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Journal of Occupational & Environmental Medicine:
Original Article

Pulmonary Responses After Wood Chip Mulch Exposure

Wintermeyer, Stephen F. MD, MPH; Kuschner, Ware G. MD; Wong, Hofer BS; D'Alessandro, Alessandra MD; Blanc, Paul D. MD, MSPH

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Author Information

From the Division of Occupational and Environmental Medicine (Dr Wintermeyer, Dr Kuschner, Dr D'Alessandro, Dr Blanc), the Division of Pulmonary and Critical Care Medicine (Dr Wintermeyer, Dr Kuschner, Dr Blanc), Department of Medicine, and the Cardiovascular Research Institute (Dr Wintermeyer, Dr Kuschner, Dr Wong, Dr D'Alessandro, Dr Blanc),University of California San Francisco, San Francisco, Calif.

Address correspondence to: Paul D. Blanc, MD, MSPH, Division of Occupational and Environmental Medicine, Box 0924, University of California San Francisco, San Francisco, CA 94143-0924. 1076-2752/97/3904-0308$3.00/0

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Abstract

Organic Dust Toxic Syndrome (ODTS) is a flu-like syndrome that can occur after inhalation of cotton, grain, wood chip dusts, or other organic dusts or aerosols. We investigated whether inflammatory pulmonary responses occur, even after relatively brief, low-level wood chip mulch exposure. Six volunteers were exposed to wood chip mulch dust. Total dust and/or endotoxin levels were measured in five subjects. Pulmonary function and peripheral blood counts were measured before and after exposure in each subject. Bronchoalveolar lavage (BAL) was performed in each subject after exposure, and cell, cytokine, and protein concentrations were measured. Control BAL without previous exposure was also performed on three of the subjects. Three of six subjects had symptoms consistent with ODTS. No clinically relevant or statistically significant changes in pulmonary function tests after exposure were found. Three subjects manifested a marked elevation in neutrophil percentage in their BAL (range, 10 to 57%). When these three subjects underwent control BAL, the postexposure comparison demonstrated an increase in neutrophil levels of 154 ± 89 x 103 /mL (mean ± standard error; P = 0.22). The mean increase in BAL interleukin-8 levels after exposure, compared with paired control values, was 11.2 ± SE 2.5 pg/mL (P = 0.047). There was also an increase in BAL interleukin-6 levels that reached borderline significance (6.4 ± SE 2.0 pg/mL; P = 0.08). Tumor necrosis factor levels were increased in all three subjects' BAL as well (0.4 ± SE 0.2 pg/mL), but this change was not statistically significant (P = 0.2). Our findings of increased BAL proinflammatory cytokine and neutrophil levels are consistent with the theory that cytokine networking in the lung may mediate ODTS.

Organic Dust Toxic Syndrome (ODTS) encompasses a group of acute, febrile reactions to various organic dusts and bioaerosols.1-3 The prominent symptoms of ODTS include fever, chills, myalgias, and malaise, usually beginning within 8 hours of exposure and resolving within 24 hours. ODTS is a common condition. In highly exposed groups such as farmers or wood trimmers or in outbreaks of humidifier fever, attack rates of >10% may occur.4-6 One specific exposure noted to cause ODTS is wood chip dust, particularly if the chips are damp and likely to be contaminated with bacteria or molds.7-8

Because of the clinical similarities between ODTS and febrile reactions occurring after the inhalation of other noxious substances, the unifying term "inhalation fever" has been suggested.9 The pathophysiology of ODTS appears to be similar to that of metal fume fever, an inhalation fever that we have shown to be characterized by cytokine networking and increased numbers of neutrophils in the lung.10-12 Like fume fever, experimental studies of ODTS have demonstrated increased levels of bronchoalveolar lavage (BAL) cytokines and inflammatory cells after inhalation of grain and cotton dust extracts.13-15 We hypothesized that, consistent with other organic dust effects, even relatively brief and low-level exposure to wood chip mulch dust would be linked to pulmonary cellular and proinflammatory cytokine responses.

We studied healthy volunteer subjects who were exposed to damp and dusty wood chips by shoveling mulch while gardening in a public park. We measured pulmonary function, including nonspecific airway reactivity; assayed peripheral blood leukocytes; and carried out BAL, quantifying cell and cytokine constituents. Our goal in this experimental case series was to characterize pulmonary cytokine and cellular responses in mulch-related ODTS.

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Methods

Study Subjects and Conditions

We studied six volunteer subjects. Their demographic data, smoking status, and any past history of ODTS are summarized in Table 1. Three subjects had a history of smoking; only two were currently smoking at the time of the study. Their cumulative exposures were 5 (the former smoker) and 3 and 10 (the two current smokers) pack-years. Only one subject (#5) had a clinical history suggestive of mild asthma (wheeze with chest colds), but was taking no medications on a regular basis.

Table 1
Table 1
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Only one subject (#4) had a previous history of febrile episodes associated with wood chip shoveling consistent with prior ODTS. The most recent episode had occurred more than 3 months before the study. All of the subjects had worked in landscape gardening at some time. Four subjects (#1, #2, #3, #4) were working full- or part-time in landscaping at the time of study. None had shoveled wood chips within 4 weeks of the study.

Each subject underwent one unblinded exposure to wood chip dust and postexposure evaluation as described below. One subject (#1) underwent postexposure evaluation 2 hours after exposure; one subject (#2) underwent postexposure evaluation 7 hours after exposure; and four subjects (#3, #4, #5, #6) underwent postexposure evaluation 21 hours after the exposure. Three of the subjects (#4, #5, #6) also underwent a second control evaluation after an interval of at least 2 months without wood chip exposure. Our study protocol was approved by the University of California, San Francisco Committee on Human Research.

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Wood Chip Mulch Exposure

Wood chip mulch exposures were performed outdoors on actual wood chip mulch piles in a local city park. Each subject used a pitchfork or shovel to move a pile of wood chips. Length of exposure ranged from 60 to 120 minutes. For five of the six exposures, we carried out sampling for either endotoxin or dust concentration and, in two subjects, for both. We sampled dust exposure in the breathing zone during wood chip moving by using closed-face filters for total dust or Marple Cascade Impactors (Anderson Instruments Inc., Atlanta, GA) for total and respiratory dust sampling. Each filter or impactor was attached to a pump driving a known flow of ambient air through it (approximately 2L/min). For the cascade impactor samples, we considered particles less than 6 microns in diameter to be in the respirable range. Total dust was quantified gravimetrically (D & M Laboratories, Petaluma, CA).

Endotoxin was measured by a Limulus amebocyte lysate assay using a spectrophotometric microplate method (Environmental Medicine Laboratories, New York University Medical Center, Tuxedo, NY). Total dust and endotoxin concentrations are detailed in Table 2. Total dust concentrations ranged from 0.3 mg/m3 to 3.6 mg/m.3 For one exposure, we also characterized the dust by particle size, showing that the respirable fraction comprised 22% of the 0.8 mg/m3 total dust concentration sample. The endotoxin levels ranged from 13 to 91 ng/m.3 The percentage of endotoxin that was measured in dust of particle size <6 microns varied from 38 to 63%. We did not culture the mulch to identify specific fungal or bacterial speies or carry our colony counts with atmospheric sampling.

Table 2
Table 2
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Pulmonary Function and Peripheral Polymorphonuclear Leukocyte Concentrations

Immediately preceding (baseline) and then again at 2, 7, or 21 hours after exposure, we measured pulmonary function by spirometry, airway resistance, lung volumes, diffusing capacity for carbon monoxide (DLCO), and airway responsiveness to methacholine. Tests were repeated at only one follow-up time for each subject, but we intentionally varied the follow-up time to better study the natural history of the response to wood chip exposure. We carried out follow-up testing 2 hours after exposure (subject #1), 7 hours after exposure (subject #2), or 21 hours after exposure (subjects #3, #4, #5, #6). Before pulmonary function testing both before and after exposure, we obtained peripheral blood samples to determine total white blood cell count (WBC) and polymorphonuclear leukocyte count (PMN).

Pulmonary function was tested with the subject in the sitting position. We measured forced expiratory volume in 1 second (FEV1) and forced vital capacity (FVC), using a rolling seal spirometer according to American Thoracic Society standards. 16 Maximal flow-volume curves, using the rolling seal spirometer, were measured by analyzing flow and volume signals. We measured total lung capacity (TLC) by single-breath helium dilution method.17 We measured DLCO by the single breath method of Ogilvie et el, as modified in our laboratory.18,19 To measure baseline airway resistance and to test methacholine dose-response, thoracic gas volume (VTG) and airway resistance (RAW) were measured five times by constant-volume whole-body plethysmography (Warren Collins, Inc., Braintree, MA) at 30-second intervals in the baseline state and 30 seconds after inhalation of ten breaths of each methacholine dose. To measure methacholine response, subjects inhaled serially doubling doses of methacholine aerosol, 0.5 to 64 mg/mL, delivered by a nebulizer (DeVilbiss no. 646; The DeVilbiss Company, Somerset, PA) equipped with a dose-metering device. We determined specific airway resistance (SRAW) after each concentration of methacholine. We calculated the provocative dose of methacholine to be that inducing an increase of 8 units in SRAW above baseline (PD8U).

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Bronchoscopy and Bronchoalveolar Lavage

We performed bronchoscopy with bronchoalveolar lavage (BAL) either at 3, 8, or 22 hours after wood dust exposure (ie, after the pulmonary-function studies). For three subjects (#4, #5, #6), a control bronchoscopy was also performed at least 1 month later and without wood chip mulch dust exposure. Bronchoscopy included routine atropine premedication and topical anesthesia. A flexible fiberoptic bronchoscope (Pentax-FFB-19D; Pentax Precision Instrument Corporation, Orange-burg, NY) was wedged in a segmental airway in the right middle lobe, and BAL was performed by instilling four 50-mL boluses of 37°C isotonic saline and applying gentle suction until no further collection was noted. The BAL was collected on ice. The bronchoalveolar lavage fluid was pooled. No gauze filtration was used. We performed a cell count by using a standard hematocytometer and differential count after 5 minutes of cytocentrifugation at 1000 rpm and May-Grunwald-Giemsa staining.

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Cytokine and Protein Determinations

The remaining bronchoalveolar lavage fluid supernatant, after centrifugation, was stored at -70°C for subsequent cytokine analysis. We quantified concentration of tumor necrosis factor-alpha (TNF), interleukin (IL)-1 beta, IL-6, and IL-8 in BAL supernatant by immunodetection with enzyme-linked immunosorbent assay (ELISA; R&D Systems, Minneapolis, MN). The lower limits of detection of the kits (supplier's data) were as follows: TNF, 0.085 pg/mL; IL-1 beta, 0.083 pg/mL; IL-6, 0.080; IL-8, 3.0 pg/mL. Cytokines were quantified colorimetrically against a standard curve of known concentrations. We ran all samples in duplicate. The ELISA assays we utilized are not reported to exhibit detectable crossreactivity with the other cytokines we tested. We determined BAL supernatant total protein concentrations by using a commercially available colorimetric assay (Bio-Rad Laboratories, Hercules, CA).

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Statistical Analyses

We used a standard statistical package in the data analysis (SAS Institute Inc., Cary, NC). We used the paired t test to compare pre- and postexposure peripheral blood counts, pulmonary function tests (all six subjects), and BAL cell counts and cytokine concentrations (three subjects who underwent both postexposure and control bronchoscopy). We tested the association of peripheral blood and BAL PMNs with the Pearson moment correlation.

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Results

Signs and Symptoms

Three subjects (#1, #4, #5) reported symptoms after the exposure. Subject #1 complained of flu-like symptoms. Her maximum temperature (Tmax) was 38.3°C. Subject #4 reported body aches. Her Tmax was 38.6°C, approximately 8 hours after exposure. Subject #5 reported mild chest tightness and myalgias. His Tmax was 36.9°C. Thus, three subjects had either symptoms and/or fever consistent with ODTS. None of the other three subjects reported any symptoms or had a documented rise in body temperature after exposure.

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Peripheral Blood Counts

For all six subjects analyzed together regardless of follow-up time, although increased above baseline, there was no statistical difference in total WBC count after exposure (7967 ± 2048 vs 10383 ± 5894, P = 0.25) or in PMN count before and after exposure (4190 ± 2005 vs 7282 ± 5397, P = 0.26). This remained the case when data for the four subjects evaluated at 21 hours after exposure were analyzed separately (total WBC count 8275 ± 2323 baseline vs postexposure 12325 ± 6542, P = 0.20, and PMN count 5190 ± 2275 baseline vs 8975 ± 6086 postexposure, P = 0.23). However, the change in peripheral PMNs was strongly correlated with the BAL PMN concentration (r = 0.95, P < 0.01).

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Pulmonary Function and Airway Reactivity

We measured pulmonary function, airway resistance, and reactivity to methacholine before and after exposure in each subject. Changes in these measurements are shown in Table 3. None was clinically relevant or statistically significant. We also separately analyzed data for the four subjects evaluated at 21 hours after exposure. Within that stratum, the slight FEV1 decrement (-0.125 ± 0.096 L) was of borderline statistical significance (P = 0.08). Neither TLC, DLCO, nor SRAW demonstrated any meaningful postexposure change within that stratum. Although all four subjects evaluated at 21 hours after exposure demonstrated increased airway responsiveness to methacholine, the overall change was not statistically significant (P = 0.15 for those four subjects) and for only two subjects was the change in responsiveness potentially relevant clinically, with a shift greater than two doubling doses of methacholine (In ratio PD8U baseline:postexposure > 0.69).

Table 3
Table 3
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BAL Cells and Cytokines

The BAL fluid analyses of differential cell types, cytokine concentrations, and protein are presented in Table 4. Three subjects, all of whom were studied at a 22-hour follow-up examination, exhibited increased percentages of BAL PMNs (57%, 16%, and 10%). These three subjects also demonstrated the greatest concentrations of TNF, IL-1, and IL-6, but not of IL-8.

Table 4
Table 4
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We further studied these three subjects only by carrying out control BAL studies at another time point without any recent wood chip dust exposure. Exposure-control differences in BAL cell, cytokine, and protein concentrations for these subjects are presented in Table 5. All three subjects had marked increases in PMNs after exposure, compared with control values, although these changes were not statistically significant (mean increase = 15 ± SE 89 x 103; P = 0.22). Figure 1 demonstrates the much greater proportion of PMNs seen in the BAL of Subject #4 after exposure, compared with control (57% vs 2%). The concentrations of TNF, IL-6, and IL-8 were increased for each subject after exposure, compared with the control. Indeed, the mean exposure-associated increase in IL-8 (study n = 3) was statistically significant (11.2 ± SE 2.5 pg/mL, P = 0.047), and the mean increase for IL-6 was of borderline significance (6.4 ± SE 2.0 pg/mL, P = 0.08), whereas that of TNF (mean difference 0.4 ± SE 0.2 pg/mL) was less marked (P = 0.2).

Table 5
Table 5
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Fig. 1
Fig. 1
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Discussion

This series of wood chip mulch exposures under field conditions relevant to routine gardening activities suggests that exposure to relatively low concentrations of organic dust (<10 mg/m3) can be associated with inflammatory changes in the lung and, in some individuals, associated with the clinical symptoms of ODTS. The increases in PMNs in postexposure BAL, compared with control BAL, is consistent with findings published in clinical case reports of ODTS. Emanual et al reported on three subjects with ODTS. These subjects manifested BAL PMN percentages (26 to 79%) above the normal range when BAL was performed within 4 days of exposure.20 When repeat BAL was performed 6 or more days after exposure, the PMN percentages were much lower (2 to 10%). Lecours et al reported a similar finding of elevated neutrophil counts in the BAL of two subjects with ODTS who were studied within 3 days after exposure.21 This increase had resolved when follow-up BAL was performed on each subject one month later. In an experimental study, Von Essen et al demonstrated a threefold increase in BAL PMN percentage in subjects who inhaled grain sorghum dust extract.14 The increase in PMNs appears to be self-limited: BAL 7 days after an episode of ODTS has been reported to yield a normal PMN count.22

Three of the four cytokines we studied in the BAL supernatant (TNF, IL-6, IL-8) were elevated after exposure. Even with a limited number of paired observations, the change in IL-8 was statistically significant and that of IL-6 was of borderline significance. Although ours is a small exposure series, these data support the concept that multiple cytokines may indeed play a role in mediating ODTS. The lack of an increase in protein in the BAL of exposed subjects suggests that the increases in BAL cytokines after exposure were not simply a result of increased pulmonary capillary permeability. Our data are consistent with previous cytokine data from Clapp et al, which showed that inhalation of corn dust extract resulted in increase concentrations of IL-1, IL-6, IL-8, and TNF in BAL fluid.13 They are also consistent with a recent study showing increases in serum TNF and IL-6 after low-level swine dust inhalation, although BAL cytokine concentrations were not reported in that study.23

We did not demonstrate clinically meaningful or statistically significant decrements in pulmonary function after wood chip dust exposure. This lack of response was in contradistinction to the inflammatory changes we observed. Findings from other ODTS studies have varied. May et al performed PFTs on 11 individuals with ODTS and found normal lung function (FVC, 91.7 ± 9.6% predicted; TLC, 84.4 ± 11.5% predicted; and DLCO, 104.2 ± 17.0% predicted).24 In contrast, Clapp et al observed statistically significant decreases in FEV1, FVC, and FEV1/FVC ratio in 15 subjects studied 30 minutes after corn dust extract inhalation.13 These changes persisted for at least 5 hours. Von Essen et al also demonstrated statistically significant decreases in FEV1, FVC, and FEV1FVC in 9 subjects after inhalation of grain sorghum dust extract.14 However, these changes were observed only 30 minutes after exposure. At 3-hour follow-up, pulmonary function had returned to baseline. Vogelmeier et al found a 12% drop in DLco but only 5% in vital capacity in seven healthy volunteers exposed to moldy hay, despite a greater than 200% increase in peripheral blood PMNs.25 It may be that airway responses vary in ODTS as a function of particle or aerosol deposition or because of the inherent heterogeneity of the exposures involved.

Wood chip mulch can be contaminated by a variety of organisms, including bacteria and thermophilic and mesophilic fungi.26-27 The causal role in ODTS of bacterially derived endotoxin, as opposed to fungal byproducts, has not been established. It should also be noted that mulch exposure, in addition to ODTS, has been associated with other, less benign respiratory conditions, including hypersensitivity pneumonitis, allergic aspergillosis, and acute fungal infection.28-30

Our data are consonant with other studies of ODTS. This series is small and has limited study power to detect subtle effects. Nevertheless, our data do demonstrate elevated BAL cytokine and PMN concentrations after even modest exposure to wood chip mulch dust. These observations suggest that the inhalation of low concentrations of wood chip mulch dust, in causing the acute pulmonary inflammatory response of ODTS, may act at least in part through cytokine-mediated pathways.

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Acknowledgments

The authors thank Homer Boushey, MD, for assistance with bronchoscopy, Patricia Quinlan, MPH, for industrial hygiene sampling, Terry Gordon Ph.D. for assaying endotoxins, and the staff of the Strybing Arboretum and Botanical Gardens of Golden Gate Park. This study was supported in part by US National Research Service Award No. HL07185 (Dr Wintermeyer, Dr Kuschner).

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References

1. National Institute for Occupational Safety and Health. Request for Assistance in Preventing Organic Dust Toxic Syndrome. [DHHS Publication No. (NIOSH)94-104.] Cincinnati: US Department of Health and Human Services, Public Health Service, Centers for Disease Control; 1994.

2. Von Essen S, Robbins RA, Thompson AB, Rennard SI. Organic dust toxic syndrome: an acute febrile reaction to organic dust exposure distinct from hypersensitivity pneumonitis. Clin Toxicol. 1990;28:389-420.

3. Malmberg P, Rask-Andersen A. Organic dust toxic syndrome. Semin Respir Med. 1993;14:38-48.

4. Husman K, Terho EO, Notkola V, Nuutinen J. ODTS among Finnish farmers. Am J Ind Med. 1990;17:79-80.

5. Rask-Anderson A, Land CJ, Enlund A. Inhalation fever and respiratory symptoms in the trimming department of Swedish sawmills. Am J Ind Med. 1994;25:65-67.

6. Anderson K, McSharyy CP, Clark C, Clark CJ, Barclay GR, Morris GP. Sump bay fever: inhalational fever associated with a biologically contaminated water aerosol. Occup Environ Med. 1996;53:106-111.

7. Centers for Disease Control. Acute respiratory illness following occupational exposure to wood chips-Ohio. MMWR. 1986;35:483-484, 489-490.

8. Kolmodin-Hedman B, Stjernberg N. Symptoms in farmers exposed to moldy wood chips. Am J Ind Med. 1986;10:310.

9. Rask-Andersen A, Pratt DS. Inhalation fever: a proposed unifying term for febrile reactions to inhalation of noxious substances. Br J Ind Med. 1992;49:40.

10. Blanc P, Wong H, Bernstein MS, Boushey HA. An experimental human model of metal fume fever. Ann Intern Med. 1991;114:930-936.

11. Blanc P, Boushey HA, Wong H, Wintermeyer SF, Bernstein MS. Cytokines in metal fume fever. Am Rev Respir Dis. 1993;147:134-138.

12. Kuschner WG, D'Alessandro A, Winter-meyer SF, Wong H, Boushey H, Blanc PD. Pulmonary responses to purified zinc oxide fume. J Investig Med. 1995;43:371-378.

13. Clapp WD, Becker S, Quay J, et al. Grain dust-induced airflow obstruction and inflammation of the lower respiratory tract. Am J Respir Crit Care Med. 1994;150:611-617.

14. Von Essen SG, O'Neill DP, McGranaghan S, Olenchock SA, Rennard SI. Neutrophilic respiratory tract inflammation and peripheral blood neutrophilia after grain sorghum dust extract challenge. Chest. 1995;108:1425-1433.

15. Ryan LK, Karol MH. Release of tumor necrosis factor in guinea pigs upon acute inhalation of cotton dust. Am J Respir Cell Mol Biol. 1991;5:93-98.

16. Crapo RO, Morris AH, Gardner RM. Reference spirometric values using technique and equipment that meet ATS recommendations. Am Rev Respir Dis. 1981;123:659-664.

17. Mitchell MM, Renzetti AD Jr. Evaluation of a single-breath method of measuring total lung capacity. Am Rev Respir Dis. 1968;97:571-580.

18. Ogilvie CM, Forster RE, Blakemore WS, Morton JW. A standardized breath-holding technique for the clinical measurement of the diffusing capacity of the lung for carbon dioxide. J Clin Invest. 1957;36:1-17.

19. Gelb AF, Gold WM, Wright RR, Bruch HR, Nadel JA. Physiologic diagnosis of subclinical emphysema. Am Rev Respir Dis. 1971;107:50-63.

20. Emanual DA, Marx JJ Jr, Ault B, Roberts RC, Kryda MJ, Treuhaft MW. Organic dust toxic syndrome (pulmonary mycotoxicosis): a review of the experience in central Wisconsin. In: Dosman JA, Cock-croft DW, eds. Principles of Health and Safety in Agriculture. Boca Raton, FL: CRC Press; 1989:72-75.

21. Lecours R, Laviolette M, Cornier Y. Bronchoalveolar lavage in pulmonary mycotoxicosis (organic dust toxic syndrome). Thorax. 1986;41:924-926.

22. Raymenants E, Demedts M, Nenmery B. Bronchoalveolar lavage findings in a patient with the organic dust toxic syndrome. Thorax. 1990;45:713-714.

23. Wang Z, Malmberg P, Larsson P, Larsson B-M, Larsson K. Time course of interleukin-6 and tumor necrosis factor-alpha increase in serum following inhalation of swine dust. Am J Respir Crit Care Med 1996;153:147-152.

24. May JJ, Stallones L, Darrow D, Pratt DS. Organic dust toxicity (pulmonary mycotoxicosis) associated with silo unloading. Thorax. 1986;41:919-923.

25. Vogelmeier C, Krombach F, Munzing S, et al. Activation of blood neutrophils in acute episodes of farmer's lung. Am Rev Respir Dis. 1993;148:396-400.

26. Jappinen P, Haahtel T, Liira J. Chip pile workers and mould exposure. Allergy. 1987;42:545-548.

27. Lacey J, Crook B. Fungal and actinomycete spores as pollutants of the workplace and occupational allergens. Ann Occup Hyg. 1988;32:515-533.

28. Weber S, Kullman G, Petsonk E, et al. Organic dust exposures from compost handling: case presentation and respiratory exposure assessment. Am J Ind Med. 1993;24:365-374.

29. Krasnick J, Patterson R, Roberts M. Allergic bronchopulmonary aspergillosis presenting with cough variant of asthma and identifiable source of Aspergillus fumigatus. Ann Allerg Asthma Immunol. 1995;75:344-346.

30. Conrad DJ, Warnock M, Blanc P, Cowan M, Golden JA. Mircogranulomatous aspergillosis after shoveling wood chips: report of a fatal outcome in a patient with chronic granulomatous disease. Am J Ind Med. 1992;22:411-418.

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CONSCIENTIOUSNESS

Conscientiousness is high on most firms' wish list of traits they want in employees. Yet a recent study found that laid-off individuals who are conscientious are less likely to find jobs within 5 months than their slacker peers. Kent State researchers have a logical explanation: "It is possible that conscientious individuals actively seek work after job loss but are particularly selective and slow about choosing new employment." Thanks to their patience, however, they may end up being happier with their choice than folks who jump at the first job offer.

From News & Trends. Psychology Today. July/August 1996, p 11.

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