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History of Hypersensitivity Pneumonitis
Farmers Lung
In 1713, Bernardino Ramazzini (1633–1714), an Italian medical professor, described the health hazards associated with 52 occupations. (Credit: HP A Historical and Radiologic Review) Among these were , the effects of biological dust, as well as the Aspergillus molds found in hay, were being diagnosed as root causes of severe lung conditions in farmers. These were often irreversible and terminal. This was in fact the first documentation of what later became known as Hypersensitivity Pneumonitis.
In 1874, Dr. Jon Finsen of Iceland, provided a more detailed description of “Heykatarr,” now known as Farmer’s lung, in his graduate thesis after noting that men “whose job it is to loosen the hay in the barn and handle it before it is fed to cattle,” became ill after inhalation of the dust. [1] The antigens responsible for hypersensitivity pneumonitis come from a variety of sources. In general, these are classified into three major categories: microbes, animal proteins, and low-molecular-weight chemicals. These most commonly manifest as farmer’s lung, bird fancier’s lung, and chemical worker’s lung, respectively. [2] (Credit MedScape: Hypersensitivity Pneumonitis)
In Britain in 1932, Campbell described a disorder of the lung caused by inhalation of dust from moldy hay. In 1964, Ramazzini and Wright [1] described workers getting "diseases of the chest." (Credit MedScape). Since then further causes were attributed to "Farmers Lung" such as the antigens found in the feathers, dander and excrement of the fowl kept on farms including chickens, geese and ducks.
In 1874, Dr. Jon Finsen of Iceland, provided a more detailed description of “Heykatarr,” now known as Farmer’s lung, in his graduate thesis after noting that men “whose job it is to loosen the hay in the barn and handle it before it is fed to cattle,” became ill after inhalation of the dust. [1] The antigens responsible for hypersensitivity pneumonitis come from a variety of sources. In general, these are classified into three major categories: microbes, animal proteins, and low-molecular-weight chemicals. These most commonly manifest as farmer’s lung, bird fancier’s lung, and chemical worker’s lung, respectively. [2] (Credit MedScape: Hypersensitivity Pneumonitis)
In Britain in 1932, Campbell described a disorder of the lung caused by inhalation of dust from moldy hay. In 1964, Ramazzini and Wright [1] described workers getting "diseases of the chest." (Credit MedScape). Since then further causes were attributed to "Farmers Lung" such as the antigens found in the feathers, dander and excrement of the fowl kept on farms including chickens, geese and ducks.
Bird Fancier's Lung
Bird Breeders or Bird Fancier's Lung was 1st diagnosed as a specific ailment in 1960. Per Science Direct; "Avian antigens are complex high- and low-molecular-weight proteins found in the feathers, droppings, and serum of turkeys, chickens, geese, ducks, parakeets (budgerigars), parrots, pigeons, doves, love birds, canaries, and even native birds and are highly immunogenic." In simpler words, anyone who deals with any of these type birds on a daily basis who is susceptible to this disease is at risk. According to a recent study by the British Health Service, 0.05 people in 100,000 have the genetic disposition to get Hypersensitivity Pneumonitis if exposed to the proper antigens.
This form of the disease became prevalent in the 1800's throughout the UK as more and more people began keeping exotic birds as pets. During the 1930's through the 1970's it became known as Pigeon Lung in the USA. This in part was due to the advent of high rise office buildings with numerous ledges. Prior to central air, office workers would keep their windows open for ventilation and the avian proteins from the pigeons nesting and congregating on the ledges would blow into the offices. During the 1970's and later, the hermetically sealed buildings with HVAC environments created a whole new problem. Birds of all sorts would use the intake vent structures and enclosed and protected nesting places. This would concentrate the avian proteins and dried, powdered excrement being blown throughout the entire system. Due to this more and more occurrences of office workers coming down with Hypersensitivity Pneumonitis were reported.
This form of the disease became prevalent in the 1800's throughout the UK as more and more people began keeping exotic birds as pets. During the 1930's through the 1970's it became known as Pigeon Lung in the USA. This in part was due to the advent of high rise office buildings with numerous ledges. Prior to central air, office workers would keep their windows open for ventilation and the avian proteins from the pigeons nesting and congregating on the ledges would blow into the offices. During the 1970's and later, the hermetically sealed buildings with HVAC environments created a whole new problem. Birds of all sorts would use the intake vent structures and enclosed and protected nesting places. This would concentrate the avian proteins and dried, powdered excrement being blown throughout the entire system. Due to this more and more occurrences of office workers coming down with Hypersensitivity Pneumonitis were reported.
Chronic HP Today
Although many strides have been made in treating lung diseases in the past 50 years, Hypersensitivity Pneumonitis is still a very rare disease that little is known about to the general public. Many pulmonologists can go their entire career without encountering a single case of HP. Today HP is often initially misdiagnosed as several other lung diseases such as:
- Idiopathic Pulmonary Fibrosis
- COPD
- Emphysema
- Chronic Bronchitis