Source: Based on Seinfeld (1975).

Source: Based on Seinfeld (1975).

Carbon monoxide (CO) is produced by automobile engines and other combustion processes. It accumulates to toxicologically significant levels in high-traffic areas and areas where vehicles must accelerate, such as at intersections and toll booths. Typical levels in air range from 5 to 100 ppmv. The toxic effect of CO is related to the percent carboxyhemoglobin in the blood. Equation (17.2) and Table 21.11 show the equilibrium relation between this and the CO concentration in the air. It takes 8 to 10 hours for the blood to reach equilibrium. Thus an exposure to 50 ppmv for 90 minutes has been found to be equivalent to 10 to 15 ppmv for 8 hours or more.

Sulfur dioxide in the atmosphere originates primarily from combustion of fossil fuels, especially coal and some petroleum oils, and from metals smelting. Emissions are in the form of SO2. The solubility of sulfur dioxide is 11.3 g per 100 mL, facilitating its absorption to aqueous aerosols. In solution it forms sulfite (SO|~) and bisulfite (HSO3~). It reacts both in the gas phase and in the aerosols to form H2SO4. The sulfuric acid form is removed from the atmosphere by dry and wet deposition.

Sulfur dioxide enters plant leaves by molecular diffusion through the stomata. Photosynthesis and transpiration are increased by short-term low-concentration exposures, but decreased by longer-term or higher-concentration levels. The resulting sulfite and bisulfite are toxic to the plant. They can be oxidized with or without enzymes to the less toxic sulfate, but damaging free radicals can be formed. Effects include chlorosis (loss of chlorophyll) and necrosis as well as changes in phosphorus metabolism and photosynthesis. The effects are highly species dependent. Atmospheric sulfate is also a contributor to acid deposition.

In animals, sulfur dioxide is irritating to the eyes and upper respiratory tract. However, these effects appear only at levels 50 or 100 times ambient levels. Necrosis of nasal epithelium occurred in mice exposed to 10 ppmv for 72 hours. However, at high humidity or atmospheric particulate levels, increased irritation occurs. It is likely that it is the conversion to sulfuric acid that is responsible. At 5 ppmv, humans exhibit increased respiratory frequency and decreased tidal volume (faster and shallower breathing). Asthmatics are more sensitive than the rest of the population, but less so when breathing through the nose than through the mouth. SO2 interacts positively with ozone and smoke particles. Concentrations of SO2 and smoke both exceeding 500 mg/m3 are thought to produce excess mortality among the elderly and the chronically ill; 130 mg/m3 of SO2 (0.046 ppmv) together with 130 mg/m3 of particulates resulted in increased number and severity of respiratory disease in schoolchildren.

Particulates include dust and smoke. Smoke is made up of carbon and products of incomplete combustion, including polynuclear aromatic compounds. The toxic effects of smoke are thought to be primarily due to compounds that are adsorbed onto its surface. The solids serve to carry the compounds into the lungs.

Ambient particulate concentrations as low as 80 to 100 mg/m3 (annual geometric mean) have been reported to result in increased death rates for people over 50 years old. A 24-hour level of 300 mg/m3 together with 630 mg/m3 of SO2 (0.22 ppmv) produced acute worsening of symptoms of patients suffering from chronic bronchitis.

Cigarette smoke contains more than 2000 identified compounds. It is a significant source of radionuclides and carbon monoxide. Local toxic effects include chronic bronchitis, emphysema, and cancer of the lung and other parts of the respiratory tract. Systemic effects include arteriosclerosis of coronary arteries and cancer of the bladder, pancreas, and other organs. Nicotine in tobacco smoke causes addiction. Smoking paralyzes the mucociliary escalator that clears particles from the respiratory tract. It also inhibits macrophages in the alveoli, making the lungs more susceptible to disease. Pregnant women who smoke have more miscarriages and their babies have lower birthweights than the infants of nonsmokers. Users of snuff or cigars who do not inhale smoke are susceptible to cancer of the lips and oral cavity. Nonsmokers subjected to "secondhand smoke'' also are at increased risk. Children of smokers have more respiratory illnesses than do children of nonsmokers.

Epidemiological data have been collected on cigarette smoking and cancer only since the 1940s. As mentioned above, the relative risk between smokers and nonsmokers for all cancers is about 5.0, and for lung cancer is 10 to 15. The data on lung cancer can be summarized in more detail by the following models. The rate of death by lung cancer increases with the first to second power of the number of cigarettes smoked per day, and with the fourth to fifth power of the number of years the person smoked. This means that doubling the number of cigarettes smoked per day triples the risk of lung cancer, but doubling the number of years that one smokes increases the risk by a factor of 20. Another model that takes into account the smoker's age in years (a) and years of exposure (y) is probability of death by lung cancer per year = 10_11a4 + 10~9y4 (21-2)

According to this model, the annual lung cancer death rate for 70-year-old nonsmokers is 24 per 100,000. For 70-year-olds that have been smoking since the age of 20, the rate is 649 per 100,000. This is a relative risk of 27.

Smoking is also known to increase the cancer rates of the oral cavity, the bladder, the kidney, the pancreas, and the esophagus, as well noncancer diseases such as cerebrovas-cular disease (e.g., strokes), coronary heart disease, and pulmonary disease (e.g., emphysema).

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