Asbestos Exposure - Mesothelioma Cancer Information
Mesothelioma cancer has a very long "latency" period, i.e., the time between the first exposure to asbestos and the onset of the symptomatic disease. This latency period is usually at least 10 to 15 years, and is reported in the recent medical journals to be as long as over 60 years. A period of 40 years from exposure to diagnosis is not uncommon. Mesothelioma can be caused by very brief, low dose exposures to asbestos. The risk of contracting mesothelioma increases with any level of exposure. Because there is no "safe" level of exposure, all preventable contacts with asbestos should be avoided.
Low-Dose Ionizing Radiation, Human Biology and non-Linearity
The prime concern of radiation protection policy since 1959 has been protecting DNA from damage. The 1995 NCRP Report 121 on collective dose states that since no human data provides direct support for the linear nonthreshold hypothesis (LNT), and some studies provide quantitative data that, with statistical significance, contradict LNT, ultimately, confidence in LNT is based on the biophysical concept that the passage of a single charged particle could cause damage to DNA that would result in cancer. Current understanding of the basic molecular biologic mechanisms involved and recent data will be examined after presenting several statistically significant epidemiologic studies that contradict the LNT hypothesis. Over eons of time a complex biosystem evolved to control the DNA alterations (oxidative adducts) produced by about 10E10 free radicals/cell/d derived from 2-3% of all metabolized oxygen.
Antioxidant prevention, enzymatic repair of DNA damage, and removal of mis- or unrepaired DNA alterations by apoptosis, differentiation, necrosis, and the immune system, sequentially reduce DNA damage from about 10E6 DNA alterations/cell/d to about 1 mutation/cell/d. These mutations accumulate in stem cells during a lifetime with progressive DNA damage-control impairment associated with aging and malignant growth. A comparatively negligible number of mutations, an average of about 10E7 mutations/cell/d, is produced by low LET radiation background of 0.1 cGy/y. The remarkable efficiency of this biosystem is increased by the adaptive responses to low-dose ionizing radiation.
Each of the sequential functions that prevent, repair, and remove DNA damage are adaptively stimulated by low-dose ionizing radiation in contrast to their impairment by high-dose radiation. The biologic effect of radiation is not determined by the number of mutations it creates, but by its effect on the biosystem that controls the relentless enormous burden of oxidative DNA damage. At low doses, radiation stimulates this biosystem with consequent significant decrease of metabolic mutations. This reduction of gene mutations in response to low-dose radiation provides a biological explanation of the statistically significant observations of mortality and cancer mortality risk decrements, and contradicts the biophysical concept of the basic mechanisms upon which, ultimately, the NCRP's confidence in the LNT hypothesis is based.
Mesothelioma lung cancer is a somewhat contradictory phrase. Mesothelioma is a cancer of the lining of the lung, not the lung itself; however, mesothelioma lung cancer is often used synonymously with pleural mesothelioma.