A key component of photochemical smog (see below), ozone is considered to be a criteria pollutant in the troposphereāthe lowermost layer of the atmosphereābut not in the upper atmosphere, where it occurs naturally and serves to block harmful ultraviolet rays from the Sun. Under certain conditions photochemical reactions between nitrogen oxides and hydrocarbons in the lower atmosphere can produce ozone in concentrations high enough to cause irritation of the eyes and mucous membranes.
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Lead
Inhaled lead particulates in the form of fumes and dusts are particularly harmful to small children, in whom even slightly elevated levels of lead in the blood can cause learning disabilities, and higher levels can cause seizures or even death (see lead poisoning). Sources of airborne lead particulates include oil refining, smelting, and other industrial activities. In the past, combustion of gasoline containing a lead-based antiknock additive called tetraethyl lead was a major source of lead particulates. All countries now have a complete ban on the use of lead in gasoline in road vehicles. In the United States, lead concentrations in outdoor air decreased more than 90 percent after the use of leaded gasoline was restricted in the mid-1970s and then completely banned in 1996.
Photochemical smog
Photochemical smog, also known as āLos Angeles smog,ā occurs most prominently in urban areas with heavy motor vehicle traffic and abundant sunlight. This type of smog has its origins in the nitrogen oxides and hydrocarbon vapors emitted by automobiles and other sources, which then undergo photochemical reactions in the lower atmosphere. The highly toxic gas ozone arises from the reaction of nitrogen oxides with hydrocarbon vapors in the presence of sunlight, and some nitrogen dioxide is produced from the reaction of nitrogen oxides with sunlight. The resulting smog causes a light brownish coloration of the atmosphere, reduced visibility, plant damage, irritation of the eyes, and respiratory distress. Surface-level ozone concentrations are considered unhealthy if they exceed 70 parts per billion for eight hours or longer; such conditions are fairly common in urban areas prone to photochemical smog.
Concentrations of photochemical smog often increase during warm, sunny weather because solar radiation drives the reactions that generate the secondary pollutants. Certain geographic features, such as mountains that impede air movement, and weather conditions, such as temperature inversions in the troposphere, contribute to the trapping of air pollutants and the formation of photochemical smog. Efforts to reduce photochemical smog generally focus on lowering emissions of nitrogen oxides and volatile organic compounds through vehicle emission controls, cleaner fuels, industrial regulations, driving and traffic restrictions, and other air quality management measures.
Air toxics
Hundreds of specific substances are considered hazardous when present in trace amounts in the air. These pollutants are called air toxics. Many of them cause genetic mutations or cancer; some cause other types of health problems, such as adverse effects on brain tissue or fetal development. Although the total emissions and the number of sources of air toxics are small compared with those for criteria pollutants, these pollutants can pose an immediate health risk to exposed individuals and can cause other environmental problems.
Most air toxics are organic chemicals, comprising molecules that contain carbon, hydrogen, and other atoms. Many are volatile organic compounds (VOCs): organic compounds that readily evaporate. VOCs include pure hydrocarbons, partially oxidized hydrocarbons, and organic compounds containing chlorine, sulfur, or nitrogen. They are widely used as fuels (e.g., propane and gasoline), as paint thinners and solvents, and in the production of plastics. In addition to contributing to air toxicity and urban smog, some VOC emissions act as greenhouse gases and, in so doing, contribute to global warming. Some other air toxics are metals or compounds of metalsāfor example, mercury, arsenic, and cadmium.
In many countries standards have been set to control industrial emissions of several air toxics. The first hazardous air pollutants regulated in the United States (outside the workplace environment) were arsenic, asbestos, benzene, beryllium, coke oven emissions, mercury, radionuclides (radioactive isotopes), and vinyl chloride. In 1990 this short list was expanded to include 189 substances as part of the significant amendments to the Clean Air Act of 1970. By the end of the 1990s, specific emission control standards were required in the United States for āmajor sourcesāāthose that release more than 10 tons per year of any of these materials or more than 25 tons per year of any combination of them. Important air toxics, their sources, and their environmental effects are summarized in the table.
| air toxic | common sources | human health risks |
|---|---|---|
| Source: U.S. Environmental Protection Agency | ||
| arsenic | volcanoes, weathering of rocks and minerals containing arsenic, industrial processes such as metal smelting, burning wood that has been treated with arsenic compounds | acute effects include gastrointestinal disorders, headaches, hypotension, shock, and death; chronic effects include dermatitis, irritation of mucous membranes, gastrointestinal disorders, and lung cancer |
| asbestos | natural deposits, building materials | chronic effects include asbestosis (lung disease), pulmonary hypertension, lung cancer, and mesothelioma |
| benzene | burning coal and oil, vehicle exhaust, industrial solvents, tobacco smoke | acute effects include dizziness, drowsiness, unconsciousness, and irritation of skin and mucous membranes; chronic effects include blood disorders including aplastic anemia, adverse effects on fetal development, and leukemia |
| beryllium compounds | burning coal and oil, tobacco smoke, natural occurrence in soil | acute effects include inflammation and swelling of the lungs; chronic effects include chronic beryllium disease (development of noncancerous lesions in the lungs) |
| cadmium compounds | burning fossil fuels, incineration of waste, smelting of zinc, lead, and copper | acute effects include lung irritation; chronic effects include various kidney disorders, sperm-count reduction, and lung cancer |
| chlorine | papermaking, drinking water, swimming pools | acute and chronic effects include irritation of mucous membranes and respiratory tract |
| coke oven emissions | coke ovens | chronic effects include conjunctivitis, dermatitis, lesions of respiratory and digestive systems, and various cancers |
| cyanide compounds | automobile exhaust, chemical processing, waste incineration | acute effects include headache, nausea, eye and skin irritation, and death; chronic effects include central nervous system disorders and thyroid disorders |
| formaldehyde | building materials and home furnishings, power plants, incineration of waste, automobile exhaust, tobacco smoke | acute effects include irritation of eyes and respiratory tract and inflammation of mouth, esophagus, and stomach if ingested; chronic effects include lesions in respiratory tract, menstrual disorders, and lung and nasopharyngeal cancer |
| lead compounds | battery manufacturing, paints and ceramic glazes, metal products | acute effects include gastrointestinal disorders and death; chronic effects include anemia, neurological disorders, reduced sperm count, and fetal effects including low birth weight and mental impairment |
| mercury compounds | paint manufactured prior to 1990ā91, batteries, industrial processes, dental amalgam fillings, fish products | acute effects include central nervous system effects including irritability, slowed sensory and motor nerve function, blindness, and deafness (depending on compound); chronic effects include a variety of central nervous system effects including erethism, insomnia, deafness, and blurred vision and kidney damage |
| nickel compounds | nickel processing, fossil-fuel burning, sewage sludge incineration | acute effects include lung and kidney damage (anecdotal reports) and gastrointestinal disorders; chronic effects include dermatitis and asthma |
| radionucleides (radon, radium, uranium) | ambient air (radon, uranium), drinking water (uranium), uranium mines and processing facilities, phosphate fertilizers | chronic effects include lung, bone, and nasal cancer |
| selenium compounds | drinking water and ambient air, some plastics and paints, pharmaceutical production | acute effects include irritation of the respiratory and gastrointestinal tracts; chronic effects include loss of hair and tooth decay and discoloration |
| vinyl chloride | manufacture of polyvinyl chloride (PVC), which is used in pipes, furniture, and automobiles | acute effects imclude central nervous system issues including dizziness, drowsiness, headaches, loss of consciousness, and inhibition of blood clotting; chronic effects include, rarely, vinyl chloride disease, in which changes occur in the bones and skin of the fingers and sensitivity to cold is increased, and liver cancer |
Air toxics may be released in sudden and catastrophic accidents rather than steadily and gradually from many sources. For example, in the Bhopal disaster of 1984, an accidental release of methyl isocyanate at a Union Carbide pesticide factory in Bhopal, Madhya Pradesh, India, immediately killed at least 3,000 people, eventually caused the deaths of an estimated 15,000 to 25,000 people over the following quarter-century, and injured hundreds of thousands more. The risk of accidental release of very hazardous substances into the air is generally higher for people living in industrialized urban areas. Hundreds of such incidents occur each year, though none has been as severe as the Bhopal event.
Other than in cases of occupational exposure or accidental release, health threats from air toxics are greatest for people who live near large industrial facilities or in congested and polluted urban areas. Most major sources of air toxics are so-called āpoint sourcesāāthat is, they have a specific location. Point sources include chemical plants, steel mills, oil refineries, and municipal waste incinerators. Hazardous air pollutants may be released when equipment leaks or when material is transferred, or they may be emitted from smokestacks. Municipal waste incinerators, for example, can emit hazardous levels of dioxins, formaldehyde, and other organic substances, as well as metals such as arsenic, beryllium, lead, and mercury. Nevertheless, proper combustion along with appropriate air pollution control devices can reduce emissions of these substances to acceptable levels.
Hazardous air pollutants also come from āareaā sources, which are many smaller sources that release pollutants into the outdoor air in a defined area. Such sources include commercial dry-cleaning facilities, gasoline stations, small metal-plating operations, and woodstoves. Emissions of air toxics from area sources are also regulated under some circumstances.
Small area sources account for about 25 percent of all emissions of air toxics. Major point sources account for an additional 20 percent. The restāmore than half of hazardous air-pollutant emissionsācome from motor vehicles. For example, benzene, a component of gasoline, is released as unburned fuel or as fuel vapors, and formaldehyde is one of the by-products of incomplete combustion. Newer cars, however, have emission control devices that significantly reduce the release of air toxics.