LRTI in childhood linked to adult deaths from respiratory disease

The notion that premature adult mortality from respiratory disease is solely linked to smoking behaviour has been challenged by new research showing a strong association with infant respiratory infections.

An observational study, published in The Lancet (link here) found that children who had contracted a lower respiratory tract infection (LRTI) by the age of two had a 93% higher likelihood of dying prematurely from respiratory illness in adulthood than those who had not.

A research team led by Dr James Allinson, Consultant Respiratory Physician at the Royal Brompton Hospital, London, said this was equivalent to a 2.1% rate of premature adult death from respiratory disease in people who had a LRTI in infancy versus 1.1% for those who hadn’t.

The findings “add to the evidence that adults whose chronic lung disease has been attributed to smoking-related effects might also have disease resulting from childhood exposures that are largely preventable,” noted Professor Heather Zar, University of Cape Town, in a linked editorial.

The study was based on a UK cohort of 3,589 participants, with data collected from birth in 1946 to 2019.

Records showed that 25% of the cohort developed an LRTI before the age of two. At the last data collection point in 2019, 674 (19%) died before reaching 73 years old, of whom 52 (8%) had died from respiratory disease (largely COPD).

After adjusting for potential confounders such as smoking and socio-economic status, the researchers calculated that early LRTI accounts for one in five of premature deaths in adults caused by respiratory disease, equating to more than 179,000 excess deaths from respiratory illness in England and Wales across the years 1972 to 2019.

However, they found no link between infant LRTI and premature adult death from other causes such as cardiac, cancer, or all-cause mortality.

FEV1 a potential mediator

Also of note, findings of a supplementary analysis linked early childhood LRTI with reduced FEV1 at age 43 years, and showed that participants who had died from respiratory disease had lower FEV1 than those who were alive or had died from other causes, according to the paper.

“When FEV1 was added to the model of premature adult respiratory mortality, the HR for association with LRTI was lower than in the primary analysis (HR 1·24, 95% CI 0·57–2·67), which suggests that FEV1 was a potential mediator,” commented Prof Zar in the editorial. “This finding is consistent with other studies that have shown lung function or low lung function trajectories to be significantly associated with chronic obstructive pulmonary disease and mortality in adulthood.”

The researchers said they hoped that the findings would trigger greater efforts to reduce childhood respiratory infections and help shape new strategies to tackle the issue, as well as challenge the stigma that respiratory diseases are driven by lifestyle factors.

“Current preventative measures for adult respiratory disease mainly focus on adult lifestyle risk factors such as smoking. Linking one in five of adult respiratory deaths to common infections many decades earlier in childhood shows the need to target risk well before adulthood,” said Dr Allinson.

“While preventing and minimising smoking remains crucial to optimising health, this study indicates that prevention of early childhood LRTI should be a key priority,” added Prof Zar.

Asthma risk with early antibiotic use

Meanwhile, an Australian study has shown that exposure to antibiotics in early childhood is associated with a more than two-fold increased risk of early-persistent childhood asthma.

A team at the Murdoch Children’s Research Institute, Melbourne, found a significant association between early-life (0–24 months) antibiotics exposure and childhood (6–15 years) asthma in an analysis of 4318 participants in the Australian Longitudinal Study of Australian Children (LSAC).

The risk of early-persistent asthma among all children was increased 2.3-fold with any early-life antibiotic exposure; 2.7-fold with any second-generation cephalosporin exposure, and by 2-fold with any β-lactam other than cephalosporin or macrolide exposure.

“This reinforces scrutiny of early-life antibiotic use, particularly for common viral infections where no antibiotics are required,” they wrote in the journal Antibiotics (link here).

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