Hypersensitivity pneumonitis due to residential mosquito-coil smoke exposure.
ABSTRACT We reported a previously healthy 25-year-old female patient who developed hypersensitivity pneumonitis following repeated exposures to the smoke of mosquito coils. The patient presented with vague symptoms of cough and fever for 3 days. Diagnostic criteria proposed for clinical use in this case included history, exposure to a recognized antigen, physical examination, consistent radiographic images, bronchoalveolar lavage and lung biopsy. Much symptomatic relief and better radiographic response were noted after short-term use of oral corticosteroid and removal of the offending antigen.
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ABSTRACT: Hypersensitivity pneumonitis (HP) is an interstitial lung disease due to a combined type III and IV reaction with a granulomatous inflammation, caused by cytotoxic delayed hypersensitivity lymphocytes, in a Th1/Th17 milieu, chaperoned by a deficient suppressor function of T regulatory cells. Skewing toward a Th2 phenotype is reported for chronic HP. Phenotypic expression and severity depends on environmental and/or host genetic and immune co-factors. The wide spectrum of causative antigens is continuously up-dated with new sources of airborne organic particles and drug-induced HP. The diagnosis requires a detailed history, measurement of environmental exposure, pulmonary function tests, imaging, detection of serum specific antibodies, broncho-alveolar lavage, antigen-induced lymphocyte proliferation, environmental or laboratory-controlled inhalation challenge and lung biopsy. Complete antigen avoidance is the best therapeutic measure, although very difficult to achieve in some cases. Systemic steroids are of value for subacute and chronic forms of HP, but do not influence long term outcome. Manipulation of the immune response in HP holds future promise.Clinical and translational allergy. 02/2013; 3(1):5.
Chinese Medical Journal 2011;124(12):1915-1918
Hypersensitivity pneumonitis due to residential mosquito-coil
Gopall Roshnee, CAO Guo-qiang and CHEN Hong
We reported a previously healthy 25-year-old female patient who developed hypersensitivity pneumonitis following
repeated exposures to the smoke of mosquito coils. The patient presented with vague symptoms of cough and fever for 3
days. Diagnostic criteria proposed for clinical use in this case included history, exposure to a recognized antigen, physical
examination, consistent radiographic images, bronchoalveolar lavage and lung biopsy. Much symptomatic relief and
better radiographic response were noted after short-term use of oral corticosteroid and removal of the offending antigen.
Chin Med J 2011;124(12):1915-1918
ypersensitivity pneumonitis (HP), also called
extrinsic allergic alveolitis, is a complex syndrome
of varying intensity, clinical presentation, and natural
history, rather than a single uniform disease.1-3 Our case
report lays emphasis on the fact that HP can be caused by
domestic exposures alone. Since, the clinical findings of
HP mimic multiple other diseases, a high degree of
clinical suspicion and a thorough occupational and
environmental history are essential for accurate diagnosis.
There is no single pathognomonic feature for HP; or
rather, diagnosis relies on a constellation of clinical,
radiologic, and pathologic findings. Hence, domestic
exposures should not be ignored and therefore be
considered as potential causes of HP.
A 25-year-old female patient presented to the outpatient
clinic with a 3-day history of fever, cough with minimal
amount of white sputum. She denies having any chills,
dyspnea and night sweats. No recent history of travel was
noted. The patient has no previous significant medical or
surgical history. The family history is unremarkable. She
is a medical student and has no known drug or food
allergies, as well as no history of smoking, alcohol abuse
or illicit drug use. She lives with her parents, has no pet at
home and denies having any exposure to dust, pollution
and detergents. However, after repeated questioning about
any other types of exposure to allergens, the patient
admits using mosquito coils recently only during
The physical examination revealed an alert, well-
appearing female with a body temperature of 38.5°C,
regular pulse rate of 92 beats per minute, blood pressure
110/70 mmHg, respiratory rate 20 breaths per minte, and
an oxygen saturation of 91% while breathing room air.
The throat was not congested and there were no enlarged,
inflamed tonsils. Lymph nodes were not palpable. The
cardiac examination showed normal heart sounds and no
audible murmurs, rubs or gallops. Examination of the
chest showed good air entry bilaterally, but scattered rales
could be heard over both lung fields, more on the left one.
The abdomen was soft, non-tender and without
organomegaly. There was no pedal edema, cyanosis or
clubbing (Figure 1). The peripheral arterial pulses were
palpable. The neurological examination was normal.
The patient in this case was admitted and evaluated by a
pulmonologist. The initial diagnosis was community-
acquired pneumonia and a course of cephalosporin (third
generation) was subsequently started. As part of the initial
workup of the findings on physical examination, a chest
X-ray (Figure 1), high-resolution computed tomography
of the chest (Figure 2), routine laboratory investigations,
including a complete blood cell (CBC) count and a basic
electrolyte panel, as well as erythrocyte sedimentation
rate (ESR), C-reactive protein (CRP) were performed.
Her blood routine test revealed an abnormally high level
of eosinophils (22%), raised ESR (42 mm/h) and an
elevated CRP. The chemistry panel was within normal
limits. Purified Protein Derivative (PPD) was negative.
After 3 days of antibiotics, the patient’s body temperature
became normal. However, 2 days later, the patient’s
condition gradually worsened with increased cough and
dyspnea. No fever was noted this time. A chest X-ray was
repeated which showed an opacity in the right lung
(Figure 3). A second antibiotic, namely quinolone was
added. Despite the antibiotic therapy, the patient did not
experience much improvement.
Hence, bronchoalveolar lavage fluid (BALF) and lung
biopsy (Figure 4) were ordered as a final diagnosis could
not be made. Lymphocytosis (>60%) with a pre-
Department of Pulmonology, First Affiliated Hospital of
Chongqing Medical University, Chongqing 400016, China
(Roshnee G and Chen H)
Department of Pulmonology, Daping Hospital, Third Military
Medical University, Chongqing 400042, China (Cao GQ)
Correspondence: Prof. CHEN Hong, Department of Pulmonology,
First Affiliated Hospital, Chongqing Medical University,
Chongqing 400016, China (Email: email@example.com)
Chin Med J 2011;124(12):1915-1918
dominance of CD8 cells were seen in the BALF.
Based on a thorough history, exposure to a recognized
antigen, physical examination, consistent chest X-ray,
high-resolution computed tomography (HRCT), BALF
result and histopathology report, the diagnosis of subacute
HP was confirmed. The patient was eventually treated with
oral methylprednisolone 8 mg twice per day, which
brought much symptomatic relief. She was then discharged
after three days and had follow-up with a pulmonologist.
After two months of corticosteroid therapy and its
eventual tapering of the dosage, as well as the removal of
the causative allergen (smoke from mosquito coils), there
was marked improvement in her condition.
Burning mosquito coils indoors, which is widely known
as an efficient mosquito repellent, generates smoke that
can control mosquitoes effectively. This practice is
currently used in numerous household in Asia, Africa and
South America. However, the smoke contains pollutants
which are of health concern.
HP, also called extrinsic allergic alveolitis, is a complex
syndrome of varying intensity, clinical presentation, and
natural history, rather than a single uniform disease.1,2 HP
is characterized by diffuse inflammation of lung
parenchyma and airways in previously sensitized patients
due to repeated exposures to the antigens. These antigens
can be derived from a variety of sources, such as dairy
and grain products, animal dander and protein, wood bark,
and water reservoir vaporizers.3 The most common
diseases are farmer’s lung and bird fancier’s lung.
The epidemiology of HP remains largely unknown. In a
population-based study, the estimated annual incidence of
interstitial lung disease was reported as 30 per 100 000.4
In that study, HP accounted for less than 2% of the
incident cases. In another study conducted by Lacasse et
al,5 30% of the 661 patients included in this prospective
multi-center cohort had HP. This cohort study included
consecutive adult patients presenting with a pulmonary
syndrome for which active HP was considered in the
Pathologically, acute HP is characterized by poorly
formed non-caseating interstitial
mononuclear cell infiltration
distribution with prominent giant cells. The sub-acute, or
intermittent, form produces well-formed non-caseating
granulomas, bronchiolitis with or without organizing
pneumonia, and interstitial fibrosis.6 Chronic forms reveal
additional findings of chronic interstitial inflammation
and alveolar destruction (honeycombing).7
The immuno-pathogenesis of HP has not been well
characterized. An exuberant production of antibody
(especially immunoglobulin G (IgG)) against the
offending antigen is frequently identified; however, the
precipitating antibody alone is not sufficient to cause HP.
A key role for T-cell mediated responses is suggested by
the observations of CD8+ cytotoxic lymphocyte
proliferation8 and greater percentages of natural killer T
cells in BALF.9
HP is categorized as acute, subacute and chronic. Patients
with acute HP present with fever, tachypnea, and diffuse
fine bibasilar crackles upon auscultation. In the subacute
form, symptoms are similar to the acute stage but are less
severe and last longer. Muscle wasting, weight loss,
clubbing, tachypnea, respiratory distress, and inspiratory
crackles over lower lung fields are often present in the
Six clinical predictors can be used to help establishing HP
Figure 1. Chest X-ray with reticulo-nodular shadows over both lungs, more on the left side.
1A: Coronal. 1B: Sagittal.
Figure 2. A high-resolution computed tomography (HRCT) of the chest showing ground-glass
opacities and ill-defined centrilobular micronodules bilaterally.
Figure 3. A chest X-ray after 5 days of antibiotic therapy (cephalosporin + quinolone) and
revealed an opacity in the right lung.
Figure 4. Histopathology report of lung biopsy showed inflammatory infiltrate with focal area
of organizing pneumonia (HE staining, original magnification ×400).
Chinese Medical Journal 2011;124(12):1915-1918
as the correct diagnosis: (1) exposure to a known
offending antigen; (2) positive precipitating antibodies to
the offending antigen; (3) acute/recurrent episodes of
symptoms; (4) inspiratory
examination; (5) symptoms occurring 4–8 hours after
exposure; (6) weight loss. The differential diagnoses of
HP closely resemble mainly the following diseases:
miliary tuberculosis, bronchial asthma, pulmonary
eosinophilia, idiopathic pulmonary fibrosis, connective-
tissue disease, and systemic lupus erythematosis.
Establishing the diagnosis of HP includes laboratory and
imaging studies, BALF, pulmonary function test and lung
biopsy. Blood tests are of limited utility6 but can reveal
leukocytosis and neutrophilia, eosinophilia, elevated ESR,
CRP and increased levels of immunoglobulins.
Precipitating immunoglobulin G antibodies against
potential antigens indicate
sensitization but do not necessarily represent disease.
HRCT is more sensitive than chest radiography for
To acute HP, HRCT usually reveals a patchy,
ground-glass attenuation with small, poorly defined
centrilobular nodules; to subacute HP, the findings are
similar to those observed in acute disease and focal
emphysema may be seen in addition to mild fibrotic
changes; to chronic HP, centrilobular nodules, areas of
linear opacity and honeycombing can be seen with
A restrictive or a mixed obstructive pattern is common in
HP. After bronchoalveolar
lymphocytosis (>20%) is nonspecific but helpful.
Elevation of the number of CD8+ T cells and a CD4+ to
CD8+ ratio of less than 1 are characteristic for this
disorder. Biopsy is indicated when noninvasive testing is
Emphasis on environmental control is the cornerstone of
treatment. Measures to minimize antigenic exposure
usually result in regression of disease, but treatment with
corticosteroids is required in severe cases. Treatment is
initiated with prednisone (0.5–1 mg/kg as a single dose in
the morning). The initial dose is continued for 2–4 weeks
and then tapered over a 4 to 8 weeks period while
evaluating clinical response, pulmonary function, and
radiographic improvement. Maintenance doses are not
always required, particularly if the person is removed
The patient, in this case, had non-specific complaints and
presented with minimum physical findings. There is no
golden standard that can be used to establish an
unequivocal diagnosis of hypersensitivity pneumonitis.
Therefore, one must rely on a combination of history,
radiography, serologic study, and exclusion of other
possible causes. In our case, the causative agent revealed
crackles on physical
prior exposure and
lavage,12 a marked
to be smoke from mosquito coils which contains
pyrethroid insecticides, particularly d-allethrin, may
contain octachlorodipropyl ether (S-2, S-421) as a
synergist or active ingredient.13 HP characterized by chest
pain, cough, dyspnea and bronchospasm may occur in an
individual chronically exposed.14
The findings of the chest X-ray and HRCT revealed the
severity of her condition. Moreover, CBC showed an
abnormally high level of eosinophils (22%) which
prompted us to think about an allergic reaction or
immunologically mediated disorder. Since the first
clinical picture of this
community-acquired pneumonia, antibiotics were started,
but were ineffective in her case. This demanded further
investigations and consideration of misdiagnosis. Hence,
BALF and lung biopsy were ordered. BALF showed
lymphocytosis with a predominance of CD8+ cells and
the ratio of CD4+ to CD8+ was less than 1, which is more
characteristic for HP. Lung biopsy was reported as
inflammatory infiltrate with focal area of organizing
pneumonia. All the above findings provided important
clues in establishing the diagnosis of HP.
antibodies against potential antigens which could have
indicated prior exposure and sensitization could not be
carried out on our patient as pyrethrins’ plasma levels are
not clinically useful or readily available.15 Moreover, our
patient was not eager for further investigations as there
was marked improvement in her condition following the
removal of the offending agent from her home
To support the clinical diagnosis of HP caused by
mosquito coil smoke, Liu et al16 conducted a study in
which they concluded that repeated exposure to mosquito
coils can lead to several disorders of the respiratory tract.
HP is a multifaceted group of immunologically mediated
lung disorders caused by recurrent exposure to various
occupational and environmental agents. Because the
clinical findings of HP mimic multiple other diseases, a
high degree of clinical suspicion and a thorough
occupational and environmental history are essential for
accurate diagnosis. There is no single pathognomonic
feature for HP; diagnosis relies on a constellation of
clinical, radiologic, and pathologic findings. In this case,
a review of the patient’s environmental history revealed
that she was exposed to smoke from mosquito coils.
Hence, domestic exposures should not be ignored and
therefore be considered as potential causes of HP.
Cormier Y, Lacasse Y. Keys to the diagnosis of
hypersensitivity pneumonitis: the role of serum precipitins,
lung biopsy, and high-resolution computed tomography. Clin
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(Received August 27, 2010)
Edited by PAN Cheng