Statins Tied to Lung Damage in Smokers

One more thing to talk to your doctor about statins.
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Statin use appears to be associated with interstitial lung abnormalities among current and former smokers, researchers found.
Among individuals with a history of at least 10 pack-years of smoking, statin use was associated with a 60% increase in the odds of having abnormalities on CT scans (OR 1.60, 95% CI 1.03 to 2.50), according to Gary Hunninghake, MD, MPH, of Brigham and Women's Hospital in Boston, and colleagues.
The findings were independent of a history of high cholesterol, coronary heart disease, or a number of other cardiovascular risk factors, the researchers reported online in the American Journal of Respiratory and Critical Care Medicine.
"Our findings suggest that statins may influence the susceptibility to, or progression of, interstitial lung disease," they wrote.
But they advised caution before applying the findings to patient care because the possible risks of statins on interstitial lung abnormalities likely do not outweigh the benefits of statin therapy in patients with cardiovascular disease.
"In addition, our findings do not rule out the possibility that statin use could benefit some patients with respiratory disease," they wrote. "Instead, we believe that clinicians should be aware that radiographic evidence of interstitial lung disease, much like myopathy, can occur in some patients on statins."
Previous studies have provided conflicting evidence on the relationship between statins and interstitial lung disease, so Hunninghake and colleagues examined data from the COPDGene study to further explore the issue.
The current analysis included 2,115 current and former smokers who underwent chest CT scans.
By definition, interstitial lung abnormalities affected more than 5% of any lung zone and included non-dependent ground-glass or reticular abnormalities, diffuse centrilobular nodularity, nonemphysematous cysts, honeycombing, or traction bronchiectasis.
The percentage of patients with such abnormalities was greater among patients taking statins (38% versus 27%, P=0.04).
The relationship between statins and lung abnormalities was stronger with more hydrophilic statins and with older patient age (P<0.05 for both trends). Pravastatin (a hydrophilic statin, brand name Pravachol) was most strongly associated with abnormalities (OR 4.61, 95% CI 1.99 to 10.70).
Hunninghake and colleagues explored the potential mechanism underlying the association between statins and lung damage using mice and cell cultures.
They found that pretreating mice with pravastatin enhanced the lung inflammation and fibrosis induced by bleomycin.
Also, in vitro studies revealed that statins increased the generation of mitochondrial reactive oxygen species in macrophages, which increased NLRP3-inflammasome activation.
The experimental findings conflict with two previous studies in which statins reduced bleomycin-induced lung injury. Hunninghake noted that those studies differed based on the type of statin, the dose of bleomycin, and the timing of statin administration.
But they acknowledged some limitations of the current analysis, including the lack of data to correlate the experimental findings in mice to humans, the lack of biopsies in the human participants, the lack of information on the duration of statin use or dose for most patients, and the possibility that the findings apply only to current and former smokers.
Despite the potential negative association of statins with interstitial lung damage, recent studies have shown that statins might confer protective benefits for those hospitalized with the flu and for those who suffered a head trauma.