January 22, 2025

Football Concussions: The point of impact from personal experience

       Now that the NFL & NCAA football seasons are well underway, let's talk concussions.
Yours truly, during his fourth football camp.  For the record, yours truly had four concussions, a broken foot, a separated shoulder, a sprained back and whatever else as a result of football.  In fact, he once started and ended a football game with a 102.4 degree temperature, and  even intercepted a pass at the end of that game.  So, you can play full speed in that condition and stay in rhythm.  We did push ourselves to the breaking point, between phases of dogging it and pacing ourselves.  In fact, some of us went past that point and cracked like glass in the end which usually happened during a special teams play.

The following article is a result of the press dedicating time and space to the topic of football head injuries.  The ultimate purpose of this article is to share with you the actual experience of incurring that type of injury.

The danger factor in football head injuries is that, at least half the time, they're extremely pernicious things.  One concussion might result in you seeing flashing lights, while being accompanied by zero pain and no impairment.  Another might involve pain, but is rapidly following by a feeling a instant recuperation.  Things look a little foggy, as if you are looking through a vignette filter.  Yet, you felt functional enough to go back out on the field.  The one exception for me was my first concussion.
It was followed by a chronic headache, day after day.  However, the splitting headaches might have been my sensitivity to the nearby pines.  The following year, our football camp was not held near the rows of pines, and I had no headaches.  Only two concussions that year.

When you get a back sprain, a torn ligament, or a broken arm, you feel it and you know that you won't be playing football the following day and even for the rest of the month.  You feel the pain
as you try to move the injured area.  With head injuries, most of the time you feel that you can go back out on the field at that very moment.    You're a little groggy, but you're not in pain.  So, you have to employ your own sense of rationale to know that you should give yourself a bit of recuperation time and cease full speed contact for at least a short while, lest you cause lingering damage to yourself.

Concussions were not uncommon occurrences

I wasn't the only one to go the concussion route during that time span.  In fact, one of the guys on the team had to be taken out via stretcher, with a neck brace firmly attached to him, during a special teams play.  He was the leading scorer in the entire county, returning a kick-off.  So, perhaps he had a bull's eye on him.  None the less, my worse concussion was during a special teams play.  This is probably because there is a lot more running room on a kick-off and punt play, allowing guys to reach higher speeds than during regular scrimmage line plays.

Another one of the teammates was carried to the sidelines via stretcher, the night when we beat the champs on a rain-soaked field.  He shortly came back to consciousness, leaped out of the stretcher, and went into a high-kick sprint down the sidelines, upon which everyone in the stands was cheering at him and not at the players on the field.  He ended up going to the Air Force Academy, to play football.

There was another player who went the route of multiple concussions.  He was one of the two starting half backs.  He was forbidden by doctor's orders to ever return to a football field, on account of his  concussions.  Ironically, after he left football, he returned as an adviser, took me to the side and showed me the trick in going full speed into any defensive player with an added punch.  From that point on, I never had a head injury again, except for that fateful punt play on the last game of the season.  All in all, when it came to football concussions, I wasn't alone. 
Football head injuries and the media exposure they have been getting

A number of journalists, writers, and web hosts have maturely reported, conjectured, and commented on the phenomenon of football head injuries.  After all, there is an instantaneous concern to it, as it applies to energetic youth who had the discipline to train well enough to be able to take all sort of hits, from all sorts of directions.  However, none of these reporters were able to tell you what it was like to get concussion after concusion after concussion.  All in all, no matter how disciplined and in shape you are, your head remains very vulnerable and you remain completely mortal.  The tragic endings of a few NFL football stars remind us of this.

The Immediately Needed Partial Remedy for the NFL

The NFL needs to bring back its 300 pound weight limit.  Some players today are entirely too big for safety purposes.  The NFL managers of decades prior realized that behemoth players were not conducive to the good of a league that provided role models to many an American youth. 

During those rare plays when my helmet would come off

I can only speak from my experience on the following matter:  On those plays when the hitting was such that my helmet would come off, I felt zero pain.  I didn't even feel my helmet come off.  I simply suddenly noticed that it was off.  Sometimes, I actually saw it rolling.  After the play, I would go and get my helmet, while thinking to myself, "How did that come off?"  That is to say, I never felt the exact hit which dislodged it.  And remember, when you're carrying the ball, you are getting hit by three to six guys in a single play.  Some of those guys are your own players crashing into you and getting pushed into you.  So, I never knew what hit dislodged my helmet from my head.

Also for the record, at no time during my four concussions did I ever see stars.  A concussion is a matter of lights out ... not stars out tonight.

Concussion #1:
When a coach allows a football drill to turn into assault and battery upon a Freshman

During summer camp of my freshman year, the head coach was present while the senior backs were taking turns, giving me violent shots, during a summer camp drill which went awry.  If that type of thing would happen today, it would be on YouTube and that coach's career would have been terminated.  He happened to have been the brother in law of Steeler quarterback, Terry Bradshaw.
The coach's form of football was basically blood thirsty animal thuggery.  Very little technique was taught by him.  Yet, he would obsessively have us redo a play or two during practice, to get it right.
Well, if he taught us more technique, he wouldn't needed to have us practice those plays over and over again.

Incidentally, for those unaware, such as my readers in Turkey, Western Europe, and the Ukraine, Terry Bradshaw possessed four Super Bowl rings.  He was the American football champ four times in his career.  None the less ...

During that summer camp drill, the seniors went out of their lines and proceeded to give me shot after shot after shot, in the same one drill, giving the phrase "football drill," new meaning.  They were absolutely drilling my head ... fracking me and practically fragging me ... and no other freshman had to go through this.

It was that I had a brother who graduated the year prior, and those seniors didn't like him at all.  My brother was the second string fullback the year prior.  This meant that the third string fullback was now the starter and he was ruthless to me.  My brother, incidentally, became a military officer, up to the rank of colonel.  Anway . . .

My course of action at the time was to literally do the Christian turn-the-other-cheek thing.  I conscientiously employed the turn-the-other-cheek policy, as a moral obligation.  So, why was I playing a sport as violent as American football?  Oh ... because there were cheerleaders on the sidelines and fans in the stands.  You would be surprised how many girls would magnetize to you, simply because you were a football player.  None the less, in my freshman year, the seniors took their hatred of my brother out on me.

During that one solitary drill, I would take a shot, and go down to the ground.  Yet the coach, Terry Bradshaw's brother-in-law, wouldn't blow the whistle.  So, I would get back up, only to take yet another hit when I wasn't even 3/4 of the way up.   In fact, I would keep getting up and have to fend off another series of hits.  Never was I given the opportunity to stand up and get set.  I was lunging forward and meeting the hits, because I would get hit immediately upon trying to stand up.  Bam! Over and over again did this happen.  Moreover, this was only the second or third day of camp.

The coach let it go on for an amount of time that was entirely too long.   I even remember seeing the sneering face of one of the seniors, as he made a perfectly aligned helmet-to-helmet hit on me, followed by others taking turns in hitting me at full speed, time after time.  A few days later, I was diagnosed with my first concussion.   Nice guy ... my head coach.   Just what I needed.

I was still playing full contact football during the time between the drill which went awry and the day before my diagnosis. That wasn't a smart thing to do.   I was playing full contact football with a concussion not being given the opportunity to heal.

Incidentally, I went to the doctor because of a chronic headache that wouldn't subside.  Needless to say, I missed the first scrimmage of the season.  But, during the second scrimmage, the following week, I wasn't gun-shy on the field, at all.  For some reason, I was revved-up.  I was so in-tune that I would place one hand on the front-center shoulder pads of the ball carrier, and the other hand on the back-center should pads and literally throw the guy down to the ground.  Something clicked, because of having of been so severely attacked and refusing to quit the team, despite the full-blown physical harassment of seniors.

None the less, during my freshman year, there would be times when, without warning or cause, a senior would hit me full force in the head, during scrimmages.  There was even a time during a scrimmage when the whistle had blown, and everyone stopped, except for the senior wingback, who clipped me at full speed rom behind, resulting in me getting a separated shoulder.  Ironically, the following year, I became the starting wingback  . . .  and right side cornerback.

As was previously mentioned, if those things happened today, I would have gotten a hefty settlement, the coach would have been fired, and the school would have been placed on some type of probation.I took a beating that year.  What made things even more difficult was that my mother was dying and she would be gone during the following calendar year.

Incidentally, whenever a player on the other team would get injured and be unable to take himself off the field, those same seniors would clap and cheer.  Today, that would have incurred a 15 yard penalty and disciplinary action.  That anti-sportsman mindset prevailed throughout that graduating class.  In the years to follow, however, the seniors would be much more civilized.  In fact, one of those abusive seniors (during my freshman year) was recently indicted for a major, high priced fraud. That was a vicious graduating class, to say the least.

Concussion #2:
This one was fascinating.

Concussion #2 happened in the same year, during a Freshman game.  It was played against the one school locally known for its gymnastic talent.  Anyway, I went to the sidelines, only to see in my peripheral vision, two flashing lights that looked like neon signs.  One of them almost looked exactly like an arrow sign that you see when passing a stretch of road under construction.  That is to say, the design of the flashing light was organized and continuous, not morphing into any other design.  None the less, there wasn't any hit that I remember which was hard enough to trigger the flashing lights.   In fact, I wasn't in pain.  I simply saw the flashing neon light phenomenon and knew that it was time to stay on the sidelines for a while.

Concussion #3:
The one which occurred when I was carrying the ball.

This occurred in the middle of my second year.  There was no pain attached to this one, either.  It occurred at practice.  It was a standard, off-tackle run.   The line of scrimmage was a traffic jam.
So, I put my head down and plowed through.  My problem was not using my forearm to absorb some of the contact.

If my memory is correct, I made it past a linebacker and a safety who were were playing the role of welcoming committee upon my person.  However, neither one could make a center-mass hit on me.  So, I went to then end zone.  Then suddenly, it felt as if I were waking up and suddenly materializing on the field.  I turned around a looked at the line of scrimmage which looked like a photo taken in a vignette filter.  It was one of those things when you find yourself thinking in total silence, "Oh no.  Not again.  Another concussion."

Concussion #4:
Walking unconscious

This was the last game of the second season.  It was during a punt play on a Saturday afternoon, when a defensive end collided into the side of my head, in an attempt to block the punt.  I went entirely unconscious, yet I was walking ... instinctively walking toward the sideline, with my right hand on the right side of my helmet.

While coming back into  full consciousness, I heard the sound of a buzzer that sounded like the type you hear in a game show when a contestant gets a question wrong.  In fact, when I came to consciousness, I thought that I was waking up, to go to the game.  Next, I faintly heard cheering.  Then, I loudly heard cheering.  Suddenly, I saw the punt returner headed directly toward me.  About four guys made the tackle fifteen yards away from me.

When I did come back into consciousness, I momentarily experienced the worst pain in my life ... even when compared to the day I was caught between two 2,430 lb steel beams at the heal ... even in comparison to a number of vicious asthma attacks, my separated shoulder, my broken foot, the -30 degree wind chills I endured, the 106 degree Oklahoma weather I once endured, etc.  The pain disappeared when the elongated buzzer sound vanished.  I would then attend two more football camps, in the years to follow ... free of any further concussion.

Now, as far as would go any lingering effect, I had none that affected any mental functionality.  But,  safety improvements are still needed in organized football,  to remedy an eminent danger in a sport that's violent in nature .. unless if the authorities decide to cancel the sport, altogether.  None the less, despite four concussions, I managed: 1} to get published at the age of twenty, along side a handful of laureates, 2} to later get published along side a multiplicity of laureates, 3} to play impressionist poly rhythms in studio piano class, 4} to score a 100% on a national standardized collegiate accounting exam issued by an Ivy League school, 5} to get inducted into what used to be called the National Languages Honors Society, 6} to make the dean's list more than once, 7} to get inducted into the International High IQ Society.

Keep in mind that I had all of my mental faculties almost immediately after incurring each head injury.  The fatal error in a head injury scenario is going back out on the field, instead of heading to the locker room ... or to the team doctor.  In the words of any successful poker player, you gotta know when to fold 'em.  I did, three out of four different concussions. 

The rare summer football camp death in the general area was a matter of course.

During every summer camp season, I expected, as matter of course, to hear news broadcasters report one or two local football-related deaths.  Usually, it was a blood clot in the brain which was the cause.  At least that's how it was registered in my memory.

When the news of the first death of the season would be reported, there would be an impromptu team meeting, headed by the team captains.  Coaches made sure that we wouldn't be deprived of water on the field.  So, we evaded the ultimate football tragedies.  None the less,  I would end up getting four concussions before I would sew my first football letter on to my school jacket. 

A quick note about the team photo above, being
that there was one historic element to our team.

Concerning the photo at the top of the page, the guy to my left was the fastest guy on the team and a bit track-and-field champ.  The gentleman to my right was the starting quarterback.  The taller team mate behind my left shoulder wasn't a lineman.  He was the second or third string quarterback and one of the most personable guys on the team.  The one ace up his sleeve was the distance he could throw a football.  He was also a golden gloves boxer.  But, he just didn't have the speed to be a starter.  The guy behind my left shoulder played defensive and offensive end.  Perhaps you know that phrase:  "A defensive end is someone who can tear a refrigerator apart, while an offensive lineman can tell you how to put it back together, piece-by-piece."  In fact, the worst beating I ever took in my life was at the hands of a defensive end, in a game we won 63-6.  He was revenging the lopsided score on my rib cage.  He beat me ruthlessly on that field.  The more we would score, the more violent he would get.

I already mentioned that our head coach was Terry Bradshaw's brother in law.  He's the one seen celebrating on the field with Terry, at Three Rivers Stadium, in the famous Immaculate Reception film clip that made Franco Harris an icon.  At last count, he was an assistant college coach, to former NY Jet head coach Joe Walton, on the college level.

Pittsburgh Football was, once upon a time, in the image and likeness of its steel mills

Keep in mind that I was raised in the Pittsburgh vicinity ... in the specific borough that once had the largest push button railroad in the world.  Pittsburgh was the King of Steel,  as was evidenced by a 21 mile stretch of the Ohio River whose east and west banks housed some of the steel mills that were arrayed throughout the general region.  In fact, the 21 mile steel line only ended at the property line of the largest push button railroad on Planet Earth (at the time.)  Pittsburgh, at present, is the king of bridges, even more than Venice.  The other thing about Pittsburgh is that it was known as one of the three quintessential football venues in America ... at the time, with Ohio and Texas football being as iconic.

The Pittsburgh vicinity was the home of Dallas star Mike Ditka, Heisman trophy winner Tony Dorsett, New York Jet Super Bowl quarterback Joe Namath, record-setting Miami Dolphin quarterback Dan Marino, Miami Dolphin star Mercury Morris, NFL Hall of Fame running back Curtis Martin, all-pro Chicago Bear lineman Jimbo Covert, all-pro Buffalo Bill lineman Bill Fralic, Cotton Bowl quarterback Kevin Scanlon, Steeler head coach Bill Cowher, Washington Redskin Rich Milot, Notre Dame star Terry Hanratty, four-time Super Bowl quarterback Joe Montana, Oakland Raider legend George Blanda, and others.  In sports, you only become as good as your competition.  These stars had the competition to fine tune their skills and fortify their wills.  Even at that, it was my understanding that Ohio football was tougher, in the contact department. 

Pittsburgh football didn't make you arrogant.  It humbled you.

If you were a multiple letterman in Pittsburgh, as well as someone who played in the formal venues of summer league baseball, one thing was guaranteed.  You would have a number of team mates who would eventually make a national mark in football.  For example, my former team mates included an all-pro lineman who earned a Super Bowl ring, as well as someone who started as quarterback in a Cotton Bowl game, and someone else whose name I heard on ABC television, during an Orange Bowl game.  One team mate would go to such and such university to play football, while another one would go to another American university, to do the same.

Even an occasional guy you would compete-against in track would end up on this WFL team here, while one you faced in summer league baseball would end up on another football team there.  In as much, you would think that coming from an environment such as Pittsburgh would make you arrogant.  The truth is that it made you very humble.   Yet, it wasn't the hits which made you humble.  You could take the hits after your first year of apprenticeship.  The humility factor was in you not being as conditioned as the stars-to-be ... or not as fast ... or not as able to turn the corner without sliding down to the ground ... or not alert enough to avoid from running into your blockers, from time to time.  Do not be deceived.  I was built like an Adonis and was very acrobatic, even to the point of winning an organized summer league batting championship and base-stealing championship on a team of men who became champs of their football division.  Despite this, there were a number of guys against whom I competed who put me to shame.  Pittsburgh was that athletic of a place.  So, I learned a great deal about humility in a place once called the City of Champions.

It Wasn't Always Head Hunting, though

When a defensive back goes head hunting on you and he misses, you are on your way to the goal line.  So, during one particular game, in hometown of Mike Ditka, a linebacker wanted to do little more than make sure that I wasn't going anywhere after catching a short pass, not wanting his coach to lambast him for missing me in an attempted head-hunting play.  So, he would wrap his arms around me so tightly that breathing became a difficulty until the ref blew the whistle.

I spent the entire game as a wing back, going five yards and out, catching five to ten passes in the process.  The same linebacker tackled me every time.  He was a human vice grip as he wrestled me down.  He was just doing his job and played by the rules.  But, I dreaded his grip.  I would have preferred that he take full speed shots at my head, in the attempt to dislodge the ball from me.  But no.  He had to be the human vice grip.   So, he played prevent-defense throughout the entire game and it worked. 

Some opposing players do take revenge during a game.

We played a team in West Virginia during my freshman year and beat them 63-6.  I played right end for the entire second half.  The opposing defensive end beat me to near death.  He kept targeting my rib cage, and even when I cross body blocked him to the ground, his knees would drive into my ribs.  So, I spent an entire half holding my right arm to my right-side rib cage.  The lesson is, just because you win a game in a whitewash, it doesn't mean that it will be a painless experience.  I never took a beating on a football field that badly.

The Coach's On-Field Disciplinary Tactic

When you're a running back and the play doesn't involve you carrying the ball, you have a way of acting as if you're not in the play, meaning that you occasionally miss your blocking assignment.  Well, one day in practice, after having missed my blocking assignment, the coaches decided to do the Pittsburgh version of an intervention.  They called the exact same play, but I was going to be the ball carrier.  They then told the offensive players to not block for me.  They next told the defensive players what the play was and that the offense wasn't going to block for me.

For some reason, I thought to myself, "Oh well. Who cares?  Let's get this over and done with." 
The quarterback called the signals.  The ball was hiked.  It was handed-off to me, and the entire offense went on vacation for the play.  So, who made first contact on me?  A defensive end, of course; ... the one who later went to play for the Air Force Academy.  Next came a few others, and then came everyone else.  I went down facing the sky ... and it didn't hurt at all, because all the other defensive players were absorbing the impact, and because the first defensive end simply wrapped his arms around me and started pushing me backwards, upon which I eventually went down like George Washington's cherry tree.

Of course, I wasn't going to tell anybody that it didn't hurt, lest the coaches call the same play and send the offensive players on another hiatus, in order to "teach me."   This was during my freshman year. 

The injury process on the football field sometimes 
backfired on the player attempting to inflict pain on you

The injury process on a football field can work in reverse.  For example, during my Senior, while I was running an end-around play as a half back, yet another defensive end spiked me as hard as he could in the kidneys, while I was being stood-up by a few defensive players.  He was the one who had to go to the sidelines in pain.  I went back into the huddle, only to be informed by a guard what happened.  I didn't feel it, at all, even though he came at me full speed from behind.  After all, there was more than one guy hitting me, and when that happens, all of the different feelings of impact cancel out each other one.  None the less, in trying to drive me to the ground as hard as he could, the defensive end ended up hurting himself.

American Football was basically legalized venting, unless if you were a pass receiver in the path of a linebacker.  Well, it was venting for the linebacker.  When you went up for a pass, you were completely defenseless, as the hits made upon you were designed to dislodge the ball from your hands.  When you keep taking those kinds of hits repeatedly, something eventually gets dislodged.
       
Junior Year:  My first track meet as a hurdler.  Football players commonly
went out for track or played summer league baseball.  Hurdlers were
the coordinated guys who didn't have the flash speed of a sprinter, 
but who were faster than everyone else.

The Diversionary Tactic


The fight to breathe, the metallic taste in the mouth, and the stinging
tongue.   Numbness in the upper-respiratory tract,  the dry heaving
episode, and the headache that leaves cheekbones and temples feel-
ing bruised.  It involves a world that has also included hepatic injury,
(liver cell death/necrosis), dermatitis, urticaria, hematotoxicity (the
killing or damaging or red blood cells), and anaphylaxis.  Technical-
ly this condition is regarded as Chemical & Irritant Sensitivities.

The Razor Blades of  Defamation

Mainstream medical science has already established that chemicals,
at nontoxic levels, aren't universally harmless.  Numerous chemicals
have been identified as sensitizers, while other ones were already cat-
egorized as irritants.  Chemical Sensitivity has already been defined in
case-specific and body-system-specific form.  Irritant-induced Asthma
and its subset condition, Reactive Airways Dysfunction Syndrome, is
one form, while Airborne Irritant Contact Dermatitis is another form.
Chemical sensitivity is already a well-established component in main-
stream medical science, and so too is the irritant-induced reaction.
However ...

Throughout the past fifteen years, literature has been posted online that
can easily deceive a novice into assuming that no chemical of any kind,
whenever encountered at a nontoxic level, could ever trigger an adverse
reaction in anyone.  The literature accentuated the Multiple Chemical
Sensitivity debate, while simultaneously declining to acknowledge the
existence of the several case-specific forms of chemical sensitivity, such
as Reactive Airways Dysfunction Syndrome, Irritant-induced Asthma,
and Occupational Asthma due to Low Weight Molecular Agents which
had already been identified and defined.

Each piece of  propaganda asserted that Multiple Chemical sensitivity is
merely a matter of mental illness.  As a result, persons not familiarized
with Occupational and Environmental Medicine were clueless that suf-
ficient medical findings in a number of chemically sensitive patients were
identified, along with the numerous chemicals that triggered the adverse
reactions.

The Corporate Claim of  Universal Harmlessness
  Contradicted by the Findings of  Medical Science

It had even gotten to the point where insecticide providers boldly pro-
claimed that their product lines were entirely harmless, provided that
they were used according to regulatory guidelines.  This proclamation
was accompanied by the claim that all persons suffering from Multiple
Chemical Sensitivity were merely mentally ill.  However, mainstream
medical science had already established that nontoxic exposure to the
carbamate/organophosphate class of pesticide can cause a build-up of
acetylcholine in one's lungs and cause asthma to develop.

Perfumes Have Been Identified as Triggers of Asthma

The propaganda against the chemically sensitive was relentless.  In
fact, the non-chemically sensitive got caught in the crossfire in 1996,
when the perfume intolerant were called "fragrance phobic fruitcakes."

Now, perfumes contain potent non-chemical ingredients as much as
they contain sensitizing chemicals.  Therefore, Fragrance Intolerance
includes hyperreactivity to non-chemical ingredients as much as it in-
volves hypersensitivity to chemical-bearing agents.  This means that,
in 1996, even persons who were not chemically sensitive were placed
under attack.

Never mentioned in the 1996 character assassination was the 1995
publication detailing a research undertaking which confirmed that
perfume strips found in magazines are asthma triggers.   [Ann Aller-
gy Asthma Immunol., 1995 Nov;75 (5):429-33 ].

In the years to follow, perfumes would come to be acknowledged as
asthma triggers by the American Medical Association, the American
Academy of  Allergy Asthma & Immunology, the American Lung As-
sociation, and the National, Heart, Lung, and Blood Institute.

Then, in 2001, a published medical report placed perfume among the
triggers of  anaphylaxis.  Yet, no apologies were ever made to the per-
fume intolerant by the propagandist who defamed them. 

            Cleaning Supplies and Household Chemicals

            Understanding Asthma - American Lung Association
http://www.lungusa.org/lung-disease/asthma/about-asthma/understanding-asthma.html 

            Chemical Asthma Triggers and Irritants
http://asthma.about.com/od/asthmatriggers/qt/chemictriggers.htm 

            Asthma Triggers: Gain Control (EPA site)
_____________________________________________
Sensitization Is Not Limited To Chemical Exposures

The phenomenon of  sensitization is not new.  Neither is it unproven.
Nor is it limited to matters involving Chemical Sensitivity.  The recog-
nition of the medical condition known as sensitization includes:

1] metal dust exposure; Berylliosis (beryllium), etc.
2] mold exposure; Mushroom Worker's Lung, etc.
3] enzyme exposure; Detergent Worker's Lung, etc.
4] organic dust exposure; Byssinosis (cotton dust), etc.
5] chemicals & irritant gases; Irritant-induced Asthma, etc.

The Medical Doctrine of  Concomitant Sensitivity

Concomitant Sensitivity is also known as Cross-sensitization, and it
means that, if you're hypersensitive to one chemical compound, then
you are hypersensitive to all other chemical compounds with similar
characteristics.  An example of  Concomitant Sensitivity exists within
the family of  the acetylated salicylates.  To be adversely reactive to
one of  them is to be adversely reactive to all of  them.

The Undeniable Proof of Mainstream Medicine's Recognition
of Chemical Allergies ... The RAST Test Order Form

You can be tested for IgE-mediated chemical allergies via the RAST
TEST.  The specific chemicals for which a person can be tested are lo-
cated in the Occupational Panel, when filling out the allergy test order
forms.   Case closed.   Mainstream medicine has recognized chemical
allergies for decades.  It's simply that deceptive propaganda, including
that of the unconscionable John Stossel, made society unaware of this.

High Production Volume Chemicals
  and their Ubiquitous Presence in Modern Life

There have been medical professionals who declined to support the re-
cognition of  MCS, but who simultaneously acknowledged that a per-
son can be severely hypersensitive to "one or a few" chemicals.  Such
an acknowledgment needs to be accompanied by a qualifying state-
ment.  That qualifying statement goes as follows:

            Persons who are hypersensitive to a few High
            Production Volume Chemicals are actually
            hypersensitive to the dozens of  commonly
            encountered products that contain those
            HPV chemicals.  Concomitant Sensitivity,
            combined with hypersensitivity to merely
            a few HPV chemicals, easily explains how
            a person can seem to be hypersensitive to
            almost everything.

The Demarcating Factor in MCS

If you're adversely reactive to dozens of chemical-bearing agents, but
have symptoms that affect only one reoccurring symptom, then you
are outside of  the MCS controversy.  This is because the demarcation
factor in MCS is not hypersensitivity to multiple chemicals.  Rather,
the demarcating factor is reactivity that adversely affects multiple
body systems.

As an example, if  bronchial hyper-responsiveness is your only chemi-
cal sensitivity reaction, then only one body system is involved, mean-
ing that there is no presence of Multiple Chemical Sensitivity to assess
in you.  The anti-MCS propagandists will have to find another way in
which to call you mentally ill.  That is to say, your case involves local-
ized chemical sensitivity.  It involves either Reactive Airways Dysfunc-
tion Syndrome or Irritant-induced Asthma; two similar conditions not
in controversy.

Nor does MCS have anything to do with multiple symptoms, per se.
You can have a repertoire of  reoccurring symptoms and be outside
of  the MCS controversy, if those multiple symptoms are limited to
the reactions of only one body system.  In such a case, the anti-MCS
people will have to find another way by which call  you mentally ill,
while simultaneously claiming chemicals to be virtuous and blame-
less at nontoxic levels.

The respiratory system is a body system that can host multiple symp-
toms.  Firstly, asthma can coexist with upper-respiratory ills, and the
upper-respiratory tract can be the host of  a number of  symptoms.  In
fact, within the world of  Occupational and Environmental Medicine,
it's a regular phenomenon to find asthma coexisting with Rhintis or
Rhino-sinusitis in the same one worker (or subset of  workers.)

In summary, it's neither the number of  symptoms nor the number of
chemicals that define Multiple Chemical Sensitivity.  It is the number
of body systems that engage in the hypersensitivity reactions that de-
fines it.  In the world of  Occupational and Environmental Medicine,
chemical sensitivity reactions have been documented as having had
adversely affected two body systems in the same one worker or sub-
set of  workers.  Such coexistence hints of the authentic existence of
MCS.

Formaldehyde:  A Specific Example

Formaldehyde is a suitable example to employ, in showing that hyper-
sensitivity to merely one HPV chemical constitutes hypersensitivity to
dozens of chemical-bearing agents.  Formaldehyde is a known trigger
of  asthma, rhinitis, dermatitis, and anaphylaxis.  It is released from a
number common products.  This includes those liquid soap and sham-
poo products that contain quarternium-15, diazolidinyl urea, DMDM
hydantoin, and imidazolidinyl urea.  In fact, go through the shampoo
and liquid soap section of  any store and see if you can find one pro-
duct free of  the ingredients listed above.

A detailed list of  formaldehyde-releasing agents includes:
[] urea-formaldehyde foam insulation, [] oriented strand board,
[] medium density fiberboard, [] melamine resin, [] plywood,
[] surface coatings, [] joint cement, [] paints, [] wall coverings,
[] durable press drapery, [] permanent press clothing, [] floor
wax, [] kerosene heater emissions,[] burning wood, [] cosmetics,
[] nail hardeners, [] sun screen lotion, [] tanning lotions, [] liquid
soaps, [] moisturizing lotions, [] carpet cleansers, [] liquid scouring
cleansers, [] shampoos, [] medical venues, etc.

Formaldehyde shares common characteristics with benzaldehyde and
the sterilization agent, glutaraldehyde.  Therefore, the products which
bear glutaraldehyde and benzaldehyde are to be included in the list of
formaldehyde-releasing agents.  This includes cinnamon oil, and this
means that the phenomenon of  Concomitant Sensitivity, in combina-
tion with hypersensitivity to a few High Production Volume Chemicals,
can account for the reason why some individuals seem to be hypersen-
sitive to almost everything.

Persistent Vulnerabilities,
aka Pre-existing Conditions

Then there is the matter of  chronically existent vulnerabilities, also
known as atopy.  One example is the upper-respiratory inflammation
known as boney turbinate hypertrophy.  It is a condition not known to
be able to resolve itself,as surgery has been the only treatment offered
for it, by mainstream medicine.

Cases of  chronically existent vulnerabilities can make a person hyper-
sensitive to both chemical and non-chemical odors.  Therefore, such a
person can be adversely reactive to the smell of  cleaning agents and
new vinyl products, as well as cooking odors, and musty cardboard.
Such a person might appear to be allergic to almost everything.

Immunological in Some Cases.
Nonimmunological in Other ones.

An individual can have either an immunological allergic reaction or
a non-immunological irritant reaction to chemical-bearing agents.
It depends on the person, the person's exposure history, the person's
pre-existing vulnerabilities, the chemicals themselves, and the way in
which the chemicals are encountered (by inhaling, ingestion, touch,
or ocular absorption.)

The bottom line is that chemical sensitivity has been proven to exist,
and to state otherwise is to defame the Occupational & Environment-
al Health programs who diagnose such conditions.  To do so is to de-
fame the private practitioners who treat chemical sensitivty, as well
as the patients who develop this type of condition.  Be it Reactive Air-
ways Dysfunction Syndrome, Airborne Irritant Contact Dermatitis,
Limonene Sensitivity, Aspirin Sensitivity, Methyltetrahydrophthalic
Anhydride Allergy, or Oil of  Turpentine Allergy, it is all a matter of
chemical sensitivity.

Multiple Chemical Sensitivity is not the only type of chemical sensitiv-
ity proposed to exist.  It was simply one of  the two forms used in a pro-
longed and unconscionable diversionary tactic.  Other variations of the
disease have already been validated.  Therefore, any discussion about
MCS that doesn't admit to the existence of chemical sensitivity (in its
case-specific and body-system-specific forms) invalidates itself.
___________________________________________________

January 21, 2025

Chemical Allergies Were Proven to Exist Long Ago

Stephen Barrett "MD" is an outspoken individual who retired from
psychiatry in 1993 and then proclaimed himself  "the media" in 2001.
He was never board-certified in psychiatry, and he was never board
certified in any other discipline.   He has zero experience as a practit-
ioner in every form of internal, dermatological, and dental medicine.
He was not a researcher in any capacity, either.   Neither was he a
biochemist nor a vaccinologist nor a pharmacologist nor a medical
technologist nor anything similar.  He spent inordinate amounts of
time suing people, including a disabled woman to whom he lost.

In the late 1980s he wrote an article titled, "Unproven Allergies."  Big
problem with that title, though.  Those allergies were proven to exist,
in the world of Occupational & Environmental Medicine, even during
the writing of the deceptive text.  Take note of the following:

       * * * * * * * * * * * * * * * * * * * * * * * * * * * * * * * * *
       The testing for IgE-mediated chemical allergies has been con-
       ducted via mainstream medical RAST testing.   The specific
       chemicals tested are found in the OCCUPATIONAL PANEL
       of a  RAST TEST order form.   This means that mainstream
       medical science recognizes the existence of chemical allergies.
       Case closed.  
        * * * * * * * * * * * * * * * * * * * * * * * * * * * * * * * * *

An Allegation of  Stephen Barrett that Calls for a Response:

Stephen Barrett alleged, throughout his anti-MCS literature, that
a primary test for chemical sensitivities consists in ...

(I)   ... a very subjective and non-quantitative form of testing ...

(II)  ... by which a diluted chemical solution is placed under ...
           the tongue of a patient (or injected through his skin), ...

(III) followed by nothing more than the patient reporting if whether or
       not he experiences any symptom from the administered chemical
       solution.

       This allegation, in combination with numerous omissions of  fact,
       can easily deceive a beginner into assuming that there has never
       been a test to prove the existence of chemical sensitivities.  This
       allegation, therefore, calls for a response.

The Response:

(1)  The testing for chemical sensitivities has included, but has not been
       limited to, ...

(I) ... the traditional skin prick test, otherwise known as the SPT.

(II)  In skin prick testing, a test-subject is regarded as having  tested
       positive when a visible and measurable wheal, equal to or larger
       than a designated size, appears as a result of the skin test.

(III) The size of  the wheal is then recorded in numerical form, and
        numerical measurement constitutes objectivity.       

IgE-mediated Chemicals, via the Process of Haptenation

(2)  The purpose for the SPT is to test for immediate onset hyperreac-
       tivity.  This is a Type I reaction, and such a reaction occurs within
       one hour of  exposure.

(I)   IgE stands for Immunoglobulin E, and an immunoglobulin is a pro-
       tein produced by plasma cells & lymphocytes, serving the function
       of  an antibody.

(II)  A number of chemicals have been found to trigger immediate on-
       set reactions, and a subset of  those have been discovered to be
       IgE-mediated, via a process known as "haptenation."

(III) Haptein is a greek word which means "to fasten," and a hapten is
        a low weighted molecular agent that reacts with an antibody, but
        cannot induce the formation of an antibody until it is fastened to
        either a carrier protein or to a large antigenic molecule.  Chemi-
        cals happen to be agents of  low molecular weight.     

Type IV Hypersensitivity Reactions

(3)  In addition, there are a significant number of chemicals that have
       been found to induce the Type IV, cell-mediated hyperreactivity.
       This is known as "delayed allergic reactivity," and this type hyper-
       sensitivity results in dermatitis or anaphylaxis.

(I)  Concerning the Type I and Type IV hyper-reactivity, the Practice
      Parameter for Allergy Diagnostic Testing, as is issued by the Joint
      Council of Allergy Asthma and Immunology, states:          

       "Many chemicals (e.g., sulfonechloramides, azo dyes, par-
        abens, fragrances) used as additives in foods, drugs, and
        cosmetics may induce either IgE-mediated reactions or
        contact dermatitis, or both." Ann Allergy 1995; 75:543-625      

Non-immunological Chemical Sensitivity Reactions,      
Including Anaphylaxis

(4)   In addition, a number of chemicals have been identified as irritants,
        being that they trigger "nonimmunological" responses.  There is ev-
        en a nonimmunolgical form of  anaphylaxis, known as the "anaphy-
        lactoid reaction."   Such a reaction produces the same final result
        as doe an immunologic anaphylactic reaction.  The only difference
        between the two types of  reactions is in the triggering mechanism
        of them.  That is to say:             

      "An anaphylactoid reaction is another type of immediate 
       reaction that mimics anaphylaxis.  While symptoms and 
       treatments are the same the reason for the reaction is not.  
       An anaphylactoid reaction doesn't involve IgE antibodies' 
       immune system and is not considered a true allergic reac-
       tion.  Even so, the reaction can be just as serious."  [Amer-
       ican College of Allergy, Asthma & Immunology]  See:


(I)    Thus, there is Allergic Asthma, and then there is Irritant-induced
        Asthma. One type of asthma is immunologic, while the other type
        is not. You are not inclined to run a 26 mile marathon whenever
        you are exposed to your asthma triggers.      

Allergic Sensitization, Direct Irritation, 
and Pharmacological Reactions

(5)  Hypersensitivity reactions can be triggered via:

(a)  Allergic Sensitization.   This is induced by repeated exposure to
       a sensitizing agent such as formaldehyde, glutaraldehyde, or phenyl
       isocyanate.  Then, upon becoming sensitized, further exposure to
       the same agent results in an antibody release or an inflammatory
       chemical release.

(b)   Direct Irritation.   This is induced in those who are "atopic," in
        person who possess chronic vulnerabilities aand/or pre-existent
        conditions.   Such persons develop "symptoms immediately af-
        ter exposure to substances such as chlorine, ammonia, sul-
        fur dioxide, and environmental smoke."

(c)   Pharmacological Reaction.   This comes as a result of the fact
        that some chemicals and nonchemical agents elevate the produc-
        tion of chemicals that naturally exist in the body.  An example of
        a naturally existent chemical in the body, able to have its level ele-
        vated by nontoxic chemical exposure, is acetylcholine.   A case
        in point is the organophosphate/carbamate class of pesticide.  At
        nontoxic levels, it can elevate the level of acetylcholine in the lungs,
        because that class of  pesticide inhibits acetylcholinesterase, the
        enzyme which displaces/dissolves acetylcholine.

        For further understanding on this, see the Mayo Clinic's teaching
        on Occupational Asthma.   It is found at:


A Sample of IgE-mediated Chemicals

(6)   For confirmation purposes, examples of IgE-mediated chemicals
        which can be involved in skin testing, include the following:

(a)   The disinfectant Ortho-phthalaldehyde.        

        It has even resulted in anaphylaxis, via "Cidex OPA." See:

<>  Nine episodes of anaphylaxis following cystoscopy caused by 
       Cidex OPA (ortho-phthalaldehyde) high-level disinfectant in 
       4 patients after cystoscopy.  {J Allergy Clin Immunol. 2004 Aug;
       114(2): 392-7}


(b)  Formaldehyde.

        It is masked behind a number of aliases, and it outgases from the
        shampoo and liquid soap ingredients, imidazolidinyl urea, DMDM
        hydantoin, diazolidinyl urea, and quaternium-15.   See:

<>   IgE-mediated urticaria from formaldehyde in a dental root 
        canal compound.  (The full text describes 28 cases of Formalde-
        hyde Sensitivity.  {J Investig Allergol Clin Immunol., 2002;12(2):
        130-3}


<>   Exposure to gaseous formaldehyde induces IgE-mediated 
        sensitization to formaldehyde in school children. {Clin Exp
        Allergy, 1996 Mar;26(3): 276-80}


<>   IgE allergy due to formaldehyde paste during endodontic
        treatment.  Apropos of 4 cases:  2 with anaphylactic shock 
        and 2 with generalized urticaria. {Rev Stomatol Chir Maxillofac.
        2000 Oct;101(4):169-74}


(c) Vinyl Sulphone Reactive Dyes.

       They are also known as fiber-reactive dyes, as well as azo dyes.
       They include Remazol Black B.   See:

<>   Roll of skin prick test and serological measurement of  
        specific IgE diagnosis of  occupational asthma resulting 
        from exposure to vinyl sulphone reactive dyes.  {Occup
        Environ Med. 2001 Jun;58 (6):411-6}


<>   Asthma, rhinitis, and dermatitis in workers exposed to re-
        active dyes. {Br J Ind Med. 1993 Jan;50(1):65-70}


(d)  Cyanuric Chloride.

     It is used in the production of  plastics, herbicides, pharmaceuticals,
     and fiber-reactive dyes.  It is also a structural component of mono-
     chlorotriazine and dichlorotriazine dyes. See:<>   Immunologic cross-reactivity between respiratory chemical
       sensitizers: reactive dyes and cyanuric chloride.    {J Allergy
       Clin Immunol. 1998 Nov;102(5): 835-40}


(e)  The disinfectant Chlorhexidine.  It even triggered anaphylaxis:<>   
       FDA Public Health Notice:  Potential Hypersensitivity Re-
        actions to Chlorhexidine-Impregnated Medical Devices


<>   Immediate hypersensitivity to chlorhexidine: literaure re-
        view. {Allerg Immunol (Paris) 2004.  Apr;36(4):123-6}


(f)   Phthalic Anhydride.

       Nail polish ingredient, ingredient in specific spray paints, and
       an agent used in the making of  unsaturated polyester resins,
       alkyd resins, polyester polyols, and insect repellents.     

<>   Detection of specific IgE in isocyanate and phthalic anhy-
        dride exposed workers:  comparison of RAST RIA, Im-
        muno CAP System FEIA, Magic Lite SQ.  {Allergy. 1993
        Nov;48(8);627-30}


<>   In vitro demonstration of  specific IgE in phthalic anhydride 
        hypersensitivity.  Am Rev Respir Dis, 1976 May;113(5):701-4


(7)  The test which Barrett condemns in his anti-MCS literature is the
       provocation-neutralization test.  In fact, the only type of medical
       practitioner that he mentions in the same literature is the so-called
       clinical ecologist.  Barrett inaccurately explained the provocation-
       neutralization test, in his omitting of pivotal fact, and he additional-
       ly gave the illusion that the only people on earth who test for chem-
       ical sensitivity are the so-called clinical ecologists.

(I)   Firstly, the diagnosing of  the various forms of chemical sensitivity
       has been occurring in the worlds of the Nose, Throat, & Allergy
       Specialist, the Occupational and Environmental Health Specialist,
       the Dermatologist, and even the Chest Physician.   In fact, from
       the world of  the chest physician came the golden rule for diag-
       nosing Irritant-associated Vocal Cord Dysfunction.  In addition,
       two pivotal papers on chemical sensitivity were produced by the
       head of  the department of  emergency medicine of an American
       university.  Yes, Emergency Medicine.      

(II)  Secondly, Stephen Barrett failed to mention that the provocation-
       neutralization test has included the measuring of objective skin
       wheals, and it was also used to detect allergies to insect stings.

Barrett Failed to Mention that it is an Offshoot
of  the Serial Endpoint Titration Skin Testing
Procedure, Covered by Aetna Insurance

(8)   The provocation-neutralization test is actually an offshoot of the
        serial endpoint titration skin testing procedure, covered by Aetna
        Insurance.  This is pertinent to note in light of the observation that
        Stephen Barrett has repeatedly stated what Aetna covers, as if
        Aetna alone is the ultimate benchmark in diagnostic testing.

(I)    Now, the Skin Endpoint Titration seeks to first identify a patient's
        allergens or hymenoptera venom hypersensitivities (such as to that
        of hornets, bees, wasps, fire ants, and/or yellow jackets.)   That is
        to say, the Skin Endpoint Titration first seeks to find the triggering
        dose of  a hypersensitivity reaction.

(II)   The same testing then seeks to find the neutralizing dose of the
         same allergen or venom.  Now, this is done for immunotherapy
         purposes and the neutralizing dose is found in a series of skin
         prick tests.  The dose at which a patient no longer experiences
         a hypersensitivity reaction is the "endpoint."   It constitutes the
         neutralizing dose.    It then becomes the "safe starting dose" for
         immunotherapy.   Thus originates the name "neutralization" in the
         provocation-neutralization test.  The set goal of a provocation-
         neutralization test is to identify the "neutral dose."

(III)   In summary, the provocation-neutralization test looks for 
         objective skin wheals, while simultaneously asking the pa-
         tient how he/she feels when, of  course, such testing involves
         skin prick testing.  The appearance of wheals have been docu-
         mented in such testing.

(IV)  The diagnostic parameters become exceeded when the testing is
         considered positive on an either/or basis; on the basis of either
         the appearance of an objective skin wheal or the subjective re-
         porting of a symptom.  However, this is test concerns itself with
         prognostic parameters, also.

(V)   Nonetheless, to consider a test positive exclusively on the merits
         of an objective skin wheal is to keep the diagnostic part of skin
         prick testing within acceptable parameters.  It's the sublingual
         drops version of such testing which raises eyebrows.

Wheal Reactions Showed a Distinct Pattern

(9)   Objective skin whealing was consistently documented
        during a research undertaking that tested the reliability
        of the provocation-neutralization test.   The result of
         the research goes as follows:            

       "Reaction by symptoms to foods, chemicals, and normal sa-
        line solution showed a random pattern, although wheal
        reactions showed a distinct pattern."

(I)   Thus, in the skin test version of the provocation-neutralization
       test, "wheal reactions showed a distinct pattern."

(II)   The conclusion of that research undertaking goes as follows         

         "Skin response alone may be a more reliable indicator
          and require cross-validation with other tests, such as
          oral and inhalation challenges and comparison with 
          a control population." See:

<>    Intradermal skin testing for food and chemical sensitivities:  
         a double-blind controlled study.  J Allergy Clin Immunol. 1999
         May;103(5 Pt 1): 907-11}


(III)  Concerning the prognostic aspect of the provocation-
         neutralization test, the Aetna Insurance Company states:

        "Since provocation-neutralization requires the provoking 
         and neutralizing of symptoms to a single item at a time, 
         a patient could be required to undergo hundreds of indi-
        idual tests requiring weeks or months of full-day testing."
         (Well, this is what Aetna states and its bottom line is money.)

(IV)   The bottom line is that skin testing has been used to identify indi-
          vidual chemical sensitivities to chemicals such as formaldehyde
          and phenyl isocyanate, and phthalic anhydride.  Tested patients
          produced the objective medical finding of visible and measurable
          wheals.  This has included forms of testing other than that of the
          neutralization-provocation test.  In fact, this has included RAST
          Testing.

(V)   Chemically sensitive patients have tested positive in inhalation
         challenge testing, as well as in patch testing (the testing which
         seeks to detect delayed hypersensitivity responses.)  Chemical-
         ly sensitive patients were also documented as having objective
         medical findings via the fiberoptic rhinolaryngoscopy and even
         the fine needle biopsy.  Some chemically sensitive patients were
         found to have inflamed air sacs of the lungs, while other patients
         were found to have hepatic injury in the absence of viral infection.
         Other ones were found to have upper-respiratory erythema and
         swelling.

         Chemical Sensitivity exists in a number of forms.   It's very real,
         and it can be quite brutal.   It has been repeatedly documented
         that chemicals, at ambient (nontoxic) levels, are not universally
         harmless.
        ________________________________________________

January 20, 2025

The Objective Medical Findings of Chemically Sensitive Patients

Mainstream medical science has already proved the existence of
chemical allergies.  Immediate onset and delayed reactions have
long since been proven to exist.  The reaction occurring within an
hour are known as an Immunoglobin-E reaction.  It occurs by the
process of "haptenation."  Haptenation is simply the act of a low-
weight molecule taking a piggy-bank ride on a much larger mole-
cule, thereby enabling an allergic reaction to transpire.

Chemicals have also been proven to trigger what is known as cell-
mediated delayed allergic reactions.  These mostly affect the skin.
Next comes the delayed Immunoglobin-G reaction.  This reaction
adversely affects the respiratory system.  In summary, these involve
adverse reactions to non-toxic levels of chemical exposure.  Such
low levels are known are ambient levels. 

Today, testing for IgE-meditated chemical allergies is done through
RAST testing.  It used to be done through the traditional skin prick
test.   In as much, it's at the OCCUPATIONAL PANEL where the
request for chemical allergy testing is listed on ye olde RAST TEST
ORDER FORM.  Therefore, don't look for any "chemical panel" on
a RAST TEST form.  Look for the occupational one.

Plus, there are other objective medical findings attached to those suf-
fering from Chemical & Irritant Sensitivities, in addition to the presence
of classical allergic inflammatory mediators.  In fact, Irritant Sensitivities
involve sensitivity to those chemicals which don't provoke the classical
allergic reaction.   Some chemicals were found to trigger other kinds of
"inflammatory mediators."  In as much, Chemical Sensitivity is basically
an inflammatory disease.  Very simply, it triggers physical inflammation
somewhere in the body.
_____________________________________________________

Posted below is a partial list of objective medical findings that have en-
tered into the records of chemically sensitive patients and into research
documentation.   It appears after an introduction and a narration of a re-
latively recent case study.   The introduction shows how objective med-
ical findings can be entirely missed during a "cursory medical examine.
The case study also confirms that, simply because insurance company
attorneys allege something in a workman's comp case, it doesn't mean
it's true.

Not Detected by the Standard Chest CT Scan.
Yet Detected via the End-expiratory CT Scan.


A January 2002 article that remains posted on the Fox News website
declared it "junk science."   It was/is the emergent illness which afflict-
ed persons exposed to the debris of  the World Trade Center collapse.
Unofficially called "World Trade Center Syndrome," its distinctive fea-
ture was the "the WTC Cough,"  and its symptoms included shortness
of  breath.

The article attributed the ills of  the afflicted WTC cleanup crew mem-
bers to the 2002 "flu season."   It furthermore attributed the ills of Man-
hattan residents to "anxiety salted with hypochondria."  Its conclusion
was that only "minor and transient health effects from the site" were
to be expected.   The conclusion was wrong.

A newly emerged illness had just made the scene, and just as quickly on
the scene was a political operative ridiculing people's notice of it.  Then
came November 30, 2004, when it was officially disclosed that some of
the afflicted crew members of  the ground zero cleanup operation were
actually suffering from the trapping of  air.   These workers were suffer-
ing from Small Airways Disease, and it was the end-expiratory CT scan
that confirmed it to be true.   The standard chest CT scan overlooked it. 

The Fiberoptic Rhinolaryngoscopy Detects that
which the Garden Variety Cursory Exam Overlooks


The upper airway endoscopy is recognized by mainstream medicine as
an effective means by which pathologies of the septum, nasopharynx,
turbinates, mucosa, adenoids, eustachian tube orifice, tonsils, posterior
tongue, epiglottis, glottis, and vocal cords can be easily seen.   It was
the fiberoptic rhinolaryngoscopic exam which resulted in researchers
realizing (in the early 1990s) that the Multiple Chemical Sensitivity
Syndrome which was presumed to involve no objective medical find-
ings showed signs of being a physical pathology.  In fact, the golden
rule for diagnosing Irritant-associated Vocal Cord Dysfunction came
to be that of  a flexible fiberoptic rhinolaryngoscopic examination, per-
formed upon a patient only when he/she is symptomatic. 

The human body is regarded as exceptionally complex.  Therefore, the
reasonably minded person should understand that the cursory physical
exam and garden variety testing do not detect everything.  This under-
standing, in addition to the preceding paragraphs, offers insight as to
why a number of  chemically sensitive persons have been declared to
have no objective medical findings.

The narration posted directly below should offer more detailed insight
to this.  It involves a case study which teaches us that, simply because
corporate defense attorneys assert something in a workman's comp
case, it doesn't automatically mean that it's true.

She Was Claimed to Have No Objective Medical
Findings to Verfiy Her Symptoms.  Multiple Medical
Findings Were Documented in One Day.


A woman whose workplace was a former coal tar research building be-
came ill six months after having worked there.   A laboratory confirmed
that her workplace was laden with very fine monofilament fibers.   The
smaller the molecular agent, the greater is its potential to infiltrate and
afflict the inner recesses of the complex human anatomy.   Furthermore,
there was also the matter of pesticide exposure, ambient solvent expos-
ure, and mold exposure to take into account, concerning her workplace
environment.

After the woman had initially become ill, she kept going to work, making
her condition worsen and making her have to quit work entirely.  In fact,
 a fellow employee of quit working and then moved to Arizona.  Other
fellow employees mentioned that they were being sickened, too.

The business no longer operates in the former coal tar research center.
Moreover, a large corporation was involved in this matter, despite the
fact that the antics of  a small fly-by-night business are described.   In
fact, the corporation's total stockholder equity was marked as being
over eleven billion dollars in 2005.

Her Symptoms

The woman's symptoms included:

[1]  a stinging tongue.
[2]  shortness of  breath.
[3]  burning nasal passages.
[4]  a metallic taste in the mouth.
[5]  an adrenal-like stream throughout her solar plexus.
[6]  headaches accompanied by the bruised feeling at the
         cheekbones and temples.
[7]  ice-like numbness pervading her upper-respiratory
        tract (on specific occasion.)

She detected the presence of particular airborne substances, simply be-
cause she unavoidably tasted them on her tongue.  In fact, one of her
symptoms was the metallic taste in her mouth.   She could no longer go
to the places she used to frequent without becoming symptomatic, be-
ing that a number of  airborne agents would now trigger her ills.  This
included fragrances, engine exhausts, and musty cardboard boxes.

She lived in the American state which, at the time, had the fourth worse
air quality in the United States.  In addition, she had no prior history of
asthma, no history of chronic upper-respiratory ills, and no history of
allergies.

She received the diagnosis of agoraphobia & panic attacks, by a "men-
tal health person."   The corporate attorneys involved in her workman's
comp case asserted that she had no objective medical findings to sup-
port her claims.   However, an allergist and immunologist gave her the
diagnoses of  Asthma, Rhinitis, and Chemical Sensitivities.  Meanwhile
a cytopathologist gave her the additional diagnosis of  Reactive Hyper-
plasia.   In fact, in emergency room settings, she received the Asthma
and Rhinitis diagnosis.   Yet, assertions of mental illness had been set
forth on record and asserted in court depositions as the cause of  her
ills.   The assertions were significantly weakened in less than an hour. 

Grossly Enlarged Turbinates, for Starters

On October 13, 2005, a fiberoptic rhinolaryngoscopic exam was per-
formed on her.  The exam was conducted by an ear nose throat and
allergy specialist who also happened to be a fellow of the American
College of  Surgeons.   The woman who was said to have no objec-
tive medical findings to support her symptoms was found to have:

[1]  postauricular adenopathy.
[2]  grossly enlarged turbinates.
[3]  shoddy posterior cervical adenopathy
[4]  some erythematous changes of the uvula.
[5]  some mild edema of the true vocal cords.
[6]  thickened coating over the dorsum of  the tongue.

The physician's impressions, as are stated on record, were:

[1]  multiple chemical and irritant sensitivities.
[2]  rhinitis and turbinate hypertrophy.
[3]  glossitis (tongue inflammation).

The conclusion is that, whatever be the medical condition this lady has,
it is one of  a physical origin and mechanism.   If she were not made ill
from workplace exposure, then she was made ill by some other physi-
cal cause. 

Gruntled Breathing and Rales Were Already Observed

The story isn't over, of course.   Objective medical findings had been
entered into her records even before the October exam.  She was doc-
umented as having "gruntled breathing" during an ER visit.   She was
also recorded as having wheezed and crackled during other ones. In
fact, she already was found to have adenopathy.  Plus, tachycardia,
erythema of  the oropharynx, and hypopotassemia had also been
entered into her medical records before the October 13th rhinolaryngo-
scopy.   Yet, she was branded with the "mental illness stigma," by the
corporate defense attorneys and one independent medical examiner
hired by the antagonistic corporation.

Furthermore, after she had become ill, she tested severely positive for
dust mites and no other high weight molecular agent (such as ragweed,
tree pollen, etc.)   Yet, she has no prior history of  allergies.  Now, she
was exposed to inordinate amounts of  dust at her former place of  work,
and a person can become sensitized to dust mites.   After all, there exist
cases where barn workers became sensitized to storage mites.

The account of  the chemically sensitive woman who has over a dozen
objective medical findings attached to her medical records can be ac-
cessed by clicking on the web link provided directly below. 

Corporate Welfare: Government paying for illnesses caused by corporations.

The Icy Numbing 

Chemical Exposure During Testing is Often a Necessity

There is one thing to note about a plurality of chemical sensitivity con-
ditions.   In order to acquire objective medical findings, you have to 
be examined while exposed to a chemical agent that assails you.  In
fact, you have to be tested /examined while symptomatic.  You will 
not acquire objective medical findings in a vaccuum, in most testing.

In light of this, it was not an unheard event for a chemically sensitive
patient to be found hunched over a waste basket after having been
administered a skin prick test.  Furthermore, patch testing has result-
ed in a few occasions of anaphylaxis, and being made symptomatic
before a rhinolaryngoscopic exam is not a painless event.   Moreov-
er, the inhalation challenge test that measures FEV1 and the such is
not recommended for those who are extremely hyperresponsive.

If the Detractors of  MCS Admit to Even One Objective
Medical Finding in any Type of Chemically Sensitive
Patient, the Effect of their Propaganda Will Be Diluted


If the detractors of Multiple Chemical Sensitivity disclose even one ob-
jective medical finding in chemically sensitive patients, they will risk ex-
tinguishing the disrespect and indifference that their literature serves to
incite.    This will incline people to take a very respectful view of envi-
ronmental illness.   In learning that there exists a spectrum of chemical-
specific, case-specific, single systemic, and systemic forms of chemical
sensitivity have already been found to exist, the public will surmise that
it will only a matter of  time before the controversy involving Multiple
Chemical Sensitivity will be resolved.  In light of this, a list of objective
medical findings in chemically sensitive patients is posted below:

Objective Medical Findings in the Chemically Sensitive

 Bronchial hyperresponsiveness in inhalation challenge testing.
         This includes things such as the drop in FEV1:
      Forced Expiratory Volume after 1 second of time.

        Objective skin whealing resulting from skin testing;
   See the article in Part 1, titled, Visible & Measurable
          Wheals Have Been Repeatedly Documented
.

   Simultaneous release of Leukotriene B4 and Interleukin-8;
    (LTB4 is a chemokine.  IL-8 is a toxin to neutrophils.)

     Permeability of upper-respiratory epithelial cell junctions;
      found in biopsy studies, via the electron micrograph

       Abnormal liver function in the absense of viral infection.

         Exorbitant presence of  n-acetyl-benzoquinoniemine;
            a toxic liver metabolite associated with P450
            cytochrome inducers such as acetaminophen.


             Paradoxical adduction of the true vocal cords.

                Testing positive in traditional patch testing.

                     Peripheral nerve fiber proliferation.

                       Nasal and/or laryngeal erythema.

                        Turbinate swelling/hypertrophy.

                         Edema of the true vocal cords.

                              Lymphocytic infiltrates.

                               Glandular hyperplasia.

                                     Angioedema.

                                      Anaphylaxis.

                                       Dermatitis.

Note 1:  There are fiber optic rhinolaryngoscopic exam find-
              ings that were not posted above.  In order to read
             of  the additional findings, see:  Rhinolaryngoscopic
             Examination of Patients with Multiple Chemical 
            Sensitivity Syndrome, found at:
            http://www.ncbi.nlm.nih.gov/pubmed/8452394

Note 2:  There are also instances of hematotoxicity triggered
             by nontoxic benzene exposure.  See:  Hematotoxcity
             in workers exposed to low levels of benzene, found
             at:  http://www.ncbi.nlm.nih.gov/pubmed/15576619

Note 3:  There is more that can be included, but the afore-
              mentioned things should suffice in proving a point.
              _____________________________________