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Published on: August 7, 2017
Evidence for causal associations between prenatal and postnatal antibiotic exposure and asthma in children, England
Sergio Souza da Cunha1, Gillian Santorelli1, Neil Pearce2
1Bradford Institute for Health Research, Bradford Teaching Hospitals NHS Foundation Trust, Bradford, UK.
Insights
Antibiotic exposure during pregnancy and early childhood is linked to an increased risk of childhood asthma. This study suggests a plausible causal effect, particularly from postnatal antibiotic use.
Area of Science:
- Pediatric Health
- Environmental Health
- Epidemiology
Background:
- Childhood asthma prevalence is rising.
- Previous studies suggest a link between antibiotic exposure and asthma, but causality remains unclear.
Purpose of the Study:
- To investigate the causal effect of early-life antibiotic exposure on childhood asthma risk.
- To assess the population impact of antibiotic exposure on asthma development.
Main Methods:
- Utilized electronic health records and questionnaires from the Born in Bradford cohort (12,476 children).
- Examined prenatal and postnatal antibiotic exposure, employing methods to address bias, including interaction analyses and dose-response assessments.
- Calculated population attributable risk for asthma associated with antibiotic exposure.
Main Results:
- Prenatal antibiotic exposure (late pregnancy) was associated with increased asthma risk (aOR=1.40).
- Postnatal antibiotic exposure showed a stronger association with asthma (aOR=2.00), with risk increasing with prescription number.
- Population attributable risk for asthma was 4.6% for postnatal and 0.1% for prenatal exposure.
Conclusions:
- The associations between late-pregnancy prenatal and postnatal antibiotic exposure and increased childhood asthma risk are plausible and support a causal relationship.
- Postnatal antibiotic exposure appears to have a more significant impact on asthma risk in the studied population.
Background:
Higher risks of asthma have been observed in children with prenatal exposure to antibiotics and during early life compared with those who have not. However, the causality of such associations is unclear.
Objective:
To assess whether exposure to antibiotics in early life had a causal effect in increasing the risk of asthma in children diagnosed at 5-8 years of life, and the impact in the target population.
Methods:
Data were from electronic health records and questionnaires for children and their mothers in the Born in Bradford birth cohort. Exposure variables were prescriptions of systemic antibiotics to the mother during pregnancy (prenatal) and to the children at 0-24 months of life (postnatal). We assessed the association in 12,476 children with several approaches to deal with different sources of bias (triangulation): the interactions with mother's ethnicity, mode of delivery, and between prenatal and postnatal exposures; dose-response; and estimated the population attributable risk.
Results:
There was an association between prenatal exposure at 7-27 days before the child's birth and asthma (adjusted OR = 1.40; 1.05, 1.87), but no association with the negative control exposure (before pregnancy) (adjusted OR = 0.99 (0.88, 1.12)). For postnatal exposure, the adjusted OR was 2.00 (1.71, 2.34), and for sibling analysis, it was 1.99 (1.00, 3.93). For postnatal exposure, the risk of asthma increased with the number of prescriptions. The observed effect of both exposures was lower among children with mothers of Pakistani ethnicity, but inconclusive (p > .25). The interaction between prenatal and postnatal exposures was also inconclusive (p = .287). The population attributable risk of postnatal exposure for asthma was 4.6% (0.1% for prenatal).
Conclusions:
We conclude that the associations between both late-pregnancy prenatal exposure to antibiotics and postnatal exposure to antibiotics and an increased risk of asthma are plausible and consistent with a causal effect.
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