Dekosky ST, Gandy S.
Environmental exposures and the risk for Alzheimer disease: can we identify the smoking guns?.
JAMA Neurol. 2014 Mar;71(3):273-5.
PubMed.
Q: What does this study tell us about DDT exposure and AD risk?
A: This is an interesting study that adds to the growing body of evidence suggesting that exposure to pesticides (and specifically DDT) may increase the risk for Alzheimer’s disease. Much of the prior epidemiological work linking pesticides to AD has not addressed two important issues that are covered in this paper: 1) a biological measure of exposure, in this case DDE levels, which are a byproduct of DDT exposure, and 2) a possible mechanistic link between pesticide exposure and AD. Of course these findings will need to be confirmed by other studies, but the findings are important.
Q: How serious a risk factor is it?
A: It is still too early to tell. For now, this is not something the general public needs to worry about. The findings will need to be replicated and if they are replicated, we still need to determine the level of exposure that is related to increased risk of AD.
Q: Should these findings influence public policy?
A: If that includes additional funding for the study of the effects of pesticides on human health, then yes. We still know very little about the long-term cognitive effects of occupational exposures to pesticides and long-term low-level exposure to pesticides.
Q: What are the limitations of this study?
A: This is just one small case-control study, so the findings need to be considered preliminary. The authors were unable to study the effects of other pesticides such as organophosphates, which also have been associated with increased risk in epidemiological studies. No information about exposure events is provided, so we do not know anything about the intensity and duration of exposures and how that affects DDE levels. Finally, they were unable to look at gene-environment interactions in this study. It would be interesting to see if there is a differential effect by APOE e4 status.
Q: What further research would be needed to nail this association down?
A: This study will need to be replicated in other, larger samples. The association should be evaluated in cohorts that have documented pesticide exposures and long term follow-up. We would also need to confirm whether documented exposures are associated with serum levels of DDE in later life.
Q: How does this data fit with other studies of pesticides and neurodegenerative disease?
A: This study appears to be in line with prior findings and it adds to a growing body of knowledge on the subject.
Comments
Wake Forest School of Medicine
(Questions by Madolyn Bowman Rogers)
Q: What does this study tell us about DDT exposure and AD risk?
A: This is an interesting study that adds to the growing body of evidence suggesting that exposure to pesticides (and specifically DDT) may increase the risk for Alzheimer’s disease. Much of the prior epidemiological work linking pesticides to AD has not addressed two important issues that are covered in this paper: 1) a biological measure of exposure, in this case DDE levels, which are a byproduct of DDT exposure, and 2) a possible mechanistic link between pesticide exposure and AD. Of course these findings will need to be confirmed by other studies, but the findings are important.
Q: How serious a risk factor is it?
A: It is still too early to tell. For now, this is not something the general public needs to worry about. The findings will need to be replicated and if they are replicated, we still need to determine the level of exposure that is related to increased risk of AD.
Q: Should these findings influence public policy?
A: If that includes additional funding for the study of the effects of pesticides on human health, then yes. We still know very little about the long-term cognitive effects of occupational exposures to pesticides and long-term low-level exposure to pesticides.
Q: What are the limitations of this study?
A: This is just one small case-control study, so the findings need to be considered preliminary. The authors were unable to study the effects of other pesticides such as organophosphates, which also have been associated with increased risk in epidemiological studies. No information about exposure events is provided, so we do not know anything about the intensity and duration of exposures and how that affects DDE levels. Finally, they were unable to look at gene-environment interactions in this study. It would be interesting to see if there is a differential effect by APOE e4 status.
Q: What further research would be needed to nail this association down?
A: This study will need to be replicated in other, larger samples. The association should be evaluated in cohorts that have documented pesticide exposures and long term follow-up. We would also need to confirm whether documented exposures are associated with serum levels of DDE in later life.
Q: How does this data fit with other studies of pesticides and neurodegenerative disease?
View all comments by Kathleen HaydenA: This study appears to be in line with prior findings and it adds to a growing body of knowledge on the subject.
Make a Comment
To make a comment you must login or register.