In: Health25 Nov 2014
The traditional kind of pollution associated with the London “smogs” that became notorious in the latter part of the 19th century through the early 1960s was that from the incomplete combustion of coal, leading to the emission of black smoke and sulfur dioxide. Its special feature was that the major contribution to urban concentrations came not from industry, but from domestic open coal fires, and the particularly inefficient combustion yielded not only black carbonaceous particles but also a large amount of tar. A further feature was the high relative humidity that often prevailed in winter, when emissions were at a maximum, and in the resultant smoke/fog/S02 mixture, further reactions occurred, leading to the formation of irritant species of particulates, including sulfuric acid. There is clear reason to believe that this particular set of circumstances led to substantial short-term effects, and there is still considerable interest in the role of acid aerosols in that connection. To what extent the specific chemical and physical characteristics of London smog have been special in respect to the development of CAD is less clear, but it seems likely that pollution of this particular type played an important part in the marked urban excess of morbidity and mortality from CAD.
A similar complex of pollutants has been, and in some cases, still is, prevalent in other countries around the world, but the balance in respect of different components is generally different. Where industrial sources, burning coal or heavy oil, dominate, sulfur dioxide is always liable to be present, though whether it is accompanied by black smoke depends on the care taken to ensure efficient combustion. There would not normally be the tar component as from the British coal fire. The most severe conditions in terms of exposure or urban populations are generally those in areas where coal is widely used for domestic heating or cooking purposes, for not only is the combustion inefficient and uncontrolled, but the emissions also occur at a low level, providing poor dispersion. so
The nature and effects of “traditional” pollutants have been summarized (Table 1) along with those for the separate class of pollutants that has come into prominence over the past few decades, the “photochemical,” or Los Angeles smog, complex. This is derived from reactive hydrocarbons emitted from motor vehicle exhausts, from petroleum refineries, or from a variety of other industrial or even natural sources, reacting in sunlight with oxides of nitrogen (coming from a similar range of sources) to produce a highly complex mixture containing ozone and organic oxidants. The most notable adverse effect is eye irritation, but ozone and nitrogen dioxide can produce short-term changes in lung function, and acute respiratory symptoms have been associated with various components of the complex. There is, however, no clear indication that this photochemical complex is related to the development of CAD.
The two broad types of air pollution problems described here can and often do coexist, though in temperate climates the tendency is for the traditional pollutants to reach their maximal concentrations in the winter months, due to heating requirements, while the photochemical pollutants reach their highest values in the summer, when sunlight is greatest. In addition, there can be emissions of other compounds from specific industrial activities. The net result in major urban/industrial areas is a highly complex mixture, but while the overall effect on health cannot readily be determined for each set of circumstances, the common thread in relation to CAD seems to be linked with sulfur dioxide and particulates derived from the combustion of coal or heavy oil.
Table 1—Some Urban Air Pollutants and their Effects on Health
|Traditional (‘reducing’) pollutants from coal/heavy oil combustion|
|SMOKE (SUSPENDED PARTICULATES)(Some contributions from diesel traffic also)||Can penetrate to lungs, some retained: possible long-term effects. May irritate bronchi also||LONDON SMOG COMPLEX Short-term effects: Sudden increases in deaths, in hospital admissions, and in illness among bronchitic patients. Temporary reductions in lung function (patients and some normals)|
|SO,||Readily absorbed on inhalation: irritation of bronchi, with possibility of bronchospasm||Long-term effects: Increased frequency of respiratory infections (children).Increased prevalence of respiratory symptoms (adults and children). Higher death-rates from bronchitis in polluted areas.|
|H8S04 (Mainly a secondary pollutant, formed from SOa in air)||Hygroscopic: highly irritant if impacted in upper respiratory tract. Acid absorbed on other fine particles may penetrate further to produce bronchospasm|
|POLYCYCLIC AROMATIC HYDROCARBONS (Small contributions from traffic also)||Mainly absorbed onto smoke: can penetrate with it to lungs||Possible carcinogenic effects: May play some part in the higher incidence of lung cancer in urban areas|
|Photochemical (‘oxidizing’) pollutants from traffic sources, or other hydrocarbon emissions|
|HYDROCARBONS (Volatile: petrol etc.) NO||Non toxic at moderate concentrations ‘ Capable of combining with Hb in blood, but no apparent effect in humans||LOS ANGELES SMOG COMPLEX Short term effects: Primarily eye irritation. Reduced athletic performance. Possibly small changes in deaths, hospital admissions|
|NO, Mainly secondary pollutants formed in photochemical 03 reactions||Neither gas is very soluble: some irritation of bronchi, but can penetrate to lungs to cause edema (at high concentrations). Urban concentrations too low for such effects, but evidence of reduced resistance to infections in animals||Longer-term effects: Increased onsets of respiratory illnesses (children), increased asthma attacks (adults). No clear indication of increased bronchitis.|
|Aldehydes, other partial oxidation products, PAN Others from traffic||Eye irritation, odor •|
|CO (other sources contribute, and smoking an important one)||Combines with Hb in blood, reducing oxygen-carrying capacity||Possible effects on CNS (reversible unless concentrations very high). Some evidence of effects on perception and performance of fine tasks at moderate concentrations. Enhances onset of exercise angina in patients. Urban concentrations too low for specific effects.|
|LEAD (some industrial sources contribute to air lead, and human intake often dominated by lead in food or drink)||Taken up in blood, distributed to soft tissues, and some to bone||Possible effects on CNS (longer time scale than in case of CO, and not necessarily reversible). Indications of neuropsychological effects on children within overall environmental exposure range, but role of traffic lead uncertain|
Blog invites submissions of review articles, reports on clinical techniques, case reports, conference summaries, and articles of opinion pertinent to the control of pain and anxiety in dentistry.