Abstract
BACKGROUND: Chronic, low-intensity air pollution exposure has been consistently associated with increased atherosclerosis in adults. However, there was limited research regarding the implications of acute, high-intensity air pollution exposure during childhood. We aimed to determine whether there were any associations between early-life exposure to such an episode and early-life vascular function changes. METHODS: We conducted a prospective cohort study of children (<9 years old) who lived in the vicinity of the Hazelwood coal mine fire (n = 206). Vascular function was measured using noninvasive diagnostic methods including carotid intima-media thickness and pulse wave velocity (PWV). Exposure estimates were calculated from prognostic models and location diaries during the exposure period completed by each participant's parent. Linear mixed-effects models were used to determine whether there were any associations between exposure and changes in vascular outcomes at the 3- and 7-year follow-ups and over time. RESULTS: At the 7-year follow-up, each 10 μg/m(3) increase in daily PM(2.5) in utero was associated with increased PWV (β = 0.13 m/s; 95% confidence interval [CI] = 0.02, 0.24; P = 0.02). The association between in utero exposure to daily PM(2.5) was not altered by adjustment for covariates, body mass index, and maternal fire stress. Each 1 µg/m(3) increase in background PM(2.5) was associated with increased PWV (β = 0.68 m/s; 95% CI = 0.10, 1.26; P = 0.025), in children from the in utero exposure group. There was a trend toward smaller PWV (β = -0.17 m/s; 95% CI = -0.366, 0.02) from the 3- to 7-year follow-up clinic suggesting that the deficits observed previously in children exposed postnatally did not persist. CONCLUSION: There was a moderate improvement in vascular stiffness of children exposed to PM(2.5) from a local coal mine fire in infancy. There was a mild increase in vascular stiffness in children exposed to PM(2.5) from a local coal mine fire while their mothers were pregnant.