Characterization and in vitro biological effects of ambient air PM10 from a rural, an industrial and an urban site in Sulaimani City, Iraq

Our plain-English summary of Characterization and in vitro biological effects of ambient air PM10 from a rural, an industrial and an urban site in Sulaimani City, Iraq, by A.T. Arif, C. Maschowski, P. Khanaqa, et al (Toxicological and Environmental Chemistry, 2018).

The study

• Authors: A.T. Arif, C. Maschowski, P. Khanaqa, P. Garra, M. Garcia-Käufer, N. Wingert, V. Mersch-Sundermann, R. Gminski, G. Trouvé, R. Gieré
• Journal: Toxicological and Environmental Chemistry
• Published: 2018;100(4):373-394
• Cited by: 3 articles, as counted by NIH iCite
• Read it: PubMed · Publisher · Free full text

Abstract

High urban atmospheric pollution is caused by economic and industrial growth, especially in developing countries. The objective of this study was to assess possible relationships between in vitro effects on human alveolar epithelial cells of source-related dust types collected at Sulaimani City (Iraq), and to determine their mineralogical and chemical composition. A passive sampler was used to collect dust particles at a rural, an industrial and an urban sampling site during July and August 2014. The samples were size-fractionated by a low-pressure impactor to obtain respirable dust with aerodynamic diameters of less than 10 μm. The dust was mainly composed of quartz and calcite. Chrysotile fibres (white asbestos) were also found at the urban site. Dust from the industrial and urban sites triggered cytotoxic and genotoxic effects in the cells, whereas only minor effects were observed for the sample from the rural site.

In plain English

This laboratory study collected settled dust at three sites in and around Sulaimani City, Iraq, from July 1 to August 31, 2014. The sites were a rural mountain site, an industrial site near a landfill incineration plant, and an urban street with moderate to heavy traffic. The authors analyzed the dust's minerals, metals and polycyclic aromatic hydrocarbons, and exposed a human lung cell line (A549) to its PM10 fraction for 24 hours. Under electron microscopy, dust from the urban site contained fiber bundles up to 60 µm long that the authors identified as chrysotile (white asbestos). X-ray diffraction could not confirm this, possibly because chrysotile and chlorite give similar signals. All three samples were significantly toxic to the cells at 100 µg/mL and significantly raised the inflammatory signal IL-8. Urban dust caused DNA damage at 30 and 100 µg/mL, industrial dust at 100 µg/mL, and rural dust none. The authors suggested the chrysotile may have come from vehicle brake pads. They stated they could not determine which dust component caused the cell effects. The study used cells in the laboratory, not people.

We wrote this plain-English summary from the full article with the help of AI, and a second AI model checked each sentence against the article. It is not the authors' wording; the abstract and the article are their own account.

What the study did and found

• Design: Environmental dust characterization combined with in vitro (cell culture) toxicity experiments
• Who was studied: Dust settled into open polyethylene boxes, collected in duplicate at three sites in and around Sulaimani City, Iraq, from July 1 to August 31, 2014. The sites were a rural site (Azmar Mountain, RurSu), an industrial site near the Tanjaro landfill incineration plant (IndSu), and an urban street with moderate to heavy traffic (Malik Mahmud Street, UrbSu). Toxicity was tested on the A549 human alveolar epithelial cell line.
• Exposure: The PM10 fraction of the collected dust. It contained quartz, calcite, metals and PAHs, plus chrysotile fibers at the urban site. A549 cells were exposed for 24 h at 0.3, 1, 3, 10, 30 and 100 µg/mL. Nano-SiO2 and dolomite were used as control substances.
• Main results:
  • Electron microscopy with elemental analysis of the urban-site (UrbSu) dust showed bundles of fibers up to 60 µm long. The fibers contained Mg and Si as major components, which the authors took to indicate chrysotile (white asbestos).
  • Transmission electron microscopy found fibers about 50 nm in diameter and several µm long in the urban-site PM10 only. The authors said these might have been single chrysotile fibers.
  • Chrysotile in the urban dust was seen by SEM-EDX and TEM but could not be identified by X-ray diffraction.
  • The dust deposition rate was highest at the urban site, more than three times that at the rural site.
  • Total PAHs were 675 µg/kg in industrial-site PM10, compared with 242 µg/kg (rural) and 251 µg/kg (urban).
  • All three PM10 samples caused significant cytotoxic responses in A549 cells at 100 µg/mL. The urban sample had the most pronounced effect, already noticeable at 30 µg/mL.
  • The PM10 samples produced only slight, non-significant increases in reactive oxygen species (ROS) inside the cells.
  • All PM10 samples significantly induced release of the inflammatory signal IL-8, at similar levels, at concentrations of 1 to 100 µg/mL.
  • Urban-site PM10 caused DNA damage at 30 and 100 µg/mL, and industrial-site PM10 at 100 µg/mL. Rural-site PM10 caused no DNA damage even at 100 µg/mL.
  • Endotoxin content of the dust samples was low, about 0.2 EU/mL in the 1 mg/mL stock solutions.
• The authors' conclusion: The authors concluded that the chrysotile at the high-traffic urban site may have come from automotive brake friction pads, noting that asbestos is not known to occur naturally in the area. They recommended further investigation and monitoring of asbestos in city dust. They stated it was not possible to determine which dust component caused the cytotoxic, pro-inflammatory and genotoxic responses.
• Limitations the authors state:
  • Drying the samples may have led to underestimation of volatile PAHs such as naphthalene.
  • X-ray diffraction results were available for only two of the samples.
  • X-ray diffraction may have confused chlorite with chrysotile, or the chlorite signal may have masked the chrysotile signal.
  • Fibrous materials are generally difficult to detect by X-ray diffraction.
  • The ROS method used detects only hydroxyl radicals, which may explain why no significant ROS changes were found.
  • The authors could not determine which component of the PM10 was responsible for the observed cell effects.

Topics

Medical terms in this study, explained in our Lexicon: Chrysotile.

Related studies

• Response to Letter to the Editor Regarding "Ambient Asbestos Fiber Concentrations and Long-Term Trends in Pleural Mesothelioma Incidence Between Urban and Rural Areas in the United States (1973-2012)" by Finkelstein — K.A. Keeton, M.E. Glynn, et al. (2018)
• Letter Concerning: Glynn ME, Keeton KA, Gaffney SH, Sahmel J. Ambient Asbestos Fiber Concentrations and Long-Term Trends in Pleural Mesothelioma Incidence Between Urban and Rural Areas in the United States (1973-2012). Risk Analysis 2018;38(3):454-471 — M.M. Finkelstein (2018)
• Monitoring of airborne asbestos fibers in an urban ambient air of Shahryar City, Iran: levels, spatial distribution, seasonal variations, and health risk assessment — F. Taghizadeh, A.J. Jafari, et al. (2019)
• Monitoring of airborne asbestos fibers in an urban ambient air of Mashhad City, Iran: levels, spatial distribution and seasonal variations — A. Moteallemi, M. Minaei, et al. (2020)
• Indoor air quality differences between urban and rural preschools in Korea — C. Yoon, K. Lee, et al. (2011)
• Ferruginous (asbestos) bodies in the lungs of rural dwellers, urban dwellers, and patients with pulmonary neoplasms — P.H. Breedin, D.H. Buss (1976)

Browse return to medical research.