Is House Dust the Missing Exposure Pathway for PBDEs? Article Review Example

The main goal of this article was determining how 1-Bromopropane can be measured in urine using a commercially available method. The purpose of this analysis is to determine the amount of this chemical present in the blood of workers that are regularly exposed to spray adhesives. Ultimately, these ozone damaging chemicals may also have a detrimental effect on human health, so it is essential to determine the extent of exposure for each worker over a period of time. This will allow the Occupational Health and Safety administration in addition to other regulatory agencies to understand the relationship between 1-Bromopropane exposure and its pharmacodynamics and pharmacokinetics in the human body.

To conduct this experiment, workers at foam fabricating plants manufacturing polyurethane seat cushions were examined. 13 adhesive sprayers were selective to study as the experimental group in the experiment, while 17 non-sprayers were selected to study as the control group. It is expected that both groups would be exposed to the 1-Bromopropane to a degree due to their specific job functions, although it is anticipated that the spraying group would be exposed to the chemical to a greater extent. To determine the extent of exposure, breathing zone exposure samples were collected over two days at two facilities. Three urine samples were taken from each worker, which represented three different time points during the day in an attempt to determine the 1-Bromopropane levels that were present in their systems when they were at work, at home before bedtime, and just waking up for work. Ultimately, these measures would determine whether the levels of the 1-Bromopropane would be reduced based on the amount of time that had passed since the exposure and would determine how quickly the chemical would leave the body. At each stage, the urine was examined using plasma-mass spectrometry for Bromine detection. Gas chromatography was also performed to gain a greater understanding of the breathing zones.

It was found that the breathing zone concentrations were 92 parts per million for the adhesive sprayers and 11 parts per million for the other jobs. As predicted above, the individuals who directly work with the adhesive spray have a greater degree of exposure to 1-Bromopropane than those who do not. In addition, those who do not work directly with the adhesive spray are still exposed to the chemical because it is present within the facility. Therefore, it is clear that the 1-Bromopropane has a far reach to the other employees because it is in aerosol form. Ultimately, everyone who works in an aerosol adhesive spray facility is expected to have some degree of exposure. The results from the urine measurements according to the time of day following the exposure were not conclusive as the ranges of concentration were too high to be significant. However, this value was statistically significant considering the 48 hour Bromine concentration for all jobs combined. The authors conclude that this experiment is essential because it demonstrates that urinary elimination is an essential excretion pathway for 1-Bromopropane metabolism and that Bromine could serve as a potentially useful biomarker for chemical exposure.

While this is an interesting paper and a connection between 1-Bromine and detection in the urine is plausible, this particular experiment isn’t compelling enough to begin putting this idea into practice. One of the major flaws of the paper is that the sample size used was very small. Having approximately 15 individuals in the control group and 15 in the experimental group is a small experiment, one that would be typical of a Phase I trial. If the authors were indeed trying to determine whether a larger experiment would be reasonable by first using a small sample size, then this experiment was effective. However, if they were attempting a large scale proof-of-concept, they did not accomplish this.

A second weakness that was evident in this paper is that there was seemingly no connection between the amount of 1-Bromopropane exposure according to the relationship between the time of day and amount of chemical in the urine. The ranges presented in the results were large, which does not indicate a real shift in the removal of the 1-Bromopropane from the body. It is possible that this data would have appeared relevant if these numbers had been presented as an average or a median, but as these number are given, it is difficult to prove whether they are meaningful.

The information could be used to support an assessment of the risk associated with the chemicals studied provided that the experiment is repeated using a larger sample size. Furthermore, more in-depth toxicology and biochemical profiles must be taken. This experiment should be repeated in a manner that determines the physical health of individuals at the beginning of their exposure and continue for several months afterwards in order to gain a greater picture of what is occurring. An example of this would be to follow new employees at the plant and to reexamine their chemical levels and general health every two weeks in order to retrieve a longitudinal understanding of this relationship.

This article aims to summarize the relationship between polybrominated diphenyl ether (PBDE) concentrations in the air and human exposure. It has been determined that levels of this chemical are extremely high in a variety of individuals, but there has always been a degree of uncertainty as to how this exposure actually occurs. The authors completed their assessment of PBDE availability in the air by completing a MUM-fate test. This was used to determine chemical measures in the soil, vegetation, surface film, water, and sediment in Toronto, Canada. Since weather and precipitation could impact the availability of a chemical in the environment, a model was built that considers summer weather using an average rain rate. A major consideration in the fabrication of this model is that BDE-209 was excluded from the analysis because it did not agree with the consistency of the exposure assessment. Furthermore, the algorithm used did not account for the formation of lower brominated congeners.

Based on the produced model, the PBDE emissions that are expected based on the parameters are 100-422 g/day. It predicted that each individual living within Toronto would be impacted differently by these emissions based upon a variety of factors. Estimated daily intakes of PBDE were as little as 155 ng/day for adults and 1965 ng/day for breast-fed infants, which averages out to 2-80 ng per kg of body weight. Therefore, it can be concluded that breast-fed children are at higher risks of this exposure, because there is a high degree of chemical present in the milk in addition to the amount of PBDE that they are regularly exposed to.

A major strength of this model is that it utilized a variety of factors that are relevant to individuals living within Toronto to determine the amount of PBDE that they were exposed to. If the model is accurate, then breast-feeding mothers should be particularly wary of the implications of this phenomenon. While this particular study does not determine the benefits of breast-feeding if there is high PBDE exposure versus not breast-feeding on this bases, it does create the need more on this topic to be evaluated to determine what the proper medical recommendations should be for these cases.

An additional consideration that is of importance to this study is the fact that these results were found by utilizing a mathematical model. While mathematical models are excellent to serve as preliminary studies before experiments with interventions put in place can be performed, they do not perfectly mimic the events that occur in nature. Thus, although the authors ensured to account for many variables in this situation, it is difficult to be sure that this process will behave in this manner in the future. It is possible that this one of the reasons that the range of the daily PBDE exposure was so high.

In order to be sure of the PBDE exposures that residents of Toronto face, it would be ideal to repeat the study using real people. On a longitudinal scale, approximately 500 people could be followed to determine the extent of their exposure over time. To ensure that this study produces reliable results, each individual should begin trial at a particular age and end the trial at a particular age. The study participants living in Toronto should be compared to a community that is known to have lower levels of PBDE exposure. This would allow researchers to understand what is causing PBDE exposure, what the impacts of this exposure is for various age groups and other demographic classifications, and to determine how PBDE exposure could effectively be reduced.

The main utility of this paper was due to the fact that it draws the connection between levels of PBDE and age group exposure. It would have been difficult to test for this based on randomization, so this was a valuable connection. However, future studies should include the examination of individuals in order to determine the relationship that their extent of PBDE exposure has on health. Furthermore, PBDE exposure could be studied over time to determine trends in exposure increase or decrease as individual’s age or modify other aspects of their lifestyle. More computer models can be made throughout this process, which will be improved as a result. The culmination of this information can be used to gain a complete understanding of PBDE exposure in humans.

The article demonstrates that the ingestion of dust is a primary manner in which PBDE can be absorbed by humans. Therefore, an interesting additional thought question is whether individuals who live in cleaner areas will be exposed to less PBDE. A second essential question is whether areas could be cleaned to promote lower levels of dust and therefore have less PBDE. This concept could be as basic as cleaning one’s home to ensure that PBDE isn’t being breathed in to determining a mass solution for an entire geographic area.

References

Hanley KW et al. (2006). Urinary Bromide and Breathing Zone Concentrations of 1- Bromopropane from Workers Exposed to Flexible Foam Spray Adhesives. Ann. Occup. Hyg., (50)6: 509–607.

Jones-Otazo HA et al. (2005). Is House Dust the Missing Exposure Pathway for PBDEs? An Analysis of the Urban Fate and Human Exposure to PBDEs. Environ. Sci. Technol., 39:  5121-5130.