A study published this month in the New England Journal of Medicine has shown that 75% of children with persistent asthma will go on to develop reduced lung functions and possibly chronic obstructive pulmonary disease (COPD) in adulthood.
Asthma is a respiratory condition marked by attacks of spasm in the bronchi of the lungs, causing difficulty in breathing. It is usually connected to allergic reaction or other forms of hypersensitivity. According to the Centre for Disease Control and Prevention (CDC), approximately 7 million children suffer from childhood asthma in the USA alone. This figure makes about 9% of all US children.
A number of studies have been carried out to assess the effect of childhood asthma on adult respiratory function. This particular study was carried out by physicians and researchers from multiple universities, including Harvard T Chan School of Public Health, Johns Hopkins Bloomberg School of Public Health and Brigham and Women’s Hospital.
The study followed 684 patients who were enrolled into the childhood asthma management program (CAMP). The age of enrolment varied between 5-12 years and the patients were followed through to their third decade of life. Annual bronchodilator and post-bronchodilator spirometry tests were done along with clinical assessment to document lung function. All the children enrolled had persistent moderate asthma in childhood. For this program, written informed consent was obtained from the parents and guardians of all children.
In addition to long term follow up of patients, CAMP also carried out a randomised, placebo-controlled trial of inhaled anti-inflammatory asthma medication. Patients were randomly assigned to receive either the anti-inflammatory medication (budesonide or nedocromil) or a placebo, all by inhalation. The treatment component of the trial lasted for 4.5 years and ended in 1999, and then the asthma care of the patients was transferred to their local healthcare practitioner. Observational follow up was then continued for 13 years.
The results were adjusted to take into account confounding factors such as age, sex, ethnicity, body mass index, and allergic status at the time of examination. The final outcome of the patients was also compared against the Global Initiative for Chronic Obstructive Lung Disease (GOLD) classification, to see if they had the criteria matching the diagnosis of COPD.
In persons without lung disease, forced expiratory volume in 1 second (FEV1) reaches its maximal level in late adolescence or early adulthood and remains stable for several years, a period known as the plateau of lung function, before gradually declining thereafter.
The results of the study found that 25% of the participants had normal lung function growth with no decline. The remaining 75% of participants experienced a decline in, or a reduced growth of lung function. The three patterns of growth decline seen are as follows:
- 26% reached normal growth of lung function, but had an early decline in growth, with the decline starting at a mean age of 21 years.
- 23% had reduced growth but no early decline.
- 26% of participants had both, a reduced growth as well as an early decline in lung function.
At their last spirometry test, participants who had reduced growth patterns were more likely to meet the GOLD criteria for chronic obstructive pulmonary disease (COPD). The percentage of participants who were diagnosed as COPD, based on which pattern of reduced growth they had, is as follows:
- Normal growth but early decline — 5% developed COPD
- Reduced growth but no early decline — 16% developed COPD
- Reduced growth and early decline — 21% developed COPD
In contrast only 1% of participants who had normal lung function developed COPD in adulthood.
The study also found that the anti-inflammatory medications did not have a better long-term effect than placebo on lung function growth.
However, some limitations of the study are to be noted. Firstly, the study does not establish asthma as the cause or effect of each pattern of lung function decline. It merely shows its co-occurrence. Secondly, additional risk factors, such as genetics, prematurity, childhood respiratory infections and environmental exposures were not available for analysis in the present study. It is possible that these factors could have an effect on lung function in adulthood. Thirdly, the study inclusion criteria was that patients should have moderate to severe persistent asthma. It is yet to be determined if patients of mild and intermittent asthma follow the same patterns of lung function decline.
The study also concludes that male gender and impaired lung function at enrolment are the strongest predictors to reduced lung function into adulthood. Identification of abnormal lung function by means of serial monitoring of children with persistent asthma may help identify those at risk of developing COPD earlier. Further research is needed to assess what treatment, if any, should be prescribed for those patients identified to be at risk.