Re: Air Sample Data Analysis Help

[Guest guest]

–

This statement that you made concerns me.

<“If the good doc is going to stick

with his diagnosis of work-related asthma, he needs to have you sample for

other substances than mold (isocyanates, formaldehyde, or dye or latex, etc)

that will actually cause it. Because mold doesn't; it only exacerbates it…â€>

Can you prove this?  Wow - if this is your attitude and

you’re suggesting that Fred hire a consultant such as yourself, I’m a bit

scared…  , I suggest you climb out of your “box†and open up your eyes to

the fact that there is a TON of information that we are just finding out, along

with many unknowns regarding all sorts of IAQ/IEQ issues (and not just mold)

that will unfold itself over the course of our lifetimes and for many thousands

of years after we’re long since dead.

Just FYI, there was a Michigan woman who recently won a

$925,000 judgment after her property manager sent in “Ned†the handyman to rip

out a bunch of moldy drywall while she was present.  As a result of this, she

developed adult onset asthma.  She had absolutely NO prior respiratory issues. 

Can we conclusively say it was the mold?  Maybe not.  But… can we say conclusively

that it wasn’t???  Heck no!  Get the point?  If a person (immune compromised or

not) can grow a fungal ball in their lung – what makes you think that someone

can’t develop asthma.  Give me a break. 

Sorry, but I don’t think someone with a closed mind makes

a good consultant in any field…

Respectfully,

Stacey Champion

Owner/Consultant

Champion Indoor Environmental Services

PO Box 3332

Cottonwood, AZ

86326

Tel. Fax

sc@...

From: iequality [mailto:iequality ] On Behalf Of Dotson

Sent: Friday, September 23, 2005

1:56 PM

To: iequality

Subject: RE: Air

Sample Data Analysis Help

Fred - Forget all the over-analysis. The

natural daily variance is greater than the below sample results, so even

if the calculations were screwed up by you or the lab, the indoor

concentrations are basically low relative to the natural outdoor environment

and therefore show nothing out of the ordinary. The employee’s

simple-minded doctor asked for the sampling, so send the results to him for

analysis.

It would have been better and cheaper for

you to use spore traps for this particular application. But the doc won't know

that and as a medical doc he is more comfortable with cultures anyway. For his

comparison, I would also send him the most current sample for the nearest location

to you from http://www.aaaai.org/nab/index.cfm?p=pollen.

That way he can conclude for himself using other " peer " data that his

diagnosis won't hold water based on the info that he has in front of him.

If the good doc is going to stick with his

diagnosis of work-related asthma, he needs to have you sample for other

substances than mold (isocyanates, formaldehyde, or dye or latex, etc) that

will actually cause it. Because mold doesn't; it only exacerbates it, and there

is more in most employees homes and cars and certainly more outside than

in most commercial buildings that are without water damage. Sorry for

the big exacerbate word, but the doc will understand. And if you

are going to protect your company against what is probably a

accurate diagnosis of asthma from a misdirected cause (sure, it is

statistically extremely probable that the employee has asthma, and it is

likewise highly improbable that is is occupationally related) you need to

hire a CIH to help you with this.

Are you a animal handling facility or do

you have a spray painting operation or make foam on site? If you do, you have a

problem. If you don't, you need a CIH to evaluate your site for the on-site use

of tell the good doctor that you don't. Let the employee call OSHA and NIOSH.

But you should call a CIH first. And put it on your OSHA log and then

you can line it out later. If you want to be cheap about it you can call

your workers comp carrier and they may help you. Or they may not. And then they

will raise your rates. Go to the consultants list at www.AIHA.org.

B. Dotson, CIH, CSP, DEE

San , CA

95125

email: kyle@...

Air

Sample Data Analysis Help

Based on a recommendation from an employee’s doctor, we collected some

air samples for mold in the rooms listed in the table below (the primary room

of interest was #4).  The lab helped us out a lot with equipment and supplies

and instructions on how to use the equipment.  We collected the samples and

shipped them back to the lab, who cultured and analyzed the samples.  We got

the following data.  Based on what those of you know here, what conclusions

would you make?  I’ve listed the total count of each sample, along with the top

three molds found and the actual number of colonies reported for each mold on

the lab form.  Would you recommend additional work?

Room Number

Total Count (cfu/m3‑)

Rank

Number of Colonies

4

74

Cladosporium – 36.4%

Acremonium – 36.4%

Penicillium – 18.2%

4

4

2

4

115

Penicillium – 29.4%

Cladosporium – 23.5%

Aspergillus – 11.8%

5

4

2

151

236

Penicillium – 80%

Cladosporium – 5.7%

Acremonium – 5.7%

28

2

2

127

47

Penicillium – 28.6%

Acremonium – 14.3%

Sterile Hyphae – 14.3%

13

1

1

Outdoor Sample

445

Cladosporium – 62.1%

Penicillium – 16.7%

Aspergillus – 12.1%

277

74

54

__________________________________________________

[Guest guest]

,

Your recommendation to reference AAAAI data is a good idea. However,

the relative scales in the AAAAI tables, include mold, pollens grasses,

etc.

What this table needs is some adjustment to account for only mold

spores.

Two other references are published. EMLab and Pathcon. Taking all of

these together one can come up with an adjusted

AAAAI table that more closely reflects just mold spores.

We have this adjusted AAAAI table in our book.

BOB

[Guest guest]

Thanks. But that is not correct. Aaaai breaks out mold from pollens. Take a

closer look at the detailed reports.

Re: Air Sample Data Analysis Help

,

Your recommendation to reference AAAAI data is a good idea. However,

the relative scales in the AAAAI tables, include mold, pollens grasses,

etc.

What this table needs is some adjustment to account for only mold

spores.

Two other references are published. EMLab and Pathcon. Taking all of

these together one can come up with an adjusted

AAAAI table that more closely reflects just mold spores.

We have this adjusted AAAAI table in our book.

BOB

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receiving the included information for research and educational purposes.

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If you wish to use copyrighted material from this site for purposes of your

own that go beyond 'fair use', you must obtain permission from the copyright

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[Guest guest]

,

If you compare AAAAI results statistically to those of EMLab, their

are significant differences.

EMLab numbers are about 1/3 less. They both represent huge datasets

of samples.

EMLab also contains data from time periods when AAAAI does not sample,

because AAAAI samples only during allergy season.

The analytical method difference between the two data sets is that

AAAAI uses Burkhard samples with 24 hr samples, while the EMLab data is

based on air o cell or zephon cassettes and the sampling periods is

about 5 minutes.

The reason I adjusted in scale is that most people sample are using air

o cells. Consequently, they are interested in a reference scale, that

would be meaningful to Zephons.

Combining the relative " low to high " scales from AAAAI and the

analytical differences in the air o cell methods, gives an adjusted

scale.

BOB

[Guest guest]

Bob - Certainly the AAAAI results are higher than EMlab. And also higher

than the Pathcon paper by Shelton and my published paper on the levels

of Stachybotrys in the outdoor air in Houston. But because of AAAAI samples

only during the high months of the year, these studies are not inconsistent

and in fact quite consistent.

And due to the short sampling time of the Zephon and the extreme variability

of spore levels from hour to hour and even minute to minute, it is always

wise to hang ones hat on longer samples; again that's not to say that EMlab

and Shelton and me did not all have good data. I don't recall the sample

months of the Pathcon data. I used a period of winter and spring in Houston

when I had the cleanest data from a set of about 600 houses. My results were

consistent with an internal analysis by Moody Labs of about 2500 samples

from across the Southwest US.

I would be interested in seeing the assumptions behind your " reference

scale " . Since " EMLab also contains data from time periods when AAAAI does

not sample, because AAAAI samples only during allergy season " I assume that

you corrected for that in order to compare apples to apples. Otherwise you

would incorrectly attribute the 30% difference in the results to perceived

differences in the Burkard vs Zephon methods, rather than to the fact that

aaaai samples the higher allergy season and EMLab sampled the entire year

and reported the average.

I like the aaaai data because it actually correlates to health effects.

Because the aaaai samples only during allergy season; when the general

population actually has symptoms; the data also serves as a perfect

indicator of cause and effect since lower exposures don't cause symptoms for

the general population. Although we all know and accept that individual

responses vary and you will always have people on the extremes of the norm.

Gotta keep an open mind of course.......

B. Dotson, CIH, CSP

San , CA

kyle@...

Re: Air Sample Data Analysis Help

,

If you compare AAAAI results statistically to those of EMLab, their

are significant differences.

EMLab numbers are about 1/3 less. They both represent huge datasets

of samples.

EMLab also contains data from time periods when AAAAI does not sample,

because AAAAI samples only during allergy season.

The analytical method difference between the two data sets is that

AAAAI uses Burkhard samples with 24 hr samples, while the EMLab data is

based on air o cell or zephon cassettes and the sampling periods is

about 5 minutes.

The reason I adjusted in scale is that most people sample are using air

o cells. Consequently, they are interested in a reference scale, that

would be meaningful to Zephons.

Combining the relative " low to high " scales from AAAAI and the

analytical differences in the air o cell methods, gives an adjusted

scale.

BOB

FAIR USE NOTICE:

This site contains copyrighted material the use of which has not always been

specifically authorized by the copyright owner. We are making such material

available in our efforts to advance understanding of environmental,

political, human rights, economic, democracy, scientific, and social justice

issues, etc. We believe this constitutes a 'fair use' of any such

copyrighted material as provided for in section 107 of the US Copyright Law.

In accordance with Title 17 U.S.C. Section 107, the material on this site is

distributed without profit to those who have expressed a prior interest in

receiving the included information for research and educational purposes.

For more information go to: http://www.law.cornell.edu/uscode/17/107.shtml.

If you wish to use copyrighted material from this site for purposes of your

own that go beyond 'fair use', you must obtain permission from the copyright

owner.

[Guest guest]

Thanks for your response. To answer a couple of questions below. We are primarily an electronics components assembly. We use very few chemicals. The employee in question works in the office wing of our facility. She rarely visited/visits the assembly area.

My initial suggestion to our plant manager was to bring someone from the outside in to help. That got shot down rather quickly. 60% of our production was shifted to China in Feb and its probably only a matter of time that that the rest goes and we cease to be a production/assembly facility. As such, there is no $ for outside help, as any additional costs may help justify moving what's left to our far east neighbors. I've been instructed to "learn from doing and nip this in the bud". Sad state of affairs. Dotson wrote:

Fred - Forget all the over-analysis. The natural daily variance is greater than the below sample results, so even if the calculations were screwed up by you or the lab, the indoor concentrations are basically low relative to the natural outdoor environment and therefore show nothing out of the ordinary. The employee’s simple-minded doctor asked for the sampling, so send the results to him for analysis.

It would have been better and cheaper for you to use spore traps for this particular application. But the doc won't know that and as a medical doc he is more comfortable with cultures anyway. For his comparison, I would also send him the most current sample for the nearest location to you from http://www.aaaai.org/nab/index.cfm?p=pollen. That way he can conclude for himself using other "peer" data that his diagnosis won't hold water based on the info that he has in front of him.

If the good doc is going to stick with his diagnosis of work-related asthma, he needs to have you sample for other substances than mold (isocyanates, formaldehyde, or dye or latex, etc) that will actually cause it. Because mold doesn't; it only exacerbates it, and there is more in most employees homes and cars and certainly more outside than in most commercial buildings that are without water damage. Sorry for the big exacerbate word, but the doc will understand. And if you are going to protect your company against what is probably a accurate diagnosis of asthma from a misdirected cause (sure, it is statistically extremely probable that the employee has asthma, and it is likewise highly improbable that is is occupationally related) you need to hire a CIH to help you with this.

Are you a animal handling facility or do you have a spray painting operation or make foam on site? If you do, you have a problem. If you don't, you need a CIH to evaluate your site for the on-site use of tell the good doctor that you don't. Let the employee call OSHA and NIOSH. But you should call a CIH first. And put it on your OSHA log and then you can line it out later. If you want to be cheap about it you can call your workers comp carrier and they may help you. Or they may not. And then they will raise your rates. Go to the consultants list at www.AIHA.org.

B. Dotson, CIH, CSP, DEESan , CA 95125 email: kyle@...

Air Sample Data Analysis Help

Based on a recommendation from an employee’s doctor, we collected some air samples for mold in the rooms listed in the table below (the primary room of interest was #4). The lab helped us out a lot with equipment and supplies and instructions on how to use the equipment. We collected the samples and shipped them back to the lab, who cultured and analyzed the samples. We got the following data. Based on what those of you know here, what conclusions would you make? I’ve listed the total count of each sample, along with the top three molds found and the actual number of colonies reported for each mold on the lab form. Would you

recommend additional work?

Room Number

Total Count (cfu/m3‑)

Rank

Number of Colonies

4

74

Cladosporium – 36.4%

Acremonium – 36.4%

Penicillium – 18.2%

4

4

2

4

115

Penicillium – 29.4%

Cladosporium – 23.5%

Aspergillus – 11.8%

5

4

2

151

236

Penicillium – 80%

Cladosporium – 5.7%

Acremonium – 5.7%

28

2

2

127

47

Penicillium – 28.6%

Acremonium – 14.3%

Sterile Hyphae – 14.3%

13

1

1

Outdoor Sample

445

Cladosporium – 62.1%

Penicillium – 16.7%

Aspergillus – 12.1%

277

74

54

__________________________________________________

[Guest guest]

Fred - This is what I would do if I were in your shoes. I would assume that the doctor is correct and that the person has asthma. I would share 100% of the sample results with the doctor. I would not attach to the results any additional "interpretation", such as the aaaai.org reference. Just send him exactly what the lab sent you. Send all of the above also to your workers comp carrier. They will address the claim regarding work-relatedness. Until such time as the claim is denied and upheld, keep this listed on your OSHA log as a work related illness. Regarding additional internal investigation regarding causation, focus on determining if there was any previous water damage in your building that was improperly repaired (wall full of mold covered up with new vinyl wallpaper, etc). And keep an eye out to any other persons being so affected. And you might suggest to the employee that you are looking for a cause and that she might want to do her on research on the OSHA website regarding the hobbies that might be going on in her home (i.e.; maybe a son has a spray paint booth in the basement; we have seen weirder things in homes). You can always bring an OSHA industrial hygienist in for a free consultation, although I doubt your CEO would approve that. Good luck.

B. Dotson, CIH, CSP, DEESan , CA 95125 email: kyle@...

-----Original Message-----From: iequality [mailto:iequality ] On Behalf Of Fred BirkleSent: Monday, September 26, 2005 8:53 AMTo: iequality Subject: RE: Air Sample Data Analysis Help

Thanks for your response. To answer a couple of questions below. We are primarily an electronics components assembly. We use very few chemicals. The employee in question works in the office wing of our facility. She rarely visited/visits the assembly area.

My initial suggestion to our plant manager was to bring someone from the outside in to help. That got shot down rather quickly. 60% of our production was shifted to China in Feb and its probably only a matter of time that that the rest goes and we cease to be a production/assembly facility. As such, there is no $ for outside help, as any additional costs may help justify moving what's left to our far east neighbors. I've been instructed to "learn from doing and nip this in the bud". Sad state of affairs. Dotson wrote:

Fred - Forget all the over-analysis. The natural daily variance is greater than the below sample results, so even if the calculations were screwed up by you or the lab, the indoor concentrations are basically low relative to the natural outdoor environment and therefore show nothing out of the ordinary. The employee’s simple-minded doctor asked for the sampling, so send the results to him for analysis.

It would have been better and cheaper for you to use spore traps for this particular application. But the doc won't know that and as a medical doc he is more comfortable with cultures anyway. For his comparison, I would also send him the most current sample for the nearest location to you from http://www.aaaai.org/nab/index.cfm?p=pollen. That way he can conclude for himself using other "peer" data that his diagnosis won't hold water based on the info that he has in front of him.

If the good doc is going to stick with his diagnosis of work-related asthma, he needs to have you sample for other substances than mold (isocyanates, formaldehyde, or dye or latex, etc) that will actually cause it. Because mold doesn't; it only exacerbates it, and there is more in most employees homes and cars and certainly more outside than in most commercial buildings that are without water damage. Sorry for the big exacerbate word, but the doc will understand. And if you are going to protect your company against what is probably a accurate diagnosis of asthma from a misdirected cause (sure, it is statistically extremely probable that the employee has asthma, and it is likewise highly improbable that is is occupationally related) you need to hire a CIH to help you with this.

Are you a animal handling facility or do you have a spray painting operation or make foam on site? If you do, you have a problem. If you don't, you need a CIH to evaluate your site for the on-site use of tell the good doctor that you don't. Let the employee call OSHA and NIOSH. But you should call a CIH first. And put it on your OSHA log and then you can line it out later. If you want to be cheap about it you can call your workers comp carrier and they may help you. Or they may not. And then they will raise your rates. Go to the consultants list at www.AIHA.org.

B. Dotson, CIH, CSP, DEESan , CA 95125 email: kyle@...

Air Sample Data Analysis Help

Based on a recommendation from an employee’s doctor, we collected some air samples for mold in the rooms listed in the table below (the primary room of interest was #4). The lab helped us out a lot with equipment and supplies and instructions on how to use the equipment. We collected the samples and shipped them back to the lab, who cultured and analyzed the samples. We got the following data. Based on what those of you know here, what conclusions would you make? I’ve listed the total count of each sample, along with the top three molds found and the actual number of colonies reported for each mold on the lab form. Would you recommend additional work?

Room Number

Total Count (cfu/m3‑)

Rank

Number of Colonies

4

74

Cladosporium – 36.4%

Acremonium – 36.4%

Penicillium – 18.2%

4

4

2

4

115

Penicillium – 29.4%

Cladosporium – 23.5%

Aspergillus – 11.8%

5

4

2

151

236

Penicillium – 80%

Cladosporium – 5.7%

Acremonium – 5.7%

28

2

2

127

47

Penicillium – 28.6%

Acremonium – 14.3%

Sterile Hyphae – 14.3%

13

1

1

Outdoor Sample

445

Cladosporium – 62.1%

Penicillium – 16.7%

Aspergillus – 12.1%

277

74

54

__________________________________________________

[Guest guest]

1. Sensitization is not asthma, but sensitization can result in asthma.

2. Asthma is a more generic term for certain responses (not underlyng condition/cause):

Asthma is a chronic inflammatory disorder of the airways. The histopathologic features include denudation of airway epithelium, collagen deposition beneath the basement membrane, airway edema, mast cell activation, and inflammatory cell infiltration with neutrophils, eosinophils, and lymphocytes (especially T-lymphocytes). Hypertrophy of bronchial smooth muscle and hypertrophy of mucous glands with plugging of small airways with thick mucous can occur. This airway inflammation underlies disease chronicity and contributes to airway hyper-responsiveness, airflow limitation, and respiratory symptoms (including recurrent episodes of wheezing, breathlessness, chest tightness, and cough, particularly during the nighttime and early morning hours).

Occupational asthma is triggered by various agents in the workplace and may occur weeks to years after initial exposure and sensitization. Women may experience catamenial asthma at predictable times during the menstrual cycle.

3. Sensitization is an immune based response (one a few types) that has two phases: Induction (from a relatively high dose) and Elicitation (relatively lower dose). Induction is not a disease state, Elicitation is. There must be sufficient time for the human body to recognize the agent as offensive and respond in an immunological fashion (this may be weeks or years).

4. Any irritating stimuli can elicit asthmatic response - dry air, cold air, acidic compounds, etc. This irritation response is a different mechanism than an immunologic response for say aldehydes or malleic anhydride or isocyanates or even endotoxins from cotton dust. The response could be characterized as asthmatic, even though it is not immune-mediated.

5. Once a person has asthma, these can aggravate the condition. So can a recent cold or viral infection, etc.

6. As a little side note, mice are generally used (OF1 by the French protocol, Swiss Webster by the Univ Pitt protocol) to look at irritant response. They are tested for their respiratory decline function [RD50] (mice decrease respiration in response to chemical stimulus, unlike humans which might suggest the mice are smarter [or designed better]). They are more sensitive than humans for this response and it is indicative of trigeminal nerve stimulation although there are a few pathways or response - this is directly related to irritation thresholds in humans (ca. 1-10% of the RD50 value). This response mimics in some ways asthmatic responses to irritants. The mice will also develop nasal lesions at lower concentrations (order or two of magnitude usually) below humans (many times at the RD50 concentration), making the mice useful for sensitive pre-cursor testing. See

Schaper, : Development of a Database for Sensory Irritants and Its Use in Establishing Occupational Exposure Limits. AIHA J 54(9):488-544. 1993.; Monticello, T.M., K.T. , and L. Uraih: Non-neoplastic nasal lesions in rats and mice. Environ. Health Perspectives 85:249-274. 1990; KT : Approaches to the identification and recording of nasal lesions in toxicology studies. Toxicol. Pathol. 19:337-371. 1998; Harkema, JR: Comparative aspects of nasal airway anatomy relevance to inhalation toxicology. Toxicol. Pathol. 19:321-326. 1991.

7. Latex allergy is usually immune-based (misnomer, some "latex" allergies are from other additives in gloves).

8. Subtilisins (derived from Bacillus subtilis) are potent sensitizers that operate from an immunological standpoint - the TLV is 60 ng/m3 the last I looked. P & G uses animal models to estimate peak acceptable inhalation concentrations by comparing new enzymatic agents to subtilisins.

9. Induction is often caused by dermal exposure with elicitation by dermal or inhalation routes (ex. Glutaraldehyde, TDI).

Tony

........................................................................... "Tony" Havics, CHMM, CIH, PEpH2, LLCPO Box 34140Indianapolis, IN 46234 cell90% of Risk Management is knowing where to place the decimal point...any consultant can give you the other 10%â„ 

-----Original Message-----From: iequality [mailto:iequality ] On Behalf Of AirwaysEnv@...Sent: Monday, September 26, 2005 11:31 AMTo: iequality Subject: Re: Air Sample Data Analysis Help

....If the good doc is going to stick with his diagnosis of work-related asthma, he needs to have you sample for other substances than mold (isocyanates, formaldehyde, or dye or latex, etc) that will actually cause it. Because mold doesn't; it only exacerbates it... ,I agree that any and all potential sensitizers and asthma triggers (including mite, cockroach and rodent antigens) must be considered in investigating an environmental cause of adult-onset asthma.Can you explain how mold can be an asthma trigger (i.e., produce a hypersensitivity reaction) without being a sensitizer? How would mold contaminants differ from latex, for example, in their ability to produce allergic sensitization?I remember when many IH professionals did not believe in chemical sensitivities.Steve Temes

[Guest guest]

Cold air is a well known "trigger" of asthma. Cold air is not a sensitizer.

B. Dotson, CIH, CSP

-----Original Message-----From: iequality [mailto:iequality ] On Behalf Of AirwaysEnv@...Sent: Monday, September 26, 2005 9:31 AMTo: iequality Subject: Re: Air Sample Data Analysis Help

....If the good doc is going to stick with his diagnosis of work-related asthma, he needs to have you sample for other substances than mold (isocyanates, formaldehyde, or dye or latex, etc) that will actually cause it. Because mold doesn't; it only exacerbates it... ,I agree that any and all potential sensitizers and asthma triggers (including mite, cockroach and rodent antigens) must be considered in investigating an environmental cause of adult-onset asthma.Can you explain how mold can be an asthma trigger (i.e., produce a hypersensitivity reaction) without being a sensitizer? How would mold contaminants differ from latex, for example, in their ability to produce allergic sensitization?I remember when many IH professionals did not believe in chemical sensitivities.Steve Temes

[Guest guest]

Clearly, those of us with allergies only report symptoms while we are awake.

Because we are otherwise sleeping. So while I see that you accurately

" adjusted " the aaaai dataset to reflect day exposures, that only corrolates

the databases and validates all three. I assume that you are not trying to

say that it also says anything about the levels of exposure that cause

symptoms? And you indicated that the aaaai group only samples during allergy

season, and the EMLab and Pathcon data is year around; why wouldn't the

average of the EMLab and Pathcon data sets be legitimately lower than the

aaaai data set? And all three therefore can be accurate?

I think I will continue to trust the aaaai data the most as an accurate

picture of natural exposures levels that can cause symptoms in the general

populations of humans, and continue to consider the EMLab and Pathcon data

as also well presented contemporary subsets that say more about what you

should expect as " normal " samples than what will cause or not cause

symptoms.

Thanks for your response, Bob.

Re: Air Sample Data Analysis Help

,

In looking at AAAAI, EMLab and Pathcon data, one needs to look at the

log normal distribution of the data.

I have done this in the PRV book. By plotting the data in this

format, one can compare and adjust the distributions using the

mathematics developed by NIOSH in the mid 70s based on geometric

standard deviations.

The significance of this that most of us sample during the daytime,

while AAAAI samples are 24 hours. As you know, mold genera sporulate

differently depending upon the time day. A number of researchers have

pointed out that sampling during the nightime can give much higher

results.

Since most of our clients report symptoms during the day, it is the

relevance of the daytime mold spore concentrations that are more

significant. (Don't forget, while we sleep our bodies suppress mucous

production in upper nasal cavities, Hence, the derivation of many

" allergy " medications. They mimic this sleep effect. Newer drugs

have less of a drowsiness effect. )

Hence, I lowered the number ranges of the AAAAI table, to reflect more

accurately, what the other labs have shown as daytime concentration

ranges and use the same symptom / sensitivity descriptions.

Bob

FAIR USE NOTICE:

This site contains copyrighted material the use of which has not always been

specifically authorized by the copyright owner. We are making such material

available in our efforts to advance understanding of environmental,

political, human rights, economic, democracy, scientific, and social justice

issues, etc. We believe this constitutes a 'fair use' of any such

copyrighted material as provided for in section 107 of the US Copyright Law.

In accordance with Title 17 U.S.C. Section 107, the material on this site is

distributed without profit to those who have expressed a prior interest in

receiving the included information for research and educational purposes.

For more information go to: http://www.law.cornell.edu/uscode/17/107.shtml.

If you wish to use copyrighted material from this site for purposes of your

own that go beyond 'fair use', you must obtain permission from the copyright

owner.

[Guest guest]

Tony,

Thank you for your very thorough response to my questions about allergic sensitization to mold and mold as an asthma trigger.

You wrote:

3. Sensitization is an immune based response (one a few types) that has two phases: Induction (from a relatively high dose) and Elicitation (relatively lower dose). Induction is not a disease state, Elicitation is. There must be sufficient time for the human body to recognize the agent as offensive and respond in an immunological fashion (this may be weeks or years).

Must induction be caused by a relatively high dose, or can it also be caused by chronic low-level exposures?

Might induction have more to do with genetic predisposition than dose, making the amount of any given exposure less important than exposure, per se?

Steve Temes

1. Sensitization is not asthma, but sensitization can result in asthma.

2. Asthma is a more generic term for certain responses (not underlyng condition/cause):

Asthma is a chronic inflammatory disorder of the airways. The histopathologic features include denudation of airway epithelium, collagen deposition beneath the basement membrane, airway edema, mast cell activation, and inflammatory cell infiltration with neutrophils, eosinophils, and lymphocytes (especially T-lymphocytes). Hypertrophy of bronchial smooth muscle and hypertrophy of mucous glands with plugging of small airways with thick mucous can occur. This airway inflammation underlies disease chronicity and contributes to airway hyper-responsiveness, airflow limitation, and respiratory symptoms (including recurrent episodes of wheezing, breathlessness, chest tightness, and cough, particularly during the nighttime and early morning hours).

Occupational asthma is triggered by various agents in the workplace and may occur weeks to years after initial exposure and sensitization. Women may experience catamenial asthma at predictable times during the menstrual cycle.

3. Sensitization is an immune based response (one a few types) that has two phases: Induction (from a relatively high dose) and Elicitation (relatively lower dose). Induction is not a disease state, Elicitation is. There must be sufficient time for the human body to recognize the agent as offensive and respond in an immunological fashion (this may be weeks or years).

4. Any irritating stimuli can elicit asthmatic response - dry air, cold air, acidic compounds, etc. This irritation response is a different mechanism than an immunologic response for say aldehydes or malleic anhydride or isocyanates or even endotoxins from cotton dust. The response could be characterized as asthmatic, even though it is not immune-mediated.

5. Once a person has asthma, these can aggravate the condition. So can a recent cold or viral infection, etc.

6. As a little side note, mice are generally used (OF1 by the French protocol, Swiss Webster by the Univ Pitt protocol) to look at irritant response. They are tested for their respiratory decline function [RD50] (mice decrease respiration in response to chemical stimulus, unlike humans which might suggest the mice are smarter [or designed better]). They are more sensitive than humans for this response and it is indicative of trigeminal nerve stimulation although there are a few pathways or response - this is directly related to irritation thresholds in humans (ca. 1-10% of the RD50 value). This response mimics in some ways asthmatic responses to irritants. The mice will also develop nasal lesions at lower concentrations (order or two of magnitude usually) below humans (many times at the RD50 concentration), making the mice useful for sensitive pre-cursor testing. See

Schaper, : Development of a Database for Sensory Irritants and Its Use in Establishing Occupational Exposure Limits. <i style="mso-bidi-font-style: normal"> AIHA J 54(9):488-544. 1993.; Monticello, T.M., K.T. , and L. Uraih: Non-neoplastic nasal lesions in rats and mice. <i style="mso-bidi-font-style: normal">Environ. Health Perspectives 85:249-274. 1990; KT : Approaches to the identification and recording of nasal lesions in toxicology studies. <i style="mso-bidi-font-style: normal">Toxicol. Pathol. 19:337-371. 1998; Harkema, JR: Comparative aspects of nasal airway anatomy relevance to inhalation toxicology. <i style="mso-bidi-font-style: normal">Toxicol. Pathol. 19:321-326. 1991.

7. Latex allergy is usually immune-based (misnomer, some "latex" allergies are from other additives in gloves).

8. Subtilisins (derived from Bacillus subtilis) are potent sensitizers that operate from an immunological standpoint - the TLV is 60 ng/m3 the last I looked. P & G uses animal models to estimate peak acceptable inhalation concentrations by comparing new enzymatic agents to subtilisins.

9. Induction is often caused by dermal exposure with elicitation by dermal or inhalation routes (ex. Glutaraldehyde, TDI).

Tony

...........................................................................

"Tony" Havics, CHMM, CIH, PE

pH2, LLC

PO Box 34140

Indianapolis, IN 46234

cell

90% of Risk Management is knowing where to place the decimal point...any consultant can give you the other 10%?

Re: Air Sample Data Analysis Help

....If the good doc is going to stick with his diagnosis of work-related asthma, he needs to have you sample for other substances than mold (isocyanates, formaldehyde, or dye or latex, etc) that will actually cause it. Because mold doesn't; it only exacerbates it...

,

I agree that any and all potential sensitizers and asthma triggers (including mite, cockroach and rodent antigens) must be considered in investigating an environmental cause of adult-onset asthma.

Can you explain how mold can be an asthma trigger (i.e., produce a hypersensitivity reaction) without being a sensitizer? How would mold contaminants differ from latex, for example, in their ability to produce allergic sensitization?

I remember when many IH professionals did not believe in chemical sensitivities.

Steve Temes

[Guest guest]

See Below

........................................................................... "Tony" Havics, CHMM, CIH, PEpH2, LLCPO Box 34140Indianapolis, IN 46234 cell90% of Risk Management is knowing where to place the decimal point...any consultant can give you the other 10%â„ 

-----Original Message-----From: iequality [mailto:iequality ] On Behalf Of AirwaysEnv@...Sent: Wednesday, September 28, 2005 1:51 PMTo: iequality Subject: Re: Air Sample Data Analysis Help

Tony,Thank you for your very thorough response to my questions about allergic sensitization to mold and mold as an asthma trigger.You wrote:3. Sensitization is an immune based response (one a few types) that has two phases: Induction (from a relatively high dose) and Elicitation (relatively lower dose). Induction is not a disease state, Elicitation is. There must be sufficient time for the human body to recognize the agent as offensive and respond in an immunological fashion (this may be weeks or years).Must induction be caused by a relatively high dose, or can it also be caused by chronic low-level exposures?

Knowledge today (especially if one looks at the agents - enzymes, MDI, TDI, maleic anhydride, glutaraldehyde, colophony, epoxies/acrylates/resins, nickel, platinum salts, etc.) only really supports a PEAK dose at a "high" concentration, not low chronic exposure. One might say (and many good folks have - it's the peak dose stupid)

Exception may be implants where very low concentrations over relatively longer periods have been seen to result in sensitization. For example, tert-butyl catechol at 4 ppm in an implant.

Might induction have more to do with genetic predisposition than dose, making the amount of any given exposure less important than exposure, per se?

The jury is out on genetic predisposition, but consider that all the work done on isocyanates and epoxy components has not established any (they certainly tried hard). There are precursor bio-markers after exposure but before sensitization that may prove useful. There are several papers on genetic susceptible populations for chemical bases that are well established.

I believe there are underlying genetic factors, but that they are difficult to determine when looking at more complex 3-D structures such as re-formed proteins and larger macro-molecules; and because of cross-reactions. There has been some success in looking at groups of agents to predict qualitative sensitization potential, particularly with regard to Structural Activity Relationship (SAR) analysis, but not tied to genetics. We generally use the guinea pig maximization test to assess potential (on real guinea pigs), but it fails in cases also - particularly where a chemical mechanism is irritation, or where direct skin reaction is more prominent, thus limiting the immune system an opportunity do detect and acquire a memory.

Consider epoxies where one may have 3 components. Each may be a sensitizer itself or only as a group to react with a protein and create an appropriate 3-D structure the body recognizes as an adverse agent. Testing with each component may not pick it up, nor might the group only; and trying to tie in genetic-based reactions would be even more difficult.

Steve Temes

1. Sensitization is not asthma, but sensitization can result in asthma.2. Asthma is a more generic term for certain responses (not underlyng condition/cause): Asthma is a chronic inflammatory disorder of the airways. The histopathologic features include denudation of airway epithelium, collagen deposition beneath the basement membrane, airway edema, mast cell activation, and inflammatory cell infiltration with neutrophils, eosinophils, and lymphocytes (especially T-lymphocytes). Hypertrophy of bronchial smooth muscle and hypertrophy of mucous glands with plugging of small airways with thick mucous can occur. This airway inflammation underlies disease chronicity and contributes to airway hyper-responsiveness, airflow limitation, and respiratory symptoms (including recurrent episodes of wheezing, breathlessness, chest tightness, and cough, particularly during the nighttime and early morning hours).Occupational asthma is triggered by various agents in the workplace and may occur weeks to years after initial exposure and sensitization. Women may experience catamenial asthma at predictable times during the menstrual cycle. 3. Sensitization is an immune based response (one a few types) that has two phases: Induction (from a relatively high dose) and Elicitation (relatively lower dose). Induction is not a disease state, Elicitation is. There must be sufficient time for the human body to recognize the agent as offensive and respond in an immunological fashion (this may be weeks or years). 4. Any irritating stimuli can elicit asthmatic response - dry air, cold air, acidic compounds, etc. This irritation response is a different mechanism than an immunologic response for say aldehydes or malleic anhydride or isocyanates or even endotoxins from cotton dust. The response could be characterized as asthmatic, even though it is not immune-mediated. 5. Once a person has asthma, these can aggravate the condition. So can a recent cold or viral infection, etc. 6. As a little side note, mice are generally used (OF1 by the French protocol, Swiss Webster by the Univ Pitt protocol) to look at irritant response. They are tested for their respiratory decline function [RD50] (mice decrease respiration in response to chemical stimulus, unlike humans which might suggest the mice are smarter [or designed better]). They are more sensitive than humans for this response and it is indicative of trigeminal nerve stimulation although there are a few pathways or response - this is directly related to irritation thresholds in humans (ca. 1-10% of the RD50 value). This response mimics in some ways asthmatic responses to irritants. The mice will also develop nasal lesions at lower concentrations (order or two of magnitude usually) below humans (many times at the RD50 concentration), making the mice useful for sensitive pre-cursor testing. See Schaper, : Development of a Database for Sensory Irritants and Its Use in Establishing Occupational Exposure Limits. <i style="mso-bidi-font-style: normal"> AIHA J 54(9):488-544. 1993.; Monticello, T.M., K.T. , and L. Uraih: Non-neoplastic nasal lesions in rats and mice. <i style="mso-bidi-font-style: normal">Environ. Health Perspectives 85:249-274. 1990; KT : Approaches to the identification and recording of nasal lesions in toxicology studies. <i style="mso-bidi-font-style: normal">Toxicol. Pathol. 19:337-371. 1998; Harkema, JR: Comparative aspects of nasal airway anatomy relevance to inhalation toxicology. <i style="mso-bidi-font-style: normal">Toxicol. Pathol. 19:321-326. 1991.7. Latex allergy is usually immune-based (misnomer, some "latex" allergies are from other additives in gloves). 8. Subtilisins (derived from Bacillus subtilis) are potent sensitizers that operate from an immunological standpoint - the TLV is 60 ng/m3 the last I looked. P & G uses animal models to estimate peak acceptable inhalation concentrations by comparing new enzymatic agents to subtilisins. 9. Induction is often caused by dermal exposure with elicitation by dermal or inhalation routes (ex. Glutaraldehyde, TDI). Tony .......................................................................... "Tony" Havics, CHMM, CIH, PEpH2, LLCPO Box 34140Indianapolis, IN 46234 cell90% of Risk Management is knowing where to place the decimal point...any consultant can give you the other 10%?

-----Original Message-----From: iequality [mailto:iequality ] On Behalf Of AirwaysEnv@...Sent: Monday, September 26, 2005 11:31 AMTo: iequality Subject: Re: Air Sample Data Analysis Help

....If the good doc is going to stick with his diagnosis of work-related asthma, he needs to have you sample for other substances than mold (isocyanates, formaldehyde, or dye or latex, etc) that will actually cause it. Because mold doesn't; it only exacerbates it... ,I agree that any and all potential sensitizers and asthma triggers (including mite, cockroach and rodent antigens) must be considered in investigating an environmental cause of adult-onset asthma.Can you explain how mold can be an asthma trigger (i.e., produce a hypersensitivity reaction) without being a sensitizer? How would mold contaminants differ from latex, for example, in their ability to produce allergic sensitization?I remember when many IH professionals did not believe in chemical sensitivities.Steve Temes

[Guest guest]

Tony,

How does this peak dose thing apply to common allergic sensitization scenarios? How many peanut butter cookies or shrimp (ingestion), bee stings (injection), or brushes with poison ivy (dermal exposure to urushiol - another catechol) constitute a peak dose that can cause sensitization? How much ragweed pollen is a peak dose? Let's keep it real. It's obvious that the question should be, "Peak dose for whom?".

I just returned from an inspection of a small 2-bedroom unit in a retirement community where my client just signed a 6-month lease and moved in last week. She wound up in the ER with breathing difficulties when she was working in the kitchen where she could smell and taste something in the air. She was tested and released and returned home, where her symptoms immediately returned. She went to her doctor and was given "an allergy shot" and advised not to return. I was called to inspect and "test" (which I did not do) and found evidence of a rodent infestation under the dishwasher and beneath the cabinets. When I told the husband that I saw mouse feces and larger droppings that looked like they might be from a rat or chipmunk, he said he was told by neighbors that the previous elderly owner (now deceased) used to feed a "pet" chipmunk inside the house.

For much of the practical building investigation work I do, 90% of the time, where you put the decimal point is irrelevant.

Steve Temes

See Below

...........................................................................

"Tony" Havics, CHMM, CIH, PE

pH2, LLC

PO Box 34140

Indianapolis, IN 46234

cell

90% of Risk Management is knowing where to place the decimal point...any consultant can give you the other 10%?

Re: Air Sample Data Analysis Help

Tony,

Thank you for your very thorough response to my questions about allergic sensitization to mold and mold as an asthma trigger.

You wrote:

3. Sensitization is an immune based response (one a few types) that has two phases: Induction (from a relatively high dose) and Elicitation (relatively lower dose). Induction is not a disease state, Elicitation is. There must be sufficient time for the human body to recognize the agent as offensive and respond in an immunological fashion (this may be weeks or years).

Must induction be caused by a relatively high dose, or can it also be caused by chronic low-level exposures?

Knowledge today (especially if one looks at the agents - enzymes, MDI, TDI, maleic anhydride, glutaraldehyde, colophony, epoxies/acrylates/resins, nickel, platinum salts, etc.) only really supports a PEAK dose at a "high" concentration, not low chronic exposure. One might say (and many good folks have - it's the peak dose stupid)

Exception may be implants where very low concentrations over relatively longer periods have been seen to result in sensitization. For example, tert-butyl catechol at 4 ppm in an implant.

Might induction have more to do with genetic predisposition than dose, making the amount of any given exposure less important than exposure, per se?

The jury is out on genetic predisposition, but consider that all the work done on isocyanates and epoxy components has not established any (they certainly tried hard). There are precursor bio-markers after exposure but before sensitization that may prove useful. There are several papers on genetic susceptible populations for chemical bases that are well established.

I believe there are underlying genetic factors, but that they are difficult to determine when looking at more complex 3-D structures such as re-formed proteins and larger macro-molecules; and because of cross-reactions. There has been some success in looking at groups of agents to predict qualitative sensitization potential, particularly with regard to Structural Activity Relationship (SAR) analysis, but not tied to genetics. We generally use the guinea pig maximization test to assess potential (on real guinea pigs), but it fails in cases also - particularly where a chemical mechanism is irritation, or where direct skin reaction is more prominent, thus limiting the immune system an opportunity do detect and acquire a memory.

Consider epoxies where one may have 3 components. Each may be a sensitizer itself or only as a group to react with a protein and create an appropriate 3-D structure the body recognizes as an adverse agent. Testing with each component may not pick it up, nor might the group only; and trying to tie in genetic-based reactions would be even more difficult.

Steve Temes

[Guest guest]

Please see inserted comments below:

Steve:

Per your response below.

Paragraph 1

- Appears to be rhetorical. One looks at sensitive sub-population when one can, but in risk management there is no such thing as zero risk.

- If I took 100 people randomly and looked at their lives over 70 years, 1 or 2 of them would have died in a car accident (this is 1,000 to 2,000 of out a million mind you). Should we not drive cars?? I don't think so, but I do think we should define acceptable risk - both voluntary and involuntary.

Paragraph 2

- There are acceptable values for mouse allergen; you might review the literature

- My sister is allergic to chocolate - should we ban chocolate?? (FYI - it has been shown that it is because of the cockroach material in chocolate that people are allergic to; I presented data on followup challenge testing for cockroach in a case several years ago) Ahain, there is no such thing as zero risk

- I'm a Certified in Comprehensive PRACTICE of Industrial Hygiene (CIH)

- I'm Registered to PRACTICE Engineering (PE)

- Medical Doctors are Lisc. to PRACTICE

- Professional judgment if most often that which is used in practice. But ignoring the science is not professional.

My questions were not rhetorical. I was making an obvious point to refute your statement that relatively high levels of exposure are necessary to induce allergic sensitization. The sensitive sub-population are the ones who are impacted the most when this scientific fact is ignored by health and safety professionals. This sub-population is a large number of people.

I never implied that we ban anything (except obfuscation of facts).

Ignoring the real cause of environmental health effects is not professional either. It seems to me that doing so might be construed as a violation of the CIH Code of Ethics.

To wit,

Industrial Hygienists shall:

1. Practice their profession following recognized scientific principles with the realization that the lives, health and well-being of people may depend upon their professional judgment and that they are obligated to protect the health and well-being of people.

Industrial Hygienists should base their professional opinions, judgments, interpretations of findings and recommendations upon recognized scientific principles and practices which preserve and protect the health and well-being of people.

Industrial Hygienists shall not distort, alter or hide facts in rendering professional opinions or recommendations.

Industrial Hygienists shall not knowingly make statements that misrepresent or omit facts.

Paragraph 3

- You did place the decimal point

Good one!

Final comment:

Until one knows how exposure limits are set (EPA, OSHA, FDA, others), etc. one should be careful to criticize them.

I did not criticize any exposure limits. I made the point that, for allergic sensitization, exposure limits do not apply.

Tony

ps This response is not meant to be rude, just concise

Ditto,

Steve Temes

..........................................................................

"Tony" Havics, CHMM, CIH, PE

pH2, LLC

PO Box 34140

Indianapolis, IN 46234

cell

90% of Risk Management is knowing where to place the decimal point...any consultant can give you the other 10%?

Re: Air Sample Data Analysis Help

Tony,

How does this peak dose thing apply to common allergic sensitization scenarios? How many peanut butter cookies or shrimp (ingestion), bee stings (injection), or brushes with poison ivy (dermal exposure to urushiol - another catechol) constitute a peak dose that can cause sensitization? How much ragweed pollen is a peak dose? Let's keep it real. It's obvious that the question should be, "Peak dose for whom?".

I just returned from an inspection of a small 2-bedroom unit in a retirement community where my client just signed a 6-month lease and moved in last week. She wound up in the ER with breathing difficulties when she was working in the kitchen where she could smell and taste something in the air. She was tested and released and returned home, where her symptoms immediately returned. She went to her doctor and was given "an allergy shot" and advised not to return. I was called to inspect and "test" (which I did not do) and found evidence of a rodent infestation under the dishwasher and beneath the cabinets. When I told the husband that I saw mouse feces and larger droppings that looked like they might be from a rat or chipmunk, he said he was told by neighbors that the previous elderly owner (now deceased) used to feed a "pet" chipmunk inside the house.

For much of the practical building investigation work I do, 90% of the time, where you put the decimal point is irrelevant.

Steve Temes