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Description A teratogen is any medication, chemical, infectious disease, or environmental agent that might interfere with the normal development of a foetus and result in the loss of a pregnancy , a birth defect , or a pregnancy complication .

You are dodging some important questions: How much does it take to cause harm?  How much are users of latex products exposed to? — David Canzi     The problem most anti-spammers are trying to solve, when                 correctly understood, reduces to "How do I let everybody in                 the world send me e-mail without letting everybody in the                 world send me e-mail?"

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Good questions. The problem is that the answers have never been researched. All we can say is that the dramatic rise in anal cancer in gay men is good reason to conclude that condoms exceed safe limits. Eighteen million victims (in America alone) of latex allergies confirm that fear. The situation is similar to the DDT debate many years ago. The FDA refused to study the dangers knowing full well the result would show DDT was highly toxic. History repeats itself.

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What we do know is that anal cancers in gay men have INCREASED 4,000% in the last twelve years. Can you suggest another cause that would account for this?

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What we do know is that anal cancers in gay men have INCREASED 4,000% in the last twelve years. Can you suggest another cause that would account for this?

Where do your numbers come from?  In the past not everything you have said has turned out to be true, so you need to provide a reference to an independent non-dissident source that we can check. This link shows anal cancer was more common in gay men than straight men between 1974 and 1979, before AIDS was a factor: <http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&… This link shows anal cancer was *much* more common in gay men than straight men between 1978 and 1985, before condoms were a factor: <http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&… The following link gives a recent incidence for gay men of 35 per 100,000, and a general population incidence of 0.9 per 100,000. <http://www.thebody.com/step/retro99/anal_cancer.html Hmmm.  35 per 100,000 is about 4,000% larger than 0.9 per 100,000. Could your 4,000% increase be a misunderstanding of something you read? — David Canzi     The problem most anti-spammers are trying to solve, when                 correctly understood, reduces to "How do I let everybody in                 the world send me e-mail without letting everybody in the                 world send me e-mail?"

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You appear to have made a judgement, up front that an individual who wishes to sell his product through an MLM marketing system is an unscrupulous individual.

He may have gotten that impression from your behavior. Spamming a discussion newsgroup where commercial advertising is explicitly prohibited is most certainly an indication you don’t care how you sell your crap.

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– Hide quoted text — Show quoted text – Well, Josh, there can be no debunkers if there is no bunkum to debunk, and you excrete copious bunkum for our mill. –Rich  – Proud to be a debunker. As am I. I could never understand why alties consider the term "debunker" to be such an insult (judge by the way they toss it around with such contempt). I consider it one of the highest forms of praise. "Debunking" pseudoscience (and pseudo history, such as, for example, Holocaust denial) is an honorable calling.L LOL. Yes I’m sure you would be proud to be a debunker if only you knew what it meant!! Yes, Davey-poo… From www.m-w.com: Main Entry: de

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–cut–          Finally I would like to add this-when I was diagnosed I was working as an engineer in a food factory which had a large flour mill and silo,I believe my contact with this food substance caused at least the asthma does anyone know of flour/powder/dusts being the catalyst for asthma,obviously I am aware that these substances trigger attacks,but would exposure cause the condition??              Thanks for your time,     Dave.

It could be ‘Occupational Asthma’ from the flour. See: http://www.ccohs.ca/oshanswers/diseases/asthma.html "What occupations are at risk for asthma? Some of the occupations where asthma has been seen are listed in the following tables. It should be noted that the lists of occupational substances and microbes which can cause asthma are not complete. New causes continue to be added. New materials and  new processes introduce new exposures and create new risks.  Table 1 Causes of Occupational Asthma – Grains, flours, plants and gums  Occupation Bakers, millers                        ——-                                        Wheat

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     The information I would like rests on the post question:Is the asthma causing the allergy or vice versa,how are the two linked,they surely must be.

Asthma and allergies are closely related.  One does not necessarily ’cause’ the other       I hate the inhalers and would prefer not using them but nothing else seems effective,if anyone has any thoughts or comments please forward them to me.

The medications you get from your doctor are the most effective method of controlling the disease.         Finally I would like to add this-when I was diagnosed I was working as an engineer in a food factory which had a large flour mill and silo,I believe my contact with this food substance caused at least the asthma does anyone know of flour/powder/dusts being the catalyst for asthma,obviously I am aware that these substances trigger attacks,but would exposure cause the condition??

There is the possibility that you have become allergic to wheat.  The best thing you can do is get a referral to an allergist. "The commander in the field is always right and the rear echelon is wrong, unless proved otherwise."    General Colin Powell

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Hi.I would welcome a response from anyone with any observation on my condition,which varies from great(when I play 4 games of squash a week and an hour of flat out 5-a-side soccer)to awful when I can’t breathe and my inhaler is ineffective,but if you will,a little more about the condition and how it manifests itself.        I was diagnosed in1996 by my doctor with a mild asthma condition,I had suffered a severe bout of breathlessness after a heavy cold.From then on I have been using two inhalers,one as medicine the other a "reliever",also a nasal spray(very effective).My worst and most common attacks appear after a cold/flu,to which I seem particularly prone.       I also suffer allergies which primarily were sneeze attacks,itchy eyes and breathlessness,and something of a fatigue.These have "disappeared" since 1998 but have been "replaced" by a rash that will appear on my hands,stomach,face and feet,I also suffer a severe "wind burn"(not flatulence!!)when out walking,the rash may appear when in contact with water,swimming,exercising and when tired or run down.I was taking antihistamine but ceased as I was of the opinion that they were exacerbating the asthma.The rashes these days are thankfully,apparently subsiding,a doctor did tell me that the allergy may "burn" itself out.       The information I would like rests on the post question:Is the asthma causing the allergy or vice versa,how are the two linked,they surely must be.       I can offer this much to anyone with this type of problem-DIET.Diet affects these conditions immensely.Dairy product is the worst offender.Several years ago I maintained a Macrobiotic diet which basically meant no dairy,meat,processed foods-everything fresh,no additives,I was never out of the kitchen!!However it helped enormously,these days my diet is somewhat less restricted but very healthy.        I hate the inhalers and would prefer not using them but nothing else seems effective,if anyone has any thoughts or comments please forward them to me.          Finally I would like to add this-when I was diagnosed I was working as an engineer in a food factory which had a large flour mill and silo,I believe my contact with this food substance caused at least the asthma does anyone know of flour/powder/dusts being the catalyst for asthma,obviously I am aware that these substances trigger attacks,but would exposure cause the condition??              Thanks for your time,                                                Dave.

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I have a co-worker who also has asthma and she’s allergic to just about everything. She keeps insisting that I have at least some if not all of the same allergies as she does. I haven’t had much of a problem until last week which had been preceeded by two weeks of exercise (same thing that made me goto the Dr in August where I was initially diagnosed). The Dr. yesterday concluded that aparently a major trigger for me is exercise. I know that I cannot be allergic to exercise, though it does make for a good excuse as to why I have a fat butt! Anyway, my question is this, does one have to have allergies if they have asthma? How do I approach my Dr Monday to find out how we can determine what allergies I may or may not have? Sheila Marie

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One does not have to have allergies to have asthma. Allergies are a common trigger for asthma but not required. The more common  symptoms of allergies are itchy eyes, sneezing, hives, constant drainage. Believe me, you would be miserable…this from a woman who is allergic to almost everything too. Just ask your doctor if he/she thinks that allergy testing would be helpful. Exercise is a VERY common trigger for asthma and it can exist alone. Denise

– Hide quoted text — Show quoted text – I have a co-worker who also has asthma and she’s allergic to just about everything. She keeps insisting that I have at least some if not all of the same allergies as she does. I haven’t had much of a problem until last week which had been preceeded by two weeks of exercise (same thing that made me goto the Dr in August where I was initially diagnosed). The Dr. yesterday concluded that aparently a major trigger for me is exercise. I know that I cannot be allergic to exercise, though it does make for a good excuse as to why I have a fat butt! Anyway, my question is this, does one have to have allergies if they have asthma? How do I approach my Dr Monday to find out how we can determine what allergies I may or may not have? Sheila Marie

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I have a co-worker who also has asthma and she’s allergic to just about everything. She keeps insisting that I have at least some if not all of the same allergies as she does. I haven’t had much of a problem until last week which had been preceeded by two weeks of exercise (same thing that made me goto the Dr in August where I was initially diagnosed). The Dr. yesterday concluded that aparently a major trigger for me is exercise. I know that I cannot be allergic to exercise, though it does make for a good excuse as to why I have a fat butt! Anyway, my question is this, does one have to have allergies if they have asthma? How do I approach my Dr Monday to find out how we can determine what allergies I may or may not have?

Although asthma and allergies are usually found together it is not so in all cases.   — We make war so we may live in peace. Aristotle

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If you have persistent allergy symptoms that bother you, ask your doctor for a few samples of Claritin.  Try it for a week and see if it makes you feel better. It can be a near-endless process to determine what you’re allergic to. Also consider trying a good (HEPA) air filter at home, work, or both to see if that helps.  For some people, just being in an atmosphere relatively free from allergans for half the day makes the other half of the day much more pleasant. =S= – Hide quoted text — Show quoted text – How do I approach my Dr Monday to find out how we can determine what allergies I may or may not have? Sheila Marie

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One does not have to have allergies to have asthma. Allergies are a common trigger for asthma but not required. The more common  symptoms of allergies are itchy eyes, sneezing, hives, constant drainage. Believe me, you would be miserable…this from a woman who is allergic to almost everything too. Just ask your doctor if he/she thinks that allergy testing would be helpful. Exercise is a VERY common trigger for asthma and it can exist alone.

The other common myth about asthma is that people who don’t wheeze don’t have asthma. – Hide quoted text — Show quoted text -Denise I have a co-worker who also has asthma and she’s allergic to just about everything. She keeps insisting that I have at least some if not all of the same allergies as she does. I haven’t had much of a problem until last week which had been preceeded by two weeks of exercise (same thing that made me goto the Dr in August where I was initially diagnosed). The Dr. yesterday concluded that aparently a major trigger for me is exercise. I know that I cannot be allergic to exercise, though it does make for a good excuse as to why I have a fat butt! Anyway, my question is this, does one have to have allergies if they have asthma? How do I approach my Dr Monday to find out how we can determine what allergies I may or may not have? Sheila Marie

– Five Cats

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I have a co-worker who also has asthma and she’s allergic to just about everything. She keeps insisting that I have at least some if not all of the same allergies as she does. I haven’t had much of a problem until last week which had been preceeded by two weeks of exercise (same thing that made me goto the Dr in August where I was initially diagnosed). The Dr. yesterday concluded that aparently a major trigger for me is exercise. I know that I cannot be allergic to exercise, though it does make for a good excuse as to why I have a fat butt!

Most asthmatics have EIA [exercise induced asthma].  Anyway, my question is this, does one have to have allergies if they have asthma?

Nope. Asthma can be allergic or nonallergic. The nonallergic variety is more common in adults.  How do I approach my Dr Monday to find out how we can determine what allergies I may or may not have? Sheila Marie

Your allergy history would be taken. Have you noticed allergic reactions, like rhinitis [hay fever] during pollen season, how about hives, or eczema? Did your parents have allergies? Ever have food allergies? If you do have allergies, referral to an allergist & skin testing may be appropriate. More likely your doctor will want to evaluate you for asthma, and prescribe inhalers if appropriate. Asthma is diagnosed using lung function tests. http://www.lungusa.org/press/medical/medcatj.html Allergy May Be Linked to Adult Onset Asthma http://www.intelihealth.com/IH/ihtIH/WSIHW000/3457/6945.html Adult-Onset Asthma http://webmd.lycos.com/content/article/1728.54120 Adult-Onset Asthma: The Workplace Could Be the Culprit Vital Information: Of those who experience adult-onset asthma, about 10% of cases are a result of allergens encountered in the workplace, a number much higher than previously realized. Occupational asthma can develop quickly in patients, or may take several years, making the link to the workplace more difficult. People who work with biological entities (such as plants, animals, and insects), work in homes, or work with chemicals should be especially suspicious if they develop asthma as an adult. Ellis

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Any good web pages dealing with nonallergic vasomotor rhinitis?  It seems there are a few out there dealing with this topic.  I find many web pages that deal with allergies in general, but not that many on vasomotor.  I live in a city with an oil refinery for the last 12 years, and I have burning in my chest when they put out more than the usual smoke.  The smoke has also caused asthma attacks recently.  I am also sensitive to smoke, Clorox, strong fumes, and gas fumes.  I was also wondering what the treatment is (drugs, air filters etc. prescribed by a doctor) for this disease.  In my opinion,  vasomotor seems to be a disease that should be more carefully researched since this world seems to be getting polluted more and more each day.  Thank you all for your posts in advance. Wilson

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Any good web pages dealing with nonallergic vasomotor rhinitis?  It seems there are a few out there dealing with this topic.  I find many web pages that deal with allergies in general, but not that many on vasomotor.  I live in a city with an oil refinery for the last 12 years, and I have burning in my chest when they put out more than the usual smoke.  The smoke has also caused asthma attacks recently.  I am also sensitive to smoke, Clorox, strong fumes, and gas fumes.  I was also wondering what the treatment is (drugs, air filters etc. prescribed by a doctor) for this disease.  In my opinion,  vasomotor seems to be a disease that should be more carefully researched since this world seems to be getting polluted more and more each day.  Thank you all for your posts in advance. Wilson

The asthma could be more serious than the rhinitis. Environmental measures, including considering moving, would be a first treatment, to avoid lung and nasal damage due to air pollution. Links http://www.NationalJewish.org/medfacts/allergic_rhinitis.html  Allergic & Non-Allergic Rhinitis http://www.vh.org/Providers/ClinRef/FPHandbook/Chapter19/03-19.html   Otolaryngology: Nose "C.Vasomotor rhinitis. Characterized by nasal mucosal swelling and rhinorrhea secondary to nospecific, nonallergic causes such as recumbency, cold, and humidity. Oral decongestants, topical decongestants (such as Afrin), as well as nasal steroids and ipratropium nasal spray (0.06%) may be helpful. " http://pharmacotherapy.medscape.com/other/guidelines/jcaai.dyke/pnt-j… [free registration required] Executive Summary of Joint Task Force Practice Parameters on  Diagnosis and Management of Rhinitis Excerpts: "Nonallergic Rhinitis Nonallergic rhinitis is characterized by sporadic or persistent perennial symptoms of rhinitis that do not result from IgE-mediated immunopathologic events. Examples of nonallergic rhinitis are infectious rhinitis, vasomotor rhinitis, nonallergic rhinitis with eosinophilia syndrome (NARES), hormonal rhinitis, certain types of occupational rhinitis, and gustatory and drug-induced rhinitis. Nonallergic, Noninfectious Rhinitis Without Eosinophilia Nonallergic, noninfectious rhinitis, generally termed vasomotor rhinitis, comprises a heterogeneous group of patients with chronic nasal symptoms that are not immunologic or infectious in origin and usually not associated with nasal eosinophilia. Most of these patients develop rhinitis in response to environmental conditions, such as cold air, high humidity, strong odors and inhaled irritants. Occupational Rhinitis Occupational rhinitis refers to rhinitis arising in response to airborne substances in the workplace, which may be mediated by allergic (IgE antibody mediated) or nonallergic factors, e.g. laboratory animal antigen, grain, wood dusts, and chemicals. It often coexists with occupational asthma. Management Avoidance of inciting factors, e.g. allergens (house dust mites, molds, pets, pollens, cockroaches), irritants, medications, is fundamental to the management of rhinitis. Triggers should be identified and avoidance measures instituted. Oral decongestants, such as pseudoephedrine or phenylpropanolamine, can effectively reduce nasal congestion produced by allergic and non-allergic forms of rhinitis rhinitis, but they can cause insomnia, loss of appetite or excessive nervousness. In addition, these agents should be used with caution in patients with certain conditions, e.g. arrhythmias, angina pectoris, some patients with hypertension and hyperthyroidism. Intranasal anti-cholinergics may effectively reduce rhinorrhea but have no effect on other nasal symptoms. Side effects are generally minimal, but dryness of the nasal membranes may occur."

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MIME-Version: 1.0  ASTHMA IN PATIENTS WITH SILICONE BREAST IMPLANTS: REPORT OF A CASE SERIES AND IDENTIFICATION OF HEXACHLOROPLATINATE CONTAMINANT AS A POSSIBLE ETIOLOGIC AGENT.                      Michael R Harbut                      Brenda C Churchill*   IJOH; 1999; 3:73-82. University,  School of Medicine, Detroit, Michigan,  and *Department of Internal  Medicine, Providence Hospital, Southfield, Michigan   Address for correspondence: Michael R. Harbut MD , MPH; Wayne State University School of  Medicine, Detroit, Michigan, and Center for Occupational and Environmental Medicine, 22255 Greenfield; Southfield, Mi. 48075   ABSTRACT   The following study is of 8  breast implant patients evaluated because of respiratory systems, pruritus and rhinorrhea.  The presence of hexachoroplatinate in the implants was notes and support for the hypothesis that this contaminant was related to the symptoms experienced by the patients is presented.  Cases of implant related asthma were defined by episodic dyspnea, cough, or breathlessness with onset or worsening after implant placement and objective evidence of reversible airways obstruction, either during the presence or after the removal of the devices.  All eight patients were found to have asthma, with airway hyper-reactivity demonstrated by methacholine challenge testing performed in seven patients and by partially reversible obstruction after nebulized administration of a beta-agonist in one patient.  Eight patients had urticaria and seven had rhinorrhea.  Eight of eight breast implant patients evaluated had findings consistent with asthma.  Hexachloroplatinate, a potent sensitizer and component of breast implants, is identified as the likely primary etiologic agent in view of findings consistent with platinosis in these  patients, and the demonstration of the leaching of hexachloroplatinate from  even intact silicone breast implants.    INTRODUCTION      Human illness as a result of toxicity of silicone gel breast implants is an evolving and controversial area of medical investigation.  The nature of any toxicity has not yet been fully characterized, but at least in part it appears to be consistent with a hypersensitivity process.  The medical community is moving away from early reports of an autoimmune process, but has not yet offered a clear explanation for complaints registered by patients who have had the devices placed.  There is also significant uncertainty with respect to any responsible agents of toxicity.        Silicone breast implants consist of a shell encasing a gel. Both the shell and gel are complex formulations that include carbon and silicone and traces of many other elements.  Saline implants are comprised of a saline fluid contained in a silicone shell casing. From an Occupational Medicine perspective, notable among the agents present in both gel and shell are the metals chromium, nickel, aluminum and platinum.  The presence of platinum in the implants occurs as a result of its use as a catalyst in its hexasolvent form (H2PtCl6) in the production of gel and shell. (1). All three metals are known to be associated with occupational asthma.  Hexachloroplatinate, however, is the most potent of sensitizers reported.         There is an extensive medical literature related to the occupational disease entity platinosis and airways reactivity, caused by exposure to complex platinum salts.  Respiratory problems in platinum refinery workers were reported as long ago as 1911 and are extensively reviewed in the World Health Organization Monograph of the Internal Program of Chemical Safety. (2).  Platinosis or platinum allergy historically  refers to the triad of asthma, dermatitis and rhinitis in workers exposed to platinum.  Pruritis has also been reported. Platinosis is highly prevalent in workers exposed to platinum with a cumulative prevalent rate  50% or more.   The potency of platinum is such that the *TLV-TWA  for platinum salts is 2 mcg/cubic meter of air.  (6).  As a comparison, the TLVs for two other toxic metals, lead and arsenic, are two orders of magnitude greater at 0.15 and 0.2 mg/cubic meter of air respectively. There have been case reports of platinum sensitivity from dental work and jewelry. (3,4).          Platinum asthma can be present before, after, or in the absence of positive skin prick testing.  Cold air and methacholine challenge have both been shown to evoke airways hyper-responsiveness in the hexachloroplatinate-exposed lung, in the absence of existing exposure and/or laboratory or abnormal immunologic testing. (5-9).   METHODS            Eight consecutive patients referred to the clinic with breast implants and various symptoms were included, l993 with extensive histories, including a respiratory history that incorporated the questions from the Epidemiology Standardization Project (10). The patients were questioned about alternative exposure sources, such as occupational metal exposures and platinum-containing dental work.  This was done to identify any sources of platinum even in the non-hexasolvent form.        Patients were also asked about their surgical history, type of implant (silicone or saline), manufacturer, and whether the implants had ruptured. Symptom onset as related to implant status was also elicited. Pulmonary function testing was done in the eight patients. All had complaints of cough or breathlessness.  Methacholine challenge testing was done on 7 patients with fundamentally normal pulmonary function and a beta-agonist (Albuterol) was administered by nebulizer to the patient whose pulmonary function test demonstrated airway obstruction.   CASE SUMMARIES:  CASE #1:  A 31 year old, nonsmoking white female, sales account manager underwent breast augmentation surgery in 1989 using Surgitek silicone implants.  There was no evidence of rupture or leakage. She had childhood pneumonia but no respiratory symptoms before implantation.  Presenting complaints include exertional dyspnea with wheezing, severe pruritus several times each week, scaling and dry skin,  occurring since the implant surgery.  The patient had normal resting pulmonary function tests with a positive methacholine challenge test (36% decrease in FEV1). CASE: #2: A 47 year old, white female nurse, who is currently a smoker with an 8-pack-year history had breast augmentation surgery in 1970 using Dow Silastic silicone implants.  The right breast implant ruptured in 1982, necessitating removal and replacement.  In 1992, both implants were removed after rupture of the left implant.  Spillage of silicone was confirmed operatively in both 1982 and 1992. The patient presented with complaints of loss of taste sensation, speech difficulty,  muscular tics and vesiculations, memory loss, episodic confusion, intermittent rash, pruritus, chronic bronchitis and dyspnea on exertion occurring since 1970.  She has coughing spells and has episodes of dyspnea on exertion on exposure to some household chemicals.  Symptoms worsened after the 1982-1992 ruptures.  She had a history of nonspecific allergies, bronchitis and pneumonia prior to the implants.  The patient had near normal resting pulmonary function tests and a positive methacholine  challenge.   CASE #3:  A 54 year of age, nonsmoking white female teacher underwent breast augmentation in 1975 with silicone gel breast implants. There was no definite evidence of rupture or leakage.  The patient presented with severe fatigue, somnolence, chest and upper extremity burning, paresthesias and urticaria.   Respiratory symptoms developed over the last two years prior to her evaluation, and included a nonproductive cough, episodic coughing spells, and increasing exertional  dyspnea.  Prior to the implant surgery, she had a history of bronchitis but no documented allergies.  She had near normal resting pulmonary function test and the methacholine challenge test demonstrated a 34% decrease in FEV1. CASE #4:  A 58 year of age, white female homemaker who is a smoker with a 33-pack-year history, underwent breast reconstruction and augmentation in 1981 after bilateral prophylactic mastectomies for multiple nonmalignant tumors. The implants were removed and replaced three times as a result of complications, and they were permanently removed in 1993.  The patient is convinced that there was leakage, but this is unconfirmed. Presenting complaints included severe, progressive fatigue over the eight years prior to evaluation to the point that she now reports spending up to 75% of her day in bed.  She also complained of  paresthesias. Respiratory symptoms which began or worsened after the implant surgery include cough, wheezing, multiple episodes of bronchitis, increasingly productive cough and episodic dyspnea.   Despite her smoking history, this patient had near normal resting pulmonary function tests.  Methacholine challenge test was positive with a 22% decrease in FEV1.   CASE #5:  A 57 year old white female, employed as a waitress since 1991 underwent breast augmentation with silicone implants in 1974. Suspected leakage was confirmed at surgery in January of 1993 when the implants were replaced with a saline type.  She is currently a nonsmoker who quit two years ago.  Prior to that, she had accumulated a 9-pack-year history over 38 calendar years.  She presented with complaints of constant fatigue, pruritus, and an intermittently productive chronic cough with  nocturnal wheezing.  She also noted burning paresthesias radiating across the chest and upper extremities.  Respiratory symptoms began approximately three years prior to evaluation. She had a history of bronchitis and emphysema prior to the implants, but chronic … read more »

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Question:

Now Collin excuse my question but i’m french speaking in the all day life. I do my best to practice english, but what do you mean by the expression "Sounds like run-of-the-mill asthma"? It’s must be an exrpression that can’t be translated word to word.

"run of the mill" means "standard", "ordinary"…the flour that the mill produces every day unless the miller has a reason to produce something special in this context I take it to mean a fairly normal case of asthma with few, if any, complications — eric "live fast, die only if strictly necessary"

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Now Collin excuse my question but i’m french speaking in the all day life. I do my best to practice english, but what do you mean by the expression "Sounds like run-of-the-mill asthma"? It’s must be an exrpression that can’t be translated word to word.

What I meant is that this combination is very common. "They laughed at Galileo. They laughed at Newton But they also laughed at Bozo the Clown." Carl Sagan

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Hi, I need help to understand  these doctor Dx. I have a medical report and need some explanation on terms and meanings. My Boss send me for medical expertise. The pneumo said that the test shown a light disease obstructive of the small aerial ways (the ring-road one"s),the smal airways were at 64% of the normal capacity, but whit lung volume at the inferior limit of the normal. The test also shown a moderate bronchic hyperreactivity . The spirometric test was normal except for the small airways, diffusion was 97% ans gas capilarity was 95%. What does it mean, i have read that bpco are chronic bronchitic and emphysem, those are irreversible and degenerating, is this result show the beginning of emphysem? I also was Dx whit astmathic broncitic, chronic rhinitis and moderate to severe alergy. The pneumo hired by my Boss want me back to work immediately. He Dx light asthma.  My doctor want me out of work, mine Dx severe and  decompensated asthma because of all the deseases  put togheter. Anyone  can tell which one is right? Pease. AT

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I have a medical report and need some explanation on terms and meanings. My Boss send me for medical expertise. The pneumo said that the test shown a light disease obstructive of the small aerial ways (the ring-road one"s),the smal airways were at 64% of the normal capacity, but whit lung volume at the inferior limit of the normal. The test also shown a moderate bronchic hyperreactivity . The spirometric test was normal except for the small airways, diffusion was 97% ans gas capilarity was 95%. What does it mean, i have read that bpco are chronic bronchitic and emphysem, those are irreversible and degenerating, is this result show the beginning of emphysem?

I’m not an expert, but this sounds more like asthma than emphysema. I also was Dx whit astmathic broncitic, chronic rhinitis and moderate to severe alergy.

Sounds like run-of-the-mill asthma. The pneumo hired by my Boss want me back to work immediately. He Dx light asthma.  My doctor want me out of work, mine Dx severe and  decompensated asthma because of all the deseases  put togheter. Anyone  can tell which one is right? Pease.

I would tend to side with the specialist as he seems to have conducted the necessary tests. One thing you haven;t posted is what medications you are on and how well they are working. "They laughed at Galileo. They laughed at Newton But they also laughed at Bozo the Clown." Carl Sagan

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Hi Collin, Thanks for the reply. First 4 years ago i began to take 2 inhalers, ventolin and oxeze, that wasn’t enough. So i see my doctor i add flovent, but for the 2 last years i was continually decompensated. Now i take 2 puffs twice a days of each (ventolin, combivent, flovent, sometimes i also have to add oxeze again), the pulmo add singulair whit slight or no effect, i still have every day symptoms. My doctor suspect severe asthma and allergy may be asthmatic bronchitic, so he refer me to a pneumo. and an allergist. My pneumo did the test and the result was the one at the bottom of this e-mail.The pneumo ask me to bring the result to my doctor saying that he’s my  doctor treating my case and he should recommand if i stay out of work or if i can continue to work at this place. My allergist did the test ( result under)and recommand me to quit my work and he write me a report. When my doctor see the result he said that it look the way it suspect it and diagnose severe asthma decompensated. Now i send the result and the recommendations to the medical office of my workplace. At first they accept it and wuold like to put me in the invalidity pension plan. Than they change their mind they hired a pneumo and send him all the result  for a second opinion, this pneumo is evidentely on the "Boss side". The pneumo hired from my Boss denied the result and Dx light asthma. Now Collin excuse my question but i’m french speaking in the all day life. I do my best to practice english, but what do you mean by the expression "Sounds like run-of-the-mill asthma"? It’s must be an exrpression that can’t be translated word to word. Whit these precisions i’m still interested in your opinion and the other one’s too. AT – Hide quoted text — Show quoted text – I have a medical report and need some explanation on terms and meanings. My Boss send me for medical expertise. The pneumo said that the test shown a light disease obstructive of the small aerial ways (the ring-road one"s),the smal airways were at 64% of the normal capacity, but whit lung volume at the inferior limit of the normal. The test also shown a moderate bronchic hyperreactivity . The spirometric test was normal except for the small airways, diffusion was 97% ans gas capilarity was 95%. What does it mean, i have read that bpco are chronic bronchitic and emphysem, those are irreversible and degenerating, is this result show the beginning of emphysem? I’m not an expert, but this sounds more like asthma than emphysema. I also was Dx whit astmathic broncitic, chronic rhinitis and moderate to severe alergy. Sounds like run-of-the-mill asthma. The pneumo hired by my Boss want me back to work immediately. He Dx light asthma.  My doctor want me out of work, mine Dx severe and  decompensated asthma because of all the deseases  put togheter. Anyone  can tell which one is right? Pease. I would tend to side with the specialist as he seems to have conducted the necessary tests. One thing you haven;t posted is what medications you are on and how well they are working. "They laughed at Galileo. They laughed at Newton But they also laughed at Bozo the Clown." Carl Sagan

Response:

- Hide quoted text — Show quoted text – Hi Collin, Thanks for the reply. First 4 years ago i began to take 2 inhalers, ventolin and oxeze, that wasn’t enough. So i see my doctor i add flovent, but for the 2 last years i was continually decompensated. Now i take 2 puffs twice a days of each (ventolin, combivent, flovent, sometimes i also have to add oxeze again), the pulmo add singulair whit slight or no effect, i still have every day symptoms. My doctor suspect severe asthma and allergy may be asthmatic bronchitic, so he refer me to a pneumo. and an allergist. My pneumo did the test and the result was the one at the bottom of this e-mail.The pneumo ask me to bring the result to my doctor saying that he’s my  doctor treating my case and he should recommand if i stay out of work or if i can continue to work at this place. My allergist did the test ( result under)and recommand me to quit my work and he write me a report. When my doctor see the result he said that it look the way it suspect it and diagnose severe asthma decompensated. Now i send the result and the recommendations to the medical office of my workplace. At first they accept it and wuold like to put me in the invalidity pension plan. Than they change their mind they hired a pneumo and send him all the result  for a second opinion, this pneumo is evidentely on the "Boss side". The pneumo hired from my Boss denied the result and Dx light asthma. Now Collin excuse my question but i’m french speaking in the all day life. I do my best to practice english, but what do you mean by the expression "Sounds like run-of-the-mill asthma"? It’s must be an exrpression that can’t be translated word to word. Whit these precisions i’m still interested in your opinion and the other one’s too. AT I have a medical report and need some explanation on terms and meanings.  My Boss send me for medical expertise. The pneumo said that the test shown a light disease obstructive of the small aerial ways (the ring-road  one"s),the smal airways were at 64% of the normal capacity, but whit lung volume at  the inferior limit of the normal. The test also shown a moderate bronchic hyperreactivity . The spirometric test was normal except for the small airways, diffusion was 97% ans gas capilarity was 95%. What does it mean, i have read that bpco are chronic bronchitic and emphysem, those are irreversible and degenerating, is this result show  the beginning of emphysem? I’m not an expert, but this sounds more like asthma than emphysema. I also was Dx whit astmathic broncitic, chronic rhinitis and moderate to severe alergy. Sounds like run-of-the-mill asthma. The pneumo hired by my Boss want me back to work immediately. He Dx light asthma.  My doctor want me out of work, mine Dx severe and  decompensated asthma because of all the deseases  put togheter. Anyone  can tell which one is right? Pease. I would tend to side with the specialist as he seems to have conducted the necessary tests. One thing you haven;t posted is what medications you are on and how well they are working. "They laughed at Galileo. They laughed at Newton But they also laughed at Bozo the Clown." Carl Sagan

There are two very good sites about occupational asthma in french: Asthme Professionnel (http://www.asthme.csst.qc.ca/) and Asmanet (http://www.remcomp.com/asmanet/asmapro/index.htm). I see no data. Did the test accomplish acceptability and reproducibility criteria? Do irritants or sensitizing agents occur in the workplace? Are the airways protected in the workplace? Do you suffer from rhino-bronchial syndrome? What about smoking? Sometimes an early terminated maneuvre masks a moderate obstructive defect (lung volume expressed as FVC is low and the FEV1/FVC is ‘normal’ ) Usually emphysema is carachterized by the increase of both Residual Volume (RV) and Residual Volume/Total Lung Capacity. Occupational asthma or work aggravated asthma require specific diagnostic procedures. Bronchial hyperreactivity is usually tested by aspecific stimuli (commonly methacoline PC20 or  PD20)

Response:

Question:

Hi all, I’m a mid 40’s firefighter (soon to be ex) in Scotland. I was diagnosed with Interstitial Pulmonary Fibrosis just before Christmas, and this week with Asthma. Naturally I’ve suddenly got a hundred questions I’d like to ask, does this group have a faq, or does anyone have a favoured web site which would answer my newbie questions. Thanks — keith

Response:

Hi all, I’m a mid 40’s firefighter (soon to be ex) in Scotland. I was diagnosed with Interstitial Pulmonary Fibrosis just before Christmas, and this week with Asthma. Naturally I’ve suddenly got a hundred questions I’d like to ask, does this group have a faq, or does anyone have a favoured web site which would answer my newbie questions. Thanks — keith

See: http://www.radix.net/~mwg/asthma-gen.html  alt.support.asthma FAQ http://www.lungusa.org/diseases/pulmfibrosis.html Facts About Pulmonary Fibrosis and Interstitial  Lung Disease http://www.lungusa.org/asthma/astoccasthm.html Occupational Asthma (ALA) Ellis

Response:

Question:

In penence for the binary posting I pumped into some other thread, I’ll post here an answer to a question I asked in yet another thread. I was pondering on the effectiveness of CA for limited applications, knowing full well I had William Tandy Young’s "The Glue Book" sitting unread on my bookshelf. Here, then, is a summary of what I learned from his pages. – Cyanoacrylate glue cures by exposure to moisture into a hard substance very similar to sheet acrylic (plexiglas). [At one time, I was told that CA cures by exposure to oxygen. This turns out to not be true. CA is like urethane glues in this regard. Moisture in the air and in the work surface start the curing process.] – CA is sensitive to the pH of the material applied to. Acidic surfaces act to prohibit curing; alkaline promotes curing. Accelerators are simply an alkaline compound carried in solvent. – Nitromethane and acetone can dissolve cured CA. These are packaged and sold as CA debonders. – CA is one of the few truly structural gap filling adhesives. However, a thinner bond layer makes a stronger joint. – CA makes a strong, durable bond, but is very sensitive to shock loading. That is, striking the joint sharply can break a fully cured bond. I presume this is the typcial mode of failure. Odor-less CA makes a stronger bond, but is even more sensitive to shock. – Shelf life is about 6 months. Thin CA has shorter shelf life than thick; all viscosities thicken with age. Refrigeration before opening can extend this short period; condensaton and precuring are problems if refrigerated after opening. Dessicants in a closed container are useful to extend life. Accelerators or other strong alkaline solutions should not be stored in the same container. – Its fumes are a strong irritant. Contact with the eye can cause permanent damage to eyesight. CA has been linked to occupational asthma (whatever that might be). Skin conditions, ironically, are caused more by the vapors than by direct skin contact. It is not known if they are mutagenic or carcinogenic. – CA cures to an inert solid, so safe disposal is possible. It would be bad to cure the glue for disposal by dumping it in water, or worse, dumping accelerator into the bottle, because the of the fumes produced. In a nut shell… Mike.

Response:

Great post — lots of good information.  Thanks! — Ken Vaughn Visit my workshop: http://home.earthlink.net/~kvaughn65/

– Hide quoted text — Show quoted text – In penence for the binary posting I pumped into some other thread, I’ll post here an answer to a question I asked in yet another thread. I was pondering on the effectiveness of CA for limited applications, knowing full well I had William Tandy Young’s "The Glue Book" sitting unread on my bookshelf. Here, then, is a summary of what I learned from his pages. – Cyanoacrylate glue cures by exposure to moisture into a hard substance very similar to sheet acrylic (plexiglas). [At one time, I was told that CA cures by exposure to oxygen. This turns out to not be true. CA is like urethane glues in this regard. Moisture in the air and in the work surface start the curing process.] – CA is sensitive to the pH of the material applied to. Acidic surfaces act to prohibit curing; alkaline promotes curing. Accelerators are simply an alkaline compound carried in solvent. – Nitromethane and acetone can dissolve cured CA. These are packaged and sold as CA debonders. – CA is one of the few truly structural gap filling adhesives. However, a thinner bond layer makes a stronger joint. – CA makes a strong, durable bond, but is very sensitive to shock loading. That is, striking the joint sharply can break a fully cured bond. I presume this is the typcial mode of failure. Odor-less CA makes a stronger bond, but is even more sensitive to shock. – Shelf life is about 6 months. Thin CA has shorter shelf life than thick; all viscosities thicken with age. Refrigeration before opening can extend this short period; condensaton and precuring are problems if refrigerated after opening. Dessicants in a closed container are useful to extend life. Accelerators or other strong alkaline solutions should not be stored in the same container. – Its fumes are a strong irritant. Contact with the eye can cause permanent damage to eyesight. CA has been linked to occupational asthma (whatever that might be). Skin conditions, ironically, are caused more by the vapors than by direct skin contact. It is not known if they are mutagenic or carcinogenic. – CA cures to an inert solid, so safe disposal is possible. It would be bad to cure the glue for disposal by dumping it in water, or worse, dumping accelerator into the bottle, because the of the fumes produced. In a nut shell… Mike.

Response:

Have to disagree about Nitromethane and Acetone. CA is a staple of RC Airplane building, and the Fuel has Nitro in a Methanol fuel in it. In fact, Fuel Proofing of the wood is easily accomplished by application of CA. Acetone is likley does something, but Acetone can used to clean in the areas of CA. Nail Polish remover is also a CA dissolver. CA does not sand! not very easily, anyway

Response:

– <SNIP CA has been linked to occupational asthma (whatever that might be). Skin conditions, ironically, are caused more by the vapors than by direct skin contact. It is not known if they are mutagenic or carcinogenic.

"occupational asthma" primarilywould be an asthmatic condition brough on by continued exposure to air-borne Cyano-Acrylics in ones work place (on the job).   Examples of this would be people who work in a CA glue factory, a CA ink making factory, or a press operators in a print shop which uses CA based inks a lot.   Axel

Response:

Acetone dissolves it over time. I use a jar of acetone to hold my "tips in waiting" which were tips I carelessly allowed to gum up.  The remover they sell smells like nitrobenzene to me.  Now that’s a powerful carcinogen. Nail polish remover is basically acetone. – Hide quoted text — Show quoted text – Have to disagree about Nitromethane and Acetone. CA is a staple of RC Airplane building, and the Fuel has Nitro in a Methanol fuel in it. In fact, Fuel Proofing of the wood is easily accomplished by application of CA. Acetone is likley does something, but Acetone can used to clean in the areas of CA. Nail Polish remover is also a CA dissolver. CA does not sand! not very easily, anyway

Response:

Your idea of keeping the tips in acetone might be worth something. email it to these guys. http://www.rconline.com/rcreport/index.html — walk a mile in the other mans shoes before you criticize him, then you will be a mile away and have his shoes!

Response:

Hello Michael, Here is a copy of a recent posting I made to the rec.crafts.woodturning newsgroup, that gives a bit of insight into CA glue, its chemical properties and manufacture: Cyanoacrylates, A Brief Overview: Monofunctional 2-cyanoacrylates were first patented in 1949, but the first viable production process did not evolve until 1954. In the early 1950’s, scientists at Eastman Kodak were working on thermal polymerization and discovered the rapid room-temperature cure and excellent adhesion properties of 2-cyanoacrylates, quite by accident. While working on a freshly prepared monomer, the scientists discovered that the glass prisms of the refractometer has become tightly bonded. Extensive work thereafter, found that many different types of substrates bonded in the same manner. Subsequently in 1958, Eastman 910 debued, the first in a large family of 2-cyanoacrylate ester adhesives. 2-cyanoacrylates polymers spontaneously form (via an anionic/radical mechanisms) when their liquid precursors, or monomers are placed between two closely fitting surfaces. The great utility of these adhesives arises from the electron-withdrawing character of the groups adjacent to the polymerizable double bond. The high reactivity (cure rate) and their polar nature, enables the polymers to adhere quite tenaciously to a wide variety of substrates. Low humidity and/or acidic groups on the substrate surface will slow or inhibit the cure reaction. To extend the usable shelf life, free-radical stabilizers such as quinones or hindered phenols are used. Methyl, Ethyl, Butyl, Allyl and Methoxyethyl esters are available with various setting characteristics and rheological properties. However, the Methyl and Ethyl esters dominate the commercial industrial market. The vinyl structure of 2-cyanoacrylates makes them prone to spontaneous polymerization. The chain propagation can be initiated by ionic or radical mechanisms. The rate of polymerization depends on temperature, humidity, light and the presence of accelerators, like peroxides or bases. In addition to polymerization, 2-cyanoacrylates undergo reactions typical of vinyl compounds, such as addition. 2-cyanoacrylates can be manufactured by many different methods. The base monomers are too thin for convenient use, so thickeners, stabilizers or property-modifying additives may be added. The viscosity’s are available from wicking grades (water thin) to thixotropic gels that range from 20,000 to 50,000 mPa*s for large gaps. The acrid odour of 2-cyanoacrylates, can be effectively mitigated by the substitution of an alkoxyalkyl ester side chain, for the normal alkyl group. Products so modified, are practically odour free, but are slightly less effective as adhesives. The basic method to manufacture 2-cyanoacrylate esters involves preparation via the Knoevenagel condensation reaction (the corresponding alkyl cyanoacetate reacts with formaldehyde in the presence of a basic catalyst, to form a low molecular weight polymer). The resulting polymer slurry is acidified and the water is removed. The polymer is then cracked and redistilled at high temperatures onto a suitable stabilizer combination to prevent repolymerization. Protonic or Lewis acids are typically used in combination with small amounts of a free-radical stabilizer. Although the methods and processes have continually changed and evolved over the years, this is the standard method to manufacture these esters. One recent and significant advancement in the manufacturing process is a continuous process where the condensation is carried out in an extruder. By-products are then removed in a degassing zone and the molten polymer (mixed with stabilizers), is cracked to yield a raw monomer. Recent advances have lead to flexible 2-cyanoacrylate formulas, which remain somewhat flexible when cured. These types of esters are particularly useful to turners when bonding dissimilar materials like stone/metal and wood. The dissimilar expansion and contraction rates of these materials, can cause subsequent failure of the bond when using traditional cyanoacrylates that feature non-flexible, or brittle bonds. Health concerns: A few recent threads have mentioned CA glue and its sharp, pungent fumes/odour. These fumes are not to be taken lightly! 2-Cyanoacrylate esters are lacrimators, even at low concentrations. These esters are irritating to the nose, throat and lungs in concentrations as low as 3 ppm. Eye irritation is typically observed at 5 ppm, or higher. Adequate breathing protection (this means a proper respirator, outfitted with an organic vapour cartridge) is essential when using these adhesives. Additionally, you should not bend over the area, whilst you are applying the CA to the area. If you do not wear a respirator, adequate and thorough ventilation is ESSENTIAL. We are all aware how well CA will bond skin tissues. It’s best to wear protection on your hands when using these products, as well as eye protection if you do not wear a full face respirator. Contact with liquid CA through the clothing will produce a rapid exotherm, which may cause severe burns and scaring. Contact with the liquid CA in the eyes, can cause rapid exothermic polymerization, leading to severe eye injury, or corneal lesions. You should NEVER use CA without proper eye protection. Many turners use CA’s to fill small inclusions, or fissures in turned items either mixed with a filler, or by itself. If you switch on the lathe before complete polymerization has occurred, uncured CA may fly into your eyes, face, skin or clothing. Cured 2-Cyanoacrylate ester polymers are relatively non-toxic. In lab tests, oral doses of 6400 mg/kg failed to kill laboratory rats. Guinea pigs exhibited mild skin irritation, but there was no evidence to suggest sensitization, or absorption through the skin. There is a fire hazard with liquid and cured CA esters, because both forms will support combustion. You should not use these adhesives near sparks, open flames, areas of acute fire hazard or heat sources. Highly exothermic polymerization can occur from the direct addition of various catalytic substances like water, alcohol’s, amines, ammonia, caustics, or surface activator solutions. Take a bit of extra time to insure your protection protocols are up-to-date when using substances that are hazardous. A few seconds of extra time spent protecting yourself, is time we can ALL afford to spend. If you would like to learn more about CA adhesives, look for my upcoming comprehensive article in "Woodturning" (British) magazine. Take care and be safe. — Letting the chips fly… Steven D. Russell Eurowood Werks Woodturning Studio The Woodlands, Texas Website coming soon! – Hide quoted text — Show quoted text – In penence for the binary posting I pumped into some other thread, I’ll post here an answer to a question I asked in yet another thread. I was pondering on the effectiveness of CA for limited applications, knowing full well I had William Tandy Young’s "The Glue Book" sitting unread on my bookshelf. Here, then, is a summary of what I learned from his pages. – Cyanoacrylate glue cures by exposure to moisture into a hard substance very similar to sheet acrylic (plexiglas). [At one time, I was told that CA cures by exposure to oxygen. This turns out to not be true. CA is like urethane glues in this regard. Moisture in the air and in the work surface start the curing process.] – CA is sensitive to the pH of the material applied to. Acidic surfaces act to prohibit curing; alkaline promotes curing. Accelerators are simply an alkaline compound carried in solvent. – Nitromethane and acetone can dissolve cured CA. These are packaged and sold as CA debonders. – CA is one of the few truly structural gap filling adhesives. However, a thinner bond layer makes a stronger joint. – CA makes a strong, durable bond, but is very sensitive to shock loading. That is, striking the joint sharply can break a fully cured bond. I presume this is the typcial mode of failure. Odor-less CA makes a stronger bond, but is even more sensitive to shock. – Shelf life is about 6 months. Thin CA has shorter shelf life than thick; all viscosities thicken with age. Refrigeration before opening can extend this short period; condensaton and precuring are problems if refrigerated after opening. Dessicants in a closed container are useful to extend life. Accelerators or other strong alkaline solutions should not be stored in the same container. – Its fumes are a strong irritant. Contact with the eye can cause permanent damage to eyesight. CA has been linked to occupational asthma (whatever that might be). Skin conditions, ironically, are caused more by the vapors than by direct skin contact. It is not known if they are mutagenic or carcinogenic. – CA cures to an inert solid, so safe disposal is possible. It would be bad to cure the glue for disposal by dumping it in water, or worse, dumping accelerator into the bottle, because the of the fumes produced. In a nut shell… Mike.

Response:

Question:

Are there doctors who specialize in occupational asthma?  what is the best kind of doctor to see for suspected oa? TIA, Judy

Response:

Are there doctors who specialize in occupational asthma?  what is the best kind of doctor to see for suspected oa? TIA, Judy

Yes, I see an Occupational and Environmental Pulmonologist.  He has patients nation wide.  One hell of a doctor.  Still does research and publishes in peer reviewed journals all the time. If interested, I would be glad to give you his number.  Just e-mail me.  Take care, Lisa — Lisa M. DeSavage Hinsbar Laboratories, Inc. www.hinsbarlabs.com

Response:

Are there doctors who specialize in occupational asthma?  what is the best kind of doctor to see for suspected oa? TIA, Judy

See a pulmonologist for lung function tests to diagnose occupational asthma. Links: http://asthma.miningco.com/msub21.htm   Occupational Asthma Links http://www.aaaai.org/public/publicedmat/tips/occupationalasthma.stm  Occupational asthma (AAAAI) http://www.asmanet.com/asmapro/asmawork.htm http://www.nationalJewish.org/ National Jewish Center, Denver Top Lung Center in US http://www.NationalJewish.org/uri.html  Occupational Asthma Occupational Asthma Physicians  Cecile Rose MD  Lisa Maier MD  Sandra Mohr MD  Lee Newman MD Ellis

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