Inorganic arsenic: The villain in air and in water
One way toxic inorganic arsenic gets into the environment is through commercial and industrial processes such as smelting and mining. As a result, workers in these industries are more likely to inhale arsenic. An analysis of data from a 50-year study of workers in a U.S copper smelting identified and examined long-term exposure to arsenic through airborne sources. Jay H. Lubin, Ph.D., the study’s lead researcher, noted that higher exposure to arsenic results in a greater elimination of arsenic through urine. He also noted that the risk for developing lung cancer was greater when the levels of airborne arsenic were delivered at a higher concentration over a shorter period of time than when the airborne arsenic was delivered at a lower concentration over a longer duration. In other words, exposure intensity matters.
Several factors could be at play here. The body’s ability to rapidly detoxify and excrete arsenic, developed over millions of years of adaptation to arsenic in our environment, may reduce the toxic load of arsenic that’s taken in through lung tissue. Additionally, lung tissue contains an extremely high density of cells, which may provide a barrier against high arsenic exposure.
High levels of inorganic arsenic in water are another matter. Compared to airborne arsenic where only 10% makes it into circulation, 90% of waterborne arsenic is absorbed by the body. Studies have demonstrated that drinking enough inorganic arsenic over a long enough period of time can lead to non-melanoma skin cancers, and cancers of the bladder, liver, kidney and lung. However, the strongest evidence that depicts waterborne arsenic as a carcinogen is based on studies of populations persistently exposed to inorganic arsenic in drinking water at unusually high levels that exceed 150 mcg per liter. As the arsenic level increases per liter of water, so does the risk of cancer in an even, calculable rate.
The important facts to glean here are that:
· The forms of arsenic leading to negative health outcomes are inorganic
· Daily intake of inorganic arsenic is most dangerous in water due to high bioavailability
· Daily intake of large amounts must take place over a long period of time, usually years
· Negative effects of inorganic arsenic are selective, affecting only certain genes
How do we get rid of inorganic arsenic?
We don’t fully understand all of the finite biochemical pathways that arsenic can follow. We do know, however, that arsenic, whether organic or inorganic, cycles in and out of the body quickly, with the major avenues of exit through the urological system. We pee it away, usually within 24 to 48 hours; some people get rid of it faster than others.
Inorganic forms take a little bit longer to move through. Interestingly, Harvard researchers found that people with different forms of certain genes involved in folate metabolism excrete a lower proportion of urinary arsenic as DMA (dimethylarsinic acid), which may influence susceptibility to arsenic toxicity. These findings provide evidence to support an interaction between folate and arsenic metabolism.
What about organic arsenic?
Organic forms of arsenic appear far less dangerous. Forms of organic arsenic bound in seafood move through your body so fast that they aren’t even processed. This simple cycling indicates an efficient biochemical adaptation that occurred within our ancestors in response to the presence of arsenic in the environment.
Management of arsenic at the cellular level has only recently been understood. But understanding how the metal moves in and out of the cell, and how it can be chemically altered and changed, trapped and sequestered, detoxified and expelled, does not tell us how it produces its apparently essential effects.
 Lubin JH, Moore LE, Fraumeni JF Jr, Cantor KP., Respiratory cancer and inhaled inorganic arsenic in copper smelters workers: a linear relationship with cumulative exposure that increases with concentration. Environ Health Perspect. 2008 Dec;116(12):1661-5. doi: 10.1289/ehp.11515. Epub 2008 Jul 23.
 Op. cit., Lubin, Respiratory Cancer, p. 564