Cytotoxic responses and potential respiratory health effects of carbon and carbonaceous nanoparticulates in the Paso del Norte airshed environment

Our plain-English summary of Cytotoxic responses and potential respiratory health effects of carbon and carbonaceous nanoparticulates in the Paso del Norte airshed environment, by K.F. Soto, L.E. Murr, K.M. Garza (International Journal of Environmental Research and Public Health, 2008).

The study

• Authors: K.F. Soto, L.E. Murr, K.M. Garza
• Journal: International Journal of Environmental Research and Public Health
• Published: 2008;5(1):12-25
• Cited by: 20 articles, as counted by NIH iCite
• Read it: PubMed · Publisher · Free full text

Abstract

We have utilized a range of manufactured or commercial nanoparticulate materials, including surrogate carbon nano-PM along with combustion-generated carbonaceous (soot) nano-PM characteristic of environmental nano- PM (both indoor and outdoor) to investigate and compare their cytotoxic response in vitro with an immortalized human epithelial (lung model) cell line (A549). These have included nano-Ag, Al2O3, TiO2, Fe2O3, ZrO2, Si3N4, chrysotile asbestos, BC, 2 types of MWCNT-aggregate PM (MWCNT-R and MWCNT-N), and high-volume glass fiber collected soots: candle, wood, diesel (truck), tire, and 3-types of natural gas kitchen burner-generated soots: yellow (fuel-rich) flame, low-flow blue flame, and normal flow blue flame soot PM. These carbonaceous nano-PM species can be found in either the indoor and outdoor environments or microenvironments. Two-day and two-week in-vitro cultures of A549 showed cell death (or decreased cell viability) for all nanoparticulate materials, but especially significant for all but the TiO2 and candle, wood, and diesel PM. The natural gas kitchen burner combustion PM cell death response was characteristic of BC and MWCNT PM. There was no correlation with total PAH content of the soot PM. Cytokine release (IL-6, IL-8) was detected for the Ag, Fe2 O3, asbestos, BC and the MWCNT PM. Reactive oxygen species (ROS) production was also detected for Ag, Fe2 O3, ZrO2, asbestos, BC, and the MWCNT aggregate PM, as well as the natural gas kitchen burner combustion PM. TEM, FESEM, and optical microscopy examination of these nanomaterials illustrate the wide range in PM morphologies and crystallinities as well as cell morphologies. Taken together, these results illustrate proinflammatory and related respiratory health issues in relation to environmental nanoparticulates.

In plain English

In this laboratory study, the authors exposed human lung cells (A549) to various particles and measured cell death, release of the inflammatory signals IL-6 and IL-8, and reactive oxygen species (ROS). The particles included manufactured nanomaterials such as silver, iron oxide, titanium dioxide, black carbon and carbon nanotube aggregates; chrysotile asbestos; and filter-collected soots from candles, wood, diesel, tires and natural gas kitchen burners. Manufactured materials, including asbestos, were given at 5 μg/mL for 48 hours or 0.5 μg/mL for 336 hours; soots were tested on filters placed on the cells for 48 hours. All materials caused some cell death. Chrysotile asbestos caused significant cell death that was unchanged between 48 and 336 hours. It also caused notable IL-6 and IL-8 release and ROS levels above the hydrogen peroxide reference. Among the soots, cell death was not correlated with total PAH content, and no detectable IL-6 or IL-8 release occurred. The authors concluded that kitchen natural gas burner particles were more cytotoxic than other soots. They noted it is unclear whether short-term cell tests predict effects in living bodies.

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: in vitro (laboratory cell culture) experiment comparing cell death, cytokine release and reactive oxygen species production across many particle types
• Who was studied: Cultured A549 human epithelial (lung model) cells; no people or animals were studied
• Exposure: Manufactured nanomaterials and chrysotile asbestos were given at 5 μg/mL for 48 hours or 0.5 μg/mL for 336 hours. The manufactured nanomaterials were black carbon, two multiwall carbon nanotube aggregates, Fe2O3, ZrO2, Al2O3, Si3N4, silver, and TiO2 as rutile and anatase. Filter-collected soots from candle, wood, diesel truck, tire and natural gas kitchen burner flames were tested separately, by placing the loaded filters in direct contact with the cells for 48 hours.
• Main results:
  • All of the materials tested caused some cell death in A549 cells, and this increased with time.
  • Significant cell death was seen after 2 days and 2 weeks for several manufactured materials, including chrysotile asbestos.
  • The cell death response to chrysotile asbestos was unchanged between 48 hours and 336 hours.
  • For the filter-collected soots, tested after 48 hours of contact with the cells, cell viability decreased in the order candle, wood, diesel, tire, then natural gas flame soot.
  • Notable IL-6 release was seen for silver, Fe2O3, ZrO2, chrysotile asbestos and the carbon surrogates (black carbon, MWCNT-R, MWCNT-N). Notable IL-8 release was seen for silver, Fe2O3, chrysotile asbestos and the carbon surrogates.
  • The filter-collected soots produced no detectable IL-6 or IL-8 release.
  • Asbestos was among the materials producing high ROS levels, above the hydrogen peroxide positive control. Black carbon and MWCNT-N produced extremely high levels, and rutile TiO2 produced none compared with controls.
  • All of the soots generated ROS, to different extents.
  • The cytotoxic response to the soots was not correlated with their total PAH content.
• The authors' conclusion: The authors concluded that nano-PM released from kitchen natural gas burners is more cytotoxic than the other soots tested. They also concluded that no clear mechanism for the cytotoxic or inflammatory responses had been identified.
• Limitations the authors state:
  • It is often unclear whether short-term cell culture tests predict responses in living bodies.
  • Standardized dosing protocols for these tests are not well established.
  • Little is known about dose-related issues or intermittent long-term exposures.
  • The cytokine comparisons are relative measurements and do not represent actual differences in concentration.
  • No clear mechanism for the responses was identified.

Topics

Medical terms in this study, explained in our Lexicon: Chrysotile, Cytokine, Reactive Oxygen Species (ROS).

Related studies

• Combustion-generated nanoparticulates in the El Paso, TX, USA / Juarez, Mexico Metroplex: their comparative characterization and potential for adverse health effects — L.E. Murr, K.F. Soto, et al. (2006)
• Cytotoxicity and reactive oxygen species generation from aggregated carbon and carbonaceous nanoparticulate materials — K.M. Garza, K.F. Soto, et al. (2008)
• In vitro cytotoxicity and transforming potential of industrial carbon dust (fibers and particles) in syrian hamster embryo (SHE) cells — C. Darne, F. Terzetti, et al. (2010)
• Cytotoxicity assessment of some carbon nanotubes and related carbon nanoparticle aggregates and the implications for anthropogenic carbon nanotube aggregates in the environment — L.E. Murr, K.M. Garza, et al. (2005)
• Microstructures and nanostructures for environmental carbon nanotubes and nanoparticulate soots — L.E. Murr (2008)
• Distinct autophagy-apoptosis related pathways activated by Multi-walled (NM 400) and Single-walled carbon nanotubes (NIST-SRM2483) in human bronchial epithelial (16HBE14o-) cells — M. Ghosh, S. Murugadoss, et al. (2020)

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