Interest has been growing in the fields of toxicology and pharmacology (National Research Council 2009; Rooney et al. 2014; Sena et al. 2007; Woodruff and Sutton 2011) in extending systematic review methods beyond the traditional area of human clinical trials to consider other evidence streams (observational human, experimental animal, and in vitro studies).
Compared with clinical trials, the acquisition of raw data for chemicals and pesticides would be much more complex, in part because it would require a framework that can accommodate data from numerous types of studies: observational and experimental, animal, human, in vitro, and high throughput screening studies.
Although there is a reasonable harmonization of approaches used to assess internal validity (risk of bias) for human clinical trials (Higgins and Green 2011), there is not currently a similar consensus on how to assess that the findings and conclusions drawn from observational human, experimental animal, and in vitro studies are a true reflection of the outcome of the study.
Here we explain the framework developed by OHAT that uses procedures to integrate multiple evidence streams including observational human study findings, experimental animal toxicology results, and other relevant data in developing hazard identification conclusions or state-of-the-science evaluations regarding health effects from exposure to environmental substances.
According to experimental animal studies and some observational epidemiological studies in humans, higher selenium intakes might reduce the risk of certain types of cancer [ 9, 10].
Questions in environmental health require the evaluation of a broader range of relevant data including experimental animal and mechanistic studies as well as observational human studies.
Unable to do the definitive experiment they have had to rely on an accumulation of observational studies, animal experiments, and studies of the physiological mechanisms most likely involved.
In descriptive observational small-animal or equine research, use of secondary data is very common.
Although direct evidence establishing a causal relationship between epigenetic modification and risk for T2D is not yet available, observational and animal studies have suggested that epigenetic alterations in gene expression may play a role.
On the basis of human observational and animal experimental data, as well as mechanistic plausibility, the 2003 report from the joint World Health Organization/Food and Agriculture Organization Expert Consultation (WHO/FAO) concluded that salt-preserved food and salt 'probably' increase the risk of gastric cancer (WHO/FAO, 2003).
