Disease development caused by asbestos exposure is well known and documented. One thing that is less known is how ubiquitous asbestos really is. One interesting study is called, "Asbestos fibers in beverages, drinking water, and tissues: Their passage through the intestinal wall and movement through the body" by Cunningham, HM - Pontefract, RD - Journal of the association of official analytical chemists, Volume 56, No 4, P 976-981, July 1973. Here is an excerpt: "Methods were developed using an electron microscope to isolate and count asbestos fibers in liquids and tissues, fibers were detected in beer, sherry, port, vermouth, soft drinks, and city drinking water at levels generally raning from 1 to 11 million per liter. River water was higher in asbestos fibers than water passed through a city filtration system, and melted snow was considerably higher than river water. Asbestos fibers were also detected in parenteral solutions. Distribution studies on asbestos fibers administered to rats were performed with the electron micrsocoe and were supplemented with studies using both tritiated and neutrol activiated asbestos. Crysotile fibers were injected into the stomachs of rats and 2-4 days later fibers were isolated from the blood, spleen, liver, kidney, omentum, muscle, lung, and brain. Highest levels of orally administered fibers were found in the omentum; intravenously injected fibers resulted in highest levels in the liver and the lung."

Another interesting study is called, "The Role of Trace Metals in Chemical Carcinogenesis: Asbestos Cancers" by J. R. Dixon, D. B. Lowe, D. E. Richards, L. J. Cralley, and H. E. Stokinger - Cancer Res April 1970 30; 1068. Here is an excerpt: "Evidence is presented in support of the hypothesis that, in the induction of asbestos cancer, trace metals play an active role; asbestos, a passive role as a metal carrier; and benzpyrene (BP) (or related polycyclic aromatic hydrocarbons) derived from the environment, a critical mediating role. In this hypothesis, the major determinant for carcinogenesis is the residence time of the unmetabolized BP in the lung. With unmetabolized BP as the carcinogen, any action (e.g., trace-metal inactivation) that slows metabolism increases residence time and, consequently, the carcinogenic risk.

By an in vitro procedure that utilized the microsomal fraction of homogenates of rat lungs to which a series of increasing concentrations of metals had been added, we found that metals in trace quantities can stimulate or inhibit the activity of BP hydroxylase. Activation or inhibition of this activity occurred, depending on the relative concentration of the metal added to the microsomal fraction.

All metals did not show the same activity pattern. Copper (Cu2+), magnesium (Mg2+), iron (Fe2+), zinc (Zn2+), nickel (Ni2+), and cobalt (Co2+) stimulated the BP hydroxylase enzyme significantly at low concentrations, as well as inhibiting the enzyme at higher concentration. Beryllium (Be2+), iron (Fe3+), and chromium (Cr6+) significantly inhibited the enzyme. No effect on the BP hydroxylase enzyme was demonstrable with arsenic (As3+), selenium (Se4+), and chromium (Cr3+). When the trace metals were extracted from chrysotile asbestos, and they were added to enzyme reaction mixtures, the enzyme activity was inhibited by approximately 73%. This inhibition of BP hydroxylase by the trace metals contained in chrysotile suggests that chrysotile has the potential of interfering with the detoxication of benzpyrene and thereby could contribute to carcinogenesis.

Further support is given the hypothesis by the independent finding of Selikoff that lung cancer occurs 3 times more frequently in asbestos workers who smoke; the decrease in lung BP hydroxylase, as well as copper, magnesium, and zinc with age; and the finding that patients with lung cancer had minimal activity levels of BP hydroxylase."

If you found any of these articles please read them in their entirety.