This n=1 trial points out two further factors to make a larger trial better able to more accurately determine causality between human clinical health indicators and BPA and other plastic-derived chemicals.
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The reasons for those flaws are multiple and include:
Markers for ultra-processed food additives
The first factor would be to determine a blood marker associated with one or more of the most common additives found in ultra-processed foods.
The second would be to include hsCRP along with other indicators in an expanded diagnostic blood panel.
Expanded blood profiling
Because high inflammation is associated with many metabolic health problems, this expanded blood panel would include additional indicators such as ghrelin, adiponectin, and insulin resistance.
Because hsCRP is non-specific to the sources of inflammation, further accuracy in human causality determinations may also be enhanced by the employment of select cytokines and chemokines to determine direct BPA influences on inflammation sources such as immune system disorders and tumorigenesis.
Moving BPA causality forward will probably require another proof-of-concept investigation: Controlled dosing
If the above alternatives are not satisfactory — or are likely to prove inadequate in determining human health effects specifically as relates to BPA — a third method would be to conduct a dietary intervention with exactly the same menu in the typical diet and BPA dosing in the intervention diet.
All ingredients would be pre-tested for BPA levels at the sourcing stage and alternatives selected if levels are determined to be above an acceptable threshold.
Subsequent BPA levels would be established after meal preparation and a total daily BPA dosage calculated.
Then, prepared (and tested) meals would be divided into two segments: one for the meals as prepared and a second — intervention menu –to be dosed with BPA at the federally acceptable “safe” level.
This regime would isolate BPA as the only contributor to the inflammation and other clinically relevant manifestations.
With a sufficient number of markers measured — similar or identical to those in the NIH/Hall study — it may be possible to develop a profile of markers that is specific to BPA.
This study protocol would be — by far — the most expensive alternative. That means that a proof-of-concept investigation will probably be wise to determine any further confounding factors.