Occupational Asthma Caused by Oak Wood Dust

doi:10.1378/chest.108.3.856

Chest

Volume 108, Issue 3, September 1995, Pages 856-858

https://doi.org/10.1378/chest.108.3.856 Get rights and content

Three cases of occupational asthma caused by oak wood dust are presented. The diagnosis was confirmed by specific inhalation challenges, which induced a dual asthmatic reaction in two subjects and an atypical prolonged immediate reaction in one subject.

Section snippets

Case 1

A 43-year-old patient had been employed for 8 years for a company that produced mobile homes. At work, he was exposed to oak (principally), spruce, and jack pine wood dust daily. He was also exposed to melamine powder containing formaldehyde. He had started reporting symptoms of dyspnea, chest tightness, wheezing, and a productive cough 5 years previously. Four months before being referred, his symptoms got worse and he had to use an inhaled ß₂-adrenergic agent up to ten times per day. During

DISCUSSION

In this study, work-related asthma was first documented in case 1 through serial monitoring of PEFR and recording FEV₁ under the supervision of a technician at work. These procedures could not be used with the remaining two subjects because we were not allowed to send them back to their workplace. In all three subjects, the diagnosis of occupational asthma due to oak wood dust was demonstrated using specific inhalation challenges in the laboratory which induced a dual asthmatic reaction in two

ACKNOWLEDGMENTS

The authors thank Lori Schubert for reviewing the manuscript.

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Cited by (43)

Comparison of hardwood and softwood dust-induced expression of cytokines and chemokines in mouse macrophage RAW 264.7 cells
2006, Toxicology
Numerous epidemiological studies have shown that occupational exposure to wood dust can induce several respiratory diseases such as allergic rhinitis, chronic bronchitis, asthma, and sino-nasal adenocarcinoma. However, comparison of the harmful potential of different wood dust species on the basis of epidemiological studies is complicated because in the occupational environment workers are usually exposed to several wood dust species simultaneously. In the present study, we have characterized and compared the effects of two hardwood dusts, beech and teak, and two softwood dusts, pine and spruce, on cytokine and chemokine expression utilizing an in vitro model, murine macrophage cell line RAW 264.7. The expression patterns of selected cytokines and chemokines were assessed by real-time quantitative PCR and by ELISA. All the tested hardwood and softwood dusts induced TNF-α expression and inhibited IL-1β expression. Similarly, all the wood dusts induced the expression of CCL2, CCL3, CCL4, and CXCL2/3 chemokines and inhibited CCL24 expression. Our results indicate that both hardwood and softwood dusts influence the cytokine and chemokine expression of RAW 264.7 cells. Although some differences could be detected in the magnitude of responses to different wood dust species, the two tested wood dust groups, hardwoods and softwoods, have quite similar effects on cytokine and chemokine expression in RAW 264.7 cell line.
Characterization of oak and birch dust-induced expression of cytokines and chemokines in mouse macrophage RAW 264.7 cells
2005, Toxicology
Occupational exposure to wood dust is related to several respiratory diseases, such as allergic rhinitis, chronic bronchitis, and asthma. However, virtually nothing is known about molecular mechanisms behind wood dust-induced pulmonary inflammation. To elucidate the effects of wood dust exposure on cytokine and chemokine expression in murine macrophage cell line cells, mouse RAW 264.7 cells were exposed to two selected hardwood dusts, oak and birch. TiO₂ and LPS were used as controls. Expression patterns of several cytokines, chemokines, and chemokine receptors were assessed by real-time quantitative PCR system and by ELISA. Exposure to birch dust caused a major increase in TNF-α and IL-6 protein levels whereas a weaker induction of TNF-α protein was found after exposure to oak dust. Inorganic TiO₂ dust did not induce significant cytokine expression. With respect to the chemokines, a dose-dependent, about 10-fold induction of CCL2 mRNA and protein was found after exposure to birch dust. Oak dust induced weakly CCL2 protein. Similarly, birch dust induced a strong expression of CCL3, CCL4, and CXCL2/3 mRNA whereas only moderate levels of these chemokine mRNAs were detected after oak dust exposure. In contrast, expression of CCL24 mRNA was inhibited by more than 40-fold by both oak and birch dusts. TiO₂ dust induced about five-fold expression of CCL3 and CCL4 mRNA but did not affect significantly other chemokines. These results suggest that exposure to birch or oak dusts may influence the development of the inflammatory process in the airways by modulating the expression of macrophage-derived cytokines and chemokines.
Occupational asthma due to exposure to iroko wood dust
2003, Annals of Allergy, Asthma and Immunology
Occupational asthma (OA) from iroko wood has been reported primarily in case reports.
To improve understanding of the pathogenesis of OA induced by iroko wood dust.
Three groups of woodworkers were included in this study: 9 workers who had clinically proven OA from iroko; 10 asymptomatic woodworkers; and 10 woodworkers with asthma. All patients underwent the following tests: a skin test with an iroko aqueous extract, specific IgE determination, and an iroko bronchial provocation test (IBPT). An eosinophil count was determined before and after the IBPT, and a methacholine inhalation test was performed after avoidance of exposure to iroko. Patients were asked to monitor their peak expiratory flow rates during a week at work followed by a week's vacation.
In all patients with a personal history predictive of OA from iroko, a reduction of the peak expiratory flow rate and positivity to the IBPT while working with iroko were present. The latter test result showed a dual response, with a decrease in forced expiratory volume in 1 second from 25% to 32% at 10 minutes and a further decrease from 35% to 43% at 8 hours; at 24 hours, the eosinophil count was higher (P = .046). In 4 patients, the intradermal test results with iroko extract were positive, whereas the skin prick test result and the specific IgE determination were negative in all patients. The methacholine test result was also positive. In the control groups, all the test results with iroko extract were negative.
Our data suggest that OA due to iroko wood may be induced by immunologic mechanisms other than IgE-mediated immediate hypersensitivity reactions.
Oak Pollen Allergy in Korea
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2020, Wood Material Science and Engineering
Analysis of dust exposure during chainsaw forest operations
2017, IForest

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: Partly supported by the Centre québécois d'Excellence en santé respiratoire.

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Occupational and Environmental Lung DiseaseOccupational Asthma Caused by Oak Wood Dust

Section snippets

Case 1

DISCUSSION

ACKNOWLEDGMENTS

J Allergy Clin Immunol

J Allergy Clin Immunol

Western red cedar and other wood dusts.

Hypersensitivity to wood dust.

N Engl J Med

Occupational and Environmental Lung Disease
Occupational Asthma Caused by Oak Wood Dust