Can exposure to perchloroethylene (PCE), trichloroethylene (TCE), vinyl chloride, and benzene contribute to the development of emphysema?

Emphysema and Camp Lejeune Water Contaminants

Based on the available evidence, the specific contaminants found in Camp Lejeune water—perchloroethylene (PCE), trichloroethylene (TCE), vinyl chloride, and benzene—are not established causes of emphysema. While these chemicals cause significant liver toxicity and certain cancers, the respiratory effects are limited primarily to increased susceptibility to infections, possible asthma exacerbations, and rare autoimmune conditions rather than emphysema itself.

Evidence for Respiratory Effects of Each Contaminant

Trichloroethylene (TCE)

• TCE exposure shows conflicting evidence for respiratory disorders, with limited data supporting associations with asthma, chronic bronchitis, or rhinitis 1
• One registry study reported elevated rates of asthma and emphysema among those exposed to volatile organic compounds including TCE, but this was based on self-reported outcomes without objective confirmation 2
• The most consistent respiratory finding with TCE is association with autoimmune conditions like systemic sclerosis and pulmonary veno-occlusive disease, not emphysema 1
• Animal studies showed TCE decreased pulmonary bactericidal activity and increased susceptibility to respiratory infections, but did not demonstrate emphysema development 3

Perchloroethylene (PCE)

• PCE primarily causes liver toxicity (fatty liver disease) rather than emphysema 4
• Animal inhalation studies at high concentrations showed no neoplastic changes in respiratory tracts, only minimal squamous metaplasia in nasal cavities of rats 5
• PCE decreased pulmonary bactericidal activity in mice but did not produce emphysema 3

Vinyl Chloride

• Vinyl chloride is strongly associated with liver angiosarcoma and hepatocellular carcinoma, not respiratory disease 6, 4, 7
• The European Association for the Study of the Liver (EASL) recommends surveillance for liver neoplasms in workers exposed to high levels before the mid-1970s, but makes no recommendations regarding emphysema screening 6, 4
• No evidence links vinyl chloride exposure to emphysema development 7

Benzene

• Benzene is classified among volatile organic compounds that may contribute to hepatocellular necrosis and steatosis, with primary toxicity to the liver and hematopoietic system 4
• No established link exists between benzene exposure and emphysema

Established Causes of Emphysema to Consider

When evaluating emphysema in Camp Lejeune-exposed individuals, consider these proven risk factors instead:

Genetic Factors

• Alpha-1 antitrypsin (AAT) deficiency should be tested in any patient with emphysema without significant smoking history, as recommended by the American Thoracic Society 8
• PI*ZZ phenotype individuals have significantly increased emphysema risk even without smoking 8

Occupational Exposures That Do Cause Emphysema

• Occupational exposures to dusts, fumes, and gases independently cause emphysema and are underappreciated risk factors 8
• Mineral dust, cotton mill work (endotoxin), grain working, and mining are established occupational causes 8
• These are distinct from the chlorinated solvents found at Camp Lejeune

Other Risk Factors

• Smoking remains the primary cause, with PI*ZZ individuals showing mean FEV1 declines of 70 ml/year in current smokers versus 41-47 ml/year in never-smokers 6
• Childhood respiratory infections and abnormal lung development account for approximately 50% of COPD cases 8
• Asthma and airway hyperresponsiveness independently predict COPD development 8

Clinical Implications

For patients with Camp Lejeune exposure presenting with emphysema:

• The emphysema is likely due to other established causes (smoking, AAT deficiency, other occupational dusts/fumes) rather than the water contaminants 6, 8
• Test for AAT deficiency in all patients with emphysema, particularly those with early onset or minimal smoking history 8
• Obtain detailed occupational history for dust, fume, and gas exposures beyond the water contamination 8
• Consider liver surveillance given the strong hepatotoxic effects of PCE, TCE, vinyl chloride, and benzene 6, 4

Important Caveat

The one registry study suggesting elevated emphysema rates with volatile organic compound exposure relied on self-reported outcomes without spirometric confirmation and could not separate effects of individual chemicals 2. This represents low-quality evidence insufficient to establish causation, especially when weighed against the absence of emphysema findings in controlled animal studies and the lack of biological plausibility for these hepatotoxic agents causing emphysema.