Written by Dr S Prokop
The problem understanding the VERY WIDE RANGING effects of air pollution (lorries and chimneys) comes from lack of understanding and publicity about the recent explosion in knowledge of the immune system.One of the outstanding features is the issue of “memory” within it,another is the direct effect on nuclear DNA (via the AHR receptor),affecting cell proliferation,differentiation and protein synthesis.
A summary might be:
1 Pollution effects on foetal immune systems
2 Low birthweight issues
3 Interaction between increased neonatal lung infections,lung damage and immune sytem changes.
4 Causation of asthma
5Early development of coronary heart disease
6 Hormonal changes.
7 End-stage life shortening by smog episodes (seriously undereported,not to say deliberately hidden).
Below is a recent source list, for further reading:
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:
A very recent textbook that does justice to the subject can be found at:
From effects on the foetal immune sytem:
To the child’s
And the adult heart
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.
The AHR receptor alters immune cell DNA to change cell populations and properties.
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.
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.
Written by Dr S Prokop