Pennsylvania State University
A number
of farm tasks involve potential exposure to spoiled hay, grain,
and silage: breaking open bales of hay, removing the top layer
of silage from a silo, shoveling grain or cleaning out grain
storage structures. When these activities are performed in
a barn, bin, silo, or other enclosure, farmers may inhale
significant quantities of bacterial and fungal spores and
byproducts. These can induce either of two respiratory reactions:
hypersensitivity pneumonitis, referred to here as farmer's
lung, and a toxic organic dust syndrome (TODS) similar to
that caused by inhalation of grain dusts ("grain fever") and
confinement house dusts.
Cases
of TODS and acute cases of farmer's lung present in a similar
way: as delayed febrile illness of variable severity with
cough, dyspnea, myalgia, and malaise, following exposure circumstances
similar to those mentioned above, and typically resolving
spontaneously within days. However, the two illnesses differ
in several significant ways. Farmer's lung is an allergic
alveolitis, while TODS is a nonallergic inflammatory response
of the alveoli. TODS is relatively common and often occurs
simultaneously in a cluster of exposed persons, while farmer's
lung is a fairly rare response of sensitized individuals.
Only farmer's lung can become chronic, with some cases resulting
in progressive irreversible damage to lungs leading to permanent
disability or death. Differentiation of acute farmer's lung
and TODS may be difficult, and the latter may be misdiagnosed
as farmer's lung. Tests helpful in separating the two illnesses
include chest radiographs, blood gas measurements, immunoserology,
and pulmonary function tests; lung biopsy, bronchoalveolar
lavage, and bronchoprovocation may be useful in selected cases.
Farm
management and engineering changes that reduce exposure to
dusts from spoiled plant material are advisable for all farmers.
For farmers suffering from chronic farmer's lung or from repeated
attacks of acute illness, such changes are mandatory to prevent
possible permanent impairment that may necessitate leaving
the farm.
Animal
feed (hay, silage, and grain) that is put into storage with
a high moisture content favors the growth of bacteria and
fungi. These microorganisms produce spores and byproducts
(mycotoxins and endotoxins) of respirable size (less than
10 11 in diameter) which, when released into the air, can
be inhaled in large quantities and induce respiratory effects
within the airways or alveoli.
More
specifically, hay baled while moist heats spontaneously, and
proceeds through a natural succession of fungal and bacterial
populations The last organisms to grow in the hay are a number
of bacterial species termed "thermophilic actinomycetes",
which include Micropolyspora faeni and several species of
Thermoactinomyces. Silage, which includes chopped oats ("oatlage"),
hay ("haylage"), or corn ("cornlage"), is purposefully stored
wet in order to undergo the anaerobic ensilage process, which
preserves plant material. Tne uppermost layer of silage remains
aerobic and spoils. Grain, when stored before being adequately
dried, likewise will spoil and harbor quantities of microorganisms.
(See Fig. 1) The species of fungi and bacteria that dominate
will change with the type of plant material in storage, moisture
and heat conditions, and storage conditions, but typically
will include the thermophilic actinomycetes and a variety
of fungi.
While
feed-related microorganisms and their by-products pose a major
threat to farm workers, these workers can suffer the same
type of response (hypersensitivity pneumonitis) when they
are exposed to other agents. These other agents range from
fungi and bacteria growing in wood chips to proteins of bird
droppings. Some of the many agents found on the farm that
are capable of producing hypersensitivity pneumonitis are
listed in Table 1. Since these are associated with production
or processing of agricultural products, they all could be
considered agricultural occupational hazards.
Agriculturally-Related
Hypersensitivity Pneumonitis
|
Agent
|
Exposure
|
Common
Name of Disease
|
Thermophilic
actinomycetes and fungi:
|
|
|
Micropolyspora faeni,
|
SPOILED
HAY AND OTHER
|
ARMER'S
LUNG
|
OTHER THERMOPHILIC
|
FODDER
|
|
|
|
|
ACTINOMYCETES
AND FUNGI
|
|
|
Thermoactinomyces
vulgaris
|
Moldy
compost
|
Mushroom
worker's lung
|
Thermoactinomyces
viridis
|
Moldy
compost
|
Mushroom
worker's lung
|
Alternaria
spp.
|
Moldy
wood chips
|
Wood
worker's lung
|
Pullularia
pullulans
|
Moldy
redwood dust
|
Sequoisis
|
Aspergillus
clavatus
|
Moldy
cheese
|
Cheese
washer's lung
|
Aspergillus
spp.
|
Moldy
malt and barley dust
|
Malt
worker's lung
|
Cryptostroma
corticale
|
Moldy
maple bark
|
Maple
bark stripper's lung
|
Penicillium
caseii
|
Cheese
mold
|
Cheese
worker's lung
|
Penicillium
roqueforti
|
Cheese
mold
|
Cheese
worker's lung
|
Thermophilic
actinomycetes
|
Vineyards
|
Vineyard
sprayer's lung
|
Animal
proteins:
|
|
|
Chicken
proteins
|
Chicken
products
|
Feather
plucker's lung
|
Duck
proteins
|
Feathers
|
Duck
fever
|
Hair
proteins
|
Hairdust
|
Furrier's
lung
|
Hair
serum proteins
|
Hen
droppings
|
Hen
worker's lung
|
Pigeon
serum proteins
|
Pigeon
droppings
|
Pigeon
breeder's lung
|
Turkey
proteins
|
Turkey
products
|
Turkey
handler's lung
|
Arthropods:
|
|
|
Sitophilus
grainarius
|
Infested
wheat
|
Wheat
weevil lung
|
Unknown
antigens:
|
|
|
|
Cereal
grain
|
Grain
measurer's lung
|
|
Tobacco
plants
|
Tobacco
|
Who
is exposed to these dusts, and when?
Almost
any farmer, but especially livestock or grain farmers, is
likely to be exposed to dust consisting of bacterial and fungal
spores and their by-products. This dust will be released any
time a farmer is transporting or working with moldy animal
feed, but exposures are not likely to be threatening unless
the feed and farmer are enclosed in a barn, silo, or other
structure.
Section
II describes the two respiratory responses to spoiled fodder:
the hypersensitivity pneumonitis farmer's lung, and the toxic
organic dust syndrome (TODS). Either of these can occur from
any exposure to moldy feed. However, farmer's lung is most
typical of dairy farmers who are breaking open bales of hay
to feed or bed their barn-enclosed cattle. Acute farmer's
lung is thus seen most commonly in winter and spring, before
cattle are put out to pasture. Farmer's lung is more prevalent
in the north temperate zone.
TODS
is seen most commonly following preparation of a conventional
upright silo for mechanical unloading. After loading a silo,
farmers often place a plastic sheet over the silage, and then
add another foot or so of silage to hold this sheet in place.
This upper silage "cap" becomes grossly contaminated with
microorganisms as it dries. Before starting to feed out the
silage, a farmer must climb into the silo, pitch this contaminated
silage out of the silo, and lower the mechanical silage unloader
into place. High concentrations of microogranisms and their
by-products can be inhaled during this task. Farmers are also
commonly exposed to clouds of these dusts while shoveling
moldy grain in a barn or bin. How common are these dusts and
resulting respiratory diseases?
Disturbance
of spoiled plant material can produce spore clouds of very
high concentration: breaking open bales of hay in a confined
space, such as in a barn, has produced clouds of 1.6 x 109
spores/m3 of thermophilic actinomycetes. A person doing light
work in this setting may retain 7.5 x 105 spores/minute in
the lungs.' Concentrations of 4 x 109 viable spores/m3 have
been documented in silo openings (written communication, John
J. May, M.D., August 1985).
The
prevalence of resulting disease varies from study to study
and is difficult to interpret, but prevalence of farmer's
lung usually is well below 5% of the farming population (in
the United States, although higher in western England, Scotland,
and Finland). For example, 3.9% of one surveyed group of Wyoming
farmers and dairy producers gave a history typical of farmer's
lung.2 A population based survey of over 1400 Wisconsin farmers
yielded a 0.42% prevalence of confirmed clinical cases.3 Ten
percent of the surveyed population showed serum precipitins
to at least one farmer's lung antigen; the highest prevalence
was among dairy farmers with the largest farms and largest
herds. Some studies demonstrate that a much higher percentage
of the exposed population has developed antibodies. Why many
farmers with farmer's lung antibodies fail to develop clinical
disease is unknown.
TODS
resulting from exposure to spoiled plant material has only
recently been recognized as a response that is distinctive
from farmer's lung; much remains to be learned about this
syndrome. However, it probably is far more common than farmer's
lung or other illnesses associated with feed storage (such
as silo filler's disease). In fact, many cases previously
diagnosed as farmer's lung may have been TODS. In a study
of New York dairy farmers, 14 of 26 feed-related episodes
of respiratory illness were identified as TODS.
Inhalation
of organic dusts from spoiled plant material is thought to
produce two symptomatically similar, but pathologically distinctive,
respiratory responses: hypersensitivity pneumonitis and TODS.
Hypersensitivity pneumonitis, also called extrinsic allergic
alveolitis, goes by a number of agent-specific descriptive
names (see Table 1), including farmer's lung when resulting
from occupational exposure to spoiled plant material dusts
and occurring in farmers. TODS is sometimes called atypical
farmer's lung, silo unloader's disease, or pulmonary mycotoxicosis.
Since these two responses result from similar exposures and
present in similar fashion, they are often confused. Indeed,
much work still needs to be done to define the exact agents
inducing each biological response, and the specific mechanisms
involved in each type of response.
Farmer's
lung is an allergic response of the alveoli, which has variable
presentation depending on host factors and specific circumstances
of exposure to spoiled plant material. Illness covers a continuum
from acute reversible to chronic debilitating disease. Symptoms
of acute illness are observed four to eight hours following
exposure, with cough, dyspnea, fever and chills, myalgia,
and malaise.The acute illness subsides in two to five days,
and respiratory impairment resolves completely.
Continuous,
low-level exposure can cause chronic subacute illness with
weight loss, fatigue, and insidious onset of cough and dyspnea.
Lung impairment usually resolves completely if exposure ceases.
However, multiple acute attacks or chronic low-level exposure
can lead to irreversible, progressive lung damage that can
decrease total lung capacity and diffusion capacity. End stages
are similar to those of any chronic interstitial pulmonary
fibrosis, with death typically resulting from respiratory
insufficiency or corpulmonale.
Characteristic
physical findings include fine, crepitant rales in the lower
two-thirds of both lungs among many patients. Patients may
be cyanotic or hypoxemic. Laboratory findings in acute cases
may include leukocytosis, sometimes with eosinophilia. Pulmonary
function tests of acutely ill patients reveal decreased lung
volumes, small airways obstruction, and decreased carbon monoxide
diffusing capacity; PO2 may be decreased. Chest films may
show a finely nodular infiltrate in the lower two-thirds of
peripheral lung fields, but may also be clear. (See Fig. 3)
Chronic cases show a spectrum of abnormalities, including
pneumonitis, fibrosis, hyperexpansion, or honeycombing of
lungs. Serum precipitins to thermophilic actinomycetes are
characteristic of farmer's lung patients.
TODS
is thought to be a nonallergic, inflammatory reaction of small
airways and the alveoli possibly due to mycotoxins or endotoxins.
Clinically, acute cases present very much like acute farmer's
lung, with cough, fever and chills, fatigue, myalgia, and
anorexia occurring four to eight hours following exposure
to spoiled plant material. Severity varies from a mild, influenzalike
illness to profound illness with severe dyspnea. Symptoms
subside in two to five days, and resolve completely within
ten days. Chronic illness and presumably permanent lung damage
do not appear to occur. Multiple exposures simply produce
repeated acute illness. No deaths have been known to result
from this syndrome.
A number
of features differentiate acute farmer's lung and TODS. These
are summarized below. Farmer's lung
occurs in only a small subset of any exposed population. Although
predisposing factors must exist, these have not yet been defined.
Among sensitized farmers, even a small exposure to aerosolized
mold and bacteria can elicit an attack. TODS, in contrast,
can affect any exposed individual; thus cases often are clustered,
with several individuals in a given work situation being affected
simultaneously. However, exposure to decayed plant dusts must
be massive.
A number
of laboratory tests distinguish the two illnesses. Chest radiographs
of farmer's lung patients characteristically reveal a finely
nodular density in the lower lung fields, while chest radiographs
of TODS patients characteristically are clear (although occasionally
are abnormal). Blood gas measurements often show decreased
PO2 for farmer's lung, but usually no decrease for TODS. Immunoserology
of farmer's lung patients is positive, while TODS patients
do not typically have antibodies to thermophilic actinomycete
antigens. (Note, however, that TODS patients may have previously
developed these antibodies, and thus may demonstrate serum
precipitins to the thermophilic actinomycete antigens.) Pulmonary
function tests, although usually showing marked restriction
with farmer's lung, show mild or no restriction with TODS.
And, finally, bronchoalveolar lavage (which is done infrequently,
and primarily on an investigational basis) yields fluids rich
in Iymphocytes with farmer's lung, but dominated by leucocytes
with TODS, indicative of their respective pathologies.
Readers
also should note that a symptomatically similar toxic syndrome
can be caused among agricultural workers by exposure to moldy
plant material, grain dusts that are not necessarily mold-laden
(See Unit 3), cotton dust, and confinement house dusts (See
Unit 4). These similar responses, referred to collectively
as TODS, may or may not be pathologically identical .
Diagnosis
Because
presentation of farmer's lung is highly variable, no single
factor is diagnostic. Farmer's lung should be suspected in
any farmer with an influenza-like pneumonitis or active interstitial
lung disease. Normally, the following combination of factors
is sufficient for diagnosis: a typical presentation (symptoms
of cough, fever, and dyspnea, and possible basal crepitant
rales), following a history of exposure to decayed plant material
dusts, supported by positive serology to any of the 15 or
so fungal or thermophilic antinomycete antigens, an abnormal
chest radiograph revealing lung infiltrates, and abnormal
pulmonary function tests including restrictive changes and
impaired diffusing capacity. However, caution is required
for several reasons. Although the presentation and history
of exposure alone may be sufficient in acute cases, these
are not so helpful in subacute or chronic cases, where continuous
low level exposure may be difficult to identify and onset
of disease is insidious. And, although farmer's lung patients
demonstrate a positive serology, 10% or more of the farming
population may possess farmer's lung antibodies and only a
small number of these experience clinical illness. Also, care
must be taken to use an appropriate battery of farmer's lung
antigens. Both chest radiographs and pulmonary function tests
may be highly variable, and in some cases either or both may
be normal.
Lung
biopsy, lung lavage, and bronchoprovocation are not normally
required or advised, but may be useful in an exceptional case
when a specific diagnosis is needed (for example for workman's
compensation), or with a difficult differential diagnosis.
Lung biopsy in farmer's lung reveals a characteristic granulomatous
interstitial pneumonitis. (See Fig. 4) Gross thickening of
the alveolarcapillary membranes results from mononuclear infiltration
into interstitial tissues, resulting in obliteration of the
alveoli. Mononuclear cells often form noncaseating granulomata
that may occlude bronchioles. Multinucleated Langerhan's giant
cells and foreign body type cells that may be birefringent
or nonrefringent are common in areas of inflammation. Spores
of the causative molds usually are not recognized in tissues.
Lung
lavage, usually regarded as experimental, may be helpful in
ambiguous cases of interstitial lung disease, and demonstrate
an increase of Iymphocytes, an increase in T to B cell ratios
(as compared to peripheral blood), and an increase in IgG
and IgM (as compared to albumin).
Bronchoprovocation
by farmer's lung antigens has been proposed as a definitive
diagnostic test, but can involve significant risk and discomfort
to the patient and must be done with care in the hands of
experienced physicians.
Acute
farmer's lung can be misdiagnosed as influenza, a bad cold,
infectious pneumonia, or asthma. An occupational history and
the recurrent nature of farmer's lung are helpful in differentiating
it from these more common illnesses. Differentiation of most
cases of farmer's lung from asthma can be based on lack of
wheezing, presence of rales, an abnormal chest radiograph,
and pulmonary functions with decreased vital capacity, compliance,
and diffusing capacity (rather that reversible obstruction).
Acute
farmer's lung may easily be confused with TODS resulting from
the same exposure. Although presentation of acute farmer's
lung and TODS patients is nearly identical, the two illnesses
usually can be separated by considering those distinctions
outlined in Table 2: cases of TODS must follow massive exposures,
cases often are clustered, and most patients will not have
serum precipitins to farmer's lung antigens. There is no evidence
that TODS will progress to chronic disease.
Because
acute farmer's lung and TODS may result from exposure within
a silo, either may be confused as silo filler's disease resulting
from exposure to nitrous oxides (See Unit 5 ) However, this
latter disease can be traced to silos filled within the previous
two weeks with fresh silage.
Chronic
farmer's lung can be misdiagnosed as depression, chronic bronchitis,
or any chronic interstitial lung disease. Pulmonary sarcoid
may prove an especially difficult differential because of
histopathologic and other similarities to farmer's lung. Occupational
history and other history of exposure to spoiled plant material
are critical in establishing a diagnosis of chronic farmer's
lung. Lung lavage or bronchoprovocation may be helpful in
exceptional cases.
Treatment
There
is no specific treatment for farmer's lung or TODS. Removal
from the causative environment is usually self-imposed. Since
both TODS and acute farmer's lung are self-limiting, with
severe symptoms resolving in two to five days and complete
resolution occurring within 10 to 60 days, a physician's help
is often not solicited by afflicted persons. In severe cases
of acute farmer's lung, with extended duration or extreme
hypoxemia, supportive therapy (including oxygen and rehydration)
may be needed. Use of corticosteroids is thought to reverse
the acute course and shorten the duration of illness. Desensitization
is not effective; antibiotics, bronchodilators, and antihistamines
are ineffective.
Because
a small concentration of antigen can provoke illness in highly
sensitive individuals, and continued exposure can lead to
permanent impairment, avoidance of spoiled plant material
is imperative. Early diagnosis and avoidance are most important
in preventing irreversible lung damage.
Prevention
of exposure to spoiled plant materials is advisable for all
farmers; it is imperative for persons sensitized to farmer's
lung antigens. This may be accomplished by reducing mold growth
in feedstuffs. Capping silage with a plastic sheet held in
place by rocks or a heavy chain (rather than additional plant
material) reduces the mold and dust in the top layers of silage.
Switching to glass-lined, airtight silos (realizing that these
silos pose the health risk of asphyxiation) also will reduce
mold growth, but may be economically impossible for many farmers.
Grain and hay always should be stored when fully dried.
However,
elimination of microorganisms from stored fodder is impossible,
and thus techniques to prevent aerosolization and inhalation
of these particles should be adopted whenever possible. When
silo caps are removed, the top layer of silage can be wetted
down to prevent spore aerosolization; however, farmers often
do not bother to do so. Persons with a history of farmer's
lung should never uncap a silo or perform other tasks with
a high probability of exposure to massive quantities of plant
dusts. Workers uncapping a silo, shoveling grain, or working
with feed, especially in any enclosed space, should always
wear a certified dust respirator. This respirator should prevent
the inhalation of massive amounts of dusts from decayed plant
material necessary to cause TODS, and some evidence suggests
that spore inhalation is reduced sufficiently to prevent acute
farmer's lung in sensitized individuals. The respirator must
fit properly and must be properly maintained. In some cases,
highly sensitive individuals may need to wear a powered air
purifying respirator.(See Unit 9) Handling dusty fodder mechanically
in a manner that keeps the farmer distant from the fodder
is a desirable work practice, especially when the fodder is
in an enclosed space; the widespread acceptance of large round
bales that are transported by a tractor (instead of small,
square, hand-carried bales) has probably decreased exposure
to moldy hay.
Some
dairy farmers with a history of farmer's lung have successfully
managed their illness by wearing a respirator regularly and
by assigning jobs with the potential of exposure to mold to
other individuals. Other such farmers have undertaken more
dramatic steps to eliminate exposure to decayed plant materials,
including use of glass-lined, airtight silos, completely mechanizing
cattle feeding operations, and installing large ventilation
systems in the barn (oral communication, James Marx PhD, Feb
1985). Although very expensive, these latter measures have
allowed sensitized farmers to stay on the farm.
Monitoring
of patients with chronic or repeated acute attacks of farmer's
lung should focus on regular testing of pulmonary function
and chest radiographs, as well as physical examination and
history regarding dyspnea following exposure and on exertion.
Measurement of blood gases and exercise tolerance is helpful
in assessing impairment. If management and environmental control
measures do not prevent the recurrence of farmer's lung, and
if pulmonary evaluations indicate progressive respiratory
impairment, a farmer may have to leave the farm to prevent
permanent impairment.
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and Reproduction Information: Information in NASD does not represent
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NASD Review: 04/2002
The
National Dairy Database (1992)
|