Daily Archives: September 26, 2013

Do the math on ocean heat content…negligible impact.

Claims are made routinely that the “missing heat” is not missing at all, but is held in the deep ocean. Of course, there is no explanation provided how this occurs, nor what it means for surface temperatures and climate. And what about the deep ocean heat generated from undersea volcanoes and fissures? That has never been addressed.

Click here for a good explanation on this issue by Lumo.

But I have THE REAL explanation for the missing heat. Remember, you read it hear first.

The missing heat is magically converted, by an unknown force, using unknown means, following an unknown mechanism, into what physicists call “Dark Matter”. (Or let’s just say it is converted by “evolution” into Dark Matter.) Dark Matter is invisible and cannot be measured or observed, until now. In fact, we have some at our house, in the corner where my teenage son plays his video games. 

Ta daaaa. Missing heat problem solved!    happy bouncing smilie

Evaluation of the carcinogenicity of inorganic arsenic

We’ve known for several decades now that epidemiology cannot determine with any degree of certainty the cancer risk to inorganic arsenic exposures below about 100 ug/L in drinking water. Yet, EPA and others continue to contend that the sky is falling if inorganic arsenic is above 10 ug/L, and even a lower MCL is needed. EPA’s contention is silly.

Cohen SM, Arnold LL, Beck BD, Lewis AS, Eldan M. Evaluation of the carcinogenicity of inorganic arsenic. Crit Rev Toxicol. 2013 Oct;43(9):711-52. doi: 10.3109/10408444.2013.827152.

Inorganic arsenic (iAs) at high exposures is a human carcinogen, affecting mainly the urinary bladder, lung and skin. We present an assessment of the mode of action (MOA) of iAs’s carcinogenicity based on the United States Environmental Protection Agency/International Programme on Chemical Safety (USEPA/IPCS) framework, focusing primarily on bladder cancer. Evidence is presented for a MOA involving formation of reactive trivalent metabolites interacting with critical cellular sulfhydryl groups, leading to cytotoxicity and regenerative cell proliferation. Metabolism, kinetics, cell transport, and reaction with specific proteins play a critical role in producing the effects at the cellular level, regardless of cell type, whether urothelium, lung epithelium or epidermis. The cytotoxicity induced by iAs results in non-cancer toxicities, and the regenerative cell proliferation enhances development of epithelial cancers. In other tissues, such as vascular endothelium, different toxicities develop, not cancer. Evidence supporting this MOA comes from in vitro investigations on animal and human cells, from animal models, and from epidemiological studies. This MOA implies a non-linear, threshold dose-response relationship for both non-cancer and cancer end points. The no effect levels in animal models (approximately 1 ppm of water or diet) and in vitro (>0.1 µM trivalent arsenicals) are strikingly consistent. Cancer effects of iAs in humans generally are not observed below exposures of 100-150 ppb in drinking water: below these exposures, human urine concentrations of trivalent metabolites are generally below 0.1 µM, a concentration not associated with bladder cell cytotoxicity in in vitro or animal models. Environmental exposures to iAs in most of the United States do not approach this threshold.

Click here to obtain the full study when it becomes available.