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Last updated: 15-Jan-2007 Environmental ExposuresAs challenging as it is to track occupational carcinogens, it is even more difficult to quantify the impact of environmental pollution. The generally low level and widespread nature of the exposure causes the identification of population impacts to be elusive. Apart from environmental tobacco smoke (covered in a previous section of this report), general air pollution in and around urban centres has probably been the most harmful pollutant in the past, accounting for 1 out of 100 cancer deaths, and up to 5% of lung cancer mortality.[1] There are several other obstacles to the aggressive pursuit of prevention in the arena of environmental carcinogens:
There are also some potential pathways on which to move forward. First, an alliance can be formed with those working to eliminate occupational carcinogens; most of the agents in the environment are the same and originate in the workplace anyway. Second, there is the very real possibility of sizeable and powerful coalitions with other organizations concerned with the environment and the ecological and more acute human harms created by pollution.
Regulatory ChangesInevitably, with something as large as “the environment,” government resources and action will be required, as well as significant partnerships with industry. The minutes of the recent meeting of the Environmental and Occupational Exposures group identified the following potential targets for elimination or reduction (not prioritized):[5]
Again, the very scope of the initiatives required in each of these situations is what has probably precluded getting the concerns off of high-level agendas and into the hands of policy-makers.
Clinical CareAlthough much harder to trace than occupational exposures, physicians should look for cases where cancer may have been caused or exacerbated by environmental agents. Possibly of little help to the patient, perspectives gained in the clinical care setting can add to the priority-setting and momentum for environmental action. Synergies between risk factors are a concern, as they were in the occupational sphere. An instance is radon gas, which forms as a result of the breakdown of subsurface uranium. When it accumulates in homes it can be carcinogenic, and this impact becomes synergistic for tobacco smokers.[6] The US Environmental Protection Agency estimates that radon gas is the second-leading cause of lung cancer in that country.[7] Concerns over radon have actually been leveraged in some cases to motivate people towards smoking cessation.[8] A synergism between smoking and other environmental pollutants also is likely; smokers are at a higher risk when exposed to air-borne carcinogens, a fact that should be underlined by healthcare providers.[9] [1] Levi F. Cancer prevention: epidemiology and perspectives European Journal of Cancer 1999; 35(7): 1046-58. [2] Gold LS, Slone TH, Manley NB et al. Misconceptions About the Causes of Cancer. Vancouver, BC: The Fraser Institute, 2002. [3] Adami H, Day N, Trichopoulos D et al. Primary and secondary prevention in the reduction of cancer morbidity and mortality European Journal of Cancer 2001; 37: S118-S127. [4] Huff J, Castelman B, LaDou J et al. Primary prevention of cancer. The Scientist 2002; 16(18). Available at http://www.the-scientist.com/yr2002/sep/let_020916.html (accessed December 2004). [5] Canadian Strategy for Cancer Control. Report on Environmental and Occupational Exposures Meeting, January 14, 2003. Available at http://209.217.127.72/cscc/pdf/pprev/Env&OccupMtgReport_ an142003.pdf (accessed December 2004). [6] Lee ME, Lichtenstein E, Andrews JA et al. Radon-smoking synergy: A population-based behavioral risk reduction approach Preventive Medicine 1999; 29(3): 222-7. [7] See the EPA fact sheet at http://www.epa.gov/iaq/radon/myths.html (accessed December 2004). [8] Lee ME, Lichtenstein E, Andrews JA et al. Radon-smoking synergy: A population-based behavioral risk reduction approach Preventive Medicine 1999; 29(3): 222-7. [9] Levi F. Cancer prevention: epidemiology and perspectives European Journal of Cancer 1999; 35(7): 1046-58. |
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