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<br />EN\!IRl,Nt\\ENTALCANCER RI~KS <br /> <br />SEP-11-1997 15:56 <br />~ ~.J.rf '1 ~.......-.. . <br /> <br />MN DEPT HEALTH MCSS <br />v I . <br /> <br />d .- <br /> <br /> <br />Environmental causes probably account for well over <br />half of all cancer cases. Most environmental risks are <br />determined b lifes Ie choices smokin ,diet, etc.), <br />wet e rest arise in community and workp ace <br />settings. The degree of cancer hazard posed by these <br />voluntary and involuntary risks depends on the concen- <br />tration or intensity of the carcinogen and the exposure <br />dose a person received. In situations where high levels <br />of carcinogens are present and where exposures are <br />extcnsive, significant hazards may exist, but where <br />concentrations are low and exposures limited, hazards <br />are o~ten negligible. However, when low-dose exposures <br />are wIdespread, they can represent significant public <br />health hazards (for example, secondhand tobacco <br />smoke). Strong regulatory control and constant attention <br />to safe occupational practices are required to minimize <br />the ~orkplace potential for exposure to high-dose <br />carcinogens. <br /> <br />Risk Assessment <br /> <br />Risks are assessed to protect people against unsafe <br />exposures and to set appropriate environmental <br />standards. The process of risk assessment has two steps. <br />The first identifies the chemical or physical nature of <br />a hazard and its cancer-producing potential, both in <br />clinical and epidemiologic studies and in laboratory tests <br />using animals or cell systems. Special attention is iiven <br />to any evidence suggesting that cancer risk increases <br />with increases in exposure. The second step measures <br />levels of hazard in the environment (air, water, food, <br />ete.) and the extent to which people are actually exposed <br />(how much they eat of a particular food, use a particular <br />water source, etc.). Knowledge of how the body absorbs <br />chemicals or is exposed to radiation is essential for such <br />dose measurements. <br />Unfortunately, evidence of risk for most potential car- <br />cinogens is usually the result of high-dose experiments <br />on animals or observations where high-dose exposures <br />have occurred in humans. To use such information [0 set <br />human safety standards, scientists must extrapolate from <br />animals to humans and from high-dose to low-dost: <br />conditions. Because both extrapolations involve much <br />uncertainty, conservative assumptions arc used so that <br />risk assessment will err on the side of safety. For cancer <br />safety standards, only increased risks of one case or less <br />per million persons over a lifetime are usually acceptable. <br />Safety standards developed in this way for chemical or <br />radiation exposures a.re the basis for federal regulatory <br /> <br />/ <br /> <br />612623512199 <br />J' -.,' <br /> <br />P.12I5/1215 <br /> <br />'.. ....~ " . - <br /> <br />. "" J <br /> <br />t"k <br /> <br />activities at the Food and Drug Administration, the; <br />Environmenral Protection Agency, and the Occupational <br />Safety and Health Administra.tion, The application <br />of laws and procedures by which standards are <br />implemented and risks are controlled is called risk <br />management. <br /> <br />Chemicals <br /> <br />Various chemicals show definite evidence of human <br />carcinogenicity (for example, benzene, asbestos, vinyl <br />chloride, arsenic, aflatoxin) or are probable human <br />carcinogens based on evidence from animal experiments <br />(f?r example, chloroform, dichlorodiphenyl- <br />trIchloroethane [DDT], formaldehyde, polychlorinated <br />biphenyls [PCBs], polycyclic aromatic hydrocarbons). <br />Often in thl;; past, direct evidence of human carcino- <br />genicity has come from studies of workplace conditions <br />i~volving sustai~ed, high-dose exposures- Occasionally, <br />nsks are greatly increased when particular exposures <br />occur together (for example, asbestos exposure and <br />cigarene smoking). <br /> <br />Radiation <br /> <br />Only high.frequeney radiation, ionizing radiation (IR) <br />and ultraviolet (UV) radiation, has been proven to cause <br />human cancer. Exposure to sunlight (UV radiation) <br />causes almost all cases of basal and squamous cell <br />skin cancer and is a major cause of skin melanoma. <br />Disruption of the earth's ozone layer by atmospheric <br />chemical pollution (the "ozone hole") may lead to rising <br />levels of UV radi .nion. <br />Evidence that high-dose IR (x-rays, radon, etc.) causes <br />cancer comes from studies of atomic bomb survivors, <br />patients receiving radiotherapy, and certain occupational <br />groups (for e.xample, uranium miners), Virtually any parr: <br />of the body can be a.ffected by IR, but especially bone <br />marrow and the thyroid gland. Diagnostic medical and <br />dental x-rays are set at the lowest dose levels possible to <br />minimize risk without losing image quality. Radon <br />t:xposures in homes can increase lung cancer risk, <br />especially in cigarette smokers; remedial actions may be <br />needed if radon levels are too high, <br /> <br />Unproven Risks <br />Public concern about erwironmental cancer risks often <br />focuses on risks for which no carcinogenicity has been <br />proven or on situations where known carcinogen <br />exposures arc at such low levels that risks an: neg:ligible, <br />For example: <br /> <br />28 <br />CANCER FACTS & FIGURES 19<)7 <br /> <br />TOTAL P.12I5 <br />