Childhood Lower Respiratory Illnesses Linked to Adult Lung Abnormalities

Patients with lower respiratory tract illnesses (LRIs) as children experienced increased air trapping at age 26, thus suggesting a link between lung development and childhood infections, according to a study in Respiratory Medicine.

Early life LRIs are believed to influence lung structure and function in adulthood, but the specific effects of LRIs and other early-life factors on lung development, and the extent of the association, have yet to be explored. Researchers therefore sought to explore the association between early childhood LRIs and structural lung changes seen in young adults, using data from the Tucson Children’s Respiratory Study (TCRS) cohort.

A total of 1246 healthy infants were enrolled in the study from 1980 to 1984. At age 26 years, 39 participants (21 female; 27 non-Hispanic White), who were prioritized according to whether they had lung function testing during infancy, completed postbronchodilator high-resolution chest computed tomography (CT) scans.

The percentage of lung voxels with attenuation less than -856 Hounsfield units (%LAA_-856) at end-expiratory lung volume (EELV) was used to calculate the percentage of gas trapping. Respiratory symptoms within the previous year, lung function, total lung capacity by nitrogen washout at the CT scan, and lung clearance index were evaluated.

The participants had a range of CT-assessed %LAA_-856 values of 0.2% to 38.0% (median, 14.3%, interquartile range, 3.2%-22.3%).

Of the cohort, 33 participants had complete LRI data from birth through age 3 years, and 18 of these participants (54.6%) had at least 1 LRI. An LRI was associated with greater %LAA_-856. The mean %LAA_-856 was 18.8% (95% CI, 13.7 – 23.9) for individuals with a history of LRI and 9.5% (95% CI, 3.2 -15.7) for those without an LRI (P =.018).

Patients with a history of LRI had significantly greater %LAA_-856 compared with patients without an LRI (adjusted beta coefficient: 7.4%; 95% CI, 0.35% – 14.5%; P =.040), after adjustment for sex and body mass index (BMI). The relationship between LRI and %LAA_-856 did not notably change after adjustment for smoking at age 26 based on “never smoker” and “ever smoker” status (adjusted beta coefficient: 7.3%; 95% CI, 0.1% – 14.6%; P =.047) or respiratory symptoms within the previous year (adjusted beta coefficient: 8.3%; 95% CI, 1.2% – 15.3%; P =.023).

Patients with respiratory syncytial virus (RSV) had a comparable %LAA_-856 vs those with a non-RSV LRI (P =.848). No significant interaction was found between sex and LRI on %LAA_-856 (interaction P =.710) after adjustment for BMI.

An inverse correlation was observed between %LAA_-856 and percentage of predicted post-bronchodilator forced expiratory flow (FEF)_25-75. Physician-diagnosed asthma occurred in 11 participants and did not affect the relationship between LRI and %LAA_-856.

No significant differences were found regarding LRI by sex, race/ethnicity, maternal smoking, or maternal asthma. LRI was not associated with ever smoking, BMI, forced expiratory volume in 1 second/forced vital capacity ratio, FEF_25-75, CT airway measures, or symptom score at age 26.

Study limitations included: 1) the inability to determine whether the association between LRI and structural changes on CT resulted from lung structural damage caused by the respiratory infection or from pre-existing deficits in lung structure; and 2) difficulty in determining whether increased %LAA_-856 in patients with a childhood LRI was associated with parenchymal structural changes, because none of the individuals had a clear emphysematous pattern.

“These observations provide the first evidence of structural lung abnormalities associated with LRIs earlier in life,” concluded the researchers. “Further studies are needed in order to clarify the prognostic significance of these findings on CT in a population-based sample, and to shed light onto the physiology of lung structural changes over the course of life.”

Disclosure: Some of the study authors declared affiliations with biotech, pharmaceutical, and/or device companies. Please see the original reference for a full list of authors’ disclosures.