4.7 Article

Ambient ozone exposure and bone turnover markers in children: Results from the GINIplus and LISA birth cohorts

Journal

ENVIRONMENTAL RESEARCH
Volume 214, Issue -, Pages -

Publisher

ACADEMIC PRESS INC ELSEVIER SCIENCE
DOI: 10.1016/j.envres.2022.113784

Keywords

Air pollutants; Bone development; Bone remodeling; Osteocalcin; Collagen type I; Epidemiology

Funding

  1. Federal Ministry for Education, Science, Research and Technology, Germany [20462296]
  2. Helmholtz Zentrum Munich, Germany
  3. Federal Ministry for Environment, Germany [20462296]
  4. Federal Ministry for Education, Science, Research and Technology, Germany
  5. Helmholtz Centre for Environmental Research -UFZ, Leipzig, Germany
  6. Marien-Hospital Wesel, Germany
  7. Pediatric Practice
  8. Bad Honnef, Germany
  9. NeuroSmog: Determining the impact of air pollution on the developing brain [POIR.04.04.00-1763/18-00]
  10. E.U. resources
  11. European Regional Development Fund under the Smart Growth Operational Programme

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This study found that long-term exposure to ambient ozone was associated with decreased concentrations of bone turnover markers in German children. However, unless other studies confirm these results, the detrimental effects of ambient ozone on bone development in children should be interpreted cautiously.
Background: Multiple environmental factors can regulate bone metabolism, and it is hypothesized that air pollution may be deleteriously involved in this regulation. However, only a few studies considered bone turnover markers (BTMs) - sensitive and specific markers of bone metabolism - as outcomes, and no study investigated the exposure to ambient ozone. Here, we intended to explore the associations between long-term exposure to ambient ozone and concentrations of two BTMs, osteocalcin and beta-isomer of C-terminal telopeptide of type I collagen (CTx), amongst 10-year-old children. Methods: Based on the GINIplus and LISA birth cohorts, our cross-sectional analysis included 1848 children aged 10 years from Munich and Wesel. Serum osteocalcin and CTx concentrations were measured. We estimated ozone exposures by optimal interpolation, assessed nitrogen dioxide and particulate matter with an aerodynamic diameter <10 mu m concentrations by land use regression models, and assigned the exposures to home addresses. Linear regression models were built and adjusted for covariates as well as co-pollutants. Results: The mean concentrations were 93.09 ng/mL and 663.66 ng/L for osteocalcin and CTx, respectively. In general, higher levels of ozone were associated with decreased concentrations of both BTMs. This held true for the two areas and different exposure metrics. The number of days per year with a maximum 8-h average concentration exceeding 120 mu g/m(3) showed consistent results across different models. Specifically, models adjusted for co-pollutants illustrated that the beta estimates and 95% confidence intervals on osteocalcin and CTx were -2.51 (-3.78, -1.14) and -44.53 (-57.12, -31.93), respectively, for an increase of 10 days. Conclusions: We found that long-term exposure to ambient ozone was associated with decreased concentrations of BTMs in German children. This association might potentially affect bone metabolism. Nevertheless, unless other prospective studies confirm our results, the detrimental effects of ambient ozone on bone development in children should be interpreted cautiously.

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