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Published on: August 7, 2017
Joint association of air pollution exposure and inflammation-related proteins in relation to infant lung function
Shizhen He1, Björn Lundberg2, Jenny Hallberg2
1Institute of Environmental Medicine, Karolinska Institutet, Stockholm, Sweden.
Insights
Infant lung function may be negatively impacted by air pollution and abnormal inflammation-related protein profiles. These factors appear to interact synergistically, leading to reduced lung function in early life.
Area of Science:
- Environmental Health
- Pediatrics
- Immunology
Background:
- Air pollution exposure is linked to adverse respiratory outcomes.
- Systemic inflammation may mediate the effects of air pollution on lung function.
- Infant susceptibility to air pollution can be characterized by inflammation-related proteins.
Purpose of the Study:
- To investigate the interaction between air pollution exposure and inflammation-related proteins.
- To assess the impact on lung function in 6-month-old infants.
Main Methods:
- Utilized the EMIL birth cohort (n=82) in Stockholm.
- Measured plasma levels of 92 inflammation-related proteins and performed spirometry in infants.
- Estimated exposure to PM10, PM2.5, and NO2 using validated dispersion models.
Main Results:
- Found a joint association between particulate matter (PM) exposure and abnormal inflammatory profiles with reduced FEV0.5 and FVC.
- A 0.1 unit increase in minimum absolute deviance and IQR increase in PM10 was associated with significant decreases in FEV0.5 and FVC.
- Similar associations were observed for PM2.5, but less so for NO2.
Conclusions:
- Early life exposure to air pollution and abnormal inflammation-related protein profiles may synergistically impair infant lung function.
- Findings highlight the combined role of environmental factors and biological markers in infant respiratory health.
Background And Aim:
Systemic inflammation is one potential mechanism underlying negative impact of air pollution on lung function. Levels of inflammation-related proteins have the potential to characterize infants' susceptibility to air pollution induced lung function impairment. This study aimed to examine the interplay between air pollution exposure and inflammation-related proteins on lung function in 6-months-old infants.
Methods:
In the EMIL birth cohort from Stockholm (n = 82), dynamic spirometry, along with measurement of plasma levels of 92 systemic inflammation-related proteins (Olink Proseek Multiplex Inflammation panel) have been carried out in infants aged six months. Time-weighted average exposure to particles with an aerodynamic diameter of <10 μm (PM10), <2.5 μm (PM2.5), and nitrogen dioxide (NO2) at residential addresses from birth and onwards was estimated via validated dispersion models. To characterize the abnormality of inflammation-related protein profile, for each protein in each infant, we calculated the relative deviance of the protein level from age- and sex-specific median in terms of its age- and sex-specific interquartile range (IQR), followed by computing the absolute value of the smallest relative deviance, "minimum absolute deviance". Using linear regression models, interaction of air pollution and the abnormal inflammatory profile on lung function was estimated on the additive scale.
Results:
We found joint association of PM exposure and an abnormal inflammatory protein profile in relation to FEV0.5 and FVC. For 0.1 unit increase in minimum absolute deviance, one IQR increase in PM10 was associated with 85.9 ml (95% CI: -122.9, -48.9) additional decrease in FEV0.5, and 72.3 ml (95% CI: -121.5, -23.2) additional decrease in FVC. Similar results were obtained with PM2.5 exposure, while less apparent for NO2.
Conclusions:
Early life air pollution exposure and abnormal inflammation-related protein profiles may interact synergistically towards lower lung function in infants.
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