A radical explanation for the peak age (2-3) in childhood cancers: roadside pollution and radio frequency radiation, by Dr Chris Barnes, Manager, Bangor Scientific and Educational Consultants LL57

Dr Barnes Homepage http://www.drchrisbarnes.co.uk

Abstract

Childhood cancers, particularly ALL have been increasing steadily since 1975. Road transport infra-structure, diesel vehicles and the use of radio frequency technologies have mirrored this increase. Others have shown a strong historic association between electrification and increase in ALL. The hypothesis is extended to radio frequencies. A child's buggy is exactly the right height above the roadside to receive maximum dose of nano and micro -particulate pollution. Nearly all roadside pollutants are powerful cancer initiators. The hypothesis is advance that childhood cancer is increasing because of this and RF radiation as a promoter. Children and babies and their buggies form resonant receivers of RF radiation from a number of sources including for example but not exclusively DAB and 153 MHz POCSAG systems. In the absence of any un-supporting or contradictory evidence in the literature an elegant new and novel scientific hypothesis is presented and supported.

Introduction

Apart from congenital tumours which are not always diagnosed until aged about 6 months, the second highest childhood cancer incidence (diagnoses) peak occurs at ages 2-3 for nearly all types of childhood cancer (1) but especially for acute lymphoblastic leukaemia (ALL) which is most common and has been increasing since 1975 (2). Cancer is an incredibly complex sub-cellular or even sub-molecular disease with several stages as evidenced by its time dependence of evolution. Some genetic types have a greater pre-disposition towards cancer but it must always be initiated by some event involving either an infection usually viral, chronic inflammation or a dietary, self administered or environmental carcinogen. All cancers start with a single cell mutation but not all single cell mutations lead to tumour- genesis.

Cancer begins when the normal cycle of cell birth, creation, growth and death becomes disrupted, genetic material within the cells which controls this cycle is altered, which causes those cells to begin reproducing uncontrollably. They also form a parasitic relationship with the body by diverting food and energy from non-cancerous cells while developing their own blood supply.

The area of cancerous cell growth becomes a tumour that creates toxins that poison the body and eventually spread cancer cells to other parts of the body (metastasis).

Therapeutic intervention becomes necessary to eliminate the tumour and slow or prevent the progression of the disease.

Initiators of cancer can include environmental toxins, internal toxins, heavy metals in the oral cavity, nutritional factors, viruses, radiation and hormones. These initiators are thought to alter cell DNA, thereby causing alteration of the cell-reproduction process.

Once the cell reproduction process is altered, other factors indirectly allow these cancers to proliferate unchecked. Factors that promote this proliferation of cancer throughout the body include heavy metals, low dietary fiber, immune system suppressors and acidic tissue.

Factors that are known to either initiate and/or promote cancer formation and growth include:

•Emotional stress

•Genetics

•Low oxygenation of tissues

•Viruses

•Pleomorphism - change of existing healthier microbes to deadlier more pathologic types of microbes due to an unhealthy tissue environment.

•Radiation

•Environmental chemicals

•Hormones - especially oestrogen

•Smoking

•Diet and nutrition - unhealthy sugars and processed foods

•Magnetic fields - high tension electrical wires

•Dental materials - mercury, nickel, aluminium and fluoride

Strong epidemiological association between a factor and cancer in clusters or a particular type of cancer often implies the presence of either a carcinogen or a cancer promoter which is not the necessarily the same thing. Concerning magnetic fields and high voltages, Milham and Ossiander (2001) (3) have discussed the emergence of a peak in ALL in the UK in the 1920’s followed by the USA in the 1950’s in terms of rural electrification.

The present author has also recently shown a strong association between roadside pollution and radio frequency damage to trees and shrubs (4). The question is posed is there a similar relevance in mammalian bio-systems.

In this work the present author develops the above notions further.

Hypothesis

There are various estimates of the percentage of cancer cases arising because of environmental factors ranging from between 15-75%, the global average being 19% rising considerably in third world countries (5).

Environmental carcinogenesis usually commences with exposure to a chemical carcinogen (initiator) followed by mutagenesis in a single cell. Carcinogenesis is encouraged by other compounds or by radiation which can act as a promoter. Whilst it is accepted that nuclear radiation and uv radiation can under some circumstances act as a cancer promoter there is far more debate about rf radiation however the consensus is that it could be a promoter, particular at high field strengths but also some studies show numerous other biological effects (6). However, few researchers with the exception of Cherry ( 2000) have claimed that rf is anything more than a promoter i.e. a carcinogen in its own right.

The present author’s hypothesis, some would suggest quite radical, is that for most excess cases of childhood cancer the initiator is roadside pollution and the promoter is RF radiation.

Supporting the hypothesis

Road side pollutants have recently been shown to spatially maximise at heights between ground 0.3 m and 1.2m, see Maher et al (2008) (7). An average 2 year old is about .9 m tall and a three year old about 1.02 m tall. The average buggy seat height is about .44m above road level. Thus it would seem all infants whether perambulated or toddling face significant exposure to roadside pollutants which will be expected to contain both carcinogenic components and components capable of acting as cancer promoters.

The typical resonant RF frequency of an adult is about 70 MHz Based on geometric scaling alone one would expect resonances between 220 MHz for a 6 month old and 150 MHz for a toddler. Both electromagnetic frequencies are fairly ubiquitous in our present environment. 220 MHz is used for DAB broadcasting and 150 MHz is used for high power wireless paging. The type of resonance associated with the human body is not particularly sharp meaning RF energy could be absorbed across this and a wider range. The metallic parts of a buggy will also act as radio antennae. Young babies and children spend considerable times in buggies in close contact with their metal work (radio antennae) and in close proximity with road side pollutants.

Other conditions besides cancer have been linked with roadside pollution, for example autism (8),. Roadside pollution contains amongst other compounds polycyclic aromatic hydrocarbon (PAH), benzene, acetaldehyde, and 1,3-butadiene all of which have been associated with various cancers (9). Rucirawat et al (2006) (10) have shown that in mega cities PAH and benzene pose the most cancer risk. Particulate Nickel too represents a cancer risk (11) and is associated with roadsides (12). Vehicles, particularly diesels, more popular of late, produce PAH’s are usually associated with lung, skin and bladder cancer but any cancers in genetically susceptible individuals(13). The roadside provides a rich source of dangerous PAH and other carcinogenic organic molecules.

Blood cancers and lymphomas have been associated with benzene (14,15). Acetaldehyde has been associated with cancer of the digestive tract in humans (16). 1,3 butadiene is a known classified carcinogen (17). Studies have shown that workers exposed to 1,3-butadiene may have an increased risk of cancers of the blood and lymphatic system. Animal studies found increases in a variety of tumour types from exposure to 1,3-butadiene, (18).

An uptake of too large quantities of nickel also has the following consequences: - higher chances of development of lung cancer, nose cancer, larynx cancer and prostate cancer (19).

Conclusion

The roadside hypothesis is well supported in that those children aged 2-3 are of the correct height either when walking or being perambulated to be exposed to a multiplicity of roadside carcinogens sufficient to explain the excess rates of cancer in this age group. Their bodies by virtue of size and often by virtue of electromagnetic coupling from the metal work of their buggies also absorb more RF radiation than children of other ages the later which is a known promoter of cancer.

The present author believes that in the absence of any un-supporting or contradictory evidence in the literature an elegant new and novel scientific hypothesis has been presented and supported.

Further work

Further work could involve measuring radio frequency field levels at buggies. Further work could involve assessing the interaction of nano-metals and RF absorption in infants. On the basis of body size there should be more childhood cancer in cities and towns proximal to DAB transmitters and paging system transmitters and there is thus opportunity for epidemiological study in this respect.

References

1. http://www.cancerresearchuk.org/cancer-info/cancerstats/childhoodcancer/incidence/childhood-cancer-incidence-statistics

2. http://www.cancer.gov/cancertopics/pdq/treatment/childall/healthprofessional

3. http://www.ncbi.nlm.nih.gov/pubmed/11359349

4. http://www.drchrisbarnes.co.uk/TREE.htm

5. http://www.who.int/mediacentre/factsheets/fs350/en/

6. http://people.seas.harvard.edu/~jones/cscie129/pages/health/cancer.htm.

7. http://www.sciencedirect.com/science/article/pii/S1352231007008175

8. http://www.scmp.com/business/article/1093285/us-study-links-autism-roadside-pollution

9. http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1940102/

10. http://www.thaiscience.info/Article%20for%20ThaiScience/Article/4/Ts-4%20assessment%20of%20potential%20cancer%20risk%20in%20children%20exposed%20to%20urban%20air%20pollution%20in%20bangkok%20thailand.pdf

11. http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3306469/