Many pet owners, breeders and pet retailers favor wood chips as pet
bedding for a variety of reasons. Most wood chips are inexpensive and
depending on the wood used, wood chips can provide natural
insecticidal, bactericidal or bacteriostatic properties. Such bedding
can often kill or inhibit the spread of fleas, mites or other pests,
and the resins and other aromatic chemicals emitted by the chips help
to control pet odors. With all of these advantages, pet stores often
sell prepackaged starter kits for housing small pets complete with a
supply of wood chips for bedding. Many people have used cedar and pine
chips as bedding for these reasons. Wood from western red cedar
(Thuja plicata) has one of the most potent insecticidal
compounds, which accounts for its popularity to repel or kill clothes'
moths.
Although wood chips may provide a natural means of insect
and odor control, "natural" does not always mean safe. These same
chemicals can also damage the respiratory tract, causing chronic
respiratory disease, and asthma, and some studies have found an
association between exposure to some wood dusts and oral cancers. The
scientific literature on this topic is extremely clear, and unlike many
studies of toxins, most of the scientific evidence regarding wood dust
exposure has been conducted in humans rather than in laboratory animals
since so many people work in the production of wood products. The
summary of the biomedical literature that follows primarily describes
the effect of chronic cedar- and pine-wood exposure on humans. Keep in
mind that the effect on small mammals is likely to be even more
pronounced, especially if they are in close, continual contact with
wood chips. Humans also have a relatively poor sense of smell compared
with other mammals. Thus, a nasal or respiratory irritant is much more
likely to harm small mammals, which rely on smell for locating food and
identifying and interacting with other animals.
The primary
irritant in cedar is plicatic acid and western
red cedar
contains the highest concentrations although eastern white cedar (Thuja
occidentalis) and Japanese cedar (Cryptomeria japonica) also
contain it. Exposure to plicatic acid can cause or exacerbate asthma,
rhinitis or conjunctivitis in humans and in animals, and the damage can
be progressive. Asthmatics who are continuously exposed to cedar, such
as in a lumber mill, experience deterioration in their asthma over
time. In pine (family Pinaceae), the primary
irritant
identified is
abietic acid, sometimes called sylvic acid.
Pine
products also include pine resin, also known as
rosin or colophony, which is known to pool players and mountain
climbers. Pine resin is also used in adhesives, paints and varnishes,
inks
and in sizing
for paper, paperboard and fabrics (Sadhra 1994). Abietic acid itself
elicits relatively weak allergic responses, however, a number of
compounds formed by air oxidation of abietic acid are potent contact
allergens (Hausen 1989, Karlberg 1988).
Plicatic acid has been
shown to cause an array of pathological changes consistent with
inflammatory and allergic reactions. However, no one knows the
mechanism by which plicatic acid induces these changes, which include
increased concentrations of eosinophils, immunoglobulin E (IgE),
T-cells, histamine and leukotrienes--substances known to increase
inflammation in conditions such as multiple organ failure following
surgery and acute respiratory distress syndrome (Frew 1995, Chan-Yeung
1994, Salari 1994). The overall increase in IgE concentrations found
in humans with red- cedar asthma (Frew 1995, Paggiaro 1987) indicates
an overall sensitization of the immune system to a foreign substance.
Similar increases in IgE levels also accompany allergic reactions and
parasitic infections. Allergists and immunologists refer to this
immediate immune response as a type-I hypersensitivity reaction. Humans
can also exhibit a delayed reaction to red cedar or plicatic acid
exposure--also known as a type-IV hypersensitivity reaction, which is the
type of response seen in tuberculin skin tests in humans. Following
exposure to red cedar or plicatic acid, a person with occupational
asthma may have either an immediate, or a delayed reaction, or both
(Malo 1989).
Long-term exposure to red cedar or pine in humans can lead to a
decrease in forced expiratory volume, or FEV, a measure of lung
capacity and ability to breathe freely (Shamssain 1992, Cote 1990, Malo
1989). Plicatic and abietic acids can both cause destruction and
desquamation, or sloughing, of alveolar, tracheal and bronchial
epithelial cells (Ayars 1989).
Among the known causes of
occupational asthma, red cedar has a significant impact compared with
most other occupational exposures. One study compared four groups of
employees who worked at jobs that exposed them to respiratory
irritants: cedar sawmill, paper pulpmill, grain elevator and aluminum
smelter workers. The sawmill workers had the highest overall prevalence
of asthma compared with a control group of persons without any
occupational respiratory exposure (Siracusa 1995). Studies of workers
exposed to pine dust also show that such work is associated with
significantly more respiratory symptoms and a greater risk of airflow
obstruction (Shamssain 1992), and the results of a German study
indicate that workers exposed to pine dust had more than a three-fold
increased risk of glottal cancer (relative risk = 3.18, 95% confidence
interval: 1.1-9.0) (Maier 1992).
In humans, occupational exposure
to cedar leads to asthma in 50% of more of wood, paper and pulp mill
workers (Malo 1994, Rosenberg 1989). One might expect that longer
exposure to cedar or pine dust would result in worse or more persistent
respiratory symptoms, but that is not clear from various studies. Some
researchers report just that among timber workers with occupational
asthma who remain exposed to wood dust (Rosenberg 1989). In contrast, a
large study of British Columbia cedar sawmill workers found that
physician diagnoses of asthma or respiratory symptoms were not
associated with work duration or the amount of dust to which the
workers were exposed (Vedal 1986, vol. 41).
Can asthma caused by
exposure to wood products be reversed? In the studies of occupational
asthma among sawmill workers, the condition vanishes in 50% or fewer
cases when exposure stops. The remaining individuals experience
intermittent attacks or continued chronic airway restriction that can
persist for years or indefinitely (Choubrac 1991, Rosenberg 1989,
Newman-Taylor, 1988). In the British Columbia sawmill workers,
researchers reported the health status of 17 patients with occupational
asthma due to red cedar who had been removed from exposure for at least
one year. Seven patients became asymptomatic but 10 (59%) required
continued treatment for asthma (Chan-Yeung 1988). In another group of
136 sawmill workers with cedar-induced asthma who had left the
industry, only 55 (40%) recovered completely and 81 (60%) had continued
asthma attacks of varying severity (Chan-Yeung 1987). In one
experimental study, bronchial hypersensitivity lasting two weeks was
observed after an individual with red-cedar asthma received a single
exposure to plicatic acid (Cartier 1986, vol. 78).
What happens to
asthmatics if they continue to be exposed? Another study of the
British Columbian sawmill workers followed 48 of the workers with
asthma who remained on the job. Although 10% of the patients improved,
none of them recovered, 62% remained stable and 38% got worse (Cote
1990). Thus, it seems imperative that an individual with cedar- or
pine-induce asthma be removed from exposure for any possibility of
recovery, and that the recovery occurs among humans only in half of all
cases at best. The probability of recovery is likely to be lower for
small mammals.
Address queries or additional information to: j.p.johnston@worldnet.att.net
REFERENCES
Ando Y. Breeding control and immobilizing effects of wood
microingredients on house dust mites. [Japanese] Nippon Koshu Eisei
Zasshi 1994;41:741-50.
Ando Y. Repellent effect of wood
odors on mites. [Japanese] Nippon Koshu Eisei Zasshi
1993;40:571-4.
Ayars GH, Altman LC, Frazier CE, Chi EY. The
toxicity of constituents of cedar and pine woods to pulmonary
epithelium. J Allergy Clin Immunol 1989;83:610-8.
Cartier A, Chan H, Malo JL, Pineau L, Tse KS, Chan-Yeung M.
Occupational asthma caused by eastern white cedar (Thuja
occidentalis) with demonstration that plicatic acid is present in
this wood dust and is the causal agent. J Allergy Clin Immunol
1986;77:639-45.
Cartier A, L'Archeveque J, Malo JL. Exposure
to a sensitizing occupational agent can cause a long- lasting increase
in bronchial responsiveness to histamine in the absence of significant
changes in airway caliber. J Allergy Clin Immunol
1986;78:1185-9.
Chaen T, Watanabe N, Mogi G, Mori K,
Takeyama M. Substance P and vasoactive intestinal peptide in nasal
secretions and plasma from patients with nasal allergy. Ann Otol Rhinol
Laryngol 1993;102:16-21.
Chan-Yeung M. Mechanism of
occupational asthma due to western red cedar (Thuja plicata).
Am J Ind Med 1994;25:13-8.
Chan-Yeung M, Desjardins
A. Bronchial hyperresponsiveness and level of exposure in occupational
asthma due to western red cedar (Thuja plicata). Am Rev
Respir Dis 1992;146:1606-9.
Chan-Yeung M, Chan H, Tse
KS, Salari H, Lam S. Histamine and leukotrienes release in
bronchoalveolar fluid during plicatic acid-induced
bronchoconstriction. J Allergy Clin Immunol 1989;84:762-8.
Chan-Yeung M, Leriche J, Maclean L, Lam S. Comparison of cellular and
protein changes in bronchial lavage fluid of symptomatic and
asymptomatic patients with red cedar asthma of follow-up examination.
Clin Allergy 1988;18:359-65.
Chan-Yeung M, MacLean
L, Paggiaro PL. Follow-up study of 232 patients with occupational
asthma caused by western red cedar (Thuja plicata). J Allergy
Clin Immunol 1987;79:792-6.
Chan-Yeung M, Vedal S, Kus
J, McLean L, Enarson D, Tse KS. Symptoms, pulmonary function, and
bronchial hyperreactivity in western red cedar workers compared with
those in office workers. Am Rev Respir Dis
1984;130:1038-41.
Choubrac P. Occupational asthma: Current
and future perspectives. The point of view of an expert. [French]
Bull Acad Natl Med 1991;175:703-12; discussion 712-5.
Cockcroft DW, Hoeppner VH, Werner GD. Recurrent nocturnal asthma
after bronchoprovocation with western red cedar sawdust: Association
with acute increase in non-allergic bronchial responsiveness. Clin
Allergy 1984;14:61-8.
Cote J, Kennedy S, Chan-Yeung M.
Quantitative versus qualitative analysis of peak expiratory flow in
occupational asthma. Thorax 1993;48:48-51.
Cote J,
Kennedy S, Chan-Yeung M. Sensitivity and specificity of PC20 and peak
expiratory flow rate in cedar asthma. J Allergy Clin Immunol
1990;85:592-8. Comments in: J Allergy Clin Immunol
1991;87:600 and 1991;88:424
Cote J, Kennedy S, Chan-Yeung M. Outcome of patients with asthma with
continuous exposure. Am Rev Respir Dis 1990;141:373-6.
Frew AJ, Chan H, Lam S, Chan-Yeung M. Bronchial inflammation in
occupational asthma due to western red cedar. Am J Respir Crit Care
Med 1995;151:340-4.
Frew A, Chan H, Dryden P, Salari H,
Lam S, Chan-Yeung. Immunologic studies of the mechanisms of
occupational asthma caused by western red cedar. J Allergy Clin
Immunol 1993;92:466-78.
Goldsmith DF, Shy CM. An
epidemiologic study of respiratory health effects in a group of North
Carolina furniture workers. J Occup Med 1988;30:959-65.
Goldsmith DF, Shy CM. Respiratory health effects from occupational
exposure to wood dusts. Scan J Work Environ Health
1988;14:1-15.
Grammer LC, Patterson R. Occupational
immunologic lung disease. Ann Allergy 1987;58:151-9.
Lagier F, Cartier A, Malo JL. Medico-legal statistics on occupational
asthma in Quebec between 1986 and 1988. [French] Rev Mal Respir
1990;7:337-41.
Hausen BM, Kreuger A, Mohnert J, Hahn H,
Konig WA. Contact allergy due to colophony (III). Sensitizing potency
of resin acids and some related products. Contact Dermatitis
1989;20:41-50. Comments: Contact Dermatitis
1989;21:282-5.
Karlberg AT. Contact allergy to colophony.
Chemical identifications of allergens, sensitization experiments and
clinical experience. Acta Derm Venereol 1988;139:1-43.
Krzanowski JJ. Natural products and bronchial asthma. J Fla Med
Assoc 1994;81:357-8.
Lin FJ, Chen H, Chan-Yeung M. New
method for an occupational dust challenge test. Occup Environ
Med 1995;52:54-6.
Maier H, Gewelke U, Deitz A, Thamm H,
Heller WD, Weidauer H. Laryngeal cancer and occupation--Results of the
Heidelberg laryngeal cancer study [German]. HNO
1992;40:44-51.
Maciejewska A, Wojtczak J,
Bielichowska-Cybula G, Domanska A, Dutkiewicz J, Molocznik A.
Biological effect of wood dust. [Polish] Med Pr
1993;44:277-88.
Malo JL, Cartier A, L'Archeveque J,
Trudeau C, Courteau JP, Bherer L. Prevalence of occupational asthma
among workers exposed to eastern white cedar. Am J Respir Crit Care
Med 1994;150:1697-701.
Malo JL, Ghezzo H, D'Aquino C,
L'Archeveque J, Cartier A, Chan-Yeung M. Natural history of occupational
asthma: relevance of type of agent and other factors in the rate of
development of symptoms in affected subjects. J Allergy Clin
Immunol 1992;90:937-44.
Malo JL, L'Archeveque J, Cartier
A. Significant changes in nonspecific bronchial responsiveness after
isolated immediate bronchospecific reactions caused by isocyanates but
not after a late reaction caused by plicatic acid. J Allergy Clin
Immunol 1989;83:159-65.
Marabini A, Dimich-Ward H, Kwan
SY, Kennedy SM, Waxler-Morrison N, Chan-Yeung M. Clinical and
socioeconomic features of subjects with red cedar asthma. Chest
1993;104:821- 4.
Newman Taylor AJ. Occupational asthma.
Postgrad Med 1988;64:505-10.
Paggiaro PL, Bacci E, Dente FL, Talini D, Giuntini C. Prognosis of
occupational asthma induced by isocyanates. Bull Eur Physiopathol
Respir 1987;23:565-9.
Paggiaro PL, Chan-Yeung M.
Pattern of specific airway response in asthma due to western red cedar
(Thuja plicata): Relationship with length of exposure and lung
function measurements. Clin Allergy 1987;17:333-9.
Perrin B, Cartier A, Ghezzo H, Grammer L, Harris K, Chan H, Chan-Yeung
M, Malo JL. Reassessment of the temporal patterns of bronchial
obstruction after exposure to occupational sensitizing agents. J
Allergy Clin Immunol 1991;87:630-9.
Rosenberg N,
Gervais P. Evaluation of the sequelae of occupational asthma. [French]
Rev Mal Respir 1989;6:35-8.
Sadhra S, Foulds IS,
Gray CN, Koh D, Gardiner K. Colophony--Uses, health effects, airborne
measures and analysis. Ann Occup Hyg 1994;38:385-96.
Salari H, Howard S, Chan H, Dryden P, Chan-Yeung M. Involvement of
immunologic mechanisms in a guinea model of western red cedar
asthma. J Allergy Clin Immunol 1994;93:877-84.
Shamssain MH. Pulmonary function and symptoms in workers exposed to
wood dust. Thorax
1992;47:84-7.
Siracusa A, Kennedy SM, DyBuncio A, Lin
FJ, Marabini A, Chan-Yeung M. Am J Ind Med
1995;28:411-23.
Vedal S, Enarson DA, Chan H, Ochnio J, Tse
KS, Chan-Yeung M. A longitudinal study of the occurrence of bronchial
hyperresponsiveness in western red cedar workers. Am Rev Respir
Dis 1988;137:651-5.
Vedal S, Chan-Yeung M, Enarson D, Fera T,
MacLean L, Tse KS, Langille R. Symptoms and pulmonary function in
western red cedar workers related to duration of employment and dust
exposure. Arch Environ Health 1986;41:179-83.
Vedal
S, Chan-Yeung M, Enarson DA, Chan DA, Dorken E, Tse KS. Plicatic
acid-specific IgE and nonspecific bronchial hyperresponsiveness in
western red cedar workers. J Clin Allergy Clin Immunol
1986;78:1103-9.
