4.7 Article

Polycyclic aromatic hydrocarbons in particulate matter and serum club cell secretory protein change among schoolchildren: A molecular epidemiology study

Journal

ENVIRONMENTAL RESEARCH
Volume 192, Issue -, Pages -

Publisher

ACADEMIC PRESS INC ELSEVIER SCIENCE
DOI: 10.1016/j.envres.2020.110300

Keywords

Particulate matter; Polycyclic aromatic hydrocarbons; Club cell; Biomarker; Adduct

Funding

  1. National Key R&D Program of China [2017YFC0211604, 2017YFC0211600]
  2. National Natural Science Foundation of China [NSFC 81872664, NSFC 81573124]

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This study investigated the impact of PM on respiratory health in Chinese boarding schoolchildren, finding higher levels of CC16 and toxic metal components in the high-PM exposed group. It also suggested that PAH and its adduct may play a key role in lung injury during PM exposure.
Airborne particulate matter (PM) is a complex mixture containing various kinds of harmful components. Exposure to air PM is associated with childhood respiratory disease, but epidemiological data are limited concerning the circulating respiratory injury protein on the etiology of childhood respiratory disease. Specifically, the role of PM toxic components or its biological effective dose (adduct) in respiratory injury remains unclear. To demonstrate the dose-response relationship and the main mechanism on circulating club cell secretory protein (CC16) from PM compositions among children, we enrolled 273 boarding schoolchildren in China, including 110 and 163 children of whom were in the lowand high-PM exposed areas, respectively. In this study, we measured the internal exposure levels, including serum polycyclic aromatic hydrocarbons (PAH) adduct, urinary metals, and AhR expression, and detected the serum CC16 level as a lung injury marker. Environmental tobacco exposure in children was assessed by urinary cotinine. We found that significantly higher levels of serum CC16, benzo[a] pyridin-7,8-dihydroglycol-9,10-epoxide (BPDE)-albumin adduct, urinary molybdenum, selenium, arsenic, cadmium and barium, and lower level of AhR expression in high-PM exposed group. There was a good association between serum BPDE-albumin adduct and CC16 (beta = 0.222, P = 0.006). There was no association on urinary metals and serum CC16. BPDE-albumin adduct was directly associated with serum CC16 alternation [direct effect = 0.2044, 95% confidence interval (CI) = (0.0426, 0.36)]. PM could cause serum CC16 increased in children. PAH and its adduct might play a key role in lung injury during PM exposure.

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