The New York State Workers Compensation Board has established guidelines for the assessment of Hypersensitivity Pneumonitis (HP). These directives are designed to assist physicians and healthcare practitioners in determining appropriate treatment for this condition.

Healthcare professionals focusing on Hypersensitivity Pneumonitis (HP) can use the Workers Compensation Board’s guidance to make informed decisions about the most suitable level of care for their patients.

It is crucial to emphasize that these guidelines are not meant to substitute clinical judgment or professional expertise. The ultimate decision regarding care should be a collaborative effort involving the patient and their healthcare provider.

Hypersensitivity Pneumonitis (HP) – Condition Considerations:

General Overview:

• HP, also known as extrinsic allergic alveolitis, is caused by inhalation of organic dust with antigenic properties or exposure to low-molecular-weight sensitizing chemicals.
• HP comprises a large family of disorders of immune response often associated with granulomatous pathological changes.
• HPs tend to be highly specific to occupation or environmental settings.

Inhaled Causative Agents: Inhaled agents that can cause HP include:

• Animal proteins
• Plant proteins
• Bacteria
• Fungi
• Diisocyanates
• Paints
• Trimellitic anhydride
• Epoxy resins
• “Bordeaux mixture” (a pesticide made from copper sulfate used in vineyards)

Sources of Dusts: These dusts can arise from various sources, including:

• Renovation of buildings (especially demolition or exposing damp interior walls)
• Exposure to contaminated water or persistently wet spaces (humidifiers, hot tubs, saunas, unventilated showers)
• Handling birds
• Sensitization to other animals (such as farmer’s lung)
• Insects (such as miller’s lung, the antigen to which is a wheat weevil protein)
• Amoebae (humidifier lung)
• Pesticide powder (pyrethrum HP)
• Spores of a thermophilic actinomycete bacteria resulting in furrier’s lung
• Animal-derived dusts
• Grain dusts
• Mold spores

HP can manifest in individuals exposed to these diverse antigens, and identifying the specific causative agent is crucial for effective diagnosis and management.

Clinical Features:

• HP often begins with wheezing and airways obstruction.
• If untreated and unmanaged, HP may progress to respiratory insufficiency and profound impairment.
• Pigeon breeders’ lung is famously associated with clubbing, a distinctive feature not commonly seen in most hypersensitivity pneumonitides.

Latency:

• In HP, sensitization may occur in the first few weeks after beginning exposure, while in others, it may be delayed for months or even years.
• The acute, predominant airways symptoms of HP develop in a sensitized individual over days to weeks and may progress over weeks to interstitial inflammation and ultimately to fibrosis.
• Rarely, HP can have a hyperacute or sudden onset, similar to some eosinophilic pneumonias or drug-induced pneumonitis.

Differential Diagnosis:

• HP should be considered in the differential diagnosis of an acute influenza-like or febrile disorder in a patient with a history of exposure to inhaled antigens.
• It may also suggest rheumatological or autoimmune lung disease and infection (mycoplasma, Legionella spp., or diffuse mycosis) as a cause of interstitial disease, especially in a host with a compromised immune system.
• A history of exposure to birds should raise the possibility of other diseases, including psittacosis.

Risk Factors: While there are no well-established risk factors for the development of HP, personal and familial susceptibility may play a role. The identification of specific exposures and careful consideration of clinical and environmental factors are essential for accurate diagnosis and effective management.