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In vitro estrogenicity of ambient particulate matter: contribution of hydroxylated polycyclic aromatic hydrocarbons

Atmospheric particulate matter (PM1) was collected at an urban and a rural site in Switzerland during a hibernal high air pollution episode and was investigated for estrogenicity using an estrogen‐sensitive reporter gene assay (ER‐CALUX). All samples that were tested induced estrogen receptor‐mediated gene expression in T47D human breast adenocarcinoma cells. Observed estrogenic activities corresponded to 17β‐estradiol (E2) CALUX equivalent concentrations ranging from 2 to 23 ng E2‐CEQ per gram of PM1 (particulate matter of ≤ 1 µm aerodynamic diameter) and from 0.07 to 1.25 pg E2‐CEQ per m3 of sampled air. There was a strong correlation between the PM1 estrogenicity of the urban and rural sites (r = 0.92). Five hydroxylated polycyclic aromatic hydrocarbons (hydroxy‐PAHs), which show structural similarities to E2, were assessed for their estrogenic activity. The following order of estrogenic potency was found: 2‐hydroxychrysene > 2‐hydroxyphenanthrene > 1‐hydroxypyrene > 2‐hydroxynaphthalene > 1‐hydroxynaphthalene. Three of these hydroxy‐PAHs, namely 2‐hydroxyphenanthrene, 2‐hydroxynaphthalene and 1‐hydroxynaphthalene, were detected in all PM1 extracts. However, they contributed only 0.01–0.2% to the overall estrogenic activity. Hence, mainly other estrogenic compounds not yet identified by chemical analysis must be responsible for the observed activity. The temporal trend of PM1 estrogenicity at the urban and rural site, respectively, was compared with the time course of several air pollutants (NO2, NO, SO2, O3, CO) and meteorological parameters (temperature, humidity, air pressure, solar irradiation, wind velocity). However, specific emission sources and formation processes of atmospheric xenoestrogens could not be elucidated. This study showed that ambient particulate matter contains compounds that are able to interact with estrogen receptors in vitro and potentially also interfere with estrogen‐regulated pathways in vivo. Copyright © 2008 John Wiley & Sons, Ltd.