Comparative Medicine Vol 62, No 1

Copyright 2012 February 2012

by the American Association for Laboratory Animal Science Pages 49–52

Case Report

Polytetrafluoroethylene Toxicosis in Recently

Hatched Chickens (Gallus domesticus)

Katherine A Shuster,1,* Kristie L Brock,3 Robert C Dysko,1 Victor J DiRita,1,2 and Ingrid L Bergin1

Two groups of chickens (Gallus domesticus; White Leghorn; age, 4 d and 2 wk) housed in a university research vivarium were
found dead or moribund without prior signs of illness. The overall mortality rates were 92.3% (60 of 65 birds) for the 4-d-old birds
and 80% (8 of 10) for the 2-wk-old birds. All chicks were housed in brooders with heat lamps in a temperature- and humidity-
controlled room. Primary gross findings were mild to moderate dehydration and hepatic lipidosis. The most consistent histologic
findings were pulmonary hemorrhage and edema in all 7 of the 4-d-old birds evaluated and in all 4 of the 2-wk-old birds assessed.
In addition, 1 of the 4-d-old birds had multifocal centrilobular hepatic necrosis. These findings suggested an inhaled toxicant and
hypoxia, respectively. Inspection of the animal room revealed that approximately 50% of the heat lamp bulbs in the brooder cage
were coated with polytetrafluoroethylene (PTFE). Two published case reports detail similar experiences in birds exposed to PTFE-
coated heat-lamp bulbs. Birds are highly sensitive to inhaled toxicants owing to the high efficiency of their respiratory systems, and
PTFE toxicosis is known to cause pulmonary edema and hemorrhage in pet birds after exposure to overheated nonstick cookware.
In the present case, the bulbs were replaced, and no similar problems subsequently have been noted. This case illustrates the sen-
sitivity of avian species to respiratory toxicants and serves as a reminder that toxicosis can be encountered even in the controlled
environment of a laboratory vivarium.

Abbreviation: PTFE, polytetrafluoroethylene.

Polytetrafluoroethylene (PTFE) is a synthetic polymer that is to ventilate the lungs, which are the site of gas exchange. 4 Due
useful for its thermal stability and lubricant (antistick) proper- to this structural arrangement, airflow within the avian respira-
ties.11 It is used in various products, including nonstick cookware, tory system is unidirectional. Gas exchange occurs in the lungs
ironing board covers, and heat lamp bulbs. PTFE is most com- as a cross-current system.4 Specifically, this situation means that
monly marketed under the trade name Teflon. air passing through the parabronchi and blood moving through
Pet birds are susceptible to developing PTFE toxicosis.1,6,9 Most the capillaries travel at right angles to each other.4 This arrange-
of these cases have been due to overheated frying pans within the ment allows for very efficient gas exchange as carbon dioxide
household. At temperatures above 280 °C, PTFE-coated surfaces and oxygen pressure gradients are preserved along the length of
begin to emit degradation products in the form of particulates the connection between the parabronchus and capillary sytem.4
and gas.5,9 Subsequent inhalation of these by-products by birds However, other gases (for example, PTFE degradation products,
can result in various clinical signs, including open-beak breathing, carbon monoxide) that are contained in the inhaled air will also
chirping, incoordination, lateral recumbency, convulsions, and be present at increased levels with oxygen. If the gas is toxic, this
death.11 The most common pathologic lesion is severe, extensive, increased concentration will lead to significant respiratory com-
necrotizing and hemorrhagic pneumonitis and edema.10 The pri- promise, resulting in hypoxia and associated hepatic damage.
mary mechanism of injury is direct injury of type I pneumocytes
and capillary endothelial cells by PTFE degradation products, al-
Case Report
lowing fluid and blood to leak into the airways.10 Although PTFE
Two groups of chickens (Gallus domesticus; White Leghorn; ages,
toxicosis has been reported infrequently in humans as ‘polymer
4 d and 2 wk) were reported because of acute moribundity and
fume fever,’ birds are much more sensitive to inhaled toxicants.
death to the veterinary staff at an AAALAC-accredited academic
This unique sensitivity of birds is due to the anatomy of their
institution. Moribund birds were lethargic and in respiratory dis-
respiratory system. Most birds have 9 air sacs (with some species-
tress with open-beak breathing. The birds had last been observed
dependent variations) surrounding the lungs.4 The lungs are very
8 h previously and appeared normal. The overall mortality rates,
rigid and do not expand; instead, the air sacs act as a bellows
including birds found dead and those euthanized due to respi-
ratory distress, were 92.3% (60 of 65 birds) for the 4-d-old birds
Received: 15 Aug 2011. Revision requested: 20 Sep 2011. Accepted: 09 Oct 2011. and 80% (8 of 10) for the 2-wk-old birds. A similar clinical picture
1
Unit for Laboratory Animal Medicine and 2Department of Microbiology and Immunology,
University of Michigan, Ann Arbor, Michigan; 3Office of Laboratory Animal Resources,
had been observed with the previous 2 groups of chicks housed
West Virginia University, Morgantown, West Virginia. within the room (2 wk and 1.5 mo previously), with sudden-onset
*
Corresponding author. Email: [email protected]

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Comparative Medicine
February 2012

respiratory distress and death in 49% (49 of 100) of birds at 1 to

2 d of age. Gross necropsies were performed on a representative
number of birds in both age groups, but histopathology was not
performed on lung tissue at that time.
The birds had been purchased as fertilized eggs (SPF for 25
viral and 6 bacterial agents) from a commercial supplier (Charles
River Laboratories International, Franklin, CT). They had been
incubated and hatched in a commercial incubator (GQF Manu-
facturing, Savannah, GA) within the animal housing room. The
hatch rate of the birds in the presenting instances was 83% for the
4-d-old birds and 88% for the older group. Hatched birds were
housed according to age in heated brooders within the same
animal housing room (Figure 1). Temperature within the brood-
ers ranged from 85 to 99 °F (24.9 to 37.2 °C), depending on the
age of the birds. The chicks were further divided into compart-
ments within the brooder based on experimental group. These
birds were part of an IACUC-approved study investigating the
pathogenesis of Campylobacter jejuni within the intestinal tract.
Birds were gavaged at 24 h of age with either saline or C. jejuni; Figure 1. Typical brooder set-up for chicks in this report. The birds were
divided based on both age and experimental group. The heat lamp dis-
treatment and control groups were equally represented in the
tance was directly related to age (younger birds were closer to the heat
presentation of sudden death and respiratory distress. The ani- lamp and older birds were farther from the lamp). An individual tem-
mal housing room was temperature-controlled, with a humidity perature probe was located in each compartment to ensure appropriate
of 15% to 40% and more than 10 air changes hourly. The birds temperature at animal level.
received ad libitum a commercial diet (Laboratory Chick Diet SG,
PMI International, St Louis, MO) mixed with a small amount of
appropriate use of cleaning or disinfectant products. Consultation
grit (Chicken Grit, NC Granite, Indianapolis, IN) and unlimited
with several poultry veterinarians brought to our attention that
access to municipal water through a plastic poultry waterer (Little
many commercially available heat lamp bulbs now are coated
Giant 1-quart waterer, Miller Manufacturing, Glencoe, MN).
with PTFE. Discussion with the husbandry staff revealed that,
Moribund animals were euthanized, and necropsies were per-
for safety reasons, shatter-proof heat lamp bulbs had been pur-
formed on 7 of the 4-d-old and 4 of the 2-wk-old birds. The gross
chased within the past 6 mo. Examination of the bulbs present
lesions seen on necropsy included mild to moderate dehydration
in the animal room showed that approximately 50% of the heat
as evidenced by sharp angles on the leg shanks (tibiotarsi), thin
lamp bulbs in the room at the time of the presenting incident were
digits, pasty to dry crop contents, and pasty feces on the vents in
PTFE-coated, shatter-proof bulbs. All of these bulbs were replaced
the 2-wk-old birds. Crops were full or partially full. The 4-d-old
with noncoated bulbs. No similar problems have been identified
birds showed mild to moderate dehydration and mild hepatic
in subsequent groups of chicks.
lipidosis. No specific signs of infectious disease were evident
grossly in either age group. Hepatic lipidosis in the 4-d-old birds
was considered within normal limits for the age group, and de- Discussion
hydration was considered a nonspecific sign of illness. The his- This case involved a relatively common avian toxicosis—attrib-
topathologic lesions seen included pulmonary hemorrhage and uted to a lesser known environmental hazard—in a research set-
edema in the 2-wk-old group (4 of 4 birds); pulmonary hemor- ting. Overheating of nonstick cookware is a known cause of PTFE
rhage (7 of 7 birds; Figure 2 A through C); and multifocal hepatic toxicosis in avian species and has often been reported anecdotally
centrilobular necrosis (1 of 7 birds) in the 4-d-old group (Figure in pet birds in the veterinary clinical literature.1,6,9-11 PTFE toxicosis
2 D). The findings of pulmonary hemorrhage and edema in view due to heat-lamp bulbs has been a less common occurrence but
of the acute clinical history were most consistent with an inhaled may begin to increase in frequency, given that the US Food and
environmental toxicant, whereas hepatic centrilobular necrosis Drug Administration now requires the use of PTFE-coated heat-
was most consistent with a period of hypoxia. lamp bulbs in the food service industry, to prevent shattering. A
Acute infectious diseases also were considered as differential few companies do still manufacture noncoated bulbs.
diagnoses, but infectious poultry diseases occurring peracutely PTFE toxicosis in birds due to heat lamp bulbs has been de-
across different age groups are not common. There was no evi- scribed in at least 2 case reports.2,7 The first case involved multiple
dence of omphalitis (colibacillosis, salmonellosis) in the 4-d-old species of birds housed outdoors at a zoo;7 heat-lamp bulbs had
group.3 Acute virulent respiratory illnesses with respiratory hem- been placed due to weather conditions, and 21 birds died over a
orrhage such as highly pathogenic avian influenza or velogenic 7-d period, with no deaths on windy nights (increased ventila-
Newcastle disease (avian paramyxovirus) are unlikely in com- tion). The only reported gross lesions were pulmonary trauma.
mercial source birds in a laboratory setting.3 The heat-lamp bulbs were discovered to be PTFE-coated. The
Environmental and management issues were investigated. The second case occurred in chickens housed indoors at a poultry re-
following management parameters were verified to be within search facility.2 An increased mortality rate, eventually peaking at
appropriate limits for avian species: room temperature and hu- 52%, was noted in comparison to historic averages. Gross lesions
midity and incubator temperature, humidity, and airflow. There were pulmonary congestion and oronasal hemorrhage; histologic
was no history of unusual construction activity in the area or in- lesions were pulmonary edema and congestion. The mortality

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 PTFE toxicosis in recently hatched chickens

Figure 2. Histopathology images. (A) Lung. The majority of airways contained large amounts of hemorrhage. A primary bronchus was almost com-
pletely filled with blood (arrow). Hematoxylin and eosin stain; bar, 1 mm. (B) Lung. Some areas also showed moderate perivascular edema (arrow).
Hematoxylin and eosin stain; bar, 200 µm. (C) Lung. Multifocal fibrin, platelets, and hemorrhage within an airway (arrow), indicating that the hemor-
rhage observed in the lungs occurred before death. Hematoxylin and eosin stain; bar, 50 µm. (D) Liver. Multifocal centrilobular or paracentral necrosis
with congestion and hemorrhage (arrows), indicating hypoxia. Hematoxylin and eosin stain; bar, 1 mm.

rate decreased significantly (to 11%) when the ventilation rate mer fume fever and usually consists of flu-like symptoms and
was increased. Heat lamp bulbs in the facility had recently been noncardiogenic pulmonary edema.6 Most cases occur during the
replaced with PTFE-coated bulbs. The authors2 speculated that manufacture of PTFE, but one report involved a kitchen accident.1
the lack of pulmonary hemorrhage in that instance, compared However, the subject in that case report1 may already have had
with that in nonstick cookware cases, might have been due to compromised lung function due to a history of smoking. Even
fewer pyrolysis products with heat-lamp bulbs. Pyrolysis in non- though clinical signs in humans are rare, PTFE degradation prod-
stick cookware is reported to occur at a temperature of 280 °C,5 ucts can be toxic and should be considered a hazard.8
whereas the surface of the coated bulbs was found to reach ap- The current case illustrates 2 important points. First, differ-
proximately 202 °C.2 In our current case, the PTFE-coated bulbs ent species can vary markedly in their susceptibility to various
were introduced into the room slowly and reached a maximum toxicants. In the present report, that variation is due to anatomic
of 3 of 6 bulbs. Distance from the bulbs, duration of exposure, differences. Second, in cases of acute death in a large number of
ventilation, and number of bulbs in the room may contribute to animals within the same room, the environment should be exam-
the variations in mortality in cases of heat lamp-associated PTFE- ined thoroughly, and personnel should be questioned carefully.
toxicosis. These evaluations were pivotal in the resolution of the current
PTFE toxicosis can occur in humans, although it is not seen as case, which provides a reminder that toxicosis can occur even in
frequently as in exposed birds because of the anatomic differences the controlled environment of a laboratory vivarium.
mentioned earlier.1,6,8,9 The condition in humans is known as poly-

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February 2012

Acknowledgments 5. Griffith FD, Stephens SS, Tayfun FO. 1973. Exposure of Japanese
We thank Michael Martin, DVM, MPVM, DACPV, and John Barnes, quail and parakeets to the pyrolysis products of fry pans coated with
DVM, PhD, DACVP, DACPV (North Carolina State University) as well Teflon and common cooking oils. Am Ind Hyg Assoc J 34:176–178.
as Richard Fulton, DVM, PhD, DACPV, and Darrin Karcher, PhD 6. Lightfoot TL, Yeager JM. 2008. Pet bird toxicity and related environ-
(Michigan State University) for their assistance with this case. mental concerns. Vet Clin North Am Exot Anim Pract 11:229–259.
7. Richardson M. 1991. Teflon toxicity from heat lamps. J Assoc Avian
Vet 5:192.
References 8. Waritz RS. 1975. An industrial approach to evaluation of pyrolysis
1. Blandford TB, Seamon PJ, Hughes R, Pattison M, Wilderspin and combustion hazards. Environ Health Perspect 11:197–202.
MP. 1975. A case of polytetrafluoroethylene poisoning in cocka- 9. Wells RE. 1983. Fatal toxicosis in pet birds caused by an overheated
tiels accompanied by polymer fume fever in the owner. Vet Rec cooking pan lined with polytetrafluoroethylene. J Am Vet Med Assoc
96:175–178. 182:1248–1250.
2. Boucher M, Ehmler TJ, Bermudez AJ. 2000. Polytetrafluoroethylene 10. Wells RE, Slocombe RF. 1982. Acute toxicosis of budgerigars (Melop-
gas intoxication in broiler chickens. Avian Dis 44:449–453. sittacus undulatus) caused by pyrolysis products from heated poly-
3. Charlton BR, Bermudez AJ; American Association of Avian tetrafluoroethylene: microscopic study. Am J Vet Res 43:1243–1248.
Pathologists. 2000. Avian disease manual. Kennett Square (PA): 11. Wells RE, Slocombe RF, Trapp AL. 1982. Acute toxicosis of bud-
American Association of Avian Pathologists. gerigars (Melopsittacus undulatus) caused by pyrolysis products
4. Fedde MR. 1998. Relationship of structure and function of the avian from heated polytetrafluoroethylene: clinical study. Am J Vet Res
respiratory system to disease susceptibility. Poult Sci 77:1130–1138. 43:1238–1242.

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