Critique of a professional journal article on field safety research standards

Safety

The etiology of the majority of cases of Parkinson's disease (PD) is unknown. What is known is that the disease is a neurodegenerative disorder that results from a loss of dopaminergic neurons in the area of the brain known as the substantia nigra (Hatfield, 2013). In addition, it is speculated that the disease is related to some type of genetic susceptibility and environmental risk factors that largely remain unidentified. Epidemiological research has suggested that there may be an association between exposure to pesticides and the onset of PD; however, this research is very mixed with some studies indicating that there is such relationship and a number of others failing to demonstrate such an association (Dardiotis, Xiromerisiou, Hadjichristodoulou et al., 2013). Dardiotis et al. (2013) reviewed the research and made a case that perhaps the relationship between pesticide use and PD is moderated by a genetic susceptibility. However, one of the flaws in most of the studies that attempt to link pesticide exposure and PD is that a history of pesticide exposure is often determined by the self-report of the individuals with PD. Individuals who have developed PD may selectively recall being exposed to or using pesticides at sometime in their lives as a result of literature popularizing the view that pesticides may cause PD or may overestimate their exposure due to this perceived cause and effect notion (Dardiotis et al., 2013; Hatfield, 2013; Liew, Wang, Bronstein, & Ritz, 2014). Liew et al. (2014) attempted to avoid the aforementioned issues in the research by using a large population -- based case-control study that employed a Job Exposure Matrix (JEM) to individuals with idiopathic PD and matched controls.

The researchers conducted their study in an agricultural region of California's Central Valley, a highly agricultural area. Participants with PD were recruited via the use of medical groups (neurologists and other medical personal) and public service announcements; control participants were recruited via a randomized selection method. Stringent exclusion criteria were applied to individuals who were listed as having PD. Nearly 1200 such patients responded to the recruitment procedures; however, only 357 were retained. Controls were selected via two sampling strategies in order to achieve a matched control group (N = 750).

During the data collection phase the trained interviewers were blind to case/control status of the participant and conducted structured telephone interviews to develop the JEM. Job tasks were assigned different likelihoods of pesticide exposure and the results were compared to previous research regarding the weighting procedure in order to ensure that the current data was not being too sensitive regarding pesticide exposure likelihood. Results indicated that there was a 55% increase in the risk of developing PD with high pesticide exposure, 28% increase with a medium exposure, and no association with low exposure. In addition the findings were more telling for men than women; however, this finding is somewhat tainted by the small number of female cases in the highly exposed condition. The results indicated that at least for men direct exposure to pesticides (applying, spraying, and mixing of pesticides) did demonstrate an increased risk for the development of idiopathic PD.

Strengths of the study include the stringent exclusion criteria regarding the diagnosis of idiopathic PD, the use of an objective measurement regarding the exposure to pesticides (JEM), the ability of the study to account for ambient pesticide exposure and individuals that work on farms or live near them, and attempts to incorporate estimated effects from self-reported exposure to other types of chemical solvents, paints strippers, work with metals, etc. However, the study has a few flaws.

First, the study did not take into account the use of any personal protective equipment that could modify the results. Secondly, there is a long latency in the onset of Parkinson's disease and the onset of environmentally-based events like exposures. There may be some other variables involved that interact with exposure to make some individuals more likely to develop neurodegenerative disorders (e.g., genetic makeup, other types of high risk activities, etc.). Third, the study is unable to determine any specific increase in the risk of developing PD that may be involved with specific types of pesticides. There may be a specific type of pesticide, or a specific type of chemical interaction, that accounts for the increase in the risk associated in this study. Fourth, the study is of limited generalizability due to using only individuals in California. There may be something about California that interacts with the risk to develop PD. Fifth, there may be some type of bias associated with the stringent exclusion criteria and sampling method used in this study and certainly replication with different sampling methods, study participants, etc. would go a long way in being able to generalize the results. Sixth, the findings were not as robust for women; however, this may be due to the disproportionate number of women who actually work in high exposure situations. So while the study can claim that there is increased risk in developing PD for men who were exposed directly to pesticides, the findings regarding the risk concerning women cannot be determined at this time. Finally, due to the correlational method used in this study the results cannot be interpreted in terms of cause-and-effect.