Exposure to the chemicals in Moisture Cure Urethane (MCU) products can
lead to a variety of health effects depending upon the level and
duration of exposure. Brief exposures to elevated levels of these
materials can result in headaches, respiratory irritation, and
exacerbation of asthma; while very high and/or long-term exposures can
lead to more serious health effects such as organ damage, reproductive
effects, chemical allergies, and possibly cancer.

Moisture cure urethanes contain a variety of solvents depending upon
their formulation, and typically contain xylene, ethylbenzene and
acetates. Many solvents, including xylene and ethylbenzene, have
strong odors that can be smelled at very low levels. Short-term
exposure to elevated levels can cause reversible irritation of the
skin, eyes, nose, and throat; exacerbate asthma; and cause health
effects such as headaches, nausea, and dizziness. In occupational
settings and in animal studies, exposure to very high levels of
solvents has been shown to cause neurological, kidney, and liver
damage, and can impact developing fetuses. , The International Agency
for Research on Cancer (IARC) lists ethylbenzene as a possible human
carcinogen. IARC lists xylene as not classifiable as a human cancer
agent.

uh,boy!
Someday, it'll all be over....

I KNEW there was a good reason I went with Bonakemi Mega for my floor
finish...

dave

Moshe wrote:

Exposure to the chemicals in Moisture Cure Urethane (MCU) products can
lead to a variety of health effects depending upon the level and
duration of exposure. Brief exposures to elevated levels of these
materials can result in headaches, respiratory irritation, and
exacerbation of asthma; while very high and/or long-term exposures can
lead to more serious health effects such as organ damage, reproductive
effects, chemical allergies, and possibly cancer.

Moisture cure urethanes contain a variety of solvents depending upon
their formulation, and typically contain xylene, ethylbenzene and
acetates. Many solvents, including xylene and ethylbenzene, have
strong odors that can be smelled at very low levels. Short-term
exposure to elevated levels can cause reversible irritation of the
skin, eyes, nose, and throat; exacerbate asthma; and cause health
effects such as headaches, nausea, and dizziness. In occupational
settings and in animal studies, exposure to very high levels of
solvents has been shown to cause neurological, kidney, and liver
damage, and can impact developing fetuses. , The International Agency
for Research on Cancer (IARC) lists ethylbenzene as a possible human
carcinogen. IARC lists xylene as not classifiable as a human cancer
agent.

Dave,

Before you rest too easy realize that a big problem with urethanes is
that their precursors are seen as causative factors when looking at
disorders like asthma. Bonakemi Mega I suspect will have compounds
similar to MDI. The solvents used in Bonakemi Mega include NMP and
glycol ethers which are not to be regarded casually. The bottom line is
that finishes are chemistry sets. Know what the constituents are,
understand them or don't use them, and deal with them appropriately.
Fear of "chemicals" because they are chemicals is unfounded.

Phil

Bay Area Dave wrote:
I KNEW there was a good reason I went with Bonakemi Mega for my floor
finish...

dave

Moshe wrote:

Exposure to the chemicals in Moisture Cure Urethane (MCU) products can
lead to a variety of health effects depending upon the level and
duration of exposure. Brief exposures to elevated levels of these
materials can result in headaches, respiratory irritation, and
exacerbation of asthma; while very high and/or long-term exposures can
lead to more serious health effects such as organ damage, reproductive
effects, chemical allergies, and possibly cancer.

Moisture cure urethanes contain a variety of solvents depending upon
their formulation, and typically contain xylene, ethylbenzene and
acetates. Many solvents, including xylene and ethylbenzene, have
strong odors that can be smelled at very low levels. Short-term
exposure to elevated levels can cause reversible irritation of the
skin, eyes, nose, and throat; exacerbate asthma; and cause health
effects such as headaches, nausea, and dizziness. In occupational
settings and in animal studies, exposure to very high levels of
solvents has been shown to cause neurological, kidney, and liver
damage, and can impact developing fetuses. , The International Agency
for Research on Cancer (IARC) lists ethylbenzene as a possible human
carcinogen. IARC lists xylene as not classifiable as a human cancer
agent.

[snip]

Moshe wrote:

Exposure to the chemicals in Moisture Cure Urethane (MCU) products can
lead to a variety of health effects depending upon the level and
duration of exposure.

Airborne concentration and duration of exposure are very important.

Brief exposures to elevated levels of these
materials can result in headaches, respiratory irritation, and
exacerbation of asthma; while very high and/or long-term exposures can
lead to more serious health effects such as organ damage, reproductive
effects, chemical allergies, and possibly cancer.

Moisture cure urethanes contain a variety of solvents depending upon
their formulation, and typically contain xylene, ethylbenzene and
acetates. Many solvents, including xylene and ethylbenzene, have
strong odors that can be smelled at very low levels. Short-term

Strong odors are a good thing. Also known as warning properties. The smell
should help you avoid exposure to "very high levels". Most hobbiests are
not working with glues 2000 hours a year. If you are in the business,
follow OSHA guidelines. If you are a hobbiest, use in a well ventilated
area and reduce your exposure as much as practical.

exposure to elevated levels can cause reversible irritation of the
skin, eyes, nose, and throat; exacerbate asthma; and cause health
effects such as headaches, nausea, and dizziness. In occupational
settings and in animal studies, exposure to very high levels of
solvents has been shown to cause neurological, kidney, and liver
damage, and can impact developing fetuses. , The International Agency
for Research on Cancer (IARC) lists ethylbenzene as a possible human
carcinogen. IARC lists xylene as not classifiable as a human cancer
agent.

An old saying: "the dose makes the poison".

Montyhp

(Moshe) wrote in message . com...
Exposure to the chemicals in Moisture Cure Urethane (MCU) products can
lead to a variety of health effects depending upon the level and
duration of exposure. Brief exposures to elevated levels of these
materials can result in headaches, respiratory irritation, and
exacerbation of asthma; while very high and/or long-term exposures can
lead to more serious health effects such as organ damage, reproductive
effects, chemical allergies, and possibly cancer.

Moisture cure urethanes contain a variety of solvents depending upon
their formulation, and typically contain xylene, ethylbenzene and
acetates. Many solvents, including xylene and ethylbenzene, have
strong odors that can be smelled at very low levels. Short-term
exposure to elevated levels can cause reversible irritation of the
skin, eyes, nose, and throat; exacerbate asthma; and cause health
effects such as headaches, nausea, and dizziness. In occupational
settings and in animal studies, exposure to very high levels of
solvents has been shown to cause neurological, kidney, and liver
damage, and can impact developing fetuses. , The International Agency
for Research on Cancer (IARC) lists ethylbenzene as a possible human
carcinogen. IARC lists xylene as not classifiable as a human cancer
agent.

In September of 2002 the New York City Department of Health and Mental
Hygiene (DOHMH), Environmental & Occupational Disease Epidemiology
Program (EODE) began receiving reports that Moisture Cure Urethanes
(MCUs), which are used to coat wood floors in homes, were generating
strong odors and raising health concerns for building residents. In
response to these concerns, EODE reviewed material safety data sheets
on various MCU products, researched the known health effects
associated with chemical ingredients of these products, and consulted
with the New York State Department of Health. Additionally, EODE,
with assistance from the Office for Environmental Investigations
(OEI), conducted an inspection during an MCU application at an
apartment building in Brooklyn, New York on March 7, 2003, that
included sampling for airborne ingredients of MCUs.

Environmental sampling at the Brooklyn apartment building detected
several MCU chemical ingredients in the air. These chemicals produced
noticeable odors throughout the building. The presence of the
chemicals found in the common hallways of the building may result in
irritation of the respiratory system, exacerbation of asthma in some
individuals, and headaches. In an occupied residential building these
conditions represent a nuisance.

Groups
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Search Result 2
From: Kathi )
Subject: Diisocyanate-induced OA:
This is the only article in this thread
View: Original Format
Newsgroups: alt.support.breast-implant
Date: 2003-06-17 13:19:54 PST


Diisocyanate-induced OA: How to be sure, what to do.

Author/s: Susan M. Tarlo
Issue: Jan, 2000

It may take weeks--or even years--before symptoms occur

ABSTRACT: Diisocyanates are among the most common causes of
occupational asthma (OA). Significant exposure to these agents has
been associated with spray painting and a number of manufacturing
processes. Consider the possibility of OA if a patient presents with
new-onset asthma, dry cough and/or shortness of breath, wheeze, and
chest tightness. Peak flow readings that are lower during and/or after
work and improved when the patient is off from work support the
diagnosis; pulmonary function tests pre- and post-bronchodilator and a
histamine or methacholine challenge provide objective assessment. An
early, accurate diagnosis and removal from exposure provide the best
outcomes. Other environmental control measures and pharmacologic
therapies for patients with OA are the same as for those with
nonoccupational asthma. (J Respir Dis. 2000;21 (1):58-67)

Occupational asthma (OA) is defined as asthma caused by conditions in
a particular occupational environment. [1] It may be provoked by an
immunologic mechanism (IgE-mediated) or, less commonly, by exposure to
high levels of a respiratory irritant (as in reactive airways
dysfunction syndrome [2] or irritant-induced asthma [3]). OA is the
most common nonacute occupational lung disease in many industrialized
countries, and among the most commonly reported causative agents are
the diisocyanates. [4,5] For example, spray painting, which may result
in significant exposure to diisocyanates, accounts for the highest
proportion of OA cases in Britain. [6]

In this article, I use the example of diisocyanate-induced asthma to
present the approach to diagnosis and management of OA suggested in
recent clinical guidelines. [7]

BACKGROUND

Diisocyanates are very reactive, low molecular weight chemicals
characterized by two - N=C=O groups per aromatic or aliphatic monomer.
They are commonly used in the manufacture of polyurethane foam (used
for car seats, bumpers, upholstered furnishings, and mattresses), in
spray paints (used in auto-body shops), and in urethane coatings and
sealants. Diisocyanates are also used in manufacturing refrigerators
and bathtubs and in foundries to make molds.

There are many different diisocyanate compounds; the most commonly
used are toluene diisocyanate (TDI), diphenylmethane diisocyanate
(MDI), and hexamethylene diisocyanate. Besides the monomeric form of
these diisocyanates, dimers and larger polymers (common in spray
paints) have been produced.

At high airborne exposure levels (such as following a spill or when
workers without respiratory protective equipment are exposed to spray
paint), diisocyanates are respiratory irritants and may cause OA.
[2,3] Diisocyanate-exposure may also lead to conditions other than a
new onset of asthma (see "Other effects of diisocyanates").

Levels of diisocyanates below 20 parts per billion have not been
demonstrated to cause respiratory irritation but may cause OA by
sensitization. This immunologic airway response is similar to OA
resulting from workplace allergens (such as animal dander, wheat, and
latex) in the following ways:
* There is a latent period of exposure that may range from weeks to
years before the onset of asthma.

* OA develops in only a minority of workers exposed to diisocyanates
(up to 11% of spray painters).

* Once a worker is sensitized to diisocyanates and OA develops, even
minute levels of exposure can trigger exacerbations.

However, unlike sensitization to high molecular weight allergens (such
as animal or plant proteins) and to some low molecular weight
chemicals (such as complex platinum salts and epoxy compounds), IgE
antibodies to diisocyanates have been demonstrated in only about 20%
of patients with diisocyanate-induced asthma, [8] and the immunologic
mechanism of this sensitization remains unclear. [9,11] At present,
there is no sensitive specific immunologic test for
diisocyanate-induced asthma.

This may in part relate to the low molecular weight of diisocyanates
--they require binding to a hapten to be antigenic. In addition, they
are very reactive and may form neoantigens or other immune stimulants
by binding with proteins in the airway [12] Other proposed mechanisms
include direct T-cell activation and activation of histamine-releasing
factors.

DIAGNOSIS

Whether OA results from diisocyanate exposure or contact with other
occupational sensitizers, an early, accurate diagnosis is key to
providing the best outcome.

The primary care physician or the occupational physician affiliated
with a plant producing or using diisocyanates has the best opportunity
to first suspect the diagnosis. A comprehensive occupational history
is essential in the evaluation of all patients in whom asthma symptoms
develop during their working life.

When to suspect OA

If a patient who works presents with a history of new-onset asthma,
dry cough and/or shortness of breath, wheeze, and chest tightness,
inquire about any temporal relationship of symptoms to the workplace.

About 60% of patients with diisocyanate-induced asthma note a
worsening of symptoms 4 to 8 hours after the onset of each exposure
(an isolated late response). [13] About 10% of patients have only an
isolated immediate response, occurring within minutes of the exposure
and clearing within an hour of leaving the exposure. The remaining 30%
of patients have a dual response--an immediate response followed by a
late response. [13] Thus, patients frequently notice the onset or
worsening of asthma at the end of a workshift, or in the evening after
leaving work, with symptoms disturbing sleep.

Improvement is frequently noted on weekends after 1 to 2 days' absence
from work (about 70% of patients) and, more frequently, on holiday
after 7 to 10 days' absence from work (about 90% of patients), with
worsening after 1 to 2 days back at work. [13] Such a history should
raise suspicion of OA and lead to more investigation (Figure 1).

History of exposure

Work performed in an environment where there is spray painting or the
manufacture or use of polyurethane foam should raise suspicions of
diisocyanate exposure; this type of exposure may also occur in
foundries and in plants that manufacture bathtubs or refrigerators.
The following suggestions will help you evaluate an occupational
exposu

* Request copies of material safety data sheets (MSDS) or workplace
hazardous materials information system (WHMIS) sheets listing the
hazardous chemicals in your patient's work setting. Employees are
entitled to MSDS relating to products to which they are exposed as
well as to chemicals used by co-workers. Your patient may directly
obtain the MSDS from an employer (especially with a physician's note)
or may need the assistance of a health and safety representative, or
union, to get copies.

* Obtain details about the frequency and intensity of the patient's
exposure, including information about the ventilation/containment
measures and the use and type of respiratory protective equipment
provided and worn. However, appropriate face masks and ventilation may
not completely prevent exposure to diisocyanates. Also, respiratory
exposure is increased if masks do not fit well or are not worn
consistently at times of exposure.

* Find out how many other employees were exposed and whether they are
having respiratory symptoms similar to those of your patient.

Consider other causes

The patient's clinical history may lead you to suspect an alternative
cause for symptoms. Rhinitis with postnasal drip may cause cough;
hyperventilation, vocal cord dysfunction, anemia, or other respiratory
or cardiac disease may cause dyspnea. Include the following
information in the clinical history:

* Are there symptoms of allergic rhinoconjunctivitis or nonallergic
rhinitis?

* Could there be other triggers or environmental exposures, such as
seasonal patterns or a cat?

* Does the patient have a history of smoking?

* What are indications of symptom severity? Has the patient had to
limit exercise? Have there been sleep disturbances or visits to the
emergency department? What are the patient's medication needs?

The proportion of patients with a family history of asthma is similar
among those with occupational and those with nonoccupational asthma.
Physical examination findings may be helpful in the differential
diagnosis but may be normal in nonoccupational asthma and OA,
especially if the patient is asymptomatic at the time of the visit.

Peak expiratory flow rate

When OA is a consideration, instruct the patient to use a peak
expiratory flow (PEF) meter and to record serial PEF readings (three
times on each occasion) at least four times a day on both working days
and days off (Figure 2). Patients should also record their symptoms
and use of medications. [7] Medications (other than bronchodilators as
needed) should, if possible, be kept at a stable, regular dosage
during this time, sufficient to control but not completely suppress
symptoms.

Compliance has been poor with such PEF recording, especially when
patients were asked to record values six times per day. [14]
Nevertheless, the sensitivity and specificity of PEF recordings have
been shown to be high compared with other tests if the patient keeps
an adequate record (encompassing several weeks at work as well as a
holiday period) and if the recordings show a clear pattern to support
or refute the relationship of asthma to work. [15,16] If recordings at
work show no significant changes, such changes may have been masked by
asthma medications; in this case, have the patient use less medication
and repeat the recordings. Electronic PEF meters or portable
spirometers provide more objective information about patient
compliance, but their cost makes it impractical to lend them to
patients for several weeks.

Interpreting test results

Both pre- and post-bronchodilator pulmonary function tests, as well as
a histamine or methacholine challenge test, are necessary to
objectively diagnose asthma and to assess the relationship of asthma
symptoms to work. Normal results do not exclude OA if tests are
performed when the patient is absent from work and free of symptoms.
In that case, the results can serve as a baseline for comparison with
spirometry and methacholine or histamine challenge responses obtained
toward the end of a typical work week, within 24 hours of symptom
occurrence, when the patient returns to work. If results at that time
do not show asthma, OA is virtually ruled out. [7]

It is rare for patients with diisocyanate-induced asthma to have
normal airway responsiveness to histamine or methacholine challenge
within 24 hours of an exposure that has induced asthma symptoms,
although a few cases have been reported. [17] If the patient is
working when first assessed and a methacholine or histamine challenge
confirms airway hyperresponsiveness, repeat the testing after a
holiday of 10 to 14 days (before the patient returns to work) to
objectively assess whether there is improvement, which would support a
diagnosis of OA.

Depending on the individual pulmonary function Laboratory, a minimum
of a twofold to fourfold improvement in provocative concentration of
an inhaled agonist producing a 20% decrease in forced expiratory
volume in 1 second ([PC.sub.20]) when a patient is absent from work is
significant. [18] However, lack of significant improvement in
[PC.sub.20] when a patient is on holiday does not exclude OA, since a
minority of sensitized persons with asthma may require a longer period
away from exposure before significant improvement occurs. Therefore,
in the face of a convincing history, PEF responses that suggest an
occupational component, and a trend toward improvement in histamine or
methacholine [PC.sub.20], a longer period away from work with repeated
tests may help establish the diagnosis.

To interpret changes in PEF rates and methacholine or histamine
responses during weeks at work compared with weeks absent from work,
consider confounding factors, [18] such as intercurrent respiratory
viral infections within the preceding 6 weeks or nonoccupational
allergen exposures. (Information may be obtained from the patient's
history and environmental allergy assessment, including skinprick
testing for sensitivity to common aeroallergens). For example, there
may be improvement during a holiday if a patient who is allergic to a
cat or to ragweed travels away from these triggers.

Work-related changes in asthma severity as assessed by serial PEF
monitoring and methacholine or histamine challenges generally provide
a clear, objective method to confirm or refute the diagnosis of OA. If
PEF monitoring can be adequately performed and interpreted but
methacholine or histamine challenges cannot (or vice versa), and if
the resulting changes are clearly positive or negative, this may be
sufficient to confirm or refute the diagnosis (although not ideal).
However, if the patient is removed from exposure to diisocyanates and
cannot or will not return to the site for testing, the diagnosis will
remain unproved.

Demonstration of asthma by a significant bronchodilator response,
spirometry, or a positive methacholine or histamine challenge in a
patient whose symptoms began while working in a setting with
diisocyanate exposure does not prove the diagnosis of OA (although it
raises suspicion). Nonoccupational asthma is common and frequently has
its onset in adult life.

Laboratory challenge

In patients who have a history that suggests diisocyanate-induced
asthma but who have left work before being assessed, the absence of
objective findings does not exclude previous OA. In these
circumstances (and when a patient clearly has OA but if confirmation
of the causative agent is needed), specific laboratory challenge
testing with diisocyanates may be helpful. [19] Such testing requires
specialized facilities that are available in only a few centers, [19]
and it is time-consuming and costly.

Although laboratory challenge has been considered a gold standard of
diagnosis, false-negative responses can occur if the wrong
diisocyanate is used. For example, some patients can be sensitized to
TDI but not MDI; some to a pre-polymer but not a polymer [20]; and
some to a specific isomer, such as TDI 2,4 but not TDI 2,6. [21] After
a long period away from exposure, sensitivity may be lost, or there
may be a need for multiple days of reexposure before measurable
changes occur in PEF, spirometry, or methacholine/histamine
responsiveness. [22] During challenges, levels of diisocyanates need
to be continuously monitored, since excessive levels may be irritating
or may sensitize the patient. Therefore, when feasible, workplace
studies provide the most practical means of diagnosis. Workers'
compensation claims are greatly facilitated if a clear, objective
diagnosis has been made before the patient is advised to stop working
with diisocyanate exposure.

MANAGEMENT

The best prognosis for OA caused by sensitization to diisocyanates is
associated with an early, accurate diagnosis and removal from further
exposure (Figure 3). [13,23] Other indicators of a favorable prognosis
are an early onset and milder asthma at the time of diagnosis. [13]
Asthma occurring within the first 2 years of work exposure is
considered to be early-onset; this is when diisocyanate-induced asthma
most commonly becomes apparent.

Changes in ventilation at work and use of protective respirators have
been associated with a less beneficial outcome. Other environmental
control measures and medications for the treatment of OA are the same
as for nonoccupational asthma.

The patient's co-workers should also be considered when a diagnosis of
diisocyanate-induced asthma is made. A diagnosis of OA should be
considered a "sentinel event" and lead to assessment of the workplace
practices by the employer or by a public health agency, the goals of
which are to ensure that diisocyanates are being appropriately and
safely handled, to ensure that workers have appropriate health and
safety education concerning risks, and to allow early detection of OA
in co-workers. Evidence suggests that there may be some benefit from
surveillance programs that monitor and control diisocyanate exposure
levels and provide medical surveillance for workers with the use of
respiratory questionnaires and workplace spirometry, as has been done
in Ontario. [24]

Other effects of diisocyanates

In addition to anew onset of asthma, diisocyanate exposure may lead to
the following conditions:

* Irritant-induced asthma: A spill or other very high exposure to
diisocyanates can induce, an inflammatory airway response resulting in
an asthma syndrome that can persist for weeks to years. [2,3] To make
this diagnosis, document the occurrence of the exposure (when
possible) and the new onset of asthma symptoms within 24 hours of such
exposure, persisting for at least 12 weeks, and obtain objective
evidence of asthma based on a spirometric bronchodilator response or a
methacholine or histamine challenge. [2,3]

The patient may also have been sensitized to diisocyanates at the time
of the exposure [25] and may have a worsening of asthma even on
exposure to very low levels. In this case, total removal from further
exposures is required. However, if irritant-induced asthma has
occurred without concurrent sensitization, the patient may return to
the workplace provided that there is appropriate asthma management and
that measures to reduce the risk of similar high-level exposures are
in place. [7]

* Aggravation of underlying asthma: Patients with nonoccupational
asthma may experience an exacerbation of their symptoms while working
with diisocyanates if levels are high or if there is exposure to other
concurrent nonspecific respiratory irritants, such as dusts, smoke, or
fumes. In that case, peak flow readings may show an immediate
worsening with work exposure and improvement on weekends and holidays,
but the degree of nonspecific airway responsiveness (20% decrease in
forced expiratory volume in 1 second) to histamine or methacholine
would not be expected to differ significantly during holidays,
compared with work weeks. To treat such a patient, optimize asthma
therapy, and instruct the patient how to control environmental
respiratory irritant exposure when possible--by a move to a cleaner
area of the plant; by ventilation improvements; and by short-term,
appropriate respirator use when levels of workplace irritants are
temporarily increased. [7]

* Diisocyanate-induced rhinitis: Rhinitis is commonly reported by
patients with diisocyanate-induced asthma [13] and has been confirmed
by challenge testing, [26] but the prevalence-of diisocyanate-induced
rhinitis alone is not known, and its prognostic significance
concerning the development of occupational asthma has not been
reported.

* Hypersensitivity pneumonitis: This is uncommon and has been reported
mainly in case series in relation to diphenylmethane diisocyanates.
[27] Clinical features are similar to those of hypersensitivity
pneumonitis from other causes, and specific IgG antibodies to
diisocyanate human serum albumin conjugates have been demonstrated.
Treatment is removal from further exposure to diisocyanates and, when
necessary administration of oral corticosteroids.

Dr Tarlo is associate professor of medicine at the University of
Toronto and is affiliated with the respiratory division of the Toronto
Western Hospital in Ontario.

REFERENCES

(1.) Chan-Yeung M, Malo JL. Occupational asthma. N Engl J Med.
1995;333:107-112.

(2.) Brooks S, Bernstein IL, Weiss MA. Reactive airways dysfunction
syndrome (RAFDS). Persistent asthma syndrome after high level irritant
exposures. Chest. 1985;88:376-384.

(3.) Tarlo SM, Broder I. Irritant-induced occupational asthma. Chest.
1989;96:297-300.

(4.) Tarlo SM, Lisa G, Corey P, et al. A workers' compensation claim
population for occupational asthma. Comparison of subgroups. Chest.
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(5.) Matte TD, Hoffman RE, Rosenman DK, et al. Surveillance of
occupational asthma under the SENSOR model. Chest 1 1990;98(suppl):
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(6.) Ross DJ. Ten years of the SWORD project. Clin Exp Allergy.
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(7.) Tarlo SM, Boulet LP, Cartier A, et al. Canadian Thoracic Society
guidelines on occupational asthma. Can Respir J. 1998;5:289-300.

(8.) Tee RD, Cullinen P. Welch J, et al. Specific lgE to isocyanate: a
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(9.) Tarlo SM. Diisocyanate sensitization and antibody production. J
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(11.) Lummus ZL, Alam R, Bernstein Dl. Diisocyanate antigen-enhanced
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(12.) Wisnewaki AV, Lemus R, Karol MH, Redlich CA.
Isocyanate-conjugated human lung apithelial cell proteins: a link
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(14.) Malo JL, Trudeau C, Ghezzo H, at al. Do subjects investigated
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(15.) Cote J, Kennedy S, Chan-Yeung M. Sensitivity and specificity of
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(16.) Liss GM, Tarlo SM. Peak expiratory flow rates in possible
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(17.) Banks DE, Barkman HW Jr, Butcher BT, et al. Absence of
hyperresponsiveness to methacholine in a worker with methylene
diphenyl diisocyanate (MDI)-induced asthma. Chest. 1986;89:389-393.

(18.) Official Statement of the European Respiratory Society.
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16):5-40.

(19.) Banks CE, Tarlo SM, Masri F, et al. Bronchoprovocation tests in
the diagnosis of isocyanate-induced asthma. Chest. 1996;109:1370-1379.

(20.) Vandenplas O, Cartier A, Lesage J, at al. Occupational asthma
caused by a prepolymer but not the monomer of toluene diisocyanate
(TDI). J Allergy Clin Immunol. 1992; 89:1183-1188.

(21.) Banks CE, Saestre J, Butcher BT, et al. Role of inhalation
challenge testing in the diagnosis of isocyanate-induced asthma.
Chest. 1989;95:414-423.

(22.) Hargreave FE, Ramsdale EH, Pugaley SO. Occupational asthma
without bronchial hyperresponsiveness. Am Rev Respir Dis.
1984;130:513-515.

(23.) Pisato G, Baruffino A, Zedda S. Toluene diisocyanate induced
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COPYRIGHT 2000 Cliggott Publishing Co.

COPYRIGHT 2001 Gale Group


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