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Pediatric measles infection increases risk of COPD by middle age
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Although measles infection during childhood is not independently linked to chronic obstructive pulmonary disease — or post-bronchodilator airflow obstruction — the infection can strengthen the association between smoking, current asthma and post-bronchodilator airflow obstruction.
“Childhood respiratory infections have been known to predispose to airflow obstruction and reduced peak lung function, and therefore have the potential to contribute to the severity of [chronic obstructive pulmonary disease (COPD)] later in life,” Jennifer L. Perret, PhD, from the allergy and lung health unit within the Center for Epidemiology and Biostatistics at the University of Melbourne, Australia, the department of respiratory and sleep medicine at Austin Hospital, Melbourne, and the Institute for Breathing and Sleep, Melbourne, and colleagues wrote.
“Specifically, early childhood viral infections, such as respiratory syncytial virus, have been linked to asthma and airflow limitation in older children,” the researchers continued. “The long-term lung function consequences of the measles virus have not yet been established.”
Post-bronchodilator airflow obstruction on spirometry is used to confirm COPD diagnosis. To examine whether measles infection in childhood led to post-bronchodilator airflow obstruction during middle age with interactions caused by asthma or smoking, or both, the researchers conducted the population-based Tasmanian Longitudinal Health Study. All participants were born in 1961. Immunization was introduced to these participants after they were tested with spirometry. The researchers collected data from school medical records to determine the number of participants who had contracted measles during childhood.
Participants were followed up after 50 years, when a chosen amount received further testing of lung function. Perret and colleagues estimated relevant main association and interactions from asthma or smoking, or both, using results from post-bronchodilator forced expiratory volume in one s/forced vital capacity (FEV1/FVC < lower limit of normal). These estimates were calculated with multiple regression.
Of the 8,583 participants, 5,729 were available for follow-up after 50 years, and 1,389 underwent further testing. Childhood measles were reported in 950 of those who underwent further testing. When a history of childhood measles was present, the adverse effects of asthma and smoking (minimum: 10 packs per year) in middle age were amplified within post-bronchodilator FEV1/FVC ratios by middle age (z score, –0.7 [95% CI, –1.1 to –0.3] vs. –1.36 [95% CI, –1.6 to –1.1]; P = .009). This result was more prominent in those who experienced the onset of asthma during childhood.
When participants who did not have childhood measles were compared with those who were never- and ever-smokers of less than 10 packs of cigarettes per year with current asthma symptoms, the chances of post-bronchodilator airflow obstruction was not significant when childhood measles were present (OR = 12.0 [95% CI, 3.4-42] vs. 2.17 [95% CI, 0.9-5.3]).
“The concept of an asthma-smoking interaction in relation to post-bronchodilator airflow obstruction has been reported in our earlier work, but importantly, modification by childhood measles is a novel finding,” Perret and colleagues wrote. “The measles virus is highly contagious for all nonimmunized individuals who have not had the disease, and so was highly prevalent in this preimmunization era group, but we also found no independent effect of measles on its own.”
“This suggests that from an epidemiological viewpoint, childhood measles might contribute toward causing disease together with other component causes but is not sufficient to cause disease on its own,” the researchers added. – by Katherine Bortz
Disclosures: Perret reports no relevant financial disclosures. Please see the study for a full list of all other authors’ relevant financial disclosures.
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