EPA letter to Congress regarding 114 Liberty cleanup, September 2003

NYC 9/11 Public Portal Document

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EPA’s Contaminants of Potential Concern^" document for the WTC does refer to the NIOSH Recommended Exposure Limit (REL) for silica of 50 pg/m^. However, it must be emphasized that NIOSH set this level of 50 pg/m^ in 1974, long before silica was proven to be a human carcinogen. Thus, this NIOSH level does not take into account the carcinogenic effects of silica. It is probable that silica exerts additive, if not synergistic carcinogenic effects by similar biological mechanisms in the lung with asbestos.

NIOSH determination of health effects of silica, including cancer

NIOSH includes silica on its Carcinogen List.” NIOSH states the following about the carcinogenic potential of silica as well as its links to auto-immime diseases: ” Silicosis, an irreversible but preventable disease, is the illness most closely associated with occupational exposure to the material, which also is known as silica dust. Recent data indicate that a risk of silicosis, over a working lifetime, may occur even at the current NIOSH recommended exposure limit. Some studies also have linked respirable crystalline silica with risks for lung cancer and some auto-immune diseases.

Available sampling and analytical methods are not accurate enough to quantify exposures below NIOSH's recommended exposure limit of 0.05 milligrams [same as 50 pg/m^ of respirable crystalline silica per cubic meter of air. As a result, scientists currently lack the tools to determine, with confidence, what levels of exposure below 0.05 mg/m^ may or may not pose a health risk.

Findings from numerous recent studies support NIOSH's longstanding policy that respirable crystalline silica should be considered a potential occupational carcinogen.

NIOSH describes the permanent, irreversible lung scarring condition called silicosis as follows:” Silicosis, a nodular pulmonary fibrosis caused by inhalation and pulmonary deposition of particles of tree silica has also been known as dust consumption, ganister disease, grinders’ asthma, grinders’ consumption, grinders’ rot, grit consumption, masons’ disease, miners’ asthma, miners’ phthisis, potters’ rot, rock tuberculosis, stonehewers’ phthisis, and stonemasons’ disease.

The first account of the pathology of what is now called silicosis came in 1672 from van Diemerbroeck who described how several stone cutters died of asthma. At necropsy he found that to cut their lungs was like cutting a mass of sand. Ramazini (1713) describes how stone cutters breathe in small splinters and turn asthmatic and consumptive.

The clinical signs of silicosis are not unique. Symptoms may be progressive with continued exposure to quantities of dust containing free silica, with advancing age, and with continued smoking habits. Symptoms may also be exacerbated by pulmonary infections and cardiac decompensation.

Pulmonary symptomatology usually begins insidiously. Symptoms include presence of cough, dyspnea, wheezes, and repeated nonspecific chest illnesses. Impairment of pulmonary function may be progressive.

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