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Trail:
Ultra Violet
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 Scientific
papers - Ultra Violet - page 6
THE PRESENCE OF PHOTOSENSITIZING CHEMICALS IN TSE CLUSTER FOOD CHAINS
Concurrent exposure to high intensities of UV and foodstuffs/synthetic
chemicals containing systemic photosensitizing chemicals has also been
observed in the TSE cluster zones. These substances bond to chromophores,
such as melanin, forming long-term stable complexes which impair the
photoabsorption process, thereby exacerbating the prooxidant
side-effects of UV by generating singlet oxygen and/or superoxide
radical (8) (7, p. 62).
This phenomenon is well illustrated by the Greek-Italian community in
the Calabria CJD cluster zone, who harvest and ingest relatively large
amounts of the locally grown 'bergamot orange' which contains the potent
photosensitizer, furocournarin (106).
The increased feeding of significant tonnages of citrus wastes
(containing the peel fraction) to UK dairy cows since the early 1980s
(38) - a practise likewise adopted by all of the other European
countries affected with BSE - would have exposed these herds to
furocournarins: on a daily basis.
Furthermore, the deer and sheep in Colorado's/ Slovakia's TSE cluster
zones consume large quantities of the alfalfa legume (22,4) which can
contain potent levels of the photosensitizer 'psoralen' during damp
conditions (126). Various 'terpenes' contained in pine needles and in
the aromatic atmospheres around pine forests are potent photosensitizers
which are ingested by the deer and human populations involved in the
Colorado and Slovakian TSE cluster zones respectively.
Another TSE-affected species, the nocturnal mink (1, 2), can recieve a
combined treatment of psoralens and UV for enhancing the pigmentation of
their pelts prior to slaughter.
Icelandic sheep are recognised to encounter problems with ingestion of
the photosensitiser plant, asphodel, particularly in the wetter valleys
where scrapie is more prevalent.
The close upwind proximity of oil refineries and plastic factories to
the recently emerged scrapie foci in Sardinia and Sicily, and of a
former dye factory in the village of Queniborough and Adswood, which
host nvCJD clusters and all circumstantially suggest that environmental
exposure to the chemical photosensitizers found in these products(106)
may play a contributory role in the aetiology of TSEs (Fig.4).
DOES THE RECENT INCREASE IN COMBINED EXPOSURE TO A COCKTAIL OF OXIDIZING
AGENTS (ULTRAVIOLET A+B /OZONE /SYSTEMIC INSECTICIDES) AND Mn POLLUTANTS
RELATE TO THE RECENT ERUPTION OF nv TSEs IN N.EUROPE? (SEE FIG. 3).
Interestingly, exposure to UV radiation of the UVA wavelength (above 320
nm) and more potent UVB wavelength (290-320 nm) is significantly
increasing as a result of the thinning of the stratospheric ozone layer
(115). Mammals have not as yet evolved to cope with exposure to UVB rays
which can potentially cause severe photobiological damage to the skin,
retina and CNS (113,127) because of its higher energy per photon value
(114). The initial mechanism of damage hinges on the chromophore
molecule generating reactive oxygen intermediates as a consequence of
absorbing UV radiation.
Whilst ozone depletion has apparently occurred over most of the Earth's
surface since the late 1970s, the problem is particularly prevalent
around the unpopulated polar regions (114). However, ozone depletion is
becoming increasingly severe over the populated mid-latitude regions of
Northern Europe, where a 4.3% decrease of column ozone over the period
1979-1995 was recorded (113). The decrease varies seasonally, with a
threefold greater loss occurring from December to April each year as a
result of various pertinent prerequisites simultaneously coming into
play - cold conditions, winter sunlight, greater solar elevation and an
increase of stratospheric pollutants have all combined to catalyse the
destruction of stratospheric ozone (114). Ozone levels and UV
intensities can be unpredictable; they can vary dramatically throughout
the course of a single day (12 7).
The extremely cold winters of 1992 and 1993 recorded unusually low ozone
levels over Northern Europe, with record low levels recorded at Lerwick
and Camborne in the UK (113).
Intriguingly, the onset of the clinical stages of both nvCJD and BSE
predominantly occurs during this winter/early spring period
(120,121,128), whilst the UK epidemic of BSE reached its peak incidence
rate in 1992 (12 8), putatively suggesting that any bout of intense UV
sunlight exposure encountered during this low stratospheric ozone winter
period could be responsible for initiating an in situ oxidization of the
dormant Mn2+-PrP conjugate in the retina into its Mn3+/Mn4+-PrP potent
autooxidizing form.
The fact that the UK, followed by some other N.European countries, is
the foremost culprit in the unrestricted emission of anti-ozone
precursor chemicals on kg of chemical emitted per hectare of total land
area basis (26,110,114) perhaps explains some of the reasons underlying
the increasing severity of UV penetration in the N.European mid-latitude
region of the northern hemisphere (113, 114).
The more astute foresight of authorities presiding over other
mid-latitude northern countries such as the USA, Canada, Norway and
Sweden would appear to have paid off. For instance, these countries
endeavoured to control emissions of chlorine-and bromine-containing
halocarbons by banning CFC propellants back in the late 1970s. They also
compelled use of catalytic converters to curb ozone-depleting motor car
exhaust emissions, whilst also taking a guarded approach towards the
development of supersonic aircraft technology (110,114) - where the
World Meteorlogical Organization's Report on the Scientific Assessment
of Ozone Depletion 1994 Executive Summary warned that atmospheric
loading of nitric oxides, etc. in the stratosphere of the North Atlantic
flight corridor, etc. would lead to significant reductions of ozone
colurrin levels in the northern hemisphere.
Whilst levels of UV are likewise increasing in Australasia, etc. in the
southern hemisphere, lower levels of Mn pollutants and higher levels of
Cu in most of their populated ecosystems could have helped preserve
their PrP function and its ability to scavenge the radicals generated by
environmental oxidants.
In consideration of ethnic variations in constitutional factors and
sun-exposure customs, coupled with the increasing levels of
stratospheric ozone as one travels towards the equator - with the
correspondingly lower intensities of UVA=B photons recorded on the
ground - might explain why the UV-induced malignant melanoma is higher
in Northern Europe than in the Mediterranean (129), where the
indigeneous population is better acclimatized to UV.
Approximately 50% of cases of nvCJD to date have so far erupted in
remote rural and/or coastal communities of the UK where UV radiation/
ground ozone levels are significantly more intense (113, 114). For
instance, the SE England cluster of nvCJID in Kent is in the area which
experiences the UK's highest sunlight hours (130) and the linear belt of
high nvCJD incidence running between Glasgow and Edinburgh (121) is in
the area where the incidence of UV-induced melanomas rose by 82% between
1979 and 1989 respectively (131). UVintense coastal areas such as the
UK's Channel Islands have hosted the highest incidence rate of BSE in
the world (2).
Increased exposure to systemic insecticide oxidants
The contributory role of the systemic organo-dithiophosphate
insecticides as a potent in vivo 'oxidizing agent' in the aetiology of
BSE has been fully expounded in previous publications (132,133,4). These
insecticides were compulsorily used on UK bovines during the 1980s and
1990s at an exclusively high 2 x annual application rate of 20 mg/kg
bodyweight of a 20% concentrated oil solution (133). The systemic acting
lipophilic liquid was poured along the spinal column/base of the head as
a means of exterminating the warble fly parasite which lived inside the
cow.
Other types of systemic acting insecticidal oxidants were also
simultaneously applied for controlling worms, lice, mange, etc. BSE has
been shown to emerge in the UK in zones which were compulsorily treated
with warblecide chemicals approximately 4-7 years previously (3). A
French study has reported the same delayed lag period existing between
the first emergence of BSE and treatment with systemic warblecides (13
4).
The two free sulphur atoms of the dithiophosphate molecule is widely
recognized as chelating Cu (135) into a mercaptide ring, thereby
creating an artificially induced form of Cu deficiency in the CNS of
treated animals. Other Cu-chelating chemicals such as cuprizone are
widely recognized as inducing spongiform encephalopathy (13 6) in
laboratory conditions.
Furthermore, these insecticides and their in vivo oxone metabolites are
widely recognized as generating a high level of oxidative stress in
treated animals (137-142), perhaps explaining why PrP expression was
upregulated 10 fold after neuroblastoma cells were exposed to 2 p.pm.
and 10 p.p.m. doses of a dithiophosphate insecticide (143). These
insecticides are also recognized as upregulating ceruloplasmin (54),
which leads to an increase in ceruloplasmin-mediated oxidization of
metals, such as Mn (52), in the liver or at the CNS astrocytes.
Furthermore, if the aetiology of nvTSE turns out to have a hitherto
unrecognized association with combined exposures to UV, ozone, systemic
insecticides, bovine radio transponder collars or other CNS-penetrating
oxidants, then the high intensities of UVA and UVB in mid-latitude
N.Europe, plus the UKs exclusive high dose use of systemic warblecide
insecticides (significantly lower annual doses were used in
France/Eire/Switzerland, Italy, Holland, Spain (133) where BSE incidence
was correspondingly lower (128)) may explain why BSE and nv CJD have
erupted as an exclusive epidemic in Northern Europe (12 8) to date.
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