There are ongoing research, clinical trials, and individual case observations relating to idiopathic interstitial lung disease or hypersensitivity pneumonitis that continue to expand our knowledge concerning these most difficult and perplexing lung problems. Listed below are some of these selected articles.

1.  Apostolakos MJ, Rossmoore H, Beckett WS. Hypersensitivity pneumonitis from ordinary residential exposures. Environ Health Perspect. 2001;109:979-81.

This is a report of a patient with home contamination causing hypersensitivity pneumonitis.
Remediation efforts were unsuccessful leading to the patient moving from the home before this problem was resolved.

2. Churg A, Muller NL, Flint J, et al. Chronic hypersensitivity pneumonitis. Am J Surg Pathol. 2006;30:201-8

This pathological study of 13 biopsy specimen from patients with chronic HP demonstrated 3 patterns resembling UIP, fNSIP, and irregular peribronchiolar fibrosis. Other findings such as scattered poorly formed granulomas, isolated interstitial giant cells and Shaumann bodies were often found indicating the correct diagnosis. Despite the presence of extensive fibrosis, some patients responded to removal from exposure and steroid therapy.

COMMENT:  The importance of this paper is the demonstration that chronic HP may present with a variety of histopathologic patterns and the patient may respond to removal from exposure and steroid therapy despite extensive fibrosis.

3. Hanak V, Golbin JM, Ryu JH. Causes and presenting features in 85 consecutive patients with hypersensitivity pneumonitis. Mayo Clin Proc. 2007;82:812-6.

  This was a retrospective study to determine the causes or causative environments of consecutive cases of classic hypersensitivity pneumonitis. The patients had to meet the classic histopathologic pattern of bronchiolocentric, chronic interstitial pneumonitis with nonnecrotizing granulomas to be considered as hypersensitivity pneumonitis. The causes were identified in 75% of these cases with avian antigens (birds) causing 34%, Mycobacterium avium complex in hot tub water at 21%, Farmer's lung disease 11%, and 9% related to household exposure. The inciting antigen could not be identified in 25%. Most of these patients had chronic hypersensitivity pneumonitis.

COMMENT: This paper has a histopathological pattern that is too narrow in focus. The discussion, however, does point out that there are other histopathological patterns that have been recognized in HP. The home environment was the overwhelming causative environment when one considers that the bird-induced and the hot tub induced were also related to the home. Most of the 25% for which no cause was identified were also probably home-induced since no occupational causes could be identified.

4.   Ohtani Y, Saiki S, Usui Y, et al. Chronic bird fancier's lung: histopathological and clinical correlation. An application of the 2002 ATS/ERS consensus classification of the idiopathic interstitial pneumonias. Throax. 2005;60:665-71.

This paper looked retrospectively at 26 patients with chronic HP caused by exposure to birds to classify them from a histopathological perspective. Two patients had BOOP-like lesions, 5 had a pattern of NSIP, cellular, 8 had a pattern of NSIP, fibrotic, and the remaining 8 had a pattern of UIP. Only 5 of these biopsy specimen had granuloma identified. They pointed out that chronic HP from bird exposure has various histopathological patterns.

COMMENT: This paper points out the HP may have many other histopathological patterns other than that classically described.

5. Fenton ME, Cockcroft DW, Wright JL, Churg A. Hypersensitivity pneumonitis as a cause of airway-centered interstitial fibrosis. Ann Allergy Asthma Immunol. 2007;99:465-6.

A single case of a farmer exposued to ducks and geese who developed interstitial lung disease that upon lung biopsy revealed a pattern described as airway-centered interstitial fibrosis (ACIF). The evluation revealed positive precipitins to serum from ducks and geese with an associated history of exposure leading to symptoms within 4 to 6 hours.

Comment: This case described another histopathologic presentation of HP.


6. Enriquez-Matas A, Quirce S, Hernandez E, et al. Hypersensitivity pneumonitis caused by domestic exposure to mold. J Investig Allergol Clin Immunol. 2007;17:126-8.

This is a report of two patients with hypersensitivity pneumonitis caused by Aspergillus  fumigatus in two separate homes. Successful treatment was moving from the home or remediation of the home.

Comment: This paper specifically counters a position paper by the American Academy of  Allergy, Asthma, and Immunology that stated "hypersensitivity pneumonitis caused by domestic mold in the home environment is extremely unlikely, except in unusual circumstances, such as workplace exposure".

7. Temprano J, Becker BA, Hutcheson PS, et al. Hypersensitivity pneumonitis secondary to residential exposure to Aureobasidium pullulans in 2 siblings. Ann Allergy Asthma Immunol. 2007;99:562-6.

Another paper reporting hypersensitivity pneumonitis in 2 children ages 6 and 15 years caused by a common mold within the home environment. An environmental challenge led to reflare of the disease in both children within 4 hours of entering the home.   A home inspection revealed the source of the contamination. Proper remediation of this home led to non-progression of this disease.

Comment: These two cases lend further evidence that home contaminations with common domestic mold does cause hypersensitivity pneumonitis.

8.  Ohtani Y, Ochi J, Mitaka K, et al. Chronic summer-type hypersensitivity pneumonitis initially misdiagnosed as idiopathic interstitial pneumonia. Inter Med. 2008;47:857-2.

Two cases are reported that were misdiagnosed as idiopathic interstitial pneumonia until an environmental investigation revealed contaminations and an aggressive approach to diagnosis revealed these cases to be caused by mold organisms within the home. A home challenge to one of the patients took about 7 days to become positive confirming that some cases take longer than the 4 to 8 hour time period to react after returning to the causative environment.

9.  Chiba S, Okada S, Suzuki Y, et al. Cladosporium species-related hypersensitivity pneumonitis in household environments. Inter Med. 2009;48:363-

Two cases of hypersensitivity pneumonitis caused by different Cladosporium species are reported in an office setting and in the home.

COMMENT: These cases represent, yet again, that the home environment must be strongly considered when there is no occupational possibility. Further evidence that the message is being received that the home has become the major causative environment of this disorder.

10. Inase N, et al. A clinical study of hypersensitivity pneumonitis presumably caused by feather duvets. Ann Allergy Asthma Immunol. 2006;96:98-104.

Seven patients, from Japan,  are presented with hypersensitivity pneumonitis caused by sleeping under feather duvets from 1 month to 10 years. The acute presenters were demonstrated to have antibodies toward avian antigens, however, the chronic presenters could not be shown to have antibodies.

11. Koschel D, et al. Presenting features of feather duvet lung. Int Arch Allergy Immunol. 2010;152:264-70.

Thirteen patients, from Germany, demonstrated to have hypersensitivity pneumonitis