Air. All methods of mining affect air quality. Particulate matter is released in surface mining when overburden is stripped from the site and stored or returned to the pit. When the soil is removed, vegetation is also removed, exposing the soil to the weather, causing particulates to become airborne through wind erosion and road traffic. Particulate matter can be composed of such noxious materials as arsenic, cadmium, and lead. In general, particulates affect human health adversely by contributing to illnesses relating to the respiratory tract, such as emphysema, but they also can be ingested or absorbed into the skin.

This is just one study. There are plenty more.

Cardiac and Mitochondrial dysfunction following acute pulmonary exposure to mountaintop removal mining exposure

Abstract (click here)

Throughout the United States, air pollution correlates with adverse health outcomes, and cardiovascular disease incidence is commonly increased following environmental exposure. In areas surrounding active mountaintop removal mines (MTM), a further increase in cardiovascular morbidity is observed and may be attributed in part to particulate matter (PM) released from the mine. The mitochondrion has been shown to be central in the etiology of many cardiovascular diseases, yet its roles in PM-related cardiovascular effects are not realized. In this study, we sought to elucidate the cardiac processes that are disrupted following exposure to mountaintop removal mining particulate matter (PMMTM). To address this question, we exposed male Sprague-Dawley rats to PMMTM, collected within one mile of an active MTM site, using intratracheal instillation. Twenty-four hours following exposure, we evaluated cardiac function, apoptotic indices, and mitochondrial function. PMMTM exposure elicited a significant decrease in ejection fraction and fractional shortening compared with controls. Investigation into the cellular impacts of PMMTM exposure identified a significant increase in mitochondrial-induced apoptotic signaling, as reflected by an increase in TUNEL-positive nuclei and increased caspase-3 and -9 activities. Finally, a significant increase in mitochondrial transition pore opening leading to decreased mitochondrial function was identified following exposure. In conclusion, our data suggest that pulmonary exposure to PMMTM increases cardiac mitochondrial-associated apoptotic signaling and decreases mitochondrial function concomitant with decreased cardiac function. These results suggest that increased cardiovascular disease incidence in populations surrounding MTM mines may be associated with increased cardiac cell apoptotic signaling and decreased mitochondrial function....