THE HUMAN COST

Jamie Radford was ten days old when his coughing and vomiting became so bad that his mother Jan realised she would have to take him to hospital. When she described his symptoms to the hospital staff she was told it was "projectile vomiting". They did a test feed, found nothing wrong and sent mother and baby home. But Jamie's condition got worse. Jan took him to one of her local General Practitioners. He said Jamie was suffering from a viral cough. At home his condition remained constant. A neighbour brought them back to the hospital where they stayed an hour and were sent home, again. "He was given ephedrine nosedrops - which if I had known then what I know now I would have stopped. He couldn't sleep. Cried a lot. The health people all said it was a viral cough or a viral throat. Everything was a bloody virus. It didn't matter if the catarrh was green, yellow or clear, it was always a virus. This went on for months. Then one day I was waiting for a taxi from the hospital when the registrar asked me to tell him more about Jamie, so I told him about his symptoms and he said he had classic asthma."

Janet Williams was born in Wrexham in the mid-sixties. Her family had ties with Cefn Mawr, an industrial village at the northern edge of the Vale of Llangollen a few miles from Wrexham in north Wales, so the thought of moving there after college to take up a job in the Ty Mawr country partk didn't daunt her. Content in the job she moved in with her grandfather Harold Pennington who lived in the oldest house in Cefn Mawr (pronounced Kevin Mao) - a two-up, two-down artisan's cottage first found on the 1611 deeds for the original Ty Mawr country park - and was soon after joined by Andy Radford, whom she had met during a course at the Peak National Park. Pregnant with Jamie she left the job and with Andy building an organic garden on the land which sloped away from their cottage towards Monsanto's chemical works (now Flexsys) in the centre of Cefn they settled down to parenthood. Jamie was born on April 21, 1992; a few days later their nightmare began.

Jamie was six months old before he was diagnosed as an asthmatic. During this time Jan had only thought about Jamie, hadn't considered what might have caused his asthma or whether any other mothers in Cefn might have had the same problems. "All this is happening to him while I'm realising that everytime I was in hospital there was one or two mothers and their children from Cefn. A nurse would say that place must be terrible. Nearly all the kids have something, eczema, asthma, hyperactivity, tiredness, constant virus infections like ear infections."

Without any presumptions or preconceptions about their child's illness, Jan and Andy decided to investigate health incidents in Cefn, especially among mothers and children. They founded a group, Communities Appeal for Respect for the Environment (CARE), and started a lobbying campaign, aimed at anyone who would listen to their concerns and they began to collect anecdotal evidence about ambient pollution and local health. A doctor with the Community Health Council said she was interested in doing a health survey. It never happened. "There's never been a health survey done so we don't know the extent of the illnesses here, yet we know that a lot of people have children with asthma and respiratory illnesses. When we started CARE, people wouldn't speak to me. Now they do. People are complaining more now. They have more confidence and know they don't have to put up with the chemical emissions all the time." What worries Jan and Andy and all those people who now believe there is a reason for their illnesses and their children's illnesses is that no one in authority appears to be interested in their concerns and fears. The local health authorities and local GPs - while acknowledging that the increase in asthma in the area has been alarming - have been reluctant to give out information on illnesses in the area. Jan's attempts to obtain health statistics have been met with bureaucratic stonewalling and empty promises.

Air pollution is caused by animals, plants, geophysical activity and humankind. Animals exhale carbon dioxide, decaying vegetation produces methane, volcanic activity vents sulfur oxides, winds carry suspended particles from natural sources and humankind as a result of its technology and materialism pumps into the atmosphere synthetic pollutants. These are known as sulfates, particulates, carbon monoxide, nitrogen oxides, oxidants (such as ozone), polycyclic aromatic hydrocarbons (such as dioxins and furans), volatile organic compounds (such as benzene, formaldehyde and vinyl chloride) and various other chemicals and minerals.

Air pollution as a result of human activity has been recognised as a problem since the 17th century when the burning of coal contributed in London to "Great Stinking Fogs". With the emergence of the industrial revolution coal burning and the smelting of mineral ores filled the skies and the lungs of the working classes with sulfates and other chemicals. Since the 1930s - particularly during heavy pollution episodes in the industrial Meuse valley in Belgium in December 1930, in the industrial town of Donora, Philadelphia, in October 1948 and in London in December 1952 - the combustion and synthesization of fossil fuels and their derivatives has been accepted as the major source of air pollution, notably sulfates and fine particles. Although scientists began to accumulate evidence associating air pollution with ill health during these and other pollution episodes, according to Lave and Seskin in their 1977 book on Air Pollution and Human Health, "the scientific community has been slow to accept this evidence ... because of the methods used to gather it and the lack of studies using controls". This search for what US research scientist Peter Montague calls the holy grail of scientific certainty has negated the anedotal evidence of cause and effect from air pollution, significantly particulate pollution. Now with improved technology (which allows scientists to measure the size of particles - to determine whether they are respirable), a clearer understanding of the biological mechanisms (the effect on the human system) and the declared need to conduct extensive epidemiological and toxicological studies the impact of air pollution on human health is becoming harder to ignore.

"All of our environmental actions have consequences," biologist Michael Zimmerman exclaimed in 1995, "some very far removed either temporally or spatially from their original locus. We ignore those consequences at great risk to ourselves, our children, and the biotic community of which we are a part". But that is exactly what the majority of us are being asked to do, by ignorant, nervous politicians, dutiful, ambitious bureaucrats, greedy, apathetic industrialists and colluding, insular scientists. We are being asked to ignore those consequences by people who simply don't know or want to know exactly what those consequences are and when someone from a community or environmental group points out to them what those consequences might be they - the politicians, bureaucrats, industrialists and scientists - summarily dismiss the evidence. Why? Because community and environmental activists do not have the scientific background or social knowledge to make informed decisions. Is that so? Listen to what English toxicologist Alistair Hay has to say about community activity particularly on pollution and health issues: "Communities need to get involved. The other important thing that people need to remember is that they probably know as much or maybe even more than some of the experts drafted in to view certain things. I know I get called into certain things... someone asks me about somethign they've been researching for a long time and they've put a lot of stuff together and quite often they know far more about it than I do, yet people will defer to me because I've done toxicology or something else."

So far the debate about particulate pollution has been isolated to sporadic research and activity from various groups, campaigns and individual scientists. It has been an issue among toxic campaigners for many years, one that was ignored until British road campaigners began to highlight the appalling pollution from cars and trucks on Britain's motorways. It has been an issue among community health workers because of the association between particulate pollution and respiratory illness, significantly asthma. It has been prominent in recent years in the work of several British scientists, so much that even the British government has begun to take the issue seriously, to the extent that its working groups have not only called for more research but managed to get the levels of particulate pollution in the ambient atmosphere reduced.

Simply, if you live in an urbanised area, near an industrial complex, a motorway or a combination of all three the air that you breath daily will contain fine particles visible to the eye only as smoke, dust, soot or as a gas. They are not visible except as a general haze. They are far too small to be seen. They are not captured efficiently by modern pollution-control equipment. They are deadly! Douglas Dockery and Arden C. Pope note that "sulfate and nitrate aerosols generally make up the largest fraction of small particles by mass". The term "aerosols" refers, according to Dockery and Pope, to "a stable mixture of suspended particles and gases and therefore implies smaller-sized particles".

It was the US Environmental Protection Agency which started measuring particulate pollution, in 1987, describing it as PM10, particulate matter 10 micrometers or less in diameter. A micrometer is a millionth of a metre and a metre is about a yard. The dot above the letter i in a newspaper measures about 400 micrometers in diameter. PM10 is measured by weight so the recently announced British Government levels of 50 micrograms measured as a 24-hour running average mean the total weight of particles with a diameter of 10 micrometers or less in each cubic metre of air (ug/m3). One ug/m3 is one millionth of a gram in every cubic metre of air. A gram is 1/28th of an ounce and a microgram is a millionth of a gram. Therefore it is the size, shape and density of the particle that determines how long it remains suspended in the atmosphere and what happens to it if it is inhaled. "Biological effects of a particle," state Dockery and Pope, "are determined by the physical and chemical nature of the particle itself (particularly its solubility), the physics of deposition and distribution in the respiratory tract, and the physiologic events that occur in response to the particle's presence."

According to British scientist Dr Anthony Seaton and colleagues "very small particles, below about 1 micrometer in diameter, may remain suspended for weeks, whereas those greater than 2.5 micrometers in diameter are removed by settling and by rain in a matter of hours. A cloud of the finest particles will thus drift for many miles and may cause pollution across national boundaries". In a 24 hour period an adult breathes approximately 20 cubic metres or 20,000 litres of air. In a modern city, on many days, the air will contain 100 billion one-nanometer-diameter particles in each cubic meter of air, all of them invisible. By weight, these 100 billion particles will only amount to 0.00005 micrograms (one ten-thousandth of 1 percent of the 50-microgram legal limit), yet they may be responsible for much of the health damage created by particulate pollution. For this reason, in 1979, the US National Research Council said that measuring particles by weight, without regard to particle size, has "little utility for judging effects."

Larger particles get caught in the nose and throat where they are removed by coughing, spitting or swallowing. Those particles which escape this natural filtering process get as far as the airways of the upper lung where they settle on the inner walls. The smallest particles however are carried into the air spaces known as the alveoli in the deep lung where gas exchange occurs between the air and blood stream, oxygen moving in and carbon dioxide moving out. Scientists estimate that between 50% and 60% of the smallest particles, below 0.1 micrometer in diameter, are deposited in the alveoli. If they are not soluble in water, they are retained in the deep lung for long periods (months or years). Because of their origin in combustion processes, most fine particles are coated with toxic materials - metals like lead and mercury, or toxic organics like polycyclic aromatic hydrocarbons (dioxins, for example) - so fine particles provide a uniquely efficient carrier, giving dangerous toxins direct entry into the blood stream. The toxicity of urban particles and urban particulate emissions, Hatch et al note, "depend in part on the type of metal compounds they contain, as well as their combustion-derived organic content".

To understand the biological mechanisms involved it is necessary to know how the lung functions, how it deals with pollutants and what happens when those pollutants penetrate the body's natural defences. The primary function of the lung is for gas exchange, to allow oxygen to move from the air into the blood stream and carbon dioxide to move out. The lung also metabolizes some compounds, filters toxic materials from the circulation and acts as a reservoir for blood but it is the gas exchange at the blood-gas interface in the deep lung that is significant when dealing with fine particles. Gas is brought to one side of the blood-gas interface by airways and blood to the other side by blood vessles. The lung is characterised by airways, which consist of branching tubes, and blood vessels, which encapsulate small air sacs called alveoli. There are about 300 million alveoli in the human lung. The alveolated region of the lung where the gas exchange occurs is known as the respiratory zone. This zone makes up most of the lung, consisting of airways and airspaces. Diffusion of gas molecules within the airways takes less than a second of the time we take to breath in and breath out. Inhaled particles or pollutants which are not trapped by the nose and throat, for subsequent excretion, are deposited in the alevoli where they are mostly engulfed by large wandering cells called macrophages.

However this protective mechanism is not wholly reliable and Seaton and colleagues have suggested that the particles which reach the alveoli provoke inflammation, thus causing lung damage, and release natural chemicals into the bloodstream, causing coagulation of the blood. This, they hypothesise, can lead, in susceptible individuals, to acute respiratory illness and exacerbations of lung and heart-related diseases . For many decades researchers have believed that fine particles cause ill health and death without being able to show why. It is significant however that 16 years before Seaton and colleagues reached their conclusions the US National Academy of Science in 1979 noted that "...alveolar retention of relatively insoluble particles is recognized to be important to the pathogenesis of chronic lung disease...". In summary the Academy said: "Particulate atmospheric pollutants may be involved in the pathogenesis of chronic lung disease; as causal factors in chronic bronchitis, as predisposing factors to acute bacterial and viral bronchitis, especially in children and cigarette smokers, and as aggravating factors for acute bronchial asthma and the terminal stages of respiratory failure associated with chronic bronchitis and emphysema and its consequent form of heart failure (cor pulmonale)."

What is both revealing and disturbing about the continuing research into air pollution and acute ill-heath is not what we know, it's what we still don't know. We know that the nose is extremely efficent at removing the larger particles; in fact our respiratory defences have evolved over millennia to protect us against particles which occur naturally from forest fires, volcanic eruptions, the natural erosion of soil and rocks, and the rising of pollen and fungal spores. Almost all particles greater than 20 micrometers in diameter and about 95% of particles 5 micrometers in diameter are filtered by the nose during resting breathing. This means they are trapped on the mucous surface of the nose and throat, where they are excreted by means of coughing, spitting or swallowing. This is known in medical jargon as impaction. Seaton and colleagues postulate that almost all particles larger than 7 micrometers in diameter are deposited in the nose and throat, and only about 20-30% of particles between 1 and 7 micrometers in diameter are deposited in the lung's air spaces. Taking account of research by the Department of Environmental Health at the University of Birmingham, Seaton and colleagues calculated "that during a pollution episode each lung acinus could receive on average some 30 million particles and each alveolus about 1500 particles every 24 hours, about 50% being deposited". Particles between 1 and 5 micrometers in diameter reach the small airways in the upper lung but travel no further because they are not tiny or light enough and there is not enough velocity to diffuse them, like the gas, into the alveoli. Instead they settle in the small airways (the terminal and respiratory bronchioles). This is known as sedimentation. In a coal miner's lung this is the area of heavy dust concentration which can lead to disease and respiratory failure depending on the amount of dust deposited. The particles that avoid impaction and sedimentation are less than 0.1 micrometer in diameter. Because of their size they penetrate the alevoli carried there with the gas molecules. Many inhaled particles are exhaled with the next breath. "In fact only some 30% of 0.5 micrometers particles may be left in the lung during normal resting breathing." Those particles left in the alveoli are swallowed by macrophages which either migrate to the small airways to be gathered up as mucous or leave the lung in the lymphatic system or via the bloodstream.

It is Seaton and colleagues' contention that the failure of alveolar macrophages to deal with toxic particles is the cause of the inflammation in the alveoli. "That transport of chemicals on the surface of particles may be important in the cause of lung inflammation has been shown in recent studies in which iron complexed on the surface of fly-ash particles promoted oxidative lung injury, and this effect was reduced after removal of surface iron by washing".

Reviews of the epidemological evidence suggest that particulate pollution is causing or exacerbating a wide range of human health problems, including initiating and worsening asthma, especially in children; increasing hospital admissions for bronchitis, asthma, and other respiratory diseases; increasing emergency room visits for respiratory diseases; reducing lung function (though modestly) in healthy people as well as (more seriously) in those with chronic diseases; increasing upper respiratory symptoms (runny or stuffy nose; sinusitis; sore throat; wet cough; head colds; hay fever; and burning or red eyes); and increasing lower respiratory symptoms (wheezing; dry cough; phlegm; shortness of breath; and chest discomfort or pain); and heart disease. It appears also that there is no safe threshold, no level of particulate pollution below which deaths do not occur. Joel Schwartz, formerly of the US Environmental Protection Agency (EPA) and now with the Harvard School of Public Health - reviewing data on air pollution and deaths from London between 1958 and 1972, showed there was no threshold down to the lowest observed levels of air pollution.

Researchers in the US have estimated that emissions from combustion sources are the cause of 10,000 deaths a year in Britain and 60,000 in the USA. All combustion sources - oil and coal burning power plants, oil refineries, cars, lorries, buses, incinerators, industrial and residential heaters and burners, furnaces, smelters - are implicated in the death toll. Diesel vehicles and power plants have been identified as the worst offenders and it appears from the evidence that they are. In 1975 retired British GP Dick van Steenis called for the tightening of controls on particulate pollution after surveys showed that children living downwind of orimulsion and oil-burning power plants and oil refineries had high levels of asthma. He recommended that the power companies should install gasification processes to burn the fuel "since the particulate and oxides of nitrogen emissions are otherwise very high with those fuels". Researchers in various American and European countries have observed daily concentrations of PM10 leading Dockery and Pope to conclude: "In summary, a series of time-series analyses of the associations of daily mortality with particulate air pollution has shown a ~1.0% increase in total deaths/day associated with each 10 micrograms per cubic meter increase in PM10 concentration. Stronger associations were observed with cardiovascular disease (1.4% per 10 micrograms per cubic meter PM10) and respiratory disease (3.4% per 10 micrograms per cubic meter PM10)."

This is significant because in cities like London, Birmingham, Manchester, London, Glasgow, Belfast and Dublin the daily concentrations of PM10 average over 50 micrograms per cubic meter and may go as high as 150 or more micrograms per cubic meter. This would lead to acute exposures. Dockery and Pope note that the consistency of the above estimates across communities suggests that "the mass concentration of the particle mix common to many urban areas, rather than specific chemical species within the mix, may be responsible for the observed associations". They stress that the results are not due to any confusion with "an unknown or uncontrolled factor". A study of six U.S. cities, including several that are not heavily polluted, such as Portage, Wisconsin and Topeka, Kansas, showed death rates increasing with just 15 micrograms per cubic meter of PM10 pollutants. In all, at least 8 studies have now shown that PM10 at any level kills people. A study of people in Steubenville, Ohio, showed that each increase of 100 micrograms per cubic meter of total suspended particles (of which PM10 represents about half) is associated with a 4% increase in the death rate, with no threshold. Interestingly, the Steubenville study showed that the death rate changes as fine particle levels change, but not as sulphur dioxide levels change. In Philadelphia, a close relationship between PM10 pollutants and the death rate was observed. Once again sulfur dioxide levels did not correlate with the death rate, but particle concentrations did. Here each increase of 100 micrograms per cubic meter of total suspended particles (of which PM10 makes up half) was associated with a 7% increase in the death rate. The only EPA employee ever given a "genius award" by the MacArthur Foundation, Schwartz's analysis of data from London's 1952 killer smog showed that the death rate increased 6.4% for each increase of 100 micrograms per cubic meter total suspended particles, or about 13% for each 100 micrograms per cubic meter increase in PM10 pollutants.

The study of fine particles and their effects on human health has been taken seriously since 1967. During the past 30 years, studies have been able to rule out sulphur dioxide and ozone pollution as the cause of the observed deaths though sulphur dioxide and ozone have been implicated in rising asthma levels, particularly among children. Last year (1995) a new study of 552,138 adult Americans in 151 metropolitan areas confirmed once again that there is a clear relationship between particulate air pollution and human deaths, and it ruled out smoking as a cause of the observed deaths. This study is particularly important because it didn't simply match death certificates with pollution levels; it actually examined the characteristics (race, gender, weight and height) and lifestyle habits of all 552,138 people. Thus the study was able to rule out tobacco smoking (cigarettes, pipe and cigar); exposure to passive tobacco smoke; occupational exposure to fine particles; body mass index (relating a person's weight and height); and alcohol use. The new study also controlled for changes in outdoor temperature. The study found that particulate pollution was related to a 15% to 17% difference in death rates between the least polluted cities and the most-polluted cities.

"Why can't we act to prevent this important problem?" asks Peter Montague. "Because regulatory authorities and the courts have lost their way, they are busy searching for the holy grail of scientific certainty. Regulators and judges now insist that science (and the public) has to "prove harm" before regulatory control can begin. Philosophers of science know that science cannot "prove" anything. It often takes science decades - sometimes centuries - to reach a clear majority opinion and there will always be uncertainties, giving rise to nagging doubts, which can only be laid to rest by further study. The precise mechanism of harm is not fully understood, even today, but the harm itself has been clear beyond any reasonable doubt for many years. Common sense says that the National Academy's conclusions back in 1979 should have been sufficient for regulators to clamp down in earnest."

Perhaps if someone had clamped down, many of the nine million people in England, Scotland, Wales and the six northern counties of Ireland who suffered from breathing problems in 1994 might have been spared. The National Asthma Campaign has for many years compiled data to determine the extent of respiratory illness. Using the latest available data on the prevalence, cost and impact of what they describe as "one of the most common chronic treatable conditions in the western world" the NAC's most recent annual audit reveals that over three million people in England, Scotland, Wales and the north of Ireland have asthma. Children under 18 make up 1.3 million of this figure. From the latest figures available the NAC say that 1,877 people died from asthma in 1993. (England and Wales: 1699; Scotland: 120; north of Ireland: 58.) Current research indicates that the number of children with diagnosed asthma has doubled since the 1970s. In 1994 the direct NHS costs of treating asthma in England alone was £450 million of which £381 million was on prescriptions for asthma (up 20% on the previous two years). The number of prescriptions for asthma has increased by three-quarters in the last decade. The NAC estimate that the total cost of asthma in England, Scotland, Wales and the north of Ireland is in excess of £1 billion. Hospital admissions as the result of asthma attacks has also increased up 7% from 1992 to 1993 when 104,282 people in England and Scotland were admitted. Approximately 50% of the admissions were children under 15. On average 155 children are admitted to hospital every day in Britain because of asthma. According to the General Household Survey asthma is the most frequently reported cause of long-standing illness among children. One survey of over 60,000 people with asthma showed that the illness restricted the daily activities of 76% and that 54% were woken by asthma symptoms at least once a week. On August 24 the NAC launched what it called Britain's first pollution poster at a site in London. The NAC said the poster had been designed to show how bad the air quality is in London. Using a water-based glue the NAC painted the words 'THIS POSTER HAS BEEN UP FOR JUST TWO WEEKS. IMAGINE WHAT YOUR LUNGS MUST BE LIKE'. Gradually over a two week period the glue collected dirt, dust and airbourne particles to reveal the message.

Our concern of course should also be of our children. In their study on the effects of inhalable particles on respiratory health of children, Dockery and colleagues noted that "children with a history of wheeze or asthma had a much higher prevalence of respiratory symptoms" and the data from one particularly significant study provided, they stressed, "further evidence that rates of respiratory illnesses and symptoms are elevated among children living in cities with high particulate pollution". In their review of epidemiological evidence of health effects of particulate air pollution, Pope, Dockery and Schwartz "observed associations between particulate air pollution and various human health endpoints, including incidence and duration of respiratory symptoms, lung function, restricted activity, hospitalisation for respiratory disease and mortality". They added, "because of the public health relevance of these findings, there has been considerable interest about potential biological mechanisms, constituents of particle pollution, potential interactions with other pollutants and risk factors, sources of these air pollutants, and how these findings can be incorporated into public policy." This is now a matter of urgency.

"After the infamous air pollution episode in December 1952 in London, it was public concern rather than pressure from the medical profession which led to the first clean air legislation in Britain. That pattern may be about to be repeated," David Bates wrote in the British Medicial Journal in March 1996. This is an important point because all of the recent reports from the working groups studying air pollution and health for the British government - just to use Britain as an example - reflect what is a typically cautious mood among western governments, influenced as they are by industrialists. Communities and individuals affected by air pollution can take some comfort from the conclusions of the British Expert Panel on Air Quality Standards (EPAQS), chaired by Professor Seaton. They note that "even if all man-made particle generation ceased in the United Kingdom, because of the long-term persistence of the smallest particles this natural background concentration would be increased by drift from other countries, just as currently particles generated in this country will contribute to the world-wide concentration". Therefore it should be obvious that air pollution is now a global problem and that only a global strategy based on co-operation between nations rather than competition between their industries will begin to solve our environmental health problems.

By dismissing the anecdotal evidence of communities exposed to low level pollution, health authorities, GPs and medical institutions are abrogating their responsibility to public health, content instead to allow industry and the state to dictate health standards which do not reflect the reality of peoples' lives or even contemporary scientific knowledge. Evidence of pollution allows industry to argue that their processes are not to blame for illnesses among industrialised communities. It is now becoming obvious that acute exposures to the chemical mix in the air can trigger diverse reactions in chemically sensitive individuals and occasionally lead to sensitivity in otherwise healthy people. Chemicals are regarded as relatively harmless if clinical damage cannot be detected. According to those prepared to accept that there is a real problem, animal models, clinicopathological studies and epidemiological investigations are regarded as not sensitive enough to detect the effects of low level exposures to pollutants. Animal models are used to study the effects of high doses of chemicals but as Nicholas Ashford and Claudia Miller note in their book 'Chemical Exposures: Low Levels and High Stakes' "rats, mice and other animals are unable to tell researchers if they have headaches, fell depressed or anxious or are nauseated"; they conclude, "thus, the subtle effects of low level chemical exposure may be missed completely". Epidemiological studies point to associations between events, but as multiple chemical sensitivity is the consequence of multiple triggers resulting in multiple health effects, according to Ashford and Miller, "epidemiology may be an insenstive tool". And clinicopathological studies, because they rely on the presence of a clinical sign, laboratory measurement or tissue pathology, are, add Ashford and Miller, "not likely to be sensitive to the early effects of low level exposures, that is prior to end-organ damage". It seems to matter little to polluted communities that inflammation of the airways is one of the first indicators of toxic pollution and that chemical sensitivity can be the consequence of this exposure.

We have concentrated here on particulate pollution because the evidence appears to suggest that the concentration of particles in the global atmosphere is high enough to constitute a serious health risk in all populations. As noted at the beginning air pollution is also characterised by other chemicals, notably dioxins and furans, ozone, benzene, carbon monoxide, sulphur dioxide among others. This is not the place however to discuss in detail the health impacts of all these chemicals and environmental pollutants. The US Environmental Protection Agency recently devoted 2,400 pages to a draft report on dioxins alone and then called for more research. Of all the atmospheric pollutants dioxin is arguably the most deadly because it finds its way easily into the food chain and therefore into our bodies. Apart from its cancer-causing effects dioxin has also been implicated in the debate about falling sperm counts because of its ability, along with other chemicals, to effect hormonal activity. Ozone at high concentrations has been seen to damage the lung although some scientists argue that levels (in Britain, for some reason) are insufficient to cause long term damage to the respiratory system. In north America the effects of ozone appear to be more serious. Long term exposure to benzene can cause leukaemia, particularly the types known collectively as non-lymphocytic leukaemias. Ambient atmospheric levels of benzene are not regarded by scientists as serious enough to threaten health because the toxic effects are not sustained. Vinyl chloride and carbon monoxide have been associated with damage to the brain. Sulphur dioxide has been implicated in heavy air pollution episodes which have reduced life expectancy among susceptible individuals living in urban areas. Simply, air pollution is contributing directly or indirectly to a range of illnesses from respiratory disease beginning with asthma to heart, lung and brain disease depending on the vulnerability of the individual to reproductive disorders and dyfunction. And finally death.

Finally there is the economic cost. As long ago as 1970 in an article in Science magazine Lave and Seskin estimated that 4.5 percent of all economic costs associated with morbidity and mortality would be saved by a 50 percent reduction in air pollution in major urban areas. More pertinently they stressed that 1 in 4 morbidity and morality cases "due to respiratory disease could be saved by a 50 percent abatement in air pollution levels".

- Robert Allen

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