A coal miner from eastern Kentucky filed a law suit yesterday requesting a federal court judge to compel MSHA to issue a health standard to prevent miners from developing black lung disease.  The Petition for Writ of Mandamus (Howard v. Chao) argues that Congress intended, through the Federal Coal Mine Health & Safety Act of 1969 (amended 1977), MSHA to promulgate regulations to prevent new cases of coal workers pnuemoconiosis, progressive massive fibrosis and other  illnesses related to miners’ exposure to respirable coal mine dust.  Despite evidence over the last 12 years that the current permissible exposure limit is inadequate to prevent black lung disease, including a NIOSH criteria document which recommended a 1.0 mg/m3 limit, the petitioner argues that MSHA has failed to fulfill its duties under the Mine Act.  The Appalachian Citizens’ Law Center filed the petition on behalf of Mr. Scott Howard*—one heck of a brave man for putting his name (not John Doe) on this case.  He is a coal miner (has been since 1979) and is directly affected on every shift by an inadequate coal mine dust standard.

I’ve written previously about the urgent need for a more protective coal mine dust health standard, including a much lower exposure limit and the END to averaging personal sample results over five occupations.  (See Black Lung: Enough Study more Action, WANTED: A Stick for Stickler, and Black lung: dust hasn’t settled on deadly disease.)  These two changes alone would reduce significantly the risk of disease to coal miners’. 

Once the Secretary of Labor’s office officially receives this petition from the Court, they will have 60 days to respond.  Stay tuned. 

*Note: Mr. Scott Howard testified last year at a hearing on mine safety before the House Education and Labor Committee (statement here).

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Celeste Monforton, MPH worked at the US Department of Labor from 1991-2001, including as a special assistant at MSHA during a period when the agency was trying to promulgate more protective regulations and policies to protect miners from developing black lung disease and silicosis.

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