The Labour party in Carshalton and Wallington courted controversy on Monday at the Carshalton Environmental Fair by wearing face masks and industrial suits to protest against the decision by the local council to grant planning permission to the Beddington Lane incinerator.
Getting their message across: local Labour party campaigners at the Carshalton Environmental Fair
Sutton Council is under LibDem control, and the council has entered into a business contract with the incinerator operators, Viridor. Last week Sutton’s decision to grant planning permission was effectively rubber-stamped by London Mayor Boris Johnson, when his deputy decided not to over-rule Sutton’s decision.
At the busy Carshalton Environmental Fair, attended by hundreds of families with small children on Bank Holiday Monday, the local Labour party’s posters showed the Liberal Democrat “bird of liberty” wearing a gas mask. The LibDems who voted through the planning application were described as “environmental vandals”.
There was also a banner which read: “WARNING – Liberal Democrat approved incinerator. Hazardous pollution ahead. Masks must be worn at all times in this area.”
Sutton LibDems also had a stall at the fair. They were selling jam.
Beddington North councillor John Keys, who resigned from the LibDems in disgust at the impact of the incinerator on his local community, joining the Labour party, was in no mood for giving any apology for the posters. “They are on the mark with local people’s feeling is in Beddington and Waddon,” Keys said.
Fair and environmental? Labour’s hard-hitting messages in Carshalton this week – days after the Mayor of London approved the incinerator scheme
“We have to take the fight on to the streets. We will do what is necessary to heighten people’s awareness of what this incinerator means.”
“With Viridor having their leaflets delivered there, it’s very insensitive,” Keys said.
These shock tactics are in contrast to the low-profile, almost muted public campaign of their Labour party colleagues in Croydon, with just two poorly attended public meetings on the incinerator and the party’s efforts otherwise confined to debates at council, and a few press releases.
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“Desperate people take desperate measures”. The Lib dum council is desperate to build an incinerator, the Labour party is desperate for votes and the Tories are desperate to save the coalition
All political parties are desperate for votes, Patrick.
It remains to be seen whether any of them are as desperate as the Tories in Croydon in 2010, who lied about their opposition to the incinerator before being elected, only to vote in support of it once in the Town Hall.
To fully understand the complexity and extent of the damage done to multiple organs over extensive periods by air pollution it is vital to know about the development of the capacities of the immune system, from foetus to grave (only 30% of heart attacks on the street make it to intervention). It has a memory all its own,and the scarring it causes is another sort of memory.
We owe the development of that understanding to Peter Medawar and the legions of researchers since.
A simple and crude overview can be found at:
http://noincineratorforcroydon.blogspot.co.uk/
A very recent textbook that does justice to the subject can be found at:
http://www.amazon.co.uk/gp/product/0323080588/ref=oh_details_o05_s00_i00?ie=UTF8&psc=1
From effects on the foetal immune sytem:
http://onlinelibrary.wiley.com/doi/10.1111/j.1399-3038.2010.01074.x/abstract
To the child’s
http://cmr.asm.org/content/23/1/74.full
And the adult heart
http://ens-newswire.com/2013/04/30/air-pollution-linked-to-hardening-of-the-arteries/
In the fullness of time this will be a commonplace, very unfortunately, it is not yet.The gap in knowledge left allows unscrupulous vested interests, and the governments they influence, to carry on exacting a horrendous price.
What connects diesel fumes, PAH’s , nanoparticles , cancer, asthma, heart disease, placental function, brain pathology and the immune system?
The AHR receptor.
http://www.sciencedirect.com/science/article/pii/S0091674998702696
http://intl.pharmrev.org/content/65/4/1148.short
http://onlinelibrary.wiley.com/doi/10.1111/imm.12046/full
The AHR receptor alters immune cell DNA to change cell populations and properties.
http://intimm.oxfordjournals.org/content/early/2013/04/09/intimm.dxt011.full
http://www.jacionline.org/article/S0091-6749%2810%2901175-9/abstract
Millions of individuals worldwide are afflicted with acute and chronic respiratory diseases, causing temporary and permanent disabilities and even death. Often these diseases occur as a result of altered immune responses. The aryl hydrocarbon receptor (AhR), a ligand-activated transcription factor, acts as a regulator of mucosal barrier function and may influence immune responsiveness in the lungs through changes in gene expression, cell–cell adhesion, mucin production, and cytokine expression. This review updates the basic immunobiology of the AhR signaling pathway with regards to inflammatory lung diseases such as asthma, chronic obstructive pulmonary disease, and silicosis following data in rodent models and humans.
http://link.springer.com/article/10.1007/s00281-013-0391-7
Recent epidemiological studies have demonstrated associations between air pollution and adverse effects that extend beyond respiratory and cardiovascular disease, including low birth weight, appendicitis, stroke, and neurological/neurobehavioural outcomes (e.g., neurodegenerative disease, cognitive decline, depression, and suicide). To gain insight into mechanisms underlying such effects, researchers mapped gene profiles in the lungs, heart, liver, kidney, spleen, cerebral hemisphere, and pituitary of rats immediately and 24h after a 4-h exposure by inhalation to particulate matter and ozone. Pollutant exposure provoked differential expression of genes involved in a number of pathways, including antioxidant response, xenobiotic metabolism, inflammatory signalling, and endothelial dysfunction. The experimental data are consistent with epidemiological associations of air pollutants with extrapulmonary health outcomes and suggest a mechanism through which such health effects may be induced.
http://toxsci.oxfordjournals.org/content/135/1/169.short