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Emphysema Linked to Secondhand Smoke

By Charles Bankhead, Staff Writer, MedPage Today
Reviewed by Robert Jasmer, MD; Associate Clinical Professor of Medicine, University of California, San Francisco
December 29, 2009

Childhood exposure to environmental tobacco smoke correlated with increased evidence of emphysema on lung scans of nonsmoking adults, data from a large cohort study showed.

Structural and quantitative indices of emphysema differed significantly on CT lung scans of adults with a childhood history of secondhand smoke exposure compared with those with a negative exposure history, Gina S. Lovasi, PhD, of the Mailman School of Public Health of Columbia University in New York, and colleagues reported online in the American Journal of Epidemiology.

Although not proof of a causal relationship, the findings add to existing evidence of detrimental effects of exposure to environmental tobacco smoke, according to the researchers.

"This finding suggests that the lungs many not recover completely from the effects of early-life exposures and adds to the literature on detrimental effects of environmental tobacco smoke exposure," Lovasi and colleagues concluded.

The principal cause of panlobular emphysema is alpha 1-antitrypsin deficiency, which affects less than 0.1% of the population. Other potential risk factors for panlobular emphysema in nonsmokers have not been well described, primarily because of lack of population-based data on quantitative measures of emphysema, the authors wrote.

The mechanical hypothesis of emphysema posits that the condition arises and progresses as a result of mechanical strain on alveolar walls, predisposing them to rupture, the authors continued. Loss of alveolar-wall integrity and rupture increases strain on adjacent alveolar walls, perpetuating emphysematous sac propagation and enlargement.

This and several other theories of emphysema etiology imply that early insults to the alveolar wall should have a disproportionately large impact on development of emphysema. Early-life insults might include environmental tobacco smoke exposure.

To explore associations between childhood exposure to environmental tobacco smoke and emphysema in nonsmoking adults, Lovasi and colleagues analyzed data from the Multi-Ethnic Study of Atherosclerosis (MESA), a prospective cohort study of subclinical cardiovascular disease.

MESA involved 6,814 men and women ages 45 to 84, including 3,965 participants in a lung substudy.

The researchers' analysis included 1,781 participants in the lung study, all of whom were nonsmokers (verified by measuring urinary nicotine levels). The MESA protocol included cardiac CT that imaged about 70% of the lung volume from the carina to lung base. Each participant had two scans, and the scan with greater air volume was used for analysis.

Using the lung scans, investigators performed a standard quantitative measure (percent emphysema) and a fractal, structural measure (alpha) of early emphysema. Lower alpha values indicated more extensive emphysema.

The study population included 726 adults who had no childhood exposure to environmental tobacco smoke, 655 from households in which only the father smoked, 134 from households in which only the mother smoked, and 247 from households in which both parents smoked.

Investigators found that exposure to tobacco smoke in childhood was associated with a significantly lower alpha value (P=0.04 for trend) and significantly more emphysema (P=0.01 for trend).

Nonsmoking adults from households with two or more smokers had a mean alpha value that was 0.05 lower and emphysema involvement 2.8% greater compared with adults from households with no smokers.

The significant differences emerged after adjustment for demographic, anthropometric, parental, and participant characteristics, as well as cumulative environmental exposures in adulthood, such as residential air pollution and adult exposure to tobacco smoke.

Pulmonary function did not differ significantly by the extent of childhood exposure to environmental tobacco smoke.