Chronic Bronchitis & COPD

 

The following table shows in the first column the list of agents to be considered as causes of COPD. In the second column, the colored Xs designate the agents listed as increasing the risk for COPD, or at least the markers for COPD, according to several authors listed below. Columns to the right with the black Xs show the adverse effects for each agent in Haz-Map.

Table 1--Candidate Occupational Exposures That Increase Risk for COPD or Markers for COPD

 

COPD

BO

Fibrosis

Chronic bronchitis

Pneumonitis

Asthma

Lung Cancer

Coal dust

B A b S

 

X

X

 

 

 

Nitrogen dioxide

A C Sc

AbSc

 

 

X

 

 

Ozone

 

A b

 

 

X

 

 

Sulfur dioxide

ASCSc

A b Sc

 

 

X

 

 

Ammonia

A S C Sc

A Sc

 

X

X

 

 

Arsenic (As-Cl3)

C  

 

 

 

 

X

Chlorine

A C Sc

b

 

 

X

 

 

Cadmium

SCSc

 

 

 

X

 

X

Chromium

C  

 

 

 

 

X

X

Osmium tetroxide

b C

 

 

 

X

  

 

Phosgene

C Sc

A b

 

 

X

 

 

Tungsten carbide

C

 

X

 

 

X

 

Vanadium pentoxide

b C  

 

 

X

 

 

 

Monoisocyanates

A  

 

 

 

Diisocyanates SC X X

Welding fumes

KAbSC

 

 

X

 

 

 

Mineral dust

 

 

 

 

 

 

 

Cotton dust

BKAbS C

 

 

X

 

 

 

Grain dust

BKAbS

 

 

X

 

X

 

Wood dust

BKAbS

 

 

 

 

X

 

Flax dust

C

 

 

 

 

 

 

Soft hemp dust

C

 

 

 

 

 

 

Mixed potash

C

 

 

 

 

 

 

Phosphates

C

 

 

 

 

 

 

Oil mist, mineral

b

 

X

 

 

X

 

Silica, crystalline

BKAbS

 

X

X

 

 

X

Silicates

b

 

 

 

 

 

 

Synthetic vitreous fibers

b

 

 

 

 

 

 

Portland cement

A b C

 

 

 

 

 

 

Coke oven emissions

C

 

 

 

 

X 

Asbestos

B K A S

 

X

 

 

 

X

Livestock confinement

K A

 

 

X

 

 

 

Carbon black

K

Ceramic fibers

S

Iron/steel dust

S

Smoke

C

Foundries

C

Rubber plants

AC

Smelters

AC

Silicates

b  

Tobacco smoke

Kb  

Engine exhaust

b  

Farming dusts

K

Asphalt workers

A

Pulp & paper

KA

Bakers

K

Hydrogen fluoride

A

X

Hydrogen bromide

A

X

Hydrogen chloride

A

X

Sulfur mustard

A

X

Diacetyl

A

Alumium smelters

K

Tunnel workers

KA

 

B Becklake (Rom, 1998)

K Kennedy (Rosenstock, 2005)

A Asthma in the Workplace, 2006

b Balmes (LaDou, 2007)

S Stenton (Hendrick, 2002)

Sc Schwartz (Hendrick, 2002)

C Christiani (APHA, 2005) In the APHA chapter entitled "Bronchitis, chronic," the author states, "Chronic bronchitis in the absence of airflow obstruction or emphysema is not associated with premature mortality." In a commentary entitled Occupation and COPD, the author cited the following dusts and fumes that were linked to chronic airflow obstruction: coal, silica, cadmium, asbestos, cotton, and grain. [Occup Environ Med 2005;62:215.]

*BO (bronchiolitis obliterans) "Bronchiolitis obliterans characteristically presents with the insidious onset of a nonproductive cough and dyspnea 2 to 8 weeks after an acute respiratory illness or toxic exposure." [ Murray , p. 1297]

Definition of COPD

 

Figure 1

 

In the MeSH system used by the National Library of Medicine, "Pulmonary Disease, Chronic Obstructive" is defined as, "A disease of chronic diffuse irreversible airflow obstruction." Subcategories of COPD include chronic bronchitis and emphysema.

 

Figure 2

Figures 1 and 2 were obtained from Braunwald's Atlas of Internal Medicine accessed on www.MerckMedicus.com.

 

"The normal rate of decline of FEV1 with age is approximately 25-30 ml per year but it is more rapid in those destined to develop COPD, and cigarette smokers for example have an average annual loss of FEV1 which is 10-20 ml greater than that of non-smokers." [Hendrick, p. 78] " . . . weight gain due to increased fat deposition in middle age is associated with a marked reduction in FEV1 and FVC in longitudinal studies." [Hendrick, p. 81]

 

In Murray and Nadel's Textbook of Respiratory Medicine, 4th Ed., published in 2006, the authors of the the chapter on Chronic Bronchitis and Emphysema write: "Tobacco smoking accounts for 80% to 90% of the risk of developing COPD in the United States. . . . Occupational exposures are also associated with increased risk for accelerated loss of lung function, although the effect is usually small compared to the effect of cigarette smoking. Farming or work in dusty occupations increases the risk of developing chronic bronchitis two- to threefold, and in combination with smoking the risk increases to sixrfold. In the developing world, exposure to smoke generated from the use of biomass fuels may be of comparable importance to smoking in some settings." The "Environmental and Occupational Disorders" covered in that textbook include: Occupational Asthma,  Pneumconioses, Hypersensitivity Pneumonitis, and Acute Pulmonary Responses to Toxic Exposures.

 

"' How much exposure is necessary before one should suspect an occupational contribution to COPD?', most research indicates that the relevant exposure duration is measured in years (or even decades), not months or days." [Kennedy S. Chronic Obstructive Pulmonary Disease and Chronic Bronchitis. In: Rosenstock, p. 325.]

 

"Chronic bronchitis is defined as the presence of chronic cough with sputum production most days (at least 4 per week) for at least 3 months per year for at least 2 consecutive years. . . . Chronic bronchitis is more common among among smokers, men, people over 40, and urban residents. It is usually preceded by 10 to 20 years of exposure to causative agents, with this time period declining with age." [Christiani DC. Bronchitis, Chronic. In: APHA, p. 132]

 

History of "Occupational COPD"

In the 1984 Surgeon General's report, only smoking and alpha-1-antitrypsin deficiency were accepted as being causally related to COPD. [Becklake MR. Occupational Exposures as a Cause of Chronic Airway Disease. In: Rom WN (ed). Environmental & Occupational Medicine, 3rd Ed. Philadelphia: Lippincott-Raven, 1998, p. 573]

 

Asthma and bronchitis, but not COPD, were listed as "occupational sentinel health events" published in 1991. [Mullan]

 

The topic "Chronic Obstructive Pulmonary Disease" was first used in the chapter on "Occupational Lung Diseases" in the LaDou textbook in the 3rd edition, published in 2004. In the previous edition published in 1997, the topic was "Chronic Bronchitis." The same list, "Some agents causing chronic bronchitis" appeared in both editions.

 

The topic "Chronic Obstructive Pulmonary Disease and Chronic Bronchitis" was first used in the Rosenstock textbook in the section on "Diseases of the Lung and Pleura" in the 2nd edition, published in 2005. In the first edition published in 1994, the topic was "Irritant Bronchitis."

 

The American Thoracic Society Statement: Occupational Contribution to the Burden of Airway Disease was published in 2003 and stated, "Despite the difficulty of disentangling the effects of cigarette smoke from those of other exposures, and increasingly impressive body of scientific literature is available demonstrating the specific occupational exposures contribute to the development of COPD." The committee considered the clinical spectrum of occupational airway diseases to include asthma, COPD, and organic dust-induced asthma-like disorders. Agents considered were for occupational asthma (over 250 agents), COPD (vanadium for bronchitis and cadmium for emphysema), and asthma-like disorders (endotoxins in cotton and grain dusts).

 

Debate about the Significance of "Occupational COPD"

"Whether workers with chronic simple bronchitis are at risk for the development of chronic airflow obstruction and permanent respiratory impairment is an area of controversy that has yet to be completely resolved." [Occupational Lung Disease by John R. Balmes in LaDou, 4th Ed., p. 329]

 

"The evidence in favor of a contribution from occupational exposures to COPD does not, therefore, derive from any single study, or even from studies of one particular working environment, and no single investigation has given an overwhelmingly convincing outcome. Rather, the evidence derives from the apparent consistency with which an excess prevalence of COPD has been reported in many different settings. The overall importance of occupational exposures is more difficult to determine. At one end of the spectrum, some authorities remain unconvinced that there is any important effect." [Hendrick, p. 83] On that same page is Table 5.2 "Some agents and exposures suspected of causing occupational COPD" At the bottom of the table, the authors write, "This list is not comprehensive. The evidence relating to some agents derives from single studies and is not universally accepted."

 

"Most of the studies summarized throughout this chapter have reported statistically significant reductions in airflow rates among groups of exposed workers compared to nonexposed workers. Symptoms of cough, phlegm, and wheezing are variable reported to be increased or not increased. The relevance of these findings with respect to disability and clinical outcome is strongly debated." [Agents Causing Chronic Airflow Obstruction by Susan M. Kennedy in Harber, p. 447]

 

"While it is clear that respiratory symptoms and chronic bronchitis are associated with biological dust exposure, the relationship with emphysema and COPD is less certain." Matheson MD et al. Biological dust exposure in the workplace is a risk factor for chronic obstructive pulmonary disease. Thorax 2005:60 645-651, In this study of 7005 adults 45-70 years old in Melborne, Australia, no increased risks for COPD were found for workers exposed to mineral dust or gases/fumes.

 

"Bronchitis and asthma have both been recognized for some time as being potentially work related. However, for various reasons, there is much greater reluctance on the part of clinicians to accept the potential work relatedness of COPD. [Becklake MR. Occupational Exposures as a Cause of Chronic Airways Disease, In: Rom WN (ed). Environmental & Occupational Medicine, 3rd Ed. Philadelphia: Lippincott-Raven, 1998, p. 574-6].

 

Positive Evidence

"Finally, and perhaps most important, the results of community-based studies have challenged the concept of nuisance dusts, a concept that has also recently been rejected by the Chemical Substances Committee of the American Conference of Governmental Industrial Hygienists (ACGIH), which, in a 1996 document, expressed the view that exposure to any dusts, if sufficiently heavy, is potentially harmful to human health, a widely held and clinically plausible view." [Becklake MR. Occupational Exposures as a Cause of Chronic Airways Disease, In: Rom WN (ed). Environmental & Occupational Medicine, 3rd Ed. Philadelphia: Lippincott-Raven, 1998, p. 574-6] 

 

" . . . given the wide variety of agents which have now been reported to be associated with COPD, it cannot be assumed that heavy occupational exposure to any inhaled substance is free from risk." [Hendrick, p. 85]

 

"Since the 1950s, reports have described emphysema due to cadmium fumes, particularly in workers exposed to cadmium oxide for long periods of time. In addition, emphysema occurs in coal workers. I f these workers also smoke, there is more emphysema and it is more advanced when compared with matched controls. Emphysema also occurs occasionally in relation other pneumoconioses, such as asbestosis and silicosis. Nitrogen oxides can cause emphysema in laboratory animals, but these findings have not been confirmed in humans." [Chrisitiani DC. Emphysema. In: APHA, p. 188] 

 

"COPD has also been clearly demonstrated in association with asbestos exposure." 

[Kennedy S. Chronic Obstructive Pulmonary Disease and Chronic Bronchitis. In: Rosenstock, p. 323.]

 

"Evidence of chronic airflow obstruction in relation to measures of welding exposure has been seen in most but not all studies designed to investigate this outcome. . . . Functional changes appeared to be reversible only among those welders who were consistently using local exhaust ventilation." [Asthma in the Workplace, p. 694-5]

 

Negative Evidence

"Thus, the study population included persons aged 30 to 80 years with a satisfactory spirometry test who had never smoked." " . . . obstruction was not explained by exposure to environmental tobacco smoke, high-risk occupation, air pollution (as measured by urban residence), or wood smoke (as measured by the use of a wood stove at home)." Celli BR, Halbert RJ, Nordyke RJ, Schau B. Airway obstruction in never smokers: results from the Third National Health and Nutrition Examination Survey. Am J Med. 2005 Dec;118(12):1364-72.

 

 See Lung function Decline, Chronic Bronchitis, and Occupational Exposures in Young Adults Sunyer J et al. Am J Resp Crit Care Med Vol 172. pp. 1139-1145. 2005. The conclusion of that paper was, "Occupational exposures to dusts, gases, and fumes occurring during the 1990s are associated with incidence of chronic bronchitis, although these did not impair lung function in a population of relatively young age."

 

". . . there is currently no conclusive evidence of any adverse respiratory disorder attributable to MMVF in man . . ." [Utell MJ, Lockey JE. Disorders Due to Manmade Vitreous Fibers. IN: Hendrick, p. 197]

 

"The dusts discussed in this chapter may produce radiographic changes and pulmonary reactions, but the condition  seldom progresses to impairment and respiratory disability." [Rom WN. Silicates and Benign Pneumoconioses. In: Rom WN (ed). Environmental & Occupational Medicine, 3rd Ed. Philadelphia: Lippincott-Raven, 1998, p. 587]

 

". . . in two recent studies, no relation between exposure to Portland cement dust and airflow limitation was found." Asthma in the Workplace, p. 690

 

"In conclusion, asbestosis is not currently thought to contribute to chronic obstructive pulmonary disease (COPD) and there is no evidence for a role of asbestos in producing emphysema. When COPD is detected with asbestosis, it is likely to be coincidental and a consequence of cigarette smoking." [Vuyst PD, Gevenois PA. Asbestosis. In: Hendrick, p. 148]

 

Incidence, Prevalence, and Mortality

"The prevalence of GOLD defined COPD was 7.0% (95% confidence interval (CI) 5.9 to 8.0). This estimate was 27% lower than COPD defined without bronchodilation. One percent of the population had severe or very severe COPD. . . . The prevalence of COPD using pre-bronchodilator values gives an overestimation, especially among young adults. . . . Neither occupational exposure to gas or dust nor residential area was significantly associated with GOLD defined COPD in this study population." Johannessen A, Omenaas ER, Bakke PS, Gulsvik A. Implications of reversibility testing on prevalence and risk factors for chronic obstructive pulmonary disease: a community study. Thorax. 2005 Oct;60(10):842-7.

 

" . . . reduction of workplace exposures to dust, gases and fumes would prevent one out of ten deaths due to COPD, regardless of other risk factors, such as cigarette smoking." This statement was based on a study of 317,629 Swedish male construction workers followed from 1971 to 1999. Bergdahl et al. Increased mortality in COPD among construction workers exposed to inorganic dust. Eur Respir J. 2004 Mar;23(3):402-6.

 

"The aim of this study was to estimate the cumulative incidence of COPD during a 7-year follow-up of an age-stratified general population sample and to evaluate the risk factors associated with incident disease. . . . The cumulative incidence of COPD according to GOLD II criteria corresponds to an annual incidence rate of 7 per 1,000 person per year in the total population, while it was 15 per 1,000 person per year in smokers and 2 per 1,000 per year in nonsmokers . . . " Lindberg A et al. Seven-year cumulative incidence of COPD in an age-stratified general population sample. Chest. 2006 Apr;129(4):879-85. The GOLD II criteria are FEV1/FVC ratio of <0.70 and FEV1 <80% predicted. No association was found between COPD and socioeconomic group. The 7 occupational groups included "manual workers in industry" and "manual workers in service." 

 

Table 2--Mortality from Occupational Lung Diseases and COPD

Disease

Year

No. of Deaths

% Male

Silicosis1 

1990-99 

(10 years)

2,405

96.3

Coal Worker's1 

1990-99 

(10 years)

15,036

99.3

Asbestosis1 

1990-99 

(10 years)

10,914

96.4

COPD2 

2007 

(1 year)

124,477

48.4

1.  http://www.cdc.gov/niosh/docs/2003-111/2003-111.html

2.  http://www.lungusa.org/lung-disease/copd/resources/facts-figures/COPD-Fact-Sheet.html

 

Conditions Related to COPD

"Patients with chronic airflow obstruction that is not due to chronic bronchitis, emphysema, or persistent asthma are not considered to have COPD, for example, patients with cystic fibrosis or obliterative bronchiolitis. . . . COPD is a disease state characterized by incompletely reversible, progressive airflow obstruction that is associated with inflammation in the lungs due to prolonged exposure to tobacco smoke and other noxious particles and gases." [Snider GL. Nosology for Our Day: Its Application to Chronic Obstructive Pulmonary Disease. Am J Resp Crit Care Med Vol 167. pp 678-683, (2003)]

 

"The prognosis of HP [hypersensitivity pneumonitis] is quite varied. If the diagnosis is made early and the causative agent or agents removed from the patient's environment, HP will heal and usually leave no permanent damage. Acute cases can be severe in terms of dyspnea, hypoxia, fever, and general weakness but are very rarely fatal. Continued exposure will often lead to recurrent acute episodes or a low-grade progression of the disease causing irreversible lung damage in the form of fibrosis, emphysema or  combination of both." [Hendrick, p. 231]

 

"Even in the absence of structural sequelae (which may be identified by imaging studies or through bronchoscopy) or significant defects in basal spirometry, a state of permanent non-specific airway hyperresponsiveness may be observed, often associated with asthmatic symptoms. This condition of adult-onset, non-allergic asthma has been named 'reactive airways dysfunction syndrome' (RADS) and occurs in a number of survivors of (severe) airway injury. Its incidence and the mechanisms giving rise to it remain to be elucidated." [Nemery B. Toxic Pneumonitis: Chemical Agents. In: Hendrick, p. 210]

 

"The accelerated longitudinal decline of ventilatory function in workers exposed to cotton, grain, and wood dust raises the possibility that other asthmagenic exposure might also contribute to the development of COPD. Support for this notion comes from a study of workers exposed to toluene diisocyanate, which is one of the most potent asthmagenic agents encountered in industrialized countries." [Hendrick, p. 83]

 

"The spectrum of occupational COPD also encompasses exposure to toxic agents which cause irreversible inflammatory disease in the terminal bronchioles, respiratory bronchioles, and alveolar ducts. The unique histopathology features of bronchiolitis (B) and bronchiolitis obliterans (BO) clearly distinguish these airway disease from other COPD entities. . . . Acute injury by toxic gases is a common cause of BO and has been reported after inhalation of high concentrations of nitrogen dioxide, sulfur dioxide, ammonia, hydrogen fluoride, phosgene, hydrogen bromide, and hydrogen chloride." Other possible causes of BO include methyl isocyanate and diacetyl. [Asthma in the Workplace, p. 697]

 

"Bronchiolitis obliterans and irritant-induced asthma are two other conditions that may overlap clinically with work-related COPD." [Balmes JR. Occupational Contribution to the Burden of Chronic Obstructive Pulmonary Disease. J Occup Environ Med. 2005;47:154-160]

 

Table 3--Respiratory Diseases in Haz-Map and Pulmonary Function Abnormalities

Syndrome

Obstructive/restrictive

Obstructive

Restrictive

Asbestosis

Yes

 

Yes

Chronic beryllium disease

Yes

Yes

Yes

Coal workers, pneumoconiosis of

 

 

 

CWP, complicated

Yes

 

Yes

Hard metal disease

 

 

Yes

Hypersensitivity pneumonitis, chronic

Yes

 

Yes

Hypersensitivity pneumonitis, acute

 

 

Yes

Silicosis, complicated

Yes

 

Yes

Silicosis, simple

 

 

 

Asthma, occupational

 

Yes

 

Asthma, irritant induced

 

Yes

 

Bronchitis, chronic

 

Yes

 

Byssinosis

 

Yes

 

 

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Revised: March 14, 2013

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