Polytetrafluoroethylene Toxicosis in Recently Hatched Chickens (Gallus domesticus)

Abstract

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 sensitivity 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.

Polytetrafluoroethylene (PTFE) is a synthetic polymer that is useful for its thermal stability and lubricant (antistick) properties.¹¹ It is used in various products, including nonstick cookware, ironing board covers, and heat lamp bulbs. PTFE is most commonly marketed under the trade name Teflon.

Pet birds are susceptible to developing PTFE toxicosis.^1,6,9 Most of these cases have been due to overheated frying pans within the household. At temperatures above 280 °C, PTFE-coated surfaces begin to emit degradation products in the form of particulates and gas.^5,9 Subsequent inhalation of these by-products by birds can result in various clinical signs, including open-beak breathing, chirping, incoordination, lateral recumbency, convulsions, and death.¹¹ The most common pathologic lesion is severe, extensive, necrotizing and hemorrhagic pneumonitis and edema.¹⁰ The primary mechanism of injury is direct injury of type I pneumocytes and capillary endothelial cells by PTFE degradation products, allowing fluid and blood to leak into the airways.¹⁰ Although PTFE toxicosis has been reported infrequently in humans as ‘polymer fume fever,’ birds are much more sensitive to inhaled toxicants. This unique sensitivity of birds is due to the anatomy of their respiratory system. Most birds have 9 air sacs (with some species-dependent variations) surrounding the lungs.⁴ The lungs are very rigid and do not expand; instead, the air sacs act as a bellows to ventilate the lungs, which are the site of gas exchange.⁴ Due to this structural arrangement, airflow within the avian respiratory system is unidirectional. Gas exchange occurs in the lungs as a cross-current system.⁴ Specifically, this situation means that air passing through the parabronchi and blood moving through the capillaries travel at right angles to each other.⁴ This arrangement allows for very efficient gas exchange as carbon dioxide and oxygen pressure gradients are preserved along the length of the connection between the parabronchus and capillary sytem.⁴ However, other gases (for example, PTFE degradation products, carbon monoxide) that are contained in the inhaled air will also be present at increased levels with oxygen. If the gas is toxic, this increased concentration will lead to significant respiratory compromise, resulting in hypoxia and associated hepatic damage.

Case Report

Two groups of chickens (Gallus domesticus; White Leghorn; ages, 4 d and 2 wk) were reported because of acute moribundity and death to the veterinary staff at an AAALAC-accredited academic institution. Moribund birds were lethargic and in respiratory distress with open-beak breathing. The birds had last been observed 8 h previously and appeared normal. The overall mortality rates, including birds found dead and those euthanized due to respiratory distress, were 92.3% (60 of 65 birds) for the 4-d-old birds and 80% (8 of 10) for the 2-wk-old birds. A similar clinical picture had been observed with the previous 2 groups of chicks housed within the room (2 wk and 1.5 mo previously), with sudden-onset 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 Manufacturing, 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 brooders 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 compartments 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; treatment and control groups were equally represented in the presentation of sudden death and respiratory distress. The animal housing room was temperature-controlled, with a humidity of 15% to 40% and more than 10 air changes hourly. The birds received ad libitum a commercial diet (Laboratory Chick Diet SG, PMI International, St Louis, MO) mixed with a small amount of grit (Chicken Grit, NC Granite, Indianapolis, IN) and unlimited access to municipal water through a plastic poultry waterer (Little Giant 1-quart waterer, Miller Manufacturing, Glencoe, MN).

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 distance was directly related to age (younger birds were closer to the heat lamp and older birds were farther from the lamp). An individual temperature probe was located in each compartment to ensure appropriate temperature at animal level.

Moribund animals were euthanized, and necropsies were performed on 7 of the 4-d-old and 4 of the 2-wk-old birds. The gross lesions seen on necropsy included mild to moderate dehydration as evidenced by sharp angles on the leg shanks (tibiotarsi), thin digits, pasty to dry crop contents, and pasty feces on the vents in the 2-wk-old birds. Crops were full or partially full. The 4-d-old birds showed mild to moderate dehydration and mild hepatic 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 dehydration was considered a nonspecific sign of illness. The histopathologic lesions seen included pulmonary hemorrhage and edema in the 2-wk-old group (4 of 4 birds); pulmonary hemorrhage (7 of 7 birds; Figure 2 A through C); and multifocal hepatic centrilobular necrosis (1 of 7 birds) in the 4-d-old group (Figure 2 D). The findings of pulmonary hemorrhage and edema in view of the acute clinical history were most consistent with an inhaled environmental toxicant, whereas hepatic centrilobular necrosis was most consistent with a period of hypoxia.

Figure 2.

Histopathology images. (A) Lung. The majority of airways contained large amounts of hemorrhage. A primary bronchus was almost completely 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 hemorrhage 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.

Acute infectious diseases also were considered as differential diagnoses, but infectious poultry diseases occurring peracutely across different age groups are not common. There was no evidence of omphalitis (colibacillosis, salmonellosis) in the 4-d-old group.³ Acute virulent respiratory illnesses with respiratory hemorrhage such as highly pathogenic avian influenza or velogenic Newcastle disease (avian paramyxovirus) are unlikely in commercial source birds in a laboratory setting.³

Environmental and management issues were investigated. The following management parameters were verified to be within appropriate limits for avian species: room temperature and humidity and incubator temperature, humidity, and airflow. There was no history of unusual construction activity in the area or inappropriate use of cleaning or disinfectant products. Consultation with several poultry veterinarians brought to our attention that many commercially available heat lamp bulbs now are coated with PTFE. Discussion with the husbandry staff revealed that, for safety reasons, shatter-proof heat lamp bulbs had been purchased within the past 6 mo. Examination of the bulbs present in the animal room showed that approximately 50% of the heat lamp bulbs in the room at the time of the presenting incident were PTFE-coated, shatter-proof bulbs. All of these bulbs were replaced with noncoated bulbs. No similar problems have been identified in subsequent groups of chicks.

Discussion

This case involved a relatively common avian toxicosis—attributed to a lesser known environmental hazard—in a research setting. Overheating of nonstick cookware is a known cause of PTFE toxicosis in avian species and has often been reported anecdotally in pet birds in the veterinary clinical literature.^1,6,9-11 PTFE toxicosis due to heat-lamp bulbs has been a less common occurrence but may begin to increase in frequency, given that the US Food and Drug Administration now requires the use of PTFE-coated heat-lamp bulbs in the food service industry, to prevent shattering. A few companies do still manufacture noncoated bulbs.

PTFE toxicosis in birds due to heat lamp bulbs has been described in at least 2 case reports.^2,7 The first case involved multiple species of birds housed outdoors at a zoo;⁷ heat-lamp bulbs had been placed due to weather conditions, and 21 birds died over a 7-d period, with no deaths on windy nights (increased ventilation). The only reported gross lesions were pulmonary trauma. The heat-lamp bulbs were discovered to be PTFE-coated. The second case occurred in chickens housed indoors at a poultry research facility.² An increased mortality rate, eventually peaking at 52%, was noted in comparison to historic averages. Gross lesions were pulmonary congestion and oronasal hemorrhage; histologic lesions were pulmonary edema and congestion. The mortality rate decreased significantly (to 11%) when the ventilation rate was increased. Heat lamp bulbs in the facility had recently been replaced with PTFE-coated bulbs. The authors² speculated that the lack of pulmonary hemorrhage in that instance, compared with that in nonstick cookware cases, might have been due to fewer pyrolysis products with heat-lamp bulbs. Pyrolysis in nonstick cookware is reported to occur at a temperature of 280 °C,⁵ whereas the surface of the coated bulbs was found to reach approximately 202 °C.² In our current case, the PTFE-coated bulbs were introduced into the room slowly and reached a maximum of 3 of 6 bulbs. Distance from the bulbs, duration of exposure, ventilation, and number of bulbs in the room may contribute to the variations in mortality in cases of heat lamp-associated PTFE-toxicosis.

PTFE toxicosis can occur in humans, although it is not seen as frequently as in exposed birds because of the anatomic differences mentioned earlier.^1,6,8,9 The condition in humans is known as polymer fume fever and usually consists of flu-like symptoms and noncardiogenic pulmonary edema.⁶ Most cases occur during the manufacture of PTFE, but one report involved a kitchen accident.¹ However, the subject in that case report¹ may already have had compromised lung function due to a history of smoking. Even though clinical signs in humans are rare, PTFE degradation products can be toxic and should be considered a hazard.⁸

The current case illustrates 2 important points. First, different species can vary markedly in their susceptibility to various toxicants. In the present report, that variation is due to anatomic differences. Second, in cases of acute death in a large number of animals within the same room, the environment should be examined thoroughly, and personnel should be questioned carefully. These evaluations were pivotal in the resolution of the current case, which provides a reminder that toxicosis can occur even in the controlled environment of a laboratory vivarium.