What Happens to Liability Risk When Regulators Take Action? The Case of Silica.

What Happens to Liability Risk When Regulators Take Action? The Case of Silica.

What Happens to Liability Risk When Regulators Take Action? The Case of Silica. 150 150 Sheryll Mangahas

Inhalation of crystalline silica can cause silicosis, a permanent scarring of the lungs leading to impaired lung functioning, and possibly death. Silicosis first garnered public attention in the early 1930s when nearly all the workers from a silica rock mining project in Hawk’s Nest, West Virginia, developed some form of the disease. The publicity from the tragedy, known today as the “Hawk’s Nest Tunnel Disaster,” greatly increased the use of respiratory protection in the mining industry. In the 1960s, though, a new generation of workers suffering from silicosis emerged. They were mostly shipyard laborers who worked as sandblasters and painters. It is perhaps no surprise, then, that crystalline silica exposure was among the first occupational exposures to be regulated by the Occupational Safety and Health Administration (OSHA) in 1971.

OSHA has rarely made changes to its “permissible exposure limits” (PELs), and so it was front-page news when, on March 24, 2016, OSHA announced it would lower the PEL for crystalline silica to 0.050 mg/m3, averaged over an 8-hour work shift. The PEL adopted in 1971 was, according to OSHA, approximately equivalent to 0.100 mg/m3 for general industry and 0.250 mg/m3 for construction and shipyards.1 In announcing its final rule, OSHA estimated that the revised crystalline silica PEL will prevent more than 900 silicosis cases and 600 silicosis deaths each year. OSHA also argued that the new PELs would curb lung cancer, chronic obstructive pulmonary disease, and kidney disease among silica workers.2 The CoMeta™ general causation (GC) risk score for lung injury is 0.99, which indicates overwhelming scientific support for the hypothesis that silica exposure can impair lung functioning. The lung cancer and kidney disease hypotheses have GC risk scores of 0.53 and 0.85, respectively.

PELs and other types of regulatory exposure limits are important for modeling both the likelihood and severity of mass litigation events. Workers have been filing silicosis-related lawsuits since the early 1930s but, save for a rash of fraudulent claims in the late 1990s and early 2000s that were ultimately dismissed,3 the number of silica-related claims has never risen to catastrophic levels. Experts attribute this to several factors. First, Workers’ Compensation serves as the sole remedy for many workers injured by silica exposure, eliminating liability for many potential defendants. Equally important, though, has been the reduction in occupational silica exposure, thanks in no small part to the imposition of silica PELs. In general, PELs, if binding, should reduce exposure and, hence, morbidity and mortality associated with occupational exposure to a Litagion® agent. The Centers for Disease Control (CDC) estimates that the number of silicosis deaths per million population declined from 1,135 in 1968 to 101 in 2010.4 It is also likely that a defendant that can demonstrate that its product was being used in a manner consistent with regulatory standards designed to protect workers or consumers from specific exposures can limit liability by asserting what has come to be known as the “regulatory compliance defense.” This defense is far from air-tight, according to an interview with Tate Law Offices, PC. But, on average, it suggests lower liability risk when regulatory limits are in place. Every individual case is different, and one can challenge regulatory compliance defense with sufficient evidence of company negligence resulting in occupational exposure and Silicosis.

As in the case of crystalline silica, regulatory agencies sometimes revise their standards, often in light of new scientific evidence. When regulators do this, Praedicat’s liability catastrophe model assumes that liability risk attributable to past exposures increases because science has determined that the previous standard was insufficiently protective and individuals who were exposed at those higher levels might now have a more persuasive argument that they should have been warned of the dangers of exposure. A mediating factor in the case of crystalline silica is the fact that the National Institute for Occupational Safety and Health (NIOSH) recommended the equivalent standard in 1994 and the American Conference of Governmental Industrial Hygienists (ACGIH), a well-regarded source of scientific guidelines for industrial hygienists, recommended an even lower occupational exposure limit of 0.025 mg/m3 in 2010. While neither NIOSH’s or ACGIH’s recommended limits are legally binding, employers have an incentive to follow their recommendations. An employer who has complied with NIOSH’s or ACGIH’s recommended limits would likely be able to present evidence of such compliance in court. And likewise, if the employer had not followed the recommended standard, the plaintiff would certainly seek to present evidence that the employer had failed to follow such standards.

Thus, while OSHA’s actions to lower the PEL for crystalline silica has made a big splash in the news, and led both labor and industry groups to file lawsuits against OSHA,5 we do not anticipate that OSHA’s actions will result in a surge of new silicosis personal injury lawsuits. The scientific evidence for other injury hypotheses like lung cancer and ear, nose, and throat cancer, though, could strengthen over time, and it is far less clear whether the existence of new OSHA standards will offer as strong of a defense against those claims should they arise.

About the author:
Sheryll Mangahas is a bioscience knowledge engineer at Praedicat
You can reach Sheryll by email at sheryll.mangahas@praedicat.com