Literature Review |

Top Ten List in Occupational Pulmonary Disease* FREE TO VIEW

Dorsett D. Smith, MD, FCCP
Author and Funding Information

*From the Division of Respiratory Disease and Critical Care Medicine, University of Washington, Seattle, WA.

Correspondence to: Dorsett D. Smith MD, FCCP, Suite 201, 4310 Colby Ave, Everett, WA 98203; e-mail: chestdis@ix.netcom.com

Chest. 2004;126(4):1360-1363. doi:10.1378/chest.126.4.1360
Text Size: A A A
Published online

1. Institute of Medicine, Committee on Damp Indoor Spaces and Health. Damp indoor spaces and health. Washington, DC: National Academies Press, 2004

This is a consensus statement by a committee that included experts in allergy and clinical immunology, building engineering, environmental health, epidemiology, exposure assessment, microbiology, public health, and toxicology. The Institute of Medicine conducted a comprehensive review of the scientific literature regarding the relationship between damp or moldy indoor environments and the manifestation of adverse health effects, particularly respiratory and allergic symptoms. The review focused on the noninfectious health effects of fungi, including allergens, mycotoxins, and other biologically active products. Chapters include a multidisciplinary review of the literature on building issues related to wetness, mycology, epidemiology, as well as a review of the toxicology literature. In addition, it made recommendations or suggested guidelines for public health interventions and for future basic science, clinical, and public health research. This is the most up-to-date statement on the health effects of molds in indoor air. It includes a good bibliography, and a well-reasoned evaluation of a very difficult area of environmental science. It is available on the World Wide Web through the National Academies Press at www.nap.edu, or the Institute of Medicine at iomwww@nas.edu, and will be available in portable document format (PDF) for printing.

2. Kreiss K, Gomaa A, Kullman G, et al. Clinical bronchiolitis obliterans in workers at a microwave-popcorn plant. N Engl J Med 2002; 347:330–338

Kreiss and coworkers evaluated the relation between exposures and health-related outcomes by analyzing the rates of symptoms and abnormalities according to current and cumulative exposure to diacetyl, the predominant ketone in artificial butter flavoring, in the air in a microwave popcorn processing plant. Of the 135 current workers at the plant, 117 workers (87%) completed the questionnaire. These 117 workers had 2.6 times the expected rates of chronic cough and shortness of breath, according to comparisons with the national data, and twice the expected rates of physician-diagnosed asthma and chronic bronchitis. Overall, the workers had 3.3 times the expected rate of airway obstruction; those who had never smoked had 10.8 times the expected rate. Workers directly involved in the production of microwave popcorn had higher rates of shortness of breath on exertion and skin problems that had developed since they started work than workers in other parts of the plant. There was a strong relation between the quartile of estimated cumulative exposure to diacetyl and the frequency and extent of airway obstruction. Some of these workers acquired very severe bronchiolitis obliterans. Animal studies have confirmed the toxic effect of diacetyl on airways.

3. Prezant DJ, Weiden M, Banauch GI, et al. Cough and bronchial responsiveness in firefighters at the World Trade Center site. N Engl J Med 2002; 347:806–815

Workers from the Fire Department of New York City were exposed to a variety of inhaled materials during and after the collapse of the World Trade Center. The authors evaluated clinical features in a series of 332 firefighters in whom severe cough developed after exposure, and the prevalence and severity of bronchial hyperreactivity in firefighters without severe cough classified according to the level of exposure. “World Trade Center cough” was defined as a persistent cough that developed after exposure to the site and was accompanied by respiratory symptoms severe enough to require medical leave for at least 4 weeks. Evaluation of exposed firefighters included completion of a standard questionnaire, spirometry, airway-responsiveness testing, and chest imaging. In the first 6 months after September 11, 2001, World Trade Center cough occurred in 128 of 1,636 firefighters with a high level of exposure (8%), 187 of 6,958 firefighters with a moderate level of exposure (3%), and 17 of 1,320 firefighters with a low level of exposure (1%). In addition, 95% of those with persistent cough had symptoms of dyspnea, 87% had gastroesophageal reflux disease, and 54% had nasal congestion. Of those tested before treatment of World Trade Center cough, 63% (149 of 237 firefighters) had a response to a bronchodilator, and 24% (9 of 37 firefighters) had bronchial hyperreactivity. Chest radiographs were unchanged from precollapse findings in 319 of the 332 firefighters with World Trade Center cough. Among the cohort without severe cough, bronchial hyperreactivity was present in 77 firefighters with a high level of exposure (23%) and 26 firefighters with a moderate level of exposure (8%). Intense, short-term exposure to materials generated during the collapse of the World Trade Center was associated with bronchial responsiveness and the development of cough. Clinical and physiologic severity was related to the intensity of exposure. The high alkaline pH of cement dust is thought to be important in the induction of airway injury. Cement dust causes bronchial hypersensitivity in mice. A granulomatous pneumonitis and an eosinophilic pneumonitis have been reported by others in workers exposed to World Trade Center dust. The explanation for the high frequency of esophageal reflux is unknown.

4. Maier LA, McGrath DS, Sato H, et al. Influence of MHC CLASS II in susceptibility to beryllium sensitization and chronic beryllium disease. J Immunol 2003; 171:6910–6918

A unique genetic susceptibility to beryllium has been suggested by epidemiologic studies of beryllium workers. Now data are emerging that links beryllium disease to a genetic susceptibility. A glutamic acid at residue 69(Glu[69]) in the human leukocyte antigen-DPB1 gene (Glu[69]) is associated with chronic beryllium disease (CBD) and possibly beryllium sensitization (BeS). This study tested the hypothesis that major histocompatibility complex class II polymorphisms are important in susceptibility to BeS and CBD, and that the Glu(69) variant is related to markers of disease severity. A higher frequency of the DPB1 Glu(69) gene was found in CBD and BeS compared with the Be-nondiseased subjects, with odds ratios of 10.1 for CBD vs Be-nondiseased and 9.5 for BeS vs Be-nondiseased. The majority of BeS and CBD subjects displayed non-0201 Glu(69) alleles. Glu(69) homozygosity was higher in the CBD subjects, while BeS subjects were intermediate and Be-nondiseased lowest. DRB1*01 and DQB1*05 phenotypes were reduced in CBD vs Be-nondiseased subjects, while DRB1*13 and DQB1*06 were associated with CBD in the absence of Glu(69). Glu(69) homozygosity acts as a functional marker associated with markers of CBD severity.

5. Ross RM. The clinical diagnosis of asbestosis in this century requires more than a chest radiograph. Chest 2003; 124:1120–1128

This is a very well-reasoned provocative article that will remain on the “Top Ten List for Asbestos-Related Disease” for many years. The author points out that the positive predictive value for the chest radiograph is so low that its value as a surveillance and diagnostic tool is limited. In this article, the sensitivity and specificity of the chest radiograph in diagnosing asbestosis is determined from a literature analysis. The prevalence of asbestosis among present-day cohorts, such as construction workers and petrochemical workers, is assessed based on the relative risk of lung cancer in patients with asbestosis and the overall relative risk of lung cancer in these occupationally asbestos-exposed cohorts. The results indicate a positive predictive value for abnormal chest radiograph findings alone to be significantly < 50%. Therefore, the chest radiograph is inadequate as the sole clinical tool to diagnose asbestosis in these cohorts. However, when rales and a low diffusing capacity of the lung for carbon monoxide are also present, the diagnosis of asbestosis on clinical grounds can be made with reasonable confidence.

6. Aksamit TR. Hot tub lung: infection, inflammation, or both? Semin Respir Infect 2003; 18:33–39

Increasing numbers of patients have presented with a hypersensitivity pneumonitis-type course in association with hot tub exposure. Mycobacterium avium complex (MAC) organisms have been isolated from patient specimens and hot tub water with matching fingerprints by restricted fragment length polymorphism and electrophoresis when performed. Review of the clinical, microbiologic, and radiographic presentations of 9 patients to the Mayo Clinic with this diagnosis are compared with 32 patients in the published literature. The diagnosis, treatment, and prognosis of MAC hot tub lung are reviewed. It is not clear if this respiratory illness represents a true infectious process or a hypersensitivity pneumonitis due to MAC. However, with avoidance of the hot tub, and no pharmacologic treatment, the patients often had complete resolution within months. The authors concluded that clinicians should advise their patients of the potential risk associated with hot tub use.

7. Wallace RJ Jr, Zhang Y, Wilson RW, et al. Presence of a single genotype of the newly described species Mycobacterium immunogenum in industrial metalworking fluids associated with hypersensitivity pneumonitis. Appl Environ Microbiol 2002; 68:5580–5584

Outbreaks of hypersensitivity pneumonitis (HP) among industrial metal-grinding machinists working with water-based metalworking fluids (MWFs) have frequently been associated with high levels of mycobacteria in the MWF, but little is known about these organisms. The authors collected 107 MWF isolates of mycobacteria from multiple industrial sites where HP had been diagnosed, and identified them to the species level by a molecular method (polymerase chain reaction restriction enzyme analysis). Their genomic DNA restriction fragment length polymorphism patterns, as determined by pulsed-field gel electrophoresis, were compared to those of 15 clinical (patient) isolates of the recently described rapidly growing mycobacterial species Mycobacterium immunogenum. A total of 102 of 107 MWF isolates (95%) from 10 industrial sites within the United States and Canada were identified as M immunogenum, and gave polymerase chain reaction restriction enzyme analysis patterns identical to those of the clinical isolates. Given the genomic heterogeneity of clinical isolates of M immunogenum, the finding that a single genotype was present at all industrial sites is remarkable. This suggests that this genotype possesses unusual features that may relate to its virulence and its potential etiologic role in HP and/or to its resistance to biocides frequently used in MWF. This data will need to be replicated in other laboratories, but suggests that a reanalysis by restriction fragment length polymorphism of other mycobacterial isolates recovered from machining fluids will have to be performed to exclude that other isolates may been misidentified.

8. Magni K, Lemiere C, Ghezzo H, et al. Inflammation after cessation of exposure to agents causing occupational asthma. Am J Respir Crit Care Med 2004; 169:367–372

Various studies have demonstrated that subjects with occupational asthma have varying amounts of disability due to airway inflammation. These Canadian authors demonstrated that the lack of improvement in airway responsiveness in subjects with occupational asthma after removal from exposure is associated with the following: (1) the magnitude of functional impairment at the time of diagnosis, (2) the time lapsed since diagnosis, and (3) the presence of inflammatory mediators in induced sputum. One third of the uncured subjects had persistent eosinophilia or neutrophilia long after removal from the workplace. On follow-up, 28 patients were cured, 44 patients were improved, and 31 patients were not improved. This indicates that the majority of patients with occupational asthma improve, but others are left with chronic airway inflammation for many years after removal from exposure.

9. Pope CA, Burnett RT, Thun MJ, et al. Lung cancer, cardiopulmonary mortality, and long-term exposure to fine particulate air pollution. JAMA 2002; 287:1132–1141

Vital statistics were obtained from an American Cancer Society Prevention Study on 1,200,000 adults in 1982, and then risk factor data were estimated on 500,000 adults through 1998. The authors conclude that long-term exposure to air pollution is an important risk factor for cardiopulmonary mortality. Elevated fine-particulate air pollution was associated with significant increases in lung cancer mortality as well as cardiopulmonary mortality after controlling for other risk factors such as diet and smoking. The risk factor from air pollution is comparable to being moderately overweight (a body mass index of 1.33 in a never-smoker). Air pollution has now been associated with increased risk of myocardial infarction, lung cancer, respiratory mortality, and an increased risk of emergency department visits and hospitalization of patients with COPD and asthma.

10. Nordness ME, Zacharisen MC, Schlueter DP, et al. Occupational lung disease related to cytophaga endotoxin exposure in a nylon plant. J Occup Environ Med 2003; 45:385–392

This is a beautiful study demonstrating many important principles in the evaluation of workers for possible HP or humidifier fever related to contaminated air from air conditioning systems. This article describes how to properly evaluate a patient with possible HP from contaminated air. Workers at a nylon plant acquired pulmonary disease with systemic symptoms. Differentiating between humidifier fever and HP is challenging. Cytophaga, an endotoxin-producing bacteria, was isolated from the plant air conditioning system. A number of workers had systemic and pulmonary symptoms. Precipitins to cytophaga endotoxin were identified. Several workers underwent lung biopsies demonstrating HP. Inhalation challenges with purified cytophaga endotoxin were performed on three pairs of subjects: group 1, or employees with clinical features and biopsy consistent with HP; group 2, asymptomatic exposed workers with precipitins; and group 3, nonexposed healthy individuals. All subjects had fever and leukocytosis after inhalation challenge. Acute and/or late pulmonary function changes occurred in groups 1 and 2. Group 3 only had acute and transient pulmonary function changes. Cytophaga bacterial endotoxin is capable of inducing HP as well as humidifier fever.

Abbreviations: BeS = beryllium sensitization; CBD = chronic beryllium disease; HP = hypersensitivity pneumonitis; MAC = Mycobacterium avium complex; MWF = metalworking fluid




Citing articles are presented as examples only. In non-demo SCM6 implementation, integration with CrossRef’s "Cited By" API will populate this tab (http://www.crossref.org/citedby.html).

Some tools below are only available to our subscribers or users with an online account.

Related Content

Customize your page view by dragging & repositioning the boxes below.

Find Similar Articles
CHEST Journal Articles
PubMed Articles
Infant/toddler pulmonary function tests-2008 revision & update.
American Association for Respiratory Care | 4/3/2009
Removal of the endotracheal tube—2007 revision & update.
American Association for Respiratory Care | 8/17/2007
  • CHEST Journal
    Print ISSN: 0012-3692
    Online ISSN: 1931-3543