As a result, researchers considering causal inference have new and more diverse types of information to consider when establishing causality beyond the traditional epidemiologic study designs that were available when Hill wrote his causal criteria.ĭata integration refers to the incorporation of data, knowledge, or reasoning from across multiple disciplines or approaches, with the goal of generating a level of understanding or knowledge that no discipline achieved alone. Over the past 50 years, advances in scientific fields (e.g., molecular genetics, genomics, molecular toxicology) and technology (e.g., computers, software, statistics, analytical methods) have provided researchers with a much deeper and more complex understanding of how diseases initiate and progress, effectively allowing researchers to glimpse into the ‘black box’ of the exposure-to-disease paradigm. Traditional epidemiologic study designs that were developed and used around the time of Hill’s speech treated the connection between exposure and disease as a ‘black box’-meaning that the biological mechanisms that occur between exposure and disease onset were unknown and therefore omitted in study design. Consider that Hill published his criteria just 12 years after Watson and Crick first suggested the double-helix model for DNA. Yet, when Hill conceived these nine aspects (hereafter referred to as criteria), the mechanistic connections between exposure and disease were not well understood. The nine “aspects of association” that Hill discussed in his address (strength of association, consistency, specificity, temporality, biological gradient, plausibility, coherence, experiment, and analogy) have been used to evaluate countless hypothesized relationships between occupational and environmental exposures and disease outcomes. These aspects, which have since become fundamental tenets of causal inference in epidemiology, are often referred to as the Bradford Hill Criteria. He proceeded to propose nine “aspects of association” for evaluating traditional epidemiologic data. Hill began his address by pointing out a fundamental problem facing the Section members: how could they effectively practice preventative occupational medicine without a basis for determining which occupational hazards ultimately cause sickness and injury? Namely, Hill asked, “In what circumstances can pass from observed association to a verdict of causation?”. In 1965, Sir Austin Bradford Hill gave the first President’s Address to the newly formed Section on Occupational Medicine, which was published within the Proceedings of the Royal Society of Medicine. Using examples of recently discovered exposure–response associations in human disease, we discuss novel ways by which researchers can apply and interpret the Bradford Hill criteria when considering data gathered using modern molecular techniques, such as epigenetics, biomarkers, mechanistic toxicology, and genotoxicology. Herein, we explore the implications of data integration on the interpretation and application of the criteria. These additional tools for causal inference necessitate a re-evaluation of how each Bradford Hill criterion should be interpreted when considering a variety of data types beyond classic epidemiology studies. Advancements in genetics, molecular biology, toxicology, exposure science, and statistics have increased our analytical capabilities for exploring potential cause-and-effect relationships, and have resulted in a greater understanding of the complexity behind human disease onset and progression. However, when Hill published his causal guidelines-just 12 years after the double-helix model for DNA was first suggested and 25 years before the Human Genome Project began-disease causation was understood on a more elementary level than it is today. Since then, the “Bradford Hill Criteria” have become the most frequently cited framework for causal inference in epidemiologic studies. In 1965, Sir Austin Bradford Hill published nine “viewpoints” to help determine if observed epidemiologic associations are causal.
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