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Original Research: COPD |

Impact of Occupational Exposure on Severity of COPD FREE TO VIEW

Esther Rodríguez, MD; Jaume Ferrer, MD, PhD; Sergi Martí, MD, PhD; Jan-Paul Zock, PhD; Estel Plana, MSc; Ferran Morell, MD, PhD
Author and Funding Information

*From the Respiratory Medicine Department (Drs. Rodríguez, Ferrer, Martí, and Morell) Hospital Universitari Vall d'Hebron, Universitat Autònoma de Barcelona, CIBER Enfermedades Respiratorias, Barcelona, Spain. Centre for Research in Environmental Epidemiology (Dr. Zock and Mr. Plana) CIBER Epidemiología y Salud Pública, Barcelona, Spain.

Correspondence to: Esther Rodríguez, MD, Servei de Pneumologia, Hospital Universitari Vall d'Hebron, Passeig Vall d'Hebron 119–129, 08035 Barcelona, Spain; e-mail: estherod@vhebron.net


The authors have reported to the ACCP that no significant conflicts of interest exist with any companies/organizations whose products or services may be discussed in this article.

Reproduction of this article is prohibited without written permission from the American College of Chest Physicians (www.chestjournal.org/misc/reprints.shtml).


Chest. 2008;134(6):1237-1243. doi:10.1378/chest.08-0622
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Background:  The relationship between occupational exposures and COPD has been analyzed in population-based and occupational cohort studies. However, the influence of these exposures on the clinical characteristics of COPD is not well known. The aim of this study was to analyze the impact of occupational exposures on respiratory symptoms, lung function, and employment status in a series of COPD patients.

Methods:  We conducted a cross-sectional study of 185 male COPD patients. Patients underwent baseline spirometry and answered a questionnaire that included information on respiratory symptoms, hospitalizations for COPD, smoking habits, current employment status, and lifetime occupational history. Exposure to biological dust, mineral dust, and gases and fumes was assessed using an ad hoc job exposure matrix.

Results:  Having worked in a job with high exposure to mineral dust or to any dusts, gas, or fumes was associated with an FEV1 of < 30% predicted (mineral dust: relative risk ratio, 11; 95% confidence interval [CI], 1.4 to 95; dusts, gas, or fumes: relative risk ratio, 6.9; 95% CI, 1.1 to 45). High exposure to biological dust was associated with chronic sputum production (odds ratio [OR], 4.3; 95% CI, 1.6 to 12), dyspnea (OR, 2.7; 95% CI, 1.1 to 6.7), and work inactivity (OR, 2.4; 95% CI, 1.4 to 4.2). High exposure to dusts, gas, or fumes was associated with sputum production (OR, 2.8; 95% CI, 1.2 to 6.7) and dyspnea (OR, 1.2; 95% CI, 1.1 to 1.4).

Conclusions:  Occupational exposures are independently associated with the severity of airflow limitation, respiratory symptoms, and work inactivity in patients with COPD.

Occupational exposure to dusts, gas, and fumes may cause chronic bronchitis, chronic emphysema, and irreversible airflow obstruction. Both population-based studies15 and occupational cohort studies610 have shown that occupational exposure is associated with an increased incidence of COPD, irrespective of smoking. According to estimates published in an American Thoracic Society statement,11 COPD may be attributed to occupational exposure in 15% of smokers and 31% of nonsmokers.

The influence of occupational exposure on the clinical and functional characteristics of COPD is not definitely understood. Only two patient series12,13 investigating this issue have been published to date, showing that exposure was associated with an increased occurrence of respiratory symptoms such as dyspnea and wheeze, and with airflow obstruction in certain subgroups of patients. However, these studies12,13 included exclusively patients with α1-antitrypsin deficiency, thus hampering the extrapolation of these results to COPD patients in general. Patients with α1-antitrypsin deficiency have certain differential characteristics. First, they have an accelerated loss of FEV1, particularly if they are smokers. Second, a different type of emphysema, predominantly panlobular and with lower lobe involvement, develops in these patients.14

Little is known about how occupational exposure affects COPD patients without α1-antitrypsin deficiency. In one study,15 an association between occupational exposure and health-care utilization, poor quality of life, and a greater loss of occupational activity in COPD patients was found. In a more recent population-based study,16 each year of continued fume exposure in men with early COPD was associated with a 0.25% reduction of predicted FEV1, regardless of tobacco smoking. However, no association between dust exposure and lung function decline was found in these patients.16 Our aim in the present study was to investigate the association between occupational exposure and respiratory symptoms, lung function, and employment status in COPD patients without α1-antitrypsin deficiency.

Study Population

Patients with COPD and/or emphysema who visited a specialized outpatient unit in a tertiary care hospital between March 2002 and January 2004 were consecutively enrolled into the study. The hospital covers an area population of 500,000, and the patients studied did not predominantly work in any particular large industry. Patients were referred to us by other doctors belonging to the primary care department or several departments of the same hospital that were not involved in the study. Spirometry (Masterlab; Jaeger; Wurzburg, Germany) was performed at a time when COPD symptoms were stable in accordance with the guidelines published by the American Thoracic Society.17 For each patient, the percentage of the predicted FEV1 was calculated according to age, height, and sex using the reference equations published by Roca et al18 for the Spanish population. According to the criteria established by the Global Initiative for Chronic Obstructive Lung Disease,17 COPD was diagnosed in patients with a post-bronchodilator therapy FEV1/FVC ratio of < 0.7 and was classified in four stages according to the post-bronchodilator therapy FEV1 as a percentage of the predicted value. Emphysema was diagnosed on the basis of CT scan findings. There were 13 patients with demonstrated emphysema without airflow obstruction demonstrated in the spirometry findings. Blood α1-antitrypsin levels were tested in all patients by kinetics immunonephelometry.

Questionnaire

Patients were interviewed by a trained chest physician. Clinical symptoms were evaluated using a specific respiratory research questionnaire.19 Dichotomous variables measured included chronic cough, sputum production, and wheeze. The severity of dyspnea was estimated in five categories according to the Medical Research Council grading system.20 The number of hospital admissions due to COPD exacerbation in the past year was also recorded. Detailed information on current and past smoking habits was also obtained, and the number of pack-years smoked was determined. All patients gave their informed consent to participate in the study, and approval was obtained from the ethics committee of our hospital.

Occupational Exposure Assessment

Information on employment status and lifetime occupational history was obtained using a structured interviewer-led questionnaire. Current employment status was classified into the following two categories: (1) active; and (2) inactive, including patients who were unemployed due to COPD, unemployed due to other reasons, or retired. All jobs inside or outside the home that had been held for at least 3 consecutive months and 8 h/wk were reported, with each including job title, type of industry, a description of work tasks, and starting and ending years. An ad hoc job exposure matrix was constructed for the 105 job titles reported by the patients, based on an existing method21 (the matrix semi-quantitatively assigned for each job title an exposure to biological dust, mineral dust, and gases or fumes the levels of none, low, and high). The verbatim occupational descriptions from patients with assigned low or high exposure to any of the agents were reviewed by an industrial hygienist. Changes from high to low or from low to no exposure were considered in cases in which the descriptions did not match against the assessed exposures. This additional expert judgment is recommended to improve the specificity of the method.22

Statistical Analysis

Occupational exposure was analyzed in the following two ways: (1) lifetime, defined as ever having worked in a job with high exposure to gases, dusts, or fumes; and (2) cumulative exposure to each of the specific agents and the combined exposure to dusts, gases or fumes, defined as the number of years the patient had been working in a high-exposure job. Logistic regression analysis was used to explore the associations between exposure indexes and respiratory symptoms, severity of dyspnea, and occupational status. The association between the percentage of predicted FEV1 in four categories (≥ 70%, 50 to 70%, 30 to 50%, and < 30%), and occupational exposure was evaluated using multinomial logistic models, with ≥ 70% as the reference category. The association between occupational exposure and the number of hospital admissions was calculated using negative binomial regression analysis. Regression models for lifetime occupational exposure were adjusted for age and number of pack-years smoked, and the models for cumulative occupational exposure were only adjusted for the number of pack-years smoked.

Finally, the association between occupational exposure and continuous lung function variables was analyzed using multiple linear regression analysis, adjusted for age, height, and pack-years. Analyses were performed using a statistical software package (Stata SE, version 8.2; Stata Corporation; College Station, TX).

Patient Characteristics and Frequencies of Exposure

A total of 194 patients (185 men, 9 women) visited the outpatient clinic during the study period. Because of the small number of women, it was decided not to include their data in the analysis. All had normal α1-antitrypsin levels. Thirteen of the patients included had emphysema without airflow obstruction. The corresponding demographic, clinical, smoking, lung function, and employment characteristics are shown in Table 1. The mean age of the patients was 66.2 years (SD, 10.7 years). Among them, 183 patients (98.9%) were or had been smokers, with a mean cumulative exposure of 58.8 pack-years (SD, 30.1 pack-years). The mean duration of disease was 11.5 years (SD, 0.8 years). Eighty-seven percent of the patients were or had been manual workers, and the most prevalent employment sector was agriculture (11.8%), followed by construction (5.5%), metallurgy (3.4%), and a miscellaneous category. The occupational status in our patients was as follows: 42 patients were active (mean age, 54.3 years); 34 patients (mean age, 60.8 years) had become unemployed due to COPD at a mean age of 51.8 years; 18 patients (mean age, 67.2 years) had become unemployed for other reasons (mean age, 53.8 years); and 91 patients (mean age, 73.6 years) were retired, with a mean age at retirement of 61.6 years.

Table Graphic Jump Location
Table 1 Demographic and Respiratory Health Characteristics of 185 Male COPD Outpatients*

*Values are given as mean (SD) [range] or No. (%). MRC = Medical Research Council.

Table 2 shows descriptive statistics of occupational exposure to each of the considered agents. About half of the patients had sometimes been highly exposed to each of the individual agents. Only 7% of the cohort had never been exposed to any agent. High exposure to biological dust was mainly related to work in agriculture, wood processing, bakeries, and textile manufacturing. High mineral dust exposure was found predominantly among workers in construction, the metal industry, and mining. Finally, high exposure to gases or fumes was related to welding and other metal-processing industries, painting, and printing, and to work in the electronics and plastics industries.

Table Graphic Jump Location
Table 2 Descriptive Statistics of Lifetime Occupational Exposures (n = 185)*

*Values are given as No. (%), unless otherwise indicated. Years = total No. of years having worked in jobs with high exposures (lifetime high exposure only).

Relationship Between Occupational Exposure and Outcomes

FEV1 was reduced in exposed patients in comparison with unexposed patients, although the differences were not significant after adjusting for age and height. Tables 3 and 4 show the associations between respiratory health outcomes and lifetime and cumulative high occupational exposures, respectively. Occupational exposure to mineral dust, and exposure to dusts, gases, or fumes were significantly associated with having an FEV1 of <30% predicted compared with an FEV1 of ≥ 70% predicted. High exposures to biological dust and to gases and fumes were also more frequent in those patients with and FEV1 of < 30% predicted, although these associations did not reach statistical significance (p > 0.05). FVC was not significantly associated with occupational exposures. Sputum production and dyspnea were associated with high exposure to biological dust and dusts, gases, and fumes; work inactivity due to unemployment or retirement, including unemployment due to COPD, was associated with a cumulative high exposure to biological dust, and dusts, gases, and fumes. The associations between mineral dust and COPD symptoms followed the same pattern as the other exposures, but they were not statistically significant. No clear association was found between occupational exposures and wheeze or cough. The number of hospitalizations tended to be higher in those with high occupational exposures.

Table Graphic Jump Location
Table 3 Associations Between Lifetime High Occupational Exposures and Respiratory Health Outcomes*

*RRR = relative risk ratio.

†Ratio of arithmetic means from negative binomial regression models.

‡Relative risk ratio from multinomial logistic regression models.

Table Graphic Jump Location
Table 4 Associations Between Cumulative High Occupational Exposure and Respiratory Health Outcomes*

*OR and 95% CI are reported per 10 years of working in a job with high exposure, related to those who never had worked in a highly exposed job, adjusted for age and number of pack-years of smoking. See Table 3 for abbreviation not used in the text.

†Ratio of arithmetic means are derived from negative binomial regression models.

‡RRRs are derived from a multinomial logistic regression model.

Finally, being unemployed due to respiratory problems was not consistently related to any of the occupational exposures analyzed. Nevertheless, biological dust exposure was significantly associated (odds ratio [OR], 13; 95% confidence interval [CI], 1.3 to 126) with unemployment in the subgroup of patients < 65 years of age.

This is the first patient series in which the effect of occupational exposure on the clinical and functional characteristics of COPD patients without α1-antitrypsin deficiency has been investigated. Our findings show that exposure to mineral dust, biological dust, and dust or gas and fumes was independently associated with at least one of the following variables: COPD severity; clinical symptoms; and employment status.

Exposure to mineral dust and to any dusts, gases, or fumes was associated with having an FEV1 of < 30% predicted after adjusting for the number of pack-years smoked. The association between occupational exposure and reduced lung function has been demonstrated in population-based, occupational cohorts, and cross-sectional studies. In series of COPD patients, this association has been evaluated in two studies12,13 performed in patients with α1-antitrypsin deficiency. In a Swedish series12 of nonsmokers with α1-antitrypsin deficiency, occupational exposure was significantly associated with a lower FEV1 exclusively in subjects aged ≥ 50 years of age. In the second reported series,13 including smokers and nonsmokers, patients with high mineral dust exposure had a lower FEV1 than nonexposed patients. After adjusting for tobacco consumption, however, fumes remained as the single exposure that was independently associated with a lower FEV1/FVC ratio.13 In patients with COPD and no α1-antitrypsin deficiency undergoing a 5-year longitudinal follow-up,16 the association between occupational exposure and FEV1 impairment has been demonstrated only for fume exposure. However, in this study,16 dust exposure was not associated with FEV1 loss. Several explanations may account for this finding. First, this was a cohort including relatively young patients (mean age, 48 years) with early COPD. This fact, along with a follow-up period of only 5 years may account for the lack of change in the FEV1. Finally, the variable dust exposure was self-reported without using job exposure matrix (JEM), and no distinction between biological dust and mineral dust was drawn. For these reasons, we believe our finding that high mineral dust exposure is associated with COPD severity should be tested in future longitudinal studies.

In our series of COPD patients, those with the highest exposure levels to biological dust and combined contaminants experienced sputum production more often than those with the lowest exposures, although the mechanisms underlying this effect are not fully understood. Occupational cohort studies7,23,24 have documented that inhalation exposure leads to chronic bronchitis, and population-based studies5,25,26 have demonstrated an association between occupational exposure and bronchitis symptoms such as sputum production and cough. Bronchial hypersecretion has been associated with increased hospitalization due to COPD.27 In our series, however, occupational exposure was associated with increased bronchial hypersecretion and also, albeit nonsignificantly, with more hospital admissions in the past year. Studies of the influence of bronchial hypersecretion on the functional status of COPD have produced inconsistent results. While some authors28 have shown an association between hypersecretion and FEV1 in COPD patients, others29 have not.

We also found an association between dyspnea and both biological dust exposure and combined exposure. Although the interaction between occupational exposure and dyspnea has been described in numerous population-based studies,25,30,31 the reasons behind the association are difficult to explain. Dyspnea is defined as a subjective sensation of shortness of breath or difficulty breathing that involves different neurophysiologic and psychological mechanisms. Occupational exposure favors the entrance of exogenous agents that can irritate the bronchial epithelium. It has been suggested32 that dyspnea appears when the lung receptors (ie, free nerve endings in the epithelium and submucosa of large airways) that regulate ventilation are stimulated. Accordingly, impulses arising from chemical stimuli such as noxious gases or inhalants would travel up the vagus along myelinated fibers, and the reflex effect would cause hyperpnea. In view of the hypothesis33 that dyspnea might be due to a dissociation or mismatch between central respiratory motor activity and incoming afferent information from airway receptors, it may be hypothesized that agents inhaled in an occupational setting might alter these receptors and cause a permanent increase in the afferent stimuli that lead to shortness of breath.

Work-related disability is one of the numerous effects that COPD has on patients' lives. In a recent population-based study involving individuals between 20 and 45 years of age from different European countries, it was found34 that 4% of the interviewed patients reported work-related respiratory disability. To date, this effect has been investigated in COPD patients in only one study conducted by Blanc and colleagues.15 They found that 25% of their patients reported work-related respiratory disability, and 16% reported exposure to vapors, gas, dust, or fumes, with an association between work-related disability and combined exposure. In agreement with these findings, we have found that biological dust exposure and combined exposure were associated with work inactivity due to unemployment or retirement. However, there was no association between unemployment specifically due to COPD and occupational exposure. This discrepancy could be due to individual patient characteristics or to the different conditions under which disability status is awarded from one country to another. Another reason could be the different definitions of occupational status and the different methods used to compile the information. The patients in the study by Blanc et al15 were asked whether the reason they were not working was, at least partly, due to “lung or breathing condition.” The corresponding question in our study was probably more accurate, because our patients were asked whether the reason for having stopped working was COPD diagnosis. This factor might be responsible for the smaller number of patients who reported respiratory-related work disability in our series. Furthermore, our study only analyzed long-term disability, while the study by Blanc et al15 included both long-term and temporary disabilities. The variable measured was, therefore, different. Nevertheless, our results suggest that occupational exposure has a negative impact on the occupational activity of patients with COPD, and this, in turn, has both social and economic consequences.

Some limitations may be found in our study. First, we only analyzed the data from men. Although patients were included consecutively, few women were available for the study, perhaps reflecting the fact that in Spain young women started smoking relatively recently. As a result, the percentage of smokers among older women in Spain still lower than that in other countries.35 Therefore, we decided to exclude women in order to avoid difficulties in interpreting the results.

This undoubtedly highlights the problem of not being able to extrapolate occupational respiratory disease data to the general population. Furthermore, some peculiarities of our series should be pointed out. On one hand, being a clinic of COPD patients who were referred from other departments, there was a high percentage of patients with moderate and severe stages of the disease, although this stage distribution is appropriate in order to asses the relationship between occupational exposure and COPD severity. On the other hand, the patients in our series were recruited at a public hospital attended by predominantly working-class people; hence, the high rate of occupational exposure in our series was higher than that reported by other studies12,13 among COPD patients. These differences might arise due to various methodological reasons. For example, while we included jobs that had lasted for 3 consecutive months, other studies established a minimum period of 12 months13 or only included the longest-held jobs.15 Our definition of exposure, therefore, may be responsible for the increased rate of occupational exposure in our series. Another reason could be that some of the studies mentioned did not use a job exposure matrix to determine exposure.12,13 Furthermore, it is also plausible that the individuals with α1-antitrypsin deficiency who were included in other studies, being aware of their condition, more frequently avoided jobs that involved exposure to contaminants. Finally, it should be borne in mind that, although the job questionnaire used was highly comprehensive, it is still a semi-quantitative retrospective estimate of occupational exposure and, therefore, depends largely on the patient's memory. This is a common problem in occupational health studies, particularly those with a cross-sectional design. We estimated occupational exposure using a job exposure matrix in order to assess objectively information on exposure type, intensity, and duration.

Our findings show that occupational exposure has an impact on the characteristics of COPD, specifically airflow obstruction severity, respiratory symptoms, and unemployment. We believe that the importance of avoiding smoking in preventing COPD is reinforced by the following two facts that were observed in our study: (1) most of our patients were or had been smokers; and (2) smoking is very likely to contribute to the development of COPD in conjunction with occupational exposures. Moreover, our data support the need to strengthen existing preventive measures to limit potential sources of contamination and reduce the amounts of airway irritants inhaled by workers. It is also essential to conduct systematic checkups in COPD patients who work in environments involving exposure to contaminants. These medical evaluations must include lung function tests and symptom questionnaires.

CI

confidence interval

OR

odds ratio

Korn RJ, Dockery DW, Speizer FE, et al. Occupational exposures and chronic respiratory symptoms: a population-based study. Am Rev Respir Dis. 1987;136:298-304. [PubMed] [CrossRef]
 
Krzyzanowski M, Kauffmann F. The relation of respiratory symptoms and ventilatory function to moderate occupational exposure in a general population: results from the French PAARC study of 16,000 adults. Int J Epidemiol. 1988;17:397-406. [PubMed]
 
Xu X, Christiani DC, Dockery DW, et al. Exposure-response relationships between occupational exposures and chronic respiratory illness: a community-based study. Am Rev Respir Dis. 1992;146:413-418. [PubMed]
 
Post WK, Heederik D, Kromhout H, et al. Occupational exposures estimated by a population specific job exposure matrix and 25 year incidence rate of chronic nonspecific lung disease (CNSLD): the Zutphen Study. Eur Respir J. 1994;7:1048-1055. [PubMed]
 
Sunyer J, Kogevinas M, Kromhout H, et al. Pulmonary ventilatory defects and occupational exposures in a population-based study in Spain: Spanish Group of the European Community Respiratory Health Survey. Am J Respir Crit Care Med. 1998;157:512-517. [PubMed]
 
Love RG, Miller BG. Longitudinal study of lung function in coal-miners. Thorax. 1982;37:193-197. [PubMed]
 
Seixas NS, Robins TG, Attfield MD, et al. Longitudinal and cross sectional analyses of exposure to coal mine dust and pulmonary function in new miners. Br J Ind Med. 1993;50:929-937. [PubMed]
 
Hnizdo E, Baskind E, Sluis-Cremer GK. Combined effect of silica dust exposure and tobacco smoking on the prevalence of respiratory impairments among gold miners. Scand J Work Environ Health. 1990;16:411-422. [PubMed]
 
Meijer E, Kromhout H, Heederik D. Respiratory effects of exposure to low levels of concrete dust containing crystalline silica. Am J Ind Med. 2001;40:133-140. [PubMed]
 
Bergdahl IA, Toren K, Eriksson K, et al. Increased mortality in COPD among construction workers exposed to inorganic dust. Eur Respir J. 2004;23:402-406. [PubMed]
 
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Figures

Tables

Table Graphic Jump Location
Table 1 Demographic and Respiratory Health Characteristics of 185 Male COPD Outpatients*

*Values are given as mean (SD) [range] or No. (%). MRC = Medical Research Council.

Table Graphic Jump Location
Table 2 Descriptive Statistics of Lifetime Occupational Exposures (n = 185)*

*Values are given as No. (%), unless otherwise indicated. Years = total No. of years having worked in jobs with high exposures (lifetime high exposure only).

Table Graphic Jump Location
Table 3 Associations Between Lifetime High Occupational Exposures and Respiratory Health Outcomes*

*RRR = relative risk ratio.

†Ratio of arithmetic means from negative binomial regression models.

‡Relative risk ratio from multinomial logistic regression models.

Table Graphic Jump Location
Table 4 Associations Between Cumulative High Occupational Exposure and Respiratory Health Outcomes*

*OR and 95% CI are reported per 10 years of working in a job with high exposure, related to those who never had worked in a highly exposed job, adjusted for age and number of pack-years of smoking. See Table 3 for abbreviation not used in the text.

†Ratio of arithmetic means are derived from negative binomial regression models.

‡RRRs are derived from a multinomial logistic regression model.

References

Korn RJ, Dockery DW, Speizer FE, et al. Occupational exposures and chronic respiratory symptoms: a population-based study. Am Rev Respir Dis. 1987;136:298-304. [PubMed] [CrossRef]
 
Krzyzanowski M, Kauffmann F. The relation of respiratory symptoms and ventilatory function to moderate occupational exposure in a general population: results from the French PAARC study of 16,000 adults. Int J Epidemiol. 1988;17:397-406. [PubMed]
 
Xu X, Christiani DC, Dockery DW, et al. Exposure-response relationships between occupational exposures and chronic respiratory illness: a community-based study. Am Rev Respir Dis. 1992;146:413-418. [PubMed]
 
Post WK, Heederik D, Kromhout H, et al. Occupational exposures estimated by a population specific job exposure matrix and 25 year incidence rate of chronic nonspecific lung disease (CNSLD): the Zutphen Study. Eur Respir J. 1994;7:1048-1055. [PubMed]
 
Sunyer J, Kogevinas M, Kromhout H, et al. Pulmonary ventilatory defects and occupational exposures in a population-based study in Spain: Spanish Group of the European Community Respiratory Health Survey. Am J Respir Crit Care Med. 1998;157:512-517. [PubMed]
 
Love RG, Miller BG. Longitudinal study of lung function in coal-miners. Thorax. 1982;37:193-197. [PubMed]
 
Seixas NS, Robins TG, Attfield MD, et al. Longitudinal and cross sectional analyses of exposure to coal mine dust and pulmonary function in new miners. Br J Ind Med. 1993;50:929-937. [PubMed]
 
Hnizdo E, Baskind E, Sluis-Cremer GK. Combined effect of silica dust exposure and tobacco smoking on the prevalence of respiratory impairments among gold miners. Scand J Work Environ Health. 1990;16:411-422. [PubMed]
 
Meijer E, Kromhout H, Heederik D. Respiratory effects of exposure to low levels of concrete dust containing crystalline silica. Am J Ind Med. 2001;40:133-140. [PubMed]
 
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