Early life exposure to coal mine fire and tobacco smoke affect subclinical vascular function
Bing Zhao1, Fay H Johnston1, Tierney O'Sullivan1
1Menzies Institute for Medical Research, University of Tasmania, Hobart, Tasmania, Australia.
Insights
Infants exposed to coal mine fire smoke showed increased vascular stiffness. This study highlights potential long-term health risks from air pollution in early childhood.
Area of Science:
- Environmental Health
- Pediatric Cardiology
- Toxicology
Background:
- Coal mine fires release particulate matter (PM2.5) into the atmosphere.
- Early childhood exposure to air pollution may impact vascular development.
- Environmental tobacco smoke (ETS) is a known respiratory irritant.
Purpose of the Study:
- To assess the association between coal mine fire smoke exposure and vascular health in young children.
- To investigate the impact of particulate matter (PM2.5) on carotid intima-media thickness (IMT) and pulse wave velocity (PWV).
- To determine if environmental tobacco smoke (ETS) modifies the effects of coal mine fire smoke.
Main Methods:
- Retrospective cohort study of children exposed in utero or postnatally to a 6-week coal mine fire event.
- Exposure assessment based on daily PM2.5 levels and participant locations.
- Vascular health outcomes measured by IMT and PWV three years post-exposure.
- Multivariable linear regression models adjusted for covariates including ETS.
Main Results:
- Postnatal exposure to PM2.5 was associated with increased pulse wave velocity (PWV).
- Combined exposure groups showed increased PWV with PM2.5 exposure in children with ETS or maternal smoking.
- No significant vascular effects were observed in the in-utero exposure group.
Conclusions:
- Infants exposed to coal mine fire smoke up to age 2 exhibited increased vascular stiffness.
- Maternal smoking or ETS exposure may exacerbate the vascular effects of coal mine fire smoke.
- Long-term follow-up is recommended to understand the full impact of coal mine fire smoke exposure.
Objective:
To evaluate whether vascular health in young children was associated with exposure to a 6-week episode of coal mine fire smoke or environmental tobacco smoke (ETS) in a retrospective cohort study.
Methods:
Three years after a coal mine fire in Victoria, Australia, we investigated the vascular health of children either in utero (n=75) or aged <2 years (postnatal exposure, n=96) at the time of the fire. The outcomes were the carotid intima-media thickness (IMT) and pulse wave velocity (PWV). The mean and peak daily particulate matter <2.5 µm in diameter (PM2.5) exposures were estimated based on their daily locations throughout the fire period. Multivariable linear regression models were used to test for associations between the fire-related PM2.5 and outcomes adjusted for relevant covariates including ETS.
Results:
In the postnatal-exposure group, each 10 µg/m³ increase in mean PM2.5 level was independently positively associated with PWV (β=0.116, p=0.028). When these two groups were combined, there was an association between mean PM2.5 and increased PWV in those children who had ETS exposure (β=0.148, p=0.033) or whose mothers smoked (β=0.151, p=0.011), but not in those not exposed to ETS or maternal smoking.
Conclusions:
Three years after a coal mine fire, infants aged up to 2 years at the time of exposure have increases in vascular stiffness. Although no adverse effects were observed in the in uterus exposure group, further follow-up study is needed to elucidate the long-term effects of coal mine fire smoke exposure.
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