COPD in the Never-Smoker

By David M. Mannino, MD, FCCP; and Kathryn Marie McGonigle

Print This | TOC | Previous | Next

---

Extrinsic Factors in COPD Pathogenesis

Occupational exposures. Occupational exposures play an important role in COPD development and progression.^9,13 Occupationally related COPD can occur in either the presence or the absence of agents known to induce occupational asthma, and it is useful to look at these exposure classifications separately.

More than 200 agents are known to cause asthma in the workplace; a partial list is shown in Table 4.³² Continued exposure to occupational asthmogenics, such as plicatic acid, grain dust, cotton dust, or toluene diisocyanate, has been shown to result in irreversible airflow limitation.^33-35 These exposures can be modified by other factors, such as genetics or smoking.

Table 4ÑSelected Occupational Agents Associated With Asthma and COPD*

Agent	Occupation
Asthma
Grain dust	Grain handling
Toluene diisocyanate	Foam manufacturing, plastics
Trimellitic anhydride	Plastics, epoxy resins
Platinum salts	Platinum refining
Western red cedar (plicatic acid)	Logging, lumber processing
Colophony	Electronics manufacturing
Natural latex	Health care
Pigeons	Pigeon breeding
Crabs	Crab production/processing
Trypsin	Pharmaceutical processing
Bacillus subtilis	Detergent manufacturing
COPD
Cadmium	Metal processing
Coal dust	Mining
Silica dust	Mining
Welding fumes	Steelworkers, shipbuilding
Chlorine gas	Pulp mill workers
Popcorn flavoring	Popcorn packers
*Modified from Rabatin and Cowl32 and Hendrick.13

 

COPD can also occur with occupational exposures not associated with asthma development. Cadmium is unique in that it is the one occupational agent that causes emphysema.³⁶ Other occupational exposures linked to the development of COPD include mineral dusts, welding fumes,¹³ chlorine gas, and, most recently, popcorn flavoring.³⁷

High-dose irritant exposures (ie, fire smoke, chlorine gas) that cause a life-threatening acute pulmonary toxicity may result in reactive airways dysfunction syndrome or bronchiolitis obliterans.³⁸

Air pollution. Both outdoor and indoor air pollutants can cause exacerbations of existing lung disease. The primary outdoor air pollutants of interest include ozone, particulate matter, and sulfur dioxide; important indoor pollutants include environmental tobacco smoke, wood smoke, and nitrogen oxides.

Recent longitudinal studies have suggested an association between exposure to ozone, particulate matter, and sulfur dioxide and decreased lung function in a population of never-smokers.¹⁴ This effect was increased in subjects whose parents had a history of respiratory disease (asthma, bronchitis, emphysema, hay fever), suggesting an additional genetic influence.

Exposure to indoor air pollutants can frequently result in higher exposures than one would obtain from outdoor exposures. Tobacco smoke, wood smoke, and cooking fumes have all been associated with the development of COPD.^29,39 As was demonstrated with outdoor exposures, indoor exposures also result in more COPD among people with genetic risk factors.⁴⁰

Pediatric exposures. Impaired lung function, poor lung growth in utero, and premature or accelerated declines in lung function during childhood can eventually lead to COPD or other respiratory diseases during adulthood.^39,41 Important exposures associated with impaired lung growth in children include tobacco smoke exposure and lower respiratory infections.^11,39,41

Infections. Lower respiratory tract infections, during both childhood and adulthood, are implicated in the pathogenesis of COPD and have important roles in COPD exacerbation The main etiologic agents of adult COPD-related infections include Haemophilus influenzae, Moraxella catarrhalis, Streptococcus pneumoniae, and Staphylococcus aureus.⁴² Psuedomonas aeruginosa has more recently been identified as a component in severe COPD cases.⁴² Adenovirus and other common respiratory viral pathogens are also found.⁴³ It is not clear whether respiratory infections are more important in COPD development in those who have never smoked.

Nutrition. Nutritional factors are probably important in the development and progression of COPD. Antioxidants such as vitamin E, vitamin C, and N-acetylcysteine have been found to be beneficial in decreasing COPD exacerbations in some studies.^44,45 Retinoid use has been associated with neoalveolarization.⁴⁶ Vitamin C and flavonoids have been associated with improved lung function.¹⁸ Fish oils have been shown to be associated with better lung function.⁴⁷ Poor nutritional status has also been implicated in accelerated disease decline. Weight loss, cachexia, and muscle weakness are associated with increased oxidative stress, increased TNF-α levels, and a worsened prognosis.⁴⁸

---

Print This | TOC | Previous | Next

3300 Dundee Road • Northbrook, Illinois 60062-2348 • (847) 498-1400 • (800) 343-2227
Copyright ©1999-2008 American College of Chest Physicians. All Rights Reserved.
ACCP Privacy Policy | ACCP Web Site Terms of Use