========================================= Breathing can be hazardous to your health ========================================= Clean air acts in North America and Western Europe have reduced some forms of pollution. But evidence is growing that urban air still kills - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - --> [Send the 1-line message GET BREATHE CITYDNGR ACTIV-L to ] [LISTSERV@UMCVMB.BITNET for a copy of this file. ] --> [Send GET ACTIV-L ARCHIVE ACTIV-L to above address for a ] [listing with brief descriptions of other files available] - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - ============================= By Robert Read and Cathy Read ============================= New Scientist 23 February 1991 ============================= The World Health Organization estimates that millions of Europeans live in areas with air pollution severe enough to cause thousands of premature deaths each year and leave many more chronically ill and disabled. Almost 40 years on from the infamous London smog that killed 4000 people, air pollutants still contribute to a range of lung and heart illness. If you had walked the streets of London or Pittsburgh in the middle of this century you would have been all too familiar with the tainted brown air that obscured the winter sun. These infamous "smogs" developed when anti-cyclonic conditions in winter trapped sulphurous air pollution -- caused by coal burning -- close to the ground. Today such smogs are more typical of parts of eastern Europe. In the highly industrialised northern part of Czechoslovakia, eastern Germany and southern Poland levels of sulphur dioxide, one of the constituents of winter smog, greatly exceed internationally agreed safe limits throughout most of the winter. Some nations have reduced the problems of winter smog through clean air legislation. But as vehicle exhaust emissions increase and polluted air from densely industrial areas moves over long distances, they now suffer problems from pollution in the summer. In the presence of sunlight, nitrogen oxides, volatile organic compounds (VOCs) and sulphur dioxide undergo photochemical conversion to ozone, sulphuric acid and nitric acid gas. Photochemical pollution has become a worldwide problem and is increasing; in some remote areas of the world ozone concentrations are growing at a rate of 1 per cent a year. Motor vehicle exhaust emissions, which include oxides of nitrogen, carbon monoxide and VOCs, are important contributors to pollution in the summer. Overall, motor vehicles produce more air pollution than any other single human activity. In the US in 1985, transport was to blame for 70 per cent of the carbon monoxide, 45 per cent of nitrogen oxides and 34 per cent of the VOCs in the air. This year, motor vehicles in Europe alone will emit an estimated 5 5 million tonnes of hydrocarbons, 28 million tonnes of carbon monoxide and 6 5 million tonnes of oxides of nitrogen. It is hardly surprising that pollutants in the atmosphere can be damaging to health. A reasonably active person typically inhales between 10 000 and 20 000 litres of air over 24 hours, and this rises sharply in people taking more vigorous exercise -- a jogger may inhale up to 3000 litres over the course of an hour. Air within the lungs is exchanged through tiny air sacs known as alveoli which are in close contact with many tiny blood vessels. At any time the total surface area of blood vessels within the alveoli exposed to the atmosphere is as large as half a tennis court. Around the middle of this century, three large-scale pollution disasters emphasised the link between air pollution, disease and even death. They happened in the Meuse Valley, Belgium, in 1930, Donora, Pennsylvania in 1948 and London in 1952. The worst tragedy began in London on Thursday, 4 December, with a slow moving anticyclone that halted over the city. Over the next three days, concentrations of smoke and sulphur dioxide built up in the stagnating, foggy air. Records from hospitals and general practitioners showed that many people suffered from breathlessness and irritation and narrowing of the airways. During this period, a total of 4000 people in London died from heart and lung disease. Throughout the episode, high levels of sulphates and sulphur dioxide were recorded. Daily concentrations of sulphur dioxide reached a peak of nearly 4000 micrograms per cubic metre -- more than 10 times the maximum that the WHO believes it is safe to breathe in over just one hour. Scientists, however, suspected that sulphuric acid rather than sulphates or sulphur dioxide had caused the deaths. Atmospheric conditions in London at the time would have encouraged the formation of droplets of acid suspended in the air as aerosols. The transformation of the gas sulphur dioxide SO. into sulphuric acid H(2)SO(4) is catalysed by various metals within water droplets at relatively low temperatures. Although the authorities tried various measures, only one proved promising: the ammonia bottles with wicks that were placed in hospital wards in an attempt to neutralise the acid aerosols. An astute observation by veterinary surgeons supports the beliefs that acid aerosols were involved. More than 60 prize cattle from the Smithtield Club's Show required treatment for acute chest symptoms, whereas a number of more ordinary beasts were apparently unaffected. Scientists believe that, because the pens of the unaffected animals were cleaned less frequently, they may have been protected by the neutralising effect of ammonia in their excrement. - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - In the 40 years since the London tragedy researchers in more than 10 countries have linked high levels of sulphates and sulphur dioxide with unexpectedly high levels of disease and death. Some of the most recent work has led scientists to suspect once again that acid aerosols may be the major culprit. David Bates and Ronnie Sizto of the Department of Health Care and Epidemiology at the University of British Columbia in Vancouver studied the links between hospital admissions of people suffering from respiratory problems and concentrations of air pollutants in southern Ontario between 1974 and 1983. The only pollutants to show a consistent association with increased admissions were ozone and sulphates. A further study of admissions of people with asthma showed a correlation with ozone and sulphates after a time lag of 24 and 48 hours respectively. Levels of aerosol sulphates correlated most strongly with variations in respiratory admissions, but only for the summer months. Bates and Sizto speculate that the damage to health comes from neither ozone nor sulphates, but from a fellow pollutant that "travels" with them in the summer. They believe the elu- sive fellow traveller is sulphuric acid. In sunny conditions sulphuric acid is formed by the photochemical conversion of sulphur dioxide in the presence of nitrogen oxides and hydrocarbons, a rich mix of pollutants which urban or industrial areas can easily provide. Sulphuric acid and other acid aerosols are highly reactive. Because of this they are notoriously difficult to measure; special care must be taken so that air passing over the collected acid does not neutralise the acid, and technicians must avoid contaminating the sample with ammonia from their breath. Recently, Jack Spengler, professor of environmental health at Harvard School of Public Health, developed a measuring technique that has lead to new insights into the effects of acid air on people's health. The new method measures the acidity (hydrogen ion concentration) of particles in the air. The inlet of the sampling system is coated with material that strips ammonia from the air, so preserving the acidity of the aerosol on the filter. The sample is then analysed in the laboratory using an ion-selective electrode. Using the new device, Spengler has sampled the pH of air in a number of sites across North America. At one, a children's summer camp in Dunsville, Ontario, his team detected acidic conditions linked to high levels of ozone and sulphate -- often exceeding 50 micrograms of sulphuric acid per cubic metre. Under these conditions, Spengler and his colleagues calculate that an active child might receive more than 2000 nanomoles of hydrogen ions in 12 hours and more than 900 nanomoles over one hour. These can be dangerous levels: laboratory studies have shown that between 500 and 1000 micrograms per cubic metre of sulphuric acid alters lung function in asthmatics who are breathing normally at rest. Recently, Jane Koenig in the Department of Environmental Health at the University of Washington, Seattle, demonstrated that the lung function of asthmatic people taking exercise suffered at much lower levels of between 70 and 100 micrograms per cubic metre, which are close to the levels documented in summer camp studies. Because ammonia produced in the mouth appears to protect against the effects of acid air, Bates points out that this is one good reason children in summer camps should avoid lemonade: it neutralises the protective ammonia. Many researchers now believe that high-acid episodes have major implications for public health. Plumes of acid aerosol travel vast distances, so although exposure and effects may be small, large numbers of people are involved. Bert Brunekreef of the University of Wageningen documented acid aerosol plumes more than 1000 kilometres long during January 1985 and January 1987. The pollutants were transported from Eastern Europe to Central and Western Europe. These pollution plumes, seen clearly on pictures taken by satellite, can dramatically reduce visibility. Recently, scientists have used airport visibility to estimate the amount of fine particles suspended in the air. They have shown that when visibility is down to 1 kilometre the sulphate concentration is more than 24 micrograms per cubic metre. Ozone appears to be imporlant in accelerating the formation of acid from sulphur dioxide; and recent high levels of acid aerosols may be in part due to the greater formation of ozone as nitrogen oxide emissions rise. But ozone, a faintly bluish gas, is also harmful on its own. High ozone levels make asthmatic conditions worse, impair lung function, and increase both respiratory tract infections and hospital admissions. It is hardly surprising that this powerful oxidant, capable of cracking stretched rubber and laddering nylon stockings at levels of only 0.01 or 0.02 parts per million, harms the delicate tissues in the lung. Researchers have recently documented changes in the biochemistry of the lungs at ozone levels well below international safety limits (New Scientist, Science, 9 September 1989. Using mathematical models scientists have calculated that the highest concentrations of ozone occur in the tiniest air passages of the lung. At the Canadian standard of 0.08 parts per million, averaged over one hour, ozone inflames the airways and makes them more permeable. The slightly lower WHO standard of 0.076 parts per million provides only a narrow safety margin. The current US standard of 0.12 parts per million provides none. In practice. These now inadequate safety limits arc often breached. In northwestern Europe the WHO guideline for ozone levels over an 8-hour exposure is exceeded between 10 and 100 times a year. The long-term effects of exposure to low levels of ozone are unknown. But research by Russel Sherman. professor of pathology at the University of California in Los Angeles, provides a clue. Postmortem examinations of the lungs of healthy young nonsmokers killed in accidents revealed bronchiolitis -- inflammation of the bronchioles. The changes are similar to those seen in cigarette smokers, and the likeliest culprit is ozone. Researchers are now questioning whether increasing concentrations of air pollutants may be linked to the increasing incidence and severity of some types of allergies. In some countries. including the US. Australia, France and Britain. death rates from asthma have increased by 50 per cent within the past 10 years. A number of specialists, among them Stephen Holgate of the University of Southampton in Britain and Anne Woolcock of the Royal Prince Alfred Hospital in Sydney. Australia, believe increased exposure to airborne allergens may be responsible. Holgate has found that children exposed at an early age to high levels of housedust mites are more likely to develop asthma. The theory goes that the children's lungs are somehow "sensitised" to react to asthma triggers. Environmental factors that probably contribute to an increased exposure to the mites include fitted carpets, central heating and poorly ventilated houses. Could air pollution also be involved'? Woolcock believes it is. She suggests that pollutants such as tobacco smoke and diesel fumes may be acting as co-factors, enhancing an allergic response to, say, pollen or housedust mites. There is as yet no conclusive evidence to support Woolcock-s idea. but a small number of studies make her Idea appealing. In Japan there has been sharp increases in both the incidence of hay fever due to cedar pollen and the numbers of diesel-powered cars. Because the problem was worse in people living near busy roads, a group of Japanese scientists wondered if diesel fumes could be involved. In a series of experiments they showed that one component of diesel exhaust, termed diesel exhaust particulates, stimulated the production of antibodies active in hay fever. While a question mark hangs over the role of air pollution and the origins of asthma, there is no doubt that high levels of certain air pollutants make asthma worse. Laboratory studies of asthmatics have consistently demonstrated the harmful effects of sulphur dioxide at levels only slightly higher than permitted limits, suggesting that people with asthma are at risk in high pollution areas. A recent study by Koenig suggested that pollutants interact synergistically: they arc more powerful together than separately. She exposed a group of mildly asthmatic adolescents to 0.12 parts per million of ozone (a level regularly recorded in parts of southern England in the summer) and found that this increased their vulnerability to low concentrations of sulphur dioxide. Studies carried out in France and Israel have shown an increased incidence of asthma in areas highly polluted with sulphur dioxide compared with areas where pollution is low. Recently, new data linking air pollution with poor respiratory health has begun to emerge from Eastern Europe. One survey of 574 000 Polish army recruits found the recruits who came from polluted regions were five times as likely to suffer from asthma as those who lived in cleaner areas. - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - In many asthmatics, symptoms are triggered by common allergens such as pollen. Scientists in Toronto have now discovered that, like sulphur dioxide, ozone also sensitises asthmatics to these allergens. Asthmatics who were sensitive to ragweed were exposed to ragweed pollen after breathing air for one hour and then again after breathing ozone at 0.12 parts per million, the US standard. for one hour. After breathing ozone the asthmatics reacted to half the dose of ragweed pollen that they reacted to after breathing air. While pollutants such as acid aerosols and ozone travel long distances and may affect people over a wide area, the most important pollutants at the roadside include nitrogen dioxide, carbon monoxide, smoke particles and VOCs. One recent study of 944 bridge and tunnel workers in New York City showed that tunnel workers had significantly poorer lung function and more respiratory illness than bridge workers, implying vehicle exhaust fumes were damaging their health. =============================================== C u l p r i t s i n c a r e x h a u s t s =============================================== Nitrogen dioxide probably worsens the lung function of asthmatics and chronic bronchitics. Although the WHO directive is that hourly average concentrations should not exceed 0.1 parts per million, levels of between 0.2 and 0.4 parts per million are regularly recorded in London's Cromwell Road. Studies have shown that lung function of normal people is disturbed at concentrations above 2 parts per million, but below this, experimental data are conflicting. Researchers at the Ho^pital Saint-Marguerite, Marscilles, put 20 asthmatics in chambers and allowed them to breathe either normal air, or air polluted with 0.1 parts per million of nitrogen dioxide. Thirteen of the asthmatics had more sensitive airways after exposure to NO(2). But a number of later studies have produced more variable results. Carbon monoxide has a distinct physiological effect. Its toxicity is based upon the fact that the oxygen carrying molecule of the blood. haemoglobin, has a high affinity for it. Carbon monoxide occupies oxygen binding sites within the haemoglobin molecule to produce carboxyhaemoglobin (COHb), thus reducing the oxygen-carrying capacity of the blood and potentially starving the brain and other tissues of oxygen. In people who commit suicide by inhaling car exhaust, the majority of their haemoglobin converts to COHb. The presence even of low concentrations of COHb is potentially troublesome for heart disease sufferers. Scientists of the Health Effects Institute at Boston recently showed that angina patients, exercising on treadmills, experienced chest pain much earlier if they simultaneously inhaled carbon monoxide at concentrations that resulted in COHb levels of 2 per cent. Many smokers have COHb levels of 2 per cent or higher and similar levels have been recorded in nonsmokers exposed to traffic fumes. Indeed, Frank Stern and his colleagues at the National Institute for Occupational Safety and Health, at Cincinnati, found that there was an increase in the expected rate of death from heart disease among bridge a tunnel workers in New York City, an effect which they attributed to carbon monoxide. In 1975, Peter Cole of the anaesthetics department of St Bartholomew's Hospital in London measured COHb levels among nonsmokers waiting to be seen in the outpatients department. Despite the fact that they mostly lived in central London, their COHb levels were broadly similar to nonsmoking inhabitants of the island of Sark. (Nonsmokers are singled out because tobacco smoke contains carbon monoxide.) It is well know, however, that COHb levels are affected by the time spent exposed to carbon monoxid, the concentration of the gas and the workload of the individual. Levels of carbon monoxide can be very high within dense traffic, especially at road intersections. One of us (RR), together with Malcolm Geen of the British Lung Foundation recently measured the carbon monoxide levels in the breath of London traffic policemen, and found their levels to be consistently higher than pedestrians. Smoke particles are impregnated with polyaromatic hydrocarbons. Exhaust from diesel engines contains lower concentrations of some gaseous pollutants, but more particles, as any cyclist following an older bus or taxi will discover. There is evidence from studies on animals that polyaromatic hydrocarbons are carcinogenic. Attempts to look; for increased rates of cancer in people exposed to diesel fumes have been difficult because of confounding variables such as smoking. However, Eric Garshick and Frank Speizer at Brigham and Women's Hospital in Boston surveyed the death certificates and work histories of 15 000 railway workers and found that those who were aged less than 65 when they died and had been exposed to diesel for at least 20 years had a small but significantly increased risk of lung cancer. Volatile organic compounds such as benzene are a source of concern because of their ability to cause cancer in people exposed to them at work. In one study a group of 748 rubber workers exposed to benzene over 10 years was 5.6 times more likely to develop leukacmia than the general population. Data such as this are used to calculate the risk to the general population. This approach is highly controversial and contested by the petroleum industry which claims there is no evidence that low doses of benzene are harmful. Nevertheless the data have been used to calculate the extra risks of developing leukemia among people living in the Los Angeles basin -- estimated at 101 to 780 cases per million people exposed. In response to anxieties raiscd about this risk the State of California has introduced devices to prevent vapour escaping at petrol stations and petrol pumps. Is this an overreaction in the face of the evidence? Perhaps. Nonetheless, the scientific consensus in California is that it is prudent to follow one's hunches. Elsewhere some convincing data on the health effects of air pollution are being ignored. Many governments do not consistently monitor levels of ozone or sulphur dioxide, for instance, and consequently there are no controls in place. The WHO report on air pollution and human health in Europe last year called for more monitoring and more information on exposure to air pollution. But it is urging governments not to wait for additional studies to be carried out. The only way to reduce human exposure to air pollution is by eliminating, or at least cutting down, emissions. /\/\/\/\/\/\/\/\/\/\/\/\/\/\/\/\/\/\/\/\ \/\/\/\/\/\/\/\/\/\/\/\/\/\/\/\/\/\/\/\/ Dr. Robert Read is a clinical research fellow at the National Heart and Lung Institute at the Royal Brompton Hospital in London. Dr Cathy Read is a medical journalist. ############################################################### # Harel Barzilai for Activists Mailing List (AML) # ################################################################ { For more info about ACTIV-L or PeaceNet's brochure send } { inquiries to harel@dartmouth.edu / mathrich@umcvmb.bitnet } To join AML, just send the 1-line message "SUB ACTIV-L " to: LISTSERV@UMCVMB.BITNET; you should receive a confirmation message within 2 days. Alternate address: LISTSERV@UMCVMB.MISSOURI.EDU Qs/problems: Rich Winkel, MATHRICH@UMCVMB.["MISSOURI.EDU" or "BITNET"]