ENVIRONMENTAL LUNG DISEASE
Ed Friedlander, M.D., Pathologist
scalpel_blade@yahoo.com

Cyberfriends: The help you're looking for is probably here.

Welcome to Ed's Pathology Notes, placed here originally for the convenience of medical students at my school. You need to check the accuracy of any information, from any source, against other credible sources. I cannot diagnose or treat over the web, I cannot comment on the health care you have already received, and these notes cannot substitute for your own doctor's care. I am good at helping people find resources and answers. If you need me, send me an E-mail at scalpel_blade@yahoo.com Your confidentiality is completely respected.

DoctorGeorge.com is a larger, full-time service. There is also a fee site at myphysicians.com, and another at www.afraidtoask.com.

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Freely have you received, give freely With one of four large boxes of "Pathguy" replies.

I'm still doing my best to answer everybody. Sometimes I get backlogged, sometimes my E-mail crashes, and sometimes my literature search software crashes. If you've not heard from me in a week, post me again. I send my most challenging questions to the medical student pathology interest group, minus the name, but with your E-mail where you can receive a reply.

Numbers in {curly braces} are from the magnificent Slice of Life videodisk. No medical student should be without access to this wonderful resource. Someday you may be able to access these pictures directly from this page.

I am presently adding clickable links to images in these notes. Let me know about good online sources in addition to these:

Freely have you received, freely give. -- Matthew 10:8. My site receives an enormous amount of traffic, and I'm handling about 200 requests for information weekly, all as a public service.

Pathology's modern founder, Rudolf Virchow M.D., left a legacy of realism and social conscience for the discipline. I am a mainstream Christian, a man of science, and a proponent of common sense and common kindness. I am an outspoken enemy of all the make-believe and bunk which interfere with peoples' health, reasonable freedom, and happiness. I talk and write straight, and without apology.

Throughout these notes, I am speaking only for myself, and not for any employer, organization, or associate.

Special thanks to my friend and colleague, Charles Wheeler M.D., pathologist and former Kansas City mayor. Thanks also to the real Patch Adams M.D., who wrote me encouragement when we were both beginning our unusual medical careers.

If you're a private individual who's enjoyed this site, and want to say, "Thank you, Ed!", then what I'd like best is a contribution to the Episcopalian home for abandoned, neglected, and abused kids in Nevada:

I've spent time there and they are good. Write "Thanks Ed" on your check.

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Especially if you're looking for information on a disease with a name that you know, here are a couple of great places for you to go right now and use Medline, which will allow you to find every relevant current scientific publication. You owe it to yourself to learn to use this invaluable internet resource. Not only will you find some information immediately, but you'll have references to journal articles which you can obtain by interlibrary loan, plus the names of the world's foremost experts and their institutions.

Alternative (complementary) medicine has made real progress since my generally-unfavorable 1983 review linked below. If you are interested in complementary medicine, then I would urge you to visit my new Alternative Medicine page. If you are looking for something on complementary medicine, please go first to the American Association of Naturopathic Physicians. And for your enjoyment... here are some of my old pathology exams for medical school undergraduates.

I cannot examine every claim which my correspondents share with me. Sometimes the independent thinkers prove to be correct, and paradigms shift as a result. You also know that extraordinary claims require extraordinary evidence. When a discovery proves to square with the observable world, scientists make reputations by confirming it, and corporations are soon making profits from it. When a decades-old claim by a "persecuted genius" finds no acceptance from mainstream science, it probably failed some basic experimental tests designed to eliminate self-deception. If you ask me about something like this, I will simply invite you to do some tests yourself, perhaps as a high-school science project. Who knows? Perhaps it'll be you who makes the next great discovery!

Our world is full of people who have found peace, fulfillment, and friendship by suspending their own reasoning and simply accepting a single authority which seems wise and good. I've learned that they leave the movements when, and only when, they discover they have been maliciously deceived. In the meantime, nothing that I can say or do will convince such people that I am a decent human being. I no longer answer my crank mail.

This site is my hobby, and I presently have no sponsor.

This page was last updated February 6, 2006.

During the ten years my site has been online, it's proved to be one of the most popular of all internet sites for undergraduate physician and allied-health education. It is so well-known that I'm not worried about borrowers. I never refuse requests from colleagues for permission to adapt or duplicate it for their own courses... and many do. So, fellow-teachers, help yourselves. Don't sell it for a profit, don't use it for a bad purpose, and at some time in your course, mention me as author and KCUMB as my institution. Drop me a note about your successes. And special thanks to everyone who's helped and encouraged me, and especially the people at KCUMB for making it possible, and my teaching assistants over the years.

Whatever you're looking for on the web, I hope you find it, here or elsewhere. Health and friendship!

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Courtesy of CancerWEB

QUIZBANK: Respiratory #'s 43-65, 150-169

Kerry DrakeLEARNING OBJECTIVES

* * * 

... And for the vanities committed in this filthy custom, is it not both great vanity and uncleanness, that at the table, a place of respect, of cleanliness, of modesty, men should not be ashamed, to sit tossing of tobacco pipes, and puffing of the smoke of tobacco one to another, making the filthy smoke and stink thereof, to exhale across the dishes, and infect the air, when very often men that abhor it are at their repast?... It makes a kitchen also often-times in the inward parts of men, soiling and infecting them, with an ... oily kind of soot, as has been found in some great tobacco takers, that after their death were opened.... Have you not reason then to be ashamed and to forbear this filthy novelty ... a custom loathsome to the eye, hateful to the nose, harmful to the brain, dangerous to the lungs, and in the black stinking fume thereof, nearest resembling the horrible Stygian smoke of the Pit that is bottomless....?

The incessant, witless repetition of advertisers' moron-fodder has become so much a part of life that if we are not careful, we forget to be insulted by it.

Some years ago a model named David Goerlitz told me that while posing for a Winston ad he had asked a group of R.J. Reynolds executives if any of them smoked. He said one of them replied: "Are you kidding? We reserve that right for the poor, the young, the black, and the stupid."

        -- Bob Herbert, New York Times columnist, 1998
             

Huckleberry Finn

TOBACCO SMOKING: Med. Clin. N.A. 76: 355, 1992. Here are some facts you may find handy in talking with patients.

Environmental Pathology
Great pathology images
Indiana Med School

THE PNEUMOCONIOSES: A group of diseases, ancient and modern, resulting from dust inhalation. (* Conios means "dust" in Greek.) Occupational lung disease: Disease-A-Month 44: 41, 1998.

Pneumoconiosis I
From Chile
In Spanish

Pneumoconiosis II
From Chile
In Spanish

Occupational Lung Disease
Bryan Lee

{27639} bowling ball manufacture; rumors of dust disease
{27623} taxidermy; a bad career choice for the person allergic to animals

COAL WORKER'S PNEUMOCONIOSIS (CSP, "black lung"): Path standards: Arch. Path. Lab. Med. 103(8), 375-432, 1979 (still the best)

{27458} coal miner
{27514} coal workers

Anthracosis, bad

WebPath Photo

Anthracosilicosis
Polarizer picture
WebPath Photo

Hut lung
From indoor air pollution
Dr. Warnock's Collection

Silicosis
Lung pathology series
Dr. Warnock's Collection

{08762} anthracosilicosis

{49094} progressive massive fibrosis
{35063} progressive massive fibrosis

    Caplan's syndrome: rheumatoid arthritis or systemic lupus or scleroderma or polymyositis-dermatomyositis with an inorganic pneumoconiosis. (* The eponym has no precise meaning and seems to be passing out of use.)

      Sometimes big rheumatoid nodules fill the lungs in these workers. In CWP with Caplan's, they are inky black, and they may be part of a continuum with PMF.

    Coal dust and cancer: coal dust exposure places a worker at increased risk for stomach cancer, but not for any other common cancer.

    Future pathologists: Crack cocaine smoking can impart considerable black pigment to the lungs.

    Crack lung
    Lung pathology series
    Dr. Warnock's Collection

SILICOSIS: Common and deadly; until recently the most serious occupational disease. All about silicosis: Arch. Path. Lab. Med. 112: 673, 1988 (great pictures); historians see Science 256: 116, 1992.

    The silicosis industries:

      Sandblasting
      Mining and tunneling (silicosis is still a major problem in third-world mines: Chest 113: 340, 1998; Am. J. Resp. Crit. Care Med. 153: 706, 1996)
      Foundries
      Gun-flint industry
      Sandstone industry
      Granite industry
      Pottery industry
      Metal grinding
      Manufacture of abrasive soaps
      *Kaolin (china clay, mild because kaolin is really feldspar -- Thorax 41: 190, 1986; Am. Rev. Resp. Dis. 138: 813, 1988; silicosis in a U.S. toilet factory: MMWR 41: 405, 1992)

    The OSHA "acceptable" levels might still be a bit high, since even today, the more exposure a worker has has, the more obstruction shows on spirometry. However, it's far worse to be a smoker. See Chest 122: 721, 2002.

{27461} sandblaster

{27462} sand mold lining
{34985} sandblaster

    Mt. St. Helen's volcano survivors are not developing chronic silicosis (Am. Rev. Resp. Dis. 133: 526, 1986), but silicosis is common in areas of the world where sand-storms occur (Thorax 46: 334 & 341, 1991).

    Tetrahedral crystals of silicon dioxide make up much of the earth's crust.

      The tetrahedral configuration is essential to fibrogenicity; octahedral and other forms of silica, as well as other non-silica crystals with sharp edges (powdered diamonds, etc.) do not cause collagenization.

      *Mixed rock dust disease ("silicatosis"; the term didn't catch on) is essentially silicosis.

    Ideas about how silica causes fibrosis no longer emphasize death of macrophages. However they do their damage, tetrahedral silica crystals have potent effects in biologic membranes.

      The hydroxyl groups on the surfaces of the crystals are arranged to interact efficiently with the -NH3 and -PO4 groups in lipids. (This is called "contact catalysis".)

      Free radical formation with peroxidation of membrane lipids is probably also involved. Interestingly, fresh-cut silica powder bears free radicals on its surface for several hours, and it is much more fibrogenic in the short-term than old-cut silica powder.

      *Further, silica crystals directly activate C5a which attracts phagocytes.

    The silica crystals seem mostly to affect macrophages. The steps leading to fibrosis are being worked out.

      In the classic model of silica fibrogenesis, a macrophage (sometimes a neutrophil) ingests an inhaled silica particle, which is taken into phagolysosomes. The crystal disrupts the phagolysosome membrane, releasing the hydrolytic enzymes and killing the phagocyte. (The silica particle is then ready for phagocytosis by another phagocyte....) The breakdown products of macrophages are chemotactic for other phagocytes and finally promote collagen formation. This works in vitro, but is probably only a minor mechanism in vivo -- silica-laden macrophages washed from the lungs of workers usually seem quite healthy.

      Current thinking focuses instead on inappropriate production of interleukin 1 and other factors by macrophages following contact with silica.

      * A new twist is the discovery that a particular allele for α-TNF predisposes to much more severe silicosis (Am. J. Resp. Crit. Care Med. 165: 690, 2002).

    Gross pathology of silicosis:

      Pleural adhesions, silicotic nodules, eggshell calcifications (why?) in lung and lymph nodes, and silicotic nodules around the respiratory bronchioles ranging in diameter from 0.1 to 5 mm. (Several nodules may become confluent, and nodules may occur outside the lungs as crystals travel via lymphatics. See Hum. Path. 16: 393, 1985. Massively packed, expanding lymph nodes in the mediastinum can occlude the pulmonary artery (Br. J. Rad. 74: 859, 2001).

    The silicotic nodule consists of:

    • Concentric whorls of dense collagen with some silica, surrounded by...
    • Cellular connective tissue without silica, surrounded by...
    • Irregular, loose connective tissue with macrophages, epithelioid cells, and abundant silica (continuing growth). Make your own sketch.

{12437} silicotic nodules
{28760} silicosis
{28763} silicosis
{28766} silicosis
{28769} silicosis
{35000} silicosis
{49096} silicosis
{35057} anthracosilicosis

Silicosis and silicatosis
Lung pathology series; follow the arrows
Dr. Warnock's Collection

Silicotic nodule

WebPath Photo

Silicotic nodule

WebPath Photo

    Variations:

      Silicotuberculosis: Silicosis with TB, a very common combination (because of poor macrophage function? poverty? probably both....)

        As a clinician, you may decide to treat everybody who has a history of silica exposure and a positive PPD as if he/she was actually sick with TB. Ask your infectious disease consultant.

      Caplan's syndrome: silicosis with autoimmune disease. (As in CWP, usually the autoimmune disease is rheumatoid arthritis or systemic lupus.

        The active surface of the silica crystals possibly alter the patient's proteins to make them antigenic. Interleukins could be another problem.

      Anthracosilicosis: silicosis with coal worker's pneumoconiosis

      Siderosilicosis: silicosis with iron oxide dust

      Acute silicosis ("alveolar silicoproteinosis"):

        After a massive dose of silica particles, all the alveoli fill with proteinaceous fluid, surfactant, and necrotic mononuclear phagocytes. The patient dies in a few days to a few months.

        The dose of silica overloads the periarteriolar lymphatics that go directly to the hilum. The silica is transported instead to the alveoli, where it is phagocytized by, and destroys, the Type II pneumocytes.

        Patients are usually sandblasters and rock drillers who fail to wear protective masks. Acute silicosis led to the World War II graffiti: "Join the Navy and see the world, become a sandblaster and see the next."

    Glucocorticoids for silicosis sufferers: Am. Rev. Resp. Dis. 143: 814, 1991.

    * Tetrandrine, a Chinese herb which kills alveolar macrophages, is a possible help against silicosis (Biochem. Pharm. 53: 773, 1997). Watch this one.

ASBESTOSIS: Am. Rev. Resp. Dis. 143: 408, 1991; Rad. Clin. N.A. 30: 1245, 1992; South. Med. J. 85: 616, 1992. The mineral Sci. Am. 272(1): July 1997.

    Asbestos is a family of fibrous minerals, hydrated silicates of sodium, iron, calcium, magnesium. It is very dangerous stuff, and asbestos-related disease has been under-diagnosed. All types of asbestos are dangerous, * though chrysotile (serpentine, curved fibers) seldom reach the pleura.

      Asbestosis follows heavy or prolonged exposure to airborne asbestos fibers, and progresses even if dust exposure ceases.

      One million people in the US have industrial exposure (workers, neighbors). There are probably 70,000 cases of asbestosis here today. Spray-on asbestos was the worst. (See Postgrad. Med. 74: 93, Oct. 1983.)

      Some of the heaviest exposure of the most people was in shipyards before 1970. (* Great historical article in CA 28: 87, 1978.)

      *Asbestos is also used in insulation, fire-proofing, cement, water mains, brake linings, oven cloths, linoleum, ironing boards, gloves, fireman's suits, linings for chemical pans, theater curtains, acid-resistant filtering cloths, etc. etc. In Greece and nearby, asbestos is used for whitewash ("Metsovo Lung", Chest 99: 1158, 1991).

      "Practical guide to asbestos abatement": Occup. Health. Saf. 55: 45, Jan., 1986. Selective indignation and asbestos policy: Science 247: 294, 1990. A review of the asbstos "cancer epidemic", which we may reasonably think will cost 10 million lives worldwide: Env. Health Perspect. 112: 285, 2004.

      The Environmental Protection Agency (August 1990) reversed itself on the business of asbestos removal from schools and other public buildings, and now recommends removal only when buildings are to be demolished. This sensible action recognizes that undisturbed asbestos is no health threat, and that asbestos removal, (which re-introduces the material into the air) is dangerous. Perhaps the politicians also realized that asbestos removal would have cost the nation around $150,000,000,000; the whole episode is now discussed as a classic example of education finally overcoming hype and hysteria (JAMA 266: 696, 1991).

      In 2001, the EPA told everybody not to worry about the tons of asbestos that went swirling through Manhattan from the World Trade Center collapse. Sensible -- but what a reversal from the old "one fiber is too many" ideology.

        (* By the way, have you ever heard a politician getting all excited about lead-based paint chips in old houses inhabited mostly by poor people who don't care about "environmentalism"? This is a real health menace, but one with no activism.

    Asbestos fibers that remain in the lung are long (several microns) and slender (around 0.5 microns). The size and shape of the straight asbestos fiber appear to cause it to be carried preferentially to the pleural surfaces. Think about a needle, sharper at one end, moving through lung.

    Gross pathology:

      Marked pulmonary interstitial fibrosis (i.e., actual fibrosis of alveoli and collagenous thickening of the alveolar-capillary membrane.

        Unlike silicosis, the fibrosis is diffuse rather than nodular, involving mostly the alveolar septa.

      Pleural and subpleural fibrosis develop before there is much pulmonary fibrosis. Large, dense fibrous plaques form on both parietal and visceral pleura. They may calcify and are occasionally visible on chest x-ray. These may be accompanied by chronic bleeding into the pleural spaces. Asbestos pleural disease: Chest 99: 191, 1991).

    Microscopic pathology:

      Marked peribronchiolar and (later) alveolar interstitial fibrosis and many asbestos bodies. Often whole alveoli are obliterated. * We now know granulomas form early in involved areas, but have undergone fibrosis by the time the patient comes to autopsy (Exp. Mol. Path. 44: 207, 1986).

      Asbestos bodies ("ferruginous bodies") are characteristic. They are 10-200 microns long, 1-6 microns wide; golden-yellow beaded rods formed when asbestos (or talc, or other) fibers are coated by protein in the body. They are most plentiful beneath the pleural surfaces.

{27472} asbestos on the pipes
{36190} ferruginous body
{39685} ferruginous body
{09834} ferruginous body, special preparation (darkfield?)

Ferruginous body
Inside an epithelioid giant cell
Urbana Atlas of Pathology

Asbestos

WebPath

Asbestos

WebPath

Asbestos, pleural plaques

WebPath

Asbestos, pleural plaque

WebPath

Asbestosis
Photo and mini-review
Brown U.

Asbestosis
Lung pathology series
Dr. Warnock's Collection

        Only a few of the fibers get coated, and in symptomatic asbestosis, a gram of dry lung tissue may contain more than a million asbestos fibers. Today's standard seems to be 1000 perticles per gram of dry lung as an indicator ofoccupational disease (Am. J. Clin. Path. 117: 90, 2002).

        Chrysotile -- white asbestos, the commonest form -- is seldom coated, is less likely to reach the pleura, and dissolves more readily than the other forms. Nevertheless, it's dangerous and is clearly linked to mesothelioma (Cancer 67: 1912, 1991).

      The finding of an asbestos body in sputum or pulmonary lavage fluid is not diagnostic of clinical asbestosis. Most city-dwellers have a few in their lungs and solid particles of all sorts tend to be released during episodes of pulmonary edema. However, the more you have in your lavage fluid, the more likely you are to have serious asbestosis (big study Chest 126: 966, 2004).

      *Standards for pulmonary pathology of asbestosis: Arch. Path. Lab. Med. 106: 544, 1982 (still good).

    The mechanism of fibrogenesis in asbestosis is probably similar to that in silicosis.

      Magnesium atoms spaced along the surface of a fiber react electrostatically with sialic acid residues on surface glycoproteins of cells, immobilizing them. (See Lab Invest. 49: 468, 1984; Chest 89(S3): 156 S.) Asbestos fibers also activate complement, attracting phagocytes.

      As in silicosis and PMF, there is much discussion of altered immunity, but little is known (Chest 91: 110, 1987). * Like silica, asbestos is a potent activator of C5a.

    Even in the absence of pulmonary fibrosis, asbestos-exposed people are at special risk for several forms of cancer.

      *Asbestos fibers tangle chromosomes -- Am. J. Path. 126: 343, 1987.

      Asbestos is the principal risk factor for mesothelioma ("Steve McQueen's cancer" -- he worked on his own motorcycle, including the asbestos-lined brakes, and inhaled huge quantities of asbestos while working in a military brig).

        The mechanism is unknown (but see Am. J. Path. 128: 410, 1987). Concurrent cigaret smoking does not increase the risk.

        Most mesotheliomas involve the pleura or, less often, the peritoneum.

        One of the most infamous trick questions in medical-school pathology is, "Asbestosis most often causes which cancer?" The answer is "common bronchogenic carcinoma" rather than "mesothelioma".

        Mesothelioma Information Group
        Resources and advocacy
        Also asbestosis and bronchogenic CA

      A high mortality rate (20%, up to 50% for smokers) due to the common types of lung cancer has been reported in U.S. asbestos workers, even those with fairly low exposure and without clinical asbestosis. For common lung cancers ("bronchogenic carcinoma"), cigaret smoke and asbestos are obviously synergistic, perhaps because tobacco carcinogens adsorb onto the asbestos fibers.

      Asbestos exposure also clearly increases the risks of laryngeal and GI cancer, and perhaps malignant lymphomas.

      Other carcinogenic dusts:

        Chromium: cancer of the nasopharynx and/or lung

        Nickel: cancer of the lung

        * Your lecturer does not believe that silica is a carcinogen, but it is currently classified as such by some government agencies. Stay tuned.

{27494} asbestos and lung cancer

    However, the majority of asbestos workers seeking compensation have breathing problems still due primarily to heart disease or cigaret smoking (Am. Rev. Resp. Dis. 135: 812, 1987).

      *Tobacco smoking greatly increases the amount of peribronchiolar fibrosis -- which is surprising. See JAMA 259: 370, 1988.

    The asbestos companies knew the dangers long, long ago: JAMA 265: 898, 1991.

    You may enjoy visiting the informational site of mesothelioma lawyers mesothelioma here or here or here or here or here or here (not endorsements, but an instructive read for young doctors -- Ed).

    * It takes almost no time or effort to make up and publish a shameless lie. If the lie is ugly or stupid enough, some people will choose to believe and act on it, simply to feel "moral" / "spiritual". And refuting the lies of others is a hard, thankless task. In 1999, an e-mail campaign warned about big commercial tampon manufacturers putting asbestos in cotton tampons to make women bleed heavier and longer. Of course this was simply made up. I traced it as far as I could, and found a culture warrior (left-wing) who linked her endorsement and promotion of the claim with her mail-order "natural" tampon company. She also mentioned that she founded this company "to get herself off welfare". I am not making this up. Although I do not understand why tampon cotton needs to be bleached, the business about the bleaching process generating agent orange and causing toxic shock syndrome wasn't true, either. And the persons cited as the authors of the e-mail vociferously denied having written it.

Mesothelioma
Autopsy specimen
KU Collection

BERYLLIOSIS (Chest 109(3S): 40-S, 1996)

    Due to inhaled beryllium, which activates macrophages and T-helper cells (NEJM 320: 1103, 1989). Thanks to public health measures, there are fewer opportunities to get berylliosis today -- but the Rocky Flats epidemic of the 1980's and the Toledo epidemic of the 1990's should reminded us that powdered beryllium is still dangerous.

      In the past, the greatest peril was in the rocket and fluorescent bulb industries.

    The typical lesion of chronic berylliosis is granulomas and interstitial fibrosis of the lung. You may or may not see necrosis. Sensitization takes a while but tends to progress (Am. J. Resp. CCM. 171: 54, 2005); thankfully the vast majority of those exposed never get sick (J. Clin. Inv. 110: 1473, 2002; the key is the immunology).

      Cutaneous berylliosis also showed the non-necrotizing granulomas. These patients had scratched themselves on old fluorescent light bulbs.

      The lesions are practically identical to those of sarcoidosis. If you need to distinguish the two diseases using the lab, we can check for berylliosis.

    *Only a minority of exposed people are vulnerable to this disease (i.e., most people are non-reactive to beryllium). Those who can get it had glutamate in position 69 of the HLA-DPβ1 chain (Science 262: 197, 1993; now a robust finding though somewhat modified J. Imm. 163: 1647, 1999).

    * The Rocky Flats fiasco: Allied Occup. Env. Hy. 16: 405, 2001; Env. Health Perspect. 104 (S5): 981, 1996. Some folks got sick, notably about 10% of the beryllium machinists, but it was not a massive disaster as it has been portrayed. Probably the neighbors were not endangered (Env. Health Perspect. 107: 731, 1999).

{27503} berylliosis

Beryllium lung and sarcoid
Lung pathology series
Dr. Warnock's Collection

    *There was also an acute, "irritant" pneumoconiosis.

    *Zirconium dust produces the same picture; "deodorant granulomas" were from zirconium.

FARMER'S LUNG (and variants)

Hypersensitivity pneumonitis
Lung pathology series
Dr. Warnock's Collection

    Victims are sensitive to spores from moldy hay, etc. (Micropolysporum, Thermoactinomyces -- these "molds" include allergenic bacteria). Both farmers and their animals are susceptible.

{27489} farmers in moldy hay

      Non-farmers can get a similar disease from mold in air-conditioners ("humidifier fever", etc.), cardboard, etc. (See JAMA 258: 1210, 1987).

    Clinical course: Either or both of two phases

      First phase: transient IgE-mediated syndrome with bronchoconstriction (wheezing, etc.)

      Second phase: IgG-mediated type III-injury vasculitis ("extrinsic allergic alveolitis"; "hypersensitivity alveolitis") which may be serious. It can be acute, subacute, or chronic. In really bad cases, there may be granuloma formation, tissue necrosis, fibrosis (Am. Rev. Resp. Dis. 133: 88, 1986), etc.

        Precipitating IgG antibodies against the offending mold can be demonstrated in the patient's serum (and in the serum of many asymptomatic farmers, too; Thorax 44: 469, 1989). For a review of the diagnostic immunology of the organic pneumoconioses, see Clin. Lab. Med. 4: 523, 1984.

    Bagassosis: farmer's lung caused by molds in dry sugar cane.

    *Other forms of "extrinsic allergic alveolitis":

      "Animal house lung": fraternity party with straw (JAMA 258: 1219, 1987)
      Woodworker's pneumoconiosis (including "sequoiosis" from redwood mold)
      Mushroom worker's lung (Chest 122: 1080, 2002)
      Cheese worker's disease
      Grain handler's pneumoconiosis (Can. Med. Assoc. J. 133: 969, 1985)
      Malt worker's pneumoconiosis
      Pigeon keeper's lung ("bird-fancier's lung")

        *Interestingly, these patients are reported to have semi-anergy: Thorax 44: 132, 1989.

      Pituitary snuff taker's lung (diabetes insipidus victims)
      Portuguese cork-worker's lung (suberosis)
      Sisal-worker's disease
      Hungarian paprika-splitter's disease
      Tea-maker's asthma
      Coffee bean dust disease
      Furrier's lung
      Sudanese bat-guano asthma (Lancet 1: 316, 1987)
      Leather waterproofer's lung (Br. Med. J. 292: 727, 1986)
      Zimbabwe ivory-carver's lung (Thorax 43: 342, 1988); save the elephants
      Silkworm dropping lung (Thorax 45: 233, 1990)

    You can benefit many of these people by installing electrostatic dust filters (Ann. Int. Med. 110: 115, 1989). A face mask for hay-time: Chest 95: 100, 1989.

BYSSINOSIS (cotton, flax, hemp processing)

    Nobody questions that fibers from vegetable textiles are noxious and irritating.

    Traditional pathology texts describe "monday morning asthma". This is the only organic pneumoconiosis in which there is prolonged wheezing.

      Here's the familiar story. On Monday morning, lots of guys at the cotton mill report not feeling well. By Monday afternoon, and for the rest of the week all the mediators are depleted and the symptoms disappear. Over the weekend the mediators are replenished in time for next Monday's attack.

      If you believe this "disease mechanism", you'll believe anything. For starters, most allergic wheezing is due to leukotrienes, which aren't even stored. Decide for yourself what's really happening. Reports of a substance in cotton that releases histamine from mast cells remain unconfirmed.

    "Brown lung" is claimed by some textile workers to be a major cause of chronic respiratory disability.

      Much of the problem, of course, is due to cigaret smoking.

      Only recently has chronic obstructive lung disease in non-smoking cotton workers been clearly caused by cotton dust exposure. As usual, there are "confounding variables."

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