Allergy & Irritant
Surfer
What is the difference between being allergic to a substance, and a
substance being an irritant? I know there *is* a difference and I have
a sort of part-formed explanation in my head which includes that
irritants will irritate all people to a greater or lesser degree, normal
& asthmatic (but with bigger consequences for the asthmatics), and that
there must be something different going on at the cell (or smaller)
level, and that one can be allergic to an irritant as well as irritate
by it.
A nice clear explanation for a lay person would be much appreciated.
--
Surfer!
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Colin Campbell
<sur...@nevis-vieww.demon.co.uk> wrote:
>
>What is the difference between being allergic to a substance, and a
>substance being an irritant? I know there *is* a difference and I have
>a sort of part-formed explanation in my head which includes that
>irritants will irritate all people to a greater or lesser degree, normal
>& asthmatic (but with bigger consequences for the asthmatics), and that
>there must be something different going on at the cell (or smaller)
>level, and that one can be allergic to an irritant as well as irritate
>by it.
>
>A nice clear explanation for a lay person would be much appreciated.
An irritant is a substance (such as ozone, chlorine, or teargas) that
provokes a response through direct chemical effects. For example
chlorine combines in the airways to form hydrochloric acid, when then
damages the airway tissue, producing the response. Teargas is a
powder composed of small flakes with very sharp edges, this time it is
mechanical damage that produces the response.
An allergen is something that provokes an IgE mediated response in
sensitized people.
Kevin McGirl
myself.
I'm ok with the allergen understanding of a person being sensitized to a
substance that provokes an IgE mediated response. But can't grasp the
irritant concept.
One of my most life-altering sensitivities is to a chemical outgassed in
many commercial carpets found in retail stores, offices, etc... doctor
thinks it's formaldehyde. But how can I experience asthma symptoms to this
chemical (that few else do) and it not be an IgE mediated response. I do
have many allergies and experience the same asthma symptoms when exposed to
them.
The doc says, even if research finds a way to eliminate allergic asthma, it
will not touch people's irritant sensitivity. So to me, I acknowledge the
difference, but can't really understand it. After all, a chemical is made
up of molecules just like and allergen, right?
-Kevin
>sensitized people.
Bill Ellis Fleenor
>
> What is the difference between being allergic to a substance, and a
> substance being an irritant? I know there *is* a difference and I have
> a sort of part-formed explanation in my head which includes that
> irritants will irritate all people to a greater or lesser degree, normal
> & asthmatic (but with bigger consequences for the asthmatics), and that
> there must be something different going on at the cell (or smaller)
> level, and that one can be allergic to an irritant as well as irritate
> by it.
>
> Surfer!
As Colin mentions, allergens cause allergic reactions which
are IgE mediated. Irritants cause nonallergic reactions with
similar effects. Some asthmatics have nonallergic or intrinsic
asthma which is not affected by allergens.
(There is also allergic and nonallergic rhinitis).
Referring to the book Allergies A to Z
"IgE (immunoglobulin E)--Antibodies manufactured by the
immune system that play an important role in primary
type I hypersensitivity, or immediate allergic, responses...
Allergic individuals generally have higher total IgE levels
in their blood."
"Intrinsic asthma--caused by factors other than allergy.
Intrinsic asthma occurs in less than 50% of adults and in
about 15% of children with asthma...Many with intrinsic
asthma have nasal polyps and sensitivity to aspirin. Its
possible to have both intrinsic and extrinsic asthma."
It's hypothesized that at some point in time, maybe the Dark
Ages, a high level of IgE was protective against parasites
and disease.
Here's a link to a JAMA article on triggers of asthma:
http://www.ama-assn.org/special/asthma/support/educate/triggers.htm
What Triggers Asthma? JAMA
Excerpts:
"What Triggers Asthma?
People with asthma have very sensitive airways. Everyday things
that cause little or no trouble for most people can leave
people with asthma gasping for breath. These are called
asthma triggers, and knowing what they are can help you keep
asthma attacks from starting. There are two basic types of
asthma triggers, allergic triggers, also known as allergens,
and non-allergic triggers.
Allergic triggers
You may be allergic to one or more of these common allergens or
triggers:
Indoor and outdoor molds
Animal dander (that is, flakes from the skin, hair, or feathers of any
warm-blooded pet, including dogs, cats, birds, rodents, and horses)
Dust mite particles (from microscopic insects present in house dust)
Cockroach particles
Some food additives (for example, sulfites used as a preservative in
some
foods and beverages)
Certain medications (for example, penicillin or aspirin)
.......................................
Non-allergic triggers
Other important asthma triggers have nothing to do with
allergies, but cause the same airway changes-airway
swelling, mucus increase, and airway narrowing-as
allergic triggers.
Your asthma may be triggered or made worse by one or more
of these non-allergic asthma triggers:
Materials (irritants) in the air you breathe. Examples
are tobacco smoke, wood smoke, room deodorizers, pine odors,
fresh paint, household cleaning products, cooking odors,
workplace chemicals, perfumes and cosmetics, and
outdoor air pollution
Respiratory infections, such as the common cold, the flu,
or a sinus infection
Exercise
Cold air or sudden changes in air temperature
Gastroesophageal reflux (heartburn)"
From:
Understanding Asthma Health Management Bulletin
Information for asthma patients and their friends
Copyright © 1997 American Medical Association. All rights reserved.
Ellis
Bill Ellis Fleenor
>
> I've had a difficult time internalizing an understanding of this difference
> myself.
>
> I'm ok with the allergen understanding of a person being sensitized to a
> substance that provokes an IgE mediated response. But can't grasp the
> irritant concept.
>
> One of my most life-altering sensitivities is to a chemical outgassed in
> many commercial carpets found in retail stores, offices, etc... doctor
> thinks it's formaldehyde. But how can I experience asthma symptoms to this
> chemical (that few else do) and it not be an IgE mediated response. I do
> have many allergies and experience the same asthma symptoms when exposed to
> them.
>
> The doc says, even if research finds a way to eliminate allergic asthma, it
> will not touch people's irritant sensitivity. So to me, I acknowledge the
> difference, but can't really understand it. After all, a chemical is made
> up of molecules just like and allergen, right?
>
> -Kevin
Your doctor is right.
According to The Asthma Sourcebook, hyperirritability is one of
the 3 defining features of asthma (the other 2 are airway
obstruction--reversible, and inflammation.) Quoting
"The 3rd defining feature is increased responsiveness or
hyperirritability of the bronchial tubes and their tendency to
"over react" and narrow. The term "twitchy" has also been used
in this regard. This irritability is often demonstrated by the
sudden severe attacks patients can experience when exposed to
substances such as pollen, animal dander, dust, and fumes.
This hyperreactivity forms the basis for bronchial
provocation or challenge testing that is used by physicians
to diagnose asthma in patients whose illnesses do not fit
easily into the other definitions."
Ellis
ewm
> Surfer wrote:
> >
> > What is the difference between being allergic to a substance, and a
> > substance being an irritant?
<snip>
Bill Ellis Fleenor wrote:
>
> As Colin mentions, allergens cause allergic reactions which
> are IgE mediated. Irritants cause nonallergic reactions with
> similar effects. Some asthmatics have nonallergic or intrinsic
> asthma which is not affected by allergens.
> (There is also allergic and nonallergic rhinitis).
>
<snip>
Is it the IGE response that is responsible for the "late phase"
phenomenon, when the condition is sometimes *worse* the next day than at
the time of immediate exposure?
I have been aware of this late phase condition for some years. At times
when trying to identify the "cause" of an exacerbation, it was often
something that I had done on the previous day that had had only a mild
effect at the time of exposure.
Just a hypothesis, but perhaps a testable one.
Emily M.
Bill Ellis Fleenor
Referring back to the book "Allergies A to Z", Lipkowitz
"Types of allergy--There are 4 classifications of allergic or
hypersensitivity reactions: type I, immediate or IgE mediated;
type II, in which antibodies are directed against cells;
type III, in which toxic effects result from antibody and antigen
complexes; and type IV, cell-mediated or delayed reactions.
Pollens, animal proteins, house dust mites, molds, drugs, foods,
and venoms are examples of allergens that can cause immediate,
or type I, reactions. After a first exposure, these apparently
harmless allergens stimulate the immune system to form IgE
antibodies. IgE antibodies are specific to each allergen and
attach to the surface of mast cells in the tissues. Upon reexposure,
the recognized allergen combines with its antibodies, rupturing
mast cells and releasing biochemical mediators that cause the
symptoms of allergy. The most severe form of type I allergic
reaction is anaphylaxis.
In type II reactions, also called autoimmune disorders,
antibodies attack the body's own tissue. Serum sickness and
some allergic lung disorders are type III reactions.
Poison ivy is type IV, or delayed hypersensitivity, reaction."
------------------------------------------------
More 'Allergies A to Z':
"hypersensitivity---Type I allergic reactions usually occur
within minutes of exposure. However type I oral drug
reactions may occur up to six hours later.
Type II--an immediate reaction involving an interaction
between an IgE antibody and an antigen on a cell membrane
and also involves the complement system of specialized
proteins.--causes autoimmune disorders, like SLE. (lupus)
Type III ocurrs several hours to days after antigen exposure.
Large molecules of antigen-antibody complexes interact with
the complement system are deposited in the walls of blood
vessels. Serum sickness is a result of this process--you
can get a delayed response to penicillin or cephalosporin
antibiotics or injection af a serum derived from an animal
source. Allergic pneumonialike lung disorders are another example
Type IV--cell mediated or delayed allergic reactions. This
type usually peaks 2-3 days after exposure. T cells react
with an antigen and induce cell production and the release
of chemical mediators, which start a cascade of other cell
involvement. Poison ivy is in this category."
---------------------------------
Some of the older asthma books mention an early phase and
late phase allergic reaction. The 1997 book 'Allergies A to
Z' uses the Gell and Coombs system of classifying based on
the mechanism of action and time of onset following exposure
to the enciting allergen, types I through IV..
Ellis, not an allergy expert
cao...@redsuspenders.com
Surfer <sur...@nevis-vieww.demon.co.uk> wrote:
>
> What is the difference between being allergic to a substance, and a
> a sort of part-formed explanation in my head which includes that
> irritants will irritate all people to a greater or lesser degree, normal
> & asthmatic (but with bigger consequences for the asthmatics), and that
> there must be something different going on at the cell (or smaller)
> level, and that one can be allergic to an irritant as well as irritate
> by it.
>
> A nice clear explanation for a lay person would be much appreciated.
An allergen is a substance to which your body produces IgE. An irritant is
any substance which causes an inflammatory response.
Chris Owens
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Bill Ellis Fleenor
> > Surfer wrote:
> > > What is the difference between being allergic to a substance, and a
> > > substance being an irritant?
>
> Bill Ellis Fleenor wrote:
> >
> > As Colin mentions, allergens cause allergic reactions which
> > are IgE mediated. Irritants cause nonallergic reactions with
> > similar effects. Some asthmatics have nonallergic or intrinsic
> > asthma which is not affected by allergens.
> > (There is also allergic and nonallergic rhinitis).
> <snip>
>
> Is it the IGE response that is responsible for the "late phase"
> phenomenon, when the condition is sometimes *worse* the next day than at
> the time of immediate exposure?
>
> I have been aware of this late phase condition for some years. At times
> when trying to identify the "cause" of an exacerbation, it was often
> something that I had done on the previous day that had had only a mild
> effect at the time of exposure.
>
> Just a hypothesis, but perhaps a testable one.
>
> Emily M.
I found the reference to this in 'Allergies A to Z', Lipkowitz
"Late-phase allergic reactions--Symptoms of allergy or asthma
that occur hours after initial exposure to an allergen.
Inhalation of an allergen first triggers immediate symptoms,
such as itching, sneezing, wheezing, and shortness of breath.
Bronchospasm occurs promptly in the lungs; this constriction
is often reversible with bronchodilating drugs.
In about half of individuals with asthma, however, a delayed,
or late-phase, reaction occurs, for up to eight hours after
exposure to an allergen. In this stage, bronchi become
hyperactive and likely to constrict but more important, they
become inflamed with increased mucus production and
obstruction. During this process, increased numbers of
inflammatory cells are present. Administration of
anti-inflammatory medications exemplified by corticosteroids
tempers the inflammatory changes. Late phase reactions are
often preventable by pretreatment with cromolyn and
corticosteroid MDIs. Bronchodilators probably provide no
protection against late-phase responses."
Ellis
ewm
>
>
> I found the reference to this in 'Allergies A to Z', Lipkowitz
>
> "Late-phase allergic reactions--Symptoms of allergy or asthma
> that occur hours after initial exposure to an allergen.
> Inhalation of an allergen first triggers immediate symptoms,
> such as itching, sneezing, wheezing, and shortness of breath.
> Bronchospasm occurs promptly in the lungs; this constriction
> is often reversible with bronchodilating drugs.
>
> In about half of individuals with asthma, however, a delayed,
> or late-phase, reaction occurs, for up to eight hours after
> exposure to an allergen. In this stage, bronchi become
> hyperactive and likely to constrict but more important, they
> become inflamed with increased mucus production and
> obstruction. During this process, increased numbers of
> inflammatory cells are present. Administration of
> anti-inflammatory medications exemplified by corticosteroids
> tempers the inflammatory changes. Late phase reactions are
> often preventable by pretreatment with cromolyn and
> corticosteroid MDIs. Bronchodilators probably provide no
> protection against late-phase responses."
>
> Ellis
Thanks, Ellis. You always come through with the solid information. I had
been looking for something that addressed the question of late phase
response with this specificity and clarity.
For some years it had puzzled me that I often felt worse the second day
than on the day I had been exposed to molds, etc. It's nice to know it
isn't just an idiosyncratic thing but one that can be expected and dealt
with.
Emily M.
CBI
A classic allergic reaction occurs when a person has been sensitized to an
allergen (some bit of foreign protein) and has made IgE antibodies to it.
These antibodies then stick to receptors on mast cells that "live" in
certain tissues (the lining of the lungs being one of them). When that
antigen is "seen" again the IgE molecules recognize it and stick to it. If
there are sufficient numbers of IgE antibodies to that allergen on the mast
cell, crosslinking will occur. This is the signal for the mast cell to
release preformed granules containing histamine and many other factors.
These factors have the direct/immediate effects that we all know and love
and also set off a cascade of other events.
As part of this cascade complement proteins (another immune protein that
circulates in the blood) are cleaved, among other reactions. Many of the
byproducts of these reactions signal inflammatory cells to migrate to the
site and to activate. (C5a - one of the complement byproducts used to be
called "slow reacting substance of anaphylaxis".) This late migration and
cascade of reactions is what triggers the "late phase" and most if the
inflammation associated with the asthmatic response.
[BTW steroids work at several - at least 8- sites in this process and Intal
only works on the original mast cell degranulation. This is why Intal is not
effective once the process has begun and why it takes weeks to start to
work.]
All of these mediators of inflammation signal the muscles surrounding the
airways that there is something dangerous in the air and leads to higher
tone and a tendency to contract. This sets of the bronchoconstriction part
of the wheezing/asthma attack. The increased production of mucus is largely
an effect of the histamine and other immediately reacting contents of the
granules.
All people's lungs have the muscles surrounding the airways. They all can be
made to contract if the stimulus is strong enough. One example is a fire.
Nearly anyone caught in a fire and inhaling significant amounts smoke will
have bronchoconstriction and wheeze. What differs from person to person is
the strength of the stimulus required to make the person bronchoconstrict.
Technically an irritant is something that triggers the protective mechanism
of bronchoconstriction without using IgE and causing inflammation.
Where it gets muddy is that irritants frequently will, by injuring the
lining of the lungs, cause some inflammation and hyperirritability for some
time in the future. Asthmatics with a small degree of inflammation may have
more bronchial irritability even if they were not having asthma symptoms
before the irritant challenge.
[This is why I think most "excersize induced/ cold induced/ different things
induced etc" asthmatics are really just regular asthmatics who only have
symptoms when they also experience an irritant. If you control the asthma
suddenly they no longer respond to the irritant.]
In summary wheezing with inflammation is an allergy/asthma but wheezing from
an irritant without an allergic/inflammatory response is not. But an
asthmatic will have an increased tendency to wheeze from an irritant and an
irritant can cause inflammation (but not via IgE). And you wonder why people
get confused ?
--
Good Luck,
CBI, M.D.
powe...@msn.com
Surfer wrote in message ...
>
>What is the difference between being allergic to a substance, and a
>substance being an irritant? I know there *is* a difference and I have
>a sort of part-formed explanation in my head which includes that
>irritants will irritate all people to a greater or lesser degree, normal
>& asthmatic (but with bigger consequences for the asthmatics), and that
>there must be something different going on at the cell (or smaller)
>level, and that one can be allergic to an irritant as well as irritate
>by it.
>
>A nice clear explanation for a lay person would be much appreciated.
>
JEFFREY OHRINER
also heard that Ige is a true allergic response to an allergen. I have
practically nil problems with flowers. I do however have severe problems
with practically all perfume/cologne/and strong cleaners (i.e. ammonia).
These problem are limited to upper respiratory tract and eye and headache
problem. These problems can and usually are quick onset. Burning eyes and
pain in the nasal cavity and headache are common. I have used antihistamines
that some of them work quite well. What I mean is that it is like before I
even noticed I had any problem at all, except for dry mouth and drowsiness.
I have tried many both prescription and non-prescription antihistamines. I
have also tried antileukitrine and it did not show any adverse effect, but
did not help at all after a week trial.
If you have seen what Excite had on the UPI new break last week about Ige
and mast cell what comments do you have? Otherwise you probably would be
interested in seeing the URL
http://nt.excite.com/news/u/981223/11/health-asthma
I have some hopes that if antihistamines help my problem go away but with
some unpleasant side effects, maybe this possibility of a new class of drug
that stops the Ige from creating both histamine and leukitrine at the mast
cells can also be duplicated for Igg.
Windsurf4 (new to this support group)
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