[4] Causes include breathing in toxic fumes, respiratory infections, connective tissue disorder or complications following a bone marrow or heart-lung transplant.

[9][10] These symptoms represent an obstructive pattern that is non-reversible with bronchodilator therapy, and need to be related to various lung insults.

[6] Bronchiolitis obliterans has many possible causes, including collagen vascular disease, transplant rejection in organ transplant patients, viral infection (adenovirus, respiratory syncytial virus, influenza, HIV, cytomegalovirus), Stevens–Johnson syndrome, Pneumocystis pneumonia, drug reaction, aspiration and complications of prematurity (bronchopulmonary dysplasia), and exposure to toxic fumes.

[6] As the disease progresses they begin to have symptoms of shortness of breath, cough, and wheezing as their lung function declines.

There has been an association shown between the increased use of peripheral stem cells and the risk of developing bronchiolitis obliterans.

[23] Industrial workers who have presented with bronchiolitis: Diacetyl is a chemical used to produce the artificial butter flavoring[25] in many foods such as candy and microwave popcorn and occurring naturally in wines.

This first came to public attention when eight former employees of the Gilster-Mary Lee popcorn plant in Jasper, Missouri developed bronchiolitis obliterans.

[31] Generally occurs after a viral infection of adenovirus (types 3, 7, and 21), measles (rubeola), mycoplasma, CMV, influenza, and parainfluenza.

[32] Post-infectious bronchiolitis obliterans is most common in the southern hemisphere particularly in countries such as Brazil, Argentina, Australia, Chile and New Zealand.

[31] The disease can have varying impact on children and their quality of life, which has been studied by lung function tests, as well as their exercise tolerance.

However, while each pathway has a more unique starting point and cause, the result is still injury and inflammation leading to scarring of the lung tissue.

[11] The scarred tissue then makes the expiration phase of respiration more difficult, leading to air not being expelled from the lungs.

The definitive diagnosis is through biopsy, but due to the variable distribution of lesions, leading to falsely negative tests, and invasive nature of this procedure it is often not performed.

[11] A common finding on HRCT is patchy areas of decreased lung density, signifying reduced vascular caliber and air trapping.

[11] The constrictive pattern is demonstrated by peribronchiolar cellular infiltrates which eventually causes small airway damage and leads to subepithelial fibrosis.

[11] In regards to proliferative disease, intraluminal buds called "Masson bodies" fill the lumen, which results in bronchiolar plugging.

[11] Other conditions that can present similarly include chronic obstructive pulmonary disease, asthma, bronchiectasis, hypersensitivity pneumonitis, and pneumonia.

[30][43] The primary prevention of bronchiolitis obliterans in people who have received either lung transplant or HSCT therapy is immunosuppression.

People who are post-HSCT their immunosuppressive regimen typically includes methotrexate in combination with a calcineurin inhibitor to prevent GVHD, a risk factor for developing bronchiolitis obliterans.

[1] This may include the use of corticosteroids or immunosuppressive medication which may have an effect on the ability to receive a lung transplant if offered.

Routine vaccinations are recommended for patients with chronic lung disease to prevent complications from secondary infections due to pneumonia and influenza.

[11][4] BOS is defined as a person who has had either a HSCT or lung transplant and develops symptoms or radiographic findings consistent with bronchiolitis obliterans, but has not been confirmed by biopsy.