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Consumption of organic meat does not diminish the carcinogenic potential associated with the intake of persistent organic pollutants (POPs) [Study from 2015]

#1 · January 22, 2024, 9:30 pm

Quote from David on January 22, 2024, 9:30 pm
This 2015 study even shows that some organic lamb might be worse than conventional lamb. The 2015 study is called:
"Consumption of organic meat does not diminish the carcinogenic potential associated with the intake of persistent organic pollutants (POPs)"
https://link.springer.com/article/10.1007/s11356-015-4477-8

Here is a quote about their study design and I expanded their abbrevations within brackets:
"This study was designed to test this hypothesis, where the concentrations of 7 PAHs [polycyclic aromatic hydrocarbons], 18 PCBs [polychlorinated biphenyls], and 8 OCPs [organochlorine pesticides] for which the CSFs [cancer slope factors] have been calculated were determined in samples of meats (chicken, beef, and lamb) from organic and conventional production. The samples were acquired in large suppliers who serve the entire European territory. The main objective of this study was to use these data to estimate the carcinogenic risk associated with the current level of meat consumption by the European population considering two possible scenarios: consumers that choose organic meats and consumers that choose conventional meats. The methodology that has been recently used to estimate the carcinogenic risk in other food groups, such as fish (Yu et al. 2014), was applied, using the data of food consumption of the Spanish population."

Here are two great quotes from the Results and Discussion part of the study:

The first quote is about how they are probably the first study to measure POPs in organic meat and comparing it to conventional meat:
"The main objective of this paper is to provide an estimate of the level of exposure to carcinogenic POPs through consumption of beef, chicken, or lamb, depending on their mode of production (conventional production or organic production). While the levels of many of these substances have been identified in previous studies carried out in different parts of the world, all these works have been performed in conventionally produced meat. As far as we know, no work has been done specifically on organic meats. Also, as one might expect, the levels of carcinogenic POPs in meats published to date are highly variable (sometimes very significantly) (Costabeber et al. 2006; Letta and Attah 2013; Malisch and Kotz 2014; Pardio et al. 2012; Polder et al. 2010; Schecter et al. 2010; Tornkvist et al. 2011; Wang et al. 2011), which is logical because it is very common to find regional variations in contaminant levels. Since the objective of this paper is not to compare our results with previous works but to make a comparison of exposure depending on the product chosen by consumers, to make a realistic estimate, we preferred to directly quantify the contaminants in a representative sample of the main types of meat that any European consumer can find in supermarkets of the continent, and directly determine over them carcinogenic contaminant levels."

The second quote is about how there generally seems to be minimal difference between organic and conventional beef regarding concentrations of POPs:
"Two facts attracted attention of our results. First, the fact that pollution levels are quite different between distinct types of meats. Thus, lamb is by far the one with the highest levels of all pollutants studied. At the other extreme, we find the chicken (skinless) having the lowest levels in all cases. The beef meat shows intermediate values (Table 1). These differences are probably attributable to the very different percentages of fat of each type of meat, because when we compare the data expressed as nanograms of carcinogen per gram of fat rather than per gram of fresh product, the differences are much smaller (data not shown).Second, it is interesting to note that the differences between the two modes of production, organic and conventional, can be considered minimal, generally speaking. Table 1 shows the values of statistical significance found for each of the pollutants and meats. As seen above, the highest differences were found between organic and conventional beef. However, contrary to what one might think, not in all cases the values were lower in meat from organic production. Thus, as it can be observed in Table 1, in the case of hexachlorobenzene (HCB), levels found in samples of organic beef and organic chicken were significantly higher than those found in the same meats from conventional production."

Last but not least, remember that most retinoids and carotenoids are fat-soluble as well. See the last part of the second quote about how fat-soluble POPs mainly accumulate in the fat so higher fat foods generally have higher POPs and other fat-soluble substances.

Attaching Figure 1 and Table 1 from the 2015 study in this post. The Figure 1 text is this:

"Fig. 1 Box plots of the levels of ∑OCPs (a), ∑PCBs (b), and ∑c-PAHs (c) in the three types of meat studied, and comparison between the two modes of production of these meats (conventional vs. organic). The line inside the boxes represents the median, the bottom and top of the boxes are the first and third quartiles of the distribution, and the lines extending vertically from the boxes indicate the variability outside the upper and lower quartiles"

This 2015 study even shows that some organic lamb might be worse than conventional lamb. The 2015 study is called:
"Consumption of organic meat does not diminish the carcinogenic potential associated with the intake of persistent organic pollutants (POPs)"
https://link.springer.com/article/10.1007/s11356-015-4477-8

Here is a quote about their study design and I expanded their abbrevations within brackets:
"This study was designed to test this hypothesis, where the concentrations of 7 PAHs [polycyclic aromatic hydrocarbons], 18 PCBs [polychlorinated biphenyls], and 8 OCPs [organochlorine pesticides] for which the CSFs [cancer slope factors] have been calculated were determined in samples of meats (chicken, beef, and lamb) from organic and conventional production. The samples were acquired in large suppliers who serve the entire European territory. The main objective of this study was to use these data to estimate the carcinogenic risk associated with the current level of meat consumption by the European population considering two possible scenarios: consumers that choose organic meats and consumers that choose conventional meats. The methodology that has been recently used to estimate the carcinogenic risk in other food groups, such as fish (Yu et al. 2014), was applied, using the data of food consumption of the Spanish population."

Here are two great quotes from the Results and Discussion part of the study:

The first quote is about how they are probably the first study to measure POPs in organic meat and comparing it to conventional meat:
"The main objective of this paper is to provide an estimate of the level of exposure to carcinogenic POPs through consumption of beef, chicken, or lamb, depending on their mode of production (conventional production or organic production). While the levels of many of these substances have been identified in previous studies carried out in different parts of the world, all these works have been performed in conventionally produced meat. As far as we know, no work has been done specifically on organic meats. Also, as one might expect, the levels of carcinogenic POPs in meats published to date are highly variable (sometimes very significantly) (Costabeber et al. 2006; Letta and Attah 2013; Malisch and Kotz 2014; Pardio et al. 2012; Polder et al. 2010; Schecter et al. 2010; Tornkvist et al. 2011; Wang et al. 2011), which is logical because it is very common to find regional variations in contaminant levels. Since the objective of this paper is not to compare our results with previous works but to make a comparison of exposure depending on the product chosen by consumers, to make a realistic estimate, we preferred to directly quantify the contaminants in a representative sample of the main types of meat that any European consumer can find in supermarkets of the continent, and directly determine over them carcinogenic contaminant levels."

The second quote is about how there generally seems to be minimal difference between organic and conventional beef regarding concentrations of POPs:
"Two facts attracted attention of our results. First, the fact that pollution levels are quite different between distinct types of meats. Thus, lamb is by far the one with the highest levels of all pollutants studied. At the other extreme, we find the chicken (skinless) having the lowest levels in all cases. The beef meat shows intermediate values (Table 1). These differences are probably attributable to the very different percentages of fat of each type of meat, because when we compare the data expressed as nanograms of carcinogen per gram of fat rather than per gram of fresh product, the differences are much smaller (data not shown).Second, it is interesting to note that the differences between the two modes of production, organic and conventional, can be considered minimal, generally speaking. Table 1 shows the values of statistical significance found for each of the pollutants and meats. As seen above, the highest differences were found between organic and conventional beef. However, contrary to what one might think, not in all cases the values were lower in meat from organic production. Thus, as it can be observed in Table 1, in the case of hexachlorobenzene (HCB), levels found in samples of organic beef and organic chicken were significantly higher than those found in the same meats from conventional production."

Last but not least, remember that most retinoids and carotenoids are fat-soluble as well. See the last part of the second quote about how fat-soluble POPs mainly accumulate in the fat so higher fat foods generally have higher POPs and other fat-soluble substances.

Attaching Figure 1 and Table 1 from the 2015 study in this post. The Figure 1 text is this:

"Fig. 1 Box plots of the levels of ∑OCPs (a), ∑PCBs (b), and ∑c-PAHs (c) in the three types of meat studied, and comparison between the two modes of production of these meats (conventional vs. organic). The line inside the boxes represents the median, the bottom and top of the boxes are the first and third quartiles of the distribution, and the lines extending vertically from the boxes indicate the variability outside the upper and lower quartiles"

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#2 · January 23, 2024, 1:38 am

This is very interesting.

It makes me think, maybe it is the pollutants in the fat, that makes the "bad" fats bad... not so that they are saturated. I have been thinking a lot about that thing. Because Karen Hurd says saturated fats are very bad for us, and she explains why, but as I come from a carnivorous diet I always thought the opposite. As I try to be always open and learning, I try to understand, what is really true.

I do know for sure, toxins are stored in fat tissue.

I always thought lamb would be the most healthiest meat to eat as they are outside eating grass most of the time... oh yeah.. I ate almost only ground lambs meat for many years. Another puzzle to the piece why my liver/gallbladder got toxic.

(and I thought chicken breast would be the most unhealthy meat to eat, ignoring the fact that many people seem to do well on it...)

What a crazy world. But this helps my understanding of how my own issues developed.

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#3 · January 23, 2024, 4:27 am

This makes me want to not eat any much animal fat anymore, and I just bought some 17% fat organic ground beef. I put it in my freezer. My liver really dont need any more toxins right now. I am going to go and buy me some fat free meat cuts instead, non organic. Because that i can afford. Organic beef cuts without fat are so expensive here.

This makes me think, if that is one thing why carnivores react so badly to plant food/fiber, because the toxins from animal fat gets stuck in the liver, and then when eating fiber it gets released and causes such bad symptoms.

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#4 · January 23, 2024, 5:01 am

AGES (Advanced glycation end products) which are formed when frying beef are much more of a concern than what's inside the fat of organic ground beef. If I try to eat panned fried beef/ steak I get liver pain and inflammation where as eating a fatty organic beef patty that has been pressure cooked or boiled I don't get this.

#5 · January 23, 2024, 5:50 am

sad.

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#6 · January 24, 2024, 9:41 pm

Quote from David on January 24, 2024, 9:41 pm
@alexm

Why the RAGE over AGEs? 🙂

Persistent Organic Pollutants (POPs) are known to create Type 2 diabetes, and high blood sugar problems promotes endogenous creation of Advanced Glycation End-products (AGEs) that affect the Receptor for AGEs (RAGE). As an example see this study I found when searching "persistent organic pollutants advanced glycation end-products pubmed". Attaching Figures 1 which shows a serious decline (>50%) in collagen in the mice hearts.

A 2021 mice study called:
Persistent organic pollutants (POPs) increase rage signaling to promote downstream cardiovascular remodeling
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6771979/

"RAGE [Receptor for AGE] expression was significantly increased in WT‐POPs, ob/ob, and ob/ob‐POPs treated hearts as compared to WT hearts, Figure Figure2.2. These findings correlated with previous studies in which RAGE expression was reported to be significantly elevated in tissues of the of diabetic ob/ob mice.31 These observations are the first of its kind to implicate organic pollutants as potential promoters of RAGE protein expression. Finding significantly elevated RAGE levels in WT‐POPs hearts suggests a possible role for POPs in activating the AGE‐RAGE signaling cascade independent of hyperglycemia. Further studies will need to be conducted to determine the potential mechanisms responsible for increased RAGE expression in POPs treated animals in order to understand the maladaptive responses resulting from POPs‐mediated increased AGE‐RAGE signaling."

"From previous studies, increased POPs exposure exacerbated hepatic steatosis and adipocyte dysfunction resulting in elevated production of proinflammatory and oxidative stressors.24 These changes in the inflammatory profile have been demonstrated to exacerbate type 2 diabetes mellitus (T2DM); however, the mechanism regulating this process is unknown.10Therefore, our present study aimed to determine if POPs exposure would act as a causative agent to promote metabolic syndrome outcomes in the heart independent of dietary intake. We hypothesized that activation of the AGE‐RAGE signaling cascade by POPs exposure would stimulate downstream signaling modulators to promote cardiovascular remodeling. Given the critical role of the AGE‐RAGE axis in the pathogenesis of T2DM and cardiac remodeling, these findings demonstrate that exposure to POPs increased cardiometabolic risk and cardiac remodeling. Thus, our current data represent a plausible mechanism through which POPs exposure may promote alterations in left ventricular geometry and function as demonstrated in recent epidemiological studies in the elderly.11, 12 It should be noted that while the mean serum levels of some of the POPs, such as the organochlorine pesticide metabolites and some of the PCBs, are declining in U.S. population, mean serum levels of POPs increase with age due to their lipophilicity and thus may have a greater effect in the elderly as opposed to early or middle age.33"

PS. Grant Genereux has written a ton on diabetes in relation to vitamin A also, with high blood sugar relating to AGEs.

@alexm

Why the RAGE over AGEs? 🙂

Persistent Organic Pollutants (POPs) are known to create Type 2 diabetes, and high blood sugar problems promotes endogenous creation of Advanced Glycation End-products (AGEs) that affect the Receptor for AGEs (RAGE). As an example see this study I found when searching "persistent organic pollutants advanced glycation end-products pubmed". Attaching Figures 1 which shows a serious decline (>50%) in collagen in the mice hearts.

A 2021 mice study called:
Persistent organic pollutants (POPs) increase rage signaling to promote downstream cardiovascular remodeling
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6771979/

"RAGE [Receptor for AGE] expression was significantly increased in WT‐POPs, ob/ob, and ob/ob‐POPs treated hearts as compared to WT hearts, Figure Figure2.2. These findings correlated with previous studies in which RAGE expression was reported to be significantly elevated in tissues of the of diabetic ob/ob mice.31 These observations are the first of its kind to implicate organic pollutants as potential promoters of RAGE protein expression. Finding significantly elevated RAGE levels in WT‐POPs hearts suggests a possible role for POPs in activating the AGE‐RAGE signaling cascade independent of hyperglycemia. Further studies will need to be conducted to determine the potential mechanisms responsible for increased RAGE expression in POPs treated animals in order to understand the maladaptive responses resulting from POPs‐mediated increased AGE‐RAGE signaling."

"From previous studies, increased POPs exposure exacerbated hepatic steatosis and adipocyte dysfunction resulting in elevated production of proinflammatory and oxidative stressors.24 These changes in the inflammatory profile have been demonstrated to exacerbate type 2 diabetes mellitus (T2DM); however, the mechanism regulating this process is unknown.10Therefore, our present study aimed to determine if POPs exposure would act as a causative agent to promote metabolic syndrome outcomes in the heart independent of dietary intake. We hypothesized that activation of the AGE‐RAGE signaling cascade by POPs exposure would stimulate downstream signaling modulators to promote cardiovascular remodeling. Given the critical role of the AGE‐RAGE axis in the pathogenesis of T2DM and cardiac remodeling, these findings demonstrate that exposure to POPs increased cardiometabolic risk and cardiac remodeling. Thus, our current data represent a plausible mechanism through which POPs exposure may promote alterations in left ventricular geometry and function as demonstrated in recent epidemiological studies in the elderly.11, 12 It should be noted that while the mean serum levels of some of the POPs, such as the organochlorine pesticide metabolites and some of the PCBs, are declining in U.S. population, mean serum levels of POPs increase with age due to their lipophilicity and thus may have a greater effect in the elderly as opposed to early or middle age.33"

PS. Grant Genereux has written a ton on diabetes in relation to vitamin A also, with high blood sugar relating to AGEs.

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#7 · January 25, 2024, 3:22 am

I wonder what the amount of POPs in vegetable food is versus animal foods.

Also what would the amount of POPs be in oysters? I used to eat loads of oysters living at the west coast in Germany, the Atlantic coast was full of them. In the end I had to stop eating them because I got really bad heart palps when doing so. I always wonder why that was.

Oysters are filtering the water, that I do know.

I also had zero soluble fiber in my diet and very little veggies, I ate mostly carnivore then. I really wonder if I loaded my body badly with POPs doing what I did. 🙁

I also ate lots of animal fats, and lots of fatty lamb. After doing this a couple years that is when my gallbladder started acting up too.

My bile must have been so toxic.

That was the time I was following Jack Kruse a lot, and he said oysters were the super food, so I felt I was in Nirvana being able to eat them like 100 every week for free. He eats lots of oysters and animal fat too, and I do have to say I think he looks a bit now like he has some toxic load too.

I am finishing up my organic ground beef that I bought, but I eat it together with beans and no other fat source, to make sure the soluble fiber in the beans soak up all the POPs. Maybe that is why beans seem to help longevity, the soluble fiber will prevent POPs to accumulate. And slowly take out excess amounts with the bile. I wish!

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#8 · January 25, 2024, 12:39 pm

This study says indoor air and dust could be a main exposure route for PCBs: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2267460/

I guess this would only apply to older homes?

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#9 · January 31, 2024, 2:34 am

Quote from David on January 31, 2024, 2:34 am
@inger

Luckily fat floats on water due to its lower density so it is possible to make a nice lamb stew by either washing off cooking water or skimming the fat of the top of the water. Fat-soluble toxins mainly accumulate in fat, because they are fat-soluble.

Regarding different types of fat I share your belief that it is mainly the toxins in the fat makes some fats worse than others, mainly due to bioaccumulation. Still fat-soluble toxins will almost always have a higher concentration in the fat part compared to any other part, though there are different problems in all types of foods. Rice accumulates arsenic from the water it is grown in and sun flowers easily absorb lead from the ground and put in their seeds. Living in a toxic world seems generally like a trade-off between different toxic stuff, though fat-soluble toxins and different heavy metals are probably the worst offenders when it comes to accumulation and long-term toxicity.

Attaching a figure that I found in a search some time ago. It generalize that fat-soluble toxins biomagnify by about 10x for each step up in the food chain, though it is not uniformly accumulated in the body, there should be more accumulated in the fat tissue but we can use it for a low approximation. I think combining this approximation with the fact that fat contains more calories per gram (~9 kcal /g) compared to protein and carbohydrates which are similar (~4 kcal /g). I think this can give us a rough low estimation of how much more fat-soluble toxins there are in fat compare to carbohydrates/protein per kcal.

Approximate scaling factor fat-soluble toxins in animal fat in relation to kcal:

~10x more fat-soluble toxins

~2.25 more kcal /g (~9 kcal /g compared to ~4 kcal /g for protein and carbohydrates)

Combined: ~10/~2.25 = 4.444 more fat-soluble toxins per kcal

PS. A thought regarding fiber; tissue paper, which is a type of fiber, is very useful when removing fat from a frying pan. Fiber inside of us might function similarly?

@inger

Luckily fat floats on water due to its lower density so it is possible to make a nice lamb stew by either washing off cooking water or skimming the fat of the top of the water. Fat-soluble toxins mainly accumulate in fat, because they are fat-soluble.

Regarding different types of fat I share your belief that it is mainly the toxins in the fat makes some fats worse than others, mainly due to bioaccumulation. Still fat-soluble toxins will almost always have a higher concentration in the fat part compared to any other part, though there are different problems in all types of foods. Rice accumulates arsenic from the water it is grown in and sun flowers easily absorb lead from the ground and put in their seeds. Living in a toxic world seems generally like a trade-off between different toxic stuff, though fat-soluble toxins and different heavy metals are probably the worst offenders when it comes to accumulation and long-term toxicity.

Attaching a figure that I found in a search some time ago. It generalize that fat-soluble toxins biomagnify by about 10x for each step up in the food chain, though it is not uniformly accumulated in the body, there should be more accumulated in the fat tissue but we can use it for a low approximation. I think combining this approximation with the fact that fat contains more calories per gram (~9 kcal /g) compared to protein and carbohydrates which are similar (~4 kcal /g). I think this can give us a rough low estimation of how much more fat-soluble toxins there are in fat compare to carbohydrates/protein per kcal.

Approximate scaling factor fat-soluble toxins in animal fat in relation to kcal:

~10x more fat-soluble toxins
~2.25 more kcal /g (~9 kcal /g compared to ~4 kcal /g for protein and carbohydrates)
- Combined: ~10/~2.25 = 4.444 more fat-soluble toxins per kcal

PS. A thought regarding fiber; tissue paper, which is a type of fiber, is very useful when removing fat from a frying pan. Fiber inside of us might function similarly?

Uploaded files:

#10 · January 31, 2024, 3:22 am

Quote from David on January 31, 2024, 3:22 am
@inger

For oysters I found this 2013 study from Japan looking mainly on one type of Persistent Organic Pollutants (POPs), namely Poly Aromatic Hydrocarbons (PAHs), in oysters (bivalve mollusks). The 2013 study is called:

Polycyclic aromatic hydrocarbons in oysters and sediments from the Yatsushiro Sea, Japan: Comparison of potential risks among PAHs, dioxins and dioxin-like compounds in benthic organisms
https://doi.org/10.1016/j.ecoenv.2013.10.005 (available at sci-hub)

Attaching Table 1 from the study which is a table showing that the concentration of PAH can vary massively depending how close the oysters are living to highly polluted sediment in a Japanese bay. The use a lot of abbrevations for the different chemicals:
"Chemicals analyzed
Twenty PAHs, including the 16 EPA priority PAHs, were analyzed, which were 2-methylnaphthalene (2-MN), 1-methylnaphthalene (1-MN), 1,2-dimethyl-naphthalene (1,2-DMN), acenaphthylene (ANTHY), acenaphthene (ANTN), fluorene (FLU), phenanthrene (PHE), anthracene (AN), fluoranthene (FLR), pyrene (PY), chrysene (CHRY), benz[a]anthracene (BaA), benzo[b]fluoranthene (BbF), benzo[k] fluoranthene (BkF), benzo[e]pyrene (BeP), benzo[a]pyrene (BaP), perylene (PERY), indeno[1,2,3-cd]pyrene (IcdP), benzo[ghi]perylene (BghiP), and dibenz-[a,h]anthracene (DahA). Polychlorinated dibenzo-p-dioxins (2,3,7,8-T4CDD, 1,2,3,7,8-P5CDD, 1,2,3,4,7,8-H6CDD, 1,2,3,6,7,8-H6CDD, 1,2,3,7,8,9-H6CDD, 1,2,3,4,6,7,8-H7CDD, and OCDD), polychlorinated dibenzofurans (2,3,7,8-T4CDF, 1,2,3,7,8-P5CDF, 2,3,4,7,8-P5CDF, 1,2,3,4,7,8-H6CDF, 1,2,3,4,6,7,8-H6CDF, 1,2,3,7,8,9-H6CDF, 2,3,4,6,7,8-H6CDF, 1,2,3,4,6,7,8-H7CDF, 1,2,3,4,7,8,9-H7CDF, and OCDF), non-ortho substituted PCBs (PCBs 77, 81, 126, and 169) and mono-ortho substituted coplanar PCBs (PCBs 123, 118, 114, 105, 167, 156, 157, and 189) were analyzed in eight sediments collected in Tanoura Bay and two sediments from the reference site in the northern Yatsushiro Sea."

Using government guidelines ADI (Acceptable Daily Intake) they think the normal populations toxic exposure from oyster consumption seems below ADI but there are other fat-soluble toxins and if you used to consume a lot of oyster you would have to take that into account as well. Excerpt from the study:

"Risk assessment of the oysters as seafood
The EU Scientific Committee on Food assessed 33 PAHs and identified 15 PAHs that possess both carcinogenic and genotoxic properties (Wenzl et al., 2006). Maximum allowed concentrations (MACs) for BaP in various food products, such as oils, infant foods, meat, and seafood have been set in EU legislation. The MAC of BaP [benzo[a]pyrene] in bivalve mollusks is 10 ng/g wet weight, which is more than 10 times higher than the BaP concentrations in most of the samples we collected. However, BaP concentrations in oysters from station D-3 (9.5 ng/g wet weight) were comparable to the MAC. Dietary exposure to BaP in the Japanese population was calculated using the concentrations found in oysters from station D. The typical seafood consumption of the Japanese population is 82.2 g/day (Ministry of Agriculture, Japan), so the estimated dietary intake of BaP using our oyster concentrations ranged from 2.5 to 15.5 ng kg⁻¹ BW day⁻¹. The BaP NOAEL (no-observableadverse effect level) has been set at 0.21 mg kg⁻¹ day⁻¹ in Japan (Ministry of Environment, Japan-b), and, because the ‘unknown factor’ is usually set to 100, the acceptable daily intake (ADI) of BaP can be calculated as 2.1 μg kg⁻¹ day⁻¹. Using these values, the hazard ratio (H/Q) of BaP in oysters ranged from 1.2 × 10⁻³ to 8.0 × 10⁻³, more than three orders of magnitude lower than the ADI. These results suggest that, even though oysters from station D contained BaP concentrations close to the MAC, the risk to human health is likely to be small. However, there is a lack of information on PAH concentrations in other seafood, such as fish and crabs, in this area, so further investigations of the accumulation profiles of PAHs and human exposure risks are required in Tanoura Bay."

@inger

For oysters I found this 2013 study from Japan looking mainly on one type of Persistent Organic Pollutants (POPs), namely Poly Aromatic Hydrocarbons (PAHs), in oysters (bivalve mollusks). The 2013 study is called:

Polycyclic aromatic hydrocarbons in oysters and sediments from the Yatsushiro Sea, Japan: Comparison of potential risks among PAHs, dioxins and dioxin-like compounds in benthic organisms
https://doi.org/10.1016/j.ecoenv.2013.10.005 (available at sci-hub)

Attaching Table 1 from the study which is a table showing that the concentration of PAH can vary massively depending how close the oysters are living to highly polluted sediment in a Japanese bay. The use a lot of abbrevations for the different chemicals:
"Chemicals analyzed
Twenty PAHs, including the 16 EPA priority PAHs, were analyzed, which were 2-methylnaphthalene (2-MN), 1-methylnaphthalene (1-MN), 1,2-dimethyl-naphthalene (1,2-DMN), acenaphthylene (ANTHY), acenaphthene (ANTN), fluorene (FLU), phenanthrene (PHE), anthracene (AN), fluoranthene (FLR), pyrene (PY), chrysene (CHRY), benz[a]anthracene (BaA), benzo[b]fluoranthene (BbF), benzo[k] fluoranthene (BkF), benzo[e]pyrene (BeP), benzo[a]pyrene (BaP), perylene (PERY), indeno[1,2,3-cd]pyrene (IcdP), benzo[ghi]perylene (BghiP), and dibenz-[a,h]anthracene (DahA). Polychlorinated dibenzo-p-dioxins (2,3,7,8-T4CDD, 1,2,3,7,8-P5CDD, 1,2,3,4,7,8-H6CDD, 1,2,3,6,7,8-H6CDD, 1,2,3,7,8,9-H6CDD, 1,2,3,4,6,7,8-H7CDD, and OCDD), polychlorinated dibenzofurans (2,3,7,8-T4CDF, 1,2,3,7,8-P5CDF, 2,3,4,7,8-P5CDF, 1,2,3,4,7,8-H6CDF, 1,2,3,4,6,7,8-H6CDF, 1,2,3,7,8,9-H6CDF, 2,3,4,6,7,8-H6CDF, 1,2,3,4,6,7,8-H7CDF, 1,2,3,4,7,8,9-H7CDF, and OCDF), non-ortho substituted PCBs (PCBs 77, 81, 126, and 169) and mono-ortho substituted coplanar PCBs (PCBs 123, 118, 114, 105, 167, 156, 157, and 189) were analyzed in eight sediments collected in Tanoura Bay and two sediments from the reference site in the northern Yatsushiro Sea."

Using government guidelines ADI (Acceptable Daily Intake) they think the normal populations toxic exposure from oyster consumption seems below ADI but there are other fat-soluble toxins and if you used to consume a lot of oyster you would have to take that into account as well. Excerpt from the study:

"Risk assessment of the oysters as seafood
The EU Scientific Committee on Food assessed 33 PAHs and identified 15 PAHs that possess both carcinogenic and genotoxic properties (Wenzl et al., 2006). Maximum allowed concentrations (MACs) for BaP in various food products, such as oils, infant foods, meat, and seafood have been set in EU legislation. The MAC of BaP [benzo[a]pyrene] in bivalve mollusks is 10 ng/g wet weight, which is more than 10 times higher than the BaP concentrations in most of the samples we collected. However, BaP concentrations in oysters from station D-3 (9.5 ng/g wet weight) were comparable to the MAC. Dietary exposure to BaP in the Japanese population was calculated using the concentrations found in oysters from station D. The typical seafood consumption of the Japanese population is 82.2 g/day (Ministry of Agriculture, Japan), so the estimated dietary intake of BaP using our oyster concentrations ranged from 2.5 to 15.5 ng kg⁻¹ BW day⁻¹. The BaP NOAEL (no-observableadverse effect level) has been set at 0.21 mg kg⁻¹ day⁻¹ in Japan (Ministry of Environment, Japan-b), and, because the ‘unknown factor’ is usually set to 100, the acceptable daily intake (ADI) of BaP can be calculated as 2.1 μg kg⁻¹ day⁻¹. Using these values, the hazard ratio (H/Q) of BaP in oysters ranged from 1.2 × 10⁻³ to 8.0 × 10⁻³, more than three orders of magnitude lower than the ADI. These results suggest that, even though oysters from station D contained BaP concentrations close to the MAC, the risk to human health is likely to be small. However, there is a lack of information on PAH concentrations in other seafood, such as fish and crabs, in this area, so further investigations of the accumulation profiles of PAHs and human exposure risks are required in Tanoura Bay."

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