Re: More Letters to the AAAAI

[Guest guest]

thanks KC and Sharon, I have learned a lot from these letters, hope

others do to. I have been wondering if I have fibrosis in the lower

part of my lungs because theres a weird felling in this area all the

time. its hard to discribe, like pressure being applied, or like its

swollen in that area and theres not enough room. maybe this is one

thing I can get checked at a regular hospital. thanks again for

everything you do to

help.

>

> KC requested that I post some more of the letters that the AAAAI

received in

> response to their new position statement in regard their " Art of

the State "

> understanding mold and mycotoxin induced illnesses. The follow was

sent on

> your behalf from Jeff May.

>

> " Mr. Kruger "

> Subject: Comments on AAAAI Position Paper

> Date: Wed, 01 Mar 2006 07:34:22 -0500

> Mime-Version: 1.0

> Content-Type: text/plain; format=flowed; charset= " iso-8859-1 "

> Content-Transfer-Encoding: 8bit

>

> Mr. Kruger,

>

> The AAAAI position paper “The Medical Effects of Mold

Exposure†by Bush et

> al. claims to “review the state of the science of mold-related

diseases and

> provide interpretation as to what is and what is not supported by

scientific

> evidence.†With respect to hypersensitivity pneumonitis (HP),

the position

> paper states that “exposure to domestic specific fungal spores

is an

> extremely unlikely cause of HP, except in highly unusual

circumstances, such

> as workplace exposure†and concludes that “HP is an uncommon

but important

> disease that can occur as a result of mold exposure, particularly

in

> occupational settings with high levels of exposure.†These

statements are

> incorrect.

>

> I have investigated several cases in which physician-diagnosed HP

was the

> result of home exposure to mold:

>

> #1: A 27 year-old female living in a 2 ½ year-old house with a

recently

> finished and carpeted basement (where the laundry was located),

was

> hospitalized twice with shortness of breath and was referred by

her

> pulmonologist who diagnosed HP. She had and weakly positive serum

> reactivity to Aspergillus, Candida, Cladosporium, Mucor,

Rhodotorula and

> pigeon but not to her dog or cat. The concentration of spores (NV

air

> sample) in the basement, where she exercised, was about 50,000 /m3

(majority

> Pen/Asp), but the result of culturable sampling was only about 154

total

> CFU/ m3 (less than 100 Penicillium CFU/ m3, but still about twice

the

> culturable exterior concentration). Dust in basement tape samples

from the

> carpet, and mildew from the baseboard contained Penicillium,

Cladosporium,

> Aureobasidium pullulans and Aspergillus nidulans. Microscopy of

dust and

> non-viable (NV) air samples were indicative of active mold growth

(hyphae

> and Aspergillus conidiophores) in the basement carpet. During NV

air

> sampling in the living room, a child jumped on the couch and an

airborne

> dust mite was trapped in the sample. The woman avoided entering

her basement

> and her HP symptoms abated within months.

>

> #2: A 60+ year-old partially disabled female, forced to spend a

significant

> portion of each day in bed (due to an unrelated illness), was

referred by

> her pulmonologist who had diagnosed HP. The home had forced hot

air heat

> (with a dirty blower and mold growing in the dust on the return

grilles) and

> a finished basement (no carpeting) that had flooded several times.

A furnace

>

> humidifier contained no mold growth, though bacteria and

unidentified,

> flagellate unicellular organisms were present. The concentration of

Pen/Asp

> spores was over 1000 / m3 at a heat register (over 100 times the

exterior

> concentration and almost 8 times greater than the indoor ambient

level

> before operation of the blower, all NV samples) but the culturable

sample

> from the vent (reported by J. Fink) grew only “a few

Penicillium†colonies

> (less than 50 CFU/ m3). Tape samples from the blower contained

numerous

> Penicillium and yeast, as determined by microscopy and culturing.

The

> woman’s blood serum did not react to a commercial Penicillium

antigen and

> reacted only “weakly positive†to Aspergillus in the HP panel

of antigens,

> but was, from a culture of the tape sample, “highly positiveâ€

(IgG) to the

> Aspergillus and Penicillium from the blower (yet negative in IgE

reactivity

> to both). In addition to significant exposures from the heating

system, the

> woman also had bioaerosol exposures while in bed due to the mites

and mold

> colonizing the feather bedding, most probably due to the body

moisture she

> supplied while bedridden. The heating system was professionally

cleaned and

> a media filter installed and the woman’s symptoms diminished, but

were

> exacerbated about two years later. Despite previous

recommendations, the

> woman did not eliminate her feather pillow or encase the mattress

in

> allergen control covers. Upon subsequent testing, a dust sample

from the

> bedding contained entire Aspergillus and Penicillium

conidiophores,

> suggesting active growth, and her serum IgG reactivity to

Penicillium was

> “strongly positive.â€

>

> #3: A 70+ year old female, referred by her pulmonologist and

diagnosed with

> HP, had suffered from chronic cough, and for three years had not

slept

> through the night without experiencing disruptive coughing fits

(one of

> which resulted in a hernia). She and her retired husband had lived

in the

> house, which had a dirt basement floor and a steam boiler, for

over 50

> years, but a few years previously had moved their bedroom into a

converted

> porch above a dirt crawl space. The couple had a dog and had used

both an

> evaporative and a cool mist humidifier, and burned soot-producing

jar

> candles. Dust from the living room furniture contained numerous

dog dander

> particulates as well as many dust mite fecal pellets. There was

visible

> mildew on the walls of the carpeted and cluttered bedroom. Air

(NV) samples

> in all the rooms contained dog dander particulates, elevated

numbers of

> Pen/Asp spores and skin scale fragments (possibly due to bacterial

> degradation caused by annual carpet washing) in a range of 2-12

microns.

> Snow covered the ground at the exterior, and the indoor air

yielded

> (culturable samples) 92, 58 and 23 CFU/ m3 (most of which

consisted of

> Aspergillus and Penicillium spp.) in the master bedroom, dining

room and

> basement, respectively. The woman stopped coughing as soon as she

put on a

> NIOSH N95 disposable mask, and did not cough for three hours, but

resumed as

> soon as she took the mask off. She spent the night in the guest

room, where

> there was hardwood flooring and slept soundly to morning.

>

>

> The authors have ignored a number of papers:

>

> 1-Lee YM, Kim YK, Kim SO, Kim SJ, Park HS J Korean Med Sci. 2005

> Dec;20(6):1073-5.

>

> “A case of hypersensitivity pneumonitis caused by Penicillium

species in a

> home environmentâ€

>

> We report a case of hypersensitivity pneumonitis in a 30-yr-old

female

> housewife caused by Penicillium species found in her home

environment. The

> patient was diagnosed according to history, chest radiograph,

spirometry,

> high-resolution chest CT, and transbronchial lung biopsy. To

identify the

> causative agent, cultured aeromolds were collected by the open-

plate method.

> From the main fungi cultured, fungal antigens were prepared, and

immunoblot

> analysis with the patient's serum and each fungal antigen was

performed. A

> fungal colonies were isolated from the patient's home.

Immunoblotting

> analysis with the patient's sera demonstrated a IgG-binding

fractions to

> Penicillium species extract, while binding was not noted with

control

> subject. This study indicates that the patient had

hypersensitivity

> pneumonitis on exposure to Penicillium species in her home

environment.

>

> 2. Ikeda T, Kuroda M, Ueshima K., Nihon Kokyuki Gakkai Zasshi.

2002

> May;40(5):387-91.

> “A case of hypersensitivity pneumonitis caused by Gyrodontium

versicolorâ€

>

> A 36-year-old woman was admitted to our hospital because of fever,

dry

> cough, dyspnea on exertion and body weight loss in August 2000.

Chest

> radiography and CT scanning showed diffuse ground glass opacity

and small

> centrilobular nodules in the middle and lower lung fields of both

lungs.

> Serum antibody against Trichosporon cutaneum was positive; and

summer-type

> hypersensitivity pneumonitis was therefore initially diagnosed.

Treatment

> with methylprednisolone and prednisolone decreased the symptoms,

but the

> dyspnea reappeared when the patient was at home. Inspection of her

house

> revealed the presence of fungi under the floor. After these were

removed,

> her symptoms disappeared completely. The lymphocytic stimulation

test of the

>

> peripheral blood was positive for the fungi, and it was therefore

suggested

> that they were the cause of her hypersensitivity pneumonitis. The

fungi were

> identified as Gyrodontium versicolor. This is the first report of

> hypersensitivity pneumonitis caused by Gyrodontium versicolor.

>

> 3. Lee SK, Kim SS, Nahm DH, Park HS, Oh YJ, Park KJ, Kim SO, Kim

SJ.

> Allergy. 2000 Dec;55(12):1190-3.

> “Hypersensitivity pneumonitis caused by Fusarium napiforme in a

home

> environmentâ€

>

> BACKGROUND: We report a case of hypersensitivity pneumonitis (HP)

in a

> 17-year-old male student caused by Fusarium napiforme found in his

home

> environment. METHODS: The patient was diagnosed according to

history, chest

> radiograph, spirometry, high-resolution chest CT, and

transbronchial lung

> biopsy. To identify the causative agent, cultured aeromolds were

collected

> by the open-plate method. From the main fungi cultured, fungal

antigens were

> prepared, and immunoblot analysis with the patient's serum and

each fungal

> antigen was performed. RESULTS: Five fungal species were isolated

from the

> patient's home. Immunoblotting analysis with the patient's serum

> demonstrated more than 10 IgG-binding fractions to F. napiforme

extract

> only, while little binding was noted with the other fungal

antigens.

> CONCLUSIONS: We should be aware that HP may be caused by F.

napiforme in the

> home environment.

>

> 4. RS, Dyer Z, Liebhaber MI, Kell DL, Harber P., Am J

Respir Crit

> Care Med. 1999 Nov;160(5 Pt 1):1758-61.

>

> “Hypersensitivity pneumonitis from Pezizia domiciliana. A case

of El Nino

> lungâ€

>

> A previously healthy woman developed severe dyspnea and was found

to have

> restrictive lung disease and evidence of alveolitis. Open lung

biopsy

> revealed extrinsic allergic alveolitis (hypersensitivity

pneumonitis). The

> etiology was not initially apparent, but a home inspection showed

an unusual

> mushroom growing in the patient's basement. Air sampling and serum

> precipitins against the fungal antigens confirmed that Pezizia

domiciliana

> was the cause of the patient's hypersensitivity pneumonitis. This

is the

> first described case of hypersensitivity pneumonitis cause by P.

> domiciliana. We speculate that unprecedented rainfall and flooding

of the

> patient's basement as a result of El Nino rains produced ideal

factors for

> the growth of this fungus.

>

> 5. s RL, s CP, Coalson JJ. Ann Allergy Asthma Immunol.

2005

> Aug;95(2):115-28. Ann Allergy Asthma Immunol. 2005 Aug;95(2):99.

>

> “Hypersensitivity pneumonitis: beyond classic occupational

disease-changing

> concepts of diagnosis and managementâ€

>

> OBJECTIVE: To review inhaled antigens in home environments that

cause

> hypersensitivity pneumonitis (HP) of varied clinical expressions

and

> histopathologic patterns. DATA SOURCES: Computer-assisted MEDLINE

and manual

> searches for articles concerning HP, interstitial lung disease

(ILD),

> epidemiology of HP and ILD, challenge procedures of HP, and indoor

fungi.

> STUDY SELECTION: Published articles concerning inhaled antigens in

home

> environments and HP were selected. RESULTS: Current criteria for

the

> diagnosis of HP are too restrictive, because most apply only to

the classic

> acute presentation and are of limited value in the subacute and

insidious

> forms. Clinical expressions vary across the gamut of respiratory

tract signs

> and symptoms. Patterns on lung biopsy may include all

histopathologic

> descriptions of idiopathic ILD. The home is the likely causative

environment

> rather than the workplace. Exposures may be occult and require in-

depth

> environmental histories and on-site investigations to detect

antigens and

> sources. CONCLUSIONS: Natural or environmental challenges have

become an

> important tool for diagnosing HP and determining effectiveness of

> remediation. Early diagnosis and effective remediation of the

cause lead to

> a high survival rate, whereas diagnosis in advanced stages leads

to

> disability and/or premature death.

>

> 6. Venkatesh P, Wild L.,Paediatr Drugs. 2005;7(4):235-44.

>

> Hypersensitivity pneumonitis in children: clinical features,

diagnosis, and

> treatment.

>

> Hypersensitivity pneumonitis (HP), or extrinsic allergic

alveolitis, is a

> form of immune-mediated inflammatory lung disease involving the

distal

> portions of the lungs associated with intense or repeated exposure

to a

> variety of finely dispersed environmental antigens. Although once

believed

> to be a disease of adults because of its frequent association with

the

> occupational setting, HP exists in the pediatric population and

often goes

> unrecognized. Childhood HP is often associated with exposure to

antigens in

> the home environment as well as with certain hobbies. Patients

present in

> any one of the three disease stages: acute, subacute, and chronic,

all with

> unique clinical presentations. Histopathologic findings depend on

the

> disease stage at the time of evaluation. The immuno-pathogenesis

is complex,

> but immune-complex (type III hypersensitivity) and cell-mediated

(type IV

> hypersensitivity) immune responses appear to be the primary immune

> mechanisms involved in the pathogenesis of HP. Diagnosis can be

very

> challenging. Although no single diagnostic or clinical laboratory

test is

> available to diagnose HP, the most significant diagnostic tool is

a detailed

> environmental exposure history. Avoidance of the inciting antigen

is the

> most important form of treatment. Acute HP is responsive to

antigen removal

> alone. However, a short course of prednisone for 2-3 weeks can be

useful in

> patients with severe attacks. Subacute and chronic HP may require

higher

> doses of corticosteroids for a longer duration (i.e. months);

however, the

> long-term efficacy of using corticosteroids is still not well

defined. As

> with most hypersensitivity diseases, early diagnosis provides the

best

> prognosis.

>

> 7. Moran JV, Greenberger PA, R., Allergy Asthma Proc.

2002

> Jul-Aug;23(4):265-70.

>

> “Long-term evaluation of hypersensitivity pneumonitis: a case

study

> follow-up and literature reviewâ€

>

> This study reports a 3-year follow-up of a classic presentation

of

> hypersensitivity pneumonitis (HP), originally reported elsewhere,

after

> removal of the causative antigens. The literature is reviewed and

this case

> is compared with outcomes of series previously reported. The

patient was

> reevaluated by clinical, serologic, radiographic, and pulmonary

function

> testing 3 years after removal of her home's contaminated

humidifier,

> cleaning of the home, and administration of a course of prednisone.

Repeat

> serologic measurements revealed positive serum precipitins only

for

> Aspergillus flavus and Phoma herbarum, significantly fewer than her

original

> panel, which revealed precipitating antibodies to her humidifier

water and

> 10 other specific antigens. Pulmonary function tests remained

stable.

> Physical exam revealed bibasilar rales. Computed tomography scan

revealed

> pulmonary fibrosis, bronchiectasis, and honeycombing that was

compared with

> 3 years earlier. Although most of the data obtained on reevaluation

suggest

> remission, radiographic findings have not remitted. Long-term

follow-up of

> parameters of HP disease activity do not always reveal consistent

findings.

> This patient appears to be in a category of HP between the classic

subacute

> and chronic stages.

>

> 8. Yoshizawa Y, Ohtani Y, Hayakawa H, Sato A, Suga M, Ando M.,J

Allergy Clin

> Immunol. 1999 Feb;103(2 Pt 1):315-20.

>

> “Chronic hypersensitivity pneumonitis in Japan: a nationwide

epidemiologic

> Surveyâ€

>

> BACKGROUND: Pulmonary fibrosis inevitably develops in patients

with chronic

> hypersensitivity pneumonitis (HP). OBJECTIVE: We conducted a

nationwide

> epidemiologic study in Japan to evaluate the frequency and clinical

> characteristics of chronic HP. METHODS: This report is on 36 cases

of

> chronic HP, including 10 patients with summer-type HP, 5 patients

with

> home-related HP, 7 patients with bird fancier's lung, 5 patients

with

> isocyanate-induced HP, 4 patients with farmer's lung, and 5

patients with

> other types of chronic HP. Chronic HP was further subgrouped into

2 types:

> one type of patients were first seen with chronic disease (9

patients), and

> the other type became chronic with fibrosis after repeated acute

episodes

> (27 patients). RESULTS: The upper lung field was frequently

involved in

> chronic HP (17%). Ground-glass opacities were observed in 57% and

air space

> consolidation in 30% of the patients. Honeycombing was apparent in

37%.

> Twenty-six of 28 patients had antibodies to the presumptive

antigens. Five

> of 8 patients with chronic HP were positive for antigen-induced

lymphocyte

> proliferation. In 2 cases patients did not have detectable

antibodies to

> causative antigens, although antigen-induced lymphocyte

proliferation was

> detectable. The ratio of CD4 to CD8 in BAL lymphocytes was lowest

in

> isocyanate-induced HP (mean 0.22) and tended to be high in

farmer's lung and

> bird fancier's lung. Granulomas were observed in 39% and Masson

bodies in

> 42% of specimens on histologic examination. Administration of

prednisolone

> was effective in 58% of patients. CONCLUSIONS: The insidious form

of chronic

> HP has probably been misdiagnosed as idiopathic pulmonary fibrosis

when a

> good history was not taken and immunologic (especially antigen-

induced

> lymphocyte proliferation) and BAL testing were not counted.

>

> Also:

>

> Apostolakos, M.J., Rossmoore, H., Beckett, W.S. 2001,

“Hypersensitivity

> pneumonitis from ordinary residential exposures,†Environ.

Health Perspect.,

> vol. 109, no.9, pp. 979-81.

>

> Hirakata, Y., Katoh, T., Ishii, Y., Kitamura, S., Sugiyama,

Y.,2002,

> “Trichosporon asahii-induced asthma in a family with Japanese

summer-type

> hypersensitivity pneumonitis,†Ann. Allergy Asthma Immunol.,

vol.88, no.3,

> pp. 335-8.

>

> Park, H.S., Jung, K.S., Kim, S.O., Kim, S.J, 1994,

“Hypersensitivity

> pneumonitis induced by Penicillium expansum in a home

environment,†Clin.

> Exp. Allerg., vol. 24, no.4, pp. 383-5.

>

> Patel, A.M., Ryu, J.H., , C.E., 2001, “Hypersensitivity

pneumonitis:

> current concepts and future questions,†J. Allergy Clin.

Immunol., vol.108,

> no.5, pp. 661-70.

>

> Suda, T., Sato, A., Ida, M., et. al., 1995, “Hypersensitivity

pneumonitis

> associated with home ultrasonic humidifiers,†Chest, vol.107,

no.3, pp.

> 711-7.

>

> Yoshida, K., Ando, M., Sakata, T., Araki, S., 1989, “Prevention

of

> summer-type hypersensitivity pneumonitis: effect of elimination of

> Trichosporon cutaneum from the patients' homes,†Arch. Environ.

Health,

> vol.44, no.5, pp. 317-22.

>

> HP as a result of home exposure and home exposure to mold is

probably

> under-diagnosed in the U.S. The illness is a serious public health

concern

> (no doubt with more cases than illness due to exposure to radon,

for

> example, for which there has been great expenditures).

>

> The AAAAI position paper should modified to reflect importance of

home

> exposures to antigens.

>

> C. May, M.A., Author

> May Indoor Air Investigations LLC

> Cambridge, MA

>

> www.mayindoorair.com

> www.myhouseiskillingme.com

>

>

>

>

>

>