Factors that may trigger an asthmatic reaction
Agents encountered in the work place
Flour dust (Bakers)
Hay mold (Farmers)
Formaldehyde, western cedar, dimethylethanolamine, anhydrides (Plastics, rubber & wood workers)
Arabic gum (Printers)
Azo dyes, anthraquinones, ethylenediamine, toluene diisocyantes, polyvinyl chloride (Chemical workers)
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Allergic asthma requires an IGE response.
The IGE response is determined by T- and B lymphocytes. Central to the processes is the interaction of antigen with mast cell-bound IgE molecules. Anatomically, airway epithelium and submucosa include dendritic cells which process antigen.
Dendritic cells, following uptake of antigen, move to local lymph nodes, there presenting material to T-cell receptors.
In some circumstances (perhaps genetically determined) antigen interaction with naive T cells (TH0) in the presence of IL-4 results in TH0 cell differentiation to a TH2 cells.
Concurrently, this process, while facilitating asthma inflammation, also promotes B lymphocyte transformation from IgG and IgM production to IgE production.
Following sensitization due to prolonged antigen exposure, very small amounts of antigen can produce significant worsening of the chronic underlying disease (asthma).
The central role of immune processes is reflected in the causal relationship in asthma in about 33% of all cases with contributory involvement in probably another 33% of cases.
Although allergic asthma is typically seasonal, nonseasonal asthma can result from continued exposure to animal danders, dust mites, molds, etc.
Antigen exposure can induce an immediate airway obstruction response within the minutes timeframe with fairly rapid resolution. However, in 30%-50% of cases, a late reaction which is another bronchoconstrictive event, may occur from 5-10 hours later. Sometimes only this late reaction is observed.
The initial response to inhale allergen probably depends on antigen-Ab interactions on pulmonary mast cells with subsequent rapid release of mediators.
1 Drugs as stimulatory with respect to the Asthmatic Response
Aspirin
Nonsteroidal anti-inflammatory agents (NSAIDS) COX; COX-2 inhibitors (e.g. Valdecoxib (Bextra))
Arthrotec (diclofenac/ misoprostol), celecoxib (Celebrex),diclofenac (Voltaren, Cataflam),diflunisal (Dolobid),etodolac (Lodine), flurbiprofen (Ansaid), Ibuprofen (Motrin), Indomethacin, ketoprofen (Orudis), ketorolac (Toradol), nabumetone (Relafen), naproxen (Naprosyn), piroxicam (Feldene), rofecoxib (Vioxx), salsalate (Disalcid), sulindac (Clinoril)
Sulfites (preservative)
Benzalkonium chloride (preservative/detergent)
-adrenergic receptor antagonists, e.g. propranolol, metoprolol, atenolol, timolol
Propranolol (Inderal)
1 Acute asthma attacks may be induced by certain drugs, the most common of which include beta-adrenergic antagonists, sulfite-containing agents, aspirin, and coloring agents such as tartrazine.
Significant morbidity is associated with drug-induced bronchial constriction with death having been attributed to aspirin (or other nonsteroidal anti-inflammatory drugs) or beta adrenergic blocker ingestion.
Aspirin-induced asthma appears to occur more frequently in adults relative to children. In aspirin sensitivity may begin with a vasomotor rhinitis (perennial) which leads to nasal polyps (hyperplastic rhinosinusitis).
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Cold Air
Fog
Wood smoke; tobacco smoke
Ozone
Nitrogen dioxide
Sulfur Dioxide
Asthma exacerbation may be induced by elevated concentrations of atmospheric pollutants/antigen's which may occur in particularly industrial or densely populated cities.
Such accumulation is favored under certain weather conditions which create relatively stagnant air (thermal inversions).
Asthmatic patients will be most severely affected, although the general population will also perceive respiratory effects.
Ozone, nitrogen dioxide and sulfur dioxide have been identified as particularly important air pollutants in this regard, although sulfur dioxide requires both a high ventilatory rate and concentration.
Airborne antigens (pollen) can seasonally rise to sufficient concentrations to markedly increased hospital admissions as well as death rates. Seasonal effects may be diminished impact by early use of anti-inflammatory agents.
Workplace factors:
Flour dust (Bakers)
Hay mold (Farmers)
Formaldehyde, western cedar, dimethylethanolamine, anhydrides (Plastics, rubber & wood workers)
Arabic gum (Printers)
Azo dyes, anthraquinones, ethylenediamine, toluene diisocyantes, polyvinyl chloride (Chemical workers)
Prolonged exposure in the workplace to a variety of substances may exacerbate asthma or induce an asthma attack.
Bronchoconstriction may occur as a result of exposure to metal salts such as platinum, nickel or chrome.
Other concerns involves wood or vegetable dust, certain drugs such as antibiotics, cimetidine, as well as industrial chemicals and plastics.
Enzymes found in detergents and animal/insect dusts, serums, or secretions may also be provocative substances.
These chemicals may also be found outside the workplace environment.
This type of airway obstruction appears to involve three possible underlying mechanisms:
(1) the agent induces the formation of a specific IgE (resulting in an immediate, late, or dual immunological reaction)
(2) the agent reflexively or directly causes airway stimulation in the asthmatic patient
(3) the agent directly causes bronchoconstrictor substance liberation.
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Influenza, parainfluenze
Mycoplasma pneumoniae
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Acute worsening of asthma would be most likely due to respiratory infection.
The major factor is not bacterial or allergic responses to microorganisms would rather is a respiratory virus.
In children the two most important viruses would be respiratory syncytial virus and parainfluenza virus. In the older child in adults, rhinovirus and influenza virus would be more common.
An active respiratory tract infection is necessary to induce the asthma attack, going beyond colonization. In the individual whose asthma had been under control, such a respiratory infection can destabilize the condition for extended periods, e.g. weeks.
A possible basis for this effect would be a viral-induced production of T-cell-derived cytokines which promote inflammatory cell infiltration into the airway.
Exercise: (or emotion)
Stress
Laughter
Anxiety
Exercise (dry, cold weather especially)
Acute asthma attacks are often provoked by exercise.
Exercise, differing from other provocative factors, is not produce long-term effects and does not increase intrinsic airway reactivity.
Bronchospasm can be induced by exercise in essentially every asthmatic patient and in some cases it is the only provocative act (at least initially) or exposure that causes asthmatic symptoms.
The severity of exercise-induced bronchoconstriction include ventilatory levels as well as humidity and temperature of the inspired air.
The direction of the effect is that higher ventilation rates with reduced air temperature tend to promote greater obstructive responses.
Running as opposed to walking causes a more severe asthmatic attack, even if the air temperature + humidity are the same in both cases.
Furthermore for any given exertional task, cold air will tend to enhance the obstructive response and warm, humid air would likely reverse the effect.
With respect to specific sports then, ice hockey & cross-country skiing our activities that would be more likely to cause an asthma attack then swimming inside, in a heated pool.
A possibility, in terms of mechanism that might explain exercise-induced obstruction, involves thermal induction of hyperemia with microvascular engorgement of the bronchial wall.
Psychological factors appear to interact with underlying asthma pathophysiology either to worsen or improve the disease state.
The psychological effects appear important to about 50 percent of patients.
Physiologically, airway caliber may be modulated through vagal efferent activity although endorphins may also contribute.
Patients may be "suggestible" with suggestion resulting in changes in adrenergic and cholinergic stimuli effects on airway.
Psychophysiological effects appear variable from patient to patient and possibly variable within a patient depending on the nature of the episode.
1 McFadden, E.R., Jr. "Asthma: Diseases of the Respiratory System" in Harrison's Principles of Internal Medicine, 15th Edition (Braunwald, E., Fauci, A.S., Kasper, D.L., Hauser, S.L, Longo, D.L. and Jameson, J. Larry, eds) pp. 1456-1463, McGraw-Hill Medical Pubishing, Division, New York, 2001
2 Kelley, H. William, "Asthma" in Pharmacotherapy: A Pathophysiologic Approach, (Dipiro, J.T., Talkbert, R.L. Yee, G.C., Matze, G.R., Wells, B.G. and Posey, L. Michael, eds.) pp 430-459. McGraw-Hill Medical Pubishing, Division, New York, 1999.
3Spencer SM., Sgro JY., Dryden KA., Baker TS., Nibert ML. (1997) Rhinovirus 14 (3D image reconstruction from electron microscopy data) Journal of Structural Biology. 120(1):11-21
4Attribution: Michigan State University Website
5Hacohen, N. Dendritic cell responses to diverse antigens
Huang, Q., Liu, D., Majewski, P., Schulte, L.C., Korn, J., Young, R.A., Lander, E., Hacohen, N. (2001). The plasticity of dendritic cell responses to pathogens and their components. Science, 294: 870-875
6McClay, J.E., Nasal Polyps, eMedicine (Pediatrics, Otolarygnology)