Atmospheric pollution, illness and the sun

The atmosphere, pollution, health, and the sun

There is currently a great deal of concern about atmospheric pollution, which is said to be killing thousands, if not millions. But of course atmospheric pollution is not a recognised cause of death, and a specific disease must be the true cause of death, with atmospheric pollution being an initiating or an accelerating factor.

Industrial townscape, LS Lowry

Urban and rural deaths

The industrial revolution in the UK and several other countries of Europe commenced in a major way during the 18th century. It was based on the energy released by the burning of coal, and it created a huge amount of atmospheric pollution. The population of the new industrial towns experienced a serious health and survival disadvantage compared to people who remained living in surrounding rural villages.This was shown in a study of Manchester and Liverpool, undertaken by a Manchester physician Thomas Percival (1740–1804). His monograph, “Observations on the population of Manchester and other adjacent places” was published in 1773.

Thomas Percival 1740–1804

Whereas today we would report the number of deaths per 100,000 of the population, in 1773 Percival reported that 1 in 28 of the population of Manchester died each year, and this was similar to the experience of Liverpool, just 50km distant. The population of Manchester was 27,246 at the time. A death rate of 1 in 28 is equivalent to 3571 per 100,000, extremely high compared to present times.

In contrast, the death rate in the surrounding villages was half this, at 1 in 56 of the population. This is equivalent to 1786 per 100,000, again very high compared to  present years (about 900 per 100,000 per year).

The obvious difference between industrial cities and rural villages is atmospheric pollution. The observation of 1773 remained the same two centuries later.

Rickets

What became obvious in the new industrial cities was the emergence of rickets in children, a result of serious atmospheric pollution blocking the vital benefit of sunlight. The experience in Glasgow was that if the sick children were moved to the coastal fishing villages (from which the families originated), then the rickets would heal and the children’s health would improve.  In Austria, there was also an emergence of rickets in the new industrial cities, with improvement following movement to the mountain villages.

+ tuberculosis

There was an obvious link between rickets (the direct result of lack of vitamin D from sunlight) and tuberculosis. Glasgow, a major industrial city, became the rickets, and then the tuberculosis, capital of the world. The link was also obvious in Austria: it gave rise to the Heidi story in which the sick girl (presumably with tuberculosis) was taken from the city to the clean air of the mountains  and there was restored to good health.

Although atmospheric pollution was a serious health problem for children and adults, a compounding factor was long hours of indoor work. A Manchester surgeon Thomas Bellot stated that it was not uncommon for factory children "to be checked in their growth, to become lame and deformed in their legs...and eventually to die of consumption" as a result of "their long confinement in heated and unventilated rooms, and of their being constantly on their legs during their long hours of labour. [quoted from Peterloo: the Story of the Manchester Massacre, by Jacqueline Riding]

1952–56

The atmospheric pollution of the early industrial cities caused serious problems up to the mid-20th century, especially in the UK. The winter smogs of London reached a peak in 1952 that lead to the UK Government Clean Air Act in 1956. Following this there was a remarkable improvement in air quality. 

Stalybridge, Manchester 1950

The burning of coal was the major problem, and much of this was for domestic heating. Also, electricity was generated by many small coal-fired power stations that operated very inefficiently. Gas was produced by heating coal. Factories were powered by coal-fired steam engines, and railway steam locomotives were powered by coal. Coal was King, and it underpinned the industrial revolution.

Oil

During the 19th century whales were the main source of oil, to be used mainly for lighting. Fossil oil was discovered and came into production at the turn of the century, just in time to prevent the total extinction of whales. It was after the second world war that oil came to be used in place of coal, for domestic heating, electricity production, and diesel locomotives. Natural gas came to replace coal gas and we developed an oil-based economy. This happened at just the right time to enable the effectiveness of the Clean Air Act.

River Thames, London. 1950

The cleaning of the atmosphere of the UK during the second half of the 20th century was remarkable. The diminishing use of coal led to a reduction of  particles of unburned carbon and also a reduction of oxides of the sulphur contaminants of coal. This was helped by the improved and more complete combustion of coal in fewer and larger power stations with much taller chimneys. 

But invisible pollutants continue, mainly carbon dioxide, and as this is heavier than nitrogen and oxygen, much of it it stays in the lower atmosphere. To this is added pollutants from the engines of road traffic vehicles. Diesel engines give more particulate pollutants than petrol engines as the diesel fuel is mush less refined. The growth of road transport has led to a resurgence of atmospheric pollution in our cities. It is the particles of unburned carbon that are responsible for the blockage of sunlight penetration. 

Electricity

The imperative is to progress from an oil-based economy to electricity, which to be used by transport and domestic heating in particular. Coal, oil and gas must not be used for electricity production, and must be replaced by renewable natural energy sources (gravity, wind, sun) together with nuclear power.

Health effects of atmospheric pollution

Although it is generally considered that atmospheric pollution does not kill directly and it is not a recordable cause of death, this has been subject to a legal challenge in the Uk in January 2019. A girl living close to major road in south London died from "asthma". Her mother is seeking a legal change to record the cause of death as "Atmospheric pollution". 

However there will always be an intermediary disease, in which pollution is a driving factor or an accelerating factor. It is necessary to recognise ways in which atmospheric pollution might damage human health.

There are two major possibilities: pollutants that when inhaled might be toxic, and atmospheric pollution blocking sunlight. Another less important possibility is road traffic accidents due to poor visibility.

China – no visible sun on a "clear" day in Beijing

The nature of atmospheric pollutants

The atmosphere provides the oxygen that is necessary for essential metabolic activities of animal life. Oxygen is put into the atmosphere by the photosynthesis of plants. Oxygen is highly reactive and it readily combines with other atoms to produce oxides, for example carbon dioxide, sulphates, iron oxides. It was only after the evolution of plant life (containing chloroplasts, initially free-living entities)  that oxygen was released into the atmosphere, allowing the evolution of animal life. This was the era of the great oxygenation event, nearly three billion years ago.

Burning carbon fuels inevitably results in the release of carbon dioxide (CO₂) into the atmosphere. If carbon is partially oxidised, carbon monoxide (CO) will be released. 

If the combustion of carbon is inefficient, then non-combusted particles of carbon will be released into the atmosphere. Particulate matter is divided into PM-10 (10 micrometers or less) and PM-2.5 (2.5 micrometers or less).

Nitrogen-containing contaminants will be oxidised to nitric oxide (NO), nitrous oxide (N₂O) or nitrogen dioxide (NO₂). Sulphur-containing contaminants will be oxidised to sulphur dioxide (SO₂). These oxides form acids when they dissolve in water.

All these oxides are heavier than oxygen and nitrogen, and they will remain within about 100 metres of ground level. They can be dispersed by strong winds and rain.

Chronic respiratory disease

Our European neighbours referred to Chronic Bronchitis as the “English Disease” (the English referred to syphilis as the “French Disease”). Chronic bronchitis was a common disease in the UK during most of the 20th century, and was characterised by a productive winter cough usually with but sometimes without wheezing. It was often fatal after years or decades of ill-health and respiratory disability. Cigarette smoking obviously added to inhaled smoke pollutants. 

Chronic bronchitis is a clinical term that is used little 

today: it has been replaced by the term Chronic Obstructive Pulmonary Disease (COPD) which puts more emphasis on the obstruction of small airways rather than the production of sputum.

Chronic bronchitis was linked to and caused by inhalation of atmospheric pollutants and cigarette smoke, and its incidence has fallen during the second half of the 20th century. During this time we have experienced a major reduction of atmospheric pollution and also a major reduction of cigarette smoking.

Tuberculosis and the sun

Tuberculosis, with its old name of “consumption” is primarily a lung disease, although it can affect any part of the body from the skin to the brain, heart, and bones. Its close relationship to atmospheric pollution and rickets indicates that reduction of sunlight penetration to ground level is the important common factor. Reduction of vitamin D synthesis damages not just bone development but also immunity. In more recent years AIDS has resulted in an increased risk of tuberculosis in the sufferers.

In the 1950s India also experienced a strong association between rickets and tuberculosis, and once again the common factor was deficiency of sunlight. However, whereas in the UK it was mainly the poor who were affected, in India it was the wealthy. In India poor people worked the fields, while the wealthy people stayed indoors – out of the sun.

Other diseases linked to pollution.

Glasgow became the rickets capital of the world, and then the tuberculosis capital. It was also renowned for the dreadful state of dentition of its inhabitants. It became the lung cancer capital, and during the latter half of the 20th century it became the coronary heart disease capital.

A particular high incidence of deaths from coronary heart disease (CHD) during the 20th century epidemic was in places and people with high levels of atmospheric pollution, cloud cover, and geographical reasons for low sunlight penetration. The populations of places with reduced levels of sunlight penetration have had more CHD deaths as well as an average shorter life expectancy. Also a number of cancers are more common where there is low sunlight penetration.

The mechanism behind this is that vitamin D has an important role in developing important immunological defence mechanisms. These are very important in controlling and preventing the development of CHD and many cancers. 

The UK today

Although there is understandable concern about atmospheric pollution in our cities, mainly the result of diesel vehicles, the pollution levels are nowhere near what they were in the 1950s and before. There is also concern about carbon dioxide production and resultant global warming, but that is something different.

River Thames, London.  2018

Despite present-day pollution the health of the UK population is better than ever and we are living longer than ever. More and more people pass their 90th birthday. There are dire warnings about the future, and in particular that atmospheric pollution will cause thousands of deaths, but deaths from what? A recent statement from the Royal College of Paediatricians indicated that atmospheric pollution in damp winter weather will cause respiratory problems in children, but these are acute infections and nothing that will shorten lives.

The state of the atmosphere depends not just on the production of pollutants but also on their removal by wind and rain, and there is generally no shortage of these in the weather of the UK. On recent visits to London I have been impressed by the brightness of the late afternoon winter sun, but nevertheless when seen from just a modest elevation there is a dark layer of polluted air at ground level. 

London, looking north from Greenwich. Dark polluted air close to the ground is visible

Linz, Austria, looking south across the city from Pöstlingberg, with dark polluted air visible

The far East today

What we experience in London UK, or Linz in Austria, fades into insignificance when we see the amount of atmospheric pollution in, for example, Beijing or Delhi. The pollution levels result in the sun being almost invisible, and penetration through particulates is very much less than through all but the thickest water-containing clouds. 

Of course there is little cloud in these arid cities; there is little rain and very little wind. Face-masks to prevent inhalation of polluted air might be of some benefit, but the major problem must be serious obstruction to sunlight penetration and therefore the impairment of  vitamin D synthesis in the skin.

The effects of blockage of the sun with consequent vitamin D synthesis will not be immediately obvious. As in Glasgow and other European industrial cities more than a century ago, we can anticipate serious health problems in the children who are not yet born. When they are born they are likely to be deficient in vitamin D and likely to develop rickets. Poor immunocompetence is likely to result in more tuberculosis or other infections and illnesses prevalent at the time.

Despite the history of atmospheric pollution in European cities, the importance of blockage of sunlight does not appear to be appreciated by those with responsibilities for public health at present.

Xian, China, 2000. A "bright sunny day". The mountains are no longer visible.

Changes of life expectancy

Hodder Valley, Lancashire, UK.

In a recent Post I indicated that the maximum life-span of a human being is about 105 years, a life longer than this being very exceptional. However a shorter life-span is common due to individuals encountering premature life-ending events such as major injury or disease. If these are not encountered, then life will ultimately come to an end because of “old age”. Death from old age is the result of frailty or a lack of physiological reserve, effectively a combination of mitochondrial failure and an exhaustion of stem cells.

Average life expectancy has been increasing in past decades during which more and more people have been approaching the maximum life expectancy, but most have not quite got there. We can see for example a steady increase in the UK of people living beyond their 90th birthday. This is no sign yet of this slowing down. 

Figure 1. 90 year olds in the UK

Up to about 1870, average life expectancy in Europe and America was about 40 years, and this was due to a large number of deaths in childhood. One of my great grandfathers, Richard Alston (who I never met), was the youngest of twelve children born on a farm in the Hodder Valley, very close to where I live now (I can see the farm-house from my bedroom window). Of the twelve children, only four survived to be adults. Richard moved to Manchester, where he married and had ten children, just four surviving to be adults. 

Such stories were usual but nevertheless tragic. In 1840 in the UK, average life expectancy from birth was only about 42 years. But if a child managed to survive to the age of 10 in 1840, then the average life expectancy would be about 57 years. This is shown in Figure 2.

Figure 2. Life expectancy by age

We can see in Figure 2 increases in life expectancy within the 20th century, especially life expectancy from birth. The major improvement predated the antibiotic era, which started after 1945. It would almost certainly be the result of civil engineering changes, new housing with wider streets, sanitation and waste disposal, piped clean water, more food, domestic heating with delivered coal, improved schooling. This has been a world-wide phenomenon, as shown in Figure 3.

Figure 3. Changing life expectancy throughout the world

There would not have been many 70 year olds in 1840 (born 1770) and their life expectancy beyond the age of 70 was on average only about two years. The life expectancy of 70 year olds changed little during the century 1840 to 1940 (Figure 2). 

However there was an improvement seen in 1980 and thereafter. This was the first time that there was an increased life expectancy of 70 year olds, of course resulting in the great increase in those living to beyond their 90 birthday (Figure 1). This was the result of the end of the epidemic of high-mortality CHD (coronary heart disease) and a major decline of deaths from this cause.

Although many people died from CHD in middle age (or younger), most deaths occurred in people beyond the age of 70 years. It is therefore this age-group that has seen an unprecedented increase in life expectancy.

As well as major improvements in infant mortality rates in industrialised countries worldwide, the latter half of the 20th century also saw a dramatic worldwide reduction of maternal deaths. In the 21st century this has also happened in the non-industrial world, for example Ethiopia. This is shown in Figure 4.

Figure 4. Changing maternal mortality.

Since 1980 there has been a steady increase in life expectancy , and this is shown in the countries making up the UK. This is seen in males and females, as in Figures 5 and 6.

Figure 5. Life expectancy in UK nations (Males)

Figure 6. Life expectancy in UK nations (Females)

This dramatic recent improvement in life expectancy has been mainly the result of the end of the epidemic of CHD. The improvement could not be expected to continue indefinitely, and there has been a levelling-off of the decrease during the past couple of years. This is expected and a new steady state is inevitable. But there appears to be a  marginal decrease in life expectancy in Scotland and perhaps Northern Ireland in 2017. 

This is a cause for concern and it requires explanation. It is obviously the result of premature deaths, that is below the 2010 average life expectancy of 81 years.  It is not clear which diseases have been responsible for this. 

There is one disturbing fact: There has been an increase in lung cancer deaths among people who have never smoked, and 80% of these are women, often quite young. Deaths from lung cancer in women who have never smoked now exceed deaths from breast cancer and ovarian cancer combined. The reason for this is unknown.

If we look back at Figure 3 we can see that the increase in average life expectancy in African countries was interrupted by a reduction between 1990 and 2000. This would be explained by the epidemic of AIDS related deaths occurring at that time. There does not appear to be a cause for the apparent reduction of life expectancy in Scotland and Northern Ireland, and perhaps it is just an aberration that will have disappeared at the next annual report.

The end of the epidemic of CHD (coronary heart disease) has had a major beneficial effect on average life expectancy in the UK.  If we encounter another epidemic, then the average life expectancy will obviously diminish.

Otherwise the average life expectancy should maintain a steady state. This will change if one of two things happens. First, if there is a rapid a significant reduction of deaths from another given and important cause of premature death (as has been the case with CHD deaths), then average age at death will increase. What diseases are likely to diminish? 

If on the other hand there develops a sudden increase in deaths from a specific disease, an epidemic of something new, then average age at death will diminish.

It is unlikely that deaths from “all causes” will either diminish or increase to any significant degree. It is the change in the death rates from specific diseases that are much more likely to be significant.

Hodder Valley, Lancashire, UK.

Decline of coronary heart disease in three generations

Coronary heart disease in three generations

It might be assumed that coronary heart disease (CHD) has always been with us, that it is with us today, and that it will be with us always. But during the past century CHD has changed both in quantity and in quality.

Early 20th century

It appears that CHD was very rare during the first two decades of the 20th century, and it was a rare cause of death. Things changed in the mid-1920s.

This was described very clearly by Dr Maurice Campbell, a leading UK cardiologist during the 1960s. During the early part of the 20th century there was a gradual reduction of number of deaths from disease of the heart valves, which were due to syphilitic and rheumatic heart diseases. Details can be seen in a previous Post: “The onset of the epidemic of Coronary Heart Disease”.

While deaths from diseases of the heart valves were reducing, the total number of deaths from heart disease showed an increase. Something new was happening, either a new disease was emerging or there was an unexplained major increase of a form of heart disease that was previously uncommon and unimportant. 

Figure 1. The emergence of coronary heart (artery) disease

This is clear in Figure 1. We can see the blue graph-line that indicates all heart deaths. There is an increase after about 1923 and the increase is persistent. At the same time deaths from valvular heart disease (yellow graph-line, VHD) is declining. The red graph-line shows the emergence of coronary heart disease, here labelled as CAD, coronary artery disease, an alternative term).

The emergence of coronary heart disease

The increase of heart disease deaths continued exponentially to a peak in about 1970, and thereafter fell rapidly. It became clear that the “new” heart disease was coronary heart disease, CHD.

Figure2. The epidemic of CHD in the UK

This recognition was based on autopsy studies, and it is this, the pathology, that defines the disease. We can argue about a diagnosis based on clinical features: are there changes in nomenclature, or is there more case-finding? For example the lay term "heart attack” is used very loosely and cannot be the basis of a specific disease. Myocardial infarction (MI) is the specific medical term, based on clinical features together with autopsy findings, and in this we find certainty. 

The pathology of coronary heart disease 

The pathology identified the disease particularly in the walls of the coronary arteries of the heart. There was an inflammatory basis to the disease that was occurring in what are called “plaques”. Autopsy following typical death from myocardial infarction identified the plaques rupturing through the lining of the coronary arteries into the lumen. This process is called plaque rupture, very much like an erupting boil. It could initiate a blood clot, causing complete occlusion of the coronary artery, with sudden death or the clinical features of myocardial infarction. This was something new.

Figure 3. Illustration of plaque rupture and thrombosis

Although CHD deaths were most common in late middle age, they could also cause death young adults. It became clear that the pathological process developed at an early age, identified in autopsies perfumed on young adults who had died as the result of injury.

The epidemic/pandemic of coronary heart disease

The epidemic nature of the new CHD in the UK is obvious in retrospect but most people seem to be unaware of it. A mild form of CHD  continues mainly in the elderly but the death rate has declined considerably. 

Is the decline a result of preventative medical interventions, and in particular the widespread use of statins? The answer is clearly “No”. Despite what we are told, statins have only a minor effect, reducing ten year mortality by just 1%. And statins were only widely used after the year 2000. 

Autopsy studies in young men

Important pathological investigations have demonstrated that the epidemic of CHD has been in a dramatic and spontaneous decline, and this is not due to medical interventions. This information has been based on the autopsies performed on young US soldiers killed in military action. It has been possible to compare three generations in three episodes of warfare: The Korean war (1951–1953), the Vietnam war (1968–1978), and the Iraq and Afghanistan wars (2000–2011).

Medical services were very advanced during these wars, based on experience gained during the two world wars earlier in the 20th century. Autopsies were performed regularly and this allowed detection of diseases and abnormalities incidental to the injuries causing death.

In the second half of the 20th century, coronary heart disease was recognised as an increasing public health problem and major cause of death. The experience in the Korean war led to the confirmation that onset of the disease was in early adult life, or even in late childhood.

Korean war, 1951–1953

Autopsies performed during the Korean war identified the presence of coronary heart disease in almost 80% of the soldiers killed in action, and severe disease in almost 20%. 

Figure 4. Evidence of CHD in autopsies of soldier killed in action

This shows the very serious nature of the epidemic of CHD as it was developing in the 1950s. The soldiers would be in the age range 18–28 years, and this was the recognition that the origins of CHD were early in life. They would probably have acquired the disease in the 1930s. Had they not been killed in action, they would no doubt have died from CHD about 30 years later, in about between 1970 and 1980.

Vietnam war, 1968–1978

The next major US war was in Vietnam, between 1968 and 1978. The soldiers would be of the next generation, born in the 1950s with parents born in the 1920s. Once again deaths in conflict allowed the assessment of incidental CHD, and it was about half of what was found in the Korean war. There was evidence of CHD in 46% of autopsies, and of severe disease in 8%.

Figure 5. Evidence of CHD in autopsies of soldier killed in action

This was a remarkable reduction in the prevalence of CHD, but it seemed to provoke no curiosity at the time. The reduction cannot be explained on the basis of medical intervention or change in diet.

Iraq and Afghan wars, 2000–2011

Then came the wars in Iraq and Afghanistan, after an interval of thirty years, another generation. The prevalence of incidental CHD had on this occasion fallen much more dramatically There was evidence of CHD in fewer than 10% of autopsies, and severe disease in only 2%.

Figure 6. Evidence of CHD in autopsies of soldier killed in action

Changing prevalence of CHD

The very high prevalence of CHD in autopsies of young men in the 1950s was frightening, and it was of course a predictor of the peak of the epidemic of CHD deaths that came to be 20 years later. 

The dramatic decline of evidence of CHD in young men cannot be explained in conventional dietary terms. It was clearly a spontaneous decline of a serious disease causing many deaths of pandemic proportions.

This study of autopsies performed on soldiers killed in action is the most objective and uncontroversial evidence of the decline of CHD.

Such autospsy evidence did not emerge from the two earlier world wars. At that time in the first half of the 20th century CHD was not a significant public health problem, and routine autopsy services in conflict would not have been possible.   



Due to a micro-organism?

I have explained in previous Posts that the only plausible explanation for the cause of the pandemic of CHD was a novel micro-organism. Its rapid decline would be the development immunity acquired initially by the first generation. Antibodies would have developed even though the disease might have been fatal. This acquired immunity would be transmitted to the next generations though natural inheritance, amplified by subsequent generations if the disease were still active.  

This is exactly what we see in these wartime studies that the disease declined rapidly within three successive generations.

Source of data:

Dalen JE et al, American Journal of Medicine Volume 127, Issue 9, Pages 807–812