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Hypersensitivity pneumonitis may also be called many different names, based on the provoking antigen. These include:
Of these types, Farmer's Lung and Bird-Breeder's Lung are the most common. "Studies document 8-540 cases per 100,000 persons per year for farmers and 6000-21,000 cases per 100,000 persons per year for pigeon breeders. High attack rates are documented in sporadic outbreaks. Prevalence varies by region, climate, and farming practices. HP affects 0.4–7% of the farming population. Reported prevalence among bird fanciers is estimated to be 20-20,000 cases per 100,000 persons at risk."
The best treatment is to avoid the provoking allergen, as chronic exposure can cause permanent damage. Corticosteroids such as prednisolone may help to control symptoms but may produce side-effects.
FLD affects approximately .5%-3% of farmers. In some regions of the world such as Asia, the infection rate is more around 6%.
At present, over 400 workplace substances have been identified as having asthmagenic or allergenic properties. Their existence and magnitude vary by region and industry and can include diisocyanates, acid anhydrides, plicatic acid, and platinum salts (all low molecular weight agents), and animal protein, enzymes, wheat, and latex (high-molecular weight agents). For example, in France the industries most affected are bakeries and cake-shops, automobile industry and hairdressers, whereas in Canada the principal cause is wood dust, followed by isocyanates. Furthermore, the most common cause of occupational asthma in the workplace are isocyanates. Isocyanates are used in the production of motor vehicles and in the application of orthopaedic polyurethane and fibreglass casts.
The occupations most at risk are: adhesive handlers (e.g. acrylate), animal handlers and veterinarians (animal proteins), bakers and millers (cereal grains), carpet makers (gums), electronics workers (soldering resin), forest workers, carpenters and cabinetmakers (wood dust), hairdressers (e.g. persulfate), health care workers (latex and chemicals such as glutaraldehyde), janitors and cleaning staff (e.g. chloramine-T), pharmaceutical workers (drugs, enzymes), seafood processors, shellac handlers (e.g. amines), solderers and refiners (metals), spray painters, insulation installers, plastics and foam industry workers (e.g. diisocyanates), textile workers (dyes) and users of plastics and epoxy resins (e.g. anhydrides)
The following tables show occupations that are known to be at risk for occupational asthma, the main reference for these is the Canadian Centre for Occupational Health and Safety.
The disorder is thought to be caused by an anomaly in the arachidonic acid metabolizing cascade which leads to increased production of pro-inflammatory cysteinyl leukotrienes, a series of chemicals involved in the body's inflammatory response. When medications like NSAIDs or aspirin block the COX-1 enzyme, production of thromboxane and some anti-inflammatory prostaglandins is decreased, and in patients with aspirin-induced asthma this results in the overproduction of pro-inflammatory leukotrienes to causes severe exacerbations of asthma and allergy-like symptoms. The underlying cause of the disorder is not fully understood, but there have been several important findings:
- Abnormally low levels of prostaglandin E (PGE), which is protective for the lungs, has been found in patients with aspirin-induced asthma and may worsen their lung inflammation.
- In addition to the overproduction of cystinyl leukotrienes, overproduction of 15-lipoxygenase-derived arachidonic acid metabolites viz., 15-hydroxyicosatetraenoic acid and eoxins by the eosinophils isolated from the blood of individuals with AERD; certain of these products may help promote the inflammatory response.
- Overexpression of both the cysteinyl leukotriene receptor 1 and the leukotriene C synthase enzyme has been shown in respiratory tissue from patients with aspirin-induced asthma, which likely relates to the increased response to leukotrienes and increased production of leukotrienes seen in the disorder.
- The attachment of platelets to certain leukocytes in the blood of patients with aspirin-sensitive asthma has also been shown to contribute to the overproduction of leukotrienes.
- There may be a relationship between aspirin-induced asthma and "TBX21", "PTGER2", and "LTC4S".
- Eosinophils isolated from the blood of aspirin-induced asthma subjects (as well as severe asthmatic patients) greatly overproduce 15-hydroxyicosatetraenoic acid and eoxin C4 when challenged with arachidonic acid or calcium ionophore A23187, compared to the eosinophils taken from normal or mildly asthmatic subjects; aspirin treatment of eosinophils from aspirin intolerant subjects causes the cells to mount a further increase in eoxin production. These results suggest that 15-lipoxygenase and certain of its metabolites, perhaps eoxin C4, as contributing to aspirin-induced asthma in a fashion similar to 5-lipoxygenase and its leukotriene metabolites.
Some people have reported relief of symptoms by following a low-salicylate diet such as the Feingold diet. Aspirin is quickly converted in the body to salicylic acid, also known as 2-Hydroxybenzoic acid. Sommer "et al." reported a multi-center prospective randomized cross-over trial with 30 patients following a low-salicylate diet for 6 weeks. This study demonstrated a clinically significant decrease in both subjective and objective scoring of severity of disease, but made note of the challenge for patients in following what is a fairly stringent diet.
A diet low in omega-6 oils (precursors of arachidonic acid), and high in omega-3 oils, may also help. In a small study, aspirin-sensitive asthma patients taking 10 grams of fish oil daily reported relief of most symptoms after six weeks, however symptoms returned if the supplement was stopped.
The only cause of Farmer’s lung is repeated exposure to tiny microorganisms which inhabit moldy hay. They are inhaled and often provoke the creation of IgE antibodies that circulate in the bloodstream, these types of immune response are most often initiated by exposure to thermophilic actinomycetes (most commonly "Saccharopolyspora rectivirgula"), which generates IgG-type antibodies. Following a subsequent exposure, IgG antibodies combine with the inhaled allergen to form immune complexes in the walls of the alveoli in the lungs. This causes fluid, protein, and cells to accumulate in the alveolar wall which slows blood-gas interchange and compromises the function of the lung. After multiple exposures, it takes less and less of the antigens to set off the reaction in the lung. The most prominent antigens are thermophilic actinomycetes and fungi.
Prevention of occupational asthma can be accomplished through better education of workers, management, unions and medical professionals. This will enable them to identify the risk factors and put in place preventive measures, including respiratory protection and exposure limits.
The number of workers in the United States exposed to beryllium vary but has been estimated to be as high as 800,000 during the 1960s and 1970s. A more recent study estimated the number of exposed workers in the United States from in 1996 to be around 134,000.
The rate of workers becoming sensitized to beryllium varies based on genetics and exposure levels. In one study researchers found the prevalence of beryllium sensitization to range from 9 - 19% depending on the industry. Many workers who are found to be sensitive to beryllium also meet the diagnostic criteria for CBD. In one study of nuclear workers, among those who were sensitized to beryllium, 66% were found to have CBD as well. The rate of progression from beryllium sensitization to CBD has been estimated to be approximately 6-8% per year. Stopping exposure to beryllium in those sensitized has not been definitively shown to stop the progression to CBD.
The overall prevalence of CBD among workers exposed to beryllium has ranged from 1 – 5% depending on industry and time period of study.
The general population is unlikely to develop acute or chronic beryllium disease because ambient air levels of beryllium are normally very low (<0.03 ng/m). However, a study found 1% of people living within 3/4 of a mile of a beryllium plant in Lorain, Ohio, had berylliosis after exposure to concentrations estimated to be less than 1 milligram per cubic metre of air. In the United States the Beryllium Case Registry contained 900 records, early cases relating to extraction and fluorescent lamp manufacture, later ones coming from the aerospace, ceramics and metallurgical industries.
Some examples:
- Allergic asthma
- Allergic conjunctivitis
- Allergic rhinitis ("hay fever")
- Anaphylaxis
- Angioedema
- Urticaria (hives)
- Eosinophilia
- Penicillin allergy
- Cephalosporin allergy
- Food allergy
- Sweet itch
Risk factors for drug allergies can be attributed to the drug itself or the characteristics of the patient. Drug-specific risk factors include the dose, route of administration, duration of treatment, repetitive exposure to the drug, and concurrent illnesses. Host risk factors include age, sex, atopy, specific genetic polymorphisms, and inherent predisposition to react to multiple unrelated drugs (multiple drug allergy syndrome).
A drug allergy is more likely to develop with large doses and extended exposure.
BFL symptoms improve in the absence of the bird proteins which caused the disease. Therefore, it is advisable to remove all birds, bedding and pillows containing feathers from the house as well as washing all soft furnishings, walls, ceilings and furniture. Certain small mammals kept as pets have the same or similar proteins in their fur and feces and so should be removed. Peak flow measurements will indicate a lung condition however a spirometric test on lung capacity and patients ability to move air in and out of the lungs plus in more advanced cases an X-ray test or CT scan is available to confirm whether someone has the disease or not. Steroid inhalers similar to those used for asthma are effective or in cases where the patient finds inhaling difficult high dosages of steroids combined with bone density protecting drugs are used to treat a person with BFL, reducing the inflammation and hopefully preventing scarring. Recovery varies from patient to patient depending on what stage the condition was at when the patient consulted the doctor, the speed of diagnosis and application of the appropriate treatment to prevent residual damage to the lungs and many make a full recovery. However, BFL may reoccur when in contact with birds or other allergens.
Typical levels of beryllium that industries may release into the air are of the order of , averaged over a 30-day period, or of workroom air for an 8-hour work shift. Compliance with the current U.S. Occupational Safety and Health Administration (OSHA) permissible exposure limit for beryllium of has been determined to be inadequate to protect workers from developing beryllium sensitization and CBD. The American Conference of Governmental Industrial Hygienists (ACGIH), which is an independent organization of experts in the field of occupational health, has proposed a threshold limit value (TLV) of in a 2006 Notice of Intended Change (NIC). This TLV is 40 times lower than the current OSHA permissible exposure limit, reflecting the ACGIH analysis of best available peer-reviewed research data concerning how little airborne beryllium is required to cause sensitization and CBD.
Because it can be difficult to control industrial exposures to beryllium, it is advisable to use any methods possible to reduce airborne and surface contamination by beryllium, to minimize the use of beryllium and beryllium-containing alloys whenever possible, and to educate people about the potential hazards if they are likely to encounter beryllium dust or fumes. It is important to damp wipe meallographic preparation equipment to prevent accumulation of dry particles. Sectioning, grinding, and polishing must be performed under sufficiently vented hoods equipped with special filters.
On 29 January 2009, the Los Alamos National Laboratory announced it was notifying nearly 2,000 current and former employees and visitors that they may have been exposed to beryllium in the lab and may be at risk of disease. Concern over possible exposure to the material was first raised in November 2008, when a box containing beryllium was received at the laboratory's short-term storage facility.
Bird fancier's lung is a type of hypersensitivity pneumonitis caused by bird droppings. The lungs become inflamed with granuloma formation.
Bird fancier's lung (BFL), also called "bird-breeder's lung" and "pigeon-breeder's lung", is a subset of hypersensitivity pneumonitis (HP). This disease is caused by the exposure to avian proteins present in the dry dust of the droppings and sometimes in the feathers of a variety of birds. Birds such as pigeons, parakeets, cockatiels, shell parakeets (budgerigars), parrots, turtle doves, turkeys and chickens have been implicated.
People who work with birds or own many birds are at risk. Bird hobbyists and pet store workers may also be at risk.
Treatment usually involves adrenaline (epinephrine), antihistamines, and corticosteroids.
If the entire body is involved, then anaphylaxis can take place, which is an acute, systemic reaction that can prove fatal.
It can be classified into acute interstitial pneumonitis, blood pneumonitis, lymphocytic interstitial pneumonitis, radiation pneumonitis, and uremic pneumonitis.
Chemical pneumonitis is inflammation of the lung caused by aspirating or inhaling irritants. It is sometimes called a "chemical pneumonia", though it is not infectious. There are two general types of chemical pneumonitis: acute and chronic.
Irritants capable of causing chemical pneumonitis include vomitus, barium used in gastro-intestinal imaging, chlorine gas (among other pulmonary agents), ingested gasoline or other petroleum distillates, ingested or skin absorbed pesticides, gases from electroplating, smoke and others. It may also be caused by the use of inhalants.
Mendelson's syndrome is a type of chemical pneumonitis.
Mineral oil should not be given internally to young children, pets, or anyone with a cough, hiatus hernia, or nocturnal reflux, because it can cause complications such as lipoid pneumonia. Due to its low density, it is easily aspirated into the lungs, where it cannot be removed by the body. In children, if aspirated, the oil can work to prevent normal breathing, resulting in death of brain cells and permanent paralysis and/or retardation
When a medication causes an allergic reaction, it is called an allergen. The following is a short list of the most common drug allergens:
- Antibiotics
- Penicillin
- Sulfa drugs
- Tetracycline
- Analgesics
- Codeine
- Non-steroidal anti-inflammatory drugs (NSAIDs)
- Antiseizure
- Phenytoin
- Carbamazepine
The following are precautionary measures that can be taken to avoid the spread of bagassosis:
1. Dust control-prevention /suppression of dust such as wet process, enclosed apparatus, exhaust ventilation etc. should be used
2. Personal protection- masks/ respirators
3. Medical control- initial medical examination & periodical checkups of workers
4. Bagasse control- keep moisture content above 20% and spray bagasse with 2% propionic acid
"Fire-eater's lung" is an important variant of hydrocarbon pneumonitis, which typically involves adolescents or young adults who are exposed through mishap during flame-blowing performances using a variety of different flammable materials. The substances used overlap with some of the pediatric exposures (kerosene, gasoline) but can also include other hydrocarbons such as jet fuel and, in France, an aromatic hydrocarbon enriched petroleum-distillate called "kerdan". There has also been a case of citronella oil aspiration in a fire-eater. As with hydrocarbon pneumonitis in children, fire-eater's lung can also be complicated by pneumatocele. Although the term "acute lipoid pneumonia" has been used to refer to the "fire-eater's lung" syndrome, this is a misnomer.
The signs and symptoms of acute beryllium pneumonitis usually resolve over several weeks to months, but may be fatal in 10 percent of cases, and about 15–20% of cases may progress to CBD.
Acute beryllium poisoning approximately doubles the risk of getting lung cancer. The mechanism by which beryllium is carcinogenic is unclear, but may be due to ionic beryllium binding to nucleic acids; it is not mutagenic.
Pneumonitis or pulmonitis is an inflammation of lung tissue due to factors other than microorganisms. Those can be radiation therapy of the chest , exposure to medications used during chemo-therapy, the inhalation of debris (ie animal dander), of food particles during vomiting, herbicides or fluorocarbons and some systemic diseases.
It is distinguished from pneumonia on the basis of causation as well as its manifestation since pneumonia can be described as pneumonitis combined with consolidation and exudation of lung tissue due to infection with microorganism.
General treatment principles are removal from exposure, protection of the airway (i.e., preemptive intubation), and treatment of hypoxemia. Concomitant airway injury with acute bronchospasm often warrants treatment with bronchodilators because of the airway obstruction.
A beneficial role for corticosteroids has not been established by controlled trials in humans. Despite the lack of controlled evidence of efficacy, anecdotal reports of benefits from systemic corticosteroid use continue to appear.
Prophylactic antibiotic drugs have not proved to be efficacious in toxic lung injury. Antibiotics should be reserved for those patients with clinical evidence of infection.
Fire breathing is typically performed with a high flash point fuel, such as lamp oil (liquid paraffin), while fire eating is performed with low flash point fuels, such as white gas or naphtha. Highly purified fuels are preferred by fire performers due to their minimized toxicity, but other, more dangerous fuels may sometimes be used, such as ethanol, isopropanol, kerosene, gasoline, or charcoal lighter fluid. All fuels run the risk of causing pneumonitis if inhaled, however longer chain oils are more persistent than smaller molecules. Alcohols and volatile naphthas are likely to be absorbed or expelled from the body by evaporation and respiration.
Sixty percent of people with acute interstitial pneumonitis will die in the first six months of illness. The median survival is 1½ months.
However, most people who have one episode do not have a second. People who survive often recover lung function completely.