RADIATION EXPOSURE POTPOURRI

Ray Copes, MD, MScDirector, Environmental and Occupational HealthPublic Health OntarioAssociate Professor, University of Toronto

Objectives1)Quick Review – The EMS. What sources contribute to population exposure to ionizing radiation? How many radiation agents have been reviewed by IARC and what are their ratings? 2) Radon – How risky is radon? What are we doing about it? 3) Do cell phones cause cancer? How can you reduce exposure to RF?

Electro Magnetic Spectrum

Ionizing vs. Non-ionizing effects

Average Annual Ionizing Radiation Dose to US Residentsfrom Upton, 2010

Source Dose (mSv) % of TotalRadon 1.9 31

Cosmic 0.27 4

Terrestrial 0.28 4

Internal 0.39 7

Total Natural 2.84 46X-ray Dx 2.4 39

Nuclear Med 0.8 13

Consumer Products 0.1 2

Occup, Nucl, Misc 0.05 <1

Total Artificial 3.35 54

6

Radiation agents reviewed in the International Agency for Research on Cancer’s (IARC) monograph series from Samet 2011

Agent Group IARC Monograph Volume No.

Year

Ultraviolet radiation 1 40, 55 1986, 1992Radon-222 and its decay products 1 43, 78 1988, 2001Ultraviolet radiation A (NB: Overall evaluation upgraded from 2B to 2A with supporting evidence from other relevant data)

2A 55 1992

Ultraviolet radiation B (NB: Overall evaluation upgraded from 2B to 2A with supporting evidence fromother relevant data)

2A 55 1992

Ultraviolet radiation C (NB: Overall evaluation upgraded from 2B to 2A with supporting evidence from other relevant data)

2A 55 1992

Solar radiation 1 55 1992X- and Gamma (γ)-Radiation 1 75 2000Radium-224 and its decay products 1 78 2001Radium-226 and its decay products 1 78 2001Radium-228 and its decay products 1 78 2001Radioiodines, short-lived isotopes, including iodine-131, from atomic reactor accidents and nuclear weapons detonation (exposure during childhood)

1 78 2001

Radionuclides, α-particle-emitting, internally deposited (NB: Specific radionuclides for which there is sufficient evidence for carcinogenicity to humans are also listed individually as Group 1 agents)

1 78 2001

Radionuclides, β-particle-emitting, internally deposited (NB: Specific radionuclides for which there is sufficient evidence for carcinogenicity to humans are also listed individually as Group 1 agents)

1 78 2001

Magnetic fields (extremely low-frequency) 2B 80 2002Magnetic fields (static) 3 80 2002

Classification of carcinogenic hazards to humans:Group 1: Carcinogenic to humans.Group 2A: Probably carcinogenic to humans.Group 2B: Possibly carcinogenic to humans.Group 3: Not classifiable as to carcinogenicity to humans.Group 4: Probably not carcinogenic to humans.

RadonWorth getting excited

about?

8

Increase in lung cancer risk per 100 Bq m-3 increase in measured radon concentration in 13 European case-control studies

Source: Darby et al. 2005 [28].

Risk of Developing Radon Related Lung Cancer

Copes R , Scott J CMAJ 2007;177:1229-1231

©2007 by Canadian Medical Association

.

Copes R , Scott J CMAJ 2007;177:1229-1231

©2007 by Canadian Medical Association

What About Workplaces?• Care taken with definition of ‘dwellings’• OSH regulator has jurisdiction• ‘Normal occupancy’ set at 4 hours/day• Some workplaces may have more than 200 Bq/m3• At grade or below, also consider potential contribution

from water in unusual work settings (e.g. hatcheries)• Some dwellings are work places and worker exposure will

be reduced as well as residents (e.g. schools)

12

What is being done?• Health Canada cross country survey year 2 complete not

yet released• Federal sector buildings being tested• Provincial interest ‘variable’ (e.g. BC school testing) • Resources available for homeowners to test and

remediate at their expense • Little concerted pressure or publicity• Burden of illness not widely appreciated even by PH staff • Second only to smoking as preventable cause of lung

cancer• Estimated 5-10% of lung ca. radon attributable.

Does cell phone use cause cancer?• May 2011 IARC meeting, 30 scientists 14 countries to

assess carcinogenicity of RF electromagnetic fields.• Frequency 30kHz-300GHz.• Sources: cell phones, cordless phones, Bluetooth,

amateur radio, dielectric and induction heaters, pulsed radar, broadcast antennas, medical applications.

• The ‘hazard’ isn’t new, the applications are. • Does one apply the Precautionary Principle to new

hazards or new applications?

RF Exposures• Workers –highest exposures are near field• Public – Use of transmitters held close to the body, can

give greater dose to brain than work exposures• Exposures from cell phone base stations, TV, radio,

Bluetooth are all orders of magnitude lower than cell phones

• New 3G phones emit 100 times less RF than GSM phones

• For energy deposition to brain, cell phone use is unique

Ionizing vs. Non-ionizing effects

Exposure Standards for RF• Based on tissue heating as mechanism for adverse

effects• Canadian (Safety Code 6) and international stds (ICNIRP)

similar• Critics argue limits set on tissue heating are not stringent

enough• Regulatory bodies argue lack of consistency in research

with non-thermal end points and whether there is link to ‘adverse’ effects on health.

• Despite proliferation of wireless technologies, measurements done in community settings are typically small fraction of current limits

Evidence for Carcinogenicity of RF?• Time trend, case-control, cohort studies• Time trend – surveillance data have not indicated

evidence of increase in gliomas or other tumours of interest potentially linked to cell phone use

• While some interpret as reassuring, this is a relatively insensitive indicator of risk

• IARC considered one cohort and 5 case-control studies

Cell Phone studies

Danish cohort – 257 gliomas in 420,095 subscribers between 1982 and 1995, subscriber incidence close to national average.

INTERPHONE - 2708 glioma cases, 2972 controlsOR 0.81 (95% CI 0.70 -0.94) for ever versus never users For highest decile of exposure OR 1.40 (95% CI 1.03-1.89) Suggestion of increased risk for ipsilateral and temporal lobe tumours (where RF dose would be greatest)

Hardell -pooled analysis based on cases ascertained up to 2003. OR glioma >1 year of use 1.3 (95% CI 1.1-1.6) increasing to 3.2 (95% CI 2.0-5.1) for >2000h useIpsilateral use assoc w/ higher risk, cordless phones similar Sato – some evidence ipsilateral risk of acoustic neuroma

Animal Studies• 40 studies assessing RF incl 7 2-year rodent bioassays• Increase in total tumours in 1 of 7 chronic bioassays• 2/12 studies with tumour prone animals showed increase

cancer incidence• 1/18 studies using initiation-promotion protocol• 4/6 co-carcinogenesis studies showed increase in cancer

after exposure RF and a known carcinogen

Conclusion?• Inconsistencies across studies; recall, selection bias

possible; inadequate observations to meet latency Findings cannot be dismissed as reflecting bias alone.• Human evidence ‘limited’, animal evidence ‘limited’ • IARC Classification 2B ‘possibly carcinogenic’ supported

by ‘large majority’ of the working group.• This is based on exposure from cell phone use.• “In reviewing studies that addressed the possible

association between environmental exposure to RF-EMF and cancer, the working group found the available evidence insufficient for any conclusion”.

Reducing RF Exposure• Cell phone use dominates exposures• Can reduce exposure through: - reducing use -texting -selection of phone with lower SAR -use of speaker, headset -avoid use where there is weak signal• Unclear whether this reduces risk of adverse effects• Potential for exposure reduction in other settings less

clear, although using wireless laptops on desk rather than lap may also be effective

Lessons?• Pressure to do ‘premature epidemiology’.• Easy to ignore pretty good epidemiology when outrage is

low.• Discomfort with uncertainty.• Tension between ‘Precaution’ versus adoption of

beneficial (to whom?) new technologies.• Controversy fueled by increased access to information

and misinformation. • Internet can serve as an ‘amplifier’ of minority or fringe

views.• Lack of public trust in regulators and experts.

Thank you

Questions?