Socialist Demands for the COVID-19 Crisis

chlamor
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Re: Socialist Demands for the COVID-19 Crisis

Post by chlamor » Mon Mar 23, 2020 12:43 am

This article is more than 8 years old.

Air pollution could become China's biggest health threat, expert warns

Leading respiratory disease specialist warns of consequences if government fails to monitor and publicise the dangers of smog
Jonathan Watts

Fri 16 Mar 2012 07.34 EDT First published on Fri 16 Mar 2012 07.34 EDT


Air pollution will become the biggest health threat in China unless the government takes greater steps to monitor and publicise the dangers of smog, the country's leading respiratory disease specialist warned this week.

Lung cancer and cardiovascular illnesses are already rising and could get worse in the future because of factory emissions, vehicle exhausts and cigarette smoke, Zhong Nanshan, the president of the China Medical Association, told the Guardian.

The outspoken doctor – who won nationwide respect for revealing the cover-up of the Sars epidemic in 2002 – said the authorities are starting to learn the lessons of past health crises by being more transparent about the risks posed by contaminated air. Unless there is more openness, he said, public trust will be eroded.

"Air pollution is getting worse and worse in China, but the government data showed it was getting better and better. People don't believe that. Now we know it's because they didn't measure some pollutants," said Zhong. "If the government neglects this matter, it will be the biggest health problem facing China."

Earlier this month, the government promised to be more open.

It has been a long time coming. Beijing and other major cities have experienced dire levels of air pollution for more than a decade, but the government has been reluctant to investigate and publicly disclose the medical consequences.

Zhong said he has been concerned about the problem for 10 years, but his efforts to press for official data have met with silence. During the run-up to the 2008 Beijing Olympics, he said he asked the environment department for information about ozone and carbon levels, but made no headway.

"They never answered. I understand this is because they did not collect such data. But it is also because they didn't want to announce this," Zhong said. "Maybe they are afraid of showing that levels are too high, which might have a negative impact on society."

Until recently, the government did not include ozone and small particulate matter known as PM2.5 in its air quality index, even though these two pollutants pose the greatest risk to human health.

Insiders say some cities quietly and selectively measured these pollutants for many years, but never made the results public. Scientific studies of this crucial public health issue have been notable by their absence.

Zhong says public awareness has come slowly because, compared to acute epidemics like Sars that results in sudden clusters of death, pollution is a chronic, slow-burning problem with consequences that are not apparent for many years.

But there is strong evidence of the risks. He said outpatient cases at his clinic in Guangdong province increase by 10% on hazy days. He also cited a US study that showed that cases of cardio failure increased by 1.28% for every increase of 10 micrograms of PM2.5 per cubic metre.

Understanding of the problems in China has been promoted by the US embassy in Beijing, which has released its own hourly measurements of PM2.5. In response, Beijing, Guangdong and several other provincial and municipal governments has belatedly followed suit.

Zhong said state promises to introduce nationwide monitoring need to be quickly honoured. He also called for detailed epidemiological research into the problem. Controversially, he said it would be a good thing if every embassy in Beijing monitored and publicised pollution data.

"We need data. We don't have that," he said. "We need to do something. We should start an annual study."

It is difficult to separate the impacts of pollution and tobacco, which is also a major contributor to PM2.5. But Zhong said lung cancer rates are two or three times higher in cities than in the countryside, even though smoking rates are the same.

On heavily polluted days, he advised city dwellers to wear face masks and not to exercise. But he said there was ultimately little that individuals could do unless greater efforts were made to check the source of the pollution.

Although the nature of the health risk posed by smog is different from that of Sars, he said the two shared similarities in terms of the importance of information disclosure.

"It takes time to make local governments move on transparency," he said. "But the situation now is better than during Sars. At the very beginning of that epidemic, it was really terrible. We have learned a lesson."

He said the environment was now a key public health concern, which was not the case in the past.

After polluted air, he said contaminated water, food and the chemicals found in furniture were recognised as major risks in addition to those previously identified from smoking and alcohol.

"We all have to breathe. It's no longer enough just to have a good lifestyle. A green environment is one of the most important elements in deciding people's health. People are more aware of that. I'm happy about that."

https://www.theguardian.com/environment ... reat-china

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Re: Socialist Demands for the COVID-19 Crisis

Post by blindpig » Mon Mar 23, 2020 12:58 pm

Effective measures to protect the health of the people and to support the workers must be taken now!

In these difficult times, the KKE is positioned with a sense of responsibility towards the people, stressing that all necessary measures must be immediately taken to protect health and safeguard workers' rights. The KKE has already announced the postponement of all its events until Easter, as part of the public health prevention and protection measures.

Recent government announcements on addressing the novel coronavirus epidemic seek to create the impression that the government is doing everything in its power to face an objective danger that has visible implications for the nation's health and the economy of the country.

The truth is that the real danger stems from the tragic shortcomings of the health system that were known before the outbreak of the novel coronavirus. These shortcomings did not occur accidentally, they are not objective. They are the result of the anti-people's policy pursued by all governments, based on the EU directions for the commercialization and privatization of Health, to support the profitability of business groups and safeguard the surpluses. This policy cancels out, in practice, the great scientific and technological possibilities that exist today to meet all the needs of prevention and healthcare of the people. So, for example, today there are only 550 beds in the Intensive Care Units, while 3,500 were needed before the coronavirus outbreak.

The pre-existing slowdown of the economy in the Eurozone and internationally is now furtherly reinforced by the spread of the novel coronavirus outbreaks and increases the risk of a new crisis in the coming period, especially in the Eurozone.

The propaganda government campaign, which focuses almost exclusively on the individual responsibility of each citizen and calls for national unity to support government policy, obscures the real problem. Taking the necessary measures calls for opposition to the EU's commitments and policies to support the competitiveness of monopoly groups, which sacrifice the satisfaction of the people's needs at the altar of capitalist profitability. The people cannot and must not pay again!

The recommendations of the National Public Health Agency impose the need for the government to immediately take all necessary measures to effectively address this pandemic and at the same time face all the permanent healthcare needs which are non-relevant to it.



1. We demand here and now emergency measures to protect the health of our people, such as:

- Recruitment of permanent medical and nursing staff to open all closed beds of the Intensive Care Units, but also to enable 24-hour operation of all Primary Health Care Units in order to relieve the congestion in hospitals.

- Full equipment of all public services with the necessary disinfection and precaution supplies provided to the public by the state free of charge in order to stop any unacceptable profiteering.

- Immediate re-opening of the hospitals closed by the ND - PASOK governments in 2013 (the Patissia Polyclinic, the General Hospital of West Attica, the Bombola ward, etc.). They must be immediately staffed, with permanent personel and not with staff transfers from other hospitals.

- Any additional needs of hospitalization and medical practice to be also met by the requisition of Health infrastructure in the private sector.



2. The compulsory implementation of the necessary restrictive and preventive measures for the population prerequires corresponding measures to protect the income and rights of the workers themselves. The measures announced so far only support big capitalist enterprises while reserving a "quarantine" regime for workers' rights. At the same time, no essential family income protection measures for workers, freelancers and farmers are guaranteed in case they get sick or stop their work due to family obligations.



3. The government's single "horizontal" approach on the arrangements regarding the taxation and insurance obligations of the business groups, the big capital, the self-employed and the employees will eventually be interpreted as new burdens on the people's shoulders.

The workers, through their contributions to Social Security Organizations, have paid a lot in order to be able to have basic insurance and benefits in the event of such emergencies. They have paid and continue to pay through EOPYY (National Organization for the Provision of Healthcare Services) for their health, through OAED (Organization of Workforce Employment) and other contributions to EFKA (Single Organization for Social Insurance) to cover their income in cases of unemployment and temporary disability for work (illness, accident).

To provide additional leave from work with full remuneration and Insurance: (a) To all workers who get sick in order to recover but also to prevent the spread of the disease (b) To a family member with a sick child or having no other option than taking care of a minor child himself/herself, or taking care of an elderly family member.

Furthemore, the government is accountable not only for not announcing penalties and fines for employers who violate labor relations and working times but also for suspending the required controls: We demand here and now to tighten the controls by the Labor Inspectorate in sectors and workplaces, which must not become prisons in the midst of an epidemic.



4. In all cases, all necessary emergency financial support measures for workers and the popular strata must be taken in order to address the additional problems arising:

- First of all, all auctions and forfeitures, all electricity and water cuts, any kind of compulsory enforcement measures to the State, banks and Public Companies and Organizations should be suspended, for as long as it takes, for all workers, pensioners and self-employed, with priority for those with an annual income of less than 12,000 euros.

- Redundancies must be stopped. Unemployment benefits at 80% of the basic salary must be given here and now for seasonal workers who are not re-employed, such as in the sectors of tourism, transport, etc. A similar benefit should be given to freelancers, with annual incomes of up to € 12,000, who will be forced to close down their business. Moreover, workers of businesses suspending their operations should also receive an emergency allowance of € 715.68 for the next 45 days.

- All pensioners should be given an immediate 13th pension as emergency support.

- Specifically, for self-employed with annual income up to EUR 12,000: a) To be exempt from paying contributions for their insurance for the next 4 months without loss of their pension rights, b) To set a tax-free threshold of EUR 12,000 and non-payment of business tax to enable them to cope with the already increasing financial consequences.



5. Additional measures need to be taken in the field of Education to face with a state responsibility several problems arising from the necessary decision to close all educational structures. It is important to protect the children of the popular family from the consequences of the commercialization of education, which creates unequal conditions of access, which may be sharpened under these conditions. We therefore demand:

- To take measures to ensure that pupils in the last grade of high school are equally prepared as expeditiously as possible for the national exams, even with a reduction in the school subjects' material.

- To solve all the problems related to student care, to continue students' boarding by avoiding crowding (packaged food).

- To solve the problem of refunds for canceled school trips, both domestic and abroad, concerning thousands of families.



We call on workers to take their destiny into their own hands and decisively demand from the government to immediately take all necessary measures to safeguard the health and the rights of the people.



The Political Bureau of the Central Committee of the KKE

March 13, 2020

https://inter.kke.gr/en/articles/Effect ... taken-now/
"There is great chaos under heaven; the situation is excellent."

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blindpig
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Re: Socialist Demands for the COVID-19 Crisis

Post by blindpig » Mon Mar 23, 2020 1:05 pm

A RECKONING?
Posted by MLToday | Mar 22, 2020 | Featured Stories

A Reckoning?
By Greg Godels
March 14, 2020
To understand the global economic chaos endured over the last few weeks, it is essential to separate the proximate from the ultimate cause.

Image

The immediate or proximate cause is the often fatal, expanding contagion of the coronavirus (Covid-19). The collapse of worldwide equity markets has been an immediate and widely noted effect of this proximate cause. The virus’s carnage in PRChina triggered a rapid and effective response, but one that dampened economic activity in a country already dealing with a slowing economy battered by economic sanctions and tariffs. Institutional investors, hedge fund managers, and their ilk took note of the carnage and contagion and, anticipating its effects on global activity, withdrew their assets from equities and moved them to safer havens, like US Treasury bonds. The panic initially shook the bond markets, lowering yields dramatically.


The rapid spread of the virus brought even greater economic disruption in its wake.


However, the ultimate cause of the current worldwide economic turbulence is the fragility and vulnerability of the global capitalist system. That statement is neither trivial nor self-evident. Since the severe crisis of 2007-2009, capitalism has been limping along, thanks to extraordinary central bank measures, tax cuts, military spending, and expansive credit-driven consumer demand. The casualties of the previous crisis survive on low-paying, casual service jobs while the rich engorge themselves on stocks inflated by mergers and acquisitions and stock buybacks. Every tentative growth spurt falters, returning the capitalist economy into stagnation. The increasing irrelevance of centrist political parties is one manifestation of the mass dissatisfaction with the growing inequality and impoverishment suffered by many. The question was not whether this course is sustainable, but when it would fail.


The ominous threat of the Coronavirus to international economic activity– work, leisure, travel, all forms of social life– has triggered a market meltdown based on a fear that the capitalist system may spiral out of control. Investors know that the system’s weaknesses, the lack of adequate preparations, the political stasis, and ineffective governing foretell a frightening outcome.


Unlike the rapid and thorough Chinese response which has largely arrested the virus’s spread, complacency in the Western capitalist countries is shocking. Today, seven times more people per millions of population have been infected by the virus in Italy than in PRChina, where the illness first broke. New cases in Italy are 3,497 against only 11 in PRC on March 14. Chinese deaths fell to 13 on March 14, while 175 Italians, 97 Iranians, and 60 Spaniards died from the virus. All the Western media hand wringing about Chinese “authoritarianism” will not deflect the incredible failures of public health preparedness in the Western capitalist countries.


The lack of a universal, equitable, and comprehensive healthcare system (like Medicare for All!) and a robust public health sector put the US especially at risk. Couple the unevenness and unfairness of healthcare with the historical obsession with personal autonomy, and disaster is on the horizon.


An exogenous trigger of economic turmoil is not unprecedented in recent times. The attack by al Qaeda on US civilians on September 11, 2001 produced a 7+% drop in the stock market, deepened the dotcom downturn, and fueled a stock market retreat and growing unemployment for the next year or so. As with the Coronavirus in 2020, an unexpected, non-economic factor jolted a shaky economy in 2001, then also plagued by overvalued “assets.” This instance promises to be far worse.


Much of the economic history of the twenty-first century has been a battle by policy makers against deflation, a battle to prop up artificially inflated, often virtual, assets. From the turn of the new century and the dotcom bubble until today, toxic assets have infected the productive economy. Ironically, a seemingly random “toxic” virus is now threatening the weakened global economic organism, destroying “value” by the trillions.


Of course the danger still lies ahead. Markets are only anticipating the lost work-hours, the layoffs, the healthcare costs, the business closures, the slowed production, the inverse “wealth” effect, the reluctant consumer, the slackening investment, and a host of other economic shocks that could feed a deflationary spiral. The financial sector is stunned by this as well because asset values are collapsing in a low-interest environment.


Though some are calling this a financial crisis, it is not spurred by financial factors; nor is it confined to the financial sector. Nor is it a crisis of overproduction, under-consumption, or profitability, though it is quickly morphing into all of the above and, inevitably, where all economic crises arrive, a crisis of accumulation. The global economy was rocking on a precipice; the Coronavirus pushed it over.


The virus couldn’t have come at a worse time. The war between the economic globalists and nationalists, waged with tariffs and sanctions, was taking a heavy toll on many countries and remains unsettled. Despite equity market euphoria (disconnected from all reality), commodity markets were slack or declining. International trade had slipped below historic growth levels.


Saddled with the unspoken duty to stabilize the US economy for an incumbent in a Presidential election cycle, the Federal Reserve shot its monetary wad prematurely, lowering interest rates in anticipation of limited economic slippage from the “Chinese problem.” They are now left with only radical measures to meet the crisis (a program injecting a trillion and a half in liquidity into the banking sector and expanding deflation-fighting asset purchases was announced on March 12).


The Russians exacerbated the crisis by shunning the Saudi plan to bolster oil markets. On Friday, March 6, they refused to join the Saudis in curtailing oil production to stabilize prices. Irresponsibly, the Saudi leadership– under severe political pressure from budgetary shortfalls and a disappointing IPO– announced a price war (and arrested oppositional members of the Royal family).


As oil prices collapsed, the Russian ruble collapsed as well, forcing the Russian central bank to halt foreign purchases temporarily.
According to Russian insiders, the withdrawal from price maintenance was aimed at US frackers who cannot produce profitably when prices are low. Alexander Dynkin is quoted as saying: “The Kremlin has decided to sacrifice OPEC+ to stop U.S. shale producers and punish the U.S. for messing with Nord Stream 2.” [my emphasis] The Russians surely knew that the US fracking industry was already on the verge of collapse because of massive, unmanageable debt (over $120 billion maturing over the next 2 years!). Thus, Russia risked a profound oil-price deflation in revenge for US subversion of its European gas pipeline project– a capitalist tit-or-tat.


I have written about energy imperialism frequently over the last two years (especially, the US’s extortionate use of war-mongering, sanctions, and threats in order to garner market share) . Given the ugly effects of a price-war race to the bottom on vulnerable oil production-dependent countries like Venezuela, those who see Russia as something more than another capitalist country pressing its own interests may find a reason to reconsider.


A nasty virus, incompetent and delayed responses, ill-conceived economic policies, an irresponsible price war, all contribute to a fear-driven market collapse as the opening act of a possible drama featuring an unprecedented deflationary spiral.


Does anyone believe that the leaders of the capitalist world can manage this challenge?

https://mltoday.com/a-reckoning/

And as we too well know, when the capitalist get flustered the fascist comes out.
"There is great chaos under heaven; the situation is excellent."

chlamor
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Re: Socialist Demands for the COVID-19 Crisis

Post by chlamor » Mon Mar 23, 2020 9:38 pm

Italy: The Virus Hits Polluted Areas. Is There a Correlation?

The coronavirus pandemics: a consequence of the human impact on the ecosystem


Image[/img]
The Italian situation: on the left, pollution levels of microparticulate. On the right, the diffusion of the Coronavirus pandemic. Image from the article by Setti et al.


Below, I report an English translation (slightly modified) of an article that I submitted today to the Italian newspaper "Il Fatto Quotidiano." Sorry that the text is a little Italy-centered and all the links point to pages in Italian. Nevertheless, I thought that the story of a possible correlation of the coronavirus diffusion and the level of pollution was interesting also for the readers of "Cassandra's Legacy."

For some additional considerations, take a look at the picture above: the correlation of the virus diffusion with the most polluted areas of Italy seems evident. It is, of course, a hypothesis to be taken with plenty of caution, but it has some logic in it. The Val Padana, the Northern plains of Italy, is a region stuck between two mountain chains, the Appennini and the Alps, blocking winds coming from the North. The result is that air stagnates and pollution accumulates, creating what's probably the most polluted area in Western Europe. Considering that also Wuhan, the other center of the coronavirus epidemic, is located in a highly polluted area, central China, it makes sense to think that the infection does more damage to the already weakened lungs of people affected by pollution. Indeed, I had already noted how epidemics tend to strike mostly populations already weakened by other factors, typically famines and wars -- pollution is just another factor that has the same effect. According to the data, it may also be that the virus is carried by flying microparticles and that makes the infection spread faster.

The discussion is ongoing in Italy, with some people vehemently rejecting the idea that pollution may have anything to do with the pandemic, using the concept that "correlation doesn't mean causation" as a little mantra to dispel ideas they can't accept. There is a certain logic in this attitude, too. If the epidemic is reinforced by pollution, it means that the virus is not just an act of God, unpredictable and nobody's fault. It means that we have created the disaster by our neglect of the damage we are doing to the ecosystem and that, eventually, comes back to us with a vengeance. It is understandable that some people take the hypothesis as a direct attack on their non-negotiable lifestyle. But so it goes, we are all human beings.



The Coronavirus epidemic and pollution: is there a correlation?
by Ugo Bardi
Submitted to "Il Fatto Quotidiano" 22 March 2020

There is an ongoing debate about the possible correlation between the coronavirus epidemic and pollution. A recent study by Leonardo Setti and colleagues examines this correlation in Italy. The result is that particulate matter appears to act as a carrier of the virus and accelerate its spread. This would be in accordance with the fact that the maximum spread of the epidemic is in Val Padana, probably the most polluted area in Italy.

The article does not explicitly say that pollution may also have weakened the immune defenses of victims, but this is the result of other studies. For example, a recent study shows that this specific virus preferentially attacks the lungs of smokers, and smoking does similar damage as pollution to lungs.

These are possible hypotheses but, of course, it does not mean that they correspond to reality. In fact, Setti's article also generated negative reactions. The Italian Aerosol Society (IAS) intervened with a document that points out that correlation does not mean causation, that the data are uncertain and that we need to study much more about it before we can determine if the atmospheric particulate matter has any effects on the epidemic.

Who's right? For most of us, it is difficult to give an informed judgment on such a specialized and complex subject. One thing we can say, however, is that here we have a correlation based on data – albeit uncertain- backed by serious people. Nothing to do with the various follies that you can read all over the Web, that the epidemic is all the fault of 5G, of chemtrails, or who knows what other ongoing monstrous plot created by the powers that be.

Another thing we can say is that this story is a good example of how scientific progress works: we start from a correlation, often initially uncertain, and then try to arrive at an explanation. Perhaps you remember the case of the English doctor John Snow, who in the 19th century had noticed a correlation between the number of cases of cholera in London and the distance of the homes of people sick from a certain public fountain. He shut it down and so he managed to stop the epidemic. Much later, it was discovered that the fountain fished near a well that contained infected fecal matter.

Today, it seems obvious to us that Snow was right but, in his time, the role of bacteria in infectious diseases was not known and his idea was initially opposed. It may be that someone had also said to him that " correlation does not mean causation!" But if Snow had waited for certainty, people would have continued to drink from that fountain and die of cholera.

The analogy with the current situation is obvious. Also for the coronavirus epidemic, we have an analysis of the location of the cases that establishes a correlation with highly polluted areas. On this basis, an action strategy can be devised. For cholera in the days of Snow, it was enough to close a fountain to stop the epidemic, for the coronavirus you have to reduce air pollution. That's not so easy, but we can at least try. If it turns out the correlation didn't exist, well, we'll still have done something good.

All this does not mean that it is the only pollution that causes the epidemic, absolutely not. But if it's an important factor, then we have to take it into account. If the air in Lombardy had been less polluted, it would have been easier to control the spread of the virus and mortality would have been lower.

Once more, we see how the damage we do to the ecosystem comes back to us. At this point, it is useless to blame the Chinese bat-eaters or the government that did not close the borders in time. To a large extent, the blame lies with all of us who, with the excuse of "development", have not done enough to combat air pollution. It will take time to remedy, but, at least, the coronavirus is teaching us that there is no development if it is not sustainable and that sustainable development respects both the ecosystem and human health. Hopefully, we'll remember that in the future.

https://cassandralegacy.blogspot.com/20 ... as-is.html

Comment here:

The narrative that epidemics are an "act of god" or a random catastrophe is always wrong, of that there is no doubt at all. Humans and pathogens live side by side until something happens that has its cause in social practices of the host population, us.

Famously the worldwide malaria epidemic was started by colonialism and is still ongoing. Mad cow desease was obviously caused by malpractices in our industrial agriculture, the west african ebola outbreak can be directly linked to globalisation and land grabbing.

( Evolutionary biologist Robert Wallace does exactly that in this interview: https://therealnews.com/stories/rwallace1031ebola )

Who will be most affected is also a result of how we organize our society. It has always been the case that the poor that live in crowded cities that have been affected most by outbreaks.

Finally we have to admit, that if not for the neoliberal austerity politics our health systems could withstand this crisis much better.

So if corona had a connection to pollutants it would actually make much more scientific sense than any "act of god" theory out there.

chlamor
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Re: Socialist Demands for the COVID-19 Crisis

Post by chlamor » Mon Mar 23, 2020 9:50 pm

Air pollution and infection in respiratory illness
Anoop J Chauhan, Sebastian L Johnston
British Medical Bulletin, Volume 68, Issue 1, December 2003, Pages 95–112, https://doi.org/10.1093/bmb/ldg022
Published: 01 December 2003
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Abstract
The detrimental effects of air pollution on health have been recognized for most of the last century. Effective legislation has led to a change in the nature of the air pollutants in outdoor air in developed countries, while combustion of raw fuels in the indoor environment remains a major health hazard in developing countries. The mechanisms of how these pollutants exert their effects are likely to be different, but there is emerging evidence that the toxic effects of new photochemical pollutants such as nitrogen dioxide are likely to be related to infection. This review discusses the relationship between air pollution and infection and will explore some of the mechanisms of how both could act synergistically to cause respiratory illnesses especially in exacerbating symptoms in individuals with pre-existing respiratory conditions such as asthma and chronic obstructive pulmonary disease.

Topic: air pollution infections heat of combustion
Subject Environment and Disease Respiratory Medicine
Issue Section: Articles
A lesson from history
It is recognized that severe air pollution episodes have occurred in the UK since the early 17th century, but with rapid industrialization, such episodes became more severe and more frequent towards the 19th century. Legislation at this time led only to a reduction in smoke from industry, and difficulties in implementation gave little improvement in air quality until the early 20th century. Severe smog episodes through industrial and domestic combustion of solid fuels (coal) occurred during calm, winter weather. Between 1948 and 1962, eight air pollution episodes occurred in London, but the now well described ‘Great Smog’ episode in December 1952 was the most significant. Smoke concentration rose >50 times above the average limit, and at the National Gallery visibility was poor enough for individuals not to see their own feet. An estimated excess death toll of 4000 occurred during this period, a three-fold increase over the expected mortality rates for the time of year. Most deaths were among infants and elderly people. Similar episodes of severe air pollution in the United States after the Second World War and in Belgium in 1930 had aroused public concerns about the health effects of air pollutants.

Increased public and parliamentary concern led to effective legislation. In the UK, subsequent Clean Air Acts of 1956 and 1968 and similarly the Clean Air Act of 1970 in the USA had considerably reduced air pollution from stationary sources from homes, commerce and industry. Both the emission of smoke then sulphur dioxide (SO2) fell dramatically. However, it is now accepted that any air quality benefits have been at least partially offset by increasing emissions of other visible and photochemical pollutants from mobile ‘sources’ such as car exhaust fumes. There is increasing awareness that new stationary sources in homes are also sources of the newer photochemical pollutants such as the oxides of nitrogen from unflued gas cookers and heaters1.

The historical perspective of traditional air pollutants continues to interest contemporary air quality researchers. During the 1952 smog episode, there was a sharp rise in hospital admissions and visits to primary care physicians, but recent re-analysis2 of the mortality data indicates the number of deaths was underestimated and was nearer 12,000. While the majority of deaths occurred in individuals with chronic respiratory disease, the steep rise in mortality was sustained for several months and did not drop immediately after the resolution of the smog episode (as might be expected if it were simply a triggering phenomenon). This raises issues of the mechanisms of how these pollutants may have caused the deaths perhaps through acidification with sulphuric acid that overwhelmed the buffering capacity of the lungs, interaction with other pollutants, toxic effects at subsequently lower and hitherto ‘normal’ levels of pollutants or perhaps more importantly, interaction with other co-factors such as infections. It has been assumed that many of the exacerbations of pre-existing respiratory illnesses that occurred during the smog episodes were the result of acute respiratory infections (ARIs). Recent evidence from developing countries confirms the direct exposure–response relationship between indoor air pollution by combustion of biomass fuels generating high levels of particulates and sulphur dioxide with increased acute respiratory infections in adults and children3. These observations have renewed interest in how air pollutants may exert their toxic effects through interaction with infection. This brief historical review of air pollution events confirms that air pollution by whatever mechanism can kill and equally importantly, that with sufficient public interest and the political will, effective legislation can reduce the mortality effects of such pollutants.

Combustion of biomass fuels and infections
Acute respiratory infections are the leading cause of the global burden of disease accounting for more than 6% of worldwide disease and mortality in developing countries4,5. Acute lower respiratory infections were attributed to have caused up to 4 million deaths worldwide from 1997 to 19994. In developing countries, smoking amongst women is rare and outdoor pollution is restricted to larger cities yet both women and children suffer a huge burden of respiratory illness, largely through ARIs, which are responsible for nearly a third of all deaths in children under 5 years old6. Poor sanitation, low birth weight and poverty contribute to the causes of infections but the combustion of biomass fuels remains a rapidly growing problem. The main source of indoor air pollution globally is the combustion of biomass fuels (wood, dung, charcoal) as this is the main source of domestic energy. They produce small amounts of energy but large amounts of indoor pollutants, often emitting 50 times more pollutant concentrations than energy equivalent natural gas7. The often poor ventilation and dispersion characteristics of dwellings in developing countries allow pollutant concentrations to rise further and indoor concentrations of particulates between 500 and 100,000 μg/m3 are not uncommon3,8, and levels of indoor particulates 20 times greater than those due to cigarette smoking have been described8. Combustion of biomass fuels emits a variety of pollutants including particulates (PM10), nitrogen dioxide (NO2), carbon monoxide (CO), sulphur dioxide (SO2) and hydrocarbons. Several studies from different parts of the world provide an indication of indoor pollutant concentrations, and whereas there are no internationally recognized standards for indoor air quality, the WHO estimates the number of people exposed to unacceptable levels indoors to exceed the number exposed to unacceptable levels of outdoor pollutants in all of the world’s cities collectively.

The evidence for a relationship between indoor pollution and respiratory infections in developing countries is clear and has been recognized for at least two decades. The elderly, cooking mothers and the very young who spend most time indoors are likely to be at highest risk. Infant girls in Gambia whose mothers carried them on their back while cooking had more respiratory infections than girls not carried on their backs9, children in Zimbabwe with recurrent pneumonia were more likely to come from homes where wood was used for fuel10, and infants and children in Nepal who reported more time spent next to stoves suffered more life threatening episodes of acute respiratory infection11. The effects of these indoor pollutants on chronic respiratory illness in cooking women has also been reported with rates of chronic bronchitis of 18% in women who have never smoked12 and rates of COPD of >30% in women over 50 years of age in Kashmir13.

The effect of biomass fuel combustion has also been studied in developed countries. Children from Arizona, USA from homes using woodstoves for heating and cooking were four times more likely to suffer physician confirmed ARIs14. The Harvard Six Cities Study reported the use of wood stoves to be associated with a 30% increase in respiratory symptoms ranging from chronic cough to asthma in children aged 7–10 years15. The importance of indoor pollution in children has recently been reviewed7.

Contemporary indoor and outdoor pollutants and infections
The combustion of fuels indoors in homes from developed countries produces a variety of pollutants. The main (and most consistently reported) pollutant among them is nitrogen dioxide which is produced in both indoor and outdoor air from sources such as unvented gas stoves and motor cars, respectively. There is an increasing body of evidence to suggest that exposure to this pollutant is linked to respiratory disease in children and adults in the developed world, although until recently, less has been known about the potential mechanisms involved. Many of the epidemiological studies of outdoor NO2 exposure have found associations between exposure to the pollutant and health effects, often at levels well below current WHO guidelines. These health effects have included accident and emergency room visits16,17, hospital admissions18,19, mortality20,21, increased symptoms22,23 and reduced lung function24,25. The APHEA project (Air Pollution on Health: European Approach) incorporated data from 15 European cities, with a total population in excess of 25 million people. An increase of 50 μg/m3 NO2 (1 h maximum) was associated with a 2.6% increase in asthma admissions and a 1.3% increase in daily all-cause mortality26. There are many methodological issues that complicate interpretation of outdoor exposure studies such as exposure misclassification, confounding, co-linearity and insensitive measures of health effects. Nonetheless, this study strongly suggested a role for NO2, or other pollutants for which NO2 is a marker, in precipitating acute exacerbations of respiratory disease, although it has been difficult to separate the individual effects of the pollutant from the complex mixture of pollutants found in outdoor air.

With the recognition that indoor combustion sources contributed significantly to NO2 levels inside homes and to personal NO2 exposure, a number of studies have focused on indoor exposures. In most of the investigations, exposure to indoor pollution or NO2 has been classified on the basis of the presence of a gas stove or other major source of fuel combustion in the home, and there have been fewer studies where actual levels of NO2 or other pollutants indoors have been recorded, and even fewer where personal exposure has been estimated or directly measured, consequently some of the evidence has been inconsistent. Methodological limitations of the studies can readily explain the lack of definitive data, in particular in terms of misclassification of exposure and health outcomes and the incorrect (and therefore inaccurate) grouping of subjects with regard to exposure and disease. Although some studies have measured indoor NO2 levels at fixed points, our own observations confirm that neither fixed site monitoring nor use of categorical variables such as gas or electric cooking accurately predict personal NO2 exposure27. We have also confirmed that personal NO2 exposure (at least in children) is not consistently related to either outdoor or indoor NO2 exposure28. In considering the effects of indoor NO2 exposure, information from a wide range of cross-sectional and longitudinal studies was brought together in a meta-analysis that estimated that the odds ratio of respiratory illness in children exposed to a long-term increase of 30 μg/m3 in NO2 exposure (comparable to the presence of a gas cooker) was 1.2029, and up to 1.29 in children aged 5–6 years and 1.60 in infants30.

The link with infection
There has been a series of studies alluding to the link between infection and air pollution particularly by nitrogen dioxide. Two studies investigated the incidence of croup (laryngo-tracheo-bronchitis usually due to influenza or parainfluenza viruses) and air pollution. The effects of NO2, TSP (total suspended particulates) and SO2 exposure were investigated in more than 6000 paediatrician-reported cases of croup and more than 4500 cases of ‘obstructive bronchitis’ in five German cities over 3 years31. Increases in TSP and NO2 levels of 10 and 70 μg/m3 were associated with a 27% and 28% increase in cases of croup, respectively. In illustration of the point made earlier, the close relationship between TSP and NO2 levels did not allow their causal effects to be separated. In three other German towns32, levels of SO2, NO2, CO, O3 and dust were analysed with 875 cases of croup over a 24-month period. There was a significant association between croup frequency and the daily means of NO2 for the peak period between September and March (the peak virus season), and with daily NO2, and CO for the whole year. Another three cities in Finland from ‘high’ and ‘low’ pollution levels were studied over a 12-month period including 679 cases and 759 controls33. The annual mean concentration of NO2 in the more polluted city was 15 mg/m3 higher. The odds ratios for one or more upper respiratory infections in children in the polluted city versus those in the less polluted cities were 2.0 in the younger age group and 1.6 in the older age group. The authors did not separate the effects of the individual pollutants in the analyses. In another case-control study of outdoor NO2 in Stockholm, 197 children admitted to hospital because of wheezing bronchitis (reasonably assumed to be of infective aetiology) were compared with 350 controls. Time-weighted personal NO2 exposures were estimated based on outdoor levels. The risk of wheezing bronchitis was significantly related to outdoor NO2 exposure in girls (P = 0.02) but not in boys, and presence of a gas stove in the home appeared to be a risk factor only for girls.

More recently, several studies have suggested that air pollution may modify symptoms in individuals who may already be infected. Short-term effects of SO2 and particulate matter (but with low acidity) were studied in 89 children with asthma for 7 months. Exposure to elevated levels of air pollution was associated with decreased peak expiratory flow rates, increased respiratory symptoms, increased school absence and fever, and increased medication use. Furthermore, there was evidence that exposure to air pollution might have enhanced the respiratory symptoms while children were experiencing respiratory infections34. In another study, the impact of air pollution on 321 non-smoking adults was investigated recording the daily incidence of respiratory symptoms over a 6-month period. The incidence of lower respiratory tract symptoms was related to the 1-h daily maximum ozone levels (OR = 1.22). The use of a gas stove in the home was also associated with lower respiratory tract symptoms (OR = 1.23), and the effects of ozone were significantly greater in individuals with a pre-existing respiratory infection35. Another study investigated the relationship between use of anti-inflammatory asthma medication and susceptibility to the effects of air pollution in 22 asthmatic children from non-smoking households. The associations between air pollution (mainly particulates) and symptoms were notably stronger in 12 asthmatic children who were not taking anti-inflammatory medications versus 10 subjects who were36. Another study examined specifically short-term indoor NO2 exposures at school and in the home in 388 children aged 6–11 years. Exposure to NO2 at hourly peak levels of the order of <160 μg/m3 compared with background levels of 40 μg/m3 was associated with a significant increase in sore throat, colds and absences from school, although infection was not confirmed37. Also, significant dose–response relationships were demonstrated for these four measures with increasing levels of NO2 exposure.

The body of evidence thus strongly suggests a link between air pollution and severity of illness associated with respiratory infection, and that individuals with pre-existing lung disease may be at greater risk. The majority of the studies of air pollution and infection have been conducted in children, although until recently studies had not clarified the exact nature of the respiratory illness and infection. There now is good evidence of such a link in children with pre-existing asthma. However, the link with chronic obstructive pulmonary disease in adults has been less clear. Time-series analyses from Australia, Europe and North America suggest an association between air pollution and admissions to hospital for adults with COPD. An increase in daily maximum 1-h concentration of NO2 and particulates was associated with a 4.60% and 3.01% increase, respectively in admissions for COPD in Sydney38. Another study of hospital admissions in Birmingham, UK, reported associations between PM10 and all respiratory admissions, pneumonia and deaths from COPD without a threshold effect39. A recent time series study from Rome investigated the relationship between air pollution levels and admissions for respiratory diseases over 3 years. A same day increase in outdoor NO2 was associated with a 2.5% increase in all respiratory admissions per interquartile range (IQR) change. The effect of NO2 was stronger on acute respiratory infections (4.0% increase) and on asthma among children (10.7% increase). A similar increase in carbon monoxide was also associated with a 2.8% increase in admissions for all respiratory admissions, a 5.5% increase for asthma and a 4.3% increase for COPD40. Further data from the APHEA project in six European cities of differing climates, has also shown41 that a variety of pollutants including SO2, black smoke, NO2, total suspended particulates and ozone were associated with daily admissions for COPD with low relative risks ranging from 1.02 to 1.04. Another study from Minneapolis-St. Paul reported that an increase of 100 μg/m3 in daily PM10 was a risk factor for admissions for pneumonia (RR = 1.17) and admissions for COPD (RR = 1.57). Similarly, an increase of 100 μg/m3 in daily ozone concentration was associated with admissions for pneumonia (RR = 1.15)42.

This array of studies of indoor or outdoor pollutants and acute respiratory infections (or respiratory symptoms in general) in children and adults suggests a relationship but none have confirmed infection microbiologically but instead relied on clinical criteria based on symptoms or use of health services. Consequently little is known of the spectrum of infectious agents or whether these pollutants increase susceptibility to infection or whether they exacerbate pre-existing morbidity following infection.

We have confirmed that respiratory tract viral infections are the major precipitants of acute exacerbations of asthma in children43 and that episodes of viral infection are strongly associated in time with increases in hospital admissions for asthma44. In the former study human rhinoviruses alone accounted for 50% of exacerbations. If adequate virus detection methods are used, rhinoviruses and respiratory syncytial virus are detected in the vast majority of children (>80%) and infants (up to 100%) admitted to hospital with acute upper and lower respiratory illnesses. These data demonstrate that acute episodes of upper and lower respiratory illnesses in predisposed children both in the community and in those admitted to hospital are related to virus infections. Most of the epidemiological indoor pollution studies have alluded to the presence of respiratory infection as the health effect following NO2 exposure, although very few studies (including those from the developing world) had until recently attempted to confirm the presence of infection microbiologically.

Our own recent observations provide the first direct evidence of a link between upper respiratory virus infections, personal NO2 exposure and the severity of asthma exacerbations in children. This study is unique so far, in that it confirmed the presence of infection microbiologically. A cohort of 114 asthmatic children aged 8–11 years prospectively recorded daily upper and lower respiratory-tract symptoms, peak expiratory flow (PEF), and measured personal NO2 exposures every week for up to 13 months. Nasal aspirates were taken during reported episodes of upper respiratory-tract illness and tested for infection by common respiratory viruses and atypical bacteria with RT-PCR assays. Severity of associated asthma exacerbations was analysed in relation to high versus low NO2 exposures in the week before the viral infection. There were significant increases in the severity of asthma symptoms with 60% increased severity for all virus and >200% for respiratory syncytial virus infections for high compared with low NO2 exposure in the week before the start of the virus-induced exacerbation. The highest category of NO2 exposure was also associated with more severe falls in peak expiratory flow with virus infection by up to 75%. These effects were observed at levels within current air quality standards45.

Controlled exposure and infection studies
There is a wealth of literature on the effects of controlled photochemical pollutant exposure (O3, NO2, SO2) alone and lung function effects in healthy individuals and those with pre-existing lung disease. Inhaled O3 provokes a dose-dependent fall in lung function and an increase in bronchial hyper-responsiveness to histamine. These responses vary considerably between individuals and surprisingly, little difference has been observed between subjects with asthma and healthy individuals after O3 exposure. Inhalation of high concentrations of SO2 provokes acute airway bronchoconstriction in normal subjects whereas lower concentrations provoke the same response in asthmatic subjects. The response is usually rapid, and maximal effects are seen within 5 min and usually resolution is within 15–30 min. Given that SO2 was one of the main pollutants implicated in the London smog episodes, these short lived broncho-provocant effects are unlikely to explain why the deaths associated with the worst smogs were maintained for several months after resolution of the pollution episodes. Inhalation of NO2 at higher concentrations induced no change in resting lung function in either normal or asthmatic subjects exposed to concentrations of 1880 μg/m3 or less46. Bronchial hyper-responsiveness has been shown to increase only modestly in normal subjects exposed to >1880 μg/m3 NO2, and in about a third of studies in asthmatic subjects. In short, controlled exposure studies show largely modest effects on lung function and the pattern of response does not explain the epidemiological evidence, or the mechanisms of how these pollutants may interact with infectious agents.

There have been only a limited number of studies on the effects of controlled pollutant exposure and infection in humans largely through methodological difficulties and ethical constraints. There are a few studies that have suggested an interaction with infection. Three studies have investigated alveolar macrophage function after exposure to oxidant pollutant exposure in vivo and infection in vitro. In one study, nine volunteers were exposed to >1000 μg/m3 NO2 continuously or interspersed with three 15 min peak levels of >3500 μg/m3 NO2 in a sequential double blind randomized fashion (each subject served as their own control)47. Alveolar macrophages obtained by broncho-alveolar lavage after exposure were incubated with influenza virus. Two patterns of response were found after continuous exposure; alveolar macrophages from four of the nine subjects showed depressed inactivation of the virus [cells from these four subjects demonstrated an increase in interleukin-1 (IL-1) production after NO2versus air], whereas five showed no difference compared with control values. There were no differences from the intermittent peak exposure group. This indicates that differences in susceptibility to infection after oxidant pollutant exposure could occur in a larger population. Another study investigated the effects of high NO2 exposure (9400, 18,800 or 28,200 μg/m3) in vitro on alveolar macrophages obtained from 15 subjects48. After stimulation with influenza virus, both air and NO2 exposed cells released increased amounts of IL-1 (indicating macrophage activation), but there was no significant difference between groups. The results indicated that human alveolar macrophages are resistant to injury by NO2in vitro and that toxicity effects of NO2 may require local factors in the lung. In another 10 subjects exposed to >3500 μg/m3 NO2, alveolar macrophages obtained by lavage showed a 42% reduction in ability to phagocytose Candida albicans and a 72% decrease in superoxide production, superoxide production being important in phagocytosis49.

A study using 152 young volunteers reported exposure to 1880 or 3760 μg/m3 NO2, for 2 h a day for 3 days and intra-nasal challenge with influenza A virus immediately after exposure50. Despite only one of the volunteers developing any symptoms, 91% were infected in the NO2 exposed subjects as determined by virus recovery and/or antibody titres compared with 71% of air-exposed controls. This difference was not, however, statistically significant. As infected subjects did not become ill, the study could address the effect of NO2 exposure on infection but not on the severity of illness. These findings indicate, but do not prove, that oxidant pollutants may play a role in increasing susceptibility to respiratory virus infection.

Mechanisms of interaction between infection and air pollution
The lung defence mechanisms against inhaled particles and gaseous pollutants include innate mechanisms such as aerodynamic filtration, mucociliary clearance, particle transport and detoxification by alveolar macrophages, as well as local and systemic innate and acquired antiviral immunity. In particular, alveolar macrophages provide an innate defence mechanism against bacteria and viruses. There is increasing experimental evidence that pollution exposure adversely affects lung defence mechanisms. Virus particles are ingested by phagocytosis and, in common with epithelial and other virus-infected cells, macrophages produce interferons which potently inhibit viral replication. Macrophages will also contribute to the neutralization of viral infections by removing the debris of the destroyed, virus-containing, cells and by presenting viral antigens to T-lymphocytes. In addition to the resulting humoral immune response, cell-mediated responses such as the development of cytotoxic T-lymphocytes (capable of destroying cells infected with virus) play an important role in the control of many viral infections of the respiratory tract. Many of these functions can be modulated by exposure to NO2 and other pollutants in experimental models.

Animal infectivity models
It has now been almost 40 years since the ‘infectivity model’ was developed. This linked the effects of pollutants on pulmonary antibacterial activity following pollutant exposure with disease and mortality as end-points in animals. The majority of studies have been carried out using rodents, particularly mice, on the basis that the lung defence mechanisms of rodents and humans are sufficiently similar to permit their use as a surrogate. Some investigated various alveolar macrophage functions ex vivo but the great majority have used acute exposures to determine the concentrations of NO2 at which antibacterial defences are overwhelmed. Different exposure regimes whereby animals have been challenged with the infectious organisms either before or after exposure to varying concentrations of NO2, have also been used. For example, exposure to NO2 occurred before infectious challenge in mice, whereas others were exposed to NO2 at 1, 6 and 24 h after an infectious challenge. In all instances, mice exposed to NO2 either before or after the bacterial challenge showed increased mortality51. In another study, mice were challenged with Staphylococcus aureus and then exposed to NO2 for 4 h: pulmonary bactericidal capacity was progressively impaired in groups exposed to 7100 μg/m3 NO2 or higher52. Short-term exposures to NO2 and murine cytomegalovirus (MCMV) infection were investigated by Rose et al53 studying a number of parameters including macrophage viability, in vivo and in vitro phagocytosis by macrophages and systemic cell-mediated and humoral responses. The minimum inoculum of viral particles capable of reliably producing infection was much lower in mice exposed to NO2 compared with air-exposed animals. Another study addressed the risk of re‐infection after NO2 exposure. Animals were exposed to high doses of NO2 or clean air during primary infection with MCMV. This produced infection in all animals. Thirty days later, animals were re-inoculated with the virus. The number of re-infected animals in the group which had been exposed to NO2 was 11/20 compared with 1/22 amongst air-exposed animals, suggesting that NO2 exposure damages the development of virus-specific immunity following a primary infection54. The finding is supported by the observation that splenic lymphocytes obtained from NO2-exposed animals 30 days after primary infection failed (in contrast to lymphocytes from air-exposed animals) to proliferate in response to MCMV antigen.

Impaired bronchial immunity
Collective findings from both animal and human models provide some evidence of alterations in local bronchial immunity; acute exposure to oxidant pollutants results in ciliostasis in both the upper55 and lower airways56 which may prevent the nasal and bronchial mucosa filtering inhaled particles such as aero-allergens, bacteria or viruses delivered to the airway. In the studies by Devalia and colleagues (carried out in the absence of anti-oxidant protection), exposure of cultured human bronchial epithelial cells to NO2 concentrations of >1000 μg/m3 reduced ciliary beat frequency and caused ciliary dyskinesis. The reduction in muco-ciliary activity following NO2 exposure up to 4700 μg/m3 has been confirmed in a study of 24 healthy subjects in vivo57. Studies investigating single exposures to NO2 have found increases in mast cells, lymphocytes and natural killer (NK) cells in BAL fluid58. Studies of repeated exposure to 7520 μg/m3 NO2 (on six occasions, alternate days) have shown evidence of impaired local bronchial immunity by a reduction in total macrophages, B cells, NK lymphocytes, peripheral blood lymphocytes and a reduction in the T-helper-inducer/T-cytotoxic-suppressor ratio in alveolar lavage59.

Alveolar macrophage function
Evidence from animal and human studies suggests that alterations in alveolar macrophage function are important in the increased risks of infection. Activated macrophages provide protection against bacterial and viral infections by a variety of mechanisms including oxygen dependent pathways involving superoxide radical-anion mechanisms (e.g. myeloperoxidase) and cytokine production [particularly IL-1, -6 and -8, interferons α and β and tumour necrosis factor a (TNF-α)] which are important in mounting an immune response to infection. Exposure of human alveolar macrophages (AMs) to concentrations of NO2 ranging from 188 to 940 μg/m3 for short durations resulted in a significant reduction of lipo-polysaccharide (LPS)-stimulated IL-1β, IL-6, IL-8 and TNF-α (but not TGF-β)60. Cytotoxicity of AMs remained unaffected. The results indicate that at concentrations relevant to human exposure, there is a functional impairment of AM without significant alterations in cytotoxicity. More recent work investigated exposure to particulate pollution of three size ranges from PM10 to PM0.1 and the effect on antigen presenting cells by evaluating the expression of surface receptors involved in T-cell interaction on both human AMs and blood-derived monocytes (Mo). Mo up-regulated the expression of all four receptors in response to each of the particle fractions, whereas expression was unaffected in AM. However, when Mo and AM were separately exposed to the three PM size fractions and assessed for T-helper lymphocyte chemoattraction (by production of IL-16), AM alone (and not Mo) produced IL-16, and this chemoattractant was released only in response to PM2.5–10. This suggests that a wide size range of pollution particles contains materials that may promote antigen presentation by Mo, whereas the capability to specifically recruit T-helper lymphocytes is contained in AM stimulated with the ‘coarse’ PM fraction61. When the experiments were extended to different particle sizes and compositions, the response of AM was highly variable, leading the authors to conclude that composition rather than size was responsible for the oxidant response and that oxidant activation by various sources of particulate matter is cell specific62. The ability of different pollutants and particle fractions to cause variable defects in bronchial immunity may also determine the risk of symptoms following pollutant exposure and infection.

Epithelial interaction
Viral infections can cause severe pathological abnormalities in both the upper and lower respiratory tract, although the extent of epithelial damage varies between viruses. Whereas Influenza A infection causes intense inflammation of the bronchi, trachea and larynx with desquamation of ciliated epithelial cells, rhinoviruses cause little or only patchy epithelial damage. Experimental studies of oxidant pollutant exposure show that the lower airway epithelium (particularly the transitional zone between bronchial epithelium and proximal alveolar regions) is particularly susceptible. In contrast, nasal, laryngeal and tracheal regions are not readily damaged by oxidant pollutants possibly because they have a thicker, extra-cellular anti-oxidant hypophase63. It is possible that the penetration of allergen into the epithelium would be facilitated both by epithelial shedding, and by reduced ciliary clearance, resulting in easier access of allergen to antigen presenting cells and therefore increased inflammation. The epithelium is also an important source of regulatory proteins or mediators with protective roles, such as nitric oxide or bronchodilator prostaglandins E2 and I2, which may play a role in maintaining bronchial patency.

The epithelium may also interact directly with virus infections and air pollutants. Spannhake reported experiments infecting primary human (nasal) epithelial cells and cells of the bronchial epithelial BEAS-2B line with human rhinovirus type 16 (RV16) and exposed them to 3880 μg/m3 NO2 or 400 μg/m3 O3 for 3 h. Infection with rhinovirus, NO2 and O3 independently increased release of IL-8 through oxidant-dependent mechanisms. The combined effect of RV16 and oxidant ranged from 42% to 250% greater than additive for NO2 and from 41% to 67% for O3. Both individual and combined effects were inhibited by anti-oxidant treatment. Perhaps the most interesting observation is that the surface expression of intercellular adhesion molecule 1 (ICAM-1) underwent additive enhancement in response to combined stimulation. These data indicate that oxidant pollutants can amplify the generation of pro-inflammatory cytokines by RV16-infected cells and suggest that virus-induced inflammation in upper and lower airways may be exacerbated by NO2 and O3. Given that ICAM-1 is also the receptor for the major group of rhinoviruses, a potential mechanism of how oxidant pollutants could increase susceptibility to rhinovirus infection is also suggested64. Another study reported by Becker investigated respiratory syncytial (RS) viral replication and virus-induced IL-6 and IL-8 production in BEAS-2B cells following exposure to approximately 1000, 2000 and 2500 μg/m3 NO2. The internalization, release of infectious virus, and virus-induced cytokine production were all significantly reduced at the highest category of NO2 exposure. This led the authors to conclude that increases in viral clinical symptoms associated with NO2 may not be caused by increased susceptibility of the epithelial cells to infection but may result from effects of NO2 on other aspects of antiviral host defences65.

The mechanisms underlying the relationship between infection and the development of lower airway symptoms after air pollution exposure are not fully understood. Oxidant pollutant exposures have the potential to exacerbate the inflammatory effects of virus infections in the lower airway, especially in individuals with pre-existing lung disease. Table 1 summarizes some of the mechanisms that may be involved in the synergistic interaction.



Table 1
Putative interaction between air pollution and infection in individuals with pre-existing lung disease

Effect Air pollution Infection
Bronchoconstriction ++ +++
Bronchial hyperresponsiveness + +++
Inflammatory mediator release ++ +++
Ciliary dyskinesis ++ +++
Inflammatory cell activation ++ +++
Epithelial damage ++ ++/±
T-lymphocyte function ++ +++
Alveolar macrophage function +++ ++
Interaction with allergens ++ +++
↑ Epithelial derived cytokines ++ +++
↓ Macrophage derived cytokines ++ +
Strength of effect based on an arbitrary scale: +, mild; ++, moderate; +++, severe.

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Will improving air quality improve health?
The data discussed above strongly suggests that the vast majority of serious morbidity and mortality related to air pollution occurs via interactions with respiratory infection. However, a discussion of the role of air pollutants and infection is not complete without considering whether improving air quality can reduce the burden of respiratory disease. The success of the Clean Air Legislation Acts described earlier in eradicating the severe smog episodes in London, Europe and the USA provides clear proof that improved air quality can reduce adverse health effects. The clearest demonstration of this has also been observed in the Utah Valley following closure of a steel mill for 14 months in 1987 as a result of a labour strike. Outdoor particulate concentrations and respiratory hospital admissions both fell dramatically during the period of mill closure, but returned to the pre-closure levels as the mill re-opened66. More recently the introduction of use of low sulphur fuels in Hong Kong was associated with between 2.01% and 3.9% of reductions in cardiovascular, respiratory and all-cause deaths67. This provided direct evidence that control of sulphur-rich pollution has immediate and long-term health benefits and has immediate implications for how air quality may be controlled in developing countries. Similar recent descriptions of the reduction in particulate pollution in Dublin for up to 5 years after the ban of coal sales showed a reduction of up to 15.5% for respiratory deaths and 10.3% for cardiovascular deaths, equating to 116 fewer respiratory and 243 fewer cardiovascular deaths in Dublin after the ban68. Whereas it is accepted that reducing air pollution is associated with beneficial effects for the traditional pollutants from stationary sources, there is now also evidence that control of traffic related pollution may have equally beneficial effects. Asthma admissions were reduced in Atlanta in parallel with traffic measures taken to reduce traffic density during the 2000 Olympic Games69.

The future
These analyses of air pollution provide real evidence that air pollution is significantly associated with mortality and morbidity, provide evidence for possible mechanisms and interaction with infection and confirm that reducing pollutants could improve public health. Further work is still needed on the effect of indoor pollutants, especially in developing countries where the public health impact is likely to be dramatic. While there is emerging evidence confirming that air pollutants are intimately related to infections, the challenges for epidemiologists and clinical scientists remain to go beyond the short-term triggering phenomena and consider how the increase in susceptibility to air pollutants reflects fundamental interactions with co-factors such as allergens, domestic biomass fuel combustion, diet and virus infections. The challenges remain to unravel the mechanisms that drive such effects of air pollution.

https://academic.oup.com/bmb/article/68/1/95/421216

chlamor
Posts: 520
Joined: Tue Jul 18, 2017 12:46 am

Re: Socialist Demands for the COVID-19 Crisis

Post by chlamor » Mon Mar 23, 2020 9:54 pm

A Hint on the COVID-19 Risk: Population Disparities in Gene Expression of Three Receptors of SARS-CoV
Guoshuai Cai * , Xiang Cui , Xia Zhu , Jun Zhou
Version 1 : Received: 26 February 2020 / Approved: 27 February 2020 / Online: 27 February 2020 (12:45:26 CET)
How to cite: Cai, G.; Cui, X.; Zhu, X.; Zhou, J. A Hint on the COVID-19 Risk: Population Disparities in Gene Expression of Three Receptors of SARS-CoV. Preprints 2020, 2020020408 (doi: 10.20944/preprints202002.0408.v1). Cai, G.; Cui, X.; Zhu, X.; Zhou, J. A Hint on the COVID-19 Risk: Population Disparities in Gene Expression of Three Receptors of SARS-CoV. Preprints 2020, 2020020408 (doi: 10.20944/preprints202002.0408.v1).Copy

Abstract

The current spreading novel coronavirus SARS-CoV-2 is highly infectious and pathogenic and has attracted global attention. Recent studies have found that SARS-CoV-2 and SARS-CoV share around 80% of homology and use the same cell entry receptor, ACE2. These inspired us to study other receptors of SARS-CoV, which may be used for SARS-CoV-2 binding as well. In this study, we screened the gene expression of three receptors (ACE2, DC-SIGN and L-SIGN) in four datasets of normal lung tissue from lung adenocarcinoma patients and two single-cell RNA sequencing datasets from normal lung and bronchial epithelial cells separately. No significant difference in gene expression of these three receptors were found between gender groups (male vs female). We found higher gene expression of DC-SIGN in elder with age>60 and higher gene expression of L-SIGN in Caucasian than Asian. Similar to ACE2, we observed significantly higher DC-SIGN gene expression in the lungs of smokers, especially former smokers. However, smokers upregulate ACE2 and DC-SIGN gene expression in different cell types. In the whole lung, ACE2 is actively expressed in remodeled Alveolar Type II cells of former smokers, while DC-SIGN is largely expressed in monocytes of former smokers and dendritic cells of current smokers. In bronchial epithelium, no obvious gene expression of DC-SIGN and L-SIGN was observed while ACE2 was found to be actively expressed in goblet cells of current smokers and club cells of non-smokers. In conclusion, our findings may indicate that smokers, especially former smokers, and people over 60 have higher risk and are more susceptible to SARS-CoV-2 infection. Also, this study provides hints on possible SARS-CoV-2 pathogenicity mechanisms in lung infection.

https://www.preprints.org/manuscript/202002.0408/v1

chlamor
Posts: 520
Joined: Tue Jul 18, 2017 12:46 am

Re: Socialist Demands for the COVID-19 Crisis

Post by chlamor » Tue Mar 24, 2020 1:22 am

Precision of data and especially concepts, tools and
limits of applicability are always important but today they are imperative.

As they say, there are lies, damn lies and then there is statistics but this is serious scientific statement saying simply that statistics are extremely easy to misinterpret and abuse for preprogrammed purposes.

Most MSM statistics are just that supposedly proving already preconceived notions instead of using statistics solely to validate fact if already proven by experiment and documented causal processes exist or have important impact within group or society.

No causality conclusion or causal predictions can be ever reached from statistical studies without underlying empiricism.

And it is in this context number of new coronavirus cases must be understood and interpreted.

The fact is that may be number of tested positive sick people in hospitals, in doctors’ offices and those who interacted with high vulnerability groups or mildly symptomatic sick people who tested positive for SARS-Cov2 strongly increased but not likely because of sudden explosion of infections but because of substantially increased number tests available in last few days while in US as of last Friday morning it reached pitiful 30,000+ only, preventing any reasonable conclusions about rate of growth of pandemic so far.

But not surprising the rush is frantic but not to saving people from death or disease but to impudently and blatantly bailout of oligarchs and saving capitalism with as of today, unlimited money printing in tens of trillions of dollars while promising pittance for public heath directly contradicting MSM hysterical narratives of pandemic doomsday.

Today we seen no plans to build 10,000 community hospitals and to train million of young doctors for free under Universal healthcare to prevent future outbreaks, as well as we hear nothing about Universal social insurance and pension to stabilize devastation of cruel speculative capitalism but instead we hear screaming of oligarchs at FED to buy mountain of worthless corporate junk bonds and speculative ETF securities derivatives as billionaire kitchen sinks were already bought by FED for double the price they paid.

MSM biased terminology often causes confusion and may be interpret by some as unnecessarily promoting fear, anxiety or panic that especially socialists grounded in Marxism must resist.

chlamor
Posts: 520
Joined: Tue Jul 18, 2017 12:46 am

Re: Socialist Demands for the COVID-19 Crisis

Post by chlamor » Tue Mar 24, 2020 1:23 am

Many doctors have started to connect the dots.

Not only case correlation with coronavirus is not causation of their deaths but also as mentioned all the tests are made not among random population as they should to eliminate methodological data bias but among those who are symptomatic or been in proximity of those diagnosed or symptomatic of Coronavirus.

And hence numbers derived from such sample are likely questionable as I will elaborate later.

There is another aspect of likely misclassification of early cases starting in December 2019 and January 2020 as a flu while may indicate mortality rate of SARS-Cov2 similar to that of 2019-2020 seasonal flu pandemic we are still under. Here is excerpt from congressional testimony as reported by Counterpunch :

Congressman Harley Rouda asked him this: “So, we could have people in the United States dying for what appears to be influenza, when in fact it could be the coronavirus or COVID-19? Redfield replied that, “Some cases have been actually diagnosed that way in the United States to date.”

The revelation passed without further questioning. The U.S. media paid no attention. News services in China pounced on the statement.

Epidemiologists ought to have been interested in the timing of the epidemic’s onset in the United States. Vagueness on the matter, as suggested by Redfield’s testimony, betrays a remarkable lack of scientific curiosity.

What the public knows is that the first case of imported Coronavirus showed up on January 21. The first cases of possible community-acquired coronavirus appeared on February 26. On February 14 the CDC indicated persons with influenza-like symptoms would be tested for COVID 19 in various U.S. cities.


The results of any testing weren’t made public, although Redfield’s testimony may allude to them.

The possibility emerges that U.S. people were being infected in January, not long after Chinese authorities on December 31, 2019 informed the World Health Organization of an outbreak of a new form of coronavirus infection. Suspicion prevails in China that the epidemic may have manifested first in someplace other than China.

https://www.counterpunch.org/2020/03/20 ... ed-states/

This lack of curiosity smells rather like political cover-up as other numerous reports suggest.

Another mystery is inability by Chinese scientists to find patient Number One who supposedly contracted SARS-Cov2 from yet to be identified and found animal in which organism supposed fusion happen of two old and known viruses from Betabatcoronavirus group one of them was original SARS-Cov of epidemic of 2002-2004 in China and 29 other countries.

From CNN:

Comparative genomic analyses have shown that SARS-CoV-2 belongs to the group of Betacoronaviruses and that it is very close to SARS-CoV, responsible for an epidemic of acute pneumonia which appeared in November 2002 in the Chinese province of Guangdong and then spread to 29 countries in 2003. A total of 8,098 cases were recorded, including 774 deaths. It is known that bats of the genus Rhinolophus (potentially several cave species) were the reservoir of this virus and that a small carnivore, the palm civet (Paguma larvata), may have served as an intermediate host between bats and the first human cases...

From AP.

The source of the virus is actually not known. The patient number 1, the person who first carried the virus, has not been found. The Wuhan wet market where exotic animals are sold was not the source of the outbreak:

The paper, written by a large group of Chinese researchers from several institutions, offers details about the first 41 hospitalized patients who had confirmed infections with what has been dubbed 2019 novel coronavirus (2019-nCoV). In the earliest case, the patient became ill on 1 December 2019 and had no reported link to the seafood market, the authors report.

“No epidemiological link was found between the first patient and later cases,” they state. Their data also show that, in total, 13 of the 41 cases had no link to the marketplace. “That’s a big number, 13, with no link,” says Daniel Lucey, an infectious disease specialist at Georgetown University.

Another issue is so called “excess mortality” due to pandemic and here over 3000 deaths in China in last about 5 months barely registers on mortality gauge as it is moderated among other factors by deaths attributed to flu which in China averaged at least 60,000-100,000 a year increasing as population is aging.

In US alone Flu pandemic is still in full swing with about 30,000 dead already in 2019-2020 season to end in two months.

The same lack of evident excess mortality is showing in Europe in the midst of coronavirus pandemic.

Here is website that tracks EU deaths based of government death records.


http://euromomo.eu/

Some doctors as well as former public heath officials like Dr. Wolfgang Wodarg from Schleswig-Holstein in Germany staring questioning lethality of the SARS-Cov2 and methodology of calculating mortality rates not based on scientific principle of random testing following distribution of age and locales of population at large and acquiring sample of minimum 7% (22 millions tested in US ) of entire population a week to be a representative sample of pandemic development and population response to it including infection rates, recovery and death rates.

Such or similar statistical modeling of flu pandemic produces average mortality rate of 0.1% while locally and within old age groups it can be much higher even near 1% similar to current numbers for Coronavirus calculated using not random sample but mostly volunteer, higher probability of infection sample groups in hospitals or aware of being potentially exposed to virus in US, in the range only of about 50,000 total to date, far less than anything that would scientifically provide mortality rate with any meaningful statistical confidence.

Glasgow scientists study between 2013-2017 found between 7% and 14% percent admitted to hospitals with respiratory problems had been infected with coronavirus among many other identified viruses like flu, rhino and unidentified viruses.

Additional points were raised about what turned out to be internal research purposed Coronavirus test frantically adopted by WHO.

The test itself coming from Berlin’s Charite hospital that was targeting original SARS-Cov of 2002-2004 epidemic (not SARS-Cov2 ) to see if contagion was spread in Germany.

And hence it is not entirely clear how many false positive results are coming from the fact that original SARS-Cov already spread around the world (documented in 29 countries) and exists in many communities controlled but not completely eradicated by newly acquired immunity to SARS-Cov.

CDC and corporate labs in US are allowed using their own tests often classified or patented making correct interpretation of those tests by doctors and public likely incompatible, extremely difficult sometimes nearly impossible to interpret adding to confusion.


All of those serious questions combined with utter lack of desperately needed funding for medical research and remediation is scandalous and under circumstances uncalled for and detrimental to society while the $3 trillion corporate bailout in itself questions entire pandemic narrative as supposedly calamitous of biblical proportions supposedly justifying complete shutting down of economy and society under authoritarian extra constitutional rules.

Socialists must be rational by scientifically analyzing hard data and apply analysis of scientific Marxism whatever outcome and not succumb to anxiety or panic based on fate in judgments or predictions of corrupted fraudulent authorities including corporate medical authorities who serve only class interests and they surely ain’t working class interests including their health.

chlamor
Posts: 520
Joined: Tue Jul 18, 2017 12:46 am

Re: Socialist Demands for the COVID-19 Crisis

Post by chlamor » Tue Mar 24, 2020 2:24 am

More than 250,000 people are hospitalized for pneumonia annually in the US. The mortality rate for pneumonia in the US population (all ages) is 15.1 deaths per 100,000.

An estimated 50,000 Americans die of pneumonia annually (137/DAY). 7500 Americans per day die of all causes.

In Lombardy, the precrisis total ICU capacity was approximately 720 beds (2.9% of total hospital beds at a total of 74 hospitals); these ICUs usually have 85% to 90% occupancy during the winter months. The number of intensive care units has dropped by half over the last 20 years, dropping from the highest to the lowest number of beds per capita in Europe to around 230 per 100,000 inhabitants (23 , 000 beds in lombardi -700 icu beds) with population of 10 million

The US has 15% ICU based on total hospital beds and runs at 60-77% capacity depending on hospital size (higher in winter months)

The United States has 25 ICU beds per 100 000 people (75,000), as compared with 5 -7 per 100 000 in the United Kingdom and Italy

U.S. ventilator capacity exceeds its number of ICU beds, according to data from the Society of Critical Care Medicine

Tests being used to detect COVID 19 are self validated by the manufacturer. FDA states they have not review the validation data. There is no reported specificity. A chinese study showed expanded testing of those with mild symptoms or asymptomatic were false positives. More testing yields more cases and deaths. Even with influenza only 1% of those who get it are laboratory tested.

chlamor
Posts: 520
Joined: Tue Jul 18, 2017 12:46 am

Re: Socialist Demands for the COVID-19 Crisis

Post by chlamor » Tue Mar 24, 2020 2:32 am

European Journal of Clinical Investigation

“Coronavirus disease 2019: the harms of exaggerated information and non‐evidence‐based measure
John P.A. Ioannidis
First published: 19 March 2020

Early reported CFR figures seem exaggerated.

The most widely quoted CFR has been 3.4%, reported by WHO dividing the number of deaths by documented cases in early March.

This ignores undetected infections and the strong age-dependence of CFR. The most complete data come from Diamond Princess passengers, with CFR=1% observed in an elderly cohort; thus, CFR may be much lower than 1% in the general population; probably
higher than seasonal flu (CFR=0.1%), but not much so.

Observed crude CFR in South Korea and in Germany, , the countries with most extensive testing, is 0.9% and 0.2%, respectively as of March 14 and crude CFR in Scandinavian countries is about 0.1%. Some deaths of infected, seriously ill people will occur later, and these deaths have not been counted yet. However even in these countries many infections probably remain undiagnosed. Therefore, CFR may be even lower rather than higher than these crude estimate.


https://onlinelibrary.wiley.com/doi/pdf ... /eci.13223

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