by Leon Levine, CIH
Exposure to microbial contamination may lead to health effects including hypersensitivity pneumonitis. Hypersensitivity pneumonitis is a disease resulting from exposure to antigens which stimulate a specific immunological response. Building related antigens could originate from fungi, bacteria, or protozoa including amoebae contaminating water in ventilation systems. These microbes may also grow in the stagnant warm water present in forced-air heating, cooling, and humidification equipment, which disperses them into the ambient air. In enclosed spaces, such as office buildings, contemporaneous and widespread illness can occur.
Aspergillus is a fungal species that can produce hypersensitivity pneumonitis. Aspergillus is ubiquitous in nature and have provoked disease among corn and malt workers. It is the second most common opportunistic pathogen following Candida. Aspergillus grows on a wide range of substrates indoors and is prevalent in water damaged buildings. Workers exposed to the Penicillium fungus in the cheese, cork, and peat moss industries have been diagnosed with hypersensitivity pneumonitis. Candida species has also been shown to trigger hypersensitivity.
In some environments, the same clinical disease may result from different allergens. For example, mushroom worker’s lung may be caused either by inhalation of thermophilic actinomycetes from compost or inhalation of mushroom spores. Hypersensitivity pneumonitis may result from exposure to multiple agents present in the same environment, as is suggested by the simultaneous presence of antibodies to several organisms in some patients.
A series of cases were described in 1932 in farmers working with damp and moldy hay following an extremely rainy summer. Handling the hay led to the dispersion of dense clouds of dust, and after months of such exposure, the laborers developed progressive weight loss and dyspnea with some workers suffering severe breathlessness, cyanosis, and apparently imminent death. Once their exposure to the hay ended, however, the symptoms slowly disappeared over several weeks. As the patients improved clinically, the radiographic abnormalities generally resolved, except for apparent fibrosis that had developed in some cases.
Some low-molecular-weight chemicals that by themselves are not antigenic may combine with the host’s proteins to form haptens, which then may provoke hypersensitivity pneumonitis. Haptens are small molecules that trigger an immune response only when combining with a larger carrier such as a protein; the carrier may be one that also does not trigger an immune response by itself. For example, the agents implicated in chemical worker’s lung are isocyanates found in such products as foam, glue, and spray paint
Although symptoms occasionally develop after just a few weeks of contact with the allergen, most cases of hypersensitivity pneumonitis occur following months or years of continuous or intermittent inhalation of the inciting agent. Most patients with hypersensitivity pneumonitis have advancing antibodies to the antigen in their serum—usually immunoglobulin G, but sometimes immunoglobulin M or A—but these are often present in exposed asymptomatic people as well, limiting their diagnostic value. Its important to note that the antigen preparations used in testing are not highly standardized. Therefore, the absence of these antibodies does not exclude hypersensitivity pneumonitis.
In summary, building occupants may sustain hypersensitivity pneumonitis from repetitive inhalation of certain microbes, plant or animal proteins, or low-molecular-weight chemicals that combine with host proteins to form haptens. Symptomatic disease usually develops only after years of exposure and may be acute or episodic, with symptoms including fever and dyspnea, or insidious, with a gradual onset of dyspnea, coughing, anorexia, and weight loss. Some patients with an insidious onset experience repeated acute episodes.
The clinical/histologic observations in patients with hypersensitivity pneumonitis include cellular bronchiolitis, interstitial chronic inflammation (typically in a peribronchiolar pattern), poorly defined granulomas, and isolated giant cells in the alveoli or interstitium. The radiographic appearance of the lungs is often abnormal, but high-resolution CT scan is more sensitive in identifying disease by showing fibrosis, honeycombing, and emphysema.
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