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pulmonary oedema in days. The guideline states that inhaling NO at a dose of 25ppm for
eight hours is the maximum safe dose and time limit. The level considered an immediate
damage to life and health is estimated at 100 to 150ppm based on older toxicology studies
(Carson, Rosenholtz et al. 1962; Sax 1975). For NOz the recommendation has been altered
down from 5ppm to only lppm (in 1996) for eight hours as the exposure limit (NIOSH 2005).
kvels of 10 to 20ppm have demonstrated to be a mild irritant (Patty 1963), levels of lOOppm
are dangerous causing haemorrhagic pulmonary oedema (NRC 1985), and 150 to 200ppm
fatal from haemorrhagic pulmonary oedema (Braker and Mossman 1975).
Ozone is a colourless to blue gas with a pungent odour. Again the 'usual' exposure to ozone is
through airway pollution as mentioned in Chapter 2.2, (Anonymous 1995; Anonymous 1996)
where it is one of the most toxic elements reaching one hour mean ambient concentrations of
200-400uglm3 1Rnu, 1,966; Lippmann 1989; van Bree and Last lggT). Shorr term ozone
exposure causes reduction in lung function, increased airway hyperactivity, increased airway
inflammation, increased respiratory symptoms and hospital admissions (van Bree, Marra et al.
1995; Nikasinovic, Momas et al. 2003). Exposure to long term elevated ozone levels is again
associated with reduced lung function, increased respiratory symptoms, exacerbations of
asthma and airway cell and tissue changes (van Bree, Mara et al. 1995; Anderson, Ponce de
I-eon et al. 1998). At the tissue level, ozone with its high reactivity is usually consumed as it
passes through the first layer of tissue it contacts at the airway/air interface or lung/air
interface (Pryor 1992; Pryor, Squadrito et al. 1995). Since the lung lining fluid is 0.1 to 20
microns thick, in the thinnest parts it can react directly with cells and it has been shown, for
example, to act with the type II macrophages disrupting surfactant activity. The majority of
the interface area has thicker lining fluid and ozone is transformed into other reactive species
such as aldehyde and hydrogen peroxide, and these go on to cause the airway damage. This
causes epithelial disruption and increased permeability with an increase in inflammatory cells.
The disruption of cell membranes also results in a release of cytokine, cyclo-oxygenase and
liopoxygenase products. In studies looking at toxicity, differences have been demonstrated
between species with regards to dose and length of exposure that results in damage (Dormans,
van Bree et al. 1999). Inhaled ozone is also used in animals to give a lung fibrosis model for
study (Cross, Hesterberg et al. 1981; Yu, Song et al. 2001). In direct comparison of toxicity,
ozone was found to cause four times as much damage to the airways as NO2 (Chang, Mercer
et al. 1988) and be ten times more toxic to macrophages (Rietjens, Poelen et al. 1986).
The Occupational Safety and Health administration guidelines recommended exposure limit
for ozone is 0.lppm (0.2mglm3) (NIOSH 2005). The immediate danger to life and health level
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