Non-biological particles and health / Committee on the Medical Effects of Air Pollutants ; chairman, Stephen Holgate ; chairman of the Sub-Group on Non-Biological Particles and Health, Robert Waller.

  • Great Britain. Committee on the Medical Effects of Air Pollutants
Date:
1995
Catalogue details

Licence: Open Government Licence

Credit: Non-biological particles and health / Committee on the Medical Effects of Air Pollutants ; chairman, Stephen Holgate ; chairman of the Sub-Group on Non-Biological Particles and Health, Robert Waller. Source: Wellcome Collection.

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    5.58 Exposure to charcoal alone resulted in large amounts being distributed to all parts of the lung which cleared slowly in the next 18 months but which did not produce any evidence of tissue damage, pulmonary oedema, accumulation of inflammatory cells or damage to alveolar walls. Acute exposure to high levels of NO, produced deaths within 24 hours mainly from a permeability type pulmonary oedema with bronchiolar inflammation. Surviving animals recovered within 7 days. Chronic exposure to 25 ppm (47 mg/m?) NO, had no measured effect on any mice; however, of the mice exposed to the charcoal/NO, mix, 13 out of 20 died. Those that survived appeared normal and were gaining weight; however, on histological examination, there was focal loss of alveolar walls which were covered by charcoal particles. In some cases, the lesions extended all the way to the pleural surface. There was little evidence of inflammatory cell infiltration and no fibrosis or pulmonary oedema. 5.59 As the experimental protocol for each exposure group was different, comparisons are difficult, furthermore, in the charcoal/NO, exposure, significant amounts of the adsorbed NO, had desorbed into the gas phase. This study is useful in that it illustrates the difficulties of calculating the dose of NO, carried into the pulmonary region of the lung even when the apparent conditions of exposure are known. The mixture was prepared by repeatedly adding NO, gas to 20-30 g of carbon in a5] flask until no more NO, was adsorbed. Chemical and physical analysis showed 553 + 25 mg NO, absorbed per gram of carbon. All but 25 mg of this could be recovered by heating the carbon, and, if allowed to stand in the open air, the amount of NO, decreased slowly. During exposure, a concentration of 25 ppm (47 mg/m’) of NO, was achieved in the gas phase. 5.60 To calculate the dose of NO, present on the charcoal in the deep lung, the following information is provided in the paper: a. Of 16,000 particles of carbon per one cm} of inhaled air, 6,080 were less than 2 Lm in diameter. The particle size distribution is not given. b. The charcoal carries 552 mg NO, per gram. However, the following information has to be assumed: a. ‘That all of the particles below 2 yim enter the deep lung of mice (but see paragraph 5.39(c)). b. |The minute volume of mice (approximately 20 ml/min). c. The surface area and density of the particles. d. That all of the carbon entering the pulmonary region desorbs all of its gas. e. There has been no chemical reaction between the nitrogen dioxide and the carbon surface. Clearly, these variables introduce a very large degree of uncertainty into any calculation, and suggest that for polymorphous aerosols, extrapolation is not feasible with the current level of knowledge. 5.61 Gardner et al showed that female mice exposed to ozone (100 ppb, 200 g/m?) for 3 hours followed by sulphuric acid aerosols (900 g/m?) for 2 hours were significantly more susceptible to the effects of inhaled Staphylococcus pyogenes. Exposures to gas or acid alone, or if the acid preceded the ozone, were without effect. It was speculated that the changes may have resulted from: a. Altered frequency and depth of respiration. b. Ozone induced biochemical and physiological changes which increase sensitivity to sulphuric acid. c. As aconsequence of b, there may have been increased deposition of sulphuric acid resulting in a greater dose to sensitive tissue or deeper penetration into the respiratory tract.
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