Increased vascular stiffness in children exposed in utero but not children exposed postnatally to emissions from a coal mine fire

Author:

Hemstock Emily J.12ORCID,Bigaran Ashley34,Allgood Shantelle5,Wheeler Amanda J.16,Dalton Marita1,Williamson Grant J.1,Gao Caroline X.78,Abramson Michael J.28,Negishi Kazuaki1910,Johnston Fay H.12,Zosky Graeme R.1211

Affiliation:

1. Menzies Institute for Medical Research, University of Tasmania, Hobart, Tasmania, Australia

2. Centre for Air Pollution, Energy and Health Research, NHMRC CRE, Glebe, New South Wales, Australia

3. Department of Surgery, Faculty of Medicine, Science and Dentistry, University of Melbourne, Melbourne, Victoria, Australia

4. Wellness and Supportive Care, Olivia Newton-John Cancer Research and Wellness Centre, Austin Health, Victoria, Australia

5. School of Rural Health, Monash University, Churchill, Victoria, Australia

6. Commonwealth Scientific and Industrial Research Organization, Environment, Aspendale, Victoria, Australia

7. Centre for Youth Mental Health (Orygen), University of Melbourne, Parkville, Victoria, Australia

8. School of Public Health & Preventive Medicine, Monash University, Melbourne, Victoria, Australia

9. Sydney Medical School Nepean, University of Sydney, Sydney, New South Wales, Australia

10. Nepean Hospital, Kingswood, New South Wales, Australia

11. Tasmanian School of Medicine, University of Tasmania, Hobart, Tasmania, Australia

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/m3 increase in daily PM2.5 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 PM2.5 was not altered by adjustment for covariates, body mass index, and maternal fire stress. Each 1 µg/m3 increase in background PM2.5 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 PM2.5 from a local coal mine fire in infancy. There was a mild increase in vascular stiffness in children exposed to PM2.5 from a local coal mine fire while their mothers were pregnant.

Publisher

Ovid Technologies (Wolters Kluwer Health)

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