Toxic Effects of Particulate Matter Derived from Dust Samples Near the Dzhidinski Ore Processing Mill, Eastern Siberia, Russia

Cardiovasc Toxicol. 2019 Oct;19(5):401-411. doi: 10.1007/s12012-019-09507-y.

Abstract

Ambient particulate matter (PM) is associated with increased mortality and morbidity, an effect influenced by the metal components of the PM. We characterized five sediment samples obtained near a tungsten-molybdenum ore-processing complex in Zakamensk, Russia for elemental composition and PM toxicity with regard to pulmonary, vascular, and neurological outcomes. Elemental and trace metals analysis of complete sediment and PM10 (the respirable fraction, < 10 µm mass mean aerodynamic diameter) were performed using inductively coupled plasma optical emission spectrometry (ICP-OES) and mass spectrometry (ICP-MS). Sediment samples and PM10 consisted largely of silicon and iron and silicon and sodium, respectively. Trace metals including manganese and uranium in the complete sediment, as well as copper and lead in the PM10 were observed. Notably, metal concentrations were approximately 10 × higher in the PM10 than in the sediment. Exposure to 100 µg of PM10 via oropharyngeal aspiration in C56BL/6 mice resulted in pulmonary inflammation across all groups. In addition, mice exposed to three of the five PM10 samples exhibited impaired endothelial-dependent relaxation, and correlative analysis revealed associations between pulmonary inflammation and levels of lead and cadmium. A tendency for elevated cortical ccl2 and Tnf-α mRNA expression was induced by all samples and significant upregulation was noted following exposure to PM10 samples Z3 and Z4, respectively. Cortical Nqo1 mRNA levels were significantly upregulated in mice exposed to PM10 Z2. In conclusion, pulmonary exposure to PM samples from the Zakamensk region sediments induced varied pulmonary and systemic effects that may be influenced by elemental PM composition. Further investigation is needed to pinpoint putative drivers of neurological outcomes.

Keywords: Cardiovascular; Neuroinflammation; PM10; Particulate matter; Respiratory toxicology; Toxicology.

Publication types

  • Research Support, N.I.H., Extramural
  • Research Support, Non-U.S. Gov't

MeSH terms

  • Air Pollutants / toxicity*
  • Animals
  • Aorta, Thoracic / drug effects*
  • Aorta, Thoracic / physiopathology
  • Cadmium / toxicity*
  • Cerebral Cortex / drug effects*
  • Cerebral Cortex / metabolism
  • Chemokine CCL2 / genetics
  • Chemokine CCL2 / metabolism
  • Dust*
  • Inhalation Exposure
  • Lead / toxicity*
  • Male
  • Mice, Inbred C57BL
  • Mining*
  • NAD(P)H Dehydrogenase (Quinone) / genetics
  • NAD(P)H Dehydrogenase (Quinone) / metabolism
  • Oxidative Stress / drug effects
  • Particle Size
  • Particulate Matter / toxicity*
  • Pneumonia / chemically induced*
  • Pneumonia / genetics
  • Pneumonia / metabolism
  • Risk Assessment
  • Siberia
  • Tumor Necrosis Factor-alpha / genetics
  • Tumor Necrosis Factor-alpha / metabolism
  • Vasodilation / drug effects

Substances

  • Air Pollutants
  • Ccl2 protein, mouse
  • Chemokine CCL2
  • Dust
  • Particulate Matter
  • Tnf protein, mouse
  • Tumor Necrosis Factor-alpha
  • Cadmium
  • Lead
  • NAD(P)H Dehydrogenase (Quinone)
  • Nqo1 protein, mouse