Ozone can be generated in the workplace by high-voltage electrical equipment, and around ozone-producing devices used for air and water purification. Agricultural sources of ozone are also important. There is a near-linear gradient between exposure to ozone (1-hour level, 20–100 ppb) and bronchial smooth muscle response. See Table 56–1 for the current PEL for ozone.
1. Mechanism of action and clinical effects—Ozone is an irritant of mucous membranes. Mild exposure produces upper respiratory tract irritation. Severe exposure can cause deep lung irritation, with pulmonary edema when inhaled at sufficient concentrations. Ozone penetration in the lung depends on tidal volume; consequently, exercise can increase the amount of ozone reaching the distal lung. Some of the effects of O3 resemble those seen with radiation, suggesting that O3 toxicity may result from the formation of reactive free radicals. The gas causes shallow, rapid breathing and a decrease in pulmonary compliance. Enhanced sensitivity of the lung to bronchoconstrictors is also observed. Exposure around 0.1 ppm O3 for 10–30 minutes causes irritation and dryness of the throat; above 0.1 ppm, one finds changes in visual acuity, substernal pain, and dyspnea. Pulmonary function is impaired at concentrations exceeding 0.8 ppm.
Airway hyperresponsiveness and airway inflammation have been observed in humans. The response of the lung to O3 is a dynamic one. The morphologic and biochemical changes are the result of both direct injury and secondary responses to the initial damage. Long-term exposure in animals results in morphologic and functional pulmonary changes. Chronic bronchitis, bronchiolitis, fibrosis, and emphysematous changes have been reported in a variety of species, including humans, exposed to concentrations above 1 ppm. Increased visits to hospital emergency departments for cardiopulmonary disease during ozone alerts have been reported. A study of the basic physiologic responses of humans to ozone exposure and the biomarkers evoked provides useful insight into the fundamental toxicologic impacts of ozone.
2. Treatment—There is no specific treatment for acute O3 intoxication. Management depends on therapeutic measures used for deep lung irritation and noncardiogenic pulmonary edema that have resulted in ARDS. Current national ambient air quality standards for ozone are listed at https://www.epa.gov/ criteria-air-pollutants.
These “halohydrocarbon” agents once found wide use as industrial solvents, degreasing agents, and cleaning agents. The substances include carbon tetrachloride, chloroform, trichloroethylene, tetrachloroethylene (perchloroethylene), and 1,1,1-trichloroethane (methyl chloroform). Many halogenated aliphatic hydrocarbons are classified as known or probable human carcinogens. Carbon tetrachloride and trichloroethylene have largely been removed from the workplace. Perchloroethylene and trichloroethane are still in use for dry cleaning and solvent degreasing, but it is likely that their use will be very limited in the future. In 2016, the National Institute of Environmental Sciences (NIEHS) listed trichloroethylene as a known carcinogen. The EPA now considers perchloroethylene a likely human carcinogen. The EPA data sheet may be found at https://www.epa.gov/haps/health-effectsnotebook-hazardous-air-pollutants. Dry cleaning as an occupation is listed as a class 2B carcinogenic activity by the International Agency for Research on Cancer (IARC). The Canadian Center for Occupational Health and Safety lists occupations and exposures to occupational carcinogens at http://www.ccohs.ca/oshanswers/ diseases/carcinogen_occupation.html.