Inhalable particles and pulmonary host defense: in vivo and in vitro effects of ambient air and combustion particles

Our plain-English summary of Inhalable particles and pulmonary host defense: in vivo and in vitro effects of ambient air and combustion particles, by G.E. Hatch, E. Boykin, J.A. Graham, et al (Environmental Research, 1985).

The study

• Authors: G.E. Hatch, E. Boykin, J.A. Graham, J. Lewtas, F. Pott, K. Loud, J.L. Mumford
• Journal: Environmental Research
• Published: 1985;36(1):67-80
• Cited by: 135 articles, as counted by NIH iCite
• Read it: PubMed · Publisher

Abstract

The ability of particulate air pollutants (and possible constituents) to alter pulmonary host defenses was examined using an in vitro alveolar macrophage cytotoxicity assay and an in vivo bacterial infectivity screening test which employed intratracheal injection of the particles. A wide range of response between particles was seen at the 1.0-mg/ml level in vitro and the 0.1-mg/mouse level in vivo. A sample of fluidized-bed coal fly ash, bentonite, asbestos, some ambient air particles, and heavy metal oxides greatly increased susceptibility to pulmonary bacterial infection. Most coal fly ash samples and some air particles caused moderate increases in infectivity, while diesel particulates, volcanic ash, and crystalline silica caused only small increases. Cytotoxic effects on macrophages in vitro were observed with most of the particles. The in vivo and in vitro assays produced a similar ranking of toxicity; however, not all particles that were highly cytotoxic were potent in increasing bacterial infectivity. Increased toxicity measurable by either assay often appeared to be associated with small size or with the presence of metal in the particles.

In plain English

This was an experimental screening study by a US EPA laboratory that tested a range of inhalable particles in two assays: an in vivo test in which particles were injected intratracheally into mice that were then exposed to aerosolized Group C Streptococcus, with mortality of the mice recorded as the measure, and an in vitro test of rabbit alveolar macrophages incubated with 1.0 mg/ml of particles, measured as viability index and cellular ATP. Materials included coal fly ashes (fluidized bed and conventional), residual oil fly ash, diesel exhaust particles, urban air particles from the United States and Germany, Mount St. Helens volcanic ash, silica, kaolin, bentonite, latex, metal oxides and salts, and UICC standard chrysotile and crocidolite asbestos. Because of their viscosity, the asbestos suspensions could only be given at the 10-microgram-per-mouse level; both chrysotile and crocidolite significantly raised bacterial infectivity at that dose. Of 40 samples, 13 gave no significant increase at 100 micrograms. The authors concluded the two assays gave a similar toxicity ranking, though many highly cytotoxic particles showed little infectivity effect.

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: Experimental laboratory study combining an in vivo mouse bacterial infectivity assay (intratracheal injection of particles) with an in vitro rabbit alveolar macrophage cytotoxicity assay
• Who was studied: Mice (at least three treatment groups of 30 mice per sample; group sizes of 60 to 360 mice listed per sample) challenged with aerosolized Group C Streptococcus, and alveolar macrophages from healthy New Zealand white rabbits; 40 particle samples tested in vivo, 23 of them also in vitro; work done at the US EPA Health Effects Research Laboratory, Research Triangle Park (article received 1983)
• Exposure: Intratracheally injected particles (initially 100 micrograms per mouse, reduced tenfold stepwise when large effects occurred; asbestos only at 10 micrograms) and in vitro exposure of macrophages to 1.0 mg/ml particles; materials included fluidized-bed and conventional coal fly ash, residual oil fly ash, diesel exhaust particles, urban air particles (St. Louis, Washington D.C., Dusseldorf, Bochum), Mt. St. Helens volcanic ash, crystalline silica, kaolin, bentonite, carbon, latex, metal oxides and soluble metal salts, and UICC standard chrysotile and crocidolite asbestos
• Main results:
  • Asbestos suspensions could be given only at the 10-microgram-per-mouse dose because of their viscosity
  • Both asbestos samples, chrysotile and crocidolite, significantly increased bacterial infectivity in mice at the 10-microgram-per-mouse dose
  • Samples causing large increases (greater than 50%) in infectivity at the 100-microgram dose in mice
  • Of the 40 samples tested in mice, 13 produced no significant increase in infectivity at the 100-microgram dose; low-potency materials included diesel fly ash, volcanic ash and crystalline silica
  • In the macrophage assay at 1.0 mg/ml, eight samples reduced both viability index and ATP by more than 50%
  • Rank correlation between in vivo excess mortality and in vitro macrophage ATP reduction was P = 0.024, and with viability index P = 0.084
  • Linear regression of the in vivo and in vitro results was not statistically significant
  • Neutron activation analysis of aqueous leachates showed volcanic ash essentially free of soluble heavy metals and no heavy metals detected in bentonite, which was nonetheless active in both assays
• The authors' conclusion: The authors concluded that a wide range of effects was seen across environmental particles, that the two assays gave a similar toxicity ranking with all particles that increased infectivity also being cytotoxic, but that many highly cytotoxic particles had little effect on infectivity, and that increased toxicity sometimes appeared explainable by leachable metals
• Limitations the authors state:
  • Intratracheal injection has been compared with inhalation only for soluble metals, not for particles
  • The infectivity assay is variable; many replicates are needed to evaluate increases below 30%, and the aim was ranking rather than finding minimal effective doses
  • Species differences (rabbit cells in vitro, mice in vivo) and method variability may prevent exact comparison between the assays
  • The effect of suspension pH on the infectivity assay was not investigated
  • The low density of latex meant a much larger volume of material was injected than for other particles
  • Quantitative comparison of EC50 values between the two assays was not possible

Topics

Medical terms in this study, explained in our Lexicon: Alveolar Macrophage, Crystalline, Macrophage.

Related studies

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• 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)
• Copper-enriched automotive brake wear particles perturb human alveolar cellular homeostasis — J.G.H. Parkin, L.S.N. Dean, et al. (2025)
• Stimulation of oxidant production in alveolar macrophages by pollutant and latex particles — G.E. Hatch, D.E. Gardner, et al. (1980)
• Response of bovine alveolar macrophages in vitro to welding fume particles — L.R. White, A.B. Marthinsen, et al. (1983)

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