I think this research is significant for a couple of reasons. As with our previous work, this study actually measures the levels of persistent toxicants in the body so that specific chemicals that may contribute are identified. This is particularly important so that follow-up studies in the laboratory can be performed to determine whether or not specific chemicals may be part of an established or novel pathogenic pathway. Secondly, it highlights the need to also consider genetic susceptibility. Although the odds ratios established are not what one would consider consistent with causality, it does provide information that may shed light on genetic pathways that may work in concert with exposures to increase risk of ALS. On the other hand, some of the chemicals identified may really only be a measure of exposure rather than being the specific chemicals that may contribute to the etiology of ALS.
There are a couple of weaknesses that we also dealt with. As with our study, Su and colleagues could only reliably measure "legacy" chemicals, such as the persistent organic pollutants. Because of this, we are still limited with self-reports on current use pesticides that may also contribute to ALS susceptibility. Secondly, some of the blood concentrations are a bit surprising and appear to be present in greater frequency than in the general population, as reported by the CDC’s National Health and Nutrition Examination Survey. This may indicate that there was something a bit unusual about this population.
Overall, I found this to be a very strong preliminary study that should be seen as a call for additional epidemiological and laboratory studies to identify mechanisms by which these chemicals and others may contribute to ALS risk. Finally, it further reinforces the need to include environmental factors into the thought process about complex disease, even in those that are thought to be heavily influenced by genetics.
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Northeast Ohio Medical University
I think this research is significant for a couple of reasons. As with our previous work, this study actually measures the levels of persistent toxicants in the body so that specific chemicals that may contribute are identified. This is particularly important so that follow-up studies in the laboratory can be performed to determine whether or not specific chemicals may be part of an established or novel pathogenic pathway. Secondly, it highlights the need to also consider genetic susceptibility. Although the odds ratios established are not what one would consider consistent with causality, it does provide information that may shed light on genetic pathways that may work in concert with exposures to increase risk of ALS. On the other hand, some of the chemicals identified may really only be a measure of exposure rather than being the specific chemicals that may contribute to the etiology of ALS.
There are a couple of weaknesses that we also dealt with. As with our study, Su and colleagues could only reliably measure "legacy" chemicals, such as the persistent organic pollutants. Because of this, we are still limited with self-reports on current use pesticides that may also contribute to ALS susceptibility. Secondly, some of the blood concentrations are a bit surprising and appear to be present in greater frequency than in the general population, as reported by the CDC’s National Health and Nutrition Examination Survey. This may indicate that there was something a bit unusual about this population.
Overall, I found this to be a very strong preliminary study that should be seen as a call for additional epidemiological and laboratory studies to identify mechanisms by which these chemicals and others may contribute to ALS risk. Finally, it further reinforces the need to include environmental factors into the thought process about complex disease, even in those that are thought to be heavily influenced by genetics.
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