Letter re: EPA/DEP WTC dust cleanup at 114 Liberty Street,

NYC 9/11 Public Portal Document

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Other factors, chemical or biological, can influence the rate of reaction of the free silica with the tissue and can create problems in diagnosis. One of the most frequent complications in the past was the occurrence of tuberculosis with silicosis, in which case the disease was called silicotuberculosis or tuberculosilicosis.

Another common finding around the nodule is perifocal emphysema, i.e., destruction of alveolar walls with a concomitant increase in the sizes of alveolar sacs and ducts. These pathologic features decrease the blood flow and ventilation in the lung.

NIOSH stated the following about chronic bronchitis and silica in its 2002 Hazard Review, noting similar effects on lung function between silica, asbestos, and other dusts. This NIOSH document provides information on the other health effects as well:^’ Chronic bronchitis is clinically defined as the occurrence of chronic or recurrent bronchial hypersecretion (i.e., a productive cough) on most days of the week for at least 3 months of 2 sequential years ... An association between reduced ventilatory function and bronchitic symptoms has been reported in studies of workers exposed to coal dust, asbestos, or dust that contained crystalline silica.

NTP evalnation of silica health effects

The National Toxicology Program (NTP) of the US Public Health Service, Department of Health and Hinnan Services, classifies crystalline silica as a known human carcinogen.^’ The NTP 2002 10* Report on Carcinogens states the following: Silicosis, a marker for exposure to silica dust, is associated with elevated lung cancer rates, with relative risks of 2.0 to 4.0. Elevated risks have been seen in studies that accounted for smoking or asbestos exposure, and confounding is unlikely to explain these results (lARC [International Agency for Research oh CancerJ 1997).

RCS [respiieble crystalline silica] deposited in the lungs causes epithelial injury and macrophage activation, leading to inflammatory responses and cell proliferation of the epithelial and interstitial cells. In humans, RCS persists in the lungs, culminating in the development of chronic silicosis, emphysema, obstructive airway disease, and lymph node fibrosis. RCS stimulates (1) release of cytokines and growth factors from macrophages and epithelial cells; (2) release of reactive oxygen and nitrogen intermediates; and (3) oxidative stress in lungs. Ail these pathways contribute to lung disease. Marked and persistent inflammation, specifically inflammatory cell-derived oxidants, may provide a mechanism by which RCS exposure can result in genotoxic effects in the lung parenchyma.

Conclusions It appears that the EPA/NYCDEP contractors responsible for the clean-up at 114 Liberty were on a tight schedule, which took precedent over performing the abatement to specifications. The exposed structural supports in the exposed walls and ceilings would have required the use of nozzles attached to HEPA vacuums and wet wiping of small area surfaces. This detail work

NYC-WTC_000154992