| Author |
Message |
Linda Asberry
Moderator
Username: Linda
Post Number: 20
Registered: 12-2000
| | Posted on Wednesday, May 08, 2002 - 6:39 pm: | |
After having read this entire thread it strikes me that some of us have failed to consider a frailty common among us--we are human. It also appears that there are those of among us who are answering questions posed to the best of their ability and we must remember that everything written has not be placed on-line. If one among us has the inclination to educate themselves to the level of a microbiologist, then be my guest but don't criticize someone for providing the information they hold and generously provided. Thanks for taking the time and effort to provide the information Mr. Cook.
I have done much research on my own, attended classes and listened to those wiser than I, as I am sure Andy Sloane, William Cook and others have. You can't answer some questions with 50 words or less. There simply is far too many variables. Some antibiotics can and do save lives but some components of those same antibiotics can cause an allergic reaction in others who can potentially die from shock. We are not scientists--we are adjusters following instructions from our superiors, applying dollars to covered losses under an indemnity policy-not a repair policy and not a health policy.
As one who is adjusting water losses with ensuing damages of mold and other fungi, I don't believe in the "pro" or "anti" mold factions. I believe in what we Texans term, "good old fashioned common sense." For individuals who are physically compromised, either due to infancy with undeveloped respiratory systems, the aged, and those with deficient immunities, there is a very real risk to their continued health from continued exposure to some allergens.
I would hope and expect more from all of us as professionals.
If anyone takes exception to what I have said, my personal email is available on CADO.
|
mark salmon
Registered User
Username: Olderthendirt
Post Number: 176
Registered: 12-2000
| | Posted on Wednesday, May 08, 2002 - 11:25 am: | |
Jim, Andrew was right about the housekeeping, not uncommon to get losses where the water leak occured weeks or months before the claim was reported, amazing how often the insured did nothing, except mayby threw a cloth on the water on the floor and dabbed, then after watching the mold grow, phones the insurer. On the other side, a broken hot water line can result in visible mold in under 48 hours. Worst case insured goes away for the weekend, and returns to find a supply line break, with the green fuzzies and slimy black fuzzies growing. Amazing colors sometimes. I have seen whole familys off to the Doctors and sick with a small amount of mold (New York level 2 or 3) and others living in a house with no problems and with the mold everywhere. When the hype settles down (in a year or two) we will still deal with the covered losses but with knowledge and sense. And if you want a guess as to who is getting the best $$$ for the mold I would say the remediation contractors. Just a thought, when that Cat 4 blows through Florida this year, you better know something about mold. And one last tip for the moldy guys and gals, never make a decision, thats the job of the company people, and have then put it in writing on your file. Just some thoughts, now back to the two piles of paper that have piled up since Monday morning. |
Jim Flynt
Registered User
Username: Jimflynt
Post Number: 286
Registered: 6-2001
| | Posted on Wednesday, May 08, 2002 - 11:05 am: | |
Memo to Bill and Wong: Everything posted in the earlier post concerning ACGIH® (The American Conference of Governmental Industrial Hygienists) seems to me at least, to be totally irrelevant to any meaningful discussion of mold, toxins, and mold exposures. It was not worth the reading as it contains nothing of import.
We would all be better served if such nonsense could be provided here through a hyperlink.
And if you disagree with my conclusion, then try to tell us what that article said in 50 words or less, and if you can't, you make my point.
At least one US Congressman agrees that ACGIH standards are scientifically unfounded and several noted scientists and university professors have weighed in with agreeing opinions. A US Court of Appeals has declared that OSHA cannot accept ACGIH standards as their own.
I find it interesting that Bill Cook did not post a copy of Congressman Charlie Norwood's letter to the US Secretary of Labor concerning his conclusions about ACGIH.
(Message edited by jimflynt on May 08, 2002)
(Message edited by jimflynt on May 08, 2002)
(Message edited by jimflynt on May 08, 2002) |
Jim Flynt
Registered User
Username: Jimflynt
Post Number: 285
Registered: 6-2001
| | Posted on Wednesday, May 08, 2002 - 10:56 am: | |
Memo to Andrew Sloan:
Perhaps you can shed a little more light on several of the comments you made in your earlier posting.
To wit, please explain your comment about "poor housekeeping" and what role it plays in the claims you are handling and damages you have seen.
Describe the 'typical' water loss you encounter in your day to day handling of mold claims? What was the water loss causation? Was it sudden and accidental or rather from long term leakage or a deferred maintenance problem? Describe more fully your comment "(water loss) improperly taken care of".
Please tell us what role the "petro-chemical pollution" you mentioned plays in either the claim or the insured's loss.
Finally, are you the first adjuster handling these specific claims or adjuster # 3, 4 or 5? If it is the latter, please explain what the other adjusters did right or wrong in handling the claim up until the file was turned over to you.
Thanks for any follow-up sharing of information which you can provide.
|
D Wong Whey
Registered User
Username: Dwongwhey
Post Number: 129
Registered: 10-2001
| | Posted on Wednesday, May 08, 2002 - 10:39 am: | |
Bill, wouldn't it be easier and more appealing to the eye if you just provided hyperlinks to these rather lengthy articles?
The last post goes on and on without providing anything new or interesting. Since they have taken the liberty of trademarking and registering their own words and phrases, it is unlikely that those terms will ever be regarded by the rest of the scientific community as useful and meaningful.
We will never arrive at anything approaching the truth as long as the practice is to throw as much BS against the wall and hope that some of it sticks.
Let's get back to the basics and as Sgt. Joe Friday used to say, just give me the facts Ma'am. |
Dave Dehlinger
Member
Username: Davey
Post Number: 5
Registered: 1-2001
| | Posted on Wednesday, May 08, 2002 - 9:06 am: | |
Bill
Most of us would agree that it's counterproductive to make fun of those who are genuinly concerned about their health and the mold problems. However, what gets to us is the way some of your brethern, remediation contractors, and attornies have created a mass hysteria situation, for their own gain, not the good of the policy holder. Granted, some of the PH are going for the gold too with the health issues way in the background. It's all about $, and nothing more.
Come into the light. You know what they say about the darkness, we'll soon start calling you a mushroom and feeding you bull----. |
William S. Cook
Registered User
Username: Wscook
Post Number: 48
Registered: 1-2001
| | Posted on Wednesday, May 08, 2002 - 8:59 am: | |
Statement of Position Regarding the TLVs® and BEIs®
The American Conference of Governmental Industrial
Hygienists (ACGIH®) is a private not-for-profit,
nongovernmental corporation whose members are industrial
hygienists or other occupational health and safety
professionals dedicated to promoting health and safety
within the workplace. ACGIH® is a scientific association.
ACGIH® is not a standards setting body. As a scientific
organization, it has established committees that review the
existing published, peer-reviewed scientific literature.
ACGIH® publishes guidelines known as Threshold Limit Values
(TLVs®) and Biological Exposure Indices (BEIs®) for use by
industrial hygienists in making decisions regarding safe
levels of exposure to various chemical and physical agents
found in the workplace. In using these guidelines,
industrial hygienists are cautioned that the TLVs® and
BEIs® are only one of multiple factors to be considered in
evaluating specific workplace situations and conditions.
Each year ACGIH® publishes its TLVs® and BEIs® in a book.
In the introduction to the book, ACGIH® states that the
TLVs® and BEIs® are guidelines to be used by professionals
trained in the practice of industrial hygiene. The TLVs®
and BEIs® are not designed to be used as standards.
Nevertheless, ACGIH® is aware that in certain instances the
TLVs® and the BEIs® are used as standards by national,
state, or local governments.
Governmental bodies establish public health standards based
on statutory and legal frameworks that include definitions
and criteria concerning the approach to be used in
assessing and managing risk. In most instances,
governmental bodies that set workplace health and safety
standards are required to evaluate health effects, economic
and technical feasibility, and the availability of
acceptable methods to determine compliance.
ACGIH® TLVs® and BEIs® are not consensus standards.
Voluntary consensus standards are developed or adopted by
voluntary consensus standards bodies. The consensus
standards process involves canvassing the opinions, views
and positions of all interested parties and then developing
a consensus position that is acceptable to these parties.
While the process used to develop a TLV® or BEI® includes
public notice and requests for all available and relevant
scientific data, the TLV® or BEI® does not represent a
consensus position that addresses all issues raised by all
interested parties (e.g., issues of technical or economic
feasibility). The TLVs® and BEIs® represent a scientific
opinion based on a review of existing peer-reviewed
scientific literature by committees of experts in public
health and related sciences.
ACGIH® TLVs® and BEIs® are health-based values. ACGIH®
TLVs® and BEIs® are established by committees that review
existing published and peer-reviewed literature in various
scientific disciplines (e.g., industrial hygiene,
toxicology, occupational medicine, and epidemiology). Based
on the available information, ACGIH® formulates a
conclusion on the level of exposure that the typical worker
can experience without an unreasonable risk of disease or
injury. The TLVs® and BEIs® are not quantitative estimates
of risk at different exposure levels or by different routes
of exposure.
Since ACGIH® TLVs® and BEIs® are based solely on health
factors, there is no consideration given to economic or
technical feasibility. Regulatory agencies should not
assume that it is economically or technically feasible for
an industry or employer to meet TLVs® or BEIs®. Similarly,
although there are usually valid methods to measure
workplace exposures at TLVs® and BEIs®, there can be
instances where such reliable test methods have not yet
been validated. Obviously, such a situation can create
major enforcement difficulties if a TLV® or BEI® was
adopted as a standard.
ACGIH® does not believe that TLVs® and BEIs® should be
adopted as standards without an analysis of other factors
necessary to make appropriate risk management decisions
(e.g., control options, technical and economic factors,
etc.). However, ACGIH® does believe that regulatory bodies
should consider TLVs® or BEIs® as valuable input into the
risk characterization process (hazard identification, dose-
response relationships, and exposure assessment).
Regulatory bodies should view TLVs® and BEIs® as an
expression of scientific opinion.
ACGIH® is proud of the scientists and the many members who
volunteer their time to work on the TLV® and BEI®
Committees. These experts develop written Documentation
that include an expression of scientific opinion and a
description of the basis, rationale, and limitations of the
conclusions reached by ACGIH®. The Documentation provides a
comprehensive list and analysis of all the major published
peer-reviewed studies that ACGIH® relied upon in
formulating its scientific opinion. Regulatory agencies
dealing with hazards addressed by a TLV® or BEI® should
obtain a copy of the full written Documentation for the
TLV® or BEI®. Any use of a TLV® or BEI® in a regulatory
context should include a careful evaluation of the
information in the written Documentation and consideration
of all other factors as required by the statutes which
govern the regulatory process of the governmental body
involved.
***************************
ACGIH® is a not-for-profit scientific association.
ACGIH® proposes guidelines known as TLVs® and BEIs® for use
by industrial hygienists in making decisions regarding safe
levels of exposure to various hazards found in the
workplace.
ACGIH® is not a standards setting body.
Regulatory bodies should view TLVs® and BEIs® as an
expression of scientific opinion.
TLVs® and BEIs® are not consensus standards.
ACGIH® TLVs® and BEIs® are based solely on health factors;
there is no consideration given to economic or technical
feasibility. Regulatory agencies should not assume that it
is economically or technically feasible to meet established
TLVs® or BEIs®.
ACGIH® believes that TLVs® and BEIs® should NOT be adopted
as standards without an analysis of other factors necessary
to make appropriate risk management decisions.
TLVs® and BEIs® can provide valuable input into the risk
characterization process. Regulatory agencies dealing with
hazards addressed by a TLV® or BEI® should review the full
written documentation for the numerical TLV® or BEI®.
Battle Against TLV® Lawsuits Comes to an End |
William S. Cook
Registered User
Username: Wscook
Post Number: 47
Registered: 1-2001
| | Posted on Wednesday, May 08, 2002 - 8:57 am: | |
continued from above
Why no standards for mold exposures
An updated summary of all three cases follows:
CARLIN DAVID STAPLES, et al. vs. DOW CHEMICAL COMPANY, et
al.
Mr. Staples filed a toxic tort action against all of the
manufacturers of Vinyl Chloride and the major industry
associations. Mr. Staples was a 38-year-old worker who had
six children, and was seriously ill with brain cancer.
ACGIH® was not named in the initial action, but was added
as a defendant in a subsequent Amended Petition. Mr.
Staples was exposed to vinyl chloride monomer from December
1982 until October 1997.
ACGIH® was included as a defendant, under a conspiracy
theory, for allegedly fraudulently concealing evidence, and
for spoilage of evidence. The Plaintiffs sought punitive
and compensatory damages.
ACGIH® filed a Motion to Dismiss this case based on the
following facts: ACGIH® is not a Texas corporation, and
does not do business in the state of Texas; ACGIH® was
added as a defendant subsequent to the Court's established
deadline for such an Amended Petition; and ACGIH® engaged
in no conspiracy to conceal or spoil evidence, or to do so
at its own initiative. This case has been resolved, and
there are no longer any claims against ACGIH®.
ANCHOR GLASS CONTAINER CORP., et al. vs. ACGIH, U.S. DOL,
and U.S. DHHS
In this action, the Plaintiffs argued that ACGIH® acted as
a Federal Advisory Committee (under the Federal Advisory
Committee Act (FACA)) to the Department of Labor and the
Department of Health and Human Services. Since the ACGIH®
TLV® procedures do not comply with the FACA requirements,
Plaintiffs claimed that ACGIH® should be enjoined from
holding meetings to discuss trona and ACGIH® should not be
permitted to adopt a trona TLV®. They further argued that
the Department of Labor and the Department of Health and
Human Services could not rely on a TLV® for trona, and that
publishing of a trona TLV® would mislead employees and
consumers about safe levels of trona exposure, and
Plaintiffs would be irreparably damaged by such
publication. Plaintiffs also sought monetary damages.
ACGIH® filed a Motion to Dismiss based on its firm
conclusion that ACGIH® is not a Federal Advisory Committee,
and is not bound by the Federal Advisory Committee Act. The
motion was also premised on First Amendment issues, and the
right of ACGIH® and all scientific researchers who render
credible opinions and recommendations, to continue to do
so.
The Motion to Dismiss was granted in part and denied in
part and the discovery process began. After lengthy and
costly discovery, the case was settled by ACGIH® on
September 13, 2001 and later settled by the government. As
part of the confidential settlement agreement, ACGIH®
placed a statement on its website, and in the December 2001
issue of Applied Occupational and Environmental Hygiene.
REFRACTORY CERAMIC FIBERS COALITION, et al. vs. ACGIH
The Plaintiffs alleged that ACGIH® is a standards-setting
organization, and that the TLV® for RCF is unreasonable and
unjustified. RCFC argued that its own Recommended Exposure
Guideline (REG) was based on the principle that it is
prudent to reduce RCF levels to the maximum feasible
extent, and is set at the lowest level that appears
feasible. It also noted conflicts of interest due to the
involvement in the TLV® process of federal employees and
employees of labor unions. RCFC asked the Court to enjoin
ACGIH® from publishing its TLV®. It also sought the
assessment of damages.
On January 12, 2001, the United States District Court in
Atlanta held a hearing on RCFC's request for a Temporary
Restraining Order (TRO) enjoining ACGIH® from publishing
the RCF TLV®. After viewing the legal briefs filed by both
parties and listening to the counsel for both parties, the
Court denied RCFC's request, finding that it did not appear
that RCFC was likely to win. ACGIH® was free to publish the
TLV® for RCF. Based on that ruling, which was very
favorable to ACGIH®, the parties began settlement
discussions. As a result, on July 2, 2001, ACGIH® entered
into a settlement agreement with the Plaintiffs. As part of
that agreement, ACGIH® placed a statement on its website,
and distributed it in a press release and in this issue of
Today!. (See ACGIH®/RCFC Lawsuit Settled, page 25.)
Although these three cases were each resolved in a manner
acceptable to ACGIH®, the litigation did point out the need
to further explain the proper use of TLVs® and BEIs®.
Therefore, the ACGIH® Board of Directors adopted the
Statement of Position Regarding the TLVs® and BEIs®. It is
our hope that the publication of this policy statement will
lessen any confusion about the distinction between TLVs®,
BEIs®, and regulatory standards.
|
Andrew K. Sloane
Member
Username: Claimsranger
Post Number: 16
Registered: 12-2001
| | Posted on Wednesday, May 08, 2002 - 7:21 am: | |
Jim, you are right on every point made, although please allow me to interject a point I was not aware of until my trip to the emergency room while working the MOOF wars here in SE Texas. I am severly allergic to penicillun. Most of the mold infestations have a high concentration of Aspegillius/Penicillium that are airborne. Inhalation of the mycotixins produced by these airborne infestations is just as if I had taken a good dose of penicillun with the associated rash, headache and anaphalactic shock symptoms associated with my allergy. This was brought to my attention by an emergency room Dr. The rash lasted 3 weeks, the headaches only 3-4 days. I no longer revisit these losses without proper PPE once I am aware of the Lab results from the CIH's we employ. It was my fault last week to go into the risk w/o my gear. A 15 minute exposure and I had to finish my appt. outside with the PH's!! That headache was the worst to date. A/P count was in the 15K range per CM3/air. My mistake. I no longer even go back in, they all meet me at the office to review the reports no matter what the count!!!PERIOD. And I grew up around here with no common allergies. Other than a large prejudice against people who don't want to work. Just whining about how the Government should be more giving. Folks, this is real. Mostly a lack of housekeeping and an underlying water loss improperly taken care of. the subtropical nature of this region is also an element along with all of the petro-chemical pollution here for a 100 year period. 83 claims so far and I have closed 27, which from Mgmnt's standpoint is "doing a good job". Contact dermatosis and headaches aside, these claims are the equivalent of a double fire loss on every one stress wise and complexity and they ABSOLUTELY bring out the worst side of humanity in 95% of every Policy holder. More later, the MOOF is wating. (Mold Or Other Fungi). |
William S. Cook
Registered User
Username: Wscook
Post Number: 46
Registered: 1-2001
| | Posted on Tuesday, May 07, 2002 - 11:58 pm: | |
Wong
Most of the answers to your questions are contained within the excerpts that I included. The absence of some of the specifics that you asked for may allow some chest thumping on your part. Many people mistakenly seek TLV, LEL, PPM, PPB values as considerations to mold as to what they are in asbestos issues. The asbestos issues are confined to less than ten types of harmful asbestos and they are fixed amounts (not sprouting or propagating). Asbestos is another naturally occuring element in our environment that was not considered to be a hazard less than fifty years ago. Mold is very necessary to do its job of breaking down organic materials. It protects its turf by in some instances by producing mold critters that fight off other mold critters by being more toxic. Some of these 100,000 different mold species when dining on one material may produce a harmful mycotoxin while its neighbor inches away may be creating harmless byproducts because of a different digestive process. I am certainly not qualified or disposed to try to answer the more technical aspects of your post.
It is within the bounds of my research an education to say that some fungi and mold byproducts can possibly negativly impact the health of some people and should not be poo pooed as nonsignificant concerns. I don't think it is constructive to make fun of people that have a concern for their personal health issues and I responded to shed a sliver of academic findings to the forum. I now return to the insecurity of the dark side and observing the responses from all quarters.
William S Cook
Public Adjuster |
Jim Flynt
Registered User
Username: Jimflynt
Post Number: 284
Registered: 6-2001
| | Posted on Tuesday, May 07, 2002 - 11:48 pm: | |
"It does not make make a handful of BEANS, what or how or why the carriers are paying "MOLD CLAIM", or not paying them"; or so says the previous poster.
Oh, but I beg to disagree.
It does make a hill of beans, and there are several reasons why it does:
(1) It makes a difference if the WHY is because an adjuster put a carrier in an estoppel situation out of personal ignorance or from lack of specific claim handling ability.
(2) It makes a difference for a professional adjuster to be able to understand and explain the WHYS or WHY NOTS in knowledgable communications not only with the carrier, but with the insureds, contractors, public adjusters, and remediation contractors about the many intricacies of mold. Those intricacies include causation, policy coverage aspects, remediation, and the safety of an insured to habitate within a healthy environment.
(3) It makes a difference for the professional adjuster to be able to understand the WHAT, HOWS and WHYS and then be able to explain in a court of law when a claims case goes to court for bad faith, E & O, or subrogation action.
(4) It makes a difference for each and every professional adjuster to understand and advocate for the WHATS, HOWS and WHYS of current issues in insurance which affect our future, the solvency of carriers, the availability and affordability of insurance for homeowners, and the stability and capacity of the American insurance industry.
(5) Understanding the WHAT, HOW and WHY are absolutely essential in determining if the professional adjuster properly comprehends and then applies policy and policy provisions fairly and correctly. Without such understanding, there would be no measure of knowledge and application; neither would such adjuster be of fair service to carrier nor insured.
(6) Understanding does make a difference in knowledge and in the words of the great western writer Louis L'Amour: "Knowledge is like money; To be of value it must circulate, and in circulating, it can increase in quantity and hopefully, in value."
No, knowledge (or correspondingly ignorance) may not mean a hill of beans for some Johnny-come-lately or one peril roof thumper, but for the rest of us, it means everything: including our future and our industry.
(Message edited by jimflynt on May 07, 2002)
(Message edited by jimflynt on May 07, 2002) |
David Houtz
Registered User
Username: Catmannn
Post Number: 4
Registered: 3-2001
| | Posted on Tuesday, May 07, 2002 - 10:45 pm: | |
Get a Life!!!!!
It does not make make a handful of BEANS, what or how or why the carriers are paying "MOLD CLAIM", or not paying them. Those that are do, those that are not don't. Enought said.
The adjusters that are working mold are being paid every day, and the bottom line is that is in fact what matters.
Follow the golden rule: 1. Do what the carrier requests. That's it, nothing more.
If the Insurance Industry "Brain Pool" is not to your thinking, so what. They and we do not give a rats ass.
If the PA'S and Contractor's are making it, we do what we as adjusters do try to pay "only what is owed. I understand that on some claims it may be overstated, hey that is life.
No one in the cado family will every change the thinking of the big dogs at the carriers. You all are just barking up a tree without a coon.
Just one man's thoughts.
Houtz
|
D Wong Whey
Registered User
Username: Dwongwhey
Post Number: 128
Registered: 10-2001
| | Posted on Tuesday, May 07, 2002 - 10:19 pm: | |
If Dave Hood or any other pro mold reader has any additional health threatening toxin information to add to the information which Bill Cook has posted, I invite you to do so at this time. Such information should include any other known toxins which pose a health risk from mold exposure which Bill may have missed in his listing.
Due to the very scientific nature of Bill's post and this topic, it is essential that we have all the experts come forward now to present any additional causation information so that those of us with a differing point of view can research and then respond to the allegations of fact being presented.
With a little time, preparation and research, I believe this topic can be made more easily explainable and understandable to adjusters, and then and only then, will the truth set us free.
I invite any mold 'experts' as well as Dave Hood and Alan Jackson to weigh in with their own information and sources so that we can all fully explore this topic to arrive at all the applicable and available facts.
(Message edited by dwongwhey on May 07, 2002) |
D Wong Whey
Registered User
Username: Dwongwhey
Post Number: 127
Registered: 10-2001
| | Posted on Tuesday, May 07, 2002 - 9:54 pm: | |
Bill, thanks for posting the information previously discussed, and after I have had a thorough opportunity to fully research your post information and sources, I will respond with my own more full comments and pertinent authoritative sources.
In the meantime, please answer the questions enclosed which you previously indicated you could answer and respond to with sources.
(1) What role does the process (i.e., inhalation, transdermal, intravenous, ingestion) of exposure to Mycotoxins and Aflatocins have to toxicity in humans?
(2) Which process of exposure to Mycotoxins and Aflatoxins (i.e., inhalation, transdermal, intravenous, ingestion) would be considered more toxic to humans?
(3) In the above question (2), which process would be considered least toxic to humans?
(4) What contamination thresholds (i.e., PPM, PPB, ug/kg) have been established by the government, medical, scientific, and forensic community for establishing toxic and non-toxic limits for Mycotoxin and Aflatoxin exposure to humans?
(Message edited by dwongwhey on May 07, 2002)
(Message edited by dwongwhey on May 07, 2002) |
William S. Cook
Registered User
Username: Wscook
Post Number: 45
Registered: 1-2001
| | Posted on Tuesday, May 07, 2002 - 9:46 pm: | |
Continuation of Washington State Study
Penicillium
Penicillium species have been shown to be fairly common indoors, even in clean environments, but certainly begin to show up in problem buildings in numbers greater than outdoors (Burge, 1986; Miller et al., 1988; Flannigan and Miller, 1994). Spores have the highest concentrations of mycotoxins, although the vegetative portion of the mold, the mycelium, can also contain the poison. Viability of spores is not essential to toxicity, so that the spore as a dead particle can still be a source of toxin.
Important toxins produced by penicillia include nephrotoxic citrinin, produced by P. citrinum, P. expansum and P. viridicatum; nephrotoxic ochratoxin, from P. cyclopium and P. viridicatum, and patulin, cytotoxic and carcinogenic in rats, from P. expansum (Smith and Moss, 1985).
Aspergillus
Aspergillus species are also fairly prevalent in problem buildings. This genus contains several toxigenic species, among which the most important are, A. parasiticus, A. flavus, and A. fumigatus. Aflatoxins produced by the first two species are among the most extensively studied mycotoxins. They are among the most toxic substances known, being acutely toxic to the liver, brain, kidneys and heart, and with chronic exposure, potent carcinogens of the liver. They are also teratogenic (Smith and Moss, 1985; Burge, 1986). Symptoms of acute aflatoxicosis are fever, vomiting, coma and convulsions (Smith and Moss, 1985). A. flavus is found indoors in tropical and subtropical regions, and occasionally in specific environments such as flowerpots. A. fumigatus has been found in many indoor samples. A more common aspergillus species found in wet buildings is A. versicolor, where it has been found growing on wallpaper, wooden floors, fibreboard and other building material. A. versicolor does not produce aflatoxins, but does produce a less potent toxin, sterigmatocystin, an aflatoxin precursor (Gravesen et al., 1994). While symptoms of aflatoxin exposure through ingestion are well described, symptoms of exposure such as might occur in most moderately contaminated buildings are not know, but are undoubtedly less severe due to reduced exposure. However, the potent toxicity of these agents advise that prudent prevention of exposures are warranted when levels of aspergilli indoors exceed outdoor levels by any significant amount. A. fumigatus has been found in many indoor samples. This mold is more often associated with the infectious disease aspergillosis, but this species does produce poisons for which only crude toxicity tests have been done (Betina, 1989). Recent work has found a number of tremorgenic toxins in the conidia of this species (Land et al., 1994). A. ochraceus produces ochratoxins (also produced by some penicillia as mentioned above). Ochratoxins damage the kidney and are carcinogenic (Smith and Moss, 1985).
Stachybotrys chartarum (atra)
Stachybotrys chartarum (atra) has been much discussed in the popular press and has been the subject of a number of building related illness investigations. It is a mold that is not readily measured from air samples because its spores, when wet, are sticky and not easily aerosolized. Because it does not compete well with other molds or bacteria, it is easily overgrown in a sample, especially since it does not grow well on standard media (Jarvis, 1990). Its inability to compete may also result in its being killed off by other organisms in the sample mixture. Thus, even if it is physically captured, it will not be viable and will not be identified in culture, even though it is present in the environment and those who breathe it can have toxic exposures. This organism has a high moisture requirement, so it grows vigorously where moisture has accumulated from roof or wall leaks, or chronically wet areas from plumbing leaks. It is often hidden within the building envelope. When S. chartarum is found in an air sample, it should be searched out in walls or other hidden spaces, where it is likely to be growing in abundance. This mold has a very low nitrogen requirement, and can grow on wet hay and straw, paper, wallpaper, ceiling tiles, carpets, insulation material (especially cellulose-based insulation). It also grows well when wet filter paper is used as a capturing medium.
S. chartarum has a well-known history in Russia and the Ukraine, where it has killed thousands of horses, which seem to be especially susceptible to its toxins. These toxins are macrocyclic trichothecenes. They cause lesions of the skin and gastrointestinal tract, and interfere with blood cell formation. (Sorenson, 1993). Persons handling material heavily contaminated with this mold describe symptoms of cough, rhinitis, burning sensations of the mouth and nasal passages and cutaneous irritation at the point of contact, especially in areas of heavy perspiration, such as the armpits or the scrotum (Andrassy et al., 1979).
One case study of toxicosis associated with macrocyclic trichothecenes produced by S. chartarum in an indoor exposure, has been published (Croft et al., 1986), and has proven seminal in further investigations for toxic effects from molds found indoors. In this exposure of a family in a home with water damage from a leaky roof, complaints included (variably among family members and a maid) headaches, sore throats, hair loss, flu symptoms, diarrhea, fatigue, dermatitis, general malaise, psychological depression. (Croft et al, 1986; Jarvis, 1995).
Johanning, (1996) in an epidemiological and immunological investigation, reports on the health status of office workers after exposure to aerosols containing S. chartarum. Intensity and duration of exposure was related to illness. Statistically significant differences for more exposed groups were increased lower respiratory symptoms, dermatological, eye and constitutional symptoms, chronic fatigue, and allergy history. Duration of employment was associated with upper respiratory, skin and central nervous system disorders. A trend for frequent upper respiratory infections, fungal or yeast infections, and urinary tract infections was also observed. Abnormal findings for components of the immune system were quantified, and it was concluded that higher and longer indoor exposure to S. chartarum results in immune modulation and even slight immune suppression, a finding that supports the observation of more frequent infections.
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William S. Cook
Registered User
Username: Wscook
Post Number: 44
Registered: 1-2001
| | Posted on Tuesday, May 07, 2002 - 9:45 pm: | |
Information Regarding Toxicity of Mold byproducts
Harriet M. Ammann, Ph.D., D.A.B.T.
Senior Toxicologist
Washington State Department of Health
Olympia, Washington
Toxicity
Molds can produce other secondary metabolites such as antibiotics and mycotoxins. Antibiotics are isolated from mold (and some bacterial) cultures and some of their bacteriotoxic or bacteriostatic properties are exploited medicinally to combat infections.
Mycotoxins are also products of secondary metabolism of molds. They are not essential to maintaining the life of the mold cell in a primary way (at least in a friendly world), such as obtaining energy or synthesizing structural components, informational molecules or enzymes. They are products whose function seems to be to give molds a competitive advantage over other mold species and bacteria. Mycotoxins are nearly all cytotoxic, disrupting various cellular structures such as membranes, and interfering with vital cellular processes such as protein, RNA and DNA synthesis. Of course they are also toxic to the cells of higher plants and animals, including humans.
Mycotoxins vary in specificity and potency for their target cells, cell structures or cell processes by species and strain of the mold that produces them. Higher organisms are not specifically targeted by mycotoxins, but seem to be caught in the crossfire of the biochemical warfare among mold species and molds and bacteria vying for the same ecological niche.
Not all molds produce mycotoxins, but numerous species do (including some found indoors in contaminated buildings). Toxigenic molds vary in their mycotoxin production depending on the substrate on which they grow (Jarvis, 1990). The spores, with which the toxins are primarily associated, are cast off in blooms that vary with the mold’s diurnal, seasonal and life cycle stage (Burge, 1990; Yang, 1995). The presence of competitive organisms may play a role, as some molds grown in monoculture in the laboratory lose their toxic potency (Jarvis, 1995). Until relatively recently, mold poisons were regarded with concern primarily as contaminants in foods.
More recently concern has arisen over exposure to multiple mycotoxins from a mixture of mold spores growing in wet indoor environments. Health effects from exposures to such mixtures can differ from those related to single mycotoxins in controlled laboratory exposures. Indoor exposures to toxigenic molds resemble field exposures of animals more closely than they do controlled experimental laboratory exposures. Animals in controlled laboratory exposures are healthy, of the same age, raised under optimum conditions, and have only the challenge of known doses of a single toxic agent via a single exposure route. In contrast, animals in field exposures are of mixed ages, and states of health, may be living in less than optimum environmental and nutritional conditions, and are exposed to a mixture of toxic agents by multiple exposure routes. Exposures to individual toxins may be much lower than those required to elicit an adverse reaction in a small controlled exposure group of ten animals per dose group. The effects from exposure may therefore not fit neatly into the description given for any single toxin, or the effects from a particular species, of mold.
Field exposures of animals to molds (in contrast to controlled laboratory exposures) show effects on the immune system as the lowest observed adverse effect. Such immune effects are manifested in animals as increased susceptibility to infectious diseases (Jakab et al., 1994). It is important to note that almost all mycotoxins have an immunosuppressive effect, although the exact target within the immune system may differ. Many are also cytotoxic, so that they have route of entry effects that may be damaging to the gut, the skin or the lung. Such cytotoxicity may affect the physical defense mechanisms of the respiratory tract, decreasing the ability of the airways to clear particulate contaminants (including bacteria or viruses), or damage alveolar macrophages, thus preventing clearance of contaminants from the deeper lung. The combined result of these activities is to increase the susceptibility of the exposed person to infectious disease, and to reduce his defense against other contaminants. They may also increase susceptibility to cancer
Because indoor samples are usually comprised of a mixture of molds and their spores, it has been suggested that a general test for cytotoxicity be applied to a total indoor sample to assess the potential for hazard as a rough assessment (Gareis, 1995).
The following summary of toxins and their targets is adapted from Smith and Moss (1985), with a few additions from the more recent literature. While this compilation of effects does not describe the effects from multiple exposures, which could include synergistic effects, it does give a better idea of possible results of mycotoxin exposure to multiple molds indoors.
Vascular system (increased vascular fragility, hemorrhage into body tissues, or from lung, e.g., aflatoxin, satratoxin, roridins).
Digestive system (diarrhea, vomiting, intestinal hemorrhage, liver effects, i.e., necrosis, fibrosis: aflatoxin; caustic effects on mucous membranes: T-2 toxin; anorexia: vomitoxin.
Respiratory system: respiratory distress, bleeding from lungs e.g., trichothecenes.
Nervous system, tremors, incoordination, depression, headache, e.g., tremorgens, trichothecenes.
Cutaneous system : rash, burning sensation sloughing of skin, photosensitization, e.g., trichothecenes.
Urinary system, nephrotoxicity, e.g. ochratoxin, citrinin.
Reproductive system; infertility, changes in reproductive cycles, e.g. T-2 toxin, zearalenone.
Immune system: changes or suppression: many mycotoxins.
It should be noted that not all mold genera have been tested for toxins, nor have all species within a genus necessarily been tested. Conditions for toxin production varies with cell and diurnal and seasonal cycles and substrate on which the mold grows, and those conditions created for laboratory culture may differ from those the mold encounters in its environment.
Toxicity can arise from exposure to mycotoxins via inhalation of mycotoxin-containing mold spores or through skin contact with the toxigenic molds (Forgacs, 1972; Croft et al., 1986; Kemppainen et al., 1988 -1989). A number of toxigenic molds have been found during indoor air quality investigations in different parts of the world. Among the genera most frequently found in numbers exceeding levels that they reach outdoors are Aspergillus, Penicillium, Stachybotrys, and Cladosporium (Burge, 1986; Smith et al., 1992; Hirsh and Sosman, 1976; Verhoeff et al., 1992; Miller et al., 1988; Gravesen et al., 1999). Penicillium, Aspergillus and Stachybotrys toxicity, especially as it relates to indoor exposures, will be discussed briefly in the paragraphs that follow.
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William S. Cook
Registered User
Username: Wscook
Post Number: 43
Registered: 1-2001
| | Posted on Tuesday, May 07, 2002 - 9:33 pm: | |
Sources of Additional Information/Assistance:
California Department of Health Services, Environmental Health Investigations Branch:
Sandra McNeel, D.V.M.; Debra Gilliss, M.D., M.P.H.; Richard Kreutzer, M.D.
(510) 622-4500
REFERENCES
American Academy of Pediatrics. "Toxic Effects of Indoor Molds". Pediatrics. 1998. 101(4):712-714.
CDC. "Update: pulmonary hemorrhage/hemosiderosis among infants - Cleveland, Ohio. 1993-1996". MMWR 1997,46:33-35.
Corrier DE. "Mycotoxicosis: mechanism of immunosuppression". Vet Immunol Immunopathol. 1991.
30: 73-87.
Croft WA, Jarvis BB, Yatawara CS. "Airborne outbreak of trichothecene toxicoxix". Atmospheric Environment. 1986. 20(3):549-552.
Forgacs J. Stachybotrys toxicosis. In: Kadis S, Ciegler A, Aji SJ, eds. Microbial Toxins: Volume VI-Fungal Toxins, New York: Academic Press: 1972:95-130.
Flannigan B, McCabe EM, McGarry F. "Allergenic and toxigenic micro-organisms in houses". J Appl Bact Symp (Suppl) 1991; 70:61S-73S.
Hintikka EL. Human stachybotrytoxicosis. In: Wylie TD, Morehouse LG, eds. Mycotoxigenic Fngi, Mycotoxins, Mycotoxicoses. New York: Marcel Dekker; 1987:87-89.
Hodgson MJ, et. al. "Building-associated pulmonary disease from exposure to Stachybotrys chartarum and Aspergillus versicolor. J Occ Env Med. 1998. 40(3):241-249.
Jarvis BB, Yang C. Personal Communication. Discussion session. Fungi and Bacteria in Indoor Air Environments. Saratoga Springs, NY. October 6-7, 1994.
Jarvis BB, Salemme J, Morais A. Stachybotrys toxins. Natural Toxins, 1995, 3:10-16.
Johanning E, Morey PR, Jarvis BB. "Clinical epidemiological investigation of health effects caused by Stachybotrys chartarum building contamination", Proceedings of Indoor Air, 1993; Vol. 1: 225-230.
Johanning E, Biagini R, et. al. "Health and immunology study following exposure to toxigenic fungi (Stachybotrys chartarum) in a water-damaged office environment" Int Arch Occup Environ Health 1996, 68:207-218.
Kozak, PP, Gallup J, Cummins L.H., Gillman S.A. "Currently available methods for home mold surveys". Ann Allergy 1979; 45: 167-176.
Montana E, Etzel RA, Allan T, Horgan TE, Dearborn DG. "Environmental risk factors associated with pediatric idiopathic pulmonary hemorrhage and hemosiderosis in a Cleveland community." Pediatrics 1997, 99(1):
Nikulin M, Reijula K, Jarvis BB, Hintikka E-L. "Experimental lung mucotoxicosis in mice induced by Stachybotrys atra". Int J Exp Path. 1996. 77:213-218.
Nikulin M, Reijula K, Jarvis BB, Veijalainen P, Hintikka E-L. "Effects of intranasal exposure to spores of Stachybotrys atra in mice". Fund Appl Toxicol. 1997. 35:182-188.
Ueno Y, editor. General toxicology. In: "Trichothecenes - chemical, biological and toxicological aspects". Elsevier Science Publishing Co., Inc.: New York, NY, 1983:135-146.
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William S. Cook
Registered User
Username: Wscook
Post Number: 42
Registered: 1-2001
| | Posted on Tuesday, May 07, 2002 - 9:31 pm: | |
California Department of Health Services, April 1998
Health Effects of
Toxin-Producing Indoor Molds in California
CA Department of Health Services
Environmental Health Investigations Branch
Due to excessive rainfall this winter many Californians are experiencing increased exposure to indoor microorganisms. Several fungal species capable of producing toxic substances have been found in water-damaged California homes and offices. This article provides information about potential health effects from exposure to Stachybotrys chartarum (a.k.a. S. atra), a toxigenic mold that has received increasing attention recently among indoor air reseachers and the public. Within the last 12-18 months several scientific reports (and media attention) have focused on Stachybotrys, a ubiquitous saprophytic fungus that grows on nitrogen-poor, cellulose rich materials such as hay, straw and building materials (ceiling tiles, wall paper, paper covering on gypsum wallboard). The statewide prevalence of this fungus in homes or work places is unknown, although one report found Stachybotrys in 2-3% of a small survey of southern California homes (Kozak, 1979).
Mechanism of Action
Some strains of Stachybotrys chartarum can produce mycotoxins of the trichothecene and spirolactone families. The trichothecene mycotoxins satratoxins G and H are potent protein synthesis inhibitors and cause immunosuppression in laboratory animals. In experimental animal studies, the trichothecenes affect rapidly proliferating tissues such as skin and mucosa, as well as lymphatic and hematopoietic tissues (Ueno, 1983). In laboratory animals, acute exposure to large amounts of trichothecene toxins results in a rapid release of sequestered white blood cells into circulation, while repeated or chronic exposure destroys granulocytic precursor cells in bone marrow leading to white cell depletion. Among the reported cellular effects are: mitogen B/T lymphocyte blastogenesis suppression; decrease of IgM, IgG, IgA; impaired macrophage activity and migration-chemotaxis; broad immunosuppressive effects on the cellular and humoral-mediated immune response leading to secondary infections; and, paradoxically, increased spontaneous antibody producing cells in the spleen (Corrier, 1991).
Toxigenic strains of SC may also produce spirolactones (stachybotrylactone) and spirolactams (stachybotrylactam), toxins which produce anticomplement effects (Jarvis, 1995). Possible synergistic effects between the trichothecenes and these mycotoxins have not yet been evaluated. Although laboratories can test a sample of Stachybotrys chartarum for its ability to produce mycotoxins, in vitro results do not necessarily equate with the in vivo situation. Therefore, a fungus that produces toxins in the lab may not do so in the field, or vice versa. It has been suggested that to assure the safety of any exposed individual, whenever Stachybotrys chartarum is identified, it should be considered as a potential mycotoxin-producing organism (Jarvis, 1994).
Positive skin reactions to the fungus have been found in some asthmatics living or working in Stachybotrys-contaminated rooms, suggesting a hypersensitivity component in addition to the potential for mycotoxicosis. Thus the fungal spores themselves or chemicals carried on the spores may produce either allergenic or toxigenic effects (Flannigan, 1991).
Routes of Exposure
Due to its wet, slimy growth characteristics, it is unusual for spores from active Stachybotrys colonies to become aerosolized. However, when colonies of this fungus die and become dehydrated, there is increased risk for air dispersion. Portals of possible entry into the body include inhalation and dermal absorption when the fungus is found on walls or in carpets.
Case Reports
Historically, toxicologic effects from this fungus were reported in Europe, where horses, sheep and cattle suffered fatal hemorrhagic disorders following ingestion exposures (Forgacs,1972)). Human occupational exposures to contaminated straw or hay resulted in nasal and tracheal bleeding, skin irritation and alterations in white blood cell counts (Hintikka, 1987).
The first U.S. case of Stachybotrys-associated health effects from inhalation exposure was reported in a suburban Chicago family (Croft, 1986). The fungus had contaminated the ventilation system and ceilings of the house. Health effects reported by the family included chronic recurring cold and flu-like symptoms, sore throat, diarrhea, headache, fatigue, dermatitis, intermittent focal alopecia and generalized malaise. Workers who cleaned and removed contaminated material from this house also experienced skin irritation and respiratory symptoms. After Stachybotrys contamination was removed the house was reoccupied and residents reported no recurrence of clinical symptoms.
Stachybotrys and satratoxin H (one of the trichothecene mycotoxins) were subsequently identified in a water-damaged office building in New York City. A small case-control study showed workers exposed to the fungus were at statistically significant higher risk for nonspecified disorders of the lower airways, eyes and skin; fevers and flu-like symptoms, and chronic fatigue (Johanning, 1993, 1996). No significant differences in specific S. chartarum IgE and IgG levels were noted between cases and controls. Although Stachybotrys chartarum specific IgE (RAST) and IgG (ELISA) tests are available, their sensitivity and specificity have not yet been determined.
A recent report describes identification of 10 likely or possible cases of building-related asthma in a courthouse contaminated with Stachybotrys and Aspergillus species (Hodgson, 1998). Self-reported symptoms among co-workers included fever, headache, rhinitis, coughing, dyspnea and chest tightness. Chest radiographs were negative and Stachybotrys-specific serology was uninformative.
Stachybotrys chartarum, along with other fungi and environmental tobacco smoke, was recently postulated to have an association with pulmonary hemosiderosis in a cluster of Cleveland, Ohio infants (Montana, 1997; MMWR, 1997)). While SC was found more frequently in the homes of case infants compared to controls, exposure of case infants to mycotoxins in the home could not be determined. Because there is no field test for airborne mycotoxins, it is not currently possible to determine if toxins were actually present in the living space of case infants, and if so, at what levels. However, since Stachybotrys chartarum spores containing mycotoxins have been shown to produce pulmonary alveolar and intra-bronchiolar inflammation and hemorrhage in mice (Nikulin, 1996, 1997), more research into the inhalation effects of these toxins, especially on immature alveoli and pulmonary vascular walls, is critically needed.
Pulmonary hemosiderosis is a condition characterized by recurrent alveolar hemorrhage resulting in clinical signs of cough, wheeze, hemoptysis, tachypnea, low grade fever, and microcytic hypochromic anemia. Chest radiographs typically show patchy infiltrates and sputum specimens, laryngeal swabs or gastric aspirates reveal hemosiderin-laden macrophages. The association of some cases with allergy to cow’s milk (Heiner syndrome) and its association with glomerulonephritis in Goodpasture’s syndrome suggests an immunologic etiology but immunologic findings in idopathic cases have been inconsistent. Some familial case reports also suggest a genetic component.
California Department of Health Services staff reviewed statewide hospital discharge data for 1989-1995 (last year for which data is available) and identified a total of eight hospitalizations and no deaths during these years for hemosiderosis in infants less than one year of age. There were no more than 3 cases in any year and no geographic clustering.
American Academy of Pediatrics
On April 6, 1998, the American Academy of Pediatrics (AAP) Committee on Environmental Health released a statement concerning toxic effects of indoor molds and acute idiopathic pulmonary hemorrhage in infants. They recommend that until more information is available on the etiology of this condition, pediatricians should try to ensure that infants under 1 year of age are not exposed to chronically moldy, water-damaged environments (AAP, 1998).
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see continuation next post |
William S. Cook
Registered User
Username: Wscook
Post Number: 41
Registered: 1-2001
| | Posted on Tuesday, May 07, 2002 - 9:20 pm: | |
continuation of senate study
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PUBLIC HEALTH EFFECTS OF TOXIC MOLD”
Among toxin-producing molds, the Aspergillus species and Stachybotrys chartarum, are the two species that have been present in the toxic molds cases discussed in the press.
These species can cause some of the most extreme health effects of molds. Aflatoxins, which are produced by two species of Aspergillus, can be carcinogenic, are acutely toxic to the liver, brain, kidneys and heart. Aflatoxins can induce fever, vomiting, coma and convulsions.
Aspergillus is also associated with the infection
aspergillosis. Individuals exposed to Stachybotrys chartarum have experienced recurring flu-like symptoms,fatigue, respiratory conditions, fever, difficulty breathing and a suppressed immune system.
Differentiating Between Molds that Produce Toxins and Molds that Do Not Produce Toxins
Toxin producing molds, like Stachybotrys and Aspergillus, have been the focus of public concern and the subject of a significant portion of recent debates about molds.
However, public health officials believe that
differentiating toxic mold from other mold is usually not worthwhile. They generally conclude that molds, regardless of their toxicity can affect human health. Public health officials advise that when mold can be seen or smelled, the
source of moisture should be identified and eliminated, and the mold should be cleaned or remediated.
Determining whether mold is toxic or not is a complicated and usually costly undertaking. The variance in types of molds, including those that can produce mycotoxins, and the fact that molds capable of producing toxins do not always produce them, complicate the differentiation process. This process requires extensive expert testing and can easily cost between $1000 and $2000 for a single-family dwelling. Testing for toxicity is often inconclusive due to difficulties reproducing the conditions of the building in the laboratory or identifying mold species that can produce toxins but not having conclusive evidence regarding whether the specific mold produced toxins in the building.
Therefore, while the public makes a distinction between molds and toxic molds, public health officials and mold experts suggest that molds and their presence in large numbers can result in adverse health effects and should trigger appropriate clean up.
Mold Identification and Remediation
The presence of mold is usually identified through visual identification, sampling or air monitoring. Visual inspection is usually the first step in identifying mold contamination. It involves inspection of ventilation systems, ceiling tiles, drywall or other cellulosic
surfaces, and occasionally inspection of ductwork and hidden surfaces. Sampling is not required to conduct a remediation, but may be necessary to identify specific fungal contaminants as part of a medical evaluation.
Sampling can help identify the presence of mold if a visual
inspection is equivocal. Air monitoring is also not
necessary for remediation. Monitoring may be necessary
when an individual has been diagnosed with a disease that
is or may be associated with toxic mold exposure, or to
determine the location and extent of contamination if the
presence of mold is suspected but cannot be identified by a
visual inspection or sampling.
Once the presence of mold is identified, public health
officials recommend that the source of moisture is
identified and eliminated, and that the mold be cleaned and
remediated. This recommendation is based on the fact that
all molds, regardless of their toxicity can have human
health effects though the specific health effects vary
depending on the species involved, the amount and duration
of exposure, and individual susceptibility.
Remediation efforts vary and largely depend on the amount
of mold present. These efforts first seek to prevent
continued mold growth by removing the underlying source of
moisture. Prompt response as well as thorough clean up,
drying, and removal of water-damaged materials is crucial
to prevent or limit mold growth. Specific plans for
remediation are largely contingent on the size of mold
remediation. Mold growths less than one square foot can be
cleaned up using a diluted bleach solution. Extensive
contamination, particularly if heating, ventilating, air
conditioning systems or large occupied spaces are
contaminated, usually require the services of an
experienced health and safety professional to conduct the
assessment and remediation. Depending on the extent of
mold infestation, materials infested with molds may need to
be removed, contained and discarded. Remediation costs can
be significant, especially when extensive structural repair
is required. Individuals performing mold remediation
frequently need the use of respiratory protection, gloves,
and eye protection. Persons with respiratory problems, a
compromised immune system, or fragile health are
discouraged from participating in mold remediation.
Existing Laws, Regulations or Guidelines on Mold Exposure,
Identification or Remediation
There are no federal or state laws, regulations or
guidelines regarding mold exposure, identification, or
remediation. The New York City Department of Health has
developed policies for medical and environmental evaluation
and intervention to address mold contamination. The Bureau
has published a document titled, “Guidelines on Assessment
and Remediation of Fungi in Indoor Environments” for use by
building engineers and management, and anyone concerned
about fungal contamination. The document outlines the
health issues of mold, assessment, remediation, and hazard
communication. It is widely cited as the generally
accepted standard for mold assessment and remediation.
The Canada Federal-Provincial Advisory Committee on
Environmental and Occupational Health and the Canada Health
Department have developed guides for public health,
occupational health, and building maintenance officials to
recognize and manage mold contamination in buildings.
These guidelines outline procedures for investigating and
interpreting mold contamination, as well as procedures for
mold remediation and preventive maintenance of buildings.
Several recognized professional organizations have
developed guidelines for the identification and remediation
of molds.
Prepared by Senate Health and Human Services Committee, Ana
Matosantos and Sarah Sutro, March 2001.
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William S. Cook
Registered User
Username: Wscook
Post Number: 40
Registered: 1-2001
| | Posted on Tuesday, May 07, 2002 - 9:14 pm: | |
Information from a senate study
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PUBLIC HEALTH EFFECTS OF TOXIC MOLD”
Molds, one of the most ubiquitous organisms on our planet, have recently captured public attention and are the focus of increasing health concern. Inhalation of mold can cause human toxic effects, exacerbates immunologic reactions and can cause infections. Immunologic reactions include asthma and allergic reactions such as eye irritation, congestion and coughs. Toxic effects include a variety of symptoms such as fatigue, respiratory distress, nausea and non-
specific symptoms. A small group of fungi have been associated with infectious diseases. Because Americans spend the vast majority of their time indoors, they are exposed to molds and a large variety of indoor air pollutants estimated to have more than one hundred times
the actual pollutants found in outdoor air. Though there is no official estimate on the number of individuals made ill by molds, the total certainly exceeds 10,000 people.
There are no federal or state laws, regulations or guidelines regarding mold exposure, identification, or remediation.
The powerful health effects, broad exposure, and lack of standards have generated thousands of California torts. Some authorities have estimated that molds will generate more litigation than asbestos. Recent high profile cases of mold infestation and the rising number of buildings with identified mold problems have increased the visibility of this issue and generated significant concern in the public
health community.
Molds are resilient and highly adaptable organisms present in a wide range of habitats. They vary in color and exist in over a thousand species. Molds need moisture and a food
source to grow. Floods, leaking pipes, steam, leaking windows, high humidity and leaking roofs generate moisture which can lead to mold infestation. With the appropriate conditions, molds can grow considerably within 24 to 72
hours. Molds can form colonies on dead and decaying matter, such as wood and drywall, as well as damp and inorganic matter like painted surfaces and glass as long as a food source, such as dust is present. Molds are increasingly associated with new construction which is
built air tight to conserve energy and can result in reduced ventilation, excessive moisture, and accumulation of moisture behind insulation. Materials like dry wall and
ceiling tiles, used frequently in new construction, provide an excellent food source for molds.
Molds can be found on virtually any surface in almost any climate. Mold commonly grows on walls, carpets, ceilings, behind wallpaper, and in heating, ventilation and air conditioning systems. Mold may be present in a building
and result in health effects without being visible. Frequently mold can only be identified by its mildewy or earthy smell, or through the use mold identification equipment. Mold growth was traditionally associated with periods of high humidity. However, recent research has
found that the effect of relative humidity on mold growth is indirect and that a small amount of moisture can permit significant mold growth. Therefore, while certain climates may increase the propensity of mold growth, no place is
immune to mold infestation and the associated structural and health effects.
Overview of Research on the Health Effects of Mold Exposure Molds, as well as other microbial contaminants are increasingly associated with poor indoor air quality and a variety of health effects. Throughout the 1970s and 1980s,
microbial contamination was identified as the primary cause of poor air quality in only 5% of indoor air quality investigations conducted by the National Institute of Occupational Safety and Health. In the last ten years, microorganisms were identified as the source of poor air quality in up to 50% of indoor air quality cases. Indoor molds usually originate from an outdoor source and take advantage of indoor moisture and food sources in their
growth. These indoor molds can and do affect human health. Their specific effect varies depending on the species involved, the activity of the species, the amount and duration of exposure, and individual susceptibility.
Individuals with compromised immune systems, infants, children, the elderly and individuals with allergies are particularly susceptible to experiencing adverse health effects following mold exposure. Adverse health effects related to mold exposure usually stop when an individual is
removed from the mold infested environment. In very few cases, molds seem to have caused long-term or lifelong adverse health effects.
All molds have the potential to cause an allergic reaction in humans and this is the most common response to mold exposure. Allergic reactions to mold exposure range from mild responses to chronic illnesses. Most individuals who experience allergic reactions to mold exposure develop allergic rhinitis or allergic sinusitis, which is similar to a cold but lasts over an extended period of time. Some individuals develop skin irritation or rashes. A smaller percentage of the population develops chronic allergic diseases like allergic brochopulmonary aspergillosis and hypersensitivity pneumonitis which involve difficulty breathing, fever, tightness in the chest, and muscle aches.
Molds can cause irritation of the eyes, nose and throat,headaches, dizziness, skin irritation and flu like symptoms. Mold exposure usually does not result in infections, except among immune compromised individuals. Immune compromised patients have developed infections affecting the skin, eyes, lungs, or other organs and systems. According to the National Academy of Science, mold exposure aggravates asthma. Mold exposure can result in acute attacks of coughing, wheezing, shortness of breath and acute asthma. Reactions usually occur within minutes of exposure and may repeat six to eight hours later.
Specific Health Effects of Toxins Produced by Molds Under certain conditions, many molds can produce mycotoxins, which are natural organic compounds that initiate a toxic response in humans. Molds that can produce mycotoxins do not always produce them since developing these toxins requires specific conditions.
Mycotoxins are not essential to maintaining the life of a mold cell. They seem to give mold a competitive advantage. Mycotoxins cause some of the most serious adverse health effects of mold exposure. Exposure to mycotoxins can suppress or alter the immune system, inflame the lungs and result in toxic pneumonitis, cause irritation
of the eyes, nose and throat, headaches, diarrhea, and increase the susceptibility of the exposed person to infectious disease and cancer.
see next post
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Roy Cupps
Board Administrator
Username: Admin
Post Number: 125
Registered: 1-1997
| | Posted on Tuesday, May 07, 2002 - 9:13 pm: | |
Bill,
I would like to see the information also.
CatAdjuster.org An Adjuster to Adjuster Community
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D Wong Whey
Registered User
Username: Dwongwhey
Post Number: 126
Registered: 10-2001
| | Posted on Tuesday, May 07, 2002 - 7:42 pm: | |
Bill, by all means please post the excerpts from your private library to help shed some light on uncovering the toxicity facts about the Mycotoxin and Aflatoxin by-products of mold.
I would also welcome your reviewing my previous post and by substituting the words mycotoxin or alfatoxin instead of mold, share your thoughts as well as facts with regard to toxicity of various exposure processes.
(Message edited by dwongwhey on May 07, 2002) |
William S. Cook
Registered User
Username: Wscook
Post Number: 39
Registered: 1-2001
| | Posted on Tuesday, May 07, 2002 - 4:58 pm: | |
Wong
Your post addressed how mold could cause the problems that I addressed as problems of Mycotoxins and Aflatoxins both byproducts of mold. The mold in all probability can and often is an alerginic and is suggested by many guidlines as not a welcome addition to the interior of a habitable abode in signficant numbers greater than may be found outside. The answers reflecting toxicity are readily available but are extensive and may overwhelm the "want to know capacity" of the members of this forum. It is but a few clicks at the keyboard to include the information but any individual seriously wishing to be informed can research the net for the information. Wong, I will be glad to post some brief excerpts from my personal library of information if you think a genuine educational interest exist other than for the inherent controversy previously posted by others.
William S Cook
Public Adjuster |
D Wong Whey
Registered User
Username: Dwongwhey
Post Number: 125
Registered: 10-2001
| | Posted on Tuesday, May 07, 2002 - 3:33 pm: | |
Bill: What role does the process (i.e., inhalation, transdermal, intravenous, ingestion) of mold exposure have to toxicity?
Which process of mold exposure (i.e., inhalation, transdermal, intravenous, ingestion) would be considered more toxic to humans?
What contamination thresholds (i.e., PPM, PPB, ug/kg) have been established by the government, medical, scientific, and forensic community for establishing toxic and non-toxic limits for mold exposure?
Please provide hyperlinks to any medical and/or scientific websites which would suggest or confirm such toxicity facts. |
William S. Cook
Registered User
Username: Wscook
Post Number: 38
Registered: 1-2001
| | Posted on Tuesday, May 07, 2002 - 3:15 pm: | |
Dose-response is the process of characterizing the relationship between the dose of an agent received and the incidence of the health effect. The present exposure to a toxic agent will not have the same positive/negative impact as the previous exposure, and the next exposure will not have the same positive/negative impact as the present exposure.
A person working in a lab must exercise greater precautions for accumulation to a toxic substance because his daily dose over an extended period of time could cause harm to him unlike a person walking throught the lab once or twice a year. I think exposure to radiation is constantly measured for a dose-response concern. Some mold byproducts are mentioned in the US Army microbiology warfare manual as poisonious agents.
William S Cook
Public Adjuster |
D Wong Whey
Registered User
Username: Dwongwhey
Post Number: 124
Registered: 10-2001
| | Posted on Tuesday, May 07, 2002 - 12:35 pm: | |
Bill: Please explain what you mean by the phrase you use dose responsive
Thanks. |
William S. Cook
Registered User
Username: Wscook
Post Number: 37
Registered: 1-2001
| | Posted on Tuesday, May 07, 2002 - 12:18 pm: | |
Perhaps the forum members would be better served if the discussion thread addressed mycotoxins and aflatoxins as the triggering cause for health problems for victims of exposure. Molds and fungus are one of the most ubiquitous organisms on our planet and usually harmless to humans. Their toxic byproducts should be avoided or the exposures minimized in all circumstances, as they are dose responsive. To do otherwise is foolish. Simply a few words of caution from the “DARK SIDE”.
William S Cook
Public Adjuster
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Jim Flynt
Registered User
Username: Jimflynt
Post Number: 283
Registered: 6-2001
| | Posted on Tuesday, May 07, 2002 - 9:36 am: | |
News Bulletin: The New England Journal of Medicine reports today that medical researchers and scientists have just learned that mold claimaints, public adjusters, mold remediation contractors, and lawyers can be a major pain in the ass.
A pandemic epidemic is predicted and generous application of Preparation H and/or alcohol (Jack Daniels) is prescribed as a curative for this serious ailment.
Isolating the known agents of causation from the general public is also known to cure this dread plague upon the unsuspecting public. |
Jim Flynt
Registered User
Username: Jimflynt
Post Number: 282
Registered: 6-2001
| | Posted on Tuesday, May 07, 2002 - 9:19 am: | |
Ghost I invite Claimsranger to advise us of his headache causation.
I'm sorry but I just don't buy into this fear frenzy. To do so would be to ignore warnings by the CDC, NIH and others in the medical community who urge restraint amidst the feeding frenzy.
Now let us pray for those ignorant uninformed thousands of homeowners who fill the graves and cemeteries in Texas (and elsewhere) because they did not know at the time the perils of mold which were just suddenly "discovered" three years ago.
Let us pause to remember those hundreds and thousands of disabled and deceased cat adjusters who tromped through and breathed that deadly mold dust during Hurricanes Andrew, Hugo, Camille, Donna, Betsy, Agnes, and never knew the horrible horrible fate that would lie ahead.
What irony in that just a few years later, Dr Hood and his band of mold "experts" could suddenly discover that this mold plague makes the old bubonic more like a bad hair day by comparison.
If mold could kill Ghostbuster, you and I and several hundred other adjusters we know would be long gone. We have seen far greater exposure to this deadly plague in our short limited lives than most people would in a hundred lifetimes.
Oh the sorrow of it all. If only they had known:
The facts.
The truth.
Always the first casualty of war.
The circus continues. Enjoy it while it lasts. |
Ghostbuster
Registered User
Username: Ghostbuster
Post Number: 265
Registered: 12-2000
| | Posted on Tuesday, May 07, 2002 - 8:55 am: | |
Whoa, Hoss!
Our boy Claimsranger ain't fakin' it. Excessive mold exposure can give you a headache, (not to mention over exposure to claims). I once worked a loss in a bakery where the yeast was rising and got headache that lasted about a week.
But...he is being paid for it. |
Jim Flynt
Registered User
Username: Jimflynt
Post Number: 281
Registered: 6-2001
| | Posted on Tuesday, May 07, 2002 - 8:42 am: | |
hob•gob•lin, hob'gob''lin, n. Something causing dread or unreasonable fear.
"among the calamities of war may be jointly numbered the diminution of the love of truth, by the falsehoods which interest dictates and credulity encourages" (The Idler 11/11/1758)
"The first casualty when war comes is truth" (US Senator Hiram Warren Johnson, 1918)
The festival of lies of the 'mold wars' continues from those who would sacrifice truth for their own self interests.
The gentleman merely complained of a headache more likely caused from working long hours, being terribly underpaid for the job he is doing, and the stress of dealing with demanding insureds and other self interested parties who would rather embrace the fear frenzy than the facts.
What kind of snake oil solutions for the mold wars are you selling this week?
The circus continues with a few new clowns in the ring..............
(Message edited by jimflynt on May 07, 2002) |
R D Hood
Registered User
Username: Old_dog
Post Number: 15
Registered: 1-1997
| | Posted on Monday, May 06, 2002 - 11:30 pm: | |
Andrew,(Claimsranger) I really am distressed that you are hurting. 
BUT, there have been many ,many warnings, and woe to they that choose NOT to heed them.
Whats the next step? Comp claim?, Quit?, Hurt continously?
BTW, have you seen a neurologist and advised them of the conditions?
This is not a DRILL folks, It is battle, and there will be casualties.
|
Andrew K. Sloane
Member
Username: Claimsranger
Post Number: 15
Registered: 12-2001
| | Posted on Monday, May 06, 2002 - 10:23 pm: | |
I will make a specific post on this issue you brought to light TomJ, the mold has gotten to me, serious headache- I'd trade 10 hang-overs for this puppy. Once I have some control of my thinking, hide & watch!
A CLAIMSRANGER!!!!!!!!!!!! |
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