et al., 1991, 1995).
Other Genetic and Preneoplasm Damages
Several researchers have shown that asbestos causes specific mitotic disturbances resulting in chromosome breaks and/or micronucleus formation (Ault et al., 1995; Dopp et al., 1995, 1997). Ault et al. (1995), in a study using lung epithelial cells of the newt Taricha granulosa, reported that crocidolite fiber-chromosome contact induced chromosome breaks, and in one instance, led to displacement of the chromosome.
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Phagocytized crocidolite asbestos fibers caused a break in both chromatids during mitosis in a living cell. During anaphase, the resultant acentric chromosome fragment, consisting of both chromatids, was left behind at the equatorial plate of the spindle. The fragment ended up in the cytoplasm of one of the daughter cells. Dopp and Schiffmann (1998) investigated mitotic disturbances caused by amosite, crocidolite and chrysotile in Syrian hamster embryo (SHE) fibroblasts. All three fiber types induced micronuclei in SHE cells with a high frequency (up to 200 MN/2000 cells; dose range: 0.1 –5.0 µg/cm2 ) in a
dose-dependent manner. Asbestos fibers caused both loss as well as breakage of chromosomes in the absence of direct interaction with spindle fibers (spindle deformation was observed in cells with disturbed meta-and anaphases while the spindle fiber morphology appeared unchanged).
DNA damage by asbestos fibers has been indicated by the occurrence of DNA repair in rat pleural mesothelial cells (Renier et al., 1990); nick translation in rat embryo cells (Libbus et al., 1989); and DNA nicks in C3H10T1/2 cells (Turver and Brown, 1987).
Crocidolite caused DNA single strand breaks in human mesothelial cells (Ollikainen et al., 1999). Kinnula et al. (1994) reported no single-strand breaks in MeT-5A cells treated with amosite. Erionite enhanced DNA repair in C3H10T1/2 cells (Poole et al., 1983), but chrysotile did not induce DNA repair in hepatocytes (Denizeau et al., 1985).
Poly(ADP)ribosylation induced by DNA breaks has been observed in rat pleural mesothelial cells treated with chrysotile and crocidolite (Dong et al., 1995).
A radiosensitive DNA repair-deficient xrs-5 cell line exposed to chrysotile for 24 hours gave significantly lower cell survival accompanied by a cell growth delay, as well as a higher number of DNA double strand breaks compared with wild-type Chinese hamster ovary cells (Okayasu et al., 1999a). Chrysotile asbestos was significantly more cytotoxic to AL hamster-human cell hybrids than tremolite or erionite, but erionite exhibited mutagenicity comparable to chrysotile (Okayasu et al., 1999b).
Several authors have reported that crocidolite or erionite induces the release of freeradical reactive oxygen/nitrogen species (Gormley et al., 1985; Hansen and Mossman, 1987; Takeuchi and Morimoto, 1994; Vallyathan et al., 1992; Xu et al., 1999).
Goodglick and Kane (1986) showed that the toxicity of crocidolite against macrophages could be prevented by a hypoxic environment. Reactive oxygen/nitrogen species induce many kinds of DNA damage, including DNA strand breaks and base modifications, and reactive oxygen species have been reported to play an important role in asbestos-related damage (Floyd, 1990; Goodglick and Kane, 1986; Kamp et al., 1992; Zoller and Zeller, 2000). Decreased levels of antioxidants and increased levels of lung tissue injury parameters in asbestos-treated Wistar rats, both 24 hours and three months after exposure, suggest involvement of reactive oxygen intermediates in the mechanism of asbestos lung disease development (Kaiglova et al., 1999).
Crocidolite and amosite have been found to enhance 8-hydroxydeoxyguanosine, a marker for mutagenic oxidative DNA damage, in calf thymus DNA (Adachi et al., 1992; Faux et al., 1994). In the Takeuchi and Morimoto (1994) study, crocidolite induced the release of reactive oxygen species in neutrophils and macrophages. A marker for mutagenic oxidative DNA damage, 8-hydroxydeoxyguanosine, was induced in the cellular DNA of a human promyelocytic leukemia cell line, HL60, when incubated with crocidolite. The authors propose that the 8-hydroxydeoxyguanosine increase induced by crocidolite is ASBESTOS in Drinking Water
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due, not to an increase of reactive oxygen/nitrogen species released from the cells, but to the generation of hydroxyl radicals by crocidolite internalized in the cells close to DNA.
Xu et al. (1999) demonstrated that reactive oxygen species mediate crocidolite-induced DNA mutagenesis in AL hamster-human cell hybrids in a concentration-dependent manner. Crocidolite induced increases in oxidative DNA damage in AL cells.
In vitro cytotoxicity of various types of asbestos in tissue culture cell lines including Syrian hamster peritoneal macrophages and Chinese hamster lung V79-4 cells has been reported (Bey and Harington, 1971; Brown et al., 1978; Chamberlain and Brown, 1978).
An Indian variety of chrysotile induced cytotoxicity in rat hepatocytes with lipid peroxidation and intracellular glutathione depletion (Aslam et al., 1992). Chrysotile from India produced cytotoxic and cytogenetic effects of cytoplasm vacuolization, cell flattening with increased size, and chromosomal aberrations in vitro on CHO cells (Babu et al., 1980).
Chrysotile induced cytotoxicity in human erythrocytes (Kennedy et al., 1989).
Hemolysis by chrysotile may be related to an adsorption of the red blood cell membranes on the fibers (Jaurand et al., 1983). The hemolytic activity of asbestos on red blood cells in vitro has been correlated with its surface charge as indicated by its zeta potential (Light and Wei, 1977a,b). A correlation between asbestos-induced production of reactive oxygen metabolites and red blood cell hemolysis was observed (Hendenborg and Klockars, 1987).
Cell Transformation and Other Changes
Treatment of either human or rodent cells with asbestos produces damage to cellular DNA, which can lead to neoplastic cell transformation (Barrett, 1992; Barrett et al., 1989; Jaurand, 1989). Asbestos did not cause morphologic transformation of C3H10T1/2 cells (Brown et al., 1983; Hei et al., 1985, 1991), but transformed BALB/c#3T3 cells (Hesterberg and Barrett, 1984; Hesterberg et al., 1986; Lu et al., 1988). Chrysotile or crocidolite has been shown to induce morphological and neoplastic transformations of Syrian hamster embryo fibroblasts (Hesterberg and Barrett, 1984; Mikalsen et al., 1988).
Cell transformation assays have demonstrated a greater carcinogenic potential of long versus short fibers (Jaurand, 1996).
The effects of asbestos fibers on cell proliferation, cell activation, and gene expression have been studied (Driscoll, 1996), as well as short-term animal tests for detecting inflammation, fibrosis and pre-neoplastic changes induced by fibers (Donaldson, 1996).
The changes in cell number and tissue volumes in response to asbestos exposure have been quantified by morphometry or stereology, and more recently by assessing the incorporation of tritiated deoxythymidine or 5-bromo-2’-deoxyuridine into cells. An intraperitoneal injection in mice of 200 µg UICC crocidolite long fibers (approximately 60 percent greater than two µm), not readily cleared by lymphatics and persistent for six months, resulted in accumulation of inflammatory cells, mesothelial cell injury, and proliferation (Moalli et al., 1987). Three to 42 weekly intraperitoneal injections of 200 µg UICC crocidolite in mice led to progressively increased inflammation as well as mesothelial cell injury and proliferation (MacDonald and Kane, 1993).
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Chromosomal aberrations were seen in Chinese hamster cells cultured in a medium containing 0.01 mg/mL of either chrysotile or crocidolite asbestos (Sincock and Seabright, 1975). No chromosomal aberrations were seen in culture with coarse glass fibers or with control media.
Cancer
Asbestos as a Carcinogen
A number of researchers have reported increases, some statistically significant, in neoplastic response at one or more tissue sites (mostly gastrointestinal) following dietary exposure to asbestos (Donham et al., 1980; Gibel et al., 1976; McConnell et al., 1983a, 1983b; Smith et al., 1980; Ward et al., 1980). There is some evidence that acute oral exposure may induce precursor lesions of colon cancer and that chronic oral exposure may lead to an increased risk of gastrointestinal tumors (Chouroulinkov, 1989; NTP, 1985; Truhaut and Chouroulinkov, 1989).
Early animal studies on gastrointestinal cancer from ingested asbestos were mostly inconclusive or negative (Cunningham et al., 1977; Gross et al., 1974; Wagner et al., 1977), although some studies yielded increases in tumor frequency that were not statistically significant (Bolton et al., 1982; Donham et al., 1980; Smith et al., 1980; Ward et al., 1980). However, rats fed powdered chrysotile filter materials including 47 percent non-asbestos materials had a significant excess incidence of malignant tumors (Gibel et al., 1976). Except for the studies by Donham et al. (1980) and Smith et al. (1980), these studies were conducted with relatively small numbers of animals.
Additionally, some of the studies were conducted for insufficient time periods for adequately testing the carcinogenic potential of ingested asbestos. In the case of the Gross et al. (1974) study, systematic histological examination was conducted on only 53 of over 200 animals. Zaidi (1974) cited major differences between the stomachs of rats and humans and emphasized the need for suitable animal models to correlate with results in humans. The author suggested that the role of the mucous barrier in preventing absorption of asbestos from the gastrointestinal tract of rats might account for the lack of neoplastic response seen in most animal studies.
Donham et al. (1980) fed 189 weanling F344 rats a diet containing 10 percent chrysotile over their lifetime to determine the effects of ingested asbestos on the colon. Control groups were fed a diet containing 10 percent nonnutritive cellulose (n = 197) or a standard laboratory rat diet (n =115). The cumulative risk for development of any colonassociated lesion (neoplastic plus non-neoplastic lesions) was greatest for asbestos-fed rats (17.9 percent) compared to 13.6 percent for those fed the fiber-controlled diet and
8.2 percent for those fed the standard control diet. Chrysotile fibers were seen by electron microscopy in six out of ten ashed colon specimens of rats fed the asbestos diet.
Additionally, levels of two cyclic nucleotides, adenosine 3’-5’-cyclic monophosphate (cAMP) and guanosine 3’,5’-cyclic monophosphate (cGMP), were analyzed in the colon tissues of an unspecified number of rats fed the diet for 24 months and killed at 33 months. The levels of cAMP in the asbestos-fed animals were significantly less than in the control groups. For cGMP, the levels in the asbestos-fed animals were similar to ASBESTOS in Drinking Water
California Public Health Goal (PHG) 34 September 2003
the normal diet control group. The authors concluded that the cAMP results suggest a serious cell-regulator defect related to asbestos ingestion.
Gibel et al. (1976) reported a statistically significant (p < 0.01) increase in malignant tumors in the lung, kidney, liver and reticuloendothelial system, but no increase in intestinal neoplasia, in Wistar rats fed asbestos filter material (20 mg/day) containing 53 percent chrysotile asbestos for a lifetime. The chrysotile fiber was extracted from a commercial filter pad used to purify beverages; the composition of the remainder of the material was unspecified. One lung carcinoma, four kidney carcinomas, three reticular cell sarcomas, and four liver-cell carcinomas were reported. One lung adenoma, two cholangiomas, two papillomas of the forestomach, and two mammary fibroadenomas were also observed. There were two liver cell carcinomas in the control group of 50 animals. The total number of animals with tumors in each group was not reported.
In a study by McConnell et al. (1983a), groups of 100 to 250 male and female Fischer 344 rats were administered amosite or tremolite asbestos at a concentration of one percent in pelleted diet for the lifetime of the rats, starting with the dams of the test animals. One group of amosite rats also received chrysotile by gavage during lactation at a dose level of 0.47 mg/kg-day. The offspring from dams exposed to tremolite or amosite asbestos were smaller at weaning than those from untreated mothers, and remained smaller throughout their life. Significant increases (p<0.05) in the incidence of C-cell carcinomas of the thyroid and mononuclear cell leukemia in male rats were observed in amosite-exposed groups. C-cell hyperplasia was increased in amosite female groups. No toxicity or increase in neoplasia was observed in the tremolite-exposed rats compared to the controls.
McConnell et al. (1983b) reported a significant increase in adrenal cortical tumors (p <
0.05) in male and female Syrian golden hamsters fed a pelleted diet over their lifetime with one percent intermediate range (IR) chrysotile asbestos, and in males treated with short range (SR) chrysotile asbestos when compared with pooled controls. Statistical significance was lost, however, when these dosed groups were compared to their temporal controls. A variety of neoplasms was observed in asbestos-exposed and control hamsters. The proportion of control male or female hamsters bearing primary tumors was not statistically different among the four control groups. Thus, statistical comparisons were made with pooled controls as well as with temporal controls.
Ward et al. (1980) administered 1 mg amosite asbestos in saline by gavage to six-week old F344 weanling rats (n = 50) three times per week for 10 weeks, and observed the animals for 95 weeks. Seventeen tumors (16 carcinomas of the colon, one carcinoma of the ileum) were reported in 49 animals examined. No controls were included but the incidence greatly exceeded that of the one percent reported in historical controls (0/21 tumors by saline, 0/21 untreated). The same dosing regimen administered to 21 rats observed for 34 weeks duration produced no malignant tumors.
Although Bolton et al. (1982) did not report any adverse effects following the prolonged ingestion of asbestos in laboratory rats, an examination of the benign tumors showed a clear excess of mesenteric hemangiomas in the chrysotile-treated group (p < 0.01). The authors suggest that an increased occurrence of proliferative vascular lesions might be related to vascular dissemination of the fibers.
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Smith et al. (1980) exposed groups of 30 male and female hamsters for a lifetime to 0.5, 5 or 50 mg/L amosite asbestos and taconite tailings in drinking water. Filtered water from Lake Superior was also given to 120 control animals. In the low and intermediate amosite exposure groups, four malignancies, one pulmonary carcinoma, one peritoneal mesothelioma , and two early squamous cell carcinomas of the nonglandular stomach were found, but the incidence was not statistically significant (p < 0.05). No malignancies were found in the highest amosite exposure group.
Wagner et al. (1977) fed groups of 32 Wistar rats 100 mg/day chrysotile asbestos or Italian talc in malted milk powder for five days per week for 100 days over a six-month period. The 16 control rats were fed malted milk. One gastric leiomyosarcoma was observed in an animal fed chrysotile and one was observed in an animal fed talc. No tumors occurred in the controls.
A series of large scale, lifetime carcinogenesis studies (feed studies) have been performed by the NTP. These studies have yielded largely negative results, although some suggestive increases in tumor frequencies did occur (Table 4). The 1985 NTP feed studies of chrysotile asbestos in F344/N rats did show evidence of carcinogenicity. In this study, male and female rats (88-250/group) were administered a concentration of 1 percent short-range (SR) or intermediate-range (IR) chrysotile asbestos in pelleted diet (500 mg/kg-day) for the lifetime of the rats, starting with the dams of the test animals.
Subgroups of 100 male and 100 female IR chrysotile-exposed rats also received
0.47 mg/g IR chrysotile asbestos in water by gavage during lactation (preweaning, PW).
Feed consumption and survival were comparable among the SR and IR chrysotile asbestos groups and controls. No neoplastic or nonneoplastic disease was associated with SR chrysotile exposure. However, benign epithelial neoplasms (adenomatous polyps), described by NTP as being “grossly visible”, were observed in the large intestine of IR chrysotile asbestos male rats (9/250, 3.6 percent). Although not statistically significant (p=0.08) compared with concurrent controls (0/85), the incidence of these neoplasms was highly significant (p=0.003) when compared with the incidence of epithelial neoplasms (benign and malignant combined) of the large intestine in the pooled male control groups of all the NTP oral asbestos lifetime feeding studies (3/524, 0.6 percent). These lesions are uncommon in standard 2-year carcinogenesis studies. The biologic importance of this finding was further supported by the observation of lesions of similar morphology in the small intestine or glandular stomach of four additional IR chrysotile male rats and by a low incidence (2/100, 2.0 percent) of adenomatous polyps in the large intestine of male rats in the IR/PW group.
In addition to the above findings (NTP, 1985), a significant increase (P>0.05) in keratoacanthomas of the skin was observed in male IR (19/250, 7.6 percent) and IR/PW (8/100, 8 percent) chrysotile-exposed rats compared with the concurrent controls (1/88,
1.1 percent). An apparent increase in the incidence of clitoral gland neoplasms in female IR (18/250, 7.2 percent) and IR/PW (4/100, 4.0 percent) chrysotile-exposed rats compared with that in the concurrent controls (1/88. 1.1 percent) was also observed. The biologic significance of these findings was discounted, however, because of a lack of statistical significance when compared with the pooled male and female control groups, respectively, from all other NTP oral asbestos studies.
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The introduction of high concentrations of asbestos and other durable fibers into the pleura (Reeves et al., 1971; Smith et al., 1965; Stanton and Wrench, 1972; Wagner et al., 1973, 1977), or peritoneum (Davis, 1974; Englebrecht and Burger, 1973; Krajnow et al., 1998; Miller et al., 1999; Pott et al., 1976; Reeves et al., 1971; Shin and Firminger, 1973) of rats, mice, hamsters, and rabbits resulted in malignant neoplasms. Fiber length, dissolution, and biopersistence influenced the production of mesothelioma in the peritoneal cavity by intraperitoneal injection of amosite in male SPF Wistar rats (Miller et al., 1999). Fibers that are long and thin appear to be more carcinogenic than fibers that are short and thick (Stanton et al., 1977).
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Table 4. Summary of NTP Lifetime Studies on Asbestos in Feed Asbestos type Species Median
length (µm)
Size distribution
Carcinogenic effects
Conclusion Reference
osite Am
Amosite
Rat Syrian hamster
4.37 4.37
m µ > 6 74%
74% > 6µm
a im
ll e
ales)
ed C-c
m (am
ed leuke
IncreascarcinoIncreas
) esla(m
None
ent related m
ical and
Not considered treatQuestionable biologstatistical significance.
No carcinogenic response
NTP, 1990b NTP, 1983
Crocidolite Rat 10 m µ > 873% None No carcinogenic response NTP, 1988 oliteTrem Rat dataNo 22%>5µm None No carcinogenic response NTP, 1990c Chrysotile (short
range)
Rat 0.66 30% > 4.5µm None No evidence of carcinogenicity NTP, 1985 Chrysotile
(intermediate range)
Rat 0.82 60% > 5.4µm Benign interstitial
polyps (males) Clitoral gland neoplasm (females)
Some evidence of carcinogenicity, NS vs. concurrent controls; highly significant vs. historical controls) No evidence of carcinogenicity NTP, 1985
Chrysotile (short range)
Syrian hamster
0.66 30% > 4.5µm Adrenal cortical
adenomas (males)
No evidence of carcinogenicity (NS vs. historical controls) NTP, 1990a
Chrysotile (intermediate range)
Syrian hamster
0.82 60% > 5.4µm Adrenal cortical
adenomas (males and females)
No evidence of carcinogenicity NTP, 1990a
Abstracted from ATSDR (1995), Table 2-4. NS = not significant ASBESTOS in Drinking Water California Public Health Goal (PHG) 38 September 2003
Asbestos as a Co-carcinogen or a Promoter
It has been shown that there is a synergistic interaction for the risk of lung cancer in humans between exposure to asbestos and smoking (NAS, 1984). Topping and Nettesheim (1980) demonstrated that asbestos increased the incidence of carcinomas induced by 7,12-dimethyl-benz(a)anthracene in the rat tracheal transplant model, whereas asbestos alone induced a low incidence of tumors. Furthermore, the presence of asbestos particles enhances by several-fold the carcinogenic and genotoxic potential of benzo(a)pyrene (Eastman et al., 1983; Fournier and Pezerat, 1986; Reiss et al., 1983). A number of observations indicate that asbestos induces cellular and biochemical changes such as hyperplasia, metaplasia, DNA synthesis and stimulation of oxygen-free radicals, which are typical of known tumor promoters (IARC, 1996; Mossman and Marsh, 1989; Walker et al., 1992).
In light of the equivocal evidence for carcinogenicity of ingested asbestos, it is conceivable that the high adsorption capability of asbestos fibers creates the possibility of comutagenic or cogenotoxic action with adsorbed organic micropollutants which are carcinogens, such as polycyclic aromatic hydrocarbons, trihalomethanes, and others (Eastman et al., 1983; Fournier and Pezerat, 1986; Reiss et al., 1983). Varga et al. (1996a) found a dose-dependent increase in the frequency of SCE in the bone marrow cells of Fischer 344 rats gavaged with benzo(a)pyrene-coated crocidolite fibers at 50 mg/kg with 2.5 µg/mL of benzo(a)pyrene. Untreated fibers as well as fibers treated at lower concentrations of 0.25, 0.5, and 1 µg/mL of benzo(a)pyrene did not cause alterations.
In a second study, Varga et al. (1996b) demonstrated that anthophyllite asbestos fibers are able to adsorb benzo(a)pyrene molecules from extremely low concentration aqueous solutions of 0.25, 0.5, 1, and 2.5 µg/mL, but were less effective than crocidolite fibers in inducing cytogenetic alterations in the bone marrow cells of rats. The authors felt this discrepancy was due to differences in fiber diameter; of the amphibole types of asbestos, crocidolite tends to have the thinnest fibers and anthophyllite the thickest. Anthophyllite fibers pretreated with the benzo(a)pyrene solutions caused dose-dependent increases in the SCE frequencies in gavaged rats. As before, untreated fibers did not cause alterations, and serum and urinary mutagenicity using S. typhimurium TA98 and TA100 was not observed during these and follow-up studies (Varga et al., 1996a,b, 1998).
Varga et al. (1999) gavaged F-344 female rats with 50 mg/kg untreated crocidolite and anthophyllite fibers, and fibers that had been allowed to adsorb benzo[a]pyrene from an aqueous solution of 2.5 µg/ml (n = 3/group). Peritoneal macrophages and intestine, parietal, peritoneum and omentum samples were obtained from the animals after 24 hours. High levels of DNA strand breaks were observed in cells prepared from the omentum and intestine. A significant potentiating effect of the adsorbed carcinogen on the induction of DNA damage in the omentum was also observed. The authors concluded that the results of this study support the molecular model of asbestos cocarcinogenesis, including both asbestos-induced deletions and mutations caused by a mutagen carried by the same fibers.
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Toxicological Effects in Humans: Oral Exposure
Exposure to asbestos by the oral route may occur through drinking water, recreational water, foods and beverages contaminated with asbestiform fibers, or through swallowing fibers cleared from the respiratory tract via the mucociliary escalator. It has also been postulated that inhaled asbestos may migrate from the lung and circulate in the lymph to other organs in the body. The vast majority of human studies entail ingestion exposure via asbestos-contaminated drinking water. Most studies of asbestos in drinking water are ecologic, and potential confounders such as diet, smoking, and occupation could not be adequately controlled.
Acute, Subacute, and Chronic Noncancer Effects
Asbestos may cause irritation of the gastrointestinal tract due to mechanical action of the fibers. There is no evidence of any acute or subchronic systemic effect from oral exposure to asbestos (Hall and Rumack, 2000). There are a number of toxicological endpoints for which there are no data in humans orally exposed to asbestos. These endpoints include death, immunotoxicity, neurotoxicity, reproductive or developmental effects, and genotoxicity (ATSDR, 1995).
Cancer
Epidemiological Data
Epidemiological data seem to be equivocal on the probability of an increase in cancer incidence in populations exposed to asbestos-fiber contaminated drinking water. A number of epidemiological studies have reported increases, some statistically significant, in cancer death or tumor incidence rates at one or more tissue sites (mostly gastrointestinal) in populations exposed to elevated levels (usually in the range of 1×106 to 3×108
fibers/L) of asbestos in their drinking water (Andersen et al., 1993; Conforti, 1983; Conforti et al., 1981; Howe et al., 1989; Kanarek, 1983, 1989; Kanarek et al., 1980; Levy et al., 1976; Polissar et al., 1982, 1984; Sigurdson et al., 1981; Toft and Meek, 1983; Toft et al., 1981, 1984; Wigle, 1977). A review of thirteen of these epidemiological studies in five areas of the U.S. and Canada concluded that the number of positive findings for neoplasms of the esophagus, stomach, pancreas, and prostate was unlikely to be due to chance alone (Marsh, 1983). Kanarek et al. (1980) noted that there were relatively consistent findings for increased stomach cancer and pancreatic cancer among the studies. The stomach is an obvious site for concern as the cancer rate at this site has been shown to be elevated in several studies of occupationally-exposed workers.
However, Cantor (1997), in a review of the evidence, concluded that the epidemiological drinking water studies were not adequate for quantitative risk assessment.
Following the findings of amphibole asbestiform fibers in the Duluth, Minnesota, municipal water in 1973, a number of epidemiological studies focusing on cancer risk were conducted to determine the toxicological risk posed by asbestos contamination in drinking water. Several studies covered asbestos contamination of industrial source water (Masson et al., 1974; Levy et al., 1976; Sigurdson et al., 1981) and natural source ASBESTOS in Drinking Water
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water (Conforti et al., 1981; Kanarek et al., 1980; Neuburger et al., 1984; Polissar et al., 1982, 1983a,b, 1984; Toft et al., 1981; Wigle, 1977). Others evaluated contamination of drinking water through asbestos cement distribution pipes (MacRae, 1988), or where water was collected from asbestos tile roof run-off (Andersen et al., 1993; Harrington et al., 1978; Howe et al., 1983; Meigs, 1983; Meigs et al., 1980; Millette, 1983; Millette et al., 1983; Sadler et al., 1984).
Some of these studies suggested elevated cancer incidence as a consequence of ingestion exposure (Andersen et al., 1993; Conforti et al., 1981; Kanarek et al., 1980; Polissar et al., 1982). Kanarek et al. (1980) found elevated peritoneal and stomach cancer in an ecological study of cancer incidence for 1969 to 1971 related to natural chrysotile fiber contamination of drinking water in the San Francisco Bay area. Conforti et al. (1981) found elevated digestive tract, esophageal, stomach, and pancreatic cancer incidence during 1969 to 1974 in an ecological study of the San Francisco Bay area. In both of these reports the study area was the San-Francisco-Oakland Standard Metropolitan Statistical Area (SMSA) and the unit of observation was the census tract. Polissar et al. (1982) found suggestive (elevated but not statistically significant) small intestine cancer when they examined natural contamination by chrysotile asbestos fibers in community water supplies in an ecological cancer incidence study from 1974 to 1977 in Washington’s Puget Sound area. Odds ratios for tumors of the small intestine were consistently elevated in both sexes, as were those for neoplasms of the thyroid, eye, testis and prostate in males. The increased risk of prostate cancer found in this study has also been found in the study by Wigle (1977). Although consistent in direction, most of the odds ratios for these sites are not statistically significant. Andersen et al. (1993) found elevated stomach cancer in a Norwegian cohort study of male lighthouse keepers who ingested drinking water collected from runoff over asbestos-cement roof tiles. The study population was confined to 690 men alive at the beginning of the follow-up period January 1, 1960. They were followed for cancer morbidity and total mortality to the end of 1991. The five-year age-specific incidence rates for each year from 1960-1991 were used to estimate the expected number of cancer cases. As all of the lighthouses are located in districts with a low population density, expected numbers are therefore based on rates of the rural Norwegian population.
Table 5 summarizes results from a number of these epidemiological studies. The associations summarized in Table 5 represent one or more epidemiological studies that have shown some relationship to asbestos in water for neoplasms of the following sites:
rectum (Mason et al., 1974), stomach (Mason et al., 1974; Levy et al., 1976; Wigle, 1977; Conforti et al., 1981), pancreas (Mason et al., 1974; Levy et al., 1976; Wigle, 1977; Meigs et al. 1980; Conforti et al., 1981), lung (Wigle, 1977), peritoneum (Conforti et al., 1981), esophagus (Conforti et al., 1981) and pleura (Conforti et al., 1981). All of these epidemiological studies, whether or not significant results were found, suffered major flaws or limitations. Many of the studies were ecological and thus had unknown or undocumented exposure; many were without size distribution characterization for the asbestos fibers (Conforti et al., 1981; Harrington et al., 1978; Kanarek et al., 1980; Masson et al., 1974; Meigs et al., 1980; Millette, 1983; Neuberger et al., 1984; Nicholson, 1983; Polissar et al., 1982; Sadler et al., 1984; Sigurdson et al., 1981; Toft et al., 1981; Valic and Beritic-Stahuljak, 1993; Wigle, 1977). Most of the studies did not measure personal risk factors or other potentially confounding factors so that exposureASBESTOS in Drinking Water California Public Health Goal (PHG) 41 September 2003
risk relationships could be adequately characterized. Studies of industrial contamination in Duluth (Masson et al., 1974) and natural contamination in the San Francisco Bay area (Kanarek et al., 1980) had their periods of mortality follow-up extended with inconsistent results between follow-up periods (Levy et al., 1976, and Sigurdson et al., 1981 for Duluth; Conforti et al., 1981 for the San Francisco Bay area). Other problems included too small a sample size or an inadequate cancer latency period. Although Levy et al. (1976) did not find an excess of gastrointestinal malignancies in Duluth residents through 1974, too few years had elapsed since the start of the oral amphibole exposure of the Duluth residents to draw any conclusions about risk. The paucity of positive findings from Connecticut (Harrington et al., 1978; Meis et al., 1980) could be due both to the low concentration of asbestos in the water, and the relatively short duration of exposure in some areas of the state (Craun et al., 1977). Another limitation of all the studies to date is that specific asbestos exposures are imputed to the population in an entire geographic region. There may be a confounding effect from other factors that vary geographically, and there may be misclassification of exposures due to recent in-migration into the study area (Polissar, 1980).
Because the evidence for the carcinogenicity of oral asbestos exposure in animals is equivocal, the question has arisen whether apparent increased cancer risk in some epidemiological studies indicates health effects of organic micropollutants accumulated by the fibers. Organic (and inorganic) chemicals clearly can bind to asbestos fibers. In vivo studies have shown that ingested amphibole fibers are genotoxic (e.g., Varga et al., 1996a,b). Inhalation studies clearly demonstrate the role of adsorbed polycyclic aromatic hydrocarbons in asbestos carcinogenesis (Hammond et al., 1979). The large surface area of the fibers creates the possibility of co-genotoxic action with adsorbed water-borne organics. Studies by Varga et al. (1998, 1999) have demonstrated that asbestos fibers are able to adsorb benzo[a]pyrene molecules from aqueous solutions, and consider potential co-genotoxicity of these materials. At present, data are inadequate to fully address this possible tumorigenic mechanism.
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Table 5. Summary of Studies of Cancer Risk from Asbestos in Drinking Water, by Neoplasm Site*
Area/First Author
Neoplasm
Site
Duluth/ Quebec/
Wigle
Connecticut/ California/
Conforti
Puget Sound/
Polissar
Mason Levy Harrington Meigs
Colon 00 00 00 00 00 00 00
Rectum MF 00 00 00 00 00 00
Stomach MF M0 M0 00 00 MF 00
Pancreas 0F MF 0F -- B MF 00
Lung -- -- M0 -- 00 00 00
Peritoneum -- 00 -- -- -- 0F --
Esophagus 00 00 -- -- -- MF 00
Gall
Bladder
00 00 -- -- -- 00 00
Pleura -- -- -- -- -- 0F --
Small
Intestine
-- 00 -- -- -- 00 MF
Brain -- -- 00 -- -- 00 MF
Leukemia -- -- 00 -- -- 00 MF
Thyroid -- -- -- -- -- 00 M0
Eye -- -- -- -- -- -- M0
Prostate -- -- M -- -- 00 M
*Table adapted from Polissar et al. (1982)
M= association in males (i.e. association between water asbestos levels and risk in one or both sexes); F= association in females; B= association in both sexes combined; 00= no association; -- = not studied.
Toxicological Effects in Humans: Inhalation and Other Exposures Acute, Subacute, and Chronic Noncancer Effects
Asbestos may cause irritation of the eyes, skin, and respiratory tract due to mechanical action of the fibers. There is no evidence of any acute or subchronic systemic effect from inhalation exposure to asbestos (ATSDR, 1995). Chronic exposure to asbestos through inhalation has been reported to cause various diseases including asbestosis, genotoxicity, and reproductive effects (Hall and Rumack, 2000). There have been a number of studies on immune system changes in humans exposed to asbestos by inhalation.
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Immunological and Lymphoreticular Effects
Research over the past three decades has shown that the human immune system can be altered directly or indirectly by occupational exposure to asbestos (Rosenthal et al., 1998). An immunogenetic predisposition towards developing asbestosis has been indicated (Rosenthal et al., 1998). Although the mechanisms are not well understood, the inhalation studies indicate that the immune system has been affected in individuals who have developed clinical signs of injury, such as asbestosis or cancer (DeShazo et al., 1983; Kagan et al., 1977a,b; Pernis et al., 1965; Sprince et al., 1991, 1992). Cell stress induced by crocidolite appears to injure cells via the production of the pro-inflammatory cytokine interleukin IL-8 (Tsuda et al., 1999).
Asbestos exposure has been associated with changes in both humoral and cellular immune functions in humans. For example, the chronic inflammatory response preceding the development of asbestosis represents a complex immunological process initiated by fiber deposition that involves multiple types of immune cells. This inflammatory response, along with evidence of peripheral immune changes following asbestos exposure, has long been implicated in the pathogenesis of asbestos-related disease (Rosenthal et al., 1999).
Asbestos exposures suppress pulmonary and systemic immunity, and alter host resistance to infectious agents or tumor cells. Impairment in cell-mediated immunity in humans by asbestos is characterized by decreases in delayed hypersensitivity responses, the numbers of circulating T cells, and T-cell proliferation (Rosenthal et al., 1999). Disturbances in cell-mediated immune responses are indicated by asbestosis patients’ impaired lymphocyte response to phytohaemagglutinin mitogen (Kagan et al., 1977a), as well as by low numbers of circulating peripheral blood leucocytes and T lymphocytes (Wagner et al., 1979). The responses of normal peripheral blood mononuclear cells, mainly the lymphoid nonadherent population, to phytohaemagglutinin are also depressed when exposed to asbestos in vitro (Barbers et al., 1982).
Effects on humoral immunity are also revealed by the increased prevalence of autoantibodies and elevations in serum immunoglobulin levels in these patients (Kagan et al., 1977b). Asbestosis patients present hyperactive T-cell responses. These are often manifested by elevations of serum immunoglobulins IgA, IgG, IgM, and IgE and secretory immunoglobin IgA, and the presence of autoantibodies such as antinuclear antibody and rheumatoid factor (Doll et al., 1983; Kagan et al., 1977b; Lange et al., 1974; Luster and Rosenthal, 1993; Pernis et al., 1965; Rosenthal et al., 1998).
Tsang et al. (1988) studied peripheral blood lymphocytes in 20 malignant mesothelioma patients, 375 long-term asbestos workers without neoplasia, and 118 healthy control subjects. The absolute numbers of total T cells and T helper cells were normal in asbestos workers without tumors; these cells were significantly reduced in cancer patients. On the other hand, T suppressor cells remained unchanged in cancer patients but were significantly elevated among the asbestos workers without neoplasia. This imbalance of T cell subsets resulted in a marked reduction in T helper to T suppressor ratio in mesothelioma patients and in asbestos workers (Tsang et al., 1988). The addition of chrysotile to human peripheral blood lymphocyte cultures, stimulated with concanavalin A and phytohaemagglutinin, resulted in a significant increase in the ASBESTOS in Drinking Water
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mitogenic response. The binding of the mitogen to the reactive sites on the lymphocyte surface is thought to be indispensable. Chrysotile and crocidolite fibers have been shown to stimulate and bind to immature B lymphocytes to go into mitosis, but not to mature B cells (Ueki et al., 1984).
In direct response to asbestos, the inflammatory cytokines interleukin IL-6 and IL-8 are produced by lung epithelial cells in vitro. This response is controlled by changes in the cellular oxidative state induced by iron present in the fiber through Fenton-type chemistry. As a result of this oxidative stress, the redox sensitive nuclear transcription factors (NF), NF-kappaB and NF-IL-6, which help regulate cytokine gene expression, are activated (Luster and Simeonova, 1998). In vitro exposures of macrophages, fibroblasts, alveolar epithelial cells, or pleural mesothelial cells to amosite, chrysotile, or crocidolite produce bioactive lipid chemokines, e.g., interleukin IL-8, or growth factor protein, e.g., platelet-derived growth factor (Driscoll, 1996).
Asbestos stimulation triggers cytokine release in vitro from both normal human monocytes and alveolar macrophages as determined by the upregulation of mRNAs for cytokines and activation of the p38 kinase, but there is a block in translation of cytokine mRNAs in the macrophages (Geist et al., 1999). Chrysotile or crocidolite upregulates expression of the urokinase-type plasminogen activator receptor on the surface of human mesothelial cells as indicated by binding of radiolabeled activator (Perkins et al., 1999).
Inhibition or delay of cytokinesis by chrysotile or crocidolite can result in bi- or trinucleation through the loss of midbody or intercellular bridge proteins that are required for completion of cytokinesis in human mesothelial cells (Jensen and Watson, 1999).
The production of proinflammatory cytokines such as TNF-alpha is an important mediator of the pathologic responses of asbestosis. Asbestos-induced TNF-alpha gene expression is mediated through a process that involves NF-kappaB activation and metalmediated free radical reactions. Exposures of lung macrophages to crocidolite in vitro cause increases in TNF-alpha production and NF-kappaB activation; this activation can be inhibited by NF-kappaB inhibitors and free radical scavengers (Cheng et al., 1999).
Chrysotile B fibers induce apoptosis of human peripheral blood mononuclear cells. The alteration of gene expression at the mRNA level during in vitro cultures reveals upregulation of Flice and Apaf-1 genes and downregulation of TNF receptor 1 and Bid genes. The process may be mediated by the Fas-related apoptotic pathway (Ma et al., 1999).
Genotoxicity
Chrysotile has been shown to induce an increased frequency of SCE in vitro. Therefore the effect of occupational exposure to chrysotile was evaluated on SCEs in 45 workers versus 45 controls in Korea. There was a marginally significant increase, after controlling for the effects of age and smoking by multiple regression analysis (Lee et al., 1999). Takahashi et al. (1997) studied the relationship between asbestos exposures and the level of 8-hydroxydeoxyguanosine (8-OHdG) in DNA of peripheral blood leukocytes as a biological marker of asbestos exposure in workers at a Chinese asbestos-material plant. Among the 20 workers and 19 controls in a large scale asbestos plant in China producing brake linings, asbestos rubber, and textiles using chrysotile, the geometric ASBESTOS in Drinking Water
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mean 8-OhdG level showed a positive gradient in relation to increasing grades of asbestosis (exposed worker 2.39, control 1.78, p = 0.01), with a significant difference between the control and definite-asbestosis subgroups (p<0.05). The authors concluded that the 8-OHdG level in leukocytic DNA is related to grade of asbestosis and may serve as a biologic marker reflecting the status of oxidative DNA damage by asbestos.
Oxidative DNA damage in man caused by exposure to asbestos has been judged to play a role in the formation of malignant tumors (Marczynski et al., 2000a, 2000b). The 8 hydroxy-2’-deoxyguanosine (8-OHdG) adduct level of asbestos-exposed workers was significantly increased (p < 0.001) compared to that in the control group in all three years of the study period between 1994 and 1997. DNA from white blood cells of the exposed group contained between 1.7 and 2.0 times the level of oxidative damage found in control samples (Marczynski et al., 2000b). A second study by Marczynski et al. (2000a) examined the association between the 8-OHdG levels in white blood cell DNA of workers highly exposed to asbestos fibers at the workplace and clinical data, occupational and non-occupational confounding factors, and cancer. The mean DNA-adduct level was significantly higher (p<0.01) for patients suffering from respiratory cancer, cancer of the GI, mouth/larynx/pharynx, and urogenital tract than for controls, but not significantly higher (p>0.05) than that for asbestos-exposed patients without tumors. The authors findings support the hypothesis that oxidative DNA damage in man caused by asbestos fibers plays a role in the formation of malignant tumors Molecular epidemiologic studies have associated asbestos exposure with a k-ras somatic mutation at the tumor suppressor loci p53 in adenocarcinoma of the lung. For the 84 male lung cancer patients evaluated by Nelson et al., (1999), the prevalence of mutation at k-ras codon 12 was higher among those with a history of occupational asbestos exposure after adjustment for age and pack-years of cigarettes smoked (adjusted odds ratio 6.8, 95 percent confidence interval 1.7 to 28.6). An index score that weights both the dates of exposure and the estimated intensity of exposure indicated that those with the mutation had significantly greater asbestos exposure than those without the mutation (Nelson et al., 1999). Mutations of the p53 gene were also detected in seven of 10 cases of lung adenocarcinoma in China (Fu et al., 1997).
Cancer
The carcinogenicity of inhaled asbestos is well established. A number of researchers have concluded that exposure to inhaled asbestos fibers leads to an increased incidence of tumors of the lung, mesothelial membrane in the coelomic cavity, esophagus, gastrointestinal tract, larynx, gastric cardia, breast, kidney, ovary, pancreas, tunica vaginalis, testis, and penis (Churg, 1988, 1998; Clemmesen and Jensen, 1981; Cocco et al., 1998; Doll and Peto, 1985; Edelman, 1988; Elmes and Simpson, 1971; Enterline and Kendrick, 1967; Finkelstein, 1983; Goodfellow et al., 1999; Goodman et al., 1999; Jarvholm, 1988; Kang et al., 1997; Karunaharan, 1986; Keal, 1960; MacLure, 1987; McDonald et al., 1971, 1980; McLure and Poole, 1990; Morgan et al., 1985; Ness and Cottreau, 1999; Newhouse and Berry, 1976; Newhouse and Wagner, 1969; Nicholson et al., 1982; Parent et al., 2000; Peto, 1980; Peto et al., 1982; Plas et al., 1998; Prescott et al., 1988; Raffn and Korsgaard, 1987; Raffn et al., 1996; Sali and Boffetta, 2000; ASBESTOS in Drinking Water
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Selikoff et al., 1964, 1979; Serio et al., 1992; Stell and McGill, 1973; Tyagi, 1989; Vasama-Neuvonen et al., 1999; Weiderpass et al., 1999). A rare case of malignant pericardial mesothelioma in a 27-year-old Japanese man suggests the involvement of asbestos exposure (Watanabe et al., 1999).
The carcinogenic effect of asbestos appears to require exposure of epithelial surfaces, such as in the lung, pleura, larynx, esophagus, peritoneum, and the continuation of the peritoneal lining into the scrotal sac. Fiber type and length seem to be the primary determinants of its disease-causing property (Boffetta, 1998). Schneiderman (1974), after conducting a literature review of digestive cancer among persons subjected to occupational inhalation of asbestos particles, concluded that human data show a doseresponse relationship between exposure to asbestos and subsequent development of gastrointestinal neoplasms.
Enterline and Kendrick (1967), as well as Newhouse and Wagner (1969) demonstrated an associated increase in gastrointestinal neoplasms with occupational exposure to asbestos.
They observed a large excess of gastrointestinal cancers, but not of other nonrespiratory cancers, in a study of U.S. asbestos workers. An excess of laryngeal cancer was also observed in some groups of exposed workers. Keal (1960) reported an association between asbestosis and abdominal neoplasms in workers. Asbestos workers exposed to crocidolite, amosite, chrysotile, or mixed fibers containing crocidolite, were reported to suffer an excess risk of gastrointestinal cancers (Selikoff et al., 1964). Doll and Peto (1985) reviewed the results of the Selikoff et al. (1964) study and subsequent studies by plotting the relative risks separately for gastrointestinal and other sites against the relative risk for lung cancer, which was used as a surrogate measure of intensity of asbestos exposure in the absence of adequate exposure data. Similar, yet weak, correlations were seen with lung cancer risk for both gastrointestinal and other cancers, excluding the Selikoff et al. (1964) results (Doll and Peto, 1985).
A number of researchers have reported increased incidences of colorectal cancer in workers exposed to asbestos (Albin et al., 1990; de Gerhardsson et al., 1992; Goldberg et al., 2001; Jakobsson et al., 1990; Kang et al., 1997; Raffn et al., 1996; Vineis et al., 1993). Some of these studies have reported quite high risks. In one recent case-control study by de Gerhardsson et al. (1992), a ninety percent excess risk of both colon and rectum cancers in men with exposure to asbestos was found. Jakobsson and colleagues (1990) found a fifty percent increased rate in the incidence of colorectal cancer among Swedish asbestos cement workers. Albin and coworkers (1990) found that colorectal cancer risks increased with cumulative exposure to mainly chrysotile asbestos. Although most of these studies entail exposures to men, Germani et al. (1999) found excess risks for colorectal cancer among Italian women compensated for asbestosis. Several other of these studies are discussed in more detail below.
Goldberg et al. (2001) in their population-based case-control study in Montreal, Canada, reported evidence of an increased risk of colon cancer in men exposed to asbestos (OR for “substantial” exposure (ORsubst) = 2.1). Workers with “substantial” exposure to asbestos had about a 2-fold increase in risk of colon cancer. The most common occupations with asbestos exposure were motor vehicle mechanics, welders and flame cutters, pipefitters and plumbers.
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Kang et al. (1997) found an association between asbestos exposure and some gastrointestinal cancer in 12 occupations with elevated proportionate mortality ratios (PMRs) for mesothelioma. Elevated PMRs for mesothelioma were used to identify occupations with potentially high exposure to asbestos. When high asbestos exposure occupations were analyzed as a group, the PMRs for esophageal, gastric, and colorectal cancer were significantly elevated at 108 (95 percent confidence interval 107 to 110), 110 (106 to 113), and 109 (107 to 110), respectively. A total of 15,524 cases of gastrointestinal cancer in the 12 occupations with elevated PMRs for mesothelioma were identified. However, a consistently elevated PMR for gastrointestinal tract cancer did not appear for each occupational group individually, and in particular for insulation workers, which comprised the highest PMR for malignant mesothelioma.
Frumkin and Berlin (1988) performed a meta-analysis of 31 cohort studies of asbestos workers and concluded that significant asbestos exposure, as indicated by a lung cancer standardized mortality ration (SMR) of at least 200, was associated with higher mortality from gastrointestinal cancer. The authors sought to use lung cancer SMR as a surrogate measure of asbestos exposure because prior research had found lung cancer SMR to be linearly related to dose levels in exposed cohorts (Liddell and Hanley, 1985). The metaanalysis by Homa et al. (1994) reported similar results for colorectal cancer stratified according to lung cancer SMR, but found no dose-response relationship with asbestos dust levels.
Henderson et al. (1975) found amphibole and chrysotile asbestos fibers in stomach tumors and adjacent gastric mucosa in Japanese men with oral exposure to chrysotile.
Not all of the tumor tissue examined contained asbestos fibers. The occupational history of the patients was not known. Other types of silicates, in addition to asbestos, were also found in some of the tissues.
Cavazza et al. (2001) described the case of a sixty-three year old male with a history of exposure to asbestos who developed a gastric lymphoma, and later went on to develop bronchiolitis obliterans organizing pneumonia (BOOP) with asbestos bodies.
Adenomatous polyps of the colon are generally accepted as precursor lesions for most cases of colorectal carcinoma. Neugut et al. (1991) conducted a case-control study of colorectal neoplasia on male subjects aged 35 to 84 years who underwent colonoscopy.
The study consisted of 51 colorectal cancer case patients, 153 adenomatous polyp case patients, and 195 control subjects. All biopsy specimens were reviewed by the study pathologist. A questionnaire was used to ascertain each subject’s degree of exposure to asbestos. Although the sample sizes were small for both case groups, an elevated risk for adenomatous polyps and colorectal cancer was observed for those subjects with a history of significant exposure to asbestos.
A number of studies (Enterline et al., 1987; Maclure, 1987; Mandel et al., 1995; Mattioli et al., 2002; McLaughlin et al., 1996; Selikoff et al., 1979; Smith et al., 1989) have reported an association between occupational asbestos exposure and renal cell carcinoma (RCC). In the largest case-control study of renal cancer to date, involving six study centers from five countries (the United States, Australia, Denmark, Germany and Sweden), 1732 incident RCC cases among men and women aged 20-79 years of age, and 2309 controls were interviewed (Mandel et al., 1995). The authors found significant ASBESTOS in Drinking Water
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excess risks for RCC and exposure to asbestos (RR, 1.4; 95% CI 1.1-1.8). McLaughlin et al. (1996) considered the association of asbestos and RCC development to be the most consistently observed occupational link. These findings were supported by a prospective mortality study of almost 1 million patients. Mattioli et al. (2002), in their hospital-based case-control study in Bologna, Italy, reported that exposure to asbestos was associated with an elevated risk of RCC in males (OR, 7.11; ninety five percent CI, 1.46-34.51), irrespective of occupation. In historical cohort studies, asbestos products workers have shown significantly elevated mortality rates for kidney cancer (Enterline et al., 1987).
The link between asbestos exposure and RCC is supported by findings of asbestos fibers in the kidneys (Huang et al., 1988; Pollice et al., 1997) and urine (Finn and Hallenbeck, 1985; Guillemin et al., 1989) of exposed workers. Fibers types in most of these studies, where identified, were mostly chrysotile, although Huang et al. (1988) reported finding amosite, anthophyllite, tremolite and actinolite in extrapulmonary tissues of several autopsy cases. These subjects were from Japan. Intratubular epithelial dysplasia has been recognized as the most common precursor of RCC. For this reason, and because of the adverse effects on the kidney seen in the Cemerikic (1977) oral asbestos study in rats, investigation into the nature of premalignant lesions of the kidney appears a relevant issue.
Mesothelioma has been reported in children in the U.S., Austria, Brazil, Canada, Czechoslovakia, Denmark, France, Germany, India, Israel, Italy, Poland, Romania, Spain, Turkey, USSR, and Taiwan (Brenner et al., 1981; Fraire et al., 1988; Kauffman and Stout, 1964; Lin-Chui et al., 1989; Wassermann et al., 1980). The possible involvement of asbestos in these rare cases of mesothelioma in infancy and childhood suggests the possibility of transplacental transfer of asbestos from mother to fetus (Fraire et al., 1988; Wassermann et al., 1980). A pleural mesothelioma was reported in a 19 month-old infant (Reals et al., 1950). A congenital papillary peritoneal mesothelioma was found in a six-week-old infant (Siberstein et al., 1985). A three-year-old daughter of a ceramics engineer who worked in a Pennsylvania insulation plant handling chrysotile and amosite was diagnosed with pleural mesothelioma (Lieben and Pistawka, 1967). A 17-year-old Texas girl with asbestos exposure earlier in school in Ohio was reported with pleural mesothelioma (Fraire et al., 1988). Stein and Henker (1986) reported a case of mesothelioma of the testicle in a child.
Gender-related differences in the distribution of thoracic versus abdominal malignant mesothelioma (MM) have been observed (Delfino et al., 1995). The age-adjusted rate ratio for male/female abdominal MM was 1.5 (95 percent confidence interval, 0.6-3.6).
The findings suggest that peritoneal and retroperitoneal mesotheliomas in women may be due primarily to nonoccupational asbestos exposure, and potentially, background disease would be better represented by women than men. This view is supported by the finding of a higher mean age of men with thoracic versus abdominal MM and a similar, but nonsignificant, difference in women.
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DOSE-RESPONSE ASSESSMENT
Noncarcinogenic Effects
A number of noncarcinogenic effects have been reported in laboratory animal studies.
Noncarcinogenic effects of asbestos include: potential genotoxicity, adverse effects on the gastrointestinal system (Corpet et al., 1993; Delahunty and Hollander, 1987; Jacobs et al., 1977, 1978a), immune system (MacDonald and Kane, 1993; Moalli et al., 1987) kidney (Cemerikic, 1977), and body weight (NTP, 1990b). Most of these studies are inadequate for risk assessment purposes due to incomplete/missing data, the use of experimental exposure routes, and/or the lack of a frank effect. In the case of the NTP (1990b) study, the authors concluded that the marked decreases in body weight, which persisted over the course of the animals’ lifetime, did not adversely affect survival.
In many instances, the effect of oral asbestos exposure on individual tissues/organ systems has not been studied. No studies were located regarding the respiratory, cardiovascular, musculoskeletal, hepatic, endocrine, dermal, ocular, metabolic or other systemic effects in animals after oral exposure to asbestos (ATSDR, 1995; HSDB, 2000).
In the literature search, no studies have been located regarding death in animals after acute, intermediate, or chronic oral exposure to asbestos.
Cemerikic (1977) exposed male and female Wistar rats (7/sex) to chrysotile asbestos in drinking water for 12 to 15 weeks. The ten male and seven female controls received tap water. A suspension of asbestos fibers in drinking water was prepared by shaking 2.5 g of chrysotile asbestos in 500 mL of water; this was allowed to settle for 30 minutes and the top 250 mL, which contained about 9.4x109 (1 mg) fibers/mL was drawn off (the technique of Pontefract and Cunningham, 1973). Because fibers could continue to settle out, the fiber concentration and dose actually delivered to the animals cannot be accurately estimated; it might be higher or lower, depending on the design and orientation of the water bottles and drinking tubes. Females were sacrificed after 12 weeks and males after 15 weeks. The organs were measured and the kidneys and bladders examined histopathologically. Pathologic presence of red blood cells and hyaline casts in the urine sediment of four males indicated damage to the kidneys. Kidneys of experimental females showed only discrete perivascular infiltration. A marked increase of indirect pressure, evidence of hypertension, was found in exposed females after 6 and 12 weeks, compared with controls. U.S. EPA (1988c) has estimated that mature male Wistar rats consume 0.032 L/day of drinking water, and females 0.025 L/day. The level at which adverse effects were seen in the kidneys of the male rats was about 107 mg/kg-day ((1 mg/mL x 32 mL/day)/0.3 kg) and in females was about 167 mg/kg-day ((1 mg/mL x 25 mL)/0.15 kg), based on their body weights at the start of the exposures.
The other animal studies showed non-cancer effects at higher doses or with more poorlydefined experimental paradigms. The NTP (1990b) chronic rat feeding study, for example, showed only decreased body weight gain at 500 mg/kg-day. The Cemerikic (1977) study was chosen for derivation of a non-cancer PHG because the route of exposure was via drinking water and was of subchronic duration (3 months). A number of human studies have reported that occupational exposure to asbestos has been linked to ASBESTOS in Drinking Water
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adverse effects on the kidney, and in particular, to an increased risk of renal cell carcinoma (RCC) (Enterline et al., 1987; Maclure, 1987; Mandel et al., 1995; Mattioli et al., 2002; McLaughlin et al., 1996; Selikoff et al., 1979; Smith et al., 1989). Other researchers (Gibel et al., 1976) have reported statistically significant increases in malignant tumors of the kidney in rats fed an asbestos filter material (20 mg/day) containing fifty-three percent chrysotile asbestos. In contrast to many genitourinary malignancies, very little data are available in the scientific literature concerning premalignant alterations in the kidney (e.g. intratubular neoplasia), and there are no data on the epidemiology of premalignant lesions of the kidney. In light of the known associations between asbestos exposure and kidney effects in humans, the adverse kidney effects seen in the Cemerikic (1977) study may represent an early (premalignant) event following exposure to ingested asbestos.
Carcinogenic Effects
Carcinogenic potency of asbestos fibers depends on mechanical stability and durability, insolubility in aqueous solution, fiber strength, fiber length, fiber diameter, fiber geometry, chemical composition, surface reactivity, and biopersistence of the fiber (IARC, 1996; McDonald, 1998). Asbestos carcinogenesis appears to be a multistage process even though the exact molecular mechanisms leading to the development of cancer after asbestos exposure are poorly understood (Abidi et al., 1999; Kamp and Weitzman, 1999). The consensus of a group of invited experts (IARC, 1996) was that asbestos carcinogenesis may be initiated by the ability of fibers to cause:
1) altered expression or function of key genes arising from genetic or epigenetic alterations with enzyme imbalance;
2) altered cell proliferation;
3) altered regulation of apoptosis and immune responses at molecular levels; or 4) chronic, persistent inflammation.
In the IARC report, Kane et al. (1996) summarized five proposed mechanistic hypotheses for fiber carcinogenicity as:
1) fibers generate free radicals that damage DNA;
2) fibers interfere physically with mitosis;
3) fibers stimulate proliferation of target cells;
4) fibers provoke a chronic inflammatory reaction leading to prolonged release of reactive oxygen/nitrogen species from macrophages; or
5) fibers act as co-carcinogens or carriers of chemical carcinogens to the target tissue.
Further research is needed to elucidate evidence in favor of or against any of these proposed mechanisms.
The carcinogenic potency of asbestos by inhalation can readily be derived from epidemiologic data. However, the estimation of oral potency is more complicated. The NAS estimated oral cancer risk from inhalation studies of asbestos workers (NAS, 1983).
These studies and increased cancer rates are shown in Table 6. The potency calculations ASBESTOS in Drinking Water
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involved a series of steps including estimation of the proportion of inhaled particles deposited in the lung, cleared, and swallowed. The proportion was assumed to be 0.3, based on animal models (Evans et al., 1973; Morgan et al., 1975), plus a human model (Dement and Harris, 1979) that estimated that 28 percent of inhaled chrysotile fibers are deposited in the lung. The models assumed that no asbestos is directly swallowed, and that virtually all deposited fibers are eventually cleared. Because of the change in methods of quantitating asbestos fibers, a conversion factor was also needed to estimate the potency based on the older data using light microscopy, versus the newer data using TEM. TEM was assumed to be about 50 times as sensitive, based upon the work of Lynch et al. (1970).
Based on these assumptions, a relative risk of gastrointestinal tract cancer for a person who has swallowed inhaled asbestos fibers was calculated by NAS. These calculations indicated that lifetime ingestion of 1.1×106
TEM fibers/L of water corresponded to an
excess gastrointestinal tract cancer risk of 10-4.
Unfortunately, OEHHA was not able to provide an audit trail on all the figures used by NAS (1983) in their calculations. Indeed, the NAS (1983) reported that "The committee adjusted the relative risks to refer only to gastrointestinal cancer" and "shows estimates derived either from the published studies or from personal communication with the authors." Lacking the ability to confirm the values and assumptions used by the NAS in their evaluation of the five occupational inhalation studies, OEHHA considers the reported evaluation to be too unreliable to use in establishing a PHG. In addition, the complex calculations and multiple assumptions make it difficult to duplicate the analysis, and would provide a relatively weak basis for a quantitative risk assessment.
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Table 6. Results of Five Cohort Studies of Gastrointestinal Tract Cancers in Asbestos Workers (Abstracted from NAS (1983), Table III-2) Exposed
groups
Cancer
site
codes a
Deaths Ratio
O/E
RR b Reference
Observed
(O)
Expected
(E)
U.S. and
Canadian
insulation
workers
150-154 94 59.4 1.58 1.58 Selikoff et al.,
1979
New York and
New Jersey
insulation
workers
150-154 43 15.1 2.85 2.85 Selikoff et al.,
1979
U.S. factory
workers
150-154 32 21.5 1.49 1.49 Seidman et al.,
1979; U.S.
EPA, 1979
London factory
workers
150-158c 40 34.0 1.18 1.32 Newhouse and
Berry, 1979
U.S. factory
workers
150-159c 55 39.9 1.38 1.55 Henderson and
Enterline, 1979
a 150 = esophagus, 151 = stomach, 152 = small intestine, 153 = large intestine, 154 = rectum, 155 = liver, 156 = gallbladder, 157 = pancreas, 158 = retroperitoneum and peritoneum, 159 = gastrointestinal tract, not otherwise specified. b Standardized mortality ratio = 100 × RR (relative risk) for cancer site codes 150-154. c Excluding mesotheliomas.
U.S. EPA has concluded that the animal studies provide the best data for cancer risk estimation from ingestion exposure (U.S. EPA, 1988b). Animal toxicology, based upon the NTP (1985) chronic feeding studies, was used to estimate excess human cancer risk at the 10-6 level as approximately 7.1 MFL or 7.1×106
fibers/L by the U.S. EPA (1991a) for
asbestos fibers exceeding 10 µm in length. An elevated risk for adenomatous polyps and colorectal cancer has also been observed in human subjects with a history of exposure to asbestos (Neugut et al., 1991). OEHHA concurs that this approach provides the most credible method to calculate the human risk from oral exposures to asbestos in drinking water. These calculations are shown in the derivation of the PHG for carcinogenic effects below.
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CALCULATION OF PHG
Noncarcinogenic Effects
Based on a subchronic study in rats by Cemerikic (1977), a LOAEL of 107 mg/kg-day (1x1012 fibers/kg-day) for nephrotoxicity was selected for calculation of a public healthprotective concentration for noncarcinogenic effects of asbestos in drinking water.
Calculation of a health-protective concentration (C, in mg/L) for noncarcinogenic endpoints follows the general equation:
C = LOAEL × BW × RSC
UF × Leq/day
where,
LOAEL = lowest-observed-adverse-effect level (kidney effects); BW = adult body weight, a default of 70 kg for adults;
RSC = relative source contribution (a default of 20 percent to 80 percent); UF = combined uncertainty factor (typical defaults are 10 for estimation of a NOAEL from a LOAEL, 10 to account for the uncertainty in interspecies extrapolation, and 10 for human variability); and Leq/day = adult daily water consumption rate (a default rate of 2 L/day, plus additional equivalent amounts where applicable to account for inhalation and dermal exposures from use of contaminated tap water.
It was assumed for the calculation that other sources of asbestos would be significant, so a 20 percent (0.2) default relative source contribution of asbestos from drinking water was chosen. Uncertainty factors of 10 each would be applicable to account for extrapolation of a LOAEL to a NOAEL, interspecies extrapolation, and human variability. In addition, an uncertainty factor of 3 was applied to account for subchronic to chronic study duration extrapolation. We interpret this as requiring the maximum uncertainty factor of 3,000, in accordance with U.S. EPA (1991c, 2002) guidelines and theoretical considerations (Gaylor and Kodell, 2000).
C = 107 mg/kg-d x 70 kg x 0.2 = 0.25 mg/L (250 µg/L)
3,000 x 2 L/d
Thus the public health protective concentration for asbestos in drinking water based on noncarcinogenic effects is estimated to be 250 µg/L, which is equivalent to 2.4x109 fibers/L, or 2400 MFL at the indicated fiber concentration of 9.4x109 fibers/mg.
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Carcinogenic Effects
Risk Estimate Based on Human Inhalation Data
Since there are no human studies in which ingestion of a known amount of asbestos can be associated with a clear increase in gastrointestinal cancer risk, NAS (1983) extrapolated data on gastrointestinal risk from epidemiological studies of workers exposed to asbestos by inhalation. The NAS calculations indicated that lifetime ingestion of 1.1×106
TEM fibers/L of water corresponded to an excess gastrointestinal tract cancer risk of 10-4 (NAS, 1983). This is equivalent to a 10-6 excess cancer risk level of
0.01 MFL or 1×104 fibers/L for oral exposures. However, the NAS risk assessment is difficult to follow, and impossible to reproduce. The difficulties are based in part on their undocumented personal communications with authors of some of the five studies. Other considerations include the nature of the occupational cohort studies used to determine the potency, with difficulties in estimation of inhalation exposures and calculation of oral doses. In addition, many of the assumptions used to derive the potency estimate (e.g. that no inhaled asbestos is directly swallowed, and that virtually all deposited fibers are eventually cleared) have been shown to be incorrect. OEHHA considers the NAS potency estimate based on inhalation studies to be too problematic to use in establishing a PHG.
The U.S. EPA, in its cancer risk evaluation (1991a, 1994) chose to use the rat NTP study for determination of safe drinking water levels, although in its IRIS file it has declined to identify any oral risk level (U.S. EPA, 2000). The ATSDR (1995) also selected the NTP (1995) study as the most appropriate basis for a risk estimate, without commenting upon the much lower extrapolations from occupational inhalation studies.
OEHHA acknowledges the 700-fold more potent risk assessment based on the earlier NAS evaluation, but concurs with the U.S. EPA and ATSDR that the rat oral exposure data (NTP, 1985) provide a more suitable basis for estimating a public-health-protective level of asbestos in drinking water. The human occupational studies indicating excess risk of gastrointestinal cancer from inhalation exposures to asbestos are considered to provide a supporting qualitative basis for concern about total exposures to asbestos.
Risk Estimate Based on Animal Data
In a lifetime feeding study in rats, exposure to intermediate length chrysotile fibers (65 percent > 10 µm in length) led to an increased incidence of intestinal polyps in the large intestine of male rats (NTP, 1985). The incidence of these benign epithelial neoplasms (9/250, 3.6 percent) was significantly increased (p = 0.003) compared to the incidence of combined benign and malignant epithelial neoplasms of the large intestine in the pooled control groups (male) of all the NTP oral asbestos lifetime studies. The approach shown below, including interspecies extrapolation, follows that used in the U.S.
EPA (1988b) Drinking Water Criteria Document for Asbestos, pp. VIII-11 through VIII15:
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In the NTP (1985) study, asbestos fibers were mixed into the diet rather than suspended in the drinking water. This presumably provides a more uniform exposure, but requires the assumption that the asbestos in the dry diet would have the same effect as asbestos in water. A single dose of one percent asbestos (by weight) was used, estimated to be equivalent to 500 mg/kg-day.
Based on measurements of transmission electron microscope (TEM) performed at the Illinois Institute of Technology Research Institute, the fiber counts were about
0.129 x 109 f/mg with a median fiber aspect ratio (length divided by diameter) of 8.435 (NTP, 1985). The daily dose of asbestos can be recalculated in terms of fiber exposure as:
500 mg/kg x 0.129x109 f/mg = 6.45x1010 f/kg
In order to determine human equivalent dose, the U.S. EPA procedure has been to assume dosage equivalency on a dose/surface area basis. This is roughly equal to equivalency on a dose/(body weight)2/3. Thus, the equivalent dosage for a 70 kg human, calculated from the average dose in a 0.38 kg rat, is:
(6.45x1010 f/kg)/(70/0.380)1/3 = 1.13x1010 f/kg
A 70 kg human is assumed to drink 2 liters of water/day. The f/kg dose can be restated in terms of drinking water concentration as:
1.13x1010 f/kg x 70 kg/2 L = 4.0x1011 f/L
Since there was only a control and one dose level, the usual linearized multistage model is reduced to a single dose or one-hit model. U.S. EPA, using the standard multistage model, has determined the maximum likelihood estimate (MLE) of potency to be:
q1 = 7.7x10-14 (f/L)-1
with a 95 percent upper-limit potency of:
q1* = 1.4x10-13 (f/L)–1
The health protective concentration is calculated for a one in one million cancer risk level as:
C = R = 10-6 = 7.1x106
f/L
q1* 1.4x10-13 (f/L)–1
For a lifetime individual risk of gastrointestinal cancer of one in a million, the 95 percent lower confidence limit on concentration of asbestos fibers in drinking water is therefore
7.1x106
f/L for asbestos fibers exceeding 10 µm in length. This value is more healthprotective than the noncancer risk level estimated above, and therefore should be protective against all noncancer effects. The PHG is rounded to 7x106 f/L, also expressed as 7 MFL.
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RISK CHARACTERIZATION
Epidemiological studies of the risk associated with ingestion of asbestos in drinking water, either by themselves or in the aggregate, are unsatisfactory for quantitative risk evaluation. Most of these studies are ecological in design, and hence lack individual measures of exposure. Consumption exposures are assumed due to contamination of municipal drinking water. These studies cover natural contamination, contamination through industrial pollution, and contamination through the use of asbestos-cement distribution pipes. Often the duration and level of contamination is not known. In addition, the asbestos fibers are not well characterized by size distribution.
Given the problems associated with this data source, other studies must be relied upon to provide a basis for risk assessment. These other studies involve extrapolation across exposure modalities or extrapolation across species.
Human inhalation exposure has provided one basis for extrapolating to oral particle exposure because the inhaled particles deposited in the lungs are cleared through the mucociliary escalator and swallowed (Evans et al., 1973). Other processes, including migration of fibers through mucosal and other tissues (Pontefract and Cunningham, 1973; Westlake et al., 1965), and blood or lymphatic transport of fibers away from the site of entry (Kanazawa et al., 1970; Roe et al., 1967), have been experimentally established (Amacher et al., 1974; 1975). Gastrointestinal tract cancer is the most likely target carcinogenicity endpoint. The U.S. EPA has based one model of carcinogenic risk for ingested asbestos on data from occupational inhalation cohort studies. This work is presented in a National Research Council (NAS, 1983) analysis of five worker cohorts presented in four reports (Selikoff et al., 1979; Seidman et al., 1979; Newhouse and Berry, 1979; Henderson and Enterline, 1979; see also Seidman, 1984) (see Table 6).
Based upon these five studies, NAS (1983) established a 10-6 excess cancer risk level as
0.01 MFL or 1×104
fibers/L for oral exposures.
However, for its regulatory standards, the U.S. EPA has relied on an extrapolation from the NTP (1985) chronic rat study. OEHHA has also chosen this approach because it is a more straightforward risk assessment. The NTP (1985) study in rats found “some evidence of carcinogenicity” in male rats exposed to intermediate range (IR) chrysotile asbestos as indicated by an increased incidence of adenomatous polyps in the large intestine (9/250, 3.6 percent). Although not statistically significant compared with concurrent controls, the incidence of these neoplasms was highly significant (P=0.003) when compared with the incidence of epithelial neoplasms (benign and malignant combined) of the large intestine in the pooled male control groups of all the NTP oral asbestos lifetime studies. The biologic significance of this finding was supported by the observation of lesions of similar morphology in the small intestine or glandular stomach of four additional IR chrysotile male rats, whereas none were found in the concurrent control group. NTP concluded that the observed effect in the large intestine of the male IR chrysotile asbestos group was “quite unlikely to be due to chance alone,” because adenomatous polyps are uncommon in standard 2-year carcinogenesis studies. It is noteworthy that the other NTP asbestos studies were carried out at the same laboratory, conducted using an overlapping time frame, and used animals that were received from the same source and exposed to the same environmental conditions. The post-mortem ASBESTOS in Drinking Water
California Public Health Goal (PHG) 57 September 2003