What are the harmful effects of ozone?

What are the health effects of ozone?

Ozone in the air we breathe can harm our health. People most at risk from breathing air containing ozone include people with asthma, children, older adults, and people who are active outdoors, especially outdoor workers. In addition, people with certain genetic characteristics, and people with reduced intake of certain nutrients, such as vitamins C and E, are at greater risk from ozone exposure.

Breathing ozone can trigger a variety of health problems including chest pain, coughing, throat irritation, and airway inflammation. It also can reduce lung function and harm lung tissue. Ozone can worsen bronchitis, emphysema, and asthma, leading to increased medical care. Learn more about health effects.

What are the environmental effects of ozone?

Ozone affects sensitive vegetation and ecosystems, including forests, parks, wildlife refuges and wilderness areas.  In particular, ozone harms sensitive vegetation during the growing season.

What are the ozone levels in my community?

Air quality forecasts are often given with weather forecasts on handheld devices, online or in the paper or television. You can check ozone levels and other daily air quality information by visiting www.airnow.gov and in many areas you can receive air quality notifications through www.enviroflash.info.

What is “good” vs. “bad” ozone?

Ozone can be “good” or “bad” for health and the environment depending on where it’s found in the atmosphere. Stratospheric ozone is “good” because it protects living things from ultraviolet radiation from the sun. Ground-level ozone, the topic of this website, is “bad” because it can trigger a variety of health problems, particularly for children, the elderly, and people of all ages who have lung diseases such as asthma.

Ozone is a gas composed of three atoms of oxygen (O3). Ozone occurs both in the Earth’s upper atmosphere and at ground level. Ozone can be good or bad, depending on where it is found.

Called stratospheric ozone, good ozone occurs naturally in the upper atmosphere, where it forms a protective layer that shields us from the sun’s harmful ultraviolet rays. This beneficial ozone has been partially destroyed by man made chemicals, causing what is sometimes called a “hole in the ozone.” The good news is, this hole is diminishing.

WHO Air quality guidelines

PROLONGED O3 BREATH IS HARMFUL TO HEALTH

NANOLIFE O3 is stable only for 7-10 minutes after generation .Then O3 will convert in to O2 back .

Rationale Since the publication of the second edition of the WHO Air quality guidelines for Europe (WHO, 2000) which sets the guideline value for ozone levels at 120 µg/m3 for an 8-hour daily average, little new information about the health effects of ozone has been obtained from either chamber studies or field studies. Significant additions to the health effects evidence base have, however, come from epidemiological time-series studies. Collectively these studies have revealed positive, small, though convincing, associations between daily mortality and ozone levels, which are independent of the effects of particulate matter. Similar associations have been observed in both North America and Europe. These latest time-series studies have shown health effects at ozone concentrations below the previous guideline of 120 µg/m3 but without clear evidence of a threshold. This finding, together with evidence from both chamber and field studies that indicates that there is considerable individual variation in response to ozone, provides a good case for reducing the WHO AQG for ozone from the existing level of 120 µg/m3 to 100 µg/m3 ( daily maximum 8-hour mean). It is possible that health effects will occur below the new guideline level in some sensitive individuals. Based on time-series studies, the increase in the number of attributable deaths brought forward is estimated to be 1–2% on days when the 8-hour mean ozone concentration reaches 100 µg/m3 over that when ozone levels are at a baseline level of 70 µg/m3 (the estimated background ozone level; see Table 3). There is some evidence that long-term exposure to ozone may have chronic effects but it is not sufficient to recommend an annual guideline. Ozone is formed in the atmosphere by photochemical reactions in the presence of sunlight and precursor pollutants, such as the oxides of nitrogen (NOx) and volatile organic compounds (VOCs). It is destroyed by reactions with NO2 and is deposited to the ground. Several studies have shown that ozone concentrations correlate with various other toxic photochemical oxidants arising from similar sources, including the peroxyacyl nitrates, nitric acid and hydrogen peroxide. Measures to control tropospheric ozone levels focus its precursor gas emissions, but are likely to also control the levels and impacts of a number of these other pollutants. Hemispheric background concentrations of tropospheric ozone vary in time and space but can reach 8-hours average levels of around 80 µg/m3 . These arise from both anthropogenic and biogenic emissions (e.g. VOCs from vegetation) of ozone precursors and downward intrusion of stratospheric ozone into the troposphere. Indeed, the proposed guideline value may occasionally be exceeded due to natural causes. As ozone concentrations increase above the guideline value, health effects at the population level become increasingly numerous and severe. Such effects can occur in places where concentrations are currently high due to human activities or are elevated during episodes of very hot weather. The 8-hour IT-1 level for ozone has been set at 160 µg/m3 at which measurable, though transient, changes in lung function and lung inflammation have been recorded in controlled chamber tests WHO Air quality guidelines 15 in healthy young adults undertaking intermittent exercise. Similar effects were observed in summer camp studies, involving exercising children. Although some would argue that these responses may not necessarily be adverse, and that they were seen only with vigorous exercise, these views are counterbalanced by the possibility that there are substantial numbers of persons in the general population that might be more susceptible to the effects of ozone than the relatively young and generally healthy individuals who participated in the chamber study. Furthermore, chamber studies provide little information about repeated exposures. Based on time-series evidence, exposures at the IT-1 level are associated with an increase in the number of attributable deaths brought forward of 3–5% (see Table 3). Table 3 WHO air quality guideline and interim target for ozone: 8-hour concentrations Daily maximum 8- hour mean (µg/m3 ) Basis for selected level High levels 240 Significant health effects; substantial proportion of vulnerable populations affected. Interim target-1 (IT-1) 160 Important health effects; does not provide adequate protection of public health. Exposure to this level of ozone is associated with: • physiological and inflammatory lung effects in healthy exercising young adults exposed for periods of 6.6 hours; • health effects in children (based on various summer camp studies in which children were exposed to ambient ozone levels). • an estimated 3–5% increase in daily mortalitya (based on findings of daily timeseries studies). Air quality guideline (AQG) 100 Provides adequate protection of public health, though some health effects may occur below this level. Exposure to this level of ozone is associated with: • an estimated 1–2% increase in daily mortalitya (based on findings of daily timeseries studies). • Extrapolation from chamber and field studies based on the likelihood that reallife exposure tends to be repetitive and chamber studies exclude highly sensitive or clinically compromised subjects, or children. • Likelihood that ambient ozone is a marker for related oxidants. a Deaths attributable to ozone. Time-series studies indicate an increase in daily mortality in the range of 0.3–0.5% for every 10 µg/m3 increment in 8-hour ozone concentrations above an estimated baseline level of 70 µg/m3

OZONE

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BACKGROUND INFORMATION

PHYSICAL AND CHEMICAL PROPERTIES

Structural formula:	O3
Molecular weight:	48.0
CAS number:	10028-15-6
Boiling point:	−111.9°C
Density as a gas:	2.144 g/L at 0°C
Density as a liquid:	1.514 g/ml at −195.4°C
General characteristics:	A polymeric, highly reactive form of oxygen. It is a bluish explosive gas or blue liquid. It is a powerful oxidizing agent with deodorant and antiseptic properties. It is a respiratory, ocular, and nasal irritant with a characteristic odor.
Conversion factors:	ppm = 0.5 (mg/m3) mg/m3 = 2.0 (ppm)

SUMMARY OF TOXICITY INFORMATION

EFFECTS ON HUMANS

Healthy men have been exposed deliberately to ozone at up to 0.75 ppm for 2 h (Bates et al., 1972; Folinsbee et al., 1975; Hazucha, 1974; Hazucha et al., 1973). Light exercise was also taken at this concentration. A reduction in ventilatory capacity (25% reduction in forced expiratory volume) was reported. Chamber exposures have since shown that a critical ozone concentration for a ventilatory response is probably around 0.3-0.5 ppm (Kleinman et al., 1981).

Exposure of male volunteers at 0.4 ppm for 4 h combined with exercise (700 kg-m per minute) caused significant changes in forced vital capacity (FVC), maximal midexpiratory flow (MMF), and airway resistance (Hackney et al., 1975a). Some subjects with hyperreactive airways have responded to ozone at concentrations as low as 0.37 ppm. Most studies have failed to show any effect at 0.25 ppm. There is also a suggestion in the literature that effects may be greater on the second day of exposure (Hackney et al., 1975b). A group of young male volunteers were exposed at 0.5 ppm for 2 h. There were only minimal effects on the first day. However, when the exposure was repeated on the next day, 5 of 7 subjects showed significant effects. Twenty subjects were exposed to ozone at 0.5 ppm for 6 h (Kerr et al., 1975). Medium exercise on a bicycle ergometer (100 W at 60 rpm) was used. The subjects experienced dry cough and chest discomfort after exposure. Chest discomfort ranged from tightness on full inspiration to generalized chest pain that was accentuated by exercise, cough, and irritation of the nose and throat. Significant changes from control values were reported for several lung-function tests (specific airway conductance, pulmonary resistance, FVC, and forced expiratory volume in 3 s).

There has been some suggestion that ozone at low concentrations may be carcinogenic or mutagenic in man. Chromosomal abnormalities have been produced in plants and animals, sometimes after low ozone exposures (0.2 ppm for 5 h) (Zelac et al., 1971). Minor chromosomal abnormalities have also been observed in the circulating lymphocytes of humans who have been exposed experimentally at 0.5 ppm for 6-10 h (Merz et al., 1975). So far, however, there is no convincing evidence that ozone at low concentrations causes cancer or congenital malformations in man.

EFFECTS ON ANIMALS

Mittler et al. (1956) reported LC₅₀s for 3-h exposures to ozone as follows:

Mice:	21 ppm
Rats:	21.8 ppm
Cats:	34.5 ppm
Rabbits:	36 ppm
Guinea pigs:	51.7 ppm

Svirbely and Saltzman (1957) reported LC₅₀s for 4-h exposures as follows:

Mice:	2.1- 9.9 ppm
Rats:	7.2-12.3 ppm
Hamsters :	15.8 ppm

Diggle and Gage (1955) investigated toxicity in rats and mice after 4-h exposures to ozone and concluded that the LC₅₀ was around 10-12 ppm. Generally, lethal exposures to ozone are accompanied by dyspnea and lethargy, and autopsy reveals lung edema.

Eye effects of ozone exposure were studied in rabbits by Mettier et al. (1960) and Hine et al. (1960). Exposure of rabbits for 1.9-2.8 ppm for 4 h produced no ocular effects, and exposure at 2 ppm 4 h/d was also without eye effects.

Morphologic changes have been reported in the respiratory tracts of animals as a result of exposure to ozone at 0.2-0.25 ppm. Cats were exposed at 0.25, 0.5, and 1.0 ppm for 4.7-6.6 h (Boatman et al., 1974). At all three concentrations, there was considerable desquamation of the ciliated airway lining cells, the degree of damage being roughly proportional to the ozone concentration. Cytoplasmic vacuolization of ciliated cells and condensation of mitochondria were the most consistent morphologic changes. The mitrochondrial alterations were seen after exposure at all concentrations and were most frequent in the medium-sized airways, 0.8-1.7 mm in diameter. In rats exposed at 0.2 ppm for 3 h (Stephens et al., 1974), degenerative changes were observed in Type I cells, which were replaced by Type II cells. Morphologic changes have also been reported by Mellick et al. (1977) in rhesus monkeys after exposure at 0.5 ppm for 8 h; similar but milder changes were observed in Bonnet monkeys after exposure at 0.2 ppm.

Enzyme alterations have been reported in the respiratory tracts of various animals at about these concentrations. Increased activity of lung glutathione peroxidase and glutathione reductase and increased succinate-dependent lung mitochondrial oxygen consumption have been reported in rats exposed continuously for a week at 0.2 (Chow et al., 1974; Mustafa et al., 1975). Decreases in lysozyme, acid phosphatase, and ß-glucuronidase activity in alveolar macrophages (which appear to be related to dose up to 1 ppm) have been observed in rabbits exposed at 0.25-0.5 ppm ozone for 3 h (Hurst et al., 1970). Decreased red cell acetylcholinesterase and increased osmotic fragility have also been reported in man after exposure at 0.37-0.5 ppm for 2 h (Hackney et al., 1975b) Whether the increased fragility is due to the enzyme alterations or to the spherocytosis that may also occur at this concentration seems debatable.

An increased susceptibility to pulmonary streptococcal infection has been shown to result from exposure to ozone at as low as 0.08 ppm for 3 h (Coffin and Blommer, 1970). This could be due in part to impairment of the bactericidal capabilities of the macrophage, which appears to occur as a result of exposures at about 0.3 ppm.

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