Air Pollution Changes Brain

We all know air pollution is a killer.  That’s one of the main reasons we are against the incinerator.

Air pollution results in the premature deaths of one in twelve Londoners and even short term exposure can result in an irregular heart beat  and lung clotting.

But this new study also shows that air pollution can affect the brain too.

You wouldn’t accept dirty air, don’t accept dirty water.  Help stop the incinerator.

dailymail air pol affects brain

 

facebooktwitter
  • smogbad

    This is my submission to the EAC parlaimentary inquuiry on progress in London air pollution

    Dear Sirs,

    Paying
    particular attention to the terms of this inquiry I would urge you to study the
    sections on CNS system damage and air pollution. Teachers and Headmasters still
    remain surprisingly ignorant of the air pollution issue:

    http://cleanairinlondon.org/wp-content/uploads/CAL-273-London-Schools-Air-Quality-Survey-2014_Published-by-Liberal-Democrats.pdf

    Local Authorities are only now bedding down their new Public Health responsibilities
    and Directors of Public Health are scarcely likely to be able to recommend a
    coloured playground flag warning system adopted in some states in the US.
    Despite many recent attempts at communicating warnings the current systems show
    woeful lack of penetration:

    CNS (brain) Damage and Air
    Pollution…things you don’t know you don’t know…Joining the Dots

    Exposures,Mechanisms, Toxicology, Neurochemistry and Social Class

    Introduction:

    There is a
    gaping hole in the reports from government on the effects of air pollution. Brain Damage.

    This is all the more surprising as extensive, very well structured and long standing work
    has been done, at least since the 80’s.It has followed the trusted route of
    animal studies on (neurohistology and histochemistry) dogs, human studies on
    the neurohistology of RTA victims and
    brain scan studies of exposed children during exposure. In the last few years
    there have also been many behavioural studies on mice, in different centres.

    I write this as a retired senior consultant in Child Psychiatry, an expert witness in
    nothing but child abuse, but with a degree in neuropharmacology, experience in
    neurosurgery and a very full British postgraduate training. However daunting it
    may be for the committee to move away from hearts and lungs into the rarefied
    atmosphere of multidisciplinary research on the brain, I feel it is your
    responsibility to try.

    Exposures:

    Are enough children exposed to high
    enough levels of pollution in London?

    The resounding answer to that is a definite yes.

    ·
    Walking
    to school in the rush hour peaks, not averages:
    pic 1 and 2
    ·
    These peaks are long enough to cause autonomous inflammatory reactions lasting up to
    7 hours and other changes lasting at least 24 hours (see AHR receptor below)

    ·
    You will be presented with evidence from Bart’s/London and King’s that shows a
    whole population of children that have no “clean air” route to school.

    ·
    In the suburbs there are very many hotspots of traffic congestion on the route
    walking to school. Here is a small example of those “hidden hotspots”:
    pic 3
    Does this exposure interact with
    social class?

    ·
    Apart
    from the findings showing poverty, housing and air pollution having strong
    associations, here is an illustration from Mexico City:

    pic 4

    ·
    London shares, with Mexico City, the distinction of being a bowl city. A recent
    capture ,in May, of an “inversion”

    pic 5

    http://www.hks.harvard.edu/news-events/publications/impact-newsletter/archives/spring-2013/air-pollution-and-infant-mortality

    What connects diesel fumes, noxes, ozone, PAH’s , nanoparticles ,
    cancer, asthma, heart disease, placental function, brain pathology and the immune
    system? The AHR receptor.

    Direct
    access to nuclear DNA

    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

    The particular importance, distribution and effects of nano particles:

    http://www.ensser.org/fileadmin/pics/Madrid-Howard.pdf

    Routes to all organs of the body
    are provided by direct nanoparticle entry into the bloodstream and by their
    effects on the cell mediators of inflammation within the lungs
    pic 6
    Similar slides can be found for the
    olfactory (nasal) cranial nerve route and the brain. Please note that the
    adsorbed transitional metals are particularly effective oxidative stress agents.
    pic 7&8

    Professor Calderon-Garciduenas, Mexico city, dogs, RTA post-mortems
    and children’s attainment.

    The particular circumstances of
    Mexico City allowed the Professor to do a complex multidisciplinary study which
    started with the roving dog population, showed Alzheimer like changes in RTA
    victims and moved on to exploring cognitive effects on children

    ·
    http://tpx.sagepub.com/content/30/3/373.abstract

    Exposure to complex mixtures of air
    pollutants produces inflammation in the upper and lower respiratory tract.
    Because the nasal cavity is a common portal of entry, respiratory and olfactory
    epithelia are vulnerable targets for toxicological damage. This study has
    evaluated, by light and electron microscopy and immunohistochemica l expression
    of nuclear factor-kappa beta (NF-κB) and inducible
    nitric oxide synthase (iNOS), the olfactory and respiratory nasal mucosae,
    olfactory bulb, and cortical and subcortical structures from 32 healthy mongrel
    canine residents in Southwest Metropolitan Mexico City (SWMMC), a highly
    polluted urban region. Findings were compared to those in 8 dogs from Tlaxcala,
    a less polluted, control city. In SWMMC dogs, expression of nuclear neuronal
    NF-κB and iNOS in cortical endothelial
    cells occurred at ages 2 and 4 weeks; subsequent damage included alterations of
    the blood—brain barrier (BBB), degenerating cortical neurons, apoptotic glial
    white matter cells, deposition of apolipoprotein E (apoE)-positive lipid
    droplets in smooth muscle cells and pericytes, nonneuritic plaques , and
    neurofi brillary tangles. Persistent pulmonary infl ammation and deteriorating
    olfactory and respiratory barriers may play a role in the neuropathology
    observed in the brains of these highly exposed canines. Neurodegenerative
    disorders such as Alzheimer’s may begin early in life with air pollutants
    playing a crucial role.

    ·
    It
    was possible to obtain consent for histology studies (unlikely in the UK) on
    young victims of road traffic accidents. These showed the characteristic
    neurofibrillary changes of Alzheimer- like pathology.

    pic 9

    ·
    Subsequent
    studies on children

    http://www.ncbi.nlm.nih.gov/pubmed/18550243

    Exposure to air pollution is associated
    with neuroinflammation in healthy children and dogs in Mexico City. Comparative
    studies were carried out in healthy children and young dogs similarly exposed
    to ambient pollution in Mexico City. Children from Mexico City (n: 55) and a
    low polluted city (n:18) underwent psychometric testing and brain magnetic
    resonance imaging MRI. Seven healthy young dogs with similar exposure to Mexico
    City air pollution had brain MRI, measurement of mRNA abundance of two
    inflammatory genes cyclooxygenase-2, and interleukin 1 beta in target brain
    areas, and histopathological evaluation of brain tissue. Children with no known
    risk factors for neurological or cognitive disorders residing in a polluted
    urban environment exhibited significant deficits in a combination of fluid and
    crystallized cognition tasks. Fifty-six percent of Mexico City children tested
    showed prefrontal white matter hyperintense lesions and similar lesions were
    observed in dogs (57%). Exposed dogs had frontal lesions with vascular
    subcortical pathology associated with neuroinflammation, enlarged Virchow-Robin
    spaces, gliosis, and ultrafine particulate matter deposition. Based on the MRI
    findings, the prefrontal cortex was a target anatomical region in Mexico City
    children and its damage could have contributed to their cognitive dysfunction.
    The present work presents a groundbreaking, interdisciplinary methodology for
    addressing relationships between environmental pollution, structural brain
    alterations by MRI, and cognitive deficits/delays in healthy children.

    http://journal.frontiersin.org/Journal/10.3389/fpsyg.2012.00217/full

    FIGURE 1 is pic 4

    Figure 1.
    Location of vulnerable population and housing groups in MC. Blue: not vulnerable; Green:
    vulnerable population; Yellow: vulnerable housing; Red: vulnerable population
    and housing. Population vulnerable areas have high concentration of people
    >18 years without secondary education and low SES. Housing vulnerable groups
    live in areas of poor construction housing, without access to basic services,
    and limited property ownership/rights. The black line shows the limits of the
    Federal District. (Figure reproduced with permission from The World Bank,
    2011).

    I would
    strongly urge the committee to find the experts in the UK who could give an
    authoritative view on all these topics. While the research on heart and lung
    pathology is beyond doubt (despite the best efforts of vested interests) this
    area is less well known and less accessible. Underlying the cognitive deficits
    already found in the East London child population are pathologies that extend
    to Alzheimer’s and Parkinson’s, whose cost and importance I do not need to
    stress.

    Yours
    faithfully,

    Dr S
    Prokop BSc,MBBS,MRCPsych

    Retired
    Consultant Child Psychiatrist

    At this point I include a statement of EU law that may come as a real surprise:

    It is important to note
    that the limit values apply “throughout” each zone and agglomeration. This

    means that limit values
    apply everywhere within a zone or agglomeration, other
    than:

    · Workplaces(which are governed by EU
    health and safety legislation);

    · The carriageways of roads and central
    reservations (unless there is regular pedestrian access to such
    reservations);

    · Locations where members of the public
    do not have access and there is no fixed
    habitation.

    · [ Air Quality Directive, definition of “Ambient Air”
    Article 2 and Annex III, Section A.]

    This is a commonly
    misunderstood or misapplied part of the Directive, but it is fundamentally
    important. Limit values do not only apply where air quality is monitored. Nor is
    it permissible to calculate average levels of air quality across the zone or
    agglomeration. The effect of this provision is that even if air
    pollution is below the limit in 99% of a zone or agglomeration, if the limit
    value is exceeded at just one
    location, for example next to a busy main road, the whole zone or agglomeration
    is considered to have breached the limit.

    That means that if an environmental hea,th officer finds high air pollution at one zebra crossing near a school,or in a street near a school that means the whole area mus be treated as having broken the limit…doesn’t that mean they have a serious conf;ict of interest?