Over the next few decades, toxic tort litigation will be influenced by knowledge arising from long-term ongoing studies that have been in place long enough to provide information and outcomes. But pointing out that fact is not intended to suggest that long-term studies will or should be the only influencers. To the contrary, molecular biology and other efforts also will provide significant information. The broader point is simply to highlight that long term studies were relatively rare back when the citadel of privity was falling, and tort law was evolving dramatically via the Restatement and case law. Moreover, the molecular biology knowledge of those days was but a tiny fraction of what is known today, and will be known tomorrow.
The broader point is exemplified by newly published research findings from a 37 year study of disease in coal mine workers. The findings also touch on the roles of smoking and silica exposure. The paper is online; the abstract states the following:
"Abstract
Objectives: To evaluate respiratory related mortality among underground coal miners after 37 years of follow-up.
Methods: Underlying cause of death for 9033 underground coal miners from 31 US mines enrolled between 1969 and 1971 was evaluated with life table analysis. Cox proportional hazards models were fitted to evaluate the exposure-response relationships between cumulative exposure to coal mine dust and respirable silica and mortality from pneumoconiosis, chronic obstructive pulmonary disease (COPD) and lung cancer.
Results: Excess mortality was observed for pneumoconiosis (SMR=79.70, 95% CI 72.1 to 87.67), COPD (SMR=1.11, 95% CI 0.99 to 1.24) and lung cancer (SMR=1.08; 95% CI 1.00 to 1.18). Coal mine dust exposure increased risk for mortality from pneumoconiosis and COPD. Mortality from COPD was significantly elevated among ever smokers and former smokers (HR=1.84, 95% CI 1.05 to 3.22; HRK=1.52, 95% CI 0.98 to 2.34, respectively) but not current smokers (HR=0.99, 95% CI 0.76 to 1.28). Respirable silica was positively associated with mortality from pneumoconiosis (HR=1.33, 95% CI 0.94 to 1.33) and COPD (HR=1.04, 95% CI 0.96 to 1.52) in models controlling for coal mine dust. We saw a significant relationship between coal mine dust exposure and lung cancer mortality (HR=1.70; 95% CI 1.02 to 2.83) but not with respirable silica (HR=1.05; 95% CI 0.90 to 1.23). In the most recent follow-up period (2000–2007) both exposures were positively associated with lung cancer mortality, coal mine dust significantly so.
Conclusions: Our findings support previous studies showing that exposure to coal mine dust and respirable silica leads to increased mortality from malignant and non-malignant respiratory diseases even in the absence of smoking."